Gastritis

dr Putra Hendra SpPD

UNIBA
Human digestive
system
 Gastro-intstinal disorders
A. Esophagial disorders E. Billiary disorders
A1. Globus E1. Gallbladder dysfunction
A2. Rumination Syndrome E2. Sphincter of Odi dysfunction
A3. Functional chest pain of presumed oesophageal origin
A4. Functional heartburn
A5. Functional dysphagia
A6. Unspecified oesophageal disorder
B. Gastroduodenal disorders F. Anorectal disorders
B1. Functional dyspepsia F1. Functional faecal incontinence
B1a. Ulcer like dyspepsia F2. Functional anorectal pain
B1b. Dysmotility like dyspepsia F2a. Levator ani syndrome
B1c. Non-specific dyspepsia F2b. Proctalgia fugax
B2. Aerophagia
B3. Functional vomiting
C. Bowel disorders
C1. Irritable bowel syndrome
C2. Functional abdominal bloating
C3. Functional constipation
C4. Functional diarrhoea
C5. Unspecified functional bowel disorder
D. Functional abdominal pain
D1. Functional abdominal pain syndrome
D2. Unspecified functional abdominal pain
Localizing pain -- epigastric
• PUD
• Gastritis
• Pancreatitis
• GERD
• Cardiac (MI,
pericarditis, etc)
Localizing pain -- epigastric
• PUD
• Gastritis
• Pancreatitis
• GERD
• Cardiac (MI,
pericarditis, etc)
 PRESENT COMPLAINT

COMMON SYMPTOMS
 Anorexia and weight loss  Abdominal pain
 Dysphagia  Wind
 Heartburn  Abdominal distension
 Dyspepsia  Altered bowel habit
 Nausea and vomiting  Rectal bleeding
 Haematemesis  Jaundice
 ANOREXIA AND WEIGHT LOSS

 Anorexia: loss of appetite

 Weight loss: energy expenditure
exceeds calorie intake
CAUSES:
 DM type 1
 Hyperthyroidism
 Malabsorption
 Diuretic therapy
 Severe burns
 Infeksi : TBC

“Do you still enjoy your meals?”

 DYSPHAGIA
 Difficulty swallowing

CAUSES:
 Oral
– Ulcers
– Mouth infections
 Neurological
– Stroke
– Bulbar palsy
 Neuromuscular
– Achalasia
– Myasthenia gravis
 Mechanical “Does food (or drink) stick when
– Oesophageal cancer you swallow?”
 HEARTBURN

 Hot burning, retrosternal discomfort

 Radiates upwards
 DYSPEPSIA

 Pain or discomfort centred in the upper abdomen

CAUSES:
 Gastro-oesophageal
reflux disease
 Peptic ulcer disease
 Functional dyspepsia
 NAUSEA AND VOMITING

 Nausea: sensation of feeling sick

 Vomiting: expulsion of gastric contents via mouth.

CAUSES:
 Dyspepsia
 Peptic ulcers
 Gastric outlet/ pylorus
obstruction
 Gastroenteritis
 Cholecystitis
 Raised intracranial
pressure
 HAEMATEMESIS
 Vomiting blood
 Above g-o sphincter (oesophageal varices)
 Below g-o sphincter (Mallory-Weiss tear)

CAUSES:
 Gastric ulcer
 Oesophagitis, gastritis
 Oesophagic, gastric
cancer
 NSAIDS
 ABDOMINAL PAIN
 Visceral abdominal pain: distension of
hollow organs, smooth muscle contraction
(deep poorly localized)
 Somatic pain: irritation of parietal peritoneum

Foregut – pain localizes to epigastric area

Midgut – pain localizes to periumbilical

area
Hindgut – pain localizes to suprapubic
area
Access its characteristics!
(site, timing, severity, what makes it
worse and what makes it better)
 WIND
 Repeated belching, excessive flatus, abdominal
distension
 Borborygmi: bowel sounds, movement of fluid and gas
along the intestine

Ask the patient to describe what is

being experienced.
 ABDOMINAL DISTENSION

 Factors (the 5 Fs) Consider

 FAT – Excessive alcohol
consumption
 FLATUS – Obstruction
 FAECES – Obstruction, constipation
 FLUID – Ascites
 FOETUS – Date of last menstrual
period
 ALTERED BOWEL HABIT

 3x each day to 1x every 3 days is considered

normal
 Constipation: infrequent passage of hard
stools
 Impaired mobility
 Physical obstruction
 Diarrhoea: frequent passage of loose stools
 Impaired water absorption
Ask for change in stool consistency,
increased frequency of defecation,
urgency, etc
 RECTAL BLEEDING

 Fresh rectal bleeding

 Haemorrhoids
 Anal fissure
 Colorectal cancer
 IBD

 Melaena: blood loss in

upper GIT tract
 JAUNDICE

 Yellow discoloration of the skin, sclerae and mucous

membrames (> 50 μmol/L)
 Hyperbilirubinaemia
 Prehepatic (haemolysis, Gillbert’s syndrome) +Ubg
 Hepatocellular (viral hepatitis, drugs, cirrhosis)
 Obstructive (drugs, gallstones, cancer) +UnBil
 Diseases of Stomach
 Indigestion
 Acute gastritis from: H.
pylori tobacco, chronic use
of drugs such as:
—Alcohol
—Aspirin
—Nonsteroidal
antiinflammatory agents
 Indigestion (Dyspepsia)
Symptoms
 Abdominal pain
 Bloating
 Nausea
 Regurgitation
 Belching
 Dyspepsia

Upset Stomach
Indigestion
 Dyspepsia

Functional Non-GI
Dyspepsia Causes of Symptoms
(cardiac disease,
muscular pain, etc.)

Structural Dyspepsia
(GERD, PUD, pancreatic
disease, gallstones, etc.)
 Definition
An international committee of clinical investigators developed
the following revised definition (Rome III criteria) of functional
dyspepsia for research purposes, which can also be applied to
clinical practice :
One or more of:
 Bothersome postprandial fullness
 Early satiation
 Epigastric pain
 Epigastric burning

AND
 No evidence of structural disease (including at upper
endoscopy) that is likely to explain the symptoms.
 Etiologi

 Gastro-oesophageal reflux disease:

(GERD) 60%+

 Non-ulcer dyspepsia: 20%+

 Ulcer dyspepsia: 4%
Symptoms of Functional Dyspepsia
Ulcer-like Dominant Dysmotility-like Dominan

Nocturnal
pain Nausea
Localized Heartburn Bloating
epigastric Early satiety
burning Retrosternal
burning Worse
Better with food
with food
 Pathophysiology
 The pathophysiology of functional
dyspepsia is unclear. Research has
focused upon the following factors:
 Gastric motor function
 Visceral sensitivity
 Helicobacter pylori infection
 Psychosocial factors
 Major Causes of Dyspepsia
Williams 1988 Stanghellini 1996 Heikkinen
1996
(n=1386) (n=1057) (n=766)
60
% of Patients with

50
Diagnosis

40

30

20

10

0
Gastric Cancer Peptic Ulcer Esophagitis/ Functional
GERD
Dyspep
Pathogenesis & Pathophysiology of
Dyspepsia

• Behavioural factors
• Gastritis
• H. pylori infection

• Increased
• Altered
visceral
motility
perception
 Diabetic Gastroparesis
(Gastroparesis Diabeticorum)
 Delayed stomach emptying of solids
 Etiology—autonomic neuropathy
 Nausea, vomiting, bloating, pain
 Insulin action and absorption of food
not synchronized
 Prescribe small frequent meals (may
need liquid diet)
 Adjust insulin
 Gastroparesis
Chronic condition with delayed gastric emptying of
solids in the absence of mechanical obstruction
symptoms. Gastric pump failure
Primary symptoms:
• nausea 92%.
•post prandial emesis 84%
• early satiety 60%
• bloating 75%
• abdominal pressure
• pain 46-89%
 (Diagram etiology)

Dig Dis Sci 43(11) Nov 1998. Soykan, McCallum et al.

 Dyspepsia Treatment
 Avoid offending foods
 Eat slowly
 Chew thoroughly
 Do not overindulge
 Gastritis
 Erosion of mucosal layer
 Exposure of cells to gastric
secretions, bacteria
 Inflammation & tissue damage
 Definition
 Epithelial cell damage and regeneration without
associated inflammation is properly referred to
as "gastropathy.“

 Gastropathy may be referred without histological

evidence and just according to gross
appearance in endoscopy or radiology

 Gastropathy is usually caused by irritants such

as drugs (eg, NSAID, Steroid, alcohol), bile
reflux, hypovolemia, and chronic congestion.
 Gastritis
 Normallygastric & duodenal mucosa
protected by:
 Mucus
 Bicarbonate (acid neutralized)
 Rapid removal of excess acid
 Rapid repair of tissue
 gastritis (ICD10)
1. Chemical gastritis (acute・chronic)
Alcoholic gastritis
Drug induced gastritis (e.g., NSAID)
Reflux ( due to duodenal juice or bile) gastritis
Other chemical gastritis
2. Radiation gastritis
3. Allergic gastritis
4. Autoimmune gastritis
5. Special forms of gastritis
6. Gastritis・NOS
7. Duodenitis
ACUTE GASTRITIS -
MORPHOLOGY
Mucosal congestion,
oedema, inflammation &
ulceration
Sequence of histological and endoscopic events in H. pylori infected
stomach with accompanying transformation of chronic atrophic gastritis
to chronic active gastritis with polyp, intestinal metaplasia and dysplasia
to cancer.
 Atrophic Gastritis
 Loss of parietal cells in stomach
 Hypochloria =  in HCl production
 Achlorhydria = loss of HCl production
 Decrease or loss of intrinsic factor production
 Malabsorption of vitamin B12
 Pernicious anemia
 vitamin B12 injections or nasal spray
 Acute hemorrhagic erosive
 specific pathogenetic factor in NSAID-
induced acute hemorrhagic and erosive
gastropathy is the inhibition of
prostaglandin production. Prostaglandins,
especially those of the E class, protect
against acute mucosal injury due to
NSAIDs and other injurious substances by
several mechanisms, including the
stimulation of mucus and bicarbonate
secretion, and maintenance of mucosal
blood flow
 Mallory-Weiss Syndrome

 Laceration
 Usually caused by
severe vomiting
 Could be life-
threatening bleeding
Peptic Ulcer Disease (PUD)
 Gastric or duodenal ulcers
 Asymptomatic or sx similar to
gastritis or dyspepsia
 Danger of hemorrhage, perforation,
penetration into adjacent organ or
space
 Melena = black, tarry stools from GI
bleeding
 Definition

 Craters extending to below the muscularis

mucosa of stomach (GU) or duodenum (DU).
 A products of self-digestion.
Peptic Ulcer Disease
 Epidemiology
 Estimated life time
prevalence :10%
 Male: female =3- 4:1
 Ratio of DU: GU = 3:1
 DU emerges 10-20 years earlier
than GU
Etiology & Pathogenesis
 Helicobacter pylori infection
 NSAIDs & Aspirin
 Acid/Pepsin
 Smoking
 Genetics
 Psychological factors
 Stress ulcer
 Two Common Forms of
Peptic Ulcer
 H.pylori – associated: 70-85%
 NSAIDs – associated: 10-25%

Non-Hp, Non-NSAID Ulcer: 5-30%

 Dictum
 No acid, no ulcer
 No acid, no Hp, no ulcer
 No Hp, No NSAIDs, no ulcer
Aggressive Factors
Defensive Factors
 Acid/Pepsin  Mucus-bicarbonate barrier
 Barrier of apical membrane
 H. pylori infection
 Mucosal blood flow
 NSAIDs  Prostaglandins

 Smoking
 Garam empedu

I
Aggressive Defensive II
Factors  Factors 

III Aggressive Factors  + Defensive Factors 

 NSAID

Loss of PGI2 induced inhibition of LTB4 media

endothelial adhesion and activation of neutr

↑ Leukocyte-Endothelial
Interactions

Capillary Proteases +
Obstruction Oxygen Radicals

Ischemic Endo/Epithelial
Cell Injury Cell Injury

Mucosal Ulceration
1. Etiology – Helicobacter pylori
 H. pylori
 Secret proteins and toxins that
interact with the stomach’s epithelial
cells
 Leads to inflammation and damage
 Smoking & Peptic Ulcer
Increasing incidence of peptic ulcer
 Delaying healing of ulcer
Increasing relapse and complication
Mechanisms:
 Facilitating bile reflux

 Decreasing mucosal blood supply

 Inhibiting synthesis of PGs

Psychological Factor in Peptic Ulcer

 Controversial
 Possible mechanisms
through vagal mechanisms,
 Stimulating acid secretion
 Decreasing mucosal blood supply
 Stress ulcer pathophysiology
 Hypersecretion of acid –head trauma.
 Defects in gastric glycoprotein mucus –In
critically ill patients, increased
concentrations of refluxed bile salts or the
presence of uremic toxins can denude the
glycoprotein mucous barrier
 Ischemia – Shock, sepsis, and trauma can
lead to impaired perfusion of the gut.
 Stress ulcer risk factors
 •Shock
• Sepsis
• Hepatic failure
• Renal failure
• Multiple trauma
• Burns over 35 percent of total body
 Memakai ventilator >48 jam
 Koagulopati
• Organ transplant recipients
• Head or spinal trauma
• Prior history of peptic ulcer disease or upper
GI bleeding
 Zollinger-Ellison Syndrome
 PUD caused by “gastrinoma”
 Gastrin producing tumor in pancreas
 Gastrin = hormone stimulates HCl prod
 Causes mucosal ulceration
 50 – 70% are malignant
 Any part of esoph., stomach, duod.,
jejun.
 Removal of tumor, gastrectomy
 Clinical Presentation
 Acid dyspepsia in DU
 Epigastric “ hunger ” pain or discomfort；
 Occurred 2-4 hours after meal，or at nigh
 Relieved by food or antacids;
 Acid dyspepsia in GU
 More severe pain；
 Occurred soon after meal；
 Less relieved by food or antacids;
 Diagnosis of H. pylori Infection
 Endoscopy  Non-invasive
 culture  serology
 biopsy  anti H. pylori IgG/IgA
 Lab ELISA or office kit
 histology and stain
 quantitative or
qualitative
 Urea breath test
 13-C
 14-C
 salivary testing
 urine testing
Helicobacter pylori and peptic ulcer disease.
Strategies for healing ulcer

 Eradicate H. pylori
 Inhibit acid secretion
 Improve mucosal defense
Peptic Ulcer Disease - Treatment
 Treatment options

Lifestyle Antacids
modifications

PPIs Approaches H2RAs

Prokinetic Surgery
motility agents
(domperidon)

Hatlebakk & Berstad, Clin Pharmacokinet 1996;31:386–406.

 Upper GI Disorders and Drugs
Heartburn & Dyspepsia
 Non pharmacological
recommendations
 Don’t eat before bedtime/lying down
 Elevate head of bed (~6 inches)
 Weight loss
 Reduce portion sizes
 Smoking cessation
 Avoid trigger foods:
 Fatty
 Spicy
 Chocolate
 Citrus
 EtOH
 Caffeine
Eradicate H. pylori infection
PPI (H2-RA) Two
or + Antibiotics
Bismuth
Clarithromycin 250-500mg
Colloidal Bismuth
Amoxicillin 500-1000mg
Subcitrate ( CBS)
(Tetracycline)
240mg
Metronidazole 400mg
Furazolidone 100mg

Triple therapy, bid for 1 week

 Inhibit acid secretion
 H2-Receptor Antagonists
 Cimetidine 400mg bid
 Ranitidine 150mg bid
 Famotidine 20mg bid DU：
4 - 6 wks
 Proton Pump Inhibitors
 Omeprazole 20mg qd GU：
 Lansoprazole 30mg qd 6 - 8 wks
 Pantoprazole 40mg qd
 Rabeprazole 10mg qd
 Esomeprazole 20mg qd
 Antiflatulent Agent
Simethicone (Mylecon)
 May be mixed in antacid
formulation or given
alone
 Causes gas bubbles to
coalesce
 Aids in the passage of
gas through the GI
 Give after meal and @ HS
 Shake liquid preparations
thoroughly
 Complications of PUD on Endoscopy

Bleeding DU Perforated GU Duodenal stricture

 Misoprostol (Cytotec)
Prostaglandin

Do not give to women of childbearing years

unless a reliable method of birth control
can be DOCUMENTED
 Surgical Therapy
 Rare event
 Indication for surgery
 Perforation
 Intractable bleeding
 Gastric outlet obstruction
(Scaring)
 Malignant transformation
 Surgical options
 Gastric Surgery
 Resective surgical procedures
 “anastamosis” – connection of two
tubular structures
 Gastrectomy – surgical removal of
part or all of stomach
 Hemigastrectomy = half
 Partial gastrectomy
 Subtotal gastrectomy = 30-90%
resected
 Gastric Surgery
 Billroth I = gastroduodenostomy
 Partial gastrectomy – anastomosis to
duodenum
 To remove ulcers, other lesions (cancer)
 Billroth II = gastrojejunostomy
 Partial gastrectomy - anastomosis to jejunum
 Allows resection of damaged mucosa
 Reduces number of acid producing cells
 Reduces ulcer recurrence
 Gastric Surgery
 Total gastrectomy
 Removal of entire stomach
 Rarely done = negative impact on
digestion, nutritional status
 In extensive gastric cancer & Zollinger-
Ellison syndrome not responding to
medical management
 Anastomosis from esophagus to
duodenum or jejunum
Gastric surgical
procedures.

Fig. 30-7. p. 661.

 Gastric surgical
procedures. (cont.)

Fig. 30-7. p. 661.