Week 4: pathology of parathyroid glands Flashcards

1
Q

normal parathyroid glands

A

~5mm in diameter

  • inferior are from 3rd pharyngeal arch and migrate with the thymus in embryology
  • superior two are from 4th pharyngeal arch
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2
Q

Cell types of parathyroid glands

A
  1. Chief cells: main functional cell
  2. Oxyphil cells: larger, with numerous mitochondria. granular appearance
  3. water-clear cells: cytoplasm appears to by empty by H and E (glycogen)
  4. transitional cells: evidence that water clear and oxyphil cells are from chief cells
  5. Adipocytes: increases with age and are diminished in hyperplasia
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3
Q

Genesis of parathyroid glands

A
  • congenital absence
  • chromosome 22
  • DiGeorge syndrome: agenesis of parathyroids and thymus
  • CATCH22: cleft palate, appearance, thymus/immunology deficiency, calcium salt low, heart defect
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4
Q

Ectopic parathyroid

A
  • inferior parathyroids may migrate with thymus and be found in the lower neck on in the mediastinum with the thymus
  • glands could also be within thyroid, in carotid bifurcation, pericardial cavity
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5
Q

Parathyroid cysts

A

small tubules that are associated with parathyroids that persist can develop cysts
-aspirate clear fluid vs thyroid cyst which would have blood/colloid in cyst

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6
Q

Primary hyperplasia of parathyroid glands

A
  • all four glands are enlarged
  • cause: adenoma, primary hyperPTH, MEN syndromes
  • microscopic: hyperplasia usually involves chief cells. Lobulated appearance. Diminished fat cells
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7
Q

Secondary hyperplasia of parathyroid glands

A
  • all four gland enlarged
  • gross: paler than brown hue in primary hyperplasia
  • causes: chronic renal disease most common, hypocalcemia, hyperphosphatemia, Vitamin D deficiency
  • can occur as a compensatory enlargement of parathyroids in conditions that tend to lower blood Ca or raise phosphorus
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8
Q

Tertiary hyperparathyroidsm

A
  • development of autonomous parathyroid hyper function in a person with secondary hyperPTH, not under influence of Ca
  • gland continues to hyper function even after stimulus is removed
  • cause: adenomas, carcinomas
  • pathogenesis obscure
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9
Q

Parathyroid adenoma

A
  • most common cause of primary hyperPTH (80-90%)
  • single enlarged gland
  • microscopic: rim of residual parathyroid tissue around adenoma
  • predominant cells: chief cells or water-clear cells or mixture
  • fat cells not really present in adenoma
  • can do Sestamibi scan
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10
Q

Parathyroid carcinoma

A
  • rare
  • difficult to diagnose: palpable mass in neck, extreme high serum calcium higher than 15mg/dl, difficult resection
  • infiltrative growth
  • high mitotic rate
  • vascular invasion, capsular invasion, metastasis
  • trabecular growth, thick fibrous septae
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11
Q

Manifestations of hyperPTH

A
  • Calcification of kidneys, soft tissues, renal stones
  • Peptic ulcer disease
  • Pancreatitis
  • Osteitis fibrosa cystica (Brown tumor of bone)
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12
Q

Bone lesions in hyperPTH

A
  • skull: salt and pepper apperance
  • vertebrae: demineralization. Look like Rugger-jersey
  • digits: erosion, resorption
  • spine fractures: compression fracture, kyphosis
  • bone: soap bubble appearance-osteitis fibrosa cystica- with cystic and hemorrhagic spaces and hemosiderin deposition that gives it brown appearance
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13
Q

osteitis fibrosa cystica

A
  • resorption of bone, replacement of marrow spaces and resorbed bone by fibrous tissue, and attempts at repair with rows of osteoblasts covering newly deposited layers
  • multinucleated giant cells
  • hemorrhage
  • hemosiderophages
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14
Q

hypercalcemia of malignancy

A
  • squamous cell carcinoma: releases PTHrP
  • renal cell carcinoma
  • ovarian tumors
  • bladder tumors
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