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Pathology of Endocrine Glands - II. Thyroid. Endocrine Pancreas. Jaroslava Dušková Inst. Pathol. 1st Med. Fac. Charles Univ. Prague https://www1.lf1.cuni.cz/~jdusk/. Thyroid Gland History I. China (2nd mill.b.C.) description of goitre (Charvát 1935) - PowerPoint PPT Presentation
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Pathology of Endocrine Glands - II
Thyroid
Jaroslava Dušková Inst. Pathol. 1st Med. Fac. Charles Univ. Prague
https://www1.lf1.cuni.cz/~jdusk/
Endocrine Pancreas
Thyroid Gland History I.
China (2nd mill.b.C.) description of goitre
(Charvát 1935)
Vitruvius (16.a.C.) goitre in the Alpine region
Warton (1656) „ Adenographia“ the term glandula thyreoidea
Luschka (1860) mechanical support of the laryngeal structures
Thyroid Gland History II.
Basedow (1840) hyperthyreosis
Köstl (1855 - Wien): Der endemische Kretinismus als Gegenstand
der öffentlichen Fürsorge (habilit. thesis)
Gull (1873) hypothyreosis
Murray (1883) Therapy with bovine thyroid extracts
Thyroid Gland History III
Hashimoto (1912) struma lymphomatosa
Kendall (1914): Tyroxine discovery
Aron a Loebe (1929) TSH discovery
Adams a Purves (1952) LATS discovery
Thyroid Gland - embryology and fetal endocrinology
mouth epithelium, end of the 1st iu. month ductus thyreoglosus
lateral pharynx ultimobranchial bodies C- cells. parathyroid glands
fetal secretion starts at 12 weeks effect on GROWTH effect on DIFFERENTIATION
Thyroid Gland - anatomy
Weight in adults 15-20g
over 60g (7g in a neonate) strumalobus dexter
isthmus et lobus pyramidalis
lobus sinister
aberant, accesory, ectopic gland (polyclonality should help to tell from ca)
Thyroid Gland - physiology and regulations
hypothalamohypophysothyreoidal axis (TRH,TSH)
enzymes - deiodases autoregulation influenced by iodine
intake immune system
Morphological Thyroid Investigation
Clinic
scintigraphy SONOGRAPHY CT
Pathology
(biopsy) FNAB histology
Main Tasks in the Thyroid Cytology
reduction of the unnecessary surgery
diagnosis of subclinical inflammation
EARLY DIAGNOSIS of NEOPLASMS
Thyroid Cytology - getting sample
needle 0.6-0.8mm min. 2 punctions
aspirationnonaspiration
cyst: evacuate and aspirate with the second punction the periphery
fluid: whole volume for cytology
Thyroid Cytology- processing
Fixation– air dried – etanol / spray
(cytospin)
CYTOBLOCK
Staining: MGG HE polychrom all histo. imunocyto
TGB,calcitonin, parathormon
Regressive changes of thyroid gland
dystrophy: amyloid deposits, calcification atrophy: due to the lack of TSH
stimmulation, postinflammatory
necrosis: only in hyperplastic or neoplastic goitre
ThyreoiditisNON-SPECIFIC purulent non-specific granulomatose de Quervain lymphocytic (Hashimoto)
hypertrophic atrofic focal
invasive sclerosing Riedel
SPECIFIC tbc syfilis sarcoidosis
Non-Specific Granulomatose Thyreoiditis de Quervain (1904)
Synonyma: „Giant cell“ „Subacute non-purulent“
Clin.features: Oedema, pain, eufunction, may be also silent
Histol. features: disperse granulomas with giant cells
Course: spontaneous healing by 2-4 weeks
Thyreoiditis lymphoplasmocellularis Hashimoto - HT
Hashimoto, H.:Zur Kenntniss der lymphomatösen Veränderung der Schilddrüse
(struma lymphomatosa)
Arch.f. klin. Chir. 97, 1912, 219
Original HT Description
Macro - diff. parenchymatose goitre firm, elastic, gray-yellow
Micro - diffuselymfoplasmocellularlymph. foliculesONCOCYTES
Etiopathogenesis of HT
Etiology: unclear - viri ?
Pathogenesis: dysregulation of T lymphocytes IL-1 expression Fas molecules on the
surface of thyreocytes (they have FasL) apoptosis
activation
Activity: CD 44 proteoglycan influencing migration and lymphocyte proliferation, and metastasizing
Course of HT
a) progressive oncocytic transformation
loss of thyreocytes, transformation to a lymph- node-with-ca- meta image
hyperfunction folowed by
hypofunction
Course of HT
b) regressive loss of parenchyma, fibrosis hypofunction
Course of HT
c) neoplasia carcinoma lymphoma (mostly B - MALT)
Thyroid Malignant Lymphomas
2% thyroid primary malignancies mostly women with HT clinically rapid growth, often hypothyreosis mostly B (MALT),
features of lymphoepithelial lesion both LG and HG diff. dg. HT clinical and cytology suspicion
dg. excision
Chronic Sclerosing Thyreoiditis Riedel (1910) Synonyma: „Invasive Fibrotising“
„ Iron hard (eisenharte) goitre“
Clin.features: slight assym. edema fixation to surrounding structures eu- or hypofunction tracheal stenosis recurrens paresis
Histol. features: tissue destruction fibrotisation fixation to surrounding structures involment of the neck vessels
Course: Stabilisation, possible progression
Thyreoidal Syndromes
hypothyreosis– inborn – cretinism
endemic, sporadic
– acquired – myxedema hyperthyreosis - thyreotoxicosis
Hypothyreosis CRETINISMUS
disturbances of growth & differentiation
BRAIN
LUNG
BONE
Acquired Hypothyreosis - MYXEDEMA
decreased metabolism – bradycardia, low blood pressure, water
retention, obstipation intolerance of cold lowered lipolysis
– weight increase
– hyperlipemia ATHEROSCLEROSIS
Thyreoidal Syndromes
hypothyreosis– inborn – cretinism
endemic, sporadic
– acquired – myxedema hyperthyreosis - thyreotoxicosis
Hyperthyreosis increased metabolism tachycardia, high blood pressure,
fibrilation,– hypercalciuria, diarrhoe
intolerance of warm increased lipolysis, glycogenolysis
– weight decrease– hyperglycemia, diabetes
muscle weekness, insomnia, exophtalmus, pretibial myxedema
Processing of Thyroid Resecate
orientation division
– lobus dx.– isthmus (+lobus pyramidalis)– lobus sin.
cutting in cca 3mm thick lamellae– revision and extensive/complete blocking
of the encapsulated nodules periphery– any suspicious focus for histology
Folicular Neoplasia (proliferating microfollicular lesion)
Histological diagnosis
– microfollicular adenoma
– follicular carcinoma
Cytological features
highly cellular smears– few colloid– microfollicular
formations– thyreocytes regular,
small or slightly enlarged
– bare nuclei– regressive changes:
mostly absent
Oncocytic Tumours
adenoma– architecture follicular, trabecular– cellular atypiae without predictive value
for biological behaviour– more risk in case of solid architecture
EXCLUDE
ANGIOINVASION, CAPSULOINVASION
Oncocytic Tumours
carcinoma– oncopapillary (may lack ground glass nuclei !)
– oncofollicular
must exhibit
ANGIOINVASION and/or
CAPSULOINVASION (all capsule thickness with extracapsular expansion)
Papillary Carcinoma
Histological variants - WHO
microcarcinoma encapsulated follicular diff. sclerosing oxyphil cell
Histological variantsadditional
tall cell
columnar cell macrofollicular with desmopl.stroma hyal. trabecular ca
Papillary CarcinomaCytological featuresgeneral
highly cellular smears few colloid waxy colloid, may be
absent
architecture phragments of papillae groups trabecular microfollicular syncytial formations squamous
metaplasia psammomata
NUCLEI
enlarged non - circular overlapping grooves pseudoinclusions
Medullary Carcinoma
origin fom C-cells
clinical forms :
(parafollicular)
sporadic familiar
– MEN 2a
– MEN 2b
Medullary Carcinoma familiar forms
MEN 2a medullary ca parathyr. adenoma pheochromocytoma
MEN 2b MEDULLARY CA marphanoid habitus mucous neuromas pheochromocytoma parathyr. adenoma -
Medullary carcinomaC-cells (parafollicular)
sporadic familiar
MEN 2a MEN 2b
Medullary carcinoma
Histological diagnosis
Calcitonin + amyloid +- argyrophilia +
Medullary Carcinoma
Histological diagnosis
architecture may mimic any otherthyroid ca!!! (WHO)
Calcitonine + amyloid +- argyrophilia +
Medullary Carcinoma
Cytological types
large cell
small cell
fusocellular
plasmocytoid
highly malignant neoplasm of the old age with rapid progression origin:
non diagnosed differentiated ca hyperplastic goitre chronic inflammation without preceeding goitre
Undifferentiated Carcinoma(anaplastic)
Undifferentiated Carcinoma
Histological variants (often combined)
fusocellular small cell (?) exclude lymphoma! giant cell (monstrous cells) squamous metaplasia composed
lmsa, rmsa,osa, chsa, hae, MFH,
classify as carcinoma!
Other Types of PrimaryThyroid Carcinomas
epidermoid mucoepidermoid mixed follicular and mucoepidermoid
Metastases into Thyroid
kidney lung breast other
Islets of Langerhans (1869)
adults 100 000 -1000 000 cell types:
B - insulin
A - glucagon
D – somatostatin
PP – pancreatic polypeptide
D – vasoactive intestinal polypeptide
Islets of Langerhans -
regressive changes
fibrosis (postinflamm.) - DM I mucoviscidosis – DM 10x frequency hyalinosis, amyloidosis
Islets of Langerhans - progressive changes hyperplasia –diabetic embryopathy nesidioblastosis
- tumours– nesidioma ( event. in MEN I)
(insulinoma, glucagonoma, somatostatinoma,VIPoma, PP-oma, G cells -gastrinoma, EC – serotonin - carcinoid
– neuroendocrine carcinoma
Islets of Langerhans - syndromes
hyperfunction – hypoglycemia (weekness , sweating, tremor,
coma)– Zollinger-Ellison, Werner Morrison, glucagonoma
hypofunction – insulin hyperglycemia – acute : polydipsia, ketoacidosis, coma, liver
steatosis , brain edema
– chronic: diabetes mellitus: microangiopathy, macroangiopathy, neuropathy, retinopathy,embryopathy
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