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4th Year Unseen Exam > Lymphomas and and multiple myeloma > Flashcards

Lymphomas and and multiple myeloma Flashcards

1
Q

What is the lymphatic system?

A

An integrated network of cells, tissues, organs and proteins. It has generative and peripheral functions

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2
Q

What are the functions of the lymphatic system?

A
  • remove and destroy waste
  • remove excess fluids from interstitial spaces
  • returns proteins and tissue fluids to the blood
  • absorbs fats and fat soluble vitamins and delivers to cells
  • important component of the immune repsonse
  • open system
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3
Q

What do b lymphocytes do?

A

When they are exposed to soluble antigens, they become sensitised to specific antigens which leads to further division of B lymphocytes into plasma cells which produce antibodies and memory cells which remain dormant until the next exposure to the antigen

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4
Q

What do t lymphocytes do?

A
  • recognise non self cells
  • helper t cells recognise self vs non self
  • suppressor prevent hypersensitivity when exposed to non self
  • cytotoxic lyse antigen cells
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5
Q

What is non-hodgkins lymphoma?

A

Diverse group of disease and treatments, incidence increased with age. 90% are of B cell origin

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6
Q

What are the clinical features of non-hodgkins lymphoma

A
  • superficial lymphadenopathy: painless asymmetric enlargement of one or more peripheral lymph nodes
  • constitutional symptoms
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7
Q

What are the constitutional symptoms of NHL?

A
  • Weight loss due to hyper-metabolic disease
  • fever
  • night sweats
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8
Q

Which symptoms are associated with organ involvement in NHl?

A

Dyspnoea, abdo symptoms, anaemia, neutropenia, thrombocytopenia, compression by lymph node

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9
Q

Which grade of lymphoma requires rapid treatment?

A

High grade

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10
Q

Which investigations are carried out for NHL?

A

Blood evaluation including lactate dehydrogenase, biopsy, imaging, prognostic evaluation

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11
Q

How is NHL staged?

A

Ann arbor staging system

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12
Q

What is stage 1 NHL?

A

1 tumour above the diaphragm

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13
Q

What is stage 2 NHL

A

More than 1 tumour above the diaphragm

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14
Q

What is stage 3 NHL?

A

Tumour below diaphragam

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15
Q

What is stage 4 NHL?

A

More than one below the diaphragam

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16
Q

What does a/b/e mean in relation to NHL staging?

A

A = absence of symptoms, b= symptoms, E = extra nodal site

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17
Q

Which drug agents are used for NHL?

A

RCHOP regimine:

rituximab, cyclophosphamide, doxirubicin, vincristine, prednisolone

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18
Q

Which supportive therapies are given alongside treatment of NHL?

A
  • Anti emetic
  • tumour lysis prevention
  • haemorrhagic cystitis prevention
  • hypersensitivty prevention - paracetamol/chloramphenamine
  • gastro protection
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19
Q

Which anti-emetics are typically given alongside the RCHOP regimen?

A

Usually give ondansertron with chemo and to take away, and metclopramide to take away. Steroid would not be given as already part of treatment regimen

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20
Q

Which drugs are given for tumour lysis prevention with NHL and when?

A

Allopurinol and rasburicase. During the first cycle only, as highest risk of tumour lysis as cellular breakdown is highest here.

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21
Q

What drugs are given for haemorhagic cystitis prevention?

A

MESNA - binds to acrolein

- hydration pre chemo

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22
Q

What is rituximab and how does it work?

A
  • targetted therapy
    1. Causes antibody dependent cellular toxicity
    2. Rituximab binds to CD20 on one side of B cell
    3. Forms a cap that draws proteins to that side
    4. Natural killer cells latch onto cap and are more successful in killing cells (enhances activity of NKCs)
    5. Complement mediated toxicity occurs which involves cascade activation of proteins
    6. Development of membrane attack complex (MAC)
    7. which causes direct lysis
    8. leads to apoptosis of cancer cells
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23
Q

What are the adverse effects of ritixumab?

A

Hypersensitivity reactions, give paracetamol and chloramphenamine

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24
Q

What is relapse associated with in NHL and how does it change treatment?

A

Worse outcomes. Treated with intensive chemo and autologous stem cell transplant

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25
Q

What is hodgkin’s lyphoma?

A

A cancer of B cell lymphocytes, characterised by Hodgkin’s reed Sternberg cells. A rare cancer common in males

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26
Q

How do clonal B cells cause cancer in Hodgkin’s lymphoma?

A

Clonal b cells lack typical b cell surface antigens and evade apoptosis by:

  • chromosomal translocations and genetic mutations
  • incorporating epstein barr virus or latent membrane proteins
  • activation of transcription factors
  • interaction with components of the microenvironment
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27
Q

What are the symptoms of hodgkins lymphoma?

A

Fever, weight loss, night sweats, alcohol induced pain, mediastinal involvement, multiple nodules within organs, lymphadenopathy

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28
Q

What must be carried out pre treatment for HL?

A
  • Blood evaluation for haematological/biochemical markers: mild anaemia, leucocytosis with raised lymphocyte count, liver function
  • staging
  • favourable/unfavourable prognosis
  • fertility preservation
  • good cardiac function check for use of anthracycline
  • check pulmonary history - bleomycin has pulmonary toxicity
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29
Q

How should a patient with favourable prognosis be treated with HL?

A

Less intensive treatment, if they have a good response then keep it the same

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30
Q

What is the prognosis for HL?

A

Generally has a good cure rate, but has potentially dehabilitating treatment. If it is diagnosed early in life it is a long term disease

31
Q

What is the risk with hodgkins lymphoma?

A

Long term disease and treatments can be carcinogenic. There is a risk of secondary malignancies and so patients should be advised to avoid cancer via lifestyle changes such as diet, exercise, not smoking

32
Q

What is the treatment for early favourable stage 1-3 hodgkins lymphoma?

A

Short course of chemo and radiotherapy

33
Q

How should early favourable patients with HL be treated if radiotherapy is contraindicated?

A

RAPID protocol: 3 cycles of ABVD regimen, then sent for a PET scan, further cycle and radiotherapy if the PET scan shows cancer still present

34
Q

How should patients with early unfavourable HL be treated?

A

4 cycles of ABVD and radiotherapy

35
Q

How should patients with advanced HL (stage 3 and 4) be treated?

A

Full course of chemo: escalated BEACOPP or ABVD

36
Q

What is the ABVD regimen and how often is it repeated?

A

Every 28 days

Doxorubicin, bleomycin, vinblastine, dacarbazine

37
Q

What should be given alongside bleomycin?

A

Iv hydrocortisone if no dexamethasone in the anti-emetic stratergy

38
Q

What is multiple myeloma?

A

A disease of plasma cells

39
Q

How does multiple myeloma occur?

A

Genetic changes during differentiation of b lymphocytes into plasma cells, which leads to expansion of malignant immature b cells, which produce monoclonal antibodies that can be detected in the blood and urine Myeloma cells accumulate in the blood and bone marrow, so antibodies cannot be produced and patients are at a risk of infection

40
Q

Why are patients with multiple myeloma at an increased risk of infection?

A

Because myeloma cells accumulate in the bone marrow and functional plasma cells are not produced, therefore antibodies cannot be produced.

41
Q

Discuss the molecular biology of multiple myeloma

A

Multiple myeloma microenvironment: clonal myeloma cells, extracellular matrix proteins, bone marrow cells, osteoblasts and clasts. There is an increased secretion of cytokines, epidermal growth factor, VEGF, tnf a, which provides protection against apoptosis

42
Q

What are the 3 stages of MM?

A

mgus, smoldering mm and active mm

43
Q

How does mgus and smoldering mm present?

A

No anaemia/bone lesions, normal calcium and kidney function

44
Q

How does active MM present?

A

Anaemia, bone lesions, high calcium, abnormal kidney function

45
Q

What is the clinical presentation of MM?

A
  • Anaemia: patients are producing more non functional plasma cells, so the production of normal cells is suppressed
  • bone disease: overexpression of RANKL leads to increased osteoclasts, lytic lesions can be seen on x rays
  • hypercalcaemia - renal dysfunction associated with monoclonal proteins which can accumulate in tubules and crystallise
46
Q

What are lytic lesions?

A

Result in bone pain/fracture

47
Q

Discuss CRAB for clinical presentation of multiple myeloma

A

hyperCalcaemia
Renal insufficiency
Anaemia
Bone lesions

48
Q

How is multiple myeloma staged?

A

Using cytogenetics and serum b2 microglobulins

49
Q

/What are serum b2 microglobulins?

A

Tumour markers, elevated in multiple myeloma

50
Q

What are the initial considerations for chemotherapy for mm patients?

A
  • stage of disease: treatment is not given for smoldering MM
  • symptomatic disease: treat the complications prior to chemo
  • is the patient a transplant candidate
51
Q

How are patients evaluated for transplant with mm?

A
  • Performance status
  • comorbidities
  • frailty
  • renal impairment: should not be used alone as it could be disease related and may improve with treatment
  • age
52
Q

What is the process of transplant for mm?

A

REMOVE stem cells from the patient and treat them pre transufsion
INDUCTION: induce complete remission or partial remission prior to transplantation using bortezomib regimens
STEM CELL HARVESTING: mobilise stem cells
HIGH DOSE MEPHALAN: destroys existing bone marrow
REINFUSE stem cells
POST TRANSPLANT CONSOLIDATION: to improve response rates
ONGOING: thaldiomide/lenalidomide for maintenance

53
Q

Does transplant cure mm?

A

No, patients will relapse

54
Q

What does the induction regime for transplant for mm involve?

A

It is complicated, includes bortezamib, thalidomide and dexamethasone

55
Q

What follow ups are carried out for hodgkins lymphoma?

A

outpatient based for up to 5 years, to check for t cell defects, malignancies, cv disease, pulmonary toxicity, thyroid dysfunction, fertility

56
Q

How are transplant non-eligible patients handled with mm?

A

Disease is controlled to achieve long term progression free survival and maintain quality of life.
Induction with thalidomide/lenalidomide, bortezomib, alkylating agent and a corticosteroid

57
Q

How do proteasome inhibitors work?

A

The ubiquitin-proteasome pathway is responsible for the degradation of the majority of regulatory proteins. Disruption of proteasome activity leads to accumulation of incompatible regulatory proteins and the induction of a cytotoxic cascade. Cancer cells have higher levels of proteasome activity, and are more sensitive to the pro apoptotic effects of proteasome inhibitors. Inhibit proteasome and tumour cells cannot regulate their proteins, which leads to apoptosis of cells

58
Q

What is an example of a proteasome inhibitor?

A

Bortezamib

59
Q

How does bortezamib work?

A

It is a reversible proteasome inhibitor, which acts via multiple mechanisms:

  • induce apoptosis
  • inhibit the NFK-kb pathway
  • reduce IL6 production and signalling
60
Q

What are the side effects of bortezamib?

A
  • peripheral neuropathy which can be dose limiting
  • GI disturbance
  • hypotension
  • bone marrow suppression
  • tumour lysis syndrome
  • pulmonary, cv and liver toxicity
  • inhibits cyp450 enzymes
  • contraception advised
61
Q

How does thalidomide work?

A
  • immunodulatory activity
  • inhibition of angiogenesis
  • anti-proliferative effects
  • can directly inhibit cytokines in the myeloma cellular environment
  • can stimulate the effects of natural killer cells
  • inhibits tumour growth
62
Q

What are adverse effects/cautions that should be given when initiating thalidomide?

A
  • it is teratogenic so a pregnancy prevention programme should be put in place
  • can cause venous thromboembolism
  • can cause constipation, so prescribe laxatives
  • rash
  • can cause somnolence so take at night
  • thyroid function
63
Q

Give examples of 2nd/3rd generation immunodulatory agents and discuss their relationship to thalidomide

A

Lenazalidomide and domalidomide. They are analogues of thalidomide, have less side effects but are more potent

64
Q

When is lenalidomide indicated and what are the side effects?

A

In myeloma cells, has reduced side effects to thalidomide but can cause myelosuppression

65
Q

When in domalidomide indicated and what are the side effects?

A

In myeloma cells resistant to thalidomide and lenalidomide. well tolerated

66
Q

Which supportive therapies are prescribed alongside multiple myeloma chemotherapy agents?

A 
Bisphosphonates
VTE prophylaxis
GI protection
Tumour lysis prevention
infection prevention
67
Q

Why are bisphosphonates prescribed in mm?

A

They inhibit bone resorption by suppressing osteoclast activity. Results in fewer lytic bone lesions but has also been found to have effects on myeloma cells. Dental checks necessary to prevent osteonecrosis of the jaw. Renal impairment considerations

68
Q

How is VTE prophylaxis prescribed in mm?

A

Thalidomide has risk of venous thromboembolism. Asses risk, avoid warfarin as you want to keep the INR stable

69
Q

Why is GI protection given alongside MM chemotherapy agents?

A

Alongside dexamethasone as theres risk of GI effects. Give a PPI

70
Q

What is given as tumour lysis prophylaxis?

A

Allopurinol

71
Q

What is given to prevent infection alongside MM treatment?

A

Antibiotics, antivirals

72
Q

What is given alongside high dose steroids?

A

Co-trimoxazole for prophylaxis of pneumocystis jirovecci

73
Q

What should happen when mm patients relapse?

A

Patients should be entered into a clinical trial wherever possible. Individualised treatment strategy should be applied. With each relapse, there likelihood of progression-free survival is shorter and the disease becomes resistant. Therapy should be swapped to a therapy with a different mechanism of action. If poor performance status, use more intensive treatments

74
Q

What are the challenges with mm?

A

We need an improved understanding of the pathophysiology, and there is a considerable symptom burden therefore supportive therapies are important.

4th Year Unseen Exam (17 decks)

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