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Pathology 1 > coagulation > Flashcards

coagulation Flashcards

1
Q

coagulation cascade is a successive series of?

A

amplifying enzymatic reactions

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2
Q

at each step in the coagulation cascade a proenzyme is?

A

proteolyzed to become an active enzyme, which in turn proteolyzes the next proenzyme

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3
Q

the end goal of the coagulation cascade leads to the activation of?

A

thrombin and the formation of fibrin

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4
Q

each reaction of the coagulation cascade depends on the assembly of what 3 complex components?

A
  • enzyme = activation coagulation factor
  • substrate= a proenzyme form of the next coagulation factor in the series
  • co-factor = a reaction accelerator
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5
Q

components of the coagulation cascade are assembled where? held together how?

A

on phospholipid surface and held together by calcium-dependent interactions

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6
Q

the ability of factors 2, 7, 9 and 10 to bind to calcium requires what vitamin?

A

vitamin K

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7
Q

coumadin and warfarin are?

A

anticoagulants

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8
Q

Major Cascade Event

A

1) activation of factor X to Xa
2) factor Xa catalyzes the conversion of prothrombin to thrombin
3) thrombin converts soluble fibrinogen to insoluble fibrin, which is stabolized by factor 13
4) stailized fibrin ‘glues’ platelet plug for greater endurance

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9
Q

describe tissue factor (extrinsic) pathway

A
  • occurs after vascular damage
  • activated by factor 3 (tissue factor) which is exposed at sites of injury
  • TF complexes with Factor 7a (extrinsic factor Xase), converging with the intrinsic pathway, leading to the activation of factor X to Xa
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10
Q

describe contact activation (intrinsic) pathway

A
  • TF- factor 7a complex activates factor 9 and 9a
  • factor 9a complexes with 8a (“intrinsic factor Xase”)
  • also activated by factor 12 (Hageman factor)
  • may be activated in the absence of tissue injury
  • important in the pathogenesis of thrombosis
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11
Q

both intrinsic and extrinsic pathways converge to activate?

A

factor 10

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12
Q

describe common pathway

A

1) factor 10 is activated by factor 9a-8a complex (intrinsic factor Xase) and TF-factor 7a (extrinic factor Xase)
2) factor 10a-5a complex activate factor 2 (prothrombin) to 2a (thrombin)
3) thrombin converts fibrinogen (factor 1) to fibrin (1a)
4) fibrin clot stabilized by factor 13a

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13
Q

what is INR?

A

international normalized ratio = standardized measurement and expression of the prothrombin time

  • patient PT/ mean normal PT)^ISI
  • normal is 0.9-1.2
  • adequate anti-coagulation generally 2.0-3.0, as high as 3.5 for high-risk conditions
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14
Q

INR is used to monitor for?

A

coumadin (warfarin) anticoagulation and screening for coagulopathies

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15
Q

INR reflects the activites of what factors?

A

2, 5, 7, and 10

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16
Q

Dental Procedures and Warfarin

A

use them! more so for outpatient dental surgery procedures like extraction or root canals
*both ACCP and BCSH agree

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17
Q

counter clotting mechanisms are set in motion simultaneously with?

A

clot formation to limit clotting to the site of injury

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18
Q

name 3 natural anticoagulants

A

1) antithrombins aka antithrimbin 3
2) Protein C and S
3) tissue factor pathway inhibitor (TFPI)

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19
Q

antithrombins aka antithrimbin 3 inhibit ____ and what factors?

A

inhibit thrombin and factors 9a, 10a, 11a, and 12a

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20
Q

antithrombins are activated by?

A

binding to heparin-like molecules on endothelial cells

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21
Q

ATT3 inhibits what?

A

inhibits thrombin and factors 9a and 10a

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22
Q

exogenous heparin binds to ____ resulting in its activation

A

ATT3

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23
Q

Protein C and S are vitamin ____ dependent and INactivates what factor?

A

vitamin K

*inactivates thrombin and factors 9a and 10a

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24
Q

1) fibrinolytic cascade limits size of?
2) fibrinolytic cascade mediated by?
3) fibrin split prodcuts (FSPs) act as ?
4) elevated FDPs are useful for?

A

1) the final clot
2) mediated by plasmin
3) fibrin split products (FSPs) can act as weak anticoagulants
4) elevated FSPs areful in diagnosing abnormal thrombotic states

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25
Q

plasmin is formed by?

A

cleaving plasminogen to plasmin by plasminogen activators

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26
Q

tissue plasminogen activator (tPA) is made by? most active when?

A

endothelial cells

*most active when attached to fibrin

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27
Q

uPA stands for?

A

urokinase-like plasminogen activator; another activator of plasminogen

28
Q

uPA and tPA are inactivated by?

A

alpha2- antiplasmin

29
Q

plasminogen activator inhibitors do what?

A

block fibrinolysis

  • increased production by inflammatory cytokines (IF-y)
  • modulates coagulation-anticoagulation balance
30
Q

define thrombosis

A

formation of blood clot in injured vessels

*pathologic converse to hemostasis

31
Q

virchow’s triad of pathogenesis of thrombosis

A

1) endothelial injury
2) stasis or turbulent blood flow
3) hypercoagulability

32
Q

endothelial injury is an important cause of?

A

thrombosis

33
Q

loss of endothelium > exposure of subendothelial ECM > ____ > _____ > reduced production of ____ and ____

A 
loss of endothelium > 
exposure of subendothelial ECM > 
plateletadhesion > 
release ofTF  > 
reduced production of prostacyclin (PGI2) and plasminogen activators
34
Q

T or F… Endothelium does not need to be denuded or
physically disrupted to contribute to
development of a thrombus

A

TRUE

35
Q

dysfunction endothelium elaborates greater or decreased amounts of procoagulant factors or anticoagulant molecules

A
  • greater procoagulant factors

* decreased anticoagulant molecules

36
Q

endothelial dysfunction can be mediated by?

A

hypertension (high BP), turbulent blood flow, bacterial products (endotoxin), radiation, hypercholesterolemia, cigarette smoking

37
Q

two major categories of abnormal blood flow we discussed

A

1) turbulence

2) stasis and turbulence

38
Q

describe turbulence? major factor in?

A
  • causes endothelial injury or dysfunction
  • formation of countercurrents and local pockets of stasis, major factor in the formation of DVTs (deep vein thrombosis, often in legs)
39
Q

describe stasis AND turbulence?

A
  • promote endothelial activation
  • platelets and WBCs in contact with endothelium
  • slows dilation of activated clotting factors
  • impedes inflow of clotting factor inhibitors
  • BF slows down
40
Q

two types of hypercoagulability

A

1) primary (genetic)

2) secondary (acquired)

41
Q

define hypercoagulability

A

infrequent contributor to arterial or intracardiac thrombosis
**important risk factor for venous thrombosis

42
Q

primary (genetic) hypercoagulability is most often caused by?

A

mutations in factor 5 and prothrombin genes

43
Q

Leiden mutation= factor ____ mutation

A

5

44
Q

factor 5 becomes resistant to what in a Leiden mutation?

A

protein C

45
Q 
\_\_\_\_% of Caucasians carry a specific factor
V mutation (Leiden mutation).
A

2-15%

46
Q

G to A single-nucelotide substitution of the

prothrombin gene increases?

A

prothrombin transcription

47
Q

G to A single-nucelotide substitution of the

prothrombin gene is in ____% of population

A

1-2%

48
Q

People are more at risk for a G to A single-nucelotide substitution of the prothrombin gene mutation when?

A

pregnant, prolonged bedrest, long plane rides

49
Q

primary (genetic) hypercoagulability has less common inherited deficiencies concerning?

A

anticoagulents

  • antithrombin 3
  • protein C
  • protein S
50
Q

Congenitally elevated levels of homocysteine > ____ and ____ thromboses

A

arterial and venous thromboses

51
Q

primary (genetic) hypercoagulability are present with ____ thromboses and?

A

Present with venous thrombosis and recurrent thromboembolism

52
Q

secondary (acquired) hypercoagulability is associated with other disease states such as:

A

■ Cardiac failure or prolonged bed rest (stasis)
■ Surgery or trauma (vascular injury)
■ Estrogen (increase hepatic production of coagulation factors and decrease production of antithrombin III)
■ Cancer (procoagulant tumor products)
■ Advanced age (increase platelet aggregation and decrease release of prostacyclin (PGI2)
■ Smoking
■ Obesity

53
Q

Heparin-induced thrombocytopenia (HIT)

syndrome and Anti-phospholipid antibody syndrome are primary or secondary hypercoagulability?

A

secondary (acquired) hypercoagulability

54
Q

Heparin-induced thrombocytopenia (HIT)

syndrome:

A

■ 5% of patients treated with unfractionated heparin.
■ Autoantibodies bind complexes of heparin and platelet membrane protein.
■ Cross-react with similar complexes on platelets and endothelial cells → platelet aggregation, activation, consumption and endothelial cell injury.

55
Q

Anti-phospholipid antibody syndrome

A 
■ Thromboses, miscarriages, cardiac valve
vegetations and thrombocytopenia.
■ PE, pulmonary HTN, stroke, bowel
infarction or renovascular HTN.
■ Renal microangiopathy → renal failure.
56
Q

Anti-Phospholipid Antibodies bind to what to create a hypercoagulable state

A

Bind to beta-2 glycoprotein I and prothrombin → hypercoagulable state

57
Q

In vitro Anti-Phospholipid Antibodies interfere with phospholipids causes an inhibition of?

A

inhibit coagulation

58
Q

what creates False-positive serologic test for syphilis?

A

Anti-Phospholipid Antibodies

59
Q

In vivo Anti-Phospholipid Antibodies interfere with phospholipids promotes?

A

promotes coagulation

60
Q

T or F… Anti-Phospholipid Antibody Syndrome has primary and secondary forms.

A

true

61
Q

secondary form of Anti-Phospholipid Antibody Syndrome is associated with?

A

associated with an autoimmune

disease (SLE)

62
Q

primary form of Anti-Phospholipid Antibody Syndrome is associated with?

A

only exhibit manifestations of

hypercoagulable state.

63
Q

Anti-Phospholipid Antibody Syndrome may appear following exposure to?

A

drugs or infections

64
Q

Anti-Phospholipid Antibody Syndrome may be noted in ____% of apparently normal individuals

A

5-15%

65
Q

treatment of Anti-Phospholipid Antibody Syndrome is?

A

Anticoagulation and immunosuppression

Pathology 1 (21 decks)

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