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Flashcards in Endocrin Pharm Deck (56):
1

What are the rapid acting insulins?

Iispro Aspart Glulisine

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Mech of lispro aspart glulisine?

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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clinical use of rapid acting insulins

DM1, DM2, GDM (postprandial glucose control)

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What are the SE of rapid acting insulins?

hypoglycemia, rare hypersensitivity

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What is the insulin, short acting?

regular

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

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

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What is the intermediate acting insulin?

NPH

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Clinical use of NPH

DM1, DM2, GDM

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What are the long acting insulins?

Glargine, Detemir

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Glargine, Detemir Clinical use?

DM1, DM2, GDM (basal glucose control)

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Biguanides (Metformin) mech of action?

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

12

Metformin clinical use?

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

13

Metformin toxicities

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

14

Whatare the first generation sulfonylureas?

Tolbutamide, Chlorpropamide

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What are the second generation Sulfonylureas?

Glyburide, Glimepiride, Glipizide

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Sulfonylureas mech

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

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Sulfonylureas clinical use

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

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Sulfonylureas SE

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

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What are the Glitazones/thiazolidinediones?

Pioglitzone, Rosiglitazone

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What is the mech of the glitzones/thiazolideinediones?

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

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Clinical use of glitzones/thiazolideinediones?

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

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SE of glitzones/thiazolideinediones?

weight gain, edema. hepatotoxicity, heart failure.

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What are the alpha glucosidase inhibitors

Acarbose. Miglitol

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What is the mech of alpha glucosidase inhibitors?

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

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What is the clinical use of the alpha glucosidase inhibitors?

monotherapy in type 2 DM or in combination with above agents

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What are the toxicities of alpha glucosidase inhibitors?

GI disturbances

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What is the Amylin analog?

Pramlintide

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Mech of the amylin analog pramlintide?

decrease gastric emptying, decrease glucagon

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Clinical use of the amylin analog pramlintide?

Type 1 DM and Type 2 DM

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SE of the amylin analog pramlintide?

hypoglycemia, nausea, diarrhea

31

What are the GLP-1 analogs?

Exenatide, Liraglutide

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Mech of the GLP-1 analogs exenatide, liraglutide?

increase insulin, decrease glucagon release

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

type 2 DM

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SE of the GLP-1 analogs exenatide, liraglutide?

nausea, vomiting; pancreatitis

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

Linagliptin, Saxagliptin, Sitagliptin

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Mech of action of Linagliptin, Saxagliptin, Sitagliptin?

Increase insulin, decrease glucagon release

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

Type 2 DM

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

Mild urinary or respiratory infections

39

Genes activated by PPAR gamma regulate what?

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

40

Propylthyiuracil, methimazole mech

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

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What is the clinical use of propylthiouracil, methimazole?

Hyperthyroidism. PTU blocks Peripheral conversion, used in Pregnancy

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What are the SE of propylthiouracil and methimazole?

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

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Levothyroxin, triiodothyronine mech

Thyroxin replacement

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Levothyroxine, triiodothyronine clinical use

Hypothyroidism, myxedmea

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Levo triiodothyronine SE

Tachycardia, heat intolerance, tremors, arrythmias

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GH use

GH deficiency, Turner

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Somatostatin (octreotide)

Acromegaly, carcinoma, gastrinoma, glucoagonma, esophageal varices.

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Oxytocin

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

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ADH (DDAVP)

Pituitary (central, not nephrogenic) DI

50

Demeclocycline mech

ADH antagonist (membrane of the tetracycline family)

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Demeclocycline clinical use

SIADH

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Demeclocycline toxicity

Nephrogenic DI, photosensitivity, abnormalties of bone and teeth

53

Glucocorticoid examples

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

54

What is the mech of the glucocorticoids

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

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Clinical use of glucocorticoids

Addison disease, inflammation, immune suppression, asthma

56

SE of glucocorticoids

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.