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Haemotology > Anaemia > Flashcards

Anaemia Flashcards

1
Q

Define anaemia

A

Anaemia is a lower than normal concentration of haemoglobin or red blood cells (Hb <130 in men, <120 women)

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2
Q

name the 5 different types of anaemia

A

Haemolytic: increased breakdown of RBC’s
Aplastic: decreased RBC, WC, platelets
Microcytic: reduced MCV
Macrocytic: raised MCV
Normocytic: normal MCV

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3
Q

most common cause of anaemia

A

Fe deficiency

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4
Q

symptoms of anaemia

A

Symptoms: fatigue, headache, dizziness, dyspnoea (especially on exertion)

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5
Q

signs of anaemia

A

Signs: tachycardia, pale skin , conjunctiva painless , intermittent claudication

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6
Q

presentation of anaemia

A

tired
cold
palpitations

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7
Q

What may specifically indicate haemolytic anaemia

A

jaundice or dark urine

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8
Q

what may specifically indicate b12 deficiency

A

lemon- yellow skin
angular stomatis - skin condition

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9
Q

what causes b12 deficiency

A

pernicious anaemia
loss of intrinsic factor production

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10
Q

what may specifically indicate iron deficiney

A

angular stomatis or koilonychia - spoon shaped nails

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11
Q

What is mcv

A

mean corpuscular volume

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12
Q

5 causes of microcytic anaemia

A

T- Thalassaemia
A- Anaemia of chronic disease
I-Iron deficiency
L-Lead poisoning
S-Sideroblastic Anaemia

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13
Q

what is thalassaema

A

defect in the production of alpha or beta chains in hb

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14
Q

What would a full blood count for Microcytic anaemia show

A

low hb
mcv <80

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15
Q

what would a blood film show for microcytic anaemia

A

small hypochromic cells

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16
Q

In iron deficiency microcytic anaemia what would iron studies show

A

Low ferratin (unless active inflammation)
Low serum iron
Low transferrin saturation
Raised transferrin

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17
Q

what is the role of ferratin

A

Ferratin = main protein that stores iron intracellularly. Predominantly in the liver. Ferratin is an acute phase reactant so will rise in acute inflammation.

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18
Q

why would transferrin be raised in anaemia

A

body tries to compensate for reduced iron levels by producing more transferrin.

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19
Q

what is the role of transferrin

A

protein mediating iron transport in the blood

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20
Q

most common cause of FE deficiency anaemia

A
  • blood loss as most common
    -malnutrition - kids
  • poor iron absorption
    elderly 60+ RARE RED FLGAG, colon cancer or bleeding
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21
Q

treatment for fe deficiency anaemia

A

oral iron - ferrous sulfate

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22
Q

SE of ferrous sulfate

A

nausea, abdo discomfort, diarrhoea, constipation

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23
Q

causes of chronic microcytic anaemia

A

Chronic infection
Chronic inflammation (connective tissue diseases)
Neoplasia

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24
Q

pathogenesis of microcytic chronic anaemia

A
  • inflammatory cytokines lead to reduced sensitivity of the marrow to epo and failure to incorporate iron into developing cells
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25
Q

what is sideroblastic anaemia

A

iron levels are normal but the body cant insert this into hb

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26
Q

what type of anaemia are alpha and beta thalassaemia

A

microcytic

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27
Q

what causes alpha thalassaemia

A

due to insufficient synthesis of alpha-hemoglobin chains and an excess of beta chains.

  • 4 genes on alpha chain, 2 from each parent
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28
Q

symptoms of b thalassaemia

A

CHIPMUNK FACE
hepatospenomegaly
massively enlarged forehead + cheekbones due to decrease in RBC

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29
Q

DIAGNOSIS for b thalassaemia

A

FBC+ blood film- hypochromic RBC
HB electrophoresis

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30
Q

pathophysiology of b thalassaemia

A
  • decreased or no b chain production
  • excess a chain
31
Q

Treatment of B thalassaemia

A
  • regular transfusion, iron chelation
32
Q

mcv value for normocytic anaemia

A

80-95mcv

33
Q

causes of normocytic anaemia

A

anaemia of chronic disease
chronic kidney disease
aplastic anaemia
haemolytic anaemia
acute blood loss

34
Q

normoblastic causes of macrocytic anaemia

A

alcohol
liver disease
hypothyroidism
pregnancy
reticulocytosis
myelodysplasia
drugs

35
Q

megaloblastic causes of macrocytic anaemia

A

b12 deficiency
folate deficiency

36
Q

what is sickle cell anaemia

A

a genetic condition that causes sickle shapes red blood cells - normocytic

37
Q

pathophysiology of sickle cell anaemia

A

Hbf is usually replaced with Hba around 6 weeks after birth in SCA it is replaced with an abnormal variant HbS

38
Q

main issue with sickle cell anaemia

A

hbS polymerises when deoxygenated

39
Q

CAUSE of sickle cell

A

single point mutation in b globin gene - HbS

40
Q

Describe the genetic background of SCA

A

AUTOSOMAL RECESSIVE
abnormal gene for beta-globin on chromosome 11
one copy results in the trait.

41
Q

Link between malaria and SCA

A

SCA more prevalent in areas where malaria is also common,

having one copy reduces the severity of malaria

42
Q

acute presentation of SCA

A

MSK: Bone pain, joint pain
Infection
Resp: dyspnoea, cough, hypoxia
CNS: stroke
GI: sequestration crisis

43
Q

WHAT IS SEQUESTRATION CRISIS

A

blood outflow from the spleen is blocked. Blood accumulates - splenomegaly

44
Q

diagnosis of SCA ?

A
  • newborn screening - heel prick test
    -sickle solubility
    -blood film + fbc, normocytic normochromic with increased reticulocytes and howell jolly bodies
    -HB electrophoresis
45
Q

MANAGEMENT OF SCA

A
  • avoid dehydration and other triggers
    -ensure vaccines are up to date
    -antibiotic prophylaxis
    -blood transfusion for severe anaemia
46
Q

treatment for acute complicated attacks of SCA

A

iv fluids
ANALGESIA
o2

47
Q

what is G6PDH DEFIEICNY

A

condition where there is a defect in the red blood cell enzyme G6PD

48
Q

what is the presentation of g6pd deficiency

A

jaundice- in neonates
gall stones
anaemia
Heinz bodies on blood film

49
Q

what does g6pd cause

A

crises that are triggered by infections medications or fava beans

50
Q

to diagnose g6pd deficiency

A

FBC AND BLOOD FILM- heinz bodies
decrease in G6PDH LEVELS

51
Q

TREATMENT FOR G6PD

A

avoid triggers and precipitans

52
Q

what is hereditary spherocytosis

A

a deficiency in structural membrane protein spectrin– increase in splenic recycling

53
Q

what does Hereditary spherocytosis cause

A

spenomegaly

54
Q

sx of hereditary spherocytosis

A

general anaemia, neonatal jaundice , splenomegaly, gall stones

55
Q

treatment of hereditary spherocytosis

A

splenectomy and folate supplementation

56
Q

what is autoimmune haemolytic anaemia

A

when antibodies are created against the patients red blood cells

leads to destruction on ones own RBC

57
Q

two types of autoimmune haemolytic anaemis

A

warm
cold

58
Q

is warm or cold more common

A

warm

59
Q

describe warm type autoimmune haemolytic anaemia

A

occurs at normal or above normal temperatures

usually idiopathic

60
Q

describe cold type autoimmune haemolytic anaemia

A

also called cold agglutin disease

at lower temperatures the antibodies against red blood cells attach themselves to RBC anc clump together

agglutination-

61
Q

management of autoimmue haemolytic anaemia

A

blood transfusions
prednisolone
rituximab
splenctomy

62
Q

what issues are associated with microcytic anaemia

A

iron deficiency
thalassaemias

63
Q

what issues are associated with normocytic anaemia

A

chronic disease
renal disease
acute bleeding

64
Q

what issues are assocaited with macrocytic anaemia

A

folate deficiency
b12 deficiency

65
Q

how much iron does a regular adult need and how much is absorbed

A

15mg a day
only 1mg is absorbed

66
Q

presentation of anaemia

A

tired
cold
palpitations

67
Q

How can kidney disease cause decrease in RBC production

A

Epo is made in the kidney so less epo then less erythropoiesis

68
Q

Intravascular haemolysis causes

A

mismatched blood transfusion
G6PD deficiency*
red cell fragmentation: heart valves, TTP, DIC, HUS
paroxysmal nocturnal haemoglobinuria
cold autoimmune haemolytic anaemia

69
Q

Extravascular haemolysis causes

A

haemoglobinopathies: sickle cell, thalassaemia
hereditary spherocytosis
haemolytic disease of newborn
warm autoimmune haemolytic anaemia

70
Q

Blood film for thalassaemia would show ?

A

Heinz bodies
Target cells
Basophiloic stippling

71
Q

Bleeding problems, normal platelets, raised bleeding time, slightly raised APTT in a question is most likely to indicate:

A

Von willerbrand disease

72
Q

10-year-old child with a history of neonatal jaundice develops pallor and jaundice after an upper respiratory tract infection associated with erythematous cheeks. Splenomegaly is noted on examination is a stereotypical history of:

A

Hereditary spherocytosis

73
Q

Presentation of hereditary spherocytsis

A

failure to thrive
jaundice, gallstones
splenomegaly
aplastic crisis precipitated by parvovirus infection
degree of haemolysis variable
MCHC elevated

Haemotology (7 decks)

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