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Y3 IWB > PATHOLOGY- Gastrointestinal disorders > Flashcards

PATHOLOGY- Gastrointestinal disorders Flashcards

1
Q

What is the oesophagus

A

Long muscular tube

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2
Q

what is the oesophagus lined with

A

Squamous epithelium

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3
Q

how long is the oesophagus

A

25cm

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4
Q

What is the sphincter at the upper end called

A

UOS, cricopharyngeus

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5
Q

What is the sphincter at the lower end called

A

Gastro-oesophageal junction

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6
Q

The bottom 1.5-2cm of the oesophagus sits where

A

Below the diaphragm

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7
Q

what is the bottom of the oesophagus lined by

A

Glandular (columnar) mucosa

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8
Q

The squamous-columnar junction is how far from the incisor teeth

A

Around 40cm

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9
Q

What is oesphagitis

A

Inflammation of oesophagus

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10
Q

What is clinical manifestation oof oesophagitis called

A

GORD

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11
Q

What is reflux oesophagitis caused by

A

Reflux of gastric acid (gastro-oesophageal reflux) and/or bile (duodenum-gastric reflux)

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12
Q

What are the risk factors for reflux oesophagus

A
  • Obesity
  • Hiatus hernia
  • Pregnancy
  • Smoking
  • Drugs (e.g. NSAIDS, aspirin etc)/ food (e.g. spicy)
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13
Q

What is the main clinical symptom of reflux oesphagitis

A

Heartburn

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14
Q

What are the other symptoms of reflux oesophagitis

A

Belching
Bloating
Cough
Can mimic heart pain

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15
Q

What is a hiatus hernia

A

When the stomach slides into thorax from the abdomen via diaphragmatic opening

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16
Q

What is hiatus hernia caused by

A

^ intra-abdominal pressures and / or decreasing diaphragm tone (age)

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17
Q

What does a hiatus hernia result in

A
  1. Decrease in sphincter competence
  2. Leading to gastric acid regurgitation
  3. Resulting in oesophagitis/GORD
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18
Q

Explain how a sliding hiatus hernia leads to reflux

A

Sliding
Lower oesophageal incompetence
Regurgitation of acid
Reflux

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19
Q

What is a paraesophageal hiatus hernia

A

Abnormal bulging of a portion of the stomach through the diaphragm

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20
Q

Explain why a paraesophageal hiatus hernia is an emergency

A

Sphincter okay but can trap the stomach, which can become ischaemic

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21
Q

What are the effects on the squamous epithelium in reflux oesophagitis

A

Basal cell hyperplasia
Elongation of papillae

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22
Q

What are the potential complications with reflux oesophagitis

A
  • Ulceration
  • Haemorrhage
  • Perforation
  • Benign stricture (narrowing)
  • Barrett’s oesophagus (^ risk Ca)
  • Erosive tooth wear / dental erosion (5-47%)
  • Upto 60% in some cohorts
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23
Q

What are the risk factors of Barrett’s oesophagus

A

As per reflux oesophagitis

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24
Q

In Barrett’s oesophagus, what do you see microscopically

A

Upward extension of the squamo-columnar junction

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25
Q

What changes in histology occur with Barrett’s oesophagus

Why

A

Squamous mucosa replaced by columnar mucosa with goblet cells

Protection from acid

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26
Q

What is metaplasia

A

Change from one differentiated cell type to another

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27
Q

What type of condition is Barrett’s

A

Premalignant

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28
Q

What are you at a higher risk of developing with Barrett’s

How many people develop it

A

Adenocarcinoma

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29
Q

What is required for pts with Barrett’s

A

Regular endoscopic surveillance for early detection of neoplasia

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30
Q

What is the 8th most common cancer in the world

A

Oesophageal carcinoma

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31
Q

What are the 2 main histological types

A
  • Squamous cell carcinoma
  • Adenocarcinoma
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32
Q

What percent of the uk pts with oesophageal carcinoma have the squamous cell carcinoma subtype

A

30%

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33
Q

Where has the incidence of adenocarcinoma increased dramatically

A

In industrialised countries

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34
Q

Who does adenocarcinoma affect more

A

Males 7:1
Caucasians

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35
Q

What are the 3 causes of adenocarcinoma

A
  • Barrett’s oesophagus
  • Smoking
  • Radiation
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36
Q

Where is adenocarcinoma located in the body

A

Lowe oesophagus

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37
Q

what does adenocarcinoma look like macroscopically

A

Plaque-like, nodular, fungating, ulcerated, depressed,Infiltrating

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38
Q

What does adenocarcinoma look like microscopically

A

Malignant cells forming glandular structures infiltrating connective tissue

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39
Q

Describe the incidence of squamous carcinoma

A

Wide geographical variation

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40
Q

what are the risk factors of squamous carcinoma

A
  • Tobacco and alcohol
  • Nutrition (potential sources of nitrosamines)
  • Thermal injury (hot beverages)
  • HPV
  • Male
  • Ethnicity (black)
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41
Q

Which part of the body does squamous carcinoma usually occur in

A

Middle to lower third

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42
Q

What is squamous carcinoma preceded by

A

Squamous dysplasia

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43
Q

What is dysplasia

A

Neoplastic change that is confined to the epithelial layer

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44
Q

What is a frequent type of gastric cancer

A

Adenocarcinoma

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45
Q

what are less frequent types of gastric cancer

A
  • Endocrine tumours
  • Lymphomas
  • Mesenchymal tumours (GIST)
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46
Q

What is the 5th most common cancer in the world

A

Gastric adenocarcinoma

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47
Q

What is the cause of gastric adenocarcinoma

A
  • Diet (smoked/cured meat or fish, pickled vegetables)
  • Helicobacter pylori infection
  • ~1% hereditary
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48
Q

What are the 2 histology cal subtypes of gastric adenocarcinoma

A

Diffuse type- invades diffusely
Intestinal type- forms a discrete mass forming glands

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49
Q

What is coeliac disease also known as

A

Coeliac sprue or gluten sensitive enteropathy

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50
Q

What type of disease is coeliac disease

A

Chronic immune-mediated enteropathy

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51
Q

Why does coeliac disease occur

A

Ingestion of gluten containing cereals
- wheat, rye or barley

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52
Q

Who does coeliac disease occur in

A

Genetically predisposed individuals
Any age

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53
Q

How common is coeliac disease

A

Estimated prevalence of 0.5%-1%

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54
Q

Explain the pathogenesis of coeliac disease

A
  1. Gluten broken down to gliadin, which is resistant to further brekadown
  2. In specific individuals, gliadin activates CD4 T cells
  3. These cause local inflammation,
    stimulate B cells to produce anti-gliadin/anti-TTF antibodies
  4. Gliadin also causes il15 to be produced by the epithelium
  5. This results in activation/proliferation of CD8/IELs
  6. The intra epithelial lymphocytes are cytotoxic and kill enterocytes (gut cells)
  7. => combo of self-reactive CD4 T-cells and gliadin-induced IL15 secretion by epithelium is the mechanism
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55
Q

What are the classical symptoms of coeliac disease

A

Diarrhoea
Abdominal pain

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56
Q

What other symptoms are associated with coeliac disease

A
  • Dermatitis herpetiformis - 10% of patients
  • Lymphocytic gastritis and lymphocytic colitis
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57
Q

What is the small link between coeliac disease and cancer

A
  • Enteropathy-associated T-cell lymphoma
  • Small intestinal adenocarcinoma
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58
Q

What oral manifestations occur due to coeliac disease

A

Enamel defects

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59
Q

How do you diagnose coeliac disease

A
  • Serologic blood tests usually performed before biopsy
  • The most sensitive tests
    • IgA antibodies to tissue transglutaminase (TTG)
    • IgA or IgG antibodies to deamidated gliadin
    • Anti-endomysial antibodies - highly specific but less sensitive
  • Tissue biopsy is diagnostic
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60
Q

What is the treatment for coeliac disease

A
  • Gluten-free diet -> symptomatic improvement for most patients
  • Reduces risk of long-term complications
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61
Q

what morphological changes can occur with coeliac disease

A

Villus atrophy
Lots of intra epithelial lymphocytes

62
Q

What is inflammatory bowel disease

A

Chronic inflammatory process within the bowel resulting from inappropriate mucosal immune-cell activation

63
Q

IBD encompasses what 2 main conditions

A

Crohn’s disease (CD)
Ulcerative colitis (UC)

64
Q

What is indeterminate colitis

A

Features of both CD and UC
Unable to classify (accounts for around 10% of IBD)

65
Q

When is the peak incidence of IBD

A

Generally young
Mean UK 29.5

66
Q

Who does ulcerative colitis occur in more

A

Equal incidence between male and female

67
Q

Who does chrohn’s disease occur in more

A

More common in females

68
Q

IBD is more common in specific geographical regions with links to ancestry, what does that imply?

A

Wrong genetic component

69
Q

What is the affected bowel region in ulcerative colitis

A

Colon only

70
Q

What is the affected bowel region in Crohn’s disease

A

Ileum and colon (but also any other region of the gastrointestinal tract from the mouth down to the anus)

71
Q

What does the mucosal surface look like in ulcerative colitis

A

Granular, red with broad flat ulcers with mucosal islands (pseudo-polyps,

72
Q

What does the mucosal surface look like in crohns disease

A

Linear fissuring ulceration (cobblestone appearance)

73
Q

What causes the difference in appearances of UC and CD

A

The different depth the inflammation extends to in the bowel wall

74
Q

How is ulcerative colitis distributed

A

Continuous from rectum

75
Q

How is CD distributed

A

Skip lesions

76
Q

Is there stricter formation in UC

A

Rare

77
Q

Describe the bowel wall in UC

A

Thinned

78
Q

Is there stricter formation in CD

A

Yes

79
Q

Describe the bowel wall in CD

A

Thickened

80
Q

What % of UC have anal lesions

A

25%

81
Q

What % of CD have anal lesions

A

75%

82
Q

What are fistuale

A

Tracts that connect anal skin to the bowel

83
Q

Are fistulae present in UC

A

no

84
Q

Are fistulae present in CD

A

yes

85
Q

What is fat wrapping

A

Thickened fat wraps around the bowel

86
Q

is there fat wrapping gin UC

A

no

87
Q

Is there fat wrapping in CD

A

Yes

88
Q

Are there granulomas in UC

A

No

89
Q

Are there graulomas in CD

A

Yes (35-60%)

90
Q

Describe the inflammation in uc

A

superficial (mucosal)

91
Q

Describe the inflammation in cd

A

Deep (trans-mural)

92
Q

Is there pseudo polyps in UC

A

Marked

93
Q

Is there pseudo polyps in cd

A

Mild/moderate

94
Q

Describe the ulceration in uc

A

Superficial/broad

95
Q

Describe the ulceration in cd

A

deep/fissuring

96
Q

What is pathognomic for CD

A

The presence of granulomas in IBD

97
Q

Describe the lymphocyte reactions in uc

A

Moderate

98
Q

Describe the lymphocyte reactions in cd

A

Marked

99
Q

Describe the fibrosis in uc

A

Mild/none

100
Q

Describe the fibrosis in cd

A

marked (thick wall/strict)

101
Q

Describe the serosal inflmmation in uc

A

Mild/none

102
Q

Describe the serosal inflmmation in Cd

A

marked (fat wrapping)

103
Q

Are there fistulas/sinus formation in cd

A

yes

103
Q

Are there fistulas/sinus formation in uc

A

No

103
Q

What are the signs/symptoms of ulcerative colitis

A
  • Diarrhoea (>66 %)
  • Rectal bleeding (>90%)
  • Abdominal pain (30-60%)
  • Weight loss (15-40%)
  • Constipation (2 %)
  • Anaemia
  • Anorexia
103
Q

Describe the clinical pattern of UC

A
  • Most commonly intermittent (<3 relapses per year: 70-80%)
  • Frequent disease less common (3 or more relapses per year: 15 %)
  • Chronic continuous disease rare (10 %)
104
Q

List the oral manifestation of uc

A
  • Association with disease severity -> severe = ^ oral manifest.
    • Ulceration, tongue coating, halitosis (up to 50% in active UC)
  • Pyostomatitis vegetans
    • Multiple small pustules on oral mucosal surface
    • May be seen CD but more commonly UC
  • Oral ulceration (most common)
  • Caries / periodontitis
104
Q

List specific oral manifestations of CD

A
  • Diffuse labial / buccal swelling
  • Cobblestoning
  • Mucosal tags
  • Deep linear ulcerations
  • Mucogingivitis
  • Granulomatous chelitis
105
Q

What are the signs/symptoms of CD

A
  • Chronic relapsing
  • Diarrhoea
  • Colicky abdominal pain
  • Palpable abdominal mass
  • Weight loss / failure to thrive
  • Anorexia
  • Fever
  • Peri-anal disease
  • Anaemia
106
Q

List non-specific oral manifestations of cd

A
  • Ulceration
  • Pyostomatitis vegitans
  • Dental caries
  • Gingivitis / periodontitis
107
Q

List potential complications with UC

A
  • Toxic megacolon and perforation
  • Haemorrhage
  • Strictures (v. rare)
107
Q

List potential complications with cd

A
  • Toxic megacolon and perforation
  • Fistula
  • Stricture (common)
  • Haemorrhage
  • Short bowel syndrome (repeated resection), causes malabsorption
107
Q

Who is at risk of colonic cancer

A

UC patients
CD patients with colonic disease

107
Q

What are the risk factors for CRC in IBD

A
  1. Early age of onset / duration of disease
  2. Pancolitis
  3. Primary sclerosing cholangitis
  4. Family history of CRC
  5. Severity of inflammation (pseudopolyps)
  6. Pre-malignant changes (dysplasia)
107
Q

What are polyps

A

Tissue masses that protrude from a surface

107
Q

What are polyps in the colon

A

A projection of mucosa that protrudes into the bowel lumen

107
Q

What are multiple polyps called

A

Polyposis

108
Q

What are the 2 types of polyps

A

Neoplastic
Non-Neoplastic

109
Q

Examples of non-Neoplastic polyps

A

Inflammatory polyps
Hamartomatous (juvenile)
Hamartomatous (Peutz-Jeghers)
Hyperplastic

110
Q

Examples of Neoplastic polyps

A

Adenomas
Adenomas (sessile AKA flat)
Malignant (cancer)

111
Q

What does sessile mean

A

Flat

112
Q

What are inflammatory polyps caused by

A

Inflammation
Mucosal prolapse

113
Q

What are pseudopolyps

A

Post-inflammatory polyps
Islands of retained mucosa following ulceration (UC)

114
Q

What are hamartomas

A

non-neoplastic tissue elements, typical for the site of origin, but that abnormal in organisation

114
Q

What is a choristoma

A

Normal tissue at a site which is not typical for its origin

115
Q

What are the 2 types of hamartomatous polyps (non-Neoplastic)

A

Juvenile polyps
Peutz-jeghers polyps

115
Q

Describe PEUTZ-JEGHERS POLYPS

A
  • Peutz-Jeghers syndrome (AD, GLM - LKB1 gene)
    • Multiple polyps (small intestine, stomach & colon)
    • Mucocutaneous hyperpigmentation
    • Positive family history
115
Q

Describe juvenile polyps

A
  • May be genetic (Juv. Polyposis Syndrome, AD)
    • SMAD4 / BMPR1A genes
      CYSTS
    • ^ Cancer risk
  • Sporadic (not inherited) - no cancer risk
  • <3cm, rectal
115
Q

What are peutz-jeghers polyps associated with (the first sign before any GI symptoms)

A

Mucocutaneous hyperpigmentation

115
Q

Describe hyperplastic polyps

A

Commonly in left colon
Often multiple
<5 mm

116
Q

Describe the characteristics of hyperplastic polyps

A
  • Shaggy / ragged
  • “Teeth-like”
  • Serrated
117
Q

What are adenomas in terms of polyps

A

Benign tumours of colonic glandular epithelium
- Polypoid but also “flat”

118
Q

What are adenomas a precursor for

A

Precursor of colorectal cancer (>80% of cases)
- 25% -35% population > 50 years
- Multiple in 20 - 30 % patients

119
Q

Small proportion of adenomas progress to what

A

Cancer

120
Q

Describe the distribution of adenomas (polyps)

A

Evenly distributed around colon, larger in recto-sigmoid and
caecum

121
Q

How are adenomas defined

A

By the presence of pre-malignant change (i.e. dysplasia), but they are still not malignant at this stage

122
Q

What can be concluded if there are dysplastic glands

A

It is Neoplastic lesion

123
Q

What is the 4th most common cancer in the uk

A

Colorectal cancer

124
Q

What diet factors can
1. Increase the risk
2. Decrease the risk
Of colorectal cancer

A
  1. Red/processed meat
    Dietary fat
    Alcohol
  2. Fibre
    Milk/calcium
    Fruit/veg
    Vitamin D
125
Q

What lifestyle factors can
1. Increase the risk
2. Decrease the risk
Of colorectal cancer

A
  1. Cigarette smoking
    Obesity
    Age
  2. Physical activity
    Screening
126
Q

What drugs can decrease the risk of colorectal cancer

A

Aspirin and nsaids
Statins/ocp

127
Q

What health conditions can increase the risk of colorectal cancer

A

Diabetes
IBD

128
Q

What % of cases of CRC are sporadic (not inherited)

What may the other % of cases be caused by

A

90-95%

Genetic predisposition

129
Q

What are the 2 main types of hereditary cancer syndromes

A
  • FAMILIAL ADENOMATOUS POLYPOSIS (FAP)
  • LYNCH SYNDROME (LS)
130
Q

What is FAP

A

Autosomal dominant CRC syndrome
- 80% FAP patients -> mutation
- Adenomatous Polyposis Coli (APC) tumour suppressor gene

131
Q

What do people with FAP develop

A

100s to 1000s of polyps in their colon

132
Q

What happens if FAP is left untreated

A

100% risk of CRC by 40 yo

133
Q

What is the molecular pathogenesis of FAP

A

Adenoma-carcinoma sequence (main pathway for CRC carcinogenesis)

134
Q

List the oral manifestations of CRC

A
  • Gardner syndrome = FAP + extra-colonic manifestations:
  • Upto 75% with GS have dental anomalies
  • Osteoma
  • Odontome
  • Supra-numerary teeth
  • Impacted teeth
135
Q

Which side of the colon do most CRC occur

A

LHS

136
Q

The vast majority of CRCs are what

A

Simple adenocarcinomas

137
Q

what are the symptoms of CRC

A

Change in bowel habits
- Diarrhoea, constipation
-Feeling that the bowel does not empty completely (tenesmus)

Stools
- Bright red or dark blood
- Narrower or thinner than usual

Abdominal pain

Unexplained weight loss, constant tiredness, or unexplained anaemia (iron deficiency)

Y3 IWB (31 decks)

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