Hypertension Flashcards

1
Q

What is the main goal of the treatment for hypertension?

A

A reduction in blood pressure and when this involves drug treatment, should inolve as few side effects as possible.

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2
Q

what are specific goals of the treatment of hypertension?

A
  • Red in cardiovascular damage
  • Preservation of renal function
  • Limitation or reversal of left ventricular hypertrophy
  • Prev of IHD
  • Red in mortality due to stroke and MIs
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3
Q

What is stage 1 Hypertension?

A
  • BP measurement > 140/90mmHg
  • Patient given ambulatory BP monitoring (ABPM) or home BP monitoring (HBPM) in the daytime over 1 week.
  • Hypertension if avg ABPM or HBPM bp>135/85
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4
Q

What is stage 2 hypertension?

A
  • BP measurement>160/100mmHg & monitoring avg BP is> 150/95
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5
Q

What is severe hypertension?

A

BP measurement>180mmHg or diastolic bp>110mmHg

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6
Q

How do you treat hypertension?

A

Lifestyle changes play a central and primary role:
* Red overall cardiovascular risk:
1. Alcohol consumption red-huge component
* Weight reduction
* Red excess caffeine
* Red fat and salt intake-DASH diet
* Inc fruit and oily fish in the diet
* Inc excercise
* smoking cessation

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7
Q

When do you use pharmacological intervention?

A
  1. Stage 1 if evidence of organ damage or renal disease/diabetes
    * Otherwise lifestyle interventions
  2. Anyone with stage 2 hypertension
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8
Q

Treatment steps for newly diagnosed hypertension.

A

Step 1: (If < 55Yo) ACEinhib
Step 1: (if >55yo or black pt) Ca2+ channel blocker
Step 2: ACEI + Ca2+ channel blocker
Step 3:ACEI + Ca2+ channel blocker + thiazide
Step 4:Add further diuretic, A-blocker or B-blocker

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9
Q

What is ACEI?

A
  • Angiotensin-converting enzyme inhibitor (e.g. captopril, enalapril, lisinopril etc)
  • Inhibits the enzyme that converts angiotensin 1 into angiotensin 2
  • Angiotensin 2 leads to vasoconstriction and aldosterone production-(leads to red in salt and water retention)
  • (also potentiate bradykinin-cough)
  • (Bradykinin:Vasodilator-cont to dec BP)
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10
Q

What are some adverse effects of ACEIs?

A
  • Cough in 10% of patients
  • First dose hypotension
  • May inc potassium-effects on kidney
  • Angioedema-swelling of lips, tongue, and face.
  • Bradykinin inc the permeability of blood vessels-more fluid into tissues.
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11
Q

What are AT1 receptor antagonists?

A
  • e.g. candesartan,losartan
  • Block action of A-II at AT1 receptor
  • These agents have similar consequences as ACEIs but do not give rise to the cough.
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12
Q

What is Aliskiren?

A
  • New to therapy
  • Acts via inhibition of renin (angiotensis activation)
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13
Q

What is Spironolactone?

A
  • Aldosterone receptor antagonist
  • Resistant hypertension
  • Main use in heart failure
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14
Q

Why are there differences in RAAS activity?

A
  • Drugs targeting RAAS are less effective in black patients. incl. aliskiren
  • Lower renin activity
  • Leads to inc salt and water retention in the kidney-inc risk of hypertension in black patients
  • Diuretics more effective in black patients as a result
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15
Q

What are Ca channel blockers?

A
  • Dihydropyridines, e.g. felodipine, nifedipine
  • Inhibit voltage gated Ca channels on smooth muscle-> vasodilation and a red in BP
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16
Q

What are Ca channel blockers (NON-DHPs)?

A
  • Verpamil-Blocks cardiac L-type Ca channel (CaV1.2)
    1. Dec HR and DEc CO
  • Diltiazem-effects heart and smooth muscle
17
Q

What are side effects of Ca channel blockers?

A
  • Constipation-block of smooth muscle in GI tract
  • Oedema-Block of smooth muscle in veins
18
Q

What are diuretics?(1)

A
  • Thiazide-like e.g. chloratidone and indapamide
  • Thiazides (e.g. bendroflumethiazide)
  • Inhibit Na+/Cl- reabsorption in distal convoluted tubule
  • Leads to diuresis
  • Red in circulating vol-red BP
  • Hypokalaemia (dec K+)
19
Q

What is vasodilation?

A
  • Mechanism not clear.
  • Continues after diuretic effect has finished(body adapts after 4-6 weeks)
  • Direct effect on smooth muscle or endothelium?
  • Indirect through reduction in plasma volume?

See PP

20
Q

What are diuretics? (2) (problems)

A
  • Dependant on good renal functions
  • Ineffective in moderate renal impairment
  • Important side effects
    1. Hypokalaemia
    2. Postural hypotension(standing up-redistribution-dizzy)
21
Q

What are B-adrenoreceptor antagonists?(beta-blockers)(1)

A
  • E.g. atenolol,propanolol
  • Block action of noradrenaline(and adrenaline) on heart
  • B1 ARs in SAN-blockers dec rate of contraction
  • B1 ARs in ventricles muscle and atria-blockers dec force of contraction
  • Dec CO
22
Q

What are problems with B-adrenoreceptor antagonists?(beta-blockers)

A
  • Limited by the fact that B-adrenoreceptors on vascular smooth muscle casues vasodilation
  • Not first line treatment for hypertension, but useful in cardiac ischaemia (e.g. angina)
  • Antagonise B-adrenoreceptors in airways-bronchoconstriction
  • Mainly B2 adrenoreceptors in airways, B1 adrenoreceptors in heart (but not exclusive)
  • Contraindicated in asthma (exacerbate breathing issues)
23
Q

What is propanolol?

A
  • Non-selective for B1 and B2 ARs
24
Q

What is Atenolol?

A
  • “Selective” but ~5X more selective than B1 over B2 ARs
25
Q

Side effects of Beta-blockers?

A
  • Bronchospasm
  • Red hypoglucaemic awareness
26
Q

What are a-adrenoreceptor antagonists?

A
  • a1-adrenoreceptors-present on vascular smooth muscle-causes vasoconstriction
  • Antagonists e.g. doxazosin, prazosin
  • Competitive receptor antagonists pf a1-adrenoreceptors
  • Last choice antihypertensives
    1. Widespread side effects, which makes them poorly tolerated.
27
Q

When are Beta-blockers used?

A
  • In patient with angina or past MI
  • Child bearing
  • Inc sympathetic drive
  • Intolerance to ACEIs/ATRA