GOITRE

Dr. Sandhya Gupta

Assistant Professor General Surgery
 Definition

The normal thyroid gland is

impalpable. The term goitre
(from the Latin guttur = the
throat) is used to describe
generalised enlargement of
the thyroid gland.
 Classification
Inflammatory
Simple goitre (euthyroid) Autoimmune
Diffuse hyperplastic Chronic lymphocytic thyroiditis
• Physiological Hashimoto’s disease
• Pubertal
• Pregnancy Granulomatous
Multinodular goitre De Quervain’s thyroiditis

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

• The daily requirement for iodine is about 0.1–0.15 mg. In

nearly all districts where simple goitre is endemic there is
a very low iodide content in the water and food.
• Endemic areas are found in the mountainous ranges,
such as the Rocky Mountains, the Alps, the Andes and
the Himalayas.
 Dyshormonogenesis

Enzyme deficiencies of varying severity may be responsible for many

congenital goitres. Genetic defects observed:

• Failure to concentrate iodide

• Defective organification of iodide due to an abnormality in the thyroid peroxidase

enzyme or in the hydrogen peroxide–generating system

• Defective thyroglobulin synthesis or transport

• Abnormal iodotyrosine deiodinase activity

Genes Responsible: TTF-1, FOXE 1, and PAX-8

Syndromes Associated: Pendred syndrome, Mc Cune Albright

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

Active lobules more vascular

and hyperplastic
 Cont..
Haemorrhage causes cental necrosis leaving a
rind of active follicles

Necrotic lobules coalesce form nodules filled with

colloid or inactive follicles

Most nodules inactive. Active follicles only in

internodular tissue.
 Clinical presentation

• 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

2. Stage of fluctuation in TSH

3. Stage of formation of nodules(inactive)

 Clinical features of MNG

• Common in middle aged women

• Slowly progressive disease with many years of
history
• Multiple nodules of different sizes are formed in both lobes,
also in isthmus, which is firm, non tender, nodular, moves
with deglutition
• Recent increase in size signifies malignant
transformation or haemorhage
Toxic thyroid
 Thyrotoxicosis/ Hyperthyroidism
• Thyrotoxicosis is a syndrome with excess FT4 & FT3.
• Hyperthyroidism indicates thyroid gland over activity
resulting in thyrotoxicosis.
• Thyrotoxicosis can result without hyperthyroidism
when stored hormone is released from damaged
thyroid.(subacute thyroiditis/ excess thyroid hormone
ect..)
 Thyrotoxicosis Causes

Primary Thyrotoxicosis without Secondary

hyperthyoridism hyperthyroidism hyperthyroidism
 Primary Hyperthyroidism
• Graves disease (commonest cause 70-80%)
• Toxic multinodular goitre
• Toxic adenoma
• Functioning thyroid metastasis
• Struma ovarii-ectopic thyroid tissue
• Activating mutation of TSH receptor
• Activating mutation of Gsa (McCune-Albright
syndrome)
• Drugs: iodine excess (Jod-Basedow phenomenon)
 Secondary Hyperthyroidism
• TSH-secreting pituitary adenoma/TSHoma
• Thyroid hormone resistance syndrome
• Chorionic gonadotropin secreting tumors
• Gestational thyrotoxicosis.
• Testicular malignancies.
Thyrotoxicosis without hyperthyroidism

• Subacute thyroiditis/de Quervain’s/post- partum

• Silent thyroiditis
• Thyrotoxicosis factitia
• Thyroid destruction: use of amiodarone, lithium,
interferon-alpha & beta, interleukin- 2, radiation &
infarction of adenoma
 Diffuse toxic goitre/ Grave’s disease
• Autoimmune disorder resulting increased
synthesis & release of thyroid hormones
• Female: male= 8:1
• Common among 20-40 years
• Accompanied by infiltrative opthalmopathy in 60%
specially in smokers.
• Subclinical opthalmopathy is detected by
CT/MRI.
• Infiltrative dermopathy /pretibial myxoedema in
1-2 % over shins, dorsum of foot. (5 P’s)
• Thyroid acropatchy- uncommon <1% resembling finger
clubbing & almost accompanied with opthalmopathy,
pretibial myxoedema
Painless palpable goitre more than 90% often with a
bruit
 Grave’s Pathophysiology
• Auto Ab’s bind to TSH receptors in thyroid cell
membrane & stimulate the gland to hyperfuncton-
TSI/TSHrAb
• Familial tendency- H/O Graves’ disease or
hashimoto’s thyroiditis
• Associates with HLA-B8 & HLA-DR3
• Thymus gland is typically enlarged & serum ANA levels
usually elevated showing underlying autoimmunity
• Dietary supplementation can trigger the disease &
treated with amioderone or KI have increased risk.
• Other organ specific autoimmune diseases
Sjogren’s syndrome
Celiac disease
Pernicious anemia
Addison’s disease
Vitiligo
T1DM/hypoparathyroidism
MG
Alopecia areata
Presentation
 Specific to Grave’s disease
Ophthalmopathy-20-40%
• upper eye lid retraction(Dalrymple sign), lid lag(von Graefe
sign)
• staring appearance(Kocher sign)
• Chemosis, Conjunctivitis
• Periorbital edema
• Proptosis( U/L in 5-10%)
• Diplopia/extra ocular muscle dysfunction impaired visual
acuity/fields
• Corneal ulceration grittiness/increased tear production
 Ophthalmopathy

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

• History and Physical examination.

clinical

• 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

• Pt is either euthyroid, hypothyroid or hyperthyroid.

• Papable smooth, firm or hard..
• Painless moves freely on swallowing
• Hardness and irregularity- calcification
• Painful nodule, sudden enlargement- haemorrhage
into simple nodule
 Clinically discreet swellings
• Discrete thyroid swellings are common and are present
in 3–4% of the adult population in the UK and USA.
• A discrete swelling in an otherwise impalpable gland is
termed isolated or solitary

• About 70% of discrete thyroid swellings are clinically

isolated and about 30% are dominant

• Their importance lies in the increased risk of neoplasia

as 15% of isolated swellings prove to be malignant, and

about 30–40% are follicular adenomas.

 Complications

SECONDARY THYROTOXICOSIS

PRESSURE SYMPTOMS

CARCINOMA ( follicular)
Risk of malignancy: rule of 12
 Investigation

THROID • SERUM TSH

• Free t3 and t4
FUNCTION

ULTRA • Subclinical nodularity, cyst

• Microcalcification, inc vascularity, nodal
SONOGRAPHY involvement

• Colloid nodules, thyroiditis, papillary,

FNA • Medullary, anaplastic carcinoma , lymphoma
C
 Classification of FNAC report
Thy1 Non-diagnostic

Thy1c Non-diagnostic cystic

Thy2 Non-neoplastic

Thy3 Follicular

Thy4 Suspicious of malignancy

Thy5 Malignant
AUTOANTIBODY • Hashimotos
TITRE • Chronic lymphocytic thyroiditis

• Toxicity+ Nodularity
ISOTOPE SCAN
• Hot, warm, cold nodule

• Chest radiograph, CT, MRI

OTHER
• Laryngoscopy, core biopsy
S
 Treatment of Euthyroid STN
Indications:
1. Risk of neoplasia (FNAC Thy 3-5)
2. Symptomatic swelling ( age & sex)
3. Pressure symptoms. ( hoarseness of voice)
4. Lymphadenopathy
5. Recurrent cyst
6. Cosmesis
Dominant nodule of
multinodular goitre

Subtotal thyroidectomy.. (inc

chances of recurrence)

Prefer total thyroidectomy (

also for FNAC thy 3 -5)
 TOTAL/COMP
HEMI BIOPSY-
LETION
THYRIDECTO FOLLICULAR
THYROIDECT
MY
OMY
CARCINOM
A
 Types of thyroiditis
• Acute infectious (painful) thyroiditis
• Subacute granulomatous thyroiditis
• Subacute lymphocytic (painless) thyroiditis
• Hashimoto (chronic lymphocytic) thyroiditis

• Fibrous (Riedel) thyroiditis

 Hashimoto’s thyroiditis
Most common cause of hypothyroidism, prevalent between 45 & 65
years of age, more common in women, can be major cause of non-
endemic goiter in children

Pathogenesis:

• Gradual hypothyroidism, secondary to autoimmune destruction of

follicular epithelial cells

• Association with other autoimmune disease like Graves disease,

SLE, RA, and Type-1 DM

• Genetic basis: more often with HLA-DR3 & HLA-DR5 alleles &
several non-HLA genes
 Hashimoto’s thyroiditis
Gross

•Thyroid diffuse and symmetrically enlarged with intact capsule

•Cut surface pale, gray-tan, firm, and somewhat friable

Microscopy
•Parenchyma shows widespread mononuclear inflammatory
infiltrate and germinal centers

•Thyroid follicles atrophic and in many areas lined by Hürthle cells

having abundant eosinophilic, granular cytoplasm
•Interstitial fibrosis is prominent
 Clinical features
•Painless, symmetric, diffuse goiter

•Hypothyroidism develops gradually, it may be preceded by

transient thyrotoxicosis caused by disruption of thyroid
follicles, with secondary release of thyroid hormones
"hashitoxicosis”
• Increased risk of NHL- B cell type lymphoma

• May predispose to Papillary Ca

 Subacute granulomatous
(de Quervain) thyroiditi s
•Self-limited disease(with in 6-8 weeks) secondary to an URT viral

infection, most common 3rd to 5th decade and frequently in women

•Gross: Enlarged firm thyroid gland, intact capsule

•Microscopic: Follicles disruption, colloid leakage, neutrophils

infiltrate, later mononuclear cells and granulomas with giant cells,

healing by resolution & fibrosis

•C/F:Onset acute, pain in neck when swallowing, fever and thyroid

enlargement. Transient hyperthyroidism may be due to disruption

of follicles and release of TH

 Subacute lymphocytic thyroiditis

•“Painless” thyroiditis which follows pregnancy,

most likely autoimmune

•Gross: Thyroid normal looking

•Microscopic: Parenchyma shows lymphocytic

infiltration and hyperplastic germinal centers

•C/F: Initial phase of thyrotoxicosis (secondary to thyroid

damage) return to euthyroid within a few months
 Riedel’s thyroiditis
• Replacement of normal thyroid parenchyma by dense
fibrosis
• C/F: Painless goitre “ Woody”, pressure symptoms
• Dx: Open biopsy
• Rx: Corticosteroids, levothyroxine, tamoxifen

Wedge resection of thyroid isthmus

THANK
YOU