GI tract cancers Flashcards
Examples of GI cancers
Oesophageal
Gastric
Colorectal cancer (CRC)
Types of oesophageal cancer
Squamous
Adenocarcinoma
Clinical presentation of oesophageal cancer
Early = no symptoms Late = dysphagia, weight loss, heartburn, Haematemesis (vomiting blood), hoarse voice
Pathophysiology of oesophageal squamous cancer
Tends to be located in the proximal 2/3rds of the oesophagus
Can locally cause pressure on Recurrent Laryngeal nerve
Aetiology of oesophageal squamous cancer
Smoking, alcohol, nitrous amines (BBQ food, tobacco)
Pathophysiology of oesophageal adenocarcinoma
Tends to be located in the distal 1/3rd of the oesophagus.
Can locally cause pressure on recurrent laryngeal nerve
Aetiology of oesophageal adenocarcinoma
Barrett’s oesophagus, obesity
Epidemiology of oesophageal adenocarcinoma
Obese people
Diagnosis of oesophageal cancer
Oesophagoscopy with biopsy
CT/MRI to stage cancer
Treatment of oesophageal cancer
Oesophagectomy with preoperative chemotherapy
Clinical presentation of gastric cancer
Nonspecific: Dyspepsia, weight loss, vomiting, dysphagia and anaemia.
Signs: Epigastric mass, hepatomegaly, jaundice, Troisier’s sign (enlarged left supraclavicular node (Virchow’s node)).
What type of cancer are most gastric cancers
90% are Adenocarcinomas
Most involve pylorus
Aetiology of gastric cancer
Multifactorial and often unknown
H.pylori can double the risk
Smoking is a risk factor
Gastritis and pernicious anaemia
Diagnosis of gastric cancer
Gastroscopy with biopsy
CT/MRI to stage cancer
Treatment of gastric cancer
Gastrectomy (partial or total) with preoperative chemo
Clinical presentation of Colorectal cancer (CRC) of left side
Most are left side of colon: rectal bleeding, increasing symptoms of intestinal obstruction (bowel habit, coliky pain).
Clinical presentation of Colorectal cancer (CRC) of right side or caecum
Right side + ceacum: iron deficiency anaemia, mass in right iliac fossa. Non specific symptoms.
Pathophysiology of CRC
Adenomatous polyps develop over time, though begnin they can become malignant through activation of oncogenes and inactivation of tumour suppressor genes. Increased no. of polyps increases chance of malignancy.
5% due to genetic syndromes:
HNPCC: accelerated progression of adenoma to CRC, >50% develop CRC after 40.
FAP: APC gene, >100 polyps develop in teenage years, 100% lifetime risk of CRC. (Both have increased risk of extracolonic malignancy).
What are polyps
abnormal tissue growths that most often look like small, flat bumps or tiny mushroomlike stalks. Most polyps are small and less than half an inch wide. Polyps in the colon are the most common
CRC risk factors
Smoking Increased Age Family hx Inflammatory Bowel Disease Streptococcus bovis bacteraemia (Western diet) Congenital polyposis syndromes Genetic predisposition
Epidemiology of CRC
mean diagnosis and how common
Mean diagnosis age 60-65
3rd most common malignancy
2nd biggest killer cancer
Diagnosis of CRC
DRE (Digital Rectal Exam), colonoscopy with biopsy
Faecal occult blood test for screening only
What does treatment of CRC depend on
Extent of the disease
Complications of CRC
Local invasion and distant metastases, often liver and lung
Obstruction
Give examples of Congenital polyposis syndromes that are risk factors for CRC
Juvenile polyposis syndrome
Peutz-Jeghers syndrome
Give examples of genetic predispositions that are risk factors for CRC
Familial adenomatous polyposis (FAP)
Hereditary non-polyposis colorectal cancer
What is CRC
Cancer of the colon and rectum
3rd most common cancer and usually an adenocarcinoma on histology
Conservative treatment of CRC
Patient education and referral to Macmillan nurses
Medical treatment of CRC
Chemotherapy (oxliplatin, folinic acid and 5-fluorouracil is most common regime)
Radiotherapy also used
Surgical treatment of CRC
Surgical resection is usually treatment of choice
Investigations of CRC
Bowel Cancer Screening Programme - faecal occult blood test in men and women aged 60-69 years
Bloods - FBC for iron deficiency anaemia and carcinoembryonic antigen (CEA) tumour marker
Endoscopy - colonoscopy/sigmoidoscopy
Imaging - double contrast barium enema study ‘apple core’ sign; virtual colonoscopy
*Describe the Dukes staging system
Stage A:
Confined to muscularis mucosa (90% 5-year survival)
Stage B:
Extends through muscularis mucosa (65% 5-year survival)
Stage C:
Lymph node involvement (30% 5-year survival)
Stage D:
Distant metastases (<10% 5-year survival)
Describe the TNM system
T = Carcinoma in situ: T1 - Submucosa invaded T2 - Muscularis mucosa inavded T3 - Tumour has invaded subserosa but other organs have not been penetrated T4 - Adjacent organs inavded
N1 = Metastatic spread to 1-3 regional lymph nodes N2 = Metastatic spread to at least 4 regional lymph nodes
M0 = No distant metastases present M1 = Distant metastases present
