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Path > week 4- coagulation part 2 > Flashcards

week 4- coagulation part 2 Flashcards

1
Q

what are some regulators of hemostasis:

A
  1. anticoagulant proteins
  2. endothelial cell
  3. fibrinolysis
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2
Q

what is a major anticoagulant

A

antithrombin

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3
Q

what does antithrombin degrade

A

IIa (thrombin) , IXa, Xa
stimulated by heparin and heparin-like proteoglycans

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4
Q

where is antithrombin made

A

liver

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5
Q

protein C

A

-made in liver
-vitamin K dependent
-activated when bound by thrombin: thrombomodulin = forms APC complexes

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6
Q

what does protein C inactivate

A

Va, VIIIa

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7
Q

Tissue factor pathway inhibitor (TFPI)

A

produced by the endothelial cell and inactivates the tissue factor VIIa complex

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8
Q

healthy endothelial cell is

A

anti thrombotic

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9
Q

how do endothelial cells prevent platelets from sticking to endothelial cells and limiting secondary hemostasis

A
  1. expression of heparin -like molecules that inhibit coagulation
  2. production of factors that reduce platelet activation
  3. enzymes that degrade ADP (ADP activates platelets)
  4. thrombomodulin (binds thrombin and activates protein C)
  5. Protein S (cofactor for Protein C)
  6. tissue factor pathway inhibitor
  7. tissue type plasminogen activator (promotes fibrinolysis)
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10
Q

what is fibrinolysis

A

removal of clots , set into motion by coagulation

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11
Q

plasmin is formed by cleavage of

A

plasminogen

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12
Q

active plasmin can

A

break down fibrin and also inhibits its polymerization

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13
Q

activation of plasminogen occurs via

A

factor XII dependent pathway
or action of plasminogen activators

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14
Q

2 main types of plasminogen activators

A

tissue type (t-PA)
urokinase (u-PA)

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15
Q

main source of t PA

A

endothelial cells

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16
Q

where is u-PA present

A

plasma

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17
Q

where is tPA most active vs uPA

A

t-PA most active when bound to fibrin
u-PA can activate plasminogen in fluid phase

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18
Q

fibrinolysis regulators act to limit production of ______

A

active plasmin

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19
Q

examples of regulators of fibrinolyssi

A
  1. plasminogen activator inhibitors (PAI-1, PAI-2)
  2. antiplasmins
  3. C1 inhibitor
20
Q

what is thrombosis

A

pathologic blood clot formation

21
Q

thrombosis causes (virchow’s triad)

A
  1. endothelial cell activation
  2. changes in blood composition
  3. altered blood flow
22
Q

what might cause endothelial injury/activation of vessel wall?

A
  1. inflammation
  2. infectious agents
  3. toxins
  4. trauma
  5. cancer cells
23
Q

changes in blood composition is also known as

A

hypercoagulability

24
Q

what may change blood composition ?

A

changes in plasma proteins , accumulation of metabolites that can alter fibrinogen structure

25
Q

protein losing nephropathy

A

-glomerulus leaks protein into urine
-antithrombin is about the same size as albumin
-animals lose antithrombin in urine
-at risk of developing blood clot

26
Q

altered blood flow

A

-turbulence and stasis
-very turbulent blood flow can mechanically damage the cell
-increases in stress can cause flow induced changes in gene expression
-stasis promotes interaction between platelets and vessel wall

27
Q

fate of thrombi

A
  1. propagation
  2. embolization
  3. dissolution
  4. organization and recanalization
28
Q

what is a downstream consequence of thrombus

A

infarts

29
Q

what is an infarct

A

-area of ischemic necrosis caused by occulusion or significant reduction in blood flow to tissue

30
Q

what is immunothrombosis

A

a blood clot that forms to entrap infectious agents and prevent their dissemination in the body

31
Q

mechanism of cytokine mediated expression of TF and activation of coagulation proteins

A
  1. bacterial infection produces cytokines that stimulate membrane expression or inc. synthesis of TF
    * in any disease state with cellular activation or damage, there is potential for activation of coagulation
32
Q

what is bacterial polyphosphates (polyP) initiation of the contact pathway

A

-polyp are negatively charged phosphorus polymers that are an important source of energy in prokaryotes
-released by activated platelets and mast cells
-large amounts can activate FXII
-can also generate thrombin independently of FXI activation

33
Q

thrombin mech:

A

-thrombin binds to PARs (protease activated receptors)
-signaling pathways triggered by thrombin: PAR promote activation of platelets
- results in all platelet changes associated with coagulation

34
Q

once a PAR is activated ____

A

it is endocytosed

35
Q

______ can activate specific PARs

A

TF-VIIa complex and Xa

36
Q

What are NETs

A

meshes of chromatin and proteins that are spit out onto a cell
-bacteria is trapped in the meshes

37
Q

DIC: disseminated intravascular coagulation

A

when inflammation triggers excessive activation of coagulation or dampens fibrinolysis, clots form in an unregulated, disseminated manner

38
Q

important points of DIC

A
  • always secondary
    -animals can be in the state where they are showering their microcirculation with small thrombi or they can be bleeding because they are no longer able to clot
39
Q

when clots dont form

A

hemorrhage

40
Q

hemorrhage defined as

A

extravasation of blood

41
Q

petechiae

A

pinpoint size hemorrhages into skin, MM, or serosal surfaces

42
Q

ecchymoses

A

subcutaneous hemorrhage at least 1 cm

43
Q

hematoma

A

accumulation of blood within tissue

44
Q

causes of bleeding

A
  1. defects in primary hemostasis
  2. defects in secondary hemostasis
  3. trauma
  4. toxins
  5. vessel wall
45
Q

why might animals with liver disease/failure bleed?

A

-no coagulation factors
-coagulation factors not carboxylated
-secondary to whatever is causing liver disease

46
Q

severity of infarcts depends on:

A

-if there are alternative routes to supply tissue
-the needs of the cell population
-if there was advance warning

47
Q

steps in wound healing:

A

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