5. Gastric clinical conditions Flashcards Preview

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Flashcards in 5. Gastric clinical conditions Deck (14)
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1
Q

what is GORD and how would a P present

A

Gastro-oesophageal reflux disease: reflux of stomach contents/acid into oesophagus causing ulceration of oesophageal mucosa (oesophagitis).
Is a result of:
- decreased tone of LOS
- delayed gastric emptying (raised intra-gastric pressure, e.g. due to obesity or pregnancy)
- hiatus hernia

Symptoms:

  • heartburn
  • cough
  • sore throat
  • dysphagia
2
Q

name 2 possible complications of GORD

A
  1. strictures (causing dysphagia)
  2. Barrett’s oesophagus: metaplasia of stratified squamous epithelium to columnar containing goblet cells, with 30-40x increased risk of developing adenocarcinoma
3
Q

describe the management of GORD

A
  1. lifestyle changes
  2. pharmacological: antacids, H2 antagonists, PPI
  3. surgery (rare)
4
Q

what is acute gastritis, why does it occur and how does it present

A

Transient bouts of acute gastric mucosa inflammation, may involve: increased HCL secretion, reduced HCO3- production, reduced blood flow (… ischaemia) or direct injury to mucosa

Can be stimulated by:

  1. NSAIDs (esp. aspirin)
  2. heavy smoking or alcohol consumption
  3. chemotherapy
  4. bile reflux

Frequently asymptomatic but may have:

  • epigastric pain
  • nausea or vomiting
  • mild to massive upper GI bleeds (can be fatal)
5
Q

what is chronic gastritis, what are the 2 main causes and how does it present

A

Chronic inflammation (lymphocytes and plasma cells) of gastric mucosa with progressive atrophy. May eventually progress to gastric carcinoma due to metaplasia and dysplasia.

2 basic aetiologies:

 1. H. pylori infection - involves immune resp. to bacteria, with MALT expansion. Asymptomatic or similar symptoms to acute gastritis.

 2. autoimmune gastritis - type II hypersensitivity reaction with autoantibody production against HK ATPase of parietal cells... decreased parietal cells... decreased production of:  - intrinsic factor (... inability to absorb vit B12... megaloblastic pernicious anaemia)  - HCL (... achlorydia) Causes symptoms of anaemia, glossitis, anorexia and neurological symptoms.
6
Q

name possible complications of chronic gastritis caused by H. pylori infection

A

peptic ulcers, adenocarcinoma, MALT lymphoma

7
Q

what is peptic ulcer disease and where does it most commonly occur. what are the main symptoms

A

Peptic ulcer = breach in gastric or duodenal mucosa that extends through muscularis mucosa.
Most common in:
1- early duodenum
2- lesser curvature of stomach

Main symptom: epigastric pain - burning/gnawing following meals, often at night

Serious symptoms: bleeding/anaemia, early satiety and weight loss

8
Q

name the causes of peptic ulcer disease, inc. an example of adenoma

A
  1. mucosal injury, e.g. stomach acid, H. pylori infection, NSAIDs (inhibit prostaglandin synthesis necessary for mucosal defence)
  2. massive physiological stress (e.g. burns, raised ICP) = STRESS ULCERATION
  3. ZOLLINGER-ELLISON SYNDROME: gastrin-secreting gastrinoma (neuroendocrine tumour) resulting in increased gastric acid secretion by parietal cells
9
Q

name 2 possible serious complications of peptic ulcers

A
  1. v. deep ulcers can erode into underlying blood vessels… rapid HAEMORRHAGE into GI tract
  2. PERFORATION if ulcer erodes all the way through wall… peritonitis
10
Q

which blood vessels are at risk of erosion in peptic ulcer disease

A

L gastric a. (from gastric ulcer in lesser curve of stomach)

Gastroduodenal a. (from post. wall duodenal ulcer)

11
Q

how does H. pylori affect the gastric mucosa

A
  1. releases cytotoxins… direct epithelial injury
  2. enzyme expression: urease - converts urea to ammonia which is toxic to epithelial cells
  3. promotes inflammatory resp. - self-injury
  4. degrades mucus layer?
12
Q

whay type of bacterium is H. pylori, how is it spread and how does it survive in stomach

A
  • GNB spread oral-oral or faecal-oral
  • survival:
    1. produces urease: converts urea to ammonium (basic in solution)… increases local pH
    2. flagellated: good motility, lives in mucus layer/adheres to gastric epithelia
13
Q

how is H. pylori eradicated

A

triple therapy with PPI + clarithromycin + amoxicillin

14
Q

name 2 mechanisms for gastric acid secretion suppression

A
  1. H2 blockers - block histamine Rs on parietal cells… decreased acid secretion
  2. proton pump inhibitors (omeprazole) - block H+/K ATPase on parietal cells… decreased acid secretion