Diabetes Medication

Question 1

MOA of acarbose

Answer 1

alpha-glucosidase inhibitor, oral hypoglycemic. Reduces intestinal absorption of starch, disaccharides by inhibiting brush border alpha-glucosidase. Reduce carb uptake and reduces post-prandial glucose rise.

Question 2

MOA of colesevelam

Answer 2

bile acid sequestrant that lowers blood cholesterol. Lowers HbA1c and LDL. Interrupts enterohepatic cycling and lowers Farnesoid X receptor activation.

Question 3

ADE of colesevelam

Answer 3

GI effects.

Question 4

MOA of exenatide

Answer 4

incretin mimetic. inhibits glucagon=stimulated glycogenolysis in liver. Preserve or increase production of new beta-cells in pancreas. Acts on GLP-1 (glucagon-like peptide-1) recepotr.

Question 5

MOA of glucagon

Answer 5

opposite effects to those of insulin. secreted by alpha-cells of pancreas. Elevated in fasting and diabetes. Sometimes used in hypoglycemic emergencies.

Question 6

MOA of glyburide

Answer 6

2nd gen sulfonylurea (oral hypoglycemic). K channel blocker increases insulin secretion

Question 7

ADE of glyburide

Answer 7

NSAIDs can cause increased hypoglycemia

Question 8

MOA of insulin detemir

Answer 8

recombinant human insulin has altered isoelectric point. When injected, acidic solution is neutralized and crystals precipitate to cause slow release.

Asp 21 is replaced by Glycine and two arginines are added to the C-terminus of the B-chain. similar to insulin glargine. Can be injected once/day.

Question 9

MOA of insulin glargine

Answer 9

recombinant human insulin has altered isoelectric point. When injected, acidic solution is neutralized and crystals precipitate to cause slow release.

Asp 21 is replaced by Glycine and two arginines are added to the C-terminus of the B-chain. Injected once/day.

Question 10

MOA of metformin

Answer 10

biguanide, oral hypoglycemic. Does not affect insulin secretion, no hypoglycemia. Decreases hepatic glucose production by acting on AMPK.

Question 11

ADE of metformin

Answer 11

few adverse effects, low risk of hypoglycemia.

Lactic acidosis! Must take them off when they come into ER

Question 12

MOA of repaglinide

Answer 12

meglitinide, oral hypoglycemic. Benzoic acid derivative. Increases insulin secretion. Very rapid GI absorption and short half-life.

Question 13

ADE of repaglinide

Answer 13

hypoglycemia

Question 14

MOA of semilente insulin

Answer 14

Pork insulin suspension with zinc chloride that is rapidly absorbed.

Question 15

MOA of sitagliptin

Answer 15

inhibitor of dipeptidyl peptidase-4 (DPP-4), the enzyme that inactivates incretin hormones.

Incretins increase insulin secretion. Two main incretins are GIP (glucose-dependent insulinotropic peptide) and GLP-1 (glucagon-like peptide 1)

Question 16

What is the reason for synthetic insulins with shifted isoelectric points?

Answer 16

to allow injection in liquid form when solution is still acidic. Once it reaches body and acid is neutralized, solution will crystalize and result in slow-release.

Question 17

What is ketoacidosis?

Answer 17

Increased release of fatty acids incraeses ketone bodies and decreases pH. Hyperglycemia due to hepatic gluconeogenesis.

Caused by LOW INSULIN. Catecholamines, GH, cortisone, and glucagon will all be elevated. Treat with insulin.

Question 18

What is a hypoglycemic coma?

Answer 18

usually caused by insulin overdose. Treat with glucose.

Question 19

What are the actions and uses of somatostatins?

Answer 19

inhibit insulin and glucagon release from pancreas. Also inhibit TSH and GH from pituitary. Secreted by D cells of pancreatic islets, GI and brain.

Octreotide is a somatostatin analog.

Question 20

What are the key differences between Type I and Type II diabetes?

Answer 20

Type I (IDDM) - insulin-dependent diabetes mellitus or juvenile diabetes. Wasting disease because glycogen, fat and muscle loss. Excretion of ketone bodies and glucose into urine. Little to no insulin release.

Type II (NIDDM) - normal/elevated insulin. Associated with age and obesity.

Question 21

What are sulfonylureas?

Answer 21

intially increas insulin reelase, but not after long-term treatment. Increase insulin sensitivity.

Question 22

What effect do NSAIDs have on diabetes medication?

Answer 22

NSAIDs will enhance the hypoglycemic action of sulfonylureas!

Question 23

What do incretins do?

Answer 23

increase insulin secretion. Two main incretins are GIP (glucose-dependent insulinotropic peptide) and GLP-1 (glucagon-like peptide 1). Both are secreted from endocine cells in epithelium of small intestine.

Question 24

What does GLP-1 do?

Answer 24

increases glucose-dependent insulin secretion.
inhibits glucagon-stimulated glycogenolysis in liver
decreases apetite and glucagon secretion

Question 25

What does amylin do?

Answer 25

amylin is a peptie hormone reelased by B-cells of pancreas along with insulin after meals. It slows gastric emptying and aids in glucose absorption. Promotes satiety via hypothalamus and inhibits inapporpriate secretion of lgucagon.

Results in weight loss, allows patients to use less insulin, and lowers average blood glucose.

Question 26

MOA of thiazolidinediones?

Answer 26

bind to PPARgamma to increase insulin sensitivity and increase glucose uptake into muscles and adipose. Pioglitazone

Question 27

MOA of pioglitazone

Answer 27

thiazolidinedione. binds to PPARy (gamma) to increase insulin sensitivity and glucose uptake by muscle/fat cells.