MN551 Unit 3: sample paper, in real form

Diabetic Ketoacidosis in a 19-Year-Old With Type 1 Diabetes: Tracing the Mechanism From Insulin Deficiency to the Presenting Findings

[Author Name]

School of Nursing, Purdue University Global

MN551 Advanced Physiology and Pathophysiology

Unit 3 Assignment

[Faculty Name]

August 11, 2026

Composite case written as a model document. No real patient, hospital or clinician is described.

The Case as Reported

The patient is a composite 19-year-old man with type 1 diabetes diagnosed at age 11, brought to a community emergency department by a roommate after 12 hours of vomiting. He reports that his insulin pump alarmed three days earlier, that he had no replacement infusion sets, and that he covered the gap with three or four injections of rapid-acting insulin before running out entirely. Over those three days he passed urine roughly every hour, drank about 5 L of water daily, and lost 3.2 kg measured against a documented clinic weight from two months earlier. Diffuse cramping abdominal pain began 18 hours ago. He denies fever, cough, dysuria, diarrhea and alcohol use, and reports no chest pain.

On arrival: temperature 37.2 C, heart rate 122 beats per minute and regular, blood pressure 102/58 mm Hg supine, respiratory rate 28 breaths per minute, oxygen saturation 99 percent on room air, weight 58 kg. He is alert and fully oriented with a Glasgow Coma Scale score of 15. Mucous membranes are dry, skin turgor over the sternum is reduced, capillary refill is 3 seconds, and the eyes appear sunken. Respirations are deep and regular rather than labored, and the breath carries a sweet acetone odor. The abdomen is soft with diffuse tenderness, no rebound, no guarding and normal bowel sounds. There is no rash, no cellulitis and no inflammation at the old infusion site.

Initial laboratory values: serum glucose 512 mg/dL, sodium 131 mEq/L, potassium 5.2 mEq/L, chloride 96 mEq/L, bicarbonate 9 mEq/L, blood urea nitrogen 28 mg/dL, creatinine 1.2 mg/dL. The venous blood gas shows a pH of 7.18 with a carbon dioxide tension of 22 mm Hg. Beta-hydroxybutyrate is 5.9 mmol/L, and urinalysis shows 4+ glucose and 3+ ketones with no nitrites and no leukocyte esterase. The calculated anion gap is 26 mEq/L and calculated serum osmolality is 300 mOsm/kg. White blood cell count is 14.2 x 10^9/L with neutrophil predominance, and hemoglobin A1C is 11.4 percent. Chest radiograph and electrocardiogram show nothing beyond sinus tachycardia.

Mechanism: From Absolute Insulin Deficiency to the Findings at the Bedside

The initiating event is an absolute insulin deficiency. When the pump stopped delivering and the injections ran out, this patient lost the one hormone that both moves glucose into muscle and adipose tissue and restrains the liver. Deficiency alone would raise the glucose; what turns hyperglycemia into ketoacidosis is the second half of the pair, a rise in the counterregulatory hormones glucagon, catecholamines, cortisol and growth hormone, driven by falling intracellular fuel and by volume loss (Rogers, 2023). Glucagon and insulin move in opposite directions here, and it is the ratio between them, not either hormone alone, that sets hepatic behavior. With that ratio inverted, the liver switches from storing fuel to manufacturing it, accelerating glycogenolysis and gluconeogenesis while peripheral uptake falls away.

Hyperglycemia explains the history before it explains the chemistry. Once the filtered glucose load exceeds the reabsorptive capacity of the proximal tubule, at a plasma concentration near 180-200 mg/dL, glucose remains in the tubular fluid and holds water and electrolytes with it (Hall & Hall, 2021). That osmotic diuresis is the hourly urination he described, and it is why he drank 5 L a day and still lost 3.2 kg. The volume that left in the urine is the volume missing from the vascular space, which appears on examination as dry membranes, reduced turgor, a capillary refill of 3 seconds and a heart rate of 122, and appears in the chemistry as a blood urea nitrogen of 28 against a creatinine of 1.2.

The acid comes from fat, not from sugar. Insulin normally suppresses hormone-sensitive lipase; without it, lipolysis releases free fatty acids into the circulation, and the glucagon-driven fall in malonyl-CoA opens carnitine palmitoyltransferase 1, the gate that admits those fatty acids to the mitochondria for beta-oxidation. Acetyl-CoA then arrives faster than the citric acid cycle can consume it, and the liver converts the surplus into acetoacetate, beta-hydroxybutyrate and acetone. Beta-hydroxybutyrate at 5.9 mmol/L is a fixed acid, and every molecule that dissociates consumes a bicarbonate ion, which is why bicarbonate sits at 9 mEq/L while the unmeasured anions push the gap to 26. Acetone is volatile and exhaled, which is the odor at the bedside.

Two of the remaining findings follow from the acidosis itself. Central and peripheral chemoreceptors respond to the falling pH by increasing tidal volume more than rate, producing breathing that is deep and unlabored at 28 per minute; the expected compensation for a bicarbonate of 9, by Winter's formula, is a carbon dioxide tension near 21-22 mm Hg, and the measured 22 says the respiratory response is appropriate rather than a second acid-base disorder layered on top. The abdominal pain and vomiting track the severity of the acidosis and the gastric stasis that accompanies it rather than an intra-abdominal catastrophe. Full alertness fits a calculated osmolality of 300 mOsm/kg, well under the range where obtundation is expected.

Three Numbers That Mislead, and What the Mechanism Predicts

The potassium of 5.2 mEq/L is the most dangerous value on the panel, because it reads as a surplus and represents a deficit. Insulin deficiency and acidemia both shift potassium out of cells into the extracellular fluid, while osmotic diuresis and vomiting strip it from the body; total body potassium in ketoacidosis is commonly depleted by 3-5 mEq per kilogram even when the serum value is normal or high (Umpierrez et al., 2024). The consequence is directional and predictable: as insulin is restored and the acidemia corrects, potassium moves back into cells and the serum value falls, sometimes steeply. The mechanism, not the single measured number, is what says this value calls for monitoring and replacement rather than reassurance.

Sodium is the second value to read twice. A measured sodium of 131 mEq/L looks like hyponatremia, but glucose held in the extracellular space draws water out of cells and dilutes the sodium against which it is measured. Correcting for a glucose of 512 mg/dL lifts the value to roughly 138 mEq/L, so this patient is not sodium depleted in the way the raw number suggests; he is water depleted. The anion gap is the third, and it behaves differently again. Glucose falls early with fluid alone, so a falling glucose is a weak marker of recovery, while the gap and beta-hydroxybutyrate follow ketone clearance and close only once ketogenesis has stopped (American Diabetes Association Professional Practice Committee, 2025).

Read in this order, the mechanism predicts the shape of treatment rather than following it. Volume is restored first because perfusion improves ketone clearance and lowers counterregulatory drive; insulin follows because it closes the gate on lipolysis, which is the source of the acid; potassium is replaced alongside insulin because insulin drives it back into cells; and alkali is reserved for extreme acidemia because giving bicarbonate does not stop the ketone production that consumed it (Umpierrez et al., 2024). The scale behind the case supports the attention it gets: an estimated 38.4 million people in the United States were living with diabetes at the most recent national count, about 11.6 percent of the population (Centers for Disease Control and Prevention, 2024).

References

American Diabetes Association Professional Practice Committee. (2025). Standards of care in diabetes 2025. Diabetes Care, 48(Suppl. 1), S1-S352. https://diabetesjournals.org/care

Centers for Disease Control and Prevention. (2024). National diabetes statistics report. U.S. Department of Health and Human Services. https://www.cdc.gov/diabetes/php/data-research/index.html

Hall, J. E., & Hall, M. E. (2021). Guyton and Hall textbook of medical physiology (14th ed.). Elsevier.

Rogers, J. L. (Ed.). (2023). McCance and Huether's pathophysiology: The biologic basis for disease in adults and children (9th ed.). Elsevier.

Umpierrez, G. E., Davis, G. M., ElSayed, N. A., Fadini, G. P., Galindo, R. J., Hirsch, I. B., Klonoff, D. C., McCoy, R. G., Misra, S., Gabbay, R. A., Bannuru, R. R., & Dhatariya, K. K. (2024). Hyperglycemic crises in adults with diabetes: A consensus report. Diabetes Care, 47(8), 1257-1275. https://diabetesjournals.org/care