Transcript The endocrine systemic disese

The endocrine
systemic disease
Li xiao yun 李晓昀
Thyroid gland disease
A.
Introduction
 Hypothalamus (TRF)
+
 Pituitary (TSH)
+
 Thyroid gland (T3,T4)
1. Anatomy and histology of thyroid
gland
 Thyroid consists of two bulky lobes.
Weight: 15~20 gram; color: red-brown.
 Histologic basic unite is thyroid follicle lined by
single layer of cuboidal epithelial cells.
 Follicular lumina contain colloid ,which is
accumulating thyroglobulins(TG) secreted by
follicular cells.
 Follicular cells produce and secrete the
thyroid hormone.
 Parafollicular cells ,located between
follicles or between follicular cells,
secrete calcitonin.
2. Physiologic function of thyroid
hormone—T3 and T4
 Enhancement of basal metabolic rate and the
nervous system excitability.
 Promotion of growth and development.
 Great influence on growth of skeleton and
central nervous system especially in the fetal
and infant period.
3. Classification of thyroid gland
diseases
Most of thyroid gland diseases are usually more
common in women than in men
 Thyroid tumor
 Goiter
 Thyroid inflammation
B. Thyroid tumor
1. Thyroid adenoma
Benigh tumor derived from thyroid follicular
epithelium
Grossly:
 Solitary,spherical nodule with intact
capsule,and 1~10 cm in diameter.
 The nodule may compress adjacent thyroid
tissue.
 The cut surface is gray–white or red-
brown,depending on the colloid content of
adenoma .
 The tumor lesion may have
hemmorage,fibrosis, calcification ,and cystic
change.
Slide 26.13
Microscopy:
(1). Embryonal adenoma:Tumor cells are small and
closely packed to form cords or trabeculae,while
follicles are seldom formed.
(2). Fetal adenoma : Tumor tissue resembles fetal
thyroid tissue. Tumor lesion is mainly composed of
small and uniform-appearing follicles with a tiny
amount of colloid. Follicular cells are cuboidal
(3). Simple adenoma: Tumor mainly consists of
follicles.The size and colloid content of follicles
are similar to those of normal thyroid follicles.
(4). Colloid adenoma: Tumor mainly consists of
large,colloid-rich follicles lined by flattened
epithelial cells.Follicles may be not the same in
size,sometimes merge into cystides.
Slide 26.14
(5). Acidophilic cell adenoma: Seldom.
Tumor cells are large, polygonal, eosinophilic,
and contain abundant cytoplasm.There are
eosinophilic granules within cytoplasm.Cells
form cords or sheets,while follicle are seldom
formed.
2. Thyroid carcinoma
Malignant tumor derived from thyroid follicular
epithelial cells or parafollicular cells,often
accompanied by hemmorage,
necrosis,fibrosis,calcification or cystis
formation.
Pathologic classification
 Papillary carcinoma:60-70%
 Follicular carcinoma:20%
 Medullary carcinoma:5%
 Undifferentiated carcinoma:15%
(1) Papillary carcinoma
Grossly:
 Tumors are usually solitary,spherical and firm
lesions with 2~3cm in diameter.
 The cut surface is gray-white,and sometimes
papillary foci may be seen.
 Most tumors have no capsules,but their
circumscriptions are still recognizable.
Microscopy:

Tumors mainly consists of a large number of papillae
with many branches.
There is fibrovascular stalk within papilla.
 Tumor nuclei are ground-glass:
loose chromatins,unclear nucleolus,big and empty
nucleus.
 A single to multiple layers of cuboidal epithelial cells
covering the papillae arrange disorderly, and are
obviously atypical.
 Calcified structures termed psammoma bodies are
often present within tumor stroma,especially within the
stalks of papillae.
Slide 26.16
Behavior:
slow growth,
low grade malignant
good prognosis
regional lymphoid nodule metastasis
5-year survival rate:90%
10 -year survival rate:85%
(2)Follicular carcinoma
Grossly:
Most tumors are single, wellcircumscribed nodules,and capsules are usually
not intact.The cut surface is gray-white.
Slide 26.17
Microscopy:
The tumor lesions have different
differentiation degree of follicles,but no
papillae.The nuclei lack ground-glass
features.
Well-differentiated carcinoma
 It resembles thyroid adenoma,but
capsules and blood vessels have been
invaded by tumor cells.
 Tumor cells form many follicles,cell
atypia is relatively less obvious.
Slide 26.18
Poor-differentiated carcinoma
Tumor cells are apparently atypical and
form solid nests or sheets,while follicles
are less seen and usually not intact.
Behavior:
Middle grade malignant
Early bloodstream metastasis
5-year survival rate: 30-40%
(3). Medullary carcinoma:
Malignant tumors derived from
parafollicular cells, APUD tumor.Tumor
cells secrete calcitonin and other hormones.
Grossly :
Tumors can arise as solitary nodules or multiple
lesions and may have fake capsules.The cut
surface is gray-white or tan, and the consistency is
soft.
Slide 26.19
Microscopy:
Tumors are composed of round, polygonal or spindle
cells,which may form solid nests or sheets. Pink amyloid
deposits are often present in tumor stroma.Electron
microscopy reveals variable number of nervous
endocrine granules within cytoplasm.
Slide 26.20
Slide 26.21
Behavior:
Middle grade malignant
5-year survival rate:50%
(4)Undifferentiated carcinoma:
Grossly:
Tumors are massive,ill-circumscribed nodules
without capsules,and surrounding tissues are
invaded by tumor cells. The cut surface is graywhite. Hemorrhage and necrosis often occur in
tumor lesions.
Microscopy:
Tumors mainly consist of highly anaplastic
cells,including 3 types of pathological
classification.
(Anaplasia: malignant tumor cells lack
differentiation and show high atypia.)
 Small cell type:
Tumor cells are small and similar to
lymphocytes,closely arranging to form nests
or cords with some abortive follicles.
 Spindle cell type :
Tumor cells are spindle and resemble
fibrosarcoma cells , so this type should
be distinguished from sarcomas.
 Giant cell type:
Tumor cells are giant and often multinuclear.
Behavior:
High grade malignant
Rapid growth
Early infiltration and metastasis
Most cases die within 2 years.
C . Goiter
Thyroid enlargement due to non-tumor
hyperplasia
1. Nontoxic goiter
(Endemic goiter)
 Definition :
The deficient secretion of thyroid hormone leads
to a compensatory rise in serum TSH
level,which ,in turn,causes hyperplasia of thyroid
follicular epithelia and colloid accumulation,and
ultimately gross enlargement of the thyroid
gland,usually without hyperthyroidism.
 Clinical symptom:
The enlargement of thyroid gland in neck.
Excessive enlargement may compress
surrounding structures of thyroid gland and
cause the difficulties in swallow and breath.
 Etiology and pathogenesis
(1) Iodine deficiency .
TSH
epithelium hyperplasia
thyroid hormone
Iodine
Deficiency
gland
enlargement
thyroglobulin within
follicular lumina can’t iodinate
and then can’t be resorbed by
epithelia
colloid accumulation within
follicles
(2) goitrogenic factions:
(3) Heredity and immunology
•Pathologic changes:
(1) Hyperplastic stage (diffuse hyperplastic goiter)
Grossly:
The thyroid gland is diffusely,
bilaterally,symmetrically and moderately
enlarged,the gland rarely exceeds 150
gram,and the surface is smooth.
 Microscopy:
Follicular epithelial cells proliferate and become
cuboidal or low and columnar, sometimes
forming small follicles and fake papillae.
Follicular lumina contain less colloid,and stroma
shows hyperemia.
(2)Colloid accumulation stage
(diffuse colloid goiter)
Involution occurs in this stage.
Grossly:
The gland is diffusely, bilaterally , symmetrically ,
and conspicuously enlarged ,and the weight is
approximately 200-300 gram.
The surface of gland is smooth,and the cut
surface is brown,somewhat glassy, translucent,
and colloidal.
Microscopy:
The majority of follicular lumina are highly
enlarged, containing abundant colloid,and the
epithelial cells involute and become flattened.
(3) Nodular stage (Nodular goiter)
The recurrent hyperplasia and involution of
follicular cells
The formation of fibre interval and nodules
Grossly:
Nodular goiters are multinodular, bilaterally,
asymmetrically enlarged,which may achieve a
weight of more than 2000 gram.
Nodules are not uniform in size and are wellcircumscribed, without capsules or with incomplete
capsules.
On cut section , hemorrhage, fibrosis,
calcification, and cystic change are often seen.
Slide 26.12
Microscopy:
Follicles are not uniform in size.
Partial follicles are highly enlarged and colloid-rich,and
the epithelial cells involute and become flattened.
Partial follicular cells proliferate and become columnar
or form fake papillae or small follicles.
The hyperplastic connective tissue divide and enclose
thyroid tissue to result in the formation of irregular
nodules.
Results:
Hypofunction of thyroid
Malignant change :1-5%.
2. Diffuse toxic goiter
 Definition :
Hyperthyroidism: Hyperthyroidism is a clinical
syndrome caused by excessive thyroid hormone in
serum acting on tissue of the whole body,
manifesting the rise of basal metabolic rate and
the nervous system excitability.
Diffuse toxic goiter (Graves disease, Exophthalmic
goiter) :
Conspicuous hyperplasia of thyroid follicular cells
makes thyroid gland enlarged,accompanied by
hyperthyroidism.
Clinical menifestation:
The enlargement of thyroid, exophthalmia,
palpitation, rapid pulse, excitable, easily
sweaty ,finger shake,eating too much,easily
hungry, emaciated.
 Pathologic changes:
Grossly:
Thyroid gland is usually diffusely, bilaterally,
symmetrically enlarged,and its surface is
smooth.The cut surface is gray-red or brown
and shows meaty appearance.The gland
usually weigh more than 80 gram.
Slide 26.8
Microscopy:
a. Follicular epithelial cells diffusely proliferate
and become tall and columnar.The hyperplasia of
epithelial cells may result in the formation of fake
papillae,small follicles ,or solid cell nests.
b. The colloid within follicular lumen is
thin with scalloped margins.
c. In the interfollicular stroma,there are
abundant blood vessels, hyperemia, the
infiltration of lymphocytes and the
formation of lymphoid follicles.
Slide 26.11
 Etiology and pathogenesis:
An autoimmune disorder produced by
autoantibodies to the TSH receptor.
Important Abs include:thyroid-stimulating
immunoglobulin(TSI),thyroid growth-stimulating
immunoglobulin(TGI).
The two Abs combine with TSH receptors to
respectively stimulate excessive secretion of
thyroid hormone and the hyperplasia of follicular
epithelia.
D .Hypothyroidism

Definition:
Hypothyroidism is a syndrome caused by
deficiency in synthesis and release of thyroid
hormone.
• Classification
1. Cretinism:
Hypothyroidism developing in fetal
period ,infancy ,or early childhood results in
impaired development of the skeleton system and
the central nervous system, characterized by
mental retardation,low intelligence,dementia
expression,stupid facial features,short
stature,and dwarf,and so on.
2. Myxedema:
Hypothyroidism developing in youth or adult
results in the decrease of basal metabolic
rate and the nervous system excitability and
the accumulation of mucoid matrix in stroma.
The clinical manifestations include
listlessness,fatigue,sleepiness,apathetic
expression,mental retardation,intolerant
cold,cool and coarse skin, edema,and other
symptoms related to mucoid matrix deposition
in other different organs.
•Cause of hypothyroidism:
Thyroid injury: thyroiditis,
thyroid surgery or radiation
Suppressed synthesis of thyroid hormone.
Autoimmune disease
Pituitary or hypothalamus disease.
E .Thyroiditis
1. Subacute thyroiditis (Granulomatous
thyroiditis):
A granulomatous inflammation usually
caused by virus infection.
 Grossly:
The gland is unilaterally or bilaterally,
asymmetrically,lightly enlarged,and may be
adherent to surrounding structures.
The cut surface is yellow-white and firm,and
may contain areas of necrosis or fibrosis.
 Microscopy :
Partial follicles are destroyed and then release
colloid. Neutrophils, macrophages,
lymphocytes,and plasma cells aggregate about
collapsed follicles.Macrophages engulf released
colloid and then convert into multinuclear giant
cells,which results in the formation of granulomas
similar to tuberculoma ,but without caseous
necrosis.
In later stages, lesions have fibrosis or scar
formation,and regeneration of follicular cells.
Slide 26.10
Clinical manifestation:
Thyroid gland is enlarged and pain.
2. Chronic lymphocytic
thyroiditis(Hashimoto’s thyroiditis):
Autoimmune disease.
 Grossly:
Gland is diffusely enlarged and firm,the cut
surface is gray-white or gray-yellow.
 Microscopy:
Thyroid gland structure is extensively
destroyed,and follicles atrophy and disappear .
In lesion,there are infiltration of a large
number of lymphocytes,formation of lymphoid
follicles,and hyperplasia of fibers.
Slide 26.9
 Clinical manifestation:
Enlargement of gland
Hypothyroidism(usually in later stage)
3. Fibrous thyroiditis (Chronic woody
thyroiditis):
 Grossly :
Gland is asymmetrically enlarged, hard
as wood, and obviously adherent to
surrounding structures.
The cut is pray-white,and show nodular
appearance.
 Microscopy:
Atrophy and destruction of the majority
of follicles.
Hyperplasia of a large amount of
fibre tissue.
Hyaline change
Scar formation
The infiltration of a tiny number
of lymphocytes
 Clinical:
Enlargement of gland,hard consistency
Hypothyroidism
Compression symptoms
The distinction between adenoma and nodular goiter
Adenoma
Nodular goiter
Capsule
Intact
Not intact
Nodular number
Usually single
Multinodular,usually
bilateral
Structure
Relatively uniform
Not uniform. Follicles of
unequal size
Adjacent thyroid tissue
Follicles are
compressed and
deformed
There are pathologic
changes similar to those
of nodules,but no
compression
phenomenon