2 - Parathyroid Gland

Parathyroid gland
 Embryology and Anatomy:

Development:
• The parathyroid glands arise from the branchial pouches Ill and IV.
• The inferior parathyroids are associated with the thymus gland and are
derived fromthe third pouches.
• The superior glands are derived from the fourth pouches
 Number and position:
• In 80% of cases there are 4 glands which are symmetrical in position on
both sides but in the remaining cases there can be more than 4
asmmetrically placed glands.
• The glands can reach up to the hyoid bone, and down to retrosternal
and retroclavicular areas to reach the pericardium.
 Blood supply:
Each gland is supplied by a branch from the inferior thyroid artery that
enters at the hilum. Sometimes the superior gland is supplied by the superior
thyroid artery.
Physiology of calcium of homeostasis
 The parathyroid glands secrete(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.
 PTH, calcitonin and vitamin D thus work in concert to modulate fluctuations
in the level of serum ionized calcium.
• The serum calcium is made of 3 fragments; ionized 50%, protein bound
45% and complexed to organic anions 5%, hence the need for
simultaneous assay of plasma proteins especially albumin.
Hyperparathyroidism
 Types:
1. Primary hyperparathyroidism. There is autonomous production of the
parathormone with loss of the feedback mechanism.
2. Secondary hyperparathyroidism. This type is due to compensatory
hypersecretion of the parathormone secondary to low serum calcium.
3. Tertiary hyperparathyroidism. This starts as secondary
hyperparathyroidism, but the hyperplastic glands develop an autonomous
function.
Primary hyperparathyroidism
 Incidence:
It is more in females, particularly in the fifth and sixth decades of life. The
disease is sometimes familial, and is sometimes a part of the multiple
endocrine neoplasia MEN either type I (Wermer's) or type II (Sipple).

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.
 Clinical presentations:
Hyperparathyroidism is more commonly detected due to measurement of
serum calcium and phosphate in screening procedures of asymptomatic
patients. in general 80% of patients have renal involvement, and 35% have
skeletal involvement.
 1. The earliest complaints are
muscle weakness, anorexia, nausea, constipation, polyuria and
polydipsia.
2. Renal presentations. These include nephrolithiasis (30-80%), or
nephrocalcinosis (5-10%), the latter is irreversible and may lead to renal failure
The patients complain of backache, haematuria, passage of renal calculi .
Hypertension due to renal impairment
 3. Bone disease. The common skeletal involvements are subperiosteal
resorption especially of the phalanges and in severe cases cysts and tufting
of terminal phalanges The skull is the second common site with diffuse
granularity and cystic changes. With advanced disease giant cell lesions
that look like osteoclastoma (brown tumours) are present. There is severe
demineralization of the whole skeleton and multiple pathological fractures
may occur. the fractures fail to heal. The patient is losing his skeleton in his
urine,
 4. Gastrointestinal manifestations. Peptic ulcer disease and pancreatitis
may occur in hyper-parathyroidism cases.
5. Emotional disturbances. Neurologic and psychiatric problems may occur.
6. Hyperparathyroid crisis occurs with high serum calcium 16-20 mg per 100
ml, It presents by rapidly developing muscular weakness, nausea, vomiting,
weight loss, fatigue and drowsiness.
To summarize hyperparathyroidism is a disease of bones, stones, abdominal
groans and psychic moans
 Parathyroid carcinoma. Patients are usually symptomatic with skeletal and
renal involvements, high elevation of PTH, calcium and alkaline phosphate.
The glands are palpable is one third to half of cases.
Differential diagnosis of hypercalcaemia:
Causes of hypercalcaemia, other than primary hyperparathyroidism, are.
1. Malignancy characterized by recent onset of hypercalcaemia, elevated
sedimentation rate, anaemia, elevated alkaline phosphatase and serum
calcium level above 14 mg/I00 ml.. Haematologic malignancies as multiple
myeloma and lymphomas. Solid tumours with lytic bone metastases as
cancers of breast, lung, kidney and pancreas.
2. Other causes of hypercalcaemia are milk alkali syndrome, Paget's disease
of bone, vitamin D intoxication and sarcoidosis.
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 hypercalcaemia.
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
 Localization:
1. High resolution ultrasound has an accuracy of 76%.
2. CT scan has 50% accuracy as and is helpful in mediastinal sites.
3. Technetium labeled sestamibi scan
4. Newer modalities of scintigraphy in combination with single photon
emission computed tomography (SPECT), SPECT with computed
tomography (SPECT/CT), and four-dimensional CT have demonstrated
higher sensitivity and positive predictive values. ·
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).
Management of asymptomatic patients is more controversial, but recent
guidelines from an expert consensus panel recommend parathyroidectomy for
those meeting one of the following criteria:
(1) Age less than 50 years;
(2) unable to participate in appropriate followup;
(3) serum calcium level >1 mg/dl above normal range;
(4) urine calcium >400 mg per 24 hours;
(5) creatinine clearance <60 ml/min; or
(6) complications of primary HPT
Secondary and tertiary
hyperparathyroidism:
 In secondary hyperparathyroidism there is increased PTH secretion in

response to low plasma serum calcium concentration. This occurs in cases
of:
1. Renal osteodystrophy especially those on haemodialysis associated with
elevated serum phosphorus.
2. Malabsorption syndrome
3. 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.
 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.
Surgery should be postponed six months after renal transplantation in
cases of tertiary hyperparathyroidism as the serum calcium may return to
normal after transplantation.
 Hypoparathyroidism
Aetiology:
The disease is generally uncommon. The commonest causes are;
1. As a complication of thyroidectomy especially for carcinoma or
recurrent goitre.
2. Radioactive iodine therapy for Graves' disease.
3. Autoimmune with adrenocortical insufficiency.
4. Following parathyroidectomy operation.
 diagnosis:
• Paraesthesia, muscle cramps, carpopedal spasm, tetany, urinary
frequency, depression, and psychoneurosis.
• Surgical neck scar, positive Chvostek's and Trousseau's signs.
• Brittle and atrophic nails, defective teeth, cataract, spotty alopecia
including loss of eyebrows.
• Hypocalcaemia and hyperphosphatemia, low or absent serum PTH.
Treatment:
 The aim of treatment is to raise serum calcium, to treat tetany and lower
serum phosphate level

2 - Parathyroid Gland

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2 - Parathyroid Gland

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Parathyroid gland

 Embryology and Anatomy:

 The parathyroid glands secrete(PTH). Parathormone elevates serum

 In secondary hyperparathyroidism there is increased PTH secretion in

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