United States Medical Licensing Examination (USMLE) Foundational Biomedical Sciences (Step 1 Core) Flashcards

24 sample cards from the Foundational Biomedical Sciences (Step 1 Core) deck

Sampled from the end of the deck, so these are different cards from the ones shown on the syllabus page.

1. Match the type of necrosis to its classic setting: coagulative, liquefactive, caseous, fat, fibrinoid, gangrenous.

   Coagulative = ischemic infarct of solid organs (not brain); liquefactive = brain infarct/abscess; caseous = TB and fungal granulomas; fat = pancreatitis/breast trauma; fibrinoid = vessel wall in vasculitis/malignant hypertension; gangrenous = ischemic limb (dry/wet).

2. Name the five cardinal signs of acute inflammation and the predominant cell type.

   Rubor (redness), calor (heat), tumor (swelling), dolor (pain), functio laesa (loss of function); the predominant cell is the neutrophil.

3. Outline the steps of neutrophil extravasation (leukocyte adhesion cascade).

   Margination, rolling (selectins/sialyl-Lewis X), activation, tight adhesion (integrins-ICAM), transmigration/diapedesis (PECAM-1), and chemotaxis (C5a, LTB4, IL-8, bacterial products) toward the injury.

4. Compare labile, stable, and permanent tissue types in regenerative capacity.

   Labile: continuously dividing, regenerate well (gut/skin epithelium, bone marrow). Stable: quiescent (G0) but can divide if stimulated (hepatocytes, renal tubules). Permanent: cannot regenerate, heal by scar (neurons, cardiac and skeletal muscle).

5. Distinguish healing by primary versus secondary intention.

   Primary intention: clean wound with apposed edges (sutured), minimal scar. Secondary intention: large gaping wound healing from the bottom up with granulation tissue, wound contraction (myofibroblasts), and a larger scar.

6. State Virchow's triad and its clinical significance.

   The three factors promoting thrombosis: endothelial injury, stasis (abnormal blood flow), and hypercoagulability. It explains predisposition to venous thromboembolism (e.g., DVT/PE).

7. Differentiate transudate from exudate in an effusion.

   Transudate: low protein, low specific gravity, due to increased hydrostatic or decreased oncotic pressure (CHF, cirrhosis, nephrotic syndrome). Exudate: high protein, high specific gravity, cellular, due to inflammation/increased vascular permeability (infection, malignancy).

8. Define the steps/hallmarks of neoplastic progression and contrast benign vs malignant tumors.

   Hallmarks include self-sufficient growth signals, evasion of apoptosis, limitless replication, angiogenesis, invasion/metastasis. Benign: well-differentiated, slow, encapsulated, no metastasis. Malignant: poorly differentiated/anaplastic, rapid, invasive, metastasizes.

9. Differentiate oncogenes from tumor suppressor genes with one example of each.

   Oncogenes: gain-of-function mutations (one allele) promoting cancer (e.g., RAS, MYC, HER2). Tumor suppressors: loss-of-function requiring both alleles inactivated/two-hit hypothesis (e.g., TP53, RB, APC, BRCA).

10. Define bioavailability (F) and volume of distribution (Vd), including their formulas.

    Bioavailability F = fraction of drug reaching systemic circulation (100% for IV). Vd = amount of drug in body / plasma drug concentration; high Vd suggests tissue/lipophilic distribution, low Vd suggests confinement to plasma.

11. Give the formulas for clearance, half-life, and loading dose.

    Clearance CL = rate of elimination / plasma concentration = Vd x ke. Half-life t1/2 = 0.7 x Vd / CL. Loading dose = (Css x Vd)/F; maintenance dose = (Css x CL)/F.

12. Compare zero-order and first-order elimination kinetics with examples.

    Zero-order: constant amount eliminated per unit time (rate independent of concentration) — phenytoin, ethanol, aspirin (high dose). First-order: constant fraction eliminated per unit time (rate proportional to concentration) — most drugs.

13. Define potency versus efficacy and how they appear on a dose-response curve.

    Potency: amount of drug needed for a given effect (related to EC50; left-shifted curve = more potent). Efficacy: maximal achievable effect (Emax; higher plateau = more efficacious).

14. Contrast competitive and noncompetitive antagonists in their effects on agonist potency and efficacy.

    Competitive antagonist: surmountable, shifts dose-response curve right (decreases potency/increases EC50), Emax unchanged. Noncompetitive (irreversible/allosteric): insurmountable, decreases Emax (efficacy), potency may be unchanged.

15. Define therapeutic index and write its formula.

    Therapeutic index (TI) = TD50 / ED50 (or LD50/ED50 in animals); the median toxic (or lethal) dose divided by the median effective dose. A higher TI means a safer drug.

16. Compare Phase I and Phase II drug metabolism reactions.

    Phase I: oxidation, reduction, hydrolysis (often via cytochrome P450) yielding slightly polar, sometimes active metabolites. Phase II: conjugation (glucuronidation, acetylation, sulfation) producing polar, usually inactive, water-soluble metabolites for excretion.

17. What is the difference between cytochrome P450 inducers and inhibitors for drug interactions?

    Inducers (e.g., rifampin, phenytoin, carbamazepine, barbiturates, St. John's wort, chronic alcohol) increase metabolism and lower drug levels. Inhibitors (e.g., azoles, macrolides, grapefruit juice, ritonavir, cimetidine) decrease metabolism and raise drug levels/toxicity.

18. Contrast the receptors and overall effects of the sympathetic versus parasympathetic autonomic nervous systems.

    Sympathetic ('fight or flight'): mostly adrenergic (alpha/beta) via norepinephrine, increases heart rate, dilates pupils/bronchi, decreases GI activity. Parasympathetic ('rest and digest'): cholinergic (muscarinic) via acetylcholine, decreases heart rate, constricts pupils, increases GI/secretions. Both ganglia and adrenal medulla use nicotinic ACh receptors.

19. Match adrenergic receptor subtypes to their primary actions: alpha-1, alpha-2, beta-1, beta-2.

    Alpha-1: vasoconstriction, mydriasis, increased sphincter tone (Gq). Alpha-2: decreased sympathetic outflow, decreased insulin/NE release (Gi). Beta-1: increased heart rate, contractility, renin (Gs). Beta-2: bronchodilation, vasodilation, uterine relaxation (Gs).

20. What are the signs of cholinergic (muscarinic) excess, and what is the antidote for organophosphate poisoning?

    Cholinergic toxicity (DUMBBELSS): Diarrhea, Urination, Miosis, Bronchospasm, Bradycardia, Excitation of muscle, Lacrimation, Sweating, Salivation. Antidote: atropine (muscarinic blocker) plus pralidoxime (regenerates acetylcholinesterase).

21. Match the toxin/overdose to its specific antidote: acetaminophen, opioids, benzodiazepines, warfarin, heparin.

    Acetaminophen = N-acetylcysteine; opioids = naloxone; benzodiazepines = flumazenil; warfarin = vitamin K and fresh frozen plasma; heparin = protamine sulfate.

22. What are the antidotes for methanol/ethylene glycol, iron, lead, and digoxin toxicity?

    Methanol/ethylene glycol = fomepizole (and ethanol); iron = deferoxamine/deferasirox; lead = EDTA, dimercaprol, succimer; digoxin = digoxin-specific Fab antibodies (Digibind).

23. What is the universal direct acceptor of high-energy electrons that yields the most ATP, and how many ATP does NADH versus FADH2 generate?

    NADH and FADH2 donate electrons to the electron transport chain. NADH yields ~2.5 ATP and FADH2 yields ~1.5 ATP per molecule (entering at Complex I vs Complex II, respectively).

24. Compare primary, secondary, and tertiary protein structure.

    Primary: linear amino acid sequence (peptide bonds). Secondary: local folding into alpha-helices and beta-sheets (hydrogen bonds). Tertiary: overall 3D shape of a polypeptide (disulfide, hydrophobic, ionic interactions). Quaternary: assembly of multiple subunits.

What this deck covers

Foundational Biomedical Sciences (Step 1 Core) flashcards FAQ