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Hemostasis > Section 11: Fibrinolytic and Thrombotic > Flashcards

Section 11: Fibrinolytic and Thrombotic Flashcards

1
Q

plasmin functions

A
  • lyses fibrin and fibrinogen
  • inactivates factors Va and VIIIa
  • degrades factor XIIa
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2
Q

primary fibrinolysis (fibrinogenolysis)

A
  • always pathological
  • overactivation of plasmin and/or
  • overwhelms plasmin inhibitors
  • other physiological causes
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3
Q

secondary fibrinolysis (fibrinolysis)

A
  • normal and pathological
  • pathological if overactivation of plasmin and/or overwhelms plasmin inhibitors
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4
Q

overactivation of plasmin in liver disease and exogenous activators

A
  • liver disease: decreased inhibitors of fibrinolytic system thereby increasing fibrinolysis, decreased alpha2-antiplasmin
    - plasmin free to attack not only fibrin, but also fibrinogen, factors V and VIII -> bleeding
  • exogenous activators: streptokinase, urokinase, tPA
  • Euglobulin test
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5
Q

stuff indicated in causing thrombosis

A
  • major tissue trauma and surgery
  • obesity
  • complications of pregnancy (immobility, dead fetus syndrome, amniotic fluid embolus, HELLP, increase in factors VII, VIII, IX, XII, and I…etc)
  • oral contraceptives
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6
Q

anti-thrombin deficiency

A
  • thrombosis
  • often family history of pathological thrombi and emboli
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7
Q

Protein C and Protein S deficiencies

A
  • thrombosis
  • can’t inactivate Va or VIIIa
  • can’t liberate tPA (fibrinolytic)
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8
Q

Protein Z and ZPI deficiencies

A
  • thrombosis
  • can’t degrade Xa
  • ZPI can’t degrade XIa
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9
Q

heparin cofactor II deficiency

A
  • thrombosis
  • decreased neutralization of thrombin
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10
Q

activated protein C resistance (APC-R)

A
  • aka Factor V Leiden
  • mutation of Factor V gene
  • Factor V resistant to lysis or inactivation by APC
  • 20% new thrombosis
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11
Q

expected APC-R PT and APTT results?

A

Normal for both because Va is functioning

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12
Q

APC-R clot based assay procedure

A
  1. Add APTT reagent + FV-depleted plasma + pt plasma
  2. Split into two aliquots
  3. Add CaCl2 to one aliquot
  4. Add CaCl2 + APC to the second aliquot
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13
Q

APC-R clot based assay principle

A

If APC-resistant, then adding APC will prolong clot time LESS than the non-resistant sample

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14
Q

XIIa function

A

convert plasminogen to plasmin

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15
Q

XII deficiency causes

A

thrombosis

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16
Q

factor XI deficiency (hemophilia C)

A

bleeding
not thrombosis

17
Q

dysfibrinogenemia

A
  • most asymptomatic
  • may be resistant to fibrinogenolysis and/or once clot is formed it is resistant to fibrinogenolysis -> thrombosis
  • can also be present as a bleeding disorder or both bleeding + thrombosis
18
Q

prekallekrein and HMWK deficiencies

A
  • typically asymptomatic
  • may see thrombosis due to lack of activation of plasminogen to plasmin
  • PT normal and APTT prolonged
18
Q

plasminogen deficiency

A
  • thrombosis
  • type 1: decrease in activity and protein (deficiency)
  • type 2: dysfunctional
19
Q

tPA deficiency

A
  • thrombosis
  • results in decreased activation of plasminogen to plasmin
20
Q

prothrombin mutation

A
  • prothrombin G20210A
  • single point mutation in prothrombin gene
  • causes increased prothrombin levels -> thrombosis
21
Q

increased homocysteine

A
  • defect in homocysteine metabolism
  • increased homocysteine levels -> thrombosis
  • mechanism unknown
22
Q

ebola association with thrombocytopenia

A

may be associated with bone marrow suppression but it’s often not enough to account for bleeding on its own

23
Q

list possible causes of bleeding in ebola

A
  • thrombocytopenia
  • platelet dysfunction
  • DIC
  • hepatic coagulopathy
24
Q

explain possible DIC cause of ebola

A
  • TF3 released from infected monos/macrophages
  • cytokine storm
  • inflammation -> vascular lesions
  • plt activation and unusually large vWF resulting in a TTP-like syndrome
  • fibrin deposited in organs
25
Q

explain possible hepatic coagulopathy cause of ebola

A

associated with viral-induced necrosis

26
Q

COVID-19 early CBC results

A

looks fairly normal

27
Q

what happens as COVID-19 progresses?

A

lymphopenia

28
Q

possible causes of lymphopenia in COVID-19 infection

A
  • virus infects and kills lymphs
  • virus destroys lymphatic organs
  • disordered inflammatory cytokines -> lymph apoptosis
  • inhibition of lymphs by metabolic molecules such as lactic acid that suppress lymph proliferation
29
Q

presence of what cell type during COVID-19 may represent a better outcome?

A

reactive lymphs
suggests virus-specific T-cell production

30
Q

hypercoagulopathy of COVID-19 infection

A
  • endothelial cell injury especially lungs
  • stasis: immobilization slows blood flow
  • hypercoagulable state
31
Q

explain endothelial cell injury in COVID-19 coagulopathy

A
  • direct invasion of ECs
  • cytokine storm -> systemic inflammatory response
  • TNF-alpha and IL-6 released, TNF-alpha strong inducer of TF3 -> plt activation and coagulation
32
Q

lab results of COVID-19 associated coagulopathy (CAC)

A
  • high D-dimer levels (poor prognosis)
  • elevated VIII:C and fibrinogen
  • vWF antigen increased due to injury to endothelium and reduced ADAMTS13 activity (large multimers)
  • excess thrombin formation and early fibrinolysis shutdown -> higher TFPI
  • decreased AT and protein C
  • possible antiphospholipid antibodies
33
Q

T/F
Severe hypoxia stimulates thrombosis in COVID-19 infection

A

True

34
Q

COVID-19 hypercoagulable state molecular events

A
  • neutrophil extracellular traps can worsen inflammation and thrombosis if not regulated
  • bradykinins in inflammation
  • hyperviscosity slows blood flow
35
Q

coagulation test results for COVID-19 infection

A
  • PT and APTT normal or sl prolonged
  • plt count normal or increased
  • fibrinogen increased
  • D-dimer increased (associated with ICU and respirator)
  • should monitor for renal impairment
36
Q

how to distinguish COVID-19 from DIC even tho both have increased D-dimer?

A
  • COVID: thrombosis, high fibrinogen, high factor VIII
  • acute DIC: bleeding, low fibrinogen, low factor VIII
37
Q

treatment of thromboinflammation

A
  • heparin antithrombotic
  • prophylactic LMWH

Hemostasis (10 decks)

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