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Block 7 Week 4 Colt > Secondary Hemostasis > Flashcards

Secondary Hemostasis Flashcards

1
Q

primary hemostasis forms a..

A

weak PLT plug

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2
Q

secondary hemostasis stabilizes the PLT plug with…

A

fibrin

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3
Q

PLTs bind vwF via what receptor?

A

GPIb

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4
Q

vwF binds exposed..

A

subendothelial collagen

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5
Q

What is the FIRST thing that happens when the endo has been damaged?

A

reflexive vasoconstriction via neural response and endothelin

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6
Q

What are the two sources of vWF?

A

Weibel-Palade bodies of endo and a-granules of PLTs

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7
Q

What are the two mediators that are released from PLTs adhesed to vWF?

A

ADPTXA2

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8
Q

ADP is released from what granule in the PLT?

A

dense granules

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9
Q

ADP release from PLTs promotes the exposure of what receptor on the PLT?

A

GPIIb

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10
Q

how do PLTs aggregate together?

A

via GPIIb

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11
Q

TXA2 is synthed by what enzyme?

A

COX

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12
Q

what is the linker molecule between GPIIb/IIIa receptors?

A

fibrinogen

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13
Q

What are the major symptoms of disorders in PRIMARY hemostasis?

A

MUCOSAL BLEEDINGepistaxis, hemoptysis, GI bleeding, hematuria, meorrhagia

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14
Q

what is a severe complication o thrombocytopenia?

A

intracranial bleed

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15
Q

Describe the size of petehcia, purprua and echymoses

A

petechiae: 1-2mmpurpura: >3mmecchymoses: >1cm

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16
Q

Are petechiae seen in QUALITATIVE d/o of bleeding?

A

NO just when PLTs are low!!!

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17
Q

what is the most common cause of thrombocytopenia in adults and kids?

A

ITPimmune thrombocytopenic purpura

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18
Q

Describe the general process of ITP

A

autoAbs produced by the spleen; coat PLTs, the spleen then eats the complex

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19
Q

what cell in the spleen produces the autoAbs in ITP?

A

plasma cells

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20
Q

after what event does acute ITP surface?

A

acute viral infection or IMMUNIZATION; self limited

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21
Q

What type of Ig is involved in ITP?

A

IgG

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22
Q

Chronic ITP is assc’d with other autoDz like….

A

SLE

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23
Q

how can newborns get ITP?

A

IgG can cross the placenta from mom with ITP/SLE

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24
Q

What is the PT/PTT like in ITP?

A

NORMAL; just not ENOUGH PLTs!

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25
Q

how does the bone marrow look in ITP?

A

increased megakaryocytes

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26
Q

what is the initial Tx for ITP?

A

corticosteroids

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27
Q

What is the Tx for symptomatic bleeding in ITP?

A

IVIG; just buys you time

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28
Q

What is the ultimate Tx for ITP?

A

splenectomy; removes the source of Abs and cuase of PLT destruction

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29
Q

What is the ultimate Tx for ITP?

A

splenectomy; removes the source of Abs and cuase of PLT destruction

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30
Q

What causes the shearing of RBCs in MAHA?

A

formation of microthrombi

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31
Q

TTP is due to decreased (blank), an enzyme that cleaves vWF for degradation

A

ADAMTS13

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32
Q

TTP is due to decreased (blank), an enzyme that cleaves vWF for degradation

A

ADAMTS13

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33
Q

MAHA is seen in what two qualitative PLT disorders?

A

TTP and HUS

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34
Q

Is decreased ADAMTS13 levels a congenital or acquired def?

A

acquired strangely enough!; seen in adult females

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35
Q

(TTP/HUS) is caused by drugs or infection

A

HUS

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36
Q

What E. coli toxin damages endothelial cells in the kidney and brain in HUS?

A

E. coli verotoxin

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37
Q

What are the common clinical findings in TTP/HUS?

A
  1. skin and mucosal bleeding2. MAHA3. fever
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38
Q

What clinical finding lets you know you have HUS and TTP?

A

renal insufficiency

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39
Q

What clinical finding lets you know you have TTP and not HUS?

A

CNS abnormalities

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40
Q

What are the lab values for TTP and HUS:PLTbleeding timePT/PTTHgbPeripheral smearBone marrow biopsy

A

low PLTincreased bleeding timenomral PT/PTT; coag cascade not involved!!!low Hgb aka anemiaschistocytes on smearincreased megakaryocytes on bone marrow biopsy

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41
Q

Bernard-Soulier syndrome is due to a genetic (blank) deficiency causing impaIred platelet ADHESION

A

GPIb

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42
Q

What finding do you see on smear in Bernard-Soulier syndrome?

A

enlarged PLTs; Big-Suckers

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43
Q

Glanzmann thrombasthenia is a genetic (blank) deficiency causing impaired PLT AGGREGATION

A

GPIIb/IIIa

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44
Q

Aspiriin irreversibly inhibits COX leading to a lack of (blank) and impairs aggregation

A

TXA2

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45
Q

T/F: both adhesion and aggregation are impaired in uremia

A

TRUE

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46
Q

secondary hemostasis generates (blank) which stabilizes the PLT plug

A

thrombin

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47
Q

Thrombin converts fibrinogen to (blank)

A

fibrin

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48
Q

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

A

cross-linked

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49
Q

Where are the coagulation factors produced?

A

in the liver

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50
Q

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

A

TRUE

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51
Q

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

A

tissue thromboplastin (TT)

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52
Q

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

A

subendothelial collagen (SEC)

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53
Q

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

A
  1. activating factor (SEC or TT)2. phospholipid surface of PLTs3. Calcium from PLT dense granules
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54
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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55
Q

What factors are in the intrinsic pathway?

A

12, 11, 9, 8

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56
Q

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

A

7; 7 is lucky, luck is extrinsic

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57
Q

What factors are in the common pathway?

A

5, 2, 1

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58
Q

What factors are activated by Vit. K?

A

2, 7, 9, 10, C, S

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59
Q

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

A

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

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60
Q

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

A

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

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61
Q

Hemophilia A is caused by a def of what factor?

A

AAAAAAAAA-8!

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62
Q

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

A

x-linked

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63
Q

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

A

TRUE

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64
Q

What is the most common presentation of hemophilia a?

A

deep tissue bleeding after surgery

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65
Q

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

A

TRUE

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66
Q

What are the lab values for hemophilia a?PT/PTTfactor levelsPLTbleeding time

A

HI PTTnormal PTlow FVIIINORMAL PLTnormal bleeding time (if superficial can use primary hemostasis)

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67
Q

How do you treat hemophilia A?

A

recombinant FVIII

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68
Q

What is Christmas disease ?

A

hemophilia B, factor 9 def

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69
Q

What is the only difference between hemophilia A and B?

A

B has a 9 def

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70
Q

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

A

TRUE

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71
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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72
Q

What is the most common anti-factor inhibitor?

A

anti-8

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73
Q

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

A

TRUE

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74
Q

What is the most common INHERITED coag disorder?

A

vW disease

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75
Q

How does vW disease normally present?

A

mild skin and mucosal bleeding

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76
Q

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

A

adhesion

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77
Q

Describe the lab values for vW diseasebleeding time PT/PTTPLT Ristocetin test

A

increased bleeding timeincreased PTT: decreased FV8 b/c vWF stabilizes 8normal PTabnormal ristocetin leading to NO agglutination

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78
Q

What is the Tx for vW disease?

A

desmopressin

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79
Q

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

A

weibel-palade

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80
Q

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

A

epoxide reductase

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81
Q

Vit. K gamma carboxylates what factors?

A

2 7 9 10 C S

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82
Q

PT is used to test (heparin/coumadin) levels

A

PT = coumadin/warfrintwo letters, two drug names

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83
Q

PTT is used to test (heparin/coumadin)

A

PTT = heparin; HEParin has three letters like PTT

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84
Q

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

A

epoxide reductase

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85
Q

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

A
  1. newborns –lack of GI bacteria to make vit. K2. long term abx therapy3. malabsorption
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86
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 PRODUCTIONDECREASED ACTIVATION

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87
Q

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

A

Works to dilute the factors

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88
Q

WHat is another name for factor I?

A

fibrinogen

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89
Q

What is another name for prothrombin?

A

factor II

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90
Q

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

A

FVIII

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91
Q

WHere is Prekalikrein made?

A

liver

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92
Q

Where is high molecular weight kininogen made?

A

liver

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93
Q

What is another name for factor XIII

A

fibrin stabilizing factor

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94
Q

What is Hagemann factor?

A

FXII

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95
Q

What is christmas factor

A

FIX

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96
Q

What is antihemophilic factor?

A

FVIII

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97
Q

What two factors make up the prothrombinase complex?

A

Va and Xa

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98
Q

What three factors make up the tenase complex?

A

VIIIa, Xa, and Ca

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99
Q

What two factors are needed to convert XII to XIIa?

A

prekallikrein and high molecular weight kininogen

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100
Q

What ion is needed to transform VIIIa to X?

A

Ca

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101
Q

What factor is needed to take cross link fibrin?

A

XIIIa

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102
Q

What factor is needed to take Fibrinogen to fibrin?

A

IIa

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103
Q

Plasmin degrades what end product of the coag cascade?

A

fibrin

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104
Q

what coag path is activated by tissue injury?

A

Extrinisc via 7

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105
Q

Which coag path is activated by contact?

A

Intrinsic path

106
Q

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

A

PTT

107
Q

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

A

PT

108
Q

What test screens for qualitative PLT disorders?

A

bleeding time

109
Q

What disease presents with this PENTAD of symptoms:1. thrombocytopenia2. hemolytic anemia3. neurologic abn.4. renal abn.5. fever

A

TTP

110
Q

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

A

Auto Dom

111
Q

(blank) is responsible for 50% of hereditary thrombophilia

A

activated protein C resistance

112
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

113
Q

An anthithrombin deficiency leads to no inactivation of what factors?

A

II, IXa, Xa, XIa, XIIIa2 9a 10a 11a 12a

114
Q

what is the MOA of anthithrombin?

A

auto dom

115
Q

Protein C is activated by the (blank) complex

A

thrombin-thrombomodulin complex

116
Q

What is the cofactor for the thrombin-thrombomodulin complex?

A

protein S

117
Q

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

A

protein C

118
Q

Antiphospholipid syndrome includes what two antibodies?

A

lupus anticoagulant syndromeanti-cardiolipin syndrome

119
Q

In what diseases do you seen antiphospholipid syndrome?

A

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

120
Q

What is the second most common causes of inherited thrombophilia?

A

prothrombin variant

121
Q

thrombin can act on what activated factors?

A

2a 9a 10a 11a 12a

122
Q

Is the protein C receptor antithrombotic or prothrombotic?

A

anithrombotic

123
Q

Is tPA antithrombotic or prothrombotic?

A

antithrombotic

124
Q

Is Thromboxane antithrombotic or prothrombotic?

A

prothrombotic

125
Q

Are NO and prostacyclin antithrombotic or prothrombotic?

A

anithrombotic

126
Q

What platelet receptor binds vWF?

A

GP1b

127
Q

What platelet receptor binds fibrinogen?

A

GpIIb/IIIa

128
Q

What platelet receptor binds fibronectin?

A

GPIc/IIa

129
Q

What platelet receptor is an adhesion molecule?

A

CD62P (P-selectin)

130
Q

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

A

thrombin receptor

131
Q

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

A

ADP receptor

132
Q

What platelet receptor binds collagen?

A

GPIa/IIa

133
Q

T/F: PLTs contain red cell antigens

A

TRUE

134
Q

T/F: PLTs contain Rh factor

A

FALSE

135
Q

What class of MHC ag is present on PLTs?

A

MHC I

136
Q

What particular MHCs are present on PLTs?

A

HLA-A, B, and C

137
Q

What is contained within the dense granules of PLTs?

A

ATPADPCaSerotonin

138
Q

What is contained within the a-granules of PLTs?

A

vWFFibrinogenFVVEGF, EGF, PDGFAngiostatin, thrombospondin, endostatinPF-4, IL-8, CCL5

139
Q

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

A

negative

140
Q

Tissue Factor Pathway Inhibitor blocks what conversion?

A

7 to 7a

141
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

142
Q

What test do you use to screen for vW disease?

A

bleeding time

143
Q

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

A

FALSE

144
Q

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

A

PLT aggregometry

145
Q

What is PLT flow cytometry used to Dx?

A

def. of PLT surface glycoproteins and disorders of PLT activation

146
Q

INR is used to monitor (heparin/coumadin) therapy

A

coumadin

147
Q

INR references the (PT/PTT)

A

PT

148
Q

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

A

aPTT

149
Q

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

A

TT

150
Q

What causes prolongation of the thrombin time?

A

heparin, hirudin, argatroban and dysfribrinogenemia

151
Q

What does a mixing study screen for?

A

presence of inhibitors

152
Q

T/F: mixing studies excludes the presence of heparin

A

TRUE

153
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

154
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

155
Q

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

A

fibrin

156
Q

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

A

monitor unfractionated or LMWH therapy

157
Q

Males tend to have (coag/PLT) bleeding disorders

A

coag

158
Q

females tend to have (coag/PLT) bleeding disorders

A

PLT

159
Q

Type I vW disease is (quantitative/qualitative) disorder

A

quantitative; not enough vWF

160
Q

Describe the lab values for Type I vW disease:PTPTTBT (bleeding time)FVIII levels

A

normal PTincreased PTTincreased bleeding timedecreased FVIII

161
Q

Type II vW disease is (quantitative/qualitative)

A

qualitative

162
Q

Type IIM vW prevents vWF from binding to (blank)

A

GpIb

163
Q

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

A

FVIII

164
Q

Type IIa vW is absence of (blank)

A

high molecular wt. vWF multimers

165
Q

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

A

ristocetin agglutination decreased

166
Q

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

A

PLTs

167
Q

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

A

TRUE

168
Q

What should you not give to someone with vW IIb?

A

DDAVP: profound thrombocytopenia and bleeding

169
Q

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

A

it is increased since there is spontaneous PLT binding

170
Q

In what disease do PLTs lack the PLA1 ag?

A

Glanzmann thrombasthenia

171
Q

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

A

Glanzmann thrombasthenia

172
Q

Hermansky-PudlakChediak-HigashiWiskott-AldrichAre all (blank) diseases with no second wave of aggregation

A

dense granule

173
Q

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

A

ADP

174
Q

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

A

alpha

175
Q

ASA and NSAIDS inhibit what enzyme?

A

COX-1

176
Q

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

A

tXA2

177
Q

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

A

ASA

178
Q

Ticlopidine and Clopidogrel inhibit (blank) mediated PLT activation

A

ADP

179
Q

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

A

GpIIb/IIIa

180
Q

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

A

all except ristocetin

181
Q

Ticlopidine & Clopidogrel will cause impaired aggregation against which agonist?

A

ADP

182
Q

What bleeding disease is made by a diagnosis of exclusion?

A

ITP

183
Q

Heparin induced thrombocytopenia is IgG binding to what complex?

A

Heparin-PF4 between the drug and the PLT

184
Q

T/F: bleeding is rare in HIT

A

TRUE

185
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

186
Q

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

A

d-dimer

187
Q

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

A

venous

188
Q

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

A

TRUE

189
Q

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

A

antiphospholipid; can be classified as lupus anticoagulant or anticardiolipin

190
Q

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

A

antiphospholipid syndrome

191
Q

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

A

protein C and S

192
Q

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

A

8a to X

193
Q

What PLT surface marker can HEP bind to?

A

PF4

194
Q

What causes PLT destruction in heparin induced thrombocytopenia?

A

IgG binding to HEP-PF4

195
Q

What activates the PLTs in HIT?

A

the fragments of the destroyed PLTs, leading to thrombosis

196
Q

DIC can lead to (blank) of downstream tissue

A

infarction and ischemia

197
Q

Where do you see bleeding in DIC?

A

IV sites and mucosal surfaces

198
Q

How does pregnancy cause DIC?

A

TT from the amniotic fluid may initiate coag cascade

199
Q

Sepsis from what two bugs can cause DIC?

A

E. coli and N. meningitidis

200
Q

Macrophages release what two cytokines during sepsis that can lead to DIC?

A

TNF-a and IL-1

201
Q

What is is about infx with E. coli and N. meningitidis that leads to DIC?

A

release of endotoxins

202
Q

(blank) from adenocarcinoma can lead to DIC

A

mucin

203
Q

Primary granules that go on to form Auer rods in (blank) can cause DIC

A

Acute promyelocytic leukemia

204
Q

what kind of snake bite can cause DIC?

A

rattlesnake

205
Q

What are the lab values for DIC?PLTPT/PTTfibrinogenwhat type of anemia

A

LOW PLT (lots of little clots)INCREASED PT AND PTT (consumption of cascade)decreased fibrinogen (making clots)MAHA

206
Q

What is the best test to screen for DIC?

A

D-dimer

207
Q

Are d-dimers formed from the splitting of fibrin or fibrinogen?

A

fibrin; FROM LYSIS OF ALREADY PRESENT CLOT

208
Q

Besides addressing the underlying condition causing the DIC, what supportive care can you give the patient?

A

transfusion of cryoprecipitate

209
Q

What converts plasminogen to plasmin?

A

tPA

210
Q

Plasmin cleaves (blank) and serum (blank), destroys coagulatoin factors, and blocks platelet (aggregation/adhesion)

A

cleaves fibrin and serum fibrinogenblocks PLT aggregation

211
Q

What inactivates plasmin?

A

a2-antiplasmin

212
Q

A radical prostatectomy resulting in large releases of urokinase or cirrhosis of the liver resulting in decreased a2-antiplasmin can both result in increased (blank)

A

bleeding

213
Q

What other disorder do issues of fibrinolysis resemble clincally?

A

DIC

214
Q

Describe the labs for fibrinolytic disorders:PT/PTTbleeding timePLTD-dimers (present/absent)

A

increased PT/PTTincreased bleeding timeNORMAL PLTS; THERE ARE NO CLOTS, JUST ACTIVATION OF CLOT BUSTERNO D-DIMER BECAUSE NO ACTUAL CLOTS

215
Q

What is the Tx for issues of tPA overdose or fibrinolytic disorders?

A

aminocaproic acid, blocks activation of plasminogen

216
Q

T/F: a thrombus may occur in an artery or vein

A

TRUE

217
Q

Where do DVTs normally occur?

A

below the knee

218
Q

DVTs are characterized by lines of (blank) and attachment to the vessel wall

A

lines of Zahn

219
Q

what are the three risk factors for thrombus that makeup Virchow’s triangle?

A
  1. disruption in blood flow2. endothelial cell damage3. hypercoagulable state
220
Q

T/F: turbulent non-laminar blood flow can cause clot formation

A

TRUE

221
Q

Immobilization, cardiac wall dysfunction, and anuerysm are all things that cause a (blank) in blood flow

A

disruption

222
Q

Endothelial cells prevent thrombosis by protecting expsoure to subendothelial (blank) and underlying tissue factor

A

SEC

223
Q

What two molecules do the endothelial cells produce that prevent thrombosis?

A

PGI2 and NO; PGI2 is opposite of TXA2 and NO causes vasodilation

224
Q

Endothelial cells secrete heparin-like molecules that augment (blank) which inactivates thrombin and coag factors

A

ATIII

225
Q

What are the three actions of tPA?

A
  1. converts plasminogen to plasmin2. cleaves fibrin and serum fibrinogen and destroys coag factors3. blocks PLT aggregation
226
Q

Atherosclerosis, vasculitis, and high levels of (blank) can cause endothelial damage

A

homocysteine

227
Q

What two vitamin defs can lead to high homocysteine?

A

Vit. B12 and folate def

228
Q

What enzyme deficiency can lead to homocysteine buildup?

A

Chystathionine beta synthase (CBS)

229
Q

Vessel thrombosis, mental retardation, lens dislocation, long slender fingers, and high levels of homocysteine are indicative of what congential enzyme def?

A

CBS

230
Q

Hypercoagulable states are due to excess (blank) or deficiencies of (blank)

A

excess procoagulants or def. anticoags

231
Q

DVTs normally ocurr below the knee or in what two arteries?

A

hepatic and cerebral

232
Q

Protein C or S def decreases (neg/pos) feedback on the coag cascade

A

negative, they are ANTICOAGS

233
Q

What factor do proteins C and S inactivate?

A

FVIII

234
Q

Protein C and S def has an increased risk of what drug reaction?

A

warfarin skin necrosis

235
Q

Warfarin works by decreasing Vit. K dependent factors. Why does a protein C or S deficiency cause concern at the beginning of warfarin Tx?

A

The half life of C and S is shorter than that of the 2 7 9 10; therefore the anticoags disappear faster than the coags and the pt is at risk of a microvessel thrombus

236
Q

What is Factor V Leidin?

A

FV that lacks the cleavage site for C and S

237
Q

What is the most common cause of hypercoagulable state?

A

Factor V Leidin

238
Q

An inherited point mutation that increases prothrombin expression is caused by (blank)

A

Prothrombin 20210A;

239
Q

ATIII def decreases the effect of what class of molecules released by the endothelium?

A

heparin like molecules

240
Q

What is unique about the PT/PTT in ATIII def when treating with heparin?

A

PTT does not rise with standard heparin dosing ATIII def; since aTIII is bound by HEPARIN-like molecules, the action of heparin is going to be limited!!

241
Q

Once high doses of heparin are given to acheive an anticoag’d state in ATIII def pts, what is given to maintain their blood viscosity?

A

coumadin

242
Q

The pill increases a hypercoagulable state via what mechanism?

A

estrogen increases the production of coagulation factors.

243
Q

What is the most common type of embolus?

A

thromboembolus

244
Q

What histo finding is characteristic of an atherosclerotic embolus?

A

cholesterol clefts in the embolus

245
Q

a (blank) embolus is common after traumatic bone fractures (long bones) and soft tissue trauma

A

soft tissue trauma

246
Q

in relation to the trauma, when does a fat embolus form?

A

while trauma is still present or during repair

247
Q

What clinical findings are associated with a fat emoblus/

A

SOB, and skin petechiae on the CHEST

248
Q

(blank) emobolus is seen in decompression sickness

A

gas embolus

249
Q

What is the chronic form of gas embolus that causes multifocal ischemic necrosis of bone/

A

Caisson disease

250
Q

Gas embolus may also form during what type surgery?

A

laparoscopic

251
Q

Amniotic fluid is rich in what coagulation precursor?

A

TT

252
Q

Amniotic fluid emboli present with what symptoms as they travel the lung, brain, and systemically?

A

SOB, neurologic symptoms, DIC

253
Q

Squamous cells and keratin debris in the embolus is characteristic of what?

A

amniotic fluid embolus

254
Q

PE normally arises from a DVT in the lower extremity involving what three veins?

A
  1. femoral2. iliac3. popliteal
255
Q

T/F: PE is normally clinically silent

A

true, b/c the lung has dual blood supply

256
Q

What percent of PEs result in infarction?

A

10%; need pre-existing compromise!

257
Q

what symptoms do pts with PE have?

A

SOB, hemoptysis, pleuritic chest pain, pleural effusion

258
Q

Describe the labs for PE:V/Qspiral CTLower extremity USD-dimer

A

V/Q mismatch; perfusion is abnormalCT shows vascular filling defectUS shows a DVTelevated D-dimer because they are trying to lyse the PE AND the DVT!!

259
Q

What type of embolus in PE causes sudden death?

A

saddle embolus; death by electromechanical dissociation

260
Q

WHat happens with chronic pulmonary emboli?

A

plumonary HTN

261
Q

Where do most systemic emoboli come from?

A

left heart, normally go to lower extremities

Block 7 Week 4 Colt (9 decks)

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