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PM2C Autumn Amy L > From Physiological Systems To Molecular Drug Targets II > Flashcards

From Physiological Systems To Molecular Drug Targets II Flashcards

1
Q

Name the 3 locations where nicotinic ACh receptors are found

A
  1. Muscle (neuromuscular junctions)
  2. Ganglion
  3. CNS
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2
Q

What is the function of nicotinic ACh receptors?

A

Excitation

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3
Q

Name an agonist for nicotinic ACh receptors

A

Acetyl Choline

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4
Q

How many transmembrane domains does a subunit of a nAChR have?

A

4

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5
Q

How many subunits does a nicotinic receptor have?

A

5: alpha, alpha, beta, delta, gamma

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6
Q

What do the nicotinic receptor subunits come together to form?

A

An ion channel

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7
Q

What is a nicotinic receptor’s ion channel permeable to?

A

Na+

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8
Q

How do nicotinic receptors cause excitation?

A
  1. 2 ACh molecules bind to the nAChR
  2. Conformational change occurs
  3. Ion channel opens
  4. Na+ enters the cell causing an increase in positive charge inside of the cell
  5. This causes excitation
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9
Q

What acts as the receptor gate in a nicotinic receptor?

A
  • 2 alpha helices, 1 in each alpha subunit
  • Conformational change when ACh binds causes them to open the ion channel
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10
Q

What is an issue when synthesising drugs targeted at the ANS ganglia nAChRs?

A

The drugs do not discriminate between sympathetic and parasympathetic nerves

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11
Q

Where do neuromuscular blocking agents work?

A

Neuromuscular junction

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12
Q

Name 2 types of neuromuscular blocking agents

A
  1. Competitive blockers
  2. Depolarising blockers
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13
Q

What are competitive blockers?

A

Competitive antagonists of nAChRs

(Increase concentration of agonist = decrease power of antagonist)

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14
Q

What are depolarising blockers?

A

Agonists which cause a depolarising block of the muscle fibre endplate

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15
Q

How do depolarising blockers work?

A
  1. Switch the receptor on = increase in Na+ entering the cell
  2. Blocker stops channel from closing so sodium keeps coming into the cell
  3. Eventually too much sodium enters the cell and prevents further excitation
  4. Activation of receptor switched off
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16
Q

Give a use of competitive blockers

A
  • Muscle relaxants as an adjunct to anaesthesia
  • In particular in obstetrics as they do not cross into the placenta
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17
Q

Name 3 examples of a competitive blocker

A
  1. Tubocurarine
  2. Pancuronium
  3. Vecuronium
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18
Q

Why are competitive blockers used as muscle relaxants?

A

They selectively work on the nAChRs at the neuromuscular junction, rather than at the ganglia and the brain/CNS

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19
Q

Why are different competitive blockers used for minor vs major surgeries

A

Some have shorter half lives than others therefore work for shorter periods of time

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20
Q

Give an example of a use of depolarising blockers

A

Cause paralysis during anaesthesia

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21
Q

How do depolarising blockers cause paralysis?

A
  1. The muscle contracts due to maintained depolarisation
  2. Muscle cannot repolarise (relax)
  3. This causes loss of excitability (sodium channels cannot inactivate)
  4. Therefore the continual stimulation of the NMJ by DB’s causes muscle paralysis
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22
Q

Name an example of a depolarising blocker

A

Succinylcholine (Suxamethonium)

Works on nAChRs

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23
Q

What is succinylcholine used for?

A

To cause paralysis during anaesthesia

Minor surgery

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24
Q

Why is suxamethonium so short acting? (10 mins)

A

Because it is rapidly hydrolysed by cholinesterases

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25
Q

What is the indication for Donepezil?

A

For the treatment of mild-moderate Alzheimer’s Disease

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26
Q

What is the mechanism of action of Donepezil?

A

Anticholinesterase = inhibits ACh-esterase

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27
Q

How does botulinum toxin type A work?

A

It blocks vesicle docking/release and therefore prevents the release of ACh

28
Q

How can botulinum toxin type A be deadly?

A

Can cause respiratory paralysis

29
Q

Why is botulinum toxin type A so toxic?

A

It has a very low LD50 value

LD50 = 10ng/kg

30
Q

List 3 therapeutic indications for botulinum toxin

A
  1. Excessive muscle spasm - can result from stroke, brain or spinal cord injury, CP
  2. Migraine/headache treatment - facial muscle contraction stimulates headaches
  3. Excessive secretion - severe underarm sweating or salivation
31
Q

What receptors does noradrenaline act on?

A

α or β-adrenoceptors

32
Q

What is noradrenaline release regulated by?

A

Inhibitory presynaptic α2-adrenoceptors

33
Q

What are β​-blockers?

A

Blockers of the β-adrenoceptors

34
Q

How is adrenaline released into the bloodstream?

A

It is secreted from the adrenal gland

35
Q

What is dopamine?

A

A precursor for noradrenaline and adrenaline

And a CNS transmitter

36
Q

Which amino acid are adrenaline, noradrenaline and dopamine generated from?

A

Tyrosine

37
Q

Describe the biogenic amine synthesis process

A

Tyrosine –> DOPA –> Dopamine –> Noradrenaline –> Adrenaline

38
Q

How can one of the substances in biogenic amine synthesis build up?

A

If the enzyme which converts the substance into something else becomes inhibited

39
Q

What acts as negative feedback in biogenic amine synthesis?

A
  • Build up of noradrenaline
  • Negative feedback on to tyrosine hydroxylase (converts Tyrosine to DOPA)
40
Q

How many subtypes of adrenoceptor are there?

A

5: α1 α2 β1 β2 β3

41
Q

Where is the β1-adrenoceptor located?

A

Heart

42
Q

Where is the β2-adrenoceptor located?

A

Smooth muscle

43
Q

Where is the α1-adrenoceptor located?

A

Smooth muscle

44
Q

Where is the α2-adrenoceptor located?

A

Smooth muscle

45
Q

What type of G protein is the α1-adrenoceptor coupled to?

A

Gαq

46
Q

What type of G protein does the α2-adrenoceptor couple to?

A

Gα​i/o

47
Q

What type of G protein do the β-adrenoceptors couple to?

A

Gαs

48
Q

What response does the α1-adrenoceptor cause when its G protein is bound?

A

Increase in IP3

49
Q

What response does the α2-adrenoceptor cause when bound to its G protein?

A

Decrease in cAMP

50
Q

What response do the β-adrenoceptors cause when their G protein is bound?

A

Increase in cAMP

51
Q

Name the enzyme that Gαs (with β​1/2/3 adrenoceptors) stimulates

A

Adenylate cyclase

52
Q

What process does adenylate cyclase carry out?

A

Converts ATP –> cAMP

53
Q

What effect does increased cAMP have?

A

Increased protein phosphorylation

54
Q

What would be the agonist of choice to activate the α1-adrenoceptor

A

Noradrenaline

55
Q

What would be the agonist of choice to activate the α2-adrenoceptor

A

Adrenaline

56
Q

What would be the agonist of choice to activate the β-adrenoceptors

A

Isoprenaline

57
Q

What effect does NA cause when bound to an α1 receptor

(α selective)

A
  • Vasoconstriction
  • This causes reflex bradycardia due to baroreceptor response
  • ACh release = slows vagal nerve
  • Overall increase in BP
58
Q

What effect does isoprenaline have when it binds to β adrenoceptors? (β- selective)

A

Causes vasodilation (β2) and tachycardia (β1) Overall decrease in BP

59
Q

What effect does adrenaline have when it binds to a β or α-adenoceptor?

A

Higher affinity for β receptor but can still bind to α

Slight increase in BP

60
Q

What are adrenergic synapses also known as?

A

Varicosities (= swelling)

61
Q

How do sympathomimetics work?

A

Mimic CNS

62
Q

What is the indication for salbutamol?

A

Asthma treatment

63
Q

What is the mechanism of action for salbutamol?

A

Selective β2 adrenoceptor agonist

Causes bronchodilation

64
Q

What is the indication for atenolol?

A

Hypertension

65
Q

What is the mechanism of action of atenolol?

A

Cardioselective β1 adrenoceptor antagonist

(= β​ blocker)

66
Q

What is the indication of pseudoephedrine?

A

Nasal decongestion

67
Q

What is the mechanism of action of pseudoephedrine? (Sudafed)

A

Substrate for biogenic amine uptake system = sympathomimetic

  1. Mimics NA and gets taken up by uptake system
  2. Therefore NA displaced from vesicles
  3. Released NA builds up in synapatic cleft = vasoconstriction of mucosal blood vessels (α1 adrenoceptors)
  4. This reduces fluid build up in the nose

PM2C Autumn Amy L (16 decks)

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