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Secondary hyperaldosteronism (also hyperreninism, or hyperreninemic hyperaldosteronism) is due to overactivity of the renin–angiotensin–aldosterone system (RAAS).. The causes of secondary hyperaldosteronism are accessory renal veins, fibromuscular dysplasia, reninoma, renal tubular acidosis, nutcracker syndrome, ectopic tumors, massive ascites, left ventricular failure, and cor pulmonale.
On the other hand, increased acid production at the pyloric antrum is associated with duodenal ulcers in 10% to 15% of H. pylori infection cases. In this case, somatostatin production is reduced and gastrin production is increased, leading to increased histamine secretion from the enterochromaffin cells, thus increasing acid production.
In healthy people, even small rises in blood glucose result in increased insulin secretion. As long as the pancreatic beta cells are able to sense the glucose level and produce insulin, the amount of insulin secreted is usually the amount required to maintain a fasting blood glucose between 70 and 100 mg/dL (3.9–5.6 mmol/L) and a non-fasting ...
Adrenal adenomas are benign tumors that start in the cortex of the adrenal gland.They fall into one of two categories: functional or non-secreting. Adenomas that are nonfunctional or have modest levels of hormone secretion may not show any symptoms at all and may remain asymptomatic.
Adrenal insufficiency is a condition in which the adrenal glands do not produce adequate amounts of steroid hormones.The adrenal glands—also referred to as the adrenal cortex—normally secrete glucocorticoids (primarily cortisol), mineralocorticoids (primarily aldosterone), and androgens.
The increased excretion of sodium at subnormal concentrations of this ion in the serum might represent an attempt to reduce extracellular tonicity to conform with a reduced cellular osmolarity. An eosinopenia response to epinephrine and the ability to reduce the excretion of sodium on a regime free of salt aids in differentiating this syndrome ...
The disease associated with this increased secretion of cortisol was described by the American neurosurgeon Harvey Cushing in 1912 after he was presented with a unique case of the disease in 1910 [28] [29] a 23-year-old woman called Minnie G. whose symptoms included painful obesity, amenorrhea, hypertrichosis (abnormal hair growth ...
The gland increases in size by 10%, thyroxine production increases by 50%, and iodine requirements increase. Many women have normal thyroid function but have immunological evidence of thyroid autoimmunity (as evidenced by autoantibodies) or are iodine deficient, and develop evidence of hypothyroidism before or after giving birth.