Endocrin Pharm

Question 1

What are the rapid acting insulins?

Answer 1

Iispro Aspart Glulisine

Question 2

Mech of lispro aspart glulisine?

Answer 2

Bind insulin receptor (tyrosine kinase activity). Liver: increase glucose stored as glycogen. Muscle: increase glycogen, protein syntesis; increase K+ uptake. Fat: increase TG storage

Question 3

clinical use of rapid acting insulins

Answer 3

DM1, DM2, GDM (postprandial glucose control)

Question 4

What are the SE of rapid acting insulins?

Answer 4

hypoglycemia, rare hypersensitivity

Question 5

What is the insulin, short acting?

Answer 5

regular

Question 6

What is the clinical use of the regular short acting insulin?

Answer 6

DM1, DM2, GDM, DKA (IV), hyperkalemia (+glucose), stress hyperglycemia.

Question 7

What is the intermediate acting insulin?

Answer 7

NPH

Question 8

Clinical use of NPH

Answer 8

DM1, DM2, GDM

Question 9

What are the long acting insulins?

Answer 9

Glargine, Detemir

Question 10

Glargine, Detemir Clinical use?

Answer 10

DM1, DM2, GDM (basal glucose control)

Question 11

Biguanides (Metformin) mech of action?

Answer 11

Exact mech is unknown. Decreased gluconeogenesis, increased glycolysis, increased peripheral glucose uptake (insulin sensitivity)

Question 12

Metformin clinical use?

Answer 12

oral. first-line therapy in type 2 DM. Can be used in patients without islet function.

Question 13

Metformin toxicities

Answer 13

GI upset; most serious adverse effect is lactic acidosis (thus contraindicated in renal failure)

Question 14

Whatare the first generation sulfonylureas?

Answer 14

Tolbutamide, Chlorpropamide

Question 15

What are the second generation Sulfonylureas?

Answer 15

Glyburide, Glimepiride, Glipizide

Question 16

Sulfonylureas mech

Answer 16

Close K+ channel in beta cell membrane, so cell depolarizes which triggers insulin release via Ca++ influx

Question 17

Sulfonylureas clinical use

Answer 17

stimulate release of endogenous insulin in type 2 DM. Require some islet function, so useless in type 1 DM

Question 18

Sulfonylureas SE

Answer 18

Risk of hypoglycemia increase in renal failure. First generation: disulfiram-like effects. Second generation: hypoglycemia

Question 19

What are the Glitazones/thiazolidinediones?

Answer 19

Pioglitzone, Rosiglitazone

Question 20

What is the mech of the glitzones/thiazolideinediones?

Answer 20

increase insulin sensitivity in peripheral tissue. binds to PPAR glamma nuclear transcription factor

Question 21

Clinical use of glitzones/thiazolideinediones?

Answer 21

monotherapy in type 2 DM comined with biguanides, sulfonylureas, or insulins.

Question 22

SE of glitzones/thiazolideinediones?

Answer 22

weight gain, edema. hepatotoxicity, heart failure.

Question 23

What are the alpha glucosidase inhibitors

Answer 23

Acarbose. Miglitol

Question 24

What is the mech of alpha glucosidase inhibitors?

Answer 24

Inhibit intestinal brush border alpha glucosidases. Delayed sugar hydrolysis and glucose absorption which leads to decrease postprandial hyperglycemia.

Question 25

What is the clinical use of the alpha glucosidase inhibitors?

Answer 25

monotherapy in type 2 DM or in combination with above agents

Question 26

What are the toxicities of alpha glucosidase inhibitors?

Answer 26

GI disturbances

Question 27

What is the Amylin analog?

Answer 27

Pramlintide

Question 28

Mech of the amylin analog pramlintide?

Answer 28

decrease gastric emptying, decrease glucagon

Question 29

Clinical use of the amylin analog pramlintide?

Answer 29

Type 1 DM and Type 2 DM

Question 30

SE of the amylin analog pramlintide?

Answer 30

hypoglycemia, nausea, diarrhea

Question 31

What are the GLP-1 analogs?

Answer 31

Exenatide, Liraglutide

Question 32

Mech of the GLP-1 analogs exenatide, liraglutide?

Answer 32

increase insulin, decrease glucagon release

Question 33

clinical use of the GLP-1 analogs exenatide, liraglutide?

Answer 33

type 2 DM

Question 34

SE of the GLP-1 analogs exenatide, liraglutide?

Answer 34

nausea, vomiting; pancreatitis

Question 35

What are the DPP-4 (dipeptidyl peptide 4) inhibitors?

Answer 35

Linagliptin, Saxagliptin, Sitagliptin

Question 36

Mech of action of Linagliptin, Saxagliptin, Sitagliptin?

Answer 36

Increase insulin, decrease glucagon release

Question 37

Clinical use of DPP-4 inhibitors Linagliptin, Saxagliptin, Sitagliptin

Answer 37

Type 2 DM

Question 38

SE of DPP-4 inhibitors Linagliptin, Saxagliptin, Sitagliptin?

Answer 38

Mild urinary or respiratory infections

Question 39

Genes activated by PPAR gamma regulate what?

Answer 39

fatty acid storage and glucose metabolism. Activation of PPAR gamma increases insulin sensitivity and levels of adiponectin

Question 40

Propylthyiuracil, methimazole mech

Answer 40

block thyroid peroxidase, inhibiting the oxidation of iodide and the organification (coupling) of iodine inhibition of thyroid hormone synthesis. Propylthiouracil also blocks 5' deiodinase which decreases peripheral conversion of T4 to T3

Question 41

What is the clinical use of propylthiouracil, methimazole?

Answer 41

Hyperthyroidism. PTU blocks Peripheral conversion, used in Pregnancy

Question 42

What are the SE of propylthiouracil and methimazole?

Answer 42

Skin rash, agranulocytosis (rare), aplastic anemia, hepatotoxicity (propylthiouracil). Methimazole is a possible teratogen (can cause aplasia cutis)

Question 43

Levothyroxin, triiodothyronine mech

Answer 43

Thyroxin replacement

Question 44

Levothyroxine, triiodothyronine clinical use

Answer 44

Hypothyroidism, myxedmea

Question 45

Levo triiodothyronine SE

Answer 45

Tachycardia, heat intolerance, tremors, arrythmias

Question 46

GH use

Answer 46

GH deficiency, Turner

Question 47

Somatostatin (octreotide)

Answer 47

Acromegaly, carcinoma, gastrinoma, glucoagonma, esophageal varices.

Question 48

Oxytocin

Answer 48

Stimulates labor, uterine contractions, milk let-down; controls uterine hemorrhage

Question 49

ADH (DDAVP)

Answer 49

Pituitary (central, not nephrogenic) DI

Question 50

Demeclocycline mech

Answer 50

ADH antagonist (membrane of the tetracycline family)

Question 51

Demeclocycline clinical use

Answer 51

SIADH

Question 52

Demeclocycline toxicity

Answer 52

Nephrogenic DI, photosensitivity, abnormalties of bone and teeth

Question 53

Glucocorticoid examples

Answer 53

hydrocortisone, prednisone, tramcinolone, dexamethasone, beclomethasone, fludrocortisone, (mineralcocorticoid and glucocorticoid activity)

Question 54

What is the mech of the glucocorticoids

Answer 54

Metabolic, catabolic, anti inflammatory, and immunosuppressive effects mediated by interactions with glucocorticoid response elements and inhibition of transcription factors such as NF-kB

Question 55

Clinical use of glucocorticoids

Answer 55

Addison disease, inflammation, immune suppression, asthma

Question 56

SE of glucocorticoids

Answer 56

Iatrogenic Cushing syndrome: buffalo hump, moon facies, trunal obesity, muscle wasting, thin skin, easy bruisabliity, osteoporosis (Treat with bisphosphonates), adrenocortical atrophy, peptic ulcers, diabetes (if chronic). Adrenal insufficiency when drug stopped abruptly after chronic use.