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Exam 1 Pharm II > Diabetes Drugs > Flashcards

Diabetes Drugs Flashcards

1
Q

What are the criterion for diagnosing Diabetes?

A

A1C>or = 6.5%
Fasting glucose of > or = 126mg/DL
Plasma glucose>or = 200mg/dL

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2
Q

What is the pathophysiology of Type 1 Diabetes?

A

No functional insulin secreting pancreatic B-Cells. (Insulin dependent) Age of onset= 12 yrs

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3
Q

Type 2 diabets is normally associated with____________ and has a ___________ association.

A
  1. Obesity

2. Family history

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4
Q

How does Hyperlipidemia occur in diabetes?

A

Increased fatty acid mobilization from fat cells and increased fatty acid oxidation=====> Ketoacidosis.

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5
Q

Name 5 complications of diabetes

A
  1. Micro and macro angiopathies
  2. Neuropathy (Increased utilization of the polyol pathway (Aldose reductase)
  3. Nephropathy
  4. Ocular
  5. Increased infections.
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6
Q

What effect does hyperglycemia have on proteins?

A

Oxidation products of glucose react reversibly with proteins to form Advanced Glycation End-productsroducts (AGE)

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7
Q

What is Methylglyoxal?

A

It is an AGE precursur that inhibits vasorelaxation stimilated by ACh/NO

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8
Q

What is the role of the Alpha subunit of the insuline receptor?

A

It is the regulatory unit of the receptor. It represses the catalytic activity of the Beta subunit. Repression is relieved by insulin binding.

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9
Q

What is the role of the Beta subunit on the Insulin receptor?

A

It contains tyrosine-kinase catalytic domains. (Autophosphorylation)

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10
Q

Outline the cellular signaling mechanism for lipogenesis on insulin binding to a cell.

A

Insulin binds====> Autophosphorylation of heat shock proteins===>MAPK activation===> Lipogenesis

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11
Q

Outline the cellular signaling mechanism for Glycolysis on insulin binding to a cell.

A

Induline binds=====> Autophosphorylation====>PI3K====>PDK1=====>PKB====> glycolysis

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12
Q

What does insulin do to liver, muscle and Fat cells on binding?

A

Increases expression of GLUT receptors.

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13
Q

What GLUT receptor is located on Skeletal Muscle?

A

GLUT4

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14
Q

What GLUT receptor is located on Adipose tissue?

A

GLUT4

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15
Q

What GLUT receptor is located in the liver?

A

GLUT2

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16
Q

What effects does insulin have on the liver?

A

Inhibits: Glycohenolysis, Ketogenesis, Gluconeogenesis
Stimulates: Glycogen synthesis, Triglyceride synthesis.

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17
Q

What effect does insulin have on skeletal muscle?

A

Stimulates: Glucose transport, amino acid transport

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18
Q

What effect insulin have on Adipose tissue?

A

Stimulates: Triglyceride storage, glucose transport

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19
Q

What effect doe insulin have on free fatty acids in the blood?

A

It decreases serum FFA: Decreased FFAs enchance insulin action on skeletal muscle, reduce hepatic glucose production.

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20
Q

Glut 1 is expressed _______________

A

Constitutively and in every damn tissue one would say it is the #1 GLUT!

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21
Q

GLUT 2 is expressed_____________

A

Constitutively and is expressed in B-cells, and Liver.

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22
Q

GLUT 3 is expressed in the ______________

A

Constitutively and in neurons.

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23
Q

GLUT 4 is expressed in the _______________

A

It is insulin induced!!!!Skeletal muscle and adipose tissue.

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24
Q

Whaich of these GLUT receptors has the highest Km?

A

GLUT2

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25
Q

What do the A cells of the Islet of Langerhans cells secrete?

A

Glucagon

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26
Q

What do the D cells of the Islet of Langerhans cells secrete?

A

Somatostatin

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27
Q

What do the B cells of the Islet of Langerhans cells secrete?

A

Insulin and Amylin

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28
Q

What is the role of glucagon?

A

Stimulate glycogen breakdown.

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29
Q

What does somatostatin do?

A

General inhibitor of secretion

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30
Q

What does insulin do?

A

Stimulates uptake and utilization of glucose.

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31
Q

What does Amylin do?

A
  • Co-secreted with insulin and:
    1. Slows gastric emptying
    2. Decreases food intake
    3. Inhibits glucagon secretion.
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32
Q

How id insulin synthesized?

A

As a single peptide and deposited in secretory granules where it is cleaved into A, B, and C (Connecting) peptide.

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33
Q

Name two recombinant human insulins?

A

Humulin

Novolin

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34
Q

What are the Ultra rapid onset/Very short action insulins?

A

Lispro, Aspart, Glulisine (they certainsly don’t LAG behind)

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35
Q

Name the rapid onset/Short action Insulin

A

Regular insulin (“R”apid “R”egular)

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36
Q

Name one intermediate onset/action insulin

A

NPH

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37
Q

Name three Slow Onset/Long action insulins

A

Glargine, Detemir, Degludee (Slow is GooDD)-Yes this may be a dirty joke

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38
Q

NPH Insuline (N)= Nautral Protamine Hagedorn

A

Has Protamine as an insoluble complex, tissue proteases cleave insulin off…..this increases it’s absorption and duration of action

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39
Q

Lispro is a _________acting insulin

A

Ultra-rapid/Short duration (USe immediately before meals

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40
Q

Insuline Aspart is a _____________acting insulin

A

Ultra-rapid/Short duration (Use immediately before meals)

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41
Q

Insulin Glulisine is a _____________acting insulin.

A

Ultra-rapid/Short duration (Use immediately before meals)

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42
Q

Insulin Glargine is a_____________acting insulin

A

Slow onset/ Slow release (24hrs duration 1X a day)

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43
Q

Insulin Detemir is a ________________acting insulin

A

slow onset/ Slow release Insulin. It binds albumin serum extensively!

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44
Q

Degludec

A

slow onset/ Slow release Insulin. Binds albumin extensively. (the DD’s love albumin)

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45
Q

When are the fast onset, short acting insulins taken

A

Before meals

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46
Q

When are the long/Intermediate acting insulins taken?

A

At bedtime and after breakfast

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47
Q

Humalog what is it?

A

A mixed fast-onset and long acting insulin

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48
Q

How are insulins administered?

A

Sub Q, Insulin infusion pump. (Buffered regular, Lyspro, Aspart, Glulisine), IV for severe hyperglycemia or ketoacedosis.

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49
Q

Which insulin can you inhale?

A

Afrezza (it’s a powder)-Contraindicated in pats with COPD as may reduce lung function (FEV)

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50
Q

Insulin is used to treat…..

A
  1. Type 1 diabetics
  2. Pts w/ ketosis and hyperosmolar coma
  3. Some type 2 diabetics
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51
Q

What 3 actions does insulin have in the body?

A

Decrease liver glucose output
Increase fat storage
Increase glucose uptake

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52
Q

What are the adverse effects of insulin?

A

Hypoglycemia (Too much insulin/not enough food)

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53
Q

Some symptoms of hypoglycemia include…..

A

Weakness, Sweating, Hunger, Tachycardia, Increased irritability, tremor, blurred vision, seizures, coma, increased sympathetic output.

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54
Q

How is hypoglycemia treated?

A

Give them some damn glucose or glucagon.

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55
Q

What are some other adverse reactions to insulin?

A

Lipodystrophy
Lipoatrophy
Insulin resistance (immune response)

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56
Q

Name some agents that increase blood glucose in diabetics

A

Catecholamines, Glucocorticoids, oral conraceptives, thyroid hormone, calcitonin, Somatropin, Isoniazid, phenothiazides, morphine.

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57
Q

Agents that may increase risk for insulin hypoglycemia

A

ETHANOL! ACE inhibitors, fluoxetine, MAO inhibitors, anabolic steroids, B-adrenergic blockers.

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58
Q

How do you manage type 2 diabetes?

A

Diet+Exercise

Diet+Exersise+oral antidiabetic drugs and or GLP-1 Analogs

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59
Q

How do you manage type 1 diabetes?

A

Insulin+ Diet+ Exercise

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60
Q

What is the pathophysiology for type 2 Diabetes?

A

Insulin resistance. Beta-cells are still functional

61
Q

When are sulfonylureas used?

A

When patient has functional Beta-cells (Type 2 diabetes)

62
Q

How do sulfonylureas work?

A

They increase Beta cell sensitivity to glucose and increase glucose stimulated insulin release from Beta cells.

63
Q

What is the MOA of Sulfonylureas?

A

Bind Sulfonylurea receptor, inactivate K+channel, decrease cell polarization===> Activate Ca++ channel which causes influx of Ca++. Ca++ causes increased activity of microfilaments and exocytosis of insulin containing granules.

64
Q

What GLUT receptor do pancreatic Beta cells use to sense glucose levels?

A

GLUT2

65
Q

Increase in ATP in the Beta cell causes_______________Increase in ADP causes______________

A

The K+channel to open.

The K+ channel to close.

66
Q

Name the 3 first generation sulfonyl ureas

A

Tolbut(amide)
Tolaz(amide)
Chlorprop(amide)
(CTT)- My CaTT is #1

67
Q

What is the most potent 1st gen sulfonylurea?

A

Chlorpropamide (lasts long too 24-72hrs)

68
Q

What is the second most potent sulfonylurea?

A

Tolazamide (Lasts 12-14hrs)

69
Q

What is the least potent sulfonylurea?

A

Tolbutamide

70
Q

Name the 3 2nd gen sulfonylureas

A

Glipizide
Glyburide
Glimepiride (The 3G’s come second)

71
Q

What is the duration of the 2nd gen sulfonylureas?

A

~24 hrs.

72
Q

How do Meglinides work?

A

Exactly like sulfonylureas, they increase Insulin secretion by Beta cells of the pancreas.

73
Q

What is the difference between glinides and sulfonylureas? When are thy taken?

A

They have a quick onset and short duration of action. Taken before each meal.

74
Q

Give two examples of Meglinides

A

Nate(glinide)
Rapa(glinide)
“Nate the Rapa”

75
Q

How does Nateglinide work?

A

It is a K+-ATP Channel blocker. It is very specific for these channels in the pancreas and CV system.

76
Q

Which has a longer halflife; Rapaglinide or Nateglinide?

A

Rapaglinide (prandin)

77
Q

Which drug is synergistic with metformin?

A

Rapaglinide (prandin)

78
Q

What are the adverse effects of sulfonylureas?

A

Lasrting and prolonged hypoglycemia (due to long 1/2 life)
In elderly has caused permanent neurological damage (Brain needs glucose)
Weight gain

79
Q

What drugs may enhance action of sulfonylureas leading to increased risk for hypoglycemia?

A 
Salicylates
Phenylbutazone*
Sulfonamides*
Clofibrate*
* May decrease metabolism of sulfonylureas by liver.
80
Q

What effect does excessive alcohol and salicylates intake have on sulfonylurea?

A

Can cause severe hypoglycemic reaction

81
Q

Which drugs cause hyperglycemia (opposing action of sulfonylureas)?

A

Oral contraceptives, Corticosteroids, Thyroid, Epinephrine, Thiazide diuretics.

82
Q

What does GPL-1 do ?

A

It increases insulin secretion from the beta cells (Incretin effect)
Supresses glucagon secretion
Reduces food intake
Enchances glucose disposal
Improves glucose sensitivity
Slows gastric emptying
Increases Beta cell mass and maintains function

83
Q

Where is GLP-1 made?

A

In the L cells in the intestine.

84
Q

What role does PI3K play in the signaling of GLP?

A

It phosphorylation ERK1/2 and leads to gene transcription enabling beta cell proliferation.

85
Q

What happens to the GLP-! levels in Type 2 diabetes?

A

The GLP-1 levels may be decresed in type 2 diabetes.

86
Q

What strategies can be used to treat the decreased GLP-1 levels in type 2 diabetes?

A

Provide a long-lasting GLP-1 analog.

Prevent degradation of endogenous GLP-1

87
Q

What is Exenatide? How does it work?

A

Exenatide is a Glucagon-Like Peptide 1 analog. It activates the GLP-1 receptor and has a longer half-life than GLP-1. It is coadministered with metformin, TzDs or sulfonylureas

88
Q

What adverse side effects are associated with Exenatide?

A

Vomiting and increased risk for pancreatitis.

89
Q

What is Victoza (liraglutide)? What’s its 1/2 life?

A

Victoza is a Glucagon-Like Peptide 1 analog.

13hrs (inject 1x daily)

90
Q

What adverse effects are associated with Victoza use?

A

Nausea, Vomiting, pancreatitis, and risk of thyroid tumors (monitor calcitonin levels!!!)

91
Q

What should you monitor when prescibing a patient Victoza?

A

Monitor Calcitonin levels due to increased risk of thyroid tumors.

92
Q

What are the benefits of GLP-1 use?

A

Reduced hyperglycemia with low risk of hypoglycemia

93
Q

What is Tanzeum (Albiglutide)? Why is it special?

A

It is a GLP-1 analog. It is resistant to DDP-IV protease cleavage. It has a very long half-life. (Injected SubQ 1x a week)

94
Q

What is Dulaglutide? What risks are associated with it’s use?

A

It is a GLP-1 Analogue. Risk for C-cell tumors. Contraindicated in patients with a family hx of medullary thyroid cancer.

95
Q

What is Dipeptidyl Peptidase 4? (DPP4)

A

DPP-4 is the enzyme that degrades GLp-1

96
Q

Name 4 inhibitors of DPP-4. How do they work?

A 
Sita"glipin" (Januvia)
Saxa"gliptin" (Onglyza)
alo"gliptin" (Nesina)
lina"gliptin" (Tradjenta)   (JOiNT)
They enhance the activity of endogenous GLP-1 activity. Administered 1X daily!!
97
Q

How is Sitagliptin (Januvia) and Alogliptin (Nesina) metabolized and excreted?

A

Not extensively metabolized. Excreted in urine (kidney)

98
Q

How is Linagliptin (Trajent) metabolized and excreted?

A

Tragenta is not metabolized extensively and is excreted via feces (liver)

99
Q

What side effects are associated with DPP-IV inhibitors?

A

Nausea, Vomiting, Constipation, Headache, Severe skin Rxns, Decreased WBCs increases infection potential and cancer risk.

100
Q

How is Saxaglipin (Onglyza) metabolized and excreted?

A

CYP3A4/5, major metabolite is active. It is excreted in urine (kidney)

101
Q

What is Symlin? How does it work?

A

It is an amylin analog. Slows gastric emptying, decreses food intake, inhibits glucagon secretion.
Blunts postprandial rise in blood glucose. Used in conjunction with insulin (Sub Q injected)

102
Q

What are a-Glucosidase inhbitors?

A

Decrease absorption f carbohydrates from intestine by inhibiting a-glucosidases in the brushborder (Sucrase, Maltase, Glucoamylase)

103
Q

Give two examples of a-Glucosidase inhibitors.

A

Acarbose

Miglitol

104
Q

Which of the a-glucosidase inhibitors is fully absorbed?

A

Maglitol is fully absorbed. Acarbose only partially.

105
Q

What are the adverse side effects of Acarbose and Miglitol?

A

Diarrhea, Nausea, Flautulence

106
Q

What is the major side effect of high doses of Acarbose?

A

Liver damage.

107
Q

How do SGLT-2 Transporters work?

A

Lower threshold for glucose excretion in urine in order to reduce blood sugar levels.

108
Q

Name all SGLT2 inhibitors.

A 
Dapa(gliflozin)
Cana(glifozin)
Ipra(gliflozin)
Empa(gliflozin)
Tofo(gliflozin)
Luseo(gliflozin)
109
Q

What side-effects are associated with SGLT2 inhibitors?

A

Increased risk for genital/UTIs (increased sugar in urine)

110
Q

When are SGLT2 inhibitors indicated and contraindicated?

A

Indicated: Type 2 diabetics in conmbo with metformin and sulfonylureas.

111
Q

What effect is observed in diabetics on SGLT2 inhibitors?

A

Decreased A1c levels as a monotherapy and significant weight loss when used in combo. with metformin, sulfonylureas too

112
Q

Which SGLT2 is contraindicated in patients with bladde cancer?

A

Dapagliflozin.

113
Q

What causes insulin resistance? How is it detected?

A

Obesity, inactivity. It is detected via an oral glucose Tolerance test (OGTT) which will show prolonged elevation of plasma glucose even with elevated insulin levels.

114
Q

How does obesity cause insulin resistance?

A

Free fatty acid level elevation in obese people cause insuline resistance. (Effect is on insulin-stimulated glucose transport)

115
Q

What causes insuline resistance at a molecular level?

A

Serine instead of Tyrosine phosphorylation of Insuline receptors and IR-signaling proteins, Inhibits signaling. This is promoted by FA uptake, lipid by-products and inflammatory mediators

116
Q

What is metformin?

A

An oral antihyperglycemic agent used in Non-Insulin Dependednt Diabetes Mellitus. It decreases blood glucose concentrations.

117
Q

What advantages of metformin?

A

Rearly causes hypoglycemia

Rarely causes weight gain

118
Q

How does Metformin work?

A

It activates AMP-activated kinases (AMPK) . It increases efficiency and sensitivity to insulin in liver, fat and muscle cells.

119
Q

What does metformin do to the liver?

A

It decreases gluconeogenesis in the liver.

120
Q

What does metformin do to the muscle and fat cells?

A

Increased glycolysis and glucose uptake.

121
Q

What cellular effects does metformin have?

A

Inhibits mitochondrial respiration (Complex 1 inhibition)
Decreases energy availability
Causes decreased glucagon receptor expression
Increases AMPK
Decreases glucose production
Decreases lipid/cholesterol production

122
Q

When is metformin indicated?

A

In type 2 diabetics.

123
Q

What does Metformin do to skeletal muscle?

A

Increased exersize causes Increased AMP which activates AMPK. AMPK phosphorylates TBC1D1/4 which promotes GTPase activity of Rab-. Rab dissociates from GLUT4, allowing translocation to the skeletal muscle cell membrane.

124
Q

When is metformin contraindicated?

A

In disorders that increase lactic acidosis.

125
Q

What are the common side effects of metformin?

A

GI discomfort, Decreased Vitamin B-12 absorption
Decresed serum triglycerides
Decresed serum LDL

126
Q

What are Thiazolidinediones? How do they work?

A

They decrease insulin resistance or improve cell response to insulin. (They activate PPAR-Gamma, a TF)

127
Q

What do Thiazolidinediones do to Adipocytes, Liver and skeletal Muscle?

A

Adipocytes (main target)- Enhance adipocyte differentiation. Enhance FFA uptake into Sub-Q which reduces serum FFA.
Liver: Reduce hepatic glucose production, enhance glucose uptake
Sk. Musckle: Enhance glucose uptake.

128
Q

Name two Thiazolidinediones

A

Rosi(glitazone)

Pio(glitazone)

129
Q

What are the adverse effects of Thiazolidinediones (TZDs)?

A

Cardiovascular toxicity
Pioglitazone is assoc. with increased bladder cancer.
Hepatotoxicity
Contraindicated in CHF

130
Q

What is the major risk associated with Pioglitazone?

A

Increased bladder cancer.

131
Q

What factors regulated by PPAR-gamma are increased in type 2 diabetes?

A

Resistin

TNFa

132
Q

What factors regulated by PPAR-gamma are decreased in type 2 diabetes?

A

Adiponectin

133
Q

What is leptin?

A

It is an adipokine. It signals a fed state to the brain. It is elevated in Type 2 diabetes/Obesity (can’t sense it). If missing leptin, you will be obese and diabetic

134
Q

What adipokines are elevated in Obesity/Type 2 diabetes?

A

Leptin
Angiotensinogen
Plasminogen Activaor Factor Inhibitor 1 (PAI-1)

135
Q

Which drug class drecreases differentiation of mesencymal stem cells into osteoblasts?

A

Thiazolidinediones (TdZs)

136
Q

What happens to insulin levels in early pregnancy and late pregancy? Why?

A

Early: Increased insuline sensitivity (Growth of placenta, increase fat storage)
Late pregnancy: Reduced sensitivity (Growth of Fetus)

137
Q

When does gestational diabetes appear?

A

Week 24, In the rapid growth phase of gestatiotion

138
Q

What can haen to the baby due to gestational diabetes?

A

The fetus can have macrosomia (Fat Baby)

139
Q

Does insulin cross the placenta?

A

No

140
Q

Does glucose cross the placenta?

A

Yes

141
Q

What do glucocorticoids do to insulin?

A

They oppose insulin action.

142
Q

What placental hormones are suspected in gestational Insulin resistance?

A

CRH- Cortisol
Progesterone
Placental GH (GH-V)-May contribute to insulin resistance
Placental Lactogen (PL)-Contribites to insulin resistance

143
Q

What does prolactin do during pregnancy?

A

It stimulates Beta-cell proliferation

144
Q

Where is Adiponectin produced?

A

In fat cells and is inversely correlated wtith Gestational diabetes mellitus

145
Q

Wheere is TNF-Alpha prodused?

A

By the placenta, directly correlated with insulin sensitivity.

146
Q

Resistin

A

Produced by the placenta no role in GDM

147
Q

Leptin

A

Produced in fatcells and placenta correlated with reduced insulin sensitivity

148
Q

How is gestational diabetes treated?

A

Diert
Insulin
Glyburide (may cross placenta)
Metformin (may cross placenta)

149
Q

Can you use Thiazoladinediones in gestational diabetes?

A

NOOOOOOO IT’S TERATOGENIC!!! Heck it just sounds evil.

Exam 1 Pharm II (8 decks)

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