Esophagitis

• - Reflux esophagitis (see GERD).

• - Infection by candida, herpes simplex and
CMV in immuno-compromised patients, This
can be treated by antifungal and antiviral.
• - Pills induced esophagitis results from
tetracycline, iron, NSAIDs, KCI tablets, and
other antibiotics, (drink sufficient fluid more
than 120m I) with oral medications to
prevent esophagitis.
 Eosinophilic Esophagitis
• eosinophilic esophagitis is more common in
children and in males.
• Younger children present with failure to thrive
and refusal to swallow.
• Older children present with regurgitation,
vomiting, and pain.
• Adult usually present with heartburn and
dysphagia.
• Diagnosis is confirmed by esophageal
mucosal biopsies that show increased
eosinophils (>15) per high-power field
• Treatment consists of a 12-week course of
swallowed fluticasone propionate (440 g
bid) using a metered dose inhaler.
• Oral prednisone can be used.
 INFECTIOUS ESOPHAGITIS
• Infectious esophagitis can be due to viral,
bacterial, fungal, or parasitic organisms.
• In severely immunocompromised
patients,multiple organisms may coexist.
 Viral Esophagitis
• Herpes simplex virus (HSV), Varicella-zoster
virus (VZV), Cytomegalovirus (CMV)
• Patients may complain of an acute onset of
chest pain, odynophagia, and dysphagia.
• Bleeding and tracheoesophageal fistula may
occur in severe cases;.
• Systemic manifestations such as nausea,
vomiting, fever, chills, and mild leukocytosis may
be present
 Investigations
• Endoscopy
• superficial ulcerations.
• In later stages, a diffuse erosive esophagitis
• Culture
• HSV becomes positive within days and is
helpful in diagnosis and to identify acyclovir-
resistant strains
 Treatment
• Spontaneous resolution may occur in 1–2
weeks.
• Acyclovir (400 mg PO 5 times a day for 14–21
days) causes early resolution of symptoms.
• Valacyclovir (1 g PO tid for 7 days).
• patients with severe odynophagia, intravenous
acyclovir, 5 mg/kg every 8 h for 7–14 days.
• Ganciclovir, 5 mg/kg every 12 h intravenously,
is the treatment of choice for (CMV)
 CANDIDA ESOPHAGITIS
• Candida albicans is most common.
• Patients may be asymptomatic or complain of
odynophagia and dysphagia.

• Endoscopy shows small, yellow-white raised

plaques with surrounding erythema in mild
disease.

• Oral fluconazole (200mg on the first day,

followed by 100 mg daily) for 7–14days.
 Mallory Weiss tear
• - It is a linear mucosal tear at the esophageo-
gastric junction produced by a sudden increase in
the intra-abdominal pressure.
• - It usually occurs after a bout of coughing,
retching or after an alcohol binge.
• It is diagnosed by endoscopy.
• - The hemorrhage stops spontaneously. Rarely
surgery with oversewing of the tear may be
required.
 Globus ( hystericus is an old name)
• - Persistent or intermittent sensation of a lump
or foreign body in the throat,
• this sensation is present between meals.
Absence of dysphagia on swallowing.
• In the majority, it is probably a functional
disease.
• - In the treated by reassurance with antiureflux
therapy.
Gastritis & Gastropathy
• The term "gastropathy" denote conditions in which there
is epithelial or endothelial damage without inflammation

• The term "gastritis" denote conditions in which there is

histologic evidence of inflammation

• In clinical practice, the term "gastritis" is commonly

applied to three categories:

(1) erosive and hemorrhagic "gastritis"

(2) nonerosive, nonspecific (histologic) gastritis
(3) specific types of gastritis, characterized by distinctive
histologic and endoscopic features diagnostic of specific
disorder
Erosive & Hemorrhagic "Gastritis"
• The most common causes of erosive
gastropathy are:

• Drugs (especially NSAIDs)

• Alcohol
• Stress due to severe medical or surgical
illness
• Portal hypertension ("portal gastropathy")
• Uncommon causes include:
• Caustic ingestion
• Radiation

• Erosive and hemorrhagic gastropathy

typically are diagnosed at endoscopy,
often being performed because of
dyspepsia or upper gastrointestinal
bleeding
• Endoscopic findings include:
• Subepithelial hemorrhages
• Petechiae
• Erosions

• These lesions are superficial, vary in size

and number, and may be focal or diffuse
 Clinical Findings
Symptoms and Signs
• Erosive gastropathy is usually asymptomatic

• Symptoms, when they occur, include anorexia, epigastric

pain, nausea, and vomiting

• There is poor correlation between symptoms and the

number or severity of endoscopic abnormalities

• The most common clinical manifestation of erosive

gastritis is upper gastrointestinal bleeding, which
presents as hematemesis, "coffee grounds" emesis, or
bloody aspirate in a patient receiving nasogastric
suction, or as melena
 Laboratory Findings

• The laboratory findings are nonspecific

• The hematocrit is low if significant

bleeding has occurred

• Iron deficiency may be found.

 Special Examinations
• Upper endoscopy is the most sensitive method
of diagnosis

• Endoscopy is generally performed within 24

hours in patients with upper gastrointestinal
bleeding to identify the source.
 Differential Diagnosis
• Epigastric pain may be due to
• peptic ulcer
• gastroesophageal reflux
• gastric cancer
• biliary tract disease
• food poisoning
• viral gastroenteritis
• functional dyspepsia

• With severe pain, one should consider a perforated or penetrating

ulcer, pancreatic disease, esophageal rupture, ruptured aortic
aneurysm, gastric volvulus, and myocardial colic

• Causes of upper gastrointestinal bleeding include peptic ulcer

disease, esophageal varices, Mallory-Weiss tear, and arteriovenous
malformations.
 Specific Causes & Treatment
Stress Gastritis
Prophylaxis

• Stress-related mucosal erosions and subepithelial

hemorrhages develop within 72 hours in the majority of
critically ill patients

• Major risk factors include mechanical ventilation,

coagulopathy, trauma, burns, shock, sepsis, central nervous
system injury, hepatic or renal failure, and multiorgan failure

• Pharmacologic prophylaxis with intravenous H2-receptor

antagonists, oral proton pump inhibitors such as omeprazole
suspension, or sucralfate in critically ill patients has been
shown to reduce the incidence of clinically overt and
significant bleeding
Treatment

• Once bleeding occurs, patients should receive

continuous infusions of a proton pump inhibitor
(esomeprazole, lansoprazole, or pantoprazole)
as well as sucralfate suspension
 NSAID Gastritis
• The rate of dyspepsia is increased 1.5- to 2-fold with NSAID
use

• Patients with alarm symptoms or signs, such as severe pain,

weight loss, vomiting, gastrointestinal bleeding, or anemia,
should undergo diagnostic upper endoscopy

• For other patients, symptoms may improve with

discontinuation of the agent, reduction to the lowest effective
dose, or administration with meals

• Empiric 2–4 week trial of a proton pump inhibitor

(omeprazole, rabebrazole, or esomeprazole, lansoprazole,
pantoprazole) is recommended for patients with NSAID-
related dyspepsia, especially those in whom continued
NSAID treatment is required
 Nonerosive, Nonspecific
Gastritis

• The diagnosis of nonerosive gastritis is based

on histologic assessment of mucosal biopsies

• The main types of nonerosive gastritis are:

• Due to H pylori infection
• Associated with pernicious anemia
• Lymphocytic gastritis
 Helicobacter pylori Gastritis
• H pylori is a spiral gram-negative rod that
resides beneath the gastric mucous layer
adjacent to gastric epithelial cells

• Although not invasive, it causes gastric mucosal

inflammation with PMNs and lymphocytes

• Transmission is from person to person, mainly

during infancy and childhood.
Pathogenesis

• Acute infection with H pylori may cause a transient

clinical illness characterized by nausea and abdominal
pain that may last for several days and is associated with
acute histologic gastritis with PMNs

• Inflammation may be confined to the superficial gastric

epithelium or may extend deeper into the gastric glands,
resulting in varying degrees of gland atrophy (atrophic
gastritis) and metaplasia of the gastric epithelium to
intestinal type epithelium

• Eradication of H pylori may be achieved with antibiotics

in over 85% of patients and leads to resolution of the
chronic gastritis
•Chronic H pylori gastritis is associated with a 3.5-
to 20-fold increased risk of gastric
adenocarcinoma and low-grade B cell gastric
lymphoma (mucosa-associated lymphoid tissue
lymphoma; MALToma)
Noninvasive Testing for H pylori

• Laboratory-based quantitative serologic ELISA

tests

• Fecal antigen immunoassay

• Urea test

• Proton pump inhibitors significantly reduce the

sensitivity of urea breath tests and fecal antigen
assays (but not serologic tests) and should be
discontinued 7–14 days prior to testing
 Chronic gastritis
• It is a chronic inflammation of gastric mucosa which
can lead to mucosal atrophy including loss of parietal
and chief cells with subsequent metaplasia which
constitutes a background for carcinoma.
• Causes:
• 1. Autoimmune (type A) leading to pernicious
anaemia.
• 2. Helicobacter (type B) i.e. bacterial.
• 3. Chemical (type C) i.e. biliary reflux (post
gastrectomy).
• 4. Chronic abuse of NSAID or aspirin.
Clinical features:
-Asymptomatic.
-Nausea, vomiting.
-Epigastric discomfort.
-Pernicious anemia (Autoimmune type).
lnvestigations:
-Upper endoscopy with biopsy.
-Parietal cell antibodies and intrinsic factor
antibodies in autoimmune gastritis.
Treatment:
-Cause. -Symptomatic treatment
 Pernicious Anemia Gastritis
• Pernicious anemia gastritis is an autoimmune disorder involving the
fundic glands with resultant achlorhydria and vitamin B12
malabsorption

• The majority have malabsorption secondary to aging or chronic H

pylori infection that results in atrophic gastritis, hypochlorhydria, and
impaired release of B12 from food

• Fundic histology in pernicious anemia is characterized by severe

gland atrophy and intestinal metaplasia caused by autoimmune
destruction of the gastric fundic mucosa

• Parietal cell antibodies directed against the H+-K+-ATPase pump

are present in 90% of patients
• Inflammation and autoimmune destruction of the
acid-secreting parietal cells leads to secondary loss
of fundic zymogen cells, which secrete intrinsic
factor

• Achlorhydria leads to pronounced hypergastrinemia

due to loss of acid inhibition of gastrin G cells

• Hypergastrinemia may induce hyperplasia of

gastric enterochromaffin-like cells that may lead to
the development of small, multicentric carcinoid
tumors

• Endoscopy with biopsy is indicated in patients with

pernicious anemia at the time of diagnosis.
 Specific Types of Gastritis
Infections
• Acute bacterial infection of the gastric submucosa and
muscularis with a variety of aerobic or anaerobic
organisms produces a rare, rapidly progressive, life-
threatening condition known as necrotizing gastritis. It
requires broad-spectrum antibiotic therapy

• Viral infection with CMV is commonly seen in patients

with AIDS and after bone marrow or solid organ
transplantation

• Fungal infection with Candida may occur in

immunocompromised patients
Granulomatous Gastritis
Chronic granulomatous inflammation may be caused by a
variety of systemic diseases, including Crohn's disease, H
pylori infection, tuberculosis, syphilis, fungal infections, or
sarcoidosis
These may be asymptomatic or associated with a variety of
gastrointestinal complaints
Eosinophilic Gastritis
This is a rare disorder in which eosinophils infiltrate the
antrum and sometimes the proximal intestine
Symptoms include anemia from mucosal blood loss,
abdominal pain, early satiety, and postprandial vomiting
Treatment with corticosteroids is beneficial in the majority of
patients.
Acute gastritis
 This Videoendoscopic image shows a severely
inflamed gastric mucosa typical of acute gastritis
After treatment normal gastric folds are
observed
Acute gastritis…..erosions
This Videoendoscopic image of the stomach shows a pale
decoloration of the mucosa typical of chronic gastritis.
Chronic Gastritis
Atrophic Gastritis
CHRONIC GASTRITIS ( Erosive)
Intestinal Metaplasia of the Pre-Piloric Antrum