pathology of the thyroid
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PATHOLOGYof the
THYROID
Dr. Mudjiwijono HE, MS, SpPA
Lab. Patologi AnatomiFKUB/RSSA
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THYROID PATHOLOGY1. Inflammation (thyroiditis)
1.Hashimoto thyroiditis2. Granulomatous (de Quervains) thyroiditis
3. Subacute lymphocytic thyroiditis
2. Hyperplasia
1. Goiter (Diffuse / Multinodular Goiter)
2. Graves disease
3. Neoplasm
1. Benign :Follicular adenoma
2. Malignant : Carcinoma
1.Papillary carcinoma2.Follicular carcinoma
3.Anaplastic (undifferentiated) carcinoma
4.Medullary carcinoma
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THYROIDITIS :HASHIMOTO THYROIDITIS
Etiology : autoimmune Incidence : > 45 - 65 y.o.
Female >> male (10 : 1 to 20 : 1)
Macros :
- >, diffuse, firm, intact caps, well defined- CS : pale, yellowish gray,
vaguely/distinctly nodular
Micros :
- Lymphocytic infiltration, germinal centers (+)
- Plasma cells, histiocytes, multinucleated giant
cells (+)
- Atrophic follicle, interstitial fibrosis
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Clinic : Thyroid > symmetric, diffuse, pain (-)
Initially : mild hyperthyroidism hypothyroidism
Sometimes :
Very firm, sudden enlargement,severe pressure symptom confused with Ca
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SUBACUTE THYROIDITIS
(Granulomatous thyroiditis; De Quervains thyroiditis) Freq : < Hashimoto thyroiditis
Incidence : > 40 -50 y.o.
Female > male (4 : 1)
Etiology : ? (initially with viral inf.) Macros :
- >, unilateral / bilateral, rubberyfirm
- Intact caps, little/no adherence to
the surrounding structures- CS : yellowish white
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Micros :- First : PMN infiltration, microabscesses (+)
lymphocytes, macrophages, plasma cells,multinucleated giant cells (+)(granulomatous inflammation)
late stage : fibrosis (+)
Clinic :- Thyroid >, pain (+)- First : hyperthyroidism : in 2 - 6 weeks
(with/without tx )- T4 dan T3 , TSH - 6 - 8 weeks, thyroid functionN
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SUBACUTE LYMPHOCYTIC THYROIDITIS More common in children Female > male Autoimmun Macros : thyroid N / slight > Micros :
- Lymphocytic infiltration, germinal center (+) Clinic :
- Pain (-)- Hyperthyroidism (transient) N- Some px :
hyperthyroidism hypothyroidismN
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HYPERPLASIAGOITER The most common thyroid disease Forms :
- Diffuse non toxic (simple) goiter
- Multinodular goiter
- Endemik / Sporadik
Etiology and pathogenesis :
- Impairment of thyroid hormone synthesis,largely caused by iodine deficiency
TSH ,hypertrophy and hyperplasia
follicular cells thyroid >
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Endemic goiter :* Goiter >10% population
* Etiology :
1. Low iodine content in soil, water, food(Andes,Himalaya)
2. Goitrogen (cabbage, cauliflower, radish, cassava)
Sporadic goiter : < endemic goiter* > female, peak : puberty / young adult
* Etiology :
- Goitrogen- Genetic
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SIMPLE GOITER (Colloid goiter)Thyroid >, nodule (-)Morphology :
* Hyperplastic phase :- Thyroid > diffuse, symmetric, rarely >100 - 150 gm- Follicle ep : columnar, dense papillary projection- Colloid >/ filled with colloid- CS : brownies, translucent- Micros : follicles epithelium flatened /cuboid
Clinic : Thyroid >, euthyroid
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MULTINODULAR GOITERSimple goiterrepeated hyperplasia and involution
multinodular goiter(nodular hyperplasia,adenomatoid goiter, adenomatous hyperplasia)
Macros :
- Thyroid > asymmetric, multilobulated, >2000 gm- Sometimes : substernal (intrathoracicgoiter)
- CS : irregular nodule, filled with colloid, brownies
and gelatinous
- Hemorrhage, fibrosis, calcification, and cystic
degeneration
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Micros :
- Distended follicles flattened epithelium,
hyperplastic follicles cuboid epithelium- Follicular hyperplasia (+)
- Irregular septae, hemorrhagic area and calcification
Clinic :- Thyroid >, usually euthyroid
sometimes toxic multinodular goiter
- Airway obstruction, dysphagia, large vascular
compression in cervical / upper thoracal (superior
vena cava syndrome)
- Incidence of malignant degeneration
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GRAVES DISEASE(Basedows disease, Thyrotoxicosis, Diffuse Toxic Goiter,
Exophthalmic Goiter) Etiology :
- autoimmune (Ab againts TSH receptor)
- Thyroid-Stimulating Immunoglobulin (TSI)
- Thyrotropin-Binding Inhibitor Immunoglobulin (TBBII) HyperplasiaT3, T4
Macros :
- Thyroid >, symmetric , diffuse (mild to moderate)
- Succulent, reddish- CS : uniformly gray or red
- Long standing cases : friable, dull yellow
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Micros :
- Hyperplastic follicles, papillary involding- Lining epithelium : columnar
- Colloid : pale, finely vacuolated, rand vacuole
- Aggregates of lymphoid tissue, germinal center (+)
- Longstanding cases : mild fibrosis
Clinic :
- > young adult female, muscle weakness, weight loss,exophthalmos, irritability, tachycardia, goiter,
appetite , atrial fibrillation (+/-)
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BENIGN NEOPLASM :
FOLLICULAR ADENOMA Etiology : ?
- > : (+) hemorrhages, fibrosis,calcification and cystic degeneration
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Micros :
- Uniform follicles, intact caps- Mitosis : dysphagia- Prognosis : very good
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THYROID CARCINOMA : Rare, USA : 1.5% all Ca Usually : young adult and middle age Female > male Follicle epithelium (except medullary ca),
majority well-diff. ca
Etiology :
* Genetic* Environment
The most common : exposure to ionizing
radiation, esp. at 1st and 2nd decade of life
(after Chernobyl disaster at 1986, incidence of
papillary ca in children)
* Iodine deficiency follicular ca
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PAPILLARY CARCINOMA The most common, USA 85% thyroid ca
Present in any age group, > in 25 50 y.o.Macros :
- Most cases : solid, whitish, firm, clearly invasive
- < 10% : encapsulated
- 10% cases : cystic changes- Sometimes : papillary formation are evident to the
naked eye
Micros :
- Papillae : lining by a single/stratified cuboidal cells- Well-differentiated /anaplastic
- Nuclei : ground-glass
- Intranuclear inclusion / intranuclear groove (+)
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Clinic :
- >> asymptomatic, first manifestation :
cervical nodal metastases- Hoarse, dysphagia, cough, or dyspnea (+) : late std.
- Metastases >> lymphogen, < hematogen (>> lung)
Lab : CT Scan/ FNAB
Prognosis :- Good, 10 ysr > 95%
- 5% - 20% cases : local recurrent
- 10% - 15% cases : distant metastases
- Prognosis, depend on :- Age (>40 y.o, prognosis
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FOLLICULAR CARCINOMA 5% - 15% thyroid ca
Female > male (3 : 1)
Age > papillary ca, peak : 40 60 y.o.
Macros :
- Single nodule, encapsulated
- CS : solid, fleshy, brownish to reddish grey,sometimes translucent or (+) central fibrosis
and calcification
Micros :
- Uniform epithelial cells, create small follicles,colloid +/- = Follicular adenoma
capsular/vascular invasion ca
- Variant : Hrthle cell / oncocytic variant
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Clinic :- Slow growing, pain (-)
- Lymphogen metastases other thyroid ca, 65 y.o.
Macros : necrotic and hemorrhagic solid tumor mass
Micros :
(1) large, pleomorphic giant cells(2) spindle cells with a sarcomatous appearance
(3) mixed spindle and giant cells
Clinic :
- Rapid growing, at the time of initial detected :>> extrathyroidal extension / pulmonal metastases
- Symptom : dyspnea, dysphagia, hoarseness and cough
- Effektive Tx (-), death < 1 yr. after diagnosed
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MEDULLARY CARCINOMA Neuroendocrine Tumor ( parafollicular cell/C cell),
produce calcitonin, serotonin, ACTH, and
vasoactive intestinal peptide (VIP) 5% thyroid caMacros :
- Solitary/bilateral, multicentric nodule- > : necrosis and hemorrhage- Solid, firm, nonencapsulated, well circumscribed- CS : grey to yellowish
Micros :- Solid proliferation of round to polygonal cells of
granular amphophilic cytoplasm- Separated by a highly vascular stroma, hyalinizedcolagen and amyloid
- Pattern of growth : carcinoid like, paraganglioma like,trabecular, glandular or pseudopapillary
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Clinic :
- Dysphagia, hoarsenes- Paraneoplastic syndrome
- Diarrhoe (caused by VIP)
- Cushing syndrome (caused by ACTH)
- Calcitonin
- CEA (+)
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