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Haematology > Finals Revision Haematology > Flashcards

Finals Revision Haematology Flashcards

1
Q

What are the Vitamin K dependent clotting factors?

A

Factors II, VII, IX, X

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2
Q

What are the 3 natural anticoagulants?

A

Antithrombin
Protein C
Protein S

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3
Q

How does LMWH act in anticoagulation?

A

It binds to antithrombin to potentiate it’s effect i.e. stops production of thrombin from prothrombin

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4
Q

True / False: Patients who are being commenced on dabigatran require an initial loading with LMWH?

A

True

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5
Q

True / False: Patients who are being commenced on a Factor Xa inhibitor e.g. Rivaroxaban require an initial loading with LMWH?

A

False - These patients do not require initial loading

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6
Q

What should be given to patients on warfarin who have a ‘major bleed’?

A

Prothrombin complex concentrate e.g. Beriplex PLUS 5mg Vitamin K

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7
Q

Why is Vitamin K given alongside prothrombin complex concentrate in patients on warfarin who have a ‘major bleed’?

A

Clotting factors in prothrombin complex concentrate only have a short half-life so although they can reverse the effects of warfarin quickly, they should be given along with Vitamin K for prolonged effects.

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8
Q

What is given to patients on warfarin who have a ‘non-major bleed’?

A

Vitamin K 1-3mg IV, combined with dose reduction or discontinuation of warfarin

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9
Q

What is the management of a patient on warfarin with INR more than 5 who is not bleeding?

A

Withhold 1-2 doses of warfarin and recommence at a reduced dose. Investigate for the cause of the raised INR.

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10
Q

What is the management of a patient on warfarin with INR more than 8 who is not bleeding?

A

Vitamin K 1-5mg orally

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11
Q

In which condition might you get a ‘pepper-pot skull’ appearance on x-ray?

A

Myeloma

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12
Q

Give some clinical features of myeloma

A

Bone marrow failure - Tiredness, fatigue, thrombocytopenia
Recurrent infections
Bone pain
Hypercalcaemia - Polyuria, polydipsia
Renal failure - Due to light chain deposition in kidney
Amyloidosis
Plasma cytomas

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13
Q

What investigations might you perform in suspected myeloma?

A 
FBC - Normocytic, normochromic anaemia
Blood film - Rouleaux formation
ESR
Calcium
U+E
Serum electrophoresis - 'M' component signifies immunoglobulins
Urine - Bence Jones protein
X-Ray - 'Pepper-pot skull', fractures
Bone marrow - Lots of plasma cells
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14
Q

What is another name for a Burr cell?

A

Echinocyte

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15
Q

What is another name for a Spurr cell?

A

Acanthocyte

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16
Q

What is a schistocyte and in which conditions might it be seen on a blood film?

A

A fragmented RBC which is broken up as it travels through intravascular fibrin. Seen microangiopathic haemolytic anaemia, mechanical valves etc.

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17
Q

In which condition might you see a Heinz body? Why?

A

G6PD deficiency - Heinz bodies are denatured haemoglobin caused in oxidative stress

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18
Q

In which conditions might you see a Burr cell (echinocyte) on blood film?

A

Uraemia
Liver damage
Artefact

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19
Q

What is ‘Rouleaux formation’ and when is it seen?

A

Clumped RBCs, seen in multiple myeloma, chronic liver disease, lymphoma, and chronic inflammatory conditions

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20
Q

What is typically seen on a blood film in a patient with hyposplenism?

A

Howell-Jolly bodies

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21
Q

What is a Howell-Jolly Body?

A

A nuclear remnant from RBCs which is normally removed when the RBC matures

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22
Q

What is the appearance of a Spurr cell (acanthocyte)?

A

Spiculated RBC

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23
Q

When might you see a Spurr cell (acanthocyte)?

A

Liver disease

Post-splenectomy

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24
Q

When might you see a Bite cell?

A

G6PD deficiency
Oxidative drugs
Unstable haemolytic states

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25
Q

Give 2 things you might find on blood film of a patient with G6PD deficiency

A

Signs of oxidative stress:

  • Bite cell
  • Heinz body
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26
Q

What is meant by anistocytosis?

A

Large size of RBCs

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27
Q

PT i.e. Prothrombin time (and INR) represent the intrinsic or extrinsic pathway in the clotting cascade?

A

Extrinsic

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28
Q

APTT (Activated partial thromboplastin time) represents the intrinsic or extrinsic pathway in the clotting cascade?

A

Intrinsic

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29
Q

Prolonged PT but normal APTT might be due to what?

A

Isolated Factor VII deficiency (rare)
Warfarin use or Vitamin K deficiency
Liver disease

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30
Q

What results would you expect to see in the clotting profile of a patient with Haemophilia A?

A

Normal PT
Prolonged APTT
Reduced Factor VIII

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31
Q

What does von Willebrand’s Factor do?

A

1) Brings platelets into contact with exposed subendothelium
2) Platelet aggregation
3) Binds to Factor VIII preventing it’s destruction

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32
Q

What results would you expect to see in the clotting profile of a patient with von Willebrand’s disease?

A 
Normal PT/INR
Prolonged APTT
Low vWF
Low Factor VIII
Bleeding time prolonged
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33
Q

What are the clinical features of von Willebrand’s disorder?

A

Bleeding - mucosal, menorrhagia, epistaxis

Bruising

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34
Q

Which clotting factor is deficient in Haeophilia B?

A

Factor IX

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35
Q

What are the 2 ‘acute’ haematological malignancies?

A

Acute myeloid leukaemia

Acute lymphoblastic leukaemia

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36
Q

Give 3 myeloproliferative disorders

A

Myelofibrosis
Polycythaemia rubra vera
Essential thrombocytosis

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37
Q

What are the 3 types of chronic lymphoid haematological malignancies?

A

Lymphoma
Chronic lymphcytic leukaemia
Myeloma

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38
Q

What are the 3 types of chronic myeloid haematological malignancies?

A

Chronic myeloid leukaemia
Myelodysplasia
Myeloproliferative disorders

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39
Q

Give some symptoms of leukaemia

A

Generalised: Tiredness, recurrent infections, bruising, bleeding
CNS infiltration: Cranial nerve IV and VII palsies, seizures
Splenomegaly
Hepatomegaly
Lymphadenopathy

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40
Q

Which cells are typical of acute leukaemias?

A

Blast cells

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41
Q

Which leukaemia typically affects children?

A

Acute lymphoblastic leukaemia

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42
Q

Auer rods are associated with which haematological malignancy?

A

Acute myeloid leukaemia

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43
Q

Children with Down’s Syndrome are at higher risk of which haematological malignancy?

A

Acute myeloid leukaemia

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44
Q

Compare blood film findings in acute myeloid Vs. acute lymphoblastic leukaemias

A

AML:

  • Blast cells with some cytoplasm
  • Auer rods
  • Stain positive

ALL:

  • Blast cells with no cytoplasm
  • Stain negative
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45
Q

How long is the treatment for acute lymphoblastic leukaemia?

A 
Boys = 3 years (due to infiltration of testes)
Girls = 2 years
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46
Q

Orchidomegaly is typical of which haematological malignancy?

A

Acute lymphoblastic leukaemia

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47
Q

Gum hypertrophy is associated with which haematological malignancy?

A

Acute myeloid leukaemia

48
Q

The Philadelphia chromosome is associated with which haematological malignancy?

A

Chronic myeloid leukaemia

49
Q

What is the Philadelphia chromosome?

A

Translocation between chromosomes 9 and 22…BCR-ABL

50
Q

Give 5 causes of massive splenomegaly

A

2 x haematological: Chronic myeloid leukaemia, myelofibrosis
2 x infective: Malaria, Leuschmaniasis
1 x lysosomal storage disorder

51
Q

Infliximab is used to treat which haematological malignancy?

A

Chronic myeloid leukaemia

52
Q

What is infliximab?

A

A tyrosine kinase inhibitor - used in the treatment of chronic myeloid leukaemia

53
Q

What are the treatment options for chronic myeloid leukaemia?

A
  • Hydroxycarbamide
  • Infliximab
  • Stem cell transplant
54
Q

What is the Richter transformation?

A

Development of aggressive lymphoma in patients with chronic lymphocytic leukaemia (usually diffuse large B-cell lymphoma)

55
Q

What is the most common type of leukaemia in adults?

A

Chronic lymphocytic leukaemia

56
Q

In which haematological malignancy might you see ‘smudge’ cells?

A

Chronic lymphocytic leukaemia

57
Q

List some features of lymphoma

A

Lymphadenopathy
General malaise, tiredness
Weight loss
Fever

58
Q

Which is more aggressive, Hodgkin’s or non-Hodgkin’s lymphoma?

A

Non-Hodgkins is more aggressive

59
Q

Reed-Sternberg cells are associated with which type of lymphoma?

A

Hodgkin’s

60
Q

EBV is associated with an increased risk of which lymphoma?

A

Hodgkin’s

61
Q

Which type of Hodgkin’s lymphoma has the worst prognosis?

A

Lymphocyte depleted

62
Q

List 5 types of Hogkin’s lymphoma

A 
Nodular sclerosing
Mixed cellularity
Lymphocyte rich
Lymphocyte depleted
Nodular lymphocyte predominant
63
Q

What are the 2 types of high grade non-Hodgkin’s lymphoma?

A

Burkitt’s lymphoma

Diffuse large B cell lymphoma

64
Q

What are the 2 types of low grade Hogkin’s lymhoma?

A

Follicular

Marginal

65
Q

What are the ‘B’ symptoms in lymphoma

A

More than 10% weight loss in 6 months
Unexplained fever more than 38 degrees
Night sweats

66
Q

How is Hodgkin’s lymphoma staged?

A

I = Confined to single lymph node region
II = 2 or more nodal areas on same side of the diaphragm involved
III = Nodes on both sides of diaphragm involved
IV = Spread beyond lymph nodes e.g. liver, bone marrow
Each stage is either ‘A’ or ‘B’ based on the absence or presence of B symptoms

67
Q

What is the treatment for Hodgkin’s lymphoma?

A 
Chemotherapy: ABVD
Adriamycin
Bleomycin
Vinblastine
Dacarbazine
68
Q

What is the definition of a myeloproliferative disorder?

A

Malignant proliferation of a particular type of myeloid stem cell in the bone marrow, which results in a dramatically increased amount of that cell

69
Q

What is the mutation in polycythaemia rubra vera?

A

JAK2 mutation, which causes malignany proliferation of RBC, WBC and platelets

70
Q

Give some features of polycythaemia rubra vera

A

May be asymptomatic and picked up on routine FBC test
Symptoms of hyperviscosity: Headache, dizziness, visual disturbance
Itch after a hot bath
Erythromelalgia
Facial plethora
Splenomegaly
Symptoms of arterial and venous thrombosis

71
Q

How might you distinguish polycythaemia rubra vera from other causes of polycythaemia?

A

In polycythaemia, there are increased numbers of WBCs and platelets, not just RBCs

72
Q

What is the treatment for polycythaemia rubra vera?

A

Venesections to keep haematocrit low

73
Q

What mutation is present in essential thrombocytosis?

A

JAK-2 mutation (same as for polycythaemia rubra vera) which causes proliferation of megakaryocytes so there is an increase in platelets

74
Q

What is erythromelalgia?

A

Burning sensation in extremities

75
Q

List some features of essential thrombocytosis

A 
Arterial and venous thrombosis
Microvascular occlusion headache
Atypical chest pain
Light headedness
Erythromelalgia
76
Q

What is the treatment for essential thrombocytosis?

A

Aspirin daily

Hydroxycarbamide if over 60 or previous thrombosis

77
Q

What happens in myelofibrosis?

A

Bone marrow is replaced with connective tissue

78
Q

What is the difference between a myeloproliferative disorder and myelodysplasia?

A

Myelodysplasia = There is increased production of abnormal cells
Myeloproliferative disorder = There is malignant proliferation of a cell type but the cells are normal

79
Q

What are the features of myelofibrosis?

A

General features of bone marrow failure:

  • Malaise, weight loss, weakness
  • Bleeding
  • Recurrent infections
  • Hepatomegaly
  • Massive splenomegaly (due to extramedullary haematopoiesis)
  • Anaemia
80
Q

What would bone marrow biopsy show in myelofibrosis?

A

A dry tap i.e. unable to obtain a sample

Trephine biopsy shows fibrosis

81
Q

What is the management of myelofibrosis?

A 
Transfusions
Hydroxycarbamide
Splenic irradiation
Splenectomy
Stem cell transplant
82
Q

Teardrop cells are typical of ….?

A

Myelofibrosis

83
Q

Give some causes of microcytic anaemia

A

Iron deficiency anaemia
Thalassemia
Sideroblastic anaemia
Lead poisoning

84
Q

How might macrocytic anaemia be divided up?

A

Megaloblastic

Non-megaloblastic

85
Q

What are the causes of megaloblastic macrocytic anaemia?

A

B12 and folate deficiency

86
Q

What are the causes of non-megalobastic macrocytic anaemia?

A 
Alcohol
Chronic liver disease
Myelodysplasia
Hypothyroidism
Drugs
Metabolic disorder
87
Q

How might normocytic anaemias be divided up?

A

Haemolytic

Non-haemolytic

88
Q

Give some causes of a non-haemolytic normocytic anaemia

A 
Anaemia of chronic disease
Aplastic anaemia
Kidney disease
Pregnancy (due to increased volume)
Lymphoma
Acute blood loss
89
Q

What do iron studies show in iron deficiency anaemia?

A

Low iron
High TIBC
Low ferritin
Low transferrin saturation

90
Q

Where is Vitamin B12 absorbed?

A

Terminal ileum

91
Q

Approximately how long do the body’s own stores of Vitamin B12 last?

A

1-2 years

92
Q

What is the significance of intrinsic factor?

A

Free Vitamin B12 becomes bound to intrinsic factor to be absorbed at the terminal iluem. A lack of intrinsic factor (in pernicious anaemia) will mean less Vitamin B12 is absorbed.

93
Q

Give some clinical features of B12 deficiency

A 
Anaemia symptoms e.g. tiredness
'Yellow tinge' to skin
Glossitis
Angula cheilitis
Neurological involvement: Paraesthesia, depression, psychosis, dementia
94
Q

What tests are specific for pernicious anaemia?

A

Parietal cell antibodies

Intrinsic factor antibodies

95
Q

Why shouldn’t you give folic acid on it’s own to a B12 deficient patient?

A

B12 deficiency worsens folate deficiency and precipitates subacute combined degeneration of the cord

96
Q

How long do the body’s own stores of foic acid last?

A

About 4 months

97
Q

What symptoms are seen in subacute combined degeneration of the cord?

A 
Sensory symptoms:
- Loss of proprioception, leads to ataxia
- Loss of vibration sense
Motor symptoms (UMN and LMN)
- Reduced knee and ankle reflexes
- Upgoing plantars
Loss of vision due to optic atrophy
Pain and temperature sensation intact
98
Q

What is the chronic management of sickle cell disease?

A
  • Analgesia
  • Avoid factors which might preciptate a crisis e.g. cold
  • Hydroxycarbamide if frequent crises
  • Pneumococcal and influenza vaccination, plus daily penicillin due to hyposplenism
99
Q

What is the treatment for thalassemia?

A

Regular blood transfusions to maintain Hb

Iron chelators to reduce iron overload e.g. desferrioxamine

100
Q

What might be seen on blood film of a patient with iron deficiency anaemia?

A

Microcytic, hypochromic red blood cells
Pencil cells
Target cells

101
Q

How might haemolytic anaemia be divided up?

A

Inherited Vs. acquired causes

102
Q

List some inherited causes of haemolytic anaemia

A

Haemoglobinopathies: Sickle cell disease, thalassemia
Membrane defects: Hereditary spherocytosis or elliptocytosis
Enzyme defects: G6PD deficiency, pyruvate kinase deficiency

103
Q

What is the inheritance pattern of glucose-6-phosphate dehydrogenase deficiency?

A

X-linked recessive

104
Q

Give some drugs which might precipitate an oxidative crisis in G6PD deficiency

A

Ciprofloxacin
Sulphonamides
Sulphonylureas
Sulfasalazine

105
Q

What is the inheritance pattern of hereditary spherocytosis?

A

Autosomal dominant

106
Q

What is the diagnostic test for hereditary spherocytosis?

A

Osmotic fragility test

107
Q

How might acquired haemolytic anaemias be divided up?

A

Immune

Non-immune

108
Q

What is the key test in diagnosing immune haemolytic anaemia?

A

Immune haemolytic anaemias will cause a positive Coombs (direct antibody) test

109
Q

Compare warm and cold autoimmune haemolytic anaemias

A

Warm:
- Extravascular haemolysis i.e. in spleen
- Treatment = Steroids, immunosuppression, splenectomy
Cold:
- Complement-mediated intravascular haemolysis
- Infections e.g. EBV might increase antibodies
- Responds less well to steroids
- Treatment is to keep warm

110
Q

List some causes of non-immune haemolytic anaemia

A

Infection e.g. malaria
Paroxysmal nocturnal haemoglobinuria
Microangiopathic haemolytic anaemia
Heart valve disorders

111
Q

What is the triad of features in haemolytic uraemic syndrome?

A

Haemolytic anaemia (jaundice, low Hb)
Renal failure
Thrombocytopenia

112
Q

List some causes of thrombocytopenia

A

Impaired production:
- Bone marrow failure, including in leukaemia, myeloma
- Megaloblastic anaemias
- Aplastic anaemia
- Myelosuppression e.g. myelodysplasia, myelofibrosis
Increased destruction:
- Non-immune: TTP, DIC, haemolytic uraemic syndrome, sequestration e.g. in hypersplenism
- Primary immune i.e. ITP
- Secondary immune i.e. SLE, CLL, viruses, drugs

113
Q

What is the treatment for immune thrombocytopenic purpura?

A
  • If platelets over 30, might not need treatment
  • Prednisolone
  • Intravenous immunoglobulin
  • Rituximab
  • Splenectomy
114
Q

Why shouldn’t you give platelets to a patient with immune thrombocytopenic purpura?

A

It’s an autoimmune condition so antibodies to the platelets surface antigens would cause any transfused platelets to be consumed so it’s pointless administering them

115
Q

What are the 5 key features of thrombotic thrombocytopenic purpura?

A 
Thrombocytopenia
Microangiopathic haemolytic anaemia
Neurological disturbance
Fever
Renal failure

Haematology (4 decks)

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