Alterations in Hemostasis Flashcards

1
Q

What does an increased mean platelet volume can indicate?

A

Consistent with increased release of large or giant platelets and usually indicates a platelet regenerative response

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2
Q

Why is the thrombocrit a better indicator of the total platelet functional potential?

A

Because larger platelets have greater functional capacity

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3
Q

What are the three basic mechanisms of thrombocytopenia?

A

Platelet sequestration, decreased platelet production, and decreased platelet lifespan due to consumption or destruction

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4
Q

What is usually the cause for increased platelet sequestration?

A

Splenomegaly

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5
Q

What are the causes of splenomegaly?

A
  • Infiltrative diseases - lymphoma, leukemia, and multiple myeloma
  • Infectious or other inflammatory diseases - IMHA
  • Lymphoid hyperplasia
  • Splenic extramedullary hematopoiesis
  • When venous outflow is compromised
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6
Q

What can cause decreased platelet production?

A

Various bone marrow disorders

  • Myelopthisis - replacement of normal marrow - often due to marrow infiltration with neoplastic cells
  • Familial myelofibrosis - pygmy goats
  • Toxic damage to the marrow (bracken fern toxicosis or NSAID administration
  • Immune-mediated destruction of megakaryocytic
  • Infectious agents - EIA, acute bovine viral diarrhea infection
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7
Q

What can decrease platelet lifespan?

A

Destruction of platelets or platelet consumption in widespread coagulation

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8
Q

What are the causes of immune-mediated thrombocytopenia?

A
  • Idiopathic

- Secondary to various etiologies, including viral and bacterial infections, drug administration, and hemic neoplasia

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9
Q

When do we have excessive consumption of platelets?

A
  • With DIC - diagnosis of DIC relies on finding evidence of both platelet and coagulation factor consumption
  • Snake envenomation directly causes platelet destruction without evidence of DIC
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10
Q

What are the clinical signs of thrombocytopenia?

A
  • Petechial or ecchymotic hemorrhages on the oral, nasal, and or vaginal mucosa
  • Epistaxis, melena, hyphema and/or hematuria
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11
Q

What are the causes of thrombocytosis?

A
  • Physiologic - increase in high altitude
  • Relative - redistribution from spleen and other organs
  • Absolute - myeloproliferative disease, infectious and inflammatory disorders, iron deficiency
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12
Q

What does the template bleeding time assess?

A

Primary hemostasis - platelet number/function and von Willebrand factor function

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13
Q

What is Glanzmann’s thrombasthenia?

A
  • Disorder resulting in poor platelet aggregation and clot retraction
  • One or more defects in quantity or quality of platelet surface glycoprotein IIb/IIIa
  • Has been reported as an hereditary dz in horses
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14
Q

Which drugs impair platelet function?

A

Aspirin, phenylbutazone, sulfonamides, estrogens, and phenotiazines

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15
Q

What does the prothrombin time assess?

A

Extrinsic and common pathways

VII, V, X, II

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16
Q

Causes of acquired coagulation factors defects

A

Liver disease, vitamin K antagonism (moldy sweet clover poisoning), and increased consumption via DIC

17
Q

Vitamin K is necessary for the production of which coagulation factors?

A

II, VII, IX and X

18
Q

Causes of vitamin K antagonism

A
Coumarin compounds acquired via moldy sweet clover hay or anticoagulant rodenticide ingestion
Therapeutic administration (warfarin in horses)
19
Q

What does the activated partial thromboplastin time measures?

A

Intrinsic and common pathways

XII, XI, IX, VII, X, II, prekallikrein

20
Q

Liver disease and vitamin K antagonism prolong PT or PTT?

A

BOTH

21
Q

What do increased fibrin degradation products and d-dimers indicate?

A

Increased fibrinolysis in response to excessive coagulation

22
Q

What is the physiologically most important inhibitor of coagulation?

A

Antithrombin or antithrombin 3 - primarily neutralizes activated factors IX, X, and II

23
Q

What causes plasma ATIII levels to be reduced?

A

Decreased liver production, excessive use, loss from the intravascular compartment, increased catabolism, heparin administration

24
Q

Major clinical sequela of ATIII deficiency?

A

Venous thrombosis

25
Q

What can lead to hypofibrinogemia?

A

Impaired hepatic synthesis, increased consumption with DIC, uncompensated loss during massive hemorrhage

26
Q

What does thromboelastography assess?

A

Global clot formation and lysis in whole blood.

27
Q

Advantage of TEG over PT, PTT, and platelets?

A

Detects hyper coagulable states and increased fibrinolysis.

28
Q

What is the second major anticoagulant mechanism?

A

Protein C pathway