Lower GI Flashcards
What are some of the congenital dosorders of the lower GI tract?
- Failure of development of lumen: atresia (=no connection/ no communication of 2 parts of bowel) /stenosis
- Duplication
What site does Hirschsprung’s diasese originate from?
What is the patholgoy?
Starts in the rectum which fails to dilate + spreds more proximally (during surgery: resection with frozen sections)
Absence of ganglion cells in the submucosal and myenteric plexuses (picture pointing to ganglions, would be abscent in hhirschsprung’s)
What is the main site of volvuli in children and adults?
Volvulus = Complete twisting of a loop of bowel at mesenteric base around vascular pedicle
Small bowel (infants)
Sigmoid colon (elderly)
What are the main causes of acute colitis?
- Infection
- Drug/toxin (especially antibiotic)
- Chemotherapy
- Radiation
What are the main causes of chronic colitis?
Crohn’s
Ulcerative colitis
TB
What are the main pathogens causing infectious colitis?
(go over mmost common)
- Viral e.g. CMV (partiuclarl in immunsoupressed / with IBD), Norovirus, Adenovirus
- Bacterial - most common)e. g. Salmonella, Campylobacter, C-diff
- Protozoal e.g. Entamoeba hystolytica
- Fungal e.g. candida
What is pseudomembranous colitis?
How is it diagnosed?
Antibiotic associated colitis
–> then caues acute colitis with pseudomembrane formation (pseudomembrane = infalmmatory protein exotoxins formed by C-diff )
Caused by protein exotoxins of Clostridiumdifficile –> detection ofC-diff toxin makes diagnosis
What is the usual inflammation seen in patients with Ischaemic colitits?
Depending on the degree of ischaemia,can be:
Mucosal, mural, transmural (perforation)
Usually occurs in segments in “watershed” zones, e.g. splenic flexure (SMA and IMA) and the rectosigmoid (IMA and internal iliac artery)
What are the pathological/histological feature of Crohn’s disease?
- Whole of GI tract can be affected (mouth to anus)
- ‘Skip lesions’
- Cobble.stone appearance (because normal parts of mucosa shine through)
- Transmural inflammation –>
- Fissure/ sinus/fistula formation
- Non-caseating granulomas
What are some of the common extra-intestinal manifestations of Crohn’s disease?
Arthritis
Uveitis
Stomatitis/cheilitis
Skin lesions
- Pyoderma gangrenosum
- Erythema multiforme
- Erythema nodosum
What are the pathological/histological feature of UC?
- Involves rectum and colon in continuous fashion
- May see mild ‘backwash ileitis’ and appendiceal involvement but small bowel and proximal GI tract not affected.
- Inflammation confined to mucosa
- Bowel wall normal thickness
- Shallow ulcers
What are the mmain complications of UC?
Severe haemorrhage
Toxic megacolon
Adenocarcinoma (20-30 x risk)
What are some of the extra-intesinal features of UC?
- Arthritis
- Myositis
- Uveitis/iritis
- Erythema nodosum, pyoderma gangrenosum
- Primary Sclerosing Cholangitis (5.5% in pancolitis –> risk of cholangiocarcinoma)
What are the 2 different types of polyps that occur in the bowel?
1.non-neoplastic
–> hyperplastic and Sessile Serrated Lesions (SSL risk factor for adenomas as they may show dysplasia)
–> Inflammatory and Hamaromaous (e.g. Peutz Jeghers)
2. Neoplastic
–> Tubular adenoma
–> tubulovillous adenoma
–> villous adenoma
What is a Sessile Serrated Lesion in the lower GI tract?
Non-neoplastic polyp that shows
- Hyperplastic polyp with architectural abnormalities
- May show dysplasia (borderline neoplastic)
What is the definition and epidemiology of lower GI adenomas?
Excess epithelial proliferation + dysplasia
20-30% prevalence before age 40
40-50% prev. after age 60
What are the different types of Neoplastic polyps (Adenoma) in the lower GI tract?
-> Tubular adenoma
–> tubulovillous adenoma
–> villous adenoma
What are the histological characteistics of a tubular adeonoma?
Flat surface
Glands
What are the characteristics of a villous adenoma?
Villous surface –> irregular surface
What are the characteristics of tubulo-villous adenoma?
some mixed components
What characteristics in a single adenoma incrase the risk that it might be a carcinoma/ progress?
Size (>1cm)
Proportion of villous component (high)
Degree of dysplasia (high)
Explain the adenoma carcinoma sequence in the development of colon cancer
multiple factors/ evidence that it is likely that carcinomas derive from adenomas
Name some familial syndromes that pre-dispose to development of colon cancer?
- Hereditary non polyposis colon cancer –> mutation in DNA repair)
Familial adenomatous polyposis
* Gardner’s
* Turcot
What are the characteristics of FAP?
(Epidemiology, genetic mutation, prognosis )
Autosomal dominant - average onset is 25 years old
Mutation in APC tumour suppressor gene (on chromosme 5q21)
Causing: Adenomatous polyps, mostly colorectal
- Minimum 100 polyps, average ~1,000 polyps
- virtually 100% will develop cancer within 10 to 15 years –> prophylactic excision of colon
- 5% periampullary Ca
What is Gardner’s syndorme and Turcot syndrome?
FAP + extra-intestinal symptoms
Gardner: osteomas
desmoid tumors
Turcot: Brain
What is Lynch syndrome?
What is the pathophysiology + inheritence pattern?
Lynch syndrome = Hereditary Non-polyposis Colorectal Cancer (HNPCC)
- Autosomal dominant mutation in t least 1 of 4 DNA mismatch repair genes involved –> not in itself oncogenic, but become cancerous because oncogenic umutations don’t get repaired
- May have polyps –> usually develop colorectal cancer at early age (in splenic flexure)
- Other extra-colonic cancers: endometrium, prostate, breast, stomach
- 3-5% of all colorectal cancers due to
- Numerous DNA replication errors
What is the most common colon cancer?
What is the epidemiology + risk factors
98% colorectral carcinoma
Peak incidence : 60-79 years
If < 50yrs consider familial syndrome
Western population
Generic risk factors
- IBD
- adenoma
- low fibre-diet, lack of exercise
What is the new staging system of colorectal carcinoma
Now only normla TNM stageing used
