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Block 7 Week 4 Colt > Secondary Hemostasis > Flashcards

Secondary Hemostasis Flashcards

1
Q

secondary hemostasis generates (blank) which stabilizes the PLT plug

A

thrombin

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2
Q

Thrombin converts fibrinogen to (blank)

A

fibrin

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3
Q

The formation of fibrin allows it to be (blanked) to generate strength

A

cross-linked

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4
Q

Where are the coagulation factors produced?

A

in the liver

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5
Q

T/F: coag factors are produced in an inactive state

A

true

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6
Q

What is the activating substance for the extrinsic (activates VII) pathway?

A

tissue thromboplastin (TT)

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7
Q

What is the activating substance for the intrinsic (activates XII) pathway?

A

subendothelial collagen (SEC)

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8
Q

What are the three things needed to activate the coag cascade?

A
  1. activating factor (SEC or TT)
  2. phospholipid surface of PLTs
  3. Calcium from PLT dense granules
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9
Q

What distinguishes 2ry hemostatic disease from 1ry?

A

2ry causes deept tissue bleeding into muscles and joints (hemarthrosis) and rebleeding after surgical procedures (circumcision and tooth extraction common)

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10
Q

What factors are in the intrinsic pathway?

A

12, 11, 9, 8

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11
Q

What factors are in the extrinsic (tissue factor) pathway?

A

7; 7 is lucky, luck is extrinsic

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12
Q

What factors are in the common pathway?

A

5, 2, 1

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13
Q

What factors are activated by Vit. K?

A

2, 7, 9, 10, C, S

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14
Q

(PT/PTT) measures the extrinsic pathway (7)

A

PT; TT activates 7, PT and TT both have 2 letters

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15
Q

(PT/PTT) measures the intrinsic pathway (12)

A

PTT; SEC activates 12, PTT and SEC both have 3 letters

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16
Q

Hemophilia A is caused by a def of what factor?

A

AAAAAAAAA-8!

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17
Q

What is the mode of inheritance in males of hemophilia A?

A

x-linked

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18
Q

T/F: hemophilia A can present with no family history

A

true

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19
Q

What is the most common presentation of hemophilia a?

A

deep tissue bleeding after surgery

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20
Q

T/F: severity of hemophilia A is in a range depending on how def you are

A

true

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21
Q 
What are the lab values for hemophilia a?
PT/PTT
factor levels
PLT
bleeding time
A 
HI PTT
normal PT
low FVIII
NORMAL PLT
normal bleeding time (if superficial can use primary hemostasis)
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22
Q

How do you treat hemophilia A?

A

recombinant FVIII

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23
Q

What is Christmas disease ?

A

hemophilia B, factor 9 def

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24
Q

What is the only difference between hemophilia A and B?

A

B has a 9 def

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25
Q

T/F: a mixing study will normalize the PTT in both hemophilia a and B

A

true

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26
Q

T/F: a mixing study will normalize PTTT in a coagulation factor inhibitor

A

FALSE; factor will overwhelm the mixed serum

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27
Q

What is the most common anti-factor inhibitor?

A

anti-8

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28
Q

T/F: inhibitor disorders can cause qualitative and quantitative disorders

A

true

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29
Q

What is the most common INHERITED coag disorder?

A

vW disease

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30
Q

How does vW disease normally present?

A

mild skin and mucosal bleeding

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31
Q

vW disease is due to impaired PLT (adhesion/aggregation)

A

adhesion

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32
Q 
Describe the lab values for vW disease
bleeding time 
PT/PTT
PLT 
Ristocetin test
A

increased bleeding time
increased PTT: decreased FV8 b/c vWF stabilizes 8
normal PT
abnormal ristocetin leading to NO agglutination

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33
Q

What is the Tx for vW disease?

A

desmopressin

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34
Q

Desmopressin increases vWF release from the (blank) bodies of endothelial cells

A

weibel-palade

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35
Q

Vit. K is activated by (blank) in the liver

A

epoxide reductase

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36
Q

Vit. K gamma carboxylates what factors?

A

2 7 9 10 C S

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37
Q

PT is used to test (heparin/coumadin) levels

A

PT = coumadin/warfrin

two letters, two drug names

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38
Q

PTT is used to test (heparin/coumadin)

A

PTT = heparin; HEParin has three letters like PTT

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39
Q

Coumadin blocks (blank) activity resulting in less activated Vit. K

A

epoxide reductase

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40
Q

what are the three scenarios in which you see a Vit. K def?

A
  1. newborns –lack of GI bacteria to make vit. K
  2. long term abx therapy
  3. malabsorption
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41
Q

How does liver failure lead to problems with the coag cascade?

A

Liver is the source of all the factors AND of Vit. K activation.
DECREASED PRODUCTION
DECREASED ACTIVATION

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42
Q

How does a large volume transfusion mimmic a coag cascade def?

A

Works to dilute the factors

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43
Q

WHat is another name for factor I?

A

fibrinogen

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44
Q

What is another name for prothrombin?

A

factor II

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45
Q

What coag factor is made by the Kuppfer cells in the liver?

A

FVIII

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46
Q

WHere is Prekalikrein made?

A

liver

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47
Q

Where is high molecular weight kininogen made?

A

liver

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48
Q

What is another name for factor XIII

A

fibrin stabilizing factor

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49
Q

What is Hagemann factor?

A

FXII

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50
Q

What is christmas factor

A

FIX

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51
Q

What is antihemophilic factor?

A

FVIII

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52
Q

What two factors make up the prothrombinase complex?

A

Va and Xa

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53
Q

What three factors make up the tenase complex?

A

VIIIa, Xa, and Ca

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54
Q

What two factors are needed to convert XII to XIIa?

A

prekallikrein and high molecular weight kininogen

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55
Q

What ion is needed to transform VIIIa to X?

A

Ca

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56
Q

What factor is needed to take cross link fibrin?

A

XIIIa

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57
Q

What factor is needed to take Fibrinogen to fibrin?

A

IIa

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58
Q

Plasmin degrades what end product of the coag cascade?

A

fibrin

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59
Q

what coag path is activated by tissue injury?

A

Extrinisc via 7

60
Q

Which coag path is activated by contact?

A

Intrinsic path

61
Q

What test is done by adding phospholipid (contact activator) to calcium and plasma?

A

PTT

62
Q

What test is done by adding tissue factor and phospholipid to plasma?

A

PT

63
Q

What test screens for qualitative PLT disorders?

A

bleeding time

64
Q

What disease presents with this PENTAD of symptoms:

  1. thrombocytopenia
  2. hemolytic anemia
  3. neurologic abn.
  4. renal abn.
  5. fever
A

TTP

65
Q

what is the mode of inheritance of activated protein C resistance?

A

Auto Dom

66
Q

(blank) is responsible for 50% of hereditary thrombophilia

A

activated protein C resistance

67
Q

What is the MOA of activated protein C resistance? (think Factor V)

A

heterozygosity of FV Leidin which makes FVL resistance to inactivation via protein C

68
Q

An anthithrombin deficiency leads to no inactivation of what factors?

A

II, IXa, Xa, XIa, XIIIa

2 9a 10a 11a 12a

69
Q

what is the MOA of anthithrombin?

A

auto dom

70
Q

Protein C is activated by the (blank) complex

A

thrombin-thrombomodulin complex

71
Q

What is the cofactor for the thrombin-thrombomodulin complex?

A

protein S

72
Q

Acquired (blank) deficiency may be due to coumadin therapy, liver disease, and pregnancy

A

protein C

73
Q

Antiphospholipid syndrome includes what two antibodies?

A

lupus anticoagulant syndrome

anti-cardiolipin syndrome

74
Q

In what diseases do you seen antiphospholipid syndrome?

A

lupus, primary APL syndrome, HIV, malignancy, collagen vascular disorders, and with drugs

75
Q

What is the second most common causes of inherited thrombophilia?

A

prothrombin variant

76
Q

thrombin can act on what activated factors?

A

2a 9a 10a 11a 12a

77
Q

Is the protein C receptor antithrombotic or prothrombotic?

A

anithrombotic

78
Q

Is tPA antithrombotic or prothrombotic?

A

antithrombotic

79
Q

Is Thromboxane antithrombotic or prothrombotic?

A

prothrombotic

80
Q

Are NO and prostacyclin antithrombotic or prothrombotic?

A

anithrombotic

81
Q

What platelet receptor binds vWF?

A

GP1b

82
Q

What platelet receptor binds fibrinogen?

A

GpIIb/IIIa

83
Q

What platelet receptor binds fibronectin?

A

GPIc/IIa

84
Q

What platelet receptor is an adhesion molecule?

A

CD62P (P-selectin)

85
Q

What platelet receptor binds initiates platelet activation when bound by thrombin?

A

thrombin receptor

86
Q

What platelet receptor binds initiates PLT activation when bound by ADP?

A

ADP receptor

87
Q

What platelet receptor binds collagen?

A

GPIa/IIa

88
Q

T/F: PLTs contain red cell antigens

A

true

89
Q

T/F: PLTs contain Rh factor

A

FALSE

90
Q

What class of MHC ag is present on PLTs?

A

MHC I

91
Q

What particular MHCs are present on PLTs?

A

HLA-A, B, and C

92
Q

What is contained within the dense granules of PLTs?

A

ATP
ADP
Ca
Serotonin

93
Q

What is contained within the a-granules of PLTs?

A 
vWF
Fibrinogen
FV
VEGF, EGF, PDGF
Angiostatin, thrombospondin, endostatin
PF-4, IL-8, CCL5
94
Q

PGI2 released by endothelial cells has a (pos/neg) effect on the coag cascade

A

negative

95
Q

Tissue Factor Pathway Inhibitor blocks what conversion?

A

7 to 7a

96
Q

tPA prevents what final step of stabilizing the PLT plug?

A

cross linking of fibrin;

tpA converts plasminogen to plasmin, and plasmin blocks the cross linking

97
Q

What test do you use to screen for vW disease?

A

bleeding time

98
Q

T/F: bleeding time is useful to predict the risk of bleeding during surgery

A

false

99
Q

What test uses ADP, epi, arachidonate, collagen, and ristocetin to determin PLT aggregation?

A

PLT aggregometry

100
Q

What is PLT flow cytometry used to Dx?

A

def. of PLT surface glycoproteins and disorders of PLT activation

101
Q

INR is used to monitor (heparin/coumadin) therapy

A

coumadin

102
Q

INR references the (PT/PTT)

A

PT

103
Q

What test is used to monitor heparin, hirudin, or argatroban therapy?

A

aPTT

104
Q

What test is used to test the presence of functional fibrinogen?

A

TT

105
Q

What causes prolongation of the thrombin time?

A

heparin, hirudin, argatroban and dysfribrinogenemia

106
Q

What does a mixing study screen for?

A

presence of inhibitors

107
Q

T/F: mixing studies excludes the presence of heparin

A

true

108
Q

If there is at least 50% activity on the mixing study, then you know that the prolongation is due to (blank)

A

a factor deficiency

109
Q

If there is less than 50% activity in the mixing study, then you know that the prolongation is due to (blank)

A

presence of an inhibitor

110
Q

D-dimers are formed by the degradation of what molecule in the clot?

A

fibrin

111
Q

The fuck do you use an Anti-Xa assay for?

A

monitor unfractionated or LMWH therapy

112
Q

Males tend to have (coag/PLT) bleeding disorders

A

coag

113
Q

females tend to have (coag/PLT) bleeding disorders

A

PLT

114
Q

Type I vW disease is (quantitative/qualitative) disorder

A

quantitative; not enough vWF

115
Q 
Describe the lab values for Type I vW disease:
PT
PTT
BT (bleeding time)
FVIII levels
A

normal PT
increased PTT
increased bleeding time
decreased FVIII

116
Q

Type II vW disease is (quantitative/qualitative)

A

qualitative

117
Q

Type IIM vW prevents vWF from binding to (blank)

A

GpIb

118
Q

Type IIN vW is shows reduced binding of vWF to (blank)

A

FVIII

119
Q

Type IIa vW is absence of (blank)

A

high molecular wt. vWF multimers

120
Q

What is the only lab value that is markedly changed in vWF IIa?

A

ristocetin agglutination decreased

121
Q

vW disease IIb is spontaneous binding of vWF to (blank)

A

PLTs

122
Q

T/F: vW IIa and IIb both have decreased high molecular wt. vWF multimers

A

true

123
Q

What should you not give to someone with vW IIb?

A

DDAVP: profound thrombocytopenia and bleeding

124
Q

What is wonky about the ristocetin test in vW IIb>?

A

it is increased since there is spontaneous PLT binding

125
Q

In what disease do PLTs lack the PLA1 ag?

A

Glanzmann thrombasthenia

126
Q

IN what disorder to PLTs fail to aggregate with all agonists except risocetin?

A

Glanzmann thrombasthenia

127
Q

Hermansky-Pudlak
Chediak-Higashi
Wiskott-Aldrich
Are all (blank) diseases with no second wave of aggregation

A

dense granule

128
Q

In alpha granule disease, aggregation is blunted with all agents except (blank)

A

ADP

129
Q

Gray PLT syndrome is a (a/dense) granule disorder

A

alpha

130
Q

ASA and NSAIDS inhibit what enzyme?

A

COX-1

131
Q

What molecule released by first wave PLTs from the dense granules signal for the second wave aggregation?

A

tXA2

132
Q

Is the effect of ASA or NSAIDS on COX-1 irreversible?

A

ASA

133
Q

Ticlopidine and Clopidogrel inhibit (blank) mediated PLT activation

A

ADP

134
Q

Abciximab, Eptifibatide, Tirofiban inhibit the (blank) receptor, aka fibrinogen receptor

A

GpIIb/IIIa

135
Q

Abciximab, Eptifibatide, Tirofiban will cause impaired aggregation to which agonists?

A

all except ristocetin

136
Q

Ticlopidine & Clopidogrel will cause impaired aggregation against which agonist?

A

ADP

137
Q

What bleeding disease is made by a diagnosis of exclusion?

A

ITP

138
Q

Heparin induced thrombocytopenia is IgG binding to what complex?

A

Heparin-PF4 between the drug and the PLT

139
Q

T/F: bleeding is rare in HIT

A

true

140
Q

T/F: thrombosis is likely in HIT

A

true, as strange as it is considering the name; PLTs will aggregate and activate the fucking cascade

141
Q

Liver disease results in chronic DIC from an impaired clearance of (blank)

A

d-dimer

142
Q

anti-thrombin def. results in (arterial/venous) thromboses

A

venous

143
Q

T/F: homozygous anti-thrombin def is incompatible with life

A

true

144
Q

antibodies against B2 glycoproteins and prothrombin are most likely what type of Ab?

A

antiphospholipid; can be classified as lupus anticoagulant or anticardiolipin

145
Q

phenytoin, quinidine, hydralazine, procainamide, phenothiazines, IFN, cocaine
can all cause secondary (blank)

A

antiphospholipid syndrome

146
Q

Coumadin therapy may result in an acquired (blank and blank) def

A

protein C and S

147
Q

Ca is necessary in the conversion of what factor from the intrinsic pathway to the common pathway?

A

8a to X

Block 7 Week 4 Colt (9 decks)

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