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CABS2: Hematology > Coagulopathies > Flashcards

Coagulopathies Flashcards

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
Q

what is the presentation of PE

A

pleuritic chest pain
SOB, hypoxia
syncope
shocks (right sided HF)
findings of DVT
cough
hemoptysis
tachycardia

26
Q

what are types of things increase your risk of bleeding

A

von willebrand disease
hemophilia
platelet disorders

27
Q

why does liver disease result in coagulopathy

A

because unable to make certain factors
Factor VII first to go
decreased thrombopoietin - decreased
megakaryocyte production - decreased platelets

28
Q

von willebran disease

A

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
Q

what is von willebrand acquired disease

A

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
Q

what is the presentation of VWD

A

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
Q

what are hemophilia A and B

A

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
Q

what is the presentation of hemophilia A And B

A

easy bleeding - acute hemarthrosis, intramuscular hemorrhage,CNS bleeding, Epistaxis

33
Q

how is hemophilia diagnosed

A

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
Q

what is thrombocytopenia

A

decreased number of platelets
associated with decreased production, increased destruction, increased sequestration

35
Q

what is the platelet count that has an increased risk of spontaneous cerebral hemorrhage

A

platelet count < 10,000

36
Q

what is TTP

A

thrombotic thrombocytopenia purpura
auto-antibodies to ADAMTS-13
causes inappropriate aggregation of platelets
- vessel obstruction, end organ damage

37
Q

what is ADAMST-13

A

proteolytic enzyme that will cause degradation - lack of this protein will cause too much VWF

38
Q

what is ITP

A

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
Q

what does ITP present with

A

purpura and petechiae

40
Q

what is the presentation of severe ITP

A

epistaxis, bleeding gums, intra-articular bleeds

41
Q

What is DIC

A

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
Q

how is DIC diagnosed

A

evidence of clotting activation
fibrinolytic activation
consumption of coagulation factors
end organ damage

43
Q

what is HIT

A

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

CABS2: Hematology (4 decks)

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