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50 Cards in this Set
- Front
- Back
Endocrine
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[MOA/Clinical Use/TOX]
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Insulin--Rapid acting
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Lispro, Aspart, Glulisine
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Insulin--short acting
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Regular
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Insulin--intermediate acting
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NPH
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Insulin--long acting
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Glargine, Detemir
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Insulin MOA
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Bind insulin receptor (tyrosine kinase activity)
Liver: INC glucose stored as glycogen MM: INC glycogen and protein synthesis, K uptake Fat: aids TG storage |
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Insulin clinical use
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Type 1 and 2 DM
Gestational diabetes Life threatening HYPERkalemia stress-induced HYPERglycemia |
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Insulin Tox
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Hypoglycemia
Very rarely--Hypersensitivity |
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Biguanides
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Metformin
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Metformin MOA
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Exact MOA unknown
DEC gluconeogensis INC glycolysis INC peripheral glucose uptake (insulin sensitivity) |
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Metformin clinical use
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First line therapy Type 2 DM
Oral Can be used in patients without islet cell function |
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Metformin TOX
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LACTIC ACIDOSIS!
-->Contraindicated in renal failure |
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Sulfonylureas (1st gen)
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Tolbutamide and Chlorpropamide
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Sulfonylureas (2nd gen)
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Glyburide, Glimepiride, Glipizide
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Sulfonylureas MOA
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Close K channel in Beta cell membrane-->depolarization-->Ca influx-->triggering insulin release
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Sulfonylureas clinical use
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Stimulate release of endogenous insulin in Type 2 DM
Requires some islet cell function (useless in Type 1) |
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Sulfonylureas TOX
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1st gen: Disulfiram like effects (drowsiness, headache, metallic/garlic taste)
2nd gen: hypoglycemia |
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Glitazones/thiazolidinediones
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Pioglitazone, Rosiglitazone
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Glitazone MOA
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INC insulin sensitivity in peripheral tissue
Binds to PPAR-gamma nuclear transcription regulator (PPAR-gamma regulates FA storage and glucose metabolism. Activation INC insulin sensitivity and levels of adiponection) |
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Glitazone clinical use
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used as monotherapy in Type 2
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Glitazone TOX
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Weight gain
Edema Hepatotox HEART FAILURE |
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a-glucosidase inhibitors
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Acarbose, Miglitol
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a-glucosidase inhibitors MOA
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Inhibit intestinal brush border a-glucosidases=
Delayed sugar hydrolysis and glucose absorption-->DEC postprandial HYPERglycemia |
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a-glucosidase inhibitor clinical use
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Monotherapy in Type 2
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a-glucosidase inhibitor TOX
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GI disturbances
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Amylin analogs
Pramlinitde MOA/clinical use/TOX |
DEC glucagon
Type I and 2 DM HYPOglycemia, N/D |
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GLP-1 analogs (Incretins)
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Exenatide, Liraglutide
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GLP-1 MOA
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INC insulin, DEC glucagon release
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GLP-1 clinical use
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Type 2 DM
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GLP-1 TOX
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N/V
Pancreatitis |
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DPP-4 inhibitors
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Linagliptin
Saxagliptin Sitagliptin |
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DPP-4 inhibitor MOA
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INC insulin, DEC glucagon release
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DPP-4 inhibitor clinical use
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Type 2 DM
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DPP-4 inhibitor TOX
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Mild urinary or respiratory infections
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Propylthiouracil, Methimazole MOA
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Block peroxidase thereby inhibiting organification of iodie and coupling of thyroid hormone synthesis
PPU also blocks 5-deiodinase (DEC peripheral conversion) |
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PPU, MMU clinical use
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Hyperthyroidism
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PPU, MMU TOX
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Skin rash
AGRANULOCYTOSIS (discontinue MMU and give Filgastrim and G-CSF) Aplastic anemia Hepatotox (PPU) MMU=teratogen |
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Levothyroxine (T4), Tiiodothyronine (T3) MOA
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Thyroxine replacement
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Levo, Triiodo clinical use
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HYPOthyroidism
Myxedema |
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Levo,Triiodo TOX
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Tachy
heat intolerance tremors arrythmias |
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GH clinical use
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GH deficiency
TURNER'S SYNDROME |
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Somatostatin/Octreotide clinical use
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Acromegaly
Carcinoid Gastrinoma Glucagonoma Esophageal varices |
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Oxytocin clinical use
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Stimulates labor
Uterine contractions milk let-down Control uterine hemorrhage |
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ADH (desmopression) clinical use
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Central DI
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Demeclocycline MOA
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ADH antagonist
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Demeclocycline clinical use
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SIADH (caused by small cell carcinoma of lung)
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Demeclocycline TOX
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Nephrogenic DI
Photosensitivity Bone and teeth abnormalities (member of tetracyclines) |
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Gluccocorticoids MOA
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DEC production of LT and PG by inhibiting phospholipase A2 and expression of COX-2
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Gluccocorticoids clinical use
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Addison's disease (DEC steroid production due to primary insufficiency)
inflammation immune suppression asthma |
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Gluccocorticoid TOX
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Iatorgenic Cushing's Syndrome
Adrenal insufficiency when drug stopped abruptly after chronic use (severe abdominal pains, vomiting, profound muscle weakness and fatigue, depression, extremely low blood pressure (hypotension), weight loss, kidney failure, changes in mood and personality, and shock) |