Leukaemia & Lymphoma Flashcards

1
Q

what 2 groups do blood stem cell differentiate into?

A
  • myeloid

- lymphoid

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2
Q

when can a haematological cell line turn neoplastic?

A

at a number of stages

earlier in the cell line this occurs the more potentially aggressive the malignancy

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3
Q

DNA mutation - translocation

A

Part of DNA strand artificially added on to the wrong DNA chain

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4
Q

what can be the result of incorrect protein synthesis?

A
  • clonal proliferation

- cancer cells (Uncontrolled proliferation; Loss of apoptosis; Loss of normal functions/products)

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5
Q

what is a subsequent issue of harder to kill off cell lines?

A

tumours reappearing later

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6
Q

acute occurs….

A

rapid, now

symptoms in 6 months

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7
Q

chronic occurs…

A

slow onset

can take 5, 10, 20 years to show

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8
Q

name for acute lymphoid disease

A

acute lymphoblastic leukaemia

- severe illness right now

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9
Q

chronic lymphocytic leukaemia

A

chronic lymphoid disease

  • Chronic white cell enlargement -; no symptoms
  • Will switch to acute - will kill - all bone marrow does is make cancer cells not any other vital blood cells
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10
Q

multiple myeloma

A

chronic lymphoid disease

- chronic malignancy of plasma cells - dissolve bones, sits in them and hollows them out

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11
Q

name for acute myeloid disease

A

acute myeloid lymphoma

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12
Q

chronic myeloid leukaemia

A

chronic myeloid disease

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13
Q

Myeloproliferative disorders

A

Thromobocythemia

  • Over producing not quite normal platelets
  • Lead to change
  • Grumbling along and change in mutation in cell to show change
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14
Q

what does Lymphocytic, lymphoblastic or myeloid describe

A

the point in the cell lines or cell type at fault

- when the mutation occurs

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15
Q

what does acute and chronic denote

A

clinical behaviour

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16
Q

what is a blast

A

immature cell

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17
Q

lymphocytic

A

looks like cell line they will be

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18
Q

lymphoblastic

A

differentiation so far up cell line can’t tell what final cell will

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19
Q

leukaemia describes

A

a group of cancers of the bone marrow which prevent normal manufacture of the blood and therefore result in:

  • anaemia (RBC)
  • infection/neutropenia (WBC)
  • bleeding/thrombocytopenia (platelets)
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20
Q

why is limited bone marrow space a factor o remember?

A

Can only produce so many cells per day, If 90% leukemic - not enough left over for healthy cells

  • Symptoms relate to shortages of normal cell types
  • Not making as so busy making these cells
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21
Q

pathogenesis of leukaemia and lymphoma

A
  • Clonal proliferation
  • Replacement of marrow
  • Increasing marginalisation of productive normal marrow (not enough bone marrow to make marrow needed to survive)
    Marrow failure
    Organ infiltration
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22
Q

6 ways to clinically present with leukaemia or lymphoma

A

Anaemia
- Carry O2

Neutropenia
- infection

Thrombocytopenia
- Problem with bleeding

Lymphadenopathy - neck lumps

  • Migration of extra WCC into tissues
  • Too many rapidly occupy bone marrow - spill out into outside world

Splenomegaly/Hepatomegaly - swollen abdomen
- Accumulating cells so increase in size

Bone pain - especially in children
- Marrow is trying to expand in closed cavity itself

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23
Q

symptoms of anaemia

A
  • breathlessness
  • tiredness
  • easily fatigued
  • chest pain/angina
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24
Q

signs of anaemia

A
  • pallor
  • signs of cardiac failure (ankle swelling, breathlessness)
  • nail changes e.g. brittle nails, koilonychia
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25
Q

what are potential portals of entry for infections>

A
  • Mouth
  • Throat - tonsillitis, pharyngitis
  • Chest - bronchitis, pneumonia
  • Skin - impetigo, cellulitis
  • Perianal - thrush, abscesses
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26
Q

what can occur after an infection seems to to be resolved?

A

reactivation of latent infection

i. e. TB never really get rid off
- Infections stay in the body and wait for chance to become active again

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27
Q

what can happen to a leukaemia patient with an infection?

A

Increased severity, frequency and can rapidly lead to systemic infection

  • E.g. May present with oral candida; Then progress to pneumonia; Then septicaemia
  • As immune system is decreasing
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28
Q

symptoms of neutropenia

A
  • recurrent infection

- unusual severity of infection e.g. no immune response to contain it

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29
Q

signs of neutropenia

A
  • Unusual patterns of infection and rapid spread (Typically wouldn’t cause healthy people an issue usually)
  • Will respond to treatment but recur
  • Signs of systemic involvement - fever, rigors, chills
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30
Q

symptoms of bleeding (thrombocytopenia)

A
  • Bruises easily or spontaneously
  • Minor cuts fail to clot
  • Gingival bleeding or nose bleeds
  • Menorrhagia
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31
Q

signs of bleeding (thrombocytopenia)

A
  • Bruising
  • Petechiae
  • BOP
  • Bleeding/bruising following procedures (E.g. after tooth brushing)
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32
Q

Petechiae

A

small red or purple spot caused by bleeding into the skin.

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33
Q

when does acute lymphoblastic leukaemia occur?

A

peak at 4, but does occur in adults

34
Q

cases of acute lymphoblastic leukaemia

A

25 per 1,000,000 per year

35
Q

time scale and clinical process of acute lymphoblastic leukaemia

A
  • develops over days or weeks

- catabolic state leads to fever, sweats, malaise (non-specific collection of symptoms)

36
Q

what are common clinical signs of acute lymphoblastic leukaemia?

A
  • lymphadenopathy

- tissue infiltration

37
Q

who has the best prognosis for acute lymphoblastic leukaemia?

A

younger patients and females

  • Girls 2-12 years do best
  • expectation you will survive initial treatment for ALL
    >80% of children are cured
38
Q

cases of acute myeloid leukaemia

A

25 cases per million per year

39
Q

age affected by acute myeloid leukaemia

A

more common in elderly, but can affect any age

40
Q

clinical presentation of acute myeloid leukaemia

A

similar clinical signs as ALL

catabolic state leads to fever, sweats, malaise (non-specific collection of symptoms)

  • lymphadenopathy
  • tissue infiltration
41
Q

prognosis of acute myeloid leukaemia

A
  • 30-40% of <60 years

- 10% cure for >70 years but improving

42
Q

what type of disease is chronic lymphocytic (lymphoid) leukaemia?

A

B-cell clonal lymphoproliferative disease

43
Q

who are more effected by chronic lymphocytic (lymphoid) leukaemia?

A

older adults, peak age >70 years

males 2:1 females

44
Q

an issue in detecting chronic lymphocytic (lymphoid) leukaemia?

A

mostly asymptomatic and only discovered in blood tests by coincidence

slow progression, may not require treatment before person dies of another cause

Occasional blast transformation makes it aggressive
- Based on monoclonal antibodies

45
Q

what occurs in chronic myeloid leukaemia?

A

Increase in neutrophils and their precursors

46
Q

who is affected by chronic myeloid leukaemia?

A
  • Peak 50-70 years but can occur at any age
  • Slight male preponderance

15 cases per 1,000,000 per year
- 95% of patients have “Philadelphia” chromosome
(Presents in fairly unspecific way)

47
Q

clinical presentation of chronic myeloid leukaemia

A
  • Fatigue, weight loss, sweating
  • Anaemia, bleeding, splenomegaly

translocation gone wrong so faulty gene products

48
Q

difference between leukaemia and lymphoma

A

Leukaemia has 3-4 times normal WCC

Lymphoma – have solid lumps (WCC normal; abnormal collections)

49
Q

lymphoma

A

Clonal proliferation of lymphocytes arising in a lymph node or associated tissue
- solid tumour but some cell in blood

50
Q

2 types of lymphoma

A
  • Hodgkin lymphoma
  • Non-hodgkin lymphoma

behaviour and clinical features are different
NHL more common 6:1

51
Q

what does staging require?

A

imaging - CT, PET/CT or MRI

need to be aware they have a lymphoma lesion
- not obvious as no blood changes, need to spot lump or pick up by accident

52
Q

what 3 things does staging assess?

A
  • No. of nodes involved and site
  • Extra-nodal involvement
  • Systemic symptoms
    Based on:
  • How far down progression line
  • Where lumps are
53
Q

why is staging important?

A

predicting prognosis and deciding treatment

54
Q

stage I

A

single lymph node region or single extralymphatic site

55
Q

stage II

A

2 or more sites, same side of diaphragm or contiguous extralymphatic site

56
Q

stage III

A

both side of diaphragm or spleen or contguous extralympatic site

57
Q

stage IV

A

diffuse involvement of extralymphatic sites and nodal disease

58
Q

who is effected by Hodgkin lymphoma more?

A
  • Peak incidence age 15-40years

- Male > Female 2:1

59
Q

clinical presentation of Hodgkin Lymphoma

A
  • Painless lymphadenopathy – typically cervical, fluctuate in size
  • Fever, night sweats, weight loss, itching
  • Infection
60
Q

Stage I and II Hodgkin Lymphoma cure prognosis

A

> 90%

older people do less well

61
Q

stage III and IV Hodgkin Lymphoma cure prognosis

A

50-70%

older people do less well

62
Q

Hodgkin lymphoma often seen as

A

lumps in head and neck

63
Q

aetiology of non-Hodgkin lymphoma

A
Microbial factors strongly implicated
- EBV, HTLV-1, H.pylori
Autoimmune disease 
- Sjögren's Syndrome, Rheumatoid Arthritis 
Immunosuppression 
- AIDS, post-transplant
64
Q

types of Non-hodgkin lymphoma

A

B-cell (85%) or T-cell (15%) types

effects any age (more laid-back in elderly)

65
Q

triggers of non-hodgkin lymphoma

A

Viral and bacterial triggers
- H pylori in stomach - causes ulcers, can lead to gastric lymphoma

If caught early and remove lymphoma will shrink away

External cause often - remove the cause and take away risk disease will spread

66
Q

presentation of non-hodgkin disease

A

Lymphadenopathy – often widely disseminated, may be “invisible”
- Unable to see or fell sometimes – incidental finding on scan

Extra-nodal disease more common

  • Oropharyngeal involvement
  • Waldeyer’s ring (noisy breathing and sore throat)

Symptoms of marrow failure

Constitutional symptoms less commo

If can identify the cause/trigger and remove it, then cancer can go away

67
Q

prognosis of non-hodgkin disease

A
  • > 50% will relapse after treatment
  • Aggressive disease poor prognosis untreated but notably often responds better to treatment
  • Indolent disease hard to cure
    Standard medical therapy not very effective – finding trigger is best route
68
Q

what is multiple myeloma

A

malignant proliferation of plasma cells

69
Q

incidence of multiple myeloma

A

50 per million per year

70
Q

features of malignant myeloma

A

Monoclonal paraprotein in blood and urine

  • Plasma cells - make antibodies. Malignant plasma - lots of antibodies, based on light and heavy chains they normally make - same as from single group clone of cells
  • Can clog kidneys as high blood level passes into urine

Lytic bone lesions can lead to pain and fracture

Excess plasma cells in bone marrow can lead to marrow failure

71
Q

who is more likely to get multiple myeloma

A

Mean age at diagnosis 70 years,

Males > Females,

blacks>whites

72
Q

process of bone failure

A

Infection, bone pain, renal failure and amyloidosis

73
Q

amyloidosis

A
  • Antibodies in excess amount
  • Accumulate tissues e.g. heart, lungs
  • And cause them to enlarge
    Like rheumatoid arthritis
74
Q

treatment of haematological malignancies (4)

A

Chemotherapy

Radiotherapy

Monoclonal antibodies
- Drug ends in MAB; Genetically manufactured to target specific features in specific cell types

Haemopoietic stem cell transplantation

  • Can replace the bone marrow. New bone marrow doesn’t believe you should be there as not matching its old host - attacks the new host from inside. Multi system problem)
  • Can take out own stem cells - clean them so only good functioning ones - And place back into host (Much less risky - less likely to reject)
75
Q

4 concepts to know about for the process of leukaemia and lymphoma treatment

A
  • induction
  • remission
  • maintenance & consolidation
  • relapse
76
Q

induction concept of leukaemia and lymphoma treatment

A
  • Intense chemotherapy

- Blast all bad cells (cancer) out of body

77
Q

remission concept of leukaemia treatment

A
  • none left (no more acute issues)
78
Q

maintenance & remission of leukaemia and lymphoma treatment

A
  • Haven’t managed to remove all the cancer cells in first places - drug doesn’t reach all leukemic cells
  • Depends if can make treatment work in certain way to reach all cells - reduce chance of relapse
79
Q

relapse concept of leukaemia and lymphoma treatment

A
  • Can have multiple relapses but then still improve
80
Q

what is supportive therapy for leukaemia and lymphoma treatment?

A
  • Nutrition
  • Psychological and social support
  • Prevention and treatment of infection
  • Managing symptoms of therapy side effects (e.g.anti-emetics)
  • correcting marked blood component deficits
  • pain control
81
Q

why is supportive therapy very important for leukaemia and lymphoma treatment?

A

as treatments are very unpleasant