His to Pathology Endocrine

7/29/2019 His to Pathology Endocrine

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Histopathology ofEndocrine System

by

Dr. Irene Suryahudaya

Pathologist-dermatologist


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Endocrine system

Primary function : control of HOMEOSTASIS

Endocrine disease ---- result from

pathogenetic mechanism----inclabnormality :in the synthesis and secretionof 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

Hyperpituitarism.

Increased production.

And releasehormones.

Gen: Cause byadenoma of theanterior pituitary.

Microscopic:monomorphadenoma ,in rutine

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 pituitaryadenomas

Present as space occupying lesions

Grossly indistinguishable frfungtional adenomas

Microscopic:

App is variable,incl some poorly

granulated,chromophobic adenomas


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Sheehanss yndrome

Usually causes by infarction of the anteriorpituitary

Ass: with obtetrichemorrhage/shock

It may also occur in male ?and nonpregnant woman ? (trauma, vascularaccident, DIC, sickle cell anemia)

Gen ass with destruction of 90 to 95 % ofthe gland


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Empty sella syndrome

Primary lessions : herniation of arachnoidand CSF through a defect in the diafragmasellae,----result compression of thepituitary

Secondary lesions following destruction ofnormal gland via ischemic injury,infarctionof adenoma or radiation

Enlargement of the sella may be mistakenradiolographically for a pituitary neoplasm


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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 of

squamous apithelial elements and delicatereticular stroma

Appearance of the enamel organ of a

developing tooth 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 anlageextending from the foramen cecum

Midline cysts anterior to the trachea

Histopatologic : varying mixtures ofsquqmous and columnar epithelialand

lymphoid cells May become secondary infection


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Hyperthyroidism

A hypermetabolic state secondary toincreased levelsof circulating T3 andt4

Clinical : nervousness,heat intolerance

excessive perspiration, fatigue,palpitation, tachycardi, weight loss despitegood 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 thyroid defisiencydevelops during perinatal period orinfancy,and myxedema in olderchidren and adults


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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,salmonella,enterobacter,mycobacteria and fungi

May be hematogenous or associatedwith 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 otherautoimun disorders eg: SLE

Clinical:symmetric or focal rubberyenlargementof the gland with an intake

capsule Microscopic:exuberant lympocytic infiltrate

with germinal centers.


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Subacute granulomatousthyroiditis

De QuervainS Thyroiditis

An inflamatory disorder of uncertainetiology;viral origin is sugested

Female predominance Clinical : fever,painfull enlargement of the

gland ,trancient T3-T4are elevated

Micoscopic:enlargement of the

gland,evokes neutophilicinfiltrates,macrophagesand multinucleatedgiant cells


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Subacutelymphocyticthyroiditis

An inflamatory disorder of unknownetiology defined histologically bynonspesific lymphoid infiltrationof the

thyroid parenchyma No germinal center formation

No significantplasma cell infiltrate

No clear with viral infection

Ri d l th iditi


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Riedels thyroiditis(struma)

An uncommon fibrosing process ofunknown etiology

Replacement of thyroid parenchyma by

dense fibrous tissue penetrating thecapsule and extending into contiguousneck structures

Female predominance(3:1)

Peak incidence fourth to seventh decades

Diffuse nontoxic goiter(simple


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Diffuse nontoxic goiter(simplegoiter)

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 adult life

Mic: The gland is modestlyenlarged,hyperemic,hypertrophyandhyperplasia of follicular epithelium


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Neoplasms

Adenomas

Multiple histologic allrepresenting follicularneoplasms

Mic: fibrous capsule Architecture distinct

from the ajacent gland

Abcence of

multinodularity in theremaining gland

Carcinomas

Female predominance

Causes 7000 U.S

deaths annually Morphologic variants:

Papillary.follicular,medullary,others(sarcoma,

lymphomas)


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Papillary carcinoma

Most common form of thyroid cancer inchildren & adults

All thyroid neoplasms with papillary

architectureTypically infiltratif;fibrosis and calcificationare common,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 follicular

adenoma.fibrosis,hemorhage,necrosis andcyst 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 producingcells of the thyroid

Blood calcitonin is high


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Parathyroid glands

Hyperfunction :

a. primary---due tohyperplasia

b.Secondary----reaction tohypocalcemia

Hypoparathyroidsm

accidental surgicalremoval of the

parathyroid duringthyroidectomi

autoimun disease

conggenital

defisiency


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Adrenal cortex

Developmentalanomalies

Hypofunction of

adrenal cortex(hypoadrenalism)

Hyperfungtion ofadrenal cortex

Hyperadrenalism

Cushings disease


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Hypofungtion of adrenalcortex

Cused by anatomicormetaboliclesions in the adrenalcortex(primaryadrenocortical

insuffisiency)

Caused by hypothalamicpituitarydisease

(secondary)


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Cushings syndrome

Pheochromocytoma


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Thymus

Thymic agenesis and hypoplasia

Thymic hyperplasia

tumors

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His to Pathology Endocrine