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Endocrine system
Congenital adrenal hyperplasia
Primary adrenal insufficiency
Waterhouse-Friderichsen syndrome
Hyperaldosteronism
Adrenal cortical carcinoma
Cushing syndrome
Conn syndrome
Thyroglossal duct cyst
Hyperthyroidism
Graves disease
Thyroid eye disease (NORD)
Toxic multinodular goiter
Thyroid storm
Hypothyroidism
Euthyroid sick syndrome
Hashimoto thyroiditis
Subacute granulomatous thyroiditis
Riedel thyroiditis
Postpartum thyroiditis
Thyroid cancer
Hyperparathyroidism
Hypoparathyroidism
Hypercalcemia
Hypocalcemia
Diabetes mellitus
Diabetic retinopathy
Diabetic nephropathy
Hyperpituitarism
Pituitary adenoma
Hyperprolactinemia
Prolactinoma
Gigantism
Acromegaly
Hypopituitarism
Growth hormone deficiency
Pituitary apoplexy
Sheehan syndrome
Hypoprolactinemia
Constitutional growth delay
Diabetes insipidus
Syndrome of inappropriate antidiuretic hormone secretion (SIADH)
Precocious puberty
Delayed puberty
Premature ovarian failure
Polycystic ovary syndrome
Androgen insensitivity syndrome
Kallmann syndrome
5-alpha-reductase deficiency
Autoimmune polyglandular syndrome type 1 (NORD)
Multiple endocrine neoplasia
Pancreatic neuroendocrine neoplasms
Zollinger-Ellison syndrome
Carcinoid syndrome
Pheochromocytoma
Neuroblastoma
Opsoclonus myoclonus syndrome (NORD)
Adrenal insufficiency: Pathology review
Adrenal masses: Pathology review
Hyperthyroidism: Pathology review
Hypothyroidism: Pathology review
Thyroid nodules and thyroid cancer: Pathology review
Parathyroid disorders and calcium imbalance: Pathology review
Diabetes mellitus: Pathology review
Cushing syndrome and Cushing disease: Pathology review
Pituitary tumors: Pathology review
Hypopituitarism: Pathology review
Diabetes insipidus and SIADH: Pathology review
Multiple endocrine neoplasia: Pathology review
Neuroendocrine tumors of the gastrointestinal system: Pathology review
Hyperaldosteronism
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Laboratory Value | Result |
Serum | |
Sodium | 147 mEq/L |
Potassium | 2.9 mEq/L |
Chloride | 105 mEq/L |
HCO3- | 32 mEq/L |
Creatinine | 0.6 mg/dL |
Glucose | 94 mg/dL |
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hyperaldosteronism p. 355
hyperaldosteronism and p. 356
with hyperaldosteronism p. 356
hypertension with p. 306
metabolic alkalosis p. 616
potassium-sparing diuretics for p. 633
hyperaldosteronism p. 356
hyperaldosteronism p. 356
hypertension with p. 306
markers in p. 615
in hyperaldosteronism p. 356
Tanner Marshall, MS
Hyperaldosteronism refers to an endocrine disorder where the adrenal gland produces above normal levels of the hormone aldosterone.
Now, there are two adrenal glands, one above each kidney, and each one has an inner layer called the medulla and an outer layer called the cortex which is subdivided into three more layers, the zona glomerulosa, zona fasciculata, and the zona reticularis.
The outermost layer is the zona glomerulosa, and it’s full of cells that make the hormone aldosterone.
Aldosterone is part of a hormone family or axis which work together and are called the renin-angiotensin-aldosterone system.
Together these hormones decrease potassium levels, increase sodium levels, and increase blood volume and blood pressure.
Aldosterone is secreted in response to elevated levels of renin, and it’s role is to bind to receptors on two types of cells along the distal convoluted tubule of the nephron.
First it stimulates the sodium/potassium ion pumps of the principal cells to work even harder.
These pumps drive potassium from the blood into the cells and from there it flows down its concentration gradient into the tubule to be excreted as urine.
At the same time, the pumps drive sodium in the opposite direction from the cell into the blood, which allows more sodium to flow from the tubule to the cell down its concentration gradient.
Since water often flows with sodium through a process of osmosis, water also moves into the blood, which increases blood volume and therefore blood pressure.
The other function of aldosterone is to stimulate the ATPase pumps in alpha-intercalated cells which causes more protons to get excreted into the urine.
Meanwhile, ion exchangers on the basal surface of the cell move the negatively charged bicarbonate ion into the extracellular space, causing an increase in pH.
Hyperaldosteronism can happen due to primary causes which is where the adrenal gland itself is responsible for the excess production of aldosterone.
The most common primary cause is called idiopathic hyperaldosteronism, because the zona glomerulosa has an increase in the number of cells secreting aldosterone, but it’s not really clear why this happens.
The second most common cause is called Conn syndrome and this is where an adenoma or tumor in the glandular epithelial cells secretes too much hormone.
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