Pathophysiology

    Cards (11)

    • Why do you get right ventricular strain in thrombosis?
      Due to increase in pulmonary vascular resistance (due to thrombus & vasoconstriction by hypoxia mediators) -> increased right ventricular afterload -> increased right ventricular muscle stretch, increased wall tension & right ventricular dilatation -> right ventricular strain
    • What are the physiological consequences of PE?
      Blocks oxygenated blood to body
      Hypoxic vasoconstriction (changes amount of ROS)
      Increases resistances in pulmonary system
      Gas exchange reduced -> increases alveolar dead space
      Pleural effusion - fluid build up between pleural layer
    • What problems can chronic thromboembolic pulmonary HTN cause?
      Right ventricle dilation
      Tricuspid valve reguritation
      Right ventricle failure
      Change in ventricular pressure -> interventricular septum to shift to left
      Compresses left ventricle -> less CO by left ventricle -> affects coronary arteries -> heart ischaemia
    • What does a decreased left ventricular compliance cause?
      Diminished diastolic performance -> less filling
    • How does the pulmonary circulation react to hypoxia?
      Pulmonary circulation reacts differently to hypoxia -> vasoconstriction -> sends blood to highly oxygenated areas in lungs
      Pulmonary resistance vessels is insensitive to sympathetic & chemical control
    • How is an air embolism resolved naturally?
      Air bubble is eventually reabsorbed by surrounding blood or tissue and recovery without intervention may occur
    • What is Virchow's triad?
      Venous stasis
      Hypercoagulability
      Endothelial injury
    • Pathophys PE
      Damage to endothelium of veins → vasoconstrictionlimit blood flowplatelets adhere to endothelium & become activated by collagen & tissue factor → recruit more platelets → activates coagulation cascade → cleave fibrinogen to fibrinfibrin clot formationclot grows, reduces blood flow → increase venous pressure
      Clot can breakdown → increased D-dimer
      OR
      High venous pressire -> part of clot breaks off to become thromboembolism -> travel towards heart & can become lodged in lungs → PE
    • What are the 2 types of thrombus?
      Arterial
      Venous
    • What are the possible fates of a thrombus?
      Lysis - thrombolytic activity of blood
      Propagation - increase in size
      Organisation - thrombus becomes firm & greyish white
      Canalisation - new lumen
      Embolisation - part/all of thrombus becomes dislodged & travels through circulation
    • Fill in the blanks
      A) Factor XII
      B) Factor XIIa
      C) Factor XI
      D) Factor XIa
      E) Factor IX
      F) Factor IXa
      G) Factor VIIIa
      H) Tissue factor
      I) Factor VII
      J) Factor VIIa
      K) Factor X
      L) Factor Xa
      M) Factor II
      N) Factor IIa
      O) Factor I
      P) Factor Ia
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