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Hemostasis/Coagulation > Exam 1 Material > Flashcards

Exam 1 Material Flashcards

1
Q

Prostaglandin and thromboxane are _____. Their synthesis occurs in _____.

A

Procoagulants

The dense tubular system of the organelle zone

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2
Q

What are the 5 steps of platelet plug formation:

A

Adhesion, Activation, Aggregation

Secretion, Stabilization of plt plug (fibrin)

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3
Q

What 3 components are involved in platelet adhesion:

A

vWF
GPIb
Collagen fibers

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4
Q

A strong agonist will take platelet plug formation straight to this step.

A

Secondary aggregation (which is permanent)

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5
Q

What happens during plt activation:

A
  • 2nd messenger pathway activated
  • shape change
  • Secrete granules
  • Organelles move to center
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6
Q

T/F Aggregation begins 10-20 seconds following injury/plt adhesion, and requires ATP from glycolysis:

A

True

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7
Q

List the 3 things required for aggregation:

A
  • Ionized Calcium
  • GPIIb/IIIa
  • Fibrinogen
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8
Q

What initiates the intrinsic pathway:

A

Exposure to subendothelial collagen

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9
Q

What initiates the extrinsic pathway:

A

Release of tissue factor

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10
Q

What is secreted during platelet plug formation:

A

Alpha granules
Dense granules
lysosomes
prostaglandins

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11
Q

List 4 tests for plt activation:

A
  • B-TG (beta thromboglobulin)
  • PF4
  • Thrombospondin
  • PDGF
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12
Q

List some conditions associated with increased levels of plt activation markers:

A

arteriosclerosis, CVD, shock, DVT, DIC

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13
Q

Where is the glycocalyx located and what glycoproteins does it contain:

A
  • Peripheral zone of plt
  • GPIb
  • GPIIb/IIIa
  • GPVa
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14
Q

List the alpha granules:

A 
PDGF
vWF
B-TG
PF4
Fibronectin
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15
Q

What is the function of the alpha granules:

A

They are contact promoting factors

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16
Q

List the Dense granules:

A

ADP
ATP
Calcium
5-HT (serotonin)

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17
Q

What are the non-protein factor type granules:

A

Dense granules

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18
Q

Where is calcium sequestered, and when released triggers plt contraction:

A

Dense tubular system (organelle zone)

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19
Q

Where are peroxisomes found:

A

Organelle zone

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20
Q

Adhesion to aggregation takes ____:

A

10-20 seconds

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21
Q

This occurs when an external agonist interacts with a plt membrane receptor, a signal is transmitted form outer to inner cell, and 2nd messenger pathway is activated:

A

Plt Activation

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22
Q

Primary aggregation is _____, and secondary aggregation is _____:

A

Primary–> reversible

Secondary–> permanent

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23
Q

Plt count for Thrombocytopenia is:

A

<100,000/uL

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24
Q

At a plt count of _______ patients will show clinical signs/symptoms, at a plt count of ______, patients run risk of spontaneous hemorrhage:

A

<50,000/uL

<20,000/uL

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25
Q

List some acquired causes of thrombocytopenia due to decreased number of megakaryocytes:

A

chemo
radiation
alcoholism
chloramphenicol

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26
Q

List causes of thrombocytopenia due to disorders of distribution/dilution of plts in circulation:

A
  • spleen pooling (enlarged spleen will hold >30% plts)
  • hypothermia
  • dilution in circulation
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27
Q

Snake venom, tissue injury, OB complications, neoplasms, intravascular hemolysis –> how do these contribute to thrombocytopenia:

A

destruction of plts

via combined consumption of plt/coag factors

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28
Q

This is one of the most common disorders causing severe isolated thrombocytopenia, and is diagnosed by exclusion:

A

ITP (idiopathic thrombocytic purpura)

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29
Q

ITP is caused by an ______ against ______:

A

autoantibody against plts

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30
Q

Bernard Soulier, vWD, and Hemophilia A all are affected in this phase of clot formation:

A

Adhesion

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31
Q

Glanzmann’s is affected in this phase of clot formation:

A

Aggregation

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32
Q

This clotting disorder is X-linked recessive:

A

Hemophilia A

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33
Q

Bernard Soulier and Glanzmann’s are both this type of inheritance:

A

Autosomal recessive

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34
Q

What type of inheritance is Type 1 vWD:

A

Autosomal dominant

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35
Q

Glanzmann’s is a deficiency of this:

A

GPIIb/IIIa complex

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36
Q

Bernard Soulier is a deficiency of this:

A

GPIb/IX complex

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37
Q

What is the deficiency is Hemophilia A:

A

Molecular absence or defect in F8:C

coagulant portion of F8

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38
Q

What is the defect in Type 3 vWD:

A

Absence of vWF multimers

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39
Q

Which clotting disorder would have giant platelets:

A

Bernard Soulier

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40
Q

Which two clotting disorders have abnormal APTT’s:

A

vWD

Hemophilia A

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41
Q

Which two clotting disorders have absent plt aggregation with ristocetin, and which can be corrected w/ normal plasma:

A

Bernard Soulier, vWD

*can correct vWD w/ normal plasma

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42
Q

Which clotting disorder has decreased Factor 8:C:

A

Hemophilia A

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43
Q

Which clotting disorder will have normal to decreased vWF:Ag:

A

vWD

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44
Q

What type of bleeding is seen with Glanzmanns:

A

mostly mucosal bleeding

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45
Q

Which clotting is treated with DDAVP or Humate P:

A

vWD

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46
Q

Which clotting disorder needs the patient to practice good dental care:

A

Glanzmann’s

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47
Q 
The following treatments can help control bleeding in what clotting disorder:
DDAVP
Estrogen therapy
Recombinant F 8a
Plt transfusion
A

Bernard Soulier

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48
Q

This disorder requires prophylactic infusions of Factor 8 in children (the dose will be tailored to activity level/risk of injury):

A

Hemophilia A

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49
Q

Bernard Soulier has normal aggregation with all the agents EXCEPT:

A

ristocetin

same as vWD

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50
Q

Will F8:C be normal in Bernard Soulier:

A

Yes

it would only be abnormal in Hemophilia A

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51
Q

Storage pool deficiency (granule defect) are classified by ___ and ___:

A

granule analysis

plt morphology

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52
Q

Alpha:

A

decreased alpha granules
Normal dense granules
GRAY PLT SYNDROME

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53
Q

Alpha-Delta:

A 
Decreased:
alpha granules
dense granules
PF4
Beta-thromboglobulin
PDGF
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54
Q

Delta:

A 
Decreased:
dense granules
ATP
ADP
Ca
Serotonin
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55
Q

What is the disorder with decreased alpha granule proteins and reduced PF3 activity:

A

Quebec Plt Syndrome

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56
Q

List the 4 storage pool deficiencies associated with other congenital abnormalities:

A
  • Hermansky-Pudlak (albinism)
  • Chediak-Higashi
  • Wiskott-Aldrich
  • TAR (missing radial bones)
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57
Q

Would plt aggregation tests be normal in storage pool deficiencies:

A

No

but PT/APTT/Plt ct would be normal

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58
Q

Genetic deficiency of cyclo-oxygenase will lead to deficiency of _______ generation:

A

Thromboxane

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59
Q

Without Thromboxane, plt aggregation tests are unresponsive to _____ as a stimulator:

A

arachidonic acid

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60
Q

What are the treatments for storage pool and secretion defects:

A 
Plt transfusions
Cryoprecipitate
DDAVP
RBC transfusions
Avoidance of NSAID's
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61
Q

Deficiency of ______ leads to deficient conversion of membrane-associated arachidonic acid to Thromboxane A2:

A

Cyclo-oxygenase

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62
Q

Where is vWF stored:

A

alpha granules

endothelial cells

63
Q

If plts fail to generate Thrombin, (which is rare) bleeding pattern will closely resemble ______, and the treatment will be:

A

Hemophilias
Plt transfusions
(abnormal PF3, prolonged PT)

64
Q

This serves as a ligand between plts, endothelial cells, and other proteins such as fibronectin:

A

vWF

65
Q

This is an important adhesive protein on chromosome 12:

A

vWF

66
Q

Circulating vWF forms complex with ____ which protects it from _____:

A

Factor 8

protects it from degredation

67
Q

Type 1 vWD makes up ___% of cases:

A

70%

68
Q

It is important to distinguish vWD from these other two clotting disorders:

A

Hemophilia A

Bernard Soulier

69
Q

What are the changes in F1 you’ll see in early/mild, moderate, and end stage liver disease:

A

Early/mild: increase F1
Mod/severe: F1 dysfunctional (coated with sialic acid)
End stage: VERY decreased F1

70
Q

Liver disease results in reduced plt ____:

A

adhesion

71
Q

List the Vitamin K dependant factors:

A

2, 7, 9, 10

72
Q

Factor ___ activity is more specific for liver disease:

A

Factor V

  • Not affected by diet
  • Not vit K dependent
73
Q

Common pathway factors:

A

1, 2, 5, 10

74
Q

Extrinsic pathway factors:

A

7

75
Q

Intrinsic pathway factors:

A

8, 9, 11, 12

76
Q

Which test measures the Extrinsic pathway?

A

PT

77
Q

Which test measures the intrinsic pathway:

A

APTT

78
Q 
What will PT/APTT results be in:
Vascular disorder
Quant plt disorder
Qual plt disorder
Factor deficiency
A

Vascular disorder: N
Quant plt disorder: N
Qual plt disorder: N
Factor deficiency: Abnormal

79
Q

With vit K defect, which would be abnormal, PT or APTT:

A

APTT

80
Q

If inhibitor is present, TT result would be:

A

Normal

81
Q

What would result for TT be in DIC:

A

abnormal

82
Q

Where is thrombopoietin produced:

A

liver

lesser degree–>spleen

83
Q

Thrombopoietin is cleared from plasma by receptors on _____, in thrombocytopenia, clearance is ____ and plasma concentration of thrombopoietin is_____:

A

megakaryoctes
low
increased

84
Q

Eczema, skin lesions,and immunodeficiency are associated with this congenital thrombocytopenic disorder:

A

Wiskott-Aldrich

85
Q

Hermansky-Pudlak syndrome is a platelet deficiency of ____:

A

nonmetabolic ADP

86
Q

This disorder will present with giant platelets, thrombocytopenia, and Dohle bodies:

A

May-Heggelin anomaly

87
Q

This typically presents in mainly women aged 20-50, with mucosal bleeding, younger platelets in circulation contribute to to BT closer to normal:

A

ITP

88
Q

This must be dx via exclusion:

A

ITP

89
Q

Post transfusion purpura is typically caused be an alloantibody to ____:

A

P1A1 (also called HPA-1a)

90
Q

How does HIV affect plt production:

A

Causes BM hypocellularity, and subsequent thrombocytopenia

91
Q

This microangiopathic disorder can present with hemolytic anemia, renal dysfunction, and neuro abnormalities:

A

TTP

92
Q

Renal dialysis is more commonly needed in which disorder, TTP or HUS:

A

HUS

93
Q

What is the treatment for TTP:

A

plasma exchange

94
Q

Is plasma exchange the main treatment for HUS:

A

No. treatment is supportive, involving dialysis, antihypertensives, blood transfusions, steroids, anticoagulants etc

95
Q

Gestational thrombocytopenia shares features with ____, but may not be immune related:

A

ITP

96
Q

____is required for the stabilization of the GPIIb/GPIIIA complex:

A

CalciumL

97
Q

List the two plt membrane defect disorders:

A

Glanzmanns

Bernard Soulier

98
Q

Associate estrogen therapy with this disorder:

A

Bernard Soulier

99
Q

Deficiency of alpha granules leads to this appearance, associated with this disorder:

A

Gray plt syndrome

*Quebec plt disorder

100
Q

What is deficient in Quebec plt disorder:

A

Alpha granules

PF3

101
Q

Which disorder has oculotaneous albinism, and which has ocular albinism w/ gray hair:

A

Hermanski-Pudlak

Chediak-Higashi

102
Q

Cyclo-oxygenase deficiency results in deficient conversion of ___ to ___:

A

arachidonic acid–>Thromboxane A2

103
Q

vWF acts as a carrier protein for ____:

A

Factor 8

104
Q

T/F

In normal individuals, plasma levels of Factor 8 closely correlate with plasma levels of ____:

A

vWF

105
Q

GPIb/IX is the receptor for ___:

A

vWF

106
Q

DDAVP stimulates release of:

A

vWF from endothelial cells

107
Q

Will PF3 be normal in liver disease:

A

No

108
Q

Which lymphoproliferative malignancies can cause both hypo/hypercoagulability:

A

Paraproteinemias

109
Q

Decreased plasma levels of F8:C, vWF:Ag, and vWF activity, and abnormalities in vWF multimeric patterns:

A

Acquired vWD

110
Q

Are the effects on plts reversible or irreversible with the use of aspirin? ibuprofen?

A

Aspirin: irreversible
Ibuprofen: reversible

111
Q

This rare congenital connective tissue disorder is due to decreased or low quality collagen:

A

Osteogenesis imperfecta

112
Q

This rare congenital connective tissue disorder is due to bleeding abnormalities of connective tissues:

A

Marfan’s

113
Q

What is the main feature of Ehlers-Danlos syndrome:

A

hyper-elastic skin

114
Q

Pseudooxanthoma elasticum afffects the elastic fibers of the ___ and ___, caused by increased ___ and ___ in elastic fibers:

A

skin & arteries

Calcium & minerals

115
Q

This disorder is caused by increased permeability of blood vessels of the GI tract, causes chronic GI bleeds, and is associated with von Willebrands:

A

Angiodysplasia

116
Q

Factitious primary purpura:

A

self induced trauma

117
Q

List the 5 types of primary purpura:

A 
Simple
Mechanical
Senile
Factitious
Schambergs
118
Q

List the 5 types of secondary purpura:

A 
Infectious
Allergic
Metabolic
Psychogenic
Secondary to dysproteinemia
119
Q

Treatment for DIC:

A

heparin

120
Q

What coag factor deficiences are possible in liver disease:

A

Vit K dependant factors (2,7,9,10, protein C & S)

*Will see change in F7 first, has shortest half life

121
Q

Bleeding in uremia is due to problem with this stage of clot formation:

A

adhesion, leads to abnormal aggregation

122
Q

EDTA elevates results for ___ and ___, and reduces factors __ and ____:

A

PT/APTT

5 and 8

123
Q

Heparin has this affect on PT/APTT:

A

prolonged

124
Q

The BT is _____ in conditions with dysfunctionl plts and in thrombocytopenia:

A

prolonged

125
Q

Can BT distinguish coag factor deficiency or bleeding risk:

A

no

126
Q

The Clotting time test measures factors of the ____ pathway:

A

intrinsic

127
Q

What are the two reagents used for PT:

A

Thromboplastin

Calcium

128
Q

What is the ref range for PT:

A

11.5-14 sec

129
Q

What is the ref range for APTT:

A

20-45 sec

130
Q

This is used to neutralize Heparin:

A

protamine sulfate

131
Q

What is the specimen for Protamine sulfate testing:

A 
PPP
plt poor (citrated) plasma
132
Q

Can protamine sulfate testing be used for LMWH:

A

No. only for unfractionated heparin.

133
Q

A positive protamine sulfate test:

A

presence of fibrin threats

134
Q

Negative protamine sulfate test:

A

opalescent appearance of plasma

no fibrin threads

135
Q

Plt aggregation requires a conformation in the _____ complex in order to allow ____ to bind:

A

GPIIb/GPIIIa (and GPV)

fibrinogen

136
Q

Plt adhesions begins in ___ seconds, aggregation in ____ seconds following vascular injury:

A

Adhesion: 1-2 seconds
Aggregation: 10-20 seconds

137
Q

List the different types of receptors found on platelets:

A 
ADP
thrombin
epinephrine
collagen
TXA2
serotonin
138
Q

What is the phospholipid component of the plt, which moves to the outer surface when plt is activated, allowing for assembly of vit k dependent factors:

A

PF3

139
Q

Which platelet factor inhibits heparin:

A

Pf4

140
Q

Primary aggregation involves stimulation by agonist, resulting in ____, and is ____:

A

ADP

Reversible (unless agonist is STRONG)

141
Q

Secondary aggregation involves _____ and is ____:

A

Granule content release

irreversible

142
Q

Secondary aggregation is dependent on the ____ of the ADP release from primary aggregation:

A

strength/amount

143
Q

Are megakaryocytes capable of synthesizing cyclo-oxygenase:

A

Yes

144
Q

ADP binding to the plt membrane allows for _____ to be converted to _____:

A

Arachidonic acid to TXA2

145
Q

Serotonin is a ____ aggregating agent, but _____ other aggregating agents:

A

weak

amplifies

146
Q

Serotonin serves as an important _____ and potent stimulator of smooth muscle ___ production:

A

vasoconstrictor

PGI2

147
Q

Coumadin/Warfarin are ______ antagonists:

A

vitamin K

148
Q

What are PIVKA’s:

A

proteins induced by vitamin k absence/antangonists

vit k deficient patients exhibit decreased production of functional prothrombin proteins

149
Q

What two factors are the last stable:

A

5 and 8:C

150
Q

Extrinsic pathways is activated by release of:

A

Tissue factor

151
Q

Plasmin is converted to plasminogen by this:

A

tPA

152
Q

What is the mechanism of coag drugs that end in -aban:

A

Direct Factor Xa inhibitors

153
Q

This drug is an ADP binding inhibitor:

A

Plavix

154
Q

What drug inhibits synthesis of vit k dependent clotting factors:

A

warfarin/ ‘Coumadin’

Hemostasis/Coagulation (3 decks)

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