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YR2 LCRS Pharmacology > 7. Cholinoreceptor antagonists > Flashcards

7. Cholinoreceptor antagonists Flashcards

1
Q

what is affinity?

A

the ability of a drug to bind to a particular receptor to form a complex

reversible reaction

both antagonists and agonists have affinity

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2
Q

what is efficacy?

A

the ability of a drug to stimulate a response after binding to the receptor

only agonists have efficacy

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3
Q

what are nicotinic receptor antagonists also called and what do they do?

A

ganglion-blocking drugs

they interfere with transmission through all ganglia (sympathetic and parasympathetic)

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4
Q

what are the 2 actions of nicotinic receptor antagonists?

A
  1. block the nicotinic receptor (ion-channel linked receptor) to prevent depolarisation as the ion channel cannot open
  2. block the channel (drug sits in the channel pore and prevents ion passage)
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5
Q

give 2 examples of nicotinic receptor antagonists

A

hexamethonium

trimetaphan

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6
Q

describe the uses and effects of hexamethonium

A
  • first anti-hypertensive drug
  • causes vasodilation because the antagonist blocks the sympathetic tone in vessels
  • causes decreased renin secretion because less aldosterone is released
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7
Q

describe the uses and effects of trimetaphan

A
  • used clinically
  • i.v. during surgery to induce hypotension
  • short-acting drug to reduce the chance of blood loss during surgery
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8
Q

describe use-dependent block

A

the more open the channel is, the more effective the block

more agonist -> ion channels open more -> antagonist blocks channels more

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9
Q

how can you overcome a block of the actual nicotinic receptor?

A

by adding more acetylcholine (competitive)

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10
Q

do ion channel blockers have affinity?

A

no

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11
Q

what widespread effects do hexamethonium and trimetaphan have on the body?

A
  • pupil constriction interference -> dilation
  • bladder dysfunction due to bladder smooth muscle impairment
  • decreased GI tone
  • decreased saliva production
  • impaired sweating capacity
  • decreased exocrine secretions
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12
Q

why are ganglion blocking drugs good anti-hypertensive drugs?

A

by blocking renin secretion and stopping vasoconstriction (sympathetic) rather than reducing heart rate and contractility (parasympathetic)

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13
Q

do hexamethonium and trimetaphan block the receptor or the channel pore?

A

hexamethonium - both

trimetaphan - receptor

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14
Q

what is alpha-bungarotoxin and how is it different to nicotinic antagonist drugs?

A

it is a poison that comes from the common krait snake (potent toxin)

DIFFERENCE:

  1. it binds irreversibly (with covalent forces)
  2. it targets both the autonomic and somatic nervous system causing paralysis
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15
Q

what do muscarinic receptor antagonists influence?

A

parasympathetic function (except sweat glands which sympathetic nerves innervate via muscarinic receptors)

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16
Q

give 2 examples of muscarinic receptor antagonists

A

atropine
hyoscine
(structurally similar to ACh)

17
Q

what are the effects of atropine on the CNS?

A

normal dose: little effect

toxic dose: mild restlessness, agitation (CNS excitation)

18
Q

what are the effects of hyoscine on the CNS?

A

normal dose: sedative, amnesia

toxic dose: CNS depression, paradoxical CNS excitation (associated with pain)

19
Q

what is tropicamide?

A

the ophthalmic drug (muscarinic receptor antagonist) that blocks muscarinic receptors in the iris and causes pupil dilation

20
Q

why is tropicamide useful?

A

it allows you to examine the retina at the back of the eye using a light

21
Q

why might muscarinic receptor antagonists be used before a surgical procedure as anaesthetic premedication?

A
  1. reverses constriction in lungs -> bronchodilation -> assists inhalation of anaesthetic
  2. dries up salivary secretions -> reduces risk of aspiration of fluid back down into the lungs
  3. counteracts the way the anaesthetic slows down HR by increasing it
  4. hyoscine is a sedative -> calms patient
22
Q

what is motion sickness due to?

A

a sensory mismatch - the sensory info coming in visually does not match the sensory info coming in through the labyrinth (regarding balance and posture) so when it doesn’t match up the vomiting centre may be activated

23
Q

how can hyoscine patches help motion sickness?

A

hyoscine gets into the brain and prevents the cholinergic system from activating the vomiting centre

24
Q

how do dopaminergic neurones control movement?

A

dopaminergic neurones originate from substantia nigra -> project down to striatum -> dopamine is released in striatum and binds to D1 receptors on striatal neurones -> control of movement

25
Q

how can muscarinic receptor antagonists be used in parkinson’s disease?

A

muscarinic receptors (M4) impair D1 receptor function which is a problem in Parkinson’s as you lose dopaminergic neurones so theres reduced D1 activation

muscarinic receptor antagonists would block the inhibitory effect so D1 receptor function is more effective

26
Q

how can muscarinic receptor antagonists be used in respiratory disease?

A

ipratropium bromide is locally administered via inhalation because it has a +ve charge so can’t enter the systemic circulation and remains in the lungs - it is modified to atropine which is a bronchodilator to treat asthma and obstructive disease

27
Q

how are muscarinic receptor antagonists used in the GI tract?

A

used to treat IBS

M3 receptor antagonists slow down the gut -> decreases motility and secretion (decreases parasympathetic activity) -> reduces symptoms of diarrhoea

28
Q

what are the unwanted side effects of muscarinic receptor antagonists?

A
  • hot as hell: inability to sweat impairs thermoregulation
  • dry as a bone: decreased secretions (salivary, exocrine)
  • blind as a bat: cycloplegia - inability to adjust lens so can’t focus
  • mad as a hatter: CNS disturbance
29
Q

what is used to treat atropine poisoning and why?

A

physostigmine because it blocks the acetylcholinesterase enzyme and increases the ACh in the synapse which can then outcompete the atropine. you can also give an agonist such as bethanechol

30
Q

why is physostigmine preferred over ecothiopate

A

the actions of ecothiopate are irreversible whereas those of physostigmine are reversible so clinically preferred

31
Q

what does botulinum toxin do?

A

it takes out parasympathetic function - it diffuses into the parasympathetic nerves and prevents ACh vesicles from fusing with the membrane therefore ACh exocytosis is prevented

32
Q

what is one of the protein complexes that normally allows vesicles to fuse with the membrane but is blocked by the botulinum toxin?

A

SNARE proteins

33
Q

what is botox?

A

a diluted, less potent form of the botulinum toxin that can be localised which is injected to cause skeletal muscle paralysis and remove wrinkles

34
Q

other than skeletal muscle, where else can botox be injected?

A

into sweat glands and salivary glands to control secretions

YR2 LCRS Pharmacology (32 decks)

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