3. Hemorrhage

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3. Hemorrhage

• - Is extravasations of blood from vessels into
  the extravascular space
• - Rupture of a large artery or vein results in
  severe hemorrhage, and is almost always due to
  vascular injury, including

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• a. Trauma,
• b. Atherosclerosis, or
• C. Inflammatory or neoplastic erosion of the
  vessel wall

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• Hemorrhage can be external or Can be confined
  within a tissue referred to as hematoma
• - Hematoma can be relatively insignificant called
  bruise or may lead to death such as
  retroperitoneal hematoma

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• Petechiae are (1- to 2-mm) hemorrhages into skin
  or, mucous membranes, and are typically
  associated with
• a. locally increased intravascular pressure,
• b. low platelet counts (thrombocytopenia),
• c. Defective platelet function
• c. clotting factor deficiencies

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• Purpura
• - (3- to 5-mm) hemorrhages
• - And can be associated with many of the same
  disorders that cause petechiae
• - In addition, purpura can occur with trauma,
  vascular inflammation (vasculitis),

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• Ecchymoses
• - Are (1- to 2-cm) subcutaneous hemorrhages
• - Erythrocytes in these local hemorrhages are
  phagocytosed and degraded by macrophages
• - The hemoglobin (red-blue )color is
  enzymatically converted into bilirubin
  (blue-green )color and eventually into
  hemosiderin (golden- brown)

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• Large accumulations of blood in one or another
  of the body cavities are called hemothorax,
  hemopericardium, hemoperitoneum, or hemarthrosis
  (in joints).
• Patients with extensive hemorrhages
  occasionally develop jaundice from the massive
  breakdown of red blood cells and systemic
  increases in bilirubin

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• The clinical significance of haemorrhage depends
  on the volume , rate of blood loss and site of
  hemorrhage.
• 1. Rapid removal of as much as 20 of the blood
  volume or slow losses of even larger amounts may
  have little impact in healthy adults
• - Greater losses, however, can cause hemorrhagic
  (hypovolemic) shock .

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• 2. The site of hemorrhage is also important
  bleeding that would be not significant in the
  subcutaneous tissues may cause death if located
  in the brain
• 3.Chronic or recurrent external blood loss (e.g.,
  a peptic ulcer or menstrual bleeding) causes a
  net loss of iron, frequently culminating in an
  iron deficiency anemia

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4. THROMBOSIS

• Pathogenesis
• Virchow Triad
• 1. Endothelial Injury
• 2. Stasis
• 3. Blood Hypercoagulability

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• 1. Endothelial injury
• - This is the dominant influence since
  endothelial loss by itself can lead to thrombosis
• - It is particularly important for thrombus
  formation in the heart or in the arterial
  circulation

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• Causes
• 1. Valvulitis
• 2. Myocardial infarction
• 3. Ulcerated plaques of atherosclerosis
• 4. Traumatic or inflammatory conditions

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• 5. Endotoxins
• 6. Hypercholesterolemia
• 7. Radiation
• 8. Smoking
• 9. High blood pressure

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• - It is important to note that endothelium need
  not to be denuded or physically disrupted to
  contribute to the development of thrombosis
• - Any disturbance in the dynamic balance of
  prothrombotic and antithrombotic properties of
  endothelium can influence local clotting events

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• - Thus dysfunctional endothelium
• a. May elaborate greater amounts of procoagulant
  factors such as platelet adhesion molecules, or
  tissue factor
• b,. Or synthesize fewer anti-coagulant effectors
  such as thrombomodulin or PGI2

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• - Endothelial dysfunction without endothelial
  loss occurs due to
• 1. Hypertension
• 2. Bacterial endotoxins
• 3. Hypercholesterolemia
• 4. Products absorbed from cigarette smoke

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• 2.Alteration in normal blood flow (turbulence)
• - Turbulence contributes to arterial and cardiac
  thrombosis by
• a. Causing endothelial dysfunction
• b. Local pockets of stasis

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• - Stasis is a major factor in venous thrombi
• - Normal Blood flow is laminas

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• Causes of Stasis
• 1. Aneurysms
• 2. Acute Myocardial infarction (MI ) (
  Noncontractile fibers)
• 3. Remote myocardial infarction may cause cardiac
  aneurysms resulting in stasis
• 3. Mitral valve stenosis (atrial dilation)
• 5. Hyperviscosity syndrome (Polycythemia and
  Sickle Cell anemia

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• 3. Hypercoagulability
• - Alteration of the coagulation pathway
• - Generally contributes less frequently to
  thrombotic states
• A. Primary (Genetic)
• 1. Factor V mutation ( Leiden mutation)
• - The mutation results in a factor Va that cannot
  be cleaved and inactivated by protein C

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• 2. Prothrombin mutation
• - A type of mutation in prothrombin results in
  increased transcription of prothrombin and causes
  threefold increased risk of venous thrombi
• 3. Antithrombin 3 Deficiency
• 4. Protein C deficiency
• 5. Protein S deficiency

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• Secondary ( Acquired)
• - Pathogenesis is multifactorial and more
  complicated
• A. High Risk for thrombosis
• 1- Prolonged bed rest or Immobilization
• 2- Myocardial infarction complicated by cardiac
  failure
• 3- Tissue damage (surgery, fracture, burns)
• 4- Cancer Release of procagulant tumor
• products.

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• 5. Lupus anticoagulant
• Antiphospholipid antibody syndrome
• - Characterized by
• 1.Recurrent thrombosis
• 2. Recurrent abortions
• 3. Cardiac valve vegetations
• 4. Thrombocytopenia

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• - Associated with autoantibodies directed against
  anionic phospholipids (cardiolipin )
• - In vivo these antibodies induce
  hypercagulability by inducing direct platelet
  activation or interference with production of
  PGI2 from endothelium

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• Primary antiphospholipid antibody syndrome----no
  associated autoimmune disease
• Secondary antiphospholipid antibody
  syndrome---patients have autoimmune diseases such
  as systemic lupus erythematosis

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• B. Low Risk for thrombosis
• 1.Hyperestrogenic states such as pregnancy and
• Oral contraceptive pills that cause Increase
  Synthesis of coagulation factors) and decreases
  synthesis of Decrease synthesis of antithrombin
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• 2.Aging Increase platelets aggregation and
  Decrease PGI 2 release by endothelium.