Autonomic Nervous System Flashcards

1
Q

Is ANS voluntary or involuntary

A

Involuntary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Where does the ANS relay information to?

A

Internal organs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the branches of the ANS

A

Parasympathetic (rest) and Sympathetic (stress)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How do the PNS and SNS differ? (3)

A

Anatomically, functionally, chemically (neurotransmitter)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

How close to the SC is ganglion in SNS?

A

GAnglion close to SC in SNS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

How close to the SC is the ganglion in PNS?

A

Ganglion far from SC - close to target organ

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

PNS neurotransmitters?

A

ACh for pre and post ganglionic

Nicotinic and muscarinic receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

SNS neurotransmitters?

A
Preganglionic Ach
Postganglionic Noradrenaline (except sweat glands, ACh
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Postsynaptic modulation methods:

A

Chemical mediators (eg NPY enhances response)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Rate limiting step at synapse:

A

Activity of transporter

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Drug that inhibits Ach packaging into vesicles

A

vesamicol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Drug that inhibits reuptake of ACh

A

hemicholinium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Drug that enhance release of ACh

A

4-aminopyrimidine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Drug that prevent release of ACh

A

botulinin toxin (Botox)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Drug that inhibits AChE to prevent breakdown of ACH

A

neostigmine (sarin is also an AChE blocker)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

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

A

pilocarpine
carbachol
atropine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
Q

Cholinergic receptor antagonist DRUG ACTIONS

A

Muscarinic receptors! (inhibit bronchial and gastric secretion. Relax smooth muscles, bronchi, pupils)
Nicotinic receptors - gang specific, no applications. Neuromuscular blockers are muscle relaxants

26
Q

Effects of cholinergic drugs on HEART (ag/antag)

A

(ag)
Slows HR
Decrease force
Vasodilation

(antag)
Increase HR
ATROPINE for bradycardia

27
Q

Effects of cholinergic drugs on SMOOTH MUSCLE (ag/antag)

A

(ag)
Contracion of SM in bronchi, bladder, etc via M3
Stimulate peristaltic GI activity

(antag)
Relaxation of SM
IPRATOPRIUM bronchodilator for asthma

28
Q

Effects of cholinergic drugs on EXOCRINE GLANDS (ag/antag)

A

(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
Q

Effects of cholinergic drugs on GI TRACT (ag/antag)

A

(ag)
Relaxes sphincters - BETHANECHOL to assist bladder emptying

(antag)
inhibit GI motility
ATROPINE - treating gastric hypermotility

30
Q

Effects of cholinergic drugs on EYE (ag/antag)

A

(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
Q

Neuromuscular Blockers (ag/antag)

A

(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
Q

Where does noradrenaline act?

A

Most sympathetic post-ganglionic neurons except sweat glands

33
Q

What receptors does ATP act on? (NA transmission)`

A

P2 Purinergic

34
Q

What are the adrenoreceptors?

A

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
Q

How is NA degraded?

A

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
Q

Activity of MOnoamine oxidase

A

Breaks noradrenaline down to metabolites in presynaptic membrane

37
Q

Post synaptic metabolism of NA

A

Aldehyde dehydrogenase -> VMA is primary metabolite

Aldehyde reductase -> MHPEG is minor metabolite

38
Q

Drug for preventing NA release

A

GUANETHIDINE

39
Q

Drug for increasing available stores of NA

A

MAO inhibitors (prevent breakdown to metabolites in presyn)

40
Q

Drug for decreasing available stores of NA

A

RESERPINE (prevent vesicles)

41
Q

Examples of non-selective NA agonists/antagonists

A

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
Q

Effects of NA on SMOOTH MUSCLE

a1 adrenergic agonists

A
CONTRACTION of SM
Decreased vascular compliance
Increased central venous pressure 
increased peripheral resistance
PHENYLEPHRINE, OXYMETAZOLINE (nasal decongestant, local)
43
Q

Effects of NA on SMOOTH MUSCLE

a1 adrenergic antagonists

A

VASODILATION etc
PRAZOCIN, DOXAZOCIN (hypertension, less tachycardia than non-selective blockers)
MAJOR side effects postural hypotension, reflex tachycardia, impotence

44
Q

Effects of NA on SMOOTH MUSCLE

a2 adrenergic agonists

A

Activate presynaptic receptors in CV control centre, reduced SNA and decreased BP
CLONIDINE (hypertension)

45
Q

Effects of NA on SMOOTH MUSCLE

a2 adrenergic antagonists

A

Block rpesynaptic a2 receptors, increase release of NA (sympathomimetic) but can also block post-synaptic a2 receptors so complex responses

46
Q

Effects of NA on HEART

b1 adrenergic agonists

A

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
Q

Effects of NA on HEART

b1 adrenergic antagonists

A

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
Q

Effects of NA on BRONCHIAL SMOOTH MUSCLE

b2 adrenergic agonists

A

Stimulate relaxation of smooth muscle

SABUTAMOL (asthma) or used to relax SM to delay premature labour

ADRENALINE (anyphylactic relations to help breathing)

49
Q

Effects of NA on BRONCHIAL SMOOTH MUSCLE

b2 adrenergic antagonists

A

would trigger bronchial constriction - no clinical application!

50
Q

b adrenergic agonists - METABOLISM

A

encourage conversion of glycogen and fat to glucose and FFAs (b3 agonists treatment for obesity?

51
Q

Drug that has effect on NA storage

A

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
Q

AMPHETAMINE and NA release

A

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