Calcification in the brain due to<unk>  Pepper & Salt, classical X-Ray appearance of<unk> m The gold standard of diagnosis is the PTH immunoassay. Once an elevated PTH has been confirmed, the goal of diagnosis is to determine whether the<unk>  is primary or secondary in origin by obtaining a serum calcium level: Serum calcium Phosphate ALP PTH Likely type ↑ ↓ ↑ ↑ Primary<unk>  ↓ ↑ ↑ ↑ Secondary<unk>  Tertiary<unk>  has a high PTH and high serum calcium. It is differentiated from primary<unk>  by a history of chronic kidney failure and secondary<unk> .<unk>  can cause hyperchloremia and increase renal bicarbonate loss, which may result in a normal anion gap metabolic acidosis. Differential diagnosis Familial benign hypocalciuric hypercalcaemia can present with similar lab changes. In this condition, the calcium creatinine clearance ratio, however, is typically under 0.01. Blood tests Intact PTH In primary<unk> , parathyroid hormone (PTH) levels are either elevated or "inappropriately normal" in the presence of elevated calcium. Typically, PTH levels vary greatly over time in the affected patient and (as with Ca and Ca++ levels) must be retested several times to see the pattern. The currently accepted test for PTH is intact PTH, which detects only relatively intact and biologically active PTH molecules. Older tests often detected other, inactive fragments. Even intact PTH may be inaccurate in patients with kidney dysfunction. Intact pth blood tests may be falsely low if biotin has been ingested in the previous few days prior to the blood test. Calcium levels In cases of primary<unk>  or tertiary<unk> , heightened PTH leads to increased serum calcium (hypercalcemia) due to: # increased bone resorption, allowing the flow of calcium from bone to blood # reduced kidney clearance of calcium # increased intestinal calcium absorption Serum phosphate In primary<unk> , serum phosphate levels are abnormally low as a result of decreased reabsorption of phosphate in the kidney tubules. However, this is only present in about 50% of cases. This contrasts with secondary<unk> , in which serum phosphate levels are generally elevated because of kidney disease. Alkaline phosphatase Alkaline phosphatase levels are usually elevated in<unk> . In primary<unk> , levels may remain within the normal range, but this is inappropriately normal given the increased levels of plasma calcium. Nuclear medicine A technetium sestamibi scan is a procedure in nuclear medicine that identifies<unk>  (or parathyroid adenoma). It is used by surgeons to locate ectopic parathyroid adenomas, most commonly found in the anterior mediastinum. Classification Primary Parathyroid adenoma. Primary<unk>  results from a hyperfunction of the parathyroid glands themselves. The oversecretion of PTH is due to a parathyroid adenoma, parathyroid hyperplasia, or rarely, a parathyroid carcinoma. This disease is often characterized by the quartet stones, bones, groans, and psychiatric overtones referring to the presence of kidney stones, hypercalcemia, constipation, and peptic ulcers, as well as depression, respectively. In a minority of cases, this occurs as part of a multiple endocrine neoplasia (MEN) syndrome, either type 1 (caused by a mutation in the gene MEN1) or type 2a (caused by a mutation in the gene RET), which is also associated with the adrenal tumor pheochromcytoma. Other mutations that have been linked to parathyroid neoplasia include mutations in the genes HRPT2 and CASR. Patients with bipolar disorder who are receiving long-term lithium treatment are at increased risk for<unk> . Elevated calcium levels are found in 15% to 20% of patients who have been taking lithium long-term. However, only a few of these patients have significantly elevated levels of parathyroid hormone and clinical symptoms of<unk> . Lithium-associated<unk>  is usually caused by a single parathyroid adenoma. Secondary Secondary<unk>  is due to physiological (i.e. appropriate) secretion of parathyroid hormone (PTH) by the parathyroid glands in response to hypocalcemia (low blood calcium levels). The most common causes are vitamin D deficiency (caused by lack of sunlight, diet or malabsorption) and chronic kidney failure. Lack of vitamin D leads to reduced calcium absorption by the intestine leading to hypocalcemia and increased parathyroid hormone secretion. This increases bone resorption. In chronic kidney failure the problem is more specifically failure to convert vitamin D to its active form in the kidney. The bone disease in secondary<unk>  caused by kidney failure is termed renal osteodystrophy. Tertiary Tertiary<unk>  is seen in those with long-term secondary<unk> , which eventually leads to hyperplasia of the parathyroid glands and a loss of response to serum calcium levels. This disorder is most often seen in patients with end-stage kidney disease and is an autonomous activity.
Hyperparathyroidism
Panic attack
Secondary hyperparathyroidism
Primary hyperparathyroidism
Hypoparathyroidism
Tertiary hyperparathyroidism
Renal osteodystrophy
Parathyroid disease