In: Biology
Case Study: Type I Diabetes Mellitus (DM1)
David Mandel was diagnosed with type 1 (insulin-dependent) diabetes mellitus when he was 12 years old. He was in middle school at that time. He was a very good student and had many friends. At a sleepover party, the unimaginable happened – David wet his sleeping bag! He was embarrassed and might not have told his parents except that he was worried about other symptoms he was having. He was constantly thirsty and was urinating every half hour or so. Furthermore, despite a voracious appetite, he seemed to be losing weight – all of his pants had become loose in the waist. His friends remarked that his breath smelled funny. David’s parents panicked because they knew that these were classic symptoms of diabetes mellitus. They took David to see his pediatrician who performed a physical examination and ordered laboratory tests.
RESULTS:
Height 5ft 3in
Weight 100 lb (previous visit 2 mo earlier he was 108 lbs)
Blood pressure 90/55 (supine); 75/45 (standing)
Fasting plasma glucose 320 mg.dL (normal: 70-110 mg.dL)
Plasma ketones 1+ (normal: none)
Urinary glucose 4+ (normal: none)
Urinary ketones 2+ (normal: none)
The findings were consistent with a diagnosis of type 1 (insulin-dependent) diabetes mellitus. David immediately started taking injectable insulin and learned how to monitor his blood glucose level with a finger stick. His mother modified his diet to increase protein intake and decrease carbohydrates. He continued to excel in high school and is currently in the pre-medical program with the goal of a career in pediatric endocrinology. He has periodic checkups with his endocrinologist, who emphasizes the importance of meticulous care of the feet, checks for cataract, and monitors his renal function.
1. How did insulin deficiency lead to an increase in David’s blood glucose concentration?
2. How did insulin deficiency lead to elevated ketones in his blood and urine?
3. Why did David have glucose in his urine (glucosuria)?
4. Why did David have increased urine production (polyuria)?
5. Why was he drinking so much water (polydipsia)?
6. Why was David’s blood pressure lower than normal?
7. Why did his blood pressure decrease further when he stood up?
8. Why can’t David take his insulin orally (instead of by subcutaneous injection)?
9. Why did his endocrinologist monitor for cataract?
10. What is the major nephrologic complication of type1 diabetes mellitus?
1. As David has Insulin Dependent diabetes mellitus, that means he has insulin deficiency to regulate the glucose in his body, thus the glucose concentration in David increased.
2. Our body constantly produces small amount of ketone bodies that can make 22 ATPs. But low insulin leads to increased in lipolysis futher there is increase in plasma free fatty acids and that leads to formation of ketone bodies.
3. Glucosuria is common symptom of patients with diabetes, as there is increse in glucose levels, sugars pills out in urine.
4. In David who has type 1 diabetes, excess glucose ends up in the urine, it pulls more water in efforts to remove glucose from body and results in more urine.
5. As he is frequently urinating, he requires more fluid in body.
6. He might have low blood pressure because of dehydration. Poyuria can cause reduction in blood volume resulting in low blood pressure.
7. It is postural hypotension ; when a person stands in more vertical position from sitting or lying.
8. Oral insulin reaches bloodstream via digestive system. The acids in your stomach break down oral insulin before it can get to your liver. That means it’s not effective via oral route.
9. Diabetes can be primary cause f blidness. Increased blood sugar can lead to blurry vision, cataract or retinopathy thus its important to visit optholmologist regularly.
10. Diabetic nephropathy is the most common complication of diabetes.