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Gastro-intestinal system (Den 303) > GI pathology > Flashcards

GI pathology Flashcards

1
Q

Barrett’s oesophagus and oesophageal cancer and mechanism

A

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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2
Q

CELLO

A

Barrett’s oesophagus

Columnar lined lower oesophagus

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3
Q

Metaplasia

A

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

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4
Q

Oesophageal cancer UK incidence

A

Rate has been increasing since 1975

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5
Q

Mechanism leading to oesophageal cancer

A

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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6
Q

Oesophageal cancer - UK age and gender distribution

A

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

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7
Q

Oesophageal cancer - geographical distribution

A

Highest in China and Southern Africa

High in Europe e.g. UK (obesity)

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8
Q

Oesophageal cancer - risk factors

A

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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9
Q

Types of oesophageal tumour

A

Polypoid

Ulcerated

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10
Q

Oesophageal cancer - UK 5 year survival rates

A

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

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11
Q

Helicobacter gastritis

A

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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12
Q

Gastric cancer UK incidence

A

Rate has been declining since 1975

~2x higher in males than females

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13
Q

European geographical distribution of gastric cancer

A

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

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14
Q

World geographical distribution of gastric cancer

A

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

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15
Q

Gastric cancer - age distribution

A

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

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16
Q

Gastric cancer mechanism

A

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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17
Q

Presentation of gastric carcinoma

A 
Presents late
Shallow gastric carcinoma (early)
Thickened wall - linitus plastica
-leather bottle stomach
-better felt than seen
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18
Q

Gastric cancer - UK 5 year survival rates

A

<20%

Due to late presentation

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19
Q

Gluten sensitive enteropathy - coeliac disease

A

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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20
Q

Inflammatory bowel disease

A

Chronic idiopathic inflammatory bowel disease

Other inflammatory conditions

21
Q

Chronic idiopathic inflammatory bowel disease

A

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

Ulcerative colitis

22
Q

Other inflammatory bowel conditions

A 
Diverticulitis
Ischaemic colitis
Infective colitis 
-bacterial
-protozoal
23
Q

Crohn’s disease -systemic complications

A

Amyloidosis (rare)

-amyloid deposited in organs

24
Q

Crohn’s disease - bowel complications

A 
Neoplasia - colorectal cancer
Anal
-skin tags
-fissure
-fistula
Fistula formation
Perforation - acute abdomen
Obstruction 
-acute swelling
-chronic fibrosis
Malabsorption
-disease extent
-surgical resentions
25
Q

Ulcerative colitis

A

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

26
Q

Crohn’s disease

A

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

27
Q

Ulcerative colitis - skin complications

A

Erythema nodusum

Pyoderma gangrenosum

28
Q

Ulcerative colitis - eye complications

A

Iritis
Uveitis
Episcleritis

29
Q

Ulcerative colitis - joint complications

A

Ankylosing spondylitis

Arthritis

30
Q

Ulcerative colitis - colon complications

A

Blood loss
Toxic dilatation
Colorectal cancer

31
Q

Ulcerative colitis - liver complications

A

Fatty change
Chronic pericholangitis
Sclerosing cholangitis

32
Q

Diverticular disease

A 
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)
33
Q

Diverticulitis can lead to

A

Peritonitis (if ruptures and faeces escapes sigmoid colon)

34
Q

Bowel cancer incidence rates

A 
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
35
Q

Who gets colorectal cancer?

A

People with colorectal adenomas at higher risk

36
Q

Colorectal cancer mechanism

A

Normal epithelium –> adenoma –> colorectal adenocarcinoma –> metastatic colorectal adenocarcinoma

37
Q

Familial adenomatous polyposis (type of colorectal cancer)

A 
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
38
Q

Hereditary nonpolyposis colorectal cancer HNPCC

A

Doesn’t have polyps

Genes code for DNA repair, if one is missing that causes a problem

39
Q

Macroscopic features of colorectal cancer

A

Mainly in rectum
Looks like tumours
Adenocarcinoma (glandular mucosa)

40
Q

Resection coding

A

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

41
Q

Prognosis and circumferential resection margin (CRM)

A 
• CRM +ve 20% 5 year
survival with 85% risk of
local recurrence
• CRM –ve 75% 5 year
survival with 10% risk of
local recurrence
42
Q

Dukes’ stage and prognosis

A
  • A 95% 5 year survival
  • B 75% 5 year survival
  • C 35% 5 year survival
  • D 25% 5 year survival
43
Q

Age-standardised 5 year survival rate colon cancer

A

Increasing over time

Now around 50%

44
Q

Treatment of colon cancer

A

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

45
Q

Method of diagnosing problem in oesophagus

A

Flexible gastroscopy

-looks red in Barrett’s oesophagus

46
Q

Symptoms of Barrett’s oesophagus

A

Heartburn
Dyspepsia
Pain after eating

47
Q

Main cause of Barrett’s oesophagus

A

Obesity

48
Q

Treatment for H. pylori infection

A

Omeprazole, amoxicillin, clarithromycin for 10 days

Gastro-intestinal system (Den 303) (3 decks)

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