ABCP Diplomate flashcards

32 cards. Read the term and the definition here. The deck at the top of this page is optional.

Bioavailability (F)

The fraction of an administered dose that reaches systemic circulation unchanged. Intravenous dosing has F equal to 1; oral F is reduced by first-pass hepatic metabolism and incomplete absorption.

Volume of distribution

A proportionality constant relating total body drug amount to plasma concentration. Large values indicate extensive tissue distribution; small values indicate the drug stays largely in plasma.

Clearance

The volume of plasma from which drug is completely removed per unit time. Total clearance is the sum of hepatic, renal, and other elimination clearances.

Elimination half-life

The time for plasma concentration to fall by half during first-order elimination. It equals 0.693 times volume of distribution divided by clearance.

Steady state

The condition where drug input equals elimination and concentrations plateau. It is reached after roughly four to five half-lives of constant dosing.

First-order kinetics

Elimination in which a constant fraction of drug is removed per unit time. Half-life is fixed and independent of dose or concentration.

Zero-order kinetics

Elimination at a constant amount per unit time because enzymes are saturated. Half-life increases with concentration, so small dose increases can cause large level rises.

Loading dose formula

Loading dose equals volume of distribution times target concentration divided by bioavailability. It fills the distribution volume rapidly without waiting for steady state.

Maintenance dose formula

Maintenance dose equals clearance times target concentration times dosing interval, divided by bioavailability. It replaces drug removed between doses.

Therapeutic index

The ratio of toxic dose to effective dose, often TD50 over ED50. A low index means effective and toxic concentrations are close, warranting drug level monitoring.

Protein binding effects

Only unbound drug is pharmacologically active and available for elimination. Highly bound drugs can be displaced by competitors, transiently raising free active fraction.

CYP450 induction

Increased enzyme synthesis after repeated exposure to an inducer, raising substrate metabolism. Effect develops over days to weeks and lowers co-administered substrate concentrations.

CYP450 inhibition

Direct blockade of metabolic enzymes, often rapid in onset. It raises concentrations of co-administered substrates and can precipitate toxicity.

First-pass metabolism

Hepatic and gut-wall metabolism of an orally absorbed drug before it reaches systemic circulation. It lowers oral bioavailability and can be saturated at high doses.

Agonist versus antagonist

An agonist binds a receptor and activates a response; an antagonist binds without intrinsic activity and blocks agonist effect. Partial agonists produce submaximal responses.

Competitive antagonism

An antagonist reversibly competes with agonist at the same binding site. It shifts the dose-response curve right without lowering the maximal response.

Beta-1 selective blockade

Preferential blockade of cardiac beta-1 receptors at usual doses. Bronchoconstriction risk is lower than with nonselective agents but rises as dose increases.

ACE inhibitor adverse effects

Cough from bradykinin accumulation, hyperkalemia from reduced aldosterone, and hypotension. Angioedema is rare but contraindicates rechallenge.

ARB versus ACE inhibitor

ARBs block the angiotensin receptor directly and do not increase bradykinin. They cause less cough but carry similar hyperkalemia and renal risks.

Aminoglycoside killing

Concentration-dependent bactericidal activity with a post-antibiotic effect. Extended-interval dosing maximizes peak-to-MIC ratio while limiting trough-related nephrotoxicity.

Vancomycin monitoring

Dosing is guided by AUC or trough levels to balance efficacy and nephrotoxicity. Risk increases with concurrent piperacillin-tazobactam or loop diuretics.

Warfarin monitoring

Effect is tracked by INR because warfarin inhibits vitamin K-dependent clotting factor synthesis. Numerous drug and dietary interactions shift the INR unpredictably.

Heparin monitoring

Unfractionated heparin is monitored by aPTT or anti-Xa activity. Low-molecular-weight heparin usually needs no routine monitoring except in renal impairment or pregnancy.

Opioid-benzodiazepine combination

Combined use produces additive central respiratory depression. Naloxone reverses opioids but its shorter half-life may require repeat dosing or infusion.

Anticholinergic burden

Cumulative exposure to drugs blocking muscarinic receptors. It worsens cognition, causes urinary retention and constipation, and is especially risky in older adults.

NSAID renal risk

Prostaglandin inhibition reduces afferent arteriolar dilation and glomerular perfusion. Risk rises with ACE inhibitors plus diuretics, dehydration, and chronic kidney disease.

Serotonin syndrome triad

Mental status change, autonomic instability, and neuromuscular excitation such as clonus and hyperreflexia. It follows serotonergic drug combinations and requires prompt discontinuation.

QT prolongation drugs

Several antiarrhythmics, antipsychotics, and antibiotics prolong the QT interval and risk torsades de pointes. Risk increases with hypokalemia, hypomagnesemia, and drug combinations.

Corticosteroid taper

Prolonged systemic steroids suppress the hypothalamic-pituitary-adrenal axis. Abrupt withdrawal risks adrenal crisis, so doses are tapered after extended use.

Metformin and lactic acidosis

Metformin increases anaerobic glucose metabolism and is renally cleared. It is held during acute kidney injury, hypoxia, or iodinated contrast to limit lactic acidosis risk.

Levothyroxine absorption

Absorption is reduced by food, calcium, iron, and proton pump inhibitors. Consistent timing on an empty stomach stabilizes thyroid-stimulating hormone control.

Statin myopathy risk

Muscle toxicity risk rises with high doses and interacting drugs such as CYP3A4 inhibitors. Creatine kinase and symptoms guide whether the statin is continued.