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Medsci 204 > Autonomic Nervous System > Flashcards

Autonomic Nervous System Flashcards

1
Q

Is ANS voluntary or involuntary

A

Involuntary

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2
Q

Where does the ANS relay information to?

A

Internal organs

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3
Q

What are the branches of the ANS

A

Parasympathetic (rest) and Sympathetic (stress)

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4
Q

How do the PNS and SNS differ? (3)

A

Anatomically, functionally, chemically (neurotransmitter)

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5
Q

How close to the SC is ganglion in SNS?

A

GAnglion close to SC in SNS

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6
Q

How close to the SC is the ganglion in PNS?

A

Ganglion far from SC - close to target organ

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7
Q

Where do the fibres leave the SC in PNS and SNS?

A

PNS - leave SC in cranial nerves and sacral spinal roots (top and bottom of SC)

SNS - leave SC in thoracic and lumbar spinal roots (middle of SC)

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8
Q

Action of SNS vs PNS?

A

SNS prepares body for strenuous activity, stress emergencies (fight or flight)

PNS for acumulation, storage, preservation of resources (rest and digest)

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9
Q

PNS neurotransmitters?

A

ACh for pre and post ganglionic

Nicotinic and muscarinic receptors

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10
Q

SNS neurotransmitters?

A 
Preganglionic Ach
Postganglionic Noradrenaline (except sweat glands, ACh
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11
Q

Presynaptic modulation methods:

A

Homotropic inhibition - transmitter acts on presynaptic to prevent further release (autoinhibition)
AND
Heterotropic - transmitter acts on presynaptic to orevent release of second neurotransmitter

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12
Q

Postsynaptic modulation methods:

A

Chemical mediators (eg NPY enhances response)

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13
Q

Non-adrenergic non-cholinrgic (NANC) transmission

A

Known because drugs that block ACh and NA do not completely block neurotransmission

Non-peptides eg ATP, NO
Peptides eg NPY, VIP

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14
Q

Rate limiting step at synapse:

A

Activity of transporter

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15
Q

Drug that inhibits Ach packaging into vesicles

A

vesamicol

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16
Q

Drug that inhibits reuptake of ACh

A

hemicholinium

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17
Q

Drug that enhance release of ACh

A

4-aminopyrimidine

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18
Q

Drug that prevent release of ACh

A

botulinin toxin (Botox)

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19
Q

Drug that inhibits AChE to prevent breakdown of ACH

A

neostigmine (sarin is also an AChE blocker)

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20
Q

Drugs that act directly at ACh recetors to minic or block te actions of ACh

A

pilocarpine
carbachol
atropine

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21
Q

Properties of ACh Muscarinic Receptors

A

GPCRs
M1, M3, M5 coupled to Gq (activate inosityl phosphate pathway)
M2, M4 coupled to Gi to inhibit AC reducing cAMP

22
Q

Properties of ACh Nicotinic Receptors

A 
LGIC with 5 subunits
Nm at neuromusclular junction
Nn neuronal in brain
ganglionic in autonomic ganglia
Ion channel activation by Na+ and K= influx leading to depolarsation of post-syn membrane and fast excitatory post-synaptic potential (FAST)
23
Q

Which cholinergic receptors are most useful drug targets?

A

MUSCARINIC

Nicotinic are not useful because of widespread distribution throughout ANS (receptor agonists affect ganglionic and neuromuscular receptors)

24
Q

Cholinergic receptor agonist DRUG ACTIONS

A

Mimic the effects of ACh.

Affinity for muscarinic and or nicotinic but fairly non-selective

25
Cholinergic receptor antagonist DRUG ACTIONS
Muscarinic receptors! (inhibit bronchial and gastric secretion. Relax smooth muscles, bronchi, pupils) Nicotinic receptors - gang specific, no applications. Neuromuscular blockers are muscle relaxants
26
Effects of cholinergic drugs on HEART (ag/antag)
(ag) Slows HR Decrease force Vasodilation (antag) Increase HR ATROPINE for bradycardia
27
Effects of cholinergic drugs on SMOOTH MUSCLE (ag/antag)
(ag) Contracion of SM in bronchi, bladder, etc via M3 Stimulate peristaltic GI activity (antag) Relaxation of SM IPRATOPRIUM bronchodilator for asthma
28
Effects of cholinergic drugs on EXOCRINE GLANDS (ag/antag)
(ag) Stimulate secretions from sweat etc (M3) (antag) Inhib salivary / sweat etc secretions ATROPINE as adjunct for anaesthesia, reduces secretions and bronchodilator PIRENZEPINE (M1) to inhibit Gastric acid production (peptic ucler treatment)
29
Effects of cholinergic drugs on GI TRACT (ag/antag)
(ag) Relaxes sphincters - BETHANECHOL to assist bladder emptying (antag) inhibit GI motility ATROPINE - treating gastric hypermotility
30
Effects of cholinergic drugs on EYE (ag/antag)
(ag) Stimulates contraction of eye muscles to accommodate (M3) PILOCARPINE (used to treat glaucoma) (antag) Dilate pupils when unresponsive to light TROPICAMIDE (short acting dilation of pupils to allow examination of retina and lens)
31
Neuromuscular Blockers (ag/antag)
(ag) depolarising blockers trigger sustained depol of muscular endplate (no new AP generation) (antag) Non-depolarising blockers, compete with ACh for nicotinic receptor binding Prevent depolarisation of the end plate Effects can be reversed by increasing ACh concentrations (AChE inhibitions) PANCURONIUM - lethal injection with barbiturate and KCl
32
Where does noradrenaline act?
Most sympathetic post-ganglionic neurons except sweat glands
33
What receptors does ATP act on? (NA transmission)`
P2 Purinergic
34
What are the adrenoreceptors?
alpha1,2 and beta1,2,3. G protein coupled Each with second messenger system (a1 is PLC, a2,3 is AC) Widespread receptor distribution
35
How is NA degraded?
no SYNAPTICALLY located NA enzyme Terminated by reuptake through two systems Noradrenaline Transporter (NET) - 75% recycled or metabolised (high affinity) Extraneuronal transporter (ENT) - 25%, taken up by non-neuronal cells (SM, Cardiac muscle, endothelium) (low affinity)
36
Activity of MOnoamine oxidase
Breaks noradrenaline down to metabolites in presynaptic membrane
37
Post synaptic metabolism of NA
Aldehyde dehydrogenase -> VMA is primary metabolite | Aldehyde reductase -> MHPEG is minor metabolite
38
Drug for preventing NA release
GUANETHIDINE
39
Drug for increasing available stores of NA
MAO inhibitors (prevent breakdown to metabolites in presyn)
40
Drug for decreasing available stores of NA
RESERPINE (prevent vesicles)
41
Examples of non-selective NA agonists/antagonists
ADRENALINE - (ag) cardiac arrest / allergic reactions PHENTOLAMINE - (antag) heart blocks alpha regulated vasoconstriction, fall in blood pressure. baroreceptor reflex and increased CO and HR
42
Effects of NA on SMOOTH MUSCLE | a1 adrenergic agonists
``` CONTRACTION of SM Decreased vascular compliance Increased central venous pressure increased peripheral resistance PHENYLEPHRINE, OXYMETAZOLINE (nasal decongestant, local) ```
43
Effects of NA on SMOOTH MUSCLE | a1 adrenergic antagonists
VASODILATION etc PRAZOCIN, DOXAZOCIN (hypertension, less tachycardia than non-selective blockers) MAJOR side effects postural hypotension, reflex tachycardia, impotence
44
Effects of NA on SMOOTH MUSCLE | a2 adrenergic agonists
Activate presynaptic receptors in CV control centre, reduced SNA and decreased BP CLONIDINE (hypertension)
45
Effects of NA on SMOOTH MUSCLE | a2 adrenergic antagonists
Block rpesynaptic a2 receptors, increase release of NA (sympathomimetic) but can also block post-synaptic a2 receptors so complex responses
46
Effects of NA on HEART | b1 adrenergic agonists
Increase contractility, increase HR Can cause ventricular fibrillation DOBUTAMINE - cardiogenic shock (increased CO without much effect on HR) ADRENALINE administered IV for cardiac arrest
47
Effects of NA on HEART | b1 adrenergic antagonists
PROPRANOLOL - b1 and b2 ATENOLOL b1 selective Cardiac dysrhythmias, MI, failure, angina Very little effect at rest (only reduce HR, CO, BP when under exercise/excitement) B blockers ONLY lower BP in patients with hypertension, don't cause hypotension in normal. No postural and exercise-induced hypotension problems as with other drugs
48
Effects of NA on BRONCHIAL SMOOTH MUSCLE | b2 adrenergic agonists
Stimulate relaxation of smooth muscle SABUTAMOL (asthma) or used to relax SM to delay premature labour ADRENALINE (anyphylactic relations to help breathing)
49
Effects of NA on BRONCHIAL SMOOTH MUSCLE | b2 adrenergic antagonists
would trigger bronchial constriction - no clinical application!
50
b adrenergic agonists - METABOLISM
encourage conversion of glycogen and fat to glucose and FFAs (b3 agonists treatment for obesity?
51
Drug that has effect on NA storage
RESERPINE Blocks transport of NA into vesicles (accumulates in cyto, broken down by MAO, levels decrease, no NTrans) ALSO DEPLETES DOPAMINE LEVELS (has antihypertensive effect but not used clinically because depressive)
52
AMPHETAMINE and NA release
Transported into nerve terminals by uptake 1, displaces NA from vesicle, broken down or diffuses out (receptor activation_. Amphetamine reduces NA reuptake via transporter so action of released NA is enhanced

Medsci 204 (4 decks)

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