GI Cancers Flashcards
What are the two different types of oesophageal cancer?
Squamous cell carcinoma:
- commonest
- can occur at any level
- possible associations include: HPV, tannin, vitamin A deficiency, riboflavin deficiency, smoking/alcohol
Adenocarcinoma:
- occurs at lower 1/3 of oesophagus
- Barrett’s oesophagus (associated with obesity)
(chronic acid reflux —> necrosis —> metaplasia to columnar epithelium)
Outline the aetiology and investigations of oesophageal carcinoma.
- 2% of malignancies in UK (male > female)
- high incidence in some parts of China & around Caspian sea (Iran, Russia, Kazakhstan, Turkmenistan, etc.) - dietary component?
Risk factors:
- Barrett’s oesophagus/smoking
- coeliac disease
- achalasia (LOJ dysfunction)
INVESTIGATIONS:
- endoscopy -> biopsy
- barium swallow (illustrate oesophageal stricture)
Clinical features:
- dysphagia (food) which gets worse
- back/throat pain
- acid reflux
- hoarseness
- haemoptysis
- chronic cough
What is the prognosis of oesophageal cancer?
Advanced presentation in most cases
Direct spread through oesophageal wall
Only 40% are resectable
Stent used to pierce tumour and facilitate swallowing (but inactivates the sphincters -> no protection against gastric reflux)
5% five-year survival
Outline the aetiology and investigations in gastric cancer.
- 15% of cancer deaths worldwide (males > females)
- high incidence in Japan, Colombia, Finland (diet/H. pylori)
- associated with gastritis (Helicobacter pylori)
- commoner in blood group A (genetic component)
- < 20% five-year survival
Clinical features: (vague)
- epigastric pain
- vomiting
- weight loss
INVESTIGATIONS:
- endoscopy -> biopsy
- barium swallow (illustrates “apple core” stricture)
What are the microscopic and macroscopic features of gastric cancer? How does early and advanced gastric cancer differ?
Macroscopic:
- fungating (infiltrated epithelium and broken through skin surface)
- ulcerating
- infiltrative —> linitis plastica (“leather wine bottle” stomach - stomach does not collapse when opened)
- early (how much the cancer has spread through the wall of the stomach)
Microscopic:
- intestinal = variable degree of gland formation (accounts for increased incidence in some countries)
- diffuse = single cells and small groups of signet ring cells (background rate through world)
EARLY:
Confined to mucosa/submucosa
Japan: increased screening due to increased incidence
Good prognosis
ADVANCED:
Spread to liver, lymph nodes (supra-clavicular nodes = Virchow’s nodes), trans-coloemic
UK
10% five-year survival rate
What is trans-coelomic spread?
Metastasis across a body cavity e.g. peritoneal/pleural/pericardial cavities
e.g. cancer cells shed into peritoneum; causing “studs” of cancer throughout peritoneum
Associated with cancer of the:
- ovaries
- endometrium
- lung
- stomach
- colon
+ may be associated with development of malignant effusion
What is the treatment for gastric cancer?
Surgery
Chemotherapy
Herceptin (HER2 gene amplified in gastric cancer & adeno-oesophageal cancer)
What are some other examples of gastric cancers apart from squamous cell/adenocarcinomas?
Lymphoma (lymphoid cells in stomach):
- commonest GI lymphoma
- starts as low-grade lesion
- better prognosis than gastric cancer
- strong association with H. pylori
note: treatment of H. pylori MAY lead to regression of tumour (but this means that technically there was not a malignant lymphoma present)
Stromal (interstitial cells of Cajal - initiate and maintain peristalsis)
- gene mutation
- behaves unpredictably (hard to predict metastasis)
- surgery + imatinib
What are adenomas? What evidence suggests a relationship between adenomas and adenocarcinomas?
Type of polyp with malignant potential
- can be sessile (broad base) or pedunculated (narrow stalk)
- variable degree of dysplasia
- incidence increases with age and certain genetic syndromes e.g. FAP
Adenomas and adenocarcinomas: occur in the same geographical/anatomical areas, occur at the same time, if adenocarcinomas are found then more likely to develop adenomas, adenocarcinomas present in groups of adenoma
Define a polyp.
Growth protruding from a mucous membrane
Give examples of genetic disorders which predispose to the development of adenomas in the large intestine.
Familial adenomatous polyposis
- autosomal dominant
- chromosome 5
- high risk of cancer (remove bowel)
Gardner’s syndrome
- variant of FAP
- also causes fibromas, osteomas, and multiple sebaceous cysts
Outline the aetiology of colorectal adenocarcinomas.
Risk factors:
- peak age 60-70yrs
- high incidence in UK/USA
- associated with ulcerative colitis/Crohn’s
- associated with low residue diet (slow transit time)/high fat intake
Histology:
- 60%-70% rectosigmoidal
- fungating (esp. right side)
- stenotic (esp. left side)
- moderate differentiation, occasionally mucinous, occasionally have signet ring cells present
- staged via Dukes’
- K-ras & N-ras present in 50% (means cetuximab will be ineffective)
Spreads directly though bowel wall to adjacent organs (e.g. bladder), to mesenteric lymph nodes, and to the liver (via portal venous system)
note: contents of colon are quite watery, so obstructive symptoms are more likely the more distal the tumour is located (rectum, sigmoid colon)
What is the treatment for colorectal adenocarcinomas?
Neoadjuvant palliative chemotherapy + local radiotherapy + resection of liver deposits
Cetuximab (if K-ras/N-ras mutation is not present)
What does (neo)adjuvant therapy mean?
Neoadjuvant therapy = before surgery
Adjuvant therapy = treatment given after primary therapy
note: an adjuvant is a substance used with another to enhance its activity
Give some examples of large intestinal tumours other than colorectal cancer.
Carcinoid (rare) - endocrine tumour
Lymphoma (rare in large intestine)
Smooth muscle/stromal (rare in large intestine)
