ANS and physiology Flashcards

1
Q

role of the ANS

A

maintain homeostasis and natural physiology

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2
Q

describe the parasympathetic ns

A
innervates facial and visceral organs eg
constricts pupils 
stimulates saliva flow 
bile release
contraction of bladder
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3
Q

describe the sympathetic ns

A

dilates pupils
inhibit saliva
relax bronchioles
inhibit bladder contraction

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4
Q

what determines the state of the organ

A

how the pns and sns work in consort and how they level out

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5
Q

describe fight/flight responses

A

dilate pupils - more light enter, see more
increase heart rate - more o2 supply
increase diameter of bronchioles - more o2
stimulate glucose release - feed the muscles
increase sweat - dont over heat

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6
Q

when does the fight/flight response occur

A

only under stress

sympathertic and parasympathetic work all of the time

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7
Q

where does the SNS come from

A

emanates from the spinal cord
thoracic spinal cord to l3
exit where synapse in the sympathetic chain /sympathetic vertebral ganglia

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8
Q

what is the sympathetic vertebral ganglia

A

cell body of the post ganglionic fibres reside

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9
Q

where does the PNS come from

A

cranial and sacral
cranial nerves 3, 7, 9, 10
scaral 2 - 4

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10
Q

what is the major part of the PNS and where does it innervate

A

vagus nerve

lung, heart, GI

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11
Q

what is the cranial nerve 3

A

ocularmotor - pupil constriction

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12
Q

what is cranial nerve 7

A

facial nerve - salvation

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13
Q

what is the cranial nerve 9

A

glossopharyngeal - salvation

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14
Q

what is the cranial nerve 10

A

vagus - bradycardia, gastric motility, digestion

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15
Q

describe the anatomy of the sympathetic ns

A

fibre out of the brain, presympathetic/preautonomic neurones
synapse into cell on spinal cord out of the spinal cord, into sympathetic ganglia, synapse in the sympathetic chain

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16
Q

describe the anatomy of the pns

A

no ganglia out of the target organ
go from brainstem to ganglia in target organ anad synapse there
post ganglionic neurons are in the target organs

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17
Q

why is it important to know there is a different nt for each stage

A

governs the pharmacology

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18
Q

what type of connection is there in the PNS

A

monosynaptic connection

because only the 1 synapse which is in the organ

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19
Q

what nt is used in the pns

A

ACh

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20
Q

what happens when the vagus nerve innervates the heart

A

ACh is released

heart rate slowed - bradycardia

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21
Q

describe the different NT in the SNS

A

presympathetic down the spinal cord - glutamate, excitatory
preganglionic - ACh in ganglia
postganglionic - \NA at the heart, kidneys, bv
at sweat glands - ACH
renel vessel - dopamine (DA)
adrenal medulla - nerves don’t go through sympathetic ganglia - ACh released in the medulla, release adrenaline and NA into blood - target organs by hormonal response

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22
Q

describe the pathway of the somatic nerves

A

travel down spinal cord
NT is glutamate in the spinal cord
synapse directly onto the target organs - ACh

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23
Q

problem with ACh in somatic and autonomic

A

when we try to target autonomic - can block somatic as well

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24
Q

NA biosynthesis

A
L-phenylalanine 
L-tyrosine 
L-DOPA 
dopamine 
noradrenaline 

phenylalanine - dopamine in cytoplasm
dopamine to NA in vesicles in presynaptic terminal just before release

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25
Q

ACh biosynthesis

A

from acteate and choline
catalysed by choline acetyltransferase
reversed by acetycholine esterase

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26
Q

what causes alzeimers

A

reduction in ACh in certain pathways in brain

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27
Q

what reduces effect of alzheiimers

A

acetylcholinesterase inhibitors
increase ACh in synapse - less degredation
delay the time taken to be broken down

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28
Q

what do people with acetylcholinesterase inhibitors suffer from and why

A

dry mouth

targets all ACh pathways

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29
Q

pathway of sympathetic neurons

A

neurons in brain control output flow of the SNS
presympathetic down spinal cord between T1 and L3
hump in lateral edge of the spinal cord - intermediolateral cell column
all sympathetic neurons emanate from ventral rootdiverted through the sympathetic ganglion out of the spinal cord
synapse onto post ganglionic neuron

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30
Q

baraoreceptors

A

mechanoreceptor

respond to changing distension and mechanical manipulation

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31
Q

where are the baroreceptors

A

aortic arch and carotid

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32
Q

which nerve do the aortic receptors use

A

vagus

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33
Q

which nerve do the carotid receptors use

A

glossopharyngeal

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34
Q

action of Baroreceptors

A

transmit beat to beat pressure info to the brain
increae in bp reaches threshold that activates the receptors
drives PNS
inhibit SNS
reduce Bp
(reduce CO and TPR)

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35
Q

describe the effect of standing up

A
big stress on the cardio system
blood drops to the legs
drop in pressure 
inhibit barareceptors
increase heart rate and TPR 
drive blood to brain
36
Q

describe the barareflex

A

bp is at a set point
brain keeps it at this level
sensitive system - when small increase in pressure - increases baroreceptor firing

37
Q

barareflex when hypertensive

A

curve shifts to R
set pount increase
brain still aims to keep it at this level

38
Q

why does brain create new set point

A

impaired cerebral blood flow - congenital abnormality

brain attempts to maintain cerebral flpw by increasing the Bp

39
Q

what innervates the GI

A

vagus nerve

40
Q

what is the cephalic response

A

site, smell and taste of food cause release of stomach acid - prime GI tract for it
impulse goes to hypothalmus to brain stem/spinal cord and regulates function
bump in insulin time graph = cephalic response
in diabetics - there is a loss of the cephalic release of insulin

41
Q

what is the peak on the insulin-time graph

A

glucose mediated response

42
Q

what do mechanoreceptors detect in the GI tract

A

distension of the stomach wall / content in the duodenum

43
Q

what happens when you eat

A

signal to brain stem
increased firing if mechanoreceptors
bloated
satietry hormones are released - chemoreceptors on the vagus nerve

44
Q

what happens to the effect of satiety hormones in obvese people

A

dampened - need a larger signal to show they’re full

45
Q

how is the vagus nerve plastic

A

changes the presentation fo the receptors
if hungry don’t express the receptors
obese - fewer receptors - less ability to respond to hormones - less full

46
Q

what are the respiratory receptors

A

pontine respiratory centre
central respiratory centre
medullaty respiratory centre - made of ventral and dorsal group (Nucleus tractus solitarius

all communicayte - overall response

47
Q

what does the pontine centre do

A

cooordinate rate and pattern of breathing

syncronicity

48
Q

what does the ventral group do

A

coordinates rhythmicity

49
Q

what does the dorsal group do

A

control of diaphragm and inspiration

physically initiate inspiriation by sending outpiuts to diaphragm and intercostal muscles

50
Q

what do the chemoreceptors in the heart detect

A

decrease in O2, pH and increase in CO2

51
Q

what do central receptors on the surface of the brainstem detect

A

low ph high co2

52
Q

effect of chemoreceptors on respiration

A

increase

53
Q

describe the NTS

A

the central and peripheral chemorespetors send signals there via vagus nerve
gives a lot of outputs

54
Q

describe the lung mechanoreceptors

A
Hering-Breuer reflex 
protective 
stop over inflation 
reduce respiration 
inhibit output from the dorsal root
55
Q

how do you know chemoreceptors are powerful

A

canbt hold breath long

56
Q

which spinal levels control which repiratory features

A

information passes down the spinal cord
C1 - 3 accessory muscles
c3- 5 diaphragm - down phrenic nerve - high so if lesion lower you can survive
T1-11 - intercostal muscles - move ribcage up
T6 - L1 abdominal muscles

57
Q

what contols each part of the bladder

A

PNS (s2-4) - detrusor muscle- around outside
SNS (T10-12) internal sphincter
voluntary motor nerves S2 S4 external sphincter

58
Q

what do the afferent mechanoreceptors do in the bladder

A

s2-4
tell brain how full the bladder is - info on distension if the bladder wall
activate PNS - contract muscle
activate SNS - contract sphincter

59
Q

describe the centrak regulation of the autonomic nervous system

A

info goes to the NTS
input CN 10
output CN 9
if haemorrhage in this area - deadd because you have lost these nerves
input goes to hypertahlamus - integrates it
th ssends signals to dorsal motor nucleus of the vagus

60
Q

how can you no the paths of nerves

A

put tracers in

61
Q

describe the sympathetic receptors

A
adrenoreceptors 
alpha and beta 
a1 - a b d 
a2 a b c 
b1 
b2
62
Q

describe the parasympathetic receptors

A

nicotinic

muscarinic

63
Q

describe ianotrophic channels

A
bind ligand 
conformational change 
influx of ions 
change in potential 
on off
64
Q

describe G protein coupled receptor

A

ligand bind to external terminal in extracellular space
activate downstream pathways
effects last for hours

65
Q

what does a post synaptic recetor respond to

A

NT from pre

66
Q

what does a presynaptic receptor biund to

A

same NT in vesicles - regulatory
stop more entering the cleft
autoreceptor

67
Q

describe cholinergic receptors in the PNS

A

at 1st synapse - nicotinic ACh

at muscle - muscarinic receptor

68
Q

describe cholinergic receptors in SNS

A

all ganglionic - nicotinic - ACh
sweat gland muscarinic
adrenal nicotinic

69
Q

describe atropine

A

competitive muscarinic receptor antagonist
gigve dry mouth
change heart rate

70
Q

describe tubocurarine

A

nicotinic receptor antagonist

which also works at NMJ - cause paralysis so rarely used

71
Q

atropine effect on heat rate

A

increase

block PNS receptor

72
Q

atropine effect on sweat

A

decrease

73
Q

tubocurarine effect on respiration

A

decrease
involved in NMJ
cause respiratory arrest

74
Q

tubocurarine effect on heart rate

A

increase
remove autonomic control of the heart
use intrinsic heart rate

75
Q

effect of ACh at nicotinic receptors

A

allow influx of non-specific ions

make AP

76
Q

what type of receptor are muscarinic receptors

A

GPCRs

stimulated by all postganglionic PNS neurons and SNS at selected sites

77
Q

describe the adrenergic receptors

A

a1 on effector organs - sm contraction, bv, ureter, bronchioles
a2 presynaptic - prevent release of more NT
B1 - exclusively heart - activation increases Bp and HR
B2 - on effector orgam relax sm, contract sphincters in GI tract

78
Q

describe medetomidine

A

a2 receptor agonist - reduce NA

used as anesthetic on animals

79
Q

atenolol

A

B1 receptor antagonist
decrease heartrate
Block SNS
given to people with angina, acute Mi and arrhythmia

80
Q

salbutamol

A

B2 receptor agonist - relax sm

81
Q

doxazosin

A

a1 receptor antagonist

antihypertensive

82
Q

what drug give to someone with an asthma attack

A

salbutamol
relax sm
sympathomimetic

83
Q

describe shy-Drager syndrome/multiple system atrophy

A

synucleopathy - disorder of alpha synucleon - protein accululate in brain and kills cells (along with parkinsons and lewy body dementia)
loss of cell in intermediolateral cell column - loss of SNS
and striatonigrial brain areas
ortostatic hypotension
impotence
hypohidrosis - don’t sweat
dry mouth
urinary retention
incontinence
1:100000 - but 13% people with parkinsons have it so maybe underdiagnosed

84
Q

primary hypertension

A

body ddefend high bp
exaggerated SNS activity to bv and renal bed
leads to increased circulating vol and vascular tone

85
Q

tpr=

A

determined by vascular diameter/vascular tone

86
Q

heart failure

A

inability to sufficiently pump to meet demand

increased symnpathetic actiuviuty to renal bed - hypervolaemia - less excreted, increase strain on cardiac tissue

87
Q

parkinsons

A

orthostatic hypotension
constipation
NTS - 1st place where cells die - where v nerve synapses
travels to regions in forebrain
bacteria/virus or metabolite travel in v nerve
might be ANS that’s causing it
if stomach ulcer severed - less likely to get PD