Acute Gastritis

Pathology

• congested, edematous gastric mucosa
• coagulation or hemorrhage of gastric mucosa
• can have many acute erosions into the gastric mucosa

Clinical Presentation

• Epigastric pain
• Tender, nausea, vomiting
• Bleeding
• Ranges from occult (hidden) to major hemorrhage
• Most common causes
• Aspirin, NSAIDS, EtOH
• Usually self-limited

Chronic Gastritis

General

• Remember H.pylori and NSAIDS are the most common cause of gastric injury
• Just because you can’t see it (endoscopy) or remove it (biopsy) doesn’t mean it is not there.
• All types of conditions play a part in classification of type of gastritis
• More than one type can exist at any given time.

Diffuse Antral Gastritis (TYPE B)

• Pathology

Ø  incidence increases with age

Ø  Mild form is asymptomatic

Ø  Affects mainly antrum – “Antral”

Ø  Lamina propria and glands have both chronic and acute inflammatory infiltrate

Ø  NOT ASSOC. WITH ATROPHY AND INTESTINAL METAPLASIA

Ø  H.pylori ID’d in 90% of biopsies

• Etiology/Pathogenesis

Ø  western hemisphere

Ø  50% of pop over the age of 60

Multifocal atrophic gastritis (TYPE C – environmental)

• Pathology

Ø  antrum and body – “multifocal”

Ø  gastric glands atrophy and they are replaced by intestinal or parietal-looking (metaplastic) epithelium

Ø  in the body of the stomach – loss of parietal and chief cells occurs

Ø  antrum – mucous glands; doesn’t help matters any!!

• Etiology/pathogenesis

Ø  freq. Incr. With age

Ø  assoc. w/ early colonization with H.pylori.

Ø  Increases the risk of gastric adenocarcinoma

Ø  hypochlorhydria

Diffuse corporal atrophic gastritis (Type A – autoimmune)

• Pathology

Ø  body and fundus (not antrum)

Ø  mucosa turns grey, becomes thin and flat

Ø  metaplasia of the epithelium occurs

Ø  hypochlorhydria occurs also; can even be achlorhydria

Ø  Decrease in acidÞstimulation of G cellsÞincreased Gastrin production/secretion

• Etiology/pathogenesis

Ø  Abs to parietal cells and IF lead to destruction of the parietal cells

Ø  10% of patients get pernicious anemia

Ø  associated with other autoimmune diseases

H.pylori and Gastritis

• Background

Ø  Marshall and Warren, 1983

Ø  Causes injury to mucosa, decrease in viscosity of mucus gel, and an increase in acid permeability

Ø  In response to meals – increased gastrin response

Ø  Increased basal levels of gastrin

Ø  Secretes urease which splits to NH₄⁺ and CO₂. (urease breath test – 91% sensitivity)

Diffuse Antral Gastritis         Multifocal Atrophic Gastritis Diffuse Corporal Atrophic Gastritis

Where              Antrum                         Antral-body                               Body & Fundus

Who                 Caucasians                  Asian, Scan., Hispanics, Blacks            Northern Europeans,

Scandinavians

Ulcer?              DU, pyloric ulcers         uncertain                                  No

Acid                 Normal to Increased      Decreased                                Decreased

Metapla?          No                                yes                                           yes

Cancer?           No                                yes                                           yes

AutoAbs           No                                No                                            yes

PernAn             No                                No                                            yes

Gastrin             Normal                         Normal to decreased                 Increased

Reactive Gastropathies

Pathology

• hyperplasia of foveolar cells
• decreased production of mucin
• erosion and ulceration/inflammed mucosa
• can co-exist with diffuse antral gastritis

Etiology/pathogenesis

• Cause: factors that injure gastric mucosa w/o producing pronounced inflammatory infiltrate
• Most common causes: NSAIDS and bile reflux

Acute Erosive (Hemorrhagic) Gastritis

Pathology

• erosion = mucosa involvement only
• ulcer = penetration of muscularis mucosa to submucosa
• usually terminal event
• INVOLVES: stomach, lower 1/3 of esophagus, and first part of duodenum

Etiology/Pathogenesis

• requires acid gastric juice
• MAJOR CAUSE: impaired mucosal vitality

Ø  leads to shock and HYPOtension

Ø  splanchnic vasoconstriction

Ø  burns – Curling’s ulcers

• certain brain diseases can lead to excessive secretion of gastrin juice
• steroid therapy leads to steroid ulcers
• EtOH, Aspirin, NSAIDS, caffeine, smoking

Clinical Features

• few patients develop massive hemorrhage
• rarely perforation occurs

Chronic Peptic Ulcer

DEFINED: ulceration located anywhere along the upper GI tract which is exposed to action of acid and gastrin.

General

• 5-10% of US pop.
• DU(duodenum):GU (stomach); 4:1
• No ethnic preference; male>female
• Factors which increase incidence

Ø  alcoholic cirrhosis, chronic renal failure, COPD, hyperparathyroidism, Zollinger-Ellison Syndrome

Ø  H.pylori indicated in more of DU cases than GU cases

• H.pylori found in 95% of patients with DU
• 80% of GU

Etiology

• immediate cause: acid:peptic digestion of GI tract ( NO ACID:NO ULCER)
• Stimuli for acid secretion

Ø  ENDOCRINE – gastrin release from antral G cells

Ø  NEURONAL (vagus) – acetylcholine

Ø  CHEMICAL – Histamine release from mast cells

• Mucosal Defenses

Ø  intercellular junction between cells

Ø  HCO₃^- to neutralize the acid

Ø  Mucus production in the antrum of the stomach

Ø  PGs stim. Secretion of HCO₃^- and Mucus (reason for NSAIDS and Aspirin’s effects)

• Disruption of this mucosal barrier

Ø  H.pylori

Ø  EtOH, NSAIDS, Aspirin

Ø  Ischemia

Pathology

• General

Ø  cut section shows abnormalities in all areas of the wall

Ø  muscularis mucosa fused with the muscularis propria

Ø  dense fibrous tissue located at the base of the ulcer.

• Gastric Ulcer (GU)

Ø  frequently found on lesser curvature and antrum

Ø  “precipitous proximal border and sloping distal border with radial converging rugae”

• Duodenal Ulcer (DU)

Ø  usually found 2 cm from the pylorus, single, and sharply demarcated

• Microscopic

Ø  4 zones

1.     granular debris and fibrinopurulent exudate

2.     fibrinoid necrosis

3.     granulation tissue

4.     dense fibrous tissue develops – leads to scar formation

Clinical features of Chronic Peptic Ulcer

• epigastric pain – alleviated by food and antacids
• periodic symptoms that persist for years
• Complications

Ø  significant hemorrhage – 25%

Ø  perforation – 10%

Ø  pyloric obstruction – 10%

Duodenal Ulcer                       Gastric Ulcer

Frequency                            4                                                          1

Age of onset                         younger                                               Older

Parietal Cell Mass Increased                                            Normal or Decreased

Acid secretion                      Increased                                            Normal or Decreased

Mucosal Defense                 ?                                                          Decreased

Genetics                               type O, HLA-B5, non-secretors          None

Gastric emptying                 rapid                                                    delayed

H.pylori incidence                >90%                                                   >80%

Neoplasms of the Stomach

General

• incidence decreasing in Western Hemisphere
• 5^th leading cause of cancer deaths world-wide

Gastric Adenocarcinoma (90%) – MOST COMMON

• General

Ø  most patients over the age of 50, but can occur in young adults

Ø  Background: chronic atrophic gastritis w/ intestinal metaplasia

Ø  90% associated with hypochlorhydria (lack of HCl in the gastric juice)

• Pathology

Ø  Intestinal Type

• fungated and ulcerated mass antrum, lesser curvature
• older patients
• BACKGROUND: chronic atrophic gastritis

Ø  Diffuse Type

• also called Signet Ring Cell Type or “limits plastica” or “leather bottle”
• prepyloric area
• high % in young adults
• omnious prognosis
• Clinical Correlation

Ø  advanced disease when the symptoms arise from the carcinoma

Ø  upper abdominal discomfort

Ø  post-prondial fullness

Ø  anorexia, nervousness, nausea

Ø  iron deficiency anemia

• How to diagnose

Ø  Barium swallow

Ø  Endoscopy w/ cytology and biopsy

Is Peptic ulcer related to Adenocarcinoma?

Ø  Neither DU or GU is related

Ø  GU and CA not entirely clear

• less than 1% become malignant

• What is the relationship of Gastritis to Adenocarcinoma?

Ø  atrophic gastritis (DCAG and MAG) predispose to dysplasia and carcinoma

Ø  3x the chance of developing gastric carcinoma when you have pernicious anemia.

• What is the relationship of H.pylori to Gastric Adenocarcinoma?

Ø  major factor in etiology of AdenoCA

Ø  H.pylori associated more with CA of the BODY AND FUNDUS (NOT gastroesophageal junction)

• Metastasis

Ø  Usu. To adjacent lymph nodes

Ø  Isolated left supraclavicular lymph nodes (Virchow’s node)

Ø  KNOW FOR TEST – Krukenberg’s tumor – involvement of stomach and bilateral ovaries)

Ø  Also spreads to liver peritoneum, adrenal glands

Ø  Prognosis affecting factors:

1.     the younger you are, the more worse the prognosis

2.     location

3.     depth of invasion

4.     size

5.     type

6.     lymph node involvement

Gastric Lymphoma

General

• 8% of gastric malignancy
• difficult to distinguish from adenocarcinoma

Pathology

• usu. Localized to antrum or body
• majority of B cell type lymphoma are well diff. Superficial MALT
• high grade, large cell type

Clinical

• epigastric pain
• post-prandiol fullness
• fatigue

Diagnosis

• neg. biopsy doesn’t exclude malignancy

Relationship to H.pylori

• 90% of all cases
• eradication of H.pylori assoc. with regression of MALT lymphoma.
• 5 year survival rate- 96%

Gastric Sarcoma

• 2% of all gastric malignancy
• usu submucosal in location
• unpredictable behavior
• can metastasize.
• Prognosis based on size, activity

Tags: Acute Erosive Hemorrhagic Gastritis, Acute Gastritis, Chronic Gastritis, Diffuse Antral Gastritis, Epigastric pain, Gastric Adenocarcinoma, gastric malignancy, Multifocal atrophic gastritis, Peptic Ulcer, splanchnic vasoconstriction, steroid ulcers

This entry was posted on Wednesday, July 1st, 2009 at 5:00 am and is filed under Pathophysiology. You can follow any responses to this entry through the RSS 2.0 feed. Responses are currently closed, but you can trackback from your own site.