Free NEET PG & INI-CET Pharmacology MCQs

Explanation

Bioavailability is the fraction of an administered dose reaching the systemic circulation unchanged. Intravenous administration bypasses absorption entirely, so its bioavailability is defined as 100% and is the reference against which other routes are measured.

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Sublingual absorption drains into the systemic circulation via the superior vena cava, bypassing the portal vein and hepatic first-pass metabolism. This is why sublingual nitroglycerin acts rapidly and reliably.

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Phenytoin, ethanol and high-dose aspirin follow zero-order kinetics because their metabolising enzymes saturate at therapeutic concentrations. A small dose increase can then cause a disproportionate rise in plasma level and toxicity.

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A competitive inhibitor competes for the active site, raising the apparent Km (lower affinity) but leaving Vmax unchanged, since the inhibition can be overcome by increasing substrate concentration.

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The insulin receptor is a receptor tyrosine kinase. Ligand binding triggers autophosphorylation of tyrosine residues, activating downstream signalling. Insulin-like growth factor and several growth factor receptors work the same way.

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Digoxin, lithium, warfarin, phenytoin and theophylline have narrow therapeutic indices, meaning the toxic dose is close to the therapeutic dose. They require plasma level monitoring to avoid toxicity.

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It takes about 4 to 5 half-lives to reach 94 to 97% of steady-state concentration, and the same number to eliminate a drug after stopping it. This principle guides dosing intervals and loading-dose decisions.

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Atropine is a competitive muscarinic (cholinergic) antagonist. It causes tachycardia, mydriasis, dry mouth and reduced secretions, and is used in bradycardia and organophosphate poisoning.

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Metoprolol, atenolol, bisoprolol and esmolol are beta-1 selective (cardioselective), causing less bronchoconstriction than non-selective agents such as propranolol. Selectivity is relative and is lost at high doses, so caution still applies in asthma.

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Tamsulosin is a selective alpha-1A blocker that relaxes smooth muscle in the prostate and bladder neck, improving urine flow in BPH. Finasteride works differently, by inhibiting 5-alpha-reductase.

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Pyridostigmine and neostigmine inhibit acetylcholinesterase, increasing acetylcholine at the neuromuscular junction and improving muscle strength in myasthenia gravis. Neostigmine also reverses non-depolarising muscle blockade.

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Adrenaline reverses anaphylaxis through alpha-1 mediated vasoconstriction (raising blood pressure and reducing mucosal oedema) and beta-2 mediated bronchodilation, while beta-1 effects support cardiac output. It is the first-line drug, given intramuscularly.

Explanation

Succinylcholine can cause hyperkalaemia (dangerous in burns, crush injury and denervation) and can trigger malignant hyperthermia in susceptible individuals, treated with dantrolene. It also causes transient fasciculations.

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ACE also degrades bradykinin. ACE inhibitors raise bradykinin levels, producing the characteristic dry cough and, rarely, angioedema. Switching to an ARB, which does not affect bradykinin, resolves the cough.

Explanation

Warfarin inhibits vitamin K epoxide reductase, reducing synthesis of the vitamin K dependent factors II, VII, IX and X. It is monitored by PT/INR and reversed with vitamin K or, urgently, prothrombin complex concentrate.

Explanation

Unfractionated heparin is monitored by aPTT; it acts by activating antithrombin III. Warfarin is monitored by PT/INR. The antidote to heparin is protamine sulphate.

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Verapamil, quinidine and amiodarone reduce digoxin clearance and displace it from tissue binding, raising serum levels. Hypokalaemia also worsens toxicity. Digoxin-specific antibody fragments treat toxicity rather than causing it.

Explanation

Labetalol, methyldopa and nifedipine are safe in pregnancy. ACE inhibitors and ARBs are teratogenic, causing fetal renal damage, and are contraindicated especially in the second and third trimesters.

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Amiodarone is iodine-rich and lipophilic, causing pulmonary fibrosis, thyroid dysfunction (both under- and over-active), corneal deposits, hepatotoxicity and blue-grey skin discolouration. Baseline and periodic thyroid, liver and lung function testing is required.

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Statins (HMG-CoA reductase inhibitors) can cause myopathy ranging from myalgia to rhabdomyolysis, especially alongside fibrates or CYP inhibitors. They also raise liver transaminases. Muscle symptoms with a high CK warrant stopping the drug.

Explanation

Intravenous lorazepam, a benzodiazepine, is first-line for status epilepticus because of its rapid onset and longer duration than diazepam. Longer-term control follows with phenytoin, fosphenytoin or valproate.

Explanation

Ethosuximide is first-line for absence seizures, acting on T-type calcium channels in thalamic neurons. Valproate is an alternative, especially when other seizure types coexist. Carbamazepine and phenytoin can worsen absence seizures.

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The triad of miosis, respiratory depression and reduced consciousness indicates opioid overdose. Naloxone, a competitive opioid antagonist, reverses it rapidly, though repeat dosing may be needed because of its short half-life.

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Thiazides reduce renal lithium clearance by increasing proximal reabsorption, raising lithium into the toxic range. NSAIDs and ACE inhibitors do the same. Lithium has a narrow therapeutic index and needs level monitoring.

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Clozapine can cause agranulocytosis and requires regular white cell and absolute neutrophil count monitoring. It is reserved for treatment-resistant schizophrenia and also carries risks of myocarditis and seizures.

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MAC is the alveolar concentration preventing movement in 50% of patients in response to a stimulus. A low MAC means high potency. MAC correlates with lipid solubility, the Meyer-Overton hypothesis.

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Isoniazid increases pyridoxine excretion, causing a deficiency neuropathy. Prophylactic pyridoxine prevents it, particularly in those at risk such as diabetics, people with alcohol dependence and pregnant women.

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Aminoglycosides accumulate in renal proximal tubule cells (nephrotoxicity, usually reversible) and in cochlear and vestibular hair cells (ototoxicity, often permanent). Once-daily dosing and level monitoring reduce the risk.

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Ethambutol causes dose-dependent retrobulbar (optic) neuritis with reduced acuity and red-green colour blindness. It is usually reversible on stopping the drug; visual acuity and colour vision should be checked before and during treatment.

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Rifampicin colours urine, sweat and tears orange-red, which is harmless but alarming if unwarned. It is also a potent CYP450 inducer, reducing the effect of oral contraceptives, warfarin and many other drugs.

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Vancomycin is first-line for serious MRSA infections, with linezolid and daptomycin as alternatives. It can cause red man syndrome with rapid infusion and is nephrotoxic at high trough levels.

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Fluoroquinolones are associated with tendinitis and tendon rupture, and cause cartilage damage in animal studies, so they are avoided in children and pregnancy. They can also prolong the QT interval.

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Amphotericin B binds ergosterol in the fungal cell membrane, forming pores that cause leakage of ions and cell death. Azoles instead inhibit ergosterol synthesis and echinocandins block beta-glucan synthesis. Amphotericin is notably nephrotoxic.

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Beta-lactams bind penicillin-binding proteins and inhibit transpeptidation, the cross-linking step of peptidoglycan cell wall synthesis, leading to bacterial lysis. Resistance often occurs through beta-lactamase enzymes.

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Cyclophosphamide's metabolite acrolein irritates the bladder, causing haemorrhagic cystitis. Mesna binds and inactivates acrolein in the urine, preventing this. Adequate hydration also helps.

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Doxorubicin, an anthracycline, causes dose-dependent cardiotoxicity and cardiomyopathy through free-radical generation, and dexrazoxane is cardioprotective. Bleomycin causes pulmonary fibrosis, vincristine causes neuropathy and cisplatin causes nephrotoxicity.

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Vincristine, a vinca alkaloid that inhibits microtubule formation, characteristically causes peripheral neuropathy, its dose-limiting toxicity. Notably it produces relatively little myelosuppression, unlike vinblastine.

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Methotrexate inhibits dihydrofolate reductase. Folinic acid (leucovorin) bypasses the blocked enzyme, rescuing normal cells from toxicity while the tumour effect is preserved with correct timing.

Explanation

Insulin lispro, aspart and glulisine are rapid-acting analogues with onset within 15 minutes, used at mealtimes. Glargine and detemir are long-acting basal insulins, and NPH is intermediate-acting.

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Metformin, a biguanide, rarely causes lactic acidosis, especially in renal impairment, and is withheld around contrast studies and surgery. Unlike sulfonylureas it does not cause hypoglycaemia when used alone, and it is weight-neutral.

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Corticosteroids raise blood glucose and are diabetogenic, so hypoglycaemia is not expected. Chronic use causes osteoporosis, Cushingoid features, immunosuppression, cataracts and adrenal suppression on withdrawal.

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Propylthiouracil is preferred in the first trimester because methimazole and carbimazole are associated with fetal malformations such as aplasia cutis and choanal atresia early in pregnancy. Radioactive iodine is contraindicated in pregnancy.

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Aspirin irreversibly acetylates cyclooxygenase, blocking thromboxane A2 synthesis in platelets. Because platelets cannot synthesise new enzyme, the antiplatelet effect lasts the platelet's lifespan of 7 to 10 days.

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Colchicine relieves acute gout by inhibiting microtubule formation and neutrophil migration into the joint. Allopurinol and febuxostat lower urate for long-term prevention and can worsen an acute attack if started during one.

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First-generation H1 antihistamines cross the blood-brain barrier and cause sedation and anticholinergic effects. Second-generation agents such as cetirizine, loratadine and fexofenadine are less sedating because they penetrate the CNS poorly.

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Gastric mucosal prostaglandins, produced via COX-1, promote mucus and bicarbonate secretion and mucosal blood flow. NSAIDs inhibit their synthesis, reducing protection and predisposing to ulcers. Misoprostol, a prostaglandin analogue, is protective.

Explanation

Organophosphates inhibit acetylcholinesterase, causing a cholinergic crisis (DUMBELS). Atropine blocks the muscarinic effects while pralidoxime reactivates the enzyme if given before ageing of the enzyme-inhibitor complex.

Explanation

N-acetylcysteine replenishes hepatic glutathione, allowing conjugation and clearance of the toxic metabolite NAPQI. It is most effective within 8 hours of ingestion and prevents hepatic necrosis.

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Fomepizole inhibits alcohol dehydrogenase, preventing conversion of methanol to toxic formic acid, which causes the visual loss and acidosis. Ethanol is an alternative competitive substrate, and haemodialysis removes methanol in severe cases.

Explanation

Glucagon raises intracellular cAMP through a receptor independent of the beta adrenergic receptor, restoring heart rate and contractility in beta blocker overdose refractory to atropine. High-dose insulin-euglycaemia therapy is an adjunct.