Hypertension Flashcards

1
Q

HTN Treatment - Drug Classes

A
  1. Diuretics;
  2. B-Blockers;
  3. RAS (Renin-Angiotensin System) Inhibitors;
  4. CCBs;
  5. a-Blockers;
  6. Other
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2
Q

MoA for Thiazide Diuretics in treatment of HTN

A

decrease Na+ reabsorption in distal tubule

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3
Q

MoA for Loop Diuretics in treatment of HTN

A

Decrease Na+ reabsorption in ascending limb, Drug of choice for reducing acute pulmonary edema of heart failure

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4
Q

MoA for K+ SparingDiuretics in treatment of HTN

A

Inhibit sodium transport at the late distal and collecting duct; or work as an aldosterone antagonist - Spironolactone (Aldactone ®) and eplerenone (Inspra ®)

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5
Q

Adverse Effects for Thiazide Diuretics in treatment of HTN

A

Hypokalemia; Hyperuriemia; may precipitate gouty attack

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6
Q

Adverse Effects for Loop Diuretics in treatment of HTN

A

Ototoxicity

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7
Q

Adverse Effects for K+ SparingDiuretics in treatment of HTN

A

Gynecomastia in males

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8
Q

MoA for B-blockers in treatment of HTN

A
  1. Reduction of cardiac output;
  2. possible reduction in sympathetic output from CNS;
  3. Some inhibition of renin release

Selective b-1 receptor blockers are most commonly prescribed: (i.e. metoprolol, atenolol)

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9
Q

MoA for ACE-inhibitors in treatment of HTN

A
  1. Decrease BP by reduction of peripheral vascular resistance;
  2. Decrease transformation of Angiotensin I to Angiotensin II;
  3. ACE is also responsible for the breakdown of bradykinin (bradykinin levels are increased with ACEI treatment > persistent dry cough)
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10
Q

MoA for ARBs in treatment of HTN

A
  1. Block AT1 receptors (where angiotensin II binds);
  2. Effects similar to ACEIs;
  3. Decreased BP thru vasodilation and reduced aldosterone;
  4. Does not increase bradykinin levels
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11
Q

MoA for Non-Dihydropyridine CCBs in treatment of HTN

A
  1. Act on Ca+ channels of vascular smooth muscle & myocardial smooth muscle;
  2. slow automaticity/AV nodal conduction
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12
Q

MoA for Dihydropyridine in treatment of HTN

A
  1. Greater affinity for vascular calcium channels than for Ca⁺⁺ channels in heart;
  2. Cause vasodilation & decreased peripheral vascular resistance;
  3. fewer drug interactions
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13
Q

MoA for Alpha Blockers in treatment of HTN

A
  1. Competitive blockade of α1-receptors;
  2. Relaxation of arterial & venous smooth muscle > Decrease peripheral vascular resistance & BP;
  3. Minimal changes to cardiac output, renal blood flow and GFR
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14
Q

Drug Classes Indicated for Treating HTN with High-Risk Angina Pectoris

A

Preferred: B-blockers & CCBs; Secondary: Diuretics & ACEIs

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15
Q

Drug Classes Indicated for Treating HTN with Diabetes

A

Preferred: Diuretics, ACEIs, & ARBs; Secondary: B-Blockers, CCBs

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16
Q

Drug Classes Indicated for Treating HTN with Recurrent Stroke

A

Preferred: ACEIs; Secondary: Diuretics

17
Q

Drug Classes Indicated for Treating HTN with HF

A

Preferred: Diuretics, B-Blockers; ACEIs; ARBs; Aldosterone-receptor antagonists

18
Q

Drug Classes Indicated for Treating HTN with Previous MI

A

B-Blockers, ACEIs, Aldosterone-receptor antagonists

19
Q

Drug Classes Indicated for Treating HTN with Chronic Renal Disease

A

ACEIs; ARBs