Pharmacology Cheat Sheet
Autonomic Receptors and Reversal
Autonomic pharmacology for NEET-PG: receptor G-protein pathways, alpha and beta blockers, physostigmine vs neostigmine, and organophosphate antidotes.
MedNext Academy | 3 min read
Clinically reviewed by Dr Shameer Deen, MBBS, MS, MRCS
Autonomic Receptors and Reversal
Autonomic pharmacology for NEET-PG: receptor G-protein pathways, alpha and beta blockers, physostigmine vs neostigmine, and organophosphate antidotes.
Autonomic nervous system pharmacology covering cholinergic and adrenergic receptors, agonists, antagonists, anticholinesterases, and their reversal agents.
High-yield lines
- Both sympathetic and parasympathetic preganglionic fibres release acetylcholine acting on nicotinic receptors at the ganglia.
- Sweat glands are an exception in the sympathetic system: they use acetylcholine on muscarinic receptors, not noradrenaline.
- The Gq pathway raising IP3 and calcium is used by muscarinic M1, M3, M5 and alpha-1, while Gi lowering cAMP is used by M2, M4, alpha-2, and D2.
- All beta receptors and the D1 receptor signal through Gs to raise cAMP.
- After an alpha-blocker, adrenaline produces a fall in blood pressure instead of a rise, which is called adrenaline reversal or Dale's vasomotor reversal.
- Phenoxybenzamine is an irreversible, non-competitive, insurmountable alpha-blocker, whereas phentolamine is reversible and competitive.
- Phentolamine is infiltrated locally to rescue tissue from noradrenaline or dopamine extravasation.
- Glucagon is the antidote for beta-blocker overdose because it raises cardiac cAMP independently of beta receptors.
- Prazosin is the specific antidote for scorpion-sting autonomic storm in the Indian context.
- Physostigmine is a tertiary amine that crosses the blood-brain barrier and reverses central anticholinergic (atropine) toxicity, unlike quaternary neostigmine.
- Pyridostigmine is the drug of choice for chronic maintenance of myasthenia gravis because it is longer-acting and oral.
- In organophosphate poisoning, atropine treats the muscarinic features and pralidoxime reactivates acetylcholinesterase before ageing occurs.
- Once an organophosphate-inhibited enzyme has undergone ageing, pralidoxime can no longer reactivate it.
- In phaeochromocytoma, alpha-blockade with phenoxybenzamine must precede beta-blockade to avoid unopposed alpha vasoconstriction.
Mapped competency codes
- PH1.13
- PH1.14
Continue into the full chapter
This summary maps to PH2-autonomic-nervous-system-pharmacology.
Frequently Asked Questions
Why is physostigmine, not neostigmine, used for atropine toxicity?
Physostigmine is a tertiary amine that crosses the blood-brain barrier to reverse central antimuscarinic delirium; quaternary neostigmine cannot enter the CNS.
What is the antidote for beta-blocker overdose?
Glucagon, which activates cardiac adenylyl cyclase and raises cAMP independently of beta receptors, plus high-dose insulin-euglycaemia and calcium as adjuncts.
Why must pralidoxime be given early in organophosphate poisoning?
Because the inhibited enzyme undergoes ageing to a permanently inactivated form, after which oxime reactivation no longer works.
Which alpha-blocker is used for scorpion-sting autonomic storm?
Prazosin, which reverses the catecholamine-driven vasoconstriction and pulmonary oedema.
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