Post on 31-Oct-2014
description
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