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27 Cards in this Set
- Front
- Back
Somatropin/Somatrem
(a) mechanism (b) indications |
(a) recombinant forms of GH; stimulates linear/skeletal growth for pediatric patients
(b) growth failure, Turner's, cachexia, somatotropin deficiency |
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Octreotide
(a) mechanism (b) indications |
(a) long acting octapeptide that mimics somatostatin; inhibits release of GH, glucagon, gastrin, thyrotropin, insulin
(b) acromegaly, carcinoid, glucagonoma, gastrinoma, other endocrine tumors |
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Thioamides
(a) examples (b) indications (c) mechanism (d) side effects |
(a) PTU, methimazole
(b) long term hyperthyroid tx (c) inhibit synth against thyroid hormones (do NOT inactivate existing T4, T3); PTU can inhibit peripheral conversion of T4 to T3 (d) skin rash (common); hematologic effects (rare) |
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Iodides
(a) examples (b) indications (c) mechanism |
(a) Lugol's solution, potassium iodide alone
(b) prep for thyroid surgery; treat thyrotoxic crisis and thyroid blocking in radiation emergency (c) inhibit release of T4 and T4 (primary); also inhibit biosynth of T4, T3 and decrease size and vascularity of thyroid gland |
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Beta blockers in thyroid treatment
(a) examples (b) indication |
(a) nadolol, propranolol
(b) nonselective beta blockers used for palpitation, anxiety, tremor and heat intolerance; partially inhibit conversion of T4 |
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Radioactive iodine
(a) indications (b) mechanism |
(a) 1st line therapy for Grave's; treatment of choice for thyrotoxicosis in adults/elderly
(b) ablation of thyroid gland |
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Glucocorticoids
(a) example (b) indications (c) mechanism |
(a) hydrocortisone
(b) adrenocortical insufficiency (Addison disease, acute adrenal insufficiency from other causes) (c) replacement therapy |
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Mineralcorticoids
(a) example (b) indications (c) mechanism |
(a) gludrocortisone
(b) chronic treatment of Addison's disease in patients requiring mineralcorticoids (c) replacement therapy |
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Glucocorticoid synthesis inhibitors
(a) examples (b) indications |
(a) aminoglutethimide, metyrapone, ketoconazole
(b) suppress adrenocortical steroid roduction (Cushing's, Cushingoid states, congenital adrenal hyperplasia) |
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Bisphosphonates
(a) examples (b) indications (c) mechanism (d) side effects |
(a) alendronate, etidronate, pamidronate, risedronate
(b) osteoporosis, Paget disease (c) decr bone resorption (d) esophageal ulceration may occur |
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Give examples
(a) short acting (b) rapid acting (c) intermediate acting (d long acting (e) ultralong acting |
(a) short acting: lispro, aspart
(b) rapid acting: regular (c) intermediate acting: NPH, Lente (d long acting: ultralente (e) ultralong acting: glargine, detemir |
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Insulin
(a) action (b) clinical use (c) toxicity |
(a) Bind insulin receptor (tyrosine kinase activity)
Liver: incr glucose (stored as glycogen) Muscle: incr glycogen and protein synth; K+ uptake Fat: aids TG storage (b) TI and TIIDM; also life threatening hyperkalemia and stress induced hyperglycemia (c) hypoglycemia, hypersensitivity (rare) |
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Name 1st generation sulfonylureas
|
Tolbutamide
Chlopropamide |
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Name 2nd generation sulfonylyreas
|
Glyburide
Glimepiride Glipizide |
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Sulfonylureas
(a) action (b) clinical use (c) toxicities |
(a) close K+ channel in beta cell membrane so cell depolarizes, triggerig insulin release via increased Ca++ influx
(b) stimulates release of endogenous insulin in type II DM. Require some islet fct so not used in TIDM (c) first generation: disulfiram like effects Second gen: hypoglycemia |
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Biguanides
(a) examples (b) mechanism of action (c) clinical use (d) toxicities |
(a) metformin
(b) possibly decr gluconeogenesis, incr glycolysis, decr serum glucose levels (acts as an insulin sensitizer) (c) oral hypoglycemic; used in patients without islet fct (d) can cause lactic acidosis |
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Glitazones/Thiazolidinediones
(a) examples (b) mechanism of action (c) clinical use (d) toxicities |
(a)rosiglitazone, pioglitazone
(b) bind PPARgamma receptor to incr target tissue sensitivity to insulin, inhibits hepatic glucose output, incr glucose uptake (c) used as monotherapy in TIIDM or combined with other agents (d) wt gain, edema, hepatotoxicity, CV toxicity |
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Alpha glucosidase inhibitors
(a) examples (b) mechanism of action (c) clinical use (d) toxicities |
(a) acarbose, miglitol
(b) inhibit intestinal brush border alpha glucosidase to delay sugar hydrolysis, glucose absorption (leads to decreased posprandial hyperglycemia) (c) used as monotherapy in TIIDM or in combo with other agnets (d) Gi disturbances (flatulence and diarrhea) |
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Pramlintide
(a) mechanism of action (b) clinical use (c) toxicity |
(a) mimetic; decreases glucagon
(b) type IIDM (c) hypoglycemia, nausea, diarrhea |
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GLP-1 mimics
(a) examples (b) mechanism of action (c) toxicity |
(a) exenatide
(b) increase insulin, decrease glucagon release (c) type IIDM (d) nausea, vomiting; |
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Orlistat
(a) mechanism (b) clinical use (c) toxicity |
(a) inhibits pancreatic lipase
(b) long term obesity management (in conjunction w/diet) (c) steatorrhea, GI discomfort, reduced absorption of fat soluble vits, HA |
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Sibutramine
(a) mechanism (b) clinical use (c) toxicity |
(a) sympathomimetic serotonin and norep reuptake inhibitor
(b) short and long term obesity management (c) HTn and tachycardia |
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PTU, methimazole
(a) mechanism (b) clinical use (c) toxicity |
(a) inhibit organification and coupling of TH synthesis; PTU also decr converstin of T4 to T3
(b) hyperthyroidism (c) skin rash, agranulocytosis (rare), aplastic anemia |
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Hypothalamic/pituitary drugs clinical uses
(a) GH (b) somatostatin (octreotide) (c) oxytocin (d) ADH (desmopressin) |
(a) GH: GH deficiency, Turner's
(b) somatostatin (octreotide): acromegaly, carcinoid, gastrinoma, glucagonoma (c) oxytocin: stimulates labor, uterine contractions, mil let down; controls uterine hemorrhage (d) ADH (desmopressin): pituitary diabetes insipidus |
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Levothyroxine, triidiothyronine
(a) mechanism (b) clinical use (c) toxicity |
(a) thyroxine replacement
(b) hypothyroidism, myxedema (c) tachycardia, heat intolerance, tremors, arrhythmias |
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Glucocorticoids
(a) examples (b) mechanism (c) clinical use (d) toxicity |
(a) hydrocortisone, prednisone, triamcinolone, dexamethasone, becomethasone
(b) decr the production of leukotrienes and prostaglandins by inhibiting phospholipase A2 and expression of COX2 (c) addison's disease, inflammation, immune suppression, asthma (d) Iatrogenic cushings;osteoporosis, adrenocorticocal atrophy, peptic ulcers, diabetes (if chronic) |
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Demeclocycline
(a) mechanism (b) clinical use (c) toxicity |
(a) ADH antagonist (member of tetracycline family)
(b) Diabetes Insipidus, SIADH (c) photosensitivity, abnormalities of bone/teeth |