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POM 3: Haematology > 2: RBC and Anaemia > Flashcards

2: RBC and Anaemia Flashcards

Covers RBC, Blood transfusion, Blood cell diseases, Blood groups and Anaemia

1
Q

Where do blood cells originate from

A

Bone marrow:
pelvis, sternum, femur
- constantly regenerated -

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2
Q

Where are RBCs derived from

A

Pluripotent haemopoietic stem cells (HSC)

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3
Q

What 2 stem cells do HCSs give rise to

A
  • lymphoid —> lymphocytes
  • myeloid —> erythrocytes, platelets, granulocytes, monocytes, eosinophils, mast cells, basophils
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4
Q

Haemopoiesis is the…

A

Formation and development of blood cells

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5
Q

Life span and function of erythrocytes

A

120 days - due to lack of organelles
Oxygen transport

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6
Q

Life span and function of platelets

A

10 days
Haemostasis

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7
Q

Life span and function of monocytes

A

Several days
Phagocytosis, kill microorganisms

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8
Q

Life span and function of neutrophils

A

7-10h

Phagocytosis, kill microorganisms

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9
Q

Life span and function of eosinophils

A

shorter than neutrophil
Defend against parasites

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10
Q

Life span and function of lymphocytes

A

Variable
Humoral and cellular immunity

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11
Q

2 characteristics of HSCs

A
  • Self renewal (some daughter cells remain as HSCs, pool not depleted)
  • Differentiate and mature progeny (other daughter cells follow differentiation pathway)

allow expansion of cells to maintain adequate population of mature cells

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12
Q

3 sites of haemopoiesis

A
  • yolk sac (mesoderm of embryo) : 3wks
  • liver ( HSC maintenance and expansion) : 6-8wks gestation - principle source of blood prior to birth
  • bone marrow —> pelvis, femur, sternum, vertebrae (adults) , all bones (children) : 10wks gestation
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13
Q

4 things controlling Haemopoiesis

A
  • genes
  • transcript factors
  • growth factors
  • microenvironment
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14
Q

Where are HSCs and progenitor cells located

A
  • ordered fashion in bone marrow
  • amongst mesenchymal cells, endothelial cells
  • interact with vasculature
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15
Q

Disruption of Haemopoiesis regulation

A

Disturbs balance between proliferation and differentiation—> leukaemia or BM failure

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16
Q

Glycoprotein hormones regulate

A
  • proliferation and differentiation of HSCs
  • function of mature blood cells
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17
Q

Growth factors affecting erythropoiesis

A

Erythropoietin - glycoprotein hormone

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18
Q

Growth factors affecting granulocyte and monocyte production

A

G-CSF
G-M
CSF
cytokines e.g interleukins

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19
Q

Growth factors affecting megakaryocytopiesis and platelet production

A

Thrombopoietin (TPO)

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20
Q

What can the common myeloid progenitor give rise to

A

Proerythroblast

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21
Q

What do proerythroblasts give rise to

A

Erythroblasts —> erythrocytes (differentiation progresses, self renewal and lineage plasticity decrease)

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22
Q

Reticulocytes are

A

Slightly immature RBCS

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23
Q

Methylene blue stains

A

RNA content ( more in immature RBCs)

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24
Q

4 things required for erythropoiesis

A
  • iron
  • folate
  • Vit B12
  • Erythropoietin EPO
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25
Q

Low iron / B12 / folic acid can lead to

A

Anaemia (reduced haemoglobin)

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26
Q

Macrocytic Anaemia
(RBCs large size)

A
  • Due to B12/folic acid deficiency
  • cells grow but don’t develop
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27
Q

Causes of microcytic Anaemia (paler and smaller RBCs)

A

-incr. blood loss
-reduced iron intake

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28
Q

Characteristics of Erythropoietin growth factor

A
  • glycoprotein synthesised by kidney cells in response to hypoxia (supply-demand feedback loop)
  • stimulates bone marrow to produce more RBCs
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29
Q

2 functions of Iron

A
  • O2 transport via Hb
  • needed in mitochondrial proteins :
    Cytochromes a,b,c, for ATP prod.
    Cytochrome P450 for hydroxylation reactions - ETC
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30
Q

Haem iron

A

Fe2+ - best absorbed form

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31
Q

Non-haem iron

A

Fe3+
best form in food
Requires reducing substances for absorption

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32
Q

Iron excretion

A
  • no physiological mechanism by which iron is excreted by
  • iron absorption is tightly controlled 1-2mg a day from diet
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33
Q

2 things B12 and folate are required for

A

-DNA synthesis - dTTP synthesis—> thymidine
-integrity of nervous system

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34
Q

B12 and folate deficiency affects:

A

All rapidly dividing cells:
- bone marrow: megaloblastic erythropoiesis
-epithelial surface of mouth and gut
-gonads

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35
Q

Where is folate absorbed

A

Small intestine: duodenum and jejunum

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36
Q

Where is B12 absorbed

A
  • stomach : cleaved by HCL, combines with IF made in gastric parietal cells
  • small intestine : B12-IF binds to receptors in ileum
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37
Q

B12 deficiency may result from:

A

-inadequate intake e.g. veganism
-inadequate secretion of IF : pernicious anaemia
-malabsorption e.g coeliac disease
-lack of stomach acid

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38
Q

RBC destruction

A

-Breakdown in spleen: old or abnormal

  • globin returns to amino acids
  • haem broken down into iron and bilirubin
    -Fe: recycled to bone marrow - transported by transferrin in blood
    -bilirubin: excreted in bile (Liver)

-destroyed by splenic macrophages

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39
Q

What does erythrocytes function depend on (3)

A
  • integrity of membrane
  • haemoglobin structure and function
  • cellular metabolism
    (Defects result in haemolysis)
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40
Q

Erythrocyte membrane structure

A
  • biconcave shape - aids manoeuvrability through small vessels
  • lipid bilayer membrane —> protein cytoskeleton cont. transmembrane proteins (maintain integrity, shape and elasticity of red cell)
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41
Q

Spheroctyes are

A

Cells approximately spherical in shape (lost area of cell membrane)

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42
Q

Structure of spherocytes

A
  • round, regular outline
  • lack central pallor
  • less flexible so removed prematurely by spleen
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43
Q

How do spherocytes arise

A

Loss of cell membrane without loss of equivalent amount of cytoplasm so cell forced to round up

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44
Q

What is hereditary spherocytosis caused by

A

Disruption of vertical linkages in membrane
(Autosomal dominant)

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45
Q

When can elliptocytes (pencil cells) occur

A

In iron deficiency

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46
Q

2 Skeletal proteins found in RBC membrane

A
  • Spectrin
  • junctional
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47
Q

2 transmembrane proteins found in RBC membrane

A
  • Band 3
  • rhesus
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48
Q

How does deficiency in G6PD affect red cells?

A
  1. G6PD is an important enzyme in HMP shunt
  2. The HMP shunt involved in metabolism of glutathione protecting the red cell from oxidant damage
  3. Therefore deficiency of G6PD causes red cells to be vulnerable to oxidant damage
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49
Q

What protects the red cells from oxidant damage?

A

Glutathione

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50
Q

What does G6PD deficiency cause?

A

Intermittent, severe intravascular haemolysis as a result of infection or exposure to an exogenous oxidant

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51
Q

What are episodes of intravascular haemolysis associated with the appearance of?

A

considerable numbers of Irregularly contracted cells/ ‘bite cells’

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52
Q

Blood is composed of

A

55% plasma
45% erythrocytes

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53
Q

Serum is

A

plasma without clotting factors

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54
Q

3 adaptations of RBCs

A

Incr. SA for gas exchange - biconcave shape
lack of organelles to allow maximum Hb
Incr. flexibility to move through narrow vessels

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55
Q

Haematocrit (HCT)

A

expresses ratio of RBCs to blood volume
- decimal or percentage
- values depend on age and sex

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56
Q

2 functions of HSC

A

self renew to replenish pool

differentiate into mature blood cells

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57
Q

What is RBC maturation guided by

A

Haematopoetic growth factors

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58
Q

Process of HSC differentiation to make erythrocytes

A

HSC
Common myeloid progenitor
Proerythroblast
Reticulocytes - appear blue, found in circulation
Erythrocytes

  • as differentiation progresses, self renewal and lineage plasticity decrease
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59
Q

When and where is EPO produced

A

By the kidneys in response to hypoxia (low oxygen)

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60
Q

What is the difference between Folate and Folic acid

A

Folate = Vit. B9
Folic acid = synthetically derived Vit. B9 (not from food)

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61
Q

Function of Hepcidin

A

Hormone regulating absorption of iron in gut according to iron body stores
Produced at liver

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62
Q

Hypersplenism

A

overactive spleen
can lead to anaemia

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63
Q

Splenic sequestration

A

sudden pooling of blood in the spleen
- can be seen in anaemia

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64
Q

Splenomegaly

A

enlargement of the spleen

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65
Q

Anaemia is

A

a blood disorder defined as a reduction in Hb conc.

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66
Q

4 causes of reduced Hb concentration

A

Impaired red cell production
Loss of red blood cells - bleeding
Increased red cell destruction
Reduced red cell survival

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67
Q

Clincal presentations of anaemia

A

Reduced HB conc. — poor oxygenation of tissues

-dyspnoea on exertion and rest
-pallor
-fatigue

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68
Q

2 clinical tests required for diagnosing haematological conditions

A

blood film and FBC

69
Q

Differentiating anaemia types

A

Based on cell size and colour

Size (MCV or compare to lymphocytes) - normocytic, microcytic, macrocytic
Colour - Normochromic, Hypochromic (paler), Polychromatic (blue tinge)

Shape - normal, abnormal, immature

70
Q

Microcytic anaemia

A

usually hypochromic
due to defects in haemoglobin synthesis
- iron deficiency anaemia (haem synthesis)
- thalassemias (globin synthesis)
- anaemia of chronic disease

71
Q

Normocytic anaemia

A

cells of normal size
acute haemorrhage - loss of RBCs

72
Q

Macrocytic anaemia

A

Subclassified as megaloblatic anaemia or non megaloblastic

73
Q

3 causes of Non megaloblastic anaemia (Macrocytic)

A

liver disease and ethanol toxicity
haemolysis/polychromasia
pregnancy

74
Q

Normal shaped RBCs on a blood film

A

central white spot -less Hb in depression
1/3 diameter should be pale
if greater proportion - hypochromic RBC

75
Q

6 shapes of immature RBCs

A

Megaloblast
Reticulocyte
Sickle cell
Target cell
Poikilocyte
Elliptocyte

76
Q

Poikilocytes are

A

RBC showing more shape variety than usual

77
Q

Management of anaemia

A

dependent on cause

blood transfusion of packed red cells to quickly increase O2 carrying capacity of blood

78
Q

3 causes of anaemia

A

Bleeding
Nutrient deficiency
Genetic causes

79
Q

3 causes of iron deficiency

A

Inadequate intake
Inadequate absorption
Excessive iron loss by gradual prolonged bleeding

MICROCYTIC ANAEMIA

80
Q

B12 and Folate deficiency usually lead to

A

Megaloblastic anaemia (macrocytic)
- larger RBC precursors released into circulation
- hypersegmented neutrophils

81
Q

2 types of anaemia resulting from acute haemorrhage

A

normocytic
normochromic anaemia
- as no pathology in RBC synthesis (yet)

82
Q

what anaemia results from gradual and prolonged bleeding?

A

(microcytic) iron deficiency anaemia
- commonly caused by excessive menstrual bleeding

83
Q

How can genetic disorders cause anaemia

A

-structural abnormality in RBC leading to premature destruction by spleen and haemolytic anaemia

84
Q

2 genetically controlled anaemias

A

Hereditary spherocytosis - vertical linkages disrupted
Hereditary elliptocytosis - horizontal linkages disrupted

  • both autosomal dominant traits that disrupt proteins in RBC membrane
85
Q

Thalassemias

A

genetic condition causing (microcytic) anaemia
- defect in alpha or beta globin chain (named subsequently)
- can be major or minor

86
Q

Sickle cell anaemia

A

autosomal recessive (HbS)
defect in Hb synthesis affecting B-chain
removed by spleen
prone to occlusion
(HbAS -sickle cell trait)

87
Q

What is classification of blood based on

A
  • controlled by same gene or set of homolygous genes
  • significance depends on ability of antibodies against the antigen to cause haemolysis
88
Q

2 most significantly blood group systems

A

ABO system
Rh system

89
Q

Blood group system

A

combination of antigens on RBC surface

90
Q

Antigen classification in ABO system

A

Group A - antigen A
Group B- antigen B
(A and B are co-dominant)
Group AB- both antigen A and B
Group O - neither antigen A or B - recessive

91
Q

Antigen classification in Rh system

A

Antigen D- recessive
RhD positive (dd) - expressed
RhD negative (Dd, DD) - not expressed

92
Q

Type of antibody in ABO System

A

Pentametric IgM

93
Q

Type of antibody in Rhesus system

A

IgG

94
Q

Occurence of antibody in ABO system

A

naturally occuring

95
Q

Occurence of antibody in Rhesus system

A

Acquired following exposure

96
Q

How are ABO antibodies naturally acquired

A

Early life exposure to sugars which mimic A/B antigens on RBC surface
body develops Anti-A or B against antigen not expressed by own RBC
Antibodies exist in small quantities in plasma

97
Q

How are Anti-RhD antibodies acquired following exposure to RhD antigen

A

antibodies only develop following exposure to RhD antigen (alloimmunisation)

98
Q

Two types of haemolysis

A

HTR - Haemolytic transfusion reaction
HDFN - Haemolytic disease of the foetus and newborn

99
Q

In a HTR

A

-incompatible RBCs transfused into patient
patient has antibodies against antigens on transfused cells leading to haemolysis of transfused cells

100
Q

Response of Anti A and Anti B to a HTR

A

Activate complement
cause severe intravascular haemolysis (acute HTR)
can be fatal

101
Q

Response of Anti-D to a HTR

A

can cause haemolysis mainly extravascular and HTR is delayed
not usually fatal

102
Q

In HDFN

A

Foetal blood cells (RhD+) cross placenta and encounter mothers D antigen
mother produced Anti-D antigen in response (alloimmunisation)
Anti-D IgG crosses placenta and can haemolyse foetal blood cells

103
Q

2 risk factors of HDFN

A

RhD - only IgG can cross placenta
Mother and newborn have incompatible blood

greater risk if :
mother is blood group AB
high titre of IgG

104
Q

What needs to happen prior to a blood transfusion

A

Group and screen
O- blood given in emergencies

105
Q

what does a group determine

A

ABO group - forward (patients RBC+anti-ABO antibodies) and reverse group (patients plasma+RBC expressing antigen A and B)
RhD status - test patients RBCs with anti-D antibodies

106
Q

what does agglutation confirm

A

interaction between antigen and antibody and therefore presence of antigen on patients RBC

107
Q

What does a blood screen entail

A

Patients serum tested against panels of RBCs that express relevant RBC antigens
To check for presence of acquired alloantibodies in blood

108
Q

What are acquired antibodies formed as a result of

A

active immunisation to non-self RBC antigens following exposure to RBCs from another individual :
pregnancy - foetal RBC antigen enters mothers circulation
incompatible transfusion

109
Q

Following a group and screen a Cross match is carried out this, includes

A

Patients plasma + RBC sample from donor
agglutation = incompatible
no change = compatible

110
Q

How can blood be collected

A

Whole donation or apheresis
in apheresis blood donor connected to machine which separates out specific blood components

111
Q

FFP is

A

Fresh Frozen Plasma
- contains all coagulation factors
-used in treatment of bleeding in patients with coagulopathies

112
Q

Cyroprecipitate contains

A

fibrinogen
Factor VIII
von Willebrand factor
Factor XIII

113
Q

Packed red cells are given to

A

increase Hb and oxygen carrying capacity of blood:
anaemia
haemorrhage

114
Q

Shelf life and storage of packed red cells

A

35 days
in fridge at 4°C

115
Q

How to know if a patient has responded to a red cell transfusion

A

Check for response clinically by assessing patient
measure Hb levels to check increase to normal range

116
Q

Platelets are

A

fragments of megakaryocytes

117
Q

Role of platelets

A

blood clotting

118
Q

How are platelets produced for transfusion

A

pooling from whole blood donations or by apheresis

119
Q

why may platelets be transfused

A

treat or reduce risk of bleeding

120
Q

Why is it preferred that platelets match the patients ABO group

A
  • can express ABO antigens (only in 4-7% of individuals)
  • suspended in plasma which contains donors Anti-ABO antibodies (only a concern if sample in high-titre positive)
121
Q

Platelet shelf life and storage

A

7 days
at room temperature, requires constant agitation to ensure continuous oxygenation

122
Q

What does seeing nucleated RBCs in blood signify

A

high demand for RBCs so immature ones released prematurely into circulation
- nucleus lost as they mature

123
Q

Why do polychromatic (immature RBCs) appear blue

A

high RNA content - shown on methylene blue stain
still reticulocytes that lose ribosomes after few days

124
Q

Where is EPO made

A

kidneys
in response to hypoxia and anaemia providing a demand-supply feedback loop

125
Q

How does EPO work

A

interacts with EPO receptors on RBC progenitors in bone marrow to increase RBC production

126
Q

what foods can reduce iron absorption

A

soya beans - contain phytates that bind to iron reducing absorption
but also have iron in them

127
Q

Negative feedback system involving Hepcidin

A

Erythropoietic activity supresses hepcidin synthesis, increasing ferroportin duodenum enterocyte, which increases iron absorption

128
Q

Hepcidin in inflammation

A

Inflammation increases hepcidin which reduces iron supply leading to anaemia of chronic disease
-transferrin reduced
-ferritin increased
-gut iron absorption reduced

129
Q

requirements for folate increase

A

pregnancy
increased RBC production - sickle cell anaemia

130
Q

What 3 things does erythrocyte function depend on

A

Membrane integrity
Haemoglobin structure and function
Cellular metabolism

131
Q

RBC membranes

A

lipid bilayer
supported by protein cytoskeleton with transmembrane proteins to maintain integrity, shape and elasticity

132
Q

Haemoglobin structure

A

4 haem groups
each with Fe2+ bound by a porphyrin ring
Fe2+ can bind 1 O2 molecule reversibly

each haem group combined to a globin chain produced by cluster genes

133
Q

Types of haemoglobin found in adults and foetuses

A

HbA - adults
HbB - foetuses

134
Q

Right shift of haemoglobin curve

A

more O2 unloading

135
Q

2 causes of Right shift

A

Bohr Effect
HbS - sickle cell haemoglobin

136
Q

Left shift of haemoglobin curve

A

more O2 loading

137
Q

2 causes of Left shift

A

Myoglobin
HbF - foetal haemoglobin

138
Q

RBC metabolism and PPP

A

G6P is oxidised to CO2 producing NADPH - this is the Pentose phosphate pathway
G6PD is the rate-limiting enzyme in this pathway

NADPH reduces oxidised glutathione into reduced glutathione - antioxidant in RBCs

139
Q

When are oxidants produced in the blood

A

During infection
exogenous e.g drugs/broad beans

140
Q

Issues of G6PD deficiency

A

Intermittent severe intravascular haemolysis from oxidant damage
- irregular contracted, small bite cells with no central pallor
- Hb denatured and forms round inclusions:
Heinz bodies

X-linked recessive = usually homozygous males

141
Q

Why is G6PD deficient present in individuals with malaria

A

Acquired immune response in order to combat malaria
better survival advantage as RBCs containing malaria removed

142
Q

What are antioxidants

A

Chemicals protecting RBC from oxidants

143
Q

Polycythaemia is

A

too many RBC in circulation

144
Q

Two types of Polycythaemia

A

Pseudo
True

145
Q

In pseudo polycythaemia

A

Reduced plasma volume

146
Q

4 branches of true polycythaemia

A

Blood doping or over transfusion - cyclists
Appropriately increased EPO - high altitude place
Inappropriate EPO synthesis or use - cyclists or renal tumour
Independent of EPO - polycythaemia vera

147
Q

What is Polycythaemia vera

A

myeloproliferative disorder of bone marrow
-drugs can be given to reduce bone marrow production of RBCs
- can cause hyperviscosity – thrombosis– requiring venesection

148
Q

MCV is

A

average volume of each RBC
MCV (L) = Hct(L/L) x1000 / RBC x (10^12/L)

149
Q

MCH is

A

mean cell haemoglobin
average mass of Hb in each RBC

MCH (g) = Hb (g/L) / RBC x (10^12/L)

150
Q

MCHC is

A

mean cell haemoglobin concentration
average conc. of Hb in each RBC

MCHC (g/L) = Hb(g/L) / Hct (L/L)

151
Q

2 mechanisms of anaemia

A

Failiure to produce RBCs
Excess RBC loss or destructuion

152
Q

What is koilonychia and when does it occur

A

spooning of nails
presentation of anaemia

153
Q

What is angular cheilitis and when does this occur

A

Inflammation of corners of mouth
presentation of anaemia

154
Q

What is landsteiners law

A

Antigens present on RBC are opposite type to antibodies present in plasma

155
Q

what antibodies and antigens are present in individuals with blood group AB

A

A AND B antigens in blood
no antibodies in plasma

156
Q

what antibodies and antigens are present in individuals with blood group O

A

no antigens in blood
A and B antibodies in plasma

157
Q

How do genes code for ABO

A

sugar residue is added to a common glycoprotein and fucose stem (H antigen) on RBC membrane

158
Q

How do genes code for O blood

A

O gene is recessive - neither A or B sugars only H stem

159
Q

How do genes code for A blood

A

A gene codes for enzyme adding N-acetyl galactosamine to common H antigen

160
Q

How do genes code for B blood

A

B gene codes for enzyme that adds galactose to common H antigen

161
Q

What patients are given RBCs

A

anaemia

162
Q

Why are patients are given FFP

A

to treat
prolonged APTT and PT
or reversal of warfarin

163
Q

Why are patients are given Cryoprecipitate

A

Replace FVIII and fibrinogen esp in heavy bleeding - also cont. VWF and FXIII

164
Q

Why are patients given platelets

A

to treat :
Bone marrow failure
thrombocytopenia
massive bleeding / DIC

165
Q

Why are patients given Factors VIII and IX

A

To treat :
haemophilia ( A and B - respectively)

166
Q

Why are patients given immunogolbulins

A

to protect against Hep A

167
Q

What are the main fluid compartments

A

Intracellular - 55%
Extracellular - 45%
(36% interstitial fluid
Transcellular fluid - 2%
Blood plasma - 7% )
of body water

168
Q

Difference in plasma and serum use

A

plasma - easy to prepare
serum - blood into tube with anticoagulant, allowed to clot then centrifuged, cleaner sample (serum separator tubes have silica coating to induce clotting and gel layer to form physical barrier between cells and serum)

POM 3: Haematology (3 decks)

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