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Medical Phys Exam 1 > Autonomic NS > Flashcards

Autonomic NS Flashcards

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USMLE® Step 1 flashcards
1
Q

Describe the three modes of innervation in the sympathetic division

A

1) Preganglionic neuron –> paravertebral ganglia (prevertebral ganglia)–> post-ganglionic neuron
2) Preganglionic neuron –> specialized ganglion (superior cervical, celiac, superior/inferior mesenteric ganglia) –> target organ
3) Preganglionic neuron –> organ: adrenal medulla

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2
Q

Sympathetic

A

thoracolumbar - located in the lateral horn (intermediolateral cell column)
- ganglia lie

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3
Q

Parasympathetic

A

Cranio-sacral

- ganglia lie close to target

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4
Q

describe the cranial outflow of the parasympathetic division

A

Preganglionic fibers in certain cranial nerves:

  • Oculomotor
  • facial and glossopharyngeal nerves
  • vagal nerve
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5
Q

Describe the sacral outflow

A
  • bladder
  • descending large intestine
  • rectum
  • genitalia
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6
Q

Describe the enteric nervous system

A

a system of ganglia sandwiches between the layers of the gut and connected by dense meshwork of nerve fibers

  • myenteric plexus: motility of gut
  • submucosal plexus: secretion of ion and fluid transport
  • receives input from both the sympathetic and parasympathetic divisions
  • can function normally without extrinsic input
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7
Q

define dual innervation

A

Most organs receive both sympathetic and parasympathetic innervation –> actions controlled by both symptoms (not antagonistic)
EXCEPTIONS
- only symptahtic = hair follicles, thermoregulatory sweat glands, liver, adrenal gland, kidney
- two systems producing similar rather than opposing effects: salivary glands

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8
Q

what is the main NT at Presynaptic

A

ACh

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9
Q

What is the key postglanglionic NT for sympathetic sweat glands

A

ACh

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10
Q

What is the key postglanglionic NT for symapthetic Cardiac and smooth muscles, gland cells, nerve terminals

A

NE

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11
Q

What is the key postglanglionic NT for symapthic to renal vascular smooth muscle

A

Dopamine

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12
Q

What is the key postglangionic NT for Parasympathetic to cardiac and smooth muscle, gland cells, nerve terminals?

A

ACh - for All parasympathetics

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13
Q

describe Cholinergic Synthesis

A

1) Choline transporter (CHT) (transports choline into cell from Extracellular matrix)
- blocked by hemicholiniums (experimental Rx)
2) acetylCoA (mito) + Choline = Acetylcholine
- Choline acetyltransferase (ChAT) (conjugates it)

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14
Q

Storage of Cholinergic

A

1) Vesicle-associated transporter (VAT) transports ACh into the lumen of a vesicle
- -> blocked by Vesamicol (experimental)

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15
Q

Release of cholinergic

A

1) depolarization of the Nerve terminal
2) voltage-dependent Ca+ entry
3) Ca+-calmodulin association with vesicle-associated membrane protein (VAMP) and synaptosome-associated proteins (SNAP)
- -> BLOCKED BY Butulinum toxin
4) vesicles fusion and neurotransmitter released (exocytosis)

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16
Q

Termination of action of cholinergic transmission

A

1) rapid hydrolysis of Ach
- Acetylcholine esterase (AchE) forms choline and acetate
- -> blocked by AchE inhibitors! (causes hyperactivation of AcH)
2) choline re-uptake into terminals

17
Q

What are the two types of choliergic receptors

A

Muscarinic - G protein coupled

Nicotinic - Ionotropic receptor (Na+ channel)

18
Q

Affects of M3 receptor in intact endothelium vs damaged endothelium

A

Intact endothelium = effects of M3 activation lead to VASODILATION
Damaged endothelium = effets of M3 activation on vascular smooth muscle cell causes VASOCONSTRICTION.

19
Q

M1 and M3 activate what receptors?

A

Gq coupled receptors –> phospholipase C which cleaves PIP2 into:
- IP3 = increases Calcium
- DAG = increaes PKC
THINGS SPEED UP

20
Q

M2 activates what receptors

A

Gi coupled receptors –>inhibits adenylyl cyclase causes decrease cAMP which Decreases PKA activity
THINGS SLOW DOWN

21
Q

Nicotinic receptor location?

A

Nicotinic receptor are located at the presynaptic terminal that causes release of Ach on postsynaptic neuron

22
Q

Describe effect of Nn on adrenal medula

A

secretions of epinephrine and NE

23
Q

Describe effect of Nn on autonomic ganlgia

A

stimulation - net effects dependent on PANS/SANS innervation and dominance

24
Q

Describe effect of Nm on NMJ

A

stimulation - twitch/hyperactivity of skeletal muscle

25
Q

catecholamine synthesis

A

1) tyrosine hydroxylase converts tyrosine to Dopa and eventually dopamine.
- -> blocked by metyrosine

26
Q

Catecholamine storage

A

1) vesicular monoamine transporter (VMAT)
- -> blocked by Reserpine
2) synthesis continues in vesicles

27
Q

Catecholamine release

A

1) similar exocytosis mechanism as Ach release

- -> VAMP inhibited by bretylium

28
Q

Termination of action of adrenergic transmission

A

1) Diffusion at synapse and metabolized by liver (via catechol-O-methyl transferase (COMT)
2) Autoreceptor –> decreases release
3) reuptake via NET1 (NE transporter) and repackaged in vesicles or
- -> metabolized by mitochondrial monoamine oxidase (MAO)

29
Q

Mechanisms of alpha1 receptor activation

A

G-protein coupled receptor (Gq)

- leads to increase in calcium and end results in vasoconstriction (hypertension)

30
Q

Mechansims of beta and alpha 2 receptor activation

A

Beta activates Gs and activates adenylyl cyclase –> increases cAMP –> increases biologic effects
alpha2 activates Gi and inhibits adenylyl cycles (similar to M2)

31
Q

Homotropic interactions

A

the transmitter, by binding to presynaptic autoreceptors, affects the nerve terminals from which it is being released.
- inhibits the release of the same NT

32
Q

Heterotropic interactions

A

one NT affects the release of another via actions on heteroreceptors e.g. NE affects Ach release and vice-versa.

33
Q

Denervation supersensitivity (withdrawal rebound hyperactivity)

A

Phenomena: Nerve cut –> supersensitive downstream structure
- sustained block of ganglionic transmission/postsynaptic receptors –> target organs become super sensitive when the blocker is removed
MECHANISM:
- proliferation of receptors
- loss of mechanism for removal of transmitter

34
Q

Co transmission

A

Neurons release more than one transmitter or modulator, each of which interacts with specific receptors and produces effects, often both pre and postsynaptically.

35
Q

what are the main functions of the ANS

A

1) assist the body in maintaining a constant internal envornment
2) accommodates coordinated responses to external stimuli (ex. pupil response to ambient light)

36
Q

Response to sympathetic/parasympathetic activation

A

Sympathetic activation = ergotropic = fight or flight

parasympathetic activation = trophotropic = rest and digest

37
Q

Describe autonomic feedback loop controlling arterial blood pressure

A

increase in blood pressure (sympathetic activation) increases baroreceptor discharge –> activates vasomotor center –> activates SANS –> decrease in sympathetic tone –> decreases vasoconstriction, decrease cardiac contraction (M2), decrease heart rate (M2)

38
Q

Whenever you have an increase in peripheral resistence you have…

A

(increase alpha1) a reflex bradycardia (tries to correct itself)
- same is true for opposite.

39
Q

describe hormonal autonomic feedback loop

A

Decrease blood pressure –> decreases renal blood flow –> increases renin production –> increases angiotension –> increase aldosterone –> increase blood volume –> increases cardiac output –> increases blood pressure.

Decrease blood pressure –> increase sympatetic drive –> increase total peripheral resistance.

ATTEMPTS TO BRING BLOOD PRESSURE UP.

Medical Phys Exam 1 (8 decks)

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