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Finals passmed > Haematology > Flashcards

Haematology Flashcards

1
Q

Why is ferritin high in anaemic of chronic disease?

A

The body stores iron outside the blood as it wants to keep it away from bacteria or blood loss

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2
Q

What is the size of the RBCs in haemolytic anaemia?

A

normal sized

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3
Q

What size are the RBCs in iron deficiency anaemia?

A

microcytic

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4
Q

Which condition is positive for the philadelphia chromosome?

A

chronic myeloid leukaemia

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5
Q

What are the features of chronic myeloid leukaemia?

A

Anaemia, weight loss, splenomegaly

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6
Q

What is the first line treatment of CML?

A

Imatinib

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7
Q

What is the management of hyperkalaemia?

A

Insulin and dextrose solution

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8
Q

What is the mechanism behind an acute haemolytic transfusion reaction?

A

RBC destruction by IgM-type antibodies - causes fever, abdopain, hypotension (ABO incompatibility)

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9
Q

What are the presenting features of myeloma?

A

CRABBI.
Hypercalcaemia, renal damage, anaemia, bleeding, bones, infection

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10
Q

What is myeloma?

A

A cancer of plasma cells

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11
Q

What investigations do you use to test for myeloma?

A
  • blood film - rouleaux formation
  • protein electrophoresis - Bence Jones proteins, raised IgA/IgG in serum
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12
Q

What are the features on blood test in beta-thalassaemia major?

A

HbA2 (variant haemoglobin with delta chains) and HbF (foetal haemoglobin) raised and HbA (normal haemoglobin) absent

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13
Q

What is the management of beta-thalassaemia major?

A
  • repeated transfusion with iron chelation therapy (desferrioxamine)
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14
Q

What test is used to confirm an acute haemolytic reaction?

A

Direct coombs test

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15
Q

What does rhesus positive mean?

A

The RBCs have the rhesus antigen on them

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16
Q

What rhesus statuses are bad in pregnancy?

A

Mum - negative
Baby - positive

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17
Q

What happens if a mum is rhesus negative and the baby is positive?

A

In first child - nothing
In second - anti-D antibodies cross the placental membrane, they attack baby’s RBCs and cause haemolytic disease of the newborn

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18
Q

Which mother’s need routine antinatal anti-D prophylaxis?

A

Rhesus negative mothers who are not sensitised

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19
Q

What is a blood product vs a blood constituent?

A

Product = pharmaceutically produces
Constituent = part of blood

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20
Q

Which type of blood is the universal donor?

A

O negative

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21
Q

Which iron study results would show iron deficiency anaemia?

A

low ferritin
raised total iron-binding capacity
low serum iron
raised transferrin (low transferrin saturation)

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22
Q

What is the management of iron deficiency anaemia?

A
  • treat underlying cause
  • oral ferrous sulfate (for 3 months after deficiency has been corrected)
  • iron-rich diet
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23
Q

What are the features of a transfusion-associated graft-versus-host disease?

A
  • fever, rash, diarrhoea, abdominal pain, pancytopenia and abnormal LFTs - occurs after the transfusion can be days usually 1-6 weeks
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24
Q

What can be done to blood products to prevent transfusion-associated graft-versus-host disease?

A

Irradiation

25
Q

What does irradiation do to blood?

A

It deactivates the white cells - mainly lymphocytes

26
Q

Which blood products do not require irradiation?

A

Fresh frozen plasma, cryoprecipitate

27
Q

Which groups of patients require CMV negative components?

A

pregnant women, neonates, granulocyte components

28
Q

What rate should you give blood transfusions in children?

A

5ml/kg/hr

29
Q

What is the Hb transfusion threshold in adults?

A

70g/L

30
Q

Why must RBCs for transfusions be less than 5 days old for IUT and neonates?

A

risk of hyperkalaemia

31
Q

What blood group platelets should be given if ABO compatibility cannot be tested?

A

Group A

32
Q

What should the Rhesus status of platelets given be?

A

negative - in children and those with childbearing potential

33
Q

What is the normal platelet count range?

A

150 to 400 x10^9/L

34
Q

What are the components of fresh frozen plasma?

A

Coagulation factors, Immunoglobulins, proteins

35
Q

What rate should red blood cells be transfused in an adult in a non-emergency situation?

A

4mL/kg

36
Q

What commonly causes transfusion related acute lung injury?

A

HLA antibodies in the donor. Causes acute dyspnoea, hypoxia and bilateral pulmonary infiltrates, within 6hrs

37
Q

What are delayed transfusion reactions?

A

Occur > 24hours after transfusion
= purpura, delayed haemolytic, Transfusion associated graft-versus host disease

38
Q

Which observations are done as standard during a transfusion?

A
  • temperature, pulse, resp rate, BP
  • 60 mins before transfusion, 15 mins after starting, 60 mins after
39
Q

When should you stop warfarin peri-operatively?

A

It should be stopped 5 days before surgery, can be swapped to LMWH which would be stopped 24hours before surgery

40
Q

What are the features of Hodgkin’s lymphoma?

A

Reed-Sternberg cells, pain in node with alcohol, B symptoms (fever, weight loss, night sweats)

41
Q

Which staging system is used for lymphoma?

A

Lugano
stages 1-4. 1 (1 node), 2 (2 or more nodes on one side of diaphragm), 3 (both sides), 4 (everywhere)
A (no symptoms), B (symptoms), E (extranodal disease), S (splenic involvement), X (bulky disease)

42
Q

What are the features of CML?

A

anaemia, splenomegaly, increased granulocytes at different stages of maturation. Philadelphia chromosome. Increased neutrophils and platelets

43
Q

What is the management of CML?

A

Imatinib

44
Q

What is polycythaemia vera?

A

myeloproliferative disorder - proliferation of stem cells causing high wcc, platelets and rbcs

45
Q

What is the definition of neutropenic sepsis?

A

neutrophil count < 0.5 with septic features

46
Q

What is the first line management of neutropenic sepsis?

A

piperacillin with tazobactam

47
Q

Myelodysplastic syndromes are at risk of progressing to which type of cancer?

A

Acute myeloid leukaemia

48
Q

What types of conditions cause a metabolic acidosis with a normal anion gap?

A

diarrhoea, renal tubular acidosis, addisons, drugs

49
Q

What conditions cause a metabolic acidosis with a raised anion gap?

A

lactate - shock, hypoxia, diabetic ketoacidosis, alcohol, renal failure, acid poisoning

50
Q

What blood results are seen in von willebrand factor disease?

A

Prolonged bleeding time, normal platelets, APTT is prolonged

51
Q

What is the inheritance pattern of von willebrand factor disease?

A

Autosomal dominant - causes reduction in VWF - does not affect platelets

52
Q

What is the long term management of sickle cell anaemia?

A

hydroxyurea - increases HbF levels
pneumococcal vaccine every 5 years

53
Q

Which factors are affected in haemophilia A and B?

A

both cause high APTT, normal PT - causes bleeding
haemophilia A (8)
haemophilia B (9)

54
Q

What are the features of G6PD deficiency?

A

X-linked recessive, causes increased rbc susceptibility to oxidative stress. neonatal jaundice, causes intravascular haemolysis. heinz bodies on blood films, bite and blister cells

55
Q

How do you diagnose G6PD?

A

G6PD enzyme assay, 3 months after acute episode of haemolysis

56
Q

What are some early signs of haemochromatosis?

A

fatigue, erectile dysfunction and arthralgia
later: bronze skin, diabetes, liver disease, dilated cardiomyopathy, hypogonadism, arthritis

57
Q

What is the pathophysiology of haemochromatosis?

A

autosomal recessive disorder of iron absorption and metabolism causing iron accumulation

58
Q

How do you treat hyperkalaemia?

A
  • IV calcium gluconate (to stabilise cardiac membrane - no effect on K+)
  • Insulin/dextrose, nebulised salbutamol to move K+ into ICF
  • calcium resonium, loop diuretics and dialysis for longer term management

Finals passmed (23 decks)

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