The calculation involves two steps. First, determine the total volume of the intravenous fluid (IVF) administered over 24 hours. At a rate of 125 mL/hour, the total volume is 125 mL/hour × 24 hours = 3000 mL. Second, calculate the amount of dextrose in this volume. A "Dextrose 5%" solution means it contains 5 grams of dextrose per 100 mL of solution (% w/v). Using this concentration, the total amount of dextrose is (5 g / 100 mL) × 3000 mL = 150 grams. The potassium chloride content is not relevant to this specific question.

A. 300gm: This would be the correct amount if the solution was Dextrose 10%, not 5%.

B. 500gm: This is an incorrect calculation, possibly confusing the percentage with the final amount in grams.

C. 50gm: This represents the amount of dextrose in only 1000 mL (1 L) of the solution, not the total 24-hour volume of 3000 mL.

E. 200gm: This is a mathematical error and does not correspond to the given concentration and infusion rate.

1. Allen

L. V.

Jr. (2018). Ansel's Pharmaceutical Dosage Forms and Drug Delivery Systems (11th ed.). Wolters Kluwer. Chapter 6

"Pharmaceutical Calculations

" Section on Percentage Strength

p. 115. This section defines percentage weight-in-volume (% w/v) as grams of a constituent in 100 mL of solution.

2. University of Washington School of Pharmacy. (n.d.). Pharm 558: Pharmaceutical Calculations - Intravenous Flow Rates. Course materials. These materials detail the standard method for calculating the total amount of a drug infused over a specific period by first determining the total volume (Rate × Time) and then multiplying by the drug concentration.

3. Zatz

J. L.

& Teixeira

M. G. (2005). Pharmaceutical Calculations (4th ed.). Wiley-Interscience. Chapter 5

"Percentage

Ratio Strength

and Other Expressions of Concentration

" pp. 67-69. This chapter provides examples for calculating the quantity of an active ingredient in a specified volume of a liquid when the concentration is expressed as a percentage.

Sodium-glucose cotransporter 2 (SGLT2) inhibitors exert their antihyperglycemic effect by directly targeting the kidneys. They selectively block the SGLT2 protein located in the proximal convoluted tubules. This inhibition prevents the reabsorption of filtered glucose from the tubular fluid back into the bloodstream. Consequently, excess glucose is excreted in the urine (glucosuria), leading to a reduction in plasma glucose concentrations. This mechanism of action is independent of insulin secretion or sensitivity, focusing solely on renal glucose handling.

A. Sulfonylureas: Act primarily on the pancreatic beta cells to stimulate insulin secretion.

B. Alpha-Glucosidase Inhibitors: Work in the brush border of the small intestine to delay carbohydrate absorption.

C. DPP4 Inhibitors: Prevent the breakdown of incretin hormones (like GLP-1), which act on the pancreas to enhance glucose-dependent insulin secretion.

D. Glucagon-like peptide-1 receptor agonists: Mimic incretin hormones, acting on the pancreas, brain, and gastrointestinal tract.

E. Thiazolidinediones: Increase insulin sensitivity in peripheral tissues, primarily adipose tissue, skeletal muscle, and the liver.

F. Biguanide: Primarily decreases hepatic glucose production and increases insulin sensitivity in peripheral tissues.

1. American Diabetes Association Professional Practice Committee. (2024). 9. Pharmacologic Approaches to Glycemic Treatment: Standards of Care in Diabetes—2024. Diabetes Care

47(Supplement1)

S158–S178. (See Table 9.3

"Mechanisms of action of noninsulin glucose-lowering medications for type 2 diabetes"). https://doi.org/10.2337/dc24-S009

2. DeFronzo

R. A.

Norton

L.

& Abdul-Ghani

M. (2017). Renal

metabolic and cardiovascular considerations of SGLT2 inhibitors. Nature Reviews Nephrology

13(1)

11–26. (See Section: "Mechanism of action of SGLT2 inhibitors

" p. 12). https://doi.org/10.1038/nrneph.2016.170

3. Brunton

L. L.

Knollmann

B. C.

& Hilal-Dandan

R. (Eds.). (2018). Goodman & Gilman's The Pharmacological Basis of Therapeutics (13th ed.). McGraw-Hill Education. (See Chapter 48

Section: "Sodium-Glucose Cotransporter 2 Inhibitors").

The protamine dose is based on the amount of active heparin in the body, which is calculated by considering the heparin administered in the last 2-3 hours and its half-life.

1. Calculate heparin rate: 13 mL/hr × 50 units/mL = 650 units/hr.

2. Calculate heparin to be neutralized:

From the most recent hour: 650 units (100% active).

From the previous hour (1-2 hours ago): 650 units / 2 = 325 units (50% active, as one half-life of 60 minutes has passed).

3. Total active heparin: 650 units + 325 units = 975 units.

4. Calculate protamine dose: 975 units / (100 units/mg) = 9.75 mg.

The closest answer is 9.7 mg.

A. 5mg: This dose is too low and would result from a significant miscalculation, leading to inadequate heparin reversal.

B. 10mg: This is a rounded value and less precise than the calculated dose based on the provided pharmacokinetic parameters.

C. 7mg: This dose is incorrect and may result from only partially accounting for the heparin administered in the last hour.

D. 13mg: This is incorrect as it reverses the total heparin given over 2 hours (1300 units) without accounting for the 60-minute half-life.

1. University of Illinois Chicago (UIC) College of Pharmacy

Drug Information Group. (2019). FAQ: What is the appropriate dose of protamine for the reversal of unfractionated heparin (UFH)? This document outlines the standard calculation method: "The dose of protamine is dependent on the amount of heparin given in the previous 2 to 3 hours... For continuous infusions

100% of the heparin administered in the last hour

50% of the heparin administered in the hour prior

and 25% of the heparin administered in the hour before that should be reversed."

2. Weitz

J. I.

& Weitz

J. I. (2018). Blood Coagulation and Anticoagulant

Fibrinolytic

and Antiplatelet Drugs. In L. L. Brunton

R. Hilal-Dandan

& B. C. Knollmann (Eds.)

Goodman & Gilman's: The Pharmacological Basis of Therapeutics (13th ed.

Chapter 32). McGraw-Hill Education. The text describes protamine dosing based on the principle that 1 mg neutralizes approximately 100 units of heparin

emphasizing that the dose must be adjusted for time elapsed due to heparin's short half-life.

3. Hirsh

J.

Bauer

K. A.

& Guyatt

G. H. (2008). Parenteral Anticoagulants: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines (8th Edition). Chest

133(6suppl)

141S-159S. https://doi.org/10.1378/chest.08-0689. Section 2.3.3 discusses heparin's pharmacokinetics (half-life of 30-90 minutes) and Section 4.3 covers management of bleeding

where protamine dosing is based on the amount of heparin recently infused.

Adalat is a brand name for the drug nifedipine. Nifedipine is a dihydropyridine calcium channel blocker used primarily for the management of hypertension and chronic stable angina. It works by inhibiting the influx of calcium ions into vascular smooth muscle and myocardial cells, leading to peripheral and coronary artery vasodilation. This vasodilation reduces peripheral resistance, lowers blood pressure, and increases coronary blood flow, thereby alleviating angina symptoms. The most common formulation is an extended-release tablet, such as Adalat CC.

B. Adalimumab is the active ingredient in Humira, a biologic medication used to treat various autoimmune diseases.

C. Digoxin is the active ingredient in Lanoxin, a cardiac glycoside used for heart failure and atrial fibrillation.

D. Simvastatin is the active ingredient in Zocor, an HMG-CoA reductase inhibitor used to lower cholesterol levels.

1. U.S. Food and Drug Administration (FDA). (2019). ADALAT CC (nifedipine) extended-release tablets

for oral use. Prescribing Information. Application No. N019955. Section 11: DESCRIPTION. Retrieved from https://www.accessdata.fda.gov/drugsatfdadocs/label/2019/019955s064lbl.pdf

2. Whalen

K.

Finkel

R.

& Panavelil

T. A. (2018). Lippincott Illustrated Reviews: Pharmacology (7th ed.). Wolters Kluwer. Chapter 21: Calcium Channel Blockers

p. 275. (This text is standard courseware in many university pharmacy programs).

3. Katzung

B. G.

& Vanderah

T. W. (2021). Basic & Clinical Pharmacology (15th ed.). McGraw-Hill Education. Chapter 12: Vasodilators & the Treatment of Angina Pectoris

Table 12-1. (This is a foundational textbook in pharmacology curricula at reputable universities).

The calculation requires three steps. First, determine the concentration of the vasopressin solution: 40 units divided by 100 mL equals 0.4 units/mL. Second, convert the ordered dose rate from minutes to hours: 0.03 units/minute multiplied by 60 minutes/hour equals 1.8 units/hour. Finally, calculate the infusion rate in mL/hr by dividing the hourly dose by the concentration: (1.8 units/hr) / (0.4 units/mL) = 4.5 mL/hr. This is the correct rate to deliver the prescribed dose.

A. 4.0 ml/hr: This rate is incorrect and would result in underdosing the patient. It may stem from a miscalculation of the hourly dose or the drug concentration.

B. 4.9ml/hr: This is a calculation error. This rate does not align with the prescribed dose and available concentration.

D. 3.5ml/hr: This is a calculation error. This rate would deliver an insufficient amount of medication to the patient.

E. 6ml/hr: This rate is incorrect and would result in overdosing the patient. It would be the correct rate for a dose of 0.04 units/min, not the prescribed 0.03 units/min.

1. University of Washington

School of Pharmacy. (n.d.). Pharmaceutical Calculations: Infusion Rate Calculations. In PHARM 559 Course Materials. This type of university courseware outlines the standard dimensional analysis method for calculating intravenous infusion rates. The formula used is Rate (mL/hr) = [Dose (units/hr)] / [Concentration (units/mL)].

2. Evans

L.

et al. (2021). Surviving Sepsis Campaign: International Guidelines for Management of Sepsis and Septic Shock 2021. Critical Care Medicine

49(11)

e1063-e1143. In Recommendation 31

the guidelines state

"For adults with septic shock on norepinephrine with inadequate mean arterial pressure levels

we suggest adding vasopressin (up to 0.03 U/min)." This peer-reviewed source validates the clinical appropriateness of the dose used in the question. (DOI: 10.1097/CCM.0000000000005337)

3. Stoklosa

M. J.

& Ansel

H. C. (2012). Pharmaceutical Calculations (14th ed.). Lippincott Williams & Wilkins. Chapter 11

"Isotonicity

Osmolality

and Intravenous Infusion Calculations

" provides the foundational principles and formulas for determining the rate of flow for intravenous infusions based on the volume of solution

quantity of drug

and desired dose.

The patient's result of 156 mg/dL on the 1-hour, 50 g glucose challenge test (GCT) is considered a positive screen for gestational diabetes mellitus (GDM), as it exceeds the commonly used thresholds of 130-140 mg/dL. A positive GCT is not diagnostic but indicates the need for further testing. The standard, accepted next step in the two-step screening approach is to perform a confirmatory 3-hour, 100 g oral glucose tolerance test (OGTT). A diagnosis of GDM is made based on the results of this second test. Initiating treatment or dietary changes before a formal diagnosis is premature.

A. Repeat the 50 g oral glucose challenge: The initial screening test was positive; repeating it is redundant and delays the necessary diagnostic evaluation.

C. Advise the patient to follow an American Diabetic Association diet plan: Dietary intervention is a primary treatment for GDM, but it should only be initiated after a confirmed diagnosis from the 3-hour OGTT.

D. Begin insulin treatment: Insulin is a pharmacological treatment for GDM that is not controlled by diet and exercise. It is inappropriate without a confirmed diagnosis.

E. Order a fetal ultrasound examination: While fetal ultrasounds are important for monitoring fetal growth in pregnancies complicated by GDM, it is not the next step for diagnosing the condition.

1. American College of Obstetricians and Gynecologists (ACOG). (2018). ACOG Practice Bulletin No. 190: Gestational Diabetes Mellitus. Obstetrics & Gynecology

131(2)

e49-e64. (Reaffirmed 2021). In the section "Screening and Diagnosis

" the bulletin outlines the two-step approach

stating that a positive 50-g screen should be followed by a 3-hour 100-g OGTT for diagnosis. DOI: 10.1097/AOG.0000000000002501

2. American Diabetes Association Professional Practice Committee. (2023). 15. Management of Diabetes in Pregnancy: Standards of Care in Diabetes—2023. Diabetes Care

46(Suppl 1)

S254–S266. Section 15.3

"Screening for and Diagnosis of GDM

" describes the two-step strategy where a positive 1-hour 50-g screen is followed by a 3-hour 100-g OGTT. DOI: 10.2337/dc23-S015

3. Landon

M. B.

& Gabbe

S. G. (2011). Gestational diabetes mellitus. Obstetrics & Gynecology

118(6)

1379–1393. This peer-reviewed article discusses the screening protocols

explicitly stating the progression from a 50-g glucose challenge to a 100-g oral glucose tolerance test for diagnosis. DOI: 10.1097/AOG.0b013e3182364d39

The patient's clinical presentation is characteristic of acute viral rhinosinusitis, commonly known as the common cold. The key indicators are the short duration of symptoms (6 days), the nature of the discharge (thin, clear rhinorrhea), the absence of high fever, and the fact that the symptoms are improving. Acute bacterial rhinosinusitis is generally suspected only when symptoms persist for 10 days or more without any improvement, are severe at onset (e.g., fever ≥39°C, purulent discharge), or worsen after a period of initial improvement ("double sickening"). Since this patient's condition is mild and resolving, a viral etiology is the most probable cause.

A. Streptococcus pneumoniae is a leading cause of bacterial sinusitis, which is inconsistent with the patient's improving, non-severe symptoms.

C. Moraxella catarrhalis is a common bacterial pathogen in sinusitis, but the clinical picture does not support a bacterial infection.

D. Haemophilus influenzae is a frequent cause of bacterial sinusitis; however, the patient's presentation points to a viral, self-limiting illness.

E. Staphylococcus aureus is a less common cause of community-acquired bacterial sinusitis and is not suggested by these mild, resolving symptoms.

1. Chow

A. W.

Benninger

M. S.

Brook

I.

et al. (2012). IDSA Clinical Practice Guideline for Acute Bacterial Rhinosinusitis in Children and Adults. Clinical Infectious Diseases

54(8)

e72–e112. (See Table 2

page e76

which outlines criteria for distinguishing viral from bacterial rhinosinusitis. Viral rhinosinusitis is characterized by a duration of less than 10 days with symptoms that are not worsening). https://doi.org/10.1093/cid/cis370

2. Rosenfeld

R. M.

Piccirillo

J. F.

Chandrasekhar

S. S.

et al. (2015). Clinical Practice Guideline (Update): Adult Sinusitis. Otolaryngology–Head and Neck Surgery

152(2suppl)

S1–S39. (See Section 2

"Distinguishing Viral vs. Bacterial Sinusitis

" which states that viral rhinosinusitis is far more common and typically resolves or improves within 10 days). https://doi.org/10.1177/0194599815572097

3. 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 Chapter 88

"Upper Respiratory Tract Infections

" the text clarifies that the vast majority of acute rhinosinusitis cases are caused by viruses and are self-limiting

with symptoms peaking at 3-6 days and resolving by day 10.

Systemic Lupus Erythematosus (Lupus) is a classic example of a type III hypersensitivity reaction. This condition is characterized by the formation of autoantibodies against nuclear antigens. These antibodies bind to the antigens, forming immune complexes that circulate and deposit in various tissues, such as the kidneys, skin, and joints. The deposition of these complexes activates the complement system and recruits inflammatory cells, leading to tissue damage and the systemic manifestations of the disease.

B. Graves disease: This is a type II hypersensitivity reaction, where autoantibodies stimulate the TSH receptor on thyroid cells, causing hyperthyroidism.

C. Hashimoto’s thyroiditis: This is primarily a type IV (T-cell mediated) hypersensitivity reaction, leading to the destruction of thyroid tissue by cytotoxic T-lymphocytes.

D. Allergic rhinitis: This is a type I (IgE-mediated) hypersensitivity reaction, where allergens trigger the release of histamine from mast cells.

E. Myasthenia gravis: This is a type II hypersensitivity reaction, where autoantibodies block or destroy acetylcholine receptors at the neuromuscular junction.

1. Abbas

A. K.

Lichtman

A. H.

& Pillai

S. (2020). Cellular and Molecular Immunology (10th ed.). Elsevier.

For Lupus (Type III): Chapter 19

"Diseases Caused by Immune Responses: Hypersensitivity and Autoimmunity

" Section on "Immune Complex-Mediated Diseases (Type III Hypersensitivity)

" states

"Systemic lupus erythematosus (SLE) is the prototypic systemic immune complex–mediated disease."

For Graves disease and Myasthenia gravis (Type II): Chapter 19

Section on "Antibody-Mediated Diseases (Type II Hypersensitivity)

" lists Graves' disease and myasthenia gravis as examples of diseases caused by antibodies against cell surface receptors.

For Hashimoto's thyroiditis (Type IV): Chapter 19

Section on "T Lymphocyte-Mediated Diseases (Type IV Hypersensitivity)

" describes Hashimoto's thyroiditis as an autoimmune disease resulting from T-cell mediated destruction of thyroid epithelial cells.

2. Justiz Vaillant

A. A.

& Zulfiqar

H. (2023). Hypersensitivity Reactions. In StatPearls. StatPearls Publishing. Retrieved from https://www.ncbi.nlm.nih.gov/books/NBK560561/

Table 1

"Gell and Coombs Classification of Hypersensitivity Reactions

" explicitly lists Systemic Lupus Erythematosus under Type III

Allergic Rhinitis under Type I

Graves' Disease and Myasthenia Gravis under Type II

and Hashimoto's Thyroiditis under Type IV.

3. Stanford University School of Medicine. (n.d.). Immunology Course (IMM 205/206) Lecture Notes: Hypersensitivity Reactions.

In lectures covering the Gell and Coombs classification

Lupus is consistently presented as the archetypal Type III reaction due to immune complex deposition in tissues like the glomeruli. Graves' disease and Myasthenia gravis are used as primary examples of Type II receptor-targeting antibody-mediated disease.

Valproic acid has a black box warning for life-threatening pancreatitis, which can occur at any time during therapy in both children and adults. This is a rare but serious adverse effect that can progress rapidly and be fatal. Patients should be counseled to report any signs or symptoms of pancreatitis, such as severe abdominal pain, nausea, vomiting, or anorexia, to their healthcare provider immediately. The drug should be discontinued if pancreatitis is diagnosed.

A. Gingival hyperplasia is a classic and common side effect associated with phenytoin, not valproic acid.

C. Kidney stones (nephrolithiasis) are a known adverse effect of other antiepileptic drugs like topiramate and zonisamide.

D. Valproic acid is commonly associated with significant weight gain, which is often a reason for non-adherence.

E. Euphoria is not a recognized side effect of valproic acid; sedation and dizziness are more common CNS effects.

1. U.S. Food and Drug Administration (FDA). (2018). DEPAKOTE (divalproex sodium) delayed-release tablets

for oral use. Highlights of Prescribing Information. Section: WARNINGS AND PRECAUTIONS

5.2 Pancreatitis. Retrieved from the FDA database. (This official vendor documentation explicitly lists pancreatitis as a boxed warning).

2. Zaccara

G.

Franciotta

D.

& Perucca

E. (2007). Idiosyncratic adverse reactions to antiepileptic drugs. Epilepsia

48(7)

1223–1244. https://doi.org/10.1111/j.1528-1167.2007.01041.x (Table 2 on page 1228 lists pancreatitis as a rare

life-threatening idiosyncratic reaction to valproate).

3. McNamara

J. O. (2018). Pharmacotherapy of the Epilepsies. In L. L. Brunton

R. Hilal-Dandan

& B. C. Knollmann (Eds.)

Goodman & Gilman's: The Pharmacological Basis of Therapeutics (13th ed.). McGraw-Hill Education. Chapter 17

Section: Valproate

Subsection: Adverse Effects. (This standard academic textbook

used in university curricula

details pancreatitis as a serious idiosyncratic toxicity of valproate).

The patient's clinical presentation of a unilateral, throbbing headache associated with photophobia and nausea is characteristic of a migraine. The question asks for an abortive therapy, which is a medication taken to stop a migraine attack after it has started. Sumatriptan is a serotonin (5-HT1B/1D) receptor agonist (a "triptan") and is a first-line abortive treatment for moderate-to-severe migraine attacks. It works by causing vasoconstriction of cranial arteries and inhibiting the release of vasoactive neuropeptides. The other medications listed are used for migraine prophylaxis (prevention), not for treating an acute attack.

B. Gabapentin: This is an anticonvulsant medication sometimes used off-label for migraine prophylaxis, not for aborting an acute attack.

C. Amitriptyline: This is a tricyclic antidepressant that is established as an effective agent for migraine prophylaxis.

D. Propranolol: This beta-blocker is a first-line, evidence-based medication used for the prophylaxis of episodic migraines.

E. Diltiazem: This calcium channel blocker is not a standard first-line therapy for either abortive or prophylactic treatment of migraine.

1. Marmura

M. J.

Silberstein

S. D.

& Schwedt

T. J. (2015). The acute treatment of migraine in adults: the american headache society evidence assessment of migraine pharmacotherapies. Headache: The Journal of Head and Face Pain

55(1)

3–20. (In Table 2

"Triptans

" including sumatriptan

are listed with a Grade A recommendation as effective for acute migraine treatment). https://doi.org/10.1111/head.12499

2. Silberstein

S. D.

Holland

S.

Lipton

R. B.

& Dodick

D. W. (2012). Evidence-based guideline update: Pharmacologic treatment for episodic migraine prevention in adults: Report of the Quality Standards Subcommittee of the American Academy of Neurology and the American Headache Society. Neurology

78(17)

1337–1345. (In Table 2

propranolol and amitriptyline are listed as having Level A evidence for migraine prevention. Gabapentin is mentioned as having inadequate evidence to support its use). https://doi.org/10.1212/WNL.0b013e3182535d20

3. VanderPluym

J. H.

Halker Singh

R. B.

& Urtecho

M. (2021). Acute Treatments for Episodic Migraine in Adults: A Systematic Review and Meta-analysis. JAMA

325(23)

2357–2369. (This meta-analysis confirms that triptans are highly effective for acute migraine treatment

specifically for pain freedom at 2 hours). https://doi.org/10.1001/jama.2021.7939

4. University of California

San Francisco (UCSF) Headache Center. (n.d.). Medications for Migraine and Headache. UCSF Department of Neurology. (This educational resource clearly distinguishes between "Abortive Medications" like triptans and "Preventive Medications" like beta-blockers

antidepressants

and anti-seizure drugs). Retrieved from https://headache.ucsf.edu/medications-migraine-and-headache (Section: "Abortive Medications" and "Preventive Medications").