Parathyroid Glands - SNguyen

Parathyroid Glands - SNguyen - Parathyroid Glands...

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Unformatted text preview: Parathyroid Glands Parathyroid Glands Scott Nguyen Dr. Lopchinsky Embryology Embryology Branchial arches and Pharyngeal pouches form in the 4th week Superior Parathyroids ­ the 4th Pharyngeal pouch w/ thyroid Inferior Parathyroids – 3rd Pharyngeal pouch w/ thymus Anatomy Anatomy 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 1­5% pts, inferior gland in deep mediastinum Histology Histology 50/50 parenchymal cells, stromal fat Chief cells – secrete PTH Waterclear cells Oxyphil cells Parathyroid Hormone Parathyroid Hormone Synthesized in chief cells as large precursor – pre­ proparathyroid hormone Cleaved intracellularly into proparathyroid hormone then to final 84 AA PTH PTH then metabolized by liver into hormonally active N­term and inactive C­term PTH function PTH function Hyperparathyroidism Hyperparathyroidism Primary Hyperparathyroidism Secondary Hyperparathyroidism Normal feedback of Ca disturbed, causing increased production of PTH Defect in mineral homeostasis leading to a compensatory increase in parathyroid gland function Tertiary Hyperparathyroidism After prolonged compensatory stimulation, hyperplastic gland develops autonomous function Primary Hyperparathyroidism Primary Hyperparathyroidism Epidemiology 25/100,000 50,000 new cases yearly F > M Incidence increases w/ age Most in > 50 years old Etiology Etiology Unknown cause Single gland adenomatous disease Multiglandular disease – exogenous stimulus Overexpression of PRAD1 oncogene – controlls cell cycle Ionizing radiation exposure Clinical Presentation Clinical Presentation Nephrolithiasis Bone Disease Peptic Ulcer Disease Psychiatric disorders Muscle weakness Constipation Polyuria Pancreatitis Myalgia Arthralgia 30 2 12 15 70 32 28 1 54 54 Hypercalcemia ­ DDx Hypercalcemia ­ DDx Hyperparathyroidism (most common) Malignancy (most common in hospitalized) Lytic metastases to bone PTHrP producer Sarcoidosis / granulomatous disease Vit D intoxication Thiazides Hyperthyroidism Familial hypocalciuric hypercalcemia Renal Complications Renal Complications Generally the most severe clinical manifestations Many have frequency, polyuria, polydipsia Usually present w/ nephrolithiasis (20­30%) Calcium phosphate or Calcium oxalate Nephrocalcinosis (in 5­10%) – calcification w/in parenchyma of kidneys Severe renal damage Hypertension secondary to renal impairment Bone Disease Bone Disease Osteitis fibrosa cystica In early descripts of disease, many had severe bone disease (50­90%), but now 5­15% Subperiosteal resorption – pathognomonic of hyperparathyroidism Gastrointestinal Manifestations Gastrointestinal Manifestations Peptic Ulcer disease Pancreatitis Cholelithiasis – 25­35% Emotional Disturbances Emotional Disturbances Hypercalcemia of any cause – assoc w/ neurologic or psychiatric disturbances Depression, anxiety, psychosis, coma Severe disturbances not usually correctable by parathyroidectomy Articular and Soft Tissue Articular and Soft Tissue Chondrocalcinosis and Pseudogout 3­7% Deposits of Calcium pyrophosphate in articular cartilages and menisci Vascular and Cardiac calcifications Neuromuscular complications Neuromuscular complications Muscular weakness, fatigue More commonly in proximal muscles Sensory abnormalities also possible Laboratory Diagnosis Laboratory Diagnosis Elevated Serum Ca and PTH Must measure Ionized Ca (subtle cases of hyperPTH will have normal Serum Ca) 50% will have hypophosphatemia Elevated Alkaline Phosphatase in 10­40% Hyperchloremic metabolic acidosis Low Mg in 5­10% High Urinary Ca in almost all cases Hyperparathyroid crisis Hyperparathyroid crisis Most pts w/ hyperparathyroidism chronically ill w/ renal and skeletal abnormalities Rarely can become acutely ill Rapidly developing weakness, N/V, weight loss, fatigue, drowsiness, confusion, Azotemia Uncontrolled PTH production, hyperCa, polyuria, dehydration, reduced renal function, worsening hyperCa Hyperparathyroid Crisis Hyperparathyroid Crisis Definitive therapy ­ resection Must reverse hyperCa first Diuresis ­ Saline hydration then Lasix to excrete Ca Calcitonin ­ rapid affect, inhibits bone resorption Steroids ­ take up to a week Mithramycin ­ rapidly inhibiting bone resorption Treatment Treatment Only Curative treatment ­ Parathyroidectomy Who should have surgery? Many found incidentally, assx Who should have surgery? Who should have surgery? NIH Consensus statement 1991 All symptomatic If Assymptomatic Markedly elevated serum Ca H/o episode life­threatening hypercalcemia Reduce renal function Kidney stone on Radiograph Markedly elevated urinary Ca excretion Substantially reduce bone mass Standard Neck Exploration Standard Neck Exploration Parathyroidectomy Parathyroidectomy Must find all four glands Intraoperative frozen section, PTH measurement useful If single gland enlarged, removal usually curative If multiple glands enlarged, removed. Normal just biopsied If all 4 enlarged (generalized parathyroid hyperplasia) ­ subtotal (3 1/2 removed) Superior parathyroid easier to find more consistent position just on dorsal surface of upper thyroid careful for superior thyroid artery and superior laryngeal nerve Inferior gland less consistent location may be near thymus or inside thyroid careful for recurrent laryngeal nerve betw trachea / esophagus inferior thyroid artery Success of Surgery Success of Surgery 95% of cases cured at initial neck exploration If failed intial procedure, can try to localize w/ Radionuclide, detect w/ gamma probe Sestamibi concentrates in parathyroid tissue Increasingly used in initial operation limits dissection Limits operative time May need mediastinoscopy ...
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  • Fall '11
  • Dr.Aslam
  • Hyperparathyroidism, Primary hyperparathyroidism, Bone Disease, glands Parathyroid glands, pouch w/ thyroid

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