GASTRITIS

Gastritis
Gastritis adalah peradangan pada mukosa
lambung.
Gastropathy: kerusakan epitel atau endotel
lambung tanpa peradangan (inflamasi)
Tiga tipe dasar gastritis :
Akut (erosif/ hemorrhagik)
Non-erosif, Non-spesifik/kronik
Bentuk-bentuk khusus
 Gastritis akut
(Erosif/Hemorrhagik)
Umumnya disebabkan oleh
NSAIDS gastric injury by diminishing
prostaglandin production in stomach and
duodenum
Alcohol use is the leading cause of gastritis
Stress from CNS injury burns, sepsis, surgery
Portal hypertension (portal gastropathy)
Other causes:
Caustic ingestion
radiation
 Chronic Gastritis
Nonerosive/nonspecific
Infectious gastritis Type B: H Pylori
Involves antrum and body of stomach
majority of patients asymptomatic
Strong association with PUD
2 to 6 fold risks of gastric adenocarcinoma and also gastric
lymphoma
Autoimmune gastritis Type A: Pernicious anemia
Body and fundus, It usually spares the antrum & affects the
parietal cells.
Pernicious anemia caused by impaired absorption of vitamin
B-12 occurs due to lack of intrinsic factor from parietal cells
and decrease in acid production
Increased risk of adenocarcinoma
Special forms of Gastritis
Infectious (Phlegmonous or necrotizing gastritis)
Emergency gastric resection, and Abx therapy
CMV, candidal (fungal) in immunocompromised pts
Larvae ingestion requires endoscopic removal
Eosinophilic Gastritis
Giant Cell (Menetriers disease) (Hypertrophic Gastropathy)
only found on biopsy
Lymphocytic Gastritis
Granulomatous Gastritis
Tuberculosis
Syphilis
Fungal
Sarcoid
Crohns
Gastritis Symptoms

Clinical features of gastritis generally reflects the underlying syndrome

rather than the gastric injury itself
Acute:
Dyspepsia and abdominal pain are common indicators of gastritis
Mild epigastric discomfort
Occasional nausea and vomitus
Headache, excessive salivation, flatus

Chronic:
Non specific symptoms c/ chronic abdominal discomfort

Key signs: (usually none)

Hematemesis, bloody nasogastric aspirate
Abdominal tenderness
Bloating
Emesis
Gastritis
Lab:
Endoscopy c/ biopsy is the gold standard
A urea breath test can be used to detect HP
Specific test for underlying conditions (e.g) B12 and CBC for
pernicious anemia

Differential Diagnosis:
1. Peptic ulcer 2. Gastroparesis
3. Gastric carcinoma 4. GERD
5. Pancreatitis 6. Lymphoma

Treatment: (same as duodenal ulcers)

Remove irritant
Treat for H pylori
Antacids & H2 blockers
Avoid smoking & alcohol
Peptic Ulcer Disease

PUD describes any ulcer of the upper

digestive tract (stomach and duodenum)
Break in the duodenal or gastric mucosa
extending through the musularis mucosae,
and are usually 5mm-1cm.
Zollinger-Ellison Syndrome

Ulcers-associated with
the Zollinger-Ellison
(ZE) Syndrome (#3) are
caused by gastrin-
releasing islet cell
tumors (gastrinomas),
& are also considered a
form of peptic ulcer.
Zollinger-Ellison Syndrome

A tumor of the pancreas that secretes gastrin (Gastrinoma)

Usually found in head of pancreas but can also be found in

duodenum, liver & lung

75-80% of ulcers produced develop in the duodenal bulb

Suspect in any patient with:

Multiple or recurring duodenal ulcers
Post bulbar or jejunal ulcers
Ulcers associated with diarrhea
Elevated serum gastrin levels
Usually only tested when suspect ZE syndrome
Peptic Ulcer Disease (PUD)

Men 1.3 : 1 Women

Most commonly occur in:

#1 Duodenum (Duodenal)
#2 Stomach (Gastric)
Esophagus
Gastroenteric anastomoses
Meckels Diverticulum
Peptic Ulcer Disease (PUD)

The spectrum of the disease is broad from mild

mucosal injury to frank ulcerations.
Symptoms vary and are not related to the severity
of tissue damage.
1-2% of population have an ulcer at the present
time
10% of population will have ulcer in their lifetime
Gastric and Duodenal ulcers tend to recur in the
same location.
Recurrent hemorrhage occurs in 50% of patients
who have had a prior bleed.
 Duodenal Ulcer vs. Gastric Ulcer

Duodenal Gastric
Increased acid production Normal or decreased acid
production
Decreased mucosal
resistance
H. pylori
H. pylori
NSAIDS
relieved by food &
typically awakens patient worsened by food
around 1:00am
Duodenal Ulcer vs. Gastric Ulcer
Duodenal Gastric
Onset more common age 25 to 55 Onset more common age 40
never malignant to 70

mostly located in the duodenal Benign more likely @ lesser

bulb or immediately post bulbar. curvature/ antrum
Ulcers distal to the duodenal bulb
should raise suspicion for Gastric ulcers are more
Zollinger-Ellison Syndrome (also c/ common @ lesser curvature
multiple frequently occurring
duodenal ulcers.)
Malignancies more likely @
greater curvature
Men 2:1 Women
Duodenal 5 times more common 1-3% occur in carcinomas
than gastric

60-80% have recurrence within

one year.
 Etiologies of Peptic Ulcer Disease

1. Helicobacter pylori (H. pylori) infection: (#1 cause)

a. Associated with 70-95% of Peptic ulcers.
b. Treatment of H. pylori improves healing rate &
markedly decreases the recurrence rate.
2. NSAIDS: (#2 cause) (inhibit prostaglandins which
normally stimulate production of mucous secretions &
bicarb.)
a. May cause gastric or duodenal ulcers (steroids also)
b. Accounts for the majority of non H. pylori ulcers
Etiologies of Peptic Ulcer Disease
3. Hypersecretion states: (#3 although uncommon)
a. Gastrinomas (Zollinger-Ellison Syndrome)
b. Multiple endocrine neoplasia (MEN-1)
c. Systemic mastocytosis (mast cells infiltrate intestinal
wall, release histamine- stimulates acid. Symptoms are
diarrhea, flushing, urticaria. Histamine in blood.
Confirmed by biopsy.)
4. Stress: physiologic stress (eg. burns, surgery, & severe
medical conditions)
5. Rare causes: viral, radiation, vascular insuff.

6. Diseases assoc. with peptic ulcers:

Cirrhosis, renal failure, pulmonary diseases.
Any patient with systemic ds. (COPD, renal failure, cirrhosis
of liver) are prone to ulcers so should be started on H2
blockers.
The pathogenesis of PUD is related to the
imbalance between normal protective factors
and injurious factors
No Ulcer
Normal

Ulcer

Defensive forces
VS Mucus
Aggressive forces
Bicarb
Gastric acid
Prostaglandins
Digestive enzymes
Epithelial
regeneration
Ulcers result from:

1. Increased aggression
H. pylori infection
NSAIDS
Cigarettes
Etc
Or

2. Impaired Defense
Ischemia
Prostaglandin Inhibition (NSAIDS)
Delayed gastric emptying
PEPTIC ULCER DISEASE

ADVERSE EFFECTS OF SMOKING

1. Interferes c/ action of H2 antagonists
2. Increases rate of gastric emptying
3. Increases duodenogastric reflux
4. Decreases pancreatic bicarb secretion
5. Decreases mucosal blood flow
6. Depresses gastric mucosal prostaglandin synthesis
HELICOBACTER pylori
Helicobacter pylori (H. pylori) is a gram
negative spiral-shaped bacillus found in
the gastric mucous layer or adherent to
the epithelial lining of the stomach.

H. pylori causes more than 90% of

duodenal ulcers and up to 80% of gastric
ulcers.
Helicobacter pylori

It is not known how H. pylori is transmitted or why

some patients become symptomatic while others
do not.

The bacteria are most likely spread from person to

person through fecal-oral or oral-oral routes.

Possible environmental reservoirs include:

contaminated water sources
Iatrogenic spread through contaminated endoscopes has
been documented but can be prevented
 Helicobacter pylori :
Prevention
Since the source of H. pylori is not yet known,
recommendations for avoiding infection have not
been made.
In general, it is always wise for persons to wash hands
thoroughly, to eat food that has been properly
prepared, and to drink water from a safe, clean source.
H. pylori infection

Before this bacterium was discovered, spicy food,

acid, stress, and lifestyle were considered the major
causes of ulcers.

The majority of patients were given long-term

medications, such as H2 blockers, and more
recently, proton pump inhibitors, without a chance
for permanent cure.

These medications relieve ulcer-related symptoms,

heal gastric mucosal inflammation, and may heal
the ulcer, but they do NOT treat the infection.
H. Pylori infection

When acid suppression is removed, the majority of

ulcers, particularly those caused by H. pylori, recur.

Since we now know that most ulcers are caused by

H. pylori, appropriate antibiotic regimens can
successfully eradicate the infection in most
patients, with complete resolution of mucosal
inflammation and a minimal chance for recurrence
of ulcers.
H. Pylori infection
Most persons who are infected with H. pylori never suffer
any symptoms related to the infection; however, H. pylori
causes chronic active, chronic persistent, and atrophic
gastritis in adults and children.

Infection with H. pylori also causes duodenal and gastric

ulcers. Infected persons have a 2- to 6-fold increased risk of
developing gastric cancer and mucosal-associated-
lymphoid-type (MALT) lymphoma compared with their
uninfected counterparts.

The role of H. pylori in non-ulcer dyspepsia remains unclear.

Peptic Ulcer Disease Symptoms
Epigastric Pain Heartburn
Burning
Chest Discomfort
Occurs 1-3 hrs p/ meals
Anorexia
Relieved by food
Weight loss
In gastric ulcers (also in
May occur @ night pancreatic ds.)
May radiate to back or Weight gain
shoulders if perforated In duodenal ulcers
Nausea Hematemesis or melena
Due to GI bleeding
Vomiting If severe = hematochezia
May be related to partial or
complete gastric outlet
obstruction
Dyspepsia
Belching/ Bloating
Who should be tested and
treated for H. pylori ?
Persons with active gastric or duodenal ulcers or
documented history of ulcers should be tested
for H. pylori, and if found to be infected, they
should be treated.

To date, there has been no conclusive evidence

that treatment of H. pylori infection in patients
with non-ulcer dyspepsia is warranted.
H.pylori diagnostic examinations

Serological tests that measure specific H. pylori IgG antibodies

can determine if a person has been infected.
The sensitivity and specificity of these assays around 80%
Fecal Antigen Assay
Urea Breath test
In this test, the patient is given either 13C- or 14C-labeled urea to drink.
H. pylori metabolizes the urea rapidly, and the labeled carbon is
absorbed.
This labeled carbon can then be measured as CO2 in the patient's
expired breath to determine whether H. pylori is present.
The sensitivity and specificity of the breath test ranges from 94% to
98%.
PPIs can give false negative results
Diagnosis H. Pylori in Peptic
Ulcer Disease
Upper endoscopy
(esophagogastroduodenal) is considered
the reference method of diagnosis.
 Peptic Ulcer Disease : Treatment
Non-Pharmacological
Diet change is of no value
Smoking Cessation
Smoking delays healing
DC medications that enhance the progression
NSAIDS
Pharmacological Therapy
Inhibit secretion of acid
Neutralizing gastric acids
Augmentation of protection of mucosa
Antibiotics prn
Maintenance Therapy
Prevention c/ colloid bismuth
Bedtime dosage of H2 blockers
 Peptic Ulcer Disease : Treatment
Non-Pharmacological
Diet change is of no value
Smoking Cessation
Smoking delays healing
DC medications that enhance the progression
NSAIDS
Pharmacological Therapy
Inhibit secretion of acid
Neutralizing gastric acids
Augmentation of protection of mucosa
Antibiotics prn
Maintenance Therapy
Prevention c/ colloid bismuth
Bedtime dosage of H2 blockers
Peptic Ulcer Disease : Treatment

Pharmacological Therapy
Inhibition of acid
H2 blockers
Antacids
Proton pump inhibitors
Anticholinergics
Prostaglandins
Augmentation protection
 Peptic Ulcer Disease : Treatment

Antacids (magnesium, aluminum, & calcium based)

cause diarrhea

Moderate to high doses of H2 blockers result in improved healing

rates
Used 1 hr PC & HS for 6-8 wks
Side effects:
Hypermagnesemia (careful in renal patients)
Aluminum causes phosphate depletion & osteoporosis
Sodium overload in CHF
Hypercalcium causing Milk alkali syndrome
Inhibits absorption of antibiotics, digoxin, warfarin
Peptic Ulcer Disease : Treatment

Proton Pump Inhibitors:

Inhibit the H,K-ATPase pump
Healing rate 80-100%
Omeprazole, lansoprazole, rabeprazole, pantoprazole,
meromeprazole

Anticholinergics: reduce acid by 50% and cause blurred

vision
pupil dilation, consider patients occupation or driving
restriction
Peptic Ulcer Disease : Treatment

Prostaglandins (Do not use in pregnancy)

Inhibit the parietal cell cyclic AMP function in response to
histamine
Healing rate are equal to H2 blockers
Primary role is to be used as a prophylactic agent to
prevent NSAID induced ulcers. Not used as a primary
therapy
Misoprostol (Cytotec)
Sucralfate : its action is unknown
It forms a viscous shield over the mucosa
Absorbs bile & pepsin
 Peptic Ulcer Disease :
Treatment Regiment for H. pylori
Current therapy for H. pylori infection consists of 10 days to 2
weeks of one or two effective antibiotics,
amoxicillin,
tetracycline
not to be used for children <12 yrs
metronidazole, or
clarithromycin,

Plus either
ranitidine bismuth citrate (H2 blocker),
bismuth subsalicylate (pepto-bismol),
or proton pump inhibitor.
Peptic Ulcer Disease :
Treatment Regiment for H. pylori

Acid suppression by the H2 blocker or proton pump

inhibitor in conjunction with the antibiotics helps
alleviate ulcer-related symptoms (i.e., abdominal
pain, nausea),
helps heal gastric mucosal inflammation,
and may enhance efficacy of the antibiotics
against H. pylori at the gastric mucosal surface.
Peptic Ulcer Disease :
Treatment Regiment for H. pylori
Currently, eight H. pylori treatment regimens are
approved by the Food and Drug Administration (FDA);
however, several other combinations have been used
successfully.
Antibiotic resistance and patient noncompliance are
the two major reasons for treatment failure.

Overall, triple therapy regimens have shown better

eradication rates than dual therapy. Longer length of
treatment (14 days versus 10 days) results in better
eradication rates.
Peptic Ulcer Disease :
Treatment Regiment for H. pylori
(FDA Approved)
1. Omeprazole 40 mg QD + clarithromycin 500 mg TID x 2
wks, then omeprazole 20 mg QD x 2 wks - OR
2. Ranitidine bismuth citrate (RBC) 400 mg BID +
clarithromycin 500 mg TID x 2 wks, then RBC 400 mg BID x
2 wks OR
3. Bismuth subsalicylate 525 mg QID + metronidazole 250 mg
QID + tetracycline 500 mg QID* x 2 wks + H2 receptor
antagonist therapy as directed x 4 wks OR
4. Lansoprazole 30 mg BID + amoxicillin 1 g BID +
clarithromycin 500 mg TID x 10 days OR
Peptic Ulcer Disease :
Treatment Regiment for H. pylori
(FDA Approved)

5. Lansoprazole 30 mg TID + amoxicillin 1 g TID x 2 wks OR

6. Rantidine bismuth citrate 400 mg BID + clarithromycin 500

mg BID x 2 wks, then RBC 400 mg BID x 2 wks OR

7. Omeprazole 20 mg BID + clarithromycin 500 mg BID +

amoxicillin 1 g BID x 10 days OR

8. Lansoprazole 30 mg BID + clarithromycin 500 mg BID +

amoxicillin 1 g BID x 10 days
Long-term consequences of H.
pylori infection?
Recent studies have shown an association between
long-term infection with H. pylori and the
development of gastric cancer.

Gastric cancer is the second most common cancer

worldwide; it is most common in countries such as
Colombia and China, where H. pylori infects over
half the population in early childhood.

In the United States, where H. pylori is less common

in young people, gastric cancer rates have
decreased.
Terima Kasih,
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