NABP NAPLEX North American Pharmacist Licensure Examination Exam Practice Test

15% dextrose = 15gm/100ml = 300gm/2000ml. Patient needs 300gm. 300gm/Xml = 20gm/100ml = 1500ml

Propylthiouracil (PTU) is recommended for treatment of hyperthyroidism in women who are in their first trimester of pregnancy by the American Thyroid Association (ATA). Methimazole has been associated with congenital malformations including aplasia cutis in rare cases and thus it is not recommended in the first trimester. The ATA recommends switching to methimazole once in the second trimester as there is a risk of liver injury associated with the use of PTU.

Acarbose is an alpha glucosidase inhibitor that inhibits carbohydrate breakdown. Metformin is a biguanide that decreases hepatic glucose production. Dapagliflozin is a SGLT2 inhibitor to decrease glucose reabsorption in

the kidney. Pioglitazone is a TZD that increases insulin sensitivity. Sitagliptin is a DPP-4 inhibitor that works on incretins/increase insulin secretion/decrease glucagon secretion.

LDL can be elevated by diuretics, cyclosporine, glucocorticoids, and amiodarone.

80kg person = 15mg/kg/day = 1200mg/day 80mg /5ml = 1200mg/X X= 75mL/day / 4 doses = 18.75 mL per dose

Mesna is administered to patients taking either ifosfamide or cyclophoshamide to conjugate toxic acrolein and therefore prevent hemorrhagic cystitis (bladder bleeding).

Clopidogrel and ticlopidine are ADP receptor pathway inhibitors. The irreversible inhibition of the ADP- dependent pathway of platelet activation is thought to be the result of covalent modification and inactivation of the platelet P2Y ADP receptor. This receptor is coupled to the inhibition of adenylyl cyclase. Both drugs are prodrugs and undergo conversion to active metabolites in the liver. However, clopidogrel must undergo oxidation by hepatic P450 enzymes to its active form. This is significant because many drugs are metabolized the hepatic P450 enzymes, including statins, and clopidogrel may interact with these medications. Clopidogrel is a second-generation thienopyridine and ticlopidine is a first-generation thienopyridine. Both drugs are indicated in combination with aspirin to prevent stent thrombosis. Eptifibatide is a GPIIb-IIIa receptor antagonist that is used to treat unstable angina and non-ST segment elevation myocardial infarction. Eptifibatide is also used to reduce ischemic events in patients who are undergoing percutaneous coronary intervention. The drug is a synthetic peptide that directly antagonizes the GPIIb-IIIa receptor on the platelet. Aspirin is an antiplatelet drug that works by inhibition of synthesis of prostaglandins. Prostaglandin G2 is the result of a synthesis pathway that is activated by platelets and endothelial cells, and results in localized

vasoconstriction and induction of platelet aggregation, as well as causing release of platelet granules. Warfarin is an anticoagulant that acts on vitamin K-dependent reactions in the coagulation pathway. Vitamin K is necessary for hepatic synthesis of coagulation factors II, VII, IX and X, protein C and protein S. Vitamin K- dependent carboxylation is necessary for induction of enzymatic activity of these coagulation factors. Take- home message: Clopidogrel, a second-generation thienopyridine ADP receptor pathway inhibitor, is indicated in combination with aspirin to prevent stent thrombosis in patients who undergo percutaneous coronary intervention after myocardial infarction. Clopidogrel is a prodrug that must undergo oxidation by hepatic P450 enzymes, and therefore may affect the activity of statins and other drugs dependent on the hepatic P450 enzymes.

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.

Primary treatment for stenotrophomonas maltophilia is SMX-TMP. Meropenem, ciprofloxacin, and vancomycin have no coverage.

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

To determine the dose conversion IV to PO, the ratio of PO to IV needs to be determined, this is 7.5 / 1.5 which is 5. This number means that the PO dose is 5 times more than the IV dose to get the same amount of drug into the bloodstream. If the patient is taking 0.5 mg IV then the PO dose would be 0.5 mg multiplied by 5, which is 2.5 mg. Since the patient is taking the medication every 4 hours the patient is receiving 6 doses, 24hrs/4hrs = 6. Since the patient is receiving 2.5 mg every dose and is receiving 6 doses a day, the patient is receiving 15 mg, 2.5 mg multiplied by 6 doses.

DPP4 Inhibitors, D 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.

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 skeletaland 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.

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.

Agents that can cause elevated triglycerides: oral estrogens, glucocorticoids, bile acid sequestrants, protease inhibitors, retinoic acid, anabolic steroids, sirolimus, raloxifene, tamoxifen, beta blockers (not carvedilol), and thiazides.

Risk factors for myopathy are hypothyroidism, reduced renal or hepatic function, rheumatologic disorders such as polymyalgia rheumatica, steroid myopathy, vitamin D deficiency, or primary muscle diseases.

Sucralfate is a drug used to treat active duodenal ulcers and may also be used to treat GERD or stress ulcers.

It is reasonable to add triglyceride-lowering medications such as fibrates or niacin to prevent pancreatitis in those with triglyceride levels >500 mg/dL, which applies to this patient as his TG level is 640 mg/dL . C. is wrong because gemfibrozil should not be initiated in patients on statin therapy because of an increased risk for muscle symptoms and rhabdomyolysis. Fenofibrate may be considered concomitantly with a low- or moderate- intensity statin when triglycerides are above 500 mg/dL,2, however he is on a high intensity statin therapy. For niacin, the IR dose should start at 100 mg TID2 and niacin does not lower triglyceride levels as much as fibrate do.4 Fenofibrates are dose adjusted for renal function lower than 60 mL/min to 54 mg/mL, so this dose is appropriate for this patient because of his renal function being above 60 mL/min. The best option is fenofibrate 162 mg daily, but this needs to be monitored for any symptoms of muscle pain exhibited by the patient, especially as the patient is at a higher risk due to being a diabetic. Fish oil is not a first line agent to treat hypertriglyceridemia.

Acetaminophen is metabolized by choices A through D. The major route is glucuronidation catalyzed by UDP- glucuronyl transferase in the liver. Sulfation is the next most common route and is the target mechanism for NAC therapy. Oxidation by cytochrome P-450 results in the formation of N-acetyl-p-benzoquinone imine, which is responsible for the hepatic necrosis caused by acetaminophen overdose. Direct renal excretion represents approximately 5% of the metabolism of acetaminophen. Plasma metabolism of acetaminophen does not generally occur.

N-acetylcysteine can be used to prevent contrast-induced nephropathy. Whilst evidence is not overwhelming for use in favor, it does appear to have a clinical impact. N-acetylcysteine is typically given the day before treatment and the day when treatment commences. Other means to prevent contrast-induced nephropathy include adequate hydration, while some studied recommend ascorbic acid.

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.

Thiamine should be administered to prevent Wernicke’s encephalopathy.

300mg is the standard loading dose of clopidogrel – an antiplatelet drug – in the treatment of acute coronary syndrome (ACS).