Antihypertensive Agents Flashcards
Diuretics
1) How effective are they?
2) How do they work?
1) lower BP 10-15 mmHG
2) deplete body sodium stores
Chlorothiazide
1) Use
2) Mechanism of action
3) Major side effects
1) First line therapy for mild to moderate HTN with normal renal and cardiac function
2) Inhibits sodium-chloride transporter in the distal tubule and early collecting duct
3) Hypokalemia, hyperglycemia
Chlorthalidone
1) Use
2) Mechanism of action
3) Major side effects
1) First line therapy for mild to moderate HTN with normal renal and cardiac function
2) Inhibits sodium-chloride transporter in the distal tubule and early collecting duct
3) Hypokalemia, hyperglycemia
Hydrochlorothiazide
1) Use
2) Mechanism of action
3) Major side effects
1) First line therapy for mild to moderate HTN with normal renal and cardiac function
2) Inhibits sodium-chloride transporter in the distal tubule and early collecting duct
3) Hypokalemia, hyperglycemia
Furosemide
1) Use
2) Mechanism of action
3) Major side effects
1) Severe HTN, renal insufficiency, cardiac failure
2) Acts upon Na/K/2Cl in the thick loop of Henle
3) Hypokalemia, ototoxicity
Torsemide
1) Use
2) Mechanism of action
3) Major side effects
1) Severe HTN, renal insufficiency, cardiac failure
2) Acts upon Na/K/2Cl in the thick loop of Henle
3) Hypokalemia, ototoxicity
Ethacrynic acid
1) Use
2) Mechanism of action
3) Major side effects
1) Severe HTN, renal insufficiency, cardiac failure
2) Acts upon Na/K/2Cl in the thick loop of Henle
3) Hypokalemia, ototoxicity
Bumetanide
1) Use
2) Mechanism of action
3) Major side effects
1) Severe HTN, renal insufficiency, cardiac failure
2) Acts upon Na/K/2Cl in the thick loop of Henle
3) Hypokalemia, ototoxicity
Spironolactone
1) Use
2) Mechanism of action
3) Side effects
1) Avoid excessive potassium depletion and enhance effects of other diuretics
2) Bind to mineralocorticoid receptors and blunt aldosterone activity to act on the collecting duct and tubules
3) hyperkalemia, hyperchloremic acidosis
Eplerenone
1) Use
2) Mechanism of action
3) Side effects
1) Avoid excessive potassium depletion and enhance effects of other diuretics
2) Bind to mineralocorticoid receptors and blunt aldosterone activity to act on the collecting duct and tubules
3) hyperkalemia, hyperchloremic acidosis
Amiloride
1) Use
2) Mechanism of action
3) Side effects
1) Avoid excessive potassium depletion and enhance effects of other diuretics
2) Inhibit Na influx through luminal channels in the collecting duct and tubules
3) hyperkalemia, hyperchloremic acidosis
Triamterene
1) Use
2) Mechanism of action
3) Side effects
1) Avoid excessive potassium depletion and enhance effects of other diuretics
2) Inhibit Na influx through luminal channels in the collecting duct and tubules
3) hyperkalemia, hyperchloremic acidosis
Aliskiren
1) Use
2) Mechanism of action
1) Hypertension
2) Oran renin inhibitor
Catopril
1) Use
2) Mechanism of action
1) Hypertension
2) ACE inhibitor = Inhibits conversion of angiotensin to angiotensin II to aldosterone AND inhibits breakdown of bradykinin
Enalapril
1) Use
2) Mechanism of action
1) Hypertension
2) ACE inhibitor = Inhibits conversion of angiotensin to angiotensin II to aldosterone AND inhibits breakdown of bradykinin
Fosinopril
1) Use
2) Mechanism of action
1) Hypertension
2) ACE inhibitor = Inhibits conversion of angiotensin to angiotensin II to aldosterone AND inhibits breakdown of bradykinin
Lisinopril
1) Use
2) Mechanism of action
1) Hypertension
2) ACE inhibitor = Inhibits conversion of angiotensin to angiotensin II to aldosterone AND inhibits breakdown of bradykinin
What are three side effects of ACE inhibitors?
Dry cough from increased bradykinin levels
Hyperkalmeia
Angioedema
Hypotension in the presence of hypovolemia
What are the effects of ACE inhibitors on CO and HR
Remain unchanged
What are additional benefits of ACE inhibitors?
1) Improved renal hemodynamics in renal disease
2) decreased hypertrophy and remodeling in MI and HF
3) protects from diabetic nephropathy
Losartan
1) Use
2) Mechanism of action
1) Hypertension
2) AT1 receptor antagonists causing vasodilation and increased sodium and water excretion
Valsartan
1) Use
2) Mechanism of action
1) Hypertension
2) AT1 receptor antagonists causing vasodilation and increased sodium and water excretion
Candesartan
1) Use
2) Mechanism of action
1) Hypertension
2) AT1 receptor antagonists causing vasodilation and increased sodium and water excretion
Irbesartan
1) Use
2) Mechanism of action
1) Hypertension
2) AT1 receptor antagonists causing vasodilation and increased sodium and water excretion
What are the side effects of ARBs?
Same as ACEs, but reduced cough and angioedema
Propranolol
1) Use
2) Mechanism
3) Effect on CO
1) Hypertension
2) Non-selective B1-B2 receptor antagonist
3) Decreases CO by decreasing HR and contractility
Metoprolol
1) Use
2) Mechanism
3) Effect on CO
1) Hypertension
2) Selective B1 receptor antagonist
3) Decreases CO by decreasing HR and contractility
Atenolol
1) Use
2) Mechanism
3) Effect on CO
1) Hypertension
2) Selective B1 receptor antagonist
3) Decreases CO by decreasing HR and contractility
1) What are the side effects of beta blockers?
2) Who should avoid beta blockers?
1) Nausea/vomiting, dizziness, sleep disorders with propranolol
2) Asthmatics, PVD, cardiac conduction delay
Prazosin
1) Use
2) Mechanism
1) HTN and pheochromocytoma
2) blockade of a1 receptors –> dilation of arterioles and capacitance veins
Terazosin
1) Use
2) Mechanism
1) HTN and pheochromocytoma
2) blockade of a1 receptors –> dilation of arterioles and capacitance veins
Doxazosin
1) Use
2) Mechanism
1) HTN and pheochromocytoma
2) blockade of a1 receptors –> dilation of arterioles and capacitance veins
What are the side effects of a1 antagonists?
Reflex tachycardia, fluid retention, orthostatic hypotension
Labetalol
1) Use
2) Mechanism
1) Hypertensive emergencies IV, HTN orally
2) B blocking and vasodilating effects of combined a and B antagonism (B>a)
Carvedilol
1) Use
2) Mechanism
1) Reducing mortality in HF, HTN
2) B blocking and vasodilating effects of combined a and B antagonism (1:1 ratio B:a)
Clonidine
1) Use
2) Mechanism
1) resistant hypertension
2) stimulate presynaptic a2 receptors decreases sympathetic outflow and baroreceptor response
Methyldopa
1) Use
2) Mechanism
1) pregnancy induced hypertension
2) stimulate presynaptic a2 receptors decreases sympathetic outflow and baroreceptor response
Nifedipine
1) Use
2) Mechanism
1) HTN esp. w low renin, AA with systolic hypertension
2) Block voltage sensitive L-type Ca++ channels in the vascular smooth muscle
Nimodipine
1) Use
2) Mechanism
1) HTN esp. w low renin, AA with systolic hypertension
2) Block voltage sensitive L-type Ca++ channels in the vascular smooth muscle
Amlodipine
1) Use
2) Mechanism
1) HTN esp. w low renin, AA with systolic hypertension
2) Block voltage sensitive L-type Ca++ channels in the vascular smooth muscle
Verapamil
1) Use
2) Mechanism
1) HTN esp. with low renin
2) Block voltage sensitive L-type Ca++ channels in the heart (cardiac and AV node selective)
Benzothiazepine
1) Use
2) Mechanism
1) HTN esp. with low renin
2) Block voltage sensitive L-type Ca++ channels in the heart (cardiac and AV node selective)
What are the effects on: 1) PVR 2) Baroreceptor Reflex 3) HR when using calcium channel blockers?
1) decrease PVR
2) decreased baroreceptor reflex increases in HR
3) decreased HR
Hydralazine
1) Use
2) Mechanism
1) mild to moderate HTN in combination with diuretic and B-blocker
2) acts through the release of NO (NO required)
Minoxidil
1) Use
2) Mechanism
1) resistant HTN in combination with diuretic and B-blocker
2) opens K channels and hyperpolarizes the cell, closing Ca++ voltage gated channels
Nitroprusside
1) Use
2) Mechanism
1) Produce hypotension in surgery and HTN emergencies
2) direct vasodilation by generating NO, increasing cGMP
Nitroglycerin
1) Use
2) Mechanism
1) Cardiac surgery and HTN emergencies
2) generates NO increasing cGMP –> vasodilation with preferential effect on veins over arteries**
Epoprostenol
1) Use
2) Mechanism
1) Primary pulmonary HTN
2) synthetic analog of prostacyclin (PGI2) –> direct vasodilation and counteracts thromboxane A2
Bosentan
1) Use
2) Mechanism
1) Primary pulmonary HTN
2) Non-selective Endothelin receptor blocker
Ambrisentan
1) Use
2) Mechanism
1) Primary pulmonary HTN
2) Selective endothelia receptor blocker of ETa receptor