Hemostasis (Wilkinson) Flashcards
Sequelae of injury to vascular endothelium
localized vasoconstriction –> reduced blood loss
What is the product of 1º hemostasis + required factors?
Platelet plug formation (temporary “bandage” to prevent further bleeding)
requires PLTs, healthy endothelium, fibrinogen, and vWF
fibrinogen: cross-links platelets together
Thrombopoietin function + origin
tells bone marrow to make new platelets (and is produced in the liver)
2º hemostasis
Reinforces the PLT plug (the clotting factors & fibrinogen produced by the liver) for conversion of prothrombin -> thrombin (= the common pathway)
2º hemostasis
What is thrombin?
Converts fibrinogen into fibrin, acticated factor XIII which cross-links fibrin together and stabilizes the intial blood clot
What are the two ways 2º hemostasis can be activated?
Via the…
1. Extrinsic pathway (factor 7)
2. Intrinsic pathway (factors 12, 9, 8)
BOTH result in activation of common pathway (10, 5, 2, 1)
What process breaks down a clot?
Fibrinolysis
end result = removal of the fibrin plug
plasmin degrades cross-linked fibrin into small fragments
What occurs in response to…
1. excessive clotting
2. excessive fibrinolysis
- thrombosis
- hemorrhage
this is why balance b/w the two are necessary
What are two products of fibrinolysis and which is a true reflection of clot formation?
FDPs: Fibrin degradation products: product of plasmin action on any circulatin fibronogen or clot-bound fibrin
D-Dimer: product of plasmin action on cross-linked fibrin ONLY (= true reflection of clot formation)
3 causes of 1º hemostasis disorder
- thrombocytopenia (decr. PLT #s)
- thrombocytopathia
- endothelial dysfunction
What causes 2º hemostasis disorder
clotting factor deficiency
how to diagnose 1º hemostasis disorder versues 2º hemostasis disorder
1º hemostasis disorder:
- Platelet count (assess quantity)
- Buccal Mucosal Bleeding Time (BMBT - assess functionality)
2º hemostasis disorder
- Prothrombin Time (PT - assess extrinsic + common pathway)
- Partial Thromboplastin Time (PTT - assess intrinsic & common pathway)
At what PLT counts do spontaneous bleeding events occur?
PLT count below 30,000 - 50,000 /uL
1º Hemostasis Disoders - pseudothrombocytopenia
Congential Macrothrombocytopenia
inherited abnormality in PLT formation –> they have lower-than-normal PLT #s // larger-than-normal sized PLTs, but NO abnormal bleeding tendencies
- CKCS, norfolk & cairn terriers
1º Hemostasis Disoders - thrombocytopenia
Causes of thrombocytopenia (4)
“SPUD”
IMTP = most common cause
1º Hemostasis Disoders - thrombocytopathia
Thrombocytopathia
- definition
- etiology
- impaired PLT function (normal PLT count + PT/PTT)
- acquired and congenital
1º Hemostasis Disoders - thrombocytopathia
Von Willebrand Disease (vWD)
- How does it cause thrombocytopathia?
- Tx?
- congenital lack of vWF –> without vWF, PLTs cannot adhere to damaged endothelium
- Tx = aimed @ addressing severe bleeding episodes or preventing hemorrhage prior to an invasive procedure
associated w/ trauma, elected sx or spontaneous (mucosal bleeding)
1º Hemostasis Disoders - thrombocytopathia
What breed is most predisposed to vWD?
Doberman pinschers
2º hemostasis disorders
Hemophilia A and Hemophilia B
Congential coagulopathies/clotting factor deficiencies causing 2º hemostasis disorder
- Hemophilia A = factor 8 deficiency
- Hemophilia B = factor 9 deficiency
associated w/ trauma, elective sx or spontaneous (cavitary bleeding)
2º hemostasis disorders
Which pathway will be affected first in a vitamin K coagulopathy?
Th Extrinsic pathway (PT) is affected first (prolonged) b/c fafctor 7 has the shortest half life
VII = 6.2h
IX = 13.9h
X = 16.5h
Clinical signs typically observed 2-5 days post ingestion
II = 42h
1º Hemostasis - Consumption
DIC pathophysiology
Systemic activation of coagulation –> excessive clotting (starts off as hypercoagulable) uses up (consumes all of) the platelets, clotting factors, etc. –> results in final hypocoagulable state + clinical bleeding
