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Pharmacology II > L2 Cholinergic Agents (Exam #1) > Flashcards

L2 Cholinergic Agents (Exam #1) Flashcards

1
Q

What are the three muscarinic agonists and what is the MOA for all three?

A

MOA: non-specific (work on N and M receptors)

  • Acetylcholine
  • Bethanechol (Urecholine)
  • Pilocarpine (Isoptocarpine)
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2
Q

What are three general contraindications for muscarinic agonists?

A
  • Asthma/COPD
  • Peptic ulcer
  • Bowel obstruction
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3
Q

What symptoms are associated with muscarinic toxicity/poisoning?

A
  • Salivation
  • Lacrimation
  • Urination
  • Defecation
  • Gastric distress
  • Emesis/vomiting
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4
Q

What two medications can be used to treat muscarinic toxicity/poisoning?

A
  • Atropine (antagonist)

- Albuterol (B-agonist)

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5
Q

Which medication has no real clinical use because of its short half-life? What CAN it be used for occasionally?

A

Acetylcholine has a very short half-life but it can be used IV to decrease BP

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6
Q

What are the two primary uses associated with Bethanechol (Urecholine)?

A
  • Increase GI motility

- Treat urinary retention

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7
Q

What is one system that is not affected by Bethanechol (Urecholine), and why?

A

CNS is unaffected because Bethanechol cannot cross the BBB

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8
Q

What are the two primary uses associated with Pilocarpine (Isoptocarpine)?

A
  • Oral: xerostoma/dry mouth

- Topical: treat closed angle glaucoma

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9
Q

What are the three primary SEs associated with Pilocarpine (Isoptocarpine)?

A
  • Sweating (oral)
  • Blurred vision (topical)
  • HA/browache (both)
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10
Q

What is the tissue order by which Atropine affects PNS tone from most to least?

A

MOST AFFECTED (highest PNS tone, lowest Atropine dose needed)
- Salivary, sweat glands, lungs
- Heart, eyes
- GI, GU
- CNS
LEAST AFFECTED (lowest PNA tone, highest Atropine dose needed)

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11
Q

What are the two primary uses of Atropine?

A
  • Decrease bradycardia due to reverse heart block OR excessive vagal stimulation
  • Block muscarinic effects (i.e. pesticide/nerve gas poisoning, mushroom poisoning)
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12
Q

What condition is treated with a combination drug involving Atropine and an opioid, and what is this combination drug called?

A

Lomotil treats diarrhea

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13
Q

What two systems does Atropine have little effect on, and why?

A
  • Blood vessels: no PNS

- CNS: cannot cross BBB

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14
Q

What is the primary use of Scopolamine (Transderm Scop), and what does this say about its pharmacokinetics/MOA?

A

Relieves motion sickness

- Good CNS penetration/can cross BBB

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15
Q

What are two primary SEs associated with Scopolamine (Transderm Scop)?

A
  • Drowsiness

- Hallucinations (toxic dose)

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16
Q

What are two primary uses of Tropicamide (Mydriacil)?

A
  • Mydriasis (for eye exams)

- Cycloplegia

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17
Q

What is the primary use of Ipratropium (Atrovent)? What is another possible use?

A

Primary: COPD to reverse bronchoconstriction (cause bronchodilation)
- Can also be used for acute asthma attacks

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18
Q

What is the primary use of Tolterodine/Fesoterodine, Darifenacin/Solifenacin? What is specific to this group of medications?

A

Treat overactive bladder

- GREAT M3 receptor specificity

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19
Q

What is the primary use of Oxybutynin (Ditropan)?

A

Treat bladder spasms

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20
Q

What is the primary use of Dicyclomine (Bentyl), and what specific condition is it used to treat?

A

Reduces abdominal cramping (reduce GI wall contraction)

- Treats diarrhea-predominant IBS

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21
Q

What is the primary MOA of OnabotuliniumtoxinA (Botox)?

A

Blocks ACh release

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22
Q

What are three potential uses of OnabotuliniumtoxinA (Botox)?

A

Not often used because $$$ but:

  • Urinary incontinence in patients refractory to antimuscarinics
  • Chronic migraine prophylaxis
  • Wrinkles
23
Q

What is the primary AE associated with OnabotuliniumtoxinA (Botox)?

A

Asthenia (speech, swallowing, numbness, ptosis)

24
Q

What are the two primary CIs associated with muscarinic antagonists?

A
  • Closed angle glaucoma (closes angle which increases IOP)

- BPH

25
Q

What are the seven primary AEs associated with muscarinic antagonists?

A
  • Dry mouth
  • Dry eyes
  • Mydriasis
  • Cycloplegia
  • Increase HR
  • Decrease GI motility
  • Urinary retention
26
Q

What is the phrase associated with the symptoms of Atropine poisoning?

A

“Hot as a hare, dry as a bone, blind as a bat, red as a beet, mad as a hatter”

27
Q

What are the six symptoms associated with Atropine poisoning?

A
  • Hot/dry skin
  • Urinary retention, constipation
  • Pupils dilated, poor vision
  • Agitation, delirium, dementia
  • Tachycardia
  • CV/Resp. issues
28
Q

What is the primary treatment for Atropine poisoning, and why?

A

Supportive care and Physostigmine (increase ACh levels in brain)

29
Q

How do receptors differ between muscarinic and nicotinic?

A
  • Muscarinic: primarily PNS (except glands)

- Nicotinic: SNS AND PNS, as well as brain and NMJ

30
Q

What characteristic is specific to nicotinic receptors?

A

They are ligand-gated Na+ channels that rapidly desensitize

31
Q

How does nicotinic activity effect the brain (hint: low (2) vs. high (4) vs. toxic doses(2))

A
  • Low: increase alertness and attention
  • High: N, V, tremor, increase breathing
  • Toxic: convulsions, seizures
32
Q

How does nicotinic activity effect SNS (2)?

A
  • HTN

- Increase HR alternating with decrease HR (baroreflex)

33
Q

How does nicotinic activity effect PNS (4)?

A
  • N
  • V
  • D
  • Urination
34
Q

How does nicotinic activity effect NMJ, and what can this potentially lead to?

A

Muscle twitch/contraction leads to depolarizing block (with possible paralysis if persistent)

35
Q

What is the primary MOA of Varenicline (Chantix), and how does this occur?

A

Partial agonist of N receptors (stimulates reward system in brain by releasing DA)

36
Q

What is the primary use of Varenicline (Chantix), and how does this occur?

A

Smoking cessation
- When smoking is stopped, less DA is released so cravings increase BUT Chantix decreases cravings and provides some N stimulation (can block some N if smoking continues)

37
Q

What are the five primary AEs associated with Varenicline (Chantix)?

A
  • N
  • V
  • Nightmares
  • Psychosis
  • SI
38
Q

What is the general MOA of all AChE inhibitors?

A

Inhibit ACh breakdown, resulting in high levels of ACh in synaptic cleft and increased ACh receptor activation

39
Q

What are the three primary uses of Neostigmine/Pyridostigmine?

A
  • Myasthenia Gravis
  • Reverse NM blockade
  • Post-op ileus
40
Q

What is the primary use of Physostigmine, and why does this occur?

A

Treat muscarinic antagonist (Atropine) poisoning

- Enters CNS so able to help the brain

41
Q

What are the two primary uses of Edrophonium?

A
  • Diagnose and determine treatment dose for Myasthenia Gravis
  • Reverse NM blockade
42
Q

How is Edrophonium used to diagnose Myasthenia Gravis?

A
  • If patient strength improves, diagnose with MG and increase dose
  • If patient strength worsens, dose may need to be adjusted (too high)
43
Q

What is the primary use of Donepezil (Aricept)?

A

Treat Alzheimer’s disease

44
Q

What is enzyme “aging”, and what type of poisoning is it associated with?

A

Organophosphate poisoning

- Within 3-4 hours of poisoning, covalent bond formed between organophosphate and AChE becomes irreversible

45
Q

What are the general toxicities associated with Organophosphates (5)?

A

Similar to M Agonist toxicity

  • SLUDGE
  • Bradycardia
  • Hypotension
  • CNS effects (confusion, ataxia, slurring, convulsions, coma)
  • NM stimulation → blockade → paralysis → respiratory arrest → death
46
Q

What is the treatment for Organophosphate poisoning (hint: 3 parts)?

A
  1. Atropine until pupils dilate
  2. 2-PAM IF LESS THAN 3-4 HOURS
  3. Diazepam (Valium) for convulsions
47
Q

Why can 2-PAM only be administered within 3-4 hours of poisoning?

What must be confirmed prior to administering 2-PAM?

A

2-PAM is able to attract the organophosphate from AChE before “aging” can occur (but must be prior to aging)
- Must confirm that it is Organophosphate-specific poisoning because 2-PAM can also inhibit AChE itself

48
Q

What is the primary use of nondepolarizing blockers, and in what order does this occur?

Is there CNS penetration?

A

Paralyze muscles during surgical procedures

  • Starts with small muscles → larger muscles → IC muscles/diaphragm
  • NOTE: recovery occurs in reverse order

NO CNS PENETRATION (does not cross BBB)

49
Q

What is the MOA of Succinylcholine (hint: 2 parts)?

A

Initial stimulation and contraction → receptor desensitization and blocked = paralysis

50
Q

What are three significant PK characteristics of Succinylcholine, and how does this relate to its use?

A
  • IV only
  • Rapid onset of action
  • Rapid recovery

Used for rapid, short-acting procedures like tracheotomy or intubation

51
Q

What are the two primary AEs associated with Succinylcholine, and why does each occur?

A
  • Hyperkalemia leading to cardiac arrest, arrhythmias (issue in burn patients, soft tissue damage because already hyperkalemic)
  • Malignant hyperthermia due to muscle rigidity and high temperature
52
Q

What are the three primary CIs associated with Succinylcholine?

A
  • History of malignant hyperthermia
  • Extensive soft tissue damage
  • Burns
53
Q

What drug is associated with possible malignant hyperthermia, and how is this treated?

A

Succinylcholine can cause malignant hyperthermia with repeated doses
- Treat with Dantrolene

Pharmacology II (20 decks)

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