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Pharmacology I > Test 2 part V > Flashcards

Test 2 part V Flashcards

1
Q

Indirect Acting Cholinomimetics cause _____ nerve activation and effects on the ________.

A

Vagal; Vasculature

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2
Q

What are the effects associated with Vagal Nerve Activation via Indirect Acting Cholinomimetics?

A
  1. Decreased CO due to bradycardia, dec atrial contraction, and some decreased ventricular contraction
  2. Prejunctional inhibition of NE release due to negative feedback on SNS ganglia (!!!!)
  3. Post-junctional inhibition of SNS effects
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3
Q

What are the effects associated with Vasculature effects from Indirect Acting Cholinomimetics?

A
  1. Most lack cholinergic innervation
  2. Increase in SNS tone due to Ach on sympathetic ganglia (increased NE in vasculature). (Remember: we have a dominant PNS System. Ach acts on both SNS and PNS. Inc Ach can have an effect of vasoconstriction due to Ach on sympathetic ganglia)
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4
Q

MR > NR in ______ (all MR Subtypes)
NR > MR in _______

A

Brain; Spinal Cord

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5
Q

A moderate dose of an Indirect Acting Cholinomimetic will cause what effects on the CV system?

A
  1. Bradycardia
  2. Decreased CO
  3. Increased PVR
  4. Increased BP
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6
Q

A high (toxic) dose of an Indirect Acting Cholinomimetic will have what effects on the CV system?

A
  1. Marked bradycardia
  2. Significantly decreased CO
  3. Severe hypotension
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7
Q

What is the prototype drug for antimuscarinics?

A

Atropine

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8
Q

Is Atropine tertiary or quaternary?

A

Tertiary

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9
Q

What is the mechanism of action for antimuscarinics?

A

Reversible blockade of the muscarinic receptor.
Prevents the release of IP3 and blocks the inhibition of adenylyl cyclase.

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10
Q

Muscarinic Blockers block ________ cholinoreceptor agonists more effectively than _______.

A

Exogenously administered; endogenously released Ach

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11
Q

Low doses of Atropine result in initial ______ as a result of the pre-junctional ____ on vagal postganglionic fibers that normally limit Ach release.

A

Bradycardia; M1

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12
Q

Which Drug?
1. A competitive antagonist at all MR
2. Prevents release of IP3 and inhibition of adenylyl cyclase.
3. Tertiary Amine

A

Atropine

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13
Q

Which Drug?
1. A competitive antagonist at muscarinic receptors.
2.Tertiary amine
3. Transdermal patch given for PONV and/or motion sickness (patch education needed)

A

Scopolamine

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14
Q

Which Drug?
1. A competitive, non-selective antagonist at M receptors
2. Reduces/prevents bronchospasm.

A

Ipratropium

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15
Q

Which Drug?
1. Blocks Ach at PNS sites in smooth muscle, secretory glands, and CNS, preventing salivation
2. Quaternary amine

A

Glycopyrrolate

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16
Q

Which Drug?
1. inhibits Ach-E, increases available Ach.
2. Tertiary amine - well absorbed throughout
3. Given for reversal of CNS anticholinergic syndrome

A

Physostigmine

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17
Q

Which Drug?
1. Forms covalent bond with Ach-E
2. Increases PNS activity, longer-acting.
3. Quaternary amine - does not enter CNS
4. Used in tx of Myasthenia Gravis

A

Neostigmine

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18
Q

What causes Cholinergic Poisoning?

A

Too much Acetylcholine

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19
Q

What are the S/Sx of Cholinergic Poisoning?

A

SLUDGE: Salivation, Lacrimation, Urination, Diarrhea, inc Gi motility, Emesis, pulm edema

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20
Q

A Medical emergency due to Insecticides, Wild mushrooms, or Nerve Gasses. Has a rapid onset of 30 min.

A

Cholinergic Poisoning

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21
Q

What is the treatment for Cholinergic Poisoning?

A
  1. Tertiary Antimuscarinic (Atropine) for CNS and peripheral effects
  2. Benzos if seizures
  3. Cholinesterase Regenerators
22
Q

What are the S/Sx if too much Muscarine?

A

N/V/D, urinary urgency, salivation, sweating, cutaneous vasodilation, bronchial constriction

23
Q

What is the treatment for too much Muscarine?

A

Atropine

24
Q

What are the S/Sx of too much Nicotine?

A

Seizure, coma, death, respiratory paralysis. Fatal dose = 40 mg

25
Q

What is the treatment for too much Nicotine?

A

Symptom management (Nicotine is rapidly metabolized)

26
Q

Which cholinergic drugs (agonists or antagonists) are Tertiary (Can cross the blood-brain barrier)

A

PAS:
Physostigmine
Atropine
Scopolamine

27
Q

T/F: if you give a muscarinic blocker, you will inhibit/slow digestion

A

false; gut motility still active d/t modulation of local hormones and NANC within the ENS

28
Q

What clinical conditions are treated with Cholinomimetics?

A
  1. closed angle glaucoma
  2. accomodative esotropia
  3. postop ileus
  4. congenital megacolon
  5. urinary retention
  6. neurogenic bladder
  7. reflux esophagitis
  8. dry mouth
  9. myasthenia gravis
  10. alzheimers
29
Q

What medication is used in the Tensilon Test to differentiate between a Myasthenia Crisis and a Cholinergic Crisis?

A

Edrophonium (an indirect acting cholinomimetic - simple alcohol)

30
Q

What clinical conditions would you use a Muscarinic Blocker for?

A
  1. mydriasis for eye exam
  2. travelers diarrhea
  3. urinary urgency and/or incontinence
  4. urolithiasis
  5. syncope
  6. chagas dz
  7. graves dz
  8. copd/asthma recovery
  9. parkinsons
  10. motion sickness
31
Q

What is the treatment for Atropine Intoxication?

A

Neostigmine

32
Q

What are the S/Sx of Atropine Intoxication?

A
  1. dry mouth
  2. mydriasis
  3. tachycardia
  4. hot/flushed skin
  5. agitation
  6. delirium
  7. fever
  8. behavioral disturbances
  9. lethal arrhythmias
33
Q

There is no effective method for blocking the ______________ effect of cholinesterase inhibitors.

A

Nicotinic (remember: Nicotinic receptors are in SNS and PNS)

34
Q

Which sympathetic receptor is most DOMINANT in the heart?

A

Beta 1

35
Q

Adrenergic stimulation on the heart ___________ coronary blood flow

A

Increases

36
Q

Direct Acting Cholinomimetics cause direct ______ of the SA and AV node.

A

Slowing

37
Q

The slowing of the SA/AV node is opposed by what?

A

Reflex SNS discharge from the decrease in MAP

38
Q

Indirect Acting cholinomimetics will cause prejunctional inhibition of _____ release, but secondarily will increase the _____ in the vasculature (as a response)

A

NE; NE

39
Q

Which adrenergic receptor causes arterial and venous vasoconstriction = increased BP?

A

Alpha 1

40
Q

What are the effects of Alpha 1 Stimulation?

A
  1. Increased arterial tone/resistance
  2. Decreased venous capacitance
  3. Decreased HR due to baroreceptor reflex
    Ex: Phenylephrine
41
Q

Stimulation of which Adrenergic receptor inhibits Renin secretion?

A

Alpha 2

42
Q

Stimulation of Beta 1 receptors does what?

A

Increases CO by increasing contractility and direct stimulation of the SA node to increase HR.

43
Q

Which adrenergic receptor stimulates Renin secretion?

A

Beta 1

44
Q

Which adrenergic receptor decreases SVR through vasodilation of certain vascular beds?

A

Beta 2

45
Q

What is the effect of Alpha 1 agonism on the eye?

A

Reduces outflow of aqueous humor and
increases intraocular pressure.

46
Q

What is the effect of Beta Blocker administration on the eye?

A

Reduces intraocular pressure through decreasing the aqueous humor.

47
Q

Why do you want to avoid stopping a beta blocker rapidly in a patient with HTN?

A

To avoid rebound HTN

48
Q

What is the effect of Alpha Blockers on the CV System?

A

Lowers BP and SVR

49
Q

Which drug often causes orthostatic hypotension and reflex tachycardia?

A

Alpha Blockers

50
Q

You should avoid which class of drugs in asthmatic patients?

A

Beta Blockers (bronchoconstriction)

Pharmacology I (16 decks)

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