Anatomy And Physiology 2 Lab Case Study Assignment

Lanatomy And Physiology 2 Lab Namecase Study Assignment You Are

You are a medical student working your way through college and are assigned to a hospital given background information on a patient. You were provided the chief complaint and long-term history of the patient outlined below. You are asked by the nurse in charge to read the case, investigate the topic (Diabetes mellitus and chronic renal failure), and complete a written report in MLA format including references addressing each of the questions listed below. Use the provided MLA guidance link for formatting. The report should be about two to three pages typed.

The purpose of this assignment is to contextualize what you are learning in your course (lecture and lab) through real-life situations, focusing on issues related to the urinary system and its diseases.

Paper For Above instruction

Rylee Langdon, a 7-year-old girl, presents with a chief complaint of unexpected weight loss and constant thirst, along with frequent urination. Over three days, she experienced nausea, vomiting, headache, and increased thirst. Her parents noted that she gets up multiple times nightly to urinate, drinks large amounts of water, and has been eating more yet losing weight. Physical examination revealed rapid, deep breathing and a fruity odor on her breath. Lab tests showed her blood glucose level was 454 mg/dL, urine glucose was positive, and urine ketones were positive. Her urine sample was clear with light yellow-amber color, pH of 6, and specific gravity of 1.008.

Initial treatments involved insulin therapy and diabetic management education, including blood-glucose monitoring, insulin injections, and dietary regulation. Rylee’s blood glucose levels showed improvement post-treatment, with fasting levels at 95 mg/dL and most daily readings in the low to mid-100s, except post-supper readings in the upper 200s. Her HbA1c later increased to 9.5%, indicating poor long-term glucose control. Over the years, her diabetes was characterized as "brittle" with wide fluctuations, increasing the risk for complications.

By her mid-forties, Rylee developed early signs of diabetic nephropathy, featuring persistent proteinuria, hypertension, and decreased renal function. At age 55, she reported fatigue, nausea, edema, and shortness of breath. Tests revealed elevated BUN at 56 mg/dL, decreased urinary output, and advancing kidney failure symptoms. She opted for hemodialysis, which reduced her BUN to 35 mg/dL, but chronic renal failure posed ongoing challenges, including calcium and phosphate imbalances.

Questions Addressed in the Report

1. Summary of Patient's Complaint and History

Rylee’s initial complaints of excessive thirst, urination, weight loss, and signs of diabetic ketoacidosis indicated poorly controlled diabetes mellitus. Her long-term history of fluctuating blood sugar levels and development of nephropathy reflect disease progression and complications of chronic hyperglycemia.

2. Explanation of Lab Results

The blood glucose level of 454 mg/dL significantly exceeds the normal range of 50-170 mg/dL, confirming hyperglycemia. The positive urine glucose indicates that blood glucose exceeded renal reabsorption capacity. Urine ketones being positive point to ketosis from fat breakdown during insulin deficiency. The specific gravity of 1.008 suggests dilute urine, common in uncontrolled diabetes, and the pH of 6 indicates a slightly acidic urine due to ketoacid production.

3. Physiological Purpose of Unusual Breathing

Rapid, deep breathing (Kussmaul respiration) is a compensatory response to metabolic acidosis caused by ketoacidosis. By increasing ventilation, the body attempts to exhale excess carbon dioxide, thereby raising blood pH toward normal.

4. Reasons for Fruity Odor of Breath

The fruity odor results from acetone, a type of ketone body produced during excessive fat catabolism in ketoacidosis. Elevated ketone levels are characteristic of untreated or poorly managed diabetes and serve as a hallmark of diabetic ketoacidosis.

5. Why Rylee Urinates Frequently

High blood glucose levels surpass the renal threshold (~180 mg/dL), leading to glucose excretion in urine (glycosuria). This osmotic diuresis causes increased urine volume and frequent urination. The kidneys fail to reabsorb the excess glucose, resulting in dehydration and electrolyte imbalance.

6. Relation Between Rylee’s Condition and Starvation; Hormonal Roles

In diabetes, lack of insulin prevents cellular uptake of glucose, resulting in cellular starvation despite high blood glucose. Consequently, the body perceives a fasting state, triggering glucagon secretion, leading to gluconeogenesis and lipolysis, which produce ketone bodies, similar to starvation. Insulin promotes glucose uptake and storage as glycogen or fat, while glucagon breaks down glycogen and fat stores to maintain blood glucose levels. Artificial insulin administration helps prevent this starvation mimicry by enabling glucose utilization, but improper dosing can cause hypoglycemia or hyperglycemia. Carrying candy and glucagon ensures immediate treatment for hypoglycemia caused by insulin overdose. Timing and dosage of insulin are crucial to maintain blood sugar stability.

7. Differences Between NPH and Regular Insulin

NPH insulin is an intermediate-acting insulin with a longer duration, providing basal insulin coverage, whereas regular insulin is short-acting, effective within 30 minutes for mealtime control. NPH has a cloudy appearance and requires gentle mixing before injection. Using both allows for flexible insulin regimens, balancing basal and bolus needs. Drawbacks include variability in absorption and risk of hypoglycemia for NPH and inconvenience of multiple injections.

8. Adjusting Rylee’s Insulin Dosing

To reduce her pre-supper glucose levels, her insulin regimen could be adjusted by increasing the insulin dose before dinner or incorporating rapid-acting insulin at meals. Monitoring postprandial glucose responses will guide precise adjustments to prevent hyperglycemia while avoiding hypoglycemia.

9. Explanation of HbA1c and Its Significance

Hemoglobin A1c (HbA1c) measures the percentage of glycated hemoglobin, reflecting average blood glucose over approximately three months. Normal ranges are typically 4-5.6%. Elevated levels (>7%) indicate poor long-term glycemic control. Unlike a single blood sugar measurement, HbA1c provides an integrated view, guiding therapy adjustments and predicting complication risks. Rylee’s HbA1c of 9.5% suggests inadequate glucose management and increased risk for complications.

10. Long-term Complications and Precautions

Persistent hyperglycemia can lead to microvascular and macrovascular complications, including retinopathy, neuropathy, nephropathy, and cardiovascular disease. Strict glycemic control and regular screenings are vital. The importance of not walking barefoot is to prevent foot injuries and infections, which can be severe due to peripheral neuropathy and poor healing in diabetics.

11. Phosphate and Calcium Balance in Diabetes

Chronic hyperglycemia and nephropathy disrupt phosphate excretion, leading to hyperphosphatemia. Elevated phosphate levels can decrease serum calcium via precipitation and secondary hyperparathyroidism. Excess phosphate may cause soft tissue calcification, including in blood vessels, exacerbating cardiovascular risks. The endocrine response attempts to regulate calcium levels through parathyroid hormone secretion, influencing bone resorption and calcium reabsorption.

12. Impact on Skeletal System and Osteodystrophy

High phosphate and dysregulated calcium balance impair bone remodeling, resulting in osteodystrophy, a condition marked by bone deformities and fragility. Bone diseases such as osteomalacia or osteoporosis are common in advanced renal failure, illustrating the broader systemic effects of diabetic nephropathy on the skeletal system.

References

• American Diabetes Association. (2022). Standards of Medical Care in Diabetes—2022. Diabetes Care, 45(Suppl 1), S1–S232.
• Brown, A., & Smith, J. (2020). Renal Failure and Diabetes: Pathophysiology and Management. Journal of Nephrology, 33(4), 567-578.
• James, P. A., et al. (2018). Diagnosis and Management of Diabetes Mellitus. The New England Journal of Medicine, 378(2), 180-192.
• Kumar, P., & Clark, M. (2019). Clinical Medicine. Elsevier.
• Malik, R. A., et al. (2019). Diabetic Nephropathy: Pathogenesis and Treatment. Advances in Chronic Kidney Disease, 26(8), 579-584.
• National Kidney Foundation. (2021). KDOQI Clinical Practice Guidelines and Clinical Practice Recommendations for Diabetes and CKD: 2020 Update. American Journal of Kidney Diseases, 76(3), S1–S107.
• Polk, B. M. & Adams, J. (2019). Endocrine Regulation of Blood Glucose. Endocrinology Reviews, 40(2), 95-125.
• Williams, G. H. (2018). Medical Biochemistry. Churchill Livingstone.
• World Health Organization. (2019). Diabetes Fact Sheet. WHO.
• Zhao, H., et al. (2020). Chronic Kidney Disease in Diabetes. Journal of Diabetes Research, 2020, 1-12.