hypertension Flashcards

1
Q

Pharmacological treatment of HTN:

A
  • Angiotensin converting enzyme inhibitors (ACE inhibitors “prils”)
  • Angiotensin II receptor antagonists (A2RA or “sartans”)
  • Calcium channel blocking agents
  • Beta adrenoceptor antagonists (beta-blockers or ‘lol”)
  • Thiazide diuretics
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2
Q

hypertension is a cardiovascular risk factor

A

High blood pressure is a major risk factor for heart disease. It is a medical condition that happens when the pressure of the blood in your arteries and other blood vessels is too high. The high pressure, if not controlled, can affect your heart and other major organs of your body, including your kidneys and brain

ckd
diabetes
MI

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3
Q

Non-pharmacological treatment of HTN

A
  • Non-pharmacological measures first – lifestyle, diet, physical activity, reduction of alcohol, healthy eating, management of OSA, smoking cessation, moderate sodium restriction, weight reduction
  • Mediterranean diet – mono, poly, omega 3 datty acids / reduced intake of saturated fat. Lots of fruits, veg, nuts, vegetables, pasta, olives, olive oil. Limited red meat, processed foods
  • Low fat not always good. Mono, poly, omega 3 fats are good. Some low-fat products have high levels of sugars
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4
Q

ACE Inhibitors

A
  • Inhibit ACE (the enzyme that converts angiotensin I to II) + inhibit the breakdown of bradykinin
  • Reduce vasoconstriction, sodium reabsorption, aldosterone release

Produce a drop in BP by:

  • Inhibiting the production of Angiontensin II leading to vasodilation + a drop in peripheral resistance
  • Reducing the secretion of aldosterone leading to diuresis + sodium loss
  • Increasing bradykinin levels leading to vasodilation + a drop in peripheral resistance
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5
Q

ACE Inhibitors side effects

A
  • Cough
  • Orthostatic (postural) hypotension – dizziness
  • Hyperkalaemia
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6
Q

Angiotensin II Receptor Antagonists

A
  • Prevent angiontensin II from binding to type 1 angiotensin (AT1) receptors on blood vessels – they have the same result as ACE inhibitors
  • Reduce vasoconstriction, sodium reabsorption, aldosterone release

Produce a drop in BP by:

  • Inhibiting angiotensin II induced vasoconstriction leading to vasodilation + a drop in PR
  • Inhibiting the secretion of aldosterone leading to diuresis and sodium loss
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7
Q

Angiotensin II Receptor Antagonists side effects

A
  • Orthostatic hypotension, dizziness

- Hyperkalaemia

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8
Q

Calcium Channel Blocking Agents (calcium channel blockers)

A

Dihydropyridines: primarily inhibit calcium entry into the vascular smooth muscle cells of blood vessels

Non-dihydropyridines: inhibit calcium entry into the vascular smooth muscle cells of blood vessels + cells in the heart, GIT

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9
Q

calcium channel blockers side effects

A

Dihydropyridines
- Hypotension, headache, flushes, reflux, peripheral oedema (ankle)

Non-dihydropyridines:

  • Bradycardia e.g. diltiazem, verapamil
  • Constipation e.g. verapamil
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10
Q

examples of CCB

A

Dihydropyridines: Amlodipine, clevidipine, nifedipine

Non-dihydropyridines: diltiazem, verapamil

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11
Q

Beta Adrenoceptor Antagonists

A
  • Block beta receptors in heart (B1 receptor), lungs (B2 receptor), bladder (B3 receptor) etc
  • Reduce HR, BP, cardiac contractility
  • Depress sinus node rate and slow conduction through AV node

Cardio-selective BBs: just block beta 1 receptors BUT in high doses they may also block beta 2 and 3

MOA in reducing BP (not fully understood):

  • Blocks beta 1 receptors in kidneys – reduces renin release
  • Blocks beta 1 receptors in heart – reduces CO
  • Reduce peripheral resistance
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12
Q

BB side effects

A
  • Wheezing, acute asthmatic attacks in pts with asthma
  • Bradycardia, fatigue, reduced exercise tolerance
  • Cold extremities, aggravation of Raynauds
  • Sleep disturbances, nightmares, impotence
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13
Q

examples of BB

A

Non-selective BBs: Propranolol, bisoprolol

Cardio-selective BBs: atenolol, metoprolol

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14
Q

Diuretics MOA

A
  • Inhibit the uptake (reabsorption) of sodium at different sites in the renal tubules – more sodium is excreted in urine
  • Increase osmotic pressure in the renal tubules + reduce passive reabsorption of water

Loop diuretics: potent, site: LOH
Thiazide diuretics: moderately potent, site: distal convoluted tubule
Potassium sparing diuretics: weak diuretics, site: late distal convoluted tubule

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15
Q

diuretics side effects

A

Thiazide diuretics: hypokalaemia, hyponatraemia, hyperuricaemia, precipitate gout, hyperglycaemia, urinary frequency/urgency

Loop diuretics: hypokalaemia, hyponatraemia, hyperuricaemia, precipitate gout, hyperglycaemia, urinary frequency/urgency

Potassium sparing diuretics: hyPERkalaemia, gynaecomastia in men

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16
Q

triple whammy

A

Triple Whammy: this combination of meds in susceptible pts may produce renal impairment

  1. ACE Inhibitors OR Angiotensin II receptor antagonists
  2. NSAIDS including COX 2 Inhibitors
  3. Diuretics
17
Q

loop diuretics MOA

A
  • Inhibits the reabsorption of sodium and chloride in the ascending limb of the LOH
  • Potent diuretics as the ascending limb of the LOH accounts for retention of approximately 20% of filtered sodium
  • Produce a rapid and intense diuresis
  • Have a short duration of action (4-6 hours)
18
Q

thiazide diuretics MOA

A
  • Moderately potent diuretic
  • Inhibits reabsorption of sodium and chloride in the proximal (diluting) segment of the distal convoluted tubule, increasing the delivery of sodium to the collecting tubules and producing a corresponding increase in potassium excretion
19
Q

potassium sparing diuretics MOA

A
  • weak diuretics

- increased excretion of sodium and water, decreased excretion of potassium