pathology of endocrine glands - ii
DESCRIPTION
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 PresentationTRANSCRIPT
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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
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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
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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
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Thyroid Gland History III
Hashimoto (1912) struma lymphomatosa
Kendall (1914): Tyroxine discovery
Aron a Loebe (1929) TSH discovery
Adams a Purves (1952) LATS discovery
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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
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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)
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Thyroid Gland - physiology and regulations
hypothalamohypophysothyreoidal axis (TRH,TSH)
enzymes - deiodases autoregulation influenced by iodine
intake immune system
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Morphological Thyroid Investigation
Clinic
scintigraphy SONOGRAPHY CT
Pathology
(biopsy) FNAB histology
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Main Tasks in the Thyroid Cytology
reduction of the unnecessary surgery
diagnosis of subclinical inflammation
EARLY DIAGNOSIS of NEOPLASMS
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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
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Thyroid Cytology- processing
Fixation– air dried – etanol / spray
(cytospin)
CYTOBLOCK
Staining: MGG HE polychrom all histo. imunocyto
TGB,calcitonin, parathormon
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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
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ThyreoiditisNON-SPECIFIC purulent non-specific granulomatose de Quervain lymphocytic (Hashimoto)
hypertrophic atrofic focal
invasive sclerosing Riedel
SPECIFIC tbc syfilis sarcoidosis
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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
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Thyreoiditis lymphoplasmocellularis Hashimoto - HT
Hashimoto, H.:Zur Kenntniss der lymphomatösen Veränderung der Schilddrüse
(struma lymphomatosa)
Arch.f. klin. Chir. 97, 1912, 219
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Original HT Description
Macro - diff. parenchymatose goitre firm, elastic, gray-yellow
Micro - diffuselymfoplasmocellularlymph. foliculesONCOCYTES
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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
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Course of HT
a) progressive oncocytic transformation
loss of thyreocytes, transformation to a lymph- node-with-ca- meta image
hyperfunction folowed by
hypofunction
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Course of HT
b) regressive loss of parenchyma, fibrosis hypofunction
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Course of HT
c) neoplasia carcinoma lymphoma (mostly B - MALT)
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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
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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
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Thyreoidal Syndromes
hypothyreosis– inborn – cretinism
endemic, sporadic
– acquired – myxedema hyperthyreosis - thyreotoxicosis
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Hypothyreosis CRETINISMUS
disturbances of growth & differentiation
BRAIN
LUNG
BONE
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Acquired Hypothyreosis - MYXEDEMA
decreased metabolism – bradycardia, low blood pressure, water
retention, obstipation intolerance of cold lowered lipolysis
– weight increase
– hyperlipemia ATHEROSCLEROSIS
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Thyreoidal Syndromes
hypothyreosis– inborn – cretinism
endemic, sporadic
– acquired – myxedema hyperthyreosis - thyreotoxicosis
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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
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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
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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
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Oncocytic Tumours
adenoma– architecture follicular, trabecular– cellular atypiae without predictive value
for biological behaviour– more risk in case of solid architecture
EXCLUDE
ANGIOINVASION, CAPSULOINVASION
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Oncocytic Tumours
carcinoma– oncopapillary (may lack ground glass nuclei !)
– oncofollicular
must exhibit
ANGIOINVASION and/or
CAPSULOINVASION (all capsule thickness with extracapsular expansion)
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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
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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
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Medullary Carcinoma
origin fom C-cells
clinical forms :
(parafollicular)
sporadic familiar
– MEN 2a
– MEN 2b
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Medullary Carcinoma familiar forms
MEN 2a medullary ca parathyr. adenoma pheochromocytoma
MEN 2b MEDULLARY CA marphanoid habitus mucous neuromas pheochromocytoma parathyr. adenoma -
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Medullary carcinomaC-cells (parafollicular)
sporadic familiar
MEN 2a MEN 2b
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Medullary carcinoma
Histological diagnosis
Calcitonin + amyloid +- argyrophilia +
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Medullary Carcinoma
Histological diagnosis
architecture may mimic any otherthyroid ca!!! (WHO)
Calcitonine + amyloid +- argyrophilia +
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Medullary Carcinoma
Cytological types
large cell
small cell
fusocellular
plasmocytoid
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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)
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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!
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Other Types of PrimaryThyroid Carcinomas
epidermoid mucoepidermoid mixed follicular and mucoepidermoid
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Metastases into Thyroid
kidney lung breast other
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Islets of Langerhans (1869)
adults 100 000 -1000 000 cell types:
B - insulin
A - glucagon
D – somatostatin
PP – pancreatic polypeptide
D – vasoactive intestinal polypeptide
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Islets of Langerhans -
regressive changes
fibrosis (postinflamm.) - DM I mucoviscidosis – DM 10x frequency hyalinosis, amyloidosis
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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
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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