Goitre: Dr. Sandhya Gupta Assistant Professor General Surgery
Goitre: Dr. Sandhya Gupta Assistant Professor General Surgery
Goitre: Dr. Sandhya Gupta Assistant Professor General Surgery
Toxic
Fibrosing
Diffuse (Graves’ disease)
Riedel’s thyroiditis
Multinodular
Toxic adenoma
Infective
Acute (bacterial thyroiditis,
Neoplastic
Benign viral thyroiditis, subacute thyroiditis)
Malignant Chronic (tubercular, syphilitic)
Other
Causes
Iodine deficiency
Dyshormonogenesis
Goitrogens
Iodine deficiency
Syndrome
Goitrogens
• Well-known goitrogens are the vegetables of the brassica
family (cabbage, kale and rape), which contain thiocyanate,
• Drugs such as para-aminosalicylic acid (PAS) and the
anti-thyroid drugs.
• Thiocyanates and perchlorates interfere with iodide
trapping
• Whereas carbimazole and thiouracil compounds interfere
with the oxidation of iodide and the binding of iodine to
tyrosine.
Pathogenesis
Diffuse hyperplasia of all lobules composed of active
follicles and uniform iodine uptake
Fluctuating stimulation..
Areas of active and inactive lobules
• Asymptomatic
• Pain
• Hypothyroidism
• Hyperthyroidism
• Pressure symptoms
Diffuse hyperplastic goitre
• Diffuse hyperplasia corresponds to the first stages of the
natural history.
• The goitre appears in childhood in endemic areas but,
in sporadic cases, it usually occurs at puberty when
metabolic demands are high.
• If TSH stimulation ceases the goitre may regress;
however, it tends to recur later at times of stress such as
pregnancy. The goitre is soft, diffuse and may become
large enough to cause discomfort.
• A colloid goitre is a late stage of diffuse hyperplasia
when TSH stimulation has fallen off and when many
follicles are inactive and full of colloid.
Multinodular Goitre
• Pathophysiology:
1. Stage of hyperplasia and hypertrophy
Exopthalmos/proptosis
Staring appearance
Chemosis/ periorbital swelling/ conjuctivitis
Graves’ dermopathy
• Glycoaminoglycans/lymphoid infiltration skin-
thickened/rough texture
• Pre tibial/dorsum of foot elephantiasis-rare
associated with high levels of TSI/opthalmopathy
Thyroid acropachy/ clubbing
• Presents with clubbing & swelling of fingers and
toes.
• Periosteal reaction of extremity bones
• Most are smokers!
• Strongly associated with thyroid dermopathy, so that an
alternative cause of clubbing should be sought in
Graves patient without coincident skin and orbital
involvement.
• Onycholysis/Plummer’s nails
Thyroid acropachy/ clubbing
Diagnosis
• Thyroid function
lab test.
s • Auto antibodies.
• Iodine
imagin uptake.
g • Thyroid USS.
• TFT-TSH/FT4 FT3
• Second generation Anti TSH ab ->95% sensitivity & specificity
for diagnosis
• Anti TBG ab/ Anti TPO ab found in up to 80% of
Graves’ disease (also 15 % healthy women & 5% of men)
• Thyroid scintiscanning with Tc 99 /I 131 in doubt about the
nature of the goiter or thyrotoxicosis without hyperthyroidism
is suspected.
• ANA/ds DNA levels are elevated without evidence
of SLE or other ARD’s.
Thyroid scintigraphy
Thyroid scanning
• The thyroid gland is diffusely enlarged, and often
homogeneous.
• Parenchymal hypervascularity is observed.
• Goiter size is variable.
Management
Toxic MNG
• A hyperfunctioning nodule may within a long
standing goitre.
• Aka Plummer Syndrome
Solitary thyroid nodule
Clinical features
SECONDARY THYROTOXICOSIS
PRESSURE SYMPTOMS
CARCINOMA ( follicular)
Risk of malignancy: rule of 12
Investigation
Thy2 Non-neoplastic
Thy3 Follicular
Thy5 Malignant
AUTOANTIBODY • Hashimotos
TITRE • Chronic lymphocytic thyroiditis
• Toxicity+ Nodularity
ISOTOPE SCAN
• Hot, warm, cold nodule
Pathogenesis:
• Genetic basis: more often with HLA-DR3 & HLA-DR5 alleles &
several non-HLA genes
Hashimoto’s thyroiditis
Gross
Microscopy
•Parenchyma shows widespread mononuclear inflammatory
infiltrate and germinal centers