Page 562 - Concise Pathology for Exam Preparation ( PDFDrive )
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20  Endocrinology  547


             •	 Cells show finely dispersed chromatin, imparting an optically clear or empty appearance
               to the nuclei (Orphan	Annie or ground	glass	nuclei).
             •	 Invaginations of the cytoplasm may in cross-sections give an appearance of eosinophilic
               intranuclear	inclusions	or	pseudoinclusions or intranuclear	grooves.
             •	 Concentrically  calcified  structures  called  psammoma	 bodies,  usually  located  within
               cores of papillae, are often seen.
             •	 Lymphatic	invasion	is	common; however, involvement of blood vessels is relatively
               rare.
             Note: Diagnosis of PTC is based on nuclear features irrespective of the presence or absence
             of papillary architecture.
             Variants
             •	 Encapsulated	variant: Well encapsulated, vascular or lymph node dissemination rare,
               and excellent prognosis
             •	 Follicular	variant: Unencapsulated tumours with a follicular architecture, characteristic
               nuclear features of PTC and psammoma bodies
             •	 Tall	 cell	 variant:  Neoplastic  epithelium  is  tall  columnar  with  intensely  eosinophilic
               cytoplasm. Large tumours, often present with vascular invasion and local and distant
               metastases. Older individuals have a worse prognosis. Hürthle cell neoplasms are a close
               differential.
             •	 Diffuse	 sclerosing	 variant:  Younger  individuals  including  children  are  affected;
               show  diffuse  fibrosis,  abundant  psammoma  bodies  and  squamous  morules
               (metaplasia).
             •	 Hyalinizing	trabecular	tumour: Organoid growth (resembles extra-adrenal paraganglioma),
               both intra- and extracellular hyalinization are seen.
             Prognosis
             •	 Ten-year survival 98%
             •	 Metastasis seen in 10–15% cases
             Follicular	Carcinoma
             Clinical features
             •	 Second most common thyroid carcinoma
             •	 Peak incidence between 40 and 50 years; females more commonly affected than males
             •	 Incidence higher in areas with iodine deficiency; indicating that follicular carcinoma
               might arise from nodular goitre
             •	 No definite evidence that follicular carcinoma arises from adenomas except for common
               RAS mutations
             •	 Presents as a slowly enlarging painless cold nodule
             •	 Regional lymph nodes rarely involved; vascular invasion common with spread to bones,
               lungs and liver
             Gross morphology:
             •	 Solitary nodule; may be well circumscribed or infiltrative
             •	 Grey-tan-pink, translucent (due to large colloid-filled follicles)
             •	 Degenerative changes, eg, central fibrosis and foci of calcification are common.
             Microscopy:
             •	 Most tumours show a follicular pattern; in some cases, follicular differentiation is less
               apparent; trabecular pattern, sheets of polygonal to spindle-shaped cells and Hürthle
               cells are more prominent.
             •	 Anaplasia is variable (generally not marked).
             •	 Blood vessels are preferentially invaded than lymphatics.
             Types
               1.  Minimally invasive
               2.  Widely invasive (extensive invasion of adjacent thyroid parenchyma or extra-thyroidal
                tissue)
             Prognosis
             •	 Most  follicular  carcinomas  are  treated  with  total  thyroidectomy  followed  by
               administration of radioactive iodine. Better differentiated lesions are treated with
               thyroid  hormones  to  suppress  endogenous  TSH  (better-differentiated  lesions  are
               stimulated by TSH).


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