Hypertension + hypertensive drugs Flashcards

1
Q

why is high BP harmful?

A

risk factor for CHD + strokes

can lead to endothelial cell damage + internal organ damage

excessive strain on heart
-> left ventricular hypertrophy
-> congestive heart failure

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2
Q

cardiovascular risk factors

A

high BP

smoking

high salt intake

alcohol

lack of exercise

obesity

dyslipidaemias

diabetes

genetics

gender/age

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3
Q

stage 1 hypertension

A

clinic BP <140/90 mmHg

ABPM/HBPM < 135/85 mmHg

lifestyle changes

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4
Q

what conditions do patients have to meet to get treatment for stage 1 hypertension?

A

age <80

target organ damage

CV/renal disease

diabetes

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5
Q

stage 2 hypertension

A

clinic BP > 180/120 mmHg

ABPM/HBPM > 150/96 mmHg

= treatment with lifestyle changes

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6
Q

what does hypertensive treatment do

A

reduces total peripheral distance (reduces after load)

reduces SV (lowers BV and preload)

reduces HR

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7
Q

when is low BP detected?

A

carotid sinus

aortic arch

juxtaglomerular cells

macular dense cells sensing less Na+ / Cl- flowing through tubules

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8
Q

what happens when renin is secreted?

A

causes angiotensinogen to be converted to angiotensin I

angiotensin I is converted to angiotensin II by ACE

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9
Q

what does angiotensin II cause?

A

efferent arterioles to constrict more than afferent arteriole

= higher GFR
= proximal tubule to reabsorb more Na+
= more thirsty
= higher BP
= aldosterone release (= kidneys to retain Na+ and H2O)

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10
Q

ACE2

A

counter-regulator of ACE

hydrolyses angiotensin II to angiotensin (1-7)

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11
Q

3 types of antihypertensive drugs

A

ACE inhibitors (ACEI)

ATI receptor blockers (ARBs)

renin inhibitors

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12
Q

ACE on bradykinin

A

reduced

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13
Q

where is bradykinin produced

A

by kiniogen protein in CVS and lungs

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14
Q

effect of ACE inhibitors on bradykinin

A

increased = dry cough

can lead to angioedema (swelling of deeper layers of skin, caused by build-up of fluid)

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15
Q

how do ARBs work

A

block AT1 receptors which lead to reduced aldosterone/vasoconstriction

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16
Q

benefits of ARBs

A

no cough

reduced risk of angioedema

improved tolerance

17
Q

cellular mechanism of potassium channel activators

A

open ATP-sensitive potassium channels

metabolism-dependent (regulated by intracellular ATP:ADP ratio)

higher cytosolic ATP keeps K+ channels closed

18
Q

antihypertensive drug mechanism

A

activation of K+ channels in vascular smooth muscle

membrane hyperpolarisation

closure of L-VACCs

vasorelaxation

19
Q

how are beta-blockers used to treat hypertension?

A

block beta-1 adrenoceptors in heart and kidneys

20
Q

mechanism for alpha-1 adrenoceptor antagonists + their benefits for treating hypertension

A

mechanism = inhibition of post-synaptic alpha-1 adrenocepto on vascular smooth muscle cells

arterial dilation - reduced TPR and cardiac overload

venodilation - reduced cardiac preload + SV