EXAM #1: ANS PHARMACOLOGY I Flashcards

1
Q

Where do the nerve terminals of the SNS originate?

A

T1-L2

“Thoracolumbar”

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2
Q

Where do the nerve terminals of the PNS originate?

A

Cranial: III, VII, IX, X
Sacral: S2, 3, 4

“Craniosacral”

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3
Q

What are the two components of the enteric division of the ANS?

A

1) Myenteric plexus
- Auerbach’s

2) Submucosal plexus
- Meissner’s

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4
Q

Where is the myenteric plexus located? What is the alternate name for this plexus?

A

Between the external longitudinal muscle and deeper circular muscle

Auerbach’s Plexus

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5
Q

Where is the submucosal plexus located? What is the alternate name for this plexus?

A

Between the circular muscularis muscoe

Meissner’s Plexus

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6
Q

What is the function of the myentric plexus?

A

Motility

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7
Q

What is the function of the submucosal plexus?

A

Ion and fluid transport

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8
Q

What is the principle of “dual innervation?”

A
  • Most organs receive SNS and PNS innervation
  • Opposing actions

**Note that though opposing actions, these are not ANTAGONISTIC*

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9
Q

What organs only have SNS innervation?

A

1) Hair follicles
2) Thermoregulatory sweat glands
3) Liver
4) Adrenal glands
5) Kidneys

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10
Q

In what organs does the SNS and PNS have similar rather than opposing effects?

A

Salivary glands

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11
Q

What NT is released by all pre-ganglionic fibers?

A

ACh

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12
Q

What NT is released by post-ganglionic fibers of the SNS?

A

NE

“Adrenergic”

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13
Q

What NT is released by post-synaptic SNS fibers on thermoregulatory sweat glands?

A

ACh

Note that this is an EXCEPTION

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14
Q

What type of ACh receptor is located on the ANS ganglia?

A

Nicotinic ACh receptor

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15
Q

What NT is released by post-synaptic PNS fibers?

A

ACh

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16
Q

What NT is released from post-synaptic SNS fibers acting on renal vascular smooth muscle?

A

DA

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17
Q

What is a homotropic interaction?

A
  • This describes a NT binding to an autoreceptor on the pre-synaptic nerve terminal from which it is being released
  • Action is to INHIBIT secretion of that NT
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18
Q

What is the effect of blocking the autoreceptor in a homotropic interaction?

A

Dramatic increase of NT released from the nerve fiber

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19
Q

What is a heterotropic interaction?

A

This is when one NT affects the release of another NT via interactions on heteroreceptors

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20
Q

What is withdrawal rebound hyperactivity/ disuse hyperactivity?

A

Sustained block of ganglionic transmission leads to increased sensitivity of target organs

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21
Q

What are the mechanisms of withdrawal rebound hyperactivity/ disuse hyperactivity?

A

1) Receptor proliferation
2) Loss of transmitter removal mechanisms
3) Increased post-junctional responsiveness i.e. increased sensitivity of the receptor

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22
Q

What is a clinical example of withdrawal rebound hyperactivity?

A

Rebound HTN following withdrawal of adrengeric receptor blockers

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23
Q

What is cotransmission?

A

Release of more than one NT from a neuron upon stimulation

E.g. NE and NPY are released from separate vesicles upon stimulation

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24
Q

What are the five steps of NT function that provide targets for pharmacologic therapy?

A

1) Synthesis
2) Storage
3) Release
4) Receptor effects
5) Termination action

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25
Q

How does choline get from the ECF into the neuron for ACh synthesis?

A

Na+ dependent Choline Transporter (CHT)

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26
Q

What drug blocks CHT?

A

Hemicholiniums

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27
Q

Once ACh is synthesized, how is it stored in vesicles?

A

Transport into the storage vesicle via “vesicle associated transporter” (VAT)

28
Q

What drug is a VAT blocker?

A

Vesamicol

29
Q

What is the mechanism of action for the Botulinum toxin?

A
  • Botulinum impaires ACh vesicle and nerve terminal fusion/release
  • Specifically, removes 2 amino acids from the SNARE fusion proteins
30
Q

What enzyme degrades ACh?

A

Acetylcholinesterase

31
Q

What drug blocks Acetylcholinesterase?

A

Neostigmine

32
Q

What are the two types of ACh receptors?

A

1) Nicotinic

2) Muscarinic

33
Q

What type of receptor is a Muscarinic receptor?

A

G-protein coupled receptor

34
Q

What type of receptor is a Nicotinic receptor?

A

Na+ channel

35
Q

What receptors control secretion of aqueous humor?

A

Adrenergic receptors

36
Q

What muscles in the eye have M3 receptors?

A
  • Sphincter muscle

- Ciliary muscle

37
Q

What does activation of M3 receptors in the eye cause?

A
  • Miosis and opening the Canal of Schlemm (sphincter)
  • Spasm of accommodation for near vision (ciliary)

*****Opens the canal of schlemm to decrease intra-ocular pressure

38
Q

What type of muscarinic receptor is located on the heart?

A

M2

39
Q

What is the effect of M2 activation in the heart? Specifically, what happens at the: SA node, AV node, Atrial muscle, and Ventricular muscle?

A

SA node= negative chronotrope

AV node= decreased conduction velocity (negative dromotrope)

Atrial muscle= decreased atrial contraction

Ventricular muscle= decreased ventricular contraction

Generally inhibitory*

40
Q

What type of ACh receptors are located in the lung?

A

M3

41
Q

What is the effect of M3 activation in the lung? Specifically, what happens to the Brconhi and Bronchioles/ Bronchiolar submucusal glands?

A

Brconhi and Bronchioles= Contraction leading to bronchospasm

Bronchiolar submucusal glands= Secretion lead to a narrower lumen

42
Q

What type of ACh receptor is located in the stomach?

A

M3

43
Q

What is the effect of M3 stimulation in the stomach?

A

Increased motility and cramps

44
Q

What type of ACh receptor is located in the glands of the GI tract?

A

M1 and M3

45
Q

What is the effect of ACh stimulation in the glands of the GI system?

A

Secretion

46
Q

What type of ACh receptor is located in the intestines?

A

M3

47
Q

What is the effect of ACh stimulation in the intestine?

A

Contraction leading to diarrhea and involuntary defection

48
Q

What PNS receptor types control gastric acid secretion?

A

M1 and M3

49
Q

What is the role of M3 receptors in gastric acid secretion?

A
  • M3 receptors are located on parietal cells

- ACh stimulation of M3 receptors on parietal cells directly leads to the secretion of gastric acid

50
Q

What is the role of M1 receptors in gastric acid secretion?

A
  • M1 receptors are located on ECL cells
  • ECL cells release histamine
  • Histamine is a key simulator of acid secretion
51
Q

What type of drugs are cimetidine or ranitidine? What is their effect on gastric acid secretion?

A
  • Both are H2R antagonists

- Thus, they block histamine induced acid secretion AND acid secretion following a normal meal

52
Q

What are the muscles of the bladder? What are their functions?

A
  • Detrusor= contraction

- Trigone= relaxation

53
Q

What ACh receptor type is located in the bladder?

A

M3

54
Q

What is the effect of PNS stimulation of the bladder?

A

1) Contraction of the detrusor
2) Relax trigone and sphincter
3) Voiding and potentially urinary incontinence

55
Q

What type of muscarinic receptors are located in blood vessels?

A

M3

56
Q

What is the effect of muscarinic receptor activation in blood vessels?

A

Generally, vasorelaxation

Specifically,

1) Increased intracelluar Ca++
2) Activation of endothelial nitric oxide synthase
3) Production of NO
4) NO diffuses to vasular smooth muscle
5) Stimulation of guanylyl cyclase
6) Increased cGMP
7) cGMP inhibits Ca++ influx
8) VASORELAXATION

57
Q

What is the difference between M3 receptor activation in intact endothelial cells vs. damaged endothelium?

A

Intact= Vasodilation

Damaged= Vasoconstriction

This is b/c the increase in Ca++ is unopposed by NO that would normally be released by the intact endothelium*

58
Q

What type of muscarinic receptors are located in the sphincters?

A

M3

59
Q

What is the effect of ACh on sphincters? What is the exception?

A
  • Relaxation

Except contraction of LES*

60
Q

What type of muscarinic receptor is located on the glands?

A

M3

61
Q

What is the effect of ACh stimulation of the glands?

A

Secretion:

  • Sweat
  • Salviation
  • Lacrimation
62
Q

What type of ACh receptor is located in the skeletal neuromuscular junction?

A

Nicotinic AChR (Nm)

63
Q

What type of receptor is the NAChR? What is the result of ACh binding to the NAChR?

A

Na+ channel

1) Na+ influx causes an EPSP
2) EPSP depolarizes the muscle membrane
3) Muscle membrane depolariation causes an action potential that triggers muscle contraction

64
Q

What ACh receptors are located on the adrenal medulla?

A

NAChR (Nn)

65
Q

What is the response of the adrenal medulla to stimulation with ACh?

A

Secretion of NE and Epi

66
Q

What ACh receptors are located on ALL autonomic ganglia?

A

NAChR (Nn)

67
Q

What is the net response of the autonomic ganglia to ACh?

A

Stimulation

Note that the net effect is dependent on whether the SNS or PNS dominates