Endocrine Flashcards
Lispro
Rapid acting insulin
Binds insulin receptor (tyrosine kinase activity).
Liver: Increases glucose stored as glycogen
Fat: Increases TG storage
Muscle: Increases glycogen and protein synthesis, increases K uptake
Post-prandial glucose control in DM1, DM2, GDM
Hypoglycemia, rare hypersensitivity reactions
Aspart
Rapid acting insulin
Binds insulin receptor (tyrosine kinase activity).
Liver: Increases glucose stored as glycogen
Fat: Increases TG storage
Muscle: Increases glycogen and protein synthesis, increases K uptake
Post-prandial glucose control in DM1, DM2, GDM
Hypoglycemia, rare hypersensitivity reactions
Glulisine
Rapid acting insulin
Binds insulin receptor (tyrosine kinase activity).
Liver: Increases glucose stored as glycogen
Fat: Increases TG storage
Muscle: Increases glycogen and protein synthesis, increases K uptake
Post-prandial glucose control in DM1, DM2, GDM
Hypoglycemia, rare hypersensitivity reactions
Insulin
Short acting insulin
DM1, DM2, GDM, DKA (IV), hyperkalemia (with glucose), stress hyperglycemia
NPH
Intermediate acting insulin
DM1, DM2, GDM
Glargine
Long acting insulin
Basal glucose control in DM1, DM2, GDM
Detemir
Long acting insulin
Basal glucose control in DM1, DM2, GDM
Metformin
Biguanide
Unknown mechanism. Decreases gluconeogenesis, increases glycolysis, increases peripheral glucose uptake (insulin sensitivity), decreases glucose absorption. Primary effects in liver.
Oral. First line therapy in DM2. Can be used patients without islet function.
GI upset, lactic acidosis (contraindicated in renal failure)
Tolbutamide
First generation sulfonylurea
Closes K channel in β cell membrane, leading to depolarization and insulin release via increased Ca influx.
Stimulates endogenous insulin release in DM2. Not useful in DM1, requires islet cell function.
Risk of hypoglycemia increased in renal failure. Disulfiram-like (nausea, flushing, tachycardia, hyperventilation) effects.
Chlorpropamide
First generation sulfonylurea
Closes K channel in β cell membrane, leading to depolarization and insulin release via increased Ca influx.
Stimulates endogenous insulin release in DM2. Not useful in DM1, requires islet cell function.
Risk of hypoglycemia increased in renal failure. Disulfiram-like (nausea, flushing, tachycardia, hyperventilation) effects.
Glyburide
Second generation sulfonylurea
Closes K channel in β cell membrane, leading to depolarization and insulin release via increased Ca influx.
Stimulates endogenous insulin release in DM2. Not useful in DM1, requires islet cell function.
Hypoglycemia. Risk of hypoglycemia increased in renal failure.
Glimepiride
Second generation sulfonylurea
Closes K channel in β cell membrane, leading to depolarization and insulin release via increased Ca influx.
Stimulates endogenous insulin release in DM2. Not useful in DM1, requires islet cell function.
Hypoglycemia. Risk of hypoglycemia increased in renal failure.
Glipizide
Second generation sulfonylurea
Closes K channel in β cell membrane, leading to depolarization and insulin release via increased Ca influx.
Stimulates endogenous insulin release in DM2. Not useful in DM1, requires islet cell function.
Hypoglycemia. Risk of hypoglycemia increased in renal failure.
Pioglitazone
Glitazones/thiazolidinedione
Increases insulin sensitivity in peripheral tissue. Bind to peroxisome proliferator activated receptor (PPAR-γ), a nuclear transcription regulator.
Mono therapy in DM2 or combined with other agents.
Weight gain, edema, hepatotoxicity, heart failure.
Rosiglitazone
Glitazones/thiazolidinedione
Increases insulin sensitivity in peripheral tissue. Bind to peroxisome proliferator activated receptor (PPAR-γ), a nuclear transcription regulator.
Mono therapy in DM2 or combined with other agents.
Weight gain, edema, hepatotoxicity, heart failure.
Acarbose
α-glucosidease inhibitor
Inhibits intestinal brush border α-glucosidases. Delayed sugar hydrolysis and glucose absorption, leading to decreases in postprandial hyperglycemia.
Monotherapy in DM2 or in combination with other agents.
Diarrhea, flatulence, bloating, increased liver enzymes. Contraindicated in cirrhosis.
Miglitol
α-glucosidease inhibitor
Inhibits intestinal brush border α-glucosidases. Delayed sugar hydrolysis and glucose absorption, leading to decreases in postprandial hyperglycemia.
Monotherapy in DM2 or in combination with other agents.
Diarrhea, flatulence, bloating, increased liver enzymes. Contraindicated in cirrhosis.
Pramlintide
Amylin analog
Decreases gastric emptying, decreases glucagon
DM1 and DM2
Hypoglycemia, nausea, diarrhea
Exenatide
GLP-1 analog
Increases insulin, decreases glucagon release
DM2
Nausea, vomiting, pancreatitis
Liraglutide
GLP-1 analog
Increases insulin, decreases glucagon release
DM2
Nausea, vomiting, pancreatitis
Linagliptin
DPP-4 inhibitor
Increases insulin, decreases glucagon release
DM2
Mild urinary or respiratory infections
Saxagliptin
DPP-4 inhibitor
Increases insulin, decreases glucagon release
DM2
Mild urinary or respiratory infections
Sitagliptin
DPP-4 inhibitor
Increases insulin, decreases glucagon release
DM2
Mild urinary or respiratory infections
Propylthiouracil
Blocks thyroid peroxidase, inhibiting oxidation of iodide and organification (coupling) of iodine, leading to inhibition of thyroid hormone synthesis. Also blocks 5’-deiodinase, which decreases peripheral conversion of T4 to T3.
Hyperthyroidism. Safe in pregnancy.
Skin rash, agranulocytosis (rare), aplastic anemia, hepatotoxicity.
Methimazole
Blocks thyroid peroxidase, inhibiting oxidation of iodide and organification (coupling) of iodine, leading to inhibition of thyroid hormone synthesis.
Hyperthyroidism.
Skin rash, agranulocytosis (rare), aplastic anemia, teratogen (aplasia cutis).
Levothyroxine
Thyroxine replacement
Hypothyroidism, myxedema
Tachycardia, heat intolerance, tremors, arrhythmias
Triiodothyronine
Thyroxine replacement
Hypothyroidism, myxedema
Tachycardia, heat intolerance, tremors, arrhythmias
GH
GH deficiency, Turner Syndrome
Octreotide
Somatostatin
Acromegaly, carcinoid, gastrinoma, glucagonoma, esophageal varices
Oxytocin
Stimulates labor, uterine contractions, milk let-down, controls uterine hemorrhage
Demeclocycline
Tetracycline. ADH antagonist.
SIADH
Nephrogenic DI, photosensitivity, abnormalities of bone and teeth
Hydrocortisone
Glucocorticoid
Metabolic, catabolic, anti-inflammatory, and immunosuppressive effects mediated by interactions with glucocorticoid response elements and inhibition of transcription factors such as NF-κB
Addison disease, inflammation, immune suppression, asthma
Iatrogenic Cushing syndrome, adrenocortical atrophy, peptic ulcers, diabetes (if chronic), adrenal insufficiency when drugs are stopped abruptly after chronic use.
Prednisone
Glucocorticoid
Metabolic, catabolic, anti-inflammatory, and immunosuppressive effects mediated by interactions with glucocorticoid response elements and inhibition of transcription factors such as NF-κB
Addison disease, inflammation, immune suppression, asthma
Iatrogenic Cushing syndrome, adrenocortical atrophy, peptic ulcers, diabetes (if chronic), adrenal insufficiency when drugs are stopped abruptly after chronic use.
Triamcinolone
Glucocorticoid
Metabolic, catabolic, anti-inflammatory, and immunosuppressive effects mediated by interactions with glucocorticoid response elements and inhibition of transcription factors such as NF-κB
Addison disease, inflammation, immune suppression, asthma
Iatrogenic Cushing syndrome, adrenocortical atrophy, peptic ulcers, diabetes (if chronic), adrenal insufficiency when drugs are stopped abruptly after chronic use.
Dexamethasone
Glucocorticoid
Metabolic, catabolic, anti-inflammatory, and immunosuppressive effects mediated by interactions with glucocorticoid response elements and inhibition of transcription factors such as NF-κB
Addison disease, inflammation, immune suppression, asthma
Iatrogenic Cushing syndrome, adrenocortical atrophy, peptic ulcers, diabetes (if chronic), adrenal insufficiency when drugs are stopped abruptly after chronic use.
Beclomethasone
Glucocorticoid
Metabolic, catabolic, anti-inflammatory, and immunosuppressive effects mediated by interactions with glucocorticoid response elements and inhibition of transcription factors such as NF-κB
Addison disease, inflammation, immune suppression, asthma
Iatrogenic Cushing syndrome, adrenocortical atrophy, peptic ulcers, diabetes (if chronic), adrenal insufficiency when drugs are stopped abruptly after chronic use.
Fludrocortisone
Glucocorticoid and mineralocorticoid
Metabolic, catabolic, anti-inflammatory, and immunosuppressive effects mediated by interactions with glucocorticoid response elements and inhibition of transcription factors such as NF-κB
Addison disease, inflammation, immune suppression, asthma
Iatrogenic Cushing syndrome, adrenocortical atrophy, peptic ulcers, diabetes (if chronic), adrenal insufficiency when drugs are stopped abruptly after chronic use.
