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hypertension pharmacology Flashcards

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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
NICE guidelines - 3rd step for hypertension in <55
ACE inhibitor, calcium channel blocker and thiazide-type diuretic
26
NICE guidelines - 1st step for hypertension in >55 or black patients of any age
calcium-channel blocker or thiazaide-type diuretic
27
NICE guidelines - 2nd step for hypertension in >55 or black patients of any age
add an ACE inhibitor to calcium -channel blocker or thiazide-type diuretic
28
NICE guidelines - 3rd step for hypertension in >55 or black patients of any age
ACE inhibitor, calcium channel blocker and thiazide- type diuretic
29
NICE guidelines for if all 3 drug types doesn't work for hypertension?
add more diuretic therapy or alpha blocker or beta blocker
30
prescribing ACE inhibitors
if not tolerated offer angio-tensin 2 receptor antagonist, if both are not tolerated consider beta blocker.
31
considerations when prescribing beta blockers
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
renin angiotensin aldosterone system
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
what does angiotensin 2 do?
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
what does aldosterone do?
increases H2O retention
35
what does ADH do?
increase H2O absorption from collecting duct
36
what is the overall result of RAAS?
water and salt retention effective circulating volume increases perfusion of juuxtaglomerular apparatus increases
37
examples of ACE inhibitors
ramipril and enalapril
38
how do ACE inhibitors work?
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
cautions of ACE inhibitors
common cause of dry cough beware of use in renal artery stenosis cannot be used in pregnancy
40
examples of Angiotensin 2 receptor blockers
losartan and candesartan
41
when are ARBs used?
as an alternative to ACE inhibitors
42
how do ARBs work?
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
how do calcium channel blockers work?
prevents calcium entry so smooth muscle contraction cannot occur and relaxes arterioles, coronary arteries and heart muscle - vasodilation
44
how do smooth muscles contract?
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
examples of calcium channel blockers
amlodipine | nifedipine
46
cautions of calcium channel blockers
commonly cause ankle swelling | beware in heart failure as reduces contractility and heart failure already shows reduced contractility
47
effect of calcium channel blockers on heart
some types - verapamil and dilitiazem slow HR and decrease contractility
48
what do diuretics do?
lead to reduced sodium and less water reabsorption so reduces blood volume
49
examples of thiazide-type diuretics
indapamide chlortalidone normally end in -ide
50
how do thiazide diuretics work?
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
beta 1 receptors in the heart
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
how do beta blockers work?
``` 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
what is chronotropy?
heart rate
54
what is inotropy?
contractility
55
what is dromotropy?
electrical conduction
56
what is lusitropy?
relaxation
57
contraindications of beta blockers
avoid in asthma | don't give with rate limiting calcium channel blocker - risk of complete heart block
58
alpha 1 antagonist examples
doxazosin
59
how do alpha 1 antagonists work?
block alpha 1 receptors so noradrenaline cannot bind reduces the sympathetic response relative vasodilation so reduces stroke volume
60
when are alpha 1 antagonists used?
in conjunction with other medications
61
examples of alpha 2 agonists
methyldopa
62
how do alpha 2 agonists work?
``` act on presynaptic autoreceptors in CNS inhibit release of noradrenaline reduces sympathetic outflow increases vagal outflow reduces peripheral arterial and venous tone ```
63
when are alpha 2 agonists used?
mainly for hypertension in pregnancy | unwanted side effects so rarely used
64
side effects of alpha 2 agonists
``` exertion/ postural hypotension dry mouth diarrhoea sedation/ drowsiness fluid retention/ oedema ```
65
hypertension in pregnancy
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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