GI Tract Cancer and Inflammatory Bowel Disease Flashcards
What is the most common form of GIT cancer?
- Bowel cancer (combination of colon and rectal cancer) is the most common form of GIT cancer
- It is the second most common form of cancer in both men and women in Australia
Describe the form of cancer most commonly seen in each region of the GI tract:
- Esophagus: sqaumous cell carcinomas are seen proximally in the esophagus and adenocarcinomas are seen distally (particularly around the gastroesophageal junction)
- Stomach: usually adenocarcimonas but ocassionally GIST of MALT (associated with H. pylori) are seen
- Liver: primary hepatomas, but also a common site of metastases
- Gall bladder: extremely rare and rapidly fatal cholangio-carcinoma
- Pancreas: usually aggressive adenocarcinoma, but cystic neoplasms an neuroendocrine tumours are also seen
- Small intestine: cancer of the small intestine is very rate, but adenocarcioma, lymphoma and neuroendocrine cancers can sometimes be seen
- Large intestine and rectum (bowel): adenocarcinoma
- Anus: sqaumous cell carcinoma
Describe the clinical features, pathology, treatment and prognosis of esophageal cancer:
Symptoms: dysphagia and weight loss
Risk factors: smoking (squamous), reflux, Barrett’s esophagus and obesity (adenocarcinoma)- lifetime risk is 0.6% in M and 0.2% in F
Barrett’s Esophagus: occurs in the distal portion of the esophagus as a result of chronic reflux, the cells of the esophagus transition to an intestinal lining phenotype
Treatment: depends on the type of cancer, SSC is much more responsive to radiotherapy, whilst adenocarcinoma can only be treated with extensive surgery and chemotherapy
Prognosis: 5 year survival rate is 20%
How have rates of esophageal cancer changes over the previous 30 years?
- There has been a gradual decrease in rates of SSC in both men and women due to decreasing rates of smoking
- The rate of adenocarcinoma in men has risen significantly, due to an increase in the rate of obesity which causes chronic reflux and Barrett’s esophagus
Describe the symptoms, risk factors, diagnosis, treatment and prognosis of gastric cancer:
Symptoms: epigastric pain, early satiety, nausea, vomiting, weight loss and anemia (due to bleeding)
Risk factors: smoking, cured meats and H. pylori. Lifetime risk in M is 0.9% and F is 0.4%
Diagnosis: CT scans unreliable, so diagnosis is done with a gastroscopy
Treatment: chemo/radiotherapy, surgery and antibiotics (if H. pylori infection is present)
Prognosis: 5 year survival rate is 30%
Describe the symptoms, risk factors, diagnosis, treatment and prognosis of pancreatic cancer:
Symptoms: epigastric pain, painless jaundice and weight loss
Risk factors: smoking, alcohol and diabetes- lifetime risk is 1.0% in M and 0.7% in F
Diagnosis: CT, MRI and endoscopic ultrasound
Treatment: chemotherapy/radiotherapy and surgery
Prognosis: 5 year survival rate is 7% (better prognosis if presentation is painless jaundice)
Describe the symptoms, risk factors, diagnosis, treatment and prognosis of primary hepatoma liver cancer:
Symptoms: RUQ pain, weight loss and jaundice
Risk factors: cirrhosis, viral hepatitis, smoking, alcohol and diabetes (non-alcoholic fatty liver disease is an emergent cause)- lifetime risk 1% in M and 0.3% in F
Diagnosis: ultrasound, CT and MRI
Treatment: early stage can be treated with transplant, later treatment limited- chemotherapy
Prognosis: 5 year survival rate is 19%
Describe the symptoms, risk factors, diagnosis, treatment and prognosis of colorectal (bowel) cancer:
Symptoms: rectal bleeding, altered bowel habits, anemia (from bleeding ulcers), pain and occult blood loss (early sign)
Risk factors: family history, previous polyps, smoking, alcohol, diet, obesity and IBD- lifetime risk 4.6% in M and 3.3% in F
Diagnosis: colonoscopy
Treatment: primary treatment-surgery and chemo(radio)therapy, radiotherapy only used for rectal cancer
Prognosis: 5 year survival rate is 69%
Describe the natural history of bowel cancer:
- Normal Tissue
- Polyp Formation
- Cancer:
Stage 0: restricted to mucosa
Stage 1: cancer within intestinal wall (penetrates muscularis mucosa)
Stage 2: cancer moves through intestinal wall
Stage 3: lymph node involvement
Stage 4: metastases occurs - Metastases
- Death
What is a FOBT and its positives?
- Fetal Occult Blood Test offered every 2 years to all Australians aged 50-75 years
- Patients with a positive FOBT will be given a colonoscopy (half of these find a pathology- 45% polyp, 5% cancer)
- The cancers diagnosed are early stage meaning they have a much better survival rate (stage 1 cancer is associated with 97% 5 year survival rate)
What are the positives and negatives of colonoscopies?
Positives:
- Most effect diagnostic tool for colorectal cancer
- Identifies and can treat polyps
- If patients are sedated, generally acceptable
Negatives:
- Cannot remove cancers (as they penetrate the muscularis mucosa)
- Cannot remove lymph nodes (for cancer staging or prevention)
- Bowel preparation neccessary
- Polyps can be subtle and difficult to identify
- Procedure has risks such as bleeding and pain
- Not an effective bowel cancer screening initiative (better to do FOBT first)
Describe the etiology of inflammatory bowel diseases:
- IBD has a complex etiology, thought to be an interaction between genetic predoposition, environmental triggers and a dysfunctional intestinal immune response
- Genes:
- Biggest risk factor for IBD is family history
- 10-25% of patients have a positive family history - Environment:
- Smoking increases the risk of CD but decreases the risk of UC
- Childhood appendicetomy decreses UC risk
- Breast feeding decreases UC and CD risk
- Recent antibiotic use increases risk of CD
Describe the differences between UC and CD Pathology:
Ulcerative collitis:
- Inflammation in colon only
- Inflammation is continuous and retrograde beginning at the anus
- Inflammation only affects the mucosal layer
- There are no granulomas (collections of macrophages)
- There is no extracolonic disease
Crohns Diseease:
- Inflammation can be anywhere along the GI tract (upper GI involvement is more common in children)
- Inflammation is discontinuous (segmental)
- Inflammation is transmural (full-thickness)
- Granulomas (collection of macrophages) may be present
- Extracolonic disease may occur (e.g. abscesses, peripheral arthritis, eye inflammation and skin complications)
Describe the clinical features of IBD:
- Symptoms are dependent on disease location and can be relapsing and remitting
- General symptoms include: weight loss, fatigue, anaemia, fever and abdominal pain
- Symptoms specific to colonic disease (UC and CD affecting colon) are: diarrhoea including overnight bowel motions, rectal bleeding, urgency, tenesmus and incontinence
- Symptoms specific to small intestine disease (CD affecting small bowel): pain due to obstruction, bloating, vomiting and weight loss
Describe the different patterns of inflammation in UC:
- Proctitis: contained in rectum (early disease)
- Left sided/distal colitis: involves descending colon and rectum
- Pancolitis: involving entire large bowel
Describe the different patterns of inflammation in CD:
- Terminal ileum: disease centred in ileum (lower small intestine)
- Ileocolon: disease in both terminal ileum and colon
- Colon: disease mainly in colon
Describe the extra-intestinal manifestions of CD:
- Peripheral arthritis:
- Monoarticular
- Usually affects large joints
- No synovial destruction - Bile duct lesions:
- Inflammation in the biliary tree causing beading: sclerosing cholangitis
- Can be associated with development of cholangiocarcinoma (gall bladder cancer) - Eye inflammation
- Often unilateral - Skin complications:
- Erythema nodosum: raised symmetrical patches with bruise-like appearance
- Pyoderma gangrenosum: large inflamed ulcers
Describe the histology and gross appearance of crohn’s disease:
Histology:
- Segmental inflammation (skip-lesions)
- Transmural inflammation (creeping/fat wrapping)
- Thick rubbery intestinal wall (oedema/inflammation/fibrosis)
- Mucosa ‘cobblestoned’
- Fissures between mucosal folds leading to sinuses/fistulae
- Noncaseating granulomas
- Lymphoid aggregates
- Chronic inflammatory change (crypt abscess/cryptitis)
Gross appearance:
- Presenceof multiple lesions and ulcers and transmural inflammation in colon
- Obliteration of villi, inflammation, ulceration and narrowing in terminal ileum
Describe the standard disease progression in Crohns Disease:
3 Main phases of behaviour:
- Inflammatory (inflammatiom only)
- Stricturing (inflammation has caused narrowing of the bowel)
- Penetrating (stricturing has lead to bowel rupturing and abscess forming)
What are clinical predictors for aggressive CD?
- Young age at diagnosis
- Strictures
- Perianal disease
- Weight loss
What are some complications of CD?
- Stricture:
- Narrowing of bowel due to inflammation - Obstruction:
- Bowel contents becoming lodged in stricture - Fistula:
- Transmural inflammation makes exterior wall of gut to become ‘sticky’
- Entero-enteric: 2 sections of bowel become struck together and begin to communicate
- Entero-cutaneous: between bowel and skin
- Entero-vesical: between bowel and urinary vesicles
- Retroperitoneal: between bowel and vagina - Perianal Fistulae and Abscess:
- Fistulae form in anus and form abscesses
Describe the histology and gross appearance of UC:
Histology:
- Inflammation begins in rectum and is continuous and retrograde
- Causes only mucosal disease: reddening, inflammation
- Serosa is normal
- Primarily mononuclear cells infiltrate lamina propria causing crypt abseses which lead to destruction of mucosa that causes ulceration
- NO granulomas
- Submucosal fibrosis
- Ulcers can progress through dysplasia
Gross appearance:
- Inflammation, reddening and ulceration all seen in the mucosa
How is IBD diagnosed?
- Cannot be done with symptoms alone
- Fetal calprotectin tests can measure inflammation in bowel
- Intestinal ultrasound
- Baseline tests including LFTs, TFTs, WCC, nutritional panels
What are the main treatments for IBD?
- 5-ASA for UC
- Corticoteroids (prednisolone)
- Immunosuppressants (thiopurine and and methotrexate)
- Biologics e.g. anti-TNFs and integrin inhibitors (Vedolizumab)
