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4th year gi > Disorders of the stomach > Flashcards

Disorders of the stomach Flashcards

1
Q

Describe the lining of the stomach

A
  • The stomach is lined with a specialised columnar epithelium, adapted with gastric pits that contain chief cells and parietal cells
  • Chief cells are responsible for producing pepsin, and parietal cells secrete hydrochloric acid and release intrinsic factor
  • Because of the stomach’s low pH environment, it is protected by surface cells that secrete mucus and bicarbonate
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2
Q

How does the stomach connect to the duodenum?

A

Via the pyloric sphincter

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3
Q

What does intrinsic factor do?

A

Intrinsic factor binds to vitamin B12, which essentially primes it to be abdorbed in the terminal ileum

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4
Q

What is dyspepsia?

A

Dyspepsia primarily refers to bloating and discomfort associated with the upper abdomen, it includes GORD symptoms.

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5
Q

How would you manage a patient presenting with dyspepsia?

A
  • Most patients do not require investigations and can be treated conservatively:
    • Medication review - steroids, NSAIDs, bisphosphonates, ect
    • Lifestyle modification - alcohol cessation, dietry change
    • Trial of antacids or alginates
  • ALARM symptoms/ >55y
    • Urgent endoscopy
  • Unresponsive to conservative therapy
    • Test for H. pylori (breath/stool)
      • Positive - Eradication therapy
      • Negative - Trial of PPI
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6
Q

What is gastritis and what are the two subtypes?

A

Gastritis refers to inflamation of the stomach and is primarily a histological diagnosis.

This can be divided into acute and chronic gastritis, each of which is caused by very different pathologies.

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7
Q

Causes of acute and chronic gastritis

A
  • Acute
    • H. Pylori infection
    • Alcohol
    • NSAIDs, aspirin
    • Stress-induced
    • Bile acid reflux (usually post-gastric surgery)
  • Chronic
    • Chronic H. pylori infection
    • Crohn’s disease
    • Sarcoidosis
    • Autoimmune (atrophic)
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8
Q

What is autoimmune gastritis?

A

Autoimmune gastritis is a chronic atrophic condition associated with the autoimmune destruction of parietal cells of the stomach. Severe gastric atrophy will result in insufficient intrinsic factor production, leading to pernicious anaemia.

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9
Q

Define peptic ulcer disease

A

Disease of the stomach or duodenal mucosa involving a break in the layer and loss of surface tissue.

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10
Q

Epidemiology of peptic ulcer disease

A
  • Accounts for 13% of investigated dyspepsia
  • Prevelence of less than 1% in the western population
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11
Q

Aetiology of peptic ulcer disease

A
  • Helicobacter pylori infection
  • Drugs - aspirin, NSAIDs
  • Rare causes
    • Zollinger-Ellison syndrome
    • Crohn’s disease
  • Secondary to
    • Intracranial neurology (known as a Cushing ulcer)
    • Burns or trauma (know as a Curling ulcer)
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12
Q

Clinical features of peptic ulcer disease

A
  • Epigastric pain with post-prandial association
  • Bloating, abdominal distension
  • Nausea
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13
Q

Peptic ulcer - does the epigastric pain get better or worse after eating?

A

The epigastric pain related to duodenal ulcers classically improves upon eating, while the pain related to gastric ulcers is typically described as worse on eating.

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14
Q

Pathophysiology of peptic ulcer due to H. pylori

A

H. pylori, a Gram-negative, urase-producing bacterium (enabling it to survive in low pH conditions), lives in the stomach and duodeal mucosa.

The pathogen stimulates gastrin production as well as inhibiting somatostain production, resulting in an increase in acid secretion, which ultimately leads to gastric and duodenal ulceration.

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15
Q

Investigations for H. pylori

A
  • Carbon-13 urea breath test (stop PPI medication 2 weeks before test as they may result in false positive tests)
  • Stool antigen testing
  • Laboratory-based serology testing
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16
Q

Stepwise management of H. pylori positive peptic ulcer disease

A
  • 7 day course of triple therapy
    • high dose PPI + amoxicillin + clarithromycin/metronidazole
  • Re-test at 6-8 weeks
    • perform re-testing at 6-8 weeks with carbon-13 urea breath test to confirm successful eradication
  • Second-line eradication therapy
    • for patients who remain symptomatic
    • bismuth (warn patients it will result in black stools)
17
Q

Stepwise management of H. pylori negative peptic ulcer disease

A
  • Stop offending medications and offer drug therapy for 8 weeks
    • Stop any offending medications (NSAIDs, aspirin) and offer full dose PPI or H2R antagonist (eg ranitidine) therapy for 8 weeks
  • Offer lifestyle advice
    • eg smoking cessation, dietry changes

Chronic or recurrent disease

  • Exclude other diagnoses
    • eg malignancy, Zollinger-Ellison syndrome, Crohn’s disease
    • Offer long term low dose PPI
18
Q

Complications of peptic ulcer disease

A
  • Acute upper GI harmorrhage
  • Perforation
  • Gastric outlet obstruction - chronic ulceration of the pylorus/duodenum will result in fibrotic stricturing
  • Malignant transformation
19
Q

Define Zollinger-Ellison syndrome

What is it associated with?

A

A rare condition caused by a gastrin secreting gastinoma usually of pancreatic origin (90%). It is thought to have an annual incidence of 1-2 per million. The syndrome is characterised by hypersecretion of gastric acid, resulting in extensive ulceration.

Multiple endocrine neoplasia (MEN) type 1.

20
Q

What is gastric cancer?

A

Gastric cancer refers to a neoplasm that arises from the stomach mucosa. It is typically of adenocarcinoma histology.

21
Q

Epidemiology of gastric cancer

A
  • the second most common cause of global cancer realted deaths
  • twice as common in men
  • higher incidence in Asia compared to western world (more common in Japan, possibly because of high consumption of raw fish)
22
Q

Risk factors for gastric cancer

A
  • Helicobacter pylori infection
  • Alcohol consumption and smoking
  • Consumption of nitrate-rich foods, such as smoked and pickled processed foods
  • Autoimmune atrophic gastritis
  • Familial adenomatous polyposis
23
Q

Clinical features of gastric cancer

A
  • Usually asymptomatic in early stages
  • Non-specific dyspepsia
  • Progressive dysphagia, vomiting +/- haematemesis
  • Weight loss, anorexia
  • Iron deficiency anaemia
24
Q

Which lymph node may be enlarged in gastric cancer?

A

Left supraclavicular lymph node (Virchow’s node)

25
Q

Investigations in suspected gastric cancer

A
  1. Check baseline bloods
    • FBC (may reveal microcytic anaemia)
    • LFTs (deranged values may indicate liver metastasis
  2. Arrange for urgent upper GI endoscopy with tissue biopsies
  3. Arrange for staging CT chest, abdomen and pelvis - to complete TNM staging
26
Q

Management of gastric cancer - early localised disease

A

Curative surgical resection with a consideration of neoadjuvant or peri-operative chemotherapy

27
Q

Management of gastric cancer - advanced inoperable disease

A

Palliative chemotherapy and palliative stenting may be offered for symptomatic relief

28
Q

Which chemotherapy regime would be used for gastic cancer?

Which drug is recommended in patients with human epidermal receptor 2 (HER2) positive metastatic disease?

A

Capecitabine in combination with a platinum based agent

Trastuzumab

4th year gi (15 decks)

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