Pharmacology: Diabetic Drugs

Front 1

where is insulin produced

Back 1

Beta cells in the Islets of Langerhans

Front 2

what messenger is used in the signaling pathway for insulin

Back 2

MAP kinase (tyrosine kinase pathway)

Front 3

insulin causes the uptake of glucose in the skeletal muscle and adipose tissue via which receptors

Back 3

GLUT-4

Front 4

insulin causes the uptake of glucose in the liver and kidney via which receptors

Back 4

GLUT-2

Front 5

insulin activates what enzyme in adipose tissue

Back 5

capillary LPL

Front 6

how does insulin affect K+ serum levels

Back 6

causes K+ to shift INTO the cell causing hypokalemia

Front 7

what are the rapid-acting insulins

Back 7

Lispro (Humalog)
Apsart
Glulisine
Crystalline zinc
Regular insulin (Humulin-R)

Front 8

what are the intermediate-acting insulins

Back 8

Lente and NPH

Front 9

what is NPL

Back 9

combination and Lispro and NPH

Front 10

what are the long-acting insulins

Back 10

Glargine (Lantus)
Detemir
Ultralente (Humulin-U)

Front 11

what's the purpose for checking C-peptide levels

Back 11

differentiate between endogenous and synthetic insulin (synthetic has NO C-peptide)

Front 12

prototype biguanide

Back 12

metformin

Front 13

4 main actions of biguanides

Back 13

decreases gluconeogenesis
increases glycolysis
increases peripheral uptake of glucose
increases insulin sensitivity

Front 14

metformin can sometimes be used to treat this condition unrelated to diabetes

Back 14

can help restore fertility in anovulatory women with polycystic ovarian disease

Front 15

most serious SE of metformin

Back 15

lactic acidosis

Front 16

most COMMON SE of metformin

Back 16

GI disturbances (nausea, vomiting, diarrhea, flatulence etc...)

Front 17

metformin is contraindicated in people with what organ dysfunctions

Back 17

contraindicated in people with renal, cardiac, and liver disease

Front 18

why should metformin NOT be given to an alcoholic

Back 18

increases risk for lactic acidosis

Front 19

does metformin cause hypoglycemia

Back 19

NO

Front 20

MOA of sulfonylureas

Back 20

closes K+ channels causing insulin release

Front 21

sulfonylureas are contraindicated in people with what organ dysfunctions

Back 21

contraindicated in people with liver disease

Front 22

do sulfonylureas cause hypoglycemia

Back 22

YES

Front 23

1st generation sulfonylureas

Back 23

Tolbutamide and Chlorpropamide

Front 24

SE of 1st generation sulfonylureas

Back 24

disulfiram-like reactions and weight gain

Front 25

2nd generation sulfonylureas

Back 25

Glyburide, Glimerpiride, and Glipizide

Front 26

newer sulfonylureas that are faster but shorter acting than 1st and 2nd generation sulfonylureas

Back 26

"Metiglinides" (eg. repaglinide and nateglinide)

Front 27

which generation of sulfonylureas have the longest half-life

Back 27

1st generations

Front 28

where in the body do alpha-glucosidase inhibitors exert their effects

Back 28

intestinal brush border

Front 29

major effect of alpha-glucosidase inhibitors

Back 29

decreases postprandial glucose absorption

Front 30

SE of alpha-glucosidase inhibitors

Back 30

GI disturbances (i.e. flatulence, diarrhea, and abdominal pain)

Front 31

which alpha-glucosidase inhibitor do you have to monitor LFTs

Back 31

acarbose

Front 32

2 main alpha-glucosidase inhibitors

Back 32

acarbose and miglitol

Front 33

MOA of thiazolidinediones

Back 33

binds to PPAR-y receptors which increases glucose uptake in muscle and fat

Front 34

which class of diabetes drugs increases your risk of MI

Back 34

thiazolidinediones

Front 35

thiazolidinediones are contraindicated in people with what organ dysfunctions

Back 35

contraindicated in people with liver and cardiac disease

Front 36

desirable SE that thiazolidinediones have on serum lipid levels

Back 36

decreases triglycerides and increases HDL

Front 37

which class of diabetes drugs induce p450 enzymes

Back 37

thiazolidinediones

Front 38

2 main thiazolidinediones

Back 38

Rosiglitazone and Pioglitazone

Front 39

how do incretins help treat type II diabetes

Back 39

increases insulin release AND decreases glucagon release

Front 40

2 main incretins

Back 40

Exenatide and Sitagliptin

Front 41

how do the MOA differ in exenatide vs. sitagliptin

Back 41

exenatide: activates GLP-1
sitagliptin: inhibits DPP-4

Front 42

prototype amylin analog

Back 42

pramlintide

Front 43

amylin analogs activate amylin by binding to what ligand

Back 43

RANK

Front 44

2 classes of diabetes drugs that can treat BOTH type I and type II diabetes

Back 44

insulins and amylin analogs (pramlintide)

Front 45

which classes of diabetes drugs can treat ONLY type II diabetes

Back 45

biguanides
sulfonylureas
alpha-glucosidase inhibitors
thiazolidinediones
incretins

Front 46

glucagon can be used to treat what overdose

Back 46

B-blocker overdose

Front 47

MOST common 1st line drug therapy for type II diabetes

Back 47

metformin combined with a sulfonylurea

Front 48

most common drug used to reverse acute severe DKA

Back 48

crystalline zinc insulin

Front 49

most common insulin drug regimen in someone with type 1 diabetes

Back 49

long-acting insulin in the morning along with rapid-acting insulin after meals

Front 50

40 year old, overweight patient presents with polyuria and polydipsia
FH is remarkable for HTN, CHF, and arrhythmias
PE reveals HTN
UA reveals 3+ glucosuria and 4+ proteinuria, but no blood in the urine
Glucose tolerance test: 225 after 2 hours

What 2 drugs should he be started on?

Later that night, he is found in a coma... upon medical stabilization, he admits to overdosing on one of his medications... which medication did overdose on, and would this coma be considered a hyper or hypoosmolar coma?

Back 50

ACE inhibitor (for the renal and HTN concerns)
Sulfonylurea (for the type II diabetes-- metformin and thiazolidinediones would be contraindicated due to his renal and cardiac risks)

He overdosed on the sulfonylurea and it was a HYPOosmolar coma (major SE of sulfonylureas is hypoglycemia)