Hyperparathyroidism

INTRODUCTION:
  1. 2:1 female:male ratio
  2. Average age at diagnosis 55
ETIOLOGY:
  • PRIMARY HYPERPARATHYROIDISM:
  1. High serum calcium (ionized calcium)
  2. Medullary carcinoma of the thyroid
  3. High or high normal PTH levels
  4. Solitary Parathyroid Adenoma ~85%
  5. Multiple Adenomas, hyperplasia ~15%(most common surgical repairable cause)
  6. Parathyroid Carcinoma ~1%
  • SECONDARY HYPERPARATHYROIDISM:
  1. Chronic renal failure, 
  2. Vitamin D deficiency, 
  3. Medullary carcinoid syndrome & 
  4. Malabsorption syndrome
  • TERTIARY HYPERPARATHYROIDISM:
  1. After renal transplant or as a progression of secondary hyperparathyroidism
CLINICAL MANIFESTATION:
Hypercalcemia:
  • Chronic thiazide therapy causes persistent hypercalcemia due to hyperparathyroidism
  • Hypercalciuria
  • Increased rate of bone turnover
  • Neurobehavioral symptoms: fatigue and weakness
  • Nephrolithiasis 20%
  • Cardiac calcification and LV hypertrophy
  • Osteopenia
  • CPPD crystals
  • Floating teeth
  • Osteitis fibrosa cystica
  • Absence of lamina dura
  • Constipation , muscle weakness ,Anorexia ,weight loss, Polydipsia & polyuria 
  • Peptic ulcer is associated with Primary hyperparathyroidism
  • Most patients asymptomatic although fatigue and weakness are undercounted as symptoms
  • 25% of asymptomatic patients have progressive disease
  • MEN I: parathyroid, pancreatic (Zollinger Ellison), pituitary (prolactinoma) 
  • tumor suppressor MENI gene, autosomal dominant inheritance
  • MEN 2A: parathyroid, pheochromocytoma, medullary thyroid cancer 
  • RET proto-oncogene, autosomal dominant inheritance
  • Familial Hypocalciuric Hypercalcemia: autosomal dominant, surgery not indicated, PTH normal
  • Neonatal Severe Hyperparathyroidism
  • Hyperparathyroidism- Jaw Tumor Syndrome
  • Brown Tumor
  1. Non neoplastic process. 
  2. On radiographic evaluation their multifocal involvement may be misconstrued as metastatic disease; however, the clinical history of renal failure and hyperparathyroidism usually establishes the diagnosis. 
  3. Hypercalcaemia: anorexia, nausea, abdominal pain, depression,Fatigue and muscle weakness.
  4. Renal presentation: polyuria, stones or nephrocalcinosis
  • Skeletal and bone:
  1. Complain of joint symptoms, due to chondrocalcinosis. 
  2. Only a minority (probably less than 10 percent) present with bone disease; this is usually generalized osteoporosis rather than the classic features of osteitis brosa, bone cysts and pathological fractures.
  • Radiological finding:
  1. They appear as single or multiple, well defined lesions, commonly affecting the facial bones, pelvis, ribs and femoral bone.
  2. With treatment Brown tumors may demonstrate healing with increased radiodensity.
  3. Osteoporosis and areas of cortical erosion.
  4. Ribs notching
  5. Secondary hyperparathyroidism causes rugger jersy spine in known case of chronic renal failure 
  6. Salt and pepper appearance of skull is a radiologic feature of hyperparathyroidism.
  7. The classical – and almost pathognomonic – feature, which should always be sought, is sub-periosteal cortical resorption of the middle phalanges.
BIOCHEMICAL TESTS:
  • Hypercalcaemia
  • Hypophosphataemia
  • Serum PTH.
  • Serum alkaline phosphatase with osteitis brosa.
TREATMENT:
  • Medical :
  1. Adequate hydration
  2. Decreased calcium intake.
  • Surgery:
  1. Parathyroidectomy
  2. Stabilisation of the lesion if mechanical damage has occured
  3. Treatment of choice for primary hyperparathyroidism secondary to parathyroid hyperplasia is Removal of all glands leaving 50 mg of tissue as remnant
  4. The initial treatment of choice for secondary hyperparathyroidism in renal osteodystrophy is Phosphate binder
Exam Question of :
  • Secondary hyperparathyroidism is seen in Chronic renal failure, Vitamin D deficiency, Medullary carcinoid syndrome & Malabsorption syndrome
  • Adenoma is the most common surgically repairable cause of hyperparathyroidism
  • Characteristic subperiosteal bone resorption in Hyperparathyroidism is best seen at Radial border of middle phalanx
  • MEN 1 is characterized by symptoms of hyperparathyroidism, tumor in pancreas, adrenal cortical hyperplasia, pituitary adenomas, islet cell tumor with cutaneous angiofibromas
  • Subperiosteal resorption and thic­kness of skull is increased in hyperparathyroidism
  • Salt and pepper appearance of the skull on Xray is seen in hyperparathyroidism
  • Chronic thiazide therapy causes persistent hypercalcemia due to hyperparathyroidism
  • Brown’s tumour is seen in hyperparathyroidism
  • Primary hyperparathyroidism, phaeochromocytoma may be associated with Medullary carcinoma of the thyroid
  • Treatment of choice for primary hyperparathyroidism secondary to parathyroid hyperplasia is Removal of all glands leaving 50 mg of tissue as remnant
  • Ca++↑ P04 ↓ is seen in hyperparathyroidism
  • Secondary hyperparathyroidism due to Vitamin D deficiency shows Hypophosphatemia
  • Hyperparathyroidism can cause nephrocalcinosis 
  • Tertiary hyperparathyroidism is Secondary hyperparathyroidism with chief cell adenoma
  • Superior rib notching is/are caused by Hyperparathyroidism
  • The symptoms of Hyperparathyroidism include Constipation , muscle weakness ,Anorexia ,weight loss, Polydipsia & polyuria
  • Subcutaneous Calcifications are seen in Hyperparathyroidism
  • Peptic ulcer is associated with Primary hyperparathyroidism
  • The initial treatment of choice for secondary hyperparathyroidism in renal osteodystrophy is Phosphate binders
  • The commonest cause of primary hyperparathyroidism is Solitary adenoma of parathyroid
  • Secondary hyperparathyroidism causes rugger jersy spine in known case of chronic renal failure 
  • Tufting of the terminal phalanges is seen in hyperparathyroidism 
  • Floating teeth is seen in hyperparathyroidism 
  • Absence of lamina dura seen in hyperparathyroidism 
  • CPPD crystals are seen in hyperparathyroidism 
  • Osteitis fibrosa cystica is seen with hyperparathyroidism
Don't Forget to Solve all the previous Year Question asked on Hyperparathyroidism