Violet Figiel
Case Study, Porth
Chapter 42, Diabetes Mellitus and the Metabolic Syndrome
Compare the actions of insulin and glucagons, including their action on glucose, fats,
and protein. How do catecholamines and GH affect blood glucose? How about
glucocorticoids?
Glucagon: causes cells to release stored food into the blood; increase in glucagon
causes an increase in glucose; increase in glucagon decreases fat and protein levels. Insulin:
allows cells to take up glucose from the blood; increase in insulin causes a decrease in
glucose; increase in insulin increases fat and protein levels.
Catecholamines: Help to maintain blood glucose levels during periods of stress.
Growth hormone: Increases protein synthesis in all cells of the body, mobilizes fatty acids
from adipose tissue, and antagonizes the effects of insulin. Glucocorticoids: stimulate
gluconeogenesis by the liver; moderately decrease tissue use of glucose. Prolonged elevation
of glucocorticoid hormones can lead to hyperglycemia
John P. is a 49-year-old male with a history of morbid obesity. He had blood work done
recently, and a random glucose test was >200. Additionally, he had glucose present on
urinalysis. He complains that he has been feeling very thirsty lately and has had to
urinate frequently.
What is John P. likely presenting with?
John P. is presenting with Diabetes Mellitus: Type 2.
Contrast Type 1 and Type 2 diabetes. Which is more common?
Type 2 is more common.
Type 1: pancreatic beta cell destruction predominantly by an autoimmune
processNo longer produce insulin; usually occurs in children, but can occur at any age;
lack of insulin in Type 1 patients means that they are particularly prone to the development of
ketoacidosis. Signs and symptoms arise suddenly.
Type 2: a combination of beta cell dysfunction and insulin resistance; usually adult
onset and associated with obesity, sedentary lifestyle, and poor diet. Develops more
insidiously than Type 1
Is adult onset ALWAYS Type 2?
No, adult onset could also be Type 1 and is referred to as latent autoimmune diabetes
in adults. This is the slowly progressive form that may actually account for up to 10% of
adults who are currently classified as having Type 2 diabetes.
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Describe the pathophysiology of Type 2 diabetes in terms of metabolic abnormalities.
Impaired insulin secretion, carbohydrate absorption, increased basal hepatic glucose
production, decreased insulin-stimulated glucose uptake
Describe the three polys of diabetes. Which one does John have? What causes these?
Polyuria: Excessive urination; when glucose levels are elevated, the amount of glucose
filtered by the glomeruli exceeds the amount that can be reabsorbed by the renal tubules
which then results in glycosuria
Polydipsia: Excessive thirst John P. has this one; as blood glucose levels rise, water is
pulled out of the body cells, then causes intracellular dehydration resulting in thirst
Polyphagia: Excessive hunger- not usually present in Type 2 patients, however in Type 1, it
probably results from cellular starvation because of the depletion of cellular stores of carbs,
fats, and proteins
Describe the meaning of glycosylated hemoglobin, or Hgb A1C. What would be the
goal for this value for John with treatment?
Hgb A1C is a measure of a patient’s blood glucose levels for 120 days. The physician
may order this to see if the patient’s levels are under control. Glucose entry into RBCs is not
insulin dependent, so the rate at which glucose becomes attached to the Hgb molecule
depends on blood glucose levels. The goal for John with treatment would be <7 and as close
to normal as possible.
What kind of diet teaching does John need? What should he be told about exercise?
Nutrition: no longer a specific diabetic or ADA diet but rather a dietary prescription
based on nutrition assessment and treatment goals. CHO counting uses product label
information that is easily available to people with diabetes. Total grams of CHO are counted.
AHA: less than 7% of daily calories should be obtained from saturated fat and dietary
cholesterol be limited to 200 mg or less. Lower protein if people have nephropathy.
Exercise in Type 2 diabetics: decrease in body fat, better weight control, and
improvement in insulin sensitivity. Integral part of therapeutic regiment for every person with
diabetes. Regular program better for CV conditioning and maintaining a muscle-fat ratio that
enhances effectiveness of insulin. However, with exercise will have an increased risk of
hypoglycemia so may need to alter diet around exercise.
Would John be more at risk for diabetic ketoacidosis or hyperosmolar, hyperglycaemic
state? Why?
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John would be more at risk for hyperosmolar, hyperglycaemic state because this is the
one more often present in Type 2 diabetic patients and happens more insidiously. His
symptoms are similar to those that would appear with this hyperglycemic complication:
excessive thirst and polyuria.
Briefly describe the actions of the following oral anti-diabetic agents:
1. Sulfonylureas- reduce blood glucose by stimulating release of insulin from beta
cells in the pancreas, however in order for this to occur, some residual beta cell
function must still remain
2. Repaglinide- require presence of insulin for their action; close the ATP-dependent
potassium channel in the beta cells rapidly absorbed and are taken shortly
before meals
3. Metformin (Biguanides)-inhibits glucose production and increases the sensitivity
of peripheral tissues to the actions of insulin secretion
4. Alpha-glucosidase inhibitors- inhibitors of alpha glucosidase, an enzyme that
breaks down complex carbs by doing this, it delays absorption of carbs in gut
and blunts the postprandial increase in plasma glucose and insulin levels
5. Thiazolidinediones- improve glycemic control by increases insulin sensitivity in
the insulin-responsive tissues and allowing the tissues to respond to endogenous
insulin more efficiently without increased output from already dysfunctional beta
cells
6. Incretins- stimulate insulin secretion by the beta cell
John gains only partial control over his diabetes in the years to come. Eventually, he
requires insulin therapy. Why might this be so?
Glycemic control cannot be achieved many times, so insulin may eventually be
needed. Insulin secretion from beta cells may decrease so far that the anti-diabetic agents just
aren’t producing enough effect anymore; insulin resistance may worsen even more too.
Describe short acting vs intermediate vs long-acting insulin. What is meant by intensive
insulin treatment?
Short-acting: usually given with meals because it has quick response and lasts a good
couple hours till it is time for the next meal.
Intermediate: NPH: onset in 2-4h, peak 4-10hr, lasts 10-24 hrs.
Long-acting: Levemir, lantus; onset 2-4 hrs, no peak, duration lantus 20-24, levemir
6-23.
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Intensive insulin treatment: multiple daily injections. Basal is met by intermediate or
long-acting insulin administered once or twice daily with boluses of rapid or short given
before meals.
Describe the macrovascular and microvascular changes John is at risk for. Is there any
special diagnostic screening John should have on a regular basis?
Microvascular: Basement membranes of blood vessels for example, Nephropathy-first
test for this is one for microalbumineria, Retinopathy, and Neuropathy.
Macrovascular: increased risk of atherosclerosis (CAD, CVD, PVD)
John should have the A/C ratio screening done that is testing for microalbuminuria
because that is one of the first manifestations of diabetic nephropathy.
Juan is a 44-year-old who works in a warehouse. He is 5’8” tall, weighs 185 pounds, and
has a waist circumference of 41”. At his last visit to the health clinic, Juan’s blood
pressure was 140/60 mm Hg. Shortly after having a series of blood tests, his physician
called him in to talk about the results. Juan had a fasting plasma glucose level of 107
mg/dL, an HDL level of 37 mg/dL, and a serum triglyceride level of 210 mg/dL.
(Learning Objectives 4, 6, 7, 8)
1.
What condition is Juan likely presenting with? Outline the wide spectrum of
physiologic abnormalities that occur with this disorder.
Juan is likely presenting with Syndrome X. The wide spectrum of physiologic
abnormalities that occur with this disorder are obesity, high levels of plasma
triglycerides and low levels of high-density lipoproteins, hypertension,
systemic inflammation, abnormal fibrinolysis, and macrovascular disease. And
as Juan’s appearance, this disorder is characterized with having a bigger waist
circumference indicating central obesity which has been shown to correlate
well with insulin resistance
2.
What is the significance of Juan’s waist diameter? Discuss how truncal obesity is
hypothesized to increase insulin resistance in the body.
The significance of Juan’s waist diameter is that it indicates central obesity
because he is wearing a size 41 pant, but yet is a pretty short man. And, a
>40inch waist circumference is a diagnosis of metabolic syndrome. Increased
insulin resistance has been attributed to the increased visceral fat that can be
detected on computed tomography scan and other imaging modalities. Waist
circumference and waist-hip ratio, both signs of central obesity, have been
shown to correlate well with insulin resistance. The increase in FFAs that
occurs in obese individuals (especially visceral obesity) with a genetic
predisposition to type 2 diabetes may eventually lead to beta cell dysfunction,
increased insulin resistance, and greater hepatic glucose production.