FA Endocrine Flashcards
Insulin, Rapid Acting
Lispro, Aspart, Glulisine
Insulin, Short Acting
Regular
Insulin, Intermediate Acting
NPH
Insulin, Long Acting
Glargine, Detemir
Insulin Mechanism
Bind insulin receptor (tyrosine kinase activity).
Liver: ↑ glucose stored as glycogen.
Muscle: ↑ glycogen, protein synthesis; ↑ K+ uptake.
Fat: ↑ TG storage.
Insulin, Rapid Acting Use
DM1, DM2, GDM (postprandial glucose control)
Insulin, Short Acting Use
DM1, DM2, GDM, DKA (IV), hyperkalemia (+ glucose), stress hyperglycemia.
Insulin, Intermediate Acting Use
DM1, DM2, GDM.
Insulin, Long Acting Use
DM1, DM2, GDM (basal glucose control).
Insulin Toxicity
Hypoglycemia, rare hypersensitivity reactions.
Biguanides
Metformin
Metformin Mechanism
Exact mechanism unknown. ↓ gluconeogenesis, ↑ glycolysis, ↑ peripheral glucose uptake (insulin sensitivity).
Metformin Use
Oral. First-line therapy in type 2 DM. Can be used in patients without islet function.
Metformin Toxicity
GI upset; most serious adverse effect is lactic acidosis (thus contraindicated in renal failure).
Sulfonylureas
First generation: Tolbutamide, Chlorpropamide
Second generation: Glyburide, Glimepiride, Glipizide
Sulfonylurea Mechanism
Close K+ channel in β-cell membrane, so cell depolarizes → triggering of insulin release via ↑ Ca2+ influx.
Sulfonylurea Use
Stimulate release of endogenous insulin in type 2 DM. Require some islet function, so useless in type 1 DM.
Sulfonylurea Toxicity
Risk of hypoglycemia ↑ in renal failure. First generation: disulfiram-like effects. Second generation: hypoglycemia.
Glitazones/thiazolidinediones
Pioglitazone, Rosiglitazone
Glitazone Mechanism
↑ insulin sensitivity in peripheral tissue. Binds to PPAR-γ nuclear transcription regulator.
Glitazone Use
Used as monotherapy in type 2 DM or combined with other agents.
Glitazone Toxicity
Weight gain, edema. Hepatotoxicity, heart failure.
α-glucosidase Inhibitors
Acarbose, Miglitol
α-glucosidase Inhibitor Mechanism
Inhibit intestinal brush-border α-glucosidases. Delayed sugar hydrolysis and glucose absorption → ↓ postprandial hyperglycemia.
α-glucosidase Inhibitor Use
Used as monotherapy in type 2 DM or combined with other agents.
α-glucosidase Inhibitor Toxicity
GI disturbances
Amylin analogs
Pramlintide
Pramlintide Mechanism
↓ gastric emptying, ↓ glucagon.
Pramlintide Use
Type 1 and 2 DM.
Pramlintide Toxicity
Hypoglycemia, nausea, diarrhea.
GLP-1 Analogs
Exenatide, Liraglutide
GLP-1 Analog Mechanism
↑ insulin, ↓ glucagon release.
GLP-1 Analog Use
Type 2 DM.
GLP-1 Analog Toxicity
Nausea, vomiting; pancreatitis.
DPP-4 Inhibitors
Linagliptin, Saxagliptin, Sitagliptin
DPP-4 Inhibitor Mechanism
↑ insulin, ↓ glucagon release.
DPP-4 Inhibitor Use
Type 2 DM.
DPP-4 Inhibitor Toxicity
Mild urinary or respiratory infections.
PTU, Methimazole Mechanism
Block thyroid peroxidase, inhibiting oxidation of iodide and organification (coupling) of iodine → inhibition of thyroid hormone synthesis. PTU also blocks 5’-deiodinase, which ↓ peripheral conversion of T4 to T3.
PTU, Methimazole Use
Hyperthyroidism. PTU blocks Peripheral conversion, used in Pregnancy.
PTU, Methimazole Toxicity
Skin rash, agranulocytosis (rare), aplastic anemia, hepatotoxicity (PTU). Methimazole is a possible teratogen (can cause aplasia cutis).
Levothyroxine, Triiodothyronine Mechanism
Thyroxine replacement.
Levothyroxine, Triiodothyronine Use
Hypothyroidism, myxedema.
Levothyroxine, Triiodothyronine Toxicity
Tachycardia, heat intolerance, tremors, arrhythmias.
GH Use
GH deficiency, Turner syndrome
Somatostatin (octreotide) Use
Acromegaly, carcinoid, gastrinoma, glucagonoma, esophageal varices.
Oxytocin Use
Stimulates labor, uterine contractions, milk let-down; controls uterine hemorrhage.
ADH (DDAVP) Use
Pituitary (central, not nephrogenic) DI.
Demeclocycline Mechanism
ADH antagonist (member of tetracycline family).
Demeclocycline Use
SIADH
Demeclocycline Toxicity
Nephrogenic DI, photosensitivity, abnormalities of bone and teeth.
Glucocorticoids
Hydrocortisone, prednisone, triamcinolone, dexamethasone, beclomethasone, fludrocortisone (mineralocorticoid and glucocorticoid activity).
Glucocorticoid mechanism
Metabolic, catabolic, anti-inflammatory, and immunosuppressive effects mediated by interactions with glucocorticoid respones elements and inhibition of transcription factors such as NF-κB.
Glucocorticoid Use
Addison disease, inflammation, immune suppression, asthma
Glucocorticoid Toxicity
Iatrogenic Cushing syndrome - buffalo hump, moon facies, truncal obesity, muscle wasting, thin skin, easy bruisability, osteoporosis (treat with bisphosphonates), adrenocortical atrophy, peptic ulcers, diabetes (if chronic).
Adrenal insufficiency when drug stopped abruptly after chronic use.
