E: Type 2 Dm Drugs

Front 1

Is there any limit (lower threshold) for the risk to the microvasculature form Ha1c? In other words, is there an amount that is ok?

Back 1

no - the most appropiate target for most patients is the lowest HbA1c possible w/o unacceptable hypoG / adverse effects.

Front 2

What are the 5 general classes of t2dm tx? Give class examples of each.

Back 2

(1) increase insulin secretion
- sulfonylureas
- meglitinides
(2) increase insulin sensitivity
- biguanide
- glitazones
(3) delay carb absorption
- a-glucosidase inhib
(4) increase incretin effect
- GLP-1 receptor agonist
- DPP IV inhibitor
(5) increase amylin
- pramlintide

Front 3

What are the two classes of insulin secretagogues? Name the common ones.
- mechanism?
- do they stimulate basal or postprandial insulin secretion?
- main risk?
- approximate HbA1c % decrease?
- generally speaking, is there a therapeutic benefit for exceeding 1/2 max dose with sulfonylureas?

Back 3

sulfonylureas and meglitinides
- glipizide, glyburide, glimepiride
+ the "gli's"
- repaglinide, nateglinide

- inhibit the outward K+ channel that's keeping the cell polarized --> depol --> ca-influx --> I release.

- both
- hypoglycemia
- 1-2%
- no

Front 4

What is metformin?
- what mechanism does it work on?
- adverse effects? main adverse risk?
- contraindications?
- titration frequency?
- WG? lipid effects?

Back 4

Biguanide
- req insulin: sensitizes liver (actv AMPK)>>muscle (^GLUT translocation) to insulin --> reduces hepatic G production
- Diarrhea and nausea, dec B12
+ lactic acidosis
- renal, cardiac, or hepatic insufficiency; IV contrast
- week(s) to months
- no WG, advantageous lipid effects.

Front 5

What are the two main thiazolidinediones (TZD/glitazones)?
- how do they help tx diabetes?
- preserve B-cell fx?
- main toxicity?
- SE's?
- which of the two has more favorable lipid effects?
+ which can ^^ LDL?
- speed of onset?

Back 5

Pioglitazone and Rosiglitazone
- insulin sensitizers: muscle & adipose >> liver
+ activate PPAR's, which are receptors for FFA and their metabolites and integrate/coordinate glucose, FFA, and chol. metabolism.
--> mainly in adipose tiss
--> 2ndar effect: ^adiponectin, \TNF-a = improve musc >> liv insulin sensitivity
- maybe
- CHF & liver tox
- edema, weight gain, rare fractures
- pioglitazone
+ rosiglitazone
- slow (titration wks to months)

Front 6

Do a-Glucosidase inhibitors effect primary postprandial or baseline G?

Back 6

postprandial; these drugs slow CHO absorption.

Front 7

What are the two a-Glucosidase inhibitors we should know?
- main risk for toxicity?
- main SE?
- small/large effect?
- best considered in which pt population(s)?

Back 7

Acarbose and Miglitol
- rare liver enzyme elevation
- flatulence
- small
- those with high CHO diet.

Front 8

What are incretins? examples?
- what stimulates their release?
- do pt's w/ t2dm have an exaggerated, normal, or blunted incretin response to ingestion of food?

Back 8

gut-derived peptide hormones that increase insulin release by the pancreas.
- glucagon like peptide (GLP) and Glucagon inhibitory peptide (GIP)
- nutrient intake
- blunted.

Front 9

GLP-1 has what effects on:
- CNS
- B-cells
- a-cells
- stomach

Back 9

- promotes satiety
- stim G-dependent Insulin secretion
- inhib glucagon secretion
- slows gastric emptying.

Front 10

What are the two GLP-1 receptor agonists?
- major adverse event?
- how are they administered?

Back 10

Exenatide and Liraglutide
- nausea, possibly pancreatitis
- INJECTION, 1 or 2x daily.

Front 11

What are DPP IV inhibitors?
- name two of 'em.
- affects baseline or posprandial G?
- requires induction by meal intake?

Back 11

*oral* drugs that prolong the effects of endogenous incretins.
- sitagliptin and saxagliptin.
- postprandial G.
- yes

Front 12

What is amylin?
- deficient in t1dm or t2dm?
- effects on CNS, B-cells, a-cells, and stomach?

Back 12

a neuroendocrine hormone co-located and co-secreted w/ insulin from B-cells.
- equivalently deficient in both.
- promotes satiety; none; inhib glucagon secretion; slows gastric emptying

Front 13

What is the name of the synthetic amylin analogue we use to tx diabetes?
- delivery mechanism?
- weight gain/loss?
- in which type of diabetes is the initial nausea worse?
- interactions w/ insulin?

Back 13

pramlintide
- injection @ each meal
- loss
- t1dm
- doubles the injections needed if the pt is on mealtime insulin.

Front 14

What is the only non-insulin therapy available for t1dm?

Back 14

Pramlintide

Front 15

What is chlorpropramide?

Back 15

a sulfonylurea no longer recommended b/c it has more side effects. It had a longer duration of action that many of the others in it's class.

Front 16

Of all these drugs used to tx diabetes, which are the only types that preserve B-cell fx?

Back 16

glitazones, earlier use of insulin, and possibly incretin mimetics.

Front 17

Of the insulin secretagogues, which are faster acting?
- how titratable are they?

Back 17

the meglitinides > sulfonylureas
- days to wks frequency.