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Pharmacology & Therapeutics Y2 > SNS Antagonists > Flashcards

SNS Antagonists Flashcards

1
Q

Difference between metabolism of NT in PSNS and SNS?

A

NA is reuptaken into tissue for metabolism, whereas ACh is broken down in the synapse

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2
Q

Which adrenoceptor is primarily responsible for increased cardiac rate and force

A

B1

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3
Q

Which adrenoceptor is primarily responsible for relaxation of the GIT

A

A1 and B1

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4
Q

Which adrenoceptor is primarily responsible for renin release from the kidney

A

B1

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5
Q

Which adrenoceptor is primarily responsible for bronchodilation

A

B2

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6
Q

Which adrenoceptor is primarily responsible for vasodilation

A

B2

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7
Q

Which adrenoceptor is primarily responsible for relaxation of visceral smooth muscle

A

B2

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8
Q

Which adrenoceptor is primarily responsible for hepatic glycogenolysis

A

B2

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9
Q

Which adrenoceptor is primarily responsible for lipolysis

A

B3

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10
Q

Which adrenoceptor is primarily responsible for CNS actions

A

A2

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11
Q

Which adrenoceptor is primarily responsible for contraction of vascular smooth muscle

A

A2

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12
Q

Which adrenoceptor is primarily responsible for inhibition of NT release

A

A2

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13
Q

Which adrenoceptor is primarily responsible for vasoconstriction

A

A1

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14
Q

What selectivity does this drug have: carvedilol

A

A1 and B1 antagonism

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15
Q

What selectivity does this drug have: phentolamine

A

A1 and A2 antagonism

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16
Q

What selectivity does this drug have: prazosin

A

A1 antagonism

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17
Q

What selectivity does this drug have: propranolol

A

B1 and B2 antagonism

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18
Q

What selectivity does this drug have: atenolol

A

B1 antagonism

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19
Q

Drug that has antagonistic selectivity for: A1 and B1

A

carvedilol

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20
Q

Drug that has antagonistic selectivity for: A1

A

prazosin

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21
Q

Drug that has antagonistic selectivity for: A1 and A2

A

phentolamine

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22
Q

Drug that has antagonistic selectivity for: B1

A

atenolol

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23
Q

name 5 adrenoceptor antagonists

A

carvedilol, phentolamine, prazosin, propranolol, atenolol

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24
Q

Main uses of SNS antagonists?

A
  • Hypertension
  • Cardiac Arrhythmias
  • Angina
  • Glaucoma
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25
Q

What adrenoceptor controls the heart sympathetically

A

B1

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26
Q

What adrenoceptor controls renin release sympathetically

A

B1

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27
Q

Tissue Targets for Anti-hypertensives (5)

A

Sympa nerves, kidneys, heart, arterioles, and CNS

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28
Q

How is the CNS involved in BP

A

baroreceptors setting BP

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29
Q

which receptor blockade has positive and which has negative of B1 and 2

A

most of the POSITIVE effects are from Beta 1 blockade and most of the NEGATIVE effects are from Beta 2 blockade

30
Q

Which adrenoceptors are found in Sympa nerves, kidneys, heart, arterioles, and CNS

A

The heart has B1 receptors, sympa nerves have B1 and B2, kidney has B1 and CNS has B1 and B2. Arterioles have no B receptor

31
Q

Blockade of what where has the biggest impact on reducing BP and why

A

B1 in the kidneys as renin secretion falls reducing TPR

32
Q

How do BB’s work to reduce BP (30

A
  • Act in the CNS to reduce sympathetic drive
  • Act on the beta 1 receptors in the heart to reduce heart rate and reduce cardiac output but this effect disappears with chronic treatment - the heart resets itself
  • Acts on the KIDNEYS on the beta 1 receptors to REDUCE RENIN PRODUCTION
33
Q

`What are Presynaptic Beta 1/2 Receptors, how common are they?

A

These presynaptic beta receptors have a positive facilitation effect on the synthesis and release of a neurotransmitter. These receptors are not found in all nerve endings but they can have a major effect.

34
Q

What effect does interfering with Presynaptic Beta 1/2 Receptors have

A

If you block the beta 1 then you remove this positive facilitation effect and reduce the amount of noradrenaline coming from the nerve terminal.

35
Q

What has superseded BB as antihypertensives and why

A

ACE inhibitors have superceded beta blockers as there are less side effects.

36
Q

Unwanted effects of Beta blockers? (6)

A

BRONCHOCONSTRICTION, CARDIAC FAILURE, HYPOGLYCAEMIA, FATIGUE, COLD EXTREMITIES, BAD DREAMS

37
Q

Which preexisting conditions mean you do not prescribe BBs (4)

A

o ASTHMA
o COPD
o CARDIAC FAILURE
o DIABETES

38
Q

Drug that is beta non-selective?

A

Propranolol

39
Q

when is the effect of propranolol particularly evident

A

when exercising

40
Q

What is a cardioselective BB

41
Q

Main areas that atenolol affects?

A

Heart and kidneys beta1 receptors

42
Q

Carvedilol is most selective for, and then followed by?

A

B1 and then A1

43
Q

How does carvedilol lower BP

A

This lowers blood pressure by blocking the alpha1 receptors in the arterioles to lower the total peripheral resistance

44
Q

Main adrenoceptor linked to TPR?

45
Q

What can cause postural hypotension?

A

Alpha antagonists blocking sympathetic drive

46
Q

a non-selective alpha antagonist ?

A

Phentolamine

47
Q

What does phentolamine do

A

non-selective alpha antagonist.

Causes vasodilation and a fall in blood pressure due to blockade of alpha-1 adrenoceptors
However, blockade of presynaptic alpha-2 receptors removes the inhibitory effect of the alpha-2 receptors on noradrenaline release and so you get an increase in noradrenaline release which leads to competitive drug-receptor interactions.
Phentolamine is outcompeted by NA as there is more of NA.

This makes reflex tachycardia stronger

48
Q

Special effect of prazosin?

A

• Unlike other anti-hypertensives, alpha-1 antagonists cause a decrease in LDL and an increase in HDL cholesterol.

49
Q

What does prazosin antagonise

A

A1 selective

50
Q

A1 selective antagonist?

51
Q

Why is an A1 selective antagonist less tachycardic?

A

There is less tachycardia than non-selective antagonists since they do NOT increase noradrenaline release from nerve terminals (no alpha-2 actions

52
Q

methyldopa synthesis and metabolism?

A

taken up by the noradrenergic neurons
form the false transmitter - alpha-methyl noradrenaline
It is NOT well metabolised within the neuron by MAO and tends to accumulate in larger quantities than noradrenaline.
It displaces noradrenaline from the synaptic vesicles when taken up

53
Q

MOA methyldopa?

A

(alpha-methyl noradrenaline) is released in the same way as noradrenaline into the synapse.
It is less active than noradrenaline on alpha-1, beta-1, and beta-2 receptors - LESS EFFECTIVE AT CAUSING VASOCONSTRICTION (as it is shit on alpha 1) so there will be a fall in BP.
it is more active on presynaptic alpha-2 receptors (the ones that mediate the negative feedback and release of NA shut down the synthesis and release).
• This means that the auto-inhibitory feedback mechanism operates more strongly and reduces noradrenaline release below normal levels
• It also has some CNS effects, it stimulates the vasopressor centre in the brainstem to inhibit sympathetic outflow

54
Q

What is the active form of methyldopa

A

alpha-methyl noradrenaline

55
Q

Other benefits to methyldopa? (3)

A

o Improves blood flow greatly.
o Renal and CNS blood flow is well maintained so it is widely used in patients with renal insufficiency or cerebrovascular disease
o It is also the recommended anti-hypertensive in pregnant women because it has no adverse effects on the foetus despite crossing the blood-placenta barrier

56
Q

Adverse effects of methyldopa (4)

A

dry mouth, sedation, orthostatic/postural hypotension (problem in the elderly), male sexual dysfunction

57
Q

Class II antiarrhythmics AKA …

58
Q

Why are BB used as antiarrhythmics

A

sympathetic drive and b1 receptors controls the pacemaker current so beta blockers are a good way of controlling arrhythmias in patients

59
Q

main cause of arrhythmias?

A

Myocardial ischaemia

60
Q

How does a BB help control arrhythmias

A

The refractory period of the AV node is increased by beta antagonists
This interferes with AV conduction in atrial tachycardias and slows down ventricular rate

61
Q

Drug that is used antiarrhythmically?

A

Propranolol

62
Q

What is angina

A

Pain that occurs when the oxygen supply to the myocardium is insufficient for its needs

63
Q

Types of angina?

A

Stable, unstable, variable

64
Q

Stable angina, pain when? Why? Heart effect?

A

o Pain on exertion
o Due to a fixed narrowing of the coronary vessels e.g. atheroma
o There is increased demand on the heart

65
Q

Unstable angina, pain when? Peak pain? Why? Risks of?

A

o Pain with less and less exertion
o Culminates with pain at rest
o The atheromatous plaque is starting to rupture and breaks away.
o You get a platelet-fibrin thrombus associated with the ruptured atheromatous plaque but without complete occlusion of the vessel
o High risk of infarction

66
Q

Variable angina, when? why? association?

A

o Occurs at rest
o Caused by coronary artery spasm not so much atherosclerosis
o It is associated with atheromatous disease

67
Q

How do BB help angina? (brief)

A

• Beta blockers do nothing about the cause of the angina (atherosclerosis) they simply lower the work the heart has to do

68
Q

How do BB help angina? (specific, 3)

A
  • Decrease heart rate
  • Decrease systolic blood pressure
  • Decrease cardiac contractile activity
69
Q

BB should not be used to treat patients with angina if they have:

A

Bradycardia, bronchospasm, hypotension, AV block

70
Q

Where is aqueous humour produced and how

A

Ciliary body by carbonic anhydrase

71
Q

What is the amount of humour produced in the eye directly related to

A

Blood flow in the ciliary body

72
Q

What SNS antagonists can be used to treat glaucoma

A

o Adrenaline can act on the alpha-1 receptors to cause vasoconstriction and reduce blood flow through the ciliary body –> this reduces the amount of aqueous humour.

There are also drugs that can act on the beta-1 receptors which drives the action of carbonic anhydrase to produce bicarbonate, , blocking these receptors reduces carbonic anhydrase activity

Pharmacology & Therapeutics Y2 (10 decks)

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