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23 Cards in this Set
- Front
- Back
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Treatment strategy for type 1 DM
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low sugar diet, insulin replacement
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Treatment strategy for type 2 DM
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dietary modification and exercise for weight loss
oral hypoglycemics and insulin replacement |
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Insulin replacement therapies
a. 3 rapid acting agents b. 1 intermediate acting agent c. 2 long acting agents |
a. lispro, aspart, regular
b. NPH c. glargine, detemir |
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Treatment for
-type 1 DM -type 2 DM -gestational diabetes -life-threatening hyperkalemia -stress-induced hyperglycemia MOA |
insulin drugs
bind insulin receptor (tyrosine kinase) |
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3 effects of insulin replacement therapies
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Binds insulin receptor
1. LIver = increases glucose stored as glycogen 2. Muscle = increased glycogen and protein synthesis, K uptake 3. fat = aids TG storage |
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2 first generation sulfonylureas
3 second gen |
first: tolbutamide, chlorporpamide
second: glyburide, glimepiride, glipizide |
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drugs that stimulate the release of endogenous insulin in type 2 DM
require some islet function, so useless in type 1 DM MOA |
sulfonylureas
close K channel in beta-cell membrane --> cell deplarizes --> triggers insulin release via increased Ca influx |
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Toxicity of insulin replacement therapies
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hypoglycemia, hypersensitivity
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Toxicities of
a. first gen sulfonylureas b. second gen |
a. disulfiram-like
b. hypoglycemia |
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Diabetes drug used orally, can be taken in patients without islet function
can cause lactic acidosis, so contraindicated in renal failure drug? MOA? |
Metformin (biguanide)
decreaess gluconeogenesis, increases glycolysis, increases peripheral glucose uptake (insulin sensitivity) |
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Monotherapy for type 2 DM by binding to PPAR-g nuclear transcription regulator -> increasing insulin sensitivity in peripheral tissue
2 drugs? adverse? |
pioglitazone, rosiglitazone (thiozaolidinediones/glitazones)
wt. gain, edema, hepatotoxicity, CV toxicity |
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a-glucosidase inhibitors
2 drugs MOA use? when is it very useful? tox |
acarbose
miglitol inhibits intestinal brush border a-glucosidases --> delayed sugar hydrolysis and gluclose absorption --> decreased post prandial hyperglycemia montherapy for type 2/useful for post prandial Gi disturbances |
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Pramlintide
a. MOA b. use c. tox |
a. decreases glucagon
b. type 2 DM c. hypoglycemia, nausea, diarrhea |
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Exenatide (GLP-1 analog)
a. action b. use c. tox |
a. inc. insulin, dec. glucagon release
b. type 2 DM c. nausea, vomiting, pancreatitis |
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Propythiouracil, methimazole
MOA USe tox |
Inhibits organification of Iodide and coupling of thyoroid hormone synth
propylthiouracil decreases peripheral conversion of T4 --> T3 Hyperthyroid Skin rash, agranulocytosis, aplastic anemia, hepatotox methimazole = teratogen |
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Levothyroxine, triiodothyronine
MOA Use Tox (4) |
Thyroxine replacement
hypothyroidism, myxedema tachycardia, heat intolerance, tremor, arrhythmia |
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Hypothalamic/pituitary drugs
what drug for: -GH deficiency, Turner syndrome |
GH
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Hypothalamic/pituitary drugs
what drug for: acromegaly, carcinoid, gastrinoma, glucagonoma |
somatostatin (octreotide)
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Hypothalamic/pituitary drugs
what drug for: stimulates labor, uterine contractions, milk let-down; controls uterine hemorrhage |
oxytocin
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Hypothalamic/pituitary drugs
what drug for: pituitary DI |
ADH (desmopressin)
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Drug for SIADH
MOA Tox |
ADH antagonist (tetracycline family)
tox = nephrogenic Di, photosensitivity, abnormal bone and teeth |
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Hydrocortison, prednisone, triamcinolone, dexamethasone, becleomethasone
a. MOA b. use c. tox |
lowers LTs and PGs by inhibiting Phospholipase A1 and COX-2 expression
b. Addison's, inflammation, immune suppression, asthma c. Iatrogenic cushing's |
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What happens if you stop glucocorticoids after chronic use
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adrenal insufficiency if stopped after chronic use
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