2804NRS · Human Pathophysiology And Pharmacology 1
Neurological and Autonomic
The brain lives in a sealed box, so pressure is everything; and the body's involuntary functions run on a two-wire autonomic system whose chemistry — noradrenaline vs acetylcholine on adrenergic vs cholinergic receptors — is the richest source of pharmacology MCQs in the unit. This chapter covers raised intracranial pressure (the Monro-Kellie doctrine, the compliance curve, CPP = MAP − ICP, and Cushing's triad as a LATE sign), then the autonomic nervous system — all preganglionic and all parasympathetic postganglionic fibres use ACh, most sympathetic postganglionic fibres use noradrenaline — and the adrenergic receptors (α1 vasoconstriction, β1 heart, β2 lungs) and cholinergic synapse with their drugs (atropine, AChE inhibitors). In 2804NRS this is Module 7 — examined by MCQ and short-answer, and autonomic pharmacology is the highest-yield drug topic.
What this chapter covers
- 017.1 Neurological dysfunction — the general picture
- 027.2 Raised ICP — Monro-Kellie & the compliance curve
- 037.3 The autonomic nervous system — two wires, two chemicals
- 047.4 Adrenergic receptors — match the drug to the receptor
- 057.5 The cholinergic synapse — ACh & its drugs
Match the adrenergic receptor to its effect and drug
- +1(a) α1: blood vessels and sphincters → vasoconstriction (↑ BP); blocker is an '-osin' (prazosin).
- +1(b) β1: the heart → ↑ rate and force; blocker is an '-olol' (metoprolol).
- +1(c) β2: bronchioles → bronchodilation; agonist is salbutamol (asthma reliever).
- +1Adrenaline in anaphylaxis: hits β2 (opens the airway) AND α1 (raises BP) — the two failing systems in anaphylaxis.
Key terms
- Monro-Kellie doctrine
- Inside the rigid skull, brain tissue + CSF + blood are in volume equilibrium: if one volume rises, another must fall or intracranial pressure (normally 7–15 mmHg) climbs.
- Cerebral perfusion pressure (CPP)
- CPP = MAP − ICP. A rising ICP lowers CPP, reducing cerebral blood flow and oxygen delivery → cerebral ischaemia.
- Cushing's triad
- A LATE, ominous sign of herniation: rising blood pressure with a widening pulse pressure, bradycardia (not tachycardia), and irregular respiration. The bradycardia is a favourite MCQ catch.
- Autonomic wiring
- All preganglionic fibres and all parasympathetic postganglionic fibres release ACh; most sympathetic postganglionic fibres release noradrenaline. The split is at the postganglionic synapse.
- Adrenergic receptors
- α1 = vasoconstriction (↑ BP, mydriasis); α2 = presynaptic negative feedback; β1 = heart (↑ rate/force); β2 = bronchodilation. '-olol' blocks β, '-osin' blocks α1, salbutamol is a β2 agonist.
Neurological and Autonomic FAQ
Why is intracranial pressure the hub of this module?
Because brain tumours, bleeds, oedema and infection all add volume to a fixed box, so they converge on one final pathway: rising ICP → falling cerebral perfusion (CPP = MAP − ICP) → ischaemia. Learn the Monro-Kellie compliance curve once — flat (compensated) then steep (decompensated) — and it explains the lot.
Why is Cushing's triad a late sign?
Cushing's triad — rising BP with widening pulse pressure, bradycardia and irregular respiration — is a reflex to force blood into an ischaemic brain, so it appears only once compensation is exhausted, signalling impending herniation. Note the bradycardia (not tachycardia), which is a common MCQ catch. Early signs are headache, reduced consciousness, projectile vomiting and papilloedema.
How is the autonomic nervous system wired chemically?
All preganglionic fibres use ACh on nicotinic receptors, and so do both ganglia. The split is postganglionic: the sympathetic system releases noradrenaline (adrenergic), the parasympathetic releases ACh (muscarinic). Exceptions to memorise: sympathetic sweat glands are cholinergic, and the adrenal medulla is nicotinic-driven.
What do AChE inhibitors do?
They block acetylcholinesterase, the enzyme that destroys ACh, so ACh accumulates at every cholinergic synapse. They are used to boost weak transmission in myasthenia gravis, slow cognitive decline in Alzheimer's (where brain ACh is low) and reverse non-depolarising neuromuscular blockade. Atropine does the opposite — it blocks muscarinic receptors ('can't see, pee, spit or poo').
Exam move
Learn the ICP compliance curve and CPP = MAP − ICP as one unit, and tag Cushing's triad firmly as LATE (with bradycardia, not tachycardia). For pharmacology, the payoff is enormous: master the autonomic wiring (ACh everywhere except sympathetic postganglionic = noradrenaline) and the adrenergic map (α1 vessels, β1 heart, β2 lungs), then read drug suffixes ('-olol' = β-blocker, '-osin' = α1-blocker, salbutamol = β2 agonist). If you can name the transmitter and the receptor, you can predict every drug effect — which is exactly how the MCQ half is built.
