Exam 1 Drug Classes Flashcards

1
Q

Diuretics

A

Aka “water pills” - MOA inc urinary output, dec circulating volume, and dec arterial resistance; dec BP by pushing out excess Na and H20; dec CO (also note, least expensive and can be added along with other hypertensives) and 1st line of therapy for many pt’s

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2
Q

Thiazaide Diuretics

A

MOA: inhibits reabsorption of K, Na, and Cl by working on the distal convoluted tubule of the kidneys; relaxes arterioles and dec peripheral vascular resistance (PVT); results in WATER LOSS and dec CO; can be used in combo w/ other anti-hypertensives; take PO

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3
Q

Loop Diuretics

A

MOA: inhibit the kidneys to reabsorb Na in the Loop of Henle; kidneys put more Na in the urine; remember: SALT SUCKS; H20 follows NA, so more NA out means more H20 out; dec fluid in the blood vessels which dec CO which drops BP; can cause hypokalemia, ototoxicity, hypotension and dehydration; nurses MUST monitor K lvls

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4
Q

Potassium -Sparing Diuretics

A

MOA: blocks retention of aldosterone (hormone that helps regulate body’s water and salt balance); leads to K retention and excretion of Na and H20; very mild diuretic and usually given in combo w/ other diuretics/hypertensives; can lead to HYPERKALEMIA which can cause impotence, irregular menstrual cycles deepened voice, gynecomastia and hirsutism and other endocrine issues

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5
Q

Sympatholytics

A

MOA: SNS blockers; dec BP by dec PVR; SNS usually vasoconstricts, so when it is blocked there is a dec in vasoconstriction; remember Sympatholytics and SNS

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6
Q

Beta-Blockers (Beta Adrenergic Blockers)

A

MOA: Blocks beta receptors, up’s nitric oxide= vasodilation resp; blocks stimulation of beta-1 receptors= dec HR and contractility;
2 types - Beta 1 found in heart (aka cardio-selective beta blockers) and Beta 2 found in lungs); remember OLOL is a “beta blocker” because “B” and “LO” are first letters of “blocker”; PO/IV

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7
Q

Vasodialtors

A

MOA: Works directly on arterial and venous smooth muscles to cause RELAXATION; direct vasodilation causes dec systemic and PVR; indicated to treat hypertension; PO/IV; IV in emergeny situation or when PO cannot be tolerated; can cause dizziness, hypotension, headache, GI upset, tachycardia, dyspnea; remember on a VAcation you RELAX

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8
Q

Calcium Channel Blockers

A

MOA: Blocks calcium from entering the cells of the heart; the heart needs calcium to contract, less calcium means less contraction so lower overall BP; dec contractility plus dec conductivity of the heart, leads to less demand for 02 and LOWER BP: PO or IV; side effects include orthostatic hypotension or peripheral edema; best for the eldlerly or those of African American descent

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9
Q

Renin Inhibitor

A

MOA: direct inhibition of renin; Induces vasodilation, dec blood volume, dec SNS, and inhibitors cardiac and vascular hypertrophy; PO; well-tolerated except for pt’s with DM; when given with ACEi watch for hyperkalemia, especially in patients with diabetes; do not take if pregnant; GI discomfort; takes a few weeks to take full affect

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10
Q

ARB’s (Angiotensin Receptor Blocker)

A

MOA: blocks the action of angiotensin 2 AFTER it is formed; dec PVR and dec CO; SARTAN common suffix for ARB’s; causes vasodilation; inc Na and H20 excretion; DOESN’T affect HR, so can be given to pt’s with weakened hearts or heart issues; can treat an array of disorders such as diabetic retinopathy/post-stoke or post-heart attack; indications include HT, heart failure, stroke progression; well-tolerated; RISK for angiodema; do not use if pregnant and pt must use contraceptive if childbearing age; use caution in pt’s with renal problems; ARB’s and AECi’s only PO

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11
Q

ACE Inhibitors

A

MOA: Blocks angiotensin-converting enzyme (ACE);
Inhibits prod of Angiotensin-2 (powerful vasoconstrictor);
Inhibits aldosterone secretion; less H20 retention; slows progression of L vent hypertrophy associated with HTN; Drug of choice for DM & has some renal protective effects;
Safe/effective; 1st line use for HT and HF; all drugs in this class end in** “-pril”**; 1st dose can give hypotension; 15-20% drop in a few hours; can cause a dry, nonproductive, PERSISTENT cough; largest complaint from patients, often reason people switch; will also cause dizziness, rash; ANGIOEDEMA rare, but more common in African Americans (5.5% in African Americans, 0.1-0.7% in others)
NOT APPROPRIATE FOR USE IN PREGNANCY

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12
Q

Alpha-2 Adrenergic Agonists (centrally acting sympatholytics)

A

MOA: Decrease sympathetic outflow resulting in decreased stimulation of adrenergic receptors (alpha and beta receptors), decreases cardiac output;
NOT a first line treatment for HTN due to high side effect profile;
Side Effects: may worsen pre-existing liver disease, causes drowsiness;
Considerations: to be given at night, do not abruptly discontinue due to rebound HTN

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13
Q

Selective Alpha-1 Blockers

A

MOA: selective alpha-1 blockade causing venous and arterial dilation;
Not a first line treatment;
Side Effects: hypotension, dizziness

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14
Q

HMG-CoA reductase Inhibitors

A

MOA: inhibits HMG-CoA reductase in the liver, causing less cholesterol to be produced, increasing the amount of LDL receptors so more LDL is removed from the blood;
Does not cause a permanent drop in cholesterol, will need to keep taking the drug;
Stabilizes already present plaques and decreases inflammation;
Side Effects: myopathy, Rhabdomyolysis, Hepatotoxicity, acute kidney failure;
Considerations: Take with food, ~2 weeks to start seeing effects, avoid alcohol, take at night

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15
Q

Cholesterol Absorption Inhibitors

A

MOA: blocks absorption of cholesterol in jejunum;
Second line defense;
Used in combination with statins;

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