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Clinical Biomedicine > W1: Anaemia > Flashcards

W1: Anaemia Flashcards

1
Q

definition of anaemia

A

reduced [Hb] in blood

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2
Q

when do symptoms of anaemia appear?

A

when [Hb] falls below 90-100g/L

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3
Q

what are the symptoms of anaemia?

A

SoB, weakness, pallor, lethargy, palpitations, headaches, heart failure & confusion

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4
Q

in young patients, how low can [Hb] get before symptoms appear?

A

60 g/L

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5
Q

what are the main clinical signs of anaemia?

A

pallor of mucous mems & nail beds

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5
Q

clinical signs that depend on type of anaemia are…

A

concave nails
jaundice (haemolytic)
leg ulcers
bone deformities
recurrent infection &/or bruising (BM failure/leukaemia)

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5
Q

which parameters are used in the classification of anaemias?

A

mean cell vol (MCV)
mean cell Hb (MCH)
mean corpuscular Hb conc (MCHC)

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6
Q

MCV normal range

A

80-101 fl

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7
Q

MCH normal range

A

27-34 pg

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8
Q

MCHC normal range

A

300-350 g/l

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9
Q

which 2 parameters are used to classify anaemia?

A

size & [Hb]

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10
Q

microcytic

A

small RBCs

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11
Q

normocytic

A

normal sized RBCs

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12
Q

macrocytic

A

large RBCs

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13
Q

hypochromic

A

reduced [Hb]

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14
Q

normochromic

A

normal [Hb]

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15
Q

hyperchromic

A

high [Hb]

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16
Q

what are RBCs like in normocytic, normochromic anaemia?

A

normal vol (MVC)
normal amount Hb (MCH)
normal [Hb] (MCHC)
RBC count reduced

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17
Q

what are the causes of normocytic, normochromic anaemia?

A

acute bleed
marrow failure
haemolysis
renal failure (epo deficiency)

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18
Q

what are RBCs like in microcytic, hypochromic anaemia?

A

reduced vol (MCV)
less Hb (MCH)
lower [Hb] (MCHC)

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19
Q

what are the causes of microcytic, hypochromic anaemia?

A

Fe deficiency (absolute or functional)
thalassemia
anaemia of chronic disorder

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20
Q

what are RBCs like in macrocytic, normochromic anaemia?

A

increased vol (MCV)
normal [Hb] (MCHC)
so MCH increased
RBC count low

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21
Q

what are the causes of macrocytic, normochromic anaemia?

A

B12 or folate defiency

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22
Q

what are the state of RBCs in anaemia due to acute blood loss?

A

normocytic, normochromic
(RBCs qualitatively normal)

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23
Q

how much acute loss can young & healthy patients tolerate w/ little/no effect?

A

500-1000ml
(10-20% blood vol)

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24
Q

effects of 1-1.5L blood loss

A

Ok if lying/sitting

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25
Q

effects of 1.5-2L blood loss

A

variable loss of consciousness
SoB
sweating

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26
Q

effects of >2L blood loss

A

severe shock
poss irreversible –> death

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27
Q

what happens 2-3 days post bleed?

A

hypovolaemia but no anaemia

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28
Q

what happens 3-5 days post bleed?

A

reticulocyte response

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29
Q

what is the state of RBCs in haematinic deficiency: iron deficiency anaemia (IDA)?

A

microcytic, hypochromic

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30
Q

what are the causes of IDA?

A

poor diet
malabsorption
chronic blood loss

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31
Q

how can iron stores be replenished in IDA?

A

oral administration (ferrous sulfate tablets)
parenteral (imferon/jectofer)

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32
Q

when is parenteral administration used over oral administration to replace iron stores?

A

when stores must be replaced rapidly
e.g. late pregnancy/oral Fe not well tolerated/absorbed

33
Q

how much should Hb rise by/week in IDA treatment?

34
Q

how is IDA treated in severe cases?

A

blood transfusion (but would be ideal to rectify underlying cause)

35
Q

what is the state of RBCs in haematinic deficiency: B12/folate defiency?

A

macrocytic, normochromic

36
Q

what is the state of RBCs in cytoskeletal RBC disorder: hereditary elliptocytosis?

A

normocytic, normochromic

37
Q

what disorders cause hereditary elliptocytosis?

A

spectrin, glycophorin C or protein 4.1 disorder

38
Q

what is the incidence of hereditary elliptocytosis?

A

1 in 3-4000

39
Q

how is elliptocytosis treated?

A

splenectomy may be required

40
Q

what is the incidence of hereditary spherocytosis?

A

200-300 cases per mil

41
Q

what disorders cause hereditary spherocytosis?

A

spectrin, ankyrin, band 3 or protein 4.1 disorder

42
Q

what are the characteristics of hereditary spherocytosis?

A

many clinically silent
genetic heterogeneity
incr osmotic fragility

43
Q

how is hereditary spherocytosis treated?

A

splenectomy may be required

44
Q

what is the state of RBCs in cytoskeletal RBC disorder: hereditary spherocytosis?

A

normocytic, normochromic

45
Q

what are 3 reasons for the acquired impairment of erythropoiesis?

A

bone marrow infiltration
transient failure
inherited (rare: fanconi anaemia & diamond blackfan anaemia)

46
Q

what happens in anaemia due to bone marrow infiltration?

A

replacement of erythropoetic tissue by tumour (metastases of e.g. Ca prostate/breast, or in leukaemia)
or fibrotic tissue (myelofibrosis)
NN

47
Q

how is acquired impairment of erythropoiesis caused by transient failure?

A

parvovirus infection (NN)
drugs (NN)
Fe deficiency (microcytic, hypochromic)
B12/folate deficiency (macrocytic, normochromic)

48
Q

what is extra-medullary haemopoiesis?

A

haemopoiesis outside BM
usually assoc w/ severe anaemia due to BM infiltration/fibrosis

49
Q

what are the 2 types of haemolytic anaemia?

A

auto-immune
‘microangiopathic’ (mechanical fragmentation)

50
Q

what are the causes of auto-immune haemolytic anaemia?

A

50% idiopathic
Lymphoproliferative disorders
Mycoplasma & EBV infection
Drug-induced, e.g. Penicillin
Other AI diseases

51
Q

what is the state of RBCs in auto-immune haemolytic anaemia?

A

normocytic, normochromic

52
Q

microangiopathic haemolytic anaemia is commonly assoc w/…

A

mechanical heart valves
DIC (in case of clot, fibrin deposited, strands of fibrin tear RBCs apart)
HUS / TTP

53
Q

what is the state of RBCs in microangiopathic haemolytic anaemia?

A

normocytic, normochromic

54
Q

what is the state of RBCs in congenital haemolytic anaemia: RBC enzymothapies?

A

normocytic, normochromic
burr cells

55
Q

how is congenital haemolytic anaemia (RBC enzymothapies) caused by pyruvate kinase deficiency?

A

leads to haemolysis thru failure of glycolytic pathway –> inadequate ATP

56
Q

how is congenital haemolytic anaemia (RBC enzymothapies) caused by G6PD deficiency?

A

Hb oxidises to MetHb
Spleen removes chunks of metHb → “bite cells” (aka keratocytes)
Challenge by oxidising agent (e.g. fava beans, some malaria medication) results in significant haemolysis

57
Q

what are the 2 categories of haemoglobinopathy?

A

Structural variations (>800), where Hb made in normal amounts but structure abnormal

thalassemia syndromes - variable loss of ability to prod particular type of globin chain

58
Q

what causes structural variations (leading to Hbopathy)?

A

aa substitutions in globin chains

59
Q

what are the most significant structural variations in Hbopathy?

A

beta chain (e.g. HbS - sickle cell, HbD, HbE, HbC)

60
Q

clinical significance of HbS hetero-/homozygote

A

he - usually asymptomatic
ho - gross haemolysis

61
Q

clinical significance of HbD Punjab hetero-/homozygote

A

he - asymptomatic
ho - may be mild haemolysis

62
Q

clinical significance of HbE hetero-/homozygote

A

he - asymptomatic
ho - asymptomatic

63
Q

clinical signifiance of HbC hetero-/homozygote

A

he - mild microcytosis (but exacerbates sickling in HbSC)
ho - mild haemolysis

64
Q

what is the state of RBCs in sickle cell disease (HbSS)?

A

normocytic, normochromic

65
Q

where is the freq of the HbS gene maintained?

A

malarial areas (despite severe consequences of homozygosity)

66
Q

SICKLE CELL

67
Q

what are some examples of unstable Hbs?

A

Hb Köln and Hb Zurich

68
Q

what type of anaemia is caused by unstable Hbs?

A

haemolytic

69
Q

what are the causes of unstable Hbs?

A

abnormality of heme pocket (heme is not firmly bound, & water can enter > metHb)

Interference in binding of α & β chains

Interference w/ α chain structure

70
Q

what is the consequence of unstable Hbs?

A

ox of heme iron - precipitates & damages cell mem
Ppts = Heinz bodies
Removal of Heinz bodies by macrophages → “bite cells”.
Assoc RBC destruction → a haemolytic anaemia

71
Q

what are thalassemias?

A

Characterised by reduced globin chain synthesis (α or β)
prevalent in pops evolved in warm, humid areas where malaria endemic, but now affects all races. (provides varying resistance to malaria)

72
Q

what is a-thalassemia?

A

impaired ability to synthesise α globin chains → excess β chains → β tetramers = Hb H
(in fetus, excess γ chains, = Hb Barts )

β tetramers (HbH bodies) aggregate

  • Usually inherit 2 α genes from each parent
  • In α-thalassemia 1 or more may be deleted.
73
Q

what type of anaemia is caused by a-thalassemia?

A

mild, microcytic hypochromic

74
Q

how many alpha genes are usually inherited from each parent? how does this differ in a-thalassemia?

A

2

1 or more may be deleted

75
Q

a-thalassemia: inheritance of 3 normal a genes –>?

A

almost no effect on Hb prod

76
Q

a-thalassemia: inheritance of 2 normal a genes –>?

A

α-thalassemia trait
Nearly normal Hb prod, but mild microcytic, hypochromic anaemia

77
Q

a-thalassemia: inheritance of 1 normal a gene –>?

A

HbH disease
Microcytic, hypochromic anaemia

78
Q

a-thalassemia: inheritance of 0 normal a gens –>?

A

incompatible w/ life, stillborn foetus

79
Q

normocytic, normochromic anaemia can be caused by…

A

bleeding
haemolysis
some drug-induced anaemia
some structural variants of Hb

80
Q

microcytic, hypochromic anaemia can be caused by…

A

Fe deficiency
thalassemia
anaemia of chronic disorder
some structural variants of Hb

81
Q

macrocytic, normochromic anaemia can be caused by…

A

B12/folate deficiency
anaemia due to alcoholism
some drug-induced anaemias
diamond blackfan

82
Q

ß-thalassemia

A
  • Impaired ability to synthesise β globin chains
  • Mutations in HBB gene on chromosome 11.
  • Many mutations identified
  • βo mutations allow no β chain prod, β+ allow some
  • Excess α-chains bind to RBC mem, damaging it → ineffective erythropoesis & reduced RBC survival
  • Decr in available β -chains → incr in γ & δ chains, so show incr in HbF & HbA2
  • Heterozygous - mild microcytic, hypochromic anaemia.
    o “Carrier” status, = thalassemia trait.
  • Homozygous – severe anaemia, usually fatal in infancy/childhood w/out intervention
    o Skeletal abnormalities due to expansion of haemopoetic spaces.
    o Transfusion dependant → Fe overload, requires Fe chelation therapy (or BM transplant, extreme case)

Clinical Biomedicine (23 decks)

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