Download Thyroid 3

CLASS 16
03/11/2015
SOLITARY THYROID NODULE
 It is a single palpable nodule in thyroid on clinical examination, in
an otherwise normal gland.
Causes
1. Thyroid adenomas
a. Follicular – colloid (commonest); embryonal; fetal.
b. Hurthle cell.
2. Papillary carcinoma of thyroid.
3. Only one nodule may be clinically palpable in an underlying
multinodular goitre.
4. Thyroid cyst.
Types
1. Toxic solitary nodule.
2. Nontoxic solitary nodule.
 Based on radioisotope study:
• Hot—Means autonomous toxic nodule.
• Warm—Normally functioning nodule.
• Cold—Nonfunctioning nodule; may be malignant
THYROTOXICOSIS AND HYPERTHYROIDISM
 It is symptom complex due to raised levels of thyroid hormones.
 Types
1. Diffuse toxic goitre—(Graves’ disease, Basedow’s disease. Primary
thyrotoxicosis).
2. Toxic multinodular goitre (Secondary thyrotoxicosis) (Plummer
disease).
3. Toxic nodule.
4. Hyperthyroidism due to rarer causes:
a. Thyrotoxicosis factitia—drug induced. Due to intake of L-thyroxine
more than normal.
b. Jod Basedow thyrotoxicosis—because of large doses of iodides
given to a hyperplastic endemic goitre.
c. Autoimmune thyroiditis or de Quervain’s thyroiditis.
d. Occasionally carcinoma thyroid.
e. Neonatal thyrotoxicosis. It subsides in 3-4 weeks as TsAb titres fall
in the baby’s serum.
f. Struma ovarii.
g. Drugs like amiodarone – an antiarrhythmic agent. [Wolf-Chaikoff
effect—Iodides inhibit the further release of hormone causing
hypothyroidism (Hokkaido goitre).]
 Grave’s disease is an autoimmune disease with increased levels
of specific antibodies in the blood (TSH receptor antibodies).
 It is often associated with vitiligo.
 It is often familial.
 Thyroid stimulating immunoglobulins (TSI)/thyroid stimulating
antibodies (Ts Ab) and long acting thyroid stimulator (LATS) cause
pathological changes in the thyroid.
 Tissues are highly vascular. Exophthalmos producing substance
(EPS) causes Grave’s ophthalmopathy.
Clinical Features
 It is eight times more common in females.
 Occurs in any age group.
 Primary type is seen commonly in younger age group.
 Secondary is common in older age group.
 Often presents without any obvious thyroid swelling in the neck.
Symptoms of Hyperthyroidism
 Gastrointestinal system
• Weight loss in spite of increased appetite.
• Diarrhoea (due to increased activity at ganglionic level).
 Cardiovascular system
• Palpitations.
• Shortness of breath at rest or on minimal exertion.
• Angina.
• Cardiac irregularity.
• Cardiac failure in the elderly (CCF).
 Neuromuscular system
• Undue fatigue and muscle weakness.
• Tremor.
 Skeletal system
• Increase in linear growth in children.
 Genitourinary system
• Oligo- or amenorrhoea.
• Occasional urinary frequency.
 Skin
• Hair loss.
• Pruritus.
• Palmar erythema.
 Psychiatry
• Irritability.
• Nervousness.
• Insomnia.
 Sympathetic overactivity causes dyspnoea, palpitation, tiredness,
heat intolerance, sweating, nervousness, increased appetite and
decrease in weight.
 Because of the increased catabolism they have increased
appetite.
 Decreased weight and so also increased creatinine level which
signifies myopathy.
 Fine tremor is due to diffuse irritability of grey matter.
 Thrill is felt in the upper pole of the thyroid and also bruit on
auscultation.
Signs of Hyperthyroidism
A.Eye signs
 Eye signs are common in primary thyrotoxicosis. Lid lag, lid spasm
can occur in secondary thyrotoxicosis also.
1. Von Graefe’s sign: (Lid Lag’s sign): It is inability of the upper eyelid
to keep pace with the eyeball when it looks downwards to follow the
examiners finger.
2. Dalrympte’s sign: Upper eye lid retraction, so visibility of upper
sclera.
3. Stellwag’s sign: Absence of normal blinking—so starring look. First
sign to appear.
4. Joffroy’s sign: Absence of wrinkling on forehead when patient looks
up (frowns).
5. Moebius sign: Lack of convergence of eye ball.
 Defective convergence is due to lymphocytic infiltration of inferior
oblique and rectus muscles in case of primary thyrotoxicosis.
 There will be diplopia.
 It may be an early sign of eventual ophthalmoplegia.
6. Jellinek’s sign: Increased pigmentation of eyelid margins.
7. Enroth sign: Oedema of eyelids and conjunctiva.
8. Rosenbach’s sign: Tremor of closed eyelids.
9. Gifford’s sign: Difficulty in everting upper eyelid in primary toxic
thyroid.
Differentiates from exophthalmos of other causes.
10. Loewi’s sign: Dilatation of pupil with weak adrenaline solution.
11. Knie’s sign: Unequal pupillary dilatation.
12. Cowen’s sign: Jerky pupillary contraction to consensual light.
13. Kocher’s sign: When clinician places his hands on patient’s eyes
and lifts it higher, patient’s upper lid springs up more quickly than
eyebrows.
14. Naffziger’s sign: With patient in sitting position and neck fully
extended, protruded eye ball can be visualized when observed from
behind.
INVESTIGATIONS
 Thyroid function tests
 Serum T3 and T4 levels are very high. TSH is very low or
undetectable.
 Radioisotope study by I131
 TRH estimation.
 ECG—To look for cardiac involvement.
 Total count and neutrophil count
 Thyroid antibodies estimation.
TREATMENT
1. Antithyroid drugs
2. Surgery
3. Radio-iodine therapy
1. ANTITHYROID DRUGS:
a. Carbimazole
b. Methimazole
c. Propyl thiouracil
Others
 Propranolol
 Lugol’s Iodine
2. SURGERY:
1. Failure of drug treatment in primary thyrotoxicosis in young patients
2. Autonomous toxic nodule
3. Nodular toxic goitre
4. When malignancy cannot be ruled out
3. RADIOIODINE THERAPY:
 Indications:
1. Primary thyrotoxicosis after 45 years of age
2. In autonomous toxic nodule
3. In recurrent thyrotoxicosis
 Usual dose is 5 to 10 millicurie, or 160 microcurie/gm of thyroid.
THYROID NEOPLASMS
 Aetiology of Thyroid Malignancy
1.Radiation either external or radioiodine can cause papillary
carcinoma thyroid.
2. Pre-existing multinodular goitre.
3. Medullary carcinoma thyroid is often familial.
4. Hashimoto’s thyroiditis may predispose to NHL/ papillary
carcinoma of thyroid.
5. Familial.
PAPILLARY CARCINOMA
 It is 60% common.
 Common in females and younger age group.
Aetiology
 Radiation either external or radioactive iodine therapy.
 TSH levels in the blood of these patients are high and so it is
called as hormone dependent tumour.
Spread
 It is a slowly progressive and less aggressive tumour.
 It is commonly multicentric.
 It spreads within the gland through intrathyroidal lymphatics to
other lobe, comes out of the capsule and spreads to cervical
lymph nodes.
 Usually there is no blood spread.
 Extrathyroidal disease – invasion into thyroid capsule can cause
blood born secondaries occasionally.
Treatment
 Total thyroidectomy.
 MRND (modified radical neck dissection) type III is required if
lymph nodes are involved.
AMES scoring
AGES scoring
MACIS scoring system
FOLLICULAR CARCINOMA
 It is 17% common.
 It is common in females.
 It can occur either de novo or in a pre-existing multinodular goitre.
 Types
a. Noninvasive—Blood spread not common.
b. Invasive—Blood spread common.
 Typical features: Capsular invasion and angioinvasion.
Spread
 It is a more aggressive tumour.
 It spreads mainly through blood into the bones, lungs, liver.
 Bone secondaries are typically vascular, warm, pulsatile, localised,
commonly in skull, long bones, ribs.
 It can also spread to lymph nodes in the neck occasionally (10%).
Investigations
 FNAC is inconclusive.
 Frozen section biopsy is very useful.
 U/S abdomen, chest X-ray.
 X-ray of skull and long bone.
Treatment
 Total thyroidectomy.
 Maintenance dose of L-Thyroxine 0.1 mg O.D or T3 80 μg/day is
given lifelong.
ANAPLASTIC CARCINOMA
 It occurs in elderly.
 It is a very aggressive tumour of short duration, presents with a
swelling in thyroid region which is rapidly progressive causing—
i. Stridor and hoarseness of voice due to tracheal obstruction.
ii. Dysphagia.
iii. Fixity to the skin.
iv. Positive Berry’s sign—involvement of carotid sheath leads to
absence of carotid pulsation.
 Swelling is hard, with involvement of isthmus and lateral lobes.
 FNAC is diagnostic.
 Tracheostomy and isthmectomy has got a role to relieve
respiratory obstruction temporarily.
 Treatment is external radiotherapy, as usually thyroidectomy is not
possible.
 Adriamycin as chemotherapy.
 However prognosis is poor.
MEDULLARY CARCINOMA OF THYROID
(MCT)
 It is uncommon (5%) type of thyroid malignancy.
 It arises from the parafollicular ‘C’ cells which is derived from the
ultimobronchial body (neural crest).
 C cells are more in upper pole of the thyroid gland.
 It contains characteristic ‘amyloid stroma’ wherein malignant cells
are dispersed.
 Immunohistochemistry reveals calcitonin in amyloid.
 In these patients blood levels of calcitonin both basal as well as
that following calcium or pentagastrin stimulation is high, a very
useful tumour marker.
 Tumour also secretes 5-H.T. (serotonin), prostaglandin, ACTH and
vasoactive intestinal polypeptide (VIP).
 It spreads mainly to lymph nodes (60%).
 It may be associated with MEN II syndrome and
pheochromocytoma with hypertension. MCT associated with MEN
type II B with phaeochromocytoma (Sipple’s disease) is most
aggressive.
 There may be mucosal neuromas in lips, oral cavity, tongue,
eyelids with marfanoid features.
 MCT is not TSH dependent and does not take up radioactive
iodine.
Clinical Features
 Thyroid swelling often with enlargement of neck lymph node.
 Diarrhoea, flushing (30%).
 Hypertension, phaeochromocytomas and mucosal neuromas
when associated with MEN II syndrome.
 Sporadic and familial types occur in adulthood whereas cases
associated with MEN syndrome II occur in younger age groups.
Types
1. Sporadic. Usualy solitary – 70%.
2. MCT with MEN II syndrome.
3. Familial MCT (20%). Commonly multicentric, autosomal dominant
in chromosome no. 10.
Investigations
 FNAC: shows amyloid deposition with dispersed malignant cells
and “C” cell hyperplasia.
 Tumour marker: Calcitonin level will be higher.
 Increased levels of calcitonin after injection of calcium 2 mg/kg or
pentagastrin 0.5 μg/kg.
 U/S abdomen.
 U/S neck to see neck nodes. CT neck and chest is preferred
method to identify neck and mediastinal nodes.
 Urinary VMA, urinary catecholamines, urinary metanephrine,
serum calcium, serum parathormone estimation.
 111 Indium octreotide scanning is useful in detecting medullary
carcinoma thyroid (70% sensitivity).
 It is also useful in postoperative follow up to find out
residual/metastatic disease.
Treatment
 Surgery is the main therapeutic modality.
 Total thyroidectomy with central node dissection in all patients
even if there are no nodes in the neck.
 + maintenance dose of L-thyroxin.
 Later regular U/S neck is done to detect early neck nodes.
 External beam radiotherapy for residual tumour disease.
 Somatostatin/octreotide
 Adriamycin
 Phaeochromocytoma -- adrenalectomy first and later only total
thyroidectomy is done.
 All family members of the patient should be evaluated for serum
calcitonin and if it is high they should undergo prophylactic total
thyroidectomy.
 MEN II A and familial MCT types, prophylactic total thyroidectomy
is done at the age of 5 years.
 MEN II B, prophylactic total thyroidectomy is done at the age of
one year.
 MCT with associated parathyroid hyperplasia (30%) in MEN IIA,
total thyroidectomy with central nodal dissection with total
parathyroidectomy and autotransplantation of half of gland.
Prognosis
 Sporadic MCT and MCT with MEN II are aggressive.
 Familial MCT not associated with MEN II has got better prognosis.
HASHIMOTO’S THYROIDITIS
Struma lymphomatosa/diffuse non-goitrous thyroiditis
 Autoimmune thyroiditis—common in women- 15 times more
common.
 Hyperplasia initially, then fibrosis, eventually infiltration with
plasma cells and lymphocytic cells.
 Askanazy cells are typical (like Hurthle cells).
Features
 Painful, diffuse, enlargement of usually both lobes of thyroid which
is firm, rubbery, tender and smooth
 Initially they present with toxic features but later, they manifest with
features of hypothyroidism.
 Hyperplasia → Hyperthyroid – Hashitoxicosis → Euthyroid--Fibrosis → Hypothyroid.
 There may be hepatosplenomegaly
Treatment
1. L-thyroxine therapy.
2. Steroid therapy often is helpful.
3. If goitre is large and causing discomfort, then subtotal
thyroidectomy is done.
DE-QUERVAIN’S SUBACUTE
 GRANULOMATOUS THYROIDITIS
 Viral aetiology either mumps or coxsackie
Clinical Features
 Painful diffuse swelling in thyroid which is tender
 Commonly seen in females.
 Initially there is transient hyperthyroidism with high T3 and T4 but
poor radioiodine uptake.
 FNAC
 It is usually a self limiting disease.
 Prednisolone 20 mg for 7 days helps
RIEDEL’S THYROIDITIS
 0.5% common
 Thyroid tissue is replaced by fibrous tissue which interestingly
infiltrates the capsule into surrounding muscles, paratracheal
tissues, carotid sheath.
 It is often associated with retroperitoneal and mediastinal fibrosis
and sclerosing cholangitis.
Clinical Features
 Hard, fixed, swelling with stridor, often Berry’s sign may be
positive.
Investigations
 T3, T4 may be low due to hypothyroidism.
 Radioisotope scan will not show any uptake.
 FNAC to rule out carcinoma.
Treatment
 Isthmectomy is done to relieve compression on the airway.
 L-thyroxine replacement
 High dose of steroid often used.
 Thyroidectomy is not necessary.
Complications of Thyroidectomy
1. Haemorrhage:
2. Respiratory obstruction: It may be due to haematoma or due to
laryngeal oedema, or due to tracheomalacia or bilateral RLN palsy.
3. Recurrent laryngeal nerve palsy:
4. Hypoparathyroidism is rare 0.5% common.
5. Thyrotoxic crisis (Thyroid storm):
6. Injury to external laryngeal nerve.
7. Hypothyroidism:
8. Wound infection, stitch granuloma formation.
9. Keloid formation.