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Pharmacology > EXAM #5: ANTIDIABETIC AGENTS > Flashcards

EXAM #5: ANTIDIABETIC AGENTS Flashcards

1
Q

What is the product of alpha cells in the pancreas?

A

Glucagon

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2
Q

What is the product of beta cells in the pancreas?

A

Insulin and amylin

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3
Q

What is the product of delta cells in the pancreas?

A

Somatostatin

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4
Q

What is the product of G cells in the pancreas?

A

Gastrin

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5
Q

What is the product of F cells in the pancreas?

A

Pancreatic polypeptide

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6
Q

What type of hormone is insulin? What are the implications?

A
  • Peptide hormone that can bind EXTRCELLULAR receptors

* Note that from a therapeutic standpoint, oral insulin is not a viable option

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7
Q

List the factors that will upregulate insulin release?

A 
Glucose 
Amino acids 
Incretins 
Epi/ B-2 adrenergic 
Vagus
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8
Q

List the factors that will downregulate insulin release?

A

NE/a-2 adrenergic

Amylin

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9
Q

Outline the response of the pancreatic beta-cell to glucose.

A

1) Glucose comes into the cell via the glucose transporter (GLUT-2)
2) Intracellular ATP increases
3) High levels of intracellular ATP cause ATP-sensitive K+ channels to CLOSE
4) Depolarization follows, opening voltage-gated Ca++ channels
5) Ca++ dependent Ca++ release of insulin packaged in secretory vesicles= insulin release

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10
Q

What is the major metabolic response to insulin?

A

Translocation of GLUT-4 transporters from the cytoplasmic compartment to the membrane

*Especially in skeletal muscle and adipose tissue

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11
Q

What is the major function of GLUT-4 transporters?

A

Insulin mediated uptake of glucose

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12
Q

Generally, what is the function of insulin action on: 1) fatty acids, 2) glucose, 3) amino acids?

A

Insulin promotes conversion of smaller molecules to their storage to the storage forms i.e:

1) Fatty acids to TAG
2) Glucose to glycogen
3) Amino acids to protein

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13
Q

What metabolic processes are favored in the absence of insulin?

A

1) Gluconeogenesis

2) Glycogenolysis

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14
Q

What is the key difference between Type I and Type II DM?

A 
I= IDDM 
II= NIDDM
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15
Q

What is the key pathologic characteristic of Type I DM?

A

Autoimmune Beta cell destruction leading to absolute insulin deficiency

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16
Q

What is the key pathologic characteristic of Type II DM?

A

Insulin resistance i.e. increased insulin needed for same effect

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17
Q

What are the signs/sx of Type I DM?

A
  • Polyuria
  • Polydipsia
  • Polyphagia

*Remember the 3 P’s of Type I DM

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18
Q

What are the signs/sx of Type II DM?

A
  • Infection
  • Neuropathy
  • Obesity/ metabolic syndrome
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19
Q

What is normal fasting blood glucose level?

A

Less than 100 mg/dL

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20
Q

What is a diabetic fasting blood glucose level?

A

Roughly 140 mg/dL

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21
Q

What plasma blood glucose level should one be at an hour or so after a meal?

A

Less than 200 mg/dL

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22
Q

What is the mainstay treatment for Type I DM?

A

Insulin

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23
Q

What is the one route that insulin cannot be administrated?

A

Oral

*Note that SQ is most common

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24
Q

What is the purpose of altering amino acids in the beta chain of insulin?

A
  • Alters the “stickiness” of the insulin
  • Will complex with other insulin or not

*Implications for duration of action/onset

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25
Q

What has been done to make rapid acting insulin?

A

Amino acid change so that insulin peptide complexes DO NOT occur

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26
Q

What are the examples of rapid-acting insulin?

A

Insulin lispro
Insulin aspart
Insulin glulisine

27
Q

What is the onset of rapid acting insulin?

A

10-30 min

28
Q

What is the duration of action of rapid-acting insulin?

A

3-5 hours

29
Q

What is an example of short-acting insulin?

A

Regular insulin

Forms complexes

30
Q

What is the duration of action for short-acting insulin?

A

4-12 hours

31
Q

What is an example of intermediate acting insulin?

A

NPH

*Forms protamine-insulin complexes

32
Q

What is the duration of action of intermediate acting insulin?

A

10-20 hours

33
Q

What are examples of long-acting insulin?

A

Glargine

Detemir

34
Q

How is insulin formulated to be long-acting?

A

Forms a precipitate at neutral pH

35
Q

What is the duration of action for long-acting insulin?

A

12-20 or 22-24 hours

36
Q

What type of insulin is used in an insulin pump vs. SQ injection?

A

Pump= rapid only

SQ= rapid and long-acting

37
Q

How would you manage eating a meal with insulin?

A

Rapid-short acting

38
Q

How are basal levels of insulin maintained?

A

Long-acting insulin

39
Q

What is intermediate duration insulin typically used for?

A

Overnight/ sleeping

40
Q

What is the most common adverse effect of insulin? What are other adverse effects seen with insulin theray?

A

Hypoglycemia*

Also, injection site reactions–lipohypertrophy or lipoatrophy– that require changing sites

41
Q

What are the signs/sx. of hypoglycemia?

A

SNS:

  • Tachycardia
  • Diaphoresis
  • Tremors
  • Nausea
  • Hunger
  • Confusion
  • Coma
42
Q

How is hypoglycemia treated?

A

Glucose or glucagon

43
Q

What is the first line agent to treat DM-II?

A

Metformin

44
Q

What is the MOA of Metformin?

A
  • Decreased hepatic glucose output
  • Increased utilization in the peripheral tissue

Not really understood, but NOT dependent on B-cell function

45
Q

What is the key adverse effect with Metformin?

A

GI disturbances

46
Q

List the sulfonylureas and meglitinides.

A

Glimepiride
Glipizide
Glyburide

Repaglinide
Nateglinide

47
Q

What is the MOA of the sulfonylureas and meglitinides?

A

Inhibit ATP-sensitive potassium channel of the Beta-cell resulting in insulin release

48
Q

What adverse effects are seen with the sulfonylureas and meglitinides?

A

Weight gain

Hypoglycemia

49
Q

What are the Glucosidase inhibitors?

A

Acarbose

Miglitol

50
Q

What is the MOA of the Glucosidase inhibitors?

A

Inhibit the brush border glucosidase enzyme the prevent absorption of glucose

51
Q

What adverse effects are seen with Glucosidase inhibitors?

A

GI disturbances

52
Q

When are Glucosidase inhibitors contraindicated?

A

Patients with pre-existing GI disorder e.g. Lactose intolerance

53
Q

What are the Thiazolindinediones?

A

Pioglitazone

Rosiglitazone

54
Q

What is the MOA of the Thiazolindinediones?

A

Generally, increase the expression of GLUT-4

*Increases peripheral glucose uptake

55
Q

What key adverse effects are associated with Thiazolindinediones?

A

Cardiovascular

Hepatotoxicity

56
Q

What is the amylinomimetic drug?

A

Pramlintide

57
Q

What is the MOA of Pramlintide?

A
  • Inhibit glucagon release
  • Inhibit gastric emptying
  • Anorectic effect
58
Q

What are the adverse effects of Pramlintide?

A
  • Anorexia
  • Hypoglycemia
  • Delayed drug absorption
59
Q

What are the incretins?

A

Exenatide

Liraglutide

60
Q

What is the MOA of the incretins?

A

Increased insulin secretion by binding to incretin receptors on beta-cells

61
Q

What adverse effects are associated with the incretins?

A

Acute pancreatitis

62
Q

What is the normal function of DPP?

A

Breakdown of incretins

*Incretins normally stimulate insulin release

63
Q

What are the DPP inhibitors?

A

Sitagliptin
Saxagliptin
Linagliptin

64
Q

What are the adverse effects of DPP inhibitors?

A
  • Acute pancreatitis

- Hemorrhagic/ necrotizing pancreatitis

Pharmacology (64 decks)

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