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First Aid > Endocrin Pharm > Flashcards

Endocrin Pharm Flashcards

1
Q

What are the rapid acting insulins?

A

Iispro Aspart Glulisine

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2
Q

Mech of lispro aspart glulisine?

A

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

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3
Q

clinical use of rapid acting insulins

A

DM1, DM2, GDM (postprandial glucose control)

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4
Q

What are the SE of rapid acting insulins?

A

hypoglycemia, rare hypersensitivity

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5
Q

What is the insulin, short acting?

A

regular

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6
Q

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

A

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

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7
Q

What is the intermediate acting insulin?

A

NPH

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8
Q

Clinical use of NPH

A

DM1, DM2, GDM

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9
Q

What are the long acting insulins?

A

Glargine, Detemir

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10
Q

Glargine, Detemir Clinical use?

A

DM1, DM2, GDM (basal glucose control)

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11
Q

Biguanides (Metformin) mech of action?

A

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

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12
Q

Metformin clinical use?

A

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

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13
Q

Metformin toxicities

A

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

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14
Q

Whatare the first generation sulfonylureas?

A

Tolbutamide, Chlorpropamide

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15
Q

What are the second generation Sulfonylureas?

A

Glyburide, Glimepiride, Glipizide

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16
Q

Sulfonylureas mech

A

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

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17
Q

Sulfonylureas clinical use

A

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

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18
Q

Sulfonylureas SE

A

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

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19
Q

What are the Glitazones/thiazolidinediones?

A

Pioglitzone, Rosiglitazone

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20
Q

What is the mech of the glitzones/thiazolideinediones?

A

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

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21
Q

Clinical use of glitzones/thiazolideinediones?

A

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

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22
Q

SE of glitzones/thiazolideinediones?

A

weight gain, edema. hepatotoxicity, heart failure.

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23
Q

What are the alpha glucosidase inhibitors

A

Acarbose. Miglitol

24
Q

What is the mech of alpha glucosidase inhibitors?

A

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

25
Q

What is the clinical use of the alpha glucosidase inhibitors?

A

monotherapy in type 2 DM or in combination with above agents

26
Q

What are the toxicities of alpha glucosidase inhibitors?

A

GI disturbances

27
Q

What is the Amylin analog?

A

Pramlintide

28
Q

Mech of the amylin analog pramlintide?

A

decrease gastric emptying, decrease glucagon

29
Q

Clinical use of the amylin analog pramlintide?

A

Type 1 DM and Type 2 DM

30
Q

SE of the amylin analog pramlintide?

A

hypoglycemia, nausea, diarrhea

31
Q

What are the GLP-1 analogs?

A

Exenatide, Liraglutide

32
Q

Mech of the GLP-1 analogs exenatide, liraglutide?

A

increase insulin, decrease glucagon release

33
Q

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

A

type 2 DM

34
Q

SE of the GLP-1 analogs exenatide, liraglutide?

A

nausea, vomiting; pancreatitis

35
Q

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

A

Linagliptin, Saxagliptin, Sitagliptin

36
Q

Mech of action of Linagliptin, Saxagliptin, Sitagliptin?

A

Increase insulin, decrease glucagon release

37
Q

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

A

Type 2 DM

38
Q

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

A

Mild urinary or respiratory infections

39
Q

Genes activated by PPAR gamma regulate what?

A

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

40
Q

Propylthyiuracil, methimazole mech

A

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

41
Q

What is the clinical use of propylthiouracil, methimazole?

A

Hyperthyroidism. PTU blocks Peripheral conversion, used in Pregnancy

42
Q

What are the SE of propylthiouracil and methimazole?

A

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

43
Q

Levothyroxin, triiodothyronine mech

A

Thyroxin replacement

44
Q

Levothyroxine, triiodothyronine clinical use

A

Hypothyroidism, myxedmea

45
Q

Levo triiodothyronine SE

A

Tachycardia, heat intolerance, tremors, arrythmias

46
Q

GH use

A

GH deficiency, Turner

47
Q

Somatostatin (octreotide)

A

Acromegaly, carcinoma, gastrinoma, glucoagonma, esophageal varices.

48
Q

Oxytocin

A

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

49
Q

ADH (DDAVP)

A

Pituitary (central, not nephrogenic) DI

50
Q

Demeclocycline mech

A

ADH antagonist (membrane of the tetracycline family)

51
Q

Demeclocycline clinical use

A

SIADH

52
Q

Demeclocycline toxicity

A

Nephrogenic DI, photosensitivity, abnormalties of bone and teeth

53
Q

Glucocorticoid examples

A

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

54
Q

What is the mech of the glucocorticoids

A

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

55
Q

Clinical use of glucocorticoids

A

Addison disease, inflammation, immune suppression, asthma

56
Q

SE of glucocorticoids

A

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.

First Aid (33 decks)

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