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27 Cards in this Set
- Front
- Back
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adverse effects of thiazides |
Metabolic: hyperuricemia (70%), hyperlipidemia, hyperglycemia (10%) Electrolyte abnormalities: hypokalemia (70%), hypomagnesia, hyponatremia Fluid abnormalities: hypovolemia |
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adverse effects of potassium sparing diuretics |
Hyperkalemia Spironolactone may cause gynecomastia |
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adverse effects of loop diuretics |
Metabolic: hyperuricemia, hyperlipidemia, hyperglycemia Electrolyte abnormalities: hypokalemia (70%), hypomagnesia Fluid abnormalities: hypovolemia |
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loop diurectics moa |
Not really used to treat HTN, more for edematous states (CHF, ascites) • Mechanism:– Inhibition of the co‐transport of Na/K/2Cl in the thick ascending limb of the Loop of Henle |
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thiazides and thiazide-like moa |
Considered 1st line therapy for treatment of HTN(along with other agents) • Mechanism:– blocks sodium and chloride absorption in the distal convoluted tubule |
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potassium sparing diuretics moa |
Prevent the secretion of potassium in the distal tubule (collecting duct) – Produce less diuretic effect than thiazides and loops – Not very effective for HTN – Often used to blunt sodium loss |
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Diuretics |
Inhibiting Na+ reabsorption in kidneys; decrease in plasma fluid volume (vasodilation) Types= thiazides, loop, K+ sparing |
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Sympatholytics Drugs |
Agents designed to interfere with increased sympathetic activity • Beta Blockers • Alpha‐blockers • Presynaptic Adrenergic Inhibitors • Centrally Acting Agents |
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Beta blockers moa |
Reduce cardiac output by reducing HR – Also may reduce sympathetic outflow from CNS and secondarilyreduce RAAS Historically 1st line for HTN -not anymore |
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Alpha blockers moa |
- Block α‐1‐adrenergic receptors resulting inrelaxation of vascular smooth muscle – Results in decreased peripheral vascularresistance and lower arterial bloodpressure Seldom used for HTN, more for treating BPH (benign prostatic hyperplasia) |
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centrally acting agents moa |
Mechanism:– α2 agonist in the brain stem, decreasingsympathetic outflow – Results in decrease in peripheral vascularresistance and heart rate |
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beta blockers adverse effects |
– Bronchoconstriction – non‐selective agents in asthmatics (Stimulation of beta‐2 receptors causes bronchodilation) – Bradycardia – Fatigue – Sexual dysfunction – Lipid abnormalities – increased TG, lowered HDL |
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alpha blockers adverse effects |
Reflex tachycardia and first‐dose syncopevery common (May be prevented by using a beta‐blocker) – Postural (orthostatic) hypotension |
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centrally acting agents adverse effects |
dry mouth dizziness sedation |
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vasodilators moa |
Mechanism:– Inhibit smooth‐muscle contraction byincreasing production of cGMP • Increased cGMP inhibits smooth musclecontraction, leading to vasodilation Drugs that directly vasodilate theperipheral vasculature– Used as last line therapy in resistant casesand emergency situations |
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vasodilators adverse effects |
Reflex tachcardia – Dizziness – Orthostatic hypotension – Headache – Hair growth with minoxidil (topicalRogaine) |
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Renin‐Angiotensin System inhibitors moa |
RAAS involves several compounds thatregulate sodium and water balance inthe body – Renin – Angiotensin I and Angiotensin II – Aldosterone Classes:– ACEI, ARB, Direct Renin inhibitor |
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ace inhibitors moa |
Block ACE that cleaves angiotensin I to formangiotensin II (powerful vasoconstrictor andstimulator of aldosterone secretion) • Results in vasodilation and reduced sodiumand water retention – Other effects: • Angiotensin II powerful stimulator of vasculargrowth, leading to vascular wall hypertrophy Considered 1st line therapy for treatmentof HTN (along with other agents) |
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ace inhibitiors adverse effects |
– Dry cough (10% of pts) • Due to build up of bradykinin – Hyperkalemia
– Angioedema • May be life‐threatening – Fetotoxic • Do not use in pregnancy |
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Angiotensin II Receptor Blockers moa |
Considered 1st line therapy fortreatment of HTN (along with otheragents) – Also referred to as “ARBs” • Mechanism: – Block the AT1 angiotesin II receptor – Effect similar to ACEI • Results in vasodilation and reduced sodiumand water retention |
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Angiotensin II Receptor Blockers adverse effects |
– Cough DO NOT cause cough • No build up of bradykinin – Hyperkalemia
– Fetotoxic • Do not use in pregnancy |
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Direct Renin Inhibitor moa |
Aliskiren (Tekturna) is the only agent • Mechanism: – Inhibits renin’s ability to convert angiotensinogen to angiotensin I – Results in actions similar to ACEI • Results in vasodilation and reduced sodium and water retention |
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Direct Renin Inhibitor adverse effects |
– Hyperkalemia – Diarrhea – Cough and angioedema less common than with ACEI |
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Calcium Channel Blockers |
Considered 1st line therapy for treatment of HTN (along with other agents) • Drugs that selectively block calcium entry into smooth muscle and myocardium – Different classes of Ca‐channel blocker have significantly different effects Classes of Ca‐channel blockers – Dihydropyridine agents – Non‐dihydropyridine agents |
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Dihydropyridine agentsmoa |
• Block calcium entry in to vascular smooth muscle • Leads to vasodilation and reduced PVR |
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Non‐dihydropyridine agents moa |
• Blocks calcium entry into myocardial cells • Leads to reduced heart rate and myocardial contraction |
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calcium channel blockers adverse effects |
– Constipation in 10% of pts taking verapamil – Dizziness, headache and fatigue more common with dihydropyridines • due to significant reduction in BP – Peripheral edema with dihydropyridines – Verapamil SIGNIFICANTLY reduces the force of cardiac muscle contraction(negative inotropic effect) • Avoid in patients with heart failure |
