Hypertension Flashcards
Atenolol
B1 receptor antagonist
B1 and B2: propranolol, B1: metoprolol, atenolol
• Mechanism of action:
– Non-selective B1- B2 or selective
Metoprolol
B receptor antagonist
B1 and B2: propranolol, B1: metoprolol, atenolol
• Mechanism of action:
– Non-selective B1- B2 or selective
Propranolol
B receptor antagonist
B1 and B2: propranolol, B1: metoprolol, atenolol
• Mechanism of action:
– Non-selective B1- B2 or selective
Doxazosin
alpha1 receptor antagonist
Mechanism of action:
– Blockade of
Prazosin
alpha receptor antagonist
Mechanism of action:
– Blockade of a1-receptors on VSM
– Dilation of arterioles and capacitance veins
• Use: alone or in combination for hypertension
– Pheochromocytoma
• Side/adverse effects:
– Reflex tachycardia, orthostatic hypotension, fluid
retention
– GI upset, palpitation, tinnitus, headache, dizziness,
urinary incontinence
– Water retention-use with diuretic or a-antagonist
Terazosin
alpha receptor antagonist
Mechanism of action:
– Blockade of a1-receptors on VSM
– Dilation of arterioles and capacitance veins
• Use: alone or in combination for hypertension
– Pheochromocytoma
• Side/adverse effects:
– Reflex tachycardia, orthostatic hypotension, fluid
retention
– GI upset, palpitation, tinnitus, headache, dizziness,
urinary incontinence
– Water retention-use with diuretic or a-antagonist
carvedilol
Mixed a/b antagonist
non-selective B and a1 receptor
antagonist
– Antioxidant and antiproliferative
• Use: hypertension and heart failure
Labetalol
Mixed a/b antagonist
non-selective B and a1 receptor
antagonist, mix of four stereoisomers
• Use: chronic hypertension and hypertensive
emergencies
reserpine
Inhibitor of peripheral transmission
Mechanism of action:
– Deplete NE from adrenergic nerve endings
– Inhibits reuptake of NE into storage terminal
– Decrease peripheral resistance and CO
• Use: mild to moderate hypertension
resurgence in use low dose in combination with
thiazide diuretic
• Adverse effects:
– Postural hypotension
– Sedation, dry mouth, nightmares
– Sodium and water retention-add diuretic
alpha-methyldopa
Central mediated agent
Brainstem a2 receptor
Mechanism of action:
– Stimulate brainstem a2 adrenergic receptors
• decrease sympathetic outflow
– Vagal activity to heart increased
– Decreased peripheral vascular resistance and CO
• Use: resistant hypertension-clonidine
– Pregnancy-induced hypertension-methyldopa
• Side/adverse effects:
– Withdrawal syndrome-rebound hypertension
– Sedation, dry mouth, depression, drowsiness
– Sodium and water retention-add diuretic
– Postural hypotension-elderly
clonidine
CNS mediated agent
Mechanism of action:
– Stimulate brainstem a2 adrenergic receptors
• decrease sympathetic outflow
– Vagal activity to heart increased
– Decreased peripheral vascular resistance and CO
• Use: resistant hypertension-clonidine
– Pregnancy-induced hypertension-methyldopa
• Side/adverse effects:
– Withdrawal syndrome-rebound hypertension
– Sedation, dry mouth, depression, drowsiness
– Sodium and water retention-add diuretic
– Postural hypotension-elderly
Guanabenz
CNS mediated agent
Mechanism of action:
– Stimulate brainstem a2 adrenergic receptors
• decrease sympathetic outflow
– Vagal activity to heart increased
– Decreased peripheral vascular resistance and CO
• Use: resistant hypertension-clonidine
– Pregnancy-induced hypertension-methyldopa
• Side/adverse effects:
– Withdrawal syndrome-rebound hypertension
– Sedation, dry mouth, depression, drowsiness
– Sodium and water retention-add diuretic
– Postural hypotension-elderly
Captopril
ACE inhibitor
Mechanism of action:
– Block conversion of angiotensin I to angiotensin II
– Elevate bradykinin levels
– Decreased peripheral resistance
– Decreased aldosterone- increase Na+ and
H2O excretion
– Reverse or reduce CV remodeling
– Increase plasma renin and renin activity
Adverse/toxic effects: – Dry cough (20%) and altered taste – Hyperkalemia-due to inhibition of aldosterone secretion – Angioedema – Hypotension – Rash – Pregnancy problems (fetal renal damage
Enalapril
ACE inhibitor
Mechanism of action:
– Block conversion of angiotensin I to angiotensin II
– Elevate bradykinin levels
– Decreased peripheral resistance
– Decreased aldosterone- increase Na+ and
H2O excretion
– Reverse or reduce CV remodeling
– Increase plasma renin and renin activity
Adverse/toxic effects: – Dry cough (20%) and altered taste – Hyperkalemia-due to inhibition of aldosterone secretion – Angioedema – Hypotension – Rash – Pregnancy problems (fetal renal damage
Fosinopril
ACE inhibitor
Mechanism of action:
– Block conversion of angiotensin I to angiotensin II
– Elevate bradykinin levels
– Decreased peripheral resistance
– Decreased aldosterone- increase Na+ and
H2O excretion
– Reverse or reduce CV remodeling
– Increase plasma renin and renin activity
Adverse/toxic effects: – Dry cough (20%) and altered taste – Hyperkalemia-due to inhibition of aldosterone secretion – Angioedema – Hypotension – Rash – Pregnancy problems (fetal renal damage
Lisinopril
ACE inhibitor
Mechanism of action:
– Block conversion of angiotensin I to angiotensin II
– Elevate bradykinin levels
– Decreased peripheral resistance
– Decreased aldosterone- increase Na+ and
H2O excretion
– Reverse or reduce CV remodeling
– Increase plasma renin and renin activity
Adverse/toxic effects: – Dry cough (20%) and altered taste – Hyperkalemia-due to inhibition of aldosterone secretion – Angioedema – Hypotension – Rash – Pregnancy problems (fetal renal damage
Candesartan
ARB
Mechanism of action: – AT1 receptor antagonists – Vasodilation – Increase Na+ and H2O excretion – Reduce plasma volume – Decrease cellular hypertrophy – Increase plasma renin and renin activity
Adverse/toxic effects: – Hypotension – NO cough or angioedema – Hyperkalemia – Fetal renal toxicity
irbesartan
ARB
Mechanism of action: – AT1 receptor antagonists – Vasodilation – Increase Na+ and H2O excretion – Reduce plasma volume – Decrease cellular hypertrophy – Increase plasma renin and renin activity
Adverse/toxic effects: – Hypotension – NO cough or angioedema – Hyperkalemia – Fetal renal toxicity
Losartan
ARB
Mechanism of action: – AT1 receptor antagonists – Vasodilation – Increase Na+ and H2O excretion – Reduce plasma volume – Decrease cellular hypertrophy – Increase plasma renin and renin activity
Adverse/toxic effects: – Hypotension – NO cough or angioedema – Hyperkalemia – Fetal renal toxicity
Valsartan
ARB
Mechanism of action: – AT1 receptor antagonists – Vasodilation – Increase Na+ and H2O excretion – Reduce plasma volume – Decrease cellular hypertrophy – Increase plasma renin and renin activity
Adverse/toxic effects: – Hypotension – NO cough or angioedema – Hyperkalemia – Fetal renal toxicity
Aliskiren
Renin Inhibitor
Mechanism of action:
– Direct, competitive inhibitor of renin
– Increase plasma renin but not renin activity
• Use: hypertension
– Not first line since long term CV outcomes unclear
• Side/adverse effects:
– Diabetic or renal impairment: hyperkalemia in combo with
ACEIs and ARBs
– Hypotension
– Dry cough but much less than with ACE inhibitors
– Rare: angioedema
– Hyperkalemia due to inhibition of aldosterone
Ambrisentan
Vasodilator
Mechanism of action:
– Direct dilators of VSM-different mechanisms
– Decrease peripheral vascular resistance
– Baroreceptor activation of compensatory mechanisms
• Use:
– Hypertension-hydralazine and minoxidil
– Hypertensive crises-nitroprusside
– Pulmonary hypertension-epoprostenol, bosentan,
ambrisentan, riociguat
– Used in combination-diuretics and B-antagonists
ETa receptor blocker:
Use: primary pulmonary hypertension • Side/adverse effects: – Edema – Headache – Spermatogenesis inhibition – Respiratory tract infection – Decreased hematocrit – Hepatic effects
Bosentan
Vasodilator
Mechanism of action:
– Direct dilators of VSM-different mechanisms
– Decrease peripheral vascular resistance
– Baroreceptor activation of compensatory mechanisms
• Use:
– Hypertension-hydralazine and minoxidil
– Hypertensive crises-nitroprusside
– Pulmonary hypertension-epoprostenol, bosentan,
ambrisentan, riociguat
– Used in combination-diuretics and B-antagonists
Non-selective ET receptor blocker
Use: primary pulmonary hypertension • Side/adverse effects: – Edema – Headache – Spermatogenesis inhibition – Respiratory tract infection – Decreased hematocrit – Hepatic effects
epoprostenol
Vasodilator
Mechanism of action:
– Direct dilators of VSM-different mechanisms
– Decrease peripheral vascular resistance
– Baroreceptor activation of compensatory mechanisms
• Use:
– Hypertension-hydralazine and minoxidil
– Hypertensive crises-nitroprusside
– Pulmonary hypertension-epoprostenol, bosentan,
ambrisentan, riociguat
– Used in combination-diuretics and B-antagonists
Prostacyclin (PGI2 ) • Mechanism of action: – Direct vasodilator via cAMP – Counteracts thromboxane A2 • Use: potent antihypertensive but must be administered continuously – Primary pulmonary hypertension
hydralazine
vasodilator
Mechanism of action:
– Direct dilators of VSM-different mechanisms
– Decrease peripheral vascular resistance
– Baroreceptor activation of compensatory mechanisms
• Use:
– Hypertension-hydralazine and minoxidil
– Hypertensive crises-nitroprusside
– Pulmonary hypertension-epoprostenol, bosentan,
ambrisentan, riociguat
– Used in combination-diuretics and B-antagonists
Mechanism of action: unclear
– Reduced intracellular calcium
– Preferential effect on arterioles vs arteries and veins
– Decreased peripheral vascular resistance, MAP
– Reflex increase in HR, contractility, CO (pronounced)
• Use: mild to moderate hypertension in
combination with diuretic and B-blocker
• Side/adverse effects: commonly occurring
– Headache, anorexia, nausea, dizziness, sweating
– Angina or ischemic arrhythmias with ischemic heart
disease due to reflex tachycardia
– Increase renin and fluid retention
– Immune response: Lupus
minoxidil
Vasodilator
Mechanism of action:
– Direct dilators of VSM-different mechanisms
– Decrease peripheral vascular resistance
– Baroreceptor activation of compensatory mechanisms
• Use:
– Hypertension-hydralazine and minoxidil
– Hypertensive crises-nitroprusside
– Pulmonary hypertension-epoprostenol, bosentan,
ambrisentan, riociguat
– Used in combination-diuretics and B-antagonists
Mechanism of action:
– Preferential effect on arterioles vs veins
– Decreased peripheral vascular resistance
– Activates K+ channels, VSM relaxation
– Reflex increase in HR, contractility, CO, renin secretion
and fluid retention
• Use: resistant hypertension in combination with
diuretic and B-blocker
• Side/adverse effects:
– Fluid retention: contraindicated in heart failure
– Pericardial effusion and cardiac tamponade
– Reflex tachycardia
– Abnormal hair growth (topical use for alopecia)
nitroglycerin
vasodilator
Mechanism of action:
– Direct dilators of VSM-different mechanisms
– Decrease peripheral vascular resistance
– Baroreceptor activation of compensatory mechanisms
• Use:
– Hypertension-hydralazine and minoxidil
– Hypertensive crises-nitroprusside
– Pulmonary hypertension-epoprostenol, bosentan,
ambrisentan, riociguat
– Used in combination-diuretics and B-antagonists
Mechanism of action: – Preferential effect on veins – Generates nitric oxide which activates guanylyl cyclase, increase in cGMP • Use: to produce hypotension in surgery and hypertensive emergencies • Pharmacokinetics: – Short duration of action – Tolerance • Side effects: – Headache
nitroprusside
vasodilator
Mechanism of action:
– Direct dilators of VSM-different mechanisms
– Decrease peripheral vascular resistance
– Baroreceptor activation of compensatory mechanisms
• Use:
– Hypertension-hydralazine and minoxidil
– Hypertensive crises-nitroprusside
– Pulmonary hypertension-epoprostenol, bosentan,
ambrisentan, riociguat
– Used in combination-diuretics and B-antagonists
Mechanism of action: – Direct vasodilator – Generates nitric oxide which activates guanylyl cyclase, increase in cGMP – Effect on veins and arteries to reduce preload and afterload • Use: to produce hypotension in surgery and hypertensive emergencies • Adverse/toxic effects: – Rapid decrease in MAP – Cyanide accumulation (infusions>48 hours and/or impaired renal function)
riociguat
vasodilator
Mechanism of action:
– Direct dilators of VSM-different mechanisms
– Decrease peripheral vascular resistance
– Baroreceptor activation of compensatory mechanisms
• Use:
– Hypertension-hydralazine and minoxidil
– Hypertensive crises-nitroprusside
– Pulmonary hypertension-epoprostenol, bosentan,
ambrisentan, riociguat
– Used in combination-diuretics and B-antagonists
Mechanism of action: – Directly stimulates guanylyl cyclase – Increases cGMP • Use: – Primary pulmonary hypertension – Thromboembolic pulmonary hypertension – Combined with ET receptor blockers • Side/adverse effects: – Headache, dizziness, nausea, diarrhea – Hypotension – Birth defects
dilitazem
Ca channel blocker (cardioselective)
Mechanism of action:
– Block voltage sensitive L-type Ca2+ channels
– Relax VSM and decrease peripheral resistance
– Decrease MAP-reflex increase sympathetic
discharge and HR
– Negative chronotropic -verapamil and diltiazem
Use:
– Hypertension (esp. low renin)
– African Americans and older patients with
systolic hypertension: dihydropyridines more
effective
• Adverse effects:
– Contraindicated in heart failure (edema)
– Depresses A-V conduction and contractility
– Headache
verapamil
Ca channel blocker (cardioselective)
Mechanism of action:
– Block voltage sensitive L-type Ca2+ channels
– Relax VSM and decrease peripheral resistance
– Decrease MAP-reflex increase sympathetic
discharge and HR
– Negative chronotropic -verapamil and diltiazem
Use:
– Hypertension (esp. low renin)
– African Americans and older patients with
systolic hypertension: dihydropyridines more
effective
• Adverse effects:
– Contraindicated in heart failure (edema)
– Depresses A-V conduction and contractility
– Headache
Amlodipine
Ca channel blocker (vasoselective)
Mechanism of action:
– Block voltage sensitive L-type Ca2+ channels
– Relax VSM and decrease peripheral resistance
– Decrease MAP-reflex increase sympathetic
discharge and HR
– Negative chronotropic -verapamil and diltiazem
Use:
– Hypertension (esp. low renin)
– African Americans and older patients with
systolic hypertension: dihydropyridines more
effective
• Adverse effects:
– Contraindicated in heart failure (edema)
– Depresses A-V conduction and contractility
– Headache
Nicardipine
Ca channel blocker (vasoselective)
Mechanism of action:
– Block voltage sensitive L-type Ca2+ channels
– Relax VSM and decrease peripheral resistance
– Decrease MAP-reflex increase sympathetic
discharge and HR
– Negative chronotropic -verapamil and diltiazem
Use:
– Hypertension (esp. low renin)
– African Americans and older patients with
systolic hypertension: dihydropyridines more
effective
• Adverse effects:
– Contraindicated in heart failure (edema)
– Depresses A-V conduction and contractility
– Headache
Nifedipine
Ca channel blocker (vasoselective)
Mechanism of action:
– Block voltage sensitive L-type Ca2+ channels
– Relax VSM and decrease peripheral resistance
– Decrease MAP-reflex increase sympathetic
discharge and HR
– Negative chronotropic -verapamil and diltiazem
Use:
– Hypertension (esp. low renin)
– African Americans and older patients with
systolic hypertension: dihydropyridines more
effective
• Adverse effects:
– Contraindicated in heart failure (edema)
– Depresses A-V conduction and contractility
– Headache
Chlorothiazide
Thiazide diuretic
Block Na/Cl symproter in distal tubule
Moderate Diuresis
Reduced by NSAIDs
Adverse: Hypokalemia, decreased uric acid excretion, sulfonamide cross-reactivity
chorthalidone
Thiazide like diuretic
Block Na/Cl symproter in distal tubule
Moderate Diuresis
Reduced by NSAIDs
Adverse: Hypokalemia, decreased uric acid excretion, sulfonamide cross-reactivity
hydrochlorothiazide
Thiazide diuretic
Block Na/Cl symproter in distal tubule
Moderate Diuresis
Reduced by NSAIDs
Adverse: Hypokalemia, decreased uric acid excretion, sulfonamide cross-reactivity
Bumetanide
Loop diuretic Mechanism of action: – Block Na+, K+ 2Cl- cotransporter in thick ascending limb of Loop of Henle • Diuretic effect: use with edema – Most effective diuretics • Adverse/toxic effects: – Hypokalemia – Decrease uric acid excretion – Deafness: more common with ethacrynic acid – Allergic reaction: all are sulfonamides except ethacrynic acid
ethacrynic acid
loops diuretic Mechanism of action: – Block Na+, K+ 2Cl- cotransporter in thick ascending limb of Loop of Henle • Diuretic effect: use with edema – Most effective diuretics • Adverse/toxic effects: – Hypokalemia – Decrease uric acid excretion – Deafness: more common with ethacrynic acid – Allergic reaction: all are sulfonamides except ethacrynic acid
furosemide
loop diuretic Mechanism of action: – Block Na+, K+ 2Cl- cotransporter in thick ascending limb of Loop of Henle • Diuretic effect: use with edema – Most effective diuretics • Adverse/toxic effects: – Hypokalemia – Decrease uric acid excretion – Deafness: more common with ethacrynic acid – Allergic reaction: all are sulfonamides except ethacrynic acid
torsemide
loop diuretic Mechanism of action: – Block Na+, K+ 2Cl- cotransporter in thick ascending limb of Loop of Henle • Diuretic effect: use with edema – Most effective diuretics • Adverse/toxic effects: – Hypokalemia – Decrease uric acid excretion – Deafness: more common with ethacrynic acid – Allergic reaction: all are sulfonamides except ethacrynic acid
Amiloride
K sparing diuretic
Mechanism of action: late distal tubule and collecting duct – Na+ channel blockers • Diuretic effect in combination with thiazides – Mild diuresis – Weak antihypertensive effect • Adverse effects: – Hyperkalemia
triamterene
K sparing diuretic
Mechanism of action: late distal tubule and collecting duct – Na+ channel blockers • Diuretic effect in combination with thiazides – Mild diuresis – Weak antihypertensive effect • Adverse effects: – Hyperkalemia
eplerenone
Aldosterone receptor antagonist
Mechanism of action: collecting duct – Block sodium and water reabsorption – Also potassium sparing • Diuretic effect: – Mild diuresis • Use: – Resistant hypertension – CHF with hypertension • Adverse effects: – Hyperkalemia
