NPLEX II key terms

The body's active maintenance of stable internal conditions, such as temperature, pH, glucose, and electrolyte balance, through coordinated feedback systems that adjust physiology in response to internal and external change.

A control mechanism in which a change in a regulated variable triggers a response that opposes the change, returning the variable toward its set point. Most endocrine and autonomic regulation works this way.

Achieving stability through change: the process by which the body adjusts its regulatory set points to meet anticipated or sustained demands, such as raising blood pressure during stress or shifting metabolic priorities during illness.

The concentration of dissolved particles per kilogram of solvent, driving water movement across membranes. Plasma osmolality near 285–295 mOsm/kg is maintained mainly by thirst, ADH, and renal water handling.

The four pressures governing fluid movement across capillary walls: hydrostatic pressure and interstitial oncotic pressure pushing fluid out, and plasma oncotic pressure and interstitial hydrostatic pressure pulling fluid in.

Palpable swelling from excess fluid accumulation in interstitial tissue, arising when capillary hydrostatic pressure rises, oncotic pressure falls, lymphatic drainage is blocked, or capillary permeability increases.

Sequestration of fluid into spaces where it is not functionally available, such as the peritoneal cavity, bowel lumen, or burned tissue, producing volume depletion despite visible or occult fluid accumulation and often requiring careful reassessment of resuscitation.

A reversible chemical pair that resists pH change by accepting or donating hydrogen ions. The bicarbonate–carbonic acid pair is the principal extracellular buffer, supplemented by hemoglobin, phosphate, and protein buffers.

The difference between measured cations and anions, calculated as sodium minus the sum of chloride and bicarbonate. An elevated gap signals unmeasured anions such as ketones, lactate, uremic acids, or toxins.

The expected fall in arterial carbon dioxide produced by increased ventilation when a primary metabolic acidosis is present. It does not correct the underlying disorder and follows predictable quantitative limits.

A posterior pituitary peptide released in response to rising osmolality or falling volume that increases renal collecting-duct water permeability, concentrating urine and conserving free water.

A hormonal cascade triggered by reduced renal perfusion, low sodium delivery, or sympathetic stimulation; renin generates angiotensin II, which constricts vessels, stimulates thirst and aldosterone, and promotes sodium and water retention.

A rapid, self-propagating change in membrane voltage produced by sequential sodium influx and potassium efflux through voltage-gated channels, transmitting signals along neurons and muscle fibers.

The interval after an action potential during which a neuron or cardiac cell cannot be re-excited, or can be re-excited only by a stronger stimulus, setting limits on firing frequency and protecting against tetanic contraction in the heart.

The narrow extracellular gap between a presynaptic terminal and postsynaptic membrane where neurotransmitter is released, diffuses, and binds receptors, determining the speed and direction of signal transfer.

An increase in the number or sensitivity of receptors on a target cell, often occurring when ligand availability is chronically low, as with prolonged beta-blockade or denervation, producing exaggerated responses when stimulation returns.

The volume of blood ejected by the heart per minute, equal to heart rate multiplied by stroke volume. It reflects the integration of preload, afterload, and contractility and determines systemic oxygen delivery.

The principle that increased ventricular filling stretches myocardial fibers and increases the force of contraction, so stroke volume rises with preload within physiologic limits, then plateaus or falls with overdistension.

Presystemic elimination of an orally administered drug by intestinal and hepatic enzymes before it reaches systemic circulation, reducing oral bioavailability and explaining large differences between oral and parenteral doses.

The fraction of an administered dose that reaches systemic circulation unchanged. Intravenous dosing is defined as complete; oral bioavailability depends on absorption and first-pass elimination.

A calculated apparent volume relating the amount of drug in the body to its plasma concentration. Large values indicate extensive tissue distribution; small values suggest confinement to plasma.

The time required for plasma drug concentration to decline by half during elimination. It determines dosing interval and time to steady state, which is roughly four to five half-lives.

The ratio of a drug dose producing toxicity to the dose producing the desired effect. A low index means small differences between therapeutic and harmful exposure, warranting monitoring of levels or clinical status.

A harmful or unintended response to a drug at doses used for prevention, diagnosis, or treatment. Reactions may be dose-related, idiosyncratic, allergic, or due to interactions with other agents.

Increased expression of hepatic drug-metabolizing enzymes after exposure to an inducing agent, accelerating clearance of coadministered substrates and potentially causing therapeutic failure or altered prodrug activation.

An immune-mediated response to an antigen that causes tissue injury or dysfunction. Types I through IV differ by mechanism: immediate IgE, antibody-mediated, immune-complex, and delayed T-cell responses.

Loss of tolerance in which the immune system attacks self-antigens, producing organ-specific or systemic disease. Mechanisms include molecular mimicry, epitope spreading, and defective regulatory T-cell function.

A coordinated vascular and cellular response to injury or infection, characterized by redness, heat, swelling, pain, and loss of function, aimed at neutralizing the insult and initiating repair.

A compact aggregate of activated macrophages, often with multinucleated giant cells and a rim of lymphocytes, formed when a persistent intracellular or foreign antigen cannot be cleared, as in tuberculosis.

New, autonomous tissue growth resulting from accumulated genetic alterations that allow cells to proliferate, evade growth suppression and apoptosis, and invade or metastasize; classified as benign or malignant.

A gene whose normal product restrains cell division or promotes DNA repair or apoptosis. Both alleles typically must be inactivated before loss of function contributes to cancer.

Spread of malignant cells from a primary tumor to distant sites through lymphatics, blood vessels, or body cavities, followed by implantation and growth; a defining feature of malignancy and a major cause of mortality.

A prioritized list of possible conditions that could explain a patient's presentation, generated from the history and examination, then narrowed by targeted testing and response to treatment.

A historical or examination finding that raises concern for serious or urgent disease and prompts expedited evaluation rather than routine management, such as unexplained weight loss, night pain, or neurologic deficit.

The proportion of people with a disease who test positive. A highly sensitive test is useful for ruling out disease when negative, because false negatives are few.

The proportion of people without a disease who test negative. A highly specific test is useful for confirming disease when positive, because false positives are few.

The probability that a person with a positive test result actually has the disease. It rises with disease prevalence and with test specificity, unlike sensitivity, which does not depend on prevalence.

The number of patients who must receive an intervention for one additional patient to benefit, calculated as the reciprocal of the absolute risk reduction. Lower values indicate greater clinical efficiency.

The arithmetic difference in event rates between a control group and a treated group, expressed as a percentage or proportion. It reflects real clinical benefit better than relative risk reduction.