Chapter 4

Question 1

Pathophysiologic categories of edema

Answer 1

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

Question 2

Difference between hyperemia and congestion

Answer 2

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)

Question 3

Steps of normal hemostasis

Answer 3

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

Question 4

Anticoagulant effects of endothelium

Answer 4

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

Question 5

Procoagulant effects of endothelium

Answer 5

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)

Question 6

Effects of stasis

Answer 6

• 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

Question 7

Clinical examples of causes of stasis

Answer 7

• atherosclerotic plaques (expose endothelial ECM and disrupt laminar flow)
• aneurysms
• 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)

Question 8

Acquired causes of hypercoagulability

Answer 8

• immobilization
• MI
• atrial fibrillation
• tissue injury
• cancer (release of procoagulant tumor products)
• prosthetic cardiac valves
• DIC
• 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

Question 9

Effects of PEs

Answer 9

• 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

Question 10

Features of fat embolism syndrome

Answer 10

• pulmonary insufficiency
• neurologic symptoms
• anemia
• thrmbocytopenia
• fatal in up to 15% of cases

Question 11

Define infarct

Answer 11

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

Question 12

Red infarcts

Answer 12

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

Question 13

White infarcts

Answer 13

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