Iran Medical Basic Sciences Exam cheat sheet

Brachial plexus: roots C5–T1; trunks (superior C5–C6, middle C7, inferior C8–T1); divisions anterior/posterior; cords named by relation to the second part of the axillary artery.

Erb palsy (C5–C6): waiter's tip posture - arm adducted and internally rotated, elbow extended, wrist flexed; from traction on the upper trunk.

Klumpke palsy (C8–T1): claw hand with intrinsic muscle wasting; T1 involvement may add Horner syndrome.

Femoral triangle borders: inguinal ligament (superior), sartorius (lateral), adductor longus (medial); floor iliopsoas and pectineus; femoral nerve lies outside the femoral sheath.

Median nerve innervates thenar muscles (opponens pollicis, abductor pollicis brevis, flexor pollicis brevis superficial head) and first two lumbricals; ulnar nerve supplies all other intrinsic hand muscles.

Epithelium classification: number of layers (simple vs stratified) plus apical surface (squamous, cuboidal, columnar) and specializations (cilia, microvilli, keratin).

Neural tube closes by end of week 4; anterior neuropore closes ~day 25, posterior ~day 27; failure of posterior closure gives spina bifida.

Pharyngeal arch nerve supply: arch 1 trigeminal (V), arch 2 facial (VII), arch 3 glossopharyngeal (IX), arch 4–6 vagus (X) and accessory (XI).

Lung maturation: surfactant from type II pneumocytes appears ~24–28 weeks; canalicular stage 16–26 weeks, saccular 26–36 weeks, alveolar from ~36 weeks to childhood.

Resting membrane potential ≈ −70 mV from K+ permeability dominance; Nernst equation E = (61/z)·log([ion]out/[ion]in) at 37 °C.

Cardiac output = heart rate × stroke volume; Fick principle: CO = VO2 / (arterial O2 content − venous O2 content).

Mean arterial pressure ≈ diastolic pressure + 1/3 (systolic − diastolic).

Frank–Starling: increased end-diastolic volume raises stroke volume up to the point of sarcomere overstretch.

Glomerular filtration rate = Kf × net filtration pressure; net pressure = glomerular capillary − (Bowman's space + oncotic) pressure.

Renal handling: glucose reabsorption saturates at transport maximum (~375 mg/min); clearance Cx = (Ux × V)/Px; inulin clearance measures GFR.

Oxygen–hemoglobin curve shifts right (decreased affinity) with ↑CO2, ↑H+, ↑temperature, ↑2,3-BPG; fetal Hb has higher affinity.

Compliance = Δvolume/Δpressure; surfactant raises compliance and reduces alveolar surface tension per Laplace law P = 2T/r.

Action potential refractory periods: absolute refractory determines maximum firing frequency; relative refractory coincides with hyperpolarization.

Glycolysis net yield: glucose → 2 pyruvate, 2 ATP, 2 NADH; committed step is phosphofructokinase-1, activated by AMP/fructose-2,6-bisphosphate and inhibited by ATP/citrate.

TCA cycle per acetyl-CoA: 3 NADH, 1 FADH2, 1 GTP; oxidative phosphorylation yields ~2.5 ATP per NADH and ~1.5 ATP per FADH2.

Rate-limiting enzymes: glycolysis PFK-1, gluconeogenesis fructose-1,6-bisphosphatase, glycogen synthesis glycogen synthase, glycogenolysis glycogen phosphorylase, fatty acid synthesis acetyl-CoA carboxylase.

Urea cycle: carbamoyl phosphate synthetase I in mitochondria; rate-limiting step; hyperammonemia with low BUN suggests proximal defect.

DNA replication is semiconservative; leading strand continuous, lagging strand in Okazaki fragments; DNA polymerase synthesizes 5′→3′ and needs a primer.

Transcription: RNA polymerase I makes rRNA, II makes mRNA (inhibited by α-amanitin at low dose), III makes tRNA and 5S rRNA.

Km is the substrate concentration at half Vmax; low Km indicates high affinity; Vmax rises with enzyme concentration.

Competitive inhibition raises apparent Km with unchanged Vmax; noncompetitive lowers Vmax with unchanged Km; uncompetitive lowers both.

Vitamin cofactors: thiamine (TPP) for pyruvate and α-ketoglutarate dehydrogenase; riboflavin (FAD), niacin (NAD), pyridoxine (PLP) for transamination, cobalamin for methylmalonyl-CoA mutase and methionine synthase.

Gram-positive cell wall: thick peptidoglycan with teichoic acid; Gram-negative: thin peptidoglycan plus outer membrane containing lipopolysaccharide (endotoxin).

Catalase-positive, coagulase-positive, Gram-positive cocci in clusters = Staphylococcus aureus.

Oxidase-positive, nonfermenting Gram-negative rods: Pseudomonas aeruginosa; oxidase-negative lactose fermenter on MacConkey = Escherichia coli.

Acid-fast staining (Ziehl–Neelsen) detects Mycobacterium; culture on Löwenstein–Jensen medium.

Viral genome types: DNA viruses replicate in nucleus (except poxvirus); RNA viruses replicate in cytoplasm (except influenza, which uses nuclear machinery).

Hepatitis B serology: HBsAg = infection present; anti-HBs = immunity; HBeAg = high infectivity; anti-HBc IgM = acute or window period.

HIV targets CD4+ T cells via gp120–CD4/CCR5 or CXCR4 binding; reverse transcriptase converts RNA to DNA; integrate enters host genome.

Fungal morphology: yeasts reproduce by budding; molds form hyphae and conidia; dimorphic fungi are mold at 25 °C and yeast at 37 °C.

Malaria: Plasmodium falciparum causes malignant tertian malaria with banana-shaped gametocytes; transmitted by female Anopheles; diagnosis by thick and thin blood films.

Innate immunity: neutrophils and macrophages, complement, Toll-like receptors; no memory. Adaptive immunity: T and B lymphocytes with clonal selection and memory.

Antibody classes: IgM (pentamer, primary response, complement fixation), IgG (placental transfer, secondary response), IgA (secretory dimer), IgE (mast cell degranulation), IgD (B-cell receptor).

MHC class I presents endogenous peptides (8–10 aa) to CD8+ cytotoxic T cells on all nucleated cells; MHC class II presents exogenous peptides (13–25 aa) to CD4+ helper T cells on antigen-presenting cells.

Complement pathways: classical (IgG/IgM–C1q), alternative (microbial surfaces, properdin), lectin (mannose-binding lectin); all converge on C3 convertase and membrane attack complex C5b–C9.

Type I hypersensitivity is IgE-mediated; type II is antibody against cell-bound antigen; type III is immune-complex deposition; type IV is delayed, T-cell mediated.

Primary immunodeficiency clues: recurrent infections, failure to thrive; Bruton agammaglobulinemia (X-linked, no B cells) and DiGeorge syndrome (thymic hypoplasia, T-cell defect, hypocalcemia).

Vaccine types: live attenuated (measles, BCG, oral polio) contraindicated in immunocompromised hosts; toxoid (tetanus, diphtheria); conjugate (Hib, pneumococcal).

Graft rejection: hyperacute (preformed antibodies, minutes), acute (cellular, days–weeks), chronic (fibrosis and vasculopathy, months–years).

Cell injury: reversible swelling and fatty change; irreversible injury shows membrane damage, mitochondrial permeability transition, and nuclear changes (pyknosis, karyorrhexis, karyolysis).

Necrosis types: coagulative (ischemia, architecture preserved), liquefactive (brain, abscess), caseous (tuberculosis), fat (pancreatitis), fibrinoid (vasculitis).

Apoptosis is energy-dependent, caspase-mediated, no inflammation; regulated by Bcl-2 (anti-apoptotic) and Bax/Bak (pro-apoptotic).

Acute inflammation: vasodilation, increased permeability, neutrophil emigration (margination, rolling via selectins, adhesion via integrins, transmigration, chemotaxis).

Granuloma: collection of activated macrophages (epithelioid cells) with giant cells and lymphocytes; causes include tuberculosis, sarcoidosis, Crohn disease, leprosy.

Tumor suppressor genes: RB (retinoblastoma), TP53 (guardian of the genome), APC, BRCA1/2; oncogenes: RAS, MYC, HER2.

Malignant features: invasion, metastasis, anaplasia, pleomorphism, high mitotic rate, loss of polarity; benign tumors are encapsulated and well differentiated.

Thrombosis triad (Virchow): endothelial injury, stasis or turbulence, hypercoagulability.

Atherosclerosis: intimal lipid plaque with foam cells, fibrous cap, and complications of rupture, thrombosis, calcification, and aneurysm.

Pharmacokinetics: volume of distribution Vd = dose/plasma concentration; clearance CL = rate of elimination/plasma concentration; half-life t½ = 0.693 × Vd/CL.

Zero-order kinetics (phenytoin, ethanol, aspirin at high dose) eliminates a constant amount per time; first-order eliminates a constant fraction.

Bioavailability is reduced by first-pass hepatic metabolism; drugs given intravenously have bioavailability 1.

Competitive antagonists shift the dose–response curve right without lowering maximal efficacy; noncompetitive antagonists reduce maximal efficacy.

Autonomic receptors: α1 vasoconstriction, β1 cardiac stimulation, β2 bronchodilation and uterine relaxation, M2 cardiac slowing, M3 secretions and smooth muscle contraction.

Organophosphate poisoning: acetylcholinesterase inhibition with SLUDGE/DUMBELS; treat with atropine plus pralidoxime.

Aminoglycosides inhibit the 30S ribosomal subunit (misreading); macrolides and chloramphenicol inhibit 50S; fluoroquinolones inhibit DNA gyrase.

Warfarin inhibits vitamin K epoxide reductase (factors II, VII, IX, X); heparin potentiates antithrombin III; protamine reverses heparin, vitamin K reverses warfarin.

Paracetamol overdose depletes glutathione, causing toxic NAPQI accumulation and centrilobular hepatic necrosis; antidote N-acetylcysteine.

Inheritance patterns: autosomal dominant (50% transmission, vertical pedigree), autosomal recessive (25% affected, consanguinity), X-linked recessive (males affected, no male-to-male transmission).

Hardy–Weinberg equilibrium: p + q = 1 and p² + 2pq + q² = 1; carrier frequency for autosomal recessive = 2pq.

Aneuploidy risk rises with maternal age; trisomy 21 accounts for most Down syndrome, with translocation forms carrying recurrence risk.

Turner syndrome 45,X: short stature, webbed neck, streak ovaries, coarctation of the aorta; no Barr body.

Klinefelter syndrome 47,XXY: tall stature, gynecomastia, small testes, infertility; one Barr body.

Fragile X syndrome: CGG repeat expansion in FMR1, premutation carriers at risk for fragile X-associated tremor/ataxia; most common inherited intellectual disability.

Mitochondrial inheritance is maternal; tissues with high energy demand (muscle, nerve, retina) are most affected, with heteroplasmy explaining variable severity.

Cystic fibrosis: autosomal recessive CFTR mutation (most commonly ΔF508); sweat chloride >60 mmol/L is diagnostic.

Sensitivity = TP/(TP+FN); specificity = TN/(TN+FP); positive predictive value = TP/(TP+FP) and depends on prevalence.

Odds ratio approximates relative risk for rare diseases; OR = (a×d)/(b×c) from a 2×2 table.

Relative risk = incidence in exposed / incidence in unexposed; attributable risk = incidence in exposed − incidence in unexposed.

Study designs: cohort (incidence, relative risk), case–control (odds ratio, rare diseases), cross-sectional (prevalence), randomized trial (causality).

Confounding is a third variable associated with both exposure and outcome; randomization and stratification control it; bias is systematic error not fixed by sample size.

Screening test criteria: important disease, accepted treatment, detectable preclinical phase, valid and acceptable test, cost-effective.

Mean, median, mode: median resists outliers; in a symmetric normal distribution mean = median = mode.

95% confidence interval for a mean ≈ sample mean ± 1.96 × standard error; standard error = SD/√n.

P-value is the probability of observing data at least as extreme as obtained if the null hypothesis is true; it is not the probability the null is true.

Four principles: autonomy (respect informed choice), beneficence (act for patient's good), non-maleficence (avoid harm), justice (fair distribution).

Valid informed consent requires capacity, adequate disclosure, comprehension, and voluntariness; refusal by a competent patient must be respected.

Confidentiality may be breached only with patient consent or a legal duty (reportable communicable disease, suspected child abuse, court order).

In emergencies with an incapacitated patient and no surrogate, treat under the doctrine of necessity, limited to what is immediately required.

Truth-telling: disclose diagnosis and prognosis honestly; therapeutic privilege is narrowly interpreted and rarely justified.

Research ethics: institutional review board approval, informed consent, risk–benefit balance, and special protection for vulnerable populations.

Medical error disclosure: inform the patient, document objectively, report through institutional channels; concealment is a professional violation.

Professional boundaries: avoid conflicts of interest, dual relationships, and accepting gifts that could influence clinical judgment.

Body mass index = weight (kg)/height (m)²; ≥25 overweight, ≥30 obesity (WHO classification).

Protein–energy malnutrition: marasmus is severe wasting without edema; kwashiorkor shows edema, hypoalbuminemia, and fatty liver.

Deficiency diseases: vitamin A - night blindness and xerophthalmia; vitamin D - rickets/osteomalacia; iron - microcytic anemia; iodine - goiter and cretinism.

Energy content: carbohydrate and protein 4 kcal/g, fat 9 kcal/g, alcohol 7 kcal/g.

Incidence measures new cases over a period; prevalence measures all existing cases; prevalence ≈ incidence × mean duration.

Screening programs require a detectable preclinical phase, an acceptable test with adequate sensitivity and specificity, and effective early treatment.

Herd immunity threshold ≈ 1 − 1/R0; higher for highly transmissible agents such as measles (R0 12–18).

Epidemiologic transition: decline in infectious disease mortality and rise in chronic disease burden as populations develop.

Primary prevention reduces exposure before disease; secondary detects early disease; tertiary limits disability and rehabilitation.