Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

BIOM 3090 > Cholinergic Drugs > Flashcards

Cholinergic Drugs Flashcards

1
Q

What are the two main types of cholinergic drugs

A
  • Cholinomimetics: mimic the action of ACh
  • Cholinergic antagonists - antimuscarinics and antinicotinics
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what do cholinomimetics typically include

A
  • agents that act directly as agonists at cholinoreceptors
  • &agents that act indirectly by inhibiting the metabolism of ACh w/ use of AChEacetylcholinesterase (AChE) inhibitors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Cholinergic drug list

A
  • Direct acting agonists: acetyl choline, bethanechol, muscarine, pilocarpine, nicotine
  • Indirecting Acting agonists: Physostigmine and Echothiophate
  • Antagonist: Atropin (M-)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

describe the drug: Acetylcholine

A
  • direct acting agonist
  • susceptible to AChE
  • +++ muscarinic activity

+++ nincotinic activity

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

describe the drug: Bethanechol

A
  • direct acting agonist
  • NOT susceptible to AChE
  • muscarinic activity ++

Nicotinic activity 0

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

describe the drug: Muscarine

A
  • direct acting agonist
  • NOT Susceptible to AChE
  • Muscarinic activity +++

Nicotinic activity 0

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

describe the drug: Pilocarpine

A
  • direct acting agonist
  • NOT susceptible to AChE
  • Muscarinic activity +++

Nicotinic activity 0

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

describe the drug: Nicotine

A
  • direct acting agonist
  • NOT susceptible to AChE
  • 0 muscarinic activity

++++ Nicotinic activity

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

describe the drug: Physostigmine

A
  • indirecting acting agonist
  • Type = carbamate
  • Duration of action = intermediate action
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

describe the drug: Echothiophate

A

indirecting acting agonist

  • Type = organophosphate

Duration of action = long action

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

describe the drug: Atropin (M-)

A
  • antagonist
  • includes trimethaphan (NN-) and D-tubocurarine (NM-)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

why are non-selective muscrinic recpetors agonists not widely used

A
  • amny cholinergic agents are capable of stimuating and blocking cholinergic receptors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

there are ____ NN or NM nicotinic receptor subtype selective agonists

  • why?
A
  • there are NONE
  • systemic receptor activation by direct-acting muscarinic and nicotinic agonists would produce the desired therapeutic effect but also undesirable side effects
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

for nicotinic agonists, receptor binding activates ____

A

PSNS and SNS branches of the autonomic nervous system

  • causes skeletal muscle contraction and stimulates nicotinic receptors int he brain
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What organs are affected by M2 and M3 receptor activation

A

M2: innervation of the heart

M3: in PSNS innervation of glads (alivary , lacrimal) smooth muscle (eg, eye, bronchi, stomach, small intestine, colon, genitals, bladder) in the SNS innervates sweat glands

*note there are alos M3 receptors on endothelial cells that line blood vessels - parasympathetic nerves do not innervate blood vessels so direct muscarinic receptor agonists result in vasodilation.

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

what results in vasodilation and why

A
  • direct muscarinic recpetor agonists result in vasodilation

bc M3 and some M5 receptors are on endothelial cells that line blood vessels and parasympathetic nerves do not innervate blood vessels

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

How will the administration of pilocarpine affect the eye, heart, blood vessels and bronchi?

A

Pilocarpine is a muscarinic receptor agonist

Eye: M3 → contraction of sphincter muscle = constriction of pupil (miosis)
→ contraction of ciliary muscle (accommodation)
Note: drugs like pilocarpine are useful treatments for glaucoma (increased ocular pressure) since contraction of the ciliary muscle opens up the canal of Schlemm, allowing excess fluid to drain out of the eye and decreasing intraocular pressure
Heart: M2 → ↓ heart rate
Blood vessels: M3 & M5 → vasodilation via endothelium-derived relaxing factor (EDRF) released from endothelial cells
Bronchi: M3 → contraction (bronchoconstriction)

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

for most organ systems ____ activation is dominant

A

PSNS

(when both systems activates the PSNS response is observed

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

describe effect of nicotine on GI tract

A
  • nicotine causes inc motility, secretion and salivation
  • tissues that do not have PSNS input will elicit a SNS response
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

vascular system does not have ____ innversation

A
  • does not have PSNS innervation
  • SNS activation is observed
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

post-ganglionic neurons release the neurotransmitter ___ involved in ___ transmission

A

post-ganglionic neurons release the neurotransmitter NE which is involved in adrenergic transmission

. If the adrendergic α1 receptor is stimulated, then vasoconstriction of the blood vessels in organs and the skin will result

if β2 receptors are stimulated, then the result will be vasodilation of the blood vessels associated with skeletal muscle.

*when both activated by soemthing like epinephrine overall effect = inc bp due to vasoconstriction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q
A
23
Q

why is increased bp observed when both α1 and β2 receptors are stimulated

A
  • occurs with epinephrine
  • inc bp bc basoconstraction is observed
  • α1 receptor stim causes vasoconstriction of blood vessels in organs and skin
  • β2 receptor stim causes vasodilation of blood vessels associated with skeletal muscle

** vascular bed of the organs and skin is much greater than that of skeletal muscle - overall effect - vasoconstriction

**SNS activation in heart will reislt in inc Hr

24
Q

what do indirect actiing cholinergic agonists do

A
  • inc levels of ACh by inhibiting the enzymatic breakdown of ACh
  • inhibitors bind to AChE which reduced ACh hydrolysis and inc local ACh conc
  • net effect = amplification of ACh and the characterisitcs of interaction between the drug and enzyme determines the duration of action of the AChE inhibitor
25
Q

how are diseases in neuromuscular junction typically treated

A
  • AChE inhibitors
  • primary defect in these diseases is an insufficient quantity of ACh or its receptor
26
Q

Describe the hydrolysis of ACh

A

* indirect acting cholinergic agonists act by inc levels of ACh by inhibiting the breakdown

  • inhibition can be reversible or irreversible
27
Q

describe reversible inhibitors

A

*indirect acting cholinergic agonist

  • include carbamate esters like physostigmine
  • covalent bond betweent he drug and AChE is somewhat resistant to hydration (step 2 of the hydrolysis) so half life ranges from 30 min to 6 hours
  • generally poorly absorbed and distributed with exception of physostigmine (longer acting and often used in treatment of chronic diseases)
28
Q

Describe irreversible inhibitors

A
  • organophosphates like echothiophate
  • covalent bond between drug and AChE is more stable and over time becomes irreversible
  • half life sig longer than the reversible - days to weeks
  • structure also affects the pharmacokinetics and drugs in this class are abs and distributed well - even in the CNS
29
Q

the action of indirect acting cholinomimetics is _____ these effects are similar to _______

what is the result

A

action of indirect acting cholinomimetics is amplification of endogenous ACh

The effects are similar to direct acting cholinomimetic drugs where ACh is released

  • result: ACh is inc in tissues innervated by autonomic ACh-releasing neurons at PSNS and SNS ganglia, at skeletal muscle and the CNS
30
Q

AChE Inhibitors Increase ACh at the Following Sites

A

PSNS: heart, eye, salivary gland, lacrimal glands, bronchi, stomach, small intestine, colon, genitals, bladder

SNS: Sweat glands

31
Q

For most tissues both SNS and PSNS innervation is present, what would be result of inc ACH levels at SNS ganglia

A

would activate post-ganglionic SNS neurons and increased norepinephrine release in tissues (except sweat glands – post-ganglionic SNS neurons release Ach).

32
Q

For most tissues both SNS and PSNS innervation is present, what would be result of inc ACH levels at PSNS ganglia

A
  • inc ACh levels stimualte post-ganglionic PSNS neurons
  • inc ACh release at an effector cell
  • emtabolism fo ACh in tissue would eb inhibited by the AChE inhibitor resulting in an inc in both level and duration fo action of ACh in these tissues
  • **demonstrated how PSNS activation is dominant in presence of AChE inhibitors

*Note: blood vessels do not have PSNS input; therefore the SNS effect will be observed

33
Q
A
34
Q

What responses will be observed in the cardiovascular system after systemic exposure to pilocarpine?

A
  • vdirect agonist
  • activates M2 receptors in heart which will ↓ rate and force of contraction
  • also activates M3 & M5 receptors on endothelial cells which ↑ EDRF in endothelial cells and cause dilation of blood vessels.
35
Q

What responses will be observed in the cardiovascular system after systemic exposure to nicotine ?

A
  • activates NN at PSNS and SNS ganglia.
  • In the blood vessels
  • SNS activation ↑ NE and epinephrine, and stimulation of α1 receptors will cause vasoconstriction in the blood vessels of the organs and skin,
  • stimulation of β2 receptors will cause vasodilation of blood vessels in skeletal muscle.

In the heart,

  • ↑ rate and force of contraction.
36
Q

What responses will be observed in the cardiovascular system after systemic exposure to physostigmine?

A

-inhibits AChE which increases ACh at ganglia and activates NN receptors that stimulates PSNS and SNS.

SNS activation

  • ↑ NE and epinephrine
    • stimulation of α1 receptors will cause vasoconstriction in the blood vessels of the organs and skin
    • stimulation of β2 receptors will cause vasodilation of blood vessels in skeletal muscle.

In the heart i

  • ↑ SNS & PSNS input
  • ↑ ACh in the heart due to AChE which will ↓ rate and force of contraction.
37
Q

describe the toxicities associated with cholinomimetics

A

*Muscarinic agonists: Muscarinic agonists have been associated with toxicities based on their effects

  • some of these agonists are naturally occuring can can cause harm
    ex: inocybe - large genus of muchrooms not safe for consumption bc of light levels of muscarine
  • pilocarpine can also cause adverse effects when overdosed
  • symptoms of muscarinic excess
38
Q

what are the symptoms of muscarinic toxicity (muscarinic excess

A

DUMBELS

Diarrhea
Urination
Miosis
Bronchoconstriction
Excitation (CNS)
Lacrimation
Sweating and salivation

*Notice that the symptoms of muscarinic excess are an extension of the pharmacological effects of muscarinic agonists on the same tissues and organs.

39
Q

describe nicotinic agonist

A
  • aslo ahs associated toxicities
  • nicotine does not have a therapeutic use but used in anti-smoking preparations
  • fatal dose of nicotine is only 40 mg equiv to 2 cig but most is nurned away
40
Q

describe outcome of ingetion of nicotine

A

activates the Nn and Nm receptor subtypes

  • initial activation causes timulation while prolonged exposure causes subsequent inactivation of the receptor

-

41
Q

symptomes of nicotinic excess

A

include symptoms of muscarinic excess (PSNS dominant in most tissues) and increased blood pressure

  • followed by convulsions, coma, and respiratory depression, which are associated with the stimulation of nicotinic receptors in the CNS and skeletal muscle contraction that is followed by paralysis.
42
Q

describe AChE inhibitors organophosphates and their initial signs of toxicity

A

Organophosphates, which are the basis of many pesticides and nerve gas

  • they are another group of nicotinic receptor agonists with severe toxicities
  • intial signs similar to mucarinic excess but followed by CNS stimulation and peripheral NN and NM receptor activation.
43
Q
A
44
Q

describe atropine - the receptors it likes and its half life

A
  • antimuscarinic drug
  • naturally occuring competitive antogaonist of muscarinic receptors derived from Atropa Belladonna and Datura Stramonium
  • equal affinity for M1, M2 and M3 receptor subtypes
  • well absorbed and distributed (even in CNS) it primarily counteracts the effects of the parasympathetic NS in the periphery
  • When administered systemically, atropine has a half-life of approximately 2 hours, but when administered topically to the eye, the half-life is several days.
45
Q
A
46
Q

Muscarinic Receptor Antagonists- what receptors do they target

A
  • inhibtis action of ACh at following sites

PNS:

  • M2 receptors at heart
  • M3 recepotrs eye, salivary gland, lacrimal glands, bronchi, stomach, small intestine, colon, genitals, bladder

SNS:

  • M3 receptors - sweat glands
47
Q

what are the two typesi fo antinicotinic drugs

A

ganglionic blockers (trimethaphan)

neuromuscular blockers (tubocurarine

48
Q

describe ganglionic blockers

A
  • antinicotinic drugs
  • rarely sued clinically bc affect the PSNS and SNS
  • only used if other drugs are ineffective or contraindicted
  • can be used if other drugs are ineffective for treating hypertensive srisis or dissecting aortic aneurysm
    ex: trimethaphen
49
Q

describe neuromuscular blockers

A
  • antinicotinic drug
  • sometimes used in surgical procedures to reduce skeletal muscle contraction
    ex: tubocurarine
50
Q

what is claucoma

A

causes increased ocular pressure and treatment involves topical cholinomimetics such as pilocarpine, physostigmine or echothiophate.

51
Q

How do these drugs decrease ocular pressure? How does the mechanism of action differ between pilocarpine and physostigmine?

A

Topical cholinomimetics activate M3 receptors on ciliary muscle which causes contraction and drains the fluid

Pilocarpine is a direct muscarinic receptor agonist while physostigmine is an AChE inhibitor, which increases ACh levels which then increases muscarinic receptor activation.

52
Q

What cholinergic drug(s) should be avoided in an individual with glaucoma?

A

* glaucome = inc ocular pressure

  • Muscarinic antagonists such as atropine should be avoided
  • block M3 receptors on ciliary muscle which prevents contraction and decreases fluid drainage, which increases intraocular pressure.
53
Q

38-year old female was having difficulty urinating (known as bladder atony) following abdominal surgery. No obstructions were found and she was given a subcutaneous injection of bethanechol. How will this drug be helpful?

A

Bethanechol activates M3 receptors on bladder smooth muscle cells which causes contraction and emptying of the bladder.

BIOM 3090 (22 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions