Card Set Information
Hemostasis in Clin Lab Lecture
complex process that stops bleeding, forms stable clot then breaks down clot.
stays where it's put
Three steps of hemostasis
: (platelet activation, adhesion and aggregation)
: cascade of enzyme conversions leading to stable clot
: breakdown of fibrin clot, activated simultaneously with hemostasis
Simple order of blood clotting
blood vessel injury, vasoconstriction, release of collagen
circulating platelets adhere to damage and collagen, form plug (Von Willebrand)
Platelets release chemicals activating blood clotting factors
cross-linked fibrin clot formed in clotting cascade
damage to tissue activates
Factor 7 (tissue thromboplastin)
Activates Intrinsic pathway
only non-protein clotting factor
in extrinsic pathway only.
Clotting factors are primarily produced by
activated by extrinsic.
damage to blood vessel, wet, anionic surface.
Factors 12, 11, 9, 8 (kmart special)
10, 5, 2, 1, 8
activated by both extrinsic and intrinsic
10a activates 5a, activates 2 (prothrombin into thrombin), activates 1 (fibrinogen into fibrin), stabilizes clot. 8 turns fibrin into clot, prolongs von willebrand's
fragments of megakaryocytes, makes platelets.
200,000 - 500,000 for most species, 100,000 is thrombocytopenia, <50,000 signs of hemmorrhage
30-40% in spleen.
Birds and reptiles have nucleated platelets.
precursor to thrombocytes
forms hemostatic plug
initiates clotting cascade
initiates clot retraction
constrict blood vessels
phagocytize some particles, particularly damaged cell membrane.
EDTA tube, used to check platelets
citrate. Used to check clotting factors
used to check fibrin split products
Whole blood clotting time test
Checks intrinsic and common (12, 11, 10, 9, 8, 5, 2, 1)
: 2-10 minutes
: 8 minutes
: 4-15 minutes
: 10-15 minutes
Buccal mucosa bleeding time test
Detect abnormalities in platelet function and von Willebrands
usually 1-5 minutes.
Long indicates thrombocytopenia (usually already know), platelet dysfunction, vWF deficiency
pinpoint bruising on gums/pinna. Look at CBC, if normal do buccal mucosa bleeding time test
Three methods for calculating platelet numbers
platelet estimate (peripheral blood smear)
platelet manual count (hemocytometer, within 5 h)
Platelet automated count (automated cell counter, trouble with overlap with RBC and clumping)
Peripheral blood smear in platelet evaluation
examine monolayer in blood smear, count min 10 microscopic fields
d/c/cw 8-10 platelets per field min
horse 5 platelets per field min
each platelet = 15,000-20,000 platelet/uL
average # x 15,000
morphology (young are macro, increased production)
cats have larger platelets
nonactivated have granules, activated may or may not.
Clot retraction test
Evaluates plately number and function in intrinsic and extrinsic.
Checks platelet function (don't use if on aspirin)
depends on interaction between platelet receptors, thrombin, fibrinogen.
1-2 hours for good clot retraction
abnormal platelet function
blotches and bruises on gums, can be pinna as well. Indicates low platelets.
thrombocytopenia, abnormal platelet distribution
splenomegaly, hypothermia (liver)
thrombocytopenia, decreased platelet production
drugs, chemo, infections, irradiation, marrow replacement
thrombocytopenia, decreased platelet survival
non-immunologic (blood loss, DIC, localized intravascular coagulation, vasculitis (leaky vessels), drugs, envenomation, rodenticide)
usually no clinical signs.
iron deficiency anemia (non-regenerative anemia, microcytic, hypochromic)
epinephrine release (fear or pain)
platelets aren't low, just not working.
Consider with prolonged bleeding time or clot retraction.
Can be hereditary or acquired.
drug exposure (NSAIDs, antihistamines, iso, phenylbutazone in horses), envenomation, hepatic disease, increased fibrin degredation products, immune mediated, Infectious (FeLV), renal failure, neoplasia
Fibrinogen/plasma test for coagulation evaluation
measure protein on refractometer (100mg-500mg/dL)
: liver disease, congenital or factors used up. Hemolysis and lipemia falsely used up.
: inflammation, hyperadrenocorticism, pregnancy, nephrotic syndrome in dogs (proteinuria, hypoalbuminemia, hypercholesteralemia, edema)
: can be any reading of platelets.
Activated clotting time test for coaguation
ACT. Evaluates intrinsic and common (all factors but 7), not very sensitive. 90-95% problem to detect
Blood into tube with diatomaceous earth, 37 degrees, check for clot time.
cats< 75 sec
Activated Partial Thromboplastin time (APTT)
tests intrinsic and common pathways.
blue top, 9:1 blood to citrate, centrifuge within 60 minutes, keep refrigerated. Analyze within 2 hours or freeze.
8-13 sec in dog, <30% normal control.
Indicates trouble in factors, substitute known deficiency factors and see if corrects.
check for liver disease, vitK deficiency, drug overdose, toxins and DIC
Prothrombin time (PT) or one stage PT (OSPT)
evaluates extrinsic and common.
citrate tube (9:1), treat sample like PTT.
normal is 6-8 sec in dog, <30% longer than normal control.
indicates deficiency of factors in extrinsic (7) or common (10, 5, 2,1)
Rodenticide affects #7 (most common)
After ingestion of rodenticide, ______________ will show up first.
Factor VII deficiency (extrinsic pathway, PT) because it has the shortest half-life. Eventually all pathways will be effected (2,7,9,10).
Early rodenticide = normal PTT, ACT
Protein Induced (Invoked) by Vitamin K Absence. Thrombotest.
Looks for built-up precurser proteins not used because of vit. K deficiency. (Pre-2, Pre-7, Pre-9, Pre-10)
rarely run, not better than PT for rodenticide. Good for subtle extrinsic/common disorders.
D-Dimer and Fibrin degradation products
formed when a clot is degraded, evidence of fibrolysis.
Used to find DIC and thromboembolism in all but horses.
d-dimer better than FDP for fibrinolysis (not DIC or TE)
Thrombocytopenia presents in the lab with
abnormal clot retraction
most common coagulopathy.
Caused by bone marrow damage, infections, immune, abnormal distribution, low production/survival, hemodilution
thrombocytopathia presents in the lab with
normal platelet count
abnormal clot retraction.
abnormal platelet function.
Congenital or acquired through drugs (Aspirin), renal failure, increased FDPs (fibrinolysis, DIC), envenomation, hepatic disease, immune, infection, neoplasia.
Intrinsic pathway coaguation defect lab findings
Intrinsic pathway coagulation defect diseases
von Willebrand's Disease
Most common intrinsic pathway defect.
Factor 8 deficiency
Severe hemorrhage and ecchymoses
sex-linked recessive--males in any breed
intrinsic pathway defect
factor 9 deficiency
mild to severe bleeding
sex-linked recessive--males in any dog and DSH cats (siamese)
von Willebrand Disease
Most common hereditary bleeding disorder in dogs (dobermans), rare in others.
Missing or ineffective von Willebrand factor, which decreases factor VIII and makes platelets not adhere.
Clinical signs of von Willebrand
mild to severe mucosal hemorrhages
prolonged hemorrhage from trauma/surgery (tail docking, tooth extraction, dewclaw removal, blood extraction)
Hemoarthrosis and hematomas in horses
von Willebrand lab results
prolonged BMBT without thrombocytopenia
normal or mildly prolonged PTT
von Willebrand antigen test (ELISA) uses anti-vWF antibodies as a % of control. 50% is positive, 70% is negative (between unclassified)
enzyme linked immuno-sorbant assay
Causes of prolonged PT, normal everything else
Factor VII deficiency (bruising not bleeding)
early hepatic disease (eventually more problems)
early vit K deficiency/antagonism/absense (Warfarin toxicity), will eventually effect all.
Common pathway lab findings
Vitamin K antagonism or deficiency
will effect II, VII, IX, X
effects VII first, shortest half-life
bleeding is common (can present as breathing problems) 3-7 days after exposure
Can come from warfarin or rodenticides
sweet clover or sweet vernal grass (large animals)
Vitamin K deficiency, not warfarin
rarely causes hemorrhage
vitK absorbed in intestine, produced/ingested by intestinal bacteria
Caused by serious, prolonged anorexia, malabsorption of vitamin K (fat-soluble, so no-fat diet)
Liver disease as common pathway deficiency
Liver makes I, II, V, VII, VIII, IX, X, XI, XII
very severe liver disease causes hemorrhage
DIC stands for
disseminated intravascular Coagulation
DIC caused by
LOTS of things. Thromboplastin in tissue exposed, sets off clotting cascade.
Septicemia, viremia, parasites, tissue injury, intravascular hemolysis, obstetric complications, malignancy, shock, liver disease, pancreaitis, GDV, abomasal displacement, toxins
starts as hypercoagulation due to activation of clotting cascades (not evident clinically)
multiple small clots form in vessels, consuming platelets and clotting factors
Fibrinolysis, leaving d-dimers and fibrin split products
fibrin split products (FDPs) are anticoagulants.
DIC lab abnormalities
decreased platelets (first sign, prolonged BMBT)
increased FDP or d-dimers