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Y4 cancer care > Haematology > Flashcards

Haematology Flashcards

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1
Q

HL epidemiology

A

Men > women

Far less common than NHL

Bimodal age distribution - peaks around 20-25 and 80 years

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2
Q

HL risk factors

A

HIV

EBV

Autoimmune conditions - RA & sarcoidosis

Family history

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3
Q

HL clinical features

A

Lymphadenopathy - painless, firm, enlarged lymph nodes → most commonly found in the neck

‘B’ symptoms - unexplained fever, night sweats and unexplained weight loss

Mediastinal mass - incidental finding on imaging or present with SoB, cough, pain or SVCO

Pruritus

Hepatosplenomegaly

Malaise

Fatigue

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4
Q

HL ix

A

Diagnostic - excision biopsy of affected lymph nodes → Reed-Sternberg cells (’owl-like’ appearance)

Bloods - FBC, U&Es, LFTs, bone profile, LDH, uric acid, ESR, HIV, hep B & hep c, HTLV-1

Imaging - CXR, PET-CT, CT neck, C/A/P, MRI brain

Additional - LP and CSF analysis, echocardiogram, PFTs, bone marrow biopsy

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5
Q

HL staging

A

Lugano staging system - describes the anatomical distribution of disease & is of both prognostic and therapeutic importance

  • attempt to update the Ann-Arbor system
  • further modified by the presence/absence of a number of features:
    • ‘B’ symptoms
    • extranodal involvement
    • bulky disease
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6
Q

HL mx

A

Chemotherapy and radiotherapy are the mainstay of management in patients with cHL

  • ABVD regimen of treatment common - doxorubicin, bleomycin, vinblastine, dacarbazine

Relapsed disease - salvage chemotherapy, radiotherapy & autologous haematopoietic cell transplantation

Blood transfusion - must receive irradiated blood → reduce the risk of transfusion-associated graft-versus-host disease

Good prognosis — >75% of patients will be cured of condition

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7
Q

NHL epidemiology

A
  • Reed-Sternberg cells are not seen in NHL
  • more than 60 subtypes, a few notable ones are diffuse large B cell lymphoma, Burkitt lymphoma & MALT lymphoma
  • more common than Hodgkin lymphoma
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8
Q

NHL clinical features

A

Lymphadenopathy

B symptoms - fever, night sweats & weight loss

Pruritus

Splenomegaly

Hepatomegaly

Pancytopenia

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9
Q

NHL ix

A

Bloods - FBC, ESR, LFTs, uric acid,

CXR

CT scan

Bone marrow aspirate & trephine - routine in NHL

Lymph node biopsy

Immunophenotyping

Immunoglobulin tests

HIV testing

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10
Q

NHL prognosis

A

Low-grade - generally not curable, median survival of 10 years, often widely disseminated at presentation due to them being asymptomatic

High-grade - more aggressive but more likely to be cured, deadly without treatment

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11
Q

NHL mx

A

Low-grade - depends on the subtype present, MDT discussion

  • symptomless → likely no treatment will be given & will just be monitored
  • radiotherapy may be curative in localised disease
  • chlorambucil (chemotherapy)

High-grade - CHOP + rituximab chemotherapy regimen

  • monoclonal antibodies can be useful for B cell lymphomas
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12
Q

ALL

A
  • most common malignancy of childhood
  • occurs due to a proliferation of malignant lymphoid progenitor cells in the bone marrow
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13
Q

ALL aetiology

A

Combination of genetic susceptibility and environmental exposure

Infection (particularly viruses) may act as a triggering event

Cytogenetic features - TEL-AML fusion gene, philadelphia chromosome (results in BCR-ABL fusion gene)

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14
Q

ALL clinical features

A

Marrow failure

  • anaemia: fatigue, breathlessness, angina
  • neutropenia: recurrent infections
  • thrombocytopenia: petechiae, nose bleeds, bruising

Tissue infiltration - lymphadenopathy, hepatosplenomegaly, bone pain, mediastinal mass & testicular enlargement

Leucostasis - altered mental state, headache, breathlessness & visual changes

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15
Q

ALL ix

A

Bloods - FBC, LDH, uric acid, U&Es, bone profile & Mg, clotting screen, d-dimer, blood borne virus screen

Imaging - CXR (may show mediastinal mass), CT C/A/P, CT/MRI head

Bone marrow aspiration & biopsy - definitive diagnostic test → samples sent for cytogenetics & flow cytometry

Further tests - blood smear, pleural tap & LP

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16
Q

ALL mx

A

Referred a specialist haemato-oncology unit for specialist management

Key aspects: pre-phase therapy (reduce the risk of TLS), leucopheresis, supportive therapy (G-CSF may be given)

Induction chemotherapy - aim to achieve complete remission/complete molecular remission

Maintenance therapy

Stem cell transplant - allogeneic stem cell transplant may be considered & reduces the risk of relapse

Palliative care - should be considered in any patient undergoing treatment without curative intent/in those with disease symptoms that are difficult to manage

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17
Q

ALL complications

A

Tumour lysis syndrome

Neutropenic sepsis

SVCO

Chemotherapy side effects - mucositis, N&V, hair loss, cardiomyopathy, secondary malignancies

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18
Q

CLL

A
  • lymphoproliferative disorder of B lymphocytes, which results from an abnormal clonal expansion of B cells
  • incidence increases with age & more common in men
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19
Q

CLL genetic alterations

A

Tp53 mutation

11q and 13q14 deletions

Trisomy 12

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20
Q

CLL clinical features

A

Symptoms - weight loss, fevers, anorexia, night sweats, lethargy

Signs - lymphadenopathy, hepatomegaly, splenomegaly

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21
Q

CLL ix

A

Majority of patients with CLL are diagnosed incidentally on a FBC

Bloods - FBC, U&Es, bone profile, LFTs, blood film, haemolysis screen, immunoglobulins

Cytogenetics & immunophenotyping

Blood film - confirm the presence of lymphocytosis & characteristically shows smear or ‘smudge’ cells

Bone marrow assessment - done if concern for an alternative diagnosis

Imaging - CT C/A/P, USS, CXR

Lymph node biopsy

Virology

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22
Q

CLL mx

A

Watch and wait → used for patients with asymptomatic, indolent disease without poor prognostic factors

Chemotherapy

Small molecule inhibitors

Monoclonal antibodies

Allogenic stem cell transplantation - potential option in patients who fail chemo & BCR inhibitor therapy

Supportive care - vaccination, antibiotics for infections, IV immunoglobulin, PJP & herpes zoster prophylaxis

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23
Q

CLL complications

A

Richter transformation - formation of an aggressive lymphoma, 5-8 month median survival

Secondary infections

Autoimmune complications

Hyperviscosity syndrome

Secondary malignancies

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24
Q

AML

A

occurs due to the malignant transformation & proliferation of myeloid progenitor cells

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25
AML risk factors
Myelodysplastic syndromes Congenital disorders - Down’s syndrome, congenital neutropenia & Fanconi anaemia Radiation exposure Previous administration of chemotherapy Toxins
26
AML clinical features
Presents with features of marrow failure/tissue infiltration Marrow failure - anaemia, neutropenia, thrombocytopenia Tissue infiltration - lymphadenopathy, hepatosplenomegaly, bone pain, gum hypertrophy, violaceous skin deposits, testicular enlargement Leucostasis (large numbers of white cells entering the blood stream) - altered mental state, headache, breathlessness, visual changes
27
AML ix
Bloods - FBC, renal function, LFTs, clotting screen, d-dimer, bone profile & Mg, uric acid, LDH, blood borne virus screen - normocytic normochromic anaemia & thrombocytopenia & reduced reticulocyte counts are common Blood smear - Auer rods is the classical finding on peripheral blood film Bone marrow aspirate & biopsy - allows for definitive diagnosis; samples used for cytogenetics, immunophenotyping & flow cytometry LP - organised if there is concern of CNS involvement
28
AML mx
Initial management - education & support, supportive care, cytoreduction (patients with leucostasis & raised WBC), CNS involvement Chemotherapy AML is most common indication for allogenic stem cell transplantation
29
CML
Slowly progressing cancer of the myeloid cell line
30
CML genetics
Hallmark cytogenetic finding in CML is the Philadelphia chromosome Results from a reciprocal translocation between chromosome 9 and chromosome 22 Abnormal chromosome 22 is characterised by the BCR-ABL1 fusion gene
31
CML clinical features
20-40% are asymptomatic & picked up incidentally during investigations B symptoms Anaemia - fatigue, breathlessness, angina Thrombocytopenia - petechiae, nose bleeds, bruising Splenomegaly - early satiety, abdominal pain Bone pain Leucostasis - headache, breathlessness, visual changes, priapism Signs - splenomegaly, hepatomegaly, lymphadenopathy
32
CML ix
Bloods - FBC, U&Es, LFTs, bone profile & Mg, LDH, urate, metabolic profile, blood borne virus screen Blood film - immature & mature myeloid cells are seen, proportion of blasts & basophils help to categorise the phase of disease Metaphase cytogenetics - identify the abnormal chromosome 22 FISH - can be used to confirm the presence of BCR-ABL1 fusion Bone marrow aspiration +/- trephine
33
CML phases
Chronic phase - clinical features are non-specific Accelerated phase - symptoms & features become more apparent, disease more difficult to treat and outcomes worse Blast crisis - resembles an acute leukaemia with the rapid expansion of blasts
34
CML mx
Tyrosine kinase inhibitors (imatinib) - blocks the enzyme created by the BCR-ABL1 fusion gene Intensive chemotherapy - typically reserved for patients with blastic transformation Allogenic stem cell transplantation
35
MM
Malignant disorder of the plasma cells Characterised by excess secretion of a monoclonal antibody → derived from a single clone of plasma cells that have undergone abnormal proliferation
36
MM pathophysiology
Development of MGUS (monoclonal gammopathy of undetermined significance) - premalignant plasma cell disorder - thought to be an abnormal plasma cell response to antigen stimulus → leads to creation of plasma cell response to antigen stimulus Progression from MGUS to MM - further cytogenetic abnormalities and changes to the bone marrow environment occur → promotes proliferation - associated with systemic problems due to plasma cell infiltration of the bone marrow & excess light chain secretion
37
MM clinical features
Constitutional symptoms - weight loss, fatigue, loss of appetite and/or generalised weakness Bone disease - lytic lesions, can lead to fractures Impaired renal function - light chain nephropathy Anaemia - seen in >90%, normal bone marrow destroyed by proliferation of malignant plasma cells, EPO deficiency due to renal disease Hypercalcaemia - MM-induced bone demineralisation Recurrent/persistent bacterial infection SLIM-CRAB
38
Emergency presentation of myeloma
Hyperviscosity syndrome - may develop with high paraprotein levels - symptoms: blurred vision, headaches, mucosal bleeding & dyspnoea due to heart failure - Requires urgent plasma exchange Spinal cord compression
39
When to suspect myeloma
Age > 60 and: - unexplained bone pain - fatigue - symptoms of hypercalcaemia - weight loss - symptoms of cord compression - symptoms of hyperviscosity - recurrent infections
40
MM ix
Protein electrophoresis - quantitative test that separates proteins into different bands using an electric current - tells us whether there is an increased number of antibodies Immunofixation - qualitative test that ‘fixes’ proteins in place by using antibodies - tells us which type of antibody is increased Serum free light chains - elevated ratio between light chains is suggestive of myeloma Urine electrophoresis - light chains within the serum may be filtered by the kidneys into the urine
41
MM diagnostic criteria
Identification of a monoclonal antibody Analysis of the bone marrow to look for a population of malignant clonal plasma cells Further lab tests and imaging to assess for myeloma-related organ damage Help differentiate between MGUS, asymptomatic myeloma & multiple myeloma
42
MM mx
Incurable condition, treatments aim to increase periods of disease remission MDT discussion Induction therapy - initial treatment option, aim to induce remission; usually combination of three drugs ASCT (autologous stem cell transplantation) - provides best option for long period of remission Maintenance - used to maintain disease remission as long as possible; given post-induction/post transplant Relapse or refractory disease - almost all patients will relapse, even if they respond to treatment; therapy indicated if a clinical relapse or rapid rise in paraproteins
43
MM complications
Myeloma bone disease - bisphosphonates used for boney pain Hypercalcaemia Cord compression Renal impairment Anaemia
44
Lymphadenopathy causes
Lymphadenopathy - condition of enlarged lymph nodes Infective - infectious mononucleosis, HIV, eczema with secondary infection, rubella, toxoplasmosis, CMV, TB, roseola infantum Neoplastic - leukaemia, lymphoma Others - autoimmune conditions (SLE, RA), graft vs host disease, sarcoidosis, drugs: phenytoin, allopurinol, isoniazid
45
Spleen functions
Immune surveillance Proliferation and maturation of lymphocytes Degradation of senescent & damaged erythrocytes
46
Hyposplenism causes
Splenectomy Sickle-cell Coeliac disease, dermatitis herpetiformis Graves’ disease SLE Amyloid
47
Hyposplenism features on blood film
Howell-Jolly bodies Siderocytes
48
Splenomegaly causes
Massive splenomegaly - myelofibrosis, CML, malaria, Gaucher’s syndrome Other causes - portal hypertension, haemolytic anaemia, infective endocarditis, thalassaemia, RA
49
MDS
Group of malignant haematopoietic stem cell disorders Affects elderly individuals, mean age of onset is 70 years
50
MDS causes
Idiopathic Secondary to exposure - toxins, genotoxic drugs, immunosuppressive agents, chemotherapy, radiation therapy Genetic defects
51
MDS complications
Pre-leukaemias, high risk of conversion to AML Progresses slowly → most succumb to bleeding & infections before AML
52
MDS clinical features
Asymptomatic in early stages Fatigue (anaemia) Infections (neutropenia) Bleeding (thrombocytopenia)
53
MDS ix
FBC - low RBCs, WBCs, platelets, normal/mildly elevated MCV, increased RDW Low reticulocyte count, dysplastic RBCs, WBCs, normal platelets, 1-20% Dysplastic cells, increased blasts Chromosomal abnormalities, gene mutations
54
MDS mx
Medications - TNF inhibitors, DNA methylation inhibitors Allogeneic haematopoietic stem cell transplant - only curative option, for young individuals - if transplant not an option → blood product transfusions, infection control (supportive)
55
PCV
polycythaemia = describes an increase in haematocrit, red cell count & Hb concentration
56
PCV reactive causes
Reactive - occurs when the Hb is elevated secondary to a low plasma volume - can be seen in dehydration, chronic alcohol intake, excess diuretic use, pyrexia, D&V - ‘stress polycythaemia’ - refers to reactive polycythaemia that is found predominantly in middle aged men with stressful occupations and chronically reduced plasma volumes of uncertain cause - Gaisbock syndrome - more common in young men (smokers & associated with HTN) → reduces plasma volume, resulting in raised Hb
57
PCV absolute causes
Absolute - classified into primary & secondary causes - primary - excess and uncontrolled erythrocytosis that is independent of EPO levels - associated with mutations in JAK2 gene → uncontrolled production of blood cells, especially RBCs - *polycythaemia rubra vera* = primary proliferative polycythaemia - secondary - excess RBC is driven by excess EPO - an appropriate rise in EPO → seen in conditions of chronic hypoxia - anabolic steroid use - inappropriate secretion of EPO: - renal neoplasma - CKS - cyanotic heart diseases - high-affinity haemoglobinopathies
58
PCV clinical features
Fatigue Headache Visual disturbances Pruritus Erythromelalgia - painful burning sensation in the fingers & toes Arterial & venous thrombosis Plethora Splenomegaly Specific clinical features of PCV: - hyperviscosity symptoms - chest pain, myalgia, weakness, headache, blurred vision & loss of concentration - ruddy complexion - splenomegaly
59
PCV ix
Bedside - pulse oximetry to look for possible secondary polycythaemia FBC - raised haematocrit, raised Hb, raised red cell mass with low/low-normal plasma volume, raised leukocytes & platelet counts - neutrophil count & platelet count are usually normal in secondary polycythaemia ! Renal function & urate Vitamin B12 EPO levels JAK-2 mutation Bone marrow biopsy - hypercellular bone marrow Important to exclude CML - cytogenetics
60
PCV mx
Possible underlying causes should be corrected Venesection PV: Regular venesection Aspirin 75mg daily Cytoreductive therapy to suppress erythropoiesis in those where venesection isn’t sufficient/those at high risk of thrombosis - 1) hydroxycarbamide - suppresses erythrocytosis & causes a macrocytosis - 2) interferon, JAK2 inhibitors (first line in younger patients) - 3) bulsulfan Other interventions - allopurinol (hyperuricaemia), antihistamines, SSRIs or interferon (for pruritus)
61
ET
myeloproliferative disorder caused by dysregulated megakaryocyte (platelet precursor) proliferation
62
ET epidemiology
Women aged 50-70 years Median survival is 10-15 years
63
ET clinical features
50% of patients are asymptomatic with only an incidental FBC finding Thrombosis (arterial or venous) Bleeding Hyperviscosity-related → dizziness/syncope, headache Splenomegaly Hyposplenism Erythromelalgia (red/blue discolouration of the extremities, often accompanied by a burning pain) Livedo reticularis (net-like purple rash)
64
ET ix
FBC - persistent platelet count significantly >450 x 10^9/L Genetic testing - JAK2 mutation Trephine biopsy - hypercellular marrow & pathological megakaryocytic clumping
65
ET mx
Based following risk stratification Low risk - treat with aspirin alone Intermediate risk - treat with either hydroxycarbamide & aspirin OR aspirin alone High risk - hydroxycarbamide & aspirin Can also used hydroxyurea & anagrelide (specialist platelet-lowering agent)
66
Myelofibrosis
chronic myeloproliferative neoplasm characterised by the gradual replacement of normal bone marrow tissue with fibrous tissue
67
Myelofibrosis aetiology
Associated with genetic mutations - JAK2 - CALR - MPL
68
Myelofibrosis clinical features
Constitutional symptoms - weight loss, fever, night sweats Marrow failure - anaemia, recurrent infection & abnormal bleeding/bruising Bone pain Haemorrhage & thrombosis (less common compared to other myeloproliferative disorders) Splenomegaly - abdominal discomfort, early satiety Hepatomegaly
69
Myelofibrosis ix
Blood film - poikilocytes (tear-shaped RBCs) & a leucoerythroblastic blood film Platelet count & WCC are often high initially, with pancytopenia occurring later Difficult to aspirate the bone marrow → resulting in a ‘dry tap’ Trephine biopsy shows evidence of fibrosis, with hypercellular tissue, reduced fat space & increased reticulin staining Urate and LDH usually high JAK2 is positive in 50% of cases
70
Myelofibrosis mx
Generally an incurable condition Allogeneic stem cell transplantation is the one exception → patients aged <70 years with good performance status & high-risk disease JAK-2 inhibitors (ruxolitinib) can have a good effect particularly in reducing splenomegaly & treating B symptoms Cytotoxic agents, immunomodulatory drugs, splenic irradiation & splenectomy can be used as treatments to lessen the need for transfusion & improve symptom control
71
Myelofibrosis complications
Transformation to acute leukaemia Splenomegaly-related complications Cardiovascular and thrombotic events

Y4 cancer care (10 decks)

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