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Local Circulatory Disturbances in Pathology

Explore manifestations, causes, and types of local circulatory disturbances like ischemia, hyperemia, and thrombosis. Learn about factors influencing vessel occlusion and hemorrhagic classifications. Study the intricate pathogenesis of hemorrhage and thrombotic events.

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Local Circulatory Disturbances in Pathology

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  1. General Pathology Circulation Disorders - II Manifestations & Causes of Local Circulatory Disturbances Jaroslava Dušková Inst. Pathol. ,1st Med. Faculty, Charles Univ. Prague

  2. Manifestations of Local Circulatory Disturbances • local hyperemia • local anemia LOCAL ISCHEMIA

  3. Manifestations of Local Circulatory Disturbances • local hyperemia • active arterial (fluxe) capillary (peristatic) • passive venous (stasis)

  4. Manifestations of Local Circulatory Disturbances • local anemia • slow development – vascular atrophy • fast development – dystrophy , necrosis

  5. Ischemia – stratification of changes • complete necrosis - central part • myomalacia • hyperemia • interstitial leucocyte infiltration – vital reaction • dystrophic steatosis (& glycogenosis) • healthy

  6. Causes of Local Circulatory Disturbances • local anemia stenosis to occlusion of artery • lumen embolism • wall atherosclerosis,thrombosis (spasmus, depositions, inflammations, tumours) • combination of previous • neighbourhood compression

  7. Causes of Local Circulatory Disturbances • local hyperemia active • function • inflammatory vasodilation passive (outflow blocade) • lumen • wall • neighbourhood

  8. Thrombosis Def.: intravital intravascular blood clotting Range: parietal obturative

  9. Haemostasis • Endotheliumdamage – vWF secretion • Thrombocytesadhesion & aggregation • Thrombocytes secretion • serotonin, PDGF, thromboxan A2vasoconstriction • fibronectin, vWF, fibrinogen aggregation • Plasma factors - proteins synthesized in hct, (vit. K dependence) cascade activation

  10. postmortem autolysis protein activation thrombin liberation no platelet thrombus fibrinogen - fibrin non adherent elastic intravital platelet based adherent to the vessel wall friable /crumbly Coagulum x Thrombus

  11. Types of Thrombi • red stagnation • white fluxe • mixed • hyaline

  12. Thrombosis - causes • blood stagnation • endothelium damage • blood composition changes

  13. Thrombosis - causes • blood stagnation • heart failure • vein insufficiency • local factors (compression) laminar flow disturbance

  14. Thrombosis - causes • endothelium damage • atherosclerosis • inflammation • injury • hemodynamic stress • high cholesterol levels

  15. Thrombosis - causes • blood composition changes • increased platelet number (over 400 000/mm3) • thromboplastin liberation (e.g. following pancreas and lung surgery) • endotoxin - DIC • amniotic fluid embolism • contraceptives……

  16. inborn mutations with increased levels of thrombocytes or lack of anticoag. proteins acquired pregnancy contraceptives disseminated neoplasms atrial flutter arteficial valves surgery……. Hypercoagulation

  17. Thrombus development • no • lysis • organisation(decoloration, recanalization, hyalinization, dystrophic calcification - phlebolith) • lysis + organisation • embolism • puriform softening • infection

  18. Natural Anticoagulant Systems • Antithrombins– e.g.antithrombin III inhibits fcts IXa,Xa,XIa,XIIa • Proteins C, S (vit K dependent) – inh. fcts Va, VIIIa • Plasminogene – plasmin system fibrin breakdown

  19. Embolism Def.: transport of a compact particle in circulation with stopping in the place of anatomic narrowing

  20. Emboli – Types • thrombotic • fat • air • amniotic fluid • cellular (neoplastic, bacterial trophoblastic) • foreign body

  21. Embolism – Fate THROMBOTIC • no • organisation • lysis , resorption • progression • fat • air • amniotic fluid life threatening

  22. Embolism – Fate CELLULAR • lysis trophoblastic • progression neoplastic METASTASES bacterial metastatic sepsis

  23. Caisson Disease (Decompression thickness – gas microembolism) • divers • underwater construction workers • unpressurized aircraft in high altitudes life threatening

  24. Factors Influencing Vessel Occlusion Result • anatomy • time • tissue/organ sensitivity to hypoxy • functional status • general circulation status • MEDICAL INTERVENTION

  25. Haemorrhagia Def.: blood extravasation (and the presence of blood in the tissue)

  26. Localisation: external internal Source: arterial capillary venous Hemorrhage – Classification

  27. Haemorrhagia per rhexin (trauma – tear of the vessel wall) per diabrosin (arosion – ulcus, neoplasm) per diapedesin (increased vessel permeability- leakage) Hemorrhage - pathogenesis

  28. Haemostasis • Endotheliumdamage – vWF secretion • Thrombocytesadhesion & aggregation • Thsecretion • serotonin, PDGF, thromboxan A2vasoconstriction • fibronectin, vWF, fibrinogen aggregation • Plasma factors - proteins synthesized in hct, (vit. K dependence) cascade activation

  29. Hemorrhagic Statuses Thrombocytopaties thrombocytopenia, thrombasthenia Coagulopaties hemofilia, hypoprothrombinemia, afibrinogenemia, Vasculopaties scurvy, m. Osler, m. Schönlein – Henoch

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