Types I And Ii Dm

Front 1

Approximately how many cases of the two types of DM occur yearly in the US?

Back 1

Approximately 150,000 type I and 1.3 million type II.

Front 2

Which is the prevalence of diabetes (both types)?

Back 2

10% of diagnosed diabetics are type 1. 90% are type 2.

Front 3

What is the “nutritional status at time of disease onset” for each type of diabetes?

Back 3

Type 1 usually happens to people who are undernourished, but type 2 is typically found in obese persons.

Front 4

Which type of diabetes has the stronger genetic predisposition?

Back 4

Type 1 is only moderate, but type 2 is very strongly linked with genetic predisposition.

Front 5

What is the frequency for ketosis in each type of diabetes?

Back 5

It is common in type 1, but rare in type 2.

Front 6

What are the “acute complications” of diabetes?

Back 6

For type 1, acute complications include ketoacidosis. Type 2 tends to be hyperosmolar state.

Front 7

What is the response to “oral hypoglycemic drugs” for each type of DM?

Back 7

Type 1 diabetics tend to be unresponsive. Type 2 diabetics tend to be responsive.

Front 8

What are the four most common types of “oral hypoglycemic drugs”?

Back 8

Sulfonylureas
Biguanides (Metformin)
Thiazolidinediones
Alpha-glucosidase inhibitors

Front 9

How do sulfonylureas work?

Back 9

The net effect is increased responsiveness of ß-cells (insulin secreting cells located in the pancreas) to both glucose and non-glucose secretagogues, resulting in more insulin being released at all blood glucose concentrations.

Front 10

How does metformin work?

Back 10

It is effective only in the presence of insulin but, in contrast to sulfonylureas, it does not directly stimulate insulin secretion. Its major effect is to increase insulin action. How metformin increases insulin action is not known but it is known to affect many tissues. One important effect appears to be suppression of glucose output from the liver. Metformin given in combination with a sulfonylurea lowers blood glucose concentrations more than either drug alone.

Front 11

How do thiazolidinediones work?

Back 11

Reverse insulin resistance by acting on muscle, fat and to a lesser extent liver to increase glucose utilization and diminish glucose production. The mechanism by which the thiazolidinediones increase insulin action is not well understood but they may be acting by redistributing fat from the visceral compartment to the subcutaneous compartment. We know that visceral fat is associated with insulin resistance.

Front 12

How do Alpha-glucosidase inhibitors work?

Back 12

They inhibit the upper gastrointestinal enzymes that converts dietary starch and other complex carbohydrates into simple sugars which can be absorbed. The result is to slow the absorption of glucose after meals.

Front 13

What is the “chemical” type of drug such as metformin or glucophage XR?

Back 13

Biguanides

Front 14

How do these two (metformin and glucophage XR) differ?

Back 14

They differ in price: one costs $11.82 (metformin), and the other costs $8.88. Others in this category cost $118 and $267.

Front 15

What is the “chemical” type of drug such as Glucotrol?

Back 15

Sulfonylureas

Front 16

What is the “chemical” type for Avandia?

Back 16

Thiazolidinediones

Front 17

How does the cost compare for these three drugs (metformin, glucotrol, and avandia)?

Back 17

Metformin and Glucotrol are about the same price as one another, but they each cost a fraction of what Avandia does ($227).

Front 18

According to LIR, slide one, how do treatment options vary for the two types of DM?

Back 18

Type 1 always requires insulin. Type 2 may be treated with diet, exercise, oral hypoglycemic drugs, and reduction of risk factors, such as smoking, high blood pressure, dyslipidemia. Insulin may or may not be necessary.

Front 19

Approximately, how many years from an initial exposure of a virus or toxin does it take to see clinical threshold of type I DM?

Back 19

7-8 years

Front 20

Is the onset slow or sudden?

Back 20

Slow

Front 21

In type I DM, what three general serum metabolites are elevated?

Back 21

Ketone bodies, hyperglucosemia, and increase chylomicrons

Front 22

What two general treatment options are available for Type I DM?

Back 22

Standard vs. intensive

Front 23

What is the basic difference between standard and intensive treatment?

Back 23

Standard treatment consists of 1-2 daily injections of insulin. Intensive monitors more frequently with 3+ injections per day.

Front 24

What is the most common complication of insulin therapy?

Back 24

Hypoglycemia due to excess insulin because appropriate dosage is hard to achieve.

Front 25

In which type of treatment does this occur more often?

Back 25

Intensive treatment

Front 26

In Type I DM, how many years post development does the role for epinephrine secretion to prevent severe hypoglycemia become prevalent?

Back 26

4 years

Front 27

What is meant by “hypoglycemia unawareness”?

Back 27

Disease progression causes diabetic autonomic neuropathy and impaired ability to secrete epinephrine in response to hypoglycemia. Combined deficiency of glucagon and epinephrine secretion creates this.

Front 28

In long term Type I DM patients, what is a common factor that promotes hypoglycemia?

Back 28

Exercise

Front 29

Which two patient populations are not appropriate for “tight control” (of hypoglycemia)?

Back 29

Children and elderly

Front 30

Which ethnic groups have the highest incidence of DM II?

Back 30

Latinos, Native Americans, African Americans, and Asian Americans

Front 31

What are the most common diagnostic symptoms of DM II?

Back 31

Polyuria, polydipsia, polyphagia.
Insulin resistance and dysfunctional beta cells

Front 32

What level of blood glucose is typically used as a diagnostic value for DM II?

Back 32

126 mg/dl

Front 33

How is Type 2 diabetes mellitus characterized?

Back 33

Hyperglycemia, insulin resistance, and relative impairment in insulin secretion

Front 34

Approximately how many times more insulin is needed in insulin-resistant obese individuals?

Back 34

3x more

Front 35

Does the obese individual have low/hi spikes of blood glucose?

Back 35

Yes

Front 36

How many years are required typically before diagnosis of DM II?

Back 36

10 years

Front 37

Approximately how many years elapse before beta cell dysfunction occurs with worsening hyperglycemia?

Back 37

20 years after diagnosis

Front 38

What are the micro- and macro- vascular complications for type 2 diabetes?

Back 38

Microvascular: retinopathy, neuropathy, nephropathy
Macrovascular: cardiovascular disease, stroke

Front 39

What is the major difference between blood metabolites between type 2 and type 1 DM?

Back 39

Fewer ketone bodies are produced in type 2; since some insulin is available, ketogenesis does not usually develop.

Front 40

What level of HbA1c is the goal of intensive therapy?

Back 40

7% or lower

Front 41

How does the benefit of exercise change with BMI?

Back 41

Benefit of exercise increases with increased BMI

Front 42

What is the role of fluoride oxalate in blood draw tubes?

Back 42

It prevents the concentration of glucose in the sample from decreasing because of glycolytic action of RBCs and WBCs. (Anticoagulant according to Wiki)

Front 43

What is the color of fluoride oxalate's cap?

Back 43

Grey

Front 44

What are colors for the tubes that contains EDTA?

Back 44

Purple/Lavendar

Front 45

What is EDTA’s role?

Back 45

It is an anticoagulant

Front 46

What is the color of the tube that contains heparin?

Back 46

Green

Front 47

What is heparin’s role?

Back 47

Anticoagulant– plasma determination of clinical chemistry (urea and electrolyte)

Front 48

What is the fasting plasma glucose level range in mM?

Back 48

2.5-6 mmol/L

Front 49

What is “Impaired fasting glycemia” (IFG)?

Back 49

6.1-6.9 mmol/L; pre-diabetes, carries cardiovascular risk

Front 50

What is “impaired glucose tolerance” (IGT)?

Back 50

The response to a standard oral glucose load is determined by measuring plasma glucose 2hrs post oral glucose; 7.8-11.0 mmol/L

Front 51

What is DKA?

Back 51

Diabetic ketoacidosis (result of elevated blood glucose because of lack of insulin)

Front 52

What is HONK?

Back 52

Hyperosmolar Non Ketotic state
Glucose levels rise very high which causes glycosuria and yields osmotic diuresis, hypovolemia, hyperosmolality, coma, and death.

Front 53

Which is common (between DKA and HONK) in Type II DM?

Back 53

HONK

Front 54

What are the common causes for hypoglycemia?

Back 54

1. Drugs: insulin, sulfonylureas, alcohol; 2. organ failure: LAP: liver, adrenal, pituitary; 3. reactive insulinoma/other tumor

Front 55

What are the common management methods for hypoglycemia?

Back 55

1. Give glucose (food/drink with sugar), 2. Hypostop gel, 3. Glucagon im, 4. Glucose IV

Front 56

What is im?

Back 56

Intramuscluar

Front 57

What is iv?

Back 57

Intravenous

Front 58

Relative or absolute lack of insulin in humans would result in which one of the following reactions in the liver?

Back 58

Increased formation of 3-hydroxybutyrate

Front 59

Which one of the following is most often found in untreated patients with type 1 and type 2 diabetes?

Back 59

Hyperglycemia

Front 60

An obese individual with type 2 diabetes:

Back 60

usually shows significant improvement in glucose tolerance if body weight is reduced to normal.

Front 61

An individual with insulin resistance and normal beta-cell function:

Back 61

usually shows elevated fasting insulin levels.

Front 62

Explain why drugs that inhibit alpha-glucosidase activity of the intestinal saccharidases aid in glycemic control in patients with diabetes.

Back 62

Alpha-glucosidase inhibitors prevent glucose production from those products of carbohydrate digestion in which glucose is attached through an alpha-glycosidic linkage, thus reducing the postprandial rise in blood glucose. Note that the digestion of lactose is unaffected because it has a beta-linkage.