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Medicine 2 > CAN Week 2 (breast Cancer) > Flashcards

CAN Week 2 (breast Cancer) Flashcards

1
Q

Triple approach for a breast lump

A

Clinical examination - palpating of breast to determine nature and feeling of abnormality

US +/- mammogram (sometimes MRI)

FNAC/B (sample lesion- cutting out cells into needle/ small tissue biopsy)

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2
Q

What clinical features would make you suspicious of a malignant lump

A
  • irregular and hard
  • fixed to the chest wall
  • skin above is tethered
  • palpable lymph nodes in axilla
  • indrawn nipple / nipple involvement
  • bone tenderness / pain
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3
Q

What is fibroadenoma

A

A benign breast tumour

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4
Q

Describe treatment of a breast lump

A

Surgery: wide local excision

Removal of lump with 2cm margin of normal breast tissue, preserving tissue

Sampling of axillary nodes same size
- specimens sent for histology for staging and grading

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5
Q

Different cancer treatments

A

Surgery

Radiotherapy

Chemotherapy

  • neo-adjuvant
  • adjuvant (chemo and surgery combined)
  • palliative

Immunotherapy

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6
Q

What are antimetabolites

A

Interfere with metabolic pathways in DNA synthesis

  • folate antagonist eg methotrexate, inhibits purine and pyrimidine synthesis
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7
Q

What are alkylating agents eg cyclophosphamide

A

Cause chemical, covalent cross-linking of DNA leading to defective DNA replication

  • dna cant be unwinded for replication
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8
Q

What is the mode of action of platinum compounds eg cisplatin

A

Inhibition of DNA synthesis by cross linking guanine residues

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9
Q

What are false substrates eg 5-fluoruracil

A

Pyrimidine analogues

Inhibits thymidylate synthase

Incorporated into DNA as false metabolites and lead to damage of the DNA

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10
Q

What are anthracycline antibiotics eg doxorubicin

A

Interfere with nucleotide synthesis by intercalated between DNA strands, inhibiting topoisomerase and generating free radicals

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11
Q

What are topoisomerase inhibitors eg etoposide

A

Inhibition of topoisomerase II prevents ligation of DNA, leading to breaks in the DNA strand

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12
Q

What are microtubule inhibitors

A

Vinca alkaloids block the formation of the mitotic spindle

- taxanes stabilise spindle fibres

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13
Q

Side effects of anticancer drugs

A
  • inhibit all fast growing cells (gut, epithelia, hair loss) myelosuppression (bone marrow) for all except vincristine
    This causes ulcers in the mouth and diarrhoea

Myelosuppression:

  • anaemia
  • decreased resistance to infection (neutropenic sepsis)
  • increasing bleeding
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14
Q

How can some of the side effects of anticancer drugs be overcome

A

Overcome reduced white counts with colony - stimulating factors

Prevents infections with antibiotics and antifungals

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15
Q

Other side effects of anti cancer drugs

A

Nausea: common esp with platinum compounds
- use of anti-emetics

Hair loss

Infertility (due to the drugs being highly damaging to rapidly dividing cells eg sperm)

Cardiotoxicity with anthracycline antibiotics

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16
Q

What is palliative care for cancer

A

Pain relief

Use strong opiods

  • morphine and diamorphine
  • oromorph for breakthrough pain
  • constipation and nausea
  • fentanyl patches
  • syringe drivers
  • hospice care
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17
Q

Symptoms of ovarian cancer

A 
Abdominal pain 
Persistent indigestion / nausea 
Bloating 
Pain during sex 
Altered bowel habits 
Back pain 
Vaginal bleeding 
Tiredness 
Unintentional weight loss
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18
Q

How do targeted approach exploit biological weakness in tumours

A

Faulty genes
Faulty signalling systems
Tumour growth
Angiogenesis

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19
Q

What do hormonal targets do

A

May antagonise hormones responsible to promoting tumour growth eg oestrogen in breast cancer

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20
Q

Describe hormone based therapy in breast cancer

A

Oestrogen can stimulate the growth of metastasised cells (proliferation)

Tamoxifen is used as it blocks oestrogen as a selective oestrogen- receptor modulator (SERM) - reduces growth of oestrogen driven breast cancer. Used in ER+ breast cancer
- prevents bone loss via oestrogenic effects

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21
Q

Why is breast cancer more common in older generation

A

Over expression of oestrogen is more common in older population and oestrogen can drive proliferation of cancer cells

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22
Q

What are aromatase inhibitors eg anastrozole

A

An inhibitor that prevents peripheral conversion of androgens into oestrogen in post-menopausal women by the enzyme aromatase

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23
Q

How is oestrogen produced before and after menopause

A

Before: produced in ovaries
After: produced via the conversion of androgens via aromatase enzyme

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24
Q

What is HER2

A

Naturally present in low levels but can be over expressed in some cancers eg breast cancer

  • more likely in older patients
  • due to oncogene (ERBB2)
  • affects gene transcription and cell cycle
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25
Q

What happens when HER2 becomes dysregulated

A

Over expression of some elements of DNA and dysregulation of cell cycle which leads to production of VEGF, COX2 and cyclins

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26
Q

What is trastuzumab

A

(MAB) large molecule approach
Selective to the HER2 receptor. (Targets it to slow down cell replication)
- manages early breast cancer and metastatic breast cancer with HER2 positive tumours

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27
Q

What is epidermal growth factor kinase eg erlotinib

A
  • small molecule approach

- has utility in some lung and pancreatic cancer if they over express the EGF receptor

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28
Q

Mode of action of epidermal growth factor receptor

A

Phosphorylates tyrosine residues which alters DNA transcription and severs the cascade signalling at that point

(Targeting the activity of the second messenger)

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29
Q

Tyrosine kinase activity

A

Philadelphia chromosome associated with chronic myeloid leukaemia (more than 90% of patients with myeloid leukaemia produce an abnormal Ph chromosome)

  • Ph chromosome produces bcr-abl protein which has tyrosine kinase activity
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30
Q

Tyrosine kinase inhibitor

A

Tyrosine kinase leads to uncontrolled cell proliferation

  • imatinib inhibits TK acitivity
  • selective inhibitor is very effective for chronic myeloid leukaemia
  • trials >90% pts with CML alive after 5 years
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31
Q

What are PARP inhibitors eg olaparib

A

PARP: poly (ADP-ribose) polymerase

  • an enzyme which repairs DNA
  • BRCA genes important in DNA repair at double strange breaks: PARP enzyme repairs single strand breaks
  • BRCA gene mutations: inhibition of PARP leads to inability of cancer cells to repair double strand breaks, leading to cell death
  • can be used in chemoresistant ovarian cancer
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32
Q

Proteasome inhibitor

A

Proteasome: cellular structures which degrade proteins
- some proteins kill cancer cells: pro-apoptosic factors
- inhibition of intracellular proteasomes alters the regulation of intracellular proteins
Eg bortezomib used in multiple myeloma

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33
Q

What is anti- VEGF

A

Vascular endothelial growth factor

- VEGF secreted to promote angiogenesis (blood vessel growth to support metastasis)

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34
Q

What are the 2 anti- VEGF approaches

A

Bevacizumab: (MAB) - advanced colonic and breast cancer

Sunitinib: inhibits VEGF-associated receptor tyrosine kinase - advanced renal carcinoma

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35
Q

What is the cause of common genetic breast cancer

A

5-10% of breast cancer cases (BRCA)- due to highly penetrant germ line mutations in cancer predisposition genes
- up to half of these families will have mutations in BRCA1 or BRCA2

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36
Q

What are the different predisposition genes for inherited cancer

A

1) proto-oncogenes - genes whose action positively promotes cell proliferation
2) tumour suppressor genes- if not working you get uncontrolled cell growth
3) mutator genes : maintain the integrity of the genome

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37
Q

Syndromes caused by mutations in Porto-oncogenes

A

Multiple endocrine neoplasia type 2

MET- hereditary papillary renal carcinoma

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38
Q

Syndromes caused by mutations in tumour suppressor genes

A

PTEN: breast cancer, skin tumours, thyroid cancer

APC: familial, adenomatous, polposis coli

BRCA1/2: breast and ovarian cancer

TP53: young onset cancers particularly sarcoma and breast

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39
Q

What is Knudsons two hit hypothesis

A

Gene mutations may be inherited or acquired during a persons life
A cell can initiate a tumour only when it contains 2 mutant alleles

1st mutation: present in all the cells of the patient
2nd mutation: arises in a somatic cell in the organ in which the tumour develops (loss of heterozygosity) - tumour only develops after 2nd mutation

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40
Q

Syndromes caused by mutations in mismatch repair genes

A

(HMLH1 and hMSH2)

Colorectal, endometrial, ovarian, uterus or renal pelvis and brain

41
Q

Patient groups likely to ask about cancer predisposition risk

A

People who present in primary care because of concerns about a family history

Affected parents about risk to siblings and offspring

42
Q

Breast cancer clinical risk categorisation.

A

Low risk- less than 2x population lifetime risk of br ca

Moderate risk 2-3x population lifetime risk of br ca

High risk - greater than 3x population lifetime risk of br ca

43
Q

Bowel cancer clinical risk categorisation

A

Low risk- risk of developing bowel ca <1 in 10

Moderate risk - risk of developing bowel ca 1 in 6 to 1 in 10

High risk - risk of developing bowel ca > 1 in 6

44
Q

What is malignancy

A

Disordered growth and differentiation of normal tissues

  • arises from genetic damage
  • arises due to increases proliferation or reduced apoptosis
45
Q

2 types of haematological malignancy

A

1) myeloid: including myeloproliferative disorders
- myelodysplasia

2) lymphoid : including lymphomas and immunosecretory disorders

46
Q

Myeloid disorders (series of malignancies)

A
  • acute myeloid leukaemia
  • chronic myeloid leukaemia
  • myeloproliferative disorders:
  • essential thrombocythaemia
  • polycythaemia rubra Vera
  • myelofibrosis
  • idiopathic hypereosinophilic syndrome
  • systemic mastocytosis
  • myelodysplasic syndromes
47
Q

Lymphoid disorders

A
  • acute lymphoblastic leukaemia
  • chronic lymphocytic leukaemia
  • plasma cell disorders eg myeloma

Non Hodgkin’s lymphomas eg

  • Hodgkin’s disease
  • diffuse large B NHL
  • follicular lymphoma
  • mantle cell lymphoma
  • marginal zone lymphoma
  • burkitts lymphoma
  • T cell lymphomas
48
Q

Myeloproliferative disorders

A

Present with an excess of mature cells in the blood:

  • polycythaemia rubra Vera: excess red cells
  • essential thrombocythaemia: excess platelets
  • both PRV and ET may progress to myelofibrosis or acute leukaemia
  • both PRV and ET have an underlying problem with the Janus kinase gene JAK2 (may cause stroke or heart attack due to abnormal clotting)
49
Q

What is myelofibrosis

A

Excess bone marrow scarring due to abnormal megakaryocyte activity- leading to bone marrow failure

50
Q

What is acute leukaemia

A

Leukaemia is malignancy of the bone marrow

  • very rapid cell growth
  • may fill marrow before spilling out into blood
  • high WBC not always present
  • present with bone marrow failure : anaemia, thrombocytopenia, neutropenia
  • may arise from pre existing conditions eg myelodysplasia
51
Q

Treating acute leukaemia

A

Delay in treatment makes infective complications worse
- commence chemo immediately

AML: strong iv chemo in short sharp bursts

  • younger patients have better prognosis as can tolerate high dose better
  • elderly may receive palliative chemo (gentler)

ALL= mix of strong chemo and persisting milder tablets ( for 3 years) to prevent relapse

52
Q

Acute lymphoblastic leukaemia

A

Commonest malignancy of children

  • peak incidence age 4-5
  • may present with cytopenias or chest masses
  • 90% can be brought into remission with infection chemo
  • 85% cured
  • higher replapse rates in older children and boys (testes and CNS are ‘sanctuary sites’)
53
Q

Chronic myeloid leukaemia

A

Chronic leukaemias present with high white cells but not usually with bone marrow failure

  • CML presents with:
  • high WBC
  • splenomegaly
  • priapism

Due to t(9:22) = Philadelphia chromosome

  • gene fusion produces BCR- ABL fusion protein
  • treatment now involves specific inhibition of this tumour cell specific enzyme by the drug IMANTINIB
54
Q

Chronic lymphocytic leukaemia

A

Relatively common (3000 cases/year in UK)

  • increases with age
  • majority of patients die of unrelated conditions
  • treatment is only required for troublesome symptoms, bulk disease or marrow failure
  • reproductive rate of most CLL is less than ordinary blood cells, but defective apoptosis means they don’t die normally
  • usually present incidentally on a routine FBC for other reasons, but may present with lymphadenopathy
55
Q

How do you diagnose chronic lymphocytic leukaemia

A

High lymphocyte count

  • smudge cells on blood film
  • appropriate cell surface markers on lymphocytes
  • hypogammaglobulinaemia (low antibody levels) common association but not diagnostic
  • may have lymphadenopathy or splenomegaly
  • may have immune disturbance
  • may have marrow suppression
56
Q

Chronic lymphocytic leukaemia prognosis (using Binet staging system)

A

Stage A: lymphocytes is only: 10 years
Stage B: lymphocytosis + 3 areas lymphadenopathy : 5 years
Stage C: lymphocytosis +LN + Hb<10 : 2 years

57
Q

Non Hodgkin’s lymphoma

A

Grouping of a variety of different disease entities all showing tumour growth of lymphoid cells

  • 30% occur outside lymph nodes
  • more common in the elderly
  • some may be related to viruses eg EBV, HTLV, HHV8, HIV
  • some related to chemical exposure
  • some related to sunlight exposure
  • B symptoms pr lymphadenopathy are the usual clue to lymphoma
58
Q

What are lymph nodes

A

The police stations of the bodies immune system

  • they may swell as part of the normal immune response
  • they may swell if the lymph system is invaded by the metastatic solid tumour
  • they can swell in lymphoid malignancy
59
Q

What are B symptoms

A

Weight loss > 10% in 6 months
Drenching night sweats - enough to change clothes

  • fevers >38c
60
Q

What is Hodgkin’s disease

A

A subtype of the non Hodgkin’s lymphomas

  • related to EBV infection
  • 2 age peaks - teens / early twenties and elderly
  • age peaks may be related to where the EBV has integrated in the lymphocyte DNA- closer or further away from the proto- oncogenes
  • presents with B symptoms + continuous nodal spread
  • the bulk of the tumour in HD are ‘normal’ white cells reacting to the presence of tumour cells
61
Q

What is stage of lymphoma

A

Defines the extent

  • spread is not the death sentence it is in other tumours as lymphocytes naturally circulate
  • worse stage implies but does not guarantee worse prognosis
  • assess stage by CT scan to locate lymphadenopathy and extra lymphatic spread + bone marrow to assess marrow involvement
  • bone marrow biopsy is not a diagnostic test for lymphoma
62
Q

What is grade of lymphoma

A

Non Hodgkin’s lymphoma is a diverse group of diseases

Grade is a shorthand way of telling how aggressive the condition is in a particular patient

Low grade = slow, grumbling
High grade = fast, aggressive

63
Q

Immunosecretory disorders

A

Myeloma

Asymptomatic myeloma

MGUS (monoclonal gammopathy of uncertain significance)

Localised plasmacytoma

Waldenstroms macroglobulinaemia

Cold haemagglutin disease (CHAD)

Amyloidosis

64
Q

List some normal antibodies

A

IgD is expressed by newly mature B lymphocytes
IGM clears pathogens from circulation
IgG clears pathogens from tissue fluid
IgA prevents pathogens invading mucosal surfaces
IgE protects against parasites

65
Q

What are paraproteins

A

Normal plasma proteins can be analysed by electrophoresis

Normal antibodies occur as a polyclonal smear on EP

Paraprotein = monoclonal antibody, causing a spike in the normal globulin pattern

Urine paraprotein = isolated light chains - bence-jones protein

66
Q

What are the 2 out of 3 conditions that must be met to diagnose myeloma

A

1) plasma cells in marrow >10%
2) detectable paraprotein in blood or urine
3) lyric lesions on skeletal survey

Skeletal survey = series of plain XR. It is not the same as a bone scan

67
Q

Diagnosing myeloma

A 
Disease of the elderly 
Think of this diagnosis whenever you see a patient with: 
- anaemia 
- high ESR 
- back pain
- unexpected renal failure 
- unusual fractures

3000 cases per year in uk, poor prognosis

68
Q

What is waldenstroms macroglobulinaemia

A

Disease of the elderly

  • clue is IgM paraprotein
  • marrow shows sparse infiltrate of lymphoplasmacytoid lymphocytes. Ie midway between lymphocytes and plasma cells
  • disease bulk is not normally a problem - health risk is hyper viscosity due to paraprotein
  • if IgM paraprotein has haemolytic activity the disease is CHAD (cold HaemAgglutinin disease)
69
Q

What is hyperviscosity syndromes

A

Due to excess plasma proteins (fibrinogen, IgM, IgA etc) or extreme polycythaemia
- blood is stickier so does not flow as easily (treacle compared to water)
Symptoms are: fatigue, headaches, confusion
May progress to stroke , heart attack
- anaemia lowers viscosity (less RBC to impede blood flow) so correcting this with transfusion is dangerous

  • severe cases treated by plasmapheresis to remove protein
70
Q

What is myelodysplasia

A

Disordered maturation of blood cells in bone marrow
- any or all cell lines may be affected eg isolated thrombocytopenia or pancytopenia

  • easy to diagnose if a chromosomal abnormality is detected or if disorganisation of marrow is severe
  • may be hard to distinguish from reactive marrow changes eg from rheumatoid arthritis, chronic infection or other systemic illness

Can progress to acute leukaemia with time

71
Q

Dietary factors causing cancer

A

Obesity / weight gain (insulin and insulin related growth factors)

Red and processed meat (nitrates + AA = nitrosamines; N-nitroso compounds; high cooking temperatures - heterolytic amines)

Saturated and animal fats- lung, colorectal, prostate and breast

Alcohol- aerodigestive tract, liver and breast

Protective: fruit, veg, phytochemicals, fibre, dairy, calcium and vit D

72
Q

Describe undernutrition in cancer patients

A

At the time of diagnosis approx 75% of cancer patients are undernourished with a significantly lower fat free mass than healthy controls

  • patients with highest weight loss are those with cancer of oesophagus, stomach and larynx
73
Q

What is cachexia

A

Chronic hypermetabolic state characterised by rapid weight loss and anorexia

Generally seen in cancer patients, certain infectious disease and chronic alcoholics

Prevalence depends on type of malignancy seen in up to 85% of gastrointestinal, pancreatic, colorectal and lung cancer patients at diagnosis

Duration, malignancy and number of anatomic sites tend to cause hyper metabolism

74
Q

What is nutrition therapy for cancer patients

A

Essential to increase the likelihood of completion of cancer treatment and improve quality of life

Support adequate energy and nutrient intake with the aim to:

  • reverse undernutrition and weight loss that have already occurred
  • prevent weight loss and promote weight gain
  • enhance immune function.
  • reduce mental and physical fatigue
75
Q

What is enteral nutrition support

A

Provided when patients are expected to or have not received adequate nutrition for 7 days

Small bowel feeding administered with pump over 8-20 hours

Formulas come in a variety of energy densities

76
Q

What is parenteral nutrition support

A

Used when GI tract is not functional, accessible or safe to use eg colon cancer

Central or peripheral vein

Energy requirement predicted from estimated daily energy expenditure

77
Q

What is the lymphatic system

A

Part of immune system
Have both superficial and deep lymphatic vessels and nodes
Superficial drains into deep vessels

78
Q

What is the lymphatic system composed of

A

Lymphatic vessels (thin walled and have valves) found throughout the body. They emerge from the:

  • lymphatic plexuses (small lymphatic vessels)
  • lymphatic capillaries (in extracellular space)
  • lymph nodes (filter the lymph)
  • lymphocytes (circulating cells)
  • lymphoid organs (where lymphocytes are produced eg spleen, thymus)
79
Q

What is the role of the lymphatic system

A
  • part of immune system
  • drains interstitial fluid from the tissues of the body and empties it into venous system
  • absorbs and transports fat from food (so via intestines)
80
Q

Describe lymphatics of breast

A

Most lymph of the lateral breast drains into axillary lymph nodes

Most lymph of the medial breast drains into parasternal lymph nodes or to other breast

Most lymph of the inferior breast drains into abdominal lymph nodes

81
Q

What does postural drainage involve

A

Person is placed in a number of different positions - so each lobe of the lung is drained

  • requires gravity so in some positions the lungs need to be lower than the hips
  • chest physiotherapist involves gentle banging or percussion of the lungs whilst in a drainage position
  • removes mucus etc from the lungs
  • helps relieve some of the symptoms in someone with eg COPD, cystic fibrosis
  • potential problems are eg acid reflux - if that leads to someone choking and getting it in their lungs, can then lead to infection
82
Q

Difference between differentiation of benign and malignant

A

Benign: resembles cell of origin

Malignant: failure of differentiation

83
Q

Difference between behaviour of benign and malignant

A

Benign: expansive; grows locally

Malignant: expansile and invasive; may metastasise

84
Q

What are the 2 main groups of lymphomas

A

Hodgkin’s disease

  • non Hodgkin’s lymphoma : the most common and important of these are the lymphocytic lymphomas
85
Q

Clinical features and behaviour of lymphoma

A

Most present clinically with lymphadenopathy : lymph node enlargement, localised or generalised

Some may also infiltrate liver (hepatomegaly), spleen (splenomegaly) or bone marrow

Bad prognosis types may diffusely infiltrate other organs

86
Q

Define myeloma

A

A tumour of mature plasma cells. Presents with bone tumours, osteolytic, painful but with interesting systemic effects

87
Q

Summarise lymphomas

A

Lymphomas are malignant diseases derived from lymphoid cells

  • 2 main types: Hodgkin’s disease and non hodgkins lymphomas
  • main effects are replacement of lymph nodes and infiltration of other tissues
  • myeloma is a bone marrow disease based on plasma cells
88
Q

What are astrocytomas

A

Brain tumours that behave in a malignant manner by local invasion but do not metastasise

89
Q

What are embryonal tumours

A

Derived from embryonic remnants of primitive ‘blast’ tissue

Mainly in young children
Highly malignant
Spread early and widely by lymphatic and veins
Sensitive to chemo
Formerly rapidly fatal, chemo has revolutionised prognosis

90
Q

Name some different embryonal tumours

A

Nephroblastoma (Wilms tumour) - in kidney, most common

Neuroblastoma - in adrenal gland, derived from primitive adrenal medullary precursors

Rarer:
Retinoblastoma - retina; often bilateral; genetic basis
Medulloblastoma - cerebellum
Hepatoblastoma- liver

91
Q

What are teratomas

A

Tumours derived from primitive germ cells which retain the capacity to differentiate along all 3 primitive embryological lines. Hence teratomas should contain representative of ectoderm, mesoderm and endoderm

As they are of germ cell origin, they mainly occur in the ovary and testis

92
Q

Describe teratomas of the ovary

A

Young women
Benign

Invariably cystic (benign cystic teratoma)

Cyst contains keratin (dermoid cyst of ovary)

Skin, hair, bronchial and gut epithelium, thyroid, neuroglia, bone, cartilage

Good prognosis

93
Q

Describe teratomas of the testis

A

Young men
Painless swelling of testis

Malignant

Malignancy varies according to type

Spreads early via blood stream (lung and liver etc)

Chemo has revolutionised prognosis

Tumour markers are important in management

94
Q

What suggests a mass might be malignant rather than benign

A

Fixation of the mass to deep tissues

95
Q

What 4 things are true about benign tumours

A

1) can cause illness and death
2) can increase pressure on adjacent vital structures in the brain
3) can secrete hormones
4) can convert to malignant tumours

96
Q

What can colorectal cancers present as

A

1) intestinal obstruction
2) fresh bleeding per rectum
3) severe anaemia of unknown cause
4) weight loss
5) hepatomegaly

97
Q

Which tumours produce the tumour marker: alpha-fetoprotein

A

1) hepatocellular carcinoma

2) germ cell tumours

98
Q

Which tumours produce harbour alterations in the MYC oncogene

A

1) burkitts lymphoma

2) neuroblastoma

Medicine 2 (16 decks)

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