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Year 1 - BRS > 11.11 - Gastrointestinal Cancers > Flashcards

11.11 - Gastrointestinal Cancers Flashcards

1
Q

Define cancer.

A
  • a term for diseases in which abnormal cells divide without control and can invade nearby tissues
  • cancer cells can also spread to other parts of the body through the blood and lymph systems
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2
Q

What is primary cancer?

A

Arising directly from the cells in an organ

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3
Q

What is secondary cancer?

A

Spread from another organ, directly or by other means (blood or lymph)

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4
Q

What are the six hallmarks of cancer? (Biological capabilities acquired by tumours)

A
  • sustaining proliferative signalling
  • evading growth suppressors
  • activating invasion and metastases
  • enabling replicative immortality
  • inducing angiogenesis
  • resisting cell death
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5
Q

What are the two emerging hallmarks of cancer? (Underlie hallmarks)

A
  • deregulating cellular energetics
  • avoiding immune destruction
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6
Q

What are the two enabling characteristics? (Underlie hallmarks)

A
  • genome instability and mutation
  • tumour-promoting inflammation
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7
Q

What are some facts about cancer?

A
  • cancer is a genetic disease
  • cancers contain multiple genetic errors
  • cancers contain more than just malignant cells e.g. there will be neurovasculature, connective tissue, fibrous tissue
  • killing cancer cells is easy
  • ONLY killing cancer cells is hard
  • developing novel therapies for cancer has many problems
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8
Q

What epithelial cell cancers of the GI tract are there and for which epithelial cell type?

A
  • squamous cells - squamous cell carcinoma (SCC)
  • glandular epithelium - adenocarcinoma
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9
Q

What neuroendocrine cell cancers of the GI tract are there and for which neuroendocrine cell type?

A
  • enteroendocrine cells - neuroendocrine tumours (NETs)
  • interstitial cells of Cajal - gastrointestinal stromal tumours (GISTs)
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10
Q

What connective tissue cancers of the GI tract are there and for which type of tissue?

A
  • smooth muscle - leiomyoma / leiomyosarcomas
  • adipose tissue - liposarcomas
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11
Q

What is cancer screening?

A
  • testing of an asymptomatic individuals to identify cancer at an early stage
  • specific screening programmes exist for those with genetic predisposition or strong family histories e.g. those with familial adenomatous polyposis (FAP) have multiple polyps in large bowel + increased cancer risk = offer colon resection to remove polyps or sigmoidoscopies to check for duodenal polyps
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12
Q

What are the seven Wilson and Jungner criteria for seeing which diseases are suitable for screening?

A
  1. the condition sought should be an important health problem
  2. there should be an accepted treatment for patients with recognised disease
  3. facilities for diagnosis and treatment should be available
  4. there should be recognisable latent or early symptomatic stage
  5. there should be a suitable test / examination
  6. the test should be acceptable to the population
  7. the natural history of the condition, including development from latent to declared disease, should be adequately understood
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13
Q

What is the screening for colorectal cancer?

A
  • offered to healthy individuals
  • faecal immunochemical test (FIT) - detects Hb in faeces, every two years for everyone aged 60-74
  • one-off sigmoidoscopy - for everyone aged >55 to remove polyps (reducing future risk of cancer)
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14
Q

What is the screening for oesopheageal cancer?

A

Regular endoscopy to patients with Barrett’s oesophagus and low-to-high grade dysplasia

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15
Q

What is the screening for pancreatic and gastric cancer?

A
  • no test exists that meets the W&J criteria
  • depends on incidence - Japan screens for gastric cancer
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16
Q

What is the screening for hepatocellular cancer?

A

Regular ultrasound and AFP for high-risk individuals with cirrhosis e.g. by viral hepatitis or alcohol hepatitis

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17
Q

What specific screening programmes exist for individuals with genetic predisposition/strong family histories?

A
  • FAP - yearly OGDs & colonoscopies
  • hereditary pancreatitis - PRSS1, SPINK1, CFTR gene mutations - 40% lifetime risk of pancreatic cancer
18
Q

What are the three parts to a patient’s cancer journey?

A
  1. diagnosis - what symptoms and signs does the patient present with? How is the diagnosis made?
  2. staging - what investigations are needed to see how advanced the cancer is?
  3. treatment - can the cancer be surgically removed? What systemic therapy (e.g. chemotherapy) or radiotherapy is available?
19
Q

What happens in real life when patients present with worrying symptoms to their GP or another doctor?

A
  1. initial presentation - patient mentions worrying symptoms to their GP/another doctor (e.g. in A&E), or the patient is identified through a screening programme (e.g. FIT for colon cancer)
  2. patient is referred through the 2-week-wait cancer pathway
  3. diagnostic tests done
  4. MDT gets involved
  5. bespoke treatment programme for patient devised
20
Q

Who are the MDT members for cancer patients?

A
  • pathologist
  • radiologist
  • surgeon
  • gastroenterologist
  • oncologist
  • cancer nurse specialist (CNS)
  • palliative care
21
Q

What does the pathologist do?

A
  • confirms the diagnosis of cancer using biopsy samples
  • provides histologic typing i.e. what type of cell does the cancer come from? - epithelium (squamous cell carcinoma) / secretory cells (adenocarcinoma), non-epithelial cells less common in GI tract - neuroendocrine cancers (pancreas), GISTs (stomach)
  • provides molecular typing i.e. what mutations does this cancer have? - can determine treatment types available alongside histological typing
  • provides tumour grade i.e. how aggressive is the cancer? - determined by how ‘abnormal’ cells and their nuclei are and how actively they are dividing
22
Q

What does the radiologist do?

A
  • review scans - if diagnosis unclear, comments on how likely the scan is to confirm cancer; suggests other imaging to clarify suspected diagnosis; should a biopsy be performed and from where?
  • provides radiological tumour stage i.e. how far the tumour has spread
  • provides re-staging after treatment - did the cancer respond completely or partially? Has it remained stable or progressed?
  • interventional radiology - percutaneous biopsies, radiological stents
23
Q

What system is used to provide radiological tumour stage?

A
  • TNM system
  • T - size of Tumour
  • N - lymph Node involvement
  • M - presence of distant Metastases
  • a T2N0M0 tumour may be fully curable, but a T3N1M1 may not
24
Q

What does the surgeon do?

A
  • decides whether surgery is appropriate - is the tumour resectable? Is the patient fit enough for surgery?
  • performs operation and cares for patient in perioperative period
25
Q

What does the gastroenterologist do?

A
  • endoscopy - diagnostic and therapeutic
  • upper GI - oesophageal and gastric biopsies, oesophageal stents put in
  • liver and pancreas - ERCP and EUS biopsies, biliary stents put in
  • lower GI - colonic biopsies and stents put in
26
Q

What does the oncologist do?

A
  • decides on whether chemotherapy/radiotherapy/other systemic therapy is appropriate - determined by scans, histological and molecular type, and whether patient is fit for full intensive therapy
  • coordinates the overall treatment plan - should chemotherapy come before surgery (neoadjuvant) or after (adjuvant)? - takes type, grade, stage, patient fitness and wishes into consideration
  • MDT decides whether plan should be for radical (curative) or palliative therapy/palliative care
27
Q

What is the difference between palliative therapy and care?

A
  • palliative therapy - trying to extend life for as long as possible with treatment even though they will die
  • palliative care - no treatment and letting patient die
28
Q

Where do squamous cell carcinomas emerge in oesophagus and from what cells?

A
  • upper 2/3 of oesophagus
  • develops from normal oesophagus squamous epithelium
  • commonest in developing world
29
Q

Where do adenocarcinomas emerge in oesophagus and from what cells and when?

A
  • lower 1/3 of oesophagus
  • emerges from squamous epithelium that has become columnar (metaplastic)
  • related to acid reflux
  • commonest in developed world
30
Q

What disease can oesophageal cancer arise from and how do they progress into cancer?

A
  1. oesophagitis (inflammation) - affects 30% of UK population, due to GORD (gastro oesophageal reflux disease)
  2. this can develop into Barrett’s oesophagus (intestinal metaplasia) - occurs in 5% of patients with GORD - metaplasia goes from mild –> moderate –> severe dysplasia –> cancer
  3. this can develop into adenocarcinoma (neoplasia) - occurs in 0.5-11% patients with Barrett’s per year
  • this disease progression increases risk of cancer by 30-100%
31
Q

How do oesophageal cancer patients present?

A
  • dysphagia (difficulty swallowing) - commonest symptom
  • presentation is normally late - 65% are at an advanced stage when diagnosed so they would not be suitable for potentially curative treatment
  • shows importance of screening patients with reflux disease/Barrett’s oesophagus
32
Q

Why do most patients present late with oesophageal cancer?

A
  • significant cancer growth needs to occur before dysphagia develops
  • often have metastases
  • most patients deemed unfit for surgery at diagnosis (malnourished)
33
Q

How is oesophageal cancer diagnosed?

A

Upper GI endoscopy (oesophagogastroduodenoscopy - OGD) - if lesion found then biopsy taken to confirm diagnosis

34
Q

What investigations can be done to stage the oesophageal cancer?

A
  • CT of chest and abdomen - done in all patients
  • PET-CT scan to exclude metastases
  • staging laparoscopy - to identify liver and peritoneal metastases
  • endoscopic ultrasound via oesophagus to clarify depth of invasion and involvement of local lymph nodes
35
Q

What are the treatment options for oesophageal cancer and how is it decided?

A
  • MDT decides - is the tumour surgically resectable with no distant metastases AND is the patient fit to undergo major surgery?
  • if YES - curative neoadjuvant chemotherapy and oesophagectomy
  • if NO - palliative chemotherapy, steroids (dexamethasone) to reduce oedema around tumour, and stent
36
Q

What is the overall pathogenesis of gastric adenocarcinomas?

A

Chronic gastritis is the main driver - leads to intestinal metaplasia which causes dysplasia and then cancer/malignancy

37
Q

What are the common pathogenesis causes of gastric cancer?

A
  • H. pylori infection - due to chronic acid overproduction (which causes metaplasia)
  • pernicious anaemia - autoantibodies against parts and products of parietal cells
  • partial gastrectomy e.g. for an ulcer - leads to bile reflux
  • Epstein-Barr virus infection
  • family history - including heritable diffuse-type gastric cancer due to E-cadherin mutations
  • high salt diet and smoking
38
Q

What is the commonest symptom of gastric cancer?

A

Dyspepsia (upper abdominal discomfort after eating or drinking)

39
Q

What are the ALARMS55 red flags for gastric cancer?

A
  • Anaemia
  • Loss of weight or appetite
  • Abdominal mass on examination
  • Recent onset of progressive symptoms
  • Melaena or haematemesis
  • Swallowing difficulty
  • 55 years of age or above
40
Q

How is gastric cancer diagnosed and staged?

A
  • similar to oesophageal cancer - endoscopy and biopsy
  • staging is exact same as oesophageal cancer
41
Q

What are the treatment options for gastric cancer?

A
  • neoadjuvant chemotherapy - may be used to reduce tumour size before surgery
  • tumour at oesophago-gastric junction - oesophago-gastrectomy
  • close (<5cm) to OG junction - total gastrectomy (cannot save sphincter mechanism)
  • further (>5cm) from OG junction - subtotal gastrectomy
  • adjuvant chemotherapy - may be needed in advanced tumours to reduce risk of relapse
  • some patients need palliative approaches e.g. stenting or gastro-jejunal anastomosis

Year 1 - BRS (73 decks)

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