D444 Adult Health I
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Free D444 Adult Health I Questions
1. Why is it important to avoid administering potassium via IV push?
- Potassium can only be given orally, not intravenously.
- Administering potassium via IV push can lead to cardiac arrest due to rapid increases in serum potassium levels.
- IV push potassium is a standard practice in emergency situations.
- IV push potassium is safe if monitored closely.
Explanation
Administering potassium via IV push is extremely dangerous because it can cause a rapid rise in serum potassium levels, which may trigger life-threatening cardiac arrhythmias or cardiac arrest. Safe administration requires dilution in IV fluids and controlled infusion rates, allowing the body to tolerate the potassium gradually. Oral potassium or a slow IV infusion is the standard practice for correcting hypokalemia, and IV push should be avoided except under very controlled, emergent protocols with continuous cardiac monitoring.
2. What is the treatment for severe cases of hyponatremia with Na levels around 115 and severe neurologic symptoms such as seizure or coma?
- 1 g IV NaCl
- 3% NaCl
- 0.45% NaCl
- 0.9% NaCl
Explanation
Severe hyponatremia with sodium levels around 115 mEq/L accompanied by neurologic symptoms such as seizures or coma is a medical emergency requiring prompt correction with hypertonic saline, specifically 3% NaCl. This concentrated solution helps raise serum sodium levels more rapidly to reduce cerebral edema and prevent further neurologic damage. The correction, however, must be carefully monitored to avoid rapid shifts that could cause central pontine myelinolysis (osmotic demyelination syndrome). Frequent sodium level assessments and controlled infusion rates are essential to ensure safe management.
3. Which of the following correctly describes the mechanism by which thiazide diuretics cause a metabolic alkalosis?
- Inhibition of sodium cotransporter→Decreased potassium backleak→Decreased luminal electropositivity
- Inhibition of luminal enzyme→Decreased carbonic acid formation→Decreased H+ recycling
- Inhibition of intracellular receptor→Decreased ENaC sodium uptake→Reduced negative luminal potential
- Inhibition of sodium cotransporter→Volume depletion→RAAS activation
Explanation
Thiazide diuretics inhibit the Na⁺/Cl⁻ cotransporter in the distal convoluted tubule, leading to increased sodium and water excretion. This causes mild volume depletion, which in turn activates the renin-angiotensin-aldosterone system (RAAS). The rise in aldosterone promotes sodium reabsorption in exchange for hydrogen and potassium secretion in the distal nephron, resulting in metabolic alkalosis and hypokalemia. Thus, the mechanism involves volume depletion leading to secondary RAAS activation rather than direct inhibition of acid-base transporters.
4. What does the A1C test measure in relation to diabetes management?
- Lipid profiles
- Current blood glucose levels
- Insulin sensitivity
- Glucose levels over the past 2–3 months
Explanation
The A1C test, also known as glycosylated hemoglobin, measures the percentage of hemoglobin that has glucose attached to it. Since red blood cells live for about 120 days, this test reflects the average blood glucose levels over the previous 2–3 months. It is a vital tool for monitoring long-term glycemic control in diabetic patients and helps assess how well treatment plans (diet, medication, insulin) are managing blood sugar over time.
5. What condition should be avoided to minimize pain following a prostatectomy?
- Dehydration
- Nausea
- Diarrhea
- Constipation
Explanation
After a prostatectomy, constipation should be avoided because straining during bowel movements increases intra-abdominal and pelvic pressure, which can cause significant pain and may disrupt the surgical site or sutures. Additionally, constipation can contribute to urinary retention, further increasing discomfort. To prevent this, patients are encouraged to maintain adequate hydration, consume a high-fiber diet, and, if necessary, use stool softeners as prescribed.
6. If a patient presents with symptoms of hypocalcemia and has a history of parathyroid dysfunction, what would you expect their PTH levels to be?
- Low
- Variable
- Normal
- High
Explanation
Parathyroid hormone (PTH) regulates calcium levels in the blood. In cases of hypocalcemia caused by parathyroid dysfunction, particularly hypoparathyroidism, the parathyroid glands fail to secrete adequate amounts of PTH. As a result, calcium levels drop, and PTH levels are low, which distinguishes it from secondary hypocalcemia caused by vitamin D deficiency or renal failure, where PTH may be elevated as a compensatory response. Low PTH confirms that the hypocalcemia is due to impaired parathyroid function rather than other causes.
7. You are taking a patient's BP and notice that the patient develops a carpal spasm. Which of the following is true?
- The patient is having nervous response to an inflating blood pressure
- The patient has hypocalcemia and this is Chvostek's Sign
- The patient has hypercalcemia and this is Trousseau's Sign
Explanation
When a patient develops a carpal spasm during blood pressure cuff inflation, this is known as Trousseau’s Sign, not Chvostek’s Sign. Trousseau’s Sign is a clinical indicator of hypocalcemia, a condition characterized by low calcium levels in the blood. The spasm occurs because low calcium increases neuromuscular excitability, leading to involuntary muscle contractions. This finding helps clinicians assess for calcium imbalances that may result from conditions such as hypoparathyroidism or renal failure.
8. A patient presents with rapid breathing and confusion. If lab results show increased pH and decreased CO₂, what condition might they be experiencing?
- Respiratory acidosis
- Metabolic alkalosis
- Respiratory alkalosis
- Metabolic acidosis
Explanation
Rapid breathing (hyperventilation) causes excessive exhalation of carbon dioxide, leading to decreased CO₂ levels in the blood. This reduction in carbonic acid results in a rise in pH, producing a state known as respiratory alkalosis. Common causes include anxiety, pain, fever, or hypoxemia. The elevated pH leads to cerebral vasoconstriction, which can explain symptoms such as confusion, dizziness, and tingling. Management involves addressing the underlying cause and restoring normal ventilation to correct the acid-base imbalance.
9. Describe the significance of holding digoxin when the apical pulse is less than 60 bpm.
- Holding digoxin is only required if the patient has other symptoms.
- Holding digoxin is important because a low heart rate may indicate potential toxicity or adverse effects of the medication.
- Holding digoxin is unnecessary as it does not affect heart rate.
- Holding digoxin can lead to increased heart rate.
Explanation
Digoxin is a cardiac glycoside used to strengthen myocardial contraction and control heart rate, especially in conditions like heart failure and atrial fibrillation. Before administering digoxin, the apical pulse should be checked for a full minute. If the pulse is below 60 beats per minute, the medication should be withheld and the healthcare provider notified. A low heart rate can indicate digoxin toxicity or an exaggerated pharmacologic effect, which can lead to bradycardia, arrhythmias, or cardiac arrest. Holding the medication allows time for evaluation and prevents further complications.
10. Which question has the most importance when the nurse admits a patient with a diagnosis of acute glomerulonephritis?
- "Do you have a susceptibility to allergies?"
- "Have you had any contact with anyone who has measles?"
- "Have you recently had strep throat?"
- "How much fluid do you drink in a day?"
Explanation
Acute glomerulonephritis is often post-infectious, most commonly following a streptococcal infection. Asking whether the patient has recently had strep throat is crucial because it can help identify the precipitating cause, guide treatment, and assist in monitoring for potential complications. While allergies, measles exposure, and fluid intake may provide useful background information, they are not directly related to the typical etiology of acute glomerulonephritis.
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