For study

1. Name- abdur rahman
Group-115

2.  The two major contributing factors to the
development of PUD are gastrointestinal
infection with H. pylori and nonsteroidal anti-
inflammatory drug (NSAID) use. Both factors
contribute to the development of PUD and
interact with other risk factors to promote
ulcer formation.
 .

3.  • Helicobacter pylori infection
 ◦ Associated with 40–70% of duodenal ulcers
and 25–50% of gastric ulcers
 ◦The rate of H. pylori infection (and,
therefore, the development of PUD) is
decreasing.

4.  Chronic NSAID use
 ◦ Associated with a fourfold risk of
developing PUD [9]
 ◦ Increases the risk for complications of PUD
(see “Complications of peptic ulcer disease”)
 For patients requiring chronic NSAID therapy,
consider acid suppression medication for
ulcer prevention. [10]
 Associated risk factors

5.  H. pylori infection or NSAID use alone do not
typically cause ulcer formation.There are
often additional risk factors present, such as
the following, that increase the probability of
developing an ulcer:
 • Shared risk factors for PUD, GERD and
gastritis (i.e., smoking, heavy alcohol use,
glucocorticoids, caffeine)

6.  Diet [11]
 • Psychological factors (e.g., anxiety, stress,
PTSD)
 • Genetic factors [12]
 Rare causes of PUD
 • Acid hypersecretory states
 ◦ Zollinger-Ellison syndrome (gastrinoma)
 ◦ Systemic mastocytosis
 ◦ Hyperparathyroidism

7.  Under typical physiological conditions, the cells
of the gastric mucosa secrete a gastric juice (an
acidic fluid composed of HCl, pepsinogen,
intrinsic factor, and mucus), which may damage
the native cells of the GI tract. Protective
mechanisms (e.g., secretion of mucus and
HCO3- to form a protective barrier) prevent the
gastric juices from digesting and eroding the
gastric epithelial cells. Ulcer formation occurs
when either the protective mechanisms are
disrupted and/or excessive acids or pepsin are
secreted.

8.  Physiological gastric secretions [13]
 • Parietal cells
 ◦ Secrete hydrochloric acid (HCl) and intrinsic
factor
 ◦ Stimulated by acetylcholine, histamine, and
gastrin
 ◦ Inhibited by prostaglandins and somatostatin
 • Mucosal cells
 ◦ Secrete protective mucus
 ◦ Stimulated by acetylcholine, prostaglandins
(which inhibit HCl secretion), and secretin

9.  Chief cells
 ◦ Secrete pepsinogen
 ◦ Stimulated by acetylcholine, gastrin,
secretin, and vasoactive intestinal
polypeptide (VIP)
 See “Secretory and regulatory products of
the gastrointestinal tract” in “Gastrointestinal
tract” for more details on typical
physiological secretions.

10.  PUD may be asymptomatic or manifest with
a variety of clinical features, e.g., general
dyspepsia or complications such as
perforation or bleeding.
 Asymptomatic PUD
 • Up to 70% of patients with peptic ulcers do
not experience symptoms. [14][15]
 • Patients who take NSAIDs are more likely
to have asymptomatic ulcers and present
with complications of PUD.

11.  Symptomatic PUD
 • Abdominal pain
 ◦The most common symptom of PUD [16]
 ◦ Commonly located in the epigastrium
 ◦ Often described as “gnawing” or “burning”
 ◦ Can be related to meal intake depending on
the location of the ulcer (see “Clinical
symptoms of gastric and duodenal ulcers”)

12.  Other associated symptoms
 ◦ Belching
 ◦ Indigestion
 ◦ Gastrointestinal reflux
 ◦ Nausea and/or vomiting
 ◦ Bloating/abdominal fullness

13.  Esophagogastroduodenoscopy (EGD)
 The most accurate test to confirm the diagnosis.
Other clinical applications include:
 • Malignancy screening: to differentiate PUD
from gastric cancer
 ◦Visualization of the lesions
 ◦ Biopsy sampling
 • Invasive H. pylori testing
 • Simultaneous therapeutic measures, e.g.,
hemostasis treatment with electrocautery for
active bleeding

14.  Gastric ulcers
 ◦ Biopsies are recommended in most cases.
 ◦ Multiple biopsies are recommended.
 From the edge and base of the ulcer (essential
to rule out malignancy, which is not uncommon
in gastric ulcers)
 Multiple biopsies from different areas of the
stomach lining, including those not surrounding
the ulcer (to test for H. pylori)


15.  • Duodenal ulcers
 ◦ Obtain biopsies from ulcers with
endoscopic features that suggest
malignancy.
 ◦ Duodenal ulcers are usually benign and do
not require routine biopsy.

16.  “Differential diagnoses of acute abdominal
pain”
 • “Differential diagnoses of dyspepsia”
 • “Differential diagnoses of nausea and
vomiting”
 • “Differential diagnoses of upper GI
bleeding”
 • “Differential diagnoses of chest pain”

17.  Approach
 • General measures
 ◦ Nonpharmacological measures: e.g., avoid
NSAIDs, restrict alcohol.
 ◦ Follow-up to confirm treatment success;
possibly endoscopic surveillance
 • H. pylori test-and-treat strategy
 ◦ Positive

18.  ▪ H. pylori eradication therapy with
antibiotics and a PPI
 ▪ Continue acid suppression medication (i.e.,
PPIs) for 4–8 weeks.
 ◦ Negative:Trial of acid suppression
medication (i.e., PPIs) for 4–8 weeks,
followed by reevaluation
 • Failure of medical treatment : Consider
elective surgery

19.  Medical treatment of PUD
 Pharmacologic therapies for uncomplicated
PUD include a trial of acid suppression therapy
and, if H. pylori is detected, eradication therapy.
These may be complemented with antacids for
rapid symptom relief, and in some cases with
cytoprotective agents for mucosal protection.
All patients should also be counseled on lifestyle
and risk factor modification.

20.  • Acid suppression medications and antacids are
covered in detail in “Treatment of dyspepsia.”
 • Cytoprotective agents (gastrointestinal mucosal
protection)
 ◦ Sucralfate : a sucrose sulfate-aluminum complex
that reacts with HCl in an acidic environment to create
a protective barrier over the gastric/duodenal mucosa
 ▪ Acts as an acid buffer and promotes HCO3
production
 ▪ Should not be taken simultaneously with a PPI or H2
blocker
 ◦ Misoprostol

21.  Antibiotics: e.g., clarithromycin triple therapy
(combined with amoxicillin and a PPI). See “H.
pylori eradication therapy” for other treatment
regimens.
 • Nonpharmacological measures [1]
 ◦ Restrict alcohol, smoking, and caffeine, and
avoid stress.
 ◦ Avoid medications that may cause or worsen
PUD (e.g., discontinue NSAIDs, reduce or stop
corticosteroids if possible).
 ◦ Avoid eating before bedtime.

22.  Surgical management of uncomplicated
peptic ulcers is rarely necessary because they
usually respond well to medical treatment.
When malignancy is confirmed or
complications such as massive bleeding or
gastrointestinal perforation occur, surgery
specific to these complications must be
performed.

23.  Indications (consider after thorough evaluation)
 ◦ Refractory symptoms or recurrence of disease
despite appropriate medical treatment
 ◦ Diseases that require the continuation of
NSAIDs
 ◦ Inability to tolerate medical treatment
 • Surgical procedures
 ◦Vagotomy: surgical division of the anterior and
posterior vagal trunk of the vagus nerve (truncal
vagotomy), both located along the lower
esophagus

24.  Denervation through truncal vagotomy results in
∼ 70% reduction of acid production.
 ▪ Complications include delayed gastric
emptying, postvagotomy diarrhea ,
postvagotomy hypergastrinemia, and dumping
syndrome.
 ▪To improve results, truncal vagotomy is
combined with one of the following drainage
procedures:
 ▪Pyloroplasty
 ▪Antrectomy
 ▪Subtotal gastrectomy