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Dr.suhaemi,SpPD,Finasim
Thrombus
red thrombus
Pendahuluan
Trombosis adalah pembentukan suatu massa
abnormal di dalam sistem peredarah darah mahluk
hidup yang berasal dari kompnen komponen darah,
Keadaan ini sering mengakibatkan kecacatan atau
kematian.
Survei KRT depkes 1998: PJK dan Stroke penyebab
kematian di Indonesia
Cardiovascular Disease
30% of all deaths in Canada
20% stroke
Thrombotic Embolic
Thrombus
Embolus
Head CT:
Ischemic Stroke
Arterial Thrombosis
Myocardial Infarction
Myocardial infarction and mural thrombosis
Clot on bicuspid aortic valve
T ooMuch Anticoagulation
in a Thromboticpatient
2 1
• Description of :
-Factor V Leiden
-Prothrombin 20210 mutation
-Protein C, Protein S and Antithrombin
Deficiencies
-Heparin-Induced Thrombocytopenia
-Antiphospholipid Antibodies
Embolus in the aorta
Risk factors?
Symptoms?
Treatment?
Outcome?
Abnormal Abnormal
Vessel Wall Blood
Immobility
Obesity
Smoking
Cancer
Pregnancy
Estrogen therapy
Types of Thrombosis
Arterial: platelet-based (white) thrombus
(scanning EM)
1964
MacFarland
“enzyme cascade”
Nature
may combine
Thrombi
Localization - detailed
Arterial – occlusive; mixed
coronary, cerebral, femoral
atherosclerosis, vasculitis, trauma
Venous – occlusive, long cast; red; 90% legs
autopsy dif. dg. postmortem clot
Heart – valves – vegetations
infective or sterile (rheum., NBTE, SLE)
Heart chambers, aneurysms of heart or aorta
Mural; infarction; embolisation: brain, kidney, spleen
1. Vessel wall – endothelial injury – dominant
exposure of subendothelial collagen
+ adherence of platelets
exposure of tissue factor, local depletion
of prostacyclin and plasminogen activator
Atherosclerosis – ulceration
Necrosis – myocardial infarction
Trauma
Inflammation – vasculitis
Hypertension, turbulent flow, bact. endotoxins
Homocystein, cholesterol, radiation, smoking
2. Alterations in normal blood flow
Normal = laminar
Turbulence – arteries, heart;
combined turb. + stasis (endot. injury + stasis)
Stasis – veins, heart
Ulcerated atherosclerotic plaques – endot. +turb.
Aneurysms – local stasis
Mitral valve stenosis – stasis – left atrial dilation
Hyperviscosity syndromes – polycythemia; sickle cell
anemia (occlusions stasis; small vessels)
3. Hypercoagulability
Any alteration of coagulation pathway
predisposing to thrombosis
Primary (genetic)
Mutations in factor V = Leiden mutation
2-15% of popul. APC resistance
antithrombin III, protein C, S deficiencies
fibrinolysis def., hyperhomocysteinemia
↑prothrombin levels - 1%, allelic variations
Thrombo(embolism) – recurrent, young,
no or insignificant other causes
Secondary (acquired) - high risk or low risk
3. Hypercoagulability
Secondary (acquired)
↑ High risk of thrombosis - immobilization, myocard
infarction, tissue damage (trauma, burns, surgery),
cancer, prosthetic cardiac valves, DIC, heparin-induced
thrombocytopenia, antiphospholipid antibody syndrome
(with/out autoimmune dis. - SLE)
↓Lower risk of thrombosis -atrial fibrillation,
cardiomyopathy, nephrotic syndrome, hyperestrogenic
states, oral contraceptives (3x), pregnancy (8x), sickle
cell anemia, smoking
Thrombus
Clot develops in intact, unbroken vessel
Blocks circulation to tissues beyond thrombus
Embolus
Thrombus that comes loose, flows
Ultimately lodges in narrow vessel, blocks
circulation
Pulmonary embolism
Cerebral embolism
Fondaparinux
Idraparinux
Antithrombine direct
Dabigatran
Müller, 1997
Choice of medication for stroke
prevention
What is the cause of the stroke?
20% 15%
0%
Ticlopidine (Ticlid)