12 Physiology of ANS. Pharmacology of ANS Flashcards

1
Q

Q: Which nerves are parasympathetic?

A

A: 4 cranial= 3,7,9,10

  • glossopharengeal 9
  • vagus 10
  • oculomotor
  • facial

S2-4 (pelvic, splanchnic nerves)

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2
Q

Q: How are nerves organised in the autonomic NS? Parasympathetic? (2) Sympathetic? (2) Another structural difference?

A

A: have pre and post ganglionic neuron where ganglion is where the nerves synapse
-cell body of pre is in vertebra (grey matter)

  • lost pre and shorter post (synapse close to target)
  • ACh is NT between N and at junction of N and effector
  • short pre and lost post (synapse in sympathetic trunk)
  • ACh innervates post ganglionic fibres but NA between N and effector

sympa can have lots of branches and synapse with other ganglia in sympathetic trunk not in line with its own exit (one pre ganglionic fibre can innervate lots of post)
-results in more of a coordinated response rather than discrete and local one caused by parasympathetic

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3
Q

Q: Describe an exception to the organisation of sympathetic neurons. Benefit?

A

A: adrenal medulla

  • only place that’s innervated by one autonomic nerve
  • just receive signal straight from ‘pre ganglionic’ neuron straight from spinal cord
  • adrenaline (and NA) released into blood -> act on tissues

effect can last longer that effect caused by post g neuron (post N is more transient in effects as NT is removed swiftly)
-when in blood-> stays for longer

there are some post ganglionic nerves that make ACh eg sweat glands

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4
Q

Q: Describe a somatic neuron.

A

A: one long neuron straight to skeletal muscle with ACh

=voluntary (not PNS)

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5
Q

Q: How do the parasympathetic and sympathetic nerves affect the pupil?

A

A: para- come down oculomotor (3)-> synapse in ganglion close to eye -> leads to para post ganglionic fibre which innervates iris muscle -> pupil constriction
-ciliary muscle also contracts to make lens bulge-> for near vision

sympa- causes pupil dilation

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6
Q

Q: How do the parasympathetic and sympathetic nerves affect gut motility?

A

A: para- vagus nerve controls -> ganglion is close to tissue
-post projects down onto stomach
-increase in secretions eg HCl, pepsin
-increase motility too
(do so sometimes by innervating glands/tissue directly or enteric nerves)

sympa does opp

  • contraction of sphincters
  • less motility
  • less secretions
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7
Q

Q: Draw a diagram showing the autonomic control of the heart.

A

A: REFER

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8
Q

Q: How do you calculate CO? BP? What controls them?

A

A: HR x SV

CO x TPR

autonomic NS

eg TPR increases with more sympa as it causes more vasoconstriction

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9
Q

Q: What’s the relationship between TPR and r?

A

A: TPR= 1/ r^4

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10
Q

Q: What doesn’t innervate the lungs? How does this system still affect oxygen delivery to lungs?

A

A: no sympa but sympa NS can still increase oxygen delivery to lungs

main method is adrenaline release from adrenals

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11
Q

Q: How does the parasympathetic NS affect the lungs? sympa?

A

A: (long pre short post)
ACh acts directly on bronchioles-> constriction

have blood vessels going through lungs-> adrenaline is carried to lungs to cause dilation-> get more oxygen to lungs

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12
Q

Q: What is the main autonomic control of the bladder? Other 2 controls?

A

A: para (long pre short post)= wants to stimulate bladder emptying
-para stimulates detrusor muscle

sympa acts of internal sphincter-> wants to inhibit emptying

voluntary motor control too of external sphincter

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13
Q

Q: What is the micturition reflex? (4)

A

A: pressure builds in bladder-> pressure

sensory info goes to spinal cord

  • get reflex activation of para NS (detrusor muscle)
  • reflex inhibition of sympa (internal sphincter)

depends of voluntary (motor) control of external sphincter if urine leaves bladder

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14
Q

Q: Name 3 catecholamines.

A

A: adrenaline, noradrenaline, dopamine

ring (6) with 2 OH groups

  • adrenaline is OH and NH-
  • nor is OH and NH2
  • dop NH2
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15
Q

Q: What are the 2 ACh receptors?

A

A: muscarinic, nicotinic

nicotinic is in all automatic ganglion, ionotropic (fast)

muscarinic between post N and effector= G protein, slower (gives cell more control)- only those that release ACh

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16
Q

Q: What are the receptors for adrenaline?

A

A: adrenoceptors

alpha 1, 2, beta 1, 2 (g protein)

alpha 1 is main in vasculature (increases TPR)

beta 2 -dilates skeletal muscle

17
Q

Q: How is ACh made? What breaks it down?

A

A: ACh transferase of choline and acetyl CoA

ACh esterase (into choline and acetate) in synapse

18
Q

Q: How is dopamine and noradrenaline made? (3) What breaks in down? (2)

A

A: 1. tyrosine from diet and tyrosine hydroxylase-> DOPA

  1. DOPA and DOPA decarboxylase-> dopamine
  2. in vesicle: dopamine and dopamine beta hydroxylase -> NA

in pre cell- MOA = monoamine oxidase
in post cell- COMT =

19
Q

Q: How is adrenaline made? Enhanced by?

A

A: adrenal medulla-chromaffin cells (sympa nerves stimulate)

one more enzyme to change NA to A
-phenylethanolamine methyl transferase

cortisol enhances PNMT