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Semester 3 - Gastrointestinal > 8. Pathophysiology of Gastric Disease > Flashcards

8. Pathophysiology of Gastric Disease Flashcards

1
Q

Define dyspepsia.

A

Term used to describe a complex of upper gastrointestinal tract symptoms which are typically present for four or more weeks, including upper abdominal pain or discomfort, heartburn, acid reflux, nausea and/or vomiting

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2
Q

What are 5 common gastric disorders?

A
  • Gord
  • Gastritis
  • Peptic ulcer disease
  • zollinger-ellison disease
  • cancer of the stomach
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3
Q

What is GORD?

A

gastro-oesophageal reflux disease

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4
Q

What are the symptoms of GORD?

A

Chest pain, acid taste in mouth, cough

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5
Q

What can trigger GORD (risk factors)? (5)

A
  • Obesity
  • Pregnancy
  • Hiatus hernia
  • LOS dysfunction
  • Delayed Gastric emptying
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6
Q

What are the possible consequences of GORD?

A
  • May not have consequences.
  • Oesophagitis
  • ulceration
  • haemorrhage
  • Strictures - due to scar tissue
  • Barrett’s oesophagus
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7
Q

what is GORD caused by?

A

ineffective LOS

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8
Q

What does the lower oesophageal sphincter consist of?

A
  • Muscular element
  • Right crus of diaphragm - closes off oesophagus when high pressures
  • Angle of entry of oesophagus into stomach
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9
Q

what does the muscular element of the LOS consist of ?

A

intrinsic smooth muscle and diaphragm

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10
Q

Is the LOS contracted or relaxed at rest?

A

Contracted

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11
Q

When are pressure of the LOS highest and lowest?

A
  • Lowest after meals

* Highest at night

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12
Q

What are the different treatment options for GORD?

A

◦ Lifestyle modifications
◦ Pharmacological
◦ Surgery (rare) (fundoplication)

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13
Q

What pharmacological interventions are available for GORD?

A

Antacids, H2 antagonists, PPIs

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14
Q

What are some lifestyle changes for treatment of GORD?

A
  • eat slower (stomach empties at a certain rate, prevents build of high pressures in stomach)
  • Have smaller meals
  • not eating before bed (lying down doesn’t help)
  • losing weight (exercise, diet)
  • stop smoking
  • reduce alcohol and caffeine
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15
Q

What are hiatal hernias?

A

herniation of the stomach and LOS into the thorax through the oesophageal hiatus in the diaphragm

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16
Q

What does moving the LOS into the thorax do to its basal tone?

A

Reduces:
• basal tone
• The normal increase in LOS tone when straining

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17
Q

What are the changes to the LOS in hiatus hernias?

A
  • weakened and shortened muscular LOS
  • Loss of diaphragmatic support
  • Loss of oblique entry of oesophagus into stomach
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18
Q

what is Barrett’s oesophagus?

A

the reversible (metaplastic) change of stratified squamous epithelia in the lower oesophagus into simple columnar epithelia due to repeated exposure to gastric contents

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19
Q

what is the risk with Barrett;s oesophagus?

A

increased risk of dysplasia into adenocarcinoma

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20
Q

What is gastritis?

A

inflammation of the gastric mucosa

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21
Q

What symptoms are present in gastritis?

A

Pain, nausea, vomiting, bleeding

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22
Q

What causes acute gastritis?

A

◦ Heavy use of NSAIDS
◦ Lots of alcohol
◦ Chemotherapy
◦ Bile reflux (irritant to the stomach)

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23
Q

What happens to gastric mucosa in exposure to chemical injury (HCL)?

A

Results in damaged epithelial cells and a reduction in mucus production

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24
Q

Which cells are seen in the gastric mucosa in response to acute gastritis?

A

Inflammatory cells, mainly neutrophils

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25
Q

what are the pathological changes of acute gastritis?

A

◦ epithelial damage
◦ some epithelial hyperplasia
◦ vasodilation
◦ neutrophil response

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26
Q

What is the treatment for acute gastritis?

A

Removal of irritant (NSAIDs, alcohol etc)

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27
Q

What are the 2 main causes of chronic gastritis?

A

◦ Bacterial - H. pylori
◦ Autoimmune (antibodies to parietal cells)
◦ (Chronic alcohol, NSAIDs etc. can also cause this)

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28
Q

what are the pathological changes seen in chronic gastritis?

A

◦ lymphocyte response
◦ glandular atrophy
◦ fibrotic changes
◦ metaplastic changes

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29
Q

how does autoimmune causes lead to gastritis?

A 
◦ antibodies to parietal cells
◦ lose parietal cells
◦reduced acid production and intrinsic factor
◦ atrophy of stomach 
◦ gastritis
30
Q

What can chronic gastritis due to autoimmune disease also lead to?

A 
Pernicious anaemia (Loss of intrinsic factor needed for B12 absorption)
- also iron deficiency anaemia, iron uptake requires acidic environment
31
Q

What are the symptoms of chronic gastritis due to autoimmune?

A
  • Symptoms of anaemia
  • Glossitis
  • Anorexia
  • Neurological symptoms
32
Q

What are the symptoms of chronic gastritis due to H. pylori?

A

Asymptomatic or similar to acute gastritis

Symptoms may develop due to complications

33
Q

What are some complications of H. pylori?

A

Peptic ulcers, adenocarcinoma, MALT lymphoma

34
Q

What type of organism is H. pylori?

A

Helix shaped/gram negative/microaerophilic - stomach has correct O2

35
Q

How does H.pylori spread?

A

• Oral to oral/faecal to oral

36
Q

What are 5 virulence factors of H. pylori?

A
  • Urease - converts urea to ammonia, increases it local pH
  • Flagella - good motility to reach optimum environment
  • Adhesins - resist peristalsis
  • Cytotoxins
  • chemotaxis - find areas with less acid
37
Q

Where in the stomach do H. pylori live?

A

in mucus layer/adheres to gastric epithelia

38
Q

How does H. pylori damage the stomach?

A
  • releases cytotoxins, cause direct epithelial injury
  • Urease, ammonia is toxic to epithelia and increases pH
  • mucinase - damage mucus layer
  • possibly degrades mucus layer
  • promotes inflammatory response (self injury)
39
Q

What are the effects of H. pylori if present in the antrum?

A
  • Increased Gastrin secretion (or decreased D cell activity)
  • Increased parietal cell acid secretion and increased acid chyme enters duodenum
  • Duodenal epithelial metaplasia due to damage (from duodenal epithelia to gastric epithelia)
  • Colonisation of duodenum
  • Duodenal ulceration
40
Q

What are the effects of H. pylori if present in the body?

A
  • Atrophic effect - atrophy of parietal cells so reduced acid production
  • Gastric ulcer
  • Leads to intestinal metaplasia
  • Dysplasia
  • cancer
41
Q

What are the effects of H. pylori if present in the antrum and body?

A

Asymptomatic - effects cancel each other§

42
Q

How can H. pylori be tested for?

A
  • Urea breath test
  • Stool antigen test
  • Serum antibodies test
  • Upper GI endoscopy with biopsy (can be used for CLO test/rapid urease test)
43
Q

How does the urea breath test work?

A

Urea with labelled carbon (C13) ingested, converted to ammonia and CO2 by H. pylori, labelled C13 detected in breath

44
Q

What is the treatment for H. pylori?

A 
Triple therapy (2 antibiotics + 1 PPI):
Amoxicillin + (clarithromycin or metronidazole)
45
Q

How is the success of the treatment checked?

A

urea breath test

46
Q

Define peptic ulcer.

A

Defects in the gastric or duodenal mucosa that extend through the muscularis mucosa

47
Q

Where do peptic ulcers commonly occur?

A

◦ Most common in first part of duodenum

◦ Commonly affects lesser curve/antrum of stomach

48
Q

What percentage of gastric and duodenal ulcers are associated with H. pylori?

A

Gastric 70%, Duodenal 95-100%

49
Q

What is the most important cause of peptic ulcers?

A

Breakdown of normal defences

- more important than excessive acid

50
Q

normal defence mechanisms of stomach

A 
◦ mucous 
◦ bicarbonate
◦  adequate mucosal bloodflow
◦ can remove acid that diffuses through injured mucosa
◦ prostaglandins
◦ epithelial renewal
51
Q

What mechanism have been implicated in duodenal ulcers?

A

Rapid gastric emptying/inadequate acid neutralisation (from bile/pancreas)

52
Q

What are the causes of peptic ulcer?

A
  • Caused by mucosal injury
    ◦ H-pylori
    ◦ NSAIDS
    ◦ Smoking (really only contributes to relapse of ulcer disease)
    ◦ massive physiological stress e.g. Burns
53
Q

what is the effect of NSAIDs on stomach defences?

A

reduces prostaglandin synthesis

54
Q

what is the effect of prostaglandin on stomach defences?

A

maintains mucosal blood flow needed for removal of H+ ions

55
Q

what is the difference in acid levels in gastric and duodenal ulcers?

A

gastric - normal/low - atrophy

duodenal - normal/high - increased gastrin release

56
Q

When do acute peptic ulcer develop?

A

•Develop as part of acute gastritis

57
Q

Where do chronic ulcers develop?

A
  • Occur most frequently at mucosal junctions
  • Where antrum meets body (on lesser curve)
  • In duodenum where antrum meets small intestine
58
Q

What is the morphology of peptic ulcers?

A

•Generally less than 2cm diameter (but can be 10cm) •Base of ulcer is necrotic tissue/granulation tissue •Muscularis propria can be replaced by scar tissue

59
Q

What are 5 clinical consequences of peptic ulcers?

A
  • scar tissue shrinks, narrow stomach or cause pyloric stenosis
  • perforation causing peritonitis
  • erosion into adjacent structure (liver, pancreas)
  • haemorrhage from vessel in base of ulcer (gastro-duodenal artery if duodenal and splenic artery if gastric)
  • malignancy (rare)
60
Q

What are the symptoms of peptic ulcers/

A

• Epigastric pain (sometimes back pain)
- Burning/gnawing
- Follows meal times
• Often at night (especially DU)

Serious symptoms
• Haematemesis or malaena-Bleeding/anaemia
• Early satiety from repeated scarring
• Weight loss (reluctance to eat due to pain)

61
Q

When does pain usually occur in peptic ulcers?

A

Following meal times, In duondenal ulcers can be 2-3 hrs after, after opening of the pyloric sphincter

62
Q

What are the different management options of peptic ulcers?

A
  • Lifestyle modification
  • Stopping any exacerbating medications (e.g. NSAIDs)
  • Testing for H-pylori (if present- eradicate)
  • PPIs
  • Endoscopy
63
Q

what is the management of peptic ulcers if active bleeding?

A

endoscopic treatment

- adrenaline injected + cautery +/- clip application

64
Q

What is functional dyspepsia?

A

Have symptoms of ulcer disease but no physical evidence of organic disease
Diagnosis of exclusion!

65
Q

What are the different methods of diagnosis of gastric pathology?

A 
Upper GI endoscopy 
- biopsies
Urease breath test
Erect CXR
- perforation
Blood test (FBC) 
- anaemia (bleeds, pernicious/iron def.)
66
Q

What pharmacological interventions can reduce acid production?

A 
H2 blockers (cimetidine, Ranitidine)
PPi (omeprazole, (zoles))
67
Q

What is Zollinger-Ellison syndrome?

A

Non beta islet cell gastrin secreting tumour of the pancreas

  • large vol acid secretion
  • severe stomach and small intestine ulceration
  • abdominal pain, diarrhoea
68
Q

What types of stress can cause mucosal damage?

A 
Symptoms of gastritis/ulceration
Following:
• Severe burns
• Raised intracranial pressure 
• Sepsis
• Severe trauma
• Multiple organ failure
69
Q

What are the symptoms of stomach cancer?

A
  • Dysphagia
  • Loss of appetite
  • Malaena
  • Weight loss
  • Nausea/vomiting/
  • Virchow’s nodes
70
Q

What are the risk factors for stomach cancer?

A
  • Male
  • H-pylori
  • Dietary factors • Smoking

Semester 3 - Gastrointestinal (17 decks)

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