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GI System > Gastric Disease > Flashcards

Gastric Disease Flashcards

1
Q

Describe the prevalence and incidence of gastric disease

A
  • up to 40% of adults suffer from dyspepsia (indigestion) a year
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2
Q

State the NICE definition of Dyspepsia

What are 5 symptoms included?

A
  • Upper GI tract symptoms, typically for 4 or more weeks
  • Abdominal pain
  • Discomfort
  • Heartburn
  • Acid reflux
  • Nausea and/ or vomiting
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3
Q

List 3 common gastric disorders

What are 2 causes of Chronic Gastritis (Can also be acute)

A
  • Gastritis
  • GORD
  • Peptic Ulcer Disease
  • Bacteria
  • Autoimmune
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4
Q

List 4 symptoms of GORD

A
  • Chest pain
  • Acid taste in mouth
  • Cough
  • Asymptomatic
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5
Q

What are 6 consequences of GORD

A
  • Nothing
  • Oesophagitis
  • Ulceration
  • Haemorrhage
  • Fibrous Strictures-> Dysphagia
  • Barrett’s Oesophagus (Strat. squamous-> Gastric columnar)
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6
Q

Name 5 risk factors for GORD

A
  • Ineffective LOS
  • Anything that increases intrabdominal pressure
  • Obesity
  • Pregnancy
  • Hiatal hernia (LOS moves into thorax)
  • Delayed gastric emptying
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7
Q

List 3 treatment mechanisms for GORD

A
  • 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 )
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8
Q

The LOS is normally contracted. When does it relax?

A

When swallowing food

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9
Q

What are 3 components of the LOS

A
  • Muscular elements (Intrinsic muscles + Part of diaphragm)
  • Right crus of diaphragm (tightens around LOS)
  • Acute angle of entry into stomach helps prevent reflux
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10
Q

What cancer can Barrets Oesophagus lead to? (Due to increased risk of dysplasia)

A

Adenocarcinoma (Normally we get squamous cell carcinoma)

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11
Q

What is Gastritis?
What is 1 way it can be diagnosed?

What are 4 typical symptoms?

A

Inflammation of stomach mucosa
Diagnosable by endoscopy

  • Pain
  • Nausea
  • Vomit
  • Haemorrhage
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12
Q

The causes of Acute Gastritis can lead to Chronic Gastritis.

List 4 causes

A
  • Heavy use of NSAIDs
  • Lots of alcohol
  • Chemotherapy
  • Bile reflux-> Chemical injury -> Damaged epithelia and reduced mucus production
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13
Q

List 3 symptoms and 1 treatment for Acute Gastritis

A
  • Asymptomatic
  • Abdominal pain, nausea, vomiting
  • Occasional bleeding (which can be fatal)
  • Removal of irritant
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14
Q

What are 3 causes of Chronic Gastritis?

A
  1. Autoimmune (Antibodies against parietal cells)
  2. Infection with H. pylori (most common)
  3. Chemical/ reactive;
    - Minimal inflammation
    - Chronic alcohol abuse, NSAIDs, Bile reflux
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15
Q

List 4 pathological changes in Acute and Chronic Gastritis

A

Acute;

  • Epithelial damage
  • Some epithelial hyperplasia
  • Vasodilation
  • Neutrophil response

Chronic;

  • Lymphocyte response
  • Glandular atrophy
  • Fibrotic changes
  • Metaplastic changes
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16
Q

Describe Autoimmune Chronic Gastritis

A
  • Antibodies target Parietal cells, which produce HCl and Intrinsic Factor
  • Can lead to Pernicious Anaemia, as Vit B12 is not absorbed in Ileum
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17
Q

List 4 symptoms of Autoimmune Chronic Gastritis

A
  • Anaemia symptoms (Megaloblastic anaemia)
  • Glossitis
  • Anorexia (Due to loss of appetite)
  • Neurological symptoms
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18
Q

What are 2 groups of symptoms of H. pylori causing Chronic Gastritis?

A
  • Asymptomatic/ similar to acute gastritis

- Peptic ulcers, Adenocarcinoma, MALT Lymphoma

19
Q

Describe H. pylori

How does it enter body?

A
  • Helix shaped
  • Gram negative
  • Microaerophilic (Needs only a little bit of O2)
  • Oral to oral OR Faecal to oral
20
Q

Where does H. pylori go once it enters the stomach?

How is it adapted to do so?

A
  • Migrates and adheres to gastric epithelia
    1. Flagella for motility
  1. Uses chemotaxis to find areas of lower acidity (Surface of
    epithelia, under mucus layer)
  2. Adhesins to attach to Gastric Epithelia and resist peristalsis
  3. Produces Urease, which converts Urea to Ammonium, raising pH around itself. (This prevents death by acid)
21
Q

What 5 problems are caused by presence of H. pylori?

A
  1. CagA gene causes cytotoxin release cytotoxins-> Direct epithelial injury + Inflammation + associated with cancer
  2. Produce ammonia-> Toxic to epithelia
  3. Promotes inflammation
  4. Produces VacA, which increases paracellular permeability and is toxic to epithelia
  5. Secretes Mucinases, Proteases, Lipases-> Mucus layer damage
22
Q

Describe what happens if H. pylori colonise predominantly in the Antrum

A
  • 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
23
Q

What if H. pylori colonise predominantly in Body of stomach?

A
  • Atrophy of Parietal cells
  • Gastric ulceration
  • Increased risk of Dysplasia-> Cancer
24
Q

What happens if H. pylori colonise predominantly in both Antrum and Body of stomach?

A

Asymptomatic

25
Q

How can we diagnose Chronic Gastritis secondary to H. pylori infection?

A
  • Stool antigen test
  • Urea Breath test (Using carbon 13)
  • Upper GI Endoscopy to get biopsy
26
Q

Describe the Urea Breath Test

A

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
27
Q

How do we treat Chronic Gastritis secondary to H. pylori infection?

A

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

28
Q

Define Peptic Ulcer Disease

Where are they most common?

Where do they commonly occur if in the stomach?

A

Defect in Gastric/ Duodenal mucosa, that extends through Mucularis Mucosa

Most common in proximal duodenum

Commonly affect Lesser Curve and Antrum of stomach

29
Q

Compare Gastric and Duodeneal ulcers in;

  • Incidence
  • Age
  • Social class
  • Blood group
  • Acid levels
  • H. pylori
A

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
30
Q

What proportion of Gastric and Duodenal ulcers are caused by H. pylori?

Describe how H. pylori colonisation in Antrum can cause Duodenal Ulcers

A

Gastric- 70%
Duodenal- 95 to 100%

  • Increased G cell stimulation-> More gastrin-> More HCl released
  • Increased acidity of chyme-> Duodenal damage
31
Q

List 3 causes/ risk factors of Peptic Ulcer Disease

A
  • Mucosal injury (H. pylori, NSAIDs)
  • Smoking (causes relapse of ulcer)
  • Massive Physiological Stress (E.g Burns)
32
Q

Compare the incidence of Acute and Chronic Peptic Ulcer Disease

A

Acute- As a result of Acute Gastritis (heals eventually)

Chronic- Occurs at Mucosal Junctions

33
Q

Describe 2 Mucosal junctions where Chronic Peptic Ulcer Disease may occur

A
  • Where Antrum meets Body of stomach

- In Duodenum where Antrum meets Small Intestine

34
Q

Describe the Morphology of Peptic Ulcer Disease

A
  • 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
35
Q

What can repeated healing of Chronic Peptic Ulcer Disease in stomach lead to?

A
  • 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)
36
Q

State how and explain why does Malaena present?

A
  • Slow Upper GI bleed, blood moves through GI Tract

- Haem component oxidised-> Tarry black stool

37
Q

What is Haematemesis? How can it happen?

A

Vomiting of blood

Haemorrhage from large vessel at base of ulcer (E.g Gastro-duodenal artery behind Duodenum)

38
Q

List 4 general symptoms of Peptic Ulcer Disease

A
  • Epigastric pain (sometimes back pain)
  • Burning/ gnawing pain
  • Often after meals
  • Often at night, especially Duodenal ulcers
39
Q

List 3 serious symptoms of Peptic Ulcer Disease

A
  • Haematemesis/ Malaena
  • Early satiety from repeated scarring (stomach can’t expand as much)
  • Weight loss (Reluctance to eat due to pain)
40
Q

In the past, why was eating food thought to reduce pain initially in patients with Duodenal Ulcers?

A
  • 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)

41
Q

List 5 ways Peptic Ulcer Disease can be managed

A
  • 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)
42
Q

What is Functional Dyspepsia?

A

When you have symptoms of ulcer disease, without any physical evidence of organic disease

43
Q

Suggest 1 way we can non-invasively look for perforation

A

Chest X-ray

GI System (26 decks)

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