Free FMGE Pharmacology questions

Explanation

In first-order kinetics, elimination rate is proportional to drug concentration, so a constant fraction is removed per unit time. Most drugs follow first-order elimination at therapeutic concentrations.

Explanation

Therapeutic index compares toxic and effective doses and provides an estimate of a drug’s safety margin. Drugs with a narrow therapeutic index require closer monitoring.

Explanation

A partial agonist has lower intrinsic efficacy than a full agonist. By competing for the same receptors, it can reduce the overall response when a full agonist is present.

Explanation

A very large apparent volume of distribution indicates that relatively little drug remains in plasma compared with the amount in the body. Extensive tissue distribution or tissue binding commonly produces this pattern.

Explanation

Atropine competitively blocks muscarinic acetylcholine receptors and rapidly treats bronchorrhea, bradycardia, and other muscarinic features of organophosphate poisoning. Oximes may be used to reactivate acetylcholinesterase when appropriate.

Explanation

Neostigmine increases acetylcholine at the neuromuscular junction and can reverse competitive non-depolarizing blockade. An antimuscarinic is commonly coadministered to limit muscarinic adverse effects.

Explanation

Propranolol is a nonselective beta blocker and can provoke bronchoconstriction through beta-2 blockade. Beta-1-selective agents are generally preferred when beta blockade is necessary in patients with airway disease.

Explanation

Phenylephrine is predominantly an alpha-1 agonist. It causes peripheral vasoconstriction and thereby increases systemic vascular resistance and blood pressure.

Explanation

ACE inhibitors reduce bradykinin breakdown, which can produce a persistent dry cough. Angiotensin receptor blockers such as losartan are much less likely to cause this effect.

Explanation

Loop diuretics inhibit NKCC2 in the thick ascending limb of the loop of Henle. This produces powerful natriuresis and reduces the medullary concentration gradient.

Explanation

Amiodarone can cause pulmonary toxicity, thyroid dysfunction, hepatic toxicity, corneal deposits, and other adverse effects. Its long half-life contributes to prolonged toxicity.

Explanation

Digoxin immune Fab binds free digoxin and is indicated in severe or life-threatening toxicity. Serious arrhythmias and significant hyperkalemia are important indications.

Explanation

Carbidopa inhibits peripheral dopa decarboxylase but does not significantly cross the blood-brain barrier. This increases levodopa availability to the CNS and reduces peripheral adverse effects.

Explanation

Flumazenil antagonizes benzodiazepine effects at the GABAA receptor complex. It must be used cautiously because it can precipitate seizures in susceptible or dependent patients.

Explanation

Valproate is an important teratogen associated particularly with neural tube defects and other fetal risks. Its use in pregnancy requires careful risk-benefit consideration.

Explanation

Thiazides promote proximal sodium and lithium reabsorption after sodium loss and can markedly increase serum lithium levels. Lithium has a narrow therapeutic index, so this interaction is clinically important.

Explanation

Vancomycin binds D-Ala-D-Ala residues and prevents proper peptidoglycan assembly. It is especially important against serious gram-positive infections.

Explanation

Aminoglycosides are well known for dose-related nephrotoxicity and vestibular or auditory toxicity. Neuromuscular blockade can also occur.

Explanation

Linezolid has monoamine oxidase-inhibiting activity and can precipitate serotonin toxicity when combined with serotonergic drugs. Hyperreflexia and clonus are useful clinical clues.

Explanation

Rifampicin is a potent inducer of hepatic drug-metabolizing enzymes and can lower concentrations of many coadministered drugs. This creates clinically important drug interactions.