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NURS 6521N-55 WEEK 11 FINAL EXAM REAL QUESTIONS + DETAILED ANSWERS - LATEST VERSION - TOP RATED

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NURS 6521N-55 WEEK 11 FINAL EXAM REAL QUESTIONS + DETAILED ANSWERS - LATEST VERSION - TOP RATED

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NURS 6521N-55 WEEK 11 FINAL EXAM REAL QUESTIONS +
DETAILED ANSWERS - LATEST VERSION - TOP RATED




1. Q: A patient with heart failure is prescribed Enalapril (Vasotec). What
is the primary mechanism of action?
ANSWER Inhibits angiotensin-converting enzyme (ACE).
Rationale: ACE inhibitors prevent the conversion of Angiotensin I to
Angiotensin II, a potent vasoconstrictor. This decreases afterload,
reduces aldosterone secretion (decreasing preload), and decreases
ventricular remodeling, making it a cornerstone in heart failure therapy.


2. Q: A patient taking Lisinopril reports a persistent, dry cough. What is
the nurse's best action?
ANSWER Contact the provider to switch to an ARB (e.g., Losartan).
Rationale: The dry cough is caused by the accumulation of bradykinin,
which is normally broken down by ACE. ARBs block the angiotensin II
receptor directly and do not affect bradykinin, eliminating the cough.


3. Q: What electrolyte imbalance requires monitoring when a patient is
taking an ACE inhibitor?
ANSWER Hyperkalemia.
Rationale: By reducing aldosterone secretion (which normally retains
sodium and excretes potassium), ACE inhibitors cause potassium
retention.
Note: Spironolactone + ACEi = high risk of hyperkalemia.


4. Q: A female patient of childbearing age is prescribed Losartan. What
is the priority teaching?

, ANSWER "This medication causes severe fetal toxicity and is
contraindicated in pregnancy."
Rationale: ARBs and ACE inhibitors are Pregnancy Category X. They can
cause renal agenesis, pulmonary hypoplasia, and fetal death in the 2nd
and 3rd trimesters.


5. Q: A patient with heart failure is started on Carvedilol (Coreg). Why is
a beta-blocker used in HF?
ANSWER It blocks the sympathetic nervous system, preventing
cardiac remodeling.
Rationale: While beta-blockers are negative inotropes, long-term use in
HF blocks the toxic effects of chronic catecholamine stimulation,
improving ejection fraction and reducing mortality. They must be
started at very low doses and titrated slowly.


6. Q: What is a contraindication for the use of Metoprolol?
ANSWER Severe asthma or 2nd/3rd degree heart block.
Rationale: Beta-1 selective blockers still have some beta-2 effects at
higher doses, which can cause bronchospasm. They also slow AV node
conduction, making them dangerous in high-degree heart blocks.


7. Q: A patient with atrial fibrillation is prescribed Diltiazem. What is the
expected effect?
ANSWER Decreased heart rate and slowed AV node conduction.
Rationale: Diltiazem is a non-dihydropyridine calcium channel blocker.
It is highly cardioselective, slowing conduction through the SA and AV
nodes, making it excellent for rate control in A-fib.


8. Q: A patient is prescribed Amlodipine for hypertension. What side
effect is most common?
ANSWER Peripheral edema.

,Rationale: Amlodipine is a dihydropyridine CCB. It causes arteriolar
dilation, leading to precapillary vasodilation. This shifts fluid into the
interstitial space, causing dependent, pitting edema that is not relieved
by diuretics.


9. Q: A patient is taking Digoxin. What sign indicates Digoxin toxicity?
ANSWER Visual disturbances (yellow-green halos) and anorexia.
Rationale: Digoxin has a narrow therapeutic index. Early signs of
toxicity are gastrointestinal (anorexia, nausea, vomiting) and
neurological (visual changes like halos, yellow vision). Late signs are
fatal cardiac dysrhythmias.


10. Q: Before administering Digoxin, the nurse notes an apical pulse of
52 bpm. What is the action?
ANSWER Hold the dose and notify the provider.
Rationale: Digoxin slows AV node conduction. The standard protocol is
to hold the dose if the heart rate is below 60 bpm (or per specific facility
protocol, sometimes 50-55 bpm) and reassess.


11. Q: A patient on Digoxin has a potassium level of 3.0 mEq/L. What is
the nurse's primary concern?
ANSWER Increased risk of severe digoxin toxicity.
Rationale: Hypokalemia potentiates the binding of digoxin to the Na+/K+
ATPase pump, effectively increasing the drug's effect and drastically
raising the risk of fatal dysrhythmias.


12. Q: What is the antidote for severe Digoxin toxicity?
ANSWER Digifab (Digoxin-specific antibody fragments).
Rationale: Digifab binds to digoxin molecules, pulling them off the
cardiac tissue and forming complexes that are excreted by the kidneys.

, 13. Q: A patient with heart failure is prescribed Furosemide. What
electrolyte must be closely monitored?
ANSWER Potassium.
Rationale: Loop diuretics block the Na/K/Cl cotransporter in the Loop of
Henle, causing massive excretion of potassium. Hypokalemia is a major
risk for cardiac dysrhythmias.


14. Q: What auditory side effect is associated with high-dose IV
Furosemide?
ANSWER Ototoxicity (tinnitus or hearing loss).
Rationale: Loop diuretics, especially when given IV at high doses or too
rapidly, can cause permanent or temporary ototoxicity.


15. Q: A patient is taking Spironolactone. What dietary teaching is
required?
ANSWER Avoid salt substitutes and foods high in potassium.
Rationale: Spironolactone is a potassium-sparing diuretic that acts as
an aldosterone antagonist. Salt substitutes are made of potassium
chloride, which combined with the drug, can cause severe
hyperkalemia.


16. Q: A patient with hyperlipidemia is prescribed Atorvastatin. When
should the nurse instruct the patient to take it?
ANSWER In the evening.
Rationale: Cholesterol synthesis occurs primarily at night. While some
statins have long half-lives, traditional teaching is to take them in the
evening to maximize efficacy during peak synthesis.


17. Q: What is the most serious adverse effect of statins that requires
immediate medical attention?

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