Gastritis

dr. Isbandiyah, SpPD

Anatomical site
CARDIA

MUCOUS SECRETING cells BODY

SPECIALISED SECRETORY PARIETAL - ACID CHIEF PEPSINOGEN ENDOCRINE HIST, SOMASTATIN

ANTRUM MUCOUS SECRETING ENDOCRINE :GASTRIN, 5HT

Definition
The term gastritis is used to denote inflammation associated with mucosal injury Gastritis is mostly a histological term that needs biopsy to be confirmed Gastritis is usually due to infectious agents (such as Helicobacter pylori) and autoimmune and hypersensitivity reactions.

Causes
H pylori (most common cause of ulceration) NSAIDs, aspirin Gastrinoma (Zollinger-Ellison syndrome) Severe stress (eg, trauma, burns), Curling ulcers Alcohol Bile reflux Pancreatic enzyme reflux Radiation Staphylococcus aureus exotoxin Bacterial or viral infection

Pathophysiology
The mechanisms of mucosal injury in gastritis are thought to be an imbalance of aggressive factors acid production or pepsin

and defensive factors mucus production bicarbonate and blood flow

IMBALANCE
FAKTOR AGRESIF

FAKTOR DEFENSIF

Robbins.Pathology Anatomy

Pathogenesis
In normal acid/pepsin attack is balanced by mucosal defences Increased attack by hyperacidity Weakened mucosal defence the major factor (H. pylori related)

Patients typically present with abdominal pain that has the following characteristics
Epigastric to left upper quadrant Frequently described as burning May radiate to the back Usually occurs 1-5 hours after meals May be relieved by food, antacids (duodenal), or vomiting (gastric)

Treatment
Drugs:
Antasid Antagonis reseptor H2 proton pump inhibitor Antikolinergic Sitoprotektor sukralfat dan rebamipid prostaglandin

Chronic gastritis
A autoimmune B bacterial (helicobacter) C - chemical

Autoimmune chronic gastritis

Autoantibodies to gastric parietal cells Hypochlorhydria/achlorhydria Loss of gastric intrinsic factor leads to malabsorption of vitamin B12 with macrocytic,megaloblastic anaemia

Morphology of chronic gastritis

Chronic inflammatory cell infiltration Mucosal atrophy Intestinal (goblet cell) metaplasia

Chemical gastritis
Commonly seen with bile reflux (toxic to cells) Prominent hyperplastic response (inflammatory cells scanty) With time intestinal metaplasia

Helicobacter pylori
Causes cell damage and inflammatory cell infiltration In most countries the majority of adults are infected

Helicobacter gastritis
2 patterns of infection
Diffuse involvement of body and antrum (pan gastritis associated with diminishing acid output) Infection confined to antrum (antral gastritis, associate with increased acid output)

Diagnostic test for H. Pilori infection

Non endoscopic
Serologic test Urea breath test (UBT) Fecal antigen test

Endoscopic
Urease based test (CLO) Histologic assessment Cultur

Tretment regimens for H. pilori infection

Standart triple drug regimen
PPI + claritomycin + amoxicillin or metronidazole

Sequential therapy for initial treatment

PPI + amoxicillin for 5 d followed by PPI + claritomycin + metronidazole for 5 d

Second line regimen for failed initial treatment

PPI + bismuth +tetracycline + metronidazole

Terapi Eradikasi H.Pylori

PPI 2x1+ amoksisilin 2x1000 mg + klaritromisin 2x500 mg PPI 2x1 + metronidazol 3x500 mg + klaritromisin 2x500 mg PPI 2x1 + metronidazol 3x500 mg + amoksisilin 2x1000 mg PPI 2x1 + metronidazol 3x500 mg + tetrasiklin 4x500 mg

Regulation of gastric acid secretion