Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
69 Cards in this Set
- Front
- Back
|
What class of diuretics is most effective in reducing blood pressure?
|
Thiazide Diuretics
|
|
|
Why are neither loop diuretics or potassium-sparing diuretics used as monotherapy for hypertension?
|
Neither are every effective, when used alone, at lowering blood pressure.
|
|
|
What class of medications, some of which are available over-the-counter, can antagonize the efficacy of diuretics? By what mechanisms does this occur?
|
NSAIDs cause sodium and fluid retention, and they compete with some diuretics for transport into the kidney tubules.
|
|
|
What monitoring is recommended when patients are using diuretics?
|
Monitor potassium (due to risk of hypokalemia) and SCr (b/c the thiazide diuretics lose efficacy at high SCr levels) upon initiation, after 2 weeks, and then periodically thereafter.
|
|
|
What electrolyte disturbances are associated with diuretics?
|
Decreased potassium and magnesium, increased calcium and uric acid.
|
|
|
On which comorbid conditions might diuretics have an unfavorable effect?
|
Diabetes, Gout, & Dyslipidemia
|
|
|
What dose should not be exceeded with hydrochlorothiazide or chlorthalidone? [Why?]
|
Do not exceed 25 mg with either hydrochlorothiazide or chlorthalidone. [The reductions in blood pressure at doses above 25 mg are marginal compared with the intensity of adverse effects they induce.]
|
|
|
What drug interaction occurs between cholestyramine and hydrochlorothiazide?
|
Cholestyramine reduces absorption of HCTZ (hydrochlorothiazide).
|
|
|
What drug interaction occurs between lithium and hydrochlorothiazide?
|
Hydrochlorothiazide increases serum lithium concentrations.
|
|
|
What drug interaction occurs between NSAIDs and diuretics?
|
NSAIDs reduce diuresis.
|
|
|
What drug interaction occurs between digoxin and diuretics?
|
Diuretics increase the toxicity of digoxin.
|
|
|
What drug interaction occurs between sulfonylureas and diuretics?
|
Diuretics reduce the efficacy of sulfonylureas.
|
|
|
What drug interaction occurs between chemotherapeutic agents, such as cyclophosphamide, fluorouracil, or methotrexate, and diuretics?
|
Worsened myelosuppression.
|
|
|
What increased risk is associated with the use of a thiazide diuretic, ACE inhibitor, and NSAID together?
|
Increased risk of acute renal injury.
|
|
|
Which thiazide diuretic, hydrochlorothiazide or chlorthalidone, is more potent, on a mg-per-mg bases, for both efficacy and adverse effects?
|
Chlorthalidone is more potent, both with respect to both the reduction of blood pressure and potassium levels.
|
|
|
What are the mechanisms of action for beta-blockers?
|
Beta-blockers decrease cardiac output by exerting negative chronotropic and inotropic effects, they decrease renin release by the kidney, and they decrease peripheral vascular resistance as well.
|
|
|
Which organ, the liver or the kidney, is primarily responsible for the clearance of propranolol?
|
Liver
|
|
|
Which organ, the liver or the kidney, is primarily responsible for the clearance of metoprolol?
|
Liver
|
|
|
Which organ, the liver or the kidney, is primarily responsible for the clearance of atenolol?
|
Kidney
|
|
|
Which beta blockers are okay to use in patients having congestive heart failure (CHF)?
|
Metoprolol, Bisoprolol, & Carbedilol
|
|
|
Which classes of antihypertensive agents are associated with withdrawal syndrome? How is it avoided?
|
Sudden discontinuation of either a beta blocker or a central alpha-2 agonist leads to rebound hypertension. Both drugs should be discontinued by a gradual taper to preclude this issue. For beta blockers, taper the dose by one-half every 2 to 3 days over a 2 week period.
|
|
|
Which commonly used beta blocker is suggested to have lower efficacy at reducing the risk of stroke? How might this be managed with the use of this agent?
|
Atenolol. Once daily dosing of atenolol appears to be ineffective at preventing stroke. If it is going to be used, it should be dosed twice daily.
|
|
|
What are some of the purported advantages of the new beta blocker nebivolol (Bystolic)?
|
Bystolic is said to effect vasodilation via nitric oxide release and have less adverse influence on glucose levels in diabetics compared to other beta blockers.
|
|
|
What drug interaction occurs between cimetidine and beta blockers?
|
Cimetidine inhibits the metabolism of metoprolol, labetalol, and propranolol.
|
|
|
What drug interaction occurs between amiodarone and beta blockers?
|
Concurrent use may result in hypotension and/or bradycardia.
|
|
|
What drug interaction occurs between ritonavir and beta blockers?
|
Ritonavir may lead to increased metoprolol concentrations via enzyme inhibition, and thereby increase risk of bradycardia and/or hypotension.
|
|
|
What drug interaction occurs between digoxin and beta blockers?
|
Concurrent use may lead to AV nodal block.
|
|
|
What drug interaction occurs between CYP2D6 inhibitors, such as SSRIs, and beta blockers?
|
CYP2D6 inhibitors may increase metoprolol concentrations, and thereby increase risk of bradycardia and/or hypotension.
|
|
|
What drug interaction occurs between St. John’s Wort and beta blockers?
|
St. John’s Wort may decrease the effectiveness of beta-blockers.
|
|
|
What drug interaction occurs between non-DHP CCBs (verapamil & diltiazem) and beta blockers?
|
Concurrent use increases risk of bradycardia, hypotension, and AV conduction abnormalities.
|
|
|
Aside from blood pressure, what vital sign should be considered before deciding whether to increase the dosage of a beta blocker?
|
Heart Rate: if the patient’s heart rate is in the low 60s, don’t increase the beta blocker dosage.
|
|
|
What are some of the beneficial effects of ACE inhibitors?
|
ACE inhibitors promote regression of left ventricular hypertrophy, improving systolic and diastolic function. They decrease mortality in CHF, slow progression of nephropathy from diabetes mellitus, decrease progression of CKD, and decrease mortality from cardiovascular causes, such as MI or stroke.
|
|
|
Why are salt substitutes not appropriate for patients on ACE inhibitors?
|
ACE inhibitors carry a risk of hyperkalemia. So salt substitutes, which contain potassium, further heighten that risk.
|
|
|
In which patients can ACE inhibitors have a profound, first-dose hypotensive effect?
|
Patients having renovascular disease or CHF, patients who are hypovolemic, and patients who are on a diuretic are at higher risk of a profound, first-dose hypotensive effect.
|
|
|
In whom are ACE inhibitors contraindicated?
|
ACE inhibitors are contraindicated during pregnancy and in patients who have bilateral renal artery stenosis.
|
|
|
What adverse effects are associated with ACE inhibitors?
|
Cough, rash, hyperkalemia, renal failure, and angioedema (swelling of the throat, lips, and tongue).
|
|
|
What monitoring is required with ACE inhibitors?
|
Monitor serum creatinine and potassium at baseline, after 2 weeks, and then periodically thereafter.
|
|
|
What subtype of Angiotensin II receptor do ARBs block?
|
AT1 receptors
|
|
|
What adverse effects are associated with ARBs?
|
Dizziness, angioedema, hyperkalemia, & cough (less than with ACE inhibitors though)
|
|
|
What are the two most commonly used non-dihydropyridine calcium channel blockers?
|
Verapamil & Diltiazem
|
|
|
What are the commonly used dihydropyridine calcium channel blockers?
|
Amlodipine & Felodipine
|
|
|
What is the mechanism of action for the Non-DHP CCBs?
|
Coronary and systemic vasodilation AND decrease myocardial contractility, heart rate, and AV node conduction.
|
|
|
What is the mechanism of action for DHP CCBs?
|
Coronary and systemic vasodilation
|
|
|
In what manner might DHP CCBs influence heart rate?
|
Because they lower blood pressure via vasodilation, DHP CCBs may prompt an increase in heart rate via reflex tachycardia.
|
|
|
What type of CCB may increase the risk of MI (and is therefore not often used anymore)?
|
Short-acting formulations, such as immediate release nifedipine, increase the risk of MI. [If you do see nifedipine used, it will likely be an extended release formulation.]
|
|
|
Which CCBs are particularly effective for treating angina symptoms in patients having coronary artery disease?
|
Verapamil or Diltiazem
|
|
|
What adverse drug reactions are associated with calcium channel blockers?
|
Constipation, especially w/ verapamil; bradycardia; AV block; CHF w/ verapamil or diltiazem; edema; dizziness; headache; tachycardia w/ amlodipine or felodipine; & gingival hyperplasia w/ nifedipine
|
|
|
What is the mechanism of action for the antihypertensive effect of alpha-1 receptor antagonist?
|
They inhibit efferent sympathetic activity by selectively blocking postsynaptic alpha-1 receptors responsible for contraction of vascular smooth muscle.
|
|
|
What first dose effect with alpha-1 antagonists should patients be warned about? How should they be advised to manage it?
|
A profound first-dose hypotensive effect may occur. Advise patients that the first dose should be taken at bedtime to reduce the risk of dizziness or fainting under dangerous circumstances.
|
|
|
What adverse effects are associated with alpha-1 antagonists?
|
Headache, fatigue, drowsiness, weakness, & vivid dreams
|
|
|
What is the mechanism of action for central alpha-2 agonists?
|
They inhibit sympathetic outflow, decreasing norepinephrine, heart rate, cardiac output, and peripheral vascular resistance.
|
|
|
Which antihypertensive agent is a drug of choice for treating hypertension during pregnancy?
|
Methyldopa (a central alpha-2 agonist)
|
|
|
What adverse effects are associated with central alpha-2 agonists?
|
Sedation; decreased alertness; depression; dry mouth; bradycardia; & sodium and fluid retention, especially with methyldopa
|
|
|
Describe how renin inhibitors function as antihypertensive agents.
|
By blocking the activity of renin, they inhibit the conversion of angiotensinogen to angiotensin I. Less angiotensin I leads to less of the vasoconstrictor angiotensin II. Less angiotensin II leads to less aldosterone, and thus less sodium and fluid retention.
|
|
|
What distinct advantages does a renin inhibitor have over an ACE inhibitor or an ARB?
|
No reflex increase in angiotensin II, little risk of hypokalemia (compared with ACE-Is or ARBs), and reduced incidence of rash, cough, or angioedema (compared with ACE-Is or ARBs).
|
|
|
What adverse effects are associated with the renin inhibitor aliskiren (Tekturna)?
|
Although it is generally well tolerated, it may cause GI upset, predominately diarrhea; cough; rash; hyperuricemia; gout; & kidney stones.
|
|
|
In what patient group should the concurrent use of a renin inhibitor with an ACE-I or an ARB be avoided? [Why?]
|
Diabetics [Increased risk of adverse renal outcomes.]
|
|
|
How should aliskiren be taken with respect to food? [Why?]
|
Aliskiren should be taken on an empty stomach. [A high fat meal reduces absorption.]
|
|
|
What enzyme metabolized aliskiren?
|
CYP3A4
|
|
|
Describe the use of direct vasodilators, such as hydralazine or minoxidil, for the treatment of hypertension.
|
Direct vasodilators relax arteriolar smooth muscle, thereby reducing peripheral vascular resistance, which lowers blood pressure. By reducing the afterload on the heart, they alleviate impedance to myocardial contractility.
|
|
|
In what group of CHF patients is the combination of a direct vasodilator, such as hydralazine, with isosorbide particularly useful?
|
They are particularly useful in patients who cannot tolerate ACE-Is or ARBs.
|
|
|
What antihypertensive agent is notorious for causing a lupus-like syndrome?
|
Hydralazine
|
|
|
What antihypertensive agent may cause hypertrichosis? [What is hypertrichosis?]
|
Minoxidil [Hypertrichosis is an abnormal amount of hair growth over the body.]
|
|
|
What are some of the adverse effects generally characteristic of direct vasodilators?
|
Dermatitis, drug fever, peripheral neuropathy, hepatitis, & headache
|
|
|
Describe the use of postganglionic sympathetic inhibitors for the treatment of hypertension.
|
They deplete norepinephrine from postganglionic nerve terminals, thereby inhibiting release of norepinephrine in response to sympathetic stimulation. This decreases both cardiac output and peripheral vascular resistance, resulting in lower blood pressure.
|
|
|
For what type of hypertension case are postganglionic sympathetic inhibitors reserved?
|
They are usually reserved for cases of refractory hypertension.
|
|
|
Why are postganglionic sympathetic inhibitors, such as guanethidine or guanadrel, rarely used?
|
They have a very unfavorable adverse effect profile. They cause profound orthostatic hypotension. They cause syncope. And they are noted for causing impotence, diarrhea, and weight gain.
|
|
|
What is the mechanism of action for the antihypertensive effect of reserpine?
|
It depleted norepinephrine from sympathetic nerve endings by blocking transport of norepinephrine to storage granules. This results in a decrease in sympathetic tone, which cardiac output and peripheral vascular resistance associated with the vasoconstriction that sympathetic tone maintains.
|
|
|
What adverse effects are associated with reserpine?
|
Sedation, depression, sodium/fluid retention, & diarrhea
|
