Coagulation Part 2: Disorders of Coagulation Flashcards

1
Q

describe abnormal morphology of platelets

A
  1. giant platelets or shift platelets
    -larger than RBCs
    -will function normally
    -suggests accelerated thrombopoiesis (platelet regeneration)
    -MPV generally increased
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2
Q

describe thrombocytopenia

A

4 causes: SPUD
Sequestration: trapping of platelets within the spleen, usually causes a mild, transient decrease in platelet counts; due to splenomegaly, splenic congestion, splenic neoplasia

Production;
-decreased production:
–bone marrow diseases; will see other cytopenias; due to aplastic anemia, toxins, and other causes
–infectious diseases: ehrlichia and other rickettsial organisms; viral organisms (FeLV/FIV, parvovirus)
–macrothrombocytopenia (CKCS): nonpathogenesis: idiopathic condition in Cavalier King Charles Spaniels due to both abnormal platelet morphology and decreased platelet production; will have fewer, larger platelets; decreased platelet count with increased MPV, normal plateletcrit; platelets normal in function

Utilization: increased
-indicates increased platelet consumption due to DIC, vasculitis, endocarditis, SEVERE acute blood loss from hemorrhage

Destruction:
-Immune-mediated thrombocytopenia: can be primary or secondary; will see marked thrombocytopenia with normal coagulation testing
-primary: autoantibodies targeting platelets and megakaryocites; breed predispositions
secondary: antibody production triggered by an inciting cause; neoplasia, infectious disease, drugs, vaccines; RULE out all secondary causes before diagnose primary

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3
Q

describe thrombocytosis

A
  1. commonly seen but not often clinically significant but can predispose to thrombosis
  2. divided int primary and secondary (reactive)
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4
Q

describe primary thrombocytosis

A
  1. very rare; associated with a persistent, extreme thrombocytosis
  2. due to a neoplastic cause: essential thrombocytopenia, acute megakaryoblastic leukemia, chronic myoproliferative diseases
  3. patients may have an increased risk of thrombosis or hemorrhage, depending on platelet function
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5
Q

describe reactive (secondary) thrombocytosis

A

several causes:
1. increased procudtion: due to inflammation, recovery from recent thrombocytopenia, chemotherapeutic drugs, iron deficiency
2. redistributive or physiologic: epinephrine mediated or exercise = splenic contraction and transient thrombocytosis
3. decreased removal: recent splenectomy, seen post-op
4. excess cortisol: endogenous (Cuhsings) or exogenous (glucocorticoud admin)

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6
Q

describe abnormal platelet function

A

thrombopathy or thrombocytopathy;

can be inherited or acquired; associated with
1. adherence or aggregation
2. surface membrane receptors
3. abilit to synthesice and release products

platelet count normally WRI or increased!

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7
Q

what are causes of congenital platelet dysfunction?

A
  1. vin willebrand disease: most common hemostatic disorder in dogs (esp dobermans, scotties, shelties, rare in others)
    -a deficinecy or abnormality of vWF due to either
    –quantitative or qualitative defect
    –acquired vWD is uncommon in vet med
  2. clinical signs of vWD:
    common: prolonged bleeding from wounds and mucosal hemorrhage
  3. diagnosis of vWD:
    -definitive requires assessment of vWF concentration and/or function
    -use vWF antigen concentration; ELIA method, eletrophoresis, functional assays, genetic assays
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8
Q

what is a cause of acquired platelet dysfunction?

A

hyporesponsive platelets

due to:
1. drugs: NSAIDs (cox inhibitors), calcium channel blockers
2. liver or renal failure
3. marked elevation in globulins
4 infectious diseases
5. DIC

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9
Q

what are the 2 disorders of the extrinsic pathway?

A
  1. inherited factor 7 deficinecy or inhibiton: seen in beagles, mild idsease associated with bruising
  2. acquired factor 7 deficiency or inhibition: associated with early vitamin K deficiency or inhibition, since factor 7 has the shortest half life it will be the first to go; only PT will be prolonged
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10
Q

give disorders of the intrinsice pathwya1

A
  1. hereditary factor 12 deficiency/Hageman’s disease: prolonged ACT or PTT with no clinical bleeding; more common in cats
  2. hereditary factor 11 deficiency/Hemophilia C: mildly prrlonged bleeding seen after surgery; seen in dogs and holstein cattle
  3. hereditary factor 9 deficiency/Hemophilia B: X chromosome linked = more common in males; affected males have variable clinical signs and spontaneous internal hemorrhage can occur; affected females are usually carriers; seen in dogs and cats
  4. hereditary factor 8 deficiency/hemophilia A: most common inherited coagulation factor disorder!; X chromosome linked = more common in males; affected males and females like hemophilia B, but seen in dogs, cats, SHEEP, CATTLE, HORSES
  5. vitamin K antagonism or deficiency: factors 2. 7, 9, 10:
    -often affects multiple pathways: both PT and PTT prolonged, but will see PT prolonged first bc factor 7 has the shortest half life
    -antagonism due to rodenticides, moldy sweet clover
    -deficiency due to liver or GI disease
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11
Q

describe common pathway disorders

A
  1. cause prolonged PT and PTT
  2. hereditary is rare but can see
    -factor 10 deficiency in dogs and cats or
    -fibrinogen deficiency in goats and dogs
  3. acquried is usually associated with multi-pathway disorders
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12
Q

describe multple pathway disorders

A

1, vitamin K antagonism or deficiency (2, 7, 9, 10)
2. liver failureL decreased production of coag factors
3. DIC consumes factors
4. multiple factor defieicnecy is very rare; usually congenital disease only affect one factor

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13
Q

describe disseminated intravascular coagulation

A
  1. syndrome in which disseminated, consumptive doagulation and fibrinolysis occurs
  2. initially starts as a hypercoagulable state with widepsread, excessive activation of hemostasis that generates excess thrombin and microvascular thrombi
  3. gradual consumption of clotting factors exceeds the rate of syntehsis and leads to hypercoagulable state and increased risk of hemorrhage
  4. always secondary to another condition that causes excessive consumption: neoplasia, heatstroke, IMHA, envenomation, sepsis, heartworm disease
  5. triggered by excessive tissue factor release from:
    -damaged endothelial cells
    -neoplastic cells
    -endotoxin stimulated cells
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14
Q

list consequences of DIC

A
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15
Q

describe diagnosis of DIC

A
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