Comsae Form 107 Part 1 | Exams Medicine

Post-viral → classic trigger for immune dysregulation

Isolated thrombocytopenia (platelets = 30k)

Symptoms: Petecehiae, mucosal bleeding, epistaxis

↑ bleeding time (15 min) → platelet problem

Normal INR and PT/PTT → coagulation cascade problem

Pathophys:

- IgG Autoabs against GpIIb/IIIa

- platelet destruction in spleen ↓ platelets

BM findings: Megakaryocytes ↑ in bone marrow (compensation)

First line treatment: steroids, IVIG; severe refractory - splenectomy

ITP vs TTP

TTP: MAHA + neuro + renal + fever (severe def in ADAMTS13 enzyme)

ITP: Isolated

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Post-viral → classic trigger for immune dysregulation Isolated thrombocytopenia ( platelets = 30k) Symptoms: Petecehiae, mucosal bleeding, epistaxis ↑ bleeding time (15 min) → platelet problem Normal INR and PT/PTT → coagulation cascade problem Pathophys :

IgG Autoabs against GpIIb/IIIa
platelet destruction in spleen ↓ platelets BM findings: Megakaryocytes ↑ in bone marrow (compensation) First line treatment: steroids, IVIG; severe refractory - splenectomy ITP vs TTP TTP: MAHA + neuro + renal + fever (severe def in ADAMTS13 enzyme) ITP: Isolated Other answers DIC: ↑ PT, ↑ PTT ↓ fibrinogen, ↑ D-dimer thrombocytopenia (yes, but NOT isolated) Hemophilia A: factor VIII def → intrinsic pathway issue ↑ PTT, normal platelets and bleeding time; deep tissue bleeding (hemathrosis), not petechiae Vitamin K deficiency: affects factor II, VII, IX, X Findings: ↑ PT (first), then ↑ PTT, normal platelets Von Willebrand Disease: defective platelet adhesion + ↓ factor VIII stability Findings: ↑ bleeding time, sometmes ↑ PTT, normal platelets Salicylate toxicity
- Tinnitus → classic aspirin toxicity
- RR: 36/min → early resp alkalosis (medullary stimulation) - Later → anion gap metabolic acidosis Pathophys: uncouples oxidative phosphorylation → ↑ heat (fever)
- Directly stimulates respiratory center → hyperventilation Tx: activated charcoal, urinary alkalization (NaHCO3 - sodium bicarb)
- If severe dialysis Why others are wrong Cocaine - it’s a sympathomimetic → agitation, CP, HTN
- No tinnitus, doens’t classically cause mixed acid-base picture
- Tx: Benzodiazepines (FIRST LINE) → ↓ CNS stimulation, ↓ BP
- Nitroglycerin or phentolamine → for severe HTN/vasospasm
- Avoid: β-blockers → unopposed α → worsening HTN Amitriptyline (TCA) - anticholinergic + Na+ channel blockade
- Would have QRS widening, arrhythmias, seizures
- Not tinnitus or hyperventilation
- Antidote: NaHCo3 - treats arrhythmias, Benzos for seizures Heroin - resp depression (↓ RR), pinpoint pupils
- Naloxone (short-acting opioid antagonist) Phencyclidine (PCP) - psychosis, violent behavior, nystagmus
- No tinnitus or classic acid-base disturbance
- Tx: Benzodiazepines (FIRST LINE) → agitation, seizures
- Supportive care (cooling if hyperthermic) Answer: Diffuse lewy body disease Sxms: visual hallucinations, fluctuating cognition, parkinsonian features, memory relatively preserved early Patho phys: a-synuclein (Lewy bodies) in cortex
- Severe sentivity to antipsychotics Alzheimer disease: early memory loss, no hallucinations early, no parkinsonism early; B-amyloid + tau (cortex + hippocampus) Creutzfeldt-Jakob Disease: rapidly progressive dementia, myoclonus, fatal in months (not 3 yrs): prions; diffuse (14-3-3 proteins) Parkinson’s Disease: motor symptoms first, demetnia later
- a-synuclein (lewy bodies), substantia nigra Frontotemporal - personality/beahvior; pick bodies (tau); frontal/temporal
- gradual/ earlier on set

Down sydnrome: ↓ AFP, estriol + ↑ β-hCG + ↑ inhibin A

↑ nuchal translucency (1st trimester); ↓ PAPP-A Edwards syndrome: everything ↓, inhibin A normal Neural tube defects AFP ↑↑ bc AFP leaks out of neural tissue
Folate deficiency Maternal serum a-feto protein (AFP) - 15-20 weeks
Screens for neural tube defects ↑ AFP
If ↓ AFP → Down syndrome Other answers: Aminocinthesis is done ≥15 weeks , BUT: Diagnostic (not routine screening)
Used after abnormal screen Chorionic villus sampling (CVS): 10-13 weeks Quantitiative B-hCG - earlier in pregeancy - part of 1st trimester screening Transvaginal ultrasound: earl pregnancy (dating and viability)
Not primary screening at 15 weeks ↑ AFP → neural tube defect (spina bifida) ↓ AFP + ↑ β-hCG → Down syndrome “Next best step after abnormal screen” → amniocentesis Pre-ecamplsia
she had new onset htn (after 20 wks gestation), proteinuria, edema Pathophys: abnormal placentation → endothelial dysfunction → vasocosntriction → HTN + protein leak Treatment: MgSo4 (seizure prophylaxis) Severe features? ↑ LFTs, ↓ platelets (HELLP) Definitive treatment → delivery Heart failure: you’d see dyspnea, crackles, JVD, no protein Renal insufficiency: you’d have ↑ creatinine, BUN; no clear pregnancy-specific trigger Eclampsia - requires seizures (plus pre-eclampsia findings) Gestatinal DM: mild glucose elevation - glucose 110 is not diagnostic; does not cause HTN + proteinuria VFs: coagulase - converts fibrinogen → fibrin
Helps bacteria wall itself off → abscess formaiton
Staph aureus = coag +, staph epi = coagulase - Protein A: binds Fc portion of IgG
Prevents opsonizaiton → immune evasion Exfoliative toxin: cleaves desmoglein → scalded skin syndrome - seen in kids Enterotxin (preformed) - food poisoning; rapid onset (1-6hrs)
vomiting >diarrhea Abx resistance - MRSA -mech altered PBP (PBP2a) - gene mecA
Tx: vancomycin - others linezolid, daptomyicn If prosthetic device valve - think staph epi not aureus Staphylococcus aureus Clues - Painful + pus / → abscess || athletes/close contact → staph aureus Classic for: folliculitis, furuncles (boils)
Gram+ cocci in clusters, coagulase positive MRSA: TMP-SMX, doxycycline, clindamycin Toxin question? Toxic shock syndrome Bacilus anthracis - painless black eschar, anmal exposure E. Coli - GI/UTI pathogen; not skin abscess H. influenza - rep infxn Neisseria meningigitiids - meningitis, petechial skin rash - not localized abscess Strep pneumoniae - pneumonia, meningitis Clues: facial/pubic hair, tall, normal testicular size → peripheral androgen source CAH b/c precocious puberty signs (hair growth, tall stature) Testes normal → not central puberty || Source = adrenal androgens Most likely 21-hydroxylase def (↑ androgens → virilization) Exogenous estrogens - causes feminization not hair growth 5-a-reductase: ↓ DHT → undervirilization, would see ambiguous genitalia, not early hair growth Androgen receptor def: XY but appears female, no pubic hair Excess inhibin: affects FSH only, no androgen excess

Fibromyalgia = dx of exclusion No specific lab test → must rule out

Hypothyroidism (weight gian, hair thinning)
RA, SLE, etc Tenderness to touch - classic finding ESR: would help find inflammatory disease | fibromyalgia = non inflammatory MRI brain: no neurologic deficits - unnecessary X-rays - no joint damage in fibro SPEP - used for multiple myeloma - bone pain, anemia Early puberty, ↑ androgens, ↓ 21-hydroxylase → ↓ cortisol 21-hydroxylase needed to make cortisol and androgens If you block → shunt to androgens ↑ estrogen/testosterone
Testosterone ↑ (not ↓) Progesterone -Actually ↑ (precursor buildup) Cholesterol not directly affected ↓ cortisol, aldosterone, ↓ cortisol Variants: Salt-wasting → hypotension, hyperkalemia Nonclassic → mild androgen excess foul-smelling sputum, seizure, cavitary lesion → anaerobes → lung abscess Seizure → aspiration risk
Aspiration - pos lung segments Foul smelling sputum → anerobes Cavitation on imaging Tx = clindamyicn Bronchiogenic carcinoma: slower onset (not 2 weeks); no foul sputum Bronchogenic cyst: congenital, not acute Hamartoma - popcorn calcification Hydatid cyst: parasitic (echionococcus); exposure history needed MOA of clopidorgrel : antiplatelet, ADP receptor → **P2Y12 inhibition
by blocking P2Y12 → GPIIb/IIIa activation, platelet aggregation** COX inhibition: aspirin Plasmin activation: thrombolytics (tPA) Lipoxygenase:leukotriene pathway Megakaryocyte differentiate: not drug related Abciximab: GPIIb/IIIa Neuronal necrosis in globus pallidus and hippocampus CO → binds Hb → ↓ O₂ delivery Also inhibits cytochrome oxidase → cellular hypoxia Brain regions most sensitive: Globus pallidus; hippocampus (memory) White matter necrosis: seen in demyelinating/toxic leukoencephalopathies Periaqueductal gray: wernicke encephalopathy - B1 def Mamillary bodies hemoorrhage - Wernike Caudate nucleus - huntington disease (degeneration - ot acute hypoxia) Treatment = 100% O

Obese, high fat diet → ↑ leptin (but resistant) Leptin is produced by adipocytes → more fat → mroe leptin

But brain becomes leptin resistant Cortisol - not necessarily elevated unless cushing Insulin: Often ↑, but question is testing satiety hormone MSH: ↓ in obesity (satiety signal impaired) Neuropeptide Y: increased appetite signal; usually suppressed by leptin (but dysregulated) MMA - classic epidural hematoma Mech: temporal bone fx → MMA rupture CT: biconvex (lens shaped) bleed Bridging vein ⇒ subdurla hematoma, crescent shaped bleed; slower onset ACA/ICA - stroke patterns, not trauma hematoma Cerebral vv - not classic for this presentation Hydrochlorothiazide → hyperuricemia b/c thiaizides ↓ uric acid excretion → hyperuricemia → gout attack Captopril → can actually ↓ uric acid slightly Colchicine → treats gout, doesn’t cause it Disulfiram → alcohol aversion Nifedipine → no uric acid effect “HTN patient + gout” → thiazide or loop diuretic Treatment question → colchicine or NSAIDs CKD, normocytic anemia → ↓ EPO Kidney makes EPO, so if you have CKD ↓ EPO → ↓ RBC production You’d see normocytic anemia EPO stimulates RBC production, dec EPO production → apoptosis of erythroid progenitor cells, → dec reticulocyte count and RBC production Other fx contributing to anemia in CKD: uremic induced inhibition of RBC production, shortened hlaf life. Aplastic anemia → pancytopenia Iron deficiency → microcytic anemia folate/b12 → macrocytic anemia Treatment → EPO (epoetin alfa)

Small vessel vasculitis Palapable purpura = vasculitis hallmark Kidney involvement - signifies kidney involvement Negative cultures - no infxn → r/o infxns Types of small vessel vasculitis IgA vasculitis (Henoch-Schonlein) : acute immune-complex mediated small vessel vasculitis that commonly occurs in children. Often rpeceded by URT or GI infx. In adults it may be idopathic.

typically develop palpable purupura, arthritis and/or arthralgai and abd pain
renal involvement is common and usually more severe in adults, manifesting in hematuria ANCA-associated vasculitis (GPA, MPA, EGPA) GPA: Wegener’s URT/LRT + kidney MPA - rapidly progressive glomerulonephritis eGPA - CHurg-Strauss - a/w asthma + high eosinophils Culture-neg pyelo would present w/ fever, elevated WBC in blood PSGN → would have infxn hx SLE → more systemic features Coccidoides - spherules w/ endospores Thick walled spherules w/ multiple endospores in inflamed tissue - pathognomonic How it’s tested: valley fever, SW US Dipmorphic fungus, endemic to arid soils of US, MExico adn S. America Acute: cough, CP, sweating, anorexia, arthralgia Skin: erythema nodusum or multiforme Dissemianted: rx inc in IC, pregnant women. Can affect bones, skins, meninges Culture: mold w/ hyphae @ 20C Mild to mod: flluconazole or itraconazole || Severe: ampB || Meningitis: lifelong azole Blastomyces → broad-based budding Histoplasma → intracellular in macrophages Cryptococcus → capsule Aspergillus → septate hyphae Gram neg rods + shock → LPS endotoxin LPS activates macrophages → TNF-a, IL-1 → septic shock There are no neutralizing Abs Why others are wrong: Lipoteichoic acid → gram + Techoic acid → gram + flagella/pili → motility/adhesion Gram neg virulence factors Pili/fimbriae - attach to cells
E.coli (UTIs); neisseria gonorrhea Exotoxin A (pseudomonoas) - inhibits EF2 → dec protein synthesis Chlorea toxin: ↑ cAMP → watery diarrhea Shiga toxin (shigella, EHEC) Inhibits 60S ribosome → cell death Capsule (immune evasion): prevents phagocytosis
N. meningitis, klebsiella, Hib Ag variation: change surface proteins → immune evasion Intracellular survival- survivesin macs - salmonella, legionella Biofilm formation: pseudomonas , e. Coli Sidepores - steals iron from host - E Coli, Klebsiella Painless ulcer, black eschar, Middle East, gram + rods in chians → bacillus anthracis Usualy exposure to animal hides Gram stain: large gram+ rods in chans (box car apperance) Non hemolytic, ground glass colonies Edema toxin + lethal thoxin Capsule made of poly-D-glutamate B. cereus → food poisoning (fried rice) C. perfringens → gas gangrene (crepitus) Francisella → ulceroglandular + lymphadenopathy Yersinia pestis → bubonic plague (painful nodes)

Toxins A + B, watery diarrhea → C. diff Tx: vancomycin (or fidaxomicin) Toxin A: enterotoxin + Toxin B: cytotoxin ⇒ causes pseudomembranous colitis Clindomycin → causes C. diff Ciprofloxaicn : not effective Others: irrelevant coverage intra-RBC parasites, NE US, splenectomy → Babesia Babesiosis: infects RBCs, asplenic pts at rx, maltese cross

fever and hemolytic anemia; predominantly in NE and N central US
asplenia increases rx of severe disease d/t inability to clear infected RBCs Vector: Tick: Ixodes Tx: atovaquine + azithromycin Lyme → rash, not RBC parasites Ehrlichiosis → intracellular in WBCs Trypanosoma → Africa Leishmania → macrophages Spindle cells → smooth muscle No mitosis/atypia → benign Leimyoma only benign option Rhabdomyosarcoma → malignant skeletal muscle Carcinoid → neuroendocrine Fibrosarcoma → malignant SCC → epithelial malignancy Answer - A Pt’s symptoms : hot flashes, amenorrhea → menopause ↓ estrogen → loss of negative feedback Pituitary → ↑ gonadotropins (LH, FSH) FSH rises more than LH Recurrent ear and throat infxns - most likely IgA IgA = mucosal immunity (resp tract, GI tract, saliva, tears, secretions) Eustachian tube, Tonsils (upper airway)
most common primary immuno def
a/w anaphylaxis to bloood transfusion IgM is wrong - 1st Ab → infants rely on it (prmary immune response)
Severe early infxns IgG - long term immunity - recurrent bacterial infxns IgE - parasites/allergy - atopy

right varicocele + retroperitoneal mass → venous obstruction Right testicular vein drains → IVC Mass compressing IVC → backup → right varicocele Right testicular vein drains direclty into IVC Left testicular vein → L renal vein IVC R renal vein drains right kidney into IVC but doesn’t receive R. testicular v R suprarenal v - not involved in testicular drainage Internal iliac v - pelvic drainage, not testicular Portal v - GI sxm. Irrelevant

Comsae Form 107 Part 1, Exams of Medicine

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Download Comsae Form 107 Part 1 and more Exams Medicine in PDF only on Docsity!