Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
11 Cards in this Set
- Front
- Back
|
Insulin- Lispro/Aspart/Regular (rapid); NPH (intermediate), Glargine/Detemir (long-acting)
|
Action- Bind insulin receptor (RTK). Liver: increase glucose stored as glycogen; Muscle: increase glycogen and protein synthesis, potassium uptake; Fat: aids TG storage
Use: Type 1 DM, type 2 DM, gestational DM, life-threatening hyperkalemia, stress-induced hyperglycemia Toxicity: hypoglycemia, hypersensitivity reaction (very rare) |
|
|
Tolbutamide/Chlorpropamide (1st gen), Glyburide/Glimepiride/Glipizide (2nd gen)
|
Sulfonylureas: Action: Close K channel in B-cell membrane so cell depolarizes, triggering of insulin release via increased Ca influx
Use: Stimulate release of endogenous insulin in type 2 DM. Require some islet function, so useless in type 1 DM Toxicities: First generation disulfiram-like effects, 2nd generation hypoglycemia. |
|
|
Biguanides- Metmorfin
|
Action: Decrease gluconeogenesis, increase glycolysis, increase peripheral glucose uptake (insulin sensitivity)
Use: Oral; can be used in patients without islet function, PCOS, okay to use in pregnancy Toxicity: Lactic acidosis (CX in renal failure) |
|
|
Glitazones/Thiazolidinediones- Pioglitazone, Rosiglitazone
|
Action: Increased insulin sensitivity in peripheral tissue. Binds to PPAR-gamma nuclear transcription regulator.
Clinical use: Monotherapy in type 2 DM or in combination with above agents. Toxicity: Weight gain, edema (dangerous in patients with CHF), hepatotoxicity (get LFTs), CV toxicity (MI) |
|
|
Pramlintide
|
Action: Mimetics- Decrease glucagon
Use: Type 2 DM Toxicity: Hypoglycemia, nausea, diarrhea |
|
|
Exenatide
|
Action: GLP-1 analogs- Increase insulin, decrease glucagon release
Use: Type 2 DM Toxicity: N/V, pancreatitis |
|
|
Propylthiouracil, methimazole
|
Mechanism: Inhibit organification of iodide and coupling of thyroid hormone synthesis (Inhibit iodination of thyroid groups). Propylthiouracil also decreases peripheral conversion of T4 to T3.
Clinical use: Hyperthyroidism Toxicity: Skin rash, agranulocytosis (rare), aplastic anemia, Methimazole is a possible teratogen |
|
|
Levothyroxine, triiodothyronine
|
Mechanism: Thyroxine replacement
Clinical use: Hypothyroidism, myxedema Toxicity: Tachycardia, heat intolerance, tremors, arrhythmias |
|
|
Hypothalamic/pituitary drugs
|
GH- GH deficiency, Turner syndrome
Somatostatin (octreotide)- Acromegaly, carcinoid, gastrinoma, glucagonoma Oxytocin- Stimulates labor, uterine contractions, milk let-down, controls uterine hemorrhage ADH (desmopressin)- Pituitary (central, NOT NEPHROGENIC) DI |
|
|
Demeclocycline
|
Mechanism: ADH antagonist (member of the tetracycline family)
Clinical use: SIADH Toxicity: Nephrogenic DI, photosensitivity, abnormalities of bone and teeth. |
|
|
Glucocorticoids- Hydrocortisone, prednisone, triamcinolone, dexamethasone, beclomethasone
|
Mechanism: Decreases the production of LKTs and PGs by inhibiting PLA2 and expression of COX-2
Clinical use: Addison's disease, inflammation, immune suppression, asthma, keloids (decreases collagen synthesis) 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). Adrenal insufficiency when drug is stopped after chronic use. Insomnia, glaucoma, acne, psychosis |
