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LCRS Pharma > SNS antagonists > Flashcards

SNS antagonists Flashcards

1
Q

where are alpha 2 receptors located?

A

presynaptic terminals

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2
Q

what effect do alpha 2 receptors have?

A

negative feedback on NA release

these can be targetted

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3
Q

normal alpha 1 function

A

vasoconstriction

relaxation of GIT

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4
Q

normal alpha 2 function

A

inhibition of NA release
contraction of VSMC
CNS

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5
Q

normal beta 1 function

A

cardiac stimulation
relaxation of GIT
renin release

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6
Q

normal beta 2 function

A

bronchodilation
vasodilation
relaxation of VSMC
hepatic glycogenolysis

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7
Q

normal beta 3 function

A

lipolysis

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8
Q

non selective antagonist example (alpha and beta)

A

carvediol

labetalol

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9
Q

non selective alpha antagonist

A

phentolamine

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10
Q

alpha 1 selective antagonist

A

prazosin

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11
Q

non selective beta antagonist

A

propanolol

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12
Q

beta 1 selective antagonist

A

atenolol

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13
Q

what are the main elements that need to be controlled to treat hypertension

A

blood volume
cardiac output
TPR

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14
Q

what tissues are targeted by anti-hypertensives?

A
  • kidney (renin) beta 1
  • heart beta 1
  • arterioles (TRP determinant) alpha 1/2
  • SNS nerves (vasoconstrictor molecule release e.g. NA) beta 1/2
  • CNS (BP set point, system regulation in BP control) beta 1/2
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15
Q

beta blocker suffix

A

-olol

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16
Q

what is used to treat hypertension

A

beta blockers
targeting the heart (beta 1)
kidney (beta 1) and CNS

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17
Q

effect of beta blockers on the heart

A

Beta 1
reduce inotropic and chronotropic effect
(this effect disappears in chronic treatment)

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18
Q

effect of beta blockers on kidney

A

beta 1

reduced renin production

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19
Q

effect of beta blockers on CNS

A

beta 1 and 2

reduce sympathetic tone

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20
Q

beta 1 blockade

A

beta 1 is also located on pre-synaptic membrane
when bound, it reduces positive feedback on NA release
this has anti-hypertensive effects

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21
Q

unwanted effects of beta blockers/antagonists

A

o Bronchoconstriction – patient has an airway disease e.g. asthmatics
o Cardiac failure – in patients with heart disease sympathetic drive is required
o Hypoglycaemia - beta blockers may mask symptoms (tremors etc.) and non-selective beta blockers will also block hepatic glycogenolysis (beta 2).
o Fatigue – reduced CO and muscular perfusion
o Cold extremities – loss of beta-receptor mediated vasodilation.
o Bad dreams- CNS

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22
Q

non selective beta blocker

A

propanolol

has equal affinities for beta 1 and 2, therefore can have adverse effects
causes little effect at rest
during exercise it reduced HR, CO and BP

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23
Q

cardiac selective beta blocker

A

atenolol

beta 1 selective
antagonises the effects of NA on the heart but affects organs with beta 1 like kidneys

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24
Q

atenolol vs propanolol

A

atenolol (beta 1 selective) is less selective for beta 2, so is less likely to give asthmatic patients an issue compared to non selective propranolol but is not entirely safe

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25
Q

change in atenolol selectivity

A

with higher concentrations, the drug becomes non-selective

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26
Q

labetalol and carvediol (mixed)

A 
alpha 1 and beta 1
more for beta 1 than alpha 1 
vasodilator effect 
lowers BP via TRP reduction 
therefore decreased HR or CO
effect wanes with chronic use
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27
Q

what is the problem with using alpha antagonists?

A

postural hypotension
arterioles are affected, decreasing the TPR

this leads to reflexive tachycardia therefore increased HR and CO (beta mediated)

28
Q

phentolamine

A

non selective alpha antagonist
causes vasodilation
fall in BP

29
Q

how does phentolamine enhance reflexive tachycardia?

A

they bind to alpha 2 receptors presynaptically

blocking the inhibition of NA

30
Q

When is phentolamine mainly used?

A

treating phaechromocytoma induced hypertension

increased GIT motility, therefore diarrhoea

31
Q

prazosin

A

alpha 1 selective
causes vasodilation by inhibiting the vasoconstrictor activity of NA
fall in BP and CO

also decreased LDL and increases HDL (good effect)

32
Q

phentolamine vs prazosin

A

prazosin causes less reflexive tachycardia as it does not bind to alpha 2, so NA release can be inhibited.

phentolamine is non-selective and will bind to alpha 2 too.

33
Q

example of false transmitter prodrug

A

methyldopa

34
Q

what is the false transmitter that methyldopa produced

A

once taken up by noradrenergic neurones, decarboxylated and hydroxylated, it becomes alpha methyl noradrenaline

35
Q

alpha methyl NA activity

A

less affinity/active to alpha 1 than NA
more affinity/active to presynpatic alpha 2 than NA
therefore less vasoconstriction and more inhibition of NA release

36
Q

why is alpha methyl NA good at its job

A

it is not degraded by MAO-O so it accumulates in the synaptic cleft in larger quantities than NA, so it displaces NA from the vesicles

37
Q

clinical use of methydopa

A

renal disease
cerebrovascular disease
[helps maintain blood flow to these regions]

hypertension, e.g. in pregnant women as it has no adverse effects despite crossing the placenta

38
Q

adverse effects of methyldopa

A 
dry mouth (reduced salivations) 
sedation 
orthostatic hypotension
male sexual dysfunction
39
Q

what is an arrhythmia?

A

abnormal or irregular heart beat mainly caused by myocardial ischaemia

40
Q

why do SNS antagonists need to be used to treat arrhythmias?

A

SNS activity exacerbates arrhythmia via beta 1, especially after ischaemia
AV conductance depends on SNS activity

41
Q

what drug is usually used to treat arrhythmias?

A

propanolol (non selective beta antagonist, class II)

  • reduced mortality of patients with myocardial ischemia
  • works particularly well in cases that occur during exercise or mental stress
42
Q

what is angina?

A

chest pain due to insufficient O2 supply to myocardium, so it is unable to meet its demands

43
Q

referred pain of angina

A

spreads down dermatome T1 in the chest, arm and neck

brought on by exertion of excitement

44
Q

types of angina

A

stable
unstable
variable

45
Q

stable angina

A

fine at rest, pain on exertion due to fixed narrowing of coronary vessels

46
Q

unstable angina

A

pain with less exertion and at rest

thrombus without the complete occlusion of the vessel

47
Q

variable angina

A

at rest, caused by coronary artery spasm , associated with atheromatous disease

48
Q

what are the 3 ways beta blockers ease angina?

A

reduce myocardial demand by:

  • decrease inotropic effect (contractility)
  • decrease chronotropic effect (heart rate)
  • decrease systolic pressure

at low effects does not affect bronchial smooth muscle

49
Q

adverse effects of beta adrenoreceptor antagonist

A 
fatigue 
insomnia 
dizziness
sexual dysfunction 
bronchospasm 
bradycardia
heart block
hypotension

therefore not used in patients where this can be exacerbated e..g congestive heart failure

50
Q

what is glaucoma?

A

an increase in intraocular pressure due to the poor drainage of aqueous humour

can permanently damage the optic nerve

51
Q

how is aqueous humour produced?

A

by blood vessels in the ciliary body
uses carbonic anhydrase
indirectly related to BP (fluid leakage used)

52
Q

what is the flow pathway of aqueous humour?

A 
ciliary body 
posterior chamber
pupil 
anterior chamber
trabecular meshwork 
into veins and canal of Schlemm
53
Q

examples of beta adr. antagonists used in glaucoma treatment

A

carteolol hydrochloride
levobunolol hydrochloride
timolol maleate

non selective of beta 1 and 2

betaxolol hydrochloride is beta 1 selective

54
Q

what is the effect of glaucoma medication?

A

reduce the rate of which aqueous humour is produced by blocking Beta-1 and stimulating alpha 2 on the ciliary body

55
Q

what effect does beta 1 blockade have?

A

vasodilation and fall in total peripheral resistance and BP

antagonises noradrenaline on the heart
also effects on kidney

56
Q

what are the main mediators of peripheral resistance?

A

alpha 1 receptors

therefore alpha blockade causes rapid fall in arterial pressure

57
Q

how does non-selective alpha antagonism lead to drop in peripheral resistance and therefore BP?

A
  • subcutaneous vasodilation

- increased flow through cutaneous and splanchnic vascular beds

58
Q

which cells of the adrenal medulla is impacted by phaechromocytoma?

A

chromaffin cells

59
Q

what is phentolamine used for?

A

phaechromocytoma induced hypertension

60
Q

what is the negative consequence of using a non selective alpha antagonist like phentolamine?

A
  • can bind to alpha 2
  • less inhibition of NA release
  • enhanced reflex tachycardia
61
Q

what is the benefit of using an alpha 1 selective antagonist over a non-selective alpha antagonist?

A

e.g. prazosin over phentolamine

less reflex tachycardia as there is no alpha 2 blockade

62
Q

what is the main effect of methyldopa?

A

as a false transmitter it is most active on pre-synaptic alpha 2

auto-inhibitor of NA release

stimulates vasopressor centre in brainstem–> reduced sympathetic outflow

63
Q

what aggravates arrhythmia?

A

increases sympathetic drive to the heart via beta 1

particularly after MI where there is an increase in sympathetic tone

64
Q

what does AV conductance depend on ?

A

sympathetic activity via beta 1

65
Q

what effect do beta antagonists have on the refractory period?

A

increases the refractory period to slow ventricular rate by interfering with AV conductance

66
Q

what effect do beta antagonists have in glaucoma?

A

reduces aqueous humour production

67
Q

how is aqueous humour production indirectly linked to blood pressure?

A

increased blood flow to ciliary body means more production of aqueous humour

LCRS Pharma (32 decks)

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