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Year 2 Medicine @ Lancaster Uni > 2.06 - Haematological disorders and Blood > Flashcards

2.06 - Haematological disorders and Blood Flashcards

1
Q

What type of bacteria is c.diff?

A
  • Gram positive bacillus
  • Spore forming and toxing producing
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2
Q

In what percentage of the population is c.diff thought to be present?

A
  • Around 2%
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3
Q

What are the two different strains of c.diff?

A
  • Toxigenic
  • Non-toxigenic
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4
Q

What is toxigenic c.diff?

A
  • C.diff colonisation that produces and releases exotoxins A + B
  • (70%-90% of cases)
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5
Q

What is non-toxigenic c.diff?

A
  • An c.diff colonisation that does not cause illness
  • (10%-30% of cases)
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6
Q

How is c.diff spread?

A
  • Faecal-oral route
  • Highly infectious
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7
Q

How are c.diff spores adapted to survive?

A
  • Resistant to acid, heat and antibiotics
  • Mature into their fully functional state in the GIT
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8
Q

What is the principle symptom related to a c.diff infection?

A
  • Diarrhoea
  • Classified as three loose bowel motions in a 24hr period
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9
Q

What is seen in a mild c.diff infection?

A
  • Diarrhoea without systemic features
  • Typically ≤ 3 bowel movements a day
  • WCC normal
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10
Q

What is seen in a moderate c.diff infection?

A
  • 3-5 bowel motions a day
  • Raised WCC but less than 15x10^19/L
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11
Q

What is seen in a severe c.diff infection?

A
  • WCC > 15x10^19
  • Increased creatinine
  • Fevers above 38.5°
  • Evidence of severe colitis
  • Bowel motions less reliable
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12
Q

What is seen in a fulminant c.diff infection?

A
  • Signs of hypotension and shock
  • Partial or complete ileus
  • Toxic megacolon
  • CT evidence of disease
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13
Q

What is the biggest risk factor for developing a c.diff infection?

A
  • The use of antibiotics
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14
Q

What are some other risk factors involved in the development of a c.diff infection?

A
  • Antibiotics
  • Age ≥ 65 = Increased risk
  • Hospitalisation
  • Severe co-morbidities
  • PPI use
  • Obesity
  • GI surgery
  • Immunosuppresion or chemotherapy
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15
Q

What is haematopoiesis?

A
  • The process of when stem cells mature to make new mature cells
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16
Q

Where does haematopoiesis occur?

A
  • Bone marrow
  • Thymus
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17
Q

What is the first cell seen in haematopoiesis?

A
  • Multipotent hematopoietic stem cell
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18
Q

What can a multipotent hematopoietic stem cell split into?

A
  • Common myeloid progenitor
  • Common lymphoid progenitor
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19
Q

What can a common lymphoid progenitor cell divide into?

A
  • NK cell
  • Small lymphocyte
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20
Q

What can a small lymphocyte differentiate into?

A
  • T cell
  • B cell
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21
Q

From which cell type are plasma cells derived?

A
  • B cells
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22
Q

What cells can a common myeloid progenitor differentiate into?

A
  • Megakaryocyte
  • Erythrocyte
  • Mast cell
  • Myeloblast
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23
Q

From which cell type are platelets derived?

A
  • Megakaryocyte
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24
Q

What cells are derived from myeloblasts?

A
  • Basophils
  • Neutrophils
  • Eosinophils
  • Monocytes
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25
Q

What cells can monocytes develop into?

A
  • Macrophages
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26
Q

What is the function of mast cells?

A
  • Play a key role in allergy response as they can release histamine granules through degranulation
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27
Q

What is the function of monocytes?

A
  • Help to break down bacteria by maturing into macrophages and then phagocytosing foreign bodies
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28
Q

What is the function of lymphocytes?

A
  • Create antibodies to fight foreign bodies found in the circulation
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28
Q

What is the function of neutrophils?

A
  • Kill and digest bacteria and fungi
  • Most numerous and they are the first line of defence in the immune system
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29
Q

What is the function of basophils?

A
  • Secrete chemicals such as histamine to help control the immune response of the body
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30
Q

What is the function of eosinophils?

A
  • Attack and kill parasites and cancer cells found in the body
  • Also play a role in allergy response
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31
Q

What are the four main components of blood?

A
  1. Plasma (55%)
  2. RBC’s (44%)
  3. WBC’s (>1%)
  4. Platelets (>1%)
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32
Q

What is the function of plasma in the blood?

A
  • Contains proteins, minerals and vitamins in soluble form
  • Suspends other components
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33
Q

What is the function of RBC’s in the blood?

A
  • Contain haemoglobin which is responsible for delivering oxygen to respiring tissues
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34
Q

What is the function of WBC’s in the blood?

A
  • Help to fight infection and disease
  • Play a role in triggering immune response
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35
Q

What is the function of platelets in the blood?

A
  • Help form blood clots and prevention of bleeding
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36
Q

What is acute lymphoblastic leukemia (ALL)?

A
  • Proliferation of immature lymphocyte progenitor cells
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37
Q

Where does acute lymphoblastic leukemia (ALL) arise from?

A
  • Arises from the bone marrow
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38
Q

What is the epidemiology of acute lymphoblastic leukemia (ALL)?

A
  • Most common type of malignancy seen in children
  • Most common in 0-4 age group
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39
Q

What is the pathophysiological process seen in acute lymphoblastic leukemia (ALL)?

A
  • A lymphoid progenitor cell undegoes malignant transformation
  • Clonal expansion occurs
  • Lymphoid precursors replace other haematopoietic stem cells in bone marrow
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40
Q

From which cells does acute lymphoblastic leukemia (ALL) arise?

A
  • Mostly from B cells but can also develop from T cells
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41
Q

What condition is acute lymphoblastic leukemia (ALL) also associated with?

A
  • Down’s syndrome
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42
Q

What are the features seen in marrow failure?

A
  • Anaemia
  • Thrombocytopenia
  • Neutropenia
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43
Q

What can acute lymphoblastic leukemia (ALL) lead to in tissues?

A
  • Can lead to tissue infiltration
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44
Q

What are the symptoms associated with acute lymphoblastic leukemia (ALL)?

A
  • Pale skin
  • Fatigue
  • Breathlessness
  • Neutropenia (Recurrent infections)
  • Frequent brusing (Thromocytopenia)
  • Bone and joint pain (Tissue infiltration)
  • Unintentional weight loss
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45
Q

What clinical signs are seen inacute lymphoblastic leukemia (ALL)?

A
  • Fever
  • Fatigue
  • Angina
  • SOB
  • Hepatosplenomegaly lymphadenopathy = tissue infiltration
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46
Q

What are some of the causes and risk factors associated with acute lymphoblastic leukemia (ALL)?

A
  • More common in causcasian
  • Boys at slightly higher risk
  • Wide range of genetic implications
  • Risk increased when another genetic condition present
  • Exposure to ionising radiation increases risk
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47
Q

What are the cytogenic features of T12:T21?

A
  • Most common translocation seen in childhood acute lymphoblastic leukemia (ALL)
  • Results in TEL-AML gene fusion
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48
Q

What are the cytogenic features of T9:T22?

A
  • Known as Philadelphia chromosome
  • Associated with poor prognosis
  • Causes BCR-ABL gene fusion
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49
Q

What are the cytogenic features of T4:T11?

A
  • Results in the MLL-AF4 gene fusion
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50
Q

What are the cytogenic features of a hyperdiploid karyotype?

A
  • Seen in 30%-40% of children
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51
Q

What are the cytogenic features seen in a hypodiploid karyotype?

A
  • May also be seen
  • Associated with a poor prognosis
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52
Q

What are some features seen in tissue infiltration?

A
  • Lymphadenopathy
  • Hepatosplenomegaly
  • Bone pain
  • Mediastinal mass -> SVC obstruction
  • Testicular enlargement
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53
Q

What is leukostasis?

A
  • WBC infiltration causes capillary blockage
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54
Q

What are some symptoms seen in leukostasis?

A
  • Altered mental state
  • SOB
  • Headache
  • Visual changes
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55
Q

What is the definitive investigation for acute lymphoblastic leukemia (ALL)?

A
  • Bone marrow aspiration and biopsy
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56
Q

What will a blood count show in acute lymphoblastic leukemia (ALL)?

A
  • Decreased RBC’s and Hb
  • Decreased platelets
  • Decreased neutrophils
  • Increased WBC’s
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57
Q

What would be seen on a blood film in acute lymphoblastic leukemia (ALL)?

A
  • Large blast cells
  • > 20% of total but can be up to 100%
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58
Q

What is a DNA mutation that could be picked up by PCR sequencing in acute lymphoblastic leukemia (ALL)?

A
  • JAK-2 mutation
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59
Q

What imaging investigations can be performed in acute lymphoblastic leukemia (ALL)?

A
  • CXR
  • CT chest, abdomen and pelvis
  • CT/MRI head
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60
Q

What factors can be associated with a poorer prognosis in acute lymphoblastic leukemia (ALL)?

A
  • Increased age
  • Performance status > 1
  • WBC count - >30 for b cell, >100 T cell
  • Cytogenics (Philadelphia chromosome etc.)
  • Immunophenotype
  • CNS involvement
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61
Q

What are the management steps for acute lymphoblastic leukemia (ALL)?

A
  • Curative therapy (Chemotherapy + Antibiotics)
  • Bone marrow transplantation
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62
Q

What are the steps of chemotherapy used in acute lymphoblastic leukemia (ALL)?

A
  1. Pre-phase
  2. Induction
  3. Maintenance
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63
Q

What happens in the pre-phase of chemotherapy?

A
  • Steroids aim to reduce chance of tumor lysis syndrome (TLS)
  • Leucopheresis to reduce WBC count
  • Supportive therapy for anaemia and throbocytopenia
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64
Q

What happens in the induction phase of chemotherapy?

A
  • Aim to achieve complete remission or ideally complete molecular remission
  • CR = >5% blasts in marrow
  • CMR = no residue detected
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65
Q

What happens in the maintenance phase of chemotherapy?

A
  • Continued treatment that aims to reduce the risk of relapse
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66
Q

What steps can be taken to reduce the risk of relapse of acute lymphoblastic leukemia (ALL)?

A
  • Maintenance therapy
  • Allogenic stem cell transplant
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67
Q

What is acute myeloid leukemia (AML)?

A
  • Abnormal proliferation of myeloid progenitor cells
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68
Q

What is the epidemiology surrounding acute myeloid leukemia (AML)?

A
  • Around 3200 cases each year in the UK
  • Much more common in the over-60’s
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69
Q

What is the pathophysiological process behind acute myeloid leukemia (AML)?

A
  • Genetic mutations in myeloid progenitor cells cause proliferation of immature cells within the bone marrow
  • Leads to marrow failure
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70
Q

What are some symptoms associated with acute myeloid leukemia (AML)?

A
  • Recurrent infections
  • Petechiae
  • Nosebleeds
  • Easy bruising
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71
Q

What are some clincal signs associated with acute myeloid leukemia (AML)?

A
  • Fatigue
  • SOB
  • Angina
  • Lymphadenopathy
  • Hepatosplenomegaly
  • Bone pain
  • Gum hypertrophy
  • Violaceous plaques
  • Testicular enlargement
72
Q

What are some risk factors and causes of acute myeloid leukemia (AML)?

A
  • Myelodysplastic syndrome
  • Radiation exposure
  • Congenital disorders
  • Previous chemotherapy
  • Toxins (Benezene etc.)
73
Q

What would be seen in blood tests of someone with acute myeloid leukemia (AML)?

A
  • Normocytic anaemia
  • Thrombocytopenia
  • Reduced reticulocyte count
  • Circulating myeloblasts
74
Q

What hallmark feature would be seen on a blood film in acute myeloid leukemia (AML)?

A
  • Auer rods
75
Q

What results would be seen in a bone marrow aspiration of someone with acute myeloid leukemia (AML)?

A
  • Reduced erythropoiesis
  • Reduced megakaryocytes
  • > 20% blast cells but can be up to 100%
76
Q

What are the management options for acute myeloid leukemia (AML)?

A
  • Education
  • Holistic support
  • Cytoreduction
  • Tumor lysis
  • Chemotherapy
  • Stem cell transplant
77
Q

What are some complications caused by acute myeloid leukemia (AML)?

A
  • Leukostasis
  • Hyperviscosity syndrome
78
Q

Who has the best prognostic outlook in acute myeloid leukemia (AML)?

A
  • Children
  • 80% without recurrence after 5 years
79
Q

What key investigation is required for the formal diagnosis of acute myeloid leukemia (AML)?

A
  • Bone marrow biopsy and aspiration
80
Q

What is chronic lymphoblastic leukemia (CLL)?

A
  • A lymphoproliferative disorder of B lymphocytes due to abnormal clonal expansion of B cells that resemble mature lymphocytes
81
Q

What does chronic lymphoblastic leukemia (CLL) cause?

A
  • Lymphadenopathy
  • Immune deficiency
  • Cytopenias
82
Q

What is the pathophysiology around chronic lymphoblastic leukemia (CLL)?

A
  • An initial trigger event leads to genetic alteration -> monoclonal B lymphocyte lymphocytosis
  • Monoclonal B cell lymphocytosis is a pre-malignant disorder
  • Becomes CLL after further genetic mutations
83
Q

What are the symptoms associated with chronic lymphoblastic leukemia (CLL)?

A
  • Weight loss
  • Fevers
  • Anorexia
  • Night sweats
  • Lethargy
84
Q

What are the clinical signs seen in chronic lymphoblastic leukemia (CLL)?

A
  • Lymphadenopathy (Main one)
  • Hepatomegaly
  • Splenomegaly
85
Q

What are some gene alterations that contribute to the development of chronic lymphoblastic leukemia (CLL)?

A
  • TP53 - Major suppression gene
  • 11q and 13q14 deletions
  • Trisomy 12
  • Overexpression of BCL2 proto-oncogene (Increases cell volume)
  • NOTCH1 mutation - Normally regulates cell cycle
86
Q

What is the hallmark feature of chronic lymphoblastic leukemia (CLL)?

A
  • Lymphadenopathy caused by maligant B lymphocytes
87
Q

What is the epidemiology around chronic lymphoblastic leukemia (CLL)?

A
  • Most common leukemia in adults
  • Incidence increase with age
88
Q

What blood results are seen in chronic lymphoblastic leukemia (CLL)?

A
  • Hb low or normal
  • Increased WBC
  • Increased platelets
89
Q

What would be seen on a blood film in chronic lymphoblastic leukemia (CLL)?

A
  • Increased lymphocytes (>5x10^9)
89
Q

What would be seen in a bone marrow aspiration in chronic lymphoblastic leukemia (CLL)?

A
  • Maybe highly infiltrated with lymphocytes
90
Q

What immunological features would be seen in chronic lymphoblastic leukemia (CLL)?

A
  • CD19/20
  • CD5+ B cells
91
Q

What are the different management options for chronic lymphoblastic leukemia (CLL)?

A
  • Intensive chemotherapy
  • Allogenic stem cell transplant
92
Q

What is the first line chemotherapy treatment for chronic lymphoblastic leukemia (CLL)?

A
  • 1st line = Imatinib - tyrosine kinase inhibitor
93
Q

What is the second line chemotherapy treatment for chronic lymphoblastic leukemia (CLL)?

A
  • 2nd line = Dasatinib
94
Q

What is the third line chemotherapy treatment for chronic lymphoblastic leukemia (CLL)?

A
  • 3rd line = Nilotinib
95
Q

What are some common complication seen in chronic lymphoblastic leukemia (CLL)?

A
  • Autoimmune haemolytic anaemia
  • Immune thrombocytopenia
  • Hypogammaglobulinaemia
96
Q

What is the main diagnostic tool used for chronic lymphoblastic leukemia (CLL)?

A
  • Flow cytometry
  • Absolute B cell count
97
Q

Which different prognostic factors can be used in the guiding of treatment in chronic lymphoblastic leukemia (CLL)?

A
  • Lymphocyte doubling time
  • Genetic testing for abnormalities
  • Beta-2 microglobulin
98
Q

In which cases does chronic lymphoblastic leukemia (CLL) not need immediate treatment?

A
  • If asymptomatic with no poor prognostic factors then a watch and wait strategy is used
99
Q

In which two ways can chronic lymphoblastic leukemia (CLL) be staged?

A
  • Binet staging
  • Rai staging
100
Q

What are the different grades seen in Binet staging for chronic lymphoblastic leukemia (CLL)?

A
  • Stage A - < 3 lymphoid sites
  • Stage B - ≥3 lymphoid sites
  • Stage C - Presence of anaemia and/or thrombocytopenia
101
Q

What are the different grades seen in Rai staging of chronic lymphoblastic leukemia (CLL)?

A
  • Stage 0 - Lymphocytosis (25%)
  • Stage I-II - Lymphocytosis + lymphadenopathy + Organomegaly (50%)
  • Stage III-IV - Lymphocytosis + anaemia / thrombocytopenia +/- lymphadenopathy/organomegaly (25%)
102
Q

What factors help to adjudge the type of treatment required in chronic lymphoblastic leukemia (CLL)?

A
  • Fitness/Performance
  • Significant health conditions
  • Mutational analysis
  • Treating relapse/refractory disease
103
Q

What are the different pharmacotherapy options available in chronic lymphoblastic leukemia (CLL)?

A
  1. Chemotherapy
  2. Small molecule inhibitors
  3. Monoclonal antibodies
  4. Corticosteroids (Dexamethasone)
104
Q

What are examples of chemotherapy agents used in chronic lymphoblastic leukemia (CLL)?

A
  • Chlorambucil
  • Fludarabine
  • Bendamustine
105
Q

What are examples of small molecule inhibitors used in chronic lymphoblastic leukemia (CLL)?

A
  • Ibrutinib - tyrosine kinase inhibitor
  • Idealalisib - phosphoinositide 3-kinase inhibitor
106
Q

What monoclonal antibodies are used in the treatment of chronic lymphoblastic leukemia (CLL)?

A
  • Rituximab - Anti CD20 antibodies
  • Targets B lymphocytes
107
Q

What corticosteroids are used in chronic lymphoblastic leukemia (CLL)?

A
  • Dexamethasone - For the treatment of complications
108
Q

What is chronic myeloid leukemia (CML)?

A
  • A clonal myeloproliferative neoplasm that is characterised by abnormal clonal expansion of cells in the myeloid lineage
109
Q

What is the epidemiology around chronic myeloid leukemia (CML)?

A
  • Annual incidence of around 1-2 cases per 100,00 people
110
Q

What is the hallmark cytogenic finding seen in chronic myeloid leukemia (CML)?

A
  • Philadelphia chromosome - translocation between chromosome 9 and 22
111
Q

What does a Philadelphia chromosome cause?

A
  • Tyrosine kinase activation
112
Q

What is the disease progression pathway seen in chronic myeloid leukemia (CML)?

A
  • Chronic phase - fatigue, weight loss (Around 3-5 years without treatment)
  • Aggressive phase - more serious symptoms (6-18 months
  • Blast phase - resembles AML, shown by rapid expansion
113
Q

What are the symptoms seen in chronic myeloid leukemia (CML)?

A
  • Fatigue
  • SOB
  • Angina
  • Thrombocytosis symptoms
  • Leukostasis symptoms
  • Weight loss
  • Night sweats
  • Bone pain
  • Abdominal pain
114
Q

What are some caues and risk factors relating to chronic myeloid leukemia (CML)?

A
  • Rare in children
  • Older age
  • Being male
  • Radiation exposure
115
Q

What blood results would be seen in chronic myeloid leukemia (CML)?

A
  • Lymphocytosis
  • Neutrophilia
  • Basophilia
  • Eosinophilia
  • Anaemia
  • Thrombocytosis
116
Q

What would be seen on a blood film in chronic myeloid leukemia (CML)?

A
  • Immature and mature myeloid cells
117
Q

What mutation helps to guide the treatment of chronic myeloid leukemia (CML)?

A
  • BCR-ABL1
118
Q

What are the three types of treatment used in chronic myeloid leukemia (CML)?

A
  1. TK inhibitors
  2. Intensive chemotherapy
  3. Stem cell transplant
119
Q

What are the types/generations of TKI’s used in chronic myeloid leukemia (CML)?

A
  • 1st gen - Imatinib
  • 2nd gen - Dasatinib
  • 2nd gen - Nilotinib
120
Q

What is the expected 5 year survival rate in those 15-64 with chronic myeloid leukemia (CML)?

A
  • Around 90%
121
Q

What is the expected 5 year survival rate seen over 65’s with chronic myeloid leukemia (CML)?

A
  • Around 40%
122
Q

At which stage of chronic myeloid leukemia (CML) is chemotherapy used?

A
  • Used for those in the blast phase of disease
  • Patients must be fit enough to handle to treatment
123
Q

What is Hodgkin’s lymphoma?

A
  • Haematological malignancy that arises from lymphoid tissue
  • Characterised by the presence of Reed-sternberg cells
124
Q

What are the different sub-types of Hodgkin’s lymphoma?

A
  • Nodular sclerosis
  • Mixed cellularity
  • Lymphocyte rich
  • Lymphocyte depeleted
125
Q

What are is nodular sclerosis in relation to Hodgkin’s lymphoma?

A
  • Most common (70%)
  • Large mediastinal masses in nodes
  • Fibrotic bands
126
Q

What is modular cellularity in relation to Hodgkin’s lymphoma?

A
  • No fibrotic bands
  • Mixed infiltrates with many leukocyte types
127
Q

What is lymphocyte-rich Hodgkin’s lymphoma?

A
  • Lots of small lymphocyte invasions seen
  • Best prognosis
128
Q

What is lymphocyte-depeleted Hodgkin’s lymphoma?

A
  • Shown by poporn cells
  • Worst prognosis
129
Q

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

A
  • Lymphocyte-rich
130
Q

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

A
  • Lymphocyte-depleted
131
Q

What is the pathophysiological process behind Hodgkin’s lymphoma?

A
  • B cells become reed-sternburg cells and stop expressing surface Ig’s due to destructional mutations of Ig genes
  • These would usually go through apoptosis but they begin to produce their own growth factors
  • Cease to perform their normal function
132
Q

What are some symptoms seen in Hodgkin’s lymphoma?

A
  • Mediastinal mass
  • Pruritis
  • Malaise
  • Fatigue
  • Alcohol induced pain at site
133
Q

What symptoms are seen with a mediastinal mass relating to Hodgkin’s lymphoma?

A
  • SOB
  • Chest pain
  • Cough
  • SVC obstructions
134
Q

What are some clinical signs seen in Hodgkin’s lymphoma?

A
  • Painless, firm lymph nodes
  • Splenomegaly
  • ‘B’ symptoms - fever, night sweats, weight loss
135
Q

What are some potential causes of Hodgkin’s lymphoma?

A
  • HIV
  • EBV
  • Autoimmune conditions
  • Family history
136
Q

What would be seen in the blood results of someone with Hodgkin’s lymphoma?

A
  • Normocytic anaemia
  • Possible lymphocytopenia
  • Eosinophilia
  • ESR may be raised
137
Q

What would be seen on the blood film of someone with Hodgkin’s lymphoma?

A
  • Reed-Sternburg cells
138
Q

What would a CT scan show in Hodgkin’s lymphoma?

A
  • Shows involvement of intrathoracic nodes
139
Q

What is Ann arbor staging in relation to Hodgkin’s lymphoma?

A
  • Stage 1 - Confined to one region
  • Stage 2 - In more than one region but same side of diaphragm
  • Stage 3 - Affects both side of diaphragm
  • Stage 4 - Widespread involvement including non-lymphatic organs
140
Q

What is the preferred biopsy type performed in Hodgkin’s lymphoma?

A
  • Excision biopsy
  • Preferred over aspiration or core biopsy
141
Q

What are the three grouping seen in Lugano staging in relation to Hodgkin’s lymphoma?

A
  • Limited disease
  • Bulky disease
  • Advanced
142
Q

What are the usual treatment options used for Hodgkin’s lymphoma?

A
  • Chemotherapy
  • Radiotherapy
143
Q

What is a common chemotherapy regimen used for Hodgkin’s lymphoma?

A

A - Adriamycin - Inhibits topoisomerase II
B - Bleomycin - Inhibits DNA synthesis
V - Vinblastine - Inhibits microtubule formation
D - Dacarbazine - Alkylating agent

144
Q

What precaution should be taken in blood transfusions with someone with Hodgkin’s lymphoma?

A
  • The blood should be irradiated to reduce transfusion associated risks
145
Q

What is the prognostic outlook for someone with limited disease in Hodgkin’s lymphoma?

A
  • 90% survival in 5 years
146
Q

What is the prognostic outlook for someone with advanced disease in Hodgkin’s lymphoma?

A
  • 75% survival in 5 years
147
Q

What is non-hodgkins lymphoma?

A
  • Haematological malignancy that arises from lymphoid tissue
  • Characterised by LACK OF Reed-Sternburg cells
148
Q

What percentage of non-hodgkins lymphoma arises from B and T cells?

A
  • 70% = B cells
  • 30% = T cells
149
Q

What are some examples of types of non-hodgkins lymphoma?

A
  • Burkitt lymphoma
  • MALT lymphoma
  • Diffuse large B cell
150
Q

How many subtypes of non-hodgkins lymphoma is there?

A
  • Over 60 subtypes
151
Q

What is the epidemiology around non-hodgkins lymphoma?

A
  • 14,000 cases in the UK
  • With 80-84 year olds most commonly affected
152
Q

What are the general symptoms associated with non-hodgkins lymphoma?

A
  • Fever
  • Night sweats
  • Weight loss
153
Q

What are the symptoms associated with B-cell non-hodgkins lymphoma?

A
  • Painless
  • Less aggressive
154
Q

What are the symptoms associated with T cell non-hodgkins lymphoma?

A
  • Usually have skin infiltrations
  • More aggressive
155
Q

What are the clinical features associated with non-hodgkins lymphoma?

A
  • Lymphadenopathy
  • Pruritis
  • Splenomegaly
  • Hepatomegaly
156
Q

What are the features of an oncological emergency associated with non-hodgkins lymphoma?

A
  • SVC obstructon
  • Cord compression
  • Tumor lysis syndrome
  • Neutropenic sepsis
  • Hypercalcaemia
157
Q

How is a distinction made between B cell and T cell non-hodgkins lymphoma?

A
  • Immunophenotyping of samples
158
Q

What test is required for a confirmed non-hodgkins lymphoma diagnosis?

A
  • Excision biopsy
159
Q

What feature is senn in very aggressive non-hodgkins lymphoma?

A
  • Very high uric acid levels -> Renal failure
160
Q

Why is Ig testing important in non-hodgkins lymphoma?

A
  • To judge whether it is IgA or IgM as this can influence treatment options
161
Q

What are causes or risk factors associated with non-hodgkins lymphoma?

A
  • HIV
  • Epstein-barr virus
  • H. Pylori
  • Hep B/Hep C infection
  • Exposure to chemicals (trichloroethylene)
  • Family history
162
Q

Exposure to which chemical can increase the risk of non-hodgkins lymphoma?

A
  • Trichloroethylene
163
Q

What are the different Lugano stages used in non-hodgkins lymphoma?

A
  1. B symptoms
  2. Extranodal involvement
  3. Bulky disease
164
Q

What is a common chemotherapy regimen used in non-hodgkins lymphoma?

A

R-CHOP (R-CDVP)
- R - Rituximab - Anti-CD20
- C - Cyclophosphamide - Alkylating agent
- D - Doxorubicin - An anthracycline (Inhibits topoiso. II)
- V - Vincristine - Inhibits microtuble formation
- P - Prednisolone - Glucocorticosteroid

165
Q

What is the most common type of non-hodgkins lymphoma?

A
  • Diffuse large B cell lymphoma
166
Q

Which type of non-hodgkins lymphoma is high grade and effects children the most?

A
  • Burkitt’s lymphoma
167
Q

How can remission be maintained in non-hodgkins lymphoma?

A
  • Alpha interferons
  • Rituximab
168
Q

How can anaemia by classified?

A
  • Mean corpuscal volume (MCV)
169
Q

What is macrocytic anaemia in terms of MCV?

A
  • Increase in MCV
  • > 99 (femtolitres)
170
Q

What is normcytic anaemia in terms of MCV?

A
  • Normal MCV
  • 80-99 (femtolitres)
171
Q

What is microcytic anaemia in terms of MCV?

A
  • Decrease in MCV
  • <82 (femtolitres)
172
Q

What are the two main types of macrocytic anaemia?

A
  • Megaloblastic
  • Non-megaloblastic
173
Q

What are some causes of megalobastic macrocytic anaemia?

A
  • B12 deficiency (Eg. Pernicious anaemia)
  • Folate deficiency (Diet insufficiency)
174
Q

What are some causes of non-megaloblastic anaemia?

A
  • Alcohol
  • Reticulocytosis
  • Liver disease
  • Hypothyroidism
175
Q

What are some causes of normocytic anaemia?

A
  • Blood loss
  • Autoimmune
  • Sickle cell
  • Aplastic
  • G6PD deficiency
  • Spherocytosis
  • Elliptocytosis
176
Q

What are some causes of microcytic anaemia?

A
  • Iron deficiency
  • Thalassaemia
  • Anaemia of chronic disease
  • Sideroblastic

Year 2 Medicine @ Lancaster Uni (15 decks)

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