NAPLEX North American Pharmacist Licensure Examination Questions and Answers

Moderate-Intensity Statin Therapy: Atorvastatin 10 (20) mg, Rosuvastatin (5) 10 mg, Simvastatin 20–40 mg,

Pravastatin 40 (80) mg, Lovastatin 40 mg, Fluvastatin XL 80 mg, Fluvastatin 40 mg bid, Pitavastatin 2–4 mg

Famotidine and Metoclopramide would need to be adjusted for poor renal function. Since his CrCl is less than 50, famotidine would need to be adjusted by decreasing the dose by 50% or increasing the interval to every 36 to 48 hours. Metoclopramide would also need to be adjusted by 50% of the normal dose since his CrCl is less than 40. ACEInhibitors and ARBs should be held if serum K is greater than 5.6 or there is a rise in serum creatinine greater than 30% after initiation.

Calcium makes up 40% of the MW of CaCO3. MW Ca / MW CaCO3 40.078 / 100.087 × 100% = 40%. 40% of 1 g CaCO3 = 0.4 g. Patient is taking 0.4 g of Ca 3 times daily. 0.4 g Ca × 3 = 1.2 g of Elemental Ca.

Relative risk can be stated as 0.77 times as likely or 0.77 times the risk, but it could also be illustrated as a relative risk reduction and stated as a 23% risk reduction or 23% lower risk by taking the medication.

A: The syndrome is an acute noninflammatory encephalopathy with hepatic failure. Although the etiology of Reye's syndrome is unknown, the condition typically follows viral illness, particularly upper respiratory tract infection (URTI), influenza, varicella, or gastroenteritis, and is associated with aspirin use during the illness. A dramatic decrease in aspirin use in children has made Reye's syndrome rare. High index of suspicion is critical for diagnosis. Consider Reye's syndrome in any child with vomiting and altered mental status. Pathogenesis is unclear, but it typically involves mitochondrial dysfunction in a viral-infected, sensitized host, usually with exposure to mitochondrial toxins (e.g., salicylates, in >80% of cases). Individuals with low levels of urea cycle enzymes are also at increased risk. Mortality has fallen from 50% to less than 20% as a result of earlier diagnosis, recognition of milder cases, and more aggressive therapy. Signs and symptoms of Reye's

syndrome include protracted vomiting, with or without significant dehydration, encephalopathy in afebrile patients with minimal or absent jaundice, and hepatomegaly in 50% of patients. Antiemetics may mask early symptoms. Liver function tests reveal elevation of ammonia levels to as much as 1.5 times normal (up to 1200g/dL) 24-48 hours after the onset of mental status changes; this is the most frequent laboratory abnormality. Transaminases (ALT and AST) increase to 3 times normal. Histologic changes include: hepatocyte cytoplasmic fatty vacuolization, astrocyte edema, loss of neurons, and edema and fatty degeneration in proximal lobules. The American Academy of Pediatrics Committee on Infectious Disease recommends that salicylate not be given to children with chicken pox or influenza B. B: Acetaminophen is incorrect. Acetaminophen acts by prostaglandin synthesis in the CNS, and this explain its antipyretic and analgesic properties, which account for its weak anti-inflammatory activity. Acetaminophen is a suitable substitute for the analgesic and antipyretic effects of aspirin in those patients with gastric complaints and to avoid Reye's syndrome in children. C: Indomethacin is incorrect. Indomethacin is more potent than aspirin as an anti-inflammatory agent (NSAID), but it is inferior to the salicylates at doses tolerated by rheumatoid arthritis patients. D: Mefenamic acid is incorrect. Mefenamic acid has no advantage over the other NSAIDS as anti- inflammatory agents. The side effects of mefenamic acid, such as diarrhea, can be severe and associated with inflammation of the bowel. E: Diclofenac is incorrect. Diclofenac is approved for long-term use in the treatment of rheumatoid arthritis, osteoarthritis, and ankylosing spondylitis.

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.

125 lb =56Kg, 56Kg × [18 units/ 1 kg] = 1022.72 units/hr, 1022.72 units × [1 mL/50 units] = 20.45 mL/hr

Statin therapy should be used as treatment in adults with primary LDL–C ≥190 mg/dL and age over 21 years. Unless contraindicated, high-intensity statin therapy should be used.

Normal serum creatinine levels are 0.6 – 1.2 mg/dL.

50 mcg/kg/min × 80 kg = 4 mg/min × 60 min/hr = 240 mg/hr 2500 mg / 250 mL = 10 mg/mL 240 mg/hr / 10 mg/ mL = 24 mL/hr Esmolol Infusion

Cisplatin. All chemotherapeutics have similar generalized side effects related to their effects on rapidly growing cells. These include hair loss, nausea, and fatigue. However, many chemotherapeutics have unique toxicities as well which are often tested. Cisplatin (C) is notable for its nephrotoxicity and ototoxicity. Cyclophosphamide

(A) is known to cause hemorrhagic cystitis. This is a distinct process from nephrotoxicity. The most noteworthy side effect of bleomycin (B) is pulmonary toxicity that can lead to pulmonary fibrosis. Vinblastine (D) is known for bone marrow suppression. Vincristine (E) causes neuropathy.

Diltiazem has a major drug interaction with Simvastatin. Diltiazem is a CYP3A4 inhibitor, and since Simvastatin is metabolized by CYP3A4, its level can build up and the risk of myopathy increases. It is recommended to switch to a non-CYP3A inhibitor such as Pitavastatin, Pravastatin, or Rosuvastatin, and if Simvastatin is to be kept on it should not exceed 10 mg/day. The same interaction also exists with lovastatin, and the recommendation is to not exceed a total dose of 20 mg/day po of Lovastatin. Given the current options, the best choice is to change to Atorvstatin 40 mg po daily.

Glucagon-like peptide-1 receptor agonists Sulfonylureas work in beta cells in the pancreas that are still functioning to enhance insulin secretion. Alpha-Glucosidase Inhibitors stop α-glucosidase enzymes in the small intestine and delay digestion and absorption of starch and disaccharides which lowers the levels of glucose after meals. DPP4 blocks the degradation ofGLP-1, GIP, and a variety of other peptides, including brain natriuretic peptide. Glucagon-like peptide-1 receptor agonists work in various organs of the body. Glucagon-like peptide-1 receptor agonists enhance glucose homeostasis through: (i) stimulation of insulin secretion; (ii) inhibition of glucagon secretion; (iii) direct and indirect suppression of endogenous glucose production; (iv) suppression of appetite; (v) enhanced insulin sensitivity secondary to weight loss; (vi) delayed gastric emptying, resulting in decreased postprandial hyperglycaemia. Thiazolidinediones are the only true insulin-sensitising agents, exerting their effects in skeletal and cardiac muscle, liver, and adipose tissue. It ameliorates insulin resistance, decreases visceral fat. Biguanides work in liver, muscle, adipose tissue via activation of AMP-activated protein kinase (AMPK) reduce hepatic glucose production. SGLT2 inhibitors work in the kidneys to inhibit sodium-glucose transport proteins to reabsorb glucose into the blood from muscle cells; overall this helps to improve insulin release from the beta cells of the pancreas.

Serum chloride levels should ideally fall between 96-106 mEq/L. For this reason, the patient’s chloride level has come back as normal.

Celexa causes dose-dependent QT interval prolongation, which can cause Torsades de Pointes, ventricular tachycardia, and sudden death. Celexa is not recommended for use at doses greater than 40 mg per day because such doses cause too large an effect on the QT interval and confer no additional benefit. Celexa should be discontinued in patients found to have persistent QTc measurements greater than 500 ms. Ondansetron and Famotidine may cause QT prolongation. Ondansetron may cause QT prolongation. However, this would be dose-dependent. Doses greater than 16 mg of Ondansetron IV are no longer recommended due to an increased risk of QT prolongation. Famotidine may prolong the QT interval; this has been reported in those with renal dysfunction. There have also been reports of torsade de pointes. Use of all three medications may result in an arrhythmia occurring since both have the potential to prolong the QT interval. Therefore, close monitoring is recommended or discontinuation of one medication. The other medications listed do not have this warning/precaution.

Benign prostatic hyperplasia (BPH) is an example of postrenal acute kidney injury (AKI). Postrenal AKI, as the name suggests, involves an effect ‘post’ or ‘beyond’ the kidney, to problems that emerge downstream from the kidney. BPH is one such example of that. Other examples include kidney stones, bladder stones and bladder cancer.

The dihydropyridine drug – nifedipine – is the active ingredient found in the medicine Adalat. Nifedipine is used to treat angina, Reynaud’s phenomenon and hypertension. It is also used as a tocolytic agent in premature labor.

A, B, C. Hepatotoxicity, including hepatic failure, has been fatal and may more commonly occur in the first 6 months of treatment. Valproic acid and its analogs are contraindicated in patients with known urea cycle disorders. Patients with urea cycle disorders have a genetic enzyme defect leading to an impaired ability to produce urea. Hyperammonemic encephalopathy has been reported following initiation of valproate therapy. Because of, inhibition of the secondary phase of platelet aggregation, and abnormal coagulation parameters complete blood counts and coagulation tests are recommended before initiating valproic acid therapy and at periodic intervals.

DPP4 Inhibitors, (D)Glucagon-like peptide-1 receptor agonists, (E)Thiazolidinediones (F)Biguanide Sulfonylureas work in beta cells in the pancreas that are still functioning to enhance insulin secretion. Alpha- Glucosidase Inhibitors stop α-glucosidase enzymes in the small intestine and delay digestion and absorption of starch and disaccharides which lowers the levels of glucose after meals. DPP4 blocks the degradation ofGLP-1, GIP, and a variety of other peptides, including brain natriuretic peptide. Glucagon-like peptide-1 receptor agonists work in various organs of the body. Glucagon-like peptide-1 receptor agonists enhance glucose homeostasis through: (i) stimulation of insulin secretion; (ii) inhibition of glucagon secretion; (iii) direct and indirect suppression of endogenous glucose production; (iv) suppression of appetite; (v) enhanced insulin sensitivity secondary to weight loss; (vi) delayed gastric emptying, resulting in decreased postprandial hyperglycaemia. Thiazolidinediones are the only true insulin-sensitising agents, exerting their effects in skeletal and cardiac muscle, liver, and adipose tissue. It ameliorates insulin resistance, decreases visceral fat.

Biguanides work in liver, muscle, adipose tissue via activation of AMP-activated protein kinase (AMPK) reduce hepatic glucose production. SGLT2 inhibitors work in the kidneys to inhibit sodium-glucose transport proteins to reabsorb glucose into the blood from muscle cells; overall this helps to improve insulin release from the beta cells of the pancreas.

Dexamethasone is used to promote fetal lung maturation. This may be necessary in cases of women who need to deliver prematurely. A tocolytic drug, such as nifedipine, may be used to suppress labor whilst dexamethasone works to accelerate fetal lung development.