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General Pathology VDMP832 > Abnormal Hemostasis > Flashcards

Abnormal Hemostasis Flashcards

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
Q

Abnormal Hemostasis:

Hemorrhage

A

the loss of blood from the vessel into extravascular sites

26
Q

Hemorrhage:

Causes

A

Vascular Injury

Platelet Disorders

Coagulation Disorders

27
Q

Causes of Vascular Injury

A
  • Trauma
  • Inflammation
    • infectious
    • non-infectious
  • Secondary invasion
    • inflammatory or neoplasitc
  • Necrosis
    • toxins
    • Infectious agents
  • Endothelial degeneration
    • endotoxin (LPS)
28
Q

Causes of Platelet Disorders

A
  • 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
Q

Causes of Coagulation Disorders

A
  • Inherited deficiency of coagulation factors
  • Acquired coagulation defects
    • decreased production due to liver disease
    • Vitamin K antagonism
    • Increased use
    • Inhibition of coagulation factors
30
Q

Hemorrhage:

Pathogensis

A
  • By rhexis:
    • Active blood loss due to tears or rents in the blood vessel
  • By Diapedesis:
    • Passive blood loss through endothelial gaps
31
Q

Hemorrhage:

Morphology

A
  • Red irregular foci in tissues characterized by extravascular erythrocytes
  • Classification:
    • petechia
    • Ecchymosis
    • Suffusive
32
Q

Hemorrhage:

Morphology:

Petechia

A

pinpoint (1-2mm) hemorrhage usually assocaited with mild injury and diapedesis

33
Q

Hemorrhage:

Morphology:

Eccymosis

A

Medium (2-3cm) hemorrhage assocaited with more severe vascular injury

34
Q

Hemorrhage:

Morphology:

Suffusive (Paint Brush)

A

Large localized hemorrhage

35
Q

Hemorrhage:

Morphology:

Into a body cavity

A

Hemopericardium

Hemothorax

Hemoperitoneum

36
Q

Hematoma

A

Hemorrhage inot tissue or interstitium

An extravascular coagulum of blood

37
Q

Hemorrhage:

Significance

A
  • 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
Q

Abnormal Hemostasis:

Thrombosis

A
  • 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
Q

Thrombosis:

Causes

A
  • 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
Q

Thrombosis:

Alterations in blood vessels

A
  • Endothelial injury
    • trauma
    • Chemical injury
    • Drugs
    • Inflammation
    • Immune reactions
    • Toxins
  • Normal endothelium is anti-thrombotic
    • platelets do not adhere
41
Q

Thrombosis:

Alterations in Blood Vessels:

Endothelial Injury Causes

A
  • Viruses
  • Bacteria
  • Fungi
  • Nematode parasites
  • Immune-mediated vasculitis
  • Endotoxin
  • Vitamin E/selemium
  • DIC
42
Q

Thrombosis:

Alterations in Blood Flow:

Decreased blood flow / stasis

A
  • Blood viscosity increases
  • Endothelium/blood component interactions increase
  • Decreased clearance of activated factors
  • Decreased local tissue oxygenation
43
Q

Thrombosis:

Alterations in blood flow:

Turbulent Blood Flow

A

enhances endothelial/blood component interactions

44
Q

Thrombosis:

Alterations in blood coagulability

A
  • 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
Q

Thrombosis:

Alterations in blood coagulability:

Hypercoagulability causes

A
  • Antithrombin deficiency
  • Hepatic disease
  • Pregnancy
  • Nephrotic syndrome/uremia
  • Anti-phospholipid antibodies
  • Endocrine disease
    • diabetes mellitus, hyperadrenocorticism, hypothyroidism
  • Neoplasia
46
Q

Thrombosis:

Alterations in blood coagulability:

Antithrombin deficiency

A

Causes of deficiency include decreased production due to liver disease, increased loss due to renal disease or enteropathy

Results in a pro-thrombotic state

47
Q

Thrombosis:

Arterial Thrombi

A

These form in arteries in association with rapidly flowing blood

48
Q

Thronbosis:

Venous Thrombi

A

These form in veins in associates with slow moving blood

49
Q

Thrombosis:

Cardiac Thormbi

A

These form in the heart chambers or on the heart valves

50
Q

Arterial Thrombi:

Morphology

A
  • 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
51
Q

Venous Thrombi:

Morphology

A
  • 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
52
Q

Cardiac Thrombi:

Morphology

A
  • 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
53
Q

Thrombus:

Outcomes

A

Lysis

Propogation and obstruction

Embolism

Organization

54
Q

Thrombus:

Lysis

A
  • 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
55
Q

Thrombus:

Progagation and Obstruction

A
  • 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
Q

Thrombus:

Embolism

A
  • 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
57
Q

Thrombus:

Organization

A
  • 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
58
Q

Thrombus:

Organization:

Process

A
  • 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)
59
Q

Thrombus:

Significance

A
  • Most significant result of thrombosis is ischemia and infarction
  • Clinical significance of thrombi depend on their size, location, and type
    *
60
Q

Significance:

Infarction

A

Pulmonary infarction

Renal infarction

General Pathology VDMP832 (26 decks)

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