Chapter 31: Insulin, Oral Hypoglycemics, and Glucagon

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1

The endocrine system of the pancreas comprises the (...), which contain four types of cells that synthesize and secrete different polypeptide hormones

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islets of Langerhans

2

Insulin is produced by the (...), which constitute most of the islet and form its central core.

β cells

3

Insulin is composed of two (...) joined by two (...).

chains (A and B); disulfide bridges

4

Proinsulin is converted to insulin when the (...) is removed, which occurs within the secretory granules of the pancreatic β cell.

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C peptide

5

C peptide has no known biologic function, but it can serve as an (...).

index of insulin secretion

6

Insulin is a member of a family of related peptides known as (...).

insulin-like growth factors (IGFs)

7

(...) is the principal stimulus to insulin secretion in humans.

glucose

8

The classic action of insulin is to (...).

decrease the blood glucose concentration

9

Insulin decreases the blood glucose production by increasing glucose (...), increasing glucose (...), and decreasing glucose (...).

uptake; utilization; production

10

The important target tissues for regulation of glucose homeostasis by insulin include (...) cells.

liver, muscle, and fat

11

Insulin affects the activities of various enzymes involved in intracellular use and storage of (...).

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glucose, amino acids, and fatty acids

12

Insulin may be given (...).

subcutaneously, intravenously, or intramuscularly

13

Endogenous insulin is secreted into the (...) circulation; injected insulin is delivered into the (...) circulation.

portal; peripheral

14

The insulin receptor is composed of two (...) and two (...) linked by (...).

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α subunits; β subunits; disulfide bonds

15

There is evidence that insulin acts by synthesis of second messengers of the (...) class.

inositolphosphoglycan (IPG)

16

(...) is a group of syndromes characterized by hyperglycemia.

diabetes mellitus

17

Virtually all forms of DM are due to either a decrease in the (...) or a decrease in the (...).

concentration of insulin (insulin deficiency); response to insulin (insulin resistance)

18

(...), occurs during pregnancy and resolves after parturition, but is important because it is a predictor of future risk of diabetes.

gestational diabetes

19

(...) is an autoimmune disease of the pancreatic β cell, resulting in degeneration and an absolute lack of insulin.

type 1 diabetes

20

In (...), impaired glucose metabolism in muscle and liver results in relative insensitivity to insulin.

type 2 diabetes

21

At elevated blood glucose concentrations, hemoglobin is glycosylated on its amino terminal valine residue to form the glycosyl valine adduct, termed (...).

hemoglobin A1c (HbA1c)

22

Because the half-life of HbA1c is the same as that of (...), its concentration can be used to assess the severity of the glycemic state over the previous (...).

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red blood cells; 8 to 12 weeks

23

Type 1 diabetes mellitus must be treated with (...); type 2 diabetes mellitus may be treated with a combination of (...).

insulin; diet and exercise, oral antihyperglycemic agents, or insulin

24

(...) insulin analogues have amino acids are substituted, or reversed.

ultrashort-acting

25

List the ultrashort-acting insulin preparations. (3)

  1. aspart
  2. glulisine
  3. lispro
26

(...) insulins are short-acting preparations.

regular

27

List the regular, short-acting insulin preparations. (2)

  1. humulin R
  2. novolin R
28

The intermediate-acting (...) insulin preparations contain particles and are cloudy suspensions at neutral pH.

NPH

29

List the intermediate-acting, NPH insulin preparations. (2)

  1. humulin N
  2. novolin N
30

(...) insulin analogues have groups added to alter their kinetics.

long-acting

31

List the long-acting insulin preparations. (3)

  1. glargine
  2. detemir
  3. degludec
32

Most commercial preparations of insulin are supplied in solution at a concentration of (...).

100 units/mL (approximately 3.47 mg/mL)

33

Insulin absorption is usually most rapid from the (...), followed by the arm, buttock, and thigh.

abdominal wall

34

(...) is the most common adverse reaction to insulin.

hypoglycemia

35

List the symptoms of hypoglycemia. (8)

  1. sweating
  2. tachycardia
  3. tremor
  4. blurred vision
  5. weakness
  6. hunger
  7. confusion
  8. altered behavior
36

What class of drug are the following?

  1. chlorpropamide
  2. tolazamide
  3. glimepiride
  4. glipizide
  5. glyburide

sulfonylureas

37

Sulfonylureas are effective only in patients with (...).

functioning pancreatic β cells

38

Sulfonylureas stimulate release of insulin by blocking (...) in pancreatic β cells.

ATP–dependent K+ current

39

Sulfonylureas have a (...) structure, which is the basis for (...) with certain antibacterial drugs.

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sulfonamide; cross-sensitivity

40

List the adverse effects of sulfonylureas. (7)

  1. hypoglycemia
  2. hypersensitivity reactions
  3. naseua and vomiting
  4. hematologic reactions
  5. cholestatic jaundice
  6. dermatologic effects
  7. weight gain
41

List some drugs that increase the effect of sulfonylureas. (6)

  1. antihistamines
  2. azole antifungals
  3. oral anticoagulants
  4. salicylates
  5. Sulfonamides
  6. β-Adrenergic receptor blockers
42

List some drugs that decrease the effect of sulfonylureas. (6)

  1. Ca2+ salts
  2. corticosteroids
  3. estrogens
  4. sympathomimetics
  5. thiazide diuretics
  6. thyroid hormones
43

Sulfonylureas cause a (...) effect by decreasing the activity of aldehyde dehydrogenase.

disulfiram-like

44

What class of drug are the following?

  1. repaglinide
  2. nateglinide
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meglitinides

45

Meglitinides are effective only in patients with (...).

functioning pancreatic β cells

46

Meglitinides stimulate release of insulin by blocking (...) in pancreatic β cells.

ATP-dependent K+ channels

47

(...) is the major adverse effect of repaglinide and is most likely to occur if a meal is delayed or skipped or in patients with hepatic insufficiency.

hypoglycemia

48

Drugs that inhibit (...) may potentiate the effect of nateglinide.

cytochrome p450 (e.g. fluconazole, amiodarone)

49

(...) drugs may potentiate the hypoglycemic effects of repaglinide.

nonsteroidal antiinflammatory drugs

50

(...) is currently the only biguanide approved for use in the United States.

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metformin

51

Biguanides stimulate (...) thereby decreasing blood glucose concentrations by several different actions.

AMP-activated protein kinase (AMPK)

52

Unlike sulfonylureas and meglitinides, biguanides do not cause (...) or (...) and do not depend on (...).

hypoglycemia; weight gain; functioning pancreatic β cells

53

List the common adverse effects of metformin. (6)

  1. nausea
  2. anorexia
  3. vomiting
  4. diarrhea
  5. flatulence
  6. cramps
54

Metformin may cause a decrease in vitamin (...) levels, possibly by decreasing absorption.

B12

55

(...) is a rare but serious complication of biguanides that is fatal in roughly 50% of patients in which it occurs.

lactic acidosis

56

Biguanides are contraindicated in patients with renal disease, hepatic disease, or conditions predisposing to tissue anoxia because of concern regarding (...).

lactic acidosis

57

What class of drug are the following?

  1. pioglitazone
  2. rosiglitazone
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thiazolidinediones

58

Thiazolidinediones act by increasing insulin sensitivity in tissues by acting on (...).

nuclear peroxisome proliferator-activated receptor-γ (PPARγ)

59

The thiazolidinediones depend on (...) for their activity.

presence of insulin

60

Thiazolidinediones now carry a “black box” warning of (...).

congestive heart failure and myocardial ischemia

(The risk is greater with rosiglitazone.)

61

List the adverse effects of thiazolidinediones. (6)

  1. congestive heart failure
  2. myocardial ischemia
  3. weight gain
  4. edema
  5. osteoporosis
  6. hepatotoxicity
62

Pioglitazone can decrease the plasma concentration of (...).

oral contraceptives

63

Hormones secreted from the gastrointestinal tract that have been shown to stimulate insulin secretion are known as (...).

incretins

64

(...) is an incretin that has been shown to augment glucose-dependent insulin secretion.

glucagon-like peptide 1 (GLP-1)

65

GLP-1 is rapidly inactivated by (...).

dipeptidyl peptidase 4 (DPP-4)

66

Incretin-related drugs that act by either stimulating (...) or inhibiting (...).

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GLP-1; DPP-4

67

What class of drug are the following?

  1. exenatide
  2. albiglutide
  3. dulaglutide
  4. liraglutide

GLP-1 receptor agonists

68

What class of drug are the following?

  1. sitagliptin
  2. saxagliptin
  3. linagliptin
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DPP-4 inhibitors

69

What class of drug are the following?

  1. canagliflozin
  2. dapagliflozin
  3. empagliflozin
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SGLT2 inhibitors

70

The SGLT2 inhibitors block (...) which facilitates (...) in the kidney.

sodium-glucose co-transporter 2; glucose reabsorption

71

List the adverse effects of SGLT2 inhibitors. (5)

  1. urinary tract infections
  2. increased urinary urgency
  3. hypotension
  4. bladder cancer
  5. hyperkalemia

(This class of drugs is not indicated for type 1 diabetics)

72

(...) is a peptide produced by pancreatic β cells and cosecreted with insulin that has a role in the maintenance of glucose homeostasis.

amylin

73

(...) is an analogue of amylin that is approved in the United States.

pramlintide

74

(...) facilitate digestion of complex starches, oligosaccharides, and disaccharides into monosaccharides, allowing them to be absorbed from the small intestine.

α-glucosidases

75

What class of drug are the following?

  1. acarbose
  2. miglitol
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α-glucosidase inhibitors

76

α-glucosidase inhibitors are competitive, reversible inhibitors of intestinal (...), which delays (...).

α-glucosidases; absorption of carbohydrates

77

List the adverse effects of α-glucosidase inhibitors.

  1. flatulence
  2. diarrhea
  3. abdominal pain
  4. hypoglycemia*

*with concurrent sulfonylurea therapy

78

The gastrointestinal adverse effects of α-glucosidase inhibitors are due to (...).

undigested carbohydrates in the lower gastrointestinal tract

79

Treatment of hypoglycemia in patients taking α-glucosidase inhibitors should be with (...), because breakdown of (...) may be inhibited.

glucose; sucrose

80

Evidence suggests that interaction of insulin with its receptor leads to the release of (...), which enter the cell and act as mediators of insulin action.

IPGs

81

(...) and (...) have been shown to delay the onset and reduce significantly the progression of diabetic nephropathy.

ACE inhibitors; angiotensin II receptor blockers

82

(...) is synthesized in the α cells of the pancreatic islets.

glucagon

83

Glucagon increases blood glucose concentration by decreasing (...), stimulating (...), and increasing (...) in the liver.

glycogenesis; glycogenolysis; gluconeogenesis

84

Glucagon may be given parenterally in the emergency treatment of (...).

severe hypoglycemic reactions (sufficient to cause unconsciousness)

85

Major risk factors for type 2 diabetes are (...) and (...).

obesity; physical inactivity

86

List the oral complications of diabetes.

  1. oral paresthesias (e.g. burning mouth)
  2. increased susceptibility to infection
  3. delayed wound healing
  4. xerostomia
  5. increased incidence and severity of caries
  6. periodontal disease
  7. periapical abscesses
87

Morning appointments are usually better for diabetic patients because that minimizes the chance of (...).

stress-induced hypoglycemia

88

Since (...) may cause an increase in blood glucose levels, short appointments may be helpful in preventing an increase in blood glucose levels.

stress

89

It is suggested that the patient’s blood glucose should be less than (...) before any invasive therapy is started.

200 mg/dL

90

Use of local anesthetic with (...) may cause transient hyperglycemia.

epinephrine

91

(...) drugs have the potential to raise blood glucose levels.

glucocorticosteroid

92
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...

93
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...