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SBB > Hemostasis and Coagulation > Flashcards

Hemostasis and Coagulation Flashcards

1
Q

aPTT

A

activated partial thromboblastin time

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2
Q

aPTT ingredients

A

1 part citrated plasma 1 part

silica contact activator plus phospholipid- incubate at 37 degrees for 5 minutes and then 1 part add calcium ions

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3
Q

PT

A

prothrombin time

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4
Q

PT ingredients

A
  1. citrated plasma to 2 parts calcium, phospholipid and tissue factor
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5
Q

what does aPTT test for?

A

2, 8, 9, 10, 11. Heparin therapy, lupus anticoagulant, hereditary or acquired deficiency, severe liver disease.

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6
Q

what does PT test for

A

2, 5, 7, 10. Warfarin therapy, vitamin K deficiency, liver disease, factors or assay inhibitors

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7
Q

Vitamin K dependent factors

A

2-7-9-10

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8
Q

Cortifact

A

drug for factor XIII deficiency

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9
Q

Factor VIII deficiency treatment

A

recombinant factor VIII or virus inactivated monoclonal antibody purified plasma derived factor VIII products.

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10
Q

GP1b

A

binds to vWF on exposed collagen - primary hemostasis

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11
Q

GPIIb/IIIa

A

binds to fibrinogen to form bridge between other platelets (complex: Gp2b/3a-fibrinogen-Gp2b/3a)

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12
Q

vwbF- what it is and what it does, where is is

A

von willebrand factor mediates platelet adherence to injured vessel wall by binging collagen and platelet receptor complex (Gp1b/V/IX) binding causes platelets to degranulate and attract more platelets. Von Willebrand factor is synthesized in the walls of the blood vessels and circulates freely in the blood in a folded form. When it encounters damage to the wall of a blood vessel, particularly in situations of high velocity blood flow, it binds to the collagen beneath the damaged endothelium and uncoils into its active form.

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13
Q

ADAMTS13

A

cleaves ULvwF multimers- if not cleaved, promotes platelet aggregation-microthrombi

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14
Q

List the Intrinsic pathway for coagulation

A

12 activates 11-(with ca)11a, which activates 9-(with ca)9a, 8+9= activation of 10a(with PS and Ca), 10+5=2-2a(with PS and Ca)- activates fibrinogen to soluble fibrin. 13 crosslinks fibrin

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15
Q

List extrinsic (trauma) coagulation cascade

A

Vascular injury- exposed Tissue Factor- activates VII-VIIa, this complex TF-VIIa activates 10- 10 and 5 make 2(with PS and Ca), activates prothrombin-thrombin and fibrinogen to fibrin, XIII- crosslinks fibrin

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16
Q

Heyde’s syndrome

A

aortic stenosis, the stenotic aortic valve becomes narrowed. Blood flow rate is increased to make up for the narrowing, the combination of narrowing and increased flow rate causes sheer stress which causes vWF to unravel like it does when it senses capillary vessel trauma, cleaved by ADAMTS13, the amount of (inactivated) vWF in the blood decreases and therefore bleeding increases. due to angiodysplasia- causes GI bleeds

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17
Q

angiodysplasia

A

small vascular malformation in the gut

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18
Q

Primary hemostasis

A

formation of the platelet plug due to platelet binding and aggregation

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19
Q

Secondary hemostasis

A

coagulation cascade- ending in crosslinking and stabilization of fibrin. Triggered by Tissue Factor released from epithelial cells with vascular trauma.

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20
Q

Tertiary hemostais

A

Fibrinolysis

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21
Q

Which part of primary hemostasis effects secondary hemostasis

A

Primary hemostasis creates Phospholipid which is used in some of the steps within the coagulation cascade.

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22
Q

gla

A

Gamma carboxyl glutamate residues on 2,7,9,10, these residues are formed by vitamin K dependent enzymes and facilitate calcium dependent complex binding to phospholipid membranes

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23
Q

which coagulation factor has the shortest half-life

A

VII, 5-8 hours, this is why FFP needs to be frozen in 8 hours. more than 8 hours, half the VII is left.

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24
Q

PCC

A

prothrombin complex concentration, factor 9 complex, medication 2,9, 10. some version contain factor 7 as well.

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25
Q

Hemophilia B

A

factor 9 deficiency”christmas disease”- joint bleeding,

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26
Q

Treatment for hemophilia B

A

PCC, recombinant factor IX- recombinant- animal derived.

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27
Q

Choice for material replacement: Fibrinogen

A

Cryo, FFP, fibrinogen concentrate

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28
Q

Choice for meterial replacement : Prothrombin

A

PCC, FFp

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29
Q

Factor 5 choice for material replacement

A

FFP

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30
Q

Factor7 choice for material replacement

A

FVIIa, FFP PCC (if it contains factor VII)

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31
Q

Factor 8 choice for material replacement (secondary name for Factor 8)

A

antihemolytic factor=factor 8, choice for material replacement= Factor VIII concentrate, rFVIII (recombinant factor VIII= drug of choice)

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32
Q

Factor 9 alternate name and choice for material replacement

A

Christmas factor and Factor 9 concentrate, rFIX, PCC

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33
Q

Factor 10 alternate name and choice for material replacement

A

Stuart factor, PCC, FFP

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34
Q

XII alternate name and choice for material replacement

A

Hageman factor and not necessary for replacement, no history of bleeding with this factor deficiency, will show a prolonged aPTT but invivo functionality is normal without this factor.

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35
Q

Non correction with plasma mixing studies

A

denotes an inhibitor, factor deficiency corrects, and stays corrected

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36
Q

Immediate correction with plasma mixing studies

A

Due to factor deficiency

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37
Q

Slow correction

A

Could be due to time sensitive inhibition.

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38
Q

Factor XIII alternate name and choice for material replacement

A

fibrin stabilizing factor, cryoprecipiate and FFP

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39
Q

vWF choice of replacement

A

Cryo, humate-P

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40
Q

humate P

A

used in treatment of vWF deficiency, combination of antihemolytic factor(VIII) and vWF complex, purified from pooled human plasma

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41
Q

HMWK

A

high molecular weight kininogen

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42
Q

Tissue Factor deficiency

A

Factor III, this is a trick question there is no such thing as TF deficiency- no known examples causing the industry to imagine that if this were a possible deficiency it is probably incompatible with life and this is why we don’t see it.

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43
Q

Plasmin

A

the active form (plasminogen is the inactive form) o

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44
Q

INR

A

international normalized ratio. used to standardize PT between different labs. INR= (PTpatient/PTcontrol)^ISI

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45
Q

ISI

A

international sensitivity index- varies between different PT reagents

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46
Q

Thrombin Time what does it measure

A

Time to fibrin clot formation, this bypasses clotting cascade

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47
Q

Thrombin Time what is involved in the testing

A

Bovine thrombin added to patient plasma

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48
Q

Elevated TT: what does it tell you

A

Heparin, Low or dysfunctional fibrinogen, DIC due to high D Dimer consumption

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49
Q

Reptilase time

A

Like thrombin time but uses snake venom, this is insensitive to heparin.

50
Q

Half life of Factor VII

A

shortest half time (5-8 hours) requirement for plasma to be frozen within 8 hours.

51
Q

Half life of Factor VIII

A

8-12 hours

52
Q

plasminogen

A

inactive form of plasmin, is produced by the liver

53
Q

TPA

A

Tissue plasminogen activator, along with urokinase converts plasminogen to active form Plasmin

54
Q

Where does TPA come from

A

TPA is released slowly into blood from damaged blood vessels, so that once bleeding has stopped it’s able to activate plasminogen and break down clots

55
Q

Plasminogen in clot

A

plasminogen gets stuck inside of the clot so when it’s activated to plasmin it is able to breakdown fibrin mesh

56
Q

D-Dimer

A

fibrin degradation product

57
Q

PAI

A

plasminogen activator inhibitor- inhibits TPA

58
Q

D-Dimer or TT which is more specific

A

more specific that TT

59
Q

Mixing studies

A

Mixes 1:1 with patient plasma and normal plasma, should allow a minimum of 50% factor activity, need approximately 30% to have normal PT/PTT

60
Q

At what points (time) do you asess the PT and PTT during mixing studies

A

0 minutes and 90 minutes

61
Q

Correction at 0 minutes and 90 minutes

A

indicates factor deficiency

62
Q

Correction at 0 minutes but not 90 minutes

A

indicated time/temperature dependent inhibitor

63
Q

No correction at 0 minutes or 90 minutes

A

Inhibitor (hepain, lupus anticoagulant)

64
Q

Unfractionated heparin

A

Binds antithrombin and accelerates it’s action against factor II (thrombin)

65
Q

What tests does unfractionated heparin prolong

A

PTT and TT

66
Q

unfractionated heparin is reversed with

67
Q

LMWH

A

low molecular weight heparin (Enoxaparin example) binds antithrombin and preferentially inactivates factor Xa. small amount binds to thrombin

68
Q

LMWH effect on PTT

A

usually does not affect PTT, needs to be montitored with anti-Xa levels

69
Q

Warfarin (Coumadin)

A

Prevents vitamin K dependent factors from being synthesized (2, 7, 9 10, protein C and S)

70
Q

Reversal of warfarin

A

Reversal with FFP, vitamin K and PCCs ( prothrombin complex concentration)

71
Q

Direct thrombin inhibitors

A

Directly binds to thrombin and inhibit it’s interaction with fibrin IV(bivalirudin, argatroban) oral (dabigatran)

72
Q

Monitoring direct thrombin inhibitors

A

PTT. thromin time is too sensitive, only necessary for IV not oral, dilute thrombin time.

73
Q

Reversal agent for direct thrombin inhibitors (oral)

A

Idarucizumab- FDA recently approved first reversal agent for Dabigatran

74
Q

Direct Factor Xa inhibitors

A

inhibits both free and bound Xa (Rivaroxaban, apixaban, edoxaban)

75
Q

Monitoring direct factor Xa inhibitors

A

anti-Xa if necessary, “heparin assay”

76
Q

Reversal agent for direct factor Xa inhibitor

A

no reversal agent yet.

77
Q

Hemophelia A

A

Factor VIII deficiency, x-linked recessive, most common severe hereditary bleeding disorder

78
Q

Classification of severity based on factor levels

A

<1% severe 1-5% moderate >5% mild

79
Q

Risk of providing factor replacement products

A

patient may develop antibodies against infused factors.

80
Q

Recombinant Factor VIII or IX

A

recombinant products are safer tahn concentrates. PCC (for IX) FFP and CRYO, both are acceptable but no longer used due to better alternatives

81
Q

Novo7

A

recombinant factor VII, for high titer inhibitor

82
Q

vWF where is it made

A

synthesized in endothelial cells and megakaryocytes

83
Q

vWF what it does

A

carrier for factor VIII, essential for interaction of platelets with damaged endothelium, binds to GP1b on surface of platelet

84
Q

vWF levels based off blood type

85
Q

bleeding risk when vWF is at what level?

86
Q

Lab tests for quantity of vWF

A

platelet function analysis (PFA100), Ristocetin cofactor activity, vWF antigen and activity levels (diagnose disease) and vWF multermer analysis (type)

87
Q

vWF disease

A

congential or acquired, classification 3 types 1) Partial quanitative deficiency 2) Qualitative deficiency 3) severe quantitative deficiency

88
Q

Therapy fro vWF disease

A

DDAVP (desmopressin) causes release of vwf from endothelial cells and platelets. Cryo- contains vwf Humate P- Factor VIII concentrate and vwf

89
Q

BiG differences in vwd and hemophelia A (VIII)

A

vwf- abnormal PFA100 and RIPA where factor VIII is normal. aPTT is increased in VIII deficiency but normal in vw disease. Decreased vwf:Ag in vw disease

90
Q

DIC

A

Disseminated intravascular coagulation, continual activation of the clotting and fibrinolytic cascades: Fibrin formation=Clotting, consumptive coagulopathy=bleeding

91
Q

Lab results of DIC

A

prolonged PT and PTT, decreased fibrinogen, increased D-Dimer, low platelet count, schistocytes

92
Q

D-Dimer

A

crosslinked fibrin molecule fragment

93
Q

Clinical associations with DIC

A

sepsis, tissue injury (trauma, surgery, burn), obstetric complication (eclampsia, placental abruption) Malignancy-leukemia, intravascular hemolysis (HTRN) cardiovascular (aortic aneurysm), miscellaneious- snake bite, heat stroke, liver disease, severe anorexia, severe acidosis.

94
Q

Treatment of DIC

A

treat underlying cause: plasma, cryo, heparin(clotting more than bleeding), anti-fibrinolytics (amicar)

95
Q

anti-fibrinolytics

A

Amicar (bleeding more than clotting in DIC)

96
Q

Cause of Elevated D-dimer

A

DIC, infection, active bleeding, thrombosis, tissue injury/surger, liver dysfunction, neoplasia

97
Q

Thrombotic Thrombocytopenic purpura symptoms

A

Fever, thrombocytopenia, microangiopathic, hemolytic anemia (schistocytes, increased reticulocyte count, increased LDH and bilirubin, low haptoglobin) Neurologic symptoms-altered mental status, renal insufficiency

98
Q

Cause of TTP

A

deficiency or inhibitor of ADAMTS-13 congenital or acquired

99
Q

Treatment of TTP

A

plasma exchange or transfusion, steroids, rituximab, platelet transfusion IS CONTRAINDICATED!! will cause thrombosis

100
Q

HIT

A

heparin induced thrombocytopenia- decreaesd platelet count after exposure to heparin count usually 50-60 K/mL or 50% of baseline. More common with unfractionated heparin but can also occur with low molecular weight heparin (enoxaparin)

101
Q

cause of HIT

A

Antibody against heparin+ PF4

102
Q

risks associated of HIT

A

high risk of thrombosis- arterial or venous

103
Q

Treatment

A

discontinue all heparin, direct thrombin inhibitors (bivalirudin, argatroban), platelets are containdicated!!!

104
Q

ITP

A

immune thromboctyopenic purpura- severely decreased platelet counts- usually <10K/mm3.

105
Q

Antibody involved in ITP

A

usually anti- GPIIB/IIIA, unclear etiology

106
Q

Treatment for ITP

A

Steroids, IVIG, Splenoctomy, platelet transfusion- risk is for bleeding not thrombosis (as in HIT and TTP)

107
Q

PFA-100

A

platelet function assay, pushes patient blood through reusable cartridge coated with Collagen and ADP- causes clot formation and aperture to close. People with VW disease have abnormal PFA-100

108
Q

RIPA

A

ristocetin induced platelet aggregation. uses patients live endogenous platelets- detect interaction between vWF and GP1B/V/IX. abnormal in patients with vWF

109
Q

DIC abnormal lab values

A

increased D dimers, Decreased platelets decreased fibrinogen. Prolonged PT and aPTT, schistocytes present. All is due to the continuous activation of clotting and fibrinolytic cascades

110
Q

MAHA

A

microangiopathic hemolytic anemia: schistocytes, increased retic count, increased LDH and bilirubin and low haptoglobin

111
Q

Lupus anticoagulant

A

anti-phospholipid antibody found in lupus patients

112
Q

Danaparoid

A

mixture of naturally occuring heparan sulfate, dermatan, chondoitin, alternative anticoagulant to HIT

113
Q

aRGATROBAN

A

anticoagulant, inhibitor of thromibin, given as alternative to HIT

114
Q

Fondapainux

A

anticoagulant amnagement of HIT

115
Q

bivalrudin

A

anticoagulant management of HIT

116
Q

what drugs can be given instead of heparin in HIT

A

Danaparoid, argatroban, fondapainux, bivalrudin

117
Q

HIT causation, why clot?

A

upon receiving heparin, can form antibodies against heparin and PF4- platelet factor 4, this causes antibodies to bind to platelets and activate them releasing procoagulatory particles that cause thrombosis (specifically bind to FcjRIIIa on platelets)

118
Q

What has a high association with HIT?

A

cardiac surgery patients.

119
Q

Cryo reduced plasma

A

after cyro is made, this is for TTP exchange fluid use

120
Q

When patient with Liver disease what coag factors are decreased

A

all except factor 8

121
Q

When patient has DIC which factors are decreased?

A

all factors are decreased

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