* The effect on bone: PTH increases bone resorption (increased hydroxyproline); the bone response to PTH is biphasic. In the second stage, the bone resorption and formation are both increased. resorption winning in general on training
* On bone cell, PTH stimulates adenylate cyclase and increase the Ca ++ influx into the cell.
* PTH increases production of lactate and especially citrate (which is a good sign of bone resorption).
* The PTH stimulates the 1-α-hydroxylation of the 25-OH-vitamin D3 in the kidney
* The PTH increases the intestinal absorption of Ca ++ indirect way (-> vitamin D3)
* The PTH increases the intestinal absorption of phosphorus; it increases phosphaturia by declining phosphorus reabsorption => hypophosphatemia.
* Other action on the kidney: increased reabsorption of magnesium and excretion of K +, Na +, bicarbonates and urinary pH elevation.
* On the lens: reduces PTH => glycolysis = the disorder> cataract
* On the pancreas: high PTH secretion of gastrin by cells D => recurrent ulcer in some hyperparathyroidism
* The main stimulus of CT secretion is hypercalcemia; others: penta-gastrin (and CCK)
* The pentagastrin test is used in the diagnosis of medullary thyroid cancer secreting calcitonin.
B- Vitamin D:
* In the bone, the calcitriol (1,25-dihydrocolécalciférol) acts primarily on bone-téoclastes. Antirachitic The effect of vitamin D is made by making available a large amount of calcium for mineralizing reactions. PTH is synergistic vitamin D.
A- Primary hyperparathyroidism:
* The single adenoma is the most common cause (80%); in 10% of adenomas are located in ectopic parathyroid (mediastinum, neck, retro-oesophageal space).
* Hyperplasia of the parathyroid glands (15-20%) covers all four parathyroid glands. Type 2a NEM (syndrome Sipple: + medullary thyroid cancer + pheochromocytoma). NEM type I (Wermer syndrome)
Disorders related to movement of calcium:
* In the bone level: geodes; bone pain, swelling and pathological fracture.
* In the kidney; nephrolithiasis, nephrocalcinosis
Disorders related to the action of calcium in the tissues:
* Increase of the action potential threshold (cell hypoexcitailité): muscle weakness, fatigue, shortening of QT;
* Digestive tract: dysphagia, nausea, vomiting, constipation, abdominal pain and cramping-minales
* At nervous level: psychasthenia, confusional disorders, depression, headache
* The polyuropolydipsic syndrome is very common and early (moderate 2 to 3 L / d); urine are hypodense (poor concentration of urine). This polyuria is insensitive to ADH.
* Renal failure is the major risk of progression
* The swellings are exceptional; They often sit on the jaw
* The bone lucency is diffuse, more marked at the cortical level (blur edge and enlargement of the spinal canal); tuft appearance before the ends of phalanges. Bleached skull of internal and external tables with “hairy appearance” (microgeodes).
* The geodes association (with a punch without condensation around) and de-mineralization is the fibrocystic osteitis Recklinghausen
* Neuropsychological Event: apathy, asthenia
Events * Digestive: anorexia, nausea, constipation are common. Recurrent ulcer of the stomach; calcific pancreatitis.
* Other: HTA;
B- biological signs:
* Hypercalcemia (between 2.57 to 2.75 mmol / L)
* The absence of hypercalciuria is possible and does not reject the diagnosis
* The hypophosphatemia is a sign of major importance
* Phosphorus reabsorption is always <80%
* Elevation of cAMP nephrogenic
* Elevated blood citrate; increased alkaline phosphatase: increased hydrocyprolinurie
* Dynamic test: calcium infusion test (calcium deprivation is abandoned).
C- The bone biopsy:
Two fundamental lesions bone resorption process and increase osteo blast activity with emphasis fibrous tissue
Location of the tumor:
* Cervical ultrasonography has value only if positive
* Cervical CT has no interest; this examination seems useful here to locate mediastinal adenomas.
* The most powerful examination is sestamibi scintigraphy
D- Clinical forms:
* Asymptomatic hyperparathyroidism
* Hyperparathyroidism with renal impairment urinary calcium and calcium levels are normal (in renal failure serum calcium is low)
* Tertiary Hyperparathyroidism: thyroid hyperplasia which follow the secondary hy-perparathyroïdies and become autonomous.
* Acute hypercalcemic crisis: significant confusion,
E- Causes of hypercalcemia:
1- malignant hypercalcemia:
* Bone Metastases
* Paraneoplastic hypercalcemia
* Hematologic malignancies
2- exogenous hypercalcemia:
* Overdose of vitamin D, calcium
* Thiazide diuretics
* Vitamin A
* Burnett Syndrome (abuse of milk and alkaline)
3- Other causes:
* Addison’s Disease
* Hypothyroidism; hyperthyroidism
* Prolonged immobilization
Formal indication for surgery in case of adenoma; hyperplasia and in case of tertiary hyperparathyroidism.
A- true Hypoparathyroidism:
* Traumatic: surgery
* Congenital: Di George syndrome
* Autoimmune: Whitaker syndrome (adrenal insufficiency + + moniliasis)
* Transient: newborn to a mother hypercalcémique-
* This device is a non-responsiveness to PTH
* Organic Table of hypoparathyroidism
* Deformities: small, rounded facies brachymétacar-pie, debility, subcutaneous calcification
* PTH is high
– Psuedo-pseudohypoparathyroidism: the dysmorphic syndrome without biological picture of the pseudo-hypoparathyroidism
* Paroxysmal manifestations of hypocalcemia: tetany
* Chronic Events:
– Neuromuscular hyperexcitability: Chvostek sign, Trousseau sign,
– Neurological disorders: Parkinson’s disease; choreiform or athetoid movement disorder
– Trophic disorders: desquamation, alopecia, leukonychia streaked teeth caries repeatedly,
– Posterior capsular Cataract
– ECG: increase the QT interval (by increasing ST)
– Heart failure if major hypocalcemia.
D- Causes of hypocalcemia:
– Chronic renal failure
– Malabsorption syndrome, cirrhosis, malnutrition
– Anticonvulsant drugs (barbiturates, phenytoin); rifampicin
– Severe acute pancreatitis;
– Blood Perfusion citrate
– Bone metastases sclerotic
– Medullary thyroid carcinoma (-> calcitonin)