After recognition, primary hyperparathyroidism should be proved or excluded.In extreme cases of primary hyperparathyroidism, removal of the parathyroid gland after surgical neck exploration is the only way to avoid death. The diagnostic program should be performed within hours, in parallel with measures to lower serum calcium. Treatment of choice for acutely lowering calcium is extensive hydration and calcitonin, as well as bisphosphonates (which have effect on calcium levels after one or two days). Causes
Primary hyperparathyroidism and malignancy account for about 90% of cases of hypercalcaemia.Causes of hypercalcemia can be divided into those that are PTH dependent or PTH independent. Parathyroid function
Primary hyperparathyroidism
Solitary parathyroid adenoma
Primary parathyroid hyperplasia
Parathyroid carcinoma
Multiple endocrine neoplasia (MEN1 & MEN2A)
Familial isolated hyperparathyroidism
Lithium use
Familial hypocalciuric hypercalcemia/familial benign hypercalcemia

Cancer
Solid tumour with metastasis (e.g. breast cancer or classically squamous cell carcinoma, which can be PTHrP-mediated)
Solid tumour with humoral mediation of hypercalcaemia (e.g. lung cancer, most commonly non-small cell lung cancer or kidney cancer, phaeochromocytoma)
Haematologic cancers (multiple myeloma, lymphoma, leukaemia)
Ovarian small cell carcinoma of the hypercalcemic type

Vitamin-D disorders
Hypervitaminosis D (vitamin D intoxication)
Elevated 1,25(OH)2D (see calcitriol under Vitamin D) levels (e.g. sarcoidosis and other granulomatous diseases such as tuberculosis, berylliosis, histoplasmosis, Crohns disease, and granulomatosis with polyangiitis)
Idiopathic hypercalcaemia of infancy
Rebound hypercalcaemia after rhabdomyolysis

High bone-turnover
Hyperthyroidism
Multiple myeloma
Prolonged immobilization
Pagets disease
Thiazide use
Vitamin A intoxication

Kidney failure
Tertiary hyperparathyroidism
Aluminium intoxication
Milk-alkali syndrome

Other
Acromegaly
Adrenal insufficiency
Zollinger–Ellison syndrome
Williams Syndrome

Diagnosis
Diagnosis should generally include either a calculation of corrected calcium or direct measurement of ionized calcium level and be confirmed after a week. This is because either high or low serum albumin levels does not show the true levels of ionised calcium.
Gastric atresia is a congenital defect with complete occlusion of the pyloric outlet of the stomach. Cause
Gastric atresia is a birth defect. It can be genetic, inherited in an autosomal recessive manner, and associated with conditions like Down syndrome and junctional epidermolysis bullosa (medicine). In about 60% of cases, the outlet of the stomach is covered by a membrane. In around 35% of cases, solid tissue blocks the outlet. In the remaining cases (less than 10%), there is a complete separation of the stomach and the small intestine. Diagnosis
Polyhydramnios is often seen during pregnancy, and prenatal diagnosis is common. Infants with gastric atresia will exhibit forceful vomiting upon the first feeding. Imaging is required for diagnosis. Treatment
Treatment is surgical and involves removing or bypassing the obstruction. Epidemiology
It is seen in approximately 1 in 100,000 live births. == References ==