lecture 2 Flashcards

peptic ulcer disease and gord (49 cards)

1
Q

dyspepsia is

A

indigestion

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2
Q

% of population with dyspepsia

A

40

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3
Q

after endoscopy , what is commonly seen

A

40% have GORD, 40 have non ulcer dyspepsia, 13 % have ulcer disease

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4
Q

symptoms of dyspepsia

A

reflux, heartburn, pain, nausea/vomiting

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5
Q

name of ulcer in stomach vs duodenum

A

gastric ulcer - stomach, duodenal ulcer - duodenum

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6
Q

what is required to form a peptic ulcer

A

acid and pepcin

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7
Q

what makes stomach corrosive

A

low pH of 1 or 2

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8
Q

name of ulcer which goes fully through stomach wall

A

perferated ulcer

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9
Q

why doesnt the stomach digest itself

A

alkaline mucus - forms a gel layer subsance on top layer of stomach/intestine to neutralise stomach acid

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10
Q

use of tight junctions

A

found between epithelial cells , they hold the epithelial cells close together so that acid cant leak between them - if these are distrupted an ulcer may form

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11
Q

peptic ulcers formed when theres impaired

A

mucosal defence and peptic acid present

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12
Q

how can nsaids cause ulcers

A

reduce prostaglandin production, which then reduces bicarbonate production ( bicarbonates neutralise the acid and prostaglandins also promote blood flow through mucosa so less of the bad stuff gets flushed away from epithelial cells)

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13
Q

what factors can increase risk of ul er

A

smoking , stress, genetics

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14
Q

mucin is

A

a genetic component which protects the musosal Layer

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15
Q

H pylori can cause ulcers because it affects

A

pepsin secretion and impairs mucosal barrier

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16
Q

how does heavy drinking or smoking cause ulcers

A

causes inflammation of the stomach which leads to breakdown of mucosal defence

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17
Q

what is the epigastrium

A

upper section of the stomach, just below the rib cage

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18
Q

peptic ulcer pain is usually located where and how is the pain described

A

in the epigastrium and usually doesnt radiate - pain described as burning, gnawing or as hunger pains

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19
Q

ulcer pain and meals

A

gastric ulcer pain is aggrevated by meals, duodenal is relieved by meals

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20
Q

H pylori is seen is 40% of individuals- how is this presented in gastric ulcer vs duodenal

A

95% of patients with gastric ulcer and 80% of those with duodenal ulcer

21
Q

where does h pylori effect and what is the effect

A

lower stomach, causes inflammation of the gastric mucosa (gastritis)

22
Q

How do you test for the presence of H pylori

A

Serologic evaluation (but this can reflect previous exposure)
Urea breath test ( - as h pylori contain large amounts of the urease enzyme which convert urea to NH3 and CO2)
Stool antigen tests ( detect antigen released by organisms present in the stomach)

23
Q

what happens if you dont get rid of h pylori

A

80% of ulcers will reoccur within a year

24
Q

How is acid secreted in the stomach

A

carbonic anhydrase produces bicarbonate and h , bicarbonate is exchanged for a cloride ion, which diffuses into the lumen , the h is pumped into lumen by h/k atpase - leads to acid in lumen

25
drugs which treat peptic ulcer disease
antacids/antisecretory agents these raise pH to promote healing , you also need to eradicate h pylori by pharmacological treatments
26
examples of histamine receptor antagonists
cimetidine, ranitidine, nizatidine, famotidine
27
now do h2 receptor antagonists work
acts competetibely on h2 receptors on gastric parietal cells and reduce the basal acid secretion by 60%
28
problem with h2 receptor antagonists as treatment
relapse is common after treatment stops can cause diarrhoea, headaches, confusion (in elderly), cimetidine - gynaecomastia (due to anti-androgen effect) and it also inhibits P450 system ( causes potential interactions with warfarin, phenytonin and theophylline)
29
PPI examples
omeprazole, lansoprazole, pantoprazole, rabeprazole, esomeprazole
30
PPIs are irreversible. How does acid secretion return?
dependent on the synthesis of new enzymes (H/K atpase) ( need to make new cells?)
31
adverse effects of PPIs
gastrointestinal upset, headache, skin rashes, gastric atrophy in long term use. omeprazole - has both stimulatory and inhibitory effecys on CYP450 system
32
Treatment to eradicate H pylori infection
Use triple therapy: PPI, amoxicillin and clarithromycin/metronidazole if pen allergic: PPi, clarithromycin and metronidazole
33
When can cytoprotectie agents not be used
in pregnancy
34
how does h pylori get trapped - effecting the stomach
it detects the pH gradient and it moves towards the raised pH (of surface of epithelial cell) where it gets into the mucus gel => trapped
35
what is serologic evaluation
blood testing
36
how is a urea blood test carried out
given a capsule containing carbon 13 form of urea. If h pylori is present the urea is broken down into 2x NH2 snf CO2 - this is better test than seologic but is more expensive
37
is an antacid or an antisecretory better at treating peptic ulcers
antisecretory agenst
38
when is acid secretion worse
during the night
39
why do males need to be wary of taking cimetidine
they can get gynaecomastia
40
which acid stimulators do PPI stop
all 3
41
eg of a cytoprotective agent
mistoprostol
42
WHen is misoprotol given
alongsided a NSAID to stop the formation of an ulcer
43
how does a cytoprotective work
enhances bicarbonate secretion in duodenum, weakly inhibits gastric acid secretion through activation of prostaglandin receptor on parietal cells , increases mucosal blood flow
44
what is zollinger-ellison syndrome
a rare disorder whoch can cause gastric/duodenal ulcers or in jejunum too due to massive gastric acid hyper secretion caused due to gastrin secreting tumour in the pancreas/duodenum (gastrinoma) which stimulates acid secretuon in the stomach
45
what causes gord
lower oesopgafeal spincter not working properly so the acid from the stomach comes back up into oesophagus - burning
46
drugs for treating GORD
antacids and antacid/alginate combinations , drugs which inhibit gastric acid secretion , drugs which act on oesophageal/ gastric motility
47
who gets diagnosed with gord
patients with long-term GORD
48
wjat is barretts oesophagus
replacement of normal stratified squamous epitheliym by columnar epithelium cells with goblet cells
49
barretts oesophagus can lead to
cancer (oesopageal adenocarcinoma)