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Cardio > Histopathology Upper Gi tract > Flashcards

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
Q

Oesophageal neoplasia: Squamous cell carcinoma prognosis

A

Poor: DXT +/- surgery

26
Q

Oesophageal neoplasia: Adenocarcinoma epi

A

80% of oesophageal neoplasia
Increasing + +
More common in the UK

27
Q

Oesophageal neoplasia: Staging

A

TNM

T3 or less = operable

28
Q

Stomach →
Inflammatory:
Histology

A

Cardiac and antral region similar mucosa

Body/fundus specialised gastric mucosa: parietal and chief

29
Q

gastritis Epi

A
  • More frequently recognised

* Now the commonest form of ‘chronic’ gastritis

30
Q

gastritis Causes

A
  • Bile reflux
  • Drugs: aspirin, other non-steroidal anti-inflammatory drugs (NSAIDS)
  • Alcohol
31
Q

gastritis Histo changes(don’t need to know)

A
  • Extension of glands

* Smooth muscle fibres extended

32
Q

Helicobacter Pylori: Disease caused by H. Pylori

A 
Gastritis
Ulcers
2 types of neoplasia:
1.	MALT lymphoma
2.	Carcinoma
33
Q

Helicobacter Pylori: MALT Lymphoma

A

Mucosa associated Lymphoid tissue

34
Q

Helicobacter Pylori: MALT lymphoma Rx

A

Eradication of HP with PPI, antibiotics +/- bismuth causes regression of MALT lymphoma

35
Q

Helicobacter Pylori: H. Pylori regional

36
Q

Carcinoma: Stages in development of gastric carcinoma

A
  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
Q

Carcinoma:H. Pylori WHO

A
  • Most common bacterial infection
  • Gastric carcinoma is the 2nd leading cause of cancer-related deaths worldwide
  • Class 1 carcinogen
38
Q

Carcinoma:Gastric Neoplasia

A
  • Adenocarcinoma
  • Lymphoma
  • Neuro-endocrine tumour (including ‘carcinoid’)
  • CIST (gastrointestinal stromal tumour)
39
Q

Adenocarcinoma of the stomach → Epi

A

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
Q

Adenocarcinoma of the stomach →Risk factors

A

Diet (high in salt, low dairy products)

Helicobacter and intestinal metaplasia

41
Q

Adenocarcinoma of the stomach → Prognosis

A

Poor (<20% 5 yr survival)

Good if early gastric cancer (90% 5 yr survival)

42
Q

Adenocarcinoma of the stomach → Use of Herceptin

A

Slows progression by inhibiting Her2 not a cure.

43
Q

GIST → Epi

44
Q

GIST →Common locations

A

Stomach> SI > oesophagus and large bowel

45
Q

GIST → Mutations

A

Tyrosine Kinase genes (KIT)

46
Q

GIST →Rx

A

Surgery +/- TKI inhibitors (e.g. imatinib)

47
Q

GIST →Histology

A

Varying histology

48
Q

Coeliac disease: Definition

A

Malabsorption (e.g. anaemia, low albumin)

Auto-immune disease with an abnormal immunological reaction to gluten

49
Q

Coeliac disease:Rx

A

Improvement on gluten-free diet

Relapses when gluten re-introduced

50
Q

Coeliac disease:Pathology in small intestine - histology

A
  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
Q

Coeliac disease:Complications

A
  1. Refractory sprue (non-responsive to gluten restriction) – could means its neoplastic.
  2. Ulcerative jejunitis
  3. Neoplasia:
    • Enteropathy – associated T-cell lymphoma (EATL)
    • Small intestine adenocarcinoma
52
Q

Giardiasis: Organisms

A

Giardia Lamblia – commonest SI protozoal infection worldwide.

53
Q

Giardiasis: Transmision

A

Contaminated water (person –to- person spreading by faecal-oral transmission)

54
Q

Giardiasis: At risk patients

A

Immunocomprimised patients more likely to be infected e.g. AIDS and common variable immunodeficiency (Ig defiency).

55
Q

Giardiasis: histology

A

Small intestinal mucosa may be normal – or inflamed.

56
Q

Small intestinal Neoplasia Types

A
  1. Adeonmas –
  2. Adenocarcinoma
  3. Lymphoma
  4. GIST – gastrointestinal stromal tumours
  5. Neuro endocrine tumours
57
Q

Small intestinal Neoplasia Adenomas

A

Duodenal (Familial adenomatous polyposis)

58
Q

Small intestinal Neoplasia Adenocarcinoma

A

Rare (coeliac disease, Crohn’s disease, FAP)

59
Q

Small intestinal Neoplasia Lymphomas

A

B cell e.g. Burkitt’s lymphoma in ileum (can be driven by Epstein barr)
T cell e.g. EATL

60
Q

Neuroendocrine tumours: Common sites

A

Small intestine

Appendix

61
Q

Neuroendocrine tumours: Macro features

A

Polyps
Masses
Smaller primary tumours
Large metastasis

62
Q

Neuroendocrine tumours: Subtypes

A

Carcinoid (liver mets)

Small cell carcinoma

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