Patho
Slide
exam


Zw
1‐
Brown
atrophy
of
the
heart

(atrophia
fusca
myocardii)

During
atrophy
and
aging,
a
brown

pigment
called
lipofuscin
accumulates

within
the
shrunken
cells.
This
is
thought

to
represent
degenerate
lipid
material
in

secondary
lysosomes
produced
by

breakdown
of
the
cell
membranes
and

organelle.
Lipofuscin
accumulated

parEcularly
in
the
atrophic
myocardial

fibers
of
the
hearts
of
elderly
people
and

gives
rise
to
the
term
brown
atrophy.


Hemotoxylin
stain
to
show
red
brown

granules
at
either
pole
of
nuclei
of
atrophic

muscle
fibers

ZW
4‐
Emphysema


‐Emph.
Lungs
demonstrate

marked
increase
in
alveolar

volume
and
consequent

B
reducEon
in
alveolar
wall

available
for
gas
exchange.

‐loss
of
elasEc
support
causes

alveolar
collapse
during

expiraEon

‐
Subpleural
bullae
(marked

B)

may
rupture
into
pleural

space
and
cause

pneumothorax

 ZW
56‐
Rickets
(rhachiEs)


Rickets
–
vitamin
D
deficiency
in
children
is
idenEcal
pathologically
to
osteomalacia
in

adults.
In
osteomalacia,
the
trabeculae
are
of
normal
or
increased
thickness,
but
there
is

deficient
mineralizaEon
so
that
each
trabecula
has
a
central
core
of
calcified
bone
(stained

black),
coated
by
an
outer
shell
of
unmineralized
osteoid
(stained
brown).

ZW
69‐
Serous
necrosis
of
lymph
node

(necrosis
caseosa
lymphonodi)

Serous
necrosis
of
lymph
node‐2


Caseous
necrosis
(top),
with

palisading
hisEocytes
below
it.

Zk
40‐
Renal
InfarcEon

The
recently
infarcted
area

stains
less
intensely
than

normal
cortex.

There
is
a

hyperemic
zone
with

purple
neutrophil
infiltrate

typical
of
early
cellular

acute
inflammatory

exudate.
The
acute

inflammatory
zone
exhibits

typically
dilated
and

congested
capillaries
and

an
influx
of
small,
dark

staining
neutrophil

polymorphs.
NecroEc

Essue
is
removed
my

macrophages
which

undergoes
fibrosis.

Renal
infarct
cont
 This
is
the

microscopic

appearance
of
an

acute
renal
infarct.

Compare
the
intact

architecure
of
the

normal
kidney
cortex

with
the
hyperemic

kidney
that
is
dying,

then
the
pale
pink

infarcted
kidney
in

which
both
tubules

and
glomeruli
are

dead.
This
is
acute

coagulaEve
necrosis,

which
iniEally
leaves

the
pale
outlines
of

the
infarcted
cells.

 Zk
46‐
lung
edema


(oedema
pumonis)


Pathology‐

the
pulmonary
capillaries
become
dilated
and
congested

with
erythrocytes
and
increased
hydrostaEc
pressure
results
in

transudaEon
of
plasma
fluid
into
the
alveolar
spaces.
–
acute

pulmonary
edema=
reversible

 Zk
15‐
Passive
CongesEon
of
the
Lung

(hyperaemia
passiva
chronica
pulmonum)

Passive
hyperemia
(congesEon),
also
termed

stasis,
is
a
consequence
of
an
impaired
venous

drainage
(heart
failure,
compression
or

obstrucEon
of
veins),
followed
by
dilataEon
of

venules
and
capillaries.

‐EEology
of
passive
conges2on
of
the
lung
:

chronic
le[
heart
(ventricular)
failure.

Alveolar
walls
are
thickened
due
to
dilated

capillaries.
Alveolar
lumens
are
filled
with

transudate
(amorphous,
eosinophilic
and

homogenous)
which
replaced
the
air,
red
blood

cells
(microhemorrhages)
and
hemosiderin‐
laden
macrophages
(also
called
"heart
failure

cells").
(H&E,
ob.
x20)

With
progression,
inters33al
fibrosis
may

appear
and,
together
with
hemosiderin

pigmentaEon,
generates
the
aspect
of
"brown

indura3on".
Extensive
fibrosis
leads
to

intrapulmonary
hypertension.

Passive
congesEon
of
lungs
2

Zk
20
–
Nutmeg
liver


(hepar
moschatum)

Nutmeg
liver
usually
results
from

right
sided
heart
failure
which
causes

a
passive
congesEon
in
the
liver.
The

result
is
a
speckled
„nutmeg”
paaern

where
there
is
congesEon
around
the

central
veins/sinusoids.


Zk
20‐
nutmeg
liver


Hepatocytes
that
have

been
replaced
with
lipid

droplets
appear
as
empty

round
white
areas.

Zk
24
fresh
thrombus


(thrombus
recens)


A[er
endothelial
injury
the
abnormal
vessel

has
become
coated
by
a
thin
layer
of
fibrin

and
platelet
thrombus
with
entrapped
RBCs.

The
fibrin
and
layer
of
platelets
and
RBC’s

alternate
to
form
lines
of
Zahn


 Zk
26‐
Thrombus
recanalizaEon

‐new
proliferaEng
vessels;
‐hemosiderin
(from
dying
RBC’s)
;
‐fibroblasts
proliferaEng;‐
endothelial
cells
migrate
into
thrombus

4

1,
AdvenEEa;
2,
tunica
media;
3,
organized
thrombus
‐
i.

e.,
replaced
by
connecEve
Essue;
4,
newly
formed
and
in

part
dilated
vessels
within
the
thrombus;
5,
disintegrated

remains
of
the
old
thrombus.

Zk48
Hemorraghic
lung
infarcEon

(Red
Infarct)

Lung
infarct
(Red
infarct)‐
characterisEc
of
organs

with
double
circulaEon


‐undegoes
coagulaEve

necrosis

‐embolism
originates
from

DVT’s

‐ Triangle
shape;
base
is

close
to
pleura
which
is

covered
by
fibrous

exudate;
apex
of
traingle

points
to
blocked
artery

‐ Pink
cells
are
necroEc
and

have
no
nuclei


 Lung
infarct
(closer
view)


In
infarct
area,
alveolar
walls,
vascular
walls
and
bronchioles
are
necroEc.
They
appear

eosinophilic
(pink),
homogenous,
lacking
the
nuclei,
but
keep
their
shapes
‐
"structured
necrosis".

Alveolar
lumens
from
infarcted
area
are
invaded
by
red
blood
cells
‐
hemorrhagic
infarct
(red).


 
Red
hepaEzaEon
describes

lung
Essue
with
confluent


Z7
Lobar
pneumonia

 acute
exudaEon
containing

neutrophils
and
red
cells

giving
a
red,
firm,
liver‐like

(hepaEzaEon)
gross

appearance.


Lobar
pneumonia
is
an
acute
exudaEve
inflammaEon
of
an
enEre
pulmonary
lobe,
produced
in
95
%
of
cases
by

Streptococcus
pneumoniae
(pneumococci).

If
not
treated,
lobar
pneumonia
evolves
in
four
stages
:CongesEon
(first
2
days);
Red
hepaEsaEon
(fibrinous
alveoliEs)
(2nd

to
4th
day);
Grey
hepaEsaEon
(leukocyEc
alveoliEs)
(4th
to
8th
day);
ResoluEon
(a[er
8th
day)

 z76A‐
Cytomegaly



In.


The
characterisEc
feature
of
CMV
is
markedly
enlarged
cells
with
large

dark
staining
intranuclear
inclusion
bodies.
In.
These
are
surrounded

by
a
clear
halo.
Cytoplasmic
inclusions
may
also
be
seen.
Focal
necrosis

is
also
someEmes
present
but
usually
minimal.
Cytomegalic
inclusions

are
usually
seen
in
epithelial
cells,
endothelial
cells
and
in

macrophages
.

Z43
–
Miliary
tuberculosis
in
liver

‐many
small

tubercles(granulomas)

in
the

liver
,
with
caseous
necrosis
in
the

center
(C)

‐ Epitheloid
macrophages
and

L E

lymphocytes
surround
the
caseous

area

(E)


C
 ‐ ‐some
macrophages
fuse
to

produce
mulEnucleated
giant
cells

called
Langhans’
giant
cell
(L)

‐ ‐spindle
shaped
fibroblasts
F

appear
in
the
peripheral

lymphocyEc
zone


Miliary
tb
liver
cont


L
F‐
fibrosis

C‐
chronic

inflammatory
 Z25
Biliary
Liver
Cirrhosis


cells


C

F


‐DestrucEve
inflammatory
changes
are
centered

primarily
on
bile
ducts,
hepatocytes
are
also
affected.

‐in
early
stages
the
epithelium
around
large
bile
ducts

undergoes
vacuolaEon
and
there
is
an
infiltraEon
of
the

wall
and
Essue
with
lymphocytes.

‐bile
pools
(yellowe
brown)
due
 ‐potal
tracts
become
progressively
expanded
by
chronic

to
obstrucEon
of
flow

 inflammatory
cells
and
later
on
by
fibrosis

 Z27‐
Portal
Liver
cirrhosis

L

F


‐features
of
cirrhosis
are
fibrous
bands(F)
connecEng
portal
areas
and

intervening
nodules
of
liver
cells(L)
showing
marked
faay
change


‐‐

Portal
liver
cirrhosis


Micronodular

cirrhosis
is

seen
along

with
moderate

faay
change.

Note
the

regeneraEve

nodule

F
 surrounded
by

fibrous

connecEve

Essue

extending

between

portal
regions.

 N54
Uterine
Leiomyoma



Micro:
whorled
(fascicular)
paCern
of
smooth

muscle
bundles
separated
by
well
vascularized

connecEve
Essue;
smooth
muscle
cells
are

elongated
with
eosinophilic
or
occasional

fibrillar
cytoplasm
and
dis2nct
cell
membranes;

may
develop
areas
of
degeneraEon
if
large,

including
hyaline
or
mucoid
change,
calcificaEon,

cysEc
change
or
faay
metamorphosis;
variable
 usually
less
than
5
mitoEc
figures
per
10
high

lymphocytes
and
mast
cells;
usually
non‐ power
fields
in
mitoEcally
most
acEve
area;
no

infiltraEve;
thick
walled
arteries
throughout;

significant
atypia;
rarely
has
focal
skeletal

cle[‐like
spaces;


muscle
differenEaEon
tubules
or
glands
are

rare

 N3‐
Lipoma



Defini2on

●
Benign
tumor
composed
of
mature
white
adipocytes
with
uniform

nuclei
resembling
normal
white
fat

●
Most
common
mesenchymal
and
so[
Essue
tumor
(100x
more

common
than
liposarcoma)

Micro

●
Mature
white
adipose
Essue
without
atypia

●
2‐5x
variaEon
in
cell
size
(more
than
normal
white
adipose
Essue),
with
obvious
large

cells
up
to
300
microns

●
Cytoplasmic
vacuoles
are
relaEvely
uniform

●
May
have
intranuclear
vacuoles,
thickened
fibrous
septa
in
buaocks,
foot
or
hand

●
May
contain
areas
of
fat
necrosis
with
hisEocytes,
infarct
or
calcificaEon;
rarely

contains
bone
or
carElage

●
No
mitoEc
figures

●
Note:
diagnosis
of
lipoma
requires
presence
of
a
mass

N85‐86
FibrocysEc
Breast
Disease

adenosis

Any
hyperplasEc
process

primarily
involving
glands

(i.e.
an
increased
number

of
glandular
components)

Loosely
structured

proliferaEon
of
acinar
or

tubular
structures,
with

epithelial
and

myoepithelial
layers,

surrounded
by
basement

membrane


Cells
resemble
apocrine
sweat
glands;
are

enlarged
with
abundant
eosinophilic

cytoplasm
and
apical
snouts,
o[en

supranuclear
vacuoles,
medium
sized

nucleus
but
prominent
nucleoli

 FibrocysEc
disease
of
breast

Benign
ductal
proliferaEve
lesion

that
typically
has
secondary
lumens

and
streaming
of
central

proliferaEng
cells

●
Streaming
(parallel
arrangement)
of
central
cells

with
indisEnct
cell
borders,
irregularly
shaped
and

sized
secondary
lumens,
o[en
peripheral;
tu[s
of

cells
project
into
lumina

●
Peripheral
elongated
cle[s
(not
round,
not

central),
irregularly
shaped
bridges
connect

opposite
porEons
of
wall
with
nuclei
parallel
to

long
axis
of
the
bridge
(not
Roman
bridges)

●
Cells
have
acidophilic
and
granular
cytoplasm,

oval
normochromaEc
nuclei
with
slight
overlap,

small
or
indisEnct
nucleoli

●
Myoepithelial
cells
and
foamy
macrophages
are

present


●
Benign,
not
neoplasEc,
but
may
be
confused
with

malignancy

●
Usually
bilateral,
although
one
breast
may
be

affected
more
than
the
other

●
Either
proliferaEve
(adenosis,
hyperplasia)
or

nonproliferaEve
(cysts)

• 
clear
or
blue
domed
cysts




N79‐
Mucinous
cystadenoma
of
ovary


The
benign
cystadenoma
has
smooth
outer
surface
composed
of

ovarian
capsule
(C).
The
cysEc
locules
are
filled
with
mucin
and
lines

with
tall
columnar
epithelium
with
uniform
basal
nuclei
and
copious

mucin‐containing
cytoplasm
at
the
luminal
aspect.


●
CysEc
spaces
lined
by
bland,
tall
columnar
cells
with
abundant

intracytoplasmic
mucin

●
Tumor
cells
exhibit
straEficaEon,
tu[ing
and
papillary
formaEon

●
Variable
cytologic
atypia

●
Columnar
cell
variant
has
round
and
convoluted
glands
in
loose

aggregates,
lined
by
tall
columnar
mucinous
epithelium
with
basal
bland

nuclei

N128‐
Squamous
cell
carcinoma
of
the

larynx
 The
features
of

squamous

differenEaEon,

observable
on

rouEne
stained

Essues
under
light

microscopy,
include

one
or
more
of
the

following:
(1)

flaaened

polyhedral,
round,

or
ovoid
epithelial

cells;
(2)

intracellular
or

extracellular

keraEnizaEon

(pearls)
(K);
and
(3)

K
 intercellular
bridges

or
desmosomes.


(blue
arrow)

‐also
lymhocytes

inflammatory

response

‐necrosis=apoptosis

Zw75A‐B
Arteriosclerosis

Z
75A
–


Fragment
of
the
Aorta
,

Simple
atheroscleroEc
plaque

‐ Pale
staining
inEma
(In)
consists

of
aggregated
myoinEmal
cells

containing
lipid,
and
some

fibrous
Essue

‐ ‐
Foam
cells
filled
with
lipid

F
 appear
as
large
pale
staining
cells

with
vacuolated
cytoplasm

‐ ‐‐purple
cells
–
accumulated

inflammatory
cells



M


In

 Zw
75
B
Arteriosclerosis


Cross
secEon
of
a
large
artery
–
no
lumer
artery
is
completely
obstructed

Destroyed
thickened
inEma
with
deposits
of
lipids
and
inflammatory
cells


‐Old
thrombus
with
recanalizaEon
(small
new
vessels)
aaached
to
plaque

‐
Yellow
brown
macrophages
with
hemosiderin
deposits


 N32
Cavernous
Hemangioma



Cavernous
hemangioma
is
a
benign
connecEve

Essue
tumor
resulted
from
endothelial
cells

proliferaEon.
It
is
a
non‐encapsulated
tumor,

with
an
infiltraEve,
lobular
growing.
The
tumor

consists
in
large
(cavernous)
spaces,
lined
by

tumor
endothelial
cells
(which
appear
very

similar
to
normal
cells).
These
interconnected

spaces
are
filled
with
blood
and
separated
by
a

fibrous
Essue

N
31
Capillary
hemangioma


Purple
areas‐
lots
of

enothelial
cells


‐lobulated
tumor

‐ Small
thin
walled
vessels

(capillaries)

‐ ‐endothelium
„plump”

N
36‐
Cavernous
lymphangioma

Micro
descrip2on

●
Large
lymphaEc

channels
in
loose

connecEve
Essue
stroma

●
Focally
disorganized

smooth
muscle
in
wall
of

larger
channels

●
Peripheral
lymphoid

aggregates

●
O[en
increased
mast

cells

Look
for
adipose
Essue

and
purple
lymphaEc

Essue
with
follicles


‐
Vascular
channels

enlarged
with
amorphous

pink
fluid


 Zk
47
Myocardial
InfarcEon


Myocardial
infarct
(healing
commencing)
‐
between
5th
and
10th
day.
In
area
of
coagula3ve
ischemic

necrosis,
myocardial
fibers
preserve
their
contour,
but
the
cytoplasm
is
intensely
eosinophilic
and
transversal

striaEons
and
nuclei
are
lost.
The
intersEEum
of
the
infarcted
area
is
iniEally
infiltrated
with
neutrophils,
then

with
lymphocytes
and
macrophages,
in
order
to
fagocitate
the
myocyte
debris.
The
necroEc
area
is

surrounded
and
progressively
invaded
by
granula3on
3ssue
which
will
replace
the
infarct
with
a
fibrous

(collagenous)
scar

 N
126
Hodgkin’s
Disease
 is
a
primary
malignant
tumor
of

the
lymph
nodes,
rarely
affecEng

L
 the
extranodal
lymphoid
Essue.

The
diagnosis
criteria
are:
tumor

component
(Reed‐Sternberg
cell
‐

typical
and
variants)
and
a
reacEve

component
(normal
mature

lymphocytes,
eosinophils,
plasma

cells,
neutrophils,
fibrosis
and

RS
 capillaries).

Histological
classificaEon
of

Hodgkin's
lymphoma
(according
to

lymph
node
architecture,
raEo

between
tumor
and
non‐tumor

components,
morphology
of
Reed‐
E Sternberg
cell
and
compositon
of

reacEve
infiltrate)
:

N (Non‐classical)
Nodular
lymphocyte

predominant
Hodgkin's
lymphoma

H
 (5
%)

Classical
Hodgkin's
lymphoma


Nodular
sclerosing
(60
‐
80

%)

Lymphocyte‐rich
(5
%)

H‐
hisEocyte(Essue
macrophage;
RS‐
Reed
Sternberg
cell

Mixed
cellularity
(15
‐
30
%)

N‐
neutrophil;
E‐
eosinophil;
L‐
lymphocyte

Lymphocyte
depleted
(<
1
%)

 ZW
61
Silico‐anthracosis

F


H
Silicosis
tends
to
occur
in
miners
and
those
with
industrial
exposure

to
silica
dusts.
Inhaled
silica
parEcles
are
engulfed
in
macrophages

which
excites
a
vigorous
focal
fibroEc
reacEon
resulEng
in
the

formaEon
of
nodules.
Center
of
each
focus
becomes
acellular
and

hyalinized
,
surrounded
by
fibrous
Essue
(F)and
inflammatory

infiltrate
in
which
black
carbon
laden
macrophages
abound.


Z48
Tuberculous
bronchopneumonia

Infected
sputum
may

gravitate
to
lower
areas

of
the
same
or
opposite

lung
where,
by

destrucEon
of
a

T bronchiolar
wall
the

organism
invades

peribronchial
lung
Essue

to
form
further
caseaEng

B
 tubercles.


B‐
bronciole

T‐
tubercle

N143‐
Non
small
cell
lung
cancer

(large
cell
undiffer.)


Large
cell
undiff.
Cancers
include
poorly
differen.
Squamous
cell

carc.
And
adenocarcinomas.
Tumors
consist
of
large
anaplasEc

epithelial
cells
growing
in
nests
and
sheets.


Tumor
cells
have
abundant
cytoplasm,
clumped
chromaEn

(blue),
and
pink
nucleoli
(arrow),
but
no
evidence
of
gland

formaEon,
mucin
producEon,
bridges,
or
pearls.
A
giant

cell
variant
occurs.

ZW77‐
Gastric
PepEc
ulcer


The
ulcerated
surface
is
covered
in
a
slough
(S)composed
of

pink
staining
necroEc
debris
combined
with
fibrin
and

neutrophils
of
and
acute
inflammatory
exudate.
Beneath

the
necroEc
slough
is
a
zone
of
vascular(V)
granulaEon

Essue,
behind
this
is
a
zone
of
fibrous
granulaEon
Essue
(F)

finally
leading
to
a
scar.
(Sc)


S
 V
F
Sc

 T


N167‐
Signet
Ring
cell
gastric
cancer

M

This
is
a
poorly
differenEated
adenocarcinoma
with
liale
or
no
discernible
gland

formaEon.
It
takes
the
form
of
a
diffuse
infiltraEon
of
the
stomach
wall
as
in
liniEs

plasEca.
The
tumor
cells
(T)
can
be
forming
a
diffuse
sheet
between
bundles
of

smooth
muscle
(M).
At
high
power
the
tumour
cells
consist
of
signet
ring
cells(S),
so

names
because
the
cytoplasm
is
occupied
with
mucin
filled
vacuole
pushing
the

nucleus
to
the
side.


 Here
is
an
adenocarcinoma
in
which
the
glands
are
much
larger

and
filled
with
necroEc
debris.


N81
Adenocarcinoma
of
colon


The
edge
of
the
carcinoma
arising
in
the
villous

adenoma
is
seen
here.
The
neoplasEc
glands
are
long

and
frond‐like,
similar
to
those
seen
in
a
villous

adenoma.
The
growth
is
primarily
exophyEc
(outward

into
the
lumen)
and
invasion
is
not
seen
at
this
point.

Microscopically,
a
moderately
differenEated

adenocarcinoma
of
colon
is
seen
here.
There
is
sEll
a

glandular
configuraEon,
but
the
glands
are
irregular

and
very
crowded.
Many
of
them
have
lumens

containing
bluish
mucin.

 N91
Mucinous
adenocarcinoma
of

stomach


.
Micro
Findings：

Intracytoplasmic
mucin
resulEng
in
the
typical
signet
ring
appearance.

 HyperchromaEc
cancer
cells

InfiltraEon
of
cancer
cells
through
whole
layers
with
occasional
glandular
 floaEng
in
pink
mucin
pools
.

formaEon
&
mucin
pooling.


Extensive
fibrosis
(desmoplasia)
&
dense
inflammatory
infiltraEon.


 Z83‐
UlceraEve
coliEs



Microscopically,
the
inflammaEon
of
ulceraEve
coliEs
is
confined
primarily
to
the
mucosa.

Here,
the
mucosa
is
eroded
by
an
ulcer
that
undermines
surrounding
mucosa.

At
higher
magnificaEon,
the
intense
inflammaEon
of
the
mucosa
is
seen.
The
colonic
mucosal
epithelium

demonstrates
loss
of
goblet
cells.
An
exudate
is
present
over
the
surface.
Both
acute
and
chronic

inflammatory
cells
are
present.
Presence
of
crypt
Abcesses
in
glands,
depleEon
of
mucus
containing

goblet
cells
and
the
presence
of
neutrophils
as
well
as
chronic
inflammatory
cells
in
lamina
propria.

 Z22‐
extracapillary
glomerulonephriEs


Cell
proliferaEon
in
the
capsular
space
of

glomerulus
especially
occurs
in
intra‐
extracapillary

(rapidly
progressive)

glomerulonephriEs.
It
is
viewed
as
a

reacEon
to
humoral
influences
reaching
the

free
capsular
space
through
defecEve

capillary
wall
in
a
severe
inflammatory

process


Rapidly progressive ("crescentic") glomerulonephritis - the majority of glomeruli present "crescents".

Formation of crescents is initiated by passage of fibrin into the Bowman space as a result of increased
permeability of glomerular basement membrane. Fibrin stimulates the proliferation of parietal cells of Bowman
capsule, and an influx of monocytes. Rapid growing and fibrosis of crescents compresses the capillary loops and
decreases the Bowman space which leads to renal failure within weeks or months.
 ZW
23K
Kidney
amyloidosis


Amyloid
(an
abnormal
protein)
accumulates
as
extra‐
cellular
deposits,
nodular
or
diffuse,
as
pink,
amorphous

material.
IniEally,
the
deposits
appear
in
the
glomeruli:

within
the
mesangial
matrix
and
along
the
basement

membranes
of
the
capillary
loops.
ConEnuous

accumulaEon
of
the
amyloid
will
compress
and
obliterate

the
capillary
tu[.
With
progression,
amyloid
deposits

appear
also
peritubular
and
within
the
arteriolar
wall,

narrowing
them.
Congo
red
is
a
special
staining,
elecEve
for

amyloid.
(Congo
Red)

N103
Renal
cell
carcinoma

Renal
clear
cell
carcinoma

(Grawitz
tumor)
is
a
malignant

epithelial
tumor
resulted
from

proliferaEon
of
tubule
cells.

Tumor
cells
form
cords,
papillae,

tubules
or
nests,
and
are
atypical,

polygonal
and
large.
Because

these
cells
accumulate
glycogen

and
lipids,
their
cytoplasm

appears
"clear",
lipid‐laden,
the

nuclei
remain
in
the
middle
of

the
cells,
and
the
cellular

membrane
is
evident.
Some
cells

may
be
smaller,
with
eosinophilic

cytoplasm,
resembling
normal

tubular
cells.
The
stroma
is

reduced,
but
well
vascularized.

The
tumor
grows
in
large
front,

compressing
the
surrounding

parenchyma,
producing
a

pseudocapsule.
(H&E,
ob.
x20)

 N78
Benign
hyperplasia
of
prostate

high
magnif‐
the
acini
are
lined
by
tall

columnar

prostaEc
epithelium(A)
with
small

basal
nuclei,
with
regular
arrangement
but

someEmes
forming
papillary
folds
(P)

adjacent
acini
seperated
by
variable
amount

of
fibromuscular
connecEve
Essue
(M)


H N

A
M

The
transiEonal
and
para‐urethral
components
of

prostate
gland
undergo
hyperplasia
accompanied
by

hypertrophy
of
fibromuscular
stroma‐peripheral
zone
 P

not
involved
and
become
atrophic/compressed.

‐Note
rounded
nodules
of
hyperplasEc
prostaEc

Essue
(H)
and
compressed
peripheral
zone
(N)

‐nodular
microcysEc
appearance
,
cysts
represenEng

dilated
hyperplasEc
glandular
acini

Normal
tesEs
appears
at
the
le[,

and
seminoma
is
present
at
the

right.
Note
the
difference
in
size

and
staining
quality
of
the

neoplasEc
nests
of
cells
compared

to
normal
germ
cells.
Note
the

N105
Seminoma

lymphoid
stroma
between
the

nests
of
seminoma.


the
tumor
consists
of
sheets
of
uniform

polygonal
cells
with
clear
cytoplasm

and
a
round
central
nucleus.
The
cells

S
 are
divided
into
clusters
by
fine
fibrous

septa
(S)
which
is
usually
infiltrated
by

small
lymphocytes



This
is
the
histologic
paaern
of
the

typical
seminoma.
Lobules
of

neoplasiEc
cells
have
an
intervening

stroma
with
characterisEc
lymphoid

infiltrates.
The
seminoma
cells
are

large
with
vesicular
nuclei,
and
pale

watery
cytoplasm.

 This
slide
is
similar
to


N114
Teratoma

 our
slide
–
an

example
of
a
mature

teratoma
in
which

ectodermal
elements

usually
predominate.

Although
ectodermal

derivaEves

predominate

parEculary
skin
and

skin
appendage

components,

mesodermal

(carElage,
smooth

muscle)
and

endodermal

(respiratory
and
gut

epithelium)
occur
in

some
tumors

 Teratoma
cont’d


Teratoma
is
a
tumor
which
arises
from

tu3potent
germinal
cells.
Frequently,
it
is

localized
in
gonads
(tesEs,
ovary).
It

contains
a
variety
of
Essues
(derived
from

one,
two
or
three
embryonic
cell
layers
‐

mesoderm,
endoderm
or
ectoderm),
Essues

which
normally
are
foreign
to
the
site
of

growth.

 Zk
3
Ectopic
pregnancy


W
H
 Cv


The
fallopian
tube
is
the
most
frequent
locaEon
of
ectopic
pregnancy.
The
tubal
lumen

becomes
filled
with
developing
embryo
(not
shown)
and
associated
membranes
as
well
as

the
chorionic
villi
(CV).
The
distended
tubal
wall
(W)
is
o[en
deeply
congested
and
thinned.

There
is
extensive
hemorrhage
(H)
into
the
lumen
of
the
tub
(haematosalpinx).
The

trophoblast
burrows
into
the
wall
of
the
Fallopian
tube
leading
to
perforaEon.

 SomeEmes
blood
clot
and
chorionic
villi,
as
seen

here,
are
recovered
outside
of
the
tube
following

rupture
of
an
ectopic
pregnancy.
Other
sites
of

ectopic
implantaEon
include
ovary,
abdominal

peritoneum,
and
cornual
(uterine)
porEon
of

fallopian
tube.


A
posiEve
pregnancy
test
(presence
of
human

chorionic
gonadotropin),
ultrasound,
and

culdocentesis
with
presence
of
blood
are
helpful
in

making
the
diagnosis
of
ectopic
pregnancy.
Seen

here
is
tubal
epithelium
at
the
right,
with
rupture

site
and
chorionic
villi
at
the
lower
le[.


CV

 Zw18
Hashimoto
thyroidiEs

Autoimmune‐
thyroid
acini

(A)are
progressively

destroyed
by
immune
system

and
glands
become
diffusely

A infiltrated
by
lymphocytes

and
plasma
cells.
In
some

areas
purple
lymphocytes

F
 aggregate
to
form
typical

lymphoid
follicles
(F)
o[en

with
germinal
centers.

Thyroid
epithelial
cell

commonly
show
oncocyEc
or

Hurthle
cell
transformaEon,

Hurthle
cells
have
strong

eosinophillic
granular

cytoplasm
and
slightly

enlarged
nuclei

 Hashimotos


F


This
high
power
microscopic
view
of
the
thyroid
with
Hashimoto's

thyroidiEs
demonstrates
the
pink
Hürthle
cells
at
the
center
and

right.
The
lymphoid
follicle
is
at
the
le[.
Hashimoto's
thyroidiEs

iniEally
leads
to
painless
enlargement
of
the
thyroid,
followed
by

atrophy
years
later.

 Zw
83S‐
Graves‐Basedow
disease
 In
Grave’s
disease
hyperplasEc
acinar

cells
are
tall
columnar
and
have
large

nuclei
reflecEng
a
greater
degree
of

metabolic
acEvity.
The
acini
themselves

are
smaller
than
normal
because
of

reduced
amount
of
colloid
resulEng
in

increased
thyroxine
secreEon.
The

hyperplasEc
acinar
cells
may
crowd
up
to

one
side
of
acini
so
as
to
project
into
the

lumen
as
a
papillary
structure
(P).


S

P


The
colloid
in
hyperplasEc
follicles
shows

peripheral
scalloping
(S)
(clear
vacuoles

next
to
colloid)
reflecEng
the
increased

uElizaEon
of
stored
thyroid
colloid
to

produce
thyroxine
by
the
acinar
cells.

 N8‐
Fibroadenoma
of
the
breast

‐benign
solitary
lesion
usually
women

<30

‐mass
is
well
circumscribed
with
a

pseudocapsule
of
connecEve
Essue
and
is

composed
of
both
epithelial
and
stromal

components

‐epithelial
components
form
glandular

structures
lined
by
mammary
type

epithelium,
whilst
the
stromal

component
is
a
loose,
cellular
form
of

fibrous
Essue
(F).


‐ Two
paaerns
of
growth
are
seen.
In
the

pericanalicular
paaern
(P),
the
epithelial

component
takes
the
form
of
rounded

P
 ducts
that
remain
small
and
undistorted,

with
stroma
around
them
in
a
roughly

In
 symmetrical
manner

‐ ‐The
intracanalicular
paaern
(In)
the

ducts
appear
elongated
but
actually

represent
secEons
cut
through
flaaened

spaces
compressed
by
nodular

proliferaEon
of
stromal
component
(more

F
 in
large
fibroadenomas)

 N84
Basal
Cell
carcinoma
of
skin

almost
always
epidermal

aaachment;
nests
or
lobules
 •  Basal
cell
carcinoma
is
a
malignant
epithelial

tumor
arising
only
in
skin,
from
the
basal
layer

of
hyperchromaEc
but
 of
the
epidermis
or
of
the
pilosebaceous

uniform
basaloid
cells
with
 adnexa.
Tumor
is
represented
by
compact

peripheral
palisading,
 areas,
well
delineated
and
invading
the
dermis,

apparent
with
no
connecEon
with
the

surrounded
by
loose
stroma,
 epidermis.
Tumor
cells
resemble
normal
basal

o[en
with
myofibroblasts
 cells
(small,
monomorphous)
are
disposed
in

palisade
at
the
periphery
of
the
tumor
nests,

N and
mucinous
changes;
also
 but
are
spindle‐shaped
and
irregular
in
the

cle[‐like
retracEon
spaces
 middle.
Tumor
clusters
are
separated
by
a

C
 (due
to
stromal
mucin)
 reduced
stroma
with
inflammatory
infiltrate.

•  ‐solid
nodular
(N),
microcysEc(C),
and

trabecular
(T)
growth
paaerns

T

N84
Basal
Cell
carcinoma


N55
JuncEonal
nevus

In
a
juncEonal

naevus
,
the

melanocytes

aggregate
in
nests


(J)in
the
lower

J layers
of
the

epidermis
but
do

not
encroach
into

J
 underlying
dermis.

The
nests
are

round
to
oval
and

well
circumscribed,

and
the

melanocytes
are

pigmented.

Z66
Trichinosis

this
micrograph
reveals

developing
Trichinella

cysts
within
human

muscle
Essue.
A[er

exposure
to
gastric
acid

and
pepsin,
the
larvae
are

released
from
the
cysts

and
invade
the
small

bowel
mucosa
where
they

develop
into
adult
worms.

A[er
one
week,
the

females
release
larvae

that
migrate
to
the

striated
muscles
where

they
encyst.

‐
Demonstrate
uncalcified

larvae
in
muscle
biopsy

Zw80
Brain
infarct


Earliest
manifestaEon‐
neurons
become
shrunken,
eosinophillic

and
exhibit
nuclear
pyknosis.


Macrophage
infiltraEon
dominates
the
cellular
reacEon

and

phagocytose
lipid‐rich
myelin
and
take
on
a
foamy
appearance

(M)
–
there
are
also
brown
hemosiderin
laden
macrophages
–

and
glial
proliferaEon

may
form
cysts
–
brain
granulaEon
Essue

Edema‐
pale
empty
spaces


Zk
1
–
Brain
hemorrhage


•  General
Microscopic
Descrip2on


•Microscopically
hemorrhages
are

surrounded
by
pallor
of
Essue,

spongiosus,
and
pericellular

vacuolizaEon.
If
the
paEent

survives
the
area
of
hemorrhage
is

walled
off
by
reacEve
astrocytes

and
macrophages.

•
There
is
a
collagenous
capsule

around
an
old
hemorrhage
with

hemosiderin
laden
macrophages

sEll
present

N69
Glioblastoma
mulEforme

Glioblastoma
mulEform

is
a
tumour
composed

of
pleomorphic
glial

cells
of
varying
sizes
.

They
vary
from
very

small
cells
which

exhibit
tendency
to

differenEaEon
to
cells

exhibiEng
astrocyEc

morphology,
to
large

bizarre
giant
tumour

cells.
Necrosis
(N)
is

typical
of
this
tumour

together
with
high

celularity
and

proliferaEon
of

endothelial
cells
in

blood
vessels.

This
glioblastoma
mulEforme
(GBM)
demonstrates

marked
cellularity
with
marked
hyperchromaEsm

and
pleomorphism.
Note
the
prominent
vascularity
 Here
is
another
example
of
pseudopalisading

as
well
as
the
area
of
necrosis
at
the
le[
with

neoplasEc
cells
palisading
around
it.
 necrosis
of
neoplasEc
cells
in
a
glioblastoma

mulEforme
(GBM).
The
cells
of
a
GBM
can

infiltrate
widely,
parEcularly
along
white
maaer

tracts,
and
even
through
the
CSF.

 •  A
Meningioma
is


N71
Meningioma

composed
of
a
mixture

of
spindle
cells
and

epithelial
cells
arranged

in
whorls.
At
the
center

of
the
whorls
there
may

be
areas
of
calcificaEon

termed
psammoma

bodies
.
MitoEc
figures

are
not
common
in

meningiomas.

At
medium
power,
this
meningioma
is
composed
of

whorled
nests
of
cells.
A
variety
of
paaerns
are
possible.


At
high
magnificaEon,
this
meningioma
has
plump

pink
cells.
A
small
amount
of
brown
granular

hemosiderin
is
present.
Meningiomas
may
also

have
psammomma
bodies.

N74
Schwannoma


Schwannomas
usually
have
two

paaerns
of
growth
.
Compact
areas

of
spindle
cells
with
pink
cytoplasm

forming
palisades
and
whorls
termed

Antoni
A
Essue,
while
degeneraEon

in
the
tumour
results
in
loosely

arranged
tomour
areas
termed

Antoni
B
Essue.


Antoni
A‐
more
common‐
nuclear

pleomorphism
low
mitoEc
acEvity


Verocai
bodies‐
cytoplasmic

processes
between
two
palisading

structures
(purple
nuclei)

These
are
the
classic
microscopic
appearances
of
a
schwannoma,
which
is
benign.
Note
the

more
cellular
"Antoni
A"
paaern
on
the
le[
with
palisading
nuclei
surrounding
pink
areas

(Verocay
bodies).
On
the
right
is
the
"Antoni
B"
paaern
with
a
looser
stroma,
fewer
cells,

and
myxoid
change.

PANCREATITIS
AND
ENZYMATIC
FAT
TISSUE
NECROSIS

N 141-2 OAT CELL LUNG CANCER
N
19

LARGE
B
CELL
LYMPHOMA

ZK
21
BROWN
INDURATION
OF
THE
LUNG

ZW
92A
Kidney
in
diabetes


Z
23
Chronic
pyelonephriEs


N100-101Hydatiform mole and choriocarcioma
Z
14
Phlegmonous
appendiciEs


LIPOSARCOMA