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S3: Gastrointestinal > 4b.) Pathology of Stomach > Flashcards

4b.) Pathology of Stomach Flashcards

1
Q

Define dyspepsia

A

Upper GI symptoms that are typically present for four or more weeks including abdo pain or discomfort, nausea/vomitting, heartburn or acid reflux

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2
Q

State some common pathologies of stomach

A
  • GORD (gastroesophageal reflux disease)
  • Gastritis (acute or chronic)
  • Peptic ulcer disease
  • Cancer
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3
Q

What do most pathologies of stomach arise from?

A

Inability of stomach to protect itself

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4
Q

For GORD, state:

  • Symptoms
  • Triggers
  • Consequences
A

Symptoms

  • Chest pain
  • Acid taste in mouth
  • Cough

Triggers

  • Obesity
  • Pregnancy
  • Hiatus hernia
  • LOS function
  • Delayed gastric emptying

Consequences

  • Nothing
  • Oesophagitis
  • Strictures
  • Barrett’s oesophagus
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5
Q

During pregnancy women can have new or worse GORD; true or false

A

True, about 50-80%

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6
Q

What does the lower oesophageal sphincter consist of?

A
  • Muscular element
  • Right crus of diaphragm
  • Angle of entry of oesophagus into stomach
  • Intra-abdominal pressure
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7
Q

State possible treatments for GORD

A
  • Lifestyle modifications: lose weight, smaller more frequent meals..
  • Pharmacological: antacids, H2 antagonists, PPI (proton pump inhibitors)
  • Surgery= fundoplication (rare)
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8
Q

Describe what a hiatus hernia is

A

Upper part of stomach pushes up through diaphragm into chest region.

Increases risk for GORD as it decreases basal tone of LOS and prevents the normal increase in LOS tone when straining

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9
Q

What is gastritis?

A
  • Inflammation of the stomach mucosa
  • Can be acute or chronic
  • Symptoms: pain, nausea, vomitting, bleeding
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10
Q

State some possible causes of acute gastritis

How do you treat acute gastritis?

A
  • Heavy use of NSAIDs
  • Excess alcohol
  • Chemotherapy
  • Bile reflux

Treat by removing the irritant

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11
Q

Describe the response of stomach mucosa to an irritant in acute gastritis

A
  • Irritant damages epithelial cells
  • Reduction in mucus production
  • Mucosa responds by vasodilation (as we know rich bood supply can remove and buffer acid that breaches mucus barrier) becomes oedematous
  • Inflammatory cells present (neutrophils)
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12
Q

State three possible causes of chronic gastritis

A
  • Helicobacterpylori infection (MOST COMMON)
  • Autoimmune: autoantibodies attack gastric parietal cells which can lead to pernicious anaemia (as parietal cells produce intrinsic factor)
  • Chemical/reactive: chronic alcohol abuse, NSAIDS, reflux of bile
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13
Q

Describe how you could differentiate between chronic gastritis caused by helicobacter pyori or autoimmune cause

A

Helicobacterpylori

  • Asymptomatic or similar to acute gastritis
  • Other symptoms may develop eg. peptic ulcers, adenocarcinoma, MALT lymphoma

Autoimmune

  • Symptoms of anaemia
  • Glossitis
  • Anorexia
  • Neurological symptoms
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14
Q

For helicobacter-pylori state:

  • Gram stain
  • Shape
  • Spread
  • Where found
  • Virulence factors
A
  • -ve
  • helix shape
  • Oral to oral/faecal to oral
  • Lives in mucus layer
  • Virulence:
    • Produces urease which allows it to convert urea in stomach into ammonium- this increases pH and helps it survive in stomach
    • Flagellum- good motility
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15
Q

Describe why helicobacter-pylori is damaging to the stomach

A
  • Damages epithelia by releasing cytotoxins
  • Produces ammonium - ammonia - toxic to epithelium
  • Pro-inflammatory -self injury
  • Degrages mucus layer
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16
Q

How do you diagnose helicobacter-pylori?

A

Diagnose:

  • urea breath test
  • stool antigen test

Treatment:

  • proton pump inhibitor
  • amoxicillin + (clarithromycin or metronidazole)
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17
Q

Contrast pathological features in acute and chronic gastristis

A
18
Q

What happens if you you H-pyrlori colonisation in the antrum?

A
  • Antrum= where G cells are
  • Increased gastrin secretion - increased parietal cell acid secretions- duodenal epithelial metaplasia- colonisation in duodenum- duodenal ulceration
19
Q

What happens if you get H-pylori colonisation in antrum and body?

A

Asymptomatic

20
Q

What happens if you get colonisation of H-pylori in body of stomach?

A
  • Atrophic effect which leads to:
    • Gstric ulcers
    • Intestinal metaplasia- dysplasia- cancer
21
Q

What is peptic ulcer disease?

A

Breach in gastric or duodenal mucosa that extends through the muscularis mucosa; it includes stomach and duodenam ulcers

22
Q

Where are peptic ulcers most commonly found?

Where, in stomach, are gastric ulcers (subdivision of peptic ulcers) most commonly found?

A
  • Peptic ulcers most commonly found in first part of duodenum (3:1)
  • Gastric ulcers most common in lesser curve/antrum of stomach
23
Q

Peptic ulcer disease is heavilyy associated with presence of Helicobacter-pylori, the effects of stomach acid and use of NSAIDs; true or false

A

True

24
Q

Do peptic ulcers always arise from high levels of acid?

A

No. Uclers can develop in people with normal or low levels of acid; rapid gastric emptying or ineffective neutralisation can increase risk for duodenal ulcers as conditions in duodenum become more acidic than what it is adapted for

25
Q

State 4 causes of peptic ulcer disease

A
  • H-pylori
  • NSAIDs
  • Smoking (generally ony contributes to relapse)
  • Stress (we mean major physiological stress e.g. burns)
26
Q

Where do chronic ulcers most commonly occur?

A

At mucosal junctions e.g.:

  • Where antrum meets body (on lesser curve)
  • Duodenum (where antrum meets small intestine)
27
Q

Descrie and explain some potential consequences of peptic ulcer disease, consider:

  • Morphology of the ulcers
  • Affects on structures
A

Morphology: generally <2cm (but could be 10cm). Base of ulcer is necrotic tissue and the muscularis propria can be replaced by scar tissue.

  • Scar tissue- stenosis
  • Perforation- peritonitis
  • Erosion into adjacent structure e.g. liver, pancreas
  • Haemorrhage from vessel in base of ulcer
  • Malignancy (RARE)
28
Q

State some symptoms of peptic ulcer disease

A
  • Epigastric pain
    • Burning/gnawing
    • Follows meal times
    • Often at night (especially DU)
  • Haematemesis
  • Malena (lead to anaemia)
  • Early satiety from repeated scarring
  • Weight loss (reluctant to eat due to pain)
29
Q

Describe the treatment for peptic ulcer disease

A
  • Lifestyle modifications (e.g. smaller meals, not smoking, weight loss etc)
  • Stopping any exacerbating medications (e.g. NSAIDs)
  • Testing for H-pylori (and removing)
  • Proton pump inhibitors
30
Q

How would you diagnose peptic ulcer disease?

A

Endoscopy

31
Q

Describe how proton pump inhibitors work

A

Inhibit proton pump in parietal cells to reduce stomach acid

32
Q

What is functional dyspepsia and how is it diagnosed?

A

Upper GI system symptoms that persist for a month or longer but no structural abnormalities are found. It is only diagnosed by exclusion of all other possibilities

33
Q

How could you diagnose a perforation?

A

Chest x-ray and look for air under diaphragm on both sides

34
Q

How could you treat functional dyspepsia?

A
  • H2 receptor blockers (cimetidine, rantidine)
  • Proton pump inhibitors (omeprazole)
35
Q

Describe Zollinger-Ellison syndrome

A

Non-beta islet cell gastrin secreting tumour of pancreas; leads to:

  • Proliferation of parietal cells
  • Lots of acid production
  • Severe ulceration- pain, diarrhoea
36
Q

What is meant by stress related mucosal damage and state some conditions which may precede it

A

Broad term used to describe spectrum of pathology attributed to acute, erosive, inflammatory insult to upper GI tract associated with critical illness e.g.:

  • Sepsis
  • Severe burns
  • Raised intracranial pressure
  • Severe trauma
  • Multi-organ failure
37
Q

How common is stomach cancer?

A

3rd most common in world

High rates in Chile/Japan/South America

38
Q

State some symptoms of stomach cancer

A
  • Dysphagia
  • Loss of apeptie
  • Malaena
  • Weight loss
  • Nausea
  • Vomitting
  • Virchow’s nodes (lymphadenopathy in left supraclavicular node)

Usually presents late

39
Q

State some risk factors for stomach cancer

A
  • Age
  • Male
  • H-pylori
  • Dietary factors
  • Smoking
40
Q

What parts make up the lower oesophageal sphincter/what does it consist of?

A

LOS consists of:

  • Muscular element
  • Right crus of diaphragm
  • Angle of entry of oesophagus into stomach
  • Intrabdominal pressure (when intrabdominal pressure rises diaphragm flattens)

S3: Gastrointestinal (18 decks)

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