Parathyroid Flashcards

1
Q

What is the parathyroid derived from?

A

pharyngeal pouches

-could be found in the carotid sheath, thymus and anterior mediatinum

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2
Q

Parathyroid histology

A

Chief cells predominate and contain glycogen and produce PTH

Oxyphil cells in small clusters, packed with mitochondria

-Fat increases with age up to 25 years, occupies 30% of adult gland

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3
Q

What does PTH do?

A
  1. Activates osteoclasts by mobilizing calcium from bone
    - increased tubular reabsorption
    - increases conversion of vitamin D to active form
    - decreases serum phosphate by increasing urinary excretion
    - Augments GI calcium absorption

-Net effect increase calcium which has negative feedback on PTH

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4
Q

What is the most common cause of clinically apparent hypercalcemia? incidental hypercalcemia?

A

clinically apparent:
malignancy

incidental:
primary hyperparathyroidism

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5
Q

Hypercalcemia of Malignancy

A
Osteolytic metastases: 
tumor
cytokines
local osteolysis
maturation of osteoclasts 

-prognosis is poor, patients present at advanced stage

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6
Q

Primary Hyperparathyroidism

age group

A
50 years old
Sporadic or familial 
1. Parathyroid adenoma (85-95%)
2. Primary Hyperplasia (diffuse or nodular) 5-10%
3. Parathyroid carcinoma 1%
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7
Q

Familial primary hyperparathyroidism
MEN1
MEN2A
Familail hypocalciuric hypercalcemia

A
  1. MEN 1-inactivation of MEN1 gene on chromosome 11q13 (tumor suppressor gene)
  2. MEN2A-activating mutation of RET (tyrosine kinase receptor) gene on chromosome 10q
  3. familial hypocalciuric hypercalcemia-autosomal dominant disorder due to mutation in parathyroid calcium-sensing receptor gene (CASR) on chromosome 3
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8
Q

Parathyroid adenoma

A

Gross
-solitary
-increased uptake of radionuclide scan
.5-5 gm

Histology:
Sheets or nests of chief cells or oxyphil cells
Encapsulated lesion with compressed normal rim of parathyroid at pituitary
Mitotic figures rare
May find endocrine atypia-rep degenerative change-not a criteria for malignancy
-

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9
Q

Parathyroid hyperplasia

A

2-4 glands
combined weight 1 gm
microscopically diffuse or multinodular chief cell hyperplasia most common

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10
Q

Parathyroid carcinoma

A

Gross:
solitary mass, may exceed 10gm
-may be circumscribed lesion or clearly invasive neoplasm

Histo:
Cells resemble normal parathyroid and are arranged in trabeculae or nodules with dense fibrous capsule with intervening fibrous bands

Diagnosis: local invasive of surrounding tissue and metastasis

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11
Q

Osteitis fibrosa cystica

A

thinned bony cortex with marrow containing fibrous tissue, hemorrhages and cyst formation

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12
Q

Brown tumor

A

collection of osteoclasts, reactive giant cells and hemorrhage debris forming masses that stimulate tumor

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13
Q

Kidney changes from hyperparthyroidism

A
  1. formation of stones
  2. calcification of interstitium and tubules
  3. metastatic calcification in organs like stomach, lung, myocardium or blood vessels
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14
Q

Primary Hyperparathyroidism

clinical manifestations

A

May be asymptomatic and identified by hypercalcemia on routine exam

bone, stones, groan, psychiatric undertones

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15
Q

Secondary Hyperparathyroidsim

Etiology

A

-process of chronic depression or decrease in calcium that causes compensatory overactivity of the parathyroid glands

  • -Renal Failure most common
    1. decreased phosphate excretion-hyperphosphatemia-decreases serum calcium-parathyroid stimulation
    2. deficiency of alpha1 hyodroxylase–deficiency of Vitamin D-less absorption of clcium from GI tract and eventually parathyroid stimulation

0ther eitologies-decreased dietary Ca, steatorrhea, vit D def

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16
Q

Secondary Hyperparathyroidsim

Clinical features

A
  • skeletal changes not as severe as in primary hyperparathyroidism
  • vascular calcification may cause significant ischemic damages to skin-calciphylaxis
17
Q

Tertiary hyperparathyroidsim

A

MInority of patients-autonomous hyperparathyroidism with symptomatic hypercalcemia

-parathyroidectomy necessary for controlling symptoms

18
Q

Hypoparathyroidism

Etiology

A

Less common than hyper
Etiology:
1. Surgically induced

  1. Autoimmune
    - mucocutaneous candidiasis
    - adrenal insufficiency (autoimmune polyendocrine syndrome 1 APS1)
  2. Autosomal dominant hypoparathyroidism-gain of function mutation in calcium sensing receptor gene (CASR)-hypercalcemia and hypocalcemia
  3. Familial isolated hypoparathyroidism-rare disorder due to the encoding PTH precursor peptide
  4. Congenital absence of parathyroid-DiGeorge or 22q11
19
Q

Hypoparathyroidism CLinical manifestations

A
  1. Tetany-numbness, paresthesias, carpopedal spasm, laryngospasm, seizures
  2. chvostek sign-occude circulation in forearm, observe carpal spasm
  3. mental status changes-emotional instability, anxiety, depression, confusion, hallucinations and frank psychosis
  4. Intracranial manifestations-calcifications of basal ganglia, parkinson like movement disorders and increased intracranial pressure with papilledema
  5. ocular disease-catarct formation
  6. cardiovascular manifestation*******-Prolonged QT interval
  7. Dental abnormalities-dental hypoplasia, failure of eruption, defective enamel and root formation and carious teeth
20
Q

Pseudohypoparathyroidism

A

Rare disease due to end organ resistance to the actions of PTH
-increased to normal PTH with hypocalcemia