RCPA BPS Exam key terms

Programmed cell death in which caspases dismantle the cell into membrane-bound bodies that are cleared without inflammation, occurring in development, immune regulation, and after irreparable DNA damage.

Uncontrolled cell death from severe injury that swells and ruptures the cell, releasing contents that provoke inflammation; classified by pattern as coagulative, liquefactive, caseous, or fat necrosis.

Reversible replacement of one mature epithelial or mesenchymal cell type by another better suited to stress, such as squamous change in smoker airways; the change itself is adaptive but may predispose to cancer.

Disordered, atypical cellular growth with loss of normal size, shape, and orientation, usually in epithelium; graded as low or high, it is not cancer but high-grade change is a precursor lesion.

Additional tissue damage caused when blood flow returns to ischaemic tissue, driven by reactive oxygen species, calcium overload, complement activation, and inflammatory cell influx, seen after infarction or transplantation.

An atom or molecule with an unpaired electron, such as superoxide or hydroxyl radical, that damages lipids, proteins, and DNA; cells defend using antioxidants, catalase, superoxide dismutase, and glutathione.

Rapid, short-lived vascular and cellular response to injury or infection, producing vasodilatation, increased permeability, and neutrophil recruitment through margination, adhesion, and transmigration.

Compact aggregate of activated macrophages, often with multinucleate giant cells and a rim of lymphocytes, formed when a stimulus resists elimination; caseating in tuberculosis, non-caseating in sarcoidosis and Crohn disease.

Proliferating tissue of healing wounds composed of new capillaries, fibroblasts, and myofibroblasts in loose matrix, together with macrophages; it fills defects before maturing into scar.

Excess deposition of collagen and other extracellular matrix replacing functional tissue after chronic injury or persistent inflammation, permanently impairing organ function in liver, lung, kidney, and heart.

Excessive scar that extends beyond the original wound margins, reflecting overactive fibroblast collagen synthesis; more common in darker skin and at sites such as sternum and earlobe.

Gene that, when activated by mutation, amplification, or translocation, drives autonomous cell proliferation; derived from proto-oncogenes such as RAS, MYC, and HER2, and typically acts dominantly.

Gene whose normal product restrains growth, repairs DNA, or promotes apoptosis; both alleles usually require inactivation before function is lost, as with RB1, TP53, and APC.

Knudson's model proposing that retinoblastoma requires inactivation of both RB1 alleles, with one hit inherited or arising early and the second acquired somatically, explaining hereditary and sporadic patterns.

Loss of the remaining normal allele at a heterozygous locus through deletion, mutation, or recombination, unmasking a recessive mutation and commonly inactivating tumour suppressor genes during carcinogenesis.

Malignant epithelial proliferation confined by the basement membrane, without stromal invasion, so metastasis cannot yet occur; high-grade dysplasia and full-thickness change are equivalent in many epithelia.

Spread of malignant cells to distant sites through lymphatics, blood, or body cavities, requiring detachment, invasion, survival in transit, arrest, extravasation, and growth in a new microenvironment.

Process in which epithelial cells lose adhesion and polarity and gain migratory mesenchymal features, contributing to invasion, metastasis, and tissue fibrosis during embryogenesis and cancer progression.

Three factors predisposing to thrombosis: endothelial injury, abnormal blood flow such as stasis or turbulence, and hypercoagulability of the blood; useful framework for assessing thrombotic risk.

Thrombus forming in deep leg or pelvic veins, favoured by immobility, surgery, malignancy, and thrombophilia; may embolise to the lungs and is treated with anticoagulation.

Acquired syndrome of widespread coagulation activation consuming platelets and clotting factors, causing both microvascular thrombosis and bleeding; triggered by sepsis, trauma, obstetric complications, and malignancy.

Blood component containing platelets suspended in plasma or additive solution, used to prevent or treat bleeding from thrombocytopenia or platelet dysfunction; stored with agitation and has short shelf life.

Matching of donor and recipient ABO blood groups to avoid haemolytic transfusion reactions; group O red cells and group AB plasma are universally acceptable, while whole blood and platelets require closer matching.

Immunoglobulin produced by plasma cells that binds specific antigen through variable regions, mediating neutralisation, opsonisation, complement activation, or cellular killing depending on isotype.

Cluster of genes encoding cell-surface molecules that present peptide antigens to T cells; class I presents to CD8 cells on most nucleated cells, class II to CD4 cells on antigen-presenting cells.

Inappropriate or exaggerated immune response causing tissue injury, classified into four types: immediate IgE-mediated, antibody-mediated, immune-complex, and delayed T-cell-mediated.

Lowest concentration of an antimicrobial that prevents visible growth of a bacterial isolate under defined conditions, used to guide therapy and define susceptibility categories.

Structured community of microorganisms attached to a surface and embedded in self-produced matrix, which reduces antibiotic penetration and immune clearance, causing persistent device-related and chronic infections.

Life-threatening organ dysfunction caused by a dysregulated host response to infection, recognised clinically by altered mentation, raised respiratory rate, and hypotension, requiring urgent antimicrobials and supportive care.

Systemic reaction to inflammation or infection, driven by cytokines such as interleukin-6, producing fever, leukocytosis, and altered hepatic protein synthesis including raised C-reactive protein and low albumin.

Calculated difference between measured cations and anions, approximately sodium minus chloride and bicarbonate, used to classify metabolic acidosis and detect unmeasured acids such as lactate or ketones.

Genetic change that reduces or abolishes the activity of the encoded protein; typically recessive when one normal allele suffices, but can act dominantly through haploinsufficiency or dominant-negative effects.

Proportion of individuals carrying a disease-causing genotype who actually show the phenotype; incomplete penetrance explains variable expression within families with dominant conditions.

Presence of two or more genetically distinct cell populations in one individual, arising from post-zygotic mutation or chromosome error and causing variable, sometimes segmental, clinical features.

Glomerular disease pattern with heavy proteinuria, hypoalbuminaemia, oedema, and hyperlipidaemia, caused by increased glomerular permeability from podocyte or basement membrane injury.

End-stage liver disease with bridging fibrosis and regenerative nodules distorting architecture, causing portal hypertension, impaired synthetic function, and risk of hepatocellular carcinoma.

Chronic arterial disease in which lipid-rich intimal plaques with inflammation, smooth muscle cells, and fibrous cap narrow vessels and can rupture, causing infarction or aneurysm.

Family of cysteine proteases that execute apoptosis by cleaving structural and regulatory proteins; initiator caspases are activated by death receptors or mitochondrial cytochrome c release.