Problem 2

Devin Alexander
405160054
LI I
Anatomy of gaster
Gaster
 dilated, saclike portion of the GI tract that exhibits significant
variation in size and configuration
 terminating at the thick, smooth muscle sphincter (pyloric sphincter)
by joining the first portion of the duodenum.
 tethered superiorly by the lesser omentum
 extending from its lesser curvature and is attached along its greater
curvature to the greater omentum and the gastrosplenic ligament
 J-shaped stomach is divided into the following regions:
 Cardiac region
 Fundus
 Body
 Pyloric region (antrum and canal)
 interior of the unstretched stomach is lined with prominent longitudinal mucosal
gastric folds called rugae
Source : netter’s
clinical anatomy 3ed
 Gaster blood supply

https://
link.springer.com/
chapter/10.1007/9
78-3-642-11202-7_
Duodenum
 is the first portion of the small intestine
 descriptively is divided into four part.
 Most of the C-shaped vduodenum is retroperitoneal
 ends at the duodenojejunal flexure, where it is tethered by a
musculoperitoneal fold called suspensory ligament of the duodenum
(ligament of Treitz)
Source : sobotta
atlas anatomi
manusia 23th ed.
Source : netter’s
clinical anatomy 3ed
Duodenum blood supply

https://anatomy
.co.uk/duodenu
m
/
Histology of gaster
 Fundus
& body

source: Eroschenko, Victor P. Difiore’s atlas of

histology with functional correlations. 11th edition.
Philadelphia: Lippincott Williams & Wilkins. 2008.
 Gaster mucosa

source: Eroschenko, Victor P. Difiore’s atlas of

histology with functional correlations. 11th edition.
Philadelphia: Lippincott Williams & Wilkins. 2008.
 Pyloric
region

source: Eroschenko, Victor P. Difiore’s atlas of

histology with functional correlations. 11th edition.
Philadelphia: Lippincott Williams & Wilkins. 2008.
Pyloric-
duodenal
junction

source: Eroschenko, Victor P. Difiore’s atlas

of histology with functional correlations.
11th edition. Philadelphia: Lippincott
Duodenum
Physiology of gaster
& duodenum
Source : lauralee, S. Fisiologi
manusia: dari sel ke sistem.6th ed.
Mechanism of H & Cl ions
secretion
 Function of HCl:
 Activate pepsiongen  pepsin
 Aids breakdown of connective tissue &
muscle fibers, reducing food into
smaller particles
 Denaturates protein
 Along with lysozyme  kills
microorganism

Source : lauralee, S. Fisiologi manusia:

dari sel ke sistem.8th ed.
Source : lauralee, S. Fisiologi
manusia: dari sel ke sistem.6th ed.
Carbohydra
te digestion

Source : lauralee, S. Fisiologi

manusia: dari sel ke sistem.6th ed.
Protein
digestion

Source : lauralee, S. Fisiologi

manusia: dari sel ke sistem.6th ed.
Lipid
digestion

Source : lauralee, S. Fisiologi

manusia: dari sel ke sistem.6th ed.
LI 2
biochemistry of
gaster & duodenum
Pancreas

Source : lauralee, S. Fisiologi manusia:

dari sel ke sistem.6th ed.
Bile

Source : lauralee, S. Fisiologi manusia:

dari sel ke sistem.6th ed.
LI 3
dyspepsia
terminology
Epigastric pain
 name for pain or discomfort right below ribs in the area of upper
abdomen
 often happens alongside other common symptoms of digestive system
 These symptoms can include heartburn, bloating, and gas.
 Epigastric pain isn’t always cause for concern. This condition has
many possible causes, especially when it happens right after eating.
Abdominal bloating
 occurs when the gastrointestinal (GI) tract is filled with air or gas
 Most people describe bloating as feeling full, tight, or swollen in the abdomen
 one of the most common gastrointestinal (GI) symptoms, which is a frequent
complaint in the patients of all ages
 possible causes of bloating are various and complicated, thus intestinal gas
production and transit, gut microflora and hypersensitivity of the patient's gut
might be the factors for the symptom generation
 Bloating is often accompanied by:

1. pain
2. excessive gas (flatulence)
https://www.ncbi.nlm.ni
3. frequent burping or belching h.gov/pmc/articles/PMC
3816178
4. abdominal rumbling or gurgles /
 Other causes of bloating may be due to medical conditions. These
include:
1. irritable bowel syndrome (IBS)
2. inflammatory bowel disease, such as ulcerative colitis or Crohn’s disease
3. other functional gastrointestinal disorders (FGIDs)
4. heartburn
5. food intolerance
Belching
 Belching is the act of expelling air from the stomach through the mouth
 It usually occurs when the stomach distends, or expands because of too much
swallowed air
 Belching releases the air to reduce the distention. Other names for belching include
burping and eructation
 There are a number of reasons why more air than normal may be swallowed. The
most common reasons are:
1. eating or drinking too quickly
2. drinking carbonated drinks
3. anxiety
 Some foods and drinks can also cause more frequent belching. These
include carbonated drinks, alcohol, and foods high in starch, sugar, or
fiber that cause gas. Common culprits include:
1. beans
2. lentils
3. broccoli
4. peas
5. onions
6. cabbage
7. cauliflower
Nausea
 Nausea is pronounced stomach discomfort and the sensation of wanting to vomit.
Nausea can be a precursor to vomiting the contents of the stomach. The condition
has many causes and can often be prevented.
 Common causes of nausea are described below.
 Heartburn or gastroesophageal reflux disease (GERD)  burning sensation  nausea
 Infection  food poisoning, bacterial/virus infection
 Medications  chemotherapy
 Motion sickness and seasickness
 Diet  spicy/ high-fat food, food allergic
 Ulcer
Vomitting
 forcible voluntary or involuntary emptying ("throwing up") of stomach contents
through the mouth
 not diseases, but symptoms of many conditions such as:

1. Motion sickness or seasickness

2. Early stages of pregnancy (nausea occurs in approximately 50%-90% of all
pregnancies; vomiting in 25%-55%)
3. Medication-induced vomiting
4. Intense pain

 The causes of vomiting differ according to age. For children, it is common for
vomiting to occur from a viral infection, food poisoning, milk allergy, motion
sickness, overeating or feeding, coughing, or blocked intestines and illnesses in
which the child has a high fever.
 the timing of the nausea or vomiting can indicate the cause. When
appearing shortly after a meal, nausea or vomiting may be caused by
food poisoning, gastritis (inflammation of the stomach lining), an
ulcer, or bulimia. Nausea or vomiting one to eight hours after a meal
may also indicate food poisoning. However, certain food- borne
bacteria, such as salmonella, can take longer to produce symptoms.
 harmless, but it can be a sign of a more serious illness.
Regurgitation & heartburn
 the sensation of acid backing up into throat or mouth.
 Regurgitation can produce a sour or bitter taste
 may experience a "wet burp" or even vomit some contents of your
stomach

 Heartburn
 Heartburn is an irritation of the esophagus
 discomfort in upper belly or below breastbone
 heartburn has nothing to do with the heart.
 Heartburn symptoms can start up because of a problem with a muscular valve called
the lower esophageal sphincter (LES)
 Normally, with the help of gravity, the LES keeps stomach acid right where it should
be
 When it's working right, the LES opens to allow food into stomach or belching then
closes again.
 But if the LES opens too often or doesn't close tightly enough, stomach acid can
seep into the esophagus and cause a burning sensation.
 Stress and lack of sleep can raise much acid in stomach  heartburn.
 Pregnant  progesterone can relax LES  heartburn
 Smoking also relaxes the LES and increases stomach acid.
LI 4
dyspepsia & GERD
pathophysiology
Functional dyspepsia
 Is usually indicates abdominal discomfort or pain with no obvious
organic cause that could be identified by endoscopy
 when a diagnosis of FD has been made, it means a number of
investigations were performed including upper gastrointestinal
endoscopy, and were found to be normal.
 Patients with dyspepsia have reduced health-related quality of life
because their symptoms like particularly abdominal pain and
indigestion can cause emotional distress, problems with food and drink.
 it may be more impaired in patients with FD than in patients with other
conditions who present for upper endoscopy 
ETIOLOGY
 Motility
 The abnormalities range from delayed to accelerated gastric emptying, abnormal antral and
fundic contractions, and accommodation issues in the fundus and antrum
 Delayed gastric emptying of solids was associated with postprandial fullness and vomiting

 Acid exposure
 might be hypersensitivity to normal acid secretion

 Food intolerance
 suggests a hypersensitivity 

 Central nervous system-stimulus processing

 Related with familial aggregation, sleep dysfunction, somatization, and anxiety.
 common triggers which may initiate pathologic cycle processes involving gastrointestinal
system
DIAGNOSTIC CRITERIA
 http://www.hopkinsmedicine.org

GERD
GERD
is an esophageal mucosal injury that occurs secondary to retrograde 
movement of gastric  content into the esophagus.
epidemiology
GERD occurs in all age groups. The prevalence of GERD increases in
people older than 40 years.
ETIOLOGY
 Poor/abnormal LES function
 short LES (the shorter the LES the lower the tonus)
 Hormonal factors (during pregnancy increase in progesterone causes decreased
LES tonus)
 hiatal hernia
 Consumption of drugs(antikolinergik, beta adrenergik, theofilin, opiat, etc)
 Poor esophageal clearance
 common in elderly population or in patients with achalasia, stroke, or collagen
vascular disease such as scleroderma.
 Delayed gastric emptying
 due to anatomic obstruction of the gastric outlet as seen in pyloric stenosis
PATHOPHYSIOLOGY
 The esophagus,LES, and
stomach can be envioned as a
simple plumbing circuit who
work together.
 The abnormalities that
contribute to GERD can stem
from any component of the
system.
1. Poor esophageal motility
decreases clearance of acidic
material.
2. A dysfunctional LES allows reflux
of large amounts of gastric
http://www.medscape.org
juice.
3. Delayed gastric emptying can
increase the volume and
SIGN & SYMPTOM
 The
most typical symptoms of
GERD(Intra esofageal)
Heartburn
Regurgitation
Disphagia

 Abnormal reflux can cause atypical

(extraesophageal)
Coughing and/or wheezing
Hoarseness, sore throat
Otitis media
Noncardiac chest pain
Enamel erosion or other dental
manifestations http://www.medscape.org
DIAGNOSIS
1. Upper gastrointestinal endoscopy
 Upper endoscopy is the first diagnostic test in the 
evaluation  of  GERD
 Evaluate Microscopic changes of the esophageal
mucosa and Eliminating other pathological conditions
that can cause gerd
 If not found Mucosa Break  NERD (Non Erosive
Reflux disease)
2. Barium Esophagram

http://www.hopkinsmedicine.org
3. PH Monitoring
also called 24-hour pH studies. It
provides information on the severity
and pattern of reflux. The information
is helpful both to confirm the
impression of reflux and to tailor
therapy for the individual patient .

Ph below 4 at a distance of 5 cm
above LES  GERD

http://www.hopkinsmedicine.org
4. PPI test.
Is an empirical therapy to assess GERD symptoms by providing high-
dose PPI for 1- 2 weeks pending the respons. Done when there is no
endoscopic modality,Ph metry etc.
 Avoid large meals.

GERD Avoid acidic foods (citrus- and tomato-

based products), alcohol, caffeinated
beverages, chocolate, onions, garlic, and
peppermint.
Therapeutic Management Decrease dietary fat intake.

Avoid lying down within three to four hours

after a meal.
 Lifestyle modifications
Avoid medications that may potentiate
GERD symptoms, including calcium
channel blockers, beta agonists, alpha-
adrenergic agonists, theophylline, nitrates,
and some sedatives.

Elevate the head of the bed 10 to 20 cm (4

to 8 inches).

Avoid wearing clothing that is tight around

the waist.
Lose weight.
Stop smoking.
GERD Therapetic Management
DRUGS
Drug Farmakokinetik
Antacid  neutralize acid or acidic food without affecting subsequent acid 
secretion. Control mild to moderate symptoms. Given2 hours after
meals and every will sleep.
Dosage: 4 x 1 tablespoon.
Antagonis Receptor H2  block  histamine-stimulated  acid  secretion.inhibit interaction of
(Ranitidine,Cimetidine,Famoti histamine at the H 2 receptors  work directly to inhibit acid scretion.
dine) Raitidine :4 x 150 mg
Simetidine :2x 800 mg or 4x 400mg
Faamotidine : 2 x 20mg
Nizatidine : 2x 150 mg
Prokinetik drugs that enhance motor activity of the smooth muscle (characteristic
(Metoclopramide) of GI tract). Increase the pressure of les and lower the reflux of gastric
contents. This drug serves to accelerate the gastric empty
Metoclopramide : 3 x10 mg
Domperidone : 3 x 10-20mg
Cisapride : 3 x10 mg
PPI (Proton Pump Inhibitor) Are drugs that block the final common pathway of acid secretion. PPIs
DOC block the effects of all three major pathways
(Omeprazole) (histamine, acetylcholine, and gastrin) for acid stimulation.
Omeprazole: 2 x 20 mg
Lansoprazole : 2x 30mg
Pantoprazole : 2 x40 mg
Rabe prazole :2x10 mg
Esomeprazole :2x40 mg
Main etiology of
Dyspepsia & GERD
Adult
Corrosive lesion of esophagus
 Injury to the oesophageal mucosa secondary to ingestion of strong acids or
bases, often with suicidal intent in adults, or accidental in children;
 with time, such injuries may evolve to strictures
 These injuries are still increasing in developing countries, related to the social,
economic, and educational variables and mainly to a lack of prevention

 Epidemiology
 Worldwide, children represent 80% of the ingestion injury population
globally, primarily due to accidental ingestion. In contrast, ingestion in
adults is more often suicidal in intent, and is frequently life-threatening .
 Pathophysiology
Ingested acid/ alkali  Acids and alkalis produce different types of tissue
damage  Injury occurs quickly, depending on the agent’s concentration
and time of exposure  alkali ingestion may lead to more serious injury and
complications, Likewise, ingestion of a strong acid  associated with a
higher incidence of systemic complications (renal failure, liver dysfunction)
Acid  coagulation necrosis, with eschar formation that may limit
substance penetration and injury depth
Alkali  combine with tissue proteins  cause liquefactive necrosis and
saponification  penetrate deeper into tissues, helped by a higher viscosity
and a longer contact time through the esophagus  alkali absorption leads
to thrombosis in blood vessels, impeding blood flow to already damaged
tissue
Esophageal injury begins within minutes and may persist for hours
marked by eosinophilic necrosis with swelling and hemorrhagic
congestion  Four to 7 d after ingestion  mucosal sloughing and
bacterial invasion  granulation tissue appears, and ulcers become
covered by fibrin  Fibroblasts appear at the injury site around day 4
day 5 “esophageal mold’’ is formed (dead cells and secretions) 
repair usually begins on the 10th day after ingestion

Scar retraction  third week and may continue for several months 
lower esophageal sphincter pressure becomes impaired, leading to
increased gastroesophageal reflux (GER)
 Clinical features
1. difficult to swallow
2. Hoarseness and stridor  laryngeal or epiglottic involvement
3. epigastric pain and bleeding
4. Burn sensation on the neck
5. esophageal or gastric perforations  occur any time during the first
2 wk after ingestion
 Diagnosis approach
 Plain chest radiography
1. Plain chest radiography may show gas shadow in the mediastinum or below the
diaphragm suggesting esophageal or gastric perforation, respectively

 USG  used to evaluate the esophageal wall

 Endoscopy

1. important and highly recommended diagnostic tool in the evaluation of caustic

injury especially during the first 12 to 48 h of caustic ingestion
2. findings of extensive damage and necrosis
Zargar classification Description
Grade 0 Normal mucosa
Grade I Edema and erythema of the mucosa
Grade IIA Hemorrhage, erosions, blisters, superficial
ulcers
Grade IIB Circumferential lesions
Grade IIIA Focal deep gray or brownish-black ulcers
Grade IIIB Extensive deep gray or brownish-black ulcers
Grade IV Perforation
 A: Zargar Grade 0: Normal mucosa;
 B: Zargar Grade I: Edema and
erythema of the mucosa;
 C: Zargar Grade IIA: Hemorrhage,
erosions, blisters, superficial
ulcers;
 D: Zargar Grade IIB:
Circumferential bleeding, ulcers.
Exudates;
 E: Zargar Grade IIIB: Focal necrosis,
deep gray or brownish black ulcers;
 F: Zargar Grade IIIB: Extensive
necrosis, deep gray or brownish
black ulcers.

Source: https
://www.ncbi.nlm.nih.gov/pmc/articl
es/PMC5421115
Treatment
 includes immediate
resuscitation and evaluation
of extent of damage

 ENDOSCOPY
 Endoscopy is important not
only in the diagnosis of
corrosive ingestion but also
in determining subsequent
management
Source: https://
www.ncbi.nlm.nih.go
v/pmc/articles/PMC5
421115 /
 Nasogastric tube
 Routine nasogastric intubation for the purpose of evacuating any remaining caustic
material is no longer warranted prior to endoscopic assessment of mucosal injury.
Moreover, insertion of a foreign body in the acute setting may act as a nidus for
infection, which may subsequently delay mucosal healing

 Gastric acid suppression and mucosal protection

 Upon admission, the patient should be kept fasting. Gastric acid suppression with
H2 blockers or intravenous proton pump inhibitors are often initiated to allow faster
mucosal healing and to prevent stress ulcers. Efficacy of these agents for caustic
ingestion has not yet been proven, although a small study done in 2013 has shown
endoscopic healing after omeprazole infusion.
 Complications
 Endoscopic dilatation
 esophageal stents

 Prognosis

1. A high white blood cell count (> 20000 cells/mm3), elevated serum C-reactive
protein, age and the presence of an esophageal ulcer have been considered
predictors of mortality in adults
2. an arterial pH less than 7.22 or a base excess lower than -12  indication of
severe esophageal injury and of emergency surgery
Reflux Esophagitis - Definition
 Reflux esophagitis is an esophageal mucosal injury that occurs secondary to
retrograde flux of gastric contents into the esophagus. Clinically, this is referred to
as gastroesophageal reflux disease (GERD). Typically, the reflux disease involves the
distal 8-10 cm of the esophagus and the gastroesophageal junction. The disease is
patchy in distribution.
 The American College of Gastroenterology has defined GERD as “chronic symptoms
or mucosal damage produced by the abnormal reflux of gastric contents into the
esophagus.” Histologically, this is referred to as “reflux esophagitis,” because it was
initially thought to cause an inflammatory (~itis) response in the esophageal
mucosa. Later in 1970s, it was noted that reflux esophagitis shows morphologic
changes unrelated to the presence of inflammation.
Etiology
 The acidic nature of the refluxed gastric contents is predominantly responsible for the esophageal
mucosal damage and subsequent development of reflux esophagitis. The frequency of acid reflux
correlates more with erosive reflux esophagitis than with nonerosive reflux disease (NERD). This is
due to the proteolytic enzyme “pepsin” in the reflux contents, which becomes activated under
acidic conditions and leads to disruption of intercellular cell junctions and cellular damage. Strong
acid (pH < 2), however, can cause mucosal damage independent of the presence of pepsin.
 The presence of bile in reflux contents is increasingly thought to contribute to reflux disease in a
subset of cases, as observed in patients on proton pump inhibitor (PPI) therapy. Bile refluxate
contains bile acids (both conjugated and unconjugated) and trypsin. Animal studies have shown
that the conjugated bile acids induce mucosal damage in an acidic environment, and the
unconjugated bile acids and trypsin are responsible for mucosal damage at more neutral pH values
(pH 5–8). At an acidic pH, the conjugated bile acids diffuse through the mucosal cells.
Subsequently, the detergent effect of bile acids leads to the dissolution of the lipid content of cell
membranes. This causes disruption of the esophageal mucosal barrier, with accumulation of more
bile acids in the mucosa. At the molecular level, bile acids stimulate squamous esophageal cells to
produce inflammatory mediators, cause oxidative stress, DNA damage, and increased apoptosis.
Etiology
 Occasional reflux of gastric contents into the esophagus is a universal
phenomenon, and the majority of people do not develop reflux
disease because of intact antireflux mechanisms, which clear the
refluxed contents back into stomach before damage is done.
Symptomatic reflux occurs when these antireflux mechanisms become
impaired, such as in the cases of weak lower esophageal sphincter
(LES) function, impaired esophageal clearance due to esophageal
dysmotility or the presence of hiatal hernia, and poor gastric
emptying.
 Poor/abnormal LES function
 Poor or abnormal LES function is the most common cause of gastroesophageal
reflux disease (GERD). This is also the most easily correctable cause and forms
the basis of antireflux surgery. The LES function can be assessed manometrically;
however, a normal manometric study does not preclude an abnormally
functioning LES undergoing transient relaxations and causing reflux disease.
Etiology
 Poor esophageal clearance
 Poor esophageal clearance due to motility disorders is common in elderly population or in
patients with achalasia, stroke, or collagen vascular disease such as scleroderma. The
presence of a large paraesophageal hernia can cause slowed emptying of esophageal
contents into stomach due to obstruction and can lead to altered esophageal motility over
a time period.
 Delayed gastric emptying
 Delayed gastric emptying can lead to the spillage of the retained gastric contents of a full
stomach back into esophagus, thereby causing reflux disease. Poor gastric emptying could
be due to anatomic obstruction of the gastric outlet — as seen in pyloric stenosis — or due
to neuromuscular dysfunction — as in gastroparesis. Gastroesophageal reflux caused by
impaired LES function can also lead to delayed gastric emptying.
Symptoms
 Esophageal
 heartburn, acid dyspepsia, regurgitation, and chest pain

 Extra-esophageal
 also referred to as “atypical” symptoms of reflux disease and
include, but are not limited to, cough, asthma, throat pain,
aspiration pneumonia, globus sensation, and hoarseness due to
pharyngitis, laryngitis, or sinus problems
Diagnosis
 esophagogastroduodenoscopy (EGD) (or, upper GI endoscopy) with biopsy, 24-hour
pH study, barium contrast study, and gastric emptying study
 EGD allows for the direct visualization of the esophageal mucosal surface and for
the obtainment of a mucosal biopsy for pathologic evaluation
 The sensitivity of endoscopy for the diagnosis of GERD is low, because 50-70% of
persons with GERD have a nonerosive reflux disease
Complication & Prognosis
 The natural course of gastroesophageal reflux disease (GERD) is variable, and
treatment typically involves the use of acid suppressor drugs. Surgical intervention
is required in patients with hiatal hernia or an incompetent lower esophageal
sphincter (LES).
 The nonerosive reflux disease is thought to be nonprogressive in its clinical course.
Erosive esophagitis, however, can become complicated by the development of
ulcers and formation of strictures due to fibrosis. About 10% of patients with
symptomatic reflux develop Barrett esophagus, which is a precursor lesion for
adenocarcinoma of the esophagus.
PEPTIC ULCERS
 peptic ulcers : Deep mucosal lesions that disrupt the
muscularis mucosa of the gastric or duodenal wall
 due to an imbalance between cytoprotective and
cytotoxic factors in the stomach and duodenum
 Classification:
 Duodenal (DU)
 Gastric (GU)
Peptic ulcer
 Ulcers in children can be classified as:
 primary peptic ulcers, which are chronic and more often
duodenal  most often associated with Helicobacter
pylori infection
 secondary, which are usually more acute in onset and
are more often gastric  can result from stress due to
sepsis, shock, or an intracranial lesion (Cushing ulcer) or
in response to a severe burn injury (Curling ulcer).
 can also occur as a result of aspirin or nonsteroidal
anti-inflammatory drug (NSAID) use, hypersecretory
states like Zollinger-Ellison syndrome, short bowel
syndrome, and systemic mastocytosis
CLINICAL FEATURES
 Epigastric pain
 Pain pattern in DU occurs 90 min to 3 h after a meal
and is frequently relieved by antacids or food.
 Pain that awakes the patient from sleep (between
midnight and 3 A.M.) is the most discriminating
symptom, with two-thirds of DU patients describing
this complaint.
 GU discomfort may actually be precipitated by food.
 Nausea and weight loss occur more commonly in GU
patients.
 Hematemesis
CLINICAL FEATURES
 Other symptoms are :
 losing weight
 not feeling like eating
 having pain while eating
 feeling sick to your stomach
 vomiting
Treatment
 Gastritis is inflammation of the lining of the
stomach

GASTRITIS

ACUTE CHRONIC

It's a common condition with a wide range of causes.

For most people, gastritis isn't serious and improves quickly if
treated – but if not, it can last for years.
Acute gastritis
 Etiology
1. H. pylori bacterial infection
2. excessive use of cocaine or alcohol
3. regularly taking aspirin, ibuprofen or other painkillers classed as
non-steroidal anti-inflammatory drugs (NSAIDs)
4. a stressful event – such as a bad injury or critical illness, or major
surgery
5. less commonly, an autoimmune reaction – when the immune system
mistakenly attacks the body's own cells and tissues (in this case, the
stomach lining)
PATHOPHYSIOLOGY
 Erosive gastritis: because of exposure to NSAIDs, alcohol,
stress, bile reflux
Exposure → reduction of prostaglandin (for protection of mucosa from
gastric acid) or reduce bicarbonate secretion → injury of mucosa
 Non erosive gastritis: generally caesed by H. pylori
Infection H. Pylori → producing toxin and enzymes → induce IL 8 →
attracts PMN and monocytes → inflammation (acute gastritis)
 Symptons: (acute & chronic)
1. indigestion
2. gnawing or burning stomach pain
3. nausea and vomiting
4. feeling full after eating
5. If the stomach lining has been worn away (erosive gastritis) and
exposed to stomach acid, symptoms may include pain, bleeding or a
stomach ulcer.
 Diagnosis
1. Physical exanimation  normal with mild epigastric pain
2. Complete blood count: to assess for anemia because of gastrointestinal bleeding
3. a stool test – to check for infection or bleeding from the stomach
4. a breath test for Helicobacter pylori (H. pylori) infection (ureum breath test) – this
involves drinking a glass of clear, tasteless liquid that contains radioactive carbon,
if H. pylori are present, the bacteria will convert the urea into carbon dioxide, and
patient breath into a bag, exhaling carbon dioxide. If the test detects the labeled
carbon atoms in the exhaled breath  confirm an H. pylori infection
5. an endoscopy – a flexible tube (endoscope) is passed down the throat and into
oesophagus and stomach to look for signs of inflammation
TREATMENT
 Antacids: containing aluminum and magnesium can help relieve
symptoms of gastritis by neutralizing gastric acids
 H2 receptor inhibitor: competitive inhibition of histamine at the
histamine 2 (H2) receptor
 Proton pump inhibitor: inhibitors of the proton (acid) pump (ie, the
enzyme H+,K+-ATPase)
H2 receptor inhibitor
Drugs Usual Dose for Usual Dose for Usual Dose for
Acute Duodenal Gastroesophagea Prevention
or l of Stress–Related
Gastric Ulcer Reflux Disease Bleeding
Cimetidine 800 mg HS or 800 mg bid 50 mg/h
400 mg bid continuous
infusion
Ranitidine 300 mg HS or 150 mg bid 6.25 mg/h
150 mg bid continuous
infusion or 50 mg
IV every
6–8 h
Nizatidine 300 mg HS or 150 mg bid -
150 mg bid
Famotidine 40 mg HS or 20 mg bid 20 mg IV every 12
20 mg bid h

HS: bedtime
PPI
Drugs Usual dosage for peptiic ulcer or
GERD
Omeprazole 20–40 mg qd
Esomeprazole 20–40 mg qd
Lansoprazole 30 mg qd
Dexlansoprazole 30–60mg qd
Pantoprazole 40 mg qd
Rabeprazole 20 mg qd
Complication
 Bleeding from an erosion or ulcer
 Limiting the adequate transfer of food from the stomach to the small
intestine
 Dehydration from vomiting
 Renal insufficiency as a result of dehydration
CHRONIC GASTRITIS
ETIOLOGY
 Chronic gastritis caused by H pylori infection
 Gastritis caused by Helicobacter heilmannii infection 
 Granulomatous gastritis associated with gastric infections in
mycobacteriosis, syphilis, histoplasmosis
 Chronic gastritis associated with parasitic infections
- Strongyloides species, schistosomiasis, or Diphyllobothrium latum
 Gastritis caused by viral (eg, CMV or herpesvirus) infection
CHRONIC GASTRITIS
 The early phase of chronic gastritis is superficial gastritis. The
inflammatory changes are limited to the lamina propria of the surface
mucosa, with edema and cellular infiltrates separating intact gastric
glands.
 The next stage is atrophic gastritis. The inflammatory infiltrate
extends deeper into the mucosa, with progressive distortion and
destruction of the glands.
 The final stage of chronic gastritis is gastric atrophy. Glandular
structures are lost, and there is a paucity of inflammatory infiltrates.
 Chronic gastritis is also classified according to the
predominant site
of involvement :

Type A refers to the body-predominant

form (autoimmune)

Type B is the antral-predominant form (H.

pylori–related).
TREATMENT
 Antibiotics:
 Amoxicillin 1 g PO q12hr for 14 days with lansoprazole (30 mg) and clarithromycin (500 mg)
or 1 g PO q8hr for 14 days with lansoprazole (30 mg) (in patients intolerant of, or resistant
to, clarithromycin)
 Proton pump inhibitor:
 Omeprazole: 20 mg PO q12hr for 10 days, w/ Amoxicillin 1000 mg PO q12hr, and
Clarithromycin 500 mg PO q12hr for 10-14 days
 Lansoprazole: 30 mg + amoxicillin 1 g + clarithromycin 500 mg PO q12hr for 10-14 days

 Bismuth

 Treatment in chronic gastritis is aimed at the sequelae and not the underlying
inflammation. Patients with pernicious anemia will require parenteral vitamin
B12 supplementation on a long-term basis. Eradication of H. Pylori.