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Flashcards in Chapter 4 Deck (13)
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Pathophysiologic categories of edema

1.) increased hydrostatic pressure
-impaired venous return (CHF, ascites, venous obstruction (thrombous))
-arteriolar dilatation (heat)
2.) Reduced plasma oncotic pressure:
-nephrotic syndrome
-liver cirrhosis
3.)lymphatic obstruction
-inflammatory, neoplastic, postsurgery/xrt
4.) sodium retention
-excess salt intake
-increased renal tubular reabsorption of sodium
5) inflammation


Difference between hyperemia and congestion

Hyperemia: active process; arteriolar dilatation causes increased blood flow with engorgement of vessels with oxygenated blood
Congestion: passive due to reduced outflow of blood frm the tissue (bluish colour because red cell stasis and the accumulation of deoxygenated hemoglobin)


Steps of normal hemostasis

1.) Vasoconstriction (reflex neurogenic mechanisms and secretion of factors such as endothelin)
2.) Exposure of thrombogenic substances on exposed ECM results in platelet adherence and activation; active platelets secrete granules that recruit additional platelets and from a hemostatic plug: Primary hemostasis
3.) TF exposed at the site of injury acts with factor VII to initiate the coagulation cascade and produce thrombin, which cleaves circulating fibrinogen to fibrin and consolidates the platelet plug: Secondary hemostasis
4.) Polymerized fibrin and platelet form the permanent plug; at this point, counterreulgatory mechanisms (tPA) are set in motion to prevent excessive clotting


Anticoagulant effects of endothelium

1.) Antiplatelet: NO and prostacyclin 1 produced by endothelial cells empeded platelet adhesion
2.) Anticoagulant effects via heparin-like molecules, thrombomodulin and tissue factor pathway inhibitor
3.) Fibrinolytic effects: endothelial cells synthesize tPA that cleaves plasminogen to make plasmin which cleaves fibrin to degrade thrombi


Procoagulant effects of endothelium

1) Platelet effects: endothelial injury allows platelets to contact ECM and interact with vWF (a product of endothelial cells)
2.) Procoagulant effects: endothelium synthesizes tissue factor in response to cytokines or bacterial endotoxin
3.) Antifibrinolytic effects: endothelial cells secrete inhibitors of plasminogen activator (PAIs)


Effects of stasis

-promote endothelial activation to produce procoagulants
-disrupt laminar flow bringing platelets in contact with endothelium
-prevent dilution and washout of clotting factors by lack of fresh flowing blood and lack of inflowing clotting inhibitors


Clinical examples of causes of stasis

-atherosclerotic plaques (expose endothelial ECM and disrupt laminar flow)
-dilated RV due to valve disease
-acute MI with wall dysfunction
-abnormal RBCs as in sickle cell disease with vascular occlusions
-hyperviscosity (e.g. in polycythemia rubra vera)


Acquired causes of hypercoagulability

-atrial fibrillation
-tissue injury
-cancer (release of procoagulant tumor products)
-prosthetic cardiac valves
-HIT (antibodies that recognize complexes of heparin and platelet factor 4 on platelets that when bound, cause activation, aggregation and consumption of platelets)
-APLA syndrome (binding of antibodies to epitopes on plasma proteins such as prothrombin; may be secondary such as associated with lupus, or primary, which may be associated with drugs)
-Lower risk: cardiomyopathy, OCP use, pregnancy, sickle cell anemia, nephrotic syndrome, smoking


Effects of PEs

-sudden death, right heart failure (cor pulmonale) or cardiovascular collapse when the emboli obstruct >60% of pulmonary circulation
-obstruction of medium-size arteries with vascular rupture can result in pulmonary hemorrhage (but not infarction due to lung's dual blood supply)
-multiple emboli over time may result in pulmonary hypertension and right heart failure


Features of fat embolism syndrome

-pulmonary insufficiency
-neurologic symptoms
-fatal in up to 15% of cases


Define infarct

An area of ischemic necrosis caused by occlusion of either the arterial supply or the venous drainage


Red infarcts

-infarcts with venous occlusions, in loose tissues where blood can collect in the infarct, in tissues with dual circulation or when flow is reestablished


White infarcts

-arterial occlusions in solid organs where tissue density limits the seepage of blood into the necrotic area