? The development and anatomy of the thyroid
glands.
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? The physiology and investigation of thyroid
function.
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? The treatment of thyrotoxicosis and thyroidfailure.
The indications for and technique of thyroid
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surgery
? The management of thyroid cancer
Mention the causes of Thyrotoxicosis. Discuss the
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clinical features and management of primary
thyrotoxicosis.
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Classify thyroid neoplasms. Discuss the management ofsolitary thyroid nodule.
Describe how wil you proceed with the diagnosis and
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treatment of a 40 y old female with multinodular goitre.
Discuss the etiology, clinical features, diagnosis and
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treatment of MNG.Discuss the etio pathology,clinical features, diagnosis
and treatment of Grave's disease.
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Discuss the classification and clinical features of
thyroiditis.
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Discuss the etio pathology,clinical features, diagnosisand treatment of thyroid malignancies.
SHORT NOTES
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Complications of thyroid surgery.
Development of thyroid and anomalies.
Ectopic thyroid
Eye signs in Grave's disease
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Jod Basedow thyrotoxicosisMEN syndrome
Thyroglossal cyst/fistula
Thyroid storm
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CLINICAL ANATOMY
VASCULAR SUPPLY
LYMPHATIC DRAINAGE
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Most important when considering surgical treatmentof thyroid carcinoma.
Paratracheal nodes; tracheoesophageal groove lymph
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nodes; mediastinal nodes in the anterior and superior
position; jugular lymph nodes in the upper, middle,
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and lower distribution; and retropharyngeal andesophageal lymph nodes.
Laterally, cervical lymph nodes within the posterior
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triangle.
Papillary carcinoma of the thyroid is commonly
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associated with adjacent nodal metastasis.Medullary carcinoma has a strong predilection for
metastatic lymphatic involvement, usually within the
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central compartment (the space between the internal
jugular veins).
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RELATIONSThe gland is enclosed in the pretracheal fascia,
covered by the strap muscles and overlapped by the
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sternocleidomastoids.
The anterior jugular veins course over the isthmus.
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On the deep aspect of the thyroid lie the larynx andtrachea, with the pharynx and oesophagus behind and
the carotid sheath on either side.
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Two nerves lie in close relationship to the gland; in
the groove between the trachea and oesophagus lies
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the recurrent laryngeal nerve and deep to the upperpole lies the external branch of the superior laryngeal
nerve passing to the cricothyroid muscle.
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PHYSIOLOGY
IODIDE TRAPPING.
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OXIDATION to iodine by thyroid peroxidase.IODINATION of tyrosine residues to mono
and di iodotyrosine.
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COUPLING.HORMONE SYNTHESIS
PHYSIOLOGY
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TRH secreted by hypothalamus.
Stimulates TSH secreted by ant pituitary.
Stimulates the thyroid gland to synthesise
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T3 and T4.T3 and T4 have negative feedback inhibition
on TSH and TRH.
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PHYSIOLOGY
The thyroid hormones secreted by the gland
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are in bound form and free form.Free form is biologically active.
The hormones once liberated are bound to
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serum proteins- name?T3 has a rapid onset of action and a much
shorter half life than T4.
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Thyroid hormone synthesis is inhibited by?
CONGENITAL DISEASES
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DEVELOPMENT
The thyroid develops
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from a bud whichpushes out from the
floor of the pharynx
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and then descends to
its definitive position
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in the neck.THYROGLOSSAL CYST
LINGUAL THYROID
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Occurs as a failure of normal descent of the thyroidPresents as a lump in the foramen caecum or in the front
of the neck near the body of the hyoid bone.
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In all cases of unexplained nodules in the line of thyroid
descent, a radio-iodine scan should be performed to
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ensure that there is normal thyroid tissue in the correctplace before the lump is removed.
Enlargement of a lingual thyroid can cause airway
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obstruction, dysphagia, or bleeding.
Most lingual thyroid glands can be suppressed with
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thyroid hormone administration.In resistant lingual thyroids, radioactive iodine treatment
may be given.
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ECTOPIC THYROID TISSUECan be found in the central compartment of the
neck, under the lower poles of normal thyroid or in
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the anterior mediastinum.
Lateral aberrant thyroid
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PENDRED'S SYNDROMEA rare autosomal recessive condition
characterised by incomplete oxidation of
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trapped iodide prior to organification.
Associated with sensorineural deafness,
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mild primary hypothyroidism with a non-toxicdiffuse goitre.
It may be confirmed by a positive
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perchlorate discharge test.
TESTS OF THYROID FUNCTION
EVALUATION OF PITUITARY- THYROID
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FEEDBACK LOOP1)Serum TSH assay
2)TRH stimulation test
SERUM T3 AND T4 LEVELS
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Only a small fraction of the total (0.03% of
T4 and 0.3% of T3) is free.
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Assays of total hormones are now obsolete.Estimation of free T3 and free T4.
T3 resin uptake test
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THYROID AUTOANTIBODIESTPO antibodies
Anti thyroglobulin antibodies
Antimicrosomal antibodies
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THYROID IMAGING
1) Chest X-Ray.
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THYROID IMAGINGUSG
Helps in determining
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the nature of swelling.USG guided FNAC.
Helps in detecting
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MetastaticLNs.Followup.
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THYROID IMAGINGCT scan
To know the extent of
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malignancy andreterosternal extension.
THYROID SCINTIGRAPHY
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Provide information about thyroid activity , the size and
extent of the gland.
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Helpful in showing retrosternal extension.Material used is Tc 99m, I123,I131.
Cold nodule: 80% benign,20% malignant.
Hot nodule: 5-9% malignant.
Warm nodule: take up the same radioactivity as rest of
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the gland.
The principal benefits of isotope scanning are in
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confirming the presence of a `hot/toxic' nodule in thethyroid gland in a thyrotoxic patient, and in identifying
metastases or residual local disease after total
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thyroidectomy for carcinoma.
THYROID SCINTIGRAPHY
A hot nodule is one that takes up isotope while the
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surrounding thyroid tissue does not.
Here, the surrounding thyroid tissue is inactive
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because the nodule is producing such high levels ofthyroid hormones that TSH secretion is suppressed.
A warm nodule takes up isotope, as does the
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normal thyroid tissue around it.
A cold nodule does not take up isotope
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FNACIOC for discrete thyroid swellings.
Thy1- Non-diagnostic
Thy2- Non-neoplastic
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Thy3 -FollicularThy4 -Suspicious of malignancy
Thy5- Malignant
MISCELLANEOUS
Serum calcitonin
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Serum thyroglobulin-concentrations > 50g/l indicateprobable residual or recurrent tumour.
Concentrations >100 g/l strongly suggest the
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presence of pulmonary or skeletal metastases.
Flow cytometry for identifying diploid tumours, which
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have a good prognosis, and aneuploid tumours,which have a poor prognosis.
CLINICAL FEATURES
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There are two broad categories of symptoms :those occurring as a result of the enlargement of
the gland itself and those related to its disordered
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endocrine activity.
The history will establish whether one or both
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classes of symptoms are present, and examinationthen aims to elicit the relevant physical signs.
NECK SYMPTOMS
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A lump in the neck
Discomfort on swallowing
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DyspnoeaHoarseness
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HYPOTHYROIDISM
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ADULT (MYXEDEMA)
? Hypothyroidism in adults THs.
? Could be:
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1ry hypothyroidism ... (diseases is in the gland)
- autoimmune disease such as "Hashimoto's thyroiditis".
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- lack of iodine.- absence of deiodination enzyme.
T3 & T4 reflex TSH.
2ry hypothyroidism ... (disease is higher up)
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TRH TSH T3 & T4.
? Follicular cells become less active.
HYPOTHYROIDISM
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Autoimmune thyroiditis (chronic lymphocyticthyroiditis)
Non-goitrous: Primary myxoedema
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Goitrous: Hashimoto's diseaseIatrogenic
After thyroidectomy
After radioiodine therapy
Drug induced (anti-thyroid drugs, para-aminosalicylic
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acid,Amiodarone,Cytokines and iodides in excess)
Dyshormonogenesis
Goitrogens
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Secondary to pituitary or hypothalamic diseaseThyroid agenesis
Endemic cretinism---- due to iodine deficiency
CRETENISM
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Inadequate thyroid hormone production during fetaland neonatal development.
2 types- Endemic and Sporadic
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A hoarse cry, macroglossia and umbilical hernia ina neonate with features of thyroid failure suggests
the diagnosis.
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Tt is by thyroxine.
ADULT HYPOTHYROIDISM
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The symptoms are:The signs are:
? tiredness;
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? bradycardia;
? mental lethargy;
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? cold extremities;? cold intolerance;
? dry skin and hair;
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? weight gain;
? periorbital puffiness;
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? constipation;? hoarse voice;
? menstrual disturbance;
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? bradykinesis, slow
? carpal tunnel syndrome
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movements;? delayed relaxation
phase of ankle jerks
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MYXEDEMA
The signs and symptoms
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of hypothyroidism are
accentuated.
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The facial appearance istypical-supraclavicular
puffiness, a malar flush
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and a yellow tinge to the
skin.
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Myxoedema coma,characterised by altered
mental state, hypothermia
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and a precipitating
medical condition, for
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example cardiac failure orinfection.
DIAGNOSIS AND TREATMENT
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Low T4 and T3 levels with a high TSH.
What will happen in Pituitary failure?
High serum levels of TPO antibodies are
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characteristic of autoimmune disease.Treatment-
Oral thyroxine (0.10?0.20 mg) as a single daily
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dose.THYROTOXICOSIS
Describe the causes
Discuss the pros and cons of the three major treatment
options
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Know how to prepare a patient for operationDescribe appropriate surgical procedures
Know about early and late postoperative management
THYROTOXICOSIS
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THYROTOXICOSIS v/s HYPERTHYROIDISM?
Hyperthyroidism is a condition in which the thyroid
gland producesand secretes excessive amounts of
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the free thyroid hormones.
Thyrotoxicosis
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hypermetabolic clinical syndrome which occurswhen there are elevated serum levels of T3 and/or
T4.
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Thyrotoxicosis can also occur without
hyperthyroidism.
THYROTOXICOSIS
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Clinical types are:
? diffuse toxic goitre (Graves' disease);
? toxic nodular goitre;
? toxic nodule;
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? hyperthyroidism due to rarer causes.THYROTOXICOSIS
Diffuse toxic goitre
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Graves' disease, occurs in younger women .Associated with eye signs.
50% of patients have a family history of
autoimmune endocrine diseases.
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The whole of the functioning thyroid tissue is
involved.
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Hypertrophy and hyperplasia are due to abnormalthyroid-stimulating antibodies (TSH-RAbs)
THYROTOXICOSIS
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Toxic nodular goitreA simple nodular goitre is present for a long time
before the Hyperthyroidism.
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Middle-aged or elderly.Very infrequently associated with eye signs.
The syndrome is that of secondary thyrotoxicosis.
In many cases of toxic nodular goitre the nodules
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are inactive and it is the internodular thyroid tissuethat is overactive.
THYROTOXICOSIS
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Toxic nodule
A toxic nodule is a solitary overactive nodule, which
may be part of a generalised nodularity or a true
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toxic adenoma.
It is autonomous and its hypertrophy and
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hyperplasia are not due to TSH-RAb.TSH secretion is suppressed by the high level of
circulating thyroid hormones and the normal thyroid
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tissue surrounding the nodule is itself suppressed
and inactive.
THYROTOXICOSIS-CLINICAL FEATURES
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The symptoms are:
The signs are:
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? tiredness;? tachycardia;
? emotional lability;
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? hot, moist palms;
v ? heat intolerance;
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? exophthalmos;? weight loss;
? lid lag/retraction;
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? excessive
? agitation;
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appetite;? thyroid goitre and
? palpitations.
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bruit.
GRAVE'S OPHTHALMOPATHY
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2 clinical phases:The inflammatory stage and the fibrotic stage
The inflammatory stage is marked by edema and
deposition of glycosaminoglycan in the extraocular
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muscles. There is orbital swelling, stare, diplopia,
periorbital edema, and at times, pain.
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The fibrotic stage is a convalescent phase and mayresult in further diplopia and lid retraction. It
improves spontaneously in 64% of patients
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PRETIBIAL MYXEDEMAElevated, firm, nonpitting, localized thickening over the
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lateral aspect of the lower leg, with bilateral involvement.Milder cases do not require therapy other than treatment
of the thyrotoxicosis.
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Therapy with topical steroids applied under an occlusive
plastic dressing film for 3-10 weeks has been helpful.
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In severe cases, pulse glucocorticoid therapy may betried.
ACROPACHY
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Clubbing of fingers with osteoarthropathy,
including periosteal new bone formation, may
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occur.This almost always occurs in association with
ophthalmopathy and dermopathy.
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No therapy has been proven to be effective.
WORKUP
TSH levels usually are suppressed to immeasurable
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levels (<0.05 ?IU/mL) in thyrotoxicosis.
Subclinical hyperthyroidism is defined as a
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suppressed TSH level (<0.5 U/mL in manylaboratories) in combination with serum
concentrations of T3 and T4 that are within the
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reference range.
Thyroid autoantibodies: The most specific
autoantibody for autoimmune thyroiditis is an
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enzyme-linked immunosorbent assay (ELISA) for
anti-TPO antibody (thyroperoxidase).
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SCANNINGGraves disease is associated with diffuse enlargement
of both thyroid lobes, with an elevated uptake .
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A toxic multinodular goiter demonstrates an enlarged
thyroid with multiple nodules and areas of both
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increased and decreased isotope uptake .Subacute thyroiditis usually demonstrates very low I-123
isotope uptake.
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A toxic adenoma demonstrates a solitary hot nodule
with suppression of function in the surrounding normal
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thyroid tissue .MANAGEMENT
ANTITHYROID DRUGS
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SURGERYRADIOIODINE
ANTI THYROID DRUGS
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Carbimazole, methimazole and propylthiouracil
are most commonly used.
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Reduce the synthesis of thyroid hormones byinhibiting the iodination of tyrosine residues.
Carbimazole also has an immunosuppresive
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action.
Clinical improvement occurs within 10-14 days.
Pt is clinical y and biochemical y euthyroid by 3-
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4 wks.
Tt is continued for 12-18 months.
ANTI THYROID DRUGS
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ADVANTAGE
No surgery and no use of radioiodine.
q DISADVANTAGE
Tt is prolonged and the failure rate is atleast 50%
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Some goitres enlarge and become more vascularduring tt.
Side effects are agranulocytosis or aplastic anemia
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SURGERY
Usually done when there is a large goitre,poor drug
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compliance,recurrence.Subtotal thyroidectomy is done.
Contraindication is previous thyroid surgery.
Complications are hypothyroidism,transient
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hypocalcemia,permanent
hypoparathyroidism,recurrent laryngeal nerve palsy.
SURGERY
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ADVANTAGE
Goitre is removed.
Cure is rapid and cure rate is high.
? DISADVANTAGE
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Recurrenc occurs in 5%Every operation carries mortality and morbidity.
Post op thyroid insufficiency
RADIOIODINE
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131I is given orally as a single dose and is
trapped and organified in thyroid.
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There is alag period of 4-12 wks before it iseffective.
During this period the symptoms are
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controlled by beta blockers.
Contraindications are pregnancy,active
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graves ophthalmopathy.Complications are
hypothyroidism,malignancies of thyroid and
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gi tract.
RADIOIODINE
No surgery and prolonged drugs.
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DISADVANTAGEIsotope facilities must be available.
High incidence of hypothyroidism which may reach 75
-80% after 10 yrs.
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Indefinite follow up.
Increased risk of malignancy.
CHOICE
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1.DIFFUSE TOXIC GOITRE-Over 45-Radioiodine
Under 45-Surgery for large goitre and drugs for small
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goitre.
2.TOXIC NODULAR GOITRE-
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SURGERY.3.TOXIC NODULE-
Surgery or Radioiodine
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4.RECURRENT THYROTOXICOSIS AFTER
SURGERY-
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Over 45-Radioiodine,Under 45-Drugs.Correction of hyperthyroidism is important for the
ophthalmopathy.
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Antithyroid drugs and thyroidectomy do notinfluence the course of the ophthalmopathy,
whereas radioiodine treatment may exacerbate
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preexisting ophthalmopathy but can be prevented
by glucocorticoids.
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In the long term, thyroid ablation may be beneficialfor ophthalmopathy because of the decrease in
antigens shared by the thyroid and the orbit in the
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autoimmune reactions.
GRAVE'S OPHTAHLMOPATHY
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For mild-to-moderate ophthalmopathy, local therapeuticmeasures (eg, artificial tears and ointments, sunglasses,
eye patches, nocturnal taping of the eyes, prisms,
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elevating the head at night) can control symptoms and
signs.
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If the disease is active (1) high-dose glucocorticoids, (2)orbital radiotherapy, (3) both, or (4) orbital
decompression
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PRE OP PREPARATIONCarbimazole in the dose of 30-40mg daily for 8-
12wks is given. when euthyroid the dose is reduced
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to 5mg t.d.s.
Iodides in the form of lugol's iodine is used 2-3 wks
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prior to surgery.dose is 30 drops t.d.s.it reduces thesize and vascularity of the gland.
Propranol acts on the target organs and not on the
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gland itself. Dose is 40mgt.d.s.it inhibits the
peripheral conversion of T4 to T3.
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POSTOPERATIVE COMPLICATIONSHaemorrhage
Respiratory obstruction
Recurrent laryngeal nerve paralysis and voice
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change
Thyroid insufficiency
Parathyroid insufficiency
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Thyrotoxic crisisWound infection
Hypertrophic or keloid scar
Stitch granuloma
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GOITRE
Know how to describe thyroid swellings
Use appropriate investigations
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Know the indications for surgery
Select the appropriate procedure
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Describe and manage postoperative complicationsCLASSIFICATION OF GOITRE
Simple goitre (euthyroid)
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Diffuse hyperplastic
Physiological
Pubertal
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PregnancyMultinodular goitre
Toxic
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DiffuseGraves' disease
Multinodular
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Toxic adenomaNeoplastic
Benign
Malignant
CLASSIFICATION OF GOITRE
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Inflammatory
Autoimmune
Chronic lymphocytic thyroiditis
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Hashimoto's diseaseGranulomatous
De Quervain's thyroiditis
Fibrosing
Riedel's thyroiditis
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Infective
Acute (bacterial thyroiditis, viral thyroiditis, `subacute
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thyroiditis')Chronic (tuberculous, syphilitic)
Inflammato Hyperplasi
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Tumours
Others
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rya
Benign
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Malignant
Graves
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Multinodular FollicularPapillary Colloid cyst
Disease
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goitre
adenoma
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Hashimoto's Non-toxicFollicular
Thyroid
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thyroiditis
goitre
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lymphomaDe
Anaplastic
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Acute
Quervain's
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suppurativethyroiditis
Medullary
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SIMPLE GOITRE
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Stimulation of the thyroid gland by TSH.
The most common cause iodine deficiency.
Increased demand.
Excess iodine or lithium ingestion, which
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decrease release of thyroid hormone
Goitrogens(cassava, lima beans, maize, bamboo
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shoots, and sweet potatoes)-Inborn errors of metabolism causing defects in
biosynthesis of thyroid hormones
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- Exposure to radiation
-Thyroid hormone resistance
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Side-effects of pharmacological therapy
such as:
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Amiodarone :inhibits peripheral conversion of thyroxine to
triiodothyronine; also interferes with
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thyroid hormone action.
Phenobarbitone, phenytoin, carbamazepine,
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Rifampcin:induce metabolic degradation of T3 and T4.
? If No Iodine T3 & T4 TRH TSH
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growth (size) of the gland simple goiter.
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HOW GOITER IS FORMED?
WITH LACK OF IODINE ...
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HypothalamusCOLD
TR
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+
H
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Anteriorpituitary
TS
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+
NO or low
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HThyroi
Lack of
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feedback
iodine
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inhibitiond gland
Poo
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+++
r
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Low T3 or T4Growth of
release
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the gland
NATURAL HISTORY
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Persistant growth stimulation cause diffusehyperplasia ,all lobules are composed of
active follicles and iodine uptake is uniform
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.This is a diffuse hyperplastic goiter .
Mixed pattern develops with areas of active
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lobules and areas of inactive lobule as aresult of fluctuating stimulation.
Active lobules become more vascular &
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hyperplastic untill haemorrhage occur
causing central necrosis & leaving only a
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surrounding rind of active follices.Necrotic lobules __
form nodules filled with
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either iodine-free colloidor a mass of new but
inactive follicles.
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Continual repetition
of this process result
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in a nodular goiter.CLINICAL FEATURES
Euthyroid.
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Neck swelling which moves on swallowing.Rule out compressive symptoms.
Hardness and irregularity, due to calcification, may
simulate carcinoma.
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A painful nodule or the sudden appearance or rapid
enlargement of a nodule may be because of
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haemorrhage or carcinoma.INVESTIGATIONS
Serum TSH.
USG neck.
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Thyroid autoantibodies.Plain X-Ray neck.
FNAC.
COMPLICATIONS
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Respiratory obstruction.
Secondary Thyrotoxicosis.
Carcinoma (Follicular).
PREVENTION AND TREATMENT OF SIMPLE
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GOITREIodised salt.
INDICATIONS OF SURGERY:
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CosmesisRetrosternal extension.
Compressive symptoms.
Suspected malignancy.
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WHAT SURGERY?Total thyroidectomy
Subtotal thyroidectomy leaving up to 4 g of
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relatively normal tissue in each remnant.
Total lobectomy on the more affected side with either
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subtotal resection (Dunhill procedure) or no interventionon the less affected side.
DISCRETE THYROID SWELLING
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WHAT IS SOLITARY SWELLING OF THYROID?
WHAT IS DOMINANT SWELLING?
About 70% of discrete thyroid swellings are
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isolated and about 30% are dominant.The importance lies in the increased risk of
neoplasia compared with other thyroid swellings.
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15% of isolated swellings are malignant, 30?40%
are follicular adenomas.
CLINICALLY DISCRETE SWELLINGS
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What are the risk factors which suggest that a
discrete swelling is malignant?
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When will you suspect malignancy in a discreteswelling?
CLINICALLY DISCRETE SWELLINGS
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Causes?
Investigation?
CLINICALLY DISCRETE SWELLINGS
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INDICATIONS OF SURGERY?All proven malignant nodules.
Cytologically proven follicular adenoma.
Suspicious nodules.
Cystic nodules which recur following aspiration.
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Nodules producing obstructive symptoms.Toxic nodule.
Cosmesis.
Patient's wish.
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RETROSTERNAL GOITRERETROSTERNAL GOITRE
Arise from the lower pole of a nodular goitre.
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Short neck and strong pretracheal muscles incresasethe negative intrathoracic pressure which tends to draw
these nodules into the superior mediastinum.
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Symptomless.
Dyspnoea, particularly at night,
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Cough and stridorDysphagia.
Engorgement of facial, neck and superficial chest wall
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veins.
Obstruction of the superior vena cava
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Recurrent nerve paralysisRETROSTERNAL GOITRE
CXR
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CT Scan.
Surgery.
THYROID INCIDENTALOMA
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THYROID INCIDENTALOMA
Due to the increased use of imaging modalities for
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non-thyroid head and neck pathology.Clinically unsuspected and impalpable thyroid
swellings.
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Generates needless anxiety.
Can be safely managed expectantly by a single
annual review.
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Thyroid incidentaloma
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on US, MRI or CT scan
Greater than 1.5 cm
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radiation exposureLess than 1.5 cm
US, MRI or CT ?cancer
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US, MRI or CT scan
benign
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FH thyroid cancerUS guided
FNAC
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Observe
HASHIMOTO'S THYROIDITIS
Characterized by the destruction of thyroid cells by
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cell- and antibody-mediated immune processes.
The thyroid gland is typically goitrous.
Antithyroid peroxidase (anti-TPO), antithyroglobulin
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(anti-Tg),TSH receptor-blocking antibodies.
Inadequate thyroid hormone production and
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secretion.Initially, (T4) and (T3) may "leak" into the circulation
from damaged cells.
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10-15 times more common in females.
The most commonly affected age range is 30-50
years.
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WORKUP
TFT.
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USG.Complete blood count.
Total and fractionated lipid profile.
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WORKUPBasic metabolic panel: Glomerular filtration rate, renal
plasma flow, and renal free water clearance are all
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decreased in hypothyroidism and may result in
hyponatremia.
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Creatine kinase: Creatine kinase levels, predominantlythe MM isoenzyme from skeletal muscle and the
aldolase enzyme, are frequently elevated in severe
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hypothyroidism.
Prolactin: Prolactin may be elevated in primary
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hypothyroidismTREATMENT
The treatment of choice for Hashimoto thyroiditis is
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thyroid hormone replacement.
The drug of choice is orally administered
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levothyroxine sodium, usually for life.Indications for surgery
A large goiter with obstructive symptoms such as
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dysphagia, voice hoarseness, and stridor from extrinsic
obstruction to airflow.
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Presence of a malignant nodule, as found by cytologicexamination by fine-needle aspiration.
Presence of a lymphoma diagnosed on fine-needle
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aspiration.
Cosmetic reasons for unsightly large goiters
REIDEL'S THYROIDITIS
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A rare, chronic inflammatory disease of the thyroid
gland characterized by a dense fibrosis that
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replaces normal thyroid parenchyma.The fibrotic process invades adjacent structures of
the neck and extends beyond the thyroid capsule.
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This feature differentiates RT from other
inflammatory or fibrotic disorders of the thyroid.
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Because of the encroachment beyond the thyroidcapsule, other problems can be associated with RT,
including hypoparathyroidism, hoarseness (due to
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recurrent laryngeal involvement), and stridor (due to
tracheal compression).
PATHOPHYSIOLOGY
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The etiology of Riedel's thyroiditis (RT) is unknown.
An autoimmune process or a primary fibrotic disorder.
The following evidence supports an autoimmune
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pathogenesis for RT:The presence of antithyroid antibodies in a significant
percentage of patients with RT (67% of 178 cases
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reviewed in one study)2
The pathological features of cellular infiltration, including
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lymphocytes, plasma cells, and histiocytesThe frequent presence of focal vasculitis on pathologic
examination
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The favorable response of a subset of patients with RT
to treatment with systemic corticosteroids
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CLINICAL FEATURESHistory
Nonpainful, rapidly growing thyroid mass.
Hard, fixed, painless goiter- stony or woody.
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Most patients are euthyroid. Hypothyroidism isnoted in approximately 30% of cases.
Local compressive symptoms.
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Hypoparathyroidism.Clinical features closely resemble those of
anaplastic carcinoma of the thyroid.
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One distinguishing feature of RT is the absence ofassociated cervical adenopathy.
CLINICAL FEATURES
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Approximately one third of patients with RT have anassociated extracervical manifestation of multifocal
fibrosclerosis (eg, retroperitoneal fibrosis,
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mediastinal fibrosis, orbital pseudotumor,
pulmonary fibrosis, sclerosing cholangitis, lacrimal
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gland fibrosis, fibrosing parotitis).MANAGEMENT
ROUTINE TESTS.
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FNAC,BIOPSY.
SURGERY.
DEQUAIRVEIN'S
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THYROIDITIS
Most common cause of a painful thyroid gland.
Pain in the region of the thyroid, which is usually
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diffusely tender with systemic symptoms.
Hyperthyroidism occurs initially, sometimes
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followed by transient hypothyroidism.Complete recovery in weeks to months is
characteristic.
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PATHOPHYSIOLOGYA viral infection like coxsackievirus, Ebstein-Barr,
mumps, measles, adenovirus, echovirus, and
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influenza.
A strong association exists with human leukocyte
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antigen (HLA)-B35.EPIDEMIOLOGY
Sex
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Female-to-male ratio of 3-5:1.
Age
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A peak incidence in the fourth and fifth decadesof life
HISTORY
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HistoryFlulike prodromal episode 1-3 weeks prior to the onset of
clinical disease. The natural course of the disease can
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be divided into the following 4 phases that usually unfoldover a period of 3-6 months:
The acute phase, lasting 3-6 weeks, presents primarily
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with pain. Symptoms of hyperthyroidism also may be
present.
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The transient asymptomatic and euthyroid phase lasts 1-3 weeks.
The hypothyroid phase lasts from weeks to months, and
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it may become permanent in 5-15% of patients.
The recovery phase is characterized by normalization of
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thyroid structure and function.S|S
Local symptoms
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Pain over the thyroid that radiates to the neck, ear, jaw,
throat, or occiput; and is aggravated by swallowing and
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head movement;pain is the presenting symptom in over 90% of cases
Dysphagia
Hoarseness (uncommon)
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Constitutional symptoms (often absent)
S|S
Symptoms of hyperthyroidism (palpitations,
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tremulousness, heat intolerance, sweating,
nervousness) occurring in the initial phase of the
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diseaseHyperthyroidism that usually is mild and rarely is severe
Transient symptoms, usually lasting 3-6 weeks
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Symptoms of hypothyroidism, occurring in the latephase of the disease
Mostly mild or moderate
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Hypothyroidism lasts weeks to months
WORKUP
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Usually, the diagnosis is made on clinical grounds,and the only laboratory studies needed initially are
those to determine whether hyperthyroidism is
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present, including TSH and free T4.
If any doubt exists as to whether de Quervain
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thyroiditis is the correct diagnosis, 2 other tests maybe helpful.
Serum thyroglobulin is almost always markedly elevated.
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Erythrocyte sedimentation rate (ESR) is usually higherthan 50 mm/h in the initial phase
WORKUP
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After the initial inflammatory phase subsides, TSHshould be monitored at intervals of 4-6 weeks for a
few months to determine whether hypothyroidism
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occurs.
Antibodies to TGB, thyroid peroxidase, and TSH
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receptor are usually absent in de Quervainthyroiditis.
In rare cases with systemic multiorgan involvement,
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elevation of serum alkaline phosphatase, gamma-
glutamyl transpeptidase, aminotransferases, and
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pancreatic enzymes may occur. Glucoseintolerance has been reported.
TT.
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Management is directed towards 2 problems--pain
and thyroid dysfunction.
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PainSome patients with mild pain require no treatment.
Nonsteroidal anti-inflammatory drugs (NSAIDs), are
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used.
If pain does not respond within 3 days, the diagnosis
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should be reconsidered.TT.
Management of thyroid dysfunction
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In the initial phase of de Quervain thyroiditis,symptomatic hyperthyroidism can be treated with beta-
blockade (propranolol 10-20 mg qid or atenolol 25-50
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mg/d).
If hypothyroidism occurs during the late phase, it is
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usually mild and transient. If symptoms are presentor TSH is elevated, the patient needs replacement
therapy with levothyroxine
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THYROID NEOPLASMS
THYROID NEOPLASMS
A.BENIGN
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a.Follicular adenoma.b.Hurthle cell adenoma.
c.Colloid adenoma.
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d.Papillary adenoma.
B.MALIGNANT(Dunhill classification)
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a.Differentiated1.Papillary CA(60%)
2.Follicular CA(17%)
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3.Papillofollicular CA
4.Hurthle cell CA
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b.Undifferentiated1.Anaplastic CA(13%)
C.Medullary CA(6%)
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D.Malignant lymphoma(4%)
E.Secondaries.
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ETIOLOGYRadiation exposure.
MNG.
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Genetic.
Hashimoto's thyroiditis.
PAPILLARY CA
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Most common cancer of thyroid.
Common in females and young age group.
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Woolner classification includesi)occult primary
ii)intrathyroidal.
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iii)extrathyroidal
PAPILLARY CA
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PATHOLOGYGrossly it can be soft,firm,solid or cystic.
Microscopically it contains cystic spaces with
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papillary projections with psammoma
bodies,malignant cells with orphan annie eye
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nuclei.PAPILLARY CA
SPREAD
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Slowly progressive tumor.Multicentric.
Spread is via lymphatics.
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PAPILLARY CA
Treatment-----
Total thyroidectomy.
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Suppressive dose of L-thyroxine.Neck dissection if LNs are positive.
PROGNOSIS is good.
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PAPILLARY CAAMES SCORING-
A-Age less than 40.
M-mets
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E-extent of primary tumorS-size less than 4cm has agood prognosis
AGES SCORING-
A-age
G-grade
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E-extentS-size
FOLLICULAR CA
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Can occur de novo or in a multinodular goitre.More aggressive tumor.
Spreads mainly by blood.
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Bone secondaries are typically vascular,warm
and pulsatile.
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FNAC is inconclusive.Tt. Is total thyroidectomy.
ANAPLASTIC CA
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Occurs in elderly.Very aggressive tumor of short duration.
Stridor and hoarseness of voice.
Dysphagia.
Fixity to skin.
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FNAC is diagnostic.Tracheostomy and isthmectomy to relieve
obstruction.
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Radiotherapy is tt.Very poor prognosis.
MEDULLARY CA
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Arises from parafollicular c cells whichare derived from ultimobranchial body.
Contains characterstic amyloid stroma.
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Calcitonin is a useful tumor marker.Tumor also secretes 5 HT,PGs,ACTH,and
VIP
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Spreads mainly via lymphatics.Can be sporadic,associated withMENII
syndrome or familial.
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Tt. Is total thyroidectomy.A 30 years old female pregnant in her 14 weeks
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developed tremors,insomnia, intolerance to hot weather and loss of
weight. On examination
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she had tachycardia and wide pulse pressure.
a. What is the possible diagnosis
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b. How would you investigate itc. Management of the condition in view of her
pregnancy
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A 35 year old housewife is suffering from TNG.She has been advised a radioiodine scan.
Which other radionuclide scans are available?
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Write two merits and two demerits of radioiodine
scan.
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