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Yes. Flashcards use active recall — retrieving an answer from memory — which research shows is one of the most effective ways to make facts stick, especially in short sessions spread over several days. That matters for Step 1's vast fact base: enzymes, organisms, drug mechanisms, antidotes, and the high-yield associations.

What topics do the USMLE Step 1 flashcards cover?

Every discipline the integrated content outline tests: pathology (the largest, 45–55%) and physiology (30–40%), plus pharmacology, microbiology, immunology, biochemistry, genetics, anatomy and neuroscience, behavioral science, and biostatistics and epidemiology — the same high-yield mechanisms and associations Step 1 vignettes reward.

Do these flashcards reflect what USMLE Step 1 actually tests?

Yes. Every card is written to the level the USMLE expects of a student applying foundational science to clinical scenarios — the high-yield mechanisms, rate-limiting enzymes, organism profiles, drug receptors, and associations — and the science is framed the way Step 1 tests it, through clinical vignettes.

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Mix the modes: flip to learn, type to test recall, match for speed, and quiz to check yourself. Weight your time toward pathology and physiology (the bulk of the exam) and the high-yield systems, and turn the rule-based facts — antidotes, hypersensitivity types, rate-limiting enzymes — into instant recall.

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Step 1 score reporting

Pass/Fail only since January 26, 2022 — no three-digit numeric score is reported.

Rate-limiting enzyme of glycolysis

Phosphofructokinase-1 (PFK-1), the committed step; activated by AMP and fructose-2,6-bisphosphate, inhibited by ATP and citrate.

Net ATP yield of glycolysis

2 ATP and 2 NADH per glucose (cytoplasm); one glucose → two pyruvate.

Citric acid (Krebs) cycle yield per turn

3 NADH, 1 FADH₂, 1 GTP, and 2 CO₂; each glucose drives two turns.

Where is the bulk of cellular ATP made?

Oxidative phosphorylation in the inner mitochondrial membrane (electron transport chain + ATP synthase).

Michaelis constant (Km)

Substrate concentration at ½ Vmax. Low Km = high affinity. On a Lineweaver-Burk plot the x-intercept is −1/Km.

Competitive vs non-competitive inhibitor (kinetics)

Competitive: ↑ apparent Km, Vmax unchanged (overcome with more substrate). Non-competitive: ↓ Vmax, Km unchanged.

Rate-limiting enzyme of fatty acid synthesis

Acetyl-CoA carboxylase (ACC); requires biotin.

Rate-limiting enzyme of fatty acid oxidation

Carnitine palmitoyltransferase I (CPT-1); inhibited by malonyl-CoA.

Rate-limiting enzyme of cholesterol synthesis

HMG-CoA reductase — the target of statins.

Rate-limiting enzyme of heme synthesis

ALA synthase (uses vitamin B6); inhibited by heme.

Rate-limiting enzyme of the urea cycle

Carbamoyl phosphate synthetase I (CPS-I) in the mitochondria.

Pyruvate dehydrogenase complex cofactors

Tender Loving Care For Nancy: Thiamine (B1), Lipoic acid, CoA (B5), FAD (B2), NAD (B3).

Glucose-6-phosphate dehydrogenase (G6PD) deficiency

X-linked; ↓ NADPH → ↓ glutathione → hemolysis with oxidative stress (fava beans, infections, sulfa/primaquine). Heinz bodies, bite cells.

Pyruvate kinase deficiency

Autosomal recessive; impaired last ATP step of glycolysis → hemolytic anemia in RBCs (which rely solely on glycolysis).

Von Gierke disease (glycogen storage type I)

Glucose-6-phosphatase deficiency → severe fasting hypoglycemia, hepatomegaly, lactic acidosis, hyperuricemia, hyperlipidemia.

Pompe disease (glycogen storage type II)

Acid α-glucosidase (lysosomal) deficiency → cardiomegaly, hypotonia, early death. 'Pompe trashes the Pump (heart).'

McArdle disease (glycogen storage type V)

Myophosphorylase deficiency → exercise intolerance, muscle cramps, myoglobinuria; flat venous lactate with exercise.

Hexosaminidase A deficiency → GM2 ganglioside accumulation; cherry-red macula, NO hepatosplenomegaly, progressive neurodegeneration.

Glucocerebrosidase deficiency → hepatosplenomegaly, bone crises; 'crumpled tissue paper' macrophages. Most common lysosomal storage disease.

Sphingomyelinase deficiency → hepatosplenomegaly, cherry-red macula, foam cells; 'No man picks his nose with his sphinger.'

Phenylketonuria (PKU)

Phenylalanine hydroxylase deficiency (or ↓ BH4) → ↑ phenylalanine; musty odor, intellectual disability. Treat: low-phenylalanine diet, avoid aspartame.

Maple syrup urine disease

Branched-chain α-ketoacid dehydrogenase deficiency → buildup of branched amino acids (Ile, Leu, Val); sweet-smelling urine.

Vitamin B1 (thiamine) deficiency

Wernicke-Korsakoff (confusion, ophthalmoplegia, ataxia + confabulation), dry/wet beriberi. Impairs PDH, α-KG dehydrogenase, transketolase.

Vitamin B12 vs folate deficiency

Both → megaloblastic anemia. B12 deficiency adds neurologic signs (subacute combined degeneration) and ↑ methylmalonic acid; folate does not.

Scurvy (vitamin C deficiency)

Impaired collagen hydroxylation (proline/lysine) → poor wound healing, bleeding gums, corkscrew hairs, perifollicular hemorrhage.

Collagen types: I, II, III, IV

I = bone/skin/tendon (most common). II = cartilage. III = reticulin/granulation (Ehlers-Danlos). IV = basement membrane.

Osteogenesis imperfecta

Defective type I collagen (often COL1A1/2) → multiple fractures, blue sclerae, hearing loss, dental problems.

Marfan syndrome defect

FBN1 (fibrillin-1); autosomal dominant. Tall, arachnodactyly, lens dislocation (up/out), aortic root dilation/dissection.

Autosomal dominant vs recessive (general)

Dominant: structural genes, often pleiotropic, vertical transmission. Recessive: enzyme deficiencies, often consanguinity, horizontal pattern.

X-linked recessive inheritance

No male-to-male transmission; sons of carrier mothers affected 50%. Examples: hemophilia A/B, DMD, G6PD, Lesch-Nyhan, Fabry.

Hardy-Weinberg: carrier frequency

p² + 2pq + q² = 1; p + q = 1. Disease allele frequency q; carrier frequency ≈ 2pq.

Trinucleotide repeat expansion diseases

Huntington (CAG), fragile X (CGG), myotonic dystrophy (CTG), Friedreich ataxia (GAA). Show anticipation.

Imprinting: Prader-Willi vs Angelman

Same 15q11-13 region. Prader-Willi: paternal deletion (hyperphagia, obesity). Angelman: maternal deletion ('happy puppet,' ataxia, seizures).

Cystic fibrosis defect

CFTR gene (chr 7, ΔF508), autosomal recessive → defective Cl⁻ channel; thick secretions, recurrent infections, ↑ sweat chloride.

DNA polymerase proofreading

DNA pol I and III (prokaryotes) have 3′→5′ exonuclease proofreading; pol I also removes RNA primers (5′→3′ exonuclease).

Lac operon regulation

Glucose absent (↑ cAMP, CAP binds, ↑ transcription) AND lactose present (allolactose removes repressor) → genes ON.

Gram-positive vs gram-negative cell wall

Gram-positive: thick peptidoglycan, stains purple. Gram-negative: thin peptidoglycan + LPS outer membrane (endotoxin), stains pink.

Catalase-positive organisms (matter in CGD)

Cats Need PLACESS: Pseudomonas, Listeria, Aspergillus, Candida, E. coli, Staph aureus, Serratia, Nocardia, Burkholderia, H. pylori.

Staph aureus vs epidermidis vs saprophyticus

All catalase-positive cocci in clusters. S. aureus = coagulase-positive. S. epidermidis = coagulase-negative, novobiocin-sensitive. S. saprophyticus = novobiocin-resistant (young women UTI).

Streptococcus classification by hemolysis

α (partial, green): S. pneumoniae (optochin-S), viridans (optochin-R). β (clear): Group A (bacitracin-S), Group B (bacitracin-R). γ (none): enterococci.

Exotoxin: diphtheria & Pseudomonas exotoxin A

ADP-ribosylate EF-2 → inhibit protein synthesis. Diphtheria: pseudomembranous pharyngitis, myocarditis.

Cholera & ETEC heat-labile toxin mechanism

ADP-ribosylate Gs → ↑ adenylate cyclase → ↑ cAMP → Cl⁻ and water secretion → watery diarrhea.

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USMLE Step 1 Flashcards

Step 1 score reporting: Pass/Fail only since January 26, 2022 — no three-digit numeric score is reported.
Rate-limiting enzyme of glycolysis: Phosphofructokinase-1 (PFK-1), the committed step; activated by AMP and fructose-2,6-bisphosphate, inhibited by ATP and citrate.
Net ATP yield of glycolysis: 2 ATP and 2 NADH per glucose (cytoplasm); one glucose → two pyruvate.
Citric acid (Krebs) cycle yield per turn: 3 NADH, 1 FADH₂, 1 GTP, and 2 CO₂; each glucose drives two turns.
Rate-limiting enzyme of the TCA cycle: Isocitrate dehydrogenase.
Where is the bulk of cellular ATP made?: Oxidative phosphorylation in the inner mitochondrial membrane (electron transport chain + ATP synthase).
Michaelis constant (Km): Substrate concentration at ½ Vmax. Low Km = high affinity. On a Lineweaver-Burk plot the x-intercept is −1/Km.
Competitive vs non-competitive inhibitor (kinetics): Competitive: ↑ apparent Km, Vmax unchanged (overcome with more substrate). Non-competitive: ↓ Vmax, Km unchanged.
Rate-limiting enzyme of gluconeogenesis: Fructose-1,6-bisphosphatase.
Rate-limiting enzyme of fatty acid synthesis: Acetyl-CoA carboxylase (ACC); requires biotin.
Rate-limiting enzyme of fatty acid oxidation: Carnitine palmitoyltransferase I (CPT-1); inhibited by malonyl-CoA.
Rate-limiting enzyme of cholesterol synthesis: HMG-CoA reductase — the target of statins.
Rate-limiting enzyme of heme synthesis: ALA synthase (uses vitamin B6); inhibited by heme.
Rate-limiting enzyme of the urea cycle: Carbamoyl phosphate synthetase I (CPS-I) in the mitochondria.
Pyruvate dehydrogenase complex cofactors: Tender Loving Care For Nancy: Thiamine (B1), Lipoic acid, CoA (B5), FAD (B2), NAD (B3).
Glucose-6-phosphate dehydrogenase (G6PD) deficiency: X-linked; ↓ NADPH → ↓ glutathione → hemolysis with oxidative stress (fava beans, infections, sulfa/primaquine). Heinz bodies, bite cells.
Pyruvate kinase deficiency: Autosomal recessive; impaired last ATP step of glycolysis → hemolytic anemia in RBCs (which rely solely on glycolysis).
Von Gierke disease (glycogen storage type I): Glucose-6-phosphatase deficiency → severe fasting hypoglycemia, hepatomegaly, lactic acidosis, hyperuricemia, hyperlipidemia.
Pompe disease (glycogen storage type II): Acid α-glucosidase (lysosomal) deficiency → cardiomegaly, hypotonia, early death. 'Pompe trashes the Pump (heart).'
McArdle disease (glycogen storage type V): Myophosphorylase deficiency → exercise intolerance, muscle cramps, myoglobinuria; flat venous lactate with exercise.
Tay-Sachs disease: Hexosaminidase A deficiency → GM2 ganglioside accumulation; cherry-red macula, NO hepatosplenomegaly, progressive neurodegeneration.
Gaucher disease: Glucocerebrosidase deficiency → hepatosplenomegaly, bone crises; 'crumpled tissue paper' macrophages. Most common lysosomal storage disease.
Niemann-Pick disease: Sphingomyelinase deficiency → hepatosplenomegaly, cherry-red macula, foam cells; 'No man picks his nose with his sphinger.'
Phenylketonuria (PKU): Phenylalanine hydroxylase deficiency (or ↓ BH4) → ↑ phenylalanine; musty odor, intellectual disability. Treat: low-phenylalanine diet, avoid aspartame.
Maple syrup urine disease: Branched-chain α-ketoacid dehydrogenase deficiency → buildup of branched amino acids (Ile, Leu, Val); sweet-smelling urine.
Vitamin B1 (thiamine) deficiency: Wernicke-Korsakoff (confusion, ophthalmoplegia, ataxia + confabulation), dry/wet beriberi. Impairs PDH, α-KG dehydrogenase, transketolase.
Vitamin B12 vs folate deficiency: Both → megaloblastic anemia. B12 deficiency adds neurologic signs (subacute combined degeneration) and ↑ methylmalonic acid; folate does not.
Scurvy (vitamin C deficiency): Impaired collagen hydroxylation (proline/lysine) → poor wound healing, bleeding gums, corkscrew hairs, perifollicular hemorrhage.
Collagen types: I, II, III, IV: I = bone/skin/tendon (most common). II = cartilage. III = reticulin/granulation (Ehlers-Danlos). IV = basement membrane.
Osteogenesis imperfecta: Defective type I collagen (often COL1A1/2) → multiple fractures, blue sclerae, hearing loss, dental problems.
Marfan syndrome defect: FBN1 (fibrillin-1); autosomal dominant. Tall, arachnodactyly, lens dislocation (up/out), aortic root dilation/dissection.
Autosomal dominant vs recessive (general): Dominant: structural genes, often pleiotropic, vertical transmission. Recessive: enzyme deficiencies, often consanguinity, horizontal pattern.
X-linked recessive inheritance: No male-to-male transmission; sons of carrier mothers affected 50%. Examples: hemophilia A/B, DMD, G6PD, Lesch-Nyhan, Fabry.
Hardy-Weinberg: carrier frequency: p² + 2pq + q² = 1; p + q = 1. Disease allele frequency q; carrier frequency ≈ 2pq.
Trinucleotide repeat expansion diseases: Huntington (CAG), fragile X (CGG), myotonic dystrophy (CTG), Friedreich ataxia (GAA). Show anticipation.
Imprinting: Prader-Willi vs Angelman: Same 15q11-13 region. Prader-Willi: paternal deletion (hyperphagia, obesity). Angelman: maternal deletion ('happy puppet,' ataxia, seizures).
Cystic fibrosis defect: CFTR gene (chr 7, ΔF508), autosomal recessive → defective Cl⁻ channel; thick secretions, recurrent infections, ↑ sweat chloride.
DNA polymerase proofreading: DNA pol I and III (prokaryotes) have 3′→5′ exonuclease proofreading; pol I also removes RNA primers (5′→3′ exonuclease).
Lac operon regulation: Glucose absent (↑ cAMP, CAP binds, ↑ transcription) AND lactose present (allolactose removes repressor) → genes ON.
Gram-positive vs gram-negative cell wall: Gram-positive: thick peptidoglycan, stains purple. Gram-negative: thin peptidoglycan + LPS outer membrane (endotoxin), stains pink.
Catalase-positive organisms (matter in CGD): Cats Need PLACESS: Pseudomonas, Listeria, Aspergillus, Candida, E. coli, Staph aureus, Serratia, Nocardia, Burkholderia, H. pylori.
Staph aureus vs epidermidis vs saprophyticus: All catalase-positive cocci in clusters. S. aureus = coagulase-positive. S. epidermidis = coagulase-negative, novobiocin-sensitive. S. saprophyticus = novobiocin-resistant (young women UTI).
Streptococcus classification by hemolysis: α (partial, green): S. pneumoniae (optochin-S), viridans (optochin-R). β (clear): Group A (bacitracin-S), Group B (bacitracin-R). γ (none): enterococci.
Exotoxin: diphtheria & Pseudomonas exotoxin A: ADP-ribosylate EF-2 → inhibit protein synthesis. Diphtheria: pseudomembranous pharyngitis, myocarditis.
Cholera & ETEC heat-labile toxin mechanism: ADP-ribosylate Gs → ↑ adenylate cyclase → ↑ cAMP → Cl⁻ and water secretion → watery diarrhea.
Pertussis toxin mechanism: ADP-ribosylates Gi (disables inhibition) → ↑ cAMP; whooping cough, lymphocytosis.
Shiga & Shiga-like toxin: Inactivate 60S ribosome (cleave rRNA) → inhibit protein synthesis. EHEC O157:H7 → HUS (thrombocytopenia, hemolysis, AKI).
Endotoxin (LPS) effects: Lipid A activates macrophages (TNF, IL-1, IL-6), complement (C3a/C5a), and the coagulation cascade → fever, hypotension, DIC, shock.
Obligate intracellular organisms: Rickettsia and Chlamydia ('stay inside, can't make own ATP'). Chlamydia also can't make peptidoglycan.
Spore-forming bacteria: Bacillus and Clostridium (gram-positive). Spores contain dipicolinic acid; resist heat and chemicals.
Lactose-fermenting enteric gram-negative rods: MacConKEE'S: Klebsiella, E. coli, Enterobacter, Serratia (pink on MacConkey). Citrobacter is a slow/late fermenter.
Pseudomonas aeruginosa: Aerobic, oxidase-positive, non-lactose fermenting gram-negative rod; blue-green pigment, grape odor. Burns, CF, hot-tub folliculitis, ecthyma gangrenosum.
DNA viruses (general rules): All DNA viruses are double-stranded except Parvovirus (ssDNA), and all replicate in the nucleus except Poxvirus (cytoplasm).
Positive-sense RNA viruses: Genome acts directly as mRNA. Examples: picornavirus, calicivirus, flavivirus, togavirus, retrovirus, coronavirus, hepevirus.
Negative-sense RNA viruses: Must carry RNA-dependent RNA polymerase. 'Always Bring Polymerase Or Fail Replication': Arenavirus, Bunyavirus, Paramyxovirus, Orthomyxovirus, Filovirus, Rhabdovirus.
HIV genes and their products: gag → p24 capsid; pol → reverse transcriptase, integrase, protease; env → gp120 (attachment) and gp41 (fusion).
Tuberculosis (M. tuberculosis): Acid-fast (mycolic acid wall), aerobic; Ghon complex; cord factor → caseating granulomas. PPD: type IV hypersensitivity.
Aspergillus fumigatus: Septate hyphae branching at acute (45°) angles; ABPA, aspergilloma in old cavities, invasive disease in neutropenia.
Cryptococcus neoformans: Encapsulated yeast; India ink / mucicarmine; meningitis in AIDS. Latex agglutination for capsular antigen.
Innate vs adaptive immunity: Innate: fast, nonspecific, no memory (neutrophils, macrophages, NK, complement, barriers). Adaptive: slower, specific, memory (T and B cells, antibodies).
MHC class I vs class II: MHC I (all nucleated cells): endogenous antigen → CD8 T cells. MHC II (APCs): exogenous antigen → CD4 T cells. 'Rule of 8': 1×8=CD8, 2×4=CD4.
Th1 vs Th2 helper T cells: Th1 (IL-2, IFN-γ): activate macrophages and CD8 cells; cell-mediated. Th2 (IL-4, IL-5, IL-13): help B cells, IgE, eosinophils; humoral/allergy.
The four hypersensitivity reactions (ACID): I Anaphylactic (IgE, mast cells); II Cytotoxic (IgG/IgM vs cell antigen); III Immune complex (antigen-antibody); IV Delayed (T cells, no antibody).
Type III hypersensitivity examples: Immune-complex deposition: serum sickness, Arthus reaction, SLE, polyarteritis nodosa, post-streptococcal glomerulonephritis.
Antibody isotype functions: IgG: most abundant, crosses placenta, opsonization. IgA: secretions/mucosa (dimer). IgM: first made, pentamer, complement. IgE: allergy/parasites. IgD: B-cell receptor.
Complement: C3b, C3a/C5a, C5-9: C3b = opsonin. C3a, C4a, C5a = anaphylatoxins; C5a = neutrophil chemotaxis. C5b-9 = membrane attack complex (lysis).
C5-C9 (terminal complement) deficiency: Recurrent Neisseria infections (meningococcemia, gonococcemia) because MAC clears Neisseria.
Chronic granulomatous disease (CGD): NADPH oxidase defect → can't make reactive oxygen species; recurrent catalase-positive infections. Diagnose: abnormal dihydrorhodamine test.
DiGeorge syndrome: 22q11 deletion; failure of 3rd/4th pharyngeal pouches → thymic and parathyroid aplasia → T-cell deficiency, hypocalcemic tetany, cardiac defects.
Live attenuated vaccines (caution): Strong cellular + humoral response but risky in immunocompromised/pregnancy: MMR, varicella, intranasal flu, oral polio (Sabin), rotavirus, yellow fever, BCG.
Apoptosis vs necrosis: Apoptosis: programmed, ATP-dependent, single cells, NO inflammation, intact membranes. Necrosis: unregulated, groups of cells, inflammatory, membrane rupture.
Coagulative necrosis: Ischemic infarction of most solid organs (heart, kidney). Cell outlines preserved; protein denaturation. (Brain → liquefactive.)
The cardinal signs of acute inflammation: Rubor (redness), calor (heat), tumor (swelling), dolor (pain), and functio laesa (loss of function); from vasodilation, ↑ permeability, leukocytes.
Acute vs chronic inflammation cells: Acute: neutrophils (PMNs), short-lived. Chronic: lymphocytes, plasma cells, macrophages, with fibrosis and angiogenesis.
Granuloma formation requires which cytokines?: Macrophages present antigen → Th1 cells release IFN-γ → macrophages become epithelioid; TNF maintains the granuloma. Anti-TNF therapy can reactivate TB.
Transudate vs exudate: Transudate: ↓ protein, from ↑ hydrostatic or ↓ oncotic pressure (CHF, cirrhosis). Exudate: ↑ protein/cells, from inflammation/infection (Light's criteria).
Amyloidosis (key stain): Misfolded protein deposits; apple-green birefringence under polarized light with Congo red stain. AL (light chains), AA (chronic inflammation).
Single defining feature of malignancy: Metastasis — spread to a distant, non-adjacent site via blood, lymph, or body cavities.
Carcinoma vs sarcoma spread: Carcinomas (epithelial) spread first via lymphatics. Sarcomas (mesenchymal) spread first hematogenously.
Oncogenes vs tumor suppressors: Oncogene: gain of function, one allele (dominant) — RAS, MYC, HER2/neu. Tumor suppressor: loss of function, both alleles (two-hit) — TP53, RB, APC, BRCA.
Philadelphia chromosome: t(9;22) → BCR-ABL fusion (constitutive tyrosine kinase) in chronic myeloid leukemia; treat with imatinib.
Lines of Zahn: Alternating layers of platelets/fibrin and RBCs — indicate a thrombus formed before death (in flowing blood), distinguishing it from a post-mortem clot.
Virchow triad: Three risk factors for thrombosis: endothelial injury, stasis, and hypercoagulability.
Edema mechanisms (Starling forces): ↑ capillary hydrostatic pressure, ↓ plasma oncotic pressure (hypoalbuminemia), ↑ permeability, or lymphatic obstruction.
Phase I vs phase II drug metabolism: Phase I (CYP450): oxidation/reduction/hydrolysis → often active or toxic metabolites. Phase II: conjugation (glucuronidation, etc.) → usually inactive, water-soluble.
Zero-order vs first-order elimination: Zero-order: constant amount removed per time (ethanol, phenytoin, high-dose aspirin). First-order: constant fraction removed; constant half-life (most drugs).
Volume of distribution (Vd): Vd = amount of drug in body ÷ plasma concentration. High Vd = lipophilic/tissue-bound; low Vd = large/charged, stays in plasma.
Loading dose vs maintenance dose: Loading dose = Cp × Vd ÷ F (independent of clearance). Maintenance dose = Cp × CL ÷ F (depends on clearance).
Competitive vs non-competitive antagonist: Competitive: ↓ potency (right-shift), Emax unchanged, surmountable. Non-competitive: ↓ efficacy (↓ Emax), insurmountable.
Therapeutic index: TI = TD50 ÷ ED50 (or LD50 ÷ ED50). Higher = safer. Low-TI drugs: warfarin, digoxin, lithium, theophylline.
Cholinergic receptor types: Nicotinic (ligand-gated ion channel) at NMJ and autonomic ganglia; muscarinic (G-protein-coupled) at parasympathetic effector organs.
Adrenergic receptor effects: α1: vasoconstriction. α2: ↓ sympathetic outflow, ↓ insulin. β1: ↑ HR/contractility, renin. β2: vasodilation, bronchodilation. β3: lipolysis.
Cholinergic crisis vs overdose treatment: Organophosphate poisoning (DUMBBELSS) → treat with atropine (muscarinic) + pralidoxime (regenerates acetylcholinesterase if given early).
Vaughan-Williams antiarrhythmic classes: I Na⁺ blockers, II β-blockers, III K⁺ blockers (amiodarone, sotalol), IV non-DHP Ca²⁺ blockers (verapamil, diltiazem).
Statins mechanism and key adverse effect: Competitively inhibit HMG-CoA reductase → ↓ cholesterol synthesis, ↑ LDL receptors. Watch for myopathy/rhabdomyolysis and hepatotoxicity.
Acetaminophen overdose antidote: N-acetylcysteine — replenishes glutathione to detoxify the toxic NAPQI metabolite that causes hepatic necrosis.
Warfarin vs heparin: Warfarin: inhibits vitamin-K epoxide reductase (factors II, VII, IX, X, C, S); oral; monitor PT/INR; teratogen. Heparin: activates antithrombin; IV/SC; monitor PTT; safe in pregnancy.
Cardiac action potential phase 0 (ventricle): Rapid Na⁺ influx → depolarization upstroke.
Cardiac action potential phase 2 (plateau): Ca²⁺ influx balances K⁺ efflux → sustained contraction; unique to cardiac muscle.
SA node phase 4 (pacemaker): Spontaneous depolarization from the funny Na⁺ current (If) and Ca²⁺; sets the heart rate.
Cardiac output (CO) equation: CO = stroke volume × heart rate = (HR × SV); also CO = rate of O₂ consumption ÷ (arterial − venous O₂) (Fick principle).
Determinants of stroke volume: Preload, afterload, and contractility. ↑ preload or contractility ↑ SV; ↑ afterload ↓ SV.
Frank-Starling relationship: ↑ venous return (preload) → ↑ ventricular end-diastolic volume → ↑ stroke volume (greater sarcomere stretch).
Mean arterial pressure (MAP): MAP = diastolic + ⅓(systolic − diastolic) = cardiac output × total peripheral resistance.
Renin-angiotensin-aldosterone system: ↓ renal perfusion → renin → angiotensin I → (ACE, lung) angiotensin II → vasoconstriction + aldosterone (Na⁺/water retention) + ADH + thirst.
Glomerular filtration rate (GFR) marker: Inulin (freely filtered, not secreted or reabsorbed). Creatinine clearance slightly overestimates GFR. GFR = Kf[(PGC − PBS) − πGC].
Where is most filtered sodium reabsorbed?: The proximal convoluted tubule (~65–70%), isosmotically with water.
Loop diuretic vs thiazide site: Loop (furosemide): thick ascending limb Na-K-2Cl. Thiazide: distal convoluted tubule Na-Cl. Thiazide can cause hypercalcemia; loops cause hypocalcemia.
Henderson-Hasselbalch / acid-base: pH = 6.1 + log([HCO₃⁻]/0.03·PCO₂). Metabolic acidosis: ↓ HCO₃⁻; respiratory acidosis: ↑ PCO₂. Use the anion gap for metabolic acidosis.
Anion gap and its causes (MUDPILES): Anion gap = Na⁺ − (Cl⁻ + HCO₃⁻); normal 8–12. High-gap acidosis: Methanol, Uremia, DKA, Propylene glycol, Iron/INH, Lactic acidosis, Ethylene glycol, Salicylates.
Oxygen-hemoglobin dissociation curve (right shift): Right shift = ↓ O₂ affinity (unloads to tissues): ↑ CO₂, ↑ H⁺ (↓ pH), ↑ temperature, ↑ 2,3-BPG (Bohr effect).
Lung volumes: FRC and residual volume: FRC = ERV + RV (volume after normal expiration). RV (residual volume) and any capacity containing it cannot be measured by spirometry.
Obstructive vs restrictive lung disease (PFTs): Obstructive: ↓ FEV1/FVC ratio (<0.7), ↑ lung volumes (asthma, COPD). Restrictive: normal/↑ ratio, ↓ all volumes (fibrosis).
Insulin vs glucagon actions: Insulin: anabolic — ↑ glucose uptake (GLUT4), glycogenesis, lipogenesis; ↓ blood glucose. Glucagon: catabolic — glycogenolysis, gluconeogenesis, lipolysis.
Anterior vs posterior pituitary hormones: Anterior (FLAT PiG): FSH, LH, ACTH, TSH, Prolactin, GH. Posterior (stores hypothalamic): ADH and oxytocin.
Cortisol functions: ↑ gluconeogenesis, ↑ blood glucose, anti-inflammatory/immunosuppressive, ↑ blood pressure (vascular sensitivity), bone loss; follows circadian rhythm.
Brachial plexus: Erb-Duchenne vs Klumpke: Erb-Duchenne: upper trunk (C5-C6), 'waiter's tip.' Klumpke: lower trunk (C8-T1), claw hand.
Radial nerve injury: Mid-shaft humeral fracture ('Saturday night palsy') → wrist drop, loss of extension and supination; sensory loss over dorsal hand.
Common peroneal (fibular) nerve injury: Fibular neck injury or leg crossing → foot drop, loss of dorsiflexion and eversion; 'PED = Peroneal Everts and Dorsiflexes.'
Horner syndrome: Ptosis, miosis, anhidrosis from interruption of the cervical sympathetic chain (e.g., Pancoast tumor, carotid dissection).
Spinal cord: dorsal columns: Carry fine touch, vibration, proprioception; ascend ipsilaterally then decussate in the medulla. Damaged in B12 deficiency and tabes dorsalis.
Spinothalamic tract: Carries pain and temperature; decussates within ~2 levels in the anterior white commissure (syringomyelia affects this first — 'cape' distribution).
Upper vs lower motor neuron lesion: UMN: spastic, ↑ tone, hyperreflexia, ↑ Babinski. LMN: flaccid, ↓ tone, hyporeflexia, atrophy, fasciculations.
Broca vs Wernicke aphasia: Broca (inferior frontal, MCA): non-fluent, comprehension intact, frustrated. Wernicke (superior temporal): fluent but nonsensical, poor comprehension.
Cerebellar lesion signs: Ipsilateral deficits: ataxia, intention tremor, dysmetria, dysdiadochokinesia, nystagmus; wide-based gait (vermis).
Parkinson disease pathology: Loss of dopaminergic neurons in the substantia nigra pars compacta; Lewy bodies (α-synuclein). TRAP: tremor, rigidity, akinesia, postural instability.
Neurotransmitter changes in disease: ↓ Dopamine/↑ ACh: Parkinson. ↓ ACh: Alzheimer. ↓ GABA + ACh: Huntington. ↑ Dopamine: schizophrenia. ↓ Serotonin/NE: depression.
Berry (saccular) aneurysm: Rupture → subarachnoid hemorrhage ('worst headache of my life'); associated with ADPKD, Ehlers-Danlos; at circle of Willis branch points.
Epidural vs subdural hematoma: Epidural: middle meningeal artery, lucid interval, lens-shaped (won't cross sutures). Subdural: bridging veins, crescent-shaped, crosses sutures (elderly, alcoholics).
Stages of sleep (REM): REM: dreaming, atonia, rapid eye movements, EEG resembles wakefulness (beta/sawtooth); ↑ throughout the night; ACh-driven; first ~90 min after sleep onset.
Classical vs operant conditioning: Classical (Pavlov): pair stimuli to elicit a reflex. Operant (Skinner): behavior shaped by reinforcement (↑ behavior) or punishment (↓ behavior).
Sensitivity and SnNout: Sensitivity = TP/(TP+FN) = true-positive rate. A highly Sensitive test, when Negative, rules a disease OUT (SnNout). High sensitivity = good screening test.
Specificity and SpPin: Specificity = TN/(TN+FP) = true-negative rate. A highly Specific test, when Positive, rules a disease IN (SpPin). High specificity = good confirmatory test.
Positive predictive value (PPV) and prevalence: PPV = TP/(TP+FP) = probability of disease given a positive test. PPV rises with prevalence; NPV falls with prevalence.
Likelihood ratios: LR+ = sensitivity/(1−specificity); LR− = (1−sensitivity)/specificity. Independent of prevalence. LR+ >10 or LR− <0.1 strongly changes probability.
Relative risk vs odds ratio: RR (cohort): risk in exposed ÷ risk in unexposed. OR (case-control): odds of exposure in cases ÷ controls; approximates RR for rare diseases.
Number needed to treat (NNT): NNT = 1 ÷ absolute risk reduction (ARR). The number of patients to treat to prevent one bad outcome; lower = more effective.
Type I vs type II error: Type I (α): rejecting a true null — false positive. Type II (β): failing to reject a false null — false negative. Power = 1 − β.
Confidence interval and significance: A 95% CI for a difference of means that includes 0 → not significant; for a ratio (RR/OR) that includes 1 → not significant.
Confounding vs effect modification: Confounding: a third variable distorts the exposure-outcome link (control with stratification, matching, multivariate). Effect modification: the effect truly differs across strata.
Selection bias examples: Berkson bias (hospital controls), healthy-worker effect, loss to follow-up; the study sample isn't representative of the target population.
Lead-time vs length-time bias: Lead-time: screening detects disease earlier, falsely lengthening apparent survival. Length-time: screening preferentially catches slow, indolent disease.
Disulfiram-like reaction drugs: Metronidazole, certain cephalosporins, sulfonylureas, griseofulvin → flushing, nausea, headache with alcohol (acetaldehyde accumulation).
Aminoglycosides: Bind 30S, inhibit protein synthesis (bactericidal); for gram-negative aerobes. Adverse: nephrotoxicity, ototoxicity; require O₂ for uptake.
Beta-lactam mechanism: Penicillins/cephalosporins bind penicillin-binding proteins → block transpeptidase (cell-wall cross-linking) → bactericidal. Resistance: β-lactamase.
Fluoroquinolone adverse effects: Inhibit DNA gyrase/topoisomerase IV. Tendon rupture (avoid in children/elderly), QT prolongation, cartilage damage; avoid with antacids.
Anticancer cell-cycle specificity: Methotrexate/5-FU (S phase, antimetabolites), vinca alkaloids (M, block microtubule assembly), paclitaxel (M, stabilize microtubules), bleomycin (G2).
Serotonin syndrome: Excess serotonergic activity (SSRIs + MAOIs/tramadol/triptans) → autonomic instability, hyperthermia, clonus, agitation. Treat: cyproheptadine.
Down syndrome (trisomy 21) features: Most common viable trisomy; intellectual disability, flat facies, single palmar crease, duodenal atresia, AV septal defect, ↑ Alzheimer/ALL risk.
Diabetic ketoacidosis vs HHS: DKA (type 1): ketones, anion-gap acidosis, Kussmaul breathing, fruity breath. HHS (type 2): profound hyperglycemia, hyperosmolarity, minimal ketones.
Nephrotic vs nephritic syndrome: Nephrotic: proteinuria >3.5 g/day, edema, hypoalbuminemia, hyperlipidemia. Nephritic: hematuria, RBC casts, hypertension, mild proteinuria, azotemia.
Goodpasture syndrome: Anti-glomerular basement membrane antibodies (type II hypersensitivity) → rapidly progressive glomerulonephritis + pulmonary hemorrhage; linear IF.
Charcot triad (cholangitis): Fever, jaundice, right-upper-quadrant pain. Add hypotension + confusion (Reynolds pentad) for suppurative cholangitis.
Cushing syndrome vs Addison disease: Cushing: excess cortisol — central obesity, striae, hyperglycemia, hypertension. Addison: adrenal insufficiency — hypotension, hyperpigmentation, hyperkalemia.
Multiple endocrine neoplasia (MEN): MEN1 (3 P's: pituitary, parathyroid, pancreas). MEN2A (medullary thyroid, pheo, parathyroid). MEN2B (medullary thyroid, pheo, mucosal neuromas, marfanoid). RET in 2A/2B.
Hyperkalemia ECG changes: Peaked T waves → widened QRS → loss of P waves → sine wave → asystole. Treat: calcium gluconate (membrane), insulin + glucose, albuterol (shift).
Reversible vs irreversible cell injury (hallmark): Reversible: cellular swelling, ribosome detachment, membrane blebbing. Irreversible (point of no return): mitochondrial damage and membrane disruption.
Standard error of the mean (SEM): SEM = standard deviation ÷ √n. SEM decreases as sample size increases; SEM < SD.
Normal distribution (empirical rule): ~68% within 1 SD of the mean, ~95% within 2 SD, ~99.7% within 3 SD. Mean = median = mode.
Positive vs negative skew: Positive (right) skew: mean > median > mode (tail to the right). Negative (left) skew: mean < median < mode.
Cori cycle: Lactate from anaerobic muscle/RBCs travels to the liver, is converted back to glucose via gluconeogenesis, and returns to tissue — shifts the metabolic burden to the liver.
Glucose-alanine cycle: Muscle transaminates pyruvate to alanine (carrying nitrogen) → liver → glucose + urea; transports amino-acid nitrogen safely to the liver.
NADPH sources and uses: Made by the pentose phosphate pathway (G6PD), malic enzyme, and isocitrate dehydrogenase. Used for fatty-acid/cholesterol synthesis, glutathione reduction, and the respiratory burst.
Fragile X syndrome: CGG repeat expansion in FMR1 (X-linked dominant); most common inherited cause of intellectual disability; long face, large ears, macroorchidism.
Mitochondrial (maternal) inheritance: Transmitted only from the mother; all offspring may be affected; heteroplasmy causes variable expression. Examples: MELAS, Leber hereditary optic neuropathy.
Lyonization (X-inactivation): Random inactivation of one X chromosome in females (forms a Barr body); explains variable expression in X-linked carriers.
Northern, Southern, Western blots: Southern = DNA, Northern = RNA, Western = protein. SNoW DRoP: Southern-DNA, Northern-RNA, Western-Protein.
Start and stop codons: Start: AUG (methionine). Stop: UGA, UAA, UAG ('U Go Away, U Are Away, U Are Gone'). The genetic code is degenerate and unambiguous.
Essential amino acids: PVT TIM HaLL: Phenylalanine, Valine, Threonine, Tryptophan, Isoleucine, Methionine, Histidine, Leucine, Lysine (and arginine in growth).
Fat-soluble vitamins: A, D, E, K — stored in fat; toxicity possible; malabsorption (steatorrhea, CF) causes deficiency. Water-soluble (B, C) wash out except B12.
Clostridium difficile: Toxins A and B → pseudomembranous colitis after antibiotics (clindamycin, fluoroquinolones). Diagnose by toxin/PCR; treat with oral vancomycin or fidaxomicin.
Clostridium tetani vs botulinum toxin: Tetanus toxin blocks GABA/glycine release (spastic paralysis, lockjaw). Botulinum blocks acetylcholine release (flaccid paralysis, floppy baby).
Neisseria meningitidis vs gonorrhoeae: Both gram-negative diplococci, oxidase-positive. Meningitidis: capsule, maltose-fermenter, vaccine. Gonorrhoeae: no capsule/vaccine, no maltose; sexually transmitted.
Helicobacter pylori: Curved gram-negative rod, urease-positive; causes gastritis, peptic ulcers, gastric adenocarcinoma/MALT lymphoma. Triple therapy: PPI + clarithromycin + amoxicillin.
Treponema pallidum (syphilis stages): Primary: painless chancre. Secondary: rash (palms/soles), condylomata lata. Tertiary: gummas, aortitis, neurosyphilis. Diagnose: dark-field, VDRL/RPR + FTA-ABS.
Borrelia burgdorferi (Lyme disease): Spirochete from Ixodes tick (deer/mouse reservoir); erythema migrans (target rash) → cardiac/neuro → arthritis. Treat: doxycycline.
TORCH infections: Congenital infections crossing the placenta: Toxoplasma, Other (syphilis), Rubella, CMV, HSV/HIV. Cause growth restriction and birth defects.
Hepatitis B serology: HBsAg, anti-HBs, anti-HBc: HBsAg = active infection. Anti-HBs = immunity (vaccine or recovery). Anti-HBc IgM = acute/window. HBeAg = high infectivity.
Plasmodium (malaria): Anopheles mosquito; cyclic fevers; ring forms in RBCs. P. falciparum is most severe; P. vivax/ovale have a dormant liver hypnozoite (add primaquine).
Pneumocystis jirovecii pneumonia: Fungal opportunist in AIDS (CD4 <200); diffuse interstitial infiltrate, ↓ O₂. Diagnose: silver stain (disc-shaped). Prophylaxis/treat: TMP-SMX.
Antibody affinity maturation & class switching: Occur in the germinal center; require CD40L (T cell) and cytokines; somatic hypermutation improves affinity. IgM → IgG/IgA/IgE.
Anergy and central vs peripheral tolerance: Central tolerance: deletion of self-reactive T cells (thymus) and B cells (marrow). Peripheral tolerance: anergy, regulatory T cells, when self-antigen encountered without costimulation.
Natural killer (NK) cells: Innate lymphocytes; kill cells lacking MHC I (virally infected, tumor) and antibody-coated cells (ADCC); enhanced by IL-2, IL-12, IFN.
Superantigens: Cross-link MHC II and the T-cell receptor outside the antigen groove → massive nonspecific T-cell activation and cytokine release. TSST-1 (S. aureus), Strep pyogenic exotoxin.
Hyperacute vs acute vs chronic transplant rejection: Hyperacute: minutes, preformed antibodies. Acute: weeks, cellular (T-cell) ± antibody. Chronic: months-years, vascular fibrosis (e.g., bronchiolitis obliterans).
Severe combined immunodeficiency (SCID): Defective B and T cells (adenosine deaminase deficiency or X-linked IL-2R γ-chain); recurrent severe infections; treat with bone marrow transplant.
Psammoma bodies: Laminated calcifications seen in papillary thyroid carcinoma, serous ovarian cystadenocarcinoma, meningioma, and mesothelioma (PSaMMoma).
Metaplasia, dysplasia, anaplasia: Metaplasia: reversible change of one mature cell type to another (Barrett esophagus). Dysplasia: disordered, pre-cancerous growth. Anaplasia: undifferentiated, malignant.
Tumor markers: AFP (HCC, yolk sac), CEA (colon), CA-125 (ovarian), PSA (prostate), CA 19-9 (pancreatic), β-hCG (choriocarcinoma), S-100 (melanoma).
Granulomatosis with polyangiitis (Wegener): c-ANCA (anti-PR3); triad of upper airway (sinusitis), lung (nodules/hemorrhage), and kidney (glomerulonephritis).
Atherosclerosis progression: Endothelial injury → LDL oxidation → macrophage foam cells (fatty streak) → fibrous plaque (smooth muscle, collagen) → complicated plaque (rupture, thrombosis).
Left vs right heart failure signs: Left: pulmonary congestion (dyspnea, orthopnea, crackles). Right: systemic congestion (JVD, hepatomegaly, peripheral edema). Left failure is the most common cause of right failure.
Iron studies in iron-deficiency vs anemia of chronic disease: Iron deficiency: ↓ ferritin, ↑ TIBC, ↓ iron. Anemia of chronic disease: ↑ ferritin, ↓ TIBC, ↓ iron (iron sequestered by hepcidin).
Acute promyelocytic leukemia (APL): AML subtype M3, t(15;17) PML-RARA; Auer rods, risk of DIC; treat with all-trans retinoic acid (ATRA).
Hodgkin vs non-Hodgkin lymphoma: Hodgkin: Reed-Sternberg cells, contiguous spread, bimodal age, better prognosis. Non-Hodgkin: B/T cells, noncontiguous, more extranodal, often older adults.
Acetaminophen vs aspirin mechanism: Aspirin: irreversible COX-1/COX-2 inhibition (antiplatelet). Acetaminophen: reversible, mostly central COX inhibition; minimal anti-inflammatory/antiplatelet effect.
ACE inhibitors: effect and adverse effects: ↓ angiotensin II and ↑ bradykinin → vasodilation, ↓ aldosterone. Adverse: dry cough, angioedema, hyperkalemia, ↑ creatinine; teratogen (avoid in pregnancy).
Digoxin mechanism and toxicity: Inhibits Na⁺/K⁺-ATPase → ↑ intracellular Ca²⁺ (positive inotrope), ↑ vagal tone. Toxicity: nausea, yellow vision, arrhythmias; worsened by hypokalemia. Antidote: digoxin Fab.
SSRIs vs MAOIs (washout): Both ↑ serotonin. MAOIs risk hypertensive crisis with tyramine and serotonin syndrome with SSRIs — need a washout period between them.
Benzodiazepines vs barbiturates (GABA-A): Benzos: ↑ frequency of Cl⁻ channel opening (safer). Barbiturates: ↑ duration of Cl⁻ channel opening (more dangerous; respiratory depression). Reverse benzos with flumazenil.
Inhaled anesthetic potency (MAC): Minimum alveolar concentration to prevent movement in 50%; ↑ lipid solubility = ↑ potency = ↓ MAC.
Cytochrome P450 inducers vs inhibitors: Inducers (↓ drug levels): rifampin, phenytoin, carbamazepine, barbiturates, St. John's wort, chronic alcohol. Inhibitors (↑ levels): macrolides, azoles, grapefruit, cimetidine, ritonavir.
Sympathomimetics: epinephrine vs norepinephrine vs phenylephrine: Epinephrine: α and β. Norepinephrine: α1 > β1 (reflex bradycardia). Phenylephrine: pure α1 (vasoconstriction).
Insulin signaling vs glucagon signaling: Insulin: receptor tyrosine kinase. Glucagon and epinephrine (β): Gs → ↑ cAMP → protein kinase A. α1: Gq → IP3/DAG → ↑ Ca²⁺.
Second messenger systems (Gs, Gi, Gq): Gs: ↑ adenylate cyclase → ↑ cAMP. Gi: ↓ cAMP. Gq: phospholipase C → IP3 (↑ Ca²⁺) + DAG. ('Qiss and Qiqq till you're Siq of Sqs.')
Skeletal muscle excitation-contraction coupling: Action potential → T-tubule → DHP receptor → ryanodine receptor → Ca²⁺ from SR → Ca²⁺ binds troponin C → tropomyosin moves → cross-bridge cycling.
Smooth vs skeletal muscle contraction: Skeletal: Ca²⁺ binds troponin C. Smooth: Ca²⁺ binds calmodulin → myosin light-chain kinase phosphorylates myosin. No troponin in smooth muscle.
Thyroid hormone synthesis: Iodide trapped, oxidized by thyroid peroxidase, organified onto thyroglobulin (MIT/DIT) → T3/T4. Wolff-Chaikoff: excess iodide ↓ synthesis.
PTH actions: ↑ bone resorption (Ca²⁺ and phosphate release), ↑ renal Ca²⁺ reabsorption + ↑ phosphate excretion, ↑ activation of vitamin D (1-α-hydroxylase). Net: ↑ serum Ca²⁺, ↓ phosphate.
Calcium and the action potential / nerve: Hypocalcemia → ↑ excitability (Chvostek, Trousseau signs, tetany). Hypercalcemia → 'stones, bones, groans, psychiatric overtones.'
Fetal circulation shunts: Ductus venosus (umbilical vein → IVC, bypass liver), foramen ovale (RA → LA), ductus arteriosus (pulmonary artery → aorta, bypass lungs). Close after birth.
Glucose transporters (GLUT): GLUT1: RBCs, brain. GLUT2: β cells, liver, kidney (bidirectional sensor). GLUT4: muscle and adipose (insulin-dependent).
Facial nerve (CN VII) palsy: central vs peripheral: Central (UMN, stroke): spares the forehead (bilateral upper innervation). Peripheral (LMN, Bell palsy): whole side of the face, including the forehead.
Cavernous sinus contents: Cranial nerves III, IV, V1, V2, and VI, plus the internal carotid artery; CN VI is most medial (first affected by thrombosis).
Internal capsule / lacunar stroke: Pure motor stroke (posterior limb) from small-vessel disease (hypertension, diabetes); contralateral hemiparesis without cortical signs.
Hippocampus and memory: The hippocampus consolidates new declarative (explicit) memories; bilateral damage → anterograde amnesia. The amygdala handles fear/emotion.
Carpal tunnel syndrome: Median nerve compression at the wrist → thenar atrophy, numbness of the lateral 3½ digits; positive Phalen and Tinel signs. Associations: pregnancy, hypothyroidism, diabetes.
Aortic arch derivatives: 3rd → common carotid. 4th → aortic arch (left) / proximal subclavian (right). 6th → pulmonary arteries and (left) ductus arteriosus.
Pharyngeal (branchial) arch nerves: Arch 1 = CN V3, arch 2 = CN VII, arch 3 = CN IX, arch 4 and 6 = CN X. ('1, 5; 2, 7; 3, 9; 4 and 6, 10.')
Defense mechanisms: mature vs immature: Mature (healthy): sublimation, suppression, altruism, humor. Immature: denial, projection, displacement, splitting, regression, acting out.
Kübler-Ross stages of grief: Denial, Anger, Bargaining, Depression, Acceptance — not necessarily in order and may occur simultaneously.
Ego defense: projection vs displacement: Projection: attributing one's own unacceptable feelings to others. Displacement: redirecting emotions to a neutral target (yelling at family after a bad day).
Informed consent and exceptions: Requires capacity, disclosure, understanding, voluntariness. Exceptions: emergencies, waiver, therapeutic privilege (rare), implied consent.
Confidence interval width and sample size: Larger sample size → narrower (more precise) confidence interval; a higher confidence level (99% vs 95%) → wider interval.
Sensitivity-specificity trade-off (ROC curve): Lowering the cutoff ↑ sensitivity, ↓ specificity. The ROC curve plots true-positive vs false-positive rate; greater area under the curve = better test.
Incidence vs prevalence: Incidence = new cases ÷ population at risk over time. Prevalence = existing cases ÷ total population. Prevalence ≈ incidence × disease duration.
Cohort vs case-control study: Cohort: follows exposed vs unexposed forward → relative risk; good for rare exposures. Case-control: looks back from disease → odds ratio; good for rare diseases.
Randomized controlled trial: Gold standard for causation; randomization minimizes confounding; blinding minimizes bias. Phase I (safety), II (efficacy/dose), III (vs standard), IV (post-marketing).
Meta-analysis and publication bias: Pools data from multiple studies for greater power; limited by the quality of included studies and publication bias (negative studies underpublished; funnel-plot asymmetry).
p-value meaning: Probability of obtaining a result as extreme as observed if the null hypothesis were true; p < 0.05 conventionally 'significant.' It does NOT give effect size.
Hardy-Weinberg assumptions: No mutation, no migration, no selection, random mating, large population. Violations cause allele frequencies to change (evolution).
Ehlers-Danlos syndrome: Defective collagen (often type III/V) → hyperextensible skin, hypermobile joints, easy bruising; vascular type risks arterial/organ rupture.
Alkaptonuria: Homogentisate oxidase deficiency → homogentisic acid buildup; dark urine on standing, ochronosis (dark cartilage), arthralgias. Benign.
Lesch-Nyhan syndrome: HGPRT deficiency (X-linked) → defective purine salvage → ↑ uric acid; gout, self-mutilation, intellectual disability, dystonia.
Wilson disease vs hemochromatosis: Wilson: copper accumulation (↓ ceruloplasmin, Kayser-Fleischer rings, hepatolenticular). Hemochromatosis: iron overload (HFE gene; 'bronze diabetes,' cirrhosis, cardiomyopathy).
Asthma vs COPD pathology: Asthma: reversible bronchoconstriction, eosinophils, Curschmann spirals, Charcot-Leyden crystals. COPD: chronic bronchitis (Reid index ↑) and/or emphysema (alveolar destruction).
Alpha-1 antitrypsin deficiency: Unopposed elastase → panacinar emphysema (especially in young nonsmokers) and liver cirrhosis (PAS-positive globules). Misfolded protein accumulates in hepatocytes.
Squamous cell vs adenocarcinoma of the lung: Squamous: central, smoking, cavitation, hypercalcemia (PTHrP), keratin pearls. Adenocarcinoma: peripheral, most common overall, mucin, can occur in nonsmokers.
Crohn disease vs ulcerative colitis: Crohn: skip lesions, transmural, anywhere (mouth-to-anus), granulomas, fistulas. UC: continuous, mucosa-only, rectum→colon, crypt abscesses, ↑ colon cancer risk.
Cirrhosis complications: Portal hypertension (varices, ascites, caput medusae, splenomegaly), hepatic encephalopathy (↑ ammonia), coagulopathy, hepatorenal syndrome, ↑ HCC risk.
Acute pancreatitis causes (GET SMASHED): Gallstones, Ethanol, Trauma, Steroids, Mumps, Autoimmune, Scorpion, Hypercalcemia/Hypertriglyceridemia, ERCP, Drugs. ↑ amylase and lipase.
Glomerular disease: minimal change vs FSGS: Minimal change: most common nephrotic in kids, normal light microscopy, effaced foot processes on EM, steroid-responsive. FSGS: HIV/obesity, segmental sclerosis.
IgA nephropathy (Berger disease): Most common glomerulonephritis worldwide; gross hematuria 1–2 days after a respiratory/GI infection; mesangial IgA deposits.
Prostate vs BPH location: BPH: transition zone (urinary obstruction). Prostate adenocarcinoma: peripheral zone (palpable on DRE); ↑ PSA, osteoblastic bone metastases.
Breast cancer receptors and prognosis: ER/PR-positive → hormone therapy (tamoxifen). HER2-positive → trastuzumab. Triple-negative → worse prognosis; BRCA association.
Antidote: opioid overdose: Naloxone (opioid receptor antagonist) reverses respiratory depression, miosis, and CNS depression.
Antidote: benzodiazepine overdose: Flumazenil (GABA-A antagonist); use cautiously — can precipitate seizures in chronic users.
Antidote: heparin vs warfarin: Heparin reversal: protamine sulfate. Warfarin reversal: vitamin K (slow) and fresh frozen plasma or PCC (fast).
Antidote: methanol/ethylene glycol: Fomepizole (alcohol dehydrogenase inhibitor), or ethanol; add dialysis. Ethylene glycol → calcium oxalate crystals, renal failure.
Sulfonylureas vs metformin: Sulfonylureas: close β-cell K⁺ channels → ↑ insulin release (risk hypoglycemia). Metformin: ↓ hepatic gluconeogenesis, ↑ insulin sensitivity (risk lactic acidosis; no hypoglycemia).
Loop vs thiazide vs K-sparing diuretic effects: Loop: ↓ Ca²⁺, ↓ K⁺. Thiazide: ↑ Ca²⁺, ↓ K⁺, hyperglycemia, hyperuricemia. K-sparing (spironolactone): ↑ K⁺, antiandrogen effects.
Chemotherapy toxicities to know: Doxorubicin (cardiotoxicity), bleomycin/busulfan (pulmonary fibrosis), cisplatin (nephro/ototoxicity), vincristine (neuropathy), cyclophosphamide (hemorrhagic cystitis).
Compliance (lung physiology): Compliance = ΔV/ΔP; the ease of lung expansion. ↑ in emphysema (lost elastic recoil); ↓ in fibrosis and surfactant deficiency.
Surfactant: Made by type II pneumocytes (dipalmitoylphosphatidylcholine); ↓ alveolar surface tension, prevents collapse. Deficiency → neonatal respiratory distress syndrome.
V/Q mismatch extremes: V/Q → 0 = shunt (airway obstruction; not corrected by O₂). V/Q → ∞ = dead space (pulmonary embolism). Apex has higher V/Q than the base.
Renal clearance of PAH: Para-aminohippuric acid is filtered AND secreted (nearly completely cleared) → estimates effective renal plasma flow.
Aldosterone vs ADH: Aldosterone: ↑ Na⁺ reabsorption (and K⁺/H⁺ secretion) in the collecting duct. ADH: ↑ water reabsorption via aquaporins in the collecting duct.
GI hormones: gastrin, secretin, CCK: Gastrin: ↑ gastric acid (G cells). Secretin: ↑ bicarbonate (S cells, neutralize acid). CCK: ↑ pancreatic enzymes, gallbladder contraction (I cells).
Baroreceptor reflex: ↓ BP → ↓ carotid sinus stretch → ↓ afferent firing → ↑ sympathetic, ↓ parasympathetic → ↑ HR and vasoconstriction to restore BP.
Reye syndrome: Aspirin given to a child with a viral illness (influenza, varicella) → mitochondrial dysfunction → hepatic encephalopathy and fatty liver. Avoid aspirin in children.
Klinefelter vs Turner syndrome: Klinefelter (47,XXY): tall, small testes, gynecomastia, infertility, ↑ FSH/LH. Turner (45,XO): short, webbed neck, streak ovaries, coarctation, ↑ FSH/LH.
Diabetes mellitus type 1 vs type 2: Type 1: autoimmune β-cell destruction (anti-GAD), absolute insulin deficiency, ketosis-prone, HLA-DR3/DR4. Type 2: insulin resistance + relative deficiency, obesity-linked.
Hemoglobin A1c: Glycated hemoglobin reflecting average glucose over ~3 months (RBC lifespan); ≥6.5% diagnoses diabetes. Falsely low with hemolysis/blood loss.
SIADH vs diabetes insipidus: SIADH: too much ADH → euvolemic hyponatremia, concentrated urine. Diabetes insipidus: too little ADH (central) or renal resistance (nephrogenic) → dilute urine, hypernatremia.
Acromegaly: Excess GH/IGF-1 after epiphyseal closure (pituitary adenoma) → enlarged hands/feet/jaw, organomegaly, glucose intolerance. In children → gigantism.
Pheochromocytoma rule of 10s: Catecholamine-secreting adrenal medulla tumor: ~10% bilateral, malignant, extra-adrenal, familial. Episodic hypertension, headache, palpitations, sweating. Diagnose: urine/plasma metanephrines.
Hashimoto vs Graves disease: Hashimoto: autoimmune hypothyroidism (anti-TPO/thyroglobulin, lymphocytic infiltrate). Graves: hyperthyroidism (TSI antibodies), exophthalmos, pretibial myxedema.
Sickle cell disease: Glutamate → valine at position 6 of β-globin (HbS); RBCs sickle when deoxygenated → vaso-occlusion, hemolysis, autosplenectomy, ↑ encapsulated-organism infections.
Thalassemia (alpha vs beta): Reduced globin chain production → microcytic anemia, target cells. α: gene deletions. β: point mutations (HbA2 ↑ in β-thalassemia minor).
DIC (disseminated intravascular coagulation): Widespread activation of coagulation → consumes platelets and factors → bleeding + thrombosis. ↓ platelets, ↑ PT/PTT, ↑ D-dimer, ↓ fibrinogen, schistocytes.
Bleeding: platelet vs coagulation disorder: Platelet/vessel (↓ platelets, vWD): mucocutaneous bleeding, petechiae, ↑ bleeding time. Coagulation factor (hemophilia): deep bleeding, hemarthrosis, ↑ PTT.
von Willebrand disease: Most common inherited bleeding disorder; defective vWF → ↓ platelet adhesion + ↓ factor VIII half-life. ↑ bleeding time, ↑ PTT; treat with desmopressin.
Hemolytic disease of the newborn (Rh): Rh-negative mother sensitized to an Rh-positive fetus → maternal anti-D IgG crosses placenta in a later pregnancy → fetal hemolysis. Prevent with anti-D (RhoGAM).
Pott disease: Tuberculous infection of the vertebral bodies → back pain, vertebral collapse, possible paraplegia and psoas abscess.
Rabies virus: Negative-sense RNA (Rhabdovirus, bullet-shaped); travels retrograde up axons to the CNS; Negri bodies; hydrophobia. Post-exposure: vaccine + immunoglobulin.
Most common cause of bacterial meningitis by age: Neonates: Group B Strep, E. coli, Listeria. Children/adults: S. pneumoniae, N. meningitidis. Elderly/immunocompromised: add Listeria.
CSF findings: bacterial vs viral meningitis: Bacterial: ↑↑ neutrophils, ↑ protein, ↓ glucose. Viral: ↑ lymphocytes, normal/↑ protein, normal glucose. Fungal/TB: lymphocytes, ↑ protein, ↓ glucose.
Vitamin D activation pathway: Skin (UV) → cholecalciferol → liver (25-hydroxylation) → kidney (1-α-hydroxylase, PTH-driven) → 1,25-(OH)₂-D (calcitriol), the active form; ↑ gut Ca²⁺/phosphate absorption.
Rickets vs osteomalacia: Both from vitamin D deficiency → defective bone mineralization. Rickets in children (bowed legs, growth plates). Osteomalacia in adults (bone pain, fractures).
Osteoporosis vs osteopetrosis: Osteoporosis: ↓ bone mass (normal mineralization), fragility fractures. Osteopetrosis: defective osteoclasts (carbonic anhydrase II) → dense, brittle bone, marrow failure.
Multiple sclerosis: Autoimmune CNS demyelination (oligodendrocytes); relapsing-remitting; periventricular plaques on MRI, oligoclonal bands in CSF; optic neuritis, internuclear ophthalmoplegia.
Guillain-Barré syndrome: Acute inflammatory demyelinating polyneuropathy (often post-Campylobacter); ascending symmetric weakness, areflexia; albuminocytologic dissociation in CSF.
Myasthenia gravis vs Lambert-Eaton: MG: antibodies to ACh receptor; worsens with use; improves with edrophonium; thymoma. Lambert-Eaton: antibodies to presynaptic Ca²⁺ channels; improves with use; small cell lung cancer.
Paraneoplastic syndromes (classic): Small cell lung cancer: SIADH (ADH), Cushing (ACTH), Lambert-Eaton. Squamous cell: PTHrP (hypercalcemia). Renal cell: EPO (polycythemia).
Wallerian degeneration: Degeneration of the axon distal to an injury; the proximal stump can regenerate in the peripheral nervous system (Schwann cells) but not effectively in the CNS.
Aminoacyl-tRNA synthetase role: Charges each tRNA with its correct amino acid (the key accuracy step of translation), using ATP; has proofreading activity.
Operon vs eukaryotic gene regulation: Prokaryotes: polycistronic operons (lac, trp). Eukaryotes: monocistronic, regulated by enhancers, promoters, transcription factors, and chromatin (histone acetylation).
Tetralogy of Fallot: Pulmonary stenosis, Right ventricular hypertrophy, Overriding aorta, VSD (PROVe); 'boot-shaped' heart; right-to-left shunt → cyanosis ('tet spells').
Left-to-right shunts (acyanotic): VSD (most common congenital), ASD (fixed split S2), PDA (continuous machine-like murmur). Can reverse to cyanotic (Eisenmenger) if untreated.
Coarctation of the aorta: Narrowing of the aorta; upper-extremity hypertension with lower-extremity hypotension/weak femoral pulses, rib notching; associated with Turner syndrome and bicuspid aortic valve.
Heart murmurs: systolic vs diastolic: Systolic: aortic stenosis, mitral regurgitation, VSD, mitral valve prolapse. Diastolic: aortic regurgitation, mitral stenosis. Maneuvers change intensity (↑ preload, afterload).
Jones criteria (acute rheumatic fever): Follows Group A Strep pharyngitis; JONES: Joints (migratory arthritis), carditis (♥), Nodules (subcutaneous), Erythema marginatum, Sydenham chorea. Type II hypersensitivity.
Anemia classification by MCV: Microcytic (<80): iron deficiency, thalassemia, anemia of chronic disease, lead, sideroblastic. Macrocytic (>100): B12/folate, alcohol. Normocytic: hemolysis, acute blood loss.
Pemphigus vulgaris vs bullous pemphigoid: Pemphigus: antibodies to desmoglein (desmosomes), intraepidermal, positive Nikolsky, oral involvement. Bullous pemphigoid: antibodies to hemidesmosomes, subepidermal, tense bullae, Nikolsky-negative.
Skin cancer: BCC vs SCC vs melanoma: Basal cell: most common, 'pearly' papule, rarely metastasizes. Squamous cell: actinic keratosis precursor, keratin pearls. Melanoma: ABCDE, depth (Breslow) predicts metastasis.
Hypersensitivity vasculitis vs PAN: Polyarteritis nodosa: medium-vessel, hepatitis B-associated, spares the lungs, 'string of beads' on angiography, p-ANCA negative typically.
Cushing reflex (↑ intracranial pressure): Hypertension (widened pulse pressure), bradycardia, and irregular respirations — the brain's response to rising intracranial pressure.
Renal tubular acidosis types: Type 1 (distal): can't secrete H⁺, ↑ urine pH, stones. Type 2 (proximal): ↓ bicarbonate reabsorption. Type 4: aldosterone resistance/deficiency, hyperkalemia.
Acute tubular necrosis: Most common cause of intrinsic acute kidney injury; ischemic or nephrotoxic; muddy brown granular casts; FENa >2%.
Prerenal vs intrinsic vs postrenal AKI: Prerenal: ↓ perfusion, BUN/Cr >20, FENa <1%. Intrinsic (ATN): tubular damage, FENa >2%. Postrenal: obstruction, hydronephrosis.
Wernicke vs Korsakoff: Wernicke encephalopathy: acute, reversible — confusion, ophthalmoplegia, ataxia (thiamine deficiency). Korsakoff: chronic, irreversible — amnesia and confabulation.
Bias: recall vs measurement vs observer: Recall: cases remember exposures differently. Measurement (information): systematic data error. Observer (Hawthorne): subjects change behavior when watched; reduce with blinding.
Sensitivity vs specificity for screening vs confirming: Screening tests should be highly sensitive (don't miss disease); confirmatory tests should be highly specific (avoid false positives). Often run a sensitive then a specific test.
Capacity vs competency: Capacity is a clinical determination (made by a physician, decision-specific). Competency is a legal determination (made by a court). A patient with capacity may refuse treatment.
Minor consent exceptions: Minors can usually consent for emergencies, STIs, contraception, pregnancy care, and substance use, or if emancipated; otherwise a parent/guardian consents.
Cell cycle checkpoints: G1/S (restriction point, RB and p53), G2/M, and the spindle (M) checkpoint. p53 arrests the cycle for DNA repair or triggers apoptosis ('guardian of the genome').
Telomerase: Reverse transcriptase that extends chromosome ends (telomeres); active in germ cells, stem cells, and most cancers; absent in most somatic cells (replicative senescence).
Free radical injury and antioxidants: Reactive oxygen species damage lipids, proteins, DNA (lipid peroxidation). Defenses: superoxide dismutase, catalase, glutathione peroxidase, vitamins A/C/E.
Ischemia-reperfusion injury: Restoring blood flow to ischemic tissue paradoxically worsens damage via a burst of reactive oxygen species, calcium overload, and inflammation.
Diabetic complications (mechanisms): Chronic hyperglycemia → nonenzymatic glycation (large vessels: atherosclerosis) and sorbitol accumulation (small vessels/nerves: retinopathy, nephropathy, neuropathy).

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By Career EmployerUpdated Jun 19, 2026

300+ free USMLE Step 1 flashcards — 4 ways to study

USMLE Step 1 Flashcard of the DayNew daily

The classic card. Do you know this one?

Click Study Flashcards above to open the flashcard hub — hundreds of USMLE Step 1 cards you can flip, match, type, or quiz yourself on. Every card is drawn from the high-yield basic science Step 1 tests, so you study exactly what the exam measures.^[1] Pair them with our free practice questions and study guide.

USMLE Step 1 Flashcard Study Modes

Most flashcard sites give you one thing: a card to flip. Ours has four modes so you can both learn the material and prove you know it — the difference between recognizing an answer and recalling it under pressure.

Flip (Study) — the classic card. Flip term ↔ definition, shuffle the deck, and mark each card “Got it” or “Still learning.”
Match (Game) — a timed game: pair each term to its definition as fast as you can. Great for cementing rule sets like antidotes and hypersensitivity types.
Type (Recall) — read the definition and type the term. Typing forces true active recall instead of passive recognition.
Quiz (Test) — multiple-choice questions generated from the cards, so you can self-test exactly like exam day.

Free USMLE Step 1 flashcards from Career Employer — active recall for the medical licensing exam

Why Flashcards Work for USMLE Step 1

Flashcards aren’t busywork — they’re built on active recall: pulling an answer out of memory strengthens it far more than re-reading notes. Pair that with spacing — short sessions across several days rather than one cram — and you retain more in less time.

That matters on Step 1, where a vast fact base (rate-limiting enzymes, organism profiles, drug receptors, antidotes, high-yield associations) must be instantly available under time pressure. Used alongside our practice questions and study guide, flashcards turn review time into measurable progress.

USMLE Step 1 Flashcards by Topic

The cards are organized by the disciplines you study. Pathology and physiology together carry most of the exam, so weight your time there — but the rule-based facts in every discipline (antidotes, hypersensitivity types, rate-limiting enzymes) are pure recall and reliable points:^[1]

USMLE Step 1 flashcard topics and their approximate discipline weight
Flashcard topic	Approx. Step 1 discipline weight
Pathology	45–55% (the largest)
Physiology	30–40%
Microbiology	10–20%
Pharmacology	10–20%
Anatomy & Neuroscience	10–20% (anatomy/embryology)
Behavioral Sciences	10–15%
Biochemistry & Genetics	5–15% (biochem) + 5–10% (genetics)
Immunology	5–15%
Biostatistics & Epidemiology	4–6% (by system)

Ranges overlap because each Step 1 question maps to several disciplines at once. Because the rule-based associations are so reliably tested, they are some of the most efficient points you can bank with flashcards.

How to Get the Most Out of These Flashcards

Start early, review daily. Begin flashcards as you cover each discipline, not the week before — a few minutes a day beats one marathon session.
Use Type and Quiz, not just Flip. Recognizing the right answer is easy; recalling and choosing it is the real test.
Drill your weakest discipline. Pick a single deck and grind it until the Match time drops and the Quiz score climbs.
Bank the rule sets. Antidotes, hypersensitivity types, rate-limiting enzymes, and organism profiles are guaranteed points — master them cold.
Stay at the Step 1 level. When a card describes a vignette, the answer is usually the mechanism, the organism, the drug, or the best next step.
Then prove it. When the cards feel easy, confirm with our practice questions — build a comfortable margin before exam day.

USMLE Step 1 Flashcards FAQ

Hundreds of free USMLE Step 1 flashcards, spanning the highest-yield basic science the exam tests — pathology, physiology, pharmacology, microbiology, immunology, biochemistry, genetics, anatomy/neuroscience, behavioral science, and biostatistics. They're free with no account required.

References

1.USMLE Program (FSMB and NBME). “Step 1 Content Outline and Specifications.” usmle.org. ↑
2.USMLE Program (FSMB and NBME). “Step 1 Overview.” usmle.org. ↑
3.National Institutes of Health (NIH). “Biochemistry, Citric Acid Cycle.” ncbi.nlm.nih.gov. ↑

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