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IBI Test 3 > B3-049 Disorders of Coagulation > Flashcards

B3-049 Disorders of Coagulation Flashcards

1
Q

VWF is synthesized from

A

endothelial cells (stored in Weibel Palade bodies)
platelets (stored in alpha granules)

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2
Q

multimers that vary in molecular weight make up

A

VWF

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3
Q

VWF is processed in the plasma by

A

ADAMTS-13

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4
Q

protease that cleaves ultra large VWF multimers into smaller sizes

A

ADAMTS-13

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5
Q

functions in platelet adhesion and stabilization of factor VIII

A

VWF

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6
Q

fibrin meshwork stabilized by crosslinking

A

secondary hemostasis

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7
Q

platelet plug formation

A

primary hemostasis

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8
Q

factors of the extrinsic pathway

A

tissue factor
factor VII

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9
Q

factors of the intrinsic pathway

A

prekallikrein
HMWK
XII
XI
IX
VIII

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10
Q

factors of the common pathway

A

X
V
II (prothrombin)
I (fibrinogen)

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11
Q

fibrin stabilization factor

A

XIII

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12
Q

Vitamin K dependent coagulation proteins

A

II
VII
IX
X
C
S

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13
Q

required for post-translation gamma carboxylation of glutamic acid residues

forming gla

A

vitamin K

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14
Q

PFA-100 is screening test for which pathway

A

primary hemostasis

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15
Q

PTT is a screening test for which pathway

A

intrinsic

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16
Q

PT is a screening test for which pathway

A

extrinsic

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17
Q

causes of abnormal PT

A

liver disease
vitamin K deficiency
warfarin

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18
Q

how to calculate INR

A
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19
Q

common causes of abnormal PTT

diseases

A

hemophilia A and B
vW disease
heparin
severe liver disease
severe vitamin K deficiency
warfarin

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20
Q

causes of prolonged thrombin time

molecular level

A

Low fibrin
dysfibrinogenemia
thrombin inhibitors
fibrin monomer polymerization inhibitors

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21
Q

fibrin degradation can be quantified using

A

D-dimer

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22
Q

D dimer has [high/low] sensitvitiy

A

high for DIC
low for inhierited disorders of increased fibrinolysis

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23
Q

D dimer has [high/low] specificity

A

low

positive in any disorder that produces intravascular clot

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24
Q

D-dimer has a [high/low] negative predictive value

A

high for PE

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25
Q

bleeding within skin or mucous membranes

A

purpura

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26
Q

pinpoint bleeding of skin or mucous membranes

A

petechiae

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27
Q

large confluent area of bleeding within skin, larger than petechiae

A

ecchymosis

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28
Q

a collection of blood in an organ, space or tissue

A

hematoma

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29
Q

bleeding into the joint space

A

hemarthrosis

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30
Q

bleeding patterns consistent with primary hemostasis problem

A

skin/mucosal bleeds
purpura, petechiae, eccymosis
spontaneous bleeding

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31
Q

bleeding patterns consistent with an issue in secondary hemostasis

A

bleeds into soft tissue, muscle, joints
hemarthrosis
bleeding with trauma

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32
Q

partial quantititative deficiency

A

type 1 von willebrand

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33
Q

inheritance pattern of type 1 vWD

A

autosomal dominant

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34
Q

type 2vWD is [qualitative/quanitative]

A

qualitative

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35
Q

type 3 vWD is [quanitative/qualitative]

A

complete quantitative deficiency

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36
Q

inheritance pattern type 3 vWD

A

autosomal recessive

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37
Q

prolonged closure time on PFA-100
prolonged PTT

A

vWD

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38
Q

petechiae
ecchymosis
prolonged bleeding after tooth extraction

associated with what disease

A

vWD

hemarthrosis and hematomas in type 3 as well

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38
Q

petechiae
ecchymosis
prolonged bleeding after tooth extraction

associated with what disease

A

vWD

hemarthrosis and hematomas in type 3 as well

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39
Q

VWF concetrate, blood derivative (pathogen activated)

vWD treatment

A

humate P

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40
Q

good source of vWF, blood product (not pathogen activated)

vWD treatment

A

cryoprecipitate

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41
Q

stimulates endothelial cells to release remaining vWF stores

vWD treatment

A

desmopressin

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42
Q

venous thrombotic disorders are

A

inherited or acquired

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43
Q

arterial thromotic disorders are caused by

A

platelet and vessel wall abnormalities

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44
Q

major acquired risk factors for venous thromboembolism

A

major surgery/trauma
hx of thrombosis
lupus anticoagulant
pregnancy
cancer

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45
Q

anatomic locations of DVT/VTE

A

deep veins of legs
pulmonary arteries
cerebral, mesenteric, hepatic veins (Budd-chiari)

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46
Q

diagnosis of DVT/VTE

A

compression ultrasound of proximal leg veins
D- dimer
Venography

+1 if non compressible

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47
Q

pain, swelling, ulceration of affected leg

A

post thrombotic syndrome

DVT/VTE

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48
Q

clinical features of PE

A

dyspnea, wheezing
pleuritic chest pain
hemoptysis
right sided heart failure
hypoxemia

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49
Q

diagnosis of PE

A

spiral CT- high PPV
D dimer- high NPV
ventilation perfusion scan
pulmonary angiography

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50
Q

point mutation leading to decreased proteolytic inactivation by protein C

A

Factor V Leiden

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51
Q

Factor V Leiden has a high prevalence in

A

caucasians

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52
Q

activated protein C resistance

A

Factor V Leiden

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53
Q

point mutation in 3’ UTR leading to instability of mRNA

A

prothrombin gene mutation

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54
Q

causes increased prothrombin levels

disease

A

prothrombin gene mutation

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55
Q

prothrombin gene mutation has a high prevalence in

A

caucasians

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56
Q

decreased activation of FVa and FVIIIa

A

protein C and protein S deficiency

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57
Q

warfarin induced skin necrosis is caused by

A

heterozygous protein C and S deficiency

antithrombin deficiency

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58
Q

neonatal purpura fulminans is caused by

A

homozygous protein C and protein S deficiency

59
Q

decreased plasma protein C or protein S level

A

protein C and protein S deficiency

60
Q

decreased in vitamin K deficiency

A

protein C and S

61
Q

decreased inactivation of FX, FII

A

antithrombin deficiency

62
Q

resistant to heparin therapy

A

antithrombin deficiency

63
Q

homozygous state is incompatible with life

A

antithrombin deficiency

64
Q

decreased plasma antithrobin level

A

antithrombin deficiency

65
Q

autoantibodies against phospholipid binding proteins

A

antiphospholipid syndrome

66
Q

venous and arterial thrombosis

A

antiphospholipid syndrome

67
Q

venous thrombosis
arterial thrombosis
recurrent spontaneous pregnancy loss

A

antiphospholipid syndrome

68
Q

lab diagnosis of antiphospholipid syndrome

A

+anticardiolipin
or + anti-B2 glycoprotein I antibody
or + lupus anticoag test

69
Q

treatment for antiphospholipid syndrome

A

anticoagulant therapy

70
Q

autoantibodies against heparin-platelet factor 4 complex

causes platelet inactivation and thrombosis

A

heparin induced thrombocytopenia

71
Q

rank the types of heparin according to risk of
heparin induced thrombocytopenia

A

UFH>LMWH>fondaparinux

72
Q

4 T’s of heparin induced thrombocytopenia

A

Timing: 5-7 days after starting heparin
Thrombocytopenia- 50% decrease from baseline or below reference range
Thrombosis: venous or arterial
exclude oTher causes

73
Q

diagnosis of heparin induced thrombocytopenia

A

clinical
Heparin-PF4 antibodies
heparin induced activation assay

74
Q

treatment heparin induced thrombocytopenia

A

d/c heparin
use direct thrombin inhibitors

75
Q

consumptive coagulopathy

A

DIC

76
Q

major causes of DIC

A

infection related sepsis
ABO incompatible reaction
acute pancreatitis
septic abortion, AFE
APL
brain injury
trauma

77
Q

Clinicial features:
bleeding
thrombosis

A

DIC

78
Q

hyaline microthrombi of microvessels

A

DIC

79
Q

platelet and fibrin rich thrombi

A

DIC

80
Q

thrombocytopenia
prolonged PT, PTT
decreased fibrinogen
elevated D dimer

A

DIC

81
Q

microangiopathic hemolysis

shistocytes

A

DIC

82
Q

differential for DIC

A

other causes of MAHA
other causes of thrombocytopenia
other causes of coagulopathy

83
Q

thrombocytopenia
normal PT, PTT
normal fibrinogen

A

ITP, TTP, HUS, aHUS

84
Q

thrombocytopenia
increased PT, PTT
normal fibrinogen

A

cirrhosis

85
Q

thrombocytopenia
normal PT
elevated PTT
normal fibrinogen

A

heparin induced thrombocytopenia

86
Q

treatment DIC

A

treat underlying disorder
blood products

if bleeding predominant, antifibrinolytic
if clotting predominant, hepar

87
Q

prolonged PTT indicates

A

presence of inhibitor

think anticoagulant or dysfunctional platlets

88
Q

warfarin therapy would causes a prolonged

A

PT

ultimately, INR as well

89
Q

if factors VIII or X caused a prolonged PTT, the 1:1 mix would show

A

correction of clotting time

90
Q

most appropriate test to monitor warfarin therapy

A

INR

91
Q

tests for these values are standardized to allow easy comparison across all labs

A

INR
factor levels

92
Q

tests for these values are highly dependent on testing systems, methodologies and reagents

cannot easily be compared across labs

A

PT
PTT
TT

93
Q

screens for primary hemostatic defects involving platelets or vWF

A

PFA-100

94
Q

factor V leiden is associated with

A

increased risk of venous thrombosis

decreased degradation of Va

95
Q

thrombin time measures

A

the conversion of fibrinogen to fibrin and its crosslinking

96
Q

deficiency of fibrin will cause

A

prolonged thrombin time

97
Q

if the D dimer is negative, exclude …. from the differential

A

PE

98
Q

positive d dimer can indicate

A

DIC
fibrinolytic disorder

99
Q

platelet adhesion to the vascular wall at the site of injury is primarily mediated by

A

Gp1b and vWF

100
Q

mediates platelet aggregation through fibrinogen binding across all platelets

A

GpIIb-IIIa

101
Q

most common inherited coagulopathy

A

vWD

102
Q

vWF is caused by ….. deficiency of vWF

A

quantitative

103
Q

vWF is exposed with

A

endothelial injury

104
Q

vFW is reponsible for

A

platelet aggregation

links gp1b to exposed collagen

105
Q

links gp1b to exposed collagen

A

vWF

106
Q

vWD causes ….. bleeding time

A

prolonged

107
Q

how does vWF affected factor VIII?

A

decreased vFW causes FVIII to have shorter half life

108
Q

vWD causes prolonged [PT/PTT]

A

PTT

decreased FVIII leads to decreased activity of intinsic pathway

109
Q

negative ristocetin test, but normal plasma can be added to cause aggregation

A

vWD

110
Q

desmopressin can be used to treat

A

vWD

111
Q

desmopressin causes

A

endothelial cells to release stored vWF

112
Q

aortic stenosis can causes

A

acquired vWD

113
Q

APL can cause

A

DIC

114
Q

DIC causes excessive

A

bleeding and clotting

115
Q

sepsis can cause

A

DIC

116
Q

obstetric complications can cause

A

DIC

117
Q

consumptive coagulopathy

A

DIC

118
Q

oozing from IVs or arterial lines
petechiae, ecchymoses, mucocutaneous bleeding

A

DIC

119
Q

DIC causes prolonged [PT/PTT}

A

both

120
Q

vitamin K dependent factors

A

2, 7, 9, 10
C and S

121
Q

causes of vitamin K deficiency

A

malabsorption
antibiotics
cirrhosis

122
Q

vitamin K deficiency causes prolonged [PT/PTT]

A

PT

123
Q

vitamin K deficiency can be treated with

A

fresh frozen plasma
vitamin K supplementation

124
Q

result of autoantibodies against cardiolipin

A

antiphospholipid syndrome

125
Q

antiphospholipid syndrome can be secondary to

A

RA
HIV
SLE

126
Q

lupus anticoagulants inhibit

A

clotting in lab, but promote clotting in situ

127
Q

antiphospholipid causes increased [PT/PTT]

A

PTT

128
Q

anti-beta2 gp

A

antiphospholipid syndrome

129
Q

often presents with arterial or venous thrombosis in young patient

A

antiphospholipid syndrome

130
Q

polycythemia vera can increase risk of thrombosis due to

A

hypereviscosity

131
Q

most common inherited thrombosis syndrome

A

factor V Leiden

132
Q

inheritance pattern of Factor V Leiden

A

autosomal dominant

133
Q

protein C is unable to destroy activated factor V

A

Factor V Leiden

134
Q

Factor V Leiden mutation elminates binding spot for

A

protein C

135
Q

in factor V Leiden, thrombin activity is [increased/decreased]

A

increased

136
Q

in factor V Leiden, increased generation of thrombin and loss of negative feedback loop cause

A

increased risk of venous thrombosis

137
Q

cause increased risk of thrombosis in Factor V Leiden

A

OCP and preganancy
smoking
prolonged immobilization

138
Q

catalyzes the conversion of fibrinogen to fibrin

A

thrombin

139
Q

leads to overproduction of thrombin –> increased risk of venous thrombosis

A

prothrombin mutation

140
Q

protein C or S deficiency causes increased

A

factor Va and VIIIa activity –> increased risk of venouns thrombosis

141
Q

in protein C and S deficiency, avoid treatment with

A

warfarin

increases thrombotic effect

142
Q

in protein C and S deficiency, administration of warfarin can cause

A

warfarin induced skin necrosis

143
Q

homozygous protein C of S deficiency can cause what in newborns?

A

neonatal purpura fulminans

144
Q

ATIII deficeincy causes

A

decreased inhibition of thrombin

145
Q

most inherited thrombosis disorders follow what inheritance pattern?

A

autosomal dominant

146
Q

heparin has not effect in

A

ATIII deficiency

heparin must bind antithrombin to function

IBI Test 3 (20 decks)

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