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
paraneoplastic expt hyper ca
 SOLITARY PULMONARY NODULE
◊ Calcifictaion
 Bull’s eye: granuloma: AFB
smear
 Popcorn: hamartoma
◊ Prev Xray or PET
◊ Non smoking <35: serial CT
◊ Smoking >35: biopsy
 Pneumomediastinum
◊ Hamman’s: SubQ emphysema
◊ Supplemental oxygen
 Pleural effusion: base, dull percussion, lag,
absent breath sounds
◊ XrayUTS (quantify)
 Pneumothorax: hyperresonant percussion
◊ Spontaneous primary pneumothorax
 Pulmo thickening: decreased breath sounds
 Pleurodesis for malignant effusion
Heart diseases
 Hypertrophic cardiomyopathy:LVOT >60
mmHg
◊ Sustained ventricular tachycardia:
most common cause of death
 Fulminant myocarditis: fever
malaiseshock
◊ Trypanosoma cruzi(Chagas)
 Acute viral myocarditis: left ventricular
segmental hypokinesia
 Clostridial myocarditis: gas bubbles
 Mesothelioma: primary malignant tumor of
the pericardium
 Stage 1: diffuse ST elevation ( Convex:
MI,Concave: Acute Pericarditis)
 Stage 2: ST baseline
 Stage 3: T wave inversions
 Stage 4: ECG returns to normal
 Beck’s triad: cardiac tamponade:
hypotension, distended neck veins and
muffled or absent heart sounds, ECG:
electrical alternans
◊ Prominent X, absent Y
 Chronic constrictive pericarditis
◊ PROMINENT X AND Y DESCENT
 RV infarction absent y descent
 Acute pericarditis: friction rub
 ABI:
◊ Normal >1
◊ Peripheral arterial disease: <1
◊ Severe ischemia: <0.5
 Peripheral arterial disease
◊ INTERMITTENT CLAUDICATION
◊ DEATH: CORONARY ARTERY DISEASE
PAD TO CAD
◊ CILOSTAZOL: PDE-I vasodilator and
antiplatelet, impro QOL
 Thromboangitis obliterans NOT
sclerodactyly
◊ Claudication, raynaud’s
phenomenon, migratorysuperficial
vein thrombophlebitis
 Fibromuscular dysplasia: string of beads
 APS sys
 Daya APR
 Increased risk of arterial embolization
◊ S. aureus
◊ Vegetations >10mm
◊ Infection involve mitral valve
 Major criteria
◊ Positive blood culture
 2 separate cultures
◊ Endocardial involvement : +
echocardiogram,new valve regurg
 Minor (PF, VIM)
◊ Predisposition (<3 conditon or Iv
drug use)
◊ Fever
◊ Vascular (janeway)
◊ Immunologic (osler, roths)
◊ Microbiologic evidence
 Dx: 2 major/ 1 major and 3 minor/ 5 minor
 TTE: not image <2mm
 TEE: safe vegetatios >90%
 IE defervecence 5-7 days
 LDL-C= Total- (TG/5)-HDL
 Cholesterol absorption inhibitor:
Sitosterolemia (anemia, enlarged spleen,
cardiomegaly)
 Abetalipoproteinemia: recurrent diarrhea,
deficiency in vit A, K and E
 Tangier disease: hepatosplenomegaly
+enlarged orange tonsils
 COMPLETE HEART BLOCK/3rd degree AV
block: bradyarrhythmia due to slow of
conduction of AV node
 Bradyarrythmia: AV node dysfuncion and 1st
and 2nd degree AV block
 SINUS EXIT BLOCK: intermittent failure of
conduction from SA node
 Automaticity: result of net inward ionic
current (phase 4)
 Reentry: impulse circuited back to reentrant
portion & disorder of impulse propagation
 Accessory pathway: abnormal connections
that allow conduction between atrium and
ventricles across the AV ring
 TRIGGERED ACTIVITY: oscillations in the
RMP during phase 3
 AV NODE REENTRY: slow and fast pathways
◊ P waves embedded in QRS complex
◊ PR prolongedslowpathwayfast
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
 BLOOD PRESSURE
◊ Office: >= 140/90
◊ Ambulatory
 Daytime >=135/85
 Nighttime >=120/70
 24 hr: 130/80
◊ Home: >=135/85
 Canadian Cardiovascular Fxnal
Classification: severity of ANGINA
 NYHA: <3 dse on fxnal capacity
 STEMI: FIBRIN RICH,
◊ Responsive to streptokinase
◊ Q waves
 NSTEMI
◊ No ST elev
◊ Myocardial necrosis
◊ UA
 PLAQUE RUPTURE: MC mechanism for
acute coronary syndrome
 Anginal equivalents: dyspnea, epi
discomfort etc, esp in women, diabetics and
elderly
 Troponin released in 2-4 hrs/ persist 7-10
days
 CPKMB/ elev 4-6 hrs/ persists 2-3 days
 PINSAN:
◊ Parasympatheticinferior wall
infarction
◊ Sympatheticanterior wall
infarction
 MULTIPLE SCLEROSIS
◊ Relapsing Remitting: discrete attacks
that evolve over days to weeks
◊ PRIMARY PROGRESSIVE: No
attacks/steady fxnal decline
◊ Secondary progressive: steady
deterioration in fxn not associated
with acute attacks
 Begin with RRMS
◊ Progressive/relapsing: steady
deterioration in condition, but with
occasional attack superimposed on
progressive course
 NEUROMYELITIS OPTICA: vasculocentric
inflammation with antibody and
complement deposition
◊ Astrocyte: Aquaporin-4
◊ Complete transverse myelopathy
◊ Tx. Acute exacerbation (IV METHYL
PREDNISOLONE)
◊ If refractory: plasma exchange and
IV immunoglobulin
 Acute disseminated encephalomyelitis
(ADEM)
◊ Polysymptomatic demyelination
with encephalopathy
◊ MULTIFOCAL WHITE MATTER
LESIONS WITH NO MASS EFFECT
◊ Perivenous localization
◊ Exanthema (post infection)
◊ Post vaccination: MEASLES
◊ Area postrema syndrome:
intractable hiccups, nausea,
vomiting
◊ Optic neuritis: extensive, frequent
posterior involvement, bilateral
 Multiple Sclerosis: dissemination in time
and space
◊ autoimmune disease of the CNS
characterized by chronic
inflammation, demyelination, gliosis
(scarring), and neuronal loss
◊ perpendicular oriented white matter
hyperintensities
◊ Tx: High dose IV methylprednisolone
and plasmapheresis
◊ Disease modifying agents: interferon
◊ T cells and macrophages
 UMN/supranuclear: spastic hyperactive
DTRs, babinski
 LMN/intranuclear: fasciculations,flaccid and
hypotonic
 Vasogenic edema: from blood vessels (inc
permeability of BBB), tumor
 Intersititial edema: obstruction of
ventricular flow
 Cytotoxic: inflammation or increased amt of
fluid inside cells
 TB tubercles burst into subpial and
subependymal areasTB meningitis
 Rifampicicn: prophylaxis contact with
meningococcal meningitis
 Neiseria gonor meningitis: PenG or
Ampicillin
 Bacterial meningitis wo rashes: 3rd gen
cephalosporin and vancomycin
 MINIMALLY CONSCIOUS STATE: mutism,
unresponsiveness, unawareness of
environment, inability to sustain social
interaction
 Heptic encephalopathy: accumulation of
intracerebral manganese
 Heavy alcohol consumption: GLUTAMYL
TRANSFERASE
 HIPPOCAMPUS: most susceptible to
ischemia
 WERNICKE ENCEPHALOPATHY: mental
status change, ophthalmoplegia and ataxia
 KORSAKOFF: inability to incorporate new
memories, immediate recall intact,
presence of confabulation
 Contraindications for administration of rtPA
◊ Sustained BP >185/110
◊ Platelets <100,000
◊ HCT <25%
◊ Glucose <50 >400
◊ Heparin 48 h
◊ Prolonged PTT
 ◊ Elevated INR
◊ Rapidly improving symptoms
◊ Prior stroke or head injury win 3
mos prior intracranial hemorrhage
◊ Major surg preceding 14 days
◊ Minor stroke symptoms
◊ GI bleeding prec 21 days
◊ Recent MI
◊ Coma/stupor
 Amyloid angiopathy: recurrent lobar
hemorrhages in elderly
 PUTAMEN: MC site hypertensive
intraparenchymal hemorrhage
 PARKINSONS: MCC of resting tremor
 DYSTONIA: hyperkinetic, involuntary,
repetitive contractions, twisting movement
and abnormal posture
 TIC : repetitive stereotyped movement
longer in duration than mycolic jerk
 MMSE dementia; 22 (LESS THAN 24)
 HYPOGLYCEMIA: MCC treatable coma
 Pseudo coma vs. Coma
◊ Eyelid-release test
◊ Flaccidity of the cheek
◊ Limb dropping test
 VASOVAGAL SYNCOPE: peripheral
vasodilation drop in BPloss of
consciousness
 LAMOTRIGINE: generalized TC normal bg
activity w gen polyspike waves
 CARBAMAZEPINE, PHENYTOIN AND
PHENOBARBITAL AVOID
 Sjs and ten related to
carbamazepinePOSITIVE ALLELE HLA
B015
 * Valproic acid: highest teratogenic
potential
 *Carbamazepine and phenytoin: dizziness
and ataxia
 *Gabapentin and Leviteracetam: NOT
hepatotoxic
 decussations
 SPINOTHALAMIC TRACT: 1-2 spinal nerve
segments above its point of entry in the
SPINAL CORD
◊ Pain and temp
 Fasciculus gracilis and cuneatus and
corticospinal tract: MEDULLA
 Central facial palsy + ipsilateral weakness
=SUPRATENTORIAL
 ABCDD for stroke
◊ Age >=60,BP >140/90,Clinsx,
unilateral weakness(2), speech
disturbance only (1), Duration >=60
min (2),10-59 (1), Diabetes
 MRI: Infarction
RHEUMA
 EBV: associated trigger of SLE
 Hydroxycholoroquine: mainstay in long
term tx of SLE
 Methylprednisilone: safest in pregnancy
 Anti-histone: drug induced lupus
◊ HYDRALAZINE
 Causes of stroke in lupus patient
◊ B2 glycoprotein antibody
◊ Systemic vasculitis
◊ Libman Sacks endocarditis
 SLE monitor for Tx side effects
◊ CBC
◊ FBS
◊ Annual ophthalmologic exam
 Pulmonary hypertension
◊ Systemic sclerosis and SLE
 Osteoarthritis
◊ Pain
◊ Weight bearing
◊ Relieved with rest
◊ Immobilitystiffness
◊ Minimal inflammation
◊ BONE ENLARGENEMT DEFORMITIES
◊ Bouchard and Heberden node?
◊ Hyaline articular cartilage loss
◊ Increase thickness and sclerosis of
subchondral bone
◊ Outgrowth of osteophytes at joint
margin
◊ Meniscal degeneration
 SEPTIC/ BACTERIAL ARTHRITIS
◊ Negative orNORMAL CUTURE: LOW
POSSIBILITY
 Rheumatoid arthritis
◊ PANNUS FORMATION
◊ CIGARETTE SMOKING
◊ ANTI CYCLIC CITRULLINATED
PEPTIDE
◊ Fusiform swelling of fingers
 ◊ Spared wrist elbow and ankle
◊ Chronic deformities: boutonniere,
swan neck and Zline
◊ MC cause of death CV disease
 Gouty arthritis
◊ SYNOVIAL FLUID LEUKOCYTE ARE
ELEVATED 2K-60K
◊ CONTROL INFLAMMATION:
PRIORITY
◊ WARM RED TENDER
◊ Attacks can be triggered by rapid
changes in urate levels
◊ NSAID, colchicine, glucocorticoids
 Ankylosing spondylitis
◊ ENTHESITIS: main patho
◊ Sacroilitis: earliest AS
◊ Syndesmophytes:AS &PA
◊ Dactylitis
 Psoriatic arthritis
◊ Syndesmophytes
◊ Dactylitis
 FIBROMYALGIA
◊ WIDESPREAD PAIN
 Systemic sclerosis: CREST syndrome
 Dermatomyositis
◊ Heliotrpe rash
◊ Gottron’s sign
◊ Colon CA
Rehab Medicine
 Disability: restriction/lack capacity
 Impairment: body function or structure
 Activity: execution of task
 Participation: involvement
 Rehab Goals #1: PAIN, #5 Conserve
energy(easy fatigability)
 PLATFORM WALKER AND FORE-ARM
CRUTCHES: Commonly used mobility asitive
devices
 PULMONARY EMBOLISM: complication in
hours, stasis
 ISOTONIC ALL LIMB AND TRUNK (large
muscles): diabetic
 MODERATE AEROBIC CONDITIONING
EXERCISE: Renal transplant overcome
chronic anemia and abnormal bone
metabolism
 TRANSCUTANEOUS ELECTRICAL
STIMUATION(TES): lessen exposure to toxic
side effects of Analgesics
Renal Medicine
 GLOMERULAR CAPILLARY HYDROSTATIC
PRESSURE
◊ Primary driving force for glomerular
filtration
 GLOMERULAR CPILLARY ONCOTIC
PRESSURE
◊ CONCENTRATION OF UNFILTERED
PLASMA PROTEINS
◊ PARTIALLY OFFSETS HYDROSTATIC
PRESSURE
◊ OPPOSES FILTRATION
 MYOGENIC REFLEX
◊ First line defense against
◊ Trigger:fluctuations in renal blood
flow
◊ Afferent arteriole
◊ HPNconstrict afferent arteriole
 TUBULOGLOMERULAR FEEDBACK
◊ Mediated by macula densa
◊ Trigger: NaCl in urine
 HIV-ASSOCIATED: FSGS
 IGA NEPHROPATHY: cardiac(murmur) and
renal
◊ Dysmorphic RBCs
 Pauci immune: Wegener, Churg Strauss,
Microscopic polyangitis
 TYPE 1 DIABETIC NEPHROPATHY: early
increase in GFR then inexorable decline+
increasing proteinuria
 CYSTATIN C: biomarkers in CKD assess
kidney fxn better
 DISTAL RTA ( hypokalemic acidosis (low K
citrate and high Ca (stone)
ENDO HUHU
 PARATHYROID HORMONE-RELATED
PROTEIN: released by CAincreased bone
resorptionhypercalcemia
 ANTICONVULSANTSincreased catabolism
of vit D
 Calcium reqt
◊ 500 young children
◊ 800 older children
◊ 1,300 adolescents and young adults
◊ 1,000 19-50
◊ 1,200 >50