Thrombosis. Dr. László Terézia

Transcription

1 Thrombosis Dr. László Terézia

2 HYPERCOAGULABILITY THROMBOSIS BLOODFLOW ENDOTHEL VIRCHOW

3 ENDOTHEL INJURY L. ventricle: Arteries: surgery infection prosthetic valve hypertension irradiation chemical: cigarette smoke cholesterol bact. Toxins IC

4 BLOODFLOW Turbulent ATS paque aneurysms Stasis AMI mitral stenosis varicouse veins hyperviscosity giant hemangioma-kassabach-merritt

5 HYPERCOAGULABILITY Inherited hypercoagulable conditions Factor V Leiden mutation Prothrombin gene mutation fibrinogen Deficiencies of anticoagulant proteins (antithrombin III, protein C and protein S) factor VIII

6 Acquired hypercoagulable conditions I. cancer Trousseau sy. recent trauma or surgery pregnancy and exogenous estrogen use (including use of oral contraceptive pills) bed rest or immobility smoking obesity age

7 Acquired hypercoagulable conditions II. Nephrosis syndrome Previous deep vein thrombosis or pulmonary embolism Myeloproliferative disorders polycythemia vera essential thrombocytosis

8 FATE OF THROMBUS Propagation Embolisation dissolution by fibrinolytic action Organisation / recanalisation

9 THROMBOHAEMORRHAGIA

10 DIC 1. Activation of coagulation - thrombosis 2. Consumption of: platelet - bleeding fibrin coagulation factors

11 Triggering menchanism Obstetric complications AML Adenocarcinoma-mucus release Sepsis (gram neg.) Trauma Endothel injury (IC) Extrinsic and intrinsic pathway

12 EMBOLIA

13 Types of embolisation I. Thromboembolisation Pulmonary Systemic Paradox

14 Types of embolisation II. Amnionic fluid Air / gas Fat, bone marrow Bits of tumor

15 SHOCK

16 Cardiogenic AMI Arrhythmia Pulm. Emb. Hemopericardium Hypovolemic Hemorrhage Fluid loss Septic Neurogenic

17 Hypovolemic & cardiogenic shock Cardiac output pale cool sweaty skin Sympathetic vasoconstriction of microcirculation

18 Stages os septic shock I. Hyperdynamic state: arteriolar dilatation systemic vascular resistance norm. or cardiac output warm, dry skin II. Dilatation of perif. microcirculation Pooling of blood effective circulatory blood volume Cardiac output Ineffective perfusion

19 Endotoxin shock Gram neg. Sepsis E. coli Klebsiella Enterobacter pseudomonas LPS release

20 endotoxin Membrane and cell demage Endothel cell platelet Macrophag, neutrophil coagulation Histamin, serotonin TNF, IL 1, PG Complement activation DIC Arteriolar dilatation permeability Effective blood volume Cardiac aoutput SHOCK

21 Stages of shock 1. Early compensated: baroreceptor reflexes release of catecholamines activation of the renin-angiotensin axis antidiuretic hormone release generalized sympathetic stimulation tachycardia, peripheral vasoconstriction renal conservation of fluid near normal blood pressure

22 2. Progressive decompensated phase: Despite arterial constriction and increased heart rate Blood pressure cardiac output tissue hypoperfusion circulatory and metabolic imbalance Anaerob glicolysis Acidosis capillary permeability transudation

23 3. irreversible stage Progressive reduction of cardiac output Progressive reduction of blood pressure Acidosis ischemic injury brain: hypoxic encephalopathy Lung: ARDS heart: contraction band necrosis kidney: acut tubular necrosis liver: fatty degeneration central hemorrhagic necrosis GI: patchy mucosal hemorrhage

24 HYPERTONIA

25 A. Essential B. Secunder 1. Renal Renoparenchymal Renin prod. tumor Renovascular 2. Endocrine Cushing sy. Aldosteronism Exogenous glycocorticosteroid Estrogens Pheocromocytoma Hypo-, hyperthyroidism Pregnancy

26 3. Cardiovascular Coarctation aortae Increased intravascular volume Increased cardiac output Rigidity of aorta 4. Neurologic Psychogenic Increased intracranial pressure Sleep apnoe Acut stress (Surgery)