Peptic Ulcer Disease and

Gastritis

Prof. Shorena Chumburidze MD, PhD

Peptic Ulcers:
Gastric & Dudodenal
PUD Demographics

 Higher prevalence in developing

countries

 H. Pylori is sometimes associated with

socioeconomic status and poor
hygiene
PUD Demographics

 In the US:

 Lifetime prevalence is ~10%.

 PUD affects ~4.5 million annually.
 Hospitalization rate is ~30 pts per 100,000
cases.
 Mortality rate has decreased dramatically in
the past 20 years
 Approximately 1 death per 100,000 cases
 2 most commonly diagnosed cause of
epigastric pain.

 Focal ulceration of stomach or duodenal

tissue

 In both types of peptic ulceration, gastric and

duodenal, there is an imbalance between
secretion and neutralization of secreted acid.
 Pain tends to occur after eating.

 With gastric ulcer it usually occurs briefly after

eating, with duodenal ulcers it tends to occur a
few hours after eating.

 You cannot differentiate between gastric and

duodenal Ulcer by symptoms alone .

 You have to scope to know definitively

Causes

 NSAIDs and Helicobacter pylori infection make

up majority of cases

 Head trauma (Cushing’s ulcer), burns (Curling’s

ulcer), mechanical ventilation, Crohn’s disease,
ZES

 All patients should be tested for H. Pylori

Comparing Duodenal
and Gastric Ulcers
Duodenal Ulcers

 Duodenal sites are 4x as common as gastric

sites

 most common in middle age

 peak 30-50 years

 Male to female ratio 4:1

 Genetic link: 3x more common in 1st degree

relatives
Duodenal Ulcers

 More common in patients with blood group O

 Associated with increased serum pepsinogen

 H. pylori infection common

 up to 95%
 Gastric Ulcers

 Common in late middle age

 Incidence increases with age

 Male to female ratio- 2:1

 More common in patients with blood group A

 Use of NSAIDs - associated with a three- to four-

fold increase in risk of gastric ulcer
Gastric Ulcers

 Less related to H. pylori than duodenal

ulcers – about 80%

 10 - 20% of patients with a gastric ulcer

have a concomitant duodenal ulcer
 Subjective Data
 Pain—”gnawing”, “aching”, or “burning”

 Duodenal ulcers: occurs 1-3 hours after a

meal and may awaken patient from
sleep. Pain is relieved by food, antacids,
or vomiting.

 Gastric ulcers: food may exacerbate the

pain while vomiting relieves it.
Subjective Data

 Nausea, vomiting, belching, dyspepsia,

bloating, chest discomfort, anorexia,
hematemesis, &/or melena may also
occur.

 Nausea, vomiting, & weight loss more

common with Gastric ulcers
Objective Data
 Epigastric tenderness

 Guaic-positive stool resulting from occult

blood loss

 Succussion splash resulting from scaring

or edema due to partial or complete
gastric outlet obstruction
Objective Data
 A succussion splash or gastric splash, describes the sound
obtained by shaking an individual who has free fluid and air
or gas in a hollow organ or body cavity.

 Usually elicited to confirm intestinal or pyloric obstruction.

 Done by gently shaking the abdomen by holding either side

of the pelvis.

 A positive test occurs when a splashing noise is heard,

either with or without a stethoscope.

 It is not valid if the pt has eaten or drunk fluid within the last
three hours.
Alarm symptoms

 Weight loss
 Anemia
 Heme+ stool or hematemesis
 Early satiety
 Odynophagia or dysphagia
 Older than age 45
 How should we test for H. pylori ?

 There are three comonly –used ways to test:

 Serology: Most sensitive

 Gastric biopsy: Most specific, but require

endoscopy

 Stooll antigen: checks for present infection.

This is a good to use if the pt does not respond to
therapy
How should we test for H. pylory ?

 The most accurate test for H.Pylori

infection is gastric biopsy
Diagnosis

 Patients w/o alarm symptoms should be

tested for H.Pylori with serology

 Pts w/alarm symptoms should receive

endoscopy

 Active bleeding should scoped right away

Treatment

 All patients should be given a PPI (i.e.

Omeprazole), pts who are test positive
for H. pylori should be given
clarithromycin and amoxicilin

 If patient is on NSAID, try to replace w/a

COX2 inhibitors (Celecoxib)
What if patients doesn’t respond to
treatment? H. pylori ulcer

 After 2 weeks if there is no improvement in sx or if

the sx recur, the pt should get endoscopy

 Antibiotic regimen should be changed

Alternative regimen:
 Metronidazole
 Tetracycline (and continue the PPI, of course)
 Bismuth can also be added, but not necessary
What if patients doesn’t respond to
treatment?

Non H. pylori (i.c. NSAID) ulcer

After 6-8 weeks if there is no

improvement in symptoms, pt should get
endoscopy
Do alcohol and tobacco
cause ulcers?

No, they delay healing

 Complications

 Perforation & Penetration—into pancreas,

liver and retroperitoneal space

 Peritonitis

 Bowel obstruction, Gastric outflow

obstruction, & Pyloric stenosis
 Complications

 Bleeding- occurs in 25% to 33% of cases

and accounts for 25% of ulcer deaths.

 Gastric CA
Complications of PUD

 Perforated ulcer: Pain is significantly

worse- progressive peritoneal pain
(generalized, very sensitive to touch,
movement, rebound tenderness),
abdominal distension, fever, shock

 This is a surgical emergency!!!

Complications of PUD

 If pt has a hx of PUD and presents w/

sudden peritoneal pain and bloating, the
best diagnostic step is to get an
abdominal film
(subdiaphragmatic air)

 Surgery will be performed immediately

thereafter given a positive dx
Complications of PUD
 Complications of PUD

 Gastric adenocarcinoma , MALT lymphoma

 Malignancy 3 % lifetime risk in patients w/

gastric ulcers

 Sx include failure to respond to treatment

 Dx: on biopsy
Complications of PUD

Gastric outlet obstruction: rare

Sx:
 Early satiety

 Weight loss

 Vomiting

 Dx: scope

 Tx: Surgical
 Gastritis

 # 3 most commonly diagnosed cause of

epigastric pain

 More generalized inflammation of the

stomach tissue

 Clinically very difficult to differentiate from

PUD
Gastritis

 Like PUD : often presents w/epigastric

pain, can be caused by all the same
things (especially NSAIDs and H.Pylori)

 Pts may have hematemesis or melena

 Gastritis

 Unlike PUD: may also be caused by EtOH,

tobacco, Vitamin B12 deficiency and
specific condition atrophic gastritis.

 Must be vary of all the same alarm sx.

 If present proceed to endoscopy

 Gastritis : Diagnosis

 First step for pts w/no alarm sx is to test for

H. Pylori (serology)

 Pts should also have CBC, CMP, B12 and

MMA (methylmalonic acid)
 Gastritis : treatment

Positive H. Pylori:
Start triple therapy (PPI, clarithromycin and
amoxicilin)

 Negative H. pylori: PPI

 Low B12 and /or high MMA: B12 replacement

 Anti- parietal cell antibodies: B12 replacement

 Gastritis due to B12 deficiency

 Gastritis caused by low B12 levels

 Hx: Malnutrition, alcoholism

 Sx: Epigastric pain, fatigue, pallor, reduced

peripheral vibratory sensation
 Gastritis due to B12 deficiency :
diagnosis

 B12 levels will be low

 MMA levels will be high
 Almost universally there will be a macrocytic
anemia (MCV>100),
 Negative antiparietal cell antibodies and
antiintrinsic factor antibodies

 Tx: B12 replacement

 Pernicious anemia

 Autoimmune gastritis

 Hx: FHX of pernicious anemia

 Sx: Epigastric pain, fatigue, pallor, reduced peripheral

vibratory sensation on px
 Pernicious anemia : diagnosis

 B12 levels will be low

 MMA level will be high
 Almost universally there will be a macrocytic anemia
(MCV>100)
 Hypochlorhydria (high gastrin)
 Positive anti- parietal cell antibodies and antiintrinsic factor
antibodies

 Tx: B12 replacement

 Atrophic gastritis

 The “ end-stage” of chronic gastritis

 Requires endoscopy and biopsy for dx

(decreases rugal folds)

 Chronic inflammatory damages the

parietal cells and therefore everything that
the parietal cells secrete will be reduced
 Atrophic gastritis

 Achlorhydria/ hydrochlorhydria: due to

decrease hydrochloric acid (HCL) secretion

 Low B12 levels : due to decrease intrinsic

factor secretion

 Increased risk of gastric carcinoma

Prevention

 Consider prophylactic therapy for the

following patients:

 Pts with NSAID-induced ulcers who

require daily NSAID therapy

 Pts older than 60 years

Prevention

 Pts with a history of PUD or a

complication such as GI bleeding

 Pts taking steroids or anticoagulants or

patients with significant comorbid
medical illnesses
 Prevention

 Prophylactic regimens that have been shown to

dramatically reduce the risk of NSAID-induced
gastric and duodenal ulcers include the use of a
prostaglandin analogue or a proton pump
inhibitor.

 Misoprostol (Cytotec) 100-200 mcg PO 4 times

per day
 Omeprazole (Prilosec) 20-40 mg PO every day
 Lansoprazole (Prevacid) 15-30 mg PO every
day
 Surgery
 People who do not respond to medication, or
who develop complications:

 Vagotomy - cutting the vagus nerve to

interrupt messages sent from the brain to the
stomach to reducing acid secretion.

 Antrectomy - remove the lower part of the

stomach (antrum), which produces a hormone
that stimulates the stomach to secrete
digestive juices. A vagotomy is usually done in
conjunction with an antrectomy.
 Surgery

 Pyloroplasty - the opening into the

duodenum and small intestine (pylorus)
are enlarged, enabling contents to pass
more freely from the stomach. May be
performed along with a vagotomy.
Evaluation/Follow-up/Referrals

 H. Pylori Positive: retesting for tx efficacy

 Ureabreath test: no sooner than 4

weeks after therapy to avoid false
negative results

 Stool
antigen test: an 8 weeks interval
must be allowed after therapy.
Evaluation/Follow-up/Referrals

 H. Pylori Negative:

 Evaluate symptoms after one month.

 Patients who are controlled should cont. 2-4

more weeks.

 If symptoms persist then refer to specialist for

additional diagnostic testing.
Question 1

 A 31- year –old male presents to the clinic

complaining of substernal pain that comes and
goes, and has been happening over the four
months.

 He notes it gets worse after meals. It is

sometimes associated with a sour, metallic
taste in his breath.

 He’s attempted over-the-counter drug (OTC)

antacids but to no avail .
Question 1

 He does eat before bed and denies

alcohol and tobacco use.

 He denies difficulty swallowing, weight

loss or blood in the vomit.

 His physical exam is unremarkable.

Question 1

 Which of the following would be the next step in

the management of this patient

 A. Calcium carbonate
 B. Omeprazole
 C. ECG
 D. CT scan of chest
 E. Esophagogastroduodenoscopy (EGD)
Question 2
 A 31- year –old male presents to the clinic
complaining of substernal pain that comes and
goes, and has been happening over the four
months.

 He notes it gets worse after meals. It is sometimes

associated with a sour, metallic taste in his breath.

 He’s attempted OTC antacids but to no avail .

 He does eat before bed and denies alcohol and

tobacco use.
Question 2

 He denies difficulty swallowing, weight loss or

blood in the vomit.

 His physical exam is unremarkable, however

he has lost 5 pounds in the past month
 Question 2
 Which of the following would be the next step in
the management of this patient

 A. Calcium carbonate
 B. Omeprazole
 C. ECG
 D. Barium swallow
 E. Esophagogastroduodenoscopy ( EGD)
Question 3
 A 52 - year -old woman complains of
substernal pain. The pain is well localized, non-
radiating, and is rated as +7/10

 She says that “a glass of milk or some bread”

help the pain, but it will come back an hour or
two.

 Her medical history includes emphysema,

obesity and osteoarthritis of the knees.
Question 3

 On physical exam, there is mild epigastric

abdominal tenderness, rales bilaterally, but
otherwise unremarkable.

 EGD reveals a 0.5 cm duodenal ulcer.

Serologic testing for H. Pylori returns positive
 Question 3
 Which of the following would be the next step in
the management of this patient

 A. Metronidazole, tetracycline and omeprazole

 B. Metronidazole, amoxicillin and bismut
 C. Clarithromycin, amoxicillin and omeprazole
 D. Clarithromycin, metronidazole and
omeprazole
 E. Metronidazole, clarithromycin and bismut