Chapter 17: GIT-Complications of Chronic Gastritis

Question 1

Complications of Chronic Gastritis

Answer 1

• PEPTIC ULCER DISEASE
• MUCOSAL ATROPHY AND INTESTINAL METAPLASIA
• DYSPLASIA
• GASTRITIS CYSTICA

Question 2

Peptic ulcer disease (PUD) is most often associated with what?

Answer 2

_H. pylori–induced hyperchlorhydric
chronic gastritis_, which is present in 85% to 100% of individuals with duodenal ulcers and in
65% with gastric ulcers.

Question 3

What can help to distinguish peptic ulcers from acute erosive gastritis or stress ulcers?

Answer 3

The presence of chronic gastritis can help to distinguish peptic ulcers
from acute erosive gastritis or stress ulcers, since the mucosa adjacent to the ulcer is generally
normal in the latter two conditions.

Question 4

To which areas of GIT can PUD occur?

Answer 4

• portion of the GI tract exposed to acidic gastric juices, but is most common in the gastric antrum and first portion of the duodenum.
• esophagus as a result of GERD or acid secretion by ectopic gastric mucosa.
• Gastric mucosa within a Meckel diverticulum can result in peptic ulceration of adjacent mucosa.

Question 5

PUD most commonly occur in what areas of GIT?

Answer 5

• *gastric antrum** and **first portion of the
  duodenum. **

Question 6

What is the epidemiology of PUD?

Answer 6

PUD is common and ranks fourth in both annual physician visits and costs among all GI diseases. [19]

In the United States, the lifetime risk of developing an ulcer is approximately 10% for males and 4% for females; the latter are typically affected during or after menopause.

PUD
affects more than 300 million people and is responsible for treatment and ongoing care of over
3 million people, 190,000 hospitalizations, and 5000 deaths in the United States each year

Question 7

What is the pathogenesis of PUD?

Answer 7

The imbalances of mucosal defenses and damaging forces that cause chronic gastritis are also
responsible for PUD.

Thus, PUD generally develops on a background of chronic gastritis.

The
reasons why some people develop only chronic gastritis while others develop PUD are poorly
understood.

Question 8

What are the primary underlying causes of PUD, and both
compromise mucosal defense while causing mucosal damage.

Answer 8

• H. pylori infection and
• NSAID use

Although more than 70% of
individuals with PUD are infected by H. pylori, fewer than 20% of H. pylori–infected individuals
develop peptic ulcer. It is probable that host factors as well as variation among H. pylori strains
determine the clinical outcomes.

Question 9

The gastric hyperacidity that drives PUD may be caused by what?

Answer 9

• H. pylori infection,
• parietal cell hyperplasia,
• excessive secretory responses, or
• impaired inhibition of stimulatory mechanisms such as gastrin release.

For example, Zollinger-Ellison syndrome, in which there are multiple peptic ulcerations in the stomach, duodenum, and even jejunum, is caused by uncontrolled release of gastrin by a tumor and the resulting massive acid production.

More common

cofactors in peptic ulcerogenesis include chronic NSAID use, which causes direct chemical irritation while suppressing prostaglandin synthesis necessary for mucosal protection;

cigarette

smoking, which impairs mucosal blood flow and healing;

and high-dose corticosteroids that suppress prostaglandin synthesis and impair healing.

Question 10

Duodenal ulcers are more frequent inindividuals with what?

Answer 10

• alcoholic cirrhosis,
• chronic obstructive pulmonary disease,
• chronic renal failure,
• and hyperparathyroidism.
• self-imposed or exogenous psychologic stress may increase gastric acid production.

Question 11

In chronic renal failure, and hyperparathyroidism what is the reason for stimulating gastrin leading to increase acid secretion?

Answer 11

In this two conditions, hypercalcemia stimulates gastrin production and therefore increases acid secretion. .

Question 12

Peptic ulcers are four times more common in the proximal duodenum than in
the stomach.

T or F

Answer 12

TRUE

Duodenal ulcers usually occur within a few centimeters of the pyloric valve and involve the anterior duodenal wall.

Question 13

Gastric peptic ulcers are predominantly located along where?

Answer 13

lesser curvature near the interface of the body and antrum.

Question 14

.

Describe the size of peptic ulcer.

Answer 14

• solitary in more than 80% of patients.
• Lesions less than 0.3 cm in diameter tend to be shallow while those over 0.6 cm are likely to be deeper ulcers

Question 15

What is the morphology of classic peptic ulcer?

Answer 15

• round to oval,
• sharply punched-out defect ( Fig. 17-14A ).
• The mucosal margin may overhang the base slightly, particularly on the upstream side, but is usually level with the surrounding mucosa.
  
  • In contrast, heaped-up margins are more characteristic of cancers.
• Hemorrhage and fibrin deposition are often present on the gastric serosa.

Question 16

How to differentiate PUD from cancer?

Answer 16

In PU the mucosal margin
may overhang the base slightly, particularly on the upstream side, but is usually level with
the surrounding mucosa.

In contrast, heaped-up margins are more characteristic of cancers.

Question 17

The depth of ulcers may be limited by the what?

Answer 17

• thick gastric muscularis propria or by
• adherent pancreas,
• omental fat,
• or the liver.

Question 18

What is present on the gastric serosa of patients with PUD?

Answer 18

Hemorrhage and fibrin deposition are often
present on the gastric serosa.

Perforation into the peritoneal cavity is a surgical emergency
that may be identified by the presence of free air under the diaphragm on upright
radiographs of the abdomen.

Question 19

What is the appearance of the base of the peptic ulcer?

Answer 19

smooth and clean as a result of peptic digestion of exudate, and blood vessels may be evident.

In active ulcers the base may have a thin layer of fibrinoid debris underlaid by a predominantly neutrophilic inflammatory infiltrate

. Beneath this, active
granulation tissue infiltrated with mononuclear leukocytes and a fibrous or collagenous scar
forms the ulcer base( Fig. 17-14B ).

Vessel walls within the scarred area are typically
thickened and are occasionally thrombosed.

Ongoing bleeding within the ulcer base may
cause life-threatening hemorrhage.

Scarring may involve the entire thickness of the wall and pucker the surrounding mucosa into folds that radiate outward.

Question 20

Size and location can differentiate benign and malignant ulcers.

T or F

Answer 20

FALSE

Size and location do not differentiate benign and malignant ulcers.

However, the gross
appearance of chronic peptic ulcers is virtually diagnostic. Malignant transformation of
peptic ulcers is very rare, and reports of transformation probably represent cases
wherein a lesion thought to be benign was actually an ulcerated carcinoma from the start.

Question 21

What is diagnostic for PUD?

Answer 21

However, the gross
appearance of chronic peptic ulcers is virtually diagnostic.

Question 22

Malignant transformation of
peptic ulcers is very rare, and reports of transformation probably represent cases
wherein a lesion thought to be benign was actually an ulcerated carcinoma from the start

Question 23

Answer 23

FIGURE 17-14 Acute gastric perforation in a patient presenting with free air under the
diaphragm.

A, Mucosal defect with clean edges

. B, The necrotic ulcer base is composed
of granulation tissue.

Question 24

What is the clinical course of Peptic Ulcer?

Answer 24

Peptic ulcers are notoriously chronic, recurring lesions with much greater morbidity than
mortality.

Question 25

What age most often is Peptic Ulcer diagnosed?

Answer 25

They may present in young adults but are most often diagnosed in middle-aged to older adults without obvious precipitating conditions.

Question 26

After a period of weeks to months of active
disease in peptic ulcer disease what happens?

Answer 26

healing may occur with or without therapy, but the tendency to develop peptic ulcers
remains.

Question 27

The majority of peptic ulcers come to clinical attention because of what?

Answer 27

epigastric burning or aching pain, although a significant fraction present with complications such as iron deficiency anemia, frank hemorrhage, or perforation.

Question 28

Describe the occurence of pain in PUD.

Answer 28

The pain tends to occur 1 to 3 hours after meals
during the day, is worse at night, and is relieved by alkali or food.

Nausea, vomiting, bloating,
belching, and significant weight loss are additional manifestations. With penetrating ulcers the pain is occasionally referred to the back, the left upper quadrant, or the chest, where it may be
misinterpreted as cardiac in origin.

Question 29

What is the treatment for PUD?

Answer 29

Current therapies for PUD are aimed at H. pylori eradication and neutralization of gastric acid,
primarily with proton pump inhibitors or H2 histamine receptor antagonists.[20]

A variety of
surgical approaches were formerly used, including antrectomy to remove gastrin-producing
cells and vagotomy to remove the acid-stimulatory effects mediated by the vagus nerve.

Proton
pump inhibitors and H. pylori eradicationhavemarkedly reduced the need for surgical
intervention,which is primarily reserved for treatment of bleeding or perforated peptic ulcers.

Question 30

Long-standing chronic gastritis that involves the body and fundus may ultimately lead to what?

Answer 30

significant loss of parietal cell mass.

Question 31

This oxyntic atrophy may be associated with what?

Answer 31

intestinal metaplasia, recognized by the presence of goblet cells, and is strongly associated with
increased risk of gastric adenocarcinoma.

Question 32

How is intestinal metaplasia reconized?

Answer 32

intestinal metaplasia, recognized by the presence of goblet cells, and is strongly associated with
increased risk of gastric adenocarcinoma.

Question 33

The risk of adenocarcinoma is greatest in what?

Answer 33

autoimmune gastritis.

This may be because achlorhydria of gastric mucosal atrophy permits overgrowth of bacteria that produce carcinogenic nitrosamines

. Intestinal metaplasia also
occurs in chronic H. pylori gastritis and may regress after clearance of the organism.

Question 34

What are the factors that contribute to the transformation of gastritis to dysplasia?

Answer 34

Chronic gastritis exposes the epithelium to inflammation-related free radical damage and
proliferative stimuli.

Over time this combination of stressors can lead to the accumulation of genetic alterations that result in carcinoma.

Pre-invasive in situ lesions can be recognized
histologically as dysplasia

.

Question 35

What are the morphologic hallmarks of dysplasia ?

Answer 35

are variations in epithelial size, shape, and orientation along with coarse chromatin texture, hyperchromasia, and nuclear enlargement.

Question 36

What is the distinction between dysplasia and regenerative epithelial changes?

Answer 36

The distinction between dysplasia and regenerative epithelial changes induced by
active inflammation can be a challenge for the pathologist, since increased epithelial
proliferation and mitotic figures may be prominent in both.

However, reactive epithelial cells
mature as they reach the mucosal surface, while _dysplastic lesions remain cytologically
immature._

Question 37

What is Gastritis cystica?

Answer 37

refers to an exuberant reactive epithelial proliferation associated with entrapment of epithelial-lined cysts.

These may be found within the submucosa (gastritis cystica polyposa) or deeper layers of the gastric wall (gastritis cystica profunda).

Because of the association with chronic gastritis and partial gastrectomy, it is presumed that gastritis cystica is trauma-induced, but the reasons for the development of epithelial cysts within deeper portions
of the gastric wall are not clear.

Question 38

How can gastritis cystica mimic invasive adenocarcinoma?

Answer 38

Regenerative epithelial changes can be prominent in the entrapped epithelium, and gastritis cystica can therefore mimic invasive adenocarcinoma