Haematology Flashcards

1
Q

What histological cells are present in Hodgkins lymphoma but not NHL?

A

Reed-Sternberg cells

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2
Q

At what age is the peak incidence of Hodgkins lymphoma?

A

Young adults

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3
Q

What type of anaemia is most common in Hodgkins lymphoma?

A

Normochronic normocytic anaemia. If bone marrow failure occurs then may develop leucoerythroblastic anaemia.

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4
Q

What distinctive cell is central to the diagnosis of the four classic type of Hodgkins lymphoma?

A

Multinucleate polypoid RS cell

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5
Q

What is the treatment for Hodgkins lymphoma?

A

Chemotherapy alone or a combination of chemotherapy with radiotherapy. Disease relapse can be treated with chemotherapy and sometimes stem cell transplantation.

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6
Q

Non-Hodgkin lymphoma are a large group of clonal lymphoid tumours. What cell-origin is most common?

A

B-cell - 85%
T or NK cell - 15%

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7
Q

What is the management for NHL?

A

Combination of chemotherapy drugs together with a monoclonal antibody directed against the tumour cell. However, various new drugs have been developed which may change the management of disease in future years.

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8
Q

Multiple myeloma is a neoplastic disease characterised by the accumulation of what kind of cell in bone marrow?

A

Plasma cell. As well as the presence of monoclonal protein in the serum and/or urine and, in symptomatic patients, related tissue damage

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9
Q

At what age is the peak incidence of multiple myeloma?

A

65-70 years

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10
Q

What acronym can be used to remember the tissue damage in myeloma?

A

CRAB:
hyperCalaemia
Renal impairment
Anaemia
Bone pain (esp. backache)

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11
Q

Name some possible lab findings in multiple myeloma?

A
  1. Presence of a paraprotein in serum/urine (IgG in 60%, IgA in 20% and light chain only in almost all the rest).
  2. Elevated serum immunoglobulin-free light chains.
  3. Bence-Jones proteins in urine
  4. Marked Rouleaux formation on blood film.
  5. Raised serum β2-microglobin (useful indicator of prognosis)
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12
Q

What is the management of multiple myeloma?

A

Intensive combination chemotherapy (mostly for patients <70) or non-intensive therapy for older patients. New drugs such as proteasome inhibitors.

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13
Q

What is the prognosis of multiple myeloma?

A

Overall median survival is 7-10 years. In patients <50 years it can be over 10 years.

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14
Q

What is the most common form of acute leukaemia in adults?

A

Acute myeloid leukaemia (AML)

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15
Q

In AMLhaematological investigations reveal what?

A

Normochronic normocytic anaemia with thrombocytopaemia in most cases. The WCC is usually increased and blood film typically shows a variable number of blast cells. The bone marrow is hyper cellular and typically contains many blast cells.

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16
Q

Acute lymphoblastic leukaemia is caused by an accumulation of lymphoblasts in the bone marrow. Which is more common, B-cell lineage or T-cell lineage?

A

B-cell lineage - 85% of cases (equal sex incidence).
T-cell lineage - 15% of cases (male predominance).

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17
Q

The characteristic presence of what chromosome on cryogenic analysis is present in 98% of chronic myeloid leukaemia (CML) cases?

A

Philadelphia (ph) chromosome

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18
Q

CML typically has increased or decreased circulating basophils?

A

Increased

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19
Q

What is the mainstay of treatment for CML?

A

Tyrosine kinase inhibitors (TKI) are the mainstay of treatment and several different drugs are now available, largely replacing chemotherapy treatment

20
Q

What is the most common form of leukaemia within Europe and USA?

A

Chronic lymphocytic leukaemia (CLL)

21
Q

What is the CLL tumour cell?

A

A mature B-cell with weak surface expression of immunoglobulins (IgM or IgD)

22
Q

CLL tumour cells accumulate where?

A

Blood, bone marrow, liver, spleen and lymph nodes

23
Q

80% of CLL cases are diagnosed following a routine blood test. What is the most frequent clinical sign?

A

Enlargement of cervical, axillary or inguinal lymph nodes

24
Q

The treatment of CLL is typically conservative, aiming for symptom control rather than a cure. Treatment may be given for troublesome symptoms or if the lymphocyte count rises rapidly. What treatment can be given?

A

Chemotherapy and an anti-DC20 monoclonal antibody establishes disease remission but is not curative.

25
Q

An increase in red cell 2,3 -diphosphoglycerate (2,3 -DPG) has what effect on the oxygen dissociation curve?

A

Rightward shift

26
Q

Name some causes of microcytic anaemia?

A

Iron deficiency.
Thalassaemia.
Other haemoglobin defects.
Anaemia of chronic disease (some cases).
Congenital sideroblastic anaemia.

27
Q

Name some causes of normocytic anaemias?

A

Most haemolytic anaemias
Anaemia of chronic disease (most cases)
Mixed cases

28
Q

Name some causes of macrocytic anaemia?

A

Megaloblastic anaemia (B12/folate deficiency)
Alcohol, liver disease, hypothyroidism, reticulocytosis, cytotoxic drugs, aplastic anaemia, pregnancy, myelodysplastic syndromes, myeloma, neonatal

29
Q

Name drugs which can cause iron-deficiency anaemia?

A

Tetracyclines, quinolone, antacids, PPIs

30
Q

Name 5 specific features of iron deficiency?

A
  1. Koilonychia (spoon-shaped nails)
  2. Angular cheilitis
  3. Atrophic glossitis
  4. Pica
  5. Hair thinning
31
Q

What may be seen on blood film in iron deficiency?

A

Hypochromic/microcytic cells, anisocytosis/poikilocytosis, target cells, ‘pencil’ cells

32
Q

In iron deficiency anaemia what happens to the levels of serum ferritin, transferrin and total iron binding capacity (TIBC)?

A

Serum ferritin - decrease
Transferrin - increase
Total iron binding capacity (TIBC) - increase

33
Q

Where is transferrin synthesised?

A

Liver

34
Q

Dietary iron may be in the form of haem or non-harm. Haem is degraded after absorption through the cell surface to release what?

A

Fe2+

35
Q

Most non-harm iron is in the form of what?

A

Fe3+

36
Q

Fe2+ is taken from the intestinal lumen into the cell across the enterocyte apical membrane by what transporter?

A

Divalent metal transporter (DMT1)

37
Q

What is the main hormonal regulator of iron homeostasis?

A

Hepcidin

38
Q

Give some examples of chronic infections which may cause anaemia of chronic disease?

A

Osteomyelitis, bacterial endocarditis, TB, chronic abscesses, bronchiectasis, chronic UTI, HIV, AIDs, malaria

39
Q

Name some chronic inflammatory disorders which can cause anaemia of chronic disease?

A

Rheumatoid arthritis, polymyalgia rheumatica, SLE, scleroderma, IBD, thrombophlebitis

40
Q

In anaemia of chronic disease what happens to the levels of serum ferritin, transferrin and total iron binding capacity (TIBC)?

A

Serum ferritin - normal or increase
Transferrin - decrease
Total iron binding capacity (TIBC) - decrease

41
Q

Name some hereditary causes of haemolytic anaemia?

A
  1. Red cell membrane (e.g. hereditary spherocytosis, hereditary elliptocytosis).
  2. Red cell metabolism (e.g. glucose-6-phosphate dehydrogenase (G6PD) deficiency, pyruvate kinase deficiency).
  3. Haemoglobin synthesis (e.g. thalassaemia, sickle cell disease).
42
Q

What condition is characterised by a positive direct Coombs test

A

Autoimmune haemolytic anaemia

43
Q

Name some acquired causes of haemolytic anaemia/

A
  1. Autoimmune
  2. Alloimmune (e.g. haemolytic disease of the newborn, haemolytic transfusion reactions).
  3. Red cell fragmentation syndromes (e.g. DIC, TTP, HUS).
  4. Infections (e.g. malaria).
  5. Drug or chemical association.
  6. Secondary to liver or renal disease.
  7. Paroxysmal nocturnal haemoglobinuria.
44
Q

Name some causes of intravascular haemolysis?

A
  1. Haemolytic transfusion reactions.
  2. G6PD deficiency reactions.
  3. Red cell fragmentation syndromes.
  4. Some severe autoimmune haemolytic anaemias.
  5. Some drug-and infection-induced haemolytic anaemias.
  6. Paroxysmal nocturnal haemoglobinuria.
45
Q

Which virus can trigger aplastic crisis?

A

Parvovirus B19