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

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.

2

II - Local effects ( appearance of ! organs ) :

Liver

Early ( C.V.C. liver) = Nut Meg liver

Late ( cardiac cirrhosis )

= focal fatty change

N/E

Size : enlarged

Shrunken ( -- size )

Shape : preserved

Distorted

Surface : smooth

Granular ( irregular ) surface

2S

Serous coat : fibrosed later

Grayish red due to fibrosis e`

Colour : dark red congested

congestion.

2C
Consistency : soft to firm

Firm

Capsule : Tense

Thick by fibrosis

C/s : ( mottled appearance )

1- white ( fibrosis )
2- show cirrhotic nodules

due to alternation of brown

(congestion) and yellow colours
(fatty change) So called
( Nut - Meg liver )

a - cells of central zone show

a - central veins and central ends

of sinusoids are

followed by fibrosis
fibrosed area
join each other by fibrous bands.

dilated
congested

b - cells of mid zone

M/E

b - compensatory hyperplasia of healthy

hepatocytes w` are encircled by fibrous
bands
cirrhotic nodules

show

( Fatty change ).

= regenerating nodules.
c - cells of peripheral zone show
(Normal OR cloudy swelling)
d - Von Kuppfer cells

necrosis

show

( Haemosidrine granules )

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
Haemosiderine

fibrosis

rupture

haemolysis of RBCs

calcification

2 - Component :

as before

3 - Prussian blue :

+ ve Prussian blue due to haemosidrine and iron.

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

I - chronic left vent. Failure

Causes

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 )
5

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.

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)
7

2 - Color :
pale thrombus

Red thrombus

* pale, grayish white

* dark red.

* granular surface

* smooth surface

* firm

* soft.

* adherent to ! intima

* adherent to ! pale

* consists of platelets & fibrin

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

Thrombus not to intima.

* consists of RBCs & fibrin

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 ).

* Two types occurs

Thrombophlebitis

Phlebothrombosis

Def

Thrombosis of infected vein

Thrombosis of non infected vein

Site

a - any vein passing through septic

inflammation( septic thrombophlebitis )

a - small veins of calf , legs in

b - any vein passing exposed to trauma or

irradiation (a septic thrombophlebitis)

b - femoral , pelvic vein after delivery.

Etiology and a - Endothelial injury due to trauma,

Pathogenesis irradiation and direct effect of organism

patients e` heart failure confined to bed.

c - varicose vein due to stasis.

a - stasis of blood due to weak heart
action and decrease muscular activity

b - Activation of co-agulation cascade by

chemical mediators of acute inflammation

b - roughness of intima d.t to

frequent traumatization agaist

c - stasis of bood that a

ccompany inflam.

def mattress.
c - hyperfibringenemia that accompany
pregnancy or after operation.

N/E

Show cardinal signs of acute inflam.

Show obstructive venous edema only

(disscused later in edema)

Complication Thromboembolism (less common) and if :

* mildly septic
mycotic aneurysm
* septic

Thromboembolism (more common)

Ischemia

pyemia,pyemic abscess

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
9

Fate of thrombus :
1 - detachment
a - septic

Embolism if :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
c - incorporation

phlebolith

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

* Stagnant blood

* platelet are essential

* platelet not essential

* platelet and fibrin

* Red cells and fibrin

* pale or Red or Both

* dark red or yellow red

* Lines of zahn

* No lines of zahn

* Friable, dry

* soft, moist

* Firmly adherent to wall

* Not adherent to wall

* granular surface

* smooth surface

11

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
11

- e` good collateral

no effect.

(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.
12

Ischemia = decrease blood supply to a part or tissue

Gradual ( chronic ) ischemia

Sudden ( acute ) ischemia

Causes : Sudden complete arterial occlusion :-

Causes : Gradual incomplete arterial occlusion :-

a - Thrombosis or embolism.

a - Pressure from outside by : tumor,

b - Surgical ligature of ! artery.

enlarged L.N. fibrosis ... etc.

c - Twisting of ! pedicle of

b - atherosclerosis.
c - Endarteritis as in syphilis ($)

movable organ as overy.

d - Arterial spasm .
effects : depends on :
1 - sufficiency of blood supply :
a - If arteries e` inefficient collaterals

effects :
The Gradual occlusion gives chance for !
collaterals to open up SO :

infarction or gangrene.

1 - insufficient collaterals

b - If arteries e` efficient collaterals

some necrosis & fibrosis occur e.g :

No tissue damage occur.

* atherosclerosis

2 - Nature of ! affected tissue :

myocardial
Infarction.

related to its metabolic rate i.e.

2 - Sufficient collaterals

- Highly specialized Cs are easily killed as

No tissue damage occurs.

Cs of nervous system die in few minutes.

* C.T cells & skin are more resistant to ischemia.

13

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 :
2S

size of obstructed artery

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
* It show post necrotic change

Liquefactive.

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 ).

14

Types :

Red ( hemorrhagic ) infarct

Pale ( anemic ) infarct

- Occur in soft & vascular organs as lung & intestine - occurs in firm & less vascular
- ! red color is d.t hemorrhage in ! substance
organs as ! kidneys & heart.
of ! infarct (! blood pass from ! dilated
marginal vessels into ! necrotic
vessels in ! infarct area).
- When hemolysis occurs in ! red Cs, &

N.B : Infarction of ! brain & spleen

may be pale or red.

its products are removed, ! infarct become pale.

Q - Compare Recent and Old infarct :

Recent infarct
Surface

Old (healed) infarct

* Raised ( edema )

* Depressed ( Fibrosis )

- Pale in heart & kidney,

Colour

- Red in lung & intestine

- greyish white.

- Pale then red in spleen

Edges

* red due to inflammation

* No hyperemia ( no inflammation)

M/E

Coagulative necrosis

* fibrous tissue, Collagen

M/E

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

15

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

Lung

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.
Kidney

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
16

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

spleen

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.

Intestine

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 :
17

- 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

18

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
cause
type
Site
Putrifaction
Mamification

Wet gangrene

Gradual occlusion of any artery

always 2ry

Sudden occlusion of Both artery and vein

1ry Or 2ry

Exposed limb

Internal organ as intestine

Slow

Rapid

Present

Absent e` edema instead

19

* line of

Marked

Poor

* line of
Separation

Present

Absent

Self amputation

may occur

Not occur

spread

Slow

Rapid

Toxemia

Mild

Severe

Fatality

Not fatal

Highly fatal

demarcation

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

2 - Renal

2 - Milroy's edema

a - Venous

a - Nephritic

b - Lymphatic

b - Nephrotic
c - Nutritional

21

Clinical classification of edema of subcutaneous tissue :-

Pitting (soft) edema

Non pitting (hard) edema

1 - accumulated fluid is present free in

1 - fluid not move on pressure.

! tissue spaces & can be moved by pressure

2 - occurs in localized edema with

obstructed lymphatics ( inflammatory ;
fibrin obstruct it and in lymphatic edema)

2 - occurs in all generalized edema & in

localized venous edema (patent lymphatics)

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.

21

# Secondary Shock :Cardiogenic Shock

= acute heart failure
Due to :* myocardial infarction
* major pulmonary embolism
* cardiac surgery.

Septic ( Endotoxic ) Shock

Hypovolemic Shock

Fatal

Causes :-

Causes : Severe bacterial infections :-

a - Hemorrhage
b - Loss of plasma
fluids e.g. Burns.

- gram - ve bact as. E-Coli.

c - Loss of fluids &

electrolytes e.g. severe
diarrhea & vomiting
Pathogenesis :-

- infected burns.
- immunodeficiency states.

Pathogenesis :-

- blood volume
decrease VR

1 - Dilatation of venules &

capillaries by chemical

decrease COP

mediators -- effective

decrease blood
flow decrease O2

blood flow.

supply to ! tissue

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.

22

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.

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