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Anaemia Flashcards

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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
features folate deficiency
same as B12 def but with no neuropathy
26
tests for causes B12 def
history, tests for IF antibody and parietal cell antibodies, upper GI endoscopy
27
tests for causes folate def
history, TTG and endomysial antibodies, duodenal biopsy. serum folate low, red cell folate low
28
treatment folate deficiency
5mg folic acid for 4 months
29
other causes raised MCV
alcohol, liver disease, myxoedema, reticulocytosis, cytotoxic drugs, aplastic anaemia, pregnancy, myeloma
30
normal red cell lifespan
120 days
31
what is haemolytic anaemia
abnormal destruction red blood cells, decreased lifespan RBCs. may be caused by fault in red cell or abnormality in its environment
32
inherited haemolytic anaemias
red cell membrane- hereditary spherocytosis, elliptocytosis; Hb- thalassaemia, sickling; G6PD
33
acquired haemolytic anaemias
immune- warm and cold autoimmune haemolytic anaemias; rhesus or ABO incompatability; trauma; infection; hypersplenism
34
features haemolytic
anaemia, jaundice, incr gallstones, splenomegaly, megaloblastic caused by decr folate
35
lab features haemolytic
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
36
causes of haemolytic anaemia- red cell fragmentation syndromes
cardiac valve, TTP, DIC, haemolytic uraemic syndrome
37
why is there jaundice in haemolytic
incr catabolism Hb releasing increased amounts bilirubin
38
what type of jaundice in haemolytic
uconjugated bilirubin so not present in urine
39
what is the most common inherited HA
hereditary spherocytosis
40
hereditary spherocytosis what is the defect in
red cell membrane protein- ankyrin
41
hereditary spherocytosis signs
splenomegaly, severe anaemia. fhx.
42
tests for hereditary spherocytosis
direct antiglobulin test- negative. EMA
43
treatment hereditary spherocytosis
splenectomy. folic acid. cholecystectomy- if gallstones
44
what happens in G6PD deficiency
red cells susceptible to oxidant stress- by drugs, infections, fava beans, neonatal period. X linked.
45
who is G6PD common in
Mediterranean, middle eastern, oriental
46
what does the blood film show in G6PD
in a crisis can be absent Hb- bite and blister cells. Heinz bodies (denatured Hb)
47
what is autoimmune haemolytic anaemia
autoantibodies against red cell membrane
48
what temp does warm AIHA work
37 degrees
49
what temp does cold AIHA work
0-5 degrees (4)
50
features warm AIHA
splenomegaly. DAT scan positive (differentiating from hereditary spherocytosis where is it negative). IgG
51
treatment warm AIHA
prednisolone 1mg/kg PO. transfusion if necessary, immunosuppressive drugs, splenectomy if fails, remove cause, treat underlying disease
52
warm AIHA antibody
IgG
53
cold AIHA antibody
IgM
54
DAT scan in cold AIHA
positive with C3d
55
features cold AIHA
acrocyanosis (purplish skin), Raynaud phenomenon. may be intravascular haemolysis and if severe- rigors, haemoglobinuria, renal failure
56
why is Hb high in intravascular haemolysis
as RBCs are broken down and released into the blood stream
57
causes of intravascular haemolysis
mismatched blood transfusion, G6PD, red cell fragmentation, autoimmune haemolytic, drug and infection
58
what are present in cold AIHA
cold agglutinins directed against red cells.
59
treatment cold AIHA
keep the patient warm, immunosuppression, plasma exchange to lower antibody titre
60
what is red cell fragmentation syndrome
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
what is thalassaemia
autosomal recessive. disorders of alpha or beta globin chain synthesis
62
alpha thalassaemia severity depends on
number of a genes deleted or dysfunctional there are 4 genes 2 on each chromosome 16
63
what happens if all 4 alpha genes are inactive
hydrops foetalis. fetus cant make fetal or adult Hb. death in utero or neonatally
64
what is the lab of thalassaemia
hypochromic microcytic
65
what is it called when 3/4 a genes are inactive
haemoglobin H disease
66
what do you get if one or 2 a genes are inactive
a thalassaemia trait
67
what is thalassaemia major
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
features thalassaemia major
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
management thalassaemia major
regular tranfusions- packed red cells, iron chelation- desferrioxamine (SC) 5-7 nights weekly. oral vit C incr iron excretion; deferiprone (oral)
70
why does anaemia present at 3-6m in thal major
switch from y to b chain synthesis
71
what is the presentation of thalassaemia intermedia
less severe. present later (2-5 years), normal bones changes and growth
72
b thalassaemia trait
asymptomatic hypochromic microcytic anaemia
73
if both parents have b thal trait, what is the chance of having thal major
25%
74
what is sickle cell disease
point mutation in B gene- substitution valine for glutamic acid. insolubility of HB S- crystallise causing sickling and vascular occlusion
75
what are the B like in sickle cell anaemia and trait
2 x BS in anaemia, BS with BA in trait
76
what are the crises in sickle cell
vaso-occlusive, sequestration, aplastic
77
what happens in vaso occlusive crises
incr sickling with blockage small vessels. infection, dehydration, acidosis, deoxygenation. abdominal pain, bone pain, CNS
78
what happens in sequestration crises
sickling with pooling red cells in liver, spleen, lungs. acute chest syndrome
79
what happens in aplastic crisis
follows infection by B19 parvovirus. temp arrest erythropoiesis. severe anaemia need transfusion
80
clinical features sickle cell
increased susceptibility to infection, gallstones, legulcers, avascular necrosis fem and hum heads, cardiomyopathy, pulm hypertension
81
diagnosis sickle cell
Hb 70-90, blood film- sickle cells, screening for sickling. can do cranial Doppler to assess for stroke, retinal exam
82
treatment sickle cell
avoid precipitants of crisis, vaccination, folic acid. red cell transfusion in severe anaemia.
83
how is vaso occlusive crisis treated
hydration, saline, analgesia
84
how is sequestration crisis treated
exchange transfusion to reduce HbS
85
what medication can be given in sickle cell to reduce freq sickle cell crises
hydroxycarbamide
86
how does sickle trait present
benign condition without anaemia, asymptomatic. can be haematuria in oxygen deprivation
87
conditions causing anaemia of chronic disease
chronic infections eg tb,osteomyelitis, HIV; ronic inflam- RA, SLE; malignant- carcinoma, lymphoma; CCF; endo- hypo and hyper thyroid
88
what is released by the liver in anaemia of chronic disease
hepicidin
89
what cells are seen on blood film in sickle cell
target cells, pencil cells

Haematology (12 decks)

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