FCPS Part-1 key terms

The coordinated physiological processes that keep the internal environment of the body stable around a set point despite changes outside it, maintained by negative feedback loops, buffers, and organ-level regulation.

A control mechanism in which the output of a system suppresses its own stimulus, so that a deviation from a set point triggers a response that reduces the deviation and restores balance.

The concentration of dissolved particles per kilogram of solvent, expressed in milliosmoles per kilogram; it determines water movement across membranes and is regulated mainly by antidiuretic hormone and thirst.

The four pressures governing fluid movement across a capillary wall: hydrostatic pressure and interstitial fluid pressure, opposed by plasma oncotic pressure and interstitial oncotic pressure, together determining net filtration.

A rapid, all-or-none reversal of membrane potential produced by voltage-gated sodium influx followed by potassium efflux, which propagates along excitable cells and triggers neurotransmitter release at axon terminals.

The steady electrical difference across a cell membrane at rest, usually about minus seventy millivolts in neurons, set largely by potassium permeability and the sodium-potassium pump.

Fast, jumping propagation of an action potential between nodes of Ranvier along a myelinated axon, which increases conduction velocity and reduces the energy cost of restoring ionic gradients.

A reduction in the number or sensitivity of cell surface receptors after prolonged exposure to a ligand, producing tolerance to drugs such as beta agonists and requiring dose escalation or withdrawal strategies.

An increase in receptor number or sensitivity, often after chronic blockade, so that abrupt withdrawal of the blocking drug can cause exaggerated responses such as tachycardia after stopping beta blockers.

A molecule that binds a receptor and activates it, producing a biological response; full agonists achieve maximal effect, whereas partial agonists produce a smaller maximal response even at full occupancy.

A molecule that binds a receptor without activating it, blocking the effect of agonists; competitive antagonists shift dose-response curves rightward, while non-competitive antagonists reduce maximal response.

The ratio of the dose producing toxicity to the dose producing the desired effect in a population; a low index, as with digoxin or lithium, demands careful monitoring of plasma levels.

Presystemic breakdown of an orally absorbed drug in gut wall or liver before it reaches systemic circulation, which lowers bioavailability and can be avoided by parenteral or sublingual routes.

The fraction of an administered dose that reaches systemic circulation unchanged; it is one hundred percent for intravenous dosing and lower for oral dosing because of incomplete absorption and first-pass metabolism.

The apparent volume relating the amount of drug in the body to its plasma concentration; a large value indicates extensive tissue uptake, as seen with lipophilic drugs such as chloroquine.

The volume of plasma from which a drug is completely removed per unit time, reflecting hepatic metabolism and renal excretion; it determines the maintenance dose needed to hold a steady-state concentration.

The time required for plasma concentration of a drug to fall by half, governed by clearance and volume of distribution; roughly four to five half-lives are needed to reach steady state.

The study of reaction rates catalysed by enzymes, described by Michaelis-Menten parameters: maximal velocity and the substrate concentration giving half maximal velocity, which together indicate affinity and capacity.

Reversible blockade in which an inhibitor competes with substrate for the active site, raising the apparent Michaelis constant while leaving maximal velocity unchanged; it can be overcome by more substrate.

Control of enzyme activity by a molecule binding at a site distinct from the active site, altering conformation and either enhancing or reducing catalysis; it underlies feedback control of metabolic pathways.

A non-protein substance, such as a metal ion or a coenzyme derived from a vitamin, that is required for an enzyme to catalyse its reaction and is often transiently bound during catalysis.

The enzyme catalysing the slowest step of a metabolic pathway, usually positioned first and subject to feedback inhibition by end products; it sets overall flux through the pathway.

The cytoplasmic pathway converting one glucose molecule into two pyruvate molecules with net production of two ATP and two NADH, functioning with or without oxygen and feeding into lactate or mitochondrial oxidation.

The mitochondrial sequence that oxidises acetyl coenzyme A to carbon dioxide, generating reduced NADH and FADH2 that drive oxidative phosphorylation; it also supplies intermediates for biosynthesis.

ATP synthesis driven by a proton gradient across the inner mitochondrial membrane, created by electron transport and used by ATP synthase; it is the main source of cellular energy and a target of poisons.

Transmission of traits controlled by single genes according to segregation and independent assortment, producing autosomal dominant, autosomal recessive, X-linked dominant and X-linked recessive patterns recognisable in pedigrees.

The proportion of individuals carrying a disease-causing genotype who actually express the phenotype; reduced penetrance explains skipped generations in dominant pedigrees and complicates genetic counselling.

The phenomenon in which a genetic disorder appears earlier or more severely in successive generations, typically caused by expansion of a trinucleotide repeat as in Huntington disease.

Parent-of-origin dependent gene expression caused by epigenetic marking, so that only the maternal or paternal copy is active; disruption produces syndromes such as Prader-Willi and Angelman.

The rapid, non-specific first line of defence comprising barriers, phagocytes, complement, natural killer cells and inflammation, recognising conserved molecular patterns rather than specific antigens and lacking memory.

Antigen-specific defence mediated by T and B lymphocytes, characterised by clonal selection, immunological memory and self-tolerance; it is slower on first exposure but faster and stronger thereafter.

A cascade of plasma proteins activated by classical, alternative or lectin pathways, producing opsonins, anaphylatoxins and a membrane attack complex that lyses cells and amplifies inflammation.

An exaggerated or inappropriate immune response causing tissue damage, classified into four types: immediate IgE-mediated, antibody-mediated cytotoxic, immune complex and delayed T-cell mediated.

Abnormal accumulation of fluid in interstitial tissue, arising from raised capillary hydrostatic pressure, reduced oncotic pressure, lymphatic obstruction or increased capillary permeability, each with characteristic clinical signs.

Inadequate blood supply to a tissue relative to its metabolic demand, causing hypoxia, accumulation of waste products and reversible or irreversible cell injury depending on duration and collateral flow.

Death of tissue caused by prolonged loss of arterial supply or venous drainage, producing a wedge-shaped pale or haemorrhagic lesion whose appearance depends on the organ's vascular anatomy.

Additional tissue damage occurring when blood flow is restored to ischaemic tissue, driven by oxygen free radicals, calcium overload, complement activation and inflammatory cell influx.

Programmed, energy-dependent cell death producing cell shrinkage, chromatin condensation and apoptotic bodies that are phagocytosed without inflammation, regulated by caspases and Bcl-2 family proteins.

Uncontrolled cell death from severe injury, marked by swelling, membrane rupture and inflammation, with subtypes such as coagulative, liquefactive, caseous and fat necrosis reflecting tissue context.

Two measures of diagnostic test performance: sensitivity is the proportion of diseased people correctly identified, and specificity is the proportion of healthy people correctly identified as disease-free.

The probability that a person with a positive test result truly has the disease; unlike sensitivity it depends on disease prevalence, rising as prevalence in the tested population increases.

The ratio of the probability of a given test result in diseased versus non-diseased people; it summarises how much a result shifts the pre-test probability of disease toward or away from diagnosis.