FCPS Part-I cheat sheet

Osmolality (mOsm/kg) ≈ 2×Na⁺ + glucose/18 + urea/2.8; effective (tonicity) omits urea because urea crosses membranes freely.

Anion gap = Na⁺ − (Cl⁻ + HCO₃⁻); normal 8–12 mmol/L; raised by lactate, ketones, urate, toxins, or renal failure; low in hypoalbuminaemia, lithium, bromide.

Henderson–Hasselbalch: pH = 6.1 + log([HCO₃⁻]/0.03×PaCO₂); compensation never fully corrects the primary disorder.

Winter's formula: expected PaCO₂ = 1.5×HCO₃⁻ + 8 ± 2; measured PaCO₂ above range indicates added respiratory acidosis.

Hb oxygen affinity: right shift (↑2,3-BPG, ↑CO₂, ↑H⁺, ↑temperature) releases O₂; fetal Hb and carboxyhaemoglobin shift left.

Starling equation: Jv = Kf[(Pc − Pi) − σ(πc − πi)]; oedema arises from ↑hydrostatic pressure, ↓oncotic pressure, ↑capillary permeability, or lymphatic obstruction.

Cell cycle checkpoints: G1/S (Rb–E2F, p53), G2/M (cyclin B–CDK1), spindle assembly checkpoint; loss of p53 permits replication of damaged DNA.

Autosomal recessive disease recurs in 25% of offspring of two carriers; autosomal dominant in 50% per child of an affected heterozygote; X-linked recessive affects males, carrier females transmit 50% risk.

Pharmacokinetics: half-life t½ = 0.693×Vd/CL; steady state reached in ~4–5 half-lives; loading dose = Vd×target concentration/bioavailability.

Zero-order kinetics (phenytoin, ethanol, salicylate at high dose) saturate enzymes: constant amount eliminated per unit time, so small dose increases raise levels disproportionately.

First-pass hepatic metabolism reduces oral bioavailability; routes bypassing it include IV, sublingual, rectal (partial), transdermal, and inhaled.

Henderson–Hasselbalch for drug trapping: acidic drugs ionise in alkaline urine (↑renal elimination); ionised species cannot cross lipid membranes.

Receptor pharmacology: agonist = intrinsic activity; competitive antagonist shifts dose–response right without lowering Emax; non-competitive lowers Emax; partial agonist has Emax below full agonist.

Enzyme kinetics: Michaelis–Menten v = Vmax[S]/(Km+[S]); Km is substrate concentration at half-Vmax; competitive inhibitors raise Km, non-competitive lower Vmax.

Volume of distribution = dose/plasma concentration; large Vd (>1 L/kg) indicates extensive tissue binding (e.g., tricyclics, chloroquine).

Microbial genetics: plasmids transfer resistance by conjugation; transposons move within genomes; transformation takes free DNA; transduction uses bacteriophages.

Shock classification: hypovolaemic (↓preload), cardiogenic (↓contractility), distributive (↓SVR, e.g., sepsis, anaphylaxis), obstructive (tamponade, tension pneumothorax, PE).

Sepsis-3: suspected infection plus SOFA rise ≥2; septic shock = persistent hypotension needing vasopressors with lactate >2 mmol/L despite fluids.

Acute chest pain: ST elevation or new LBBB triggers reperfusion; serial high-sensitivity troponin with dynamic change defines acute myocardial infarction.

Head injury: GCS ≤8 warrants airway protection; pupillary asymmetry with bradycardia and hypertension (Cushing triad) signals raised intracranial pressure.

Hyponatraemia: assess volume status and urine osmolality; urine osmolality >100 mOsm/kg with euvolaemia suggests SIADH; correct slowly to avoid osmotic demyelination.

Jaundice: unconjugated hyperbilirubinaemia implies haemolysis or Gilbert syndrome; conjugated implies hepatocellular or cholestatic disease; ultrasound first for cholestasis.

Acid–base stepwise: identify primary pH, calculate expected compensation, then anion gap; delta ratio = ΔAG/ΔHCO₃⁻ (>2 suggests metabolic alkalosis, <1 non-gap acidosis).

Paediatric dehydration: assess percentage loss, capillary refill, skin turgor, and mental state; oral rehydration is first line in mild-moderate cases without shock.

Sensitivity = TP/(TP+FN); specificity = TN/(TN+FP); positive predictive value depends on prevalence, so screening tests in low-prevalence populations yield many false positives.

Likelihood ratio positive = sensitivity/(1−specificity); LR >10 strongly rules in, LR <0.1 strongly rules out; LRs are prevalence-independent.

Number needed to treat = 1/absolute risk reduction; NNH = 1/absolute risk increase; ARR = control event rate − treatment event rate.

Therapeutic index = TD50/ED50; narrow-index drugs (digoxin, lithium, warfarin, aminoglycosides, phenytoin) require level monitoring.

CYP interactions: CYP3A4 inhibitors include macrolides, azoles, grapefruit, and ritonavir; inducers include rifampicin, carbamazepine, phenytoin, and St John's wort.

Warfarin: monitor INR; target 2–3 for most indications, 2.5–3.5 for mechanical mitral valves; vitamin K and prothrombin complex concentrate reverse major bleeding.

Heparin-induced thrombocytopenia: platelet fall 5–10 days after exposure with paradoxical thrombosis; stop heparin and start a non-heparin anticoagulant.

Patient safety: WHO surgical safety checklist (sign in, time out, sign out) reduces wrong-site surgery; medication reconciliation at transitions cuts prescribing errors.

Reporting: adverse drug reactions go to the national pharmacovigilance scheme; serious incidents require duty-of-candour disclosure to the patient.