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
what are the pathological changes of acute gastritis?
◦ epithelial damage ◦ some epithelial hyperplasia ◦ vasodilation ◦ neutrophil response
26
What is the treatment for acute gastritis?
Removal of irritant (NSAIDs, alcohol etc)
27
What are the 2 main causes of chronic gastritis?
◦ Bacterial - H. pylori ◦ Autoimmune (antibodies to parietal cells) ◦ (Chronic alcohol, NSAIDs etc. can also cause this)
28
what are the pathological changes seen in chronic gastritis?
◦ lymphocyte response ◦ glandular atrophy ◦ fibrotic changes ◦ metaplastic changes
29
how does autoimmune causes lead to gastritis?
``` ◦ antibodies to parietal cells ◦ lose parietal cells ◦reduced acid production and intrinsic factor ◦ atrophy of stomach ◦ gastritis ```
30
What can chronic gastritis due to autoimmune disease also lead to?
``` Pernicious anaemia (Loss of intrinsic factor needed for B12 absorption) - also iron deficiency anaemia, iron uptake requires acidic environment ```
31
What are the symptoms of chronic gastritis due to autoimmune?
* Symptoms of anaemia * Glossitis * Anorexia * Neurological symptoms
32
What are the symptoms of chronic gastritis due to H. pylori?
Asymptomatic or similar to acute gastritis | Symptoms may develop due to complications
33
What are some complications of H. pylori?
Peptic ulcers, adenocarcinoma, MALT lymphoma
34
What type of organism is H. pylori?
Helix shaped/gram negative/microaerophilic - stomach has correct O2
35
How does H.pylori spread?
• Oral to oral/faecal to oral
36
What are 5 virulence factors of H. pylori?
* 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
Where in the stomach do H. pylori live?
in mucus layer/adheres to gastric epithelia
38
How does H. pylori damage the stomach?
- 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
What are the effects of H. pylori if present in the antrum?
* 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
What are the effects of H. pylori if present in the body?
* Atrophic effect - atrophy of parietal cells so reduced acid production * Gastric ulcer * Leads to intestinal metaplasia * Dysplasia * cancer
41
What are the effects of H. pylori if present in the antrum and body?
Asymptomatic - effects cancel each other§
42
How can H. pylori be tested for?
- Urea breath test - Stool antigen test - Serum antibodies test - Upper GI endoscopy with biopsy (can be used for CLO test/rapid urease test)
43
How does the urea breath test work?
Urea with labelled carbon (C13) ingested, converted to ammonia and CO2 by H. pylori, labelled C13 detected in breath
44
What is the treatment for H. pylori?
``` Triple therapy (2 antibiotics + 1 PPI): Amoxicillin + (clarithromycin or metronidazole) ```
45
How is the success of the treatment checked?
urea breath test
46
Define peptic ulcer.
Defects in the gastric or duodenal mucosa that extend through the muscularis mucosa
47
Where do peptic ulcers commonly occur?
◦ Most common in first part of duodenum | ◦ Commonly affects lesser curve/antrum of stomach
48
What percentage of gastric and duodenal ulcers are associated with H. pylori?
Gastric 70%, Duodenal 95-100%
49
What is the most important cause of peptic ulcers?
Breakdown of normal defences | - more important than excessive acid
50
normal defence mechanisms of stomach
``` ◦ mucous ◦ bicarbonate ◦ adequate mucosal bloodflow ◦ can remove acid that diffuses through injured mucosa ◦ prostaglandins ◦ epithelial renewal ```
51
What mechanism have been implicated in duodenal ulcers?
Rapid gastric emptying/inadequate acid neutralisation (from bile/pancreas)
52
What are the causes of peptic ulcer?
- Caused by mucosal injury ◦ H-pylori ◦ NSAIDS ◦ Smoking (really only contributes to relapse of ulcer disease) ◦ massive physiological stress e.g. Burns
53
what is the effect of NSAIDs on stomach defences?
reduces prostaglandin synthesis
54
what is the effect of prostaglandin on stomach defences?
maintains mucosal blood flow needed for removal of H+ ions
55
what is the difference in acid levels in gastric and duodenal ulcers?
gastric - normal/low - atrophy | duodenal - normal/high - increased gastrin release
56
When do acute peptic ulcer develop?
•Develop as part of acute gastritis
57
Where do chronic ulcers develop?
* Occur most frequently at mucosal junctions * Where antrum meets body (on lesser curve) * In duodenum where antrum meets small intestine
58
What is the morphology of peptic ulcers?
•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
What are 5 clinical consequences of peptic ulcers?
- 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
What are the symptoms of peptic ulcers/
• 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
When does pain usually occur in peptic ulcers?
Following meal times, In duondenal ulcers can be 2-3 hrs after, after opening of the pyloric sphincter
62
What are the different management options of peptic ulcers?
* Lifestyle modification * Stopping any exacerbating medications (e.g. NSAIDs) * Testing for H-pylori (if present- eradicate) * PPIs * Endoscopy
63
what is the management of peptic ulcers if active bleeding?
endoscopic treatment | - adrenaline injected + cautery +/- clip application
64
What is functional dyspepsia?
Have symptoms of ulcer disease but no physical evidence of organic disease Diagnosis of exclusion!
65
What are the different methods of diagnosis of gastric pathology?
``` Upper GI endoscopy - biopsies Urease breath test Erect CXR - perforation Blood test (FBC) - anaemia (bleeds, pernicious/iron def.) ```
66
What pharmacological interventions can reduce acid production?
``` H2 blockers (cimetidine, Ranitidine) PPi (omeprazole, (zoles)) ```
67
What is Zollinger-Ellison syndrome?
Non beta islet cell gastrin secreting tumour of the pancreas - large vol acid secretion - severe stomach and small intestine ulceration - abdominal pain, diarrhoea
68
What types of stress can cause mucosal damage?
``` Symptoms of gastritis/ulceration Following: • Severe burns • Raised intracranial pressure • Sepsis • Severe trauma • Multiple organ failure ```
69
What are the symptoms of stomach cancer?
* Dysphagia * Loss of appetite * Malaena * Weight loss * Nausea/vomiting/ * Virchow's nodes
70
What are the risk factors for stomach cancer?
* Male * H-pylori * Dietary factors • Smoking