The document discusses parathyroid disease and hyperparathyroidism. It notes that the parathyroid glands secrete parathormone (PTH) which regulates calcium levels. There are three types of hyperparathyroidism: primary, secondary, and tertiary. Primary hyperparathyroidism is usually caused by a single adenoma and can present with muscle weakness, nausea, kidney stones, or bone disease. Secondary hyperparathyroidism is caused by low calcium levels stimulating excess PTH production, while tertiary develops from long-term secondary hyperparathyroidism causing autonomous PTH overproduction. The document also discusses hypoparathyroidism, its causes, symptoms, and treatment focused on calcium

1. PARATHYROID DISEASE
Section 11 Group 2

2. INTRODUCTION:
 The parathyroid glands secrete parathormone (PTH). Parathormone
elevates serum calcium through bone resorption and increased
calcium reabsorption in the renal tubules.Together with vitamin D
they regulate calcium and phosphorus absorption
 Vitamin D also increases serum calcium by promoting calcium
absorption from the gut
 On the contrary calcitonin from the parafollicular cells of the thyroid
decreases serum calcium through reversing the PTH effect on the
bone and kidneys

3. HYPERPARATHYROIDISM
Types:
 Primary hyperparathyroidism:There is autonomous production of
the parathormone with loss of the feedback mechanism.
 Secondary hyperparathyroidism:This type is due to compensatory
hypersecretion of the parathormone secondary to low serum
calcium.
Tertiary hyperparathyroidism:This starts as secondary
hyperparathyroidism, but the hyperplastic glands develop an
autonomous function.

4. PRIMARY HYPERPARATHYROIDISM
Incidence: It is more in females, particularly in the fifth and
sixth decades of life
Aetiology:
1. A single adenoma [92%]. 2. Multiple adenomata [4%].
3. Hyperplasia [3%]. 4. Parathyroid carcinoma [1 %].
5. Rarely ectopic PTH production by cancers especially of lung,
kidney and bladder may produce manifestations of the disease.

5. CLINICAL PRESENTATIONS:
 The earliest complaints are muscle weakness, anorexia, nausea, constipation, polyuria
and polydipsia.
 Renal presentations. These include nephrolithiasis (30-80%), or nephrocalcinosis (5-
10%
 Bone disease. The common skeletal involvements are subperiosteal resorption
especially of the phalanges and in severe cases cysts and tufting of terminal phalanges
Gastrointestinal manifestations. Peptic ulcer disease and pancreatitis may occur in
hyper-parathyroidism cases.
 Emotional disturbances. Neurologic and psychiatric problems may occur.The severe
forms are not correctable by parathyroidectomy.
 Hyperparathyroid crisis occurs with high serum calcium 16-20 mg per 100 ml

6. LABORATORY DIAGNOSIS:
1. Serum calcium level. The normal level is 8.5-10.5 mg/100 ml,
values above 13 mg/100 ml are strongly suspicious.
2. Parathormone immunoassay. Elevated plasma level of PTH
does not establish diagnosis of hyperparathyroidism except with
hypercalcemia.
3. Serum chloride to phosphate ratio above 33 suggests
hyperparathyroidism.
4. Increased excretion of calcium in urine.
5. Serum alkaline phosphatase is raised with skeletal lesions

7. TREATMENT:
Treatment is surgical
Indications for surgery:Parathyroidectomy is indicated for
patients with classic symptoms of primary HPT (i.e.,
nephrolithiasis, pathologic fracture, neuromuscular
disturbances, and hypercalcemic crisis).
 Postoperative care. Following removal of the parathyroid
glands the serum calcium concentration falls to normal in 24-48
hours.

8. SECONDARY &TERTIARY HYPERPARATHYROIDISM:
In secondary hyperparathyroidism there is increased PTH secretion in
response to low plasma serum calcium concentration.This occurs in cases of:
 Renal osteodystrophy especially those on haemodialysis associated with
elevated serum phosphorus.
 Malabsorption syndrome
 Rickets and osteomalacia associated with diminished serum phosphorus.
In tertiary hyperparathyroidism the prolonged parathyroid stimulation
causes the chief cell hyperplasia to be autonomous, with elevated serum PTH
and calcium.

9. TREATMENT
The treatment of both conditions is essentially medical by:
 Law phosphate diet and phosphate binders
 Adequate calcium intake.
 1.25 dihydroxy vitamin D.
 Calcimimitic drugs as cinacalcit which diminish the sensitivity of the
parathormone receptors to calcium.
Surgery is indicated for failure to respond to medical treatment by
removal of all but about 50 mg of parathyroid or 15 slices 1 mm each.

10. HYPOPARATHYROIDISM
Etiology:
The disease is generally uncommon.The commonest causes are;
 As a complication of thyroidectomy especially for carcinoma or recurrent
goitre.
 Radioactive iodine therapy for Graves' disease.
 Autoimmune with adrenocortical insufficiency.
 Following parathyroidectomy operation.
 Neonatal tetany associated with maternal hyperparathyroidism.

11. ESSENTIALS OF DIAGNOSIS:
 Paraesthesia, muscle cramps, carpopedal spasm, tetany,
urinary frequency, depression, and psychoneurosis.
 Surgical neck scar, positive Chvostek's andTrousseau's signs.
 Brittle and atrophic nails, defective teeth, cataract, spotty
alopecia including loss of eyebrows.
 Calcification of basal ganglia, cartilage and arteries.
 Hypocalcaemia and hyperphosphatemia, low or absent serum
PTH.

12. TREATMENT:
The aim of treatment is to raise serum calcium, to treat tetany and lower
serum phosphate level to prevent metastatic calcification
In acute tetany the aim is attained by 10-20 ml of 10% calcium chloride IV
and if the response is poor, addition of Mg sulfate 2-4 g/day IV is needed.
 In chronic hypoparathyroidism, that is persistent for more than 3 weeks
oral calcium as gluconate, lactate or carbonate is indicated 3 times daily,
together with vitamin D. Episodes of hypocalcaemia may occur and need .
control by dihydrotachysterol. Phosphorus should be limited in the diet by
ehmrnat1on of dairy products. Aluminum hydroxide is prescribed to combine
with phosphates and lead to their faecai loss

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