ANS and physiology Flashcards
role of the ANS
maintain homeostasis and natural physiology
describe the parasympathetic ns
innervates facial and visceral organs eg constricts pupils stimulates saliva flow bile release contraction of bladder
describe the sympathetic ns
dilates pupils
inhibit saliva
relax bronchioles
inhibit bladder contraction
what determines the state of the organ
how the pns and sns work in consort and how they level out
describe fight/flight responses
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
when does the fight/flight response occur
only under stress
sympathertic and parasympathetic work all of the time
where does the SNS come from
emanates from the spinal cord
thoracic spinal cord to l3
exit where synapse in the sympathetic chain /sympathetic vertebral ganglia
what is the sympathetic vertebral ganglia
cell body of the post ganglionic fibres reside
where does the PNS come from
cranial and sacral
cranial nerves 3, 7, 9, 10
scaral 2 - 4
what is the major part of the PNS and where does it innervate
vagus nerve
lung, heart, GI
what is the cranial nerve 3
ocularmotor - pupil constriction
what is cranial nerve 7
facial nerve - salvation
what is the cranial nerve 9
glossopharyngeal - salvation
what is the cranial nerve 10
vagus - bradycardia, gastric motility, digestion
describe the anatomy of the sympathetic ns
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
describe the anatomy of the pns
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
why is it important to know there is a different nt for each stage
governs the pharmacology
what type of connection is there in the PNS
monosynaptic connection
because only the 1 synapse which is in the organ
what nt is used in the pns
ACh
what happens when the vagus nerve innervates the heart
ACh is released
heart rate slowed - bradycardia
describe the different NT in the SNS
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
describe the pathway of the somatic nerves
travel down spinal cord
NT is glutamate in the spinal cord
synapse directly onto the target organs - ACh
problem with ACh in somatic and autonomic
when we try to target autonomic - can block somatic as well
NA biosynthesis
L-phenylalanine L-tyrosine L-DOPA dopamine noradrenaline
phenylalanine - dopamine in cytoplasm
dopamine to NA in vesicles in presynaptic terminal just before release
ACh biosynthesis
from acteate and choline
catalysed by choline acetyltransferase
reversed by acetycholine esterase
what causes alzeimers
reduction in ACh in certain pathways in brain
what reduces effect of alzheiimers
acetylcholinesterase inhibitors
increase ACh in synapse - less degredation
delay the time taken to be broken down
what do people with acetylcholinesterase inhibitors suffer from and why
dry mouth
targets all ACh pathways
pathway of sympathetic neurons
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
baraoreceptors
mechanoreceptor
respond to changing distension and mechanical manipulation
where are the baroreceptors
aortic arch and carotid
which nerve do the aortic receptors use
vagus
which nerve do the carotid receptors use
glossopharyngeal
action of Baroreceptors
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)
describe the effect of standing up
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
describe the barareflex
bp is at a set point
brain keeps it at this level
sensitive system - when small increase in pressure - increases baroreceptor firing
barareflex when hypertensive
curve shifts to R
set pount increase
brain still aims to keep it at this level
why does brain create new set point
impaired cerebral blood flow - congenital abnormality
brain attempts to maintain cerebral flpw by increasing the Bp
what innervates the GI
vagus nerve
what is the cephalic response
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
what is the peak on the insulin-time graph
glucose mediated response
what do mechanoreceptors detect in the GI tract
distension of the stomach wall / content in the duodenum
what happens when you eat
signal to brain stem
increased firing if mechanoreceptors
bloated
satietry hormones are released - chemoreceptors on the vagus nerve
what happens to the effect of satiety hormones in obvese people
dampened - need a larger signal to show they’re full
how is the vagus nerve plastic
changes the presentation fo the receptors
if hungry don’t express the receptors
obese - fewer receptors - less ability to respond to hormones - less full
what are the respiratory receptors
pontine respiratory centre
central respiratory centre
medullaty respiratory centre - made of ventral and dorsal group (Nucleus tractus solitarius
all communicayte - overall response
what does the pontine centre do
cooordinate rate and pattern of breathing
syncronicity
what does the ventral group do
coordinates rhythmicity
what does the dorsal group do
control of diaphragm and inspiration
physically initiate inspiriation by sending outpiuts to diaphragm and intercostal muscles
what do the chemoreceptors in the heart detect
decrease in O2, pH and increase in CO2
what do central receptors on the surface of the brainstem detect
low ph high co2
effect of chemoreceptors on respiration
increase
describe the NTS
the central and peripheral chemorespetors send signals there via vagus nerve
gives a lot of outputs
describe the lung mechanoreceptors
Hering-Breuer reflex protective stop over inflation reduce respiration inhibit output from the dorsal root
how do you know chemoreceptors are powerful
canbt hold breath long
which spinal levels control which repiratory features
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
what contols each part of the bladder
PNS (s2-4) - detrusor muscle- around outside
SNS (T10-12) internal sphincter
voluntary motor nerves S2 S4 external sphincter
what do the afferent mechanoreceptors do in the bladder
s2-4
tell brain how full the bladder is - info on distension if the bladder wall
activate PNS - contract muscle
activate SNS - contract sphincter
describe the centrak regulation of the autonomic nervous system
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
how can you no the paths of nerves
put tracers in
describe the sympathetic receptors
adrenoreceptors alpha and beta a1 - a b d a2 a b c b1 b2
describe the parasympathetic receptors
nicotinic
muscarinic
describe ianotrophic channels
bind ligand conformational change influx of ions change in potential on off
describe G protein coupled receptor
ligand bind to external terminal in extracellular space
activate downstream pathways
effects last for hours
what does a post synaptic recetor respond to
NT from pre
what does a presynaptic receptor biund to
same NT in vesicles - regulatory
stop more entering the cleft
autoreceptor
describe cholinergic receptors in the PNS
at 1st synapse - nicotinic ACh
at muscle - muscarinic receptor
describe cholinergic receptors in SNS
all ganglionic - nicotinic - ACh
sweat gland muscarinic
adrenal nicotinic
describe atropine
competitive muscarinic receptor antagonist
gigve dry mouth
change heart rate
describe tubocurarine
nicotinic receptor antagonist
which also works at NMJ - cause paralysis so rarely used
atropine effect on heat rate
increase
block PNS receptor
atropine effect on sweat
decrease
tubocurarine effect on respiration
decrease
involved in NMJ
cause respiratory arrest
tubocurarine effect on heart rate
increase
remove autonomic control of the heart
use intrinsic heart rate
effect of ACh at nicotinic receptors
allow influx of non-specific ions
make AP
what type of receptor are muscarinic receptors
GPCRs
stimulated by all postganglionic PNS neurons and SNS at selected sites
describe the adrenergic receptors
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
describe medetomidine
a2 receptor agonist - reduce NA
used as anesthetic on animals
atenolol
B1 receptor antagonist
decrease heartrate
Block SNS
given to people with angina, acute Mi and arrhythmia
salbutamol
B2 receptor agonist - relax sm
doxazosin
a1 receptor antagonist
antihypertensive
what drug give to someone with an asthma attack
salbutamol
relax sm
sympathomimetic
describe shy-Drager syndrome/multiple system atrophy
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
primary hypertension
body ddefend high bp
exaggerated SNS activity to bv and renal bed
leads to increased circulating vol and vascular tone
tpr=
determined by vascular diameter/vascular tone
heart failure
inability to sufficiently pump to meet demand
increased symnpathetic actiuviuty to renal bed - hypervolaemia - less excreted, increase strain on cardiac tissue
parkinsons
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
