King of pathology

By\King of pathology( Legand Hazem )

Cell injury
(N) Cs are constantly change their structure & function according to various demands & stress.
The Cs react to injury by:
1-AA!"A"#$% =altered state that preserve vitality of Cs in response to !T"#!! (physiologic or
pathological).
"ype& of 'ell adaptation are:
A-Hypertrophy: $$ in organ si%e d.t $$ in si%e of its Cs .
B-Atrophy: && in organ si%e of an organ d.t && in si%e of its Cs.
C- Hyperpla&ia: $$ in si%e of an organ d.t $$ in number of Cs
(-)*)%)+A"#$%= reversible injury of Cs.
,-C)LL )A"H= 'rreversible injury. There are ( patterns for cell death:
)poptosis (single cell death).
Necrosis (*eath of group of Cs)
egeneration
ef- "eversible injury of living Cs leading to metabolic+ functional & morphological changes.
Cla&&ifi'ation- A- "ypi'al
,)Cloudy s-elling & hydropic degeneration: d.t $$ intracellular -ater.
().atty change: d.t $$ intracellular fat.
B- Atypi'al ('ntracellular accumulation & e/tracellular depositions)
,. 0ucoid degeneration & my/omatous degeneration: disturbance of mucopolysaccharides.
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King of pathology
(. 1yaline degeneration (or change).
2. .ibrinoid degeneration.
3. )myloid degeneration.
CL$./ 01)LL#%* (ALB.2#%$.0 )*)%)+A"#$%)
)tiology:
!hy&i'al: e.g. cold+ heat+ electrical+ & irradiation.
Chemi'al: e.g. poisons+ drugs+ acids & al4alis )tiology of
#nfe'tiou&: e.g. bacteria+ virus+ & fungi 3 degeneration.
#mmunologi'al:)g&)b reaction
Hypo4ia: e.g. in anemia & loss of 5( carrying capacity.
2yo'ardial infar'tion and ne'roti' ti&&ue
!athogene&i&:
2ito'hondrial theory: mitochondrial damage && )T6 production failure of Na78 pump
accumulation of Na & 1(9 in cell.
55 intra'ellular o&moti' pre&&ure d.t: accumulation of metabolites.
Both intracellular accumulation of -ater.
$rgan& affe'ted: parenchymatous organs (e.g. liver+ 4idney+ heart & pancreas) are mainly affected
because Cs of these organs are highly active containing $$ number of mitochondria.
%6): &5rgan is $$ in si%e e tense capsule & smooth surface.
& !oft in consistency+ e rounded borders & bulging cut surface
26)& Cs are s-ollen e granular cytoplasm. Nucleus is normal (N)
&in 8idneytubules sho-( !tar shaped appearance)
Hydropi' degeneration (Ballooning 78a'uolar(
ef- severe form of degeneration+ severer than cloudy s-elling.
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%6)926): !ame as cloudy s-elling e/cept cytoplasm is vascular not granular
)4ample& are: )ccumulation of $$ fluid in epidermal Cs as in burns or herpes simple/.
.atty change (*egeneration or infiltration)
ef: $$ accumulation of intracellular neutral fat (Triglycerides) in parenchymatous cells
transforming into fat li4e cells
0ite&: parenchymatous organs+ most commonly in liver.
Cau&e& : !ame aetiology as degeneration :ut :
'rritant is severe e short duration of action 5"
'rritant is mild e long duration of action
$ )tiology of fatty li:er (di&'u&&ed after)
!athogene&i&
)& ;atty degeneration = 2ito'hondrial theory: injurious agent injury to mitochondria release
of mitoch. lipid in cytoplasm.
:&;atty infiltration : 0pe'ial me'hani&m& in < li:er-
,&$$ entry of free fatty acids into liver. e.g. $$ inta4e or mobili%ation of fat from depots.
(&$$ fatty acid synthesis in liver from glucose(*0) & amino acids
2&$$ rate of conversion of fatty acids to triglycerides (esterification).
3& && fatty acid o/idation.
;& && conjugation of fatty acids e apo&protein.
<& && lipoprotein secretion from liver.
The above causes can act by , or more mechanisms+ e.g. chronic alcoholism acts through ,+( & 2.
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26)- of fatty 'hange in any organ-
.at is dissolved during preparation:
,&#n H46):cells containing fat are enlarged
cytoplasm contain empty vacuoles = enlarge7coalesce7push nucleus to one side
of cell giving (!ignet ring appearance)
(&#n ;rozen &e'tion:the fat appear in cytoplasm as droplet= enlarge7coalesce7push
nucleus to one side of cell giving (!ignet ring appearance)
- can be stained by = $&mi' a'id blac4
- > 0udan ### 5range .
- > 0'arlet red "ed.
!athologi'al feature&-
Li:er- ;atty Li:er
%6): !i%e:enlarged
(0
!hape:preserved
Border:rounded
Colour:pale yello-
(C
Consistency:soft
C60 :bulges out+ greasy to touch+diffuse or focal
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26)- !ame as before 5
i&tri>ution:
-;o'al: as in viral hepatitis.
-?onal: to/emia & anemia.
-iffu&e: Nutritional cases
%3B: (%ut-meg li:er) 't is morphological term describe .ocal .atty change of liver in case of
chronic venous congestion of liver (@ill >e di&'u&&ed in 'ir'ulatory di&order)

1eart: T-o types:
1) iffu&e: occurs in severe injury
)arly: 1eart becomes flabby+ soft+ $$ rupture)1..
Late: 0yocardial fibers are replaced by fibrosis && in heart si%e.
2) !at'hy ("a>>y 'at) or tigroid appearan'e or fru&h >rea&t. occurs in moderate injury
%6): yello- strea4s(fat) alternating e bro-n (intact ms fibers) areas mottled appearance.
26)- !ame as before e/cept ( %o &ignet ring appearan'e)
N.::
,-$>e&ity fat deposition in fat deposits.
(-fatty 'hange fat deposition in parenchymatous cells.
,-adepo&ity fat deposition in tissue of parenchymatous organ.

;atty 'hange of Aidney
%6): &ame a& li:er $ Cut surface sho-s yello- strea4s in corte/.
26): &ame a& >efore $ .at vacuoles appear in cytoplasm of pro/imal convoluted tubular Cs.
i&tur>an'e of mu'opoly&a''haride&
ef -55accumulation of mucopolysaccharides in epithelial Cs (mucoid degeneration) or CT
(my/omatous degeneration)
,)0ucoid degeneration: ()0y/omatous degeneration
ef
)B-
$''ur
26)
)ffect epithelial cell.
,&catarrhal inflammation
(&mucoid adenocarcinoma
intracelluar
( signet ring appearance)
!-ollen cells filled #? mucin
6ushing nucleus to one side
5f the cell
)ffect C.T
,&0y/edema.
(&0y/oma(tumour).
#/tracellular
( =harton@s Aelly)
:ranching cells #? pale blue
cytoplasm
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King of pathology
Hyaline degeneration (hyalino&i&)
ef :!tructural changes of dead tissue into homogenous+pin4+refractile+structurless material
Cau&e:!till Bn4no-n
"ype&:
,&)4tra'ellular(C3" hyalino&i&)
C8a&'ular:
&arteries #C. )therosclerosis
&arterioles . #C. ,&benign hypertension
(&splenomegally(central arteriole of spleen)
&capillaries ,&*.0
(&:enign hypertension
2&glomerulonephritis
B-)4tra:a&'ular-)B
,&leiomyoma
(&old thrombus or infarction
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(& 'ellular
+u&&el >odie& in +hino&'leroma-def of ru&&el >odie& hyaline degeneration of plasma cells
Coun'ilman >odie& in :iral hepatiti& in li:er: def of councilman bodies hyaline degeneration
of hepatocytes (it is proved to be apoptosis than degeneration)
Corpora amyla'ia in >enign pro&tati' hyperpla&ia
#&let& of langerhan& of pan'rea& in 32
zenAerD& hyaline degeneration (%e'ro&i&)
=1yalinosis in voluntary muscles occurs in severe infections & fevers+ especially typhoid.
0ite& -- "ectus abdominus *iaphragm. 'ntercostal muscles.
'ompli'ation: "upture of muscles & hemorrhage
;i>rinoid degeneration
ef- homogenous or granular+ eosinophilic material e staining properties li4e fibrin (destroyed
collagen).
)4ample&-
Collagen diseases: e.g. "h fever+ polyarteritis nodosa+ systemic lupus erythematosis (!D#).
0alignant hypertension: in -alls of arterioles.
Amyloido&i&
ef: disease comple/ (not a single disease) characteri%ed by abn protein deposited ( ) Cs in many
tissues & organs of body variable clinical pictures
't has a uniform morphological appearance but different chemical composition.
Chemi'al nature of amyloid protein-
&E9F of amyloid structure is formed from protein called fibrillary protein -? is ( types:
a-2ajor 'omponent--
&)D:amyloid derived from light chain 'g.
&)):amyloid derived from !))(serum associated amyloid).
't is deposited in case of chronic inflamatory disease.
&).:amyloid of familian medetrian fever(..0..).
&)#:amyloid of endocrine glands.
&)!:amyloid of senility.
B-2ajor 'omponent--
&amyloid endocrine thyroid:& in medullary carcinoma of thyroid.
&pre&albumin.
&:( microglobulin.
&:( amyloid protein in al%ehemir disease.
Clinical types of amyloidosis:
A-Lo'alized:occur in vocal cord
Thyroid gland
1eart
B-0y&temi':2types & primary amyloidosis
- !econdary amyloidosis
- .amilial(..0..
Be&t @i&he&
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0e'ondary amyloido&i& primary amyloido&i&
5ccur in any age
Common
1 - 'nfective granuloma as T.:&G&Deprosy .
2 - allergic granuloma as arthritis .
3 - chronic suppurative granuloma as :
- chronis lung abscess
- chronic osteomylitis
- hodg4in@s lymphoma
- bronchiectasis
))(amyloid associated) .
!olid organ than 1ollo- organ e/cept heart
5ccur due to renal or hepatic failure .
Be&t @i&he& .
5ccur in old age
"are
5f un4no-n cause associated # `
dse c?h by production of 'g as :
multiple myeloma7non 1odg4in@s
lymphoma(malignant tumour of
:&lymphocyte)
)D(light chain)
1ollo- organ than !olid organ :
- hollo- organ as
heart+H'T+muscle .
- solid organ as
Diver+spleen+4idney
5ccur due to heart failure .
Be&t @i&he& .

Age :
#n'iden'e :
Cau&e :
"ype7nature
of protein :
$rgan
affe'ted :
eath :
%6)- of any amyloid organ :
!i%e:enlarged
(0
!hape:preserved
Cap&ule:tense
Colour:bro-n or gray
(C
Cosistency:firm+rubbery or -a/y
Border:sharp .
Cut &urfa'e:flat .
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26)-of any amyloid organ :
1 - 0ite of depo&ition: differ according to the organ .
2 - 0hape of amyloid material :
!pread for-ard +bac4-ard+laterally enclosing original cells
ischemia + atrophy + degeneration and necrosis .
3 - 0tain&(method of demon&tration of amyloid material) :
* gro&& &taining : (@rite it )E %6) )
a&Lugol& iodine- stain amyloid: dar4 bro-n .
stain rest of tissue: dar4 bro-n .
b&iodine eE 1F &ulphuri' a'id: stain amyloid:blue .
* mi'ro&'opi' &taining- (@rite it )E 26))
a-HB6)- amyloid appear homogenous refractile pale pin4 material .
>-Congo red &tain- amyloid appear orange red .
'-2eta'hromati' &tain: stain amyloid rose red .

stain rest of tissue violet .
d-#mmunohi&tologi'al- momclonal )b is directed against various chemical
form of amyloid .
Be&t @i&he&
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King of pathology
!athologi'al feature& of amyloido&i& in &ome organ&-
1)Li:er-
%3B-cause:&e'ondary amyloidosis more than primary amyloidosis.( ).
%6): )s before $gross staining (-rite them) .

26): ,&&ite of depo&ition of amyloid material:&!pace of disse&arterioles&venules.
&'t begins in intermediate %one then spread in both direction.
(&&hape of amyloid material: (@rite them)3
2&mi'ro&'opi' &taining-
Clini'al effe't&: &don@t affect liver function e/cept very late
&liver failure is rare..
() Kidney- < mo&t 'ommon 9 &eriou&3
%3B-cause: &e'ondary amyloidosis more than primary amyloidosis.( )
%6): & A& >efore5gro&& &taining (@rite them)$ e4'ept only that(0#?)) #arly no change in si%e+
later 4idney is $$ in si%e. 'n prolonged course it may become small d.t ischemic changes ( ( ry
'ontra'ted Aidney)3
26)- 1-0hape of amyloid material: (@rite them)3
(-2i'ro&'opi' &taining-
,-0ite of depo&ition of amyloid material: diffu&e depo&ition of amyloid material in:
a- Afferent arteriole&
thic4ening of the -all & narro-ing of the lumen.
>- *lomerular 'apillarie&:
)myloid deposit in basement membrane
'- Colle'ting tu>ule& -
)myloid deposit in basement membrane.
1yaline casts in tubular lumen.
Clini'al effe't&: a-dep&oition in afferent arteriole (Nephrotic syndrome)occur.
>-depo&ition in glomerular 'apillary (*iabetic insipidus)occur.
'-depo&ition in afferent arteriole ("enal failure)occur Dater.
%3B- %ephroti' &yndrome 7 generalized edema.
G& patient e? chronic lung abscess +!uddenly develop hea:y proteinuria and generalized edema
1hat i& 26) of AidneyI =rite 07# of ()myloid 4idney)
Be&t @i&he&
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King of pathology
,) 0pleen- one of t@o pattern& de:elop-
%3B-cause:&e'ondary amyloidosis more than primary amyloidosis.( ).
&there are ( pattern of amyloid spleen:
a&!ago spleen=.ocal type.
:&*iffuse amyloid spleen.
c&may be mi/ed type.
%6): A& >efore $gro&& &taining (@rite them) e/cept only one differen'e accordind to pattern:

C60: &'f focal type :ro-n dots on bac4round.
& 'f diffuse type :ro-n strea4s on bac4ground.
26): - 1-0hape of amyloid material: (@rite them)3
(-2i'ro&'opi' &taining-
,-0ite of depo&ition-differ a''ording to pattern -
#f fo'al type amyloid is present in central arteriole then replace lymphoid follicle !o called
.ocal type.
#f diffu&e type amyloid is present in basement membrane of splenic sinusoids and blood vessel
Then compress lymphoid follicle !o called diffuse type.
Clini'al effe't&: Cause splenomegally.
0ago 0pleen. iffu&e amyloid &pleen.
#n'iden'e-
0ize-
Lymph
folli'le-
C60-
26):
Common
0oderately enlarged.
)trophied by pressure.
6lenty bro-n dots.
)myloid in central
)rteriole.
"are
0ar4ed enlarged.
Not atrophy.
*iffuse bro-n strea4s.
)myloid in blood vessel
and blood sinusoids.
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H) Heart-
)myloid is deposited ( ) cardiac muscle fibers & -alls of blood vessels. !ubendocardium is mainly
affected especially seen in atria.
1eart is $$ in si%e. 't may lead to heart failure or conduction defect.
I) Alimentary tra't (0toma'h 9 inte&tine)-
The mucosa is thic4ened by deposition of amyloid in basement membrane of capillaries. This lead to:
J )trophy of epithelium causing malabsorption.
J )ltered permeability causing diarrhea & electrolyte disturbance.
J)"ongue- "hi& may 'au&e 2a'roglo&&ia (55 tongue)3
K) Hingiva: Thic4ened gingiva.
K) 6eripheral nerve: Thic4ened+ associated e neuropathy & a/onal degeneration
!athologi'al 'al'ifi'ation
ef : *eposition of Ca$$ salts (phosphate & carbonate) in tissues other than bone & teeth.
%6): Calcified area resembles chal4. 't is dull opaLue+ -hite+ e finely granular surface & hard in
consistency.
26): 't is dar4 bluish+ granular+ e hemato/ylin.
"ype&- ,& *ystrophic calcification. 't is commonest type.
(&0etastatic calcification.
2&!tone formation.
1-y&trophi' 'al'ifi'ation3

(- 2eta&tati' 'al'ifi'ation
ef-
Cau&e:
)4-
*eposition of Ca in dead or
degenerated tissue e? normal Ca
level.
1-Lo'al alAalinity of ne'roti'
ti&&ue3
(-in'rea&e a'ti:ity of alAaline
pho&phata&e3
a-in degenerated ti&&ue:
&old scar.
&leiomyoma.
&@all of chronic abscess.
>-in dead7ne'roti' ti&&ue:
&infarction.
&fat necrosis.
&pu& of chronic abscess.
'-'al'ino&i& of unAno@n 'au&e-
&Lo'alized('al'ino&i&
'ir'um&'ripta) in s4in&!.C
tissue.
&generalized('al'ino&i&
uni:er&ali&) in muscle and
tendon.
*eposition of Ca in normal tissue e?
elevated Ca level.
,&in'rea&e >lood Ca >y-
&increase inta4e from diet.
&increase mobili%ation from bone.
&!arcoidosis.
1-ga&tri' mu'o&a3
(-ranal tu>ule&3
,-lung al:eoli3
H-arterie&3
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,) 0tone formation:
Ca$$ salt deposition in biliary tract+ urinary tract & rarely in other ductal systems+
!igmentation
ef: 6igments are colored substances that stain tissue. These II accumulate intracellularly.
6athological pigmentation includes t-o major fs:
#))B$*)%$.0:
a&)nthracosis: :lac4 pigmentation of lung d.t inhalation of carbon+ -hich is engulfed by
macrophages. 't is d.t air pollution. 'n $$ e/posure lead to pulmonary fibrosis or emphysema.
b&Tattooing: 'njection of colored pigments into s4in+ ta4en by dermal macrophages
())%$*)%$.0 :
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King of pathology
A-2elanin - B) Lipo'hrome pigment
(Lipofu&'in)3
C) hemoglo>in - deri:ed pigment& :
.ormed by melanocytes
from tyrosine by action of
tyrosinase.
"esponsible for (N)
color of s4in+ hair+ eyes
meninges & basal ganglia.
Causes of melanin
hyperpigmentatlon:
, & #/posure to sun.
(&)ddisons disease.
2&Chloasma of pregnancy:
6igmentation around nipple+
face & genitalia.
3&Tumors of melanocytic
origin:
:enign: pigmented nevus.
0alignant: 0alignant
melanoma.
;&Cafe au lait s4in patches: in
multiple neurofibromatosis+
Causes of melanin
hypopigmentation:
,&)lbinism: This is a
generali%ed hypopigmentation
d.t congenital tyrosinase
deficiency. 0elanin pigment is
absent from s4in+ hair & eyes.
(&Deu4oderma: congenital or
acLuired (as in leprosy).
ef - yello-ish bro-n pigment -
present (N) in heart+
testis+seminal vesicles+ & adrenal
corte/.
)4ample- >ro@n atrophy of <
heart3 -
Cau&e: !enile atrophy.
%6)-
1-Heart small in si%e.
(-@all of heart thin
,-peri'ardial ;at disappear
)nd replaced by( edematous jelly
li4e tissue).
H-2yo'ardium bro-n in
colour
I-$rifi'e& of heart still large
J-'oronary artery is tortuous
26):
,&mu&'le fi>er of heart are
thin+atrophy.
(&nu'lei are pyAnoti'
(small+eccentric+dar4 stained).
2&yello-ish bro-n lipochrome
pigment on both sides of
nucleus(peri&nuclear distal)
3&'nterstitial tissue sho- area of
fibrosis.
;&The section is stained e? 1C7#
only or.at stain.
26): affected cell undergo
necrosis and fibrosis.
)ffe't:
&Diver pigmentary cirrhosis.
hepatoma in (9F of cases.
&6ancreas diabetes mellitus.
&1eart heart failure.
&!4in 1as a bron%ed color d.t $$
melanin & 1emosiderin
deposition.
1)Biliru>in: $$ in jaundice. Mve e?6russian
blue test.
()hemozoin (hematin ): bro-nish iron containing
pigment associated e bilhar%iasis & malaria.
The pigment is produced by -orm released
into blood+ then engulfed by macrophages in
liver & spleen (6arasitic pigmentation). &ve e?
6russian blue test+ .
,) Hemo&iderin-
&) bro-nish iron containing pigmen.$ve
6russian blue test.
& "ype&:
a& Lo'alized hemo&idero&i&:
& 'n areas of hemorrhage
&blood leave bl.vessel to tissue fibrosis
&hemosiderin is phagocytosed by macrophage
b& *eneralized hemo&idero&i& (!rimary 9 (ry
type&)
1)(ry hemo&idero&i&:
Cau&e&- 'ron overload d.t:
&"epeated blood transfusions.
&1emolytic animas.
&:one marro- hypofunction ('mpaired
utili%ation of iron).
!athology:
a&normally+iron is stored in cells binding e?
apoferrtin to form haemosidrine.
b&#/cess haemosiderine appear in mononuclear
phagocytic cells and in advanced cases affect
parenchymal cells.
()1ry hemo&idero&i&7Bronzed
dia>ete&:

'au&e&: inborn error ch?by defect in apoferrtin&
ferrtin system e/cess absorption of iron.
!athogene&i&:
#/cess absorption of iron saturation of
macrophage system deposition of iron in
phagocytes and in parenchymatous organ (more
severe) injury and manifestation.
'ncidence: & male above 39 years
&.emale is protected by
0enstruation.
%6): affected organ is ( 2" ) enlarged&hard&
:ro-n.
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King of pathology
Cell death in'lude
A-%e'ro&i&3
B-Apopto&i&3
%)C+$0#0
ef : *eath of a group of Cs e in a living body.
Cau&e& :
0ame etiology of degeneration ( discussed before ) e/cept only ( difference:&
1-#rritant ha& 0e:ere inten&ity3
!rolonged duration3
(-Chemi'al agent& are proteolyti' enzyme of amoe>a3
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King of pathology
!oi&on&-drug&3
!an'reati' &e'retion3
!athogene&i&-
1-!evere mitochondrial damage and mar4ed reduction of )T6 production
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King of pathology
$$ anaerobic glycolysis &&of most en%ymes e/cept lysosomal en%ymes.
(&destruction of cell membrane en%ymes become free.
2&increase intracellular Ca $$ of follo-ing en%ymes:&
a-protea&e brea4do-n of cytos4eleton protein.
>-pho&pholipid& destruction f membrane phospholipids.
'-)ndonu'lea&e& brea4do-n of *N) chromatin fragmentation
py4nosis&4aryorrhe/is&4aryolysis.
3&( processes underlie the basic morphological change:&
a-enaturation of protein.
>-)nzymati' dige&tion of organelle& and other 'yto&oli' 'omponent >y:&
>cellular lysosome autolysis.
>polymorphs lysosome.
=hen denaturation predominates the cells retain their outline e? loss of cellular details
and the area is firm+pale+s-ollen.
=hen en%ymatic digestion predominates there is loss of architectural and structural detail
)nd the area is soft and filled e? turbid fluid.

!athologi'al 'hange&-
%6): the necrotic area is >dfined.
> dull+opaLue.
> firm.
> &-ollen.
> &urrounded by %one of hyperemia(acute inflamation).
26) = po&t ne'roti' 'hange:&
1- Cellular-
A-%u'lear-
=pyAno&i&-small&dar4 stained nucleus.
=Aaryorrhe4i&-fragmentation of nucleus in cytoplasm3
=Aaryoly&i&-nucleus disappear due to chromatin hydrolysis3
B-'ytopla&m-
=Cytomegaly-s-ollen of the cell.
=>e'ome more eosinophilic.
C-'ell mem>rane-
=#t disappear and en%ymes become free.
(- Ar'hite'ture-
A-denaturation o''ur $+
B-ly&i&- autolysis- release proteolytic en%yme from ti&&ue3
Heterolysis: release proteolytic en%yme from ma'rophage3
;ate of ne'roti' ti&&ue :&
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King of pathology
#f &mall part-
>DiLuifaction occur.
>)bsorped by macrophage Then undergo:
-+egeneration $+
-;i>ro&i&3
#f large part-
>#ncapsulation occur= !urrounded by fibrous capsule.
Then undergo: LiKuifa'tion $+
Cal'ifi'ation $+
!utrifa'tion o''ur gangrene $+
Ba'terial infe'tion o''ur pu& a>&'e&& o''ur.
"ype& of ne'ro&i&-
1-Coagulati:e ne'ro&i& (-liKuefa'ti:e ne'ro&i&
)tiology:
)B3and
pathogene&i& .
%6)-
26)-
a&Cut of blood supply (ischemia)
-all infarction e4'ept brain infarction3
a->lo'Aage of action of most en%ymes
due to denaturation of cellular
protein by irritant.
>&)s hydrolytic en%ymes are bloc4ed
6reserved ararchitecture of
dead tissue it appear paler than
normal tissue li4e boiled meat.
!ame as before
1-!o&t ne'roti' 'hange:
Nuclear+cytoplasmic+denaturation+
But %o lysis.
(-Lo&& of cellular details e?
!re&er:ed architecture.
,->lood :e&&el persist for long time:&
(more resistant)
a& Cut of blood supply (ischemia).
b& 6roteolytic en%yme -? liLuify necrotic
tissue.
,&:rain infarction:due to high lipid 'ontent
and la'A of lymphati'&.
(&pyogenic abscess:due to proteolytic
en%ymes from pus cells.
2&amoebic abscess:due to liLuifactive
en%ymes produced by parasite.
DiLuified tissue and it is soft.
1-!o&t ne'roti' 'hange:
Nuclear+cytoplasmic+lysis+
But %o denaturation.
(-Complete lo&& of cellular details and
Lo&& of architecture.

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King of pathology
,) Ca&eation ne'ro&i&-
)tiology : allergy follo-ed by liLuefaction
)B : T.: and !yphilis(G).
%6) : the necrotic area is >yello-+dry.
>friable.
>%ot surrounded by hyperaemia.

26) :,&6ost necrotic change3
(&homogenous structurless pin4 eo&inophili' area.

H);at ne'ro&i&- %e'ro&i& of fat
"ype&-
a-"raumati' fat ne'ro&i&-
trauma to adipose tissue of subcutaneous fat & breast rupture of fat Cs release of lipase self
digestion of fat Cs.
% 6)- 1ard mass in breast$ retraction of nipple. II mi&taAen for 'ar'inoma.
26)- Necrotic fat Cs appear cloudy e infiltration by neutrophils+ macrophages & foreign body giant
Cs. Hranulation tissue is formed around lesion+ & mature to form a fibrous tissue. II calcified.
>-)nzymati' fat ne'ro&i&-
5ccurs in acute hemorrhagic pancreatitis. #scape of lipases & protease en%ymes from ruptured
pancreatic ducts digestion of surrounding peritoneal fat Cs. liberated fatty acids have a high
affinity to combine e Ca$$ forming Ca$$ soaps.
I)?enAer& degeneration or ne'ro&i&- (de&'ri>ed >efore)3
J);i>rinoid degeneration or ne'ro&i&- (de&'ri>ed >efore)3
"3B 0yphili&(L)
=)4tent of
%e'ro&i&3
='ellular
detail&3
>o''urren'e
:
>giant 'ell&:
=ide
Complete loss
"apid.
55
Dimited.
6artial loss.
Ta4e longer time
5(less)

19
King of pathology
Apopto&i&
ef: > !ingle cell death. 5"
=6rogrammed cell death.5"
=Cell suicide.
't occur e?out inflammatory reaction in surrounding tissue.
)62: &Chromatin condensation $ .ragmentation of *N) by endonuclease
&.ormation of membrane blebs.
&)poptotic bodies consist of nuclear fragment surrounded by part of cell+ -hich separate
engulfed by phagocytic Cs. #n H9) appear as &mall rounded eo&inophili' >odie& .
)4ample&
!hy&iologi' pathologi'
,& )m>ryogene&i&: atresia of
some structures
(& #ndometrium during
menstruation
2& phy&iologi' atrophy of
lactating breast after -eaning
,& death of tumor cells (competition
for nutrition)
(& death by cytoto/ic T cells in
rejection
2& viral (councilman bodies in viral
hepatits)
3& pathologi' atrophy after duct
obstruction and after & & hormone
production
ifferen'e& >et@een ne'ro&i& and apopto&i&--
%e'ro&i& Apopto&i&
Cau&e-
2e'hani&m-
"i&&ue rea'tion:
2orphology-
%6)-
26)-
!athologi'al e3g Hypo4iaMto4in&
,&0embrane injury.
(&)T6 depletion.
'nflammation.
& pale+ dry + -ell defined.
&cellular s-elling.
&coagulation of protein.
&destruction of organelles
!hy&iologi'al or pathologi'al3
,&#ndonuclease activation.
No inflammation but phagocytosis of
apoptotic bodies by adjacent cells.
-No changes & area appear normal.
&cell shrin4age.
&chromatin condensation.
&)poptotic body.
Be&t @i&he&

By\King of pathology( Legand Hazem )
20