Brainscape's Knowledge GenomeTM

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


See full index

Semester 2 Year 1 > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

3 ways to block neuromuscular transmission:

A

Presynaptically - inhibiting ACh synthesis or release

Postsynaptically

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

How can you block neuromuscular transmission presynaptically through inhibiting ACh SYNTHESIS?

A

Block rate-limiting step of choline uptake

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

How can you block neuromuscular transmission presynaptically through inhibiting ACh RELEASE?

A

Not much specificity

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

How can you block neuromuscular transmission postsynaptically?

A

Interfering with actions of ACh on receptor - more specific

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

What can you use to inhibit ACh release?

A

Local anaesthetics

General inhalation also anaesthetics

Inhibitors/competitors of calcium

Neurotoxins

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

Examples of Inhibitors/competitors of calcium:

A

Magnesium ions

Some antibiotics

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

Some examples of Neurotoxins:

A

Botulinum toxin

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

What does BOTOX stand for?

A

Botulinum toxin - relaxes muscles underneath skin

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

Clinical uses of neuromuscular blocking drugs:

A

Endotracheal intubation

During surgical procedures

Intensive care

During electroconvulsive therapy

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

Structure of Nicotinic acetylcholine receptor:

A

Pore in centre

5x subunits

2 binding regions for ACh

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

Types of blockers for Nicotinic ACh receptors:

A

Agonists - depolarising

Antagonists - non-depolarising

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

Why are agonist drugs depolarising?

A

Stimulate pore opening

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

Why are antagonists non-depolarising?

A

Prevent ACh binding - pore remains closed

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

Examples of competitive non-depolarising antagonist blockers:

A

Tubocuraine

Atracurium

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

How do antagonists result in no activation of muscle action potential?

A

Prevent ACh binding by occupying site

Decrease motor end plate potential

Decreases depolarisation of motor end plate region

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

Example of depolarising agonist blocker:

A

Suxamethonium

17
Q

How do agonists over-stimulate the cell?

A

Not metabolised by Acetylcholine esterase- prolongs activity of ACh at neuromuscular junction

18
Q

How do depolarising agonist blockers result in no more action potentials being generated?

A

Persistent depolarisation of motor end plate and muscle membrane

Prolonged end plate potential

19
Q

What does the prolonged depolarisation of muscle membrane caused by depolarising agonists result in?

A

Membrane potential above threshold for resetting voltage-gated sodium channels

Channels remain refractory - can’t reset

20
Q

Phase 1 of depolarising block:

A

Muscle fasciculatations, then blocked

Repolarisation inhibited

Sodium channels remain inactivated

21
Q

Phase 2 of depolarising block:

A

Desensitisation blockade - no depolarisation as receptors are refractory

22
Q

Examples of non-depolarising blockers:

A

PARVM

P = Pancuronium (SE Tachycardia)

A = Atracurium (SE hypotension)

R = Rocuronium (SE Tachycardia)

V = Vecuronium (SE few)

M = Mivacurium (SE hypotension)

23
Q

Side effects of Suxamethonium:

A

Bradycardia

24
Q

Ways of degrading Atracurium:

A

Ester hydrolysis and Hofmann elimination

Rapid degradation

25
Q

Ways to degrade Mivacurium:

A

Plasma cholinesterases

26
Q

Ways to degrade suxamethonium:

A

Plasma cholinesterases

27
Q

Ways to degrade Pancuronium:

A

Hepatic metabolism

Slow - longer duration of immobility

28
Q

Ways to degrade Vecuronium:

A

Hepatic metabolism

Slow - longer duration of immobility

29
Q

Ways to degrade Recuronium:

A

Unchanged in bile/urine

30
Q

What do cholinesterases degrade?

A

Mivacurium

Suxamethonium

31
Q

Types of cholinesterases:

A

Acetylcholinesterase - hydrolysis of ACh

Plasma cholinesterases

32
Q

What inhibits cholinesterases enzymes?

A

Anticholinesterase drugs

33
Q

What do anticholinesterase drugs do?

A

Increase ACh at neuromuscular junction

Decrease degradation - longer duration of ACh

Reversible or irreversible effects on enzyme

34
Q

Effects of anticholinesterases:

A

CNS = convulsions

ANS - many effects

35
Q

Effects of anticholinesterases on ANS:

A

SLUDGE

Salivation
Lacrimation
Urination
Defecation
GI upset
Emesis
36
Q

Clinical uses of anticholinesterases:

A

Anaesthesia

Alzheimer’s disease

Myasthenia Gravis

37
Q

What is Myasthenia gravis?

A

Auto-immune reaction

Block receptor to ACh -> muscle weakness

38
Q

What reverses effect of rocuronium and Vecuronium?

A

Selective binding agent

Semester 2 Year 1 (12 decks)

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