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Pharmacology 1 - Exam 2 > Chapt 41: Pancreatic Hormones, Antidiabetics, Glucagon > Flashcards

Chapt 41: Pancreatic Hormones, Antidiabetics, Glucagon Flashcards

1
Q

In the endocrine pancreas, what are the 4 types of endocrine cells contained in the islets of Langerhans?

A

A (alpha, glucagon producing)
B (beta, insulin, and amylin producing)
D (delta, somatostatin producing)
F (pancreatic polypeptide producing).

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2
Q

Of the 4 types of endocrine cells, which is the most numerous?

A

B (insulin-producing)

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3
Q

Diabetes mellitus, a deficiency of _______.

A

insulin production or effect.

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4
Q

What is glucagon and how is it used in hypoglycemia?

A

It is a hormone that affects the liver, cardiovascular system, and gastrointestinal tract, can be used to treat severe hypoglycemia.

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5
Q

Drugs for diabetes mellitus are split into which two categories?

A

Insulins and Noninsulin Antidiabetic Drugs

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6
Q

What are the 3 Insulin Categories

A

Rapid, Short acting
Intermediate acting
Slow, long acting

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7
Q

What are the rapid, short-acting insulins?

A

Rapid: lispro, aspart, glulisine
Short: regular

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8
Q

What are the Intermediate-acting Insulins

A

NPH, lente

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9
Q

What are the slow, long-acting insulins?

A

glargine and deter

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10
Q

What are the categories of non insulin anti diabetic drugs? Identify the 4 “well-established” groups of oral anti diabetics used to treat Type 2.

A

Well Established: Insulin secretagogues, Biguanides, Alpha-glucosidase inhibitors, Thiazolidinediones
Additional Groups: Amylin analogs, Incretin modulators, SGLT2 inhibitors.

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11
Q

What are the Insulin secretagogue drugs?

A

2nd Generation Sulfonylureas: GlipizIDE, GlimepirIDE, GlyburIDE.
Meglitinide: RepaglinIDE
D-Penylalanine Derivative: NateglinIDE

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12
Q

What are the Biguanide Drugs?

A

Metformin (Remember Big-Formin)

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13
Q

What are the Alpha-glucosidase Inhibitors?

A

Pioglitazone

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14
Q

What are the amylin analog drugs?

A

Pramlinitide

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15
Q

What are the incretin modulators?

A

GLP-1 Analog: Exenatide

DPP-4 Inhibitor: Sitagliptin

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16
Q

What are the SGLT2 Inhibitor Drugs?

A

Canagliflozin

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17
Q

What are the categories of Diabetes Mellitus?

A

Type 1, Type 2, Other, Gestational Diabetes Mellitus

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18
Q

When does onset of Type 1 occurs?

A

during childhood

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19
Q

How does Type 1 occur?

A

From autoimmune destruction of pancreatic B cells

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20
Q

What is Type 2?

A

Progressive disorder characterized by increasing insulin resistance and diminishing insulin secretory capacity.

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21
Q

Type 2 is frequently associated with ______ and is much _______ common than _______.

A

obesity; more; type 1

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22
Q

Type 2 is only seen in adults? (T/F)

A

Its onset is usually in adults, but incidence in children and adolescents is rising with increased childhood obesity.

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23
Q

Treatment for both Type 1 and 2 require _______.

A

Careful attention to diet, fasting and postprandial blood glucose concentrations, and serum concentrations of hemoglobin A1c, a glycosylated hemoglobin that
serves as a marker of glycemia.

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24
Q

Which type of diabetes requires treatment with insulin?

A

Type 1 requires insulin. Though later stages of type 2 often require addition of insulin to drug regimen.

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25
Q

Insulin is not used to treat Type 2 DM? (T/F)

A

Although early stages of Type 2 are usually controlled with non insulin drugs, later stages of Type 2 may require addition of insulin to drug regimen.

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26
Q

What is proinsulin?

A

An 86-AA single-chain polypeptide and is the pro hormone that insulin arises from.

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27
Q

What results form the cleavage of proinsulin and cross-linking?

A

2-chain 51-peptide insulin molecule, and a 31-AA residual C-peptide.

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28
Q

What do pro-insulin and C-peptide have in common?

A

Neither have any physiologic action

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29
Q

What results from the activation of insulin receptor?

A

When activated by the hormone, the insulin receptor, a transmembrane tyrosine kinase, phosphorylates itself and a variety of intracellular proteins when activated by the hormone.

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30
Q

What type of receptor is the insulin receptor?

A

Transmembrane tyrosine kinase

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31
Q

What are kinases?

A

Enzymes that phosphorylate

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32
Q

What are the major target organs for insulin action?

A

Liver, skeletal muscle, and adipose tissue

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33
Q

How does insulin effect the liver?

A

Insulin increases the storage of glucose as glycogen in

the liver.

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34
Q

How does insulin increase storage of glucose and glycogen in the liver?

A

By the insertion of additional GLUT2 glucose transporter molecules in cell plasma membranes.
By increased synthesis of enzyme pyruvate kinase, phophofructokinase, and glucokinase.
by suppression of several other enzymes.

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35
Q

What is insulins effect on protein catabolism?

A

Decreases

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36
Q

What is Insulins effect on skeletal muscle?

A

stimulates glycogen synthesis and protein synthesis

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37
Q

How is glucose transport into muscle cells facilitated?

A

By insertion of GLUT4 transporters into cell plasma membranes

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38
Q

What is insulins effect on adipose tissue?

A

Insulin facilitates triglyceride storage by activating plasma lipoprotein lipase, increasing glucose transport into cells via GLUT4 transporters, and reducing intracellular lipolysis.

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39
Q

How is human insulin manufactured?

A

By bacterial recombinant DNA technology; E Coli

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40
Q

What is the goal of insulin therapy?

A

To control both basal and postprandial (after meals) glucose levels while minimizing the risk of hypoglycemia.

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41
Q

Rapid acting insulins have _____ onsets and _____ peaks of activity.

A

rapid; early

42
Q

Rapid acting insulins permit control of _________.

A

postprandial glucose levels

43
Q

What is the purpose of the small alterations in AA sequences between the 3 rapid-acting insulins?

A

To speed up their entry into circulation without affecting their interactions with the insulin receptors.

44
Q

When are rapid-acting insulins injected?

A

immediately before a meal

45
Q

Which insulin category is preferred for continuous SQ infusion devices?

A

Rapid-acting

46
Q

Rapid-acting insulins are used for treatment of which emergency.

A

Uncomplicated Diabetic Ketoacidosis

47
Q

What category is regular insulin and when is it used?

A

Category: Short-acting
Used IV use in emergencies
Used SQ in ordinary maintenance

48
Q

Regular Insulin can be given as a mixture? (T/F)

A

True.

Can be given alone or as a mixture with intermediate- or long-acting preparations

49
Q

Which insulin type is Intermediate-acting?

A

Neutral protamine Hagedorn insulin (NPH insulin)

50
Q

What is NPH?

A

Neutral protamine Hagedorn insulin.

A combination of regular insulin and protamine that exhibits a delayed onset and peak of action.

51
Q

What is protamine?

A

A highly basic protein also used to reverse the action of unfractionated heparin

52
Q

NPH insulin is often combined with ______ and ______.

A

Regular; rapid-acting insulins.

53
Q

What are Insulin Glargine and Detemir?

A

Long-acting Insulin. Modified forms of human insulin that provide a peak less basal insulin level lasting more than 20 hours, which helps control basal glucose levels without producing hypoglycemia.

54
Q

List the different insulin delivery systems?

A

SQ injection with disposable needle and syringe
Portable pen-sized injector
Continuous SQ insulin infusion device: programable pump.

55
Q

What is the most common complication of insulin use?

A

Hypoglycemia, from excessive insulin effect

56
Q

What is the treatment for severe hypoglycemia?

A

Prompt administration of glucose (candy, sugar or IV glucose) or of glucagon (IM injection)

57
Q

Who is most at risk for complications of hypoglycemia?

A

Patients with advanced renal disease, the elderly, and children younger than 7.

58
Q

What is the most common form of insulin-induced immunologic complication?

A

The formation of antibodies to insulin or noninsulin

protein contaminants, which results in resistance to the action of the drug or allergic reactions.

59
Q

Which 3 oral anti diabetics target endogenous regulators or glucose homeostasis?

A

Amalyn Analog: Pramlintide
GLP-1 Analog: Exenatide
DPP-4 Inhibitor: Sitagliptin

60
Q

What is the MOA of Insulin Secretagogues?

A

Insulin secretagogues stimulate the release of endogenous insulin by promoting closure of potassium channels in the pancreatic B-cell membrane. Channel closure depolarizes the cell and triggers opening of Ca2+ channels, triggering insulin release from vesicles via exocytosis.

61
Q

Insulin secretagogues are not effective in which types of patients?

A

patients who lack functional pancreatic B cells.

62
Q

Most insulin secretagogues are in which chemical class?

A

sulfonylureas

63
Q

Which are more potent, the second-generation or the older agents? Give examples of both.

A

Second-generation > Older agents

Second-Gen: glyburide, glipizide, glimepiride)
Older agents: tolbutamide, chlorpropamide

64
Q

What insulin secretagogues have a rapid onset and short duration of action? Why are they useful?

A

Repaglinide (a meglitinide) and Nateglinide (a d-phenylalanine derivative)
Useful for administration just before a meal to control postprandial glucose levels.

65
Q

Older sulfonylureas cause less of a hypoglycemic effect than 2nd Generation Antidiabetic drugs. (T/F)

A 
False. 
Older sulfonylureas (Tolbutamide and Chlorpropamide) are extensively bound to serum proteins, and drugs that compete for protein binding may enhance their hypoglycemic effects.
66
Q

What are the adverse effects associated with Insulin Secretagogues?

A

Hypoglycemia, skin rash, weight gain

67
Q

What is the MOA of Biguanides?

A

Reduces postprandial and fasting glucose by inhibiting hepatic and renal gluconeogenesis.
Also stimulates glucose uptake and glycolysis in peripheral tissues, slowing of glucose absorption from the gastrointestinal tract, and reduction of plasma glucagon levels.

68
Q

What is the molecular mechanism of biguanide reduction in hepatic glucose production?

A

Appears to involve activation of an AMP-stimulated protein kinase.

69
Q

What effect does metformin have in patients with insulin resistance?

A

metformin reduces endogenous insulin production presumably through enhanced insulin sensitivity.

70
Q

Why is Metformin the drug of first choice in overweight patients with Type 2?

A

Because of this insulin-sparing effect and because it does not increase weight (unlike insulin, secretagogues, or the thiazolidinediones)

71
Q

When is metformin used to restore fertility?

A 
In anovulatory women with polycystic
ovary disease (PCOD) and evidence of insulin resistance.
72
Q

The side effect of hypoglycemia is greater in Secretagogues than in Biguanides? (T/F)

A

True. Unlike sulfonylureas, biguanides DO NOT cause hypoglycemia.

73
Q

What are the toxic side effects of Biguanides?

A

Most common: GI Distress (nausea, diarrhea)
Most Severe: LACTIC ACIDOSIS, especially in patients with renal or liver disease, alcoholism, or conditions that predispose to tissue anoxia and lactic acid production (e.g. chronic cardiopulmonary dysfunction)

74
Q

What are the Thiazolidinedione drugs?

A

Rosiglitazone and Pioglitazone

75
Q

What is the MOA of Thiazolidinediones?

A

Increase target tissue sensitivity to insulin by activating the peroxisome proliferator-activated receptor-gamma nuclear receptor (PPAR-gamma receptor)

76
Q

What is the function of the nuclear receptor PPAR-gamma?

A

It regulates the transcription of genes encoding proteins involved in carbohydrate and lipid metabolism.

77
Q

What is the effects of thiazolidinediones?

A

Primary: Increasing glucose uptake in muscle and adipose tissue
Secondary: Inhibit hepatic gluconeogenesis and have effect on lipid metabolism and distribution of body fat.

78
Q

How do Thiazolidiediones effect hyperglycemia?

A

Reduce both fasting and postprandial hyperglycemia

79
Q

Thiazolidinediones are NEVER used as mono therapy. (T/F)

A

False.

They are used as mono therapy or in combination with insulin or other oral anti diabetic drugs.

80
Q

Hypoglycemia is increased with Thiazolidinediones. (T/F)

A

False.

When used alone, hypoglycemia is extremely rare.

81
Q

How do Thiazolidinediones increase the risk of heart failure?

A

Thiazolidinediones can cause fluid retention, which presents as mild anemia and edema and may increase the risk of heart failure.

82
Q

Which Thiazolidinedione has been linked to MI?

A

Rosiglitazone

83
Q

What is the concern between Thiazolidinediones and liver dysfunction?

A

The original thiazolidinedione, Troglitazone, has caused hapatotoxicity and is no longer used.
Newer, Rosiglitazone and pioglitazone have not been linked to serious liver disease but require regular monitoring.

84
Q

Female patients taking thiazolidinediones appear to have an increased risk of ________.

A

bone fractures.

85
Q

What is the effect of Pioglitazone and troglitazone on cytochrome P450 activity?

A

Induce CYP450 activity (especially the CYP3A4 isozyme) and can reduce the serum concentrations of drugs that are metabolized by these enzymes (eg, oral contraceptives, cyclosporine).

86
Q

What is the MOA of Alpha-Glucosidase Inhibitors?

A

Acarbose and miglitol are carbohydrate
analogs that act within the intestine to inhibit alpha-glucosidase, and as a result of slowed absorption, postprandial hyperglycemia is reduced.

87
Q

What is the function of Alpha-Glucosidase?

A

It is an enzyme necessary for the conversion of complex starches, oligosaccharides, and disaccharides to the monosaccharides that can be transported out of the intestinal lumen and into the bloodstream.

88
Q

Alpha-Glucosidase Inhibitors primarily effect fasting blood sugar. (T/F)

A

False.

These drugs lack an effect on fasting blood sugar

89
Q

Alpha-glucosidase inhibitors are used as mono therapy and in combination with other anti diabetic drugs. (T/F)

A

True

90
Q

What is the relation between metformin, thiazolidinediones, and α-glucosidase inhibitors with respect to pre diabetic patients?

A

Like metformin and the thiazolidinediones, the α-glucosidase inhibitors have been shown to prevent type 2 diabetes in prediabetic persons.

91
Q

What are the primary adverse effects of the Alpha-glucosidase inhibitors?

A

Flatulence, diarrhea, and abdominal pain resulting

from increased fermentation of unabsorbed carbohydrate by bacteria in the colon.

92
Q

How is hypoglycemia treated in patients taking an alpha-glucosidase inhibitor?

A

Treated with oral glucose (dextrose) and not sucrose, because the absorption of sucrose will be delayed.

93
Q

What is Pramlintide? is an injectable synthetic analog of amylin, a 37-amino acid hormone produced by pancreatic B cells.

A

An injectable synthetic analog of amylin, a 37-amino

acid hormone produced by pancreatic B cells.

94
Q

How does Amylin contributes to glycemic control?

A

By activating high-affinity receptors involved in both glycemic control and osteogenesis. Pramlintide suppresses glucagon release, slows gastric emptying, and works in the CNS to reduce appetite.

95
Q

How is Pramlintide absorbed?

A

After subcutaneous injection, it is rapidly absorbed and has a short duration of action.

96
Q

Pramlintide is used as mono therapy. (T/F)

A

It is used in combination with insulin to control postprandial glucose levels.

97
Q

What are the major adverse effects associated with pramlintide?

A

Hypoglycemia and gastrointestinal disturbances.

98
Q

What is GLP-1?

A

Glucagon-like peptide-1 (GLP-1) is a member of the incretin family of peptide hormones, which are released from endocrine cells in the epithelium of the bowel in response to food.

99
Q

What is the function of incretins?

A

The incretins augment glucose-stimulated insulin release from pancreatic B cells, retard gastric emptying, inhibit glucagon secretion, and produce a feeling of satiety.

100
Q

What is the function of the GLP-1 receptor?

A

The GLP-1 receptor is a G-protein coupled receptor (GPCR) that increases cAMP and also increases the free intracellular concentration of calcium.

101
Q

What is Exenatide?

A

A long-acting injectable peptide analog of GLP-1, used in combination with metformin or a sulfonylurea for treatment of type 2 diabetes.

102
Q

What are the adverse effects of Exenatide?

A

Major: GI disturbances
Hypoglycemia when combined with a sulfonylurea.
Serious or fatal acute pancreatitis.

Pharmacology 1 - Exam 2 (4 decks)

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