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Phase 2a > Haematology > Flashcards

Haematology Flashcards

1
Q

Define anaemia

A

Reduced red cell mass due to reduced haemoglobin concentration or plasma volume

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2
Q

Pathophysiology of anaemia

A

Reduced RBC’s -> reduced O2 transport -> tissue hypoxia

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3
Q

What 3 compensatory changes happen in anaemia?

A

o Increase tissue perfusion
o Increase O2 transfer to tissues
o Increase red cell production

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4
Q

List the 3 main causes of microcytic anaemia

A

o Iron deficiency
o Chronic disease
o Thalassaemia

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5
Q

List the 3 main causes of normocytic anaemia

A

o Acute blood loss
o Chronic disease
o Combined haematinic deficiency

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6
Q

List 4 causes of macrocytic anaemia

A 
o   B12/folate deficiency 
o   Alcohol excess/liver disease 
o   Hypothyroid 
o   Haematological – haemolysis, bone marrow failure 
     or infiltration
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7
Q

General symptoms of anaemia

A

Fatigue, faintness, dyspnoea, reduced exercise tolerance, palpitations, headache

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8
Q

General signs of anaemia

A

Pale skin, pale mucus membranes, tachycardia

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9
Q

List the 3 main causes of iron deficiency anaemia

A

o Blood loss – menorrhagia, GI bleeding
o Poor diet/poverty
o Malabsorption – Coeliac

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10
Q

Specific signs of iron deficiency anaemia

A

Koilonychia (spooned nails), atrophic glossitis, angular cheilosis (ulcers at side of mouth)

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11
Q

Investigations and diagnosis of iron deficiency anaemia

A

o Blood film – microcytic hypochromic anaemia
o Bloods - low ferritin
o Check Coeliac serology

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12
Q

What is the diagnostic result for iron deficiency anaemia?

A

Low ferritin

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13
Q

Management of iron deficiency anaemia

A

o Oral iron (ferrous sulphate)

o Improve diet – red meat, spinach

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14
Q

What are the common side effects of ferrous sulphate?

A

Nausea, diarrhoea, constipation

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15
Q

List the 3 main causes of folate deficiency

A

o Poor diet
o Increased demand – pregnancy
o Malabsorption – Coeliac

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16
Q

In which part of the gut is folate absorbed?

A

duodenum/proximal jejunum

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17
Q

What investigation confirms a diagnosis of folate deficiency anaemia?

A

Bloods - low folate

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18
Q

How is folate deficiency prevented in pregnancy?

A

Folate given during first 12 weeks of pregnancy to prevent spina bifida and anaemia

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19
Q

Management of folate deficiency anaemia

A

Oral folic acid for 4 months w/ B12 (unless known to have normal B12 level)

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20
Q

Pathophysiology of B12 deficiency anaemia

A

B12 helps synthesize thymidine -> DNA -> slow RBC production in deficiency

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21
Q

Pathophysiology of pernicious anaemia

A

lack of intrinsic factor in stomach (autoimmune) -> lack of B12 absorption -> anaemia

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22
Q

Causes of B12 deficiency

A

o Dietary - vegan
o Malabsorption - pernicious
o Congenital metabolic disorders

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23
Q

Signs and symptoms of B12 deficiency

A

o Lemon tinge to skin – pale and mild jaundice
o Glossitis and angular cheilosis
o Neurological and psychological problems

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24
Q

Investigations for diagnosis of B12 deficiency anaemia

A

o Bloods – low B12, high MCV, low haemoglobin

o IF antibodies if pernicious

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25
Q

Management of B12 deficiency

A

Diet, then B12 injections or tablets (hydroxocobalamin)

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26
Q

Pathophysiology of thalassaemia

A

Unbalanced Hb synthesis, under or over production of one globin chain -> unmatched globins precipitate -> damaged RBCs -> haemolysis in marrow

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27
Q

Epidemiology of thalassaemia

A

Common in areas from the Mediterranean to the Far East

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28
Q

Causes of thalassaemia

A

Genetic, inherited

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29
Q

Signs and symptoms of thalassaemia

A

Same as anaemia - fatigue, faintness, syncope ect.

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30
Q

Investigations for diagnosis of thalassaemia

A

o Blood film – microcytic

o Genetic testing

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31
Q

Management of thalassaemia

A

o Regular, life-long transfusions
o Iron-chelators and ascorbic acid for iron overload
o Stem cell transplant if severe

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32
Q

What is the cause of sickle cell anaemia?

A

Genetic - autosomal recessive deformity of RBC

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33
Q

What is the pathophysiology of sickle cell disease?

A

Autosomal recessive deformity of RBC -> HbS instead of HbA -> HbS polymerises when deoxygenated -> RBCs deform -> sickle cells fragile and haemolyse -> block small blood vessels

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34
Q

Which population is sickle cell disease most common in?

A

African, 1:700 have sickle cell

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35
Q

Signs and symptoms of sickle cell disease

A

o Normal anaemia symptoms
o Vaso-occlusive – hand and feet pain
o Avascular necrosis -> shortened bones
o Recurrent infections (spleen infarction)
o CKD

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36
Q

What investigation is used to screen for sickle cell disease in babies?

A

Heel prick screening, blood film shows sickle cells

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37
Q

Management of sickle cell disease

A

o Hydroxycarbamide if frequent crises -> increases
production of fetal haemoglobin
o Prophylaxis if splenic infarction
o Bone marrow transplant

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38
Q

What is intravascular haemolytic anaemia?

A

Premature breakdown of RBCs in circulation

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39
Q

What is extravascular haemolytic anaemia?

A

Premature breakdown of RBCs in the reticuloendothelial sustem

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40
Q

What are the main causes of haemolytic anaemia?

A

o Acquired – drug-induced, autoimmune, Malaria,
infections
o Hereditary – enzyme defects (G6DP), membrane
defects, haemoglobinopathy (sickle-cell,
thalassaemia)

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41
Q

Signs and symptoms of haemolytic anaemia

A

o Normal anaemia symptoms
o Jaundice, gallstones, leg ulcers, signs of underlying
cause

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42
Q

Investigations for suspected haemolytic anaemia

A

o Blood film

o Malaria screen

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43
Q

Management of haemolytic anaemia

A

o Folate and iron supplements
o Immunosuppressants if autoimmune
o Splenectomy if hereditary spherocytosis or other
approaches fail

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44
Q

Symptoms of DVT

A

Non-specific, pain, swelling

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45
Q

Signs of DVT

A

Non-specific, tenderness, swelling, warmth, discolouration

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46
Q

Risk factors for DVT

A

o Surgery, immobility
o OC pill, HRT, pregnancy
o Long haul flights/ travel
o Inherited thrombophilia

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47
Q

Investigations for suspected DVT

A

o D-dimer – normal excludes, +ve does not confirm
o Ultrasound compression test proximal veins
o Venogram for calf, recurrence, uncertain

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48
Q

Management of DVT

A 
o   LMW Heparin for min 5 days
o   Oral warfarin for 6 months
o   Compression stockings, hydration and early 
     mobilisation
o   Treat/seek underlying cause
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49
Q

What is the target INR range for a patient on warfarin?

A

2-3

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50
Q

Epidemiology of ALL

A

Most common in age 3-7

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51
Q

What cells are affected in ALL?

A

B and T lymphocytes

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52
Q

What is the pathophysiology of ALL?

A

uncontrolled proliferation of B or T-lymphocytes -> leukaemia cells accumulate -> bone marrow failure and tissue infiltration

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53
Q

What are the causes of ALL?

A

Ionising radiation in pregnancy, Down’s syndrome

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54
Q

List 3 symptoms of ALL

A

Anaemia, recurrent infections, bleeding

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55
Q

List 3 signs of ALL

A

Hepatosplenomegaly, CNS involvement (meningism), lymphoadenopathy

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56
Q

Investigations for diagnosis of ALL

A

o Blood film and marrow biopsy – blast cells
o CXR and CT – lymphadenopathy
o Lumbar puncture – check for CNS involvement
o FBC - ↓RBC, ↓platelets, WCC variable

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57
Q

Management of ALL

A

o Support – transfusions/fluids
o Infections – immediate IV antibiotics, prophylaxis
o Chemo – methotrexate
o Bone marrow transplant

58
Q

Epidemiology of CLL

A

Most common leukaemia, mostly elderly, more common in women

59
Q

Pathophysiology of CLL

A

Progressive accumulation of malignant functionally incomplete B cells in blood, bone marrow, lymph glands (incl. spleen)

60
Q

What are the causes of CLL?

A

Genetic mutations, infection, autoimmune, hypogammaglobulinaemia

61
Q

List 4 symptoms of CLL

A

Anaemic, infection-prone, weight loss, sweats

62
Q

List 2 signs of CLL

A

Enlarged rubbery nodes, hepatosplenomegaly

63
Q

Investigations for diagnosing CLL

A

o Blood film – increased lymphocytes, ‘smear cells’

o Low HB, low neutrophils, low platelets

64
Q

Management of CLL

A

o Nothing if asymptomatic – monitor
o Chemotherapy
o Monoclonal antibodies (rituximab)
o Bone marrow transplant

65
Q

What cells are affected in CLL?

A

B lymphocytes

66
Q

What cells are affected in AML?

A

Myeloblasts

67
Q

Pathophysiology of AML

A

Neoplastic proliferation of blast cells derived from marrow myeloid elements -> rapidly progresses

68
Q

Epidemiology of AML

A

Commonest acute leukaemia of adults, incidence increases with age

69
Q

What are the causes of AML?

A

Long-term complication of chemo, haematological disorders, radiation

70
Q

List 3 symptoms of AML

A

Anaemia, recurrent infections, bleeding

71
Q

List 3 signs of AML

A

Lymphadenopathy, hepatosplenomegaly, CNS involvement

72
Q

Investigations for diagnosis of AML

A

o Blood film – thrombocytopenia, Auer Rods
o Bone marrow biopsy – blast cells
o ↓RBC, ↓platelets, WCC variable

73
Q

Management of AML

A

o Supportive – transfusions, fluids, prophylaxis
o Human mononuclear leukocytes
o Chemotherapy
o Transplantation

74
Q

What cells are affected in CML?

A

Basophils, eosinophils and neutrophils

75
Q

Epidemiology of CML

A

40-60yrs, slight male predominance, rare in childhood

76
Q

What is the main cause of CML?

A

80% have Philadelphia chromosome

77
Q

What are the symptoms of CML?

A

Weight loss, tiredness, fever, sweats, gout, bleeding, abdominal discomfort

78
Q

What are the signs of CML?

A

Hepatosplenomegaly, anaemia, bruising

79
Q

Investigations for diagnosis of CML

A

o Bloods – high WBC, high urate, low Hb
o Blood film – left shift + basophilia
o Philadelphia Chromosome -> activated tyrosine
kinase

80
Q

Management of CML

A

o Target molecular therapy – tyrosine kinase inhibitors
– Imatinib (Glivec)
o Chemotherapy if in acute stage
o Stem cell transplant

81
Q

What is the main difference between Hodgkin’s and non-Hodgkin’s lymphoma?

A

Reed-Sternberg cells are seen in biopsy of Hodgkin’s lymphoma and not in non-Hodgkin’s

82
Q

List 3 symptoms of Hodgkin’s lymphoma

A

o Painless lymphoedema
o Sweats
o Weight loss

83
Q

List 3 signs of Hodgkin’s lymphoma

A

o Lymphadenopathy
o Anaemia
o Hepatosplenomegaly

84
Q

Investigations for suspected lymphoma

A

o Tissue diagnosis – lymph node biopsy
o Bloods – FBC, film, ESR, LFT, LDH
o Imaging – CT/PET, for mets and staging

85
Q

What is the diagnostic feature of Hodgkin’s lymphoma?

A

Reed-Sterberg cells

86
Q

Management of Hodgkins’s lymphoma

A

o ABVD chemo - length determined by stage
o Radiotherapy
o Stem cell transplant

87
Q

Complications of radiotherapy

A

Increased risk of second malignancies, IHD, hypothyroidism, lung fibrosis

88
Q

Complications of chemotherapy

A

Myelosuppression, nausea, alopecia, infection

89
Q

Causes of non-Hodgkin’s lymphoma

A

o Immunodeficiency – drugs, HIV
o HTLV-1
o H.pylori

90
Q

Symptoms of non-Hodgkin’s lymphoma

A

o Extranodal disease
o Systemic features – fever, sweats, weight loss
o Infection
o Bleeding

91
Q

Signs of non-Hodgkin’s lymphoma

A

o Anaemia
o Superficial lymphadenopathy
o Bleeding and easy bruising

92
Q

Management of non-Hodgkin’s lymphoma

A

o Low grade – nothing, radiotherapy if localised
o High grade – R-CHOP chemotherapy
o Remission maintained using interferon alfa or
rituximab

93
Q

Definition of myeloma

A

Malignant proliferation of bone marrow plasma cells, leading to the overproduction of Ig, causing the dysfunction of many organs

94
Q

Which organs are most affected in myeloma?

A

The kidneys

95
Q

Signs and symptoms of myeloma (CRAB)

A

• Calcium (hypercalcaemia) - bones, stones, groans,
moans
• Renal impairment -↓urine output, oedema,
dehydration
• Anaemia
• Bone disease - backache and pathological fractures

96
Q

Investigations in suspected myeloma

A 
• X-Ray > CT/MRI
• Bone marrow biopsy 
• Blood film
• Monoclonal protein band in serum protein 
  electrophoresis
97
Q

How is umsymptomatic myeloma managed?

A

Watch and wait

98
Q

What is the main treatment for myeloma?

A

o Chemo/Radiotherapy with autologous stem cell
transplant
o Treat complications
o Supportive treatments

99
Q

List 4 complications of myeloma

A

o Hypercalcaemia
o Spinal cord compression
o Hyperviscosity
o AKI

100
Q

What supportive treatments are used to manage myeloma?

A

o Bone Pain: Analgesia and bisphosphonates
o Anaemia: Blood transfusion/Erythropoietin
o Infections: Abx/Regular IV Immunoglobulin infusions

101
Q

Why can myeloma cause hypercalcaemia?

A

Increased bone resorption and decreased formation -> more calcium in blood

102
Q

Why can myeloma cause anaemia?

A

Bone marrow infiltration

103
Q

Why might myeloma cause renal failure?

A

Light chain deposition

104
Q

What is malaria?

A

Infection by plasmodium transmitted by mosquito (protozoa)

105
Q

Pathology of malaria cycle

A
  1. Bite by infected mosquito
  2. Sporozoites in saliva travel to liver to mature (in
    hepatocytes)
  3. Rupture to release merozoites into the blood
  4. Invade RBC and undergo asexual reproduction to
    create sporozoites a mosquito can pick up (cycle)
106
Q

List 5 symptoms of malaria

A

FEVER, chills, cough, myalgia, abdominal discomfort

107
Q

List 3 signs of malaria

A

Anaemia, thrombocytopenia, hepatosplenomegaly

108
Q

How long is the incubation period for malaria?

A

A few weeks to 3 months

109
Q

Investigations for suspected malaria

A
  • Urine dip – blood and leukocytes
  • Bloods - LFTS, AKI, anaemia
  • Thick and thin blood smears
110
Q

Management of malaria

A
  • Fluids and road spectrum antibiotics
  • Chloroquine to treat acute infection
  • Primiquine to kill hypnozoites
111
Q

What medication is used to treat complicated malaria?

A

IV artesunate

112
Q

When is an exchange transfusion needed to treat malaria?

A

When the disease burden is huge

113
Q

What is a complication of malaria?

A

Multiple organ and failure -> death

114
Q

What causes polycynthaemia vera?

A

Genetic mutation in JAK2 gene -> increased proliferation of RBC in bone marrow

115
Q

What is polycynthaemia?

A

An abnormally increased concentration of haemoglobin in the blood, either through reduction of plasma volume or increase in RBC

116
Q

Symptoms of polycynthaemia

A

• Hyperviscosity – headaches, dizziness, tinnitus,
visual disturbances
• Itching after a hot bath, burning sensation in fingers
and toes

117
Q

Signs of polycynthaemia

A

Facial plethora, splenomegaly

118
Q

Investigations for suspected polycynthaemia

A
  • Genetic testing for JAK2 gene
  • Bone marrow biopsy
  • FBC – high haematocrit, haemoglobin and platelets
  • Serum EPO – low
119
Q

Management of polycynthaemia

A
  • Venesection in younger low risk
  • Hydroxycarbamide in higher risk
  • Aspirin
  • Treat cause if not genetic
120
Q

What are the most common anticoagulation medications?

A

Warfarin and NOACs

121
Q

What is warfarin?

A

Vitamin K antagonist

122
Q

What is the main benefit of using a NOACs instead of warfarin?

A

Review is needed much less regularly

123
Q

What are the 2 main causes of over-anticoagulation?

A

o Poor patient compliance

o New/interacting drugs

124
Q

Symptoms of over-anticoagulation

A

Bleeding, bruising, melena (black stool), epistaxis (nose bleeds), hematemesis (vomiting blood), haemoptysis (coughing up blood)

125
Q

Investigations for suspected over-anticoagulation

A 
o  APTT (activated partial thromboplastin time) – 
    intrinsic pathway 
o  PTT (prothrombin time) – extrinsic pathway
126
Q

What is disseminated intravascular crisis (DIC)?

A

Generation of fibrin within blood vessels and consumption of platelets/coagulation factors -> secondary activation of fibrinolysis

127
Q

List 4 causes of DIC

A

Malignancy, septicaemia, trauma, infections

128
Q

Management of DIC

A

Treat cause, transfusion, activated protein C

129
Q

What is thrombocytopenia?

A

Deficiency of platelets in the blood

130
Q

List 3 general causes of thrombocytopenia

A

o Reduced platelet production in bone marrow
o Excessive peripheral destruction of platelets
o Splenomegaly

131
Q

What is immune thrombocytopenia?

A

Autoimmune destruction of platelets

132
Q

Signs and symptoms of thrombocytopenia

A

Easy bruising, purpura, epistaxis/menorrhagia

133
Q

Investigations for suspected thrombocytopenia

A

o Bloods – low platelets

o May have detection of platelet autoantibodies

134
Q

Management of immune thrombocytopenia

A

o Splenectomy
o IV IG
o Corticosteroids i.e. prednisolone
o Anti D

135
Q

What is thrombotic thrombocytopenia?

A

Extensive microvascular clots form in small vessels -> low platelet count and organ damage

136
Q

Management of thrombotic thrombocytopenia

A

Plasma exchange and immunosuppression

137
Q

What are the 2 types of haemophilia?

A

A (VIII) and B (IX)

138
Q

What causes haemophilia?

A

Inherited, X-linked recessive -> more common in males

139
Q

Symptoms of haemophilia

A

Easy bruising, bleeding

140
Q

Investigations for suspected haemophilia

A

Normal PTT but prolonged APTT

Genetic testing

141
Q

What cells are typically seen on a blood film from a patient with thalassaemia?

A

Target cells

Phase 2a (9 decks)

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