Free NAPLEX Exam Braindumps (page: 7)

Page 7 of 39

A 50-year-old female has been receiving a diuretic for the treatment of essential hypertension. This drug acts by increasing the calcium content of urine and is the drug of choice for reducing acute pulmonary edema in congestive heart failure. Its side effects include ototoxicity and hyperuricemia. What is the most likely mechanism of action of this drug?

  1. Aldosterone receptor antagonist
  2. Inhibition of the Na/K/2Cl cotransporter
  3. Inhibition of carbonic anhydrase
  4. Acts as osmotic diuretic
  5. Blocking of the NACL cotransporter

Answer(s): B

Explanation:

B: Loop diuretics inhibit the Na/K/2Cl cotransporter of the luminal membrane in the ascending limb of the loop of Henle. Therefore, reabsorption of Na, K, and CL is decreased. The loop diuretics are the most efficacious of the diuretic drugs because the ascending limb accounts for the reabsorption of 25–30 % of filtered NaCl and downstream sites are not able to compensate for this increased Na load. Loop diuretics are the drugs of choice for reducing acute pulmonary edema in congestive heart failure. Loop diuretics act promptly, even among patients who have poor function or who have not responded to thiazides or other diuretics. Adverse side effects include ototoxicity, particularly when used in conjunction with the aminoglycoside antibiotics. Furosemide and ethacrynic acid compete with uric acid for the renal and biliary secretary system, thus blocking its secretion, and thereby causing or exacerbating gouty attacks. A: Aldosterone receptor antagonist is incorrect. Spironolactone is a synthetic aldosterone antagonist that competes with aldosterone for intracellular cytoplasmic receptor sites. Because spironolactone chemically resembles some of the sex steroids, it does have minimal hormonal activity and may induce gynecomastia in males and menstrual irregularities in females. C: Inhibition of carbonic anhydrase is incorrect. Acetazolamide inhibits carbonic anhydrase, which is located intracellulary and on the apical membrane of the proximal tubular epithelium. The decreased ability to exchange NA for H in the presence of acetazolamide results in a mild diuresis. The adverse side effects of acetazolamide include metabolic acidosis (mild), potassium depletion, renal stone formation, drowsiness, and paresthesia. D: Acts as osmotic diuretic is incorrect. A number of simple, hydrophilic, chemical substances that are filtered through the glomerulus, such as mannitol and urea, result in some degree of diuresis. This is due to their ability to carry water with them into tubular fluid. Osmotic diuretics are a mainstay of treatment for patients with increased intracranial pressure or acute renal failure due to shock, drug toxicities, or trauma. E: Blocking of the NaCl cotransporter is incorrect. The thiazide derivatives act mainly in the distal tubule to decrease the reabsorption of Na by inhibition of an Na/Cl cotransporter on the luminal membrane. As a result, these drugs increase the concentration of NA and CL in the tubular fluid. Hypokalemia is the most frequent problem encountered with the thiazide diuretics and can predispose patients on digitalis to ventricular arrhythmias. Thiazides increase serum uric acid by decreasing the amount of acid excreted by the organic acid secretory system. The thiazides inhibit the secretion of calcium, sometimes leading to elevated levels of Ca in the blood.



A 54-year-old male with a long history of mild persistent asthma on daily fluticasone therapy has been using his albuterol inhaler every day for the past month, and presents requesting a refill. What changes should be made to his current regimen?

  1. Add ciclesonide to current regimen
  2. Add salmeterol to current regimen
  3. Discontinue fluticasone and instead use salmeterol
  4. Add cromolyn to current regimen
  5. Discontinue fluticasone and add ipratropium to current regimen

Answer(s): B

Explanation:

Add salmeterol to the current regimen. This patient had mild persistent asthma but was using his albuterol daily, which indicates that a step up in therapy is warranted. The preferred first line treatment regimen for moderate persistent asthma are low to medium dose inhaled corticosteroids plus a long acting beta2 agonist, as well as a short acting beta2 agonist as needed. A is incorrect. Ciclesonide is an inhaled corticosteroid. The patient in the case is already using fluticasone, so adding ciclesonide would be therapeutic duplication. C is incorrect. Long-acting beta2 agonists should only be used as adjunctive therapy in patients who are currently receiving but not adequately controlled on an inhaled corticosteroid. These medications should not be used as monotherapy, due to an increased risk of asthma related deaths. D is incorrect. Cromolyn prevents the release of vasoactive mediators from mast cell and is primarily used for exercise-induced asthma, it is not indicated as an alternative agent in patientswith moderate persistent asthma. E is incorrect. Ipratropium is a short-acting anticholinergic, which is often used in COPD or in asthma exacerbations. It is not indicated for maintenance treatment of moderate persistent asthma.



LN is 84 YOM who is in hospital for a back surgery. His height is 5 feet and 4 inches, weight 85 kg and NKDA. His past medical history includes hypertension, diabetes mellitus, major depression, hypothyroidism and chronic back pain. Post-op day 1, LN’s medication includes Dexamethasone 8 mg iv q6h with taper dosing, Ondansetron 4 mg iv q6h prn for N/V, Levothyroxine 0.075 mg po daily, Lisinopril 10 mg po daily, Citalopram 20 mg po daily, Docusate sodium / Senna 1 tab po twice a day, Bisacodyl 10 mg suppository daily prn for constipation, Famotidine 20 mg iv q12hr, Metoclopramide 10 mg iv q6h, Metformin 500 mg po bid, D51/2NS with 20 K at 125 mls/hour and Hydromorphone PCA at 0.2 mg/hour of basal rate, demand dose 0.1 mg. lock-out every 6 min, one hour limit 2.2 mg/hour. Pertinent morning labs includes serum creatinine 1.4 mg/dl, Mg 1.5 mg/dl, K5.0 mmol/L, Na 135 mmol/L.
Which of the following medication may increase LN’s Blood glucose?

  1. Lisinopril
  2. Dexamethasone
  3. Famotidine
  4. Metoclopramide
  5. Hydromorphone

Answer(s): B

Explanation:

Dexamethasone can increase LN’s blood glucose. All glucocorticosteroids are known to increase blood glucose. Blood glucose would need to be monitored while LN is being treated with dexamethasone.



LN is 84 YOM who is in hospital for a back surgery. His height is 5 feet and 4 inches, weight 85 kg and NKDA. His past medical history includes hypertension, diabetes mellitus, major depression, hypothyroidism and chronic back pain. Post-op day 1, LN’s medication includes Dexamethasone 8 mg iv q6h with taper dosing, Ondansetron 4 mg iv q6h prn for N/V, Levothyroxine 0.075 mg po daily, Lisinopril 10 mg po daily, Citalopram 20 mg po daily, Docusate sodium / Senna 1 tab po twice a day, Bisacodyl 10 mg suppository daily prn for constipation, Famotidine 20 mg iv q12hr, Metoclopramide 10 mg iv q6h, Metformin 500 mg po bid, D51/2NS with 20 K at 125 mls/hour and Hydromorphone PCA at 0.2 mg/hour of basal rate, demand dose 0.1 mg. lock-out every 6 min, one hour limit 2.2 mg/hour. Pertinent morning labs includes serum creatinine 1.4 mg/dl, Mg 1.5 mg/dl, K5.0 mmol/L, Na 135 mmol/L.
Which of the following medication may cause tardive dyskinesia when given at a higher dose and for a long duration?

  1. Lisinopril
  2. Dexamethasone
  3. Famotidine
  4. Metoclopramide
  5. Hydromorphone

Answer(s): D

Explanation:

Metoclopramide may cause tardive dyskinesia when given at a higher dose and for a long duration of time of more than 3 months. Tardive dyskinesia is also listed as a Boxed Warning for metoclopramide. Tardive dyskinesia is a serious movement disorder that is irreversible. The risk increases with duration of treatment
and the total cumulative dose. If signs or symptoms of tardive dyskinesia develop, then metoclopramide should be discontinued. There is currently no known treatment for it, but symptoms can lessen or resolve after metoclopramide is stopped. Treatment should not be more than 12 weeks unless the benefits outweigh the risks of developing tardive dyskinesia.



Page 7 of 39



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