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Year 1 NME > Histopathology of the gut > Flashcards

Histopathology of the gut Flashcards

1
Q

What cells line lumen of the oesophagus?

A
  • non keratinising stratified squamous epithelium
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2
Q

In Barrett’s Oesophagus the cells lining the lumen at the distal end of the oesophagus undergo metaplasia, which is the replacement of one cell type to another from the basal cells due to a stimulus. The normal non keratinising stratified squamous epithelium of the lower oesophagus undego metaplasia and become what type of cell and why this type of cell?

A
  • columnar cells
  • more equipped to protection of organ such as in the intestines
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3
Q

In Barrett’s Oesophagus the cells lining the lumen at the distal end of the oesophagus undergo metaplasia, which is the replacement of one cell type to another from the basal cells due to a stimulus. The normal non keratinising stratified squamous epithelium of the lower oesophagus undego metaplasia and become columnar cells. What is the pathological cause of this?

A
  • acid from stomach causes oesophagitis
  • long standing gastro-oesophageal reflux disease
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4
Q

In the image below of the oesophagus we can see where metaplasia has occured and there has been a switch from non keratinising stratified squamous epithelium to column cells. Which number in the image below related to squamous and columnar cells?

A

1 = columnar cells

2 = non keratinising stratified squamous epithelium

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5
Q

In the image below we can see a healthy Oesophageal- gastric junction (OGJ) and a OGJ in a patient with Barrett’s Oesophagus. Between A and B, which is the healtht and which is the Barrett’s Oesophagus?

A
  • A = normal
  • B = Barrett’s Oesophagus
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6
Q

What is the single most important risk factor for Oesophageal adenocarcinoma?

A
  • Barrette oesophagus
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7
Q

What are the 2 most common clinical presentations of Barretts oesophagus?

A
  • heartburn
  • dysphagia (difficulty swallowing)
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8
Q

What is the normal development of Barrettes Oesophagus from squamous cells?

A
  • reflux of gastric contents into the lower oesophagus
  • reflux oesophagitis
  • metaplasia of squamous epithelium to columnar cells
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9
Q

What is the normal development of squamous cells to Barrettes Oesophagus and then onto Adenocarcinoma?

A
  • squamous epithelium exposed to gastric acid
  • reflux disease/oesophagitis
  • metaplasia causing Barrettes Oesophagus
  • low grade dysplasia
  • high grade dysplasia
  • adenocarcinoma
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10
Q

Patients with Barrettes Oesophagus undergo regular screening. Why is this?

A
  • biopsies of oesophagus are taken
  • screen for dysplasia
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11
Q

What is coeliac disease?

A
  • disease where GIT is sensitive to gluten (specifically gliadin)
  • immune-mediated disorder
  • causes ucosal lesion of the small intestine and impaired nutrient absorption
  • improves on withdrawal of gluten
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12
Q

Coeliac disease is associated with the genes that code for 2 human leukocyte antigens (HLA). What are these genes?

A
  • HLA-DQ2
  • HLA-DQ8
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13
Q

In coeliac disease where are biopsies generally taken from?

A
  • duodenum or proximal jejunum
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14
Q

What are the most common histopathological presentation of coeliac disease?

A
  • villi atrophy
  • increase inflammatory cells in lamina propria
  • increased number of intraepithelial lymphocytes
  • elongated and hyperplastic crypts
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15
Q

Diagnosis of ceoliac disease is based on clinical, histological and serological findings. What are the clinical symptoms patients present with?

A
  • sensitivity to gluten
  • diarrohoea
  • flatulence
  • weight loss
  • fatigue
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16
Q

Diagnosis of ceoliac disease is based on clinical, histological and serological findings. What are the 4 histological features that will be present on patients biopsies?

A

1 - atrophy or loss of villi

2 -increased number of intraepithelial lymphocytes

3 - crypts – Elongated and hyperplastic

4 - lamina propria shows increased chronic inflammatory cells

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17
Q

Diagnosis of ceoliac disease is based on clinical, histological and serological findings. What is a key sign of this diease if you remove gluten?

A
  • everything improves
18
Q

Diagnosis of ceoliac disease is based on clinical, histological and serological findings. What is the serology (study of bodily fluids) diagnosis of celiacs?

A
  • anti tissue transglutaminase (TTG)
  • anti-endomysial antibodies
19
Q

Patients with ceoliacs disease is at risk of complications. What are some of the complications associated with this disease?

A
  • anaemia
  • osteoporosis
  • primary biliary cirrhosis
  • Non-Hodkins lymphoma - Enteropathy-associated T-cell lymphoma
  • adenocarcinoma of the small intestine
20
Q

What are the 2 types of inflammatory bowel disease?

A

1 - Ulcerative colitis

2 - Crohn’s disease

21
Q

Who does inflammatory bowel disease affect?

A
  • common in early 20s
22
Q

Is inflammatory bowel disease a constant disease or is it intermittent?

A
  • chronic, relapsing inflammatory condition
23
Q

Where crohns and ulcerative colitis (UC) generally affect in the GIT?

A
  • crohns = anywhere
  • UC = large bowel only
24
Q

In crohns disease what do the histopathologists do with biopsies of the the whole GIT?

A
  • macroscopic examination
  • from outer to inner side of bowel wall
  • disease is intramural (affecting whole wall)
25
Q

In crohns disease what how does the GIT wall appear?

A
  • rubbery and thick
  • inflammation, fibrosis and hypertrophy of the muscularis propria
  • stricture formation
26
Q

In crohns disease what can happen to the mucosa?

A
  • focal mucosa ulcer (aphthous ulcer) form
  • can progress to elongated, serpentine ulcers oriented along the axis of the bowel
27
Q

In crohns disease when looking at the lumen what appearance will we see?

A
  • cobblestone appearance of the mucosa
  • due to ulceration with sparing of interspersed mucosa
28
Q

When studying histological sections of the GIT in Crohns and Ulcerative Colitis, do we see granulomas in both?

A
  • no
  • just Crohns
29
Q

In ulcerative colitis is the disease continous through the affected area or is it cobblestone appearence like in crohns disease?

A
  • continous
30
Q

Pseudopolps can appear in ulcerative colitis. What are these?

A
  • ulcers form on mucosa
  • mucosa tries to regenerate
  • regenerative mucosa forms pseudopolyps
31
Q

What are the 3 major complications of ulcerative colitis that we need to be aware of?

A

1 - pancolitis - involving the entire colon

2 - toxic megacolon – gangrenous changes

3 - low and high grade dysplasia leading to adenocarcinoma

32
Q

What is a common extraintestinal complication of inflammatory bowel disease?

A
  • skin and joint problems
33
Q

What is the most common malignancy of the GIT?

A
  • adenocarcinoma
  • cancer forms from mucus-producing glandular cells
34
Q

Dietary wise, what is a risk factofor the risk of colon cancer?

A
  • low intake of fibres
  • high intake of refined carbohydrates and fat
35
Q

Cyclooxygenase-2 (COX-2) levels are high in colorectal cancer. What common medication have been shown to inhibit COX-2 and potentially offer protection againt colorectal cancer?

A
  • NSAIDs and Aspirin
36
Q

In colon cancer, what are the 2 most common genes that can cause colon cancer?

A

1 - Adenomatous polyposis coli (APC) (tmour supressor)

2 - Mismatch repair gene pathway (check damaged DNA)

37
Q

What is the staging method used for colon cancer?

A
  • TNM
  • T = tumour size
  • N = nodal involvement
  • M = metastatic
38
Q

What are diverticula?

A
  • small, bulging pouches
  • can form in the lining of your digestive system
  • most common in the lower part of the large intestine
  • very common >40 years but generally benign ,
39
Q

Where in the world is diverticular disease most common?

A
  • western world
40
Q

What age is diverticular disease most common?

A
  • >60 years old
41
Q

What region of the colon is diverticular disease most common?

A
  • sigmoid

Year 1 NME (61 decks)

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