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Patho 2 > 3 - Hemostasis/Coagulation > Flashcards

3 - Hemostasis/Coagulation Flashcards

1
Q

Hemostasis is achieved through four main mechanisms:

A
  1. Vasoconstriction
  2. Platelet Plug
  3. Blood clot
  4. Fibrous tissue to close the hole permanently
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2
Q

How do platelets contribute to vasoconstriction in small vessels?

A

release thromboxane A2, which is a vasoconstrictor

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3
Q

Very small holes are closed with what type of plug?

A

Almost always platelet, and rarely blood

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4
Q

Platelets are formed in the _____ from _____

A

bone marrow

Megakaryocytes

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5
Q

What is the half life of a platelet?

A

8-12 days

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6
Q

Why does thrombocytopenia cause petechiae?

A

Normally very small wounds would be closed off with platelets adhering the endothelium to itself. When platelets are absent, the only other option is a blood clot, hence the bruised appearance

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7
Q

There are three essential steps to blood clotting:

A
  1. Production of prothrombin activator in response to vessel damage
  2. prothrombin activator catalyzes the conversion of prothrombin to thrombin
  3. thrombin acts as an enzyme to convert fibrinogen into fibrin, which forms the clot
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8
Q

In the presence of sufficient ____, prothrombin activator converts ____ to _____

A

calcium

Prothrombin

thrombin

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9
Q

What is the rate limiting factor in the coagulation cascade?

A

the formation of prothrombin activator

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10
Q

Prothrombin is formed continually by which organ?

A

The liver

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11
Q

Where is fibrinogen formed?

A

The liver

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12
Q

What is thrombin?

A

A proteolytic enzyme

Breaks fibrinogen into four fibrin monomers

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13
Q

initial fibrin fibers are weak and not cross linked. What changes this?

A

fibrin stabilizing factor from platelets

acts as an enzyme to form covalent bonds between the monomers and cross linkage with other fibrin fibers

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14
Q

The extrinsic pathway begins _______

The intrinsic pathway begins _______

A

with trauma to the vascular wall and surrounding tissues

in the blood in response to the presence of collagen

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15
Q

What’s the difference between factor VIII and factor VIIIa?

A

The “a” denotes the activated form

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16
Q

What is GpIIb/IIIa?

A

Glycoprotein 2b/3a

protein on the membrane of the platelet that binds fibrin linkages between platelets and facilitates aggregation

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17
Q

What is GpIa?

A

Glycoprotein 1A

Protein on the platelet membrane that binds with vWF

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18
Q

When platelets bind with vWF secreted by endothelial cells, they produce:

A

ADP, Thromboxane A2, Serotonin

All of these promote platelet aggregation and/or vasoconstriction

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19
Q

The first step of the extrinsic pathway is:

A

the release of Factor III (tissue factor) from damaged endothelial cells

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20
Q

What activates factor XII?

A

Contact with polyanions

Activated platelets secrete polyphosphates (polyanions) which activate factor XII

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21
Q

The first step of the intrinsic pathway is:

A

Activation of Factor XII and release of platelet phospholipids

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22
Q

The common pathway of coagulation is:

A

the activation of factor X

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23
Q

What are the growth factors produced by platelets?

What do they do?

A

VEGF: vascular regrowth

PDGF: collagen and muscle regrowth

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24
Q

What is tPA?

A

tissue plasminogen activator

it’s an enzyme that converts plasminogen to plasmin, which digests fibrin

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25
Q

What are the byproducts of fibrinolysis?

A

fibrin

D-Dimer

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26
Q

Someone with hemophilia would have a breakdown where in the coagulation cascade?

A

In the activation of factor X

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27
Q

Calcium is required for which stages of the coagulation cascade?

A

All of them, except the first two steps of the intrinsic cascade

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28
Q

Which is faster: extrinsic or intrinsic

A

the extrinsic, activated in about 15 seconds

intrinsic takes 6-10 minutes

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29
Q

What prevents intravascular coagulation?

A
  1. the smoothness of the endothelium
  2. the glycocalyx repels clotting factors and platelets
  3. thrombomodulin binds with thrombin, removing it from circulation and activating plasma protein C
  4. Plasma protein C inactivates factors 5 and 8
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30
Q

Intact endothelial cells produce ____ and ____ which inhibit platelet aggregation

A

NO

PGI2

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31
Q

There are two substances that remove thrombin from circulation:

A
  1. the fibrin fibers that are forming a clot
  2. antithrombin III
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32
Q

By itself heparin has no anticoagulant properties, but when it binds with ______, its effectiveness increases exponentially

A

Antithrombin III

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33
Q

Why does exogenous heparin prevent clotting?

A

In the presence of excess heparin, free thrombin is instantaneously removed from the blood by antithrombin III

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34
Q

Endogenous heparin is mostly produced by:

A

basophilic mast cells

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35
Q

Why do the lungs and the liver have an abundance of mast cells?

A

They receive lots of minor embolic clots that need to be broken down

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36
Q

______ causes fibrinolysis

A

plasmin

very similar to trypsin, which makes sense since it’s eating proteins

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37
Q

Spontaneous major bleeding episodes generally occur when platelets are less than:

A

20,000

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38
Q

The state of platelet activation is primarily under the control of:

A

the endothelium

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39
Q

Platelets adhere when _____ binds to _____

A

platelet surface receptor FP1b

vWF in the subendothelial matrix

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40
Q

What happens when platelets are activated?

A
  1. reorganizes the platelet cytoskeleton from sphere-like to spiky
  2. degranulation, releasing various biochemicals
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41
Q

Platelets contain three types of granules.

What are their roles?

A

dense bodies (ADP, serotonin, calcium)

alpha granules (fibrinogen, factor V, VEGF, PDGF)

lysosomes (degrade extracellular matrix and remodel the vasculature)

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42
Q

Once activated, platelet aggregation is induced by:

A

platelet release of TXA2

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43
Q

_____ and ____ initiate the extrinsic pathway

A

Tissue Factor

Factor VII

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44
Q

____ and ____ initiate the intrinsic pathway

A

Factor XIIa (activated by HK)

Prekallikrein (PK)

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45
Q

The intrinsic pathway is activated in the ____ by contact with _____

A

blood vessels

negatively charged molecules

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46
Q

How do intrinsic pathway deficiencies effect hemostasis?

A

They generally don’t, except for hemophilia C (only causes mild bleeding)

The intrinsic pathway is not a significant pathway for normal hemostasis

pg. 915

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47
Q

What factor is responsible for blood clots in ECMO or CRRT circuits?

A

Factor XII

exogenous artificial surfaces activate factor XII

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48
Q

The major regulatory factors that control hemostasis reside where the greatest probability of clotting would occur:

A

on the endothelial cell surface

p. 916

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49
Q

What are the three types of primary anticoagulant mechanisms?

A
  1. Thrombin inhibitors
  2. tissue factor inhibitors
  3. mechanisms for degrading activated clotting factors
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50
Q

______ binds with endogenous heparan or exogenous heparin to prevent thrombosis

A

Antithrombin III

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51
Q

How does tissue factor pathway inhibitor effect coagulation?

A

Produced by endothelial cells and platelets

forms complexes with and inhibits Xa

The TFPI/Xa complex goes on to inhibit TF/VIIa and prothrombinase

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52
Q

How does heparin impact TFPI?

A

About 20% of TFPI circulates in the bloodstream on lipoproteins

Heparin increases the plasma levels of TFPI

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53
Q

What happens when thrombomodulin on the surface of endothelial cells binds to thrombin?

A

When thrombin binds to thrombomodulin, it is inactivated

Protein C binds to this thrombomodulin-thrombin complex and is rapidly activated

Activated protein C interacts with protein S to inactivate factors Va and VIIIa

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54
Q

Inherited hypercoagulation is caused by deficiency of _____ (3)

A

AT-III

Protein C

Protein S

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55
Q

If the body needs to clot or become inflamed, how does it overcome the body’s natural anticoagulants?

A

Cytokines and inflammatory mediators down regulate expression of thrombomodulin and protein C receptors

decreased expression leads to decreased protein C production, which leads to coagulation

56
Q

How does the fetus tolerate the hypoxic environment of the placenta/uterus?

A

polycythemia

57
Q

A newborn infant would be expected to have high levels of ______ on a CBC

A

reticulocytes

58
Q

Why is there an increased incidence of VTE in the elderly?

A

platelet adhesiveness is elevated

Higher levels of factors V, VII, and IX and vWF

thrombin generation and platelet activation enhanced

p. 922

59
Q

Which is worse: insufficient platelets or a clotting cascade abnormality?

A

Clotting cascade abnormalities tend to cause more serious internal bleeding than platelet defects

60
Q

Define thrombocytopenia and thrombocythemia

A

T-cytopenia: decrease platelets

T-cythemia: too many platelets

61
Q

Why is a manual differential done for patients with low platelets?

A

to rule out pseudothrombocytopenia

happens with the automated cell counter misreads clumps of platelets and gives a falsely low platelet count

62
Q

Which is more common: acquired or congenital thrombocytopenia?

A

Acquired

63
Q

What are some common causes of acquired thrombocytopenia?

A

Viral infection (EBV, rubella, CMV, HIV)

Drugs (thiazides, estrogens, quinines, chemo, ethanol)

Nutritional (B12, folate)

Chronic renal failure

bone marrow cancer/hypoplasia

64
Q

HIT is mediated by which antibodies?

A

IgG antibodies against the heparin-platelet factor 4 complex that leads to platelet activation

65
Q

The hallmark sign of HIT is:

A

thrombocytopenia

66
Q

Which is more common in HIT: bleeding or clotting?

A

Clotting

High risk for VTE and arterial thromboses

bleeding is uncommon, even with low platelet counts

67
Q

HIT begins after _____ days of heparin administration

A

5-10

68
Q

Why should coumadin not be used in patients with HIT?

A

Increased incidence of skin necrosis

69
Q

Which drugs should be used to decrease the chance of thrombosis in a patient with HIT?

A

Thrombin inhibitors (argatroban etc)

70
Q

Hit decreases the platelet count by increasing platelet _____

A

activation (consumptive)

71
Q

Immune thrombocytopenia purpura decreases platelet count by ______

A

destroying platelets

72
Q

What usually causes acute Immune thrombocytopenic purpura (ITP)?

A

secondary to a disease (usually viral infection) that leads to large amounts of antigen in the blood (can also be SLE or drug allergies)

Immune complexes bind to platelet receptors, and then that platelet is destroyed by the spleen

73
Q

What is the treatment for acute ITP?

A

Usually resolves with the illness (as immune complex load decreases)

74
Q

What causes chronic ITP?

A

Autoantibodies against platelet antigens

75
Q

In chronic ITP, auto-antibodies are usually of the _____ class

A

IgG

76
Q

What are the initial manifestations of ITP?

A

petechiae and purpura, which progress to epistaxis, hematuria, bleeding gums etc.

77
Q

If a woman develops ITP during pregnancy, what are the implications for her infant?

A

newborn will also be thrombocytopenic

The IgG antibody cross the placenta

78
Q

What are the symptoms of ITP?

A

weight loss

headache

fever

79
Q

What is the treatment for chronic ITP?

A

glucocorticoids

IVIG

These are transient, and don’t fix the problem permanently. Some patients may need splenectomy

80
Q

What is thrombotic thrombocytopenia purpura?

A

a.k.a Moschcowitz disease

combination of severe thrombocytopenia AND thrombotic microangiopathy caused by platelet aggregation

81
Q

What is the difference in clots formed by DIC and clots formed by TTP?

A

TTP clots are mostly composed of platelets and RBCs with minimal fibrinolysis

In DIC, there is a massive amount of fibrinolysis

82
Q

What causes TTP?

A

dysfunction in the protein that breaks down vWF

Causes an excess of vWF on the endothelium, which attracts clumps of platelets

These clumps can detach and cause microemboli

83
Q

The classic pentad of TTP symptoms is:

A

extreme thrombocytopenia (<20)

intravascular hemolytic anemia

ischemic s/s in the CNS

kidney failure

fever

DO NOT NEED ALL FIVE TO DIAGNOSE

84
Q

A blood smear of a patient with TTP will show:

A

schistocytes (fragmented RBCs)

elevated LDH

85
Q

What is the death rate for TTP if left untreated?

A

90%

86
Q

What is the treatment for TTP?

A

infusion with FFP, which replenishes functional ADAMTS13 (vWF proteinase)

87
Q

When does secondary thrombocythemia often occur?

A

After a splenectomy

The spleen is a storage site for platelets, so after splenectomy all those platelets are circulating instead of sequestered

88
Q

What causes reactive thrombocythemia?

A

infections and inflammatory conditions (RA in particular)

excessive production of cytokines induces increased production of thrombopoietin in the liver, causing increases megakaryocyte proliferation

89
Q

What is the most severe form of thrombocythemia?

A

primary / essential

90
Q

What causes primary thrombocythemia?

A

excess platelet production d/t defective bone marrow megakaryocyte progenitor cells

91
Q

What is common in thrombocythemia: bleeding or clotting?

A

clotting

microvasculature thrombosis, BUT they are also at risk for large vessel thrombi

Bleeding can occur more rarely

92
Q

The primary presenting symptoms of essential thrombocythemia are:

A

erythromelalgia (hot burning hands and feet)

headache

paresthesias

93
Q

Which is more common with thrombocythemia: venous or arterial clotting?

A

arterial

94
Q

Vitamin K is necessary for the synthesis of:

A

prothrombin

Factor 7, 9, 10

Proteins C and S

95
Q

What is the most common cause of Vit K deficiency?

A

Parenteral Nutrition and Abx that wreck the gut

96
Q

Liver disease can cause complications in three aspects of coagulation:

A
  1. coagulation system decreased factor production
  2. fibrinolysis system decreased plasminogen production
  3. platelet function decreased thrombopoietin and ADAMTS13 and sequestration in spleen due to portal HTN
97
Q

Factor ____ is most sensitive to liver damage due to its short half life

A

VII

98
Q

For patients with liver disease, what is the optimal way to treat hemostatic alterations?

A

FFP

Contains all the aspects absent in liver failure (clotting, fibrinolysis and platelets)

99
Q

TTP causes ____ clots

DIC causes ____ clots

A

Platelet

Fibrin

100
Q

What is the most common condition associated with DIC?

A

sepsis, usually from gram (-) endotoxins causing endothelial damage

101
Q

The common pathway to DIC is _____

A

excessive and widespread exposure to TF due to vascular injury

102
Q

Why do inflammatory disorders lead to DIC?

A

Normally, endothelial cells and monocytes don’t express surface TF, but they do in response to cytokines

a large majority of the cells produced in response to inflammatory cytokines have TF on their cell surfaces

103
Q

In DIC, TF binds to factor ______. What happens next?

A

VII

leads to conversion of prothrombin to thrombin and formation of fibrin clots

104
Q

Inhibition of _____ or _____ completely halts the path of DIC

A

TF

Factor VIIa

105
Q

List the coagulation problems present in DIC:

A
  1. Extensive activation of the clotting cascade
  2. Anticoagulants (TFI, ATIII and protein C) are profoundly diminished
  3. Fibrinolysis is diminished d/t increased production of plasminogen inhibitor (PAI1)
  4. Activation of clotting causes activation of complement which induces platelet destruction
106
Q

Besides consumption of clotting factors and platelets, what are other reasons hemorrhage occurs in DIC?

A

Fibrin degradation products (FDPs) are natural anticoagulants

107
Q

DIC will continue until:

A

whatever started it stops

108
Q

What things are you looking for on a blood panel to determine DIC?

A

platelet count

PT/PTT

D-Dimer

pg. 596

109
Q

Treatment of DIC is directed toward three goals:

A
  1. Removing the underlying cause
  2. controlling thrombosis
  3. maintaining organ perfusion
110
Q

Once the stimulus for DIC is gone, how long does it take for plasma to normalize?

A

24-48 hours

111
Q

Why is heparin not the drug of choice for septic DIC?

A

It acts by binding to and activating AT-III, which is deficient in DIC

112
Q

Arterial thrombi form under conditions of ______ blood flow

Venous thrombi form under conditions of _____ blood flow

A

High, composed of platelets

Low, composed of red cells

113
Q

What is Virchow’s triad?

A
  1. Vessel Injury
  2. Abnormal blood flow
  3. Hypercoaguability
114
Q

Why does turbulent flow lead to thrombi?

A

Turbulent flow platelets and endothelial cells activated

115
Q

Why does stasis lead to thrombi?

A

platelets remain in contact with the endothelium longer than normal

clotting factors aren’t as diluted as normal and become activated when they come into contact with one another

116
Q

What are three disorders that cause both stasis and turbulent flow?

A

Myocardial infarction

polycythemia

sickle cell

117
Q

Which two inherited thrombophilias pose the greatest risk of developing an MI or stroke?

A

F2 gene mutation Prothrombin (G20210A)

Factor V Leiden

118
Q

What happens when a Factor V leiden mutation takes place?

A

Its binding site for protein C (which normally inactivates Factor Va) is altered and it becomes resistant

results in high levels of factor Va and prolonged clot formation

119
Q

What does an F2 gene mutation cause?

A

causes too much prothrombin to be produced

increased prothrombin → increased thrombin → increased clotting

120
Q

Antiphospholipid Syndrome is an example of a ______ disease

A

acquired hypercoaguability

121
Q

What is antiphospholipid syndrome?

A

autoimmune syndrome

autoantibodies against plasma membrane phospholipids and phospholipid-binding proteins

122
Q

What are the implications of having APS in pregnancy?

A

Autoantibodies attack the placental surface

Leads to pregnancy loss, pre-E or eclampsia

123
Q

What is the treatment for Antiphospholipid syndrome in pregnancy?

A

unfractionated or LWMH with low-dose aspirin

124
Q

Deficiencies of which three coagulation factors account for 95% of hemophilias?

A

VIII

IX

XI

125
Q

What is the most common hemophilia?

A

Hemophilia A (Factor VIII deficiency)

126
Q

Mutations in the F8 gene cause hemophilia ____

Mutations in the F9 gene cause hemophilia ____

A

A

B

pg. 1007

127
Q

Hemophilia B is a deficiency of factor:

A

IX

128
Q

How are hemophilia A and B inherited?

A

X-linked recessive

129
Q

Normal hemostasis is achieved in hemophilia without excessive bleeding. How?

A

The extrinsic coagulation cascade does not rely on factors VIII, IX or XI

130
Q

In Hemophilia A or B, the PT will be __ and the PTT will be __

A

normal

prolonged

131
Q

What is the primary goal of administering rFVIII/IX to hemophiliacs?

A

Prevent joint bleeding

132
Q

Why is von Willebrand disease sometimes said to be a factor VIII deficiency?

A

Because vWF binds factor VIII and platelets to the blood vessel wall as part of the clotting process

Factor VIII activity is decreased in individuals with von Willebrand disease. Not factor VIII quantity

133
Q

What are the two types of protein C deficiency?

A

Type 1: quantitative deficiency

Type 2: qualitative deficiency

134
Q

What causes neonatal purpura fulminans?

A

presence of both types 1 and 2 protein C deficiency

135
Q

What is the treatment for protein C deficiency?

A

Long term or short term anticoagulation, depending on severity

136
Q

Which thrombocytopenia has a high probability of neonatal death?

A

neonatal alloimmune thrombocytopenic purpura (NATP)

137
Q

Which neonatal thrombocytopenia is relatively benign?

A

autoimmune neonatal thrombocytopenia

Patho 2 (24 decks)

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