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1st Year Medicine > Gastric Cancer And Peptic Ulcer Disease. > Flashcards

Gastric Cancer And Peptic Ulcer Disease. Flashcards

1
Q

What are we looking for in the physical examination of gastric cancer?

A

Weight loss, lymph nodes and abdominal mass.

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2
Q

What imaging studies do we do for gastric cancer?

A

Barium meal and an MRI scan.

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3
Q

What are the alarm features for gastric cancer?

A

Aged over 55, dysphagia, evidence of GI blood loss, persistent vomiting, unexplained weight loss, upper abdominal mass and anaemia.

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4
Q

What are contraindications for surgery for gastric cancer?

A

Widely metastatic disease, malignant ascites or brief life expectancy.

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5
Q

What surgery is done for proximal gastric lesions?

A

Total gastrectomy.

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6
Q

What surgery is done for distal gastric lesions?

A

Partial gastrectomy.

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7
Q

What are non surgical treatments of gastric cancer?

A

Tariff therapy, chemotherapy and intubation of proximal lesions.

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8
Q

What is the 5 year survival rate for gastric cancer?

A

15%

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9
Q

What are the adverse prognostic factors for gastric cancer?

A

Metastatic disease, short history, advanced age, proximal lesion and superficial gross appearance.

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10
Q

What criteria do we use to define dyspepsia?

A

Rome III criteria.

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11
Q

What are the Rome III criteria for functional dyspepsia?

A 
No evidence of structural disease (on endoscopy) AND presence of one of the following:
Epigastric pain
Epigastric burning.
Postprandial fullness
Early satiety

Last two known as postprandial distress syndrome.

Criteria must be filled for past three months with onset of symptoms 6 months before diagnosis.

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12
Q

What are tow common causes of dyspepsia and peptic ulcer disease?

A

H pylori and NSAIDS

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13
Q

What percentage do organic causes of dyspepsia account for?

What are the causes?

A

25%

Peptic ulcer disease, drugs or cancer.

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14
Q

What percentage of dyspepsia is functional?

What are the causes?

A

75%

no evidence of cause but are often associated with IBS.

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15
Q

What drugs can cause organic dyspepsia?

A

NSAIDS and COX2 inhibitors.

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16
Q

What does uncomplicated dyspepsia show on examination?

A

Only epigastric tenderness.

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17
Q

What does complicated dyspepsia show on examination?

A

Cachexia, mass, evidence of gastric outflow obstruction and peritonitis.

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18
Q

What is the management for dyspepsia in the absence of alarm symptoms?

A

Check H pylori status and eradicate it which will cure the disease.
If no h pylori then treat with acid inhibition as required.

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19
Q

What are some hypothesised causes of functional dyspepsia?

A

Combination of genetic factors, visceral hypersensitivity, disrupted gut immune reactions, altered brain gut reactions, psychological factors and abnormal upper GI motor and reflex reactions.

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20
Q

What are the symptoms of peptic ulcer disease?

A

Pain predominant dyspepsia (to back), often nocturnal pain and dyspepsia, aggravated or relieved by eating. Relapsing and remitting chronic illness.

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21
Q

What patients is peptic ulcer disease more common in?

A

Lower socioeconomic groups and those with a family history.

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22
Q

What kind of bacteria is helicobacter pylori?

A

Gram neg microaerophillic flagellated bacillus.

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23
Q

How is helicobactor pylori spread?

A

Oral to oral and faecal to oral spread.

24
Q

What are the consequences of helicobactor pylori?

A 
Majority have no pathology.
20-40% Peptic ulcer disease
95% Duodenal ulcers
75% of gastric ulcers.
Gastric cancer e.g. Non carina adenocarcinoma and low grade gastric B cell lymphomas (maltoma)
25
Q

What other 2 cancers is helicobactor possibly involved in?

A

Gastric cardia adenocarcinoma and oesophageal adenocarcinoma.

26
Q

What non invasive test do we do for helicobactor pylori?

A

Urea breath test as the urease enzyme is present with helicobactor pylori.

27
Q

What drug treatments have been shown to help in helping duodenal ulcers?

A

Antacids and sucralfate.

Misoprostol has also been shown useful but has no advantage over PPIs or H2RAs.

28
Q

What is the pharmacological treatment of a helicobactor pylori infection?

A

Triple therapy for 1 week: PPI plus amoxycillin 1g bd and clarithromycin 500mg bd. OR PPI plus metronidazole 400mg bd and clarithromycin 250mg bd.

Above has an 85% success rate. 2 week regimens have a higher eradication rate but poorer compliance.

2 week therapies:
Dual therapy - PPI plus 1 antibiotic not recommended.
Quadruple therapy plus culture directed therapy.

29
Q

What are the side effects of H pylori treatment?

A

Nausea and diarrhoea.

30
Q

What are complications of peptic ulcer disease?

A

Anaemia, bleeding, perforation and gastric outlet/duodenal obstruction from Fibrotic scarring.

31
Q

What is the follow up following therapy for a duodenal ulcer?

A

Uncomplicated needs no follow up, only if there is ongoing symptoms.

32
Q

What is the follow up following therapy for a gastric ulcer?

A

Endoscopy at 6-8 weeks to ensure healing and no malignancy.

33
Q

When should we suspect gastric cancer?

A

If there is dyspepsia plus alarm symptoms such as weight loss, anaemia, mass or recurrent vomiting.
Family history is always a big factor.

34
Q

What is correas hypothesis For the development of gastric cancer?

A

Normal ==> chronic gastritis ==> atrophy ==> intestinal metaplasia (all involving h pylori) ==> dysplasia and then neoplasia.
From atrophy onwards are exacerbated by smoking.

35
Q

What histological findings are seen with gastric cancer?

A

Body predominant or pangastritis.
Atrophy
Intestinal metaplasia.

36
Q

What physiological findings are seen with gastric cancer?

A

Decreased or no acid production.

37
Q

What bacterial findings are seen with gastric cancer?

A

H pylori and mixed bacterial overgrowth.

38
Q

What two ways does H pylori inhibit gastric secretion?

A

The direct affect of the bacterial products.

Inflammation caused by the bacteria also inhibits acid.

39
Q

What bacterial products of H pylori inhibit acid secretion?

A

Ammonia, caves factor and alpha methyl histamine.

40
Q

How does the inflammation caused by H pylori inhibit acid secretion?

A

IL 1 beta production is stimulated by H pylori and this is a powerful inhibitor of acid secretion.

41
Q

How do host factors alter the affect of helicobactor pylori and IL-1B on acid production?
What happens in affected and unaffected patients?

A

Some parents have genetic polymorphisms in IL-1B giving it differing pro inflammatory activities.
the people with polymorphisms in IL-1B get acid hyposecretion, body predominant gastritis, atrophic gastritis and then cancer.
In those without the polymorphism there is normal or high acid causing antral predominant gastritis and either DU or no disease.

42
Q

What can cause acute gastritis?

A

Irritant chemical injury, severe burns, shock, severe trauma and head injury.

43
Q

What are rare causes of gastritis?

A

Lymphocytic, eosinophilic and granulomatous.

44
Q

What cells produce anti h pylori antibodies?

A

Lamina propria plasma cells.

45
Q

Where are chronic peptic ulcers often found?

A

1st part of the duodenum, stomach at the junction of the body and the Antrum and oesophagogastric ulcers.

46
Q

What kind of ulcers are often seen with chronic peptic ulcers?

A

2-10 cm across, edges are punched out and clear cut.

Ulceration is often long standing and deep.

47
Q

What is the pathogenesis of chronic peptic ulcers?

A

Half of patients have raised acid production, excess acid leads to gastric metaplasia, h pylori infection, inflammation, epithelial damage and ulceration.
The pathogenesis is not just due to the acid production but also due to failure of defences.

48
Q

What is the microscopic appearance of peptic ulcers?

A

Layered appearance, floor of fibrotic fibrinopurulent debris. Base of inflamed granulation tissue and the deepest layer is fibrotic scar tissue.

49
Q

What benign gastric polyps do we get?

A

Hyperplastic polyps and cystic fundic gland polyps.

50
Q

What malignant gastric tumours do we get?

A

Carcinomas, lymphomas and gastrointestinal stromal tumours (GISTs).

51
Q

What countries have high incidence of gastric adenocarcinomas?
What does this imply?

A

Japan, China, Columbia and Finland.

Suggest genetic factors.

52
Q

What are the two subtypes of gastric adenocarcinomas?

A

Intestinal type - exophytic/polyploid mass.
Diffuse types- expands /infiltrates the stomach walls.

15% are mixed.

53
Q

What do benign peptic ulcers look like?

A

Mimics cancer but is more punched out and lacks the raised, rolled edge.

54
Q

What type of adenocarcinomas of the stomach have a better prognosis?

A

Intestinal type.

55
Q

What are the signs and symptoms of gastric cancer?

A

Dyspepsia, abdominal pain, weight loss, emesis, anorexia, dysphagia, early satiety, upper GI haemorrhage, abdominal mass, jaundice and paraneoplastic syndromes.

1st Year Medicine (64 decks)

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