Naveed's Siminar PUD(1)

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PUD

(Pepic Ulcer Disease)


Definition_x0000_
A break in the lining of the lower part of the
esophagus, the stomach, or the upper part of the
small intestine. Peptic ulcers form when cells on
the surface of the lining become inflamed and die.

The term peptic ulcer disease (PUD) refers to


both duodenal ulcer and gastric
ulcer disease.
‫ﻋﺒﺎرت از ﺿﺎﯾﻌﻪ ﻏﺸﺎی ﻣﺨﺎﻃﯽ اﺳﺖ اﮐﺜﺮا از اﺛﺮ اﻟﺘﻬﺎب ﺣﺎد‬
‫ﺑﻪ وﺟﻮد ً در ﻣﻌﺪه وﯾﺎ اﺛﻨﺎ ﻋﺸﺮه‬
_.‫ ﻣﯿﮕﺮدد‬Focal defect ‫آﻣﺪه وﻣﻨﺠﺮ ﺑﻪ اﯾﺠﺎد‬
Causes

1.Most common causes


a. Helicobacter pylori infection
b. NSAIDs—inhibit prostaglandin production, which
leads to impaired mucosal defenses
c. Acid hypersecretory states, such as Zollinger–
Ellison syndrome
Other Causes.

a. Smoking—ulcers twice as likely in cigarette


smokers as in nonsmokers

b. Alcohol and coffee—may exacerbate


symptoms,but causal relationship as yet
unproven

c. Other potential but unproven causes include


emotional stress, personality type
(“type A”), and dietary factors.
Clinical featurs.
1 Epigastric pain

a. Aching or gnawing in nature


b. Nocturnal symptoms and the effect of food
on symptoms are variable

2. May be complicated by upper GI bleeding

3. Other symptoms: nausea/vomiting, early


satiety, and weight loss.
Diagnosis
1.... Endoscopy
A. Most accurate test in diagnosing ulcers.

B. Essential in diagnosis of gastric ulcers


because biopsy is necessary to rule out
malignancy—duodenal ulcers do not require biopsy.

C. Preferred when severe or acute bleeding


is present (can perform electrocautery
of bleeding ulcers).

D. Can obtain endoscopic biopsy for


diagnosis of H. pylori.
Dx. contin.....
• 2. Barium swallow

a. Sometimes used initially but is less reliable


than endoscopy.

b. Double-contrast techniques preferred due


to improved accuracy.
Dx. contin....

3. Laboratory test—for diagnosis of H. pylori


infection

a. Biopsy: Histologic evaluation of endoscopic


biopsy is the gold standard.

b. Urease detection via urea breath test is the


most convenient test (sensitivity and specificity >
95%). It documents active infection and helps to
assess the results of antibiotic therapy._
• c. Serology (lower specificity)—The presence
of antibodies to H. pylori does not necessarily
indicate current infection—Antibodies to H.
pylori can remain ele vated for months or even
years after eradication of infection (90%
sensitive).

• The following may lead to false-negative test


results: proton pump inhibitors (PPIs), bismuth,
many antibiotics and upper GI bleeding.

4. Serum gastrin measurement—if


considering Zollinger–Ellison
syndrome as a diagnosis_
Note.

If a peptic ulcer is uncomplicated, a barium


study or endoscopy is not needed initially.

Initiate empiric therapy. However,


if you suspect any of the complications of
PUD, order confirmatory studies._
Treatment
1. Medical—Majority of patients with PUD can
be successfully treated by curing H. pylori
infection, avoidance of NSAIDs, and appropriate
use of antisecretory drugs.

A. Supportive (patient directive)


٠ Discontinue aspirin/NSAIDs.
• Restrict alcohol use but do not restrict any
foods.
• Stop smoking, decrease emotional stress.
• Avoid eating before bedtime (eating stimulates
nocturnal gastric acid levels);
decrease coffee intake (although no strong link
has been established with ulcer disease).
B. Acid suppression therapy
• H2 receptor blockers—Cimetidine (Tagamet) and
Ranitidine (Zantac). Block
histamine–based parietal cell acid secretion.
Accelerate healing of ulcers.
• PPIs—omeprazole (Prilosec), lansoprazole
(Prevacid), Block H+/K+ ATPase
pump directly in parietal cell membrane. Most
effective antisecretory agents
(although expensive).
• Antacids—somewhat outdated for primary therapy
and more appropriately
used for adjunctive therapy/symptomatic relief.
Examples include alumi num hydroxide (Mylanta),
calcium carbonate (Tums), Bismuth subsalicylate
(Pepto-Bismol).
C. Eradicate H. pylori with triple or quadruple
therapy Once infec tion is cleared, the rate of
recurrence is very low.
• For initial therapy, triple therapy (PPI, amoxicillin
and clarithromycin) for 10
days to 2 weeks.
• For retreatment, quadruple therapy (PPI, bismuth,
metronidazole, and tetra cycline).
D. Cytoprotection
• Sucralfate—facilitates ulcer healing, must be taken
frequently, is costly, and
can cause GI upset.
• Misoprostol—reduces risk for ulcer formation
associated with NSAID therapy,
is costly, and can cause GI upset (common side
effect).
E.. Treatment regimens
• If H. pylori test is positive, begin eradication
therapy with either triple or qua druple therapy
. Also begin acid suppression with antacids, an
H2 blocker, or a PPI.
• If the patient has an active NSAID-induced
ulcer, stop NSAID use (may
switch to acetaminophen). Also begin with
either a PPI or misoprostol.
Continue for 4 to 8 weeks, depending on
severity. Treat the H. pylori infection
as above if present.
E........

• Antisecretory drugs can be discontinued after 4


to 6 weeks in patients with uncomplicated ulcers
who are asymptomatic. Patients at increased risk
of recurrence (especially if underlying cause of
ulcer is not reversed) may ben efit from
maintenance therapy.

• H. pylori-negative ulcers that are NOT caused


by NSAIDs can be treated with
antisecretory drugs (either H2 blockers or PPI).
2. Surgical

a. Rarely needed electively

b. Required for the complications PUD,


(perforation, bleeding, gastric outlet
obstruction)

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