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Anticholinergic Agents Flashcards

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1
Q

What is the function of anticholinergic drugs?

A

Oppose the physiological action of neurotransmitter acetylcholine

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2
Q

What are the classes of anticholinergic drugs?

A

Cholinoceptor blockers
Cholinesterase regenerators

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3
Q

What are cholinoceptor blockers?

A

Antagonists or inverse agonists that bind to muscarinic or nicotinic receptors and prevent the effects of ACh

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4
Q

What are cholinesterase regenerators?

A

Not receptor blockers but instead chemical antagonists of AChE inhibitors

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5
Q

What are the different classes under cholinoceptor blockers?

A

Antimuscarinic agents
Neuromuscular blockers
Ganglionic blockers

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6
Q

Which two classes make up the anti-nicotinic drugs?

A

Neuromuscular blockers and ganglionic blockers

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7
Q

Why are most antimuscarinic drugs non selective?

A

The amino acids composing the ligand binding pocket are conserved among all muscarinic receptor types

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8
Q

What is another name given to the cholinoceptor blockers?

A

Parasympatholytic agents

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9
Q

What is the main effect of Parasympatholytic agents?

A

Reduce the activity of the parasympathetic nervous system

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10
Q

Which organs do the parasympatholytic agents target?

Why?

A

Many organs like the eyes, respiratory, GIT, heart and the bladder

Because parasympathetic nerves are widely distributed

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11
Q

What does the response of the parasympatholytic agents depend on?

A

Specific drug and the dose used

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12
Q

What does Scopolamine usually cause?

A

Excitement and delirium

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13
Q

What are examples of antimuscarinic agents?

A

Atropine
Scopolamine
Tropicamide
Darifenacin / Oxybutynin
Ipratropium / Totropium
Benztropine / Trihexyphenidyl
Pirenzepine

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14
Q

What is Atropine?

A

An alkaloid found in a plant

Non-selective, reversible and competitive antagonist

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15
Q

What is the MOA of Atropine?

A

Binds to all five muscarinic receptors with high affinity

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16
Q

How can the blocking effect of the muscarinic receptors by Atropine be overcome?

A

Increasing concentration of muscarinic agonists

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17
Q

What are the PK of Atropine?

A

Lipid-soluble
Crosses membranes, including CNS, eye and other organs
Well distributed

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18
Q

What are the therapeutic uses of Atropine?

A

Antidote in treatment of AChE poisoning, overdose if muscarinic agonists or poisoning caused by consumption of mushrooms

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19
Q

What are the side effects of Atropine?

A

Dry mouth
Urinary retention
Blurred vision
Tachycardia
Constipation

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20
Q

What is Scopolamine?

A

Belladonna alkaloid

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21
Q

What are the therapeutic uses of Scopolamine?

A

Prevention of morning sickness and nausea

Treatment of poisoning by AChE

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22
Q

Why is Scopolamine recommended for the treatment of AChE poisoning compared to Atropine?

A

Readily crosses BBB
Greater action on CNS
Longer duration

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23
Q

What are the side effects of Scopolamine?

A

Short-term memory block
Sedation
Euphoria

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24
Q

What is Tropicamide?

A

Short acting antimuscarinic drug

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25
What is the therapeutic use of Tropicamide?
Eye drops prior to retinal exams
26
What is the function of Tropcamide?
Produces mydriasis (dilation of pupil) for 6 hours Inhibition of contraction of iris sphincter muscles
27
What are Darifenacin & Oxybutynin?
Synthetic atropine-like drugs
28
What is the therapeutic use of Darifenacin & Oxybutynin?
Treatment of overactive bladder
29
What are the clinical uses Ipratropium and Tiotropium?
Approved as bronchodilators for maintenance treatment of bronchospasm Ashma & COPD
30
What are the clinical uses of Benzotropine and Trihexyphenidyl?
Treatment of Parkinson's disease
31
What is Pirenzepine?
M1 selective antagonist
32
What is the therapeutic use of Pirenzepine?
Treatment of peptic ulcers
33
Which drugs under natural alkaloids?
Atropine Scopolamine
34
Which drugs are under tertiary amines?
Tropicamide Oxybutynin Benzotropine
35
Which drugs are under quaternary amines?
Ipratropium Tiotropium
36
Which classes of antimuscarinic drugs are well absorbed from the GIT and conjunctival membranes?
Natural alkaloids and tertiary amines
37
How are quaternary amines absorbed?
10 to 30% after oral administration
38
Which antimuscarinic agent are widely distributed?
Atropine and tertiary amines Significant levels are achieved in CNS within 30 minutes to 1 hour
39
Which antimuscarinic agent is rapidly and gully distributed into CNS where it has greater effects than the rest?
Scopolamine
40
Which antimuscarinic agents are poorly taken up by the brain?
Quaternary, they have no effect on the brain at low doses
41
How is Atropine metabolised?
Partly by the liver and partially unchanged in the urine
42
What are the two phases of Atropine elimination from the blood?
1. The half-life of the RAPID phase is 2 hours 2. The SLOW phase is approximately 13 hours
43
How do Atropine's effects decline?
Rapidly all organs (4 to 8 hours) Except of the eye, where it lasts for days
44
What are the contraindications of anticholinergic drugs?
Glaucoma, GIT disease, and urinary retention
45
Why is narrow angle glaucoma a contraindication of anticholinergic drugs?
Even moderate doses can induce acute glaucoma which is a medical emergency
46
Why are GIT disease or urinary retention contraindications for anticholinergic drugs?
Antimuscarinic drugs reduce contractility of bladder smooth muscle --> acute urinary retention Reduction of GI motility may worsen symptoms of individuals with intestinal obstruction
47
Why is Atropine contraindicated in narrow angle glaucom?
Atropine relaxes the ciliary muscles causing complete drainage obstruction of aqueous humor.
48
What are neuromuscular blockers?
Quaternary amines that are structurally related to ACh. Most are antagonists
49
What is the prototype of neuromuscular blockers?
Tubocurarine
50
Which is the neuromuscular blocker which is clinically used today?
Succinylcholine, agonist at the nicotinic receptor
51
What is the MOA of nondepolarizing neuromuscular blockers?
Competitively block ACh transmission at the nicotinic receptors --> prevent depolarisation at the muscle cell membrane --> inhibit muscular contraction
52
What can overcome the effects of the nondepolarizing neuromuscular blockers?
Increasing the amount of agonist, ACh or administrating cholinesterase inhibitors
53
What are the general PK of the nondepolarizing neuromuscular blockers?
Given IV or IM Quaternary amine structure prevents absorption from the gut Poor penetration of the membranes, do not cross BBB Eliminated in the bile
54
What are the PK of Cisatracurium?
Degrades in the plasma Onset: 2 to 8 minutes Type: Intermediate, Competitive Duration: 45 to 90 minutes Mode of Elimination: Renal
55
What are the PK of Rocuronium?
Onset: 0.9 to 1.7 minutes Type: Intermediate, competitive Duration: 36 to 73 minutes Mode of Elimination: Hepatic (bile)
56
What are the PK of Pancuronium?
Onset: 3 to 4 minutes Type: Long, competitive Duration: 85 to 100 minutes Mode of Elimination: Renal & hepatic
57
What are the PK of Succinylcholine?
Onset: 0.8 to 1.4 minutes Type: Ultrashort, depolarising Duration: 6 to 11 minutes Mode of Elimination: Hydrolysis by plasma cholinesterases Injected IV
58
What is the only example of depolarising neuromuscular blocking drugs?
Succinylcholine
59
What are the steps that Succinylcholine follows?
1. signaling 2. desensitization 3. internalisation 4. a) degradation 4. b) recycling
60
What is the MOA of depolarising neuromuscular blocking drugs?
Agonist bind to nicotinic receptors --> opening of the sodium channels --> depolarises the junction
61
What is the difference between Succinylcholine and ACh?
Unlike ACh, Succinylcholine is more resistant to degradation by AChE --> remains attached for longer time --> depolarisation is longer
62
What causes resistance to Succinylcholine, phase II (desensitisation) ?
Tension cannot be maintained in skeletal muscles without periods of repolarization --> muscle relaxation and paralysis
63
What are the differences between the PK of Atropine & Succinylcholine?
Action of Succinylcholine is longer than that of ACh
64
What will happen to Succinylcholine upon discontinuation?
Because it is still brief --> redistribution and rapid hydrolysis Drug effects will rapidly disappear
65
What are the side effects of neuromuscular blockers?
1. Respiratory paralysis --> asphyxiation 2. Autonomic effects --> cardiac muscarinic receptors are affected 3. Hyperkalemia --> Succinylcholine
66
What are the drug interactions of the Neuromuscular blockers?
Inhaled anesthetics --> potentiate and prolong the blockade Aminoglycoside antibiotics Antiarrhythmic drugs
67
What happens if succinylcholine interacts with inhaled anaesthetics?
Malignant hypothermia Early sign is contraction of jaw muscles
68
What are the examples of ganglionic blockers?
Hezamethonium Mecamylamine
69
What do ganglionic blockers do?
Block nicotinic receptors at sympathetic and parasympathetic autonomic ganglia
70
What were ganglionic receptor developed to treat?
Hypertension
71
What limits their clinical use?
The lack of selectivity
72
What are the effects of nicotine?
Increases alertness Reduces circulation to extremities Increases BP and HR Relaxes muscles and enhances the release of dopamine & NE Suppresses apetite
73
What is the prototype of Cholinesterase regenerators?
Pralidoxime
74
What is the MOA of Cholinesterase regenerators?
Reactivate AChE by an organophosphate agent
75
How is the organophosphate agent reactivated?
The oxide group of Pralidoxime has high affinity for the phosphate group of organophosphate Hydrolyses the bond if aging has not occurred Enzyme is regenerated
76
Why is Pralidoxime not as effective against the chemically different "carbamate" type AChE?
Carbamates do not have a phosphate group

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