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ASPHO Lectures 2021 > Blood Coagulation Overview and Acquired Hemorrhagic Disorders > Flashcards

Blood Coagulation Overview and Acquired Hemorrhagic Disorders Flashcards

1
Q

What are the natural coagulation inhibitors?

A
  • Tissue factor pathway inhibitor (TFPI)
  • Antithrombin
  • Protein C
  • Protein S
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2
Q

What does antithrombin inhibit?

A

Mainly thrombin and factor Xa, other plasma proteins

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3
Q

What converts protein C to it’s activated form?

A

Thrombin

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4
Q

Other name for thrombin?

A

Factor IIa

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5
Q

What does protein C inhibit, along with protein S?

A

Factor Va and Factor VIIIa

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6
Q

Catalysts of the coagulation cascade?

A

Factor V and Factor VIII

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7
Q

Which antithrombotic factors are made in endothelial cells?

A
  • Protein S

- Tissue plasminogen activator (TPA)

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8
Q

What is the inhibitor of TPA?

A

Plasminogen activator inhibitor 1 (PAI-1)

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9
Q

What compound acts with antithrombin to inhibit thrombin and factor Xa?

A

Heparin SULFATE

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10
Q

Main enzyme in fibrinolytic pathway? What is it converted to?

A

Plasminogen –> Plasmin

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11
Q

Plasmin along with what compounds lyses clots?

A

tPA

uPA (in the urine)

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12
Q

What does plasmin dissolve clots into?

A
  • Fibrin split products

- D-dimer

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13
Q

Inhibitor of Plasmin?

A

alpha2-antiplasmin

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14
Q

What is TAFI? what does it get converted to? What does it inhibit?

A
  • Thrombin activatable fibrinolysis inhibitor–> TAFIa

- Inhibits plasmin ability to dissolve clots

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15
Q

Which fibrinolytic proteins can have rare congenital deficiency states? What are they associated with in theory?

A
  • Plasmin
  • tPA

-Thrombosis

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16
Q

What fibrinolytic inhibitors can be deficient in rare congenital disorders? What are they associated with?

A
  • PAI-1*
  • alpha-2 antiplasmin
  • Associated with bleeding
  • *PAI-1 deficiency found effect in Amish, mucocutaneous bleeding and bruising
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17
Q

What are the antifibrinolytic drugs? What are they biochemically? How do they work?

A
  • Epsilon-aminocaproic acid
  • Tranexamic acid
  • amino acid analogs of lysine
  • inhibit fibrinolysis by blocking plasmin’s binding site for fibrin
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18
Q

How does plasmin work in fibrinolysis?

A

Recognizes exposed lysine residues on fibrinogen

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19
Q

Which factor deficiency does not cause a prolonged PTT and PT?

A

Factor XIII

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20
Q

Which factors does PTT measure?

A 
Intrinsic pathway = 
-Contact factors
--PK
--HWMK
--FXI
--FXII
-Factor VIII
-Factor IX
Common pathway = 
-Factor X
-Factor V
-Prothrombin (Factor II)
-Fibrinogen
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21
Q

Which factors does PT measure?

A 
Extrinsic pathway=
-Factor VII
Common pathway = 
-Factor X
-Factor V
-Prothrombin (Factor II)
-Fibrinogen
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22
Q

Which test assess presence and function of fibrin? Which disorders is it abnormal in? Which disorder in particular is it helpful in, and why?

A
  • Thrombin Time
  • Hypofibrinogenemia
  • Afibrinogenemia
  • Dysfibrinogenemia - fibrinogen level might be normal, but thrombin time abnormal
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23
Q

If PTT is normal and PT is prolonged, which factor deficiency?

A

Factor VII

24
Q

What assays do you use to measure factor XIII deficiency?

A
  • Urea clot lysis assay (qualitative only; only abnormal in seveere deficiency)
  • Chromogenic assay (Quantitative but only available in selected laboratories)
25
Q

What does vitamin K do to PIVKA (protein induced in vitamin K absence) factor precursors?

A

Adds a second carboxyl (COOH) group in the gamma position and makes them functional

26
Q

Which test comes back very high in Vitamin K deficiency?

A

Protein induced in vitamin K absence (PIVKA)

27
Q

How does warfarin work?

A

it inhibits Vitamin K Epoxide Reductase

28
Q

What does vitamin K epoxide reductase do?

A
  • Converts Vitamin K epoxide back to Vitamin K

- Converts Vitamin K to Vitamin K hydroxyquinone

29
Q

What is the INR?

A

A mathematical calculation of the PT based on the sensitivity of the PT reagent the lab uses

30
Q

What can lead to an early rapid rise in the INR? Why does this happen?

A

Decrease in factor VII due to half life of 3-6hours

31
Q

How long does therapeutic warfarin effect take? Why?

A
  • 5-7 days
  • When factor X level falls
  • Factor X has half life of 40 hours
32
Q

Vitamin K dependent factors?

A

II, VII, IX, X, Protein C and Protein S

33
Q

Why does warfarin-induced skin necrosis develop?

A

Drop in protein C early after warfarin initiation

34
Q

Effects of desmopressin?

A
  • Increases vWF
  • Increased FVIII (probably due to increased vWF)
  • Increases tPA release
35
Q

What do the PT, PTT, TT rely on?

A

Sample has proper ratio of plasma to citrate (9:1)

36
Q

What will happen to the PT, PTT and TT if there is too little plasma in the sample? What are causes of this?

A

-Elevated levels

  • Tube not properly filled
  • Patient has polycythemia
37
Q

What will happen to the PT, PTT and TT if there is too much plasma? What can cause this?

A
  • Falsely normal

- Anemia

38
Q

Pre-analytic factors that can lead to a falsely elevated PT, PTT or TT?

A
  • Sample not processed quickly (temperature artifact)
  • Difficult lab draw (sample begins to clot consuming the factors)
  • Heparin in sample (Use heparin neutralization procedure)
39
Q

Important limitations for PT, PTT as pre-op tests?

A
  • screen for factor deficiencies but NOT bleeding - e.g. no bleeding in Factor XII deficiency but very prolonged PTT, severe bleeding in factor XIII deficiency but normal screening
  • Subject to false positives
  • Can be truly abnormal, but no increased risk for bleeding e.g. lupus anticoagulant
40
Q

Which factors are acute phase reactants?

A
  • Factor VIII
  • vWF
  • Fibrinogen
41
Q

Mechanism by which DIC causes bleeding?

A

Consumption of prohemostatic clotting factors and platelets

42
Q

Mechanisms by which DIC causes thrombosis?

A
  • Consumption of anticoagulant clotting factors

- Disruption of endothelial cell anticoagulant surface

43
Q

Typical causes of DIC in children?

A
  • Sepsis
  • Kasabach-Merritt syndrome (unique to neonates)
  • Trauma (brain, burns, gunshot wounds)
  • Malignancy (APML)
  • Severe hemolysis
  • Severe protein C deficiency (unique to neonates)
44
Q

What does severe protein C deficiency cause in neonates?

A

Purpura fulminans

  • skin necrosis due to microvascular thrombosis
  • acute onset
45
Q

In addition to bleeding and thrombosis, what other symptom comes with DIC?

A

Hemolytic anemia

46
Q

Diagnosis of DIC?

A

-No one lab test

  • Common lab findings (none required):
  • -Prolonged PT and PTT
  • –Any clotting factor can be reduced
  • -Decreased fibrinogen
  • -Thrombocytopenia
  • -Elevated fibrin degradation products, d-dimer, fibrinopeptide A and B
  • Decreased protein C and S and antithrombin
47
Q

Why are neonates slightly more at risk for DIC?

A

-Physiologically deficient in proteins C/S and antithrombin - impairs their protective mechanisms for DIC

48
Q

Treatment of DIC?

A

-Treating the underlying disease is the main therapeutic option (and this will be the exam answer - e.g. antibiotics for sepsis)

49
Q

Management of coagulopathy in DIC?

A
  • No clear consensus
  • Platelet transfusion not generally indicated (risk for increasing thrombosis)
  • FFP
  • -Provides balanced replacement of all prohemostatic clotting factors and their inhibitors (standard risks for FFP)
  • -No evidence if it affects outcome
  • Cryo
  • -Can be given for low fibrinogen (if bleeding occurs)
  • -No clear evidence of benefit (standard risks for cryo)
  • Anticoagulation is NOT indicated
50
Q

Factors leading to vitamin K deficiency?

A
  • Fat soluble
  • Tissue stores limited - can become deficient quickly
  • Human milk has little to no vitamin K
51
Q

Lab findings in early and classical vitamin K deficient bleeding?

A
  • PT and PTT very prolonged (often unclottable,i.e. >200 seconds)
  • In less severe cases, PT can be as long or longer than PTT (absence of factor VII)
  • Vitamin K dependent factors (II, VII, IX, X, Pn C, PnS) severely deficient
52
Q

Lab findings in late vitamin K deficient bleeding?

A
  • PT is always prolonged (factor VII has the shortest half life)
  • PTT is variably prolonged (depends on severity)
  • Vitamin K dependent factors deficient
  • Elevated PIVKA (sent only if diagnosis is in question)
53
Q

Treatment of VKDB? How long does it take to correct the deficiency?
What to give if need to give something immediately due to bleeding?

A
  • Oral/parenteral Vit K (Phytonadione/Vit K1)
  • 12-24 hours after a parenteral dose to correct the deficiency
  • Prothrombin complex concentrates
  • -Plasma-derivd products containing factors II, VII, IX and X
  • -Can be given if immediate correction is warranted (ICH)
  • -Carries a risk for thrombosis
54
Q

What can cause prolonged severe coagulopathy if accidentally ingested? Treatment?

A
  • Pesticides (rats, mice)
  • Contain warfarin-like drugs that are more potent and with much longer half-lives than human warfarin (weeks)
  • Treatment is prolonged therapy with vitamin K (until poison cleared)
55
Q

Mechanisms responsible for bleeding in liver disease?

A
  • Decreased production of liver synthesize factors
  • -most factors decreased
  • -FVIII elevated (Acute phase reactant and not made in liver)
  • Thrombocytopenia
  • -Various causes
  • –Hypersplenism (e.g. with portal vein hypertension)
  • –Decreased TPO production (made in hepatocytes)
  • Hyperfibrinolysis
  • -Increased tPA release from endothelial cells
56
Q

Lab features of liver disease?

A
  • Elevated PT (early marker, short half life of Factor VII)
  • Elevated PTT (decreased production of most other factors)
  • Low fibrinogen (varies with severity of liver failure)
  • -Can be high as acute phase reactant
  • Thrombocytopenia
  • Elevated D-dimer
  • -Liver clears D-dimers
  • -Hyperfibrinolysis
57
Q

Treatment for bleeding in liver disease?

A
  • FFP (contains all plasma clotting factors)
  • Cryoprecipitate (to correct low fibrinogen; has factor VIII, vWF, factor XIII and fibrinogen)
  • Platelet transfusions
  • rFVIIa (useful if Factor VII particularly low)
  • PCCs
  • -Contain all VKD factors
  • -Cases of thrombosis have been reported with PCC use in liver failure - ABP outline states contraindicated in the treatment of bleeding due to liver disease!)

ASPHO Lectures 2021 (10 decks)

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