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GI Cancers Flashcards

1
Q

Whats the difference between a primary cancer and a secondary cancer?

A

Primary cancer: arising directly from the cells in an organ

Secondary: spread from another organ, directly or by other means

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2
Q

What are the 6 hallmarks of cancer?

A 
Sustaining proliferative signalling
Evading growth suppressors
Activating invasion and metastasis
Enabling replicative immortality
Inducing angiogenesis
Resisting cell death
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3
Q

What 4 factors underlie the hallmarks of cancer?

A

Deregulating cellular energetics
Avoiding immune destruction
Tumour- promoting inflammation
Genome instability and mutation

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4
Q

What are different types of cancers that can be found in the GI tract?

A

Epithelial cells:
Squamous cell carcinoma
Adenocarcinoma

Neuroendocrine cells:
Neuroendocrine tumours
Gastrointestinal stromal tumours

Connective tissue:
Leiomyoma/ leiomyosarcomas
Liposarcomas

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5
Q

Which GI cancer has the best prognosis?

A

Colorectal

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6
Q

Which GI cancer has the worst prognosis?

A

Pancreatic

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7
Q

What is the purpose of cancer screening?

A

Tests asymptomatic individual to identify cancer at early stage
To decide which diseases are suitable for screening- Wilson and Jungner criteria
Depends on epidemiology of the disease and features of the test

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8
Q

What screening options are there for colorectal cancer?

A

Offered to healthy individuals:
Faecal immunochemical test (FIT)- detects haemoglobin in faeces, every 2 years for everyone ages 60-74

One off sigmoidoscopy for everyone aged >55 to remove polyps (reducing future risk of cancer)

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9
Q

What screening options are there for oesophageal cancer?

A

Regular endoscopy to patients with:
Barrett’s oesophagus
Low- high- grade dysplasia

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10
Q

What screening options are there for pancreatic and gastric cancer?

A

No tests exist that meet W&J criteria

Depends on incidence

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11
Q

What are screening options for hepatocellular cancer?

A

Regular ultrasound and AFP for high risk individuals with cirrhosis:

  • viral hepatitis
  • alcoholic hepatitis
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12
Q

What are examples of specific screening programmes for individuals with genetic predispositions or strong family histories?

A

Individuals with hereditary pancreatitis (caused by mutation in CFTR, PRSS1 AND SPINK1) have a 40-50% risk on pancreatic cancer so need to be screened regularly

Individuals with familial adenomatous polyposis (FAP) have many polyps. They are at high risk of cancer so have routine colonoscopies and sigmoidoscopes and perhaps a prophylactic resection (removal of organ/ part of organ before cancer to reduce risk of cancer)

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13
Q

What is the journey a cancer patient takes?

A

Initial presentation- through screening programme or referral
Patient is referred through 2-week-wait cancer pathways
Diagnosis tests
MDT
Treatment

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14
Q

What individuals may be involved in the cancer multi-disciplinary team?

A 
Pathologist
Cancer nurse specialist
Surgeon
Radiologist
Palliative care
Gastroenterologist 
Oncologist
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15
Q

What is the role of the pathologist?

A
  1. Confirms diagnosis of cancer using biopsy
  2. Provides histological typing, i.e. what type of cell cancer comes from:
    - non-epithelial cells less common in GI tract
    - Epithelium (squamous cell carcinoma) or secretory cells (adenocarcinoma)
    - Neuroendocrine tumours
    - Gastrointestinal cancer
  3. Provides molecular typing i.e. what mutations does this cancer have? It can also determine types of treatment available
  4. Provides tumour grade- determined by how abnormal cells are and their nuclei are and how actively they are dividing
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16
Q

What is the role of the radiologist?

A

Reviews scans:

  • if diagnosis is unclear comment on how likely scan is to confirm cancer
  • suggest other imaging to clarify suspected diagnosis
  • should a biopsy be performed and where?

Provides radiological tumour stage i.e. how far has it spread? :

  • T size of tumour
  • N lymph node involvement
  • M presence of metastasis

Provides re-staging after treatment:

  • has cancer responded completely or partially?
  • has it stayed stable or progressed?

Interventional radiology

  • percutaneous biopsies
  • radiological tests
17
Q

What is the role of the surgeon?

A

Decides whether surgery is appropriate

Performs operation and cares for patient in preoperative period

18
Q

What is the role of the gastroenterologist?

A 
Endoscopy- therapeutic and diagnostic:
Upper GI
- oesophageal and gastric biopsies
-oesophageal stents
Liver and Pancreas
-ERCP and EUS biopsies
-Biliary stents
Lower GI
-Colonic biopsies
-Colonic stents
19
Q

What is the role of the oncologist?

A

Decides whether chemotherapy, radiotherapy or other systemic therapy is appropriate

  • determined by scans, histology and molecular types
  • is the patient fir for full intensity therapy?

Coordinates the overall treatment plan- should chemo come before surgery (nonadjuvant) or after (adjuvant). Considers:

  • type, grade, stage
  • patient fitness and wishes

MDT decided whether plan should be radical (curative) or palliative therapy (tying to extend life) or palliative care (no treatment)

20
Q

What is the pathogenesis of oesophageal cancer?

A

Squamous cell carcinoma:
Upper 2/3 of oesophagus
Develops from normal oesophageal squamous epithelium
commonest in developing world

Adenocarcinoma:
Lower 1/3 of oesophagus
Squamous epithelium that has become columnar (metaplastic)
Related to acid reflux
Commenest in developed world
21
Q

What are different conditions that can increase the risk of oesophageal cancer?

A

Oesophagitis- affects 30% of population, due to GORD

Barrette’s oesophagus (intestine metaplasia)- occurs in 5% of pts with GORD. Metaplasia can lead to mild/moderate/severe dysplasia which can lead to cancer

Adenocarcinoma (neoplasia)- occurs in 0.5-11% patients with Barrett’s per year

These can increase risk of cancer by 30-100 fold

22
Q

How does oesophageal cancer present?

A

Dysphagia (difficulty swallowing) is comments symptom

Late presentation- 65% at an advanced stage when diagnosed- palliative treatment

23
Q

Why do so many patients present with oesophageal cancer late?

A

Significant cancer growth needs to occur before dysphagia develops
Often have metastsis
Most patients deemed unfit for surgery at diagnosis

24
Q

How is oesophageal cancer diagnosed and screened?

A

Upper GI endoscopy (OGD)- if lesion found, biopsy is taken to confirm diagnosis

Investigations to stage the cancer:

  • CT of chest and abdomen
  • PET-CT scan to exclude metastases
  • Staging laparoscopy- to identify peritoneal metastasis
  • Endoscopic ultrasound- via oesophagus to clarify depth of invasion and involvement of local lymph nodes
25
Q

What are treatment options for oesophageal cancer?

A

If tumour is surgically resectable with no distant metastasis and patient is fit for surgery:
- Curative: neoadjuvant chemotherapy- oesophagectomy

If not:
-Palliative: palliative chemotherapy and steroids and stent

26
Q

What is the pathogenesis of gastric cancer?

A

Gastric adenocarcinoma

Chronic gastritis is the major driver:

  • H. pylori infection- due to chronic acid overproduction
  • Pernicious anaemia- antibodies against parietal cells
  • Partial gastrectomy- leading to bile reflux
  • Epstein- Barr virus
Family history (inc, heritable diffuse-type gastric cancer) due to E-cadherin mutations)
High salt diet and smoking
27
Q

What is the presentation of gastric cancer?

A 
Dyspepsia (upper abdominal discomfort after eating or drinking) commonest symptom
Red flags: ALARMS55
Anaemia
Loss of weight or apetite
Abdominal mass on examination 
Recent onset of progressive symptoms
Melaena (black stool) or haematemesis (vomiting blood)
Swallowing difficulty
55yrs old or above
28
Q

How is gastric cancer diagnosed and staged?

A

Diagnosis: endoscopy and biopsy

Staging:

  • CT of chest, abdomen and pelvis
  • PET-CT
  • Diagnostic laparoscopy- for peritoneal and liver metastasis disease prior to full operation
  • Endoscopic ultrasound- will give most detail about local invasion and node involvement
29
Q

What are treatment options for gastric cancer?

A

Oesophageal- gastrectomy: for tumour at oesophago- gastric junction
Non-adjuvant chemotherapy (shrink tumour before surgery)
Subtotal gastrectomy- further from OG junction
Total gastrectomy- close to OG junction
Adjuvant chemotherapy (in advanced tumours to reduce relapse risk)

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