1

Circulatory disturbances
( disturbances of blood flow & body fluids)
# Hyperemia = ++ amount of blood in a vessel : -
(1) Active (arterial) : increase in bl.flow to organ d.t vasodilation of arterioles
Physiologic a- muscular exercise
b- glands during secretion
Pathologic c- acute inflammation
(2) Passive (venous congestion ) : ++ bl flow to organ d.t obstruction of venous out flow
Veins become passively dilated
Local . . . . . . . a - acute b - chronic
General . . . . . . a - acute b - chronic
# Passive Hyperemia = ( venous congestion )
I - LOCAL = LOCALIZED CONGESTION IN ANY PART OF ! BODY D.T ITS VENOUS OUT FLOW OBSTRUCTION.

Acute
a - Causes : Sudden complete venous obstruction d.t :
- Thrombosis
- Ligature
- Twisting of Pedicle movable organ (ovary)
- Strangulated hernia .
b - Pathology : Rapid severe dilatation of ! veins & capillaries w may rupture edema
c - Fate : (1) sufficient venous anastomosis
no harmful effect.
(2) insufficient venous anastomosis (as in mesenteric veins)
venous infarction of intestine







2
Chronic
a - Causes :
gradual incomplete venous obstruction as compression by :
- Tumor
- Enlarged L.N.
- Pregnant uterus
- Liver cirrhosis & fibrosis.
b - Pathology : 1) ! veins, venules & capillaries proximal to
obstruction become dilated & congested edema
2) Gradual opening of ! collaterals & anastomatic veins
c - Examples of chronic local venous congestion :
1 - Liver cirrhosis or fibrosis : obst. of veins portal hypertension
2 - C V.C. of ! lungs ( brown induration )



II- General : d.t total ( congestive = Rt & Lt ) heart failure So Congestion occurs all over ! body.
1- Acute
in acute H.F all organs show acute congestion.
2- Chronic
Def : gradual venous congestion affecting ! whole venous system.
Causes : both Rt. Sided & left sided H.F.
Rt. Sided H.F : show chronic venous congestion ( v. c. ) all over ! body except lungs.
Left sided. H.F : show chronic venous congestion ( v. c. ) of lungs

Pathology of Rt. Sided H.F.
I - General effects
1 - Congested neck veins
2 - Cyanosis = (purple - blue coloration) of lips, bed of nails ... etc. d.t ++ reduced Hb
& inadequate tissue perfusion & - - oxygenation.
3 - Cardiac edema : in dependent parts of ! body =
Gravitational edema ( discussed later in edema )
4 - increase blood volume Na & H2o retension.

3
II - Local effects ( appearance of ! organs ) :
Liver


Early ( C.V.C. liver) = Nut Meg liver
= focal fatty change
Late ( cardiac cirrhosis )

N/E
















M/E









Size : enlarged
2S
Shape : preserved
Surface : smooth
Serous coat : fibrosed later
Colour : dark red congested
2C
Consistency : soft to firm
Capsule : Tense
C/s : ( mottled appearance )
due to alternation of brown
(congestion) and yellow colours
(fatty change) So called
( Nut - Meg liver )
a - central veins and central ends
of sinusoids are dilated
congested
b - cells of mid zone show
( Fatty change ).

c - cells of peripheral zone show
(Normal OR cloudy swelling)
d - Von Kuppfer cells show
( Haemosidrine granules )




Shrunken ( -- size )

Distorted
Granular ( irregular ) surface

Grayish red due to fibrosis e`
congestion.
Firm
Thick by fibrosis
1- white ( fibrosis )
2- show cirrhotic nodules



a - cells of central zone show necrosis
followed by fibrosis fibrosed area
join each other by fibrous bands.
b - compensatory hyperplasia of healthy
hepatocytes w` are encircled by fibrous
bands cirrhotic nodules
= regenerating nodules.
4
Spleen
N/E : Size : enlarged (2 times)
2S
Shape : preserved
Surface : smooth
Colour : dark red congested
2C
Consistency : firm
Capsule & trabeculae : thick
C/S : Lymphoid follicle is not apparent

M/E:
* Thick capsule & trabeculae.
* Atrophy of lymphoid follicles.
* Fibrous tissue of ! red pulp.
* Rupture of congested capillaries disintegrate hemosiderin
leading to fibrosis & formation of fibrosiderotic nodules
(Gamna Gandy nodules). This contains : 2 minerals
iron + calcium.
2 fibers collagen + elastic.
1 pigment hemosiderin.
Giant cells.
Q : give account on ( Gama Gandy nodules ) :
1 - pathogenesis :
Severe congestion in splenic sinusoids rupture haemolysis of RBCs
Haemosiderine fibrosis calcification
2 - Component : as before
3 - Prussian blue : + ve Prussian blue due to haemosidrine and iron.


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Kidneys
N/E : Size : enlarged.
2S
Shape : preserved.
Surface : smooth.
Colour : dark red congested.
2C
Cosistency: soft.
Capsule : stretched
Borders : rounded
C/S : a - yellow cortex (d.t fatty change) containing dark red dots &
streaks w` are ! glomeruli & ! congested vessels
b - dark red medulla.
M/E : * Congestion of ! glomerular capillaries.
* Fatty change of ! proximal convoluted tubules.
Chronic venous congestion lungs ( Brown induration ) = Pulmonary congestion
Causes I - chronic left vent. Failure
2 - Mitral stenosis
Pathogenesis :
- Blood accumulates in Lt. Atrium pulmonary veins venules
capillaries becomes congested & dilated rupture
disintegration of RBCs hemosiderin w` cause fibrosis & taken by
macrophages w` appear swollen & brown & are called heart failure Cs.
- Some of ! Heart F. Cs go to draining lymph nodes. Some of them die & ! released
hemosiderin fibrosis in ! interstitial tissue.So lung becomes brown
& tough a condition called "Brown induration"
N/E : 1S Size : enlarged
Colour : Brown ( d.t hemosiderin )
2C
Consistency : Heavy, firm ( d.t fibrosis )
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C/S : oozes blood - stained frothy fluid
bronchial mucosa congested, edematous & covered by a layer of mucous
M/E :
# Inter alveolar septa : thickened by :
Edema ( transudate ) & fibrosis. contain dilated congested capillaries
# The alveoli : Contains
- Orange ( intact & hemolyzed RBCs )
- brown ( hemosidrin granules & heart failure cells )
- pink, homogenous ( transudate )
The heart failure cells :
Groups of Large, rounded, phagocytic cells engulfing brown hemosidrin granules & red cells
# Interstitium shows :
- Bronchial mucosa congested, edematous e` H.F. Cs

Thrombosis
Def : formation of a solid mass ( thrombus ) of blood elements ( mainly platelets & fibrin ) in ! CVS
during life.
Causes of thrombosis : ( Virchows triad )
1) Damage of ! vascular endothelium : i.e. roughness of ! intima ! platelets adhere to !
damaged endothelium.
a - Mechanical : trauma, pressure as (ligature).
b - Inflammatory ( phlebitis, arteritis, endocardites )
c - Degenerative (atheroma)

N.B : Normal prostacyclin secreted by ! vascular endothelium - - thrombosis.
Thromboxane A2 liberated from ! platelets helps their aggregation ++ thrombosis.



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2) Slowing of blood flow = Stasis :-
- In normal blood stream : ! blood Cs occupy ! central part, & ! plasma in ! peripheral part.
- In a slow stream : ! platelets cross ! plasmatic zone & come in contact to endothelium.
Slowing occurs in ! following :
- In heart failure ( weak pump) stasis esp. in leg veins ( most far )
- In auricles of ! heart in valve diseases
- In aneurysms, varicose veins
- In portal vein 2ry to liver cirrhosis & bilharziasis
- In acute inflammation
3) Composition changes of blood :
I) ++ blood elements :
a) Platelets After severe hemorrhage ( major operations ) ! bone marrow produces
new platelets w` are more sticky adhere to ! vascular endothelium.
b) RBCs ++ in polycythemia ++ viscosity & stasis.
c) WBCs ++ in leukemia ++ viscosity & stasis.
d) All blood elements In dehydration d.t hemoconcentration.
II) Biochemical factors as activation of clotting system as in Disseminated
intravascular coagulation " DIC " in w` there is thrombosis of many small B.Vs. So it is fatal
Cause : endotoxins, septicemia, liver & kidney diseases . . . . etc.
# Mechanism of thrombus formation :
Platelets adhere to ! damaged endothelium & release
thromboxane A2 helps their aggregation.
More platelets are deposited in columns perpendicular to blood
stream w` appear as homogenous reddish streaks = Lines of Zahn.
Stasis of blood occurs ( ) ! lines of Zahn e` deposition of fibrin threads & blood Cs
TYPES OF THROMBI : Thrombi are classified according to:
1 - Presence of organism : i.e. infection
- Septic (contains pyogenic bacteria)
- Aseptic (no micro - organism)

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2 - Color :
pale thrombus Red thrombus Mixed or laminated
* pale, grayish white
* granular surface
* firm
* adherent to ! intima
* consists of platelets & fibrin

* dark red.
* smooth surface
* soft.
* adherent to ! pale
Thrombus not to intima.
* consists of RBCs & fibrin

* Consists of alternating
layers of red &
white thrombi
* found in aneurysms


3 - Extension :
a - Mural thrombus : adherent to ! wall
b - Occluding thrombus : occlude ! lumen
c - Propagating thrombus : extend to reach !
nearby venous tributary
thrombosis starts again in moving blood stream clotting in stagnant blood
another thrombus is produced & ! process is repeated until reach ! heart.

Sites of thrombus formation :
1 - Arteries :
* Less common than venous thrombosis d.t rapid flow in ! arteries, & roughness of intima is rare
* Thrombosis occurs in arteries caused by :
(I) Atheroma : d.t roughness of intima
(ii) Aneurysm : d.t stasis & roughness
(iii) Syphilitic arteritis : roughness of intima (i.e. End arteritis oblitrans = EAO + inflammation)
2 - Veins :
* commonest site d.t slow blood flow & easy roughness of ! intima
(as veins are thin walled, superficial & collapsible ).



9
* Two types occurs

Thrombophlebitis Phlebothrombosis
Def
Site

Etiology and
Pathogenesis




N/E
Complication
Thrombosis of infected vein
a - any vein passing through septic
inflammation( septic thrombophlebitis )
b - any vein passing exposed to trauma or
irradiation (a septic thrombophlebitis)
a - Endothelial injury due to trauma,
irradiation and direct effect of organism
b - Activation of co-agulation cascade by
chemical mediators of acute inflammation
c - stasis of bood that a
ccompany inflam.

Show cardinal signs of acute inflam.

Thromboembolism (less common) and if :
* mildly septic mycotic aneurysm
* septic pyemia,pyemic abscess
Thrombosis of non infected vein
a - small veins of calf , legs in
patients e` heart failure confined to bed.
b - femoral , pelvic vein after delivery.
c - varicose vein due to stasis.
a - stasis of blood due to weak heart
action and decrease muscular activity
b - roughness of intima d.t to
frequent traumatization agaist
def mattress.
c - hyperfibringenemia that accompany
pregnancy or after operation.
Show obstructive venous edema only
(disscused later in edema)
Thromboembolism (more common)
Ischemia

3 - Heart = cardiac thrombi
# usually in ! left side. ! following types occur :
a) Mural thrombi : on non - valvular endocardium. Occurs over infarcts in ! left ventricle
b) Vegetation : Occurs over ! valves in rheumatic & infective endocarditis
c) Auricular thrombi : Occur in left atrium in mitral stenosis mainly rheumatic
# They develop in auricular appendage, on Mac callum's patch & a ball valve thrombus
when thrombus detach & remains in ! dilated atrial cavity
4 - capillaries
Occurs in acute inflammation, severe cold & frost bite.
called hyaline thrombi as they are formed of RBCs & occur d.t : stasis,
endothelial damage & hemoconcentration
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Fate of thrombus :
1 - detachment Embolism if :-
a - septic pyemia abscess
b - mildly septic mycotic aneurysm
c - Aseptic emboli :
e`poor collateral ischemia
e` good collateral no effect
2 - Undetachment thrombi :
- a - If small dissolved by fibrinolysis & absorbed
b - dystrophic calcification phlebolith
c - incorporation arterial thrombi may be covered by endothelium and
incorporated into atheroma.
d - Organization due to invasion of thrombus by granulation tissue
e - Large occluding thrombus may :-
1 - undergo recanalization by - wide capillary loop derived from granulation tissue.
- Retraction of organized thrombus.
2 - become complicated by: * propagation.
* congestion : in case of occlusion of vein.
* Ischemia : in case of occlusion of an artery e` poor collateral.

Thrombus Clot
* Blood in motion
* platelet are essential
* platelet and fibrin
* pale or Red or Both
* Lines of zahn
* Friable, dry
* Firmly adherent to wall
* granular surface
* Stagnant blood
* platelet not essential
* Red cells and fibrin
* dark red or yellow red
* No lines of zahn
* soft, moist
* Not adherent to wall
* smooth surface
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Embolism
Def : circulation of an insoluble material in ! blood + sudden Impaction in a narrow vessel. !
material is called an embolus.
Types & Sources of Emboli :
(I) - Thrombo embolism : A detached thrombus may originate from :
1 - Veins :
* from systemic veins Rt side of heart lungs
occlude pulmonary arteries pulm. Embolism
* If ! embolus passes through atrial or ventricular septal defect
( from Rt. to Lt side of ! heart) to ! systemic circulation
to any organ = paradoxical embolism e` out passing to ! lung.
* Detached thrombus from ! portal vein or its branches
passes to ! liver ( portal embolism )
2 - Cardiac thrombi :
* Usually Lt side of ! heart
* carried by ! systemic arterial circulation to any organ.
N.B : rare sites of embolism are: Coronary artery ( filled during diastole )
Bronchial artery ( small side way branch )
3 - Arteries :
Emboli originating from arteries are uncommon due to :
* Arterial thrombosis is rare.
* Arteries get narrower in their course & ! thrombus does not move.
# effects of emboli of thrombotic origin : depends on
- Size of embolus.
- Nature of ! embolus, septic or aseptic.
- State of ! collateral circulation in ! affected organ so w;
a - septic emboli pyemia abscess.
b - mildly septic mycotic aneurysm.
c - Aseptic emboli :
- e`poor collateral - ischemia - e` good collateral no effect.
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(II) - Fat embolism: common in sites containing fat as:-
* cutaneous burns
* bone fractures
* in abdomen d.t acute pancreatitis
* fatty change liver.
Fat globules enter through ! ruptured veins pulmonary or systemic embolism.
! fatty acids from fat damage ! capillaries hemorrhagic edema.
(III) - Tumor emboli:
Malignant Cs pass as emboli in ! circulation & give metastases in ! organs.
(IV) - parasitic emboli
As bilharzial ova & worms.
(V) - Air embolism : Causes
1 - Injury of large neck veins gaping as they are embedded in
fascia preventing their collapseair is sucked into ! heart.
2 - Faulty technique in doing artificial pneumothorax & in blood transfusion.
3 - Air passes into ! uterine veins in criminal abortion.
* Caisson 'S disease :-
Deep divers & bridges builders work under a high atmospheric pressure where
their nitrogen gas is dissolved in ! tissues & blood SO
sudden ascent produces nitrogen bubbles w act as gas emboli.
and Spinal cord is mainly affected.
(VI) - Amniotic fluid embolism :
during delivery fatal pulmonary embolism.
(VII) - Pulmonary embolism
- Sources of ! embolus : thrombi of calf veins in ! lower limbs.
- Effects:
1 - Large embolus : Occludes ! pulmonary trunk or one of its main branches produces
sudden death d.t acute Rt. sided H.F. No time for an infarct to occur.
2 - Medium sized emboli : a - If ! lung is healthy no effect as ! lung has
double blood supply ( pulmonary & bronchial )
b - if ! lung shows chronic V.C. lung infarcts
3 - Recurrent small sized emboli pulmonary hypertension d.t lung fibrosis. No Infarction.
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Ischemia = decrease blood supply to a part or tissue


Sudden ( acute ) ischemia
Gradual ( chronic ) ischemia
Causes : Sudden complete arterial occlusion :-
a - Thrombosis or embolism.
b - Surgical ligature of ! artery.
c - Twisting of ! pedicle of
movable organ as overy.
d - Arterial spasm .
effects : depends on :
1 - sufficiency of blood supply :
a - If arteries e` inefficient collaterals
infarction or gangrene.
b - If arteries e` efficient collaterals
No tissue damage occur.
2 - Nature of ! affected tissue :
related to its metabolic rate i.e.
- Highly specialized Cs are easily killed as
Cs of nervous system die in few minutes.
* C.T cells & skin are more resistant to ischemia.
Causes : Gradual incomplete arterial occlusion :-
a - Pressure from outside by : tumor,
enlarged L.N. fibrosis ... etc.
b - atherosclerosis.
c - Endarteritis as in syphilis ($)

effects :
The Gradual occlusion gives chance for !
collaterals to open up SO :
1 - insufficient collaterals
some necrosis & fibrosis occur e.g :
* atherosclerosis myocardial
Infarction.
2 - Sufficient collaterals
No tissue damage occurs.


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Infarction

Def : area of coagulative necrosis ( liquefactive in ! brain ) d.t acute sudden ischemia
in an organ e` endarteries = ( arteries e` Insufficiet collateral ) Like brain, retina,
heart, spleen, kidney & intestine.
General features of infarction = N/E :
Site : Sub - capsular ( in the periphery of affected organ )
Size : depend on : size of obstructed artery
2S sensitivity of tissue to ischemia.

Shape : wedge (pyramidal) shaped as ! arteries have a fan - like distribution. !
base is directed towards ! surface of ! organ & ! apex towards the hilum.
Surface : raised ( swollen ) when recent d.t edema & depressed when healed d.t fibrosis.
Covering Serosa : shows Serofibrinous inflammation
Surrounding : red zone of inflammatory hyperemia as ! necrotic tissue irritates ! adjacent
living tissue by diffusion of ! chemical products of necrosis.
Colour : pale or red.
2C
Consistency : firm in all organ except C.N.S Soft.

C/S : Show 3 zones ( infarct area & zone of inflammation around & surrounding tissue).
M/E of infarction :
1 - The infarct area : * Coagulative necrosis in all organ except C.N.S Liquefactive.
* It show post necrotic change
2 - The margins of infarct : * show M/E of acute inflammation
3 - The rest of organ : * is normal except in lung infarction( the lung show C.V.C ).




15
Types :
Red ( hemorrhagic ) infarct Pale ( anemic ) infarct
- Occur in soft & vascular organs as lung & intestine
- ! red color is d.t hemorrhage in ! substance
of ! infarct (! blood pass from ! dilated
marginal vessels into ! necrotic
vessels in ! infarct area).
- When hemolysis occurs in ! red Cs, &
its products are removed, ! infarct become pale.

- occurs in firm & less vascular
organs as ! kidneys & heart.

N.B : Infarction of ! brain & spleen
may be pale or red.



Q - Compare Recent and Old infarct :


Recent infarct Old (healed) infarct
Surface

Colour

Edges
M/E
* Raised ( edema )
- Pale in heart & kidney,
- Red in lung & intestine
- Pale then red in spleen
* red due to inflammation
Coagulative necrosis
M/E
* Depressed ( Fibrosis )

- greyish white.

* No hyperemia ( no inflammation)
* fibrous tissue, Collagen
Bundles & fibroblasts.



@ Fate of infarct : 2H 3 - 2F -6
1 - Healing by organization :
a - Small infarct : replaced by fibrosis
b - Large infarct : surrounded by fibrous capsule
2 - Hyaline degeneration

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3 - Dystrophic calcification.
4 - 2ry infection Abscess
5 - putrefaction Gangrene
6 - In ! brain d.t high lipid content, leaves a cyst surrounded by glial tissue.
@ Infarcts in different organs

Causes : The lung have double blood supply ( pulmonary & Bronchial arteries ) SO for infarction to
occur Both arteries have to be occulded :-
* Thrombosis or embolism of pulmonary artery.
* Left ventricular failure or mitral stenosis Lung congestion & decrease C.O.P
insufficient bronchial blood flow.
N/E : The infarction show same general feature ( as before ) except Colour is Red

M/E : 1 - The infarct area : - the alveoal wall show Coagulative necrosis ) M/E).
- the lumen is filled e` blood ( haemorrhagic infarction ).
2 - The margins of infarct : * show M/E of acute inflammation
3 - The rest of the lung : * show chronic venous congestion ) M/E).
C/P
- Chest pain ( pleurisy )
- Dyspnea , Hemoptysis , Hemolytic jaundice.


Causes :
a - Emboli originating from left side of ! heart.
b - Thrombosis complicating atheroma of a branch of ! renal artery.
N/E :
No single or multiple
1S wedge shaped
Colour : pale
2C Consistency : firm
Surrounding : red zone of inflammatory hyperemia
Lung
Kidney
17
Capsule not affected so painless ( has a different BI. Supply )
M/E : 1 - The infarct area : the glomeruli & tubules appear as ghosts
Coagulative necrosis ) M/E)
2 - The margins of infarct : * show M/E of acute inflammation
3 - The rest of the kidney : * normal



Causes :
(a) Emboli from left side of ! heart.
(b) Leucocytic thrombi in leukemia.

N/E : As w` of ! kidney but capsule is affected so painful ( capsule and the organ
have the same blood supply)

M/E : 1 - The infarct area : the lymphoid follicle & vessels appear as ghosts
Coagulative necrosis ) M/E).
2 - The margins of infarct : * show M/E of acute inflammation
3 - The rest of the spleen : * normal.



Causes :
a - Mesenteric thrombosis or embolism ( artery )
b - Thrombosis of superior mesenteric vein.
c - Strangulated hernia , intussusception & volvulus.
N/E :
* Infarction is hemorrhagic, ! affected loop appear dark red, thick & edematous.
* ! serous coat is covered by fibrinous exudate.
* ! wall, lumen & peritoneal cavity show hemorrhage.

C/P :
spleen
Intestine
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- Acute intestinal obstruction
- Gangrene d.t bacterial invasion.
- peritonitis & toxemia.

Rare types of infarctions:
1) Infarction e`out acute ischemia :
- occur in ! brain d.t sever hypotension during surgical operations (shock)
2) Venous infarction :
- Follow acute local venous obstruction occur in intestine d.t
thrombosis or ligature of superior mesenteric vein w
have insufficient anastomosis
venous congestion, edema, hemorrhage & thrombosis.
This acute local ischemic necrosis.
3) Infected infarction :
- Septic thrombi detached septic infarct abscess
- putrefaction of infarct intestine or leg gangrene
Gangrene = Necrosis + putrefaction

Causes:
1 - Necrosis is due to : a - Acute ischemia ( 2ry )
b - Bacterial infection ( 1ry )
2 - Putrefaction is due to saprophytic bacteria w` active in necrotic tissue.
They digest ! necrotic tissue liberating hydrogen sulfide (H2S) w gives ! tissue a foul odor.
H2S + iron of Hb iron sulfide w` stain ! gangrenous tissue black.
Types of gangrene : according to ! amount of blood & tissue fluids
(nutritive to saprophytic bacteria) in ! affected part.
1 - Dry gangrene
2 - Moist gangrene



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I - Dry gangrene
- Site : Occurs in areas e`
* poor in ! blood supply & tissue fluids.
* Poor collateral circulation
- Cause : due to acute ischemia = sudden complete occlusion of artery in a dry lower limb.

- Pathogenesis : arterial supply is only occluded venous & lymphatic drainage & surface
evaporation occur, so ! gangrene is dry
- Examples of Dry gangrene :

II - Moist gangrene ( Wet gangrene )

- due to sudden arterial & venous occlusion.
- occurs anywhere in ! body mainly in ! internal organs as ! intestine from
w` no evaporation of fluids can occur.
- ! presence of ++ tissue fluids rapid putrefaction.
- Toxemia is severe.
NB : Bed Sores : type of gangrene occurs e` prolonged confinement to bed
)paralysis, senility .etc). ! continuos pressure of bed mattress over
bony prominence (sacrum, greater trochanter) produces Bl. stasis e`
thrombosis & necrosis.
Dead tissue sloughs leaving a sore (superficial ulcer). Underlying bone may be exposed. 2ry
bacterial infection occure.

Dry gangrene Wet gangrene
cause
type
Site
Putrifaction
Mamification
Gradual occlusion of any artery
always 2ry
Exposed limb
Slow
Present
Sudden occlusion of Both artery and vein
1ry Or 2ry
Internal organ as intestine
Rapid
Absent e` edema instead
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line of *
demarcation
* line of
Separation
Self -
amputation
spread
Toxemia
Fatality
Marked

Present

may occur
Slow
Mild
Not fatal
Poor

Absent

Not occur
Rapid
Severe
Highly fatal

Edema
Def : abnormal ++ of interstitial fluid in the tissue spaces.
Causes of edema
1) vascular factors :
a - increase capillary hydrostatic pressure.
b - increase capillary permeability
c - decrease Colloid OP of plasma proteins
d - Obstruction of draining veins & lymphatic vessels
2) Tissue factors :
Increase tissue osmotic pressure.
Classification of edema

Local Generalized Miscellaneous
1 - Inflammatory 1 - Cardiac 1 - Angioneuretic (Allergic)
2 - Obstructive
a - Venous
b - Lymphatic
2 - Renal
a - Nephritic
b - Nephrotic
c - Nutritional
2 - Milroy's edema
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Clinical classification of edema of subcutaneous tissue :-
Pitting (soft) edema Non pitting (hard) edema
1 - accumulated fluid is present free in
! tissue spaces & can be moved by pressure
2 - occurs in all generalized edema & in
localized venous edema (patent lymphatics)
1 - fluid not move on pressure.
2 - occurs in localized edema with
obstructed lymphatics ( inflammatory ;
fibrin obstruct it and in lymphatic edema)

Generalized edema..
Localized edema..

M/E :
- Edema fluid is pale red homogenous.
- separates ! tissue Cs & may enter them ( intracellular ).
Milory's edema : = congenital obstruction of ! lymphatics of ! lower limbs dating since birth
Shock = Acute peripheral circulatory failure d.t reduction in cardiac output
Types :
# 1ry Shock
= Neurogenic = Vaso-Vagal Attack :-
an immediate fainting attack w` lasts few minutes & recovery is rapid.
Causes : * Severe pain as testicular trauma.
* Psychogenic stimuli as fright.
Pathogenesis : Neurogenic stimuli ++ VD blood stagnation -- circulating blood volume
decrease COP cerebral anoxia & loss of consciousness.


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# Secondary Shock :-
Cardiogenic Shock
= acute heart failure
Hypovolemic Shock
Septic ( Endotoxic ) Shock
Fatal
Due to :-
* myocardial infarction
* major pulmonary embolism
* cardiac surgery.

Causes :-
a - Hemorrhage
b - Loss of plasma
fluids e.g. Burns.
c - Loss of fluids &
electrolytes e.g. severe
diarrhea & vomiting
Pathogenesis :-
- blood volume
decrease VR
decrease COP
decrease blood
flow decrease O2
supply to ! tissue

Causes : Severe bacterial infections :-
- gram - ve bact as. E-Coli.
- infected burns.
- immunodeficiency states.

Pathogenesis :-
1 - Dilatation of venules &
capillaries by chemical
mediators -- effective
blood flow.
2 - Endothelial damage DIC
(disseminated intravascular
coagulation = DIC ).
3 - Toxic cell injury including !
heart damage to
parenchymal Cs.


Pathogenesis of 2ry Shock : occurs after few hours, & passes into :
# Reversible Stage: ! following compensatory mechanisms occur :
1 - V.D of bl. V in vital organs ( heart and CNS ).
2 - V.C of rest of bl.v by vasoactive agents as :
- Catecholamines
- renin-angiotensin-aldosterone mechanism
- antidiuretic hormone (ADH) ++ venous blood flow into heart ++ blood pressure.
3 - ++ of aortic arch & carotid sinus ++ HR ++ blood volume.


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If this stage fails, ! patient enters into :
# Irreversible Stage :
1 - decrease B.P decrease blood supply to organs
hypoxia & capillaries dilate & ++ permeability.
2 - heart, respiratory , renal failures increase ischemic brain damage.
Post - Mortem picture of shock :
* Hypoxia degeneration & necrosis in ! heart, liver, kidney, brain.etc.
* Capillary dilatation congestion, edema, hemorrhage of ! viscera.
* Absence of lipids from ! adrenal cortex as they are used in ! formation of hormones
* ischemic entero - colitis .
Hemorrhage
Def : Escape of blood outside ! cardio - vascular system.
Causes :
1 - Traumatic hemorrhages d.t mechanical injury of ! either accidental or surgical.
2 - Spontaneous hemorrhage d.t : affection of vascular wall by :
a - Diseases of ! vascular wall : atheroma, aneurysms , varicose veins..etc.
b - Destruction of ! vascular wall : TB, malignancy, peptic ulcer... etc.
c - Systemic diseases characterized by hemorrhage :
blood diseases as hemophilia & purpura.
vit. C & K deficiency.
hypertension & fevers.
Types of hemorrhage :
Interstitial Blood escape into ! tissues
According to ! size of ruptured vessel :
a - Petechiae ( purpuras) = tiny or pin's head size hemorrhages of capillary origin.
b - Ecchymosis = moderate amount of blood from large vessel.
c - Hematoma = ++ hemorrhage forming a swelling (oma).


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Internal Blood escape in ! serous sacs

a - Hemothorax Hemorrhage into ! pleura
b - Hemopericardium pericardium
c - Hemoperitonium peritoneum
d - Hemoarthrosis joint cavity
e - Hematocele tunica vaginalis

External escape of blood outside ! body
Respiratory System :
a - Epistaxis (bleeding from nose)
b - Hemoptysis = coughing of blood from lung or bronchi. !
blood is red, frothy, alkaline
Gastrointestinal Tract :
a - Hematemesis = vomiting of blood from esophagus, stomach, duodenum.
The stomach blood is.
* brown due to HCL digestion
* contains food remnants
* acidic
b - Melena = digested blood passing e stools. originates from stomach or duodenum.
c - Blood per Rectum : undigested blood passing e stools. originates below ! duodenum.
Urinary System :
hematuria = blood passing e` urine.
Female Genital Tract :
- Menorrhagia : ++ amount of menstrual bleeding.
- Metrorrhagia : irregular uterine bleeding not related to menstruation.

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Hemostasis : = natural arrest of hemorrhage from a small B.V.
Mechanism :
a - Temporary arrest : platelets aggregation together platelet plug to close ! tear
serotonin released from platelets local V.C.
b - Permanent arrest : d.t formation of ! clot, healing of the tear

Effects of hemorrhage : This depends on ! amount & velocity of ! blood loss :-
1 - Repeated loss of small amount (10%) iron deficiency anemia.
2 - Loss of 15 % of blood volume - - COP - - blood pressure this is compensated by
The same compensatory mech in reversible stage of shock
3 - Loss of 25 % or more of blood volume :
- may recover or decrease VR decrease COP decrease B.P shock & death.
Post - mortem Picture of Hemorrhage :
Similar to ! post-mortem picture of shock but ! organs are pale from blood loss.