**_💊Pharmacology💊 - Hypertension Flashcards

1
Q

What are the therapeutic objectives with hypertension?

A

Set reasonable blood pressure reduction goals
Reduce cardiovascular risk associated with increased morbidity and mortality

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2
Q

What is the first threshold for blood pressure management?

A

Under 135/85mmHg - monitor at least every 5 years

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3
Q

What is the threshold for stage 1 hypertension, and what are the treatment options?

A

135/85 to 149/94
BP above 140/90, ABPM/HBPM offered
Start drug treatment if any of the following:
Target organ damage
CVD
Renal disease
Diabetes
10 year CVD risk >10%

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4
Q

What is the threshold for stage 2 hypertension?

A

150/95
Start drug treatment immediately

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5
Q

What are the NICE guideline first line hypertension treatments?

A

Calcium channel blockers
Amlodipine & felodipine common examples

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6
Q

What is the mechanism of action of calcium channel blockers?

A
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7
Q

What is drug clearance?

A

Clearance is the measure of the ability of the body to eliminate a drug
Clearance by means of various organs of elimination is additive
Elimination of drug may occur as a result of processes that occur in the liver, kidney, and other organs

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8
Q

What is the elimination half-life of a drug?

A

Elimination half-life is the length of time required for the concentration of a particular drug to decreasetohalf of itsstarting dose in the body

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9
Q

What is a drug’s time to peak plasma levels?

A

The time required for a drug to reach peak concentration in plasma
The faster the absorption rate, the lower is the time to peak plasma concentration

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10
Q

What does this information tell us about the difference between amlodipine and felodipine?

A

Felodipine is faster acting and shorter lasting - shorter half-life, possibly due to plasma clearance
Plasma clearance and elimination half-life always linked

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11
Q

What advantages does amlodipine have over felodipine?

A

Longest lasting
Less pronounced reflex tachychardia due to slower onset

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12
Q

What is reflex tachycardia?

A

Drop in systolic and diastolic blood pressure stimulates baroreceptors in the heart
Causes heart to increase rate of contraction to maintain blood flow and perfusion

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13
Q

What is the most common next line treatment after calcium channel blockers to manage hypertension?

A

ACE inhibitors

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14
Q

What is the mechanism of action of ACE inhibitors in the treatment of hypertension?

A

Prevents production of Angiotensin II
Prevents degradation of bradykinins

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15
Q

How does stopping the production of angiotensin 2 lower blood pressurs?

A

Angiotensin 2 causes:
Vasoconstriction
Salt (and therefore water) retention in the kidneys
Stimulates aldosterone secretion in the adrenals

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16
Q

When should ARB (andgiotensin 2 receptor blockers) be used instead of ACE inhibitors?

A

Patients over 65
Patients of African or Caribbean descent
Renin system is less sensitive making ARBs more effective

17
Q

When are ACE inhibitors contraindicated?

A

Patients with renal artery stenosis need increased BP to maintain renal perfusion

18
Q

What is the difference between a pro drug and an active drug?

A
19
Q

Why might someone waiting for surgery not take ACE inhibitors?

A

Can raise serum potassium levels
Can lead to cancellation of surgery

20
Q

What are the next treatment options for hypertension after calcium channel blockers?

A

Thiazide-like diuretics

21
Q

What is the mechanism of action of Thiazide-like diuretics?

A

Inhibits Na+/Cl- co transporter it DCT
Increased Na+ and therefore H2O loss
Lowers blood volume, decreases BP

22
Q

Why is it important that thiazide-like diuretics are excreted unchanged in urine?

A

Need to move from the blood, to basolateral transporter, to the apical transporter to reach the sodium chloride transporter (i.e. it is in the filtrate/urine when it has its effect, so must be present there unchanged)

23
Q

Why do thiazide-like diuretics increase potassium excretion?

A
24
Q

What is an important note about the length of time for which thiazides can be used?

A

The diuretic effect of thiazides only lasts for 1-2 weeks
The kidney becomes tolerant to the diuretics because there is a rebound activation of the renin angiotensin system which counteracts the diuretic effect due to increasing sodium reabsorption
Any continuing anti-hypertensive effect is due to a further (less well understood) vasodilating action

25
Q

What is the primary mechanism of action of ACE inhibitors?

A

Inhibits angiotensin converting enzyme, and therefore production of angiotensin 2

26
Q

What is the primary mechanism of action of calcium channel blockers

A

Blocks L-type calcium channels, predominantly on vascular smooth muscle
Prevents calcium influx, therefore stopping contraction and promoting vasodilation

27
Q

What is the primary mechanism of action of thiazide/thiazide-like diuretics?

A

Block the Na+/Cl- co transporter
Na+ reabsorption limited

28
Q

What is the primary mechanism of action of angiotensin receptor blockers?

A

Non-competitive antagonists of the AT1 receptor (found in kidneys and vasculature)

29
Q

What is the target of ACE inhibitors?

A

Angiotensin converting enzyme

30
Q

What is the target of calcium channel blockers?

A

L-type calcium channels
(Predominantly in vascular smooth muscle)

31
Q

What is the target of thiazide/thiazide-like diuretcs?

A

Sodium/chloride cotransporter

32
Q

What is the target of angiotensin receptor blockers?

A

Angiotensin receptors

33
Q

What are the side effects of ACE inhibitors?

A

Cough
Hypotension
Hyperkalaemia
Foetal injury (AVOID IN PREGNANT WOMEN)
Renal failure (in cases of renal artery stenosis)
Urticaria/angioedema

34
Q

What are the side effects of calcium channel blockers?

A

Ankle oedema
Constipation
Palpitations
Flushing/headaches

35
Q

What are the side effects of thiazide/thiazide-like diuretics?

A

Hypokalaemia
Hyponatraemia
Metabolic alkalosis (due to increased H+ excretion)
Hypercalcaemia
Hyperglycaemia
Hyperuricaemia

36
Q

What are the side effects of ARBs?

A

Hypotension
Hyperkalaemia
Foetal injury (AVOID IN PREGNANT WOMEN)
Renal failure (in cases of renal artery stenosis)