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Cancer and Continuing Care > Blue Book Questions: Big 4 Cancers > Flashcards

Blue Book Questions: Big 4 Cancers Flashcards

1
Q

How common is Lung cancer?
What is it second to in men and women?
How many new cases are there each year and what proportion does it account for in new cancer cases?
Is it more common in women or men?

A

Second/third commonest (13%)

Prostate in men and breast in women

42000 new cases each year

More common in men, 1 in 11 approximately will develop lung cancer.

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2
Q

What are the risk factors for lung cancer?

A

Age - incidence rises steeply after the age of 40

Smoking - 80-90% of cases are caused by smoking

Occupation - Asbestos exposure, uranium mining, ship building and petroleum refining

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3
Q

What is the aetiology of lung cancer?

A

Chromosomal deletions of 3p and to a lesser extent 13q and 17p result in the loss of tumour suppresor genes.

Over expression of many oncogenes such as ras, myc, and c-erb-b2.

Certain activating mutation in the EGFR associated with small proportion of lung cancers.

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4
Q

Where do tumours arise in lung cancer and how does the the WHO classify them?

A

Arise from the epithelium of the large and medium sized bronchi, and rarely from the lung parenchyma itself.

Small cell LC
Non small cell LC
Carcinoid, sarcoma, lymphoma

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5
Q

What percentage of lung cancers are small cell and what is their histology?

A

~18%
These may derive from neuro-endocrine cells within the lung. They are therefore associated with neuropeptide secretion such as ADH or ACTH

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6
Q

What percentage of lung cancers are non small cell lung cancer and what is their histology and subgroups?

A

~82%
These types can be further subdivided into:
Squamous cell carcinoma (32%)
Adenocarcinoma (26%) may arise in areas of lung damage, are often peripheral and are more frequent in women.
Large cell carcinoma (10%)
NSCLC not otherwise specifice

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7
Q

What symptoms do the majority of patients present with with lung cancer?

A

Present with non-specific symptoms of the primary tumour such as cough, dyspnoea, haemoptysis, chest pain, or recurrent chest infection.

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8
Q

What other symptoms may patients with lung cancer at specific sites present with?

A

Apical tumours - may invade brachial plexus producing Horner’s syndrome and pain in the distribution of the nerve routes (Pancoast’s tumour)

Mediastinal disease - recurrent laryngeal nerve palsy and superior vena cava obstruction.

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9
Q

What symptoms can be associated with specific histologies of lung cancer?

A

Clubbing is more frequent with squamous cell carcinoma.

Sputum production may be excessive in bronchiolo-alveolar carcinoma.

SCLC may present with manifestations related to the production of neuro-endocrine factors.

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10
Q

What investigations are indicated in lung cancer?

A

CXR - more than 95% of lung tumours are visible on a CXR at presentation

Sputum cytology - over 80% of patients with LC have malignant cells detectable in sputum

Bronchoscopy - allows visualisation, tumour biopsy and bronchial washings to be taken

Other biopsy techniques - trans-thoracic biopsy, mediastinoscopy.

CT chest and upper abdomen

PET scan

Other diagnostic tests - head scans or isotope bone scans for mets

Tumour markers - neuron specific enolas (NSE) and lactate dehydrogenase (LDH) indicate tumour activity, not routine

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11
Q

How is accurate staging of lung cancer tumours performed?

What staging system is used?

A

CT scans of chest and upper abdomen and sometimes isotope bone scans or head scans are required.
Patients considered for surgical resection require assessment of cardiopulmonary function.

TNM for non-small cell lung carcinoma and small cell carcinoma.

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12
Q

What do the T stages range from in lung cancer and what are the parameters?

A

T1-4

T1 - 3cm or less, surrounded by lung or visceral pleura and not invading a main bronchus

T2 - More than 3cm but less than 7cm or invading a main bronchus (but >2cm from the carina) or invading visceral pleura or causing atelectasis of some but not all of one lung

T3 - More than 7cm or local invasion of particular structures (irrespective of size of tumour):
Chest wall, diaphragm, phrenic nerve, mediastinal pleura, parietal pericardium, main bronchus within 2cm of carina, atelectasis of entire lung or separate tumour nodule in same lobe

T4 - Organ invasion (inoperable): mediastinum, heart, great vessels, recurrent laryngeal nerve, oesophagus, vertebral body, carina or separate tumour nodules in a different ipsilateral lobe

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13
Q

What do the N stages range in from in lung cancer and what are the parameters?

A

N1-3

NI - Ipsilateral bronchopulmonary and hilar nodes

N2 - Ipsilateral mediastinal node (operable) or subcarinal

N3 - Contralateral mediastinal or contralateral hilar nodes, or supraclavicular nodes (inoperable)

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14
Q

What do the M stages range from in lung cancer and what are the parameters?

A

M0-M1a/1b

M0 -No metastases

M1a - Separate tumour nodules in contralateral lung, malignant pleural of pericardial effusion

M1b - Distant metastases

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15
Q

What stage grouping is used for non-small cell lung cancers, how many stages are there and what are their parameters?

A

VICC/AJCC group staging

Stage I: TI NO MO, T2 (if ≤5cm,) N0 M0

Stage 2: TI NI MO, T2 (if 5-7cm) N0 M0, T2 NI MO, T3 N0 M0

Stage 3a: T1/2/3 N2 MO, or T3 N1 M0, or T4 N0 M0, or T4 N1 M0

Stage 3b (inoperable):T4 N2 M0, any N3 MO

Stage 4: any M1

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16
Q

Why was the TNM previously not used in small cell lung cancer?

A

Small Cell Lung Cancer (SCLC) metastasises extremely early in its clinical course and most patients will have occult metastases at presentation.

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17
Q

What are the two classifications for small cell lung cancer put forward by the Veterans Administration Lung Cancer Study Group?

A

Limited: Tumour confined to one hemi-thorax with local extension confined to ipsilateral or contralateral mediastinal nodes or ipsilateral supraclavicular lymph nodes.
Extensive: Disease at sites beyond the definition of limited disease. Two thirds of patients present with extensive disease.

Traditionally the difference between extensive or limited stage disease was whether or not the tumour could be encompassed within a radical radiotherapy field (limited) or not (extensive).

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18
Q

What is small cell lung cancer considered at presentation and what is its treatment?

A

Considered systemic disease at presentation.

One of the most chemo sensitive solid tumours but also highly radiosensitive

Chemotherapy, with radiotherapy in limited stage disease

Can treat SVCO and spinal cord compression with chemo too in contrast to NSCLC

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19
Q

What is the response rate to combination chemotherapy in small cell lung cancer?

A

90% will respond, with complete response rates approaching 50%

Most will relapse, many within 12 months of chemo with disease that is chemo-resistant and die from rapidly progressive disease

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20
Q

When is radiotherapy indicated in small cell lung cancer?

A
  1. Treatment of primary tumour. Thoracic radiotherapy as consolidation after chemotherapy or as concurrent treatment improves overall survival in patients with limited disease. Local control is achieved with radiation such that relapse occurs at a site distant to that of the primary disease. This pattern of relapse may result in improved palliative symptom control.
  2. Prophylactic cranial irradiation (PCI). Brain metastases are frequent in SCLC and cause significant morbidity. PCI reduces the frequency of brain metastases and improves survival, but is associated with toxicities such as memory impairment, functional deficit and dementia. It is usually applied in good prognosis limited and chemotherapy sensitive disease.
  3. Palliative. Radiotherapy may be used to palliate the symptoms of advanced SCLC, unresponsive to other treatments.
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21
Q

What is the median survival of small cell lung cancer without treatment and how is it improved with systemic chemo?

A

2-4 months without treatment

Approximately 11 months with chemo

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22
Q

What are the prognostic factors for small cell lung cancer treatment?

A

Extent of disease at presentation
Number of metastatic sites
Performance status
Degree of weight loss Biochemical abnormalities (elevated LDH or low sodium or albumin).

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23
Q

Within how much time from diagnosis will most patients with non small cell lung cancer die?

A

12 months

24
Q

How would you treat stage 1 and 2 non small cell lung cancer and what is the prognosis?

A

Surgical resection

80% 5 year survival

25
Q

What is offered to patients who are not suitable for surgery and what is the prognosis in non small cell lung cancer?

A

Radical radiotherapy

20% 5 year survival in patients with stage 1 or 2 disease

26
Q

How is the radiotherapy administered and what is it called?

A

CHART (continuous, hyperfractionated accelerated radiotherapy)

Three times a day for 12 consecutive days.

27
Q

What are the response rates of chemotherapy in non small cell lung cancer and what types are used?

A

Chemotherapy can produce response rates of up to 30% with combination regimes such as carboplatin and gemcitabine or carboplatin and paclitaxel.

28
Q

What can be used in non-small cell lung cancer as a second line choice for palliation after chemo?

A

Tyrosine kinase inhibitors (erlotinib or gefitinib)

29
Q

How common is prostate cancer?

How many new cases a year in the UK?

A

Most common cancer in men second/third commonest overall (13%).
More than 10000 new cases diagnosed in the UK each year. More than 50% occurring over the age of 75.

30
Q

What are the aetiological factors in prostate cancer@?

A

There are no clear etiological agents although radiation exposure, diet and anabolic steroids have all been implicated. These may alter the level of the male hormone testosterone which controls the growth, and function of the prostate. Mutations of BRCA II and the pTEN genes are associated with an increased risk but familial prostate cancer is rare.

31
Q

What is the most common histological type of prostate cancer?

A

Adenocarcinomas (95%)

32
Q

What score is used to assess prostate cancer?

A

Gleason grading system

33
Q

How does prostate cancer present?

A

Frequently asymptomatic and diagnosed by routine rectal examination.

Prostatism (poor stream, nocturia, dribbling and increased frequency)

In some patients metastatic symptoms, e.g bone pain

34
Q

What is felt on prostate examination in prostate cancer?

A

An enlarged, hard, craggy gland is felt, with obliteration of the median sulcus.

35
Q

How do you investigate prostate cancer?

A

Histological diagnosis is mandatory with transrectal biopsy ideally performed under ultrasound guidance.

PSA (serum prostate-specific antigen)
Radionucleotide scans may be useful to detect bone mets.
MRI

36
Q

How does the gleason system score tumours?

A

From 2 to 10 on the basis of histological patterns in the two most predominant areas of the tumour, (e.g. Gleason 4 + 3 means main area is 4 with the second area 3).

37
Q

How is prostate cancer managed?

A

Locally advanced disease (T2 or less) treated with surgery, radiotherapy and/or systemic therapy.

Observation, in asymptomatic disease confined to the prostate.

Radiotherapy, as an alternative to surgery

Hormonal therapy

Chemotherapy in castrate-refractory metastatic disease.

38
Q

What types of surgery are used and what are side effects in prostate cancer?

A

Radical prostatectomy

Impotence and incontinence

39
Q

Why is hormonal therapy indicated in prostate cancer?

What types of hormonal therapy are used?

A

To achieve castrate state (no testosterone. Inhibition of the growth-stimulatory effect of endogenous androgens may effectively treat prostatic cancer with a response rate of approximately 80%. Hormonal methods can also be used in a neoadjuvant manner to ‘downstage’ a tumour prior to surgery.

LHRH agonists
Oestrogen therapy
Anti-androgens
Bilateral orchidectomy

40
Q

What are LHRH agonists and what are their side-effects?

A

Luteinizing-hormone releasing hormone (LHRH) interferes with the normal release of gonadotropins from the pituitary. This reduces the level of circulating testosterone to those following castration. Agents include goserelin and buserelin.

Side effects include impotence, loss of libido and tumour flare. Tumour flare occurs on initiation of treatment (prior to the down regulation of gonadotropin and may be treated by short -term concomitant anti-androgen therapy.

41
Q

What is oestrogen therapy and what are their side-effects?

A

Oestrogens inhibit LHRH production from the hypothalamus.

They are rarely used because of their side effects - impotence, loss of libido, gynaecomastia, myocardial infarction, cerebro-vascular accidents (CV A’s) and pulmonary emboli.

LHRH agonists have replaced the use of oestrogens.

42
Q

What are some examples of anti-androgens and how do they work?

A

These compounds compete with androgens for sites on the androgen receptor. They include bicalutamide, cyproterone acetate, megestrol acetate and medroxyprogesterone acetate

43
Q

What is median survival for patients with locally advanced tumours metastatic disease in prostate cancer?

A

4.5 years
Following radical surgery or radiotherapy, the 10 year survival for localised disease reaches 80-90%

Patients with metastatic disease 2.5 years

44
Q

How common is colorectal carcinoma?

How many new cases a year in the UK?

A

Fourth most common malignancy (11%)

28000 new cases are diagnosed in the UK every year.

45
Q

What are the main risk factors for colorectal cancer?

A
  1. Diet. A diet rich in animal fats and meat and poor in fibre.
  2. Inflammatory disease. There is an association with ulcerative colitis
  3. Familial association. (FAP, HNPCC)
46
Q

What proportion of colorectal cancers occur in what part of the bowel?

A

Rectum (40%)
Sigmoid colon (20%)
Caecum (6%)
The rest in the remaining colon

90-95% are adenocarcinomas

47
Q

What are the different histological types of colorectal cancer?

A
  • Epithelial: far away most frequently- adenocarcinoma (mucinous or signet ring). Rare others include squamous cell carcinoma and adenosquamous carcinoma.
  • Carcinoid
  • Gastrointestinal stromal tumour
  • Primary malignant lymphoma
48
Q

How does colorectal cancer normally spread?

A

Local invasion
Lymphatic
Venous
Coelemic spread

49
Q

How does colorectal cancer normally present?

A

Classical features of altered bowel habit, weight loss, rectal bleeding and vague abdominal pain.

More occult tumours, typically of the right side of the colon and the caecum, can present with iron deficiency anaemia.

50
Q

What investigations are indicated in colorectal cancer?

A

Rectal examinations is essential (3/4 can be felt)
Rigid and flexible sigmoidoscopy, and colonoscopy allows biopsy and visualisation of suspicious lesions
CT provides staging and evaluation of the bowel
Monitoring CEA (carcino-embryonic antigen) can be useful to monitor disease

51
Q

How is colorectal cancer managed?

A

Radical resection is the standard operation for primary colorectal carcinoma.

52
Q

When is radiotherapy indicated in colorectal cancer?

A

Treatment of rectal carcinomas.
Not commonly used in colonic cancers due to toxicity to adjacent organs.
Adjuvant chemotherapy

53
Q

What is the staging system for colorectal cancer?

What are the stages?

A

Duke’s staging system

stage A: limited to mucosa
stage B1: extending into muscularis propria but not penetrating through it; nodes not involved
stage B2: penetrating through muscularis propria; nodes not involved
stage C1: extending into muscularis propria but not penetrating through it; nodes involved
stage C2: penetrating through muscularis propria; nodes involved
stage D: distant metastatic spread

54
Q

When is chemotherapy indicated in colorectal cancer?

A

Adjuvant chemotherapy for high-risk colorectal carcinoma. Oxaliplatin and Irinotecan are now in standard use.

55
Q

What are the prognostic factors for colorectal cancer?

A 
Stage of tumour	: 5-year survival
Stage A		: 80%
Stage B 		: 50%
Stage C 		: 15-40%
Stage D		: 5%
56
Q

What is the screening tool for colorectal cancer?

A

Faecal occult blood testing, demonstrated a reduction of mortality between 15-18%

Cancer and Continuing Care (5 decks)

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