A nurse is discussing the use of docusate sodium (Colace) with a client who is recovering from a non-ST elevation myocardial infarction (NSTEMI). What is the rationale for administering this medication during the recovery from a myocardial infarction?
Treats hyperlipidemia to reduce the risk of new plaques
Prevents the formation of clots to reduce the risk of stroke
Prevents vagal stimulation to reduce e risk of dysrhythmias
Removes excess sodium to reduce the risk of hypertension
The Correct Answer is C
A. This statement refers to medications like statins (e.g., rosuvastatin, atorvastatin) which are used to lower cholesterol levels and reduce the risk of atherosclerosis progression. Docusate sodium does not treat hyperlipidemia or affect plaque formation directly.
B. This refers to anticoagulant medications (e.g., heparin, warfarin, direct oral anticoagulants) which are used to prevent clot formation and reduce the risk of thromboembolic events such as stroke. Docusate sodium does not have anticoagulant properties.
C. After a myocardial infarction (MI), especially in the early recovery phase, vagal stimulation can exacerbate bradycardia or contribute to dysrhythmias. Stool softeners like docusate sodium help prevent constipation, which can stimulate the vagus nerve during straining, potentially leading to vagally mediated dysrhythmias such as bradycardia or atrioventricular blocks.
D. Diuretics (e.g., furosemide, hydrochlorothiazide) are used to reduce fluid retention and lower blood pressure by increasing urine output. Docusate sodium does not remove excess sodium or affect blood pressure regulation.
Nursing Test Bank
Naxlex Comprehensive Predictor Exams
Related Questions
Correct Answer is D
Explanation
A. Dopamine is primarily associated with other neurodegenerative disorders such as Parkinson's disease, not Alzheimer's disease. In Alzheimer's disease, the focus is on changes related to beta-amyloid plaques and neurofibrillary tangles rather than alterations in dopamine levels.
B. Glial cells, including astrocytes and microglia, play a role in the brain's immune response and support of neurons. In Alzheimer's disease, there is evidence of increased activation and proliferation of glial cells in response to neuroinflammation and the presence of beta-amyloid plaques and neurofibrillary tangles. This reactive gliosis is a secondary response to the underlying pathology.
C. Glutamate is an excitatory neurotransmitter involved in various brain functions, including memory and learning. In Alzheimer's disease, there is evidence of dysregulation in glutamate metabolism and
signaling pathways. This dysregulation can lead to excitotoxicity, which contributes to neuronal damage and cell death seen in the disease.
D. Neurofibrillary tangles are one of the hallmark pathological features of Alzheimer's disease. These tangles are aggregates of hyperphosphorylated tau protein that accumulate inside neurons, disrupting their normal functioning and eventually leading to cell death. Neurofibrillary tangles, along with beta- amyloid plaques, contribute to the progressive cognitive decline observed in Alzheimer's disease.
Correct Answer is D
Explanation
A. Heparin is an anticoagulant medication used primarily to prevent and treat blood clots. It does not directly affect cardiac output or ejection fraction.
B. Adenosine is used to treat supraventricular tachycardia (SVT) by slowing conduction through the AV node. It does not directly affect cardiac output or ejection fraction in the context of heart failure.
C. Warfarin is an anticoagulant used to prevent blood clots. Similar to heparin, it does not affect cardiac output or ejection fraction.
D. Digoxin is a medication that increases the strength and efficiency of heart contractions (positive inotropic effect) and slows the heart rate (negative chronotropic effect). It is commonly used in heart failure to improve symptoms and increase cardiac output by enhancing the heart's ability to pump blood effectively.
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