High yield review 3 Flashcards

Question

Alport syndrome

Answer 1

Defect in Type IV collagen Affects basement membranes of kidney, inner ear, and eye Most common: X-linked dominant (COL4A5 gene) Can also be AR or AD (rare) 👉 Type IV collagen is key in the glomerular basement membrane (GBM)

Answer 2

Type Where Found USMLE Buzzwords Type I Bone, skin, tendon "Bone = One" Type II Cartilage "CarTWOlage" Type III Blood vessels, skin Ehlers-Danlos Type IV Basement membrane Alport, Goodpasture’s Hematuria (persistent, microscopic or gross) → nephritic syndrome Sensorineural hearing loss Ocular defects (e.g., anterior lenticonus) 🧠 Mnemonic: “Can’t see, can’t pee, can’t hear a bee”

Answer 3

Thinning and splitting of GBM on EM "Basket-weave" appearance (very testable buzzword!) Family history of renal failure or hearing loss No immune deposits (distinguishes from other nephritic syndromes)

Answer 4

Treatment IVIG + aspirin (only time kids routinely get aspirin) Follow-up with echo 🎯 USMLE Tips If child has fever >5 days + conjunctivitis + rash + strawberry tongue, always consider Kawasaki Coronary aneurysms = fatal complication IVIG prevents cardiac sequelae Differentiate from viral exanthems and scarlet fever

Answer 5

Diagnostic Criteria (≥5 days of fever + 4 of 5) Bilateral non-purulent conjunctivitis Rash (polymorphous, not vesicular) Cervical lymphadenopathy (usually unilateral) Oral changes: "strawberry tongue", red cracked lips Extremity changes: edema, erythema, desquamation

Answer 6

Etiology Caused by Group A Strep (GAS) producing erythrogenic exotoxins 📌 Clinical Features Fever + pharyngitis + sandpaper rash Strawberry tongue (also in Kawasaki) Rash begins on trunk, spares palms/soles Often follows strep throat 👉 Circumoral pallor, Pastia’s lines (in skin folds) Treatment Penicillin (prevents rheumatic fever) USMLE Tips If the rash follows pharyngitis → Scarlet Fever If conjunctivitis + hand/foot edema + fever >5 days → Kawasaki Both can have strawberry tongue, but conjunctivitis = Kawasaki Scarlet fever does not cause coronary aneurysms

Answer 7

Catalyzes: Acetaldehyde → Acetate (part of ethanol metabolism) 👉 Works after alcohol dehydrogenase (ADH) converts ethanol → acetaldehyde

Answer 8

Leads to: ↑ acetaldehyde Facial flushing, tachycardia, nausea after drinking alcohol 🧠 USMLE Tip: Seen in questions where someone avoids alcohol due to “unpleasant symptoms” — classic for ALDH2 deficiency

Answer 9

Inhibits ALDH → ↑ acetaldehyde after alcohol → aversive reaction Used in alcohol dependence treatment 🧠 USMLE Tip: If patient is on disulfiram and drinks → flushing + nausea + vomiting + hypotension

Answer 10

Ethanol → Acetaldehyde (by Alcohol dehydrogenase, NAD⁺ → NADH) Acetaldehyde → Acetate (by Aldehyde dehydrogenase, NAD⁺ → NADH) ⚠️ Both steps generate NADH, which leads to: Lactic acidosis Hypoglycemia Fatty liver 🧠 USMLE Tip: Chronic alcohol use → ↑ NADH/NAD⁺ ratio → blocks gluconeogenesis & promotes lipogenesis USMLE Step 1 Tips Flushing after alcohol → ALDH2 deficiency Disulfiram = ALDH inhibitor → ↑ acetaldehyde → aversive reaction Know the link to ↑ NADH and its metabolic effects: lactic acidosis, hypoglycemia, fatty change If question describes "unpleasant reaction to alcohol" or treatment for alcoholism → think ALDH

Answer 11

🧠 USMLE Connection: Not directly involved in MS pathology MS = demyelination; not a GABA or neurotransmitter problem BUT GABA agonists like baclofen are used to treat spasticity in MS 💊 GABA & MS: Treatment Link Drug Mechanism Use in MS Baclofen GABA-B agonist → CNS muscle relaxant ↓ Spasticity in MS Benzodiazepines GABA-A agonist → ↑ Cl⁻ influx Sometimes used for MS-related muscle symptoms or anxiety 🎯 USMLE Step 1 Tips MS = demyelination in CNS (oligodendrocytes), NOT a GABA problem Baclofen = GABA-B agonist → used for spasticity in MS (test favorite) GABA = inhibitory, glutamate = excitatory MS: think white matter, T cells, periventricular plaques

Answer 12

utoimmune hyperthyroidism (TSI → TSH receptor stimulation) Histology: Tall, crowded follicular epithelium (columnar) Scalloped colloid (due to active reabsorption) 🧠 USMLE Tip: Tall, hyperactive follicles + scalloped colloid = Graves Often shows up with exophthalmos, pretibial myxedema

Answer 13

Autoimmune hypothyroidism, anti-TPO/anti-Tg Abs Histology: Hurthle cells (eosinophilic metaplasia of follicular cells) Lymphoid aggregates with germinal centers 🧠 USMLE Tip: Chronic inflammation + Hurthle cells = Hashimoto ↑ risk of B-cell lymphoma

Answer 14

Painful thyroid after viral infection Histology: Granulomatous inflammation with multinucleated giant cells 🧠 USMLE Tip: Painful thyroid + granulomas = de Quervain Transient hyperthyroid → euthyroid → hypothyroid phases

Answer 15

Rare fibrosing condition → “rock-hard” painless thyroid Histology: Dense fibrosis, replaces thyroid & invades local structures 🧠 USMLE Tip: Mimics anaplastic carcinoma but with normal cells + fibrosis Associated with IgG4-related disease

Answer 16

Good prognosis, radiation exposure risk Histology: Orphan Annie eye nuclei (empty/cleared out) Psammoma bodies Nuclear grooves 🧠 USMLE Tip: Papillary = P’s: Psammoma, Palpable nodes, Positive prognosis, Previous radiation

Answer 17

econd most common Hematogenous spread Histology: Invasion through capsule and vasculature is diagnostic (not seen on FNA) 🧠 USMLE Tip: FNA can’t distinguish adenoma vs. carcinoma — you need capsular invasion

Answer 18

From parafollicular C cells → secretes calcitonin Associated with MEN 2A/2B (RET mutation) Histology: Sheets of cells in amyloid stroma Congo red stains amyloid (calcitonin) 🧠 USMLE Tip: Thyroid mass + diarrhea or MEN syndrome → think medullary Look for amyloid deposits

Answer 19

Elderly, aggressive, poor prognosis Histology: Undifferentiated giant cells with high mitotic rate Invasion of local structures 🧠 USMLE Tip: Older patient + rapidly enlarging neck mass + compressive symptoms → anaplastic Must distinguish from Riedel (painless & fibrous)

Answer 20

Scalloped colloid → Graves Hurthle cells + lymphoid follicles → Hashimoto Granulomas + pain → de Quervain Fibrosis + normal cells → Riedel Orphan Annie + Psammoma → Papillary Capsular invasion → Follicular carcinoma Amyloid + calcitonin → Medullary (MEN 2) Giant undifferentiated cells → Anaplastic

Answer 21

Possible due to presence of Schwann cells After injury, Wallerian degeneration occurs: Distal axon degenerates Macrophages clean debris Schwann cells proliferate → guide axon regrowth via endoneurial tubes 🧠 USMLE Tip: Wallerian degeneration = PNS only Schwann cells = key for regeneration Axonal regrowth = ~1–3 mm/day

Answer 22

No significant regeneration due to: Oligodendrocytes → inhibit growth (release Nogo, MAG, OMgp) Astrocytes → form glial scar No endoneurial tubes in CNS 🧠 USMLE Tip: CNS cannot regenerate due to inhibitory molecules & glial scarring Oligodendrocytes = inhibit Schwann cells = promote

Answer 23

“Cape-like” bilateral loss of: Pain and temperature (due to spinothalamic tract damage) Preserved fine touch & proprioception (dorsal columns spared) May also cause: Lower motor neuron signs (flaccid weakness, atrophy) in hands → anterior horn involvement 🧠 USMLE Tip: "Cape-like distribution of sensory loss" = buzzword for syringomyelia

Answer 24

Non-malignant enlargement of the periurethral (transition zone) of the prostate due to DHT-driven hyperplasia of stromal and epithelial cells Testosterone → DHT (via 5α-reductase) ↓ DHT stimulates prostate growth, especially in transition zone Leads to urethral compression → urinary obstruction 🧠 USMLE Tip: BPH occurs in transition zone (vs. peripheral zone in prostate cancer) 🧠 USMLE Tip: Lower urinary tract symptoms + smooth, enlarged, non-tender prostate = BPH 🧠 USMLE Tip: Finasteride = ↓ DHT (also used in male pattern baldness) Tamsulosin = selective α1A blocker (less hypotension than non-selective) α-blockers work fast, 5α-reductase inhibitors work slow

Answer 25

🧠 USMLE Tips & Buzzwords Case-control = Disease → Risk (Backwards) → Use Odds Ratio (OR) → Classic for rare diseases → Example: “200 women with breast cancer, 200 without – compare OCP use” Cohort = Risk → Disease (Forward) → Use Relative Risk (RR) → Strong for studying incidence → Example: “Smokers vs. non-smokers followed for 10 years” Cross-sectional = Snapshot → Use Prevalence, not incidence → Example: “What % of teens currently smoke?” Randomized Controlled Trial (RCT) = Highest-quality evidence for treatment → Randomization reduces bias → Blinding prevents placebo effect Meta-analysis = Most statistically powerful → Combines RCTs, gives pooled RR or OR → USMLE may ask about heterogeneity or publication bias Case series = No comparison group → Can suggest hypotheses, not causality Ecological fallacy = Assuming population-level data applies to individuals → Common USMLE trick question 🎯 Quick Memory Aid Case-Control → "Start with the Case" Cohort → "Start with the Exposure" Cross-Sectional → "Crossroads in Time" (snapshot) RCT → "Randomized for Results"

Answer 26

Gram-positive (G⁺): Thick peptidoglycan wall → retains crystal violet (purple/blue) Gram-negative (G⁻): Thin peptidoglycan + outer membrane → loses crystal violet, takes up safranin (red/pink) USMLE Tip: Decolorizer step is key → Gram⁺ stays purple, Gram⁻ gets decolorized

Answer 27

Cocci: Staph (clusters) Strep (chains or pairs) Rods: Bacillus, Clostridium, Corynebacterium, Listeria, Mycobacterium (weakly Gram⁺) Gram⁺ = thick wall = retains crystal violet = purple “Clusters of Gram⁺ cocci” = Staph “Chains of Gram⁺ cocci” = Strep

Answer 28

Cocci: Neisseria Rods (Enteric): E. coli, Salmonella, Shigella, Klebsiella, Proteus, Pseudomonas, etc. Gram⁻ = thin wall + outer membrane = pink Gram⁻ rods = think enterics (E. coli, Klebsiella, etc.)

Answer 29

Organism Why It Doesn’t Stain USMLE Clue Treponema Too thin ***Use dark field or fluorescent Ab*** Mycobacteria Mycolic acid (lipid-rich wall) ***Acid-fast stain*** Mycoplasma No cell wall ***Cholesterol membrane*** Legionella Intracellular, poor uptake ***Silver stain*** Chlamydia / Rickettsia Intracellular + no classic peptidoglycan ***Giemsa stain*** Bartonella, Plasmodium, Borrelia Use Giemsa 🧠 USMLE Tip: “Doesn’t Gram stain” → Always consider Mycoplasma, Mycobacteria, Treponema, Chlamydia, Rickettsia

Answer 30

Classification (by Hemolysis) Type Hemolysis Key Species Alpha-hemolytic Partial (green) Streptococcus pneumoniae, Streptococcus viridans Beta-hemolytic Complete (clear) Streptococcus pyogenes (Group A), S. agalactiae (Group B) Gamma-hemolytic None Enterococcus faecalis, S. bovis

Answer 31

Beta-hemolytic, bacitracin sensitive Virulence: M protein (antiphagocytic), streptolysin O (ASO titers) 🧠 Causes: Pharyngitis → rheumatic fever (type II HSR) Impetigo → glomerulonephritis (type III HSR) Scarlet fever: sandpaper rash, strawberry tongue Necrotizing fasciitis, TSS 🧠 USMLE Tip: Post-strep GN can follow skin OR throat infection Rheumatic fever follows only pharyngitis ASO titer Recent S. pyogenes infection (e.g., rheumatic fever)

Answer 32

Beta-hemolytic, bacitracin resistant Colonizes vagina 🧠 Causes: Neonatal sepsis, pneumonia, meningitis 🧠 USMLE Tip: Screen pregnant women at 35–37 weeks Give intrapartum penicillin prophylaxis CAMP test Positive in S. agalactiae

Answer 33

Alpha-hemolytic, optochin sensitive, bile soluble Lancet-shaped diplococci Encapsulated → quellung positive 🧠 Causes: “MOPS” Meningitis Otitis media v Pneumonia (lobar) Sinusitis 🧠 USMLE Tip: Rusty sputum, sepsis in sickle cell or asplenic patients Vaccine: PCV13 (kids), PPSV23 (adults, asplenia) Quellung reaction Detects pneumococcal capsule

Answer 34

Alpha-hemolytic, optochin resistant Includes S. mutans, S. sanguinis 🧠 Causes: Dental caries, subacute endocarditis (esp. after dental work) 🧠 USMLE Tip: Adheres to damaged valves via dextrans (made from glucose)

Answer 35

Gamma-hemolytic, grows in bile and NaCl 🧠 Causes: “Do U ♥ Trees?” UTIs, endocarditis, biliary infections 🧠 USMLE Tip: Often nosocomial, can be vancomycin-resistant (VRE)

Answer 36

Group D; causes endocarditis 🧠 USMLE Tip: If found in blood → screen for colon cancer

Answer 37

M protein → Rheumatic fever (S. pyogenes) Bacitracin sensitive → Group A (pyogenes) Bacitracin resistant → Group B (agalactiae) Optochin sensitive → S. pneumoniae Optochin resistant → Viridans Dextrans → Damaged valves → Viridans Quellung positive, capsule → S. pneumoniae S. bovis + endocarditis → Colon cancer screen

Answer 38

Mitochondrial disorder affecting the nervous system and muscles Caused by mitochondrial DNA mutations (esp. tRNA^Leu(UUR) gene) 🧠 USMLE Tip: Mitochondrial disorders = always maternal inheritance Variable expression due to heteroplasmy 🧠 USMLE Tip: Stroke in a child or young adult with lactic acidosis = think MELAS Not confined to vascular territories (unlike embolic strokes) “Ragged red fibers” = mitochondrial myopathy, seen in MELAS and other mitochondrial disorders

High yield review 3 Flashcards

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