Pharmacology Test 3 Flashcards

1
Q

alpha-blockers

A

[alpha adrenergic antagonists]

blood vessels (blocks constriction)

bladder and prostate (blocks contraction)=BPH

eyes- (blocks dilation)

male sex organs (blocks ejaculation)

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2
Q

alpha blockers

A

Drug Interactions: increased hypotension wih alcohol

Adverse Effects: orthostatic hypotension, first dose phenomenon, flushing, reflex tachycardia, vertigo, inhibition of ejaculation (major reason for non-adhearance)

Nurse: orthostatic hypotension, easy on the caffiene, take at bedtime to avoid drowsiness, discontinue slowly, fist dose effect

examples: phentanolamine (antidote for alpha agonist extravasation), doxazosin, prazosin, Flomax (no orthostatic hypotension)

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3
Q

ARB’s

A

=Angiotensin II Receptor Blockers

block angiotensin II receptors on blood vessels, causing blood vessels to dilate, reducing BP, making it easier for heart to pump blood-can improve heart failure. In addition, progression of kidney disease due to high blood pressure or diabetes is slowed-prevent kidney failure. Decrease release of aldosterone, thereby increase renal excretion of sodium and water.

approved for: HTN, MI, HF, diabetic neuropathy, prevention of MI,

Effect is similar to angiotensin converting enzyme (ACE) inhibitors. ACE inhibitors work by preventing the formation of angiotensin II rather than blocking it.

***ARB’s cost more than ACE inhibitors and are 2nd line. Used when pt develops cough from ACE inhibitors. ARB’s DO NOT cause hyperkalemia, but may increase risk of cancer.

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4
Q

Angiotensin II

A

Part of the RAAS. Most importantly: vasoconstriction and aldosterone release (ie. increase BP)

Directly causes muscles surrounding blood vessels to contract, thereby narrowing blood vessels=high blood pressure

Indirectly: acts on sympathetic nervous system to promote NE release, adrenal medulla to promote Epi release and the CNS to increase sympathetic outflow to blod vessels.

Acts on adrenal cortex to promote synthesis and release of aldosterone (even when angiotensin II is too low to cause vasoconstriction)

Can cause hypertrophy of cardiac muscle and remodeling of of mass within the heart., thickening of blood vessel walls.

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5
Q

ARB’s

A

indications: HTN (Benicar and Cozaar), diabetic nephropathy (Cozaar), stroke prevention (Cozaar)

Adverse Effects: headache, dizziness, fainting, hypotension, fetal harm (2nd/3rd trimester), renal failure (if pt has renal artery stenosis) , cancer

Drug Interactions: additive with other antihypertensive (diuretics, sympatholytics, vasodilators, CCB’s), reduced serum level with phonbarbital

Nursing Implications: rule out pregnancy, monitor for first dose phenomenon, advise-wt loss, smoking cessation, reduce alcohol, salt, increase exercise. Monitor electrolytes, hepatic and renal function

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6
Q

Antihypertensives

A

Calcium Channel Blockers (nifedipine=Procardia)

Vasodilators (sodium nitroprusside=Nitropress, hydralazine=Apresoline)

alpha-blockers

beta-blockers

ACE inhibitors

ARB’s

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7
Q

Beta Blockers

(sympatholytics)

A

Actions: Block sympathetic nervous system catecholamines (Epi, NE)=reduced renin and aldosterone release, decreased fluid volume, vasodilation of arterioles=decrease in PVR and BP, reduce HR, reduce force of contraction, reduce velocity of impulse conduction through AV node

Indications: HTN, long-term angina treatment, dysrhythmias (suppress sinus and atrial tachydysrhythmias), MI, HF, hyperthyroidism, migraine prophylaxis, stage fright, pheochromocytoma, glaucoma

Contraindications: AV block, bradydysrhythmias

Adverse Effects: Beta1-bradycardia (AV block), reduced CO, symptoms of HF (cough, SOB, edema, fatigue), drowsiness, depression, Beta2-bronchospasm/bronchoconstriction, hypoglycemia from inhibition of glycogenolysis

Nurse: VS (esp. with CCB), report dizziness, bradycardia, fainting, take before meals, report edema/dypsnea, diabetes: tachycardia (symptom of hypoglycemia) is masked bc of Beta1 blockade

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8
Q

RAAS

(renin-angiotensin-aldosterone-system)

A

Renin + Angiotensin
(kidney) (liver)

Angiotensin I
(weak vasoconstrictor)
↓(ACE)
** Angiotensin II**
(potent vasoconstrictor)
↓ ↓
Peripheral Aldosterone
Vasoconstriction
↓ ↓
Increased BP Sodium Retention
+
Water Retention

Restored Fluid
Volume

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9
Q

Beta1 and Beta2 Blockers

A

Non-selective (first generation)

propanolol-angina, HTN, dysrhythmias, MI, migraine prophylaxis

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10
Q

Beta1 Blockers

A

Cardioselective (2nd Generation)

Atenolol-HTN, Angina MI

Metoprolol-HTN, Angina, MI, HF

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11
Q

Beta Blockers with Vasodilation Actions

A

Third Generation

Carvedilol-HTN, MI, HF

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12
Q

Beta1 agonist

A

Selective activation of Beta1 receptors (heart)

beta1 receptors can be activated by epinephrine, NE, isoproterenol, dopamine, dobutamine, and ephedrine.

Indications: HF, Shock, AV heart block, asystole

Adverse Effects: tachycardia, dysrhythmias, angina

Drug Interatctions:

Nurse:

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13
Q

dobutamine

(Dubutrex IV)

A

Beta-1 agonist (catecholamine)

Indication: HF

Adverse Effects: tachycardia

Drug Interactions: intensified by MAOI’s (reduce dobutamine dosage at least 90%), TCA, and general anesthesia

Nurse: monitor BP and ECG

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14
Q

Antidysrhythmics

A

in their most severe forms, dysrhythmias can disable the heart that no blood is pumped at all. Because of their ability to compromise cardiac function, dysrhythmias are associated with a high degree of morbidity and mortality. virtually all of the drugs used to treat dysrhythmias can also cause dysrhythmias-use only when benefits outweigh risks

Sodium Channel Blockers

Beta-Blockers

Potassium Channel Blockers

Calcium Channel Blockers

Adenosine and Digoxin

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15
Q

inotropic

chronotropic

A

force of contraction

rate of contraction

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16
Q

Anti-Anginals

A

BB’s

Nitrates

CCB’s

ranolazine