Case study: Endocrine function
C.B. is a significantly overweight, 48-year-old woman from the Winnebago Indian tribe who had high blood sugar and cholesterol levels three years ago but did not follow up with a clinical diagnostic work-up. She had participated in the state’s annual health screening program and noticed that her fasting blood sugar was 141 and her cholesterol was 225. However, she felt “perfectly fine at the time” and could not afford any more medications. Except for a number of “female infections,” she has felt fine until recently. Today, she presents to the Indian Hospital general practitioner complaining that her left foot has been weak and numb for nearly three weeks and that the foot is difficult to flex. She denies any other weakness or numbness at this time. However, she reports that she has been very thirsty lately and gets up more often at night to urinate. She has attributed these symptoms to the extremely warm weather and drinking more water to keep hydrated. She has gained a total of 65 pounds since her last pregnancy 14 years ago, 15 pounds in the last 6 months alone.
Case study questions
- In which racial and ethnic groups is diabetes mellitus (DM) more prevalent? Based on C.B.’s clinical manifestations, compile the signs and symptoms she is exhibiting that are compatible with a diagnosis of type 2 diabetes mellitus.
- If C.B. develops a bacterial pneumonia in her right lower lobe, how would you expect her glycemia values to be? Explain and support your answer.
- What would be the best initial non-pharmacologic and pharmacologic therapy to recommend to C.B.?
1. Racial and ethnic groups with higher diabetes prevalence
In the United States, diabetes is not distributed equally. Prevalence of diagnosed diabetes among adults is highest in American Indian and Alaska Native people, followed by non-Hispanic Black, Hispanic and Asian American adults, and lowest in non-Hispanic White adults (Centers for Disease Control and Prevention [CDC], 2024).
| Group (U.S. adults) | Approximate prevalence of diagnosed diabetes |
|---|---|
| American Indian / Alaska Native | About 13.6%, the highest of any group |
| Non-Hispanic Black | About 12.1% |
| Hispanic / Latino | About 11.7% (highest among people of Mexican and Puerto Rican descent) |
| Asian American | About 9.1% (higher in some subgroups, such as South Asian and Filipino) |
| Non-Hispanic White | About 6.9% |
Source: CDC National Diabetes Statistics Report, age-adjusted estimates for 2019–2021 (CDC, 2024). The CDC updated the report in September 2026; check it for the newest figures, although the ranking of groups has been consistent for many years. Rates among American Indian communities vary by region and tribe, and some communities have among the highest rates of type 2 diabetes in the world. These disparities reflect a combination of genetic susceptibility and powerful social and historical factors: loss of traditional foodways, poverty, limited access to healthy food and healthcare, and the effects of historical trauma.
C.B.’s risk factors for type 2 diabetes
- Ethnicity: American Indian (Winnebago/Ho-Chunk).
- Age: 48 (risk rises after 35–45).
- Obesity with progressive weight gain: 65 lb since her last pregnancy, 15 lb in 6 months. Excess visceral fat drives insulin resistance.
- Possible history of gestational diabetes or a large baby, which should be asked about.
- Dyslipidemia: cholesterol of 225 mg/dL, part of the metabolic syndrome picture.
- Barriers to care: cost of medications and lack of follow-up.
Signs and symptoms compatible with type 2 diabetes
| Finding | Explanation |
|---|---|
| Elevated fasting blood glucose (141 mg/dL) three years ago | A fasting plasma glucose of 126 mg/dL or higher, confirmed by repeat testing, meets diagnostic criteria for diabetes (American Diabetes Association [ADA], 2025). Her value was never confirmed, so the diagnosis was missed. |
| Polydipsia (excessive thirst) | High blood glucose raises serum osmolality and causes fluid loss through the kidneys, which triggers thirst. |
| Polyuria and nocturia (urinating more at night) | When glucose exceeds the renal threshold (about 180 mg/dL), it spills into the urine and pulls water with it (osmotic diuresis) (Rogers, 2023). |
| Recurrent “female infections” | Likely vulvovaginal candidiasis. Glucose in urine and secretions feeds yeast, and hyperglycemia impairs neutrophil function. |
| Numbness and weakness of the left foot, difficulty flexing it | Consistent with diabetic neuropathy. Chronic hyperglycemia damages nerves and the small vessels that supply them. Unilateral weakness with difficulty dorsiflexing (possible foot drop) suggests a mononeuropathy, such as of the peroneal nerve. Because neuropathy usually appears after years of high glucose, it suggests she has had undiagnosed diabetes for some time. |
| Obesity and recent weight gain | Strongly associated with insulin resistance and type 2 diabetes. |
| Elevated cholesterol (225 mg/dL) | Insulin resistance is associated with dyslipidemia and raises cardiovascular risk. |
Signs to assess that are not described: polyphagia (excessive hunger), blurred vision, fatigue, slow-healing wounds, skin infections, acanthosis nigricans (dark, velvety skin at the neck or armpits, a sign of insulin resistance), hypertension, and kidney involvement (albumin in the urine).
Diagnostic work-up: HbA1c (6.5% or higher is diagnostic), repeat fasting plasma glucose, a random glucose (200 mg/dL or higher with symptoms is diagnostic), lipid panel, kidney function and urine albumin-to-creatinine ratio, liver enzymes and TSH. Her foot needs a full neuropathy assessment: monofilament and vibration testing, reflexes, a foot exam, and B12 to rule out other causes. Nerve conduction studies or referral are warranted given the focal weakness (ADA, 2025).
2. Expected glycemia if C.B. develops right lower lobe bacterial pneumonia
Her blood glucose would be expected to rise, often significantly (stress hyperglycemia). Acute infection worsens glucose control in people with diabetes through several mechanisms:
- Counter-regulatory stress hormones: infection activates the stress response, increasing cortisol, epinephrine, glucagon and growth hormone. These hormones stimulate gluconeogenesis and glycogenolysis in the liver and reduce glucose uptake by muscle, which raises blood glucose.
- Inflammatory cytokines: pneumonia releases cytokines such as IL-1, IL-6 and TNF-α, which interfere with insulin signaling and worsen insulin resistance.
- Existing insulin resistance and limited reserve: as a person with untreated type 2 diabetes, C.B. already has insulin resistance and impaired insulin secretion, so she cannot increase insulin output enough to offset the stress response.
- Reduced activity and dehydration: bed rest reduces glucose use by muscles, and fever, rapid breathing and osmotic diuresis cause dehydration, which concentrates blood glucose further.
- Medications: if corticosteroids are given, they raise glucose further.
Risks: severe hyperglycemia can progress to hyperosmolar hyperglycemic state (HHS), the typical hyperglycemic emergency in type 2 diabetes, marked by very high glucose (often above 600 mg/dL), dehydration and confusion. Diabetic ketoacidosis is less common in type 2 diabetes but can occur with severe infection. Hyperglycemia also impairs neutrophil and macrophage function, which slows recovery from pneumonia and creates a vicious cycle of infection and worsening glucose control.
Management: frequent glucose monitoring; insulin therapy in hospital, typically targeting 140–180 mg/dL for most hospitalized patients; hydration; and treatment of the infection (ADA, 2025). As the infection resolves, glucose levels usually improve. If she eats very little, hypoglycemia is also possible, so insulin doses must be adjusted to her intake.
3. Best initial therapy for C.B.
Non-pharmacologic therapy
- Diabetes self-management education and support (DSMES): refer at diagnosis to learn glucose monitoring, medications, recognition of hypo- and hyperglycemia, sick-day rules and foot care. Use culturally respectful approaches, and partner with community programs such as the Indian Health Service Special Diabetes Program for Indians.
- Medical nutrition therapy with a registered dietitian: a culturally tailored eating plan that values traditional foods. It should reduce refined carbohydrates, sugary drinks and saturated fat, increase vegetables, fiber and lean proteins, and use portion guidance such as the plate method.
- Weight management: losing at least 5–7% of body weight improves glucose control and cardiovascular risk, and greater loss (10–15% or more) can lead to remission in some people (ADA, 2025).
- Physical activity: build gradually toward 150 minutes a week of moderate activity, plus resistance training 2–3 times a week, and reduce sitting time. Exercise must be adapted to her foot weakness. Refer to physical therapy and consider an ankle-foot orthosis for safety and fall prevention.
- Foot care: daily foot inspection, proper footwear, and podiatry referral because of her neuropathy.
- Screening and prevention: dilated eye exam, kidney screening, blood pressure control, vaccinations (influenza, pneumococcal, hepatitis B, COVID-19), dental care, and smoking cessation if applicable.
- Address cost and access: as a tribal member, she may be eligible for medications and services through the Indian Health Service or tribal health programs at little or no cost. Connect her with a case manager to remove the cost barrier that prevented follow-up three years ago.
Pharmacologic therapy
Treatment choice depends on her confirmed HbA1c, kidney function, cardiovascular and kidney risk, weight goals, cost and preference (ADA, 2025):
- Metformin remains a common, affordable first-line agent for type 2 diabetes if kidney function allows (eGFR 30 or above). It lowers hepatic glucose production, improves insulin sensitivity, rarely causes hypoglycemia and is weight-neutral. Start low (500 mg daily with meals) and titrate, or use the extended-release form to reduce GI side effects. Monitor B12 long term, because deficiency can worsen neuropathy.
- A GLP-1 receptor agonist (such as semaglutide or dulaglutide) or a dual GIP/GLP-1 receptor agonist (tirzepatide) should be strongly considered because of her obesity and weight gain. These agents provide substantial glucose lowering and weight loss, and some have proven cardiovascular benefit. They can be combined with metformin.
- SGLT2 inhibitors (such as empagliflozin) offer heart and kidney protection, but they increase the risk of genital fungal infections. Given C.B.’s recurrent “female infections,” they should be used cautiously, if at all, with close monitoring.
- Insulin should be considered if HbA1c is very high (above 10%), glucose is 300 mg/dL or higher, or there are signs of catabolism such as weight loss or ketosis.
- Statin therapy: adults aged 40–75 with diabetes should receive at least a moderate-intensity statin to reduce cardiovascular risk. Her cholesterol of 225 mg/dL and multiple risk factors may justify high-intensity therapy.
- Neuropathy management: the best way to slow progression is good glucose control. If neuropathic pain develops, options include pregabalin, duloxetine or gabapentin.
Summary of the best initial plan: confirm the diagnosis with HbA1c; start metformin with lifestyle therapy (DSMES, culturally tailored nutrition, gradual activity and weight loss); consider adding a GLP-1 receptor agonist or tirzepatide for weight and cardiovascular benefit; start a statin; evaluate and protect her foot; and remove cost barriers through IHS and tribal resources.
Conclusion
American Indian and Alaska Native people have the highest prevalence of diabetes in the United States, and C.B. has many classic risk factors and manifestations of undiagnosed type 2 diabetes: a previously elevated fasting glucose, polydipsia, polyuria and nocturia, recurrent yeast infections, obesity with rapid weight gain, dyslipidemia, and possible diabetic neuropathy affecting her left foot. If she developed pneumonia, stress hormones and inflammation would cause marked hyperglycemia, with a risk of HHS. The best initial approach combines culturally tailored self-management education, nutrition, activity and weight loss with metformin, possibly a GLP-1 receptor agonist or tirzepatide, and a statin, while addressing the cost and access barriers that delayed her care.
Note: Prevalence figures and treatment recommendations are summarized from the CDC and the ADA Standards of Care in Diabetes. Check the most recent editions, which are updated every year. This case analysis is for education only.
References
American Diabetes Association Professional Practice Committee. (2025). Standards of care in diabetes—2025. Diabetes Care, 48(Suppl. 1). https://diabetesjournals.org/care/issue/48/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/php/data-research/
Rogers, J. L. (Ed.). (2023). McCance & Huether’s pathophysiology: The biologic basis for disease in adults and children (9th ed.). Elsevier.
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