Coagulopathies Flashcards

(43 cards)

1
Q

What does tPA stimulate

A

plasminogen

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2
Q

what is the active form of plasminogen

A

Plasmin

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3
Q

what is plasmin

A

an enzyme that will break down the formed clot (fibrinolysis)

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4
Q

when do you transfuse a patient

A

7

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5
Q

when do you transfuse a patient with a cardiac issue

A

8

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6
Q

What is virchow’s triad

A

endothelial injury
hyper coagulability
stasis

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7
Q

what are the types of hypercaogulable states

A

disseminated intravascular coagulation
inherited thrombophilias
acquired thrombophilias

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8
Q

What are inherited thrombophilias

A

Factor V Leiden
Protein C deficiency
Protein S deficiency
Antithrombin deficiency
Prothrombin 20210A

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9
Q

What to protein C and S inactivate

A

factor Va

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10
Q

what is factor V leiden

A

genetic mutation of F5 gene - more likely to be symptomatic, 8x increase risk of DVT

works with factor X to produce thrombin - clot

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11
Q

what are protein C and Protein S deficiency

A

*much more rate than Factor V leiden
increased clotting

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12
Q

what is a venous thromboembolism

A

thrombotic disease typically associated with Virchow triad
included DVT and pulmonary embolism (PE)

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13
Q

what is a provoked clot

A

*know why it happened
one of the corners of Virchow’s triad - trauma, recent surgery, immobilization, cancer, estrogen use

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14
Q

what is an unprovoked clot

A

dont know why they are clotting

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15
Q

what is the effect of estrogen and blood clots

A

increases circulating plasma fibrinogen, factor VII and X, and platelet aggregation

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16
Q

what is a DVT

A

thrombos forms on the valves which disrupts valvular function and venous blood will pool more

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17
Q

what is the presentation of DVT

A

increased swelling, distended (varicose) veins, pain, skin hyperpigmentation

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18
Q

what is phlegmasia alba dolens

A

white swollen leg associated with proximal DVT

19
Q

what is phlegmasia cerulea dolens

A

dusky or blue

20
Q

what is superficial thrombophlebitis

A

clot within a superficial vein (typically of the lower extremity)
can cause inflammatory changes that are seen on clinical exam

21
Q

What is an arterial thrombotic event

A

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

22
Q

What is a PE

A

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

23
Q

what are the classifcations of PE

A

Massive: hemodynamic instability wiht hypotension
Submassive with right heart strain: elevated troponin, BNP, strain on imaging
Submassive without right heart strain: subsegmental

24
Q

what are the risk factors for PE

A

time of immobility
surgery
trauma
cancer
estrogen replacement
procoagulant syndromes
hx of DVT or PE

25
what is the presentation of PE
pleuritic chest pain SOB, hypoxia syncope shocks (right sided HF) findings of DVT cough hemoptysis tachycardia
26
what are types of things increase your risk of bleeding
von willebrand disease hemophilia platelet disorders
27
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
28
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
29
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
30
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
31
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
32
what is the presentation of hemophilia A And B
easy bleeding - acute hemarthrosis, intramuscular hemorrhage,CNS bleeding, Epistaxis
33
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)
34
what is thrombocytopenia
decreased number of platelets associated with decreased production, increased destruction, increased sequestration
35
what is the platelet count that has an increased risk of spontaneous cerebral hemorrhage
platelet count < 10,000
36
what is TTP
thrombotic thrombocytopenia purpura auto-antibodies to ADAMTS-13 causes inappropriate aggregation of platelets - vessel obstruction, end organ damage
37
what is ADAMST-13
proteolytic enzyme that will cause degradation - lack of this protein will cause too much VWF
38
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
39
what does ITP present with
purpura and petechiae
40
what is the presentation of severe ITP
epistaxis, bleeding gums, intra-articular bleeds
41
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
42
how is DIC diagnosed
evidence of clotting activation fibrinolytic activation consumption of coagulation factors end organ damage
43
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