Treatment of different types of medical problems that occur when too much of the hormone prolactin is produced. It can be used to treat certain menstrual problems, fertility problems in men and women, and pituitary prolactinomas (tumors of the pituitary gland).
Cabergoline is administered orally and undergoes significant first-pass metabolism following systemic absorption. Extensively metabolized in the liver. Elimination is primarily in the feces. Half-life: 63-69 hr.
Prepare a 10-international units/ml dilution; withdraw 0.05 ml from a 200-international units/ml vial in a tuberculin syringe; fill up to 1 ml with 0.9% NaCl. Take 0.1 ml and inject intracutaneously on inner aspect of forearm. Observe after 15 min; a positive response is the appearance of more than mild erythema or wheal.
Therapeutic Effect: Stimulates calcium and phosphate absorption from small intestine, promotes secretion of calcium from bone to blood, promotes renal tubule phosphate resorption, acts on bone cells to stimulate skeletal growth and on parathyroid gland to suppress hormone synthesis and secretion.
! Later signs of overdosage are evidenced by polyuria, polydipsia, anorexia, weight loss, nocturia, photophobia, rhinorrhea, pruritus, disorientation, hallucinations, hyperthermia, hypertension, and cardiac arrhythmias.
• Monitor the patient’s BUN, serum alkaline phosphatase, serum calcium, serum creatinine, serum magnesium, serum phosphate, and urinary calcium levels. Know that the therapeutic serum calcium level is 9 to 10 mg/dl.
Rapidly, completely absorbed. Protein binding: greater than 99%. Undergoes minor hepatic metabolism to inactive metabolite. Excreted unchanged in urine and in the feces through the biliary system. Not removed by hemodialysis. Half-life: 9 hr.
First-line treatment of patients with metastatic colorectal cancer and metastatic breast cancer resistant to both paclitaxel and anthracycline-containing chemotherapy regimens; colorectal cancer when treatment with a fluoropyrimidine alone is preferred
! Serious reactions may include myelosuppression (evidenced by neutropenia, thrombocytopenia, and anemia), cardiovascular toxicity (marked by angina, cardiomyopathy, and deep vein thrombosis), respiratory toxicity (marked by dyspnea, epistaxis, and pneumonia), and lymphedema.
Axona is a prescription medical food containing a proprietary formulation of medium chain triglycerides (MCTs) that are metabolized to ketone bodies to induce hyperketonemia, thus providing an alternate glucose substrate and energy source to the brain when its ability to process glucose is impaired. Brain-imaging scans of older adults and those with Alzheimer’s disease reveal a dramatically decreased uptake of glucose.
Allergy to milk or soy (contains caseinate, whey, and lecithin) and/or hypersensitivity to palm or coconut oil. Use with caution in patients at risk for ketoacidosis (alcoholics, poorly controlled diabetics) and in patients with a history of GI inflammatory conditions (IBS, diverticulitis, chronic gastritis, GERD). May increase serum triglycerides. May increase BUN, uric acid, or serum creatinine.
An ACE inhibitor that suppresses the renin-angiotensin-aldosterone system and prevents conversion of angiotensin I to angiotensin II, a potent vasoconstrictor; may also inhibit angiotensin II at local vascular and renal sites. Decreases plasma angiotensin II, increases plasma renin activity, and decreases aldosterone secretion.
Rapidly, well absorbed from the GI tract (absorption is decreased in the presence of food). Protein binding: 25%–30%. Metabolized in the liver. Primarily excreted in urine. Removed by hemodialysis. Half-life: less than 3 hr (increased in those with impaired renal function).
Initially, 12.5–25 mg 2–3 times a day. After 1–2 wk, may increase to 50 mg 2–3 times a day. Diuretic may be added if no response in additional 1–2 wk. If taken in combination with diuretic, may increase to 100–150 mg 2–3 times a day after 1–2 wk. Maintenance: 25–150 mg 2–3 times a day. Maximum: 450 mg/day.