- Q. Who gets colorectal cancer?
Q. Name 3 risk factors associated with colorectal cancer
A. People with polyps, can develop into adenocarcinoma
A. Diet (fibre, red meat, alcohol, smoking), PMH (adenoma, ulcerative colitis), family history
Name two features of bowel cancer presentation, what differences occur depending on tumour location?
A. Bleeding, mucous, narrowing, metastasise, (closer to rectum = increased symptoms)
B. Later presentation: thin stools, tenesmus (continual inclination to evacuate the bowels)
C. Rectal: PR bleed (blood in or on stool, altered blood - dark), mucus, … thin stool, tenesmus
D. Lt side/sigmoid: change of bowel habit, diarrhoea, alternating constipation and diarrhoea, thin/altered stool – more likely to present in A&E with obstruction
E. Rt side: anaemia, mass, possibly blood at later presentation = huge mass before presentation, perforation is first presentation
- Q. Name a genetic condition with a high risk of GI cancer
A. Familial adenomatous polyposis: born with normal colon, presents in teens with thousands of polyps, high levels of epithelial proliferation
B. Hereditary nonpolyposis colorectal cancer HNPCC, autosomal dominant, 80% lifetime risk of colon cancer (AKA Lynch syndrome)
- Q. Where do most colorectal cancers occur?
A. L: presents earlier – obstruction
- Q. Describe DUKEs staging of cancer
A. Tumour confined to mucosa
B. Tumour growth into muscularis propria
C. Tumour growth through muscularis and serosa
1. Tumour spread to 1-4 regional lymph nodes
2. Tumour spread to more than 4 regional lymph nodes
D. Distant metastases (liver, lung, bones)
- Q. Name two investigations for bowel cancer
A. Faecal occult blood
a. Guaiac test – poor practice as diagnostic
B. Tumour markers – follow up not diagnosis
C. Colonoscopy: gold standard for diagnosis, permits biopsy of leisons and removal of small polyps (bleed risk)
D. Double contrast barium enema – 2nd line alternative to colonoscopy
E. CT colonoscopy `– 2nd line alternative to colonoscopy in elderly
Q. Name four causes of diarrhoea
A. Infectious: rota virus, shigella, E.coli 0157, salmonella Typhi, salmonella paratyphi, hep A/E, vibriocholerae
B. Malignancy
C. Irritable bowel
- Q. Name some digestive causes of malabsorption
A. Pancreatic insufficiency: CF (secretions block pancreatic duct), pancreatitis (lack of amylase)
B. Defective bile secretion: biliary obstruction, ileal resection
- Q. Name some causes of malabsorption related to insufficient absorptive area
A. Cealiac’s disease: villi destruction due to gliaden, antibodies and transglutaminase produced
B. Crohn’s disease: extensive surface parasitisation, inflammatory damage
C. Giardia lamblia: pathogen coats surface of villi preventing absorption
D. Small intestinal resection or bypass: reduced SA
- Q. Name 3 causes of malabsorption related to lack of digestive enzymes
A. Disaccharidase deficiency (lactose intolerance)
B. Bacterial border damage: brush border damage
C. Defective epithelial transport: abetalipoproteinaemia, primary bile acid malabsorption (mutations in bile acid transporter protein – lipoproteins)
- Q. Name 2 causes of malabsorption related to lymphatic obstruction
A. Lymphoma, tuberculosis
- Q. Describe the pathophysiology of chron’s disease
A. Patchy inflammation: can occur anywhere from mouth to anus
B. Endoscope: patchy within individual areas, (can be seen in mouth), fibrosis, (cobble stone mucosa)
C. Histo: deep fissure ulcers, fibrosis, granulomatous inflammation
D. Numerous complications: due to damage to GI – malabsorption (due to diease and surgical resections), obstruction (acute swelling and chronic fibrosis), perforation (acute abdo), neoplasia (colorectal cancer risk), skin tags, systemic (amyloidosis – rare)
E. Anastomosis: less common due to drugs
- Q. Describe the pathophysiology of ulcerative colitis
A. ?Genetic, mucosa link
B. Pan colitis: entire colon
C. Distinct cut off between inflamed mucosa and normal mucosa – spread through mucosa? –Unknown pathology
D. Diffuse inflammation
E. Affects mucosa – does not go down further (unlike Chron’s disease)
F. Complications: colon (blood loss, toxic dilatation, colorectal cancer), joints (ankylosing spondylitis, arthritis), eyes (iritis, uveitis, episcleritis), skin (erythema nodosum, pyoderma gangrenosum) , liver (fibrosis, fatty change, chronic pericholangitis, sclerosis cholangitis)
- Q. Describe two differences between Chron’s disease and ulcerative colitis
A. Chron’s: mouth to anus, UC: rectum to large colon (not small bowel)
B. Chron’s: appears patchy, UC: continuous pan colitis (distinct cut off between inflamaed mucosa and normal mucosa)
C. Chrons: inflammation can descend into other layers of GI tract, US: cannot penetrate further than mucosa
D. Chrons complications: malabsorption, obstruction, skin tags, systemic amyloidosis
E. UC complications: colon dilation and cancer, arthritis, iritis/uveitis, erythema nodosum, liver fibrosis/fatty/chronic pericholangitis etc
- Q. What is dyspepsia?
A. One or more of the following: postprandial fullness, early satiation, epigastric pain or burning > 4/52
- Q. Name 2 causes/risk factors of gastric ulcers
A. Excess acid production, large volume meals, eating habits, drugs (nitrates, CCBs, NSAIDS), obesity & pregnancy -(both due to smaller tolerated gastric volume) smoking & alcohol,
B. Causes: PUD, GORD, gastritis/NSAID induced dyspepsia
- Q. Describe 3 features of a clinical presentation of dyspepsia
A. Reflux, indigestion, heartburn, acid taste (points to reflux), bloating
B. Acute or chronic, detect alarm features, atypical symptoms (?)
- Q. Name 4 alarm features in dyspepsia history
A. Unexplained weight loss B. Iron deficiency Anaemia/ Evidence of GI blood loss C. Dysphagia D. Upper Abdominal Mass E. Persistent Vomiting F. >55 years old G. Epigastric mass
- Q. Describe the management of dyspepsia
A. Suspend NSAIDS
B. Endoscopy (others: barium, microcam etc)
C. Treat ulcer, GORD, non-ulcer dyspepsia (NUD)
D. Life style advice!! – weight loss, compliance
E. Full dose PPI for one month – change in symptoms?
F. H.Pulori (common infection) – breath test/stool antigen test (stool test in Shef) – if +ve, prescribe antibiotics and PPI to clear infection
G. Treatment variable – dependent on flare ups and symptoms (may be once a day, some days may be 3 or 4 times)
H. GORD – PPI/ Lifestyle measures/ Antireflux surgery
a. Avoid eating large meals before bed
b. Antireflux – last resort
c. PPI – best but failure is common – timing is important! Must be taken half an hour before morning and evening meal (knocks out proton pumps)
I. Cancer
a. MDT referral
J. Functional (Non-Ulcer) d yspepsia
a. Reassurance (can relieve symptoms - anxiety)/ Dietary Review/ Antidepressants (TCA/SSRI’s – can desensitize gullet)
- Q. What protein are patients with coeliac’s disease sensitive to? What foods contain this protein?
A. Protein Gliaden (and glutenin)
B. Found in wheat, oats, barley and rye
- Q. Describe the pathogenesis of coeliac’s disease
A. Uncertain, results in damage to surface enterocytes of small intestine, resulting in a severely reduced absorptive state
B. Causes disruption of tight junctions between enterocytes, combined immune response have direct effects on intestinal permeability
C. Most pts have prior infection with adenovirus type 21
D. Combination of genetic factors and infection triggers onset
E. Total malabsorption: sugars, fatty acids, monoglycerides, amino acids, water, electrolytes
F. Onset: 40s-60s
- Q. What cells are found in the degenerative surface epithelium? (Coeliac’s)
A. T lymphs and inflammatory cells
- Q. What coeliac-specific tests are available?
A. Serology: Tissue transglutaminase (tTG) Anti-endomysial antibody (EMA) Immunoglobulins (must have gluten in diet 6 weeks before for +ve tests)
B. Endoscopy + Duodenal biopsies
C. Histology: Villous atrophy
- Q. Name 2 macroscopic signs of Coeliac’s diease on endoscopy
A. Reduced folds in duodenum, scalloping
