Download THYROID TUMOURS

THYROID TUMOURS
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Benign – adenomas
Malignant
Solitary thyroid nodule – discrete nodule within normal thyroid gland.
Mostly non neoplastic e.g. Hyperplasia, cysts etc as well as benign neoplasms
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Solitary Thyroid Nodule - more likely to be neoplastic than multiple nodules
Nodules in younger patients have likelihood of being neoplastic than those in
older patients
Nodules in males - likelihood of being neoplastic
DXT to head, neck - incidence of thyroid Cancer
“Hot” nodules - likelihood of being benign
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ADENOMAS
Follicular adenomas
Discrete solitary masses; often non-functioning hence “cold” nodules
Small no. may be functional  thyrotoxicosis (“toxic adenomas” – “hot” nodules).
This is independent of TSH stimulation
Morphology
Well-circumscribed nodule, surrounded by well-defined capsule; adjacent
compressed thyroid tissue (diff from MNG); also growth pattern is distinct from
adj non neoplastic thyroid*.
Histo shows uniform closely packed colloid filled follicles of different sizes
(macro, micro, trabecular, foetal)
Variants – Hurthle cell, clear cell, signet ring cell etc.
Nuclear pleomorphism & atypia may be present in few cases (does NOT imply
malignancy)
Important to examine capsule for integrity – INTACT CAPSULE NECESSARY
TO QUALIFY AS AN ADENOMA
Evaluation of adenomas
Radioactive iodine uptake scan – usually “cold nodule”
U/S – cystic/solid
FNAC
Biopsy – definitive diagnosis of adenoma vs. Cancer can ONLY BE MADE ON
HISTOLOGY – adenoma should show NO capsular or vascular invasion
CARCINOMAS
 Papillary Ca
 Follicular Ca
 Medullary Ca
 Anaplastic Ca
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PATHOGENESIS OF CA’S
Genetic factors
Follicular Ca – 50% have RAS mutations; translocations between PAX8 & the
peroxisome proliferatorPPAR
present in 30%
Papillary Ca – mutations of tyrosine kinase receptors RET or NTRK1; mutations
of BRAF oncogene; mutations of RAS oncogenes
Medullary Ca – arise from parafollicular (C cells); familial cases associated with
MEN 2; 95% show RET proto-oncogene mutations
Anaplastic Ca – De Novo or de-differentiation of well differentiated papillary/
follicular Ca; p53 mutations impt.
Environmental factors
DXT – esp during 1st 2 decades of life (radiation to head and neck was used to treat
tonsillar enlargement, acne, tinea capitis!) DXT as a risk factor – atom bomb,
Chernobyl nuclear disaster (1986)  associated with markedly high incidence of
paediatric thyroid Cancer
Papillary Ca
 Commonest thyroid Ca
 20–40 yrs age
 Solitary/multifocal, often cystic
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Papillary structures (diff from those in hyperpl – fibrovasc cores, more complex,
epithelium may be atypical)
Psammoma bodies
Characteristic nuclear features :
Optically clear / “empty”/ ground glass/ “orphan Annie eye” nuclei
 Intranuclear pseudoinclusions (due to invagination of cytoplasm)
 Longitudinal grooving of nuclei
*Diagnosis of papillary Ca based on these nuclear features even in absence of
papillary structures.
 Lymphatic spread favoured.
 Usually cold nodules
 Unlike follicular Ca’s they can accurately be diagnosed on FNAC
Follicular Cancer
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2nd commonest cancer
F>M, tend to be a decade older than pts with papillary Ca
Morphology – uniform cells forming follicles with dense eosinophilic colloid
No nuclear features of papillary Ca, no psammoma bodies
Presence of capsular or vasc invasion
May be minimally or widely invasive
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Medullary Carcinoma
Neuroendocrine origin, from C cells  calcitonin (useful in diagnosis & follow-up)
80% sporadic, remainder associated with MEN 2A or 2B or as familial tumours
without assoc MEN synd (FMTC)
MEN2 associated cases occur in young pts
Familial cases – bilateral & multicentric
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Histo – polygonal to spindle shaped cells  nests, trabeculae, follicles; amyloid
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deposition; surrounding thyroid tissue shows C cell hyperplasia in familial cases;
presence of calcitonin – IHC
Clin – mass effects, paraneoplastic synd caused by secretion of a peptide
hormone eg VIP, serotonin, hypocalcaemia not prominent despite raised
calcitonin levels
Anaplastic Cancer
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Undifferentiated tumours
Aggressive
50% have h/o MNG; 20% have h/o de-differentiated Ca; 20-30% have concurrent
de-diff Ca, freq papillary
Poor prognosis
Histo – anaplastic cells, GC’s, MF’s, sarcomatoid appearance
Clin – rapidly growing bulky neck mass, compression sympt common
REFERENCE
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Robbins Basis of Pathology 8th edition
Pages 1118 - 1126
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