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GI: stomach > Peptic Ulceration > Flashcards

Peptic Ulceration Flashcards

1
Q

This is a breach in the gastrointestinal mucosa as a result of ___ and _____ attack. Ulceration is longstanding and often deep

A

This is a breach in the gastrointestinal mucosa as a result of acid and pepsin attack. Ulceration is longstanding and often deep

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2
Q

The pathogenesis involves consideration of a number of factors including mucosal defence mechanisms, -____ metabolism, mucosal ___ flow and crucially the effect of ______

A

The pathogenesis involved consideration of a number of factors including mucosal defence mechanisms, prostaglandin metabolism, mucosal blood flow and crucially the effect of H.pylori

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3
Q

how are acute ulcers distinguished from chronic ones?

A

the absence of fibrosis

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4
Q

acute ulcers can occur in ___ ____ . and also in ____ ____

A

acute gastritis (NSAIDS or alcohol)

acute hyperacidity

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5
Q

what is the most common cause of acute hyperacidity?

A

most often due to gastrin-secreting neuroendocrine tumours (zollinger ellison)

but also in cushing’s

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6
Q

what are the symptoms of PUD

A

dyspepsia - very common cause of this

pain aggravated or relieved by eating

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7
Q

pain can be ____

A

nocturnal

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8
Q

what does pain that keeps you awake suggest about the cause of dyspepsia ?

A

it is organic .

People with functional dyspepsia can go back to sleep

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9
Q

duodenal ulcers are ____ by eating

A

relieved

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10
Q

gastric ulcers ____ by eating

A

aggravated

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11
Q

what accounts for most cases of PUD?

A

H.pylori

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12
Q

H.P is acquired in ______

A

infancy

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13
Q

what do HP look like ?

A

Gram negative microaerophilic flagellated bacillus

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14
Q 
with H.P 
Can either have no pathology
- the majority of people 
- Peptic ulcer disease - \_\_ -\_\_% 
- Gastric cancer - \_\_ %
A

Can either have no pathology - the majority of people
Peptic ulcer disease - 20-40%
Gastric cancer - 1%

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15
Q

what kinds of gastric cancer can be caused by HP ?

A

almost all non-cardia gastric adenocarcinoma

low gradeB cell gastric lymphoma - MALTOMA

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16
Q

what are some other causes of PUD?

A

NSAIDS (COX1, COX2 and PGE)

17
Q

why is the duodenum the commonest site for PUD?

A

because the mucosa in the duodenum is much weaker when faced with acid

18
Q

where in the stomach are ulcers common?

A

antrum and junction of body

19
Q

where else can you get ulcers/

A
  • oesophago-gastric junction
20
Q

which cells are responsible for the secretion of acid

A

parietal cells

21
Q

HP when infecting the stomach causes intense _____, increased ___ ____ and causes a _____ state. In duodenal ulcer pathology increased gastrin leads to increased ____ but no ___ of the cells

A

inflammation, blood flow, hyperacidic, acid, atrophy

22
Q

In gastric cancer, there is increased ___ production which causes _____. This means that even though there is lots of ____ cells do not produce ____

A

gastrin, atrophy, gastrin, acid

23
Q

duodenal ulcers

  1. Get increased gastrin release due to:
    - decreased _______
    - Cag +ve > Cag -ve - oncogenic, highly antigenic
  2. Increased gastrin leads to
    - Increased acid secretion
    - Increased _____ cell mass
    - No ____ gastritis
  3. Leads to increased _____ acid load
    - Get gastric _____
    - HP colonisation and ulceration
A
  1. Get increased gastrin release due to:
    - decreased somatostatin
    - Cag +ve > Cag -ve - oncogenic, highly antigenic
  2. Increased gastrin leads to
    - Increased acid secretion
    - Increased parietal cell mass
    - No body gastritis
  3. Leads to increased duodenal acid load
    - Get gastric metaplasia
    - HP colonisation and ulceration
24
Q

how is H.Pylori diagnosed?

A
  • gastric biopsy
  • urease breath test
  • FAT (faecal antigen test)
  • serology (IgA antibodies)
25
Q

how does the urease test work?

A

HP increases the pH of its environment so the urease enzyme can work and is thus present in the breath when it wouldn’t normally

26
Q

what is the metaplastic change in chronic duodenal acid exposure?

A

turn from goblet and absorptive to barrier

27
Q

how big are ulcers, what range?

A

between 2-10 cm

28
Q

what do ulcers look like?

A

edges are clear cut, punched out

29
Q

in ulcers you get thickening of the ____ below and ____ tissue at the base

A

muscle, granular

30
Q

what are the microscopic layers of the ulcer?
1 - floor of necrotic _____ debris
2 - this overlies a base of ____ ____ tissue
3- deepest layer of ____ ____ tissue
These changes almost always extend into the _____ and commonly beyond to involve the surrounding tissues and organs in a chronic inflammatory mass.

A
  1. fibropurulent debris
  2. inflamed granulation
  3. fibrotic scar

muscularis

31
Q

how is PUD treated?

A
  • ALL anti-secretory therapy (PPI)
  • ALL tested for presence of H pylori
  • H pylori +ve - eradicate and confirm
  • H pylori -ve - anti-secretory therapy
  • Triple therapy is 80-85% effective
  • withdraw NSAIDs
  • lifestyle (difficult)
  • non-HP/non-NSAID ulcers - nutrition and optimise comorbidities
  • no firm dietary recommendations
  • surgery - infrequent
32
Q

what are the options for anti-secretory therapy ?

A
  • can use H2 receptor antagonists
  • PPI
  • antacids and sucralfate
33
Q

what is the treatment for hp 1 week commonest (85% success) ?

A

PPI and amoxicillin 1g bd + clarithromycin 500mg bd

PPI and metronidazole 400mg bd + clarithromycin 250mg bd

34
Q

what are the side effects of HP treatment?

A

nausea, diarrhoea

35
Q

what are the complications of peptic ulcers?

A
  • Perforation
  • Penetration
  • Haemorrhage
  • Stenosis
  • Intractable pain
  • Anaemia
36
Q

how do you get haemorrhages with ulcers?

A

if ulcer digests through an artery

37
Q

DU if uncomplicated requires no ____ __

A

follow up

38
Q

what is the follow up for GU?

A

endoscopy at 6-8 weeks

GI: stomach (3 decks)

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