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Histopathology of

Endocrine System
by
Dr. Irene Suryahudaya
Pathologist-dermatologist

Endocrine system
Primary function : control of HOMEOSTASIS
Endocrine disease ---- result from
pathogenetic mechanism----incl
abnormality :in the synthesis and secretion
of hormonal stimulation.
Homeostasis ??-------------

In general;
endocrine disorder
Production of
hormone :

Clinical apearance
Hypofungtional

Underproduction
Overproduction

Hyperfungtional
state

PITUITARY GLAND
Embryology and anatomy of pituitary gland

Diseases of pituitary gland


Hyperpituitarism.
Increased production.
And release
hormones.
Gen: Cause by
adenoma of the
anterior pituitary.
Microscopic:monomorph
adenoma ,in rutine
section HE can app as
eosinophilic,basophilic
or chromophobic
appearance.

Hypopytuitarism.
May result fr hypothalamic
/primary pitutari disorder.
Lesion as
craniopharyngioma
or,glioma.
Primary pit disorders
underline most cases ;
causes include a; Non
secretory
adenomas,sheehans
syndrome,empty sella
syndrome.
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 poorly
granulated,chromophobic adenomas

Sheehanss yndrome
Usually causes by infarction of the anterior
pituitary
Ass: with obtetrichemorrhage/shock
It may also occur in male ?and non
pregnant woman ? (trauma, vascular
accident, DIC, sickle cell anemia)
Gen ass with destruction of 90 to 95 % of
the gland

Empty sella syndrome


Primary lessions : herniation of arachnoid
and CSF through a defect in the diafragma
sellae,----result compression of the
pituitary
Secondary lesions following destruction of
normal gland via ischemic injury,infarction
of adenoma or radiation
Enlargement of the sella may be mistaken
radiolographically for a pituitary neoplasm

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 delicate
reticular 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


Congenital lesions

Thyroiditis

Hyperthyroidism

Goiter

hypothyroidism

Neoplasm

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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 epithelialand
lymphoid cells
May become secondary infection
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Hyperthyroidism
A hypermetabolic state secondary to
increased levelsof circulating T3 andt4
Clinical : nervousness,heat intolerance
excessive perspiration, fatigue, palpitation,
tachycardi, weight loss despite good
appetite.Wide-eyed
Laboratory:elevated T3 and T4
Thyroid storm

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Hypothyroidism
A hypometabolic state caused by
deficiency of thyroid hormones
Clinic: Cretinism if thyroid defisiency
develops during perinatal period or
infancy,and myxedema in older
chidren 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: staphylococus
aureus,streptococci,salmonella,enter
obacter,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 intake
capsule
Microscopic:exuberant lympocytic infiltrate
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 of the
gland ,trancient T3-T4are elevated
Micoscopic:enlargement of the
gland,evokes neutophilic
infiltrates,macrophagesand multinucleated
giant cells
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Subacute
lymphocyticthyroiditis
An inflamatory disorder of unknown
etiology defined histologically by
nonspesific lymphoid infiltrationof the
thyroid parenchyma
No germinal center formation
No significantplasma cell infiltrate
No clear with viral infection

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Riedels thyroiditis
(struma)
An uncommon fibrosing process of
unknown etiology
Replacement of thyroid parenchyma by
dense fibrous tissue penetrating the
capsule and extending into contiguous
neck structures
Female predominance(3:1)
Peak incidence fourth to seventh decades

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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 deficiency
e.g;Alps,himalaya)
Sporadic goiter is less common than
endemic goiter
Female predominance(8:1)
Peak incidence in puberty/young adult life
Mic: The gland is modestly
enlarged,hyperemic,hypertrophyand
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hyperplasia of follicular epithelium

Neoplasms
Adenomas
Multiple histologic all
representing follicular
neoplasms
Mic: fibrous capsule
Architecture distinct
from the ajacent gland
Abcence of
multinodularity in the
remaining gland

Carcinomas
Female predominance
Causes 7000 U.S
deaths annually
Morphologic variants:
Papillary.follicular,med
ullary,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
are common,often multifocal
Clearground-glassnuclei are common and
diagnostic of papillary carcinoma
Psamomas 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 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 the
parathyroid during
thyroidectomi
autoimun disease
conggenital
defisiency

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Adrenal cortex
Developmental
anomalies
Hypofunction of
adrenal 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
Pheochromocytoma

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Thymus
Thymic agenesis and hypoplasia
Thymic hyperplasia
tumors

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