NR 565 VERIFIED EXAM QUESTIONS AND ANSWERS
Thiazide Monitoring
Monitor blood pressure and pulse rate; also, patients should weigh themselves daily
and evaluate for decreased edema. Have patients monitor for signs or symptoms of
HYPOKALEMIA
Angiotensin-Converting Enzyme (ACE) Inhibitors Therapeutic Goal
Decrease blood pressure;
Improve hemodynamics in patients with heart failure, Drug of choice for patients w/ CKD
or DM
Reduce mortality, and treat heart failure after myocardial infarction.
Angiotensin-Converting Enzyme (ACE) Inhibitors Adverse Effects
cough, angioedema, first-dose hypotension (arteriolar dilation), hyperkalemia (due to
inhibition of aldosterone release which can cause potassium retention by the kidney.)
ACE Inhibitor Mechanism of Action
produce their beneficial effects and adverse effects by (1) reducing levels of angiotensin
II (through inhibition of ACE) and (2) increasing levels of bradykinin (through inhibition of
kinase II)
Angiotensin-Converting Enzyme (ACE) Inhibitor Prototype Drug
Lisinopril; Ramipril; Catopril;
Angiotensin-Converting Enzyme (ACE) Inhibitors Monitoring
checking creatinine 2-4 weeks after starting. Have patients track blood pressure values;
patients w/ diabetic nephropathy, monitor proteinuria and glomerular filtration rate
Angiotensin-Converting Enzyme (ACE) Inhibitors Contraindication
contraindicated during the second and third trimesters of pregnancy and in patients with
bilateral renal artery stenosis.
ACE Inhibitor Drug Interactions
Diuretics may intensify first-dose hypotension; other antihypertensive agents;
HYPERKALEMIA RISK: AVOID Drugs That Raise Potassium Levels;
Lithium;
NSAIDS (may reduce antihypertensive effects of ACE I)
Angiotensin II Receptor Blockers (ARBs)
,Indicated for individuals that cannot tolerate ACE Inhibitors due to cough/angioedema;
Similar mechanism of action;
Angiotensin II Receptor Blockers Mechanism of Action
block the actions of angiotensin II at receptor site; block access of angiotensin II to its
receptors in blood vessels, the adrenals, and all other tissues.
Angiotensin II Receptor Blockers Therapeutic Goal
Reduce blood pressure in patients with hypertension, improve hemodynamics in
patients with heart failure, slow progression of established diabetic nephropathy, reduce
mortality, and treat heart failure after myocardial infarction
Angiotensin II Receptor Blockers Difference from ACE Inhibitors
do not inhibit kinase II and hence do not increase levels of bradykinin in the lung. a
lower risk for cough; do not cause clinically significant hyperkalemia
ARBs Adverse Effects
Angioedema; can cause renal failure in patients with bilateral renal artery stenosis or
stenosis in the artery to a single remaining kidney;
ARBs/ACE Inhibitor Black Box Warning
Fetal Toxicity; Cannot be taken during pregnancy
ARBs Drug Interaction
Other antihypertensive agents
Angiotensin II Receptor Blockers Monitoring
Renal Montioring;
ARBs Prototype Drug
Losartan
Labetalol
third generation β blocker; act on both alpha and beta receptors; acts on β1, β2, α1
causing vasodilation
Labetalol Contraindication
asthma, hypotensive, 2nd/3rd degree "AV block," uncontrolled heart failure,
bradycardia.
Adverse Effects of α Blockade
, most significant adverse effect is orthostatic hypotension; other adverse effects include
reflex tachycardia, nasal congestion, inhibition of ejaculation; sodium retention and
increased blood volume
Metabolism of Labetalol, Propanolol, Metoprolol
Hepatic
Labetalol Lipid Solubility
Moderate
Drugs Used to Treat Heart Failure
(1) agents that inhibit the RAAS (ACE Inhibitors/ARBs), (2) diuretics (3) β blockers.
Prototype Drugs for HF
RAAS Inhibitors:
Captopril (angiotensin-converting enzyme inhibitor)
Losartan (angiotensin II receptor blocker)
Eplerenone (aldosterone antagonist)
Diuretics:
Hydrochlorothiazide
Furosemide
Inotropic Agent:
Digoxin (a cardiac glycoside)
β Blocker:
Metoprolol
Drugs that precipitate or exacerbate Heart Failure
NSAIDS, Alcohol, CCB,
HF ACE Inhibitor Mechanism of Action
Inhibit ANG1-->ANG2;
Decrease preload/afterload and increase cardiac output;
Decrease VSM tone =decrease BP;
Decrease Aldosterone production = Decrease NA/H20 retention
Thiazide Monitoring
Monitor blood pressure and pulse rate; also, patients should weigh themselves daily
and evaluate for decreased edema. Have patients monitor for signs or symptoms of
HYPOKALEMIA
Angiotensin-Converting Enzyme (ACE) Inhibitors Therapeutic Goal
Decrease blood pressure;
Improve hemodynamics in patients with heart failure, Drug of choice for patients w/ CKD
or DM
Reduce mortality, and treat heart failure after myocardial infarction.
Angiotensin-Converting Enzyme (ACE) Inhibitors Adverse Effects
cough, angioedema, first-dose hypotension (arteriolar dilation), hyperkalemia (due to
inhibition of aldosterone release which can cause potassium retention by the kidney.)
ACE Inhibitor Mechanism of Action
produce their beneficial effects and adverse effects by (1) reducing levels of angiotensin
II (through inhibition of ACE) and (2) increasing levels of bradykinin (through inhibition of
kinase II)
Angiotensin-Converting Enzyme (ACE) Inhibitor Prototype Drug
Lisinopril; Ramipril; Catopril;
Angiotensin-Converting Enzyme (ACE) Inhibitors Monitoring
checking creatinine 2-4 weeks after starting. Have patients track blood pressure values;
patients w/ diabetic nephropathy, monitor proteinuria and glomerular filtration rate
Angiotensin-Converting Enzyme (ACE) Inhibitors Contraindication
contraindicated during the second and third trimesters of pregnancy and in patients with
bilateral renal artery stenosis.
ACE Inhibitor Drug Interactions
Diuretics may intensify first-dose hypotension; other antihypertensive agents;
HYPERKALEMIA RISK: AVOID Drugs That Raise Potassium Levels;
Lithium;
NSAIDS (may reduce antihypertensive effects of ACE I)
Angiotensin II Receptor Blockers (ARBs)
,Indicated for individuals that cannot tolerate ACE Inhibitors due to cough/angioedema;
Similar mechanism of action;
Angiotensin II Receptor Blockers Mechanism of Action
block the actions of angiotensin II at receptor site; block access of angiotensin II to its
receptors in blood vessels, the adrenals, and all other tissues.
Angiotensin II Receptor Blockers Therapeutic Goal
Reduce blood pressure in patients with hypertension, improve hemodynamics in
patients with heart failure, slow progression of established diabetic nephropathy, reduce
mortality, and treat heart failure after myocardial infarction
Angiotensin II Receptor Blockers Difference from ACE Inhibitors
do not inhibit kinase II and hence do not increase levels of bradykinin in the lung. a
lower risk for cough; do not cause clinically significant hyperkalemia
ARBs Adverse Effects
Angioedema; can cause renal failure in patients with bilateral renal artery stenosis or
stenosis in the artery to a single remaining kidney;
ARBs/ACE Inhibitor Black Box Warning
Fetal Toxicity; Cannot be taken during pregnancy
ARBs Drug Interaction
Other antihypertensive agents
Angiotensin II Receptor Blockers Monitoring
Renal Montioring;
ARBs Prototype Drug
Losartan
Labetalol
third generation β blocker; act on both alpha and beta receptors; acts on β1, β2, α1
causing vasodilation
Labetalol Contraindication
asthma, hypotensive, 2nd/3rd degree "AV block," uncontrolled heart failure,
bradycardia.
Adverse Effects of α Blockade
, most significant adverse effect is orthostatic hypotension; other adverse effects include
reflex tachycardia, nasal congestion, inhibition of ejaculation; sodium retention and
increased blood volume
Metabolism of Labetalol, Propanolol, Metoprolol
Hepatic
Labetalol Lipid Solubility
Moderate
Drugs Used to Treat Heart Failure
(1) agents that inhibit the RAAS (ACE Inhibitors/ARBs), (2) diuretics (3) β blockers.
Prototype Drugs for HF
RAAS Inhibitors:
Captopril (angiotensin-converting enzyme inhibitor)
Losartan (angiotensin II receptor blocker)
Eplerenone (aldosterone antagonist)
Diuretics:
Hydrochlorothiazide
Furosemide
Inotropic Agent:
Digoxin (a cardiac glycoside)
β Blocker:
Metoprolol
Drugs that precipitate or exacerbate Heart Failure
NSAIDS, Alcohol, CCB,
HF ACE Inhibitor Mechanism of Action
Inhibit ANG1-->ANG2;
Decrease preload/afterload and increase cardiac output;
Decrease VSM tone =decrease BP;
Decrease Aldosterone production = Decrease NA/H20 retention
