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MDCM626 > Oral Hypoglycemics > Flashcards

Oral Hypoglycemics Flashcards

1
Q

What are the 3 possible modes of actions for oral hypoglycemics?

A
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2
Q

5 oral hypoglycemic agents

A
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3
Q

Sulfonyl

Overview

The name is derived from what 2 structural features?

A
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4
Q

Why are sulfonylureas weak acids?

A
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5
Q

Features of sulfonlyl

Like other weak acids they are?

How many generations of them?

A
  • Weak acids protein bound
  • 1,2,3
    • 1 and 2 are similar 3 is very different
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6
Q

Sulf MOA

A
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7
Q

4 first gen Sulfonylureas

A
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8
Q

Tolbutamide (gen?)

What metabolite is formed?

What does this mean for its activity?

A
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9
Q

Tolazamide (Gen?)

Metabolism?

A
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10
Q

Metablized Tolazamide vs. Tolbutamide

Which one has the longer DOA and why?

A
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11
Q

Chlopropamide (gen?)

What block metabolism of the carboxylic acid?

What does this do?

A
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12
Q

What does the n-propyl chain of chlorpropamide do?

So what does this mean for the drug?

A
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13
Q

Acetohexamide (gen)

What group is rapidly reduced?

A
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14
Q

Acetohexamide metabolite and DOA

A
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15
Q

What first generation sulf provides the core for second gen?

A

Acetohexamide

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16
Q

2nd gen

What features do they all share?

A
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17
Q

Are second generations more potent than first?

These 2nd gen agents undergo similar biotranformations but its important to note that the metabolites?

A
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18
Q

Second gen sulfs 2

A

Glipizide and Glyburide

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19
Q

Glipizide

Structural featurs and DOA

3 things we need to know

A
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20
Q

Glyburide Structural features and DOA

A
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21
Q

SAR of 1st and second gen

What must be on the urea nitrogen?

A
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22
Q

SAR 1st and 2nd

Where must substitution be present?

A
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23
Q

SAR 1st and 2nd

For second gen what appears to be important?

A
24
Q

3rd Gen

Structural features similar to?

What is the chief example

What 2 good things does this drug have?

A
25
Q

3rd gen

Where is binding?

How does it exert its hypoglycemic effects?

What is Glimepiride less likely to produce?

Notes on Glimepiride

A
26
Q

Glimiperide

DOA

Structural features

A
27
Q

Glimepiride

Metabolism?

Enzymes?

What metabolite has activity and what one doesnt?

A
28
Q

Problems with sulfs 4

A
29
Q

Meglitinides Given example?

Difference compared to other hypoglycemics?

Potency?

What is it free of?

A
30
Q

Meglitinides MOA?

Sites of binding?

A
31
Q

Repaglinide

Metabolism

how is it metabolized?

A
32
Q

Nateglinide?

MOA?

Like repaglinide free of?

A
33
Q

Biguanides

Goats rue

Galegine

A
34
Q

What by itself was know to lower sugar?

Example shown?

A
35
Q

Metformin

MOA?

What is it dependent on?

has no effect on what three things?

A
36
Q

3 important components of Metformins Action

  1. Inhibits
  2. Increases
  3. Increase
  4. Overall metformin increases?
A
37
Q

Metformin doesnt induce?

Protein binding and metabolism?

Elimination where?

Drug is active in pts that dont have?

DOA?

A
38
Q

A glucosidase Is

MOA

To be absorbed from the GI tract what has to happen with carbs?

A
39
Q

Actual A-Glucosidase I MOA

A
40
Q

A-glucosidase Inhibitors MOA

What to Type II pts have that make this type of drug useful?

A
41
Q

A-GI notes

What do they not cause?

What is the main SE? Think about where its working

A
42
Q

3 A-GIs

A
43
Q

Acarbose

Why is it poorly absorbed?

A
44
Q

Acarbose

What unit is important for activity?

What type of drug?

A
45
Q

Miglitol and Voglibose

What is a key part of its structure?

What about it compared to Acarbose?

A
46
Q

Thiazolidine

Glitazones

What functionality do they have?

A
47
Q

NO

A
48
Q

Metabolic path of troglitazone

What enzymes metabolize it?

What metabolite may have toxicity? what is the toxicity?

A
49
Q

Glitazone MOA

What does it do? What does it target?

What are they called?

A
50
Q

What do glitazones bind to?

A
51
Q

Glitazone MOA

What is the main action of this drug? What does it increase?

What are these drugs dependent on?

A
52
Q

Pioglitazone and Rosiglitazone both undergo?

A
53
Q

Pioglitazone

Metabolic pathway

A
54
Q

Rosiglitazone pathway

A
55
Q

Big picture

A

MDCM626 (26 decks)

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