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Pharmacology Test #5 > Insulin and Diabetes > Flashcards

Insulin and Diabetes Flashcards

1
Q

Criteria for the Diagnosis of Diabetes

A
  1. A1C greater than or equal to 6.5%
  2. Fasting plasma glucose greater than or equal to 126 mg/dL
  3. 2-h plasma glucose greater than 200 mg/dL during an OGTT
  4. A random plasma glucose greater than 200 mg/dL
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2
Q

Glucose intolerance in type 1 diabetes characterized by

A

no functioning insulin-secreting pancreatic beta cells, dependency on exogenous insulin and a tendency towards ketoacidosis

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3
Q

Type 1 diabetes is thought to be caused by

A

antibodies that destroy pancreatic beta cells that may be triggered by viruses, chemicals etc. in genetically predisposed individuals

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4
Q

Role of glucagon

A

increased glucagon levels in the presence of increased blood glucose levels

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5
Q

Hyperlipidemia in diabetes

A

increased fatty acid mobilization from fat cells; increased fatty acid oxidation - ketoacidosis

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6
Q

What happens in hyperglucemia (due to lack of insulin)

A
  1. decreased glucose uptake in cells where glucose uptake is insulin-dependent
  2. decreased glycogen synthesis
  3. increased conversion of amino acids to glucose
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7
Q

Cardiovascular complications from diabetes

A

micro and macro angiopathies

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8
Q

Neuropathy complications from diabetes

A

increased blood glucose levels lead to increased utilization of the polyol pathway (Aldose Reductase); increased cytosolic water in neural cells

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9
Q

Nephropathy complications from diabetes

A

renal vascular changes and changes in the glomerular basement membrane

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10
Q

Ocular complications from diabetes

A

cataracts, retinal microaneurysms and hemorrhage

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11
Q

Increased susceptibility to what? with diabetes

A

increased susceptibility to infections

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12
Q

Conventional therapy goals of insulin therapy and monitoring

A

reduce acute symptoms - polyuria, dehydration and ketoacidosis

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13
Q

Intensive therapy goals of insulin therapy and monitoring

A

keep blood glucose levels below 150 mg/dL; prevent/delay onset of complications; increased risk of hypoglycemia

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14
Q

Oxidation products of glucose react irreversibly with proteins to form

A

Advanced glycation end-products (AGE)

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15
Q

Advanced glycation end-products (AGE) results in

A

loss of normal protein function; acceleration of aging process; theorized to account for many long-term complications of diabetes

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16
Q

AGE precursor, methylglyoxal, inhibits

A

vasorelaxation stimulated by acetylcholine/NO

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17
Q

Role of the alpha subunits in the insulin receptor

A

regulatory unit of the receptor; represses the catalytic activity of the beta subunit; repression is relieved by insulin binding

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18
Q

Role of the beta subunits in the insulin receptor

A

contain the tyrosine kinase catalytic domains (autophosphorylation)

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19
Q

Insulin effects on the liver

A

inhibits: glycogenolysis; ketogenesis; and gluconeogenesis
stimulates: glycogen synthesis and triglyceride synthesis

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20
Q

Insulin effects on the skeletal muscle

A

glucose transport; amino acid transport

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21
Q

Insulin effects of the adipose tissue

A

triglyceride storage and glucose transport

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22
Q

Glucose disposal in a fasting state

A

75% is non-insulin dependent (Liver, GI, brain)

25% is insulin-dependent (skeletal muscle)

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23
Q

Glucagon is secreted in a fasting state to prevent

A

hypoglycemia

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24
Q

Glucose disposal in a fed state

A

80-85% is insulin-dependent (skeletal muscle)
4-5% is insulin-dependent in adipose tissue
Glucagon secretion is inhibited

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25
Q

In a fed state, insulin inhibits the release of what?

A

inhibits release of FFA from adipose tissue

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26
Q

What does decreased serum FFA regulate?

A

enhances insulin action of skeletal muscle; reduces hepatic glucose production

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27
Q

GLUT1

A

constitutive; widely expressed

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28
Q

GLUT2

A

constitutive; beta-cells and liver

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29
Q

GLUT3

A

constitutive; neurons

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30
Q

GLUT4

A

insulin-induced; skeletal muscle and adipocytes

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31
Q

Pancreatic polypeptide hormones

A

glucagon; somatostatin; insulin; amylin

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32
Q

Actions of glucagon

A

Stimulates glycogen breakdown; increases blood glucose

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33
Q

Actions of somatostatin

A

general inhibitor of secretion

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34
Q

Actions of insulin

A

stimulates uptake and utilization of glucose

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35
Q

Actions of amylin

A

co-secreted with insulin; slows gastric emptying; decreases food intake; inhibits glucagon secretion

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36
Q

Where is insulin synthesized?

A

synthesized as a single peptide and deposited in secretory granules in the beta cells

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37
Q

What happens to insulin in the beta cell secretory granules?

A

insulin is cleaved to A and B chains, and C (connecting) peptide by proconvertases

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38
Q

Human insulin cDNA in plasmid expressed in E. coli

A

Humulin

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39
Q

Human insulin cDNA in plasmid expressed in transformed yeast

A

Novolin

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40
Q

Units/concentration of insulin

A

100 units/ml

28 units/mg insulin

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41
Q

Lispro

A

Humalog

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42
Q

Aspart

A

Novolog

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43
Q

Glulisine

A

Apidra

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44
Q

Glargine

A

Lantus

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45
Q

Detemir

A

Levemir

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46
Q

Degludec

A

Tresiba

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47
Q

Ultra rapid onset/very short action insulins

A

Lispro (Humalog); Aspart (Novolog); Glulisine (Apidra)

48
Q

Rapid onset/short action insulin

A

Regular

49
Q

Intermediate onset/action insulin

A

NPH

50
Q

Slow onset/long action insulin

A

Glargine (Lantus); Detemir (Levemir); Degludec (Tresiba)

51
Q

What happens when you delay the absorption of insulins

A

prolong the onset and duration

52
Q

What happens when you increase the absorption of insulins

A

decrease time to onset and duration

53
Q

Absorption and duration of action of NPH

A

slow absorption, long duration of action

54
Q

What decreases the self-association of Lispro (Humalong)?

A

reversing positions of P28 and K29 on insulin B chain

55
Q

Onset of Humalog (Lispro) compared to regular insulin

A

regular: 30-60 minutes
Lispro: 5-15 minutes

56
Q

Difference between human insulin and Aspart (Novolog)

A

Proline 29 in B chain is switched to Aspartate

57
Q

Onset of Aspart (Novolog)

A

rapid onset: 5-15 min, short duration

58
Q

Difference between human insulin and Glulisine (Apidra)

A

Asn 3 and Lys 29 in B chain are switched to Lys and Glu

59
Q

Difference between human insulin and Glargine (Lantus)

A

Asn 21 of alpha-chain is changed to Gly

2 Arg residues added to the end of the beta-chain

60
Q

Difference between human insulin and Detemir (Levemir)

A

Thr 30 of beta-chain is deleted, and Lys 29 is myristylated

Binds serum albumin extensively

61
Q

Difference between human insulin and Degludec (Tresiba)

A

Thr 30 of beta-chain is replaced by gamma-Glu/C16 fatty acid

Binds serum albumin extensively

62
Q

Routes of administration for insulins

A
  1. subcutaneous - all preparations
  2. insulin infusion pump - rapidly acting
  3. IV - regular
  4. Inhalation - Afrezza
63
Q

Afrezza (Regular Human Insulin) is contraindicated in which patients?

A

contraindicated in patients with asthma and COPD; may reduce lung function (decrease FEV)

64
Q

Inhaled insulin

A

Afrezza

65
Q

Types of patients using insulin

A
  1. Type 1 diabetics
  2. Patients with ketosis and hyperosmolar coma
  3. Some Type II diabetics
66
Q

Mode of action of insulin in a diabetic patient

A
  1. decreased liver glucose output
  2. increase fat storage
  3. increase glucose uptake
67
Q

Hypoglycemia treated with

A

glucose or glucagon

68
Q

Adverse reactions to insulin

A

Lipodystrophy; lipoatrophy; insulin resistance

69
Q

lipodystrophy

A

lump of fat at overused injection site

70
Q

lipoatrophy

A

concavities in subcutaneous tissue

71
Q

insulin resistance

A

immune response to insulin

72
Q

Agents that increase blood glucose in diabetics

A

catecholamines; glucocorticoids; oral contraceptives; thyroid hormone; calcitonin; somatropin; isoniazid; phenothiazines; morphine

73
Q

Agents that increase the risk of insulin hypoglycemia

A

ethanol; beta blockers; ACE inhibitors; fluoxetine; somatostatin; anabolic steroids; MAO inhibitors; exercise

74
Q

Overview of treatment of type II diabetes

A
  1. Diet + exercise
  2. Diet + exercise + oral antidiabetic drugs/GLP-1 analogs
  3. Diet + exercise + insulin
75
Q

Effects of sulfonylurea receptors

A
  1. binds to sulfonylurea receptors
  2. inactivates K+ channel
  3. decreased cell polarization
  4. activates voltage sensitive Ca2+ channels
  5. increase Ca2+ and activity of microfilaments
  6. increased exocytosis of insulin containing granules
76
Q

1st generation sulfonylureas

A
  1. Tolbutamide
  2. Tolazamide
  3. Chlorpropamide
77
Q

2nd generation sulfonylureas

A
  1. Glipizide
  2. Glyburide/Glibenclamide
  3. Glimepiride
78
Q

Repaglinide

A

a non-sulfonylurea hypoglucemic agent

79
Q

Sulfonylureas vs. “Glinides”

A
  1. mechanism of action is the same
  2. glinides have a quick onset and a short duration of action
  3. glinides are taken before each meal
80
Q

Starlix (Nateglinide)

A

non-sulfonylurea Katp channel blocker

81
Q

Starlix (Nateglinide) is synergistic with

A

metformin

82
Q

Adverse effects of sulfonylureas

A

lasting and prolonged hypoglycemia (due to long half life); G.I. problems; weight gain and increased numbers of secondary failures

83
Q

Lasting and prolonged hypoglycemia with sulfonylureas has been mistaken for what in the elderly?

A

has been misdiagnosed as stroke and has lead to permanent neurological damage and death with elderly patients

84
Q

Drugs which may enhance the action of sulfonylureas and increase the risk of hypoglycemia

A

salicylates; phenylbutazone; sulfonamides; clofibrate

85
Q

Drugs having their own hypoglycemic effects which may be additive to the sulfonylureas

A

alcohol (associated with severe sulfonylurea hypoglycemic reactions); and high dise salicylates

86
Q

Drugs which cause hyperglycemia which in turn oppose the action of sulfonylureas and insulin therapy

A

oral contraceptives; epinephrine; thiazide diuretics; corticosteroids; thyroid

87
Q

The incretin effect

A

oral glucose stimulates a larger insulin response than IV glucose in humans

88
Q

Why does the incretin effect happen?

A

GLP-1 (from the L-cells in the intestine) potentiates excitation-secretion and excitation-transcription coupling in the beta-cell

89
Q

The incretin effect is diminished in which patients

A

Type II diabetic patients

90
Q

Benefits of GLP-1 analog treatment in type II diabetics

A

reduce hyperglycemia with low risk of hypoglycemia; weight loss; increase beta cell mass(?)

91
Q

GLP-1 analogs

A

Exenatide; Victoza (Liraglutide); Tanzeum (Albiglutide); Dulaglutide (Trulicity)

92
Q

Exenatide co-administered with

A

metformin, TzDs, or sulfonylureas

93
Q

Adverse effects of Exenatide

A

nausea and vomiting; risk of pancreatitis

94
Q

Victoza (Liraglutide) co-adminstered with

A

metformin, TzDs, and sulfonylureas

95
Q

Adverse effects of Victoza (Liraglutide)

A

nausea and vomiting, pancreatitis, risk of thyroid tumors - monitor calcitonin levels

96
Q

Adverse effects of Dulaglutide (Trulicity)

A

risk of thyroid C-cell tumors, contraindicated in patients with a family history of medullary thyroid cancer

97
Q

Inhibitors of Dipeptidyl Peptidase 4 (DPP-4) - the enzyme that degrades GLP-1

A

Januvia (Sitagliptin); Onglyza (Saxagliptin); Tradjenta (Linagliptin); Nesina (Alogliptin)

98
Q

Side effects of DPP IV inhibitors

A

nausea, vomiting, constipation, headache, severe skin reactions; reduced WBC counts (infections); potential increased risk of cancers

99
Q

Symlin (Pramlintide) is what kind of analog

A

amylin analog

100
Q

MOA of alpha-glucosidase inhibitors

A

decrease the absorption of carbohydrate from the intestine via inhibition of gut alpha-glucosidases on the brush border (sucrase, maltase, glucoamylase)

101
Q

Strategy for inhibition of sodium glucose transporter 2 (SGLT2)

A

decrease the threshold for glucose excretion in urine; reduce blood glucose levels

102
Q

SGLT2 inhibitors

A

Dapagliflozin; Empagliflozin; Canagliflozin

103
Q

Adverse effects of Canagliflozin

A

increase risk of genital/UT infections; increased urine flow/volume depletion; increased risk of hypoglycemia with SU and insulin; contraindicated in patients with renal impairement

104
Q

Do not use Dapagliflozin in patients with

A

bladder cancer

105
Q

Causes of insulin resistance

A
  1. Polymorphisms in insulin signaling pathway proteins (rare)
  2. Obesity - especially accumulation of fat in the abdominal cavity
  3. inactivity
106
Q

Role of fatty acids in obesity-induced insulin resistance

A

FFA levels are increased in obese people; acutely raising FFA levels causes insulin resistance; acute lowering of plasma FFA levels reduces chronic IR

107
Q

Oral antidiabetic drugs - non-hypoglycemic agents

A

Metformin

108
Q

Advantages of biguanides over sulfonylureas

A

rarely causes hypoglycemia; rarely causes weight gain

109
Q

MOA of metformin

A

activator of AMP-activated kinase (AMPK); increase the efficiency of sensitivity to insulin in liver, fat and muscle cells

110
Q

Metformin contraindications

A

contraindicated in those disorders which increase the tendency toward lactic acidosis

111
Q

metformin effects on blood lipid profile

A

decreased serum triglycerides; decreased serum LDL

112
Q

Thiazolidinediones

A

Rosiglitazone (Avandia); Pioglitazone (Actos)

113
Q

MOA of Thiazolidinediones

A

decrease insulin resistance or improve target cell response to insulin (activators of PPARy)

114
Q

Main target of Thiazolidinediones

A

adipocytes - enhances adipocyte differentiation; enhances FFA uptake into subQ fat; reduces serum FFA; shifts lipids into fat cells from non-fat cells

115
Q

Why is thiazolidinedione prescribing restricted?

A

due to cardiovascular toxicities; both are contraindicated in CHF

116
Q

Factors regulated by activation of PPARy

A

Resistin; Adiponectin; TNFalpha; Leptin; Angiotensinogen; Plasminogen Activator Inhibitor 1

Pharmacology Test #5 (11 decks)

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