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Clinical pathology > Upper gastrointestinal pathology > Flashcards

Upper gastrointestinal pathology Flashcards

1
Q

Oesophagitis definition

A
  • Inflammation of the oesophagus

- Classification: acute or chronic (depends on aetiology and duration)

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2
Q

Oesophagitis aetiology

A
  • Infectious (not the most common)
  • Bacterial, viral (Herpes: HSV1, fungal - candida
  • Chemical – most common
  • Ingestion of corrosive substances
  • Reflux of gastric contents: commonest cause; stomach contents works through sphincter into lower oesophagus, sometimes upper oesophagus
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3
Q

Reflux Oesophagitis definition

A
  • Commonest form of oesophagitis - caused by reflux of gastric acid = gastro-oesophageal or bile = duodeno-gastric reflux
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4
Q

Reflux Oesophagitis risk factors

A
  • Defective lower oesophageal sphincter
  • Hiatus hernia
  • Increased intra-abdominal pressure
  • Increased gastric fluid volume due to gastric outflow stenosis
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5
Q

Two types of Hiatus hernia

A
  • Sliding hiatus hernia = reflux symptoms

- Para-oesophageal hernia = strangulation and reflux

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6
Q

Barrett’s Oesophagus

A
  • Cause: longstanding gastro-oesophageal reflux
  • Risk factors: same as reflux, male, Caucasian, overweight
  • Squamous replaced by columnar mucosa = glandular metaplasia
  • Barret’s goblet cells
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7
Q

Oesophageal Carcinoma

A
  • Squamous Cell Carcinoma – carcinoma of endemic tissue
  • Adenocarcinoma – almost always from Barrett’s as glandular tissue shouldn’t be there – most common
  • Adenocarcinoma more common in richer countries due to lifestyle
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8
Q

Oesophageal Adenocarcinoma

A
  • Mainly lower oesophagus
  • Higher incidence in main: male/female ratio: 7:1 and among Caucasians
    Aetiology:
    o Barrett’s oesophagus: most originate from this
    o Tobacco/Obesity
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9
Q

Oesophageal Squamous Carcinoma

A
  • Location: middle and lower third
  • Squamous carcinoma preceded by squamous dysplasia
  • Risk factors include tobacco and alcohol, HPV
  • Polypoidal, ulcerating and stricturing
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10
Q

TNM system

A
  • T = depth of invasion of the primary tumour (how far through muscularis propria, deeper connective tissue = worse) – grade of tumour
  • N = regional lymph nodes
  • M = distant metastasis
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11
Q

4 gastric anatomic regions

A
  • Cardia: area around the GO junction
  • Fundus: located in the upper part of the body of the stomach
  • Body: main part of the stomach
  • Antrum: near the pylorus
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12
Q

Acute gastritis

A
  • Usually due to chemical injury
  • Drugs e.g. NSAIDS, alcohol, initial response to helicobacter pylori infection
  • Effects depend on severity of the injury: can get erosions and haemorrhage
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13
Q

Gastritis type

A

Organ wide inflammation

  • Normal - Balance of aggressive (acid) and defensive forces
  • Increased aggression
  • Impaired defences
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14
Q

Chronic Gastritis

A
  • Autoimmune - B12 deficiency

- Helicobacter pylori - Increased risk of gastric cancer and MALT lymphoma

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15
Q

Helicobacter pylori

A
  • Infection itself damages the epithelium leading to chronic inflammation of the mucosa (destruction of cells = decreased acid levels)
  • Treat with a combination of antibiotics and PPIs
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16
Q

Peptic Ulcer Disease definition

A
  • Localised defect extending at least into submucosa
  • Only part of the lining = erosion, full lining = ulcer
    Major sites:
  • First part of duodenum
  • Junction of antral and body mucosa
  • Distal oesophagus (GOJ)
17
Q

Peptic Ulcer Disease aetiology

A
  • Anything that increases gastric acid levels:

- H. pylori infection, duodeno-gastric reflux, drugs: NSAIDs, smoking

18
Q

Acute gastric ulcer histology

A
  • Full thickness coagulative necrosis of mucosa or deeper layers
  • Granulation tissue at ulcer floor
19
Q

Chronic gastric ulcer histology

A
  • Clear cut edges overhanging the base

- Extensive granulation and scar tissue at ulcer floor

20
Q

Peptic Ulcer Complications

A
  • Perforation = peritonitis
  • Penetration into an adjacent organ e.g. liver or pancreas
  • Stricturing = hour glass deformity
  • Haemorrhage - chronic can lead to anaemia
21
Q

Most frequent gastric cancer

A

adenocarcinoma, as columnar epithelium in the stomach

22
Q

Gastric Adenocarcinoma aetiology

A
  • Diet (smoked/cured meat or fish, pickled vegetables)
  • Helicobacter pylori infection (Western mainly)
  • Bile reflux (e.g. post Billroth II operation)
  • Hypochlorhydria (allows bacterial growth)
23
Q

Carcinoma of GOJ

A
  • Similar to lower oesophagus carcinoma
  • White males
  • Association with GO reflux - no association with H pylori/ diet
24
Q

Carcinoma of gastric body/antrum

A
  • Association with H. pylori/diet - no association with GO reflux
25
Q

Hereditary Diffuse Type Gastric Cancer (HDGC)

A
  • Germline CDH1/E-cadherin mutation

- Increased risk of other cancers

26
Q

Coeliac Disease

A
  • Gluten sensitive enteropathy
  • Ingestion of gluten containing cereals
  • Fairly common - prevalence of 0.5-1%
27
Q

Pathogenesis of Coeliac Disease

A
  • Immune-mediated reaction to gliadin
  • Causes epithelial cells to produce IL-15
  • Causes activation of CD8+ intra-epithelial lymphocytes
  • Attack tissue transglutaminase on the bowel epithelium
28
Q

Diagnosis of coeliac disease

A
  • Tissue biopsy is diagnostic - Gold standard test
  • Look down microscope to see the effects of the coeliac on the epithelium
  • Gluten free diet and take biopsy weeks later to see if improvement
29
Q

Clinical Features and Associations of Coeliac

A
  • Dermatitis herpetiformis
  • Lymphocytic gastritis and lymphocytic colitis
  • Coeliac disease is linked with cancer of the small intestine and T cell lymphoma
30
Q

Treatment of Coeliac

A
  • Gluten-free diet symptomatic = improvement for most patients
  • Reduces risk of long-term complications including anaemia, female infertility, osteoporosis, and cancer
31
Q

Gastric cancer epidemiology

A
  • More common with ageing, male:female = 2:1

- High rates in Eastern Asia/South America/Eastern Europe

32
Q

Gastric cancer aetiology

A
  • lifestyle factors (75% of cases) – diet (smoked/cured meat, pickled veg.), smoking, alcohol, obesity
  • H.pyori, bile reflux and low levels of stomach acid
33
Q

Gastric cancer pathogenesis

A
  • Depends on location
  • GOJ = GO reflux, no association with H.pylori or diet
  • Body and antrum = associated with H.pylori and diet, not GO reflux
34
Q

Gastric cancer types

A
  • Intestinal type = well differentiated, have intestinal architecture e.g. glands
  • Diffuse type = poorly differentiated, scattered growth, cadherin mutation
35
Q

Gastric cancer clinical features

A
  • Dysphagia, weight loss, indigestion, feeling full, vomiting
  • If ulcerating = bleeding (haematemesis) and meleana
36
Q

Gastric cancer treatment

A
  • If early = resection with a clear margin. If advanced = partial or total gastrectomy.
  • Often, it has spread further = chemotherapy
  • 20% live for 5 years – poor prognosis with gradual increase in survival

Clinical pathology (69 decks)

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