THYROIDITIS AND

PARATHYROID GLAND
Dr NAGALEKSHMI M. S.
ASSISTANT PROFESSOR
DEPARTMENT OF GENERAL SURGERY
TIRUNELVELI MEDICAL COLLEGE
CHRONIC LYMPHOCYTIC
(AUTOIMMUNE) THYROIDITIS
• This common condition is usually associated with raised titres of
thyroid antibodies.
• Not infrequently there is a family history of other autoimmune
disease.
• It commonly presents as a goitre, Which may be diffuse or nodular
with a characteristic ‘bosselated’ Feel or with established or
subclinical thyroid failure.
• The diagnosis often follows investigation of a discrete swelling.
• Features of chronic lymphocytic (focal) thyroiditis are commonly
present on histological examination in association with other thyroid
disease, notably toxic goitre.
• Primary myxoedema without detectable thyroid enlargement
represents the end stage of the pathological process.
CLINICAL FEATURES
• The onset, thyroid status and the type of goitre vary profoundly from
case to case. The onset may be insidious and asymptomatic, or so
sudden and painful that it resembles the acute form of
granulomatous thyroiditis.
• Mild hyperthyroidism may be present initially, but hypothyroidism is
inevitable and may develop rapidly or extremely slowly.
• The goitre is usually lobulated, and may be diffuse or localised to one
lobe. It may be large or small, and soft, rubbery or firm in consistency,
depending upon the cellularity and the degree of fibrosis.
• The disease is most common in women at the menopause, but may
occur at any age.
• Papillary carcinoma and malignant lymphoma are occasionally
associated with autoimmune thyroiditis
DIAGNOSIS
• Biochemical tests of thyroid function vary with the thyroid status and
are of diagnostic value only if hypothyroidism is present. Significantly,
raised serum levels of one or more thyroid antibodies are present in
over 85 per cent of cases.
• Nevertheless, differential diagnosis from nodular goitre, carcinoma
and malignant lymphoma of the thyroid is not always easy.
• FNAC is the most appropriate investigation although abundant
lymphocytes may make the cytological distinction between
autoimmune thyroiditis and lymphoma difficult.
• When there is doubt about neoplastic disease, which may coexist
with thyroiditis, diagnostic lobectomy may be necessary
TREATMENT
• Full replacement dosage of thyroxine should be given for
hypothyroidism and if the goitre is large or symptomatic, because
some (under TSH stimulation) may subside with hormone therapy.
• More minor manifestations of the condition such as a small goitre
with raised antibody titres, or histological evidence of thyroiditis in
association with other thyroid disease, do not justify thyroxine
replacement if thyroid function is biochemically normal; however,
long-term surveillance is necessary because of the risk of late thyroid
failure
• Thyroidectomy may be necessary if the goitre is large and causes
discomfort.
• Increase in size of a long-standing lymphocytic goitre should be
assessed urgently because of the possibility of the development of
malignant lymphoma.
GRANULOMATOUS THYROIDITIS /DE QUERVAIN
THYROIDITIS /SUBACUTE THYROIDITIS
• This may follow a viral infection.
• In a typical subacute presentation, there is pain in the neck, fever,
malaise and a firm, irregular enlargement of one or both thyroid
lobes.
• There are raised inflammatory markers, absent thyroid antibodies, the
serum T4 is high normal or slightly raised, and the 123I uptake of the
gland is low.
• The condition is self-limiting and, in a few months, the goitre subsides
and there may be a period of months of hypothyroidism before
eventual recovery.
• In 10 per cent of cases the onset is acute, the goitre very painful and
tender and there may be symptoms of hyperthyroidism. One-third of
cases are asymptomatic but for the presence of the goitre.
• If diagnosis is in doubt, It may be confirmed by FNAC, radioactive
iodine uptake and by a rapid symptomatic response to prednisone.
• The specific treatment for the acute case with severe pain is to give
prednisone l0–20 mg daily for 7 days and the dose is then gradually
reduced over the next month. If thyroid failure is prominent,
treatment with thyroxine may be required until function recovers
RIEDEL’S THYROIDITIS
• This is very rare, accounting for 0.5 per cent of goitres.
• Thyroid tissue is replaced by cellular fibrous tissue, which infiltrates
through the capsule into muscles and adjacent structures, including
parathyroids, recurrent nerves and carotid sheath.
• It may occur in association with retroperitoneal and mediastinal
fibrosis and is most probably a collagen disease.
• The goitre may be unilateral or bilateral and is very hard and fixed.
• The differential diagnosis from anaplastic carcinoma can be made
with certainty only by biopsy, when a wedge of the isthmus should
also be removed to free the trachea.
• If unilateral, the other lobe is usually involved later and subsequent
hypothyroidism is common.
• Treatment is with high-dose steroid, tamoxifen and thyroxine
replacement. Reduction in size of the goitre and longterm
improvement in symptoms are to be expected if treatment is
commenced early
PRIMARY HYPERPARATHYROIDISM
• Primary hyperparathyroidism is commonly a sporadic rather than
familial condition associated with hypercalcaemia and inappropriately
raised serum PTH levels due to enlargement of one or more glands
and hypersecretion of PTH.
• The normal response to hypercalcaemia is PTH suppression
PATHOLOGY
• The majority (85 per cent) of patients with sporadic primary
hyperparathyroidism have a single adenoma, approximately 13 per
cent have hyperplasia affecting all four glands and about 1 per cent
will have more than one adenoma or a carcinoma. In familial disease,
multiple gland enlargement is usual.
• There is a weak correlation between the size of an adenoma and the
level of PTH . The histological differentiation between adenoma and
hyperplasia can be difficult and the macroscopic findings are an
important determinant in making the diagnosis.
• A single enlarged gland with three small normal glands is
characteristic of a single adenoma regardless of the histology which
may show considerable overlap between a hyperplastic and
adenomatous gland.
• Multiple adenomas occur more frequently in older patients
• Parathyroid carcinomas are large tumours and typically much more
adherent or even frankly invasive than large adenomas.
• Histology demonstrates a florid desmoplastic reaction with dense
fibrosis and capsular and vascular invasion.
PARATHYROID ADENOMA
CLINICAL FEATURES
• The classic quartet of ‘stones, bones, abdominal groans and psychic
moans’ is rarely observed in developed countries.
• Diagnosis is usually detected on serum calcium estimation well before
the full picture of severe bone disease (von Recklinghausen’s disease),
renal calculi and calcinosis, pancreatitis and psychiatric disorder.
Incidentally detected hypercalcaemia is rarely truly ‘asymptomatic’
and most patients experience an improved sense of well-being after
surgery.
DIAGNOSIS
• Although ionised calcium is the physiologically active circulating
element, total serum calcium is a satisfactory measure.
• PTH levels in the
• Serum phosphate level
• urine calcium excretion
• parathyroid hormone-related peptide (PTHrP) , PTH level
TREATMENT
• At present surgery is the only curative option .
• simple expectant treatment until the calcium level or symptoms
reach a level at which surgery becomes more attractive, low calcium
diet, withdrawal of drugs (diuretics and lithium) which aggravate
hypercalcaemia and, more recently, calcium reducing agents such as
bisphosphanates and the calcium receptor agonist cinacalcet
• Intravenous saline and bisphosphonate therapy (pamidronate) are
required to correct the dehydration and hypercalcaemia.
INDICATIONS OF SURGERY
• Urinary tract calculi
• Reduced bone density
• High serum calciuma
• All in younger age group <50 years
• Deteriorating renal function
• Symptomatic hypercalcaemia
CONSENT FOR SURGERY
• persistent hyperparathyroidism (5 per cent);
• recurrent laryngeal nerve injury (1 per cent);
• postoperative haemorrhage (1 per cent);
• permanent hypoparathyroidism;
• recurrent hyperparathyroidism
SECONDARY
HYPERPARATHYROIDISM
• Chronic renal failure results in secondary hyperparathyroidism.
• The kidney cannot convert vitamin D into the physiologically active
1,25-cholecalciferol.
• Reduced intestinal absorption of calcium resulting in a low serum
calcium and elevated phosphate due to renal failure to excrete
phosphate increases secretion of parathyroid hormone. Prolonged
stimulation results in parathyroid hyperplasia.
• Secondary hyperparathyroidism also occurs in vitamin D-deficient
rickets, malabsorption and pseudohypoparathyroidism.
PARATHYROID CARCINOMA
• Accounts for 1 per cent of cases of hyperparathyroidism.
• Typical features are very high calcium and PTH levels often with a
palpable neck swelling or occasionally lymphadenopathy.
• The diagnosis is rarely known at the time of exploration but, if
suspected, operation should include excision of the tumour mass with
en bloc thyroid lobectomy and node dissection when indicated.
• The diagnosis is difficult to make histologically and may only become
apparent when recurrent disease presents with hypercalcaemia,
increased serum PTH and evidence of local recurrence.
• Adjuvant or palliative radiotherapy may be indicated and overall
survival as in most endocrine cancers is reasonable with 85 per cent
five-year survival.
HYPOPARATHYROIDISM
• While there are rare congenital (DiGeorge) and medical (autoimmune
polyglandular and Wilson) syndromes causing hypoparathyroidism,
for practical purposes postoperative hypoparathyroidism is the
dominant management issue in surgical practice.
• This results from removal, trauma or devascularisation of the
parathyroid glands which may be deliberate but is more often
inadvertent.
SIGNS AND SYMPTOMS
• Ranges through mild circumoral and digital numbness and paraesthesia, to
tetanic symptoms with carpopedal or laryngeal spasms, cardiac arrhythmia
and fits.
• abnormal bone demineralisation, cataracts, calcification in basal ganglia and
consequent extrapyramidal disorders.
• Percussion of the facial nerve just below the zygoma causes contraction of the
ipsilateral facial muscles (Chvostek’s sign).
• Carpopedal spasm can be induced by occlusion of the arm with a blood
pressure cuff for 3 minutes (Trousseau’s sign).
• Electrocardiogram changes include prolonged QT intervals and QRS complex
changes
TREATMENT
• Acute symptomatic hypocalcaemia is a medical emergency and
requires urgent correction by intravenous injection of calcium.
Magnesium supplements may also be required.
• Oral calcium supplements (1 g three or four times daily)
supplemented by1–3 µg of 1-alpha-vitramin D if necessary should be
given with gradual withdrawal over the next 3–12 months.
• Lesser degrees of asymptomatic hypocalcaemia can be treated with
oral calcium supplements of 3–4 g calcium per day in divided doses .
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