Diabetes brand/generic/class/MOA

Question 1

Clorpropamide (gen)

Answer 1

Sulfonylurea (1st gen), Stimulate insulin secretion in beta cells (secretagogues) by binding to K+channels causing depolarization, leads to Ca2+ influx increasing insulin release.
Also decreases insulin resistance and hepatic glucose output

Question 2

Glucotrol

Answer 2

Glipizide, Sulfonylurea (2nd gen), Stimulate insulin secretion in beta cells (secretagogues) by binding to K+channels causing depolarization, leads to Ca2+ influx increasing insulin release.
Also decreases insulin resistance and hepatic glucose output

Question 3

Diabeta, Glynase

Answer 3

Glyburide, Sulfonylurea (2nd gen), Stimulate insulin secretion in beta cells (secretagogues) by binding to K+channels causing depolarization, leads to Ca2+ influx increasing insulin release.
Also decreases insulin resistance and hepatic glucose output

Question 4

Amaryl

Answer 4

Glimeperide, Sulfonylurea (2nd gen), Stimulate insulin secretion in beta cells (secretagogues) by binding to K+channels causing depolarization, leads to Ca2+ influx increasing insulin release.
Also decreases insulin resistance and hepatic glucose output

Question 5

Glucophage

Answer 5

Metformin, Biguanide, -enhances insulin sensitivity of both hepatic and muscle tissues (possibly by activating AMPK)

-allows for an increased uptake of glucose into these insulin-sensitive tissues

Question 6

Actos

Answer 6

Pioglitazone, TZD, act on ppar gamma which results in glucose uptake (fat cells) and decreases hepatic glucose output and ultimately increases insulin sensitivity

Question 7

Avandia

Answer 7

Rosiglitazone, TZD, act on ppar gamma which results in glucose uptake (fat cells) and decreases hepatic glucose output and ultimately increases insulin sensitivity

Question 8

Prandin

Answer 8

Repaglinide, Meglitinide, stimulate the release of insulin from the β pancreatic cells in the same manner that the sulfonylureas do: they are also
secretagogues

bind to/blocks K channel > depolarization of cell > opens Ca channel > Ca influx causes relase of insulin

Question 9

Starlix

Answer 9

Nateglinide, Meglitinide, stimulate the release of insulin from the β pancreatic cells in the same manner that the sulfonylureas do: they are also
secretagogues

bind to/blocks K channel > depolarization of cell > opens Ca channel > Ca influx causes relase of insulin

Question 10

Precose

Answer 10

Acarbose, Alpha-glucosidase inhibitor, competitively inhibit enzymes (maltase, isomaltase, sucrase, and glucoamylase) in the small intestine, delaying the breakdown of sucrose and complex carbohydrates. results in reduction of the postprandial blood glucose rise

Question 11

Glyset

Answer 11

Miglitol, Alpha-glucosidase inhibitor, competitively inhibit enzymes (maltase, isomaltase, sucrase, and glucoamylase) in the small intestine, delaying the breakdown of sucrose and complex carbohydrates. results in reduction of the postprandial blood glucose rise

Question 12

Humalog

Answer 12

Insulin Lispro, rapid acting insulin (onset 15-30 min)

Question 13

Novolog

Answer 13

Insulin aspart, rapid acting insulin, (onset 15-30 min)

Question 14

Apidra

Answer 14

Insulin Glulisine, rapid acting insulin, (onset 15-30 min)

Question 15

Humulin R

Answer 15

Short acting insulin (onset 30 min- 1 hr)

Question 16

Novolin R

Answer 16

Short acting insulin, (onset 30 min- 1 hr)

Question 17

Humulin N

Answer 17

NPH Insulin (onset 2-4 hr)

Question 18

Novolin N

Answer 18

NPH insulin (onset 2-4hr)

Question 19

Lantus

Answer 19

Insulin Glargine, long acting insulin (22-24 hr)

Question 20

Levemire

Answer 20

Insulin detemir, long acting insulin (14-24 hr).

Question 21

Symlin

Answer 21

Pramlintide, amylinomimetic, Pramlintide is a synthetic analog of amylin (amylinomimetic), a neurohormone co-secreted from the cells with insulin. It suppresses inappropriately high postprandial glucagon secretion, increases satiety, which may result in weight loss, and slows gastric emptying so that the rate of glucose appearance into the plasma better matches the glucose disposition

Question 22

Byetta

Answer 22

Exenatide, GLP-Agonist, GLP-1 analogue, enhances glucose dependent insulin secretion while suppressing inappropriately high postprandial glucagon secretion in the presence of elevated glucose concentrations, resulting in a reduction in hepatic glucose production

Question 23

Victoza

Answer 23

Liraglutide, GLP-1 receptor agonist, enhances glucose-dependent insulin secretion while suppressing inappropriately high glucagon secretion in the presence of elevated glucose concentrations, resulting in a reduction in hepatic glucose production

Question 24

Trulicity

Answer 24

Dulaglutide, GLP-1 receptor agonist, enhances glucose-dependent insulin secretion while suppressing inappropriately high glucagon secretion in the presence of elevated glucose concentrations, resulting in a reduction in hepatic glucose production

Question 25

Tanzeum

Answer 25

Albiglutide, GLP-1 receptor agonist, enhances glucose-dependent insulin secretion while suppressing inappropriately high glucagon secretion in the presence of elevated glucose concentrations, resulting in a reduction in hepatic glucose production

Question 26

Januvia

Answer 26

Sitagliptin, Dipeptidyl peptidase IV inhibitor, DPP-4 inhibitors prolong the half-life of endogenously produced GLP-1 and GIP (normally only minutes). As these agents block nearly 100% of the DPP-4 enzyme activity for at least 12 hours, normal physiologic, nondiabetic GLP-1 levels are achieved. DPP-4 inhibitors significantly reduce the inappropriately elevated glucagon postprandially, though not back to nondiabetic levels, and improve insulin response to a high glucose level. Insulin levels tend to be unchanged with DPP-4 inhibitors, but glucose levels are reduced.

Question 27

Onglyza

Answer 27

Saxagliptin, Dipeptidyl peptidase IV inhibitor, DPP-4 inhibitors prolong the half-life of endogenously produced GLP-1 and GIP (normally only minutes). As these agents block nearly 100% of the DPP-4 enzyme activity for at least 12 hours, normal physiologic, nondiabetic GLP-1 levels are achieved. DPP-4 inhibitors significantly reduce the inappropriately elevated glucagon postprandially, though not back to nondiabetic levels, and improve insulin response to a high glucose level. Insulin levels tend to be unchanged with DPP-4 inhibitors, but glucose levels are reduced.

Question 28

Nesina

Answer 28

Alogliptin, Dipeptidyl peptidase IV inhibitor, DPP-4 inhibitors prolong the half-life of endogenously produced GLP-1 and GIP (normally only minutes). As these agents block nearly 100% of the DPP-4 enzyme activity for at least 12 hours, normal physiologic, nondiabetic GLP-1 levels are achieved. DPP-4 inhibitors significantly reduce the inappropriately elevated glucagon postprandially, though not back to nondiabetic levels, and improve insulin response to a high glucose level. Insulin levels tend to be unchanged with DPP-4 inhibitors, but glucose levels are reduced.

Question 29

Tradjenta

Answer 29

Linagliptin, Dipeptidyl peptidase IV inhibitor, DPP-4 inhibitors prolong the half-life of endogenously produced GLP-1 and GIP (normally only minutes). As these agents block nearly 100% of the DPP-4 enzyme activity for at least 12 hours, normal physiologic, nondiabetic GLP-1 levels are achieved. DPP-4 inhibitors significantly reduce the inappropriately elevated glucagon postprandially, though not back to nondiabetic levels, and improve insulin response to a high glucose level. Insulin levels tend to be unchanged with DPP-4 inhibitors, but glucose levels are reduced.

Question 30

Invokana

Answer 30

Canagliflozin, Sodium Glucose Transporter, Inhibits SGT2 in proximal renal tubules and reduces reabsorption of glucose which lowers the renal threshold for glucose

Question 31

Farxiga

Answer 31

Dapagliflozin, Sodium Glucose Transporter, Inhibits SGT2 in proximal renal tubules and reduces reabsorption of glucose which lowers the renal threshold for glucose

Question 32

Whelcol

Answer 32

Colesevelam, Bile Acid Sequestrant, Binds bile acid in the intestinal lumen, decreasing the bile acid pool for reabsorption. MOA is to lower plasma glucose levels is in the intestinal lumen or a systemic effect due to the intestinal lumen effect or some combination of these two. We don’t know.

Question 33

Cycloset, Parlodel

Answer 33

Bromocriptine Mesylate, Dopamine agonist, Bromocriptine is thought to act on the circadian neuronal activities in the hypothalamus, to reset an abnormally elevated hypothalamic drive for increased plasma glucose, free fatty acids, and triglycerides in insulin-resistant patients