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
how does the urease test work?
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
what is the metaplastic change in chronic duodenal acid exposure?
turn from goblet and absorptive to barrier
27
how big are ulcers, what range?
between 2-10 cm
28
what do ulcers look like?
edges are clear cut, punched out
29
in ulcers you get thickening of the ____ below and ____ tissue at the base
muscle, granular
30
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.
1. fibropurulent debris 2. inflamed granulation 3. fibrotic scar muscularis
31
how is PUD treated?
- 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
what are the options for anti-secretory therapy ?
- can use H2 receptor antagonists - PPI - antacids and sucralfate
33
what is the treatment for hp 1 week commonest (85% success) ?
PPI and amoxicillin 1g bd + clarithromycin 500mg bd PPI and metronidazole 400mg bd + clarithromycin 250mg bd
34
what are the side effects of HP treatment?
nausea, diarrhoea
35
what are the complications of peptic ulcers?
- Perforation - Penetration - Haemorrhage - Stenosis - Intractable pain - Anaemia
36
how do you get haemorrhages with ulcers?
if ulcer digests through an artery
37
DU if uncomplicated requires no ____ __
follow up
38
what is the follow up for GU?
endoscopy at 6-8 weeks