D236 Task 1 Pathophysiology Paper Example

Type 2 Diabetes Mellitus in a 52-Year-Old Adult: How Insulin Resistance Produces the Presenting Signs, Laboratory Values and Nursing Priorities

[Author Name]

Leavitt School of Health, Western Governors University

D236 Pathophysiology

Task 1

[Course Instructor]

August 11, 2026

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

Case Summary and Presenting Data

The patient is a composite 52-year-old woman who works as an office administrator and comes to a primary care clinic for a check she has put off for three years. For about three months she has been thirsty most of the day, drinks close to four liters of water, and gets up three times a night to pass urine. She is tired by early afternoon, her vision blurs and clears at different times of day, and she has lost 3.5 kg without trying. She also reports tingling in both feet that began around four months ago, and a shallow sore under her right great toe that has stayed open for more than a month.

On examination she weighs 96 kg at a height of 166 cm, for a body mass index of 34.8, with a waist circumference of 104 cm. Blood pressure is 142/88 mm Hg, heart rate 82 beats per minute, temperature 36.9 C, and respirations 16 per minute. The sore under the right great toe measures 1.5 cm across, has a clean pink base with thickened callus at its edge, and is not tender when pressed. She cannot feel a 10 g monofilament at three of ten sites on the right foot and two of ten on the left. Pedal pulses are present on both sides, and the skin of both lower legs is dry with a few small scratches.

Laboratory results support the picture. Fasting plasma glucose is 214 mg/dL, hemoglobin A1C is 9.4 percent, and a random glucose drawn at the visit is 268 mg/dL. Urinalysis shows 3+ glucose with no ketones. Triglycerides are 285 mg/dL, high density lipoprotein cholesterol is 34 mg/dL, and low density lipoprotein cholesterol is 138 mg/dL. Serum creatinine is 0.9 mg/dL and the urine albumin to creatinine ratio is 62 mg/g. Her mother and her older brother both live with type 2 diabetes. A fasting glucose of 126 mg/dL or higher, or a hemoglobin A1C of 6.5 percent or higher, meets the diagnostic threshold, and she is above both.

How Type 2 Diabetes Develops

Normal control starts with a meal. Glucose absorbed from the small intestine raises blood glucose, and beta cells in the islets of the pancreas release insulin in response. Insulin binds to receptors on muscle and fat cells and signals GLUT4 transporters to move to the cell surface, where they carry glucose into the cell. At the same time insulin tells the liver to store glucose as glycogen and to stop releasing new glucose, and it tells fat cells to stop breaking down stored fat. Blood glucose returns to its usual range within about two hours, and the whole process depends on cells answering insulin, not simply on insulin being present.

In type 2 diabetes the cells stop answering. Excess fat stored inside the abdomen releases free fatty acids and inflammatory chemicals into the circulation, and these interfere with the signal that follows the insulin receptor, so fewer GLUT4 transporters reach the cell surface. Muscle then takes up less glucose after a meal, and the liver keeps releasing glucose overnight even though insulin is telling it to stop. The beta cells answer by making more insulin, and for years that extra output holds blood glucose close to normal. This silent compensated stage is why a person can carry the disease for a decade before any symptom appears.

Compensation eventually fails. Beta cells exposed to years of high demand, high glucose and high fatty acid levels lose both mass and function, and by the time type 2 diabetes is diagnosed a large share of that function is already gone. Insulin output can no longer match the resistance, so fasting glucose rises first, driven by a liver that is no longer restrained overnight, and after meal glucose rises next. Once blood glucose passes the reabsorption threshold of the kidney near 180 mg/dL, the tubules cannot reclaim it all and glucose spills into the urine. This patient's family history and central fat distribution are the two risk factors that set the process in motion.

Why This Patient Has These Findings, and What They Mean for Nursing Care

Three of her symptoms come from one mechanism. Glucose that spills into the filtrate pulls water with it, an osmotic diuresis, which is why she passes urine three times a night and why the urinalysis reads 3+ glucose. The water lost that way concentrates the blood, and rising serum osmolality stimulates the thirst centers of the hypothalamus, which is why she drinks four liters a day. The weight loss and the fatigue share a cause as well: glucose is in the blood but cannot get into muscle and fat cells, so the body breaks down fat and muscle protein for fuel while blood glucose stays high.

The rest of her findings map just as directly. High blood glucose pulls water into the lens of the eye and changes its shape, so vision blurs and clears as glucose swings, which is why a new eyeglass prescription is held until glucose is steadier and the refraction has stopped moving. The tingling in both feet is early distal symmetric neuropathy, produced by sorbitol building up inside nerve cells and by damage to the small vessels that supply those nerves. The albumin to creatinine ratio of 62 mg/g is early kidney involvement, where years of high pressure filtration and a thickened glomerular basement membrane let albumin leak through.

The open sore under her toe is the same disease reaching the skin. Sensory loss means she does not feel the repeated pressure of walking, so the injury keeps reopening, and the callused rim is the record of that pressure. High glucose also slows healing directly: neutrophils move and kill bacteria less effectively, collagen is laid down more slowly, and small vessel disease limits the oxygen a healing wound needs. Her missing monofilament sensation at three of ten sites on the right foot is therefore not a minor finding; it is the reason a painless sore was allowed to stay open for more than a month.

Two conclusions follow for nursing care. First, this is type 2 rather than type 1: onset was gradual, ketones are absent, and enough insulin remains to hold ketone production down, so the acute danger to watch for is a hyperosmolar hyperglycemic state with very high glucose and severe dehydration rather than diabetic ketoacidosis. Second, the priorities here are assessment and teaching. The prescriber decides the medication plan, while the nurse checks glucose and reviews the log with her, inspects both feet at every visit, teaches daily foot checks and well fitted footwear, teaches the signs of high and low blood glucose, arranges wound follow-up, and evaluates at the next visit whether any of that teaching changed her practice at home.

References

American Diabetes Association Professional Practice Committee. (2024). Standards of care in diabetes-2024. Diabetes Care, 47(Supplement 1). https://diabetesjournals.org/care/issue/47/Supplement_1

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

Hinkle, J. L., Cheever, K. H., & Overbaugh, K. J. (2022). Brunner and Suddarth's textbook of medical-surgical nursing (15th ed.). Wolters Kluwer.

National Institute of Diabetes and Digestive and Kidney Diseases. (2023). Type 2 diabetes. U.S. Department of Health and Human Services, National Institutes of Health. https://www.niddk.nih.gov/health-information/diabetes/overview/what-is-diabetes/type-2-diabetes

Norris, T. L. (2020). Porth's essentials of pathophysiology (5th ed.). Wolters Kluwer.