Anti-Hypertension Drug Therapy Flashcards
Most patient will require more than
one BP medication to reach goal BP
Initial Therapy
Thiazide-type diuretics
Angiotensin-converting enzyme (ACE)inhibitors/angiotensinII receptor blockers (ARBs)
Calcium channel blockers
First line therapy for HF and HTN
diuretics
reduces extracellular flid
diuretics
ADR for Diuretics
electrolyte imbalance
drug interactions diruetics
protentional additive hypotensive effects with other drugs that lower BP
Diuretics’ MOA
Blockade of sodium and chloride reabsorption
Diuretics site of action
Proximal tubule produces greatest diuresis
Diuretics adverse effects
Hypovolemia
Acid-base imbalance
Electrolyte imbalances
Classifications of Diuretics
Thiazide diuretics
Loop diuretics
Potassium sparing diuretics
Loop Diuretic Example
Furosemide, bumetanide, torsemide
Potassium-Sparing Diuretics useful response
Useful responses
Modest increase in urine production
Substantial decrease in potassium excretion
Potassium-Sparing Diuretics are rarely used
Rarely used alone for therapy
Potassium-Sparing Diuretics example
Amiloride,triamterene,spironolactone, andeplerenone
Potassium-Sparing Diuretics act on
Primary used in combination with a loop or thiazide diuretic
Potassium-Sparing Diuretics primary used in combination with
combination with a loop or thiazide diuretic
Potassium-Sparing Diuretics monitor
serum potassium
Spironolactone is a
Aldosterone antagonist
Spironolactone MOA
Blocks aldosterone in the distal nephron
Retention of potassium
Increased excretion of sodium
Spironolactone Uses
Edematous states Heart failure (decreases mortality in severe failure) Primary hyperaldosteronism Premenstrual syndrome Polycystic ovary syndrome Acne in young women
Spironolactone ADR
Hyperkalemia
Benign and malignant tumors
Endocrine effects
Interactions
Thiazide and loop diuretics
Agents that raise potassium levels
ACE Effects and MOA
Reduce levels of angiotensin II
Increase levels of bradykinin
ACE Use
HTN, HF, MI, diabetic and non-diabetic nephropathy; prevention of MI, stroke, and death in patients at high CV risk
ACE ADR
diuretics, anti-HTN agents, drugs that raise potassium, lithium, NSAIDs.
ACE Interactions
diuretics, anti-HTN agents, drugs that raise potassium, lithium, NSAIDs.
Angiotensin II Receptor Blocker MOA
Block access of angiotensin II Cause dilation of arterioles and veins Prevent angiotensin II from inducing pathologic changes in cardiac structure Reduce excretion of potassium Decrease release of aldosterone Increase renal excretion of sodium and water Do not inhibit kinase II Do not increase levels of bradykinin
Angiotensin II Receptor Blockers use
Therapeutic uses: HTN, HF, MI, diabetic nephropathy, patient unable to tolerate ACE inhibitors, may prevent development of diabetic retinopathy
Angiotensin II Receptor Blockers ADR
angioedema, fetal harm, renal failure
Angiotensin II Receptor Blockers benefit
Lower incidence of cough
CCB are drugs that
Drugs that prevent calcium ions from entering cells
CCB greatest impact is on the
Greatest impact on heart and blood vessels
CCB used to treat
Used to treat hypertension, angina pectoris, and cardiac dysrhythmias
CCB is also known as
calcium antagonists and slow channel block`ers
Types of calcium channel blockers
Dihydropyridines
non-Dihydropyridines
dihydropyridines example
nifedipine,isradipine,felodipine,nicardipine,nisoldipine, lacidipine, andamlodipine
non-dihydropyridines example
verapamil and diltiazem
Dihydropyridines are
Potent vasodilators
Dihydropyridines little or no
Little or no negative effect upon cardiac contractility or conduction.
Dihydropyridines use to treat
Use to treat hypertension or chronic stable angina.
Dihydropyridines are longer-
Longer-acting agents are generally safer and are increasingly preferred.
Non-dihydropyridines use
Uses: HTN, chronic stable angina, cardiac arrhythmias, proteinuria reduction
Non-dihydropyridines less potent
Less potent vasodilation
Non-dihydropyridines greater
depression effect on cardiac condution and contractility
Dihydropyridines SE
headache, lightheadedness, flushing, and dose-dependent edema
Non-dihydropyridines SE
dose-dependent constipation, bradycardia and worsening cardiac output
Non-dihydropyridines CI
pt beta blockers or who have heart failure with reduced ejection fraction , sick sinus syndrome, and second- or third-degree atrioventricular block