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 - thrombocytopenia
IMTP
- definition
- CBC result
- primary etiology
- what 2º infections (dog vs cats) can potentially cause it
Immune-Mediated Thrombocytopenia: abnormal IR directed against platelets
- lab findings = severe thrombocytopenia (PLT # 0-20,000/uL); regen anemia due to hemorrhage or concurrent IMHA (can see spherocytes or ghost cells)
- Primarily usually idiopathic, but a 2º rickettsial (dogs) or FeLV (cats) disease can cause it
rickettsial dz: ehrlichia, anaplasmosis, RMSF
1º Hemostasis Disoders - thrombocytopenia
How can IMTP be treated (4)?
- Doxycycline (rickettsial dzs)
- Prednisone or dexamethasone (to increase PLT count – ~7 days for >40k)
- Vincristine (chemotherapy agent for adjunctive ER tx - shortens PLT count recovery time)
- Blood transfusion (when CS related to blood loss anemia are present – use fresh whole blood > pRBCs)
vincristine admin w/ corticosteroid can shorten hospitalization time
Vincristine is a vesicant (causes blistering) –> AVOID EXTRAVASATION!! Place an IVC solely dedicated to administering vincristine
1º Hemostasis Disoders - thrombocytopathia
Thrombocytopathia
- definition
- etiology
- impaired PLT function (normal PLT count + PT/PTT)
- acquired and congenital
1º Hemostasis Disoders - thrombocytopathia
Test that can assess PLT function
BMBT - Sf incision made into buccal mucosa and time for bleeding to stop is recorded
assess both enodthelial & PLT functions
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
how are hemophilia A and B diagnosed?
young animal w/ unexplained bleeding and prolonged PTT only, or via a factor assay (to confirm presumptive dx)
2º hemostasis disorders
Vitamin K coagulopathies
- definition
- VitK role in clotting factor pathway
- most common cause
- acquired coagulopathy causing 2º hemostasis disorder
- VitK is required for production/activation of VitK-dependent coag factors (2, 7, 9, 10)
- Causes: anticoagulant rodenticide ingestion
Primary hemostasis involves the formation of a platelet plug at the site of an injured blood vessel, and secondary hemostasis involves the coagulation cascade which is where a protein net called a fibrin mesh forms over the platelet plug to reinforce it - forming a blood clot.
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
How does liver disease cause hemostasis/clotting disorders?
The liver synthesizes several clotting factors –> multi-factorial acquired coagulopathy
- 1º defects = thrompocytopenia (decr. thrombopoietin; DIC), thrombocytopathia (uncommon)
- 2º defects = decr. clotting factor synthesis; hypofibrinogenemia
tx = underlying hepatic dz
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
