Week 3: Haematology Flashcards
1
Q
What is haemopoiesis?
A
The process of blood cell formation
2
Q
What are the different sites of haemopoiesis throughout life?
A
FOETUS: 0-2 months = yolk sac 2-7 months = liver, spleen 5-9 months = bone marrow INFANT = all bone marrow ADULT = red bone marrow (vertebrae, ribs, sternum, femur)
3
Q
What are the characteristics of haemopoietic stem sells?
A
Self renew, unspecialised, ability to differentiate, rare, quiescent
4
Q
Where are haemopoietic stem cells found?
A
Red bone marrow
Peripheral blood after treatment with G-CSF
Umbilical cord blood
5
Q
What is symmetrical and asymmetrical division?
A
Symmetrical = contraction of stem cell number/ expansion of stem cell number Asymmetrical = maintenance of stem cell numbers
6
Q
What is the stroma?
A
The bone marrow microenvironment that supports the developing haemopoietic cell
Rich environment for growth and development of stem cells
7
Q
What are some stromal cells?
A
macrophages fibroblasts endothelial cells fat cells reticulum cells
8
Q
What is leukaemogenesis?
A
A multi step process
Neoplastic cell is HSC or early myeloid/lymphoid cell
Dysregulation of cell growth and differentiation
Proliferation of leukaemic clone with differentiation blocked at early stage
9
Q
What is a CLONAL stem cell disorder?
A
Haematological malignancy arising from a single ancestral cell
10
Q
What is the evidence of a clonal stem cell disorder?
A
- Carry unique rearrangement of immunoglobulin or TcR gene
- In leukaemia clonal proliferation carries an active maternal or paternal X chromosome
- Acquired cytogenetic/molecular change arising during development of a malignancy [eg philadelphia translocation in CML]
11
Q
Define myeloproliferative disorders
A
Clonal disorders of haemopoiesis leading to increased numbers of one or more mature blood progeny
12
Q
What mutations are myeloproliferative disorders associated with?
A
JAK2V617F and calreticulin
13
Q
What is essential thrombocytosis?
A
High platelets (>600x10^9)
Features:
Thrombotic complication
Haemorrhagic complications
Splenomegaly
14
Q
How is high risk essential thrombocytosis managed?
A
1st line = hydroxycarbamide + aspirin
2nd line = anagrelide + aspirin
IFNa - useful in management during pregnancy
JAK2 inhibitors
15
Q
What are JAK2 mutations?
A
JAK 2 mutations result in continuous activation of JAK receptor regardless of ligand binding
16
Q
What are JAK 2 inhibitors?
A
Eg ruxolitinib
Inhibits JAK1/2
Side effect = thrombocytopaenia
17
Q
Define myelodysplastic syndromes
A
Characterised by dysplasia dn ineffective haemopoiesis in >1 of the myeloid series.
Characterised by progressive bone marrow failure
18
Q
What are the clinical features of MDS?
A
predominantly affects elderly
Majority present with fatigue due to anaemia
19
Q
How is MDS managed?
A
Supportive care - blood and platelet transfusion
Growth factors: EPO + granulocyte colony stimulating factor (G-CSF)
Immunosuppression
Low dose chemotherapy (eg hydroxycarbamide)
Demethylating agent
Intensive chemo
Allogeneic stem cell transplantation
20
Q
What is Fanconi Anaemia?
A
Aplastic anaemia
Bone marrow failure
Autosomal recessive
21
Q
What are the characteristics of Fanconi anaemia?
A
Somatic abnormalities Bone Marrow Failure Short Telomeres Malignancy Chromosome Instability
22
Q
What are some abnormalities in Fanconi Anaemia?
A
microphthalmia
GU/GI malformation
Mental retardation
Hearing loss
23
Q
How is Fanconi anaemia treated?
A
Gold standard = allogeneic stem cell transplant
Other options: supportive care, corticosteroids, androgens
Lifetime surveillance for secondary tumours
24
Q
Name the main types of stem cell transplant and define them
A
Autologous: use patients own blood stem cells
Allogeneic: stem cells come from donor
25
What are the different types of donors?
```
Syngeneic: between identical twins
Allogeneic: HLA identical
Haplotype identical: half matched family member
Volunteer unrelated
Umbilical cord blood
```
26
Explain autologous stem cell transplants
Indications: relapsed Hodgkins disease, non Hodgkins Lymphoma, myeloma
Almost all use mobilised peripehral blood stem cells harvested by apheresis
Patients receive G-CSF to make stem cells leave bone marrow to be collected from blood
27
Explain allogeneic stem cell transplants
Can use peripheral blood stem cells, bone marrow or umbilical cord blood
Indications: acute/chronic leukaemias, relapsed lymphoma, aplastic anaemia, hereditary disorders
In malignant disease it has the benefit of graft vs leukaemia effect (at the expense of graft vs host disease)
28
Explain volunteer unrelated donor transplants
70% chance of finding a VUD
Increased risk of GvHD compared to family donor
Majority are caucasian
29
What are some recent advances in stem cell transplants?
Non-myeloablative SCT: low dose, less toxic, prove immunosuppression
Cord blood transplant
Donor lymphocyte infusion after SCT: prevents or treates relapse after SCT
30
Explain umbilical cord blood transplants
Blood collected from umbilical cord and placenta
Cells are tissue types and frozen in liquid nitrogen in cord blook banks
Advantage: more rapidly available than VUD, less rigorous matching to patient as immune system naive
Disadvantage: small amount (often need double cord transplant), slower angraftment, can't have DLI if relapsed
31
Explain graft versus host disease
Occurs in patients with allogeneic transplant
Donor's immune system recognises hosts body as foreign and starts to attack it
Manifestation: rash, jaundice, diarrhoea
Types: acute (1st 100 days), chronic (after first 100 days)
Treated with immunosuppressants
32
Explain graft versus leukaemia
Cels which cause GvHD also attack leukaemia cells
| Doesn't occur in autologous transplant as there's no GvHD
33
What are the problems with a stem cell transplant?
```
Limited donor availability
Risk of mortality
GvHD
Immunosuppression
Infertility
Risk of cataracts/osteoporosis
Hypothyroidism
Relapse
```
34
What does normal red cell production involve?
EPO, genes, iron, B12, folate, minerals, functioning bone marrow
35
What is the difference between anaemia and polycythaemia?
```
Anaemia = not enough red cell production
Polycythaemia = too much red cell production
```
36
What is the main function of red blood cells?
Gas transfer: CO2 removal, O2 delivery from lungs to tissues
37
What is haemoglobin made from?
4 globin chains (2a, 2B), 4 haem groups (1/globin chain)
38
Explain Hb binding with oxygen
Hb can reversibly bind to oxygen without undergoing oxidation or reduction
39
How is iron transported in plasma?
Transferrin
40
What is transferrin?
```
Used in plasma iron transport
Glycoprotein
Synthesised in hepatocytes
2 iron binding domains
Delivers iron to all tissues, erythroblasts, hepatocytes, muscle
```
41
How is iron stored in macrophages?
As derritin
| Serum ferritin is in proportion with RES iron. The problem is that serum ferritin is an acute phase protein
42
How is iron absorbed from the intestine?
Fe2+ (haem iron) diffuses into enterocyte, Fe3+ (non haem iron) is transported into the enterocyte by DMT1
Fe2+ is transported out of the enterocyte by hepcidin
43
How are effete red blood cells removed from the blood?
By macrophages of the reticuloendothelial system
44
How is RES iron stored?
as ferritin/haemosiderin
45
How is Tf-iron taken up?
via Tf receptors on erythroblasts, hepatocytes etc
46
How is iron metabolism regulated?
Hepcidin is most important in regulating iron metabolism.
It reduces levels of iron in plasma
Hepcidin binds ferroportin and degrades it (- reduces iron absorption and decreases iron release from RES)
Synthesised in liver
47
What is IDA?
Commonest anaemia where there aren't enough healthy RBCs.
| Microcytic Hypochromic
48
What could microcytic hypochromic RBCs mean?
IDA (not enough haem)
Thalassaemia (not enough globin)
ACD (anaemia of chronic disease)
Sideroblastic anaemia
49
What is the link between serum ferritin and IDA?
Low serum ferritin always indicated low RES iron stores (but remember it's an acute phase protein)
50
What are some physical signs of iron deficiency anaemia?
Koilonychia
Atrophic glossitis
Angular stomatitis
51
What are some causes of IDA?
DIetary (premature neonates, adolescent females), malabsorption, blood loss
52
What is the golden rule of IDA?
IDA in males and post-menopausal females is due to GI blood loss until proven otherwise
53
How is IDA treated?
The treatment is iron replacement and not blood transfusion
Ferrous sulphate 200mg
Ferrous gluconate 300mg
IV iron
54
When would you use IV iron replacement?
Intolerance of oral iron
Compliance issues
Renal anaemia and EPO replacement
55
What is anaemia of chronic disease?
Failure of iron utilisation eg Fe trapped in RES
56
What are the basic causes of anaemia of chronic disease?
Infection
Inflammation
Neoplasia
57
What does anaemia of chronic renal failure involve?
ACD + reduced EPO
58
What would the lab values be in anaemia of chronic disease?
```
MCV/MCH (mean corpuscular volume) N/down
ESR up
Ferritin N/up
Iron down
TIBC (total iron binding capacity) down
```
59
What are RBC rouleaux?
Aggregations of RBCs
| These occur when ESR is raised
60
What mechanisms cause anaemia of chronic disease?
RES iron blockade; iron trapped in macrophage; raised hepcidin levels
Reduced EPO response
Depressed marrow activity
61
why are B12 and folate needed?
They're essential for DNA synthesis and nuclear maturation
Required for all dividing cells, deficiency noted first in red cells
Deficiency results in megaloblastic anaemia initially
62
What processes is vitamin B12 needed for?
B12 = cobalamin
Methylation of homocysteine to methionine
Methylmalonyl-CoA isomerisation
63
How is vitamin B12 absorbed in the gut?
Binds to intrinsic factor
Absorbed in ileum
Binds to transcobalamin
64
How is folate absorbed in the gut?
Mostly in the small bowel. No carrier molecule is required.
65
How does lack of B12/folate cause anaemia?
Disparity in rate of synthesis of precursors of DNA - leads to abnormal cell division
ie dissociation between nuclear and cytoplasmic development
66
What is B12/folate deficiency anaemia?
Dissociation between nuclear and cytoplasmic development
Ineffective eryhtropoiesis - death of mature cells while still in marrow
Raised bilirubin, raised LDH
67
What tissues are affected by B12/folate deficiency?
Bone marrow, epithelial surfaces (mouth, stomach, small intestine, urinary, female genital tract)
68
What does clinical B12 deficiency result in?
Blood abnormalities: megaloblastic anaemia (leucopaenia, thrombocytopaenia)
Neurological manifestations: bilateral peripheral neuropathy or demyelination of posterior and pyramidal tracts of spinal cord
69
What does clinical folate deficiency result in?
Blood abnormalities: megaloblastic anaemia (leucopaenia, thrombocytopenia)
Growing foetus: in 1st 12 weeks deficiency causes neural tube defects
70
What are the symptoms/signs of anaemia/cytopaenia?
```
tired (macrocytic/megaloblastic),
easy bruising (thrombocytopaenic),
mild jaundice (haemolysis),
neurological problems (nerve disturbance after B12 deficiency)
```
71
What are some causes of general deficiency?
Intake
Absorption
Utilisation
Loss
72
What is pernicious anaemia?
Anaemia caused by vitamin B12 deficiency
73
What are causes of folate deficiency?
Dietary
Extensive small bowel disease (coeliac/severe Crohns)
Increased cell turnover (haemolysis, skin disorders)
74
What are the causes of B12 deficiency?
Dietary
Pernicious anaemia
Gastrectomy/achlorhydria
Terminal ileum problem (Crohn's/resection)
75
What are causes of macrocytosis other than B12/folate deficiency?
Reticuocytosis
| Cell wall abnormality
76
What are haemoglobinopathies?
Relative lack of normal globin chains due to absent genes
77
What does the severity of haemoglobinopathies depend on?
Amount of abnormal haemoglobin
Type of abnormal haemoglobin
Ameliorating factors
78
What are the genetics of Hb production?
Haem synthesis takes place from proerythroblast to reticulocyte stage of red cell precursor
Transcription of each gene is controlled by promoter genes at 5' end and influenced by upstream locus control elements
79
What are thalassaemias?
A relative lack of globin genes
4 alpha globin genes
2 beta globin genes
80
What is the clinical significance of alpha thalassaemia?
missing one gene = mild microcytosis
missing two genes = microcytosis, inc red cell count, ver mild anaemia
missing three genes = significant anaemia and bizarre shaped small red cells
missing four genes = incompatible with life
81
What is HbH disease?
Haemoglobin H disease
Missing 3 alpha genes
Lack of alpha chains -> excess beta chains
Beta chains end up joining together
82
What is beta thalassaemia?
Missing B genes
| Common in Greek Cypriots (1/7)
83
What is beta thalassaemia major?
```
Missing both beta globin genes
Autosomal recessive
Unable to make adult haemoglobin
Significant dyserythropoiesis
Transfusion dependant from early life (iron overload has major effect on life expectancy)
```
84
What are some haemoglobin variant diseases?
```
Thalassaemia
Sickle cell anaemia
Hb C
Hb D
Hb E
```
85
What is the pathogenesis of sickle cell disease?
Polymerisation of Hb S occurs which results in altered beta Hb chains
86
What is the clinical result of sickle cell anaemia?
Reduced red cell survivial (haemolysis), vasoocclusion (tissue hypoxia/infarction)
87
How does sickle cell anaemia affect other systems?
Brain - stroke, moya moya
Lungs - acute chest syndrome
Bones - dactilytis
Spleen - hyposplenic
88
What is the treatment of sickle cell disease?
1. PREVENTING CRISES - hydration, prophylactic vaccine/antibiotics, folic acid
2. MANAGING CRISES - O2, fluids, analgesia, antibiotics, bone transfusion
3. BONE MARROW TRANSPLANT
89
What is haemolytic anaemia?
Increased red cell destruction
Anaemia related to reduced RBC lifespan
No blood loss
No haematinic deficiency
90
What is congenital haemolytic anaemia?
Abnormality of RBC membrane
91
What is hereditary spherocytosis?
```
A congenital haemolytic anaemia
Abnormality of RBC membrane
Autosomal dominant
RBC spherocytic and polychromatic
Jaundice
Splenomegaly
Treatment = splenectomy and hyposplenic prophylaxis
```
92
What is the hyposplenic state?
Hyposplenism = acquired disorder
caused by several haematological and immunological diseases
Rises from encapsulated organisms - pneumococcus, meningococcus, haemophilus, immunisation, long term penicillin V
93
What is pyruvate kinase deficiency anaemia?
Chronic/extravascular haemolytic anaemia
ATP depletion
Autosomal recessive
94
What is Glucose-6-phosphate dehydrogenase deficinecy?
Acute episodic intravascular haemolysis
X linked recessive
Acute haemolysis from oxidative stress (Favism, Drugs - antimalarials, sulphonamides)
95
What are the types of acquired haemolytic anaemia?
Autoimmune - warm type (IgG), cold type (IgM)
Isoimmune - haemolytic disease of newborn
Non-immune - fragmentation haemolysis
96
What is cold autoimmune haemolytic anaemia?
Autoantibody IgM + complement
Mycoplasma infection
Idiopathic
Treatment: self limiting mycoplasma, idiopathic, keep warm
97
What are cold agglutinins?
Autoantibodies that mistakenly target red blood cells.
They cause RBCs to clump together when exposed to cold temperatures and increase the likelihood that the affected RBCs will be destroyed by the body.
98
What is warm autoimmune haemolytic anaemia?
```
Autoantibody IgG (+/- complement)
Cause: Idiopathic 30%, lymphoproliferative disorder, other autoimmune disease, drug induced
RBC spherocytic and polychromatic
```
Treatment: stop drugs, steroids, immunosuppression, splenectomy
99
What is the direct coombs test?
Purpose is to detect antibody on RBC surface. Positive means AIHA or haemolytic disease of newborn
100
What is the purpose of the indirect coombs test?
To detect RBC antibodies in plasma
101
How can leukaemia be classified?
Acute - AML, ALL
| Chronic - CML, ALL
102
What is leukaemia?
Accumulation of white blood cells (leucocytes)
Blood cancer
Accumulation of abnormal leucocytes in marrow/blood/other tissues
103
What's the difference between chronic and acute leukaemia?
```
Chronic = symptoms from accumulation of cells
Acute = symptoms from marrow failure
```
104
What is MDS (myelodysplastic syndrome)?
A clonal blood disorder
| Characterised by failure of effective haemopoiesis and dysplastic blood and marrow
105
How do you establish between low risk and high risk MDS?
Proportion of blast cells in marrow and cytogenetic profile
106
How is MDS treated?
It is untreatable other than stem cell transplant
107
What are myeloproliferative disorders?
Clonal blood disorders. The JAK2 mutation is prevalent. Characterised by too much haemaopoiesis
108
What are examples of MPDs?
Too many platelets = essential thrombocythaemia
Too many RBC = polycythaemia vera/ primary polycythaemia
Too much fibrous tissue = myelofibrosis
109
What is myelofibrosis?
```
Too much fibrous tissue
Difficult to manage
Large spleen
Systemic symptoms
Incurable other than SCT
Can use JAK2 inhibtors
```
110
What is acute leukaemia?
A clonal blood disorder
Blastic proliferation in bone marrow
Rapid onset
Serious compromise of normal marrow elements
111
What is the aetiology of AML?
largely unkown
Chemicals
Chemo/radiotherapy
genetics
112
What are signs of AML?
```
rapid onset of symptoms
lethargy
infection
bone pain
lymphadenopathy
```
113
How is AML diagnosed?
Peripheral bloods - anaemia, neutropaenia, thrombocytopaenia, blasts
114
How is AML managed?
Intensive chemo
Low dose chemo
Supportive care only
115
What is the clinical presentation in ALL?
Limping child
purpuric rash
Unexplained bone pain
116
How is ALL managed?
Chemo: Prednisolone, cyclophosphamide, vincristine. Initial aggressive therapy then oral maintenance
Supportive: blood transfusion, platelet transfusion, ABx, G-CSF
117
What are the presenting features of CLL?
```
none
lethargy
night sweats
weight loss
anaemia symptoms
lymphadenopathy
infection
```
118
How is CLL diagnosed?
Clonal population of B lymphocytes
| Unique immunophenotype
119
How is CLL staged?
```
With BINET staging
Stages:
A = <3 nodes involved
B = >3 nodes involved
C = anaemia or thrombocytopaenia
```
120
What is BINET?
A type of clinical staging for CLL
A = <3 nodes involved
B = >3 nodes invovled
C = anaemia or thrombocytopaenia
121
What are the immune complications of CLL?
Autoimmune haemolytic anaemia
| Autoimmune thrombocytopaenia
122
When do you treat patients with CLL?
Symptoms = sweat, weight loss, symptomatic nodes
Bone marrow failure = anaemia, thrombocytopaenia
Don't treat asymptomatic patients
123
What is the clinical presentation of CML?
```
Fatigue
Weight loss
Night sweats
Abdominal discomfort
Splenomegaly
Asymptomatic
```
124
What is the natural history of CML?
1. 3-5 years = chronic phase
2. 12 - 18 months = accelerated phase
3. 3-6 months = myeloid blast phase
125
How is CML diagnosed?
Blood film and clinical features
MOlecular test on blood (BCR-ABL)
Cytogenetic analysis (karyotype)
126
What mutation must people have for CML
Philadelphia translocation - BCR-ABL
127
How is CML treated?
Imatinib - blocks action of BCR-ABL
128
What are complications in CML treatment?
Imatinib resistance
Imatinib intolerance
Need for 2nd/3rd line TKI inhibitors
Accelerated phase/blast crisis
129
In what ways do chronic and acute leukaemias differ?
```
Cell of origin
Biology and genetics
presentation
complications
management
outcome
```
130
What are lymphocytes
White blood cells that form part of the immune system
They help protect the body against infective and other foreign agents
Some produce antibodies and others have a direct action against pathogens
131
Describe B cells
Produced in bone marrow from stem cell progenitor
mature B cells circulate in peripheral blood and populate lymphoid and other organs
Interaction with antigens results in: memory B cells, plasma cells
132
Describe T cells
T cells originate in bone marrow from stem cell progenitor
Precursor T cells migrate to the thymus where they develop into mature T cells
Mature T cells circulate in peripheral blood and populate lymphoid and other organs
133
What is the size of a lymphocyte population determined by?
Rate of division
| Rate of programmed cell death/apoptosis
134
What is lymphoma?
Malignancy derived from lymphocytes.
Generally presents with a tumour mass
Commonly in lymph nodes
135
What are risk factors for lymphoma?
Immuno-suppressive disorders/treatments
Infections
Age
Genetics
136
How does lymphoma arise?
Genetic abnormalities in lymphocytes result in altered gene expression. So there's altered growth and the balance between cell birth and death favours net growth of the tumour
137
What's the difference between leukaemia and lymphoma?
```
Leukaemia = widespread involvement of bone marrow and peripheral blood
Lymphoma = discrete tissue masses
```
138
How is lymphoma diagnosed?
Biopsy (excision or core)
139
What are the problems in diagnosis of lymphoma?
Malignant lymphocytes in NHL look like normal lymphocytes
| Morphology alone may not be able to tell if tissue is malignant
140
How is lymphoma classified?
Based on: morphology, immunophenotype, genetic features
141
What are the general categories of lymphoma?
Non Hodgkins
| Hodgkins
142
What is low grade lymphoma?
Neoplastic cells mostly of small side (low rate of proliferation, low rate of apoptosis)
Cell cycle characteristics result in slow accumulation of neoplastic lymphocytes
143
What is high grade lymphoma?
Neoblastic cells usually of large size with activated blast like appearance (dispersed nuclear chromatin, prominent nucleoli)
Cell cycyel characteristics result in rapid accumulation of neoplastic lymphocytes
144
What is Ki67?
A protein expressed by cells in the S phase (ie dividing or proliferating cells)
145
What is follicular lymphoma?
```
Neoplasm of follicle centre B cells
Presents as painless lymphadenopathy
Incurable bur indolent course
Treatment: alleviate symptoms
Low grade lymphoma characterised by: low rate of proliferation, low rate of cell death
```
146
What is diffuse large B-cell lymphoma?
Biologically heterogenous group of lymphoma
Prsents with rapidly enlarging mass at single nodal or extranodal site
Varied immunophenotype
Usually a complex karyotype and many other genetic abnormalities are also present
147
What is Burkitt lymphoma?
Neoplasm of proliferating follicle centre (germinal centre) B cells
Highly aggressive but curable (with intensive chemo)
148
What are the epidemiological variants of Burkitt lymphoma?
Endemic Burkitt lymphoma - equatorial Africa and Papua new Guinea, associated with EBV
Sporadic Burkitt lymphoma - in Western Europe and North America
Immunodeficiency Burkitt lymphoma - HIV, post transplant
149
What are the genetics of Burkitt lymphoma?
Majority have chromosomal translocation involving MYC and IG gene partner
150
What is Hodgkin lymphoma?
Lymphoid neoplasm affecting lymph nodes.
| Characterised by: large neoplastic B cells (Reed Sternberg cell), prominent background of reactive WBC
151
What are the 2 subtypes of Hodgkins lymphoma?
Nodular lymphocyte predominant Hosgkin lymphoma
| Classic Hodgkin lymphoma
152
What is classic Hodgkin lymphoma?
A subtype of Hodgkin lymphoma
Bimodal age incidence (peaks in YA, elderly)
Usually presents with painless lymphadenopathy
May have systemic symptoms
153
What is the morphology of classic Hodgkin lymphoma?
Neoplastic cell is very large with blast like morphology - Reed Sternberg cells
Abundant cytoplasm
Binucleate
Prominent nucleolus
154
What is nodular sclerosing?
Bands of sclerosis divide node into cellular nodes
155
What is plasma cell myeloma?
A neoplastic proliferation of plasma cells in bone (lytic bone lesion)
Abnormal immunoglobulin detectable in peripheral blood or urine
Incurable
156
What are plasma cells?
Immunoglobulin producing cells of the immune system: IgG>IgA>IgM
157
What is plasma cell myeloma diagnosis based on?
Neoplastic plasma cells in bone marrow
Evidence of end organ damage attributable to plasma cell proliferation: hypercalcaemia, renal insufficiency, anaemia
Biomarkers of malignancy
158
What is plasma cell myeloma morphology?
Neoplastic cells resemble normal mature plasma cells
Eccentric nucleus with clock face chromatin
Abundant cytoplasm with perinuclear clearing
159
What is smouldering (asymptomatic) myeloma?
Presence of 10-60% clonal plasma cells in bone marrow but no other myeloma defining event
May be stable for many years but ultimate progression to symptomatic plasma cell myeloma
160
What is monoclonal gammopathy of uncertain significance?
Serum M protein <30g/l
Clonal plasma cells in bone marrow <10%
Absence of end organ damage
Low risk of progression to myeloma
161
What is plasmacytoma?
Single localised tumours consisting of monoclonal plasma cells
M protein may be detectable but no other typical features of plasma cell myeloma present
Normally managed by local radiotherapy
162
How do patients with lymphoma normally present?
Lymphadenopathy: painless, rubbery
Splenomegaly
B symptoms: night sweats, weight loss, fever
Anaemia
163
What do you need to consider when deciding fitness for treatment?
```
renal function
liver function
bone marrow function
cardiac disease
respiratory disease
```
164
What system is used to stage lymphoma?
Ann-Arbor classification system
I: single lymph node group
II: more than one lymph node group same side of diaphragm
III: lymph node groups both side of the diaphragm (inc spleen)
IV: extranodal involvement eg liver, bone marrow
A or B can be added to signify presence of B symptoms
