Ravilya_1_Gastro_Peptic Ulcer

Front 1

what could lead to PUD

Back 1

The strongest causal relationship for the development of ulcers is the use of
NSAIDs,Helicobacter pylori infection, cancer of the stomach, Zollinger-Ellison syndrome, Crohn
disease,burns, head trauma, and prolonged intubation and mechanical ventilation.

Front 2

do Tobacco smoking, alcohol,and the use of steroids lead to PUD?

Back 2

Tobacco smoking, alcohol,and the use of steroids by themselves do not cause ulcer disease.Tobacco
and alcohol use can delay healing and are associated with the development of gastritis, but they do
not cause ulcers.

Front 3

NSAIDs lead to ulcer formation -- mechanism?

Back 3

NSAIDs lead to ulcer formation because they decrease the normal production of the mucous
barrier that protects the epithelial cells of the gastric mucosa. Prostaglandins, the major stimulant
for mucous production that forms this protective barrier, are inhibited by NSAIDs and
hence diminish the protective barrier ofthe stomach lining.

Front 4

stress ulcers from burns and head - mechanism formation of ulcer

Back 4

of stress ulcers from burns and head trauma is that there is an intense vasoconstriction
of the vasculature that supplies the gastric mucosa, leading to the sloughing of these cells
and ulceration

Front 5

is there a routine indication for stress ulcer prophylaxis during steroid tratment?

Back 5

Steroid use by itself does not lead to peptic ulcer disease and is therefore not a
routine indication for stress ulcer prophylaxis.

Front 6

what produced by parietal cells in stomach?
what are 3 stimulants for prpduction of acid?

Back 6

Parietal cells in the stomach produce acid.

The three stimulants to the production of acid from the parietal cells are gastrin, acetylcholine, and histamine.

Front 7

gastrin production?

Back 7

Gastrin is produced by G cells in the
stomach, and its release is stimulated by distention of the stomach, the presence of amino acids,
and vagal stimulation.

Front 8

what is released by vagal stimulation

Back 8

Vagalstimulation also releases acetylcholine and gastrin-releasing peptide.

Front 9

what is the single most important stimulant to gastrin release

Back 9

However, the single most important stimulant to gastrin release is distention of the stomach.

Front 10

Histamine is released by

Back 10

Histamine is released by enterochromaffin-like cells present in the same glandular elements of
the stomach that have the parietal and chief cells.

Front 11

Chief cells release

Back 11

Chief cells release pepsinogen, which is converted
to pepsin by the acid environment of the gastric lumen.

Front 12

why H2 blockers, such as cimetidine, famotidine, and ranitidine, have such
a large effect on inhibition of acid release.

Back 12

Histamine directly stimulates the
parietal cells to both release acid and potentiate the effects of acetylcholine and gastrin on the
parietal cells. This is why H2 blockers, such as cimetidine, famotidine, and ranitidine, have such
a large effect on inhibition of acid release.

Front 13

Zollinger-Ellison syndrome is the excessive production and release of

Back 13

Zollinger-Ellison syndrome is the excessive production and release of gastrin from G cells.

Front 14

Somatostatin inhibits

Back 14

Somatostatin is the counterbalance to this system. Somatostatin inhibits the release of gastrin
and histamine, as well as having a direct inhibitory effect on the production of acid from the
parietal cells.

Front 15

Secretin is released from

The main stimulant to
the release of secretin is

Secretin inhibits

Back 15

Secretin is released from the S cells of the duodenal lining. The main stimulant to
the release of secretin is the presence of acid in the duodenum. Secretin inhibits the production
of gastrin, as well as stimulates pancreatic and biliary bicarbonate production and release

Front 16

The most common cause of ulcer disease is

Back 16

The most common cause of ulcer disease is Helicobacter pylori followed by the use of NSAIDs.
Eighty to 90% of duodenal ulcers and 70 to 800/0 of gastric ulcers are associated with H. pylori

Front 17

The most common presentation of ulcer disease is...

differnce in pain ( gastric/ duodenum)

Back 17

The most common presentation of ulcer disease is midepigastric pain.


gastric ulcers have been associated with pain on eating, and
duodenal ulcers were thought to be relieved by eating. Because gastric ulcers were thought to
be associated with pain on eating, this more frequently led to weight loss.
More than 80% are not
associated with abdominal tenderness in the absence of a perforation. Nausea and vomiting are
occasionally found with both of them.

Front 18

how to ds the PUD
what is superior- endosc or BA

Back 18

Ulcer disease is best diagnosed with upper endoscopy. Barium studies are inferior.

Front 19

In generally
healthy patients younger than 45 years of age with epigastric pain, what to do first?
what to do if the symptoms persists?

if P with alarm symptoms or . 45 years. what to do first?

Back 19

In generally
healthy patients younger than 45 years of age with epigastric pain, endoscopy can be deferred in
favor of a trial of Hz blockers or proton-pump inhibitors (PPIs). If the symptoms persist, then
endoscopy can be performed. In those older than 45 years or those with alarm symptoms (weight
loss, anemia) heme-positive stools, or dysphagia), endoscopy should be performed.

Front 20

what test for Helicobacter is least expensive, is the least invasive, and has a very high degree
of sensitivity.

when we could say that Helicob Pilory is negative as etiology for
PUD

can the serology distinguish between old or new disease?

Back 20

The diagnosis of H. pylori is based on either serology, urea breath testing, stool antigen testing)
or biopsy with histology. Knowing which diagnostic test to perform first for Helicobacter is not
definitively clear. Serology is the least expensive, is the least invasive, and has a very high degree
of sensitivity. This means a negative test for the Helicobaeter antibody effectively excludes this
agent as an etiology of the ulcer disease. The drawback to serology is that it does not reliably
distinguish between old disease and new disease and therefore lacks specificity

Front 21

what tests are able to easily distinguish new versus old
disease

Back 21

The advantage of both breath testing and stool antigen detection methods is
that they have the same sensitivity as serology and are able to easily distinguish new versus old
disease.When H. pylori has been treated, both the breath and stool tests readily become negative.
This means they can be used to evaluate eradication of the organism post treatment and
can test for cure of the infection.

Front 22

what is the
most sensitive and specific test

Back 22

Biopsy with histology is the
most sensitive and specific test. Further, it can exclude cancer

Front 23

rapid test on the biopsy,

Back 23

there is a rapid test on the biopsy, known as a CLO
test, that can exclude Helicobacter. The CLO is performed to see if the organisms present in the
biopsy specimen can produce urease) demonstrating the presence of the bacterium.

Front 24

tx for helicob pilory

Back 24

the first
choice is a PPI combined with clarithromycin and amoxicillin. Omeprazole, lansoprazole, pantoprazole,
rabeprazole, and esomeprazole are all equal in efficacy

The other two choices of antibiotics are tetracycline and metronidazole. Bismuth subsalicylate
is not necessary. Regimens that contain PPIs are superior to those that use Hzblockers) such as
ranitidine or cimetidine. The PPI/clarithromycin/amoxicillin regimen should be effective in
>900/0 of patients. Duration of therapy is 10 to 14 days.

Front 25

In those who fail therapy, what to do
after re-treatment of helicob and no improving what to do

Back 25

In those who fail therapy, a urea breath test should be performed to see if the reason for failure
was the inability to eradicate the organism. If the organism was not eradicated, then re-treatment
should occur with different antibiotics and the addition of bismuth subsalicylate. In addition)
sensitivity testing for the organism should be explored. If the organism was eradicated and the
ulcer persists, recurs, or worsens) the patient may need evaluation for Zollinger-Ellison syndrome.

Front 26

Ordinary ulcers not related to Helicobacter can be treated

Back 26

Ordinary ulcers not related to Helicobacter can be treated with PPIs alone

Front 27

what drug could prevent the development o f NSAID-induced ulcers.

Back 27

Misoprostol is a
prostaglandin analog that was developed to prevent the development of NSAID-induced ulcers.
It is rarely used.

Front 28

COX-1 COX2

Back 28

Cyclooxygenase 1 (COX-1) is the enzyme that produces the prostaglandins that
protect the gastric mucosa. COX-2 is the enzyme implicated in the development of pain. COX-2
inhibitors, such as celecoxib and valdecoxib, were developed to relieve pain without damaging
the gastric lining. They have the same degree of analgesic effect, but do not damage the ability
to produce the protective mucous barrier of the stomach. COX-2 inhibitors also have no effect
on platelets.

Front 29

INDICATION FOR OPERATION

Back 29

Front 30

ds of H pylori inf gold standart

Back 30

gastric mucosal biopwith rapid urease testing

Front 31

non invasive test for H .pylori infection
best initia test

Back 31

stoll antogen testing - to prove irradication after tx
or urease breath testing( must be antisecretory therapy for 2 weeks)

IG serology- positive for life, confirm exposure
serum antibody test is the best initial test

Front 32

best test to confirm eradication

Back 32

urease breath test or stool antigen