Coagulopathies Flashcards
What does tPA stimulate
plasminogen
what is the active form of plasminogen
Plasmin
what is plasmin
an enzyme that will break down the formed clot (fibrinolysis)
when do you transfuse a patient
7
when do you transfuse a patient with a cardiac issue
8
What is virchow’s triad
endothelial injury
hyper coagulability
stasis
what are the types of hypercaogulable states
disseminated intravascular coagulation
inherited thrombophilias
acquired thrombophilias
What are inherited thrombophilias
Factor V Leiden
Protein C deficiency
Protein S deficiency
Antithrombin deficiency
Prothrombin 20210A
What to protein C and S inactivate
factor Va
what is factor V leiden
genetic mutation of F5 gene - more likely to be symptomatic, 8x increase risk of DVT
works with factor X to produce thrombin - clot
what are protein C and Protein S deficiency
*much more rate than Factor V leiden
increased clotting
what is a venous thromboembolism
thrombotic disease typically associated with Virchow triad
included DVT and pulmonary embolism (PE)
what is a provoked clot
*know why it happened
one of the corners of Virchow’s triad - trauma, recent surgery, immobilization, cancer, estrogen use
what is an unprovoked clot
dont know why they are clotting
what is the effect of estrogen and blood clots
increases circulating plasma fibrinogen, factor VII and X, and platelet aggregation
what is a DVT
thrombos forms on the valves which disrupts valvular function and venous blood will pool more
what is the presentation of DVT
increased swelling, distended (varicose) veins, pain, skin hyperpigmentation
what is phlegmasia alba dolens
white swollen leg associated with proximal DVT
what is phlegmasia cerulea dolens
dusky or blue
what is superficial thrombophlebitis
clot within a superficial vein (typically of the lower extremity)
can cause inflammatory changes that are seen on clinical exam
What is an arterial thrombotic event
arterial occlusion leading to increase risk of limb loss, ischemic limb
often associated with preexisting narrowing such as a plaque formation
can occur at site of aneurysm
hypercoagulable states as previous discussed
What is a PE
Virchows triad cause of clotting
clot becomes loose and travels through the circulation to lodge in the pulmonary vasculature
the severity of grading depends on the patient
what are the classifcations of PE
Massive: hemodynamic instability wiht hypotension
Submassive with right heart strain: elevated troponin, BNP, strain on imaging
Submassive without right heart strain: subsegmental
what are the risk factors for PE
time of immobility
surgery
trauma
cancer
estrogen replacement
procoagulant syndromes
hx of DVT or PE
what is the presentation of PE
pleuritic chest pain
SOB, hypoxia
syncope
shocks (right sided HF)
findings of DVT
cough
hemoptysis
tachycardia
what are types of things increase your risk of bleeding
von willebrand disease
hemophilia
platelet disorders
why does liver disease result in coagulopathy
because unable to make certain factors
Factor VII first to go
decreased thrombopoietin - decreased
megakaryocyte production - decreased platelets
von willebran disease
hallmarked by deficiency in or malfunction in von willebrand factor
most common inherited bleeding disorder
VWF helps with clot adherence as well as activating factor 8
can be acquired or inherited
what is von willebrand acquired disease
may be due to high circulatory shear stress
may also be associated with chronic systemic diseases such as: Leukemia, non-hodgkin lymphoma, MM, etc
what is the presentation of VWD
hemostasis is impaired
may be mild and not recognized
may note increased bleeding with ASA or NSAID
inappropriate bleeding:
- epistaxis
- easy bruising
- bleeding after dental procedures
-if severe, may have mucocutaneous and joint bleedings, GI bleeding
what are hemophilia A and B
X linked recessive disorders
A= deficiency in factor VIII
B = deficiency of factor IX
deficiency in these factors will decrease the ability to form the fibrin mesh over the platelet plug
what is the presentation of hemophilia A And B
easy bleeding - acute hemarthrosis, intramuscular hemorrhage,CNS bleeding, Epistaxis
how is hemophilia diagnosed
prolonged aPTT (activated partial thromboplastin time)
reduced factor VIII = hemophilia A
reduced factor XI = hemophilia B
PT, platelet count, vwf are normal (unless another coexisting disease)
what is thrombocytopenia
decreased number of platelets
associated with decreased production, increased destruction, increased sequestration
what is the platelet count that has an increased risk of spontaneous cerebral hemorrhage
platelet count < 10,000
what is TTP
thrombotic thrombocytopenia purpura
auto-antibodies to ADAMTS-13
causes inappropriate aggregation of platelets
- vessel obstruction, end organ damage
what is ADAMST-13
proteolytic enzyme that will cause degradation - lack of this protein will cause too much VWF
what is ITP
Immune Thrombocytopenic purpura
most common type of elevated platelet destruction
IgG antibodies against platelet glycoproteins
typically associated with viral illness
antigen against immune complex similar to platelets - platelets tagged - platelets broken down by phagocytes in spleen
what does ITP present with
purpura and petechiae
what is the presentation of severe ITP
epistaxis, bleeding gums, intra-articular bleeds
What is DIC
disseminated intravascular coagulation
secondary disease process associated with systemic illness or disease state - most commonly sepsis that leads to ischemia and necrosis
hallmarked by inappropriate activation of coagulation factors
leads to bleeding - results in prolonged PT/PTT
how is DIC diagnosed
evidence of clotting activation
fibrinolytic activation
consumption of coagulation factors
end organ damage
what is HIT
heparin induced thrombocytopenia
more common with UF than LMWF
IgG mediated response to Heparin resulting in platelet activation, platelet consumption - thrombocytopenia
may see clotting then thrombocytopenia
