PH2.1-5 | Autonomic and Peripheral Pharmacology — Practice Quiz

Correct. Adrenaline's non-selective adrenoceptor agonism is precisely what makes it indispensable in anaphylaxis — no other single drug can simultaneously reverse vasodilation, bronchospasm, and cardiac depression.

Adrenaline is the drug of choice in anaphylaxis because it simultaneously addresses all three life-threatening components: α1-mediated vasoconstriction restores BP, β2-mediated bronchodilation relieves bronchospasm, and β1-mediated inotropy improves cardiac output.

Incorrect. In anaphylaxis, you need to reverse three simultaneous threats: vasodilatory shock (α1), bronchospasm (β2), and reduced cardiac output (β1). Only adrenaline's broad receptor profile achieves all three.

Correct. OPCs irreversibly phosphorylate the serine residue at AChE's esteratic site, preventing ACh hydrolysis and causing sustained cholinergic overstimulation at all cholinergic synapses — muscarinic, nicotinic, and central.

Organophosphate compounds (OPCs) cause SLUDGE/DUMBELS features through irreversible AChE inhibition. The classic presentation combines muscarinic (SLUDGE: salivation, lacrimation, urination, defecation, GI cramps, emesis), nicotinic (fasciculations, weakness), and central effects.

Incorrect. The clinical picture — miosis, bradycardia, bronchospasm, excessive secretions, AND muscle fasciculations — is the toxidrome of AChE inhibition by an organophosphate. The combination of muscarinic + nicotinic features is the key diagnostic clue.

Correct. The primary goal of atropine in OPC poisoning is to dry bronchial secretions and relieve bronchospasm — the two features that cause death by asphyxia. These muscarinic endpoints are the correct titration target.

Atropine titration in OPC poisoning targets the muscarinic (not nicotinic) endpoints. The life-threatening features are bronchospasm and excessive bronchial secretions. Tachycardia, mydriasis, and skin dryness are unreliable; fasciculations require pralidoxime, not atropine.

Incorrect. Atropine titration should target bronchial secretions and chest auscultation, not heart rate or pupils. Fasciculations are a nicotinic feature not reversed by atropine; they require pralidoxime (oxime therapy).

Correct. α1 blockers have dual utility: antihypertensive via arterial vasodilation, and BPH symptom relief via relaxation of bladder neck and prostate smooth muscle (α1A subtypes). Prazosin treats both; tamsulosin is uroselective (α1A/D) with minimal BP effect.

α1 receptors mediate smooth muscle contraction in both blood vessels (vasoconstriction → hypertension) and the bladder neck/prostate (urethral resistance → BPH symptoms). α1 blockers reduce peripheral vascular resistance AND relax urethral smooth muscle, addressing both conditions.

Incorrect. The key insight is that α1 receptors mediate smooth muscle tone in both vessels and the lower urinary tract. Only α1 blockade addresses both pathologies simultaneously.

Correct. Phase 1 depolarisation block is unique to depolarising NMBDs. The fasciculations are the clinical signature of the initial depolarisation; flaccid paralysis follows as end-plate Na+ channels become inactivated during sustained membrane depolarisation.

Succinylcholine is a depolarising NMBD: it mimics ACh and depolarises the NMJ end-plate (phase 1 block). The initial depolarisation produces disorganised unsynchronised fasciculations. Because succinylcholine is not hydrolysed by AChE (only by plasma cholinesterase), sustained depolarisation keeps Na+ channels inactivated → flaccid paralysis.

Incorrect. Succinylcholine is a depolarising NMB, not a competitive blocker or AChE inhibitor. The sequence (fasciculations then paralysis) specifically reflects the two phases of depolarisation block at the NMJ.

Correct. Atracurium/cisatracurium are the preferred NMBDs in renal failure precisely because Hofmann elimination is organ-independent. The drug is safely metabolised regardless of renal function.

Atracurium (and cisatracurium) undergo Hofmann elimination — a spontaneous non-enzymatic chemical degradation at physiological pH and temperature, independent of renal or hepatic function. This makes them the NMBDs of choice in renal and hepatic failure. Pancuronium is 80% renally excreted and must be avoided in renal failure.

Incorrect. For a patient with renal failure, you need an NMBD that does NOT rely on kidneys for elimination. Atracurium's Hofmann elimination is the only organ-independent route among the standard NMBDs.

Correct. 3 mg/kg is the standard maximum for lignocaine plain (without vasoconstrictor). For a 70 kg adult: 3 × 70 = 210 mg. With adrenaline, this rises to 7 mg/kg. Both figures are high-yield for clinical practice.

The maximum safe dose of lignocaine (lidocaine) is 3 mg/kg WITHOUT adrenaline and 7 mg/kg WITH adrenaline. Adrenaline causes local vasoconstriction, slowing systemic absorption and allowing a higher total dose. Exceeding these limits risks systemic LA toxicity (CNS excitation → convulsions → CNS depression → cardiovascular collapse).

Incorrect. The standard dose limits for lignocaine are: 3 mg/kg plain, 7 mg/kg with adrenaline. Exceeding the plain limit in well-vascularised areas risks CNS toxicity (tinnitus, perioral numbness, convulsions).

Correct. Lipid emulsion rescue (20% Intralipid, 1.5 mL/kg IV bolus) is the established intervention for LA cardiovascular toxicity, particularly bupivacaine. The lipid sink pulls bupivacaine away from cardiac myocytes, allowing channel recovery.

Bupivacaine is highly cardiotoxic because it preferentially binds the inactivated state of cardiac Na+ channels with slow dissociation ('fast-in, slow-out' kinetics), causing refractory arrhythmias. The definitive rescue therapy is 20% lipid emulsion (Intralipid) — the 'lipid sink' mechanism draws bupivacaine out of cardiac tissue into a lipid aqueous compartment.

Incorrect. Standard ACLS measures are often insufficient for bupivacaine cardiotoxicity. The specific antidote is 20% lipid emulsion (Intralipid) — all areas using bupivacaine must have it immediately available per AAGBI guidelines.

Correct. This is a classic high-yield pharmacology principle. The 'alpha-first' rule exists because β2-vasodilation provides a partial safety buffer against catecholamine-induced hypertension. Remove β2 before controlling α1, and the resulting unopposed α1 vasoconstriction can be catastrophic.

In phaeochromocytoma, massive catecholamine secretion activates both α and β receptors. β2-mediated vasodilation partially counterbalances α1-mediated vasoconstriction. If beta blockers are given first, β2 vasodilation is removed, leaving α1 vasoconstriction completely unopposed — resulting in a potentially lethal hypertensive crisis (BP can exceed 300/200 mmHg).

Incorrect. The reason is mechanistic: in a catecholamine-rich state, β2 vasodilation is keeping blood vessels partially open. Beta blockade removes this vasodilatory buffer, leaving only α1-mediated vasoconstriction — a potentially fatal scenario.

Correct. Pralidoxime reactivates AChE by removing the organophosphate from the serine esteratic site before ageing. It is particularly important for nicotinic/NMJ effects (muscle weakness, fasciculations) that atropine cannot reverse because atropine only blocks muscarinic receptors.

Pralidoxime (an oxime) reactivates AChE by nucleophilically attacking the phosphate group binding AChE, releasing the active enzyme — but ONLY before the phosphorylated enzyme 'ages' (hydrolysis of a side chain makes the bond irreversible, typically within 24–48 h for most OPCs). Pralidoxime addresses nicotinic (NMJ) effects that atropine cannot; together they provide complementary coverage.

Incorrect. Pralidoxime is an oxime AChE reactivator, not a receptor blocker. Its role is to physically reverse AChE inhibition before ageing renders it permanent. Time is critical — pralidoxime must be given early.