Thrombosis Dr. László Terézia
HYPERCOAGULABILITY THROMBOSIS BLOODFLOW ENDOTHEL VIRCHOW
ENDOTHEL INJURY L. ventricle: Arteries: surgery infection prosthetic valve hypertension irradiation chemical: cigarette smoke cholesterol bact. Toxins IC
BLOODFLOW Turbulent ATS paque aneurysms Stasis AMI mitral stenosis varicouse veins hyperviscosity giant hemangioma-kassabach-merritt
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
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
Acquired hypercoagulable conditions II. Nephrosis syndrome Previous deep vein thrombosis or pulmonary embolism Myeloproliferative disorders polycythemia vera essential thrombocytosis
FATE OF THROMBUS Propagation Embolisation dissolution by fibrinolytic action Organisation / recanalisation
THROMBOHAEMORRHAGIA
DIC 1. Activation of coagulation - thrombosis 2. Consumption of: platelet - bleeding fibrin coagulation factors
Triggering menchanism Obstetric complications AML Adenocarcinoma-mucus release Sepsis (gram neg.) Trauma Endothel injury (IC) Extrinsic and intrinsic pathway
EMBOLIA
Types of embolisation I. Thromboembolisation Pulmonary Systemic Paradox
Types of embolisation II. Amnionic fluid Air / gas Fat, bone marrow Bits of tumor
SHOCK
Cardiogenic AMI Arrhythmia Pulm. Emb. Hemopericardium Hypovolemic Hemorrhage Fluid loss Septic Neurogenic
Hypovolemic & cardiogenic shock Cardiac output pale cool sweaty skin Sympathetic vasoconstriction of microcirculation
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
Endotoxin shock Gram neg. Sepsis E. coli Klebsiella Enterobacter pseudomonas LPS release
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
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
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
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
HYPERTONIA
A. Essential B. Secunder 1. Renal Renoparenchymal Renin prod. tumor Renovascular 2. Endocrine Cushing sy. Aldosteronism Exogenous glycocorticosteroid Estrogens Pheocromocytoma Hypo-, hyperthyroidism Pregnancy
3. Cardiovascular Coarctation aortae Increased intravascular volume Increased cardiac output Rigidity of aorta 4. Neurologic Psychogenic Increased intracranial pressure Sleep apnoe Acut stress (Surgery)