Parathyroid Glands 1849 Sir Richard Owen 1879 Anton

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Parathyroid Glands

Parathyroid Glands

 • 1849 - Sir Richard Owen • 1879 - Anton Wölfler documented that

• 1849 - Sir Richard Owen • 1879 - Anton Wölfler documented that tetany • 1879 -Ivar Sandstrom • Hyperparathyroidism and the bone disease osteitis fibrosa cystica -1903

FELIX MANDL-1925

FELIX MANDL-1925

u Superior parathyroid glands 4 th branchial pouch u Inferior parathyroid glands -3 rd

u Superior parathyroid glands 4 th branchial pouch u Inferior parathyroid glands -3 rd branchial pouch u 80% of these glands - posterior aspect of the upper and middle thyroid lobes, cricoid cartilage u 1% of normal upper glands may be found in the paraesophageal or retroesophageal space

 • Common location of inferior glands is within a distance of 1 cm

• Common location of inferior glands is within a distance of 1 cm from a point centered where the inferior thyroid artery and recurrent laryngeal nerve cross. • 15% of inferior glands are found in the thymus. Skull base, Angle of the mandible, Superior to the superior parathyroid glands, Along with an undescended thymus

ANATOMY • 4 Parathyroid glands • 2 superior, 2 inferior • Superior parathyroid -dorsal

ANATOMY • 4 Parathyroid glands • 2 superior, 2 inferior • Superior parathyroid -dorsal to RLN at cricoid cartilage • Inferior parathyroid are ventral to RNL • Parathyroid glands are gray and semitransparent in newborns • Golden-yellow to light-brown in adults.

 • 5 to 7 mm in size • Weigh approximately 40 to 50

• 5 to 7 mm in size • Weigh approximately 40 to 50 mg each • Blood supply : branches of the inferior thyroid artery. Branches from the thyroidea ima, vessels to the trachea, esophagus, larynx, and mediastinum. The parathyroid glands drain ipsilaterally by the superior, middle, and inferior thyroid veins.

Hyperparathyroidism • is due to increased activity of parathyroid (hypercalcemia) • Types 1. Primary

Hyperparathyroidism • is due to increased activity of parathyroid (hypercalcemia) • Types 1. Primary 2. Secondary 3. Tertiary

 • Primary -unstimulated , high, PTH secreation due to primary hyperplasia/adenoma • Secondary

• Primary -unstimulated , high, PTH secreation due to primary hyperplasia/adenoma • Secondary -chronic hypocalcemia CRF, malabsorption, vid D deficiency rickets • Tertiary - autonomous reactive hyperplasia (renal transplantation)

C/F • Bones, Stones, Abdominal groans & psychic moans • • • common in

C/F • Bones, Stones, Abdominal groans & psychic moans • • • common in females 4: 1 age 20 -60 , 5 th decay incidence 1: 10000 manifestation; asymptomatic >50% behavioural problems osteitis fibrosa cystica (von recklinghausen disease) single or multiple cyst pseudo tumour in jam, skull, middle phalanges

 • B/L multiple renal caliculi • peptic ulcer, pancreatitis , MEN 1 syndrome

• B/L multiple renal caliculi • peptic ulcer, pancreatitis , MEN 1 syndrome • skin necrosis, band keratopathy, pseudo gout, myalgia, arthralgia, glycosuria, hypertension

 • Investigation Se. calcium, phosphate, albumin Se. PTH assay Alkaline phosphatase X-ray of

• Investigation Se. calcium, phosphate, albumin Se. PTH assay Alkaline phosphatase X-ray of bones TO LOCALISE PARATHYROID GLAND USG neck Thallium & technetium scan Selective venous sampling for PTH Sestamibi scanning

 • Differential diagnosis Secondaries in bone Multiple myeloma Vit-D intoxication Sarcoidosis paraneoplastic syndrome

• Differential diagnosis Secondaries in bone Multiple myeloma Vit-D intoxication Sarcoidosis paraneoplastic syndrome Familial hypocalciuric hypercalcaemia

 • Medical Management Primary HPT • Estrogen– Dose required is high • SERMs

• Medical Management Primary HPT • Estrogen– Dose required is high • SERMs – Reduction in serum calcium and markers of bone turnover after 4 weeks • Bisphonates – Studies have shown increase in lumbar spine and femoral neck mineral density • Calcium/Vitamin DCalcium/D • Calcimimeticagents (agents Cinacalcet) – Under investigation for primary HPT

 • All symptomatic • If Assymptomatic Markedly elevated serum Ca. Markedly Ca H/o

• All symptomatic • If Assymptomatic Markedly elevated serum Ca. Markedly Ca H/o episode life. H/life-threatening hypercalcemia Reduce renal function. Reduce function Kidney stone on Radiograph. Kidney Radiograph Markedly elevated urinary Ca excretion. Markedly excretion Substantially reduce bone mass. Substantially mass

 • serum calcium > 1 mgserum 1 mg/d. L above normal • history

• serum calcium > 1 mgserum 1 mg/d. L above normal • history of life threatening hypercalcemia • abnormal serum Cr • elevated urine calcium, > 400 mgelevated 400 mg/day • kidney stones • < 50 years old< old • bone density less than two standard deviations below the normbelow norm • neuromuscular symptoms

Surgical Management • Adenoma – Unilateral vs. Bilateral Exploration – r. PTH vs. Frozen

Surgical Management • Adenoma – Unilateral vs. Bilateral Exploration – r. PTH vs. Frozen Section • Hyperplasia/Multiple adenomata – Subtotal – less hypocalcemia – Subtotal w/ autotransplantation – MEN, Renal Failure – Total w/ Cryopreservation – up to 1 year

Autotransplantation • Iced saline bath • 20 20 -30 mg; 10 10 -20 1

Autotransplantation • Iced saline bath • 20 20 -30 mg; 10 10 -20 1 1 -2 mm slices • SCM vs. Brachioradialis • Pockets marked with clips • Up to 50% failure rate