USMLE Step 1 Journal

 Warfarin/Coumadin Skin necrosis  patient already deficient in Protein C & S,

so when given warfarin, vitamin K dependent factors (VII, Protein C &S) cannot
function so  Thrombosis (hypercoagulable state occurs) within the skin.
Treatment  vitamin K and fresh frozen plasma

 Hepatitis C virus is genetically unstable because it lacks proofreading 3’—5’

exonuclease activity in the RNA polymerase. Its envelope glycoprotein contains a
hyper variable region prone to frequent genetic mutation.

 Hib Vaccine consists of PRP capsular polysaccharide conjugated with either

tetanus or diphtheria toxoid  protein conjugation causes T cell mediated
response leading to immunoglobulin class switching  generation of memory B-
lymphocytes. (This response will not occur if only a pure polysaccharide
immunization was given).

 Only Naked + single stranded RNA molecules are infectious acts directly as an
mRNA.
 Only +sense single RNA’s act like an mRNA. –ssDNA or –ssRNA do not.

 Mutations of Parkin, PINK1, DJ1

Autosomal recessive forms of Parkinson’s disease with an early stage of
onset <50 years old.
Parkin, PINK1, DJ1 is ubiquitin proteins.

 SnRNP ( Splicing) are synthesized by RNA polymerase II in the nucleus. They

help to remove introns from the RNA transcript and are thus necessary for
synthesis of mRNA.

 N-acetylglutamate is an essential activator of carbomyol phosphate synthetase 1

(Urea cycle) and is formed by the enzyme N-acetyglutamate synthase from the
precursor acetyl coA and glutamate.
o Without this enzymes there will be no disposal of Ammonia  lethargy,
vomiting, seizures early in life. Hyperammoniemia
o Hyperammonemia  advanced liver failure from cirrhosis  inability to
metabolize nitrogenous waste products. Can be triggered by large protein
meat/diet, GI bleeding
 Ammonia crosses BBB and causes excess glutamine to accumulate
in within astrocytes  decreases the amount of glutamine
available for conversion to glutamate in the neurons  disruption
of excitatory neurotransmission.
 Tremor, slurring of speech, somnolence, vomiting, cerebral edema,
blurring of vision
  N-acetylglutamate synthase deficiency  in neonates  poorly
regulated respiration & body temperature, poor feeding,
developmental delay, intellectual disability (identical to the
presentation of carbamoyl phosphate synthetase I deficiency).
 Rifaximin  decreases the colonic/intraluminal ammonia
production by intestinal bacteria.
 Lactulose  lowers colonic pH and increases the conversion of
ammonia to ammonium

 Tetrahydrobiopterin needed for tyrosine, dopamine, and norepinephrine, and

serotonin synthesis.

 HMP shunt  liver, adrenal cortex, gonads, adipose tissue, and erythrocytes.

 Methemoglobinemia, the partial pressure of O2 in blood is normal because

amount of dissolved O2 in the plasma will be the same and normal.

 Folate deficiency  inhibits formation of dTMP, which limits DNA synthesis and
Promotes megaloblastosis and erythroid apoptosis.
o Thymidine supplementation can moderately increase dTMP levels, which
decrease erythroid apoptosis.
 SMX (sulfonamides)  Dihydropteroate synthetase inhibitor
 Drugs that inhibit folate synthesis, Methotrexate, Trimethoprim,
pyrimethamine. Inhibit dihydrofolate reductase
 5-fluorouracil (5-FU), inhibits thymidylate synthase, also decrease
dTMP.
 Methotrexate  treated with severe RA, SE: stomatitis, bone
marrow suppression, and liver function abnormalities.

 Delta G= -RTInkeq,
 ^G (-) negative (pretty much doesn’t use energy, so goes down to make more
products)= favors products,
 ^G (+)positive (pretty much uses energy so the substrates are more favored so
less energy is used)= favors substrates
o ^G-, keq = >1 (concentration of products increased compared to
substrates).
o ^G+, keq = <1 (concentration of substrates increased compared to
products).

 Lysine + leucine  exclusively ketogenic, would not increase blood lactate levels
in patients suffering pyruvate dehydrogenase deficiency.

 Amino Acids with 3 Titrable acids  histadine, arginine, lysine, aspartic acid,
glutamic acid, cysteine, and tyrosine.
o Mnemonic  Hot Allergic Llamas Ameliorate Gorgeous Conditioned Toes
 PILE:
o Proteasomes degrade Intracellular proteins.
o Lysosomes degrade Extracellular proteins.

 Methylation of DNA  heterochromatin  low transcriptional activity, cytosine

& adenine are methylated in DNA allows mismatch repair enzymes to
distinguish between old and new strands in prokaryotes.
 Acetylation of histone  euchromatin  high transcriptional activity

 Transverse Spinal cord Sections:

o The more proximal thoracic/upper levels cervical have increasing
amount of white matter (a lot) with more ovoid sections.
o Lower cervical/lumbosacral levels have large ventral horns, innervate
muscles of arms and legs respectively.
o Thoracic & early lumber levels T1-L2, contain lateral grey matter horns
with larger white matter. Sympathetic preganglionic neurons.
o Sacral spinal level, gray matter occupies most of the transverse section
and white matter exists as a thing mantle at the periphery of the cord. No
lateral horns.
o Gracile and cuneate fasciculi are present above the T7 spinal level,
whereas only the gracile fasciculus is present below this level.
 RPGN: Prominent fibrin deposition.
 T-lymph, monocytes, and eosinophilic infiltration seen in AIN, Acute interstitial
nephritis secondary to antibiotics such as penicillin’s and cephalosporin’s 
fever, maculopapular rash, and symptoms of acute renal failure 1-3 weeks after
beginning treatment with ß-lactam antibiotics.
 Hyaline, acellular deposits composed of plasma proteins, Kimmelstiel-Wilson
nodules of Diabetic nephropathy.
 Lipid droplet (hyperlipidemia) in renal tubules in nephrotic syndrome.
 Electron-dense deposits on epithelial side of the glomerular basement
membrane (subepithelial humps, lumpy bumpy), seen in patients with PSGN,
nephritic syndrome with hematuria and hypertention.
o This deposit represents IgG, IgM, and C3.

 Vision problems
o Frontal eye fields lesions  eye deviates toward the lesion, loss of
conjugate gaze movement.
 Normally the right eye field generates conjugate gaze movement
to the left
 The left eye field generates conjugate gaze movement to the right
 o Lesions: (pupillary light reflex normal)  hemianopia’s must occur
before the lateral geniculate nucleus
 Lateral geniculate nucleus contralateral homonymous
hemianopia
 Dorsal Optic radiation (right parietal lobe MCA) inferior
quadrantonopia (pie on the floor)
 Meyers loop (temporal lobe MCA) contralateral upper
quadrantonopia (pie in the sky)
 Visual cortex (occipital lobe PCA)  contralateral homonymous
hemianopia with macular sparing
o Lesions (pupillary light reflex problems) 
 Retina, optic nerve, optic chiasm, optic tract  all this leads to
normal pupillary light reflex, anything after (lateral geniculate this
results in pupillary light reflex problems.
o The pupillary light flex assessed by shinning light in one eye and
observing both eyes.
 Optic nerve responsible for afferent limp of pupillary reflex
 Oculomotor nerve responsible for efferent limp of pupillary reflex.

 Amaurosis fugax  Painless, transient, mononuclear vision loss caused by

small embolus to the ophthalmic artery. It usually does not last more than a
few seconds.
 Central retinal artery occlusion  sudden, painless, permanent monocular
blindness. Funuscopic exam reveals a pale retina and cherry-red macula
usually a result from athero-thormboemoblis; this artery arises from internal
carotid artery  ophthalmic artery  retinal artery (supplies the inner
retina and surface of the optic nerve).

 Ears
o Scala vestibule and Scala tempani  Na+ fluid filled
o Scala media  K+ fluid filled
 Low frequency sounds  detected at the apex of the cochlea at the
helicotrema
 High frequency sounds  detected at the base of the cochlea near
oval & round window
 Prolonged exposure to loud noises causes hearing loss due to
damage to the stereociliated hair cells of the organ of corti.

 Case-control  past exposure  “what happened”

 Cross-sectional  particular point in time  “what is happening”
 Cohort  future problems  “What will happen”
 Crossover study  randomly allocated to a sequence of 2 or more treatments
given consecutively.
o A washout (no treatment) period is often added between treatment
intervals to limit the confounding effects of prior treatment.
 Mode is RESISTENT to OUTLIERS
 Mean is most sensitive to outliers

 Mannitol  Osmotic diuretic, decreases ICP by increasing urine flow by

increasing plasma or tubular fluid osmolality.
o SE: Pulmonary edema

 Imatinib  treats BCR-ABL

 MDR1 gene  Human multidrug resistance gene  P-glycoprotein that is a

transmembrane ATP-dependent efflux pump, for hydrophobic compounds.
o Can reduce the influx of drugs into the cytosol and can increase efflux
from cytosol, thereby preventing the action of chemotherapeutic agents.
o By this gene human cells develop resistance to chemotherapy drugs.
o Verapamil, diltiazem, and ketoconazole  shown to reduce action of this
gene in experimental models.

 Competitive antagonist = change ED50  shifts graph to the right, deceases

potency.
 Noncompetitive antagonist = change Vmax  shifts graph down, decrease
efficacy

 Antimuscarinic = Oxybutynin (M3 receptors)  treatment for urge incontinence

 Muscarinic agonist = Bethanechol  treatment for urinary retention or also can
use a1 antagonist.

 Disulfiram-like effects  can happen with Metronidazole treatment combined

with Alcohol, when treating for giardiasis, trichomonas vaginitis, and bacterial
vaginosis. (Remember metronidazole treats anaerobes below the diaphragm,
Clindamycin treats anaerobes above the diaphragm)

 Warfarin, Cyclosporin, Phenobarbitual, Tacrolimus, phenytoin, isoniazid,

rifampin universal enhancers of CYP450 all metabolized by CYP450 liver
enzymes so avoid inhibitors of this enzyme.

o Inhibitors: Valproate, isoniazid, cimetidine, azoles, sulfonamides, alcohol

(acute), Ciprofloxacin, Chloramphenical, Erythomycin, Amiodarone,
omeprazole, Grapefruit juice, Quinidine.
o Inducers: Barbituates, St. Johns wart, Carbamazepine, rifampin, alcohol
(chronic), phenytoin, Griseofulvin, Sulfonylureas.

 Non-selective B-adrenergic blockers cause bronchoconstriction, peripheral

vasospasm, and can predispose diabetic patients to hypoglycemia
 Propanolol, timolol, nidolol
 o Use selective B-blockers in patients with COPD, Asthma
 Metoprolol, atenolol, acebutolol, esmolol

 Antimuscarinic effects: atropine, tricyclic antidepressants (e.g. Amitriptyline),

H1 receptor blockers (eg. Diphenhydramine), neuroleptics, and antiparkinsonian
drugs  contraindicated in patients that have shallow anterior chamber angle or
increased intraocular pressure  results in closed-angle glaucoma.

 Heparin  acute management of venous thrombosis or thromboembolism

activates antithrombin III.
o Water soluble materials, such as conjugated bilirubin, do not readily cross
the placenta while lipophilic materials, such as unconjugated bilirubin,
may easily cross the placenta. Warfarin is a lipophilic molecule while
heparin sulfate, a charged molecule, is water soluble and is safer for
pregnancy.
 Warfarin  Long-term prevention of recurrences of venous thromboembolism
 inhibits vit K dependent carboxylation of glutamic acid residues of clotting
factors. II, VII, IX, X, C, S

 Colchicine  cytoskeleton

 NNRTI’s  antiretroviral drugs that do not require activation of intracellular

phosphorylation,
o Nevirapine, Efavirenz, Delavirdine
o SE= Rash SJS, hepatotoxicity (abrupt onset flulike symptoms, abdominal
pain, jaundice, fever life-threatening hepatic failure), neuropsychiatric
effects & teratogenicity (Efavirenz).
 NRTI’s  require activation of intercellular phosphorylation by thymidine
kinase, abacavir, tenofovir, emtricitabine, didanosine, stavudine, lamivudine,
zidovudine
 Protease inhibitors  prevent assembly and maturation of virus. Atazanavir,
darunavir, indinavir, ritonavir
 Enfuvirtide  HIV fusion inhibitor that binds to HIV envelop gp41 and blocks
conformational changes for the fusion of viral and cellular membrane no entry
of HIV into uninfected CD4+ T cells (outside the cytoplasm).
 Maraviroc  inhibits HIV entry by allosteric blocking of HIV gp120 interaction
with CCR5 (tropism testing required).
 Raltegravir  is an integrase inhibitor that disrupts HIV genome integration into
the host cells chromosomes, thereby preventing host cellular machinery from
being used to synthesize HIV mRNA.

 Foot in cast, became atrophied, what was the reason?

o Increased protein degradation via proteasomes, they have to first be
modified by ubiqitination. So Increased polyubiquitination in the muscle
cells.
 I cell disease: will show dilated RER, defect in N-acetylglucosaminyl-1-
phophotransferase  failure of the golgi to phosphorylate mannose residues on
glycoproteins  proteins are secreted extracellulary rather than delivered to the
lysosomes. High plasma levels of lysosomal enzymes.

 Glucagon  stimulates hepatic glucose release/production, must be used for

emergency hypoglycemia and/or fainting because of it.

 Long-chain acyl-coA dehydrogenase deficiency, inherited defect in transport of

LCFA”s into the mitochondria. Toxic accumulation. After starvation for 24 hours
patients cannot oxidize fatty acids for energy or produce ketone bodies
o Weakness, hypotnia, hypoketotic hypoglycemia.
o Impaired ß-oxidation of fatty acids  hypoglycemia.
o Systemic primary carnitine deficiency, LCFA’s require a carnitine
dependent transport from the cytosol to the mitochondria for beta-
oxidation
o Acyl-CoA accumulation to toxic levels
o Medium-chain triglycerides administered for treatment
o Also Acyl-CoA dehydrogenase deficiency  also limits break down of
fatty acids, increased dicarboxylic acids, has decreased glucose and
ketones.

 Peroxisomal diseases  rare inborn errors of metabolism where peroxisomes

are either absent of nonfunctional. Very-long-chain fatty acids are fatty acids
with branch points at odd-numbered carbons cannot undergo mitochondrial
beta-oxidation; these fatty acids are metabolized by a special form of beta
oxidation (very long chain fatty acids) or by alpha oxidation (branched chain
fatty acids such as phytanic acid) within peroxisomes.  Neurologic defects
from improper CNS myelination, such as seizures and hypotonia.

 Ataxia telangiectasia & fanconi anemia, have mutations in nonhomologous end

joining of broken DNA.

 Anti-smith antibodies = antibodies to spliceosomal snRNP’s. SLE.

 Panhypopituitarism with failure of lactation (low prolactin) in a new mother,

central hypothyrioidism, and adrenal insufficiency  Ischemic necrosis of the
pituitary gland.  Sheehan syndrome  pituitary enlarges during pregnancy
due to estrogen stimulation, but the blood supply does not increase so very
vulnerable to ischemia, from peripartum hemorrhage. Also cortisol and thyroid
deficiency, but cortisol deficiency manifests rapidly with nausea, postural
hypotension, fatigue, and weight loss.
 Chronic pancreatitis chronic alcohol use  alcohol-induced secretions of
protein rich fluids, which precipitate within the pancreatic ducts. That may
calcify. (hint: calcifications in the epigastric area).

o Digestive enzymes deficiency, steatorrhea, weight loss, bulky, forthy

stools.
o Pancreatic exocrine insufficiency : low amylase, lipase, and proteases.

 Uric acid precipitation in the renal tubules in the collecting duct of the
nephron, because of its low urine ph. Tumor lysis syndrome usually results
massive uric acid crystals in the serum
o Uric acid acidic crystals.

 Possible causes of hypoxemia in the setting of normal A-a gradient include

o Alveolar hypoventilation
o Inspiration of air at high altitude
 Gas diffusion impairment  high A-a gradient, thickening of alveolar capillaries
o O2 cannot be transported into the blood
 V/Q mismatch also a common cause of hypoxemia, poor ventilation of the lung
segment with normal perfusion. i.e. pneumonia, COPD,  also an increase in A-a
gradient.
o Normal value of A-a gradient =5-15 mmhg

 Fatty streaks  earliest lesion of atherosclerosis, 2nd decade of life  that

usually progresses to atherosclerotic plaques
o Lipid-laden macrophages (foam cells)
o In the intima

 Atherosclerosis  initiated by repetitive endothelial cell injury  leads to

chronic inflammatory state in the underlying intima of large elastic arteries as
well as large and medium-size muscular arteries.
o Lower abdominal aorta and coronary arteries develop the highest burden
of atherosclerosis

 Blunt trauma to the orbit in a blowout fracture orbital contents herniate into
the maxillary sinus (mainly, orbital floor, inferior wall) or Ethmoid sinuses
(medial wall).

 Septic abortion: abortion of pregnancy, but retained products of conception in

the uterine cavity.
o Fever, chills, lower abdominal pain, bloody or purulent vaginal discharge.
o Gram-negative bacilli or staph aureus.

 Brain
o Arteriovenous malformation m/c cause of intracranial hemorrhage in
children.

o Carotid artery atherosclerosis & cardiac embolism  Ischemic stroke

which resemble hemorrhagic stroke

o Cerebral amyloid angiopathy  lobar/cortical spontaneous parenchymal

hemorrhage, older patients, occipital/parietal lobes.

o Hypertensive encephalopathy progressive headache, nausea/vomiting,

nonlocalizing neurologic syndrome (confusion).

 Brain edema, petechial hemorrhages throughout the gray/white

matter found on autopsy.

o Hypoxic ischemic encephalopathy  decreased O2 in the brain due to

cardiac arrest, decreased consciousness, coma, and vegetative stage.
 Pyramidal cells of the hippocampus (first area damaged),
neocortex, and Purkinje cells of the cerebellum are the most
vulnerable to ischemic injury, affected first
 Necrosis of the watershed areas of the brain results between the
ACA-MCA, and MCA-PCA,  bilateral wedge-shaped strips of
necrosis over the cerebral convexity, parallel and adjacent to the
longitudinal cerebral fissure.

o Saccular aneurysm rupture (berry aneurysm or arteriovenous

malformation)  leads to subarachnoid hemorrhage. Severe headache
 Arterial severe vasospasm 4-12 days after the initial insult is the
major cause of morbidity and mortality in patients recovering
from SAH. It’s in the vessels surrounding ruptured aneurysm. 
 Causes cerebral ischemia, new onset confusion and focal
and neurological deficit weakness in one area of body 4-12
days after the initial  give Ca2+ channel blocker to
prevent this (especially nimodipine).
o Will not show on CT scan,
o Only transcranial color Doppler is needed
 Rebleeding of SAH or hydrocephalus will show on CT scan

o Charcot-bouchard aneurysm rupture, (deep intraparenchymal

hemorrhage, basal ganglia, cerebellar nuclei, thalamus, and pons), due to
hypertensive vasculopathy of small penetrating branches of cerebral
arteries.
 Acute bleeding, hyperattenuated, bright red
 Neurological deficits, hand/leg weakness, followed by
nausea/vomiting.
 o Intracranial vasculitis  can lead to intraparenchymal hemorrhage.
(rare)
o Hypertensive arteriolar sclerosis  patients with long-standing
hypertension.
 Occlusion of small (leniculostriate arteries), perforating branches
of major cerebral arteries.
 Lacunar infarcts (small ischemic infarcts) occur in basal ganglia,
internal capsule, pons, and thalamus  due to lipohyalinosis and
microatheroma formation secondary to leakage of plasma proteins
through damaged endothelium  hyaline thickening of vascular
wall.
 Initial CT scan does not show any abnormalities, but repeat CT
imaging of brain after weeks show 9mm lakelike cavitary lesion in
the left internal capsule.

 Q# 1525, Gallstone ileus  cholesterol containing large gallstone through a

cholecystenteric fistula ino the small bowel  stuck in the intestinal lumen,
ileocecal valve  small bowel obstruction  fistula between gallbladder and
gastrointestinal tract gas within the biliary tree and gallbladder.
o Results in pneumobilia  air in the biliary tree, which makes high bowel
sounds.
o Obstruction at the common bile duct by a gallstone (choledocholithaisis)
can lead to pancreatitis and/or cholangitis. Presents with fever, right
upper quadrant abdominal pain and jaundice (charcot triad).

 Autosomal recessive => 25% chance of unborn child getting the disease
 Autosomal dominant => 50% change of unborn child getting the disease,
because they only need 1 allele affected to get disease.
o Achondroplasia  Endochondral ossification affected  short-limbed
dwarfism  Point mutation in FGFR3 fibroblast growth factor receptor 3
inhibits chondrocytes proliferation  leading to prevention of
endochondral ossification. 80% increased paternal age, 15% sporadic
o 2 copies of the mutant allele lead to death shortly after birth. Normal
sized head and trunk because no problem with membranous ossification

 Anaphylaxis  histamine release, and tryptase release (preformed

inflammatory mediators).
o Tryptase is an enzyme specific to mast cells and can be used as a marker
for mast cell activation
o Multiple membrane bond IgE antibodies  receptor aggregation of IgE
leads to trigger vasoactive mast cell release by these cells.  Histamine
released from mast cells and basophils.
 Bacterial mRNA  polycistronic mRNA (lac operon in E.coli)  1 mRNA codes
for several proteins, such as enzymes B-galactosidase and galactoside permease,
and transacetylase).
o Low glucose  increase cAMP  increases CAP (catabolite activator
protein  increases transcription
o High lactose unbinds repressing protein from the repressor/operator
site  increase transcription
 Lac operon  regulated by 2 distinct mechanisms  negatively by binding of
the repressor protein to the operator locus and stopping transcription and
positively by cAMP-CAP binding upstream from the promoter region increasing
the transcription. Constitutive expression of the structural genes of the lac
operon occurs with mutations that impair the binding of the repressor protein
(Lac I) to its regulatory sequence in the operator region.
 Repressor proteins, when bound to operator region, prevent biding of RNA
polymerase to the promoter region, thus decreasing transcription of the lac Z, Y,
and A genes.

 Capped, tailed, and spliced hnRNA is  mRNA

 Q#, 11595, microRNA’s and Small interfering RNA (siRNA)  degradation or
activation of a target mRNA  abnormal expression leads posttranscriptional
gene silencing by base-pairing with complementary sequences to certain
malignancies by silencing, tumor suppressor genes.

 Hypophosphorylated Rb= is activated and arrests cell cycle transcription from

G1-S phase

 Ulcers
o Stomach ulcers
 Deep peptic ulcer localized proximally on the lesser curvature of
the stomach, at the border of acid secreting and gastrin secreting
mucosa. Most gastric ulcers arise along the lesser curvature of the
stomach.
 Ulcer penetrated the left gastric artery. (proximal lesser
curvature)
 Distal lesser curvature  right gastric artery.
 The right and left gastric arteries perfuse the lesser curvature of
the stomach. Likely to be penetrated by an ulcer, leading
hemorrhage.
 Gastric ulcers DO NOT commonly occur in the greater curvature.
o Duodenal ulcers
 Gastroduodenal artery supplies the blood to the pylorus and
proximal part of the duodenum.
 Ulcers in the duodenal bulb can erode into the
gastroduodenal artery and case hemorrhage/bleeding.
  A perforated ulcer would cause the acidic juice to hit the
gastroduodenal artery, portal vein, and the inferior vena
cava, and the common bile duct.
 Posterior duodenal ulcers is hemorrhage secondary to
gastroduodenal artery damage.
o 3rd part of the duodenum courses horizontally across the abdominal aorta
and inferior vena cava at the level of the third lumbar vertebra.
 Superior mesenteric vessels lie anterior to the 3rd part of the
duodenum at this location.
 So anterior tumor invasion could compromise the SMV,
o 1st part of the duodenum is the only part that is not retroperitoneal
o 2nd part of duodenum  head of pancreas, ampulla of vater where
pancreatic and common bile duct secretions are released
o 4th part becomes jejunum

 Type 1 muscle fibers  slow twitch

o Actions requiring low level sustained force, aerobic metabolism  high
myoglobin oxygen storage and mitochondrial aerobic respiration
concentrations.
 postural maintenance  paraspinal muscles, and soleus muscles.
 Type 2 muscle fibers  fast twitch
o Rapid forceful pulses of movement.
o Type IIa  intermediate between Type IIb and Type I, ATP through
aerobic metabolism.
o Type IIb fibers derive ATP energy through anaerobic glycogenolysis and
glycolysis. Fastest muscle fibers.
 Biceps brachii, Latissimus dorsi, pectoralis major, deltoid.

 Jervall and Lange-Nielsen syndrome: M/c congenital long-QT syndrome. AR,

congenital neurosensory deafness.
o Syncopal episodes, palpitations, seizures, or sudden cardiac death from
torsades de pointes.
 Romano-Ward syndrome  AD, pure cardiac phenotype. No deafness.
 Drugs that causes QT-prolongation:
o AntiArrhythmics (class IA, III)
o AntiBiotics (e.g. Macrolides)
o Anti “C” ychotics (haloperidol, Ziprasidone)
o AntiDepressants (e.g. TCA’s)
o AntiEmetics (e.g. ondansetron)

 Carbamazepine  blocks voltage-gated sodium channels in neuronal

membranes.
o SE: Anemia, agranulocytosis, thrombocytopenia, hepatotoxic
 Low hemoglobin, leukopenia, and thrombocytopenia.
 Graves Disease: autoimmune response that results in accumulation of
glycosaminoglycan’s by deposition by orbital fibroblasts leading to orbital
edema and enlargement of the extraocular muscles, and also within the affected
tissues.
o Pretibial myxedema  specific features of hyperthyroidism due to
graves.
 Pretibial myxedema are lower leg thickening and induration of
TSH receptors there
o Exophthalmos also specific for graves disease
 Autoimmune response directed against the TSH receptors
 Treatment  high dose glucocorticoids, such as prednisone 
decreases the severity of inflammation and decreases extraocular
volume.
 Conventional antithyroid drugs and propranolol do not
improve opthalmopathy.

 Bleeding problems:
o Factor VIII deficiency, Hemophilia A deep-tissue bleeding (bleeding
into joints/muscles, gastrointestinal bleeding, hematuria)
o Factor IX deficiency, Hemophilia B Christmas Disease  AR, clot
instability. Delayed recurrent bleeding after trauma, or surgery. Also deep
tissue bleeding.
 For both hemophilia A and B  leads to failure of to convert
prothrombin into thrombin and deficient thrombus formation.
 Adding thrombin to the blood of a patient with hemophilia
results in clotting when in emergency situations.
o vWD mutation in vWF  qualitative defect in platelet binding, and
aggregation. Bleeding in skin and mucosal sites (mucocutaneous
bleeding), vWF normally binds to collagen with cross linked platelet
glycoproteins GpIb. Ristocetin aggregation test will show decreased
aggregation of platelets.
 gingivae, nasal mucosa, gastrointestinal and endometrium
 heavy menstrual bleeding (menorrhagia), epistaxis, Anemia
 Severe forms of vWD can result in factor VIII deficiency, because
factor VIII is protected from degradation by vWF.
o Protein C or S deficiency  natural anticoagulant protein
 Procoagulant state, recurrent deep venous thrombosis.
o Immune thrombocytopenia purpura  produces isolated
thrombocytopenia with episodic bleeding mucocutaneously.
 Petechiae, purpura, epistaxis.

 First generation H1 histamine receptor antagonist, including diphenhydramine

(Benadryl) and chlorpheniramine  can cause significant sedation.
 o AVOID taking it with CNS depressants such as benzodiazepines
(Diazepam).
o In general benzodiazepines shouldn’t be used with alcohol, barbiturates,
neuroleptics, or 1st generation antihistamines.
 May increase Frequent falls in the elderly.
 Benzodiazepines substitute the action of alcohol on GABA
receptors and are indicate for treatment of withdrawal.

 Pulmonary embolism: Respiratory CO2 decreased, and increased pH, and normal
HCO3-, which means its Respiratory alkalosis yet not compensated with
metabolic metabolism.

 Antihyperlipidemic agents:
o Bile acid-binding resins inhibit enterohepatic circulation of bile acids by
binding bile acids in the GIT, inhibiting enterohepatic circulation 
increased LDL cholesterol uptake.
 SE: GI upset, impaired absorption of nutrients and drugs, and
increase production in triglycerides and release of VLDL particles
into the circulation hypertriglyceridemia.
o Statins  LDL decreases and triglycerides by inhibition of rate limiting
step of cholesterol enzyme HMG-CoA reductase. SE: myopathy (myalgia,
elevated creatine kinase). Increased LDL density
o Ezetimibe  inhibits intestinal absorption of cholesterol and lowers LDL
levels at the brush border of the small intestine Lowers triglyceride
levels.
o Fibrates  inhibit cholesterol 7a-hydroxlyase enzyme (rate limiting step
in synthesis of bile acids), lowers triglycerides and is first line treatment
for hypertriglyceridemia.
o Niacin  reduces blood triglycerides, raises HDL and lowers VLDL
conversion to LDL.
 SE  skin flushing and warmth  caused by mediation of
Prostaglandins
o Simvastatin  decreases hepatic cholesterol synthesis, cholestyramine
 increases hepatic cholesterol synthesis.

 ORBA  segmented viruses  can undergo genetic shift through reassortment.

o Orthomyxoviruses (influenze A&B), reoviruses (rotavirus), bunyavirus,
and arenaviruses
 Reassortment  coinfected with 2 segmented viruses, exchange of a whole
genome segments  sudden alterations in surface antigens of the viral progeny,
with highly mutagenic influenza virus which can lead to pandemics.
 Recombination  crossing over or exchange of genes between 2 double-
stranded DNA chromosomes within homologous regions.
o Crossing-over of 2 double stranded DNA molecules.
 Transformation  uptake of a naked DNA by prokaryotic or eukaryotic cell 
incorporation of viral DNA into host cells chromosome.
o Bacterium to take up exogenous DNA fragments, integrate the DNA into
the genome and express encoded proteins
o E.g. Is streptococcus pneumonia of a non-capsule-forming strains can
aquire the genes that code for the capsule and thus gain virulence.
 Conjugation and transduction are 2 additional mechanisms by which bacteria
can obtain new genetic material.

 Neuroleptic malignant syndrome: Diffuse muscle rigidity, hyperthermia,

autonomic instability, and altered sensorium, high fevers, hypertention, and
tachycardia. Creatinine kinase elevation due to rhabdomyolysis.
o Also malignant hyperthermia treat with dantrolene.
o Treat with Dantrolene  antagonizing, blocks the ryanodine receptors 
inhibits calcium release from sarcoplasmic reticulum of the skeletal
muscle.

 Serotonin syndrome  life-threating, tremors/myoclonus, diaphoresis,

hypertension, hyperthermia, tachycardia, nausea, diarrhea, and altered mental
status. NO diffuse muscle rigidity.
o Cyproheptadine  serotonin receptor antagonist used to treat this
syndrome.

 MCA left stroke have expressive and receptive aphasia due to infarction of the
broca and Wernicke areas, respectively.
 MCA right stroke have contralateral hemiparesis, hemisensory loss involving
face and upper limps due to infarction, spatial neglect of the contralateral side
due to damage of the nondominant right parietal love.

 Thyroglossal duct  persistence  Throglossal cyst  midline neck mass

o This cyst moves upward with swallowing.

 Branchial cleft cyst  persistence of second branchial cleft (2nd pharyngeal

groove)  branchial cleft cyst between angle of mandible and
sternocleidomastoid muscle, later neck mass.

 Nitric oxide  synthesized by nitric oxide  cGMP  vasodilation

 Pharm resistance

o Isoniazid (INH): inhibition of mycolic acid synthesis

 Resistance Decreased activity of bacterial catalase-peroxidase,
this enzyme is required for conversion of INH to its active
metabolite within mycobacterial cells.
  SE: Neurotoxicity  give B6, hepatotoxicity  direct hepatotoxic,
causing acute, mild hepatic dysfunction in 10-20% of patients and
frank hepatitis (fever, anorexia, and nausea, sometimes
progressing to hepatic failure) in a small percentage of patients.
o Rifampin: Inhibition of bacterial DNA-dependent RNA polymerase
 Resistance  structural alteration of enzymes involved in RNA
synthesis
 SE: GI upset, red-orange body fluids, cytopenias
o Ethambutol: Inhibition of arabinosyl transferase
 Increased activity of enzymes involved in cell wall poylysaccaride
synthesis.
 SE: optic neuropathy
o Pyrazinamide: unclear MOA,
 SE: hepatotoxicity
o Streptomycin: an aminoglycoside, inhibits protein synthesis by
inactivating the 30s ribosomal subunit.
 Resistance: Altered structure of bacterial ribosomal protiens and
aminoglycoside-modifying enzymes (transferases) and mutated
porins.

 Dehydration stimulates ADH secretion. ADH acts on the collecting ducts,

increasing their permeability to water.
o Thus, in the presence of ADH  collecting ducts contain the most
concentrated fluid in the nephron, while the thick ascending limb of the
loop of henle and distal convoluted tubule contain the most dilute fluid.

 Great saphenous vein  originates in the medial side of the foot, courses
anterior to the medial malleolus and travels up the medial aspect of the leg and
thigh.
o Drain into the femoral vein within the region of the femoral triangle, few
centimeters inferolateral to the pubic tubercle.

 Pulmonary vascular resistance (PVR) is lowest at the functional residual

capacity.
o Increased lung volumes increase PVR due to the longitudinal stretching of
alveolar capillaries by the expanding alveoli.
o Decreased lung volumes also increase PVR due to the decreased radial
traction from adjacent tissues on the large extra-alveolar vessels.

 Breast cancer treatments:

o Trastuzumab: Monoclonal antibody used in management of pts with
HER2-positive breast cancer.
 Prevents activation of transmembrane tyrosine kinase receptor 
down regulates cellular proliferation and promotes apoptosis.
 o Bevacizumab: VEGF vascular endothelial growth factor inhibitor, also a
tyrosinse kinase receptor.
 Metastatic cancers (colon, lungs)
o Denosumab: RANKL receptor activator of nuclear factor kappa-B ligand
which activates osteoclasts  may contribute to bone metastases by
binding to RANK on tumor cells.
 RANKL receptor blocker.
o Tamoxifen: selective estrogen receptor modulator treats pts with
Estrogen receptor/progesterone receptor tumor expression.
o Anastrozole: aromatase inhibitor, for postmenopausal patients who have
breast cancer with ER/PR tumor expression.
 Venous thromboembolism  Virchow triad of endothelial injury, venous stasis
and hypercoagulable state only perfusion is limited, so pulmonary function
tests are unaffected.

 Proto-oncogenes  single nucleotide substitution causing and activation

mutation.
 Tumor-suppressors (anti-oncogenes)  inactivation, loss of function mutation.
 Growth factors that promote angiogenesis:
o VEGF & FGF
o Proinflammatory cytokines can indirectly promote angiogenesis through
increased VEGF expression.
o Laminin in the basement membrane may pose a physical barrier to the
sprouting of new blood vessels.
 Hyperacusis caused by stapedius nerve injury a branch of the facial nerve. So
paralysis of this muscle oscillates more widely producing very loud noises with
normal volume.
o Treatment  retraining to sound therapy using broadband noise (white
noise).
o Ipsilateral hyperacusis associated with Bell’s palsy  unilateral facial
paralysis, decreased tearing, hyperacusis, and/or loss of taste sensation
over the anterior two-thirds of the tongue.
 Antigen presentation to macrophages  produce IL-12  stimulates
differentiation into a Th1 (cell mediated immunity)
o So if a patients T-lymphocytes lack IL-12, then supplement the patient
with Interferon-g (IFN-Gamma), because helper T-cells cannot
differentiate into Th1 cells.
o Thus, pts with IL-12 deficiency suffer from severe mycobacterial
infections.
 Other antigen presenting cells release IL-4 (Humoral (antibody-mediated
immunity)  facilitates differentiation into the Th2 subset.
o If any deficiency  administering immunoglobulin’s or IL-4 would
immove the immune response.
 Kidneys are more likely than other organs to suffer embolic infarctions as they
are perfused at a higher rate to support adequate Glomular filtration rate.
o Systemic thromboembolism occurs with atrial fibrillation as the irregular
heart contractions can lead to clot formation.
 Cause  recent stroke with emboli traveling to peripheral arteries
in the brain, intestinal or foot ischemia, renal infarction
 Can occur also following a myocardial infarction.
 Kidneys lead to coagulative infarcts  pale wedge shaped.

 Aortic valve stenosis due to aging  cell necrosis, with normal Ca2+ levels.
o Dystrophic calcification  damaged or necrotic tissue.

 Lactase deficiency  osmotic diarrhea and stool pH low, acidification.

 Severe hypertention  can lead to flame-shaped hemorrhages in the orbits,

from precapillary arterioles which causes endothelial disruption.

 Bruise color green  caused by a release of Biliverdin which is released from

break down of heme by Heme oxygenase.

 Q# 1374, Parvovirus- Hydrops Fetalis, stillbirth of a fetus with autopsy of pleural

effusion, pulmonary hypoplasia, heart failure and ascites
o Due to nonenveloped, single-stranded DNA virus  Parvovirus B19.
o Lead to interruption of erythropoiesis, profound anemia, fetal hydrops

 BRCA1 and BRCA2 involved in double-stranded DNA breaks, they are tumor
suppressor genes, AD,
o High risk of breast and ovarian cancers.

 Resistance by acetyl group transfer to exogenous substances  bacteria

resistance to aminoglycosides.

 Hereditary spherocytosis HS  lead to pigmented gallstones from the hemolytic

anemia with all the bilirubin increased from the lysed RBC’s which precipitates
as calcium bilirubinate (all hemolytic anemia’s in risk with pigment stones).
o Aplastic crisis with Parvovirus B19.
o Aplastic anemia  kidneys respond with increasing erythropoietin levels
due to hypoxia.

 Sickle cell anemia AR, both parents must be carriers! Hemoglobin

electrophoresis of both parents is best to know if they are carriers.
o Autoinfarction of the spleen and avascular necrosis of the femur.
 Osteonecrosis (avascular necrosis)  impaired blood supply to a
segment of the bone, mainly femoral head.
  Can also result form glucocorticoid therapy, vasculitis, and
alcoholism.
o Sickling episodes result in hemolysis, which leads to increased indirect
bilirubin and lactate dehydrogenase and decreased levels of haptoglobin.
o Vaso-occulsive crisis  treat with oxygen supplementation, IV fluids and
high dose narcotics,  repetitive splenic infarction caused by splenic
microvessel occlusion  Fibrosis, brown discoloration and eventual
autosplenectomy.
o Salmonella osteomyelitis may be a complication that needs antibiotics,
this bacteria is resistant to opsonization
 Vaso-occlusion results in a relative immunodeficiency as the
spleen suffers widespread infarction (functional asplenia), putting
patients at an increased risk for infection by encapsulated
organisms such as streptococcus pneumoniae as well as Neisseria,
Haemophilus, and Salmonella spp. (resistance to opsonization).
o HbS aggregates in the deoxygenated state (low oxygen levels or low blood
volumes)  HbS polymers form fibrous strands that reduce red blood
cell membrane flexibility and promote sickling.
 Anoxia, low pH and high 2,3BPG.
 Microvascular occlusion and microinfracts
 Valine instead of glutamic acid promotes hydrophobic
interaction among Hb molecules and results in HbS
polymerization and erythrocyte sickling.
 Hydroxyurea increases hgb F, and Gardos ca2+ dependent K+ channel blockers
prevents intracellular dehydration, it regulates the transport of potassium and
water throught the rbc membrane and when blocked, K+ and water efflux is
reduced and it prevents dehydration of erythrocytes and reduces the
polymerization of Hb S.

 Staph epidermidis synthesis of extracellular polysaccharide matrix  biofilms

 Ubiquitin proteasome pathway controlled by ubiquitin ligases  recognizes

specific protein substrates and attach a ubiquitin tag.
o Then coupled with MHC 1 in the endoplasmic reticulum, which is cell
surface recognition by cytotoxic CD8+ lymphocytes.

 Stable angina/acute coronary syndrome 

o Acute plaque change, often with superimposed thrombosis.
o Fixed atherosclerosis
o plaques obstructing >75% of the lumen or a coronary artery
 Asymptomatic 
o Plaques occluding less than 75% of the coronary artery lumen
 Unstable angina or subnendocardial infarction 
o An ulcerated atherosclerotic plaque with partially obstructive thrombus
 Transmural myocardial infarction  ruptured atherosclerotic plaque with a
fully obstructive thrombus.
 Significant coronary artery vasospasm causing flow obstruction  Prinzmetal’s
angina  episodic angina that generally occurs at rest.

 Gastric bypass surgery can cause small intestinal bacterial overgrowth due to
excessive bacterial proliferation in the blind-ended gastroduodenal segment.
SIBO results in deficiency of most vitamins, (B12, A, D, and E) and iron, but
increased production of folic acid and vitamin K are observed.

 Acidophilic bodies = eosinophilic bodies = councilman bodies  apoptotic

bodies.

 Methomoglobinemia dusky discoloration of the skin (similar to cyanosis),

methomoglobin is unable to carry oxygen becuz iron is in the ferric state (Fe3+),
anemia is induced.
o The bound fraction of oxygen and its delivery to the peripheral tissues
will also decrease due to methemoglobin’s inability to carry and deliver
oxygen.
o Blood partial pressure of oxygen is unchanged as it is a measure of
oxygen dissolved in the plasma and is unrelated to hemoglobin function.
o Nitrites are oxidizing agents that are effective in treating cyanide
poisoning due to their ability to induce methemoglobinemia. Cyanide
binds to ferric (Fe3+) more avidly than mitochondrial cytochrome
enzymes (cytochrome c oxidase, which is essential for oxidative
phosphorylation,  inhibition of this enzyme results in severe lactic
acidosis and death as a result of cells switching to anaerobic metabolism).

 CFTR protein is a transmembrane ATP-gated chloride channel.

 Paradoxical embolism occurs when a thrombus form the venous system crosses
into the arterial circulation via an abnormal connection between the right and
left cardiac chambers (patent foramen ovale, ASD, or VSD). Atrial left –to-right
shunts (ASD) cause wide fixed splitting of S2 and can facilitate paradoxical
embolism due to periods of transient shunt reversal (during straining or
coughing).
 Wide splitting of S1 accentuated by inspiration  sign of delayed closure of the
tricuspid valve.

 mRNA transcription 
o 5’-capping, poly A tail addition, and intron splicing all take part in the
nucleus
o In the cytoplasm mRNA’s associate with P bodies, which play an
important role in mRNA translation regulation and mRNA degradation
and storage.
 o Poly-A tail is not transcribed from DNA, instead it is added as a post-
transcriptional modification downstream of the consensus sequence
(AAUAAA) near the 3’ end of the mRNA molecule.
 This tail protects mRNA from degradation within the cytoplasm
after it exits the nucleus.
 Most likely to bind latex beads of the adenine residues on the tail
would form complementary base pairs with the repeated
deoxythymine (double stranded thymines) residues fixed to the
beads.

 AR heterozygotes parents on both parents

o ¼ of the children will be affected (homozygous)
o ½ of the children will be carriers
o ¼ of the children will not be affected nor carriers

 A holosystolic murmur that increases in intensity on inspiration most likely

represents tricuspid regurgitation.
 The other holosystolic murmurs (which are secondary to mitral regurgitation or
a ventricular septal defect) do not typically increase in intensity during
inspiration.
 Oxygenated blood from the placenta is delivered to the fetus via the umbilical
vein.
o The umbilical vein has the highest oxygen content in the fetal circulation.
 The ligamentum teres is th remnant of the umbilical vein in the
adult.
o Blood from the umbilical vein is first delivered to the liver, where it
bypasses the hepatic circulation via the ductus venosus and enters the
inferior vena cava. (IVC). So the IVC is the second to have the highest
oxygenated content
o From the IVC, blood is pumped into the heart  to the pulmonary
circulation  or bypasses from the right heart to the left heart directly
via the foramen ovale.
o A fraction of the blood in the pulmonary circulation may bypass the lungs
via ductus arteriosus and pass directly into the descending aortablood
circulates to all of the fetal tissues.
 Q# 1885, Psoas abscess can occur as a result of hematogenous or lymphatic
seeding from a distant site or by spread from an adjacent site.
o Presentation of fever, back or flank pain, inguinal mass, and difficulty
walking, pain is caused when the hip is extended (psoas sign).
o Originates at the anterior surface of the transverse processes and lateral
surface of the vertebral bodies at T12-L5.
o Spread of pus along the psoas muscle may lead to formation of an abscess
in the groin and pain referred to that region.

 Proximal ureter  blood supply from renal artery

 Distal ureter  blood supply by superior vesical artery.
 Middle part is anastomotic.

 Gonadal artery  arises from abdominal aorta  twisting of the testis around
the spermatic cord  ischemia  Testicular torsion

 Glucagon increases serum glucose by increasing hepatic glucose production via

glycogenolysis (break down of glycogen) and gluconeogenesis (production of
glucose from noncarbohydrate sources).
o Glucagon induced glycogenolysis is the predominant initial means of
rapidly increasing blood glucose levels during hypoglycemia.
o Glucagon functions by stimulating G protein-coupled receptors on
hepatocytes, increasing intracellular cAMP concentration and activating
protein kinase A.
o Glycogen phosphorylase (glycogenolysis), pruvate carboxylase,
phosphoenolpyruvate carboxykinase (gluconeogentic).
o 12 hours of fasting  hepatic glycogenolysis is the source
o After 12 hours of sustained fasting  Gluconeogenesis in renal cortex is
the source
 Epinephrine is more effective than glucagon in stimulating renal
gluconeogenesis.

 Obstructive sleep apnea with loud snoring and gasping respirations is due to
oropharyngeal
o Electrical stimulation of the hypoglossal nerve increases the diameter of
the oropharyngeal airway and decreases the frequency of apneic events.
o Increases risk for pulmonary HTN and right heart failure if not treated.

 Pilocytic astrocytoma primary child brain tumor, have both solid and cystic
components, good prognosis, pilocytic astrocytes and Rosenthal fibers are seen
on histology.
 Medulloblastoma second most child brain tumor, have only solid component,
most malignant and poor prognosis  cerebellum, sheets of small blue cells. Bad
prognosis.

 Congestive heart failure & left ventricular ejection fraction  use

mineralocorticoid receptor anatagonists (spironolactone, eplerenone), to
improve survival in these patients.
o Use these drugs also for aldosterone secreting tumors (adenoma) leading
to hyperaldosteroninsm (conns syndrome)  decreased renin,
hypokalemia, alkalosis, and hypertension  type IV renal tubular
acidosis  use this drug to replenish K+.
 C-jun and c-fos are nuclear transcription factors that directly bind DNA via
leucine zipper motif. Genes that code for this are proto-oncogenes. They directly
bind DNA
o Basic-region leucine zippers are a class of eukaryotic transcription factors
composed of 2 alpha-helical proteins that combine to form a dimer. Each
dimer has a DNA binding region composed of basic amino acids and a
leucine zipper dimerization domain that contains repeated leucine
residues at every seventh position. Other motifs are helix-loop-helix and
zinc finger, each of these permit interaction of the DNA-binding protein
with the major groove in DNA. Mutations may result in malignant
transformation or cell death.
o Southwestern blotting is used to detect DNA-binding proteins such as a
transcription factors, nucleases, and histones.

 Bicuspid aortic valves  most common complication is aortic stenosis at an

early age around 50 years.
 Compared to senile calcific stenosis of normal valves, generally becomes
symptomatic age >65.
o Calcific degeneration of the trileaflet aortic valve  valve leaflet
thickening leading to restricted leaflet excursion and mobility.
o Harsh ejection-type systolic mumur heard best at the base of the heart in
aortic area  2nd right intercoastal space radiates to the carotid
arteries.

 Right-sided colon cancer (ascending colon) exophytic masses that present

with occult bleeding and symptoms of iron deficiency anemia.
 Left-sided colon cancer (rectosigmoid colon) infiltrates the intestinal wall and
encircles the lumen, causing constipation and symptoms of intestinal
obstruction.
 Rectosigmoid involment often causes hemochezia.
 Anti-HBs is a neutralizing antibody that prevents viral entry into the cells.
Therefore, individuals who receive vaccination will develop immunity and be
positive for anti-HBs but neg for HBsAg.
o But those who recover from an infection have both anti-HBs as well as
anti-HBc antibodies.

 In left ventricular failure, fluid accumulation in the lung interstitium results in

decreased compliance.

 Neotnatal diabetes mellitus have identified mustations of the K+ ATP channels in

which elevated glucose levels do not lead to appropriate depolarization and
insulin release.  And no opening of voltage-gated calcium channels which
increases intracellular calcium and then facilitates the release of insulin.
 Pericarditis  m/c cardiovascular manifestation associated with systemic lupus
erythematosus  sharp pleuritic chest pain the is relieved by sitting up and
leaning forward.

 Amphotericin B  nephrotoxitiy  due to decrease in glomerular filtration rate

and direct toxic effects on the tubular epithelium creating pores in the fungal cell
membrane, fungal cell wall is caspofungin 
o Anemia, hypokalemia, and hypomagnesemia, reflects and increase in
distal tubular membrane permeability.

 ACE inhibitors decrease renal filtration fraction by blocking angiotensin

mediated efferent arteriole vasoconstriction
o Those dependent on efferent arteriole constriction to maintain renal
perfusion (renal artery stenosis), then ACE inhibitors can be detrimental
by precipitating acute renal failure.
o May cause first-dose hypotension in patients taking diuretics or have
heart failure  start patients off with low dose
o Patients with evidence of diffuse atherosclerosis may have bilateral renal
artery stenosis  GFR dependent of angiotensin II-mediated arteriolar
vasoconstriction in RAS  because of this ACE and ARBs cause efferent
arteriolar vasodilation  then GFR decreases  acute renal failure.
o Efferent arteriole dilation decreasing GFR, can precipitate acute renal
failure in patients with reduced intrarenal perfusion pressure.

 In patients with infection or surgery (stressful situations) that are normally

treated with glucocorticoids should have their dose increased when in these
situations to avoid adrenal insufficiency and adrenal crisis.

 Adenomyosis  presence of endometrial glandular tissue within the

myometrium.
o Common in middle-aged parous females. Heavy menstrual bleeding,
dysmenorrhea, uniformly enlarged uterus.
o Can only be diagnosed definitively by microscopic examination of a
hysterectomy specimen.

 Polysaccharides must be degraded to monosaccharides by pancreatic and brush

border amylases before they can be absorbed.

 Monosaccharides can be absorbed directly. D-xylose is a monosaccharide whose

absorption is not affected by exocrine pancreatic insufficiency, and can be used
to differentiate between pancreatic versus mucosal causes of malabsorption.

 Acute hemodynamic changes can produce functional heart murmurs, in the

absence of any fixed valve lesion. Dilatation of the left ventricle in response to
increased preload can result in functional mitral regurgitation, which can be
 eliminated by preload reduction and afterload reduction by using a diuretics and
vasodilators.

 Rheumatoid arthritis MTP, PIP, writs, elbow, knees, and ankles. Cervical spine
is involved  which may lead to severe disability due to pain and spinal
instability and potential to radiculopathy and cord compression.
 Osteoarthritis  lumbar spine involvement, progressive erosion of articular
cartilage, often due to repeated biochemical trauma over time. Relative
overactivity of metalloproteases in the joint space also appears to contribute,
joint space narrowing, subchondral bony sclerosis, and osteophyte formation.
 Seronegative spondyloarthropathies  Ankylosing spondylitis, reactive
arthritis, arthritis associated with inflammatory bowel disease, psoriatic
arthritis  HLA-B27 human leukocyte antigen class I to CD8+ cytotoxic T cells.
 involve sacroiliac joints
o Psoriasis hyperparakeratosis, acanthosis, rete ridge elongation, mitotic
activity above basal cell layer and reduced or absent stratum granulosum.
 TNF-a, IL-12, IFN-g, IL-23, IL017 and keratinocyte growth factors.
 Treatment includes topical vitamin D analogs (calcipotriene,
calcitriol, and tacalcitol) binds to vit D receptors and inhibit
keratinocyte proliferation and stimulate differentiation.

o Ankylosing spondylitis  stiffness and fusion of axial joints (ankylosis)
and inflammation at the site of insertion of tendons into bone (enthesitis).
 Thoracic spine and costoverterbral and costosternal junctions can
limit chest wall expansion, leading to hypoventilation.

 Extramedullary hematopoiesis is most frequently caused by severe chronic

hemolytic anemia’s, such as B-thalassemia.
o EMH can cause a range of skeletal abnormalities. Expanding mass of the
progenitor cells in the bone marrow thins the bony cortex and impairs
bone growth.
o Maxillary overgrowth and frontal bossing are associated with the
characteristic “chipmunk facies”.

 Chronic bronchitis  thickened bronchial walls, lymphocytic infiltration,

mucous gland enlargement, and patchy squamous metaplasia of the bronchial
mucosa.
o Cigarette smoking is the leading cause of chronic bronchitis. (Always
cigarette smoking is the major risk factor to almost everything).

 Normal tracheal pO2 = 150 mmHg

 Normal alveolar pO2 = 104 mmHg.
 Normal alveolar pCO2 = 40 mmHg
 Equilibration of O2 in a normal individual at rest is perfusion-limited.
o When perfusion is poor, equilibrium will occur slowly or not at all
 o PE, which blocks all blood flow to a given segment of the lung that aerates
normally.
o The tracheal air and alveolar air would be approximately the same.
 Diffusion-limited gas exchange, alveolar does not equilibrate with the blood gas
by the time that given volume of blood reaches the end of alveolar.
o Include disease states, such as emphysema, pulmonary fibrosis, and
exercise.
 Interscalene nerve block anesthetizes the brachial plexus as it passes through
the scalene triangle. It is used to provide anesthesia to for the shoulder and
upper arm
o Nearly all patients develop transient ipsilateral diaphragmatic paralysis
dude to involvement of the phrenic nerve roots as they pass through the
interscalene sheath.
o This nerve block should be avoided in patients with chronic lung disease
or with contralateral phrenic nerve dysfunction.

 Menotropins (human menopausal gonadotropin)

o Mimics FSH and triggers the formation of a dominant ovarian follicle.
o This followed by a single injection of human chorionic gonadotropin
(hCG) mimics LH surge  so that ovulation can occur.

 Antibodies to acetylcholine receptor  Reduced motor end-plate potential

myasthenia gravis
o Treatment is cholinesterase inhibitors  which may cause adverse
effects to muscarinic overstimulation  scopolamine can be used  anti-
muscarinic agent without messing with cholinesterase inhibitors
 Antibodies to cardiolipin  antiphospholipid antibody syndrome  recurrent
venous thrombosis and/or pregnancy loss  associated with Systemic lupus
erythematosus.
 Antibodies to Desmoglein  1 and 3, these help form desmosomal junctions, the
primary structures by which epidermal keratinocytes adhere to one another
Pemphigus vulgaris skin blistering and desquamation. Light microscopy show
intraepithelial cleavage with detached keratinocytes (acantholysis) and retained
keratinocytes along the basement membrane.
 Anti-histidyl-tRNA synthetase (Anti-Jo1) and anti-ANA  Polymyositis &
dermatomyositis with skin findings endomysial mononuclear inflammatory
infiltrate and patchy muscle fiber necrosis.
o These are paraneoplastic manifestation of an underlying malignancy
(especially adenocarcinoma) particularly lung, colorectal, and ovarian
cancers.
o Polymyositis causes symmetric proximal muscle weakness. Biopsy
reveals inflammation, necrosis, and regeneration of muscle fibers.
Overexpression of MCH class I proteins on sarcolemma leads to
infiltration with CD8+ T lymphocytes and myocyte damage.
  It is an inflammatory myopathy triggered by unknown possibly
viral, or antigens. Cell-mediated immune response

 Antimitochondrial antibodies are seen in patients with primary biliary cirrhosis,

which typically present with cholestatic symptoms
o Pruritis, jaundice, steatorrhea and abnormal hepatic enzymes. Liver
biopsy is characterized by lymphocytic infiltrates and destruction of
small and mid-sized intrahepatic bile ducts. This biopsy is similar to graft
vs. host disease highlighting the immunologic etiology of the disorder.
 Anti-smooth muscle antibodies autoimmune hepatitis,
o Middle-aged women as chronic progressive hepatitis.
 Hypocalcemia during thyroid surgery, the parathyroid glands can get injured
due to direct trauma, devascularization or inadvertent removal. Also,
autoimmunie hypoparathyroidism, sepsis, tumor lysis syndrome, acute
pancreatitis and severe vitamin D or magnesium deficiency may occur.
o Chvostek sign  facial muscle contraction elicited by tapping on the facial
nerve anterior to the ear.
o Trousseau sign  carpopedal spasm triggered by prolonged inflation of
blood pressure cuff around the arm.
o Muscle cramps, perioral paresthesias, hypotension and neuromuscular
hyperexcitability.

 Hibernating myocardium refers to the presence of the left ventricular systolic

dysfunction due to reduced coronary blood flow at rest that is partially or
completely reversible by coronary revascularization.
o Decreased expression and disorganization of the contractile and
cytoskeletal proteins, altered adrenergic control, and reduced calcium
responsiveness.

 Q# 11795, Gastric Varices  Short gastric veins drain blood from the gastric
fundus into the splenic vein. Pancreatic inflammation (pancreatitis, pancreatic
cancer) can cause a blood clot within the splenic vein, which can increase
pressure in the short gastric veins and lead to gastric varices only in the fundus
of the stomach.
 Esophageal varices  portal hypertension  collateral drainage from the portal
venous system to the azygos system.
 Left gastric vein  drains blood from upper stomach, lower esophagus into the
portal vein  from portal hypertension  causes both esophagus and gastric
varices.
 Superior mesenteric veins (SMV) blockage could lead to variceal formation in
the lower stomach, but not the upper regions. So pancreaticoduodenal vein
drains the pancreas and duodenum into the SMV. SMV drains lower stomach
from right gastroepiploic vein and small intestine.
 Lung transplantation chronic rejection  months to years, immune reaction
affects the small airways, causing bronchiolitis obliterans syndrome.
o Dyspnea and wheezing
o Acute rejection  pulmonary and bronchial vessels are the main targets
 pervascular infiltration with lymphocytes, macrophages, and plasma
cells, diffuse lymphocytic infiltration
 Renal allograft rejection  chronic rejection  months to years, worsening
hypertension and slowly progressive rise in serum creatinine.
o Obliterative intimal thickening, tubular atrophy, and interstitial vascular
fibrosis.

 AR probability of it being transmitted  an unaffected individual with

unaffected parents who has a sibling affected by an AR condition has a 2/3
chance of being a carrier for that condition.
o 2/3 of being a carrier, transmit the mutant allele ½
o 2/3 x 1/3 = 1/3

 CD14 a surface marker for monocyte-macrophage cell linage  caseating

granuloma in TB caused by macrophages.

 DNA polymerase 1 has both 5’-3’ exonuclease activity and 3’-5’ exonuclease
activity  can remove RNA primers by using the 5’-3’ exonuclease activity that
DNA polymerase 3 lacks.

 Intussusception intermittent, severe, colicky abdominal pain, “current jelly

stools, and sometimes palpable mass in the right lower abdominal quadrant.

 Q#2047, Schizoaffective disorder  psychosis must occur in the absence of

major mood episodes, but mood symptoms must be present for the most of the
illness.
o > 2 weeks but < than 1 month.
o Major depressive or bipolar disorder with psychotic features, psychotic
symptoms occur exclusively during manic or depressive episodes, but
when the patient is not having a mood episode than there are not
psychotic symptoms.

 Norepinephrine stimulates cardiac ß1 adrenoreceptors, which utilize the cAMP

signal transduction pathway  increase in cAMP concentration within the
cardiac myocytes

 Complete molar pregnancy  empty ovum fertilized with a haploid sperm

sperm is then duplicated with the paternal genetic complement 23X  46XX
genotype.
o No fetal structures large edematous and disordered chorionic villi 
clusters of vesicular structures  bunch of grapes
 o Pelvic pain and vaginal bleeding, uterus is larger than expected for
gestational age, ß-hCG extremely high  due to trophoblastic
hyperplasia.
o Ultrasound swiss cheese or snowstrome
 Partial molar pregnancies have 69XXX or 69XXY  fertilization of an ovum by 2
sperms
o Contain fetal tissue and normal placental villi intermixed with hydropic
villi and edematous villi with focal trophoblastic proliferation, and
normal appearing villi.

 Positive skewed  tail shifted to the right +Pos side.

o Mean>median>mode
 Negative skewed  tail shifted to the left –Neg side
o Mode>median>mean

 Helicobactor pylori infection and nonsteroidal anti-inflammatory drug (NSAID)

use causes proximal duodenal ulcers, these bacteria found in the gastric antrum
will likely lead to duodenal ulcers due to increased gastric acidity.

 Zollinger-Ellison syndrome ZES  ulcers beyond the duodenal bulb  multiple

ulcers and ulcers refactory to therapy. Abdominal pain/acid reflux, and diarrhea.
This is usually associated with MEN type 1 so check calcium and prolactin levels.
o Elevated gastrin levels that rise in response to exogenous secretin
administration, in contrast to secretin inhibiting release of gastrin from
the normal gastric G cells.
o Parietal cell hyperplasia with enlargement of gastric rugal folds due to
hypersecretion

 Class 1 antiarrhythmics  sodium channel binding strength is 1C> 1A > 1B.

o 1C demonstrates the most use dependence, and class 1B drugs have the
least. They are strong use-dependence by prolonging the QRS duration to
a greater extent at higher heart rates during exercise. They are used to
treat atrial fibrillation.

 Chest tube for drainage of pleural effusion is placed through the skin and
subcutaneous fat into the 4th and 5th intercostal space in the anterior axillary or
midaxillary line.
o Tube traverses through  serratus anterior muscle, intercoastal muslces,
and parietal pleura.

 Alpha-1 antitrypsin (AAT) deficiency  severe panacinar emphysema due to

unchecked destruction of alveolar walls and liver disease
o Intrahepatocyte accumulation of polymerized AAT molecules can
progress to cirrhosis and heaptocelluar carcinoma.
o Reddish pink with PAS and resist digestion by diastase
 Pulsus paradoxus  decrease in systolic blood pressure of >10 mmHg with
inspiration. Korotkoff sounds
o Seen in cardiac tamponade, severe asthma, COPD, and contrictive
pericarditis.
o Treatment  beta-adrenergic agonists control acute asthma and COPD
exacerbations by causing bronchial smooth muscle relaxation via
increased intracellular cAMP.

 Seborrheic keratosis is a benign epidermal tumor that presents as a tan or

brown, round lesion with well-demarcated border and stuck on appearance.
o Cause not fully known, but rapid onset and multiple oone of these can
mean undiagnosed internal malignancy (leser-Trelat sign).
 Vitamin B2 Riboflavin  component of favins FAD and FMN
o Used as cofactors in redox reactions
o e.i Succinate dehydrogenase reaction in the TCA cycle.
 Vitamin B6 used in transamination eg ALT, AST.

 Peau d’orange is an erythematous, itchy breast rash with skin texture changes
analogous to an orange peel.
o Inflammatory breast cancer is caused by cancerous cells obstructing
lymphatic drainage due to spread of the dermal lymphatic spaces.

 Proliferation signals activate CDK4 (cyclin-dependent kinase 4), resulting in

hyperphosphorylation of the Rb protein. Because hyperphosphorylation Rb is
inactive, cells are allowed to transition unchecked from the G1 phase to the S
phase in the cell cycle.

 Hot tub folliculitis  caused by self-limited Pseudomonas aeruginosa infection

of the hair follicles that tends to occur in minor outbreaks following exposure to
a pool or spa in which the chemicals have not been maintained at appropriate
concentrations.

 Dihydroergotamine  ergot alkaloid used to tread acute migraine headaches 

may induce vasospastic angina (prinzmetal angina) as it constricts the vascular
smooth muscle via stimulation of both alpha-adrenergic (partial agonist) and
serotonergic receptors.
o Treatment is cessation of smoking and vasodilator therapy (nitrates,
calcium channel blockers).

 Mallory-weiss tears account for about 10% of cases of upper GI hemorrhage.

o Occur due to increased intraluminal gastric pressure due to retching,
vomiting, or other abdominal straining.

 Sucrose  fructose + Glucose

 Lactose  Galactose + Glucose, lactose intolerance  abnormality in gene
expression process.
 Maltose  Glucose + Glucose
 Essential Fructosuria  fructokinase deficiency  urine will test positive for
reducing sugar due to presence of unmetabolized fructose  some of the dietary
fructose load is converted by hexokinase to fructose-6-phosphate, which can
then enter glycolysis; this pathway is not significant in normal individuals.

 Congenital toxoplasmosis  transplacental infecetion (acquired in utero).

o Classic triad  intracranial calcifications, hydrocephalus, and
chorioretinitis.
o Mothers should avoid cat feces to help prevent exposure to toxoplasma.
 When flow is reduced by a factor of 16, the radius of the lumen is decreased to
r/2 (50% of the original radius).
o Blood flow is directly proportional to the vessel radius raised to the
fourth power.
o Resistance to the blood flow is inversely proportional to the vessel radius
raised to the fourth power.
 Flow (Q) = P1 – P2 x r^4/ nL
 Flow (Q) = P1 – P2/R =constant
 Flow = r^4
 Flow/16 =(r^4/16) = (r/2)^4

 Nitroglycerin is primarily a venodilator. It decreases preload which decreases

myocardial oxygen demand and thereby treats angina pectoris.
o Large veins are the most susceptible and modest effect on arteriolar
dilation , which can cause a decrease in systemic vascular resistance
and CO.
o Patients taking daily maintenance nitrates need to have a nitrate-free
period everyday to avoid tolerance to the drug.
o Avoid in patients with Hypertrophic cardiomyopathy (increased outflow
tract obstruction), RV infarction (reduction in preload, impairing cardiac
output), and phosphodiesterase inhibitors sildenafil (synergism increases
risk of severe hypotension).

 Hepatic metabolism and clearance desired  then the drug needs to have a high
lipophilicity. (high Vd, good penetration into CNS).

 AV nose ventricular pacemaker  interarterial septum near the opening of the

coronary sinus.

 Porcelain gallbladder  chronic cholecystitis  multiple gallstones,

o Dystrophic intramural deposition of calcium salts in the setting of chronic
inflammation.
o Increased risk of adenocarcinoma of the gallbladder.
 Acute acalculous cholecystitis  acute inflammation of the gallbladder in the
absence of gallstones.
o Usually occurs in critically ill patients (sepsis, severe burns, trauma,
immunosuppression) due to gallbladder stasis and ischemia.
o Fever, right upper quadrant pain and leukocytosis.

 Treatment choice for diabetic ketoacidosis is intravenous normal saline and

insulin and replace potassium, these pts have increased serum K+ and decreased
intracellular K+
 Increase serum bicarbonate and sodium and decrease serum glucose, osmolality
and potassium

 Rapidly progressive glomerularnephritis RPGN

o  antibodies to glomerular basement membrane anti-GBM  linear IgG
and C3 on immunofluorescence.
o Anti-GBM (target alpha3-chain of collagen type IV) cross-react with
pulmonary alveolar basement membrances  pulmonary hemorrhage 
Goodpasture syndrome.
o Pauci-immune RPGN  no immunoglobulin or complement deposits.
 Have Antineutrophil cytoplasmic antibodies ANCA in their serum.
 Wegners granulomatosis with polyangiitis or microscopic
polyangitis 
 a patient with nasal ulcer (or sinusitis and hemoptysis) that
is not healing, new onset oligouria, high serum creatinine
level  antibodies to neutrophils protease 3 C-ANCA

 Beta-thalassemia affects beta-chain production and can be caused by a variety of

DNA mutations affecting the transcription, processing, and translation of beta-
globin mRNA.
o Increased formation of A2 and in some patient’s hemoglobin F.
o DNA replicates normally despite the mutation in the beta-globin gene, it
is not until the DNA is transcribed into the mRNA that hemoglobin
production becomes abnormal.
 DNA synthesis defect mutations are noted in megaloblastic anemias.

 Proliferative diabetic retinopathy  Increased formation of new blood vessels at

the optic disc is the characteristic feature of proliferative diabetic retinopathy.

o Blurry vision, black spots, floaters, and decreased peripheral vision.

 Glaucoma  A form of optic neuropathy characterized by increased intraocular

pressure associated with increased production or decreased outflow of aqueous
humor.
 o Latanoprost (prostaglandins)  increases outflow of aqueous via
uveoscleral pathway and are the preferred treatment for open-angle
glaucoma.
o Carbonic anhydrase inhibitors (dorzolamide)  decrease the formation
of HC03- in the ciliary body  leading to decreased sodium and fluid
transport and subsequently decreased production of aqueous humor due
to vasoconstriction in the ciliary body.
o Alpha-adrenergic agonists (eg, brimonidine)  inhibit production of
aqueous humor due to vasoconstriction in the ciliary body.
o Beta-blockers (timolol)  decrease production of aqueous humor.

 Strawberry hemangiomas (capillary hemangiomas)  benign vascular tumors of

childhood. Appear during the first few weeks of life and grow rapidly, and
regress by 5-8 years of age.
 Cherry hemangiomas  benign vascular proliferation in adults. Small bright red
cutaneous papules that appear in adulthood.
o Dilated capillaries and post-capillary venules in the papillary dermis and
do not regress spontaneously.
 Spider angiomas  in pregnancy, liver diseases, and pts taking OCP’s or
estrogen supplements.
o Dilated cutaneous arterioles present as central papule with radiating
blanching capillaries.
 Cavernous hemangiomas  at birth or develop later in life.
o Soft blue compressible masses up to a few cm in size. Large dilated
vascular spaces/malformation that m/c within the brain parenchyma;
carry an increased risk of intracerebral hemorrhage and seizure.
o M/c benign liver tumor  consists of blood filled vascular spaces of
variable size lined by a single epithelial layer. Biopsy not advisable as the
procedure has been known to cause fatal hemorrhages and is of low
diagnostic yield.

 Brachiocephalic vein obstruction  formed by the union of right sbuclavian

vein and right internal jugular vein. It drains the ipsilateral jugular and
subclavian veins.
o Obstruction is similar to SVC syndrome, but only on one side, from apical
lung tumor or and external compression
 Ride-sided face and arm swelling, engorgement of subcutaneous
veins on same side of the neck.

 A Kegels exercise targets the lavetor ani to improve support around the urethra
and bladder. Lavetor ani muscle is part of the pelvic floor muscles.
 A patient with hyperthyroidism (graves disease)  taking antithyroid drugs
(methimazole, propylthiouracil) presenting with sudden onset fever and sore
throat
o Should raise suspicion of agranulocytosis with the SE of the drugs.
 o Completely discontinue and drugs and do a CBC count to confirm
diagnosis.
o Both these drugs inhibit thyroid peroxidase, but PPU also decreases
peripheral conversion of T4/T3.
 So give to patients with life=threatening thyroid storm
 Thyroid peroxidase  responsible for the oxidation of iodide to
iodine, the iodination of thyroglobulin tyrosine residues, and
the iodotyrosine coupling reaction that forms T3 and T4.
Antibodies against thyroid peroxidase are present in more than
90% of patients with autoimmune (hashimoto’s) thyroiditis.s

 MRSA  resistant to all ß-lactam antibiotics  including beta-lactamase-

resistant antibiotics,
o Has an altered penicillin-binding protein in its peptidoglycan cell wall
that does not bind ß-lactams effectively.
o Penicillins  structurally similar to D-alanine-D-alanine  inhibit
transpeptidase by binding covalently to its active site.  failed synthesis
of bacterial peptidoglycan cell wall.

 Neck of the fibula or trauma to the lateral aspect of leg  injury to the common
peroneal nerve as it courses superficially and laterally to this structure.
o Weakness in foot dorsiflexion and eversion
o Impaired sensation over the lateral leg and dorsal foot (top of the foot)
and lateral shin, “PED” peroneal, everts, dorsiflex
 Tibial nerve injury, knee trauma  courses through the popliteal fossa
o Impaired planter flexion and inversion, and decreased sensation at the
sole (bottom of the foot). “TIP” Tibial, inverts, Planterflex

Diabetes medications
 Thiazolidinediones  pioglitazone and rosiglitazone  Intracellular nuclear
receptors
o Activates transcription regulator (modulation) PPAR-gamma, decreasing
insulin resistance, and increases adiponectin levels so insulin secretion
can increase.
o SE Fluid retention/heart failure precipitation and weight gain & edema.
o Check liver function tests.
o This drug is dependent on alteration of gene expression and subsequent
protein synthesis; there can be a delay in action of several days to few
weeks.
 Sodium-glucose cotransporter 2 (SGLT2) inhibitors  Canagliflozin,
dapagliflozin  oral anti-diabetic agents that work by decreasing proximal
tubular reabsorption of glucose therapy promoting urinary glucose loss.
o SE urinary tract and genital mycotic infections due to glucosuria,
symptomatic hypotension.
 o Avoided in patients with moderate to severe renal impairment due to lack
of efficacy and increased risk of adverse effects.
 Sulfonylyureas  increase insulin release from pancreatic beta cells  long-
acting meds causes hypoglycemia (glyburide, glimepridie)
 Meglitinides short acting glucose-lowering meds that act by closing the
ATP=dependent K+ channels in the pancreatic beta cell membrane induces
depolarization and stimulating insulin release. Give with meals for postprandial
glucose control
o Works by membrane ion channels.
 Metformin  noncompetitive inhibitor of mitochondrial glycerol-3-phosphate
dehydrogenase, an enzyme important for maintaining the hepatocellular redox
state.
o Molecular target: Intracellular mitochondrial enzymes.
 Acarbose, miglitol  decrease enzyme activity of disaccharidases found on the
plasma membranes of the intestinal brush border.
o Surface membrane-bound enzymes

 Q# 0628, Q# 0721, Hematogenous osteomyelitis  metaphysis of long bones

most common in children due to the slower blood flow and capillary fenestrae in
this region, due to Staphylococcus aureus infections.
o Without proper treatment infection can progress to chronic suppurative
osteomyelitis.
o In adults the vertebral body is the most common location for
hematogenous osteomyelitis  Potts disease  caused by
mycobacterium tuberculosis.

 Chlamydia trachomatis serotypes L1-L3 cause lymphogranuloma venereum, a

sexually transmitted disease characterized initially by painless ulcers with later
progression to painful inguinal lymphadenopathy (buboes).

 Pertussis  Paroxysmal cough lasting >2 weeks associated with post-tussive

emesis or inspiratory whoop after a severe coughing episode.
o Considered in adults who have not booster’s vaccinations.

 Schistosomiasis freshwater sources that contain snails infected with

schistosoma larvae.
o S. japonicum and S. mansoni cause intestinal/hepatic
o S. haematobium causes urinary

 Janeway lesions  nontender, macular, and erythematous lesions typically

located on the palms and soles. Usually in patients with acute infective
endocarditis.
o Result of septic embolization from valvular vegatations, which are
composed, of bacteria, neutrophils, and necrotic material and
subcutaneous hemorrhage.
 o Infective endocarditis can result from rheumatic heart disease that
resulted in chronic valvular inflammation and scarring.
 Rheumatic  Aschoff bodies  macrophages with abundant
cytoplasm and central, slender ribbons of chromatic (Anitschokow
cells)
 Valvular vegetation’s with destruction of the underlying cardiac
tissue.
 Fever, progressive weakness, dyspnea
 Macroscopic vegetations consist of fibrin and platelets on
the surface with RBC debris, WBC, and clusters of
microorganisms embedded deep within the lesion.
 Rupture of chordae tendineae is a complication of endocarditis or myocardial
infarction, it is not a risk factor for development of IE.

 Elastin  rubber-like properties due to extensive cross-linking between elastin

monomers, facilitated by lysyl oxidase.
o Early onset lower-lobe predominant emphysema due to excessive
alveolar elastin degradation.

 Q# 1684, Caudal regression syndrome  Sacral and lumbar spine agenesis 

flaccid paralysis of the legs, dorsiflexed contractures of the feet, and urinary
incontinence.
o Due to poorly controlled maternal diabetes

 Calcium-sensing receptors (CaSR) are transmembrane G-protein coupled

(metabotropic) receptors that help regulate the secretion of parathyroid
hormone in response to changes in circulating calcium levels.
o Bind calcium to CaSR  inhibiton of PTH release
o Low calcium  increased PTH release
 Familial hypocalciuric hypercalcemia is a benign autosomal dominant disorder
caused by defective calcium-sensing receptors in the parathyroid gland and
kidneys
o Mild asymptomatic hypercalcemia, reduced excretion of calcium and
normal or mildly high PTH.

 ADHD = inattentive, distractible, disorganized, forgetfulness, hyper-talkativeness

o Norepinephrine and dopamine are the key neurotransmitters involved in
pathophysiology, reduced levels of these in the prefrontal cortex.
o Treatment  methylphenidate and amphetamines  increasing release
of norepinephrine and dopamine from vesicular storage sites and
blocking norepinephrine and dopamine reuptake

 ACE inhibitors and angiotensin II receptor blockers have an additional

protective effects on the remodeling that is independent of blood pressure
 o They significantly reduce mortality in patients with systolic HF and are
therefore recommended in all such patients.
o They inhibit chronic angiotensin II-mediated adverse cardiac remodeling
that occurs with HF, which provides an additional mortality benefit.

 Hypothalamus is located in the diencephalon  it regulates the temperature,

appetite, emotion, growth, and circadian rhythm.
o Ventromedial  monitors blood glucose and is thought to be the center
of satiety (fullness)  lesions here cause hyperphagia and obesity.
o Later nuclei  signals hunger, lesions here can result in loss of appetite.

 Sarcoplasmic reticulum Ca2+-ATPase pump SERCA transfers Ca2+ from the

cytosol to the lumen of the sarcoplasmic reticulum at the expense of ATP
hydrolysis.
 Calcium efflux from the cardiac cells prior to relaxation is primarily mediated via
a Na+/Ca2+ exchange pump and Sarcoplasmic reticulum Ca2+-ATPase pump.

 CO poisoning increases carboyhemoglobin concentrations and reduces oxygen

unloading from the hemoglobin in the tissues, but it does not affect the partial
pressure of dissolved oxygen PaO2 and does not precipitate
methemoglobinemia.

 Health insurance plans:

o Health maintenance organization (HMO)
 Low monthly premiums, low copayments and deductibles, and low
total cost for the patients.
 Limited panel of providers, requiring referrals, and denying
payment for services that do not meet the established guidelines
o Point-of-service (POS) plans:
 Require pts to have a primary care provider and obtain referrals
for specialty consultations.
 Pts may see out-of-network providers,
 Higher premiums than HMO’s and significant costs to see out of
network specialists.
o Preferred provider organization (PPO):
 Most flexible choices both in-network and out-of-network.
 Higher premiums and deductibles.

 Ethylene glycol ingestion  toxic acute tubular necrosis with vacuolar

degeneration and ballooning of the PCT.
o High anion gap metabolic acidosis and increased osmolar gap, and
calcium oxalate crystals in the urine.

 ARDS  increased pulmonary capillary permeability.

 o Decreased lung compliance, increased work of breathing, worsened
ventilation to perfusion mismatching
o Deposition of fibrin, blood, and exudate in the alveolus from
Atelectasis injury which causes hyaline membrane
o But normal pulmonary capillary wedge pressure, but increased
alveolar dead space and hypercapnia.

 ADH acts on the medullary segment of the collecting duct to increase urea
and water reabsorption

 Intra-abdominal infections are polymicrobial with B. Fragilis and E. coli being

the most prominent organisms isolated

 Internal hemorrhoids  covered by columnar epithelium  innervated by

inferior hypogastric plexus

 External hemorrhoids  modified squamous epithelium  Inferior rectal

nerve a branch of the pudendal nerve.

 Renal artery stenosis  renal hypoperfusion and activation of RASS.

o Modified smooth muscle (juxtaglomerular) cells of the afferent
arteriole of the afferent glomerular arterioles synthesize renin.
o Chronic renal artery stenosis will cause hypertrophy and hyperplasia
of the juxtaglomerular cells.

 Some patients with non-small cell lung carcinoma (neuroendocrine origin)

(NSCLC) harbor a chromosomal rearrangement that creates a fusion gene
between EML4 (echinoderm microtubule-associated protein-like 4) and ALK
(anaplastic lymphoma kinase). This results in a constitutive active tyrosine
kinase that causes malignancy.
o This is similar to CML, the BCR-ABL fusion protein with tyrosine
kinase activity.

 Q# 11779, Giant cell arteritis (temporal arteritis, large vessel arteritis) 

o Polymyalgia rheumatica occurs in more than half of patients with
temporal arteritis. It is characterized by myalgias of the neck, torso,
shoulder, and pelvic girdle pain and morning stiffness. Fatigue, fever,
and weight loss may also occur. Occurs exclusively in patients older
than 50.
o Mononuclear vision loss is a common complication of temporal
arteritis.
o Erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP)
have very high sensitivity for this disease.
 o Cell mediated primary mechanism underlying giant cell arteritis –
production of cytokines  IL-6 (fever) is an important driver of this
process and closely correlates with the severity of symptoms.

 Oseltamivir  neuraminidase inhibitor useful in treatment and prevention of

both influenza A and B virus infections.
o Impairs the release of newly formed virions from infected host cells
and impairs viral penetration of mucous secretions that overlie the
respiratory epithelium
o Major adaptive immune mechanism that prevents reinfection with the
influenza virus include anti-hemagglutinin antibodies. Not
Neuraminadase because they are not the main source of protection
against reinfection although they have some protective effect
(decrease extent of viral invasion and shedding).

 Measles presents with fever, cough, rhinorrhea, and conjunctivitis followed

by a maculopapular rash that spreads on the face and spreads downwards.
Koplik spots are pathognomonic for measles and characterized by tiny white
or blue-gray lesions on the buccal mucosa.

 Failure to acidify lysosomes would lead to deficient expression of MHC class

II bound to foreign antigen and subsequent lack between antigen presenting
cells and T cells.

 Gout  increased frequency in patients with activating mutations involving

phosohoribosyl pyrophosphate synthetase due to increased production and
degradation of purines.
o Neutrophils are the primary cells responsible for the intense
inflammatory response seen in patients with gout.

 N-myc is a transcription factor that is by definition, capable of binding DNA,

because of its DNA-binding ability, N-myc can be detected by DNA probes.
o N-myc is overexpressed in Burkitts lymphoma.

 Candida infections
o Local defense against Candida is performed by T cells, whereas
systemic infection is prevented by neutrophils.
 Common in patients who are HIV positive
o Neutropenic individuals are more likely to have the systemic form of
the disease.
 Disseminated candidiasis
 Lower extremeties 
o Superficial lymphatic system
 Medial tracks  runs up to the superficial inguinal lymph
nodes, bypassing the popliteal nodes.
  Lateral tracks superficial nodes and popliteal nodes.
o Lesions from the medial foot cause inguinal lymphadenopathy,
whereas, lateral lesions are more likely to cause lymphadenopathy in
both the popliteal and inguinal areas.

 Mothers who are positive for HBsAg and HBeAg have a high risk of
transmitting hepatitis B virus during delivery. Infected neonates experience
high levels of HBV replication, demonstrate mildly elevated liver enzymes,
and are at high risk for chronic infection >90%.

 Dandy-walker malformation development anomaly characterized by

hypoplasia/absence of the cerebellar vermis and cystic dilation of the 4 th
ventricle with posterior fossa enlargement.
o Developmental delay and progressive skull enlargement
(macrocephaly) during infancy. Also, cerebellar dysfunction and non-
communicating hydrocephalus (common symptom is CN 6 palsy ) due
to atresia of the foramina of luschka and magendie, (elevated
intracranial pressure irritability, and vomiting.
o Hydrocephalus in infants  macrocephaly, poor feeding  enlarged
ventricles  if untreated leads to stretching of the pyramidal tracts,
developmental delays and seizures  muscle hypertonicity.

 Arteriovenous malformation  development of vascular lesions that usually

present at age 10-30 with intracranial hemorrhage, seizures, headache or
focal neurologic deficits

 Coronary sinus communicates freely with the right atrium and will become
dilated secondary to any factor that causes increased right atrial pressure.
The most common cause is pulmonary hypertension leading to elevated right
heart pressures.
o It’s a venous drainage from the myocardium traverses that delivers
deoxygenated blood to the right atrium

 Ribavirin mechanism of action is multifactorial 

o Lethal hypermutation to RNA viruses
o Inhibits RNA polymerase directly by ribavirin triphosphate
o Inhibits inosine monophosphate dehydrogenase by depleting
intracellular pools of GTP by ribavirin monophosphate
o Inhibits viral RNA guanyltransferease and methlytransferase resulting
in defective 5’cap formation on viral mRNA transcripts and, therefore
inefficient viral translation.
o Enhances Th1-cell mediated immunity while it inhibits Th2 cytokine
production, thus modulating a more effective immune response.
 Treats HCV and RSV in children use palivizumab
 SE: hemolytic anemia and severe teratogen
 Nose bleeds  irritation of the highly vascular mucosa at the anterior nasal
septum. Anterior nasal septum contains the kiesselbach plexus that is an
anastomosis of anterior ethmoidal, sphenopalantine, and superior labial
arteries.
o The most common nosebleed is picking at it in the anterior
compartment and the way to stop it is through direct compression of
the nasal alae in the nasal septum or cautery silver nitrate of the area.
o Bleeding from the posterior nose is more severe and does not usually
stop with cautery treatment.

 Tabes dorsalis  degeneration of dorsal columns and dorsal roots of the

spinal cord.
o Loss of proprioception and vibration senses, ataxia, and Argyll
Robertson pupils may be seen.
o Severe tabbing pains in his extremities.
 Live attenuated oral (sabin) poliovirus vaccine produces a stronger mucosal
secretory IgA immune response thatn deos the inactivated polipvorus (salk)
vaccine.
o The increase in mucosal IgA offers immune protection at the site of
viral entry by inhibiting attachment to intestinal epithelial cells.
o Difference between sabin (live) or salk (killed) vaccine is the duodenal
luminal IgA.

 Probability of at least 1 event turning out differently is given as 1-P (all

events being the same). 1-(0.95^8) for 1 standing for that one event that
turns different than the rest.

 High levels of dietary aflatoxin exposure from high dietary mold of

Aspergillus growing on food in certain temperatures is associated G:C T:A
transversion in codon 249 of the p53 gene, a mutation thought to greatly
increase the risk of hepatocellular carcinoma.
o Allergic bronchopulmonary aspergillosis ABPA due to aspergillus
fumigatus may complicate asthma and can result in transient
recurrent pulmonary infiltrates and eventual proximal bronchiectasis
with eosinophilia. Forms a fungus ball within a preexisting lung cavity.

 Autism spectrum disorder  Refuses to play with other children or go to

their homes, has temper tantrums when not allowed to watch his favorite
movie repeatedly.

o Impaired social communication/interactions and restricted/repetitive

interest or behaviors

 Cytosolic acetyl-CoA carboxylase converts acetyl-CoA to malonyl-CoA during

the rate-limiting step of de novo fatty acid synthesis.
 o Malonyl-CoA inhibits the action of mitochondrial carnitine
acyltransferase (an enzyme of the fatty acid degradation step right
before the carnithine shuttle), which prevents the transfer of acyl
group into the mitochondria and inhibits the beta-oxidation of newly
formed fatty acids.
o Malonyl-CoA inhibits this step in the fed-state so no beta-oxidation is
necessary.
o So the steps is that when there is excess ATP in the liver than inhibits
isocitrate dehydrogenase  leads to high levels of citrate in the
mitochondria which is than transferred to the cytosol via citrate
shuttle and cleaved by ATP citrate lyase to form acetyl-CoA (fatty acid
synthesis). Than upregulation of Acetyl-CoA carboxylase (rate-
limiting enzyme) converts acetyl-CoA to malonyl-CoA which than
inhibits and malonyl-coA inhibits b-oxidation by inhibiting carnithine
acyltransferase.
o Carnithine deficiency impairs fatty acid transport from the cytoplasm
into the mitochondria, preventing B-oxidation of fatty acids into the
acetyl CoA. This leads to cardiac and skeletal myocyte injury (lack of
ATP from citric acid cycle) and impaired ketone body production by
the liver during fasting periods.

 T-tubules are uniformly distributed in skeletal muscle fibers and ensure

that a depolarizing signal reaches each fiber at the same time. They transmit
depolarizing signals to the sarcoplasmic reticulum and trigger the release of
calcium
o A lack of T-tubules in some myofibrils would lead to uncoordinated
contraction of individual fibers.

 ETEC  LT, Cholera-like toxin and heat stable enterotoxin

o LT activated adenylate cyclase  increased intracellular cAMP and ST
activates cGMP  increased intracellular cGMP.
o Watery diarrhea.

 ARB’s  Losartan, Candesartan, Valsartan

 Only Muscarinic blockade leads to flushed skin and mydriasis even when
using an anti-histamine, so not H1 blockade, but a muscarinic blockade.

 Celiac disease abdominal pain, diarrhea, vomiting, and weight loss

o Crypt hyperplasia, villous atrophy in duodenum (diagnostic biopsy),
and intraepithelial lymphocyte infiltration.
o Treatment gluten-free diet resolves symptoms

 Patients with heart failure CHF exacerbation and significant fluid overload
should be treated with intravenous loops diuretics  most potent type of
 diuretic and provide the maximum amount of diuresis in shortest period of
time.
o Compensatory activation of RAAS and Sympathetic nervous system
results in increased afterload from excessive vasoconstriction, excess
fluid retention, and deleterious cardiac remodeling.

 Attributable risk percent (ARP) in exposed represents the excess risk in the
exposed population that can be attributed to the risk factor. Easily derived
from the relative risk RR.
o ARP exposed = 100 x [(RR-1)/RR]

 pO2 in the left atrium and ventricle is lower than that in pulmonary
capillaries due to mixing of oxygenated blood from the pulmonary veins with
deoxygenated blood arising from the bronchial arteries and thebesian veins.

 Speed of hemoglobin movement on gel electrophoresis is

o Hemoglobin A > hemoglobin S > Hemoglobin C

 Hepcidin is a polypeptide synthesized by the liver that acts as the central

regulator of iron hemostasis.
o High iron levels  synthesis of hepcidin
o Low iron levels  increase intestinal iron absorption and stimulate
iron release by macrophages.

 Cromolyn and nedocromil  mast cell-stabilizing agents that inhibit mast

cell degranulation independent of the triggering stimulus.

 Erythrocytosis is defined as a hematocrit level >52% in men and 48% in

women. Measuring the RBC mass is necessary to distinguish between
absolute from relative erthrocytosis.
o Absolute, Normal RBC mass  plasma volume expansion like
transfusion or IV fluids
o Relative  high RBC mass

 Accessory nipples are the most common congenital breast anomaly resulting
from failed regression of the mammary ridge in utero. They are usually
asymptomatic but can become tender along with breast tissue during times
of hormonal fluctuations.

 Alzheimer disease  early-onset APP on Ch21, presenilin 1 and presenilin 2

o Late-onset  Apolipoprotein E4 genotype.
o Hippocampus is the area of the brain demonstrating the greatest
degree of atrophy in this disease.
o Treat with Donepezil, Vitamin E, and memantine (NMDA receptor
antagonist.
 o Amyloid plaques/neuritic plaques and neurofibrillary tangles which
are aggregates of hyperphosphorylated tau protein.

 Mitral valve prolapse (with or without regurgitation) is the most common

predisposing condition for native valve infective endocarditis (IE) in
developed nations. Rheumatic heart disease remains a frequent cause of IE in
developing countries.  defects in mitral valve connective tissue proteins
predispose to myxomatous degeneration of the mitral leaflet and chordae
tendineae.

 Respiratory distress syndrome in neonates with the use of concentrated

oxygen therapy may be complicated by retinopathy of prematurity.
o Abnormal retinal neovascularization is a major cause of blindness in
developed nations

 The supraspinatus tendon is vulnerable to injury due to impingement

between the acromion and the head of the humerus.
o Supraspinatus tendionpathy is the most common cause of rotator cuff
syndrome.

 HPV 16 and 18 are strongly associated with anal and cervical squamous cell
carcinoma. HIV infection increases the prevalence of HPV infection and risk
of anal carcinoma.
o Risk is augmented with homosexual men.
o Condyloma acuminatum  itchy, few, small, red weeping and painless
bumps on the shaft of the penis, after applying 5% acetic acid the
lesions turn white (cauliflower-like appearance).

 Obesity, particularly morbid, central obesity, can cause a pattern of extrinsic

restrictive pulmonary function tests. Most common indicator of obesity-
related disease is 
o Reduction in ERV, and FRC, Total and residual lung volumes are
reduced also.
o Also decrease in FEV1, FVC, and TLC
 However in COPD  FEV1 is <50%, FVC normal or mildly decreased
o TLC, RV are increased with emphysema are due to destruction of
interalveolar walls.

 Wide fixed splitting of S2  ASD  creates a left-to right shunt cuz of high
pressure in left atrium  increased blood flow through pulmonary artery.
o Laminated medial hypertrophy
o Shunt can reverse  Eisenmenger syndrome
  TCA’s tricyclic antidepressant overdose  cardiac arrhythmias and
refractory hypotension  inhibition of fast sodium channels in cardiac
myocytes is thought to be the major underlying cellular event.

 ACA  supply medial portion of the 2 hemispheres (frontal and parietal) 

o Occlusion  contralateral motor/sensory deficits of the lower
extremities, behavioral changes, and urinary incontinence.

 Addison’s Disease  Adrenal insufficiency  patients not able to increase

glucocorticoid production in response to acute stress (illness, surgery).
o Adrenal crisis  severe hypotension, abdominal pain, vomiting,
weakness, and fever.
o Treatment aggressive fluid resuscitation and immediate
glucocorticoid supplementation or dexamethasone.

 Medullary chromaffin cells (catecholamines) are stimulated by Ach released

by sympathetic preganglionic neurons.

 CGD chronic granulomatous disease  recurrent bacterial and fungal

infections with catalase positive organisms.
o 5 catalase pos+ organisms  Staphylococcus aureus, Burkholderia
cepacia, Serratia marcescens, nocardia, and Aspergillus. BANS!

 Theophylline (methylxanthines)  seizures and tachyarrhythmias is the

major cause of morbidity and mortality.

Vasculitis:
 Takayasu arteritis  Pulseless disease in lower extremites typically affects
the aortic arch, coronary, and renal arteries (large vessels). Occurs in females
of Asian decent less than 40 years of age. Medial granuloma is seen
o GCA and Takayasu artritis have similar presentation
 Giant cell arteritis or Temporal arteritis  Large vessels  granuloma
inflammation of the media, develops in patients older than 50.  Jaw
claudication, headache, facial pain, and vision loss.
 Leukocytoclastic vasculitis  microscopic polyangiitis, microscopic
polyarteritis, hypersensitivity vasculitis  segmental fibrinoid necrosis of
the small vessels
o Microscopic polyangiitis and polyarteritis nodosa PAN have similar
presentation.
 PAN  segmental transmural necrotizing inflammation of medium to small-
sized arteries. Smudgy eosinophilic deposit (fibrinoid necrosis)  immune
complex vasculitis.
o Renal artery involvement is prominent, heart,liver and GIT are
involved, but the lung is very rarely involved.
 Thromboangiitis obliterans or Buerger’s disease (segmental thrombosing
vasculitis  small and medium sized arteries  tibial and radial arteries 
seen among heavy smokers onset prior to age of 35  hypersensitive to
intradermal injections of tobacco extracts.

 Potter sequence  renal anomaly  decreased fetal urine output leading to

oligohydramnios  no amniotic fluid  compression of the fetus, pulmonary
hypoplasia,

 Cholestatic liver disease can cause malabsorption and nutritional deficiencies

of fat-soluble vitamins.

 Organophosphates  inhibit breakdown of Ach  cholinergic excess.

 Atropine  Anticholinergic agents  block post-junctional Ach receptors,
antidote for organophosphates.
 Botulinum toxin inhibits Ach release from the presynaptic neurons. 
descending skeletal muscle paralysis.

 Cushing syndrome 
o Exogenous glucocorticoids
o ACTH-secreting pituitary adenomas, ^ACTH
 Suppresses with high dose dexamethasone
o Ectopic production of ACTH (paraneoplastic), ^ACTH
 Does not suppress with any dose of dexamethasone
o Primary adrenocortical hyperplasia, malignancy -> low ACTH 
cushing syndrome

 Hydrogen bonds are the principal stabilizing force for the secondary
structure of proteins
 Intermittent muscle pain reproducibly caused by exercise and relieved by
brief period of rest defines claudication.
o It is almost always the result of atherosclerosis of larger, named
arteries. Fixed stenotic lesions produced by atheromas, lipidp-filled
intimal plaques  stenosis prevents sufficient increases in blood flow
to exercising muscles, resulting in ischemic muscle pain.

 Pulmonary fibrosis present with gradually progressive dyspnea and bilateral

reticulonodular opacities on chest x-ray. PFT  restrictive pattern and lung
biopsy shows patchy interstitial lymphocytic inflammation and fibrosis of the
alveolar walls

 Enterobius vermicularis  school-age children with perianal pruritus 

diagnose with scotch tape test  Albendazole 1st line treatment and pyrantel
pamoate for pregnant patients.
  Treacher-Collins syndrome  Neural crest dysfunction  mandibular
hypoplasia, facial abnormalities  abnormal development of the first and
second pharyngeal arches.

 HBV surface antigen must coat the HDV antigen before it can infect
hepatocytes and multiply.

 Urachus is a remnanat of the allantois that connects the bladder with the yolk
sac during fetal development. Failure of the urachus to obliterate at birth
results in a patent urachus  discharge of urine from the umbilicus 
Straw-colored discharge from umbilicus.

 Q# 1900 Androgenetic alopecia  Polygenic with variable expressivity 

m/c hair loss in both males and females. The pattern and severity of the
baldness depend on both hormonal (circulating androgens) and genetic
factors and very between males and females.

Hearing loss
 Normal hearing  Rinne’s test Air conduction better than bone conduction
o Tuning fork weber’s test lateralizes to the midline of both ears
 Sensorineural hearing loss  Rinnes test Air conduction is better than
bone conduction
o Weber’s test lateralizes to the unaffected ear.
o R AC>BC, W unaffected ear
 Conduction hearing loss  Rinne’s test  in affected ear bone conduction is
better, in unaffected ear  air conduction is better
o Weber’s test  lateralizes to the affected ear.

 Elderly patients with dementia or hemiparesis may have dysphagia, which is

a risk factor for aspiration pneumonia. Dependent lung consolidation is
commonly seen in aspiration pneumonia.

 Fabry’s Disease  alpha-galactosidase A deficiency causes accumulation of

the sphingolipid globotriaosylceramide.
o Neuropathic pain and angiokeratomas, renal failure, left ventricular
hypertrophy, transient ischemic attacks in adulthood.

 Conversion disorder (functional neurological symptom disorder) 

neurological symptoms that are incompatible with a neurological disease.
 Somatic symptom disorder  excessive anxiety & preoccupation with ≥1
unexplained symptoms

 Piriformis syndrome  passes through the greater sciatic foramen and

involved in external hip rotation.
 o Injury or hypertrophy can compress the sciatic nerve in the foramen
 pain, tingling, and numbness in buttocks along the nerve
distribution.
 Injury to superior gluteal nerve  paralysis of gluteus medius and minimus
and tensor fasciae latae muscles.
o Pelvis to tilt downward towards contralateral side (positive
Trendelenburg sign)
 Injury to inferior gluteal nerve  paralysis of gluteus maximus 
o Difficulty in rising from a seated position and climbing stairs.

 Cholesteatoma  squamous (desquamated keratin debris) cell debris that

form a mass behind the tympanic membrane within the middle ear space.
o May erode ossicles, mastoid air cells  causes conduction hearing
loss, if mass grows sufficiently large, it can erode into the vestibular
apparatus or facial nerve, causing vertigo or facial palsies.

 Coagulase-negative staphylococcal infection initial empiric treatment should

include vancomycin due to widespread methicillin resistance, especially in
nosocomial infections.
o If susceptibility results indicate a methicillin-susceptible isolate, then
switch vancomycin to naficillin or oxacillins

 Dobutamine  ß-adrenergic agonist  ß1 receptors and weak ß2 and a1

receptors  Increased production of cAMP and cytosolic Ca2+  increased
myocardial contractility leading to increase in myocardial oxygen
consumption. Increased HR and cardiac contractility.

 Chronic myelogenous leukemia (CML)  decreased ALP, t(9,22), BCR-ABL

fusion gene or mRNA.
o Markedly elevated WBC counts, in neutrophils, increased myelocytes
and absolute basophilia and eosinophilia. Tyrosine Kinase inhibitor
 Leukemoid reaction  elevated or normal ALP.
o Benign leukocytosis that occurs in response to an underlying
condition such as severe infection/hemorrhage, malignancy, or acute
hemolysis.
o Increased neutrophil bands and early mature neutrophil precursors.
o Dohle bodies  light blue periphearal granules in neutrophils.
 Ribosomes bound with RER.

 Indirect hernias  Lateral to the inferior epigastric vessels 

o Failure of processus vaginalis to obliterate and internal inguinal ring
to close. Protrude through internal inguinal ring
o Infants, children, and young adults
 Direct hernias  medial to the inferior epigastric vessels 
 o Weakness in transversalis fascia in hesselbach’s triangle
o Protrude only through external inguinal ring, covered with external
spermatic fascia
o Older men
 Femoral hernias below the inguinal ligament and protrude through the
femoral ring  which is medial to the femoral sheath (femoral artery and
vein) and lateral to the lacunar ligament.

 Direct arteriolar vasodilators (hydralazine, minoxidil)  lower blood

pressure in uncontrollable patients  but trigger reflex sympathetic
activation and stimulate the RASS.
o SE: tachycardia and edema from fluid retention.
o To conteract the SE, they are given in combination with
sympatholytics and diuretics

TCA cycle
 GTP  synthesized by succinyl-CoA synthetase  succinyl-CoA to succinate
in TCA cycle.
o In gluconeogenesis  phosphoenolpyruvate carboxykinase uses GTP
to synthesize phosphoenolpyruvate from oxaloacetate. Gets its GTP
from succinyl-CoA synthetase
 NADH  synthesized by a-ketogluterate dehydrogenase  a-ketogluterate
to succinyl-CoA
 Isocitrate dehydrogenase  isocitrate to a-ketogluterate
 Malate dehydrodenase  malate to oxaloacetate
 During anaerobic conditons, NADH transfers electrons to pyruvate to
form lactate and regenerate NAD+. NAD+ is required to convert
glyceraldehyde-3-phosphate to 1-3-bisphosphoglycerate in glycolysis. So
NAD+ is regenerated when pyruvate is converted to lactate via LDH. So in
patients with LDH deficiency, glycolysis is inhibited in strenuously
exercising muscle as muscle cells cannot regenerate NAD+  muscle
breakdown, pain, and fatigue.
 FADH2  synthesized by succinate dehydrogenase  succinate to fumarate

 Multiple sclerosis  urge incontinence due to loss of central nervous system

inhibition of detrusor, hyperreflexias (bladder hypertonia) and contraction
in the bladder.
o Disease progression  leads to overflow incontinence  atonic
bladder.
o Loss of myelin sheaths and depletion of oligodendrocytes. Oligoclonal
bands of IgG may be detected in CSF.
 Paroxysmal breathlessness and wheezing in a young pts unrelated to
ingestion of aspirin, pulmonary infection, inhalation of irritants, stress, or
exercise  strong suspicion for extrinsic allergic asthma.
o Eosinophils  Charcot-leyden crystals
 o Eosinophil recruited by IL-5 secreted by Th2 cells.

 Panic disorder  unexpected panic attacks  abrupt surge of fear

accompanied by physical and cognitive symptoms.
o Shaky, dizzy, nauseated, sweaty
o Restrict their activities as a result of future attacks

 COPD  increased TLC and Residual volume which is the lung volume
remaining after maximal exhalation, everything else is decreased so a curve
would show that at the end which is the exhalation is larger than the normal
when everything else is not too off.

 Osteoporosis  fall femoral neck fracture in elderly patients

Osteonecrosis  blood supply to the femoral head  medial femoral
circumflex artery  which is derived from the femoral artery, this and lateral
femoral circumflex arteries.

 Insulin  stimulates glycogen synthesis by activating protein phosphatase,

an enzyme that dephosphorylates (activates) glycogen synthase.

 Strongyloides stercoralis infection begins following skin penetration by

filariforn (infectious) larve  diagnosed by finding rhabditiform
(noninfectious) larvae in the stool.
o Can result in hyperinfection syndrome by massive dissemination of
the organism leading to multiorgan dysfunction and septic shock.
o Treatment  ivermectin

 NBTE, nonbacterial thrombotic endocarditis  a form of noninfectious

endocarditis characterized  deposition of sterile platelet thrombi on
cardiac valves.
o Associated with advanced malignancies, chronic inflammatory
disorders (Lupus, antiphospholipid syndrome) and sepsis.
o Compared to infective endocarditis, vegetation’s can dislodge and
cause embolization, causing infarction.

 Wernicke encephalopathy  oculomotor dysfunction, ataxia, and confusion

all resolve after thiamine administration.
 Korsakoff syndrome  permanent memory loss, and confabulation
o Does not resolve even with treatment, so permanent.

 Thiazides (hydrochlorothiazide, chlorthalidone)  increase serum calcium,

uric acid, glucose, cholesterol, and triglyceride levels. They lower serum
sodium, potassium, and magnesium levels.
o Chlorthalidone is more potent in lowering blood pressure than the
others.
 Lead poisoning from homes built before 1978  lead inhibits ferrochelatase
and delta-aminolevulinic acid (ALA) dehydratase  this results in anemia,
ALA accumulation, and elevated zinc protoporphyrin levels.
o Neurotoxicity is also a significant long-term complication.

 Henoch-schonlein purpura  ages 3-10, IgA immune complex- mediated

vaculitis (type III hypersensitivity reaction)
o Follows upper respiratory or minor infections
o Palpable purpura, arthralgias, abdominal pain, and hematuria.
Intussusception may occur.
o Skin biopsy  IgA deposition in blood vessels
o Treatment is supportive.

 IVC courses through the abdomen and inferior thorax in a location anterior
to the right half of the vertebral bodies. Renal veins join the IVC at the level of
L1/L2 and common iliac veins merge to become the IVC at the level of L4.
o IVC filters are placed in patients with deep venous thrombosis or
pulmonary embolism who have bleeding problems and
anticoagulations are contraindicated for them.

 Renal cell carcinoma’s or clear cell carcinomas originate from the epithelial
cells of the proximal renal tubules.
o Macroscopically golden-yellow due to its high glycogen and lipid
content. High glycogen or lipid content that dissolves during routine
tissue preparation and makes it into a clear cell.
o Microscopically large rounded polygonal cells clear cells with
abundant cytoplasm and eccentric nuclei.
o Hematuria, flank pain and palpable mass occur in minority of people.
Nonspecific symptoms and paraneoplastic (polycythemia from
erythropoietin production by the tumor) syndromes are more
common. Lung metastatsis is m/c site for metastasis.
 Renal pelvis lining tumors  90% transitional cell carcinomas  papillary
tumors of urothelium supported by a thin fibrobascular stalk.

 Triptans are serotonin 5-HT 1b/5-HT 1d agonists used as abortive therapy

during an acute migraine. Beta-blockers, antidepressants (amitriptyline and
venlafaxine), and anticonvulsants (valproate and topiramate) are commonly
used for migraine prophylaxis.

 Carotid sinus pressure or massage stimulates the baroreceptors and

increases the firing rate from the carotid sinus  increase in
parasympathetic output and withdrawal of sympathetic output to the heart
and peripheral vasculature.
 o Carotid sinus  dilation of internal carotid artery  afferent sensory
fibers  glossopharyngeal nerve XI  the efferent sensory fibers 
vagus nerve X.
o Decreased blood pressure, decreased cardiac output
 In sensitive individuals, severe bradycardia can result and
hypotension and syncope.

 Ovarian torsion  twisting of infundibulopelvic ligament (suspensory

ligament).  Due to weight of a large adnexal mass 
o Leads to occlusion of blood and nerve supply  severe, acute pelvic
pain and ovarian ischemia
 Nausea, vomiting, and fever

 Vaginitis 
o Bacterial vaginosis  off-white discharge with fishy odor, no
inflammaition
 Clue cells with bacteria around it, pH>4.5
 Metronidazole or clindamyacin
o Trichomoniasis  yellow-green malodorous, frothy discharge,
inflammation,
 Motile trichomonads pH >4.5
 Metronidazole treat partner
o Candida  white cottage cheese like discharge, inflammation
 Normal pH, pseudohyphae
 Fluconazole

 Cytosine methylation is used in genomic imprinting  offspring’s genes are

expressed in a parent-specific manner. DNA methylation, DNA –muted or
silenced by attaching methyl groups to cytosine residues in the DNA
molecule.
o Cytosine and adenine are methylated in DNA replication  allows
mismatch repair enzymes to distinguish between old and new strands
in prokaryotes.
 DNA methylation at the CpG islands represses/silences
transcription of those genes.

 When a person gets in contact with TB the first time what happens is that the
small droplets of bacterial organisms deposit in the alveoli of the lower lung
fields. Then they get engulfed by alveolar macrophages , which allow for
the bacteria to proliferate intracellularly.
o After 2-4 weeks, ingested organisms by macrophages are presented to
specific Th1 lymphocytes.

 IgE-independent mast cell degranulation  opioids, radiocontrast agents,

and some antibiotics (vancomycin).
 o Diffuse itching, pain, bronchospasm, localized swelling (urticaria).

 Liquefactive necrosis  complete digestion and removal of necrotic tissue

with formation of cystic cavity.
o CNS injury  liquefactive necrosis.
o Abscess formation  bacterial or fungal infection  also liquefactive
necrosis.

 BNP  Endogenous natriuretic peptides promote vasodilation and

natriuresis and provide a beneficial counter-regulatory mechanism in
patients with heart failure. They are metabolized by the enzyme Neprilysin
inhibition of this enzyme improves outcomes in patients with chronic
systolic heart failure.
o Neprilysin inhibitors is a metalloprotease that cleaves and inactivates
endogenous peptides including natriuretic peptides Sacubitril
o BNP, ANP, an NO activate guanyly cyclase and increase conversion of
cGMP, sildenafil decreases the degradation of cGMP  all lead to
vascular smooth muscle vasodilation
o ANP secreted by atrial cardiomyocytes in response to atrial stretch
induced by hypertension or hypervolemia.

 Q# 11819, Osgood-schlatter disease  focal pain and swelling at the tibial

tuberosity of the knee. Repetitive quadriceps contraction and chronic
avulsion causes the proximal patellar tendon to separate from the tibial
tubercle.
o Patella fractures are most commonly due to a direct impact to the
anterior aspect of the knee, signs are acutely swollen knee, focal
patella tenderness, inability to extend the knee against gravity, and a
palpable gap in the extensor mechanism.

 Silicosis impairs the macrophage effector arm of cell-mediated immunity,

which is integral to the immune response against mycobacteria.

 Most important opsonins (coating proteins)  IgG and complement C3b.

o Occurs when host proteins bind to foreign cells such as bacteria and
coat the surface to enhance phagocytosis.

 Enveloped viruses sensitive to ether and other organic solvents, and they
lose their infectivity after ether exposure
 Non-enveloped viruses are resistant to action of ether.

 Congentital torticollis is typically noted by 2 to 4 weeks of age  child

prefers to hold the head tilted to one side. Resulted from a malposition of the
head in utero or birth trauma. They resolve with conservative therapy and
stretching exercises.
 Desmopressin (DDAVP)  treatment of hemophilia A and type 1 vWF 
increases circulating factor VIII and endothelial secretion of vWF to stop
bleeding. Also works on renal tubule collecting ducts increased aquaporin
channels to increase water and decrease urine output for diabetes insipidus
and nocturnal enuresis.

 HPV 6 & 11 small DNA virus verrucous genital warts  has a predilection
for stratified squamous epithelium  so it infects the true vocal cords the
only ones in the respiratory tract that’s stratified squamous epithelium.
o Infants born to mothers with warts can get respiratory papillomatosis
via passage from the birth canal  grow warts on the true vocal cords
which leads to weak cry, hoarseness, and stridor.

 LV pacemaker course through the coronary sinus atrioventricular groove

on the posterior aspect of the heart.

 MPTP toxic substance that induces parkinsonism-like syndrome by

destroying dopaminergic neurons in the CNS.
o A metabolite of MPTP produced by MAO type B  called MPP+ that
causes the neurological damage.
o Pretreat it with Selegiline an inhibitor of MAO type B to prevent
dopaminergic neuron damage.
o Selegiline, anticholinergics, amantadine are used to delay the
symptoms of parkinsons disease until they no longer produce control
of symptoms then levodopa/carbidopa are introduced  anxiety and
agitation are not decreased by adding carbidopa because it result
from more dopamine available to the brain.

 Chromaffin cells of the adrenal medulla and parafollicular C cells of the

thyroid originate from embryonic neural crest tissue.

 Osteoporosis  loss of total bone mass  trabecular thinning with few

interconnections normal serum calcium, phosphorus, and PTH.
 Hyperparathyroidism  subperiosteal resorption with cystic degeneration
 Vitamin D deficiency  excessive unmineralized osteoid low mineral
density
 Osteopetrosis  the persistence of primary unmineralized spongiosa in the
medullary canals

 Angiosarcoma (stewart-Treves-syndrome) usually results from axillary

lymph node dissection  results in chronic lymphedema involving ipsilateral
arm
o Usually happens after radical mastectomy.
  Reid index  ratio of thickness of the mucous gland layer in bronchial wall
submucosa to the thickness of the bronchial wall between the respiratory
epithelium and bronchial cartilage.
o (b/a+b+c)

NMBE 16 wrong answers:

 Use TNFa to treat failed Rheumatoid arthritis disease.
 Anal fissures  venous obstruction  increased red blood cell mass
decrease outflow from organ dude to hyperviscousity increased body mass
and blood volume in pregnant woman.
 Gastrin stimulates enterochromaffin cells to secrete acid.
 Bias measurements of the exposure  because the exposure status was
determined by interviewing the subjects. So the researcher is more biased
towards the exposure
 Pulmonary embolism  ventilation perfusion relationship in the right lower
lobe is dead space because the lung is getting air but is it not putting it in the
blood because of the obstruction
 Branching filamentous, gram+ rod causes respiratory problems and skin
abscesses, and CNS disease in immunocompromised  nocardia
o Pulmonary nocardiosis can present as cavitary pneumonia
(misdiagnosed as TB); branching gm+ organisms on sputum
examination.sx
 Berry aneurysm that includes oculomotor problems  from posterior
communicating aneurysm
 Ureteral calculus abdominal pain, nausea, vomiting, pain orginaties left
flank, radiates to the groin, high BP, pain in left lower quadrant of the
abdomen. Mildly hypoactive
 Spinal needle insertion between L-3 to L-4 vertebral arches  ligamentum
flavum
 During swallowing the glottis (vocal cords)  closed, immideately after
laryngeal irritation glottis is closed, and while coughing its open.
 Precontemplation not acknowledging that there is a problem
o Contemplation  acknowledging there is a problem but not willing to
change
o Preparation/determination  getting ready to change behaviors
o Action/willpower changing behaviors
o Maintenance maintaining the behavior changes
o Relapse  returning to old behaviors and abandoning new changes.
 Volume depletion in low urine output possible cause of dehydration with dry
mucous membranes
 Small cell carcinoma  neither glandular nor squamous  SIADH, so
hyponatremia normal body fluid volume, inappropriately concentrated
urine, low sodium and osmolality.
 Increased risk for liver injury because of induction of cytochrome P450
enzymes that activate acetaminophen to a hepatotoxic metabolite
 Type 1 hypersensitivity  immediate (min)
 Delayed (after 2-4 hours) due to release of cytokines and here
macrophages are the one releasing acute phase cytokines, IL-1, IL-6; TNFa
 49 year old woman, breast cancer, taking chemo 3rd-4th time, sensation to
pinprick fine touch decreased over the hands, wrists, ankles, and feet 
adverse affect of chemo  microtubules for axonal transport  vincristine
 peripheral neuropathy.
 Polycystic ovarian syndrome  hyperinsulinemia due to insulin resistance
from increased glucose from adipose tissue with increased glucose and
insulin (obesity), too much acne and facial hair  increased androgens  ^
LH &FSH & testosterone  oligomenorrhea, polycystic ovaries.
o Increased (endometrial hyperplasia) endometrial cancer 2nd to
unopposed estrogen and decreased progesterone secretion from
repeated anovulatory cycles.
 Leg in cast for a while  atrophy of myoctyes  increased protein
(cytoskeleton degradation)  protein degraded through proteasomes 
have to be modified through ubiquitination  increased polyubiquitination
in muscle cells.
 Puberty starts at the age of 8-13 in girls and 9-14 in boys, precocious puberty
starts before age 7.
 Vitamin D absorps calcium & phosphate in the gastrointestinal tract, ^ bone
mineralization at low levels, ^ bone resorption at high levels.
 Small cell carcinoma  lambart-eaton  proximal upper and lower
extremeity muscles that augments(gets better) with repetitive use,
o Small blue cell neoplasm, cytokeratin, chromogranin, and
synaptophysin.
 Obstructive bowels signs with GI bleeding = possible polyps.
Hyperpigmented macules + polyposis= peutz-jeghers  hamartomatous GI
polyps, hyperpigmentation of mouth/feet/hands/genitalia
o ^ risk of GI cancer.
 Clomiphene  prevents normal feedback inhibition and ^ release of LH and
FSH from pituitary, which stimulates ovulation  treatment for fertility due
to anovulation (PCOS).
o SE; hot flashes, ovarian enlargement, multiple simultaneous
pregnancies, visual disturbances.
 Q#2 -Horseshoe kidney  anomalous origins of multiple renal arteries to
each kidney. Inferior mesenteric artery
 I-cell disease  electron microscopy shows  dilated RER  failure of
transport of vesicles to the golgi  everything remains in the RER thus it
becomes dilated.
 Increase the pulmonary lymph flow by infusing 0.9% of saline for 5 minutes
because it increases hydrostatic pressure (not the osmolarity). So net
lymphatic increases and that should increase lymph flow.
 o Saline  ^ P hydrostatic in the capillaries  freely filtered 
increases filtration  increses fluid volume in the ECS  increases
flow of lymph.
 Diaphragmatic hernia  congenital defect pleuroperitoneal membrane 
m/c on left side due to relative protection of right hemidiaphragm by liver 
o Abdominal structures enter the thorax
o Bowel sound heard over the left hemithorax
o Multiple cystic-appearing areas on the left with decreased aeration on
the right  air in the intestine
 Occult blood test  low sensitivity
 Graft vs. host disease  Donor T lymphocytes reacting against host cells so
the donor graft must be irradiated before transplantation.
 Vinblastine attacks rapidly dividing cells  so resistant to permanent
(stable) cells  ventricular cardiac muscle fibers  heart cells do not divide
 Glycolytic intermediates that are indirectly inhibited by increasd glucose
concentrations  both pyruvate and 1,3-bisphosphoglycerate  so the
enzyme glyceraldehyde-3-phosphate dehydrogenase is inhibited
 Costochondritis  left-sided chest pain and tenderness, pain radiates to the
back and is exacerbated when she reaches over her head or behind her back.
 Leukotrienes LTC4, LTD4, LTE4 are cause asthma
o Tenderness to palpation 2 cm lateral to the midline and 10 cm below
the clavicle on the left.
 Resperidone  atypical antidepressant treatment for schizophrenia both
positive and negative symptoms
 Defect in pro-collagen synthesis  blue sclera  easily broken bones 
osteogenesis imperfect  impairment in bone matrix formation.
 Corticalspinal tract  ipsilateral movement, dorsal column  vibration,
prioperaception, spinothalamic tract pain and temperature.
 Severe abdominal pain after meals  unintentional weight loss, relieved
when she decreases the amount of food that she eats. Pedal pulses
diminished.  stenosis of the superior mesenteric artery
 Fish oil to treat triglycerides  Anagonizes VLDL cholesterol secretion
 Pseudofolliculitis barbae  razor burn after shaving, African American men
usually get it…
 Renal cell carcinoma  polycythemia, hypercalcemia, microscopic
hematuria, positive for epithelial membrane antigen and negative for
carcinoembryonic antigen
 Poliovirus is the simplest and most significant RNA virus = lacks 5’m7G cap
but is translated efficiently the host cell’s mRNA’s the 5’ end of poliovirus
RNA is extremely long-over 700 nucleotides – and is highly structured.
o Called internal ribosome entry site (IRES) and it directs translation of
the viral RNA without the 5’end cap.
 Morphine  is metabolized to active metabolites that accumulate caused by
overdose and deterioration
 ARDS in a newborn younger than 35 weeks old  caused by decreased
numbers of lamellar bodies  because surfactant is stored in lamellar bodies
in type 2 pneumocysts.
 Dilated cardiomyopathy  both ventriculars enlarged  S3 gallop, HF
holosystolic murmur  mitral regurgitation  systolic dysfunction
o Balloon appearance on CXR  eccentric hypertrophy
 Hypertrophic cardiomyopathy ventricular hypertrophy  ß-myosin
heavy-chain mutation  sudden death in athletes  S4, systolic murmur 
mitral regurgitation diastolic dysfunction
o Maneuvers that increase preload or afterload will decrease murmur
intensity by increasing LVED volumes and lessening outflow tract
obstruction  Valsalva, abrupt standing, and nitroglycerin.
o Dynamic left ventricular outflow tract obstruction is due to abnormal
systolic anterior motion of the anterior leaflet of the mitral valve
toward a hypertrophied interventricular septum towards the aorta.
 Restrictive cardiomyopathy thick fibroelastic tissue in endocardium 
diastolic dysfunction
o Causes Diastolic heart failure (DHF), with decreased ventricular
compliance with normal left ventricular ejection fraction and normal
LVED volume, and elevated LV filling pressures.
o TTR  protein produced by liver, carrier of thyroxine and retinol,
mutation in this gene  increases the tendency to misfold and
produce amyloid protein that infiltrates the myocardium (infiltrative
cardiomyopathy).
o Sarcoidosis, amyloidosis, hemochromatosis
 Hypertension taking already hydrochlorothiazide but not enough lowering of
the bp, and has DM  give ARBs or ACEI  because it’s good for pts that
have DM.
 Microglial cells clear necrotic tissue in the area of the brain with the damage.
 African American woman 70 years  Postmenopausal woman
osteoporosis  predisposing risk factor
 If only 4 measurements are taken  The range increases its width cause the
values that are out of range have a higher impact on the mean and the
deviation
o If 10 or more measurements are taken  the range decreases its
width because of less very high/very low values
 Syringomeliya  cape-like bilateral loss of pain and temperature sensation
in upper extremities  syrinx of the central region of the spinal cord from C4
to T5 distribution
o The syrinx damages the ventral white commissure, leading to bilateral
loss of pain and temperature of the arms and hands, also destruction
of the ventral horns due to extension of syrinx  flaccid paralysis and
atrophy of the intrinsic muscles of the hand,
o Damage of the spinal cord is usually in the center where the little
white dot or opening is at!
 o Associated with chiari malformation
o Also upper extremity lower motor neuron signs, and or lower
extremetiy upper motor neuron signs with scoliosis, loss of vibration
and position in the feet
 Differentiate syringomyelia from brown-sequard syndrome
which is a unilateral, contralateral loss of pain and
temperature below the level of the lestion.

 Heteroplasmy  variable expression in a population or even within a family

with one disease  mitochondrial inheritance
o MELAS  mitochondrial encephalopathy, lactic acidosis, stroke-like
episodes  secondary to failure in oxidative phosphorylation.
o Ragged red fibers.

 McArdle’s disease type V  deficiency in skeletal muscle Glycogen

phosphorylase (myophophorylase)  blood glucose not effected, no increase
in lactate during exercise, compared to pre-exercise values, so no breakdown
of glycogen to use glucose as an ATP, so glycogen phosphorylase problem to
break it down.
o Painful muscle cramps esp. after exercise, myoglobinuria, serum
creatine kinase increased,

 Left main coronary artery  branches into

1. Left circumflex coronary artery  supplies lateral/posterior walls of
left ventricle.
2. Left marginal artery
3. Left anterior descending artery (LAD)  supplies anterior 2/3 of
interventricular septum towards the apex of the heart and anterior
surface of left ventricle
 Right coronary artery (RCA) 
1. Right marginal artery  supplies right ventricle (SA & AV nodes)
2. Posterior descending/interventricular artery (PDA)  supplies 1/3 of
interventricular septum, post. walls of ventricles.
a. Inferior diaphragmatic surface of the heart is formed by the left
ventricle so occlusion of RCA  ischemia of inferior surface of
the heart
 Based on these finding, if you want to visualize the anterior interventricular
(LAD) artery  the tip of the angiographic catheter would need to be placed
into the orifice of left main coronary artery

 Infraspinatus and teres minor (adducts also) laterally rotates the arm
 Subscapularis  medially rotates and adducts arm
 Wegener polyangiitis granulomatosis  perforation of nasal septum, chronic
sinusitis, otitis media, mastoiditis, hemoptysis, cough, dyspnea, hematuria,
red cell casts
o Necrotizing granulomas in the lung and upper airway. C-ANCA post 
anti-proteinase
 Goodpastures syndrome  type 2 HSR  antibodies to GBM and alveolar
basement membrane  hematuria/hemoptysis  emergent plasmapheresis.
o IgG and C3 in glomerular capillary loops
 Ghrelin  hunghre  stimulates hunger, after the consumption of food, its
levels will start to drop
 Leptin  stimulates fullness, keeps you thin without leads to obesity, cuz
you will eat and not know when you are full…
 Radical prostatectomy  greatest risk of injury during removal of the
prostate is pelvic parasympathetic nerves (mediate pupil dilation and eyelid
elevation and retraction)  due to pudendal nerve damage.
 Due to exposure to smoking animals/humans have increased mucus
production and secretion but low ciliary clearance which results in mucus
plugs with no clearance and the macrophages function in the alveoli decrease
because macrophages exprese VEGF receptors and blockade of these
receptors drastically reduces the ability of macrophages to phagocytize
apoptotic cells which results in less clearance and more build up and plugs 
which leads to COPD.
o Mucus production increased
o Ciliary activity  decreased
o Macrophage function in alveoli  decreased
 End of Review for NBME 16 –

 Trypanosoma cruzi  Chagas disease  sedonary achalasia, megacolon, and

megaureter because parasite destroys myenteric plexi

 Naloxone  pure opioid receptor antagonist  treats opioid intoxication or

overdose binds mu, kappa, and delta receptors but has greatest affinity
for mu receptors.

 Krukenberg tumor  gastric signet ring cell tumor that metastasizes to the
ovaries
o Unintentional weight loss, epigastric pain, adnexal masses, and
anemia, unlike clear cell carcinoma which results in increased with
hematocrit.
o Large amounts of mucin with displaced nuclei (signet ring)
 Mutations that decrease positive charge of binding sites of 2,3-BPG increases
hemoglobin oxygen affinity  normally 2,3BPG binds positive sites and
decreases hemoglobin oxygen affinity to increase oxygen loading to tissues
o This mutation resembles hemoglobin F rather than hemoglobin A
  Normally hgbF binds oxygen higher to extract more oxygen
from the mother to have adequate supply of oxygen and
 Decreased oxygen loading  more oxygen extracting
from mother.

 Bone pain in older man with osteoblastic lesion of metastasis on imaging is

highly suspicicous of prostate cancer.

 Syphilis  vasa vasrum endarteritis and oblieteration  inflammation,

ischemia, and weakening of aortic adventitia.

 RANK receptor and RANK-ligant interaction  formation and differentiation

of osteoclasts
o Osteoclasts increases bone remodeling which is then followed by
increased osteoblastic activity, which forms poor-quality bone.
 Decrease in bone mass osteoporosis
 Osteoblasts  mesenchymal origin
o So Osteoprotegrin blocks the binding of RANK-L with RANK on
osteoclasts and decreases the formation and differentiation of
osteoclasts
o So when there is low estrogen states  osteoporosis results because
osteoprotegrin (OPG) (decoy receptor) is decreased which then
RANK-L binds on RANK receptors on osteoclasts and increases
osteoclast precursors and bone remodeling and decreased bone mass
results because of the poor quality bone made by osteoblasts that
followed osteoclast bone resorption
o RANK on osteoclasts, RANK-L is blocked by OPG
 Q#0987 Pagets Disease of bone -Osteoclasts originate from hematopoietic
progenitor cells  macrophage colony-stimulating factor and receptor for
activated nuclear factor kappa-ß ligand (RANK-L) play an important role in
osteoclast differentiation. Paget’s disease of bone is characterized by
increased numbers of abnormal osteoclasts, excessive bone turnover and
disorganized bone remodeling, eventually osteoblasts also increase as the
disease progresses.
o Deformity of long bones and hearing loss.

 Bisphosphonates  alendronate  Inhibit osteoclastic activity and reduce

both formation and resorption of hydroxyapatite  used for malignancy-
associated hypercalcemia, postmenopausal osteoporosis, pagets disease of
bone. SE  Corrosive esophagitis and necrosis of the jaw so stay upright for
30 mins after ingestion.
o Chemical structure similar to pyrophosphate and attach to
hydroxyapatite binding sites on bony surfaces to inhibit bone
resorption by mature osteoclasts.
 Cancer cells may develop the ability to splice out a particular exon that codes
for the transmembrane domain of the Fas receptor (FasR), converting it to a
soluble form that is not expressed on the cell surface, which allows the cells
to evade apoptosis.
o Extrinsic apoptotic pathway  Fas receptor-Fas ligand drives
programmed cell death via the cytotoxic T-cell mediated extrinsic
pathway.
 Also, defective binding of Fas-FasL interactions cause
lymphoproliferative syndromes
o Intrinsic apoptotic pathway  Bim, Bax, Bak  proapoptotic
 Bcl-2  antiapoptotic  Binds to and inhibits APAF-1 
APAF-1 normally binds cytochrome c  activates caspase 9 
initiates caspase cascade  leads to apoptosis
 Bcl-2 overexpressed in Follicular lymphoma t(14;18), so then
APAF-1 is overly inhibited by bcl-2  decreases caspase
tumorigenesis

 Polyhydramnios (excess accumulation of amniotic fluid)  increased

abdominal circumference due to decreased/impaired fetal swallowing which
can be caused by 
o Gastrointestinal obstruction (duodenal, esophageal, intestinal atresia)
and anencephaly.

 Aplastic anemia  toxic effect or autoimmune response  pancytopenia 

hypocellular bone marrow with abundant fat cells.

 On-off phenomenon with long-term treatment of parkinsons disease with

levodopa  decreased therapeutic window for levodopa from progressive
nigrostriatal neurodegeneration  drug response is unpredictable

o Nigrostriatal degeneration in Parkinson disease reduces activity of the

thalamus and its projections to the cortex, resulting in bradykinesia
and rigidity. Brain shows lewy bodies
 Patients with medically intractable symptoms of parkinsons
disease my benefit from high frequency deep brain stimulation
of the globus pallidus internus or subthalamic nucleus as it
promotes thalamo-cortical disinhibition with improved
mobility.

 Spleen  blood filter for removing circulating pathogens and major site of
opsonizing antibody synthesis. Splenectomy  increased infections with
encapsulated bacteria.
 Milrinone  selective phosphodiesterase-3 enzyme inhibitor (PDE-3) 
inotrophic agent in patient with refractory heart failure due to left
ventricular systolic dysfunction
o Decrease the rate of degradation of cyclic adenosine monophosphate
(cAMP) in cardiac tissues. So increased levels of cAMP promotes
calcium influx into the cardiac myocytes, which in turn increases
myocardial contractility.
o Also inhibits PDE-3 in vascular smooth muscle cells  systemic
arterial and venous dilation  decreased BP
o This drug is limited in patients with severe hypotension as it
decreases the blood pressure even more.

 HIT heparin induced thrombocytopenia  paradoxical thrombosis rather

than bleeding so all forms of heparin must be stopped.  It’s a serious
disorder caused by antibodies to heparin and platelet factor IV.
o Treat with direct thrombin inhibitors  Hirudin, lepirudin, and
argatroban.
o These patients need ongoing anticoagulation due to the presence of or
possibility of thrombosis.

 L5 radiculopathy occurs due to compression of the L5 nerve root usually as a

result of vertebral disc herniation (prolapse nucleus pulposus) or spinal
foraminal stenosis.
o Vertebral disc herniation  acute back pain, classically affects the S1
nerve, which results in  S1 radiculopathy as opposed to L5
radiculopathy.
o Spinal foraminal stenosis  back pain radiating down the leg with
sensory loss over the buttocks, lateral thigh and calf, and dorsal foot.
 Weakness on dorsiflexion, inversion, eversion, and toe
extension.

 High mutability of HIV-1 allows for the evasion of host humoral and cellular
immune responses and the development of resistance to anti-retroviral
drugs. In HIV replication cycle, polyprotein precursors are encoded by the
structural genes, (gag, pol, env). Only the env gene polyprotein product is
glycosylated to gp160 and proteolytically cleaved within the ER and Golgi
apparatus to form the envelop glycoprotein gp120 and gp41.
o Pol gene mutations  responsible for acquired resistance of HIV
reverse transcriptase inhibitors and HIV protease inhibitors.
o Env gene mutations  enable escape from host neutralizing
antibodies

 Active transports  requires hydrolysis of ATP and therefore an active

transport mechanism
 o Omeprazole or proton pump inhibitors suppress the activity of gastric
parietal cell H/K ATPase leading to an increase in the pH of the gastric
lumen.

 Inherited defects involving Interferon-gamma signaling pathway (IFN-g) 

disseminated mycobacterial disease in infancy or early childhood.
o Patients require a life-long treatment with antimycobacterial agents.

 Alanine  glucose is inhibited in increased concentrations of fructose 2,6-

bisphosphate within hepatocytes.
o F2,6bisphosphate activates PFK-1 increasing glycolysis and inhibits
fructose 1,6bisphosphatase decreasing gluconeogenesis.
o This is regulated by bifunctional enzyme complex:
 PFK-2 increases levels of F2,6BP in response to insulin  so
glycolysis favored
 Fructose2,6Phosphatase decreases its levels in response to
glucagon so gluconeogenesis is favored.

 Tetralogy of Fallot  RVH, overriding of the aorta, pulmonary stenosis, and

VSD.
o What determines the degree of cyanosis in these infants it the right
ventricular hypertrophy that leads to obstruction  right ventricular
outflow tract obstruction (harsh systolic ejection murmur in mid-left
upper sternal border)  degree of right to left intracardiac shunting
and resulting cyanosis.
o VSD usually accentuated during hand grip
o Anterior and cephalad deviation of the infundibular septum 
malaligned VSD with overriding aorta. Squatting increases systemic
vascular resistance (afterload) without changing peripheral vascular
resistance and it also decreases right – left shunting across the VSD,
which increases pulmonary blood flow and improves the oxygenation
status.

 Antriretroviral therapy  enzyme inhibitor drug during pregnancy reduces

the risk of perinatal transmission of HIV to 1-2% and is recommended for all
pregnant women with HIV.
o Infant born with oral thrush, interstitial pneumonia, and severe
lymphopenia during the first year of life. Mother to child vertical
transmission of HIV-1

 Frontal lobe injury  executive dysfunction and personality changes,

impairment of organizational, restraint, and motivational systems.
o Changes in social behavior, left-sided more often associated with
apathy and depression and right-sided lesions with disinhibited
behavior.
 Atazanavir  Protease inhibitors for HIV treatment  causes lipodystrophy
 which leads to cushings syndrome
o Hyperglycemia and inhibition of cytochrome P450
 Vascular smooth muscle cells VSMC’s are the only cells within atherosclerotic
plaque capable of synthesizing fibrous cap with extracellular matrix and
collagen. VSMC’s have PDGF and FGFs
o but first all this starts off with endothelial cell injury or dysfunction
 Endothelial cell dysfunction  macrophages & LDL accumulation  foam
cell formation  fatty streaks  Smooth muscle cell migration, proliferation,
extracellular matrix deposition  fibrous plaque  complex atheromas

 PrP normal cellular protein found in neuron and has a-helical structure 
undergoes conformational change to ß-pleated sheet  and accumulation
results and makes it resistant to proteases  prion disease  Cruetzfeldt-
jakob disease  vacuoles in gray matter spongiform encephalopathy.

 Hypothyroidism  decrased T4, increased TSH, and normal T3 in early

disease. Hypothyroidism itself can cause hypertension due to an increase in
peripheral vascular resistance.

 H band  contains only thick myosin filaments, it is part of the A band,

where thick filament have overlapped thin actin filaments.
 I band  contains only the thin actin filaments, no overlap
 M line  myosin attachment, Z line  actin attachment, A band overlap of
both myosin and actin, A band always stays the same length

 Transamination reaction  occur between amino acids and a-keto acid 

amino group transferred to the a-keto acid so it becomes amino acid. B
o Vitamin B6 pyridoxal phosphate serves as a cofactor for amino acid
transamination and decarboxylation reactions.

 Dengue viruses are single-stranded RNA viruses with 4 different serotypes.

Primary (first) infection can be asymptomatic or cause a self-limited disease
in most adults. Secondary infection is due to infection with a different viral
serotype and usually causes more severe illness.

 Androgen insensitivity syndrome  46, XY males, phenotypically females

due to androgen receptor defect. Minimal axillary or pubic hair, cryptorchid
testes no uterus, or ovaries.

 Mullerian aplasia as known as (vaginal agenesis or Mayer-Rokintansky-

Kuster-Hauser syndrome) no upper vagina (short vagina), variable uterine
development. 46, XX female’s normal ovaries and secondary sexual
characteristic.
 Leuprolide  GHRH  transient increase in LH and rise in testosterone, then
continuous use suppresses LH release and decreases testosterone
production which decreases testosterone conversion to DHT.

 Pregnancy increases the risk of venous thromboembolic disease due to

increased venous stasis, endothelial injury and hypercoagulability.
o Low-molecular-weight heparins such as enoxaparin are treatment of
choice, esp during early stages of pregnancy.

 Beta-blockers ameliorate symptoms of thyrotoxicosis by decreasing effect of

sympathetic adrenergic impulses on target organs and decrease peripheral
conversion of T4 to T3.

 Necrotizing enterocolitis  one of the most common gastrointestinal

emergencies affecting newborns that are premature and initiation of enteral
feeding happened  bacteria is introduced into the bowel and they
proliferate excessively due to compromised immune clearance.
o Pneumatosis intestinalis  air in the bowel wall, curvilinear areas of
lucency parallel to the lumen. Bloody stools, abdominal distention,
o Congested, gangrenous intramural gas collection, transmural
necrosis!

 Hyper-IgM syndrome  inability for B-lymphs to undergo isotype switching

from IgM to other immunoglobulins  IgD, IgG, IgE, IgA.
o Lymphoid hyperplasia and recurrent sinopulmonary infections.s
o Genetic absence of CD-40 ligand on T-lymphocytes or from a genetic
deficiency in enzymes responsible for the DNA modification that takes
place during isotype switching.

 Pulsion divertulosis  composed of mucosal and submucosal layers that are

covered by serosa.
 Meckel’s diverticulum  true, congenital  fetal development  contains all
3 gut layers  mucosal, submucosal, and muscularis
o Results from a failed obliteration of the vitelline (omphalomesenteric)
duct and usually presents with spontaneous but painless lower
gastrointestinal bleeding. Tc-pertechnetate localizes ectopic gastric
mucosa and its increased uptake is diagnostic for meckel
diverticulum.

 Vimentin  mesenchymal tissue

 Chromogranin  neuroendocrine
 cytokeratin  epithelial cells/skin
 Desmin  muscle
 GFAP neuroglia
  Neurofilaments  neurons

 HER2/neu oncogene  185-kD transmembrane glycoprotein  intracellular

tyrosine kinase activity and is a member of the family of epidermal growth
factor receptors.  Increase rates of breast and ovarian cancer.

 Airway resistance along the bronchial tree is:

o Increased in the trachea due the high surface diameter
o Increases even more in the medium sized bronchi
o And starts to decrease in the bronchioles and terminal bronchioles.

 SLE  Pancytopenia  autoantibodies against blood cells (type 2 HSR),

lupus nephritis (diffuse proliferative glomerulonephritis) caused by 
immune complex deposition within the glomerulus (type III HSR). Low
complement C3 and C4.

 Intestinal malrotation results  midgut undergoes incomplete

embryological counterclockwise rotation intestinal obstruction & midgut
volvulus (intestinal ischemia around blood vessels). Midgut rotation around
the superior mesenteric artery.

 CD8+ interacts with MHC class 1 proteins which are consistent of heavy
chain and ß2-microglobulin.
o MHC class 2 is consistent of alpha and beta polypeptide chains

 Inulin freely filtered so can be used to calculate a substance excretion rate

that is also freely filtered = excretion rate = filtration rate (total filtration
rate) – total tubular reabsorption rate.
 Excretion = (filtration + secretion) – reabsorption

Transplantation of organs:
 Graft vs. host  donor T cells attacks recipients organs (skin, liver, GI) 
develops diffuse maculopapular eruption that begins with palms, soles, back
and neck.
 Immediate type 1 HSR  vasodilation, vascular leakage, and edema
 Hyperacute  min to hours  type 2 HSR/preformed antibodies against
graft in recipient circulation  gross mottling and cyanosis and thrombotic
occlusion.
o Acute hemolytic transfusion reactions is a antibody-mediated (type II)
HSR caused by pre-existing anti-ABO antibodies that bind antigens on
transfused donor RBC’s. Subsequent complement activation results in
red cell lysis, vasodilation, symptoms of shock. Common findings
include fever, hypotension, chest & back pain, and hemoglobinuria.
 Acute  months <6  immune cells  type 3 HSR  humoral and cellular
deposition  either neutrophil infiltration or lymp infiltration
 Chronic  month-years T cells  delayed  vascular wall thickening and
luminal narrowing, interstitial fibrosis & parenchyma atrophy.

 Glucokinase  glucose sensor in pancreatic beta cells by controlling the rate

of glucose entry into the glycolytic pathway.
o AD, impaired insulin secretion with minimal or no defects in insulin
action, presents with noninsulin-dependent diabetes in lean young
adults.
o Mutations in the glucokinase gene are cause of maturity-onset of
diabetes of the young, MODY. Hyperglycemia in these groups is
usually mild, does not usually require medication and is not
associated with an elevated risk of long-term diabetic complications.

 P50 of hemoglobin is 26mmHg, while P50 of myoglobin is 1mmHg  this

indicates that myoglobin has a much higher affinity for oxygen than
hemoglobin.
o Hemoglobin dissociation curve is sigmoid, while myoglobin is
hyperbolic cuz it has only single heme group and binds oxygen tightly
o Hemoglobin molecule are structurally analogous to myoglobin, if
separated, the monomeric subunits will demonstrate a hyperbolic
oxygen-dissociation curve similar to myoglobin and it will be
hyperbolic instead of sigmoid
o So it will shift all the way to the left for tight affinity with oxygen.

 The liver is the second most common site of metastatic spread after the
lymph nodes because of its large size, dual blood supply, high perfusion rate,
and the filtration function of Kupffer cells.
o Multiple nodules throughout liver, and may replace more than 80% of
the hepatic parenchyma often resulting in marked hepatomegaly.

 Cocaine withdrawal  development of acute depression, fatigue, vivid

dreams, hypersomnia, and hyperphagia.
o Minor physical symptoms unlike in opiates, alcohol, and benzo’s.
o Opiate withdrawal  abdominal cramps, nausea, vomiting, yawning,
muscle aches, piloerection, lacrimation, dilated pupil
 Withdrawal is not life-threatening.
 Cocaine  indirect sympathomimetic by inhibiting the presynaptic reuptake
of norepinephrine, dopamine, and serotonin. Intoxication  agitation,
tachycardia, hypertension, light-responsive mydriasis due to increased
sympathetic activity. Cocaine is also potent vasoconstrictor that can cause
myocardial ischemia & atrophy of the nasal mucosa and septum.

 Prior history of attempted suicide is the strongest single factor predictive for
suicide, 5-6 more likely to make another attempt.
 As sample size n increases, the standard error SE decreases, so the
confidence interval becomes narrower and more precise.
o SD – reflects spread of individual values in a normal distribution
o SE of mean – reflects the variability of means and helps estimate the
true mean of underlying population.
o 95% CI  mean +/- 1.96*SE = mean +/- 1.96*SD/^n
o 99% CI  mean +/- 2.58*SE= mean +/- 2.58*SD/^n
o 68% 1 SD, 95% 2 SD, and 99.7% 3 SD’s.

 Loss of cardiomyocyte contractility occurs within 60 seconds after the onset

of total ischemia. When ischemia lasts less than 30 minutes, restoration of
blood flow leads to reversible contractile dysfunction (myocardial stunning),
with contractility gradually returning to normal over the next several hours
to days. However, after 30 minutes of total ischemia, ischemic injury
becomes irreversible.
 Systemic mastocytosis  abnormal proliferation of mast cells and increased
histamine release  hypersecretion of gastric acid by parietal cells in the
stomach  hypotension, flushing, rash, pruritis.
 Zollinger-Ellison secretes gastrin  peptic ulcers refractory to treatment
 Insulinoma  hypoglycemia
 Glucagonaoma  hyperglycemia with rash
 Somatostatinoma  diarrhea, cholelithiasis, hyperglycemia
 Vasoactive intestinal peptide  watery diarrhea, hypokalemia, achlorhydria

 Removal of excess cholesterol form the body occurs via excretion of free
cholesterol into bile and conversion of cholesterol into bile acids.
o When there is > cholesterol that can be made soluble then it
precipitates into crystals that form gallstones.
o High level of bile salts and phosphatidylcholine increases cholesterol
solubility and decreases risk of gallstones.
o Someone with gallstones has:
 High cholesterol content, low bile salts, and low
phosphatidylcholine

 HBV  accumulation of HBsAg  appears as finely granular, homogeneous,

dull eosinophilic inclusions that are ground glass appearance. Hepatocyte
necrosis (ballooning degeneration), apoptosis, steatosis, portal inflammation
with mononuclear inclusions with macrophages and lymphocytes.
 HCV  lymphoid aggregates within portal tracts and focal areas of
macrovesicular steatosis.

 Aspirin intoxication  traid of fever, tinnitus, and tachypnea, mixed

respiratory alkalosis and anion gap metabolic acidosis.
 o Both PaCO2 and HCO3- are outside the normal range suggesting
mixed with no compensatory response.
o At first these patients have respiratory alkalosis in the first 3 hours
o After 3 hours patient develops metabolic acidosis.

 Large cell carcinoma  undifferentiated, large polygonal tumor cells that

form solid sheets or nests. Located peripherally.
 Adenocarcinoma of the lungs  m/c lung cancer in general population. m/c
in woman and in nonsmokers, located peripherally and consists of tumor
cells with glandular/papillary structures.

 Papillary thyroid cancer branching papillary structures with interspersed

calcified bodies (psammoma bodies) & follicular hyperplasia with tall cells
forming intrafollicular papillary projections.
o The thyroid gland is one of the most radiation-sensitive, and radiation
exposure to the head and neck during childhood is the most important
risk factor for primary thyroid maliganancy.
 Reidels thyroiditis  hard nodule no symptoms  extensive stromal fibrosis
extending beyond the thyroid capsule.
 Subacute thyroiditis granulomatosis  de Quervain thyroiditis  painful
thyroid enlargement, follows illness  lymphocytic infiltrate with
macrophages and multinucleated giant cells.
 Hashimoto’s thyroiditis  mononuclear, parenchymal infiltration with well-
developed germinal centers. Hurthle cells (large oxyphilic cells filled with
granular cytoplasm).
 Deep brachial (profunda brachii) artery and radial nerve run together along
the posterior aspect of the humerus. Midshaft fractures of the humerus risk
injury to these structures.

 Isotype switching  germinal centers of lymph nodes  CD40 receptor on

B-cells with CD40 ligand on T-cells.

 Alanine is the major amino acid responsible for transferring nitrogen to the
liver for disposal. It is transaminated by alanine aminotransferase to
pyruvate with the amino group being transferred to a-ketogluterate to form
glutamate.
o Almost all aminotransferase anzymes use a-ketogluterate as the
amino group acceptor.
o Glutamine is then processed in the liver to form urea primary
disposal form of nitrogen in humans.

 Arsenic  inhibits lipoic acid vomiting, rice water stools, garlic breath and
QTc prolongation which can progress to torsades de pointes and it also
causes glycolysis to produce zero net ATP. It impairs cellular respiration.
Insecticides and contaminated water are common sources of arsenic.
 Dimercaprol is the chelating agent of choice  the sulfhydryl group of this
drug combines with arsenic and displaces the ions form the sulfhydryl
groups of enzymes involved in cellular respiration. Arsenic binds to
sulfhydryl groups, impairing cellular respiration via inhibition of pyruvate
dehydrogenase.
 Lead poisoning  EDTA, Deferoxamine  iron overdoses, Cyanide poisoning
 hydroxycobalamin, metheglobinemia  methylene blue, TCA’s  sodium
bicarbonate which works by increasing serum pH and extracellular sodium.

 Pyruvate dehydrogenase deficiency  X-linked  increased lactic acidosis,

and increased serum alanine in infancy,
o Treatment  ketogenic diet, lysine and leucine  only purely
ketogenic amino acids

 Menopause  average age 51  diagnosable after 12 months of

amenorrhea elevated FSH confirms diagnosis

 Pick disease  frontotemporal dementia  changes in personality/behavior

and abnormal speech. Frontotemporal brain atrophy of the frontal lobe
diagnosed with silver staining shows aggregates of tau protein (pick bodies).

 Northern blot  mRNA, Southern blot  DNA, Western blot  protein, DNA-
bound protein  southern blot

 Non-neoplastic polyps  hyperplastic, hamartomatous, inflammatory do not

progress into adenocarcinoma of the colon.

 Adenomatous polyps  Villous and tubular  villous is more likely to

progress to adenocarcinoma.

 Familial dysbetalipoproteinemia  defect in ApoE3 and ApoE4 found on TG

rich lipoproteins  liver cannot efficiently remove chylomicrons and VLDL
remnants from the circulation.
o Pancreatic lipase -> degradation of TG in small intestine
o Lipoprotein lipase  degradation of TG circulating in chylomicrons
and VLDL’s
o Hepatic TG lipase --> degradation of TG remaining in IDL
o Hormone sensitive lipase  degradation of TG stored in adipocytes.
o Lipoprotein lipase  needs CII degrades TG in chylomicrons and
VLDL

 Glycosylase (removes defective base), endonuclease, lyase, DNA polymerase,

and ligase
 Iron absorption in duodenum and proximal jejunum  gastrojejunostomy
results in iron deficiency anemia  so supplement long term
o Also for gastric bypass, malabsorption of B12, folate, fat-solube vit D,
and calcium can occur.

 Neonatal abstinence syndrome  neurologic, gastrointestinal, and

autonomic symptoms  tremors, irritability, diarrhea, poor feeding
mother was taking opiates while pregnant so baby is dependent on it, so has
to be replaced now and slowly weaned off  treatment is with methadone or
morphine  long-half life. Also a drug of choice for maintenance treatment
of opioid abuse  long half-life, and a good bioavailability and given once-
daily oral dosing prolonged effects suppress withdrawal symptoms and
cravings, allowing for productive patient functioning.

 Q# 803, Hirschsprung disease  abnormal migration of neural crest cells

during embryogenesis  failure to pass meconium within 48 hours of birth.
o Bowel filled with stool, rectum empty. Rectal biopsy reveals
aganglionic segment of bowel.
o Rectum and anus always involved.
o Biopsy narrowed part of submucosa.
 Vs. Meconium ileus caused by CF  distal small bowel obstruction due to
abnormally dehydrated meconium, persistent, treatment-resistant infectious
pneumonias, bronchiectasis, or cor pulmonale account for most deaths due
to CF. Abnormalities in chloride, sodium, and water transport by the ductal
epithelium of intestinal mucous glands cause isotonic dehydration of the
lumen contents. This results in secretion of abnormally viscous mucus into
the small bowel.

 Green discoloration of pus or sputum due to bacterial infection 

myeloperoxidase/ blue-green heme based enzyme released from neutrophil
azurophilic granules and forms hypocholorous acid. Step pneumo
 Klebsiella  current jelly sputum extravasation of RBC’s and hemoglobin.

 Short acting benzodiazepines  Lorazepam, oxazepam, and temazepam and

not metabolized by hepatic metabolism so preferred in pts with hepatic
impairment. Triazolam has a short-half lie  but undergoes hepatic
metabolism and not preferred in pts with hepatic impairment.

 Zolpidem hypnotic  for insomnia and is like the same as a benzodiazepine

mechanism of action but with a lower risk of tolerance

 Damage to posterior pituitary  only transient central DI, whereas damage

to the hypothalamic nuclei causes permenant central DI. Usually following
car accidents.
 Blood flow in the LV myocardium is maximum during diastole and minimum
during systole. LV wall pressure is increased during this time all other organs
have a constant blood flow except in RV, which has a lower pressure than LV.

 Cephalic and gastric phases  stimulate gastric acid secretions

 Intestinal influences  reduce gastric acid secretion.

 Type 2 pneumocytes  regeneration of alveolar lining following damage and

surfactant production.

 Latissimus dorsi  innervated by thoracodorsal nerve.

 Biceps & brachioradialis reflex done at the mid elbow  innervated C5, C6
 C7,C8  triceps reflex

 Clostridium difficile requires additional contact precautions, including hand

washing with soap and water, nonsterile gloves thrown away after use, and a
gown for any patient contact because  hand sanitizers do not kill the
spores. Same with MRSA, VRE, and Scapies.
o Causes pseudomembraneous colitis  white/yellow plaques with
fibrin on colonic mucosa.
o Hand dygiene is the single most important measure to reduce the risk
of transmission of hospital-acquired infections such as MRSA.

 Etanercept  TNF-a inhibitor to treat rheumatoid artritis  it is a decoy

receptor protein for TNF
o Monoclonal antibody  mab, receptor molecule  cept, kinase
inhibitor  nib
o May reactivate latent TB

 Reperfusion injury  cell membrane damage  CK increases with a dislodge

of thrombus

 Ixodes Tick transmit both babesiosis and Lyme disease.

 Medication noncompliance with ARBs and diuretics  block RAAS  which

increases renin  so if no change in renin and no increase is seen  meds
are not complaint
o ARBs  angiotensin II blocker, so it’ll have increased renin,
angiotensin I, angiotensin II, decreased aldosterone and no change for
bradykinin.

 PCR  requires primers that are complementary to the regions of DNA

flanking the segment of interest, and it also requires thermostable DNA
polymerase, deoxynucleotide triphosphate, and a source of DNA template
 strand. It amplifys target DNA segments via repeated replication. It requires
2 primers that are complementary to the flanking regions of the target DNA
sequence. DNA Pol synthesizes DNA strans in a 5’to3’ direction, so that new
nucleotides are added only to the 3’hydroxyl end of the elongating strand.

 Narcolepsy treatment  scheduled daytime naps and psychostimulants such

as modafinil for daytime sleepiness

 Hyaline arteriolosclerosis  Homogenous deposition of eosinophilic hyaline

material in the intima and media of small arteries and arterioles, PAS positive
stain.
o Due to poorly controlled HTN or Diabetes Mellitus.

 Cerebellar hemisphere are responsible for motor planning and coordination

of ipsilateral extremities via their connections with lateral descending motor
systems. Lesions result in ipsilateral dysdiadochokinesia, limp dysmetria,
and intention tremor.

 It is important to have high sensitivity in all screening tests.

 Sertoli cells produce MIF mullerian-inhibiting factore that prevents the

development of female internal genitalia and leydig cells secrete testosterone
necessary for development of male internal genitalia.
o Absence of sertoli cells will produce internal genitalia of a female
because the mullerian ducts are not inhibited so the paramesonephric
ducts goes on to develop.
o Testosterone  DHT  external male genitalia.
 Incidence = # of new cases/total population at risk
 T lymphocytes deficiency  poor development of lymph node paracortex.
 Macrophages that from granulomas giant cells are activated by CD4+ Th1
lymphocytes.  IFN-gama, IL-12, TNF-a is critical for formation of
granulomas.

 LV free wall rupture usually occurs within 5-14 days after an initial
myocardial infarction and presents with sudden onset of chest pain,
profound shock, and rapid progression to death.
o Slit-like tear in the infarcted myocardium, with a preference for the
left ventricle due to higher systolic pressures.

 Tetrahydrobiopterin (BH4) is a cofactor used by hydroxylase enzymes in the

synthesis of tyrosine, dopamine, and serotonin.
o Phenylketonuria can result from BH4 deficiency due to
dihydropteridine reductase deficiency.
 Intellectual diability results, serotonin deficiency, and
hyperphenylalanemia,
  Treatment  low phenylalanine diet and supplementation
with BH4.

 Hypocretin-1 (orexin-A) and hypocretin-2 (orexin-B)  neuropeptides

produced in the lateral hypothalamus to function to promote wakefulness
and inhibit REM sleep.
o Narcolepsy patients with cataplexy have undetectable levels of
hypocretin-1 in their CSF.

 Children develop gender identity by age 4  but experimenting with

opposite-gender activities is a normal form of exploration.
o Incontrast- gender dysphoria is the prolonged and intense feeling that
one is the opposite gender from birth sex.

 Vertigo  sensation that the room is spinning with intractable vomiting 

most commonly due to dysfunction within the vestibular system.

 Creatinine and inulin are freely filtered and completely excreted in the urine
regardless of its serum concentration.
 PAH  filtered and actively secreted into the tubular lumen so even at low
serum concentration, urinary excretion exceeds total filtered amount.
o PAH is primarily secreted into the nephron by the PCT, but some is
also freely filtered by the glomerulus. Any portion of the nephron
does not reabsorb it; therefore, Bowman’s space has the lowest PAH
concentration.
 Glucose is filtered and reabsorbed entirely as its below the maximum tubular
reabsorption, TmG, but at higher plasma concentrations, glucose is excreted
into the urine when filtered amount exceeds the TmG.
o Incases of inhibition of sodium-coupled, carrier mediated transport of
glucose by the proximal tubule would cause the glucose clearance to
approach the value of the GFR, which is typically estimated by
calculating the clearance of inulin.

 Foramen cecum is usually in the anterior tongue in the median sulcus, the
part where taste is innervated by facial nerve VII, and sensation is innervate
by mandibular division of the trigeminal nerve V3.

 Infection from burns are caused by pseudomonas aeruginosa  treat with

ticaracillin, piperacillin, ceftazidime, cefempime, ciprofloxacin, levofloxacin,
imipenem, meropenem

 HSV-1 encephalitis  potentially fatal complication from primary infection

or reactivation of latent disease.
o Necrosis of temporal lobe, which can result in aphasia and personality
changes in addition to classic features of encephalitis
  Headache, fever, altered mental status, seizures.

 Thiazide diuretics (hydrocholorthiazide)  increase calcium reabsorption

form the nephron  treats patients with calcium renal stones by decreasing
calcium excreted in the urine  contraindicated in hypercalcemia.

 Urethral injury  foley catheter is contraindicated because it can worsen the

injury  first perform a retrograde urethrogram to assess urethral integrity.
o Posterior urethra  usually injured in pelvic fractures
 Prostatic and membranous segment and membranous segment
is relatively unsupported by the adjacent tissues and is the
weakest point of the post. urethra  inability to void with a
full bladder sensation, a high-riding boggy prostate, and blood
at the urethral meatus.
o Anterior urethra  injured in straddle injuries.
 Bulbous and penile segments

 Which parameters should be similar between the systemic and pulmonary

circulation during rest and exercise?
o Circulatory system is a continuous circuit and therefore the volume
output of the LV must closely match the output of the RV. This
balance is necessary to maintain continuous blood flow through the
body and exists both at rest and during exercise. Blood flow per
minute. Normal cardiovascular response to exercise is increased
cardiac output, vasodilation in exercising muscles, end-diastolic
volume and HR are both increased while end-systolic volume and
systemic vascular resistance are decreased.

 COX-2 inhibitors (celecoxib)  anti-inflammatory effect with less risk of

bleeding and GI ulceration. Recommended for patients at risk for GI
complications such as prior peptic ulcer disease.

 Rabies binds Ach receptors after the virus stays in the local for a period of
days or weeks then binds it and travels retrograde to the CNS. In the US bats
are the source of rabies, prophylactic vaccination is recommended for
individuals at high risk for exposure to rabid animals or their tissues. Vaccine
is inactivated vaccine consists of various rhabdovirus strains grown in tissue
cell culture and then inactivated. Eosinophilic cytoplasmic inclusions (negri
bodies) in the hippocampal neurons which are consistent of nucleocapsid
material from the rabies virus.

 Vitiligo skin lesion  absence of melanocytes in the skin/loss of epidermal

melanocytes due to something effecting it, whereas in albinism there is
normal number of melanocytes but produce decreased number of melanin or
 never made it to their destination because of failure of neural crest cell
migration.

 Combined use of non-dihydropryidine L-type Ca2+ channel blockers

(verapamil, diltiazem) and ß-adrenergic blockers (atenolol) can have
additive negative chronotropic effects yielding severe bradycardia and
hypotension.
o Verapamil & Diltiazem cause constipation and severe AV block leading
to bradycardia (negative chronotropic effect)  worsens heart failure
in pts with reduced LV function.

 CREST syndrome  calcinosis, raynaud’s phenomenon, esophageal

dysmotility, sclerodactyly and telangiectasias. Anti-centromere antibodies
are found in about 40% of patients with CREST syndrome. Anti-DNA
topoisomerase I (Scl-70) antibodes are higly specific for systemic sclerosis.
Pulmonary hypertension develops in patients with systemic sclerosis as a
result of damage to the pulmonary arterioles. It manifests with an
accentuated pulmonary component of the second heart sound and signs of
right-sided heart failure due to cor pulmonale Intimal thickening of
pulmonary arterioles.

 HIV-associated dementia  in AIDS patients with progressive cognitive

decline. Microglial nodules, groups of activated macrophages/microglial cells
formed around small areas of necrosis that may fuse to form multinucleated
giant cells.

 Intestinal microbiome effectively suppress overgrowth of clostridium difficle

and other potentially pathogenic bacteria by competing for nutrients and
adhesion sites within the gut.

Breast pathology 
 Intraductal papilloma  papillary cells with fibrovascular core, focal atypia,
cyst wall/dut
o Most common cause of bloody nipple discharge
 Fibroadenomas  small, firm, mobile breast masses due to proliferation of
breast stroma and ducts due to slits, cellular or myxoid stroma that encircles
and sometimes compresses epithelium-lined glandular and cystic spaces.
 Fat necrosis  trauma  irregular breast mass, no nipple discharge.
o Liquefactive necrosis of adipocytes with hemorrhage.
 Fibrocystic change  diffuse small cysts with/without metaplasia, cyclic
breast pain, no nipple discharge
 Paget disease of the nipple eczematous exudate over nipple & areola and is
due to ductal spread of malignant cells to the nipple surface. Bloody nipple
discharge may be present
 Invasive breast carcinoma typically presents as an irregularly shaped
adherent breast mass, m/c in the upper outer quadrant. Malignant
infiltration of the suspensory ligaments of the breast causes dimpling of the
overlying kin.

 Patients with adult-type coarctation of the aorta  commonly die of

hypertension-associated complications, including left ventricular failure,
ruptured dissecting aortic aneurysm and intracranial hemorrhage. These
patients are at increased risk for ruptured intracranial aneurysms because of
the increased incidence of congenital berry aneurysms of the Circle of Willis
as well as aortic arch hypertension. Berry aneurysms are particularly prone
to rupture when associated with coarctation, because of hypertension in
branches of the aortic arch proximal to the coarct, subarachnoid hemorrhage
is the result.

 Pityriasis versicolor (tinea versicolor)  superficial skin infection  by

Malassezia species, “spaghetti and meatballs” forms spores and hyphae
appearance on KOH  hyper or hypopigmented macules and patches to sun
exposed skin

 Intertrigo well-defined erythematous plaques with satellite vesicles or

pustules in warm, moist skin areas (axillae, groin, skin folds)  due to
Candida species, which is m/c after use of antibiotics or immunosuppression
states (diabetes).

 The liver makes ketone bodies, but it lacks the enzymes to use the ketones
for fuel.

 Marfan syndrome  most common life threatening complications are early-

onset cystic medial degeneration of the aorta  aortic dissection.

 Homocystinuira  thrombosis/atherosclerosis  Myocardial infarction,

mafanoid habitus, ectopia lentis, developmental delay. Many pts respond to
pyridoxine B6 supplementation.

 Clozapine  2nd generation antipsychotics  used in treatment-resistant

schizophrenia 
o SE neutropenia and agranulocytosis (must be monitored), weight
gain and metabolic effects.

 Retroperitoneal hematoma large fluid collection  displaces kidney

anteriorly  Femoral mononeuropathy femoral nerve compressed from
the fluid  weakness of the quadriceps muscle, loss of paterllar reflex and
loss of sensation over the anterior and medial thigh and medial leg 
 o Groin & lower abdomen pain and back pain, difficulty with stairs and
frequent falling.
o Common complication for retroperitoneal hematoma is abdominal
and pelvic trauma  pancreas is a retropertoneal organ and injury to
this organ can cause bleeding. The abdominal aorta is also a
retroperitoneal organ but injury to this would cause massive and
rapid blood loss leading to hemorrhagic shock.

 Highly lipophilic drug  will be rapidly distributed to organs with high blood
flow (brain, liver, kidneys, and lungs)  then this drug is slowly
redistributed to the tissues with relatively lower blood flow (skeletal muscle,
fat, and bone)  short duration of action  such as propofol.

 Dextrocardia  (situs inversus) cardiac point of maximal impulse that is

palpated at the right 5th intercostal space. Kartageners syndrome  Dynein
arms defect with primary ciliary dyskinesia. Chronic sinusitis and
bronchiectasis

 Zone 1 of lungs = Palv > Part > Pv  arterial pressure is low in this region as
the heart must pump blood uphill against the force of gravity because this
zone of the lungs is higher in the chest than the heart.  So pulmonary
capillaries are collapsed and there is no blood flow in this zone.
 Zone 2 = Part> Palv> Pv  because alveolar pressure is greater than venous
pressure, the pulmonary are obstructed near the venous end of the capillary
bed. Blood flow here is pulsatile fashion.
 Zone 3 = Part> Pv> Palv  blood flows continuously through the pulmonary
capillaries.
 In a supine person, lung is entirely composed of zone 3 blood flow. For this
reason the ventilation/perfusion ratio decreases in the lung from apex to the
base.

 Actinomyces israelii  Gram positive organism  causing cervicofacial

actinomycosis after dental manipulation or oral trauma  slow growing or
firm-feeling abscess in the face or neck region  forms cutaneous sinus
tracts. Use long-term penicillin and surgical debridement.

 MCL medial collateral ligament resists force that pushes the knew medially
 increased laxity of the knew with the valgus stress test  Knee extended
by placing one hand along the lateral thigh pressing inward while other hand
is placed on medial aspect of ankle and pushed outward.

 Acute compartment syndrome  increased pressure within the fascial

compartment of the limbs of leg leading to impaired perfusion  severe pain,
myonecrosis, and nerve injury. Anterior most compartment of the leg 
contains the deep peroneal (fibular) nerve m/c site of ACS. The deep
 posterior compartment contains the posterior tibial artery, perineal artery,
and tibial nerve  decreased sensation in the plantar surface, decreased toe
flexon, and pain with passive toe extension.
o Common perineal (fibular) nerve divides into superficial perineal
nerve which innervates muscles of the lateral compartment of the leg
and evert the foot, and sensory innervation to dorsum of the foot.
Than the deep peroneal nerve innervates anterior compartment of the
leg and dorsiflex the foot and toes, and gives sensory innervation to
region between the first and second digits of the foot.

 In females, the paramesonephric ducts fuse to form the fallopian tubes,

uterus, cervix, and upper vagina. Disruption of this process can lead to a
variety of mullerian tract anomalies, and renal anomalies are a common
comorbidity.
o Incomplete lateral fusion of the paramesonephric ducts result in a
bicornuate uterus characterized by an indentation in the center of the
fundus.
o Septate uterus  incomplete resorption of septum  treat with
septoplasty, decreased infertility.
o Uterus didelphys  complete failure of fusion  double uterus,
vagina and cervix. Pregnancy is possible

 B-FLAT = basophils  FSH, LH, ACTH, TSH

 Acidophils= GH, PRL prolactin.

 Beta-endorphin is one endogenous opioid peptide that is derived from

proopiomelanocortin (POMC) which is a polypeptide precursor that goes
through enzymatic cleavage and modification to produce not only beta-
endorphins (endogenous endorphins in the body), but also ACTH and MSH.
o The fact that beta-endorphin and ACTH are derived from the same
precursor suggest that there may be a close physiological relationship
between the stress axid and the opioid system.
 ACTH, MSH, and Opioid receptors all have the same molecular origin.

 Q#186, Diastolic heart failure  Left ventricular end-diastolic pressure =

Increased, Left-ventricular end-diastolic volume = normal, left ventricular
ejection fraction = normal.
o Systolic HF= decreased LV ejection fraction by <50%, increased LV
volume, and elevated LV end diastolic pressure.

 The optimal site for obtaining vascular access in the lower extremity during
cardiac catheterization is the common femoral artery below the inguinal
ligament. Cannulation (penetration) above the inguinal ligament can
significantly increase the risk of retroperitoneal hemorrhage.
 Strep Viridans produce dextrans that aid them in colonizing host surfaces
such as enamel and heart valves  subacute bacterial endocarditis.
o This bacteria can adhere to fibrin-platelet aggregates and establish
infection

 Erythema multiform is a cell-mediated inflammatory CD8+ T cells, disorder

of the skin characterized by erythematous papules that evolve into target
lesions  most commonly associated with Herpes simplex virus,
mycoplasma pneumonia, drugs ( Sulfa drugs, b-lactams, phenytoion),
cancers, and autoimmune diseases.

 Cystic fibrosis  3 base pair deletion in transmembrane conductance

regulartor (CFTR) gene at amino acid position 508  impairs
posttranslational processing of CFTR  shunting of CFTR toward the
proteasome with complete absence of protein in apical membrane of affected
epithelial cells.

 In the lungs the binding of oxygen to hemoglobin drives the release of H+ and
CO2 from hemoglobin, in peripheral tissues, high concentrations of CO2 and
H+ facilitate oxygen unloading from hemoglobin.

 Daptomycin  lipopeptide antibiotic activity limited to gram-positive

organism  MRSA. Causes depolarization of bacterial cellular membrane
that cause intracellular ion leakage and inhibiton of DNA, RNA, and protein
synthesis.
o Associated with increased CPK levels and myopathy so should do CPK
level monitoring with assessment for muscle pain and weakness
regularly.

 Amyotrophic lateral sclerosis (ALS)  causes both upper and lower motor
neuron lesions  loss of anterior horns of the spinal cord LMN lesions causes
muscle weakness and atrophy. Demylination of lateral corticospinal tract
(UMN lesion) leads to spasticity and hyperreflexia. Loss of motor nuclei of
CN V, IX, X, XII

 Vit A maintains differentiation of specialized epithelia including mucus-

secreting columnar epithelia of the ocular conjunctive, respiratory and
urinary tracts, and pancreatic and other exocrine ducts. Avitaminosis A 
causes squamous metaplasia of such epithelia to a kertinizing epithelium.

 Neonatal intraventricular hemorrhage  fragile germinal matrix & increases

in frequency with decreasing age and birth weight. Common complication of
prematurity  long-term neurodevelopment impairment.
 Hypo-acetylated histones bind tightly to DNA and prevent transcription of
genes in their associated regions. Alteration of gene expression in Huntington
disease occurs in part due to deacetylation of histones  prevent
transcription of certain genes that code for neurotrophic factors,
contributing to neuronal cell death.

 Cholelithiasis during pregnancy or taking OCPs is influenced by estrogen-

induced cholesterol hypersecretion and progesterone-induced gallbladder
hypomotility.

 Diffuse esophageal spasm periodic, simultaneous, non-peristaltic

contractions of the esophagus due to impaired inhibitory innervation within
the esophageal myenteric plexus. Solid/liquid dysphagia and chest pain due
to inefficient propulsion of food into the stomach.

 Specific phobia  exposure based behavorial therapy with confrontation on

their feared objects or situations.

 Legionella pneumonia  cruise ships, high fevers, hyponatremia, headache,

confusion, watery diarrhea.

 Ramelteon  melatonin agonist to treat insomnia in elderly patients  safe

and effective in reducing time to sleep onset in the elderly.
o Avoid benzo’s, antihistamines, and sedating antidepressants in this
population to avoid SE.
 Ulner nerve  Posterior displacement of the proximal humerus or fracture
of the medial epicondyle.
 Radial nerve  lateral supracondylar humeral fractures. Radial nerve
injury with a lateral displacement of the proximal fracture fragment. Radial
runs laterally, medial nerve and brachial artery runs medially.
o Brachial artery injury  pulseless hand due to vascular insufficiency.
 Median Nerve  Suprcondylar fractures in the anteromedial
displacement of the proximal fracture fragment  median nerve and
brachial artery injury.

 Influenza vaccine  inhibiton of viral entry into the cells  generate a

humoral immune response

 Echinocandins (caspofungin, micafungin) are antifungal meds that inhibit

synthesis of polysaccharide glucan, an essential component of the fungal cell
wall.

 Q# 0973, Pseudomonas Aeruginosa, Ecthyma gangrenosum  cutaneous

necrotic disease with a strong associated with Pseudomonas aeruginosa
bacteriemia. Occurs from perivascular invasion and release of tissue-
 destructive exotoxins, causing vascular destruction and insufficient blood
flow to patches of skin that become edematous and subsequently necrose.
o Common in neutropenic patients, hospitalized, burn, and indwelling
catheter patients.

 Zidovudine  NRTI to treat HIV, competitively binds to reverse transcriptase

and incorportated into the viral genome as a thymidine analog. AZT does not
have 3’-OH group, making a 3’-5’ phosphodiester bond formation is
impossible.

 Diastolic sound S4  left ventricular wall stiffness/hypertropny 

presystolic meaning it’s a diastolic sound. Precedes immediately after the
first heart sound.

 Delirium  acute reversible confusional state involving a reduced or

fluctuating level of consciousness with difficulties sustaining attention and
impaired memory, sleep disturbances, and agitation.
o Occurs due to underlying medical condition like UTI, elderly have a
higher risk for delirium and people with a history of cognitive
impairment.
o Low dose haloperidol is the treatment to treat behavioral and
psychotic manifestations.

 Duodenal S-cells secrete secretin in response to H+ concentration. Secretin

 increases pancreatic HCO3-secretion and decreases Cl- content of the
pancreas.

 Presbyopia & skin wrinkles  age related changes  Presbyopia due to

denaturation of structural proteins within the lens, leading to loss of
elasticity. Decreased synthesis and increased breakdown of collagen fibril
production and elastin contribute to the development of skin wrinkles.

 Roseola infantum  age less than 2 years old, 2-5 days of high fevers with
seizures followed by blanching maculopapular rash, treatment is supportive
care, usually in infants. Caused by HHV-6 and rash starts on the trunk and
spreads to the face and extremeties.

 MRSA anterior nares are the most common site of colonization for both
MRSA or MSSA.

 Sirolimus binds to the immunophilin FK-506 binding protein (FKBP) in the

cytoplasm, forming a complex that binds and inhibits mTOR. Inhibition of
mTOR signaling blocks IL-2 signal transduction and prevents cell cycle
progression and lymphocyte proliferation.
 Superfiical and deep inguinal rings are physiologic openings in the external
abdominal oblique aponeurosis and the transversalis fascia, respectively.
Surgical repair of an undescended testicle lodged in the inguinal canal
involves reducing the testis through the superficial inguinal ring (external
oblique muscle aponeurosis) and fixing it in the scrotum (orchiopexy).

 Californian’s like girls in string bikini’s  Stratum corneum, Stratum

lucidum, stratum granulosom, stratum spinosum, stratun basalis 
epidermal layers of the skin

 LV afterload is the major determinant of the forward-to-regurgitant flow

ratio in the patients with mitral regurgitation. Decreasing the afterload will
increase forward flow while reducing regurgitant flow.
o Increasing LVED volume will contribute to or worsen mitral
regurgitation.

 Gallstone ileus  obstruction at the ileum, symptoms of small bowel

obstruction and has within the gallbladder and biliary tree.
 Malformation  primary intrinsic defect in cells or tissues that form a
structure leading to a chain of downstream anomalies,
o Agenesis  complete absence
o Deformation  fetal anomalies that occur due to extrinsic mechanical
forces.
o Disruption  secondary breakdown of previously normal tissue or
structure. E.g rupture of amnion leading to amniotic bands, which
compress or even amputate fetal limbs.
o Sequence  number of abnormalities result from a single primary
defect  like in oligohydramnios

 Strong pulse on the sternocleidomastoid muscle  carotid artery derived

from the Third pharyngeal and aortic arch.

 Saline microscopy  wet mount

 Progressive inflammation in the appendix irritates the parietal peritoneum

and abdominal wall to cause severe somatic pain shifting from the umbilicus
to McBurney point

 Lung infarction are rare in PE because of the collateral blood circulation of

the pulmonary artery and bronchial artery.

 Insulin decreases glucagon secretion, but in type 1 diabetes mellitus that fact
that insulin is deficient  there will not be a decrease in glucagon secretion
leading to an increase glucose
 IL-10  anti-inflammatory and immunomodulatory roles  and
pathogenesis in inflammatory bowel disease. IL-10 attenuates the immune
response through inhibition of Th1 cytokines, reduction of MHC-II
expression, and suppression of activated macrophages and dendritic cells.

 ICP increased intracranial pressure leads to compression of the ipsilateral

3rd CN (PCA) resulting in oculomotor nerve palsy with a  dilated pupils
o Can result from temporal lobe lesions from transtentorial herniation
of uncus from hemorrhage. Around the MCA/ACA area.
o An (actively enlarging intracranial aneurysm) aneurysm arising from
either artery can lead to a non-pupil-sparing 3rd nerve palsy, which
clinically present with unilateral headache, eye pain, diplopia, dilated
pupil and ptosis with ipsilateral down and out, an aneurysm
compressing ipsilateral PCA.
o Lateral striate artery  common location of lacunar infarcts 2ndary
to unmanaged HTN, weakness on one side of body, and cavity lesion
on repeat CT couple of days after.
o Neoplastic lesions of the central nervous system can promote
vasogenic edema by disrupting the blood-brain barrier. Increased
vascular leakage into the cerebral interstitium contributes to the
elevated intracranial pressure, which typically presents with
headache, nausea/vomiting, and papilledema.

 Calcium kidney stones  normocalcemia, hypercalciuria.

 Restless leg syndrome  uncomfortable sensation in the legs accompanied

by urge to move them  treatment dopamine agonist Pramipexole or
ropinirole. A number of drugs worsen RLS like glucocorticoids, SSRI’s, and
lithium.

 Orotic aciduria  rare AR disorder of de novo pyrimidine synthesis that

occurs due to a defect in uridine 5’-monophosphate (UMP) synthase.
o Physical and mental retardation, megaloblastic anemia, and large
amounts of urinary orotic acid.
o Uridine supplementation  uridine converts to UMP via nucleoside
kinases.
o CPSII in de novo pyrimidine synthesis are located in the cytosol, while
the CPSI of the urea cycle is located in the mitochondria.

 Acyclovir competes with deoxyguanosine triphosphate for viral DNA

polymerase  it becomes incorporated into replicating viral DNA and the
replication is terminated  phosphorylated to acyclovir monophosphate by
thymidine kinase TK, only for HSV, VZV, but for CMV and EBV they do not
produce the same kinase, which is why CMV and EBV are treated with
gangcyclovir and other antivirals
 Appendectomy can damage iliohypogastric nerve  which provides
sensation to the suprapubic and gluteal regions and motor function to the
anterolateral abdominal wall muscles.  Decreased sensation and burning
pain at the suprapubic region.

 Clopidogrel  irreversibly blocks P2Y12 of ADP receptors and prevents

platelet aggregation. As effective as aspirin in the prevention of
cardiovascular events in patients with stable angina.
 Warfarin and apixaban  prevention/treatment of thromboembolic events
 Cilostazol  peripheral vascular disease (claudication)
 Heparin  unstable angina and MI
 Eptifibatide and abmixamab  acute coronary syndrome but not stable
angina.

 ACE inhibitors promote efferent arteriolar dilation, causing GFR reduction.

 Pulsatile administration of GnRH stimulates FSH and LH release 

infertility.
o Nonpulsatile constant infusion of GnRH is a long acting analog and
suppresses FSH and LH and used to suppress gonadal function such as
cancers of the prostate, endometriosis, precocious puberty, or
premenopausal breast cancer.

 ACA, MCA, PCA are large vessels arising from the circle of willis  ischemic
stroke due to thrombotic or embolic vessel occlusion
 Penetrating branches of these major arteries cause hypertensive
vasculopathy and affect basal ganglia putamen, cerebellar nuclei, thalamus,
and pons. Basal ganglia are supplied by lenticulostriate arteries and are small
branches off of MCA.

 Clostridium Difficile infection treated with metronidazole, vancomycin,

fidaxomicin, first 2 are first line treaments

 Fidaxomicin used in recurrent infection of C. Difficile, macrocylic antibiotic

inhibits subunit of RNA polymerase  leading to protein synthesis
impairment and cell death  bacteriocidal, minimal systemic absorption,
and narrow spectrum.

 Vibrio Cholerae  purely toxin-mediated watery diarrhea  modify

electrolyte handling by enterocytes  no erythrocytes or leukocytes are
typically noted  Mucus and some sloughed epithelial cells.

 Metabolic alkalosis  high pH, HCO3-, and pCO2  vomiting/nasogastric

suctioning and thiazide/loop diuretic use cause volume and Cl-depletion,
 resulting in metabolic alkalosis that is saline-responsive. In contrast,
hyperaldosteronism leads to metabolic alkalosis that is saline-unresponsive.
o Determine patient’s volume status and measure urinary Cl-
concentrations to help identify cause of metabolic alkalosis.

 Patients with a history of irregular menses are at risk of inaccurate

pregnancy dating, do an ultrasound to check the accurate dating of the fetus.

 Cleft lip  maxillary prominence fails to fuse with the intermaxillary

segment during the 5-6th week of embryonic development.
 Cleft palate  palatine shelves fail to fuse with one another or with primary
palate.

 Reduction in slope of curve depicting lung volume vs distending peressure

indicates decreased lung compliance  hallmark of pulmonary fibrosis,
increase in lung compliance means emphysema.

 Achalasia  reduced numbers of inhibitory ganglion cells in esophageal wall

 decreased amplitude of peristalsis in the mid esophagus, and increased
tone and incomplete relaxation at the LES.

 Long cutaneous adverse effects of chronic tropical corticosteroid

administration include atrophy/thinning of the dermis that is associated
with loss of dermal collagen, drying, cracking, and tightening of the skin,
telangiectasias and ecchymosis.

 Shingles develops in a dermatomal distribution and before vesicles appear

that part of the body has a burning itching sensation and then develops the
vesicles.  Intranuclear inclusions in keratinocytes and multinucleated giant
cells are seen  persistent local pain persists for up to 6 months. The risk of
developing herpes zoster increases with advancing age and/or
immunosuppression. Young patients with herpes zoster should be tested for
HIV. Patients with HIV are also at increased risk for developing disseminated
varicella zoster disease.

 Extended-spectrum beta-lactamases (ESBL) can be produced by gram-

negative bacteria, rendering cephalosporin’s and other beta-lactam
antibiotics inactive. These genes can be transmitted between organisms
through plasmid conjugation. Carbapenems (eg. Imipenem) are the
treatment of choice for ESBL-producing organisms, although unfortunately,
organism with carbapenem resistance have emerged.
o Beta-lactam antibiotics improve aminoglycosides efficacy by
compromising the integrity of the bacterial cell wall and allowing the
aminoglycoside to penetrate into the bacterium where it can bind the
ribosomal 30s subunit and inhibit bacterial protein synthesis.
 Digital clubbing  prolonged hypoxia  large-call lung cancer, TB, cystic
fibrosis, suppurative lung diseases empyema, bronchiectasis, and chronic
lung abscesses.

 Serotonin-releasing neurons in CNS  located in the raphe nuclei.

 NE  locus ceruleus, Dopamine  Substantia nigra, ACh Basal nucleus of

meynert, GABA  nucleus accumbens

 MAO inhibitors (Tranylcypromine, phenelzine) {affect the degradation of

monamine} are particularly useful in patients with treatment-resistant and
atypical depression. Increased appetite and sleep, leaden paralysis, rejection
sensitivity, and mood reactivity are hallmarks of atypical depression.
o It’s a mitochondrial enzyme that degrades excess monoamine
neurotransmitters in presynaptic nerve terminals and also detoxifies
tyramine in the GI tract.
o Tyramine hypertensive crisis can occur in pts taking MAO inhibitors
and eat foods containing high amounts of tyramine (aged cheese,
cured meats, draft beer).

 Mifepristone progesterone antagonist, misoprostol prostaglandin

analog causes cervical softening and uterine contractions leading to
expulsion of the pregnancy

 Injury to the intercoastal vein, artery, and nerve all lie in the lower border of
the rib not the upper part of the rib.
 Thoracentesis should be performed 
o Between 6th -8th ribs along the midclavicular line
o Between 8th-10th ribs along the midaxillary line  risk of injuring right
hepatic lobe.
o Between 10-12th ribs along the paravertebral line.
 If needle is inserted higher there is a risk of lung injury and inserted at these
levels, there is a risk of penetrating abdominal structures like the liver.

 Epihelial ovarian cancer  frequency of trauma and repair at the ovarian

surface. Oral contraceptive, multiparity, breastfeeding are protective by
decreasing the frequency of ovulation. Risk factors include BRCA mutation,
nulliparity and infertility.

 Wolff-Parkinson-White syndrome = accessory AV conduction pathway 

recurrent paroxysmal supraventricular tachycardia in an otherwise healthy
individual. So the heart skips the AV nodal conduction which slows down the
HR, and some of the circuit under cuts and excites the ventricular and they
undergo a partial depolarization.
 o Traid of abnormalities  ventricular pre-excitation, shortened PR-
interval, a delta wave at the start of QRS complex, and a widened QRS
interval.

 In multiple sclerosis  causes optic neuritis in usually one optic nerve. The
afferent limp of the light reflex is pathway is the optic nerve, efferent limp is
parasympathetic fibers of CN3. When one optic nerve is damaged, light in
that eye will cause neither pupil to constrict (nerve can’t sense the light).
However, light in the contralateral eye will cause both pupils to constrict the
motor pathways are intact.

 Bacillus and Clostridium bacteria are commonly found in soil and are able to
survive high temperatures, desiccation, and chemical agents by forming
spores, can be killed only by autoclaving.

 Bacillus anthracis produces an antiphagocytic capsule that contains

antiphagocytic D-glutamate capsule. It causes pulmonary anthrax
(woolsorters disease by inhalation of spores while working with goat hair or
hides). Hemorrhagic mediastinitis (widened mediastinum) and bacteria is
long chains serpentine or medusa head.

 Cortisol binds to an intracellular receptor and are located within the

cytoplasm  bind to hormone-responsive DNA elements altering gene
transcription to enhance hepatic glucose production and limit peripheral
glucose utilization.

 Absorbed copper used to form ceruloplasmin  90-95% of circulating

copper  anything unabsorbed are secreted into bile and excreted in the
stool  primary route for copper elimination.

 Pigment gallstones 10-25% m/c in rural Asian population  unconjugated

bilirubin in bile  calcium bilirubinate 

o Brown pigment stones  biliary tract infection (microbes producing

ß-glucuronidases, liver fluke Clonorchis sinesis.
o Black pigment stones  chronic hemolysis from sickle cell anemia, ß-
thalassemia, HS and increased enterohepatic cycling of bilirubin ileal
disease.
o Cholesterol gallstones significant risk factor from obesity/metabolic
syndrome, multiparity, OCP, rapid weight loss.

 1st generation of anti-histamines  hydroxyzine, promethazine,

chlorpheniramine, diphenhydramine
 2nd generation of anti-histamines  loratadine, cetirizine, fexofenadine,
desloratadine.
 Panic attacks  hyperventilation  decreased pCO2  hypocapnia causes
cerebral vasoconstriction and decreased cerebral blood flow.

 Pulmonary artery occlusion pressure (pulmonary capillary wedge pressure

{PCWP}) is measured at the distal tip of the pulmonary artery catheter
after it enters the right atrium, RV, pulmonary artery into the branch and
then its inflated and the balloon occludes the blood flow through the
pulmonary artery branch.
o Measures the pressure in the left atrium and left ventricle end-
diastolic pressure

 Tracheoesophageal fistula with esophageal atresia  results from failure of

the primitive forgut to appropriately divide into separate trachea and
esophageal structures.
o Infants shortly after birth present with excessive salivation and
choking/cyanosis during feeds. Diagnosis can be confirmed by x-ray
after the inability to pass a nasogastric tube into the stomach.

 Choanal atresia/obstruction of posterior nasal passages  upper airway

obstruction and cyanosis with feeding but not excessive drooling. Inability to
pass a nasogastric tube through the nares is suggestive of the diagnosis.

 HPV  basal cervical cells can progress to premalignant and cancerous

lesions  CIN refers to atypical squamous cells and is classified as low-grade
squamous intraepithelial lesions (if extending < 1/3 of the epithelium) or
high-grade squamous intraepithelial lesions (if extending beyond).
Basement membrane breach signifies invasive disease.
o High grade expansion of immature basal cells to the epithelial
surface

 Q# 1754, Monoclonality and Cancer: Benign lymph node enlargement in

response to antigenic stimulation is associated with a polyclonal
proliferation of lymphocytes.
 Monoclonal lymphocytic proliferation and T-cell receptor gene
rearrangement is a strong evidence of malignancy.

 Tuberous sclerosis  mutations in tuberin and harmartin  cardiac

rhabdomyomas, bening tumor composed of blood vessels, smooth muscle,
and fat. Bilateral renal angiomyolipomas  AD.

 Complete AV atrioventricular septal defect comprises an ostium primum ASD

with VSD  endocardial cushion syndrome  m/c congenital cardiac
anomaly.
 Lichen planus  Pruritic, Purple, Polygonal, Papules. Sawtooth infiltrate of
lymphs at dermal  associated with HCV

 Neutrophil chemotaxis  CILK  C5, LTB4,

 Probenecid (uric acid drug inhibits reabsorption of uric acid in PCT) inhibits
secretion of penicillin, by blocking the anion transporters on renal tubular
cells to inhibit tubular secretion of certain antibiotics (eg, penicillin) in cases
of penicillin resistance gonorrhea, neurosyphilis.

 The primary somatosensory cortex (postcentral gyrus) is responsible for

processing of all somatic sensory modalities (touch, temp/pain,
vibration/proprioception) on the contralateral body. A partial focal seizure
originating in this region can result in contralateral sensory disturbance such
as numbness and paresthesias.

 Chronic mesenteric ischemia  atherosclerosis of the mesenteric arteries

resulting in diminished blood flow to the intestine after meals  causes
postprandial epigastric pain (intestinal angina) with associated food
aversion/weight loss.  Pathogenesis is similar to angina pectoris.

 Skeletal muscle is not dependent on extracellular calcium influx to cause

calcium release from the SR  therefore its not blocked by Ca2+ channel
blockers.

 Enteropeptidase  jejunal brush border enzyme  activates trypsin from

trypsinogen  Deficiency impairs both protein and fat absorption leading to
diarrhea, failure to thrive, and hypoproteinemia.

 Acute allergic contact dermatitis  type IV delayed hypersensitivity

reactions to an antigen on the skin surface.  Erythematous,
papulovesicular, weeping lesion characterized y spongiosis , which is an
accumulation of edema fluid in the intercellular spaces of the epidermis.
Chronic exposure  lesions become less edematous with thickening of the
stratum spinosum and stratum corneum.

 Amatoxins (amanita phalloides, death cap which are poisionous mushrooms)

 potent inhibitors of RNA polymerase II halting mRNA synthesis.

 Androgenic steroid abuse  erythrocytosis, testicular atrophy, acne, and

virilization in woman (clitoromegelay, hirsutism).

 Primary (psychogenic) polydipsia  psychological disorder  increased

intake of free water leading to hyponatremia and production of a large
volume of dilute urine. Water restriction will correct the serum sodium
 levela and lead to a significant increase in urine osmolality. Diabetes
insipidus has increased sodium unlike this one with decreased sodium.

 Methacholine  challenge test negative can help exclude and rule out
diagnosis of asthma. It is a muscarinic cholinergic agonist, which induces
bronchial smooth muscle contraction and increased bronchial mucus
production. Can induce bronchoconstriction and airway obstruction on
spirometry.

 Norepinephrine extravasation blanching of veins, induration and pallor of

tissues surrounding IV sites, which resulted in vasoconstriction  Tissue
necrosis is best prevented by local injection of alpha-1 blocking drug such as
phentolamine.

 If undescended testes are not surgically moved to the scrotal sac, the
seminiferous tubules which are temperature sensitive and prone to heat-
induced damage, will become atrophic and hyalinized over time, which
results in low sperm count and decrease levels of inhibin and increased FSH
levels. Cryptorchidism should be corrected surgically early in life to prevent
damage to seminiferous tubules and decrease pts risk of testicular cancer.

 Q# 0680, Staphylococcus scalded skin syndrome SSSS occurs in infants

and children from the production of exotoxin exfoliatin by staph species.
Widespread spidermal sloughing, esp with gentle pressure (nikolsky’s sign).

 Dyskeratosis  squamous cell carcinoma.

 Pleiotropy  instances where multiple phenotypic manifestations result

from a single genetic mutation. Most syndromic genetic illnesses exhibit
pleiotropy. Ex. PKU

 Inferior epigastric artery  1 of 2 branches of external iliac artery takes off

immediately proximal to the inguinal ligament. Provides blood to lower
anterior abdominal wall

 Fetal unilateral hydronephrosis inutero  detected 2nd trimester 

narrowing or kinking of the proximal ureter at the ureteropelvic junction, if
not diagnosed during in utero, infants present with palpable abdominal mass
reflecting and enlarged kidney. Usually from inadequate canalization of the
connection site between the kidney and ureter. M/c cause usually.

 Posterior urethral valves  m/c cause of bilateral fetal hydronephrosis in

boy’s  obstructive, persistent urogenital membrane at the junction of the
bladder and urethra. Usually results from urethral strictures, meatal stenosis,
 bladder neck obstruction, and uropathy from spinal cord damage from
bilateral hydronephrosis.

 Acute bacterial Parotitis  elderly postoperative patients who are intubated

or dehydrated. Staph aureus is the most common bacterial etiology. An
elevated serum amylase level with a normal serum lipase level and no
evidence of pancreatitis can confirm diagnosis.

 Effective discharge planning requires collaboration of multiple disciplines

such as physician, nurse, and social worker. A social worker can be
instrumental in assessing whether the patient has adequate family or
caregiver support at home.

 Ehlers-Danlos syndrome  Defectvie collagen synthesis  procollagen

peptidase deficiency  impaired cleavage of terminal propeptides in the
extracellular space. N-terminal propeptides removal.
o Joint laxity, hyperextensible skin, and tissue fragility due to formation
of soluble collagen that does not properly crosslink.

 Most enveloped nucleocapsid viruses acquire their lipid bilayer envelop by

budding through the plasma membrane of the host cell.
 Herpesviruses, however bud through and acquire there
envelop from the host cell nuclear membrane.

 Nondisjunction of chromosome pairs fail to separate during meiosis I

(inheriting both of one parents bands or chromosomes) or failure of sister
chromatids to separate during meiosis II or mitosis (darker band of one of
the child’s bands indicate fetus inherited he inherited 2 sister chromatids).

 Ataxia telangiectasia  cerebellar ataxia, telangiectasias, increased risk of

sinopulmonary infection with IgA deficiency, predisposes infections to upper
and lower airways. ATM gene mutation which plays a role in DNA break
repair.

 Erythrocytes use glycolysis as major pathway to generate energy, but they do

not have mitochondria so therefore cannot use citric acid cycle (TCA cycle).
They use bisphophoglycerate mutase to convert 1,3-BPG to 2,3-BPG in a step
that does not produce ATP. 2,3-BPG decreases hemoglobins affinity for
oxygen, which increases O2 delivery to peripheral tissues. So RBC’s bypass
the net gain in ATP in glycolysis. So when this enzyme bisphosphoglycerate
mutase is deficient than 2,3-BPG is also low which favors less oxygen
unloading which is the same as the fetal hemoglobin and shifts the
hemoglobin-dissociation curve to the left.
 Erythropoiesis-stimulating agenst (ESA’s) can substantially improve anemia
symptoms, avoiding the need for transfusion in chronic kidney disease and
dialysis patients. However, due to the increase in RBC mass , which results
in increased blood, viscosity can lead to thromboembolic events and develop
hypertension. (same concept as being pregnant  high RBC mass 
increased viscosity  thromboembolic events).

 Exercise  increased HR & cardiac output, constant arterial blood gas

because O2 is decreased and CO2 is increased so balances out.

 Borderline personality disorder  persistent pattern of unstable

relationships, mood liability, and impulsivity. May exhibit suicidal ideation or
interpersonal crisis in which the person feels rejected or abandoned.

 Pulmonary vascular bed  tissue hypoxia  vasoconstriction response 

happens in small muscular arteries to divert blood flow away from under-
ventilated regions of the lung toward better-ventilated areas where gas
exchange happens, but in the systemic circulation, vasodilation occurs and
blood is diverted towards underventilated regions so that hypoxic tissues
receive increased blood flow.
o As vascular resistance decreases = tissue oxygen content increases.
 Administration of excessively high oxygen concentrations in patients with
COPD can lead to increased CO2 retention (oxygen-induced hypercapnia),
resulting in confusion and depression consciousness. This is due in part to
reversal of hypoxic pulmonary vasoconstriction, which increases physiologic
dead space as the poorly ventilated alveoli are perfused (ventilation-
perfusion mismatch).
o Increased PaO2 decreases hemoglobins affinity for CO2, resulting in
dissociation of bound CO2 from hemoglobin and increased blood
pCO2 levels.
o Peripheral chemoreceptors in the carotid and aortic bodies sense
arterial PaO2 and are normally stimulated by hypoxemia. High-flow
oxygen reduces chemoreceptor stimulation, resulting in decreased
respiratory rate and minute ventilation.

 Infront of the esophagus and can even cause compression of the esophagus is
left atrium  posterior to the esophagus is descending aorta. The esophagus
passes through the esophageal hiatus of the diaphragm at the level of the T10
vertebra. This opening also contains the anterior and posterior trunks of the
vagus nerve, so dissection in this right crus/esophageal hiatus can cause
damage to the vagus nerve.

 Trigeminal nerve CN 5  arises at the level of middle cerebellar peduncle at

the lateral aspect of mid-pons. Infarcts involving the anterior portion of the
medial pons can produce dysarthria and contralateral ataxic hemiparesis.
 Diphtheria toxin  AB exotoxin that inhibit protein synthesis by ADP-
ribosylation of EF-2 (pseudomonas similar). This inhibits protein synthesis
and ultimately leads to cell death.

 Schwann cells destroyed in  Guillain-Barre syndrome  demyelination of

peripheral nerves  Endoneural inflammatory infiltrate.

 Polymyositis  endomysial inflammation with CD+ T cells.

 D1 direct pathway = inhibit the Gpi, then the GPi can no longer inhibit the
thalamus (- - = +) so excites the thalamus

 D2 indirect pathway = inhibits the GPe usually inhibit the subthalamus

nucleus  so no longer inhibits the STN  activates the GPi and inhibits the
thalamus.

 On the homunculus  the legs are medial, hands are in the middle and face is
most lateral. ACA/MCA junction mediates the proximal arm and leg = man in
a barrel syndrome  arms and legs dangle but are able to walk. PCA/MCA
junction = mediates occipital lobe = visual agnosia can’t recognize common
objects

 Broca’s  intact comprehension (understands) but nonfluent aphasia 

inferior frontal gyrus of the superior division of the MCA of dominant
hemisphere.
 Wernicke’s aphasia (word sandwhich)  fluent aphasia, impaired
comprehension  superior temporal gyrus of the infarcts of the inferior
division of the MCA of the dominant hemisphere.
 Global aphasia  when both are impaired so no comprehension and
nonfluent aphasia
 Conduction aphasia lesion in the arcuate fasciculus which connects the
broca’s and Wernicke so poor repetition but fluent speech and intact
comprehension.

 ACA and MCA  from internal carotid artery, PCA  basilary artery

 Medial medullary syndrome  ASA anterior spinal artery  Lateral

corticospinal tract  contralateral hemiparesis of the lower limbs, medial
lemniscus  decreased proprioception from the dorsal column lesion, caudal
medulla  hypoglossal nerve so tongue deviates side of lesion.

 Wallenberg syndrome or Lateral medullary syndrome  PICA (posterior

inferior cerebral artery)  vestibular nuceli  vomiting, vertigo, &
nystagmus, lateral spinothalamic tract (contralateral limbs) & spinal
 trigeminal nucleus (ipsilateral face)  decreased pain and temp on face and
limbs, sympathetic lesions  horner’s syndrome
o Nucleus ambiguous specific to PICA lesions and causes dysphagia,
hoarseness, and decreased gag flex,
o Inferior cerebellar peduncle  ipsilateral ataxia

 Lateral pontine syndrome  AICA  vestibular nuclei, facial (VII) nucleus

decreased lacrimation, salivation & taste from anterior 2/3 of tongue, and
ipsilateral facial paralysis, spinal trigeminal (V) nucleus, cochlear nuclei
(VIII) decreased ipsilateral hearing, and sympathetic, Middle and inferior
cerebellar peduncle  ipsilateral ataxia
o Potine hemorrhage typically cause pinpoint pupils, loss of horizontal
gaze, guadriparesis, decerebrate posturing, and rapidly evolving coma
that culminates in death within hours.
 Posterior communicating artery lesion  3rd nerve palsy, Acomm artery 
berry aneurysm’s

 Prokaryotes  circular DNA with single origin of replication, Eukaryotes 

linear DNA with multiple origins of replication.

 Gastric adenocarcinoma  intestinal type  solid mass that projects into the
stomach lumen and composed of glandular-forming cuboidal or columnar
cells. Diffuse carcinoma Linitis plastic  infiltrates the stomach wall and
displays signet-ring cells on light microscopy =infiltrative growth within the
stomach wall.

 Patients with Crohn disease affecting the terminal ileum are prone to
developing gallstones. Decreased bile acid reabsorption and wasting
promote supersaturation of bile with cholesterol, resulting in gallstone
formation.  Oxalate kidney stones  by impaired bile acid absorption in
terminal ileum.

 McCune-Albright syndrome  Triad of Fibrous dysplasia of the bone,

endocrine abnormalities (precocious puberty <age 8), and unilateral café-au-
lait spots. Activating mutation in the mosaic somatic GNAS gene stimulating
the a subunit of G protein/cAMP/adenylate cyclase singlaing pathway.

 Serum TSH level is most sensitive screening test diagnosing primary

hypothyroidism. Decreased T4 levels and increased TSH levels, T3 is
primarily produced by conversion from T4 in peripheral tissues, and levels
may be normal in early hypothyrioidism.

 Cori disease Debranching enzyme deficiency  accumulation of glycogen

with abnormally short outer chains (limit dextrins) due to inability to
degrade a-1,6-glycosidic branch points.  Hypoglycemia, ketoacidosis,
 hepatomegaly, muscle weakness and hypotonia. It is a milder form of Von
Gierke disease  hypoglycemia, lactic acidosis, hyperlipidemia,
hyperuricemia.

 Avoiding the use of unsafe abbreviations and trailing zeros in medication

orders can help reduce the incidence of medication errors.

 Acanthosis nigricans  thickening and hyperpigmentation of the skin in the

flexural areas (axilla, groin, posterior neck). Classic velvety texture 
associated with insulin-resistant states  diabetes mellitus, acromegaly,
obesity, and gastrointestinal malignancies.

 Acute interstitial pancreatitis the pancreas is grossly edematous  Focal

areas of fat necrosis, calcium deposition, and intestinal edema are seen on
light microscopy. In necrotizing hemorrhagic pancreatitis, chalky white
areas of fat necrosis are interspersed with hemorrhage.

 Power (1-ß) is the probability of rejecting null hypothesis when it’s truly
false. Depends on sample size and difference between outcomes.

 Unexplained oral thrush in healthy patient caused by Candida 

immunosuppression so HIV infection.

 Cardiogenic shock due to MI in the inferior leads of occluded Right coronary

artery  RV MI  elevated right atrial and central venous pressures 
reduced pulmonary capillary wedge pressure and reduced cardiac output.

 Congenital adrenal hyperplasia 

1. 21-hydroxylase deficiency (high level of 17-hydroxyprogestrone is
diagnostic) low mineralocorticoids (cortisol and aldosterone) 
salt wasting and increased serum K+, hypotension  increased
testosterone and 17-hydroxyprogesterone  ambiguous genitalia in
girls.
a. Classic, non-salt-wasting form of disease  males with this
variety typically present during the first few years of life with
early virilization and accelerated linear growth due to shunting
of corticosteroid precursors toward androgen production in
the adrenal cortex. Female’s ambiguous genitalia at birth. All
patients with 21-hydroxylase deficiency  increased serum
concentrations of 17-hydroxyprogesterone and androgens.
i. ACTH excess secretion  treatment of congenital
adrenal hyperplasia involves low doses of exogenous
corticosteroids to suppress excessive ACTH secretion
and reduce stimulation of the adrenal cortex.
 b. Leydig cell hyperplasia would result in masculinization due to
excessive production of testosterone, androstenedione, and
dehydroepiandrosterone. However, there would be no excess
of the adrenal hormone 17-hydroxyprogesterone.
2. 11ß-hydroxylase deficiencies  increased 11-dexoycorticostreone
leads to weak mineralocorticoids and 11-dexcortisol  fluid & salt
retention  hypertension  ambiguous genitalia in girls.
3. 17a-hydroxylase deficiency  decrease cortisol & testosterone  all
patients phenotypically female (ambiguous genital in boys) 
increased mineralocorticoids & corticosterone (weak glucocorticoid)
 fluid and salt retention  hypertension

 Ventral posterior lateral nucleus receives input from the spinothalamic tract
and dorsal columns and ventral posterior medial nucleus receives input from
the trigeminal pathway of the thalamus send somatosensory projections to
the cortex via thalamocortical fibers. Damage to these nuclei results in
complete contralateral sensory loss of the face and lower and upper limbs.

 Calcineurin  essential protein in the activation of IL-2, which promotes the

growth and differentiation of T cells. Immunosuppressant’s such as
cyclosporine and tacrolimus work by inhibiting calcineurin activation.
o Used to prevent organ transplants of solid organs and in inflammatory
disorders (severe psoriasis).
o Calcineurin inhibitor nephrotoxicity is dose-related and manifests as a
rise in serium BUN and Creatinine levels as well as increased blood
pressure.

 5a-reducatase deficiency small phallus (penis) and hypospadias.

 Hemoglobin O2 dissociation-curve
o Left shift  Decreased CO2, temperature, 2,3-BPG, H+ (increased pH),
and increased O2 affinity less loading. Examples : hypothermia,
hyperventilation.
o Right shift  increased CO2, temp., 2,3BPG, H+ (decreased pH), and
decreased O2  more oxygen loading to peripheral tissues. Examples:
High attitude (elevated 2,3BPG), Anemia, hypoventilation, exercise
(increased CO2, more O2 released so more available to tissues).

 Aortic regurgitation  early diastolic mumur  caused by aortic root

dilation or bicuspid aortic valve in developed countries, wide pulse pressure
(systolic arterial pressure – diastolic arterial pressure)  which leads to
involuntary head bobbing due to the forceful ventricular contractions
ejecting large stoke volumes.
 Metalloproteinases are zinc-containing enzymes that degrade the
extracellular matrix. They participate in normal tissue remodeling and in
tumor invasion through the basement membrane and connective tissue, 
reduce plaque stability and degrade extracellular matrix proteins.

 Zinc-finger Motifs (transcription finger motif)  composed of chains of

amino acids bound together around a zinc atom via linkages with cysteine
and histidine residues. They recognize specific DNA sequences and are used
by many transcription factors to bind DNA and alter activity of target genes.
Intracellular receptors that bind steroids (estrogen, aldosterone, cortisol),
thyroid hormone, and fat-soluble vitamin receptors act directly as
transcription factors and contain zinc-finger binding domains.

 Foscarnet pyrophosphate analog inhibit DNA polymerase in herpesvirus

and reverse transcriptase in HIV and does not require intracellular activation
by viral or cellular kinase.

 Lead poisioning  hypochromic microcytic anemia  basophilic stippling 

abnormal degradation of ribosomal RNA due to lead induced inhibition of a
nucleotidase. Inhibition of delta-aminolevulinate dehydratase and reduced
incorporation of iron into heme  decreased hemoglobin synthesis.

 Q# 395, HFE protein mutations are the most common cause of primary
hemochromatosis, HFE protein is on the basolateral surface of hepatocytes
and enterocytes  interacts with transferrin receptor, decreased expression
 reduced endocytosis of the iron-transferrin complex.  Primary
hemochromatosis  inactivation of this protein results in decreased
hepcidin synthesis by hepatocytes and increased DMT1 expression by
enterocytes  iron overload.  increased risk of cirrhosis and
hepatocellular carcinoma.

 Raloxifene  is a selective estrogen modulator that binds to estrogen

receptors and imitates or antagonizes the effects of endogenous estrogen. in
the bone its an agonist and prevents osteoporosis and in mammary tissues,
its an antagonist of estrogen and can prevent estrogen receptor positive
breast cancer.

 Tamoxifien  strong estrogen antagonist activity in the breast and is used in

the treatment of estrogen receptor-positive breast cancer. It can reduce risk
of osteoporosis but its agonist activity on the uterus increases its risk of
endometrial hyperplasia/cancer and limits its potential in osteoporosis
management.

 Lateral ankle sprain due to inversion of a planter-flexed foot  injured

ligament  anterior talofibular ligament.
 Actinic keratosis  develops chronically sun-exposed areas of the skin in
predisposed individuals. Lesions consist of erythematous papules with
central scale and rough sandpaper-like texture.  Premalignant lesions and
have a potential to progress to squamous cell carcinoma.

 Cyclothymic disorder  2 years of fluctuating, mild hypomanic and

depressive symptoms that do not meet criteria for hypomanic episodes or
major depressive episodes.

 Bipolar II disorder  hypomanic episodes and more than 1 major depressive

episodes

 Hydrocephalus ex vacuo  no ICP but a hole in the brain that gets filled with
CSF and the whole is usually a damage/atrophy from a brain damage, for ex:
Alzhiemers, HIV, Picks disease

 Vertebral disc herniation  between L5-S1 most commonly.

 Poliomyelitis  asymmetric weakness, both of these anterior horn lesions.

 Werdnig-hoffman disease symmetric weakness

 CN 3  parasympathetic more compression injury, ocular muscles 

ischemia, metabolic = diabetes, HTN

 Blepharospasm  involunatary forcible closure of the eyelids 

uncontrollable blinking.

 Gallbladder actively absorbs water from bile  gallbladder hypomotility

causes bile concentration promotes bile precipitation & accumulation of
viscous biliary sludge that predisposes to gallstone formation and bile duct
obstruction.

 Odds ratio (OR)  ad/bc

 Heroin overdose  respiratory acidosis with no metabolic compensation,

low pH, high pCO2, and normal HCO3-, but for COPD  initially low pH, high
Pco2, and normal Hco3-, but after a sustained hypoventilation, metabolic
compensation happens and needs 24 hours to kick in normal pH, high
Pco2, and high Hco3- to compensate.

 Rett syndrome  X-linked dominant exclusively in girls, (boys die in utero),

apparent in ages 1-4  regression of loss of development, loss of verbal
abilities, intellectual disability, ataxia, and stereotyped hand-wringing  loss
 of motor skills that were developed first, deceleration of head growth
associated with  mutations in the MECP2 gene.

 Fragile X syndrome  CGG trinucleotide repeats  FMR1 gene is

hypermethylated and inactivated FMR1 happens which prevents
transcription and production of fragile x mental retardation protein thereby
impairing neural development.

 Postoperative hypoparathyroidism is common after thyroidectomy. Surgical

removal of or damage to parathyroid glands results in a drop in parathyroid
hormone levels, resulting in deceased calcium and phosphate resorption
form the bone and decreased calcium reabsorption by the kidneys/urine.

 Internal hemorrhoids drains into the middle & superior rectal veins 
communicate with internal iliac and inferior mesenteric veins, respectively.

 Dysplasia is a reversible change in epithelial cells  low-grade dysplasia

high-grade dysplasia/carcinoma in situ  invasive carcinoma.

 Nucleolus  dense intranuclear body visible by electron microscopy that

functions as the primary site of ribosome synthesis and assembly  all
ribosomal RNA except 5S rRNA is transcribed in the nucleolus.

 The arteriovenous concentration gradient reflects the overall tissue

solubility of an anesthetic. Anesthetics with high tissue solubility are
characterized by large arteriovenous concentration gradient and slower
onset of action. But those with low peripheral tissue solubility and uptake
have small AV gradient  so less anesthetic is required to replace the
amount absorbed by the peripheral tissue and so blood saturation occurs
quickly, allowing concentrations in the brain to equilibrate faster.

 Volume contraction  loss of free water with retention of electrolytes 

seen in diabetes insipidus and in states of excessive sweating without fluid
replacement.  Hyperosmotic volume contraction.

 After a ligand binds to a-1 receptors of G protein-coupled receptor that

activates phospholipase C, membrane phospholipids are broken down into
tdiacylglycerol DAG and inositol triphosphate (IP3). Protein kinase C is
subsequently activated by DAG and Ca2+, the latter is released from
endoplasmic reticulum under the influence of IP3.

 Melanoma  malignancy of melanocytes  embryologically derived from

neural crest cells. Dysplastic nevus syndrome with numerous dysplastic nevi
in a young person who has family history of melona in more than 3 first-
 degree relatives. This syndrome is associated with mutations in the CDKN2A
gene on chromosome 9p21.

 Loss of sensation with anesthetics  A-delta (fast) lost first, C fiber (slow),
than A-gamma, than A-beta.

 Muscarine  toxin found in certain mushrooms  muscarinic agonists,

Activation of muscarinic receptors by acetylcholine or cholinergic agonists
result in peripheral vasodilation due to synthesis of nitric oxide in
endothelial cells, which leads to vascular smooth muscle relaxation
(hypotension).

 Absolute risk reduction = event rate in the control group – event rate in the
treatment group  4%=6%- trt grp, = 2% in this case 24/0.02 = 1200

 Crohns disease = associated with mutations in NOD2 (encodes an

intracellular microbial receptor), resulting in decreased activity of the NF-kB
protein (proinflammatory transcription factor) with reduced cytokine
production. Impairs the innate barrier function of the intestinal mucosa and
allows intestinal microbes to induce an exaggerated response by the adaptive
immune system, resulting in chronic gastrointestinal inflammation.
o Prolonged diarrhea, abdominal pain, low-grade fever, fatique,
malabsorption, weight loss. Formation of fistulas, abcesses, and
fibrotic strictures.

 Chronic lithium toxicity = confusion, ataxia, neuromuscular excitability 

can be precipitated by volume depletion and drug interactions with thiazide
diuretics, ACE inhibitors, and NSAIDs, by decreasing GFR, so anything that
decreases sodium reabosorption will decrease lithium/sodium reabsorption.
o Lithium can also cause nephrogenic diabetes insipidus by impairing
aquaporin-2 water channels and reducing responsiveness to
endogenous and exogenous vasopressin.

 HSV-2 recurrence of genital herpes can be reduced through daily treatment

with oral valacyclovir, acyclovir, or famciclovir. Condoms do not prevent
reactivation of latent infection.

 In males, incomplete fusion of the urethral (urogenital) folds result in

hypospadias, and abnormal opening of the urethra proximal to the glans
penis along the ventral shaft of the penis.

 Q# 1407, Congenital hypothyroidism is usually asymptomatic at birth.

After maternal T4 wanes, infants develop constipation, lethargy, hypotonia,
macroglossia, and umbilical hernia, and a large anterior fontanella.
 Suspensory ligament of the ovary contains the ovarian artery, vein,
lymphatics, and nerves. Ovarian artery is major blood supply and must be
ligated during an oophorectomy to prevent heavy bleeding.

 Patients with type 1 DM are prone to developing other autoimmune

endocrinopathies including hashimoto thyroiditis, graves, & primary adrenal
insufficiency (addison’s disease)  hyponatremia, hyperkalemia,
hyperchloremia, and non-anion gap metabolic acidosis.
o Metabolic acidosis  hyperkalemia, metabolic alkalosis 
hypokalemia.
o Lactic acidosis in septic shock results from tissues hypoxia which
impairs oxidative phosphorylation and causes shunting of pyruvate to
lactate following glycolysis. Hepatic hypoperfusion also contributes to
the buildup of lactic acid as the liver is the primary site of lactate
clearance.

 Both 6-MP and 6-thioguanine Azthioprine require activation by

hypoxanthine-guanine phosphoribosyl transferase HGPRT by xanthine
oxidase. So allopurinol can increase concentrations of these.

 Compound nevi  benign proliferation of melanocytes that involve both the

dermis and epidermis  slightly raised papules with uniform pigmentation
and symmetrical sharp borders.

 NK cells recognize and kill cells with decreased MHC class 1 antigen cell
surface expression, such as virus-infected cells and tumors.

 Glucagon  drug of choice for ß-blocker overdose  G protein-coupled

receptors  increases cAMP and thus increasing the release of intracellular
calcium  increases HR and contractility.

 Waterhouse-friderichsen syndrome  meningococcal septicemia causes

bilateral hemorrhagic infarction of the adrenal glands from Neisseria
meningitides infection with DIC.

 Cutaneous neurofibromas in neurofibromatosis type 1  multiple raised

fleshy tumors in Schwann cells (loose disorganized proliferation of schwann
cells, fibroblasts, and neuritis) Café-au-lait spots  derived from neural
crest.

 Q#1730, Valsalva maneuver increases vagal tone and can be used to abolish
paroxysmal supraventricular tachycardia. The rectus abdominis is the most
important muscle in achieving the increased intraabdominal and
intrathoracic pressure of the valsalva maneuver.
 o Forcibly exhaling against a closed glottis  taking a full inhalation,
holding ones breath, and bearing down-without exhaling as one
would during a bowel movement.

 G6PD is the rate-limiting enzyme in the pentose phosphate pathway, the

major source of cellular NADPH. This reducing molecule is necessary for the
reducing glutathione (preventing oxidative damage) and for the biosynthesis
of cholesterol, fatty acids, and steroids.

 Root cause analysis is a quality improvement measure that identifies what,

how and why a preventable adverse outcome occurred. The first step
involves collecting data mainly through interviewing multiple individuals
involved in the steps leading to the outcome.

 Because exercising muscle extracts additional O2, the venous blood O2

content is decreased. The venous blood CO2 content is increased due to
increased CO2 production. The venous blood pH is decreased.

 Acute ureteral constriction or obstruction decreases the glomerular filtration

rate and filtration fraction. FF= GFR/RPF so if GFR decreases than FF also
decreases. But when renal perfusion pressure falls/drops, (by systemic
hypotension, renal artery stenosis/obstruction) will cause efferent arteriolar
constriction, which helps GFR, therefore the FF will increase as renal
perfusion pressure drops.

 The superior mesenteric artery and inferior mesenteric artery are the 2 main
vessels supplying the small and large intestines. They are connected by a pair
of anastomoses; the marginal artery of Drummond (marginal artery), which
is the principal anastomosis, and the inconsistently present arc of Riolan
(mesenteric meandering artery).

 Isopropyl alcohol  disruption of cell membranes on skin, denaturation f

proteins
 Chlorhexidine disruption of cell membranes, coagulation of cytoplasm,
 Hydrogen peroxide produces destructive free radicals that oxidize cellular
components sporicidal,
 Iodine  halogenation of proteins & nucleic acids  sporicial.

 Binding of growth factor  autophophorylation of tyrosine residues 

activation of phosphoinositide 3-kinase  activation of protein kinase B
(Akt)  activation of X (mTOR, mammalian target of rapamycin)
translocation to the nucleus and gene transcription (cell survival, anti-
apoptosis, and angiogenesis). Important for anti-apoptosis, cellular
proliferation and angiogenesis, mutations in growth factor receptors, Akt,
 mTOR, or PTEN that enhance the activity of this pathway contribute to
cancer pathogenesis.

 Superoxide dismutase  neutralizes reactive oxygen species.

 Major determinant of whether or not coronary artery plaque will cause

ischemic myocardial injury is the rate at which it occludes the artery. A slow
developing occlusion would allow for formation of collaterals that could
prevent myocardial necrosis. A thin fibrous cap, a rich lipid core, and active
inflammation in the atheroma would all decrease plaque stability and thus
potentially promote rapid coronary occlusion via superimposed thrombosis
if the plaque were to rupture.

 Mitral stenosis  best and most reliable auscultatory indicator of the degree
of mitral stenosis is the (S2) A2-OS interval, OS= opening snap. A short
interval indicates more severe stenosis.
o Diastolic rumbling murmur with presystolic accentuation due to left-
atrial contraction can also occur.

 Drug-induced lupus slow acetylators, have more of this  procainamide,

hydralazine, isoniazid, minocycline, TNF-a inhibitors (etanercept), 
positive anti-histone antibodies

 Splenic artery branches  originates from the celiac artery

1. Pancreatic branches  body and tail of pancreas
2. Left gastroepiploic artery  middle part of curvature of the stomach
3. Short gastric branches  upper part of greater curvature of the
stomach.
 The short gastric arteries have very poor anastomoses, and the gastric
tissues supplied by them are vulnerable to ischemic injury following splenic
artery blockage. In contrast, tissues supplied by the left gastroepipolic can be
alternatively supplemented by its strong anastomotic connection with right
gastroepiploic artery, which is given off by the gastroduodenal artery.

 Non-pathogenic Corynebacterium can cause severe pseudomembranous

pharyngitis after acquiring the Tox gene via lysogenization by a temperate
bacteriophage. It aquires virulence via bacteriophage-mediated “infection”
with the Tox gene which codes for the diphtheria AB exotoxin, and the
bacteriophage responsible is called Corynephage beta.

 Polycythemia vera (PV) is a clonal myeloproliferative disease of pluripotent

hematopoietic stem cells  increased RBC mass, increased plasma volume,
increased platelets and WBC count, pruritus due to histamine release from
basophils, and low erythropoietin levels  Majority of patients have JAK2
V617F mutation, rendering hematopoietic stem cells more sensitive to
 growth factors. Secondary polycythemia  misnomer, not all cell lines are
increased but only red blood cells (better term, secondary erythrocytosis).
o JAK2  non-receptor cytoplasmic tyrosine kinase associated with the
erythropoietin receptor.

 Amniotic fluid embolism (AFE) rare and catastrophic pregnancy

complication that results from amniotic fluid entering the maternal
circulation. Hypoxia, hypotensive shock, DIC all result and fetal squamous
cells are seen in the pulmonary vasculature during histologic evaluation.

 Lipofuscin product of lipid peroxidation and are yellow-brown finely

granular perinuclear pigments (product of free radical injury), accumulating
in aging cells of the heart and liver of aging and cachectic, malnourished
patients.

 Acid/base  high altitude exposure  hypoxemia with respiratory alkalosis

from hyperventilation  over a few days, chronic respiratory alkalosis sets
in with a corresponding decrease in serum bicarbonate level reflecting renal
compensation.

 Hereditary nonpolyposis colon cancer (HNPCC) or lynch syndrome, leads to

occurrence of colonic adenocarcinomas at a young age (age <50) along with a
predisposition for extraintestinal malignancies (colorectal cancer,
endometrial cancer, and ovarian cancer). Mutations of DNA mismatch repair
genes are responsible for HNPCC. This is a microsatellite instability and is a
short DNA sequence containing a repetitive pattern of nucleotides, it is prone
to mutations due to slippage of DNA polymerase.

 Biopsy  mass reveals uniform, round, medium-sized tumor cells with

basophilic cytoplasm and proliferation fraction (Ki-67 fraction) of >99%. 
EBV infection -> Burkitts lymphoma, c-myc translocation of t (8; 14) 
diffuse medium-sized lymphocytes and high proliferative index represented
by high Ki67 fraction. Starry sky appearance, benign macrophages.

 Coronary dominance is determined by the coronary artery supplying the

posterior descending artery (PDA), which also supplies blood to the
atrioventricular AV node via the AV nodal artery. The PDA originates from
the right coronary artery in approximately 70% of patients (right dominant);
both the right coronary and left circumflex artery in 20% (codominant); and
the left circumflex artery in 10% (left dominant circulation).

 Glucose-6-phosphate dehydrogenase deficiency causes hemolytic anemia

and jaundice secondary to increased oxidative stress due to lack of NADPH.
Glutathione reductase deficiency has a similar clinical consequence as its
absence results in inability to utilize NADPH to reduce glutathione.
 Phenotypic mixing refers to coinfection of a host cell by 2 viral strains,
resulting in progeny virions that contain nuceocapsid proteins from one
strain and the unchanged parental genome of the other strain. Because there
is no change in the underlying viral genomes (no genetic exchange), the next
generation of virions revert to their original, unmixed phenotypes.

 Hypercalcemia can present with mental status changes, muscle weakness,

constipation, polyuria/polydipsia, and dehydration. Activated macrophages
in sarcoidosis and other granulomatous disease produce excess 1,25-
dihydroxyvitamin D from PTH-independent conversion, which can cause
hypercalcemia by increasing intestinal absorption of calciym and phosphate.

 Whipple disease distended macrophages in the intestinal lamina propria

are typical finding  malabsorptive diarrhea, weight loss, and joint pain
caused by Tropheryma whippelii  the glycoprotein in the cell walls of the
actinomyete colors magenta with PAS and is diastase-resistant (an excellent
stain for evaluating this disease).

 Confounding  matching is used in case-control studies in order to control

confounding. Matching variables should always be the potential confounders
of the study (eg, age, race). Cases and controls are then selected based on the
matching variables so that both groups have similar distribution in
accordance with the variables.

 Gardos channel blockers hinder efflux of K+ and water from the cell,
preventing dehydration of rbc’s and reducing polymerization of Hb S.

 Mycoplasma & ureaplasma genus lack peptidoglycan cell walls  resistant to

penicillins, cephalosporins, carbepenems, and vancomycin  treated with
tetracyclines, and macrolides.
o Mycoplasma  cold agglutinins  anemia since it mounts immune
response so treatment leads to cessation of anemia.

 Minute ventilation = product of tidal volume respiratory rate and includes

dead space. Alveolar ventilation = product of respiratory rate and difference
between tidal volume and dead space.

 Chest x-ray in acute decompensated heart failure with secondary pulmonary

edema  cepalization of the pulmonary vessels, perihilar alveolar edema
(batwaing distribution), and blunting of costophrenic angles due to pleural
effusions.

 Hepatic abscesses caused by staph aureus  through hematogenous seeding

of the liver.
 PTHrP  hypercalcemia of malignancy  squamous cell cancers of the lungs
caused by smoking

 Organ susceptibility to infarction after occlusion of a feeding artery (from

greatest to least)  CNS, myocardium, kidney, spleen, than liver (liver has
dual blood supply by hepatic and portal veins.

 Reticulocytes bluish cytoplasm and reticular precipitates of residual

ribosomal RNA.

 Phosphorylation of serine and threonine residues of insulin receptor and

insulin receptor substrate by serine kinase leads to insulin resistance. This
type of phosphorylation can be induced by TNF-a, catecholamines,
glucocorticoids, and glucagon. TNF-a is a proinflammatory cytokine that
induces insulin resistance through the activation of serine kinases, which
then phosphorylate serine residues on the beta subunits of IR and IRS-1. This
inhibits tyrosine phosphorylation of IRS-1 by IR and subsequently hinders
downstream signaling, resulting in resistance to the normal actions of
insulin. Phosphorylation of threonine residues has similar effects.

 Bladder control is influenced by descending cortical fibers that run in the

distended paraventricular area  leads to loss of cortical inhibition on the
sacral micturition center causes the development of urge incontinence.

 Dietary fructose is phosphorylated in the liver to F1P and is rapidly

metabolized because it bypasses PFK-1, the major rate-limiting enzyme of
glycolysis. Other sugars such as glucose, galactose, and mannose enter
glycolysis prior to PFK-1 and as a result are metabolized more slowly.

 Q# 302, Inflammation and Abscess  Tissue damage and resultant abscess

formation is primarily caused by lysosomal enzyme release from neutrophils
and macrophages. Pulmonary ascesses are local suppurative collection
within lung, which are caused by release of lysosomal enzyme release by
neutrophils and macrophages.

 Aspergillus fumigatus  CML chemotherapy usually loses neutrophils 

neutropenia  and infection with this organism  thin, septate hyphae, with
V-shaped branching  invasive aspergillosis.

 Anesthetics  poor blood solubility  amount of gas needed to saturate

blood is small and brain saturation occurs quickly.
o Highly soluble anesthetics are absorbed to a greater degree by the
blood, delaying saturation of the CNS  slow onset.
 o Onset of action of gas anesthetic depends on its solubility in the blood
(blood/gas partition coefficient). Drugs with high blood/gas partition
coefficients are more soluble in the blood, demonstrate slower
equilibrium with the brain, and have longer onset times.

 Q# 530, Pulmonary arterial hypertension 2-hit hypothesis  abnormal

BMPR2 gene acts as the first insult and predisposes to excessive endothelial
and smooth muscle cell proliferation. A second insult (infection, drugs, ion
channel defects) is then thought to activate the disease the disease process,
resulting in vascular remodeling, elevated pulmonary vascular resistance,
and progressive pulmonary hypertension.

 The Sympathetic nervous system typically regulates visceral function via 2-

neuron signal transmission involving cholinergic preganglionic neurons
and adrenergic postganglionic neurons. Eccrine sweat glands and the
adrenal medullae are exceptions to this rule as they are both innervated by
cholinergic neurons. The parasympathetic system uses both preganglionic
and postganglionic cholinergic neurons.

 HELLP syndrome  pregnancy in patients with severe preeclampsia or

eclampsia. MAHA hemolysis, elevated liver enzymes, and low platelets.
o Swollen fenestrae in renal glomerular capillary endothelial cellsa re
implicated in preeclampsia (presents with new-onset hypertension
and proteinuria or end-organ dysfunction at >20 weeks gestation).

 TTP, Thrombotic thrombocytopenic purpura  microangiopathic hemolytic

anemia, thrombocytopenia. ADAMTS13 decreased or deficient. Large vWF
multimers—platelet rich thrombi, which are prothrombotic and cause
microvascular thrombosis, other manifestations are renal failure, neurologic
manifestations, and fever. Plasma exchange therapy is life-saving and a rapid
diagnosis.
o Primary thrombotic microangioapathy (TMA) syndromes share
common clinical and pathologic features and result in platelet
activation and diffuse microthrombosis in arterioles and capillaries.
TMA syndromes present with hemolytic anemia with schistocytes,
thrombocytopenia and organ injury (brain, kidney, and heart). 
TTP-HUS, one of the thrombotic microangiopathy syndromes.

 Vitamin B12 deficiency  myelopathy  subacute combined degeneration.

“combined”  degeneration of both ascending (dorsal columns) and
descending (corticospinal tract) pathways. Loss of position and vibration
sensation, ataxia, and spastic paresis are common manifestations.

 Wernicke  mammillary body usually under the thalamus off to the left side
(my left) a little bulb is the mammillary body.
 Myxomatous changes with pooling of proteoglycans in the media layer of
large arteries are found in cystic medial degeneration, which predisposes to
the development of aortic dissection and aortic aneurysms. Medical
degeneration is frequently seen in younger individuals with marfan
syndrome.

 Isoniazid inhibits pyridoxine phosphokinase, leading to pyridoxine (vitamin

B6) deficiency. Pyridoxines active form is the cofactor for delta-
aminolevulinate synthase, the enzyme that catalyzes the rate-limiting step of
heme synthesis. Inhibition of this step can result in sideroblastic anemia.

 Suprachiasmatic nucleus regulates the circadian rhythem  processes light

information received from the retina and relays it to the other hypothalamic
nuclei and the pineal gland to modulate body temperature and production of
hormones such as cortisol and melatonin.  melatonin supplementation is
recommended for treatment of insomnia associated with jet lag.

 Pineal gland tumors (pinealomas) are often accompanied by headache and

nausea/vomiting due to obstruction of the cerebral aqueduct and resulting
hydrocephalus. These are due to mass effect on the dorsal midbrain in the
superior colliculus region. Findings are and upward gaze palsy, absent
pupillary reflex, and impaired convergence.

 Patient experiencing a major depressive episode should be carefully

screened for past manic episodes to rule out bipolar disorder. Antidepressant
monotherapy should be avoided in pts with bipolar disorder due to the risk
of precipitating mania.

 Intrinsic factor (IF) is a glycoprotein that is normally secreted by parietal

cells in the stomach and is necessary for the absorption of vitamin B12 in the
ileum. Patients who have undergone a total gastrectomy require lifelong
vitamin B12 supplementation due to inability to produce IF.

 Topical preparations of a-adrenergic agonists cause vasoconstriction of the

nasal mucosa vessels and are used as decongestants.  Overuse  negative
feedback  decreased norepinephrine synthesis and release from nerve
endings, which diminishes their effect  tachyphlaxis.

 Alcoholic cirrhosis  Increased pressure in the portal system portal vein

identified on cross-sectional scans lying medial to (or just within) the right
love of the lier and anterior to the IVC.

 Central pontine myelinolysis (osmotic demyelination syndrome) Spastic

quadriplegia and pseudobulbar palsy.
 Asthma  short-term relief  ipratropium (antimuscarinic M3 blocker),
long-term relief  Zafirlukast and montelukast  leukotriene D4 receptor
antagonist increases airway caliber and reducing mucosal inflammation.
LTC4, LTD4, and LTE4 are associated with asthma.
o Ipratropium, an anticholinergic agent and derivative of atropine,
blocks the action of acetylcholine at muscarinic receptors, preventing
bronchoconstriction and reducing the parasympathetic stimulation of
tracheobronchial submucosal glands in the lungs. So it would not
cause any change in a post-vagotomy patient since the vagus nerve is
not there anymore. Hence  Muscarinic works on
parasympathetic vagus nerve!

 Bartonella henselae  cat-scratch disease, bacillary angiomatosis, and

culture-negative endocarditis. Cat-scratch disease  low fever,
lymphadenopathy, and self-limited course.

 Li-fraumeni syndrome  AD mutation in the tumor suppressor gene TP53

leukemia, sarcomas, and tumors of the breast, brain, and adrenal cortex.

 Pressure-volume loops 
o normal saline infusion increases preload and causes rightward
widening of the pressure-volume loop
o decreased contractility narrow loop with a shift from the left
indicating smaller ejection fraction.
o Dobutamine infusion increase contractility  increased volume of
ejection and widening of the loop.
o Clamping the abdominal aorta  increase afterload  narrowing and
upward shift of the ventricular ejection phase.

 Neuroblastoma  spontaneous bursts of non-rhythmic conjugate eye

movements, hypotonia, myoclonus  abdominal mass  increased copies of
N-myc gene  most common extracranial neoplasm in children.

 Ulcerative colitis  increased risk of colorectal cancer depends on the extent

of colitis. Unlike sporadic colorectal carcinomas, colitis-associated
carcinomas more likely to arise from non-polypoid dysplastic lesions, be
multifactorial in nature, develop early p53 mutations and late APC gene
mutations opposite that of sporadic colorectal carcinoma’s, and be of a
higher histological grade. Erythema nodosum and pyoderma gangrenosum
and neutrophils accumulate in the crypt lumina, a finding termed “crypt
abscesses”. Endoscopy reveals erythematous, edematous, friable, and
granular mucosa that begins at the anal verge and extends proximally and its
limited to the mucosa on the rectum and sigmoid colon.
 Hyperplastic arteriolosclerosis in renal arterioles can result from and
perpetuate malignant hypertension  onion-like concentric thickening of
arteriolar walls in the renal vasculature and elsewhere.

 Transforming growth factor-ß (TGF-ß) is critical for fibroblast migration,

proliferation, and connective tissue synthesis. Increased TGF-ß activity is
responsible for the hypertrophic/keloid scarring and fibrosis of the lung,
liver, and kidney that occur with chronic inflammation.

 Standard deviation  68% = 1 SD from the mean

o 95% 2 SD from the mean
o 99.7% 3 SD from the mean
 Since 95% of values must be within 2 SD’s (200-400), what’s left from the
95% is 5% so divide it in half and 2.5% of values must lie below 200 mg/dl
and 2.5 above 240. So when the study has 400 patients, 400 x 0.025 is 10, so
10 patients will have above 240.

 COPD= hypoxia sufficient to stimulate increased erythropoietin production

by cortical cells of the kidney.

 Herpetic gingivostomatitis  severe vesicular or ulcerative disease following

primary infection with HSV-1  involves gingiva, tongue, palate, and
pharynx along with systemic symptoms (fever, malaise). Reactivation of the
latent infection in the trigeminal ganglia  mild perioral vesicles.

 Long-standing RA can affect the cervical spine causing vertebral

malalignment (subluxation) that can affect the atlantoaxial joint. Extention of
the neck during endotracheal intubation can worsen the subluxation 
leading to acute compression of the spinal cord/vertebral arteries patients
can develop paralysis with decreased or absent reflexes below the level of
the compression (spinal shock), hypotension due to loss of sympathetic tone,
and sudden death.

 Atypical lymphocytes on peripheral blood smears of patients with infectious

mono  CD8+ cytotoxic T lymphs  destroy virally infected B-lymphocytes.

 Diabetic nephropathy  end-stage renal disease diagnosed by checking the

albumin level since diabetic nephropathy is a nephrotic syndrome. Urine
albumin <300 mg/day is the earliest manifestation of diabetic nephropathy.

 Nephritis  PSGN, RPGN, IgA nephropathy (bergers),

membranoproliferative glomerulonephritis, and alport syndrome
o Both Nephritis and Nephrotic  Diffuse proliferative
glomerulonephritis, and membranoproliferative glomerulonephritis.
 Nephrotic syndrome  FSGN, MCD, Membranous nephropathy, amyloidosis,
Diabetic glomerulonephropathy.
o Increased permeability of glomerular to plasma proteins, decreased
plasma oncotic pressure of the blood  fluid shift into the
interstitium, increased aldosterone synthesis, increased ADH
release sodium and water retention and subsequent hyperlipidemia
and lipiduria.
o Frothy, foamy urine may be caused by proteinuria  nephrotic
syndrome  regional or generalized interstitial edema because the
decrease in serum albumin and total protein concentrations lowers
the plasma oncotic pressure and increases net plasma filtration
capillary beds.

 Carcinoid tumors  islands of sheets of uniform cells with eosinophilic

cytoplasm and oval-to-round stippled nuclei. Neuroendocrine cells of the GIT.
Appendiceal carcinoids typically have a benign course but may cause
appendicitis or rarely, carcinoid syndrome only with metastasis (with liver
metastasis).

 Carcinoid syndrome typically presents with episodic flushing, secretory

diarrhea, and wheezing. It can lead to pathognomonic plaque-like deposits of
fibrous tissue on the right-sided endocardium, causing tricuspid
regurgitation and right-sided heart failure. Elevated 24-hour urinary 5-
hydroxyindoleacetic acid can confirm the diagnosis.

 Isolated mitral stenosis elevates left atrial diastolic pressure and can
therefore cause elevated pulmonary capillary wedge pressure, pulmonary
HTN, decreased pulmonary vascular compliance, RV dilatation and functional
tricuspid regurgitation. Diastolic pressure in left is usually decreased or near
normal.
o However, when there’s both mitral valve and aortic valve problems
then it will show increased LV diastolic pressure.

 Lobar pneumonia  inflammation involves an entire lobe of the lung. A pale

and firm lobe  gray hepatization phase with exudates that have
neutrophils, fibrin and fragmented RBC’s.

 Hereditary hemochromatosis  excessive intestinal iron absorption and

organ damage due to iron accumulation within parenchymal tissues.
Although iron loss occurs through sloughing of the intestinal lining and
during menstruation in women, there are no regulated mechanisms to
excrete iron from the body.
 Folic acid deficiency  commonly in alcoholics  megaloblastic anemia that
can develop within weeks  macrocytosis, ovalocytosis, and neutrophils
with hypersegmented nuclei

 Glycine  most abundant amino acid in collagen, occupies every 3rd amino
acid position (gly-X-Y).

 Alkaptonuria  AR disorder  lack of homogentisic acid dioxygenase

blocks the metabolism of tyrosine, leading to an accumulation of
homogentisic acid. The Pathway that is deficient is tyrosine to fumarate.
Features are black urine color when exposed to air, a blue-black
pigmentation on the face, and ochronotic arthropathy.

 Chiari type 1  benign and presents during adulthood with occipital

headache and cerebellar dysfunction. Chiari type 2 is more severe that
affects neonates and associated with lumbar myelomeningocele and
hydrophalus.  congenital  underdevelopment of posterior fossa causing
parts of the cerebellum and medulla to herniate through the foramen
magnum.

 Both unfractionated heparin and LMWH can bind antithrombin to increase

its activity against factor X, but only unfractionated heparin is able to bind
both antithrombin and thrombin to allow antithrombin to inactivate
thrombin.

 Fibrinolytics may cause reperfusion arrhythmia on arterial re-opening after

restoration of blood flow after a clot lysis  it is a benign arrhythmia
fibrinolytics are effective when given within six hours of ST elevation MI 
CI in hemorrhagic stroke, ischemic stroke within one year, active internal
bleedind, blood pressure of 180/110mmhg and dissecting aneurysm

 Antibodies to citrullinated peptides/proteins have a high specificity for

rheumatoid arthritis  diagnosis tool for it; RA has poor specificity, as it is
contained in many other diseases.

 Anxiety due to a general medical condition  hyperthyroidism  weight

loss, tachycardia; warm moist skin; tremor, frightened stare, and
restlessness. Other diseases that can cause anxiety is hypoglycemia,
pheochromocytoma, hypercortisolism, and cardiac arrhythmias.

 Fenoldopam  selective peripheral dopamine-1 receptor agonist. It is given

intravenously to lower blood pressure in hypertensive emergency,
especially in patients with renal insufficiency. Fenoldapam causes arteriolar
dilation, increases renal perfusion, and promotes diuresis and natriuresis.
 The HCV is genetically unstable and have variant strains that are
hypervairable  it has no proofreading 3’—5’ exonuclease activity built into
the virion-encoded RNA polymerase  as a result RNA polymerase makes a
lot of errors during replication and several dozen subspecies of HCV are
typically present in the blood of infected individuals at any one time. Its
envelope glycoprotein sequences also contain a hypervariable region prone
to frequent genetic mutation.

 Autoimmune platelet destruction  common cause of thrombocytopenia

and should be suspected in patients with ecchymoses, petechiae, mucosal
bleeding, and no other obvious causes of thrombocytopenia (meds, bone
marrow failure).

 Metabolic acidosis  acidosis stimulates renal ammoniagenesis  a process

by which renal tubular epithelial cells metabolize glutamine to glutamate,
generating ammonium that is excreted in the urine and bicarbonate that is
absorbed into the blood. This process is responsible for the vast majority of
renal acid excretion in chronic acidotic states. Increased ammonium
production is almost entirely responsible for the increase in renal acid
excretion seen with chronic acidosis.

 SVC syndrome, Q#565, Intrathoracic spread of bronchogenic carcinoma

(usually lung cancer followed by non-hodgkins lymphoma is the most
common cause) may lead to compression of the superior vena cava, causing
impaired venous return from the upper part of the body  mediastinal mass
o Dyspnea, bilateral facial swelling, neck and upper extremities,
dilated collateral veins in the upper trunk, cough, headache, dizziness,
confusion, cerebral edema, elevated intracranial pressure and
laryngeal edema. Mainly on the lateral side of ascending aorta.

 Foramen ovale is patent in approximately 25% of normal adults. Although

the foramen ovale usually remains functionally closed, transient increase of
right atrial pressure above left atrial pressure can produce a right-to-left
shunt. This can lead to paradoxical embolization of venous clots into the
systemic arterial circulation.
o Stroke in the setting of venous thromboembolism  usually when
normal saline is injected into the peripheral vein then bubbles are
seen passing into the left side of the heart.

 Listeria monocytogenes produces a very narrow zone of beta-hemolysis on

blood agar, shows tumbling motility at 22C, and can be cultured at
temperatures as low as 4C. Intact cell-mediated immunity is essential for the
elimination of the bacterium from the body. Neonates up to 3 months of age
are especially vulnerable, as their cell-mediated immunity is not yet fully
developed.
 Phencyclidine (PCP)  N-methyl-D-aspartate receptor antagonist, with
lesser effects on the reuptake inhibition of biogenic amines and other
receptors. It can have dissociative and anesthetic effects but may also cause
psychosis and severe agitation leading to dissociative and anesthetic effect
but may also cause psychosis, severe agitation leading to violent trauma.
Ataxia, horizontal and vertical nystagmus, and delirium can also be present.

 Normally, metabolic acidosis is partially compensated for by respiratory

alkalosis. When the steady-state PaCO2 persists above the range, the patient
has superimposed respiratory acidosis (respiratory failure indicated by not
having a respiratory compensation).

 Vd= Amount of drug given (mg)/ plasma concentration of drug (mg/L) 

characteristics of a drug such as high molecular weight, high plasma protein
binding, high charge, and hydrophilicity tend to trap the drug in the plasma
compartment resulting in a low Vd (3-5L). A high molecular weight and
lipophilic drugs and high tissue binding and have a high Vd.

 Pregnant women  compression of IVC  gravid uterus while supine

position  reduces venous return and cardiac output  hypotension and
syncope.

 CCR5 enables HIV virus to enter cells. Deletion of both these genes 
resistance to HIV infection, deletion of one allele  delayed manifestation of
the disease in infected individuals.

 A scotoma  visual field defect that occurs due to pathologic process that
involves parts of the retina of the optic nerve resulting in a discrete area of
altered vision surrounded by zones of normal vision. Lesions of the macula
cause central scotomas.

 Acoustic schwannomas are commonly located at the cerebellopontine angle

and arise from cranial nerve VIII. Patients may have ipsilateral sensorineural
hearing loss/tinnitus and vertigo (CN VIII), loss of facial sensation (CN V),
and facial paresis (CN VII). Bilateral acoustic neuromas are associated with
neurofibromatosis type 2.

 Communicatin hydrocele  serious fluid accumulation within the tunica

vaginalis in patent processus vaginalis. Painless swelling of one scrotum that
transilluminates on examination.

 ALL type T or B, ALL subtype T cell (CD4, CD3, CD5, CD7, and CD*) 15-17%
of all cases of ALL, it presents with fever, malaise, bleeding, bone pain and
hepatosplenomeglay and mediastinal mass that can cause compression and
 lead to SVC syndrome, esophagus compression, and trachea leading to
dyspnea and stridor. They both have TdT positive
o B-cell ALL (CD10, CD19, CD20) 70-80% of all ALL  fever, malaise,
bleeding, bone pain, and hepatosplenomegaly. No symptoms of
mediastinal compression.

 Diptheria  cardiomyopathy, pharyngeal exudate, neck swelling, palatal

paralysis. Passive immunization  process of administering antitoxin
represents transfer of pre-existing, neutralizing antibodies. Passive
immunization has the greatest effect on prognosis on someone who is
infected. Active immunization with DPT vaccine (IgG against circulating
protiens) provides lasting immunity against future diphtheria infection.

 Stress-related mucosal disease is usually casued by local ischemia in the

setting of severe physiologic stress (shock, extensive burns, sepsis, severe
trauma). Ulcers arising in the setting of severe trauma/burns are called
Curlings ulcers. Ulcers arising form intracranial injury are caused by direct
vagal stimulation and are called Cushing’s ulcers  Ach release and
hypersecretion of gastric acid.

 Reye syndrome in children with febrile illness treated with salicylates

(ASPIRIN). It consists of hepatic failure and encephalopathy. 
Microvesicular steatosis of hepatocytes without inflammation and cerebral
edema is the hallmark of this disease.

 Reactive arthritis  classic traid of nongonococcal urethritis, conjunctivitis,

and arthritis. HLA-B7 positive, genitourinary or enteric infection and causes
sacroiliitis in 20% of the patients. Cutaneous findings (keratoderma
blennorrhagica and balanitis circinata) are also common. Reactive arthritis is
triggered by urogenital and gastrointestinal infections.

 Glucocorticoids  predominately catabolic  muscle weakness, skin

thinning, impaired wound healing, osteoporosis, and immunosuppression.
However they increase hepatic gluconeogenesis and glycogenesis. This along
with peripheral antagonism of insulin contributes to the development of
hyperglycemia.

 Methylmalonic academia is an organic academia due to the complete or

partial deficiency of methylmalony-CoA mutase. Complete deficiency
classicaly presents with lethargy, vomiting, and tachypnea in a newborn.
Laboratory testing shows hyperammonemia, ketotic hypoglycemia and
metabolic acidosis and an increased elevated urine methymalonic acid and
propionic acid.
 Propionyl-CoA is derived from the metabolism of valine, isoleucine,
methionine, threonine, and odd-chain fatty acids. Congential deficiency of
propionyl-CoA carboxylase, the enzyme responsible for the conversion of
propionyl-CoA to methylmalonyl-CoA, leads to the development of propionic
academia.

 Cardiac action potential conduction  slowest in AV node and fastest in the

purkinje system. Conduction speed of the atrial muscle is faster than that of
the ventricular muscle. Point 1: AV node = 0.05m/sec, point 2: Ventricular
muscle= 0.3m/sec, point 3: atrial muscle 1.1 m/sec, point 4: purkinje system
= 2.2 m/sec

 Cataract formation in diabetic’s  aldose reductase converts glucose into

sorbitol, which is further metabolized into fructose by sorbitol
dehydrogenase. (This pathway is most active in seminal vesicles). Lens has a
lot of sorbitol dehydrogenase and become overwhelmed in the setting of
hyperglycemia.  Other tissues  retina, renal papilla, Schwann cells have
much less sorbitol dehydrogenase activity.

 Paroxysmal nocturnal hemoglobinuria (PNH)  results from acquired

mutation in the PIGA gene that causes absence of the
glycosylphosphatidylinositol (GPI) anchor and associated deficiency of CD55
(decay-accelerating factor) and CD59 (MAC inhibitory protein) complement
inhibitor proteins. These proteins inactivate complement and prevent
membrane attack complex from forming on normal cells. Absence of these
results in uncontrolled complement-mediated hemolysis.
o Fatique, hemolytic anemia, hemoglobinuria, low haptoglobin, high
bilirubin and LDH, thrombocytopenia, pancytopenia.
o Chronic hemolysis can cause iron deposition in the kidney
(hemosiderosis), which can increase the risk of chronic kidney
disease.

 Power= 1-ß; study determines mean blood cholesterol level is 195mg/dl in

200 non-diabetic hospitalized patients and 210 mg/dl in 180 diabetic
patients. Probability that the observed difference is due to chance alone is
reported to be 5% (å ), and probability of rejecting the null hypothesis when
there is really a different is 20% (ß), so there is a higher number of it really
having a problem that is accidently being rejected  P= 1- ß so in this case ß
is 20% and 1-20% is equal to 0.80. (type II error p=1-ß) (type 1 error p= 1-
å ).

 Pancreatic islet amyloid deposition is characteristic of type 2 diabetes

mellitus. A strong linkage with HLA class II gene makeup, pancreatic islet
infiltration with leukocytes (insulitis), and antibodies against islet antigens
are frequently seen in type I diabetes.
 Opioid analgesics can cause contraction of smooth muscles in the sphincter
of Oddi, leading to increased pressures in the common bile duct and
gallbladder.

 Q#952 Coronary steal syndrome = Collateral microvessels form adjacent

pathways for blood flow to areas distal to an occluded vessel. Adenosine and
Dipyridamole are selective vasodilators of coronary vessels that can cause
coronary steal, a phenomenon in which blood flow in ischemic areas is
reduced due to arteriolar vasodilation in nonischemic areas. Coronary steal
can lead to hypoperfusion and worsening of existing ischemia.  Allows for
detection of ischemic areas that would otherwise not be seen in a resting
heart. So pretty much induces ischemia.

 Plummer-Vinson syndrome  dysphagia form esophageal webs and iron

deficiency anemia. Koilonychia (spoon-shaped nails) and shiny red tongue.
Most symptoms resolve following iron supplementation.

 Radial head subluxation (nursemaid’s elbow) result from sudden traction on

the outstretched and protonated arm of a child. Affected children are usually
in little distress unless attempts are made to move the elbow. The annular
ligament is torn and displaced in this injury.

 Cause of fistulas in crohn’s disease  transmural inflammation of any area of

the GIT with involvement of all layers of the intestinal wall explains the most
common cause of the fistula’s and strictures.

 Progressively weakening diaphragmatic contractions during maximal

voluntary ventilation with intact phrenic nerve stimulation indicates
neuromuscular junction pathology (myasthenia gravis) or abnormally rapid
diaphragmatic muscle fatigue.

 3’CCA tail of tRNA serves as the amino acid binding site by aminoacyl tRNA
synthetase.

 Closteridium perfringens  Lecithinase = alpha toxin  degrade lecithin a

component of cellular phospholipid membranes, leading to membrane
destruction, cell death and widespread necrosis and hemolysis.

 Ivabradine selectively inhibits funny Na+ sodium channels (If), prolonging

the slow deplorazation phase 4 and slowing the SA node-firing rate.  Has
negative chronotropic effect with little effect on cardiac contractility and
relaxation.
o With no effect on cardiac contractility and/or relaxation.
 Idiopathic pulmonary fibrosis  dyspnea, dry cough, restrictive profile,
interstitial fibrosis with cystic air space enlargement dense fibrosis
(honeycomb) are prominent in subpleural and paraseptal spaces.

 Rivaroxaban and Apixaban both direct and Fondaparinux indirect are factor
Xa inhibitors. These drugs are used in long-term treatments DVT and stroke
prophylaxis in patients with atrial fibrillation who are at risk for embolic
stroke.

 At age 2, children should have a vocab of 50-200 words and be using 2-word
phrases. Parents concerns about delayed milestones should be validated;
they should be reassured that children often catch up but may need help.
Further evaluation and regular monitoring are essential.

 IFN-gamma released by T lymphocytes and activates macrophages to make

granulomas  TB tests.

 A drug that binds to and activate GABA-A receptors (or enhances their
activity) will increase the conductance of chloride ions, leading to increased
passive transport of chloride into the cell interior. This causes the membrane
potential to become hyperpolarized (more negative than resting membrane
potential) by approaching or reaching the equilibrium potential for chloride.

 Wilson’s disease (copper toxicity)  cystic degeneration of the putamen and

other basal ganglia structures. Putamen is medial to the insula and lateral to
the globus pallidus on coronal sections. Kayser-Fleischer rings brownish or
grey-green rings of fine granular copper deposits in descemet’s membrane in
cornea.

 Common cardinal veins of the developing embryo drain directly into the
sinus venosus. These cardinal veins ultimately give rise to SVC and other
constituents of the systemic venous circulation. In the embryo the umbilical
vein degenerates and vitelline veins becomes the portal system.

 Strep pneumoniae leading cause of community acquired pneumonia, otitis

media, and meningitis in adults  lancet-shaped, GM+ cocci in pairs.

 Clinicians have legal and ethical obligation to report elder abuse, neglect, and
exploitation. If there is reason to suspect abuse or neglect, the patient should
be interviewed alone to avoid intimidation by possible abusers.

 Zenker’s diverticulum (false) diminished relaxation of cricopharyngeal

muscles during swallowing results in increased intraluminal pressure in the
oropharynx. This may eventually cause the mucosa to herniate through a
zone of muscle weakness in the posterior hypopharynx. Usually presents in
 elderly patients with oropharyngeal dysphagia, halitosis, regurgitation, and
recurrent aspiration pneumonia.

 Varicose veins are dilated; tortuous veins resulting form impairment of the
venous valves and reflux of venous blood. This leads to venous
stasis/congestion, edema, and increased incidence of superficial venous
thrombosis. Thromboembolism is a very infrequent complication of varicose
veins, while venous stasis ulcers are very common and often occur over the
medial malleolus. Complication are skin ulcerations, poor wound healing and
superficial infections.

 Atrial fibrillation  associated with increased risk of systemic

thromboemobolism  left atrial appendage is the most common site of
thrombus formation  would lead to left atrial enlargement, and normal left
ventricle systolic function and mild mitral regurgitation. With AF, there is an
ineffective atrial contraction and absence of the end-diastolic atrial kick,
resulting in loss of the “a” wave from jugular venous pulse tracing.

 Isoproterenol  nonselective B adrenergic agonist  increases cardiac

contractility by acting on the myocardial ß-1 adrenergic receptors. It relaxes
the vascular smooth muscle by binding to B-2 causes decrease in vascular
resistance and mean arterial blood pressure.

 Q# 2116, Lung cancer, An obstructive lesion in the mainstem bronchus can

prevent ventilation of an entire lung, leading to obstructive atelectasis and
complete lung collapse. Characteristic findings on chest x-ray  unilateral
pulmonary opacification (cloudy lung) and deviation of the mediastinum
toward the opacified lung.

 Damage to the brainstem at/below the level of the red nucleus e.g (midbrain
tegmentum, pons) typically results in decerebrate (extensor) posturing 
loss of descending excitation to the upper limb flexors (via the rubrospinal
tract) and predominance of the extensors (controlled by the vestibulospinal
tract). Limps are flat and off to the side of the body.
 Damage to neural structures above the red nucleus (cerebral hemispheres)
 decorticate flexor posturing due to loss of descending inhibition of the red
nucleus and subsequent hyperactivity of upper-extremity flexor muscles, so
tight fist with arms on top of the body.

 Gaucher disease  AR lysosomal storage disorder that is characterized by ß-

glucocerebrosidase deficiency and presents with pancytopenia and
hepatosplenomegaly  distended macrophages with a wrinkled tissue paper
appearance  gaucher cells.
 Some individuals demonstrate increased activity of specific intracellular
enzyme more susceptible to developing benz(o)pyrene-induced lung cancer
and the enzyme most overactive is microsomal monooxygenase cytochrome
P450 most chemicals enter the body in an inactive state (pro-carcinogens).
These chemicals are converted into active metabolite by the cytochrome
P450 oxidase system.

 Dietary lipids (triglycerides, phospholipids, cholesterol esters) are primarily

digested in the duodenum via pancreatic enzymes. Bile salts emulsify lipid
breakdown products, forming water-soluble micelles that facilitate lipid
absorption in the jejunum. Most cholecystectomy patients can tolerate fatty
foods in the diet as bile is constantly being released into the duodenum. 
Dietary lipids absorbed in the jejunum.

 Ethanol inhibits citric acid cycle TCA and inhibits gluconeogenesis and can
cause hypoglycemia once hepatic glycogen stores are depleted.

 4 calories per gram of protein/carbohydrate, 9 caloreis per gram of fat, 7

calories per gram of ethanol. When someone is constructed to consume
3000 cal per day and 30% of that to be protein and they want to know the
gram per day of protein person needs to take 
o 3000 x 30% = 900 / 4 cal/gram of protein = 225 g/day of protein

 prostacyclin vasodilates, inhibits platelet aggregation and increases

vascular permeability, thromboxane A2  vasoconstricts, aggregates
platelets and decreases vascular permeability. They are in homeostasis.

 Chronic kidney disease  osteodystrophy from secondary

hyperparathyroidism, hyperphosphatemia and hypocalcemia.

 Anatomic of functional vesicoureteral reflux is almost always necessary for

the development of acute pyelonephritis.

 ADH acts primarily on collecting ducts, increasing their permeability to

water. In the absence of ADH, the tubular fluid is most concentrated at the
junction between the descending and ascending limbs of the loop of henle
and most dilute in the collecting ducts.

 Transfer RNA (tRNA) is a small, noncoding form of RNA that contains

chemically modified bases (dihyfrouridine, ribothymidine, pseudouridine).
tRNA has a CCA sequence at its 3-end that is used as a recognition sequence
by proteins. The 3’ terminal hydroxyl group of the CCA tail serves as the
amino acid binding site.
 Oppositional defiant disorder  behavioral disorder of childhood
characterized by argumentative and defiant behavior toward authority
figures. It does not involve the more severe violation of basic rights of others
seen in conduct disorder.

 Conduct disorder  like PDD but behaviors are more severe and aggressive,
physical aggression or cruelty towards people or animals, destruction of
property, stealing or deceit which can lead to antisocial disorder if older than
18 year of age.

 Antisocial disorder  disregard for and violation of the rights of others,

criminality, impulsivity, males>females and is not diagnosed in individuals
under age 18 and a history of conduct disorder.

 Thoracic outlet syndrome  due to compression of the lower trunk of the

brachial plexus in the scalene triangle, the space bordered by the anterior
and middle scalene muscles and the first rib  symptoms, upper extremity
numbness, tingling, and weakness.

 Resting membrane  potassium (-70), than sodium (+60), then Cl- (-90),

 Normally rectus abdominis muscle is transected vertically, but a horizontal

transection of the rectus abdominus muscle must be performed with great
caution as the inferior epigastric arteries enter this muscle at the level of the
arcuate line. The inferior epigastric arteries below the arcute line are
susceptible to injury (eg, hematoma) due to lack of support posterior rectus
sheath.

 Spinal accessory nerve is vulnerable to injury in the posterior triangle of the

neck. Injury results in weakness of the trapezius muscle, which presents with
drooping of the shoulder, impaired abduction of the arm above horizontal
(due to weakness in rotating the glenoid upward), and winging of the
scapula.

 RRR =standard care 8% recurrences, new drug + standard care together

need to bring down 40% = .4x0.08=0.032  0.08-0.032 = 0.048 or 4.8%

 ARF  migratory arthritis, new onset mitral regurgitation, fever, and anti-
streptolysin O titer. Acute morbidity is most likely due to pancarditis
(inflammation of the endocardium, myocardium, and epicardium). Mitral
stenosis develops years or decades after the original illness.

 Topical capsaicin  causes desfunctionalization of afferent pain fibers and

depletion of substance P. Initial application results a burning and stinging
sensation, but chronic exposure leads to reduced pain transmission.
 Colchicine  treatment of gouty arthritis in patients who cannot take
NSAIDs due to peptic ulcer disease. It inhibits leukocyte migration and
phagocytosis by blocking tubulin polymerization , which disrupts
cytoskeletal-dependent fuctions such as chemotaxis and phagocytosis.
Significant side effects of colchicine include nausea and diarrhea, also
reduces the formation of leukotriene B4.

 Low serum levels of C1 esterase inhibitor are diagnostic of hereditary

angioedema an inherited AD condition that causes episodes of painless, non-
pitting, well-circumscribed edema. Face, neck, lips, tongue are most
commonly affected, but internal organs may also be involved.
o Hereditary angioedema, low C1 esterase inhibitor activity leads to
increases in bradykinin activity. ACE inhibitors should not be used in
these patients.

 Decompensated systolic heart failure due to nonischemic cardiomyopathy 

after initial stabilization, give beta blockers (carvedilol, and metoprolol)
should be started in all HF patients with LV systolic dysfunction to improve
survival. Also ACE inhibitors, ARBs, and aldosterone antagonists.
 Beta-blockers should not be initiated in patients with unstable HF and should
be introduced slowly to avoid worsening of patients condition by further
impairing cardiac output.

 Sertoli-leydig cell tumors of the ovary arise from the sex cord stroma and
secrete testosterone. Typical features include a large ovarian mass and signs
of virilization. Tubular structures lined by round sertoli cells and surrounded
by a fibrous stroma are seen on pathology.

 Maturing erythrocytes lose their ability to synthesize heme when they lose
their mitochondira, which are necessary for the first and final 3 steps of
heme synthesis.

 Neisseria gonorrhea  IgA protease which cleaves IgA at its hinge region,
rendering it ineffective  IgA exits on mucosal surfaces and bind and inhibits
the action of pili and other cell surface antigens that normally mediate
mucosal adherence and subsequent penetration. Neisseria meningitides,
strep pneumo, and haemophilus influenza all have IgA protease.

 The splenic flexure and rectosigmoid junction lie between regions of

perfusion of major arteries. Watershed areas are susceptible to ischemic
damage during hypotensive states, esp in patients with underlying arterial
insufficiency.
 Carotid sinus massage  increase in parasympathetic tone causing
temporary inhibition of SA node activity, slowing of conduction through the
AV node, and prolongation of the AV node refractory period. Its useful vagal
maneuver for termination of paroxysmal supraventricular tachycardia.

 Thromboemolism  perfusion limited  ventilation/perfusion mismatch.

 Horseshoe kidney fused at poles  the inferior mesenteric artery (IMA)

limits the ascent of the horseshoe kidney.

 Acute HBV from an unprotected sex can cause serum sickness-like

syndrome with joint pain, lymphadenopathy, and pruritic urticarial rash,
upper right quad pain, hepatomegaly, and elevated transaminase levels.

 Cardiac tamponade  hypotension with pulsus paradoxus, elevated jugular

venous pressure, muffled heart sounds (beck’s traid). Pulsus paradoxus 
exaggerated decrease in systolic blood pressure >10 mmhg on inspiration.
Also common in pericardial effusion.

 Left-sided heart disease can cause pulmonary HTN  increasing pulmonary

venous pressure and congestion  leads to passive increase in pulmonary
arterial pressure, which is made worse by reactive vasoconstriction and
structural remodeling of the pulmonary vasculature secondary to impaired
nitric oxide availability and increased endothelin expression.

 Sickle cell  asplenic (atrophy or asplenia)  infections with encapsulated

bacteria  strep pneumo, hemophilus influenza. Salmonella  m/c cause of
osteomyelitis, than staph aureus and e. coli next m/c cause of osteomyelitis.

 Q#1874, During wound healing  excessive matrix metalloproteinase

activity and myofibroblast accumulation in the wound margins can result in
contracture. Contractures produce deformities of the wound and
surrounding tissues, on palms, soles, anterior thorax and or at serious burn
sites.
o Wound dehiscence  rupturing of previously closed wound 
insufficient granulation and scar formation, inadequate wound
contraction, or excessive mechanical stress.

 Cleavage of pro-insulin in the islet cell secretory granules yields insulin and
C-peptide, which are stored in the granule until they are secreted in
equimolar amounts.
 PAD peripheral arterial disease -> give cilostazol  reduces platelet
activation by inhibiting platelet phosphodiesterase, the enzyme responsible
for the breakdown of cAMP. It is also a direct arterial vasodilator decreases
claudication symptoms and increase in pain-free walking distance. These
 patients should also be initiated on a graded exercise program, which has
also been shown to improve symptoms.
 Abciximab, heparin, and tPA are all not used for long-term management.
 Aspirin antiplatelet agent for CAD not useful for PAD.

 Dopamine agonists  ergot = bromocriptine, nonergot = pramipexole &

ropinirole  chemical structure similar to neurotransmitter dopamine and
directly stimulate dopamine receptors.

 Diabetic mononeuropathy  CNIII, caused central ischemia affects the

somatic nerve fibers but spares peripheral parasympathetic fibers.
Symptoms  ptosis, down and out gaze, and normal light and
accommodation reflexes.

 Cell surface cytotoxic T-lymphocytes stimulate a response that results in

rapid cell death  by effectors of caspases.

 Low doses of dopamine  stimulate D1 in renal and mesenteric vasculature

 vasodilation and increased blood flow to these sites.
 High doses of dopamine  increase cardiac contractility by stimulation of
beta-1 adrenergic receptors  generalized vasoconstriction by alpha-1
ultimately.

 Adenocarcinoma in situ (bronchioalveolar carcinoma) of lung  well-

differentiated dysplastic columnar cells that line alveolar septa without
vascular or stromal invasion  aerogenous spread and can progress to
invasive disease if not resected.

 Cavernous sinus  houses CN 3, 4, 5(1), and 6  headache, fever, proptosis,

ptosis, mydriasis, ipsilateral deficits, and eye cannot move in any direction,
by usually thrombosis or infection sometimes from mucormycosis if the
patients has diabetes type 1 which always leads to DKA.

 Renal cortical cells sense hypoxia and respond by synthesizing and releasing
erythropoietin which stimulates production of erythrocytes in bone marrow.

 Stretch injury of the pudendal nerve due to stress placed on pelvic floor
during labor  weakness of the perineal musculature causing fecal and
urinary incontinence, perineal pain, and sexual dysfunction.

 Lepromin skin test  + in pts with tuberculoid leprosy strong CD+ T cells
immune response  increase IL-2 and IFN-gamma in skin lesions
o Lepromatous leprosy  Negative to their weak Th1 cell-mediated
immune response so no reaction.
 Phrenic nerve  C3-C5  intrathoracic spread of lung cancer may affect the
phrenic nerve  hiccups, diaphragmatic paralysis with dyspnea. Brachial
plexus  pain in distribution of C8-T1, T2 nerve roots. Involvement of
recurrent laryngeal nerve may cause hoarseness.

 Physicians are ethically and legally obligated to report impaired colleagues in

a timely manner. Reporting protects safety and can assist the impaired
physician in receiving appropriate evaluation and treatment.

 Pufferfish poisioning is caused by tetrodotoxin, a neurotoxin produced by

microorganisms associated with the fish. Tetrodotoxin binds to voltage-gated
sodium channels in nerve and cardiac tissue, preventing sodium influx and
depolarization. Voltage-gated sodium channels are important for the
generation and propagation of action potentials. When the action potential
reaches the axon terminal, voltage-gated calcium channels open and allow
the influx of calcium, which is essential for the fusion and release of
neurotransmitter vesicles into the synaptic cleft.

 Synaptophysin  protein found in presynaptic vesicles of neurons,

neuroendocrine, and neuroectodermal cells. Glail orgin  astrocytes,
ependymomas, and oligodendrogliomas stain positive for GFAP.

 Disulfirm-like reaction  metronidazole, cephalosporins, and 1st generation

sulfonylureas shortly after alcohol consumption  symptoms are abdominal
cramps, nausea, headache, facial flushing, and vomiting.

 Risk is the probability of developing disease over a certain period of time. To

calculate this probability, divide the number of affected subjects by the total
number of subjects in the corresponding exposure group.

 Norovirus  viral gastroenteritis  watery diarrhea with no blood or

mucus, vomiting, fever, malaise, and headache outbreaks in crowded
places like schools.

 Q# 0760, Immunity to Tetanus, C. tetani produces the protein exotoxin

tetanospasmin that blocks release of inhibitory (glycine and GABA) motor
interneurons in the CNS. Tetanus is prevented by immunization with toxoid
that triggers the production of antitioxin antibodies (active immunity). So a
vaccinated person does not develop tetanus because of circulating antibodies
that neutralize bacterial products. Toxin blocks release of glycine & GABA
from the spinal inhibitory interneurons that regulate the lower motor
neurons  increased motor neurons cause increased activation of muscles
 leading to spasms and hyperreflexia.
 Hydroxylationof proline and lysine residues in collagen helps it attain its
maximum tensile strength. This process occurs in the rough endoplasmic
reticulum and requires vitamin C as a cofactor. Impaired collagen synthesis
resulting from vitamin C deficiency (scurvy) can lead to fragile vessels,
predisposing to gingival bleeding, ecchymosis, and petechia. Defective
proline hydroxylation leads to failure of triple helix formation and
stabilization by pro-alpha chains during collagen synthesis.

 Atherosclerotic plaques  develop predominately in large elastic arteries

(aorta, carotid, and iliac arteries), and in large or medium-sized muscular
arteries (coronary and popliteal arteries. In humans the most heavily
involved vessels is the abdominal aorta> coronary> popliteal > internal
carotid > and circle of Willis. ACPCCW

 Helicobacter pylori can cause duodenal ulcers and is typically found in

greatest concentration in the prepyloric area of the gastric antrum. As a
result, biopsy of the prepyloric area would have the greatest yield of the
organism.

 Hepatocellular carcinoma is strongly associated with HBV infection.

Integration of viral DNA into genome of host hepatocytes triggers neoplastic
changes including suppression of the p53 tumor suppressor. Other risk
factors for hepatocellular carcinoma include HCV, alcoholic cirrhosis,
aflatoxins, and hemochromatosis.

 The facial nerve (CN VII) exits the stylomastoid foramen and courses through
the substance of the parotid gland, where it divides into its 5 terminal
branches that innervate the muscles of facial expression.
o Malignant tumors of the parotid gland often compresses and disrupts
the facial nerve and its branches, causing  ipsilateral facial droop.

 Early Lyme disease causes flu-like symptoms and erythema chronicum

migrans. The second stage of Lyme disease may involve atrioventricular
block and facial palsy. Late Lyme disease can cause chronic asymmetric large
joint arthritis and encephalopathy. Lyme disease is easily treated with
doxycycline at first and when facial palsy results than treat with penicillin-
type antibiotics like ceftriaxone to prevent late Lyme disease. Also
tetracyclines/doxycycline are the first-line treatment for lyme disease, they
are contraindicated in pregnancy due to the potential for fetal tooth
discoloration. Amoxicillin should be given instead for treatment of Lyme
disease in pregnant women.
 Down syndrome  chromosomal anomaly  low levels of maternal serum
alpha-fetoprotein and estriol and increased levels of ß-hCG and inhibin A.
Elevated a-fetoprotein  multiple gestations, open neural tube defects,
abdominal defects. Also low levels of a-fetoprotein  trisomy 18.
 Cardiac pacemaker cells  have only phase 4 (Na+/K+ inward slow current),
phase 0 (Ca+ voltage gated inward channels for depolarization), and phase 3
(K+ efflux for repolarization). Slope of phase 4 in the SA node determines
heart rate. ACh/adenosine decreases diastolic depolarization and decreases
HR, while catecholamines increases depolarization and increases HR.
Verapamil  calcium CH blocker slows depolarization of cardiac slow-
response tissue (SA & AV) nodes and the latter part of phase 4. Verapamil
also decreases the amount of intracellular calcium available within
cardiomyocytes (fast-response tissue), which can reduce myocardial
contractility.

 Cystinuria  AR disorder caused by defective transportation of cysteine,

ornithine, arginine, and lysine (COAL) across the intestinal and renal tubular
epithelium in proximal convoluted tubule PCT. Recurrent nephrolithiasis is
the only clinical manifestation. Urinalysis shows pathognomonic hexagonal
cysteine crystals.

 Ampicillin for listeria only, resistant to cephalosporins.

 Q# 11920, Ovarian Vein Thrombosis, Venous stasis  hypercoagulability

from pregnancy in addition to endothelial damage from delivery can cause
ovarian vein thrombosis in puerperium. Symptoms include fever and
localized abdominal or flank pain. Most thrombosis is right-sided and can
extend to the inferior vena cava; however left ovarian vain thrombosis can
extend into left renal vein. Mostly right sided, and can dislodge into the IVC,
but pulmonary emboli is uncommon and morbidity/mortality is low.

 Pulmonary emboli typically appear  multiple wedge-shaped hemorrhagic

lesions in the periphery of the lung. Intravenous drug users are at risk for
developing septic pulmonary emboli as a complication of tricuspid valve
endocarditis.

 Above pectinate line internal hemorrhoids and adenocarcinoma 

supplied by superior rectal vein venous drainage from superior rectal vein
to inferior mesenteric vein to portal system.

 Below pectinate line  external hemorrhoids  squamous cell

carcinomainferior rectal artery (branch of pudendal artery) and drains
into the inferior rectal vein to internal pudendal vein to internal iliac vein to
IVC.

 Type 1 HSR  Cell surface-bound antibody bridging by antigen  allergen

with preexisting IgE bound to basophils and mast cells.
 Homocystinuira  elevated levels of plasma homocysteine  risk for
thrombotic events. Homocysteine can be metabolized to methionine via
remethylation or to cystationine via transsulfuration.
Hyperhomocysteinemia is most commonly due to genetic mutations in
critical enzymes or deficiencies of vitamin B12, vitamin B6, and folate.

 The ions that will flow out of the cell after opening their respective ion
channels are potassium only.

 Professional medical organization with published ethics guidelines

consistently recommend that treatment of friends should be limited to
emergency situation when no other physician is available. Providing informal
treatment to friends is ethically problematic and should generally be limited
to emergency situations in which no other physician is available.

 Syphilis  primary = chancre lesion, secondary = condylomata lata, and

tertiary syphilis = gumma with cardiovascular involvements, and
neurosyphilis.

 Febrile seizures  most common neurologic disorder affecting children and

are benign sequelae of fever. Children who experience a febrile seizure are at
risk for recurrence but have a low risk of developing epilepsy. Antipyretics
(acetaminophen and ibuprofen) can improve patients during fever but do not
prevent future seizures. Heat strokes however, like when a child is left in a
hot car will need actively cooling right away with water sponging, and ice
packs.

 Superior mesenteric artery syndrome occurs when the transverse portion of

the duodenum is entrapped between the SMA and aorta, causing symptoms
of partial intestinal obstruction. This syndrome occurs when the
aortamesenteric angle critically decreases, secondary to diminished
mesenteric fat, pronounced lordosis, or surgical correction of scoliosis.

 Cremasteric reflex  lightly stroking the medial thigh, which causes

contraction of the cremaster muscle to pull the ipsilateral testis. This reflex is
mediated by genitofemoral nerve, which originates from the L1-L2 spinal
nerves. Loss of the cremasteric reflex is most commonly seen with testicular
torsion or L1-L2 spinal injury.

 Prostatic plexus lies within the fascia of the prostate and innervates the
corpus cavernosa of the penis, which facilitates penile erection. As a result,
prostatectomy or injury to the prostatic plexus can cause erectile
dysfunction.
 Emphysema/COPD  increased TLC, RV and FRC (functional residual
capacity = RV + ERV (expiratory reserve volume). All increased!

 Prepatellar bursitis causes anterior knee pain and is usually due to repetitive
or prolonged kneeling. A bursa  fluid filled synovial sac that serves to
alleviate pressure from bony prominences and reduce friction between
muscles and tendons.

 Transference is the unconscious shifting of emotions associated with a

significant person from ones past to a person in the present.

 Malignant mesothelioma  rare neoplasm from the pleura or peritoneum 

strongly associated with asbestos exposure  Hemorrhagic pleural effusions
and pleural thickening are characteristic  tumor cells with numerous, long
slender microvilli and abundant tonofilaments.

 Ulcerative colitis  Erythema nodosum and pyoderma gangrenosum

 Diabetes  acanthosis nigricans and necrobiosis lipoidica diabeticorum.
 Dermatitis herpetiformis  celiac disease  erythematous pruritic papules,
vesicles, and bullae that appear bilaterally and symmetrical on the extensor
surfaces.

 Chronic kidney disease with mineral bone disease usually presents with
hyperphosphatemia. Secondary hyperparathyroidism and decreased
calcitriol levels. Patients can be asymptomatic or develop weakness, bone
pain, and fractures. ^PTH, PO4, and decreased calcitriol.

 Reflux nephropathy  vesicoureteral reflux is caused by retrograde urine

flow from the bladder into the ureter. The hydrostatic pressure of refluxing
urine along with infections due to ascending bacteria causes inflammation.
The compound papillae in the upper and lower poles of the kidney are most
susceptible to reflux-induced damage, which appears as dilated calyces with
overlaying renal cortical scarring  hypertension from pyelonephritis.

 Toxic megacolon well-recognized complication of ulcerative colitis 

abdominal pain/distention, bloody diarrhea, fever, and sings of shock. Plain
abdominal x-ray is the preferred diagnostic imaging study. Barium contrast
studies and colonoscopy are contraindicated due to the risk of perforation.

 Chronic pericarditis  pericardial knock = high frequency, precordial sound

heard in early diastole, acute pericarditis = friction rub.

 Restrictive lung disease  interstitial lung disease  decreased lung

volumes and increased lung elastic recoil caused by fibrotic interstitial
tissues. The increased elastic recoil results in increased radial traction
 (outward pulling) on the airways, leading to increased expiratory flow rates
when corrected for the low lung volumes.

 Q# 197, Fat emboli  statin black with osmium tetroxide.

 Succinylcholine  fast-acting depolarizing neuromuscular blocking agent

used for rapid-sequence intubation  equal reduction of all 4 twitches
during train-of four stimulation. Prolonged administration in patients with
abnormal plasma cholinesterase activity  transition to a phase II
(nondepolarizing) block, seen as a progressive reduction in each of the 4
twitches.

 Patients with sickle trait  asymptomatic  protected from Plasmodium

falciparum  normal hemoglobin, reticulocytes, and RBC indices.

 KRAS  bound to GTP. Regulation of the Ras-MAPK signal transduction

pathway requires a balance between active (GTP-bound) and inactive (GDP-
bound) Ras proteins. RAS gene mutations, which result in constitutively
activated Ras proteins, are implicated in the development of malignant
tumors.

 A P50 shift from 26mmHg to 20mmHg indicates that the affinity of

hemoglobin for oxygen is increased (left shift of the O2 dissociation curve)
which means less oxygen loading to tissues and more RBC produced from
bone marrow to compensate  erythrocytosis.

 Fractures of orbital floor  direct frontal trauma to the orbit  infraorbital

nerve runs along the orbital floor in a groove in the maxilla  CN V2 which
innervates from under the eye to the top of the lips so this patient would
have paresthesias of the upper cheek, upper lip, and upper gingiva. Inferior
rectus muscle entrapped  limiting superior gaze.

 Duodenal ulcers not associated with increased risk of carcinoma in the same
location in contrast, esophageal, gastric, colorectal cancers are frequently
identified as ulcerative lesions on endoscopy.

 Hepatitis B  reverse transcriptase of RNA template  partially double-

stranded circular DNA and reverse transcriptase.

 Alcohol- induced hepatic steatosis  decrease free fatty acid oxidation

secondary to excess NADH production by the 2 major alcohol metabolism
enzymes, alcohol dehydrogenase and aldehyde dehydrogenase.

 During exercise --> Shorter duration of diastole during tachycardia becomes

the major limiting factor for coronary blood supply to the myocardium.
 Neutropenia is a significant adverse effect of ganciclovir therapy, and its
incidence is increased with co-administration of zidovudine or
trimethoprim-sulfamethoxazole.

 Atrial Myxoma  m/c primary cardiac neoplasm and 80% arises at the left
atrium. A mid-diastolic rumbling murmur head best at apex (MS), positional
cardiovascular symptoms (dyspnea and syncope), embolic symptoms, and a
large pedunculated mass in the left atrium.  Scattered cells within
mucopolysaccharide stroma, abnormal blood vessels, and hemorrhaging.

 Hamartomas  m/c benign lung tumors  coin lesion in pts 50-60 years old
 composed of disorganized cartilage, fibrous and adipose tissue.

 UMN lesion  contralateral spastic rigidity, hyperreflexia and paresis. They

can affect any part of they pyramidal motor system, including the
corticospinal tracts of the spinal cord; the medulla, pons, and midbrain; the
internal capsule; the precentral gyrus (primary motor cortex).
o Clasp-knife spasticity with initial resistance to passive extension
followed by sudden release of resistance  internal capsule stroke
pure motor weakness affecting contralateral arm, leg, and lower face.

 Adolescents have low treatment adherence rates related to issues with

autonomy, rebellion against authority figures, and lack of understanding of
potential risks. Peer behavior has a strong influence on adherence at this age
due to adolescents’ desire to fit in with their social groups.

 Differential clubbing and cyanosis without blood pressure or pulse

discrepancy are pathognomonic for a large patent ductus arteriosus
complicated by Eisenmenger syndrome (reversal of shunt flow from left-to-
right to right-to-left). Severe coarctation of the aorta can cause lower
extremity cyanosis. Right-to-left shunting in patients with large septal
defects and tetralogy of fallot results in whole-body cyanosis.

 Neurocysticercosis  common cause of seizures in patients from central and

south America and should be considered in patients with suggestive
symptoms and imaging (cystic brain lesion) and characteristic
epidemiological risk factors  exposure to infected stool.

 M/c trigger for DIC in pregnancy is release of tissue factor (thromboplastin)

from an injured placenta (placental abruption) into the maternal circulation.
DIC bleeding form incision sites, intravenous line sites, mucosal surfaces
due to rapid consumption of clotting factors and platelets. Placental
abruption may result from severe hypertension and one that leads to fetal
demise is the most common cause of DIC in pregnancy.
 o However, amniotic fluid embolism is associated with hypotension and
cardiogenic shock rather than the hypertension.

 Q# 1518 AV shunts increase preload and decrease afterload by routing blood

directly from the arterial system to the venous system, bypassing the
arterioles. High-volume AV shunts can eventually  high-output cardiac
failure.

 A cerebellar hemangioblastoma in association with congenital cysts of the

kidneys, liver, pancreas  highly suggestive of VHL disease, a rare AD
condition.

 3 variables that affect the total oxygen content of blood are hemoglobin
concentration, oxygen saturation of hemoglobin (SaO2), and the partial
pressure of oxygen dissolved in blood (PaO2). Anemia  decreased
hemoglobin concentration in the setting of normal SaO2 and PaO2.

 Highly active antiretroviral therapy (HAART) for HIV is commonly associated

with body fat redistribution. Subcutaneous lipoatrophy involving the face
and extremities is associated with nucleoside reverse transcriptase
inhibitors (especially stravudine and zidovudine) and protease inhibitors.
Central fat accumulation in the trunk and viscera can occur with any HAART
regimen.

 Postpartum hemorrhage is an obstetrical emergency. Bilateral ligation of the

internal iliac artery can decrease uterine blood flow and control postpartum
hemorrhage that is unresponsive to medial management (Uterine massage,
uterotonic medications).

 Poststreptococcal glomerulonephritis presents with edema, hypertension,

and hematuria after a streptococcal infection. Most children recover
completely but adult patients have a relatively poor prognosis and higher
risk of chronic hypertension and renal insufficiency.

 Pseudomonas  motile and oxidase positive

 X-linked (Bruton) agammaglobulinemia caused by defect in B cell

maturation, resulting in the absence of mature B cell with severe deficiency
of all immunoglobulin types. T cell number and function remain intact. Due
to the absence of B cells, primary lymphoid follicles and germinal centers will
not form within the lymph nodes. T cell  Paracortical zones, B cells 
follicles and germinal centers.

 Hemolytic uremic syndrome  common cause of acute renal failure in

children. It is characterized by the triad of: microangiopathic hemolytic
 anemia, thrombocytopenia, and acute kidney injury. Most cases develop
following a diarrheal illness caused by shiga toxin-producing organisms
(E.coli 0157:H7, shigella dysenteriae) microthormbi in small vessels.

 To prevent future cardiovascular events in lipidemia  an enzyme inhibitor

 statin drugs, which inhibit HMG-Co Reductase, leads to lowering LDL
levels and prevent cardiovascular events for the future.

 Malignant cells with nuclei contain prominent, round, basophilic bodies of

the nucleus  Nucleolus  site of ribosomal subunit maturation and
assembly  RNA polymerase I synthesizes the vast majority of rRNA from
within the nucleolus.

 New-onset odynophagia (pain with swallowing food) in the setting of chronic

gastroesophageal reflux disease usually indicates the presence of erosive
esophagitis and formation of an ulcer. Diagnosis is made by upper
endoscopy.

 Postpartum hemorrhage is an obstetric emergency and can result from

abnormal placentation. Prior uterine surgery can impair decidualization,
resulting in myometrial invasion by villous tissue and a placenta that is
abnormally attached to the myometrium (placenta accreta).

 Vitamin A can be beneficial in the treatment of measles infection by reducing

comorbidities (e.g. Ocular complications, diarrhea, pneumonia), recovery
time, and length of hospital stay.

 Human chorionic gonadotropin (hCG) has a structure similar to TSH. Patients

with testicular germ cell tumors or gestational trophoblastic disease may
develop very high serum HCG concentrations, which can stimulate TSH
receptors and cause hyperthyroidism.

 The aedes aegypti mosquitoes can transmit the viruses that cause dengue
fever and chikungunya. Classic dengue fever presents as an acute febrile
illness with headache, retro-orbital pain, and joint and muscle pain.
Chikungunya is a febrile illness with flulike symptoms, prominent
polyarthralgias, and diffuse macular rash.

 Typhoid fever  caused by salmonella typhi and usually acquired from

contaminated food or water, typically in areas with poor sanitation 
escalating fevers with initial diarrhea or constipation then abdominal pain,
formation of rose spots on the chest/abdomen, and hemorrhagic enteritis
and possible bowel perforation.
 Epinephrine increases systolic blood pressure (a1 + B1), increases heart rate
(B1), and either increases or decreases diastolic blood pressure depending
on the dost (either a1 or B2 predominates). Pretreatment with propranolol
eliminates the B effects of epinephrine (vasodilatation and tachycardia),
leaving only the a effect (vasoconstriction).

 Class 1C antiarrhythmics are potent sodium channel blockers  exhibit

strong use-dependence by prolonging the QRS duration to a greater extent at
higher heart rates. Class II (beta blockers) use during exercise can limit
maximal heart rate that is achieved. Digoxin  false positive ST segment
depression during exercise. Class III prolong QT interval duration,
verapamil class IV  block or slow SA and AV nodal conduction.

 Acetyl-CoA  allosteric activator of gluconeogenesis that acts by increasing

the activity of pyruvate carboxylase when acetyl-CoA is abundant. This
regulatory step allows pyruvate to be shunted toward acetyl-CoA production
when acetyl-CoA levels are low, preventing the cell from becoming depleted
of energy.

 Cellular compartmentalization allows multiple biochemical processes to

occur simultaneously at maximum efficiency.
o Beta-oxidation of fatty acids, TCA cycle, decarboxylation of pyruvate
all occur in mitochondria.
o Glycolysis, fatty acid synthesis, and pentose phosphate pathway (HMP
Shunt) reside in the cytosol. Transketolase is in the HMP pathway and
uses B1 vitamin (thiamine) to shuttle 2-carbon fragment between
sugar molecules.
o Heme synthesis, urea, and gluconeogenesis  both mitochondria and
cytosol.

 Telomerase  RNA-dependent DNA polymerase  synthesizes telomeric

DNA sequences that can replace the lost chromosomal ends of the telomeres.
Telomerase  prevents chromosomal shortening.

 Liver functionality  tests by PT, bilirubin, albumin, and cholesterol.

Structural integrity and cellular intactness of the liver  transaminases, or
biliary tract  alkaline phosphatase (both in liver and bone), gamma-
glutamyl transferase (GGTP). GGTP is not present to a significant extent in
bone. It is therefore particularly useful in determining whether an elevated
alkaline phosphatase is of hepatic or bony origin. A moderately elevated ALP
of unclear etiology should be followed up with GGTP.

 Cardiac Leads in MI 
1. Leads I and aVL  lateral aspect of LV  occlusion of left circumflex
artery  acute lateral myocardial infarction.
 2. Leads V1-V4  LAD  anterior aspect of the LV and interventricular
septum.
a. Leads V1-V2  anteroseptal  LAD occlusion
b. Leads V3-V4  Anteroapical  distal LAD occlusion
3. Left main coronary artery  give rise to LAD (anterior) and left
circumflex arteries (lateral) occlusion here  anterolateral
infarction ST elevation in anterior V1-V4, and lateral V5-V6, I, and aVL
leads.
4. Right coronary artery  RV and inferior aspect of LV  inferior MI
ST elevation in lead II, III, and aVF.

 SA node  specialized pacemaker cells located at junction of right atrium

and SVC  site of earliest electrical activation in patients with sinus rhythm.

 Inhaled anesthetics  almost all-volatile anesthetics increase cerebral blood

flow  undesirable effect as it results in increased ICP. Other SE are
myocardial depression, hypotension, respiratory depression, and decreased
renal function.

 Tolcapone and entacapone  prevent L-dopa degradation to 3-O-

methyldopa by inhibiting COMT  decreases peripheral levodopa
degradation.

 Wallerian degeneration  refers to the process of axonal degradation and

breakdown of the myelin sheath that occurs distal to a site of injury. Axonal
regeneration does not occur in the central nervous system due to the
persistence of myelin debris, secretion of neuronal inhibitory factors, and
development of the dense glial scarring (formed by astrocytes).

 IL-6, IL-1, TNF-a  systemic inflammatory response and stimulate hepatic

secretion of acute-phase proteins (fibrinogen).

 Ballotable left flank mass after hysterectomy  causes hydronephrosis 

ureters run in close proximity to the pelvic lymph nodes and the uterine
artery in the female pelvis, which predisposes them to injury during pelvic
surgery.

 Silicosis  inhalation of mineral dusts  pneumoconiosis dyspnea on

exertion and productive cough  calcification of the rim of hilar nodes
(eggshell calcification) and birefringent silica particles surrounded by fibrous
tissues on histology.

 Asbestosis  dyspnea on exertion  lower zones  pleural plaques =

ferruginous bodies- fusiform rods with translucent asbestos center and iron-
containing coating.
 Berylliosis  ill-defined nodular or irregular opacities on chest x-ray 
noncheasting epitheloid granulomas without obvious particles.

 Coal workers pneumoconiosis  exertional dyspnea and nodular interstitial

opacities on chest- X ray  nodal interstitial infiltrates on chest x- ray
noncaseating granuloma.

 Organic dust  hypersensitivity pneumonitis  exertional dyspnea and

diffuse nodular interstitial infiltrates.

 Varenicline  partial agonist of nicotinic acetylcholine receptors  can

assist patients with cessation of tobacco use by reducing withdrawal cravings
and attenuating the rewarding effects of nicotine.

 Kaposi’s sarcoma (HHV-8) involves the skin and GI tract and is common in
HIV patients not on antiretroviral therapy. Endoscopy reveals characteristic
lesions, which range from reddish/violet flat maculopapular lesions to raised
hemorrhagic nodules or polypoid masses. Biopsy can show spindle cells,
neovascularization, and extravasated red blood cells.

 Various forms of cardiac rupture from m/c to l/c

o Free wall rupture  hemopericardium and cardiac tamponade
o Ventricular septal rupture  acute ventricular septal defect and left-
to-right shunting.
o Papillary muscle rupture  acute onset of severe MR.
 Rupture of LV free wall  catastrophic mechanical complication of anterior
wall myocardial infarction (MI) that usually occurs within the first 3-14 days
after MI. Rupture leads to hemopericardium and cardiac tamponade, causing
profound hypotension and shock with rapid progression to pulseless
electrical activity and death.

 Major depressive disorder consists of a >2 week period with >5 of the
following symptoms: depressed mood, loss of interest, sleep disturbance,
appetite disturbance, loss of energy, psychomotor agitation or retardation,
impaired concentration, guilt, and suicidal thoughts.

 Pituitary apoplexy  acute hemorrhage into the pituitary gland 

preexisting pituitary adenoma. Presents acutely with severe headache,
cranial nerve involvement, (bitemporal hemianopsia, opthalmoplegia),
decreased libido for a while, and signs of meningeal irritation. Pts often have
chronic symptoms associated with underlying pituitary tumor.
Cardiovascular collapse can occur due to adrenocortical deficiency.
 Merocrine glands release a watery secretory product via exocytosis with no
loss of cell membrane. Apocrine glands release membrane-bound vesicles
containing the secretory product. Holocrine gland release the entire content
of cells via cell lysis (sebaceous glands, Ace vulgaris inflammatory acne).

 Q# 1879, Factor V Leiden  heterozygote with single amino acid

substitution (glutamine for arginine) near protein C cleavage site 
hypercoagulable  DVT PE.

 Iron deficiency anemia  most dangerous overlooked mechanism  blood

loss (in postmenopausal women and older men) in the GIT due to
malignancy. Women of childbearing age lose iron through menstruation, but
older men and postmenopausal women have no reason to be iron deficient.
o Decreased serum iron, increased transferrin, and increased TIBC.

 Pneumococcal conjugate vaccines are strongly immunogenic in infancy due

to both B and T cell recruitment. They provide higher, longer-lasting
antibody titers relative to pneumococcal polysaccharide vaccines. The
pneumococcal polysaccharide vaccine is poorly immunogenic in infants due
to their relatively immature humoral antibody response.

 Sturge-weber syndrome  congenital vascular disorder  facial port-wine

stain, leptomeningeal capillary-venous malformation.

 Osler-weber-rendu syndrome  hereditary hemorrhagic telangiectasia

multiple telangiectasia’s of the skin and mucosa membranes of the lips,
oronasopharynx, respiratory tract, GI tract, and urinary tract. Rupture of
these telangiectasias may cause epistaxis, GI bleeding or hematuria.

 MI  sharp decrease in cardiac output and no difference in venous return on

the curve.
 Anaphylaxis  venous and arteriolar dilatation & increased capillary
permeability  significant drop in venous return.
 Phenylephrine infusion  vasoconstriction = increased TPR and systolic
blood pressure decreased CO due to increased afterload & decrease in
venous return and decreases pulse pressure and HR.
 GI bleeding  decrease in circulating blood volume shift to the left.
 Chronic arteriovenous shunt would increase CO and increase venous return.
Would also cause venous return to shift to the right because of circulating
blood volume.

 Left intercostal space of left midclavicular line  injury to the left lung.

 Teniae coli a surgical landmark next to the appendix (appendicitis).

 Congenital pyloric stenosis  hypertrophy of the pyloric muscularis
mucosae and prominent peristalsis in the epigastrium and an olive-sized
mass on deep palpation.

 Cardiac ischemia  Ion pump failure due to ATP deficiency  intracellular

accumulation of Na+ and Ca2+  cellular and mitochondrial swelling.

 Theophylline  adenosine receptor antagonist and indirect adrenergic agent

with narrow therapeutic index. Metabolized by hepatic cytochrome oxidases
so can be increased to toxic levels by inhibition of P450 system 
ciprofloxacin.

 Staph aureus  protein A virulence factor in peptidoglycan cell wall 

binds to the Fc portion of IgG.

 Radioactive iodine therapy  pretreat with potassium perchlorate to

decrease the effects of radiotherapy through competitive inhibition of iodine
transportation.

 Biliary atresia or obstruction of extrahepatic bile ducts  jaundice, dark

urine, acholic stools in 1st 2 months of life due to conjugated
hyperbilirubinemia.

 Tocar and cannula will penetrate the bladder wall and anterior abdominal
aponeurosis.

 Corticosteroids  increase neutrophils and decrease other WBC’s.

 Furosemide  ototoxicity, inhibits Na-K-2Cl symporters in the loop of henle

effectively causing increased Na, Cl, and Fluid excertion. Additionally, loop
diuretics also stimulate prostaglandin release. By stimulating renal
prostaglandin release, loop diuretics also increase renal blood flow leading to
increased GFR and enhanced drug delivery. Thus, concurrent use of NSAIDs
with loop diuretics can result in a decreased diuretic response. High doses
predispose to hypokalemia and contraction alkalosis, with early signs of
hypokalemia with muscle weekness, cramps, myalgias and fatique. Prompt
treatment is necessary to prevent respiratory depression and ventricular
arrhythmias.

 Primary hyperparathyroidism  subperiosteal resorption with cystic

degeneration, excess secretion of parathyroid hormone by parathyroid
adenomas can cause Hypercalcemia. This may lead to atrophy of the
remaining 3 parathyroid glands due to feedback inhibition.
 In CHF  more of angiotensin II potent vasoconstrictor  more in
pulmonary vein than in artery to rise BP.

 Acute tubular necrosis (ATN)  recovery phase has hypokalemia,

hypomagnesaemia important complications due to high volume, hypotonic
urine.

 Wet age-related macular degeneration  retinal neovascularization due to

VEGF levels. Acute vision loss, grayish-green subretinal membrane and
subretinal hemorrhage. VEGF inhibitor therapy is the treatment like
ranibizumab and bevacizumab.

 Diphtheria toxin and pseudomonal exotoxin A  ribosylating and

inactivating elongation factor 2 EF2, inhibiting host cell protein synthesis and
causing cell death.

 Coxiella burnetii  farm workers waste from cattle and sheep. Myalgia’s,
retroorbital headache, fatigue, and fever, thrombocytopenia increased liver
enzymes  acute Q fever.

 Demyelination of axons decreases length constant and increases time

constant.

 Myocardial oxygen extraction exceeds that of any other tissue or organ in the
body. Due to the high degree of oxygen extraction, increases in myocardial
oxygen demand (during exercise) are met by a nearly proportionate increase
in coronary blood flow/coronary sinus.

 Rhino Virus naked SS+ sense RNA  has a purified RNA molecule to induce
viral protein synthesis in a host cell; it must be able to act directly as mRNA
using the host’s intracellular machinery for translation. Therefore, in general,
purified single-stranded positive-sense RNA can be infectious; single-
stranded negative sense or double-stranded RNA is not.

 Adult patients with capacity have the authority to refuse any form of
treatment, including life-saving therapies. In an emergency situation in which
the patient does not have capacity, consent is not required to provide life-
saving treatment. In an emergency, the physician should always provide
potentially life-saving therapy to a minor.

 An elderly patient with nutrient deficiency most likely with normal blood
counts with decreased light touch, vibration sense in the feet, decreased knee
and ankle reflexes bilaterally  thiamine B1 deficient  dry beriberi is
symmetrical peripheral neuropathy; wet beriberi includes the addition of
high-output congestive heart failure.
 Pressure in the left renal vein may become elevated due to compression
where the vein crosses the aorta beneath the superior mesenteric artery.
This “nutcracker effect” can cause hematuria and flank pain. Pressure can
also be elevated in the left gonadal vein, leading to formation of varicocele.

 Corticosteroids have the strongest and most predictable effects on the

inflammatory component of asthma. Inhaled corticosteroids form the
cornerstone of chronic therapy for patients with persistent asthma and can
reduce the number and severity of acute asthma exacerbations. (Fluticasone)

 Overflow incontinence  impaired detrusor contractility (detrusor muscle

inactivity), (diabetic autonomic neuropathy), or bladder outlet obstruction
(tumor obstructing urethra) causing incomplete bladder evacuation. 
Involuntary and continuous urinary leakage when the pressure inside the full
bladder exceeds that of the sphincters.

 Urge incontinence  detrusor overactivity that causes sudden and/or

frequent urge to urinate and empty the bladder. Triggers can include running
water, hand washing, or exposure to cold water. Loss of inhibitory central
nervous system input to the bladder, due to frontal lobe and internal capsule
infarcts, commonly cause detrusor hyperreflexia and urge incontinence. Also
small frontal lobe infarct that loses inhibitory function to the bladder.

 Stress incontinence  loss of pelvic floor support and incompetence of the

urethral sphincter (urethral sphincter dysfunction). Increased abdominal
pressure (coughing, sneezing, vigorous effort) greater than urethral
sphincter pressure can cause brief involuntary urine loss, which is virtually
diagnostic of stress incontinence.

 Hemoglobin A2 elevated in beta-thalassemia as beta-globin chain

underproduction leads to decreasing hemoglobin A synthesis.

 CLL  lymphoproliferative disorder involving B-lymphocytes. The most

significant laboratory finding is marked lymphocytosis with smudge cells
seen on peripheral blood smear. Increased expression of proto-oncogenes
BCL-2 similar to follicular lymphomas.

 Chronic myeloproliferative disorders (polycythemia vera, essential

thrombocytosis, and primary myelofibrosis) often have a mutation in Janus
kinas 2 (JAK2), a cytoplasmic tyrosine kinase  results in constitutive
tyrosine kinase activity, and consequently, in the cytokine-independent
activation of signal transducers and activators of transcription (STAT)
proteins. (JAK-STAT signaling pathway).
 Both gynecomastia and spider angiomata are caused by hyperestrinism
(this can be due to liver cirrhosis due to increases in androstenedione
production, androgen aromatization, and sex hormone-binding globulin
concentration (binds testosterone). This is due to decreased metabolism of
estrogen by the failing liver, decreased production of sex hormone binding
globulin by the liver which causes increased free sex hormone levels.

 Scarlet fever  fever, pharyngitis, sandpaper-like rash, circumoral pallor,

and a strawberry tongue. It is caused by strains of Group A streptococcus
that produce pyrogenic exotoxins. Scarlet fever can predispose to acute
rheumatic fever and glomerulonephritis.

 Kawasaki disease  fever, strawberry tongue, bilateral conjunctival

injections, coronary aneurysm.

 An increase in estrogen activity  pregnancy, oral contraceptive use, post-

menopausal hormone replacement therapy increases the synthesis and
sialylation of TBG, leading to decreased clearance of the protein and elevated
TBG levels  increase in total thyroid hormone levels (increased in total T4
pool), but feedback control maintains normal levels of free thyroid hormone.

 In patients with mitral regurgitation MR, the most reliable auscultatory

finding indicating a high regurgitant volume (Severe MR) and LV volume
overload is left-sided S3 gallop. The intensity of the holosystolic murmur
does not correlate well with regurgitant volume as larger regurgitant orifices
often present with softer murmurs.

 Most of the K+ absorbed in the PCT and loop of henle  100% in Bowman’s
capsule, 35% in PCT, 10% in loop of henle, and 110% in collecting ducts.

 First-generation antipsychotics can be classified according to high or low

potency and have characteristic side effect profile. Low-potency
(chlorpromazine) more likely to cause non-neurological side effects
(sedation, anticholinergic side effects, orthostatic hypotension). High-
potency (fluphenazine) antipsychotics are more likely to cause
extrapyramidal symptoms (potency= extrapyramidal).

 Open-angle glaucoma  characterized by progressive loss of peripheral

vision from elevated intraocular pressure. Timolol and other nonselective
beta-blockers work by diminishing the secretion of aqueous humor by the
ciliary epithelium. Acetazolamide, a carbonic anhydrase inhibitor, also
decreases aqueous humor secretion by the ciliary epithelium. Prostaglandin
F2a (latanoprost, travoprost) and cholinomimetics (pilocarpine, carbachol)
decrease intraocular pressure by increasing the outflow of aqueous humor.
 Right atrium, RV  periodic pressure of maximum of 25mmhg and minimum
of 2mmhg, Pulmonary artery  pressure of maximum 25mmhg and
minimum of 10mmhg, LV 90-140 mmhg and LEDV pressure of 6-12mmhg.

 Abnormal bleeding in patients with uremia is due to a qualitative platelet

disorder that causes prolonged bleeding time with normal platelet count,
prothrombin time, and activated partial thromboplastin time. Uremic
bleeding can be improved with dialysis, as it removes the toxins and partially
reverses the bleeding abnormality.

 Digoxin is used to for ventricular rate control in atrial fibrillation as it

decreases atrioventricular nodal conduction by increasing parasympathetic
vagal tone. Digoxin is also used in heart failure due to its positive inotropic
effect. This is accomplished by inhibition of the Na+/K+ ATPase pump, which
leads to increased intracellular calcium and greater contractility.

 Subacute sclerosing panencephalitis is rare complication of measles infection

that occurs several years after recovery from initial infection. Oligoclonal
bands of measles virus antibodies are found in the cerebrospinal fluid of
these patients. Proteins of membrane-bound hemagglutinin.

 Nephrotic syndrome is characterized by massive proteinuria >3.5

hypoalbuminemia, generalized edema, hyperlipidemia, and lipiduria.
Depending on the ratio of low-to-high molecular weight proteins in the urine
with Nephrotic syndrome, proteinuria can be either highly or poorly
selective proteinuria. Minimal change disease is an example of highly
selective proteinuria selective albuminuria: mostly low-molecular weight
proteins, such as albumin and transferrin, are excreted.

 Orthopnea (shortness of breath when lying flat, person has to sit up or prop
up on pillows to feel better) a specific sign of left-sided heart failure. Bilateral
lower extremity edema and congestive hepatomegaly are more specific for
right-sided heart failure. Left-sided heart failure may also produce a
productive cough and exertional wheezing or chest tightness, but these are
nonspecific signs seen in a variety of disorder.

 Abetalipoproteinemia inherited inability to synthesize apolipoprotein B,

an important component of chylomicrons and VLDL. Lipids absorbed by the
small intestine cannot be transported into the blood and accumulate in the
intestinal epithelium, resulting in enterocytes with clear or foamy cytoplasm.
Usually in infants with malabsorption, abdominal distention, foul-smelling
stool, deficiency of fat-soluble vitamins particularly vitamin E and essential
fatty acids. Acanthocytes, progressive ataxia, and retinitis pigmentosa.
 Follicular lymphoma  m/c indolent non-hodkins lymphoma in adults. It is
of B-cell origin and presents with painless waxing and waning
lymphadenopathy. The cytogenetic change t (14; 18) is characteristic and
results in in overexpression of bcl-2 oncogene.

 Testes para-aortic retroperitoneal lymph nodes, glans penis & cutaneous

posterior calf drain into the deep inguinal lymph nodes. All skin from the
umbilicus down including the anus  below the dentate/pectinate line
drains into the superficial inguinal lymph nodes, which then drains into the
deep inguinal lymph nodes later.

 Renal papillary necrosis  classically presents with gross hematuria, acute

flank pain, and passage of tissue fragments in urine. It is most commonly
seen in patients with sickle cell disease or trait, diabetes mellitus, analgesic
nephropathy, or severe obstructive pyelonephritis.

 Indwelling bladder catheters urinary tract infection pseudomonas

aeruginosa

 Primary biliary cirrhosis  potential cause of hypercholesterolemia leading

to xanthelasma of the upper eyelid. Destruction of intrahepatic, interlobular
bile ducts by granulomatous inflammation  insidiously with pruritus (at
night esp.) and fatigue in middle-aged women, develop signs of jaundice, pale
stools, and dark urine and hypercholesterolemia (xanthelasma).

 Pancreatitis  major risk factor for ARDS  release of large amounts of

inflammatory cytokines and pancreatic enzymes, which leads to activation of
neutrophils in the alveolar tissues  interstitial and intaalveolar edema,
inflammation, and fibrin deposition cause the alveoli to become lined with
way hyaline membranes.

 Ureter can be injured during hysterectomy due to its close proximity to the
uterine structures. Distal ureter may be severed during ligation of the uterine
vessels because the ureter passes inferior and lateral to the uterine artery at
the level of the internal cervical os prior to entering the bladder (water under
the bridge).

 Ducts distended by pleomorphic cells with prominent central necrosis that

do not penetrate the basement membrane are characterized ductal
carcinoma in situ. It is the precursor to invasive ductal carcinoma, the most
common type of breast cancer.

 Metformin inhibits hepatic gluconeogenesis and increases peripheral glucose

utilization. Lactic acidosis is a rare complication of metformin therapy, but its
risk is increased in patients with underlying renal insufficiency, but first
 before initiation of the drug you must first test the patients serum Creatinine
to check if he kidneys are functioning well.

 Q# 903, Idiopathic pulmonary artery hypertension  increased arteriolar

smooth muscle thickness (medial hypertrophy), intimal fibrosis, and
significant luminal narrowing. If severe HTN  lesions can form interlacing
tufts of small vascular channels called plexiform lesions.

o Women age 20-40, dyspnea and exercise intolerance, inactivating

mutations involving pro-apoptotic BMPR2 gene. Increase in
endothelial and smooth muscle cell proliferation leads to vascular
remodeling, elevated pulmonary vascular resistance, and progressive
pulmonary hypertension.
o Treat with Bosentan  competitive antagonist of endothelin
receptors used for treatment of idiopathic pulmonary arterial
hypertension. Decreases pulmonary arterial pressure and lessens the
progression of vascular and right ventricular hypertrophy.

 Pseudogout  Synovial fluid analysis shows rhomboid-shaped calcium

pyrophosphate crystals is diagnostic. Positively birefringent under polarized
light, knee joint is involved >50% of cases, whereas in gout it’s the toe that
mainly involved and in gout its monosodium urate (needle shaped and
negatively birefringent).

 S3 gallop  LV systolic heart failure  occurs after S2 associated with

increased left ventricular end-systolic volume:
1. Forceful, rapid filling of a ventricle that has normal or elevated
compliance.
2. Normal or even decreased filling rates when ventricular compliance is
low.
3. Blood flowing into an overfilled ventricle with high end-systolic volume.

 Efficacy is a measure of the maximum pharmacodynamics effect achievable

with a drug. Potency refers to the dose of drug that is required to produce a
given effect. Drugs that bind their receptors with a higher affinity or are
better able to gain access their target tissues will have greater potency
(lower ED50).
o The more to the left it is  higher potency
o The higher the curve is  higher efficacy
o 2 curves same efficacy  competitive antagonist added to the drug so
shifts it to the right
o 2 curves one with higher efficacy and one wit lower 
noncompetitive inhibitor
o Partial agonist also has lower efficacy.
 Q# 1133. Clavicle fracture Clavicle most commonly fractured bone in
children  sternocleidomastoid muscle causes superior displacement of the
medial fragment; the weight of the arm and the pectoralis major muscle
cause inferior displacement of the lateral fragment. Also in distal clavicle
fracture, the deltoid will draw a distal fragment inferolaterally, this can cause
displacement of the fracture and lead to possible nonunion.

 A pudendal nerve block  performed by injecting an anesthetic

intravaginally, medial to the ischial spine, through the sacrospinous ligament.
This provides anesthesia to most of the perineum for perineal laceration
repair.

 Diabetes insipidus DI  unable to concentrate their urine in response to

dehydration. Following desmopressin administration during the water
deprivation test, urine osmolality increases to normal levels in central DI but
does not change in complete nephrogenic DI. And in Primary polydipsia 
exhibits an increase in serum and urine osmolality on water deprivation that
is similar to partial nephrogenic DI.

 Glucagonoma (alpha-cells of pancreatic islets of Langerhans) Necrolytic

migratory erythema  papules/plaques on face, perineum, extremities
(elevated painful and pruritic rash, large lesions with central clearing of
bronz-colored induration). Lesions enlarge & coalesce, leaving a bronze-
colored, central indurated area with peripheral blistering and scaling. Causes
diabetes mellitus, GI symptoms, and markedly elevated glucagon levels.

 Medullary thyroid cancer  neuroendocrine tumor  arises from

parafollicular calcitonin-secreting C cells  nests or sheets of polygonal or
spindle-shaped cells with extracellular amyloid deposits derived form
calcitonin.

 Persistent granulomatous inflammation with subsequent fibrosis can cause

organ dysfunction, which is seen in a number of granulomatous diseases, so a
boy with sutures comes in for a painful subcutaneous nodule is caused by
foreign body causes granuloma. CD 4+ cells secrete INF-g  activates
macrophages  secretes TNF-a  further macrophage maturation and
formation of granuloma.

 The change in the body of neuron after axons has been severed are called
axonal reaction.  Increased protein synthesis that facilitates axon repair.
Results in enlarged, rounded cells with peripherally located nuclei and
dispersed finely granular Nissl substance are seen.
 Cirrhosis  diffuse hepatic fibrosis with replacement of normal lobular
architecture by fibrous-lined parenchymal nodules composed of proliferating
hepatocytes.

 Pyrimidine dimers  (nucleotide excision repair) formed in DNA as a result

of ultraviolet light exposure. They are recognized by a specific endonuclease
complex that initiates the process of repair by nicking the damaged strand on
both sides of the pyrimidine dimer. The damaged segment is then excised,
and replaced by DNA polymerase.

 Renal vein thrombosis  Nephrotic syndrome  new-onset left varicocele

associated with ipsilateral flank pain, hematuria, left-sided varicocele  loss
of antithrombin III is responsible for the thrombotic and thromboembolic
complications of nephrotic syndrome. But normally left-sided varicoceles are
relatively common in healthy pubertal men as the aorta and SMA can
compress the left renal vein (nutcracker effect), resulting in increased
intravascular pressure in the left gonadal vein (pampiniform plexus) with
retrograde blood flow and varicocele formation.

 Portal vein thrombosis  hypertension, splenomegaly, varicosities at

portocaval anastomoses. It does not cause histologic changes to the hepatic
parenchyma. Ascites is uncommon as the obstruction is presinusoidal.

 Heart failure backup of fluid in the pulmonary  transudate of plasma into

the lung interstitium and alveoli.

 E. Coli  lactose fermenter and indole-positive gram-negative rods  m/c

cause of UTI

 Symmetrical enlargement of ventricle  communicating hydrocephalus 

secondary to dysfunction or obliteration of subarachnoid villi  usually from
Tb meningitis or subarachnoid/intraventricular hemorrhage.

 Iron is absorbed in the duodenum, folate in the jejunum and B12 in the ileum

 Growth hormone (GH) is used to treat turners syndrome  binds to cell

surface receptors, leading to intracellular activation of the JAK-STAT
pathway. Cytokines (interferon) and hematopoietic growth factors (e.g.
Erythropoietin, G-CSF) also use this pathway.
o Mosaicism presence of multiple genetically different cell lines
within the body, can be either germline mosaicism or somatic
mosaicism, if its germline, it can be passed on to offspring, but somatic
does not pass on.
  For example, turner’s syndrome 45,X/46, XX can be both found
in sex chromosome  usually a milder form or a
asymptomatic.

 Medullary respiratory center controls the depth and rate of respiration based
on the input from central and peripheral chemoreceptors and airway
mechanoreceptors.

o Central chemoreceptors  increased PaCO2 is the major stimulator of

central chemoreceptors, leading to an increase in respiration.
o Peripheral chemoreceptors (in the carotid bodies, CN IX) carotid
and aortic bodies  primary sites for sensing arterial PaO2 and
stimulated by hypoxemia.
o Pulmonary stretch receptors  militated & myelinated C fibers in the
lungs and airway  regulate the duration of inspiration and act to
predominately to protect the lung from hyperinflation.
 PaCO2 is the major stimulator of respiration in healthy people. Even a slight
increase in PaCO2 results in increased pulmonary ventilation. In patients
with chronic obstructive pulmonary disease, response to PaCO2 is blunted
and hypoxemia becomes an important contributor to the respiratory drive.
Peripheral chemoreceptors are primarily responsible for sensing arterial
PaO2 and can be suppressed with O2 administration.

 Nitroprusside on the LV pressure/volume relationship curve treats

hypertension heart failure short-acting balanced venous and arterial
vasodilator. Decreases left ventricular preload and afterload so that enough
cardiac output is delivered at a lower LVEDP. So the curve shifts to the left
and down, so afterload (ejection fraction) is decreased, and preload is also
decreased but compliance is unchanged.

 Infectious esophagitis (odynophagia, dysphagia is common in patients with

HIV and immunocompromised patients. The most common cause is Candida
albican, also cytomegalovirus, and HSV too.
o CMV esophagitis  large, shallow linear ulcerations in distal(lower)
esophagus with intranuclear cytoplasmic inclusion microscopically.
o Candida  grey, white pseudomembranes on erythematous mucosa,
yeast cell and pseudohyphae
o HSV-2 small vesicles “punched out” ulcers, eosinophilic
intranuclear inclusions (Cowdry type A) in multinuclear squamous
cells at ulcer margins.

 The celiac trunk is the first main branch of the abdominal aorta; it provides
oxygenated blood to the spleen, stomach, liver, abdominal esophagus, and
parts of the duodenum and pancreas. The proper hepatic artery is a distal
branch of the celiac trunk that supplies arterial blood to the liver; it also runs
 with the portal vein and common bile duct to form the portal triad in the
liver.

 A femoral nerve block to repair the quadriceps muscle  should be in the

inguinal crease to anesthetize the skin and muscles of the anterior thigh
(quadriceps), femur, and knee, also the saphenous nerve (terminal extension
of the femoral nerve) to decrease sensation in the medial leg below the knee.

 Constrictive pericarditis  a chronic condition in which the normal

pericardial space is replaced by a thick, fibrous shell that restricts ventricular
volumes and eventually causes heart failure. Impaired right ventricular filling
leads to increased jugular venous pressure and often results in a positive
Kussmaul sign. There may also be a pericardial knock, which occurs earlier in
diastole than the S3 heart sound. Kussmaul sign Increased JVP.

 Class IB (lidocaine, mexilitine) highly efficacious in inhibiting ischemia-

induced ventricular arrhythmias. It binds inactivated sodium channels and
rapidly dissociates  as a result it is effective in suppressing ventricular
tachyarrhythmia’s induced by rapidly depolarizing and ischemic
myocardium. Amiodarone has replaced lidocaine as the drug of choice in
acute management of ventricular arrhythmias during myocardial infarction.

 Regular insulin and neutral protamine Hagedorn (NPH) are the only human
recombinant insulin’s. And usually curve point B, and ends in about 5-7
hours. The rest of the insulin’s given are usually referred to as insulin
analogs. When given NPH insulin starts working within 30 mins, peaks 2-4
hours and lasts 5-8 hours. Human form insulin should be used in patients
with DKA as they are usually volume depleted and have erratic subcutaneous
absorption.

 Alport syndrome  disorder of type IV collagen  hearing loss and ocular

abnormalities  EM = lamellated basement membrane with irregular
thinning and thickening basket-weave appearance).

 IgA nephropathy (Berger disease) frequently presents as recurrent, self-

limited, painless hematuria within 5 days after an upper respiratory infection
(synpharyngitis hematuria). Kidney biopsy will show mesangial IgA deposits
on immunofluorescense. In contrast, PSGN is seen 1-3 weeks after strep
pharyngitis and is usually not recurrent.

 Endometriosis refers to the presence of endometrial glands and stroma

outside the uterus. It may be asymptomatic or present with dysmenorrhea,
dyspareunia (pain with intercourse), and/or infertility.
 Type 2 diabetes mellitus is due to insulin resistance and relative insulin
deficiency. Chronically elevated free fatty acid levels contribute to insulin
resistance by impairing insulin-dependent glucose uptake and increasing
hepatic gluconeogenesis  acanthosis nigracans can also present due to DM
on axillary and skin folds.

 Gilbert syndrome  no apparent liver disease that has mild unconjugated

hyperbilirubinemia that appears provoked by one of the classic triggers.

 Dubin-johnson syndrome  black liver conjugated chronic

hyperbilirubinemia associated with hemolysis.

 Melanoma  early horizontal phase with low metastatic potential followed

by a nodular, vertical growth phase  increased risk of metastasis. Depth of
invasion is the most important prognostic indicator of malignant melanoma.

 Acute erosive gastropathy  NSAID, head trauma, severe burns, acute stress,
and alcohol/tobacco use. Erosions are mucosal defects that do not fully
extend through the muscularis mucosa. Acute erosive gastropathy can cause
upper GI hemorrhage that leads to melena. Gastric ulcers extend into the
submucosal layer and muscularis propria  but in erosion do not fully
penetrate the muscularis mucosa.

 Reed-Sternberg cells are large binucleated cell with “owls’ eyes” appearance
that appear on a background of lymphocytic infiltrates. Reed-Sternberg cells
must be present histopathologically in order to make the diagnosis of
hodkins lymphoma. Abnormality is in the lymphoid tissue.

 The risk of progression of diabetic nephropathy in patients with proteinuria

can be reduced by appropriate glycemic and blood pressure control. ACE
inhibitors and angiotensin II receptor blocker are the preferred
antihypertensive agents due to their blood pressure-independent anti-
proteinuric effects.

 Parvovirus B19 (erythema infectiosum) 5th disease presents with a

nonspecific prodrome malaise, fever, and congestion followed by classic
“slapped-cheek” facial rash and lacy, reticular body rash. It is highly tropic for
erythrocyte precursor cell and replicates predominantly in the bone marrow.

 Both schwannomas (biphasic pattern of cellularity antoni A and B areas) and

melanomas are S-100 positive due to their neural crest cell origin. Optic
nerve is covered with oligodendrocytes not schwann cells, but the rest of the
CN are schwann cells. Most common site for this tumor is cerebellopontine
angle at CN VIII  acoustic neuromas and can present with tinnitus, vertigo,
and sensorineural hearing loss.
 Medicare is different from Medicaid  state-run medical insurance program
that covers the homeless, undocumented immigrants, pregnant women, and
low-income families. Medicare  federal socialized medical insurance
program that covers individuals age 65 and older who have a work history
and younger individuals with disabilities.

 Universal vaccination of children against HBV would likely cause a steep

decline in the worldwide incidence of hepatocellular carcinoma

 Paraneoplastic syndromes  occur due to production of hormone-like

substances from tumor cells. They can also result from immune reactions
against tumor cells that cross-react with normal cells, causing dysfunction
and/or damage to healthy organs and tissues. Neurological paraneoplastic
syndromes (paraneoplastic cerebellar degeneration) are autoimmune 
o Progressively worsening dizziness, limb and truncal ataxia,
dysarthria, and visual disturbances, they cross-react with Purkinje
neuron antigens  leading to acute-onset rapid degeneration of the
cerebellum, Anti-Yo, anti-P/Q, and anti-Hu are m/c antibodies
detected in the serum.

 Urate nephropathy  tubular obstruction from urate crystals deposition is

usually seen in individuals with acute hyperuricemia (tumor lysis syndrome).
The classic presentation is acute renal failure during chemotherapy for a
malignancy.

 Invasive vascular procedures can be complicated by atheroembolic renal

disease, which may involve the kidneys (most common), GIT, and CNS and
the skin. Light microscopy shows a partially or completely obstructed
arterial lumen with needle-shaped cholesterol clefts within the atheromatous
thrombus.

 Migratory superficial thrombophlebitis  indication of visceral cancer,

paraneoplastic syndrome of hypercoagulability may be seen in
adenocarcinomas of the pancreas, colon, or lungs. Superficial venous
thrombosis may therefor appear in one site and then resolve only to recur in
another site.

 The diagnosis of tetanus is clinical of history and physical. It is based on the

history of penetrating wound in a patient who has not been vaccinated,
clinical features consistent with tetanus such as trismus, sardonic smile and
muscle spasms, and high clinical suspicion.
 Hypercalcemia  sarcoidosis is caused by PTH-independent formation of
1,25-dihydroxyvitamin D by activated macrophages. This leads to increased
intestinal absorption of calcium.

 Presence of hemosiderin-laden macrophages in pulmonary alveoli indicates

chronic elevation of pulmonary capillary hydrostatic pressures, m/c as a
result of left-sided heart failure.

 P450 microsomal oxidase system plays an important role in detoxification,

but in carbon tetrachloride poisoning, however, it produces free radicals that
start a vicious cycle of hepatic injury.

 Q# 1933, Trochlear nerve CN IV palsy superior oblique muscle  eye to

internally rotate and depress while adducted. CN 4 palsy  traumatic or
idiopathic and presents with vertical diplopia that worsens when the affected
eye looks down and towards the nose (down and in) (walking downstairs,
up-close reading). Tucking the chin in and tilting the head away from the
affected eye can compensate this.

 Aortic dissection severe retrosternal pain that radiates to the back

tearing of the aortic intima. Hypertension is the primary risk factor for aortic
dissection  medial hypertrophy of the aortic vasa vasorum Blood
pressure discrepancy in both arms, BP higher in the left arm and lower in the
right arm. Signs are cardiomegaly, abnormal aortic contour, and widened
superior mediastinum.

 Chronic rejection is a major problem in lung transplant recipients; it affects

small airways, causing bronchiolitis obliterans. It is characterized by
lymphocytic inflammation, fibrosis, and ultimately, destruction of the
bronchioles. Symptoms include dyspnea and wheezing.

 In PCOS  OCP’s is 1st choice for treating hirsutism  works by suppressing

LH secretion from the pituitary decreasing ovarian androgen production.
Increase sex hormone-binding globulin synthesis by the liver, decreasing free
testosterone levels.

 Craniopharyngiomas  suprasellar tumors found in children and composed

of calcified cysts containing cholesterol crystals. They arise from remnants of
Rathke’s pouch, an embryonic precursor of the anterior pituitary.

 Alternative splicing is a process where the exons of a gene are reconnected in

multiple ways during post-transcriptional processing. This creates different
mRNA sequences and subsequently, different protein isoforms. It is a normal
phenomenon in eukaryotes that greatly increases the biodiversity of proteins
encoded by the genome.
 Maternal diabetes  baby gets transient hypoglycemia.

 Thiazide diuretics decrease intravascular fluid volume  stimulates

aldosterone secretion and leads to increased excretion of potassium and
hydrogen ions in the urine. This results in hypokalemia and metabolic
alkalosis.

 Mycobacterial TB infection  granulomatous inflammation with caseous

necrosis containment of macrophages, multinucleated giant cells, and CD4
T lymphocytes (together with aggregation of activated leukocytes), 
results in collateral tissue damage, resulting in caseous necrosis with
formation of cavitary lung lesions.

 Pancreatic adenocarcinoma  of the head of the pancreas  compresses

common bile duct  most common risk factor  smoking than age >50,
chronic pancreatitis, DM, genetic predisposition.

 BPH  leads to bladder outlet obstruction and overflow incontinence 

increased pressure in the urinary tract and resultant reflux nephropathy 
hydronephrosis, renal parenchymal interstitial atrophy and scarring ensure.

 Bacterial vaginosis (gardnerella vaginalis)  anaerobic gram-variable rod.

 Glioblastoma multiforme  primary brain tumor in adult’s  areas of

necrosis and hemorrhage and pseudopalisading tumor cells around areas of
necrosis. Can become significantly large and cause mass effect, midline shift
and may cross the corpus callosum (butterfly glioma).

 Somatostatinoma  reduced gallbladder contractility, due to decreased CCK

secretion  responsible for biliary stones.

 Gastric acid  neutralized by HCO3- from the submucosal glands of the

duodenum (Brunner glands) and from pancreatic duct secretions. Chronic
overproduction of gastric acid  hyperplasia of the submucosal glands.

 Absence of normal enteral stimulation in patients receiving total parenteral

nutrition leads to decreased CCK release, biliary stasis, and increased risk of
gallstones. Resection of the ileum can also increase the risk of gallstones due
to disruption of normal enterohepatic circulation of bile acids.

 80% of acute pancreatitis  from gallstones or chronic alcoholism.

Inherited/acquired hypertriglyceridemia can cause acute pancreatitis if the
serum level of triglycerides exceeds 1000 mg/dL.
 Scabies  highly contagious disease that presents with an intensity pruritic
rash usually worse at night in the flexor surfaces of the wrist, lateral surfaces
of the fingers, and the finger webs.  Excoriations with small, crusted, red
papules scattered around the affected areas. Skin scrapings from the
excoriated lesions that show mites, ova, and feces under light microscopy
confirm diagnosis.

 A person walking on a crutches for a leg broken or whatnot  radial nerve

injury  repetitive pressure/trauma at the axilla and absent triceps reflex.

 Nuclear factor-kappa B (NF-kB) is a transcription factor with a critical role in

the immune response to infection. It is normally present in the cytoplasm in a
latent, inactive state bound to its inhibitor protein, IkB. Extracellular
substances such as lipopolysaccharide can initiate a signal cascade that
results in the destruction of IkB and translocation of free NF-kB to the
nucleus. NF-kB enters the nucleus and promotes the synthesis of a number of
inflammatory proteins such as cytokines, acute phase reactants, cell adhesion
molecules and leukocyte-related growth factors.

 Irritable bowel syndrome  chronic abdominal pain associated with altered

bowel habits (diarrhea and/or constipation). Pain is often relieved with
bowel movements. IBS is not an inflammatory condition and does not cause
fistulas.

 In Hypertrophic cardiomyopathy HCM hypertrophied  causes

obstruction of LV so a decreased LV volume  less blood and O2 to the
body so dyspnea, fatigue, sudden death  avoid giving Nitroglycerin
(Isosorbide dinitrate,) and dihydropyridine Ca2+ channel blockers
(nefidepine, amlodipine) cause it decreases blood flow venous return (dec.
afterload) which will decrease preload and already obstructed LV and
diuretics (dec LV venous filling (preload) and result in greater outflow
obstruction) even less more blood going to the body  more problems.

 Rasburicase is a recombinant version of urate oxidase, an enzyme present in

many mammals, but not in humans. It catalyzes the conversion of uric acid to
allantoin, which is 5-10 times more soluble than uric acid. Effective in
preventing and treating hyperuricemia and resulting renal manifestations of
Tumor lysis syndrome.

 Q# 1159 Osteocyte connections  Gap junctions because they send signals

to exchange nutrients and waste products with other osteocytes.

 Q# 1158 Granulosa cell tumors, unilateral large sex-cord stromal tumors of

the ovary that secrete estrogen, which can lead to endometrial hyperplasia
by the unopposed estrogen. Small and cuboidal cells in sheets that form
 follicle or rosette-like structures (Call-Exner bodies) with gland-like
structures containing acidophilic material (coffee bean nuclei). Mass is
yellow due to the theca cells plump with lipid contents.

 Q#2130 Blunt Aortic Injury  traumatic aortic rupture is most often caused
by the rapid deceleration that occurs in motor vehicle collision and the most
common site of injury is the aortic isthmus because it is tethered or held firm
by the ligamentum arteriosum and is relatively fixec and immobile compared
to the adjacent descending aorta.

 Q # 1744, Gastrointestinal hemorrhage  Hindgut (distal one-third of the

transverse colon, descending colon, and sigmoid colon and rectum, they
receive their main arterial blood supply from the IMA. A catheter
embolization through the femoral artery would go through  External iliac,
common iliac, abdominal aorta, and inferior mesenteric.

 If a significant increase in blood oxygen saturation between 2 right-sided

vessels or chambers indicates the presence of a left-to-right shunt, than a
VSD is most likely responsible. VSD would produce a holosystolic murmur
that is loudest over the left mid-sternal border.

 Q# 12046, Subclavian steal syndromeoccurs due to severe stenosis of the

proximal subclavian artery which leads to reversal in blood flow from the
contralateral vertebral artery to the ipsilateral vertebral artery. Patients may
have symptoms related to arm ischemia in the affected extremity (eg,
exercise-induced fatigue, pain, paresthesias) or vertebrobasilar insufficiency
(eg, dizziness, vertigo). Usually the left subclavian artery.

 Q#528, Blood gases interpretation (pulmonary & critical care)  Arterial

PaCO2 is a direct indicator of alveolar ventilation status. Hypocapnia implies
ongoing alveolar hyperventilation. Upper airway obstruction, reduced
ventilator drive, respiratory muscle fatique, and decreased chest wall
compliance are possible causes of alveolar hypoventilation and hypercapnia.

 Perfusion greatly increases from the apex of the lung to the base; ventilation
increases slightly from the apex to the base. For this reason,
ventilation/perfusion ratio decreases from 2.5 to 0.6 in the lungs from the
apex to the base.

 Cheyne-stokes breathing is a cyclic breathing in which apnea is followed by

gradually increasing than decreasing tidal volumes until the next apneic
period. It is commonly seen in the setting of advanced CHF, strokes, brain
tumors, and traumatic brain injury.
 Q# 11814, Learning disorder  difficulites with key academic skills (reading,
writing, or mathematics), resulting in performace well below expectations
for age level. Children commonly display symptoms of anxiety, inattention, or
hyperactivity when under stress. If a child is showing these symptoms, a
learning disorder should be ruled out. So child doesn’t want to go to school
but is fine to go to soccer practice or anywhere else.

 Synchronization of glycogen degradation with skeletal muscle contraction

occurs due to release of sarcoplasmic calcium following neuromuscular
stimulation. Increased intracellular calcium causes activation of
phophorylase kinase, stimulating glycogen phosporylase to increase
glycogenolysis.

 Bloom syndrome  a rare AR condition caused by mutation in the BLM gene

encoding helicase, an enzyme that unwinds the double helix during DNA
replication. Patients present with growth retardation, facial anomalies,
photosensitive skin rash, and immunodeficiency due to chromosomal
instability and breakage.

 The Kozak consensus sequence occurs on eukaryotic mRNA and is defined by

the following sequence: (gcc)gccRccAUGG, in which R is either adenine or
guanine. This sequence helps initiation translation at the methionine start
codon (AUG).

 Q# 955, Fetal-placental aromatase deficiency  Aromatase converts

androgens into estrogens in the ovaries, testes, and placenta, and other
peripheral tissues. Placental aromatase deficiency causes accumulation of
androgens during pregnancy, resulting in ambiguous external genitalia in
female infants and maternal virilization. Maternal virilization (hirsutism)
commonly occurs during pregnancy due to transfer of excess androgens into
the maternal circulation. Affected newborn girls will have normal internal
genitalia, ambiguous or male-type external genitalia. At puberty  ovarin
estrogen synthesis causes primary amenorrhea, osteoporosis, tall stature.
And in men they will have tall stature and osteoporosis but no genital
abnormalities.

 Lateral epicondylitis (tennis elbow) is caused by overuse of the extensor

carpi radialis brevis and is characterized by angiofibroblastic tendinosis at its
origin on the lateral epicondyle.

 Buprenorphine is a partial opioid receptor agonist that binds with high

affinity but has low intrinsic activity. In patients on long-term opioid therapy,
buprenorphine can displace other opioids from their receptor and
precipitate withdrawal.
 Piperacillin-Tazobactam is a combination of extended-spectrum penicillin
with B-lactamase inhibitor. It is effective against most gram-negative enteric
rods (including Pseudomonas aeruginosa) and against Bacteriodes fragilis.

 Regurgitant flow into the left atrium in acute mitral regurgitations leads to
increased left atrial pressure and increased left ventricular end-diastolic
volume (preload). The low-resistance regurgitant pathway also decreases
left ventricular afterload, end-systolic volume, and forward stroke volume.
Increased left atrial pressure and decreased cardiac output result in
pulmonary congestion and severe hypotension, respectively.

 Q# 12024, High altitude and decompression sickness  People traveling to

elevations >2,500 m (8000ft) are at risk for developing high-altitude
sickness, characterized by headache, fatique, nausea, dizziness, and sleep
disturbances. Hypobaric hypoxia is the primary cause; it leads to an increasd
respiratory rate with development of respiratory alkalosis, which is
compensated by renal excretion of bicarbonate within 24-48 hours.

 Q# 12255, Cutaneous small vessel vasculitis is associated with medication

(eg, penicillins, cephalosporins) use and typically presents with palpable
purpura in the lower extremities. Characteristic histopathologic findings
include marked perivascular inflammation of small blood vessels with
fibrinoid necrosis and predominance of neutrophils and fragmented
neutrophilic nuclei (leukocytoclastic vasculitis).

 Chronic alcoholism can cause Cerebellar degeneration of the nervous system

by atrophy of the anterior lobes and cerebellar vermis resulting in gait ataxia,
truncal instability, intention tremor, and rhythmic, postural “parkinsonian”
tremor of the fingers and hands.

 Metoclopramide  D2 receptor antagonist, increased resting tone,

contractility, LES tone, motility, promotes gastric emptying. (does not
influence colon transport time. Used for diabetic and postsurgery
gastroparesis, antiemetic, and persistent GERD.
o It increases Parkinsonian effects, tardive dyskinesia, Restlessness,
drowsiness, fatique, depression, and diarrhea. Drug interaction with
digoxin and diabetic agents. CI in pts with small bowel obstruction or
Parkinson disease (due to D2-receptor blockade).

 Tissue ischemia increases the extracellular K+ concentrations via reduced

functionality of membrane Na+-K+-ATPase and subsequent K+ leakage from
affected cells. Ischemia may reduce extracellular Na+, Ca++, and HCO3-.
Cytoplasmic Ca++ accumulation is a hallmark of ischemic injury.
 The foam stability index evaluates surfactant functionality. To perform this
test, multiple wells containing mixtures of ethanol and amniotic fluid are
shaken and then examined to find the highest value well that contains a ring
of stable foam.

 Pancreatic pseudocysts are well-circumscribed fluid collections that typically

develop following acute pancreatitis due to walling off of necrotic pancreatic
tissue/peripancrreatic fat. These collections usually resolve on their own but
may become infected or expand, causing abdominal pain, small
blowel/biliary obstruction, or fistula formation into neighboring structures.
o It is a collection of fluid rich in enzymes and inflammatory debris
which consist of granulation tissue and fibrosis, they are not lined by
epithelium like a true cyst, instead it is lined by granulation tissue.

 Bowel epithelial stem cells are in the crypts of liberkuhn which are
responsible for regeneration of mucosal epithelium.

 Cystic hygromas  turner syndrome trisomies, soft compressible masses

that transilluminate found on the head and neck, typically on the left side.

 Because sodium’s equilibrium potential contributes to the most to the

neuron’s membrane potential during deplorization, a decrease in
extracellular concentration will reduce the amplitude of the action potential,
and decreasing intracellular sodium concentration will increase the
concentration gradient across the cell membrane, raising the equilibrium
potential of sodium above its normal value of +65 mV, this will result in
increased action potential during deplorization.

 Kluver-bucy syndrome can result from bilateral damage to the temporal

lobes, particularly the amygdalae that are right below the globus pallidus on
both sides. Potential causes include herpes simplex virus encephalitis and
traumatic brain injury. Symptoms include oral fixation, hyperphagia,
hypersexuality, visual agnoisa, placidity, and amnesia.

 Tardive dyskinesia  medication-induced movement disorder characterized

by abnormal involuntary movements of the mouth, tongue, trunk, and
extremities. Due to prolonged exposure to dopamine-blocking agents causing
the upregulation and supersensitivity of dopamine receptors.

 Dopamine beta hydroxylase is responsible for the synthesis of

norepinephrine from dopamine. A congenital deficiency of this enzyme will
impair synthesis of NE and EPi and lead to impaired sympathetic adrenergic
activity such as hypotension, ptosis, and hypothermia in infants and children,
and in adults postural hypotension, exercise intolerance, nasal congestion,
and ejaculatory difficulites.
 When normal cells are cultured in a petri dish, they reproduce until the
medium is covered with a single layer of cells that just touch one another. At
that point, mitosis halts. Mediated by cadherins and catenins, this
phenomenon is termed “contact inhibition”. Malignant cells, however, behave
differently. They will cover the medium with a single layer of cells and then
continue to divide, eventually pilling up into mounds.

 To compensate for the additional X chromosome in women, one X

chromosome is inactivated in each somatic cell. The selection of the
inactivated X chromosome is ransom, but a portion of women may have
significantly skewed inactivation, making them more susceptible to
displaying manifestations of X-linked diseases like hemophilia A & B.

 Orlistat is an intestinal lipase inhibitor that reduces absorption of dietary fat.

It is often recommended as a 1st line medication due to favorable safety
profile; however, it has significant gastrointestinal side effects (diarrhea,
fecal incontinence, oily spotting). Produces moderate weight loss in most
cases 2.2-6.6Ibs 1-3kg in the first year but it is associated with slight
reduction in the incidence of diabetes and hypertension. SE  steatorrhea,
dec absorption of fat-solube vitamins, abdominal discomfort, flatulence.

 Membranous glomerulonephritis is a common cause of nephrotic syndrome

that is associated with solid tumors. Edema, weight gain due to severe
proteinuria. Glomerular capillary loops appear thickened and demonstrate
glomerular basement membrane “spikes” as a result of subepithelial immune
complex deposition.

 Venous drainage of the rectum above the dentate line occurs through the
superior rectal vein, which drains into the portal venous system via the
inferior mesenteric vein. As a result cancers arising in the proximal rectum
typically metastasize to the liver first due to hematogenous dissemination
through the portal system. Structures below the dentate line drain into the
middle and inferior rectal veins, which drain into the systemic circulation
(drain into the caval system) via the internal iliac veins, as a result cancers
arising below the dentate line metastasize to the lungs.

 Insulin activates the Phosphofructokinase-2 (PFK-2) domain, which

converts fructose-6p to fructose-2,6-bisphosphate (fructose-2,6BP).
Fructose-2,6BP activates PFK-1 and inhibits F-1,6-Pase, increasing the
production of fructose-1,6,BP and driving the cell towards glycolysis.

 Glucagon activates the F-2,6-BPase domain, which degrades fructose-2,6BP

(to fructose-6P). Therefore, glucagon has the opposite effect of insulin and
favors gluconeogenesis.
 Cell surface receptors with 7 alpha-helical transmembrane domains are
typically G protein-coupled receptors. Transmembrane or membrane-
associated domains of any protein are composed of hydrophobic amino
acids, such as alanine, valine, leucine, isoleucine, phenylalanine, tryptophan,
methionine, proline, and glycine.

 Mumps-induced orchitis in an unvaccinated patient can result in leydig cell

atrophy and decreased testosterone production. Testosterone therapy
maybe indicated.

 In cough syncope, increased intrathoracic pressure during a cough episode

decreases venous return to the heart thereby transiently decreasing cardiac
output and cerebral perfusion.

 Premature ovarian insufficiency occurs in women age <40 and presents with
amenorrhea and an elevated FSH level. It may result from follicular depletion
through accelerated atresia, and apoptotic process.

 In an agglutination inhibition test, the presence of agglutination is considered

a negative result.

 Paclitaxel-Eluting stent Q#6689, both Paclitaxel and sirolimus are used both
as a coat drug-eluting stents, for myocardial ischemia due to stenosis of his
right coronary artery done by angiography. Paclitaxel is an antineoplastic
agent that function by binding b-tubulin and preventing microtubule
breakdown so it prevents stent restenosis by preventing intimal hyperplasia.

 Insulin increases cellular uptake of glucose in adipocytes and skeletal muscle

by increasing the translocation of GLUT4, a passive glucose transporter, from
intracellular vesicles to the cell membrane. Increased translocation of the
protein to the cell membrane. Than GLUT4 is re-internalized via clathrin-
coated pits.

 Uncal herniation, Q#6804, of the tentorium cerebelli of the innermost

portion of the right temporal lobe results in palsy of the ipsilateral
oculomotor nerve (CN III), causing dilation and fixation of the ipsilateral
pupil. Contralateral muscle paresis is most often seen due to direct
compression of the ipsilateral cerebral peduncle by the herniated temporal
lobe.

 HLA haplotypes (MHC class I and II molecules) participate in immunologic

recognition of specific antigens by T lymphocytes. MHC molecules do not
undergo somatic recombination, and individuals with HLA haplotypes that
cannot bind certain polypeptide fragments will be unable to mount a T cell-
 dependent (eg, IgG, cell-mediated) immune response against these antigens
 so antigen presentation is the problem.

 Eye problems:
o Iris  iris Hamartomas (lisch nodules) in neurofibromatosis type I.
o Conjunctivae  inflamed in conjunctivitis by infectious organisms,
allergies, and traumatic insult.
o Sclerae bluish tinge in patients with osteogenesis imperfect or
nevus of Ota.
o Retina numerous pathologic conditions  diabetic retinopathy,
HTN (retinal hemorrhage), and pseudoxyanthoma elasticum (angioid
streaks) and tays-sachs disease (cherry red macular spot).
o Cornea  kayser-fleischer rings  wilsons disease

 Retioniods are vitamin A analog that bind nuclear receptors, which

subsequently function as transcription factors. In patients with acne,
retinoids decrease sebum production and increase cellular turnover and the
shedding of cells from the strum corneum. This reduces hyperkeratinization,
opens blocked pores, and prevent formation of microcomedones.
 Benzoyl peroxide is converted to benzoic acid when applied to the skin. It
oxidizes bacterial proteins, making it bacteriostatic against
propionibacterium acnes. A number of topical and oral antibiotics also have
activity against P acnes and are useful in treating papulopustular
inflammatory acne.

 The cervix has stratified squamous non-keratinized epithelium in the

exocervix and simple columnar mucus-secreting epithelium in the
endocervical canal. The transformation zone contains both epithelial types
and is vulnerable to cervical malignancy due to metaplasia.

 Supply of blood to the cerebellum and brain stem is the vertebral artery’s
and basilar artery.

 Internuclear opthalmoplegia is a disorder of conjugate horizontal gaze in

which the affected eye (ipsilateral to the lesion) is unable to adduct and the
contralateral eye abducts with nystagmus. Convergence and the pupillary
light reflex are preserved. This typically occurs with damage to the medial
longitudinal fasciculus.

 Increased osteoclastic activity in multiple myeloma leads to elevated serum

calcium and reduced parathyroid hormone production. This decreases
renal calcium reabsorption causing hypercalciuria. Hypercalemia and light
chain cast nephropathy cause progressive renal failure, leading to reduced
1,25-dihydroxyvitamin D synthesis.
 DNA-binding proteins include transcription factors (Myc, CREB), steroid
receptors (cortisol, aldosterone, progesterone) thyroid hormone receptors,
fat-soluble vitamin receptors (vit D, retinoic acid), and DNA transcription and
replication proteins.

 Isosorbide dinitrate has a low bioavailability due to extensive first-pass

hepatic metabolism prior to release in systemic circulation. Sublingual
nitroglycerin is absorbed directly from oral mucosa into the venous
circulation and has a higher bioavailability.

 Functional hypothalamic amenorrhea results from loss of pulsatile

gonadotropin-releasing hormone release from the hypothalamus and is
caused by weight loss, strenuous exercise, systemic illness, or abnormal
eating habits. Loss of cyclic gonadotropin releases leads to a decrease in FSH
and LH secretion from the pituitary, which in turn causes low circulating
estrogen levels.

 Renal calculi occur due to an imbalance of the factors that facilitate and
prevent stone formation. Increased urinary concentration of calcium, oxalate,
and uric acid promote salt crystallization whereas, increased urinary citrate
concentration and high fluid intake prevent calculi formation.

 Idiopathic intracranial hypertension (pseudotumor cerebri) presents in

young obese women with daily headache (which worsen during Valsalva),
bilaterally symmetric papilledema, and transient visual disturbances.
Increased intracranial pressure compresses the optic nerves, resulting in
impaired axoplasmic flow and optic disc edema.

 Telomerase is an RNA-dependent DNA polymerase enzyme and contains

TTAGGG repeats and critical shortening of the telomerase is signal
programmed cell death.

 The circulatory system is a continuous circuit, and therefore the volume

output of the left ventricle must closely match the output of the right
ventricle. This balance is necessary to maintain continuous blood flow
through the body and exists both at rest and during exercise, so blood flow
per minute is the same for systemic and pulmonary circulation.

 Pure red cell aplasia (PRCA) is a rare form of marrow failure characterized by
severe hypoplasia of marrow erythroid element in the setting of normal
granulopoiesis and thrombopoiesis. Pure red cell aplasia is associated with
thymoma, lymphocytic leukemias, and parvovirus B19 infection.
 Galactocele is a mass filled with breast milk and can occur with
hyperprolactinemia but is more often associated with pregnancy and
breastfeeding.

 Morphine is an opiate analgesic that is commonly used to treat severe

chronic pain in patients with cancer, mu, delta, and kappa mediate analgesia
at the spinal and supraspinal levels, and they are transmembrane receptors
coupled to inhibitory G proteins. In the spine they result in the closure of
voltage-gated calcium channels, which reduces calcium influx, and decrease
excitatory neurotransmitter release. They also bind on the postsynaptic
membrane and open potassium channels and lead to membrane
hyperpolarization due to potassium efflux.

 Friedreich ataxia  AR, mutation of frataxin (FXN) gene which codes for an
essential mitochondrial protein involved in the assembly of iron-sulfur
enzymes, increased number of trinucleotide repeats (GAA) causing
decreased FXN expression. This leads to decreased mitochondrial energy
production and increased oxidative stress, resulting in degeneration of
neural tracts and peripheral nerves.
o Spinocerebellar and lateral corticospinal tract degeneration leading to
gait ataxia and spastic muscle weakness.
o Degeneration of dorsal columns and dorsal root ganglia  loss of
position and vibration.
o Kyposcholiosis and foot abnormalities (pes cavus) skeletal
deformities.
o Hypertrophic cardiomyopathy and congestive heart failure and
diabetes mellitus develop in about 10% of patients with friedreich
ataxia.

 After gallstones, alcohol abuse is the second most common cause of acute
pancreatitis. Macrocytosis and an AST:ALT ratio>2 are indirect indicators of
chronic alcohol consumption. Alcohol-related macrocytosis can occur
independently of folate deficiency.

 The binding of programmed death receptor 1 (PD-1) to its ligand (PD-L1)

downregulates the immune response against tumor cells by inhibiting
cytotoxic T cells. Many types of cancers evade the immune system by
increasing expression of PD-L1. Monoclonal antibodies blocking PD-1 help
prevent T cell inhibition and promote apoptosis of tumor cells.

 So inducers of the cytochrome P450 system will lead to toxicity of

acetaminophen and codeine because it will break it down and cause toxic
metabolites of acetaminophen and codeine. Also for inhibitors will cause
failure in this situation. But for the other drugs inducers usually lead to
failure of the drug and inhibitors will lead to toxicity.
 Cytochrome P450 enzymes found in the liver are responsible for the majority
of drug. Polymorphisms occurring in the genes coding for these enzymes
result in various phenotypes that differ in their rates of metabolism;
individual differences in phenotypes alter treatment efficacy and drug
toxicity.
o Tamoxifen, a SERM used in the treatment of estrogen receptor-
positive breast cancer, is a prodrug metabolized by CYP2D to its active
metabolite, endoxifen. Patients with genetic polymorphisms resulting
in poor CYP2D activity are exposed to decreased levels of the active
metabolite and have a higher risk of disease relapse.

 Interferons a and B are produced by most human cells in response to viral

infections. The production of a and B interferons helps suppress viral
replication by halting protein synthesis and promoting apoptosis of infected
cells, limiting the ability of viruses to spread through the tissues.

 An indicator of the severity of mitral stenosis is the S2 to opening interval

between the closure of the aortic valve A2 and the abrupt halthing of leaflet
motion during opening of a stenotic mitral valve.

 An indicator of the severity of mitral regurgitation indicating a high

regurgitant volume and left ventricular volume overload is a left-sided S3
gallop. Usually the intensity of the holosystolic murmur does not correlate
well with regurgitant volume as larger regurgitant orifices often present with
softer murmurs.

 Dress syndrome Q# 508, Drug reaction with eosinophilia and systemic dress
syndrome typically occurs 2-8 weeks after exposure to high-risk drugs such
as anticonvulsants (eg, phenytoin, carbamazepine), allopurinol, sulfonamides
(eg Sulfasalazaline), and antibiotics (eg, minocycline, vancomycin). Patients
typically develop fever, generalized lymphadenopathy, facial edema, diffuse
skin rash, eosinophilia, and internal organ dysfunction.

 Stimulation of beta-2 receptors promotes insulin secretion while stimulation

of alpha-2 receptors inhibits insulin release. However, the alpha-2-mediated
inhibitory effect is predominant, causing sympathetic stimulation to lead to
overall inhibition of insulin secretion. Likewise, epinephrine administration
activates both alpha-2 and beta-2 receptors, but the overriding inhibitory
effect results in decreased insulin secretion. So following pretreatment
with an alpha-2 receptor blocker (drug A), epinephrine’s effect on beta-
2 receptors would become dominant, resulting in increased insulin
secretion.

 Diuretics taken for a long time can lead to hypotention and hypovolemia.
 TrkA Tropomyosin receptor kinase A  has high affinity nerve growth factor
receptor encodes a member of the neurotrophic tyrosine kinase receptor is a
membrane bound receptor that upon neurotrophin binding, phosphorylates
itself and members of the MAPK pathway.

 Estrogens increases expression of uterotonic (eg, oxytocin) receptors, which

mediate calcium transport through ligand-activated calcium channels. The
combination of an increase in gap junction density and uterotonic receptors
results in coordinated, synchronous labor contractions.

 Tight junctions are comprised of claudins and occludin and serve as a

paracellular barrier to water and solutes. The endotoxin from clostridium
perfingens, a common cause of food poisoning, bind claudin and interferes
with tight junctions in the intestinal barrier. So water loss from the tissue to
the intestinal lumen results in watery diarrhea.

 Round ligament maintains the anteflexion of the uterus from the uterus to
the inguinal ring to the labia majora, and that uterosacral ligaments connect
the posterior aspect of the uterus to the anterior portion of the sacrum and
hold the uterus in an anteverted or retroverted position and loss of this
support contributes to uterine prolapse into the vagina.

 Short gastric veins drain the fundus of the stomach into the splenic vein,
splenic vein thrombosis can increase pressure in the short gastric veins and
cause gastric varices only in the fundus.
 Left gastric vein drains blood from the upper stomach and lower esophagus
into the portal vein. Portal HTN can increase pressure here and usually
causes both gastric and esophageal varices.

 Hoffman elimination = non-depolarizing neuromuscular blocking agent

(atracurium) that spontaneously degrades in plasma and organ tissue, a type
of metabolism.

 Evidence has long accumulated to point toward a pivitol role for E-cadherin and
the catenin complex in the control of cancer cell dissociation and spread. Tumor
invasion and metastasis, both hallmarks of tumor malignancy, frequently coincide
with the loss of E-cadherin-mediated cell-cell adhesion. Expression of E-cadherin,
the most abundant adhesion molecule in adherens junctions of epithelia, is
downregulated in most, if not all, epithelial cancers.39 Several studies have shown
that reconstitution of a functional E-cadherin adhesion complex suppresses the
invasive phenotype of many different tumor cell types.40-42 In the context of cancer,
E-cadherin has been categorized as a tumor suppressor, given its essential role in
the formation of proper intercellular junctions, and its downregulation in the
 process of epithelial-mesenchymal transition (EMT) in epithelial tumor
progression.

 Q# 12062, Dumping syndrome= after gastric bypass surgery or damage to

the pyloric sphincter, emptying of hyperosmolar chime into the small
intestine causes a rapid shift of fluid from the serum to the intestine,
resulting in postprandial gastrointestinal (eg, nausea/vomiting, cramps,
diarrhea) and vasomotor symptoms (diaphoresis, flushing).

 Sialoliths can form both in the submandibular or parotid, but parotid is more
common and the pain would be reproduced if lemon juice is squirted into the
oral cavity, but for submandibular, the patient would have pain under the
tongue at the base of the frenulum.

 Berry aneurysm on the left posterior communicating artery patients left

oculomotor nerve would be affected  lead to ptosis, mydriasis and
diplopia.

 Berry aneurysm of the anterior communicating artery in a person would lead

to bitemporal hemianopia due to compression of the optic chiasm,
contralateral lower extremity hemiparesis, and sensory deficits.

 Management of tension pneumothorax is needle decompression followed by

a chest tube placement. The preferred site for needle decompression is the
2nd intercoastal space mid-clavicular line, and the preferred site for chest
tube placement is 5th intercostal space mid-axillary line.

 Digoxin toxicity can result with the use of Quinidine, Amiodarone, and
verapamil, and spironolactone. Can result in confusion, hallucination, blurred
vision and seizures, anorexia, nausea, and vomiting.