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My Haem Cue Cards > Anaemia > Flashcards

Anaemia Flashcards

1
Q

sites of haemopoesis in the embryo 1. all sites 2. where from 3rd to 7th month

A
  1. Yolk sac then liver then marrow

3rd to 7th month - spleen

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2
Q

ordre of maturation in granulopoesis

A

myeloblast to promyelocyte to myelocyte through metamyelocyte forms eventually to band forms and neutrophils that are seen in the blood

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3
Q

order of maturation in erythropoiesis

A 
Pronormoblast
early normoblast
intermediate normoblast
late normoblast
Reticulocyte
erythrocyte
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4
Q

platelets form from what type of cells

A

megakaryocytes

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5
Q

what are the 3 granulocytes?

A

eosinophils
basophils
neutrophils

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6
Q

structure and function of neutrophil

A 
Segmented nucleus (polymorph)
Neutral staining granules
Phagocytose invaders
Kill with granule contents and die in the process
Attract other cells
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7
Q

structure and function of eosinophils

A

Usually bi-lobed
Bright orange/red granules

parasitic/ hypersensitivity

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8
Q

structure and function of basophils

A

Infrequent in circulation
Large deep purple granules obscuring nucleus
Circulating version of tissue mast cell

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9
Q

structure and function of monocytes

A

Large single nucleus
Faintly staining granules, often vacuolated
Circulate for a week and enter tissues to become macrophages
Phagocyose invaders
Kill them
Present antigen to lymphocytes

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10
Q

structure of lymphocytes

A

Mature – small with condensed nucleus and rim of cytoplasm
Activated (often called atypical) – large with plentiful blue cytoplasm extending round neighbouring red cells on the film, nucleus more ‘open’ structure

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11
Q

recognise primitive precursers

A

immunophenotyping bioassays

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12
Q

why is the red cell only restricted to glycolysis?

A

no mitochondria

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13
Q

why do rbcs hve a limited life span ?

A

no nucleus

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14
Q

is haemoglobin a pentamer?

A

no tetramer

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15
Q

adult hb

A

2 alpha and 2 beta

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16
Q

where is fe2+ in hb?

A

in the porphyrin ring

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17
Q

how many o2 can bind to fe2+

A

one

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18
Q

what cells are involved in red cell destruction?

A

macrophages

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19
Q

breakdown of rbcs

A

haem - iron + porphyrin

globin - amino acids

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20
Q

what are the 3 things that can happen to iron?

A

stored in ferritin
recycled by transferrin
added to proteins

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21
Q

breakdown of haem

A

haem + fe2+
porphyrin
biliverdin
bilirubin – liver to conjugate it

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22
Q

what is epo produced in response to?

A

hypoxia

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23
Q

how does a red cell produce energy?

A

glycolysis - ATP

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24
Q

A way to keep Fe2+ from becoming Fe3+ (ie stop it oxidising) for rbcs

A

nadph

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25
Q

fe3+ other name

A

metHb - doesn’t carry o2

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26
Q

To prevent oxidative damage to enzymes from free radicals (hydrogen peroxidase)

A

glutathione reacts to produce water

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27
Q

what replenishes the glutathione to water process?

A

production of nadph via hexose monophosphate shunt

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28
Q

what is the rate limiting enzyme for the hexokinase monophosphate shunt?

A

G6PD

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29
Q

rate limiting enzyme for co2 to bicarb

A

carbonic anhydrase

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30
Q

Fully saturated 1g Hb will bind

A

1.34ml o2

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31
Q

fetal hb

A

2 alpha 2 gamae

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32
Q

haemoglobin graph is

A

sigmoidal

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33
Q

describe the fetal hb saturation

A

Fetal Hb (a2g2) saturates more at the same pO2 so effectively takes O2 from the maternal circulation.

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34
Q

1,3 BPG to 2,3 BPG is called the

A

rapapoport lumbering shunt

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35
Q

Curve is shifted right by

A

molecules that interact with
Hb (H+, CO2, 2,3 DPG, increased temp). This results in more O2
delivered to tissues.

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36
Q

what is increased in chronic anaemia?

A

2,3 BPG

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37
Q

haem synthesis

A

precursers
porphobilinogen
protoporphyrin
fe + iron

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38
Q

iron absorption occurs mainly in the

A

duodenum

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39
Q

what enhances iron absorption

A

Haem vs non-haem iron
dedicated haem iron transporter
Ascorbic acid (reduces iron to Fe2+ form)
Alcohol

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40
Q

what inhibits iron absorption

A

Tannins eg tea
Phytates eg cereals, bran, nuts and seeds
Calcium eg dairy produce

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41
Q

what reduces iron from fe3+ to fe2+

A

duodenal cytochrome B

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42
Q

what transports ferrous iron into the duodenal enterocyte

A

DMT1

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43
Q

Facilitates iron export from the enterocyte

A

ferroportin

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44
Q

what picks up iron from ferroportin ?

A

transferrin

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45
Q

The major negative regulator of iron uptake

A

hepcidin

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46
Q

hepcidin increases/decreases when iron deficient

A

decreases

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47
Q

how many binding sites does transferrin have for iron?

A

two

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48
Q

transferrin transports iron from ……. to ……..

A

Transports iron from donor tissues (macrophages, intestinal cells and hepatocytes) to tissues expressing transferrin receptors

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49
Q

holotransferrin

A

iron bound

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50
Q

apotransferrin

A

iron unbound

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51
Q

consequences of a negative iron balance

A 
Exhaustion of iron stores
Iron deficient erythropoiesis
Falling red cell MCV
Microcytic Anaemia
Epithelial changes
skin
Koilonychia
Angular stomatitis
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52
Q

what causes hypochromic microcytic anaemia?

A

Haem deficiency
Lack of iron for erythropoiesis
Iron deficiency (low body iron)‏
Anaemia of Chronic Disease (normal body iron)‏
Congenital sideroblastic anaemia (very rare)

Globin deficiency
Thalassaemias

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53
Q

how do you confirm iron deficiency

A

a combination of anaemia (decreased haemoglobin iron) and reduced storage iron (low serum ferritin)

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54
Q

causes of iron deficiency

A

dietary
bleeding
malabsorption

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55
Q

causes of chronic blood loss

A 
Menorrhagia
Gastrointestinal
Tumours
Ulcers
Non-steroidal anti-inflammatory agents (NSAIDs)
Parasitic infection
Haematuria
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56
Q

what is iron malutiisation

A

anaemia of chronic disease

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57
Q

what happens in anaemia of chronic disease

A

due to the amount of inflammatory mediators in chronic disease this in turn leads to increased ferritin/ increased hepcidin/ and hence impaired iron supply to the marrow erythroblasts

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58
Q

causes of iron overload

A 
Primary
Hereditary haemochromatosis
Secondary
Transfusional
Iron loading anaemias
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59
Q

gene causing haemochromatosis

A

HFE gene = decreases synthesis of hepcidin and increased iron absorption

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60
Q

mutations in haemochromatosis other than the HFE gene

A

C282Y or H63D

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61
Q

diagnose haemochromatosis

A

Risk of iron loading: transferrin saturation >50% (sustained on repeat fasting sample)‏
Increased iron stores: serum ferritin >300 g/l in men or >200 g/l in pre-menopausal women

Liver biopsy: rarely needed, non-invasive techniques such as Fibroscan available to assess for cirrhosis

family screening

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62
Q

treat haemochromatosis

A

venesection

to keep ferritin below 50 ug /l

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63
Q

name the iron loading anaemias

A

Massive ineffective erythropoiesis
Thalassaemia syndromes
Sideroblastic anaemias

Refractory hypoplastic anaemias
Red cell aplasia
Myelodysplasia (MDS)

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64
Q

what do you give patients along side transfusions to prevent iron overload>

A

iron chelation

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65
Q

what is the literal meaning of anaemia

A

without blood - reduced total red cell mass - hb and haematocrit

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66
Q

what is the haematocrit?

A

Ratio (or commonly expressed as the percentage) of the whole blood that is red cells if the sample was left to settle

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67
Q

what is the bodies natural response to anaemia?

A

reticulocytosis (increased rbc production)

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68
Q

why is the blood film polychromic in reticulocytes?

A

have rna so stain purple

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69
Q

what are the two main causes of anaemia?

A 
decreased production (low retic count) 
increased loss or destruction (high retic count)
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70
Q

what are the two main causes of decreased production of rbcs?

A

hypoproliferative

maturation abn

71
Q

cytoplasmic defects

A

impaired haemoglobinisation

72
Q

nuclear defects

A

impaired cell division

73
Q

what are the main causes of increased loss of destruction of rbcs?

A

bleeding

haemolysis

74
Q

what is the main reson for a microcytic and hypochromic anaemia

A

shortage of building blocks needed for hb production = deficient hb synthesis = cytoplasmic defect

75
Q

heavy menstrual loss

A

> 60ml

76
Q

nadph in red cell generated by what pathway

A

ebden myerhoff pathway

77
Q

anaemia with an increased retic response –?

A

hameolysis

blood loss

78
Q

anaemia with a reduced retic response

A

maturation abnormality (microcytic or macrocytic)

or

hyporpoloferative (normocytic)

79
Q

what type of bilirubin is in the urine?

A

urobilinogen

80
Q

what type of bilirubin is in faeces?

A

stercobilinogen

81
Q

if you suspect haemolytic anaemia look for …

A

evidence of rbc breakdown products and a reticulocytosis

82
Q

MCH can either be

A

hypochromic or normochromic

83
Q

macrocytic anaemia - megaloblastic anaemia causes

A

B12 or folate deficiency

84
Q

causes of macrocytic anaemia

A 
myelodysplasia
myeloma
aplastic anaemia
reticulocytosis
cold agglutinins
85
Q

microcytosis without anaemia

A

alcohol
liver disease
hypothyroidism

86
Q

normocytic normochromic anaemia causes

A

[Acute blood loss/early iron deficiency]
Hypoproliferative (low retic):
Chronic diseases -inflammatory, infective, malignant disorders
Anaemia of renal failure
Hypometabolic states (e.g. hypothyroidism)
Marrow failure (e.g. aplasia or infiltration)

87
Q

sources of folate

A

liver green leafy veg cereal

synthetic - folic acid

88
Q

women planning pregnancy folic acid supplements

A

400 ug/d pre conception up to the 12th week of pregnancy

89
Q

main general causes of microcytosis

A

genuine - megaloblastic or non megaloblastic

spurious

90
Q

developing erythroblasts undergo what three things

A

Accumulate Hb
Reduce in size
Stop dividing and lose nucleus (once Hb content optimal)

91
Q

define megaloblast

A

An abnormally large nucleated red cell precursor with an immature nucleus

92
Q

megaloblastic anaemia are characterised by defects in

A

dna synthesis and nuclear maturation

93
Q

B12 and folate are essential co-factors for

A

nuclear maturation - they enable chemical reactions for dna synthesis and gene activity

94
Q

Folate cycle important for

A

nucleoside synthesis (eg uridine to thymidine conversion)

95
Q

Methionine cycle important for producing a

A

methyl donor called ‘S-adenosyl methionine’ (impact on DNA, RNA, proteins, lipids, folate intermediates)

96
Q

what are the two cycles involved with B12 and folate

A

methionine cycle

folate cycle

97
Q

what is pernicious anaemia?

A

Autoimmune condition with resulting destruction of gastric parietal cells - Results in intrinsic factor deficiency with B12 malabsorption and deficiency

98
Q

folate absorption

A

converted to monoglutamate

absorbed in jejunum and duodenum

99
Q

source of b12

A

animal

100
Q

absorption of b12

A

ileum

101
Q

what drugs can induce a folate deficiency?

A

anticonvulsants

102
Q

what can cause excessive utilisation of folate?

A

haemolysis
exfoliating dermatitis
pregnancy
malignancy

103
Q

main feature of b12/folate deficiency

A

jaundice

104
Q

what deficiency is associated with neurological problems?

A

b12 deficiency

105
Q

macroovalocytes and hypersegmented neutrophils

A

b12/folate deficiency

106
Q

if you suspect b12 or folate deficiency what tests do you do ?

A

assay b12 and folate levels in serum
autoantibodies
schilling test
bone marrow exam

107
Q

autoantibodies seen in pernicious anaemia

A

anti intrinsic factor

anti gastric parietal cell

108
Q

what is given for life in pernicious anaemia

A

vitamin b12 (hydroxycobalamin)

109
Q

non megaloblastic anaemia causes

A 
Alcohol
Liver disease
Hypothyroidism
Marrow failure:`
Myelodysplasia
Myeloma
Aplastic anaemia
110
Q

what is spurious macrocytosis?

A

The volume of the mature red cell is NORMAL, but the MCV is measured as high!

111
Q

causes of spurious macrocytosis

A 
reticulocytosis 
cold agglutinins (clumps of red cells)
112
Q

what is haemolysis?

A

premature red cell destruction

113
Q

what is compensated haemolysis?

A

Increased red cell destruction compensated by increased red cell production
i.e. Hb Maintained

114
Q

what is decompensated haemolysis (or haemolytic anaemia)?

A

Increased rate of red cell destruction exceeding bone marrow capacity for red cell production
i.e. Hb Falls

115
Q

what are the consequences of haemolysis?

A

erythroid hyperplasia

excess rbc breakdown products

116
Q

how do you diagnose haemolysis?

A

increased red cell production

detection of breakdown products

117
Q

extravascular

A

Taken up by reticuloendothelial system (spleen and liver predominantly)

118
Q

intravascular

A

destroyed in circulation

119
Q

what is seen in extravascular haemolysis?

A

hyperplasia at site of destruction
jaundice (unconjugated)
gall stones
urobilinogenuria

– normal products in excess

120
Q

what is seen in intravascular haemolysis?

A

Haemoglobinaemia (free Hb in circulation)
Methaemalbuminaemia
Haemoglobinuria: pink urine, turns black on standing
Haemosiderinuria
– abnormal products so life threatening

121
Q

causes of intravascular haemolysis

A

ABO incompatible blood transfusion
G6PD deficiency
Severe falciparum malaria (Blackwater Fever)
Rarer still PNH,PCH

122
Q

HbS

A

sickle cell

123
Q

spherocytes

A

membrane damage

124
Q

red cell fragments

A

mechanical damage

125
Q

Heinz bodies

A

oxidative damage

126
Q

autoimmune causes of haemolysis

A

Warm (IgG) - Idiopathic (commonest); Autoimmune disorders (SLE); Lymphoproliferative disorders (CLL); Drugs (penicillins, etc); Infections
Cold (IgM) - Idiopathic; Infections (EBV, mycoplasma); Lymphoproliferative disorders

127
Q

what is the direct coombs test ?

A

Identifies antibody (and complement) bound to own red cells

128
Q

causes of alloimmune haemolysis?

A 
Immune response (antibody produced)
Haemolytic transfusion reaction
Immediate (IgM) predominantly intravascular
Delayed (IgG) predominantly extravascular
Passive transfer of antibody
Haemolytic disease of the newborn
Rh D
ABO incompatibility
Others eg anti-Kell
129
Q

causes of acquired haemolysis

A 
Mechanical red cell destruction
Disseminated intravascular coagulation
Haemolytic uraemic syndrome (eg E. coli O157)
TTP
Leaking heart valve
Infections e.g. Malaria
130
Q

Mechanical valve related Microangiopathic haemolytic anaemia (MAHA)

A

Red cell fragmentation as a result of mechanical (extrinsic) damage

131
Q

microspherocytes

A

severe burns

132
Q

membrane defects causing haemolysis

A 
Liver Disease (Zieve’s Syndrome)
Vitamin E deficiency
Paroxysmal Nocturnal Haemoglobinuria
133
Q

Haemolysis, Alcoholic liver disease, hyperlilidaemia

A

zieves syndrome

134
Q

hams test

A

paroxysmal nocturnal haemoglobinuria

135
Q

genetic causes of haemolysis

A

hereditary spherocytosis

136
Q

what is the result of g6pd deficiency

A

failure to cope with oxidant stress

137
Q

describe sickle cell

A

abnormal polymerisation of haemoglobin resulting in shortened red cell survival
caused by a point mutation in beta globin chain

138
Q

trait sickle cell symptoms

A

asymptomatic

139
Q

film hypo/micro targets nucleated rbc’s pappenheimer bodies (red) alpha chain precipitates (blue)

A

beta thal major

140
Q 
22 yrs female. 
Splenomegaly
Intermittent mild jaundice
Gallstones
Father had splenectomy in young adulthood for gallstones
A

hereditary spherocytosis

141
Q

what is hereditary spherocytosis?

A

defect in red cell membrane affecting its flexibility - dominant inheritance - chronic extravascular haemolysis

142
Q

black water fever

A

falciparum malaria - intravascular hamolysis

143
Q

thai girl intermittent jaundice fever unwell oxidant drugs

A

thalasaemia

144
Q

HbH

A

alpha thalassaemis

145
Q

HbH genes

A

3 of 4 genes not working - excess of beta chains (B4)

146
Q

golf balls

A

HbH

147
Q

what are the main haemoglobinopathies?

A

Alpha thalassaemia
Beta thalassaemia
Sickle cell anaemia

148
Q

HbA

A

2 alpha 2 beta

149
Q

HbA2

A

2 alpha 2 delta

150
Q

HbF

A

2 alpha 2 gamma

151
Q

alpha genes are on

A

chromosome 16

2 per chromosome so 4 per cell

152
Q

beta like genes

A

chromosome 11

one beta gene per chromosome 2 per cell

153
Q

aut dom or aut rec for haemoglobinopathies

A

aut rec

154
Q

what are the two main groups of haemoglobinopathies and what are they caused?

A

Thalassaemias; decreased rate of globin chain synthesis

Structural haemoglobin variants; normal production of structurally abnormal globin chain → variant haemoglobin eg HbS

155
Q

what type of anaemia is thalassaemia?

A

hypochromic microcytic anaemia

156
Q

mutation in alpha thalassaemia

A

Unaffected individuals have 4 normal α genes (αα/αα)
Results from deletion of one α+ (-α) or both α0 (–) alpha genes from chromosome 16
Reduced α+ or absent α0 alpha chain synthesis
α chains present in all adult forms of Hb therefore HbA, HbA2 and HbF all affected

157
Q

alpha thal trait

A

one or two missing genes - asymptomatic with mild anaeima

158
Q

HbH disease

A 
only one alpha gene affected 
severe 
anaemia with very low mcv and mch  
splenomegaly
jaundice
159
Q

Hb barts hydrops fetalis

A 
most severe 
no alpha genes from either parent 
Hb barts (gamma 4)
HbH (beta 4)
almost
160
Q

what happens to the beta chains in HbH disease?

A

Excess β chains form tetramers (β4) called HbH which can’t carry oxygen

161
Q

what is the genetic cause of beta thal?

A

point mutation

162
Q

beta thal trait

A

asymptomatic

mild anaemia low mcv mch

163
Q

management of beta thal major

A 
transfusions 
iron chelation (desferrioxamine)
164
Q

genetics of sickling disorders

A

Point mutation in codon 6 of the β globin gene that substitutes glutamine to valine producing S
This alters the structure of the resulting Hb→ HbS (α2βs2)
HbS polymerises if exposed to low oxygen levels for a prolonged period
This distorts the red cell, damaging the RBC membrane

165
Q

sickle cell trait

A

HbAS

166
Q

sickle cell trait

A

HbAS

may sickle in severe hypoxia

167
Q

HbSS

A

sickle sell anaemia

168
Q

what is sickle crisis

A

Episodes of tissue infarction due to vascular occlusion

169
Q

what causes hyposplenism in sickle cell?

A

splenic infarcts

170
Q

precipitants of sickle crisis

A 
hypoxia 
dehydration
infection
cold exposure
stress/fatigue
171
Q

treat sickle crisis

A 
Opiate analgesia 
Hydration 
Rest
Oxygen 
Antibiotics if evidence of infection 
Red cell exchange transfusion in severe crises eg chest crisis or stroke
172
Q

long term management of sickle cell

A

hyposplenism - long term prophylactic penicillin
folic acid supplements
Hydrocycarbamide
regular transfuison

173
Q

haemoglobinopathy diagnosis

A

high performance liquid chromatography or gel electrophoresis

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