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Histopathology Upper Gi tract Flashcards

1
Q

Oesophagus length

A

40 cm, this is used to assess degree of change in the oesophagus during endoscopy.

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2
Q

inflammatory oesophagus conditions

A
  1. Reflex Oesophagitis

2. Achalasia

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3
Q

Oesophageal histology

A

Non-keratinized squamous epithelium

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4
Q

Reflux oesophagitis

A

Reflux of bile salts and stomach acid

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5
Q

Risk factors forReflux oesophagitis

A 
Hiatus hernia
Peptic ulcer
Smoking and alcohol
Excessive vomiting
Pregnancy
Diabetes
Surgery of/around GOJ
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6
Q

Endoscopy findings Reflux oesophagitis

A

Normal patches with red inflamed areas

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7
Q

Reflux oesophagitis Histologically

A
  1. Increased number of inflamed cells
  2. Basal hyperplasia
  3. Upward extension of vascular papillae
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8
Q

Reflux oesophagitis Complications

A

Stricture
Barrett’s
Neoplasia

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9
Q

Achalasia: Aetiology

A

Unknown potentially autoimmune

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10
Q

Achalasia: Definition

A

Inflammatory destruction of myenteric ganglion cells – reduced peristalsis

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11
Q

Achalasia: Long-term complication

A

Squamous cell carcinoma

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12
Q

Achalasia: Macroscopically

A

Lower oesophagus: Destruction = stricture/obstruction distally
Upper oesophagus: Dilation with stagnation of food =
• Inflammation of squamous epithelium which leads prolonged neoplasia – dysplasia – squamous cell carcinoma develops/

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13
Q

Infection of oesophagus Types of organisms

A

Candida
Herpes simplex virus
Trypanosomiasis

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14
Q

Candida and HSVpresent in

A

Immunosuppressed patients:

  1. Elderly
  2. Young – think more serious
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15
Q

Endoscopic appearance of candida →

A

Cottage cheese

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16
Q

Trypanosoma cruzi transmitted by

A

Transmitted in faeces of ‘blood sucking’ reduviid bug – via its bite

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17
Q

Trypanosoma cruzi effects

A
  • Myocardium: increased inflammation and fibrosis = cardiac failure
  • Smooth muscle of GI: inflammation and fibrosis = strictures (pseudo-achalasia)
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18
Q

Barretts metaplasia/columnar lined oesophagus Definition

A

Metaplastic replacement of oesophageal lining by glandular mucosa.

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19
Q

Barretts metaplasia/columnar lined oesophagus Aetiology

A

Reflux of gastric (acid) and duodenal (bile) contents into the oesophagus

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20
Q

Barretts metaplasia/columnar lined oesophagus Endoscopically

A

Transition of squamous to columnar cells (SCJ) is above the gastrooesophageal junction (GOJ)

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21
Q

Barretts metaplasia/columnar lined oesophagus Subtypes

A
  1. Gastric Cardia
  2. Gastric Body
  3. Pancreatic (v. Rare)
  4. Intestinal: most likely to form in cancer
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22
Q

Barretts metaplasia/columnar lined oesophagus Developmental stages to carcinoma

A

Normal squamous
Barretts
Dysplasia
Adenocarcinoma

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23
Q

Oesophageal neoplasia: Types of neoplasia

A 
•	Squamous cell carcinoma
•	Adenocarcinoma
Rare:
•	Mesenchymal neoplasms (e.g. leiomyoma)
•	Lymphoma
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24
Q

Oesophageal neoplasia: Squamous cell carcinoma epi

A

205 of oesophageal cancers
M:F = 3:1
Lower>upper>middle
China, Japan, Iran, South Africa

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25
Oesophageal neoplasia: Squamous cell carcinoma prognosis
Poor: DXT +/- surgery
26
Oesophageal neoplasia: Adenocarcinoma epi
80% of oesophageal neoplasia Increasing + + More common in the UK
27
Oesophageal neoplasia: Staging
TNM | T3 or less = operable
28
Stomach → Inflammatory: Histology
Cardiac and antral region similar mucosa Body/fundus specialised gastric mucosa: parietal and chief
29
gastritis Epi
* More frequently recognised | * Now the commonest form of ‘chronic’ gastritis
30
gastritis Causes
* Bile reflux * Drugs: aspirin, other non-steroidal anti-inflammatory drugs (NSAIDS) * Alcohol
31
gastritis Histo changes(don’t need to know)
* Extension of glands | * Smooth muscle fibres extended
32
Helicobacter Pylori: Disease caused by H. Pylori
``` Gastritis Ulcers 2 types of neoplasia: 1. MALT lymphoma 2. Carcinoma ```
33
Helicobacter Pylori: MALT Lymphoma
Mucosa associated Lymphoid tissue
34
Helicobacter Pylori: MALT lymphoma Rx
Eradication of HP with PPI, antibiotics +/- bismuth causes regression of MALT lymphoma
35
Helicobacter Pylori: H. Pylori regional
Antrum
36
Carcinoma: Stages in development of gastric carcinoma
1. Normal gastric mucosa (H pylori infiltrates post this) 2. Superficial gastritis 3. Atrophic gastritis (precancerous) 4. Intestinal metaplasia (precancerous) – similar to barretts 5. Dysplasia (precancerous) 6. Carcinoma
37
Carcinoma:H. Pylori WHO
* Most common bacterial infection * Gastric carcinoma is the 2nd leading cause of cancer-related deaths worldwide * Class 1 carcinogen
38
Carcinoma:Gastric Neoplasia
* Adenocarcinoma * Lymphoma * Neuro-endocrine tumour (including ‘carcinoid’) * CIST (gastrointestinal stromal tumour)
39
Adenocarcinoma of the stomach → Epi
M:F = 3:1 7th commonest cancer killer in UK; was 4th Japan, Korea, Chile – shows environmental aspect e.g. food when they migrated to the states
40
Adenocarcinoma of the stomach →Risk factors
Diet (high in salt, low dairy products) | Helicobacter and intestinal metaplasia
41
Adenocarcinoma of the stomach → Prognosis
Poor (<20% 5 yr survival) | Good if early gastric cancer (90% 5 yr survival)
42
Adenocarcinoma of the stomach → Use of Herceptin
Slows progression by inhibiting Her2 not a cure.
43
GIST → Epi
RARE
44
GIST →Common locations
Stomach> SI > oesophagus and large bowel
45
GIST → Mutations
Tyrosine Kinase genes (KIT)
46
GIST →Rx
Surgery +/- TKI inhibitors (e.g. imatinib)
47
GIST →Histology
Varying histology
48
Coeliac disease: Definition
Malabsorption (e.g. anaemia, low albumin) | Auto-immune disease with an abnormal immunological reaction to gluten
49
Coeliac disease:Rx
Improvement on gluten-free diet | Relapses when gluten re-introduced
50
Coeliac disease:Pathology in small intestine - histology
1. Flat mucosa 2. Reduction in the normal villous height to crypt depth ratio from 5:1 to <3:1 3. Crypt Hyperplasia 4. Increased intraepithelial lymphocytes 5. Infiltration of the lamina propria by plasma cells and lymphocytes
51
Coeliac disease:Complications
6. Refractory sprue (non-responsive to gluten restriction) – could means its neoplastic. 7. Ulcerative jejunitis 8. Neoplasia: • Enteropathy – associated T-cell lymphoma (EATL) • Small intestine adenocarcinoma
52
Giardiasis: Organisms
Giardia Lamblia – commonest SI protozoal infection worldwide.
53
Giardiasis: Transmision
Contaminated water (person –to- person spreading by faecal-oral transmission)
54
Giardiasis: At risk patients
Immunocomprimised patients more likely to be infected e.g. AIDS and common variable immunodeficiency (Ig defiency).
55
Giardiasis: histology
Small intestinal mucosa may be normal – or inflamed.
56
Small intestinal Neoplasia Types
1. Adeonmas – 2. Adenocarcinoma 3. Lymphoma 4. GIST – gastrointestinal stromal tumours 5. Neuro endocrine tumours
57
Small intestinal Neoplasia Adenomas
Duodenal (Familial adenomatous polyposis)
58
Small intestinal Neoplasia Adenocarcinoma
Rare (coeliac disease, Crohn’s disease, FAP)
59
Small intestinal Neoplasia Lymphomas
B cell e.g. Burkitt’s lymphoma in ileum (can be driven by Epstein barr) T cell e.g. EATL
60
Neuroendocrine tumours: Common sites
Small intestine | Appendix
61
Neuroendocrine tumours: Macro features
Polyps Masses Smaller primary tumours Large metastasis
62
Neuroendocrine tumours: Subtypes
Carcinoid (liver mets) | Small cell carcinoma

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