Gastric Disease Flashcards
Describe the prevalence and incidence of gastric disease
- up to 40% of adults suffer from dyspepsia (indigestion) a year
State the NICE definition of Dyspepsia
What are 5 symptoms included?
- Upper GI tract symptoms, typically for 4 or more weeks
- Abdominal pain
- Discomfort
- Heartburn
- Acid reflux
- Nausea and/ or vomiting
List 3 common gastric disorders
What are 2 causes of Chronic Gastritis (Can also be acute)
- Gastritis
- GORD
- Peptic Ulcer Disease
- Bacteria
- Autoimmune
List 4 symptoms of GORD
- Chest pain
- Acid taste in mouth
- Cough
- Asymptomatic
What are 6 consequences of GORD
- Nothing
- Oesophagitis
- Ulceration
- Haemorrhage
- Fibrous Strictures-> Dysphagia
- Barrett’s Oesophagus (Strat. squamous-> Gastric columnar)
Name 5 risk factors for GORD
- Ineffective LOS
- Anything that increases intrabdominal pressure
- Obesity
- Pregnancy
- Hiatal hernia (LOS moves into thorax)
- Delayed gastric emptying
List 3 treatment mechanisms for GORD
- Lifestyle modifications (weight loss, smaller meals, less alcohol and caffeine, stop smoking, avoid trigger foods)
- Surgery (Rare) (Fundoplication where fundus is wrapped around LO to assist sphincter mechanism)
- Pharmacological (Antacids, H2 antagonists, Proton pump inhibitors )
The LOS is normally contracted. When does it relax?
When swallowing food
What are 3 components of the LOS
- Muscular elements (Intrinsic muscles + Part of diaphragm)
- Right crus of diaphragm (tightens around LOS)
- Acute angle of entry into stomach helps prevent reflux
What cancer can Barrets Oesophagus lead to? (Due to increased risk of dysplasia)
Adenocarcinoma (Normally we get squamous cell carcinoma)
What is Gastritis?
What is 1 way it can be diagnosed?
What are 4 typical symptoms?
Inflammation of stomach mucosa
Diagnosable by endoscopy
- Pain
- Nausea
- Vomit
- Haemorrhage
The causes of Acute Gastritis can lead to Chronic Gastritis.
List 4 causes
- Heavy use of NSAIDs
- Lots of alcohol
- Chemotherapy
- Bile reflux-> Chemical injury -> Damaged epithelia and reduced mucus production
List 3 symptoms and 1 treatment for Acute Gastritis
- Asymptomatic
- Abdominal pain, nausea, vomiting
- Occasional bleeding (which can be fatal)
- Removal of irritant
What are 3 causes of Chronic Gastritis?
- Autoimmune (Antibodies against parietal cells)
- Infection with H. pylori (most common)
- Chemical/ reactive;
- Minimal inflammation
- Chronic alcohol abuse, NSAIDs, Bile reflux
List 4 pathological changes in Acute and Chronic Gastritis
Acute;
- Epithelial damage
- Some epithelial hyperplasia
- Vasodilation
- Neutrophil response
Chronic;
- Lymphocyte response
- Glandular atrophy
- Fibrotic changes
- Metaplastic changes
Describe Autoimmune Chronic Gastritis
- Antibodies target Parietal cells, which produce HCl and Intrinsic Factor
- Can lead to Pernicious Anaemia, as Vit B12 is not absorbed in Ileum
List 4 symptoms of Autoimmune Chronic Gastritis
- Anaemia symptoms (Megaloblastic anaemia)
- Glossitis
- Anorexia (Due to loss of appetite)
- Neurological symptoms
What are 2 groups of symptoms of H. pylori causing Chronic Gastritis?
- Asymptomatic/ similar to acute gastritis
- Peptic ulcers, Adenocarcinoma, MALT Lymphoma
Describe H. pylori
How does it enter body?
- Helix shaped
- Gram negative
- Microaerophilic (Needs only a little bit of O2)
- Oral to oral OR Faecal to oral
Where does H. pylori go once it enters the stomach?
How is it adapted to do so?
- Migrates and adheres to gastric epithelia
1. Flagella for motility
- Uses chemotaxis to find areas of lower acidity (Surface of
epithelia, under mucus layer) - Adhesins to attach to Gastric Epithelia and resist peristalsis
- Produces Urease, which converts Urea to Ammonium, raising pH around itself. (This prevents death by acid)
What 5 problems are caused by presence of H. pylori?
- CagA gene causes cytotoxin release cytotoxins-> Direct epithelial injury + Inflammation + associated with cancer
- Produce ammonia-> Toxic to epithelia
- Promotes inflammation
- Produces VacA, which increases paracellular permeability and is toxic to epithelia
- Secretes Mucinases, Proteases, Lipases-> Mucus layer damage
Describe what happens if H. pylori colonise predominantly in the Antrum
- Increased G cell/ decreased D cell activity-> More Gastrin made
- Parietal cells make more HCl and increase in number
- Chyme more acidic-> Duodenum damage and metaplasia (to be more like gastric epithelia)
- H. pylori colonise Duodenum-> Duodenal ulcers
What if H. pylori colonise predominantly in Body of stomach?
- Atrophy of Parietal cells
- Gastric ulceration
- Increased risk of Dysplasia-> Cancer
What happens if H. pylori colonise predominantly in both Antrum and Body of stomach?
Asymptomatic
How can we diagnose Chronic Gastritis secondary to H. pylori infection?
- Stool antigen test
- Urea Breath test (Using carbon 13)
- Upper GI Endoscopy to get biopsy
Describe the Urea Breath Test
Gastric Urea normally contains Carbon 12 mainly with only 1% Carbon 13
- In test, patient ingests Urea that is mainly Carbon 13
- If H. pylori present, this is broken down into NH4 and CO2
- If Carbon 13 detected in exhaled CO2, H. pylori are present
How do we treat Chronic Gastritis secondary to H. pylori infection?
Proton Pump Inhibitor + 2 Antibiotics (Clarithromycin/ Metronidazole/ Amoxicillin)
Side effects: Diarrhoea and nausea
Course can be extended from 7 to 14 days, but minimal additional effect
Define Peptic Ulcer Disease
Where are they most common?
Where do they commonly occur if in the stomach?
Defect in Gastric/ Duodenal mucosa, that extends through Mucularis Mucosa
Most common in proximal duodenum
Commonly affect Lesser Curve and Antrum of stomach
Compare Gastric and Duodeneal ulcers in;
- Incidence
- Age
- Social class
- Blood group
- Acid levels
- H. pylori
Gastric;
- More common with increasing age
- More common in low social classes
- More common with Blood Grp A
- Normal/ low acid levels
- 70% caused by H. pylori
Duodenal;
- 3 times more common than gastric ulcers
- More common with age up to 35 years
- No correlation with social class
- More common with Blood Grp O
- Normal/ High levels (More incidence with higher levels)
- 100% caused by H. pylori
What proportion of Gastric and Duodenal ulcers are caused by H. pylori?
Describe how H. pylori colonisation in Antrum can cause Duodenal Ulcers
Gastric- 70%
Duodenal- 95 to 100%
- Increased G cell stimulation-> More gastrin-> More HCl released
- Increased acidity of chyme-> Duodenal damage
List 3 causes/ risk factors of Peptic Ulcer Disease
- Mucosal injury (H. pylori, NSAIDs)
- Smoking (causes relapse of ulcer)
- Massive Physiological Stress (E.g Burns)
Compare the incidence of Acute and Chronic Peptic Ulcer Disease
Acute- As a result of Acute Gastritis (heals eventually)
Chronic- Occurs at Mucosal Junctions
Describe 2 Mucosal junctions where Chronic Peptic Ulcer Disease may occur
- Where Antrum meets Body of stomach
- In Duodenum where Antrum meets Small Intestine
Describe the Morphology of Peptic Ulcer Disease
- Generally<2cm, but can be up to 10cm
- Ulcer base is Necrotic or Granulation tissue
- When healing, Muscularis Propria/ Externa can be replaced by Scar Tissue
What can repeated healing of Chronic Peptic Ulcer Disease in stomach lead to?
- Scar tissue in Muscularis Externa can shrink-> Narrowing of stomach lumen or Pyloric Stenosis-> Vomiting
- Perforation of stomach/ duodenal wall-> Peritonitis
- Erosion/ Ulceration into adjacent structure (Liver or Pancreas)
- Haemorrhage from vessel in base of ulcer-> Malaena (Slow Upper GI bleed)
- Malignancy (Rare)
State how and explain why does Malaena present?
- Slow Upper GI bleed, blood moves through GI Tract
- Haem component oxidised-> Tarry black stool
What is Haematemesis? How can it happen?
Vomiting of blood
Haemorrhage from large vessel at base of ulcer (E.g Gastro-duodenal artery behind Duodenum)
List 4 general symptoms of Peptic Ulcer Disease
- Epigastric pain (sometimes back pain)
- Burning/ gnawing pain
- Often after meals
- Often at night, especially Duodenal ulcers
List 3 serious symptoms of Peptic Ulcer Disease
- Haematemesis/ Malaena
- Early satiety from repeated scarring (stomach can’t expand as much)
- Weight loss (Reluctance to eat due to pain)
In the past, why was eating food thought to reduce pain initially in patients with Duodenal Ulcers?
- Food intake causes Pyloric Sphincter to close
- Less chyme/ irritation to Duodenal Ulcer
(However pain would return later once Sphincter relaxes and chyme enters duodenum)
List 5 ways Peptic Ulcer Disease can be managed
- Lifestyle modification
- Avoid exacerbating medications
- Test for H. pylori (Use PPIs and ABs to eradicate if present, this promotes Ulcer Healing)
- Endoscopy (if actively bleeding, repair if perforated)
What is Functional Dyspepsia?
When you have symptoms of ulcer disease, without any physical evidence of organic disease
Suggest 1 way we can non-invasively look for perforation
Chest X-ray
