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Haematology > Anaemia > Flashcards

Anaemia Flashcards

1
Q

causes microcytic anaemia

A

iron deficiency, thalassaemia

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2
Q

causes normocytic anaemia

A

blood loss, haemolysis, chronic disease, marrow infiltration

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3
Q

causes macrocytic anaemia

A

megaloblastic anaemia

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4
Q

causes of iron deficient anaemia

A

bleeding from GI tract- benign, malignant; menorrhagia; pregnancy; malabsorption; malnutrition; bleeding urinary tract; hookworm, pulmonary haemosiderosis

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5
Q

symptoms/ signs iron deficient

A

koilonychia, glossitis, angular stomatitis, gastritis

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6
Q

investigations iron defi

A

endoscopy/colonoscopy, if GIT normal- test urine for haematuria; CXR

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7
Q

what can you give to correct iron deficiency

A

ferrous sulphate 200mg. give for 6 months

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8
Q

side effects ferrous sulphate

A

nausea, epigastric pain, diarrhoea constipation

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9
Q

what is the MCV for macrocytic

A

> 98

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10
Q

MCV for normocytic

A

78-98

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11
Q

MCV for microcytic

A
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12
Q

what is megaloblastic anaemia caused by

A

B12 or folate deficiency

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13
Q

what are folate and B12 needed for

A

synthesis DNA

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14
Q

what is the name for B12

A

cobalamin

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15
Q

what do you get B12 from

A

animal sources- meat, fish, eggs, butter, milk

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16
Q

what does B12 combine with and where is it absorbed

A

combines with intrinsic factor (secreted by parietal cells), absorbed in the terminal ileum

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17
Q

causes of B12 deficiency

A

inadequate diet, intestinal malabsorption- ileal resection, crohns, congenital malabsorption, deficient gastric intrinsic factor- pernicious anaemia, gastrectomy

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18
Q

what is pernicious anaemia

A

autoimmune gastritis- reduced gastric secretion IF

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19
Q

presentation pernicious anaemia

A

patient is often early greying of the hair, blue eyes, fhx, associated autoimmune disorders- myxoedema, vitiligo, Addisons, thyrotoxicosis

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20
Q

features B12 deficiency

A

gradual onset symptoms. jaundice. glossitis and angular cheilosis. neuropathy- tingling in the feet, gait, visual.

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21
Q

treatment B12 deficiency

A

1mg hydroxycobalamin. then vit B12

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22
Q

where is folate in diet

A

in most foods. especially liver and green veg

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23
Q

where is folate absorbed

A

upper small intestine

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24
Q

causes of folate deficiency

A

malabsorption- coeliac, small bowel disease/resection, tropical sprue; dietary; liver disease; increased demand- pregnancy, haemolytic anaemia, malignancy, inflammatory diseases

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25
Q

features folate deficiency

A

same as B12 def but with no neuropathy

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26
Q

tests for causes B12 def

A

history, tests for IF antibody and parietal cell antibodies, upper GI endoscopy

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27
Q

tests for causes folate def

A

history, TTG and endomysial antibodies, duodenal biopsy. serum folate low, red cell folate low

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28
Q

treatment folate deficiency

A

5mg folic acid for 4 months

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29
Q

other causes raised MCV

A

alcohol, liver disease, myxoedema, reticulocytosis, cytotoxic drugs, aplastic anaemia, pregnancy, myeloma

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30
Q

normal red cell lifespan

A

120 days

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31
Q

what is haemolytic anaemia

A

abnormal destruction red blood cells, decreased lifespan RBCs. may be caused by fault in red cell or abnormality in its environment

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32
Q

inherited haemolytic anaemias

A

red cell membrane- hereditary spherocytosis, elliptocytosis; Hb- thalassaemia, sickling; G6PD

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33
Q

acquired haemolytic anaemias

A

immune- warm and cold autoimmune haemolytic anaemias; rhesus or ABO incompatability; trauma; infection; hypersplenism

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34
Q

features haemolytic

A

anaemia, jaundice, incr gallstones, splenomegaly, megaloblastic caused by decr folate

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35
Q

lab features haemolytic

A

extravascular- hb may be normal or reduced, raised reticulocyte, blood film, bone marrow shows incr erythropoiesis, bilirubin raised, haptogloibin absent. intravascular- raised Hb, positive Schumm test, haemosiderin in urine

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36
Q

causes of haemolytic anaemia- red cell fragmentation syndromes

A

cardiac valve, TTP, DIC, haemolytic uraemic syndrome

37
Q

why is there jaundice in haemolytic

A

incr catabolism Hb releasing increased amounts bilirubin

38
Q

what type of jaundice in haemolytic

A

uconjugated bilirubin so not present in urine

39
Q

what is the most common inherited HA

A

hereditary spherocytosis

40
Q

hereditary spherocytosis what is the defect in

A

red cell membrane protein- ankyrin

41
Q

hereditary spherocytosis signs

A

splenomegaly, severe anaemia. fhx.

42
Q

tests for hereditary spherocytosis

A

direct antiglobulin test- negative. EMA

43
Q

treatment hereditary spherocytosis

A

splenectomy. folic acid. cholecystectomy- if gallstones

44
Q

what happens in G6PD deficiency

A

red cells susceptible to oxidant stress- by drugs, infections, fava beans, neonatal period. X linked.

45
Q

who is G6PD common in

A

Mediterranean, middle eastern, oriental

46
Q

what does the blood film show in G6PD

A

in a crisis can be absent Hb- bite and blister cells. Heinz bodies (denatured Hb)

47
Q

what is autoimmune haemolytic anaemia

A

autoantibodies against red cell membrane

48
Q

what temp does warm AIHA work

A

37 degrees

49
Q

what temp does cold AIHA work

A

0-5 degrees (4)

50
Q

features warm AIHA

A

splenomegaly. DAT scan positive (differentiating from hereditary spherocytosis where is it negative). IgG

51
Q

treatment warm AIHA

A

prednisolone 1mg/kg PO. transfusion if necessary, immunosuppressive drugs, splenectomy if fails, remove cause, treat underlying disease

52
Q

warm AIHA antibody

A

IgG

53
Q

cold AIHA antibody

A

IgM

54
Q

DAT scan in cold AIHA

A

positive with C3d

55
Q

features cold AIHA

A

acrocyanosis (purplish skin), Raynaud phenomenon. may be intravascular haemolysis and if severe- rigors, haemoglobinuria, renal failure

56
Q

why is Hb high in intravascular haemolysis

A

as RBCs are broken down and released into the blood stream

57
Q

causes of intravascular haemolysis

A

mismatched blood transfusion, G6PD, red cell fragmentation, autoimmune haemolytic, drug and infection

58
Q

what are present in cold AIHA

A

cold agglutinins directed against red cells.

59
Q

treatment cold AIHA

A

keep the patient warm, immunosuppression, plasma exchange to lower antibody titre

60
Q

what is red cell fragmentation syndrome

A

when red cells are exposed to an abnormal surface eg artificial heart valve, DIC, damaged small vessels eg TTP. haemolysis is intra and extra vascular

61
Q

what is thalassaemia

A

autosomal recessive. disorders of alpha or beta globin chain synthesis

62
Q

alpha thalassaemia severity depends on

A

number of a genes deleted or dysfunctional there are 4 genes 2 on each chromosome 16

63
Q

what happens if all 4 alpha genes are inactive

A

hydrops foetalis. fetus cant make fetal or adult Hb. death in utero or neonatally

64
Q

what is the lab of thalassaemia

A

hypochromic microcytic

65
Q

what is it called when 3/4 a genes are inactive

A

haemoglobin H disease

66
Q

what do you get if one or 2 a genes are inactive

A

a thalassaemia trait

67
Q

what is thalassaemia major

A

complete or almost complete failure B globin chain synthesis. severe imbalance a:b chains and a chains are deposited in erythroblasts. innefective eryhthropoiesis, severe anaemia, extra medullary haemopoiesis

68
Q

features thalassaemia major

A

anaemia (3-6m), failure to thrive, infection, pallor, jaundice, hepato and splenomegaly, frontal bossing and hair on end appearance on x ray. iron overload

69
Q

management thalassaemia major

A

regular tranfusions- packed red cells, iron chelation- desferrioxamine (SC) 5-7 nights weekly. oral vit C incr iron excretion; deferiprone (oral)

70
Q

why does anaemia present at 3-6m in thal major

A

switch from y to b chain synthesis

71
Q

what is the presentation of thalassaemia intermedia

A

less severe. present later (2-5 years), normal bones changes and growth

72
Q

b thalassaemia trait

A

asymptomatic hypochromic microcytic anaemia

73
Q

if both parents have b thal trait, what is the chance of having thal major

A

25%

74
Q

what is sickle cell disease

A

point mutation in B gene- substitution valine for glutamic acid. insolubility of HB S- crystallise causing sickling and vascular occlusion

75
Q

what are the B like in sickle cell anaemia and trait

A

2 x BS in anaemia, BS with BA in trait

76
Q

what are the crises in sickle cell

A

vaso-occlusive, sequestration, aplastic

77
Q

what happens in vaso occlusive crises

A

incr sickling with blockage small vessels. infection, dehydration, acidosis, deoxygenation. abdominal pain, bone pain, CNS

78
Q

what happens in sequestration crises

A

sickling with pooling red cells in liver, spleen, lungs. acute chest syndrome

79
Q

what happens in aplastic crisis

A

follows infection by B19 parvovirus. temp arrest erythropoiesis. severe anaemia need transfusion

80
Q

clinical features sickle cell

A

increased susceptibility to infection, gallstones, legulcers, avascular necrosis fem and hum heads, cardiomyopathy, pulm hypertension

81
Q

diagnosis sickle cell

A

Hb 70-90, blood film- sickle cells, screening for sickling. can do cranial Doppler to assess for stroke, retinal exam

82
Q

treatment sickle cell

A

avoid precipitants of crisis, vaccination, folic acid. red cell transfusion in severe anaemia.

83
Q

how is vaso occlusive crisis treated

A

hydration, saline, analgesia

84
Q

how is sequestration crisis treated

A

exchange transfusion to reduce HbS

85
Q

what medication can be given in sickle cell to reduce freq sickle cell crises

A

hydroxycarbamide

86
Q

how does sickle trait present

A

benign condition without anaemia, asymptomatic. can be haematuria in oxygen deprivation

87
Q

conditions causing anaemia of chronic disease

A

chronic infections eg tb,osteomyelitis, HIV; ronic inflam- RA, SLE; malignant- carcinoma, lymphoma; CCF; endo- hypo and hyper thyroid

88
Q

what is released by the liver in anaemia of chronic disease

A

hepicidin

89
Q

what cells are seen on blood film in sickle cell

A

target cells, pencil cells

Haematology (12 decks)

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