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Pharmacology: Exam 2 > Lecture 4: Cholinergic > Flashcards

Lecture 4: Cholinergic Flashcards

1
Q

List the drug classes of the Cholinergics

A
  • Direct Acting Cholinomimetics
  • Indirect-Acting Cholinomimetics
  • Muscarnic Inhibitors
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2
Q

Which drug(s) are Direct acting Cholinomimetics?

A
  • Acetycholine
  • Bethanechol
  • Nicotine
  • Pilocarpine
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3
Q

Which drug(s) are Indirect acting Cholinomimetics?

A
  • Edrophonium
  • Physostigmine
  • Echothiophate
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4
Q

Which drug(s) are Muscarnic Inhibitors?

A
  • Atropine
  • Ipratropium
  • Titotopium
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5
Q

Acetylcholine is a _

A

NT that is released from the nerve from presynaptic terminal to bind to postsynaptic receptor

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6
Q

Explain how ACh is made

A
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7
Q

What are the ACh receptors?
What terminates the ACh signal?

A

Receptors:

  • Nicotinic (Ion channels)
  • Muscarinic (GPCR)

Terminates: acetylcholine esterase

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8
Q

What are the choline ester and alkaloid direct acting acetylcholine receptor agonist?

A
  • Choline Ester: acetylcholine, methacholine, bethanechol, carbachol
  • Alkaloid: Muscarine, pilocarpine, nicotine
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9
Q

Does the alkaloid class use AChE metabolism

A

NO

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10
Q

Does nicotine have muscarinic AChR activity?
Does muscarine have nicrotinic AChr activity?

A

NO and NO

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11
Q

Which one (choline ester or alkaloid) can cross the membrane

A
  • Alkaloid will distrub throughout the body
  • Choline ester is charged so it cannot cross the membrane
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12
Q

What are the different muscarinic receptors?

A
  • M1, M3, M5 (odd): Gq-coupled, PLC activation, ↑ DAG & IP3 production, ↑ Ca2+
    * mobilizes calcium to cause contraction and glandular secretion
  • M2, M4 (even): Gi-coupled, ↓ cAMP, ↓ PKA
    * inhibits Adlyl cyclase
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13
Q

Where are the muscarinic receptor location

A

End organs

  • cardiac and smooth muscle, gland cells, nerve terminals
  • Sweat glands, skeletal muscle arterioles (sympathetic)
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14
Q

fill in

A
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15
Q

What is the action of mAChr with muscosal gland

A

M1

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16
Q

What is the inn, action of mAChR and effect of the heart with muscarinic receptors

A
  • Inn: para
  • Action of mAChR: decrease contraction, conduction (M2)
  • Effect: decrease BP and bradycardia
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17
Q

What is the inn, action of mAChR and effect of the vasc. endothelium with muscarinic receptors

A
  • Inn: none but can be de/activated by agonist ot antagonist
  • ActionL EDRF/NO release, VSM dilation (M3)
  • Effect: decrease BP and reflex tachycardia
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18
Q

What is the inn, action of mAChR and effect of the sweat glands with muscarinic receptors

A
  • Inn: symp
  • Action: stimulation (M3)-> sym but ACH
  • effect: increase secretion
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19
Q

What is the mechanisms of action and pharmacology of Direct-Acting Cholinomimetics?

Acetylcholine, Bethanechol, Pilocarpine

A
  • Activate muscarinic receptors
    – Affect all muscarinic receptor subtypes
  • Mainly evoke parasympathetic effects
  • Mild or no desensitization
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20
Q

What does high IOP causes?
How is it caused?

A
  • High IOP causes loss of optic nerve and permanent blindness, open angle glaucoma
  • Caused by increase aqueous humor
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21
Q

How can we reduce the ocular hypertension?

A
  • Ocular hypertension can be reduced by increasing aqueous humor flow OUT via Canal of Schlemm
  • Contraction of cillary muscle (via activation of M3 receptor) opens the Trabecular meshwork and facilitates aqueous humor outflow
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22
Q

What are drug class+ drug name that can be used to treat glaucoma? Which ones cannot and why?

A
  • Alkaloids (uncharged, lipophilic)-> drug name: pilocarpine can be used to treat
  • Choline esters (charged)-> drug name Bathanechol cannot be used to treat becasue unable to penetrate to the eye cillary muscle
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23
Q

What is the AE, contradinication and interactions with Bethanechol, methacholine and pilocarpine?

A
  • AD: Parasympatheitic effects, bronchospasms, hypotension (vasodilation), reflex tachycardia, decrease secretion
  • Cont: Asthma, COPD, peptic ulcer, hypotension
  • Interactions: B-Blockers
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24
Q

What is the drug class and drug name of direct action nicotinic agonists

A
  • Class: alkaloid-> increase bioav (not charged/lipophilic
  • Drug name: Nicotine
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25
Q
  • Where is the distribution of nicotinic receptors?
  • What type of effect will they cause?
A
  • NMJ
  • Autonomic ganglia
  • Brain
  • Symp and para
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26
Q

Nictonic ace Receptor are what type of receptors

A

Pentameric cation channels

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27
Q

Does nic ace receptor desensitize?

A

Yes they can desensitize with ptolonged agonist

28
Q

Explain what happens at the NMJ

A

Ach binds to cause Na to come in then cause AP and Ca+Na flow in which causes contraction

29
Q

Nm=
Nn=

A

Nm= muscle contraction
Nn=ganglia, ESPS (depolarization)

30
Q
  • Nicotinic agonist activat what?
  • What does it stimulate?
A
  • Activate nicotinic receptors
  • Stimulate CNS, all peripheral ganglia (and adrenal medulla) and skeletal muscle (NMJ)
    * Parasympathetic
    * sympathetic
    * Catecholamine release
    * Skeletal Muscle (somatic NS)
31
Q

Where do we evoke parasympathomimetic effect?

A

GI, GU, glands, lungs

32
Q

Where do we evoke sympathomimetic effect?

A

CV ( increase cardiac output and blood pressure, sweat glands)

33
Q

What is the major clinical use of nicotinic agonists

A

smoking cessation

34
Q

What do antimuscarinics (muscarinic antagonist) do?

A
  • Inhibit muscarinic receptors
    – Drugs available clinically generally act on
    all receptor subtypes (limited selectivity)
  • Evoke parasympatholytic effects
35
Q

Antagonists only have an effect if there is also an _ present

A

agonist

36
Q

Explain what happens to the eye, urinary, gut, muscosal glands and lungs when we give antimuscarinic?

A
37
Q

Explain what happens to heart, vasc. endothelium, sweat glands, and CNS when we give an antimuscarinic

A
38
Q

What is naturally occurring muscarinic antagonists? Explain the structure

A

Belladonna alkaloids: atropine
* Tropic acid will bind to receptor
* Base gives bioavibility

39
Q

What amine (+drugs) are good absorptors and which amines (+drugs) are poor absorptors

A

Good: Tertary amine
* Tropicamide (eye examination)
* Beztropine (parkinson’s)

Poor: Quaternaty amine
* Ipratropium (asthma)
* Propantheline (gut)

40
Q
  • What drug is used for eye examination?
  • What drug is used for parkinson’s?
  • What drug is used asthma?
  • What drug is used for gut?
A
  • Tropicamide
  • Benztropine
  • Ipratropium (poor absorption is it good becasue it will stay in lungs)
  • Propantheline
41
Q

Explain what happens in lung repair in asthmas/COPD

A
  • Irritant in lungs-> afferent-> CNS-> parasymp efferent-> contracts smooth muscle-> produce mucous
  • uses M3 agonist (ach) for this
42
Q

What is atropine used for and what is the amine type?

A
  • Bradycardia to increase HR
  • 3 degree
43
Q

What is benztropine used for and what is the amine type?

A
  • Parkinson’s disease, extrapyramidal symptoms
  • 3 degree
44
Q

What is scopolamine used for and what is the amine type?

A
  • Motion Sickness
  • 3 degree
45
Q

What is ipratropium+titropium used for and what is the amine type?

A
  • Bronchospasm in Chronic obstructive pulmonary disease (COPD), and asthma
  • 4 degree

quartary stays local

46
Q

What does ipratropium block

A

ACh mediated secretion and contraction

autonomatic ganglion

47
Q

What are the toxic effects of muscarinic antagonist?

A
  • Blurred vision, photsensitivity
  • Agitation, hallucination, delirium, coma
  • Tachycardia, angina
  • Dry mouth, nasal congestion, hot/flush skin, hyperthermia
  • Dysuria, retention (no peeing)
  • Nausea, distention, cramps, constipation

Abolish parasym

“Dry as a bone, blind as a bat, red as a beet, mad as a hatter, and hot as a hare.”

48
Q
  • What are muscarinic antagonist contradicated for?
  • What is an example and how it works?
A

Open angle glaucoma

Atropine prevents activation of M3
* Causes dilation of cillary muscle
* decreases humor outflow-> increase IOP

49
Q

Glaucome+atropine=

A

NOOOOOOOO

50
Q

What does AChE inhibitors cause?

A

inhibits the breakdown of ACh therefore increase in Ach for muscarnic receptors

51
Q

What is the ach signal terminated by?

A

acetylcholine esterase

52
Q

What are the key sites on the achE

A
  • Anionic site
  • choline subsite
  • Acyl pocket
53
Q

What needs to be down in order for acetyl choline esterase to be active again?

A

Acetate needs to leave
* This is where drugs target

54
Q

What does edrophonium do?

A
  • will bind to the choline subsite to get in the way and slow down the breaking down
  • Bind to choline subsite and H+ bond to acyl pocket
  • short acting (Temporary blocking)
55
Q

What does neostigmine(4) or Physostigmine (3degree) do?

A
  • It is a carbamate so it will bind to the serine in the acyl pocket to block
  • Bind like ACh with covalent bond, decarbamoylation rate slower than deacetylation rate.
  • Longer time than edrophonium
56
Q

What does echothiophate do?

A
  • Organophophates
  • Some bind like ACh some only to acyl pocket with covalent bond, dephosphorylation rate slower than decarbamoylation and deacetylation rate.
  • Perment so irreversible
57
Q

Which cholinesterase inhibitors are reversible and which ones are not

A

reversible:
* Edrophonium (4 degree alcohol)
* Physosostigmine (3) and neostigmine (4)- carbamates

Irr: echothiophate (organophosphates)

58
Q

What are the effects of cholinesterase inhibition?

A
  • Brain: increase EEG and alertness
  • NMJincrease strength
  • Parasympathomimetic: bradycardia (dec. HR)
  • Stimulation of all automotic ganglia
  • decrease IOP, increase motility of bowels and peeing, contriction
  • Low dose: indirect dec BP
  • Higher dose: increase symp drive (inc BP)
59
Q

What do we do to test myasthenia gravis and what do we give to fix it (general)

A
  • Looking up eye test shows muscle fatigue
  • Fixes it by adding AChE inhibitor-> boosts NMJ function
60
Q
  • What does the NMJ look like in Myasthenia gravis patient compared to a normal patient?
  • What do we do to help?
A
  • Less nic receptors and not as dense
  • Less Ach release so no ESPS for muscle contraction so loss of muscle contraction
  • If we block AChE, then we incre the hald life of Ach so we can have bigger activation of receptors leading to ESPS and better muscle contractions
61
Q
  • What drug do we use to diagnose MG?
  • What is the absoprion, fate and excretion?
  • MOA?
  • Duration?
A

Edrophonium (alcohols)
* absorbed poorly, destroyed by plasma esterases
* Binds to choline subsite of active center and H+ bond to acyl pocket
* 5-15 min

62
Q
  • What drugs are used to treat MG?
  • What is the absoprion, fate and excretion?
  • MOA?
  • Duration?
A

Carbamates: Physostigmine (3), Neostigmine (4),
Pyridostigmine (4)
* Physo: Absorbed readily,
destroyed by plasma esterases, enters CNS
* Neo+Py: Absorbed poorly,
destroyed by plasma esterases, excreted in urine, does not enter CNS.
MOA: Bind to acyl pocket of active center via covalent bond and hydrolyzed by enzyme

Other: Donepezil
* Well absorbed, enters CNS, metabolized in liver and kidneys

63
Q

Besides the activation of M3 receptors, what can help open agle glaucoma?

A

AChE inhibitors (physostigmine/echothiophate, in eye drops) increase half-life of endogenous ACh → increase cillary contraction → decrease IOP

64
Q

What are the toxic effects of cholinesterase inhibition

A

Excess acetylcholine causes desensitization for nicotinic receptors, not muscarinic
* Convulsions-> coma
* Blockage of nic (desensitized)-> diaphragm doesnt work and die
* parasympathomimetic: decrease HR-> block gangion for sympathic but para is not blocked
* depression
* Increase vomit, peeing, pooping, secretions
* decrease BP->hypotesion

65
Q

Explain the different between MG and cholineesterase crisis

A
66
Q
  • What is used to treat muscarinic inhibitor poisioning?
  • What are the Symptoms?
  • What is needed to increase?
A
  • AChE inhibitors: Physostigmine (3)
  • Atropine toxicity: Dry as a bone, blind as a bat, red as a beet, mad as a hatter, and hot as a hare
  • Need to increase endogenous ACh
67
Q
  • What is used to treat AChE inhibitor poisioning?
  • What are the Symptoms?
  • What is needed to increase?
A
  • Muscarinic inhibitors: Atropine(3)
  • Organophosphate toxicity:
    Irreversible AChE inhibition – Paralysis, bronchospasm, diarrhea, hypotension
  • Need to block actions of endogenous ACh at muscarinic receptors (increase Ach)

Pharmacology: Exam 2 (10 decks)

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