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Dyspepsia & peptic ulcer disease Flashcards

1
Q

what is dyspepsia?

A

indigestion

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2
Q

what are 3 symptoms of dyspepsia?

A
  • epigastric pain or burning (epigastric pain syndrome)
  • post-prandial fullness (post-prandial distress syndrome)
  • early satiety (post-prandial distress syndrome)
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3
Q

what are 5 foregut structures?

A
  • oesophagus
  • stomach
  • duodenum
  • pancreas
  • gallbladder

= cico-pharyngeus to ampulla of Water

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4
Q

when is dyspepsia more common?

A

1) if H. pylori infection

2) if NSAID drugs are used

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5
Q

what are 3 causes of dyspepsia?

A

1) peptic ulcer disease
2) drugs (esp NSAIDs, COX2 inhibitors)
3) gastric cancer

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6
Q

what are the causes of functional dyspepsia?

A
  • no evidence of culprit structural diseases

= associated with other functional gut disorders e.. IBS

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7
Q

what are the 2 other possible differential diagnosis of dyspepsia?

A
  • heartburn or reflux

- GORD

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8
Q

what might you find on examination of dyspepsia?

A

Uncomplicated;
= epigastric tenderness only

Complicated;

  • cachexia
  • mass
  • evidence gastric outflow obstruction
  • peritoneum
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9
Q

in the absence of alarm symptoms how would you treat dyspepsia?

A

test and treat method;

  • check H. pylori status
  • eradicate if infected

= cure ulcer disease
= remove risk of gastric cancer

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10
Q

if HP is negative in dyspepsia what would you treat it with?

A

= acid inhibition as required

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11
Q

what is the diagnostic criteria for functional dyspepsia?

A

Presence of at least one of the following;
- bothersome post-prandial fullness
- early satiation
- epigastric pain
- epigastric burning
and
no evidence of structural disease that is likely to explain symptoms

= criteria must be fulfilled for past 3 months, with symptom for at least 6 months before diagnosis

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12
Q

what are peptic ulcers?

A

break in the inner lining of the stomach, 1st part of the small intestine or lower oesophagus.

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13
Q

what are peptic ulcers a common cause of?

A

= organic dyspepsia

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14
Q

describe the symptoms of peptic ulcers?

A
  • pain predominant dyspepsia (to back)
  • often nocturnal
  • aggravated or relieved by eating
    = relapsing & remitting chronic illness
    + family history common
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15
Q

what are the causes of peptic ulcers?

A

1) H. pylori infection
2) NSAIDSs (COX1, COX2, PGE)

+ gastric dysmotility, outflow obstruction

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16
Q

when is H. pylori commonly acquired and when do consequences of infection arise?

A

acquired = in infancy

consequences arise = later in life

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17
Q

what type of bacteria is H, pylori and how is it spread?

A

= gram negative microaerophilic flagellated bacillus

Spread
= oral-oral/faecal oral spread

18
Q

what are the 2 main consequences of H. pylori infections?

A

1) peptic ulcers
- 95% duodenal ulcers
- 75% gastric ulcers

2) gastric cancers
- almost all = non-cardia gastric adenocarcinoma
- low grade B cell gastric lymphoma (MALT-oma)

19
Q

what cells are involved in acid secretion?

A

G cells, parietal cells and gastrin

20
Q

describe the 2 different outcomes of H. pylori infection.

A 
OUTCOME 1
1) Acid in stomach increases 
(gastrin increases)
2) no atrophy
3) duodenal ulcer

OUTCOME 2

1) Acid in stomach decreases (gastrin increases)
2) atrophy
3) gastric cancer

21
Q

what is the Cag A gene?

A

= cytotoxin associated gene A (oncogene)

22
Q

describe what happens in duodenal ulcers.

A

1) duodenal acid load increases
- gastric metaplasia
- H. pylori colonisation
- ulceration

2) gastrin release increases
= gastrin increases
- due to decreased somatostatin
- Cag +ve > Cag -ve

3) acid secretin increases
- due to increase parietal cell mass
= no body gastritis

23
Q

how would you diagnose H. pylori infection?

A

= gastric biopsy

  • urease test
  • histology
  • culture/sensitivity

= urease breath test
= FAT (faecal antigen test)
= serology (IgA antibody) - not accurate with increasing patient age

24
Q

what does H. pylori do to the pH of its microenvironment?

  • look at equations on slide 32
A

= increases the pH

  • look t equations on slide 32
25
Q

how would you treat peptic ulcer disease?

A
  • ALL anti-secretory therapy (Proton pump inhibitor - PPI)
  • ALL test for H. pylori
    = H. pylori +ve eradicate
    = H. pylori -ve anti-secretory therapy
  • withdraw NSAIDS
  • lifestyle
  • non-HP/non-NSAIDS ulcers
    = nutrition & optimise co-morbidities

(surgery is infrequent)

26
Q

what are 4 H2 receptor antagonists (H2RAs) used as anti-secretory therapy?

A

1) cimetidine
2) ranitidine
3) famotidine
4) nizatidine

27
Q

what are 6 examples of effective PPIs?

A

1) omeprazole
- 20-40mg/daily

2) esomeprazole
3) lansoprazole
4) dexlansoprazole
5) pantoprazole
6) rabeprazole

28
Q

what heals duodenal and gastric ulcers faster - omeprazole or ranitidine?

A

duodenal ulcers are healed faster by = omperazole

gastric ulcers = omperazole but difference is not as great as for duodenal ulcers

29
Q

what else can be used to help healing other duodenal ulcers - that has not yet been established for Gastric ulcers, NSAIDS or non.H.pylori/ non-NSAID ulcers?

A

1) anti-acids

2) sucralfate

30
Q

what else enhances duodenal healing, but no advantage over PPIs or H2RAs?

A

misoprostol

31
Q

how would you treat H. pylori infections - with the aim to eradicate it?

A

1) triple therapy for 1 week
= PPI + amoxycillin 1g bd + clarithromycin 500mg bd
= PPI + metronidzole 400mg bd + clarithromycin 250mg bd

  • 2 week regimens
    + higher eradication rates
    + poor compliance

2) Dual therapy
= PPI + 1 antibiotic not recommended

3) quadruple therapy + culture directed therapy

Side effects are common = nausea and diarrhoea.

32
Q

what are 4 complications of peptic ulcer disease?

A

1) anaemia
2) bleeding
3) perforation
4) gastric outlet/duodenal obstruction - fibrotic scar

33
Q

describe the post-therapy follow up in duodenal and gastric ulcers?

A

Duodenal ulcers
= uncomplicated DU requires no f/u
- only if ongoing symptoms

gastric ulcers
= f/u endoscopy at 6-8 weeks
= ensure healing and no malignancy

34
Q

what are the alarm symptoms of gastric cancer?

A
  • dyspepsia
  • weight loss
  • anaemia
  • mass
  • recurrent committing
35
Q

what increases the risk of getting gastric cancer?

A

= achlorhydria (absence of HCL in gastric secretions)
- pernicious anaemia, previous gastric surgery

+ family history

36
Q

what are 3 histological, 2 physiological features and bacteriology of gastric cancer?

A

Histology
= body predominant or pangastritis
= atrophy
= intestinal metaplasia

Physiology
= deceased of no acid secretions
= increased gastrin

Bacteriology
= H. purloined disappear
= mixed bacterial overgrowth

37
Q

True or False.

those with H. pylori who develop peptic ulcer disease are somehow protected from developing gastric cancer.

A

Yes.

38
Q

how does H. pylori inhibit gastric secretions?

A

1) direct effect of bacterial product
- ammonia
- caves factor
- alpha methyl histamine

2) effect of body inflammation induced by H. pylori
- IL-1B = increased in H. pylori gastritis
- powerful inhibitor of acid secretion

(1B = recognised polymorphisms of IL- gene with different pro-inflammatory activities)

39
Q

how does inflammation, induced by H. pylori, inhibit gastric secretion?

A

= IL-1 beta production is stimulated by H. pylori

= IL-1 is a powerful inhibitor of acid secretion

40
Q

describe the progression that happens as a result of H. pylori infection, mucosal inflammation and then IL-1B pro-inflammatory host-genotype?

A 
IL-1B pro-inflammatory host genotype
= acid hypo-secretion
= body predominant gastritis
= atrophic gastritis 
= cancer

NO IL-1B pro-inflammatory host genotype
= normal or high acid
= antral predominant gastritis
= duodenal ulcer or no disease

GI (43 decks)

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