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30 Cards in this Set
- Front
- Back
treatment of type I diabetes
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low-sugar diet, insulin replacement
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type II diabetes
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dietary modification, exercise, wl, oral hypoglycemics and insulin replacement
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insulin lispro
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rapid acting
Action: Bind insulin receptor (tyrosine kinase activity). Liver: increase glucose stored as glycogen. Muscle: increase glycogen and protein synthesis, K+uptake. Fat: aids TG storage. Clinical use: Type I DM, type 2 DM , gestational diabetes, Iife-threatening hyperkalemia, and stress-induced hyperglycemia. Toxicities: hypoglycemia, hypersensitivity reaction (very rare) |
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insulin aspart
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rapid-acting
Action: Bind insulin receptor (tyrosine kinase activity). Liver: increase glucose stored as glycogen. Muscle: increase glycogen and protein synthesis, K+uptake. Fat: aids TG storage. Clinical use: Type I DM, type 2 DM , gestational diabetes, Iife-threatening hyperkalemia, and stress-induced hyperglycemia. Toxicities: hypoglycemia, hypersensitivity reaction (very rare) |
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regular insulin
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rapid-acting
Action: Bind insulin receptor (tyrosine kinase activity). Liver: increase glucose stored as glycogen. Muscle: increase glycogen and protein synthesis, K+uptake. Fat: aids TG storage. Clinical use: Type I DM, type 2 DM , gestational diabetes, Iife-threatening hyperkalemia, and stress-induced hyperglycemia. Toxicities: hypoglycemia, hypersensitivity reaction (very rare) |
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NPH insulin
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intermediate acting
Action: Bind insulin receptor (tyrosine kinase activity). Liver: increase glucose stored as glycogen. Muscle: increase glycogen and protein synthesis, K+uptake. Fat: aids TG storage. Clinical use: Type I DM, type 2 DM , gestational diabetes, Iife-threatening hyperkalemia, and stress-induced hyperglycemia. Toxicities: hypoglycemia, hypersensitivity reaction (very rare) |
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insulin glargine
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long-acting
Action: Bind insulin receptor (tyrosine kinase activity). Liver: increase glucose stored as glycogen. Muscle: increase glycogen and protein synthesis, K+uptake. Fat: aids TG storage. Clinical use: Type I DM, type 2 DM , gestational diabetes, Iife-threatening hyperkalemia, and stress-induced hyperglycemia. Toxicities: hypoglycemia, hypersensitivity reaction (very rare) |
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insulin detemir
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long-acting
Action: Bind insulin receptor (tyrosine kinase activity). Liver: increase glucose stored as glycogen. Muscle: increase glycogen and protein synthesis, K+uptake. Fat: aids TG storage. Clinical use: Type I DM, type 2 DM , gestational diabetes, Iife-threatening hyperkalemia, and stress-induced hyperglycemia. Toxicities: hypoglycemia, hypersensitivity reaction (very rare) |
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tolbutamide
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Sulfonylurea; first generation
Action: Close K+ channel in B-cell membrane, so cell depolarizes --> triggering of insulin release vie increased Ca2+ influx Clinical use: Stimulate release of endogenous insulin in type 2 DM. Requires some islet function, so USELESS IN TYPE I DM. Toxicities: disulfiram like effects |
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chlorpropamide
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Sulfonylurea; first generation
Action: Close K+ channel in B-cell membrane, so cell depolarizes --> triggering of insulin release vie increased Ca2+ influx Clinical use: Stimulate release of endogenous insulin in type 2 DM. Requires some islet function, so USELESS IN TYPE I DM. Toxicities: disulfiram like effects |
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Glyburide
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Sulfonylurea, Second generation
Action: Close K+ channel in B-cell membrane, so cell depolarizes --> triggering of insulin release vie increased Ca2+ influx Clinical use: Stimulate release of endogenous insulin in type 2 DM. Requires some islet function, so USELESS IN TYPE I DM. Toxicities: hypoglycemia |
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Glimepiride
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Sullfonylurea, Second generation
Action: Close K+ channel in B-cell membrane, so cell depolarizes --> triggering of insulin release vie increased Ca2+ influx Clinical use: Stimulate release of endogenous insulin in type 2 DM. Requires some islet function, so USELESS IN TYPE I DM. Toxicities: hypoglycemia |
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Glipizide
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Sulfonylurea, Second generation
Action: Close K+ channel in B-cell membrane, so cell depolarizes --> triggering of insulin release vie increased Ca2+ influx Clinical use: Stimulate release of endogenous insulin in type 2 DM. Requires some islet function, so USELESS IN TYPE I DM. Toxicities: hypoglycemia |
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Metformin
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Biguanide
Action: Exact mechanism is unknown. decreased gluconeogenesis, increased glycolysis, increased peripheral glucose uptake (insulin sensitivity). Clinical use: Oral can be used in patients WITHOUT islet function Toxicities: Most grave adverse effect is lactic acidosis (CI in renal failure) - lactate is taken up into liver for gluconeogenesis, which is inhibited by metformin, therefore it builds up in the blood. |
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Pioglitazone
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glitazones/thiazolidinediones
Action: Increase insulin sensitivity in peripheral tissues (by causing a release of adipnectin from adipocytes). Binds to PPAR-gamma nuclear transcription regulator. Overall decreased gluconeogenesis and increased uptake in muscle. Clinical use: Used as monotherapy in type 2 DM or combined with other agents. toxicity: weight gain, edema, hepatotoxic. CI in class III/IV HF |
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Rosiglitazone
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glitazones/thiazolidinediones
Action: Increase insulin sensitivity in peripheral tissues (by causing a release of adipnectin from adipocytes). Binds to PPAR-gamma nuclear transcription regulator. Overall decreased gluconeogenesis and increased uptake in muscle. Clinical use: Used as monotherapy in type 2 DM or combined with other agents. toxicity: weight gain, edema, hepatotoxic. CI in class III/IV HF |
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Acarbose
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alpha-glucosidase inhibitors
Action: Inhibit intestinal brush border alpha-glucosidases. Delayed sugar hydrolysis and glucose absorption leads to DECREASED postprandial hyperglycemia. Clinical use: used as a monotherapy in type 2 DM or in combo. toxicity: GI disturbances |
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Miglitol
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alpha-glucosidase inhibitors
Action: Inhibit intestinal brush border alpha-glucosidases. Delayed sugar hydrolysis and glucose absorption leads to DECREASED postprandial hyperglycemia. Clinical use: used as a monotherapy in type 2 DM or in combo. toxicity: GI disturbances |
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Pramlintide
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amylin mimetic
Action: decreases release of glucagon Clinical use: type 2 DM toxicities: hypoglycemia, nausea, diarrhea |
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Exenatide
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GLP-1 analog
Action: increases insulin by stimulating release from beta cells decreases glucagon release slows gastric emptying clinical use: type 2 DM toxicities: nausea, vomiting, pancreatitis |
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propylthiouracil
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Mechanism: inhibit organification of iodide (I- --> I) and coupling (iodination) of thyroid hormone synthesis.
Also decreases peripheral conversion of T4 to T3 (methimazole does not) Clinical use: hyperthyroidism Toxicity: skin rash, agranulocytosis (rare severe and dangerous leukopenia), aplastic anemia |
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methimazole
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Mechanism: inhibit organification of iodide (I- --> I) and coupling (iodination) of thyroid hormone synthesis.
Clinical use: hyperthyroidism Toxicity: skin rash, agranulocytosis (rare severe and dangerous leukopenia), aplastic anemia Possible teratogen (PTU is not) |
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levothyroxine
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T4
Mechanism: thyroxine replacement Clinical use: hypothyroidism, myxedema Toxicity: tachycardia, heat intolerance, tremors, arrhythmias |
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triiodothyronine
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T3
Mechanism: thyroxine replacement Clinical use: hypothyroidism, myxedema Toxicity: tachycardia, heat intolerance, tremors, arrhythmias |
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GH
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GH deficiency
Turner's |
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Somatostatin (octreotide)
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acromegaly
carcinoid gastrinoma glucagonoma |
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oxytocin
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stimulates labor
uterine contractions milk let-down controls uterine hemorrhage |
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ADH (desmopressin)
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pituitary (central) DI
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Demeclocycline
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Mechanism: ADH antagonist (a tetracycline antibiotic)
clinical use: SIADH toxicity: nephrogenic DI, photosensitivity, abnormalities of bone and teeth conivaptan also used to treat SIADH |
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Hydrocortisone
Prednisone Triamcinolone dexamethasone beclomethasone |
Mechanism: decrease the production of leukotrienes and prostaglandins by inhibiting PLA2 and expression of COX2.
Clinical use: Addison's disease, inflammation, immune suppression, asthma. Toxicity: Iatrogenic Cushing's syndrome - buffalo hump, moon facies, truncal obesity, muscle wasting, thin skin, easy bruisability, osteoporosis, adrenocortical atrophy, peptic ulcers, diabetes (if chronic - GCs are primarily catabolic; also increase the enzymes for gluconeogenesis and glycogen synthesis, thereby antagonizing insulin, leading to hyperglycemia). Adrenal insufficiency when drug stopped after chronic use. |