Transcript Parathyroid Glands

Parathyroid Glands
HUSSEN.S.ALNAKHLY
PARATHYROID GLAND
Location:
•Usually paired.
•Very small (less than 5 mm).
•Called parathyroid glands because of their position on
posterior margins outer surface of thyroid gland.
•More superior of each pair usually near middle of
margin of lobe.
•More inferior of each pair usually at inferior apex of
lobe.
Development: Like thyroid gland, develop from
endodermal thickening in floor of early pharynx and
epithelium of 3rd and 4th gill slit pouches.
Anatomy
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Arterial supply usually from
inferior thyroid art
Superior glands usually
imbedded in fat on posterior
surface of middle or upper
portion of thyroid lobe
Lower glands near the lower
pole of thyroid gland
In 1-5% pts, inferior gland in
deep mediastinum
Histology
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50/50 parenchymal cells,
stromal fat
Chief cells – secrete PTH
Waterclear cells
Oxyphil cells
Parathyroid Hormone
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Synthesized in chief cells as large precursor – preproparathyroid hormone
Cleaved intracellularly into proparathyroid hormone
then to final 84 AA PTH
PTH then metabolized by liver into hormonally
active N-term and inactive C-term
PTH function
Hyperparathyroidism
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Primary Hyperparathyroidism
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Normal feedback of Ca disturbed, causing increased
production of PTH
Secondary Hyperparathyroidism
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Defect in mineral homeostasis leading to a
compensatory increase in parathyroid gland function
Etiology
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Unknown cause
Single gland adenomatous disease
Multiglandular disease – exogenous stimulus
Ionizing radiation exposure
Clinical Presentation
Nephrolithiasis
Bone Disease
Peptic Ulcer Disease
Psychiatric disorders
Muscle weakness
Constipation
Polyuria
Pancreatitis
Myalgia
Arthralgia
Hypercalcemia
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Hyperparathyroidism (most common)
Malignancy (most common in hospitalized)
Lytic metastases to bone
 PTHrP producer
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Sarcoidosis / granulomatous disease
Vit D intoxication
Thiazides
Hyperthyroidism
Familial hypocalciuric hypercalcemia
Renal Complications
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Generally the most severe clinical manifestations
Many have frequency, polyuria, polydipsia
Usually present w/ nephrolithiasis (20-30%)
Calcium phosphate or Calcium oxalate
Nephrocalcinosis (in 5-10%) – calcification w/in
parenchyma of kidneys
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Severe renal damage
Hypertension secondary to renal impairment
Bone Disease
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Osteitis fibrosa cystica
In early descripts of disease, many had severe
bone disease (50-90%), but now 5-15%
Subperiosteal resorption – pathognomonic of
hyperparathyroidism
Gastrointestinal Manifestations
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Peptic Ulcer disease
Pancreatitis
Cholelithiasis – 25-35%
Neuromuscular complications
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Muscular weakness, fatigue
More commonly in proximal muscles
Sensory abnormalities also possible
Laboratory Diagnosis
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Elevated Serum Ca and PTH
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Must measure Ionized Ca (subtle cases of hyperPTH
will have normal Serum Ca)
50% will have hypophosphatemia Elevated
Alkaline Phosphatase in 10-40%
Hyperchloremic metabolic acidosis
Low Mg in 5-10%
High Urinary Ca in almost all cases