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Physiology > hypertension pharmacology > Flashcards

hypertension pharmacology Flashcards

1
Q

why does hypertension need treating?

A

accounts for more CV deaths than any other modifiable cardiac risk factor. It is responsible for over half of the deaths due to coronary heart disease and stroke

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2
Q

stage 1 hypertension

A

clinical BP = 140/90mmHg

home BP = 135/85mmHg or higher

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3
Q

what is ambulatory BP monitoring?

A

constant BP monitoring

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4
Q

stage 2 hypertension

A

clinical BP = 160/100mmHg or higher and home BP = 150/95mmHg

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5
Q

severe hypertension

A

clinical BP = 180mmHg or higher systolic or diastolic over 110mmHg

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6
Q

what to do if someone has severe hypertension?

A

look for concerning signs of hypertension emergency

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7
Q

what are concerning signs of severe hypertension?

A 
papilloedema 
retinal haemorrhage 
MI
aortic dissection
Stroke
rapid renal failure
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8
Q

when to treat stage 1 hypertension with anti-hypertensives?

A

patients younger than 80 and target-organ damage. Those with other cardiovascular risks - renal disease, diabetes or a 10 year cardiovascular risk over 20%

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9
Q

when to treat stage 2 hypertension?

A

always treat, regardless of age

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10
Q

when/ how to treat severe hypertension?

A

treat promptly

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11
Q

lifestyle modification

A 
smoking cessation
weight reduction
reduction of excessive intake of alcohol and caffeine
reduction of dietary salf
reduction of total and saturated fat
increasing exercise
increasing fruit and veg intake
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12
Q

what determines cardiac output?

A

heart rate
contractility - stroke volume
arterial pressure - afterload
filling pressure - preload

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13
Q

how to calculate BP?

A

Cardiac output x total peripheral resistance

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14
Q

how to calculate cardiac output?

A

HR x stroke volume

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15
Q

what is a decrease in blood volume?

A

hypovolaemia

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16
Q

what happens during hypovolaemia?

A

decreases cardiac filling - preload

reduces stroke work, cardiac output and arterial BP

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17
Q

what is starling’s law?

A

stroke volume of the heart increases in response to an increase in the volume of blood in the ventricles before contraction when all other factors remain constant
as a larger volume of blood flows into the ventricle the blood stretches the cardiac muscle fibres leading to an increase in force of contraction

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18
Q

what is hypervolaemia?

A

increase in blood volume

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19
Q

what happens during hypervolaemia?

A

increases cardiac filling

increases stroke work, cardiac output and arterial BP

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20
Q

what is preload?

A

initial stretching of cardiac myocytes prior to contraction. related to ventricular filling

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21
Q

what is after load?

A

force or load against which the heart has to contract to expel blood

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22
Q

how to decrease BP?

A 
decrease arterial pressure - afterload
decrease filling - preload
decrease blood volume
decrease HR
decrease sympathetic activity
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23
Q

NICE guidelines - 1st step for hypertension in <55

A

ACE inhibitor

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24
Q

NICE guidelines - 2nd step for hypertension in <55

A

ACE inhibitor and calcium channel blocker or ACE inhibitor and thiazide-type diuretic

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25
Q

NICE guidelines - 3rd step for hypertension in <55

A

ACE inhibitor, calcium channel blocker and thiazide-type diuretic

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26
Q

NICE guidelines - 1st step for hypertension in >55 or black patients of any age

A

calcium-channel blocker or thiazaide-type diuretic

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27
Q

NICE guidelines - 2nd step for hypertension in >55 or black patients of any age

A

add an ACE inhibitor to calcium -channel blocker or thiazide-type diuretic

28
Q

NICE guidelines - 3rd step for hypertension in >55 or black patients of any age

A

ACE inhibitor, calcium channel blocker and thiazide- type diuretic

29
Q

NICE guidelines for if all 3 drug types doesn’t work for hypertension?

A

add more diuretic therapy or alpha blocker or beta blocker

30
Q

prescribing ACE inhibitors

A

if not tolerated offer angio-tensin 2 receptor antagonist, if both are not tolerated consider beta blocker.

31
Q

considerations when prescribing beta blockers

A

especially in combination with thiazide-type diuretics beta blockers should not be given to people with uncomplicated hypertension and diabetes or those who have a high risk of developing diabetes

32
Q

renin angiotensin aldosterone system

A

RAAS
liver secretes angiotensinogen which causes the kidney to release renin.
angiotensinogen forms angiotensin 1 due to renin which then forms angiotensin 2 in response to ACE

33
Q

what does angiotensin 2 do?

A

increases sympathetic activity
increases tubular sodium and chlorine ion reabsorption and potassium excretion
causes H2O retention
causes the adrenal cortex to produce aldosterone
increases arteriolar vasoconstriction to increase BP
increases release of ADH from posterior pituitary

34
Q

what does aldosterone do?

A

increases H2O retention

35
Q

what does ADH do?

A

increase H2O absorption from collecting duct

36
Q

what is the overall result of RAAS?

A

water and salt retention
effective circulating volume increases
perfusion of juuxtaglomerular apparatus increases

37
Q

examples of ACE inhibitors

A

ramipril and enalapril

38
Q

how do ACE inhibitors work?

A

interfere with renin-angiotensin-aldosterone system
block conversion of angiotensin 1 to 2
reduces circulating angiotensin 2
causing arterial dilation
ACE also converts bradykinin so reduced ACE increases bradykinin increasing vasodilation so reduces vascular resistance

39
Q

cautions of ACE inhibitors

A

common cause of dry cough
beware of use in renal artery stenosis
cannot be used in pregnancy

40
Q

examples of Angiotensin 2 receptor blockers

A

losartan and candesartan

41
Q

when are ARBs used?

A

as an alternative to ACE inhibitors

42
Q

how do ARBs work?

A

block angiotensin 2 receptors
angiotensin 2 normally causes constriction of blood vessels and released of aldosterone which increases sodium and water reabsorption from kidney so these drugs prevent this

43
Q

how do calcium channel blockers work?

A

prevents calcium entry so smooth muscle contraction cannot occur and relaxes arterioles, coronary arteries and heart muscle - vasodilation

44
Q

how do smooth muscles contract?

A

increase in free intracellular calcium
calcium binds to calmodulin binding protein
calcium-calmodulin activates myosin light chain kinase which phosphorylates myosin light chain in the presence of ATP
this leads to cross-bridge formation between myosin heads and actin filaments so causes smooth muscle contraction

45
Q

examples of calcium channel blockers

A

amlodipine

nifedipine

46
Q

cautions of calcium channel blockers

A

commonly cause ankle swelling

beware in heart failure as reduces contractility and heart failure already shows reduced contractility

47
Q

effect of calcium channel blockers on heart

A

some types - verapamil and dilitiazem slow HR and decrease contractility

48
Q

what do diuretics do?

A

lead to reduced sodium and less water reabsorption so reduces blood volume

49
Q

examples of thiazide-type diuretics

A

indapamide
chlortalidone
normally end in -ide

50
Q

how do thiazide diuretics work?

A

block NaCl co-transporter
reduce sodium ion absorption at distal convoluted tubule in kidney
results in higher osmolarity of urine and decreased water reabsorption
effect is self-limiting as lower blood volume activates RAAS

51
Q

beta 1 receptors in the heart

A

noradrenaline or adrenaline bind to the receptors in the heart. They are GPCRs - Gs so activate adenyl cyclase to form cAMP from ATP . cAMP activates a cAMP-dependent protein kinase A which phosphorylates L-type calcium channels and cause increased calcium entry into the cell. This increases contractility and heart rate.

52
Q

how do beta blockers work?

A 
block sympathetic activation of beta 1 receptors, prevent binding of adrenaline or noradrenaline. 
reduce HR
reduce strength of contractions
decrease conduction velocity
decrease relaxation rate
53
Q

what is chronotropy?

A

heart rate

54
Q

what is inotropy?

A

contractility

55
Q

what is dromotropy?

A

electrical conduction

56
Q

what is lusitropy?

A

relaxation

57
Q

contraindications of beta blockers

A

avoid in asthma

don’t give with rate limiting calcium channel blocker - risk of complete heart block

58
Q

alpha 1 antagonist examples

A

doxazosin

59
Q

how do alpha 1 antagonists work?

A

block alpha 1 receptors so noradrenaline cannot bind
reduces the sympathetic response
relative vasodilation so reduces stroke volume

60
Q

when are alpha 1 antagonists used?

A

in conjunction with other medications

61
Q

examples of alpha 2 agonists

A

methyldopa

62
Q

how do alpha 2 agonists work?

A 
act on presynaptic autoreceptors in CNS 
inhibit release of noradrenaline 
reduces sympathetic outflow 
increases vagal outflow
reduces peripheral arterial and venous tone
63
Q

when are alpha 2 agonists used?

A

mainly for hypertension in pregnancy

unwanted side effects so rarely used

64
Q

side effects of alpha 2 agonists

A 
exertion/ postural hypotension
dry mouth
diarrhoea
sedation/ drowsiness
fluid retention/ oedema
65
Q

hypertension in pregnancy

A

hypertensive complications in pregnancy can be hazardous for the mother and fetus and are associated with a significant risk of morbidity and mortality
can cause premature labour

Physiology (46 decks)

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