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haematology > lecture 2- anaemias > Flashcards

lecture 2- anaemias Flashcards

1
Q

what is haemoglobin

A

haemoprotein composed of globin

haem gives red blood cells their characteristic colour

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2
Q

what is the function of haemoglobin

A

transport oxygen from lungs to body tissues

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3
Q

what is the name of the shape used to describe normal adult haemoglobin

A

tetramer

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4
Q

what is normal adult haemoglobin made up of

A

4 polypeptide chains- 2 unlike pairs
2 alpha chains
2 beta chains

each globin chain has 1 iron-containing molecule (haem)

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5
Q

in normal adult hameoglobin, where is the haem (iron-containing molecule) located

A

within a hydrophobic cavity

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6
Q

what is the function of haemoglobin

A

carry oxygen around the body

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7
Q

how does haemoglobin carry oxygen around the body

A

iron (Fe) has the ability to bind oxygenit unloads its oxygen changing from ferrous state (Fe2+) to its ferric state (Fe3+) and back again

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8
Q

how many haemoglobin molecules does each red cell contain

A

640 million

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9
Q

what must red blood cells be able to do in order to allow gaseous exchange

A

be able to pass repeatedly through microcirculation

have to come into close contact with tissues

maintain haemoglobin in its reduced ferrous state (Fe2+)

maintain osmotic equilibrium

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10
Q

how many miles does a red cell pass in its life cycle

A

300 miles in its 120 day lifespan

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11
Q

in order to fulfill its function, what features does a red cell have

A

is a biconcave disc

has to generate energy as ATP

generate reducing power as NADPH

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12
Q

why does a red cell use the embden-meyerhorf pathway

A

to generate energy as ATP

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13
Q

why does a red cell use the hexose-monophosphate pathway

A

generate reducing power as NADPH

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14
Q

why is iron important for health

A

plays vital role in normal function/metabolism of every cell in body

essential for haemoglobin production

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15
Q

what is the function of transferrin

A

transports iron to developing cells which has transferrin receptors

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16
Q

what is the function of transferrin receptors

A

present on blood cellbinds to transferrin/iron complex

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17
Q

where is iron stored in the body

A

66% as ferritin in liver, bone marrow, spleen and muscles

33% stored as haemosiderin, found in cells not circulating the blood

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18
Q

how much iron does an average western diet contain

A

10-15mg

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19
Q

what percentage of iron is absorbed through the small intestine

A

5-10%

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20
Q

how is absorption of iron adjusted

A

according to bodys’ needs

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21
Q

which products is iron more readily absorbed from

A

meat rather than veg

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22
Q

how much iron is lost daily and through what

A

1mg

through hair, skin, urine, faeces and menstrual blood loss

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23
Q

name some sources of dietary iron

A 
red meat- liver
fish- salmon, sardines, pilchards, 
tuna
egg yolk
wholemeal bread
fortified cereals
vegetables and 
pulses
nuts and prunes
marmite
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24
Q

describe normal blood cells in terms of:nucleusdiametershapepallor

A

anucleate

6.7-7.7µm
biconcave disc

central area of pallor- 1/3rd of red cell diameter

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25
Q

what is anaemia

A

a below normal level of haemoglobin

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26
Q

what is the normal range of haemoglobin for adult males and females

A

males- 130-170g/Lfemales- 120-155g/L

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27
Q

how is anaemia classified

A

by the size of red cels (mean cell volume)

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28
Q

what are the 3 MCV classfications of anaemia

A

microcytic- small red cells (MCV<78fl)

macrocytic- large red cell (MCV>100fl)

normocytic- normal sized red cells (MCV 78-100fl)

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29
Q

what are the causes of microcytic anaemia

A

iron deficiency

thalassaemia

haemoglobin defects

anaemia of chronic disease

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30
Q

what are the causes of macrocytic anaemia

A 
megaloblastic anaemia:
folic acid deficiency
B12 deficiency
auto-immune disease 
pernicious anaemia

non megaloblastic anaemia:
MDS- myelodysplastic syndromes
liver disease

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31
Q

what are the causes of normocytic anaemia

A

haemolytic anaemia

acute blood loss

anaemia of chronic disease

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32
Q

what is the most common cause of anaemia worldwide

A

iron deficiency

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33
Q

what are the most common causes of microcytic anaemia

A

reduced mean cell volume (MCV)- small red cells

reduced MCH (mean cell haemoglobin)- pale empty red cells

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34
Q

why does iron deficiency anaemia occur

A

iron supply doesnt meet the demand

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35
Q

how long does it take for iron deficiency anaemia to become apparent

A

takes a long time to use up all the body iron stores (ferritin)

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36
Q

what are the 3 phases for iron deficiency anaemia

A

iron replete

iron deplete

iron deficient

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37
Q

what are the causes of iron deficiency anaemia

A

chronic blood loss e.g. menorrhagia, GI bleed

increased demands e.g. growth, pregnancy

malabsorption e.g. post gastrectomy

poor diet- contributory cause

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38
Q

iron deficiency anaemia develops slowly, what are the clinical features

A 
pallor- eyes
sore mouth
brittle nails
dysphagia
glossitis
abnormal apetite
hair thinning
lassitude
fatigue
tachycardia
39
Q

what are the laboratory findings in iron deficiency anaemia

A

hypochromic microcytic anaemia

raised platelet count

bone marrow shows absence of stored iron

bone marrow shows erythroblasts with ragged irregular cytoplasm

reduced serum ferritin level

low serum iron level

raised serum transferrin receptor

40
Q

what dye would be used to stain bone marrow filmwhat would be seen

A

prussion blue

iron stores

41
Q

for iron deficiency anaemia, what would be the treatment

in which cases would IV iron be used

A

oral iron 3 times daily
reticulocyte response within 7 days
treatment continued for 4-6 months
treatment of cause

patients with malabsorption

42
Q

what are the side effects of oral/IV iron

A

abdominal pain

diarrhoea

constipation

43
Q

what is vitamin B12

A

cobalaminconsists of cobalt atom situated in centre of a corrin nucleus

44
Q

draw out the molecular structure of vitamin B12 molecule

A
45
Q

what is the function of vitamin B12

A

it is a coenzyme for 2 biochemical reactions

  1. methylation of homocysteine to methionine
  2. converts methylmalomyl coenzyme A to succinyl coenzyme A
46
Q

what happens to the body without vitamin B12

A

without the 2 necessary reactions taking place body has reduced supply of precursors required for DNA synthesis and Myelin production

47
Q

how does reduced DNA synthesis in the body, effect red cell production

A

erythrocytes in the bone marrow show abnormal maturation- maturation arrest

maturation of nucleus being delayed relative to cytoplasm

no reticulocytes produced

48
Q

what is the adult daily requirement of B12

A

1µg

49
Q

how much B12 does a normal mixed diet contain

A

10-15µg

50
Q

where is B12 stored in the body and for how long

A

liver2-4 years

51
Q

where is B12 absorbed in the body

A

absorbed in ileum attached to intrinsic factor which is secreted in the stomach

52
Q

how is B12 lost from the body

A

through urine
faeces
excretion of bile

53
Q

how is B12 transported in the body

A

in plasmabound to transcoalbumin

54
Q

name some dietary sources of B12

A 
liver
kidney
heart
clams
oysters
red meat
sea food
eggs
milk
cheese
yoghurt
fortified foods
55
Q

what are the causes of a B12 deficiency

A

inadequate diet- vegans

malabsorption- gastrectomy, intrinsic factor deficiency/antibody

intestinal causes- tapeworm, crohns disease, illeal resection

excess utilisation- pregnancy, haematological disease

liver disease

drug treatments

56
Q

what are the clinical features of B12 deficiency

A 
gradual onset of anaemia
mild jaundice
glossitis
tingling in feet/hands
difficulty in gait
visual disorders
psychiatric disorders
may be asymptomatic
57
Q

what are the laboratory findings of B12 deficiency

A 
macrocytic anaemia with oval red cells
reticulocyte absence
hypersegmented neutrophils
moderarely reduced white blood cell count
moderately reduced platelet count
raised bilirubin
low serum B12
hypercellular bone marrow- maturation arrest
raised serum methylmalonic acid
raised serum homocysteine levels
58
Q

what is the treatment for B12 deficiency

A

1 mg hydroxycobalamin intramuscularly
every 3 days until 6 injections have been given
then every 3 months for life, unless cause of deficiency has been treated

59
Q

why are potassium supplements given at the same time as B12 deficiency treatment in some patients

A

in severe cases

because some patients die suddenly after starting treatment due to the drop in potassium levels

60
Q

what is vitamin B12 deficiency neuropathy

A

progressive damage to peripheral sensory nerves (sensory chord, brain and peripheral nerves)

affects lower limbs in main (tingling feet, difficulty walking, falls, optic atrophy psychiatric symptoms)

61
Q

what is the cause of vitamin B12 deficiency neuropathy

A

accumulation of homocysteine and reduction of methionine in nervous tissues

defective methylation of myelin

causes abnormal fatty acids to form around cells and nerves

62
Q

what is pernicious anaemia

A

auto-immune disease

auto antibodies attack the gastric parietal cells- parietal cells secrete intrinsic factor

cannot absorb B12

63
Q

what is the ratio that pernicious anaemia affects females and males

A

1.6 : 1

64
Q

what age is pernicious anaemia most commonly found at

A

over 60 years of age

65
Q

which race is pernicious anaemia commonly found in

A

all races, particularly northern Europeans

66
Q

an increased incidence in carcinoma of the stomach is found in which type of anaemia

A

pernicious anaemia

67
Q

what is folic acid

A

vitamin B9

pteorglutamin acid

parent compound of large group of compounds- the folates

68
Q

name 2 special properties of folic acid

A

humans cannot synthesise it

heat-labile- destroyed by cooking

69
Q

where is folic acid absorbed

A

in jejunum

70
Q

which diseases is folic acid deficiency often seen

A

diseases of small intestine

coeliac disease

tropical sprue

crohns disease

71
Q

how long does the body store folic acid for

A

3 months

72
Q

which biochemical reactions is folic acid required for in the body

A

homocysteine-methionine

serine-glycine

synthesis of DNA precursors

73
Q

what other processes is folic acid required for in the body

A

production of new cells

deficiency hinders DNA synthesis/cell division

substrate in important reactions that involved B12

74
Q

name the sources of folate

A 
leafy veg- spinach
turnip
lettuce
beans
peas
breakfast cereals
fruit
liver
75
Q

what are the clinical features of folate deficiency

A

same as B12 deficiency, often less severe

76
Q

why does folate deficiency develop rapidly

A

due to low body stores

77
Q

what causes folate deficiency

A

dietary

alcoholism

disorders of intestine

78
Q

which periods of time is folate demand particularly increased

A

pregnancy

periods of rapid cell division

79
Q

what is meant by spina bifada

A

neural tube defect

opening in spinal cord or brain

80
Q

what is the cause of spina bifada

A

B12 or folic acid deficiency in early pregnancy

lower maternal serum B12/folate- greater incidence

build up of homocysteine in foetus

impairs methylation of various proteins and lipids

81
Q

how is spina bifada treated

A

dietary supplements in early prengnayc reduce incidence by 75%

82
Q

state the other tissue abnormalities associated with B12/folic acid deficiency

A

sterility (either sex)

mophological abnormalities of cervix, bladder and other epithelia

cleft lip and palate in foetus/newborn

widespread reversible melanin pigmentation

associated with cardiovascular and malignant disease

83
Q

what happens in normocytic anaemia

A

normal sized RBCs (MCV in normal range)

not enough of them

84
Q

what are the causes of normocytic anaemia

A

acute blood loss

premature destruction of red cells- haemolytic anaemia

chronic disease

85
Q

what are the causes of haemolytic anaemia, which causes red cell destruction, leading to normocytic anaemia

A

sickle cell

hereditary spherocytosis

auto immune disease

86
Q

what are the chronic diseases which may cause normocytic anaemia

A

rhuematoid arthritis

cancer

kidney disease

drug treatment

87
Q

what is haemolytic anaemia

A

anaemias that result from increased rate of red cell destruction

88
Q

what is haemolytic anaemia classified as

A

hereditary or acquired

89
Q

what are the causes of hereditary haemolytic anaemias

A

red cell membrane defects- spherocytosis, elliptoctosis

defective red cell metaboism- G6PD deficiency, pyruvate kinase deficiency

disorders of haemoglobin synthesis- sickle cell, thalassaemia

90
Q

what are the 2 types of acquired haemolytic anaemias

A

extracorpuscular

environmental

91
Q

name the causes of acquired exracorpuscular haemolytic anaemia

A

haemolytic disease of newborn

autoimmune haemolytic anaemia

DIC- disseminated intravascular coagulation

heart valve replacements

92
Q

name the causes of environmental haemolytic anaemia

A

drug induced

march haemoglobinuria

infections such as malaria and E. coli 0157

93
Q

what are the clinical features of haemolytic anaemias

A

pallor

mild fluctuating jaundice

94
Q

what are the laboratory findings or haemolytic anaemia

A

increased RBC breakdown- raised bilirubin, LDH raised, haptoglobin reduced

increased RBC production- reticulocytosis, bone marow erythroid hyperplasia

damaged red cells- morphology shows fragments, microspherocytes, elliptocytes

haematology (3 decks)

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