More clin path Flashcards
requirements for hemostasis
- intact and healthy vessels
- normal platelet numbers
- normal platelet function
- normal amount and function of clotting factors
petechiae and echymoses
pin point red spots on skin/mucus membranes
indicating problem with platelets
megakaryocytes
in bone marrow
pinched off parts of cytoplasm containing granules turns into platelets
thromboxane A2 and ADP
activates platelets
vonWillebrands factor
platlets bind to receptor on vWF when exposed
platelets
from cytoplasm of metakaryocytes
binds to vWF and fibrinogen (cross linking)
+ charge to bind to - charge
automated platelet count
hematology analyzer
pro: quick and easy
cons: clumping = false decrease
estimated platelet count
stained blood smear
pro: cheap, small sample volume, subjective if clumping
cons: clumping, time and technical skill
look at monolayer under 100x objective
multiply number in field by 15,000
thrombopathy
platelets are not working properly
can be extrinsic or intrinsic
extrinsic platelet thrombopathy
something from outside the platelet is not working
most common: vonWillebrands disease
diagnosis:
* normal platelet count, PT, PTT
* prolonged buccal mucosal bleeding time (BMBT)
* measure vWF
problem with PRIMARY hemostasis
intrinisc hereditary thrombopathy
- uncommon
- various mechanisms
- specialized testing
diagnosis
* bleeding, poor clot formation, normal platelets, normal PT/PTT, normal vWF
intrinsic acquired thrombopathy
drugs: COX inhibitors (NSAIDs, steroids), b-lactam antbiotics, calcium channel blockers
uremia (renal failure, toxins in circulation impairs platelets)
DIC: fibrin and fibrinogen in excess interfere with platelts
liver dz
infections
thrombocytopenia main causes
Sequestration
Decreased Production
Utilization/consumption
Destruction
SPUD
sequestration thrombocytopenia
platelets trapped in spleen
splenomegaly
decreased production thrombocytopenia
selective and generalized marrow injury
severy thrombocytopenia
utilization/consumption thrombocytopenia
DIC (hypercoagulation forms microclots, then runs out and hemorrhage)
moderate thrombocytopenia
schistocytes/fragmenatation RBCs
destruction thrombocytopenia
severe
immune mediated usually
infection, drugs
Thrombocytosis causes
Not Neoplasia (Common)
* Physiologic/Excitement (splenic contraction)
* Inflammation (reactive, most common)
* Hemorrhage (regeneration)
* Iron deficiency
* Vincristine
* Glucocorticoids
Neoplasia (rare)
* Essential Thrombocythemia (Chronic megakaryocytic leukemia)
* >1,000,000/uL
Where are clotting factors produced?
liver
coagulation factor I
fibrinogen
coagulation factor II
thrombin
coagulation factor III
tissue factor (TF)
Coagulation factor VIII 8
factor A
coagulation factor IX 9
factor B
Intrinsic coagulation pathway
inside the blood vessel
initiated by contact with - charged substances (exposed collagen, platelet, endotoxins)
extrinsic coag cascade
things outside of the blood vessel (ex tissue factor III)
Intrinsic cascade coagulation factors
12 > 11> 9 > 8
Its not $12, its $11.9
common coagulation cascade factors
10 > 5 > 2 > 1
common coagulation cascade factors
10 > 5 > 2 > 1
extrinsic coag pathway factors
3 > 7
vitamin K dependent factors
2, 7, 9, 10
which vit k dependent coag factor has the shortest half life?
7
will shoe deficiency first
blue top tube
contains citrate, stops clotting
coagulation test for intrinsic and common cascades?
Activated clotting time (ACT): not as sensitive, can do at clinic
Partial thromboplastin time (PTT): must go to lab
coagulation test for extrinsic and common cascades?
Prothrombin time (PT)
coagulation test for fibrinogen concentration?
Thrombin time (TT)
prolonged PTT/ACT, normal PT
Problems with intrinsic pathway
usually hemophilia A (8) or B (9)
prolonged PT, normal PTT/ACT
problem with extrinsic pathway
factor 7 or 3 (TF) deficiency
early vit K deficiency (7 has shortest half life)
prolonged TT
Fibrinogen deficiency/dysfunction
Thrombin inactivation
liver failure, DIC
NOT vit k deficiency
Increased PTT/ACT and PT
vit K deficiency (if normal TT)
DIC (schistocytes, thrombocytopenia, increased TT, increased D dimers)
liver failure (low other liver products- glucose, BUN, albumin, cholesterol)
Causes of intravascular coagulation
Thrombosis:
Initially unbalanced hemostasis
Virchow’s triad
* Stasis of blood flow
* Endothelial injury
* Hypercoagulability
Inciting processes
* Congestive heart failure
* Heartworm
* Protein-losing nephropathy
DIC
Initially balanced hemostasis
Massive coagulation initiation
* Massive TF exposure or release
Inciting processes
* Trauma
* Cancer
* Shock
* Sepsis
DIC causes
Initially balanced hemostasis
Massive coagulation initiation
* Massive TF exposure or release
Inciting processes
* Trauma
* Cancer
* Shock
* Sepsis
TISSUE FACTOR
Thrombosis causes
Initially unbalanced hemostasis
Virchow’s triad
* Stasis of blood flow
* Endothelial injury
* Hypercoagulability
Inciting processes
* Congestive heart failure
* Heartworm
* Protein-losing nephropathy
plasminogen activator
in endothelial cells
converts plasminogen into plasmin
plasmin chops up fibrin and makes d dimers
fibrinogenolysis/fibrinolysis
- plasma activator released from endothelial cells
- PA cleaves plasminogen into plasmin
- plasmin breaks down fibrin and fibrinogen into D dimers and fibrin degredation factors (FDP)
increased fibrin degredation products
fibrin and fibrinogen degredation products
increased when there is plasmin mediated cleavage of fibrinogen/fibrin
increase = clot formation and breakdown
suggest DIC
increased D dimers
specific type of fibrin degredation product
suggest clot formation and breakdown
suggest DIC
heparin
anticoagulant
antithrombin III
MOST POTENT antihemostasis protein in body
destroys thrombin
anticoagulant
amplified by heparin
lose by: Protein-losing disorders
* Protein-losing nephropathy (PLN)
* Protein-losing enteropathy (PLE)
