GI tumours lower tract Flashcards
Small intestine - benign
Adenoma (25%) Mesenchymal tumours (leiomyoma, lipoma, angioma)
Small intestine - Malignant
Adenocarcinoma and carcinoid
Lymphoma
Sarcomas
Large intestine Benign
Non-neoplastic polyps: hyperplastic and hamartomatous (juvenile or peutz-jeghers)
Neoplastic - Adenoma (tubular, villous, tubulovillous)
Large intestine malignant
Adenocarcinoma (98%) Carcinoid Anal zone carcinoma Lymphoma Leiomyosarcomas
Adenoma – benign tumour small intestine
- 30 to 60 yo; occult blood loss (often the only symptom)
- Usually affects ampulla of Vater: enlarged and presents a velvety surface
- Malignant potential adenocarcinoma
Adenocarcinoma – malignant tumour of small intestine
- 40-70 yo; in duodenum
- Napkin-ring encircling pattern
- Polypoid exophytic masses
- Causes intestinal obstruction cramping pain, nausea, vomiting, weight loss, obstructive jaundice (blicking ampulla of Vater, presents early as compressing ducts)
- 70% five-year survival (good, because spotted so early, before metastasis)
Hyperplastic polyps
Non-neoplastic polyps – benign tumour of large intestine (90%)
- longer finger like projections – often accidental findings
- > 60 yo, <5mm
- Nipple-like, hemispheric, smooth, moist protrusions of the mucosa
- 1/2 in rectosigmoid colon
- Histology: well formed glands and crypts, lined by non-neoplastic epithelial cells most of which show differentiation into mature globet or absorptive cells
- No malignant potential
- Normal under microscope – slightly crowded
Juvenile polyps (hamartomatous - non-neoplastic, benign large intestine)
Malformations of the mucosal epithelium and lamina propria
- In children under 5
- 80% in rectum
- Histologically: abundant cystically dilated glands (containing mucus), inflammation is common, surface may be congested or ulcerated
- No malignant potential, often an accidental finding
Hamartomatous (2): Peutz-Jeghers polyps
An autosmal dominant syndrome, mutation of gene STK11 (LKB1) on chromosome 19
- 30% in colon, 25% in stomach; small bowel
- Involves mucosal epithelium, lamina propria and muscolaris mucosa – tend to be large and pedunculated
- No malignant potential but increased risk of pancreas, breast, lung, ovary and uterus carcinoma. Maybe relates to mutation q19
Neoplastic polyps – adenoma – benign of colon and rectum
Classification, overview, arise from>
Classified into Tubular (75%), Villous (1-10%) and Tubulovillous adenomas (5-15%)
They are intraepithelial lesions. Large neoplasms, usually sessile. 20-30% before 40 years of age; 40-50% after 60. Equal m/f.
Arise as the result of epithelial proliferative dysplasia.
Is a precursor lesion invasive colorectal adenocarcinoma: risk correlated to
- polyp size
o rare in tubular adenomas <1cm,
o high risk (40%) in sessile villous adenomas >4cm
- histological architecture,
- severity of epithelial dysplasia (if severe is often found in villous areas).
Impossible from gross inspection of a polyp to determine its clinical significance (whether benign or malignant – need biopsies)
Adenomas - large intestine (neoplastic polyps)
Tubular (75%)
- Colon (90%), stomach, small intestine
- Usually <2.5cm – PEDUNCULATED??
- Small tubular adenomas – smooth contoured and sessile
- Large tubular adenomas – coarsely lobulated and have slender stalks, raspberry-like
- Histologically:
o stalk is composed of fibromuscular tissue and prominent blood vessels
o presence of dysplastic epithelium, lines galnds as a tall, hyperchromatic, disordered epithelium that may show mucin vacuoles
o degree of dysplasia is low-grade (high-degree dysplasia may be present)
o invasive when malignant cells in the submucosal stalk of polyp
Villous (1-10%)
- Affects older persons
- Rectum and rectosigmoid
- Sessile, up to 10cm
- Velvety or cauliflower-like masses projecting 1-3cm above the surrounding normal mucosa
- Histology
o Frond like villiform extensions (finger like projections see normal vs abnormal) of the mucosa
o Covered by dysplastic (sometimes very disorderly) columnar epithelium
o All degrees of dysplasia
o When invasive carcinoma occurs (40%) there is no stalk as a buffer zone and invasion is directly into the wall of the colon - More symptomatic than tubular and tubulovillous (may be asymptomatic), may be discovered from overt rectal bleeding (others discovered during evaluation of anaemia
When are tubular or villous said to be invasive (or not)?
Tubular: invasive when malignant cells in the submucosal stalk of polyp
Villous: Intramucosal carcinoma with
lamina propria invasion only is regarded also as having little or no metastatic potential
Neoplastic polyps – adenomas – treatment
Impossible from gross inspection of a polyp to determine its clinical significance (whether benign or malignant – need biopsies)
Endoscopic removal of a pedunculated adenoma is regarded as adequate if
1. Adenocarcinoma is superficial and does not approach the margin of excision across the base of the stalk
2. There is no vascular of lymphatic invasion
3. The carcinoma is not poorly differentiated
Invasive adenocarcinoma arising in a sessile polyp cannot be adequately resected by polypectomy and further surgery may be required (because they are flat!)
Familial Adenomatous Polyposis (FAP)
- Mutation of APC gene on 5q21-22
- Patients develop 500-2500 colonic adenomas that carpet the mucosal surface
- Most are tubular adenomas
- 100% risk of developing adenocarcinoma before age 30 – total colectomy indicated
Colorectal (adeno)carcinoma:
- 98% of all cancers in large intestine are adenomcarcinoma
- Peak incidence between 60 and 79 yo
- Rectum m:f is 1.2:1, more proximal is 1:1
- Most deaths in Us, Australia, New Zealand and Eastern European countries (rare in Africa)
Adenocarcinoma aetiology and pathogenesis. Dietary:
- Excess dietary intake
- Low content of vegetable fibre
- High content of refined carbohydrates
- Intake of red meat (especially if heated eg fried)
- Decreased intake of protective micronutrients (vit C, D)
How does colorectal adenocarcinoma start and what are the most common sites?
All begin as carcinoma in situ lesions
- Rectosigmoid colon 55%
- Caecum/ascending colon 22%
- Transverse colon 11%
- Descending colon 6%
- Other sites 6%
Morphology of colorectal carcinoma in proximal colon:
- Polypoid, exophytic masses
- Obstruction uncommon
- Penetrate the bowel wall as subserosal and serosal white, firm masses
Morphology of colorectal carcinoma in distalcolon:
- Annular, encircling lesions – napkin-like constrictions
- The margins are classically heaped up, beaded and firm, with ulcerated mid-region
- Lumen markedly narrowed – proximal bowel may be distended – obstruction more common
- Penetrate the bowel as subserosal and serosal white firm masses
Diagnostic procedures for GI lower tract tumours
In colonoscopy – give drugs to relax patient/make them forget as can be very painful
Also use Barium enema technique (X-ray) for diagnosis, should be followed by endoscopy. See classic “apply core” lesion.
Histology of colorectal adenocarcinoma
- Range from tall, columnar cells (resembling their counterpart in adenomatous lesions) to undifferentiated, anaplastic masses
- Many cells produce mucin
- Invasive tumour incites a strong desmoplastic stroma response
Clinical features of colorectal adenocarcinoma
- Asymptomatic for years
- Caecum and right colonic: fatigue, weakness, iron deficiency anaemia
- Left sided lesions: occult bleeding (only picked up in stool occult bleeding test, doesn’t save NHS money but saves lives!), changes is bowel habit, crampy left lower quadrant discomfort
- Iron-deficiency anaemia, in older males this is a red flag and means GI cancer until proven otherwise!!
- Systemic manifestations (weakness, malaise, weight loss) signify more extensive disease
What is a red flag for colorectal adenocarcinoma?
- Iron-deficiency anaemia, in older males means GI cancer until proven otherwise
