his to pathology 2

7/29/2019 His to Pathology 2

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Histopathology of EndocrineSystem

by

Dr. Irene Suryahudaya

Pathologist-dermatologist


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Endocrine system

Primary function : control ofHOMEOSTASIS .

Endocrine disease ---- result frompathogenetic mechanism----inclabnormality :in the synthesis and

secretion of hormonal stimulation.

Homeostasis ??-------------.


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In general;endocrine

disorder Production of

hormone :

Underproduction

Overproduction

Clinical apearance

Hypofungtional

Hyperfungtionalstate


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Pituitary gland

Embryology and anatomy of pituitary gland


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Diseases of pituitary gland

Hyper pituitarism.

Increased production.

And releasehormones.

Gen; Cause byadenomaof theanterior pituitary.

Microscopic:monomorphadenoma ,in rutin

section HE can app aseosinophilic,basophilicor chromophobicappearance.

Hypopytuitarism. May result fr hypothalamic

/primary pitutari disorder.

Lesion ascraniopharyngioma

or,glioma.

Primary pit disordersunderline most cases ;causes include a; Nonsecretory

adenomas,sheehanssyndrome,empty sellasyndrome.

Radiation and accident.


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Non secretory pituitary

adenomas Present as space occupying lesions

Grossly indistinguishable fr

fungtional adenomas

Microscopic:

App is variable,incl some poorlygranulated,chromophobicadenomas


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Sheehanss yndrome

Usually causes by infarction of theanterior pituitary

Ass: with obtetrichemorrhage/shock It may also occur in male ?and non

pregnant woman ? (trauma, vascularaccident, DIC, sickle cell anemia)

Gen ass with destruction of 90 to 95 %of the gland


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Empty sella syndrome

Primary lessions : herniation of arachnoidand CSF through a defect in thediafragma sellae,----result compression

of the pituitary Secondary lesions following destruction

of normal gland via ischemicinjury,infarction of adenoma or radiation

Enlargement of the sella may bemistaken radiolographically for a pituitaryneoplasm


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Craniopharyngioma 5% of intracranial neoplasm

Most are found in patients during 2-3 decades

Characteristic: cystic ,calsification 75%

Microscopically: composed of a mixture ofsquamous apithelial elements and delicatereticular stroma

Appearance of the enamel organ of a developingtooth

Gliosis is common at the perifer Malignancy is rare


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THYROID GLAND

Embryologi and anatomi


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Diseases of thyroid gland

Thyroiditis

Goiter

Neoplasm

Congenital lesions

Hyperthyroidism

hypothyroidism


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Congenital lesions

Thyroglossal duct cysts

Represent persistence of thyroid anlage

extending from the foramen cecum Midline cysts anterior to the trachea

Histopatologic : varying mixtures of

squqmous and columnar epithelialandlymphoid cells

May become secondary infection


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Hyperthyroidism

A hypermetabolic state secondary toincreased levelsof circulating T3 andt4

Clinical : nervousness,heat intoleranceexcessive perspiration, fatigue,palpitation, tachycardi, weight lossdespite good appetite.Wide-eyed

Laboratory:elevated T3 and T4

Thyroid storm


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Hypothyroidism

A hypometabolic state caused bydeficiency of thyroid hormones

Clinic: Cretinism if thyroiddefisiency develops duringperinatal period or infancy,and

myxedema in older chidren andadults


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Thyroiditis

Infectious thyroiditis

Hashimotos Thyroiditis

Subacute granulomatous thyroiditis Lymphocytic thyroiditis

Riedel thyroiditis


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Infectious thyroiditis

Agents: staphylococusaureus,streptococci,sarmonella,ent

erobacter,mycobacteria and fungi May be hematogenous or

associated with local trauma RRR


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Hashimoto thyroiditis

Autoimun disorder

Female predominance(10:1)

Peak incidence is 30 to50 years of age Associated with HLA-DR5 and other

autoimun disorders eg: SLE

Clinical:symmetric or focal rubbery

enlargementof the gland with an intakecapsule

Microscopic:exuberant lympocyticinfiltrate with germinal centers.


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Subacute granulomatous

thyroiditis De QuervainS Thyroiditis

An inflamatory disorder of uncertain

etiology;viral origin is sugested Female predominance

Clinical : fever,painfull enlargement ofthe gland ,trancient T3-T4are elevated

Micoscopic:enlargement of thegland,evokes neutophilicinfiltrates,macrophagesandmultinucleated giant cells


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Subacute

lymphocyticthyroiditis An inflamatory disorder of

unknown etiology defined

histologically by nonspesificlymphoid infiltrationof the thyroidparenchyma

No germinal center formation

No significantplasma cell infiltrate

No clear with viral infection


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Riedels thyroiditis(struma)

An uncommon fibrosing process ofunknown etiology

Replacement of thyroid parenchyma bydense fibrous tissue penetrating thecapsule and extending into contiguousneck structures

Female predominance(3:1) Peak incidence fourth to seventhdecades


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Diffuse nontoxic

goiter(simple goiter) The gland is diffusely enlarged

No evidence of hyper or hypothyroidism

Occurs in endemic and sporadic forms Endemic goiter is most prevalent in

areas with dietary iodine deficiencye.g;Alps,himalaya)

Sporadic goiter is less common thanendemic goiter

Female predominance(8:1)

Peak incidence in puberty/young adultlife


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Neoplasms

Adenomas

Multiple histologic allrepresenting

follicular neoplasms Mic: fibrous capsule

Architecture distinctfrom the ajacent

gland Abcence ofmultinodularity inthe remaining gland

Carcinomas

Femalepredominance

Causes 7000 U.Sdeaths annually

Morphologicvariants:

Papillary.follicular,medullary,others(sarcoma,lymphomas)


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Papillary carcinoma

Most common form of thyroid cancer in children &adults

All thyroid neoplasms with papillary architecture

Typically infiltratif;fibrosis and calcification arecommon,often multifocal

Clearground-glassnuclei are common and

diagnostic of papillary carcinomaPsamomas bodies are found in papillaein one half of

patients


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Follicular carcinoma

One fourth of thyroid malignancies

Peak incidence in the fith to sixth decades

Gross resembling follicularadenoma.fibrosis,hemorhage,necrosis and cyst

formation are relatively common

Ground glass nuclei and psamomas bodies are

absent

Clinical features,more aggressive than papillary ca


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Medllary carcinoma

Rare tumor

Arising from calcitonin producing cells of

the thyroid

Blood calcitonin is high


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Parathyroid glands

Hyperfunction :

a. primary---due to

hyperplasia b.Secondary----

reaction to

hypocalcemia

Hypoparathyroidsm

-accidental surgical

removal of theparathyroid

duringthyroidectomi

-autoimun disease

-conggenital

defisiency


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Adrenal cortex

Developmental

anomalies

Hypofunction ofadrenal cortex

(hypoadrenalism)

Hyperfungtion of

adrenal cortex

Hyperadrenalism Cushings disease


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Hypofungtion of adrenal cortex

Cused by anatomic ormetaboliclesions in

the adrenal cortex(primaryadrenocortical

insuffisiency) Caused by hypothalamicpituitary disease

(secondary)


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Cushings syndrome


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Pheochromocytoma


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Thymus

Thymic agenesis and hypoplasia

Thymic hyperp[lasia

tumors


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The skin


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his to pathology 2

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