19. ANS Pt 2 Flashcards

1
Q

What are the targets of PNS?

A
  1. Smooth muscle (gut, resp. syst, vasculature)
  2. Cardiac muscle
  3. Glands (hormones, digestive enzmes, tears)
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2
Q

What are PNS effects?

A
  • PNS brings body to most efficient state
  1. Salivation
  2. Lacrimation
  3. Urination
  4. Digestion (metabolism, peristalsis, breakdown + uptake of nutrients)
  5. Defecation
  6. Pupillary constriction
  7. Vasomotor control (balanced by SNS output: BP, blood flow)
  8. Bronchial control (balanced by SNS: bronchial dilation for bigger breaths)
  • SNS wastes E + takes away from organ reserve
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3
Q

What is the major parasympathetic nerve?

A
  • Vagus = “wandering”
  • Comes out of brainstem + Innervates thoracic + abd structures (SNS ganglia tend to be more organ sp.)
  • Recurrent laryngeal nerve supplies motor innervation to all nerves of larynx except cricothyroid (–> superior laryngeal)
    • Damage –> closing of vocal cords (nerve keeps cords open)
  • Neck surgery, tumors, trauma involving carotid sheath (carotid artery, jugular vein + vagal nerve) –> hoarse voice
    • Bilateral damage results in midline position of vocal cords, stridor, laryngeal obstruction
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4
Q

What are PNS NT + receptors called?

A
  • NT = Ach
    • B/c ACh = NT for neuromuscular jxn, anything that impacts PNS will also affect motor end plates
  • Receptor = cholinergic receptor
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5
Q

How is ACh synthesized?

A
  • Synthesized in cholinergic neurons
  • Acetyl Co-A + choline –(choline acetyltransferase)–> ACh
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6
Q

Where are ACh stored?

A

ACh stored in vesicles at nerve end terminals (both pre + post-ganglionic nerve terminals)

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7
Q

What 2 types of receptors are found on distal organs interfacing w 2nd nerve?

A
  1. Muscarinic receptors
  2. Nicotinic receptors
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8
Q

ACh re-uptake is facilicated by _____ coupled to Na-K-ATPase pump.

A

High affinity Na-choline co-transport

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9
Q

How is ACh released?

A
  1. Depolarization of nerve terminal –> influx of Ca++
  2. Ca++ stimulates + promotes vesicular exocytosis of NT into cleft
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10
Q

What is 1 example of a toxin that prevents acetylcholine release? What happens as result?

A
  • Botulinum Toxin A
  • Binds to vesicles + prevents exocytosis (–> no neuromuscular jxn fxn)
  • Leads to flaccid paralysis + resp. failure
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11
Q

How is ACh activity terminated?

A
  1. Reuptake –> can be reused
  2. Hydrolysis to acetate + choline –> can be reused
    • Accel. by acetylcholinesterase prim. in synapse
    • Butyrylcholinesterase (pseudocholinesterase) –> circulating hydrolysis in bloodstream
    • Diffusion away is minimal due to high enzyme activity
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12
Q

What is 1 parasymathetic consequence of using muscle relaxant reversals?

A

Increase in ACh affects both neuromuscular jxn + PNS –> huge parasympathetic output (=reason we give glyco)

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13
Q

What are 4 cholinesterase inhibitors?

A
  1. Neostigmine
  2. Edrophonium
  3. Pyridostigmine
  4. Physostigmine

Increased ACh leads to increased ACh diffusing away from synapse into bloodstream –> more distal + PNS effects

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14
Q

What kind of receptors are nicotinic receptors?

A
  • Nicotinic receptors = ligand-gated ion channels
    • Ligand: nicotine or ACh
    • ACh binds ⍺-subunits
  • Location: neuromuscular jxn + autonomic ganglia (PNS + SNS)
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15
Q

What happens when nicotinic receptors are activated?

A
  1. Stimulation (ACh binds ⍺-subunits)
  2. Nicotinic receptor ion channel opens
  3. Na + K flow down concentration gradient –> depol
  4. Further stim of another nerve or other outcome (secretion, smooth muscle contraction…)
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16
Q

What kind of receptors are muscarinic receptors?

A
  • At least 5 types:
    • M1 - autonomic ganglia + CNS
    • M2 - supraventricular cardiac (brady + negative inotropic effect)
    • M3 - smooth muscle + glands (depending on location –> constraction or dilation of smooth muscles + release of secretions from glands)
17
Q

What happens when muscarinic receptors are activated?

A
  1. Stimulation
  2. G-protein activation
  3. Pospholipase C activation: phosphatidylinositol 4,5-bisphosphate –> IP3 + DAG
  4. IP3 –> increased Ca++ from SR
  5. Smooth muscle contraction + glandular secretion
18
Q

(T/F) Binding of ACh to muscarinic receptor leads to vasoconstriction.

A

False.

ACh stim. production of NO by endoendothelial cells –> vasodilation. Without endothelial cells, ACh leads to smooth muscle contraction

  • NO = very potent but shortlived vasodilator, works on smooth muscle cells
19
Q

(T/F) ACh induced NO release by endothelial cells can cause systemic vasodilation.

A

False.

NO can’t cause systemic vasodilation b/c breaks down quickly –> would breakdown as diffusing away

20
Q

Does release of Ca++ by ACh binding to muscarinic receptor increase contraction + conduction?

A

No. Slows conduction + decrease HR!

M2 receptors mediate inhibition via G-proteins –> hyperpolarization + slower spontaneous depol

21
Q

What is a cholinergic crisis?

A
  • Upregulated + uncontrolled increase in PNS
  • Causes:
    1. Mydriasis (crying)
    2. Miosis (pupillary dilation)
    3. Perspiration
    4. Salivation
    5. Bronchoconstriction
    6. Broncial secretions –> bronchospasm + laryngospasm
    7. Flaccid paralysis
    8. Respiratory failure
  • Treatment: anticholinergic drugs to block side effects
22
Q

Summary of cholinergic receptor action.

A