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ISCM > HEMATOLOGY > Flashcards

HEMATOLOGY Flashcards

1
Q

blood cells and their function

A

red blood cells- oxygen and carbon dioxide transport
platelets-haemotosis
neutrophils- protection from bacteria and fungi
monocytes- protection from bacteria and fungi
eosinophils- protection against parasites
lymphocytes-B cells-immunoglobulin synthesis
-T cells -protection against viruses

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2
Q

what is the difference of lifespan between red blood cells and platelets

A

red blood cells- 120 days

platelets- 10 days

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3
Q

What is a decrease/increase in myeloid cells

A

Pancytopenia/pancytosis

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4
Q

What is a decrease/increase in red cell count

A

Anaemia/ erythrocytosis

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5
Q

What is a decrease/increase in neutrophils

A

Neutropenia/neutrophilia

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6
Q

What is a decrease/increase in white cells

A

Leukopenia/leukocytosis

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7
Q

Whats an increase in eosinophil

A

Eosinophilia

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8
Q

What is an increase in basophils

A

Basophilia

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9
Q

Whats a decrease/increase in monocytes

A

Monocytopenia/monocytosis

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10
Q

Whats a decrease/increase in lymphocyte

A

Lymphopenia/lymphocytosis

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11
Q

Whats a decrease/increase in platelet

A

Thrombocytopenia/thrombocytosis

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12
Q

What is haematopoiesis

A

Is the commitment and differentiation process that leads to the formation of all blood cells from haematopietic stem cells

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13
Q

When does haematopoiesis take place

A

In the egg yolk in a fetus and in the bone marrow of an adult

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14
Q

What is the role of pluripotent haematopoietic stem cells

A

Can self renew and differentiate into a variety of cell types and the oath is determined by a range of growth factors present

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15
Q

What are the types of growth factors

A

Colony stimulating factors (CSF)- mutli CSF (IL-3) and GM-CSF (granulocyte macrophage)

EPO(erythropoietin) induces production of RBCs (red blood cells)

TPO(thrombopoietin) induces the production of megakaryocytes

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16
Q

what is erythropiesis

A

the differentiation of proerythroblast cells into mature red blood cells

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17
Q

describe the cells in order in erythropiesis

A

proerythroblst-basophlic erythroblast-polychromatphilic erythrobloast- normoblast-reticulocyte-mature erythrocyte

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18
Q

what is present in a normoblast

A

nuclear DNA, RNA in cytoplasm, its in one marrow and not in the blood

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19
Q

whats present in a reticulocyte

A

no nuclear DNA, RNA in cytoplasm and is present in blood and bone marrow

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20
Q

what is present in a mature RBC

A

no nuclear dna and no rna in cytoplasm it is present in bone marrow and blood

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21
Q

where is EPO produced

A

in the kidney in response to anoxia caused by anemia

it acts to stimulate erythropoiesis and stimulates haemoglobin synthesis

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22
Q

is the reticulocyte present in blood

A

yes and it later develops into mature blood cells within 24 to 48

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23
Q

what factors affect erthrocyte production

A

iron, vitamin B12 and folic acid

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24
Q

what are the reasons for thrombocytopenia

A

result of decreased bone marrow production usually in an enlarged spleen or an increases platelet destruction due to infection, drugs, immune mechanisms

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25
Q

what are the reasons for thrombocytosis

A

due to iron deficiency, imflammation, cancer or infection

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26
Q

what could be the cause of changes in leukocytes

A

infection, trauma, malignancy, autoimmunity, allergy and drugs

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27
Q

what does mean cell volume mean

A

how big the cells are on average

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28
Q

what does packed cell volume/haematocrit mean

A

how much of the blood volume is cells

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29
Q

what does mean cell haemoglobin mean

A

average amount of Hb per RBC

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30
Q

what does mean cell Hb concentration mean

A

conc of Hb in a given volume of RBC’s

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31
Q

what does red cell distribution width mean

A

how variable are individual cell size measurements

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32
Q

what is anemia

A

reduction in RBC Hb concentration

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33
Q

what are cells with low MCV called

A

microcytic

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34
Q

what are cells with high MCV called

A

macrocytic

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35
Q

what is microcytic hypochromic anemia

A

smaller RBC and decreased colour

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36
Q

what is normocytic normochromic anemia

A

individual rbc normal but fewer in number

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37
Q

what is hemolytic anemia

A

usually an increase in reticulocytes

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38
Q

what are the causes of acquired anemia

A

iron, folate deficiency- blood loss, anemia of chronic disease, haemolysis, marrow infiltration

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39
Q

what are the causes of inherited anemia

A

haemoglobinpathies eg thalassemia, sickle cell disease and RBC membrane defects

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40
Q

what is the normal reticulocyte percentage in blood

A

0.5-2%

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41
Q

what happens to reticulocyte count if anemia is caused by bleeding

A

reticulocyte count increases

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42
Q

what does a low reticulocyte number suggest

A

anemia due to failure of production of RBC. this could be due to iron deficiency, VitB12 deficiency, folate deficiency or kidney disease

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43
Q

what kind of anemia does iron deficiency cause

A

microcytic hypochromic anemia

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44
Q

how is iron recycled in the body

A

the iron is transported to the blood where it is carried by transferrin to the bone marrow for erythropoiesis and the destruction of RBCs leads to iron recycling

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45
Q

what usually causes iron deficiency

A

blood loss or heavy menstrual periods

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46
Q

what are the other causes of microcytic anemia

A

anemia of chronic disorders-failure of iron release to serum by macrophages

sideroblastic anemia- failure of protoporphyrin synthesis for haem ring

thalassaemias- failure of globin synthesis due to genetic defect

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47
Q

what is sideroblastic anemia

A

disordered incorporation of iron into haem within the mitochondria of developing erythroblasts

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48
Q

what are causes of sideroblastic anemia

A

hereditary- X linked

drugs-isoniazid

lead poisoning

idiopathic-common form and disease of the elderly

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49
Q

what causes chronic disorder anemia

A

typically normocytic and normochromic

pathogenesis related to decrease release of iron from macrophages to plasma and reduced RBC lifespan

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50
Q

what type of macrocytic anemia is there and what causes it

A

megaloblastic anemia caused by vit B12 and folate deficiency

51
Q

how does folate or b12 deficiency lead to megaloblastic anemia

A

reduces the rate of conversion of dUMP to dTMP which is the rate limiting step in DNA synthesis. dTMP is converted into dTTP and a failure of this conversion leads to the inclusion of dUTP which can lead to DNA fragmenting and premature death of cell

52
Q

what are causes of vitamin B12 deficiency

A

pernicious anemia-the failure of gastric parietal cells to synthesise intrinsic factor

total or partial gastrectomy- removes the source of IF production

some drugs impair b12 absorption

53
Q

what are causes of folic acid deficiency

A

dietary

demand-folic acid deficiency is common in pregnancy as there is an increased demand

drugs- some drugs affect the absorption eg methotrexate as well as alcohol

54
Q

what is haemolytic anemia

A

anemias that result from an increase in the rate of red cell destruction

55
Q

why is it difficult to notice HA (haemolytic anemia)

A

normal adult bone marrow can produce red cells at 6-8 times the normal rate during a HA episode and so unless the lifespan reaches below 30 days it may not be noticeable

56
Q

what is immune haemolytic anemia

A

caused by the presence of auto-antibodies or complement on the surface of the RBC leading to cell death

57
Q

what is drug induced haemolytic anemia

A

antibody directed against drug-red cell membrane complex eg penicillin

deposition of complement by drug protein antibody complex

58
Q

what is haemostasis

A

is the stopping of excessive bleeding from a cut or severed vessel to prevent excessive blood loss

59
Q

what are the three phases of haemostasis

A
  • formation of a temporary platelet aggregate
  • formation of a fibrin mesh
  • dissolution of the haemostatic plug
60
Q

what happens after a vascular injury

A

reflex vasoconstriction as well as the endothelium cells releasing endothelin which causes vasoconstriction

61
Q

what happens in primary haemostasis

A

-platelets bind to collagen via von willebrand factor (vWF) and are activated then undergo a shape change and release granules. the released granules then induce additional platelet aggregation and through binding fibrinogen form the primary haemostatic plug

62
Q

what happens in secondary haemostasis

A

local activation of the coagulation cascade (involving exposed tissue factorand platelet phospholipids) results in fibrin polymerisation due to the action of thrombonin. this solidifies the platelets into a definitive secondary haemostatic plug

63
Q

what is a coagulation cascade

A

the coagulation cascade by clotting factors lead to a proteolytic conversion of prothrombin to thrombin. thrombin catalyses fibrinogen to to initiate fibrin clot formation

64
Q

what are inactive proteins involved in coagulation cascade called

A

zymogens

65
Q

how are zymogens activated

A

by cleavage into the same number but with a so zymogen 11 to 11a

66
Q

how does the intrinsic pathway work (use roman numerals)

A

zymogen 12 is activated to by a negatively charged surface eg phospholipids into 12a which activates 11 into 11a which activates 9 to 9a. 9a and 8a convert 10 into 10a which combined with 5a converts prothrombin into thrombin

67
Q

which activated zymogen is involved in both the intrinsic and extrinsic process

A

10a

68
Q

how does the extrinsic pathway work

A

it is activated by tissue factor which activates 7 into 7a which combined with another tissue factor converts 10 into 10a which then combines with 5a to convert prothrombin into thrombin

69
Q

how does coagulation cascade happen in vivo(real time)

A

the same pathways occur and there is an amplification loop so the same thing is happening multiple times due to the activity of thrombin.

70
Q

what stabilizes the fibrin clot

A

the thrombin converts the 13 into 13a which stabilizes the fibrin clot

71
Q

what is the fibrinolytic system

A

the fibrin clot is broken down to restore normal function to a vessel

72
Q

what happens during the fibrinolytic process

A

the zymogen plasminogen is converted into plasmin which degrades fibrin to form fibrin degradation products including D dimers

73
Q

how is plasminogen activated

A

by tissue and urinary plasminogen activator (tPA) produced by endothelial cells

74
Q

how do we prevent the formation of primary haemostatic plug

A

intact endothelium releases factors, prostacyclin, NO that inhibit platelet aggregation

75
Q

how do we confine clotting to site of injury

A

control mechanisms mediated by tissue plasminogen activator (tPA) and thrombomodulin confine the haemostatic process to the site of injury

76
Q

how do we limit the coagulation cascade ( name the three proteins that stop it )

A

thrombomodulin binds to thrombin and this complex leads to the degradation of factors 5a and 8a via activation of protein C.

  • anithrombin inhibits 10a.
  • tissue factor pathway inhibitor (TFPI) inhibits 10a via interaction with TF-7a complex
77
Q

how do we regulate the fibrinolytic system

A

plasminogen activator inhibtors (PAI) that inhibit tPA

alpha-antiplasmin binds to and inhibits plasmin

78
Q

how can we access the haemostasis process in patients

A
  • full blood count (platelet numbers)
  • quantify fibrinogen. deficiency due to liver disease or DIC ( when proteins responsible for clotting become overactivated)
  • D-dimers increased due to DIC
79
Q

what is involved in the coagulation test prothrombin time (PT)

A

measures extrinsic pathway and measures the time for clot formation after adding phospholipids and tissue factor. we use a international normalized ratio (INR) to compare times

80
Q

what is involved in the coagulation test activated partial thromboplastin time (APTT)

A

measures intrinsic pathway aclcium and contact surface activator

81
Q

what is involved in the coagulation test thrombin clotting time

A

measures common pathway. calcium and thrombin added

82
Q

what are examples of genetic disorders of haemostasis

A

haemphilia A
haemophilia B
von willebrand disease

these are X linked so affect mostly males

83
Q

what is affected in haemophilia A and haemophilia b

A

factor 8 and factor 9

84
Q

how does von willebrand disease affect haemostasis

A

it affects the primary haemostatic plug as its responsible for binding the platelets to the collagen but it also affects factor 8

85
Q

what are examples of acquired haemostasis disorders ( more common)

A
  • liver disease
  • thromboctytopenia due to : impaired production of platelets, immune mediated destruction of platelets and excessive coagulation in DIC
86
Q

how does liver disease affect haemostasis

A

may increase prothrombin time due to deficiency in coagulation factors as the liver synthesizes bile salts which absorb the vitamin K from the blood which synthesizes clotting factors

87
Q

what can happen in severe liver disease

A

-if severe we see decrease in fibrinogen levels and may also cause thrombocytopenia

88
Q

what happens in thrombosis

A

it is the formation of a blood clot inside a blood vessel obstructing the flow of blood through the circulatory system

89
Q

what are the three factors in virchows triad

A

stasis (reduced blood flow ), vessel wall injury and hypercoagubility

90
Q

what is disseminated intravascular coagulation (DIC)

A

a life threatening disorder of haemostasis. it occurs when there is a sytemic activation of coagulation and can be triggered by a variety of conditions eg bacterial sepsis and metabolic stress

91
Q

what is leukodepletion

A

when the white blood cells are removed before transferring blood components to reduce an immune reaction and infection

92
Q

how are specific blood components seperated

A

anticoagulated blood undergoes centrifugation and the dense RBCs go to the bottom and the white blood cells and platelets form a buffy coat and the free cell plasma collects at the top

93
Q

when would you use RBCs thats been seperated

A
  • hypovolaemia due to blood loss
  • severe anemia
  • anemia that cant be corrected by bone marrow function
94
Q

when would the fresh frozen plasma be used ( rich in coagulation proteins and inhibitors)

A
  • massive transfusion and dilutioal coagulapathy
  • liver disease
  • DIC
95
Q

when would the cryoprecipitate be used (rich in fibrinogen)

A
  • in DIC

- hypofibrinogenaemia

96
Q

when would platelets be used

A

-lack of production or peripheral consumption

97
Q

what are the most important antigens on a RBC

A
  • ABO blood group antigen

- rhesus D antigen

98
Q

what are ABO antigens

A

they are carbohydrates

99
Q

what antigen do all blood groups have and what is it

A

H antigen and its fucose

100
Q

what antigen is present in group O

A

only H

101
Q

what antigen is present in group A

A

N-acetylgalactosamine and H

102
Q

what antigen is present in group B

A

D-galactose and H

103
Q

what antigen is present in group AB

A

both N-acetygalactosamine and D-galactose as well as H

104
Q

what enzyme do A and B alleles encode for

A

glycosyltrasferase which then adds the respective antigens

105
Q

why can we not add any more sugars to the O group

A

the O allele doesnt code for a functional protein so nothing is added to the H

106
Q

what is landsteiners rule

A

individuals will form immune antibodies to ABO blood group antigens they dont possess

107
Q

why are antibodies to A and B blood group called natural anitbodies

A

you do not need prior exposure to either the A or B antigen to have anti-A or anti-B and are naturally produced

108
Q

what happens when incompatible blood is transfused and whats it called

A

the antibodies wil bind to the RBC and will lyse it through the use of complement. its called intravascular hemolysis

109
Q

what are the five major Rh antigens

A

D,C,c,E,e

110
Q

which is the most common rh antigen

A

D

111
Q

what does the D gene produce

A

a single protein the D antigen

112
Q

what does the CE gene produce

A

two proteins generation one of four combinations CE,Ce,cE,ce

113
Q

what gene do rh negative individuals have

A

lack the D gene but have a CE gene

114
Q

whats the difference between C and c and E and e

A

C and c differ by 4 amino acids

E and e differ by 1 amino acid

115
Q

whats the difference between the CE and D

A

differ by 400 amino acids

116
Q

whats the name of the antibodies created for the ABO antigen and the Rh antigen

A

ABO-IgM

Rh-IgG

117
Q

what process does IgG lead to

A

extravascular remval via spleen

118
Q

how does blood group typing work

A

mix sample of the patients blood with anti A, anti B and anti AB. if the anti -antigen stick together is is present

119
Q

what is a hemolytic transfusion reaction

A

inflammatory cascade which may cause disseminate intravascular coagulation

120
Q

what is a febrile non haemolytic transfusion reaction

A

antibody mediated recognition of leukocytes transfused as part of RBC/platelet units

121
Q

what is an allergic transfusion reaction

A

may be present with hives

122
Q

what is a transfusion related acute lung injury

A

sudden acute respiratory distress due to transfused antibodies and leads to granulocyte activation in the lungs

123
Q

What’s the function of tPA

A

Breakdown of the clot

ISCM (19 decks)

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