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general path > hemostasis and thrombosis > Flashcards

hemostasis and thrombosis Flashcards

1
Q

what is hemostasis

A

Ability to maintain blood in a fluid state and prevent loss

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2
Q

what are the 3 major components of hemostatic system

A

Vascular wall
Platelets
Coagulation proteins

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3
Q

how does vascular injury seal off the damged site to prevent futher blood loss

A

Exposes subendo collagen

  • activated platelets
  • activates coagulation proteins to create a more stable mesh with platelet plus
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4
Q

what is the primary hemostatic plug

A

the intial platelets coming together

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5
Q

what are the two aspects of hemostatic balance

A

Procoagulant

Regulatory

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6
Q

what is the first part of the platelet response

A

Adhesion of platelets to damaged endothelial site

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7
Q

what is needed for adhesion of platelets

A 
surface membrane receptor (glycoprotein Ib/IX)
adhesive protein (von willbrand factor)
appropriate surface (subendo collagen)
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8
Q

what is the roll of vWF

A

mediates adherence of platelets to subendo collagen

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9
Q

what happens when platelts are bound to vWF

A 
become activated
release second messenger molecules
shape change from discoid to spherical
secrete cytoplasmic ADP
activate glycoprotein IIb//IIIa recetpor
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10
Q

what mediates contraction of the platelet

A

actin fibers

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11
Q

what does release of cytoplasmic ADP into the local milieu by activated platelets do

A

activate adjectent platelets

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12
Q

what mediates platelet to platelet bind

A

Fibrinogen

gp IIb/IIIa receptor

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13
Q

what happens when soluble coagulation proteins within plasma is activated

A

Generate thrombin in an amplification reaction

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14
Q

what does thrombin to

A

converts fibrinogen to fibrin

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15
Q

what is the roll of fibrin

A

adds stability to the clot after fibrin monomers by covalently crosslinking by factor XIII

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16
Q

what is the intrinsic pathway

A

sequence of activation of Factor XII by kalikrein

activation of factor XI by factor XIIa

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17
Q

what is the extrinsic pathway

A

sequence of activation of factor VII by tissue factor

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18
Q

what is the common pathway

A

activation of X to Xa
conversion of prothrombin (II) to thrombin
conversion of fibrinogen to fibrin

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19
Q

how is a fibrin clot formed

A

fibrin monomers generated by thrombin polymerize to form a long strand

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20
Q

what makes the fibrin monomers stable

A

covalent crosslinking by factor XIII

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21
Q

what does primary hemostasis regulate

A

platelets

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22
Q

what does secondary hemostasis regulate

A

coagulation pathways

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23
Q

what molecules regulate primary hemostasis

A

NO
Prostacyclin (PGI2)
ADPase

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24
Q

what molecules regulate secondary hemostasis

A

Serine protease inhibitors (antithrombin)
protein C pathway (Controls Va and VIIIa)
fibrinolytic system (removes excess clot)

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25
Q

how does antithrombin regulate secondary hemostasis

A

Inhibit activity of thrombin and other serine proteases of the coagulation cascade by forming inactive enzyme-inhibitor complex

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26
Q

what is the action of antithrombin III in the presence of heparin

A

becomes activated so that it can form a complex with thrombin
- desotrys thrombin’s ability to participate in generation of fibrin monomers

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27
Q

what does Protein C regualte specifically

A

Factors Va and VIIIa

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28
Q

what are the parts of the protein C system( major effecor and coenzyme

A

Protein C: major effector

Protein S: major cofactor

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29
Q

what do protein C and S deficincies lead to

A

Hypercoaguable states

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30
Q

what does Factor V leiden mutation lead to

A

Promotes coagulation

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31
Q

what does tissue plasminogen activator do in presence of fibrin

A

Binds to plasminogen and converts it to active enzyme plasmin

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32
Q

what does active plasmin do

A

breaks down previsouly cross linked fibrin into fibrin degradation prodcuts
- breaks down previously formed clot

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33
Q

what does uncontrolled activation of plasmin lead to

A

bleeding complicactions

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34
Q

when is a TPA infusion done

A

recent myocardial infarcts

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35
Q

what tests are done for hemostasis

A 
Prothrombin time
international normalised ratio
partial thromboplastin time
platelet cound
bleeding time
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36
Q

what does prothrombin time screen for

A

Activity of proteins in the extrinsic pathway (factors V, VII, II, X, and fibrinogen)

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37
Q

what is done in a prothrombin time test

A

Phospholipid and tissue factor added to patient’s plasma with Ca++
- time noted for a clot(11-13 sec)

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38
Q

what does partial thromboplastin time screen for

A

actiivity in the intrinsic pathway (factors XII, XI, IX, VIII, X, V, II, and fibrinogen

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39
Q

what is done in a partial thromboplastin time tests

A

addition of negatively charged activator of factor XII to patient serum with Ca++
- clot form after 28-35 sec

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40
Q

when do we tend to do partial thromboplastin time

A

monitor patients on heparin

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41
Q

what does a problem being corrected in a mixing study show about hemostasis

A

PAtient deficiency exists

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42
Q

what happens if their is no correction of hemostasis in a mixing study

A

Inhibitor is present( factor specific or lupus anticoagulant type)

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43
Q

what is the most important part of defining the cause of a bleeding disorder

A

Careful clinical history

  • bleeding manifestation (evidence and nature of bleeding)
  • age of onset of symptoms
  • bleeding frequecy
  • family history
  • med history
  • predisposing causes
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44
Q

what kind of patient do you use prothrombin time on

A

patients with oral anticoagulants

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45
Q

how is a mixing study done

A

mix 50:50 with patient plasma and extra plasma

  • if a change in the PT and PTT test occurs a deficiency of some factors is present
  • if no hange, inhibitor is present, either factor specfic of lupus anticoagulant
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46
Q

how are congenital dissorders developed

A

hereditated and seen at birth

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47
Q

when do acquired disorders appear

A

after birth

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48
Q

what causes acquired disorders to come to be

A

Meds

pathologic processes

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49
Q

how do disorders of primary hemostasis manifest clinically

A

mucocutaneous bleeding

bleeding associated with trauma

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50
Q

hwo do disorders of primary hemostasis manifest laboratory

A

prolonged bleedingtime/PFA-100

thrombocytopenia

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51
Q

how do secondary hemostasis disorders manifest clincally

A

soft tissue bleeding

bleeding associated with trauma

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52
Q

how do secondary hemostasis disorder manifest clinically

A

include prolonged PT/PTT/thrombin time

53
Q

what are the clinical manifestation of disorders of the regulatory system

A

Soft tissue bleeding

Bleeding associated with trauma

54
Q

what are the laboratory manifestations of disorders of the regulatory system

A

Normal in screening tests

55
Q

how is von willebrand disease transmitted

A

Autosomal dominant disorder (usually)

56
Q

what does von willebrand disease result for

A

abnormalities of vW factor (wuantitiative, qualitative or both)

57
Q

what is the dominant clincial manifestation of von willebrand disease

A

Mucocutaneous bleeding

58
Q

what is the factor VIII complex made of

A

VonWillebrand factor

Factor VIII procoagulant

59
Q

are vWF and factor VIII made by the same gene

A

No, but different genes on the same chromosome

60
Q

what does vWF do

A

carrier molecule for factor VIII

glue between damaged endothelium and platelets (primary hemostasis)

61
Q

when is factor VIII procoagulant released for associated with vWF

A

when a clot is formed

62
Q

what does Factor VIII do once release from vWF

A

participated in the generation of factor X(secondary hemostasis)

63
Q

where is factor VIII synth and vWF synth

A

Factor VIII in liver

vWF in endothelial cells

64
Q

how mant people are affected by von willebrand disease

A

less than 1% (the most common inherited bleeding disorder

65
Q

when do symtoms of von willebrand disease improve

A

after adolescence

66
Q

what is the most common of von Willebrand disease types

A

most common: decreased vWK

67
Q

what does a decrease in vWK do to factor VIII

A

decreases the level of it in the blood

68
Q

what type of von willebrand disease is autosomal recessive

A

Type III (total absence)

69
Q

what are the laboratory manifestations of Von Wilebrand disease

A

prolonged bleeding time
Prolonged PTT(due to decreased Factor VIII)
Decreased vWF
Decreased factor VIII

70
Q

what do platelet studies show during von willebrnad disease

A

abnormal in 1/3

71
Q

what therapies can be used in von willebrand disease

A

desmopressin (releases vWF from endothelial cells)
antibrinolytic agents in mild cases
factor VIII concentrates containing vWF and cryoprecipitate in more sereve cases

72
Q

hows is hemophilia A transmitted

A

X-linked recessive

73
Q

what causes hemophilia A

A

deficiency of factor VIII

74
Q

what happens when you have hemophilia A

A

recurrent soft tissue bleeding

75
Q

when do symptoms of hemophilia A start

A

early childhood

76
Q

clinical manifestation of hemophilia A

A 
hemarthrosis
Soft tissue bleeding
excessive bleeding with trauma
intramuscular hematomas
intracerebral hemorrhage
bleeding into other tissues
77
Q

Lab results of Hemophilia A (BT/PFA-100, PTT, Factor VIII, vWF:Ag, vWF:Rcof, Factor IX)

A 
BT/PFA-100: normal
PTT: prolonged
Factor VIII: decreased
vWF:Ag: normal
vWF:RCof: normal
Factor IX: normal
78
Q

how much factor VIII is there in severe hemophilia A

A

less than 1 percent

79
Q

what happens in severe hemophilia A

A

recurrent spontaneous soft tissue and joint space bleeding (hemarthrosis)

80
Q

how much factor VIII is there in moderate Hemophilia A

A

1-5% factor VIII

81
Q

what happens in moderate hemophilia A

A

bleeding with minor trauma

82
Q

how much factor VIII is there in mild Hemophilia A

A

greater than 5% Factor VIII

83
Q

what happens in mild hemophilia A

A

bleeding with major trauma

84
Q

how does one treat hemophilia A

A

factor VIII concentrates
Recombinant Factor VIII
Inhibitors of fibrinolysis

85
Q

what are the disease related Hemophilia A complications

A

Arthritis and joint destruction
Pseudotumors
Intracranial bleeding
Retroperitoneal bleeding

86
Q

what are the treatment related complications

A

antibodies to Factor VIII
infectious diseases
hemolysis
allergic reaction

87
Q

what is the most common hereditary cause for serious bleeding

A

Hemophilia A

88
Q

how is hemophilia B transmitted

A

Sex linked recessive disorder

89
Q

what causes hemophilia B

A

deficiency of factor IX

90
Q

what are the clinical presentation of hemophilia B

A

similar to Hemophilia A

91
Q

what are the laboratory presentation of Hemophilia B

A

similar to hemophilia A

92
Q

what are the classifications of mehophilia B

A

mild
moderate
Severe

93
Q

what case of hemophilia can be difficult yo recognize clinically

A

Mild Hemophilia B

94
Q

what are the disease related complications of hemophilia B

A

arthritis and joint destruction
pseudotumors
intracranial bleeding
retroperitoneal bleeding

95
Q

what are the treatment related complications of hemophilia B

A

antibodies to factor IX

Infectious diseases

96
Q

how can one treat hemophilia B

A

factor IX concetrates
Recombo Factor IX
Inhibitors of fibrinolysis

97
Q

what causes thrombocytopenia

A

decreased platelet production

98
Q

what is the mechanisms of thrombocytopenia

A

increased destruction
decreased production
sequesttration

99
Q

how can evaluate thrombocytopenia

A 
- Clinical history/setting of 
prolonged bleeding or hemorrhage (petechial)
 - peripheral blood smear
 - Bone marrow examination
 - Platelet autoantibody determination
100
Q

what is the platelet count for thrombocytopenai

A

less than 100,000 per microleter

101
Q

when does spontaneous bleeding occur for thrombocytopenia

A

below 20,000

102
Q

how does bleeding due to thrombocytopenia appear

A

petechial hemorrhages in skin and muccous membranes

103
Q

what causes immune thrombocytopenia Purpura

A

immune mediated destruction of platelets by autoantibodies directed at the platelet membrane antigens

104
Q

what is the target for immune thrombocytopenic Purpura(ITP)

A

GPIb/IX and IIb/IIIa

105
Q

what happens to the platelets that are coated with

A

sequested in the speel and reticuloendothelial system

106
Q

when does Acute and chronic immune thrombocytopenic purpura form

A

acute: childhood
chronic: adult

107
Q

what follows acute immune thrombocytopenic Purpura

A

Viral prodrome and severe thrombocytopenia

108
Q

what follows chronic immune thrombocytopenia Purpura

A

no antecedent infection

109
Q

how does acute and chronic ITP come on

A

acute is sudden

Chronic is gradual

110
Q

how severe is acute and chronic Immune thrombocytopenic purpura

A

acute has severe thrombocytopenia

chronic is moderate thrombocytopenia

111
Q

does acute and chronic ITP remiss on its own

A

Acute: frequently undergoes spontaneous remission
Chronic: infrequent spontaneous remission

112
Q

M/F ratio of acute and chronic ITP

A

Acute: M/F is 1 to 1
chronic: more females

113
Q

what are the clinical features of ITP

A

petchial hemorrhages
Gingival bleeding
Ecchymoses (bruising)
bleeding with trauma or surgery

114
Q

what happens to Megakaryocytes in ITP

A

normal to increased

115
Q

microangiopathic changes on a blood smear for ITP

A

No changes

116
Q

how does one treat ITP

A

corticosteroids
Intravenous immunoglobulin
Immunosuppression
Splenectomy

117
Q

what is thrombotic thrombocytopenic purpura

A

acute disorder characterized by intravascular platelet activation with formation of plaetelet-rich microthrombi throughout the circulation

118
Q

what causes thrombotic thrombocytopenic purpura

A

deficiency of ADAMTS 13

119
Q

what is ADAMTS 13

A

metalloproteinase that normally degrade very high molecular weight vWF

120
Q

how is thrombotic thrombocytopenic purpura transmitted

A

inherited or acquired

121
Q

what happens if thrombotic thrombocytopenic purpura is leaf untreated

A

High mortality

122
Q

what is disseminated inctravascular coagulation

A

Unregulated, widespread intravascular activation of the hemostatic system

123
Q

what happens in disseminated intravascular coagulation

A
  • Systemic formation of thrombin and plasmin with simultaenous microthrombi formation
  • consumption of clotting factors that promote bleeding
124
Q

what are the clinical settings for DIC

A

Infections(gram negative sepsis)
tissue injury (trauma, burn, surgery)
obstetrical complications
Certain malignancies

125
Q

clinical manifestations of DIC

A 
bleeding from multiple sites
Thromboembolic problems
Hypotension and shock
Respiratory dysfunction
Hepatic dysfunction
Renal dysfunction
CNS dysfunction
126
Q

how to treat DIC

A

remove/reverse initaiting stimulus

Supportive therapy with transfusions of blood products(FFP, Cryoprecipiatates, Platelets)

127
Q

what is FFP

A

coagulation and regulatory proteins

128
Q

what are Cryoprecipitates

A

fibrinogen
VIII
vWF

general path (16 decks)

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