Brainscape's Knowledge GenomeTM

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


See full index

Pharmacology > Cholinoceptor Antagonists > Flashcards

Cholinoceptor Antagonists Flashcards

1
Q

Where are nicotinic receptors present?

A

at all autonomic ganglia

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

What are nicotinic receptor antagonists also known as?

A

ganglion blocking drugs

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

What are the two ways in which ganglion blocking drugs work?

A

Antagonise the receptor and/or physically block the ion-channel itself (nicotinic)

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

What does use dependant blockage mean?

A

The drug works best when the channel is open so the more the receptor is used, the more it is blocked.

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

What is incomplete blocking?

A

Ion-channel blockade is only partial (as some ions still pass through)

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

Why do some GBDs not have affinity?

A

They don’t bind to the receptor, just block the ion-channel itself

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

What does the effect of GBDs depend on?

A

Which system is more dominant e.g. PNS or SNS

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

Give some of the effects of the PNS

A

eye: constriction of pupil and contraction of ciliary muscle

trachea and bronchioles: constriction

salivary glands: copious watery secretion

ureters and bladder: contraction of detrussor and relaxation of trigone and sphincter

heart: reduced HR and contractility

GI: increases motility/tone and more secretions

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

Give some of the effects of the SNS

A

eye: pupil dilation

trachea and bronchioles: dilation

salivary glands: thick viscous secretion

skin: piloerection and more sweating
adipose: lipolysis
liver: glycogenolysis and gluconeogenesis
kidney: increased renin

ureters and bladder: relaxation of detrussor and constriction of trigone and sphincter

heart: increased HR and contractility

GI: reduces motility/tone and less secretions

blood vessels (skeletal m): dilation

blood vessels (skin, mucous membrane and splanchnic area): constriction

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

What are the CVS effects of GBDs?

A

Hypotension – blood vessel vasoconstriction inhibited and kidney renin secretion inhibited

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

What are the smooth muscle effects of GBDs?

A

Pupil dilation, decreased GI-tone, bladder dysfunction, bronchodilation

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

What are the exocrine effects of GBDs?

A

Decreased secretions

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

Give examples of ganglion blocking drugs and what they were originally used for

A

hexamethonium and trimetaphan

Anti-hypertensives - both blocks channels and antagonise them

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

How did hexamethonium work and what was its flaw?

A

First anti-hypertensive drug used but lots of side effects as very general
An ion-channel blocker (so not a lot of affinity)

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

How did trimetaphan work and when was it used?

A

Used for when you want hypotension during surgery, IV-administered, short acting.
A receptor antagonist (so has affinity)

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

What is alpha bungarotoxin?

A

A GBD that is irreversible (used by snakes)

Binds mainly to somatic nicotinic receptors (NRs) whereas the GBDs above bind to autonomic NRs

17
Q

What do muscarinic receptor antagonists mainly work on?

A

PNS - only found in SNS in sweat glands

18
Q

Give two examples of MRAs (muscarinic receptor antagonists)

A

atropine

hyoscine

19
Q

How can MRAs be useful in treating Parkinson’s? Explain briefly what Parkinson’s involves

A
  • In Parkinson’s disease, the substantia nigra neurones are lost which usually produce dopamine for the striatum to allow fine movement control
  • The lack of dopamine gives the Parkinson’s disease symptoms
  • Muscarinic receptor antagonist drug decreases the negative inhibition on release of dopamine into the striatum from another source meaning dopamine can continue to be released into the striatum
20
Q

What are the CNS effects of atropine and hyoscine (high and low doses)?

A

Atropine:
Normal dose – little effect
Toxic dose – mild restlessness and agitation

Hyoscine:
Normal dose – sedation, amnesia
Toxic dose – CNS depression or paradoxical CNS excitation (associated with pain). Maybe due to a greater permeability through the BBB into the brain

21
Q

What are the opthalmic effects of tropicamide and how is this useful?

A

Used in examination of the retina – causes dilation/miosis

22
Q

How can MRAs be used in anesthetic pre-medication?

A

The MRAs block the PNS and so block; bronchoconstriction (so bronchodilates), watery secretions (more thick secretions decreases chance of aspirations), decreased HR and contractility (protect the heart from slowing effects of other drugs) and also sedates the patient

23
Q

How can hyoscine be used to treat motion sickness?

What causes motion sickness?

A

Inhibits the muscarinic receptors in the vomiting centre so the sensory mismatch (from a mismatch from what the eyes see and what the labyrinth reports in balance) cannot induce vomiting when suffering from motion sickness.

24
Q

What are the respiratory effects of Ipratropium bromide and what is it used for?
What is its relationship to atropine and why is it preferred to atropine?

A
  • Used for Asthma and COPD as it causes bronchodilation
  • Similar molecular shape to atropine but has an extra nitrogen-containing polar group attached that allows it to linger more in the lungs as it cannot cross the mucosa as easily as atropine would
25
Q

What are the GI uses of MRAs?

A

Treats irritable bowel syndrome as the MRA decreases GI tone and secretions.

26
Q

What are the unwanted effects of MRAs?

A

Hot as hell – decrease in sweating and thermoregulation defects

Dry as a bone – decreased secretions

Blind as a bat – cyclopegia (paralysis of eye muscles so no accommodation/focusing)

Mad as a hatter – CNS disturbance (i.e. tremors etc.)

27
Q

Which drug can be used to treat an atropine overdose?

A

A drug that either enhances ACh activity (anticholinesterase) or inhibits atropine so: 1. bethanechol (muscarinic receptor agonist),
ecothiopate (Irreversible anticholinesterase - less preferred as irreversible) and physostigmine (anticholinesterase)

28
Q

What is botulinum toxin and what does it do?

A

Parasympatholytics - reduces the activity of the PNS

  • One of the most toxic proteins known
  • Binds to the ACh vesicles and stops them docking with the inner membrane forming a SNARE complex

Pharmacology (26 decks)

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