GI pathology Flashcards by Rachel Sladden

Barrett’s oesophagus and oesophageal cancer and mechanism

Squamous epithelium of oesophagus changes to glandular mucosa to protect from acid (produce mucin) due to acid reflux
-type of metaplasia
-columnar lined lower oesophagus
-adaptive change at bottom of oesophagus
Precursor to oesophageal cancer- x100 risk
-rising due to obesity
-mainly in males

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CELLO

Barrett’s oesophagus

Columnar lined lower oesophagus

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Metaplasia

Change in differentiation of a cell from one fully-differentiated type to a different fully differentiated type

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Oesophageal cancer UK incidence

Rate has been increasing since 1975

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Mechanism leading to oesophageal cancer

Normal oesophageal squamous epithelium –GO reflux–> metaplastic oesophageal glandular epithelium –continuing GO reflux and other factors–> dysplastic oesophageal glandular epithelium –continuing GO reflex and other factors–> neoplastic oesophageal glandular epithelium

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Oesophageal cancer - UK age and gender distribution

Increases with age
-mostly in 60s and 70s
Rate almost doubled amongst men than women

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Oesophageal cancer - geographical distribution

Highest in China and Southern Africa

High in Europe e.g. UK (obesity)

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Oesophageal cancer - risk factors

Squamous cell carcinoma (more in Asia):
-smoking
-heavy alcohol intake (particularly conc. distilled spirits)
-heavy smoking + alcohol increases the risk 10x
Adenocarcinoma
-severe reflux i.e. Barrett’s oesophagus
-obesity

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Types of oesophageal tumour

Polypoid

Ulcerated

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Oesophageal cancer - UK 5 year survival rates

Decreases with age
Higher amongst females
~ 20% for 15-39s
<5% for 80-99s

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Helicobacter gastritis

Stomach
Caused by helicobacter pylori (lives in mucin)
-release chemicals that induce stomach inflammation
-attract neutrophil polymorphs from surrounding blood
-leads to acute inflammation / infection
2-3 weeks of intense stomach pains
Can kill cells and form little ulcers
Eventually metaplasia may occur –> intestinal cells

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Gastric cancer UK incidence

Rate has been declining since 1975

~2x higher in males than females

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European geographical distribution of gastric cancer

Highest in Eastern Europe
Lowest in Scandinavia
-smoked/ pickled foods
-sausages cooked in cast iron frying pans (carcinogens)

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World geographical distribution of gastric cancer

Highest in Eastern Asia and Eastern Europe
Lowest in Africa
Due to professions/ diet
-smoked/ pickled foods

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Gastric cancer - age distribution

Sharp rise >40
Highest amongst 70-85
-must be something to do with environmental factors

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Gastric cancer mechanism

Normal gastric mucosa –> intestinal metaplasia due to
-smoked/ pickled food diet
-helicobacter pylori
-pernicious anaemia
Intestinal metaplasia –genetic change–> dysplasia –genetic change–> intramucosal carcinoma –genetic change–> invasive carcinoma

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Presentation of gastric carcinoma

Presents late
Shallow gastric carcinoma (early)
Thickened wall - linitus plastica
-leather bottle stomach
-better felt than seen

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Gastric cancer - UK 5 year survival rates

<20%

Due to late presentation

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Gluten sensitive enteropathy - coeliac disease

Villous atrophy + Crypt hyperplasia
Affects ~1% of population
Hugely increased number of lymphocytes
Immune reaction to gliadine component of gluten (found in wheat)
-sensitised T cells ready to react with it and injure and kill adjacent cells (bystander effect)
Treatment: exclude gluten

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Inflammatory bowel disease

Chronic idiopathic inflammatory bowel disease

Other inflammatory conditions

Chronic idiopathic inflammatory bowel disease

Crohn’s disease - can appear in mouth (aphthous ulcers)

Ulcerative colitis

Other inflammatory bowel conditions

Diverticulitis
Ischaemic colitis
Infective colitis 
-bacterial
-protozoal

Crohn’s disease -systemic complications

Amyloidosis (rare)

-amyloid deposited in organs

Crohn’s disease - bowel complications

Neoplasia - colorectal cancer
Anal
-skin tags
-fissure
-fistula
Fistula formation
Perforation - acute abdomen
Obstruction 
-acute swelling
-chronic fibrosis
Malabsorption
-disease extent
-surgical resentions

Ulcerative colitis

Ulcerative colitis is a long-term condition, where the colon and rectum become inflamed The colon is the large intestine (bowel), and the rectum is the end of the bowel where stools are stored Small ulcers can develop on the colon's lining, and can bleed and produce pus

Crohn's disease

It causes inflammation of your digestive tract, which can lead to abdominal pain, severe diarrhea, fatigue, weight loss and malnutrition. Inflammation caused by Crohn's disease can involve different areas of the digestive tract in different people

Ulcerative colitis - skin complications

Erythema nodusum | Pyoderma gangrenosum

Ulcerative colitis - eye complications

Iritis Uveitis Episcleritis

Ulcerative colitis - joint complications

Ankylosing spondylitis | Arthritis

Ulcerative colitis - colon complications

Blood loss Toxic dilatation Colorectal cancer

Ulcerative colitis - liver complications

Fatty change Chronic pericholangitis Sclerosing cholangitis

Diverticular disease

``` In sigmoid colon Muscularis layer Occurs in older people Outpouchings of bowel mucosa -sac-like structures Inflammation --> resection -little holes in bowel wall (for BVs) -internal pressure increased (low fibre) ```

Diverticulitis can lead to

Peritonitis (if ruptures and faeces escapes sigmoid colon)

Bowel cancer incidence rates

``` Higher amongst men than females in general Increases with age -mainly environmental Highest in developed countries -high fibre diet? -higher life expectancy Mortality rates decreasing -increase in treatment and diagnosis ```

Who gets colorectal cancer?

People with colorectal adenomas at higher risk

Colorectal cancer mechanism

Normal epithelium --> adenoma --> colorectal adenocarcinoma --> metastatic colorectal adenocarcinoma

Familial adenomatous polyposis (type of colorectal cancer)

``` People with genetic abnormality --> 1000s of polyps apc gene --> apc protein affected -not there at all -or doesn't work properly 1% of colorectal cancer ```

Hereditary nonpolyposis colorectal cancer HNPCC

Doesn't have polyps | Genes code for DNA repair, if one is missing that causes a problem

Macroscopic features of colorectal cancer

Mainly in rectum Looks like tumours Adenocarcinoma (glandular mucosa)

Resection coding

• R0 - tumour completely excised locally • R1 - microscopic involvement of margin by tumour • R2 - macroscopic involvement of margin by tumour

Prognosis and circumferential resection margin (CRM)

``` • CRM +ve 20% 5 year survival with 85% risk of local recurrence • CRM –ve 75% 5 year survival with 10% risk of local recurrence ```

Dukes' stage and prognosis

* A 95% 5 year survival * B 75% 5 year survival * C 35% 5 year survival * D 25% 5 year survival

Age-standardised 5 year survival rate colon cancer

Increasing over time | Now around 50%

Treatment of colon cancer

Normal epithelium: prevention Endoscopic resection: adenoma Colorectal adenocarcinoma: surgical resection Metastatic colorectal adenocarcinoma: chemotherapy and palliative care

Method of diagnosing problem in oesophagus

Flexible gastroscopy | -looks red in Barrett's oesophagus

Symptoms of Barrett's oesophagus

Heartburn Dyspepsia Pain after eating

Main cause of Barrett's oesophagus

Obesity

Treatment for H. pylori infection

Omeprazole, amoxicillin, clarithromycin for 10 days