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I3 Exam 1 > Coagulation Lecture Mauro > Flashcards

Coagulation Lecture Mauro Flashcards

1
Q

What is the vascular response to damage?

A

vasoconstriction to cause narrowing to reduce blood flow

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2
Q

What occurs during primary hemostasis?

A

the formation of the platelet plug

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3
Q

What occurs when endothelium is damaged

A

when endothelium is damaged it exposes collagen, VWF, and tissue factor

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4
Q

What is the first step in primary hemostasis

A

platelets will undergo platelet adhesion and combine the GP1b/IX to the vWF that is incorporated into the subendothelium

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5
Q

What occurs after the platelets undergo a shape change?

A

release granules = ADP, TXA2, serotonin, fibrinogen

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6
Q

How do platelets undergo adhesion?

A

as other platelets get recruited they expose GP11b/IIIa complex and link to fibrinogen to form the platelet plug

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7
Q

What does secondary hemostasis do?

A

Forms fibrin scaffolding that will help bind the platelet plug to keep it on the site of injury

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8
Q

Where is tissue factor release from

A

the subendothelium at the site of injury

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9
Q

What starts the coagulation cascade

A

release of the TF from the subendothelium in the extrinsic pathway and TF will also help start the intrinsic pathway by activating 9 to 9A
- once you have a small amount of thrombin produced by extrinsic pathway and this will go back and help activate the intrinsic pathway with 9, 11, cleaving of 8 from VWF

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10
Q

What does increased production of thrombin lead to

A

more intrinsic pathway activation

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11
Q

Which factor helps with platelet activation?

A

Factor Xa and it also helps with exposure of phospholipids on platelet surface

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12
Q

What does anti-thrombin do

A

circulating plasma protease inhibitor that neutralizes factors

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13
Q

Activated protein C

A

in the presence of protein S, can help neutralize 8a and 5a

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14
Q

TFPI

A

circulating in blood, inhibits and neutralizes Xa and TF:VIIa

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15
Q

What increases when heparin is given?

A

concentration of TFPI

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16
Q

What does fibrinogen do?

A

Finds to the fibrin clot via exposure of lysine residues

and gets converted to plasmin

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17
Q

What does plasmin do

A

starts breaking up fibrin clots and release degradation products including D-dimer

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18
Q

PAI

A

Plasminogen activator inhibitor

  • released by the endothelium
  • inhibits plasminogen to plasmin actiation
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19
Q

Alpha 2 antiplasmin

A

released by some of the platelets

- inhibits plasmin activation

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20
Q

TAFI (thrombin activatible fibrinolysis inhibitor)

A

removes lysine residues

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21
Q

What is a normal platelet count

A

normal 150,000-400,000 microL

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22
Q

Thrombocytopenia with prolonged bleeding

A

when platelets drop below 100,000

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23
Q

When are platelets below 50,000 a concern?

A

before surgery

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24
Q

What is the platelet count at which we are worried about spontaneous bleeding

A

below 10,000

*hemorrhage

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25
Q

What does PT test look at

A

looks at extrinsic and final common pathway

  • see how well the factors in the extrinsic and final common pathway are acting
  • factor VII, X, V, thrombin, fibrinogen
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26
Q

What does PTT test look at

A

looks at intrisic and final common pathway

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27
Q

Mixing studies

A
  • take part of patients blood and add it to normal blood and remeasure whatever test is prolonged
  • if you’re only looking at a factor deficiency, the test will normalize
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28
Q

If you do mixing study and it doesn’t correct, what is the issue in the blood?

A

you have an inhibitor - an antibody that is preventing the factors from acting appropriately
- you can tell the strength of an inhibitor based upon how much normal blood you have to add to normalize your blood

29
Q

What is a d-dimer

A

fibrin monomer, part of the fibrin degradation products

30
Q

When is d-dimer elevated

A

presence of clot turnover, marker of fibrinolysis, and a marker of recent/ongoing blood coagulation

31
Q

What is measured in the intrinsic pathway

A

PTT - partial thromboplastin time

32
Q

What is measured in the extrinsic pathway

A

PT - prothrombin time

33
Q

If you have a prolonged PT and the mixing study corrects then you have a deficiency in:

A

you have a factor deficiency (factor VII), vitamin K deficiency, or liver disease

34
Q

What is vitamin k required for?

A

post-translational modification of factors II, VII, X, PC, PS

35
Q

What is the first thing that drops with vitamin K deficiency

A

factor VII so you develop long PT first

36
Q

coumadin

A

blood thinner

  • inhibits vitamin K
  • monitor with PT
37
Q

What can lead to vitamin K deficiency

A

antibiotics, malnutrition, and coumadin

38
Q

liver disease

A

all of the proenzymes are created in the liver

  • decreased production of factors
  • factor VII is the most sensitive
  • pt will prolong
39
Q

If you have a prolonged PTT and the mixing study corrects but you have no bleeding
then you have a deficiency in:

A

factor XII, pre-kallikrein, klinonogen

  • body can compensate and go around the initial step of the intrinsic system
  • tissue factor will activate lower down so you can bypass the upper step
40
Q

If you have a prolonged PTT and the mixing study corrects but you have bleeding
then you have a deficiency in:

A

factor XI, IX, VIII, vWD (because it can lower factor VIII)

41
Q

If you have a prolonged PTT and the mixing study doesn’t correct you have:

A
  • factor inhibitor of VIII, IX, XI
  • heparin
  • lupus anticoagulant - prolongs PTT and causes clotting
42
Q

lupus anticoagulant

A

prolongs PTT and causes clotting

- look for this in patient that is coming in with tons of clotting

43
Q

prolonged PT and PTT

A

deficiencies of final common pathway

  • severe vitamin K deficiency
  • severe liver disease
  • DIC (disseminated intravascular coagulation)
44
Q

What sort of defect will give you mucocutaneous bleeding

A

platelet defect

- oral cavity, nasal, GI, GU bleeding

45
Q

What sort of defect will give you excessive bleeding after cuts

A

primary hemostasis - platelet defect

- initial platelet cut is not forming

46
Q

What sort of defect will give you petechaie

A

primary hemostasis platelet defect

47
Q

What sort of defect will give you immediate bleeding with surgery

A

platelet defect, primary hemostasis

48
Q

What sort of defect will you deep tissue bleeding and joint and muscle bleeding

A

coagulation disorder, secondary hemostasis

- can make initial platelet plug

49
Q

What sort of bruising will you get with coagulation disorders and secondary hemostasis

A

large hematomas

50
Q

What sort of defect will give you delayed bleeding with invasive surgery

A

coagulation disorder, secondary hemostasis

  • not a stable clot after surgery
  • need fibrin scaffolding and you don’t have that and then you have hemmorhaging
51
Q

allo vs autoantibody

A

auto antibody - made it against your own body and allo antibody is making it against something foreign

52
Q

What are the symptoms of a patient with a fVIII inhibitor

A

ecchymoses, epistaxis, GI, hematuria, intracranial

53
Q

What is the treatment for a patient with FVIII inhibitor

A

give immunosuppression to suppress body’s response

  • give FEIBA which is a bypassing agent
  • give NOVO seven which ramps up the extrinsic system
54
Q

What is caused by a deficiency in factor VIII

A

hemophilia A

55
Q

what is caused by a deficiency in factor IX

A

hemophilia B

56
Q

What is hemarthrosis a symptom of

A

hemophilia

  • present first year of life
  • muscle bleeds
  • intracranial bleeds
  • dental bleeding
  • post surgery bleeding
57
Q

What is the treatment of choice for hemophilia

A

give factor: factor VIII or IX concentrates
or DDAVP in mild hemophilia A to stimulate release of FVIII from endothelium
- prophylaxis for surgery and for children to prevent spontaneous bleeds

58
Q

What does VWF do

A

helps bind the platelet to the subendothelium and carrier for FVIII and increases half life of FVIII

59
Q

What is the most common type of VWD

A

type 1 - partial quantitative deficiency of vWF

  • AD
  • vWF antigen low and activity low
  • fVIII low
60
Q

What is the treatment for type 1 vWD

A
  • DDAVP to release vWF and FVIII from endothelial cells

- intermediate purity FVIII concentrates

61
Q

What is DIC

A

diffuse activation of thrombin which leads to consumptive coagulopathy and secondary fibrinolysis

  • fibring degradation products can impact the whole clotting system
62
Q

What can cause DIC

A

thromboembolism, sepsis, malignancy/leukemia, pregnancy complications (exlampsia, HELLP, placental abruption), severe liver failure, trauma

63
Q

Symptoms of DIC

A

bleeding, renal and liver and pulm dysfunction, thromboembolism (arterial and venous)

64
Q

What are symptoms of pulm embolism

A

pleuritic chest pain, SOB, tachychardia, cough

65
Q

What does antiphospholipid antibody lead to

A

increases clotting and vascular tone

66
Q

What is the clinical criteria for APLS

A

arterial or venous thrombosis or pregnancy morbidity: unexplained fetal death, premature birth due to preeclampsia, 3 or more unexplained miscarriages

67
Q

What tests confirm lupus anticoagulant

A
  • prolonged PTT that doesn’t correct with mixing
  • proloned dRVVT assay that doesn’t correct with mixing
  • correction of clotting time by adding phospholipid
68
Q

What are the two syndromes that can cause both arterial and venous clotting

A

DIC and APLS

69
Q

FVL mutation

A

abolishes cleaving site of APC

- FVL has 20 fold slower degradation time than normal FV so extended thrombin generation

I3 Exam 1 (12 decks)

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