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HYPERPARATHYROIDISM
- Dr NIKHIL.S.U
PARATHYROID GLANDS
• Two pairs of glands
• Behind the left and right lobes of the thyroid
• About 6 mm long and 3 to 4 mm ...
HYPERPARATHYROIDISM
• Primary
– Single adenoma- MC
– Multiple adenomas
– Nodular hyperplasia
– Carcinoma
• Secondary
– chr...
• Both sexes affected
• 2-3> women
• Middle aged
• Features
o Bones, stones, abdominal groans, psychic
moans
• Bones
 Severe pain, tenderness
 Gen weakness
 Deformity of limbs & spine
 Pathological # & delayed union
• Stones
 ...
Bone pathology
• Rapid progressive resorption, softening of the
bones with deformity
• Osteoclastic – conversion into fibr...
• Gland pathology- single adenoma-mc, pale,
clear- chief cells.
• Lab findings
• Hypercalcemia
• Hypophosphatemia
• Hyperp...
Radiologic findings of
HYPERPARATHYROIDISM
• The M/C radiologic abnormality is generalized osteopenia.
• Bone resorption, ...
Radiologic findings of
HYPERPARATHYROIDISM
• Subperiosteal resorption - M/C
– Usually occurs in the hands and feet.
– M/C ...
AP radiograph of the hand in a 66-year-old woman with primary hyperparathyroidism owing to
parathyroid adenoma shows subpe...
AP radiograph of the knee in a child with hyperparathyroidism shows subperiosteal
bone resorption ( arrow) along the proxi...
Lateral radiograph of the skull in a 23-year-old man with secondary hyperparathyroidism
shows trabecular resorption of the...
Dental radiograph in another child with hyperparathyroidism shows resorption (
arrow) of the lamina dura of the mandible.
Radiologic findings of
HYPERPARATHYROIDISM
Secondary
• Bony sclerosis; focal or
generalized.
• Rugger-jersey
appearance of...
AP radiograph of the wrist in an 83-year-old woman with primary hyperparathyroidism shows
chondrocalcinosis ( arrow) of th...
Secondary HPT. Radiograph of the pelvis and hips showing diffuse osteosclerosis( coarse striations)
A, AP radiograph of the spine in a patient with secondary hyperparathyroidism shows generalized bone
sclerosis, small kidn...
AP radiograph of the hand in a 50-year-old man with renal osteodystrophy shows acro-osteolysis
( short arrows), subperiost...
Secondary HPT. Radiograph of the hand showing resorption of the first to third tufts with soft tissue
calcification (1). T...
The differential diagnosis of
HYPERPARATHYROIDISM
• Focal subperiosteal resorption involving a single bone
– Neoplasms or ...
• Osteoporosis – late onset, Ca++ -N
• Osteitis Deformans(Pagets disease)- Se Ca++ -
N, ALP , X ray- mainly pelvis, lumbar...
TREATMENT
1. Management of acute hypercalcemia by
rehydration with normal
saline,bisphosphonates,haemodialysis.
2. Medical...
3. Surgery : -Is indicated in patients with
complications and in younger age group.
-Minimally invasive surgery to excise
...
SECONDARY HYPERPARATHYROIDISM
• It occurs when PTH secretion is increased to
compensate for prolonged hypocalcemia.
• It i...
• Secondary hyperparathyroidism can also
result from malabsorption of vitamin D
due to chronic pancreatitis, small bowel
d...
• INVESTIGATIONS : Serum calcium levels are
low.PTH levels are raised. Phosphate levels depend
on etiology (e.g. high in r...
TERTIARY HYPERPARATHYROIDISM
• In a small proportion of cases of secondary
hyperparathyroidism,continuous stimulation
of t...
• CLINICAL FEATURES : Symptoms and signs are
due to hypercalcemia so presentation is similar
to primary hyperparathyroidis...
THANK YOU
Hyperparathyroidism
Hyperparathyroidism
Hyperparathyroidism
Hyperparathyroidism
Hyperparathyroidism
Hyperparathyroidism
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Hyperparathyroidism

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Primary, Secondary, Tertiary, rugger Jersey spine, hypercalcemia.

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Hyperparathyroidism

  1. 1. HYPERPARATHYROIDISM - Dr NIKHIL.S.U
  2. 2. PARATHYROID GLANDS • Two pairs of glands • Behind the left and right lobes of the thyroid • About 6 mm long and 3 to 4 mm wide, and 1 to 2 mm anteroposteriorly • Chief cells- synthesize and release parathyroid hormone • Single chain polypeptide -84 a.a
  3. 3. HYPERPARATHYROIDISM • Primary – Single adenoma- MC – Multiple adenomas – Nodular hyperplasia – Carcinoma • Secondary – chronic renal insufficiency. – Malabsorption – Osteomalacia & rickets • Hyperparathyroidism may result in either bone resorption or bone formation, bone resorption usually dominates. • Normal values are 10 to 55 pg/ml
  4. 4. • Both sexes affected • 2-3> women • Middle aged • Features o Bones, stones, abdominal groans, psychic moans
  5. 5. • Bones  Severe pain, tenderness  Gen weakness  Deformity of limbs & spine  Pathological # & delayed union • Stones  Renal colic  Polyuria, dypsia, nocturia, hypercalcemia  Renal failure • Abdominal groans  Anorexia, nausea, vomiting, constipation, dyspepsia, peptic ulceration • Psychic moans  Depression, drowsiness, impaired cognitive function
  6. 6. Bone pathology • Rapid progressive resorption, softening of the bones with deformity • Osteoclastic – conversion into fibrous tissue cylinder • Width of bones increased- Normal periosteum • Haversian canal gets enlarged- osteoblasts - vascular –becomes fibrous • Deformities-gravity, weight bearing • Cysts of varying size occur- thin brownish fluid filled
  7. 7. • Gland pathology- single adenoma-mc, pale, clear- chief cells. • Lab findings • Hypercalcemia • Hypophosphatemia • Hyperphospaturia • Hypercalcuria • ALP- increased
  8. 8. Radiologic findings of HYPERPARATHYROIDISM • The M/C radiologic abnormality is generalized osteopenia. • Bone resorption, bone sclerosis, brown tumors, chondrocalcinosis, soft tissue calcification, and vascular calcification. • Brown tumors appear as well-defined lytic lesions. – After resection of parathyroid adenomas, the lesions may become sclerotic and may mimic blastic metastasis. – (Brown tumors are composed mostly of osteoclasts ) • Bone resorption, the most characteristic finding, is usually classified as – subchondral, trabecular, endosteal, intracortical, subperiosteal, subligamentous, and subtendinous.
  9. 9. Radiologic findings of HYPERPARATHYROIDISM • Subperiosteal resorption - M/C – Usually occurs in the hands and feet. – M/C affected site: radial aspects of the middle phalanges. – Acro-osteolysis or phalangeal tufts resoption may also be present. • Trabecular resorption – Often seen in the diploic space of the skull, where it has a characteristic salt and pepper appearance. • Subchondral resorption – May be seen in the sacroiliac joints, sternoclavicular joints, acromioclavicular joints, symphysis pubis, and discovertebral junction .
  10. 10. AP radiograph of the hand in a 66-year-old woman with primary hyperparathyroidism owing to parathyroid adenoma shows subperiosteal bone resorption ( arrows) along the radial aspect of 2nd, 3rd, and 4th middle phalanges.
  11. 11. AP radiograph of the knee in a child with hyperparathyroidism shows subperiosteal bone resorption ( arrow) along the proximal medial tibia.
  12. 12. Lateral radiograph of the skull in a 23-year-old man with secondary hyperparathyroidism shows trabecular resorption of the diploic space ("salt and pepper" appearance).
  13. 13. Dental radiograph in another child with hyperparathyroidism shows resorption ( arrow) of the lamina dura of the mandible.
  14. 14. Radiologic findings of HYPERPARATHYROIDISM Secondary • Bony sclerosis; focal or generalized. • Rugger-jersey appearance of spine. • Soft tissue and vascular calcification. Primary • Chondrocalcinosis • usually seen in the menisci of the knee, the triangular fibrocartilage of the wrist, and the pubic symphysis
  15. 15. AP radiograph of the wrist in an 83-year-old woman with primary hyperparathyroidism shows chondrocalcinosis ( arrow) of the triangular fibrocartilage.
  16. 16. Secondary HPT. Radiograph of the pelvis and hips showing diffuse osteosclerosis( coarse striations)
  17. 17. A, AP radiograph of the spine in a patient with secondary hyperparathyroidism shows generalized bone sclerosis, small kidneys, and left renal calculi. B, Lateral radiograph of the lumbar spine in another patient with secondary hyperparathyroidism shows horizontal, bandlike ("rugger jersey") sclerosis of the vertebral bodies ( arrows).
  18. 18. AP radiograph of the hand in a 50-year-old man with renal osteodystrophy shows acro-osteolysis ( short arrows), subperiosteal bone resorption ( long arrows), and vascular calcifications.
  19. 19. Secondary HPT. Radiograph of the hand showing resorption of the first to third tufts with soft tissue calcification (1). There is articular calcification (2), and subperiosteal and subligamentous resorption (3).
  20. 20. The differential diagnosis of HYPERPARATHYROIDISM • Focal subperiosteal resorption involving a single bone – Neoplasms or osteomyelitis. • Bone sclerosis in patients with secondary hyperparathyroidism. – Metastatic disease, radiation-induced bone disease, hypoparathyroidism, myelofibrosis, mastocytosis, sickle-cell disease, and Paget's disease. • Chondrocalcinosis – Pyrophosphate arthropathy (CPPD) or hemochromatosis. • Brown tumors – includes other focal lytic lesions, such as giant cell tumor and fibrous dysplasia.
  21. 21. • Osteoporosis – late onset, Ca++ -N • Osteitis Deformans(Pagets disease)- Se Ca++ - N, ALP , X ray- mainly pelvis, lumbar spine, femora, skull involved, deformities r common • Osteomalasia- Ca++ , ALP , response to Vitamin D (+), X ray- bending of bones (+) • Osteogeneis imperfecta- multiple fractures, childhood disease, blue sclera.
  22. 22. TREATMENT 1. Management of acute hypercalcemia by rehydration with normal saline,bisphosphonates,haemodialysis. 2. Medical line : -Monitor serum creatinine levels and calcium levels every 6 months.DEXA scan on an annual basis. -Avoid thiazide diuretics. -Maintain high oral fluid intake. -Improving bone mineral density and achieving calcium homeostasis by calcimimetics and HRT.
  23. 23. 3. Surgery : -Is indicated in patients with complications and in younger age group. -Minimally invasive surgery to excise solitary adenoma, Subtotal parathyroidectomy in case of diffuse hyperplasia are being done.
  24. 24. SECONDARY HYPERPARATHYROIDISM • It occurs when PTH secretion is increased to compensate for prolonged hypocalcemia. • It is seen in patients with chronic renal failure where the failing kidneys do not convert vitamin D to its active form and they do not excrete phosphate. Excess phosphate combines with calcium to form calcium phosphate. • Both processes lead to hypocalcemia,cause hyperplasia of all parathyroid tissue and hence secondary hyperparathyroidism.
  25. 25. • Secondary hyperparathyroidism can also result from malabsorption of vitamin D due to chronic pancreatitis, small bowel disease, bariatric surgery. • CLINICAL FEATURES : are mostly of renal failure. If it is due to vitamin D deficiency, limb deformities, pathological fractures occur.
  26. 26. • INVESTIGATIONS : Serum calcium levels are low.PTH levels are raised. Phosphate levels depend on etiology (e.g. high in renal disease, low in vitamin D deficiency). Radiology shows evidence of bone disease. • TREATMENT : Medical line is the mainstay. The underlying condition needs to be treated -correcting vitamin D deficiency. -treatment of chronic kidney disease (Calcium supplementation. Treatment with vitamin D and its analogues. Calcimimetics)
  27. 27. TERTIARY HYPERPARATHYROIDISM • In a small proportion of cases of secondary hyperparathyroidism,continuous stimulation of the parathyroids results in adenoma formation and unregulated PTH secretion. • Even correction of the underlying cause will not stop excess PTH secretion i.e parathyroid gland hypertrophy becomes irreversible.
  28. 28. • CLINICAL FEATURES : Symptoms and signs are due to hypercalcemia so presentation is similar to primary hyperparathyroidism. • INVESTIGATIONS : Serum calcium and PTH levels are raised. Phosphate levels are often high. • TREATMENT : Total or subtotal parathyroidectomy is the recommended treatment. Autotransplantation of parathyroid tissue in the forearm is also commonly carried out.
  29. 29. THANK YOU

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