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.

5

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 ).

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* 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 ).

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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

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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

18

- 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.