UNIT 4 NCLEX REVIW QUETIONS

The nurse is caring for a patient whose physician has just ordered Cyclomen PO 800 mg daily in 2 divided doses.  What disease process would the physician be ordering the Cyclomen for?

Endometriosis

Loop diuretic first-line in Step Care Management program to treat hypertension.

False

3 controls of blood pressure

Heart rate, stroke volume, and peripheral resistance.

ACE inhibitors effect

Prevent conversion of angiotensin I to angiotensin II → ↓vasoconstriction and ↓aldosterone → ↓BP.

ARBs effect

Block angiotensin II receptors → ↓vasoconstriction and ↓aldosterone → ↓peripheral resistance and BP.

Calcium channel blockers effect

Block Ca entry into muscle cells → vasodilation, ↓peripheral resistance, ↓BP.

Vasodilators effect

Directly relax vascular smooth muscle → ↓peripheral resistance and ↓BP.

Antihypertensives across lifespan (children)

lifestyle changes first; CCBs if needed.

Antihypertensives across lifespan (Adults)

ACE/ARBs contraindicated in pregnancy.

Antihypertensives across lifespan (Older adults)

↑toxicity risk due to renal/hepatic impairment; need dose reduction.

The primary treatment for congestive heart failure is to make the heart beat harder and faster.

False

Drug concern in acute MI

Milrinone (Primacor); Rationale: Contraindicated due to, ↑oxygen demand and contractility, worsening condition.

Heart failure pathophysiology

CAD causes hypoxia; cardiomyopathy weakens contraction; HTN enlarges heart; valve disease overloads ventricles. Right-sided failure → edema, liver congestion. Left-sided → pulmonary edema, dyspnea.

Heart failure compensatory mechanisms

↑HR, ↑BP, ↑respirations, ↑contractility; activation of renin-angiotensin system → ↑BP and fluid retention. Failure leads to worsening HF.

Digoxin toxicity symptoms

Anorexia, nausea, vomiting, malaise, depression, arrhythmias (heart block, atrial arrhythmias, ventricular tachycardia).

Why older adults risk digoxin toxicity

Higher risk due to decreased renal function, drug accumulation, and increased sensitivity.

Cardiac action potential phases

Na influx (depolarization); Na equalization; Ca influx (plateau); K efflux (repolarization); resting state.

Antiarrhythmic classes effect

Class I: block Na (phase 0); Class II: depress phase 4; Class III: prolong phase 3; Class IV: block Ca (phases 1–2).

Coronary artery disease definition

Narrowing of coronary vessels due to atherosclerosis → ↓blood flow → myocardial hypoxia → angina.

Stable angina

exertion-related, relieved by rest.

unstable angina

occurs at rest, high risk MI.

Prinzmetal angina

coronary artery spasm.

Antianginal drug indications

Nitroglycerin: acute angina; Metoprolol: stable angina, HTN, post-MI; Diltiazem: Prinzmetal’s, chronic angina, HTN.

The patient asks the nurse to explain the type of angina he is experiencing. The nurse explains the pain is due to the imbalance of myocardial supply and demand. What type of angina does this describe?

Stable

Nitrates mechanism

Vasodilation → ↓preload and myocardial oxygen demand → improved oxygen supply.

Nitrates adverse effects

Headache, dizziness, hypotension, flushing, nausea, tachycardia.

Nitroglycerin administration routine

1 SL tablet every 5 minutes up to 3 doses; call 911 if no relief after 15 minutes.

Beta blockers mechanism

Block SNS → ↓HR, ↓contractility, ↓renin → ↓BP and ↓oxygen demand.

Beta blockers adverse effects

Bradycardia, hypotension, fatigue, bronchospasm, depression, decreased libido.

Calcium channel blockers mechanism

Block calcium → vasodilation, ↓workload, ↓oxygen demand.

Calcium channel blockers adverse effects

Hypotension, arrhythmias, GI upset, headache.

Nursing implications antihypertensives

Monitor BP/HR, change positions slowly, avoid alcohol/heat, report symptoms, track angina episodes.

Nitroglycerin teaching

Do not swallow SL, store properly, sit/lie during use, rotate patches, allow nitrate-free period.

Older adults are more likely to develop adverse effects associated with the use of these drugs—dysrrhythmias, hypertension, and congestive heart disease.

False

Low density lipoproteins (LDL) enter circulation as a tightly packed unit consisting of cholesterol, triglycerides, and lipids.

True

What would cause a drug-drug interaction with bile acid sequestrants?

Thyroid hormones

Bile acid sequestrants mechanism

Bind bile acids → excreted → liver uses cholesterol to replace → ↓serum cholesterol.

The nurse is caring for a patient taking a HMG-CoA inhibitor. What would be an appropriate intervention for this patient?

Arrange for periodic ophthalmic examinations

Bile acid sequestrants adverse effects

GI irritation, constipation, vitamin deficiency, fatigue.

HMG-CoA inhibitors (statins) mechanism

Block cholesterol synthesis in liver → ↓LDL, ↓triglycerides, ↑HDL.

Statins adverse effects

GI upset, headache, liver toxicity, rhabdomyolysis.

Statin teaching

Monitor liver, report muscle pain, avoid grapefruit juice, take at bedtime.

Cholesterol absorption inhibitors mechanism

Block cholesterol absorption in intestine → ↓serum cholesterol.

Cholesterol absorption inhibitors adverse effects

Abdominal pain, diarrhea, headache, fatigue, muscle pain.

Niacin effects

↓LDL, ↓triglycerides, ↑HDL.

Niacin adverse effects

Flushing, nausea, abdominal pain.

Fibrates mechanism

↓triglyceride synthesis, ↑HDL, ↑fat breakdown.

CAD cause of death

Lead in Western world due to atherosclerosis.

LDL vs HDL

contributes to plaque formation; removes cholesterol and is protective.

Fat metabolism

broken into micelles → absorbed → chylomicrons → used for energy, stored, or processed by liver into lipoproteins.

Hyperlipidemia definition

Elevated lipids in blood contributing to CAD.

Statin nursing intervention

Arrange for periodic ophthalmic examinations; Rationale: Monitor for cataract development.