Endocrin Pharm Flashcards
What are the rapid acting insulins?
Iispro Aspart Glulisine
Mech of lispro aspart glulisine?
Bind insulin receptor (tyrosine kinase activity). Liver: increase glucose stored as glycogen. Muscle: increase glycogen, protein syntesis; increase K+ uptake. Fat: increase TG storage
clinical use of rapid acting insulins
DM1, DM2, GDM (postprandial glucose control)
What are the SE of rapid acting insulins?
hypoglycemia, rare hypersensitivity
What is the insulin, short acting?
regular
What is the clinical use of the regular short acting insulin?
DM1, DM2, GDM, DKA (IV), hyperkalemia (+glucose), stress hyperglycemia.
What is the intermediate acting insulin?
NPH
Clinical use of NPH
DM1, DM2, GDM
What are the long acting insulins?
Glargine, Detemir
Glargine, Detemir Clinical use?
DM1, DM2, GDM (basal glucose control)
Biguanides (Metformin) mech of action?
Exact mech is unknown. Decreased gluconeogenesis, increased glycolysis, increased peripheral glucose uptake (insulin sensitivity)
Metformin clinical use?
oral. first-line therapy in type 2 DM. Can be used in patients without islet function.
Metformin toxicities
GI upset; most serious adverse effect is lactic acidosis (thus contraindicated in renal failure)
Whatare the first generation sulfonylureas?
Tolbutamide, Chlorpropamide
What are the second generation Sulfonylureas?
Glyburide, Glimepiride, Glipizide
Sulfonylureas mech
Close K+ channel in beta cell membrane, so cell depolarizes which triggers insulin release via Ca++ influx
Sulfonylureas clinical use
stimulate release of endogenous insulin in type 2 DM. Require some islet function, so useless in type 1 DM
Sulfonylureas SE
Risk of hypoglycemia increase in renal failure. First generation: disulfiram-like effects. Second generation: hypoglycemia
What are the Glitazones/thiazolidinediones?
Pioglitzone, Rosiglitazone
What is the mech of the glitzones/thiazolideinediones?
increase insulin sensitivity in peripheral tissue. binds to PPAR glamma nuclear transcription factor
Clinical use of glitzones/thiazolideinediones?
monotherapy in type 2 DM comined with biguanides, sulfonylureas, or insulins.
SE of glitzones/thiazolideinediones?
weight gain, edema. hepatotoxicity, heart failure.
What are the alpha glucosidase inhibitors
Acarbose. Miglitol
What is the mech of alpha glucosidase inhibitors?
Inhibit intestinal brush border alpha glucosidases. Delayed sugar hydrolysis and glucose absorption which leads to decrease postprandial hyperglycemia.
What is the clinical use of the alpha glucosidase inhibitors?
monotherapy in type 2 DM or in combination with above agents
What are the toxicities of alpha glucosidase inhibitors?
GI disturbances
What is the Amylin analog?
Pramlintide
Mech of the amylin analog pramlintide?
decrease gastric emptying, decrease glucagon
Clinical use of the amylin analog pramlintide?
Type 1 DM and Type 2 DM
SE of the amylin analog pramlintide?
hypoglycemia, nausea, diarrhea
What are the GLP-1 analogs?
Exenatide, Liraglutide
Mech of the GLP-1 analogs exenatide, liraglutide?
increase insulin, decrease glucagon release
clinical use of the GLP-1 analogs exenatide, liraglutide?
type 2 DM
SE of the GLP-1 analogs exenatide, liraglutide?
nausea, vomiting; pancreatitis
What are the DPP-4 (dipeptidyl peptide 4) inhibitors?
Linagliptin, Saxagliptin, Sitagliptin
Mech of action of Linagliptin, Saxagliptin, Sitagliptin?
Increase insulin, decrease glucagon release
Clinical use of DPP-4 inhibitors Linagliptin, Saxagliptin, Sitagliptin
Type 2 DM
SE of DPP-4 inhibitors Linagliptin, Saxagliptin, Sitagliptin?
Mild urinary or respiratory infections
Genes activated by PPAR gamma regulate what?
fatty acid storage and glucose metabolism. Activation of PPAR gamma increases insulin sensitivity and levels of adiponectin
Propylthyiuracil, methimazole mech
block thyroid peroxidase, inhibiting the oxidation of iodide and the organification (coupling) of iodine inhibition of thyroid hormone synthesis. Propylthiouracil also blocks 5’ deiodinase which decreases peripheral conversion of T4 to T3
What is the clinical use of propylthiouracil, methimazole?
Hyperthyroidism. PTU blocks Peripheral conversion, used in Pregnancy
What are the SE of propylthiouracil and methimazole?
Skin rash, agranulocytosis (rare), aplastic anemia, hepatotoxicity (propylthiouracil). Methimazole is a possible teratogen (can cause aplasia cutis)
Levothyroxin, triiodothyronine mech
Thyroxin replacement
Levothyroxine, triiodothyronine clinical use
Hypothyroidism, myxedmea
Levo triiodothyronine SE
Tachycardia, heat intolerance, tremors, arrythmias
GH use
GH deficiency, Turner
Somatostatin (octreotide)
Acromegaly, carcinoma, gastrinoma, glucoagonma, esophageal varices.
Oxytocin
Stimulates labor, uterine contractions, milk let-down; controls uterine hemorrhage
ADH (DDAVP)
Pituitary (central, not nephrogenic) DI
Demeclocycline mech
ADH antagonist (membrane of the tetracycline family)
Demeclocycline clinical use
SIADH
Demeclocycline toxicity
Nephrogenic DI, photosensitivity, abnormalties of bone and teeth
Glucocorticoid examples
hydrocortisone, prednisone, tramcinolone, dexamethasone, beclomethasone, fludrocortisone, (mineralcocorticoid and glucocorticoid activity)
What is the mech of the glucocorticoids
Metabolic, catabolic, anti inflammatory, and immunosuppressive effects mediated by interactions with glucocorticoid response elements and inhibition of transcription factors such as NF-kB
Clinical use of glucocorticoids
Addison disease, inflammation, immune suppression, asthma
SE of glucocorticoids
Iatrogenic Cushing syndrome: buffalo hump, moon facies, trunal obesity, muscle wasting, thin skin, easy bruisabliity, osteoporosis (Treat with bisphosphonates), adrenocortical atrophy, peptic ulcers, diabetes (if chronic). Adrenal insufficiency when drug stopped abruptly after chronic use.
