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Pharm II > Pancreatic Hormones & antidiabetic drugs-DONE > Flashcards

Pancreatic Hormones & antidiabetic drugs-DONE Flashcards

0
Q

hyperglycemic factor that mobilized glycogen

A

glucagon

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1
Q

involved in storage and anabolic hormone of the body

A

insulin

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2
Q

modulates appetite, gastric emptying, insulin, and glucagon secretion

A

amylin

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3
Q

stimulates gastric acid secretion

A

gastrin

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4
Q

universal inhibitor of secretory cells

A

somatostatin

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5
Q

facilitates digestive processes

A

pancreatic peptide

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6
Q

proinsulin = _____

A

A & B chains linked by C-peptide

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7
Q

what is synthesized and stored in B-cells of pancreas?

A

insulin

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8
Q

describe the release of insulin

A

it has a slow basal release of 5-15 uU/ml but rapid release of 60-90 uU/ml upon stimulation

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9
Q

What are some stimulants of insulin?

A
  1. glucose and other sugars
  2. amino acids
  3. glucagon-like peptide
  4. glucagon
  5. cholecystokinin
  6. vagal nerve stimulation
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10
Q

What are the inhibitors or insulin?

A
  1. somatostatin
  2. leptin
  3. chronically elevated glucose or amino acid levels
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11
Q

Almost all tissues have insulin receptors but primary tissues are…

A

liver, adipose, and skeletal muscle

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12
Q

What are the physiological and signaling effects of insulin at the liver?

A

inhibits glucose production (gluconeogensis and glyogenolysis), promotes glucose storage

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13
Q

What are the signaling and physiological effects of insulin at the muscle?

A

increase glucose uptake

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14
Q

What is the signaling and physiological effects of insulin in adipose?

A

increase TG storage and glucose uptake

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15
Q

Which insulin receptor regulation insulin release from b-cells?

A

GLUT2

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17
Q

Which receptor is involved with insulin stimulated glucose uptake in glucose disposing tissue?

A

GLUT4

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18
Q

Which type of diabetes mellitus is due to autoimmune dysfunction where B-cells are destroyed?

A

T1DM

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19
Q

Witch T1DM what can you expect the levels of insulin and glucose to be in the blood?

A

hyperglycemia (>126 mg/dL fasting)

hypoinsulinemia

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20
Q

90-95% of cases of DM involves which type?

A

T2DM

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21
Q

T2DM is highly associated with ______.

A

obesity and dyslipidemia

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22
Q

T/F: With T2DM, exogenous insulin may or may not be required depending on degree of resistance and effect of sensitizers.

A

TRUE

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23
Q

What lifestyle changes are often beneficial with treating T2DM?

A

dietary intervention and exercise

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24
Q

hyperglycemia during pregnancy with NO prior history = _____.

A

gestational diabetes

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25
Q

What induces insulin resistance in gestational diabetes?

A

placenta and placental hormones

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26
Q

What is the most common complication of insulin therapy?

A

hypoglycemia

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27
Q

_____ develops in people with frequent hypoglycemic episodes.

A

hypoglycemic unawareness (normal symptoms of hypoglycemia are absent)

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28
Q

How is hypoglycemia treated?

A

with oral or IV glucose

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29
Q

What causes immune insulin resistance?

A

Anti-insulin IgG antibodies neutralize insulin

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30
Q

What is the first line of therapy for T2DM?

A

Biguanides (Metformin)

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31
Q

What is the primary MOA of Metformin (Glucophage)?

A

it decreases hepatic glucose production by activating AMP-activated protein kinase (AMPK)

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32
Q

What are the secondary effects of Metformin (Glucophage)?

A

increases insulin sensitivity in the skeletal muscle, decrease renal gluconeogensis, slow glucose absorption from GI, and reduces plasma glucagon

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33
Q

T/F: Metformin depends on functioning beta cells

A

FALSE (does NOT)

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34
Q

Does metformin (Glucophage) cause hypoglycemia?

A

NO!! pts are euglycemic

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35
Q

What are the adverse effects of Metformin (Glucophage)?

A

N/V/D, anorexia, lactic acidosis, decreased B12 absorption

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36
Q

Sulfonylureas = ____

A

insulin secreatogues

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37
Q

What is the MOA of sulfonylureas?

A

binds to ATP sensitive inward rectifier K+ channel in B-cells blocking K+ efflux, depolarizing cell, Ca 2+ influx, insulin secretion

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38
Q

Major adverse effect of sulfonylureas = ___.

A

hypolgycemia

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39
Q

T/F: Weight gain secondary to increased adipose insulin sensitivity occurs with sulfonylureas.

A

TRUE

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40
Q

What is the major differences between the two generations of sulfonylureas?

A

potency and adverse effects (2nd generation is more potent with less adverse effects)

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41
Q

What are the three second generation sulfonylureas?

A
  1. glyburide
  2. glipizide
  3. glimepiride
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42
Q

A 45 yr old WM present with obesity, polyuria, polydipsia, and hyperglycemia. You decide to place him on a sulfonylurea but you notice it is stated in his record that he has renal insufficiency. Which sulfonylurea is best for this patient?

A

Glimepiride

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43
Q

What are the principal types of injected insulin?

A

rapid acting
short acting
intermediate acting
long acting

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44
Q

Which type of injectable insulin is used for physiologic prandial replacement?

A

rapid acting

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45
Q

What was the first monomeric insulin analog marketed?

A

Humalog (insulin Lispro)

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46
Q

Which type of injectable insulin has a 30 min onset and makes a SQ depot with three rates of absorption because hexamers must be diluted with ECF?

A

Short acting insulin

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47
Q

When must short acting injectable insulins be administered?

A

30-45 min. before meals

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48
Q

Which type of injectable insulin is the only insulin preparation that should be given IV?

A

short acting insulin

49
Q

NPH insulin = ____.

A

intermediate acting insulin

50
Q

Which type of injectable insulin is used to provide basal replacement?

A

long acting insulin

51
Q

Which long acting injectable insulin is soluble in acidic solutions but precipitates at physiological pH? It forms a depot where molecules slowly dissolve away.

A

Insulin glargine (Lantus)

52
Q

Which long acting insulin is usually given once daily but can be given BID for insulin sensitive or resistant patients?

A

insulin glargine (Lantus)

53
Q

Which long acting injectable insulin has the most reproducible effect of the NPH and long acting insulins with less hypoglycemia than NPH?

A

insulin detemir (Levemir)

54
Q

Which long acting injectable insulin lasts the longest?

A

insulin detemir (Levemir)

55
Q

Which treatment regimen is thought to achieve tighter gylcemic control and prevent long term end organ complications?

A

intensive

56
Q

Which treatment regimen with insulin typically calls for more injections but is more physiologically relevant?

A

intensive

57
Q

Which treatment regimen with insulin is known as the “sliding scale”?

A

conventional

58
Q

Which type of DM is conventional treatment regimen with insulin usually more beneficial?

A

T2DM

59
Q

Which treatment regimen with insulin allows for more meal flexibility?

A

intensive

60
Q

How is the total daily insulin requirement determined with intensive treatment with insulin?

A

body wt. (lbs)/4

(1/2 of daily insulin requirement is typically administered as a long acting insulin to cover basal insulin requirement. Remainder covers meal and snack requirements)

61
Q

What are meal and snack insulin boluses calculated bases on for intensive treatment with insulin?

A

based on carbohydrate load of meal

insulin to carbohydrate ratio

62
Q

Which treatment regimen with insulin usually involves a fixed dose of long acting insulin?

A

conventional

63
Q

Which insulin treatment regimen can involve a variable dose of short or rapid insulin depending on blood glucose and not meal carbohydrate content?

A

conventional

64
Q

This insulin treatment regimen typically utilizes insulin pumps or pens for injections because of ease?

A

intensive

65
Q

Like sulfonylureas, which other oral antihyperglycemics inhibit ATP sensitive inward rectifier K+ channel on B-cells?

A

Meglitinides

66
Q

Of the 2 Meglitinides, which one is approved for monotherapy or in combo with metformin?

A

Repaglinide (Prandin)

67
Q

Which meglitinide causes amplified insulin secretion in response to glucose BUT diminished effect in euglycemia?

A

Nateglinide (Starlix)

[has less rebound hypoglycemia than other secretagogues]

68
Q

Which Meglitinide has a longer duration of action?

A

Repaglinide (Prandin) [5-8 hrs]

69
Q

What is the mechanism of action of Meglitinides?

A

like sulfonylureas, inhibit ATP sensitive inward rectifier K+ channel on beta cell
- bind to different sites on the channel

70
Q

What are two oral antihyperglycemic Meglitinides?

A

Repaglinide

Nateglinidide (D-Phenylalanine derivative)

71
Q
  1. What is the peak of Repaglinide?
  2. How long does it last?
  3. Where is it metabolized?
A
  1. peak after 1 hour
  2. lasts 5-8 hours
  3. hepatic metabolism
72
Q

What is Repaglnide used for clinically?

A

b/c of its rapid onset it is indicated for controlling post prandial glucose excursions

73
Q

When should Meglitinides be taken?

A

before meal

74
Q

In a hyperglycemic patient that is allergic to sulfer, what is the alternative oral medication for this patient?

A

Repaglinide

75
Q

Repaglinide can be used alone or in combination. What drug can it be used in combination with?

A

biguanides

76
Q

Which drug used to treat hyperglycemia is a D-phylalanine derative?

A

Nateglinide

77
Q

What are the two mechanisms by which Nateglinide restores euglycemia?

A

increase insulin secretion from beta cells by closing ATP-sensitive potassium channels
Partially Restores initial insulin in response to glucose IV tolerance test

78
Q

Is Nateglinide useful in treating fasting glucose levels and post-prandial hyperglycemia?

A

NO!! only post-prandial hyperglycema

79
Q

Nateglinide can be used alone or in combination with what other drug?

A

can be given with a nonsecretous oral agent (Metformin)

80
Q

What is the one thing that Nateglinidie does not require that most other diabetic drugs do?

A

DOSE TITRATION NOT REQUIRED

  • **less rebound hypoglycemia
  • *amplified insulin secretion in response to glucose BUT diminished effect in euglycemia
81
Q

What is the peak of Nateglinide?
How long does it last?
Where is it metabolized?

A

peak in less than one hour
lasts less than 4 hours
hepatic metabolism

82
Q

What is the mechanism of action of Thiazolidinediones?

Name the two discussed in lecture.

A

reduce insulin resistance (insulin sensitizers)
ligand of peroxisome proliferator-activated receptor -gamma (PPAR-gamma)
-mediate the expression of genes involved in lipid and glucose metabolism, insulin signal transduction, and adipocyte and other tissue differentiation
1. Pioglitizone and Rosiglitazone

83
Q

What is the primary effect of Thiazolidinediones in diabetic patients?

A

increase insulin sensitivity in adipose;

84
Q

Where are PPAR-gamma receptors found?

A

liver, muscle, fat

85
Q

Where are Pioglitizone and rosiglitazone (Thiazolidinediones) metabolized?

A

liver

86
Q

What is Pioglitizone specificially metabolized by?

A

CYP 3A4 ….. and

book: CYP2C8

87
Q

What are Rosiglitazone specifically metabolized by?

A

CYP2C8 and to a lesser extent CYP2C9

88
Q

Which Thiazolidinediones has a triglyceride lowering effect that is aboserved more than the other becasue of PPAR-alpha binding?

A

Pioglitizone

89
Q

What is the effect of food taken with Pioglitizone?

A

may slow down absorption, but will NOT effect bioavailability

90
Q

A 23 year old woman with comes in complaining to heat intolerance, weight gain, deceased appetite, labs showed increase in T4. Patient is currently taking daily dose of vitamin D, fish oil, adderall, and oral contraceptive yaz. You prescribe the patient Piglitizone. What drug interaction would u advise this patient on when prescribing Piglitizone based on her patient history?

A

Drug interaction with oral contraceptive; PA should advice use of alternate contraceptive

91
Q

Prioglitizone can be used alone or in combination with what other drug in treatment for Type 2 Diabetes?

A

metformin, sulfonyureas, and insulin for treatment of type 2 diabetes

92
Q

What is a major adverse effect of Rosiglitazone?

A

Cardio Vascular Disease

93
Q

What are the adverse effects associated with Thiazolidinediones?

A

weight gain, edema, increased risk of heart failure, increased bone fracture in women

94
Q

What is the mechanism of action of Alpha-glucosidase inhibitors?
Name the two drugs from lecture.

A

ALpha-glucosidase breaks down starches and other polysaccharides into monosaccharides for absorption at intestinal brush border.
BLOCKING THIS minimizing upper intestinal digestion and defers digestion (and thus absorption) of the ingested starch and disaccarides to the distal small intestine, thereby lowering post meal glycemic excursions, creating an INSULIN SPARING effect.

Drugs: Miglitol and Acarbose

95
Q

Slides: T/F Alpha Glucosidase inhibitors reduce post-meal glucose increases by delaying absorption.

A

TRUE!!!!

96
Q

What are the adverse effects of Acarbose and miglitol? What causes these adverse effects?

A

Flatulence, Diarrhea, and abdominal pain due to undigested carbohydrates in the colon that ferment producing gasess

97
Q

T/F Alpha Glucosidase Inhibitors may prevent diabetes in prediabetics.

A

TRUEEEEE

98
Q

In type 2 diabetes, the release of glucagon-like polypeptide is diminished postprandially, which leads to inadequate glucagon suppression and excessive hepatic glucose output. Two synthetic anoalots of glucagon like polypeptide, ______ and ______ are commercially available to help RESTORE GLP-1 activity.

A

Exenatide (Byetta) and Liraglutide (Victoza)

99
Q

What are the 4 effects of Exenatide (Byetta) and Liraglutide (Victoza)?

A
  1. increase in glucose dependent insulin secretion
  2. decrease in glucagon secretion
  3. slows gastric emptying
  4. decrease in appetite
100
Q

What are the adverse effects of “Incretin Therapy” ?

Incretin therapy = Exenatide (Byetta) and Iiraglutide (Victoza)

A

nausea (44% of patients; usually decreases with extended use), vomiting, diarrhea
***WEIGHT LOSS in some patients

101
Q

What are the three inhibitors of DPP-4, the enzyme that degrades incretin hormones, used to treat Type 2 daibetic patients?

A
  1. Sitagliptin (Januvia)
  2. Saxagliptin (onglyza)
  3. Linagliptin (tradjenta)
102
Q

What are the 3 effects of DPP-4 Inhibotors in treating Type 2 Diabetic Patients?

A
  1. Increase circulating levels of native GLP-1 and GIP levels
  2. Decreases post prandial glucose
  3. Decrease glucagon levels
103
Q

T/F Monotherapy of DPP-4 Inhibitors cause hypoglycemia in Type 2 diabetic patients.

A

false! .. THEY DO NOT

104
Q

What are the adverse effects associated with DPP-4 Inhibitors?

A

Nasopharyngitis, upper respiratory infections, headache

105
Q

When is glucagon give in treatment of hypoglycemia?

A

severe hypoglycemia when oral or IV glucose is not an option

106
Q

How is glucagon administered?

A

IM, IV, or SC

107
Q

What is the MOA of Glucagon?

A

promotes hepatic glycogenolysis, increases gluconeogenesis

—–Glycogenolysis is primary, immediate effect

108
Q

T/F Glucagon increases blood glucose transiently.

A

true

109
Q

What are the adverse effects of Glucagon?

A

Transient nausea, vomiting…generally mild

110
Q

What is an injectable amylin analog?

A

Pramlintide

111
Q

What is the effect of Pramlintide?

A
  1. slows gastric emptying
  2. reduces postprandial glucagon release
  3. promotes satiety
112
Q

When is Pramlintide administered?

A

before meals

113
Q

What is the most common adverse effect of Pramlintide?

A

nausea

114
Q

T/F Pramlintide can cause hypoglycemia when administered with other antihyperglycemics, and dosage of other insulin secretagogues or insulin may need to be decreased.

A

TRUE

115
Q

What is the MOA of SGLT2?

A

increases urinary glucose secretion by inhibiting sodium glucose co-transporter 2.

116
Q

When is SGLT2 taken?

A

taken prior to first meal of the day

117
Q

What is first in class of SGLT2?

A

Canagliflozin

118
Q

In what patient is SGLT2 contraindicated in?

A

severe renal impairment

119
Q

What are the adverse effects of SGLT2?

A

polyuria, UTI, mycosis

Pharm II (13 decks)

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