Alterations in Hemostasis Flashcards

(28 cards)

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?

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
What can lead to hypofibrinogemia?
Impaired hepatic synthesis, increased consumption with DIC, uncompensated loss during massive hemorrhage
26
What does thromboelastography assess?
Global clot formation and lysis in whole blood.
27
Advantage of TEG over PT, PTT, and platelets?
Detects hyper coagulable states and increased fibrinolysis.
28
What is the second major anticoagulant mechanism?
Protein C pathway