King of pathology

By\King of pathology( Legand – Hazem )
CIRCULATOR !I"TURBA#C$"
% ( di&t'()an*e& of )lood flo+ , )ody fl'id&)-
Hype(emia % .. amo'nt of )lood in a /e&&el 0 1
(1) Active (arterial) : ++ in bl.flow to organ d-t 2-! of a(te(iole&
phy&iologi* 0 e.g:
- muscular exercise.
- glands during secretion
3athologi* : e.g:
-A*'te inflammation
(2) Passive (venous congestion ): ++ bl flow to organ d-t o)&t('*tion of /eno'& o't flo+  /ein&
)e*ome pa&&i/ely dilated
Lo*al :
♦ Acute
♦ Chronic
4ene(al :
♦ Acute
♦ Chronic
3a&&i/e Hype(emia % ( /eno'& *onge&tion )
I1 Local =Localized congestion in any pa(t of 5 )ody d-t it6& /eno'& o't flo+ o)&t('*tion-
(7) A*'te (8)Ch(oni*
a1 Ca'&e& : Sudden complete enous
obstruction d.t :
- !hrombosis
- Ligature
- !wisting of " pedicle of moable
organ #oar$%
- Strangulated hernia.
)1 pathology : &apid seere dilatation of "
eins ' capillaries w ma$ rupture edema
*1 9ate : #(% &'ffi*ient enous
anastomosis no harmful effect.
#)%in&'ffi*ient enous anastomosis #as in
mesenteric eins% venous infarction of
intestine
a1 Ca'&e& : gradual incomplete enous
obstruction as compression b$ :
- !umor
- *nlarged L.+.
- ,regnant uterus
- Lier cirrhosis ' fibrosis.
)1 3athology : #(% " eins- enules ' capillaries
proximal to obstruction become dilated '
congested  edema.
#)%.radual opening of " collaterals '
anastomatic eins.
*1 $:ample& of *h(oni* lo*al /eno'&
*onge&tion :
(-Lier cirrhosis or fibrosis :  obst. of eins
portal h$pertension.
)-C /.C. of " lungs # brown induration %.
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King of pathology
I71 General : d-t total ( *onge&ti/e% Rt , Lt ) hea(t fail'(e So Congestion occurs all o/e( 5 )ody.
71 A*'te
in a*'te H-9 all organs show acute congestion.
81 Ch(oni*
Def : gradual enous congestion affecting " whole enous s$stem.
Causes : both &t. Sided ' left sided 0.1.
Rt- "ided H-9.: show chronic enous congestion # . c. % all oer " bod$ e:*ept l'ng&-
Left &ided- H-9.: show chronic enous congestion # . c. % of l'ng&
Pathology of t! "i#e# $!%! 0
&'General effects
(- Conge&ted ne*; /ein&
)- Cyano&i& = purple - blue coloration of lips- bed of nails ... etc. d.t ++ reduced 0b ' inade2uate
tissue perfusion ' - - ox$genation.
3- Ca(dia* edema : in dependent parts of " bod$ =4(a/itational edema ( di&*'&&ed late( in edema )
4- in*(ea&e )lood /ol'me +a ' 0)o retension.
&&' Local effects ( appearance of ( organs ) :
Li/e(0
$a(ly ( C-2-C- li/e()%#'t <eg
li/e( % fo*al fatty *hange-
Late ( *a(dia* *i((ho&i& )-
#=$
<=$0
Size: enlarged.
8"
Shape: presered
"'(fa*e: smooth.
"e(o'& *oat: fibrosed later.
Colour:dar5 red congested
8C
Consistenc$:soft to firm.
Cap&'le0Tense.
C=&: # mottled appearance %
due to alternation of )(o+n
(*onge&tion)and yello+ colours
(fatty *hange) So called
( )ut'*eg liver )!
A1central eins and central ends
of sinusoids are dilated
congested.
B1*ell& of mid zone show
# 1att$ change %.
C1*ell& of pe(iphe(al zone show
#+ormal OR cloud$
swelling%
!-2on K'ppfe( *ell& show
# 0aemosidrine granules %
Shrun5en# - - size %
distorted
.ranular# irregular % surface.
.ra$ish red due to fibrosis e6
congestion.
1irm.
Thic5 b$ fibrosis.
C=&0 (-+hite # fi)(o&i& %.
)-show *i((hoti* nod'le&-
A1*ell& of *ent(al zone show necrosis
followed b$ fibrosis fibrosed area
7oin each other b$ fibrous bands.

B1*ompen&ato(y hype(pla&ia of health$
hepatoc$tes w6 are encircled b$ fibrous
bands cirrhotic nodules
=regenerating nodules.
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King of pathology
"pleen 0
#=$ 0 Size : enlarged#) times%
8"
Shape : presered.
"'(fa*e : smooth.
Colour: dar5 red congested.
8C
Consistenc$ : firm.
Cap&'le,t(a)e*'lae:thic5.
C=" : L$mphoid follicle is not apparent.
<=$0
8 !hic5 capsule ' trabeculae.
8 Atroph$ of l$mphoid follicles.
8 1ibrous tissue of " red pulp.
8 &upture of congested capillaries disintegrate hemosiderin leading to
fibrosis ' fo(mation of fi)(o&ide(oti* nod'le& #4amna 4andy nod'le&%. !his
contains : ) minerals iron + calcium.
) fibers collagen + elastic.
( pigment hemosiderin.
.iant cells.
>0 gi/e a**o'nt on( 4ama 4andy nod'le& )0
71pathogene&i&0
Seere congestion in splenic sinusoids rupture haemol$sis of &9Cs
0aemosiderine fibrosis calcification
81Component0 as before.
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King of pathology
?13('&&ian )l'e : +e ,russian blue due to haemosidrine and iron.
Kidney& 0
#=$ 0 Size:enlarged.
8"
Shape:presered.
"'(fa*e:smooth.
Colour:dar5 red congested.
8C
Cosistenc$:soft.
Cap&'le : stretched.
Bo(de(&:rounded
C=" : a- $ellow cortex #d.t fatt$ change% containing dar5 red dots ' strea5s w6 are "
glomeruli ' " congested essels
b-dar5 red medulla.

<=$ 0 8 Congestion of " glomerular capillaries.
8 1att$ change of " proximal conoluted tubules.
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King of pathology
Ch(oni* /eno'& *onge&tion l'ng& ( B(o+n ind'(ation )%3'lmona(y *onge&tion
Ca'&e& :- chronic left ent. 1ailure.
)-<it(al &teno&i&.
3athogene&i& :
-+loo# accumulates in Lt! Atrium  pulmonar$ eins enules  capillaries becomes
congested ' dilated rupture  disintegration of &9Cs  hemosi#erin ,- cause fi)(o&i& ' ta5en
b$ macrophages ,- appear s,ollen . /ro,n ' are called heart failure Cs!
'"ome of ( $eart %! Cs go to draining l$mph nodes. Some of them die ' " released hemo&ide(in 
fi)(o&i& in " interstitial tissue.So lung becomes brown ' tough a condition called0+ro,n in#uration0
#=$ 0 7" Size: enlarged.
Colour: 9rown # d-t hemo&ide(in %.
8C
Consistenc$: 0ea$- firm # d-t fi)(o&i& %

C=": oozes blood-stained froth$ fluid.
)(on*hial m'*o&a  congested- edematous ' coered b$ a la$er of mucous.
<=$0
 Inte( al/eola( &epta : thic5ened b$ :
*dema # transudate % ' fibrosis. contain dilated congested capillaries
 The al/eoli : Contains
− ;range # intact ' hemol$zed &9Cs %-
− brown # hemosidrin granules ' heart failure cells %-
− pin5- homogenous # transudate %.
1he heart failure cells :
.roups of Large- rounded- phagoc$tic cells engulfing brown hemosidrin granules ' red cells
 Inte(&titi'm &ho+& :
-9ronchial mucosa  congested- edematous e6 0.1. Cs
THRO<BO"I"
!ef : formation of a solid mass # thrombus % of blood elements ( mainly platelet& , fi)(in % in " C/S.
during life.
Ca'&e& of th(om)o&i& : ( 2i(*ho+@& t(iad )
7) Damage of ( vascular en#othelium : i.e. roughness of " intima " platelets adhere to " damaged
endothelium.
a- <echanical : trauma- pressure #as ligature%.
b- :nflammator$ # phlebitis- arteritis- endocardites %
C- =egeneratie # atheroma%
#-B : #o(mal p(o&ta*y*lin &e*(eted )y 5 /a&*'la( endotheli'm  - - thrombosis.
Th(om)o:ane A8 li)e(ated f(om 5 platelet& help& thei( agg(egation  ++ thrombosis.
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King of pathology
2) "lo,ing of /loo# flo, 2 "tasis :'
• In no(mal )lood &t(eam: " )lood C& occup$ " central part- ' 5 pla&ma in " peripheral part.
• In a &lo+ &t(eam 05 platelet& cross " plasmatic zone ' come in contact to endothelium.
"lo,ing occurs in ( follo,ing :
- :n heart failure # wea5 pump% stasis esp. in leg eins # most far %.
- :n auricles of " heart in ale diseases.
- :n aneur$sms- aricose eins.
-
- :n portal ein )r$ to lier cirrhosis ' bilharziasis.
- :n acute inflammation.
34) Changes of composition of /loo# :
i1 .. )lood element& 0
a1 ,latelets After seere hemorrhage # ma7or operations % " bone marrow produces new platelets w6 are
more stic5$ adhere to " ascular endothelium.
)1 &9Cs ++ in pol$c$themia  ++ iscosit$ ' stasis.
*1 >9Cs ++ in leu5emia ++ iscosit$ ' stasis.
d1 All blood elements :n deh$dration d.t hemoconcentration.
ii1- Bio*hemi*al fa*to(& as actiation of clotting s$stem as in =isseminated intraascular coagulation
A !IC ? in w6 there is thrombosis of man$ small 9./s. "o it i& fatal
Ca'&e : endotoxins- septicemia- lier ' 5idne$ diseases. . . . etc.
<e*hani&m of th(om)'& fo(mation 0
 ,latelets adhere to " damaged endothelium ' release th(om)o:ane A8 helps their aggregation.
 <ore platelets are deposited in columns perpendicular to blood stream w6 appear as homogenous
reddish strea5s = Line& of Bahn-
 Stasis of blood occurs # % " lines of @ahn e6 deposition of fibrin threads ' blood Cs
Type& of th(om)i 0
!hrombi are classified according to:
71 3(e&en*e of o(gani&m : i.e. infection
- septic # contains p$ogenic bacteria %.
- Aseptic # +o micro-organism %
81Colo( 0
(a) pale th(om)'& #))Red th(om)'& (*)<i:ed o(
laminated
8pale- gra$ish white
8granular surface.
8firm.
8adherent to "
intima.
8consists of
platelets ' fibrin.
8dar5 red.
8smooth surface.
8soft.
8adherent to " pale thrombus
not to intima.
8consists of &9Cs ' fibrin.
8Consists of
alternating la$ers of
red ' white thrombi
8found in aneur$sms.
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King of pathology
?1$:ten&ion :
a'*ural throm/us : adherent to " wall
/' 5cclu#ing throm/us : occlude " lumen
c'Propagating throm/us : extend to reach " nearb$ enous tributar$ thrombosis starts
again in moing blood stream clotting in stagnant blood another thrombus is produced ' "
process is repeated 'ntil (ea*h 5 hea(t.
Be&t +i&he&
"ite& of th(om)'& fo(mation 0
71 A(te(ie&
8 Less common than venous throm/osis d-t rapid flow in " arteries- ' roughness of intima is rare
8 !hrombosis occurs in arteries caused b$ :
#:% Atheroma : d.t roughness of intima
#ii% Aneurysm : d.t stasis ' roughness
#iii% "yphilitic arteritis : roughness of intima #i.e. *nd arteritis oblitrans = *A; + inflammation%
81 2ein&0
6 commonest site d-t slow blood flow ' eas$ roughness of " intima #as eins are thin walled-
superficial ' collapsible %.
6 1,o types occurs!
71Th(om)ophle)iti& 813hle)oth(om)o&i&
!ef0
"ite :
$tiology and
3athogene&i&0
#=$0
Compli*ation
0
!hrombosis of infe*ted /ein-
a-an$ ein passing through septic
inflammation# &epti* thrombophlebitis %
)-an$ ein passing exposed to trauma
or
irradiation.#a &epti* thrombophlebitis%
a'7n#othelial in8ury due to trauma-
irradiation and direct effect of organism
)-A*ti/ation of *o1ag'lation *a&*ade
b$
chemical mediators of acute inflammation
*1stasis of /oo# that accompan$ inflam.
Show cardinal signs of acute inflam. بتكت
!hromboembolism#less common% and if:
8mildl$ septic m$cotic aneur$sm
8septic p$emia-p$emic abscess.
!hrombosis of non infe*ted /ein
a-&mall /ein& of *alf C leg& in patients e6
heart failure confined to bed.
b-femo(al C pel/i* /ein after delier$.
c-/a(i*o&e /ein due to stasis.
a1stasis of /loo# due to wea5 heart action
and decrease muscular actiit$.
)-roughness of intima d.t to fre2uent
traumatization agaist def mattress.
c'hyperfi/ringenemia that accompan$
pregnanc$ or after operation.
Show obstructie enous edema onl$ 9:;<
#di&&*'&ed late( in edema%
!hromboembolism#more common%
I&*hemia
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King of pathology
?1 Hea(t % *a(dia* th(om)i
usually in ( left si#e. " following t$pes occur:
a) *ural throm/i: on non1/al/'la( endo*a(di'm. ;ccurs o/e( infa(*t& in 5 left /ent(i*le-
)) =egetation: ;ccurs o/e( 5 /al/e& in (he'mati* , infe*ti/e endo*a(diti&.
*) Auricular throm/i: ;ccur in left at(i'm in mit(al &teno&i& mainly (he'mati*. !he$ deelop in
auricular appendage- on <ac callumAs patch ' a )all /al/e th(om)'& when thrombus detach '
remains in " dilated atrial cait$.
D1 *apilla(ie&
• ;ccurs in acute inflammation- seere cold ' frost bite.
• called hyaline th(om)i as the$ are formed of &9Cs ' occur d.t: stasis- endothelial damage '
hemoconcentration
9ate of th(om)'& :
1'#etachment *mbolism if :-
a-septic p$emia abscess.
b-mildl$ septic m$cotic aneur$sm.
c-Aseptic emboli:
e6poor collateral ischemia
e6 good collateral no effect.
2'>n#etachment throm/i :
- a1 If &mall dissoled b$ fibrinol$sis ' absorbed.
)1dy&t(ophi* *al*ifi*ation phlebolith
*1in*o(po(ation arterial thrombi ma$ be coered b$ endothelium and
incorporated into atheroma.
d1O(ganization due to inasion of thrombus b$ granulation tissue
e1La(ge o**l'ding th(om)'& may 01
(-undergo recanalization b$ - wide capillar$ loop deried from granulation tissue.
- &etraction of organized thrombus.
)-become complicated b$: E p(opagation.
E*onge&tion : in case of occlusion of ein.
E I&*hemia : in case of occlusion of an arter$ e6 poor collateral.
Th(om)'& Clot
8Blood in motion.
8platelet are essential.
8platelet and fibrin.
8pale or &ed or 9oth.
8Lines of zahn.
89riable- dr$
89irml$ adherent to wall.
8granular surface.
8Stagnant blood.
8platelet not essential.
8&ed cells and fibrin.
8dar5 red or $ellow red.
8+o lines of zahn.
8soft- moist.
8+ot adherent to wall.
8smooth surface.
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King of pathology

$<BOLI"<
!ef : circulation of an insolu/le material in " blood + sudden impaction in a narrow essel. " material
is called an embolus.
Type& , "o'(*e& of $m)oli0
A1Th(om)o – em)oli&m : A detached thrombus ma$ originate from:
712ein&0
- from s$stemic eins  &t side of heart lungs occlude pulmonar$ arteries  pulm.
*mbolism
- :f " embolus passes through atrial or entricular septal defect # from &t. to Lt side of "
heart%  to " s$stemic circulation to any o(gan% para#o?ical em/olism e- out passing to ( lung!
- =etached thrombus from " portal ein or its branches passes to 5 li/e( # portal em/olism %
81Ca(dia* th(om)i 0
- Bsuall$ Lt side of " heart
- carried b$ " s$stemic arterial circulation to an$ organ.
Be&t +i&he&
#-B: rare sites of embolism are: Coronar$ arter$. # filled during diastole %
9ronchial arter$. # small side wa$ branch %.
?1A(te(ie& 0
*mboli originating from arteries are uncommon due to :
♦ Arterial thrombosis is rare.
♦ Arteries get narrower in their course ' " thrombus does not moe.
7ffects of em/oli of throm/otic origin : depends on
♦ "ize of embolus.
♦ #ature of " embolus- septic or aseptic.
♦ "tate of " collateral circulation in " affected organ so wC
a-septic emboli p$emia abscess.
b-mildl$ septic m$cotic aneur$sm.
c-Aseptic emboli:
e6poor collateral ischemia
e6 good collateral no effect.
B19at em)oli&m: common in sites containing fat as:-
8 cutaneous burns
8 bone fractures
8 in abdomen d.t acute pancreatitis
8 fatt$ change lier.
1at globules enter through " ruptured eins  pulmonar$ or s$stemic embolism. " fatt$ acids from fat
 damage " capillaries  hemorrhagic edema.
C1 T'mo( em)oli0
<alignant Cs pass as emboli in " circulation ' gie metastases in " organs.
d1 pa(a&iti* em)oli
As bilharzial oa ' worms.
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King of pathology
e1 Ai( em)oli&m 0Causes
(- :n7ur$ of large nec5 eins  gaping as the$ are embedded in fascia preenting their collapseair
is suc5ed into " heart.
)-1ault$ techni2ue in doing artificial pneumothorax ' in blood transfusion.
3-Air passes into " uterine eins in criminal abortion.
8Cai&&on F" di&ea&e:-
=eep diers ' bridges builders wor5 under a high atmospheric pressure where their nitrogen gas is
dissoled in " tissues ' blood S; &'dden a&*ent produces nitrogen bubbles w act as gas emboli.
and Spinal cord is mainl$ affected.
91 Amnioti* fl'id em)oli&m0
during delier$  fatal pulmonar$ embolism.
Be&t +i&he&
3'lmona(y em)oli&m
♦ "o'(*e& of 5 em)ol'& : thrombi of calf eins in " lower limbs.
♦ $ffe*t&0
1' Large em/olus : ;ccludes " pulmonar$ trun5 or one of its main branches produces sudden death
d.t acute &t. sided 0.1. #o time fo( an infa(*t to o**'(.
2'*e#ium si@e# em/oli :
a1 If 5 l'ng i& healthy no effe*t as " lung has double blood suppl$ # pulmonar$ ' bronchial %
)1if 5 l'ng &ho+& *h(oni* 2-C-  l'ng infa(*t&
4'ecurrent small si@e# em/oli  pulmonar$ h$pertension d.t lung fibrosis- #o Infa(*tion-
I"CH$<IA % 11 )lood &'pply to a pa(t o( ti&&'e
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King of pathology
"'dden ( a*'te )
i&*hemia
4(ad'al ( *h(oni* ) i&*hemia
Ca'&e& : "u##en complete
arterial occlusion :-
a-!hrombosis or embolism.
b-Surgical ligature of " arter$.
c-!wisting of " pedicle of
moable organ.
d- Arterial spasm .
$ffe*t&0 depends on
1- &'ffi*ien*y of )lood
&'pply:
a-:f arteries e6 inefficient
collaterals  infa(*tion o(
gang(ene.
b-:f arteries e6 efficient
collaterals  +o tissue
damage occur.
8-#at'(e of 5 affe*ted
ti&&'e : related to its
metabolic rate i.e.
♦ 0ighl$ specialized Cs are
easil$ 5illed as Cs of nerous
s$stem die in few minutes.
8 C.! cells ' s5in are more
resistant to ischemia.
Ca'&e& : Gra#ual incomplete
arterial occlusion :-
a-,ressure from outside b$ : tumor-
enlarged L.+. fibrosis ... etc.
b-atherosclerosis.
c-*ndarteritis as in s$philis# D %
$ffe*t&0
!he .radual occlusion gies chance
for " collaterals to open up "O0
71in&'ffi*ient *ollate(al& 
some necrosis ' fibrosis occur
e-g0
8atherosclerosis m$ocardial
:nfarction.

81 "'ffi*ient *ollate(al& +o tissue
damage occurs.
I#9ARCTIO#
!ef: area of coagulatie necrosis # li2uefactie in " brain % d-t a*'te &'dden i&*hemia in an organ e6
enda(te(ie& % ( a(te(ie& eG In&'ffi*iet *ollate(al % Li5e brain- retina- heart- spleen- 5idne$ ' intestine.
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King of pathology
4ene(al feat'(e& of infa(*tion % #=$0
"ite : Sub-capsular # in the peripher$ of affected organ %
Size:depend on: &ize of obstructed arter$
8" &ensitiit$ of tissue to ischemia.
Shape : wedge #p$ramidal%shaped as " arteries hae a fan1li;e di&t(i)'tion. " base is
directed towards " surface of " organ ' " apex towards the hilum.
"'(fa*e 0 raised# swollen % when recent d.t edema ' depressed when healed d.t fibrosis.
Co/e(ing "e(o&a : shows Serofibrinous inflammation
"'((o'nding : red zone of inflammator$ h$peremia as " necrotic tissue irritates " ad7acent
liing tissue b$ diffusion of " chemical products of necrosis.

Colour: pale or red.
8C
Consistenc$: firm in all organ except C.+.S Soft.
C=" : Show 3 zones# infarct area ' zone of inflammation around ' surrounding tissue%.
<=$ of infa(*tion0
71The infa(*t a(ea:8 Coagulatie necrosis in all organ except C.+.S Li2uefactie.
8 :t show po&t ne*(oti* *hange 9:;A

81The ma(gin& of infa(*t:8show <=$ of a*'te inflammation 9:;A

?1The (e&t of o(gan:8is normal e?cept in lung infarction# the lung show C./.C %.
Type&0
I) Red ( hemo((hagi* ) infa(*t0 ii) 3ale ( anemi* ) infa(*t0
- ;ccur in &oft , /a&*'la( organs as
lung 'intestine.
- " red color is d.t hemorrhage in "
substance of " infarct #" blood pass
from " dilated marginal essels into "
necrotic essels in " infarct area%.
- >hen hemol$sis occurs in " red Cs-
' its products are remoed- " infarct
become pale.
-occurs in fi(m , le&& /a&*'la(
organs as " 5idne$s ' heart.
#-B 0 :nfarction of " brain '
spleen ma$ be pale or red.
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King of pathology
Be&t +i&he&
>1Compa(e Re*ent and Old infa(*t0
&ecent infarct ;ld #healed% infarct
71 "'(fa*e:

81Colo'(0
?1$dge&:
D1<=$0
8 &aised # edema %
13ale in heart '
5idne$-
1Red in lung '
intestine
13ale then (ed in
spleen
8(ed due to
inflammation
Coagulatie necrosis
9:;A <=$
8 =epressed # 1ibrosis %
1g(eyi&h +hite-
E#o hype(emia # no
inflammation%
8 fibrous tissue- Collagen bundles
' fibroblasts.
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King of pathology
9ate of infa(*t 0 8H1?1891H
(- Healing b$ organization:
a1"mall infa(*t : replaced b$ fibrosis
)1 La(ge infa(*t : surrounded b$ fibrous capsule
)- H$aline degeneration
?- =$strophic calcification.
4- )r$ infection Abscess
E- putrefaction .angrene
H- :n " brain d.t high lipid content- leaes a c$st surrounded b$ glial tissue.
Infa(*t& in diffe(ent o(gan&
♦ L'ng 0
Ca'&e& : !he lung hae double blood suppl$ # pulmonar$'9ronchial arteries % S; for infarction to
occur Both a(te(ie& ha/e to )e o**'lded :-
8!hrombosis or embolism of pulmonar$ arter$.
ELeft /ent(i*'la( fail'(e o( mit(al &teno&i& L'ng *onge&tion, C-O-3 in&'ffi*ient )(on*hial )lood flo+.
#=$ 0 !he infarction show same general feature # as before % 9:;A e:*ept Colo'( is Red
<=$ 0 71The infa(*t a(ea : -the aleoal wall show Coagulatie necrosis 9:;A) <=$)-
-the lumen is filled e6 blood # haemorrhagic infarction %.

81The ma(gin& of infa(*t :8show <=$ of a*'te inflammation 9:;A
?1The (e&t of the l'ng :8show chronic enous congestion 9:;A) <=$)-
C=3
- Chest pain # pleuris$ %
- =$spnea - 0emopt$sis - 0emol$tic 7aundice.

Kidney 0
Ca'&e& 0
a- *mboli originating from left side of " heart.
b- !hrombosis complicating atheroma of a branch of " renal arter$.
#=$ 0
#o single or multiple.
7" wedge shaped.
Colour:pale.
8C
Consistenc$:firm
"'((o'nding : red zone of inflammator$ h$peremia
Cap&'le not affe*ted &o  painless. # has a different 9:. Suppl$ %

<=$0 71The infa(*t a(ea0the glomeruli&tubules appear as ghosts Coagulatie necrosis بتكي% <F*%.
81The ma(gin& of infa(*t:8 show <=$ of a*'te inflammation 9:;A
?1The (e&t of the ;idney:8 normal.
"pleen 0
Ca'&e& :
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King of pathology
#a%*mboli from left side of " heart.
()) Le'*o*yti* th(om)i in le';emia-
#=$ 0 As w6 of " 5idne$ but capsule is affected so painful # capsule and the organ hae the same blood
suppl$%
<=$:(-!he infarct area:the l$mphoid follicle'essels appear as ghosts Coagulatie necrosis بتكي)
<F*%.
81The ma(gin& of infa(*t:8show <=$ of a*'te inflammation 9:;A
?1The (e&t of the &pleen ::8 normal.
Inte&tine 0
Ca'&e&0
(a) <esenteric thrombosis or embolism # arter$ %
#b% !hrombosis of superior mesenteric ein.
(c) Strangulated hernia - intussusception- ' olulus.
#=$0
8 Infa(*tion is hemorrhagic- 5 affe*ted loop appear dar5 red- thic5 ' edematous.
E5 &e(o'& *oat is coered b$ fibrinous exudate.
E5 +allC l'men , pe(itoneal *a/ity show hemorrhage.
C=30
- Acute intestinal obstruction
- .angrene d.t bacterial inasion.
-peritonitis ' toxemia.
Ra(e type& of infa(*tion&0
1)&nfarction e-out acute ischemia :
-occur in " brain d.t seer h$potension during surgical operations #shoc5%
Be&t +i&he&
2) =enous infarction :
-1ollow acute local enous obstruction occur in intestine d.t thrombosis or
ligature of superior mesenteric ein w hae insufficient anastomosis enous
congestion- edema- hemorrhage ' thrombosis. !his  acute local ischemic
necrosis.
4)&nfecte# infarction :
- Septic thrombi  detached  septic infarct  abscess
- putrefaction of infarct intestine or leggangrene.
4A#4R$#$ % #e*(o&i& . p't(efa*tion-
Ca'&e&0
(-)ecrosis is #ue to :a- Acute ischemia # )r$ %
b-9acterial infection # (r$ %
)-Putrefaction is #ue to saproph$tic bacteria w6  actie in necrotic tissue. !he$ digest " necrotic
tissue liberating  h$drogen sulfide #0
)
S% w gies " tissue a foul odor.
0)S + iron of 0b  iron sulfide w6 stain " gangrenous tissue blac5.
Type& of gang(ene 0according to ( amount of /loo# ' tissue flui#s #nutritie to saproph$tic bacteria%
in " affected part.
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King of pathology
(- =r$ gangrene.
)- <oist gangrene.
I 1 !(y gang(ene
1"ite: ;ccurs in areas e6
 poor in " blood suppl$ ' tissue fluids.
 ,oor collateral circulation
1 Ca'&e: due to a*'te i&*hemia = &'dden *omplete o**l'&ion of a(te(y in a d(y lo+e( lim)-
1 3athogene&i&0 arterial suppl$ is onl$ occluded  enous ' l$mphatic drainage ' surface
e/apo(ation o**'r- so " gangrene is dr$
1$:ample& of !(y gang(ene: BCDEFGH BIJKGH LMNH
II1 <oi&t gang(ene ( Iet gang(ene )
- d'e to &'dden a(te(ial , /eno'& o**l'&ion.
- o**'(& any+he(e in " bod$ mainl$ in " internal organs as " intestine from w6 no e/apo(ation of fluids
can occur.
- 5 p(e&en*e of .. ti&&'e fl'id&  rapid putrefaction.
- To:emia i& &e/e(e-
8 BCDEFGH BIJKGH LMNH
#B0 Bed "o(e&?: OHLJGH PLQ t$pe of gangrene occurs e6 prolonged confinement to bed #paral$sis-
senilit$ G.etc%. " continuos pressure of bed mattress oer bon$ prominence #sacrum- greater
trochanter% produces 9l. stasis e6 thrombosis ' necrosis.
=ead tissue sloughs leaing a sore #superficial ulcer%. Bnderl$ing bone ma$ be exposed. )r$
bacterial infection occure.
!(y gang(ene Iet gang(ene
71*a'&e0
2 - type :
3 - "ite :
4 -
p't(ifa*tion :
5 -
mamifi*ation
:
6 - line of
dema(*ation :
7 - line of
"epa(ation :
8 - &elf1
amp'tation :
9 - &p(ead :
10 -
To:emia :
11 - 9atality :
4(ad'al occlusion of any a(te(y.
alwa$s )r$ .
*xposed limb
Slow
,resent
<ar5ed .
,resent .
ma$ occur .
Slow .
<ild .
+ot fatal
"'dden o**l'&ion of Both a(te(y and /ein.
(r$ ;r )r$ .
:nternal organ as intestine .
&apid
Absent e6 edema instead .
,oor .
Absent .
+ot occur .
&apid .
Seere .
0ighl$ fatal .
16
King of pathology
$dema
!ef : abnormal++ of interstitial fluid in the tissue spaces.
Ca'&e& of edema
7) /a&*'la( fa*to(&:
a- ++ capillar$ h$drostatic pressure.
b- ++ capillar$ permeabilit$
c- - -Colloid ;, of plasma proteins
d- ;bstruction of draining eins ' l$mphatic essels
8) Ti&&'e fa*to(&
++ tissue osmotic pressure.
Cla&&ifi*ation of edema
Lo*al 4ene(alized <i&*ellaneo'&
7 1Inflammato(y 7 1 Ca(dia* 71 Angione'(eti* (Alle(gi*)
81O)&t('*ti/e 81 Renal 81 <il(oyF& edema
a-/enous a- +ephritic
b-L$mphatic b- +ephrotic
3-+utritional
Clini*al *la&&ifi*ation of edema of &')*'taneo'& ti&&'e01
I) 3ITTI#4 ("O9T) $!$<A 8) #O# 3ITTI#4 (HAR!) $!$<A
1- accumulated fluid is present free in " tissue
spaces ' can be moed b$ pressure
)- occurs in all generalized edema ' in localized
enous edema#patent l$mphatics%
(- fluid not moe on pressure.
2- occurs in localized edema with obstructed
l$mphatics # inflammator$ C fibrin obstruct it
and in l$mphatic edema%
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King of pathology
4ene(alized edema
BCDEFGH BIJKGH LMNH
Lo*alized edema
BCDEFGH BIJKGH LMNH
<=$0
-*dema fluid is pale red homogenous.
-separates " tissue Cs ' ma$ enter them # intracellular %.
<ilo(yF& edema : =congenital obstruction of " l$mphatics of " lower limbs dating since birth

"HOCK = Acute peripheral circulator$ failure d.t reduction in cardiac output.
Type&0
 7(y "ho*; %#e'(ogeni*% 2a&o12agal Atta*; 01
an immediate fainting attac5 w6 lasts few minutes ' recoer$ is rapid.
Ca'&e&0 8Seere pain as testicular trauma.
8,s$chogenic stimuli as fright.
3athogene&i&: +eurogenic stimuli ++/= blood stagnation -- circulating blood olume
-- C;, cerebral anoxia ' loss of consciousness.
 "e*onda(y "ho*;01
71Ca(diogeni*
"ho*;0
% a*'te hea(t fail'(e
8- Hypo/olemi* "ho*;0 ?1 "epti* ( $ndoto:i* ) "ho*;0
9atal
!'e to01
8 m$ocardial
infarction
8ma7or pulmonar$
embolism
8cardiac surger$.
a- 0emorrhage
b-Loss of plasma fluids
e.g. 9urns.
c-Loss of fluids '
electrol$tes e.g. seere
diarrhea ' omiting
3athogene&i& :- - blood
olume --/&--
C;, -- blood flow
--;) suppl$ to "
tissue
Ca'&e&:Seere bacterial
infections:-
♦ gram He bact as. *-Coli.
♦ infected burns.
♦ immunodeficienc$ states.
3athogene&i&01
(-=ilatation of enules '
capillaries b$ chemical
mediators -- effectie
blood flow.
)-*ndothelial damage 
=:C #disseminated
intraascular coagulation
= =:C %.
3-!oxic cell in7ur$
including " heart 
damage to parench$mal
Cs.
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King of pathology
3athogene&i& of 8(y "ho*; : occurs after few hours- ' passes into:
♦ Re/e(&i)le "tage0 5 follo+ing *ompen&ato(y me*hani&m& o**'(:
(-/.= of bl. / in ital organs # heart and C+S %.
)-/.C of rest of bl. b$ asoactie agents as:
-Catecholamines
-renin-angiotensin-aldosterone mechanism
- antidiuretic hormone #A=0%.++ enous blood flow into heart  ++ blood pressure.
3-++ of aortic arch ' carotid sinus ++0&++ blood olume.
:f this stage fails- " patient enters into :
♦ I((e/e(&i)le "tage0
(---9., - - blood suppl$ to organs  h$poxia ' capillaries dilate '++permeabilit$.
)-hea(t- (espirator$ - (enal failures + ischemic b(ain damage.
3o&t1 <o(tem pi*t'(e of &ho*;0
80$poxia  degeneration ' necrosis in " heart- lier- 5idne$- brain etc.
8Capillar$ dilatation congestion- edema- hemorrhage of " iscera.
8 Absence of lipids from " adrenal cortex as the$ are used in " formation of hormones
8 ischemic entero-colitis .
Be&t +i&he&
Hemo((hage
!ef0 *scape of blood outside " cardio-ascular s$stem.
Ca'&e&0
(-!raumatic hemorrhages d.t mechanical in7ur$ of " either accidental or surgical.
)-Spontaneous hemorrhage d.t: affection of ascular wall b$:
a-=iseases of " ascular wall :atheroma- aneur$sms- aricose eins etc.
b-=estruction of " ascular wall : !9- malignanc$- peptic ulcer... etc.
C-S$stemic diseases characterized b$ hemorrhage:
I blood diseases as hemophilia ' purpura.
I it. C ' J deficienc$.
I h$pertension ' feers.
Be&t +i&he&
19
King of pathology
Type& of hemo((hage:
I1$:te(nal $&*ape of )lood o't&ide 5 )ody- Il1Inte(nal0 Blood e&*ape in
5 &e(o'& &a*&-
III1Inte(&titial0 Blood
e&*ape into 5 ti&&'e&-
Re&pi(ato(y "y&tem:
a1$pi&ta:i&#bleeding from
nose%
)1Hemopty&i& = coughing of blood from lung or
bronchi. " blood is red- froth$-al5aline
4a&t(ointe&tinal T(a*t0
a1Hemateme&i& = omiting of blood from
esophagus- stomach- duodenum. !he stomach
blood is.
8brown due to 0CL digestion
8contains food remnants
8acidic
)1<elena = digested blood passing e stools.
originates from stomach or duodenum.
*1Blood pe( Re*t'm: undigested blood passing e
stools. originates below " duodenum.
U(ina(y "y&tem0
hematuria = blood passing e6 urine.
9emale 4enital T(a*t0
♦ <eno((hagia : ++ amount of menstrual
bleeding.
♦ <et(o((hagia : irregular uterine bleeding
not related to menstruation.
a1Hemotho(a: 0emorrhage into "
pleura.
b-0emopericardiumpericardium.
C-0emoperitonium peritoneum.
d-0emoarthrosis7oint cait$.
e-0ematoceletunica aginalis.
According to " size of
ruptured essel:
a13ete*hiae ( p'(p'(a&%
= tin$ or pinAs head size
hemorrhages of capillar$
origin.
)1$**hymo&i& =
moderate amount of
blood from large essel.
*1Hematoma = ++
hemorrhage forming
a swelling #oma%.
Hemo&ta&i&0% natural arrest of hemorrhage from a small 9./.
<e*hani&m0
a-!emporar$ arrest: platelets aggregation together platelet plug to close " tearserotonin released
from platelets local /.C.
b-,ermanent arrest. d.t formation of " clot- healing of the tear.
$ffe*t& of Hemo((hage : !his depends on " amount ' elocit$ of " blood lossC
(. &epeated loss of small amount #(KL% iron deficienc$ anemia.
). Loss of (E L of blood olume  - - C;, - - blood pressure this is compensated b$
!he same compensator$ mech in reersible stage of shoc5
3. Loss of )E L or more of blood olume:
♦ ma$ recoer or
♦ - H/&--C;, --9.,shoc5 ' death.
3o&t1mo(tem 3i*t'(e of Hemo((hage0
Similar to " post-mortem picture of shoc5 but " organs are pale from blood loss.

Be&t +i&he&
By\King of pathology( Legand – Hazem )
20