Internal Medicine Quick Tables

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Chronic venous stasis

 Obesity
 Advanced age
Risk factors  Varicose veins
 History of DVT

 Leg pain (achy, heavy)


 Edema
 Venous dilation (varicosities, telangiectasias)
Clinical features  Dermatitis: erythema, pruritus, scaling, weeping
 Chronic woody induration and brown discoloration
 Ulcers

 Elevation
Management  Compression stockings

DVT = deep vein thrombosis.


Primary sclerosing cholangitis
 Asymptomatic
 Fatigue & pruritus
Clinical features
 Associated with IBD, particularly UC (~90% of patients)

 Cholestatic liver injury (↑ alkaline phosphatase, ↑ bilirubin)


 Multifocal stricturing/dilation of intrahepatic &/or
Laboratory/imaging
extrahepatic bile ducts on cholangiography

 Fibrous obliteration of small bile ducts, with concentric


Liver biopsy replacement by connective tissue in onion-skin pattern

 Biliary stricture
 Cholangitis or cholelithiasis
Complications  Cholangiocarcinoma, colon cancer, biliary cancer
 Cholestasis (eg, ↓ fat-soluble vitamins, osteoporosis)

IBD = inflammatory bowel disease; UC = ulcerative colitis.


Laboratory evaluation of hypertension
 Serum electrolytes (Na, K, Ca)
 Serum creatinine
Renal function tests  Urinalysis
 Urine albumin/creatinine ratio (optional)

 Fasting glucose or hemoglobin A1c


 Lipid profile
Endocrine tests
 TSH
 ECG
Cardiac tests  Echocardiography (optional)

 Complete blood count


Other tests  Uric acid (optional)

Cryoglobulinemia
(immunoglobulins that precipitate at <37 C)
Type I Mixed = type II or III
 Chronic viremia (eg, HCV,
 Plasma cell dyscrasias
HIV)
Associated (eg, Waldenström, multiple
 Autoimmunity (eg, SLE,
diseases myeloma)
Sjögren)

 B-cell lineage malignancy:  B-cell hyperactivation: IgM


Pathogenesis:
monoclonal IgM RF* bound to polyclonal IgG
cryoglobulin
 Cryoprecipitates → vascular
occlusion  Immune complexes →
(eg, livedo reticularis, retiform vasculitis
purpura, digital ischemia) (eg, palpable purpura, GN,
Clinical
 High cryocrit → arthralgia, neuropathy)
findings
hyperviscosity  Viral hepatitis →
(eg, blurred vision, vertigo, hepatomegaly
ataxia)

 + Cryocrit, normal
 + Cryocrit, ↓ C4
complement
 + RF autoantibodies
Laboratory  ↑ Erythrocyte sedimentation
 + Viral or antinuclear
findings rate
antibodies
 + Monoclonal spike on SPEP

*Monoclonal RF (type II), polyclonal RF (type III).


GN = glomerulonephritis; HCV = hepatitis C virus; RF = rheumatoid factor; SLE = systemic
lupus erythematosus; SPEP = serum protein electrophoresis.
Pneumocystis pneumonia
 AIDS (CD4 <200/mm3)*
Epidemiology  Immunosuppressive medications (eg, chronic glucocorticoids)

 Indolent (AIDS) or acute respiratory failure (immunosuppressive


treatment)
 Dyspnea, hypoxia, dry cough, fever
Manifestations
 ↑ Lactate dehydrogenase level
 Diffuse bilateral reticulonodular infiltrates on pulmonary imaging
 Induced sputum or bronchoalveolar lavage
Diagnosis
 Trimethoprim-sulfamethoxazole ± corticosteroids
Treatment  Antiretroviral initiation (in AIDS)

*Patients with AIDS (CD4 <200/mm3) & those on chronic glucocorticoid therapy generally
receive primary
prophylaxis against Pneumocystis pneumonia with trimethoprim-sulfamethoxazole.
Fat embolism syndrome
 Fracture of marrow-containing bone (eg, femur)
 Orthopedic surgery
Etiology
 Pancreatitis

 24-72 hr following inciting event


 Clinical triad
Clinical o Respiratory distress
presentation o Neurologic dysfunction (eg, confusion)
o Petechial rash 

 Based on clinical presentation


Diagnosis
 Early immobilization of fracture
Prevention
 Supportive care (eg, mechanical ventilation)
& treatment
Bladder cancer
 >90% urothelial carcinoma
Epidemiology  ↑ Risk with smokers & exposure to industrial carcinogens

 Painless hematuria throughout micturition


 Irritative voiding symptoms (eg, frequency, urgency, dysuria)
Manifestations
 Regional pain

 Flexible cystoscopy with biopsy (gold standard)


Diagnosis  Urine cytology

 TURBT
Staging  Upper urinary tract imaging (eg, IVP, MRI, CT)

 No muscle invasion: TURBT & intravesical immunotherapy


 Muscle invasion: radical cystectomy & systemic chemotherapy
Treatment
 Metastatic: systemic chemotherapy & immunotherapy

IVP = intravenous pyelogram; TURBT = transurethral resection of bladder tumor.


Milk-alkali syndrome
 Excessive intake of calcium & absorbable alkali
 Renal vasoconstriction & decreased GFR
Pathophysiology
 Renal loss of sodium & water, reabsorption of bicarbonate

 Nausea, vomiting, constipation


 Polyuria, polydipsia
Symptoms
 Neuropsychiatric symptoms

 Hypercalcemia
 Metabolic alkalosis
Laboratory
 Acute kidney injury
findings
 Suppressed PTH

 Discontinuation of causative agent


Treatment  Isotonic saline followed by furosemide

GFR = glomerular filtration rate; PTH = parathyroid hormone.


Community-acquired pneumonia
Setting Recommended therapy
 Healthy patients
o Amoxicillin or doxycycline
Outpatient  Comorbid conditions (eg, diabetes, malignancy)
o Fluoroquinolone or beta-lactam + macrolide

 Fluoroquinolone

Inpatient     OR
(non-ICU)
 Beta-lactam + macrolide

 Beta-lactam + macrolide

Inpatient     OR
(ICU)
 Beta-lactam + fluoroquinolone

ICU = intensive care unit.


Tetanus prophylaxis
Clean or minor wound Dirty or severe wound
 Tetanus toxoid-  Tetanus toxoid-
containing vaccine* containing vaccine*
only if last dose >10 only if last dose >5
>3 tetanus toxoid doses
years ago years ago
 No TIG  No TIG
 Tetanus toxoid-
 Tetanus toxoid- containing vaccine*
containing vaccine*
Unimmunized, uncertain, or <3
only PLUS
tetanus toxoid doses
 No TIG
 TIG

*Booster given as tetanus/diphtheria (Td) toxoids adsorbed or tetanus toxoid/reduced diphtheria


toxoid/acellular pertussis (Tdap)
TIG = tetanus immune globulin.
Laboratory evaluation of hypertension
 Serum electrolytes (Na, K, Ca)
 Serum creatinine
Renal function tests  Urinalysis
 Urine albumin/creatinine ratio (optional)

 Fasting glucose or hemoglobin A1c


 Lipid profile
Endocrine tests
 TSH

 ECG
Cardiac tests  Echocardiography (optional)

 Complete blood count


Other tests  Uric acid (optional)

Iron studies in microcytic anemia


Transferrin
saturation
Cause MCV Iron TIBC Ferritin
(Iron/TIBC)
Iron deficiency ↓ ↓ ↑ ↓ ↓
Thalassemia ↓↓ ↑ ↓ ↑ ↑↑
Anemia of chronic disease
Normal/↓ ↓ ↓ Normal/↑ Normal/↓
(inflammation)
MCV = mean corpuscular volume; TIBC = total iron binding capacity.
Cerebrospinal fluid analysis
Diagnosis Cell count Cell type Glucose Protein
Bacterial meningitis ↑↑ Neutrophils ↓ ↑↑
Viral meningitis ↑ Lymphocytes Normal Normal or ↑
Fungal or tuberculous
↑ Lymphocytes ↓ ↑
meningitis
Lymphocytes &
Herpes encephalitis ↑ Normal ↑
erythrocytes
Guillain-Barré syndrome Normal Normal Normal ↑
Clinical features of dermatomyositis
 Proximal, symmetric
Muscle weakness  Weakness in UE = LE

 Gottron sign/papules
Skin findings  Heliotrope rash

 Interstitial lung disease


 Dysphagia
Extramuscular findings
 Myocarditis

 ↑ CPK, aldolase, LDH


 Anti-Mi2, anti-Jo-1
Diagnosis
 Diagnostic uncertainty: EMG/MRI, biopsy (skin/muscle)

 High-dose glucocorticoids plus glucocorticoid-sparing


agent
Management
 Screening for malignancy

CPK = creatine phosphokinase; EMG = electromyography; LDH = lactate dehydrogenase; LE


= lower extremity; UE = upper extremity.
Malignant biliary obstruction
 Cholangiocarcinoma
 Pancreatic/hepatocellular carcinoma
Etiologies
 Metastasis (eg, colon, gastric)

 Jaundice, pruritus, acholic stool, dark urine


 Weight loss
 RUQ pain
Manifestations
 RUQ mass or hepatomegaly
 ↑ Direct bilirubin, ALP, GGT

 Serum tumor markers (CEA, CA 19-9, AFP)


 Abdominal imaging (ultrasonography, CT scan)
Diagnosis
 EUS or ERCP for tissue diagnosis if unclear

AFP = α-fetoprotein; ALP = alkaline phosphatase; CEA = carcinoembryonic antigen; ERCP =


endoscopic retrograde cholangiopancreatography; EUS = endoscopic ultrasonography; GGT =
γ-glutamyltransferase; RUQ = right upper quadrant.

Idiopathic intracranial hypertension


Risk factors  Women of childbearing age
 Recent weight gain/obesity
 Medications (eg, retinoids/vitamin A, tetracyclines, growth hormone)

 Impaired CSF resorption & intracranial venous hypertension


Pathophysiology
 Headache/nausea/vomiting
 Visual changes (transient obscurations; vision loss; diplopia due to
Clinical abducens nerve [CN VI] palsy)
features  Pulsatile tinnitus
 Retrobulbar pain/neck pain/back pain

 Papilledema & enlarged blind spots


 MRI to rule out mass lesions/hydrocephalus
Diagnosis  MR venography to rule out venous thrombosis
 Lumbar puncture: elevated opening pressure

 Weight loss, including bariatric surgery


Treatment  Carbonic anhydrase inhibitor (acetazolamide, topiramate)

CSF = cerebrospinal fluid.


Multiple sclerosis
 Sensory disturbances (trigeminal neuralgia), motor weakness,
bowel/bladder dysfunction
 Ocular manifestations: optic neuritis, internuclear ophthalmoplegia
Clinical
 Uhthoff phenomenon: symptom worsening with increased body
features
temperature
 Lhermitte sign: electrical sensation in limbs or back

 Neurologic symptoms disseminated in space & time


 Periventricular white matter lesions on MRI
Diagnosis
 Oligoclonal IgG bands on cerebrospinal fluid analysis

 Acute exacerbation: high-dose corticosteroids


 Disease-modifying therapies: interferon β, fumarates, biologics (eg,
Management
natalizumab)

Temporomandibular joint disorder


 Joint trauma (eg, injury, bruxism)
 Psychiatric illness (eg, anxiety, history of
Risk factors
abuse)

Clinical  Facial pain (worsens with jaw motion)


manifestations  Ear pain, tinnitus
 Headache (unilateral, worse on
awakening)
 Jaw dysfunction

 Clinical, imaging not typically needed


 Tenderness of mastication muscles
Diagnosis  Tooth wear (evidence of bruxism)
 Crepitus or clicking with TMJ motion

 Education (eg, avoidance of triggers, soft


diet)
Management  Dental splints (if bruxism suspected)
 NSAIDs (eg, naproxen)

NSAIDs = nonsteroidal anti-inflammatory drugs;


TMJ = temporomandibular joint.
Legionella pneumonia
 Contaminated water
o Hospital
Epidemiology
o Travel (cruise, hotel)

 Fever >38.8 C (101.8 F)


 Relative bradycardia
Clinical features  Gastrointestinal: diarrhea, vomiting, cramps
 Pulmonary: delayed symptoms

 Hyponatremia
 Chest x-ray: lobar infiltrate
Diagnosis  Sputum Gram stain: PMNs, few/no organisms
 Urine Legionella antigen

 Respiratory fluoroquinolone or newer macrolide


Treatment
PMNs = polymorphonuclear leukocytes.
Acute exacerbation of chronic obstructive pulmonary disease
 Infectious (70%): respiratory viruses (eg, rhinovirus) &
commensal bacteria (eg, nontypable Haemophilus influenzae)
Precipitants  Noninfectious (30%): sterile inflammation (underlying
disease), pulmonary embolism, inhaled irritants

 Bronchial inflammation: systemic response (eg, fever,


leukocytosis) usually absent
 Cardinal symptoms: ↑ dyspnea, ↑ sputum volume, ↑ sputum
Pathophysiology &
purulence
presentation
 ↑ WOB (hyperinflation) & impaired gas exchange (hypoxemia
[↓ V/Q], hypercapnia [↑ VD])
 Maximize expiratory flow: inhaled bronchodilators
 Reduce airway inflammation: systemic glucocorticoids
 Treat underlying triggers: ± antibiotics* &/or antivirals
(influenza, COVID-19)
Management
 Maintain adequate oxygenation: SpO2 target 88%-92%
 Maintain adequate ventilation: NIPPV or invasive mechanical
ventilation

*Antibiotics generally indicated if: (1) increased sputum purulence + ≥1 other cardinal
symptoms; or (2) patient requires hospitalization.

NIPPV = noninvasive positive pressure ventilation; VD = alveolar dead space ventilation; V/Q =
ventilation/perfusion ratio; WOB = work of breathing.
Meningococcal meningitis
 Neisseria meningitidis
Epidemiology  Most common in young children & young adults

 Initial: nonspecific fever, headache, vomiting, myalgia, sore throat


Clinical features  Within 12-24 hr: petechiae/purpura, meningeal signs, AMS

 Ceftriaxone
Treatment
 Shock
 Disseminated intravascular coagulation
Complications
 Adrenal hemorrhage

 Droplet precautions
Prevention  Chemoprophylaxis* for close contacts

*Rifampin, ciprofloxacin, or ceftriaxone.

AMS = altered mental status.


Drug-induced, immune-mediated hemolytic anemia
 Drug coats erythrocytes → IgG binding → splenic
destruction of RBCs (extravascular hemolysis)
 Drug triggers immune complexes → complement-
Pathogenesis
mediated destruction of RBCs (intravascular
hemolysis)

Manifestations  Sudden onset (within hours of exposure)


 Anemia: fatigue, pallor, dyspnea
 Hemolysis: jaundice, dark urine, abdominal or back
pain
o ↑ Reticulocytes, indirect bilirubin & LDH
o ↓ Haptoglobin
o Spherocytes on peripheral blood smear
o + Direct Coombs test (anti-IgG, anti-C3)

 Discontinue offending drug


 Transfusion (if severe)
Treatment
 ± Glucocorticoids, IVIG

IVIG = intravenous immunoglobulin; LDH = lactate dehydrogenase;


RBC = red blood cell.
Mitral stenosis in adults
 Rheumatic heart disease (vast majority of cases)
Etiology  Age-related calcification, radiation induced

 Exertional dyspnea, orthopnea, paroxysmal nocturnal dyspnea,


hemoptysis
Clinical  Pulmonary edema ± right-sided heart failure (eg, lower extremity
presentation edema)
 Atrial fibrillation, ↑ risk for systemic embolization

 Opening snap with middiastolic rumble at the apex


Diagnosis  Echocardiography: ↑ transmitral flow velocity

 Percutaneous valvotomy or surgical repair/replacement


Treatment
Bronchiectasis
 Pathophysiology: airway insult (eg, infection, inhalation)
with impaired clearance (eg, mucostasis,
immunodeficiency)
 Chronic: daily production of voluminous, thick ± blood-
Clinical features
tinged mucus
 Acute exacerbations: recurrent infections with
mucopurulent sputum ± frank hemoptysis

 Airway obstruction (eg, cancer, foreign body) &


mucostasis (eg, CF, ABPA)
 Immunodeficiency (eg, ↓Ig) & autoinflammatory disease
Etiologies/contributory
(eg, Sjögren syndrome)
conditions
 Chronic/past infection (eg, mycobacteria) or toxic
inhalation

Evaluation  High-resolution CT scan of the chest (needed for


diagnosis): airway dilation
 Pulmonary function testing: obstructive pattern
 Investigation of etiologies (eg, Ig levels, respiratory
cultures, bronchial obstruction)

 Address underlying disorders (eg, Ig replacement)


 Airway clearance (eg, chest physiotherapy), mucolytics
Treatment  Antibiotics to suppress bacterial overgrowth & treat
exacerbations

ABPA = allergic bronchopulmonary aspergillosis; CF = cystic fibrosis; Ig = immunoglobulin;


RA = rheumatoid arthritis.
Infectious epiglottitis
 Streptococcus pneumoniae, Haemophilus influenzae
Epidemiology  Risk reduced with H influenzae vaccination

 Rapidly progressive & life-threatening


 Fever, sore throat, drooling, muffled voice
 Airway obstruction (stridor, dyspnea)
Clinical
 Pooled oropharynx secretions
 Laryngotracheal tenderness

 Direct visualization
Diagnosis  Imaging (lateral neck x-ray)

 Early artificial airway (if needed)


Treatment  Intravenous antibiotics (ceftriaxone plus vancomycin)

Causes of gout
 Primary gout (idiopathic)
Increased  Myeloproliferative/lymphoproliferative disorders
 Tumor lysis syndrome
urate production  Hypoxanthine guanine phosphoribosyltransferase deficiency

Decreased  Chronic kidney disease


 Thiazide/loop diuretics
urate clearance
Diagnosis of brain death
 Known cause (eg, TBI, stroke)
 Evidence (eg, clinical, neuroimaging) of devastating CNS event
 Exclusion of confounding conditions (eg, electrolyte abnormality,
Clinical criteria
intoxication, paralytics)
 Core temperature >36 C (96.8 F), SBP >100 mm Hg

Clinical  Coma
examination  Absent brainstem reflexes:
o Pupillary
o Corneal
o Oculocephalic, oculovestibular
o Jaw jerk
o Cough
o Gag
 Absent brain-originating* motor responses (including decerebrate &
decorticate posturing)
 Apnea test: no respiratory response to PaCO2 >60 mm Hg

*Movements originating from the spinal cord (eg, deep tendon reflexes) may still be present.

SBP = systolic blood pressure; TBI = traumatic brain injury.


Syphilis: diagnostic serology
 Antibody to cardiolipin-cholesterol-lecithin antigen

Nontreponemal
 Quantitative (titers)
 Possible negative result in early infection
(RPR, VDRL)
 Decrease in titers confirms treatment

 Antibody to treponemal antigens


Treponemal  Qualitative (reactive/nonreactive)
 Greater sensitivity in early infection
(FTA-ABS, TP-EIA)  Positive even after treatment

FTA-ABS = fluorescent treponemal antibody absorption; RPR = rapid plasma reagin;


TP-EIA = Treponema pallidum enzyme immunoassay.
 
Common causes of recurrent pneumonia
Bronchial obstruction

 Extrinsic: neoplasm, adenopathy


 Intrinsic: bronchiectasis, foreign body

Recurrent aspiration
Same
lung lobe*  Altered consciousness: seizure, sedatives, antipsychotics, alcohol,
illicit drugs

 Dysphagia: neurologic disorder, esophageal motility issue


 Poor dental hygiene
 Gastroesophageal reflux

 Immunodeficiency: HIV, leukemia, CVID


Different  Sinopulmonary disease: cystic fibrosis, immotile cilia
lung lobes  Noninfectious: vasculitis, BOOP
*Recurrent aspiration can lead to pneumonia in different dependent regions of the lung
depending on the position of the patient during the aspiration event.

BOOP = bronchiolitis obliterans with organizing pneumonia; CVID = common variable


immunodeficiency.
Klinefelter syndrome
 Nondisjunction of the sex chromosomes, resulting in a 47,XXY
Pathogenesis male

 Primary hypogonadism
 Increased long bone length
Clinical features  Gynecomastia
 Learning & socialization difficulties

 ↓ Testosterone
 ↑ LH & FSH (due to loss of feedback inhibition)
Laboratory findings
 ↑ Estradiol

Common causes of hypogonadism in men


 Congenital (eg, Klinefelter syndrome, cryptorchidism)
Primary  Drugs (eg, alkylating agents, ketoconazole)
 Orchitis (eg, mumps), trauma, torsion
(testicular)  Chronic kidney disease

 Gonadotroph damage: Tumor, cranial trauma, infiltrative


Secondary diseases (eg, hemochromatosis), apoplexy
 Gonadotropin suppression: Exogenous androgens,
(pituitary/hypothalamic) hyperprolactinemia, diabetes mellitus, morbid obesity

Combined  Hypercortisolism
 Cirrhosis
(primary & secondary)
Toxic alcohol ingestion (methanol or ethylene glycol)
 Methanol: windshield wiper fluid, contaminated homemade liquor
 Ethylene glycol: automotive coolant/antifreeze, brake fluid
Typical sources  Industrial solvents & deicing solutions may contain either toxic
alcohol

 Early: CNS sedation & inebriation, osmolar gap


 Late: anion gap metabolic acidosis, compensatory tachypnea
Clinical features o Ocular toxicity (methanol)
o Urine oxalate crystals, hypocalcemia, AKI (ethylene glycol)

Management  Fomepizole (inhibits ADHase) is preferred therapy


 Ethanol solution (competes for ADHase) if fomepizole unavailable
 IV sodium bicarbonate for acidemia (eg, pH <7.3)
 Hemodialysis for severe cases (eg, acidosis, end-organ damage)

ADHase = alcohol dehydrogenase; AKI = acute kidney injury; IV = intravenous.


Common inflammatory eyelid conditions
Etiology Clinical findings
 Redness, swelling &/or
 Inflammation of the eyelid
scaling of lid margin, often
Blepharitis margin
with crusting of eyelashes

 Solitary, rubbery nodule


 Granulomatous reaction to
deep to eyelid margin
obstructed meibomian
Chalazion  Usually painless, most
gland
common on upper eyelid

 External hordeolum (sty):


 Tender, erythematous
focal infection of Zeis
nodule/pustule at lid margin
gland
(external hordeolum) or
Hordeolum  Internal hordeolum: focal
internal surface of eyelid
infection of meibomian
(internal hordeolum)
gland

 Painful swelling & redness


 Acute
around medial canthal
inflammation/infection of
Dacryocystitis region ± purulent discharge
nasolacrimal sac
from punctum

Uric acid kidney stones


 Low urine pH: chronic diarrhea (GI bicarbonate loss), metabolic
syndrome/
diabetes mellitus
Risk factors
 Increased uric acid excretion: gout, myeloproliferative disorders
 Increased urine concentration: hot, arid climates; dehydration

 Acidic urine favors formation of uric acid (insoluble) over urate


(soluble)
Pathophysiology
 Supersaturation of urine with uric acid precipitates crystal formation

 Radiolucent stones (not visible on x-ray)


Clinical  Uric acid crystals on urine microscopy (diamond/rhomboid shaped)
characteristics  Urine pH usually <5.5

 Alkalinization of urine (eg, potassium citrate)


Treatment  Reduction of uric acid production (eg, low-purine diet, allopurinol)
GI = gastrointestinal.
Cardiac syncope
Etiology Clues to diagnosis
 Exertional syncope
Aortic stenosis or HCM  Systolic murmur on examination

 No preceding symptoms
Ventricular tachycardia  Cardiomyopathy or previous MI

 Preceding fatigue or dizziness


Sick sinus syndrome  Sinus pauses on ECG

 Bifascicular block or ↑ PR interval on ECG


Advanced AV block  Dropped QRS complexes on ECG

 No preceding symptoms
 Medications that prolong QT interval
Torsades de pointes
 Hypokalemia or hypomagnesemia

AV = atrioventricular; HCM = hypertrophic cardiomyopathy; MI = myocardial infarction.


Myasthenic crisis
 Infection or surgery
 Pregnancy or childbirth
Precipitating
 Tapering of immunosuppressive drugs
factors
 Medications (eg, aminoglycosides, beta blockers)

 ↑ Generalized & oropharyngeal weakness


Signs/symptoms  Respiratory insufficiency/dyspnea

 Intubation for deteriorating respiratory status


Treatment  Plasmapheresis or IVIG as well as corticosteroids

IVIG = intravenous immunoglobulin.


Nonbacterial thrombotic endocarditis
 Hypercoagulable state due primarily to underlying malignancy (80%) or
SLE
Etiology
 Noninfectious thrombi form on healthy valve

 Usually asymptomatic until embolism to kidney, spleen, skin,


extremities, or brain occurs
Manifestations  Uncommon: fever, leukocytosis, significant valve insufficiency (eg,
murmur)

Diagnosis  Blood cultures: no growth


 Echocardiography: small, mobile vegetations on aortic/mitral valves
 Evaluate for hypercoagulable state &/or malignancy

 Anticoagulation
Treatment
SLE = systemic lupus erythematosus.
Acute kidney injury
Prerenal Acute tubular necrosis
BUN/creatinine ratio Typically >20 Typically normal (~10-15)
Urine sodium <20 mEq/L >40 mEq/L
Fractional excretion of sodium <1% >2%
Urine osmolality >500 mOsm/kg ~300 mOsm/kg
Urine specific gravity >1.020 <1.020
Microscopy Bland Muddy brown casts
Indications for statin therapy in prevention of ASCVD
 Established ASCVD
o Acute coronary syndrome
o Stable angina
Secondary prevention
o Arterial revascularization (eg, CABG)
o Stroke, TIA, PAD

 LDL ≥190 mg/dL


 Age ≥40 with diabetes mellitus
Primary prevention
 Estimated 10-year risk of ASCVD >7.5%-10%

ASCVD = atherosclerotic cardiovascular disease; CABG = coronary artery bypass grafting;


PAD = peripheral artery disease; TIA = transient ischemic attack.
Rectovaginal fistula
 Pelvic radiation
 Obstetric trauma
 Pelvic surgery
Risk factors  Colon cancer
 Diverticulitis
 Crohn disease

 Uncontrollable passage of gas &/or feces from the vagina


Clinical features
 Physical examination
 Fistulography
Diagnostic studies  Magnetic resonance imaging
 Endosonography

Common causes of pleural effusions


Transudate Exudate
 Infections
 Malignancy
 Congestive heart failure
 Connective tissue diseases
 Cirrhosis
 Inflammatory disorders
 Nephrotic syndrome
 Movement of fluid from abdomen to pleural space
 Peritoneal dialysis
 Coronary artery bypass surgery
 Pulmonary embolism (usually)

Syndrome of inappropriate antidiuretic hormone


 CNS disturbance (eg, stroke, hemorrhage, trauma)
 Medications (eg, carbamazepine, SSRIs, NSAIDs)
 Lung disease (eg, pneumonia)
Etiologies
 Ectopic ADH secretion (eg, small cell lung cancer)
 Pain &/or nausea

 Mild/moderate hyponatremia: nausea, forgetfulness


 Severe hyponatremia: seizures, coma
Clinical features
 Euvolemia (eg, moist mucous membranes, no edema, no JVD)

 Hyponatremia
 Serum osmolality <275 mOsm/kg H2O (hypotonic)
Laboratory findings  Urine osmolality >100 mOsm/kg H2O
 Urine sodium >40 mEq/L

 Fluid restriction ± salt tablets


Management  Hypertonic (3%) saline for severe hyponatremia

ADH = antidiuretic hormone; JVD = jugular venous distension; NSAIDs = nonsteroidal anti-


inflammatory drugs; SSRIs = selective serotonin reuptake inhibitors.
 
Distinguishing features of fibromyalgia, polymyositis
& polymyalgia rheumatica
Clinical features Diagnosis
 Young to middle-aged women
 Chronic widespread pain  ≥3 months of symptoms with
 Fatigue, impaired concentration widespread pain index or
Fibromyalgia  Tenderness at trigger points symptom severity score
(eg, midtrapezius, costochondral  Normal laboratory studies
junction)

Polymyositis  Proximal muscle weakness  Elevated muscle enzymes


(eg, increasing difficulty (eg, creatine kinase, aldolase,
climbing stairs) AST)  
 Pain mild/absent  Autoantibodies (anti–Jo-1,
ANA)
 Biopsy: endomysial infiltrate,
patchy necrosis

 Age >50
 Systemic signs & symptoms  Elevated ESR, C-reactive
 Stiffness > pain in shoulders, hip protein
Polymyalgia
girdle, neck  Rapid improvement with
rheumatica
 Association with giant cell glucocorticoids
(temporal) arteritis

ANA = antinuclear antibody; AST = aspartate aminotransferase; ESR = erythrocyte


sedimentation rate.
Hepatorenal syndrome
 Advanced cirrhosis with portal hypertension
Risk factors  Acute liver failure, severe alcoholic hepatitis

 Splanchnic vasodilation* → renal hypoperfusion →


RAAS
activation → overwhelming renal vasoconstriction →
Pathophysiology
AKI
 Precipitants: gastrointestinal bleed, infection (eg, SBP)

 Bland urinalysis
 Very low urine Na+ (<10 mEq/L)
Diagnosis  Exclusion of other causes of AKI
 No improvement with trial of volume expansion

 Albumin + splanchnic vasoconstrictors**


(temporizing)
Treatment
 Liver transplantation (curative)

*Due to excess local release of vasodilators (eg, nitric oxide).

**Midodrine plus octreotide, terlipressin, or norepinephrine.

AKI = acute kidney injury; RAAS = renin-angiotensin-aldosterone system; SBP = spontaneous


bacterial peritonitis.
Spontaneous bacterial peritonitis
 Temperature >37.8 C (100 F)
 Abdominal pain/tenderness
Clinical presentation  Altered mental status (abnormal connect-the-numbers test)
 Hypotension, hypothermia, paralytic ileus with severe infection

Diagnosis from ascitic  PMNs >250/mm3


fluid  Positive culture, often gram-negative organisms (eg,
Escherichia coli, Klebsiella)
 Protein <1 g/dL
 SAAG >1.1 g/dL

 Empiric antibiotics - third-generation cephalosporins (eg,


cefotaxime)
Treatment
 Fluoroquinolones for SBP prophylaxis

PMN = polymorphonuclear leukocytes; SAAG = serum-ascites albumin gradient; SBP=


spontaneous bacterial peritonitis.
Cor pulmonale
 Right-sided heart failure due to primary pulmonary disorder
Pathophysiology  Absence of left-sided heart disease

 Parenchymal disease/chronic hypoxia


o COPD (most common)
o Cystic fibrosis
Common
o Interstitial lung disease
etiologies
o Obstructive sleep apnea
 Pulmonary vascular disease: pulmonary embolism

 Dyspnea & fatigue on exertion


 Exertional angina (due to ↑ cardiac demand)
Symptoms
 Exertional syncope (due to ↓ cardiac output)

 Jugular venous distension


 Peripheral edema
Examination  Palpable RV heave, loud P2, tricuspid regurgitation murmur
 Hepatomegaly with pulsatile liver

 Electrocardiography
o Incomplete/complete right bundle branch block
o Right axis deviation, RV hypertrophy, RA enlargement
 Echocardiography
Diagnostic o Pulmonary hypertension, RV dilation/dysfunction, tricuspid
evaluation regurgitation
 Catheterization (gold standard)
o Elevated filling pressures, decreased cardiac output,
pulmonary hypertension

COPD = chronic obstructive pulmonary disease; RA = right atrial; RV = right ventricular.


Clinical features of FMD
Patients to Women age <50 with 1 of the following:
screen
 Severe or resistant hypertension
 Onset of hypertension before age 35
 Sudden increase in blood pressure from baseline
 Increase in creatinine (≥0.5-1 mg/dL) after starting angiotensin-
converting enzyme inhibitor or angiotensin receptor blocker & without
significant effect on blood pressure
 Systolic-diastolic epigastric bruit

 Resistant hypertension from renal artery involvement


 Cerebrovascular FMD with symptoms of brain ischemia (eg, amaurosis
fugax, Horner’s syndrome, transient ischemic attack, stroke)
Clinical
 Nonspecific symptoms (eg, headache, pulsatile tinnitus, dizziness)
presentation
from carotid or vertebral artery involvement
 Can also involve iliac, subclavian & visceral arteries

 Noninvasive testing preferred (eg, computed tomography angiography,


duplex ultrasound)
 Catheter-based digital subtraction arteriography for patients with
Diagnosis &
inconclusive noninvasive testing
follow-up
 Medically treated patients need follow-up blood pressure & creatinine
every 3-4 months & renal ultrasound every 6-12 months

FMD = fibromuscular dysplasia.


Clinical features of acromegaly
Local tumor
Headache, visual field defects, cranial nerve defects
effect
Gigantism, frontal bossing, malocclusion of jaw, macrognathia, arthritis,
Musculoskeletal
carpal tunnel syndrome, enlargement of hands/feet
Skin Skin thickening, hyperhidrosis (odor), skin tags
Cardiovascular Cardiomyopathy, hypertension, heart failure
Respiratory Sleep apnea
Gastrointestinal Colon polyps/cancer, diverticulosis
Endocrine Galactorrhea, hypogonadism, diabetes mellitus, hypertriglyceridemia
Additional
Enlarged tongue, thyroid, salivary glands, liver, spleen, kidney, prostate
features
Clues to etiology of syncope
Reflex syncope  Trigger (eg, emotional stress, prolonged
standing)
Vasovagal
 Prodrome (eg, nausea, sweating, warmth)

 Occurs with micturition, defecation,


Situational swallowing, or coughing

Carotid  Tactile stimulation of carotid sinus while


hypersensitivity standing
 Advanced age, carotid atherosclerosis

 Vasodilators (eg, alpha-1 blockers,


antihypertensives)
Medications  Inotropic/chronotropic blockade (eg, beta
blockers)
Orthostatic
syncope  History consistent with volume loss
Hypovolemia
 Advanced age
Autonomic
 Predisposing disease (eg, DM, Parkinson)
dysfunction
 Syncope with exertion
LV outflow
 Systolic ejection murmur
obstruction
 No warning symptoms
 Cardiomyopathy or ischemic HD
Ventricular
(monomorphic)
Cardiac syncope tachycardia
 QT-interval prolongation (polymorphic)

 Preceding fatigue or light-headedness


Conduction  ECG abnormalities (eg, sinus pauses, dropped
impairment* QRS complexes)

*Sick sinus syndrome or advanced atrioventricular block.

DM = diabetes mellitus; HD = heart disease; LV = left ventricular.

Clinical features of crystal-induced acute kidney injury


 Acyclovir
 Sulfonamides
 Methotrexate
Common etiologies  Ethylene glycol
 Protease inhibitors
 Uric acid (tumor lysis syndrome)

 Usually asymptomatic
 AKI ≤7 days of starting drug
Clinical presentation  UA: Hematuria, pyuria & crystals
 Increased risk with volume depletion, CKD

Management  Discontinuation of drug


 Volume repletion
 Loop diuretic

AKI = acute kidney injury; CKD = chronic kidney disease; UA = urinalysis.


Neisseria meningitidis postexposure prophylaxis
 Household members
 Roommates or intimate contacts
Recommended  Childcare center workers
populations*  Persons directly exposed to respiratory or oral secretions
 Person seated next to affected person for ≥8 hr (eg, airline traveler)

 Rifampin
Prophylaxis  Ceftriaxone
options  Ciprofloxacin (adults only)

*Regardless of vaccination status.


Acute exacerbation of chronic obstructive pulmonary disease
 Infectious (70%): respiratory viruses (eg, rhinovirus) &
commensal bacteria (eg, nontypable Haemophilus influenzae)
Precipitants  Noninfectious (30%): sterile inflammation (underlying
disease), pulmonary embolism, inhaled irritants

 Bronchial inflammation: systemic response (eg, fever,


leukocytosis) usually absent
 Cardinal symptoms: ↑ dyspnea, ↑ sputum volume, ↑ sputum
Pathophysiology &
purulence
presentation
 ↑ WOB (hyperinflation) & impaired gas exchange (hypoxemia
[↓ V/Q], hypercapnia [↑ VD])

 Maximize expiratory flow: inhaled bronchodilators


 Reduce airway inflammation: systemic glucocorticoids
 Treat underlying triggers: ± antibiotics* &/or antivirals
(influenza, COVID-19)
Management
 Maintain adequate oxygenation: SpO2 target 88%-92%
 Maintain adequate ventilation: NIPPV or invasive mechanical
ventilation

*Antibiotics generally indicated if: (1) increased sputum purulence + ≥1 other cardinal
symptoms; or (2) patient requires hospitalization.

NIPPV = noninvasive positive pressure ventilation; VD = alveolar dead space ventilation; V/Q =
ventilation/perfusion ratio; WOB = work of breathing.
Primary adrenal insufficiency
Etiology  Autoimmune adrenalitis (most common)
 Infection (eg, tuberculosis)
 Metastatic infiltration

 Fatigue, weakness, anorexia/weight loss


 Nausea, vomiting, abdominal pain
Clinical  Salt craving, postural hypotension
features  Hyperpigmentation
 Acute adrenal crisis: confusion, hypotension/shock

 Hyponatremia, hyperkalemia, eosinophilia


Laboratory
 Low morning cortisol, high ACTH
findings
 Glucocorticoids (eg, hydrocortisone, prednisone)
Treatment  Mineralocorticoids (eg, fludrocortisone)

ACTH = adrenocorticotropic hormone.


Milk-alkali syndrome
 Excessive intake of calcium & absorbable alkali
 Renal vasoconstriction & decreased GFR
Pathophysiology
 Renal loss of sodium & water, reabsorption of bicarbonate

 Nausea, vomiting, constipation


 Polyuria, polydipsia
Symptoms
 Neuropsychiatric symptoms

 Hypercalcemia
 Metabolic alkalosis
Laboratory
 Acute kidney injury
findings
 Suppressed PTH

 Discontinuation of causative agent


Treatment  Isotonic saline followed by furosemide

GFR = glomerular filtration rate; PTH = parathyroid hormone.

Tinea versicolor (pityriasis versicolor)


 Malassezia globosa skin flora grows in exposure to
Pathogenesis hot & humid weather

 Hypopigmented, hyperpigmented, or mildly


erythematous lesions (face in children, trunk & upper
Clinical extremities in adolescents & adults)
features  ± Fine scale
 ± Pruritus

Diagnosis  KOH preparation shows hyphae & yeast cells in a


"spaghetti & meatballs" pattern

 Topical ketoconazole, terbinafine, or selenium


Treatment sulfide

KOH = potassium hydroxide.


Pharmacotherapy for chronic heart failure with reduced ejection fraction
Agent Mortality benefit
Angiotensin receptor-neprilysin inhibitor

(eg, sacubitril-valsartan)

OR

ACE inhibitor
Yes
(eg, lisinopril)

OR

Angiotensin II receptor blocker

(eg, losartan)
Beta blocker
Yes
(eg, metoprolol, carvedilol)
Mineralocorticoid receptor antagonist
Yes
(eg, spironolactone, eplerenone)
Sodium-glucose cotransporter-2 inhibitor
Yes
(eg, dapagliflozin, empagliflozin)
Diuretic
No*
(eg, furosemide, metolazone)
Digoxin No**
*Improves symptoms & reduces hospitalization.

**Reduces hospitalization.
Primary hyperparathyroidism
 Parathyroid adenoma (most common), hyperplasia, carcinoma
Etiology  Increased risk in MEN types 1 & 2A

Symptoms  Asymptomatic (most common)


 Mild, nonspecific symptoms (eg, fatigue, constipation)
 Abdominal pain, renal stones, bone pain, neuropsychiatric
symptoms

 Hypercalcemia
 Elevated or inappropriately normal PTH
Diagnostic findings
 Elevated 24-hour urinary calcium excretion

MEN = multiple endocrine neoplasia; PTH = parathyroid hormone.


Stress-induced (takotsubo) cardiomyopathy
 Postmenopausal woman
Risk factors  Recent physical or emotional stressor

 Chest pain mimicking myocardial infarction


 Decompensated heart failure
Clinical features  Moderate troponin elevation
 ECG: ischemic changes in precordial leads

 Catheterization: no obstructive CAD


Diagnosis  Echo: LV apical hypokinesis, basilar hyperkinesis

 Resolves in several weeks with supportive care


Treatment
CAD = coronary artery disease; LV = left ventricular.
Thyroid effects of amiodarone
Disorder Features Treatment
 ↑ T4 None needed
 ↓ T3
Decreased T4-T3 conversion
 Normal/↑ TSH

 ↑ TSH Levothyroxine
Inhibition of thyroid hormone
 ↓ T4
synthesis
 ↓ TSH Antithyroid drugs
 ↑ T3 & T4
AIT type 1
 ↓ RAIU
(iodine-induced increase
 Increased vascularity on
in thyroid hormone synthesis)
ultrasound

 ↓ TSH Glucocorticoids
 ↑ T3 & T4
AIT type 2  Undetectable RAIU
(destructive thyroiditis)  Decreased vascularity on
ultrasound

AIT = amiodarone-induced thyrotoxicosis; RAIU = radioactive iodine uptake.


Conditions associated with aspiration pneumonia
Trigger Related conditions
 Sedatives or antipsychotics
 Illicit drugs or alcohol
Reduced
 Anesthesia
consciousness
 Generalized seizure

 Neurologic disorders
 Esophageal motility defects
Dysphagia  Protracted vomiting
 Gastroesophageal reflux

 Tracheostomy
Pharyngeal or  Intubation
glottal dysfunction  Nasogastric feeding

 Gingivitis
Dental issues  Poor dental hygiene

Acute pericarditis
 Viral or idiopathic
 Autoimmune disease (eg, SLE)
 Uremia (acute or chronic renal failure)
Etiology  Post myocardial infarction
o Early: peri-infarction pericarditis
o Late: Dressler syndrome

 Pleuritic chest pain (↓ when sitting) ± fever


 Pericardial friction rub (highly specific)
Clinical features
 ECG: diffuse ST-segment elevation & PR-segment
& diagnosis
depression
 Echocardiography: pericardial effusion

 NSAIDs & colchicine for viral or idiopathic etiology


Treatment  Variable for other etiologies

NSAIDs = nonsteroidal anti-inflammatory drugs; SLE = systemic lupus erythematosus.


Major pathologic mechanisms of foodborne illness
Staphylococcus aureus  Quick onset (1-6 hours)
Enterotoxin ingested  Vomiting predominant
Bacillus cereus
Enterotoxin made in intestine Clostridium perfringens  Delayed onset (>1 day)
 Watery/bloody diarrhea
ETEC/STEC

Vibrio cholerae
Campylobacter jejuni  Variable onset
 Watery/bloody diarrhea
Bacterial epithelial invasion Nontyphoidal salmonella  Fever
 Systemic illness (Listeria)
Listeria monocytogenes
ETEC = enterotoxigenic Escherichia coli; STEC = Shiga toxin-producing E coli.
Cardiovascular effects of hyperthyroidism
 Tachycardia/palpitations
Increased rate  Atrial fibrillation

 ↑ Ejection fraction & cardiac output


 ↑ Myocardial oxygen demand & angina
Increased contractility
 ↑ Pulmonary artery pressure

 ↓ Systemic vascular resistance


Peripheral vasodilation
 ↓ Diastolic pressure
 ↑ Systolic pressure
Additional effects  ↑ Pulse pressure
 High-output heart failure

Anterior uveitis
 Symptoms: ocular pain, photophobia, decreased acuity
Presentation  Examination: ciliary flush, pupillary constriction, hypopyon

 Infections: herpesviruses, toxoplasmosis, syphilis


 Sarcoidosis
Common causes/
 Spondylarthritis (eg, ankylosing spondylitis, reactive arthritis)
associations
 Inflammatory bowel disease

 Slit-lamp examination
 As indicated: HLA-B27, pelvis/spine x-ray, chest x-ray, HIV,
Evaluation/testing
syphilis serology

 Dilating eye drops (eg, cyclopentolate)


Treatment  Topical glucocorticoids

HLA-B27 = human leukocyte antigen B27.


Spinal epidural abscess
Epidemiology  Staphylococcus aureus (65%)
 Immunosuppression (HIV, diabetes, alcohol use, old age)
 Inoculating sources
o Distant infection (eg, cellulitis, joint/bone)
o Spinal procedure (eg, epidural catheter)
o Injection drug use

 Classic triad
o Fever (~50%)
o Focal/severe back pain
Manifestations o Neurologic findings (eg, motor/sensory change, bowel/bladder
dysfunction, paralysis)
 ↑ Erythrocyte sedimentation rate

 MRI of the spine with contrast


Diagnosis  Blood & aspirate cultures

 Broad-spectrum antibiotics (eg, vancomycin + ceftriaxone)


Treatment  Urgent aspiration/surgical decompression

Type of stress Mechanism Best for Not for


Exercise ECG test  ↑ HR  Patients able to  LBBB
 ↑ BP reach tHR  Pacemaker
(tHR = 85% of  Patients unable to
220 − age) reach tHR

Pharmacologic stress  Nonselective  LBBB  Reactive airway


test with adenosine or adenosine  Pacemaker disease
dipyridamole agonist  Patients unable  Patients on
 Dilates to reach tHR dipyridamole or 
coronary theophylline
arteries without
↑ HR or BP

Dobutamine stress  Β-1 agonist  Reactive  Tachyarrhythmias


echocardiography  ↑ HR ± BP airway disease
 Patients unable
to reach tHR

BP = blood pressure; HR = heart rate; LBBB = left bundle branch block; tHR = target HR.
Drugs for neuropathic pain
Drug Mechanism of action
Tricyclic antidepressants  ↓ Reuptake of serotonin & norepinephrine
(eg, amitriptyline, nortriptyline)  Inhibition of pain signals

 
SNRIs (eg, duloxetine)
Anticonvulsants  Decreased depolarization of neurons in the CNS
(eg, gabapentin, pregabalin)
 Activation of central opioid receptors
Opioids
 Loss of membrane potential in nociceptive fibers
Capsaicin (topical)
 Decreased depolarization of neurons in peripheral nerves
Lidocaine (topical)
SNRIs = serotonin-norepinephrine reuptake inhibitors.
Infective endocarditis with intravenous drug use
 Injected particles cause microdamage to right-sided
valves before being filtered out by the lungs
Pathogenesis  Microdamage facilitates bacterial attachment
 Increased risk with HIV

 Tricuspid valve most commonly affected


 Staphylococcus aureus is the most common organism
 Septic pulmonary emboli present in up to 75% of cases
 Audible murmur may be absent in 50% of cases
Clinical features
 Few peripheral manifestations
(eg, splinter hemorrhages, Janeway lesions)
 Heart failure uncommon

Management of hypercalcemia
Short-term (immediate) treatment

 Normal saline hydration plus calcitonin


Severe  Avoid loop diuretics unless volume overload (heart failure) exists
(calcium >14 mg/dL)
or symptomatic Long-term treatment

 Bisphosphonate (zoledronic acid)

Moderate  Usually no immediate treatment required unless symptomatic


(calcium 12-14  Treatment is similar to that for severe hypercalcemia
mg/dL)
 No immediate treatment required
Asymptomatic or
 Avoid thiazide diuretics, lithium, volume depletion & prolonged
mild
bed rest
(calcium <12 mg/dL)
Causes of polyuria & dilute urine
Primary polydipsia Central DI Nephrogenic DI
Cause  ADH  ADH  ADH
independent deficiency
resistance
(excessive (CNS
(renal disease)
water intake) pathology)

 Chronic
 Idiopathic
lithium use
 Antipsychotics  Trauma
 Hypercalcemia
(dry mouth)  Pituitary
 Hereditary
Etiology  Psychiatric surgery
(AVPR2 &
conditions  Ischemic
aquaporin 2
encephalopathy
mutations)

Results  High urine  Low urine  Low urine


of water osmolality osmolality osmolality
deprivation
 Increased urine
Response to  No change  No change
osmolality
desmopressin
ADH = antidiuretic hormone; AVPR2 = vasopressor V2; DI = diabetes insipidus.
 
Hereditary spherocytosis
 Usually autosomal dominant
Epidemiology
 Hemolytic anemia
 Jaundice
Clinical presentation
 Splenomegaly

 ↑ MCHC
 Negative Coombs test
 Spherocytes on peripheral smear
Laboratory findings
 ↑ Osmotic fragility on acidified glycerol lysis test
 Abnormal eosin-5-maleimide binding test

 Folic acid supplementation


 Blood transfusion
Treatment
 Splenectomy

MCHC = mean corpuscular hemoglobin concentration.


Clinical features of psoriatic arthritis
 Distal interphalangeal joints
 Asymmetric oligoarthritis
 Symmetric polyarthritis, similar to rheumatoid arthritis
Arthritis
 Arthritis mutilans (deforming & destructive arthritis)
 Spondylarthritides (sacroiliitis & spondylitis)
 Enthesitis (inflammation at site of tendon insertion into
bone)
Soft tissue & nail  Dactylitis ("sausage digits") of toe or finger
involvement  Nail pitting & onycholysis
 Swelling of the hands or feet with pitting edema

 Arthritis precedes skin disease in 15% of patients


 Skin lesions are present but not yet diagnosed in 15% of
Skin lesions
patients

Metformin
 Inhibits mitochondrial glycerophosphate dehydrogenase
Mechanism of action  Upregulates AMP-activated protein kinase

 ↓ Hepatic glucose production


 ↓ Intestinal glucose absorption
Metabolic effects  ↑ Peripheral glucose uptake/utilization
 ↓ Lipogenesis

 Renal clearance
Pharmacokinetics  No significant metabolites

 Diarrhea
 Lactic acidosis
Adverse effects
 Vitamin B12 deficiency

 Renal insufficiency (check serum creatinine)


 Hepatic insufficiency
Precautions/ contraindications
 Decompensated heart failure

 
Thyroiditis
Clinical features Diagnostic testing
Chronic autoimmune  Predominant hypothyroid  TPO antibody
thyroiditis features  Variable radioiodine
 Diffuse goiter uptake
(Hashimoto thyroiditis)
   Variant of chronic autoimmune
 Positive TPO
thyroiditis
antibody
Painless thyroiditis  Mild, brief hyperthyroid phase
 Low radioiodine
 Small, nontender goiter
uptake
(silent thyroiditis)  Spontaneous recovery
 
Subacute thyroiditis  Likely postviral inflammatory  Elevated ESR & CRP
(de Quervain thyroiditis) process
 Prominent fever & hyperthyroid
symptoms  Low radioiodine
 Painful/tender goiter uptake
 

CRP = C-reactive protein; ESR = erythrocyte sedimentation rate; TPO = positive thyroid
peroxidase.
Wilson disease
 Autosomal recessive mutation of ATP7B → hepatic copper accumulation
→ leak from damaged hepatocytes → deposits in tissues (eg, basal
Pathogenesis
ganglia, cornea)

 Hepatic (acute liver failure, chronic hepatitis, cirrhosis)


Clinical  Neurologic (parkinsonism, gait disturbance, dysarthria)
findings  Psychiatric (depression, personality changes, psychosis)

 ↓ Ceruloplasmin & ↑ urinary copper excretion


 Kayser-Fleischer rings on slit-lamp examination
Diagnosis
 ↑ Copper content on liver biopsy

 Chelators (eg, D-penicillamine, trientine)


Treatment  Zinc (interferes with copper absorption)

Characteristics of chronic headache


Headache
Clinical presentation
subtype
 Female predominance
 Unilateral, throbbing
Migraine
 Nausea/vomiting, photophobia

 Gradual onset, bilateral pressure


Tension-type  Mild to moderate without pericranial muscle tenderness

 Male predominance
 Unilateral, trigeminal distribution with ipsilateral
autonomic symptoms
Cluster
 Duration 15 min to 3 hr, circadian periodicity
 Improves with oxygen therapy

 Develops or worsens with daily medication use


Medication  Similar pattern to chronic migraine or tension-type
overuse headache

Myasthenic crisis
Precipitating  Infection or surgery
 Pregnancy or childbirth
 Tapering of immunosuppressive drugs
factors
 Medications (eg, aminoglycosides, beta blockers)

 ↑ Generalized & oropharyngeal weakness


Signs/symptoms  Respiratory insufficiency/dyspnea

 Intubation for deteriorating respiratory status


Treatment  Plasmapheresis or IVIG as well as corticosteroids

IVIG = intravenous immunoglobulin.


Fatal asthma: risk factors
 Prior respiratory failure: NIPPV, intubation, ICU admission
 Poor asthma control: ↑ inhaler use, frequent oral
Patient history
corticosteroids or acute care visits

 Examination: respirations >30/min, SaO2 ≤90%, accessory


muscle use, AMS, "silent chest"
Clinical status (impending
 ABG: ↑ or inappropriately normal PaCO2 relative to WOB
respiratory failure)
 Peak flow: ≤50% of baseline

ABG = arterial blood gas; AMS = altered mental status; ICU = intensive care unit; NIPPV =
noninvasive positive pressure ventilation; SaO2 = arterial saturation of oxygen; WOB = work of
breathing.
Clinical features of acute opioid intoxication
 Substance abuse
 Chronic opioid use
Risk factors  Hospitalized patients (especially postoperative)
 Hepatic or renal insufficiency

 Somnolence, AMS
 Pinpoint pupils (miosis)
 Shallow breathing & ↓ respiratory rate
Clinical findings
 Bradycardia, hypothermia, ↓ bowel sounds
 Respiratory acidosis on ABG

 Naloxone (may need repeated dosings)


 Airway management & ventilation
Management
 Exclude other AMS causes (eg, hypoglycemia)

ABG = arterial blood gas; AMS = altered mental status.


 
Infective endocarditis with intravenous drug use
Pathogenesis  Injected particles cause microdamage to right-sided
valves before being filtered out by the lungs
 Microdamage facilitates bacterial attachment
 Increased risk with HIV

 Tricuspid valve most commonly affected


 Staphylococcus aureus is the most common organism
 Septic pulmonary emboli present in up to 75% of cases
 Audible murmur may be absent in 50% of cases
Clinical features
 Few peripheral manifestations
(eg, splinter hemorrhages, Janeway lesions)
 Heart failure uncommon

Takayasu arteritis
 Female
 Asian
Risk factors
 Age 10-40

 Constitutional (eg, fever, weight loss, fatigue)


 Arterioocclusive (eg, claudication, ulcers) in upper
Symptoms extremities
 Arthralgias/myalgias

 Blood pressure discrepancies


 Pulse deficits
Examination findings
 Arterial bruits

 Elevated inflammatory markers (eg, ESR, CRP)


 Chest x-ray: aortic dilation, widened mediastinum
Diagnosis  CT/MR angiography: wall thickening, narrowing of
lumen

 Systemic glucocorticoids
Treatment
CRP = C-reactive protein; ESR = erythrocyte sedimentation rate.
Secondary causes of hypertension
Condition Clinical clues/features
 Elevated creatinine level
Renal parenchymal disease  Abnormal urinalysis (proteinuria, red blood cell casts)

 Recurrent flash pulmonary edema


 Elevated creatinine level (particularly with ACE inhibitor
Renovascular disease use)
 Abdominal bruit

Primary  Hypokalemia (spontaneous or thiazide induced)


hyperaldosteronism
 Metabolic alkalosis

 Daytime somnolence
Obstructive sleep apnea  Increased neck circumference

 Paroxysmal hypertension & tachycardia


Pheochromocytoma  Headaches, palpitations, diaphoresis

 Cushingoid body habitus & proximal muscle atrophy


Cushing syndrome  Hyperglycemia

 Hyperthyroidism: anxiety, heat intolerance, weight loss,


tachycardia
Thyroid disease  Hypothyroidism: fatigue, cold intolerance, weight gain,
bradycardia

 Mild hypercalcemia ± symptoms (eg, constipation)


Primary
 Kidney stones
hyperparathyroidism
 Upper extremity hypertension with brachial-femoral pulse
delay (common)
Coarctation of the aorta
 Lateralizing hypertension (less common)

Lead poisoning in adults


Risk  Occupational exposure (eg, lead paint, batteries, ammunition, construction)
factors
 Gastrointestinal (abdominal pain, constipation, anorexia)
Clinical  Neurologic (cognitive deficits, peripheral neuropathy)
features  Hematologic (anemia)

 Anemia
 Elevated venous lead level
Laboratory
 Elevated serum zinc protoporphyrin level
findings
 Basophilic stippling on peripheral smear

Common cognitive errors in medicine


Type of bias Definition Example
 Fixating on initial  Burning throat pain
impressions to make a diagnosed as acid reflux
diagnosis despite weight loss
Anchoring
 Related to confirmation  Correct diagnosis is lung
bias & premature closure malignancy

Availability  Allowing recently seen or  Dyspnea diagnosed as


memorable (high-stakes) influenza during peak
influenza season
cases to sway diagnosis  Correct diagnosis is
pulmonary embolism

 Emphasizing evidence that  Burning throat pain after


supports presumed eating spicy food diagnosed
diagnosis & overlooking as acid reflux despite
Confirmation information that supports weight loss
other diagnoses  Correct diagnosis is
 Related to anchoring bias malignancy

 Abdominal pain diagnosed


 Allowing diagnostic as opioid withdrawal in
approach to be influenced patient described as drug
Framing by context & presentation seeking
of information  Correct diagnosis is bowel
obstruction

Mechanical complications of acute myocardial infarction


Involved
Time Echocardiography
Complication coronary Clinical findings
course findings
artery
 Severe pulmonary edema,
respiratory distress
Papillary muscle Acute or  New early systolic
rupture/ within 3- RCA murmur Severe MR
dysfunction 5 days  Hypotension/cardiogenic
shock

LAD  Chest pain


Acute or (apical  New holosystolic murmur
Interventricular Left-to-right
within 3- septal) or  Hypotension/cardiogenic
septum rupture ventricular shunt**
5 days RCA (basal shock
septal)
 Chest pain
Within 5
 Distant heart sounds Pericardial
days* or
Free wall rupture LAD  Shock, rapid progression effusion with
up to 2
to cardiac arrest tamponade
weeks
 Heart failure
Up to
Left ventricular  Angina Thin & dyskinetic
several LAD
aneurysm  Ventricular arrhythmias myocardial wall
months
*50% occur within 5 days.
**Right heart catheterization shows step up in O2 concentration from right atrium to right
ventricle.

LAD = left anterior descending; MR = mitral regurgitation; RCA = right coronary artery.
Infectious keratitis
Pathogen Risk factors Clinical features*
 Central, round ulcer
 Improper contact lens use  Stromal abscess
Bacteria (eg, Staphylococcus  Corneal trauma, foreign  Mucopurulent
aureus, Pseudomonas) body discharge
 Acute presentation

 Branched dendritic
ulcerations
 Immunocompromised, HIV  ↓ Corneal sensation
Herpes simplex virus
 Watery discharge
 Recurrent episodes

 Ulcerations with
 Immunocompromised with feathery margins &
corneal injury involving satellite lesions
Fungi (eg, Candida) contaminated soil (eg,  Mucopurulent
gardening) discharge
 Indolent course

*Eye pain/redness, blurred vision & photophobia are features of all infectious keratitis.
Jarisch-Herxheimer reaction
 6-48 hours after initiating treatment for syphilis (most commonly
primary or secondary)
Epidemiology  May also be seen with treatment of other spirochete diseases (eg,
Lyme disease, leptospirosis)

 Acute onset of fever, chills, myalgias


Clinical
 Rash progression in secondary syphilis
presentation
 Supportive (IV fluids, acetaminophen, NSAIDs)
Treatment  Typically self-limiting within 48 hours of onset

IV = intravenous; NSAIDs = nonsteroidal anti-inflammatory drugs.


 
Acute bronchitis
 Preceding respiratory illness (90% viral)
Etiology
Clinical presentation  Cough for >5 days to 3 weeks (± purulent sputum)
 Absent systemic findings (eg, fever, chills)
 Wheezing or rhonchi, chest wall tenderness

 Clinical diagnosis, CXR only when pneumonia suspected


 Symptomatic treatment (eg, NSAIDs &/or bronchodilators)
Diagnosis & treatment
 Antibiotics not recommended

CXR = chest x-ray; NSAIDs = nonsteroidal anti-inflammatory drugs.


Bacterial meningitis
Risk group Common organisms Empiric antibiotics
 
Streptococcus pneumoniae, Vancomycin + 3rd-
Neisseria meningitidis generation cephalosporin
Age 2-50
Vancomycin + ampicillin +
S pneumoniae, N meningitidis,
Age >50 3rd-generation
Listeria
cephalosporin
 
S pneumoniae, N meningitidis, Vancomycin + ampicillin +
Listeria, gram-negative rods cefepime
Immunocompromised
Gram-negative rods, MRSA,
Neurosurgery/penetrating
coagulase-negative Vancomycin + cefepime
skull trauma
staphylococci
 3rd-generation cephalosporins: ceftriaxone or cefotaxime
 Alternatives to cefepime: ceftazidime or meropenem
 Alternative to ampicillin: trimethoprim-sulfamethoxazole for Listeria

MRSA = methicillin-resistant Staphylococcus aureus.


 
Esophageal cancer
 Adenocarcinoma
o Distal esophagus, arises from Barrett esophagus

Subtypes
 Squamous cell carcinoma
o Most commonly proximal and mid esophagus

 Uncontrolled gastroesophageal reflux, obesity, male (adenocarcinoma)


Risk factors  Smoking, alcohol use, n-nitroso containing food (squamous cell)

 Progressive solid-food dysphagia


 GI bleeding, iron deficiency anemia
Symptoms
 Weight loss, aspiration

 Endoscopy with biopsy


Diagnosis  CT (PET/CT) is used for staging (not initial diagnosis)
GI = gastrointestinal; PET = positron emission tomography.
Infectious mononucleosis
 Epstein-Barr virus most common
Etiology
 Fever
 Tonsillitis/pharyngitis ± exudates
 Posterior or diffuse cervical lymphadenopathy
Clinical features  Significant fatigue
 ± Hepatosplenomegaly
 ± Rash after amoxicillin

 Positive heterophile antibody (Monospot) test (25% false-negative


rate during 1st week of illness)
Diagnostic
 Atypical lymphocytosis
findings
 Transient hepatitis

 Avoid sports for ≥3 weeks (contact sports ≥4 weeks) due to the risk of
Management splenic rupture

 
Sickle cell trait
 Usually asymptomatic
Clinical features  No change in overall life expectancy

 Normal hemoglobin, reticulocyte count, RBC indices & morphology


Laboratory
 Hemoglobin electrophoresis: Hb A > Hb S
findings
 Hematuria/papillary necrosis, hyposthenuria
 Splenic infarction (especially at higher altitudes), venous
Complications thromboembolism, priapism
 Exertional rhabdomyolysis

Hb A = hemoglobin A; Hb S = hemoglobin S; RBC = red blood cell.


Thyroiditis
Clinical features Diagnostic testing
 Predominant hypothyroid  Positive TPO
Chronic autoimmune
features antibody
thyroiditis
 Diffuse goiter  Variable radioiodine
uptake
(Hashimoto thyroiditis)
Painless thyroiditis  Variant of chronic autoimmune  Positive TPO
thyroiditis antibody
(silent thyroiditis)  Mild, brief hyperthyroid phase  Low radioiodine
 Small, nontender goiter uptake
 Spontaneous recovery

 Likely postviral inflammatory  Elevated ESR & CRP


process  Low radioiodine
Subacute thyroiditis  Prominent fever & uptake
(de Quervain thyroiditis) hyperthyroid symptoms
 Painful/tender goiter

CRP = C-reactive protein; ESR = erythrocyte sedimentation rate; TPO = thyroid peroxidase.
Waldenström macroglobulinemia Multiple myeloma
 Hyperviscosity syndrome
 Osteolytic lesions/fractures
 Neuropathy
 Anemia
 Bleeding
Major manifestations  Hypercalcemia
 Hepatosplenomegaly
 Renal insufficiency
 Lymphadenopathy

Monoclonal antibody IgM IgG, IgA, light chains


Peripheral smear Rouleaux Rouleaux
Bone marrow biopsy >10% clonal B cells >10% clonal plasma cells
Age-related dry eye syndrome vs Sjögren syndrome
Age-related dry eye syndrome Sjögren syndrome
 Common  Uncommon to rare
Prevalence
Age of  50s-80s  30s-60s
onset
 Mucosal dryness often severe
 Parotid enlargement
Clinical  Mild to moderate mucosal dryness  Comorbid autoimmune disease
features (eg, scleroderma, rheumatoid
arthritis)

 Normal ESR and autoimmune  Abnormal ESR and autoimmune


markers* markers*
Diagnostic  Secretory function objectively  Secretory function objectively
features normal/near-normal (eg, normal decreased (eg, abnormal
Schirmer test) Schirmer test)

*Examples: antinuclear antibody, anti-SSA (Ro), anti-SSB (La).

ESR = erythrocyte sedimentation rate.


Clinical features of cocaine use
Clinical presentation  Sympathetic hyperactivity: tachycardia, hypertension, dilated
pupils
 Chest pain due to coronary vasoconstriction
 Psychomotor agitation, seizures

 Acute myocardial ischemia


 Aortic dissection
Complications
 ICH

 Benzodiazepines for blood pressure & anxiety


 Aspirin for inhibition of cocaine-induced platelet aggregation
 Nitroglycerin & calcium channel blockers for vasoconstrictive
Management of chest pain
pain  Immediate cardiac catheterization if indicated (eg, STEMI)
 Caution with: fibrinolysis (↑ risk of ICH), beta blockers (↑ risk
of coronary vasoconstriction*)

*Theoretical risk due to unopposed alpha stimulation.  Mixed alpha/beta blockers are sometimes
considered.

ICH = intracranial hemorrhage; STEMI = ST-segment elevation myocardial infarction.


Paget disease of bone
 Most patients are asymptomatic
 Bone pain & deformity
o Skull: headache, hearing loss
Clinical
o Spine: spinal stenosis, radiculopathy
features
o Long bones: bowing, fracture, arthritis of adjacent joints
 Giant cell tumor, osteosarcoma

 Osteoclast dysfunction
Pathogenesis  Increased bone turnover

 Elevated alkaline phosphatase


Laboratory  Elevated bone turnover markers (eg, PINP, urine hydroxyproline)
testing  Calcium & phosphorus: usually normal

 X-ray: osteolytic or mixed lytic/sclerotic lesions


Imaging  Bone scan: focal increase in uptake

 Bisphosphonates
Treatment
PINP = procollagen type I N-terminal propeptide.
Hemophilia A & B
 X-linked recessive
Inheritance
Clinical  Delayed/prolonged bleeding after mild trauma
features o Hemarthrosis, intramuscular hematomas
o Gastrointestinal or genitourinary tract bleeding
o Intracranial hemorrhage
 Complications: hemophilic arthropathy

 ↑ Activated PTT
 Normal platelet count & PT
Laboratory
 Absent or ↓ factor VIII (hemophilia A) or factor IX
findings
(hemophilia B) activity

 Factor replacement
Treatment  Desmopressin for mild hemophilia A

Parkinson disease Essential tremor


 Rest tremor, decreases with
voluntary movement  Action tremor
Characteristics
 "Pill-rolling"

 Hands, legs  Hands, head, voice


Distribution  Often asymmetric  Usually bilateral

 Bradykinesia  Family history often present


Associated features  Rigidity  Improves with alcohol

Clinical features of cocaine use


 Sympathetic hyperactivity: tachycardia, hypertension, dilated
pupils
Clinical presentation  Chest pain due to coronary vasoconstriction
 Psychomotor agitation, seizures

 Acute myocardial ischemia


 Aortic dissection
Complications
 ICH

 Benzodiazepines for blood pressure & anxiety


 Aspirin for inhibition of cocaine-induced platelet aggregation
 Nitroglycerin & calcium channel blockers for vasoconstrictive
Management of chest pain
pain  Immediate cardiac catheterization if indicated (eg, STEMI)
 Caution with: fibrinolysis (↑ risk of ICH), beta blockers (↑ risk
of coronary vasoconstriction*)

*Theoretical risk due to unopposed alpha stimulation.  Mixed alpha/beta blockers are sometimes
considered.

ICH = intracranial hemorrhage; STEMI = ST-segment elevation myocardial infarction.


Hereditary hemochromatosis
 Hyperpigmentation
 Arthropathy
 Hepatomegaly, cirrhosis, hepatocellular carcinoma
Clinical manifestations  Diabetes mellitus
 Hypopituitarism, secondary hypogonadism
 Cardiomyopathy

 Elevated liver transaminases


 Elevated serum ferritin, transferrin saturation
Diagnosis
 HFE genetic mutations

 Therapeutic phlebotomy (urgent if ferritin >1,000 ng/mL)


Management
Infectious mononucleosis
 Fever
 Tonsillitis/pharyngitis ± exudates
 Posterior or diffuse cervical lymphadenopathy
Clinical features  Significant fatigue
 ± Hepatosplenomegaly
 ± Rash after amoxicillin

 Acute airway obstruction


 Autoimmune hemolytic anemia & thrombocytopenia
Complications
 Splenic rupture

Clinical features of asbestosis


 Prolonged asbestos exposure (eg, shipyard, mining)
 Symptoms develop >20 years after initial exposure
Clinical presentation  Progressive dyspnea, basilar fine crackles, clubbing
 Increased risk for lung cancer & mesothelioma

 Pleural plaques on chest imaging


Diagnostic evaluation  Imaging, PFT & histology consistent with pulmonary fibrosis

PFT = pulmonary function testing.


Lung cancer
Tumor type Incidence Location Clinical associations
 Clubbing
Adenocarcinoma 40%-50% Peripheral  Hypertrophic osteoarthropathy

 Hypercalcemia
Squamous cell carcinoma 20%-25% Central  Necrosis & cavitation
 Cushing syndrome
 SIADH
Small cell carcinoma 10%-15% Central
 Lambert-Eaton syndrome

 Gynecomastia
Large cell carcinoma 5%-10% Peripheral  Galactorrhea

SIADH = syndrome of inappropriate antidiuretic hormone.


 
Infective endocarditis
 Congenital heart disease or prosthetic valve
 Previous endocarditis
Risk factors  Intravascular catheters
 Intravenous drug use

 New regurgitant murmur


 Skin: Janeway lesions, Osler nodes
 Roth spots (eyes), splinter hemorrhages (nails)
Physical examination
 Splenomegaly
 ± Signs of embolic phenomenon

 Hematuria/proteinuria (glomerulonephritis)
 Positive blood cultures
Diagnostic testing
 TEE > TTE for detecting vegetation

 Acute: Empiric treatment with vancomycin  


Treatment  Subacute: Treatment based on culture results

TEE = transesophageal echocardiogram; TTE = transthoracic echocardiogram.


 
Reactive arthritis
 Genitourinary infection: Chlamydia trachomatis
 Enteritis: Salmonella, Shigella, Yersinia,
Preceding infection Campylobacter, Clostridioides (formerly Clostridium)
difficile

 Asymmetric oligoarthritis
 Enthesitis
Musculoskeletal
 Dactylitis

Extraarticular symptoms  Ocular: conjunctivitis, anterior uveitis


 Genital: urethritis, cervicitis, prostatitis
 Dermal: keratoderma blennorrhagicum, circinate
balanitis
 Oral ulcers

 
Reactive arthritis
 Genitourinary infection: Chlamydia trachomatis
 Enteritis: Salmonella, Shigella, Yersinia,
Preceding infection Campylobacter, Clostridioides (formerly Clostridium)
difficile

 Asymmetric oligoarthritis
 Enthesitis
Musculoskeletal
 Dactylitis

 Ocular: conjunctivitis, anterior uveitis


 Genital: urethritis, cervicitis, prostatitis
 Dermal: keratoderma blennorrhagicum, circinate
Extraarticular symptoms
balanitis
 Oral ulcers

Acute liver failure


 Viral hepatitis (eg, HSV; CMV; hepatitis A, B, D, E)
 Drug toxicity (eg, acetaminophen overdose, idiosyncratic)
 Ischemia (eg, shock liver, Budd-Chiari syndrome)
Etiology  Autoimmune hepatitis
 Wilson disease
 Malignant infiltration

 Generalized symptoms (eg, fatigue, lethargy, anorexia,


nausea)
 Right upper quadrant abdominal pain
 Pruritus & jaundice due to hyperbilirubinemia
Clinical presentation
 Renal insufficiency
 Thrombocytopenia
 Hypoglycemia

 Severe acute liver injury (ALT & AST often >1,000 U/L)
 Signs of hepatic encephalopathy (eg, confusion, asterixis)
Diagnostic requirements
 Synthetic liver dysfunction (INR ≥1.5)

ALT = alanine aminotransferase; AST = aspartate aminotransferase; CMV = cytomegalovirus;


HSV = herpes simplex virus; INR = international normalized ratio.
Subdural hematoma
 Rupture of bridging veins (head trauma)
Pathogenesis
Risk factors  Elderly & alcoholic use disorder (cerebral atrophy, ↑ fall risk)
 Infants (thin-walled vessels)
 Anticoagulant use

 Acute: gradual onset 1-2 days after injury


o Impaired consciousness (eg, coma), confusion
o Headache, nausea & vomiting (↑ intracranial pressure)
Clinical
 Chronic: insidious onset weeks after injury
features
o Headache, somnolence, confusion, lightheadedness
o Focal neurologic deficits

 CT scan of the head: crescent-shaped hyperdensity (acute) or


Diagnosis hypodensity (chronic) crossing suture lines

 Reverse/discontinue anticoagulants
Treatment  Surgical evacuation of symptomatic or large bleeds

Differential diagnosis & features of chest pain


 Substernal
Coronary artery  Precipitated by exertion
disease  Relieved by rest or nitroglycerin

 Sharp/stabbing pain
Pulmonary/pleuritic
 Worse with inspiration
(pleurisy, pneumonia,
 Pericarditis: worse when lying flat
pericarditis, PE)
 Abrupt (maximal at onset), severe "tearing" pain
Aortic
 May radiate to back
(dissection,
 Hypertension and/or inherited aortopathy
intramural hematoma)
 Substernal, may refer to neck
 Associated with regurgitation
Esophageal  Provoked by recumbent position
 Nonexertional, relieved by antacids

 Persistent pain
Chest wall/  Worse with movement or change in position
musculoskeletal  Often follows repetitive activity

PE = pulmonary embolism.
Acute pericarditis
Etiology  Viral or idiopathic
 Autoimmune disease (eg, SLE)
 Uremia (acute or chronic renal failure)
 Post myocardial infarction
o Early: peri-infarction pericarditis
o Late: Dressler syndrome

 Pleuritic chest pain (↓ when sitting) ± fever


 Pericardial friction rub (highly specific)
Clinical features
 ECG: diffuse ST-segment elevation & PR-segment
& diagnosis
depression
 Echocardiography: pericardial effusion

 NSAIDs & colchicine for viral or idiopathic etiology


Treatment  Variable for other etiologies

NSAIDs = nonsteroidal anti-inflammatory drugs; SLE = systemic lupus erythematosus.


Next-of-kin surrogate decision maker
 Inability to communicate wishes regarding medical
decision-making
Patient selection  Advance directive not available or applicable
 No previously designated surrogate decision maker

 Priority to patient's spouse


 Alternate: adult children, parents, adult siblings, other
Surrogate selection
family members

 Substituted judgment: what the patient, not family, would


have wanted
Implementation
 Decisions in the patient's best interest

Primary biliary cholangitis


 Autoimmune destruction of intrahepatic bile ducts
Pathogenesis
 Affects middle-aged women
 Insidious onset of fatigue & pruritus
Clinical features  Progressive jaundice, hepatomegaly, cirrhosis
 Cutaneous xanthomas & xanthelasmas

 Cholestatic pattern of liver injury (↑↑ alkaline phosphatase,


↑ aminotransferases)
Laboratory findings  Antimitochondrial antibody
 Severe hypercholesterolemia

 Ursodeoxycholic acid (delays progression)


Treatment  Liver transplantation for advanced disease

Complications  Malabsorption, fat-soluble vitamin deficiencies


 Metabolic bone disease (osteoporosis, osteomalacia)
 Hepatocellular carcinoma

Giardiasis
 Contaminated food or water
 Fecal incontinence & crowding (eg, day care, nursing home)
Risk factors
 Immunodeficiency (eg, CVID, IgA deficiency, CF, HIV)

 Villous blunting, disruption of epithelial tight junctions, loss of brush


Pathogenesis border enzymes → malabsorption

 Subacute (<4 weeks) or chronic (months)


 Loose, oily, nonbloody stools
Clinical features  Bloating, flatulence
 Weight loss, decreased linear velocity (children), vitamin deficiencies

 Stool antigen or PCR testing (↑ sensitivity)


Diagnosis
 Stool microscopy (↓ sensitivity)

 First-line: tinidazole or nitazoxanide


 Alternate: metronidazole (children)
Treatment
 Pregnancy (first trimester): paromomycin
 Refractory/recurrent symptoms: evaluation for immunodeficiency

CF = cystic fibrosis; CVID = common variable immunodeficiency.


Normal pressure hydrocephalus
 Gait instability (wide-based) with frequent falls
 Cognitive dysfunction
Clinical  Urinary urgency/incontinence
features  Depressed affect (frontal lobe compression)
 Upper motor neuron signs in lower extremities

 Marked improvement in gait with spinal fluid


removal: Miller Fisher (lumbar tap) test
Diagnosis  Enlarged ventricles out of proportion to the
underlying brain atrophy on MRI

 Ventriculoperitoneal shunting
Treatment
Common cognitive errors in medicine
Type of bias Definition Example
Anchoring  Fixating on initial  Burning throat pain
impressions to make a diagnosed as acid reflux
diagnosis despite weight loss
 Related to confirmation  Correct diagnosis is lung
bias & premature closure malignancy

 Dyspnea diagnosed as
 Allowing recently seen or influenza during peak
memorable (high-stakes) influenza season
Availability
cases to sway diagnosis  Correct diagnosis is
pulmonary embolism

 Emphasizing evidence that  Burning throat pain after


supports presumed eating spicy food diagnosed
diagnosis & overlooking as acid reflux despite
Confirmation information that supports weight loss
other diagnoses  Correct diagnosis is
 Related to anchoring bias malignancy

 Abdominal pain diagnosed


 Allowing diagnostic as opioid withdrawal in
approach to be influenced patient described as drug
Framing by context & presentation seeking
of information  Correct diagnosis is bowel
obstruction

Prosthetic joint infection


Early onset Delayed onset Late onset
Time to onset
<3 months 3-12 months >12 months
after surgery
 Acute pain  Chronic joint pain  Acute symptoms in
 Wound infection  Implant loosening previously
or breakdown  Sinus tract asymptomatic joint
Presentation
 Fever formation  Recent infection at
distant site

 Staphylococcus  Coagulase-  Staphylococcus


aureus negative aureus
Most  Gram-negative staphylococci  Gram-negative rods
common rods  Propionibacterium  Beta-hemolytic
organisms  Anaerobes species streptococci
 Enterococci

Regulation of calcium metabolism


 ↑ Bone resorption
 ↑ Renal reabsorption of calcium & ↓ reabsorption of phosphate
Parathyroid hormone
 ↑ Conversion of 25-hydroxyvitamin D to 1,25-dihydroxyvitamin D
 ↑ Intestinal absorption of calcium & phosphate
 ↑ Renal reabsorption of calcium & phosphate
Vitamin D  ↓ Parathyroid hormone secretion
 ↑ Mineralization of bone

 ↓ Bone resorption
Calcitonin  ↓ Renal calcium reabsorption

Rhabdomyolysis
Skeletal muscle lysis/necrosis due to:

 Crush injury or prolonged immobilization


Etiology
 Intense muscle activity (eg, seizure, exertion)
 Drug/medication toxicity (eg, statins)

 Muscle pain & weakness


 Dark urine (myoglobinuria/pigmenturia)
 + Blood on urinalysis & no RBCs on microscopy
Clinical features
 ↑ Serum K & PO4, ↓ serum Ca, ↑ AST > ALT
 Acute kidney injury

 Serum creatine kinase >1,000 U/L


Diagnosis  Consistent clinical features

 Aggressive intravenous fluid resuscitation


Management  Sodium bicarbonate in some cases

ALT = alanine aminotransferase; AST = aspartate aminotransferase; RBCs = red blood cells.
Clinical features of pulmonary hypertension
 Pulmonary arterial hypertension (WHO group 1)
 Due to left heart disease (group 2)
 Due to chronic lung disease or hypoxemia (eg, COPD, OSA)
Classification (group 3)
 Due to chronic thromboembolic disease (group 4)
 Due to other causes (eg, sarcoidosis) (group 5)

 ↓ Cardiac output: exertional syncope/presyncope, fatigue,


weakness
 ↑ PA pressure: chest tightness, hemoptysis (rare)
Symptoms  RV demand ischemia: exertional angina/tightness
 Venous congestion: abdominal distension (bowel edema), early
satiety

Signs  Precordial heave due to RV hypertrophy


 Loud P2, right-sided S3 &/or S4
 Holosystolic murmur of tricuspid regurgitation
 JVD, ascites, peripheral edema, hepatomegaly

COPD = chronic obstructive pulmonary disease; JVD = jugular venous distension; OSA =
obstructive sleep apnea; PA = pulmonary artery; RV = right ventricular.
Clinical clues to renovascular disease
 Resistant HTN (uncontrolled despite 3-drug regimen)
 Malignant HTN (with end-organ damage)
HTN-related  Onset of severe HTN (>180/120 mm Hg) after age 55
symptoms  Severe HTN with diffuse atherosclerosis
 Recurrent flash pulmonary edema with severe HTN

Physical examination

 Asymmetric renal size (>1.5 cm)


 Abdominal bruit

Laboratory results
Supportive evidence
 Unexplained rise in serum creatinine (>30%) after starting ACE
inhibitors or ARBs

Imaging results

 Unexplained atrophic kidney

ARBs = angiotensin II receptor blockers; HTN = hypertension.


Septic arthritis
 Advanced age
 Abnormal joint (eg, OA, RA, prosthetic joint)
Risk factors  Immunocompromise (eg, diabetes mellitus)
 Bacteremia (eg, intravenous drug use)

 Hot, swollen joint with ↓ ROM


 Fever
Clinical features
 ↑ ESR & CRP

 Synovial fluid analysis


o Leukocytosis (>50,000/mm3)
o Gram stain (sensitivity ~30%-50%) & culture
Diagnosis
 Blood cultures

Initial treatment  Intravenous antibiotics


 Joint irrigation & drainage (eg, arthroscopy, open
arthrotomy)

CRP = C-reactive protein; ESR = erythrocyte sedimentation rate; OA = osteoarthritis; RA =


rheumatoid arthritis; ROM = range of motion.
Features of constrictive pericarditis
 Recurrent idiopathic or viral pericarditis
 Cardiac surgery or radiation therapy
Etiology
 Tuberculous pericarditis (where endemic)

 Fatigue, dyspnea on exertion


 Peripheral edema, ascites, hepatic congestion
 Pericardial knock in early diastole
Clinical presentation
 JVD with positive Kussmaul sign* & prominent y
descent

 ECG: low-voltage QRS complexes


 Chest x-ray/CT: pericardial calcification
Diagnostic findings  Echocardiogram: biatrial enlargement, normal
ventricular wall thickness & cavity size

*Increase in JVD with inspiration.

JVD = jugular venous distension.


 
Mycoplasma pneumonia
 Respiratory droplets
 Close quarters/young (eg, school, military)
Epidemiology
 Fall or winter

 Indolent headache, malaise, fever, persistent dry cough


 Pharyngitis(nonexudative)
Clinical
 Macular/vesicular rash

 Normal leukocyte count


 Subclinical hemolytic anemia (cold agglutinins)
Diagnostic
 Interstitial infiltrate (chest x-ray)

 Usually empiric
Treatment  Macrolide or respiratory fluoroquinolone

 
Disseminated gonococcal infection
Manifestations  Purulent monoarthritis
      OR

 Triad of tenosynovitis, dermatitis, migratory polyarthralgia

 Detection of Neisseria gonorrhoeae in urine, cervical, or urethral sample


Diagnosis  Culture of blood, synovial fluid (less sensitive)

 3rd-generation cephalosporin intravenously


Treatment
Clinical features of rheumatoid arthritis
 Pain, swelling & morning stiffness in multiple joints
 Small joints (PIP, MCP, MTP); spares DIP joints
 Systemic symptoms (fever, weight loss, anemia)
Clinical presentation
 Cervical spine involvement: subluxation, cord
compression

 Positive rheumatoid factor & anti–CCP antibodies


 C-reactive protein & ESR correlate with disease activity
Laboratory/
 X-ray: soft tissue swelling, joint space narrowing, bony
imaging studies
erosions

anti–CCP = anti–cyclic citrullinated peptide; DIP = distal interphalangeal; ESR = erythrocyte


sedimentation rate; MCP = metacarpophalangeal; MTP = metatarsophalangeal; PIP = proximal
interphalangeal.
Beta blocker toxicity
 2-6 hr after ingestion
Symptom onset
 Hypotension
 Bradycardia
Signs and  Bronchospasm
symptoms  Altered mental status
 Seizures

 Hypoglycemia
Laboratory findings
 Prolonged PR interval
ECG findings  Bradycardia

 Secure airway
 GI decontamination
 IV fluid boluses
Management
 IV atropine
 IV glucagon
GI = gastrointestinal; IV = intravenous.
Hodgkin lymphoma
 Bimodal peak incidence: age 15-35 & >60
Epidemiology  Association with EBV in immunosuppression

 Painless lymphadenopathy
 Mediastinal mass
Manifestations  B symptoms (ie, fever, sweats, weight loss)
 Pruritus

 Lymph node biopsy


Diagnosis  Reed-Sternberg cells on histology

EBV = Epstein-Barr virus.


Prevention of calcium stone (calcium oxalate, calcium phosphate) recurrence
Intervention Mechanism
All calcium stones:
↑ Fluid (produce >2 L/day urine) ↑ Urine flow, ↓ solute concentration
↓ Sodium (<2,300 mg/day) ↑ Renal calcium reabsorption
Binds urinary calcium to inhibit stone
↑ Citrate (fruits & vegetables)
formation
Dietary
↑ Potassium ↑ Urinary citrate excretion
interventions
↓ Animal protein ↓ Urinary calcium excretion
Calcium oxalate stones:
Adequate calcium intake (1,200
↓ Oxalate absorption in GI tract
mg/day)
↓ Oxalate (spinach) ↓ Urinary oxalate excretion
Pharmacologic Thiazide diuretics ↑ Renal calcium reabsorption
interventions Potassium citrate ↑ Urinary citrate concentration
GI = gastrointestinal.
Medication-induced esophagitis
Drug class Drug
Antibiotics Tetracyclines
Anti-inflammatory Aspirin & many nonsteroidal anti-
agents inflammatory drugs
Bisphosphonates Alendronate, risedronate
Others Potassium chloride, iron
Distinguishing features of fibromyalgia, polymyositis
& polymyalgia rheumatica
Clinical features Diagnosis
Fibromyalgia  Young to middle-aged women  ≥3 months of symptoms with
 Chronic widespread pain widespread pain index or
 Fatigue, impaired concentration symptom severity score
 Tenderness at trigger points
(eg, midtrapezius, costochondral  Normal laboratory studies
junction)

 Elevated muscle enzymes


(eg, creatine kinase, aldolase,
 Proximal muscle weakness
AST)  
(eg, increasing difficulty
 Autoantibodies (anti–Jo-1,
Polymyositis climbing stairs)
ANA)
 Pain mild/absent
 Biopsy: endomysial infiltrate,
patchy necrosis

 Age >50
 Systemic signs & symptoms  Elevated ESR, C-reactive
 Stiffness > pain in shoulders, hip protein
Polymyalgia
girdle, neck  Rapid improvement with
rheumatica
 Association with giant cell glucocorticoids
(temporal) arteritis

ANA = antinuclear antibody; AST = aspartate aminotransferase; ESR = erythrocyte


sedimentation rate.
Blastomycosis
 South/South Central states, Mississippi & Ohio River valleys, Upper
Midwest states, Great Lakes states & Canadian provinces
Epidemiology  Disseminated disease may occur even in immunocompetent patients
 Generally more severe in immunocompromised patients

 Lung: acute & chronic pneumonia (usually mild to moderate but may be
severe)
 Skin: wart-like lesions, violaceous nodules, skin ulcers
Clinical
 Bone: osteomyelitis
features
 Genitourinary: prostatitis, epididymoorchitis
 CNS: meningitis, epidural or brain abscesses

 Culture (blood, sputum, tissue specimens)


 Microscopy (body fluids, sputum, tissue specimens)
Diagnosis
 Antigen testing (urine, blood)

 Mild pulmonary disease in immunocompetent patients: may consider


not treating
 Mild-to-moderate pulmonary disease, mild disseminated disease: oral
Treatment itraconazole
 Severe pulmonary disease, moderately severe to severe disseminated
disease, immunocompromised patients: intravenous amphotericin B
Clinical features of trichinellosis
 Ingestion of undercooked meat (usually pork)
 More endemic in Mexico, China, Thailand, parts of central Europe &
Argentina
Epidemiology  Gastric acid releases larvae (within 1st week of ingestion) that invade the
& life cycle small intestine & develop into worms
 Female worms release larvae (up to 4 weeks later) that migrate & encyst
in striated muscle

Intestinal stage (within a week of ingestion)

 Can be asymptomatic or include abdominal pain, nausea, vomiting &


diarrhea

 
Clinical
Muscle stage (up to 4 weeks after ingestion)
presentation
 Myositis
 Fever, subungual splinter hemorrhages
 Periorbital edema
 Eosinophilia (usually >20%) with possible elevated creatine kinase &
leukocytosis

Rocky Mountain spotted fever


 Rickettsia rickettsii infection
 Transmitted by tick bite
Epidemiology
 Peaks in summer

 Nonspecific fever, headache, myalgia, arthralgia


 Macular & petechial rash on wrists/ankles
Clinical features  Can develop complications of encephalitis, pulmonary edema,
bleeding, shock

 ↓ Platelets
Laboratory  ↓ Sodium
findings  ↑ AST & ALT

 Rickettsia serology
Diagnosis  Skin biopsy

 Doxycycline
Treatment
ALT = alanine transaminase; AST = aspartate transaminase.
Overview of chronic pancreatitis
 Alcohol use
 Cystic fibrosis (common in children)
 Ductal obstruction (eg, malignancy,
Etiology
stones)
 Autoimmune

 Chronic epigastric pain with intermittent


pain-free intervals
Clinical
 Malabsorption: steatorrhea, weight loss
presentation
 Diabetes mellitus

 Amylase/lipase can be normal &


nondiagnostic
Laboratory
 CT scan or MRCP can show calcifications,
results/imaging
dilated ducts & enlarged pancreas

 Pain management
 Alcohol & smoking cessation
Treatment  Frequent, small meals
 Pancreatic enzyme supplements

MRCP = magnetic resonance cholangiopancreatography.


Hepatorenal syndrome
 Advanced cirrhosis with portal hypertension
Risk factors  Acute liver failure, severe alcoholic hepatitis

 Splanchnic vasodilation* → renal hypoperfusion →


RAAS
activation → overwhelming renal vasoconstriction →
Pathophysiology
AKI
 Precipitants: gastrointestinal bleed, infection (eg, SBP)

 Bland urinalysis
 Very low urine Na+ (<10 mEq/L)
Diagnosis  Exclusion of other causes of AKI
 No improvement with trial of volume expansion

 Albumin + splanchnic vasoconstrictors**


(temporizing)
Treatment
 Liver transplantation (curative)

*Due to excess local release of vasodilators (eg, nitric oxide).


**Midodrine plus octreotide, terlipressin, or norepinephrine.

AKI = acute kidney injury; RAAS = renin-angiotensin-aldosterone system; SBP = spontaneous


bacterial peritonitis.
Cutaneous larva migrans
 Hookworm larvae
o Dog (Ancylostoma caninum) or cat (A braziliense)
Epidemiology  Humans are incidental hosts
 Barefoot contact with contaminated sand or soil

 Primarily lower extremity


 Cutaneous (deeper infection rare)
Clinical
 Erythematous, pruritic papule at site of entry
 Intensely pruritic, migrating, serpiginous, reddish-brown tracks

 History & clinical findings


Diagnosis  Eosinophils usually normal

 Antihelmintic (eg, ivermectin)


Treatment
Acute coronary syndromes
Primary diagnostic finding Management
ST-segment elevation in ≥2
STEMI Emergency reperfusion (eg, PCI)
contiguous ECG leads
Non-STEMI Troponin elevation*
Medical management initially,
Consistent history (eg, rest
Unstable angina reperfusion within 24 hr
angina)**
*ECG shows nonspecific ischemic changes but no ST-segment elevation.

**ECG shows nonspecific changes & troponin is not elevated.

PCI = percutaneous coronary intervention; STEMI = ST-segment elevation myocardial


infarction.
Clues to etiology of syncope
Reflex syncope  Trigger (eg, emotional stress, prolonged
standing)
Vasovagal
 Prodrome (eg, nausea, sweating, warmth)

 Occurs with micturition, defecation,


Situational swallowing, or coughing

Carotid  Tactile stimulation of carotid sinus while


hypersensitivity standing
 Advanced age, carotid atherosclerosis

 Vasodilators (eg, alpha-1 blockers,


antihypertensives)
Medications  Inotropic/chronotropic blockade (eg, beta
blockers)
Orthostatic
syncope  History consistent with volume loss
Hypovolemia
 Advanced age
Autonomic
 Predisposing disease (eg, DM, Parkinson)
dysfunction
 Syncope with exertion
LV outflow
 Systolic ejection murmur
obstruction
 No warning symptoms
 Cardiomyopathy or ischemic HD
Ventricular
(monomorphic)
Cardiac syncope tachycardia
 QT-interval prolongation (polymorphic)

 Preceding fatigue or light-headedness


Conduction  ECG abnormalities (eg, sinus pauses, dropped
impairment* QRS complexes)

*Sick sinus syndrome or advanced atrioventricular block.

DM = diabetes mellitus; HD = heart disease; LV = left ventricular.


Colon cancer screening
 Start at age 45:
o Colonoscopy every 10 years
o gFOBT or FIT every year
o FIT-DNA every 1-3 years
Patients at
o CT colonography every 5 years
average risk
o Flexible sigmoidoscopy every 5 years (or every 10
years with annual FIT)

 Colonoscopy at age 40 (or 10 years prior to age of


diagnosis in FDR, whichever comes first)
Patients with FDR with CRC or
 Repeat every 5 years (every 10 years if FDR
high-risk adenomatous polyp*
diagnosed at age >60)

 Start screening 8-10 years after diagnosis


Patients with ulcerative colitis  Colonoscopy every 1-3 years
*Adenomatous polyp ≥10 mm, high-grade dysplasia, villous elements (for example).

CRC = colorectal cancer; FDR = first-degree relative; FIT = fecal immunochemical test; FIT-


DNA = multitarget stool DNA test; gFOBT = guaiac-based fecal occult blood test.
Coarctation of the aorta
 Congenital
Etiology  Acquired (rare) (eg, Takayasu arteritis)

 Upper body
o Well developed
o Hypertension (headaches, epistaxis)
 Lower extremities
o Underdeveloped
Clinical features
o Claudication
 Brachial-femoral pulse delay
 Upper & lower extremity blood pressure differential
 Left interscapular systolic or continuous murmur

 ECG: Left ventricular hypertrophy


 Chest x-ray
o Inferior notching of the 3rd to 8th ribs
Diagnostic studies o "3" sign due to aortic indentation

 Echocardiography: diagnostic confirmation

 Balloon angioplasty ± stent placement


Treatment  Surgery

Health maintenance in diabetes mellitus


 Check A1c every 3-6 months
 Goal A1c:
Glycemic control o ≤7% (younger, otherwise healthy)
o ≤8% (older, limited life expectancy, comorbidities)

 Annual random urine albumin/creatinine ratio*


Nephropathy o Normal value: <30 mg/g
screening  Periodic serum creatinine level

Retinopathy  Dilated eye examination every 1-2 years*


screening
 Visual inspection at each visit
Neuropathy
 Annual comprehensive foot examination
screening
Cardiovascular  Address lifestyle factors (eg, tobacco, obesity, diet & exercise)
risk reduction  Annual lipid & BP screening
 Aspirin and statin (depending on other risk factors)

*Begin at time of diagnosis for type 2 diabetes mellitus & 5 years after diagnosis for type 1.

BP = blood pressure.
Polycythemia vera
 ↑ Blood viscosity
o Hypertension
o Erythromelalgia (burning cyanosis in hands/feet)
o Transient visual disturbances
Manifestations
 ↑ RBC turnover (gouty arthritis)
 Aquagenic pruritus
 Bleeding

 Facial plethora (ruddy cyanosis)


Examination  Splenomegaly

   Elevated hemoglobin
 Leukocytosis & thrombocytosis
Laboratory  Low erythropoietin level
 JAK2 mutation positive
findings
 Thrombosis
Complications  Myelofibrosis & acute leukemia

 Phlebotomy
Treatment  Hydroxyurea (if ↑ risk of thrombus)

RBC = red blood cell.


Diffuse alveolar hemorrhage
 Pulmonary capillaritis: ANCA vasculitis, SLE,
antiphospholipid antibodies
 Bland hemorrhage: mitral stenosis, anticoagulation
Etiology & pathogenesis
 Alveolar damage: viral pneumonitis, ARDS, drug-induced
(eg, cocaine, amiodarone)

 Dyspnea, hypoxemia, hemoptysis (absent in ~50%) & blood


loss anemia
Clinical presentation &
 CXR or CT: diffuse ground-glass opacities
diagnosis
 Bronchoscopy: progressive blood on serial lavage

 Treat underlying (eg, rheumatologic, infectious) cause


 Supportive care: oxygen, mechanical ventilation; avoid
Management
anticoagulation
ANCA = antineutrophil cytoplasmic antibody; ARDS = acute respiratory distress syndrome;
CXR = chest x-ray; SLE = systemic lupus erythematosus.
Clinical features of VIPoma
 Watery diarrhea
 Hypo- or achlorhydria due to ↓ gastric acid secretion
Clinical
 Associated flushing, lethargy, nausea, vomiting, muscle
presentation
weakness/cramps

 Hypokalemia (↑ intestinal potassium secretion)


 Hypercalcemia (increased bone resorption)
Laboratory  Hyperglycemia due to increased glycogenolysis
findings  Stool studies show secretory diarrhea with ↑ sodium & osmolal gap
<50 mOsm/kg

 Watery diarrhea with VIP level >75 pg/mL


 CT or MRI scan of the abdomen to localize tumor in pancreas
Diagnosis
(usually in pancreatic tail)

VIP = vasoactive intestinal peptide.


Dependent variable
Qualitative
Quantitative
(categorical)
Qualitative Chi-square, logistic t test, ANOVA, linear
(categorical) regression* regression
Independent variable
Correlation, linear
Quantitative Logistic regression*
regression
*Dependent variable must be dichotomous.

ANOVA =  analysis of variance.


Atrioventricular block
Clinical presentation ECG features Management
First degree Asymptomatic PR interval prolongation Observation
Observation
Progressive PR interval
Mobitz type I
Usually asymptomatic lengthening followed by dropped
second degree (rarely PPM
QRS complex
placement)
Fatigue,
Mobitz type II Constant PR interval with
lightheadedness, PPM placement
second degree randomly dropped QRS complexes
syncope
Fatigue,
Third degree Complete dissociation of P waves
lightheadedness, PPM placement
(complete) & QRS complexes
syncope
PPM = permanent pacemaker.
Contrast-associated acute kidney injury
 Creatinine elevation 24-48 hr after arterial contrast administration
Presentation  Gradual return to baseline within 3-7 days

 Chronic kidney disease (particularly diabetic nephropathy)


 High contrast load
Risk factors  Hypovolemia
 NSAID use

 Prerenal vasoconstriction
Pathophysiology  Direct tubular cytotoxicity

 Clinical diagnosis (ie, biopsy usually not needed)


 FeNa <1% & muddy brown, granular casts
Diagnosis
 Patchy necrosis of renal tubular cells on biopsy

 Optimize renal perfusion (eg, 0.9% saline)


 Hold NSAIDs
Prevention
 Use lowest volume of contrast agent possible

FeNa = fractional excretion of sodium; NSAID = nonsteroidal anti-inflammatory drug.


Behavioral interventions for weight loss
 Maintain stocks of easy-to-prepare, healthy foods
 Store healthy foods in prominent locations
Stimulus control
 Limit stocks of less healthy foods

 Moderate-to-intense aerobic exercise


 Resistance/strength training
Physical activity
 Lifestyle activity (eg, take stairs, reduce sitting time)

Regular documentation of:

 Weight
Self-monitoring
 Food intake
 Exercise

Accountability/  Provider visits, phone calls, Internet contacts


 Group participation sessions
follow-up
Vaccines for adults with HIV
Vaccine Indications
 All patients without documented immunity
HAV to HAV

HBV  All patients without documented immunity


to HBV

 All patients age 11-26


HPV
 Inactivated vaccine annually
Influenza
Meningococcus
 All patients
(serogroups A, C, W, Y)
 Pneumococcal conjugate vaccine once
 Pneumococcal polysaccharide vaccine 8
Pneumococcus
weeks later, 5 years later & at age 65

 Varicella (live): patients born after 1979


without evidence of immunity*
Varicella-zoster
 Recombinant zoster: all patients age ≥50

*Live vaccines (eg, MMR, varicella) contraindicated if CD4 <200/mm3.

HAV = hepatitis A virus; HBV = hepatitis B virus; HPV = human papillomavirus;


MMR = measles, mumps & rubella.
Lacunar stroke
 Small penetrating artery occlusion due to hypertensive arteriolar
Etiology sclerosis

 Basal ganglia
Affected  Subcortical white matter (eg, internal capsule, corona radiata)
areas  Pons

Risk  Hypertension
factor
 Absence of cortical signs (eg, aphasia, agnosia, neglect, apraxia,
hemianopia), seizure, or mental status changes
 Common syndromes:
Clinical o Pure motor hemiparesis (most frequent)
features o Pure sensory stroke
o Ataxic hemiparesis
o Dysarthria–clumsy hand syndrome

Anaphylaxis
 Food (eg, nuts, shellfish)
 Medications (eg, β-lactam antibiotics)
Triggers
 Insect stings

Clinical  Cardiovascular
o Vasodilation → hypotension & tissue edema
o Tachycardia
 Respiratory
o Upper airway edema → stridor & hoarseness
o Bronchospasm → wheezing
manifestations
 Cutaneous
o Urticarial rash, pruritus, flushing
 Gastrointestinal
o Nausea, vomiting, abdominal pain

 Intramuscular epinephrine
 Airway management & volume resuscitation
Treatment
 Adjunct therapy (eg, antihistamines, glucocorticoids)

Diagnostic criteria for anaphylaxis


Anaphylaxis is likely if there is rapid symptom onset & any 1 of the following criteria:
Skin/mucosa involvement (eg, hives, lip/tongue swelling)  & either hypotension or
1
respiratory distress
Involvement of ≥2 organ systems after exposure to a likely allergen

 Skin/mucosa (eg, hives, lip/tongue swelling)


2  Respiratory (eg, wheezing, stridor, dyspnea)
 Cardiovascular (eg, hypotension, tachycardia, syncope)
 Gastrointestinal (eg, abdominal pain, vomiting, diarrhea)

3 Hypotension after exposure to a known allergen


Treatment of hypertriglyceridemia
Triglycerides 150-499 mg/dL 500-999 mg/dL ≥1,000 mg/dL
 Limit dietary sugar/tight
glycemic control in diabetes
 Limit saturated fat
 Regular aerobic exercise
General
 Weight loss of 5%-10% of
measures
body weight
 Treat with statins based on
ASCVD risk

Specific  Limit alcohol  Abstain from  Abstain from


measures intake alcohol alcohol
 Ω-3 acids if high  Ω-3 acids or  Fibrates to reduce
risk of ASCVD fibrates, depending pancreatitis risk
on ASCVD risk

ASCVD = atherosclerotic cardiovascular disease; Ω-3 acids = omega-3 fatty acids.


Immune thrombocytopenic purpura
 Commonly acquired form of thrombocytopenia
 Autoantibody formation
Epidemiology
 Often recent viral infection or comorbidity (eg, HIV, HCV, CLL)

 Frequently asymptomatic
 Mucocutaneous bleeding (eg, menorrhagia, epistaxis)
Manifestations  Ecchymoses, petechiae, purpura
 Severe hemorrhage is rare

 Diagnosis of exclusion
 Normal coagulation tests, platelet morphology (peripheral smear)
Diagnosis
 HIV, HCV testing (commonly induces ITP)

 Observation if no bleeding & platelets >30,000/mm3


 Corticosteroids if platelets <30,000/mm3
Treatment
 IVIG & platelet transfusion if hemorrhage

CLL = chronic lymphocytic leukemia; HCV = hepatitis C virus; ITP = immune


thrombocytopenic purpura; IVIG = intravenous immunoglobulin.
 
Clinical findings for heart failure
Sensitivity Specificity
Dyspnea High Low
Serum BNP >100 pg/mL High Moderate
Lower extremity edema Moderate Moderate
Jugular venous distension Moderate Moderate
Pulmonary crackles Moderate Moderate
Orthopnea Moderate High
Audible S3 Low High
BNP = brain natriuretic peptide.
 
Pseudogout (acute calcium pyrophosphate crystal arthritis)
 Acute mono- or oligoarticular arthritis
Symptoms  Peripheral joints (knee most common)

 Inflammatory effusion (15,000-30,000/mm3)


 CPPD crystals (rhomboid shape, positive birefringence)
Diagnosis
 Chondrocalcinosis on imaging

Treatment  Intraarticular glucocorticoids


 Nonsteroidal anti-inflammatory drugs
 Colchicine

CPPD = calcium pyrophosphate dihydrate.


Vascular & immunologic manifestations of infective endocarditis
 Systemic emboli (cerebral, pulmonary, or splenic infarcts)
 Mycotic aneurysm
Vascular phenomena  Janeway lesions: macular, erythematous, nontender lesions on
the palms & soles

 Osler nodes: painful, violaceous nodules seen on the fingertips


Immunologic & toes
phenomena  Roth spots: edematous & hemorrhagic lesions of the retina

Disseminated gonococcal infection


 Purulent monoarthritis

      OR
Manifestations
 Triad of tenosynovitis, dermatitis, migratory polyarthralgia

 Detection of Neisseria gonorrhoeae in urine, cervical, or urethral sample


Diagnosis  Culture of blood, synovial fluid (less sensitive)

 3rd-generation cephalosporin intravenously


Treatment
Conditions that alter TBG concentration
Increased TBG Decreased TBG
 Androgenic hormones
 Estrogens (eg, pregnancy, OCs, HRT)  High-dose
& estrogenic medications (eg, glucocorticoids/hypercortisolism
tamoxifen)  Hypoproteinemia (eg, nephrotic
 Acute hepatitis syndrome, starvation)
 Chronic liver disease

HRT = hormone replacement therapy; OCs = oral contraceptives; TBG = thyroxine-binding


globulin.
Adults at high risk for influenza complications
 Age ≥65
 Women who are pregnant & up to 2 weeks postpartum
 Underlying chronic medical illness (eg, chronic pulmonary, cardiovascular, renal,
hepatic)
 Immunosuppressed
 Morbidly obese
 Residents of nursing homes or long-term care facilities

Acute pancreatitis
 Chronic alcohol use (~40%)
 Gallstones (~40%)
 Hypertriglyceridemia
Etiology  Drugs (eg, azathioprine, valproic acid, thiazides)
 Infection (eg, CMV, Legionella, Aspergillus)
 Iatrogenic (post-ERCP, ischemic/atheroembolic)

Diagnosis (requires 2 of the following)

 Acute epigastric pain radiating to the back


 Amylase or lipase >3× normal limit
 Abnormalities on imaging consistent with pancreatitis

Clinical presentation  

Other findings

 ALT level >150 U/L suggests biliary pancreatitis


 Severe disease: fever, tachypnea, hypoxemia, hypotension

ALT = alanine aminotransferase; CMV = cytomegalovirus; ERCP = endoscopic retrograde


cholangiopancreatography.
Opportunistic infections in HIV
Infection CD4 cell count Prophylaxis
Trimethoprim-sulfamethoxazole
 <200/mm3 OR
Alternate therapies:
 Oropharyngeal candidiasis
Pneumocystis
OR
jirovecii  Dapsone
 History of PCP infection
 Atovaquone
 Pentamidine

Trimethoprim-sulfamethoxazole

Alternate therapies:
Toxoplasma
<100/mm3 & positive IgG antibody  Dapsone plus pyrimethamine
gondii
plus leucovorin
 Atovaquone ± pyrimethamine
plus leucovorin

Histoplasma <150/mm3 & endemic area Itraconazole


capsulatum
Close contact with person with
chickenpox or shingles & no history VariZIG or IVIG administered within 4
VZV
of prior disease or negative antibody days of exposure
to VZV
IVIG = intravenous immune globulin; PCP = Pneumocystis jirovecii pneumonia; VariZIG
= human varicella immune globulin; VZV = varicella-zoster virus.
Cervicofacial Actinomyces
 Dental infections & trauma (extraction)
Risk factors  Immunosuppression, diabetes mellitus, malnutrition

 Upper/lower jaw (mandible)


 Slowly progressive, nonpainful, indurated mass
Manifestations  Sinus tracts with sulfur granules
 Fever/lymphadenopathy are uncommon

 Fine-needle aspiration
Diagnosis  Culture >14 days

 Penicillin 2-6 months


Treatment  Surgery (severe disease)
common adverse transfusion reaction
Stevens-Johnson syndrome & toxic epidermal necrolysis
<10% of BSA:   SJS

Nomenclature       10%-30%:   SJS/TEN overlap

            >30%:   TEN


 4-28 days after exposure to trigger (2 days after repeat exposure)
 Acute influenza-like prodrome
Clinical  Rapid-onset erythematous macules, vesicles, bullae
features  Necrosis & sloughing of epidermis
 Mucosal involvement

Common Drugs
triggers
 Allopurinol
 Antibiotics (eg, sulfonamides)
 Anticonvulsants (eg, carbamazepine, lamotrigine, phenytoin)
 NSAIDs (eg, piroxicam)
 Sulfasalazine

Other

 Mycoplasma pneumoniae
 Vaccination
 Graft versus host disease

BSA = body surface area; NSAIDs = nonsteroidal anti-inflammatory drugs;


SJS = Stevens-Johnson syndrome; TEN = toxic epidermal necrolysis.
Wilson disease
 Autosomal recessive mutation of ATP7B → hepatic copper
accumulation → leak from damaged hepatocytes → deposits
Pathogenesis
in tissues (eg, basal ganglia, cornea)

 Hepatic (acute liver failure, chronic hepatitis, cirrhosis)


Clinical  Neurologic (parkinsonism, gait disturbance, dysarthria)
findings  Psychiatric (depression, personality changes, psychosis)

 ↓ Ceruloplasmin & ↑ urinary copper excretion


 Kayser-Fleischer rings on slit-lamp examination
Diagnosis
 ↑ Copper content on liver biopsy

 Chelators (eg, D-penicillamine, trientine)


Treatment  Zinc (interferes with copper absorption)

Tumor lysis syndrome


 Tumors with high cell burden or rapid turnover
Risk  Combination chemotherapy/immunotherapy

 Severe electrolyte abnormalities


o ↑ Phosphorus, potassium, uric acid
o ↓ Calcium
Manifestations  Acute kidney injury
 Cardiac arrhythmias
 Seizures

 Intravenous fluids
Prophylaxis  Xanthine oxidase inhibitor* or rasburicase

 Intravenous fluids + rasburicase


 Continuous telemetry
Treatment
 Aggressive electrolyte monitoring & treatment

*Allopurinol or febuxostat.
Microscopic colitis
 Watery, nonbloody diarrhea; fecal urgency & incontinence
Clinical
 Abdominal pain, fatigue, weight loss, arthralgias
findings
 Smoking, medications (eg, NSAIDs, PPIs, SSRIs)
Triggers
 Colonoscopic biopsy with lymphocytic infiltration of lamina propria
o Collagenous: thickened subepithelial collagen band
Diagnosis
o Lymphocytic: high levels of intraepithelial lymphocytes

 Remove possible triggers


Management  Antidiarrheal medications & budesonide  

NSAIDs = nonsteroidal anti-inflammatory drugs; PPIs = proton pump inhibitors; SSRIs =


selective serotonin reuptake inhibitors.
Culture-positive infective endocarditis
 Prosthetic valves
 Intravascular catheters
Staphylococcus aureus  Implanted devices (eg, pacemaker/defibrillator)
 Intravenous drug users

 Gingival manipulation
Viridans streptococci  Respiratory tract incision or biopsy

 Prosthetic valves
 Intravascular catheters
Staphylococcus epidermidis
 Implanted devices

 Nosocomial urinary tract infections


Enterococci
 Colon carcinoma
Streptococcus gallolyticus
 Inflammatory bowel disease
(formerly S bovis)
 Immunocompromised host
Fungi  Intravascular catheters
(eg, Candida)  Prolonged antibiotic therapy

Granulomatosis with polyangiitis


 Upper respiratory: sinusitis/otitis, saddle nose
 Lower respiratory: lung nodules/cavitation, interstitial lung
Clinical disease, diffuse alveolar hemorrhage
manifestations  Renal: rapidly progressive GN
 Skin: livedo reticularis, nonhealing ulcers
 ANCA: PR3 (~70%), MPO (~20%)
 Biopsy:
o Skin (leukocytoclastic vasculitis)
Diagnosis
o Kidney (pauci-immune GN)
o Lung (granulomatous vasculitis)

 Corticosteroids & immunomodulators (eg, cyclophosphamide)


Management
ANCA = antineutrophil cytoplasmic antibody; GN = glomerulonephritis;
MPO = myeloperoxidase; PR3 = proteinase-3.
Differential diagnosis of myopathy
Pain & Creatine
Weakness ESR Other features
tenderness kinase
 Prominent atrophy
Glucocorticoid-  Lower extremities
Yes No Normal Normal
induced myopathy most affected

 Stiffness of shoulders
& hips with restricted
motion
Polymyalgia  Often coexists with
No Yes ↑ Normal
rheumatica GCA
 Rapid improvement
with glucocorticoids

 Multisystem
involvement (arthritis,
Polymyositis & Normal
Yes Uncommon ↑ rash, ILD)
dermatomyositis or ↑
 ↑ Malignancy risk

 Additive risk with


Statin-induced Normal or
Variable Yes Normal fibrates
myopathy ↑
 Delayed DTRs;
myoedema
 Hypothyroid
Hypothyroid
Yes Yes Normal ↑ symptoms &
myopathy
abnormal thyroid test
results

DTR = deep tendon reflex; ESR = erythrocyte sedimentation rate; GCA = giant cell arteritis;
ILD = interstitial lung disease.
Distinguishing features of fibromyalgia, polymyositis
& polymyalgia rheumatica
Clinical features Diagnosis
 Young to middle-aged women
 Chronic widespread pain  ≥3 months of symptoms with
 Fatigue, impaired concentration widespread pain index or
Fibromyalgia  Tenderness at trigger points symptom severity score
(eg, midtrapezius, costochondral  Normal laboratory studies
junction)

 Elevated muscle enzymes


(eg, creatine kinase, aldolase,
 Proximal muscle weakness
AST)  
(eg, increasing difficulty
 Autoantibodies (anti–Jo-1,
Polymyositis climbing stairs)
ANA)
 Pain mild/absent
 Biopsy: endomysial infiltrate,
patchy necrosis

 Age >50
 Systemic signs & symptoms  Elevated ESR, C-reactive
 Stiffness > pain in shoulders, hip protein
Polymyalgia
girdle, neck  Rapid improvement with
rheumatica
 Association with giant cell glucocorticoids
(temporal) arteritis

ANA = antinuclear antibody; AST = aspartate aminotransferase; ESR = erythrocyte


sedimentation rate.
Drugs associated with drug-induced pancreatitis
 Acetaminophen
 Nonsteroidal anti-inflammatory drugs
Analgesics  Mesalamine, sulfasalazine
 Opiates

 Isoniazid
 Tetracyclines
Antibiotics  Metronidazole
 Trimethoprim-sulfamethoxazole

 Valproic acid
Antiepileptics  Carbamazepine

 Thiazides, furosemide
Antihypertensives  Enalapril, losartan

 Lamivudine
Antivirals  Didanosine

Immunosuppressants  Azathioprine, mercaptopurine


 Corticosteroids

 Asparaginase
Others  Estrogens

Cerebrospinal fluid analysis


WBC count Glucose Protein
Diagnosis
(mm ) 3
(mg/dL) (mg/dL)
Normal 0-5 40-70 <40
Bacterial
>1,000 <40 >250
meningitis
Tuberculous
100-500 <45 100-500
meningitis
Viral meningitis 10-500 40-70 <150
Guillain-Barré
0-5 40-70 45-1,000
syndrome
WBC = white blood cell.
Major drug interactions of levothyroxine
 Bile acid–binding agents (eg, cholestyramine)
↓ Levothyroxine  Iron, calcium, aluminum hydroxide
absorption  Proton pump inhibitors, sucralfate

 Estrogen replacement, oral contraceptives


↑ TBG
 Tamoxifen
concentration
 Androgens, glucocorticoids
↓ TBG
 Anabolic steroids
concentration
 Rifampin
↑ Thyroid hormone  Phenytoin
metabolism  Carbamazepine

TBG = thyroxine-binding globulin.


Clues to etiology of syncope
Reflex syncope  Trigger (eg, emotional stress, prolonged
standing)
Vasovagal
 Prodrome (eg, nausea, sweating, warmth)

 Occurs with micturition, defecation,


Situational swallowing, or coughing

Carotid  Tactile stimulation of carotid sinus while


hypersensitivity standing
 Advanced age, carotid atherosclerosis

 Vasodilators (eg, alpha-1 blockers,


antihypertensives)
Medications  Inotropic/chronotropic blockade (eg, beta
blockers)
Orthostatic
syncope  History consistent with volume loss
Hypovolemia
 Advanced age
Autonomic
 Predisposing disease (eg, DM, Parkinson)
dysfunction
 Syncope with exertion
LV outflow
 Systolic ejection murmur
obstruction
 No warning symptoms
 Cardiomyopathy or ischemic HD
Ventricular
(monomorphic)
Cardiac syncope tachycardia
 QT-interval prolongation (polymorphic)

 Preceding fatigue or light-headedness


Conduction  ECG abnormalities (eg, sinus pauses, dropped
impairment* QRS complexes)

*Sick sinus syndrome or advanced atrioventricular block.

DM = diabetes mellitus; HD = heart disease; LV = left ventricular.


Clinical features & management of tricyclic antidepressant overdose
 Mental status changes (eg, drowsiness,
delirium, coma)
CNS
 Seizures, respiratory depression

 Sinus tachycardia, hypotension


Clinical  Prolonged PR/QRS/QT intervals
presentation Cardiovascular  Arrhythmias (eg, ventricular tachycardia,
fibrillation)

 Dry mouth, blurred vision, dilated pupils


Anticholinergic  Urinary retention, flushing, hyperthermia

Management Supportive care &  Supplemental oxygen, intubation


therapy  Intravenous fluids
 Activated charcoal for patients within 2 hours
of ingestion (unless ileus present)
 Intravenous sodium bicarbonate for QRS
interval widening or ventricular arrhythmia

Management of ST-segment elevation myocardial infarction


 Caution with hypotension (eg, RV infarction)
Nitrates
 Oral cardioselective (eg, metoprolol, atenolol)
Beta blockers  Contraindicated in heart failure & bradycardia

 Aspirin & P2Y12 receptor blocker (eg, ticagrelor)


Antiplatelet therapy
 Unfractionated heparin, enoxaparin, or bivalirudin
Anticoagulation
 High potency (eg, atorvastatin, rosuvastatin)
Statin therapy
 PCI ≤90 min from first medical contact
Coronary reperfusion  Fibrinolytics (eg, alteplase) if PCI is unavailable

PCI = percutaneous coronary intervention; RV = right ventricular.


Carbon monoxide poisoning
 Smoke inhalation
 Defective heating systems
Epidemiology
 Gas motors operating in poorly ventilated areas

Mild-moderate

 Headache, confusion
 Malaise, dizziness, nausea
Manifestations
Severe

 Seizure, syncope, coma


 Myocardial ischemia, arrhythmias

 ABG: carboxyhemoglobin level


Diagnosis  ECG ± cardiac enzymes

 High-flow 100% oxygen


Treatment  Intubation/hyperbaric oxygen (severe)

ABG = arterial blood gas.


Overview of chronic pancreatitis
Etiology  Alcohol use
 Cystic fibrosis (common in children)
 Ductal obstruction (eg, malignancy,
stones)
 Autoimmune

 Chronic epigastric pain with intermittent


pain-free intervals
Clinical
 Malabsorption: steatorrhea, weight loss
presentation
 Diabetes mellitus

 Amylase/lipase can be normal &


nondiagnostic
Laboratory
 CT scan or MRCP can show calcifications,
results/imaging
dilated ducts & enlarged pancreas

 Pain management
 Alcohol & smoking cessation
Treatment  Frequent, small meals
 Pancreatic enzyme supplements

MRCP = magnetic resonance cholangiopancreatography.


Lupus nephritis
 Affects ~50% of patients with SLE
Epidemiology  Can be the presenting manifestation of SLE

 Loss of immune tolerance to nuclear antigens (eg, nucleosomes)


 Renal deposition of circulating ICs (eg, anti-dsDNA bound to
Pathogenesis DNA)
 Complement activation & inflammatory injury

 Mesangial: microscopic hematuria &/or asymptomatic hematuria


Clinical features  Subendothelial: glomerulonephritis ± proteinuria
(related to site of ICs)  Subepithelial: nephrotic syndrome

 ANA, anti-dsDNA, anti-Smith


 Low serum complement (C3 & C4)
Diagnostic tests
 Kidney biopsy

ANA = antinuclear antibody; ds = double-stranded; IC = immune complex; SLE = systemic


lupus erythematosus.
Analgesic nephropathy
Pathophysiology  Prolonged use of combination analgesics
o Acetaminophen: direct oxidative renal toxicity
o Aspirin/NSAIDs: depletion of glutathione impairs
deactivation of reactive acetaminophen metabolites
 Manifests as chronic interstitial nephritis ± papillary necrosis

 History of chronic pain (eg, headaches, lower back pain)


 Often asymptomatic, may have malaise, fatigue, flank pain
 Urinalysis: WBCs & WBC casts ± mild proteinuria
Clinical
 Hematuria & urine RBCs if papillary necrosis is present
presentation
 Imaging: small kidneys ± papillary calcification & irregular
contours

NSAIDs = nonsteroidal anti-inflammatory drugs; RBCs = red blood cells; WBCs = white blood
cells.
Pheochromocytoma
 Classic triad: episodic headache, sweating & tachycardia
 Resistant HTN or HTN accompanied by unexplained ↑
glucose
Indications for testing
 Family history or familial syndrome (eg, MEN2, NF1,
VHL)

 Urine or plasma metanephrine levels


Diagnostic approach  Confirmatory abdominal imaging for ↑ metanephrines

 10% bilateral, 10% extraadrenal, 10% malignant


Notable features
 Preoperative alpha blockade prior to beta blockade
Management  Laparoscopic or open surgical resection

HTN = hypertension; MEN2 = multiple endocrine neoplasia type 2; NF1 = neurofibromatosis


type 1; VHL = von Hippel-Lindau syndrome.
 
Common causes of vertigo
 Recurrent episodes lasting 20 minutes to several hours
 Sensorineural hearing loss
Ménière disease
 Tinnitus &/or feeling of fullness in the ear

 Brief episodes triggered by head movement


BPPV  Dix-Hallpike maneuver causes nystagmus

 Acute, single episode that can last days


Vestibular  Often follows viral syndrome
neuritis  Abnormal head thrust test

 Vertigo associated with headache or other migrainous phenomenon


(eg, visual aura)
Migraine
 Symptoms resolve completely between episodes
 Sudden-onset, persistent vertigo
Brainstem/
 Usually other neurologic symptoms
cerebellar stroke
BPPV = benign paroxysmal positional vertigo.
Monomorphic nonsustained ventricular tachycardia
 ≥3 consecutive ventricular beats (wide QRS complex)
Identification  Rate >100/min & duration <30 sec

 Heart failure with reduced ejection fraction


 Ischemic heart disease
Predisposing conditions
 Other cardiomyopathy (eg, HCM)

 Serum electrolyte abnormalities (eg, ↓ K, ↓ Mg)


 Hypoxemia or acute myocardial ischemia
Precipitating factors
 Elevated sympathetic tone (eg, sepsis)

 Address precipitating factors (eg, replace electrolytes)


Management  Consider adding (or increasing dose of) beta blockade

HCM = hypertrophic cardiomyopathy.


Medication-induced orthostasis
Mechanism Examples
 Terazosin, prazosin, doxazosin
 Antipsychotics (eg, risperidone)
α1 blockade–mediated vasodilation
 Antihistamines, TCAs

 ACE inhibitors & ARBs


 Dihydropyridine CCBs
Other vasodilation  Hydralazine, nitrates
 Phosphodiesterase inhibitors

 Diuretics
Volume depletion  SGLT-2 inhibitors

 Beta blockers
Sympathetic blockade  Clonidine

ARBs = angiotensin II receptor blockers; CCBs = calcium channel blockers;


SGLT = sodium-glucose cotransporter; TCAs = tricyclic antidepressants.
Effect of intensive glycemic control in type 2 diabetes
Macrovascular complications
No change (short-term)
(eg, acute myocardial infarction, stroke)
Microvascular complications Improve
(eg, nephropathy, retinopathy)
Mortality No change or increased
Pulmonary  examination findings
Tactile
Condition Breath sounds Percussion Mediastinal shift
fremitus
Bronchovesicular
Normal lung (hilar), vesicular Normal Resonance None
(peripheral)
Consolidation
(eg, lobar Increased Increased Dullness None
pneumonia)
Pleural Away from
Decreased or absent Decreased Dullness
effusion effusion (if large)
Away from
Pneumothorax Decreased or absent Decreased Hyperresonance tension
pneumothorax
Atelectasis
Toward atelectasis
(eg, mucus Decreased or absent Decreased Dullness
(if large)
plugging)
Acute pyelonephritis
 Otherwise healthy, nonpregnant
 Primarily Escherichia coli
Uncomplicated  Oral fluoroquinolone, trimethoprim-sulfamethoxazole
 Intravenous antibiotics if vomiting, elderly, septic

 Diabetes, urinary obstruction/instrumentation, renal failure,


immunosuppression, hospital-acquired
 ↑ Risk of antibiotic resistance/treatment failure
Complicated
 Intravenous fluoroquinolone, aminoglycoside, extended
spectrum beta-lactam/cephalosporin

Sjögren syndrome
 Keratoconjunctivitis sicca
Exocrine  Dry mouth, salivary hypertrophy
features  Xerosis

 Raynaud phenomenon
 Cutaneous vasculitis
Extraglandular  Arthralgia/arthritis
features  Interstitial lung disease
 Non-Hodgkin lymphoma

Diagnostic  Objective signs of decreased lacrimation (eg, Schirmer test)


 Positive anti-Ro (SSA) &/or anti-La (SSB)
 Salivary gland biopsy with focal lymphocytic sialoadenitis
findings  Classification: primary if no associated CTD, secondary if comorbid
CTD (eg, SLE, RA, scleroderma)

CTD = connective tissue disease; RA = rheumatoid arthritis; SLE = systemic lupus


erythematosus; SSA/SSB = Sjögren syndrome (antibody) A/B.
 
Necrotizing (malignant) otitis externa
 Elderly (age >60)
 Diabetes mellitus
Risk factors
 Aural irrigation (cerumen removal)

 Pseudomonas aeruginosa
Microbiology
 Severe, unremitting ear pain (worse at night & with
chewing)
 Deficits of lower cranial nerves (eg, facial
Clinical [CN VII], glossopharyngeal [CN IX], vagus
manifestations [CN X])
 Granulation tissue in the external auditory canal
 Elevated erythrocyte sedimentation rate

 Intravenous antipseudomonal antibiotics (eg,


ciprofloxacin)
Treatment
 ± Surgical débridement

 
Complications of Graves disease treatment
Treatment Adverse effects
 Agranulocytosis
Antithyroid drugs  Methimazole: 1st-trimester teratogen, cholestasis
(thionamides)  Propylthiouracil: hepatic failure, ANCA-associated vasculitis

 Permanent hypothyroidism
Radioiodine  Worsening of ophthalmopathy
ablation  Possible radiation side effects

 Permanent hypothyroidism
 Risk for recurrent laryngeal nerve damage
Surgery
 Risk for hypoparathyroidism

ANCA = antineutrophilic cytoplasmic antibodies.


Acute urticaria
Etiologies  Medications, insect stings
 Infections, rheumatologic diseases
 Many cases are idiopathic

 Mast cells release histamine → dermal edema


Pathophysiology
 Pruritic, erythematous plaques (ie, wheals)
 Each wheal lasts <24 hr, urticaria duration <6 weeks
Clinical features
 Diffuse or localized

 No workup for 1st episode


 Allergy testing if specific trigger (eg, food) is suspected
Evaluation  Laboratory testing/biopsy if systemic symptoms are
present

 2nd-generation H1 antihistamines
Treatment &  Add H2 antihistamines or systemic corticosteroids if severe
prognosis  Two-thirds of cases self-resolve

Hepatitis A
 Fecal-oral transmission
Transmission  Poor sanitation/hygiene, travel to endemic areas
& risk factors  Contaminated food & water

 Fever, nausea, right upper quadrant pain


Clinical
 Jaundice, hepatomegaly
presentation
 Elevated liver transaminases (>1,000 U/L)
Diagnostic
 Anti–hepatitis A serology
testing
 Supportive/expectant
Management  Spontaneous recovery in most patients

Management of diabetic ketoacidosis


 Rapid infusion of 0.9% normal saline
IV fluids  Add dextrose 5% when serum glucose is ≤200 mg/dL

 Start continuous IV insulin infusion; hold if K <3.3 mEq/L


 Switch to SQ (basal bolus) insulin for the following: able to eat, glucose
Insulin <200 mg/dL, anion gap <12 mEq/L & serum HCO3− ≥15 mEq/L
 Overlap SQ & IV insulin by 1-2 hr

 Add IV K if serum K+ <5.3 mEq/L; hold if ≥5.3 mEq/L


Potassium  Nearly all patients' K+ depleted, even with hyperkalemia

Bicarbonate  Consider for patients with pH ≤6.9


 Consider for serum phosphate <1.0 mg/dL, cardiac dysfunction, or
respiratory depression
Phosphate
 Monitor serum calcium frequently

IV = intravenous; SQ = subcutaneous.
Obstructive sleep apnea
 Relaxation of pharyngeal muscles, leading to closure of airway
Pathophysiology  Loud snoring with periods of apnea

 Daytime somnolence
 Nonrestorative sleep with frequent awakenings
Symptoms  Morning headaches
 Affective & cognitive symptoms

 Systemic hypertension
Sequelae  Pulmonary hypertension & right-sided heart failure

Causes of normal anion gap metabolic acidosis


 Diarrhea
 Fistulae (eg, pancreatic, ileocutaneous, etc.)
 Carbonic anhydrase inhibitors
 Renal tubular acidosis
 Ureteral diversion (eg, ileal loop)
 Iatrogenic

Acute pericarditis
 Viral or idiopathic
 Autoimmune disease (eg, SLE)
 Uremia (acute or chronic renal failure)
Etiology  Post myocardial infarction
o Early: peri-infarction pericarditis
o Late: Dressler syndrome

 Pleuritic chest pain (↓ when sitting) ± fever


 Pericardial friction rub (highly specific)
Clinical features
 ECG: diffuse ST-segment elevation & PR-segment
& diagnosis
depression
 Echocardiography: pericardial effusion

 NSAIDs & colchicine for viral or idiopathic etiology


Treatment  Variable for other etiologies
NSAIDs = nonsteroidal anti-inflammatory drugs; SLE = systemic lupus erythematosus.
Clinical features of irritable bowel syndrome
Recurrent abdominal pain/discomfort ≥1 days/week for past 3 months
& ≥2 of the following:
Rome IV diagnostic
 Related to defecation (improves or worsens)
criteria
 Change in stool frequency
 Change in stool form

 Older age of onset (≥50)


 Gastrointestinal bleeding
 Nocturnal diarrhea (ie, fasting state)
 Worsening pain
 Unintended weight loss
Alarm features
 Iron deficiency anemia
 Elevated C-reactive protein
 Positive fecal lactoferrin or calprotectin
 Family history of early colon cancer or IBD

IBD = inflammatory bowel disease.


Primary pulmonary tuberculosis
 Immunosuppression (eg, HIV)
 Travel from endemic area
Risk factors  Exposure to infected household contact
 Resident/employee of prison, homeless shelter, health care facility

 Chronic cough
Clinical  Prolonged fever
manifestations  Weight loss, failure to thrive

 Positive screening PPD or interferon-γ release assay


 Chest x-ray: hilar adenopathy, effusion, consolidation, cavitation
Diagnosis
 Positive AFB smear & mycobacterial culture

 Multidrug therapy: isoniazid, rifampin, pyrazinamide, ethambutol


Treatment
AFB = acid-fast bacilli; PPD = purified protein derivative.
Molluscum contagiosum
Children Adults
 Trunk
 Intertriginous areas (eg,  Lower abdomen, genitals, upper
Typical
axillae) thighs
location
 Face (including eyelids)

Evaluation  Clinical diagnosis (ie,  Clinical diagnosis


firm, domed, papule with
 Genital lesions: STI testing
central umbilication)
 Extensive lesions: HIV testing
 No further evaluation

 Cryotherapy
 Curettage
 Reassurance
Treatment  Topical therapy (eg, cantharidin,
podophyllotoxin)

STI = sexually transmitted infection.


Primary Raynaud Secondary Raynaud
phenomenon phenomenon
 Connective tissue diseases
 Occlusive vascular conditions
 Sympathomimetic drugs
 No underlying cause
Etiology  Vibrating tools
 Hyperviscosity syndromes
 Nicotine

 Usually men age >40


 Usually women age <30  Symptoms of underlying disease
Clinical  No tissue injury  Tissue injury or digital ulcers
presentation  Negative ANA & ESR  Abnormal nail fold capillary
examination

 Evaluate & treat underlying


disorder
 Avoid aggravating factors
 CCB for persistent symptoms,
Management  CCB for persistent symptoms
aspirin for patients at risk for
digital ulceration

ANA = antinuclear antibody; CCB = calcium channel blocker; ESR = erythrocyte sedimentation
rate.
Hepatic encephalopathy
 Drugs (eg, sedatives, narcotics)
 Hypovolemia (eg, diarrhea)
 Electrolyte changes (eg, hypokalemia)
Precipitating factors  ↑ Nitrogen load (eg, GI bleeding)
 Infection (eg, pneumonia, UTI, SBP)
 Portosystemic shunting (eg, TIPS)

Clinical presentation  Sleep pattern changes


 Altered mental status
 Ataxia
 Asterixis

 Correct precipitating causes (eg, fluids, antibiotics)


Treatment  ↓ Blood ammonia concentration (eg, lactulose, rifaximin)

GI = gastrointestinal; SBP = spontaneous bacterial peritonitis; TIPS = transjugular intrahepatic


portosystemic shunt; UTI = urinary tract infection.
Multiple myeloma
 Plasma cell neoplasm produces monoclonal paraprotein
Pathophysiology (immunoglobulin)

 Bone pain, fractures


 Constitutional symptoms (weight loss, fatigue)
Manifestations
 Recurrent infections

 Normocytic anemia
 Renal insufficiency
Laboratory  Hypercalcemia (constipation, muscle weakness)
 Monoclonal paraproteinemia (M-spike)

 Osteolytic lesions/osteopenia (osteoclast activation)


Radiology
Causes of pancytopenia
 Aplastic anemia
 Infection (eg, parvovirus, HIV, viral hepatitis)
Bone marrow aplasia  Nutritional deficiency (eg, vitamin B12/folate)
 Medications (eg, hydroxyurea)

 Cancer (eg, hematologic, metastatic)


 Myelofibrosis
Bone marrow infiltration
 Infection (eg, tuberculosis, fungal infection)

 Intravascular (eg, DIC, TTP)


Mature blood cell destruction  Extravascular (eg, hypersplenism)

DIC = disseminated intravascular coagulation; TTP = thrombotic thrombocytopenic purpura.


HIV-associated neurocognitive disorders
 Impaired memory & attention/concentration
 Personality & behavior changes
Manifestations
 Motor symptoms (eg, ataxia, slowed movement)

 Asymptomatic neurocognitive impairment


 Mild neurocognitive disorder
Severity
 HIV-associated dementia
 Long-standing HIV disease
 Age ≥50
Risk factors
 CD4 count <200/mm3

 Clinical presentation
Diagnosis  Neuropsychological testing

Major types of systemic amyloidosis


Primary Secondary Age related Dialysis related
Chronic
Disease
Plasma cell dyscrasia infection/ Elderly men ESRD on dialysis
association
inflammation
Precursor
Immunoglobulin Serum Transthyretin
protein
light chains amyloid A (prealbumin) β2-Microglobulin


↓ ↓ ↓
Decreased
Misfolding
Increased Increased Accumulation clearance
mechanism
production production over time


↓ ↓ ↓
Aβ2M
Amyloid
AL AA ATTR*
fibril type
Cardiomyopathy,
Nephropathy, hepatosplenomegaly,
Clinical CTS, other Scapulohumeral
cardiomyopathy (AL > AA), peripheral
manifestations peripheral arthritis, CTS
neuropathy, macroglossia, skin bruising
neuropathy
Amyloid names begin with "A" followed by the precursor protein abbreviation.

*ATTR also occurs in a hereditary form that affects younger patients.

CTS = carpal tunnel syndrome; ESRD = end-stage renal disease.


Risk factors for gout
 Medications (eg, diuretics, low-dose aspirin)
 Surgery, trauma, recent hospitalization
 Volume depletion
 Diet: High-protein foods (meat, seafood), high-fat foods,
Increased risk fructose or sweetened beverages
 Heavy alcohol consumption
 Underlying medical conditions (eg, hypertension, obesity,
chronic kidney disease, organ transplant)

Decreased risk  Dairy product intake


 Vitamin C (≥1,500 mg/day)
 Coffee intake (≥6 cups/day)

Viral myocarditis
 Relatively young adults (eg, age <55)
 Viral prodrome (eg, fever, malaise, myalgias)
Clinical  Heart failure (eg, dyspnea, orthopnea, edema)
presentation  Chest pain
 Sudden cardiac death

 ECG: nonspecific
 Echocardiography: 4-chamber dilation
Diagnosis  Cardiac MRI: late enhancement of the epicardium
 Biopsy: lymphocytic infiltration, viral DNA or RNA

 Medication (eg, diuretics, ACE inhibitor, beta blocker)


 Temporary ventricular assist device, if needed
Treatment
 Heart transplant if no recovery

Chronic dyspnea in sickle cell disease


Cause Symptoms Diagnostic findings
 Intermittent/chronic wheezing
 Pulmonary function testing
 May be worse at night or with
showing reversible airway
Asthma exercise or upper respiratory
obstruction
infection

 Tricuspid regurgitation on
 Exertional dyspnea
echocardiography
 Signs of right-sided heart
Pulmonary  ↑ Pulmonary arterial pressure
failure (eg, jugular venous
hypertension on right-sided heart
distension, edema)
catheterization

 Honeycomb pattern on chest


 Exertional dyspnea CT scan
Pulmonary
 Progressive  Pulmonary function testing
fibrosis
showing restrictive pattern

Disseminated histoplasmosis
 Temperate regions worldwide
 Soil contaminated by bird or bat droppings
Epidemiology
 ↑ Dose exposure or immunocompromised (eg, AIDS)

Symptoms  Systemic (fever, chills, malaise)


 Weight loss & cachexia
 Pulmonary (cough, dyspnea)
 Mucocutaneous lesions (papules, nodules)
 Reticuloendothelial (HSM, LAD)

 Laboratory findings:
o Pancytopenia
o Transaminase elevation
o ↑ LDH & ferritin

Diagnosis
 Chest x-ray (reticulonodular or interstitial infiltrate)
 Urine/serum histoplasma antigen (↑ sensitivity/rapid)
 Serology
 Culture (takes 4-6 weeks)

 Amphotericin B (moderate to severe disease &/or HIV positive)


Treatment  Itraconazole (mild disease/maintenance)

HSM = hepatosplenomegaly; LAD = lymphadenopathy; LDH = lactate dehydrogenase.


 
Autoimmune hepatitis
 Asymptomatic
 Symptomatic (eg, anorexia, nausea, abdominal pain,
Presentation
jaundice)

 Hepatocellular pattern (↑↑ AST & ALT, ± mildly elevated


alkaline phosphatase & total bilirubin)
Laboratory
 Hypergammaglobulinemia with elevated gamma gap
findings
 Elevated anti–smooth muscle autoantibodies

 Portal & periportal lymphoplasmacytic infiltration


Histology
ALT = alanine aminotransferase; AST = aspartate aminotransferase.
Major types of systemic amyloidosis
Primary Secondary Age related Dialysis related
Chronic
Disease
Plasma cell dyscrasia infection/ Elderly men ESRD on dialysis
association
inflammation
Precursor Immunoglobulin Serum Transthyretin β2-Microglobulin
protein light chains amyloid A (prealbumin) ↓

↓ ↓ ↓ ↓ Decreased
clearance
Misfolding Increased Increased Accumulation
mechanism production
production over time

↓ ↓
↓ ↓
Amyloid
AL Aβ2M
fibril type
AA ATTR*
Cardiomyopathy,
Nephropathy, hepatosplenomegaly,
Clinical CTS, other Scapulohumeral
cardiomyopathy (AL > AA), peripheral
manifestations peripheral arthritis, CTS
neuropathy, macroglossia, skin bruising
neuropathy
Amyloid names begin with "A" followed by the precursor protein abbreviation.

*ATTR also occurs in a hereditary form that affects younger patients.

CTS = carpal tunnel syndrome; ESRD = end-stage renal disease.


 
Clinical features of severe pancreatitis
 Fever, tachycardia, hypotension
 Dyspnea, tachypnea &/or basilar crackles
 Abdominal tenderness &/or distension
 Cullen sign: periumbilical bluish coloration indicating
Clinical presentation
hemoperitoneum
 Grey Turner sign: reddish-brown coloration around flanks
indicating retroperitoneal bleed

 Age >75
 Obesity
 Alcoholism
 C-reactive protein >150 mg/dL at 48 hr after presentation
Associated with ↑ risk of
 Rising blood urea nitrogen & creatinine in the first 48 hr
severe pancreatitis
 Chest x-ray with pulmonary infiltrates or pleural effusion
 CT scan/magnetic resonance cholangiopancreatography with
pancreatic necrosis & extra pancreatic inflammation

 Pseudocyst
 Peripancreatic fluid collection
 Necrotizing pancreatitis
Complications  Acute respiratory distress syndrome
 Acute renal failure
 Gastrointestinal bleeding

Clinical features of alcoholic hepatitis


Clinical presentation  Jaundice, anorexia, fever
 Right upper quadrant &/or epigastric pain
 Abdominal distention due to ascites
 Proximal muscle weakness from muscle wasting (if
malnourished)
 Possible hepatic encephalopathy

 Elevated AST & ALT, usually <300 U/L


 AST: ALT ratio ≥2
 Elevated gamma-glutamyltransferase, bilirubin, &/or
Laboratory/ imaging international normalized ratio
studies  Leukocytosis, predominantly neutrophils
 Decreased albumin if malnourished
 Abdominal imaging may show fatty liver

Pseudogout (acute calcium pyrophosphate crystal arthritis)


 Acute mono- or oligoarticular arthritis
Symptoms  Peripheral joints (knee most common)

 Inflammatory effusion (15,000-30,000/mm3)


 CPPD crystals (rhomboid shape, positive birefringence)
Diagnosis
 Chondrocalcinosis on imaging

 Intraarticular glucocorticoids
 Nonsteroidal anti-inflammatory drugs
Treatment
 Colchicine

CPPD = calcium pyrophosphate dihydrate.


Clostridioides difficile colitis
 Recent antibiotic use or hospitalization
 Advanced age (>65)
 Gastric acid suppression (eg, PPI, H2 blocker)
Risk factors
 Underlying inflammatory bowel disease
 Chemotherapy

 Profuse watery diarrhea


Clinical  Leukocytosis (~15,000/mm3)
presentation  Fulminant colitis or toxic megacolon

 Stool PCR for C difficile genes*


 Stool EIA for C difficile toxin & glutamate
Diagnosis
dehydrogenase antigen

 Hand hygiene with soap & water


Infection  Contact isolation
control  Sporicidal disinfectants (eg, bleach)

*Genes specific to toxigenic strains are assessed.


EIA = enzyme immunoassay; H2 = histamine-2 receptor; PPI = proton
pump inhibitor.
Felty syndrome
 Rheumatoid arthritis
o Severe erosive joint disease & deformity
o Rheumatoid nodules
Clinical
o Vasculitis (mononeuritis multiplex, necrotizing skin lesions)
features
 Neutropenia (ANC <2000/µL)
 Splenomegaly

 Anti-CCP & RF are positive in >90% of patients


 Markedly elevated ESR, often >85 mm/hr
Diagnosis  Peripheral smear & bone marrow biopsy to rule out other causes of
neutropenia

ANC = absolute neutrophil count; anti-CCP = anticyclic citrullinated peptide;


ESR = erythrocyte sedimentation rate; RF = rheumatoid factor.
Acute aortic dissection
 Chronic hypertension (strongest overall risk factor)
 Underlying aortopathy (eg, Marfan syndrome)
Risk factors
 Cocaine use

 Severe, tearing chest or back pain, maximal at onset


 ± Variation in SBP between arms >20 mm Hg
Clinical presentation
 Hypertension usually present*

 ECG: normal or nonspecific ST-segment & T-wave changes


 Chest x-ray: mediastinal widening
Diagnosis
 CT angiography or TEE for definitive diagnosis

 Pain control (eg, morphine)


 Intravenous beta blockers (eg, esmolol)
Treatment  ± Sodium nitroprusside (if SBP >120 mm Hg)
 Emergency surgical repair for ascending dissection

*Hypotension on presentation suggests aortic rupture or other complication (eg, cardiac


tamponade, acute aortic regurgitation).

SBP = systolic blood pressure; TEE = transesophageal echocardiography.


Manifestations of systemic lupus erythematosus
Clinical  Constitutional: fever, fatigue & weight loss
symptoms  Symmetric, migratory arthritis
 Skin: butterfly rash & photosensitivity
 Serositis: pleurisy, pericarditis & peritonitis
 Thromboembolic events (due to vasculitis & antiphospholipid antibodies)
 Neurologic: cognitive dysfunction & seizures

 Hemolytic anemia, thrombocytopenia & leukopenia


 Hypocomplementemia (C3 & C4)
 Antibodies:
Laboratory
o Antinuclear antibodies (sensitive)
findings
o Anti-dsDNA & anti-Smith (specific)
 Renal involvement: proteinuria & elevated creatinine

dsDNA = double-stranded DNA.


Hemodynamic measurements in shock
Distributive
Hypovolemic Cardiogenic Obstructive
Parameter
shock shock shock
shock
CVP
(right-sided ↓ ↑ ↑ ↓
preload)
PCWP
(left-sided ↓ ↑ ↓* ↓
preload)
Cardiac index
↓ ↓ ↓ ↑**
(LV output)
SVR
↑ ↑ ↑ ↓
(afterload)
SvO2 ↓ ↓ ↓ ↑**
*In tamponade, left-sided preload is decreased, but measured PCWP is paradoxically increased
due to external compression by pericardial fluid.

**Cardiac index & SvO2 are usually decreased in neurogenic shock due to impaired sympathetic
reflexes.

CVP = central venous pressure; LV = left ventricular; PCWP = pulmonary capillary wedge


pressure; SvO2 = mixed venous oxygen saturation; SVR = systemic vascular resistance.
Nonalcoholic fatty liver disease
 Hepatic steatosis on imaging or biopsy
Definition  Exclusion of other etiologies (eg, alcohol, hepatitis C, glucocorticoids)

 Mostly asymptomatic
 Metabolic syndrome
Clinical
 AST/ALT ratio <1
features
 Hyperechoic texture on ultrasound examination

Treatment  Weight loss (eg, diet modification, exercise)


 Consider bariatric surgery if BMI ≥35

 Hepatic fibrosis associated with increased risk for cirrhosis & liver-
Prognosis related death

ALT = alanine aminotransferase; AST = aspartate aminotransferase.


Comparison of left ventricular & right ventricular myocardial infarction
Left ventricular MI Right ventricular MI
 Pulmonary edema  Clear lungs & JVD
Clinical features  S3 & S4  Marked hypotension

 Inferior ischemic changes


 Ischemic changes in
 ST-segment elevation in
anterior, lateral, or inferior
ECG findings V4R
leads
 Bradyarrhythmias

 ↑ LV & RV preload  ↑ RV preload, ↓ LV preload


Hemodynamic findings  ↑ SVR  ↑ SVR

 Fluid restriction
 Fluid resuscitation
 Preload & afterload
 Avoid preload reduction
Management reduction
 Reperfusion therapy
 Reperfusion therapy

JVD = jugular venous distension; LV = left ventricular; MI = myocardial infarction; RV = right


ventricular; SVR = systemic vascular resistance.
Features of lumbosacral radiculopathy
Nerve
Reflex affected Sensory loss* Weakness
Root
 Anteromedial  Hip flexion (iliopsoas)
 Patellar thigh  Hip adduction
L2-L4**
 Medial shin  Knee extension (quadriceps)

 Foot dorsiflexion & inversion


 Lateral shin (tibialis anterior)
 None  Dorsum of the  Foot eversion (peroneus)
L5
foot  Toe extension (extensor
hallucis & digitorum)

 Hip extension (gluteus


 Posterior calf maximus)
 Achilles  Sole & lateral  Knee flexion (hamstrings)
S1
foot  Foot plantarflexion
(gastrocnemius)
 Urinary or fecal incontinence
 Anocutaneous  Perineum
S2-S4**  Sexual dysfunction

*Radicular pain typically has a similar distribution to sensory loss.

**Difficult to distinguish between individual nerve roots clinically.


Plaque psoriasis
 Well-defined, erythematous plaques with silvery scale
Skin lesions  Extensor surfaces (knees, elbows), hands, scalp, back, nail plates

 Nail pitting
Extradermal  Conjunctivitis, uveitis
manifestations  Psoriatic arthritis

 Topical: high-potency glucocorticoids, vitamin D analogs, tar, retinoids,


calcineurin inhibitors, tazarotene
 Ultraviolet light/phototherapy
Treatment
 Systemic: methotrexate, calcineurin inhibitors, retinoids, apremilast,
biologic agents

Symptoms of digoxin toxicity


 Life-threatening arrhythmias
Cardiac
 Anorexia
 Nausea & vomiting
Gastrointestinal
 Abdominal pain

 Fatigue
 Confusion
Neurologic  Weakness
 Color vision alterations

Clinical features of vertebral compression fracture


 Trauma (often trivial)
 Osteoporosis, osteomalacia
 Bone metastases
Etiologies
 Metabolic (eg, hyperparathyroidism)
 Paget disease

Clinical Acute
presentation
 Back pain & decreased spinal mobility
 Pain increasing with standing, walking, lying on
back
 Referred pain to abdomen/flank
 Spinal tenderness at affected level

Chronic/gradual

 Painless
 Progressive kyphosis
 Loss of height

 Increased risk for future fractures


 Hyperkyphosis → protuberant abdomen, early
Complications
satiety, weight loss, decreased respiratory capacity

Management of diabetic ketoacidosis


 Initial: give isotonic intravenous fluids
 Subsequent:
o Continue isotonic fluids if serum Na+ <135 mEq/L
Fluids
o Switch to half normal saline if serum Na+ ≥135 mEq/L
o Add dextrose when serum glucose <200 mg/dL

 Reduce insulin infusion rate when serum glucose <200 mg/dL


 Hold insulin infusion if serum K+ <3.3 mEq/L
Insulin
 Switch to subcutaneous insulin on DKA resolution*

 Give replacement when serum K+ <5.3 mEq/L**


Potassium
 Consider replacement for severe DKA with blood pH ≤6.9
Bicarbonate
*Normalization of anion gap & patient able to eat.

**Due to total body potassium depletion and risk of insulin-induced hypokalemia.

DKA = diabetic ketoacidosis.


Hyperosmolar hyperglycemic state
 Type 2 diabetes mellitus
Patient
 Older age
characteristics
 Gradual hyperglycemic symptoms (eg, polyuria, polydipsia)
Clinical
 Altered mentation (eg, coma, focal signs, seizures)
symptoms
 Glucose >600 mg/dL (frequently >1,000 mg/dL)
 Normal pH & bicarbonate
Laboratory  Normal anion gap
studies  Negative or small serum ketones
 Serum osmolality >320 mOsm/kg
 Aggressive hydration with normal saline*
Initial  Intravenous insulin
management  Potassium replacement if level is <5.3 mEq/L

*Normal saline for the first hour regardless of sodium levels; fluid choice may change thereafter.
Heart failure with preserved ejection fraction
 LV diastolic dysfunction due to impaired relaxation
Etiology
 Chronic hypertension (concentric LV hypertrophy)
 Obesity & sedentary lifestyle (myocardial interstitial fibrosis)
Risk factors
 CAD & related risk factors (eg, diabetes mellitus)

 Specific therapies to reduce hospitalization & possibly mortality:


o MRAs (eg, spironolactone)
o SGLT2 inhibitors (eg, dapagliflozin)
 Loop diuretics as needed to treat volume overload
Management
 Additional antihypertensives PRN to reduce afterload
 Treatment of exacerbating conditions (eg, CAD, OSA, A-fib)
 Exercise training/cardiac rehabilitation

A-fib = atrial fibrillation; CAD = coronary artery disease; LV = left ventricular;


MRAs = mineralocorticoid antagonists; OSA = obstructive sleep apnea; PRN = as needed;
SGLT2 = sodium-glucose cotransporter 2.
Clinical features of acute pancreatitis
 Chronic alcohol use
 Gallstones
 Hyperlipidemia (types I, IV & V)
 Drugs (eg, didanosine, azathioprine, valproic acid)
Etiology  Infections (eg, cytomegalovirus, Legionella,
Aspergillus)
 Trauma
 Iatrogenic (post-ERCP)

Clinical Diagnosis requires 2 of the following:


presentation
 Acute epigastric abdominal pain often radiating to the
back
 ↑ Amylase/lipase >3 times normal limit
 Abdominal imaging showing focal or diffuse pancreatic
enlargement with heterogeneous enhancement with
intravenous contrast (CT scan) or diffusely enlarged &
hypoechoic pancreas (ultrasound)

 
Other findings:

 Nausea, vomiting, leukocytosis


 Severe disease with possible abdominal tenderness,
fever, tachypnea, hypoxemia & hypotension

 ALT level >150 U/L → biliary pancreatitis

 Pleural effusion
 Ileus
Complications  Pancreatic pseudocyst/abscess/necrosis
 Acute respiratory distress syndrome

ERCP = endoscopic retrograde cholangiopancreatography; ALT = alanine


aminotransferase.
ADH-related causes of polyuria & polydipsia
Primary polydipsia Central DI Nephrogenic DI
↓ ADH release from
Defect ↑ Water intake ADH resistance in kidney
pituitary
 Idiopathic
 Chronic lithium use
 Antipsychotics  Trauma
 Hypercalcemia
 Anxious, middle-  Pituitary surgery
Etiology  Hereditary (AVPR2
age women  Ischemic
mutations)
encephalopathy

Clinical
Low serum Na High serum Na Normal serum Na
features
ADH = antidiuretic hormone; DI = diabetes insipidus.
Kaposi sarcoma
 Endothelial tumor caused by human herpesvirus 8
 Most common malignancy in patients with untreated HIV
Etiology
 Endemic in certain African & Mediterranean regions

 Cutaneous lesions:
o Violaceous, red, or brown flat lesions grow into papules
o Most common along skin folds
o Pruritus, pain & friability are rare
Manifestations o Lymphedema distal to lesions
 Visceral lesions:
o Lungs & gastrointestinal tract most common
o May cause life-threatening bleeding

Treatment  HIV-associated KS:


o Antiretroviral therapy initiation
o Local or systemic chemotherapy rarely required
 Endemic KS:
o Surgery & local therapy are primary modalities

KS = Kaposi sarcoma.
Diagnostic tests for pulmonary tuberculosis
 Low cost & rapid (minutes to hours)
 Low sensitivity because high burden (>10,000/mL) of organisms required
AFB smear
in sample
microscopy
 Cannot differentiate TB from non-TB mycobacteria

 Higher cost & slightly less rapid (1-2 days)


Nucleic acid
 Higher sensitivity (only ~10 bacilli/mL required for positive test)
amplification
 Can differentiate TB from non-TB mycobacteria
testing
 Gold standard, quantitative & allows for drug sensitivity testing
Sputum
 Slow: takes 3-8 weeks
culture
AFB = acid-fast bacillus (stain); TB = tuberculosis.
Echinococcus granulosus
 Dog tapeworm (sheep intermediate host)
 Rural, developing countries (eg, South America, Middle East)
Epidemiology
 Humans are incidental hosts (egg ingestion)

 Initially asymptomatic (often for years)


 Liver cyst (most common)
o Mass effect: RUQ pain, nausea, vomiting, hepatomegaly
Manifestations
o Rupture: fever, eosinophilia
 Lung cyst: cough, chest pain, hemoptysis

 Large, smooth hydatid cyst often with internal septations on imaging


Diagnosis  IgG E granulosus serology

 Albendazole
 Percutaneous therapy (>5 cm or septations)
Treatment
 Surgery (if rupture)

RUQ = right upper quadrant.


Common causes of myopathy
 Polymyositis/dermatomyositis
 Inclusion body myositis
Connective tissue diseases  Vasculitis
 Overlap syndrome (mixed connective tissue disease)
 Hypothyroidism, thyrotoxicosis
Endocrine/
 Cushing syndrome
 Electrolytes (↓ potassium, calcium, phosphorus)
metabolic
 Corticosteroids, statins
 Zidovudine, colchicine
Drugs/toxins
 Alcohol, cocaine, heroin

 Infections, trauma, hyperthermia


Miscellaneous
Stage Lyme disease clinical features
 Erythema migrans
Early localized  Fatigue, headache
(days to 1 month)  Myalgia, arthralgia

 Multiple erythema migrans


 Unilateral/bilateral cranial nerve palsy (eg, CN VII)
Early disseminated  Meningitis
(weeks to months)  Carditis (eg, AV block)
 Migratory arthralgia

 Arthritis
Late  Encephalitis
(months to years)  Peripheral neuropathy

AV = atrioventricular.
Hyperosmolar hyperglycemic state
 Type 2 diabetes mellitus
Patient
 Older age
characteristics
 Acute illness, trauma, infection
Inciting  Insulin nonadherence
factors  Medications: glucocorticoids, diuretics, atypical antipsychotics

Subacute or acute onset of:

Clinical  Altered mentation


features  Hyperglycemic symptoms (eg, polyuria)
 Volume depletion

Laboratory  Glucose >600 mg/dL (33.3 mmol/L)


studies  Bicarbonate >18 mEq/L (18 mmol/L)
 Normal anion gap
 Negative or small serum ketones
 Serum osmolality >320 mOsm/kg (320 mmol/kg)

Rheumatologic diseases & commonly associated autoantibodies


Sensitivity (%) Specificity (%)
Rheumatoid arthritis RF: 70-80 Anti-CCP: 95
Systemic lupus erythematosus ANA: 95 Anti-dsDNA/anti-Sm: 96
Drug-induced lupus ANA: 95 Antihistone: 95
Diffuse systemic sclerosis ANA: 95 Anti–Scl-70: 99
Limited systemic sclerosis ANA: 95 Anticentromere: 97
Polymyositis/dermatomyositis ANA: 75 Anti–Jo-1: 99
ANA = antinuclear antibodies; anti-CCP = anti–cyclic citrullinated peptide; anti-
dsDNA = anti–double-stranded DNA; anti–Scl-70 = anti–topoisomerase I; anti-Sm =
anti-Smith; RF = rheumatoid factor.
Symptoms/signs of ankylosing spondylitis
 Low back pain (onset age <40, insidious onset, improves with exercise but not with rest,
pain at night)
 Hip & buttock pain
 Limited chest expansion & spinal mobility
 Enthesitis (inflammation at the site of insertion of a tendon to the bone)
 Systemic symptoms (eg, fever, chills, fatigue, weight loss)
 Acute anterior uveitis (unilateral pain, photophobia, blurry vision)

Clinical features of pulmonary hypertension


 Pulmonary arterial hypertension (WHO group 1)
 Due to left heart disease (group 2)
 Due to chronic lung disease or hypoxemia (eg, COPD, OSA)
Classification (group 3)
 Due to chronic thromboembolic disease (group 4)
 Due to other causes (eg, sarcoidosis) (group 5)

 ↓ Cardiac output: exertional syncope/presyncope, fatigue,


weakness
 ↑ PA pressure: chest tightness, hemoptysis (rare)
Symptoms  RV demand ischemia: exertional angina/tightness
 Venous congestion: abdominal distension (bowel edema), early
satiety

 Precordial heave due to RV hypertrophy


 Loud P2, right-sided S3 &/or S4
Signs  Holosystolic murmur of tricuspid regurgitation
 JVD, ascites, peripheral edema, hepatomegaly

COPD = chronic obstructive pulmonary disease; JVD = jugular venous distension;


OSA = obstructive sleep apnea; PA = pulmonary artery; RV = right ventricular.
Cryptococcal meningoencephalitis
 Headache, fever & malaise
 Develops over 2 weeks (subacute)
Presentation
 Can be more acute & severe in patients with HIV

Cerebrospinal fluid:

 High opening pressure


 Low glucose, high protein
Diagnosis  White blood cells <50/mm3 with mononuclear predominance
 Transparent capsule seen with India ink stain
 Cryptococcal antigen positive
 Culture on Sabouraud agar

 Initial: amphotericin B with flucytosine


Treatment  Maintenance: fluconazole

Comparison of leukemoid reaction & chronic myeloid leukemia (CML)


Leukemoid reaction CML
Elevated
Leukocyte count >50,000/mm3 (>50 × 109)
(often >100,000/mm3 [>100 × 109])
Cause Severe infection BCR-ABL fusion
LAP score High Low
More mature Less mature
Neutrophil precursors
(metamyelocytes > myelocytes) (metamyelocytes < myelocytes)
Absolute basophilia Not present Present
LAP = leukocyte alkaline phosphatase.
Diagnostic challenges in anaphylaxis
 No prior allergic reactions (ie, first episode)
Nonclassic  Absence of hypotension, respiratory symptoms, or cutaneous signs
presentation  Protracted or biphasic presentation

 Preexisting conditions with similar symptoms (eg, asthma, COPD)


Challenging  Ongoing physiologic shifts (eg, childbirth, hemodialysis)
clinical situations  Impaired communication (eg, sedation, severe psychiatric illness)

 Directly activate mast cells (eg, opiates, NSAIDs)


Medication  Interfere with epinephrine effect (eg, β-blockers,
effects α-adrenergic blockers)

COPD = chronic obstructive pulmonary disease; NSAIDs = nonsteroidal anti-inflammatory


drugs.
Common complications of infective endocarditis
Local (cardiac)  Heart failure
 Perivalvular abscess
 Pericarditis
 Intracardiac fistula

 Septic embolism
 Metastatic abscess
Distant (embolic)  Mycotic aneurysm
 Organ infarction

Causes of QT-interval prolongation


 Medications
o Macrolides & fluoroquinolones
o Antiemetics (eg, ondansetron)
o Azoles (eg, fluconazole)
o Antipsychotics, TCAs & SSRIs
Acquired o Some opioids (eg, methadone, oxycodone)
o Class Ia antiarrhythmics (eg, quinidine)
o Class III antiarrhythmics (eg, dofetilide, sotalol)
 Electrolyte abnormalities
o ↓ Magnesium, ↓ potassium, ↓ calcium

 Romano-Ward syndrome (autosomal dominant)


Congenital  Jervell & Lange-Nielsen syndrome (autosomal recessive)*

*Associated with sensorineural hearing loss.

SSRI = selective serotonin reuptake inhibitor; TCA = tricyclic antidepressant.


Vasospastic angina
 Hyperreactivity of coronary smooth muscle
Pathogenesis
 Young patients (age <50)
 Smoking (minimal other CAD risk factors)
Clinical  Recurrent chest discomfort
presentation o Occurs at rest or during sleep
o Spontaneous resolution ≤15 min

 Ambulatory ECG: ST-segment elevation


Diagnosis  Coronary angiography: no CAD

 Calcium channel blocker (preventive)


Treatment  Sublingual nitroglycerin (abortive)

CAD = coronary artery disease.


Giant cell arteritis
Symptoms  Systemic: fever, fatigue, malaise, weight loss
 Headaches
 Jaw claudication
 PMR

 Visual disturbances: amaurosis fugax, AION

 Normochromic anemia
Diagnostic  Elevated ESR & CRP
tests  Temporal artery biopsy

 PMR only: low-dose oral glucocorticoids (eg, prednisone 10-


20 mg daily)
Treatment  GCA: intermediate- to high-dose oral glucocorticoids (eg,
prednisone 40-60 mg daily)

AION = anterior ischemic optic neuropathy; CRP = C-reactive protein; ESR =


erythrocyte sedimentation rate; GCA = giant cell arteritis; PMR = polymyalgia
rheumatica.
Secondary iron overload
 Chronic anemia that requires repeated transfusions
(eg, sickle cell disease, thalassemia)
 Ineffective erythropoiesis (eg, thalassemia)
Risk factors
 Chronic liver disease
 Excess iron supplementation

 Liver: hepatomegaly, cirrhosis


 Heart: cardiomyopathy, heart failure
 Endocrine: hypopituitarism (eg, secondary
Clinical features* hypogonadism), diabetes mellitus
 Skin: hyperpigmentation
 Joint: arthropathy

 ↑ Ferritin & transferrin saturation


 Imaging/biopsy of affected organs consistent
Diagnosis
with iron overload

*Same as in hereditary hemochromatosis (primary iron overload).


Obstructive sleep apnea
 Relaxation of pharyngeal muscles, leading to closure of airway
Pathophysiology  Loud snoring with periods of apnea

Symptoms  Daytime somnolence


 Nonrestorative sleep with frequent awakenings
 Morning headaches
 Affective & cognitive symptoms

 Systemic hypertension
Sequelae  Pulmonary hypertension & right-sided heart failure

Acute management of acute coronary syndrome

(STEMI, NSTEMI, or unstable angina)


 Rapid chest pain relief
Nitrates  Caution with hypotension (eg, RV infarction)

 Cardioselective (eg, metoprolol, atenolol)


 Decreases myocardial O2 demand to limit infarct size
Beta blocker
 Contraindicated in cardiogenic shock & bradycardia

 Aspirin + P2Y12 inhibitor (eg, prasugrel, clopidogrel)*


Antiplatelet therapy  Reduces platelet activity

 Unfractionated heparin, bivalirudin, or enoxaparin


Anticoagulation  Limits thrombus expansion

 High potency (eg, atorvastatin, rosuvastatin)


Statin therapy  Stabilizes atherosclerotic plaque

STEMI

 PCI <90 min from 1st medical contact


 Fibrinolytics (eg, alteplase) if PCI is unavailable
Coronary reperfusion
NSTEMI or unstable angina

 Coronary angiography often within 24 hr

*In patients with NSTEMI or unstable angina, P2Y12 inhibitor therapy is often held until after
coronary angiography in case the atherosclerotic coronary anatomy indicates the need for
coronary artery bypass grafting.

NSTEMI = non–ST-segment elevation myocardial infarction; PCI = percutaneous coronary


intervention; RV = right ventricular; STEMI = ST-segment elevation myocardial infarction.
Causes of hypercapnia
Mechanism Examples
 Drugs (eg, opioids, benzodiazepines)
↓ Central respiratory drive  CNS trauma, stroke, or encephalitis
 Spinal cord lesions
↓ Respiratory neuromuscular  Amyotrophic lateral sclerosis
function  Myasthenia gravis

 Obesity hypoventilation syndrome


 Pneumothorax
↓ Thoracic cage or pleural function
 Rib fractures, flail chest

 Obstructive sleep apnea (upper airway)


 Chronic obstructive pulmonary disease (lower
Airway obstruction
airway)

 Cardiogenic pulmonary edema


Impaired gas exchange  Interstitial lung disease

Primary versus secondary adrenal insufficiency


Primary Secondary
 Destruction of bilateral  Disruption of hypothalamic-
Mechanism adrenal cortex pituitary axis

 Autoimmune adrenalitis  Chronic glucocorticoid therapy


Possible
 Infection, malignancy  Infiltrative disease
etiologies
Cortisol ↓ ↓
Aldosterone ↓ Normal
ACTH ↑ ↓
 More severe symptoms  Less severe symptoms
 Hypovolemia  Euvolemia
Clinical
 Hyperkalemia, hyponatremia  Minimal electrolyte disturbance
features
 Hyperpigmentation  No hyperpigmentation

Medications for osteoporosis


 First-line treatment for most patients
 Taken with water on an empty stomach an hour before food
Bisphosphonates & other medications
(eg, alendronate,  Not recommended for patients with renal impairment
risedronate)  Atypical fractures possible with prolonged use
 Oral & parenteral options available

 Risk of infection & skin reactions


Denosumab  Close monitoring for hypocalcemia needed

 Useful in severe osteoporosis


Anabolic agents
 Monitor serum calcium, uric acid & renal function
(eg, teriparatide)
 Modest reduction in fracture risk
Nasal calcitonin  Reduces pain from fracture

 Less effective than bisphosphonates


Selective estrogen
 May lower risk of breast cancer
receptor modulators
 Increased risk of DVT
(eg, raloxifene)
DVT = deep vein thrombosis.
Features of drug-induced lupus erythematosus
Acute onset of:

 Constitutional symptoms (eg, fever, malaise)


Clinical features*  Arthralgias
 Serositis (eg, pleuritis, pericarditis)
 Rash (less common compared with SLE)

 High drug dose, prolonged use (>3 months)


Risk factors  Slow acetylator status

 Antihistone antibodies (>90%)


Laboratory
 Antinuclear antibodies (>95%)
findings
 Most common: procainamide, hydralazine, penicillamine
 Others: minocycline, TNF-α inhibitors (eg, etanercept, infliximab),
Implicated drugs
isoniazid

*No minimum number of SLE criteria is needed for diagnosis.

SLE = systemic lupus erythematosus; TNF-α = tumor necrosis factor-alpha.


Causes of hemolysis
 Microangiopathic hemolytic anemia (eg, disseminated intravascular
coagulation)
 Transfusion reactions
Intravascular
 Infections (eg, clostridial sepsis)
hemolysis
 Paroxysmal nocturnal hemoglobinuria
 Intravenous Rho(D) immunoglobulin infusion

 Intrinsic RBC enzyme deficiencies (eg, G6PD)


 Hemoglobinopathies (eg, sickle cell, thalassemia)
 Membrane defects (eg, hereditary spherocytosis)
Extravascular
 Hypersplenism, intravenous immunoglobulin infusion
hemolysis
 Warm- or cold-agglutinin autoimmune hemolytic anemia (most cases)
 Infections (eg, Bartonella, malaria)

G6PD = glucose-6-phosphate dehydrogenase; RBC = red blood cell.


Patterns of intracranial hemorrhage by location
 Lobar: CAA (less common: AVM, tumor)
Intraparenchymal hemorrhage  Basal ganglia, pons, thalamus: hypertension

 Aneurysm (80% of SAH)


 Trauma
Subarachnoid hemorrhage
 AVM

AVM = arteriovenous malformation; CAA = cerebral amyloid angiopathy; SAH = subarachnoid


hemorrhage.
Features of carcinoid syndrome
 Skin: flushing, telangiectasias, cyanosis
 Gastrointestinal: diarrhea, cramping
 Cardiac: valvular lesions (right > left side)
Clinical
 Pulmonary: bronchospasm
manifestations
 Miscellaneous: niacin deficiency (dermatitis,
diarrhea, dementia)

 Elevated 24-hr urinary excretion of 5-HIAA


 CT scan/MRI of abdomen & pelvis to
localize tumor
Diagnosis  OctreoScan to detect metastases
 Echocardiogram (if symptoms of carcinoid
heart disease are present)

 Octreotide for symptomatic patients & prior


to surgery/anesthesia
Treatment
 Surgery for liver metastases

Chronic silicosis
 Occupation: quarry work, stone cutting, glass & ceramic
manufacturing
 Pathogenesis: respired silica crystals → inflammatory activation of
Risk factors &
alveolar macrophages
pathogenesis
 Associations: lung cancer, mycobacterial disease, rheumatoid
arthritis

 Slowly progressive symptoms beginning 10-30 yr after exposure


 Annular (eggshell) calcification of hilar & mediastinal nodes
Clinical
 Simple silicosis: small, nodular fibrotic opacities in upper lung zones
presentation
 PMF: coalescent fibrotic masses with severe respiratory impairment

Prevention &  Respiratory protection (minimize exposure, NIOSH respirator)


management  Smoking cessation, pulmonary rehabilitation, oxygen
 Lung transplantation

NIOSH = National Institute of Occupational Safety & Health; PMF = progressive massive


fibrosis.

Asthma vs COPD
Asthma COPD Late-stage COPD
FVC Normal/↓ Normal/↓ ↓/↓↓
FEV1 ↓ ↓ ↓↓
FEV1/FVC ↓ ↓ ↓↓
Bronchodilator Partially reversible/ Usually
Reversible
response nonreversible nonreversible
Hyperinflation, loss
Chest x-ray Normal Normal
of lung markings
DLCO Normal/↑ Normal/↓ ↓
COPD = chronic obstructive pulmonary disease; DLCO = diffusion capacity of the lung for
carbon monoxide.
Hypersensitivity pneumonitis
 Immunologic response to inhaled antigen (eg, mold, animal protein)
Etiology
Acute

 Abrupt-onset fever, chills, cough, dyspnea, fatigue, leukocytosis


 Episodes often recurrent and self-resolving
 Chest x-ray: scattered micronodular interstitial opacities
Clinical
presentation Chronic

 Progressive cough, dyspnea, fatigue, weight loss


 Hypoxemia that worsens with exertion
 Chest x-ray: diffuse reticular interstitial opacities

 PFT: restrictive pattern, ↓ DLCO (chronic only)


 BAL: high relative lymphocyte count
Diagnosis  Lung biopsy: lymphocytic infiltrate, poorly formed noncaseating
granulomas, interstitial inflammation or fibrosis (chronic only)

 Remove antigen exposure (resolves acute disease)


Treatment  Glucocorticoids and/or lung transplantation (chronic only)

BAL = bronchoalveolar lavage; DLCO = diffusion capacity of the lung for carbon monoxide;
PFT = pulmonary function testing.
Vasospastic angina
 Hyperreactivity of coronary smooth muscle
Pathogenesis
 Young patients (age <50)
 Smoking (minimal other CAD risk factors)
Clinical  Recurrent chest discomfort
presentation o Occurs at rest or during sleep
o Spontaneous resolution ≤15 min

 Ambulatory ECG: ST-segment elevation


Diagnosis  Coronary angiography: no CAD

 Calcium channel blocker (preventive)


Treatment  Sublingual nitroglycerin (abortive)

CAD = coronary artery disease.


Metabolic acidosis
Type Normal anion gap Elevated anion gap
 Accumulation of
 Loss of bicarbonate unmeasured acidic
Mechanism
compounds

 Severe diarrhea
 Lactic acidosis
 Renal tubular acidosis
 Diabetic ketoacidosis
 Excess saline infusion
 Renal failure (uremia)
Etiologies  Intestinal or pancreatic
 Methanol, ethylene glycol
fistula
 Salicylate toxicity
 CAI & MRA diuretics

CAI = carbonic anhydrase inhibitor; MRA = mineralocorticoid receptor antagonist.


 
Inflammatory bowel disease subtype characteristics
Crohn disease Ulcerative colitis
 Anywhere mouth to anus (mostly
ileum & colon)  Rectum (always) & colon
Involvement  Perianal disease with rectal sparing  Continuous lesions
 Skip lesions

 Noncaseating granulomas  No granulomas


Microscopy
 Transmural inflammation  Mucosal & submucosal
Gross  Linear mucosal ulcerations inflammation
findings  Cobblestoning, creeping fat  Pseudopolyps
 Abdominal pain (varying
 Abdominal pain (often RLQ)
Clinical locations)
 Watery diarrhea (bloody if colitis)
manifestations  Bloody diarrhea

 Fistulae, abscesses
Intestinal  Toxic megacolon
 Strictures (bowel obstruction)
complications
RLQ = right lower quadrant.
 
Second-degree atrioventricular block:
distinguishing features of Mobitz types I & II
Mobitz type I Mobitz type II
Below AV node (eg, His
Level of block AV node
bundle)
Progressive prolongation of PR Constant PR interval with
ECG findings interval followed by dropped randomly dropped QRS
QRS complex complexes
QRS complexes Usually narrow Narrow or wide
Decreased vagal tone (eg,
Block improves Block worsens
exercise, atropine)
Increased vagal tone (eg,
Block worsens Block improves
carotid massage)
Risk of complete block Low High (indication for PPM)
AV = atrioventricular; PPM = permanent pacemaker.
Bacterial aspiration pneumonia
 Oropharyngeal/gastric microbes aspirated into lungs → host
Pathophysiology defenses overwhelmed due to large inoculum size

 Reduced consciousness (eg, anesthesia)


 Dysphagia (eg, neuromuscular disorder)
 Impaired glottic closure (eg, intubation)
Major risk factors
 Protracted vomiting
 Poor dental hygiene

 Fever & cough ± foul-smelling sputum


 Infiltrate in dependent portions of lung
Clinical features
 Aerobic + anaerobic pathogens on sputum studies

 No empyema or lung abscess: treat for community-acquired


pneumonia
Management  Empyema or lung abscess present: extend coverage to
include anaerobes (eg, ampicillin-sulbactam)

Epidemiology and extrapulmonary clinical manifestations of endemic mycoses


Syndrome Epidemiology Clinical clues
 Cutaneous plaques/ulcerations
Mississippi/Ohio River Valley  Bone lesions with sinus tracts
Blastomycosis  Genitourinary involvement
Midwestern United States  CNS involvement (very rare)

 Hilar/mediastinal lymphadenopathy
Mississippi/Ohio River Valley  Hepatosplenomegaly
Histoplasmosis  Pancytopenia
Central & South America  Adrenal insufficiency

 Skin lesions
Southern Arizona/California  Lymph node involvement
Coccidioidomycosis  Meningitis
Northern Mexico  Osteoarticular infection

 
Laboratory evaluation of hypertension
 Serum electrolytes (Na, K, Ca)
 Serum creatinine
Renal function tests  Urinalysis
 Urine albumin/creatinine ratio (optional)

 Fasting glucose or hemoglobin A1c


 Lipid profile
Endocrine tests
 TSH

 ECG
Cardiac tests  Echocardiography (optional)

 Complete blood count


Other tests  Uric acid (optional)

Pulmonary involvement in systemic sclerosis


PAH alone ILD
 Dyspnea  Dyspnea
Clinical  Exertional syncope  Cough
presentation  Clear lungs  Velcro-like crackles

 Normal FEV1 & FVC  ↓ FEV1 & FVC


Pulmonary
 Normal FEV1/FVC ratio  Normal or ↑ FEV1/FVC ratio
function
 ↓ DLCO  ↓ DLCO
testing
DLCO = diffusion capacity of the lungs for carbon monoxide; ILD = interstitial lung
disease; PAH = pulmonary arterial hypertension.
Clues to etiology of syncope
 Trigger (eg, emotional stress, prolonged
standing)
Vasovagal
 Prodrome (eg, nausea, sweating, warmth)

 Occurs with micturition, defecation,


Reflex syncope Situational swallowing, or coughing

 Tactile stimulation of carotid sinus while


Carotid standing
hypersensitivity  Advanced age, carotid atherosclerosis

 Vasodilators (eg, alpha-1 blockers,


antihypertensives)
Medications  Inotropic/chronotropic blockade (eg, beta
blockers)
Orthostatic
syncope  History consistent with volume loss
Hypovolemia
 Advanced age
Autonomic
 Predisposing disease (eg, DM, Parkinson)
dysfunction
 Syncope with exertion
LV outflow
 Systolic ejection murmur
obstruction
 No warning symptoms
 Cardiomyopathy or ischemic HD
Ventricular
(monomorphic)
Cardiac syncope tachycardia
 QT-interval prolongation (polymorphic)

 Preceding fatigue or light-headedness


Conduction  ECG abnormalities (eg, sinus pauses, dropped
impairment* QRS complexes)

*Sick sinus syndrome or advanced atrioventricular block.

DM = diabetes mellitus; HD = heart disease; LV = left ventricular.


Osteoarthritis
 >40; prevalence increases with age
Age of onset
 Knees
 Hips
Joint
 Distal interphalangeal joints
involvement
 1st carpometacarpal joint
Morning  None/brief (<30 min)
stiffness
Systemic  Absent
symptoms
 Hard, bony enlargement of joints
Examination
 Reduced range of motion with crepitus
findings
Sick sinus syndrome
 Elderly patients
 Bradycardia
o Fatigue, dyspnea, dizziness, syncope
Clinical features  Bradycardia-tachycardia syndrome
o Atrial arrhythmias (eg, atrial fibrillation)
o Palpitations

 Sinus bradycardia
 Sinus pauses (delayed P waves)
ECG findings
 Sinoatrial nodal exit block (dropped P waves)

 Pacemaker
Treatment  +/- Rate-control medication (if tachyarrhythmias)

Disseminated gonococcal infection


 Purulent monoarthritis

      OR
Manifestations
 Triad of tenosynovitis, dermatitis, migratory polyarthralgia

 Detection of Neisseria gonorrhoeae in urine, cervical, or urethral sample


Diagnosis  Culture of blood, synovial fluid (less sensitive)

 3rd-generation cephalosporin intravenously


Treatment
Gastroparesis
 Diabetes mellitus (autonomic neuropathy)
 Medications (eg, opioids, anticholinergic drugs)
 Traumatic/postsurgical injury (ie, vagus nerve injury)
Causes
 Neurologic (eg, multiple sclerosis, spinal cord injury)
 Idiopathic/postviral

Clinical  Nausea & vomiting, epigastric abdominal pain


features  Early satiety, bloating, weight loss
 Labile glucose (diabetes mellitus)
 Epigastric distension & succussion splash

 Exclude obstruction: upper endoscopy ± CT/MR enterography


Diagnosis  Assess motility: nuclear gastric-emptying study

 Frequent small meals (low fat, soluble fiber only)


 Promotility drugs (eg, metoclopramide, erythromycin)
Treatment  Gastric electrical stimulation &/or jejunal feeding tube (refractory
symptoms)

Renal cell carcinoma


 Flank pain, hematuria & a palpable abdominal renal mass
 Scrotal varicoceles (left sided)
 Paraneoplastic symptoms
o Anemia or erythrocytosis
o Thrombocytosis
o Fever
o Hypercalcemia
o Cachexia

First-time seizure in adults


 Metabolic (eg, hypoglycemia, electrolyte disorders)
 Toxic (eg, substance use/withdrawal, medications)
 Acute brain injury (eg, hemorrhage, meningoencephalitis,
Etiology stroke)
 Structural (eg, temporal sclerosis, dysplasia, tumor)
 Idiopathic/unknown (eg, juvenile myoclonic epilepsy)

 Laboratory: glucose, complete blood count, electrolytes,


renal function, liver function, ± urine drug screen
 Neuroimaging: CT scan (for acute injury; faster) or MRI
Evaluation (for smaller lesions; more time-consuming)
 ± Lumbar puncture (for fever or nuchal rigidity)
 EEG

 Abnormal EEG or neuroimaging


Indication to start  Nocturnal seizure
antiepileptic medications  Focal neurologic examination

EEG = electroencephalography.
Frostbite
 Superficial pallor & anesthesia
Clinical  Blistering, eschar formation
findings  Deep tissue necrosis & mummification
 Rapid rewarming in water bath at 37-39 C (98.6-102.2 F)
 Analgesia & wound care
 Angiography or technetium-99m scan to assess for thrombosis if
Management
rewarming is unsuccessful
 Thrombolysis in severe, limb-threatening cases

Inflammatory bowel disease subtype characteristics


Crohn disease Ulcerative colitis
 Anywhere mouth to anus (mostly
ileum & colon)  Rectum (always) & colon
Involvement  Perianal disease with rectal sparing  Continuous lesions
 Skip lesions

 Noncaseating granulomas  No granulomas


Microscopy
 Transmural inflammation  Mucosal & submucosal
Gross  Linear mucosal ulcerations inflammation
findings  Cobblestoning, creeping fat  Pseudopolyps

 Abdominal pain (varying


 Abdominal pain (often RLQ)
Clinical locations)
 Watery diarrhea (bloody if colitis)
manifestations  Bloody diarrhea

 Fistulae, abscesses
Intestinal  Toxic megacolon
 Strictures (bowel obstruction)
complications
RLQ = right lower quadrant.
Advance directives
 Legally binding instructions regarding patient's own health care
 Considered determinative for giving consent/refusal for treatment
Definition
 Takes priority over family's/friends' preferences

 Patient is competent at time directive is prepared


Requirements  Enacted only when patient lacks capacity for decision-making

 Living will: written document with consent/refusal of specific services


Types  Health care proxy: designation of a surrogate decision maker

Gilbert syndrome
 Most common inherited disorder of bilirubin metabolism
Epidemiology
 ↓ Hepatic UDP glucuronosyltransferase activity → ↓ conjugation of
Pathogenesis bilirubin
 Recurrent episodes of mild jaundice
 Provoked by stress (eg, febrile illness, fasting, dehydration, vigorous
Clinical findings
exercise, menstruation, surgery)

 ↑ Unconjugated bilirubin (ie, indirect hyperbilirubinemia)


 Normal CBC, blood smear, reticulocyte count
Diagnosis
 Normal AST, ALT, alkaline phosphatase

 Benign; no treatment required


Treatment
ALT = alanine aminotransferase; AST = aspartate aminotransferase; CBC = complete blood
count; UDP = uridine diphosphogluconurate.
Infectious genital ulcers
 Pustules, vesicles, or small ulcers on
erythematous base
Herpes simplex virus  Tender lymphadenopathy
 Systemic symptoms common

 Larger, deep ulcers with gray/yellow


Painful
exudate
 Well-demarcated borders & soft, friable
Haemophilus ducreyi
base
(chancroid)
 Severe lymphadenopathy that may
suppurate

 Usually single ulcer (chancre)


Treponema pallidum
 Indurated borders & hard, nonpurulent base
(syphilis)
Painless
Chlamydia trachomatis  Initial small, shallow ulcers (often missed)
serovars L1-L3  Then painful & fluctuant adenitis (buboes)
(lymphogranuloma venereum)
Lead poisoning in adults
Risk  Occupational exposure (eg, lead paint, batteries, ammunition, construction)
factors
 Gastrointestinal (abdominal pain, constipation, anorexia)
Clinical  Neurologic (cognitive deficits, peripheral neuropathy)
features  Hematologic (anemia)

 Anemia
 Elevated venous lead level
Laboratory
 Elevated serum zinc protoporphyrin level
findings
 Basophilic stippling on peripheral smear

Hypersensitivity pneumonitis
Etiology  Immunologic response to inhaled antigen (eg, mold, animal protein)
Acute

 Abrupt-onset fever, chills, cough, dyspnea, fatigue, leukocytosis


 Episodes often recurrent and self-resolving
 Chest x-ray: scattered micronodular interstitial opacities
Clinical
presentation Chronic

 Progressive cough, dyspnea, fatigue, weight loss


 Hypoxemia that worsens with exertion
 Chest x-ray: diffuse reticular interstitial opacities

 PFT: restrictive pattern, ↓ DLCO (chronic only)


 BAL: high relative lymphocyte count
Diagnosis  Lung biopsy: lymphocytic infiltrate, poorly formed noncaseating
granulomas, interstitial inflammation or fibrosis (chronic only)

 Remove antigen exposure (resolves acute disease)


Treatment  Glucocorticoids and/or lung transplantation (chronic only)

BAL = bronchoalveolar lavage; DLCO = diffusion capacity of the lung for carbon monoxide;
PFT = pulmonary function testing.
Classification of multiple endocrine neoplasia
 Primary hyperparathyroidism (parathyroid adenomas or
hyperplasia)
Type 1  Pituitary tumors (prolactin, visual defects)
 Pancreatic tumors (especially gastrinomas)

 Medullary thyroid cancer (calcitonin)


 Pheochromocytoma
Type 2A
 Primary hyperparathyroidism (parathyroid hyperplasia)

 Medullary thyroid cancer (calcitonin)


 Pheochromocytoma
Type 2B
 Mucosal neuromas/marfanoid habitus

Syndrome of inappropriate antidiuretic hormone


 CNS disturbance (eg, stroke, hemorrhage, trauma)
 Medications (eg, carbamazepine, SSRIs, NSAIDs)
 Lung disease (eg, pneumonia)
Etiologies
 Ectopic ADH secretion (eg, small cell lung cancer)
 Pain &/or nausea
 Mild/moderate hyponatremia: nausea, forgetfulness
 Severe hyponatremia: seizures, coma
Clinical features
 Euvolemia (eg, moist mucous membranes, no edema, no JVD)

 Hyponatremia
 Serum osmolality <275 mOsm/kg H2O (hypotonic)
Laboratory findings  Urine osmolality >100 mOsm/kg H2O
 Urine sodium >40 mEq/L

 Fluid restriction ± salt tablets


Management  Hypertonic (3%) saline for severe hyponatremia

ADH = antidiuretic hormone; JVD = jugular venous distension; NSAIDs = nonsteroidal anti-


inflammatory drugs; SSRIs = selective serotonin reuptake inhibitors.
Acute intermittent porphyria
 Autosomal dominant disorder with low penetrance
Etiology  Reduced activity of porphobilinogen deaminase

 Medications (eg, cytochrome P-450 inducers, progesterone)


Exacerbating  Physiologic stress (eg, fasting, surgery, illness)
factors  Alcohol, tobacco

 Abdominal pain
 Peripheral neuropathy most pronounced in the proximal upper
extremities
 Autonomic dysfunction (eg, tachycardia, diaphoresis,
Manifestations
hypertension)
 Neuropsychiatric (eg, hallucinations, anxiety, psychosis)
 Red-tinged urine that oxidizes with light/air exposure

 Elevated serum & urinary PBG, ALA, porphyrins


Laboratory findings  ± Hyponatremia, elevated transaminases

 Glucose & hemin (heme analogue)


Management
ALA = aminolevulinic acid; PBG = porphobilinogen.
Varicocele
 Soft scrotal mass ("bag of worms")  
o ↓ In supine position  
Clinical o ↑ With standing/Valsalva maneuvers
presentation  Subfertility
 Testicular atrophy

Ultrasound  Retrograde venous flow


findings  Tortuous, anechoic tubules adjacent to testis
 Dilation of pampiniform plexus veins

 Gonadal vein ligation (boys & young men with


testicular atrophy)
Treatment  Scrotal support & NSAIDs (older men who do
not desire additional children)

NSAIDs = nonsteroidal anti-inflammatory drugs.


Hemodynamic measurements in shock
Distributive
Hypovolemic Cardiogenic Obstructive
Parameter
shock shock shock
shock
CVP
(right-sided ↓ ↑ ↑ ↓
preload)
PCWP
(left-sided ↓ ↑ ↓* ↓
preload)
Cardiac index
↓ ↓ ↓ ↑**
(LV output)
SVR
↑ ↑ ↑ ↓
(afterload)
SvO2 ↓ ↓ ↓ ↑**
*In tamponade, left-sided preload is decreased, but measured PCWP is paradoxically increased
due to external compression by pericardial fluid.

**Cardiac index & SvO2 are usually decreased in neurogenic shock due to impaired sympathetic
reflexes.

CVP = central venous pressure; LV = left ventricular; PCWP = pulmonary capillary wedge


pressure; SvO2 = mixed venous oxygen saturation; SVR = systemic vascular resistance.
Diabetic ketoacidosis
 Young age
 Brittle type 1 diabetes mellitus
Patient characteristics
 May be initial manifestation of diabetes

 Acute to subacute onset


o Initial: polydipsia/polyuria, blurred vision, weight loss
Clinical symptoms o Later: altered mentation, hyperventilation, abdominal
pain

Diagnosis  ↑ Glucose (typically 300-800 mg/dL)


 Metabolic acidosis (bicarbonate <18 mEq/L)
 ↑ Anion gap
 Positive serum ketones

 High-flow IV fluids (normal saline)


 IV insulin
Treatment
 Follow & replace potassium

IV = intravenous.
Hyperosmolar hyperglycemic state
 Type 2 diabetes mellitus
Patient
 Older age
characteristics
 Gradual hyperglycemic symptoms (eg, polyuria, polydipsia)
Clinical
 Altered mentation (eg, coma, focal signs, seizures)
symptoms
 Glucose >600 mg/dL (frequently >1,000 mg/dL)
 Normal pH & bicarbonate
Laboratory  Normal anion gap
studies  Negative or small serum ketones
 Serum osmolality >320 mOsm/kg

 Aggressive hydration with normal saline*


Initial  Intravenous insulin
management  Potassium replacement if level is <5.3 mEq/L

*Normal saline for the first hour regardless of sodium levels; fluid choice may change thereafter.
Systemic small-vessel vasculitides
Usual vasculitic patterns &
Laboratory & biopsy findings
associated findings
Primary
 Palpable purpura, GN,
PN  ANCA (PR3 or MPO)
ANCA-associated  3 types with variable  Pauci-immune vasculitis (±
vasculitis lung, heart & sinus granulomas)
involvement

 Palpable purpura, GN,


 No serologic test
abdominal pain
IgA vasculitis (Henoch-  IgA immunofluorescence on
 More common in
Schönlein purpura) skin or kidney biopsy
children

 GN ± pulmonary
hemorrhage  Serum anti-GBM antibodies
Anti-GBM disease  No palpable purpura or  Linear IgG on kidney biopsy
PN
Secondary
 Palpable purpura, GN,
 +Cryoglobulins, +rheumatoid
PN
factor, low complement
Cryoglobulinemic  Hepatitis C, HIV,
 +Viral or autoimmune
vasculitis (MCS) autoimmune disease*
serologies
(SLE, RA)

 Most common cause,


can be seen with most  No specific test
drug classes  ± Antihistone or ANCA, low
Drug-induced vasculitis
 Often isolated to one complement
organ

*Vasculitis secondary to autoimmune disease can be mediated by either cryoglobulins or other


nonprecipitating immune complexes.

ANCA = antineutrophil cytoplasmic antibodies; GBM = glomerular basement membrane; GN =


glomerulonephritis; MCS = mixed cryoglobulinemia syndrome; MPO = myeloperoxidase; PN =
peripheral neuropathy; PR3 = proteinase 3; RA = rheumatoid arthritis; SLE = systemic lupus
erythematosus.
Antiphospholipid antibody syndrome
Venous or arterial thromboembolic disease

 Deep venous thrombosis


 Pulmonary embolism
 Ischemic stroke/transient ischemic attack

Clinical features  

Adverse pregnancy outcomes

 Unexplained embryonic or fetal loss


 Premature birth due to placental insufficiency or preeclampsia

 Lupus anticoagulant effect: paradoxical activated PTT prolongation


not reversed on plasma mixing studies
Laboratory  Presence of specific antiphospholipid antibodies
findings o Anticardiolipin antibody
o Anti-beta2-glycoprotein-I antibody

Mycobacterium avium complex


 M avium, M intracellulare
Epidemiology  Patients with advanced AIDS (CD4 <50/mm3)

Manifestations  Fever & weight loss


 Abdominal pain & diarrhea
 LAD & (often) hepatosplenomegaly
o ↑ Alkaline phosphatase

 Blood/lymph node culture → nontuberculous mycobacteria


Diagnosis
 Macrolide + ethambutol
Treatment  Primary prophylaxis (azithromycin) no longer recommended

LAD = lymphadenopathy.
Chronic mesenteric ischemia
 Atherosclerosis (smoking, dyslipidemia)
Etiology
 Crampy, postprandial epigastric pain
Clinical features  Food aversion & weight loss

 Signs of malnutrition, abdominal bruit


Diagnosis  CT angiography (preferred), Doppler ultrasonography

 Risk reduction (eg, tobacco reduction), nutritional support


Management  Endovascular or open surgical revascularization

Management of hypercalcemia
Short-term (immediate) treatment

 Normal saline hydration plus calcitonin


Severe  Avoid loop diuretics unless volume overload (heart failure) exists
(calcium >14 mg/dL)
or symptomatic Long-term treatment

 Bisphosphonate (zoledronic acid)

Moderate  Usually no immediate treatment required unless symptomatic


(calcium 12-14  Treatment is similar to that for severe hypercalcemia
mg/dL)
 No immediate treatment required
Asymptomatic or
 Avoid thiazide diuretics, lithium, volume depletion & prolonged
mild
bed rest
(calcium <12 mg/dL)
Differential diagnosis of myopathy
Pain & Creatine
Weakness ESR Other features
tenderness kinase
Glucocorticoid- Yes No Normal Normal  Prominent atrophy
induced myopathy
 Lower extremities
most affected

 Stiffness of shoulders
& hips with restricted
motion
Polymyalgia  Often coexists with
No Yes ↑ Normal
rheumatica GCA
 Rapid improvement
with glucocorticoids

 Multisystem
involvement (arthritis,
Polymyositis & Normal
Yes Uncommon ↑ rash, ILD)
dermatomyositis or ↑
 ↑ Malignancy risk

 Additive risk with


Statin-induced Normal or
Variable Yes Normal fibrates
myopathy ↑
 Delayed DTRs;
myoedema
 Hypothyroid
Hypothyroid
Yes Yes Normal ↑ symptoms &
myopathy
abnormal thyroid test
results

DTR = deep tendon reflex; ESR = erythrocyte sedimentation rate; GCA = giant cell arteritis;
ILD = interstitial lung disease.
Pemphigus vulgaris vs bullous pemphigoid
Pemphigus vulgaris Bullous pemphigoid
 40-60  >60
Age of onset
 Painful
 Flaccid bullae →  Pruritic
erosions  Tense bullae
Clinical features
 Mucosal involvement  Mucosal involvement rare
common

 Intraepidermal cleavage  Subepidermal cleavage


Histology
 Linear IgG against
 Net-like intercellular
hemidesmosomes along
Immunofluorescence IgG against desmosomes
basement membrane

Treatment of urinary tract infection in nonpregnant women


 Nitrofurantoin
 Trimethoprim-sulfamethoxazole
Uncomplicated  Fosfomycin (single dose)
UTI  Fluoroquinolones only if previous options cannot be used
 Urine culture only if initial treatment fails

 Outpatient: fluoroquinolones
 Inpatient: ceftriaxone, piperacillin-tazobactam, carbapenems (eg,
Complicated imipenem)
UTI*  Culture obtained prior to therapy, with adjustment  of  antibiotic as
needed

*Infection above the bladder (eg, pyelonephritis), pelvic pain in men, other signs or symptoms of
systemic illness.

UTI = urinary tract infection.


Renal vein thrombosis
 Hypercoagulability
o Nephrotic syndrome (particularly membranous nephropathy)
o Malignancy (particularly renal cell)
Causes
o Other (eg, inherited thrombophilia, oral contraceptive pills)
 Trauma

 Acute: renal infarction symptoms (flank pain, hematuria, ↑ LDH, ↑


kidney size on imaging)
Clinical
 Chronic: renal symptoms typically absent  (may cause pulmonary
features
embolus)

 CT scan or MR angiography
Diagnosis  Renal venography

 Anticoagulation
Treatment  Local thrombolysis/thrombectomy (if AKI present)

AKI = acute kidney injury; LDH = lactate dehydrogenase.


Toxoplasma encephalitis
 Headache
 Confusion
Symptoms  Fever
 Focal neurologic deficits/seizures

 AIDS with CD4 count <100/mm3


 Positive Toxoplasma gondii IgG
Diagnosis
 Multiple ring-enhancing brain lesions (MRI)
 Sulfadiazine & pyrimethamine (plus
leucovorin)
 Antiretroviral initiation within 2 weeks
Treatment
 Prophylaxis: TMP-SMX (CD4 count
<100/mm3)

TMP-SMX = trimethoprim-sulfamethoxazole.
IgA nephropathy APSGN
 Several days after upper  Weeks after group A
respiratory tract infection or Streptococcus infection (eg,
spontaneous pharyngitis, impetigo)
Onset
 Most common in young  Most common in school-aged
adults children

 IgA-based immune complex  Immune complex deposition


Pathogenesis deposition in mesangium along GBM (ie, subepithelial)

 Gross hematuria (often  Gross hematuria


recurrent)  Edema (periorbital or
 ± Flank pain, low-grade generalized)
Clinical features
fever, hypertension  Hypertension
 May be asymptomatic  May be asymptomatic

 Urinalysis: + protein, RBCs,


 Urinalysis: + protein, RBCs,
RBC casts
RBC casts
 Serum:
 Serum:
Laboratory findings o ↓ C3 & CH50
o Normal C3 & C4
o ↓ Or normal C4
o ↑ Creatinine
o ↑ Creatinine

APSGN = acute poststreptococcal glomerulonephritis; CH50 = total complement; GBM =


glomerular basement membrane; RBC = red blood cell.
Guillain-Barré syndrome
 Immune-mediated demyelinating polyneuropathy
Pathophysiology  Preceding gastrointestinal (Campylobacter) or respiratory infection

 Paresthesia, neuropathic pain


 Symmetric, ascending weakness
 Decreased/absent deep tendon reflexes
Clinical features
 Autonomic dysfunction (eg, arrhythmia, ileus)
 Respiratory compromise

Diagnosis  Clinical
 Supportive findings
o Cerebrospinal fluid: ↑ protein, normal leukocytes
o Abnormal electromyography & nerve conduction
o MRI: normal or enhancement of anterior nerve roots/cauda
equina

 Monitoring of autonomic & respiratory function


Management  Intravenous immunoglobulin or plasmapheresis 

Clinical features of hypopituitarism


 Pituitary causes
o Primary (eg, adenoma) or metastatic mass
o Infiltration (eg, hemochromatosis, lymphocytic hypophysitis)
o Hemorrhage (pituitary apoplexy) or infarction (Sheehan
syndrome)
 Hypothalamic causes
Etiology
o Mass lesions
o Radiation therapy
o Infiltration (sarcoidosis)
o Trauma to skull base
o Infections (tuberculosis meningitis)

 ACTH deficiency (secondary adrenal insufficiency)


o Postural hypotension, tachycardia, fatigue, weight loss,
hypoglycemia, eosinophilia
 Hypothyroidism (central)
Clinical o Fatigue, cold intolerance, constipation, dry skin, bradycardia,
presentation slowed deep tendon reflexes
 Gonadotropins
o Women: Amenorrhea, infertility
o Men: Infertility, loss of libido

Clinical features of paroxysmal nocturnal hemoglobinuria


 Hemolysis → fatigue

Clinical  Cytopenias (impaired hematopoiesis)


manifestations
 Venous thrombosis (intraabdominal, cerebral veins)

 Complete blood count (hypoplastic/aplastic anemia,


thrombocytopenia, leukopenia)
 Elevated lactate dehydrogenase and low haptoglobin
(hemolysis)
Workup
 Indirect hyperbilirubinemia
 Urinalysis (hemoglobinuria)
 Flow cytometry (absence of CD55 & CD59)
 Iron & folate supplementation
 Eculizumab (monoclonal antibody that inhibits
Treatment
complement activation)

Comparison of left ventricular & right ventricular myocardial infarction


Left ventricular MI Right ventricular MI
 Pulmonary edema  Clear lungs & JVD
Clinical features  S3 & S4  Marked hypotension

 Inferior ischemic changes


 Ischemic changes in
 ST-segment elevation in
anterior, lateral, or inferior
ECG findings V4R
leads
 Bradyarrhythmias

 ↑ LV & RV preload  ↑ RV preload, ↓ LV preload


Hemodynamic findings  ↑ SVR  ↑ SVR

 Fluid restriction
 Fluid resuscitation
 Preload & afterload
 Avoid preload reduction
Management reduction
 Reperfusion therapy
 Reperfusion therapy

JVD = jugular venous distension; LV = left ventricular; MI = myocardial infarction; RV = right


ventricular; SVR = systemic vascular resistance.
Alcohol withdrawal syndrome
Onset since last
Manifestations Symptoms/signs
drink (hr)
Mild Anxiety, insomnia, tremors, diaphoresis, palpitations,
6-24
withdrawal gastrointestinal upset, intact orientation
Seizures Single or multiple generalized tonic-clonic 12-48
Alcoholic Visual, auditory, or tactile; intact orientation; stable vital
12-48
hallucinosis signs
Delirium Confusion, agitation, fever, tachycardia, hypertension,
48-96
tremens diaphoresis, hallucinations
Rhabdomyolysis
Skeletal muscle lysis/necrosis due to:

 Crush injury or prolonged immobilization


Etiology
 Intense muscle activity (eg, seizure, exertion)
 Drug/medication toxicity (eg, statins)

Clinical features  Muscle pain & weakness


 Dark urine (myoglobinuria/pigmenturia)
 + Blood on urinalysis & no RBCs on microscopy
 ↑ Serum K & PO4, ↓ serum Ca, ↑ AST > ALT
 Acute kidney injury

 Serum creatine kinase >1,000 U/L


Diagnosis  Consistent clinical features

 Aggressive intravenous fluid resuscitation


Management  Sodium bicarbonate in some cases

ALT = alanine aminotransferase; AST = aspartate aminotransferase; RBCs = red blood cells.
AIDS-defining malignancies
Malignancy Viral association
Kaposi sarcoma Human herpesvirus 8
Invasive cervical carcinoma Human papillomavirus
Non-Hodgkin lymphoma Epstein-Barr virus
Primary CNS lymphoma Epstein-Barr virus

Progressive multifocal leukoencephalopathy


 JC virus reactivation
Epidemiology  Severe immunosuppression (eg, untreated AIDS)

 Confusion, paresis, ataxia, seizure


Manifestations
 MRI/CT of the brain with contrast: asymmetric white
matter lesions; no enhancement/edema
Diagnosis  Lumbar puncture: CSF PCR positive for JC virus
 Brain biopsy (rarely needed)

 Often fatal
Treatment  If HIV positive: antiretroviral therapy

CSF = cerebrospinal fluid.


Focal segmental glomerulosclerosis
 Primary FSGS: circulating factor causing immune injury to
podocytes
 Secondary FSGS: glomerular hyperfiltration (eg, obesity,
Pathogenesis
solitary kidney, reflux nephropathy), podocyte toxin (eg,
heroin), infection (eg, HIVAN)

 Primary FSGS: usually nephrotic syndrome*


Clinical features  Secondary FSGS: proteinuria ± nephrotic syndrome

Diagnosis  LM: segmental scarring in <50% of glomeruli**


 IF: usually negative
 EM: podocyte foot process effacement

 Renin-angiotensin blockade, loop diuretics


 Primary FSGS: immunosuppression
Treatment  Secondary FSGS: risk factor modification (eg, weight loss,
ART)

*Proteinuria >3.5 g/day, generalized edema & hypoalbuminemia.

**Glomerular tuft collapse is also seen in HIVAN.

ART = antiretroviral therapy; EM = electron microscopy; FSGS = focal segmental


glomerulosclerosis; HIVAN = HIV-associated nephropathy; IF = immunofluorescence
microscopy; LM = light microscopy.

Acute bacterial prostatitis


 Intraprostatic reflux of pathogens in urine
Etiology  Primarily gram-negative bacilli (Escherichia coli ~75%)

 Flu-like illness (eg, fever, chills, malaise, myalgia)


 Lower urinary symptoms (eg, dysuria, urine retention, pelvic
Manifestations
pain)

 Digital rectal examination: tender, swollen prostate


Diagnosis  Urine culture

 6 weeks of TMP-SMX or fluoroquinolone


Treatment
 Bacteremia/systemic spread
 Prostatic abscess
Complications
 Chronic prostatitis

TMP-SMX = trimethoprim-sulfamethoxazole.
Paget disease of bone
 Most patients are asymptomatic
 Bone pain & deformity
o Skull: headache, hearing loss
Clinical
o Spine: spinal stenosis, radiculopathy
features
o Long bones: bowing, fracture, arthritis of adjacent joints
 Giant cell tumor, osteosarcoma

Pathogenesis  Osteoclast dysfunction


 Increased bone turnover

 Elevated alkaline phosphatase


Laboratory  Elevated bone turnover markers (eg, PINP, urine hydroxyproline)
testing  Calcium & phosphorus: usually normal

 X-ray: osteolytic or mixed lytic/sclerotic lesions


Imaging  Bone scan: focal increase in uptake

 Bisphosphonates
Treatment
PINP = procollagen type I N-terminal propeptide.

Tumor lysis syndrome


 Tumors with high cell burden or rapid turnover
Risk  Combination chemotherapy/immunotherapy

 Severe electrolyte abnormalities


o ↑ Phosphorus, potassium, uric acid
o ↓ Calcium
Manifestations  Acute kidney injury
 Cardiac arrhythmias
 Seizures

 Intravenous fluids
Prophylaxis  Xanthine oxidase inhibitor* or rasburicase

 Intravenous fluids + rasburicase


 Continuous telemetry
Treatment
 Aggressive electrolyte monitoring & treatment

*Allopurinol or febuxostat.

Effect of maneuvers on hypertrophic cardiomyopathy


Left ventricular
Physiologic effect Murmur intensity
blood volume
Valsalva
(strain phase)
Abrupt
↓ Preload ↓ ↑
standing
Nitroglycerin
administration
Sustained ↑ Afterload ↑ ↓
hand grip
Squatting ↑ Afterload & preload
Passive
↑ Preload
leg raise
Toxic alcohol ingestion (methanol or ethylene glycol)
 Methanol: windshield wiper fluid, contaminated homemade liquor
 Ethylene glycol: automotive coolant/antifreeze, brake fluid
Typical sources  Industrial solvents & deicing solutions may contain either toxic
alcohol

 Early: CNS sedation & inebriation, osmolar gap


 Late: anion gap metabolic acidosis, compensatory tachypnea
Clinical features o Ocular toxicity (methanol)
o Urine oxalate crystals, hypocalcemia, AKI (ethylene glycol)

 Fomepizole (inhibits ADHase) is preferred therapy


 Ethanol solution (competes for ADHase) if fomepizole unavailable
Management  IV sodium bicarbonate for acidemia (eg, pH <7.3)
 Hemodialysis for severe cases (eg, acidosis, end-organ damage)

ADHase = alcohol dehydrogenase; AKI = acute kidney injury; IV = intravenous.


Common agents with anticholinergic properties
 Diphenhydramine, cyproheptadine
Antihistamines
 1st generation: chlorpromazine, haloperidol
 2nd generation: clozapine
Psychotropics
 Tricyclic antidepressants: amitriptyline, clomipramine

 Benztropine, trihexyphenidyl
Antiparkinson
 Ipratropium (bronchodilator)
 Oxybutynin, darifenacin (overactive bladder)
Antimuscarinic  Dicyclomine, hyoscyamine (antispasmodics)
 Scopolamine (antiemetic)

 Atropine, cyclopentolate
Mydriatics
 Muscarinic mushroom species
 Jimsonweed
Plant-based
 Nightshade species

Common causes of vertigo


 Recurrent episodes lasting 20 minutes to several hours
 Sensorineural hearing loss
Ménière disease
 Tinnitus &/or feeling of fullness in the ear
 Brief episodes triggered by head movement
BPPV  Dix-Hallpike maneuver causes nystagmus

 Acute, single episode that can last days


Vestibular  Often follows viral syndrome
neuritis  Abnormal head thrust test

 Vertigo associated with headache or other migrainous phenomenon


(eg, visual aura)
Migraine
 Symptoms resolve completely between episodes

 Sudden-onset, persistent vertigo


Brainstem/
 Usually other neurologic symptoms
cerebellar stroke
BPPV = benign paroxysmal positional vertigo.
Wernicke encephalopathy
 Chronic alcoholism (most common)
 Malnutrition (eg, anorexia nervosa)
Associated conditions
 Hyperemesis gravidarum

 Thiamine deficiency
Pathophysiology
 Encephalopathy
 Oculomotor dysfunction (eg, horizontal nystagmus
Clinical features & bilateral abducens palsy)
 Postural & gait ataxia

 Intravenous thiamine followed by glucose infusion


Treatment
Hypokalemic, hypochloremic metabolic alkalosis
 Gastric suction or severe vomiting
Common etiologies  Loop or thiazide diuretic overuse

 Gastric or renal H+ losses initiate alkalosis


 Volume depletion activates RAAS
 ↑ Renal K+ & H+ losses cause hypokalemia & worsen alkalosis
Pathophysiology
 Relatively greater loss of Cl− than Na+ → profound Cl− depletion
 ↓ Cl− impairs renal HCO3− excretion to perpetuate alkalosis

 Remove or treat initiating factor


Management  Cl− replenishment with normal saline corrects alkalosis

RAAS = renin-angiotensin-aldosterone system.


Common skin infections
Infection Organism Manifestations
 Superficial dermis & lymphatics
 Streptococcus  Raised, sharply demarcated edges
Erysipelas pyogenes  Rapid spread & onset
 Fever early in course

 Deep dermis & subcutaneous fat


 S pyogenes  Flat edges with poor demarcation
Cellulitis
 MSSA  Indolent (over days)
(nonpurulent)
 Localized (fever later in course)

 Purulent drainage
 Folliculitis: infected hair follicle
 MSSA
 Furuncles: folliculitis → dermis →
Cellulitis (purulent)  MRSA
abscess

 Carbuncle: multiple furuncles

MRSA = methicillin-resistant Staphylococcus aureus; MSSA = methicillin-sensitive S aureus.


Features of glucagonoma
 Weight loss
 Necrolytic migratory erythema: erythematous papules that coalesce
Clinical to form large, indurated plaques with central clearing
presentation  Diabetes mellitus/hyperglycemia
 Gastrointestinal symptoms (eg, diarrhea, anorexia, abdominal pain)

 Markedly elevated glucagon level


Diagnosis  Abdominal imaging (MRI or CT scan)

Clinical manifestations of amyloidosis (primary & secondary)


 Heavy proteinuria with nephrotic syndrome
Renal  Peripheral edema

 Restrictive cardiomyopathy
Cardiac  Conduction defects, low voltage

 Peripheral &/or autonomic neuropathy


CNS  Stroke

 Hepatomegaly
 Dysmotility, malabsorption
GI
 GI bleeding due to vascular fragility

Pulmonary  Pulmonary nodules, tracheobronchial infiltration, pleural effusions


 Enlarged tongue, shoulder pad enlargement
Musculoskeletal
 Thickening of skin, subcutaneous nodules/plaques
Skin  Ecchymoses, periorbital purpura

 Anemia, thrombocytopenia
Heme
CNS = central nervous system; GI = gastrointestinal.
 
Overview of subarachnoid hemorrhage
 Ruptured arterial saccular (berry) aneurysm (most common)
 Severe headache at onset of neurologic symptoms
Clinical features  Meningeal irritation (eg, neck stiffness)
 Focal deficits can be present

 Rebleeding (1st 24 hr)


 Delayed cerebral ischemia due to vasospasm (after 3 days)
 Obstructive hydrocephalus/increased ICP
Complications
 Seizures
 Hyponatremia (usually from SIADH)

 Noncontrast CT scan of the head initially


 Lumbar puncture required to definitively rule out SAH if CT scan is
negative
Diagnosis
 Xanthochromia in CSF confirms diagnosis
 Cerebral angiography to identify bleeding source

 Angiographic procedure to stabilize aneurysm (coiling or clipping)


Treatment  Nimodipine & euvolemia to reduce delayed cerebral ischemia

CSF = cerebrospinal fluid; ICP = intracranial pressure; SAH = subarachnoid hemorrhage;


SIADH = syndrome of inappropriate antidiuretic hormone secretion.
 
Acute aortic dissection
 Chronic hypertension (strongest overall risk factor)
 Underlying aortopathy (eg, Marfan syndrome)
Risk factors
 Cocaine use

 Severe, tearing chest or back pain, maximal at onset


 ± Variation in SBP between arms >20 mm Hg
Clinical presentation
 Hypertension usually present*

Diagnosis  ECG: normal or nonspecific ST-segment & T-wave changes


 Chest x-ray: mediastinal widening
 CT angiography or TEE for definitive diagnosis

 Pain control (eg, morphine)


 Intravenous beta blockers (eg, esmolol)
Treatment  ± Sodium nitroprusside (if SBP >120 mm Hg)
 Emergency surgical repair for ascending dissection

*Hypotension on presentation suggests aortic rupture or other complication (eg, cardiac


tamponade, acute aortic regurgitation).

SBP = systolic blood pressure; TEE = transesophageal echocardiography.


Amyloidosis
 Extracellular deposition of insoluble protein fibrils
o AL:  produced by clonal plasma cells
o AA:  secondary to chronic inflammation
Etiology
o ATTR:  age-related or hereditary
o AB2-m:  dialysis-related

 Nephrotic syndrome (AL & AA)


 Hepatomegaly with/without splenomegaly (AL & AA)
Clinical  Restrictive cardiomyopathy (AL & ATTR)
 CTS, scapulohumeral periarthritis (AB2-m)
presentation*  Peripheral/autonomic neuropathy
 Periorbital purpura, waxy skin, macroglossia

*Clinical presentation varies depending on the type of amyloid present.

AA = amyloid A; AB2-m = amyloid beta2-microglobulin; AL = amyloid light chain;


ATTR = amyloid transthyretin; CTS = carpal tunnel syndrome.
Mechanical complications of acute myocardial infarction
Involved
Time Echocardiography
Complication coronary Clinical findings
course findings
artery
 Severe pulmonary edema,
respiratory distress
Papillary muscle Acute or  New early systolic
rupture/ within 3- RCA murmur Severe MR
dysfunction 5 days  Hypotension/cardiogenic
shock

Interventricular Acute or LAD  Chest pain Left-to-right


septum rupture within 3- (apical  New holosystolic murmur ventricular shunt**
5 days septal) or  Hypotension/cardiogenic
RCA (basal
shock
septal)
 Chest pain
Within 5
 Distant heart sounds Pericardial
days* or
Free wall rupture LAD  Shock, rapid progression effusion with
up to 2
to cardiac arrest tamponade
weeks
 Heart failure
Up to
Left ventricular  Angina Thin & dyskinetic
several LAD
aneurysm  Ventricular arrhythmias myocardial wall
months
*50% occur within 5 days.

**Right heart catheterization shows step up in O2 concentration from right atrium to right
ventricle.

LAD = left anterior descending; MR = mitral regurgitation; RCA = right coronary artery.
Acute pericarditis
 Viral or idiopathic
 Autoimmune disease (eg, SLE)
 Uremia (acute or chronic renal failure)
Etiology  Post myocardial infarction
o Early: peri-infarction pericarditis
o Late: Dressler syndrome

 Pleuritic chest pain (↓ when sitting) ± fever


 Pericardial friction rub (highly specific)
Clinical features
 ECG: diffuse ST-segment elevation & PR-segment
& diagnosis
depression
 Echocardiography: pericardial effusion

 NSAIDs & colchicine for viral or idiopathic etiology


Treatment  Variable for other etiologies

NSAIDs = nonsteroidal anti-inflammatory drugs; SLE = systemic lupus erythematosus.


Common hereditary cancer syndromes
Syndrome Associated neoplasms
 Colorectal cancer
 Endometrial cancer
Lynch syndrome
 Ovarian cancer

Familial adenomatous polyposis  Colorectal cancer


 Desmoids & osteomas
 Brain tumors

 Hemangioblastomas
 Clear cell renal carcinoma
von Hippel-Lindau syndrome
 Pheochromocytoma

 Parathyroid adenomas
 Pituitary adenomas
Multiple endocrine neoplasia type 1
 Pancreatic adenomas

 Medullary thyroid cancer


 Pheochromocytoma
Multiple endocrine neoplasia type 2
 Parathyroid hyperplasia (type 2A)

 Breast cancer
BRCA1 & BRCA2  Ovarian cancer

Bullous pemphigoid
 Age >60
 Pruritic, tense bullae
Clinical
 Rare mucosal involvement
features
 Prodrome of eczematous/urticaria-like rash

 Dementia
Associated
 Parkinson disease
 Depression, bipolar disorder
disorders
 Histology: subepidermal cleavage
 Immunofluorescence: linear IgG/C3 deposition along basement membrane
Diagnosis
 Serology: autoantibodies to bullous pemphigoid antigens (hemidesmosomes)

 Topical therapies: high-potency corticosteroids


Treatment  Systemic therapies: corticosteroid, doxycycline

Stevens-Johnson syndrome & toxic epidermal necrolysis


<10% of BSA:   SJS

Nomenclature       10%-30%:   SJS/TEN overlap

            >30%:   TEN


Clinical  4-28 days after exposure to trigger (2 days after repeat exposure)
features  Acute influenza-like prodrome
 Rapid-onset erythematous macules, vesicles, bullae
 Necrosis & sloughing of epidermis
 Mucosal involvement

Drugs

 Allopurinol
 Antibiotics (eg, sulfonamides)
 Anticonvulsants (eg, carbamazepine, lamotrigine, phenytoin)
 NSAIDs (eg, piroxicam)
Common  Sulfasalazine
triggers
Other

 Mycoplasma pneumoniae
 Vaccination
 Graft versus host disease

BSA = body surface area; NSAIDs = nonsteroidal anti-inflammatory drugs;


SJS = Stevens-Johnson syndrome; TEN = toxic epidermal necrolysis.
Common causes of primary acid-base disturbance
Elevated anion gap

 Poor tissue perfusion (ie, lactic acidosis)


 Diabetic ketoacidosis
 Renal failure (ie, uremia)
 Certain toxicities (eg, methanol, ethylene glycol)
Metabolic acidosis
Normal anion gap

 Severe diarrhea
 Renal tubular acidosis
 Excess normal saline infusion

 Nasogastric suctioning or severe vomiting


 Diuretic overuse
Metabolic alkalosis
 Primary hyperaldosteronism

 Central respiratory depression (eg, opioid overdose)


Respiratory acidosis
 OHS, neuromuscular weakness
 Chronic obstructive pulmonary disease
(hypoventilation)
Respiratory alkalosis  Acute V/Q mismatch (eg, PE, pneumonia)

(hyperventilation)  Anxiety, inadequate pain control


 High altitude, pregnancy

OHS = obesity hypoventilation syndrome; PE = pulmonary embolism;


V/Q = ventilation/perfusion.
Multiple endocrine neoplasia type 1
Manifestation Clinical features
 Secretion of prolactin, growth hormone, ACTH (or
Pituitary adenomas “nonfunctioning” tumors)
(10%-20%)  Mass effects (eg, headache, visual field defects)

 Multiple parathyroid adenomas or parathyroid


hyperplasia
Primary hyperparathyroidism
 Hypercalcemia (eg, polyuria, kidney stones,
(>90%)
decreased bone density)

 Gastrinoma - recurrent peptic ulcers


 Insulinoma - hypoglycemia
Pancreatic/gastrointestinal  VIPoma - secretory diarrhea, hypokalemia,
neuroendocrine tumors hypochlorhydria
(60%-70%)  Glucagonoma - weight loss, necrolytic migratory
erythema, hyperglycemia

Mixed primary acid-base disorders


HCO3− PaCO2 pH Example
Metabolic acidosis + Sepsis (lactic acidosis)
↓ ↑ Very low
respiratory acidosis with respiratory failure
Metabolic alkalosis + Hyperemesis gravidarum &
↑ ↓ Very high
respiratory alkalosis hyperventilation of pregnancy
Metabolic acidosis +
↓ ↓ Near normal Salicylate toxicity
respiratory alkalosis
Metabolic alkalosis + Overdiuresed heart failure
↑ ↑ Near normal
respiratory acidosis & underlying COPD
Metabolic acidosis +
Diabetic ketoacidosis
↔ ↔ Near normal
with severe vomiting
metabolic alkalosis
COPD = chronic obstructive pulmonary disease.
Common drugs associated with photosensitivity reactions
Antibiotics Tetracyclines (eg, doxycycline)
Antipsychotics Chlorpromazine, prochlorperazine
Diuretics Furosemide, hydrochlorothiazide
Others Amiodarone, promethazine, piroxicam
Features of carcinoid syndrome
Clinical  Skin: flushing, telangiectasias, cyanosis
manifestations  Gastrointestinal: diarrhea, cramping
 Cardiac: valvular lesions (right > left side)
 Pulmonary: bronchospasm
 Miscellaneous: niacin deficiency (dermatitis,
diarrhea, dementia)

 Elevated 24-hr urinary excretion of 5-HIAA


 CT scan/MRI of abdomen & pelvis to
localize tumor
Diagnosis  OctreoScan to detect metastases
 Echocardiogram (if symptoms of carcinoid
heart disease are present)

 Octreotide for symptomatic patients & prior


to surgery/anesthesia
Treatment
 Surgery for liver metastases

Tinea corporis (ringworm)


 Athletes who have skin-to-skin contact
 Humid environment
Risk factors
 Contact with infected animals (eg, rodents)

 Scaly, erythematous, pruritic patch with


centrifugal spread
Presentation  Subsequent central clearing with raised, annular
border

 First-line/localized: topical antifungals


(eg, clotrimazole, terbinafine)
Treatment
 Second-line/extensive: oral antifungals
(eg, terbinafine, griseofulvin)

 
Thyrotoxicosis with normal or ↑
Thyrotoxicosis with ↓ RAIU
RAIU
 Painless (silent) thyroiditis
 Subacute (de Quervain) thyroiditis
 Amiodarone-induced thyroiditis
 Graves disease
 Excessive dose (or surreptitious intake) of
 Toxic multinodular goiter
levothyroxine
 Toxic nodule
 Struma ovarii
 Iodine-induced
 Extensive thyroid cancer metastasis

RAIU = radioactive iodine uptake.


Budd-Chiari syndrome
 Hepatic venous outflow obstruction
 Usually due to:
o Myeloproliferative disorder (eg, PV)
Etiology
o Malignancy (eg, hepatocellular carcinoma)
o Oral contraception use/pregnancy

 Acute
Jaundice, hepatic encephalopathy, variceal bleeding
o
Prolonged INR/PTT; elevated transaminases
o
 Subacute/chronic
Manifestations
o Vague, progressive abdominal pain
o Hepatomegaly, splenomegaly, ascites
o Mild/moderate elevation in bilirubin, transaminases

 Abdominal Doppler ultrasound – ↓ hepatic vein flow


Diagnosis  Investigation for underlying disorders (eg, JAK2 testing for PV)

INR = international normalized ratio; PTT = partial thromboplastin time; PV =


polycythemia vera.
Clinical features of asbestosis
 Prolonged asbestos exposure (eg, shipyard, mining)
 Symptoms develop ≥20 years after initial exposure
Clinical presentation  Progressive dyspnea, basilar fine crackles, clubbing
 Increased risk for lung cancer & mesothelioma

 Pleural plaques on chest imaging


Diagnostic evaluation  Imaging, PFT & histology consistent with pulmonary fibrosis

PFT = pulmonary function testing.


Spinal cord compression
 Mechanical (eg, disc herniation, spinal stenosis)
 Malignancy (eg, lung, breast, prostate cancers)
Causes
 Infection (eg, epidural abscess)

 Gradually worsening, severe back pain


Symptoms  Pain worse in recumbent position/at night

Physical  Early signs


examination o Symmetric extremity weakness
o ↓ Deep tendon reflexes

 Late signs
o ↓ Rectal tone
o ↑ Deep tendon reflexes, bilateral Babinski reflex
o Paralysis

 Emergency MRI of the spine


 Emergency surgical ± radiation oncology consultation
Management  Intravenous glucocorticoids (eg, malignancy) or antibiotics (eg,
infection)

Diagnostic approach to abnormal liver function tests


 Detailed alcohol intake assessment (frequency, quantity)
 Hepatitis risk factor assessment (eg, sexual history)
History  Medication review (eg, acetaminophen, supplement use)
 Family history (eg, autoimmune disease)

 Assess for:
o Stigmata of cirrhosis (eg, palmar erythema, spider
angiomata)
Physical
o Signs of malignancy (eg, lymph node enlargement)
examination
o Volume overload (eg, elevated jugular venous pressure)
o Visceral obesity (eg, truncal obesity)

 Selective laboratory testing based on risk factors


 Hepatocellular pattern: viral serologies, antinuclear antibody, iron
studies
Diagnostic testing
 Cholestatic pattern: γ-glutamyltransferase, pancreatic enzymes, liver
ultrasonography

Polycythemia vera
 ↑ Blood viscosity
o Hypertension
o Erythromelalgia (burning cyanosis in hands/feet)
o Transient visual disturbances
Manifestations
 ↑ RBC turnover (gouty arthritis)
 Aquagenic pruritus
 Bleeding

 Facial plethora (ruddy cyanosis)


Examination  Splenomegaly

   Elevated hemoglobin
 Leukocytosis & thrombocytosis
Laboratory  Low erythropoietin level
 JAK2 mutation positive
findings
 Thrombosis
Complications  Myelofibrosis & acute leukemia

 Phlebotomy
Treatment  Hydroxyurea (if ↑ risk of thrombus)

RBC = red blood cell.


Causes of acute, painless vision loss
Diagnosis Symptoms Clinical findings Management
 Possible
intraarterial
 Severe vision
thrombolytics
loss with  Pale fundus
Central retinal  Ocular massage
temporal sparing with cherry-red
artery  Reduction of IOP
 History of spot
occlusion (eg, anterior
amaurosis fugax
chamber
paracentesis)

 Fundus with
retinal  Observation ±
 Blurred vision to hemorrhages & intravitreal
Central retinal
severe vision loss optic disc injection of VEGF
vein occlusion
edema ("blood inhibitors
& thunder")

 Floaters,  Fundus with


photopsia vitreous  Surgical correction
(flashing lights) hemorrhage & (eg, retinopexy,
Retinal
 Progressive marked vitrectomy)
detachment
visual field elevation of typically required
defect retina

 ↓ or absent red
 Bed rest, HOB
reflex
 Hazy vision ± elevation 30-45
 RBCs/floating
red hue or vision degrees
Vitreous debris in
loss  Photocoagulation
hemorrhage vitreous,
 Floaters/shadows or vitrectomy in
obscured view
some cases
of fundus

HOB = head-of-bed; IOP = intraocular pressure; RBCs = red blood cells; VEGF = vascular


endothelial growth factor.
Spontaneous bacterial peritonitis
Clinical presentation  Temperature >37.8 C (100 F)
 Abdominal pain/tenderness
 Altered mental status (abnormal connect-the-numbers test)
 Hypotension, hypothermia, paralytic ileus with severe infection

 PMNs >250/mm3
 Positive culture, often gram-negative organisms (eg,
Diagnosis from ascitic Escherichia coli, Klebsiella)
fluid  Protein <1 g/dL
 SAAG >1.1 g/dL

 Empiric antibiotics - third-generation cephalosporins (eg,


cefotaxime)
Treatment
 Fluoroquinolones for SBP prophylaxis

PMN = polymorphonuclear leukocytes; SAAG = serum-ascites albumin gradient; SBP=


spontaneous bacterial peritonitis.
Hairy cell leukemia
 Clonal B-cell neoplasm
 Middle-age/older adults
Features
 BRAF mutation

 Pancytopenia due to bone marrow fibrosis


o Granulocytopenia (infections)
o Anemia (fatigue, weakness)
Manifestations o Thrombocytopenia (bleeding, bruising)
 Splenomegaly (early satiety)
 Hepatomegaly/lymphadenopathy rare

 Peripheral smear – "hairy" leukocyte cells


Diagnosis  Bone marrow biopsy with flow cytometry

 Chemotherapy (for moderate/severe)


Treatment
 Life expectancy is often near-normal

Infectious mononucleosis
 Epstein-Barr virus most common
Etiology
 Fever
 Tonsillitis/pharyngitis ± exudates
 Posterior or diffuse cervical lymphadenopathy
Clinical features  Significant fatigue
 ± Hepatosplenomegaly
 ± Rash after amoxicillin

Diagnostic  Positive heterophile antibody (Monospot) test (25% false-negative


rate during 1st week of illness)
 Atypical lymphocytosis
findings
 Transient hepatitis

 Avoid sports for ≥3 weeks (contact sports ≥4 weeks) due to the risk of
Management splenic rupture

Comparison of leukemoid reaction & chronic myeloid leukemia (CML)


Leukemoid reaction CML
Elevated
Leukocyte count >50,000/mm3 (>50 × 109)
(often >100,000/mm3 [>100 × 109])
Cause Severe infection BCR-ABL fusion
LAP score High Low
More mature Less mature
Neutrophil precursors
(metamyelocytes > myelocytes) (metamyelocytes < myelocytes)
Absolute basophilia Not present Present
LAP = leukocyte alkaline phosphatase.
Nonalcoholic fatty liver disease
 Hepatic steatosis on imaging or biopsy
Definition  Exclusion of other etiologies (eg, alcohol, hepatitis C, glucocorticoids)

 Mostly asymptomatic
 Metabolic syndrome
Clinical
 AST/ALT ratio <1
features
 Hyperechoic texture on ultrasound examination

 Weight loss (eg, diet modification, exercise)


Treatment  Consider bariatric surgery if BMI ≥35

 Hepatic fibrosis associated with increased risk for cirrhosis & liver-
Prognosis related death

ALT = alanine aminotransferase; AST = aspartate aminotransferase.


IgM IgG
Anti- Anti-
HBsAg HBeAg HBV DNA
anti- anti- HBs HBe
HBc HBc
Acute HBV
Early phase + + + +++
Window phase + +
Recovery phase + + + Likely +
Chronic HBV carrier + +
Acute flare of chronic HBV + Likely + + + +
Vaccinated for HBV +
Immune due to natural HBV
+ +
infection
anti-HBc = hepatitis B core antibody; anti-HBe = hepatitis B e antibody; anti-HBs = hepatitis B surface
antibody; HBeAg = hepatitis B e antigen; HBsAg = hepatitis B surface antigen; HBV = hepatitis B virus.
Chronic lymphocytic leukemia
 Lymphadenopathy (cervical, supraclavicular, axillary)
 Hepatosplenomegaly
Clinical features  Mild thrombocytopenia & anemia
 Often asymptomatic

 Severe lymphocytosis & smudge cells


 Flow cytometry
Diagnosis
 Lymph node & bone marrow biopsy not generally needed

 Median survival 10 years


 Worse prognosis with:
o Multiple chain lymphadenopathy
Prognosis
o Hepatosplenomegaly
o Anemia & thrombocytopenia

 Infection
 Autoimmune hemolytic anemia
Complications
 Secondary malignancies (eg, Richter syndrome)

Hypokalemia
 Diuretic therapy (eg, thiazides)
 Vomiting/diarrhea
 Hypomagnesemia
Etiologies  Hyperaldosteronism
 Increased beta-adrenergic activity
(eg, albuterol)

 Muscle weakness & cramps


Clinical  Hyporeflexia
 Rhabdomyolysis
features  Cardiac palpitations/arrhythmias

 Broad, flat T waves


ECG
 Prominent U waves
findings
 Potassium replacement
Treatment
Invasive aspergillosis Chronic pulmonary aspergillosis*
Risk factors  Immunocompromise  Lung disease/damage
(neutropenia, glucocorticoids,
HIV) (cavitary tuberculosis)

 Triad of fever, chest pain,


 >3 months: weight loss
hemoptysis
(>90%), cough, hemoptysis,
 Pulmonary nodules with halo
fatigue
sign
Manifestations  Cavity lesion ± fungus ball
 Positive cultures
 Positive Aspergillus IgG
 Positive cell wall biomarkers
serology
(galactomannan, β-D-glucan)

 Resect aspergilloma (if


possible)
 Azole medication
 Voriconazole ± caspofungin
Management (voriconazole)
 Embolization (if severe
hemoptysis)

*Simple aspergilloma (fungus ball in preexisting lung cavity) is a form of chronic pulmonary
aspergillosis but is usually quiescent with occasional hemoptysis.
Clinical features of alcoholic hepatitis
 Jaundice, anorexia, fever
 Right upper quadrant &/or epigastric pain
 Abdominal distention due to ascites
Clinical presentation  Proximal muscle weakness from muscle wasting (if
malnourished)
 Possible hepatic encephalopathy

 Elevated AST & ALT, usually <300 U/L


 AST: ALT ratio ≥2
 Elevated gamma-glutamyltransferase, bilirubin, &/or
Laboratory/ imaging international normalized ratio
studies  Leukocytosis, predominantly neutrophils
 Decreased albumin if malnourished
 Abdominal imaging may show fatty liver

Management of ascites in cirrhosis


 Imaging for confirmation (eg, abdominal ultrasound)
 Diagnostic paracentesis to confirm etiology & rule out infection
Initial evaluation
o SAAG, cell count & differential, total protein

 Spironolactone with furosemide


 Alcohol abstinence, sodium restriction
Medical therapy
 Avoid ACE inhibitors, angiotensin receptor blockers, NSAIDs

Refractory ascites  Large-volume paracentesis


 Transjugular intrahepatic portosystemic shunt

NSAIDs = nonsteroidal anti-inflammatory drugs; SAAG = serum-ascites albumin gradient.


Acute respiratory distress syndrome: pathogenesis & diagnosis
 Direct (eg, pneumonia, inhalation) or indirect (eg, sepsis, pancreatitis,
trauma) lung injury
Risk factors &
 Inflammatory cell activation & ↑ permeability ↔ fluid & cytokine
pathogenesis
leakage into alveoli

 ↓ Lung compliance (alveolar flooding) → ↑ work of breathing


 Severe V/Q mismatch (intrapulmonary shunt) → severe hypoxemia
Pathophysiology  ↑ Hypoxic pulmonary vasoconstriction → ↑ RV afterload & acute
PHTN

 New bilateral alveolar opacities within 1 week of inciting insult


 Edema not explained by cardiac failure or volume overload
Diagnosis
 Hypoxemia with PaO2/FiO2 ≤300

PHTN = pulmonary hypertension; RV = right ventricular; V/Q = ventilation/perfusion.


Acute pancreatitis
 Chronic alcohol use (~40%)
 Gallstones (~40%)
 Hypertriglyceridemia
Etiology  Drugs (eg, azathioprine, valproic acid, thiazides)
 Infection (eg, CMV, Legionella, Aspergillus)
 Iatrogenic (post-ERCP, ischemic/atheroembolic)

Diagnosis (requires 2 of the following)

 Acute epigastric pain radiating to the back


 Amylase or lipase >3× normal limit
 Abnormalities on imaging consistent with pancreatitis

Clinical presentation  

Other findings

 ALT level >150 U/L suggests biliary pancreatitis


 Severe disease: fever, tachypnea, hypoxemia, hypotension

ALT = alanine aminotransferase; CMV = cytomegalovirus; ERCP = endoscopic retrograde


cholangiopancreatography.
Acute cholangitis
 Ascending infection due to biliary obstruction
Etiology
 Fever, jaundice, RUQ pain (Charcot triad)
Clinical presentation  ± Hypotension, AMS (Reynolds pentad)

 Cholestatic liver function abnormalities


o ↑ Direct bilirubin, alkaline phosphatase
Diagnosis o Mildly ↑ aminotransferases
 Biliary dilation on abdominal ultrasound or CT scan

 Antibiotic coverage of enteric bacteria


Treatment  Biliary drainage by ERCP within 24-48 hr

AMS = altered mental status; ERCP = endoscopic retrograde cholangiopancreatography; RUQ


= right upper quadrant.
Acute aortic dissection
 Chronic hypertension (strongest overall risk factor)
 Underlying aortopathy (eg, Marfan syndrome)
Risk factors
 Cocaine use

 Severe, tearing chest or back pain, maximal at onset


 ± Variation in SBP between arms >20 mm Hg
Clinical presentation
 Hypertension usually present*

 ECG: normal or nonspecific ST-segment & T-wave changes


 Chest x-ray: mediastinal widening
Diagnosis
 CT angiography or TEE for definitive diagnosis

 Pain control (eg, morphine)


 Intravenous beta blockers (eg, esmolol)
Treatment  ± Sodium nitroprusside (if SBP >120 mm Hg)
 Emergency surgical repair for ascending dissection

*Hypotension on presentation suggests aortic rupture or other complication (eg, cardiac


tamponade, acute aortic regurgitation).

SBP = systolic blood pressure; TEE = transesophageal echocardiography.

Chronic lymphocytic leukemia


 Lymphadenopathy (cervical, supraclavicular, axillary)
 Hepatosplenomegaly
Clinical features  Mild thrombocytopenia & anemia
 Often asymptomatic

Diagnosis  Severe lymphocytosis & smudge cells


 Flow cytometry
 Lymph node & bone marrow biopsy not generally needed

 Median survival 10 years


 Worse prognosis with:
o Multiple chain lymphadenopathy
Prognosis
o Hepatosplenomegaly
o Anemia & thrombocytopenia

 Infection
 Autoimmune hemolytic anemia
Complications
 Secondary malignancies (eg, Richter syndrome)

Rhino-orbital-cerebral mucormycosis*
 Diabetes mellitus (ketoacidosis)
 Hematologic malignancy
Risk factors
 Solid organ or stem cell transplant

 Acute/aggressive
 Fever, nasal congestion, purulent nasal discharge, headache, sinus pain
Manifestations
 Necrotic invasion of palate, orbit, brain

 Sinus endoscopy with biopsy & culture


Diagnosis
 Surgical debridement
 Liposomal amphotericin B
Treatment
 Elimination of risk factors (eg, ↑ glucose, acidosis)

*Largely due to Rhizopus species.


Herpes simplex virus (HSV) encephalitis
 Fever
 Headache
 Seizure
Clinical findings  Altered mental status (eg, confusion, agitation)
 ± Focal neurologic findings (eg, hemiparesis, cranial nerve palsies,
ataxia)

 CSF analysis:
o ↑ WBCs (↑ lymphocytes), ↑ RBCs
Diagnostic o ↑ Protein, normal glucose
findings o HSV DNA on PCR
 Brain MRI: temporal lobe hemorrhage/edema

 Intravenous acyclovir
Treatment
CSF = cerebrospinal fluid; WBCs = white blood cells; RBCs = red blood cells.
Clinical manifestations of hereditary hemochromatosis
Skin Hyperpigmentation (bronze diabetes)
Musculoskeletal Arthralgia, arthropathy & chondrocalcinosis
Elevated hepatic enzymes with hepatomegaly (early), cirrhosis (later) &
Gastrointestinal
increased risk of hepatocellular carcinoma
Endocrine Diabetes mellitus, secondary hypogonadism & hypothyroidism
Cardiac Restrictive or dilated cardiomyopathy & conduction abnormalities
Infections Increased susceptibility to Listeria, Vibrio vulnificus & Yersinia enterocolitica
Common causes of recurrent pneumonia
Bronchial obstruction

 Extrinsic: neoplasm, adenopathy


 Intrinsic: bronchiectasis, foreign body

Same Recurrent aspiration


lung lobe*
 Altered consciousness: seizure, sedatives, antipsychotics, alcohol,
illicit drugs

 Dysphagia: neurologic disorder, esophageal motility issue


 Poor dental hygiene
 Gastroesophageal reflux

 Immunodeficiency: HIV, leukemia, CVID


Different  Sinopulmonary disease: cystic fibrosis, immotile cilia
lung lobes  Noninfectious: vasculitis, BOOP

*Recurrent aspiration can lead to pneumonia in different dependent regions of the lung
depending on the position of the patient during the aspiration event.

BOOP = bronchiolitis obliterans with organizing pneumonia; CVID = common variable


immunodeficiency.

Common features of sarcoidosis


 Young adults
Epidemiology  African Americans

Clinical  Constitutional symptoms


 Cough, dyspnea & chest pain
 Extrapulmonary findings
o Skin lesions
o Anterior/posterior uveitis
o Löfgren syndrome
 Parotid gland swelling

 Bilateral hilar adenopathy


Imaging  Pulmonary reticular infiltrates

 Hypercalcemia/hypercalciuria
Laboratory  Elevated serum ACE level

 Biopsy showing noncaseating granulomas


Pathology that stain negative for fungi & acid-fast bacilli

Interstitial lung disease


 Sarcoidosis, amyloidosis, alveolar proteinosis
 Vasculitis (eg, granulomatosis with polyangiitis)
 Infection (eg, fungal, tuberculosis, viral pneumonia)
Common etiologies  Environmental exposure (eg, silicosis, HP)
 Connective tissue disease (eg, SLE, scleroderma)
 IPF, cryptogenic organizing pneumonia

 Progressive exertional dyspnea, dry cough


 >50% of patients have significant smoking history
Clinical presentation
 Fine inspiratory crackles ± digital clubbing

 Chest x-ray: reticulonodular interstitial opacities


 HRCT: fibrosis, honeycombing, traction bronchiectasis
Diagnosis
 PFT: restrictive pattern with ↓ DLCO

DLCO = diffusion capacity of the lung for carbon monoxide; HP = hypersensitivity


pneumonitis;
HRCT = high resolution CT scan; IPF = idiopathic pulmonary fibrosis; PFT = pulmonary
function
testing; SLE = systemic lupus erythematosus.

Tuberculin skin test (TST) thresholds


Induration
Patient population
size
 Individuals with HIV infection
 Recent contacts of patient with known TB
 Persons with nodular or fibrotic changes on chest x-ray consistent with
≥5 mm
previously healed TB
 Organ transplant recipients & other immunosuppressed persons

≥10 mm  Recent immigrants (<5 years) from TB-endemic areas


 Injection drug users
 Residents & employees in high-risk settings (eg, prisons, nursing homes,
hospitals, homeless shelters)
 Mycobacteriology laboratory personnel
 Persons with conditions that result in higher risk for TB reactivation (eg,
diabetes mellitus, leukemia, end-stage renal disease, chronic malabsorption
syndromes, low body weight)
 Children age <5 or those exposed to adults in high-risk categories

 All of the above plus healthy persons


≥15 mm
PPD = purified protein derivative; TB = tuberculosis.
Clinical features & management of tricyclic antidepressant overdose
 Mental status changes (eg, drowsiness,
delirium, coma)
CNS
 Seizures, respiratory depression

 Sinus tachycardia, hypotension


Clinical  Prolonged PR/QRS/QT intervals
presentation Cardiovascular  Arrhythmias (eg, ventricular tachycardia,
fibrillation)

 Dry mouth, blurred vision, dilated pupils


Anticholinergic  Urinary retention, flushing, hyperthermia

 Supplemental oxygen, intubation


 Intravenous fluids
 Activated charcoal for patients within 2 hours
Supportive care &
Management of ingestion (unless ileus present)
therapy
 Intravenous sodium bicarbonate for QRS
interval widening or ventricular arrhythmia

Granulomatosis with polyangiitis


 Upper respiratory: sinusitis/otitis, saddle nose
 Lower respiratory: lung nodules/cavitation, interstitial lung
Clinical disease, diffuse alveolar hemorrhage
manifestations  Renal: rapidly progressive GN
 Skin: livedo reticularis, nonhealing ulcers

 ANCA: PR3 (~70%), MPO (~20%)


 Biopsy:
o Skin (leukocytoclastic vasculitis)
Diagnosis
o Kidney (pauci-immune GN)
o Lung (granulomatous vasculitis)

Management  Corticosteroids & immunomodulators (eg, cyclophosphamide)


ANCA = antineutrophil cytoplasmic antibody; GN = glomerulonephritis; MPO =
myeloperoxidase; PR3 = proteinase-3.
Chronic aortic regurgitation
 Congenital bicuspid aortic valve
 Postinflammatory (eg, rheumatic heart disease, endocarditis)
Common etiologies
 Aortic root dilation (eg, Marfan syndrome, syphilis)

 Backflow from aorta into LV → ↑ LV end-diastolic volume


 LV initially compensates with eccentric hypertrophy → ↑ SV &
Pathophysiology CO
 Eventual LV dysfunction → ↓ SV & CO → heart failure

 Decrescendo diastolic murmur


 Widened pulse pressure (↑SBP & ↓DBP)
Clinical
 Rapid rise-rapid fall (“water-hammer”) pulsation
 Abrupt carotid distension & collapse, “pistol-shot” femoral
findings
pulses

CO = cardiac output; DBP = diastolic blood pressure; LV = left ventricle; SBP = systolic blood
pressure; SV = stroke volume.
Multifocal atrial tachycardia
 Exacerbation of pulmonary disease (eg, COPD)
 Electrolyte disturbance (eg, hypokalemia)
Etiology
 Catecholamine surge (eg, sepsis)

 Typically asymptomatic
 Rapid, irregular pulse
Clinical findings
 ECG: >3 P-wave forms & atrial rate >100/min

 Correct underlying disturbance


Treatment  AV nodal blockade (eg, verapamil) if persistent

AV = atrioventricular; COPD = chronic obstructive pulmonary disease.


Primary hyperaldosteronism (Conn syndrome)
 Bilateral adrenal hyperplasia (~60%) or unilateral adenoma
 Difficult-to-control hypertension
Clinical features  Hypokalemia & metabolic alkalosis*
 No extravascular volume overload (aldosterone escape)

Diagnosis  Elevated plasma aldosterone & low plasma renin (ratio >20)
 Absence of aldosterone suppression with oral saline load
 CT scan of adrenal glands to determine bilateral hyperplasia vs
adenoma

 Bilateral adrenal hyperplasia: MRA (eg, spironolactone)


Treatment  Unilateral adenoma: surgical resection preferred

*In some patients, the characteristic electrolyte abnormalities are apparent only after a thiazide
is initiated for blood pressure management.

MRA = mineralocorticoid receptor antagonist.


Differential diagnosis of neck pain
Condition Clinical clues
 Antecedent history of neck injury
Strain  Pain/stiffness with neck movement

 Older individuals
 Pain/stiffness worse with movement
Facet osteoarthritis
 Relieved with rest

 Pain radiates to shoulder/arm


 Dermatomal sensory/motor/reflex findings
Radiculopathy
 Positive Spurling test

 LE weakness, gait/bowel/bladder dysfunction


Spondylitic myelopathy  Lhermitte sign

 Young men
 HLA-B27
Spondyloarthropathy  Relieved with exercise
 Prolonged morning stiffness

 Constant pain
 Worse at night
Spinal metastasis
 Not responsive to position changes

 Focal tenderness
 Fevers & night sweats
Vertebral osteomyelitis
 IVDU, immune compromise, or recent infection

IVDU = intravenous drug use; LE = lower extremity.


Common causes of esophagitis in patients with HIV
 Oral thrush usually present
 White plaques throughout esophagus
Candida albicans
 Biopsy: pseudohyphae

Herpes simplex virus  Orolabial lesions usually present


 Vesicular or ulcerative round/ovoid lesions ("volcano-like")
 Biopsy: multinucleated giant cells

 Large, linear ulcers in distal esophagus


Cytomegalovirus  Biopsy: intranuclear/intracytoplasmic inclusions

Parvovirus B19 infection


 Most patients are asymptomatic or have flulike symptoms
 Erythema infectiosum (fifth disease): Fever, nausea & “slapped
cheek” rash (more common in children)
Signs &  Acute, symmetric arthralgia/arthritis: Hands, wrists, knees & feet
symptoms (resembles RA)
 Transient pure red cell aplasia; aplastic crisis in patients with
underlying hematologic disease (eg, sickle cell)

 Acute infection
o B19 IgM antibodies in immunocompetent patients
o NAAT for B19 DNA in immunocompromised patients
Diagnosis
 Previous infection: B19 IgG antibodies (documents immunity)
 Reactivation of previous infection: NAAT for B19 DNA

NAAT = nucleic acid amplification testing;  RA = rheumatoid arthritis.


Neurogenic & vascular claudication
Neurogenic claudication
Vascular claudication
(pseudoclaudication)
 Posture-dependent pain
 Exertionally dependent
 Lumbar extension
pain
worsens pain (eg,
 Pain relieved with rest but
walking downhill)
not with bending forward
 Lumbar flexion relieves
while walking
pain (eg, walking while
 Lower extremity
Symptoms bent forward)
cramping/tightness
 Lower extremity
 No significant lower
numbness & tingling
extremity weakness
 Lower extremity
 Possible buttock, thigh,
weakness
calf, or foot pain
 Low back pain

 Decreased pulses
 Normal pulses
 Cool extremities
 Frequently normal
Examination  Decreased hair growth
examination
 Pallor with leg elevation

 MRI of the spine  Ankle-brachial index


Diagnosis
Human monocytic ehrlichiosis
 Transmitted by tick vector (Lone Star tick)
Epidemiology  Seen in southeastern & south central United States

 Flu-like illness (high fever, headache, myalgias, chills)


 Neurologic symptoms (confusion)
Clinical
 Rash (<30% in adults) is uncommon ("Rocky Mountain spotted
manifestations
fever without the spots")

 Leukopenia & thrombocytopenia


Laboratory findings  Elevated liver enzymes & lactate dehydrogenase

 Intracytoplasmic morulae in monocytes


Diagnosis  PCR testing for Ehrlichia chaffeensis/E ewingii

 Empiric doxycycline while awaiting confirmatory testing


Treatment
Stage Lyme disease clinical features
 Erythema migrans
Early localized  Fatigue, headache
(days to 1 month)  Myalgia, arthralgia

 Multiple erythema migrans


 Unilateral/bilateral cranial nerve palsy (eg, CN VII)
Early disseminated  Meningitis
(weeks to months)  Carditis (eg, AV block)
 Migratory arthralgia

 Arthritis
Late  Encephalitis
(months to years)  Peripheral neuropathy

AV = atrioventricular.
Babesiosis
 Babesia microti
 Ixodes scapularis tick bite (Lyme disease & HGA)
Epidemiology
 Northeastern United States

 Fever, fatigue, myalgia, headache (flu-like


symptoms)
Clinical  If severe: ARDS, CHF, DIC, splenic rupture
manifestations  Anemia, thrombocytopenia, increased
bilirubin/LDH/LFTs

Diagnosis  Thin blood smear: intraerythrocytic rings ("Maltese


cross")

 Atovaquone + azithromycin
Treatment  Quinine + clindamycin (if severe)

ARDS = acute respiratory distress syndrome; CHF = congestive heart failure;


DIC = disseminated intravascular coagulation; HGA = human granulocytic
anaplasmosis; LDH = lactate dehydrogenase; LFTs = liver function tests.
Joint fluid characteristics
Noninflammatory Inflammatory
Normal  Septic joint
(eg, OA) (eg, crystals, RA)
Translucent or
Appearance Clear Clear Opaque
opaque
WBCs
<200 200-2,000 2,000-100,000 50,000-150,000
(mm3)
PMNs <25% 25% Often >50% >80%-90%
OA = osteoarthritis; PMNs = polymorphonuclear leukocytes; RA = rheumatoid arthritis; WBCs
= white blood cells.
Disease-modifying antirheumatic drugs
Agent Mechanism Adverse effects
 Hepatotoxicity
 Folate antimetabolite  Stomatitis
Methotrexate
 Cytopenias

 Hepatotoxicity
 Pyrimidine synthesis
Leflunomide inhibitor
 Cytopenias

 TNF & IL-1 suppressor  Retinopathy


Hydroxychloroquine
 Hepatotoxicity
 TNF & IL-1 suppressor  Stomatitis
Sulfasalazine
 Hemolytic anemia

 Infection
TNF inhibitors  Demyelination
(eg, adalimumab, certolizumab,  Congestive heart
etanercept, golimumab, failure
infliximab)  Malignancy

IL-1 = interleukin 1;TNF = tumor necrosis factor.


Distinguishing acid reflux from angina
GERD Angina
 Substernal burning or dull
 Substernal pressure; may radiate
pain; may radiate to arms,
to arms, neck, jaw
neck, jaw
Symptoms  Frequently accompanied by
 Frequently accompanied by
dyspnea
cough or reflux

 Short, intermittent (eg, 2-5 min


 Prolonged, constant (eg, >1
Symptom for chronic angina; >15 min
hr)
duration suggests ACS)

 Recumbency
 Physical exertion
Precipitating  Trigger foods (eg, alcohol,
 Stress
factors coffee)

 Rest
Alleviating  Antacids
 Nitroglycerin
factors
ACS = acute coronary syndrome; GERD = gastroesophageal reflux disease.
Bronchiectasis
 Pathophysiology: airway insult (eg, infection, inhalation)
with impaired clearance (eg, mucostasis,
immunodeficiency)
 Chronic: daily production of voluminous, thick ± blood-
Clinical features
tinged mucus
 Acute exacerbations: recurrent infections with
mucopurulent sputum ± frank hemoptysis

 Airway obstruction (eg, cancer, foreign body) &


mucostasis (eg, CF, ABPA)
 Immunodeficiency (eg, ↓Ig) & autoinflammatory disease
Etiologies/contributory
(eg, Sjögren syndrome)
conditions
 Chronic/past infection (eg, mycobacteria) or toxic
inhalation

 High-resolution CT scan of the chest (needed for


diagnosis): airway dilation
 Pulmonary function testing: obstructive pattern
Evaluation
 Investigation of etiologies (eg, Ig levels, respiratory
cultures, bronchial obstruction)

Treatment  Address underlying disorders (eg, Ig replacement)


 Airway clearance (eg, chest physiotherapy), mucolytics
 Antibiotics to suppress bacterial overgrowth & treat
exacerbations

ABPA = allergic bronchopulmonary aspergillosis; CF = cystic fibrosis; Ig = immunoglobulin;


RA = rheumatoid arthritis.
Ankylosing spondylitis
 Insidious onset at age <40
 Symptoms >3 months
Inflammatory back pain  Relieved with exercise but not rest
 Nocturnal pain

 Arthritis (sacroiliitis)
 Reduced chest expansion & spinal mobility
 Enthesitis (tenderness at tendon insertion sites)
Examination findings
 Dactylitis (swelling of fingers & toes)
 Uveitis

 Osteoporosis/vertebral fractures
 Aortic regurgitation
Complications
 Cauda equina syndrome

 Elevated ESR & CRP


Laboratory  HLA-B27 association

 X-ray of sacroiliac joints


Imaging  MRI of sacroiliac joints

CRP = C-reactive protein; ESR = erythrocyte sedimentation rate.


 
Assessment of malignancy risk for solitary pulmonary nodule
Variable Low risk Intermediate risk High risk
Nodule size (cm) <0.8 0.8-2.0 >2.0
Age (yr) <40 40-60 >60
Smoking status Never smoked Current Current
Smoking cessation (yr) >15 5-15 <5
Nodule margin Corona radiata or
Smooth Scalloped
characteristics spiculated
Spinal cord compression
 Mechanical (eg, disc herniation, spinal stenosis)
 Malignancy (eg, lung, breast, prostate cancers)
Causes
 Infection (eg, epidural abscess)

 Gradually worsening, severe back pain


Symptoms  Pain worse in recumbent position/at night
 Early signs
o Symmetric extremity weakness
o ↓ Deep tendon reflexes

Physical
 Late signs
examination
o ↓ Rectal tone
o ↑ Deep tendon reflexes, bilateral Babinski reflex
o Paralysis

 Emergency MRI of the spine


 Emergency surgical ± radiation oncology consultation
Management  Intravenous glucocorticoids (eg, malignancy) or antibiotics (eg,
infection)

Acute respiratory distress syndrome: management & prognosis


 Lung protection: limit alveolar distending volume (VT 6 mL/kg)
& pressure (Pplat ≤30 cm H2O)
 Ventilation: tolerate permissive hypercapnia (ie, ↑ PaCO2 & ↓
Mechanical
pH acceptable) to avoid excessive VT
ventilation
 Oxygenation: set lowest feasible FiO2 (goal SpO2 92%-96%) to
avoid O2 toxicity

 Treat underlying etiology: source control (eg, sepsis)


 Prevent iatrogenic harm: negative fluid balance, timely
extubation (eg, minimize sedation)
Supportive care
 ± Corticosteroids: select patients with moderate-to-severe early
ARDS

 Mortality rate: 40% in hospital, death mostly due to multiorgan


failure
 Morbidity rate: 50% with chronic cognitive impairment &
Prognosis
physical debility, 25% with chronic pulmonary dysfunction
(restriction & ↓ DLCO)

ARDS = acute respiratory distress syndrome; DLCO = diffusion capacity of lung for carbon
monoxide; Pplat = plateau pressure; SpO2 = oxygen saturation as measured by pulse oximetry;
VT = tidal volume.
Male hypogonadism
Primary Secondary

(testicular disease) (pituitary/hypothalamic disease)


Findings  ↓ Energy/libido, ↓ body hair  ↓ Energy/libido, ↓ body hair
 Gynecomastia more likely  Gynecomastia less likely
 ↑ LH/FSH  ↓ Normal LH/FSH
 ↓↓ Testosterone/sperm count  ↓ Testosterone/sperm count

 Congenital
 Congenital
o Kallman syndrome
o Klinefelter syndrome
 Gonadotropin suppression
o Varicocele
o Hyperprolactinemia
 Acquired
o Glucocorticoids/opiates
o Radiation
 Gonadotroph cell damage
o Infection (eg, mumps)
Causes o Benign/malignant
o Trauma
tumors
o Medications (eg,
o Pituitary apoplexy
alkylating agents,
o Infiltration (eg,
glucocorticoids)
hemochromatosis)
o Chronic disease
o Systemic disease

 Karyotype  Prolactin
 Others based on clinical  Transferrin
Evaluation
suspicion  ± MRI

 
Pancreatic adenocarcinoma
 Smoking
 Hereditary pancreatitis
Risk factors  Nonhereditary chronic pancreatitis
 Obesity & lack of physical activity

 Systemic symptoms (eg, weight loss, anorexia)


(>85%)
 Abdominal pain/back pain (80%)
Clinical  Jaundice (56%)
presentation  Recent-onset atypical diabetes mellitus
 Unexplained migratory superficial thrombophlebitis
 Hepatomegaly & ascites with metastasis

 Cholestasis (↑ alkaline phosphatase & direct


bilirubin)
 ↑ CA-19-9 (not as a screening test)
Laboratory
studies
 Abdominal ultrasonography (if jaundiced) or CT scan
(if no jaundice)

Syphilis treatment
Stage First line Alternate
Primary (chancre) Penicillin G IM × 1 Doxycycline × 14 days
Secondary (diffuse rash)
Early latent (asymptomatic)*
Late latent (asymptomatic)*
Penicillin G IM × 3 Doxycycline × 28 days
Tertiary (eg, CV, gummata)
Neurosyphilis
Penicillin G IV × 10-14 days Ceftriaxone IV × 14 days**
(eg, meningitis, ocular)
*Early latent = asymptomatic with infection <1 year; Late latent = asymptomatic with unknown
duration of infection or infection >1 year.

**Penicillin desensitization followed by IV penicillin is preferred for those with penicillin


allergy who have neurosyphilis; ceftriaxone can be used in those unable to be desensitized.

CV = cardiovascular; IM = intramuscular; IV = intravenous.


Causes of hirsutism in women
Etiology Clinical features
 Oligomenorrhea, hyperandrogenism, obesity
 Associated with type 2 diabetes, dyslipidemia,
Polycystic ovary syndrome
hypertension

 Normal menstruation
Idiopathic hirsutism  Normal serum androgens

 Similar to polycystic ovary syndrome


Nonclassic
 Elevated serum 17-hydroxyprogesterone
21-hydroxylase deficiency
 More common in postmenopausal women
Androgen-secreting ovarian  Rapidly progressive hirsutism with virilization
tumors, ovarian hyperthecosis  Very high serum androgens

 Obesity (usually of the face, neck, trunk, abdomen)


Cushing syndrome  Increased libido, virilization, irregular menses

Post–cardiac injury syndrome


 Myocardial infarction (ie, Dressler syndrome)
 Cardiac surgery or trauma
Causes
 Percutaneous coronary intervention

 Latent period of several weeks to months


 Pleuritic chest pain, fever, leukocytosis
Clinical
 Chest x-ray: pleural effusion ± enlarged cardiac silhouette
features
 Echocardiography: pericardial effusion

 NSAID (usually high-dose aspirin) ± colchicine


Treatment  Corticosteroids in refractory disease
 Usually self-limited disease course
Prognosis  May cause chronic/recurrent disease leading to constrictive pericarditis

NSAID = nonsteroidal anti-inflammatory drug.


Mixed connective tissue disease
 Autoimmune disorder with variable features of:
o Systemic lupus erythematosus
o Systemic sclerosis
Definition
o Polymyositis
o Rheumatoid arthritis

 Raynaud phenomenon*
 Hand/finger swelling*
 Arthritis/synovitis*
 Inflammatory myopathy*
Clinical features
 Pulmonary hypertension
 Malar or discoid rash
 Mild CNS &/or kidney disease

 Anti–U1 ribonucleoprotein
 Antinuclear antibody
 Rheumatoid factor, anti–cyclic citrullinated peptide
Laboratory findings
 Elevated creatine kinase
 Anemia/cytopenia

*Diagnostic criteria.
Systemic sclerosis
 Progressive tissue fibrosis
Pathogenesis
 Vascular dysfunction

 Skin: telangiectasia, sclerodactyly, digital ulcer, calcinosis cutis


 Extremities: arthralgia, myalgia, contracture
 Gastrointestinal tract: esophageal dysmotility, dysphagia, acid
Clinical features reflux
 Lungs: dyspnea, dry cough
 Vascular system: Raynaud phenomenon

 Antinuclear
 Anti–topoisomerase type I (anti–Scl-70) (diffuse SSc)
Autoantibodies
 Anticentromere (limited SSc)

Complications  Lungs: interstitial lung disease, pulmonary arterial HTN


 Kidneys: HTN, scleroderma renal crisis (severe HTN, AKI,
MAHA)
 Heart: myocardial fibrosis, pericarditis, pericardial effusion

AKI = acute kidney injury; HTN = hypertension; MAHA = microangiopathic hemolytic


anemia; SSc = systemic sclerosis.
Occupational HIV postexposure prophylaxis
Exposure of:

 Mucous membrane, nonintact skin, or percutaneous exposure


High-risk contact
Exposure to:
(prophylaxis
recommended)  Blood, semen, vaginal secretions, or any body fluid with visible
blood (uncertain risk: cerebrospinal fluid, pleural/pericardial
fluid, synovial fluid, peritoneal fluid, amniotic fluid)

Exposure to:
Low-risk contact
 Urine, feces, nasal secretions, saliva, sweat, tears (with no
(prophylaxis not
visible blood)
recommended)
 Initiate urgently, preferably in the first few hours
Timing  Continue for 4 weeks

Treatment with ≥3-drug regimen recommended:

 Two nucleotide/nucleoside reverse transcriptase inhibitors (eg,


tenofovir, emtricitabine)
Regimen
PLUS:

 Integrase strand transfer inhibitor (eg, raltegravir), protease


inhibitor, or nonnucleoside reverse transcriptase inhibitor

Bronchiectasis
 Pathophysiology: airway insult (eg, infection, inhalation)
with impaired clearance (eg, mucostasis,
immunodeficiency)
 Chronic: daily production of voluminous, thick ± blood-
Clinical features
tinged mucus
 Acute exacerbations: recurrent infections with
mucopurulent sputum ± frank hemoptysis

Etiologies/contributory  Airway obstruction (eg, cancer, foreign body) &


conditions mucostasis (eg, CF, ABPA)
 Immunodeficiency (eg, ↓Ig) & autoinflammatory disease
(eg, Sjögren syndrome)
 Chronic/past infection (eg, mycobacteria) or toxic
inhalation

 High-resolution CT scan of the chest (needed for


diagnosis): airway dilation
 Pulmonary function testing: obstructive pattern
Evaluation
 Investigation of etiologies (eg, Ig levels, respiratory
cultures, bronchial obstruction)

 Address underlying disorders (eg, Ig replacement)


 Airway clearance (eg, chest physiotherapy), mucolytics
Treatment  Antibiotics to suppress bacterial overgrowth & treat
exacerbations

ABPA = allergic bronchopulmonary aspergillosis; CF = cystic fibrosis; Ig = immunoglobulin;


RA = rheumatoid arthritis.
Dyspepsia
 Epigastric pain or burning
 Postprandial fullness, early satiety, bloating
Symptoms
 ≥1 months

 Functional/idiopathic (75%)
 Malignancy (eg, gastric, esophageal)
Etiology  Peptic ulcer (eg, Helicobacter pylori infection, NSAIDs)
 Drug-induced (eg, NSAIDs, bisphosphonate)

 Low malignancy risk (eg, age <60 & no alarm symptoms*)


o Testing & treatment for H pylori
Work-up  High malignancy risk (eg, age >60 or alarm symptoms)
o Gastroenterology referral/upper endoscopy

 Treatment of underlying cause


Treatment  Trial of proton pump inhibitor if no cause found

*GI bleeding, weight loss, iron deficiency anemia, lymphadenopathy, dysphagia, odynophagia,
persistent vomiting, palpable mass, family history of upper GI cancer.

GERD = gastroesophageal reflux disease; GI = gastrointestinal; NSAIDs = nonsteroidal anti-


inflammatory drugs.
Euthyroid sick syndrome
Early/mild Prolonged/severe
T3 ↓ ↓
T4 Normal ↓
TSH Normal ↓
Reverse T3 ↑ ↑
Clinical features of osteomalacia
 Malabsorption
 Intestinal bypass surgery
 Celiac disease
Causes
 Chronic liver disease
 Chronic kidney disease

 May be asymptomatic
 Bone pain & muscle weakness
Symptoms/signs  Muscle cramps
 Difficulty walking, waddling gait

 ↑ Alkaline phosphatase, ↑ PTH


 ↓ Serum calcium & phosphorus, ↓ urinary calcium
 ↓ 25(OH)D levels
 Imaging
Diagnosis
o Cortical thinning & reduced bone density
o Bilateral symmetric pseudofractures (Looser
zones)

25(OH)D = 25-hydroxycholecalciferol; PTH = parathyroid hormone.


Causes of altered mental status
 Prescription drugs (eg, opioids, lithium, antipsychotics)
 Drugs of abuse (eg, ethanol, hallucinogens)
Drugs/toxins
 Drug withdrawal (eg, ethanol, benzodiazepines)

 Sepsis, systemic infections


Infections  Meningitis, encephalitis, brain/epidural abscess

 Electrolyte disturbances
 Hypo-/hyperglycemia
 Endocrine (eg, hypo/hyperthyroid, pituitary, adrenal)
Metabolic  Hypoxemia, hypercarbia
 Nutritional (eg, thiamine, vitamin B12 deficiency)
 Hepatic or renal failure

 Seizure, head injury


 Hypertensive encephalopathy
Central nervous system
 Psychiatric disorders

Leprosy
Epidemiology  Mycobacterium leprae
 Primarily developing world (eg, Asia, Africa, South America)
 Respiratory droplets/nine banded armadillo
 Low infectivity

 Macular, anesthetic skin lesions with raised borders


Manifestations  Nodular, painful nearby nerves with loss of sensory/motor function 

 Full thickness biopsy of skin lesion (active edge)


Diagnosis  M leprae is not culturable

 Dapsone + rifampin
Treatment  Add clofazimine if severe ("multibacillary")

Polymyalgia rheumatica
Clinical features Findings
 Age >50
 Bilateral pain & morning stiffness >1 month
 Involvement of 2 of the following:
o Neck or torso
Symptoms
o Shoulders or proximal arms
o Proximal thigh or hip
o Constitutional (fever, malaise, weight loss)

 Decreased active ROM in shoulders, neck & hips


Physical examination
 Elevated ESR
 Elevated CRP
Laboratory studies
 Normocytic anemia

 Oral glucocorticoids
Treatment
CRP= C-reactive protein; ESR = erythrocyte sedimentation rate; ROM = range of motion.
Polymyalgia rheumatica
Clinical features Findings
 Age >50
 Bilateral pain & morning stiffness >1 month
 Involvement of 2 of the following:
o Neck or torso
Symptoms
o Shoulders or proximal arms
o Proximal thigh or hip
o Constitutional (fever, malaise, weight loss)

 Decreased active ROM in shoulders, neck & hips


Physical examination
Laboratory studies  Elevated ESR
 Elevated CRP
 Normocytic anemia

 Oral glucocorticoids
Treatment
CRP= C-reactive protein; ESR = erythrocyte sedimentation rate; ROM = range of motion.
Common skin infections
Infection Organism Manifestations
 Superficial dermis & lymphatics
 Streptococcus  Raised, sharply demarcated edges
Erysipelas pyogenes  Rapid spread & onset
 Fever early in course

 Deep dermis & subcutaneous fat


 S pyogenes  Flat edges with poor demarcation
Cellulitis
 MSSA  Indolent (over days)
(nonpurulent)
 Localized (fever later in course)

 Purulent drainage
 Folliculitis: infected hair follicle
 MSSA
 Furuncles: folliculitis → dermis →
Cellulitis (purulent)  MRSA
abscess

 Carbuncle: multiple furuncles

MRSA = methicillin-resistant Staphylococcus aureus;MSSA = methicillin-sensitive S aureus.


Malaria prevention
 Travelers new to endemic regions
 Travelers returning to endemic region after long absence
High-risk groups
 Pregnant women

 Avoid being outside from dusk → dawn


 Cover skin with clothing
Mosquito bite  Wear insect repellant
avoidance  Use insecticide-treated bed nets
 Sleep in screened/air-conditioned rooms

 Atovaquone-proguanil
 Mefloquine
Chemoprophylaxis  Doxycycline
 Tafenoquine

Glucose-6-phosphate dehydrogenase deficiency


Epidemiology  Hemolytic anemia due to oxidative stress
(infection, sulfa drugs, fava beans)
 X-linked: Asian, African, or Middle Eastern
descent

 Pallor & fatigue


 Dark urine, jaundice & icterus
Manifestations
 Abdominal/back pain

 Hemolysis: ↓ hemoglobin, ↓ haptoglobin,


↑ bilirubin & LDH, ↑ reticulocytes
 Peripheral smear: bite cells & Heinz bodies
Laboratory
 Negative Coombs test
findings
 ↓ G6PD activity level (may be normal during
attack)

 Remove or treat responsible agent/condition


Management  Provide supportive care

G6PD = glucose-6-phosphate dehydrogenase; LDH = lactate dehydrogenase.


Extraintestinal manifestations of inflammatory bowel disease
 Erythema nodosum*
 Pyoderma gangrenosum**
Dermatologic  Hidradenitis suppurativa
 Oral aphthous ulcerations*

 Primary sclerosing cholangitis**


Hepatobiliary
 Inflammatory axial &/or peripheral arthritis
Musculoskeletal
 Episcleritis
Ophthalmic  Anterior uveitis*

 Venous thromboembolism (increased risk)


Vascular
*More commonly seen with Crohn disease.

**More commonly seen with ulcerative colitis.


Medical therapy for benign prostatic hyperplasia
 Relax smooth muscle in bladder neck, prostate capsule &
α-Adrenergic
prostatic urethra
antagonists
 Usual first-line therapy
(eg, terazosin,
 Adverse effects: orthostatic hypotension, dizziness
tamsulosin)
5-α Reductase  Inhibit conversion of testosterone to dihydrotestosterone
inhibitors  Reduce prostate gland size & vascularity (reduced hematuria)
(eg, finasteride,  Effectiveness may take 6-12 months
 Adverse effects: decreased libido, erectile dysfunction
dutasteride)
 Used to treat overactive bladder (urinary frequency, urgency &
Antimuscarinics incontinence)
(eg, tolterodine)  Adverse effects: urine retention, dry mouth

Paget disease of bone


 Most patients are asymptomatic
 Bone pain & deformity
o Skull: headache, hearing loss
Clinical
o Spine: spinal stenosis, radiculopathy
features
o Long bones: bowing, fracture, arthritis of adjacent joints
 Giant cell tumor, osteosarcoma

 Osteoclast dysfunction
Pathogenesis  Increased bone turnover

 Elevated alkaline phosphatase


Laboratory  Elevated bone turnover markers (eg, PINP, urine hydroxyproline)
testing  Calcium & phosphorus: usually normal

 X-ray: osteolytic or mixed lytic/sclerotic lesions


Imaging  Bone scan: focal increase in uptake

 Bisphosphonates
Treatment
PINP = procollagen type I N-terminal propeptide.
Common causes of diarrhea in patients with AIDS
Organism CD4 count Symptoms
 Severe watery diarrhea
 Low-grade fever
Cryptosporidium <180/mm3
 Weight loss

 Watery diarrhea
 Crampy abdominal pain
Microsporidium/Isosporidium <100/mm3  Weight loss
 Fever is rare

 Watery diarrhea
 High fever (>39 C [102.2 F])
Mycobacterium avium complex <50/mm3
 Weight loss

Cytomegalovirus <50/mm3  Frequent, small-volume diarrhea


 Hematochezia
 Abdominal pain
 Low-grade fever
 Weight loss

Causes of recurrent pregnancy loss


 Uterine: fibroids, adhesions, polyps
Structural  Cervical insufficiency

 Aneuploidy
 Translocations/rearrangements
Chromosomal
 Mosaicism

 Hypercoagulable disorders (eg, antiphospholipid syndrome)


Immunologic/
 Alloimmune intolerance
Hematologic
 Thyroid disease
 Polycystic ovary syndrome
Endocrine  Diabetes mellitus
 Hyperprolactinemia

 Advancing maternal age


 Defective endometrial receptivity
Other  Decreased ovarian reserve
 Celiac disease

Modified Wells criteria for pretest probability


of deep venous thrombosis
 Previously documented DVT
 Active cancer
 Recent immobilization of the legs
 Recently bedridden >3 days
Score 1 point for  Localized tenderness along vein distribution
each feature  Swollen leg
present  Calf swelling >3 cm compared to other leg
 Pitting edema
 Collateral superficial nonvaricose veins
 Alternate diagnosis more likely (−2 points)

 0 points = Low probability


Total score for  1 or 2 points = Moderate probability
clinical probability  ≥3 points = High probability

DVT = deep venous thrombosis.


Acute HIV infection
 Typically presents 2-4 weeks after exposure
Epidemiology
 Mononucleosis-like syndrome (eg, fever, lymphadenopathy, sore throat,
arthralgia)
Clinical
 Generalized macular rash
features
 Gastrointestinal symptoms

 Viral load is markedly elevated (>100,000 copies/mL)


 HIV antibody testing may be negative (not yet seroconverted)
Diagnosis
 CD4 count may be normal

 Combination antiretroviral therapy


Management  Partner notification; consider secondary prophylaxis

Primary adrenal insufficiency


 Autoimmune adrenalitis (most common)
 Infection (eg, tuberculosis)
Etiology
 Metastatic infiltration

 Fatigue, weakness, anorexia/weight loss


 Nausea, vomiting, abdominal pain
Clinical  Salt craving, postural hypotension
features  Hyperpigmentation
 Acute adrenal crisis: confusion, hypotension/shock

 Hyponatremia, hyperkalemia, eosinophilia


Laboratory
 Low morning cortisol, high ACTH
findings
 Glucocorticoids (eg, hydrocortisone, prednisone)
Treatment  Mineralocorticoids (eg, fludrocortisone)

ACTH = adrenocorticotropic hormone.

Clinical features of Marfan syndrome


 Arachnodactyly
 ↓ Upper/lower body segment ratio
 ↑ Arm/height ratio
Skeletal
 Pectus deformity, scoliosis, kyphosis
 Joint hypermobility

 Ectopia lentis
Ocular
Cardiovascular  Aortic dilation, regurgitation, or dissection
 Mitral valve prolapse

 Spontaneous pneumothorax from apical blebs


Pulmonary
 Incisional or inguinal hernias
Skin/fascia  Skin striae

Sexually transmitted infection screening*


 Neisseria gonorrhoeae (eg, NAAT)
 Chlamydia trachomatis (eg, NAAT)
All patients  Syphilis (eg, RPR)
 HIV (eg, 4th-generation antigen/antibody)

 Women only: Trichomonas vaginalis (eg, wet mount)


Additional testing for  Herpes simplex virus screening (eg, serology) only when
certain populations history of characteristic lesions

*For patients with active sexually transmitted infection or those who request screening.

NAAT = nucleic acid amplification testing; RPR = rapid plasma reagin.


Major side effects of amiodarone
Cardiac  Sinus bradycardia, heart block
 Risk of proarrhythmias: QT
prolongation & risk of torsade
de pointes

 Chronic interstitial
pneumonitis (cough, fever,
Pulmonary dyspnea, pulmonary
infiltrates) most common

 Hypothyroidism
Endocrine  Hyperthyroidism

 Elevated transaminases,
Gastrointestinal/
hepatitis
hepatic
 Corneal microdeposits
Ocular  Optic neuropathy

 Blue-gray skin discoloration


Dermatologic
 Peripheral neuropathy
Neurologic
Mitral stenosis in adults
 Rheumatic heart disease (vast majority of cases)
Etiology  Age-related calcification, radiation induced

 Exertional dyspnea, orthopnea, paroxysmal nocturnal dyspnea,


hemoptysis
Clinical  Pulmonary edema ± right-sided heart failure (eg, lower extremity
presentation edema)
 Atrial fibrillation, ↑ risk for systemic embolization

 Opening snap with middiastolic rumble at the apex


Diagnosis  Echocardiography: ↑ transmitral flow velocity

 Percutaneous valvotomy or surgical repair/replacement


Treatment
Clinical features of hyperkalemia
 Tall, peaked T waves with shortened QT interval
 PR interval prolongation
Sequence of  QRS complex widening
ECG changes  Disappearance of P wave
 Conduction blocks, ectopy, or sine wave pattern

Cardiac membrane  Calcium infusion


stabilization
Rapidly acting  Insulin with glucose
 β2-adrenergic agonists
treatment options  Sodium bicarbonate

 Diuretics
Removal of potassium  Gastrointestinal cation exchangers
from body (slow acting)  Hemodialysis

Malaria
 Vector: female Anopheles mosquito
 4 major species of Plasmodium: P falciparum, P
vivax, P ovale, P malariae
Epidemiology
 Highest burden of disease is in Africa but is found
in most tropical/subtropical areas worldwide

 Periodic febrile paroxysms


 Nonspecific malaise, headache, nausea, vomiting,
Manifestations
abdominal pain, diarrhea, myalgia

 Cerebral (eg, delirium, seizure), hypoglycemia,


ARDS, acidosis, renal/hepatic failure,
Complications
coagulopathy

 Thin & thick peripheral blood smears


Diagnosis  Rapid testing

ARDS = acute respiratory distress syndrome.


Atrioventricular block
Clinical presentation ECG features Management
First degree Asymptomatic PR interval prolongation Observation
Observation
Progressive PR interval
Mobitz type I
Usually asymptomatic lengthening followed by dropped
second degree (rarely PPM
QRS complex
placement)
Fatigue,
Mobitz type II Constant PR interval with
lightheadedness, PPM placement
second degree randomly dropped QRS complexes
syncope
Fatigue,
Third degree Complete dissociation of P waves
lightheadedness, PPM placement
(complete) & QRS complexes
syncope
PPM = permanent pacemaker.
Idiopathic intracranial hypertension
 Women of childbearing age
 Recent weight gain/obesity
Risk factors
 Medications (eg, retinoids/vitamin A, tetracyclines, growth hormone)

 Impaired CSF resorption & intracranial venous hypertension


Pathophysiology
 Headache/nausea/vomiting
 Visual changes (transient obscurations; vision loss; diplopia due to
Clinical abducens nerve [CN VI] palsy)
features  Pulsatile tinnitus
 Retrobulbar pain/neck pain/back pain

 Papilledema & enlarged blind spots


 MRI to rule out mass lesions/hydrocephalus
Diagnosis  MR venography to rule out venous thrombosis
 Lumbar puncture: elevated opening pressure

 Weight loss, including bariatric surgery


Treatment  Carbonic anhydrase inhibitor (acetazolamide, topiramate)

CSF = cerebrospinal fluid.


Management of sickle cell anemia
 Vaccination
 Penicillin (until age 5)
Maintenance  Folic acid supplementation
 Hydroxyurea (for patients with recurrent vaso-occlusive crises)

 Hydration
 Analgesia
Acute pain crises
 +/- Transfusion

Behçet disease
 Young adults
Epidemiology  Turkish, Middle Eastern, or Asian descent

 Recurrent, painful oral aphthous ulcers


 Genital ulcers
Clinical  Eye lesions (eg, uveitis)
findings  Skin lesions (eg, erythema nodosum, acneiform lesions)
 Thrombosis

 Pathergy: Exaggerated skin ulceration with minor trauma (eg,


needlestick)
Evaluation
 Biopsy: Nonspecific vasculitis of different sized vessels

Cardiovascular risk factor management in type 2 diabetes mellitus


 Healthy weight
 Exercise
General measures
 Smoking cessation

 Medication + lifestyle changes to target of 125-130/<80 mm


Hg
Blood pressure  ACE inhibitor or ARB recommended if diabetic kidney
disease is present

 High-intensity statin:* established CVD or 10-year CVD risk


≥20%
Cholesterol  Moderate-intensity statin:** all other patients with diabetes
mellitus age ≥40

 Lifestyle measures
 SGLT2 inhibitor
Glycemic control
 GLP-1 agonist

*Atorvastatin 40-80 mg or rosuvastatin 20-40 mg daily.

**Atorvastatin 10-20 mg, rosuvastatin 5-10 mg, simvastatin 20-40 mg, pravastatin 40-80 mg,
lovastatin 40 mg, fluvastatin XL 80 mg, or pitavastatin 2-4 mg daily.

ARB = angiotensin receptor blocker; CVD = cardiovascular disease; GLP-1 = glucagon-like


peptide-1; SGLT2 = sodium-glucose cotransporter-2.
Secondary causes of hypertension
Condition Clinical clues/features
 Elevated creatinine level
Renal parenchymal disease  Abnormal urinalysis (proteinuria, red blood cell casts)

Renovascular disease  Recurrent flash pulmonary edema


 Elevated creatinine level (particularly with ACE inhibitor
use)
 Abdominal bruit

 Hypokalemia (spontaneous or thiazide induced)


Primary
 Metabolic alkalosis
hyperaldosteronism
 Daytime somnolence
Obstructive sleep apnea  Increased neck circumference

 Paroxysmal hypertension & tachycardia


Pheochromocytoma  Headaches, palpitations, diaphoresis

 Cushingoid body habitus & proximal muscle atrophy


Cushing syndrome  Hyperglycemia

 Hyperthyroidism: anxiety, heat intolerance, weight loss,


tachycardia
Thyroid disease  Hypothyroidism: fatigue, cold intolerance, weight gain,
bradycardia

 Mild hypercalcemia ± symptoms (eg, constipation)


Primary
 Kidney stones
hyperparathyroidism
 Upper extremity hypertension with brachial-femoral pulse
delay (common)
Coarctation of the aorta
 Lateralizing hypertension (less common)

Paraneoplastic
Involved site Clinical features
syndrome
 Fluctuating muscle weakness
o Ocular (ptosis, diplopia)
Acetylcholine receptor in o Bulbar (dysphagia,
Myasthenia gravis
postsynaptic membrane dysarthria)
o Facial, neck & limb muscles

 Proximal muscle weakness


 Autonomic dysfunction (eg, dry
mouth)
Presynaptic membrane
Lambert-Eaton  Cranial nerve involvement
voltage-gated calcium
syndrome (eg, ptosis)
channels
 Diminished or absent deep-
tendon reflexes

Dermatomyositis/ Muscle fiber injury  Symmetrical & more proximal


muscle weakness
 ILD, Raynaud phenomenon
 Polyarthritis
polymyositis  Dysphagia
 Skin findings (eg, Gottron papules,
heliotrope rash) in dermatomyositis

ILD = interstitial lung disease.


Somatic symptom disorder
 Female
 Lower educational level
 Chronic childhood illness or family history of chronic illness
Risk factors
 Childhood abuse/neglect
 Sexual trauma

 ≥1 somatic symptom(s) causing distress/functional impairment


 Excessive thoughts, anxiety, or behaviors (time & energy) related to
Key features symptoms
 ≥6 months duration

 High health care utilization/multiple providers


Associated
features  Repeated testing rarely reassuring

 Schedule regular visits (not symptom driven) with same provider


 Limit unnecessary workup & specialist referrals
 Legitimize symptoms but focus on stress reduction/coping strategies
Management
 Antidepressants, cognitive-behavioral therapy if treatment resistant

Adverse effects of inhaled corticosteroids


~75% of dose deposited in oropharynx

 Dysphonia: steroid-induced laryngeal myopathy; common (50%) & usually


minor
Local  Thrush: affects tongue & pharynx (esophagus: very rarely); prevent by
rinsing & gargling with water, using spacer (decrease local deposition)
 Other: contact dermatitis (budesonide hypersensitivity); cough & reflex
bronchoconstriction

Systemic* ~25% of dose deposited in peripheral lung & systemically absorbed

 HPA axis: secondary adrenal insufficiency (usually subclinical); can coexist


with ICS-induced Cushing syndrome
 Skeletal: small ↑ osteoporosis & fracture risk
 Other: dermal thinning (fragile skin, purpura), ocular effects (cataract
formation, ↑ IOP), small ↑ CAP risk in COPD patients

*Uncommon. Typically only seen with prolonged (years) of high-dose ICS, superimposed oral
glucocorticoid use, or concurrent administration of potent cytochrome P-450 3A4 inhibitor.

CAP = community-acquired pneumonia; COPD = chronic obstructive pulmonary disease; HPA


= hypothalamic-pituitary-adrenal; ICS = inhaled corticosteroid; IOP = intraocular pressure.
Clinical manifestations of hereditary hemochromatosis
Skin Hyperpigmentation (bronze diabetes)
Musculoskeletal Arthralgia, arthropathy & chondrocalcinosis
Elevated hepatic enzymes with hepatomegaly (early), cirrhosis (later) &
Gastrointestinal
increased risk of hepatocellular carcinoma
Endocrine Diabetes mellitus, secondary hypogonadism & hypothyroidism
Cardiac Restrictive or dilated cardiomyopathy & conduction abnormalities
Infections Increased susceptibility to Listeria, Vibrio vulnificus & Yersinia enterocolitica
Entamoeba histolytica
 Resource-limited regions (contaminated food/water)
Risk factors
 Most are asymptomatic
 Colitis: prolonged bloody/mucoid diarrhea
Clinical  Liver abscess: RUQ pain, fever
manifestations o Complications: pleural effusion, rupture into peritoneum/pleural
space

 Stool PCR/antigen: preferred


 Stool microscopy: low sensitivity
Diagnosis
 Serology*: useful for isolated liver abscess

 Metronidazole or tinidazole

     PLUS
Treatment
 Intraluminal antibiotic (eg, paromomycin)

*Does not distinguish between prior & current infection.

RUQ = right upper quadrant.


Common causes of diarrhea in patients with AIDS
Organism CD4 count Symptoms
Cryptosporidium <180/mm3  Severe watery diarrhea
 Low-grade fever
 Weight loss

 Watery diarrhea
 Crampy abdominal pain
Microsporidium/Isosporidium <100/mm3  Weight loss
 Fever is rare

 Watery diarrhea
 High fever (>39 C [102.2 F])
Mycobacterium avium complex <50/mm3
 Weight loss

 Frequent, small-volume diarrhea


 Hematochezia
 Abdominal pain
Cytomegalovirus <50/mm3
 Low-grade fever
 Weight loss

Infectious urethritis in men


 Neisseria gonorrhoeae
 Chlamydia trachomatis
Etiology  Mycoplasma genitalium
 Trichomonas vaginalis

 Dysuria
Manifestations  Discharge

 Gram stain & culture


Diagnosis  Nucleic acid amplification testing

 GU alone: ceftriaxone
 GU + Chlamydia*: ceftriaxone +
doxycycline
Treatment
 Chlamydia/Mycoplasma: azithromycin
 Trichomonas: metronidazole

*GU + uncertain Chlamydia status is also treated with ceftriaxone +


doxycycline.

GU = gonococcal urethritis.
Autosomal dominant polycystic kidney disease
Clinical  Most patients asymptomatic until age 30-40
presentation  Flank pain, hematuria
 Hypertension
 Palpable abdominal masses (usually bilateral)
 Chronic kidney disease (CKD)

 Cerebral aneurysms
 Hepatic & pancreatic cysts
Extrarenal  Mitral valve prolapse, aortic regurgitation
features  Colonic diverticulosis
 Ventral & inguinal hernias

 Ultrasonography showing multiple renal cysts


Diagnosis
 Aggressive control of risk factors for CV & CKD
 ACE inhibitors preferred for hypertension
Management
 Hemodialysis, renal transplant for ESRD

CV = cardiovascular; ESRD = end-stage renal disease.


Tabes dorsalis
 Years → decades after initial infection
Epidemiology  Increased incidence/more rapid progression in those with HIV

 Treponema pallidum directly damages dorsal sensory roots


Pathogenesis  Secondary degeneration of the dorsal columns

 Sensory ataxia
 Lancinating pains
Clinical findings  Neurogenic urinary incontinence
 Associated with Argyll Robertson pupils

 10-14 days of intravenous penicillin G


Treatment
AL amyloidosis AA amyloidosis
 Chronic inflammatory
 Multiple myeloma conditions: rheumatoid
arthritis, inflammatory
  bowel disease
Associated
conditions
 Waldenström  Chronic infections:
macroglobulinemia osteomyelitis,
tuberculosis

 Abnormally folded
proteins: beta-2
 Light chains
Composition microglobulin,
of amyloid apolipoprotein or
(usually lambda)
transthyretin
AA amyloidosis = inflammatory amyloidosis; AL amyloidosis = amyloid
light-chain amyloidosis.
Lumbosacral strain
 Strain of paraspinal muscles, tendons, intervertebral ligaments
 Sudden or unbalanced muscle contraction (eg, lifting, twisting)
Causes  Risk factors: obesity, spinal deformity or degeneration, muscle
weakness

 Pain in lumbar area; may radiate to buttocks, hips, thighs (above knee)
 Paraspinal tenderness
Clinical features
 No neurologic deficits; negative straight-leg raising test

 Moderate activity
 Nonsteroidal anti-inflammatory drugs
Management
 Nonbenzodiazepine muscle relaxants

Comorbidities that encourage atrial fibrillation


 Advanced age
 Systemic hypertension
 Mitral valve dysfunction
 Left ventricular failure
Precipitants of atrial dilation  Coronary artery disease & related factors (eg, DM,
&/or conduction remodeling smoking)
 Obesity & obstructive sleep apnea

 Chronic hypoxic lung disease (eg, COPD)

 Hyperthyroidism
 Excessive alcohol use
 Increased sympathetic tone
Triggers of increased o Acute illness (eg, sepsis, PE, MI)
automaticity o Cardiac surgery

 Sympathomimetic drugs (eg, cocaine)

COPD = chronic obstructive pulmonary disease; DM = diabetes mellitus; MI = myocardial


infarction;
PE = pulmonary embolism.
Prerenal acute kidney injury
Etiology  Decreased renal perfusion
o True volume depletion
o Decreased EABV (eg, heart failure, cirrhosis)
o Displacement of intravascular fluid (eg, sepsis, pancreatitis)
o Bilateral renal artery stenosis with ACE inhibition
o Afferent arteriole vasoconstriction (eg, NSAIDs)

 Increase in serum creatinine (eg, 50% from baseline)


 Decreased urine output
 Blood urea nitrogen/creatinine ratio >20:1
Clinical features
 Fractional excretion of sodium <1%
 Unremarkable ("bland") urine sediment

 Restoration of renal perfusion


Treatment
EABV = effective arterial blood volume; NSAIDs = nonsteroidal anti-inflammatory drugs.
Cholesterol crystal embolism (atheroembolism)
 Comorbid conditions (hypercholesterolemia, hypertension, type 2
diabetes mellitus)
Risk factors
 Cardiac catheterization or vascular procedure

 Dermatologic (livedo reticularis, ulcers, gangrene, blue toe syndrome)


 Renal (acute or subacute kidney injury)
Clinical  CNS (stroke, amaurosis fugax)
features  Ocular involvement (Hollenhorst plaques)
 Gastrointestinal (intestinal ischemia, pancreatitis)

Laboratory findings

 Elevated serum creatinine, eosinophilia, hypocomplementemia


 Urinalysis, typically benign with few cells or casts, may have
eosinophiluria
Diagnosis
Skin or renal biopsy

 Biconvex, needle-shaped clefts within occluded vessels


 Perivascular inflammation with eosinophils

Amyotrophic lateral sclerosis


Clinical manifestations  Upper motor neuron signs
o Spasticity
o Hyperreflexia
o Pathologic reflexes (eg, jaw jerk, extensor plantar
reflex)
 Lower motor neuron signs
o Atrophy
o Fasciculations
 Bulbar symptoms
o Dysarthria
o Dysphagia

 Clinical evaluation
 EMG
Diagnosis
 MRI of brain & spinal cord (to exclude other causes)

 Riluzole
 Respiratory support (eg, NIPPV)
Treatment
 Nutritional support (eg, PEG tube)

EMG = electromyography; NIPPV = noninvasive positive pressure ventilation; PEG =


percutaneous endoscopic gastrostomy.
Inflammatory bowel disease subtype characteristics
Crohn disease Ulcerative colitis
 Anywhere mouth to anus (mostly
ileum & colon)  Rectum (always) & colon
Involvement  Perianal disease with rectal sparing  Continuous lesions
 Skip lesions

 Noncaseating granulomas  No granulomas


Microscopy
 Transmural inflammation  Mucosal & submucosal
Gross  Linear mucosal ulcerations inflammation
findings  Cobblestoning, creeping fat  Pseudopolyps

 Abdominal pain (varying


 Abdominal pain (often RLQ)
Clinical locations)
 Watery diarrhea (bloody if colitis)
manifestations  Bloody diarrhea

 Fistulae, abscesses
Intestinal  Toxic megacolon
 Strictures (bowel obstruction)
complications
RLQ = right lower quadrant.
Internal validity External validity
Describes causality (ie, if change in Describes generalizability (ie, if
independent variable causes change in observed relationship applies to
dependent variable) situations or people outside study)
Characteristics ↑ As study becomes more tightly ↓ As study becomes more tightly
controlled controlled
↓ As study becomes more like the real ↑ As study becomes more like the real
world world
Threats to Bias due to: Bias due to:
validity
 Confounding  Artificial research
 History
 Maturation
 Measurement environment
 Regression toward the mean  Measurement effects
 Repeated testing  Nonrepresentative sample
 Selection

Acute pericarditis
 Viral or idiopathic
 Autoimmune disease (eg, SLE)
 Uremia (acute or chronic renal failure)
Etiology  Post myocardial infarction
o Early: peri-infarction pericarditis
o Late: Dressler syndrome

 Pleuritic chest pain (↓ when sitting) ± fever


 Pericardial friction rub (highly specific)
Clinical features
 ECG: diffuse ST-segment elevation & PR-segment
& diagnosis
depression
 Echocardiography: pericardial effusion

 NSAIDs & colchicine for viral or idiopathic etiology


Treatment  Variable for other etiologies

NSAIDs = nonsteroidal anti-inflammatory drugs; SLE = systemic lupus erythematosus.


Systemic sclerosis subtype characteristics
 Scleroderma on head & distal upper extremities
 Prominent vascular manifestations
o Raynaud phenomenon
o Cutaneous telangiectasia
Limited cutaneous o Pulmonary arterial hypertension
 CREST syndrome
 Anticentromere antibodies
 Better prognosis

 Scleroderma on trunk & upper extremities


 Prominent internal organ involvement
o Scleroderma renal crisis
o Myocardial ischemia & fibrosis
Diffuse cutaneous o Interstitial lung disease
 Anti–Scl-70 (topoisomerase type I) antibodies
 Anti–RNA polymerase III antibodies
 Worse prognosis
CREST = Calcinosis, Raynaud phenomenon, Esophageal dysmotility, Sclerodactyly &
Telangiectasia.
Focal segmental glomerulosclerosis
 Primary FSGS: circulating factor causing immune injury to
podocytes
 Secondary FSGS: glomerular hyperfiltration (eg, obesity,
Pathogenesis
solitary kidney, reflux nephropathy), podocyte toxin (eg,
heroin), infection (eg, HIVAN)

 Primary FSGS: usually nephrotic syndrome*


Clinical features  Secondary FSGS: proteinuria ± nephrotic syndrome

 LM: segmental scarring in <50% of glomeruli**


 IF: usually negative
Diagnosis
 EM: podocyte foot process effacement

 Renin-angiotensin blockade, loop diuretics


 Primary FSGS: immunosuppression
Treatment  Secondary FSGS: risk factor modification (eg, weight loss,
ART)

*Proteinuria >3.5 g/day, generalized edema & hypoalbuminemia.

**Glomerular tuft collapse is also seen in HIVAN.

ART = antiretroviral therapy; EM = electron microscopy; FSGS = focal segmental


glomerulosclerosis; HIVAN = HIV-associated nephropathy; IF = immunofluorescence
microscopy; LM = light microscopy.
Dependent variable
Qualitative
Quantitative
(categorical)
Qualitative Chi-square, logistic t test, ANOVA, linear
(categorical) regression* regression
Independent variable
Correlation, linear
Quantitative Logistic regression*
regression
*Dependent variable must be dichotomous.

ANOVA =  analysis of variance.


Huntington disease
 Motor: chorea, delayed saccade
 Psychiatric: depression, irritability, psychosis,
Clinical features obsessive-compulsive symptoms
 Cognitive: executive dysfunction

Findings  Genetic: autosomal dominant CAG trinucleotide repeat


expansion disorder
 Neuropathology: loss of GABA-ergic neurons
 Imaging: caudate nucleus & putamen atrophy

 Treatment: supportive
Management & prognosis  Survival: 10-20 years

Acute interstitial nephritis


 Medications (eg, antibiotics, NSAIDs, PPIs)*
 Rheumatologic disease (eg, SLE, Sjögren syndrome,
Causes sarcoidosis)
 Infections (eg, Legionella, tuberculosis, CMV)

 New medication exposure


 Acute kidney injury
 Arthralgias, malaise
Clinical features
 Classic triad of fever, skin rash & eosinophilia rarely
present**

 Clinical presentation
 Urinalysis: WBCs & WBC casts ± mild RBCs &
proteinuria
Diagnosis
 Peripheral eosinophilia ± urine eosinophils
 ± Renal biopsy: tubulointerstitial inflammation & edema

 Discontinue offending drug or treat underlying condition


 Systemic glucocorticoids
Management
 Supportive hemodialysis if needed

*Medications account for ~75% of cases.

**Classic triad is present in only ~10% of cases.

CMV = cytomegalovirus; NSAID = nonsteroidal anti-inflammatory drug; PPI = proton pump


inhibitor; RBC = red blood cell; SLE = systemic lupus erythematosus; WBC = white blood cell.
Alcoholic cerebellar degeneration
 >10 years heavy alcohol use
Epidemiology  Degeneration of Purkinje cells (cerebellar vermis)

 Usually develops over weeks to months


 Wide-based gait
Manifestations  Incoordination in legs
 Cognition usually intact

Diagnosis  Clinical:
o Impaired tandem walking/heel-knee-shin
o Preserved finger-nose testing
 CT/MRI - cerebellar atrophy

 Alcohol cessation
 Nutritional supplements
Treatment
 Ambulatory assistance devices (eg, walker)

Multiple myeloma
 Plasma cell neoplasm produces monoclonal paraprotein
Pathophysiology (immunoglobulin)

 Bone pain, fractures


 Constitutional symptoms (weight loss, fatigue)
Manifestations
 Recurrent infections

 Normocytic anemia
 Renal insufficiency
Laboratory  Hypercalcemia (constipation, muscle weakness)
 Monoclonal paraproteinemia (M-spike)

 Osteolytic lesions/osteopenia (osteoclast activation)


Radiology
Statistical significance:
Relationship between confidence intervals and p-values
"A ___ confidence interval that does not include the null value…" 95% 99%
"…corresponds to p < ___." 0.05 0.01

Avascular necrosis
Etiology  Steroid use
 Alcohol abuse
 Systemic lupus erythematosus
 Antiphospholipid syndrome
 Hemoglobinopathy (eg, sickle cell)
 Infection (eg, osteomyelitis, HIV)
 Kidney transplantation
 Decompression sickness

 Groin pain on weight bearing


 Pain on hip abduction & internal rotation
Clinical manifestations
 No erythema, swelling, or point tenderness

 Normal white blood cell count


Laboratory findings  Normal ESR & CRP

 Crescent sign seen in advanced stage


Radiologic imaging  MRI is most sensitive modality

CRP = C-reactive protein; ESR = erythrocyte sedimentation rate.


Hereditary thrombophilias*
 Most common in white patients
Factor V Leiden  Activated protein C resistance

 2nd most common in white patients


Prothrombin mutation  ↑ Prothrombin levels

 Inherited form is rare


Antithrombin deficiency  Acquired: DIC, cirrhosis, nephrotic syndrome

 ↓ Inactivation of factors Va & VIIIa


Protein C or S deficiency  Warfarin-induced skin necrosis (protein C only)

*Typically autosomal dominant with variable penetrance.

DIC = disseminated intravascular coagulation.


Cardiovascular effects of thyrotoxicosis
 Sinus tachycardia
 Premature atrial & ventricular complexes
Rhythm
 Atrial fibrillation/flutter

 Systolic hypertension & ↑ pulse pressure


 ↑ Contractility & cardiac output
Hemodynamic effects  ↓ Systemic vascular resistance
 ↑ Myocardial oxygen demand

 High-output failure
Heart failure  Exacerbation of preexisting low-output failure
 Coronary vasospasm
Angina symptoms  Preexisting coronary atherosclerosis

Viral myocarditis
 Relatively young adults (eg, age <55)
 Viral prodrome (eg, fever, malaise, myalgias)
Clinical  Heart failure (eg, dyspnea, orthopnea, edema)
presentation  Chest pain
 Sudden cardiac death

 ECG: nonspecific
 Echocardiography: 4-chamber dilation
Diagnosis  Cardiac MRI: late enhancement of the epicardium
 Biopsy: lymphocytic infiltration, viral DNA or RNA

 Medication (eg, diuretics, ACE inhibitor, beta blocker)


 Temporary ventricular assist device, if needed
Treatment
 Heart transplant if no recovery

Acute bacterial prostatitis


 Intraprostatic reflux of pathogens in urine
Etiology  Primarily gram-negative bacilli (Escherichia coli ~75%)

 Flu-like illness (eg, fever, chills, malaise, myalgia)


 Lower urinary symptoms (eg, dysuria, urine retention, pelvic
Manifestations
pain)

 Digital rectal examination: tender, swollen prostate


Diagnosis  Urine culture

 6 weeks of TMP-SMX or fluoroquinolone


Treatment
 Bacteremia/systemic spread
 Prostatic abscess
Complications
 Chronic prostatitis

TMP-SMX = trimethoprim-sulfamethoxazole.
Prevention of calcium stone (calcium oxalate, calcium phosphate) recurrence
Intervention Mechanism
Dietary All calcium stones:
interventions ↑ Fluid (produce >2 L/day urine) ↑ Urine flow, ↓ solute concentration
↓ Sodium (<2,300 mg/day) ↑ Renal calcium reabsorption
↑ Citrate (fruits & vegetables) Binds urinary calcium to inhibit stone
formation
↑ Potassium ↑ Urinary citrate excretion
↓ Animal protein ↓ Urinary calcium excretion
Calcium oxalate stones:
Adequate calcium intake (1,200
↓ Oxalate absorption in GI tract
mg/day)
↓ Oxalate (spinach) ↓ Urinary oxalate excretion
Pharmacologic Thiazide diuretics ↑ Renal calcium reabsorption
interventions Potassium citrate ↑ Urinary citrate concentration
GI = gastrointestinal.
Nocardiosis
 Gram-positive rod (beaded or branching)
 Partially acid-fast
Microbiology
 Aerobic

 Endemic in soil
 Disease from spore inhalation or traumatic inoculation into skin
Epidemiology
 Immunocompromised or elderly patients

 Pneumonia: similar to tuberculosis


 CNS involvement: brain abscess
Clinical features
 Cutaneous involvement

 Trimethoprim-sulfamethoxazole
Treatment  Surgical drainage of abscesses

Otitis externa
 Water exposure
 Trauma (eg, cotton swabs, ear candling)
 Foreign material (eg, hearing aid, headphones)
Risk factors
 Dermatologic conditions (eg, eczema, contact
dermatitis)

 Pseudomonas aeruginosa
Microbiology  Staphylococcus aureus

 Otalgia, pruritus, discharge, hearing loss


 Pain with auricle manipulation
Clinical  Ear canal erythema, edema, debris
manifestations  Tympanic membrane spared (clear, not inflamed, no
middle ear fluid)

Treatment  Remove debris


 Topical antibiotic (eg, fluoroquinolone)
 ± Topical glucocorticoid
 Consider wick placement to facilitate medication
delivery

Treatment of rosacea
 Avoidance of sun exposure, hot/spicy foods,
alcohol
General measures
 Gentle cleansers & emollients

 Topical brimonidine
Erythematotelangiectatic rosacea
 Laser/intense pulsed light therapy
(flushing, erythema, telangiectasia)
 First line: topical metronidazole, azelaic
Papulopustular rosacea acid, ivermectin
(small papules & pustules)  Second line: oral tetracyclines

 Oral isotretinoin
Phymatous rosacea
 Laser therapy/surgery
(irregular thickening of skin)
Ocular rosacea  Lid scrubs & ocular lubricants
(burning/foreign body sensations,  Topical or systemic antibiotics (eg,
blepharitis, keratitis, conjunctivitis, corneal metronidazole, macrolides)
ulcers)
Myotonic dystrophy
 Autosomal dominant CTG trinucleotide repeat expansion
Pathogenesis  Longer repeat length correlating with earlier & more severe disease

 Classic (adult): myotonia & weakness (eg, face, hands, ankles)


 Childhood: cognitive & behavioral difficulties (classic symptoms
Presentation develop over time)
 Infantile: hypotonia, respiratory failure, inverted V–shaped upper lip

 Cardiac: arrhythmias, cardiomyopathy


 Gastrointestinal: dysphagia, constipation
Associated  Respiratory: pharyngeal weakness, hypoventilation
findings  Nonmuscular: insulin resistance, hypogonadism, cataracts, frontal
balding, excessive daytime sleepiness

 Genetic testing
Diagnosis &
 Supportive management
treatment
CTG = cytosine-thymine-guanine.
Hodgkin lymphoma
 Bimodal peak incidence: age 15-35 & >60
Epidemiology  Association with EBV in immunosuppression
 Painless lymphadenopathy
 Mediastinal mass
Manifestations  B symptoms (ie, fever, sweats, weight loss)
 Pruritus

 Lymph node biopsy


Diagnosis  Reed-Sternberg cells on histology

EBV = Epstein-Barr virus.


Carbon monoxide poisoning
 Smoke inhalation
 Defective heating systems
Epidemiology
 Gas motors operating in poorly ventilated areas

Mild-moderate

 Headache, confusion
 Malaise, dizziness, nausea
Manifestations
Severe

 Seizure, syncope, coma


 Myocardial ischemia, arrhythmias

 ABG: carboxyhemoglobin level


Diagnosis  ECG ± cardiac enzymes

 High-flow 100% oxygen


Treatment  Intubation/hyperbaric oxygen (severe)

ABG = arterial blood gas.


Kaposi sarcoma
Type Risk group Features
 Mediterranean or
 Indolent
Central/Eastern European
Classic  Visceral lesions rare
 Age >60

 Indolent or aggressive
 Equatorial Africa
Endemic  Visceral lesions can occur

Iatrogenic  Immunosuppression  Can be aggressive


 Particularly after organ  Visceral lesions common
transplantation  Usually improves when
immunosuppressives reduced

 Can be aggressive
 Men who have sex with men  Visceral lesions common
AIDS  CD4 <200/mm3  Usually improves with antiretroviral
therapy

Clues for increasing index of suspicion for Legionella pneumonia


 Recent travel (especially cruise or hotel stay) within
the previous 2 weeks
Exposure to possibly
 Contaminated potable water in hospitals/nursing
contaminated water
homes

 Fever >39 C (102.2 F)


 Bradycardia relative to high fever
 Neurologic symptoms (especially confusion)
Clinical clues  Gastrointestinal symptoms (especially diarrhea)
 Unresponsive to β-lactam & aminoglycoside
antibiotics

 Hyponatremia
 Hepatic dysfunction
 Hematuria & proteinuria
Laboratory clues
 Sputum Gram stain showing many neutrophils but
few or no microorganisms

Common medications that cause hyperkalemia


Medication Mechanism
Decreases aldosterone secretion (inhibition of AT II/AT II
ACE inhibitor, ARB
receptor) + inhibits ENaC
Cyclosporine Blocks aldosterone activity
Digitalis Inhibits Na+/K+-ATPase
Heparin Blocks aldosterone production
Nonselective
Interferes with β2-mediated intracellular potassium uptake
β-adrenergic blocker
Decreases renal perfusion → decreased potassium delivery to the
NSAID
collecting ducts
Potassium-sparing diuretic Inhibits ENaC or aldosterone receptor
Causes extracellular leakage of potassium through acetylcholine
Succinylcholine
receptors
Trimethoprim Inhibits ENaC
ARB = angiotensin II receptor blocker; AT = angiotensin; ENaC = epithelial sodium channel;
Na+/K+-ATPase = sodium-potassium pump; NSAID = nonsteroidal anti-inflammatory drug.
Physical examination features of LVOT obstruction
due to aortic stenosis & hypertrophic cardiomyopathy
Aortic stenosis Hypertrophic cardiomyopathy
Decreased preload*
↓ Murmur intensity ↑ Murmur intensity
(eg, Valsalva strain phase)
Increased afterload
↓ Murmur intensity ↓ Murmur intensity
(eg, handgrip)
S4 Often present Often present
Ejection click* Usually present Absent
Carotid pulses* Soft & delayed Brisk
*Distinguishing feature.

LVOT = left ventricular outflow tract.

Polyarteritis nodosa
 Correlation with underlying hepatitis B/C (immune complexes)
 Fibrinoid necrosis of arterial wall → luminal narrowing & thrombosis
→ tissue ischemia
Pathophysiology
 Internal/external elastic lamina damage → microaneurysm formation 
→ rupture & bleeding

 Constitutional: fever, weight loss, malaise


 Skin: nodules, livedo reticularis, ulcers, purpura
 Renal: hypertension, renal insufficiency, arterial aneurysms
Clinical
 Nervous: headache, seizures, mononeuritis multiplex
features
 Gastrointestinal: mesenteric ischemia/infarction
 Musculoskeletal: myalgias, arthritis

 Negative ANCA & ANA


 Angiography: microaneurysms & segmental/distal narrowing
Diagnosis
 Tissue biopsy: nongranulomatous transmural inflammation

ANA = antinuclear antibodies; ANCA = antineutrophil cytoplasmic antibodies.


 
Management of AMA discharges
 Financial concerns: involve social workers
Investigate/address  Substance withdrawal: offer medication-assisted treatment
reasons for leaving  Care delay dissatisfaction: apologize for unmet expectations

Ensure/document  Determine that patient:


patient's o Has capacity for medical decision-making
informed refusal o Understands benefits of staying & risks of leaving
o Communicates reasoned basis for refusing treatment
 Document informed refusal in chart, including signed AMA
form

 Offer appropriate treatments/prescriptions


Provide best possible  Offer assistance with follow-up care
alternative treatment  Offer to resume treatment at any time

AMA = against medical advice.


Exudative & transudative pleural effusions
Exudate Transudate
 Pleural protein/serum protein >0.5

OR

 Pleural LDH/serum LDH >0.6  Exudate criteria not


Light criteria met
OR

 Pleural LDH >2/3 upper limit of normal


of serum LDH

 Change in
 Inflammatory increase in membrane
hydrostatic or
Pathophysiology permeability
oncotic pressure

 Heart failure
 Infection (eg, pneumonia, TB)
 Cirrhosis (hepatic
 Malignancy
Common causes hydrothorax)
 Rheumatologic disease
 Nephrotic syndrome

LDH = lactate dehydrogenase; TB = tuberculosis.


Clostridioides difficile colitis
 Recent antibiotic use or hospitalization
 Advanced age (>65)
 Gastric acid suppression (eg, PPI, H2 blocker)
Risk factors
 Underlying inflammatory bowel disease
 Chemotherapy

 Profuse watery diarrhea


Clinical  Leukocytosis (~15,000/mm3)
presentation  Fulminant colitis or toxic megacolon

Diagnosis  Stool PCR for C difficile genes*


 Stool EIA for C difficile toxin & glutamate
dehydrogenase antigen

 Hand hygiene with soap & water


Infection  Contact isolation
control  Sporicidal disinfectants (eg, bleach)

*Genes specific to toxigenic strains are assessed.

EIA = enzyme immunoassay; H2 = histamine-2 receptor; PPI = proton


pump inhibitor.
 
Sporotrichosis
 Sporothrix schenckii (dimorphic fungus)
 Decaying plant matter/soil
Epidemiology
 Gardeners, farmers & landscapers

 Subacute/chronic manifestations
 Inoculation → skin papule → ulceration → nonpurulent, odorless
drainage
Manifestations
 Proximal lesions form along lymphatic chain
 Distant spread & systemic symptoms are rare

 Cultures (aspirate fluid or biopsy) → cigar-shaped yeast with narrow-


Diagnosis based budding at 37 C (98.6 F)

 Prolonged course of itraconazole


Treatment
Causes of delirium
 Dementia
 Parkinson disease
Predisposing  Prior stroke
risk factors  Advanced age
 Sensory impairment

 Drugs (eg, narcotics, sedatives, antihistamines, muscle relaxers,


polypharmacy)
 Infections (eg, pneumonia, urinary tract infection, meningitis)
 Electrolyte disturbances (eg, hyponatremia, hypercalcemia)
Precipitating  Metabolic derangements (eg, volume depletion, vitamin B12
factors deficiency, hyperglycemia)
 Systemic illnesses (eg, congestive heart failure, hepatic failure,
malignancy)
 CNS conditions (eg, seizure, stroke, head injury, subdural hematoma)

Treatment of acute deep vein thrombosis/pulmonary embolism


Oral factor Xa inhibitors Warfarin
Mechanism
Direct factor Xa inhibition Vitamin K antagonism
of action
Therapeutic onset 2-4 hr 5-7 days
Yes, overlap with UFH
Overlap needed? No
or LMWH for ~5 days
Laboratory monitoring No PT/INR
LMWH = low molecular weight heparin; UFH = unfractionated heparin.

SGLT-2 inhibitors*
 Increased urinary glucose excretion (block proximal tubule
Mechanism of action glucose reabsorption)
 Reduced progression of nephropathy & albuminuria
 Reduced cardiovascular morbidity & mortality
Possible benefits  Reduced hospitalizations for heart failure
 Weight loss

 Euglycemic ketoacidosis
Adverse effects  Increased risk of genitourinary infections

 Type 1 DM
 History of DKA
Contraindications
 Impaired renal function (eGFR <30-45 mL/min/1.73 m2)

*For example, canagliflozin & empagliflozin.

DKA = diabetic ketoacidosis; DM = diabetes mellitus; eGFR = estimated glomerular filtration


rate; SGLT-2 = sodium-glucose cotransporter 2.
Achalasia
 Inflammatory degeneration of inhibitory ganglions of the myenteric
Pathophysiology plexus

 Chronic dysphagia to solids & liquids, regurgitation


Clinical
 Heartburn, weight loss
presentation
 Manometry: incomplete LES relaxation, ↓ peristalsis of distal
esophagus
 Barium esophagography: smooth "bird-beak" narrowing at
Diagnosis
gastroesophageal junction
 Upper endoscopy to exclude malignancy

 Myotomy or pneumatic balloon dilation


Management  Botulinum toxin injection, nitrates & CCB

CCB = calcium channel blocker; LES = lower esophageal sphincter.


Skin conditions & associated diseases
Skin conditions Associated conditions
 Insulin resistance
 Acanthosis nigricans
 Gastrointestinal malignancy

 Insulin resistance
 Multiple skin tags  Pregnancy
 Crohn disease (perianal)

 Porphyria cutanea tarda  Hepatitis C


 Cutaneous leukocytoclastic vasculitis
(palpable pupura) secondary
to cryoglobulinemia

 Dermatitis herpetiformis  Celiac disease

 Sudden-onset, severe psoriasis


 Recurrent herpes zoster  HIV infection
 Disseminated molluscum contagiosum

 HIV infection
 Severe seborrheic dermatitis
 Parkinson disease

 Explosive onset multiple, itchy


 Gastrointestinal malignancy
seborrheic keratoses

 Pyoderma gangrenosum  Inflammatory bowel disease

Causes of polyuria & dilute urine


Primary polydipsia Central DI Nephrogenic DI
 ADH  ADH
 ADH
independent deficiency
resistance
Cause (excessive (CNS
(renal disease)
water intake) pathology)

 Chronic
 Idiopathic
lithium use
 Antipsychotics  Trauma
 Hypercalcemia
(dry mouth)  Pituitary
 Hereditary
Etiology  Psychiatric surgery
(AVPR2 &
conditions  Ischemic
aquaporin 2
encephalopathy
mutations)

Results  High urine  Low urine  Low urine


of water osmolality osmolality osmolality
deprivation
 Increased urine
Response to  No change  No change
osmolality
desmopressin
ADH = antidiuretic hormone; AVPR2 = vasopressor V2; DI = diabetes insipidus.
Distinguishing features of common upper respiratory illnesses
Viral upper respiratory Streptococcal
Influenza
syndrome pharyngitis
Onset of Slow, stepwise, migratory,
Abrupt & often dramatic Variable
symptoms or evolving
Upper Rhinorrhea, coryza, Usually mild Predominantly
respiratory
sneezing, mild pharyngitis pharyngeal symptoms
symptoms
Prominent with possible
Systemic Variable with possible
Usually mild high fever, myalgias,
symptoms fever & myalgias
headache
Pharyngeal erythema,
Nasal edema with normal
Examination Variable but often tonsillar hypertrophy &
or slightly erythematous
findings unremarkable exudates, tender cervical
pharynx
lymph nodes
Porphyria cutanea tarda
 Blisters, bullae, scarring, hypopigmentation/hyperpigmentation on sun
Clinical exposed skin (eg, back of hands, forearms, face)
presentation  Scarring & calcification similar to scleroderma

 Hepatitis C
 HIV
Associated  Excessive alcohol consumption
conditions  Estrogen use
 Smoking

 Mildly elevated liver enzymes & iron overload


Diagnostic
 Elevated plasma or urine porphyrin levels
testing
Esophageal perforation
 Instrumentation (eg, endoscopy), trauma
 Effort rupture (Boerhaave syndrome)
Etiology
 Esophagitis (infectious/pills/caustic)

 Chest/back &/or epigastric pain, systemic signs (eg, fever)


Clinical  Crepitus, Hamman sign (crunching sound on auscultation)
presentation  Pleural effusion with atypical (eg, green) fluid

 Chest x-ray or CT scan: widened mediastinum, pneumomediastinum,


pneumothorax, pleural effusion
 CT scan: esophageal wall thickening, mediastinal fluid collection
Diagnosis
 Esophagography with water-soluble contrast: leak from
perforation

 NPO, IV antibiotics & proton pump inhibitors


Management  Emergency surgical consultation

Common variable immunodeficiency


 Abnormal differentiation of B cells into plasma cells →
Pathophysiology decreased immunoglobulin production
 Symptom onset classically age 20-40, as early as puberty
 Recurrent respiratory infections (eg, pneumonia, sinusitis,
otitis)
 Recurrent GI infections (eg, Salmonella, Campylobacter,
Clinical Giardia)
manifestations  Chronic disease:
o Autoimmune (eg, RA, thyroid disease)
o Pulmonary (eg, bronchiectasis, fibrosis)
o GI (eg, chronic diarrhea, IBD-like conditions)

 ↓↓ IgG, ↓ IgA/IgM
Diagnosis  No response to vaccination

 Immunoglobulin replacement therapy


Management
GI = gastrointestinal; IBD = inflammatory bowel disease; RA = rheumatoid arthritis.
Systemic sclerosis
 Progressive tissue fibrosis

Pathogenesis
 Vascular dysfunction

 Skin: telangiectasia, sclerodactyly, digital ulcer, calcinosis cutis


 Extremities: arthralgia, myalgia, contracture
 Gastrointestinal tract: esophageal dysmotility, dysphagia, acid
Clinical features reflux
 Lungs: dyspnea, dry cough
 Vascular system: Raynaud phenomenon

 Antinuclear
 Anti–topoisomerase type I (anti–Scl-70) (diffuse SSc)
Autoantibodies
 Anticentromere (limited SSc)

 Lungs: interstitial lung disease, pulmonary arterial HTN


 Kidneys: HTN, scleroderma renal crisis (severe HTN, AKI,
Complications MAHA)
 Heart: myocardial fibrosis, pericarditis, pericardial effusion

AKI = acute kidney injury; HTN = hypertension; MAHA = microangiopathic hemolytic


anemia; SSc = systemic sclerosis.
Symptoms of digoxin toxicity
 Life-threatening arrhythmias
Cardiac
Gastrointestinal  Anorexia
 Nausea & vomiting
 Abdominal pain

 Fatigue
 Confusion
Neurologic  Weakness
 Color vision alterations

Acute management of acute coronary syndrome

(STEMI, NSTEMI, or unstable angina)


 Rapid chest pain relief
Nitrates  Caution with hypotension (eg, RV infarction)

 Cardioselective (eg, metoprolol, atenolol)


 Decreases myocardial O2 demand to limit infarct size
Beta blocker
 Contraindicated in cardiogenic shock & bradycardia

 Aspirin + P2Y12 inhibitor (eg, prasugrel, clopidogrel)*


Antiplatelet therapy  Reduces platelet activity

 Unfractionated heparin, bivalirudin, or enoxaparin


Anticoagulation  Limits thrombus expansion

 High potency (eg, atorvastatin, rosuvastatin)


Statin therapy  Stabilizes atherosclerotic plaque

STEMI

 PCI <90 min from 1st medical contact


 Fibrinolytics (eg, alteplase) if PCI is unavailable
Coronary reperfusion
NSTEMI or unstable angina

 Coronary angiography often within 24 hr

*In patients with NSTEMI or unstable angina, P2Y12 inhibitor therapy is often held until after
coronary angiography in case the atherosclerotic coronary anatomy indicates the need for
coronary artery bypass grafting.

NSTEMI = non–ST-segment elevation myocardial infarction; PCI = percutaneous coronary


intervention; RV = right ventricular; STEMI = ST-segment elevation myocardial infarction.
Opioid medications in patients with impaired kidney function
Recommended Avoid
 Fentanyl  Morphine
 Hydromorphone  Meperidine
 Methadone  Codeine
 Buprenorphine  Tramadol

Arthropathy of hereditary hemochromatosis


 Onset at age <40
 Chronic pain & bony swelling
Clinical features  Most common at 2nd & 3rd MCP joints
 Occasional acute flare

 Joint space narrowing


 Chondrocalcinosis
X-ray signs
 Hook-shaped osteophytes at metacarpal heads

 Oral analgesics (eg, acetaminophen, NSAIDs)


Management  Therapeutic phlebotomy (to prevent other complications)

MCP = metacarpophalangeal; NSAIDs = nonsteroidal anti-inflammatory drugs.


Manifestations of systemic lupus erythematosus
 Constitutional: fever, fatigue & weight loss
 Symmetric, migratory arthritis
 Skin: butterfly rash & photosensitivity
Clinical
 Serositis: pleurisy, pericarditis & peritonitis
symptoms
 Thromboembolic events (due to vasculitis & antiphospholipid antibodies)
 Neurologic: cognitive dysfunction & seizures

 Hemolytic anemia, thrombocytopenia & leukopenia


 Hypocomplementemia (C3 & C4)
 Antibodies:
Laboratory
o Antinuclear antibodies (sensitive)
findings
o Anti-dsDNA & anti-Smith (specific)
 Renal involvement: proteinuria & elevated creatinine

dsDNA = double-stranded DNA.


Clinical features of thyroid storm
 Thyroid or nonthyroidal surgery
Precipitating  Acute illness (eg, trauma, infection), childbirth
factors  Acute iodine load (eg, iodine contrast)

 High fever
 Tachycardia, hypertension, congestive heart failure, cardiac
arrhythmias (eg, atrial fibrillation)
Clinical
 Agitation, delirium, seizure, coma
presentation
 Goiter, lid lag, tremor
 Nausea, vomiting, diarrhea, jaundice
Hyperosmolar hyperglycemic state
 Type 2 diabetes mellitus
Patient
 Older age
characteristics
 Acute illness, trauma, infection
Inciting  Insulin nonadherence
factors  Medications: glucocorticoids, diuretics, atypical antipsychotics

Subacute or acute onset of:

Clinical  Altered mentation


features  Hyperglycemic symptoms (eg, polyuria)
 Volume depletion

 Glucose >600 mg/dL (33.3 mmol/L)


 Bicarbonate >18 mEq/L (18 mmol/L)
Laboratory  Normal anion gap
studies  Negative or small serum ketones
 Serum osmolality >320 mOsm/kg (320 mmol/kg)

Indications for statin therapy in prevention of ASCVD


 Established ASCVD
o Acute coronary syndrome
o Stable angina
Secondary prevention
o Arterial revascularization (eg, CABG)
o Stroke, TIA, PAD

 LDL ≥190 mg/dL


 Age ≥40 with diabetes mellitus
Primary prevention
 Estimated 10-year risk of ASCVD >7.5%-10%

ASCVD = atherosclerotic cardiovascular disease; CABG = coronary artery bypass grafting;


PAD = peripheral artery disease; TIA = transient ischemic attack.
Sheehan syndrome
 Obstetric hemorrhage complicated by hypotension
Pathogenesis  Postpartum pituitary infarction

 Lactation failure (↓ prolactin)


 Amenorrhea, hot flashes, vaginal atrophy (↓ FSH, LH)
Clinical  Fatigue, bradycardia (↓ TSH)
features  Anorexia, weight loss, hypotension (↓ ACTH)
 Decreased lean body mass (↓ growth hormone)

Pulmonary changes in pregnancy


Pathophysiology  Progesterone-induced hyperventilation
 Dyspnea of pregnancy
Clinical features  ↑ PaO2, ↓ PaCO2 (respiratory alkalosis)

 ↑ Minute ventilation (mostly via ↑ tidal volume)


 ↓ Residual volume & functional residual capacity
Lung volumes
 Normal vital capacity & FEV1

Hypercalcemia of malignancy
Cause Tumor type Mechanism Diagnostic
 Squamous cell
 Renal & bladder  ↓ PTH
 PTH mimic
PTHrP*  Breast &  ↑ PTHrP
ovarian

 Breast  ↓ PTH &


 Multiple  ↑ Osteolysis PTHrP
Bone metastases
myeloma  ↓ Vitamin D

 ↑ Calcium  ↓ PTH
1,25-dihydroxyvitamin  Lymphoma
absorption  ↑ Vitamin D
D
*PTHrP causes approximately 80% of malignancy-associated hypercalcemia.

PTH = parathyroid hormone; PTHrP = parathyroid hormone-related protein.


Pulmonary  examination findings
Tactile
Condition Breath sounds Percussion Mediastinal shift
fremitus
Bronchovesicular
Normal lung (hilar), vesicular Normal Resonance None
(peripheral)
Consolidation
(eg, lobar Increased Increased Dullness None
pneumonia)
Pleural Away from
Decreased or absent Decreased Dullness
effusion effusion (if large)
Away from
Pneumothorax Decreased or absent Decreased Hyperresonance tension
pneumothorax
Atelectasis
Toward atelectasis
(eg, mucus Decreased or absent Decreased Dullness
(if large)
plugging)
Clinical features of psoriatic arthritis
 Distal interphalangeal joints
 Asymmetric oligoarthritis
 Symmetric polyarthritis, similar to rheumatoid arthritis
Arthritis
 Arthritis mutilans (deforming & destructive arthritis)
 Spondylarthritides (sacroiliitis & spondylitis)

 Enthesitis (inflammation at site of tendon insertion into


bone)
Soft tissue & nail  Dactylitis ("sausage digits") of toe or finger
involvement  Nail pitting & onycholysis
 Swelling of the hands or feet with pitting edema

 Arthritis precedes skin disease in 15% of patients


 Skin lesions are present but not yet diagnosed in 15% of
Skin lesions
patients

Primary versus secondary adrenal insufficiency


Primary Secondary
 Destruction of bilateral  Disruption of hypothalamic-
Mechanism adrenal cortex pituitary axis

 Autoimmune adrenalitis  Chronic glucocorticoid therapy


Possible
 Infection, malignancy  Infiltrative disease
etiologies
Cortisol ↓ ↓
Aldosterone ↓ Normal
ACTH ↑ ↓
 More severe symptoms  Less severe symptoms
 Hypovolemia  Euvolemia
Clinical
 Hyperkalemia, hyponatremia  Minimal electrolyte disturbance
features
 Hyperpigmentation  No hyperpigmentation

Autosomal dominant polycystic kidney disease


 Most patients asymptomatic until age 30-40
 Flank pain, hematuria
Clinical  Hypertension
presentation  Palpable abdominal masses (usually bilateral)
 Chronic kidney disease (CKD)

 Cerebral aneurysms
 Hepatic & pancreatic cysts
Extrarenal  Mitral valve prolapse, aortic regurgitation
features  Colonic diverticulosis
 Ventral & inguinal hernias
 Ultrasonography showing multiple renal cysts
Diagnosis
 Aggressive control of risk factors for CV & CKD
 ACE inhibitors preferred for hypertension
Management
 Hemodialysis, renal transplant for ESRD

CV = cardiovascular; ESRD = end-stage renal disease.


Common causes of esophagitis in patients with HIV
 Oral thrush usually present
 White plaques throughout esophagus
Candida albicans
 Biopsy: pseudohyphae

 Orolabial lesions usually present


 Vesicular or ulcerative round/ovoid lesions ("volcano-like")
Herpes simplex virus
 Biopsy: multinucleated giant cells

 Large, linear ulcers in distal esophagus


Cytomegalovirus  Biopsy: intranuclear/intracytoplasmic inclusions

Common causes of ulceroglandular syndrome


Syndrome Transmission Manifestations
 Hunting/skinning wild animals  Single skin ulcer
(eg, hares, rabbits)  Regional suppurative
Tularemia  Tick/mosquito bite lymphadenitis
 Bioterrorism weapon  Fever

 Subacute/chronic
 Papuloulcerative lesion
 Gardening or landscaping  New lesions up lymphatic
Sporotrichosis
chain
 No fever or purulence

 Papule in area of transmission


 Feline scratch/bite
Catscratch  Prominent, tender regional
 Flea bite from infected feline
disease lymphadenopathy

Complex regional pain syndrome


 Trauma: fracture, sprain
Triggers  Surgery

 Pain: severe, regional (not dermatomal), burning/stinging


 Edema, abnormal sweating
Clinical features  Vasomotor changes, altered skin temperature
 Trophic skin, hair & nail changes
 Primarily based on clinical features
 X-ray: patchy demineralization
Diagnosis
 Bone scintigraphy: ↑ uptake in affected limb

 Physical & occupational therapy, exercise


 Medications: NSAIDs, antineuropathic medications (eg, pregabalin,
Management
TCAs)

NSAIDs = nonsteroidal anti-inflammatory drugs; TCAs = tricyclic antidepressants.


Waldenström macroglobulinemia Multiple myeloma
 Hyperviscosity syndrome
 Osteolytic lesions/fractures
 Neuropathy
 Anemia
 Bleeding
Major manifestations  Hypercalcemia
 Hepatosplenomegaly
 Renal insufficiency
 Lymphadenopathy

Monoclonal antibody IgM IgG, IgA, light chains


Peripheral smear Rouleaux Rouleaux
Bone marrow biopsy >10% clonal B cells >10% clonal plasma cells
Spinal cord compression
 Mechanical (eg, disc herniation, spinal stenosis)
 Malignancy (eg, lung, breast, prostate cancers)
Causes
 Infection (eg, epidural abscess)

 Gradually worsening, severe back pain


Symptoms  Pain worse in recumbent position/at night

 Early signs
o Symmetric extremity weakness
o ↓ Deep tendon reflexes

Physical
 Late signs
examination
o ↓ Rectal tone
o ↑ Deep tendon reflexes, bilateral Babinski reflex
o Paralysis

 Emergency MRI of the spine


 Emergency surgical ± radiation oncology consultation
Management  Intravenous glucocorticoids (eg, malignancy) or antibiotics (eg,
infection)

Reversible causes of asystole/pulseless electrical activity


5 Hs 5 Ts
Hypovolemia Tension pneumothorax
Hypoxia Tamponade, cardiac
Hydrogen ions (acidosis) Toxins (narcotics, benzodiazepines)
Hypokalemia or hyperkalemia Thrombosis (pulmonary or coronary)
Hypothermia Trauma
Brain abscess
 Staphylococcus aureus
 Viridans streptococci
Microbiology
 Anaerobes

 Direct spread (eg, otitis media, mastoiditis, sinusitis)


Pathogenesis  Hematogenous spread (eg, endocarditis)

 Headache, vomiting
 Fever
Clinical findings   Focal neurologic deficits, seizure
 Ring-enhancing lesion on neuroimaging (CT, MRI)

 Aspiration/surgical drainage
Treatment  Prolonged antibiotic therapy

Acute respiratory failure due to transfusion


Feature TRALI TACO
Pulmonary symptoms Acute dyspnea Acute dyspnea
Chest x-ray Diffuse bilateral infiltrate Diffuse bilateral infiltrate
Jugular venous distension Absent Present
Auscultation Crackles/rales Crackles/rales ± S3
Ejection fraction Normal Decreased
BNP Normal High
BNP = brain natriuretic peptide; TACO = transfusion-associated circulatory overload; TRALI
= transfusion-related acute lung injury.
Risk factors for cellulitis
 Diabetes mellitus
 HIV infection
Immune suppression
 Chronic glucocorticoid therapy

 Dry skin
 Chronic inflammation (eg, eczema, radiation therapy)
Breaches in
 Chronic wounds (eg, pressure ulcer, venous ulcer)
skin barrier
 Dermatophyte infection (eg, tinea pedis)

Chronic edema  Postsurgical lymphedema (eg, lymph node dissection)


 Chronic venous insufficiency
 Congestive heart failure, chronic kidney disease
 Prior cellulitis with lymphatic scarring

 Obesity
Other
Features of constrictive pericarditis
 Recurrent idiopathic or viral pericarditis
 Cardiac surgery or radiation therapy
Etiology
 Tuberculous pericarditis (where endemic)

 Fatigue, dyspnea on exertion


 Peripheral edema, ascites, hepatic congestion
 Pericardial knock in early diastole
Clinical presentation
 JVD with positive Kussmaul sign* & prominent y
descent

 ECG: low-voltage QRS complexes


 Chest x-ray/CT: pericardial calcification
Diagnostic findings  Echocardiogram: biatrial enlargement, normal
ventricular wall thickness & cavity size

*Increase in JVD with inspiration.

JVD = jugular venous distension.


Thrombotic thrombocytopenic purpura
 ↓ ADAMTS13 level → uncleaved vWF multimers → platelet
trapping & activation
Pathophysiology
 Acquired (autoantibody) or hereditary

 Hemolytic anemia (↑ LDH, ↓ haptoglobin) with schistocytes


 Thrombocytopenia (↑ bleeding time, normal PT/PTT)

Sometimes with:
Clinical features
 Renal failure
 Neurologic manifestations
 Fever

 Plasma exchange
 Glucocorticoids
Management  Rituximab
 Caplacizumab

LDH = lactate dehydrogenase; vWF = von Willebrand factor.


Cardiac tamponade
Etiology  Blood in pericardial space (eg, LV rupture, cardiac surgery)
 Pericardial effusion (eg, malignancy, infection, uremia)

 Beck triad: hypotension, JVD, ↓ heart sounds


Clinical
 Pulsus paradoxus: SBP ↓ >10 mm Hg during inspiration
signs
 ECG: low-voltage QRS complex, electrical alternans
 Chest x-ray: enlarged cardiac silhouette,* clear lungs
Diagnosis
 Echocardiography: right atrial & ventricular collapse, IVC plethora

 Intravenous fluids to increase right-sided preload


Treatment  Drainage via pericardiocentesis or pericardial window

*Subacute but not acute tamponade.

IVC = inferior vena cava; JVD = jugular venous distension; LV = left ventricular;


SBP = systolic blood pressure.
Wernicke encephalopathy
 Chronic alcoholism (most common)
 Malnutrition (eg, anorexia nervosa)
Associated conditions
 Hyperemesis gravidarum

 Thiamine deficiency
Pathophysiology
 Encephalopathy
 Oculomotor dysfunction (eg, horizontal nystagmus
Clinical features & bilateral abducens palsy)
 Postural & gait ataxia

 Intravenous thiamine followed by glucose infusion


Treatment
Cerebrospinal fluid analysis
WBC count Glucose Protein
Diagnosis
(mm3) (mg/dL) (mg/dL)
Normal 0-5 40-70 <40
Bacterial
>1,000 <40 >250
meningitis
Tuberculous
100-500 <45 100-500
meningitis
Viral meningitis 10-500 40-70 <150
Guillain-Barré
0-5 40-70 45-1,000
syndrome
WBC = white blood cell.
Multiple sclerosis
Common  Sensory disturbances, motor weakness, bowel/bladder dysfunction
 Ocular manifestations:  optic neuritis (painful eye movement),
internuclear ophthalmoplegia (impaired adduction on lateral gaze)
presenting  Lhermitte sign:  electrical sensation in limbs or back
symptoms  Uhthoff phenomenon:  symptom worsening with increased body
temperature

 Female, HLA-DRB1
 Environmental factors (United States, Europe, Australia)
Risk factors  Low vitamin D levels
 Epstein-Barr infection

 Episodic/progressive symptoms disseminated over time & space


 Hyperintense lesions on T2-weighted MRI
Diagnosis
 Oligoclonal IgG bands on cerebrospinal fluid analysis

Calcific uremic arteriolopathy (calciphylaxis)


 Arteriolar & soft tissue calcification
Pathophysiology  Local tissue ischemia & necrosis

 End-stage renal disease


 Hypercalcemia, hyperphosphatemia
Risk factors  Hyperparathyroidism
 Oral anticoagulants (eg, warfarin)

 Painful nodules & ulcers


 Soft tissue calcification on imaging
Clinical
 Diagnosis requires skin biopsy: arteriolar calcification/occlusion,
manifestations
subintimal fibrosis

 Analgesia & wound care


 Treatment of risk factors (eg, high phosphorus, high calcium)
Management
 Optimization of dialysis

Hypertrophic cardiomyopathy
 Genetic mutations affecting cardiac sarcomere proteins
 Autosomal dominant inheritance
Pathophysiology
 Variable phenotypic penetrance

 Many patients are asymptomatic


 Exertional dyspnea, fatigue, angina, light-headedness, syncope
 Systolic ejection murmur accentuated by ↓ LV blood volume
Clinical features
 Diastolic dysfunction with audible S4
 ↑ Risk for atrial fibrillation & ventricular tachycardia

Diagnosis  ECG: left axis deviation, abnormalities of depolarization


(eg, Q waves) or repolarization (eg, inverted T waves)
 Echocardiography: septal LV hypertrophy, dynamic LVOT
obstruction, LA dilation

 Beta blocker or nondihydropyridine CCB (facilitate ↑ LV blood


volume)
 Avoidance of dehydration & vasodilators (avoid ↓ LV blood
Management volume)
 ICD placement for increased risk for SCD
 Septal ablation, cardiac transplantation

CCB = calcium channel blocker; ICD = implantable cardiac defibrillator; LA = left atrial;


LV = left ventricular; LVOT = left ventricular outflow tract; SCD = sudden cardiac death.
Clinical features of rheumatoid arthritis
 Pain, swelling & morning stiffness in multiple joints
 Small joints (PIP, MCP, MTP); spares DIP joints
 Systemic symptoms (fever, weight loss, anemia)
Clinical presentation
 Cervical spine involvement: subluxation, cord
compression

 Positive rheumatoid factor & anti–CCP antibodies


 C-reactive protein & ESR correlate with disease activity
Laboratory/
 X-ray: soft tissue swelling, joint space narrowing, bony
imaging studies
erosions

anti–CCP = anti–cyclic citrullinated peptide; DIP = distal interphalangeal; ESR = erythrocyte


sedimentation rate; MCP = metacarpophalangeal; MTP = metatarsophalangeal; PIP = proximal
interphalangeal.
Manifestations of sarcoidosis
 Hilar lymphadenopathy*
Pulmonary  Interstitial infiltrates

 Papules, nodules & plaques


Cutaneous  Erythema nodosum*

 Anterior & posterior uveitis


Ophthalmologic  Keratoconjunctivitis sicca

 Facial nerve palsy


 Central diabetes insipidus
Neurologic
 Hypogonadotropic hypogonadism

 AV block
Cardiovascular  Dilated or restrictive cardiomyopathy
 Hepatosplenomegaly
Gastrointestinal  Asymptomatic LFT abnormalities

 Hypercalcemia
 Peripheral lymphadenopathy
 Parotid gland swelling
Other
 Polyarthritis*
 Constitutional symptoms (fever,* malaise)

*Manifestations of Löfgren syndrome.

AV = atrioventricular; LFT = liver function test.


Acute pericarditis
 Viral or idiopathic
 Autoimmune disease (eg, SLE)
 Uremia (acute or chronic renal failure)
Etiology  Post myocardial infarction
o Early: peri-infarction pericarditis
o Late: Dressler syndrome

 Pleuritic chest pain (↓ when sitting up) ± fever


 Pericardial friction rub
Clinical features
 ECG: diffuse ST-segment elevation
& diagnosis
 Pericardial effusion on echocardiogram

SLE = systemic lupus erythematosus.


Myasthenic crisis
 Infection or surgery
 Pregnancy or childbirth
Precipitating
 Tapering of immunosuppressive drugs
factors
 Medications (eg, aminoglycosides, beta blockers)

 ↑ Generalized & oropharyngeal weakness


Signs/symptoms  Respiratory insufficiency/dyspnea

 Intubation for deteriorating respiratory status


Treatment  Plasmapheresis or IVIG as well as corticosteroids

IVIG = intravenous immunoglobulin.


Rhabdomyolysis
Etiology Skeletal muscle lysis/necrosis due to:

 Crush injury or prolonged immobilization


 Intense muscle activity (eg, seizure, exertion)
 Drug/medication toxicity (eg, statins)

 Muscle pain & weakness


 Dark urine (myoglobinuria/pigmenturia)
 + Blood on urinalysis & no RBCs on microscopy
Clinical features
 ↑ Serum K & PO4, ↓ serum Ca, ↑ AST > ALT
 Acute kidney injury

 Serum creatine kinase >1,000 U/L


Diagnosis  Consistent clinical features

 Aggressive intravenous fluid resuscitation


Management  Sodium bicarbonate in some cases

ALT = alanine aminotransferase; AST = aspartate aminotransferase; RBCs = red blood cells.
Factors associated with poor outcome after witnessed out-of-hospital sudden cardiac arrest
 Time elapsed prior to effective resuscitation (delayed bystander CPR, delayed
defibrillation)

 Initial rhythm of pulseless electrical activity or asystole


 Prolonged CPR (>5 min)
 Absence of vital signs
 Advanced age
 History of cardiac disease
 ≥2 Chronic illnesses
 Persistent coma after CPR
 Need for intubation or vasopressors
 Pneumonia or renal failure after CPR
 Sepsis, cerebrovascular accident, or class III or IV heart failure

CPR = cardiopulmonary resuscitation.


Female & male pattern hair loss
 Polygenetic inheritance
Etiology  Hormonal factors (dihydrotestosterone)

 Chronic, progressive thinning of hair


 Men: vertex, frontal hairline, temporal areas
Clinical features
 Women: vertex, center of scalp (sparing of hairline)

 Men: minoxidil, finasteride


Management  Women: minoxidil

Secondary causes of hypertension


Condition Clinical clues/features
Renal parenchymal disease  Elevated creatinine level
 Abnormal urinalysis (proteinuria, red blood cell casts)

 Recurrent flash pulmonary edema


 Elevated creatinine level (particularly with ACE inhibitor
Renovascular disease use)
 Abdominal bruit

 Hypokalemia (spontaneous or thiazide induced)


Primary
 Metabolic alkalosis
hyperaldosteronism
 Daytime somnolence
Obstructive sleep apnea  Increased neck circumference

 Paroxysmal hypertension & tachycardia


Pheochromocytoma  Headaches, palpitations, diaphoresis

 Cushingoid body habitus & proximal muscle atrophy


Cushing syndrome  Hyperglycemia

 Hyperthyroidism: anxiety, heat intolerance, weight loss,


tachycardia
Thyroid disease  Hypothyroidism: fatigue, cold intolerance, weight gain,
bradycardia

 Mild hypercalcemia ± symptoms (eg, constipation)


Primary
 Kidney stones
hyperparathyroidism
 Upper extremity hypertension with brachial-femoral pulse
delay (common)
Coarctation of the aorta
 Lateralizing hypertension (less common)

Anorexia nervosa
Significantly low weight
Diagnostic
Fear of weight gain
criteria
Distorted views of body weight & shape
Complications Cardiovascular: myocardial atrophy, bradycardia, hypotension,
arrhythmias
Renal: poor urinary concentration, dehydration

Neurological: seizures, cognitive impairment

Dermatological: dry skin, lanugo

Gynecological: amenorrhea, infertility

Gastrointestinal: gastroparesis, constipation

Hematological: cytopenia

Other: electrolyte depletion, osteopenia, hypercholesterolemia,


hypercarotenemia
 
Assessment of intimate partner violence
Location of injuries (eg, genitals, torso, face, head, neck)

Inconsistent explanation, evasive, fearful

Nonadherence to follow-up, emergency department visits


Signs
Partner who resists patient being seen alone

Discomfort in examination, sexually transmitted infections, chronic pelvic


pain
Ensure privacy

Nonjudgmental, empathic, open-ended questions


Interview
Avoid pressuring to disclose abuse or report or leave partner
strategies
Assess immediate safety; determine emergency safety plan, provide referrals
for resources as needed (eg, shelters, domestic violence agency, mental
health)
Risk factors for community-acquired pneumonia
Age >65

Impaired immunity HIV

Diabetes mellitus
Impaired pulmonary Chronic obstructive pulmonary disease
function
Bronchiectasis/cystic fibrosis

Recent upper respiratory viral infection

Smoking
Substance/alcohol use disorder

Increased microaspiration Seizure disorder or stroke

Esophageal dysmotility
Acid suppressants

Medications Sedatives

Immunomodulatory agents
Acute vs chronic disseminated intravascular coagulation (DIC)
Acute DIC Chronic DIC
Sepsis

Common etiologies Severe trauma Malignancy (eg, pancreatic)

Obstetric complications
Coagulation studies Prolonged Often normal
Platelets Low Often normal
Fibrinogen Low Often normal
D-dimer High High
Bleeding risk Very high Mildly increased
Thromboembolism risk Mildly increased Very high
Causes of peripheral edema
Primary mechanism Clinical examples
Heart failure (left ventricular & cor pulmonale)
Increased capillary hydrostatic
Primary renal sodium retention (renal disease & drugs)
pressure
Venous obstruction (eg, cirrhosis & venous insufficiency)
Protein loss (eg, nephrotic syndrome & protein-losing
Decreased capillary oncotic enteropathy)
pressure (hypoalbuminemia)
Decreased albumin synthesis (eg, cirrhosis & malnutrition)
Increased capillary Burns, trauma & sepsis
permeability
Allergic reactions
Acute respiratory distress syndrome

Malignant ascites
Malignant ascites
Lymphatic
obstruction/increased Hypothyroidism
interstitial oncotic pressure
Lymph node dissection
Complications of Graves disease treatment
Treatment Adverse effects
Agranulocytosis
Antithyroid drugs
Methimazole: 1st-trimester teratogen, cholestasis
(thionamides)
Propylthiouracil: hepatic failure, ANCA-associated vasculitis
Permanent hypothyroidism
Radioiodine
Worsening of ophthalmopathy
ablation
Possible radiation side effects
Permanent hypothyroidism

Surgery Risk for recurrent laryngeal nerve damage

Risk for hypoparathyroidism


ANCA = antineutrophilic cytoplasmic antibodies.
Myoclonus status epilepticus
Etiology Severe neurologic injury (eg, cardiac arrest)
Comatose patient

Appears within 72 hr of injury


Clinical
features
Involuntary muscle contraction in a joint or limb

Generalized, symmetric
Electroencephalography
Management
Antiepileptic medications
Hypoglycemia in patients without diabetes mellitus
Drugs: quinolones, quinine, beta blockers

Alcohol (usually with prolonged starvation)


Sepsis/critical illness

Adrenal insufficiency

Insulinoma

Surreptitious insulin, sulfonylurea, or meglitinide use

Depleted glycogen stores (anorexia nervosa)

Severe hepatic failure


Exertional heat stroke
Strenuous activity during hot & humid weather

Dehydration, poor acclimatization


Risk factors
Lack of physical fitness, obesity

Medications: anticholinergics, antihistamines,


phenothiazines, tricyclics, antipsychotics
Core temperature >40 C (104 F) with CNS
dysfunction (eg, AMS, seizure)
Clinical
manifestations Organ or tissue damage: renal or hepatic failure,
disseminated intravascular coagulation, acute
respiratory distress syndrome
Rapid cooling: ice water immersion preferred; can
consider high-flow cold water dousing, ice-wet
towel rotation, evaporative cooling

Management Fluid resuscitation, electrolyte correction

Management of end-organ complications

No role for antipyretic therapy


AMS = altered mental status.
Common medications that cause hyperkalemia
Medication Mechanism
Decreases aldosterone secretion (inhibition of AT II/AT II
ACE inhibitor, ARB
receptor) + inhibits ENaC
Cyclosporine Blocks aldosterone activity
Digitalis Inhibits Na+/K+-ATPase
Heparin Blocks aldosterone production
Nonselective Interferes with β2-mediated intracellular potassium uptake
β-adrenergic blocker
Decreases renal perfusion → decreased potassium delivery to the
NSAID
collecting ducts
Potassium-sparing diuretic Inhibits ENaC or aldosterone receptor
Causes extracellular leakage of potassium through acetylcholine
Succinylcholine
receptors
Trimethoprim Inhibits ENaC
ARB = angiotensin II receptor blocker; AT = angiotensin; ENaC = epithelial sodium channel;
Na+/K+-ATPase = sodium-potassium pump; NSAID = nonsteroidal anti-inflammatory drug.
Clinical features of tremors
Bilateral action tremor of the hands

Head tremor without dystonia


Essential
No other neurologic signs

Improves with alcohol


Resting tremor; ↓ with voluntary movement

Parkinson disease Pill-rolling

Asymmetric; hands & legs


Usually associated with ataxia &/or dysmetria
Cerebellar
↑ Steadily as hand approaches target
Legs & trunk
Orthostatic
Occurs only when standing
Low amplitude, not visible under normal conditions

↑ With sympathetic activity (eg, drugs, hyperthyroidism, anxiety,


caffeine)
Physiologic
Worse with movement

Most common cause of action tremor


Acute myeloid leukemia
Most common adult acute leukemia
Background
Median age 65
Manifestations Fatigue is common (other B symptoms unusual)

Often presents with symptoms from cytopenias:


Fatigue, weakness (anemia)

Bleeding, bruising (thrombocytopenia)

Infection (granulocytopenia)

Hepatosplenomegaly/lymphadenopathy rare

Disseminated intravascular coagulation (if APML)


Cytopenias (leukocytes may be ↑, normal or ↓)

Laboratory Elevated lactate dehydrogenase

Peripheral smear - usually myeloblasts with Auer rods


Diagnosis Bone marrow biopsy - usually hypercellular with myeloid blasts
APML = acute promyelocytic leukemia.
Stimuli for secretion of antidiuretic hormone
Osmotic Serum osmolality > ~285 mOsm/kg H2O
Nausea

Pain

Physical or emotional stress

Nonosmotic Hypotension

Hypovolemia

Hypoxia

Hypoglycemia
Actinic keratosis
Erythematous, scaly papules; rough plaques
Clinical
features
Sun-exposed areas
Clinical appearance
Diagnosis
Biopsy if features of possible SCC (eg, size ≥1 cm,
rapid growth, ulceration, tenderness)
Chronic/persistent

Prognosis Progression to SCC

Spontaneous resolution
Isolated lesions: cryotherapy
Treatment
Diffuse lesions: topical fluorouracil, imiquimod,
tirbanibulin
SCC = squamous cell carcinoma.
Iron deficiency anemia & thalassemias
Iron
Alpha-thalassemia Beta-thalassemia
Parameter deficiency
minor minor
anemia
MCV ↓ ↓ ↓
RDW ↑ Normal Normal
RBCs ↓ Normal Normal
Peripheral Microcytosis,
Target cells Target cells
smear hypochromia
↓ Iron & ferritin
Serum iron Normal/↑ iron & ferritin Normal/↑ iron & ferritin
studies (RBC turnover) (RBC turnover)
↑ TIBC
Response to iron
↑ Hemoglobin No improvement No improvement
supplementation
Hemoglobin
Normal Normal ↑ Hemoglobin A2
electrophoresis
MCV = mean corpuscular volume; RBCs = red blood cells; RDW = red blood cell distribution
width; TIBC = total iron-binding capacity.
High-output heart failure
↓ SVR leads to ↑ cardiac output & ↑ venous
Pathophysiology
return
Morbid obesity (most common)

Arteriovenous fistula (congenital or acquired)


Causes
Hyperthyroidism, severe anemia, advanced
cirrhosis

Paget disease, thiamine deficiency


Hyperdynamic circulation (↑ PP, warm
extremities)
Clinical presentation
Peripheral & pulmonary edema

Laterally displaced PMI, systolic flow murmur


Dilated LV, RV & inferior vena cava
Echocardiographic findings
Elevated resting cardiac index
LV = left ventricle; PMI = point of maximal impulse; PP = pulse pressure; RV =
right ventricle; SVR = systemic vascular resistance.
Optimal medical management following myocardial infarction
Medication Indication
All patients (regardless of stent placement)
Dual antiplatelet therapy
Low-dose aspirin continued indefinitely
(low-dose aspirin + P2Y12 inhibitor)
P2Y12 inhibitor continued for 12 months
All patients, continued indefinitely
Beta blocker
(eg, metoprolol, carvedilol) Reduces myocardial oxygen demand, decreases
arrhythmia risk & inhibits remodeling
All patients, continued indefinitely for reduced LVEF
ACE inhibitor or angiotensin II
receptor blocker
Inhibits post-MI remodeling
All patients, continued indefinitely
High-intensity statin
(ie, atorvastatin, rosuvastatin) Stabilizes atherosclerotic plaque & reduces recurrent
MI
Reduced LVEF with symptoms or comorbid DM
Mineralocorticoid antagonist
(eg, spironolactone)
Inhibits post-MI remodeling
DM = diabetes mellitus; LVEF = left ventricular ejection fraction; MI = myocardial infarction.
 
Acute management of acute coronary syndrome

(STEMI, NSTEMI, or unstable angina)


Rapid chest pain relief
Nitrates
Caution with hypotension (eg, RV infarction)
Cardioselective (eg, metoprolol, atenolol)

Beta blocker Decreases myocardial O2 demand to limit infarct size

Contraindicated in cardiogenic shock & bradycardia


Aspirin + P2Y12 inhibitor (eg, prasugrel, clopidogrel)*
Antiplatelet therapy
Reduces platelet activity
Unfractionated heparin, bivalirudin, or enoxaparin
Anticoagulation
Limits thrombus expansion
High potency (eg, atorvastatin, rosuvastatin)
Statin therapy
Stabilizes atherosclerotic plaque
Coronary reperfusion STEMI
PCI <90 min from 1st medical contact

Fibrinolytics (eg, alteplase) if PCI is unavailable

NSTEMI or unstable angina

Coronary angiography often within 24 hr


*In patients with NSTEMI or unstable angina, P2Y12 inhibitor therapy is often held until after
coronary angiography in case the atherosclerotic coronary anatomy indicates the need for
coronary artery bypass grafting.

NSTEMI = non–ST-segment elevation myocardial infarction; PCI = percutaneous coronary


intervention; RV = right ventricular; STEMI = ST-segment elevation myocardial infarction.
Urinary incontinence
Type Symptoms Treatment
Lifestyle modification

Leaking with Valsalva maneuver Pelvic floor exercises


Stress (coughing, sneezing,
laughing) Pessary

Pelvic floor surgery


Lifestyle modification
Sudden, overwhelming, or
Urgency Bladder training
frequent need to void
Antimuscarinic drugs
Features of stress & urgency Variable treatment depending on
Mixed
incontinence predominant symptoms
Identification and correction of underlying
cause
Constant involuntary dribbling &
Overflow
incomplete emptying Cholinergic agonists

Intermittent self-catheterization
Clinical features of irritable bowel syndrome
Rome IV diagnostic Recurrent abdominal pain/discomfort ≥1 days/week for past 3 months
criteria & ≥2 of the following:

Related to defecation (improves or worsens)

Change in stool frequency


Change in stool form
Older age of onset (≥50)

Gastrointestinal bleeding

Nocturnal diarrhea (ie, fasting state)

Worsening pain

Alarm features Unintended weight loss

Iron deficiency anemia

Elevated C-reactive protein

Positive fecal lactoferrin or calprotectin

Family history of early colon cancer or IBD


IBD = inflammatory bowel disease.
Distal symmetric polyneuropathy
Diabetes mellitus (diabetic neuropathy)

Long-standing HIV infection

Uremia
Triggers
Medications (eg, fluoroquinolones, metronidazole)

Chemotherapy (eg, cisplatin, paclitaxel)

Toxicity (eg, alcohol abuse, heavy metal exposure)


Pathophysiology Damage to distal sensory peripheral nerve axons
Symptoms begin in toes/feet; progresses proximally over time

Distal numbness, tingling, pins & needles sensation


Manifestations
↓ Pain, temperature, touch & vibration sensation

↓ Ankle/Babinski reflexes
Treat underlying cause
Treatment
Pain management: gabapentinoid, tricyclic antidepressant, duloxetine &/or
capsaicin cream
Sjögren syndrome
Immune-mediated destruction of the lacrimal & salivary glands
Pathogenesis
Can occur as primary disease or secondary with other autoimmune
disorders (eg, SLE, RA)
Dry eyes (keratoconjunctivitis sicca)

Dry mouth (xerostomia), salivary hypertrophy

Dry skin (xerosis)


Clinical
features
Raynaud phenomenon

Cutaneous vasculitis

Positive anti-Ro (SSA) &/or anti-La (SSB)


Non-Hodgkin lymphoma
Complications
Corneal damage, dental caries
RA = rheumatoid arthritis; SLE = systemic lupus erythematosus; SSA/SSB = Sjögren syndrome
(antibody) A/B.
Salicylate toxicity
Excess ingestion of aspirin or other salicylates (eg, oil of wintergreen)
Epidemiology
Liver metabolism gets overwhelmed → slower renal excretion → prolonged
elevated salicylate levels
Nausea/vomiting

Hyperventilation

Manifestations Hyperthermia

Altered mental status

Anion gap metabolic acidosis (elevated lactate)


Diagnosis Serum salicylate level
Activated charcoal (alert patients within 2 hr of ingestion)

Treatment Intravenous sodium bicarbonate (enhances salicylate excretion)

Hemodialysis (severe ingestions, pulmonary edema, renal failure)


Valve replacement in aortic stenosis
Severe AS criteria Aortic jet velocity ≥4.0 m/sec, or

Mean transvalvular pressure gradient ≥40 mm Hg


Valve area usually ≤1.0 cm2 but not required
Severe AS & ≥1 of the following:

Onset of symptoms (eg, angina, syncope)  


Indications for valve replacement
Left ventricular ejection fraction <50%

Undergoing other cardiac surgery (eg, CABG)


AS = aortic stenosis; CABG = coronary artery bypass grafting.
Conditions commonly associated with digital clubbing
Bronchogenic carcinoma

Metastatic cancers
Intrathoracic
neoplasms
Malignant mesothelioma

Lymphoma
Lung abscess

Empyema
Intrathoracic
Bronchiectasis
suppurative
diseases
Cystic fibrosis

Chronic cavitary infections (eg, fungal,


mycobacterial)
Idiopathic pulmonary fibrosis

Lung diseases Asbestosis

Pulmonary arteriovenous malformations


Cardiovascular
Cyanotic congenital heart disease
disease
Features of constrictive pericarditis
Recurrent idiopathic or viral pericarditis

Etiology Cardiac surgery or radiation therapy

Tuberculous pericarditis (where endemic)


Clinical presentation Fatigue, dyspnea on exertion

Peripheral edema, ascites, hepatic congestion


Pericardial knock in early diastole

JVD with positive Kussmaul sign* & prominent y descent


ECG: low-voltage QRS complexes

Chest x-ray/CT: pericardial calcification


Diagnostic findings
Echocardiogram: biatrial enlargement, normal ventricular
wall thickness & cavity size
*Increase in JVD with inspiration.

JVD = jugular venous distension.


Overview of running injuries of the foot & ankle
Injury Clinical features
Insidious onset

Focal pain in navicular or metatarsals


Stress fracture
Risk factors: abrupt increase in intensity of training, poor running
mechanics, female with eating disorder
Plantar surface of the heel
Plantar fasciitis
Worse when initiating running or first steps of the day
Achilles
Burning pain or stiffness 2-6 cm above the posterior calcaneus
tendinopathy
Numbness or pain between the 3rd & 4th toes
Morton neuroma
Clicking sensation when palpating space between 3rd & 4th toes while
squeezing the metatarsal joints
Compression of the tibial nerve at the ankle
Tarsal tunnel
syndrome Burning, numbness & aching of the distal plantar surface of the
foot/toes
Light criteria for pleural effusions
Transudate Exudate
Protein
≤0.5 >0.5
(pleural/serum)
LDH ≤0.6 >0.6
Pleural LDH ≤ two-thirds upper limit Pleural LDH > two-thirds upper limit
(pleural/serum) of normal serum LDH of normal serum LDH
Common causes Hypoalbuminemia Infection (parapneumonic, TB,
(cirrhosis, nephrotic fungal, empyema)
syndrome)
Malignancy
Congestive heart failure
PE
LDH = lactate dehydrogenase; PE = pulmonary embolism; TB = tuberculosis.
Carbon monoxide poisoning
Smoke inhalation

Epidemiology Defective heating systems

Gas motors operating in poorly ventilated areas


Mild-moderate

Headache, confusion

Malaise, dizziness, nausea


Manifestations
Severe

Seizure, syncope, coma

Myocardial ischemia, arrhythmias


ABG: carboxyhemoglobin level
Diagnosis
ECG ± cardiac enzymes
High-flow 100% oxygen
Treatment
Intubation/hyperbaric oxygen (severe)
ABG = arterial blood gas.
Infectious genital ulcers
Pustules, vesicles, or small ulcers on
erythematous base
Herpes simplex virus
Tender lymphadenopathy

Painful Systemic symptoms common


Larger, deep ulcers with gray/yellow exudate
Haemophilus ducreyi
Well-demarcated borders & soft, friable base
(chancroid)
Severe lymphadenopathy that may suppurate
Painless Usually single ulcer (chancre)
Treponema pallidum
(syphilis)
Indurated borders & hard, nonpurulent base
Chlamydia trachomatis Initial small, shallow ulcers (often missed)
serovars L1-L3
(lymphogranuloma venereum)
Then painful & fluctuant adenitis (buboes)
Anion gap metabolic acidosis
Anion gap = sodium – (chloride + bicarbonate)
Calculation
(normal: 10-14 mEq/L)
Methanol

Uremia

Diabetic ketoacidosis

Common causes Propylene glycol/paraldehyde

Mnemonic: MUDPILES Isoniazid/iron

Lactic acidosis

Ethylene glycol (antifreeze)

Salicylate (aspirin)
General manifestations of hyperthyroidism
Anxiety & insomnia

Palpitations

Symptoms Heat intolerance

Increased perspiration

Weight loss without decreased appetite


Goiter

Hypertension

Tremors involving fingers/hands

Physical examination Hyperreflexia

Proximal muscle weakness

Lid lag

Atrial fibrillation
Clues to etiology of syncope
Trigger (eg, emotional stress, prolonged standing)
Vasovagal
Prodrome (eg, nausea, sweating, warmth)
Occurs with micturition, defecation, swallowing,
Reflex syncope Situational
or coughing
Tactile stimulation of carotid sinus while standing
Carotid
hypersensitivity
Advanced age, carotid atherosclerosis
Vasodilators (eg, alpha-1 blockers,
antihypertensives)
Medications
Inotropic/chronotropic blockade (eg, beta
Orthostatic blockers)
syncope
Hypovolemia History consistent with volume loss
Advanced age
Autonomic
dysfunction
Predisposing disease (eg, DM, Parkinson)
Syncope with exertion
LV outflow
obstruction
Systolic ejection murmur
No warning symptoms
Ventricular
Cardiomyopathy or ischemic HD (monomorphic)
Cardiac syncope tachycardia
QT-interval prolongation (polymorphic)
Preceding fatigue or light-headedness
Conduction
impairment* ECG abnormalities (eg, sinus pauses, dropped
QRS complexes)
*Sick sinus syndrome or advanced atrioventricular block.

DM = diabetes mellitus; HD = heart disease; LV = left ventricular.


Testicular cancer
Age 15-35
Epidemiology
Risk factors: family history, cryptorchidism
Unilateral, painless testicular nodule or swelling

Manifestations Dull lower abdominal ache

Metastatic symptoms (eg, dyspnea, neck mass, low back pain)


Diagnosis Examination: firm, ovoid mass or unilateral swelling
Scrotal ultrasound

Tumor markers (AFP, β-hCG)

Staging imaging (CT scan, chest x-ray)


Radical orchiectomy

Treatment Chemotherapy

Cure rate ~95%


AFP = alpha-fetoprotein.
Foodborne botulism
Clostridium botulinum toxin inhibits presynaptic
Pathogenesis
acetylcholine release at neuromuscular junction
Improperly canned foods (eg, fruits, vegetables)
Sources
Aged seafood (eg, cured fish)
Acute onset within 36 hr of ingestion

Bilateral cranial neuropathies

Blurred vision, diplopia


Clinical
features
Facial weakness, dysarthria, dysphagia

Symmetric descending muscle weakness

Diaphragmatic weakness with respiratory failure


Diagnosis Serum analysis for toxin
Treatment Equine serum heptavalent botulinum antitoxin
Rocky Mountain spotted fever
Rickettsia rickettsii infection

Epidemiology Transmitted by tick bite

Peaks in summer
Nonspecific fever, headache, myalgia, arthralgia

Macular & petechial rash on wrists/ankles


Clinical features
Can develop complications of encephalitis, pulmonary edema,
bleeding, shock
Laboratory ↓ Platelets
findings
↓ Sodium

↑ AST & ALT


Rickettsia serology
Diagnosis
Skin biopsy
Treatment Doxycycline
ALT = alanine transaminase; AST = aspartate transaminase.
Gastroesophageal reflux disease
Decreased tone or excessive transient relaxations of LES

Pathophysiology Anatomic disruption to gastroesophageal junction (eg, hiatal hernia)

↑ Risk with obesity, pregnancy, smoking, alcohol intake


Regurgitation of acidic material in mouth

Heartburn
Manifestations
Odynophagia (often indicates reflux esophagitis)

Extraesophageal manifestations: cough, hoarseness, wheezing


Esophageal: erosive esophagitis, Barrett esophagus, strictures
Complications
Extraesophageal: asthma exacerbation, laryngitis
Lifestyle (eg, weight loss) & dietary changes
Initial treatment
H2R blocker or PPI
H2R = histamine 2 receptor; LES = lower esophageal sphincter; PPI = proton pump inhibitor.
Common causes of recurrent pneumonia
Same Bronchial obstruction
lung lobe*
Extrinsic: neoplasm, adenopathy

Intrinsic: bronchiectasis, foreign body

Recurrent aspiration

Altered consciousness: seizure, sedatives, antipsychotics, alcohol,


illicit drugs

Dysphagia: neurologic disorder, esophageal motility issue

Poor dental hygiene


Gastroesophageal reflux
Immunodeficiency: HIV, leukemia, CVID
Different
Sinopulmonary disease: cystic fibrosis, immotile cilia
lung lobes
Noninfectious: vasculitis, BOOP
*Recurrent aspiration can lead to pneumonia in different dependent regions of the lung
depending on the position of the patient during the aspiration event.

BOOP = bronchiolitis obliterans with organizing pneumonia; CVID = common variable


immunodeficiency.
General manifestations of hyperthyroidism
Anxiety & insomnia

Palpitations

Symptoms Heat intolerance

Increased perspiration

Weight loss without decreased appetite


Goiter

Hypertension

Tremors involving fingers/hands

Physical examination Hyperreflexia

Proximal muscle weakness

Lid lag

Atrial fibrillation
Distinguishing hypertrophic cardiomyopathy from athlete's heart
Hypertrophic cardiomyopathy Athlete's heart
Family history Common Usually unremarkable
LVH criteria + depolarization &/or LVH criteria without other
ECG findings
repolarization abnormalities* abnormalities
Left atrial size Enlarged Normal
LV cavity size Usually decreased Slightly enlarged
LV wall
≥15 mm <15 mm
thickness
Focal septal Yes No
hypertrophy
LV diastolic
Impaired Normal
function
*Common depolarization abnormalities include prominent Q waves; common repolarization
abnormalities include T-wave inversions.

LV = left ventricular; LVH = left ventricular hypertrophy.


Delayed hemolytic transfusion reaction
Anamnestic antibody response: antibody production
Pathogenesis against minor RBC antigen to which patient was
previously* exposed
Onset >24 hr to a month after transfusion

Often asymptomatic
Clinical
Fatigue, dyspnea, tachycardia
findings
Jaundice

Low-grade fever
Hemolytic anemia

↑ Indirect bilirubin, LDH, reticulocyte count


Laboratory
findings
↓ Hemoglobin, haptoglobin

New positive direct antiglobulin (Coombs) test


Management Supportive (eg, fluids)
Review transfusion history & prior antibody screens
Prevention
Transfuse when necessary with extended-antigen cross-
matched blood
*Prior transfusion (eg, sickle cell disease), pregnancy, or transplant.

LDH = lactate dehydrogenase; RBC = red blood cell.


Complications due to extension of acute aortic dissection
Complication Stroke (carotid artery)

(involved structure) Horner syndrome (carotid sympathetic plexus)

Acute aortic regurgitation (aortic root/valve)

Myocardial ischemia/infarction (coronary artery ostia)


Pericardial effusion/tamponade (pericardium)

Hemothorax (pleural cavity)

Renal infarction (renal arteries)

Intestinal ischemia (mesenteric arteries)

Lower extremity paralysis (spinal arteries)


Necrotizing (malignant) otitis externa
Elderly (age >60)

Risk factors Diabetes mellitus

Aural irrigation (cerumen removal)


Microbiology Pseudomonas aeruginosa
Severe, unremitting ear pain (worse at night & with
chewing)

Deficits of lower cranial nerves (eg, facial [CN VII],


Clinical
glossopharyngeal [CN IX], vagus [CN X])
manifestations
Granulation tissue in the external auditory canal

Elevated erythrocyte sedimentation rate


Intravenous antipseudomonal antibiotics (eg,
ciprofloxacin)
Treatment
± Surgical débridement
Chikungunya virus infection
Tropical/subtropical parts of the Caribbean region,
Central/South America, Africa & Asia
Epidemiology
Vector: Aedes mosquitoes (also transmit dengue, yellow
fever & Zika viruses)
Incubation period: 3-7 days

High fever & severe polyarthralgia (almost always


present)
Manifestations
Headache, myalgia, conjunctivitis, maculopapular rash

Lymphopenia, thrombocytopenia, transaminitis


Management Supportive care (initial symptoms usually resolve in 7-10
days)

Chronic arthralgia/arthritis frequently occurs (may require


methotrexate)
Disease-modifying antirheumatic drugs
Agent Mechanism Adverse effects
Hepatotoxicity

Methotrexate Folate antimetabolite Stomatitis

Cytopenias
Hepatotoxicity
Pyrimidine synthesis
Leflunomide
inhibitor
Cytopenias
Hydroxychloroquine TNF & IL-1 suppressor Retinopathy
Hepatotoxicity

Sulfasalazine TNF & IL-1 suppressor Stomatitis

Hemolytic anemia
Infection
TNF inhibitors
Demyelination
(eg, adalimumab, certolizumab,
etanercept, golimumab,
Congestive heart failure
infliximab)
Malignancy
IL-1 = interleukin 1;TNF = tumor necrosis factor.
Transfusion reactions associated with hypotension
Reaction Onset* Cause Clinical features
Shock,
Seconds to Recipient anti-IgA
Anaphylaxis angioedema/urticaria
minutes antibodies
& respiratory distress
Respiratory distress &
noncardiogenic
Transfusion- Donor
Minutes to pulmonary edema
related acute lung antileukocyte
hours
injury antibodies
Bilateral pulmonary
infiltrates
Fever, flank pain,
Minutes to ABO
Acute hemolysis hemoglobinuria &
hours incompatibility
DIC
Bacterial
Minutes to Fever, chills, septic shock
Bacterial sepsis contamination of
hours & DIC
donor product
*Time after transfusion initiation.

DIC = disseminated intravascular coagulation.


Upper extremity deep venous thrombosis
Central venous catheters

Repetitive arm motions (eg, baseball pitching)


Risk factors
Weight lifting

Malignancy
Acute arm edema, heaviness, pain & erythema

Manifestations Dilated subcutaneous collateral veins in chest/upper extremity

Pulmonary embolism
Diagnosis Duplex or doppler ultrasonography
3 months of anticoagulation
Treatment
Thrombolysis (non–catheter-related)
Clinical features of chronic hepatitis C
Asymptomatic or nonspecific symptoms (eg, fatigue, anorexia,
arthralgia/myalgia)

Hepatic manifestations: cirrhosis, hepatocellular carcinoma

Extrahepatic manifestations
Clinical
manifestations
Hematologic: mixed cryoglobulinemia, ITP, autoimmune hemolytic
anemia

Renal: membranoproliferative glomerulonephritis

Dermatologic: porphyria cutanea tarda, lichen planus


Laboratory Anti-HCV IgG antibodies (screening): current or past infection
findings
HCV RNA PCR (confirmatory/diagnostic): active infection

Elevated AST, ALT

Thrombocytopenia (cirrhosis or ITP)

False-positive antinuclear antibodies & rheumatoid factor

Liver biopsy: portal triad lymphocytic inflammation, lymphoid follicles,


fibrosis & regenerative nodules (cirrhosis)
ALT = alanine aminotransferase; AST = aspartate aminotransferase; HCV = hepatitis C virus;
ITP = immune thrombocytopenia.
Clues to secondary causes of bone loss
Diarrhea, weight loss
Malabsorption
↓ 25-Hydroxyvitamin D, ↓ urine calcium excretion
Weight loss, heat intolerance, tremor
Hyperthyroidism
Goiter
Central obesity/cushingoid habitus
Hypercortisolism
Hyperglycemia
Hypercalcemia, hypercalciuria
Hyperparathyroidism
Kidney stones
Joint pain, morning stiffness
Inflammatory disorder
(eg, rheumatoid arthritis)
↑ ESR, CRP
♀: amenorrhea, weight loss/anorexia
Hypogonadism
♂: ↓ libido, erectile dysfunction, loss of body hair
Anemia
Multiple myeloma
Hypercalcemia, ↑ creatinine
CRP = C-reactive protein; ESR = erythrocyte sedimentation rate.
Osteoarthritis
Age of onset >40; prevalence increases with age
Knees

Hips
Joint
involvement
Distal interphalangeal joints

1st carpometacarpal joint


Morning
None/brief (<30 min)
stiffness
Systemic
Absent
symptoms
Hard, bony enlargement of joints
Examination
findings
Reduced range of motion with crepitus
Primary adrenal insufficiency
Autoimmune adrenalitis (most common)

Etiology Infection (eg, tuberculosis)

Metastatic infiltration
Fatigue, weakness, anorexia/weight loss

Nausea, vomiting, abdominal pain


Clinical
Salt craving, postural hypotension
features
Hyperpigmentation

Acute adrenal crisis: confusion, hypotension/shock


Hyponatremia, hyperkalemia, eosinophilia
Laboratory
findings
Low morning cortisol, high ACTH
Glucocorticoids (eg, hydrocortisone, prednisone)
Treatment
Mineralocorticoids (eg, fludrocortisone)
ACTH = adrenocorticotropic hormone.
Syphilis manifestations
Primary Painless genital ulcer (chancre)
Diffuse rash (palms & soles)

Lymphadenopathy (epitrochlear)

Secondary Condyloma latum

Oral lesions

Hepatitis
Latent Asymptomatic
CNS (tabes dorsalis, dementia)

Tertiary Cardiovascular (aortic aneurysm/insufficiency)

Cutaneous (gummas)
CNS = central nervous system.
ECG effects of antiarrhythmic drugs
PR interval
QRS duration QT interval
(prolonged via Ca2+
(prolonged via Na+ (prolonged via K+
channel inhibition or
channel inhibition) channel inhibition)
sympathetic blockade)
Class IA − ↑ ↑
(eg, procainamide)
Class IB
− − −
(eg, lidocaine)
Class IC
− ↑
(eg, flecainide)
Class II
↑ − −
(eg, metoprolol)
Amiodarone ↑ ↑ ↑
Sotalol ↑ − ↑
Other class III
− − ↑
(eg, dofetilide)
Class IV
↑ − −
(eg, verapamil)
Culture-positive infective endocarditis
Prosthetic valves

Intravascular catheters
Staphylococcus aureus
Implanted devices (eg, pacemaker/defibrillator)

Intravenous drug users


Gingival manipulation
Viridans streptococci
Respiratory tract incision or biopsy
Prosthetic valves

Staphylococcus epidermidis Intravascular catheters

Implanted devices
Enterococci Nosocomial urinary tract infections
Colon carcinoma
Streptococcus gallolyticus
(formerly S bovis)
Inflammatory bowel disease
Immunocompromised host
Fungi
Intravascular catheters
(eg, Candida)
Prolonged antibiotic therapy
Hyperosmolar hyperglycemic state
Type 2 diabetes mellitus
Patient
characteristics
Older age
Inciting Acute illness, trauma, infection
factors
Insulin nonadherence

Medications: glucocorticoids, diuretics, atypical antipsychotics


Subacute or acute onset of:

Altered mentation
Clinical
features
Hyperglycemic symptoms (eg, polyuria)

Volume depletion
Glucose >600 mg/dL (33.3 mmol/L)

Bicarbonate >18 mEq/L (18 mmol/L)


Laboratory
Normal anion gap
studies
Negative or small serum ketones

Serum osmolality >320 mOsm/kg (320 mmol/kg)

Diffuse esophageal spasm


Uncoordinated, simultaneous
Pathophysiology
contractions of esophageal body
Intermittent chest pain
Symptoms
Dysphagia for solids & liquids
Manometry: Intermittent peristalsis,
multiple simultaneous contractions
Diagnosis
Esophagram: "Corkscrew" pattern
Calcium channel blockers
Treatment
Alternates: Nitrates or tricyclics
 
Opioid withdrawal
4 to 48 hr after opioid cessation
Time course
Immediately after opioid antagonist (life-threatening)
Clinical Gastrointestinal: nausea, vomiting, cramping, diarrhea, ↑ bowel
presentation sounds

Cardiac: ↑ pulse, ↑ blood pressure, diaphoresis


Psychologic: insomnia, yawning, dysphoric mood

Other: myalgia, arthralgia, mydriasis, lacrimation, rhinorrhea,


piloerection
Diagnosis History & examination alone (clinical diagnosis)
Opioid agonist: methadone or buprenorphine
Management
Nonopioid: clonidine or adjunctive medications (antiemetics,
antidiarrheals, benzodiazepines)
 
Tuberculous meningitis
Occurs in ~5% of patients with disseminated TB
Epidemiology
↑ Risk with HIV, immunomodulatory medications, malnutrition,
substance abuse
Subacute fever, vomiting, headache, lethargy

Manifestations Cranial nerve palsy

Stroke
Imaging: basilar meningeal enhancement & hydrocephalus

CSF: WBC count 100-500/mm3, mildly ↑ protein, ↓ glucose, ↑ adenosine


Diagnosis
deaminase

NAAT or AFB CSF smear


AFB = acid-fast bacillus; CSF = cerebrospinal fluid; NAAT = nucleic acid amplification test;
TB = tuberculosis; WBC = white blood cell.
 
Reducing antibiotic use in URI & acute bronchitis
Careful history & examination to rule out pneumonia & other serious illnesses
Patient
assessment
Patient's understanding of causes & natural history of illness
Explain expected duration & self-limited course of illness
Patient
Explain potential harm & lack of efficacy of antibiotics
education
Refer to infection as a "cold" or "chest cold"
Symptomatic treatment: OTC (eg, guaifenesin, tea with honey) & prescription
(eg, benzonatate) options
Management
Consider delayed antibiotic prescription (ie, prescription to be filled only if no
improvement occurs after predetermined time)
OTC = over-the-counter; URI = upper respiratory infection.
Anemia of chronic disease
↑ inflammatory cytokines (eg, hepcidin)

Inhibition of ferroportin on enterocytes and macrophages


Pathogenesis
↓ iron absorption and ↑ iron sequestration

Reduced circulating iron → impaired erythropoiesis


Malignancy

Chronic infection

Rheumatic disease
Common Etiologies
Obesity

Diabetes mellitus

Congestive heart failure


Normocytic/slightly microcytic anemia

↓ serum iron, iron-binding capacity, reticulocyte count


Laboratory findings
↑ bone marrow iron

Lower than expected erythropoietin for degree of anemia


Treatment Treat underlying condition causing inflammation
Pulmonary function tests in chronic lung disease
Pulmonary Restrictive
Interstitial
Asthma COPD arterial chest wall
lung diseases
hypertension disease
TLC Normal/↑ ↑ ↓ Normal ↓
FEV1/FVC ↓* ↓ Normal Normal Normal
DLCO Normal/↑ ↓† ↓ ↓ Normal
COPD = chronic obstructive pulmonary disease; DLCO = diffusing capacity for carbon
monoxide; TLC = total lung capacity.

*With positive bronchodilator response.



Normal in early COPD.
Drug-induced rhabdomyolysis
Major mechanism Examples
Direct myotoxicity Statins, fibrates
Colchicine

Ethanol

Cocaine
Cocaine
Vasoconstrictive ischemia
Amphetamines
Ethanol
Prolonged immobilization
Opioids
(compression ischemia)
Benzodiazepines
Cor pulmonale
Right-sided heart failure due to primary pulmonary disorder
Pathophysiology
Absence of left-sided heart disease
Parenchymal disease/chronic hypoxia

COPD (most common)

Cystic fibrosis
Common
etiologies
Interstitial lung disease

Obstructive sleep apnea

Pulmonary vascular disease: pulmonary embolism


Dyspnea & fatigue on exertion

Symptoms Exertional angina (due to ↑ cardiac demand)

Exertional syncope (due to ↓ cardiac output)


Jugular venous distension

Peripheral edema
Examination
Palpable RV heave, loud P2, tricuspid regurgitation murmur

Hepatomegaly with pulsatile liver


Diagnostic Electrocardiography
evaluation
Incomplete/complete right bundle branch block
Right axis deviation, RV hypertrophy, RA enlargement

Echocardiography

Pulmonary hypertension, RV dilation/dysfunction, tricuspid


regurgitation

Catheterization (gold standard)

Elevated filling pressures, decreased cardiac output, pulmonary


hypertension
COPD = chronic obstructive pulmonary disease; RA = right atrial; RV = right ventricular.
Peritoneal dialysis–related peritonitis
Touch contamination of catheter lumen
Pathophysiology
Extension of catheter site skin infection
Abdominal pain ± fever & nausea

Clinical presentation Diffuse abdominal tenderness ± rebound

Cloudy peritoneal fluid


Gram-positive bacteria (~65%)

Microbiology Gram-negative bacteria (~30%)

Fungal organism (~5%)


Clinical presentation (ie, abdominal pain, cloudy fluid)

Diagnosis Relative neutrophilia on fluid analysis

Positive fluid Gram stain or culture


Treatment Intraperitoneal antibiotics (eg, vancomycin + gentamicin)*
*Empiric therapy should cover both gram-positive & gram-negative organisms.
Hepatic encephalopathy
Precipitating factors Drugs (eg, sedatives, narcotics)

Hypovolemia (eg, diarrhea)

Electrolyte changes (eg, hypokalemia)

↑ Nitrogen load (eg, GI bleeding)

Infection (eg, pneumonia, UTI, SBP)


Portosystemic shunting (eg, TIPS)
Sleep pattern changes

Altered mental status


Clinical presentation
Ataxia

Asterixis
Correct precipitating causes (eg, fluids, antibiotics)
Treatment
↓ Blood ammonia concentration (eg, lactulose, rifaximin)
GI = gastrointestinal; SBP = spontaneous bacterial peritonitis; TIPS = transjugular intrahepatic
portosystemic shunt; UTI = urinary tract infection.
Pertussis
Microbiology Bordetella pertussis (gram-negative coccobacilli)
Catarrhal (weeks 1-2): mild cough, rhinitis

Paroxysmal (weeks 2-8): severe coughing spells


Clinical
phases ± Inspiratory whoop, posttussive emesis, apnea/cyanosis (infants);
posttussive syncope (older patients)

Convalescent (weeks 8+): symptoms resolve gradually


Clinical: cough + paroxysmal symptoms &/or pertussis exposure

Supportive findings: low-grade/no fever, leukocytosis with


Diagnosis
lymphocytosis, normal/nonspecific chest x-ray

Confirmatory: pertussis PCR (sensitive) & culture (specific)


Treat empirically with macrolide (eg, azithromycin)
Treatment
Droplet precautions
Acellular pertussis vaccine
Prevention
Macrolides for close (home/health care) contacts regardless of
vaccination status
Cyanide poisoning
Structure fires (eg, combustion of plastics)

Common etiologies Occupational exposure (eg, mining)

Cyanide-containing medications (eg, sodium nitroprusside)


Pathophysiology Inhibits oxidative phosphorylation & forces anaerobic metabolism
Rapidly lethal if untreated
Hypertension, tachycardia, tachypnea → circulatory collapse, death

Headache, confusion, anxiety → seizures, coma


Clinical features
Cherry-red skin

Elevated anion gap metabolic acidosis with ↑ lactic acid


Decontamination

Management Supportive care (eg, 100% oxygen, intravenous fluids, vasopressors)

Empiric treatment with hydroxocobalamin ± sodium thiosulfate*


*Sodium nitrite + sodium thiosulfate is an alternate treatment but is contraindicated in carbon
monoxide poisoning.
Hypertrophic cardiomyopathy
Genetic mutations affecting cardiac sarcomere proteins

Pathophysiology Autosomal dominant inheritance

Variable phenotypic penetrance


Many patients are asymptomatic

Exertional dyspnea, fatigue, angina, light-headedness, syncope

Clinical features Systolic ejection murmur accentuated by ↓ LV blood volume

Diastolic dysfunction with audible S4

↑ Risk for atrial fibrillation & ventricular tachycardia


ECG: left axis deviation, abnormalities of depolarization (eg, Q waves)
or repolarization (eg, inverted T waves)
Diagnosis
Echocardiography: septal LV hypertrophy, dynamic LVOT obstruction,
LA dilation
Beta blocker or nondihydropyridine CCB (facilitate ↑ LV blood
volume)

Avoidance of dehydration & vasodilators (avoid ↓ LV blood volume)


Management
ICD placement for increased risk for SCD

Septal ablation, cardiac transplantation


CCB = calcium channel blocker; ICD = implantable cardiac defibrillator; LA = left atrial;
LV = left ventricular; LVOT = left ventricular outflow tract; SCD = sudden cardiac death.
Prerenal acute kidney injury
Decreased renal perfusion

True volume depletion

Decreased EABV (eg, heart failure, cirrhosis)


Etiology
Displacement of intravascular fluid (eg, sepsis, pancreatitis)

Bilateral renal artery stenosis with ACE inhibition

Afferent arteriole vasoconstriction (eg, NSAIDs)


Increase in serum creatinine (eg, 50% from baseline)

Decreased urine output

Clinical features Blood urea nitrogen/creatinine ratio >20:1

Fractional excretion of sodium <1%

Unremarkable ("bland") urine sediment


Treatment Restoration of renal perfusion
EABV = effective arterial blood volume; NSAIDs = nonsteroidal anti-inflammatory drugs.
Osteoarthritis vs rheumatoid arthritis
Osteoarthritis Rheumatoid arthritis
Age of onset >40; increases with age 40-60; often younger
Knees & hips MCP joint

Joint involvement DIP joint PIP joint

First CMC joint Wrists


Morning stiffness None/brief Prolonged
Fever

Systemic symptoms Absent Fatigue

Weight loss
Examination Hard, bony enlargement of joints Soft/spongy, warm joints
Narrowed joint space
X-ray Periarticular erosions
Osteophytes
CMC = carpometacarpal; DIP = distal interphalangeal; MCP = metacarpophalangeal; PIP =
proximal interphalangeal.
Initial pharmacotherapy for acute asthma exacerbation
Class Medication Use
Bronchodilator
Short-acting ꞵ2-agonist Inhaled albuterol
Continuous (if severe) or
repeated dosing
Bronchodilator

Repeated dosing only in


Anticholinergic Inhaled ipratropium bromide
acute setting & in
conjunction with
albuterol
Anti-inflammatory
Prednisone,
Delayed effect (6 hr)
methylprednisolone,
Glucocorticoid
dexamethasone
Multiday dosing for control
(oral/intravenous)
of late-phase
inflammation
Serum sickness & serum sickness–like reaction
SS SSLR
Common Foreign proteins in antivenom, Medications, particularly cefaclor,
triggers antitoxin, or monoclonal antibody penicillin & TMP-SMX
Immune
High titer Mild or none
complexes
Complement
Extensive Minimal or none
activation
Onset 5-14 days after exposure 5-14 days after exposure
Fever High Low-grade
Arthralgia Yes Yes
Urticaria Yes Yes
Spontaneous (discontinue drug if still
Resolution Spontaneous
receiving)
SS = serum sickness; SSLR = serum sickness–like reaction; TMP-SMX = trimethoprim-
sulfamethoxazole.
Risk factors for dermatophyte infection
Warm, humid environments

Environmental exposures Direct contact with infected person, fomites, or public showers

Contact with animals (eg, kittens)


Patient factors Concurrent dermatophyte infection (autoinoculation)

Occlusive clothing
Obesity

Peripheral artery disease


Diabetes mellitus

Immune deficiency HIV infection

Systemic glucocorticoid therapy


Mechanical complications of acute myocardial infarction
Involved
Time Echocardiography
Complication coronary Clinical findings
course findings
artery
Severe pulmonary edema,
respiratory distress
Papillary muscle Acute or
rupture/ within 3- RCA New early systolic murmur Severe MR
dysfunction 5 days
Hypotension/cardiogenic
shock
Chest pain
LAD (apical
Acute or
Interventricular septal) or New holosystolic murmur Left-to-right
within 3-
septum rupture RCA (basal ventricular shunt**
5 days
septal) Hypotension/cardiogenic
shock
Chest pain
Within 5
days* or Distant heart sounds Pericardial effusion
Free wall rupture LAD
up to 2 with tamponade
weeks Shock, rapid progression
to cardiac arrest
Heart failure
Up to
Left ventricular Thin & dyskinetic
several LAD Angina
aneurysm myocardial wall
months
Ventricular arrhythmias
*50% occur within 5 days.

**Right heart catheterization shows step up in O2 concentration from right atrium to right
ventricle.

LAD = left anterior descending; MR = mitral regurgitation; RCA = right coronary artery.
Cyanide poisoning
Common etiologies Structure fires (eg, combustion of plastics)
Occupational exposure (eg, mining)

Cyanide-containing medications (eg, sodium nitroprusside)


Inhibits oxidative phosphorylation & forces anaerobic metabolism
Pathophysiology
Rapidly lethal if untreated
Hypertension, tachycardia, tachypnea → circulatory collapse, death

Headache, confusion, anxiety → seizures, coma


Clinical features
Cherry-red skin

Elevated anion gap metabolic acidosis with ↑ lactic acid


Decontamination

Management Supportive care (eg, 100% oxygen, intravenous fluids, vasopressors)

Empiric treatment with hydroxocobalamin ± sodium thiosulfate*


*Sodium nitrite + sodium thiosulfate is an alternate treatment but is contraindicated in carbon
monoxide poisoning.
Kaposi sarcoma
Endothelial tumor caused by human herpesvirus 8

Etiology Most common malignancy in patients with untreated HIV

Endemic in certain African & Mediterranean regions


Cutaneous lesions:

Violaceous, red, or brown flat lesions grow into papules

Most common along skin folds

Pruritus, pain & friability are rare


Manifestations
Lymphedema distal to lesions

Visceral lesions:

Lungs & gastrointestinal tract most common

May cause life-threatening bleeding


Treatment HIV-associated KS:
Antiretroviral therapy initiation

Local or systemic chemotherapy rarely required

Endemic KS:

Surgery & local therapy are primary modalities


KS = Kaposi sarcoma.
Acute respiratory distress syndrome: management & prognosis
Lung protection: limit alveolar distending volume (VT 6 mL/kg) &
pressure (Pplat ≤30 cm H2O)

Mechanical Ventilation: tolerate permissive hypercapnia (ie, ↑ PaCO2 & ↓ pH


ventilation acceptable) to avoid excessive VT

Oxygenation: set lowest feasible FiO2 (goal SpO2 92%-96%) to


avoid O2 toxicity
Treat underlying etiology: source control (eg, sepsis)

Prevent iatrogenic harm: negative fluid balance, timely extubation


Supportive care (eg, minimize sedation)

± Corticosteroids: select patients with moderate-to-severe early


ARDS
Mortality rate: 40% in hospital, death mostly due to multiorgan
failure
Prognosis
Morbidity rate: 50% with chronic cognitive impairment & physical
debility, 25% with chronic pulmonary dysfunction (restriction &
↓ DLCO)
ARDS = acute respiratory distress syndrome; DLCO = diffusion capacity of lung for carbon
monoxide; Pplat = plateau pressure; SpO2 = oxygen saturation as measured by pulse oximetry;
VT = tidal volume.
Arsenic poisoning
Binds to sulfhydryl groups
Mechanism
Disrupts cellular respiration & gluconeogenesis
Pesticides/insecticides

Sources Contaminated water (often from wells)

Pressure-treated wood
Manifestations Acute: garlic breath, vomiting, watery diarrhea, QTc prolongation
Chronic: hypo-/hyperpigmentation, hyperkeratosis, stocking-glove
neuropathy
Dimercaprol (British anti-Lewisite)
Treatment
DMSA (ie, meso-2,3-dimercaptosuccinic acid, succimer)
Hemodynamic measurements in shock
Distributive
Hypovolemic Cardiogenic Obstructive
Parameter
shock shock shock
shock
CVP
(right-sided ↓ ↑ ↑ ↓
preload)
PCWP
(left-sided ↓ ↑ ↓* ↓
preload)
Cardiac index
↓ ↓ ↓ ↑**
(LV output)
SVR
↑ ↑ ↑ ↓
(afterload)
SvO2 ↓ ↓ ↓ ↑**
*In tamponade, left-sided preload is decreased, but measured PCWP is paradoxically increased
due to external compression by pericardial fluid.

**Cardiac index & SvO2 are usually decreased in neurogenic shock due to impaired sympathetic
reflexes.

CVP = central venous pressure; LV = left ventricular; PCWP = pulmonary capillary wedge


pressure; SvO2 = mixed venous oxygen saturation; SVR = systemic vascular resistance.
Adults at high risk for influenza complications
Age ≥65

Women who are pregnant & up to 2 weeks postpartum

Underlying chronic medical illness (eg, chronic pulmonary, cardiovascular, renal, hepatic)

Immunosuppressed

Morbidly obese

Residents of nursing homes or long-term care facilities


Indications for urgent dialysis (AEIOU)
Metabolic acidosis
Acidosis
pH <7.1 refractory to medical therapy
Symptomatic hyperkalemia

ECG changes or ventricular arrhythmias


Electrolyte abnormalities
Severe hyperkalemia

Potassium >6.5 mEq/L refractory to medical therapy


Toxic alcohols (methanol, ethylene glycol)

Salicylate
Ingestion
Lithium

Sodium valproate, carbamazepine


Overload Volume overload refractory to diuretics
Symptomatic:

Encephalopathy
Uremia
Pericarditis

Bleeding
Red blood cell transfusion thresholds
Hemoglobin
Recommendation
(g/dL)
<7 Generally indicated
Cardiac surgery

7-8 Oncology patients in treatment

Heart failure
Symptomatic anemia

Ongoing bleeding
8-10
Acute coronary syndrome

Noncardiac surgery
>10 Not generally indicated
Primary adrenal insufficiency
Etiology Autoimmune adrenalitis (most common)

Infection (eg, tuberculosis)
Metastatic infiltration
Fatigue, weakness, anorexia/weight loss

Nausea, vomiting, abdominal pain


Clinical
Salt craving, postural hypotension
features
Hyperpigmentation

Acute adrenal crisis: confusion, hypotension/shock


Hyponatremia, hyperkalemia, eosinophilia
Laboratory
findings
Low morning cortisol, high ACTH
Glucocorticoids (eg, hydrocortisone, prednisone)
Treatment
Mineralocorticoids (eg, fludrocortisone)
ACTH = adrenocorticotropic hormone.
Clues to surreptitious cocaine use
Personality & mood changes

Changes in sleep patterns


Behavioral
features
Unexplained weight loss

Financial difficulties
Chest pain
Reported
Epistaxis, rhinitis (intranasal use)
symptoms
Headaches
Hypertension, tachycardia
Examination
Dilated pupils
signs
Psychomotor agitation
Seizures

Acute myocardial ischemia


Emergent
complications
Aortic dissection

Intracranial hemorrhage
Organophosphate poisoning
Common Pesticide: farmer/field worker, pediatric ingestion, suicide attempt
exposures
Nerve agent: multiple patients presenting with similar symptoms
Muscarinic:

Diarrhea/diaphoresis

Urination

Miosis

Manifestations Bronchospasms, bronchorrhea, bradycardia

Emesis

Lacrimation

Salivation

Nicotinic: muscle weakness, paralysis, fasciculations


Remove patient's clothes, irrigate skin

Atropine reverses muscarinic symptoms


Management
Pralidoxime reverses nicotinic and muscarinic symptoms (administer
after atropine)
Extraarticular manifestations of rheumatoid arthritis
Fever

Systemic Weight loss

Fatigue
Fibrotic lung disease

Pleural effusions
Pulmonary
Lung nodules

Pulmonary hypertension
Atherosclerosis
Cardiovascular
Vasculitis
Musculoskeletal Osteopenia/osteoporosis
Dermatologic Rheumatoid nodules
Hematologic Anemia
Depression
Neuropsychiatric
Neuropathy
Sjögren syndrome

Other Raynaud phenomenon

Scleritis, episcleritis
Management of pulmonary hypertension
Evaluate for autoimmune CTD, toxins (eg, amphetamines), HIV,
schistosomiasis, etc.
Group 1
PAH
Pulmonary vasodilator therapy, treat underlying (eg, autoimmune)
cause
Echocardiography (± RHC if diagnosis unclear)
Group 2
Left-sided
Optimize left ventricular function (eg, heart failure therapy), treat
heart disease
significant valve disease
Group 3 Pulmonary function tests, chest imaging, polysomnography
Lung disease &/or
chronic hypoxemia Treat underlying respiratory condition (eg, obstructive sleep apnea)
V/Q scan, pulmonary angiography
Group 4
CTEPH Pulmonary thromboendarterectomy surgery (curative),
anticoagulation
Refer to accredited PH center

Maintain normoxia, euvolemia & sinus rhythm


General
measures
Contraceptive counseling, immunization, cardiac rehabilitation

Refractory PH: bilateral lung transplant


CTD = connective tissue disease (eg, scleroderma); CTEPH = chronic thromboembolic
pulmonary hypertension; PAH = pulmonary arterial hypertension; PH = pulmonary
hypertension; RHC = right-sided heart catheterization; V/Q = ventilation-perfusion.
Recommendations for lung cancer screening
Recommended
Low-dose CT scan of the chest
test
Recommended interval Yearly
Age for
50-80
screening
Eligibility ≥20-pack-year history
&

Currently smoking or quit smoking within the past


15 years
Patient successfully quit smoking for ≥15 years
OR
Termination of
screening
Patient has medical conditions that significantly limit life
expectancy
Hemodynamic effects of adrenergic agonists
α1: peripheral vasoconstriction, ↑ SVR

β1: ↑ heart rate & contractility, ↑ cardiac output

β2: peripheral vasodilation, ↓ SVR

D1: renal arteriolar vasodilation


Receptor Cardiac Renal
Agonist SVR
binding output blood flow
Dobutamine β1 > β 2 ↓ ↑ –
D1 > β1 > α1
–/↓ ↑ ↑
(low-dose)
Dopamine
α 1 > β1 > D 1
↑ –/↓ ↓
(high-dose)
β1 > β 2 > α 1
–/↓ ↑ –
(low-dose)
Epinephrine
α1 > β 1 > β 2
↑ –/↓ ↓
(high-dose)
Isoproterenol β1 = β 2 ↓ ↑ –
Norepinephrine α1 = β1 > β2 ↑ – ↓
Phenylephrine α1 ↑ ↓ ↓
SVR = systemic vascular resistance.
Infective endocarditis with intravenous drug use
Injected particles cause microdamage to right-sided
valves before being filtered out by the lungs
Pathogenesis
Microdamage facilitates bacterial attachment

Increased risk with HIV


Clinical features Tricuspid valve most commonly affected

Staphylococcus aureus is the most common organism

Septic pulmonary emboli present in up to 75% of cases


Audible murmur may be absent in 50% of cases

Few peripheral manifestations


(eg, splinter hemorrhages, Janeway lesions)

Heart failure uncommon


Acute mitral regurgitation
Ruptured mitral chordae tendineae from:

Mitral valve prolapse

Infective endocarditis
Etiology
Rheumatic heart disease

Trauma

Papillary muscle displacement or rupture due to MI


Rapid onset of pulmonary edema

Clinical features Acute LV failure (also causing acute RV failure)

Hypotension, cardiogenic shock


Jugular venous distension, pulmonary crackles

Hyperdynamic cardiac impulse


Physical examination
Apical systolic murmur (often absent)

Diaphoresis, cool extremities (if shock is present)


Bedside echocardiography
Management
Emergency surgical intervention
LV = left ventricular; MI = myocardial infarction; RV = right ventricular.
Myasthenia gravis
Fluctuating & fatigable proximal muscle weakness:

Ocular (eg, diplopia, ptosis)


Clinical
presentation
Bulbar (eg, dysphagia, dysarthria)

Respiratory (myasthenic crisis)


Causes of Medications: antibiotics (eg, fluoroquinolones,
exacerbations aminoglycosides), neuromuscular blocking agents, cardiac
medications (eg, BBs), MgSO4, penicillamine

Physiologic stress: pregnancy/childbirth, surgery (especially


thymectomy), infection
Ice pack test (bedside), AChR-Ab (highly specific)
Diagnosis
CT scan of chest (thymoma)
AChE inhibitors (eg, pyridostigmine) ± immunotherapy (eg,
corticosteroids, azathioprine)
Treatment
Thymectomy
AChE = acetylcholinesterase; AChR-Ab = acetylcholine receptor antibodies; BBs
= beta blockers; MgSO4 = magnesium sulfate.
Post–cardiac injury syndrome
Myocardial infarction (ie, Dressler syndrome)

Causes Cardiac surgery or trauma

Percutaneous coronary intervention


Latent period of several weeks to months

Pleuritic chest pain, fever, leukocytosis


Clinical
features
Chest x-ray: pleural effusion ± enlarged cardiac silhouette

Echocardiography: pericardial effusion


NSAID (usually high-dose aspirin) ± colchicine
Treatment
Corticosteroids in refractory disease
Usually self-limited disease course
Prognosis
May cause chronic/recurrent disease leading to constrictive pericarditis
NSAID = nonsteroidal anti-inflammatory drug.
Hemodynamic measurements in shock
Distributive
Hypovolemic Cardiogenic Obstructive
Parameter
shock shock shock
shock
CVP
(right-sided ↓ ↑ ↑ ↓
preload)
PCWP
(left-sided ↓ ↑ ↓* ↓
preload)
Cardiac index
↓ ↓ ↓ ↑**
(LV output)
SVR
↑ ↑ ↑ ↓
(afterload)
SvO2 ↓ ↓ ↓ ↑**
*In tamponade, left-sided preload is decreased, but measured PCWP is paradoxically increased
due to external compression by pericardial fluid.

**Cardiac index & SvO2 are usually decreased in neurogenic shock due to impaired sympathetic
reflexes.

CVP = central venous pressure; LV = left ventricular; PCWP = pulmonary capillary wedge
pressure; SvO2 = mixed venous oxygen saturation; SVR = systemic vascular resistance.
Management of hospital delirium
Reduce noise, improve room lighting, open window blinds during the day & avoid frequent
room changes

Constant observation by a familiar person at the bedside, preferably a family member 

Nonpharmacologic sleep aids for insomnia

Early mobilization & minimal use of physical restraints

Visual & hearing aids when appropriate

Early volume repletion for dehydrated patients

Adequate pain control

Aggressive chronic disease management (eg, diabetes, COPD)

Reduce polypharmacy

Monitor & treat for metabolic disturbances, infections & drug toxicity
COPD = chronic obstructive pulmonary disease.
Localization of ST-segment elevation myocardial infarction
Involved Occluded
ST-segment elevation leads
myocardium vessel
Septal V1, V2 LAD
Anterior V3, V4 LAD
Lateral* V5, V6, I, aVL, V7 through V9 LAD or LCx
V1 through V3 (reciprocal ST-segment depression), V7
Posterior RCA or LCx
through V9 (ST-segment elevation)
Inferior II, III, aVF RCA or LCx
Right ventricle** II, III, aVF, V4R through V6R RCA
*Most lateral/posterolateral STEMIs are electrically silent due to poor coverage, usually
corresponding to LCx territory.

**Involved in ~50% of inferior STEMIs; confirmed by ST-segment elevations in leads V4R


through V6R placed on right precordial area.

LAD = left anterior descending artery; LCx = left circumflex artery; RCA = right coronary
artery; STEMI = ST-segment elevation myocardial infarction.
Hospice model
Focus on quality of life, not cure or life prolongation

Symptom control (eg, pain, nausea, dyspnea, agitation, anxiety, depression)

Interdisciplinary team (eg, medical, nursing, psychosocial, spiritual, bereavement care)

Services provided at home, assisted-living facility, or dedicated facility

Requires survival prognosis of ≤6 months


Allergic contact dermatitis
Type IV hypersensitivity reaction
Pathophysiology
Common triggers: poison ivy/oak, nickel, dyes,
topical medications, skin care products
Acute: pruritic red, indurated plaques with
Clinical vesicles/bullae
presentation
Chronic: lichenification, fissuring
Clinical findings
Diagnosis
Patch testing for persistent cases
Avoidance of suspected allergen
Treatment
Topical or systemic corticosteroid
Hyponatremia
Serum
ECV Urine findings Cause
osmolality
Low Nonrenal salt loss (eg, vomiting,
UNa <40 mEq/L
(<275 diarrhea, dehydration)
Hypovolemic
mOsm/kg) Renal salt loss (eg, diuretics, primary
UNa >40 mEq/L
adrenal insufficiency)
Psychogenic polydipsia
UOsm <100 mOsm/kg
Euvolemic Beer potomania
UOsm >100 mOsm/kg SIADH (rule out hypothyroidism,
& UNa >40 mEq/L secondary adrenal insufficiency)
Hypervolemic Variable CHF, hepatic failure, nephrotic
syndrome
Pseudohyponatremia (eg,
Normal
paraproteinemia, hyperlipidemia)
High Variable Hyperglycemia
(>295
mOsm/kg) Exogenous solutes (eg, mannitol)
CHF = congestive heart failure; ECV = extracellular volume; SIADH = syndrome of
inappropriate antidiuretic hormone; UNa = urine sodium; UOsm = urine osmolality.
Ascites fluid characteristics
Bloody: trauma, malignancy, TB (rarely)

Milky: chylous
Color
Turbid: possible infection

Straw color: likely more benign causes


Neutrophils ≥250/mm3: peritonitis (secondary or spontaneous bacterial)
≥2.5 g/dL (high-protein ascites)

CHF, constrictive pericarditis, peritoneal carcinomatosis, TB, Budd-


Chiari syndrome, fungal
Total protein
<2.5 g/dL (low-protein ascites)

Cirrhosis, nephrotic syndrome


≥1.1 g/dL (indicates portal hypertension)

Cardiac ascites, cirrhosis, Budd-Chiari syndrome


SAAG
<1.1 g/dL (absence of portal hypertension)

TB, peritoneal carcinomatosis, pancreatic ascites, nephrotic syndrome


CHF = congestive heart failure; SAAG = serum-ascites albumin gradient; TB = tuberculosis.
Diagnostic criteria for antiphospholipid-antibody syndrome

(1 clinical & 1 laboratory criterion must be met)


Clinical Vascular thrombosis

Arterial or venous

Pregnancy morbidity

≥3 consecutive, unexplained fetal losses before 10th


week
≥1 unexplained fetal losses after 10th week

≥1 premature births of normal neonates before 34th


week due to preeclampsia, eclampsia, or placental
insufficiency
Lupus anticoagulant

Laboratory Anticardiolipin antibody

Anti–beta-2 glycoprotein antibody I


Acute respiratory distress syndrome: management & prognosis
Lung protection: limit alveolar distending volume (VT 6 mL/kg) &
pressure (Pplat ≤30 cm H2O)

Mechanical Ventilation: tolerate permissive hypercapnia (ie, ↑ PaCO2 & ↓ pH


ventilation acceptable) to avoid excessive VT

Oxygenation: set lowest feasible FiO2 (goal SpO2 92%-96%) to


avoid O2 toxicity
Treat underlying etiology: source control (eg, sepsis)

Prevent iatrogenic harm: negative fluid balance, timely extubation


Supportive care (eg, minimize sedation)

± Corticosteroids: select patients with moderate-to-severe early


ARDS
Mortality rate: 40% in hospital, death mostly due to multiorgan
failure
Prognosis
Morbidity rate: 50% with chronic cognitive impairment & physical
debility, 25% with chronic pulmonary dysfunction (restriction &
↓ DLCO)
ARDS = acute respiratory distress syndrome; DLCO = diffusion capacity of lung for carbon
monoxide; Pplat = plateau pressure; SpO2 = oxygen saturation as measured by pulse oximetry;
VT = tidal volume.
Indications for statin therapy in prevention of ASCVD
Secondary prevention Established ASCVD

Acute coronary syndrome

Stable angina

Arterial revascularization (eg, CABG)


Stroke, TIA, PAD
LDL ≥190 mg/dL

Primary prevention Age ≥40 with diabetes mellitus

Estimated 10-year risk of ASCVD >7.5%-10%


ASCVD = atherosclerotic cardiovascular disease; CABG = coronary artery bypass grafting;
PAD = peripheral artery disease; TIA = transient ischemic attack.
Bacillary angiomatosis
Bartonella henselae/quintana

Cat exposure or homelessness (lice)


Epidemiology
Severe immunocompromise

Advanced HIV (CD4 <100/mm3)


Vascular cutaneous lesions (papular, nodular, peduncular)

Manifestations Systemic symptoms (fever, night sweats, fatigue)

Organ involvement rarely (liver, bone, CNS)


Diagnosis Lesional biopsy with microscopy/histopathology
Doxycycline or erythromycin
Treatment
Antiretroviral therapy
CNS = central nervous system.

Complications of nephrotic syndrome*


Mechanism
Urinary loss of anticoagulant proteins (eg, antithrombin
III)
Hypercoagulability
(↑ thromboembolism risk)
Hepatic synthesis of prothrombotic proteins (eg,
fibrinogen)
Hyperlipidemia
Hepatic synthesis of lipoproteins
(↑ atherosclerosis risk)
Infection Urinary loss of immunoglobulins & opsonizing factors
Protein malnutrition Negative nitrogen balance
Intravascular volume depletion Low oncotic pressure
*Nephrotic syndrome results from glomerular filtration barrier (eg, podocyte) injury that leads to
heavy proteinuria (>3.5 g/day), hypoalbuminemia & peripheral edema.
 
Extra (gallop) heart sounds
Features Associated pathology*
Heard just after S2 Heart failure with reduced EF

S3 Caused by reverberant sound as blood High-output states (eg, thyrotoxicosis)


fills an enlarged LV cavity during
passive diastolic filling Mitral or aortic regurgitation
Concentric LV hypertrophy
Heard just before S1
S4 Restrictive cardiomyopathy
Caused by blood striking a stiff LV
wall during atrial contraction
Acute myocardial infarction
*S3 can be normal in children, young adults & during pregnancy.  S4 can be normal in the
elderly (eg, age >70).

EF = ejection fraction; LV = left ventricular.


 
Autosomal dominant polycystic kidney disease
Most patients asymptomatic until age 30-40

Flank pain, hematuria


Clinical
Hypertension
presentation
Palpable abdominal masses (usually bilateral)

Chronic kidney disease (CKD)


Cerebral aneurysms

Hepatic & pancreatic cysts


Extrarenal
Mitral valve prolapse, aortic regurgitation
features
Colonic diverticulosis

Ventral & inguinal hernias


Diagnosis Ultrasonography showing multiple renal cysts
Aggressive control of risk factors for CV & CKD

Management ACE inhibitors preferred for hypertension

Hemodialysis, renal transplant for ESRD


CV = cardiovascular; ESRD = end-stage renal disease.
 
This patient with thrombocytopenia and thrombus progression 3 days into heparin therapy likely
has type 2 heparin-induced thrombocytopenia (HIT).  Heparin induces a conformational
change to a platelet surface protein (platelet factor 4 [PF4]), which exposes a neoantigen.  In
patients with type 2 HIT, the immune system responds by forming an IgG autoantibody (HIT
antibody) that then coats the surface of platelets and forms complexes (heparin-PF4-HIT
antibody), resulting in:

Thrombocytopenia - the reticuloendothelial system (largely the spleen) removes antibody-


coated platelets, causing a mild to moderate thrombocytopenia (rarely <20,000/mm3).

Arterial and venous thrombus - HIT antibodies activate platelets, resulting in platelet
aggregation and the release of procoagulant factors.  The risk of thrombus is as high as
50% in untreated HIT.

Typically, type 2 HIT manifests with a >50% drop in platelets 5-10 days after the initiation of
heparin, but it may occur earlier (sometimes <1 day) in patients previously exposed.  This
patient with end-stage renal disease likely receives heparin with hemodialysis.  If HIT is
suspected, all heparin products should be discontinued immediately and anticoagulation should
be initiated with an alternate anticoagulant (eg, argatroban, fondaparinux).

Heparin works by binding antithrombin, which inactivates factor Xa; this prolongs activated
partial thromboplastin time.

Thrombotic thrombocytopenic purpura


↓ ADAMTS13 level → uncleaved vWF multimers → platelet
trapping & activation
Pathophysiology
Acquired (autoantibody) or hereditary
Hemolytic anemia (↑ LDH, ↓ haptoglobin) with schistocytes

Thrombocytopenia (↑ bleeding time, normal PT/PTT)

Sometimes with:
Clinical features
Renal failure

Neurologic manifestations

Fever
Plasma exchange

Glucocorticoids
Management
Rituximab

Caplacizumab
LDH = lactate dehydrogenase; vWF = von Willebrand factor.
Differential diagnosis of polycythemia
Primary (↓ EPO) Secondary (normal/↑ EPO)
Hypoxemia

Cardiopulmonary disease

Obstructive sleep apnea

Polycythemia vera (JAK2 mutation) High altitude

EPO receptor mutations EPO-producing tumors (renal, hepatic)

Congenital (high-affinity hemoglobin)

Following renal transplantation

Androgen supplementation
EPO = erythropoietin.
Common variable immunodeficiency
Abnormal differentiation of B cells into plasma cells →
Pathophysiology
decreased immunoglobulin production
Symptom onset classically age 20-40, as early as puberty

Recurrent respiratory infections (eg, pneumonia, sinusitis,


otitis)

Recurrent GI infections (eg, Salmonella, Campylobacter,


Giardia)
Clinical
manifestations
Chronic disease:

Autoimmune (eg, RA, thyroid disease)

Pulmonary (eg, bronchiectasis, fibrosis)

GI (eg, chronic diarrhea, IBD-like conditions)


↓↓ IgG, ↓ IgA/IgM
Diagnosis
No response to vaccination
Management Immunoglobulin replacement therapy
GI = gastrointestinal; IBD = inflammatory bowel disease; RA = rheumatoid arthritis.

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