General Pathology VDMP832 > Abnormal Hemostasis > Flashcards

Abnormal Hemostasis Flashcards

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1
Q

Abnorma Hemostasis

A

Inadequate hemostasis can lead to hemorrhage

Excessive or inappropriate hemostasis can lead to thrombosis

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2
Q

Platelet Diorders:

A
  • Platelet deficiency:
    • decreased production
    • excessive utilization
    • premature destruction
  • Abnormal platelet function (Thrombocytopathy)
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3
Q

Decreased Platelet Numbers

A
  • Adequate numbers of platelets are necessary for successful response to vascular injury
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4
Q

Causes of Thrombocytopenia:

Decreased Production

A
  • Myelophthesis
    • Bone marrow neoplasia myelofibrosis
  • Chemicals:
    • Estrogen, bracken fern, trichothecene mycotoxins
  • Drugs:
    • Chloramphenicol, sulfonamides, phenybutazone
  • Radiation and chemotherapy
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5
Q

Causes of Thrombocytopenia:

Increased consumption

A
  • Endothelial activation:
    • Vasculitis, infectious agents.
  • localized intravascular coagulation
    • vascular neoplasia, hemorrhage, thrombosis
  • Disseminated Intravascular Coagulation:
    • Endotoxemia, shock
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6
Q

Causes of Throbmycytopenia:

Increased Destruction

A
  • Immune mediated:
    • primary
    • Secondary:
      • Infectious agent or chmical
  • Infection:
    • BVD virus, Canine distemper virus, canine parvovirus, ehrlichia sp. FIV, FeLV, EIA,
    • Thrombocytopenia is often associated with endotoxemia
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7
Q

Abnormal Platelet Function

A
  • Most platelet function defects are associated with an inability to adhere or aggregate at a site of injury
  • Other functional defects can affect granule content of the degranulation process
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8
Q

Causes of Thrombocytophathy:

Inherited problems of adhesions

A
  • GpIb deficiency:
    • bernard-soulier syndrome of humans
  • Defective GPIIb and GPIIa
    • glanzmann’s thrombasthenia of humans
    • Has been rarely reported in otterhounds and great pyrenees
  • Von Willebrand factor deficiency
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9
Q

Von Willebrand Disease

A
  • Most common inherited bleeding disorder of dogs
  • Abnormal primary hemostasis due to a functional deficiency of VWF
    • platelets do not efficiently bind to damaged endothelium
  • Signs include mucosal hemorrhage, bruising and prolonged bleeding
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10
Q

Causes of Thrombocytopathy:

Acquired platelet function problems

A
  • Drugs
  • Uremia assocaited with renal failure
  • Increased FDPs
  • Hepatic disease
  • Immune-mediated thrombocytopenia
  • Megakaryocytic neoplasia
  • Infection
    • BVDV and FeLV
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11
Q

Acquired Platelet Dysfunction

A

Antiplatelet drugs:

Aspirin

Irreversible inhibition of the cyclooxygenase pathway of arachidonic acid metabolism in platelets

Thromboxane A2 synthesis is inhibited

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12
Q

Coagulation Disorders

A
  • Inherited deficiency of coagulation factors
  • Acquired coagulation defects
    • decreased production due to liver disease
    • Vitamin K antagonism or deficiency
      • rodenticided, sweet clover poisoning, biliary or bowel disease
    • Increased use
    • Inhibition of coagulation factors
      • heparin, FDPs, antiphospholipid antibody to coagulation factors
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13
Q

Causes of Coagulation Disorders

A
  • Inherited Coagulation Factor deficiencies in animals include:
    • Extrinsic pathway:
      • Factor VII
    • Intrinsic Pathway:
      • Prekallikrein and Factors XII, XI, IX, VIII
    • Common Pathway:
      • Factors X, II, I
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14
Q

Inherited Coagulation Factor Deficiences:

Hemophilia A

A
  • Factor VII deficiency, X-linked recessive
  • Most common inherited coagulopathy in animals
    • reported in dogs, cats, horses, cattle
    • Best documented in dogs (German Shepherd)
  • Considerable vairability in the degree of loss of Factor VII activity:
    • Mild:
      • no spontaneous bleeding and usually maintian normal hemostasis
    • Moderate:
      • Can have serious hemorrhage after trauma, acheiving hemostasis is prolonged
    • Severe:
      • Spontaneous bleeding may occur
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15
Q

Inherited Coagulation Factor Deficiencies:

Intrinsic:

Hemophilia B

A
  • Factor IX deficiency, x-linked recessive
  • Reported in dogs and cats
  • Similar signs to Hemophilia A
  • Most cases Factor IX activity is very low
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16
Q

Inherited Coagulation Factor Deficiencies:

Intrinsic:

Hemophilia A and B

A
  • In these conditions the female is an unaffected carrier
  • The male may or may not be affected
  • When a female carrier is mated to an unaffected male, 50% will get a defective X chromosome.
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17
Q

Acquired Coagulation Disorders

A
  • Decreased production
    • extensive liver disease
    • Vitamin K deficiency
  • Increased Utilization
    • widespread endothelial injury
    • severe trauma or burns
    • Disseminated intravascular Coagulation
  • Inhibition of coagulation factors
    • heparin, FDPs, Antiphospholipid antibody, antibody to coagulation factors
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18
Q

Acquired Coagulation Disorders:

Liver Disease

A
  • Decreased production of both pro- and anti- coagulation factors
  • Bleeding is uncommon unless liver disease is severe or associated with DIC
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19
Q

Acquired Coagulation Disorders:

Vitamin K deficiency

A
  • Antagonists inhibit conversion of oxidized vitamin K to reduced (Active) form
  • These include:
    • moldy sweet clover
    • Rodenticides
    • Sulfaquinoxaline and other drugs
      *
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20
Q

Acquired Coagulation Disorder:

Increased Utilization

A

Widespread endothelial injury

Severe Trauma or burns

Disseminated Intravascular Coagulation

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21
Q

Hemostatic Dyshomeostasis:

Disseminated Intravascular Coagulation

A
  • DIC is a profound disruption of hemostasis
  • Major stimulus is widespread vascular injury
    • can occur as a priamry event
    • Commonly occurs as a termianl event in shock
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22
Q

Disseminated Intravascular Coagulation

A
  • Fundamental change is accelerated or unbalanced coagulation
    • there are elevated levels of both procoagulation and fibrinolytic substances
  • Thrombin plays a central role in DIC
    • activated platelets and coagulation factors
    • activates fibrinolysis
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23
Q

DIC:

Morphology

A

There are subclinical to severe hemorrhage

Shock

Organ failure

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24
Q

DIC:

significance

A

Is a life-threatening and rapidly progressing event

one of the most dramatic examples of dyshomeostasis in animals

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25
Abnormal Hemostasis: Hemorrhage
the loss of blood from the vessel into extravascular sites
26
Hemorrhage: Causes
Vascular Injury Platelet Disorders Coagulation Disorders
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Causes of Vascular Injury
* Trauma * Inflammation * infectious * non-infectious * Secondary invasion * inflammatory or neoplasitc * Necrosis * toxins * Infectious agents * Endothelial degeneration * endotoxin (LPS)
28
Causes of Platelet Disorders
* Platelet deficiency: * decreased production * bone marrow injury * Excessive utilization * widespread injury or DIC * Premature destruction * damage due to viruses, or other infectious agents * Immune-mediated * Abnormal platelet function (Thrombocytopathy)
29
Causes of Coagulation Disorders
* Inherited deficiency of coagulation factors * Acquired coagulation defects * decreased production due to liver disease * Vitamin K antagonism * Increased use * Inhibition of coagulation factors
30
Hemorrhage: Pathogensis
* By rhexis: * Active blood loss due to tears or rents in the blood vessel * By Diapedesis: * Passive blood loss through endothelial gaps
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Hemorrhage: Morphology
* Red irregular foci in tissues characterized by extravascular erythrocytes * Classification: * petechia * Ecchymosis * Suffusive
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Hemorrhage: Morphology: Petechia
pinpoint (1-2mm) hemorrhage usually assocaited with mild injury and diapedesis
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Hemorrhage: Morphology: Eccymosis
Medium (2-3cm) hemorrhage assocaited with more severe vascular injury
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Hemorrhage: Morphology: Suffusive (Paint Brush)
Large localized hemorrhage
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Hemorrhage: Morphology: Into a body cavity
Hemopericardium Hemothorax Hemoperitoneum
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Hematoma
Hemorrhage inot tissue or interstitium An extravascular coagulum of blood
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Hemorrhage: Significance
* Can be insignificant to life-threatening * Factors influencing clinical outcome: * Location * Vital vs. non-vital tissues and organs * Volume: * Loss of large blood volumes can lead to shock * Rate of loss * Slow rates of loss can have some compensation
38
Abnormal Hemostasis: Thrombosis
* The formation of a solid mass of blood components within a blood vessel or the heart * Thrombosis is a reflection of excessive or inappropriate hemostasis
39
Thrombosis: Causes
* Shift in the normal hemostatic balance towards thrombosis * endothelial activation/injury * Platelet activation * Coagulation pathways activated * Stasis * Decreased fibrinolysis * Abnormal Anti-coagulant proteins * “Virchows Triad” * Alterations in blood vessels * Alterations in blood flow * Alterations in blood coagulability
40
Thrombosis: Alterations in blood vessels
* Endothelial injury * trauma * Chemical injury * Drugs * Inflammation * Immune reactions * Toxins * Normal endothelium is anti-thrombotic * platelets do not adhere
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Thrombosis: Alterations in Blood Vessels: Endothelial Injury Causes
* Viruses * Bacteria * Fungi * Nematode parasites * Immune-mediated vasculitis * Endotoxin * Vitamin E/selemium * DIC
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Thrombosis: Alterations in Blood Flow: Decreased blood flow / stasis
* Blood viscosity increases * Endothelium/blood component interactions increase * Decreased clearance of activated factors * Decreased local tissue oxygenation
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Thrombosis: Alterations in blood flow: Turbulent Blood Flow
enhances endothelial/blood component interactions
44
Thrombosis: Alterations in blood coagulability
* Hypercoagulation reflects an increase or decrease in concentrations of activated hemostatic proteins * coagulation factors or coagulation inhibitors * Most commonly occurs due to increased activation or decrease degradation of pro-coagulant factors * Enhanced platelet activity can also contribute
45
Thrombosis: Alterations in blood coagulability: Hypercoagulability causes
* Antithrombin deficiency * Hepatic disease * Pregnancy * Nephrotic syndrome/uremia * Anti-phospholipid antibodies * Endocrine disease * diabetes mellitus, hyperadrenocorticism, hypothyroidism * Neoplasia
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Thrombosis: Alterations in blood coagulability: Antithrombin deficiency
Causes of deficiency include decreased production due to liver disease, increased loss due to renal disease or enteropathy Results in a pro-thrombotic state
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Thrombosis: Arterial Thrombi
These form in arteries in association with rapidly flowing blood
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Thronbosis: Venous Thrombi
These form in veins in associates with slow moving blood
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Thrombosis: Cardiac Thormbi
These form in the heart chambers or on the heart valves
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Arterial Thrombi: Morphology
* Generally pale and firm * Consist of alternating layer of fibrin and platelets * The often have a head (attached to endothelium) and a tail that grows downstream
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Venous Thrombi: Morphology
* These are dark red and gelatinous * They consist of fibrin and platelets intermixed with erythrocytes * Often occlusive form the point of origin * They look similar to a postmortem clot
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Cardiac Thrombi: Morphology
* Mural cardiac thrombi form in the heart chambers * these often mold to the outline of the chamber * Valvular Cardiac thrombi form on the heart valves * these are pale and irregular, and are often associated with infection of the valve
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Thrombus: Outcomes
Lysis Propogation and obstruction Embolism Organization
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Thrombus: Lysis
* thrombus is removed by the dissolution of the fibrin matrix and the platelet plug * plasmin is a major participant in the process * Most common and efficient with new or small thrombi * Large more mature thrombi are not easily lysed
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Thrombus: Progagation and Obstruction
* Thrombus grows until it obstructs the vessel lumen * This is most common with venous thrombi * rapid blood flow past arterial thrombi makes total obstruction more difficult, particularly in larger vessels * Dependent tissue is often deprived of oxygen
56
Thrombus: Embolism
* Occurs when a thrombus or protion of a thrombus breaks loose into the circulation and lodges in another blood vessel * This can occur with arterial, venous, and cardiac thrombi * Embolus can damage and occlude the vessel that it lodges within
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Thrombus: Organization
* This is the process of resolution and healing for large thrombi that can not be lysed * Organization reduces the size of the thrombus and converts it to a fibrous scar
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Thrombus: Organization: Process
* Endothelium grows over the surface of the thrombus * Capillaries grow itno the thrombus at it's point of attachment * Macrophages and fibroblasts enter the site to remove debris and produce collagen * New blood vessels can grow into and through the organizing mass (recanalization)
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Thrombus: Significance
* Most significant result of thrombosis is ischemia and infarction * Clinical significance of thrombi depend on their size, location, and type *
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Significance: Infarction
Pulmonary infarction Renal infarction
General Pathology VDMP832
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