Preparatory Mindset
The autonomic nervous system controls everything you don't consciously think about. The key is understanding the RECEPTOR types (α1, α2, β1, β2, M1-M3, Nn, Nm) and what each does when stimulated. Agonists activate, antagonists block. Memorize the distribution: β1 = heart, β2 = lungs/vessels, α1 = vessels, M2 = heart, M3 = glands/smooth muscle.
Core Concepts
Ch02: Autonomic Nervous System
Purpose: Key drug tables + Extra MCQs + Case-based MCQs
Key Drug Table
| Drug Class | Drug(s) | MOA | Key Effects | Key Side Effects |
|-----------|---------|-----|-------------|-----------------|
| Cholinomimetic (Direct) | Pilocarpine | M-receptor agonist | ↑ Secretions, miosis, ↓ IOP, spasm of accommodation | ↑ Salivation, sweating, bradycardia |
| Cholinomimetic (Indirect) | Neostigmine | AChE inhibitor | ↑ ACh at synapse → ↑ cholinergic effects | Bradycardia, hypersalivation (Myasthenia gravis treatment) |
| Organophosphates | Parathion, Malathion | Irreversible AChE inhibitor | Massively ↑ ACh → cholinergic crisis | Salivation, lacrimation, urination, defecation, GI upset, emesis (SLUDGE) |
| Muscarinic Antagonist | Atropine | Competitive M-receptor blocker | ↑ HR, ↓ secretions, mydriasis, cycloplegia | Dry mouth, blurred vision, tachycardia, heat intolerance |
| Muscarinic Antagonist (synthetic) | Pirenzepine | M1-selective blocker | ↓ Gastric acid secretion | Less systemic side effects than atropine |
| α1 Agonist | Phenylephrine | α1-selective agonist | Vasoconstriction → ↑ BP, mydriasis (no cycloplegia) | Reflex bradycardia |
| α2 Agonist (Central) | Clonidine | α2 agonist (central) | ↓ Sympathetic outflow → ↓ BP | Rebound hypertension on withdrawal; dry mouth, sedation |
| β1 Agonist | Dobutamine | β1-selective agonist | ↑ Contractility, ↑ HR | Arrhythmias, ↑ O2 demand |
| β2 Agonist | Salbutamol (Albuterol) | β2-selective agonist | Bronchodilation, vasodilation in muscle | Tremor, tachycardia (mild β1), hypokalemia |
| Non-selective β Agonist | Isoprenaline (Isoproterenol) | β1+β2 agonist | ↑ HR, ↑ contractility, bronchodilation | Tachycardia, arrhythmias |
| α/β Agonist | Adrenaline (Epinephrine) | α1+α2+β1+β2 agonist | Low dose: β2 vasodilation → ↓ DBP; High dose: α1 vasoconstriction → ↑ BP | Anxiety, tachycardia, hypertension, arrhythmias |
| α/β Agonist | Dopamine | D1+D2 + β1 + α1 (dose-dependent) | Low dose: renal/mesenteric vasodilation (D1); Moderate: β1 inotropy; High: α1 vasoconstriction | Tachycardia, arrhythmias, extravasation necrosis |
| α1 Blocker | Prazosin | Selective α1 blocker | Vasodilation → ↓ BP | Orthostatic hypotension, reflex tachycardia, dizziness |
| Non-selective α Blocker | Phentolamine | α1+α2 blocker | Vasodilation → ↓ BP; used for pheochromocytoma diagnosis | Reflex tachycardia; NOT for primary hypertension |
| α1+β Blocker | Labetalol, Carvedilol | α1 + β1+β2 blocker | ↓ BP via dual mechanism | Bronchospasm (β2 block), bradycardia, orthostatic hypotension |
| β Blocker (Non-selective) | Propranolol | β1+β2 blocker | ↓ HR, ↓ contractility, ↓ O2 demand; bronchoconstriction (β2) | Bronchospasm (CI in asthma), bradycardia, fatigue, mask hypoglycemia |
| β Blocker (Cardioselective) | Metoprolol, Atenolol | β1-selective blocker | ↓ HR, ↓ contractility | Less bronchospasm (safer in asthma at low doses) |
Adrenaline Effects (High-Yield: MUST KNOW)
| Dose | Heart Rate | Systolic BP | Diastolic BP | Peripheral Resistance |
|------|-----------|-------------|-------------|---------------------|
| Low/Moderate | ↑ (β1) | ↑ (β1 → ↑ CO) | ↓ (β2 vasodilation) | ↓ (β2 dominant) |
| High | ↑↑ (β1) | ↑↑ | ↑ (α1 vasoconstriction overrides β2) | ↑ (α1 dominant) |
Exam-Frequency Core Points (from exam notes)
- ① Drug of choice for cardiac arrest (rescue);
- ② Drug of choice for anaphylactic shock;
- ③ Acute bronchial asthma attacks;
- ④ Topical hemostasis for gingival and nasal bleeding;
- ⑤ Combined with local anesthetics to delay their absorption, prolong their duration of action, and reduce toxicity risk.
- Major adverse reactions: At therapeutic doses, palpitations, restlessness, headache, and elevated blood pressure may occur. Overdose can cause a sudden sharp rise in blood pressure, inducing cerebral hemorrhage, arrhythmias, and even ventricular fibrillation.
- ① Block cardiac β₁ receptors, inhibiting cardiac contractility, slowing heart rate, and reducing cardiac output;
- ② Block vascular smooth muscle β₂ receptors (long‑term use lowers peripheral vascular resistance, contributing to antihypertensive effect);
- ③ Block bronchial smooth muscle β₂ receptors, causing bronchoconstriction;
- ④ Reduce renin release, inhibiting the RAAS system;
- ⑤ Reduce metabolic responses – blunting the increases in blood glucose and free fatty acids induced by sympathetic stimulation.
- Clinical applications:
- ② Angina pectoris and myocardial infarction – reduce long‑term mortality in post‑MI patients;
- ③ Tachyarrhythmias;
- ④ Hyperthyroidism – control the sympathetic overactivity symptoms;
- ⑤ Timolol ophthalmic solution for glaucoma.
- Contraindications: Bronchial asthma, severe sinus bradycardia, second‑degree or higher AV block, and severe congestive heart failure.
- ① Drug of choice for myasthenia gravis;
- ② Postoperative abdominal distension and urinary retention – promotes contraction of gastrointestinal and bladder smooth muscle;
- ③ Paroxysmal supraventricular tachycardia – slows heart rate;
- ④ Reversal of poisoning due to overdose of competitive neuromuscular blocking agents (e.g., tubocurarine).
- Contraindications: Mechanical intestinal obstruction, urinary tract obstruction, and bronchial asthma.
- At therapeutic doses: dry mouth, blurred vision, tachycardia, mydriasis, skin flushing, etc.
- As dosage increases, adverse effects intensify: central excitation, restlessness, delirium, convulsions; severe poisoning may cause central depression, coma, and respiratory paralysis.
- Contraindications: Glaucoma and prostatic hypertrophy (may increase intraocular pressure and worsen dysuria).
High-Yield Points
- β1 receptors: heart (↑ HR, ↑ contractility) — blockade treats HTN, angina, HF
- β2 receptors: lungs (bronchodilation), vessels (vasodilation) — agonists treat asthma
- α1 receptors: vessels (vasoconstriction) — antagonists treat HTN
- M2 receptors: heart (↓ HR) — anticholinergics block this → tachycardia
- M3 receptors: glands, smooth muscle — anticholinergics block → dry mouth, constipation, urinary retention
- Atropine: antimuscarinic — used for organophosphate poisoning, bradycardia
- Adrenaline reversal: α-block unmasks β2 vasodilation → BP drops
Topic Summary
Autonomic drugs work through specific receptors. Sympathetic (adrenergic) receptors: α1 (vasoconstriction), β1 (heart), β2 (bronchodilation). Parasympathetic (cholinergic) receptors: M2 (heart), M3 (secretions/motility). Anticholinergics block parasympathetic effects; sympathomimetics mimic sympathetic effects.