January 2007

GANGGUAN HEMODINAMIK, CAIRAN TUBUH DAN TROMBOSIS

BAGIAN PATOLOGI ANATOMIK

FKUGM

January 2007

HEMOSTASIS NORMAL

HEMOSTASIS NORMAL : HEMOSTASIS NORMAL : mempertahankan darah dalam mempertahankan darah dalam kondisi cair dan membentuk kondisi cair dan membentuk jendalan darah pada tempat/ jendalan darah pada tempat/ pembuluh darah yang pembuluh darah yang mengalami jejasmengalami jejas

January 2007

HEMOSTASIS NORMAL

1. Integritas pembuluh darah kecil

2. Jumlah platelet yang mencukupi

3. Jumlah normal faktor koagulasi

4. Jumlah normal inhibitor koagulasi

5. Jumlah ion kalsium dalam darah yang mencukupi

January 2007

KANDUNGAN PEMBULUH DARAH DAN KOAGULASI

• SEL-SEL ENDOTEL BERSIFAT ANTITROMBOTIK– Efek antiplatelet– Efek antikoagulan– Efek fibrinolitik

• BISA JUGA BERSIFAT PROTROMBOTIK– Pro adesi platelet -

VWF – Prokoagulan –

teraktifasi untuk sekresi faktor jaringan

• ANTIFIBRINOLITIK – INHIBITOR AKTIFATOR PLASMINOGEN YANG MENEKAN FIBRINOLISIS

January 2007

HEMOSTASIS DAN PLATELET

• BERPERAN PENTING DALAM HEMOSTATIN– Fragmen sitoplasma

megakarosit– Setelah jejas

vaskular:• Platelet melekat• Platelet

mensekresi produk granul

• Agregat platelet– Sumbat

hemostatik primer

M

January 2007 Downloaded from: Robbins & Cotran Pathologic Basis of Disease (on 31 January 2005 07:03 PM)

© 2005 Elsevier

January 2007 Downloaded from: Robbins & Cotran Pathologic Basis of Disease (on 31 January 2005 07:03 PM)

© 2005 Elsevier

January 2007 Downloaded from: Robbins & Cotran Pathologic Basis of Disease (on 31 January 2005 07:03 PM)

© 2005 Elsevier

January 2007

GANGGUAN KOAGULASI

• ABNORMALITAS PEMBULUH DARAH KECIL

• ABNORMALITAS JUMLAH PLATELET – TROMBOSITOPENIA

• Penurunan produksi• Destruksi perifer

• PENURUNAN FAKTOR-FAKTOR KOAGULASI

– HEMOFILIA– DEFISIENSI PROTROMBIN

• ANTIKOAGULAN• SINTESIS ATAU ABSORPSI K YANG TIDAK

MENCUKUPI• PENYAKIT HATI YANG BERAT

January 2007

URUTAN KOAGULASI

• RENTETAN REAKSI ENZIMATIK DENGAN HASIL AKHIR PEMBENTUKAN TROMBIN YANG MERUBAH FIBRINOGEN (SOLUBLE) MENJADI FIBRIN (INSOLUBLE)

January 2007

January 2007 Downloaded from: Robbins & Cotran Pathologic Basis of Disease (on 31 January 2005 07:03 PM)

© 2005 Elsevier

January 2007

BAGAIMANA CARA MENGHENTIKAN PROSES

KOAGULASI

• SISTEM FIBRINOLITIK– TERUTAMA OLEH AKTIFASI

PLASMIN•PLASMIN DIBENTUK OLEH AKTIFASI

AKTIVATOR PLASMINOGEN JARINGAN DAN UROKINASE

•MENYEBABKAN PEMECAHAN FIBRIN MENJADI PRODUK PECAHAN FIBRIN

January 2007

THROMBOSIS

• PENYIMPANGAN AKTIFASI PROSES HEMOSTASIS PADA PEMBULUH DARAH YANG UTUH ATAU PEMBENTUKAN TROMBUS PADA PEMBULUH DARAH MINIMAL

January 2007 Downloaded from: Robbins & Cotran Pathologic Basis of Disease (on 31 January 2005 07:03 PM)

© 2005 Elsevier

January 2007

FAKTOR PREDISPOSISI TROMBOSIS

• HIPERKOAGULABILITAS– SEMUA PERUBAHAN PATHWAY

KOAGULASI YANG MENIMBULKAN KECENDERUNGAN TROMBOSIS•PRIMER (GENETIK)

– MUTASI GENA FAKTOR V DAN MUTASI GENA PROTROMBIN» F V resisten thd inaktifasi protein C» Kadar protrombinmeningkat

•SEKUNDER (AKUISITA)– Bed rest – immobilisasi, obesitas, canker,

fibrilasi atrium, infark miokardium, kerusakan jaringan (bedah, lk bakar)

January 2007

FAKTOR PREDISPOSISI TROMBOSIS• ABNORMALITAS ALIRAN

DARAH• TURBULENSI

– Jejas endothelial– Stasis aliran darah lokal– Aliran laminar yang

kacau• Platelet bergerak dari

pusat aliran ke dinding pembuluh darah

• Mencegah pengenceran faktor penjendalan teraktifasi

• Memperlambat masuknya inhibitor faktor penjendalan

• Merangsang aktifasi sel endotel.

January 2007

Thrombi Morphology: Venous

• Venous thrombi– Usually occlusive– Red (because they form

in stasis syndrome and have more associated enmeshed RBCs)

– Long - forming a cast of vein with markings on them from venous valves

– Red blood cells alternating with peripheral areas of fibrin

January 2007

Venous Thrombi: Clinical

January 2007

Venous Thrombi: Fates

• Organization– Ingrowth of cells

into thrombus with incorporation into wall

• Resolution – It goes away

• Embolization– Travels from its site

of origin to a distal part of circulation

January 2007

VENOUS THROMBI FATES

January 2007

Arterial Thrombi Morphology

• Adherent masses of blood that demonstrate areas of pale alternating with areas of red– Lines of Zahn

January 2007

Arterial Thrombi Morphology

January 2007

Arterial Thrombi Outcome

• Similar to venous thrombi– Resolution– Organization/Incorporation/

Recanalization– Embolization (arterial)– Propagation

January 2007

Disseminated Intravascular Coagulation

• Sudden onset of fibrin thrombi in the microcirculation with consumption of coagulation factors and formation of fibrin degradation products

• A potential complication of any disease state/process associated with the widespread activation of thrombin

January 2007

EMBOLISM

• A DETACHED SOLID, GASEOUS OR LIQUID MASS THAT IS CARRIED BY THE BLOOD FROM SITE OF ORIGIN TO A DISTAL SITE– Thrombi, fat, amniotic

fluid, foreign substances, bone marrow

– May lodge in pulmonary or systemic circulation

January 2007

Pulmonary Thromboembolism

• 20-25 per 100,000 hospitalized patients

• May be fatal if 60% of pulmonary circulation is obstructed (acute cor pulmonale)

• Saddle PE straddles the bifurcation of the main Pulmonary arteriae

• Sequelae: Sudden death, clinically silent – resolution – organization, shortness of breath, pulmonary infarction

• Pathogenesis: Deep venous thrombi usual cause –often following immobilization-bed rest from hospitalization

January 2007

PULMONARY EMBOLISM

January 2007

PULMONARY INFARCT

• EMBOLIZATION TO SMALL DISTAL VESSELS IN LUNG MAY CAUSE ISCHEMIC NECROSIS OF TISSUE OR INFARCT

January 2007

Other Emboli

January 2007

PARADOXICAL EMBOLI

• EMBOLI WHICH TRAVEL FROM VENOUS TO ARTERIAL CIRCULATION VIA A COMMUNICATION BETWEEN ARTERIAL AND VENOUS CIRCULATION

January 2007

Infarction

• Ischemic necrosis of tissue distal to an area of arterial occlusion or in an area of obstructed venous outflow– Red (Hemorrhagic)

• Organs with dual blood supply

• Soft aerated tissues

– Anemic (White)• Organs with single

blood supply

January 2007

Infarction due to venous obstruction

January 2007

Infarction

• Microscopically see coagulative necrosis

January 2007

Edema

• Excess fluid in the interstitial spaces of the body

• Major factors keeping fluid in vessel – Oncotic (albumin)

• Major factor pushing fluid out of vessel – Hydrostatic pressure

January 2007

Edema: Hydrostatic

January 2007

EDEMA

January 2007

Edema: Lymphatic Obstruction

January 2007

Congestion and Hyperemia

January 2007

CONGESTION AND HYPEREMIA

January 2007

CONGESTION: MORPHOLOGY

January 2007

CONGESTION MORPHOLOGY

January 2007

Shock

• A situation in which the circulatory system can no longer supply nutrients and oxygen to the peripheral tissues– Hemorrhagic (hypovolemic) shock

•No blood volume

– Cardiogenic shock•Pump failure

– Septic shock•Failure of microcirculation to retain pressure