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Endocrine Pharmacology > Diabetes Medications > Flashcards

Diabetes Medications Flashcards

1
Q

Natural Regular (soluble) insulins for injection are?

A
  1. bovine (beef) insulin
  2. porcine (pork) insulin
  3. ovine (sheep) insulin
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2
Q

Modified crystal size insulins are?

A
  1. NPH insulin, NPH/Reg (50/50), NPH/Reg (70/30)
  2. lente insulin
  3. semilente insulin
  4. ultralente insulin
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3
Q

Synthetic Human insulin and analogs are?

A
  1. recombinant human insulin.
  2. human insulin made by switching aa of pork insulin
  3. insulin lispro
  4. insulin aspart
  5. insulin glargine
  6. insulin detemir
  7. Insulin glulisine
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4
Q

Antidiabetic Drugs Sulfonylureas First Generation

A

CATT

  1. chlorpropamide
  2. acetohexamide
  3. tolazamide
  4. tolbutamide
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5
Q

Antidiabetic Drugs Sulfonylureas Second Generation

A
  1. glyburide
  2. glipizide
  3. gliclazide
  4. glimepiride
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6
Q

Antidiabetic Drugs Meglitinides

A
  1. repaglinide

2. nateglinide

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7
Q

Antidiabetic Drugs Biguanides

A

metformin

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8
Q

Antidiabetic Drugs Thiazolidinediones

A
  1. rosiglitazone (black box warning)
  2. pioglitazone
  3. rosiglitazone + metformin
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9
Q

Diabetes Type I

A

Insulin-Dependent Diabetes Mellitus (IDDM),

also called Juvenile Diabetes

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10
Q

Diabetes Type II

A

Non-Insulin-Dependent Diabetes Mellitus (NIDDM), also called Maturity Onset Diabetes

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11
Q

Type I Diabetes (IDDM) Define?

A

A “wasting” disease with loss of glycogen, body fat, muscle mass. Excretion of glucose and ketone bodies into urine.

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12
Q

Alpha Cells:

A

Glucagon

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13
Q

Beta Cells:

A

Insulin

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14
Q

Delta Cells:

A

Somatostatin

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15
Q

Insulin Secretion occurs?

A

Secreted from the beta cells of the pancreas.

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16
Q

Stimulants of Insulin release?

A

– Glucose, mannose
– Leucine
– Vagal stimulation
– Sulfonyl ureas

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17
Q

Amplifiers of insulin release?

A

– Enteric hormones–cholecystokinin, secretin, gastrin

– Neural stimulation (beta-adrenergic)

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18
Q

Inhibitors of insulin release?

A

– Somatostatin
– Some drugs such as diazoxide
– Catecholamines

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19
Q

Diabetes Mellitus Patients Type I (IDDM)

Describe

A

– Little or no insulin release, β cells degenerate

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20
Q

Diabetes Mellitus Patients Type I (IDDM)

Percentage of Patients?

A

– 10-20% of diabetic patients

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21
Q

Diabetes Mellitus Patients Type I (IDDM)

Onset?

A

– Juvenile onset

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22
Q

Diabetes Mellitus Patients Type I (IDDM)

Management?

A

– Difficult management

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23
Q

Diabetes Mellitus Patients Type I (IDDM)

Treatment?

A

– Insulin is the only treatment

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24
Q

Diabetes Mellitus Patients Type II (NIDDM)

Describe

A

– Normal or elevated insulin

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25
Q

Diabetes Mellitus Patients Type II (NIDDM)

Percentage of Patients?

A

– Majority of diabetic patients

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26
Q

Diabetes Mellitus Patients Type II (NIDDM)

Onset?

A

– Onset usually after 35 years

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27
Q

Diabetes Mellitus Patients Type II (NIDDM)

Associations?

A

– Usually associated with obesity

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28
Q

Diabetes Mellitus Patients Type II (NIDDM)

Treatment?

A

– Treatment includes diet, exercise, insulin and oral

hypoglycemic drugs

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29
Q

Hoe do animal and human insulin differ?

A

– Porcine insulin differs from human in 1 aa
– Bovine insulin differs in 3 aa
– Ovine insulin differs in 3 aa

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30
Q

Three principal types of insulin preparations are?

A

– Short acting: rapid onset of action, short half-life
– Intermediate acting: slower onset, longer half-life
– Long acting: longest half-life, largest crystals

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31
Q

Describe short-acting insulin and how is it administered?

A

– Soluble, clear, crystalline zinc-insulin
– Called Regular Insulin, the only preparation that can be injected IV. All others SC or IM
– All other preparations have been modified to provide prolonged action and are dispensed as turbid suspensions

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32
Q

Describe Intermediate-acting insulin and what are its characteristics?

A

– NPH insulin [Neutral, Protamine, Hagedorn]
– Lente insulins [mixture of 30% semilente (short-acting) and 70% ultralente (long-acting) zinc insulin crystals
– Long-acting = large crystals = slow absorption

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33
Q

Insulin Replacement Therapy is Based on?

How many times a day?

A

Patient measurement of blood glucose. Measurements made 4 times a day, BEFORE each meal. Two insulin injections each day.

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34
Q

Blood glucose before lunch reflects?

A

morning regular insulin dose

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35
Q

Blood glucose before supper reflects?

A

the morning NPH insulin dose

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36
Q

Blood glucose before bedtime reflects?

A

the evening regular insulin dose

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37
Q

Blood glucose before breakfast reflects?

A

the evening NPH insulin dose

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38
Q

If “before lunch” is too high?

A

increase morning dose of regular insulin.

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39
Q

If “before supper” is too high?

A

increase morning dose of NPH insulin.

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40
Q

If “before bedtime” is too high?

A

increase evening dose of regular insulin.

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41
Q

If “before breakfast” is too high?

A

increase evening dose of NPH insulin.

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42
Q

If glucose is to low?

A

Decrease insulin

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43
Q

Humulin is made using?

A

Recombinant DNA to produce the hormone in bacteria or yeast.

44
Q

Novolin is made by?

A

Switching the aa that is different in pork insulin.

45
Q

Insulin lispro is an analogue?

A

Of Humulin in which the normal Proline B28 and Lysine B29 are switched. Switching is done by mutations of hrDNA. Insulin lispro doesn’t form hexamers. (Exists in
circulation as monomer only.)

46
Q

Humalog has a faster?

A

Onset of action and shorter halflife than Regular Insulin.

47
Q

Insulin aspart is another?

A

Rapid acting insulin analog (Asp substituted for Pro). It also exists only as a monomer.

48
Q

Insulin glulisine is still another?

A

Rapid-acting insulin analogue that differs from human insulin in that the amino acid asparagine at position B3 is replaced by lysine and the lysine in position B29 is replaced by glutamic acid. It also does not form hexamers.

49
Q

Insulin lispro, insulin aspart and insulin glulisine all have the same?

A

Pharmacokinetic properties–faster onset of action and shorter onset of action– because they exist in the monomeric state.

50
Q

Insulin glargine is a? What is different about it?

A

Recombinant human insulin analog for use as an injection. Insulin glargine differs from human insulin because Asparagine 21 is replaced by glycine & two arginines are added to the C-terminus of the B-chain.

51
Q

What is special about Insulin detemir and what is it good for?

A

Long-acting (up to 24-hour duration of action). Low peak insulin concentration decreases chances
of nocturnal hypoglycemia.

52
Q

Ketoacidosis (diabetic coma) caused by and made worse by?

A

– Caused by LOW INSULIN
– Catecholamines, growth hormone, cortisone and glucagon (all elevated in diabetes) exaggerate metabolic effects of low insulin in diabetic patient.

53
Q

Ketoacidosis (diabetic coma) increases the release?

A

Fatty Acids causes increased Ketone Bodies and decreased pH.

54
Q

Ketoacidosis (diabetic coma) Treatment?

A

– Hyperglycemia due to hepatic gluconeogenesis.

– Treatment: Insulin

55
Q

Hypoglycemic coma caused by?

A

– Usually caused by INSULIN OVERDOSE

– So common that all comatose patients are given glucose first while blood glucose is being measured.

56
Q

Hypoglycemic coma Treatment?

A

Treatment: Glucose

57
Q

Glycosylated Hemoglobin (A1C) test for?

A

Test for long-term control of blood glucose. Higher average blood glucose yields more extensive glycosylation of hemoglobin.

58
Q

Glycosylated Hemoglobin (A1C) measures?

A
  • HbA1c is the hemoglobin measured.

* Red blood cells live an average of 3-4 months which allows long-term glycosylation to be tested.

59
Q

Normal (non-diabetic) glycosylation of HbA1c is?

A

About 6%. Over 8% for a diabetic patient is not good,

over 10% is dangerous. ADA recommends an A1C target of ≤6.5% (2010).

60
Q

Glucagon is?

A

A 29 a.a. peptide secreted by α-cells of the pancreas

61
Q

Glucagon causes?

A

– Has opposite effects to those of insulin.

– Elevated in fasting and diabetes.

62
Q

Glucagon used for?

A

– Rarely used for treatment.
– Sometimes used in emergency situations for
hypoglycemia, but most often glucose infusion is
used instead.

63
Q

Sulfonylureas causes?

A
  • Initially increase insulin release, but not after longterm treatment. May decrease insulin metabolism by liver.
  • Increase insulin sensitivity by enhancing the effect of insulin on glucose uptake.
64
Q

Sulfonylureas absorption and metabolized?

A

• Rapidly absorbed from GI tract. Once or twice daily.
• Second generation drugs 10 to 100 x more potent.
• Extensively protein bound, Metabolized in liver,
excreted by kidney.

65
Q

Meglitinides are?

A

Benzoic acid derivatives. Not related to sulfonylureas.

66
Q

Meglitinides cause and are absorbed & metabolized by?

A
  • Increase insulin secretion.
  • Very rapid GI absorption. Short half-life. Taken before each meal to control post-prandial glucose level.
  • Metabolized by liver
67
Q

Meglitinides major side effect?

A

Major side effect is hypoglycemia.

68
Q

Meglitinides Currently available:

A

Repaglinide

Nateglinide

69
Q

Biguanides mechanism and absorption?

A

Does not affect insulin secretion, no hypoglycemia.
Decreases hepatic glucose production.
Absorbed from GI tract. Little metabolism.

70
Q

Biguanides currently available?

A

Metformin

71
Q

Thiazolidinediones mechanism and absorption?

A

Bind specifically to Peroxisome Proliferator-Activated Receptor-γ (PPARγ).Increase insulin sensitivity. Increase glucose transport into muscles, adipose tissue.
Absorbed from GI tract. Little metabolism.

72
Q

Thiazolidinediones currently available?

A

Rosiglitazone (BB Warning)
Pioglitazone
Rosiglitazone + metformin

73
Q

α-Glucosidase Inhibitors mechanism?

A

Reduce intestinal absorption of starch, disaccharides by inhibiting brush border α-glucosidase.
Reduces uptake of carbohydrate and reduces postprandial glucose rise.

74
Q

α-Glucosidase Inhibitors are used with?

A

Usually used in combination with other hypoglycemic drugs and/or insulin.

75
Q

α-Glucosidase Inhibitors currently available?

A

Acarbose

Miglitol

76
Q

NSAIDs enhance hypoglycemic action of?

A

Sulfonylureas.

77
Q

Somatostatin secreted by?

A

Secreted by D cells of pancreatic islets. Also in GI and in brain.

78
Q

Somatostatin function?

A

Somatostatin inhibits release of TSH and GH from pituitary. Inhibits release of insulin and glucagon
from pancreas.

79
Q

Therapeutic Uses of Somatostatin include?

A

Inhibit insulin in insulinomas.

Inhibit glucagon release in glucagonomas.

80
Q

Somatostatin half life?

A

Has a short half-life (3-6 minutes)

81
Q

Octreotide (Sandostatin) is a?

A

Long-acting analogue. Used for glucagonomas. Octreotide also controls excess secretion of GH (useful in acromegaly).

82
Q

Diazoxide mechanism?

A

Antihypertensive antidiuretic that has potent hyperglycemic actions. Diazoxide inhibits insulin secretion (but does not inhibit insulin synthesis). Insulin builds up in β-cells.

83
Q

Diazoxide used?

A

To treat various forms of hypoglycemia. Used for inoperable insulinomas.

84
Q

GLP-1 is a?

A

New Target for Hypoglycemic Drugs

85
Q

GLP-1 mechanism?

A

Increases glucose-dependent insulin secretion.
Inhibits glucagon-stimulated glycogenolysis in the liver.
Slows gastric emptying.
Decreases appetite.
Decreases glucagon secretion.
All these actions decrease postprandial blood glucose.

86
Q

The incretins are hormones?

A

That can increase insulin secretion.

87
Q

Exenatide is

A

a synthetic peptide of 39 aa (the natural peptide is exendin-4 isolated from Gila monster venom)

88
Q

Exenatide mechanism?

A

It inhibits glucagon-stimulated glycogenolysis in the liver. May preserve or increase production of new beta-cells in the pancreas.

89
Q

Incretins are endogenous compounds, such as?

What is a potent form?

A

GLP-1, that improve glycemic control. They act on the GLP-1 receptor (Glucagon-like peptide-1), but exenatide is even more potent than GLP-1.

90
Q

Sitagliptin phosphate is an inhibitor of? .

A

Dipeptidyl peptidase-4 (DPP-4), the enzyme that inactivates incretin hormones.

91
Q

Incretins (2 types) are?

A

GLP-1 receptor agonists:

Dipeptidyl peptidase-4 inhibitors:

92
Q

GLP-1 receptor agonists:

A
  • exenatide

* liraglutide

93
Q

Dipeptidyl peptidase-4 inhibitors:

A
  • sitagliptin
  • saxagliptin
  • linagliptin
94
Q

Pramlintide is an?

A

Analogue of amylin, a peptide hormone released by β-cells of the pancreas along with insulin, after a meal.

95
Q

Like insulin, amylin is?

A

Deficient in individuals with type 1 diabetes.

96
Q

Pramlintide aids in the?

A

Absorption of glucose by slowing gastric emptying, promoting satiety via hypothalamic receptors (different receptors than for GLP-1), and inhibiting inappropriate secretion of glucagon, which opposes the effects of insulin and amylin.

97
Q

Pramlintide used for?

A

Type 1 and type 2 diabetics who use insulin.

98
Q

Pramlintide treatment results in?

A

Weight loss, allows patients to use less insulin, lowers average blood glucose, and substantially reduces the postprandial glucose rise.

99
Q

Bile Acid Sequestrants include?

A

Colesevelam hydrochloride

100
Q

Colesevelam hydrochloride was developed to

A

Lower blood cholesterol.

101
Q

Colesevelam hydrochloride Now approved for?

A

Type 2 diabetes patients who are taking other medications. (2 grams/day).

102
Q

Colesevelam hydrochloride effect is diabetes?

A

It lowers HbA1c 0.5% and lowers LDL cholesterol 15%.

103
Q

Colesevelam hydrochloride mechanism & side effects?

A

Assumed to interrupt enterohepatic cycling and lower Farnesoid X Receptor activation.
Side effects are gastrointestinal.

104
Q

Cinagliflozin is?

A

SGLT-2 Inhibitor: SGLT-2 is a Na-Glucose transporter in the kidney responsible for 90% glucose reabsorption. Causes you to pee glucose.

105
Q

Cinagliflozin Adverse Effects & Contraindicated:

A

Hypotension, Hyperkalemia, Hypoglycemia, Increase LDL.

Contraindicated in renal disease/dialysis.

Endocrine Pharmacology (5 decks)

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