Cancers Flashcards

1
Q

Risk factors of lung cancer

A
asbestos
scarring from eg. tb
smoking
air polution
radon gas
arsenic
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2
Q

Presentation of lung cancer

A
  • haemoptysis, pleuritic chest pain, SOB, unexplained cough for 3 weeks
  • 10% weight loss in 6 months, night sweats, fevers, fatigue, anaemia (iron def)
  • recurrent chest infections, not better with antibiotics
  • hoarse voice = recurrent laryngeal nerve
  • cachexia, clubbing, lymphadenopathy
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3
Q

Investigations for lung cancer

A
  • 1st line CXR (mass + raised hemidiaphragm from phrenic nerve)
  • Endobronchial US guided bronchcoscpy for biopsy
  • Serum calcium (raised if PTHrP from squamous)
  • U&Es (na for siadh in small cell)
  • FBC = anaemia
  • LFTs
  • pulse ox and ecg
  • Contrast CT CAP (adrenals + liver for mets!)
  • spirometry
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4
Q

When would you refer suspected lung cancer? + areas of spread

A

Liver, adrenals, bone, brain spread

2ww cxr if >= 40 and 2 of the following (1 if ever smoked)…
cough/fatigue/sob/chest pain/anorexia/weight loss

OR >40 and 1 of the following…
recurrent chest infections/ finger clubbing/ >6 week lymphadenopathy/ chest signs consistent with lung cancer/ thrombocytosis

2ww cancer pathway if

  • > = 40 and unexplained haemoptysis
  • suspicious cxr
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5
Q

Management of non small cell lung cancer

A

stage 1-3

  • lobectomy (or wedge resection in reduced lung function)
  • neo-adjuvant chemo
  • adjuvant chemo and radio for stage 2 and 3
  • or can use stereotactic ablative radiotherapy as curative therapy

stage 4

  • immunotherapy, targeted therapy, chemotherapy
  • palliative = chemo and radiotherapy for mets and symptoms
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6
Q

Management of small cell lung cancer

A

surgery if it is local but most present as mets
so do palliative chemo
do prophylaxis cranial irradiation

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7
Q

Complications of small cell lung cancer

A
  • siadh
  • lambert eaton syndrome
  • cushings
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8
Q

Complications of non-small cell lung cancer

A
  • hypertrophic pulmonary osteoarthropathy = squamous and adeno
  • PTHrP from squamous (hypercalcaemia)

most pancoast are non small cell

  • horners if sympathetic compression
  • hoarseness if recurrent laryngeal nerve compression
  • svco
  • arm pain from brachial plexus compression
  • vagus nerve compression
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9
Q

Risk factors for breast cancer (male too)

A

Male = gynaecomastia, klinefelters, BRCA1/2, fhx prostate cancer, cirrhosis, radiation

Female =

  • nulliparity, never breastfed
  • increased exposure to oestrogen (early menarche, late menopause, hrt (combined), cocp, obesity or high fat diet, first baby >30)
  • fhx of relative <50 years old
  • older age
  • BRCA1,2
  • p53 mutation
  • chest radiation
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10
Q

Presentation of breast cancer and some other differentials of breast lumps

A
  • painless fixed hard lump in the breast
  • skin changes like dimpling
  • nipple discharge or bleeding
  • nipple changes or inversion
  • Pagets disease of the nipple (ductal carcinoma in situ)
  • oedema or erythema or colour changes
  • Ulceration is a late sign
  • lump in the axilla

fibroadenomas, lipomas, phillodes tumours, fat necrosis

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11
Q

When would your refer suspected breast lump?

A

> =30 2ww
unexplained lump in the breast or axilla

> =50 2ww
unexplained skin or unilateral nipple changes suggestive of malignancy (discharge, retraction, etc)

<= 30 Not urgent
unexplained breast lump

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12
Q

What is the breast screening available?

A

47-73 every 3 years
Mammogram

also for those with brca1/2, fhx of first degree relative <50 years old, previous cancer

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13
Q

How would you investigate breast cancer?

A

Triple assessment

  • mammogram (<35 do US as there is thicker breast tissue)
  • breast examination
  • fine needle aspiration (cytology) or core needle biopsy (histology)
  • CTCAP
  • TNM staging
  • Receptor status (her, oestrogen, progesterone)
  • LFTs, U&Es, FBC
  • bone scan
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14
Q

What are the types of breast cancer?

A

Ductal carcinoma in situ

  • microcalcifications on mammogram
  • associated with pagets disease

Invasive ductal carcinoma
- invaded through basement membrane

Lobular carcinoma in situ

  • may be no lump or discharge, hard to detect
  • often multifocal and bilateral

Invasive lobular carcinoma

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15
Q

How would you manage breast cancer?

A

Wide local excision or mastectomy

  • can do neoadjuvant chemo to reduce tissue
  • adjuvant chest wall radiation afterwards
  • can do sentinel node biopsy or axillary node clearance if indicated
  • adjuvant chemo improves survival

Advanced breast cancer

  • chemo and radiotherapy +/- targeted therapies
  • HER2 +ve = herceptin (tratuzumab)
  • Oestrogen +ve = SERM tamoxifen for premenopausal, Aromatase inhibitor letrozole or anostrozole for post menopausal
  • If triple negative = chemo with platinum and anthracycline
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16
Q

Where does breast cancer spread?

A

lungs, liver, bones

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17
Q

What are some risk factors for colorectal cancer?

A
  • low fibre
  • high processed meat, high fats, alcohol, smoking
  • IBD
  • diabetes
  • old, male
  • familial adenomatous polyposis, HNPCC
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18
Q

How does colorectal cancer present? (L,R,Rectal)

A

Sister Mary Joseph Nodule = lymphadenopathy

R = caecal

  • faecal occult bleeding
  • iron def anaemia/ fatigue
  • appendicitis
  • RIF mass and abdo pain

L = sigmoid

  • colicky pain
  • LIF mass
  • tenesmus
  • bowel changes (diarrhoea, mucus), obstruction etc

Rectal

  • rectal mass
  • tenesmus then persistent pain
  • rectal bleeding
  • if invades anal sphincter = incontinence
  • can invade into sacral plexus = back pain
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19
Q

When would you refer for suspected colorectal cancer?

A
  • palpable rectal mass
  • man with iron deficiency
  • non menstruating woman with iron deficiency
  • > 40 and unknown rectal bleeding or changes in bowel habit for >6 weeks
  • > 50 and unknown rectal bleeding for >6 weeks
20
Q

How would you investigate for colorectal cancer?

A
  • 1st line = flexi or rigid colonoscopy + biopsy
  • barium enema if that was not possible
  • Faecal Occult blood
  • FBC, U&Es, LFTs
  • Cea to monitor treatment
  • CTCAP
  • MRI for rectal cancers
21
Q

What is the colorectal screening system available?

A

60-75 every 2 years

faecal immunochemistry test

22
Q

How would you manage colorectal cancer?

A

Dukes Scale and TNM

Dukes A-C

  • surgical resection (use laxatives before and prophylactic antibiotics after)
  • emergency = hartmanns
  • FOLFOX adjuvant chemo for B and C

Radiotherapy for rectal cancer +/- chemo

Obstruction = decompression colostomy or endoscopic stenting

23
Q

What are some risk factors for prostate cancer?

A

BRCA 2
fhx of prostate cancer, breast cancer, colorectal
Black, male, high bmi, old age

24
Q

How would prostate cancer present?

A
LUTS (hesitancy, resistance)
ED, haematospermia
haematuria
lower back pain
asymptomatic with a randomly raised PSA
anorexia, weight loss, lethargy
25
Q

When would you refer for prostate cancer?

A

Do a PSA and DRE for…
men with LUTS, haematuria, ED

Refer for 2ww if…

  • PSA>=3 in a <70 year old
  • PSA>5 in >70s
  • abnormal DRE
26
Q

What kinds of things can raise a PSA

A

Urinary retention, BPH, Chronic prostatitis, prostate cancer
Vigorous exercise, recent ejaculation
recent medical procedure like TURP or DRE or catheterisation

27
Q

How would you investigate for prostate cancer?

A
  • PSA
  • free PSA (if free PSA<15% and PSA is high, suggestive of malignancy)
  • DRE (BPH is smooth generally enlarged, chronic prostatitis is boggy and tender, cancer is craggy hard irregular nodular)
  • 1st line is Multiparametric MRI of prostate (Linkerts scale if >=3 then do a biopsy too for TNM and Gleason staging)
  • Used to be a Trans Rectal US Guided Biopsy (higher infection than trans perineal)
  • FBC, U&Es (obstruction or hydronephrosis), LFTs
  • Xray for osteosclerotic lesions, bone scan
  • CT CAP
28
Q

How would you manage prostate cancer

A

PSA<10, Gleason<=6, T1-T2a

  • watchful waiting (dres, psa)
  • active surveillance (dres, psa, biopsy)
  • radical prostatectomy or curative external beam radiotherapy +/- brachytherapy

PSA 10-20, Gleason 7, T2b

  • active surveillance
  • radical prostatectomy or curative EBRT+/- brachy

PSA>20, Gleason 8-10, >=T2c

  • radical prostatectomy or curative EBRT+/-brachy
  • hormonal for mets

Hormonal

  • LHRH agonists like goserelin (zolidex) but give androgen antagonist first to avoid testosterone spike
  • or you could do an bilateral orchidectomy to block androgens
  • Androgen receptor antagonists like Bicalutamide

Palliative
bisphosphonates and radiotherapy

29
Q

What are some risk factors for myeloma?

A
  • radiation
  • long term hair dye exposure
  • petrochemical industries or agriculture industry exposure
30
Q

How would myeloma present?

A

CRABBI

Calcium is high

  • osteoclast overactivity, results in bone pain and pathological fractures.
  • stones, moans, bones, psychic groans, polydipsia etc.

Renal dysfunction

  • nephrocalcinosis and nepholithiasis (hyperuricaemia) don’t help
  • light chains get deposited in renal tubules and cause damage

Anaemia
- pancytopaenia due to bone marrow overcrowding, stopping erythropoiesis

Bones

  • bone pain due to osteoclast overactivity and bone marrow overcrowding
  • Lytic lesions seen on xray

Bleeding
- pancytopaenia due to bone marrow overcrowding

Infections
- reduced production of normal immunoglobulins

31
Q

When would you refer about myeloma?

A

do Ca2+, FBC, ESR, PV if >60 and…
unknown pathological fractures or unexplained back pain

do Bence Jones proteins or serum electrophoresis within 48 hours if >=60 and…
- unknown hypercalcaemia/leukopenia AND suspicious myeloma presentation

do Bence Jones proteins or serum electrophoresis within 48 hours for anyone if…
- PV and ESR were suspicious AND suspicious myeloma presentation

do 2ww myeloma if…
- Bence Jones and serum electrophoresis were suspicious for myeloma

32
Q

How would you investigate for myeloma?

A
  • FBC, U&Es, LFTs, Ca2+, PV, ESR, LDH
  • Bone marrow aspiration and trephine biopsy = plasma infiltration of bone marrow
  • Serum protein electrophoresis (monoclonal paraproteins) + Immunofixation (Iga or igg) = raised monoclonal IgG and IgA production
  • Urine protein electrophoresis for Bence Jones proteins
  • peripheral blood film = Rouleaux formation (due to increased paraproteins)
  • Xray = lytic lesions like “raindrop skull”
  • DEXA Bone scan
  • Whole body MRI
33
Q

What results are diagnostic for myeloma?

A
  • monoclonal proteins present in serum or urine from electrophoresis
  • monoclonal plasma cells in bone marrow >10%
  • end organ damage eg. hypercalcaemia, lytic lesions, renal damage
34
Q

How would you manage myeloma?

A

Stem cell transplant (autologous best but risk of neutropenic sepsis)

  • Bortezomib + dexmethasone induction therapy
  • monitor for 3 months after with electrophoresis and bloods

if relapse after initial therapy

  • 1st line Bortezomib
  • or repeat stem cell transplant

Symptom management

  • anaemia = erythropoietin analogues, blood transfusions
  • infection = influenza vaccine, prophylaxis antibiotics, immunoglobulin replacement therapy
  • bone pain = bisphosphonates (+ppi), vit d, calcium
  • lytic lesions already happened = kyphoplasty
  • VTE prophylaxis
35
Q

What are some risk factors for Hodgkins and Non-Hodgkins lymphoma?

A

both:

  • HIV, EBV, Ra, sarcoidosis, autoimmune
  • FHX

non-hodgkins specific:

  • MALT = h pylori
  • Hep B, C
  • hx chemo or radio
  • exposure to pesticides and trichloroethylene
  • old age
36
Q

How would a hodgkins and non-hodgkins lymphoma present? compare and differentiate

A

Hodgkins

  • bimodal distribution (20s then 70s)
  • painless asymmetrical lymphadenopathy non tender
  • pain on drinking alcohol
  • B symptoms prominent like weight loss, night sweats, fatigue, malaise

Non Hodgkins

  • painless asymmetrical lymphadenopathy non tender
  • B symptoms later on
  • Extranodal presentations like hepatosplenomegaly, testicular enlargement, abdo pain, pancytopaenia, SOB
37
Q

When would you refer for query lymphoma?

A

Hodgkins
- unexplained lymphadenopathy (consider B symptoms and alcohol pain)

Non Hodgkins
- unexplained lymphadenopathy or splenomegaly (consider B symptoms)

38
Q

How would you investigate for hodgkins vs non hodgkins lymphoma?

A

Hodgkins

  • FBC, U&Es, LFTs normal, LDH high, ESR high
  • excisional Lymph node biopsy = Reed Sternberg Cells
  • CXR = mediastinal widening
  • CT CAP to stage

Non hodgkins

  • FBC, U&Es, LFTs, LDH, ESR
  • excisional Lymph node biopsy
  • Urea breath test for H Pylori (MALT)
  • Microscopy shows starry sky appearance (Burkitts)
  • Bone marrow aspiration and trephine biopsy
  • Immunophenotyping (B or T cells)
  • Immunoglobulin tests (Igm or Igg)
  • HIV test as it is a risk factor
  • CT CAP to stage
39
Q

How would you manage hodgkins and non hodgkins lymphoma?

A

Ann Arbor staging

Hodgkins:
ABVD Chemo (adriamycin, bleomycin, vinblastine, dascarbazine)

Non Hodgkins:

  • Radiotherapy for localised disease
  • Stem cell transplant
  • CHOP Chemo + rituximab (monoclonal antibody) for high grade
  • flu/pneumococcal vaccines
  • prophylactic antibiotics for neutropenia
40
Q

what are some risk factors for acute vs chronic leukaemia?

A

AML =

41
Q

what are some risk factors for acute vs chronic leukaemia?

A

Acute:
radiation, benzene, genetic mutations like downs and klinefelters

Chronic:
Philadelphia chromosome (BRC-ABL), etc
42
Q

how would ALL and AML present? how would CML and CLL present?

A

ALL = kids!

  • lymphadenopathy, hepatosplenomegaly, testicular enlargement
  • bone pain and bone marrow failure = pancytopaenia (petechiae, bleeding, bruising, infection, fatigue)

AML

  • bone marrow failure and pancytopaenia signs
  • violaceous skin lesions

CLL

  • typically asymptomatic
  • pancytopaenia
  • painless lymphadenopathy more marked than CML
  • very big hepatosplenomegaly

CML typically presents in chronic phase

  • SOB (anaemia), dyspnoea, abdo discomfort, hepatosplenomegaly, lymphadenopathy
  • gout due to increased purine breakdown
  • bruising, bleeding, pallor, infection, fatigue
43
Q

How would you investigate acute leukaemias and how would AML and ALL vary?

A

peripheral blood films =

  • ALL = leukoblasts
  • AML = Auer rods

FBC (low hb, low platelets, high wcc)
U&Es, LFTs, LDH, ESR

Bone marrow aspirate =

  • low erythropoiesis and low megakaryocytes
  • Flow Cytometry Immunophenotyping for myeloid or lymphoid
  • Fluorescent Insitu Hybridisation for mutations like Jak2

ALL has mediastinal widening on CXR

44
Q

How would you investigate chronic leukaemias and how would CML and CLL vary?

A

FBC = low rbc, low platelets, high wcc
(CLL wcc is very very high)

Blood film

  • CLL = smudge cells or smear cells
  • CML = neutrophilia with myeloid precursor like blasts

Bone marrow aspiration =

  • CLL = high lymphocytic infiltration
  • CML = increased cellularity

Immunophenotyping

Fluorescent insitu hybridisation =

  • CLL = trisomy 12, 13q deletion, mutated IgVH
  • CML = philadelphia chromosome (BRC-ABL)

Urate raised

45
Q

How would you manage acute leukaemias?

A

Remission induction using chemo to destroy tumour= huge bone marrow hypoplasia

Then once haematopoesis is acheived, remission consolidation = huge bone marrow hypoplasia

After remission, watch for 3 years. then continue to watch ALL patients closely

AML = high risk are only give treatment if they have an HLA match for bone marrow transplant

ALL = need intrathecal chemo prophylaxis as soon as blasts are cleared from blood

Symptom management

  • bleeding = prophylactic platelet transfusion (esp AML)
  • fresh frozen plasma to maintain APTT and INR<1.5x normal
  • cryoprecipitate to keep fibrinogen >1.5g/dl
  • Norethisterone for women to avoid menorrhagia
  • infection = Prophylactic antibiotics and handwashing education
  • hyperuricaemia = prophylactic allopurinol, rasburicase, hydration
46
Q

How would you manage chronic leukaemias?

A

CML = ph chromosome

  • 1st line = Imatinib for chronic phase
  • if no ph chromosome then interferon a
  • SOKAL index for prognosis

CLL

  • 1st line = Rituximab
  • Rai or Binet staging systems
  • watch for richters syndrome (EBV involved) –> NHL