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I3 Exam 1 > Coagulation Pre-work Mauro > Flashcards

Coagulation Pre-work Mauro Flashcards

1
Q

What does endothelin release cause?

A

vasoconstriction at the site of vessel injury

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2
Q

What provides the initial tethering of platelets to form a platelet plug (platelet adhesion)?

A

Glycoprotein1b/ IX complex

- binds platelets to the vWF in the exposed subendothelium

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3
Q

What do platelets granule release after they undergo a shape change?

A

ADP, serotonin, TXA2, fibrinogen, platelet derived growth factor

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4
Q

What do ADP and serotonin do upon release?

A

recruit additional platelets

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5
Q

What does TXA2 do upon release?

A

promotes vasoconstriction

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6
Q

What links platelets together

A

Fibrinogen through GP11b/IIIa complex

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7
Q

What does the GP2IIb-IIIa complex do?

A

platelets aggregate when linked with fibrinogen to eachother through this complex

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8
Q

What cell released platelets?

A

megakaryocytes

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9
Q

What initiates hemostasis?

A

exposure of tissue factor to blood which activates proenzymes

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10
Q

Where are all of the coenzymes for the clotting cascade synthesized?

A

liver except for VWF

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11
Q

Where is VWF synthesized

A

megakaryocytes and endothelial cells

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12
Q

What does tissue factor bind upon its release in the extrinsic pathway?

A

factor VIIa which activates factor X which enters the common final pathway

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13
Q

What plasma factors are activated first in the intrinsic pathway?

A

kininogen, kallikrein, and factor XIIa

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14
Q

What does factor XIIa activate?

A

Factor XI which activates factor IX

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15
Q

What does factor IXa complex with to activate factor X?

A

in complex with factor VIIIa

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16
Q

What releases factors VIII

A

VWF

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17
Q

What is factor Va released by

A

platelet alpha granules

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18
Q

What binds together as the first step in the final common pathway?

A

Factors X and Va to form thrombin from prothrombin

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19
Q

What does thrombin convert in the final common pathway?

A

fibrinogen to fibrin

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20
Q

What factor stabilizes and cross links the overlapping fibrin monomers?

A

factors XIIIa

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21
Q

What starts the clotting cascade?

A

the extrinsic pathway when tissue factor is released from the endothelium which forms factors Xa

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22
Q

What is the role of factor Xa

A

activates platelets = exposure of phospholipids on platelet surface which supports assembly of enzyme complexes

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23
Q

What leads to increased production of factor VIII and factor IX

A

more factor X and thrombin formation

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24
Q

What does factor Xa cleave?

A

FVIII from vWF to activate platelet to expose phospholipid on its surface

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25
Q

What does thrombin activate?

A

FIX, FXI, FVIIII which starts the intrinsic pathway

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26
Q

What is the role of antithrombin

A

circulating plasma protease inhibitor

- neutralizes thrombin, Xa, IXa, XIIa, XIa by forming irreversible complexes

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27
Q

Heparin

A

binds to anti-thrombin and increases its rate of inactivation by 1000x fold and can bind to thrombin simultaneously to inactive it

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28
Q

Protein C and S system

A

as more thrombin is formed, thrombin will bind to thrombomodulin causing a structural change and then this complex with Ca2+ can activate protein C which is attached to endothelial surface via EPCR and activated protein C with protein S inactivates factor Va and VIIIa so it impairs the final common pathway from moving forward

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29
Q

What does protein S do?

A

increased the cleaving rate of protein VIIIa by protein C

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30
Q

What would a deficiency of protein S or C lead to?

A

impairment of termination of clotting and lead to an increase of hyper coagulable states

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31
Q

What is the role of TFPI

A

circulates in the plasma and inhibits factor Xa directly and factor VIIa

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32
Q

What does TFPI inhibit directly?

A

FXa and then when bound to Fxa it inhibits tissue factor:FVIIa impairing the triggering method of extrinsic pathway

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33
Q

What leads to an increase in TFPI

A

heparin

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34
Q

What initiates fibrinolysis

A

when plasminogen via a lysine residue binds to the fibrin clot with tPA which leads to the conversion of plasminogen to plasmin which can then cleave fibrin and fibrinogen and clotting factors and releases fibrin degradation productions

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35
Q

What is tPA released by?

A

the endothelial cells

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36
Q

What does PAI-1 inhibit

A

tPA

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37
Q

What does a deficiency of PAI-1 lead to?

A

bleeding problems because no check to fibrinolytic pathway

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38
Q

Where is alpha-2-antiplasmin made

A

liver

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39
Q

What does alpha-2-antiplasmin inhibit

A

plasmin

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40
Q

TAFI

A

circulates in the plasma and is activated by thrombin

- removes the lysine residues from the fibrin clot to impair the ability of plasminogen and tPA to bind leads to a delay

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41
Q

What does thrombin activate in fibrinolysis

A

TAFI

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42
Q

What initiates the extrinsic pathway to initiate the whole clotting cascade?

A

tissue factor

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43
Q

What are the 4 pro-thrombotic properties of endothelium

A
  1. synthesizes vWF and FVIII
  2. releases tissue factor
  3. produces PAI
  4. contains phospholipids that facilitate clot formation
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44
Q

When endothelium is intact how does it impair clot formation and binding of platelets

A
  • not conducive to binding

- prostacyclin and nitric oxide inhibit platelet binding

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45
Q

What are the general bleeding symptoms for platelet defects

A

mucocutaneous bleeding: oral cavity, nasal, GI, GU

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46
Q

Which type of defect will cause excessive bleeding from minor cuts?

A

primary hemostasis - platelet defects

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47
Q

What type of defect will have petechia

A

primary hemostasis - platelet defect

  • small capillary hemorrhages on the legs
  • asymptomatic
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48
Q

Which type of defect will have small and superficial ecchymoses

A

primary hemostasis - platelet defects

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49
Q

Which type of defect will have hemarthroses and muscle hematomas

A

secondary hemostasis - coagulation disorder

- common in severe deficiency or mild/moderate factor deficiency

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50
Q

Which type of defect will lead to immediate bleeding with surgery?

A

primary hemostasis, platelet defect

- usually delayed with secondary hemostasis

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51
Q

Which type of defect will have large subcutaneous and soft tissue hematomas

A

secondary hemostasis coagulation disorders

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52
Q

What is a normal platelet count

A

150,000 - 400,000 platelets per microliter

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53
Q

What level is prolonged bleeding seen at

A

less than 100,000

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54
Q

What is a platelet less than 50,000 a concern for

A

bleeding with surgery

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55
Q

What is the concern if platelets are less than 10,000

A

concern for spontaneous bleeding

56
Q

What is a normal bleeding time

A

7.5 minutes

57
Q

When is bleeding time prolonged?

A

thrombocytopenia, qualitative platelet disorders, and von Willebrand disease

58
Q

What is prothrombin time looking at?

A

extrinsic and common pathways

factors VII, X, V, prothrombin and fibrinogen

59
Q

What does a coagulation test measure for

A

factor VII deficiency - liver disease

vitamin K deficiency

or factor deficiencies

60
Q

what is the partial thromboplastin time looking at

A

factors XII, XI, IX, X, V, prothrombin and fibrinogen

  • intrinsic pathway
61
Q

mixing study

A

on any patient with prolonged PT or PTT

- patients blood is mixed with equal amounts of normal blood and the prolonged test is repeated

62
Q

What will you expect to see in a factor deficiency if a patient’s blood has 0% of the factor level and is mixed with normal blood that has 100% of the factor level

A

this will lead to product having 50% normal factor level if there is a deficiency

63
Q

What does thrombin time measure

A

conversion of fibrinogen to fibrin which is the final step in clotting cascade

64
Q

What would cause prolonged TT

A
  • heparin
  • direct thrombin inhibitors
  • hypofibrinogenemia
  • circulating light chains or paraproteins
65
Q

What is a D-dimer test

A
  • elevated in presence of clot turn over
  • marker of fibrinolysis
  • marker of blood clotting
66
Q

In which primary hemostasis problems will you have a normal PT and PTT

A

thrombocytopenia, qualitative platelet defect and von willebrand disease

67
Q

In which secondary hemostasis problem will you have normal PT and PTT

A

factor XIII deficiency - helps cross link fibrin monomers into fibrin polymer

68
Q

What type of vascular problem do you see a normal PT and PTT

A

-vascular purpuras = structural problems with vessels, vasculitis, collagen problems

69
Q

What does an isolated prolonged PT tell you

A

extrinsic pathway problem

  • FVII deficiency
  • if mixing study is correct you can have a factor deficiency, vitamin K deficiency, liver deficiency
  • if mixing doesn’t correct , you have a factor VII inhibitor
70
Q

What does an isolated prolonged PTT tell you

A

intrinsic pathway problem

- if mixing study doesn’t correct

71
Q

What does a patient with prolonged PTT that corrects with mixing that has no bleeding have a deficiency of?

A

factor XII, pre-kallikrein, kininogen deficiency

72
Q

What does a patient with prolonged PTT that corrects with mixing that has bleeding have a deficiency of?

A

factor XI, IX, VIII deficiency

- VWD

73
Q

What does a patient with prolonged PTT that doesn’t correct with mixing have an inhibitor of?

A

factor inhibitor: factor VIII, IX, XI

  • heparin - binds to antithrombin to increase inactivation
  • Lupus anticoagulants
74
Q

What do patients with prolonged PT and PTT have deficiencies of?

A
  • deficiency final common pathway factors
  • severe vitamin K deficiency
  • severe liver disease
  • disseminated intravascular coagulation
75
Q

Which factor is deficient in hemophilia A

A

FVIII

76
Q

Which factor is deficiency in hemophilia B

A

FIX

77
Q

Are women affected by hemophilia

A

no, they are carriers if their father has hemophilia

- only males are affected

78
Q

What percent of factor levels is present in patients with severe hemophelia?

A

less than 1%, they have spontaneous bleeding

79
Q

What percent of factor levels is present in patients with moderate hemophelia?

A

1-5%, bleed after slight trauma

80
Q

What percent of factor levels is present in patients with mild hemophelia?

A

5-30%, bleed after surgery or moderate trauma

81
Q

What PT and PTT will patients with hemophelia have

A

prolonged PTT and normal PT

82
Q

What are symptoms of hemophelia

A
  • hemarthrosis - joint bleeding
  • muscle bleeds
  • mucocutaneous bleeding
  • intracranial bleeds
  • post-dental bleeding
  • post-surgical bleeding can be delayed by days
83
Q

Do patients with hemophelia bleed after minor cut or abrasions?

A

NO, their platelets are working normally

84
Q

What is a treatment for hemophelia

A
  • give factor VIII or IX

- give DDAVP (in mild hemophelia A) which stimulates the release of factor VIII

85
Q

What is DDAVP used for?

A

mild hemophelia A, stimulates the release of FVIII from endothelium

86
Q

What do you do for a patient that comes in with an acute bleed with hemophelia

A

give appropriate factor to try and get 30% of normal factor levels

87
Q

Von Willebrand disease

A
  • most common inherited bleeding disorder
  • vWF = huge molecule involved in primary and secondary hemostasis
  • binds platelets to exposed subendothelium
  • carrier for FVIII
88
Q

What can deficiencies in vWF lead to

A

mucocutaneous bleeding

89
Q

What is type 1 VWD

A
  • partial deficiency of VWF
  • AD
  • vWF antigen low and vWF activity low
  • FVIII level low
90
Q

What is type 2 VWD

A
  • usually AD

- activity lower than antigen level with normal or low FVIII

91
Q

What is type 3 VWD

A
  • total deficiency of vWF
  • rare, severe, AR
  • decreased or absent vWF antigen and activity
92
Q

What is a treatment for type 1 VWD

A

DDAVP to release vWF and FVIII

- intermediate purity FVIII concentrates that contain VWF

93
Q

What is a treatment for type 2 or 3 vWD

A
  • intermediate purity FVIII concentrates that contain vWF
94
Q

What clotting factors are synthesized by the liver?

A

all clotting factors except FVIII and vWF

95
Q

What will the PT and PTT look in a patient with liver disease

A

PT will prolong because FVII is affected the most

- PTT is prolonged in severe disease

96
Q

Which factors require vitamin K

A

post translational modification of factors II, VII, IX, X, protein C and protein S

97
Q

What can cause a vitamin K deficiency

A

biliary tract disease/fat malabsorption, drugs (abx, cholestyramine), severe malnutrition

98
Q

Which factor is most sensitive to vitamin K deficiency

A

FVII so you get a prolonged PT first

99
Q

FVIII inhibitors - alloantibodies

A

alloantibodies in 25% of patients with severe hemophelia after numerous exposures to foreign FVIII

100
Q

FVIII inhibitors - autoantibodies

A

patients were not born with deficiency in factor VIII

  • acquired inhibitor to their own FVIII
  • occurs in post-partum, lupus, RA, malignancy, allergic rxn, lymphoproliferative disease
101
Q

What are the symptoms of FVIII inhibitors

A

ecchymoses, epistaxis, GI, hematuria, intracranial, rare themarthroses (unlike hemophelia)

102
Q

What is the diagnostic test for FVIII inhibitors

A

prolonged PTT that doesn’t correct with mixing

103
Q

What is the treatment for FVIII inhibitors

A
  • can’t use factor to treat because of inhibitors
  • use immunosuppresion
  • FEIBA = factor 8 bypassing agent
  • NovoSeven
104
Q

What is the first step of DIC

A

diffusion activation of coagulation (uncontrolled production of thrombin) leading to arterial and venous clotting and tissue ischemia

105
Q

What causes bleeding in DIC

A
  • consumptive coagulopathy (platelets, fibrinogen, prothrombin, factors get used tup)
  • secondary fibrinolysis to break clots down - large amount of fibrin degradation products can impair normal platelet aggregation
106
Q

What causes DIC

A
  • thromboembolism
  • AML
  • sepsis
  • placental abruption
  • severe liver failure
107
Q

What are the symptoms of DIC

A

bleeding, renal and liver dysfunction, pulm dysfunction, shock, thromboembolism

108
Q

What are the diagnoses for DIC

A

prolonged PT, PTT, low fibrinogen, low platelets, increased FDP and DDimer

109
Q

What is the treatment for DIC

A
  • treat underlying disease

- supportive care (platelet, FFP, cryofibrinogen transfusion)

110
Q

Does the venous system consist of muscular vessels?

A

no the venous system is non-muscular with valves, the artery system has muscular vessels

111
Q

Which system has a lower rate of blood loss associated with trauma?

A

venous system

112
Q

Which system uses platelets for critical rapid response?

A

arterial system

113
Q

The generation of what is critical in the venous system?

A

the clotting cascade, rate of thrombin generation is critical i the venous system but secondary in the artery system

114
Q

What is the treatment for venous problems

A

anticoagulants to impair clotting cascade

115
Q

What happens with problems in the arterial system

A

MI, CVA, PVD

116
Q

What is the treatment for anti-platelet agents?

A

Asprin and plavix

117
Q

What is venous stasis

A

decreased blood flow throughout the venous system

118
Q

What causes vascular injury

A

trauma, surgery, infection, hypotension

119
Q

What are inherited risk factors for thrombophilia

A

FVL deficiency - homozygous = increased risk for VTE compared to heterozygous

PT gene mutation = increases risk of VTE

Protein S and C deficiency - increase risk of clotting

120
Q

Factor V Leiden

A

most common inherited cause for thrombophilia

  • point mutation that abolishes cleaving site of activated protein C
  • slower degradation time because activated protein C isn’t able to inactive it
  • extended thrombogeneration
121
Q

Prothrombin gene mutation

A
  • point mutation

- causes a 30% increase in prothrombin levels = increased clot formation

122
Q

Protein C and S deficiency

A
  • deficiency = sustained movement through the clotting cascade
  • increased clotting risk by 8 fold
123
Q

What does activated protein C inactive?

A

inactives FVa and FVIIIa

124
Q

What does protein S inactivate?

A

increases rate of inactivation of APC

- deficiency = decreased APC = increased FVa and FVIIIa

125
Q

Antithrombin deficiency

A

circulating plasma protease inhibitor that neutralizes thrombin
- deficiency leads to increased amount of activating clotting factors

126
Q

What are acquired transient risk factors for VTE

A

orthopedic surgery, trauma and serious accidents, central lines, acute medical illness, immobility, prolonged travel

127
Q

What are acquired persistent risk factors for VTE

A

obesity, cancer, myeloproliferative neoplasms, paralysis, nephrotic syndrome

128
Q

What can cause arterial clotting in addition to venous clotting?

A

DIC, MPN (myoproliferative neoplasms, antiphospholipid syndrome)

129
Q

What is the effect of hormones on clotting

A

increased estrogen increases the risk of clotting = birth control

  • pregnancy deliveries and postpartum
  • hormone replacement therapy
  • infertility treatment
130
Q

PE/DVT treatment

A

2 or more unprovoked events = indefinite anticoagulation

1 unprovoked life threatening event = indefinite anticoagulation

1 unprovoked event with APLS, AT, combined thrombophilia = indefinite anticoagulation

1 provoked event (paralysis, MPN, metastatic cancer) = indefinite anticoagulation

1 provoked event with transient risk factor = 3-6 months of anticoagulation

131
Q

Anti-phospholipid syndrome

A

can be primary with no underlying cause or secondary to immune disease, medications, infections, malignancy

132
Q

What does the antiphospholipid antibody increase in the body?

A

increases pro-coagulants and vascular tone

133
Q

What is the clinical diagnosis for APLS

A

arterial or venous thrombosis OR significant pregnancy morbidity (premature birth less than 34 weeks, embryonic miscarriages)

134
Q

What is the laboratory criteria for APLS

A

one or more of the following present on two occasions atleast 12 weeks apart:
anticardiolipin Ab or
Beta 2 glycoprotein Ab or
Lupus anticoagulant

135
Q

What is the treatment for APLS if the clinical diagnosis is thrombosis

A

anticoagulation for 6 months if not indefinite

136
Q

Prolonged dRVVT assay

A
  • venom is added to the blood and activates factor X directly = looks at clotting pathway below that and it is prolonged by lupus coagulants
137
Q

What is the treatment for APLS if the clinical diagnosis is pregnancy morbidity

A

LMWH (heparin) and baby aspirin during pregnancy and post partum

I3 Exam 1 (12 decks)

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