Gastritis

Gastritis

dr. Isbandiyah, SpPD

Anatomical site

ANTRUM

CARDIA

BODY

MUCOUS SECRETING cells

SPECIALISED SECRETORY PARIETAL - ACIDCHIEF -

PEPSINOGEN ENDOCRINEHIST,

SOMASTATIN

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

FAKTOR DEFENSIF

FAKTOR AGRESIF

“IMBALANCE”

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