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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
What does a prolonged prothrombin time indicate
decreases or abnormalities in factors VII, X, V, II and/or fibrinogen
26
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
partial thromboplastin time (PTT)
27
What is partial thromboplastin time used to measure
the degree of anticoagulation in patients receiving heparin
28
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
platelet count
29
This refers to a decrease in platelet number
thrombocytopenia
30
This refers to an increase in platelet number
thrombocytosis and thrombocythemia
31
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
bleeding time
32
When is a mixing study used
when either PT or PTT is prolonged
33
What is a mixing study
Mixing of normal plasma and patient plasma in a 1:1 ration
34
If the problem is corrected after a mixing study, what does this mean
that there is a deficiency
35
If the problem is not corrected after a mixing study, what does this mean
an inhibitor is present, either factor specific or lupus anticoagulant type
36
These types of bleeding disorders are present at birth, and are usually heredity
congenital disorders
37
These types of bleeding disorders occur after birth, and are more often related to medication or other pathologic processes
acquired disorders
38
What are the clinical manifestations of primary hemostasis disorders
mucocutaneous bleeding and/or bleeding associated with trauma
39
What are the laboratory manifestations of primary hemostasis disorders
prolonged bleeding time and thrombocytopenia
40
What are the clinical manifestations of secondary hemostasis disorders
soft tissue bleeding and/or bleeding associated with trauma
41
What are the laboratory manifestations of secondary hemostasis disorders
prolonged PT and/or PTT and/or thrombin time
42
What are the clinical manifestations of regulatory system disorders
soft tissue bleeding and/or bleeding associated with trauma
43
What are the laboratory manifestations of regulatory system disorders
normal in screening test
44
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
von Willebrand disease
45
What are the clinical manifestations of vWD
``` epistaxis (bleeding from the nose) ecchymoses mucosal bleeding bleeding with trauma or surgery symptoms improve after adolescence ```
46
True or False | vWD is the most common inherited bleeding disorder; 1% of the population is affected
True
47
What are the three types of vWD
type 1: quantitative (partial) type 2; qualitative type 3; quantitative (total)
48
Because in vWD there is decreased vWF, what else is decreased
factor VIII
49
What is the laboratory finding the BT/PFA-100 in vWD
prolonged
50
What is the laboratory finding in PTT in vWD
usually prolonged; due to decreased factor VIII
51
What are four treatment options of vWD
desmopressin anti-fibrinolytic agents factor VIII concentrates cryoprecipitate
52
This is a sex-linked recessive disorder with a deficiency of factor VII, it is the most common heredity cause of serious bleeding
hemophilia A
53
What is the clinical hallmark of hemophilia A
recurrent soft tissue bleeding with symptoms starting earlier in life
54
What are the other clinical manifestations of hemophilia A
``` hemarthrosis excessive bleeding with trauma intramuscular hematomas intracerebral hemorrhage bleeding into other tissues ```
55
What is the laboratory finding in PTT of hemophila A
prolonged, due to a decrease in VIII
56
What classifies severe hemophilia A
<1% factor VIII | recurrent spontaneous soft tissue and joint space bleeding
57
What classifies moderate hemophilia A
1-5% factor VIII | bleeding with minor trauma
58
What classifies mild hemophilia A
>5% factor VIII | bleeding with major trauma
59
What are two therapies for hemophilia A
factor VIII concentrates | fibrinolytic inhibitors
60
What are four disease related complications of hemophilia A
arthritis and joint destruction pseudotumors intracranial bleeding retroperitoneal bleeding
61
What are two treatment related complications of hemophilia A
antibodies to factor VIII | infectious disease
62
This is a sex linked recessive disorder concerned with deficiency of factor IX
hemophilia B
63
What are four disease related complications of hemophilia B
arthritis and joint destruction pseudotumors intracranial bleeding retroperitoneal bleeding
64
What are two treatment related complications of hemophilia B
antibodies to factor IX | infectious diseases
65
When is a platelet disorder considered thrombocytopenia
when platelet count is <100,000/µL | spontaneous bleeding may not manifest until the count is below 20,000
66
What are the four mechanisms of thrombocytopenia
decreased platelet production increased destruction sequestration congenital versus acquired
67
In which four ways can you evaluate for thrombocytopenia
clinical history/setting of prolonged bleeding or hemorrhage (petechial) peripheral blood smear bone marrow examination platelet antibody determination
68
This disorder is characterized by immune mediated destruction of platelets
immune thrombocytopenic purpura
69
What are the characteristics of the acute/childhood form of immune thrombocytopenic purpura
``` viral prodrome common sudden onset severe thrombocytopenia frequently undergoes spontaneous remission 1:1 M:F ```
70
What are the characteristics of the chronic/adult form of immune thrombocytopenic purpura
``` no antecedent infection gradual onset moderate thrombocytopenia infrequent spontaneous remission more common in females ```
71
What are the three clinical features of immune thrombocytopenic purpura
petechiae ecchymoses bleeding with trauma/surgery
72
In immune thrombocytopenic purpura there are autoantibodies directed at what
platelet membrane antigens | GPIb/IX and IIb/IIIa are also targests
73
In immune thrombocytopenic purpura there is increased IgG bound to platelet surface, which promotes what
increased sequestration/destruction by the reticuloendothelial system
74
What are the two bone marrow and blood finding of immune thrombocytopenic purpura
megakaryocytes normal to increased | no microangiopathic changes on blood smear review
75
What are the four therapies for immune thrombocytopenic purpura
corticosteriods IV Ig immunosuppression splenectomy
76
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
thrombotic thrombocytopenic purpura
77
What causes thrombotic thrombocytopenic purpura
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
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
disseminated intravascular coagulation
79
What are the four clinical settings of DIC
infections (gram (-) sepsis) tissue injury obstetrical complications certain malignancies
80
What are some clinical manifestations of DIC
bleeding from multiple sites thromboembolic problems hypotension and shock respiratory, hepatic, renal, and CNS dysfunction
81
What are two therapies for DIC
removal/reverse of initial stimulus | supportive therapy with transfusions of blood products

SP15 Pathology (17 decks)

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