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Phase 2a Sheffield Medicine > Haematology > Flashcards

Haematology Flashcards

1
Q

What is DVT?

A

A blood clot that develops within a deep vein in the body, usually the leg.

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2
Q

What is the differential diagnosis of DVT?

A

Cellulitis

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3
Q

What score determines the possibility of having DVT?

A

Wells score

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4
Q

What affects the Wells score?

A

Affected by active cancer, tenderness along DV system, swollen leg/calf, unilateral pitting oedema and recently bedridden.

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5
Q

What are the symptoms of DVT?

A
  • Nonspecific symptoms
  • Pain and swelling
  • Tenderness
  • Warmth
  • Slight discolouration
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6
Q

What investigations for DVT?

A
  1. D-dimer – look for breakdown of fibrin products, if normal it excludes DVT
  2. Ultrasound compression scan – if you can’t squash the vein it’s a clot.
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7
Q

What is the treatment of DVT?

A
  1. LMWH
  2. Oral Warfarin or DOAC (direct oral anti-coag)
  3. Compression stockings
  4. Treat underlying cause e.g. malignancy
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8
Q

What are 3 risk factors for DVT?

A
  1. Surgery, immobility, leg fracture
  2. OCP,HRT
  3. Long Haul flights
  4. Genetic predisposition
  5. Pregnancy
  6. Age
  7. Obesity
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9
Q

How can you prevent DVT’s?

A
  1. Hydration
  2. Mobilisation
  3. Compression stockings
  4. Low dose LMWH (Low weight molecular heparin
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10
Q

What is the major consequence of a dislodged DVT?

A

Pulmonary embolism

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11
Q

What is the best prophylaxis for DVT?

A

LMWH

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12
Q

Describe arterial thrombosis?

A

Platelet rich - white

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13
Q

Describe venous thrombosis?

A

Fibrin rich - red

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14
Q

What are 3 major consequences of arterial thrombosis?

A
  1. MI
  2. Stroke
  3. Peripheral vasc disease-e.g. gangrene
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15
Q

What is the treatment for arterial thrombosis?

A

Aspirin, LMWH, Thrombolytic therapy.

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16
Q

What is a consequence of venous thrombosis?

A

PE.

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17
Q

How does warfarin work?

A

producing non functional clotting factors 2,7,9,10

Agonist of Vit K.

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18
Q

Why is warfarin difficult to work with?

A

Lots of interactions
Needs constant monitoring
Teratogenic

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19
Q

What is myeloma?

A

Malignancy of plasma cells leading to progressive bone marrow failure, associated with paraprotein, bone disease and renal disease.

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20
Q

What preceding disease is associated with myeloma?

A

monoclonal gammopathy of undetermined significance (MGUS)

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21
Q

What is MGUS?

A

Common disease of paraprotein present in serum but no myeloma, often asymptomatic

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22
Q

What is the treatment for MGUS?

A

Watch and wait.

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23
Q

What are the symptoms of myeloma?

A
  1. Tiredness
  2. Bone/back pain
  3. Infections
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24
Q

What are the signs of Myeloma?

A
  1. Calcium is elevated – increased bone resorption and decreased formation causing raised Ca
  2. Renal failure – light chain deposition
  3. Anaemia – bone marrow infiltrated with plasma cells
  4. Bone lesions
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25
Q

Why is calcium elevated in myeloma?

A

increased bone resorption and decreased formation causing raised Ca

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26
Q

Why is renal failure caused by myeloma?

A

Light chain deposition

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27
Q

Why is anemia caused by myeloma?

A

Bone marrow infiltrated with plasma cells

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28
Q

What investigations would you order in suspected myeloma?

A
  1. Blood film – Rouleaux formation (Aggregations of RBC)
  2. Bone marrow aspirate and trephine biopsy - increased plasma cell
  3. Electrophoresis – Monoclonal protein band
  4. X-ray – bone lesions
  5. CT scan
  6. MRI scan
  7. Chromosomal abnormalities
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29
Q

What would you expect to see in a bone marrow biopsy in suspected myeloma?

A

Increased plasma cell proliferation

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30
Q

What would you expect to see using electrophoresis in myeloma?

A

Monoclonal protein band

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31
Q

How would you diagnose myeloma?

A

Positive investigations

Must be evidence of mono-clonality (abnormal proliferation of plasma cell leading to IG secretion causing organ dysfunction

In 2/3 of people urine contains ig light chains with kappa or lamda lineage

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32
Q

What is the management of symptomatic myeloma?

A

Chemotherapy, analgesia, bisphosphates

Radiotherapy and bone marrow transplant to be done

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33
Q

What is lymphoma?

A

A malignant growth of WBC predominantly in the lymph nodes

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34
Q

What organs are often effected in lymphoma?

A

blood, liver, spleen, bone marrow

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35
Q

What are the risk factors for lymphoma?

A
  1. Primary immunodeficiency
  2. Secondary immunodeficency e.g. HIV
  3. Infection e.g. EBV
  4. AI disorders e.g. RA
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36
Q

What is the pathophysiology of lymphoma?

A

Impaired immunosurveillance and infected B cells escape regulation and proliferate

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37
Q

What are the symptoms of lymphoma?

A
  1. Enlarged lymph nodes in arms/neck
  2. Symptoms of compression syndromes
  3. General systemic B symptoms e.g. weight loss, night sweats and malaise
  4. Liver and spleen enlargement
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38
Q

What are the investigations in lymphoma?

A
  1. Blood film
  2. Bone marrow biopsy
  3. Lymph node biopsy
  4. Immunophenotyping
  5. Cytogenetics
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39
Q

What are the two subtypes of lymphoma?

A
  1. Hodgkins lymphoma

2. Non-hodgkins lymphoma

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40
Q

Describe Low grade non hodgkins lymphoma

A

Slow growing, advanced at presentation, often incurable

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41
Q

Describe High grade hodgkins lymphoma

A

Aggressive, nodal presentation, patient unwell, often curable

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42
Q

What is the treatment of Low-grade NHL?

A

If symptomless – do nothing

Radiotherapy, combination chemotherapy and mAb may be used if symptomatic

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43
Q

What is the treatment for High-grade NHL?

A

Early – short course chemotherapy and radio therapy

Advanced – combination chemotherapy and mAb

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44
Q

What are the symptoms of Hodgkins lymphoma?

A

Painless lymphadenopathy, Presence of B symptoms

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45
Q

What must be present for a diagnosis of Hodgkin’s lymphoma?

A

Reed-sternberg cells.

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46
Q

What is the staging of Hodgkin’s lymphoma

A
  1. Confined to a single lymph node region
  2. Involvement of two or more nodal areas on same side of diaphragm
  3. Involvement of nodes on both sides of diaphragm
  4. Spread beyond the lymph nodes e.g. liver

Each stage is either A (absent of B symptoms) or B (presence of B symptoms).

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47
Q

What is the treatment of Stage 1-2a Hodgkin’s lymphoma?

A

Short course chemo followed by radiotherapy

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48
Q

What is the treatment of Stage 2b-4 Hodgkin’s lymphoma?

A

Combination chemotherapy

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49
Q

What are the possible complications of treatments for lymphoma?

A 
Secondary malignancies 
IHD
Infertility 
Nausea
Alopecia
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50
Q

What is leukaemia?

A

A malignant proliferation of haemopoietic stem cells

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51
Q

What are the sub types of leukaemia?

A

AML – Acute-myeloid leukaemia

CML – Chronic-myeloid leukaemia

ALL – Acute lymphoblastic leukaemia

CLL – Chronic lymphoblastic leukaemia

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52
Q

What are the symptoms of Leukaemia?

A
  1. Anaemia
  2. Infection
  3. Bleeding
  4. Hepatomegaly
  5. Splenomegaly
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53
Q

Why do you get anaemia, bleeding and infection in leukaemia?

A

Anaemia, bleeding and infection are all due to bone marrow failure

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54
Q

Why do you get hepatomegaly and splenomegaly in leukaemia?

A

Tissue infiltration

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55
Q

What investigations would you order for leukaemia?

A
  1. Blood film
  2. Bone marrow biopsy
  3. Lymph node biopsy
  4. Immunophenotyping
  5. Cytogenetics
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56
Q

What is Acute myeloid leukaemia?

A

Neoplastic proliferation of blast cells

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57
Q

What increases the risk of AML?

A

Prior chemo, exposure to ionising radiation and preceding haematological disorders

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58
Q

What is the treatment for AML?

A
  1. Supportive care
  2. Chemotherapy – curative v palliative
  3. Bone marrow transplant
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59
Q

What is Chronic myeloid leukaemia?

A

Uncontrolled clonal proliferation of basophils, eosinophils and neutrophils

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60
Q

What would you expect to see in the FBC of someone with CML?

A

High WBC

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61
Q

Where is the Philadelphia chromosome present?

A

In over 80% of people with CML

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62
Q

What is the treatment of CML?

A

Tyranise Kinase inhibitors

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63
Q

What is Acute lymphoblastic leukaemia?

A

Uncontrolled proliferation of immature lymphoblast cells

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64
Q

What is the treatment of ALL?

A

CNS directed therapy and stem cell transplant

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65
Q

What is Chronic lymphoblastic leukaemia?

A

Proliferation of B lymphocytes leads to accumulation of mature B cells that have escaped apoptosis

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66
Q

What is the treatment of Chronic lymphoblastic leukaemia?

A
  • Do nothing
  • Chemotherapy
  • mAb
  • Bone marrow transplant
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67
Q

What is Anaemia?

A

Decrease in the amount of Hb in the blood below the reference range.

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68
Q

What is the role of Hb in the body?

A

Carries oxygen to tissues

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69
Q

What organ’s are responsible for the removal of RBC?

A

Spleen
Liver
Bone marrow
Blood loss

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70
Q

What are the causes of microcytic anaemia?

A
  1. Iron deficiency
  2. Anaemia of chronic disease
  3. Thalassaemia
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71
Q

What are the causes of normocytic anaemia?

A
  1. Acute blood loss
  2. Anaemia of chronic disease
  3. Combined hematinic deficiency
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72
Q

What are the causes of macrocytic anaemia?

A
  1. B12/Folate deficiency
  2. Alcohol excess/liver disease
  3. Hypothyroid
73
Q

When might a patient present with reduced Hb but increased RCM?

A

In the 3rd trimester of pregnancy

74
Q

What are the consequences of anaemia?

A
  • Reduced o2 transport

- Tissue hypoxia

75
Q

What are 3 physiological compensatory changes as a result of anaemia?

A
  • Increase tissue perfusion
  • Increase O2 transfer to tissues
  • Increase red cell production
76
Q

Where is B12 absorbed at?

A

The terminal ileum

77
Q

How does pernicious anaemia lead to B12 deficiency?

A
  • Loss of parietal cells –> reduced intrinsic factor production –> B12 Malabsorption
78
Q

What are 5 causes of iron deficiency?

A
  1. Blood loss
  2. Poor absorption
  3. Decreased intake in diet
  4. Hook worm
  5. Breast feeding
79
Q

What are 4 symptoms of Iron deficiency?

A
  1. Fatigue
  2. Faintness
  3. Breathlessness
  4. Reduced exercise tolerance
80
Q

What investigations would you carry out in someone with suspected anaemia?

A
  1. Blood tests – FBC + blood film
  2. Biopsies
  3. Reticulocyte count
  4. B12 levels
  5. Serum ferritin
81
Q

What is the treatment of anaemia?

A
  • Treat the underlying cause e.g. if iron deficient give ferrous sulphate
82
Q

What is polycythaemia?

A

Too many RBC - increase in Hb

83
Q

What makes RBC?

A

Erythropoietin

84
Q

What is EPO stimulated by?

A

Tissue hypoxia

85
Q

What is the primary cause of polycythaemia?

A

Polycythaemia rubra vera – overactive bone marrow

86
Q

What is a secondary cause of polycythaemia?

A
  • Heavy smoking
  • Lung disease
  • Cyanotic heart disease
  • High altitude
87
Q

What is the treatment of polycythaemia?

A

If primary – treatment aims to maintain a normal blood count and prevent complications e.g. aspirin

If secondary – Treat the underlying cause

88
Q

What is neutrophillia?

A

Too many neutrophils

89
Q

What are the causes of neutrophillia?

A
  1. Infection
  2. CML
  3. Cancer
  4. Inflammation
90
Q

What is lymphocytosis?

A

Too many lymphocytes

91
Q

What are the causes of lymphocytosis?

A
  1. Viral infection
  2. Inflammation
  3. Malignancy
  4. CLL
92
Q

What is neutropenia?

A

Not enough neutrophils

93
Q

What are the causes of neutropenia?

A
  1. Marrow failure
  2. Marrow infiltration
  3. Marrow toxicity
94
Q

What is a major risk of neutropenia?

A

Infection.

95
Q

Where are platelets produced?

A

Bone marrow

96
Q

What is platelet regulation controlled by?

A

Thrombopoietin

97
Q

Where is Thrombopoietin produced?

98
Q

What is Thrombocytopenia?

A

Not enough platelets

99
Q

What is the lifespan of a platelet?

100
Q

What removes platelets?

A

The Spleen

101
Q

What are the causes of Thrombocytopaenia?

A

Production failure e.g. marrow suppression or marrow failure

Increased removal – splenomegaly, immune response, consumption (DIC)

102
Q

What are the two types of platelet dysfunction?

A
  • Reduced platelet number (thrombocytopenia)

- Reduced platelet function

103
Q

What are the causes of Decreased platelet numbers?

A
  1. Congenital causes e.g. malfunctioning megakaryocytes
  2. Infiltration of bone marrow e.g. leukaemia
  3. Alcohol
  4. Infection e.g. HIV/TB
104
Q

What are the causes of increased platelet destruction?

A
  1. Autoimmune e.g. ITP
  2. Hypersplenism
  3. Drug related e.g. heparin induced
  4. DIC and TTP –> increased consumption
105
Q

What are the causes of reduced platelet function?

A
  1. Congenital abnormality
  2. Medication e.g. aspirin
  3. VWF disease
  4. Uraemia
106
Q

What are the symptoms of platelet dysfunction?

A
  1. Mucosal bleeding
  2. Easy bruising
  3. Petechiae/purpura – blood spots
107
Q

What are the causes of bleeding?

A
  1. Trauma
  2. Platelet deficiency e.g. thrombocytopenia
  3. Platelet dysfunction e.g. aspirin induced
  4. Vascular disorders
108
Q

What is febrile neutropaenia?

A

Temperature over 38 degrees with low neutrophils

109
Q

What are the risk factors of febrile neutropaenia?

A
  1. Patient had chemo less than 6 weeks ago
  2. Patient who had a stem cell transplant in last year
  3. Any haematological condition causing neutropenia
  4. Bone marrow infiltration
110
Q

What is the presentation of Febrile neutropaenia?

A
  1. Pyrexia 38 degrees
  2. Generally unwell
  3. Confusion
  4. Hypotensive
  5. Tachycardia
111
Q

What is the management of Febrile neutropaenia?

A
  1. Thorough history and examination
  2. Bloods
  3. Antibiotics within 1 hour
112
Q

What is thalassemia?

A

Haemoglobin disorder of quantity –> reduced synthesis of one or more globin chains which leads to a reduction in Hb –> anaemia.

113
Q

What is Beta thalassemia?

A

Very few beta chains, alpha chains in excess

114
Q

What is the classification of B Thalassemia?

A
  1. Thalassemia major – relies on regular transfusions
  2. Thalassemia intermedia
  3. Thalassemia carrier/heterozygote – often asymptomatic
115
Q

When do people with Thalassemia major present?

A

Very young - severely anaemic and failure to thrive.

116
Q

Why must Thalassemia major be monitored constantly?

A

To prevent iron overload after blood transfusions

117
Q

What blood tests would you see in someone with thalassemia?

A
  • Raised reticulocyte count

- Microcytic anaemia

118
Q

What is Sickle cell disease?

A

A haemoglobin disorder of quality. HbS polymerises  sickle shaped RBC

119
Q

What is the genetic inheritance of sickle cell disease like?

A

Autosomal recessive and homozygous.

120
Q

What is sickling induced by?

A

Trauma, cold, stress and exercise

121
Q

What are the chance of offspring having SSA if both parents are carriers?

122
Q

What are the chance of offspring carrying SSA if both parents are carriers.

123
Q

What is an advantage of sickle cell anaemia?

A

Protection against falciparum malaria

124
Q

How long does Sickle cells last for?

125
Q

How long does a normal red blood cell last for?

126
Q

Why is Sickle cell anaemia not present until after 6 months of age?

A

Due to the fact HbF is not affected by sickle cell disease as its made out of 2 A and 2 G chains

127
Q

What are the acute complications of sickle cell disease?

A
  1. Very painful crisis
  2. Stroke in children
  3. Cognitive impairment
  4. Infections
128
Q

What are the chronic complications of sickle cell disease?

A
  1. Renal impairment
  2. Pulmonary hypertension
  3. Joint damage
129
Q

What is the treatment of Sickle cell disease?

A
  • Transfusion
  • Hydroxycarbamide – prevents crisis
  • Stem cell transplant
130
Q

What are the investigations necessary in sickle cell anaemia?

A

FBC/Blood film

Raised reticulocyte count due to increased RBC degradation

131
Q

Why is the parovirus significant?

A

Common infection in children

Leads to decreased RBC production

Cause’s a drop in Hb in patients who have an already reduced RBC lifespan

132
Q

What is a membranopathy?

A

Deficiency of red cell membrane proteins caused by genetic lesions

133
Q

What are two examples of membranopathies?

A
  1. Spherocytosis

2. Elliptocytosis

134
Q

Are membranopathies autosomal dominant or recessive?

135
Q

What are enzymopathies?

A

Enzyme deficiencies leading to shortened RBC lifespan

136
Q

What is an example of an enzymopathy?

A

G6PD Deficency

137
Q

What are the signs of G6PD deficiency?

A
  1. Haemolysis
  2. Jaundice
  3. Anaemia
138
Q

Name 3 categories of red cell disorders

A

Haemoglobinopathies
Membranopathies
Enzymopathies

139
Q

What is normal adult haemoglobin made of?

A

2 alpha and 2 beta chains

140
Q

What is foetal haemoglobin made of?

A

2 alpha and 2 gamma chains.

141
Q

What is Haemoglobin S?

A

Variant of Hb arising from point mutation in b globin gene

Mutation causes single AA change from valine to glutamine.

142
Q

What is a risk factor for spinal cord compression?

A

Any malignancy that can cause compression e.g. bone metastasis

143
Q

What is the presentation of spinal cord compression?

A
  1. Back pain
  2. Weakness in legs
  3. Inability to control bladder
  4. Spastic paresis
  5. Sensory level
144
Q

Describe the management of spinal cord compression

A
  1. Bed rest
  2. High dose steroids
  3. Analgesia
  4. Urgent MRI of the whole spine
145
Q

What is tumour lysis syndrome?

A

Break down of malignant cells –> Content release –> metabolic disturbances which can cause

Hyperuricaemia
Hyperkalaemia
Hypocalcaemia

146
Q

What are the risk factors for tumour lysis syndrome?

A
  1. High tumour burden
  2. Pre-existing renal failure
  3. Increasing age.
147
Q

What is the treatment for Tumour lysis syndrome?

A
  1. Agressive hydration
  2. Monitor electrolytes
  3. Drugs to reduce uric acid production e.g. allopurinol
148
Q

What is hyperviscosity syndrome?

A

Increase in blood viscosity usually due to high levels of Ig

149
Q

Consequences of hyperviscosity syndrome

A

Vascular stasis

Hypoperfusion

150
Q

What is the presentation of hyperviscosity syndrome?

A 
Mucosal bleeding
Visual change 
Neurological distrubances
Breathlessness
Fatigue
151
Q

What investigations would you do in someone who has hyperviscosity syndrome?

A
  1. FBC and blood film –> look for rouleaux formation
  2. U and E
  3. Immunoglobulins
152
Q

What is the treatment of hyperviscosity syndrome?

A

Keep hydrated
Avoid blood transfusion
Treat the underlying cause

153
Q

What does rituximab target?

A

Targets CD20 on the surface of B2.

154
Q

How is myeloma bone disease usually asssessed?

155
Q

Haemophilia A is due to a deficiency of what clotting factor?

A

Factor 8 deficiency

156
Q

Haemophilia B is due to a deficiency of what clotting factor?

A

Factor 9 deficiency

157
Q

What anaemia could methotrexate cause?

A

Macrocytic due to folate deficiency

158
Q

Causes of folate deficiency

A
  1. Dietary
  2. Malabsorption
  3. Increased Requirement e.g. in pregnancy
  4. Folate antagonists e.g. methotrexate.
159
Q

Give 3 signs of haemolytic anaemia

A
  1. Pallor
  2. Jaundice
  3. Splenomegaly
160
Q

Give 4 causes of Haemolytic anaemia

A
  1. GP6D deficiency
  2. Sickle cell aenmia
  3. Sphereocytosis/eliptocytosis
  4. AI haemolytic anaemia.
161
Q

What 3 disorders can cause coagulation disorders?

A
  1. Vit K deficiency
  2. Liver disease
  3. Congenital e.g. Haemophilia.
162
Q

How does Heparin work?

A

Activates Antithrombin which inhibits thrombin and factor Xa

163
Q

What is disseminated intravascular coagulation?

A

Pathological activation of coagulation cascade –> Fibrin in vessel walls .

There is platelet and coagulation factor consumption

164
Q

Give 3 causes of disseminated intravascular coagulation (DIC)

A

Sepsis
Major Trauma
Malignancy

165
Q

What is the affect on TT, PTT and APTT in someone with DIC.

A

All increased

166
Q

What is the affect in fibrinogen in someone with DIC

167
Q

What is the affect of iron deficiency anaemia on iron binding capacity?

A

Iron binding capacity will be raised

168
Q

Why might measuring serum ferritin be inaccurate for looking at iron levels?

A

Ferritin is an acute phase protein so its concentration will increase in response to inflammation.

169
Q

What is aplastic anaemia?

A

When bone marrow stem cells are damaged –> Pancytopenia.

170
Q

How can multiple myeloma cause AKI?

A
  1. Deposition of Lighht chain
  2. Hypercalcaemia
    Hyperuricaemia
171
Q

Some patients with myeloma can present with blurred vision, gangrene and bleeding. What is the pathology behind this?

A

Paraproteins form aggregates in the blood which increase visoosity.

172
Q

Why are patients with myeloma be susceptible to recurrent infections.

A

Reduction in polyclonal Ig levels.

173
Q

What anaemia is seen in patients with multiple myeloma?

A

Normochromic normocytic.

174
Q

What chemotherapy agent is used in patients with myeloma?

A

VAD or CTD.

175
Q

What combination therapy is used in patients with non HL?

176
Q

Give 3 environmental causes of leukaemia

A

Radiation exposure
Benzene compounds
Drugs

177
Q

Give 3 clinical features of membranopathy

A
  1. Jaundice
    Anaemia
    Splenomegaly
178
Q

Why does a deficiency in Glucose-6-phosphate dehydrogenase cause shortened red cells life span

A

G6PD protects against oxidative damage

179
Q

What 3 blood test values are increased in polycythaemia?

Phase 2a Sheffield Medicine (10 decks)

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