vascular system Flashcards

vasoactive drugs: identify the drugs that impact vascular tone, their mechanisms of actions and their side-effects

1
Q

step 1 hypertension treatment for under 55s

A

ACE inhibitor or angiotensin receptor blocker (ARB)

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2
Q

step 1 hypertension treatment for over 55s or afro-Caribbean’s

A

Ca2+ channel blocker (CCB) or thiazide-like diuretic

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3
Q

step 2 hypertension treatment

A

CCB or thiazide-like diuretic and ACE inhibitor or ARB

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4
Q

step 2 hypertension treatment for afro-Caribbean’s

A

same, but ARBs preferred to ACE inhibitors

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5
Q

step 3 hypertension treatment

A

combination of ACE inhibitor/ARB with CCB and thiazide-like diuretic

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6
Q

step 4 resistant hypertension treatment

A

low dose spironolactone, B-blocker or a-blocker

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7
Q

2 reactions ACE inhibitors prevent

A

angiotensin I -> angiotensin II; bradykinin -> inactive metabolites

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8
Q

3 stimuli for renin

A

decreased renal Na+ reabsorption, decreased renal perfusion pressure, increased SNS

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9
Q

4 normal angiotensin II actions

A

SNS activation and thirst, vasoconstriction, direct salt and water retention, aldosterone secretion (indirect salt and water retention)

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10
Q

6 uses of ACE inhibitors

A

hypertension, heart failure, post-myocardial infarction, diabetic nephropathy, progressive renal insufficiency, patients at high risk of cardiovascular disease

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11
Q

example of ACE inhibitor

A

enalapril (usually -pril)

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12
Q

what will ACE inhibitors help treat by decreasing TPR and venous return

A

hypertension and heart failure

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13
Q

how do increased TPR and increased venous return worsen hypertension

A

increased TPR directly contributes to increased BP, and increased venous return leads to increased cardiac contractility (via Starling’s Law), and thus cardiac output and BP

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14
Q

how do increased TPR and increased venous return worsen heart failure

A

increased vasoconstriction increases afterload and cardiac work, and increased venous return leads to long term fluid retention and congestion, leading to oedema

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15
Q

example of ARB

A

iosartan

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16
Q

mechanism of ARB action

A

antagonist of type 1 (AT1) receptors for angiotensin II, preventing renal and vascular actions of angiotensin II (same outcome as ACE inhibitors)

17
Q

2 uses of ARB

A

hypertension, heart failure (same as ACE inhibitors)

18
Q

are ACE inhibitors and ARB well tolerated

A

yes, particularly ARB

19
Q

3 side effects of both ACE inhibitors and ARB

A

hypotension (e.g. dizziness, postural), hyperkalaemia, renal failure in patients with renal artery stenosis

20
Q

how do ACE inhibitors and ARB cause renal failure in patients with renal artery stenosis

A

angiotensin II controls pressure in glomerulus (constricts efferent arteriole, increasing pressure), so if pressure falls then can’t regulate glomerular filtration pressure

21
Q

side effect of just ACE inhibitors and why

A

build up of bradykinin so cough

22
Q

how do ACE inhibitors and ARB cause hyperkalaemia

A

by stopping Na+ reabsorption to lower blood volume, K+ exchange is not occuring so builds up in blood

23
Q

how is hyperkalaemia cared with

A

K+ supplements or K+ sparing diuretics

24
Q

process of smooth muscle contraction

A

membrane depolarisation opens VGCC -> Ca2+ enters -> binds to calmodulin (CaM) -> Ca2+-CaM complex binds to and activates myosin light chain kinase (MLCK) -> MLCK mediated phosphorylation -> smooth muscle contraction

25
Q

2 classes of Ca2+ channel blockers

A

dihydropyridines, non-dihydropyridines (rate-limiting)

26
Q

uses of dihydropyridine Ca2+ channel blockers

A

hypertension, prophylaxis of angina, as more selective for blood vessels

27
Q

example of dihydropyridine Ca2+ channel blocker

A

amiodipine

28
Q

example of non-dihydropyridine Ca2+ channel blocker

A

verapamil

29
Q

what doesn’t amiodipine cause in heart, which verapamil does

A

negative inotropy

30
Q

how do dihydropyridine Ca2+ channel blockers treat hypertension

A

inhibit Ca2+ entry into VSMCs, decreasing TPR and BP

31
Q

side effect of using dihydropyridine Ca2+ channel blockers to treat hypertension

A

powerful vasodilation can lead to reflex tachycardia and increased inotropy, thus increasing myocardial oxygen demand

32
Q

how are anti-hypertensives selected for treatment

A

based on compliance (usually due to side effects); select CCB or thiazide-type diuretic (e.g. afro-Caribbeans) because of low plasma renin activity; evidence of effects on heart failure, stroke, death etc.

33
Q

drugs for hypertension: RAS inhibitors vs CCBs outcomes on SBP, heart failure, stroke and all-cause death

A

CCBs decrease SBP more than RAS inhibitors, RAS inhibitors decrease heart failure but increase stroke, with no difference for all-cause death

34
Q

drugs for hypertension: RAS inhibitors vs thiazides outcomes on SBP, heart failure, stroke and all-cause death

A

thiazides decrease SBP more than RAS inhibitors, RAS inhibitors increase heart failure and stroke; no difference for all-cause death

35
Q

drugs for hypertension: RAS inhibitors vs B-blockers outcomes on SBP, CV events, stroke and all-cause death

A

no difference in SBP reduction, RAS inhibitors decrease CV events and stroke; no difference for all-cause death

36
Q

why might a1-adrenoceptor antagonists e.g. prazosin be used as anti-hypertensives

A

a1 adrenoceptors cause vasoconstriction, so this is blocked, lowering TPR