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

Correct. Salbutamol's β2 selectivity targets bronchial smooth muscle with minimal cardiac stimulation — the ideal profile for chronic asthma management.

Selective β2 agonists (salbutamol, terbutaline) provide bronchodilation with minimal β1-mediated cardiac stimulation. Non-selective β agonists (isoprenaline) and mixed α/β agonists (adrenaline) carry significant cardiac side effects and are reserved for specific emergencies.

Incorrect. For isolated bronchospasm with minimal cardiac side effects, selectivity matters. β2-selective agonists confine the pharmacological action to bronchial smooth muscle.

Correct. This is the classic pharmacological pairing: neostigmine reverses NMBD at the NMJ via AChE inhibition; glycopyrrolate prevents the muscarinic side effects of the same AChE inhibition elsewhere.

Neostigmine inhibits AChE everywhere, raising ACh at both NMJ (nicotinic — desired: reversal) and peripheral parasympathetic synapses (muscarinic — undesired: bradycardia, salivation, bronchospasm). A muscarinic antagonist is co-administered to block these side effects. Glycopyrrolate's quaternary structure prevents CNS penetration; atropine (tertiary) is an alternative but crosses the BBB.

Incorrect. The combination relies on complementary pharmacology: neostigmine raises ACh (NMJ reversal), glycopyrrolate blocks the resulting muscarinic side effects. They act at different receptor types.

Correct. Succinylcholine is a proven malignant hyperthermia trigger and is absolutely contraindicated in susceptible patients. Rocuronium (1.2 mg/kg) is the standard alternative for RSI in MH-susceptible patients.

Malignant hyperthermia (MH) is a pharmacogenetic disorder triggered by volatile halogenated anaesthetics and depolarising NMBDs (succinylcholine). Non-depolarising NMBDs are NOT MH triggers. When RSI is needed in a patient with MH susceptibility, high-dose rocuronium (1.2 mg/kg) is used instead, with sugammadex available for reversal.

Incorrect. The key risk factor here is MH susceptibility. Succinylcholine is a classic trigger for the hypermetabolic crisis of malignant hyperthermia; non-depolarising agents are safe alternatives.

Correct. Pilocarpine's M3-mediated ciliary muscle contraction directly expands the trabecular network, facilitating aqueous drainage — the classical mechanism of cholinomimetics in open-angle glaucoma.

Pilocarpine is a direct-acting muscarinic agonist that acts on M3 receptors in the ciliary muscle. Ciliary muscle contraction tightens the trabecular meshwork, opening aqueous humour outflow channels in the conventional pathway, reducing IOP. Note: pilocarpine causes miosis (not mydriasis) via the iris sphincter; it is contraindicated in angle-closure glaucoma if the iris blocks flow.

Incorrect. Pilocarpine reduces IOP by increasing aqueous outflow (not reducing production). The pathway is M3 → ciliary muscle contraction → trabecular meshwork opens → outflow increases.

Correct. The calculation chain is: 7 mg/kg × 60 kg = 420 mg; 2% = 20 mg/mL; 420 ÷ 20 = 21 mL. This is a high-yield calculation for clinical practice and written examinations.

Maximum dose of lignocaine WITH adrenaline = 7 mg/kg. For 60 kg: 7 × 60 = 420 mg. A 2% solution contains 20 mg/mL (2 g/100 mL = 20 mg/mL). Volume = 420 mg ÷ 20 mg/mL = 21 mL. The 3 mg/kg limit (9 mL) applies to lignocaine WITHOUT adrenaline.

Incorrect. Apply the correct formula: maximum dose (mg/kg) × patient weight ÷ concentration (mg/mL). With adrenaline the limit is 7 mg/kg; a 2% solution contains 20 mg per mL.

Correct. This is the mechanistic rationale for noradrenaline as first-line vasopressor in septic shock. The α1:β2 receptor selectivity profile determines which catecholamine best restores SVR with minimal adverse effects.

In distributive (septic) shock, the pathophysiology is massive vasodilation with maintained or elevated cardiac output. Restoration of SVR is the therapeutic goal. Noradrenaline (α1 >> β1, minimal β2) achieves this without counterproductive β2-mediated vasodilation. Adrenaline adds β2 vasodilation, worsening the core problem, and causes lactic acidosis at higher doses.

Incorrect. The pharmacological choice here is based on receptor selectivity profile. In septic shock (vasodilation predominant), you need α1 vasoconstriction without additional β2 vasodilation — noradrenaline provides this; adrenaline does not.

Correct. PABA — the ester hydrolysis product — explains the higher allergy rate with ester LAs. Because amides don't produce PABA, true amide allergy is rare. This distinction is essential when a patient reports an 'LA allergy.'

The ester/amide classification is clinically important for allergy prediction. Esters (procaine, cocaine, chloroprocaine, benzocaine) are hydrolysed by plasma cholinesterase to para-aminobenzoic acid (PABA), a common allergen. Amides (lignocaine, bupivacaine, ropivacaine, prilocaine) are metabolised in the liver by cytochrome P450 enzymes — true allergy is extremely rare, and they produce NO PABA.

Incorrect. The metabolic and allergy profiles differ fundamentally between ester and amide LAs. Esters → plasma hydrolysis → PABA (allergenic). Amides → hepatic CYP → no PABA → rare allergy.

Correct. In cardiogenic shock, the heart cannot pump adequately. Inotropes (dobutamine, dopamine) are the pharmacological priority; noradrenaline may be added if severe hypotension persists despite inotropes.

Cardiogenic shock is pump failure — the fundamental problem is reduced cardiac output, not vasodilation. The solution is inotropic support. Dobutamine (β1 dominant, some β2) increases contractility and reduces afterload. Dopamine at intermediate doses (5–10 mcg/kg/min) provides inotropy + some vasoconstriction. Pure vasoconstrictors (phenylephrine) worsen afterload and worsen a failing heart.

Incorrect. Cardiogenic shock is pump failure — the pathophysiology is depressed contractility, NOT vasodilation. Pure vasopressors increase afterload against an already failing heart. Inotropic support (dobutamine/dopamine) addresses the primary deficit.

Correct. This is a clinically critical distinction: treating a cholinergic crisis with more pyridostigmine (thinking it is a myasthenic crisis) would worsen the patient dangerously. Look for muscarinic features (SLUDGE signs) to identify cholinergic crisis.

Worsening weakness in a patient on AChE inhibitor therapy can represent either a myasthenic crisis (under-treated, too little ACh at NMJ → give more pyridostigmine) or a cholinergic crisis (ACh toxicity — sustained depolarisation blocking NMJ, with added muscarinic features: excessive secretions, miosis, bradycardia → reduce or stop pyridostigmine + atropine for muscarinic effects). The edrophonium (Tensilon) test was historically used to differentiate but is now rarely done due to the availability of clinical assessment and ICU support.

Incorrect. The immediate clinical priority is distinguishing myasthenic from cholinergic crisis because the treatments are diametrically opposite. Additional AChE inhibitor in a cholinergic crisis is potentially fatal.