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GI > Dyspepsia and PUD > Flashcards

Dyspepsia and PUD Flashcards

1
Q

What is dyspepsia?

A 
Epigastric pain or burning (epigastric pain syndrome)
Postprandial fullness (postprandial distress syndrome)
Early satiety (postprandial distress syndrome
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2
Q

What are the foregut structures?

A

Oesophagus, stomach, duodenum, pancreas and gallbladder

Cricopharyngeus to ampulla of Vater

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3
Q

When is dyspepsia more common?

A

In those infected with H pylori, those who used NSAIDs
Overlap with IBS/GORD.
No age sex,smoking, alcohol association

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4
Q

What are the organic causes of dyspepsia (25% of cases)?

A

PUD
Drugs (esp. NSAID, COX2 inhibators)
Gastric cancer

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5
Q

What is functional dyspepsia (75%)?

A

Idiopathic dyspepsia.

Same symptoms but with no evidence of structural disease. Associated with other functional gut disorders eg IBS

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6
Q

Can GORD coexist with dyspepsia?

A

Yes

You can have heart burn and indigestion. They are not the same thing

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7
Q

What would you find on examination of a patient with uncomplicated dyspepsia?

A

Epigastric tenderness only

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8
Q

What would you find on examination of a patient with complicated dyspepsia?

A

Cachexia
Mass
Evidence gastric outflow obstruction
Peritonism- symptom complex characterized by vomiting, pain or abdominal tenderness, and shock.

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9
Q

What are the alarm symptoms for dyspepsia?

A 
Dysphagia
Evidence of GI blood loss- haematemisis or melaena
Persistent vomiting 
Unexplained weight loss
Upper abdominal mass
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10
Q

How do you manage dyspepsia without alarm symptoms?

A

Non invasive test and treat.
CHeck H pylori status If positive, eradicate
If negative treat with antacids or histamine receptor antagonist

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11
Q

What is the Rome III classification of functional dyspepsia?

A

Epigastic pain, epigastric burning, early satiation and postprandial fullness
WITH no evidence of structural disease.
Criteria must be fulfilled for the last 3 months with symptom onset 6 months before diagnosis

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12
Q

WHat are the possible causes of functional dyspepsia?

A

Visceral hypersensitivity, altered brain gut interactions
Genetic factors
Psychosocial factors
Abnormal upper GI motor and reflex functions
Disrupted gut immune interactions

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13
Q

What is Peptic ulcer disease?

A

PUD is a common cause of organic dyspepsia associated with epigastic pain radiating to the back

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14
Q

If PUD a relapsing and remitting chronic illness?

A

Yes

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15
Q

What are the characteristic symptoms of of PUD?

A

Pain orse at night
Relapsing and remitting
Aggravated or relieved by eating
Family history common and more common in lower socio economic groups

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16
Q

What are the causes of PUD?

A

H pylori causes 90% of duodenal ulcers and 60% of gastric ulcers
NSAIDs (COX1, COX2, PGE) cause the majority of the rest. The ratio of NSAID: H pylori is rising

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17
Q

What type of bacteria is H pylori?

A

Gram negative microaerophilic flagellated bacillus

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18
Q

When is H pylori acquired and how is it spread?

A

Usually in infancy and oral-oral or faecal-oral spread. The consequences of infection do not arise until later in life

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19
Q

What are the consequences of H pylori infection?

A

1) No pathology- majority
2) PUD = 20-40%
3) Gastric cancer -1%

20
Q

What are the most typical gastric cancers associted with H pylori infection?

A

Non- cardia gastric adenocarcinoma

Low grade B cell gastric lymphomas (Maltoma)

21
Q

How does the prevalence of H pylori change in the developed and developing world?

A

Developed world = slowly increases with age

Developing world = the majority of people infected by age 15

22
Q

There is greater H pylori infection and PUD in people of lower socioeconomic status?

A

True

23
Q

Acid is produced by the parietal cells of the stomach and this signals to G cells of the stomach to do what?

A

Reduce gastrin release which intern signals to the parietal cells to reduce the acid secreted. Negative feedback.

24
Q

What are the different outcome of H. pylori infection?

A

1) No clinical disease
2) Increased acid production => Gastrin production. No atrophy and duodenal ulcers in 20-40% of cases
3) Decased acid production => increased gastrin production. Atrophy and incidence of gastric cancer in 1% of cases

25
Q

What is the pathophysiology of duodenal ulcers?

A

Increased acid secretion in the stomach which leaves. Decreased somatostatin leads to higher levels of gastrin which maintains acid production.
When acid enters the duodenum => Gastric metaplasia, h pylori collenisation and ulceration

26
Q

What are the causes of duodenal ulceration?

A

H pylori infection
NSAIDs
Severe stress

27
Q

How is H pylori diagnosed?

A

1) Gastric biopsy- urease test, histology and culture/sensitivity
2) Urease breath test
3) FAT= faecal antigen test
4) Serology (IgA antibodies)- not accurate with increasing patient age

28
Q

H pylori increases the pH of its microenvironment. How does the body counter act this?

A

Urea is broken down with water and H+ to ammonium bicarbonate by the urease enzyme. It is the urease enzyme which you can test for the presence of .

29
Q

What is the treatment for PUD?

A

1) All antisecretory therapy (PPI)
2) All tested for presence of H pylori and treated if positive
3) Lifestyleis difficult. no firm dietary recommendations.
4) Surgery infrequent
5) Non H pylori/non-NSAID ulcers. => Nutrition and optimse co morbidities.

30
Q

What are teh types of antisecretory therapy?

A

Histamine receptor agonists (Cimetidine, ranitidine, famotidine and nizatidine)
Proton pump inhibatrs (omeprazole, lansoprazole, dexlansoprazole)
PPI inhibators are more effective for healing DU and also slightly better for GU

31
Q

How are antacids used in therapy for DU/GU?

A

Help with symptoms but not as effective for healing.

32
Q

Is misoprostol used in DU/GU treatment?

A

No- its less effective than PPIs or histamine receptor antagonists

33
Q

How is H pylori infection treated in one week?

A

Triple therapy for 1 week (most common)

1) PPI + amoxycillin 1g bd + clarithromycin 500mg bd.
2) PPI + metronidazole 400mg bd + clarithromycin 250mg bd

34
Q

Is two weeks of tripple therapy more effective for erradiaction of H pylori?

A

Yes- higher eradication rates but poorer complience

35
Q

Why is complience poor for tripple therapy for H ylori?

A

Side effects are common (nausea and diahoea.

If they are still symptomatic after the course you must retest.

36
Q

Dual therapy is not recommended for H pylori erradication. T or F?

A

True

37
Q

What are the cmplications of PUD?

A

Anaemia, bleeding, perforation, gastric outlet/duodenal obstruction- fibrotic scar

38
Q

Do duodenal ulcers adn gastric ulcers require a follow up?

A

Uncomplicated DU only requires follow up if ongoing symptoms.
Gastric ulcers require a follow up endoscopy at 6-8 weeks to check healing and check for malignancy

39
Q

What may raise your suspicions of gastric cancer?

A

Dyspepsia + alarm symptoms (weight loss, anaemia, mass, recurrent vommiting)
Achlorhydria (due to pernicious anaemia or previous gastric surgery)
Family history

40
Q

What is achlorhydria?

A

absence of hydrochloric acid in the gastric secretions.

41
Q

What is the phenotype of gastric cancer?

A

Atrophy,
Intestinal metaplasia
H pylori disappear and mixed bacterial overgrowth takes over
Low acid secretion due to increased gastrin release

42
Q

Those with H pylori infection with PUD are somehow protected from developing gastric cancer. T or F?

A

True

43
Q

H pylori often inhibits gastric acid secretion. T or F?

A

True. Inflamation => IL-1 beta production which inhibits acid secretion

44
Q

Are there genetci factors which may predispose an individual to hypochlorhydric response to h pylori?

A

Yes the IL-1B gene as IL-1beta production is increased which inhibits acid secretion

45
Q

If your H pylori causes increased acid secretion what disease will you get?
If your H pylori causes decreased acid secretion what disease will you get?
NB: bodies response is down to genetics?

A

High acid => DU/GU

Low acid => Atrophy and cancer

46
Q

What medications do you need to stop and when before a H pylori test?

A

Antibiotics- 4 weeks before
PPI 2 weeks before
Histamine receptor antagonists 24 hours before.

47
Q

Where is alkaline phosphate found?

A

Liver and the bone

GI (48 decks)

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