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27 Cards in this Set

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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
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
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)
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
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
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
Glucocorticoids
(a) example
(b) indications
(c) mechanism
(a) hydrocortisone
(b) adrenocortical insufficiency (Addison disease, acute adrenal insufficiency from other causes)
(c) replacement therapy
Mineralcorticoids
(a) example
(b) indications
(c) mechanism
(a) gludrocortisone
(b) chronic treatment of Addison's disease in patients requiring mineralcorticoids
(c) replacement therapy
Glucocorticoid synthesis inhibitors
(a) examples
(b) indications
(a) aminoglutethimide, metyrapone, ketoconazole
(b) suppress adrenocortical steroid roduction (Cushing's, Cushingoid states, congenital adrenal hyperplasia)
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
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
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)
Name 1st generation sulfonylureas
Tolbutamide
Chlopropamide
Name 2nd generation sulfonylyreas
Glyburide
Glimepiride
Glipizide
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
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
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
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)
Pramlintide
(a) mechanism of action
(b) clinical use
(c) toxicity
(a) mimetic; decreases glucagon
(b) type IIDM
(c) hypoglycemia, nausea, diarrhea
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;
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
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
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
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
Levothyroxine, triidiothyronine
(a) mechanism
(b) clinical use
(c) toxicity
(a) thyroxine replacement
(b) hypothyroidism, myxedema
(c) tachycardia, heat intolerance, tremors, arrhythmias
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)
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