FA Endo Pharm Flashcards
Exact mechanism is unknown.
Dec gluconeogenesis, inc glycolysis, inc peripheral glucose uptake (insulin sensitivity); first line in type 2 DM.
SE: lactic acidosis (CI in RF, LF, CHF, check BUN/Cr before starting)
Metformin
Close K+ channel in beta cell membrane, so cell depolarizes –> insulin release via Ca2+ influx.
Sulfonylureas (2G: glyburide, glimepiride, glipizide)
Inc insulin sensitivity in peripheral tissue. Binds to PPAR-gamma nuclear transcription regulator –> increased insulin sensitivity and adiponectin.
SE: fluid retention, hepatox, hear failure
TZDs ( -glitazones)
Inhibit intestinal brush border alpha glucosidases.
SE: GI disturbances
Acarbose and miglitol
Decrease gastric emptying, decrease glucagon.
SE: hyoglycemia, nausea, diarrhea
Amylin analogs (Pramlintide)
Increase insulin, decrease glucagon release.
GLP-1 analogs (Exenatide, Liraglutide)
- SE: N/V, pancreatitis
DPP-4 inhibitors (-gliptans)
- SE mild UTI or URTI
Insulin - Lispro, Aspart, Glulisine
Rapid acting
Insulin - Regular
Short acting
Insulin - NPH
Intermediate acting
Insulin - Glargine, Detemir
Long acting
Ex: Glyburide, Glimepiride, Glipizide
Sulfonylureas
Ex: Pioglitazone, Rosiglitazone
TZDs
Ex: Acarbose, Miglitol
alpha-glucosidase inhibitors
Ex: Pramlintide
amylin analog
Ex: Exenatide, Liraglutide
GLP-1 analog
Ex: Linagliptin, Saxagliptin, Sitagliptin
DPP-4 inhibitors
Block thyroid peroxidase, inhibiting the oxidation of iodide and the organification (coupling) of iodine –> inhibition of thyroid hormone synthesis; ALSO blocks peripheral conversion of T4 to T3
PTU
Block thyroid peroxidase, inhibiting the oxidation of iodide and the organification (coupling) of iodine –> inhibition of thyroid hormone synthesis; does NOT block peripheral conversion of T4 to T3
Methimazole
Thyroxine replacement
Levothyroxine, triiodothyonine
ADH antagonist (member of the tetracycline family). SE: nephrogenic DI, photosensitivity, abnormalities of bone and teeth
Demeclocycline
Metabolic, catabolic, anti-inflammatory, and immunosuppressive effects mediated by interactions with glucocorticoid response elements and inhibition of transcription factors such as NF-kappaB.
SE: iatrogenic cushings - osteoporosis, diabetes, adrenal crisis if stopped
Glucocorticoids
