Lecture 15: Cardiovascular Disease II Flashcards
Types of hemodynamic disturbances
- Edema
- Hyperemia
- Hemorrhage
- Thrombosis
- Embolism
- Infarction
- Shock
Edema
Increased fluid in interstitial tissue spaces; effusion = fluid collection in body cavities
Anasarca
Severe general edema w/ subQ tissue swelling
Transudate vs exudate
Transudate = fluid leaving vessels due to pressure changes
Exudate = fluid leaving vessels due to inflam. processes (cell/protein content)
Hyperemia
Active process secondary to arteriole dilation; red tissue color
- Increased inflow
Congestion
Passive process due to slow moving blood; cyanosis
- Impaired outflow; chronic leads to chronic hypoxia, scarring
Pulmonary congestion phases
- Acute:
- Cap. engorgement
- Septal edema
- Intra-alveolar hemorrhage - Chronic:
- Alveolar septal fibrosis
- Hemosiderin-laden mφ’s (heart failure cells)
Hepatic congestion phases
- Acute:
- Central vein/sinusoid distension
- Central hepatocyte dropout (necrosis) - Chronic:
- Pressure atrophy
- Centrilobular necrosis
- Nutmeg liver
- Fibrosis/cirrhosis
Hemorrhage
Blood outside vessel;
- Hematoma: blood accumul. w/in tissue
- Bruises: skin, mucosal surfaces
Effects of different types of hemorrhage
Acute: shock
Chronic: anemia
Loss w/in closed space: mass effects
Types of bruises
- Petechiae
- Ecchymoses
- Purpura
Petechiae
Minute (1-2 mm) hemorrhages into skin, mucous membranes, serosal surfaces
Assoc. w/ local increased intravasc. P, thrombocytopenia, platelet defect., clotting factor defect.
Ecchymoses
Larger (1-2 cm) subQ hematomas
Enzymatic conversion of RBCs to hemosiderin by mφ’s produces color changes
Purpura
Slightly larger hemorrhages (3-5 mm); same disorders as petechiae + trauma, vasculitis, vascular fragility
Normal vs pathologic hemostasis
Normal: Tight regulation maintains fluid, clot-free blood w/ rapid local plug formation at vascular injury sites
Path.: thrombosis
Components of normal hemostasis
- Vascular wall
- Platelets
- Clotting cascade
Anti-thrombotic properties of endothelial cells
- Anti-platelet (physical barrier, NO, prostacyclin)
- Anti-coagulant (heparin-like, thrombomodulin, tissue factor pathway inhib.)
- Fibrinolytic effects (tissue tPA)
Events at site of vascular injury
- Vasoconstriction
- Primary hemostasis
- Secondary hemostasis
- Thrombosis (coag.)
- Anti-thrombotic events (fibrinolysis)
Formation of primary hemostatic plug
- Platelet adhesion
- Granule release
- Platelet aggregation
Pro-thrombotic clotting mediators
- Thrombin (cleaves fibrinogen)
- Plasminogen activator inhibitors
- Tissue factor (clotting cascade activation)
- von Willebrand’s factor (platelet adhesion)
Fibrinolytic proteins
- Plasmin (fibrinolysis)
- Plasminogen
- Plasminogen activators
Virchow’s Triad of thrombosis
- Endothelial injury
- Hypercoagulability
- Abnormal blood flow
Pathogenesis of thrombus formation
- Endothelial cell injury
- Abnormal blood flow
- Hypercoagulable state (primary genetic, secondary acquired)
Primary (inherited) hypercoagulable states
- Factor V Leiden mutation
- Prothrombin mutation
- Antithrombin III deficiency
- Protein C deficiency
- Protein S deficiency
Secondary (acquired) hypercoagulable states
- Immobility/bedrest
- MI
- A-Fib
- Tissue damage (surgery, burns)
- Cancer
- Prosthetic valves
etc.
Arterial thrombi
Arise at site of injury, w/ Lines of Zahn
- Pale
- Retrograde propagation
- Usually results in infarction
- Coronary, cerebral, femoral arteries; atherosclerotic plaques
Venous thrombi
Arise at sites of stasis (lower extremity veins), less firmly attached
- Red/stasis
- Almost always occlusive
- Anterograde propagation
Superficial venous thrombosis
- Local pain/swelling
- Varicose veins, eczema, ulcers
- Rarely embolize
Deep vein thrombosis
- 50% asymptom. due to collateral vessels
- Thromboembolism
Fates of thrombi
- Propagate
- Embolize
- Dissolution
- Organize + recanalize
Embolism
Detached intravasc. solid/liquid/gas mass carried by blood to distant site (99% dislodged thrombi)
- In systemic circ. typically result in end organ infarct
