IM DERMA  LUPUS VULGARIS: APPLE JELLY

 ERYTHRASMA: CORAL RED

 Measles (Rubeola): Koplik spots fever+rash  ATOPIC DERMATITIS: Clinical features:3 or 4
sabay PCF LA(pruritus, chronic relapsing, Family hx
 RUBELLA: prodrome the n rash _ atopy, location and appearance)
forscheimer spots (soft palate and uvula)  SEBORRHEIC DERMATITIS: scalp eyebrows,
 EXANTHEM SUBITUM: Human herpesvirus 6 nasolabial folds, side burn areas, flexural,
◊ Palpebral edema “stress”
◊ Nagayama spots(erythematous  STASIS DERMATITIS:
papules in soft palate) ◊ Lesion in medial ankle (distended
◊ Exanthema: 1 before to 1-2 days vein)
after fever fades lasts for 3-5 days ◊ Bipedal edema
◊ Rose red macules or papules with  IRRITANT CONTACT DERMATITIS
WHITE HALO (neck and trunk) ◊ Non-allergic inflammatory
◊ NO desquamation ◊ Irritating substance(detergents)
 HERPANGINA:  ERYTHRODERMA
◊ Coxsackievirus ◊ Widespread erythematous scaling
◊ Fever sorethroat headache, ab pain patches
vomiting and body aches  PSORIASIS
◊ Yellow white with ◊ Red scaling
erythemaerosons on anterior ◊ Elbows and knees
pillars of tonsillar fauces(uvula, ◊ Mild: Glucocrotocids, Topical
tonsils and soft palate) ◊ Moderate to Severe: Systemics and
 VARICELLA ZOSTER Biologicals, Phototherapy
◊ Facetrunk ◊ Associated ARTHRITIS AND
◊ SPARE EXTREMITIES METABOLIC SYNDROME
◊ Dewdrop on rose petal ◊ Increased risk of <3 dses
◊ Umbulicated pustule and crust  NECROLYTIC MIGRATORY ERYTHEMA (NME)
 HERPES ZOSTER ◊ Pancreatic glucagonoma
◊ Unilateral and along a single sensory ◊ Alpha cell
ganglion  DERMATOMYOSITIS
◊ V1 ◊ Muscle weakness
◊ T3 to L2 ◊ Gottron papules: IP &/ MCP
 HERPES SIMPLEX  JAUNDICE: scleara and hard palate bilirubin
◊ HSV 1: orofacial  SWEET SYNDROME:
◊ HSV 2: genital ◊ Red plaque on face, neck, upper
 MOLLUSCUM CONTAGIOSUM trunk, extremities
◊ Molluscipoxvirus ◊ Leukocytosis
◊ Central umbilication ◊ Acute myelogenous leukemia
◊ Koebnerization  ACANTHOSIS NIGRICANS
 PEDICULOSIS CAPITIS ◊ Thickening of the skin induced by
◊ Scalp with nits insulin-like growth factors
◊ Itching: saliva by louse  XANTHELASMA PALEBRARUM
 TINEA CAPITIS ◊ associated with dyslipidemia
◊ Dermatophytosis  NECROBIOSIS LIPOIDICA
 Piedra: ◊ Yellowish annular plaques with
◊ Fungal, asymptomatic atrophic enter
◊ Trichomycosis ◊ Telangiectasia
 ◊ Pre-tibial  Ampicillin
◊ Represents; degeneration of  Azithro
collagen in the dermis  Ceftriaxone
 PEUTZ JEGHER’S  Cefotaxime
◊ Multiple intestinal polyps  TYPHOID
◊ Brown oval macules on lip and ◊ Blood culture 40-80%, : GOLD
buccal mucosa STANDARD FIRST WEEK OF ILLNESS
IM INFECTIOUS DISEASES ◊ Stool cultures (+) during 3rd week of
 CONTACT PRECAUTIONS: skin! Poop infection,
 AIRBORNE PRECAUTIONS: Measles, ◊ Bone marrow highest sensitivity,
varicella, TB, Bird flu yield NOT reduced up to 5 days Ab
 DROPLET: INFLUENZA! PNEUMONIA, therapy
meningitis, pharyngitis, mumps ◊ Salmonella can be cultured from
 Strongly recommended for Filipino rose spots
healthcare workers: Tdap, Hep B, Influenza, ◊ Hyperplasia, ulceration and necrosis
Varicella, MMR of ileocecal Peyer’s patches at initial
 LEPTOSPIROSIS site of Salmonella infiltration
◊ Post exposure prophylaxis symptoms
 Low-risk ◊ CIPROFLOXACIN: most cost effective
 Single exposure ◊ Fluoroquinolones: most effective
 No wounds class of agents
 Doxycycline 2 caps  TETANUS
100mg in 1-3 days ◊ Clostridium tetani obligate anerobic
 Moderate risk gram + with mult flagellae
 Single ◊ 2nd week of severe tetanus:
 (+) Wounds cuts Autonomic disturbance
 Doxycycline 2 caps for ◊ TETANOSPASMIN: responsible for
3-5 days clinical manifestation
 High risk ◊ Culture not useful
 Continuous exposure ◊ Kille dby iodine, glutaraldehyde,
 Doxycycline 2 caps agua oxinada, autoclaving
once weekly until end ◊ COLE STAGING
of exposure ◊ Stage I
◊ LEPTOMAT: when negative request  >14 d incbation
for repeat LEPTO MAT, increase  mild/localized stiffness
sensitivity 10-12 days  mild brief transient spasm
◊ Renal fxn returns to normal in ◊ Stage II
survivors  10-14 d
◊ Jaundice but no heaptic necrosis  moderate trismus,
◊ *conjunctival suffusion pronounced rigidity with
◊ Treatment opisthotonus
 Mild  more severe and longer
 Doxycycline 100mg spasms
 Amox ◊ Stage III
 Azithromycin  <10 days
dehydrate  RISUS SARDONICUS
 Moderate-severe  Aspiration
 Pen G 1.5 MU  Veretbrla fracture
  Violent spasms ◊ Paralytic/dumb flaccid paralysis
 SYMPATHETHIC NERVOUS ◊ 5 injections
SYSTEM OVERACTIVITY  FILARIASIS
◊ Tx ◊ OBSTRUCTION: GRANULOMATOUS
◊ Prevent exotoxin and PROLIFERATIVE PROCESSES to
 Aq Pen G 5M ADULT WORM (Schistosoma to egg)
 Metronidazole 500 mg ◊ Big balls (big belly schistosomiasis)
◊ Tetanus immune globulin or equine  SCHISTOSOMIASIS
antitoxin: neutralized unbound ◊ Onchomelania (snails)
toxins ◊ DOC Praziquantel
 Syndromic approach: best and practical ◊ Symptoms from granulomatous host
 Etiologic approach: ideal immune response to EGGS
 GONOCOCCAL deposited In tissues
◊ N. gonorrhea ◊ Kato thick smears miss light infxns
◊ Mucopurulent Urethral discharge  MALARIA
◊ Cefixime ◊ P falciparum: trophozoites and
◊ Doxycycline schizonts in vital organs
◊ INTRACELLULAR gram negative ◊ See page 15 2017 ratio
diplococci ◊ CQ+SP: not severe
◊ + leukocyte esterase ◊ Co-Artem: 2nd line
 CHLAMYDIA ◊ Quinine: cerebral malaria
◊ Mucopurulent Urethral discharge ◊ Primaquine+Chloroquine: confirmed
◊ Azithromycin and Doxycycline vivax
 HERPES  Aspergillosis
◊ Painful genital ulcer ◊ Aspergilloma: surgical rsection
 SYPHILIS ◊ Invasive aspergillosis: Voriconazole+
◊ Painless genital ulcer Ampho B
◊ VDRL: DIAGNOSTIC TEST OF CHOICE  Cryptococcosis
FOR NEUROSYPHILIS ◊ Ampothericin B + Flucytosine
 VDRL and RPR Correlate with ◊ India ink
disease activity  See page 18 2017 ratio
◊ Primary: Chancre GI SYSTEM 1
◊ Secondary skin  PREFORMED TOXIN (B cerecus. S aureus C
◊ Late cardiac ophthalmic gumma perfringens) & ENTEROTOXIN( V cholatr,
 Vaginal discharge ETC, Klebsiella, Aeromonas) VOMITING,
◊ Trichomonas WATERY DIARRHEA
◊ Bacterial vaginosis  ENTEROADHERENT( EPEC, EAEC, Giardia,
◊ Candidiasis Cryptospordiosis, Helminths): AB PAIN +
 TB MUSHY DIARRHEA
◊ Pan susceptible: sensitive to all  Cytotoxin (Clostridium difficile, EHEC):
◊ MDR: >2 drugs (with INH and RFP) ABDOMINAL PAIN, WATERY THEN
◊ XDR: >4 drugs (INH RFP KM FQ) BLOODY(QUICKLY: EHEC, OCCULT: DIFFI)
◊ TB meningitis, military, bone/joint: 2  Invasive (Rota, Norwalk, salmonella,
HRZE/ 10 HR (12 mos) campylobacter, yersionia parahemolyticus):
 RABIES FEVER, WATERY DIARRHEA
◊ Can be confirmed by IFAT  SEVERE: Shigella, EIEC, Entamoeba
◊ Encephalitic/furiosu type: histolytica, AB PAIN FEVER AND BLOOFY
aerophobia nd hydrophobia DIARRHEA
 SECRETORY: derangemet in fluid and  NON MECHANICAL /ADYNAMIC ILEUS: (-)
electrolyte transport, kahit di kumain may colicky pain, discomfort from distention,
diarrhea, frequent vomiting
◊ Painless, watery large volume PULMONARY
PERSISTS WITH FASTING  TB
◊ Stimulant laxatives, bowel resection,  PRESUMPTIVE TB: signs/symptoms
mucosal disease or enterocolic  BACTERIOLOGICALLY CONFIRMED
fistula, metastatic GIT carcinoid  CLINICALLY DIAGNOSED: diagnosed with
tumors, gastrinom, panc cholera, active TB: abnormal chest Xray findings
 OSMOTIC: ingested poorly absorbable  LATENT TB/TB INFECTION: POSITIVE TST (no
osmotically active solutes fluid lumenward s sx)
to exceed resorption of colon  TB EXPOSURE: close contact
◊ STOPS with FASTING  TB DISEASE: presumptive+clinical and
◊ Health supplements, osmotic diagnostic CONFIRMATION
laxatives, CHO malabsorption
 STEATORRHEAL: greasy foul smelling diff to
DRTB
flush,weight loss and nutritional deficiencies
CURED: (-) smear at last *18 mos tx, no
◊ FAT MALABSORPTION
month of tx & 1 in failure
◊ Pancreatic
continuation phase, *>3 cultures, 30
◊ Celiac sprue, post mucosal lymphatic
days (-) after
obstruction
intensive phase
 INFLAMMATORY:
TREATMENT No record
◊ pain fever and bleeding
COMPLETED: complete culture taken
◊ ANASARCA,
no record
◊ (+) LEUKOCYTES or leukocyte
TREATMENT FAILURE: (+) *need for
derived protein
smear 5 months or later permanent
◊ Eosinophilic Gastroenteritis: Charcot
in tx, not show clinical regimen change
Leyden crystals
improvement of at least 2
◊ Hypogammaglobulinemia antiTB drugs:
 DYSMOTILITY ADRs, lack
◊ Rapid transit either secondary or conversion,
contributory bacteria revr
◊ IRRITABLE BOWEL SYNDROME LOST TO FOLLOW UP:
◊ HYPERTHYROIDISM AND DIABETES interrupted for 2
 FACTITIAL consecutive months or
◊ Munchausen more
◊ Bulimia  Isoniazid preventive therapy
◊ Decreased stool osmolality(H2O ◊ With HIV
added) ◊ <5 years old
◊ Increase urea(urine contaminated)  COAL WORKERS PNEUMOCONIOSIS: chest
◊ Increased mg (laxative) Xray looks worse than the patient
 ADHESIONS: prior surgery  Silicosis and Caplan syndrome: progressive
 Vomiting more profuse: higher obstruction assive fibrosis
 COLICKY PAIN, MECHANICAL BOWEL  SILICOSIS
OBSTRUCTION ◊ Upper lobes
 OBSTIPATION: complete lower gut  VARY among individuals: immunological rxn
obstruction  EVERYONE: toxic exposure
 WORSENING DURING WEEKDAYS: ◊ Chest xray finding of bilateral
occupational asthma, sick building infiltrates consistent with pulmo
syndrome, stress-related asthma edema
 ASBESTOSIS ◊ PaO2/FiO2 ratio <= 300mmHg
◊ LOWER LOBES ◊ Respi failure cannot be fully
◊ PLEURAL PLAQUES and effusion explained by <3 failure
◊ LATE(dose dependent) ◊ + Neuromuscular blockade
 RECURRENT HYPERSENISITIVITY  TIDAL VOLUME <=6ML/KG: low mortality
PNEUMONITIS  TYPE 1
◊ Even with psych ◊ HYPOXEMIC RF
 POSITIVE METACHOLINE TEST ◊ PaO2 <60
◊ Asthma ◊ PNEUMONIA,sepsis, near drowning,
◊ Reactive airways dysfunction muly blood transfusions and panx
syndrome  TYPE 2
 PFT ◊ Hypercapneic
◊ FEV1 and FVC LOW; FEV1/FVC: ◊ Severe respi acidosis normal
normal: RESTRICTIVE PATTERN oxygenation to mild hypoxemia
◊ Normal FVC,FEV1/FVC:  TYPE 3
lowobstruction ◊ Peri operative RF
 CURB 65 ◊ POST OP
◊ Confusion ◊ Post anesthetic depression
◊ Urea >7mmol/L  TYPE 4
◊ RR >= 30 bpm ◊ Hypoperfusion
◊ BP <=90/60 mmHg ◊ Shock
◊ Age >=65 years  BRONCHIAL ASTHMA
 Tx ◊ (Actual post BD-Actual pre BD )/
◊ 0-1 home Actual pre
◊ 2:hospital supervised, admit ward IV  Intermittent: daytime monthly,nocturnal
antibiotic awakening less than monthly, agonist use
◊ 3+: manage in hospital ssevere less weekly, PEF or FEV1 >80%
pneumonia, assess ICU admission ◊ Tx: occasional prn B2 only
(CURB 4 or 5)  Mild to Moderate Persistent: PEF FEV1: 60-
 BRONCHIECTASIS 80% predicted
◊ Focal:obstruction ◊ Tx: regular ICS +LABA
◊ Diffuse: widespread  Severe Persistent: PEF FEV1: <60%
◊ Persistent productive cough with ◊ Tx: ICS+ LABA+OCS
prod of thick tenacious sputum  Symbicort: Formoterol+Budesonide
◊ HRCT ◊ Single inhaler maintenance and
◊ CYLINDRICAL MOST COMMON relief therapy strategy
 LUNG ABSCESS  STEP 3: RELIEVER MEDICATION + 1 OR 2
◊ Primary: aspirate and anaerobic CONTROLLERS
bacteria (H. INFLUENZAE AND  VARIABLE EXPIRATORY FLOW:
PSEUDOMONAS AEROGINOSA) bronchoconstriction, airway thickening and
◊ Secondary: underlying increased mucus
 ARDS  Typical presentation: cough + wheeze and
◊ Acute onset chest tightness
 Controlled: no s/sx
 Partly: <3
 Uncontrolled: 3 or more ◊ Ocula rinvolvement
 Post bronchodilator improve = 12% ◊ NEUTROPHIL infiltration
 Risk factors for developing future asthma ◊ ENDOTHELIAL SWELLING
◊ FEV1 low ◊ Involve all kinds of vessels small me
◊ Near fatal asthma dand large
 Pulmonary vascular diseases  Takayasu arteritis
 D-dimer ◊ Pulseless disease
◊ DVT or Pulmonary embolism ◊ Panarteritis with inf mononuclear
◊ Virchows triad(SHE) and occasional giant cells
 Stasis (confinement) ◊ Medium and large
 Hypercoagulable  Pulmonary arterial hypertension
 Endothelial ◊ Responsive to NO
dysfxn(smoking/surgery) ◊ Tx: Ca channel blocker: Nifedipine
◊ Not use: INCREASED in AML, sepsis, ◊ Increased PAP
Pneumonia, CA, post-op and ◊ Normal PCWP
pregnancy  Pulmonary venous HPN
◊ (CA P P P) ◊ No effective therapy
◊ Increased PAP and PWP
 Venous UTS  LUNG NEOPLASMS
◊ GOLD STANDARD FOR  SCLC : central
DIAGNOSISNG DVT ◊ LIMITED: chemoradio
◊ NO PULMO SX  One hemithorax
◊ RFs:immbolization,  Regional lymph nodes
pregnant,polycythemia ◊ EXTENSIVE: chemo
 Ct angiogram of lung  Exceed boundaries
◊ Principal imaging test for diagnosing 
PE ◊ No surgery
◊ Pulmo sx.  NSCLC: peripheral
◊ Note Ci to D dimer ◊ TNM
 Ventilation/perfusion lung scan  CHEMOTHERPAY ALONE
◊ If allergic to dye and CI to d-dimer  RADIOTHERPAY ALONE
◊ Pulmonary embolism ◊ NSCLC Stage IV
◊ Alternative is MRI  SURGICLA RESECTION ALONE
 Wegener Syndrome  CHEMO +RADIO
◊ Glomerulonephritis ◊ Small cell CA
◊ Granulomatosis vasculitis ◊ LIMITED: one hemithorax, ipsi
mediastinal
 Microscopic Polyangitis ◊ NSCLC:
◊ Glomerulonephritis  N2 nodes: subcaribal
◊ Necrotizing vasculitis mediastinal STAGE 3A
◊ capillaries and venules  N3 nodes: CONTRALATERAL
 Churg-Staruss Syndrome STAGE 3B
◊ ASTHMA  SURGERY+CHEMO+RADIO
◊ EOSINOPHILIA ◊ NSCLC Stage 2b
◊ Extravascular granuloma  T2b(5-7cm) N1 M0
 Behcet’s syndrome  Squamous: hypercalcemia as
◊ Recurrent oral and genital paraneoplastic, EGFR mutation
ulcerations +  AdenoCA EGFR mutation
 Small cell: MYC mutation, other ◊ Normal >1
paraneoplastic expt hyper ca ◊ Peripheral arterial disease: <1
 SOLITARY PULMONARY NODULE ◊ Severe ischemia: <0.5
◊ Calcifictaion  Peripheral arterial disease
 Bull’s eye: granuloma: AFB ◊ INTERMITTENT CLAUDICATION
smear ◊ DEATH: CORONARY ARTERY DISEASE
 Popcorn: hamartoma PAD TO CAD
◊ Prev Xray or PET ◊ CILOSTAZOL: PDE-I vasodilator and
◊ Non smoking <35: serial CT antiplatelet, impro QOL
◊ Smoking >35: biopsy  Thromboangitis obliterans NOT
 Pneumomediastinum sclerodactyly
◊ Hamman’s: SubQ emphysema ◊ Claudication, raynaud’s
◊ Supplemental oxygen phenomenon, migratorysuperficial
 Pleural effusion: base, dull percussion, lag, vein thrombophlebitis
absent breath sounds  Fibromuscular dysplasia: string of beads
◊ XrayUTS (quantify)  APS sys
 Pneumothorax: hyperresonant percussion  Daya APR
◊ Spontaneous primary pneumothorax  Increased risk of arterial embolization
 Pulmo thickening: decreased breath sounds ◊ S. aureus
 Pleurodesis for malignant effusion ◊ Vegetations >10mm
Heart diseases ◊ Infection involve mitral valve
 Hypertrophic cardiomyopathy:LVOT >60  Major criteria
mmHg ◊ Positive blood culture
◊ Sustained ventricular tachycardia:  2 separate cultures
most common cause of death ◊ Endocardial involvement : +
 Fulminant myocarditis: fever echocardiogram,new valve regurg
malaiseshock  Minor (PF, VIM)
◊ Trypanosoma cruzi(Chagas) ◊ Predisposition (<3 conditon or Iv
 Acute viral myocarditis: left ventricular drug use)
segmental hypokinesia ◊ Fever
 Clostridial myocarditis: gas bubbles ◊ Vascular (janeway)
 Mesothelioma: primary malignant tumor of ◊ Immunologic (osler, roths)
the pericardium ◊ Microbiologic evidence
 Stage 1: diffuse ST elevation ( Convex:  Dx: 2 major/ 1 major and 3 minor/ 5 minor
MI,Concave: Acute Pericarditis)  TTE: not image <2mm
 Stage 2: ST baseline  TEE: safe vegetatios >90%
 Stage 3: T wave inversions  IE defervecence 5-7 days
 Stage 4: ECG returns to normal  LDL-C= Total- (TG/5)-HDL
 Beck’s triad: cardiac tamponade:  Cholesterol absorption inhibitor:
hypotension, distended neck veins and Sitosterolemia (anemia, enlarged spleen,
muffled or absent heart sounds, ECG: cardiomegaly)
electrical alternans
◊ Prominent X, absent Y
 Chronic constrictive pericarditis
◊ PROMINENT X AND Y DESCENT
 RV infarction absent y descent
 Acute pericarditis: friction rub
 ABI:
 Abetalipoproteinemia: recurrent diarrhea, ◊ PR prolongedslowpathwayfast
deficiency in vit A, K and E rhythm
 Ventricular Premature Beat: wide QRS
complex+bundle branch w/ negative T wave
 Ventricular Tachycardia: >= 3 consecutive
beats at rate faster than 100 beats/min
 Wolff-Parkinson-White Syndrome:
supraventricular rhythm + wide QRS
complex due to pre-excitation
 P wave atrial depo
 QRS ventricular depo
 ST ventricular repo
 ATRIAL FIBRILLATION: irregularly irregular
◊ Supraventricular
◊ Irregular RR
◊ No discernible P waves
 Sinus tachycardia: regular
 Junctional tachycardia: narrow QRS with VA
block
 Ventricular Tachycardia: regular rhythm
faster than 100 beats/min from bundle of
His
 MULTIFOCAL ATRIAL TACHYCARDIA
◊ Irregular <3 rhythm
◊ 3 distinct P wave morphologies
◊ 100-150 beats/min
 Tangier disease: hepatosplenomegaly  BLOOD PRESSURE
+enlarged orange tonsils ◊ Office: >= 140/90
 COMPLETE HEART BLOCK/3rd degree AV ◊ Ambulatory
block: bradyarrhythmia due to slow of  Daytime >=135/85
conduction of AV node  Nighttime >=120/70
 Bradyarrythmia: AV node dysfuncion and 1st  24 hr: 130/80
and 2nd degree AV block ◊ Home: >=135/85
 SINUS EXIT BLOCK: intermittent failure of  Canadian Cardiovascular Fxnal
conduction from SA node Classification: severity of ANGINA
 Automaticity: result of net inward ionic  NYHA: <3 dse on fxnal capacity
current (phase 4)  STEMI: FIBRIN RICH,
 Reentry: impulse circuited back to reentrant ◊ Responsive to streptokinase
portion & disorder of impulse propagation ◊ Q waves
 NSTEMI
 Accessory pathway: abnormal connections ◊ No ST elev
that allow conduction between atrium and ◊ Myocardial necrosis
ventricles across the AV ring ◊ UA
 TRIGGERED ACTIVITY: oscillations in the  PLAQUE RUPTURE: MC mechanism for
RMP during phase 3 acute coronary syndrome
 AV NODE REENTRY: slow and fast pathways  Anginal equivalents: dyspnea, epi
◊ P waves embedded in QRS complex discomfort etc, esp in women, diabetics and
elderly
 Troponin released in 2-4 hrs/ persist 7-10 inflammation, demyelination, gliosis
days (scarring), and neuronal loss
 CPKMB/ elev 4-6 hrs/ persists 2-3 days ◊ perpendicular oriented white matter
 PINSAN: hyperintensities
◊ Parasympatheticinferior wall ◊ Tx: High dose IV methylprednisolone
infarction and plasmapheresis
◊ Sympatheticanterior wall ◊ Disease modifying agents: interferon
infarction ◊ T cells and macrophages
 MULTIPLE SCLEROSIS  UMN/supranuclear: spastic hyperactive
◊ Relapsing Remitting: discrete attacks DTRs, babinski
that evolve over days to weeks  LMN/intranuclear: fasciculations,flaccid and
◊ PRIMARY PROGRESSIVE: No hypotonic
attacks/steady fxnal decline  Vasogenic edema: from blood vessels (inc
◊ Secondary progressive: steady permeability of BBB), tumor
deterioration in fxn not associated  Intersititial edema: obstruction of
with acute attacks ventricular flow
 Begin with RRMS  Cytotoxic: inflammation or increased amt of
◊ Progressive/relapsing: steady fluid inside cells
deterioration in condition, but with  TB tubercles burst into subpial and
occasional attack superimposed on subependymal areasTB meningitis
progressive course  Rifampicicn: prophylaxis contact with
 NEUROMYELITIS OPTICA: vasculocentric meningococcal meningitis
inflammation with antibody and  Neiseria gonor meningitis: PenG or
complement deposition Ampicillin
◊ Astrocyte: Aquaporin-4  Bacterial meningitis wo rashes: 3rd gen
◊ Complete transverse myelopathy cephalosporin and vancomycin
◊ Tx. Acute exacerbation (IV METHYL  MINIMALLY CONSCIOUS STATE: mutism,
PREDNISOLONE) unresponsiveness, unawareness of
◊ If refractory: plasma exchange and environment, inability to sustain social
IV immunoglobulin interaction
 Acute disseminated encephalomyelitis  Heptic encephalopathy: accumulation of
(ADEM) intracerebral manganese
◊ Polysymptomatic demyelination  Heavy alcohol consumption: GLUTAMYL
with encephalopathy TRANSFERASE
◊ MULTIFOCAL WHITE MATTER  HIPPOCAMPUS: most susceptible to
LESIONS WITH NO MASS EFFECT ischemia
◊ Perivenous localization  WERNICKE ENCEPHALOPATHY: mental
◊ Exanthema (post infection) status change, ophthalmoplegia and ataxia
◊ Post vaccination: MEASLES  KORSAKOFF: inability to incorporate new
◊ Area postrema syndrome: memories, immediate recall intact,
intractable hiccups, nausea, presence of confabulation
vomiting  Contraindications for administration of rtPA
◊ Optic neuritis: extensive, frequent ◊ Sustained BP >185/110
posterior involvement, bilateral ◊ Platelets <100,000
 Multiple Sclerosis: dissemination in time ◊ HCT <25%
and space ◊ Glucose <50 >400
◊ autoimmune disease of the CNS ◊ Heparin 48 h
characterized by chronic ◊ Prolonged PTT
 ◊ Elevated INR  Central facial palsy + ipsilateral weakness
◊ Rapidly improving symptoms =SUPRATENTORIAL
◊ Prior stroke or head injury win 3  ABCDD for stroke
mos prior intracranial hemorrhage ◊ Age >=60,BP >140/90,Clinsx,
◊ Major surg preceding 14 days unilateral weakness(2), speech
◊ Minor stroke symptoms disturbance only (1), Duration >=60
◊ GI bleeding prec 21 days min (2),10-59 (1), Diabetes
◊ Recent MI  MRI: Infarction
◊ Coma/stupor RHEUMA
 Amyloid angiopathy: recurrent lobar  EBV: associated trigger of SLE
hemorrhages in elderly  Hydroxycholoroquine: mainstay in long
 PUTAMEN: MC site hypertensive term tx of SLE
intraparenchymal hemorrhage  Methylprednisilone: safest in pregnancy
 PARKINSONS: MCC of resting tremor  Anti-histone: drug induced lupus
 DYSTONIA: hyperkinetic, involuntary, ◊ HYDRALAZINE
repetitive contractions, twisting movement  Causes of stroke in lupus patient
and abnormal posture ◊ B2 glycoprotein antibody
 TIC : repetitive stereotyped movement ◊ Systemic vasculitis
longer in duration than mycolic jerk ◊ Libman Sacks endocarditis
 MMSE dementia; 22 (LESS THAN 24)  SLE monitor for Tx side effects
 HYPOGLYCEMIA: MCC treatable coma ◊ CBC
 Pseudo coma vs. Coma ◊ FBS
◊ Eyelid-release test ◊ Annual ophthalmologic exam
◊ Flaccidity of the cheek  Pulmonary hypertension
◊ Limb dropping test ◊ Systemic sclerosis and SLE
 VASOVAGAL SYNCOPE: peripheral  Osteoarthritis
vasodilation drop in BPloss of ◊ Pain
consciousness ◊ Weight bearing
 LAMOTRIGINE: generalized TC normal bg ◊ Relieved with rest
activity w gen polyspike waves ◊ Immobilitystiffness
 CARBAMAZEPINE, PHENYTOIN AND ◊ Minimal inflammation
PHENOBARBITAL AVOID ◊ BONE ENLARGENEMT DEFORMITIES
 Sjs and ten related to ◊ Bouchard and Heberden node?
carbamazepinePOSITIVE ALLELE HLA ◊ Hyaline articular cartilage loss
B015 ◊ Increase thickness and sclerosis of
 * Valproic acid: highest teratogenic subchondral bone
potential ◊ Outgrowth of osteophytes at joint
 *Carbamazepine and phenytoin: dizziness margin
and ataxia ◊ Meniscal degeneration
 *Gabapentin and Leviteracetam: NOT  SEPTIC/ BACTERIAL ARTHRITIS
hepatotoxic ◊ Negative orNORMAL CUTURE: LOW
 decussations POSSIBILITY
 SPINOTHALAMIC TRACT: 1-2 spinal nerve  Rheumatoid arthritis
segments above its point of entry in the ◊ PANNUS FORMATION
SPINAL CORD ◊ CIGARETTE SMOKING
◊ Pain and temp ◊ ANTI CYCLIC CITRULLINATED
 Fasciculus gracilis and cuneatus and PEPTIDE
corticospinal tract: MEDULLA ◊ Fusiform swelling of fingers
 ◊ Spared wrist elbow and ankle  TRANSCUTANEOUS ELECTRICAL
◊ Chronic deformities: boutonniere, STIMUATION(TES): lessen exposure to toxic
swan neck and Zline side effects of Analgesics
◊ MC cause of death CV disease Renal Medicine
 Gouty arthritis  GLOMERULAR CAPILLARY HYDROSTATIC
◊ SYNOVIAL FLUID LEUKOCYTE ARE PRESSURE
ELEVATED 2K-60K ◊ Primary driving force for glomerular
◊ CONTROL INFLAMMATION: filtration
PRIORITY  GLOMERULAR CPILLARY ONCOTIC
◊ WARM RED TENDER PRESSURE
◊ Attacks can be triggered by rapid ◊ CONCENTRATION OF UNFILTERED
changes in urate levels PLASMA PROTEINS
◊ NSAID, colchicine, glucocorticoids ◊ PARTIALLY OFFSETS HYDROSTATIC
 Ankylosing spondylitis PRESSURE
◊ ENTHESITIS: main patho ◊ OPPOSES FILTRATION
◊ Sacroilitis: earliest AS  MYOGENIC REFLEX
◊ Syndesmophytes:AS &PA ◊ First line defense against
◊ Dactylitis ◊ Trigger:fluctuations in renal blood
 Psoriatic arthritis flow
◊ Syndesmophytes ◊ Afferent arteriole
◊ Dactylitis ◊ HPNconstrict afferent arteriole
 FIBROMYALGIA  TUBULOGLOMERULAR FEEDBACK
◊ WIDESPREAD PAIN ◊ Mediated by macula densa
 Systemic sclerosis: CREST syndrome ◊ Trigger: NaCl in urine
 Dermatomyositis  HIV-ASSOCIATED: FSGS
◊ Heliotrpe rash  IGA NEPHROPATHY: cardiac(murmur) and
◊ Gottron’s sign renal
◊ Colon CA ◊ Dysmorphic RBCs
Rehab Medicine  Pauci immune: Wegener, Churg Strauss,
 Disability: restriction/lack capacity Microscopic polyangitis
 Impairment: body function or structure  TYPE 1 DIABETIC NEPHROPATHY: early
 Activity: execution of task increase in GFR then inexorable decline+
 Participation: involvement increasing proteinuria
 Rehab Goals #1: PAIN, #5 Conserve  CYSTATIN C: biomarkers in CKD assess
energy(easy fatigability) kidney fxn better
 PLATFORM WALKER AND FORE-ARM  DISTAL RTA ( hypokalemic acidosis (low K
CRUTCHES: Commonly used mobility asitive citrate and high Ca (stone)
devices ENDO HUHU
 PULMONARY EMBOLISM: complication in  PARATHYROID HORMONE-RELATED
hours, stasis PROTEIN: released by CAincreased bone
 ISOTONIC ALL LIMB AND TRUNK (large resorptionhypercalcemia
muscles): diabetic  ANTICONVULSANTSincreased catabolism
 MODERATE AEROBIC CONDITIONING of vit D
EXERCISE: Renal transplant overcome  Calcium reqt
chronic anemia and abnormal bone ◊ 500 young children
metabolism ◊ 800 older children
◊ 1,300 adolescents and young adults
◊ 1,000 19-50
◊ 1,200 >50