ANS Flashcards
(53 cards)
Somatic NS
- voluntary
- conscious body functions
ex: posture, locomotion - no pre/post ganglionic fibres
Autonomic NS
- involuntary
- unconscious body functions
- pre + post ganglion fibres
divided into parasymp and sympathetic NS
Parasympathetic NS
- cranio-sacral
- rest and digest
Cholinergic –> (Nicotinic receptors) –> Cholinergic –> (M receptors)
increases SLUDGE response
- salivation
- lacrimation
- urination
- diaphoresis/sweating
- GI motility
- emesis/vomitting
Sympathetic NS
- thoraco-lumbar
- fight or flight
Cholinergic –> (Nicotinic receptors) –> Adrenergic fibres –> A and B adrenergic receptors
Adrenergic neurotransmission is terminated by:
1) Re-uptake via U1 receptor (pre-synaptic cell)
2) Removal via U2 receptor (target cell)
3) COMT in target cell degrades it
4) a2 adrenergic receptors in presynaptic cell inhibits further release of NT
5) degradation via MOA in mitochondria
Cholinergic receptors
Muscarinic receptors
- GPCRs
- M1, M2, M3, M4, M5 (1,3,5 coupled to IP3 and DAG, excitatory, 2 and 4 are inhibitory)
- subtype selective drugs UNCOMMON
Nicotinic receptor
- ligand gated ion channels (Na+/K+)
- Nn (peripheral ganglia)
- Nm (neuromuscular junction)
- both coupled to Na+/K+ depolarizing channels
- subtype selective drugs are COMMON
Drugs stimulating PNS
- synthetic choline esters and plant alkaloids
- ACT ONLY ON THE M RECEPTORS
- less sensitive to metabolism, have a longer half life than ACh
Direct acting cholinergic agonists
-bind directly to the M receptors
Indirect acting cholinergic agonists
- inhibit acetylcholinerase
- Group A: reversible, ionic site
- Group B: reversible, both sites
- Group C: irreversible, covalent site
*NOT ALL CAN CROSS BBB
Use of muscarinic agonists
- Xerostomia, dry mouth
- activates parasympathetic NS
Stimulates vasodilation
- acetylcholine binds to the endothelial cell –> Nitric oxide to be produced by nitric oxide synthase –> causes relaxation of your smooth muscle, vasodilation bitch
- indirect acetylcholinesterase inhibitors are not effective at vasodilation (do a good job at inhibiting break down, don’t do anything to receptor
Cevimeline
- selective M1 and M3 agonist
- causes salivation in treatment of xerostomia
- should NOT BE USED IN ASTHMA (cholinergic stimulation causes bronchoconstriction)
Uses of acetylcholinesterase inhibitors
MYASTHENIA GRAVIS
- autoimmune loss of N receptors
- muscle gets paralyzed because ACh not being used
- AChE inhibitors keep ACh in synapse longer –> increases muscle contraction
GLAUCOMA
- intra-ocular pressure build up
- AChE inhibitors cause MIOSIS (constriction of pupil)
DEMENTIA OF ALZHEIMERS DISEASE
- patients lose cholinergic neurons
- AChE inhibitors prolongs ACh, not a permanent cure, will not improve the number of neutron viability
Neostigmine
increases ACh at end plate
-group B acetylcholinesterase inhibitor
Symptoms of overdose of AChE inhibitors
MUSCARINIC EFFECTS
- increased sludge response
- blurred vision
- miosis
NICOTINIC EFFECTS
- muscle weakness
- tachycardia
CNS EFFECTS
-anxiety, tremors, decreased respiratory
nicotinic antagonists
block the PNS
Nn receptor blockers
- ganglion blockers
- block the Nn receptors, bad consequences, not used
Nm receptor blockers
- block the Nm receptors at the neuromuscular junction
- loss of skeletal muscle control
- muscle relaxation (helps intubation, i.v drips)
- two types, non depolarizing NMJ and depolarizing NMJ blockers
Succinyl choline
- depolarizing NMJ blocker
- short acting, weakly acts like ACh
- intrinsic activity: stimulates depolarization like ACh
PHASE 1: PROLONGED DEPOLARIZATION
- fasciculations= tiny disorganized twitches
- muscle cell contracting, using up all energy stores, use up all the ATP
- leads to DEPOLARIZATION BLOCK: muscle becomes flaccid
PHASE 2: DESENSITIZATION/CHANNEL BLOCK
- locks channel closed, no more depolarization
- muscle relaxation
Non depolarizing NMJ blockers
- no intrinsic activity (no ability to produce functional response)
- competitive inhibitors, bind to the Nm receptor, lock gate so it doesn’t open
- muscle can’t contract
OLD: tubocurarine
-1 to 2 hrs
NEW: cisatracurium
- 30-45min
- dont release histamine from mast cells
- dont block ganglia
Muscarinic antagonists
-competes with ACh for M receptors
ALKALOIDS (naturally occurring)
-atropine
SYNTHETIC
- charged
- not absorbed through gut
- less CNS effects
Atropine
- anti-muscarinic drug, naturally occurring
- antidote for nerve gase poisoning
- decreases SLUDGE response
TREATS ASTHMA
-cause bronchodilation
CAUSES MYDRIASIS
-dilation of pupil via radial muscle
parasympathetic system causes
- bronchoconstriction
- vasodilation
- miosis
sympathetic system causes
- bronchodilation
- vasoconstriction
- mydriasis
ANS pathway of adrenal gland
preganglionic cholinergic –> releases ACh to adrenal gland, causes adrenal medulla to release catecholamines (NE and E)
Biosynthesis of catecholamines
Tyr –> DOPA –> DOPAMINE –> Norepinephrine —> Epinephrine (in the adrenal gland)
catecholamines
-catechol derivatives of phenylethylamine
alpha 1 adrenergic receptors
- GPCRS
- in the smooth muscle of BV
Activation causes
- vasoconstriction (skin, viscera, veins)
- pupil dilation
- salivary secretion
- *via IP3**
Phenylephrine
- alpha 1 selective agonist
- causes vasoconstriction, nasal decongestion
- smooth muscle contraction, causes mydriasis (pupil dilation)
