NAPLEX Practice Questions

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.
Reference:
Inzucchi S, Bergenstal R, Buse J, et al. Management of hyperglycemia in type 2 diabetes: a patient- centered approach. Diabetes Care 2012;35:1364-79.

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.
Reference:
Metoclopramide hydrochloride tablet package insert. Rockford, IL: Mylan Institutional Inc.; 2016 Oct.

Dexamethasone is associated with psychiatric disturbances. Corticosteroids may exacerbate pre-existing psychiatric conditions.
Reference:
Cerullo MA, Corticosteroid-induced mania: Prepare for the unpredictable, Current Psychiatry. 2006 June;5(6):43-50.

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.
Reference:
I. FDA Drug Safety Communication: Revised recommendations for Celexa (citalopram hydrobromide) related to a potential risk of abnormal heart rhythms with high doses. Available at: http://www.fda.gov/Drugs/DrugSafety/ucm297391.htm Accessed January 17, 2017.
II. Nachimuthu S, Assar MD, et al. Drug-induced QT interval prolongation: mechanisms and clinical management. Ther Adv Drug Saf. 2012 Oct; 3(5): 241–253. doi: 10.1177/2042098612454283. Available at: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4110870

LN should be on docusate sodium/Senna for constipation and ondansetron for N/V. Dexamethasone has an off label use for N/V that is chemotherapy-associated. It is mostly used as an anti-inflammatory or immunosuppressant agent. Hydromorphone does not cause hyperglycemia. The most common side effect of opioids are nausea, vomiting and constipation.
Reference:
Dilaudid and Dilaudid HP (hydromorphone) injection package insert. Stamford, CT: Purdue Pharma L.P.; 2016 Oct.

Lisinopril may increase LN’s potassium. One of the warnings/precautions of lisinopril is hyperkalemia. ACE inhibitors block the formation of circulating angiotensin II, which can lead to a decrease in aldosterone secretion that can result in an increase in potassium. Risk factors for hyperkalemia while taking lisinopril include renal impairment, diabetes, and concomitant use of potassium-sparing diuretics, potassium supplements and/or potassium containing salts. Potassium should be monitored closely when taking any of the other agents listed. Hyperkalemia is not listed in the warnings/precautions section for the other medications.
Reference:
Raebel MA. Hyperkalemia associated with use of angiotensin-converting enzyme inhibitors and angiotensin receptor blockers.Cardiovasc Ther. 2012 Jun;30(3):e156-66. doi: 10.1111/j.1755-5922.2010.00258.x. Epub 2011 Jan 26.

Metformin is held in patients with reduced renal function due to an increased risk of lactic acidosis. Metformin has a Boxed Warning for lactic acidosis, which is a rare but serious metabolic complication. Lactic acidosis can occurs due to an accumulation of metformin (5 mcg/mL or more). It is fatal in about 50% of cases. Lactic acidosis has also been reported to occur in those with diabetes who have significant renal function impairment. Lactic acidosis occurs when there are elevated blood lactate levels of 5 mmol/L or more, decreased blood pH, electrolyte disturbances with an increased anion gap, and an increased lactate/pyruvate ratio. Normal lactic acid level <2.0 mmol/L
Reference:
Misbin RI. The Phantom of Lactic Acidosis due to Metformin in Patients with Diabetes. Diabetes Care 2004 Jul; 27(7): 1791-1793. https://doi.org/10.2337/diacare.27.7.1791. Accessed Oct 2016

Metformin may impair the absorption of vitamin B12, especially in those with inadequate vitamin b12 or calcium intake/absorption. Vitamin b12 deficiency can be treated with discontinuation of therapy or supplementation. Vitamin b12 serum concentrations should be monitored periodically with long-term therapy.
Reference:
Glucophage and Glucophage XR (metformin HCl tablets and extended-release tablets) package insert. Princeton, NJ: Bristol-Myers Squibb Company; 2015 June

0.2 mg/hour basal rate = 0.2mg/hour (24 hours) = 4.8 mg
Demand dose of 0.1 mg x 5 = 0.5 mg
4.8 mg + 0.5 mg = 5.3 mg
Reference:
Cohen MR. Patient-Controlled Analgesia: Making It Safer for Patients. Institute for Safe Medication Practices (ISMP), May 2006. Retrieved Oct 2016 from: https://www.ismp.org/profdevelopment/PCAMonograph.pdf

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.
Reference:
Munar, Myrna Y., and Harleen Singh. "Drug dosing adjustments in patients with chronic kidney disease." American family physician 75.10 (2007).

Since the bioavailability of levothyroxine is roughly 50% (given in the question).To convert the home dose to intravenous, it would be 50% of the oral dose. So 50% of oral 75 mcg would be 37.5 mcg intravenously.
Reference:
Fish LH, Schwartz HL, Cavanaugh J, et al. Replacement dose, metabolism, and bioavailability of levothyroxine in the treatment of hypothyroidism. N Engl J Med 1987;316:764-70.

Since LN used 3 mg of hydromorphone, this would be equivalent to a total of morphine 60 mg po daily. Since you would start with 70-80% of that dose, Morphine 15mg ER po q12hr and morphine 5mg po q6h prn breakthrough pain would be appropriate regimen.
Reference:
American Pain Society. Principles of Analgesic Use in the Treatment of Acute Pain and Cancer Pain, 4th ed. Glenview, Ill. 1999.

ABW = 85 kg
IBW = 50 kg + 2.3 kg (4) = 59.2 kg
85/59.2 = 1.44
AdjBW = 59.2 kg + 0.4(85 kg-59.2 kg) = 69.52 kg
CrCl (IBW) = [(140-84) 59.2]/(72 x 1.4) = 32.8
CrCl (AdjBW) = [(140-84) 69.52]/(72 x 1.4) = 38.6
Reference:
Jelliffe RW. Creatinine clearance: Bedside estimate. Ann Inter Med. 1973; 79:604

0.05 (1000 mL) = 50 g
1000 mL x (1 hour/125 mL) = 8 hours
50x 3 = 150 g

1mEq NaCl= 58.5 ; Valence = 1.
mg = mEq x molecular weight / valence.
mg = 51.3mEq x 58.5mg / 1 = 3001.05mg = 3g.
23.4 g/100ml = 3g/Xml
X = 12.825mL

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.
Reference:
Stone N, Robinson J, Lichtenstein A et al. 2013 ACC/AHA Guideline on the Treatment of Blood Cholesterol to Reduce Atherosclerotic Cardiovascular Risk in Adults. Circulation. 2013;129(25 suppl 2):S1-S45. doi:10.1161/01.cir.0000437738.63853.7a.

ATP4 found that the use of statins for prevention of ASCVD is extensive and consistent. Statin therapy is recommended for patients at a higher risk of ASCVD who are most likely to experience a net benefit in terms of the potential for risk reduction vs the potential for adverse effects. Non-statin therapies do not provide sufficient benefits in the reduction of ASCVD risk in regards to their potential for adverse effects.
Reference:
Stone N, Robinson J, Lichtenstein A et al. 2013 ACC/AHA Guideline on the Treatment of Blood Cholesterol to Reduce Atherosclerotic Cardiovascular Risk in Adults. Circulation. 2013;129(25 suppl 2):S1-S45. doi:10.1161/01.cir.0000437738.63853.7a.

Lidocaine: 30g x 0.05 = 1.5g.
Hydrocortisone: 90g x 0.005 = 0.45g.
90g+30g = 120g.

1.5g/120g = 0.0125 x100 = 1.25% Lidocaine.
0.45g/120g = 0.00375 x 100 = 0.375% Hydrocortisone.

Relative risk reduction: 0.71 = 71%
Relative risk: (Event rate in rivaroxaban group)/(Event rate in enoxaparin group) = (17/1513)/(57/1473) = 0.2903
Relative risk reduction: 1 – (relative risk) = 1 – 0.2903 = 0.7097 = 0.71
Reference:
I. Barratt A, Wyer PC, Hatala R, et al. Tips for learners of evidence-based medicine: 1. Relative risk reduction, absolute risk reduction and number needed to treat. CMAJ. 2004;171(4):353-8. doi: 10.1503/cmaj.1021197.
II. Stone N, Robinson J, Lichtenstein A et al. 2013 ACC/AHA Guideline on the Treatment of Blood Cholesterol to Reduce Atherosclerotic Cardiovascular Risk in Adults. Circulation. 2013;129(25 suppl 2):S1-S45. doi:10.1161/01.cir.0000437738.63853.7a.

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

Statin therapy should be used as treatment in adults with with primary LDL–C ≥190 mg/dL and age over 21 years. Unless contraindicated, high-intensity statin therapy should be used.
Reference:
Stone N, Robinson J, Lichtenstein A et al. 2013 ACC/AHA Guideline on the Treatment of Blood Cholesterol to Reduce Atherosclerotic Cardiovascular Risk in Adults. Circulation. 2013;129(25 suppl 2):S1-S45. doi:10.1161/01.cir.0000437738.63853.7a.

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

Ceftaroline covers MRSA, but it does not cover pseudomonas. Ertapenem does not cover pseudomonas. Cefazolin does not cover MRSA nor Pseudomonas. Cefepime has pseudomonas coverage. Vancomycin does not cover gram negative bacteria.
Reference:
Gilbert D. The Sanford Guide to Antimicrobial Therapy 2014. Sperryville, Va.: Antimicrobial Therapy; 2014

SG= weight/mL, 1.27 = X/1000ml
X = 1270gm

This patient belongs in one of the four statin benefit groups because his estimated 10-year ASCVD risk is over 7.5%. Adults 40 to 75 years of age with LDL–C 70 to 189 mg/dL, with an estimated 10-year ASCVD risk ≥7.5% and without clinical ASCVD or diabetes should receive either a moderate-intensity or high-intensity statin. Since the extent of reducing the risk of ASCVD is proportionally related to the degree of LDL-C reduction, risk could be reduced more so with a high intensity statin.Considering the given options, Atorvastatin 80 mg PO QHS is the best choice.
Reference:
Stone N, Robinson J, Lichtenstein A et al. 2013 ACC/AHA Guideline on the Treatment of Blood Cholesterol to Reduce Atherosclerotic Cardiovascular Risk in Adults. Circulation. 2013;129(25 suppl 2):S1-S45. doi:10.1161/01.cir.0000437738.63853.7a.

50% = 50g/100ml = 0.5g/ml = 500mg/ml mEq = (mg/MW) x valence = (500mg/120.4) x 2 = 8.3mEq/ml

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.
Reference:
Stone N, Robinson J, Lichtenstein A et al. 2013 ACC/AHA Guideline on the Treatment of Blood Cholesterol to Reduce Atherosclerotic Cardiovascular Risk in Adults. Circulation. 2013;129(25 suppl 2):S1-S45. doi:10.1161/01.cir.0000437738.63853.7a.

Categorical data includes ordinal (ordered categories) and nominal (unordered categories). NYHA I-IV and grade of breast cancer are considered ordinal data because the categories for the answer choice are in order, you can have NYHA class I, II, III, or IV. Grade of breast cancers are also in order, grade 1, 2, or 3. Sex, Improvemnet Yes/No, Alive or Dead is considered nominal, unordered data because the answer choices are female or male, and do not have a set order.
Reference:
"Statistics at Square One | The BMJ". Bmj.com. 2016. Web. 7 Nov. 2016. Available at: http://www.bmj.com/about-bmj/resources-readers/publications/statistics-square-one

40mEq X 1 equiv/1000mEq X 74.5g/1 equiv = 2.98 gm of KCl in 100ml.
Calculate: mOsm/L.
2.98g/100ml X 1 mol/74.5g x 2Osm/1 mol X 1000mOsm/1 Osm X 1000ml/1L = 800mOsm/L

LDL can be elevated by diuretics, cyclosporine, glucocorticoids, and amiodarone.
Reference: Stone N, Robinson J, Lichtenstein A et al. 2013 ACC/AHA Guideline on the Treatment of Blood Cholesterol to Reduce Atherosclerotic Cardiovascular Risk in Adults. Circulation. 2013; 129(25 suppl 2):S1-S45. doi:10.1161/01.cir.0000437738.63853.7a.

In a normal distribution sample, within 1 standard deviation 68% of the sample falls within 1 standard deviation, 95% within 2 standard deviations, and 99.7% within 3 standard deviations of the mean.
Reference:
I. "Mean, Mode And Median - Measures Of Central Tendency - When To Use With Different Types Of Variable And Skewed Distributions | Laerd Statistics". statistics.laerd.com. 2016. Web. 7 Nov. 2016. Available at: https://statistics.laerd.com/statistical-guides/measures-central-tendency-mean-mode-median.php
II. "Statistics at Square One | The BMJ". Bmj.com. 2016. Web. 7 Nov. 2016. Available at: http://www.bmj.com/about-bmj/resources-readers/publications/statistics-square-one

[1 mg/ 1 min] x60min= 60mg/hr. 60 mg/hr x [1 mL/ 1.8 mg] = 33.33 mL/hr
0.5 mg/min x [60 min/ 1 hr] = 30 mg/hr
30 mg/hr x [1 mL/1.8 mg] = 16.67 mL/hr
Infusion rates: 33.33 mL/hr for 6 hours, then 16.67 mL/hr

Seizure threshold can be lowered by bupropion, chlorpromazine, clozapine, maprotiline, olanzapine, thioridazine, thiothixene, and tramadol.
Reference:
American Geriatrics Society 2015 Updated Beers Criteria for Potentially Inappropriate Medication Use in Older Adults. Journal of the American Geriatrics Society. 2015;63(11):2227-2246. doi:10.1111/jgs.13702.

Patients with heart failure should avoid taking NSAIDs (which includes naproxen), COX-2 inhibitors, nondihydropyridine calcium channel blockers (for reduced EF), thiazolidinediones (which includes pioglitazone), cilostazol, and dronedarone (for severe or recently decompensated heart failure).
Reference:
American Geriatrics Society 2015 Updated Beers Criteria for Potentially Inappropriate Medication Use in Older Adults. Journal of the American Geriatrics Society. 2015;63(11):2227-2246. doi:10.1111/jgs.13702

Because SGLT2 inhibitors work by preventing reabsorption of glucose in the kidneys, this increases frequency of urination. All of the options are monitoring requirements since the hydration status, blood pressure, blood glucose, and renal function may all be changed from increased urination (from the mechanism of the drug).
Reference:
Garber AJ, et al. Consensus Statement by the American Association of Clinical Endocrinologists and American College of Endocrinology on the Comprehensive Type 2 Diabetes Management Algorithm – 2016 Executive Summary. Endocr Pract. 2016; 22(1):84-113

Dichotomous data is considered categorical data that only has two categories, or two answer choices. All 3 answer choices have only 2 categories: sex has male or female, pain is yes or no, and alive or dead is only two options also.
Reference:
"Statistics at Square One | The BMJ". Bmj.com. 2016. Web. 7 Nov. 2016. Available at: http://www.bmj.com/about-bmj/resources-readers/publications/statistics-square-one

Empagliflozin is a SGLT2 inhibitor to decrease glucose reabsorption in the kidney. Linagliptin is a DPP-4 inhibitor that works on incretins/increase insulin secretion/decrease glucagon secretion. Pioglitazone is a TZD that increases insulin sensitivity. Exenatide is a GLP-1 agonist which increase insulin secretion/decrease glucagon secretion/increase satiety.
Reference: 1. American Diabetes Association. In Standards of Medical Care in Diabetes 2016. Diabetes Care 2016;39(Suppl. 1)

0.9%= 0.9g/100mL, 120mL/h x 24hrs = 2880mL
0.9g/100ml= X/2880ml
X=25.92g of NaCl

Thiazolidinediones may cause fluid retention through proposed mechanism of increasing reabsorption in the collecting duct of the kidney and increasing vascular permeability in adipose tissue. Bile acid sequestrants work in the intestine to bind bile acids which doesn’t affect fluid retention. GLP-1 receptor agonists work to activate these receptors to secrete insulin from beta pancreatic cells/decrease glucagon secretion/ increase satiety and doesn’t affect fluid retention. SGLT2 inhibitors actually cause increase of fluid elimination through the kidneys. Alpha-glucosidase inhibitors work in the gut to decrease carb absorption/digestion and have no affect on fluid retention.
Reference:
I. Yang T, Soodvilai S. Renal and Vascular Mechanisms of Thiazolidinediones- Induced Fluid Retention. PPAR Research. 2008. Article ID 943614.
II. American Diabetes Association. In Standards of Medical Care in Diabetes 2016. Diabetes Care 2016;39(Suppl. 1)

ACE-inhibitors (such as lisinopril), NSAIDs (such as naproxen) and loop diuretics (furosemide) can all increase the risk of lithium toxicity.
Reference:
American Geriatrics Society 2015 Updated Beers Criteria for Potentially Inappropriate Medication Use in Older Adults. Journal of the American Geriatrics Society. 2015;63(11):2227-2246. doi:10.1111/jgs.13702.

The only bile acid sequestrant, colesevelam (Welchol), has been shown to increase triglycerides through mechanism of: activation of phosphatidic acid phosphatase with promotes triglyceride synthesis. GLP-1 agonists work on GLP 1 receptors to increase insulin secretion, decrease glucagon secretion, and increase satiety. Thiazolidinediones activate nuclear transcription factor PPAR gamma to increase insulin sensitivity. SGLT2 inhibitors inhibit glucose reabsorption in the kidney. Alpha-glucosidase inhibitors slow down digestion and absorptions of carbs in the gut.
Reference: 1. Welchol (colesevelam) tablets and powder for oral suspension package insert. Parsipanny, NJ: Daiiki Sankyo 2014.
2. Sheperd J. Mechanism of action of bile acid sequestrants and other lipid-lowering drugs. Cardiology. 1989; 76 Suppl 1:65-71; discussion 71-74.

68 kg x [5 mcg/kg/min] = 340 mcg/min
Bag concentration = 2 mg/ml or 2000 mcg/ml
340 mcg x [1 mL/2000 mcg] = 0.17 mL/min
60 in x [0.17 mL/min] = 10.2 mLs in one hour

Metformin should be stopped when eGFR falls below 30. This is the only cutoff that is recommended for absolute discontinuing. If the eGFR falls between 30-44 while ontherapy, benefits and risks of discontinuing should be evaluated. New initiation is only recommended when eGFR >45.
Reference:
I. US Food and Drug Administration (FDA) MedWatch for Metformin-containing Drugs: Revised Warnings for Certain Patients With Reduced Kidney Function. Retrieved April 8, 2016. Available at: http://www.fda.gov/Safety/MedWatch/SafetyInformation/SafetyAlertsforHumanMedicalProducts/ucm494829.htm?source=govdelivery&utm_medium=email&utm_source=govdelivery
II. Eknoyan G, Lameire N, et al. KDIGO 2012 Clinical Practice Guideline for the Evaluation and Management of Chronic Kidney Disease. Journal of International Society of Nephrology. Jan 2013;3(1): 91-111

Pt’s weight in Kg 76.4.
76.4 x [5 mcg/kg/min] = 381.18 mcg/min
Concentration of the bag [400 mg/250 mL] = 1.6 mg/ml or 1600mcg
381.18 mcg x [1 mL/1600 mcg] = 0.2382 mL/ml
60 in x [0.0.2382 mL/min] = 14.29 mL in one hour

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.
Reference:
American Diabetes Association. In Standards of Medical Care in Diabetes 2016. Diabetes Care 2016;39(Suppl. 1)

Cefepime, levofloxacin, cefazolin does not provide good coverage of anaerobes. Ampicillin-sulbactam and piperacillin-tazobactam provide anaerobic coverage.
Reference:
Gilbert D. The Sanford Guide to Antimicrobial Therapy 2014. Sperryville, Va.: Antimicrobial Therapy; 2014.

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

25g/100ml = 300g/Xml
Xml = 1200mL

Metformin is associated with vitamin B12 deficiency because it affects the calcium dependent membrane uptake of it. All other drug classes are not associated with this.
Reference:
Liu KW, Lok KD, Jean W. Metformin-related vitamin B12 deficiency. Age Aging. 2006. 35(2): 200-201.

The concentration is the first thing to calculate, using 1 mL of octreotide solution containing a concentration of 0.5mg/mL is really using 0.5mg of octreotide. If this is placed in 50 mL NS then it is 0.5mg/50mL which is 0.01mg/mL or 10 mcg/mL. If the patient needs 50 mcg of octreotide per hour then the patient will need 5, 10 mcg/mL doses or 5 mLs. So the rate for this patient would be 5 mL/hr.

Nadolol is not proven to reduce mortality in patients with systolic CHF. The efficacy of nadolol in HF has not been determined. For patients taking nadolol, it should be used with caution in those with compensated heart failure and patients should be monitored for a worsening of the condition. Bisoprolol, carvedilol, and sustained-release metoprolol succinate are the beta-blockers that have been proven to reduce mortality in patients with systolic CHF. These 3 beta-blockers have been effective in reducing the risk of death in patients with chronic HFrEF. Other beta-blockers were found to be less effective. Bucindolol did not exhibit uniform effectiveness across different populations. Metoprolol tartrate was found to be less effective in HF clinical trials.
Reference:
Yancy CW, Jessup M, Bozkurt B, et al. 2013 ACCF/AHA Guideline for the Management of Heart Failure: A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines.J Am Coll Cardiol. 2013;62(16):e147-e239. doi:10.1016/j.jacc.2013.05.019. Retirved on Feb 6th from :http://circ.ahajournals.org/content/128/16/e240

68kg x 0.9mg/kg = 61.2mg dose x 1mg/mL = 61.2mL 61.2mg x 0.1 = 6mL IV bolus 61.2mg x 0.9 = 55mL IV over 60 minutes

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.
Reference:
I. FDA Drug Safety Communication: New restrictions, contraindications, and dose limitations for Zocor (simvastatin) to reduce the risk of muscle injury. December 15, 2011. Retrieved on Feb 8th, 2017 from : http://www.fda.gov/Drugs/DrugSafety/ucm256581.htm
II. Stone N, Robinson J, Lichtenstein A et al. 2013 ACC/AHA Guideline on the Treatment of Blood Cholesterol to Reduce Atherosclerotic Cardiovascular Risk in Adults. Circulation. 2013;129(25 suppl 2):S1-S45. doi:10.1161/01.cir.0000437738.63853.7a. Retrieved on Feb 6th 2017 from : http://circ.ahajournals.org/content/129/25_suppl_2/S1

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

Influenza vaccine is recommended annually, thus, WM should not skip it this year, and B is incorrect. Also, per the CDC, seasonal influenza outbreaks can occur as early as October, however, most activity peaks in January or later. Thus, it is not too late for WM to receive his vaccine in December, thus A is incorrect. Lastly, antiviral medications such as Tamiflu are an important adjunct to vaccinations. They are recommended as early as possible for any patient with confirmed or suspected influenza who, is 1) Hospitalized, 2) has severe, complicated, or progressive illness or 3) is at higher risk for influenza complications. Thus, WM is not a candidate with the given information and C is incorrect. Starting Tamiflu or Amantadine is not recommended for prevention. It has indication for treatment and prophylaxis.
Reference:
Key Facts About Seasonal Flu Vaccine. Centers for Disease Control and Prevention. 2016. Available at: http://www.cdc.gov/flu/protect/keyfacts.htm. Accessed September 27, 2016.

70% of 70 units = 49 units of Insulin Glargine daily 30% of 70 units = 21 units of Insulin Lispro daily. Dived in 3 doses would be 7 units three times a day. FT’s Insulin regimen should be 49 units of Insulin Glargine subcutaneous daily and 7 units of Insulin Lispro subcutaneous three times a day with meals

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.
Reference:
Irwig, Les. Chapter 18: Relative risk, relative and absolute risk reduction, number needed to treat and confidence intervals. Smart health choices: making sense of health advice. Judy Irwig, 2007. Retrieved Jan. 24, 2017 from: https://www.ncbi.nlm.nih.gov/books/NBK63647/

RR = rate of an outcome occurring in an exposed group (treatment group/intervention group) divided by the rate of an outcome occurring in an unexposed group (control group) Ex: Relative Risk = Rate of UTI in patients taking drug XYZ / rate of UTI in patients not on drug XYZ
Reference:
I. 2x2 Contingency Table with Odds Ratios, etc. (n.d.). Retrieved Jan. 24, 2017 from: http://www.vassarstats.net/odds2x2.html
II. Szumilas, M. "Explaining odds ratios." J Can Acad Child Adolesc Psychiatry 19 (2010): 227. Retrieved Jan. 24, 2017 from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2938757/

22 x 2 + 7 = 51 units of total insulin per day Decrease by 10% 51 units x 0.9 = 45.9 units per day round up to 46 units 46 units x 0.50 = 23 units, administer 23 units of insulin glargine once daily 46 units x 0.50 = 23 units total Insulin Lispro. Round down, divided by three times a day, 7 units 3 times a day with meals

As the patient is over the age of 60 and he does not have CKD or diabetes, his goal BP should be SBP < 150 mmHg or DBP < 90 mmHg, and he is not currently at this goal with his medication regimen. Options are to maximize the current medication dosage (option A), or to add a second agent. Since calcium channel blockers like Norvasc are recommended as initial treatment options in African Americans, choosing Norvasc over lisinopril would probably be the more effective option.
Reference:
James P, Oparil S, Carter B et al. 2014 Evidence-Based Guideline for the Management of High Blood Pressure in Adults. JAMA. 2014;311(5):507. doi:10.1001/jama.2013.284427. Retrieved Jan. 24, 2017 from: http://jamanetwork.com/journals/jama/fullarticle/1791497

Odds ratio of 0.44 (44%) means that this group was associated with an event happening 44% of the time, compared to 1 (an event happening 100% of the time if unexposed), therefore 100 - 44 = 56%, which is the reduction caused by the exposure. Exposure is the use of ascorbic acid.
Reference:
Davies, Huw Talfryn Oakley, Iain Kinloch Crombie, and Manouche Tavakoli. "When can odds ratios mislead?." Bmj 316.7136 (1998): 989-991. Retrieved Jan. 24, 2017 from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1112884/

Calcium makes up 40% of the MW of CaCO3. MW Ca / MW CaCO3 40.078 / 100.087 x 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 x 3 = 1.2 g of Elemental Ca

Incidence rate = New reported cases / summed person-years of observation (avg population during time interval). Prevalence = Cases in a population in a given time period / total population at that time Mortality rate = deaths during specified time interval / population size at risk for death
Reference:
Dicker, R. C., Coronado, F., Koo, D., et al. Principals of Epidemiology in Public Health Practice, Third Edition: An Introduction to Applied Epidemiology and Biostatistics; Lesson 3, Section 2. Oct. 2006 Retrieved Jan. 24, 2017 from: https://www.cdc.gov/ophss/csels/dsepd/ss1978/lesson3/section2.html Updated: Nov. 2011

KCl: Osmoles = number of particles in solution Convert 40meq to weight in g: 40meq x 1equiv/1000 mEq x 74.5g/1 equiv = 2.98g of KCL Calculate mOsm/L : 2.98g/L x 1mol/74.5g x 2Osm/1 mol x 1000mOsm/1 Osm = 80mOsm/L
NaCl: 0.9g/100ml x 1mol/58.5 g x 2 Osm/1mol x 1000 mOsm/ 1Osm x 1000ml/1L = 308 mOsm/L 80 mOsm/L + 308 mOsm/L = 388 mOsm/L

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.
Reference: Stone N, Robinson J, Lichtenstein A et al. 2013 ACC/AHA Guideline on the Treatment of Blood Cholesterol to Reduce Atherosclerotic Cardiovascular Risk in Adults. Circulation. 2013;129(25 suppl 2):S1-S45. doi:10.1161/01.cir.0000437738.63853.7a. Retrieved on Feb 6th 2017 from : http://circ.ahajournals.org/content/129/25_suppl_2/S1
Miller M, Stone N, Ballantyne C et al. Triglycerides and Cardiovascular Disease: A Scientific Statement From the American Heart Association. Circulation. 2011;123(20):2292-2333. doi:10.1161/cir.0b013e3182160726.

If 40mg of amoxicillin are needed per kg of body weight then the dose of amoxicillin is 40mg multiplied by the patient’s body weight. This patient weighs 18 lbs, based on the conversion of 2.2 lbs = 1 kg, the patient weighs 8.2 kg. 40 mg multiplied by 8.2 kg is equal to 328 mg, this is one dose of amoxicillin. If the amoxicillin comes in 250 mg/5 mL, then it needs to be determined how many mLs it will take to get 328 mg of amoxicillin. In order to do this 328 mg needs to be divided by 250 mg to get a ratio. This comes out to be 1.312. This ratio can be multiplied by the number of mLs it takes to make up 250 mg, which is 5 mLs. 1.312 multiplied by 5 mLs is 6.56 mL, this is how many mLs it will take to have 328 mg. This volume is for 1 single dose of amoxicillin. The patient is receiving 2 doses per day and for a total of 10 days, this means the patient will be receiving 20 doses. 20 doses multiplied by 6.56 mL doses equals the total volume the patient will be receiving, which is 131.2 mL.

LDL can be elevated by diuretics, cyclosporine, glucocorticoids, and amiodarone.
Reference:
Stone N, Robinson J, Lichtenstein A et al. 2013 ACC/AHA Guideline on the Treatment of Blood Cholesterol to Reduce Atherosclerotic Cardiovascular Risk in Adults. Circulation. 2013;129(25 suppl 2):S1-S45. doi:10.1161/01.cir.0000437738.63853.7a. Retrieved on Feb 6th 2017 from : http://circ.ahajournals.org/content/129/25_suppl_2/S1

Nominal data is considered unordered categories. Sex answers fall into male or female which is unordered. Race can be multiple answers such as Caucasian, African American, Asian, etc which is unordered. Blood group can only have blood type O, A, B, or AB which is also unordered. Ordered, or ordinal data would have categories that are in some sort of order
Reference:
"Statistics at Square One | The BMJ". Bmj.com. 2016. Web. 7 Nov. 2016. Available at: http://www.bmj.com/about-bmj/resources-readers/publications/statistics-square-one

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.

Incidence rate = New reported cases / summed person-years of observation (avg population during time interval) Prevalence = Cases in a population in a given time period / total population at that time
Reference:
I. Dicker, R. C., Coronado, F., Koo, D., et al. Principals of Epidemiology in Public Health Practice, Third Edition: An Introduction to Applied Epidemiology and Biostatistics; Lesson 3, Section 2. Oct. 2006 Retrieved Jan. 24, 2017 from: https://www.cdc.gov/ophss/csels/dsepd/ss1978/lesson3/section2.html Updated: Nov. 2011
II. Numerators, denominators and populations at risk. Jun. 20, 2010. Retrieved Jan. 24, 2017 from: http://www.healthknowledge.org.uk/public-health-textbook/research-methods/1a-epidemiology/numerators-denominators-populations

Primary treatment for stenotrophomonas maltophilia is SMX-TMP. Meropenem, ciprofloxacin, Ampicillin and vancomycin have no coverage.
Reference:
Gilbert D. The Sanford Guide to Antimicrobial Therapy 2014. Sperryville, Va.: Antimicrobial Therapy; 2014

Thiamine should be administered to prevent Wernicke’s encephalopathy.
Reference:
Management of moderate and severe alcohol withdrawal syndromes. Uptodate.com. 2016. Available at: http://www.uptodate.com/contents/management-of-moderate-and-severe-alcohol-withdrawal-syndromes Accessed May 24, 2016.

(A) Sulfonylureas, (C) 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 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.
Reference:

• Eur Heart J (2015) 36 (34): 2288-2296. DOI: https://doi.org/10.1093.eurheart
• Ferrannini, E, DeFronzo, R. Impact of glucose-lowering drugs on cardiovascular disease in type 2 diabetes. Eur Heart J (2015) 36 (34): 2288-2296Eur Heart J (2015) 36 (34): 2288-2296. DOI: https://doi.org/10.1093/eurheartj/ehv239.
• Kennedy M, Masharani U. Pancreatic Hormones & Antidiabetic Drugs. In: Katzung BG, Trevor AJ. eds. Basic & Clinical Pharmacology, 13e New York, NY: McGraw-Hill; 2015.
• Powers AC, D'Alessio D. Endocrine Pancreas and Pharmacotherapy of Diabetes Mellitus and Hypoglycemia. In: Brunton LL, Chabner BA, Knollmann BC. eds. Goodman & Gilman's: The Pharmacological Basis of Therapeutics, 12e New York, NY: McGraw-Hill; 2015.

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.
Reference:

• Eur Heart J (2015) 36 (34): 2288-2296. DOI: https://doi.org/10.1093.eurheart
• Ferrannini, E, DeFronzo, R. Impact of glucose-lowering drugs on cardiovascular disease in type 2 diabetes. Eur Heart J (2015) 36 (34): 2288-2296Eur Heart J (2015) 36 (34): 2288-2296. DOI: https://doi.org/10.1093/eurheartj/ehv239.
• Kennedy M, Masharani U. Pancreatic Hormones & Antidiabetic Drugs. In: Katzung BG, Trevor AJ. eds. Basic & Clinical Pharmacology, 13e New York, NY: McGraw-Hill; 2015.
• Powers AC, D'Alessio D. Endocrine Pancreas and Pharmacotherapy of Diabetes Mellitus and Hypoglycemia. In: Brunton LL, Chabner BA, Knollmann BC. eds. Goodman & Gilman's: The Pharmacological Basis of Therapeutics, 12e New York, NY: McGraw-Hill; 2015.

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.
Reference:

• Eur Heart J (2015) 36 (34): 2288-2296. DOI: https://doi.org/10.1093.eurheart
• Ferrannini, E, DeFronzo, R. Impact of glucose-lowering drugs on cardiovascular disease in type 2 diabetes. Eur Heart J (2015) 36 (34): 2288-2296Eur Heart J (2015) 36 (34): 2288-2296. DOI: https://doi.org/10.1093/eurheartj/ehv239.
• Kennedy M, Masharani U. Pancreatic Hormones & Antidiabetic Drugs. In: Katzung BG, Trevor AJ. eds. Basic & Clinical Pharmacology, 13e New York, NY: McGraw-Hill; 2015.
• Powers AC, D'Alessio D. Endocrine Pancreas and Pharmacotherapy of Diabetes Mellitus and Hypoglycemia. In: Brunton LL, Chabner BA, Knollmann BC. eds. Goodman & Gilman's: The Pharmacological Basis of Therapeutics, 12e New York, NY: McGraw-Hill; 2015.

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.
Reference:

• Eur Heart J (2015) 36 (34): 2288-2296. DOI: https://doi.org/10.1093.eurheart
• Ferrannini, E, DeFronzo, R. Impact of glucose-lowering drugs on cardiovascular disease in type 2 diabetes. Eur Heart J (2015) 36 (34): 2288-2296Eur Heart J (2015) 36 (34): 2288-2296. DOI: https://doi.org/10.1093/eurheartj/ehv239.
• Kennedy M, Masharani U. Pancreatic Hormones & Antidiabetic Drugs. In: Katzung BG, Trevor AJ. eds. Basic & Clinical Pharmacology, 13e New York, NY: McGraw-Hill; 2015.
• Powers AC, D'Alessio D. Endocrine Pancreas and Pharmacotherapy of Diabetes Mellitus and Hypoglycemia. In: Brunton LL, Chabner BA, Knollmann BC. eds. Goodman & Gilman's: The Pharmacological Basis of Therapeutics, 12e New York, NY: McGraw-Hill; 2015.

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.
Reference:

• Eur Heart J (2015) 36 (34): 2288-2296. DOI: https://doi.org/10.1093.eurheart
• Ferrannini, E, DeFronzo, R. Impact of glucose-lowering drugs on cardiovascular disease in type 2 diabetes. Eur Heart J (2015) 36 (34): 2288-2296Eur Heart J (2015) 36 (34): 2288-2296. DOI: https://doi.org/10.1093/eurheartj/ehv239.
• Kennedy M, Masharani U. Pancreatic Hormones & Antidiabetic Drugs. In: Katzung BG, Trevor AJ. eds. Basic & Clinical Pharmacology, 13e New York, NY: McGraw-Hill; 2015.
• Powers AC, D'Alessio D. Endocrine Pancreas and Pharmacotherapy of Diabetes Mellitus and Hypoglycemia. In: Brunton LL, Chabner BA, Knollmann BC. eds. Goodman & Gilman's: The Pharmacological Basis of Therapeutics, 12e New York, NY: McGraw-Hill; 2015.

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.
Reference:

• Eur Heart J (2015) 36 (34): 2288-2296. DOI: https://doi.org/10.1093.eurheart
• Ferrannini, E, DeFronzo, R. Impact of glucose-lowering drugs on cardiovascular disease in type 2 diabetes. Eur Heart J (2015) 36 (34): 2288-2296Eur Heart J (2015) 36 (34): 2288-2296. DOI: https://doi.org/10.1093/eurheartj/ehv239.
• Kennedy M, Masharani U. Pancreatic Hormones & Antidiabetic Drugs. In: Katzung BG, Trevor AJ. eds. Basic & Clinical Pharmacology, 13e New York, NY: McGraw-Hill; 2015.
• Powers AC, D'Alessio D. Endocrine Pancreas and Pharmacotherapy of Diabetes Mellitus and Hypoglycemia. In: Brunton LL, Chabner BA, Knollmann BC. eds. Goodman & Gilman's: The Pharmacological Basis of Therapeutics, 12e New York, NY: McGraw-Hill; 2015.

SGLT2 inhibitors 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.
Reference:

• Eur Heart J (2015) 36 (34): 2288-2296. DOI: https://doi.org/10.1093.eurheart
• Ferrannini, E, DeFronzo, R. Impact of glucose-lowering drugs on cardiovascular disease in type 2 diabetes. Eur Heart J (2015) 36 (34): 2288-2296Eur Heart J (2015) 36 (34): 2288-2296. DOI: https://doi.org/10.1093/eurheartj/ehv239.
• Kennedy M, Masharani U. Pancreatic Hormones & Antidiabetic Drugs. In: Katzung BG, Trevor AJ. eds. Basic & Clinical Pharmacology, 13e New York, NY: McGraw-Hill; 2015.
• Powers AC, D'Alessio D. Endocrine Pancreas and Pharmacotherapy of Diabetes Mellitus and Hypoglycemia. In: Brunton LL, Chabner BA, Knollmann BC. eds. Goodman & Gilman's: The Pharmacological Basis of Therapeutics, 12e New York, NY: McGraw-Hill; 2015.

Thiazolidinediones 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.
Reference:

• Eur Heart J (2015) 36 (34): 2288-2296. DOI: https://doi.org/10.1093.eurheart
• Ferrannini, E, DeFronzo, R. Impact of glucose-lowering drugs on cardiovascular disease in type 2 diabetes. Eur Heart J (2015) 36 (34): 2288-2296Eur Heart J (2015) 36 (34): 2288-2296. DOI: https://doi.org/10.1093/eurheartj/ehv239.
• Kennedy M, Masharani U. Pancreatic Hormones & Antidiabetic Drugs. In: Katzung BG, Trevor AJ. eds. Basic & Clinical Pharmacology, 13e New York, NY: McGraw-Hill; 2015.
• Powers AC, D'Alessio D. Endocrine Pancreas and Pharmacotherapy of Diabetes Mellitus and Hypoglycemia. In: Brunton LL, Chabner BA, Knollmann BC. eds. Goodman & Gilman's: The Pharmacological Basis of Therapeutics, 12e New York, NY: McGraw-Hill; 2015.

Primidone is an anticonvulsant drug that is structurally related to phenobarbital. Primidone is metabolized to phenobarbital and therefore shares its anticonvulsant and sedative properties. Primidone may be more effective than therapy with phenobarbital alone because primidone and both of its metabolites, phenobarbital and phenylethylmalonamide (PEMA), possess anticonvulsant activity.
Reference:
 Mysoline (primidone) package insert. Bridgewater, NJ: Valeant Pharmaceuticals, LLC; 2016 Nov.

Corrected phenytoin (mg/L) = Observed phenytoin (mg/L) /(0.2 x albumin [g/dL]) + 0.1
         = 17.8/(0.2 x 2.1)+ 0.1
     = 17.8/0.42 + 0.1
= 42.48mg/L ← phenytoin level is high.
Normal therapeutic range is:  10-20mg/dL
Reference:
Von Winckelmann SL, Spret I, Willems L. Therapeutic drug monitoring of phenytoin in critically ill patients. Pharmacotherapy 2008;28(11):1391–400.

The delayed-release action of divalproex allows for less frequent dosing than valproic acid in some patients. Divalproex sodium contains sodium valproate and valproic acid in a 1:1 molar stable co-ordination compound. Valproic acid, sodium valproate, and divalproex share the same pharmacology; however, there are pharmacokinetic differences among products.
Reference:
Depakote (divalproex sodium tablets) package insert. North Chicago, IL: AbbVie Inc.; 2016 Nov.

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.
Reference:
Depacon (valproate sodium injection) package insert. North Chicago, IL: Abbvie Inc.; 2017 April.

Rate of infusion: 100mL/40U x 0.03U/min x 60min/1 hr = 4.5mL/hr

Cases of life-threatening pancreatitis have been reported in both pediatric and adult patients receiving valproic acid or its analogs. Patients should be warned that abdominal pain, nausea, vomiting, and/or anorexia can be symptoms of pancreatitis that require prompt medical evaluation. If pancreatitis is diagnosed, valproate should be discontinued.
Reference:
Clinical Pharmacology, Available at: http://www.clinicalpharmacology-ip.com/Forms/Monograph/monograph.aspx?cpnum=637&sec=moncontr&t=0 Accessed May 2017

Common GI side effects of Valproic Acid and Divalproex Sodium are Weight gain, Nausea, Vomiting, Diarrhea, abdominal pain, dyspepsia. Divalproex sodium or valproic acid affects reproductive endocrine function in women. Menstrual irregularities defined as amenorrhea, oligomenorrhea, and prolonged cycles were common. Gynecomastia is not a side effect of Divalproex Sodium. For list of drugs that causes gynecomastia refer the reference. Gingival hyperplasia is a well-known side effect of phenytoin.
Reference: Depakote (divalproex sodium tablets) package insert. North Chicago, IL: AbbVie Inc.; 2017 May. Drug-induced gynecomastia. Giuseppe R, Mauro M. Available at: http://www.pharmaco-vigilance.eu/content/drug-induced-gynecomastia . Accessed May 2017

The diagnosis of Zollinger-Ellison syndrome is suggested when plasma gastrin is > 1000 pg/ml and the basal acid output is > 15 mEq/h or when associated with a pH < 2. The treatment is focused on controlling gastric acid hypersecretion and localisation of the tumour and its metastases. Proton pump inhibitors are the most effective antisecretory drugs and can be administered at high dosages
Reference:
I. Tomassetti P, Campana D. Treatment of Zollinger-Ellison Syndrome. World J Gastroenterol 2005 Sep 21; 11(35): 5423–5432.
II. Jensen RT, Gardner JD, Raufman JP, Pandol SJ, Doppman JL, Collen MJ. Zollinger-Ellison syndrome: current concepts and management. Ann Intern Med. 1983;98:59–75

Use proton pump inhibitors (PPIs) in patients with or who have risk factors for osteoporosis cautiously. PPIs have been associated with a possible increased risk of bone fractures of the hip, wrist, and spine. Daily treatment with a gastric acid-suppressing medication over a long period of time may lead to hypomagnesemia. Vitamin B12 deficiency has been reported with long term use of PPIs in the literatures. The use of PPIs, may increase the risk of enteric infection by encouraging the growth of gut microflora and increasing susceptibility to organism including Clostridium Difficile. There are recent FDA warnings regarding C. Diff infection with use of PPIs. H. Pylori infection is not a complication of PPIs. PPIs in combination with certain antibiotics are used to treat H. pylori Infections.
Reference:
I. Targownik LE, Lix LM, Metge CJ, et al. Use of proton pump inhibitors and risk of osteoporosis-related fractures. CMAJ 2008;179:319—26.
II. Howden CW. Vitamin B12 levels during prolonged treatment with proton pump inhibitors. J Clin Gastroenterol. 2000;30:29–33.
III. Haag S, Andrews JM, Katelaris PH, et al. Management of reflux symptoms with over-the-counter proton pump inhibitors: issues and proposed guidelines. Digestion 2009;80:226-34.

Omeprazole is CYP2C19 inhibitor which can prolong the elimination of warfarin, particularly R-warfarin. R-warfarin is partially metabolized by CYP2C19. The combined use of omeprazole and warfarin has been associated with reports of increased INR and prothrombin time (PT).
Reference:
 Prilosec (omeprazole) package insert. Wilmington, DE: AstraZeneca; 2016 Dec.

Non-pharmacological measure that may control symptoms of gastroesophageal reflux disease are: Avoid aggravating foods/beverages that may reduce LES pressure alcohol, citrus juices caffeine, garlic, onions or cause direct irritation such as spicy foods or tomato juice should be avoided. Reduce fat intake, remain upright after meals, avoid meal before bedtime. Avoid tight fitted cloths, decrease intra-abdominal pressure. Discontinue nicotine use. Reduce intake of food or beverage that may reduce lower esophageal sphincter tone.
Reference:
American Gastroenterological Association Institute. Medical position statement on the management of gastroesophageal reflux disease. Gastroenterology 2008;135:1383-91.

1st hour
13mL/hr x 1 hr= 13mL
50U/mL=XU/13mL 650U Heparin given in hours
since the half life of protamine is 60min
2nd hour 650/2 =325 units
650 units + 325 units =975 units needs to be reveresed
**1mg of protamine reverses 100U of Heparin
(1mg protamine/100U Heparin) = (Xmg protamine/975U Heparin given)
= x = 9.7mg protamine

Absolute risk reduction: 0.027 = 2.7%
(Event rate in enoxaparin group) – (Event rate in rivaroxaban group) = (57/1473) – (17/1513) = 0.02746
Reference:
Barratt A, Wyer PC, Hatala R, et al. Tips for learners of evidence-based medicine: 1. Relative risk reduction, absolute risk reduction and number needed to treat. CMAJ. 2004;171(4):353-8. doi: 10.1503/cmaj.1021197.

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
Reference:
Stone N, Robinson J, Lichtenstein A et al. 2013 ACC/AHA Guideline on the Treatment of Blood Cholesterol to Reduce Atherosclerotic Cardiovascular Risk in Adults. Circulation. 2013;129(25 suppl 2):S1-S45. doi:10.1161/01.cir.0000437738.63853.7a.

Cefazolin or an antistaphylococcal penicillin (oxacillin or nafcillin) is recommended for this patient because the C&S results indicate MSSA. Since the patient develops a rash to penicillins, it would be acceptable to use cefazolin in this case. .
Reference: Stevens, Dennis L., et al. "Practice guidelines for the diagnosis and management of skin and soft tissue infections: 2014 update by the Infectious Diseases Society of America." Clinical Infectious Diseases (2014): ciu296. Available at: https://academic.oup.com/cid/article/59/2/e10/2895845/Practice-Guidelines-for-the-Diagnosis-and

Osmolarity = mOsmol/L = (wt of substance (g/mL))/(MW(g/mol)) x (# of particles) x 1000
Weight of substance: 3% = (3g/100mL) = (xg/1000mL) = x = 30g/L
# of particles NaCL Na+ + Cl- (2 particles) mOsmol/L = (30g/L)/(58.5g/mol) x 2 x 1000 = 1,025.6
1026 mOsmol/L

Primary treatment for stenotrophomonas maltophilia is SMX-TMP. Meropenem, ciprofloxacin, and vancomycin have no coverage.
Reference:
Gilbert D. The Sanford Guide to Antimicrobial Therapy 2014. Sperryville, Va.: Antimicrobial Therapy; 2014

*Patient dose: 0.75mcg x 115kg = 86.25mcg/min
(100mL/20mg) x (86.25mcg/1hr) x (60min/1hr) x (1mg/1000mcg)
= 25.875mL/hr Rate of infusion of Milrinone

This patient is displaying signs of a severe case of cellulitis. Severe cellulitis is defined as having one of the following: failed oral antibiotic treatment, immunocompromised, clinical signs of deeper infection, or meeting the SIRS criteria. Based on this patient’s presentation they have failed antibiotic treatment and meet SIRS criteria. For severe cellulitis, IDSA SSTI guidelines recommend using Vancomycin along with Zosyn.
Reference:
Stevens, Dennis L., et al. "Practice guidelines for the diagnosis and management of skin and soft tissue infections: 2014 update by the Infectious Diseases Society of America." Clinical Infectious Diseases (2014): ciu296. Available at: https://academic.oup.com/cid/article/59/2/e10/2895845/Practice-Guidelines-for-the-Diagnosis-and

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.