Endocrine Drug Introduction Endocrine medications can be broken down into the following categories diabetic agents hormone agonists hormone antagonists Endocrine Drug Table Diabetic Agents Sulfonylureas (1st Generation) Name Mechanism of Action Key Indication(s) Key Toxicity Chlorpropamide Tolazamide Tolbutamide Inhibits ATP-sensitive K+ channels resulting in β-cell depolarization and insulin release Second-line treatment for type II diabetes Hypoglycemia (long-lasting) Renal failure Disulfiram effects Sulfonylureas (2nd Generation) Name Mechanism of Action Key Indication(s) Key Toxicity Glipizide Glyburide Inhibits ATP-sensitive K+ channels resulting in β-cell depolarization and insulin release Second-line treatment for type II diabetes Hypoglycemia (long-lasting) Renal failure Disulfiram effects Biguinides Name Mechanism of Action Key Indication(s) Key Toxicity Metformin Exact mechanism unknown ↓ gluconeogenesis ↑ insulin sensitivity ↑ glycolysis ↓ serum glucose levels ↓ postprandial glucose levels First-line treatment for type II diabetes and metabolic syndrome Lactic acidosis in patients with poor renal function Alpha-Glucosidase Inhibitor Name Mechanism of Action Key Indication(s) Key Toxicity Acarbose Miglitol Prevents breakdown of carbohydrates into single glucose molecules decreasing rate of absorption Refractory type II diabetes mellitus Osmotic diarrhea Flatulence Thioglitazones Name Mechanism of Action Key Indication(s) Key Toxicity Pioglitazone Troglitazone Rosiglitazone Stimulates PPAR-γ which controls insulin-sensitive genes resulting in increased insulin sensitivity in peripheral tissues Type II diabetes combination therapy Heart failure Hepatotoxicity Weight gain Other Name Mechanism of Action Key Indication(s) Key Toxicity Repaglinide Inhibits ATP-sensitive K+ channels resulting in β-cell depolarization and insulin release Type II diabetes combination therapy Hypoglycemia Hormone Agonists Estrogen Name Mechanism of Action Key Indication(s) Key Toxicity Polyestradiol Inhibits actions of dihydrotestosterone Blocks LH secretion by pituitary Decreases testosterone synthesis Blocks testosterone uptake into prostate cells Inhibits 5α-reductase Induces chemical castration Palliative prostate cancer therapy Feminization Nausea Headache Water retention Diethylstilbestrol Inhibits HPG axis Blocks testosterone synthesis Induces chemical castration Believed to decrease incidence of stillbirth No longer used in the US Clear cell carcinoma (of the fetus) Vaginal adenosis T-shaped uterus Progestins Name Mechanism of Action Key Indication(s) Key Toxicity Megestrol acetate Synthetic progestin suppresses leuteinizing hormone by inhibition of pituitary function Anorexic mechanism unknown Appetite stimulant Anti-neoplastic agent Weight gain Nausea Vomiting Gonadotropin Releasing Hormones Name Mechanism of Action Key Indication(s) Key Toxicity Leuprorelin Acts as a gonadotropin releasing hormone agonist which inhibits gonadotropin secretion Hormone responsive cancer (non-pulsatile) Fertility (pulsatile) Flushing Sweating Fatigue Edema Skin reaction Hormone Antagonists Anti-Estrogens Name Mechanism of Action Key Indication(s) Key Toxicity Tamoxifen Competitively binds to estrogen receptors inhibiting effects of estrogen ER/PR positive breast cancer Endometrial cancer Growth plate fusion Increased bone density Anti-Androgens Name Mechanism of Action Key Indication(s) Key Toxicity Flutamide Blocks action of testosterone by binding to adrogen receptors Prostate cancer (used prior to GnRH analogues) Gynecomastia GI disturbance Enzyme Inhibitors Name Mechanism of Action Key Indication(s) Key Toxicity Anastrozole Inhibits aromatase ER/PR positive breast cancer Fertility Osteoporosis Bone fracture
QUESTIONS 1 of 2 1 2 Previous Next (M2.PH.15.8) A 45-year-old diabetic man presents to your office for routine follow-up. One year ago, the patient’s hemoglobin A1C was 7.2% and the patient was encouraged to modify his diet and increase exercise. Six months ago, the patient’s HA1C was 7.3%, and you initiated metformin. Today, the patient has no complaints. For which of the following co-morbidities would it be acceptable to continue metformin? QID: 102587 Type & Select Correct Answer 1 Hepatitis C infection 5% (2/39) 2 Mild chronic obstructive pulmonary disease 56% (22/39) 3 Recent diagnosis of NYHA Class II congestive heart failure 5% (2/39) 4 Prior hospitalization for alcoholic hepatitis 8% (3/39) 5 Headache and family history of brain aneurysms requiring CT angiography 18% (7/39) M 7 Question Complexity E Question Importance Select Answer to see Preferred Response SUBMIT RESPONSE 2 Review Tested Concept Review Full Topic (M2.PH.14.70) A 66-year-old man presents to the emergency department with abdominal pain, nausea, and vomiting. He endorses diffuse abdominal tenderness. His past medical history is notable for diabetic nephropathy, hypertension, dyslipidemia, depression, and morbid obesity. He also is currently being treated for an outbreak of genital herpes. His temperature is 99.0°F (37.2°C), blood pressure is 184/102 mmHg, pulse is 89/min, respirations are 18/min, and oxygen saturation is 98% on room air. Physical exam is notable for an obese man in no acute distress. A CT scan of the abdomen with contrast is performed and is unremarkable. The patient is admitted to the observation unit for monitoring of his pain. Notably, the patient's abdominal pain improves after an enema and multiple bowel movements. The patient's evening laboratory values are ordered and return as seen below.Serum:Na+: 141 mEq/LCl-: 99 mEq/LK+: 4.8 mEq/LHCO3-: 11 mEq/LBUN: 65 mg/dLGlucose: 177 mg/dLCreatinine: 3.1 mg/dLWhich of the following is the most likely etiology of this patient's laboratory derangements? QID: 104517 Type & Select Correct Answer 1 Acyclovir 23% (8/35) 2 Atorvastatin 51% (18/35) 3 Insulin 6% (2/35) 4 Metformin 11% (4/35) 5 Metoprolol 6% (2/35) M 6 Question Complexity E Question Importance Select Answer to see Preferred Response SUBMIT RESPONSE 4 Review Tested Concept Review Full Topic