Lecithin is primarily used in pharmaceutical compounding as an emulsifying agent, surfactant, or wetting agent. Its main function is to stabilize mixtures of oil and water (emulsions). While some components of lecithin may exhibit minor antioxidant properties, it is not classified or utilized as an antimicrobial preservative. The other options are all well-established preservatives used to prevent the growth of bacteria, yeast, and mold in pharmaceutical preparations, thereby ensuring their stability and safety.

A. Benzalkonium chloride is a quaternary ammonium compound widely used as an antimicrobial preservative, particularly in ophthalmic, otic, and nasal preparations.

C. Sodium benzoate is a common preservative used to inhibit the growth of mold and yeast in acidic oral liquid preparations, foods, and cosmetics.

D. Benzyl alcohol is an aromatic alcohol frequently used as a bacteriostatic preservative in multi-dose parenteral (injectable) formulations and topical products.

1. Rowe

R. C.

Sheskey

P. J.

& Quinn

M. E. (Eds.). (2012). Handbook of Pharmaceutical Excipients (7th ed.). Pharmaceutical Press.

Lecithin: "Functional category: Emulsifying agent; emollient; solubilizing agent." (p. 417).

Benzalkonium Chloride: "Functional category: Antimicrobial preservative; antiseptic; disinfectant; solubilizing agent; wetting agent." (p. 56).

Sodium Benzoate: "Functional category: Antimicrobial preservative." (p. 627).

Benzyl Alcohol: "Functional category: Antimicrobial preservative; disinfectant; solvent." (p. 64).

2. Allen

L. V. (2018). Ansel's Pharmaceutical Dosage Forms and Drug Delivery Systems (11th ed.). Wolters Kluwer.

Chapter 18: Pharmaceutical Excipients: This chapter lists benzalkonium chloride

benzyl alcohol

and benzoic acid/its salts (like sodium benzoate) in the table of "Antimicrobial Preservatives." Lecithin is discussed and categorized under "Emulsifying and Suspending Agents." (Section: "Excipients Used in Liquid Dosage Forms").

3. United States Pharmacopeia and National Formulary (USP-NF). USP Pharmaceutical Dosage Forms.

This general chapter describes the typical components of various dosage forms. Preservatives are defined as substances added to inhibit microbial growth. Emulsifying agents

like lecithin

are defined as substances that promote and maintain the dispersion of one immiscible phase in another.

Systemic corticosteroids, such as dexamethasone, are well-documented to cause a wide range of dose-dependent neuropsychiatric adverse effects. These can range from mild mood changes and insomnia to severe reactions like mania, depression, delirium, and frank psychosis, often termed "steroid psychosis." The symptoms described in the question—emotional lability, hallucinations, mania, and mood swings—are classic manifestations. The patient's high dose of dexamethasone (32 mg/day) and advanced age increase this risk significantly. While other medications listed can cause CNS disturbances, the specific constellation of symptoms, particularly mania and significant mood swings, is most characteristic of corticosteroid therapy.

A. Lisinopril: While mood changes can occur, ACE inhibitors are not commonly associated with causing severe psychotic episodes.

C. Famotidine: Can cause confusion and delirium, especially in elderly patients with renal impairment, but is less likely to induce mania or a full psychotic syndrome.

D. Metoclopramide: Can cause CNS effects like confusion and hallucinations, but is more characteristically associated with extrapyramidal symptoms and tardive dyskinesia.

E. Hydromorphone: Opioids are a common cause of sedation, confusion, and delirium in the elderly, but are less frequently implicated in causing mania or complex mood disorders.

1. DiPiro

J. T.

Yee

G. C.

Posey

L. M.

Haines

S. T.

Nolin

T. D.

& Ellingrod

V. (2020). Pharmacotherapy: A Pathophysiologic Approach (11th ed.). McGraw-Hill. In the chapter on "General Principles of Endocrine Pharmacology

" the adverse effects of glucocorticoids are detailed

including behavioral and personality changes

euphoria

insomnia

and psychosis.

2. Kenna

H. A.

Poon

A. W.

de la Rue

O. P.

& Rasgon

N. L. (2011). Neuropsychiatric effects of corticosteroids: a review. Comprehensive Psychiatry

52(5)

519–528. (See Abstract and Section 3

"Psychiatric Disturbances"). This review states that corticosteroid-induced psychiatric disturbances include mania

depression

psychosis

and delirium

with risk increasing at higher doses (e.g.

>40 mg of prednisone or equivalent per day). https://doi.org/10.1016/j.comppsych.2010.10.004

3. Warrington

T. P.

& Bostwick

J. M. (2006). Psychiatric adverse effects of corticosteroids. Mayo Clinic Proceedings

81(10)

1361–1367. (See Table 1

page 1362). This article categorizes the psychiatric adverse effects of corticosteroids

listing psychosis

mania

and mood lability as established complications. https://doi.org/10.4065/81.10.1361

The question requires calculating the subcutaneous insulin regimen based on the patient's recent intravenous (IV) insulin requirement and the physician's suggested ratio. The patient's average total daily dose (TDD) from the IV insulin drip was 70 units. The suggested split is 70% for long-acting (basal) insulin and 30% for short-acting (bolus) insulin.

1. Calculate Basal Dose (Insulin Glargine):

TDD × Basal Percentage = 70 units × 0.70 = 49 units.

2. Calculate Total Bolus Dose (Insulin Lispro):

TDD × Bolus Percentage = 70 units × 0.30 = 21 units.

3. Calculate Per-Meal Bolus Dose:

Total Bolus Dose / Number of meals = 21 units / 3 meals = 7 units per meal.

This calculation results in a regimen of 49 units of Insulin Glargine daily and 7 units of Insulin Lispro three times a day with meals.

B. This option represents a 36:64 basal-to-bolus ratio (25 units / 70 units ≈ 36%), which is incorrect.

C. This option represents a 57:43 basal-to-bolus ratio (40 units / 70 units ≈ 57%), which is incorrect.

D. This option represents a 66:34 basal-to-bolus ratio (46 units / 70 units ≈ 66%), which is incorrect.

E. This option represents a 74:26 basal-to-bolus ratio (52 units / 70 units ≈ 74%), which is incorrect.

1. American Diabetes Association Professional Practice Committee. (2023). 15. Diabetes Care in the Hospital: Standards of Medical Care in Diabetes—2023. Diabetes Care

46(Supplement1)

S247–S257. https://doi.org/10.2337/dc23-S015. (Section: "Transitioning From Intravenous to Subcutaneous Insulin

" which discusses basing the initial subcutaneous dose on the IV infusion rate over the preceding hours).

2. UCSF Division of Hospital Medicine. (2023). Hyperglycemia & Diabetes. In The UCSF Hospitalist Handbook. University of California

San Francisco. Retrieved from https://hospitalmedicine.ucsf.edu/manual/ch15hyper.html. (Chapter: "Transitioning from Insulin Drip to Subcutaneous Insulin

" which outlines the method of calculating the TDD from the 24-hour IV requirement and then splitting it into basal and bolus components).

3. Kitabchi

A. E.

Umpierrez

G. E.

Miles

J. M.

& Fisher

J. N. (2009). Hyperglycemic crises in adult patients with diabetes. Diabetes Care

32(7)

1335–1343. https://doi.org/10.2337/dc09-9032. (Section: "Transition to Subcutaneous Insulin

" which describes the general principles for initiating a multiple daily injection regimen after DKA resolution).

Thiazolidinediones (TZDs), such as pioglitazone and rosiglitazone, are peroxisome proliferator-activated receptor-gamma (PPAR-γ) agonists. A well-documented and clinically significant adverse effect of this class is fluid retention. The mechanism involves the upregulation of the epithelial sodium channel (ENaC) in the renal collecting ducts, leading to increased sodium and water reabsorption. This can manifest as peripheral edema, weight gain, and hemodilution. Importantly, this side effect can exacerbate or precipitate congestive heart failure, leading to a boxed warning for this drug class.

A. Bile acid sequestrants primarily cause gastrointestinal side effects, such as constipation and bloating, not systemic fluid retention.

B. GLP-1 agonists are associated with gastrointestinal side effects (nausea, vomiting) and weight loss; they do not cause fluid retention.

D. SGLT2 inhibitors work by promoting urinary glucose excretion, which induces an osmotic diuresis, leading to fluid loss, not retention.

E. Alpha-glucosidase inhibitors act locally in the intestine to delay carbohydrate absorption, causing gastrointestinal side effects like flatulence and diarrhea.

1. American Diabetes Association. (2023). 9. Pharmacologic Approaches to Glycemic Treatment: Standards of Medical Care in Diabetes—2023. Diabetes Care

46(Supplement1)

S140–S157. (See Table 9.2

"Drug-Specific and Patient Factors to Consider When Selecting Antihyperglycemic Treatment

" which lists "Edema/Heart Failure" as a side effect for Thiazolidinediones). https://doi.org/10.2337/dc23-S009

2. Katzung

B. G.

& Vanderah

T. W. (2021). Basic & Clinical Pharmacology (15th ed.). McGraw Hill. In Chapter 41

"Pancreatic Hormones & Antidiabetic Drugs

" under the section "Thiazolidinediones

" it states

"The major adverse effect of the thiazolidinediones is fluid retention

which presents as a mild anemia and peripheral edema."

3. Nesto

R. W.

Bell

D.

Bonow

R. O.

Fonseca

V.

et al. (2003). Thiazolidinedione use

fluid retention

and congestive heart failure: a consensus statement from the American Heart Association and American Diabetes Association. Circulation

108(23)

2941-2948. (See "Pathophysiology of Fluid Retention" section

which details the renal mechanism). https://doi.org/10.1161/01.CIR.0000103549.88423.75

Sucralfate is an aluminum salt of a sulfated disaccharide. Although its action is primarily local on the gastrointestinal mucosa, a small amount of aluminum is absorbed systemically. In patients with normal kidney function, this absorbed aluminum is excreted by the kidneys. However, in patients with chronic renal failure or those on dialysis, the excretion of aluminum is impaired. Chronic administration of sucralfate in this patient population can lead to the accumulation of aluminum to toxic levels, potentially causing serious adverse effects such as aluminum-induced osteomalacia, adynamic bone disease, and encephalopathy.

B. Bismuth subgallate: This medication contains bismuth, not aluminum. Overuse can lead to bismuth toxicity, which has different clinical manifestations.

C. Docusate sodium: This is a surfactant-type stool softener that does not contain aluminum or affect its systemic absorption or excretion.

D. Lactulose: This is an osmotic laxative used for constipation and hepatic encephalopathy; it has no association with aluminum metabolism.

E. Alginates: Alginates are used for gastroesophageal reflux. While some formulations may be combined with aluminum-containing antacids, alginates themselves are not a source of aluminum.

1. U.S. Food and Drug Administration (FDA). (2013). CARAFATE® (sucralfate) Tablets Prescribing Information. Section: WARNINGS. "In patients with chronic renal failure or those receiving dialysis

aluminum accumulation and toxicity (aluminum osteodystrophy

osteomalacia

encephalopathy) have been described." Available from the FDA website.

2. Brunton

L. L.

Dandan

R.

& Knollmann

B. C. (Eds.). (2017). Goodman & Gilman's The Pharmacological Basis of Therapeutics (13th ed.). McGraw-Hill Education. Chapter 49

Pharmacotherapy of Gastric Acidity

Peptic Ulcers

and Gastroesophageal Reflux Disease

Section: Mucosal Protective Agents. "Because a small amount of Al3+ is absorbed

sucralfate should be used with caution in patients with renal insufficiency

who are at risk for Al3+ overload."

3. DiPiro

J. T.

Yee

G. C.

Posey

L. M.

Haines

S. T.

Nolin

T. D.

& Ellingrod

V. (Eds.). (2020). Pharmacotherapy: A Pathophysiologic Approach (11th ed.). McGraw-Hill Education. Chapter 25

Peptic Ulcer Disease

Section: Mucosal Protective Agents. "Systemic absorption of aluminum is minimal but may be problematic in patients with chronic renal failure because of the risk of accumulation and toxicity."

Intravenous (IV) dextrose is supplied as dextrose monohydrate. While pure, anhydrous carbohydrates provide 4 kcal per gram, the water molecule in dextrose monohydrate adds to the total weight without contributing calories. This "hydration" effectively dilutes the caloric density. Therefore, the standardized caloric value used in all clinical and pharmaceutical calculations for IV dextrose is 3.4 kcal per gram. This value is critical for accurately calculating the energy provided to patients receiving parenteral nutrition.

A. 0.9 kcal/g: This value is incorrect. It may be confused with the percentage concentration of Normal Saline (0.9% sodium chloride), not a caloric value.

B. 1.2 kcal/g: This is an arbitrary and incorrect caloric value for any macronutrient used in parenteral nutrition.

C. 1.5 kcal/g: This is an arbitrary and incorrect caloric value for any macronutrient used in parenteral nutrition.

1. American Society for Parenteral and Enteral Nutrition (A.S.P.E.N.). (2017). The A.S.P.E.N. Adult Nutrition Support Core Curriculum (3rd ed.). In Chapter 11

Parenteral Nutrition Formulations

it is explicitly stated

"Dextrose monohydrate is the carbohydrate source used in PN solutions in the United States

providing 3.4 kcal/g."

2. Mueller

C. M. (Ed.). (2012). The A.S.P.E.N. Nutrition Support Practice Manual (2nd ed.). American Society for Parenteral and Enteral Nutrition. In Chapter 20

Parenteral Nutrition Formulas

Table 20-1

"Macronutrient Sources for Parenteral Nutrition

" lists Dextrose Monohydrate as providing 3.4 kcal/g.

3. University of Illinois Chicago

College of Pharmacy. (2021). PGY1 Pharmacy Residency Program Educational Materials: Parenteral Nutrition Basics. This university courseware consistently uses 3.4 kcal/g for dextrose in all parenteral nutrition calculation examples and teaching modules.

4. Worthington

P.

Balint

J.

Bechtold

M.

et al. (2017). When is parenteral nutrition appropriate? Journal of Parenteral and Enteral Nutrition

41(3)

324–377. In the section on "Parenteral Nutrition Components

" the caloric value of dextrose is cited as 3.4 kcal/g. https://doi.org/10.1177/0148607117695251

Sodium-glucose cotransporter 2 (SGLT2) inhibitors lower blood glucose by inducing glucosuria. This mechanism has several physiological consequences that require monitoring. The induced osmotic diuresis can lead to volume depletion, dehydration, and hypotension, making it essential to monitor hydration status (A) and blood pressure (B). As these are antidiabetic medications, blood glucose (C) must be monitored to assess efficacy and the risk of hypoglycemia, especially when used with other glucose-lowering agents. Since SGLT2 inhibitors act directly on the kidneys and can cause an initial decline in the estimated glomerular filtration rate (eGFR), renal function (D) must be assessed at baseline and periodically thereafter. Therefore, all listed parameters are critical for safe and effective therapy.

A. Incorrect because it is an incomplete answer; blood pressure, glucose, and renal function also require monitoring.

B. Incorrect because it is an incomplete answer; hydration status, glucose, and renal function also require monitoring.

C. Incorrect because it is an incomplete answer; hydration status, blood pressure, and renal function also require monitoring.

D. Incorrect because it is an incomplete answer; hydration status, blood pressure, and glucose also require monitoring.

1. U.S. Food and Drug Administration (FDA). (2023). JARDIANCE® (empagliflozin) tablets

for oral use. Prescribing Information. Boehringer Ingelheim Pharmaceuticals

Inc. See Sections 2.2 (Recommended Dosage and Administration - Renal Function)

5.2 (Hypotension)

and 5.4 (Acute Kidney Injury and Impairment in Renal Function). Available at: https://www.accessdata.fda.gov/drugsatfdadocs/label/2023/204629s033lbl.pdf

2. American Diabetes Association Professional Practice Committee. (2023). 9. Pharmacologic Approaches to Glycemic Treatment: Standards of Medical Care in Diabetes—2023. Diabetes Care

46(Supplement1)

S140–S157. See Table 9.3

which outlines drug-specific and patient factors to consider for SGLT2 inhibitors

including eGFR

volume depletion risk

and blood pressure effects. DOI: https://doi.org/10.2337/dc23-S009

3. Heerspink

H. J. L.

Stefánsson

B. V.

Correa-Rotter

R.

Chertow

G. M.

Greene

T.

Hou

F. F.

Mann

J. F. E.

McMurray

J. J. V.

Lindberg

M.

Rossing

P.

Sjöström

C. D.

Toto

R. D.

& Wheeler

D. C. (2020). Dapagliflozin in Patients with Chronic Kidney Disease. New England Journal of Medicine

383(15)

1436–1446. This article discusses the renal and cardiovascular effects of SGLT2 inhibitors

highlighting the importance of monitoring renal function (eGFR) and blood pressure. DOI: https://doi.org/10.1056/NEJMoa2024816

Prevalence is an epidemiological measure that quantifies the proportion of a population with a particular disease or condition at a specific point in time (point prevalence) or over a specified period (period prevalence). It is calculated as the total number of existing cases (both new and pre-existing) divided by the total population. The question's definition of "proportion of people in a population who have a particular disease at a specified point in time" is the exact definition of prevalence.

A. Incidence rate: Measures the rate of new cases of a disease in a population over a specific time period, not the total proportion of existing cases.

C. Mortality rate: Measures the frequency of death in a population, not the proportion of individuals living with a disease.

D. Relative risk: Is a measure of association that compares the risk of disease in an exposed group to the risk in an unexposed group.

E. Odds ratio: Is a measure of association that quantifies the odds of an outcome occurring given an exposure compared to the odds of it occurring without the exposure.

1. Centers for Disease Control and Prevention (CDC). (2012). Principles of Epidemiology in Public Health Practice

Third Edition. Lesson 3: Measures of Risk

Section 2: Frequency Measures. "Prevalence refers to the proportion of persons in a population who have a particular disease or attribute at a specified point in time or over a specified period of time."

2. Boston University School of Public Health. (n.d.). Measures of Disease Frequency. PH717 Module 2. Retrieved from the Boston University website. The module states

"Prevalence is the proportion of a particular population that has the condition of interest at a specified time."

3. Noordzij

M.

Dekker

F. W.

Zoccali

C.

& Jager

K. J. (2010). Measures of disease frequency: prevalence and incidence. Nephron. Clinical practice

115(1)

c17–c20. Page c17

Abstract. "Prevalence is the proportion of a population that has a specific characteristic at a given point in time." https://doi.org/10.1159/000286345

The 2013 ACC/AHA Guideline on the Treatment of Blood Cholesterol identifies four major statin benefit groups. One of these groups comprises adults aged 21 years and older with primary, severe elevations of low-density lipoprotein cholesterol (LDL-C) at a concentration of 190 mg/dL or greater. For this group, the guideline recommends initiating high-intensity statin therapy to achieve at least a 50% reduction in LDL-C, as this level of hypercholesterolemia confers a high lifetime risk for atherosclerotic cardiovascular disease (ASCVD).

A. ≥ 100 mg/dL: This was a treatment target in older guidelines (ATP III) but is not the 2013 threshold for initiating high-intensity statin therapy based on LDL-C alone.

B. ≥ 130 mg/dL: This was another treatment target in older guidelines, not the specific threshold for this indication in the 2013 guideline.

D. ≥ 200 mg/dL: This value is incorrect; the guideline specifically defines the threshold for severe hypercholesterolemia as ≥190 mg/dL.

E. ≥ 150 mg/dL: This value is incorrect and does not represent a specific threshold for high-intensity statin initiation in the 2013 guideline.

1. Stone

N. J.

Robinson

J. G.

Lichtenstein

A. H.

Bairey Merz

C. N.

Blum

C. B.

Eckel

R. H.

... & Wilson

P. W. (2014). 2013 ACC/AHA guideline on the treatment of blood cholesterol to reduce atherosclerotic cardiovascular risk in adults: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Circulation

129(25suppl2)

S1-S45. https://doi.org/10.1161/01.cir.0000437738.63853.7a (See Table 3: "The 4 Statin Benefit Groups

" page S15

and Recommendation #3

page S18).

Stenotrophomonas maltophilia is an opportunistic, multidrug-resistant Gram-negative bacillus. The agent of choice for treating infections caused by this organism is sulfamethoxazole/trimethoprim (TMP-SMX). This recommendation is based on its consistent in vitro activity and established clinical efficacy. S. maltophilia is characteristically and intrinsically resistant to carbapenems (e.g., meropenem) due to the production of two beta-lactamases. While other agents like fluoroquinolones may show some activity, resistance is common and can emerge during therapy, making TMP-SMX the most appropriate and reliable first-line treatment.

A. Meropenem: S. maltophilia is intrinsically resistant to carbapenems due to its production of metallo-β-lactamases (L1) and serine-β-lactamases (L2).

B. Vancomycin: This antibiotic is primarily active against Gram-positive bacteria and has no clinically significant activity against Gram-negative organisms like S. maltophilia.

C. Ciprofloxacin: Resistance rates to fluoroquinolones are high and can develop rapidly during treatment, making it a less reliable option than TMP-SMX.

E. Ampicillin: S. maltophilia is resistant to most penicillins due to the production of beta-lactamases that hydrolyze the antibiotic.

1. Brooke

J. S. (2012). Stenotrophomonas maltophilia: an emerging global opportunistic pathogen. Clinical Microbiology Reviews

25(1)

2–41. (See page 20

"Therapy

" which states

"Trimethoprim-sulfamethoxazole (SXT) is currently the antimicrobial agent of choice for the treatment of S. maltophilia infections."). DOI: https://doi.org/10.1128/CMR.00019-11

2. Looney

W. J.

Narita

M.

& Mühlemann

K. (2009). Stenotrophomonas maltophilia: an emerging opportunist human pathogen. The Lancet Infectious Diseases

9(5)

312–323. (See page 318

Table 2

which lists Trimethoprim-sulfamethoxazole as the "Drug of choice" and notes intrinsic resistance to carbapenems). DOI: https://doi.org/10.1016/S1473-3099(09)70083-0

3. DiPiro

J. T.

Yee

G. C.

Posey

L. M.

Haines

S. T.

Nolin

T. D.

& Ellingrod

V. L. (2020). Pharmacotherapy: A Pathophysiologic Approach (11th ed.). McGraw-Hill Education. In Chapter 95

"Nosocomial Pneumonia

" the section on Stenotrophomonas maltophilia identifies trimethoprim-sulfamethoxazole as the drug of choice.