ANS: OVERVIEW, CHOLINERGIC, ADRENERGIC Flashcards
(38 cards)
What are the two main divisions of the autonomic nervous system (ANS)?
The sympathetic (“fight or flight”) and parasympathetic (“rest and digest”) divisions.
What are cholinoceptors and what are their two main types?
Cholinoceptors are receptors that respond to acetylcholine. They include:
Muscarinic receptors (mAChRs): G-protein-coupled receptors
Nicotinic receptors (nAChRs): Ligand-gated ion channels
What are the locations and effects of muscarinic receptors
Excitatory: GIT motility, bladder contraction
Inhibitory: Bronchoconstriction, reduced heart rate
Locations include GIT, bladder, and bronchial smooth muscle
What are the types and roles of nicotinic receptors?
Nicotinic N (neuronal): Autonomic ganglia, adrenal medulla
Nicotinic M (muscle): Neuromuscular junction
Both respond to acetylcholine and nicotine
What are the two major classes of cholinergic agonists?
Direct-acting: Mimic ACh and bind to receptors (e.g. bethanechol, pilocarpine)
Indirect-acting: Inhibit acetylcholinesterase (e.g. neostigmine, physostigmine)
Which cholinergic drugs reduce intraocular pressure in glaucoma?
Pilocarpine (muscarinic agonist)
Physostigmine (indirect cholinomimetic)
How is ACh synthesized and released?
Synthesis: Choline + Acetyl-CoA via choline acetyltransferase
Storage: Vesicles
Release: Triggered by calcium influx and exocytosis
Termination: Acetylcholinesterase degrades ACh to acetate and choline
Differentiate between reversible and irreversible AChE inhibitors.
Reversible: Neostigmine, donepezil — shorter action, used in Myasthenia gravis, Alzheimer’s
Irreversible: Organophosphates (e.g. echothiophate) — long action, toxic unless reversed with pralidoxime
What cholinergic drugs are used in Alzheimer’s?
Donepezil, Rivastigmine, Galantamine — all reversible AChE inhibitors
What are examples of nicotinic agonists and their effects?
Nicotine: Stimulates autonomic ganglia and neuromuscular junctions
Effect: CNS stimulation, increased HR and BP
What are muscarinic antagonists and where do they act?
Atropine: Eye (mydriasis), heart (↑HR), GIT (↓motility)
Ipratropium: Bronchodilation in asthma/COPD
Scopolamine: Motion sickness
What are the therapeutic uses of muscarinic antagonists?
Bradycardia, asthma, COPD, motion sickness, eye exams, Parkinson’s disease
How does the ANS control the following:
Bladder, lungs, GIT, Heart?
Bladder:
Parasympathetic: Contracts detrusor
Sympathetic: Contracts internal sphincter
Lungs:
Parasympathetic: Bronchoconstriction
Sympathetic: Bronchodilation
GIT:
Parasympathetic: ↑ Motility and secretion
Sympathetic: ↓ Motility
Heart:
Parasympathetic: ↓ HR
Sympathetic: ↑ HR & contractility
What are neuromuscular blockers and how are they used?
Non-depolarizing: Tubocurarine — blocks ACh at nicotinic M receptors
Depolarizing: Succinylcholine — initial stimulation followed by paralysis
Use: Muscle relaxation in surgery/intubation
What are the common adverse effects of cholinergic agonists?
DUMBBELLS mnemonic
Diarrhea, Urination, Miosis, Bradycardia, Bronchorrhea, Emesis, Lacrimation, Lethargy, Salivation
What are the adverse effects of anticholinergics?
Dry mouth, blurred vision, constipation, urinary retention, confusion, tachycardia (“dry as a bone, blind as a bat, red as a beet, mad as a hatter”)
What is the synthesis pathway for noradrenaline (NA)?
Tyrosine → DOPA (via tyrosine hydroxylase)
DOPA → Dopamine (via DOPA decarboxylase)
Dopamine → Noradrenaline (in vesicles via dopamine β-hydroxylase)
How is noradrenaline stored, released, and inactivated?
Stored: In synaptic vesicles
Released: Exocytosis triggered by calcium influx
Terminated: Reuptake by NET and enzymatic degradation via MAO & COMT
What are catecholamines and examples?
Compounds with a catechol (benzene + 2 OHs) and amine group
Examples: Adrenaline, Noradrenaline, Dopamine
What are the types of adrenoceptors and their major locations/actions?
α1: Smooth muscle contraction (blood vessels, uterus, eye radial muscle)
α2: Presynaptic inhibition, ↓ insulin, platelet aggregation
β1: ↑ Heart rate and contractility
β2: Smooth muscle relaxation (bronchi, uterus, blood vessels), glycogenolysis
β3: Lipolysis (adipose), detrusor relaxation (bladder)
What are the effects of α1 receptor activation?
Vasoconstriction (↑ BP)
Mydriasis
Contraction of bladder sphincter
Uterine and GIT sphincter contraction
What are the effects of α2 receptor activation?
↓ Sympathetic outflow (CNS)
↓ Insulin secretion (pancreas)
Platelet aggregation
Give examples and indications of α-adrenoceptor agonists.
Phenylephrine: Nasal decongestion, mydriasis
Clonidine: Hypertension (central α2 agonist)
Oxymetazoline, pseudoephedrine: Decongestants
Effects of β1 activation?
↑ HR (chronotropy), ↑ contractility (inotropy)
