Hypertension Flashcards by Katherine Chulack

What is a QRISK?

a prediction algorithm for cardiovascular disease (CVD)

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What factors does QRISK take into consideration?

age
systolic BP
smoking status
cholesterol
-
BMI
ethnicity
measures of deprivation
family history
CKD
RA
AF
diabetes
antihypertensive treatment

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What is a normal QRISK score?

<10%

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What is HBPM?

Home Blood Pressure Monitoring

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What is ABPM?

Ambulatory Blood Pressure Monitoring

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If clinic BP is above 140/90 what do we offer pts?

AMPM or HBPM

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What are the 2 most commonly prescribed calcium channel blockers? What are the starting doses for each?

amlodipine and felodipine

5mg each

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What are the target, location and effect of amlodipine and felodipine?

target: L type Ca2+ channel
location: vascular smooth muscle cell
effect: decreased muscular contraction -> reduced vasoconstriction -> reduced peripheral resistance -> reduce bp

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Pharmacokinetic parameters:

What is “clearance”?

a measure of the ability of the body to eliminate a drug

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Pharmacokinetic parameters:

What is “elimination half-life”?

the length of time required for the conc of a particular drug to decrease to half of its starting dose in the body

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What is the term used to describe the measure of the ability of the body to eliminate a drug?

clearance

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What is the term used to describe the length of time required for the conc of a particular drug to decrease to half of its starting dose in the body?

elimination half-life

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Pharmacokinetic parameters:

What is “time to peak plasma concentration levels”?

Time to peak concentration is the time required for a drug to reach peak concentration in plasma.

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How does absorption rate affect time to peak conc?

The faster the absorption rate the lower the time to peak plasma concentration.

What term to we used to describe the time required for a drug to reach peak concentration in plasma?

time to peak plasma concentration levels

What term to we used to describe the time required for a drug to reach peak concentration in plasma?

time to peak plasma concentration levels

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

(target, location, effect)

target: ACE
location: lungs + kidney
effect: less angiotensin II, which is causes vasoconstriction and also stimulates aldosterone production

Why are ACEi typically used ahead of ARBs?

cost
evidence shows ACEi more effective

What does ARB stand for?

angiotensin 2 receptor blocker

What demographic of pts would we use ARB over ACEi for?

African or caribbean descent

ACEis and ARBs are contraindicated with bilateral renal artery stenosis. Why?

pressure in glomerulus is dependent on angiotensin 2, so with ACEI, eGFR will decrease

ACEis and ARBs are contraindicated with bilateral renal artery stenosis. Why?

pressure in glomerulus is dependent on angiotensin 2, so with ACEI, eGFR will decrease

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

prodrug: inactive before metabolism

Name an example of a thiazide-like diuretic.

indapamide

What is the mechanism of action of indapamide? (target, location, effect)

target: NaCl symporter on apical side location: distal tubule cell effect: Na+ and H2O loss -> decreased blood vol, venous return andcardiac output

Why might ACE inhibitors have a negative effect on eGFR and serum potassium?

pressure in glomerulus is dependent on angiotensin 2, so with ACEI, eGFR will decrease "ACE inhibitors and ARBs reduce proteinuria by lowering the intraglomerular pressure, reducing hyperfiltration. These drugs tend to raise the serum potassium level and reduce the glomerular filtration rate (GFR)."

Why do thiazides increase potassium excretion?

The diuretic effect of thiazides only lasts about 1-2 weeks. Why? Why do we continue treatment as an anti-hypertensive if this is the case?

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. The continuing anti-hypertensive effect of thiazides is due to a further (less well understood) vaso-dilating action.

Indapamide (and other thiazide-like diuretics) are excreted unchanged in the urine. Why is this a vital part of the therapeutic action of thiazide-like diuretics?

The diuretic (labelled OA) needs to move from; - The blood - Transported on basolateral side - Transporter on apical side Only then can it access the sodium chloride transporter on the apical side of distal tubule