Lecture 5 - Insulin & Oral Hypoglycemics

Question 1

What is the MOA of Insulin?

What receptors, what does it trigger, how does it affect metabolism

Answer 1

• at tyrosine kinase cell membrane receptors
• leads to phosphorylation and activation of GTP binding proteins
• cascade events stimulates transcription factors to control gene expression
• metabolic actions increase glucose transport and gylcogen synthetase

Question 2

What is Type I Diabetes and how is it treated?

Answer 2

• insulin dependent diabetes mellitus
• No beta cell production = lack of insulin
• treated with insulin, usually develops in childhood

Question 3

What is Type II Diabetes and how is it treated?

Answer 3

• non-insulin dependent diabetes mellitus

- treated with oral agents or insulin and may reduce or eliminate need for drugs

Question 4

What is duration of regular insulin (crystalline zinc or lispro), isophane insulin suspension (NPH) and insuline glargine (Lantus)?

(Short, intermediate, long acting)

Answer 4

• regular: short acting 5-7 hours
• Isophane: intermediate 18-24 hours
• Insulin glargine: long acting 36 hours

Question 5

What are the CV and CNS symptoms of hypoglycemia or insulin shock (blood sugar falling)

(Also, what is the result if not treated)

Answer 5

• CV effects: tachycardia, pallor, sweating
• CNS effects: tremor, nervousness, unrest, convulsions
• coma and death if not treated

Question 6

Which type of insulin prep is least likely to have allergic hypersensitivity?

A. Human insulin
B. Regular insulin
C. Isophane insulin suspension
D. Insulin Glargine

Answer 6

A. Human insulin

Question 7

Oral agents for control of blood glucose is only effective for what type of diabetes?

A. Type I
B. Type II

Answer 7

B. Type II

patient must have functional beta cells

Question 8

Which of the following is true about Type II Diabetes?

A. Due to decreased sensitivity of insulin receptors (either decreased receptors of effector tissue or decreased efficiency of signal transduction)
B. Type II is controlled with diet and body weight reduction.
C. Sulfonylyreas, biguanides, glucosides inhibitors and glitazones are used to treat Type II.
D. All of the above.

Answer 8

D. All of the above.

A. Due to decreased sensitivity of insulin receptors (either decreased receptors of effector tissue or decreased efficiency of signal transduction)
B. Type II is controlled with diet and body weight reduction.
C. Sulfonylyreas, biguanides, glucosides inhibitors and glitazones are used to treat Type II.

Question 9

What is the MOA for sulfonylureas?

Tolbutamide, Glipizide, Glyburide, Glimepiride

Answer 9

• Sulfonylureas bind to ATP-dependant K+ channel. Leads to decrease in K+ effluc and Ca2+ influx.
• Gives greater insulin release upon stimulation by glucose
• Enhanced glucose uptake at peripheral tissues from increased sensitivity

Question 10

List 4 sulfonylureas?

Answer 10

• Tolbutamide
• Glipizide
• Glyburide
• Glimepiride

Question 11

What are the toxicities of sulfonylureas?

Blood sugar, blood, skin, muscles, CNS

Answer 11

• hypoglycemia
• nausea, rash
• blood disorders
• jaundice
• muscle weakness and ataxia
• dizziness and mental confusion

Question 12

What is the least likely toxicity from sunfonylurea?

A. hypoglycemia
B. diarrhea
C. jaundice
D. Muscle weakness and ataxia
E. Mental confusion

Answer 12

B. diarrhea

Question 13

Which sulfonylurea is most likely to cause toxic effects?

A. Tolbutamide
B. Glipizide
C. Glyburide
D. Glimepiride

Answer 13

A. Tolbutamide

Question 14

List 2 secretagogues

Answer 14

• Repaglinide
• Nateglinide

(Key: -glinide)

Question 15

What is the MOA for Secretogogues?

Repaglinide, Nateglinide

Answer 15

• stimulates insulin release from beta cells (same channel binding)

Question 16

What are the differences between secratogogues and sulfanylureas?

(duration, toxicities)
Hint: secreatogogues have GI effects

Answer 16

• short duration
• not sulfa drugs
• cause hypoglycemia, nausea dyspepsia (indigestion), diarrhea