What is the most effective preventative intervention in all patients, especially those with DM?
Pt presents with HTN, low plasma renin, hypokalemia, and metabolic alkalosis. What is the diagnosis?
Primary hyperaldosteronism caused by:
- adrenal adenoma
- bilateral adrenal hyperplasia
What are the hormone/lab findings in Klinefelter syndrome? What is the cause of these hormone findings?
- low testosterone
- elevated LH
- elevated FSH
- dysgenesis of seminiferous tubules causes decreased inhibin B
- abnormal leydig cell function leads to decreased testosterone
- low levels=no feedback inhibition= high levels of FSH and LH (estrogen) from the hypothalamus
*common cause of hypogonadism seen in infertility workup
what are the physical sx of a person with Klinefelter syndrome?
- primary hypogonadism
- long lower extremities
- small, firm testes
sx of excess vitamin D intake
- mental status change
- muscle weakness
explain Vitamin D metabolism in a person with granulomatous disease (sarcoidosis, tuberculosis)
Normally, 25-hydroxyvitamin D is converted to 1,25-dihydroxyvitamin D (active form) by 1-alpha-hydroxylase in the kidneys, a process regulated by parathyroid hormone.
Activated macrophages in sarcoidosis and other granulomatous diseases express 1-alpha-hydroxylase, leading to excess production of 1,25-dihydroxyvitamin D (active form) and hypercalcemia.
When is glycogenolysis the primary source of glucose?
the first 12-18 hours of fasting
explain how cataracts are formed
in teh polyol pathway ,aldose reductase converts glucose into sorbitol, which is slowly metabolized into fructose by sorbitol dehydrogenase. Chronic hyperglycemia overwhelms this pathway, causing intracellular sorbitol accumulation and increased osmotic/oxidative stress. This accelerates cataract development in patients with diabetes, and contributes to the pathogenesis of diabetic retinopathy, neuropathy, and nephropathy.
Which blood cell will be elevated in a person taking steroids?