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Parathyroid gland
Emberyology of Parathyroid
The upper parathyroid has its origin in the fourth branchial
pouch
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 hyperparathyroidism
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
Weight:
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
calcium
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
hypercalcaemia.
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
Malignancy:
A. Solid tumours with or without bony metastasis Multiple
myeloma
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
Miscellaneous:
A. Benign familial hypocalcuric hypercalcemia Paget's
disease
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
Vit.D.
H. Treatment of hypercalcaemic crises: Usually by
haemodialysis
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.
Etiology:
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
diseases.
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
calcium.
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
hyperparathyrodism
MEN. II B.
Medullary carcinoma of thyroid + Pheochromocytoma
hyperparathyroidism
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
Asymptomatic
The patient should be diagnosed before "Renal stones,
painful hones, abdominal groans and psychic moans".
Early symptoms
Fatiguability, weakness, depression, polyurea, polydepsia,
constipation.
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
helpful.
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
ectopic.
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
goitre.
For inexperienced Surgeon and single tumour, localization
could be used.
Surgical treatment of Primary hyperparathyroidism:
Needs:
Experiencedsurgeon
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
thyroid
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