RCPA BPS Exam cheat sheet

Reversible cell injury: ATP depletion, cell swelling, fatty change, ribosomal detachment; mitochondria and nucleus remain intact.

Irreversible injury markers: mitochondrial permeability transition pore opening, membrane integrity loss, lysosomal enzyme leakage, nuclear pyknosis/karyorrhexis/karyolysis.

Necrosis vs apoptosis: necrosis is passive, involves swelling and inflammation; apoptosis is ATP-dependent, caspase-mediated, non-inflammatory.

Adaptations: hypertrophy (increase in cell size), hyperplasia (increase in cell number), atrophy (decrease in size/number), metaplasia (reversible change of one mature cell type to another, e.g., Barrett oesophagus).

Cellular ageing mechanisms: telomere shortening, oxidative stress, DNA damage accumulation, defective autophagy; caloric restriction delays ageing in model organisms.

Basic histology: four tissue types-epithelium (covering/lining, glandular), connective tissue (ECM, fibroblasts, collagen), muscle (skeletal, cardiac, smooth), nervous (neurons, glia).

Epithelial junctions: tight junctions (zonula occludens) seal paracellular space; adherens junctions (zonula adherens) link actin; desmosomes link intermediate filaments; gap junctions allow ionic coupling.

Fixation and staining: formalin cross-links proteins; H&E stains nuclei blue (haematoxylin) and cytoplasm pink (eosin); PAS highlights glycogen and mucin.

Acute inflammation: vasodilation, increased vascular permeability, neutrophil recruitment (margination, rolling, adhesion, transmigration, chemotaxis).

Mediators: histamine (mast cells) causes vasodilation; prostaglandins cause pain and fever; leukotrienes are potent chemotactic and vasoactive agents; TNF and IL-1 induce endothelial adhesion molecules.

Chronic inflammation: mononuclear infiltrate (macrophages, lymphocytes, plasma cells), tissue destruction, fibrosis; granulomas consist of epithelioid macrophages with Langhans giant cells.

Wound healing phases: haemostasis, inflammation, proliferation (granulation tissue, angiogenesis, fibroblast collagen), remodelling (matrix metalloproteinases, type III to type I collagen switch).

Healing by primary intention: clean apposed edges, minimal granulation tissue, thin scar; secondary intention: large defect, abundant granulation, wound contraction, larger scar.

Factors impairing repair: infection, poor perfusion, diabetes, corticosteroids, malnutrition (protein, vitamin C), foreign bodies, mechanical stress.

Regeneration capacity: labile cells (skin, gut) continuously divide; stable cells (liver, kidney) enter G0 but can re-enter cell cycle; permanent cells (neurons, cardiac myocytes) cannot regenerate.

Granuloma formation: persistent intracellular pathogens or foreign bodies trigger Th1 response, IFN-γ activates macrophages to epithelioid cells, surrounded by lymphocytes and fibrosis.

Hallmarks of cancer: self-sufficiency in growth signals, insensitivity to growth inhibition, evasion of apoptosis, limitless replicative potential, sustained angiogenesis, tissue invasion/metastasis, altered metabolism, immune evasion.

Oncogenes vs tumour suppressors: oncogenes are gain-of-function (RAS, MYC, HER2); tumour suppressors are loss-of-function (TP53, RB1, APC, BRCA1/2).

Carcinogenesis stages: initiation (irreversible genetic damage), promotion (reversible clonal expansion), progression (additional mutations, invasion).

Metastatic cascade: local invasion, intravasation, survival in circulation, extravasation, colonisation of distant site; organ tropism follows 'seed and soil' hypothesis.

Tumour grading vs staging: grade describes differentiation (low to high); stage describes anatomical extent (TNM: tumour size, node involvement, metastasis).

Paraneoplastic syndromes: ectopic hormone production (ACTH, ADH, PTHrP), hypercalcaemia, cachexia, Trousseau syndrome (migratory thrombophlebitis).

Tumour markers: AFP (hepatocellular carcinoma, yolk sac tumour), CEA (colorectal), CA-125 (ovarian), PSA (prostate), hCG (choriocarcinoma).

Angiogenesis and invasion: VEGF drives neovascularisation; matrix metalloproteinases degrade basement membrane; E-cadherin loss promotes epithelial-mesenchymal transition.

Primary haemostasis: platelet adhesion (von Willebrand factor to collagen), activation (shape change, granule release), aggregation (GPIIb/IIIa with fibrinogen).

Coagulation cascade: intrinsic (XII, XI, IX, VIII), extrinsic (III, VII), common (X, V, II, I); thrombin converts fibrinogen to fibrin and activates factors V, VIII, XIII.

Anticoagulant pathways: antithrombin inhibits thrombin and Xa; protein C/S degrade factors Va and VIIIa; tissue factor pathway inhibitor limits initiation.

Fibrinolysis: plasminogen converted to plasmin by tPA/uPA; plasmin degrades fibrin into D-dimers; α2-antiplasmin inhibits plasmin.

Virchow's triad: endothelial injury, abnormal blood flow (stasis/turbulence), hypercoagulability.

Thrombophilia: factor V Leiden (activated protein C resistance), prothrombin G20210A, antithrombin deficiency, protein C/S deficiency, antiphospholipid syndrome.

Transfusion: ABO compatibility mandatory; crossmatch detects recipient antibodies against donor red cells; RhD-negative females of childbearing age receive RhD-negative blood.

Transfusion reactions: acute haemolytic (ABO mismatch, fever, haemoglobinuria, DIC), febrile non-haemolytic, allergic/anaphylactic, TRALI, TACO, delayed haemolytic.

Innate immunity: physical barriers, phagocytes, NK cells, complement, cytokines; rapid, non-specific, no memory.

Adaptive immunity: T lymphocytes (cell-mediated, CD4 helper, CD8 cytotoxic) and B lymphocytes (humoral, antibody production); specificity and memory.

Hypersensitivity types: I IgE-mediated (anaphylaxis), II antibody-mediated (haemolytic anaemia), III immune complex (SLE, glomerulonephritis), IV delayed T-cell (contact dermatitis, TB).

Autoimmunity mechanisms: loss of self-tolerance, molecular mimicry, epitope spreading, defective regulatory T cells; HLA associations (e.g., HLA-B27 with ankylosing spondylitis).

Immunodeficiency: primary (e.g., X-linked agammaglobulinaemia, SCID, chronic granulomatous disease) and secondary (HIV/AIDS, malnutrition, immunosuppression).

Transplant rejection: hyperacute (preformed antibodies), acute (cellular/humoral within weeks), chronic (fibrosis, graft vasculopathy); graft-versus-host disease in bone marrow transplant.

Complement pathways: classical (antibody-antigen), alternative (microbial surfaces), lectin (mannose-binding lectin); all converge on C3 convertase and membrane attack complex.

Tumour immunology: tumour antigens recognised by CD8 T cells; immune editing (elimination, equilibrium, escape); checkpoint inhibitors (anti-PD-1/PD-L1, anti-CTLA-4) restore T-cell activity.

Bacterial classification: Gram stain (positive thick peptidoglycan, negative thin layer with outer membrane), shape (cocci, bacilli, spirochaetes), oxygen requirement.

Virulence factors: adhesins, capsules (antiphagocytic), toxins (endotoxin LPS, exotoxins), siderophores, secretion systems, biofilm formation.

Viral replication: attachment, penetration, uncoating, genome replication, assembly, release; DNA viruses replicate in nucleus, RNA viruses in cytoplasm (except retroviruses).

Fungal infections: superficial (dermatophytes), subcutaneous, systemic (Aspergillus, Cryptococcus, Candida); dimorphic fungi (Histoplasma) switch between mould and yeast.

Parasites: protozoa (malaria, Giardia, Toxoplasma), helminths (nematodes, cestodes, trematodes); eosinophilia suggests helminth infection.

Sterilisation vs disinfection: sterilisation kills all microorganisms including spores (autoclave 121°C, 15 psi, 15 min); disinfection reduces pathogens on inanimate objects.

Antimicrobial resistance mechanisms: enzymatic inactivation (β-lactamase), efflux pumps, target modification, reduced permeability; horizontal gene transfer via plasmids, transposons.

Notifiable diseases and infection control: isolation precautions (contact, droplet, airborne), hand hygiene, PPE; MRSA, VRE, C. difficile require contact precautions.

Reference intervals: 95% of healthy population; results outside may be normal for individual; interpret with clinical context and biological variation.

Diabetes diagnosis: fasting plasma glucose ≥7.0 mmol/L, 2-h OGTT ≥11.1 mmol/L, HbA1c ≥6.5% (48 mmol/mol), or random ≥11.1 with symptoms.

Acid-base: Henderson-Hasselbalch pH = 6.1 + log([HCO3-]/0.03×pCO2); metabolic acidosis: low HCO3-, respiratory compensation lowers pCO2; anion gap = Na+ - (Cl- + HCO3-), normal 8-12 mmol/L.

Electrolyte disorders: hyponatraemia (assess volume status, urine osmolality), hyperkalaemia (ECG changes, treat with calcium gluconate, insulin-dextrose, salbutamol), hypokalaemia (arrhythmia, weakness).

Liver function tests: ALT/AST (hepatocellular), ALP/GGT (cholestatic), bilirubin (conjugation), albumin (synthetic function), INR (synthetic function).

Renal function: creatinine, eGFR (CKD-EPI), urea; AKI staged by KDIGO criteria (creatinine rise ≥26.5 µmol/L in 48h or ≥1.5× baseline in 7 days).

Lipids: LDL calculated by Friedewald formula (LDL = TC - HDL - TG/2.2 in mmol/L) valid if TG <4.5 mmol/L; cardiovascular risk assessed by ratio TC/HDL.

Tumour markers and hormones: TSH and free T4 for thyroid; cortisol diurnal variation; troponin for myocardial injury; BNP for heart failure.

Mendelian inheritance: autosomal dominant (vertical transmission, 50% risk), autosomal recessive (25% risk, consanguinity), X-linked recessive (males affected, carrier females).

Chromosomal abnormalities: aneuploidy (trisomy 21, 18, 13), structural (deletions, duplications, translocations, inversions); Philadelphia chromosome t(9;22) BCR-ABL in CML.

Mutation types: missense (amino acid change), nonsense (premature stop), frameshift (insertion/deletion not multiple of three), splice-site; consequences range from benign to lethal.

Cancer genetics: proto-oncogenes activated by mutation/amplification; tumour suppressors inactivated by two-hit hypothesis (Knudson); hereditary cancer syndromes (BRCA, Lynch, FAP).

Molecular techniques: PCR (amplification), Sanger sequencing (single gene), next-generation sequencing (panel/exome/genome), FISH (copy number, translocations), microarray (CNV).

Pharmacogenomics: CYP2C19 variants affect clopidogrel activation; HLA-B*5701 predicts abacavir hypersensitivity; TPMT deficiency increases thiopurine toxicity.

Epigenetics: DNA methylation (gene silencing), histone acetylation (gene activation), imprinting (Prader-Willi/Angelman syndromes), X-inactivation.

Prenatal and carrier screening: karyotype, chromosomal microarray, cell-free fetal DNA (NIPT), carrier panels for recessive conditions; genetic counselling addresses risk and options.

Cardiovascular: atherosclerosis (endothelial injury, lipid accumulation, inflammation, plaque rupture), myocardial infarction (coagulative necrosis, troponin rise, complications by day), hypertension (vascular remodelling).

Respiratory: COPD (emphysema and chronic bronchitis), asthma (eosinophilic inflammation, bronchoconstriction), pneumonia (lobar vs bronchopneumonia), pulmonary embolism.

Gastrointestinal: peptic ulcer disease (H. pylori, NSAIDs), coeliac disease (villous atrophy, anti-tTG), inflammatory bowel disease (Crohn transmural, UC mucosal), colorectal carcinoma adenoma-carcinoma sequence.

Hepatobiliary: cirrhosis (fibrosis, nodules, portal hypertension), viral hepatitis (B, C), alcoholic liver disease (steatosis, hepatitis, cirrhosis), gallstones (cholesterol, pigment).

Renal: glomerulonephritis (immune complex, crescentic), nephrotic syndrome (proteinuria >3.5 g/day, hypoalbuminaemia, oedema), acute tubular necrosis, chronic kidney disease.

Endocrine: diabetes mellitus (type 1 autoimmune β-cell destruction, type 2 insulin resistance), thyroid disorders (Graves, Hashimoto), adrenal insufficiency (Addison).

Neurological: ischaemic stroke (liquefactive necrosis), Alzheimer disease (amyloid plaques, neurofibrillary tangles), Parkinson disease (substantia nigra loss), multiple sclerosis (demyelination).

Musculoskeletal and skin: osteoarthritis (cartilage loss, osteophytes), rheumatoid arthritis (pannus, symmetric), osteoporosis (reduced bone mass), psoriasis (epidermal hyperplasia).