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PDA Block 1 > Cholinergics > Flashcards

Cholinergics Flashcards

1
Q 
Muscarinic Receptors
Eye:
Heart:
Lung:
Bladder:
GI tract:
Sweat Glands:
Blood Vessels:
A

Eye: Contraction of the ciliary muscle focus lens for near vision; Contraction of the iris sphincter muscle
Heart: Decreased rate
Lung: Constriction of bronchi; secretion
Bladder: Voiding
GI tract: Salivation; Increased gastric secretion; increased intestinal motility
Sweat Glands: Generalized sweating
Blood Vessels: Vasodilation

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2
Q

Nicotinic Receptors
Nm:
Nn:
CNS:

A

Nm: Skeletal muscle - End-plate depolarization
Nn: Autonomic ganglia and Adrenal medulla - depolarization and firing of post-ganglionic neurons; Depolarization and secretion of catecholamines
CNS: Control of neurotransmitter release

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3
Q

Cholinergic Agonists and Antagonists

A 
Muscarinic Receptor Agonists
Acetylcholinesterase inhibitors
- Reversible inhibitors
- Irreversible inhibitors
Muscarinic Receptor Antagonists
Ganglionic Blocking Agents
Neuromuscular Blocking Agents
- Competitive blockers
- Depolarizing blockers
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4
Q

Muscarinic Agonists

A

Direct agonists of muscarinic receptors; produce effects similar to activating post-ganglionic parasympathetic nerves (parasympathomimetics)

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5
Q

Choline Esters

A

Acetyclcholine; Bethanechol

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6
Q

Bethanechol
Primarily Effects:
Therapeutic Uses:

A

Primarily effects G.I/G.U systems

Therapeutic Uses: Orally or subcutaneous treatment for urinary retention in the absence of obstruction

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7
Q

Alkaloids

A

Muscarine; Pilocarpine

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8
Q

Pilocarpine - Therapeutic Effects

A
  • Orally for xerostomia

- Miotic agent used opthalmically to treat wide-angle glaucoma as well as emergency treatment for narrow-angle glaucoma

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9
Q

Bethanechol and Pilocarpine: Route of administration

A

Not IV
Oral (bethanechol, pilocarpine) or Subcutaneous (Bethanechol)
Opthalmic: pilocarpine, acetylcholine

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10
Q

Bethanechol and Pilocarpine: Side Effects

A

Salivation, Lacrimation, Urination, Defacation, Gastrointestinal upset, Emesis (SLUDGE)
Also… Hypotension, bradycardia and blurred vision
Toxicity: treated with muscarinic receptor antagonist (atropine)

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11
Q

Bethanechol and Pilocarpine: Use with caution in patients with…

A

Athsma and COPD
Urinary or GI obstruction and peptic ulcer
Cardiovascular diseases involving bradycardia or hypotension

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12
Q

Acetylcholinesterase Inhibitors

A

Enhance the effects of endogenously released acetycholine by blocking its natural breakdown by acetylcholinesterase

  • Effective at any site where acetycholine is the neurotransmitter
  • Also termed anticholinesterase agents
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13
Q

Acetylcholinesterase Sites of action

A
  • Post-ganglionic parasympathetic neuroeffector junction
  • Ganglia (Sympathetic and Parasympathetic)
  • Neuromuscular junction
  • CNS (if able to penetrate)
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14
Q

Reversible acetycholinesterase inhibitors

A

Edrophonium
Physostigmine
Neostigmine

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15
Q

Edrophonium - Therapeutic Use

A
  • Diagnosis of myasthenia gravis
  • Distinguish cholinergic from myasthenic crisis
  • Reverse paralysis by competitive neuromuscular blocking agents
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16
Q

Administration of Edrophonium

A

Rapid onset and short duration of action
Does not penetrate into CNS
Not orally active (IV administration)

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17
Q

Physostigmine - Therapeutic Use:

A

Treatment of chronic wide-angle glaucoma

Toxicity by antimuscarinic drug poisoning

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18
Q

Physostigmine: Structure

A

Tertiary Amine (lipophilic) - CNS effects

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19
Q

Neostigmine: Structure

A

Synthetic: Quarternary amine so no CNS penetration

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20
Q

Neostigmine - Therapeutic Use:

A

Treatment of myasthenia gravis (oral)
Prevention and treatment of post-operative atony of gut and bladder (oral)
Reversal of paralysis by neuromuscular junction blocking agents

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21
Q

Reversible Acetycholinesterase Inhibitors - Side Effects

A

SLUDGE

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22
Q

Irreversible Acetycholinesterase Inhibitors are all….

A

Lipophilic and can pass through mucosal membranes and skin

23
Q

Nerve gas used in attacks in Japan and Syria

24
Q

Malathion

A

Insecticide - greater safety than Sarin because it is detoxified in higher organisms

25
Toxicity of Irreversible Acetycholinesterase Inhibitors (Organophosphate)
- SLUDGE - Hypotension; Bradycardia; Bronchoconstriction; Blurred vision - Death due to respiratory failure - Medullary respiratory center depression - Symptom onset depends on method of exposure
26
Treatment for Organophosphate
- Remove poisoning - Maintain open airway; artificial respiration - Treat convulsions and shock Antidotes - Atropine - Pralidoxime
27
Pralidoxime
Reactivates Acetycholine esterase peripherally | Must treat quickly (2-3 hours)
28
Muscarinic Receptor Antagonists
Competitively block muscarinic receptors (Parasympatholytics)
29
Effects of Muscarinic antagonists
- Relax iris sphincter and ciliary muscles - Relax non-vascular smooth muscle - Inhibit exocrine gland secretion - Increase heart rate - CNS effects (Sedation (low doses); Excitement, delirium, psycohsis (high hoses))
30
Atropine - Therapeutic Uses
- Bradyarrhythmias - Opthalmic uses - mydriasis and cycloplegia - Block vagal reflexes and reduce secretions during anesthesia - Acetylcholinesterase and muscarinic toxicity
31
Scopolamine - Therapeutic Use
Motion sickness and vestibular diseases
32
Muscarinic Receptor Antagonists: Alkaloids
Atropine; Scopolamine
33
Muscarinic Receptor Antagonists: semi-synthetic derivative
Ipratropium
34
Ipratropium - Therapeutic Use
COPD | Less effective for athsma
35
Ipratropium administration and actions
Administered by inhalation No CNS penetration and poor systemic absorption when inhaled Reduces bronchial secretions and reduces bronchoconstriction
36
Muscarinic Receptor Antagonists: Synthetics
Tropicamide Oxybutynin Darifenacin Glycopyrrolate
37
Tropicamide - Therapeutic Use
``` Mydriatic and Cycloplegic Fast onset (20-40 min) and short duration of action (4-6 hours) ```
38
Oxybutynin Therapeutic Use: Side-effects
Therapeutic use: Overactive bladder, incontinence | SE: xerostomia, blurred vision, constipation
39
Darifenacin (Has some M3 selectivity) | Therapeutic use:
Overactive bladder, incontinence | Less CNS side effects
40
Glycopyrrolate - Therapeutic Use:
Used to block parasympathomimetic effects when neostigmine is used to reverse+ skeletal muscle paralysis by neuromuscular blocking agents No CNS penetration
41
Muscarinic Receptor Antagonists: Side Effects
``` Hot as a hare (no sweating) Dry as a bone (Dry mouth) Red as a beet (Due to excess heat) Blind as a bat (Mydriasis, cycloplegia) Drowsiness (CNS actions) Mad as Hatter (at high concentrations) ```
42
Muscarinic Receptor Antagonists: Use with caution
Glaucoma Benign Prostatic hyperplasia Any disease where tachycardia is a problem (angina)
43
Neuromuscular blocking agents
Block neurotransmission at the neuromuscular junction producing paralysis of skeletal muscle - Used as adjuvant in surgical anesthesia
44
All competitive neuromuscular blocking agents are...
Quartenary amines, so no CNS effects, not absorbed
45
Competitive Neuromuscular blocking agents differ in:
``` Duration of action (Short, medium, long) Side Effects (Cardiovascular, histamine) Elimination route (Metabolism, renal excretion) ```
46
``` Rocuronium Duration of action: Elimination: CV effects: Histamine Release: ```
Duration of action: Intermediate (30-60 min) Elimination: Liver metabolism CV effects: Minimal Histamine Release: None
47
``` Atracurium Duration of action: Elimination: CV effects: Histamine Release: ```
Duration of action: Intermediate (30-60 minutes) Elimination: Spontaneously degrades in plasma CV effects: Minimal Histamine Release: Slight
48
``` Vercuronium Duration of action: Elimination: CV effects: Histamine Release: ```
Duration of action: Intermediate (60-90 minutes) Elimination: Liver metabolism CV effects: Minimal Histamine Release: None
49
``` Pancuronium Duration of action: Elimination: CV effects: Histamine Release: ```
Duration of action: Long (120-180 min) Elimination: Renal excretion CV effects: Slight increase in HR and BP Histamine Release: Slight
50
Depolarizing Neuromuscular Blockers
Activate nicotinic receptors at the neuromuscular junction maintaining motor end plate depolarization and thus prevents transmission of another action potential
51
Succinylcholine (Depolarizing Neurmuscular Blocker) Duration of Action: Metabolized by:
Ultra short duration of action (5-8 minutes) - Rapid onset (1 - 1.5 minutes) Metabolized by pseudocholinesterase
52
Competitive Neuromuscular blockers - Adverse Effects and Toxicity
- Prolonged apnea - Toxicity or overdose with competitive antagonists can be reversed by administering an acetylcholinesterase inhibitor - If treat with an acetylcholinesterase inhibitor, treat with glycopyrrolate to minimize muscarinic actions
53
Depolarizing Neuromuscular blockers - Adverse Effects and Toxicity
- Prolonged apnea - Malignant hyperthermia - Post operative muscle pain due to muscle fasciculation - Hyperkalemia

PDA Block 1 (13 decks)

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