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Simona Gurzu Ioan Jung

INTRODUCTION IN
HISTOPATHOLOGY

2012

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Authors:
Simona Gurzu, MD, PhD
Ioan Jung, MD, PhD
Reviewers: Emeric Egyed-Zsigmond, MD, PhD
Mihai Turcu, MD, PhD

Descrierea CIP a Bibliotecii Naionale a Romniei

GURZU, SIMONA
Introduction in histopathology/ Simona Gurzu, Ioan
Jung - Trgu-Mure: University Press, 2011
Bibliogr.
ISBN 978-973-169-166-4
I. Simona, Gurzu
II. Ioan, Jung

Production Editors: Simona Gurzu, Ioan Jung

Cover design: Ioan Jung, Magdalena One

University Press, U.M.F Trgu Mure, Romania

Head of Publishing House: Prof. Alexandru chiopu
Corresponding address: U.M.F Trgu Mure, Gh. Marinescu 38, 540130
E-mail: schiopua2000@yahoo.com
Tel. 0744527700, 0265215551 126, Fax: 0265210407

Printed at Digital Color Company, Tg. Mure, Gh. Doja 185, Romania

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Contents

INTRODUCTION.......................................................................................................4

GENERAL PATHOLOGY.......................................................................................5

DISORDERS OF BLOOD CIRCULATION..............................................................6

Acute pulmonary edema...............................................................................6
Chronic pulmonary congestion.....................................................................8
Hepatic congestion.....................................................................................10
Acute infarction of the kidney....................................................................12
Acute infarction of the lung........................................................................14
Mixed thrombus..........................................................................................16

DISORDERS OF CELL AND TISSUE METABOLISM.........................................18

Hyperkeratosis...........................................................................................18
Fatty liver (hepatic steatosis).....................................................................20
Renal amyloidosis......................................................................................22

INFLAMMATION................................................................................................... 24
Fibrinous pericarditis................................................................................24
Hepatic abscess.........................................................................................26
Foreign body granuloma...........................................................................28
Tuberculous lymphadenitis.......................................................................30

CONGENITAL MALFORMATIONS......................................................................32

BENIGN TUMORS...................................................................................................36
Ovarian cystadenoma ................................................................................36
Breast fibroadenoma..................................................................................38
Leiomyoma of the uterine body.................................................................40
Cavernous hemangioma of the liver...........................................................42

MALIGNANT TUMORS..........................................................................................44
Squamous cell carcinoma of the lip............................................................44
Basal cell carcinoma...................................................................................46
Colorectal adenocarcinoma.........................................................................48
Hodgkins lymphoma - nodular sclerosis type...........................................50

SYSTEMIC PATHOLOGY....................................................................................53

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PATHOLOGY OF THE HEART..............................................................................54

Acute myocardial infarction.........................................................................54
Scarring myocardial infarction.....................................................................56

PATHOLOGY OF BLOOD VESSELS....................................................................58

Atherosclerosis............................................................................................58
Coronarosclerosis........................................................................................60
Hemorrhoids................................................................................................62

PATHOLOGY OF THE RESPIRATORY SYSTEM...............................................64

Bronchopneumonia.....................................................................................64
Lung emphysema........................................................................................66
Respiratory distress syndrome....................................................................68
Miliary tuberculosis of the lung..................................................................70
Squamous cell carcinoma of the lung.........................................................72
Small cell lung carcinoma...........................................................................74

PATHOLOGY OF THE GASTROINTESTINAL TRACT......................................76

Chronic superficial gastritis.........................................................................76
Chronic gastric ulcer....................................................................................78
Gastric adenocarcinoma..............................................................................80

PATHOLOGY OF LIVER AND PANCREAS.........................................................82

Liver cirrhosis.............................................................................................82
Acute pancreatitis........................................................................................84

PATHOLOGY OF KIDNEY AND URINARY TRACT..........................................86

Crescentic glomerulonephritis......................................................................86
Renal cell carcinoma, clear cell type............................................................88

PATHOLOGY OF THE FEMALE GENITAL TRACT AND BREAST.................90

Squamous cell carcinoma of the uterine cervix.............................................90
Endometrial adenocarcinoma........................................................................92
Fibrocystic changes of the breast..................................................................94

PATHOLOGY OF THE MALE GENITAL SYSTEM.............................................96

Nodular (benign) prostatic hyperplasia........................................................96
Seminoma.....................................................................................................98

PATHOLOGY OF THE THYROID GLAND........................................................100

Multinodular goiter.....................................................................................100
Hashimotos thyroidits................................................................................102

REFERENCES.......................................................................................................104

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INTRODUCTION

We have prepared this book to help our students in medical school to

understand the basic lesions of Pathology. The short descriptions which
accompany the pictures are very simple and easy to be understood. Our goal
as authors, scientists and educators, was to reveal the characteristics of those
main disorders which are present in the daily diagnosis. We revealed those
thinks that the students must know to be able to make a correct differential
diagnosis.

This book contain two parts: General Pathology and Systemic Pathology and
represents only a introduction in the complexity of challenging Pathology.
We should mention that the book is only a supplemental material for practical
labs and the presentation is adapted for third-year medical school pathology
courses.

We hope that our students will find this book to be useful to the learning of
pathology.

You chose to be, you chose to see

To be a branch of the diagnosis tree
You chose to understand;
Please be yourself
This is the secret of the health.

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GENERAL PATHOLOGY

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I. DISORDERS OF BLOOD CIRCULATION

1. Acute pulmonary edema

Macroscopic view:
- distended and heavy lungs
- at compression, releasing of foamy liquid from the cut surface (bubble of
air + serum)

Microscopic morphology
- dilated capillaries and serum extravasation in alveolar septa (septal edema)
- the alveoli are filled with blood serum, which appears as a smooth pink
material (alveolar edema)

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serum

air

Fig. 1. Acute pulmonary edema with releasing of foamy liquid (upper).

Under microscope, the pink-stained fluid fils the alveolar spaces and dilated
capilaries are seen in alveolar septa
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2. Chronic pulmonary congestion

(brown induration of the lungs)

Macroscopic view
- heavy and firm lungs (induration)
- brown color, due to iron pigment (siderophages)

Microscopic morphology
- thick alveolar septae due to fibrosis as a result of long-time hypoxia
- interstitial and alveolar large brown cells represent macrophages inglobating
hemosiderin (hemosiderin-laden macrophages, siderophages or heart failure
cells)

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Fig. 2. Brown indurated lung (upper). Under microscope (below), alveolar

septal fibrosis and brown siderophages are observed

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2. Hepatic congestion

Macroscopic view
- acute and chronic congestion: enlarged liver; on section: the alternance
between yellow (hepatic parenchyma) and red colored areas (dilated central
vein and sinusoid capillaries)
- prolonged congestion liver induration (hardening); on section: irregular
gray-bluish areas of connective tissue (regeneration)

Microscopic morphology
- acute congestion - dilatation of the central veins (CLV) in hepatic lobules
- chronic congestion (nutmeg liver) - dilatation of the central veins and
sinusoid capillaries (C) and their fusion with neighboring lobules
- prolonged congestion (cardiac cirrhosis) - areas of fibrosis, respectively
connective tissue (F) followed by destruction of hepatocytes in those areas

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CLV

ACUTE

C
C
CLV

CLV

CHRONIC

F F
F

F
F

PROLONGED

Fig. 3. In hepatic congestion, in acute stages, central veins (CLV) of the

hepatic lobules are dilated; in chronic stages, sinusoid capillaries (C) are also
dilated and nutmeg liver can be observed. In prolonged congestion, pale areas
of fibrosis (F) replaces the congested liver

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3. Acute infarction of the kidney

Macroscopic view
- the infarcted area is pale, bulged, surrounded by a red, hyperemic narrow
rim (pale or white infarction due to end-arterial circulation and solid tissue)

Microscopic morphology
- small power view: the infarcted area is pale and is well defined, being
surrounded by a red narrow rim composed by dilated capillaries,
extravasated blood and neutrophils
- high power view: in the infarcted area the cellular architecture of
glomerules and tubules is preserved but the nuclei are missing (necrosis); the
narrow rim is composed by dilated capillaries, extravasated blood and
neutrophils

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infarct

narrow rim
narrow rim

infarct

narrow rim

infarct

Fig. 4. In the left upper part, infarcted area of kidney is pale, surrounded by a
hyperemic narrow rim; Microscopically, the rim is composed by dilated
capilaries and neutrophils. No nuclei are observed in the infarcted area

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5. Acute infarction of the lung

Macroscopic view
- the infarcted area is red, triangular shape, soft, with occluded vessel at the
apex (red or hemorrhagic infarction)

Microscopic morphology
- the infarcted area is red and well defined
- in the infarcted area the cellular architecture of the alveoli and septa is
preserved but the nuclei are missing (necrosis); in both alveolar lumen and
septa extravasated blood is observed
- in the non-infarcted area, features of chronic pulmonary congestion are
present (see the previous pages)

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Fig. 5. The lung infarcted area is red, triangular-shape, well defined (upper).
At high magnification, no nuclei and extravasated blood into alveoli and
septa (below)

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6. Mixed thrombus

Macroscopic view
- it is formed in living body
- solid friable red mass, occluding or partially occluding the blood vessels

Microscopic morphology
- it is located into the lumen of vessels
- alternated pink (platelets+fibrin) and red layers (erythrocytes)

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Fig. 6. A mixed arterial thrombus (upper), with an alternance between red

(erythrocytes) and pink layers (platelets) in the lower microphotographs

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II. DISORDERS OF CELL AND TISSUE METABOLISM

1. Hyperkeratosis (callosity)

Macroscopic view
- the affected skin area is hardening at palpation and is pale

Microscopic morphology
thickening of the stratum corneum (corneal layer), without nuclei in this
layer

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Basal layer
Corneal layer
Spinosum layer

Granulosum layer

Lucidum layer

Normal skin

Corneal layer

Hyperkeratosis - callosity

Fig. 7. Compared to normal skin, in hyperkeratosis a thickening of corneal

layer may be observed

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2. Fatty liver (hepatic steatosis)

Macroscopic view
- large, soft, greasy, yellow, and friable liver

Microscopic morphology
- several clear vacuoles (lipid droplets) within hepatocytes (ballooning
degeneration)
- the whole surface of hepatic lobules (central and peripheral areas) is
affected (fatty liver or hepatic steatosis)

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Fig. 8. Fatty liver is enlarged, yellow and friable (upper). Under microscope,
clear fatty vacuoles are accumulated in hepatocytes (below)

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3. Renal amyloidosis

Macroscopic view
- the kidney are enlarged, pale-shinny-glassy on section

Microscopic morphology
- accumulation of amyloid within the walls of glomerular capillaries as well
as small renal arterioles; both of them become thickened
- in Hematoxylin-Eosine the amyloid is an amorphous eosinophil material
- with Congo Red dye the amyloid is orange-stained

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Congo Red dye

l

Hematoxylin-Eosine

Fig. 9. Renal amyloidosis is characterized by a pale enlarged kidney (upper).

Under microscope, amyloid is an acellular substance stored in the glomeruli,
being eosinophil in H&E and orange in Congo Red staining
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III. INFLAMMATION

1. Fibrinous pericarditis

Macroscopic view
villous dry, dull roughened membrane on the epicardial surface (bread and
butter appearance)

Microscopic morphology
eosinophil fibrin deposits on the epicardial surface
- dilated vessels and neutrophils in subepicardial layer

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fibrin membrane

epicardium

myocardium

Fig. 10. Fibrinous pericarditis. Covering the epicardial surface, fibrinous

membranes with bread-butter appearance (upper). Under microscope, low-
power view shows fibrin deposits on the epicardial surface

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2. Hepatic abscess

Macroscopic view
- multiple well-defined cavities with pus and necrotic tissue, within liver
parenchyma

Microscopic morphology
- into the cavities, several neutrophils and necrotic debris, with hepatocyte
destruction
- around the cavity, necrotic area (acute abscess)

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abscess

abscess

abscess

Fig. 11. Several yellow ill-defined pus-containing cavities (abscesses) may be

seen on the liver cut surface (upper). Under microscope, an well defined
cavity with neutrophils and cellular debris compresses the surrounded
hepatocytes (left below)

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3. Foreign body granuloma

Macroscopic view
- a small palpable and well-defined nodule
- in this case, there are cholesterol crystals precipitate into the mammary
gland

Microscopic morphology
- several elongated clear spaces (cholesterol crystals) surrounded by
inflammatory cells and giant multinucleated histiocytes (foreign body giant
cells)

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granuloma

foreign body giant cells

cholesterol crystals

Fig. 12. The microphotographs show foreign body granulomas, which are
collection of activated macrophages and giant multinucleated cells localized
around cholesterol cristals precipitated in a female breast

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4. Tuberculous lymphadenitis

Macroscopic view
- enlargement of the lymph node (lymphadenopathy)
- on section, yellow-gray, shalky, cheesy-looking necrosis (caseous
necrosis)

Microscopic morphology of mixed tubercle

- several granulomas composed by central areas of caseous necrosis
(eosinophil material) surrounded by epithelioid cells (elongated,
uninucleated), multinucleated Langhans cells with horeseshoe arrangement
of peripheral nuclei and lymphocytes

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lymphocytes

Langhanscell

Caseous
epitheloid cells necrosis

Fig. 13. Tuberculosis in lymph node. Upper: one of the hilar lymph nodes is
enlarged, with cheesy-loking aspect on section (caseous necrosis). Under
microscope, at low power-view (upper right) the lymph node architecture is
destroyed by irregular tubercles. Below: at high-power view, the mixed
tubercle is composed by the succesive layers indicate in the figure

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IV. CONGENITAL MALFORMATIONS

Embryopathies = malformations which occur in first three months (12

weeks)

Fetopathies = diseases which occur in the second period of the intrauterine

life

Inhibition of development
Aplasia = failure of an organ development during embrionic life
Agenesis = failure of an organ and its embriological structures
Hypoplasia = development of a smaller organ during embriogenesis
Atresia = failure of recanalization of one lumen (ex: billiary atresia)
Stenosis = narrowing of a lumen

Excess of development
Polydactyly = one or more extradigits
Polymastia = accessory breasts
Polythelia = extra nipples
Macrocephaly = abnormally large head
Macroglossia = enlargement of the tongue

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Development of organs in abnormal places

Dystopia = abnormal position of an organ or a body part
Heterotopia = the presence of a tissue in an abnormal location
Situs inversus = right to left reversal of the thoracic and abdominal organs

Malformations of the cranium and brain

Anencephaly = congenital absence of the cerebral cranium
Exencephaly = the brain is located outside of the skul
Cranioschisis = incomplete closure of the skul (schixo, gr. = to split)
Meningocele = protrusion of the meninges through a defect in the cranium or
vertebral column
Myelocele = protrusion of the spinal cord through a defect in the vertebral
column

Malformations of the face and mouth

Cheiloschisis (cleft lip) = congenital cleft in the middle of the upper lip
(cheilos, gr. = lip)
Gnathoschisis (cleft jaw) = congenital cleft of the jaw (gnathos, gr. = jaw)
Palatoschisis (cleft palate) = congenital cleft of the palate (roof of the mouth)
Prosoposchisis = congenital cleft of the face (prosopon, gr. = face)
Macrognathia = abnormally large lower jaw
Agnathia = lack of the lower jaw
Synotia = fusion of the lobe of the ears
Cyclopia = presence of one eye in central part of the face; above it, a tubular
apendage replaces the missing nose
Aprosopia = lack of the face
Anophtalmia = lack of one or both eyes

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Malformations of the neck

Branchial cyst = a cavity developed under the skin, in the cervical area
Congenital hygroma = fluid accumulation in the soft tissue of the neck

Malformations of the vertebral column

Rachischisis = incomplete closure of the vertebral arches and covered skin
Spina bifida = the vertebral defect is covered by the skin

Malformations of the limbs

Syndactyly = fusion of fingers
Oligodactyly = lack of one or more fingers
Amelia = absence of one or more limbs
Abrachius = absence of both upper limbs
Monobrachius = absence of one of the upper limbs
Apus = absence of one or both lower limbs
Phocomelia = congenital absence of the proximal portion of a limb; the hands
are attached to abbreviated arms
Sympus = fusion of the lower extremities

Malformations of the twins

Holoacardius = an unequal twin fetus in which the heart is entirely absent
Fetus papyraceus = mummification and compression of one of the twins
Conjoined twins= Siamese twins = twins whose bodies are conjoined
Thoracopagus = conjoined twins in thorax region
Pygopagus = conjoined twins in the sacral region (pygos, gr. = posterior)
Dicephalic parapagus = one trunk and two heads

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Fig. 14. Rachischisis (left) and omphalocele (right), two of congenital

malformations

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V. BENIGN TUMORS

1. Ovarian cystadenoma

Macroscopic view
- large, encapsulated tumor with a smooth surface
- cut surface reveals multiple mucin- or serum-filled cavities with smooth
walls and rare papillary excrescences

Microscopic morphology
- the cysts and papillary structures are lined by a single layer of columnar
cells with apical mucin and small basally located nuclei (mucinous
cystadenoma)
- no atypical cells are observed

Immunohistochemistry
- the tumor cells are marked by Cytokeratin

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Fig. 15. Ovarian cystadenoma. Grossly, the tumor is large, multiloculated,

with papillary excrescences on cut surface, indicated by the arrows (upper).
Microscopically, the cyst wall is lined by a single layer of columnar cells
with basally arranged nuclei.

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2. Breast fibroadenoma

Macroscopic view
- an well circumscribed, usually encapsulated, movable round mass, which
occurs especially in young women
- on section, grayish lobulated nodule that bulge above the surrounding tissue
and may present slit-like spaces

Microscopic morphology
- proliferation of both mammary ducts and connective tissue
- depends on the growth type, there are two histological types:
a) pericanalicular fibroadenoma - proliferation of fibroblastic stroma around
ducts in a circumferential fashion
b) intracanalicular fibroadenoma - the proliferating fibroblastic stroma
compresses the ducts into clefts

Immunohistochemistry
- ductal cells are marked by Cytokeratin; fibroblast are marked by Vimentin

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Fig. 16. Breast fibroadenoma. Upper: pericanalicular fibroadenoma - note the

glandular and stromal proliferation, without deformities of ducts. Below,
intracanalicular fibroadenoma with ductal clefts.

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3. Leiomyoma of the uterine body

Macroscopic view
- well-circumscribed nodules, often multiple, firm, without capsule, which
bulge above the surrounding myometrium
- the sectioned surface shows white nodules with whorled trabecular texture
- depends on the growth, three types are described:
subserosal: located beneath the serosa
intramural: within myometrium
submucosal: located immediately beneath the endometrium

Microscopic morphology
- proliferation of spindle smooth muscle cells in interlacing fascicles
- mitoses are infrequently observed

Immunohistochemistry
- the tumor cells are marked by Vimentin and Smooth Muscle Antigen

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leiomyoma

normal myometrium

Fig. 17. Leiomyomas. In the uterine body, the arrows show two well-
circumscribed round nodules (upper left). Microscopically, interlacing
fascicles of smooth muscle cells without atypia may be seen (upper right and
lower microphotographs)

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4. Cavernous hemangioma of the liver

Macroscopic view
- well-defined red-blue, soft, spongy mass
- on section, the tumor mass is composed of compact tangles of vessels filled
with venous blood

Microscopic morphology
- the tumor is sharply defined by the surrounding hepatocytes, but is not
encapsulated
- it is composed of network of thin-walled, dilated (cavernous) veins, covered
by endothelial cells, partly filled with blood

Immunohistochemistry
- the endothelial cells are marked by CD31 and CD34 (CD = Clusters of
Differentiation)

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haemangioma

normal hepatocytes

Fig. 18. Cavernous hemangioma. Upper, the arrow shows a blue-red well-
defined tumor mass within liver. Below, in the low-power view note several
dilated thin-walled blood vessels filled with blood

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VI. MALIGNANT TUMORS

1. Squamous cell carcinoma of the lip

Macroscopic view
- a nodular lesion which can be ulcerated or can present hyperkeratosis
- it is most common located on the skin of the face or the lip and also on the
mucosa of oral cavity
- in this case the tumor was located on the lower lip

Microscopic morphology
- small power view: tumor clusters which exhibits large areas of keratin pearl
formation (well-differentiated squamous cell carcinoma)
- high power view: the tumor cells resemble those of the spinosum layer of
the squamous epithelium; they are large, polygonal-shaped, with atypical
nuclei

Immunohistochemistry
- the tumor cells are marked by Cytokeratin

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keratinization

Fig. 19. Squamous cell carcinoma. Histologic sections reveals clusters of

tumor cells which infiltrates the deep tissues (upper). In central part of lower
picture, the arrows indicate large areas of keratin pearls which are
characteristically seen in well-differentiated squamous cell carcinoma

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1. Basal cell carcinoma

Macroscopic view
- a slow growing nodular or ulcerated lesion which is usually located on the
sun-exposed skin (e.g. face)
- it does not occur on mucosal surfaces

Microscopic morphology
- the tumor cells are arranged in small nests located beneath the overlying
epidermis which invade the dermis
- the cells resemble those of the basal layer of the epidermis; they are small,
atypical cells, with scant cytoplasm
- the tumor nests have a pallisaded arrangment of cells around their periphery

Immunohistochemistry
- the tumor cells are marked by Cytokeratin

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pallisaded
arrangement

Fig. 20. Basall cell carcinoma has a nodular shape (upper) and is composed
of nests of basaloid cells showing peripheral pallisading (lower)

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2. Colorectal adenocarcinoma

Macroscopic view
- the colorectal carcinomas can be described as polypoid, ulcerated or
infiltrative tumors
- in this case, an ulcerated infiltrative tumor may be seen in the large bowel

Microscopic morphology
- proliferation of atypical glands which infiltrate the mucosa, submucosa and
muscularis of the colon wall (well-differentiated adenocarcinoma)

Immunohistochemistry
- the tumor cells are marked by Cytokeratin and Cytokeratin 20

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Fig. 21. Colorectal adenocarcinoma. Grossly, it is an ulcerated tumor which

infitrates the colonic wall (upper). Under microscope, at low-power view, in
the left part of below picture the normal aspect of colonic mucosa may be
seen. In the right part, the normal structure is replaced by atypical glands
which infiltrate mucosa, submucosa and muscularis propria

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3. Hodgkins lymphoma nodular sclerosis type

Macroscopic view
- enlarged lymph nodes (lymphadenopathy) with fleshy or hard consistency
and a smooth surface
- cervical and axillary lymph nodes are especially involved
- on cut surface: sclerotic bands which confer a nodular architecture

Microscopic morphology
- thick nodal capsule
- the normal architecture of the lymph nodes is replaced by cellular nodules
separated by large bands of pink collagen fibers
- into the cellular nodules following cells can be observed:
Reed-Sternberg cells - lacunar variant - uninucleated cells with large
multilobated nuclei, prominent nucleoli and clear cytoplasm
Hodgkins cells - large uninucleated cells
background reactive cells: lymphocytes, eosinophils, plasma cells, etc.

Immunohistochemistry
- Reed-Sternberg cells are specifically marked by CD15 and CD30

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Fig. 22. Hodgkins lymphoma, nodular sclerosis type. At low-power view

(upper) the lymph node architecture is replaced by large sclerotic bands
which divide the lymph node in small nodules. High-magnification (below)
shows lymphocytes and large cells with clear cytoplasm (Reed-Sternberg
cells)

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SYSTEMIC PATHOLOGY

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I. PATHOLOGY OF THE HEART

1. Acute myocardial infarction

Macroscopic view
- the infarcted area is pale, surrounded by a hyperemic narrow rim

Microscopic morphology
- in the infarcted area, the architecture of myocardial fibers is preserved but the
cytoplasm is intense eosinophilic from loss of proteins (coagulative necrosis) and no
nuclei are observed (karyolysis)
- the hyperemic narrow rim is composed by neutrophils and extravasated blood
- the non-necrotic myocardial fibers present a normal structure, with blue nuclei

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2
1

Fig. 23. Acute myocardial infarction. In the upper picture, the infarcted area
(1) is pale, surrounded by a hyperemic narrow rim (2). Microscopically, the
necrotic myocytes (1) present intense eosinophilia, without nuclei (below,
right). Compare them with the normal myocytes (3). The narrow rim (2) is
composed by extravasated neutrophils

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2. Scarring myocardial infarction

Macroscopic view
- the infarcted area is hard and white, the normal myocardium is red-brownish

Microscopic morphology
- in the scarring area the myocardial fibers being replaced by connective tissue (scar)
- at periphery of the picture, normal myocardial fibers have a normal structure, with
blue nuclei

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normal myocardium scarring infarcted area

Fig. 24. The scarring myocardial infarction is pale (upper). Microscopically,

the myocardial fibers are replaced by connective tissue

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II. PATHOLOGY OF BLOOD VESSELS

1. Atherosclerosis

Macroscopic view
- the intimal layer is covered by yellow elevated plaques (atheromas)

Microscopic morphology
- the atherosclerotic plaques are localized in the intimal layer of elastic and
medium-sized arteries and are partially covered by endothelium
- the atheroma is composed by cholesterol crystals (elongated clear spaces)
and cellular debris

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intima
media

endothelium

atheroma

Fig. 25. Aortic atherosclerosis. In gross photograph, the arrows indicate the
yellow atheromas. Microscopically (below), several cholesterol crystals and
cellular debries are stored in the intimal layer

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2. Coronarosclerosis

Macroscopic view
- the lumen of coronary artery is narrowed
- the intimal layer contain white hard raised plaques (hyaline atherosclerotic
plaques); their rupture can lead to thrombogenesis

Microscopic morphology
- small power view: thick wall, narrow lumen
- high power view: the hyaline plaques are composed by a glassy-like
acellular substance (hyaline)

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myocardium
coronary artery

Fig. 26. Coronarosclerosis. In the upper picture, narrowing of coronary lumen

is produced by atherosclerotic plaques and an associated thrombus. Below,
on cross-section, atherosclerotic plaques and stenosis of the artery (left). The
plaque is composed by hyaline (right below)

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3. Hemorrhoids

Macroscopic view
- the hemorrhoidal veins are dilated and elongated (varicose veins)

Microscopic morphology
- the veins located within inferior rectum and anal canal are dilated
- within venous lumen red thrombi can be observed

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rectum

anal canal

varicose veins

rectum

anal canal

Fig. 27. Hemorrhoids. Macroscopically, dilated hemorrhoidal veins can be

seen in anal canal (upper). Microscopically, several dilated veins, some of
them with red thrombi (below)

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II. PATHOLOGY OF THE RESPIRATORY SYSTEM

1. Bronchopneumonia

Macroscopic view
- on section, an alternance between yellow-gray patchy consolidated friable
areas and pale normal spongy pulmonary parenchyma (spotted lung)

Microscopic morphology
- leukocytic exudate within alveolar lumen
- dilated capillaries in alveolar septa
- pulmonary edema may be associated

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Fig. 28. Bronchopneumonia has a patchy distribution, gray congested area

alternating with normal lung parenchyma (upper-left). Microscopically, note
the same patchy distribution on low-power view (upper-right).
Below, high magnification shows hyperemia in the alveolar septae and
leukocytes in alveolar spaces

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2. Lung emphysema

Macroscopic view
- overdistended lungs, with sea-spongy aspect on section (distended air
spaces)

Microscopic morphology
- abnormal, permanent enlargement of alveolar spaces, distal to the terminal
bronchioles
- the alveolar septa are very thin

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Fig. 29. Emphysema. Macroscopically, the air spaces are distended and the
cut section aspect is similar to sea sponge (upper). In below picture, the
microphotograph shows markedly enlarged alveolar spaces and loss of some
alveolar septae

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3. Respiratory distress syndrome

(Hyaline membrane disease)

Macroscopic view
- firm and heavy dystelectasic lungs, without friability

Microscopic morphology
- the alveoli are linning by thick eosinophil membranes which represent
precipitated proteins due to surfactant destruction (hyaline membranes)

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Fig. 30. Hyaline membrane disease. The alveolar septae are focally lined by
acellular membranes (below) which decrease the air content into alveoli, this
aspect being seen in the upper image (dystelectasia)

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4. Miliary tuberculosis of the lung

Macroscopic view
- small diffuse gray-white pulmonary parenchymal nodules, with cheesy-
looking necrosis (caseous necrosis)

Microscopic morphology
- in this slide, small caseating tubercles are present in lung parenchyma
- the tubercles consist in large areas of caseous necrosis surrounded by
epithelioid cells (elongated, uninucleated macrophages) which ofteh fuse to
form multinucleated Langhans giant cells with horeseshoe arrangement of
peripheral nuclei; at the periphery of tubercles, lymphocytes may be observed

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caseous necrosis

Langhans cell

epithelioid cells

Fig. 31. Pulmonary miliary tuberculosis. Upper: on the cut surface of lung
several miliary tubercles with cheesy-like appearance. Below: the panoramic
view from left shows multiple small tubercles with central caseous necrosis,
epithelioid cells and one Langhans cell (right)

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5. Squamous cell carcinoma of the lung

Macroscopic view
- a nodular poorly-defined gray-white mass which is usually located central
or at or near to the lung hilum
- sometimes, the tumor can cavitates due to necrosis

Microscopic morphology
- proliferation of atypical cells arranged in clusters which do not exhibit
keratin pearls (nonkeratinizing variant)
- the tumor cells resemble those of the spinosum layer of the squamous
epithelium but are poorly differentiated

Immunohistochemistry
- the tumor cells are marked by Cytokeratin and Cytokeratin 5/6

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Fig. 32. Squamous cell carcinoma of lung. Note the central gray-white mass
in the hilum of the lung (upper-left). Microscopically, the tumor proliferation
around the central bronchi may be seen (upper-right). The poorly
differentiated tumor cells are arranged in clusters (lower)

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6. Small cell lung carcinoma (SCLC)

Macroscopic view
- poorly-defined masses, with extensive necrosis, usually located central,
along bronchi

Microscopic morphology
- proliferation of atypical small cells which show a sheet like arrangement
- the tumor cells are less than three resting lymphocytes
- the proliferating cells have round-shaped nuclei and scant cytoplasm
- in the tumor cells, the nuclear to cytoplasmic ratio is high, the mitotic rate
is high and necrotic areas are extensive

Immunohistochemistry
- the tumor cells are infrequent marked by Cytokeratin but express
neuroendocrine markers (Chromogranin, Synaptophysin, CD56)

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Fig. 33. The small cell lung carcinoma is a white infiltrating mass located in
the lung hilus, along the bronchi (upper-left). Microscopically, proliferation
of small round cells with sheetlike growth and scant cytoplasm (upper-right
and below microphotographs)

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IV. PATHOLOGY OF THE GASTROINTESTINAL TRACT

1. Chronic superficial gastritis

Macroscopic view
- infrequent sweling mucosa

Microscopic morphology
- lymphocytes in the foveolar layer of mucosa
- lymphoid aggregates with germinal centers within glandular layer of
mucosa are common in infection with Helicobacter pylori
- no inflammatory infiltrate in submucosa or muscularis

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SM

SM M

Fig. 34. Chronic superficial gastritis. Upper, note mild swelling mucosa. In
microphotographs, infiltration of the superficial foveolar layer with
lymphocytes and some lymphoid structures in the deep glandular layer. The
other layers are not involved in the inflammatory process

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2. Chronic gastric ulcer

Macroscopic view
- round sharply defect with straight walls
- the margins are flat, not ulcerated or elevated
- the base is smooth and clean
- the surrounding mucosal folds radiate from the ulcer in spokelike fashion

Microscopic morphology
- the chronic ulcer involves the mucosa, submucosa and muscularis
- the active ulcers have four layers, which reveal steps from inflammation to
repair: 1. neutrophils and cellular debris (on the luminal surface)
2. fibrinoid necrosis
3. granulation tissue
4. fibrous scar (in the basis of the ulcer, the deepest layer)

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1 2

Fig. 35. In the superior images, the arrows indicate a chronic ulcer, with
sharply demarcated margins, clean base and spokelike radiation od the gastric
folds. Microscopically, the four layers, from superficial to deep, are: 1.
neutrophilic exudate, 2. fibrin, 3. granulation tissue and 4. fibrosis

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3. Gastric adenocarcinoma

Macroscopic view
- in this case, a protruding ulcerated mass (polypoid tumor)

Microscopic morphology
- atypical glands infiltrate mucosa, submucosa, muscularis and subserosa
- the subserosal lymph node presents metastases

Immunohistochemistry
- the tumor cells are marked by Cytokeratin and Cytokeratin 20, which is
specifically for carcinomas of the gastro-intestinal tract

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SM

muscularis
lymph node with
metastases

subserosa

Fig. 36. Gastric adenocarcinoma. Upper: the arrow shows a giant protruding
ulcearated tumor mass. Below: note the presence of atypical glands in all
layers of the gastric wall and lymph node invasion.
(M = mucosa; SM = submucosa)
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V. PATHOLOGY OF LIVER AND PANCREAS

1. Liver cirrhosis

Macroscopic view
- enlarged or shrunken hard liver with diffuse nodularity
- on section, irregulary sized yellow nodules separated by fibrous septa

Microscopic morphology
- irregular nodules of regenerating hepatocytes, without centrolobular veins
- the regenerative nodules are surrounded by fibrous bands
- into connective bands, small bile ductules and minimal inflammatory cells

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bile ductules

regenerative nodules

Fig. 37. Cirrhosis. Uper: The liver has a nodular surface and cross-section
reveals that parenchyma is replaced by innumerable small nodules. Below:
these microphotographs shows several restant hepatocytes with nodular
appearance, surrounded by connective bands containing small bile ductules

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2. Acute pancreatitis

Macroscopic view
- enlarged edematous pancreas with fat necrosis (yellow-white patches) and
hemorrhagic areas

Microscopic morphology
- fat necrosis or steatonecrosis (soaps) are eosinophil homogeneous areas,
without nuclei which produce destruction of pancreatic parenchyma; they are
surrounded by inflammatory cells

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fat necrosis

Fig. 38. Acute pancreatitis. Upper: in the gross photographs, the arrows show
small steatonecrotic areas (yellow-white patches). Large areas of
hemorrhages may be seen in the upper right picture. Below, the steatonecrotic
areas are homogeneous and eosinophil

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VI. PATHOLOGY OF KIDNEY AND URINARY TRACT

1. Crescentic glomerulonephritis
(Rapidly progressive glomerulonephritis)

Macroscopic view
- enlarged kidneys with several minute hemorrhages on their surface (spotted
kidney)

Microscopic morphology
- proliferation of epithelial cells of the parietal layer of Bowmans capsule
- thickening of the Bowmans capsule (crescent-like structures)
- compression of the glomerular capillaries by the crescent structures
- droplets of hyaline in the renal tubes

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Fig. 39. Crescentic glomerulonephritis. Upper: enlarged kidney with minute

hemorrhages on surface (spotted kidney). In the below microphotograph, the
arrows show that all three glomerules present crescent-like proliferation of
epithelial cells within Bowmans space and compression of the capilary tuft.
The eosinophilic hyaline droplets seen in renal tubules are indicative of
proteinuria
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2. Renal cell carcinoma, clear cell type

(Grawitz tumor)

Macroscopic view
- yellow tumor which is well-defined and localized in the upper pole in early
stages; in this case, the tumor is in advanced stage and infiltrates most part of
the kidney parenchyma

Microscopic morphology
- clusters of large atypical cells with clear cytoplasm and pleomorphic nuclei
interspersed by delicate vascular network

Immunohistochemistry
- the tumor cells are marked by Cytokeratin 7 and Vimentin

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Fig. 40. Grawitz tumor. Upper: the yellow tumor infiltrates the kidney
parenchyma. Below: the tumor is composed by large clear cells interspersed
by a scanty vascular network

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VII. PATHOLOGY OF THE FEMALE GENITAL TRACT

AND BREAST

1. Squamous cell carcinoma of the uterine cervix

Macroscopic view
- in this case, an ulcerated-infiltrative tumor which protrudes into vagina and
also infiltrates the uterine body

Microscopic morphology
- proliferation of atypical cells arranged in nests which exhibit keratin pearl
formation (keratinizing type)
- the tumor cells resemble those of the spinosum layer of the squamous
epithelium

Immunohistochemistry
- the tumor cells are marked by Cytokeratin and p63

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ovaries and fallopian tubes
w. w.
A B B Y Y.c A B B Y Y.c

uterine body

cervical tumor

vagina

endocervix
(tumor)

exocervix
(squamous epithelium)

Fig. 41. Invasive squamous cell carcinoma of the uterine cervix.

Macroscopically, an ulcerated tumor which infiltrates vagina and the uterine
body (upper image). In the below low-power view microphotograph note
central keratin pearls indicate by arrow into clusters of pleomorphic
squamous cells
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2. Endometrial adenocarcinoma

Macroscopic view
- in this case, an exophytic infiltrative tumor mass in the uterine cavity

Microscopic morphology
- the tumor is composed by well-differentiated atypical glands and solid areas
(atypical columnar cells without glandular structures)
- the tumor involves the endometrium and myometrium;

Immunohistochemistry
- the tumor cells are marked by Cytokeratin and sometimes by Vimentin

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exophytic tumor
in uterine body

cervix

Fig. 42. Endometrial adenocarcinoma. Upper: an exophytic infiltrative tumor

mass. Below: the tumor consists on invasive proliferation of atypical glands
and solid undifferentiated areas

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3. Fibrocystic changes of the breast

Macroscopic view
- fibrotic areas with cystic structures on cut-section

Microscopic morphology
1. proliferation of ducts
2. cystic ducts dilatation
3. hyperplasia of the ductal epithelium with papillary and cribriform (slitlike)
pattern
4. apocrine metaplasia of some ducts and cysts (large, polygonal cells with
abundant eosinophilic cytoplasm replace the lining epithelium)
5. periductal and perilobular fibrosis

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Fig. 43. Fibrocystic changes of the breast. The dilated spaces are cysts lined
either by epithelial hyperplasia with slitlike aspect (upper right) or flat
epithelia (below right). In the central part of picture, apocrine metaplasia with
papillary pattern

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VIII. PATHOLOGY OF THE MALE GENITAL SYSTEM

1. Nodular (benign) prostatic hyperplasia

Macroscopic view
- enlarged prostate, with multinodular cut surface
- the peripheral zone of prostate is compressed by the hyperplastic tissue
- the urethra is compressed and the mucosa of urinary bladder is hypertrophic

Microscopic morphology
- well-defined, nonencapsulated nodules composed of proliferation of glands
with columnar-lining epithelium without atypia, surrounded by fibroblasts
and smooth muscle cells
- some proliferated glands are dilated

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urinary bladder

Fig. 44. Benign (nodular) prostatic hyperplasia. In the left picture, the
prostate is enlarged and the bladder presents compensatory hypertrophy. In
the right, nodular structures with proliferation of glands, smooth muscle cells
and connective tissue

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2. Seminoma

Macroscopic view
- enlarged testis
- the gray-white cut surface of tumor devoid of hemorrhage and necrosis

Microscopic morphology
- nests of atypical spermatocyte-like cells separated by thin fibrous septa
which contains lymphocytes
- preservation of seminiferous tubules may be seen at the periphery of the
tumor

98
 F T ra n sf o F T ra n sf o
PD rm PD rm
Y Y
Y

Y
er

er
ABB

ABB
y

y
bu

bu
3.0

3.0
to

to
re

re
he

he
k

k
lic

lic
C

C
w om w om
w

w
w. w.
A B B Y Y.c A B B Y Y.c

Fig. 45. Seminoma. Upper: gray-white homogeneous tumor. Below: the

tumor consists in proliferation of large monotonous population of
spermatocyte-like cells separated by fibrous septae

99
 F T ra n sf o F T ra n sf o
PD rm PD rm
Y Y
Y

Y
er

er
ABB

ABB
y

y
bu

bu
3.0

3.0
to

to
re

re
he

he
k

k
lic

lic
C

C
w om w om
w

w
w. w.
A B B Y Y.c A B B Y Y.c

IX. PATHOLOGY OF THE THYROID GLAND

1. Multinodular goiter

Macroscopic view
- enlargement of the thyroid gland (hyperplasia)
- cut surface shows nodular architecture, often with colloid substance

Microscopic morphology
- a nodular hyperplasia of the thyroidal colloid-filled follicles

100
 F T ra n sf o F T ra n sf o
PD rm PD rm
Y Y
Y

Y
er

er
ABB

ABB
y

y
bu

bu
3.0

3.0
to

to
re

re
he

he
k

k
lic

lic
C

C
w om w om
w

w
w. w.
A B B Y Y.c A B B Y Y.c

Fig. 46. Goiter. In the left picture, the arrow shows enlargement of the right
lobule compared with the normal left lobule of the thyroid gland.
Microscopically, in the right, proliferation of thyroidal follicles separated by
fibrous septae

101
 F T ra n sf o F T ra n sf o
PD rm PD rm
Y Y
Y

Y
er

er
ABB

ABB
y

y
bu

bu
3.0

3.0
to

to
re

re
he

he
k

k
lic

lic
C

C
w om w om
w

w
w. w.
A B B Y Y.c A B B Y Y.c

2. Hashimoto`s thyroiditis
(Chronic autoimmune thyroiditis)

Macroscopic view
- the thyroid gland may be diffusely enlarged, normal size or atrophic,
sometimes with inhomogeneous nodular pattern

Microscopic morphology
- the thyroid gland is destroyed by lymphocytes arranged in follicles with
germinal centers

102
 F T ra n sf o F T ra n sf o
PD rm PD rm
Y Y
Y

Y
er

er
ABB

ABB
y

y
bu

bu
3.0

3.0
to

to
re

re
he

he
k

k
lic

lic
C

C
w om w om
w

w
w. w.
A B B Y Y.c A B B Y Y.c

Fig. 47. Hashimoto thyroiditis. The microscopic low-power view shows

infiltration of thyroid parenchyma by lymphocytes arranged in round
lymphoid follicle structures

103
 F T ra n sf o F T ra n sf o
PD rm PD rm
Y Y
Y

Y
er

er
ABB

ABB
y

y
bu

bu
3.0

3.0
to

to
re

re
he

he
k

k
lic

lic
C

C
w om w om
w

w
w. w.
A B B Y Y.c A B B Y Y.c

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