Endo Pharm mechanisms/toxicity

Question 1

Lispro

Answer 1

rapid acting insulin

Question 2

Insulin mechanism

Answer 2

M:Bind insulin receptor (tyrosine kinase act)
Liver - increase glucose stored as glycogen
mm - inc glycogen & protein synth; K+ uptake
Fat - aids TG storage

Question 3

Insulin Toxicity

Answer 3

Hypoglycemia; hypersensitivity (rare)

Question 4

Insulin Clinical use

Answer 4

DM I, DM II, gestational diabetes, life-threatening hyperkalemia, stress-induced hyperglycemia
Always injected

Question 5

Aspart

Answer 5

Rapid acting insulin

Question 6

Glulisine

Answer 6

rapid acting insuling

Question 7

Regular Insulin

Answer 7

short acting; only one used IV

Question 8

NPH

Answer 8

intermediate insulin

Question 9

Glargine

Answer 9

long acting insulin

Question 10

Detemir

Answer 10

long-acting insulin

Question 11

Biguanide mechanism

Answer 11

(Metformin)

decrease GNG, increase Glycolysis, increase peripheral glucose uptake (insulin sensitivity)

Question 12

Biguanide clinical use

Answer 12

(Metformin)

oral 1st line for type 2. Can be used if no islet fx

Question 13

Biguanide tox

Answer 13

(Metformin)

GI upset, lactic acidosis (serious), Contraindicated in renal failure so CHECK creatinine!

Question 14

Sulfonylurea mechanism

Answer 14

closes K+ channel in beta cell membrane –> depolarization –> insulin release via Ca2+ influx. Also increases protein C

Question 15

Sulfonylurea Use

Answer 15

stimulate endogenous insulin in type 2 diabetes. Requires some islet fx

Question 16

Sulfonylurea tox

Answer 16

1st gen: disulfiram-like

2nd gen: hypoglycemia

Question 17

Tolbutamide, Chlorpropramide

Answer 17

1st gen sulfonylurea

Question 18

Glyburide, Glimepiride, Glipizide

Answer 18

2nd Gen sulfonylurea

Question 19

Glitazones/thiazolidinediones mech

Answer 19

increase insulin sensitivity in peripheral tissue by binding PPAR gamma nuclear transcription regulator

Question 20

Glitazones/thiazolidinediones use

Answer 20

monotherapy in DM 2 or in combo

Question 21

Glitazones/thiazolidinediones tox

Answer 21

weight gain, edema, hepatotox, Heart failure (makes this last choice)

Question 22

Pioglitazone, rosiglitazone

Answer 22

Glitazones/thiazolidinediones

Question 23

alpha glucosidase inhibitors mechanism

Answer 23

inhibit intestinal brush border on surface membrane. delayed sugar hydrolysis & glucose absorption –> decreases postprandial hyperglycemia

Question 24

alpha glucosidase inhibitors use

Answer 24

monotherapy DM 2 or in combo

Question 25

alpha glucosidase inhibitors tox

Answer 25

GI disturbances

Question 26

Acarbose, miglitol

Answer 26

alpha glucosidase inhibitors

Question 27

Amylin analogs (Pramlintide)

Answer 27

decrease glucagon in DM 1&2; hypoglycemia, nausea, diarrhea

Question 28

GLP-1 analogs

Answer 28

increase insulin, decrease glucagon; DM2; tox = nausea, vomit, pancreatitis

Question 29

Exenatide, Liraglutide

Answer 29

glucose-like peptide 1 analogs

Question 30

DPP-4 inhibitors

Answer 30

increase insulin, decrease glucagon; DM2; tox mild urinary/respiratory infection

Question 31

Linagliptin, saxagliptin, sitagliptin

Answer 31

DPP-4 inhibitors

Question 32

TNF-alpha

Answer 32

decreases glucose uptake by increasing sering p'lation

Question 33

Propylthiouracil, methimazole mech

Answer 33

block peroxidase, inhibits organification of iodide & TH synth. (Prop. also blocks 5'-deiodinase, decreasing peripheral T4->T3)

Question 34

Propylthiouracil, methimazole Tox

Answer 34

Skin rash, agranulocytosis, aplastic anemia, hepatotox, teratogen

Question 35

Levothyroxine, triiodothyronine

Answer 35

Thyroxine replacement hypothyroid, myxedema Tox: tachy, heat intolerance, tremor, arrythm

Question 36

Growth hormone

Answer 36

Gh deficiency, Turner's

Question 37

Octreotide

Answer 37

Somatostatin analog; | Tx- Acromegaly, carcinoid, gastrinoma, glucagonoma, esophageal varices

Question 38

oxytocin

Answer 38

stimulates labor & contractions, milk letdown, controls uterine hemorrhage

Question 39

Desmopressin

Answer 39

ADH | Tx-central DI (not nephrogenic)

Question 40

Demeclocycline

Answer 40

M: ADH antag (tetracycline) TX: SIADH TOX: Nephrogenic DI, photsens, bone/teeth abnorm

Question 41

Glucocorticoids mechanism

Answer 41

decreases LTs & PGs by inhibiting phospholipase A2, and expression of COX-2

Question 42

Glucocorticoid use

Answer 42

Addison's. inflammation, immune suppression, asthma, adrenal crisis

Question 43

Glucocorticoid Tox

Answer 43

Iatrogenic Cuching's syndrome | Adrenal insufficiency if stopped abruptly after chronic use