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C.C.C > Blue Book: Management of individual cancers > Flashcards

Blue Book: Management of individual cancers Flashcards

1
Q

What is the incidence of breast cancer?

A
  • Most common cancer in women, 19% of all new female cancer.
  • UK 26,000 new each yr, 16,000 women die from the disease.
  • 1/12 women will develop breast cancer.
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2
Q

Risk Factors

A
  • Age
  • Increased periods of oestrogen exposure (late childbearing, nulliparity, early menace, late menopause, obesity)
  • Ionising radiation
  • Family Hx (1st degree relative, especially if b4 meanouase)
  • Inherited mutations: BRCA 1=breast and ovarian. (BRAC2)
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3
Q

Histology

A
  • Infiltrating or invasive ductal carcinoma (IDC): 70-80%
  • Locular Carcinoma (10%): higher incidence of multi-centric tumours.
  • Medullary, colloid, pappilary

Graded 1-3: well-differentiated to poor.

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4
Q

Clinical features: presentation

A 
Breast mass
Nipple discharge
Regional lymphadenopathy (axillary or supraclavicular)
Symptoms of metastatic disease.
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5
Q

Investigate

A

Mammography
Fine needle aspiration cytology/needle biopsy/excisional biopsy

CT if risk of dissemination.
Isotopic bone scan
Liver imaging

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6
Q

Staging

A 
TNM
TO	No primary tumour
Tis	In situ disease, non invasive
TI	Invasive tumour less than 2 cm
T2	Tumour between 2 and 5 cm
T3	Primary tumour greater than 5 cm
T4	Skin involvement
NO	No lymph nodes
NI	Mobile axillary nodes
N2	Fixed axillary nodes
N3	Internal mammary nodes
MO	No metastases
MI	Distant metastases
Stage 0: Tis, N0, M0 
Stage I: T1, N0, M0
Stage II: T2/3, N0, M0 or T0/1/2, N1, M0 
Stage III: T or N > stage II, M0
Stage IV: Any T, Any N, M1
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7
Q

Management:

Surgery

A

Surgery:
1) mastectomy (radical/simple), wide local excision (conservative),

2) assessment of axillary lymph node.
3) Axillary node clearance.

Depends on location, size. breast size, appearance on mammogram, extent of in-situ change and patient preference.

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8
Q

Radiotherapy:

A

Breast:
Conservative: then radiotherapy of residual tissue.
Mastectomy if high risk of recurrence.

Axilla:
Not if full axillary dissection. But consider if risk of local recurrence is high.
Risk of lymphedema.
Sentinel lymph node biopsy, lymph nodes selected for biopsy depending on lymphatic drainage, reduces morbidity.

Palliation of locally recurrent and controlling symptoms of pain.

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9
Q

Systemic therapy: endocrine treatment or cytotoxic chemotherapy. When used?

A

Used in micro metastatic disease and recurrent/metastic disease.

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10
Q

What facts must be considered before selecting treatment?

A
  • Hormone receptor status [oestrogen receptor (ER) status]
  • HER-2 receptor status
  • Menopausal status
  • Sites of recurrent disease (e.g. visceral or soft tissue lesions)
  • Disease-free interval
  • Response to previous treatment
  • Performance status
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11
Q

Endocrine therapy:

A

Tamoxifen 20 mg/day: primary tumours that are ER positive. Increased thrombotic complications and increased endometrial carcinoma.

Aromatase inhibitors: anastrozole and letrozole: better in post menopausal women: toxicity profile: osteoporosis.

After 2-5 years swap from tamoxifen to AI.

Ovarian ablation shown to reduced risk in premenopausal women.: oophorectomy or radiotherapy-induced response. Or LHRH agonist.

Trastuzamab: Herceptin is effective in metastatic/localize disease that over express HER-2 (epithelial growth factor)

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12
Q

Metastatic disease: how many respond to endocrine therapies. What is the median duration of response to single endocrine therapy?

Difference between ER-positive and ER-negative.

A

1/3, 1-2 years.

ER-positive tumours (50-60%)
ER-negative tumours (5-10%)

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13
Q

Chemotherapy

A

Adjuvant: decreases annual risk of recurrence (by 28%) in adjacent setting. Greater in under 50.

Metastatic: palliate symtoms and importve QoL.

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14
Q

Prognostic Factors:

A 
Stage of tumour: 5 year survival
Stage I		: 84% 
Stage II 		: 71 % 
Stage III		: 48 % 
Stage IV		: 18 %

Also dependant on histological grade, nuclear grade, HER-2 and oestrogen receptor status.

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15
Q

Screening:

A

In women age 50+ should reduce breast mortality form 15-20%. Effects remain uncertain.

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16
Q

Colorectal Carcinoma

Incidence

A
  • Second most common malignancy after lung, 10-15% of all malignancies.
  • 28,000 new cases, 19,000 death each year in UK.
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17
Q

Risk Factors:

A
  1. Diet: diet rich in animal fats and poor in fibre.
  2. Inflammatory diseaseL UC related to extent of bowel involvement.
  3. Familial association: Hereditary non-polyposis colon cancer (HNPCC), Familial adenomatous polyposis (FAP) Garder’s syndrome.
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18
Q

Histology

A
  • 40% rectum
  • 20% sigmoid colon
  • 6% caecum

90-95% are adenocarcinomas.

Normally spreads by local invasion, lymphatic, venous and coelomic spread.

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19
Q

Presentation

A

Altered bowel habit
rectal bleeding
vague abdominal pain
Occult tumours on R side can present with iron deficiency anaemia.

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20
Q

Investigations

A

PR exam: 3/4 lesions can be felt.
Visualisation: Rigid sigmoidoscopy (25cm), flexible sigmoidoscopy and colonoscopy + biopsy.
CT
Tumour marker CEA: useful for monitoring

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21
Q

Managentment

A

Surgery:
- Radical resection for primary. If early stage all that is needed.

  • Maybe indicated in advanced patients. Resection of liver mets.
  • Palliative: surgery or colonic stenting to prevent obstruction.

Radiotherapy:
Rectal carcinomas.
Not often used in colon cancers due to toxicity to adjacent organs. Maybe used in bone mets.

Chemotherapy:
Adjuvant for high-risk carcinoma Dukes C

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22
Q

Prognostic: 5 year survival

A 
Stage of tumour: 5-year survival
Stage A		: 80%
Stage B 		: 50%
Stage C 		: 15-40%
Stage D		: 5%

Age below 40 is a poor prognostic factor.

23
Q

Screening:

A

Faecal occult blood testing of average populations have demonstrated a reduction of mortality between 15-18%.

24
Q

Incidence of prostate cancer.

A
  • 3rd most common cancer in males.
  • 10,000 new cases each year in UK
  • Mostly older men, 50% over 75
25
Q

Risk factors

A 
Age
Radiation exposure
Diet
Anabolic steroids
Mutations in BRAC II, pTEN genes
26
Q

Histology

How does it compare to benign prostatic hyperplasia.

Grading system

A

-95% adenocarcinomas in glandular tissue in posterior peripheral glad.

(NB Benign prostatic hyperplasia more commonly arises in the centre)

Grade + architecture defined by Gleason Grade. Effects prognosis

27
Q

Clinical Presentation:

A 
Asymptomatic 
Prostatism:
poor stream
Nocturia 
dribbling 
increased frequency

Some have metastatic symptoms: pathological fracture or bone pain.

28
Q

Examination

A

Rectal examination: enlarged, hard, craggy with obliteration of median sulcus.

29
Q

Investigation

A

Histological diagnosis: transrectal biopsy (US guided)

Tumour markers:
PSA (if low in biopsied tissue but high systemically need radical treatment as likely occult metastases)

Radiological bone scans for bone mets.

MRI: extra-capsular spread

30
Q

TMN Scale

A

Staging
The TNM staging system:
TX: Primary tumor cannot be assessed
T0: No evidence of primary tumor
T1: Clinically unapparent tumor not palpable nor visible by imaging
T1a: Tumor incidental histologic finding in ≤5% of tissue resected
T1b: Tumor incidental histologic finding in >5% of tissue resected
T1c: Tumor identified by needle biopsy (e.g., because of elevated PSA)
T2: Tumor confined within prostate
T2a: Tumor involves 50% of one lobe or less
T2b: Tumor involves >50% of one lobe but not both lobes
T2c: Tumor involves both lobes
T3: Tumor extends through the prostate capsule
T3a: Extracapsular extension (unilateral or bilateral)
T3b: Tumor invades seminal vesicle(s)
T4: Tumor is fixed or invades adjacent structures other than seminal vesicles: bladder neck, external sphincter, rectum, levator muscles, and/or pelvic wall

NO No regional lymph node involvement.
NI Regional lymph node involvement

MX: Distant metastasis cannot be assessed (not evaluated by any modality)
M0: No distant metastasis
M1: Distant metastasis
M1a: Nonregional lymph node(s)
M1b: Bone(s)
M1c: Other or multiple site(s) with or without bone disease

31
Q

Managment

A
  • Relatively indolent, elderly patients may die from different co-morbidity
  • Locally advance disease: surgery, radiotherapy and/or systemic therapy.

Guided by age, performance status, presence of other medical conditions and preference.

32
Q

Observation

A

Asymptomatic disease, confined to prostate.

33
Q

Surgery

A

Localised disease T2 or less, radical prostatectomy. Side effects of impotence and incontinence, 12% mortality.

Palliative (transurethral) to relieve urinary obstruction.

34
Q

Radiotherapy:

A

Radical T1/T2, and PSA is low.
Control of advanced local disease: adjuvant.

External beam or brachytherapy.

Palliative: primary or mets.

35
Q

Hormonal treatment:

A

Advanced disease: inhibition of growth stimulation form endogenous androgens with response rate of 80%.

  • LHRH agonist: (from pituitary) Goserelin/buserelin. SE impotence, loss of libido, tumour flare. Flare: give short term anti-androgen.
  • Anti-androgens
  • Bi-lateral orchidectomy
36
Q

Chemotherapy

A

Cytotoxic therapy with docetaxel (with prednisolone) and cabazitaxel.

37
Q

Prognosis

A

Released to extent of disease.
Median survival for locally advance is 4.5 years. Following radical radiotherapy/surgery 10 year survival is 80-90%.

Patients with metastatic disease have median survival of 2.5 years. High levels of PSA are associated with poorer prognosis.

38
Q

Testicular cancer is predominantly which type of tumour?

What are the classic characteristics of these tumours?

A

Germ cell tumour which accounts for 95% of cases.

Testicular germ cell tumours are classically highly metastatic, sensitive to treatment and can be cured.

39
Q

What is the incidence of testicular cancer?

A

20 per million. 2000 new cases each yr in UK. Predominantly occurring in 15-45 year olds.

40
Q

Risk Factors for TC

A

Maldescent of testes
Testicular atrophy
Family Hx

41
Q

What is the name of the pre-invasive lesion that is often seen in the testis in association with the invasive tumour.

When should it be biopsied? What is the management and why?

A

Intratubular germ cell neoplasia

Biopsy if the contralateral testis is small.

Treat with radiotherapy as otherwise will progress to invasive cancer (10 yrs)

42
Q

Histology.

Name the 2 most common testicular tumours (bonus mark for 2 rare)

A

Germ cell tumour (95%)
Lymphoma (4%)
Leydig & Sertoli cell (1%)

43
Q

There are two histological classification of testicular germ cell tumours. Describe them.

A

Seminomas (40%)

Non-seminomatous germ cell tumours (NSGC1). (60%)

  • Malignant teratoma
  • Combined seminoma/non-seminoma
  • Yolk sac tumours

Tumours may have a mixed histological appearance.

44
Q

Describe the how testicular cancers spread.

A

Early spread is common via lymphatics to para-aortic nodes (reflecting embryological origin from para-renal tissues)

Blood borne spread to lungs, liver, bone & brain is common in advanced disease

45
Q

How does testicular cancer normally present?

A

Painless testicular swelling.

If metastatic:

  • dyspnoea: lung mets
  • low back pain: para-aortic involvement.
46
Q

Investigations

A

Testicular ultrasound- differentiates solid and fluid filled masses & can differentiate between teratoma & seminomas

Tumour markers (next Q)

Trans-scrotal biopsy contra-indicated (risk of dissemination)
Orchidectomy required for tissue diagnosis and for definitive therapy. Biopsy of contralateral testicle is indicated in patients with cryptorchidism or Hx of testicular maldescent (↑risk of bilateral disease)

CT chest, abdo & pelvis post-op.

47
Q

Tumour Markers

A

B-human chorionic gonadotrophin (B HCG): raised in seminomas and non-seminomas.

A-Fetoprotein (AFP) is only raised in the presence of non-seminomatous

Lactate dehydrogenase is a useful marker to assess prognosis, response to treatment and detect relapse.

48
Q

What are the 2 grading systems used for testicular cancer

A

Royal Marsden Staging System

‘Prognostic grouping’

49
Q

Describe the Royal Marsden Staging System

A

Stage I confined to testicle.
Stage II involving para-aortic lymph nodes below the diaphragm.
Stage III involving para-aortic lymph nodes above the diaphragm.
Stage IV Involving visceral metastases.

50
Q

What three factors does the ‘prognostic grouping’ look at?

A

Site of primary
Presence of non-pulmonary visceral mets
Markers

51
Q

Markers are more useful for grading which type of TGC cancer

A

Non-seminomas

52
Q

There are three stages good prognosis, intermediate prognosis and poor prognosis.

Whats is the 5 year survival for each stage?

A

Non-seminoma:
Good: 92%
Intermediate: 80%
Poor: 50%

Seminoma
Good: 86%
Intermediate: 70%
Poor: V poor

53
Q

Treatment

A

Surgery: Orchidectomy
Chemotherapy: Adjuvant
Radiotherapy: para-aortic nodes

54
Q

prognosis

A

Bulky tumour: worse prognosis

Adverse histological markers: yolk sac elements, vascular invasion, lymphatic invasion.
For seminomas size >4cm and rete involvement.

Tumour markers: AFP, BHCG, LDH

NB: presence of pulmonary metastases does not affect prognosis

C.C.C (28 decks)

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