Hypertension Flashcards
HTN Treatment - Drug Classes
- Diuretics;
- B-Blockers;
- RAS (Renin-Angiotensin System) Inhibitors;
- CCBs;
- a-Blockers;
- Other
MoA for Thiazide Diuretics in treatment of HTN
decrease Na+ reabsorption in distal tubule
MoA for Loop Diuretics in treatment of HTN
Decrease Na+ reabsorption in ascending limb, Drug of choice for reducing acute pulmonary edema of heart failure
MoA for K+ SparingDiuretics in treatment of HTN
Inhibit sodium transport at the late distal and collecting duct; or work as an aldosterone antagonist - Spironolactone (Aldactone ®) and eplerenone (Inspra ®)
Adverse Effects for Thiazide Diuretics in treatment of HTN
Hypokalemia; Hyperuriemia; may precipitate gouty attack
Adverse Effects for Loop Diuretics in treatment of HTN
Ototoxicity
Adverse Effects for K+ SparingDiuretics in treatment of HTN
Gynecomastia in males
MoA for B-blockers in treatment of HTN
- Reduction of cardiac output;
- possible reduction in sympathetic output from CNS;
- Some inhibition of renin release
Selective b-1 receptor blockers are most commonly prescribed: (i.e. metoprolol, atenolol)
MoA for ACE-inhibitors in treatment of HTN
- Decrease BP by reduction of peripheral vascular resistance;
- Decrease transformation of Angiotensin I to Angiotensin II;
- ACE is also responsible for the breakdown of bradykinin (bradykinin levels are increased with ACEI treatment > persistent dry cough)
MoA for ARBs in treatment of HTN
- Block AT1 receptors (where angiotensin II binds);
- Effects similar to ACEIs;
- Decreased BP thru vasodilation and reduced aldosterone;
- Does not increase bradykinin levels
MoA for Non-Dihydropyridine CCBs in treatment of HTN
- Act on Ca+ channels of vascular smooth muscle & myocardial smooth muscle;
- slow automaticity/AV nodal conduction
MoA for Dihydropyridine in treatment of HTN
- Greater affinity for vascular calcium channels than for Ca⁺⁺ channels in heart;
- Cause vasodilation & decreased peripheral vascular resistance;
- fewer drug interactions
MoA for Alpha Blockers in treatment of HTN
- Competitive blockade of α1-receptors;
- Relaxation of arterial & venous smooth muscle > Decrease peripheral vascular resistance & BP;
- Minimal changes to cardiac output, renal blood flow and GFR
Drug Classes Indicated for Treating HTN with High-Risk Angina Pectoris
Preferred: B-blockers & CCBs; Secondary: Diuretics & ACEIs
Drug Classes Indicated for Treating HTN with Diabetes
Preferred: Diuretics, ACEIs, & ARBs; Secondary: B-Blockers, CCBs