Parathyroid gland by nikeborome


									           Parathyroid gland
Emberyology of Parathyroid

     The upper parathyroid has its origin in the fourth branchial
     and moves to a position in adult life adjacent to the middle
     third of the lateral thyroid lobe.
     The lower parathyroid originates from the third branchial
     pouch to travel in a longer distance to the lower pole of
     thyroid. It has more frequent ectopic positions

Historical background
     Since Von Ricklinghouse at 1891, who described fibro
     cystic disease of the bones produced by hyper-
     But he did not define the nature of association , till the full,
     good description done by Albright 1932 describing the
     association between renal stones and parathyroid glands
     Many trials done in between

Anatomy of parathyroid glands
      Number 4 in nearly 80% 3 in nearly 13% 5 in nearly 6%
      Very rare more or less
      Upper more stationary post above the inferior thyroid
      artery or behind or between branches
      Lower parathyroid: Highly variables
  50% lateral or posterior to the lower pole 12.5% below the
lower pole < > 1 cm
  May be inside the capsule but never under the tissue
 Average for opne = 35 mg Average for 4 = 120 - 140 mg
      Blood supply:
  Superior glands ---> Superior thyroid a. Inferior glands ----->
Inferior thyroid a.
  Some ectopic ----> by other vessels Rare inferior by ---->
superior thyroid

Calcium metabolism
     Body contains 1,000,gm calcium Extracellular -- 1 gm
     Average intake 0.5 - 1 gm / day
     Average urinary output 100 - 200 mg / day
     In plasma, about 47% ionized Phosphorus metabolism
     Body contains 500 gm of phosphorus Intracellular fluid
     0.4 gm 15% are protien bound
     Serum value varies: 3 - 3.5 mg% in adult
                    5 - 6 mg% in children

Parathyroid hormone

      Each hormone contains 84 amino acids with molicular
      weight about 9,500
      C - terminal fragment is the easiest to measure
      N - terminal fragment is the biologically active
      Serum calcium homeostasis:
  Physiologically there. is feed back mechanism between S.
calcium and the PTH. Also calcitonin has a rule to antoganize
      PTH experimentally leads to hypercalcemia
  hypophosphataemia and phosphaturia

mechanisms of action of PTH

  A. Direct action on bone - increased bone resorption
  B. Increased calcium absorption from intestine
  C. Decreased tubular absorption of phosphate
  D. Effect of PTH on kidney and bone through activation of
     cyclic AMP.
Causes of hypercalcaemia
     Endocrine causes:
  A. Hyperparathyroidism
  B. Hyper or hypothyroidism
  C. Addison's disease
  D. VI Pomas and pheochromocytomas
  A. Solid tumours with or without bony metastasis Multiple
  B. Lymphoma and leukaemias

Causes of hypercalcaemia
     Granulomatous disease:
  A. Sarcoidosis
  B. Tuberculosis
     Increased intake:
  A. Calcium
  B. Vit. D. and Vit. A intoxication Milk alkali syndrome
  A. Benign familial hypocalcuric hypercalcemia Paget's
  B. Immobilization
  C. Thiazides
  D. Lithium

Medical treatment of hypercalcemia
  A. Parenteral solut. and diuretics
  B. Phosphate:either I.V. or oral side effect
  C. EDTA (Elhylene Diaminotetracetic Acid)
  D. Sulfate and citrate therapy
  E. Calcitonin:best in combination with phosphate prolonged
     use leads to CT escape
  F. Dialysis:especially in severe renal failure
  G. Corticosteroids:It's effect is by antagonizing the effects of
  H. Treatment of hypercalcaemic crises: Usually by
  I. Treatment of persisted or recurrent hyper-parathyroidism
     by trans catheter staining with contrast agent Through the
     feeding artery of the parathyroid either The internal
     mammary branch or the inferior thyroid branch, either by
     gelfoam or silicone or by radiographic contrasts best used
     in an ectopic parathyroid adenoma.

Hypercalcaemic crises

     Rapid and sudden elevation to 14 mg%
     Symptoms: Many ending by coma.
  A. Primary hyperthyroidism
  B. Other causes
     The second type responds adequately to steorids
     The first type responds to calcitonin, Mithramycin,
     intravenous phosphate with adequate hydration.
     Then parathyroidectomy Hyperparathyroidism with other
     First to treat the disease before the complications To avoid
     the hypercalcaemic crises

Pathology of primary hyperparathyroidism
     Hyperplasia Multiglandular disease 15-20% Adenoma
     single in 80-85%
     Carcinoma less than 1%
     Ectopic hyperparathyroidism
     Now hyperplasia is chief cell and oxyphil cell hyperplasia
     The activity of the gland depends upon the fat either
     extracellular or intracellular.
     It is very difficult to differentiate between adenoma and
     hyperplastic gland and the normal one.
     Also microscopic differentiation between adenoma and
     hyperplasia is difficult.
carcinoma of parathyroid
     there is high serum calcium above 14 mg% palpable neck
     mass in about 50% of cases.
     Carcinoma of parathyroid very difficult to diagnose
     histologically and to differentiate from benign adenoma
     local infiltration, recurrence, distant metastasis are the only
     acceptable criteria.
     Complications which are agressive i.e. pancreatitis, renal
     stones and renal failure, bone diseases more common.
     Adequate resection of the parathyroid with adjacent safety
     margin including the thyroid lobe in that side.

Secondary hyperparathyroidism
     Defined as a state of compensatory hyper Secretion of
     PTH which could occur in any clinical condition in which
     there is a tendency to hypocalcaemia.
     Possible causes:
  A. Chronic renal failure
  B. Ricket's osteomalacia
  C. Intestinal malabsorption
  D. Fanconi's syndrome and renal tubular acidosis
  E. Some said that main causes of hypocalcaemia - mainly the
     ionic part is due to phosphate retention - which lowers free
     The most important indication of parathyroidectomy is
     severe bone pain unresponsive to Vit. D administration.
     Medical treatments:
  Dialysis, Vit. D. Phosphate binder

Tertiary hyperparathyroidism:
      It is autonomous increase of the activity of chief cell
      hyperplastic gland in secondary hyperparathyroidism
      ending in Adenomatous change. The main trigger factor is
      the hypocalcaemia.
      Sometimes, this autonomous hyperactivity stopped after
      renal transplantation and the gland gradually involuted.
     In other conditions, the autonomous activity continues, and
     parathyroidectomy is recommended.

Multiple endocrine neoplasia syndromes

     MEN. I Wermer's syndrome
 Pituitary + Pancreatic (Gastrinoma) hyperparathyroidism
     MEN . II A. Sipple's syndrome
 Pheochromocytoma + Medullary carcinoma of thyroid
     MEN. II B.
 Medullary carcinoma of thyroid + Pheochromocytoma
 Ganglion neuroma Neuroma of tongue Marfanoid habit
     All are inherited and autosomal dominant with variable
     percentage of each tumour.

Clinical picture of hyperparathyroidism:
     Renal stones, nephrocalcinosis
     Bone disease pain, cysts, 'brown tumours, fractures
     Peptic ulcer Pancreatitis Fatigue
     Muscle weakness Hypertension usually renal
     Central nervous symptoms and signs
     Mental disturbance, till coma
     Other of MEN Neck swelling Hypercalcaemic crises
     Polyurea, Polydipsia, hypokalemia
     The patient should be diagnosed before "Renal stones,
     painful hones, abdominal groans and psychic moans".
     Early symptoms
     Fatiguability, weakness, depression, polyurea, polydepsia,
Diagnosis of Primary hyperparathyroidism:
    Hypercalcaemia with elevated PTH concentration is
    usually diagnostic of hyperparathyroidism.
    Estimation of the ionized fracture of CA++ usually help to
    exclude         the       so-called      Normocalcaemic
    hyperparathyroidism. Estimation of serum protein is
    Serum phosphate is low in most cases
    Alakaline phosphatase in case of bone disease elevated
    Urinary calcium output above 200 mg/day, mainly to
    exclude familial hypocalcuric hypercalcaemia
    Plasmachloride: Usually elevated Cyclic AMP level:
    elevated in urine Bone biopsy mainly from iliac crest

Localization studies
     Localization studies valuable mainly in tumours, but in
     hyperplasia highly misleading.
     Ultrasound could localize up to 80%, mainly in the neck,
     needle aspiration could he done also.
     Thallium - Technetium, subtraction technique, Technetium
     will be taken by both.
     Thallium by the thyroid only.
     Subtraction will give the parathyroid only. excellent for
     Good number false positive results.
     CT, for mediastinal or substernal tumours highly valuable
     Venous catherization with blood sampling for PTH,
     difficult, but best to lateralize in difficult cases i.e. nodular
     For inexperienced Surgeon and single tumour, localization
     could be used.
Surgical treatment of Primary hyperparathyroidism:
     Needs:                  Experienced-                 surgeon
     Experienced Pathologist
     Requirements to improve neck exploration:
     Absolute haemostasis
     Complete exploration, extensive elevation of the flaps up
     and down
     An unhurried time schedule
     Knowledge of the anatomy of the parathyroid glands
     A systemic exploration in an attempt to identify all glands
     Possible sites of the glands:
     At site of crossing of recurrent laryngeal and interior
     thyroid artery
     Upper posterior capsular region of the superior pole of
     Subcapsular position
     In the superior mediastinum after cleaning the inferior
     poles of thyroid gland. In the thymus
     Paraeosopharyngeal, parapharyngeal, retrooesopharyngeal
     or retro-pharyngeal regions
     Incision of carotid sheath. Included in the glands?
     Mediastinotomy in other session How much excision
     Single adenoma
     3 1/2 glands subtotal .Total with autograft Frozen section
     is better
     Complications of Surgery:
  A. Hypocalcaemia
  B. Recurrent laryngeal injury
  C. Haematoma
  D. Wound infection

To top