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SP15 Pathology > Exam 2; Hemostasis and Thrombosis > Flashcards

Exam 2; Hemostasis and Thrombosis Flashcards

1
Q

This refers to the ability to maintain blood in a fluid state and prevent loss from sites of vascular damage

A

hemostasis

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2
Q

What is primary hemostasis

A

platelet response to vascular injury (adhesion and aggregation)

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3
Q

What is the membrane receptor for primary hemostasis adhesion

A

glycoprotein 1b

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4
Q

What is the adhesive protein for primary hemostasis adhesion

A

Von Wildebrand factor

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5
Q

What is the appropriate surface for primary hemostasis adhesion

A

sub endothelial matrix (collagen)

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6
Q

Secretion of these drive platelet activation

A

alpha-granules and dense bodies

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7
Q

As platelets are activated by binding to vWF, there is release of 2nd messenger molecules which lead to what four changes

A

shape change from discoid to spherical
secretion of cytoplasmic ADP
activation of the glycoprotein IIb/IIIa receptor
contraction of the platelet mediated through actin fibers

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8
Q

What is platelet aggregation mediated by

A

the release of cytoplasmic ADP into local milieu causes activation of adjacent platelets and platelet-platelet binding is mediated through fibrinogen and GP IIb/IIIa receptor

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9
Q

What is secondary hemostasis

A

fibrin clot formation

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10
Q

How is the fibrin clot formed

A

with cross linking of fibrin monomers by factor XIIIa

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11
Q

What is thrombin converted to

A

thrombin to fibrinogen to fibrin

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12
Q

What is the intrinsic pathway

A

the sequence of activation of factor XII by kallikrein followed by activation of factor XI by XIIa, factor XIa activates factor IX

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13
Q

What is the extrinsic pathway

A

the sequence of activation of factor VII by tissue factor

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14
Q

What is the common pathway

A

it involves the activation of X to Xa, followed by conversion of prothrombin II to thrombin, followed by conversion of fibrinogen to fibrin

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15
Q

This is formed when fibrin monomers generated by thrombin polymerize to form a long strand, made more stable by covalently cross linking with factor XIII

A

fibrin clot

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16
Q

Primary hemostasis regulates what

A

platelets

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17
Q

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

A

antithrombins

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18
Q

This molecule, in the presence of heparin becomes activated so that it can form a complex with thrombin, thus destroying the ability of thrombin to participate in the generation of fibrin monomers

A

antithrombin III

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19
Q

This regulates the major cofactors of the coagulation cascade, factors and VIIIa

A

protein C system

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20
Q

Deficiencies in protein C or protein S can result in what

A

hypercoaguable states

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21
Q

This mutation also promotes coagulation; resistance to enzymatic inactivation by the protein C/S complex

A

Factor V leiden mutation

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22
Q

In the presence of fibrin, this can bind to plasminogen and convert it to an active enzyme, plasmin

A

tissue plasminogen activator (TPA)

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23
Q

What does plasmin do

A

it breaks down previously cross-linked fibrin monomers into fibrin degradation products, providing a mechanism to break down previously formed clots.

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24
Q

This is a measurement of the time needed for plasma to form a clot in the presence of added tissue thromboplastin, to initiate the extrinsic cascade and calcium ionsl used to measure degree of anticoagulation in patients receiving oral anticoagulants

A

prothrombin time (PT)

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25
Q

What does a prolonged prothrombin time indicate

A

decreases or abnormalities in factors VII, X, V, II and/or fibrinogen

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26
Q

This is a measurement of the time needed for plasma to form a clot in the presence of added ground glass or kaolin (factor XII), cephalin, and Ca; to initiate the intrinsic cascade

A

partial thromboplastin time (PTT)

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27
Q

What is partial thromboplastin time used to measure

A

the degree of anticoagulation in patients receiving heparin

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28
Q

This is a measurement of the platelet number in anti coagulated blood quantified by an automated instruments ; the normal range is 150,000 to 400,000

A

platelet count

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29
Q

This refers to a decrease in platelet number

A

thrombocytopenia

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30
Q

This refers to an increase in platelet number

A

thrombocytosis and thrombocythemia

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31
Q

This is a measurement of platelet function, as determined by the time taken for a standardized skin incision to stop bleeding, the normal range is 2-8 minutes, its prolonged when there are abnormalities of platelet number and function

A

bleeding time

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32
Q

When is a mixing study used

A

when either PT or PTT is prolonged

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33
Q

What is a mixing study

A

Mixing of normal plasma and patient plasma in a 1:1 ration

34
Q

If the problem is corrected after a mixing study, what does this mean

A

that there is a deficiency

35
Q

If the problem is not corrected after a mixing study, what does this mean

A

an inhibitor is present, either factor specific or lupus anticoagulant type

36
Q

These types of bleeding disorders are present at birth, and are usually heredity

A

congenital disorders

37
Q

These types of bleeding disorders occur after birth, and are more often related to medication or other pathologic processes

A

acquired disorders

38
Q

What are the clinical manifestations of primary hemostasis disorders

A

mucocutaneous bleeding and/or bleeding associated with trauma

39
Q

What are the laboratory manifestations of primary hemostasis disorders

A

prolonged bleeding time and thrombocytopenia

40
Q

What are the clinical manifestations of secondary hemostasis disorders

A

soft tissue bleeding and/or bleeding associated with trauma

41
Q

What are the laboratory manifestations of secondary hemostasis disorders

A

prolonged PT and/or PTT and/or thrombin time

42
Q

What are the clinical manifestations of regulatory system disorders

A

soft tissue bleeding and/or bleeding associated with trauma

43
Q

What are the laboratory manifestations of regulatory system disorders

A

normal in screening test

44
Q

This is an autosomal dominant disorder associated with production of decreased amounts of a normal protein (quantitative abnormality) or production of a protein with abnormal function (abnormal function), or both

A

von Willebrand disease

45
Q

What are the clinical manifestations of vWD

A 
epistaxis (bleeding from the nose)
ecchymoses
mucosal bleeding
bleeding with trauma or surgery
symptoms improve after adolescence
46
Q

True or False

vWD is the most common inherited bleeding disorder; 1% of the population is affected

A

True

47
Q

What are the three types of vWD

A

type 1: quantitative (partial)
type 2; qualitative
type 3; quantitative (total)

48
Q

Because in vWD there is decreased vWF, what else is decreased

A

factor VIII

49
Q

What is the laboratory finding the BT/PFA-100 in vWD

A

prolonged

50
Q

What is the laboratory finding in PTT in vWD

A

usually prolonged; due to decreased factor VIII

51
Q

What are four treatment options of vWD

A

desmopressin
anti-fibrinolytic agents
factor VIII concentrates
cryoprecipitate

52
Q

This is a sex-linked recessive disorder with a deficiency of factor VII, it is the most common heredity cause of serious bleeding

A

hemophilia A

53
Q

What is the clinical hallmark of hemophilia A

A

recurrent soft tissue bleeding with symptoms starting earlier in life

54
Q

What are the other clinical manifestations of hemophilia A

A 
hemarthrosis
excessive bleeding with trauma
intramuscular hematomas
intracerebral hemorrhage
bleeding into other tissues
55
Q

What is the laboratory finding in PTT of hemophila A

A

prolonged, due to a decrease in VIII

56
Q

What classifies severe hemophilia A

A

<1% factor VIII

recurrent spontaneous soft tissue and joint space bleeding

57
Q

What classifies moderate hemophilia A

A

1-5% factor VIII

bleeding with minor trauma

58
Q

What classifies mild hemophilia A

A

> 5% factor VIII

bleeding with major trauma

59
Q

What are two therapies for hemophilia A

A

factor VIII concentrates

fibrinolytic inhibitors

60
Q

What are four disease related complications of hemophilia A

A

arthritis and joint destruction
pseudotumors
intracranial bleeding
retroperitoneal bleeding

61
Q

What are two treatment related complications of hemophilia A

A

antibodies to factor VIII

infectious disease

62
Q

This is a sex linked recessive disorder concerned with deficiency of factor IX

A

hemophilia B

63
Q

What are four disease related complications of hemophilia B

A

arthritis and joint destruction
pseudotumors
intracranial bleeding
retroperitoneal bleeding

64
Q

What are two treatment related complications of hemophilia B

A

antibodies to factor IX

infectious diseases

65
Q

When is a platelet disorder considered thrombocytopenia

A

when platelet count is <100,000/µL

spontaneous bleeding may not manifest until the count is below 20,000

66
Q

What are the four mechanisms of thrombocytopenia

A

decreased platelet production
increased destruction
sequestration
congenital versus acquired

67
Q

In which four ways can you evaluate for thrombocytopenia

A

clinical history/setting of prolonged bleeding or hemorrhage (petechial)
peripheral blood smear
bone marrow examination
platelet antibody determination

68
Q

This disorder is characterized by immune mediated destruction of platelets

A

immune thrombocytopenic purpura

69
Q

What are the characteristics of the acute/childhood form of immune thrombocytopenic purpura

A 
viral prodrome common
sudden onset
severe thrombocytopenia
frequently undergoes spontaneous remission
1:1 M:F
70
Q

What are the characteristics of the chronic/adult form of immune thrombocytopenic purpura

A 
no antecedent infection
gradual onset
moderate thrombocytopenia
infrequent spontaneous remission
more common in females
71
Q

What are the three clinical features of immune thrombocytopenic purpura

A

petechiae
ecchymoses
bleeding with trauma/surgery

72
Q

In immune thrombocytopenic purpura there are autoantibodies directed at what

A

platelet membrane antigens

GPIb/IX and IIb/IIIa are also targests

73
Q

In immune thrombocytopenic purpura there is increased IgG bound to platelet surface, which promotes what

A

increased sequestration/destruction by the reticuloendothelial system

74
Q

What are the two bone marrow and blood finding of immune thrombocytopenic purpura

A

megakaryocytes normal to increased

no microangiopathic changes on blood smear review

75
Q

What are the four therapies for immune thrombocytopenic purpura

A

corticosteriods
IV Ig
immunosuppression
splenectomy

76
Q

This is an acute disorder characterized by intravascular platelet activation with formation of platelet-rich micro thrombi throughout the circulation; if left untreated, is associated with high mortality

A

thrombotic thrombocytopenic purpura

77
Q

What causes thrombotic thrombocytopenic purpura

A

a deficiency of ADAMTS 13, a metalloproteinase that normally degrades very high mw vWF, resulting in accumulation of the abnormally large vWF
can be inherited or acquired

78
Q

This is unregulated, widespread intravascular activation of the hemostats system, resulting in both systemic formation of thrombin and plasmin with consumption of clotting factors and bleeding; platelets are consumed resulting in thrombocytopenia

A

disseminated intravascular coagulation

79
Q

What are the four clinical settings of DIC

A

infections (gram (-) sepsis)
tissue injury
obstetrical complications
certain malignancies

80
Q

What are some clinical manifestations of DIC

A

bleeding from multiple sites
thromboembolic problems
hypotension and shock
respiratory, hepatic, renal, and CNS dysfunction

81
Q

What are two therapies for DIC

A

removal/reverse of initial stimulus

supportive therapy with transfusions of blood products

SP15 Pathology (17 decks)

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