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Year 2 - LCRS - Pharmacology > Cholinoreceptor antagonists > Flashcards

Cholinoreceptor antagonists Flashcards

14.10.2019

1
Q

What qualities do agnoists/antagonists have?

A

Agonist: affinity and efficacy
antagonist: affinity but no efficacy

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2
Q

Does the drug stay attached for a long time?

A

No, mostly there is constant binding and unbinding which allows for competition.

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3
Q

Where are nicotinic receptors found?

A
  • within the ganglions in the ANS

- on the adrenal gland

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4
Q

What are nicotinic receptor antagonists also called sometimes?

A

Ganglion blocking drugs

=> ganglion blocking effect in both the sympathetic and parasympathetic nervous system.

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5
Q

In what ways can nicotinic receptor antagonists work?

A
  • by blocking the receptor

- by blocking the ion channel (so name is slightly wrong)

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6
Q

Name 2 nicotinic receptor antagonists

A
  • hexamethonium (historical drug) -> better at blocking the ion channel
  • trimetaphan -> better at blocking the receptor
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7
Q

Hexamethonium

A
  • one of the first antihypertensives

- is better at blocking the ion channel

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8
Q

Trimetaphan

A
  • at the moment most commonly used nicotinic receptor antagonist.
  • fairly short acting
  • better at blocking the receptor
  • Hypotension during surgery - Short acting!
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9
Q

Use dependent block

A
  • refers to the ability to block the ion channel, not the receptor.
  • the more open the channels are the better the drug works
  • more ACh (agonist) -> drug more effective because the
    channels are open and allow entry
  • Here: incomplete block: the sodium can get through but not as effectively
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10
Q

Do hexamethonium and trimetaphan have affinity?

A

Hexamethonium: no, it is a physical blockade of the ion channel
Trimetaphan: Yes, it binds to the receptor

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11
Q 
Which of the following effects would 
be observed at rest after treatment 
with a ganglion blocking drug?
a) Increased heart rate
b) Pupil constriction
c) Bronchodilation
d) Detrusor contraction
e) Increased gut motility
A

a)

c)

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12
Q

Why do nicotinic receptor antagonists cause hypotension?

A
  • act on kidney - Renin Angiotensin system
  • act on the blood vessles and cause vasodilation - decrease in TPR leads to a decrease in BP
  • act on the heart?
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13
Q

What are the effects of nicotinic receptor antagonists on the CVS?

A
  • Hypotension (due to effects on kidney and blood vessles)

- also: affect the heart

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14
Q

What are the effects of nicotinic receptor antagonists on smooth muscle?

A
  • Pupil dilation
  • decreased G.I. tone
  • bladder dysfunction
  • bronchodilation
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15
Q

What do the effects of nicotinic receptor antagonists depend on?

A 
Which system (PS or S) is dominant at that time.
If PS is dominant then it blocks these effects.
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16
Q

What are the effects of nicotinic receptor antagonists on secretions?

A
  • decreased secretions (sweat, saliva, GI secretions)
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17
Q

What is a clinical use of trimetaphan?

A
  • Hypotension during surgery -> Short acting!
18
Q

Alpha - bungarotoxin

A
  • most powerful nicotinic receptor antagonist on the planet
  • binds covalently to nicotinic receptor (true receptor antagonist) -> tissue would have to replace the receptor to restore function
  • there are ANS effects
  • Real issue: skeletal muscle!
19
Q

Are there many venoms and toxins targeting the nicotinic receptor?

A

Yes.

20
Q

What is the most powerful nicotinic receptor antagonist toxin on the planet?

A

alpha bungarotoxin

-> from the common krait (Bungarus carelueus)

21
Q

What are venoms/toxins designed to do?

A
  • affect your skeletal muscle so that you cannot move
22
Q

Are nicotinic receptor antagonists used widely clinically?

A
  • no

- because they are quite messt and have too many side effects

23
Q

Where are muscarinic receptors found?

A
  • at the end of PS nerves
  • sweat glands

-> generally for blocking PS effects

24
Q

What are the main muscarinic receptor antagonists?

A
  • Atropine

- Hyascine

25
Q

CNS effects of atropine?

A
  • Normal dose – Little effect
  • Toxic dose - Mild restlessness -> Agitation
    (Less M1 selective)
26
Q

CNS effects of Hyascine?

A
  • Normal dose – Sedation, amnesia
  • Toxic dose – CNS depression or paradoxical CNS excitation (associated with pain)

(Greater permeation into CNS. Influence at
therapeutic dose)

27
Q

Why does Hyascine have greater permeation into the CNS?

A
  • slightly more lipid soluble -> can enter deeper in the brain
28
Q

Why do atropine and hyoscine have such different effects?

A
  • not entirely sure
  • maybe because Hyoscine is far more M1 selective (perhaps that is where the sedation comes form)
  • Hyoscine is more lipid soluble and perhaps can penetrate deeper into the brain and have effects there.
29
Q

Ophthalmic effects of muscarinic receptor antagonists?

A
  • e.g. tropicamide
  • allows for examination of the retina
  • causes pupil dilation
  • tropic amide paralyses a muscle
30
Q

Uses of muscarinic receptor antagonists as anaesthetic pre-medicaiton?

A
  • trachea and bronchioles - blocks constriction
  • salivary glands - blocks copious, watery secretion
  • heart - blocks decreased rate and contractility (hyptensive effect, protects HR)

+ Sedation (if the right antimuscarinic is used)

31
Q

How can muscarinic receptor antagonists be used in motion sickness?

A
  • motion sickness = sensory mismatch
  • cholinergic nerve goes to vomiting center
  • Hyoscine patch can help
32
Q

Muscarinic receptor antagonists in PD?

A
  • PD = loss of dopaminergic neurones that project from the substantial migrant
  • M4R has a suppressive effect on D1R
  • blocking the M4R makes D1R more responsive to Dopamine, upregulates D1R function
  • reduces the effects of PD
33
Q

Muscarinic receptor antagonists in respiratory disease?

A
  • e.g. Asthma it obstructive airway disease
  • blocks trachea and bronchiole constriction
  • e.g. Ipratropium Bromide (more likely to stay in the lungs -> better side effect profile)
  • e.g. Atropine

-> local effect wanted, side effects occur if it enters the systemic

34
Q

Unwanted effects of muscarinic effector antagonsits

A

Hot as hell - decreased sweating, thermoregulation

Dry as a bone - decreased secretions

Blind as a bat - cyclopegia

Mad as a hatter- CNS disturbance

35
Q

Cyclopegia

A
  • paralysis of the ciliary muscle of the eye

- resulting in a loss of accommodation.

36
Q

Muscarinic receptor antagonists in GI disease

A
  • e.g. IBS
  • decreases motility and tone
  • decreases secretions

M3 receptor antagonists:
Reduce side effects

37
Q 
Which of the following drugs would you
administer to treat an atropine overdose?
a) Bethanechol
b) Ecothiopate
c) Hyoscine
d) Physostigmine
e) Pralidoxime
A

a) Bethanecol looks like ACh
b) Ecothiopate (irreversible, not used in practice)
d) Physostigmine: main drug used in atropine poisoning

38
Q

How does Botulinum toxin work?

A
  • blocks SNARE complex

- prevents ACh exocytosis

39
Q

How can you treat atropine poisoning?

A
  • with anticholinersterase (e.g. physostigmine)

- establishes competitive receptor agonism

40
Q

Botulinum toxin facts

A
  • most toxic protein known
  • 1 gram of crystalline toxin, evenly dispersed and inhaled, would kill more than 1 million people
  • 2 molecules are enough to shut down a nerve
  • used commonly to remove wrinkles.
  • prevents ACh exocytosis
41
Q

How can you get atropine posioning?

A
  • e.g. berries from atropine plant
42
Q

SNARE complex

A
  • involved in exocytosis

- blocked by botulinum toxin

Year 2 - LCRS - Pharmacology (34 decks)

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