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LSM3211 - AP_2024 > Cholinergic Pharmacology > Flashcards

Cholinergic Pharmacology Flashcards

1
Q

What are the two major parts of the autonomic nervous system?

A

Sympathetic and parasympathetic systems.

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2
Q

Name 2 KEY neurotransmitters in the autonomic nervous system?

A

Acetylcholine and noradrenaline.

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3
Q

Which neurons are cholinergic in the autonomic nervous system?

A

Preganglionic neurons and postganglionic parasympathetic neurons.

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4
Q

What inhibits the rate-limiting step of choline uptake into the nerve terminal?

A

Hemicholinium.

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5
Q

How is ACh transported into its vesicles for storage?

A

By the vesicular acetylcholine transporter (VAChT).

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6
Q

What is the major mechanism for the termination of ACh’s action?

A

Inactivation via acetylcholinesterase (AChE).

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7
Q

How do reversible AChE inhibitors work?

A

They prevent the breakdown of ACh, enhancing its action.

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8
Q

Name two families of cholinoceptors.

A

Muscarinic receptors and nicotinic receptors.

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9
Q

What are the effects of muscarinic agonists on the cardiovascular system?

A

Decrease in cardiac output via M2 receptors

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10
Q

How do muscarinic agonists affect the eye?

A

Contraction of the ciliary muscle and constrictor pupillae, reducing intraocular pressure via M3 receptors.

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11
Q

What are the side effects of the non-selective muscarinic agonist bethanechol?

A

Blurred vision, increased salivation, bronchial constriction, hypotension, abdominal cramping, diarrhea, urinary urgency.

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12
Q

What are the main effects of muscarinic antagonists like atropine?

A

Reduced secretions, urinary retention, mydriasis, relaxation of the gut

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13
Q

What is the primary action of pralidoxime?

A

To reactivate cholinesterase inactivated by organophosphates.

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14
Q

What distinguishes muscarinic from nicotinic receptors?

A

Muscarinic receptors are G-protein-coupled, while nicotinic receptors are ligand-gated ion channels.

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15
Q

What is the role of nicotine in ganglion stimulation?

A

It stimulates both sympathetic and parasympathetic ganglia.

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16
Q

What is the mechanism of action for nondepolarizing neuromuscular blockers?

A

They act as competitive antagonists at ACh receptors, without depolarizing the motor end plate preventing muscle contraction.

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17
Q

How does succinylcholine work as a depolarizing blocker?

A

It binds to nicotinic receptors, causing persistent depolarization and eventual transmission block.

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18
Q

What is the primary cause of myasthenia gravis?

A

Autoimmune production of antibodies that destroy/block nicotinic acetylcholine receptors.

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19
Q

How are cholinesterase inhibitors used in the treatment of myasthenia gravis?

A

They enhance communication between nerves and muscles by preventing ACh degradation (increase ACh levels).

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20
Q

What is the clinical application of edrophonium?

A

Diagnosis of myasthenia gravis. (It is a short acting acetylcholinesterase inhibitor)

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21
Q

Describe the therapeutic use of neostigmine.

A

Treatment of myasthenia gravis and reversal of neuromuscular block. (It is an intermediate acting acetylcholinesterase inhibitor)

22
Q

What are the adverse effects of organophosphates like parathion?

A

Parasympathetic effects, muscle paralysis, and coma.

23
Q

What is the action of sarin?

A

Like parathion, but more rapid and lethal, used as a nerve gas.

24
Q

What differentiates direct-acting from indirect-acting cholinergic drugs?

A

Direct-acting drugs act on receptors, while indirect-acting drugs inhibit cholinesterase to prolong ACh action.

25
Q

Why are antimuscarinic drugs like atropine used in cholinergic poisoning?

A

As an antidote for cholinesterase inhibitor toxicity and to relieve symptoms of organophosphate poisoning.

26
Q

How do neuromuscular blocking drugs aid in surgery?

A

They facilitate muscle relaxation and tracheal intubation

27
Q

What is the main pharmacological action of muscarinic agonists on smooth muscle?

A

Contraction of smooth muscles.

28
Q

How does botulinum toxin affect acetylcholine release?

A

It prevents the release of ACh, used in treating dystonia and cosmetic applications.

29
Q

What is the role of cholinesterase inhibitors in cholinergic function?

A

Enhance cholinergic function by preventing ACh degradation, affecting muscarinic and nicotinic receptors.

30
Q

What is the primary use of pilocarpine (non selective M agonist)?

A

Treatment of acute angle glaucoma

31
Q

How does atropine affect heart rate?

A

Causes modest tachycardia by blocking M2 receptors.

32
Q

What are the effects of muscarinic antagonists on gastrointestinal motility?

A

Inhibit gastrointestinal motility at larger doses

33
Q

Describe the action of depolarizing blockers like succinylcholine on muscle fibers.

A

They cause persistent depolarization, leading to flaccid paralysis.

34
Q

How do nondepolarizing blockers work?

A

They block Nic receptors competitively without depolarizing the motor endplate, inhibiting muscular contraction.

35
Q

How does mydriasis affect intraocular pressure?

A

IO pressure may rise due to relaxation of the ciliary muscle.

36
Q

What are the primary signal transduction pathways for muscarinic receptors?

A

Phosphatidylinositol pathway (M1, M3) and cAMP pathway (M2).

37
Q

What is the significance of acetylcholinesterase inhibitors in the treatment of Alzheimer’s disease?

A

They enhance cholinergic neurotransmission by preventing ACh breakdown.

38
Q

What distinguishes muscarinic agonists from antagonists in their effects on the eye?

A

Agonists induce miosis (pupil constriction) and may decrease intraocular pressure, while antagonists cause mydriasis (pupil dilation) and may increase intraocular pressure.

39
Q

How does the presence of choline acetyltransferase (ChAT) affect acetylcholine synthesis?

A

ChAT catalyzes the synthesis of ACh from choline and acetyl-CoA.

40
Q

How do competitive (non-depolarizing) neuromuscular blockers achieve muscle relaxation, and what can potentially reverse their effects?

A

Block ACh receptors without depolarization; reversed by cholinesterase inhibitors.

41
Q

Analyze the clinical significance of reversible AChE inhibitors in the management of Myasthenia Gravis.

A

Increase ACh concentration, improving muscle strength by enhancing neuromuscular transmission.

42
Q

How does botulinum toxin’s mechanism of action in preventing ACh release contribute to its cosmetic and therapeutic uses?

A

Reduces muscle contraction and wrinkles by inhibiting ACh release at neuromuscular junctions.

43
Q

Evaluate the use of muscarinic antagonists in asthma management considering their mechanism of action.

A

They relax bronchial muscles by blocking M3 receptors, reducing constriction.

44
Q

Considering the side effects, discuss the practicality of using cholinergic drugs for specific gastrointestinal disorders.

A

Effective in stimulating GI motility but can cause cramping and diarrhea.

45
Q

Discuss the rationale behind the use of cholinergic drugs in treating dry mouth conditions.

A

Stimulate saliva production by activating M3 receptors in salivary glands.

46
Q

How do cholinergic agonists’ effects on the cardiovascular system illustrate the principle of selective action?

A

They decrease heart rate and blood pressure by selectively activating M2 receptors in the heart.

47
Q

Evaluate the therapeutic approach of using cholinergic drugs for bladder dysfunction.

A

Improve urination by stimulating bladder muscle contraction but may cause abdominal discomfort.

48
Q

How does the action of cholinergic drugs on the gastrointestinal system support their use in specific disorders?

A

Increase GI motility and secretion, beneficial in conditions like gastroparesis.

49
Q

Why are cholinergic drugs like atropine used in ophthalmic exams avoided in patients with glaucoma?

A

Atropine causes pupil dilation and paralysis of accommodation, aiding in diagnostics and treatment, but is used cautiously in glaucoma due to potential intraocular pressure increase.

50
Q

Evaluate the impact of cholinergic drugs on salivary and sweat glands in treating disorders.

A

Increase secretion, useful in dry mouth or eye conditions but can cause excessive sweating.

51
Q

How does the differentiation between M1, M2, and M3 receptors influence the design of cholinergic drugs?

A

Allows for targeted drug development to minimize side effects by selective receptor activation/inhibition.

LSM3211 - AP_2024 (2 decks)

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