Hematology/Oncology Flashcards

1
Q

Where does hematopoiesus occur in embryo?

3rd-7th month?

7th month?

at birth?

adulthood?

A

Embryo: Yolk sac

3rd-7th month: spleen and liver

7th month: Marrow cavity

Birth: Mostly bone marrow, liver/spleen as back-up

Adulthood: Bone marrow (Skull, ribs, sternum, vertebral columns, proximal ends of the femur)

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2
Q

Hematopoiesis starts with a ________ stem cell.

A

Pluripotent

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3
Q

This is a bone marrow stem cell that has the potential to become any blood cell.

A

Hematocytoblast

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4
Q

Hematocytoblasts can differentiate into ________ or ________

A

Myeloid stem cells

Lymphoid stem cells

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5
Q

A myeloblast will become a _______, ________, or _________.

A Monoblast will become a ____________ or ________

A erythroblast will become a ___________.

A Megakaryoblast will become a ___________.

A

Neutrophil, Eosinophil, Basophil

Monocyte or macrophage

Erythrocyte

Megakaryocyte

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6
Q

WBC precursors outnumber RBCs :

A

3:1

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7
Q

How long is a WBC’s life span?

A

3 days

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8
Q

What is the main growth factor for erythroblasts?

A

Erythropoietin (EPO)

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9
Q

Where is EPO formed?

When is it released?

A

Kidney (by peritue)

When pO2 decreases

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10
Q

Once a blast is committed to becoming an erythrocyte, ____-____ also stimulates cell division

A

GM-CSF

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11
Q

What is the main growth factor for thromboblasts?

A

Thrombopoietin

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12
Q

What FOUR “cytokines” work to increase platelet numbers?

Which one is a fever inducer?

A

GM-CSF
IL-3
IL-6 (fever inducer)
IL-11

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13
Q

What THREE “cytokines” work as the main growth factors for myeloblasts?

A

G-CSF
GM-CSF (increases monocytes = more macrophages)
IL-3

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14
Q

What SIX molecules are important to RBC formation?

A
Iron
EPO
Heme
Hemoglobin
Folate 
B12
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15
Q

T/F: Folate and B12 are made by the human body

A

False (they are not)

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16
Q

Where is B12 obtained from?

A

Small Intestines

Stomach

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17
Q

What most B12 be bound to in order to be absorbed?

Where is this made?

Where does B12 ultimately end up being absorbed?

A

Intrinsic factor

Stomach

Ilium

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18
Q

T/F: B12/Folate deficiencies cause anemia because of decreased RBC production, not due to absence of iron

A

True

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19
Q

______ anemia is described as larger cells than usual (seen in labs as high MCV)

A

Macrocytic

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20
Q

______ anemia is described as more Hb per cell than normal (seen in labs as high MCH)

A

Hyperchromic

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21
Q

What is the main component of RBCs?

A

Hemoglobin

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22
Q

Typically hemoglobin is made up of 2 _____ and _______ chains.

A

Alpha

Beta

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23
Q

What are SIX hemoglobin variants?

A
Four α-Hb genes
Two β-Hb genes
Four γ-Hb genes
Two δ-Hb genes
Two ε-Hb genes
Two ζ-Hb genes
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24
Q

This Hgb variant begins in the third trimester and can have a normal adult range of 1.5 - 3.5%

A

Hemoglobin A2 (alpha 2 delta 2)

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25
Q

This Hgb variant is also referred to as fetal hemoglobin and can be elevated in patients with sickle cell disease or beta-thalassemia.

A

Hemoglobin F (alpha 2 gamma 2)

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26
Q

This is referred to a large chemical group called a porphyrin, made of 4 rings of porphobilinogen attached to a central iron ion

A

Heme

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27
Q

What are 4 others molecules that use heme?

A
  1. Myoglobin (o2 binding in muscle)
  2. NO synthase (vasodilation)
  3. Cytochromes
  4. Catalase
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28
Q

Where is heme primarily synthesized?

A

Liver and bone marrow

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29
Q

During the process of heme formation, glycine binds to SuccCoA (Kreb’s Cycle) to form ________, which join together to form _______. Four of these come together to form __________ and then ___ is added to the middle to form heme.

A

D-ALA

Porphobilinogen

Porphyrin

Fe2+

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30
Q

This is an inherited or acquired disease affecting heme production, has multiple subtypes, and is unique for turning feces purple when it is exposed to light.

A

Porphyria

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31
Q

What are the Sx of porphyria?

A
Muscle Pain
Tooth Changes
Increased Hair growth
Anemia
Sun Intolerance
Neuropathies
Personality changes
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32
Q

T/F: Iron for heme is not absorbed in the GI tract

A

False (It is absorbed in the GI tract)

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33
Q

Heme is stored as _______ and transported as _______

A

Ferrin

Transferrin

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34
Q

What vitamin increases iron absorption?

What decreases it?

A

Increases: Vitamin C

Decreases: Ca2+, Mg2+

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35
Q

Microcytic hypochromic anemia is often a result of _____ deficiency

A

Iron

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36
Q

What is the lifespan of a RBC?

A

100-120 days

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37
Q

What unique feature of a RBC’s plasma membrane allows it to pass through small capillaries?

What allows it to have an easier time during O2 exchange?

A

Flexibility

High Surface area

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38
Q

___ of RBCs hemolyze during circulatory life.

___ of RBCs survive long enough to have their shape altered by wear and tear.

A

10%

90%

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39
Q

______ is the apoptosis of a RBC

A

Eryptosis

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40
Q

Where are the sites of RBC breakdown (FOUR)?

A
  1. Liver
  2. Spleen
  3. Bone Marrow
  4. Lymph Nodes
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41
Q

Hemoglobin is recycled by separating heme from ______ and then turning that into amino acids.

The heme is then carried to the ______ by a protein which is brocken down into ________ then into bilirubin to be used in the bile, however some is converted to a brown pigment by _______ and excreted in the feces.

A

Globin

Liver

Biliverdin

Bacteria

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42
Q

_____ anemia is when you do not make enough RBCs mostly do to dysfunctioning bone marrow.

A

Aplastic

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43
Q

________ anemia occurs when there is not enough Hgb.

A

Microcytic

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44
Q

________ ________ anemia occurs when RBCs die too fast.

A

Autoimmune hemolytic

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45
Q

This is the congenital absences of the protein spectrin that give RBC’s their shape.

A

Hereditary Spherocytosis

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46
Q

If the Hgb dissociation curve shifts to the left then Hgb is holding onto 02 more ______

A

tightly

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47
Q

If the Hgb dissociation curve shifts to the right then Hgb is holding onto 02 more ______

A

loosely

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48
Q

An increase in DPG levels will cause Hgb to hold onto O2 ________ shifting the dissociation curve to the _____.

A

loosely

right

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49
Q

As temperature decreases, Hgb will hold onto 02 ________ shifting the curve to the ______

A

tightly

left

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50
Q

As pH decreases becoming more acidic, Hgb will hold onto O2 _______ shifting the curve to the ______.

A

loosely

right

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51
Q

Between myoglobin, hemoglobin F, and hemoglobin A, which is the “strongest holder” of 02?

A

Myoglobin

fetal hemoglobin is next strongest

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52
Q

This disease occurs when there is 2 alpha and beta chains that make up Hgb however the beta chains are abnormal

(Also called Hemoglobin SS)

A

Sickle Cell Disease

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53
Q

This abnormal form of hemoglobin occurs when there are 2 alpha and beta chains that compose Hgb however only ONE beta chain is some hemoglobins are abnormal.

(Also called Hemoglobin AS)

A

Sickle Cell Trait

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54
Q

T/F: HgbS tends to change shape at a higher pH

A

False (They change shape at a lower pH)

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55
Q

_____ thalassemia occurs when one or more of the four alpha globin genes.

A

Alpha

56
Q

Hemoglobin H is 4 _____ chains bonded together.

A

beta

57
Q

Hemoglobin Barts is four _____ chains bonded together.

A

gamma

58
Q

______ thalassemia occurs when one or more of the two beta globin genes are missing.

A

Beta

59
Q

_________ is Hgb that exists with Fe3+ rather than Fe2+.

Will this form of Hgb hold onto oxygen better or worse than Fe2+ binded Hgb?

A

Methemoglobin (HbM)

Worse (Fe3+ will essentially not hold 02 at all and will remain in the doxygenated shape)

60
Q

How is methemoglobin corrected?

What Pathway?

A

Using NADH made it the Embden-Meyerhof Pathway

61
Q

T/F: Usually involves a defect on cytochrome B5 Reductase (methemoglobin reductase)

A

True

62
Q

What is considered the normal amount of methemoglobin?

When would you become cyanotic?

Death?

A

<1.5 (10% of hemoglobin)

1.5 - 3.0 (10-20% of hemoglobin)

> 10.5 (>70% of hemoglobin)

63
Q

What are three common causes of methemoglobin?

A
  1. Hb variants [rare]
  2. Cytochrome B5 Reductase deficiency [rare]
    Toxic substances [more common]
64
Q

High exposures to what three oxidizing chemicals increase the risk for methemoglobin?

Anesthetics?

Abx?

A
  1. Nitrates
  2. Benzocaine
  3. Dapsone

Prilocaine

Trimethoprin and sulfas

65
Q

What is the name of the pathway RBCs use to get fuel?

What molecule do they use as fuel?

A

Embden-Meyerhof Pathway

Glucose

66
Q

________ _________ ______ is a “detour” that some G6P take instead of going through glycolysis that occurs to generate NADH, a reducing agent that detoxes free radicals

A

Hexose Monophosphate Shunt

67
Q

This is a deficiency most commonly found in men, is X-linked, and affects infants more than children and children more than adults.

A

G6PD Deficiency

68
Q

Being heterozygous for G6PD deficiency protects against _____.

Why?

A

Malaria, because G6PD deficiency destabilizes the RBC membrane making it difficult for the parasite to reproduce.

69
Q

______are fragments of megakaryocytes that leave the bone marrow and move into systemic circulation w/o nuclei or membrane bound organelles, w/ a lot of surface receptors and many granules

A

Platelets

70
Q

What is the lifespan of a platelet?

What is the lifespan of a Neutrophil?

What is the lifespan of a Basophil?

What is the lifespan of a Eosinophil?

A

10 days

1-3 days

3-10 days

10 - 21 days

71
Q

Myeloblasts in the peripheral blood is a sign of what?

A

Leukemia

72
Q

Should Promyelocytes or Myelocytes be found in the peripheral blood?

Should Metamyelocytes, bands, or segmented neutrophils be found in the peripheral blood?

A

No

Yes

73
Q

An increase in bands in the peripheral blood is indicative of what?

A

Acute infection

74
Q

______ is a decrease in myeloid cells (RBCs, Neutrophils, and/or platelets)

What are THREE examples of this?

A

Cytopenia

Leukopenia
Anemia
Thrombocytopenia

75
Q

What are THREE ways cytopenia can occur?

A
  1. Increased destruction
  2. Increase sequestration
  3. Decreased production
76
Q

______ is a decrease in all THREE myeloid lines.

A

Pancytopenia

77
Q

_______ pancytopenia occurs when there is increased destruction of myeloid cells, likely autoimmune.

_______ pancytopenia occurs when there is decreased production of myeloid cells, likely due to environmental exposures (chemicals chemo, disease, etc…)

A

Idiopathic

Secondary

78
Q

Which or what growth factors are decreased in iron deficiency?

Kidney disease?

Liver disease?

A

Folate/B12

EPO

CSFs

79
Q

___________ syndrome occurs when there are dysfunctional stem cell lines in the bone marrow, is a precursor to acute myeloid leukemia, and can require a bone marrow transplant.

A

Myeloidysplastic

80
Q

_______ anemia is totally dysfunctional stem cells in the bone marrow.

A biopsy of the bone marrow in this condition would show decreased stem cell replace by ______.

A

Aplastic

Fat

81
Q

What are the most common causes of aplastic anemia?

There are Seven

A
  1. Idiopathic (>65%)
  2. Chemicals (Benzene)
  3. Drugs (Chemo, etc…)
  4. Radiation
  5. Viruses (Hep C, Paravirus B19, EBV)
  6. Inheritied Disease (Fanconi Anemia()
  7. Other (Connective tissue disorders, pregnancy)
82
Q

How is aplastic anemia treated?

A
  1. Androgens and CSFs
  2. Cyclophosphamide (a chemo agent)
  3. Bone Marrow Transplant
83
Q

Idiopathic pancytopenia (also referred to as _________ ______) appears to be an autoimmune destruction of myeloid elements in the peripheral blood by macrophages that were inappropriately amplified by helper T cells. Decrease in all myelocytic cell lines

A

Hemophagocytic Syndrome

84
Q

What would you expect the bone marrow, spleen, and liver to be filled with in a patient with hemophagocytic syndrome?

A

macrophages that have phagocytosed RBCs

85
Q

T/F: Hepatosplenomegaly is not common in patients with hemophagocytic syndrome

A

False (It is common)

86
Q

What organ is the most common site of RBC sequestration in a patient with sickle cell disease?

A

Spleen

87
Q

What commonly triggers sickling episodes?

A

Infection

Hypoxia

88
Q

What are three risks for splenic sequestration?

How would this be treated?

How fast would the spleen die without treatment?

A
  1. Acute/Severe hypovalemia
  2. Hypovolemic shock
  3. Splenic rupture

Tx:

  1. Transfusion
  2. BP Support

Splenic death in 2 hours

89
Q

T/F: Sickle cell disease that does not cause blood vessel occlusion

A

False (It does)

90
Q

This is known as spleen death due to narrow blood vessels in spleen.

(It has often died by the time a sickle cell pt is 2-5 y/o)

A

Autosplenectomy

91
Q

T/F: Platelets contain nuclei and organelles

A

False

92
Q

T/F: Platelets contain granules which contain secretory products to aid in clotting

A

True

93
Q

This is a potent platelet aggregator and vasoconstrictor that is localized to the site of injury and activated platelets

A

TXA2

94
Q

_____ is produced by endothelial cells around the clot to reverse the effects of TXA2

A

PGI2

95
Q

What enzyme does ASA inhibit?

A

COX-1

96
Q

Why can’t platelets produce more COX-1 enzymes in a patient taking ASA?

A

Platelets have no nucleus, and come “pre-loaded” with enzymes they will need, and cannot make more

97
Q

What is the extrinsic pathway in the clotting cascade?

Intrinsic?

A

Trigger→ 7→ 9→ 10→ 2→ 1

Trigger→ 12→ 11→ 9→ 10→ 2→ 1

98
Q

What factors in the clotting cascade are amplifiers?

stabilizers?

A

Factor 5, 8

Factor 13

99
Q

Where are clotting factors produced?

Are they secreted in their active or inactive forms?

A

Liver

Inactive Forms

100
Q

What is used to treat factor disorders?

A

FFP

101
Q

_________ is a genetic disorder characterized by deficiencies in clotting factors (usually Factor VIII)

A

Hemophilia

102
Q

PT is used to measure ________ pathway activity and asses vitamin ___ status.

A

Extrinsic

K

103
Q

aPTT is used to measure the _______ pathway and is useful in checking factor __.

A

Intrinsic

8

104
Q

A low PT is indicative of a ______ ability to clot

A high PT is indicative of a _____ ability to clot

A

high

Low

105
Q

T/F: Hemophilia A (Factor VIII deficiency) is a X linked disorder

A

True

106
Q

By what age are patients typically diagnosed with Hemophilia A?

A

3 y.o.

107
Q

What is a hallmark of hemophilia A?

A

Hemarthrosis

108
Q

Less than 50% Factor VIII activity is considered?

6-49% Factor VIII activity is considered?

2-5% Factor VIII activity is considered?

0-1% Factor VIII activity is considered?

A

Disease

Mild

Moderate

Severe

109
Q

How is hemophilia A treated?

A

Factor VIII replacement

110
Q

T/F: von Willebrand disease is the most common inherited clotting disorder

A

False (It is the most common inherited bleeding disorder)

111
Q

von Willebrand disorder involves an autosomal dominant of chromosome ____.

A

16

112
Q

How is von Willebrand factor improtant in the clotting cascade?

What happens in von Willebrand disorder?

A

vWF allows Factor VIII to travel through the blood bound to it

Without vWF, Factor VIII has a very short lifespan

113
Q

What are classic presenting Sx in some with vWF deficiency?

What is the classic complaint in women with vWF deficiency?

A

Epistaxis
Bleeding gums

Heavy menstrual cycle

114
Q

Vitamin ____ is necessary for synthesis of multiple clotting factors.

Lack of this vitamin can present as severe bleeding that is difficult to control

A

Vitamin K

115
Q

Protein __ and __ require vitamin K to be produced.

A

Protein C and S

116
Q

What are good sources of vitamin K

A

Leafy Green Vegetables
Cauliflower
Bacteria in the colon

117
Q

T/F: Fetuses can create and store vitamin K before birth

A

False (They can not, it travels through the placenta)

118
Q

Why are fetuses given Vitamin K injections at birth?

A

To protect again hemolytic diseases

119
Q

28-y/o woman admitted due to a tendency to hemorrhage. She used to be obese in childhood but a fear of obesity forced her to go on a diet after she entered high school. For the past few years, she has had episodes of self-induced vomiting after each meal, often in conjunction w/ purgative (ipecac) use. Her menstruation is irregular, occurring only a few times/year. On admission, she is 5’0” and 77 lb. PE reveals numerous ecchymoses of her extremities, right flank and hip and hemarthrosis of her rt. knee.

Labs:

Hematocrit 28%
Platelet count was 574 x 109/l
PT = 99.1sec (normal, 10-13 sec)
aPTT = 52.9 sec (normal, < 45)
Coag factors II, VII, IX and X markedly reduced
Fibrinogen normal

Why are her lab values abnormal?

How would you treat this?

A

The body’s Vit K stores tend to be small, thus frequent vomiting/purging episodes can result in deficiency of Vit K & Vit K-dependent coagulation factors

Tx: IV Vit K w/ rapid resolution of her coagulopathy

120
Q

______ & ________ inactivate unbound thrombin in the systemic system

A

Antithrombin III & protein C

121
Q

______ is an anticoagulant contained in mast cells, basophils, and on surface of endothelial cells which enhances antithrombin III and inhibits the intrinsic pathway

A

Heparin

122
Q

T/F: Heparin will dissolve clots

A

False

123
Q

When ______ __ is activated it turns off the amplification activity of Factors V and VIII, which greatly ____ the clot formation process

A

Protein C

Slows

124
Q

T/F: Protein C cannot function with Protein S

A

True

125
Q

Would a person with Protein C deficiency be at risk for increased bleeding or increased clotting?

A

Increased clotting

126
Q

______ is a clot that forms and persists in an unbroken blood vessel, which can block the vessel if large enough, leads to ischemia and tissue death downstream from clot

A

Thrombus

127
Q

_____ is a clot that is free-floating in bloodstream

A

Embolus

128
Q

Are inflammation, atherosclerosis, DM, and HTN all risk factors of clotting?

What are TWO “non-disease” risk factors for clotting?

A

Yes

Bed ridden patient
Long flights

129
Q

What are three drugs commonly used to prevent clotting?

A
  1. ASA
  2. Warfarin
  3. Heparin
130
Q

TPA converts plasminogen to _____ and is typically used to _____ clots.

A

Plasmin

Dissolve

131
Q

How do you treat Protein C deficiency?

A

Anticoagulants (Heparin followed by warfarin)

132
Q

This disorder is a mutation of Factor V in which is has “no shut off valve” for protein C to bind to?

A

Factor V Leiden Mutation

133
Q

T/F: DVTs, Thrombophlebitis, and PEs less common in patients with Factor V Leiden

A

False (Those are more common)

134
Q

What are two tests used to diagnose Factor V Lieden?

A
  1. Dilute Russell’s Viper Venom Test

2. DNA Electrophoresis with restriction endonucleases

135
Q

What composes Virchow’s Triad?

THREE Things

A
  1. Stasis of blood flow
  2. Endothelial Injury
  3. Hypercoagubalility