Thrombosis, Embolism and Infarction 1

Beschreibung

Processes in Diseases Mindmap am Thrombosis, Embolism and Infarction 1, erstellt von Daniel Elandix G am 03/10/2013.
Daniel Elandix G
Mindmap von Daniel Elandix G, aktualisiert more than 1 year ago
Daniel Elandix G
Erstellt von Daniel Elandix G vor etwa 11 Jahre
78
1

Zusammenfassung der Ressource

Thrombosis, Embolism and Infarction 1
  1. Thrombosis

    Anmerkungen:

    • Solid or a semi-solid mass formed from the constituents of blood within the vascular system during life.
    1. Differences from haemostassis

      Anmerkungen:

      • Similar to haemostassis but then it is not adaptive like thrombosis but maladaptive.
      1. Factors inhibiting thrombosis

        Anmerkungen:

        • Intact endothelial cells to prevent platelet adhesion and it also produces anticoagulant molecules (like heparin-like) It also produces Tissue Factor Pathway Inhibitor (TFPI). Fibrinolysis: Clear fibrin deposits from endothelial surfaces Laminar flow to stop platelets to come in contact with walls and deliver anticoagulant molecules.
        1. Virchow's Triad

          Anmerkungen:

          • Factors predisposing thrombosis (this may occur anywhere in the Cardiovascular system)
          1. Changes in vessel walls

            Anmerkungen:

            • Either injury or dysfunction of the endothelium with exposure of sub-endothelial layers (collagen) Might be due to atherosclerosis, inflammation, trauma.
            1. Change in flow

              Anmerkungen:

              • Normal flow is laminar with plasma layer at edges and central column of cells. This like before said, removes clotting factors. Prevent platelets to come in contact with wall. Changes in flow occur mostly at branch points where there are loads of turbulence. At valves, or at aneurysm.
              1. Change in constituents of blood

                Anmerkungen:

                • Hereditary: Factor V mutation like (factor V Leiden) Inherited deficiency of anti-coagulant molecules. Acquired: Increased coagulation factors such as IL-12 or TNF-alpha. Or increased liver synthesis Hyperviscosity: Due to increase in blood cells (polycytaemia) or dehydration (decrease in plasma)
            2. Responses to Haemorrhage

              Anmerkungen:

              • 3 steps: Reflex vasoconstriction Primary Haemostassis (by which a platelet plug form) Secondary Haemostassis (protein aggregation and activation)
              1. Thrombi
                1. Venous

                  Anmerkungen:

                  • Occur due to low flow Mostly originate in the deep veins of the calf i.e DVT
                  1. Predisposing factors

                    Anmerkungen:

                    • Immobilization, decreased flow Post-surgical, Increased clotting factors and platelets plus the factor above Poor peri-operative care Cancer Pregnancy Heart failure Dehydration.
                    1. Type

                      Anmerkungen:

                      • Starts by attachment to valves or damaged endothelium. Propagates in the direction of flow. Occlusive.
                      1. Outcomes

                        Anmerkungen:

                        • 1. Resolution: Regular degradation, to restore normal function. 2. Organised and incorporated into wall. 3. Organized and recanalized. 4. Embolism in the lungs.
                        1. DVT
                          1. Clinical

                            Anmerkungen:

                            • Wells' Criteria: Swollen Tender Predisposing Factors Plus it may have associated warmth and redness....
                            1. Investigations

                              Anmerkungen:

                              • Venous Doppler
                              1. Prevention

                                Anmerkungen:

                                • Graduated compression stockings Heparin intermittent calf pressure Early mobilisation
                            2. Arterial Thrombus

                              Anmerkungen:

                              • Forms under high flow. Usually due to injured endothelium especially caused by atheroscelerosis. Usually really really laminated appearance with alternate layers of white fibrin and platelets, increased numbers of red cells.
                              1. Outcomes

                                Anmerkungen:

                                • Occlusion Embolism Coronary circulation Cerebral circulation Femoral arteries
                              2. Mural

                                Anmerkungen:

                                • Occurs in heart. Commonly in left ventricle after myocardial infarction due to low flow injured endothelium TNF and IL-12
                              3. Embolism

                                Anmerkungen:

                                • Transportation by the blood of the abnormal material and the point 
                                1. Arterial embolism

                                  Anmerkungen:

                                  • Moves with flow of blood, lodges in vessel fo matching size. Cause distal ischaemia
                                  1. Source

                                    Anmerkungen:

                                    • 80% Heart: From mural thrombus in Left ventricle after MI. or Mural thrombus in LA related to atrial fibrillations. From valvular vegetations. 20% Atherosclerosis
                                    1. Infarction

                                      Anmerkungen:

                                      • Circumscribed area of ischaemic necrosis in an organ or tissue resulting from interference of blood flow.
                                      1. Effects/Outcomes

                                        Anmerkungen:

                                        • Leg: Ischaemia/gangrene Brain: Cerebral infarct Kidney/spleen: Wedge shaped infarct. Gut: Infarct.
                                    Zusammenfassung anzeigen Zusammenfassung ausblenden

                                    ähnlicher Inhalt

                                    Atherosclerosis
                                    Daniel Elandix G
                                    Injurious Agents
                                    Daniel Elandix G
                                    Healing and Repair
                                    Daniel Elandix G
                                    Acute inflammation
                                    Daniel Elandix G
                                    Tuberculosis
                                    Daniel Elandix G
                                    Introduction to the immune system
                                    Daniel Elandix G
                                    Appendicitis
                                    Daniel Elandix G
                                    Concepts and Classification
                                    Daniel Elandix G
                                    Biology of Neoplasia
                                    Daniel Elandix G
                                    Breast Cancer
                                    Daniel Elandix G
                                    Pneumonia
                                    Daniel Elandix G