Thyroid

kusumarani 714 views 71 slides Sep 11, 2017
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About This Presentation

disorders of thyroid


Slide Content

PATHOLOGY OF THE THYROID
GLAND
Dr. Kusuma K N

DISEASES OF THE THYROID
GLAND
Congenital diseases
Inflammation
Functional abnormality
Diffuse and Multinodular goiters
Neoplasia

CONGENITAL THYROID DISEASES
Agenesis /Aplasia
Hypoplasia
Accessory or aberrant thyroid glands
Thyroglossal duct cyst

THYROGLOSSAL DUCT CYST
Children
Failure of regression
Squamous or
columnar lining
Complications:
inflammation, sinus
tracts

INFLAMMATION
Thyroiditis
Acute illness with pain
Infectious
Acute
Chronic
Subacute or granulomatous (De Quervain’s)
Little inflammation with dysfunction
Subacute lymphocytic thyroiditis
Fibrous (Riedel) thyroiditis
Autoimmune
Hashimoto thyroiditis

HASHIMOTO THYROIDITIS
Most common cause of hypothyroidism
Autoimmune
45-65 years
F:M = 10-20:1
Painless symmetrical enlargement

PATHOGENESIS
Immune systems reacts against a variety of
thyroid antigens.
circulating autoantibodies against thyroglobulin
and thyroid peroxidase
Progressive depletion of thyroid epithelial cells
which are gradually replaced by mononuclear
cells → fibrosis

HASHIMOTO THYROIDITIS
Diffuse enlargement
Firm or rubbery
Pale, yellow-tan, firm & somewhat nodular cut
surface

HASHIMOTO THYROIDITIS
Massive lymphoplasmcytic infiltration with
lymphoid follicles formation
Destruction of thyroid follicles
Remaining follicles are small and many are lined
by Hurthle cells
Increased interstitial connective tissue

Risk of developing
B-cell non-Hodgkin’s lymphoma
Other concomitant autoimmune diseases
Endocrine and non-endocrine

SUBACUTE THYROIDITIS
Granulomatous thyroiditis / De Quervain
thyroiditis
less frequent than Hashimoto disease
40 and 50
F: M = 4 : 1
triggered by a viral infection
history of an upper respiratory infection just
before the onset of thyroiditis

FUNCTIONAL ABNORMALITY
Hyperfunction- hyperthyroidism
Thyrotoxicosis : hypermetabolic state caused by
elevated circulating levels of free T
3
and T
4

Hypofunction- hypothyroidism
¯ in level of hormone → impair development in
infants and slowing of physical and mental
ability in adults
Cretinism
Myxedema

GRAVES DISEASE
Most common cause of endogenous hyperthyroidism
F:M = 7:1
3rd to 4th decades
Characterized by
Hyperthyroidism
ophthalmopathy with exophthalmos
dermopathy (pretibial myxedema)
Autoimmune disease with genetic susceptibility
associated with HLA-B8 and DR3

GRAVES DISEASE….
Diffuse enlargement with audible bruit
Wide,staring gaze,lid lag,exophthalmos,pretibial
myxedema
↑ levels of free T
4
& T
3
and ↓ levels of TSH in blood
↑ uptake of radioactive iodine

Autoimmune disease with breakdown of helper-T-cell tolerance
Excessive production of TWO thyroid autoantibodies:
1)Thyroid-stimulating antibody (TSAb) &
2)Growth-stimulating antibody (GSAb)
Antibodies bind to the TSH receptor of the follicular cell
Stimulation of the cell resulting in:
Increased levels of thyroid hormones &
Hyperplasia of the thyroid gland
Hyperthyroidism and Thyroid gland enlargement

GRAVES DISEASE
Symmetrical
enlargement of thyroid
gland
C/s: homogenous, soft
and appear meaty
Hyperplasia and
hypertrophy of follicular
cells

DIFFUSE & MULTINODULAR
GOITERS
Reflects impaired synthesis of thyroid hormone most
often caused by iodine deficiency
Impairment leads to compensatory ↑ in TSH levels →
hypertrophy and hyperplasia of follicular cells →
gross enlargement of gland
Euthyroid metabolic state
Degree of enlargement is proportional to level and
duration

DIFFUSE NONTOXIC GOITER
Diffuse non-toxic (simple) goiter
colloid goiter
Endemic
sporadic (dyshormonogenetic)

ENDEMIC GOITER
Low iodine content in drinking water & food
(Himalayas, Alps, Andes, areas far from the sea)
Prevalence decreasing due to prophylactic
iodination of salt
Iodine deficiency causes decreased hormone
levels & consequent elevation in TSH

SPORADIC GOITER
Commonest type of goiter
Euthyroid, but may be hypo- or hyper-
Mostly idiopathic, but RARELY, may be caused
by:
Drugs used in Rx of hyperthyroidism
Goitrogens e.g. cauliflower, cabbage, cassava
Suboptimal iodine intake
Hereditary enzymatic defects

MULTINODULAR GOITER
Recurrent episodes of hyperplasia and involution
leads to irregular enlargement
All long standing diffuse endemic and sporadic
goiter may eventually convert to multinodular
goiter
Causes most extreme enlargement and may be
mistaken for neoplasm

May arise due to variable response of follicular
cells to external stimuli such as trophic hormones
With uneven follicular hyperplasia, generation of
new follicles and uneven accumulation of colloid
→ rupture of follicle and vessels →hemorrhage,
scarring & calcification → nodularity

MULTINODULAR GOITER
Asymmetric
enlargement
Multinodular
Haemorrhage
Calcification
Fibrosis
Cystic degeneration

MULTINODULAR GOITER
Numerous follicles varying in size
Recent haemorrhage
Haemosiderin
Calcification
Cystic degeneration
+/- dominant nodule

THYROID NEOPLASMS
I.Primary
Epithelial
Malignant Lymphomas
Mesenchymal tumors
II.Metastatic Tumors

EPITHELIAL THYROID NEOPLASMS
Tumours of follicular cells
Benign (adenomas)
Follicular adenoma
Malignant (carcinomas)
Follicular carcinoma (10-20%)
Papillary carcinoma (75-85%)
Undifferentiated (anaplastic) carcinoma (<5%)
Tumours of C-cells
Medullary thyroid carcinoma (MTC - 5%)

FOLLICULAR ADENOMA
Benign, encapsulated tumor showing evidence of
follicular differentiation
Common
Predominantly young to middle women
Presents as solitary thyroid nodule
Painless nodular mass, cold on isotopic scan

FOLLICULAR ADENOMA
Solitary, Variably sized,
encapsulated, well-
circumscribed with
homogenous gray-white to
red-brown cut-surface
+/- degenerative changes

Hurthle cell/ oxyphil adenoma

FOLLICULAR CARCINOMA
Second most common form, 10-20%
Females > Males
45 - 55 yrs.
Rare in children
Solitary nodule, painless, cold on isotopic
scan
Widely invasive Vs minimaly invasive
Haematogenous route is preferred mode of
spread

FOLLICULAR CARCINOMA
Solitary round or oval
nodule
Thick capsule
Composed of follicles
Capsular invasion or
vascular invasion

PAPILLARY CARCINOMA
Commonest thyroid malignancy, 75-85%
Female:Male = 2.5:1
Mean age at onset = 20 - 40 yr
May affect children
Prior head & neck radiation exposure
Indolent, slow-growing painless mass cold
on isotopic scan
Cervical lymphadenopathy may be
presenting feature

PAPILLARY CARCINOMA
Variable size
(microscopic to
several cm)
Solid or cystic
Infiltrative or
encapsulated
Solitary or
multicentric (20%)

PAPILLARY CARCINOMA
Papillae or follicles
Psammoma bodies
NUCLEAR
FEATURES***

PAPILLARY CARCINOMA
Nuclear Features
Optically clear (ground glass, Orphan Annie)
nuclei
Nuclear pseudoinclusions or nuclear grooves

VARIANTS
Follicular variant
tall-cell variant
diffuse sclerosing variant
papillary microcarcinoma

ANAPLASTIC CARCINOMA
Rare; < 5% of thyroid carcinomas
Highly malignant and generally fatal < 1yr.
Elderly » 65 yrs; females slightly > males
Rapidly enlarging bulky neck mass
Dysphagia, dyspnoea, hoarseness

ANAPLASTIC CARCINOMA
Large, firm, necrotic mass
Frequently replaces entire thyroid gland
Extends into adjacent soft tissue, trachea and
oesophagus
Highly anaplastic cell on histology with:
Giant, spindle,small or mix cell population
Foci of papillary or follicular differentiation

Cellular pleomorphism
+/- multinucleated giant cells
High mitotic activity
Necrosis

MEDULLARY THYROID
CARCINOMA (MTC)
Malignant tumour of thyroid C cells producing
cacitonin
5 % of all thyroid malignancies
Sporadic (80%)
Rest in the setting of MEN IIA or B or as familial
without associated MEN syndrome

MEDULLARY THYROID
CARCINOMA (MTC)
Sporadic MTC
Middle-aged adults
Female:male = 1.3:1
Unilateral involvement of gland
+/- cervical lymph node metastases
Indolent course with 60-70% 5-yr survival after
thyroidectomy

MEDULLARY THYROID
CARCINOMA (MTC)
Associated with MEN IIA
Younger patients in twenties
Multicentric and bilateral
Slow growing
Associated with MEN IIB
Even younger patients in teens
Aggressive with early metastasis
Poor prognosis

Histology same for sporadic & familial
Solid, lobular or insular growth
patterns
Tumour cells round, polygonal or
spindle-shaped
Amyloid deposits in many cases

Amyloid deposits stain
orange-red with Congo
Red stain

PROGNOSIS OF THYROID
CARCINOMAS
Papillary Best prognosis
Follicular
Medullary
Anaplastic Worst prognosis

SECONDARY TUMOURS
Direct extensions from: larynx, pharynx,
oesophagus etc.
 Metastasis from:
renal cell carcinoma, large intestinal
carcinoma, malignant melanoma, lung
carcinoma, breast carcinoma etc.

SOLITARY THYROID NODULE
Papillary carcinoma
Follicular carcinoma
Medullary carcinoma
Follicular adenoma
Hyperplastic (dominant) nodule
Metastatic neoplasms

MULTIPLE ENDOCRINE
NEOPLASIA TYPES IIA & IIB
Germ-line mutation in Ret
protooncogene on chromosome 10q11.2
MEN IIA: MTC, phaeochromocytoma,
parathyroid adenoma or hyperplasia
MEN IIB: MTC, phaeochromocytoma,
mucosal ganglioneuromas, Marfanoid
habitus, other skeletal abnormalities
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