Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Autonomic Drugs > Cholinergic > Flashcards

Cholinergic Flashcards

1
Q

Bella Donna Alkaloids

A

Antimuscarinic. Naturally occurring. Very potent. Includes atropine, hyoscyamine, scopalamine.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Atropine

A

Antimuscarinic. Used to treat tachycardia in critical care situations with pronounced vagal activity. Also used to dilate pupils, and as a pre-anesthetic topical prep (reduces respiratory secretions and facilitates intubation).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Hyoscyamine

A

Antimuscarinic. Used to treat overactive GI tracts (IBS, chronic gastric cramping).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Scopalamine

A

Antimuscarinic. Anti-nausea, anti-seasickness.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Synthetic antimuscarinics

A

Benztropine, Ipratropium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Benztropine

A

Antimuscarinic. Used to manage sx of movement disorders (e.g. extrapyramidal syndrome caused by antipsychotics and others)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Ipratropium

A

Antimuscarinic. Inhaled anticholinergic used to treat pts with COPD to keep secretions under control. Avoids taking a systemic anticholinergic.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Therapeutic effects M-receptor antagonists: ulcers

A

Selective blockage of the M1 receptors of parietal cells; inhibits acid secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Therapeutic effects M-receptor antagonists: asthma

A

Blockade of m-receptors on bronchioles SM inhibits the constricting effects of parasympathetic innervation. (Ipratropium)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Therapeutic effects M-receptor antagonists: 1st degree AV block

A

Blockade of m-receptors on the AV node prevents in an antagonistic fashion the slowing of conduction caused by the PSNS. This improves conduction in minor blocks (atropine).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Therapeutic effects M-receptor antagonists: pre-surgery

A

Inhibits secretions in the upper airways. Inhibits reflex-induced bradycardia and/or cardiac arrest during surgery. (atropine, glycopyrrolate)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Therapeutic effects M-receptor antagonists: IBS

A

Inhibits propulsive contractions and hypersecretion caused by PSNS. Use of quaternary ammonium derivatives retards absorption and limits systemic effects. (methscoplomine)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Quaternary derivatives

A

Antimuscarinic drugs that are polar, and therefore do not readily cross the blood brain barrier to enter the CNS.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Therapeutic effects M-receptor antagonists: hyperhidrosis

A

Inhibits sweating

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Therapeutic effects M-receptor antagonists: ocular exams

A

Causes pupil dilation. (homatropine)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Therapeutic effects M-receptor antagonists: mushroom poisoning

A

Some mushrooms contain potent m-receptor agonists, which can cause hypersalivation, bradycardia, bronchospasm, hallucinations). Treated with atropine as antidote.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Therapeutic effects M-receptor antagonists: anticholinesterase poisoning

A

Anticholinesterases include insecticides and nerve gas. Atropine is used to treat ODs from these drugs.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Therapeutic effects M-receptor antagonists: motion sickness

A

Prophylactic effectiveness against motion sickness (scopolamine–lipid soluble, CNS effects).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Adverse effects M-receptor antagonists: tachycardia

A

Blockade of m-receptors in the SA node inhibits vagal effects on the heart. Tachycardia can result.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Adverse effects M-receptor antagonists: Xerostomia (dryness of the mouth)

A

Blockade of m-receptors in salivary glands inhibits salivation of vagal innervation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Adverse effects M-receptor antagonists: blurred vision

A

Can inhibit actions of the ciliary muscles (control lens shape), and therefore cause blurry vision. (Cycloplegia: paralysis of accommodation). Also causes dilation of pupils.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Adverse effects M-receptor antagonists: Sedation

A

Anticholinergic agents that are lipid soluble can cross into the brain and have sedative effects.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Adverse effects M-receptor antagonists: Anhydrosis

A

Blockade of m-receptors on the sweat glands inhibit sweat production.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Adverse effects M-receptor antagonists:

A

Tachycardia, Xerostomia (dry mouth), blurred vision, sedation, anhydrosis (decrease in sweating).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Primary receptor at ganglia:
Nicotinic (Nn)
26
Ganglionic blockers reduce transmission at which ganglia?
Sympathetic and parasympathetic
27
Nicotine
Depolarizing ganglionic blocker. Agonist. Initial stimulation followed by a polarization blockade. At moderate doses can produce arousal (agonistic effect). At high doses can cause depression and coma (antagonistic effect).
28
Mecamylamine
Non-depolarizing blocker. Antagonist. No initial response. Used in the past to treat HTN, but there are better drugs now.
29
Effects of ganglionic blockage on: systemic arterioles
Predominant innervation: SNS | Vasodilation and reduction of blood pressure
30
Effects of ganglionic blockage on: cardiac ventricles
Predominant innervation: SNS | Depressed contractility
31
Effects of ganglionic blockage on: cardiac SA node
Predominant innervation: PSNS | Tachycardia
32
Effects of ganglionic blockage on: salivary glands
Predominant innervation: PSNS | Xerostomia
33
Effects of ganglionic blockage on: sweat glands
Predominant innervation: SNS cholinergic | Anhydrosis
34
Effects of ganglionic blockage on: somatic cells
Very high doses of mecamylamine can block NMJ receptors and cause paralysis
35
Bethanechol
Muscarinic receptor agonist
36
Muscarine
Muscarinic receptor agonist - no therapeutic use
37
Pilocarpine
Muscarinic receptor agonist
38
Arecoline
Muscarinic receptor agonist - psychoactive
39
Therapeutic uses of muscarinic receptor agonists:
Gastric Atony: stimulates tonic movement of gastric muscles (bethanechol) Urinary retention: stimulates SM of GU tract, leading to contractile activity and urinary excretion (bethanechol) Xerostomia: stimulates secretion of saliva by salivary glands (pilocarpine eye drops) Glaucoma: stimulates meiosis and ciliary body constriction, which allows for better fluid drainage through the canal of Schlemm, and relieving some intraocular pressure.
40
Adverse effects of muscarinic receptor agonists
Marked meiosis Respiratory distress: overstimulation of bronchial SM leads to bronchospasm and hypersecretion Hypersalvation Sweating Intestinal hyperactivity: overstimulation of intestinal SM and glands leads to abdominal cramps and diarrhea. Hypotension: overstimulation of vascular endothelial cells leads to NO-dependent vasodilation Bradycardia: overstimulation of the SA node and other cardiac cells can lead to severe bradycardia and other arrhythmias.
41
Nicotine cardiac effects:
Tachycardia (primary due to Epi released from the adrenal medulla)
42
Nicotine blood vessel effects:
Vasoconstriction (due to increased sympathetic stimulation from ganglia, as well as Epi released by the adrenal medulla, resulting in increased blood pressure)
43
With continued use of nicotine, what can happen?
Tolerance to nicotine can develop
44
Nicotine somatic effect:
At toxic doses, leads to muscle twitching and eventually a polarizing blockade of ganglia and in the NMJ.
45
Nicotine CNS effects:
Low concentration: increased attention, performance, ability to concentrate Positive reinforcement due primarily to stimulation of dopamine release Decreased appetite and increased metabolic activity. Withdrawal from nicotine can cause HA, restlessness, irritability, insomnia, and increased appetite.
46
Varenicline
Partial nicotinic agonist. (Chantix). Antagonist action blocks reinforcing properties, agonist action helps to relieve withdrawal symptoms.
47
Acetylcholinesterase inhibitors
Prevent the breakdown of acetylcholine, producing a pro-cholinergic effect. Not M or N receptor specific, increase ACh levels at all synapses.
48
Activation of M receptors
Parasympathetic stimulation
49
Activation of N receptors
Initial stimulation followed by depolarization blockade
50
Cholinesterase inhibitors are broken into four categories:
Short acting competitive inhibitor at active site of enzyme (Edrophonium) Noncompetitive inhibitors block entry to active sites of AChE noncompetitively, lasting hours. Used to treat Alzheimer's dz (Donepezil, Tacrine, Galantamine, Rivastigmine) Carbamates produce a slow hydrolysis of a carbamate enzyme (Physostigmine, neostigmine, pyridostigmine, carbaryl [insecticide]) Organophosphates produce very slow hydrolysis of phosphorylated enzyme (days to weeks, adding a phosphate bond that cannot be removed). Two categories: Insecticides (malathion, parathion: prodrugs). Nerve gases (Sarin, VX: extremely toxic, very lipid soluble and volatile, high degree of dermal and pulmonary absorption).
51
Edrophonium
AChE inhibitor. Very short acting (minutes) competitive inhibitor. Used primarily for diagnosis and dose adjustment in Myasthenia Gravis
52
Donepezil
Noncompetitive AChE inhibitor. Lipophilic reversible inhibitor which produces effective inhibition of AChE in the CNS. Used to treat Alzheimer's dz, duration of action 6-8 hours
53
Physostigmine
AChE inhibitor. Used for treatment of glaucoma. Lipid soluble, safe.
54
Rivastigmine
AChE inhibitor. Used for treatment of Alzheimer's dz. Route via patch and pill.
55
Neostigmine, Pyridostigmine
AChE inhibitor. Quaternary derivative of physostigmine: does not cross BBB. Used for treatment of myasthenia gravis, and to reverse paralysis from non-depolarizing muscle blockers (tubocurarine, pancuronium, atracurium)
56
Carbaryl
Carbamate AChE inhibitor. Home and garden insecticide
57
Malathion, Parathion
Organophosphate AChE inhibitor. Prodrug (metabolized quickly to inactive compound by mammals and birds, but not insects or fish). Used in aerial crop dusting, mosquito control spraying, home and garden, and lice treatment.
58
Sarin, VX
Organophosphate AChE inhibitor. Nerve gases. Irreversible AChE inhibitor. Extremely toxic, lipid soluble, high potency, volatile. Used in warfare, large stockpiles in US and Russia.
59
Therapeutic uses of AChE inhibitors
Belladonna poisoning: AChE inhibitors increase ACh levels, competitively overriding the receptor blockade in atropine poisoning. Nerve gas poisoning: it's thought that prophylactic treatment with reversible AChE inhibitors protects against subsequent phosphorylation of the enzyme by organophosphates. Alzeheimer's dz: CNS acting anticholinesterases increase brain levels of ACh, thought to overcome some deficits from Alzheimer's (tacrine, donepezil) Myasthenia gravis: muscle weakness associated with deficits in Nm receptors at the NMJ. AChE inhibitors increase the ACh levels at the junction, activating a greater percent of the remaining Nm receptors.
60
Side effects of AChE inhibitors (acronym)
``` DUMBELS Diarrhea, Diaphoresis Urination Miosis Bradycardia, Bronchospasm, Bronchorrhea Emesis Lacrimation Salivation, Sweating ``` ``` SLUDGE Salivation, Sweating Lacrimation Urination Diarrhea, Diaphoresis Gastrointestinal upset Emesis ```
61
AChE inhibitor toxicity: respiratory paralysis/asphyxia mechanism:
Paralysis of diaphragm and intercostal muscles. Respiratory congestion and bronchoconstriction CNS respiratory depression
62
Treatment for AChE inhibitor toxicity
Respiratory support, atropine (sx relief) and pralidoxime (2-PAM). 2-PAM restores AChE by having a higher affinity for the organophosphate than AChE. Before aging occurs, 2-PAM is able to rip away the organophosphate.
63
Treatment for myasthenia gravis:
Immunosuppressants and AChE inhibitors. Immunosuppressants decrease the destruction of remaining Nm receptors. AChE inhibitors increase the amount of ACh in the NMJ. (Neostigmine, Pyrodostigmine, Ambenonium). Dx with edrophonium (nml pt would have decreased muscle strength due to depolarization blockade. Pt with MG would have increased muscle strength).

Autonomic Drugs (3 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions