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Key facts Phase 2a > Haematology > Flashcards

Haematology Flashcards

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1
Q

give 3 causes of microcytic anaemia

A

TICS
Thalassaemia
Iron-deficiency
Chronic disease (20% will be microcytic)
Sideroblastic anaemia.

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2
Q

give 3 causes of normocytic anaemia

A
  1. bleeding
  2. anaemia of chronic disease (80% is normocytic)
  3. bone marrow failure; - renal failure (decreased erythropoietin)
  4. hypothyroidism
  5. haemolytic anaemia
  6. pregnancy
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3
Q

give 3 general symptoms of anaemia

A

classic = fatigue, dyspnoea, faintness

+ palpitations, headache, tinnitus, anorexia

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4
Q

give 3 general signs of anaemia

A

classic = conjunctival pallor

pallor, tachycardia

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5
Q

give a physiological cause of anaemia

A

Pregnancy

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6
Q

give some causes of iron-deficiency anaemia

A
  1. inadequate intake: poor diet, poverty
  2. poor absorption: poor acid production, gastric surgery, coeliac
  3. excessive loss: GI bleeding, peptic ulcers (NSAID use), diverticulosis, neoplasm, menorrhagia
  4. increase requirement: infancy, pregnancy, hookworm
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7
Q

possible presenting features of iron deficiency anaemia?

A

koilonychias (spoon nails)
mouth changes - angular stomatitis, atrophic glossitis
fatigue, pallor, faintness, dyspnoea
pica (classic = ice craving)

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8
Q

In iron deficiency anaemia, what will happen to the iron, ferritin and total iron binding capacity (TIBC) (aka iron studies)?

A

iron and ferritin are decreased.
TIBC is increased.
transferrin saturation = low.

NB - ferritin is acute phase protein so may be raised in inflammation/infection/malignancy

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9
Q

how would you treat iron deficiency anaemia? how long would this treatment be given?

A

oral ferrous sulphate - given until anaemia resolved + further 3-6/12

consider transfusion if symptomatic at rest w/ dyspnoea and chest pain.

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10
Q

what are some side effects of ferrous sulphate?

A

nausea, abdominal discomfort, diarrhoea/constipation, black stools

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11
Q

what causes pernicious anaemia?

A

autoimmune atrophic gastritis - autoantibodies against intrinsic factor (and parietal cells), so these are destroyed leading to achlorydia and B12 malabsorption.

associated with other AI disease - thyroid, vitiligo, DM.

risk of gastric cancer.

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12
Q

how does B12/folate deficiency lead to anaemia?

A

B12 and folate needed for DNA synthesis - developing red cells can’t divide, they are stuck as large immature cells (megaloblastic) which then become macrocytic RBCs

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13
Q

what signs characterise pernicious anaemia?

A

mild jaundice due to haemolysis - pallor + jaundice = “lemon tinged skin” is classic.

headache is hallmark of megaloblastic anaemia.

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14
Q

what specific tests would you perform if you suspected pernicious anaemia?

A

BC, blood film etc and:
- intrinsic factor antibody
- antiparietal cell antibody (90% sensitive, but not specific as elevated in atrophic gastritis)

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15
Q

give some causes of folate deficiency

A
  1. poor diet.
  2. increased demand - pregnancy or increased cell turnover.
  3. malabsorption (coeliac)
  4. drugs, alcohol, methotrexate (inhibits folic acid synth)
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16
Q

how would you investigate and treat folate-deficiency anaemia?

A

blood film shows macrocytic RBCs, hypersegmented neutrophils.
do other anaemia bloods.

oral folic acid (1-5mg) + B12 for 4 months min. treat cause.

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17
Q

give some hereditary causes of haemolytic anaemia

A
  1. Enzyme defects - G6PD deficiency, pyruvate kinase deficiency
  2. Membrane defects - hereditary spherocytosis, elliptocytosis
  3. Abnormal Hb production - sickle cell disease, thalassaemia
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18
Q

what is aplastic anaemia?

A

anaemia due to bone marrow failure
triad = pancytopenia with hypoplastic marrow and no abnormal cells
marrow stops making all cells

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19
Q

what is sickle cell anaemia?

A

autosomal recessive disorder causing production of abnormal beta globin chains.
HbSS instead of HbA

sickle shaped cells disrupt the blood cell, haemolyse earlier and causes varying degrees of anaemia.
obstruction of small blood capillaries leads to painful crises, organ damage and increased vulnerability to infection

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20
Q

being a carrier of sickle cell protects you against what disease?

A

p. falciparum malaria

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21
Q

what is the pathogenesis of sickle cell anaemia?

A

HbS causes RBCs to sickle - rigid, fragile cells that occlude small vessels and have short lifespan (haemolyse).

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22
Q

describe the clinical features of vaso-occlusive crises seen in sickle-cell anaemia

A
  1. severe pain due to effect on marrow of microvascular occlusio
  2. acutely painful hands and feet
  3. dactylitis
  4. visual floaters
  5. chest/abdo pain (mesenteric ischaemia)
  6. chronic renal failure.
  7. avascular necrosis femoral head/bone infarcts.

general symps/signs - parent with sickle cell anaemia/trait. symps of anaemia + haemolysis = jaundice, pallor, lethargy, tachycardia.

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23
Q

what is splenic sequestration?

A

a type of sickle-cell crisis:
vaso-occlusion produces acute painful enlargement of spleen.
pooling of RBCs in spleen = hypovolaemia = circulatory collapse and death.
immediate transfusion needed.

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24
Q

give 3 long-term complications of sickle-cell disease

A

poor growth, bone problems, infections, leg ulcers, neurological complication, gallstones, retinal disease, lung fibrosis, pulmonary hypertension

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25
what tests would you perform in a case of sickle cell disease? what would you see?
FBC. - low Hb. blood film - sickle cells and target cells (pale centre). Howell-Jolly bodies. sickle solubility test - HbSS/HbAS instead of HbA Hb electrophoresis - distinguishes HbSS and HbAS.
26
how would you treat sickle cell disease?
Hydroxyurea - increases HbF production Blood transfusions
27
describe the genetics of beta thalassaemia
Mutation in beta-globin gene on chromosome 11 leading no reduced (minor) or no (major) beta chain production
28
how does beta thalassaemia cause anaemia?
decreased/absent synthesis of beta-globin leads to excess alpha production + membrane damage/cell destruction. get ineffective erythropoeisis and increased haemolysis
29
how would you treat beta thalassaemia?
1) minor/trait = genetic counselling, iron advice (avoid unless deficient) 2) medium = genetic counselling, transfusion if symptomatic anaemia (e.g. infection, periop) + iron monitoring with chelation (desferrioxamine) 3) major = genetic counselling + regular transfusion to >10g/dL + iron monitoring with chelation. ± splenectomy ± assess for haematopoeitic stem cell transplant (curative)
30
what are the genetics of alpha thalassaemia?
Gene deletion in alpha globin chain genes on chromosome 16
31
what is glucose-6-phosphate dehydrogenase (G6PD) deficiency?
X linked haemolytic condition caused by mutation in the G6PD gene leading to G6PD enzyme deficiency. common in parts where malaria is common as it’s protective!
32
What does G6PD do?
Important for red cells to protect from oxidative stress
33
does G6PD deficiency affect mainly men or women?
men
34
give some precipitants of G6PD deficiency crises
1. henna. 2. favism (ingesting fava/broad beans) 3. Drugs (cephalosporins) 4. infections
35
Features of acute G6PD deficiency
Anaemia, fever, jaundice, dark urine Bite and blister cells Heinz bodies on blood film
36
why do polycythaemia patients get gout?
Increased urate from RBC turnover
37
How would you treat polycythaemia rubra vera?
Rx aims to keep low haematocrit + reduce risk of thrombosis. venesection hydroxycarbamide (cytoreduction, used if high risk) low dose aspirin (75mg) manage CV RFs
38
Which condition is associated with Heinz bodies?
G6PD deficiency
39
Which condition is associated with Howell Jolley
Sickle cell anaemia or splenectomy Remnant of RBC
40
Which condition is associated with auer rods?
Acute myeloid leukaemia
41
Which condition is associated with rouleaux formations?
Multiple myeloma Stacking of RBCs
42
Which condition is associated with hypersegmented neutrophil polymorphs?
Megalobastic anaemia (B12/folate)
43
What's the inheritance pattern for G6PD deficiency?
X-linked recessive
44
What's the inheritance pattern for Haemophilia A and B?
X-linked recessive
45
What's the inheritance pattern for Von Willebrand's disease?
Autosomal dominant
46
What's the inheritance pattern for Sickle Cell anaemia?
Autosomal recessive
47
Which condition is associated with Janus Kinase 2?
Polycythemia vera
48
Which condition is associated with monoclonal gammopathy of unknown significance?
Multiple myeloma
49
Which condition is associated with philadelphia chromosome/BCR-ABL gene?
Chronic myeloid leukaemia
50
What's the Ann harbour staging for lymphoma
Stage I - confined to single lymph node Stage II - involvement of 2 or more nodal areas on same side of diaphragm Stage III - involvement of nodes on both sides of diaphragm Stage IV - spread beyond lymph nodes A or B - depends on whether patient has B symptoms (weight loss, fever)
51
Features of multiple myeloma
OLD CRAB Old age, calcium raised, renal failure, anaemia, bone lytic lesions (back pain)
52
When would you suspect tumour lysis syndrome?
Cancer patient undergoing chemo start developing infections easily and severe neutropenia (low platelets)
53
1st line treatment for chronic myeloid leukaemia
Imatinib
54
Features of Hodgkin's lymphoma
Painful cervical lymphadenopathy after alcohol consumptions
55
Which virus is Hodgkin's lymphoma most associated with?
EBV
56
Which clotting factor is Haemophilia A associated with?
8
57
Which clotting factor is Haemophilia B associated with?
9
58
Which condition is associated with occasional blast cells on blood film?
Acute lymphoblastic leukaemia
59
Which condition is associated with Reed-Stenberg?
Hodgkin's lymphoma
60
-xaban suffix anticoagulant medication MOA
Direct Factor Xa inhibitor
61
What causes hypercalcaemia in multiple myeloma?
Increased osteoclast activity in response to cytokines released by myeloma cells
62
What condition is associated with smudge cells in blood film?
Chronic lymphoid leukaemia (proliferation of B cells)
63
Is vWF disease hereditary or acquired?
Hereditary
64
Which condition is associated with URINE Bence-Jones proteins?
Multiple myeloma
65
Pathophysiology of G6PD deficiency
G6PD deficiency causes decreased levels of reduced glutathione → increased susceptibility to oxidative stress

Key facts Phase 2a (5 decks)

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