NEOPLASMS OF THYROID Flashcards
(33 cards)
Most common benign thyroid neoplasia
follicular adenoma
list Most common malignant thyroid neoplasia in order:
- Papillary Carcinoma:>85%
- Follicular carcinoma: 5%-15%
- Medullary carcinoma:5%
- Anaplastic carcinoma:< 5%
history of radiation of the head and neck, especially first two decades of life.
* Usually presents as a distinct solitary nodule.
thyroid neoplasms
features suggessting malignancy in hyroid neoplasms
✓young age, Male, cold nodule
✓Pain, rapid rate of growth and change in voice
Radio Iodine uptake studies used to further categorize nodules:
* Hot nodule( increased uptake)
- graves / nodular goiter
Radio Iodine uptake studies used to further categorize nodules:
* COLD nodule( dec. uptake)
Adenoma / carcinoma
Clinical features of follicular adenoma
- Usually painless solitary
nodules - May be functional &
cause hyperthyroidism
(toxic adenoma)
microscopy of follicular adenoma
- Solitary nodules; Well capsulated tumor;
Compressed normal gland.
1 nodule + capsule - No capsular and vascular invasion & papillary carcinoma nuclear features
- Occasional atypia ( Endocrine atypia)
- Variant- Hurthle cell adenoma
Follicular Adenomas is a benign neoplasm derived from ___________
follicular epithelium
pathogenesis of follicular adenoma
Most adenomas are Cold nodules ( Toxic- hot).
* Toxic adenomas:
TSH receptor pathway mutations —> autonomy
* Non Functional Adenoma: <20% express RAS gene mutations
genetic pathogenesis of papillary carcinoma
Activation of MAP kinase pathway either by
* Rearrangement of tyrosine kinase RET gene
* Point mutation in BRAF gene
**FOLLICULAR CELL DERIVED
genetic pathogenesis of Follicular carcinoma
- RAS gene – frequent ( HRAS, N RAS, KRAS)
- P13K/AKT signaling pathway components including its negative
regulator PTEN - PAX8 gene
list 3 FOLLICULAR CELL DERIVED carcinomas
papillary
follicular
anaplastic
genetic pathogenesis of anaplastic carcinoma
- De novo / progression from Papillary/ Follicular carcinoma
- TP53 mutation in additions
genetic pathogenesis of medullary carcinoma
Parafollicular C cells derivation
- Familial ( MEN-2) – RET gene ( Chr 10) – tyrosine kinase receptor activation
- Non Familial
diagnosis:
* 5% -15% of malignant thyroid tumors
* F > M; 40-60yrs
* Hematogenous spread to bones or lungs is common
* Genetic basis
* ~50% cases harbor mutations in RAS family
of oncogenes
* HRAS, NRAS, and KRAS
* NRAS mutations are most common
follicular carcinoma
Gross morphology of follicular carcinoma
Single well circumscribed
nodules or widely infiltrative
Microscopic morphology of follicular carcinoma
- Uniform cells forming small
follicles containing inspissated
colloid - Rule out capsular and/or vascular invasion to distinguish follicular adenomas from minimally invasive follicular carcinomas
- Hematogenous spread
Gross morphology of papillary carcinoma
- Solitary / Multifocal
- Circumscribed – encapsulated / infiltrating surrounding
parenchyma - Papillary excrescences
microscopic morphology of papillary carcinoma
- Branching papillae with fibrovascular core covered with uniform cuboidal epithelial cells
- Psammoma bodies - Concentrically calcified structures
termed within the cores of papillae - Cells: Nucleus - optically clear (ground-glass or Orphan Annie eye nuclei)
- intranuclear inclusions (“pseudo-inclusions”)
- intranuclear grooves
determine diagnosis:
* 80% of malignant thyroid tumors
* F > M
* Age 20-50
* Risk factor
-Radiation exposure
PAPILLARY CARCINOMA
pathogenesis of PAPILLARY CARCINOMA
Activation of MAP kinase pathway is
feature of all papillary carcinomas.
-RET protooncogene on chr.10
-Point mutations in BRAF(MAP-Kinase pathway)
papillary carcinoma is commonly spread via
cervical lymphnodes
RX: for papillary carcinoma
- Resection is curative in most cases
- Radiotherapy with iodine 131 is effective for metastasis
