Lecture Pathology BMS III

7/30/2019 Lecture Pathology BMS III

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Hemodinamic disorder

C.Murtono

Pathology DeptAtma Jaya Med.Faculty


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HEMODINAMIC

DISORDERS

OXIGEN DISTRIBUTION IS VERY

IMPORTANT60% OF BODY WEIGHT AN ADULT IS

WATER ( 40% INTRA- AND 20%

EXTRACELLULAIR )

MANY DISEASES AND MORTALITY ARE

BASED ON HEMODINAMIC DISORDER


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EDEMA

ACCUMULATION OF ABNORMALAMOUNT OF FLUID IN THE

INTERCELLULER TISSUE SPACES ORBODY CAVITY.

CLASSIFICATION OF EDEMA :

I. GENERALIZED ORLOCALIZED

II. INFLAMMATORY AND NONINFLAMMATORY


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CAUSE OF EDEMA

1. INCREASE IN INTRAVASCULAIR

HYDROSTATIS PRESSURE

2. A FALL OF OSMOTIC PRESSURE OF

THE PLASMA

3. LYMPHATIC OBSTRUCTION

4. RENAL RETENTION OF SALT


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1.INCREASE OF INTRAVASCULAR

HYDROSTATIC PRESSURELOCAL INCREASE, e.c. trombosis of

lower leg. The result is edema of lower leg

GENERALIZED EDEMA, e.c.systemic

edema caused by increased systemic venous

pressure, as seen by congestive heartfailure.


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2. REDUCED PLASMA OSMOTIC

PRESSURETHE LOSS OF ALBUMIN, like in nephrotic

syndrome, a kidney disorder with leaky of

glomerular basement membrane and generelizededema.

THE REDUCED SYNTHESIS OF SERUM

PROTEIN, due diffuse disease of the lever, such

as cirrhosis. Also in malnutrition ( proteindeffensiasi ). Fluid move from intravascular to

interstitial tissue.


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3. LYMPHATIC OBSTRUCTION

FROM THE LUMEN, like filariasis cause fibrosis

of lymph channel in inguinal region. Resulting

edema of external genital and lower limb (elephantiasis )

FROM THE WALL, like tumour of the wall (

myoma, fibroma cs )

FROM OUTSIDE, ,fibrosis of perilymphatic

tissue ( ec .due radiation in mamma Ca )


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4. SODIUM AND WATER

RETENTION

SALT RETENTION BY ACUTEREDUCTION OF RENAL FUNCTION

CAUSED EDEMA.

RETAINED SALT AND WATER

EXPANSION OF INTRAVASCULARFLUID VOLUME INCREASEDHYDROSTATIC PRESSUREEDEMA.


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MORPHOLOGY

SUBCUTANEOUS EDEMA , prominent

manifestation of cardiac failure, particularly right

ventricel. Distribution of edema influenced by

gravity.

RENAL DYSFUNCTION AND NEPHROTICSYNDROME ,initially periorbital edema, but later

generalized edema ( anasarca ). FINGER

PRESSURE caused pitting edema.


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MORPHOLOGY

PULMONARY EDEMA, mostly in the lower

lobe. On sectioning, frothy ,sanguinous fluid.Microscopic, wide septal capillair with proteinous

fluid in alveoli.

BRAIN EDEMA, could be localized ( localizedprocess like abscess or neoplasma). If generalized

, like encephalitis, hypertensive crisis, or venous

obstruction. Brain is heavier than normal, gyri

flattened with narrowed sulci. Peri vascular spaceswidened.


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HYPEREMIA-CONGESTION

HYPEREMIA, OR ACTIVE HYPEREMIA, an

arterial dilatation caused an increased blood flow.Excessive body heat, as exercise or febrile.

Blushing , due neurogenic mechanism.

CONGESTION, OR PASSIVE HYPEREMIA, anvenous dilatation. Congestion could be classified

as localized or generalized. Also acute or chronic.


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CONGESTION

Closely related with edema, commonly

occur together.

Localized congestion ec venous return of

blood obstructed or portal hypertension by

cirrhosis

Systemic congestion ec decompensatiocordis right or left.


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MORPHOLOGY

congestion of the lungALVEOLAR CAPILLARIES CONGESTED ,

RUPTURED, ALVEOLI FILLED WITH

BLOOD.EDEMA FLUID COLLECTS IN THE

ALVEOLAIR SEPTA.

RUPTURED ERITROCYTES INGESTED BY

MACROPHAGE ( HEART FAILURE CELL )

SEPTA FIBROUS ( BROWN INDURATION )


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MORPHOLOGY

congestion of the liverCausa : right sided heart failure , obstruction ofvena cava inferior , or hepatic vein.

Around v.centralis is red blue , surroundeduncongested lever cells ( nutmeg liver )

V. centralis distended wiwh blood, the cells areatrophic due chronic hypoxia. Periferi : fatty

changes. Advance : hemorrhagic necrosis


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MORPHOLOGY

congestion of the spleenSpleen enlarged : congestive splenomegali

Causa : obstruction of v splenica ( trombus ),

intrahepatic (cirrhosis ), or systemic ( heartfailure )

Spleen enlarged ( until 5000 gram), firm, capsulthickened, hemorrhage with organization ( Gamna

Gandhi , fibrosis+ iron+ calcium )


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HEMORRHAGE

IMPLIES RUPTURE OF BLOOD VESSEL.CAN BE EXTERNAL OR HEMATOMA

IN THE CAVITY : HEMOTHORAX ,

HEMOPERICARDIUM , HEMARTHROSIS ,

HEMOPERITONEUM .

MINUTE: PETECHIAE, SLIGHTLY LARGER :

PURPURA,

SUBCUTANE HEMATOMA 1 - 2cm :ECCHYMOSES


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HEMORRHAGE

RELEASED HEMOGLOBINBILIRUBINHEMOSIDERIN SO THE PATIENT WITHLARGE HEMORRHAGE BECOMESJAUNDICE.

CLINICAL : DEPEND ON VOLUME OF THEBLOOD, RATE OF LOSS , SITE OFHEMORRHAGE..

SLOW LOSSES : - , LARGER/ ACUTE :

SCHOK , VERY LARGE : DEATH. REPEATED: IRON DEFFICIENCY.


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THROMBOSIS

FORMATION OF CLOTTED MASS OFBLOOD WITHIN THE NON INTERUPTEDVASCULAR SYSTEM

CAUSES : 1. ENDOTHELIAL INJURY

2. ALTERATIONS IN NORMAL

BLOOD FLOW

3. HYPERCOAGULABILITY


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ENDOTHELIAL INJURY

MOST THROMBI IN THE HEART ANDULCERATED PLAQUES OF

ATHEROSCLEROTIC ARTERI

EXOGEN INJURY:CHEMICALS ( SMOKING ),

ENDOGEN INJURY :

HYPERCHOLESTEROLEMI, BACTERIAL

TOXINS, IMMUNOLOGIC INJURY (

TRANSPLANT )


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ALTERATIONS OF BLOOD FLOW

TURBULENCE - ARTERIAL THROMBI

SLUGGISH / STASIS - VENOUS THROMBI


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HYPERCOAGULABILITY

PRIMARY : antithrombin defficiency, protein c

defficiency, Fibrinolysis deffect

SECUNDAIR : prolonged bed rest , myocardinfarct, leukemia, cancer

diss intrav ,coagul,thromb.

thromboc.pur, oral contrasepsisickle cell anemia,smoking

late pregnancy


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Morphology of thrombus

ARTERIIL THROMBUS : ENDOTHELIAL INJURY,

TURBULENCE, BIFURCATIO, OT BRANCH.

INTERSPERSE BETWEEN DARKER LINES

(AGGREGATED PLATELETS ) WITH PALER LAYER(COAGULATED FIBRIN ) LINES OF ZAHN.

ON SURFACE MURAL THROMBI , IN SMALLER

ARTERI :OCCLUSIVE THROMBI , ON HEART

VALVE ( WITH BACTERI )VEGETATION , IN

BRANCHSADDLE THROMBUS


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VENOUS THROMBUS

( PHLEBOTHROMBOSIS )MOSTLY IN LOWER EXTREMITIES :

v.femoralis , poplitea , deep calf , iliac veins

ATTACHED TO UNDERLYING VESSEL thetail fragmented EMBOLUS

Diff Diagnosis with post mortal clot. Clot is

rubbery , or gelatinous. Clot not attached to the

underlying tissue.


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WHAT HAPPENS WITH THROMBUS

may propagate , cause obstruction

May embolize

Removed by fibrinolytic activityOrganized , fibroblast and endothelial cellsingrowth vascularized connective tissue (

recanalization


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CLINICAL CORRELATION

CAUSE OBSTRUCTION, cause myocardialinfarction , encephalomalacia ( strokes

PROVIDE SOURCE OF EMBOLI superficial, causelocal swelling, pain, tenderness

DEEP VEIN THROMBOSIS, cause edema foot,ankle , Homan sign.

MULTIPEL THROMBOSIS : phlebitis migrans : Capancreas.


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DISSEMENATED INTRAVASCULAR

COAGULATION ( D.I.C. )MINUTE THROMBI FORMED INMICROCIRCULATION, ESPECIALLYCAPILLAIR, AND VENULE

COMPLICATION OF UNDERLYING DISEASE.

CIRCULATORY INSUFFISIENCY,lung,

brain,heart, kidney.SIMPTOM: HEMORRHAGIC DIATHESEAND OCCLUSION IN MICROCIRCULATION


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Morphology of thrombus

THROMBUS ARTERIIL :

ENDOTHELIAL INJURY,

TURBULENCE, BIFURCATIO, OTBRANCH. INTERSPERSE BETWEEN

DARKER LINESM (AGGREGATED

PLATELETS ) WITH PALER LAYER (COAGULATED FIBRIN ) LINES OF

ZAHN.

ON SURFACE

MURAL THROMBI ,


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EMBOLISM

OCCLUSION OF SOME PART OF

CARDIOVASCULAIRE SYSTEM BY

EMBOLUS TRANSPORTED TO THE SITETHROUGH THE BLOODSTREAM.

95% ARISE FROM THROMBUS, THE REST

ARISE FROM: BAT, BUBBLE OF GAS ,

ATHEROSCLEROTIC DEBRIS , BONEMARROW FRAGMENTS, TUMOUR CELLS.


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PULMONARY EMBOLISM

64% OF AUTOPSIES , SOMEASIMPTOMATIC

15% DEATH OF HOSPITALIZED PATIENT.

SMALLER EMBOLIES CAUSE PULMONARYHEMORRHAGE AND INFARCTION. LARGEEMBOLIES CAUSE ACUTE COR

PULMONALE WITH SUDDEN , SEVEREHYPOXEMIA.

AMONG THE SURVIVER: RAPIDFIBRINOLYSIS


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SYSTEMIC EMBOLI

Mostly ( 85% ) due the heart thrombus, secondary

to myocardial infarction.

Also arrythmia , like atrial fibrillation.Atrial emboli cause infarction, in lower

extremities ( 70%) that cause gangren , brain (

10%) that fatal, viscera (10%).


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AMNIOTIC FLUID EMBOLISM

UNCOMMON :( 1 : 50.000 labor) with fatalityrate 86%. Suddenly, respiratory difficulty withcyanosis, cardiovascular shock, convul sion,

coma, pulmonary edema.

Tear of placenta membrane, amniotic fluid intomaternal circulation ( epitel, lanugo fat,muconium). Death due anaphylaxis.


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Air embolism ( Caisson )

Gas obstructs vascular flow.

Causa: gas breathing under pressure,

during delivery/abortionduring pneumothorax

injury to chest wall.

Lead to multiple foci ischemic necrosis.


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FAT EMBOLI

Following fracture of the shaft long bone

Sudden onset of tachypeu ,dyspneu and

tachycardia. Accompanied by rest

less, delirium, coma.


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INFARCTION

AREA OF ISCHEMIC NECROSIS

produced by occlusion ( by either arteri al

supply or venous drainage).Nearly 99% caused by thromboembolic

event , and mostly by arterial occlusion.

Ovary, testis have single venous outflowchance for venous thrombosis.


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TYPES OF INFARCT ( I )

1. White vs hemorrhagic

2. Presence vs absance of bacterial

infection.White infarct : arterial occlusion in solidorgan , ec kidney , heart , spleen.

Blood from anastomosis

initialhemorrhage lyses hemoglobinehemosiderin


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TYPES OF INFARCT ( II )

HEMORRHAGIC INFARCT:

- with venous occlusion

- in loose tissue

- tissue with double circulation

- tissues previously congested.

In lung , small intestine


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MORPHOLOGY OF INFARCT

WEDGE shaped, apex the focus of vascularocclusion.

The next 24 hours , the sharp define , withhyperemia and inflammatory infiltration

Fibroblastic reparative response fromperiphery and replaced the infarct area withscar tissue.

Exception : brain liquefaction. Septicconvert to abscess


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MAJOR DETERMINANTS OF

INFARCT1. The nature of vascular supply, ec 2 arteries in lung, liver , hand ( not end arteri).

2. Rate of development of occlusion, slowlydevelopment of occlusion less likely toinfarction

3. Vulnerability of the tissue to hypoxia ,ecbrain,neuron, myocard is sensitif.


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CLINICAL SIGNIFICANT

CORONARY heart disease : 33% of all.

Cerebral infarction.

Pulmonary infarction

Ischemic necrosis ( + gangren in DM )

Kidney infarction

Gut hemorrhagic infarction.


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SHOCK ( I )

Hypoperfusion of tissue due to reduction of

blood volume or cardiac output or

redistribution of blood, resulting in anadequate effective circulating volume.

Defficiency in oxygen deliveryaerobic to

anerobic metabif worsenirreversibelinjury / cell death.


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SHOCK ( II )

3 types:

1. Cardiogenic, failure of myocardial pump

due myocardial damage, arryth mia,orpulmonary embolism

2. Hemorrhagic,due fluid loss

3. Septic shock, most commonly gramnegative / or endotoxin


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SHOCK ( III )

RARELY :

1. neurogenic shock due anaesthetic

accident or spinal cord injury massiveperipheral dilatation.

2. Anaphylactic shock : initiated by type 1hypersensitivity reaction.


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MORPHOLOGY OF SHOCK

Hypoxic failure of multiple organ system

Brain : hypoxic encephalopathy

Heart: subendocardial necrosis/hemorrh

Kidney:acute tubular necrosis

Lung: shock lung

Adrenal : stress response

Intestinal: hemorrhagic enteropathy


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Lecture Pathology BMS III