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SBM Pharm term 1 > cholinergic inhibition > Flashcards

cholinergic inhibition Flashcards

1
Q

what are the direct acting anticholinergics?

A

none

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2
Q

muscarinic receptors are what kind of receptor?

A

GPCRs

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3
Q

where are M1 receptors found?

A

gastric parietal cells

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4
Q

where are M2 receptors found?

A

heart

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5
Q

where are M3 receptors found?

A

most tissues

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6
Q

where are M4 and M5 receptors found?

A

CNS

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7
Q

Gi vs Gq

A
  • M1, M3, M5 use Gq and stimulate phospholipase C (elevates Ca++)
  • M2, M4 use Gi and inhibit adenylyl cyclase (activate K+ channels)
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8
Q

are there muscarinic blockers specific for subsets of M receptors?

A
  • in vitro yes, but not in clinical practice
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9
Q

how do muscarinic blockers work?

A
  • block parasympathetic transmission at end organs

- produce inhibitory effect

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10
Q

how does atropine work?

A
  • anti-DUMBBELSS

- unopposed sympathetic actions

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11
Q

effects of atropine toxicity

A

1) delirium (mad as a hatter)
2) mydriasis, blurred vision (blind as a bat)
3) dry mouth, skin, eyes, bronchi (dry as a bone)
4) temp up (hot as a hare)
5) redness (red as a beet)
6) pee pee dance

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12
Q

clinical uses for atropine

A

1) bronchodilation Rx for asthma
2) constipation Rx for IBS
3) tachycardia and hypertension Rx for bradycardia

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13
Q

what are the M specific anticholinergics?

A

1) atropine

2) scopolamine

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14
Q

what are the two subclasses of Nm specific anticholinergics?

A

depolarizing and non-depolarizing

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15
Q

what are the depolarizing Nm specific anticholinergics?

A

succinylcholine - cholinolytic agonist

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16
Q

what are the non-depolarizing Nm specific anticholinergics?

A 
benzylisoquinolines
- d-Tubocurarin
- cisatracurium
aminosteroids
- pancuronium
- vercuronium
- rocuronium
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17
Q

what are the Nn specific anticholinergics?

A

trimethaphan - ganglionic blocker

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18
Q

what are the major clinical uses for scopolamine?

A

1) motion sickness

2) inducing anesthesia

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19
Q

how is scopolamine given?

A

transdermal patch

20
Q

side effects of scopolamine

A
  • same as atropine

- plus CNS depression/excitation

21
Q

muscarinic blockers for urgency and bladder spasms?

A

1) oxybutynin

2) glycopyrrolate

22
Q

muscarinic blocker for parkinsons

A

benztropine

23
Q

muscarinic blockers for asthma/COPD

A
  • ipratropium - short action

- tiotropium - long action

24
Q

muscarinic blockers for cholinergic poisoning

A
  • atropine

- pralidoxime (when organophospates are involved)

25
Q

what is the one clinical use of Nm blockers?

A

inhibit skeletal muscle activity during surgery

26
Q

how does succinylcholine work?

A

acts like ACh at Nm receptors but binds and depolarizes longer and stronger causing paralysis. ACh can’t bind because succinylcholine is already there

27
Q

what are some possible adverse effects of succinylcholine?

A

1) muscle fasciculations
2) hyperkalemia
3) histamine release
4) malignant hyperthermia (rare)

28
Q

contraindications for succinylcholine

A

1) family hx of malignant hyperthermia
2) hyperkalemia
3) burns, trauma, tissue injury
4) heart failure

29
Q

how do non-depolarizing Nm blockers work on receptors?

A

reversible competitive inhibition

30
Q

what does d-Tubocurarine do?

A

paralysis in fully conscious patients

31
Q

what is the best way to reverse non-depolarizing Nm blockers?

A

neostygmine

32
Q

what is the best way to reverse depolarizing Nm blockers?

A

time - neostygmine will produce muscarinic syndrome

33
Q

side effects of non-depolarizing Nm blockers

A
  • tachycardia
  • hypertension
  • histamine release
  • ganglionic and muscarinic side effects
34
Q

what are the routes of excretion for the non depolarizing Nm blockers?

A

pancuronium - renal
vecuronium - hepatic
rocuronium - hepatic
cisatracurium - inactivated by plasma ChE

so……

renal disease - not pancuronium
liver disease - not vecuronium or rocuronium
renal AND liver disease - cisatracurium
plasma ChE deficiency - not cisatracurium

35
Q

when is trimethaphan used?

A
  • hypertensive crisis

- dissecting aortic aneurysm

36
Q

atropine F

A

25%

37
Q

atropine half life

A

2 hours

38
Q

atropine metabolism/excretion

A
  • 50% metabolized to tropine and tropic acid

- 50% excreted unchanged in urine

39
Q

atropine routes

A

oral, IV, IM, rectal

40
Q

ipratropium indications

A
  • COPD

- acute asthma

41
Q

ipratropium metabolism

A

hepatic

42
Q

ipratropium half life

A

2 hours

43
Q

ipratropium pharmacodynamics

A
  • non-selective muscarinic blocker
  • promotes degradation of cGMP
  • decreased contractility of smooth muscle
  • does not cross blood brain barrier
44
Q

ipratropium special considerations

A

not a short acting bronchodilator, cannot be used as a rescue drug for acute asthma

45
Q

trimethaphan routes

A

oral, IM, IV

46
Q

trimethaphan pharmacodynamics

A
  • blocks Nn receptors at ganglion shutting down both SANS and PANS.
  • causes vasodilation and histamine release
47
Q

two other drugs that work like tubocurarine

A
  • rocuronium

- cisatracurium

SBM Pharm term 1 (9 decks)

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