General Pathology > Abnormal Hemostasis > Flashcards

Abnormal Hemostasis Flashcards

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1
Q

Abnormal Hemostasis

A
  • Hemostasis is a complex balance that once distrubed, can lead to various problems
  • Inadequate hemostasis can lead to hemorrhage
  • Excessive or inappropriate hemostasis can lead to thrombosis
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2
Q

Platelet disorders

A
  • Platelet deficiency (Thrombocytopenia)
    • Decreased production
      • Bone marrow injury or susppression
    • Excessive utilization
      • Widespread injury or Disseminated Intravascular Coagulation (DIC)
    • Premature destruction
      • Damage due to viruses or other infectious agents
      • Immune-mediated
  • Abnormal platelet function (Thromboctopathy)
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3
Q

Decreased Platelet numbers

A
  • Adequate numbers of plateletsare necessary for successful response to vascular injury
    • For mild, localized injury, and animals may be slightly thrombocytopenic and still respond adequtely
    • For sever, widespread injury, even nd animal that originally had adequate platelet numbers may rapidly deplete the number necesary for succesful response
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4
Q

Cause of Thrombocytopenia

A
  • Decreased production:
    • Myelphthesis
      • Bone marrow neoplasia, myelofibbrosis
    • Chemicals
      • Estrogen, bracken fern, trichothecene mycotoxins
    • Drugs
      • chloramphenicol, sulfonamides, phenylbutazone
    • Radiation and chemical durgs
  • Increased destruction:
    • Immune medaiated - Primary
      • sefonday- Infectious aget or chemical drug-inuduced (various antibodies and anti0infalmmaorties
    • Infection -
      • BVD, virus, canine distemper birus, canin parvovirus, Ehrlichia spl FIV, FELV, EIA, ansaplasma sp. histoplasma capsulateum, Babesia sp..
      • Thrombocytopenia is often associated with endotoxemia
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5
Q

Causes of thrombocytopenia

A
  • Increased Consumption
    • Endothelial activation
      • Vasculitis: infectiou agents (RMSF, canine herpes, canine adenovirs, Dirofilaria)
      • Endocarditis
    • Localized intravascular coagulation
      • Vascular neoplasia, hemorrhage, thrombosis
    • Disseminated Intravascular Coagulation
      • Endotoxemia, Shock
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6
Q

Abnormal Platelet function

A
  • Most platelet function defects are associated with an inability to adhere or aggregate at a sigte of injury
  • Other functional efects can afffect granule content or the degrnulation process
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7
Q

Causes of Thrombocytopathy

A
  • Inherited problems of adhesion and/or
  • Aggregation include;
    • GpIbdeficiency
      • Bernard-Soulier syndrome of humans
      • rarely reported in Otterhounds d Gread Pyreneese dogs and horses
        • CA+2 binding domain of GPIIb is defective
    • Von WIllebrand Factor deficiency
  • Acquired platelet function problems include:
    • Drugs: anti-inflammatories, anesthetics and antibiotics
    • Uremia associated with renal failure
    • Increased FDPs
    • Hepatic disease
    • Immune-mediated thrombocytopeni
    • Megakaryocytic neoplasia
    • Infection
      • BVDV and FeLV
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8
Q

Von Willebrand Disease

A
  • Most common inherited bleeding disorder of dogs
    • Gorgi, Doberman Pinsher, GSD, German Shrothaired and Wirehaired pointers, Golden retriever, Shetland sheepdog, and stradard pooddel are commonl affected
  • Abnormal primary hemostatis du to functional deficiency of vWF
    • Pltelets do not efficiently bind to damage endothelium
  • Signs include mucosal hemmorhge, bruising and prolonged bleeding
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9
Q

Aquired Platelet Dysfunction

A
  • Antiplatlet drugs
    • Aspirin
      • Irreversible inhibition of the cyclooxygenase pathway of arachidonic acid metabolism in platelets
      • Thromboxane A2 synthesis is inhibited
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10
Q

Coagulation Disorders

A
  • Inherited deficiency of coagulation factors
  • Acquired coagulation defects
    • Decreased production due to liver diease
    • Vitamin K antagonism or deficiency
      • Rodentifcides, sweet clover poisoning, biliary or bowel diease
    • Increased Use (Consumption: DIC)
    • Inhibition of coagulation factors
      • Heparin, FDPs, antiphospholipid antibody, antibody to coagulation factors
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11
Q

Causes of Coagulation Disorders

A
  • Inhrited Coagulation Factor Deficiencies in andimals include:
    • Extrinsic pathway (Factor VII)
    • Intrinsic Pathway
      • Prekallikrein
      • Factors XII, XI, IX, VIII
    • Commno Pathway
      • Factors X, II, I
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12
Q

Hemophilia A

A
  • Inherited Coagulation Factor Deficiency
  • Factor VIII deficieny, X-linked recessive
  • Most common inherited coagulopathy in animals
    • Reported in dogs, cats, horses, cattle
    • Best documented in dogs
  • Considerable variability in the degree of loss of Factor VIII activity
    • Mild (>5% activity): no spontaneous bleeding and usually maintain normal hemostasis
    • Moderate (2-5% activity): Can have serious hemorrhage after trauma, achieving hemostasis is prolonged
    • Severe (<2% activity): Spontaneous bleeding may occur
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13
Q

Hemophilia B

“Christmas Disease”

A
  • Intrinsic Inherited Coagulation Factor Deficiency
  • Factor IX deficiency, X-linked recessive
  • Reported in DOgs and cats
  • Similar signs to Hemophilia A
  • In most cases, Factor IX activity is very low
    • It lacks the variability in activity associated with Factr VIII in hemophilia A
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14
Q

X-linked Inherited Coagulation Factor Deficiencies

A
  • In these conditions the female is an unaffected carrier
  • Males may or may not be affected
  • When a female carrier is crossed with an unaffected male:
    • 50% of offspring will get defective X
      • 50% of females will be carriers
      • 50% of males will be affected
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15
Q

Severity of Inherited Coagulation Factor Deficiencies

A
  • Many deficiencies are autosomal recessive (incomplete penetrance)
  • Severity varies based on inheritance pattern:
    • Homozygous animals typically have 5-10% enzyme activiy
    • Heterozygous animals typically have 40-50% enzyme activity
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16
Q

Aquired Coagulation Disorders

A
  • Decreased Production
    • Extensive liver disease
    • Vitamin K deficiency
  • Increased utilization
    • Widespread endothelial injury
    • Severe trauma or burns
    • Disseminated Intravasculatr Coagulation
  • Inhibition of coagulation factors
    • Heparin, FDPs, antiphospholipid antibody, antibody to coagulation factors
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17
Q

How do Acquired Coagulation DIsorders affect the Liver

A
  • Decreased production fo both pro- and anti- coagulant factors
  • Bleeding is uncommon unless liver disease is sever or associated with DIC
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18
Q

Vitamin K antagonist - Acquired Coagulation Disorders

A
  • VitK antagonists inhibit conversion of oxidized vitamin K to reduced (active) form
    • reduced vit K is required to interact with Vit K-dependent carboxylase
  • Antagonists include:
    • Moldy sweet clover
      • bishydroxycoumarin
    • Rodenticides
      • Coumarins (warfarin) or Indanediones (bromadiolone)
    • Sulfaquinoxaline and other drugs
  • Vit K deficiency can also be induced by :
    • Anorexia
    • Enteric antimicrobials
    • Decreased fat digestion or absorption
      • Malabsorption
      • Cholestasis
      • Pancreatic insufficiency
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19
Q

Increased Utilization

A
  • Widespread endothelial injury
  • Severe trauma or burns
  • Disseminated Intravascular Coagulation
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20
Q

Disseminated Intravascular Coagulation

A
  • a profound disruption of hemostais
  • Major stimulu is widespread (systemic) vascular injury
    • can occur as a primary event
      • infectious agents or toxins that cause widespread vscular injury
    • Commonly occurs as a terminal event in shock
  • Causes:
    • Necrosis
    • Heat stroke
    • Neoplasia
    • Endotoxemia/spticemia
    • Pancreatitis
    • Hepatic disease
    • Venoms
    • trauma
    • Burns
  • Fundamental change is accelerated o unbalaned cagulation
    • elevated levels of both procoagulant and fibrinolytic substances
  • Thrombin play a central role in DIC
    • activates platelets and coagulation factors
    • Activates fibrinolysis
  • Widespread nature of the response results in rapid consumption of hemostatic proteins
    • consumption coagulopathy
  • Widespread, uncontrolled hemorrhage occurs in later stages
    • There are inadequate platelet or coagulation factors available to seal up the injured areas
    • There are increased levels of FDPs and other degradation products
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21
Q

DIC Morphology

A
  • There are subclinical to severe hemorrhages
    • Often large, widespread hemorrhages
  • Shock
  • Organ failure
    • due to thromboembolism or hemorrhage
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22
Q

DIC Significance

A
  • DIC is life-threatening and rapidly progressing event
    • one of the most dramatic examples of dyshomeostasis in animals
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23
Q

Hemorrhage

A
  • Loss of blood from the vessel into extravascular sites
  • Causes:
    • Vascular injury
    • Platelet disorders
    • Coagulation disorders
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24
Q

Causes of Vascular Injury

Study These Flashcards
A
  • Trauma
  • Inflammation (Vasculitis)
    • Infectious (Bacteria, viruses)
    • Non-infectious (Immune-mediated)
  • Secondary invasion
    • Inflammatory or neoplastic
  • Necrosis
    • Toxins
    • Infectious agents (viruses)
  • Endthelial degeneration
    • Endotoxin
25
Causes of Platelet disorders
* Platelet deficency (thrombocytopenia) * Decreaed production * bone marrow injury or supperession * Excessive utlization * Widespread injury or DIC * Premature destruction * Damage due to viruses or other infectious agents * Immune-mediated * Abnormal Platelet function (Thrombocytopathy)
26
Causes of Coagulation Disorders
* Inherited deficiency of coagulation factors * Acquired coagulation defects * Decreased production due to liver disease * Vitamin K antagonism or deficiency * Rodenticides, sweet clover poisoning, biliary or bowel disease * Increased use (consumption; DIC) * Inhibition of coagulation factors * Heparin, FDPs, antiphospholigpid antibody, antibody to coagulation factors
27
What is the Pahogenesis of hemorrhages?
* By rhexis: * Active blood loss due to tears of rents in the blood vessel * By diapedesis: * Passive blood loss through endothelial gaps
28
What is the Morphology of Hemorrages?
* Red irregular foci in tissues characterized by extravascular erythrocytes
29
How are hemorrhages classified?
* Petechia * Ecchymosis * Suffusive
30
What is the morphology of petechia hemorrhages
* Pinpoint (1-2 mm) hemorrhage usually associeated with mild injury and diapedesis
31
What is the morphology of Eccymsis hemorrhage?
* Medium (2-3cm) hemorrhage associated with more sever vascular injury
32
What is the morphology of suffusive hemorrhage?
* Paint brush * large localized hemorrhage
33
How do you name hemorrhages into body cavities?
Based on cavity * Hemopericardium * Hemothorax * Hemoperitoneum
34
What is a hematoma?
* hemorrhage into tissue or interstitium * extravascular coagulum of blood
35
What is the significance of hemorrhage?
* Can be insignificant to lig-threatening
36
What Factors influence clinical outcomes of hemorrhages?
* Location: * vital vs. non-vital tissues or organs * Volume: * Loss of large blood volumes can lead to shock * Rate of Loss: * Slow rates of loss can have some compensation
37
What is a Thrombosis?
* The formation of **a solid mass of blood componentss** within a blood vessel or the heart * A reflection of excessive or inppropriate hemostasis
38
What causes Thrombosis?
* A shift in normal hemostatic balance towards thrombosis * Endothelial activation/injury * Platelet activation * Coagulation pathways activated * Stasis * Decreased fibrinolysis * Abnormal anti-coagulant proteins
39
What is Virchows Triad?
* Alterations in blood vessels * Alterations in blood flow * Alterations in blood coagulability Cause of Thrombosis
40
What are some alterations in blood vessels that lead to Thrombosis?
* Endothelial injury * Trauma * Chemical injury * Drugs * inflammatino * Immune reactions * Toxins
41
Why do thrombi not form normally in blood vessels?
* Normal endothelium is anti-thrombotic * platelets do not dhere and coagulation is not activated
42
What causes endothelial injury?
* Viruses (Ex: Canine adenovirus-1) * Bacteria (Ex: Salmonell) * Fungi (Ex: Aspergillus) * Nematode Parasites (Ex: Dirofilaria) * Immune-mediated vasculitis * Endotoxin * Vitamin E/Selenium deficiency * DIC
43
What changes in blood flow can lead to the formation of Thrombi?
* Decreased blood flow or stasis * inceased blood viscosity * increased endothelium/blood component interactions * Decreased clearance of activated factors * Decreased local tissue oxygenation * Turbulent blood flow * Enhanves endothelial/blood component interactions
44
What can cause altered blood flow?
* Gastrointestinal displacement * gastric or intestinal dilation and volvulus * Cardiac disease * Aneurysm * Strongylus vulgaris * Hypovolemia * shock, diarrhea
45
How does alteration in bood cogulability lead to formation of thrombi?
* Hypercoagulability reflects an increase or decrease in concentrations of activaed hemostatic proteins * Coagulatino factors or coagulation inhibitors * This most commonly occurs due to increased activation or decreased degradation of pro-cogulant factors * Enhanved platelet activity can also contribure
46
What can cause Hypercogulability?
* Antithrombin deficiency * Hepatic disease * Pregnancy * Nephrotic syndrome/uremia * Anti-phospholipid antibodies * Endocrine disease * Diabetes mellitus, hyperadrenocorticism, hypothyroidism * Neoplasia
47
How does Antithrombin deficieny cause alteration in blood coagulability?
* Results in a pro-thrombotic state * **Decreased inactivation of activated factors** * Causes of dificiency include decreased production due to liver disease, increased loss due to liver disease, increased loss due to renal disease or enteropathy (protein-losing nephropathy or enteropathy)
48
What are the categories of Thombi?
* Arterial Thrombi * Form in arteries in association with rapidly flowing blood * Venour Thrombi * Form in veins in association with slow moving blood * Cardiac Thrombi * Form in the hear chambers or on the heart valves
49
What is the morphology of Arterial Thrombi
* Generally pale and firm * Consist of alternating layers of fibrin and platelts * RBCs are washed away due to rapid blood flow * Ofent have a head (attached to endothelium) and a tail that gros downstream
50
What is the morphology of Venous Thrombi?
* Dark red, gelatinous * Consist of fibrin and platelets intermixed with erythrocytes * Often occclusiveand grow upstream from the point of origin * Look similar to a postmortem clot
51
What is the morphology of Cardiac Thrombi?
* Mural cardiac thrombi form in the heat chambers * Often mold to the outline of the chamber * Valvular cardiac thrombi from on teh heart valves * Pale and irregular * Often associated with infction of the valve
52
What are the outcomes of Thrombi?
* Lysis * propogation and Obstruction * Embolism * organization
53
What happens when a thrombus is lysed?
* The thrombus is removed by the dissolution of the fibrin matrix (fibrinolysis) * Plasmin is a major participantin the process * This is most common and efficient with new or small thrombi * Large more mature thrombi are not easily lysed
54
What happens during propagation ad obstruction with a thrombus?
* The Thrombus grows until ist obstructs teh vessel lumen * Most common with Venous thrombi * rapid blood flow past arterial thrombi makes total obstruction more difficult, particularly in larger vessels * Dependent tissue is often depreived of oxygen
55
What is an Embolism?
* Embolism occurs when a thrombus or portion of a thrombus breaks loose into the circulation and lodges into another blood vessel * This can occur with arterial, venous, and cardiac thrombi * The embolus can damage and occlude the vessel that it lodges within
56
What is Thrombus organization?
* The process of resolution and healing for large thrombi that cn not be lysed * Organization reduces the size of the thrombus and converts it to a fibrous scar
57
Describe the process of Thrombus Organization
1. Endothelium grows over teh surface of the thrombus 2. Capillaries grow into the thrombus at its point of attachment 3. Macrophages and gicroblasts enter the site to remove debris and produce collagen 4. New blood vessels can grow into and through the organizing mass (recanalization)
58
What is the significance of a thrombus?
* The most significant result of a thrombosis is ischemia and infarction * Thrombi are the most common cause of infarction * Clincal significance of thrombi depend on their size, location, and type * Large thrombi tend to be occlusive and more serious * Thrombi in tissues with poor collateral circulation are more serious * Venous thrombi tend to be occlusive
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