Miscellaneous Topics in

Gastroenterology

Waseem Hamoudi M.D

Consultant Internal Medicine

Gastroenterology & Hepatology

• Peptic Ulcer Disease.

• Inflammatory Bowel Disease.

• Acute diarrhea.

Peptic Ulcer Disease

• Peptic ulcerations are excavated defects (holes) in the gastrointestinal mucosa that result when epithelial cells succumb to the caustic effects of acid and pepsin in the lumen.

• Peptic ulcer disease commonly used term to refer to ulcerations of the stomach, duodenum, or both, that is caused by acid-peptic injury.

• Histological, ulcers are necrotic mucosal

defects that extend through the muscularis

mucosa and into the submucosa or deeper

layers.

• More superficial necrotic defects are

named erosions.

History

• In the early part of the 20th century, stress and diet were considered to be the pathogenetic factors for PUD, so treatment was with bed rest and diet.

• 1950, clinicians had focused their attention on the pathogenetic role of gastric acid, so antacid therapy had become the treatment of choice.

• 1970, histamine H2 receptor antagonists became available, and acid suppression with antisecretory therapy was the treatment of choice for UD.

• 1980, proton pump inhibitors (PPI) were discovered, with more potent acid suppression and higher rates of ulcer healing.

• Using alone antisecretory drugs, will have recurrence within one year in most patients

• H. pylori was discovered in April 1982 by two Australian physicians, Dr. Barry Marshall and Dr. Robbin Warren.

• In 1983 the two doctors proposed that the bacterium is the cause of peptic (duodenal and gastric) ulcers.

• Dr. Marshall even went so far as to inoculate himself with the bacterium to prove his point.

• it soon became apparent just how widespread and serious the H. pylori threat is.

• Researches confirm that over 90 per cent of people with peptic ulcers are infected with the bacterium.

• In 1987 the Sydney gastroenterologist Thomas Borody invented the first triple therapy for the treatment of duodenal ulcers.

Causes

• United Kingdome United states

• Duodenal ulcer Peptic ulcer disease

• Gastric ulcer( Benign) Gastroesophageal

varices

• Esophagitis Angiomas

• Mallory-Weiss tear Mallory-Weiss tear

• Gastroesophageal varices Tumors

• Gastritis or gastric erosions Erosions

• Tumors Dieulafoy's lesion

Jordan (Al Bashir Hospital)

• Duodenal ulcer 41.90%

• Esophageal varices 16.07%

• Erosive gastritis/duodenitis 14.09%

• Esophagitis 8.64%

• Gastric ulcer 5.87%

• Gastric and duodenal ulcers 3.60%

• Esophageal ulcer 3.25%

• Anastomotic ulcer 2.26%

• Mallory-Weiss tear 1.55%

• Esophageal tumor 1.41%

• Gastric tumor 1.27%

Waseem H. et al. Upper G.I Bleeding in Jordan- Retrospective statistical analysis 1996-2000

• Peptic Ulcer Disease.

• Inflammatory Bowel Disease.

• Acute diarrhea.

Main types of inflammatory bowel

disease (IBD)

• Ulcerative colitis

• Crohn’s disease

Endoscopic features of ulcerative colitis

(reproduced with permission, Schiller et al, 1986)

Anatomical location of ulcerative colitis

Intestinal complications of

ulcerative colitis

• Fibrosis

• Shortening of the colon

• Bleeding

• Stricture

• Bowel perforation

• Toxic megacolon

Systemic complications of

ulcerative colitis

• Arthritis

• Iritis

• Erythema nodosum

• Pyoderma gangrenosum

• Sclerosing cholangitis

• Aphthous stomatitis

• Thromboembolic disorders

Clinical presentation of

ulcerative colitis

• Bloody diarrhoea

• Fever

• Cramping abdominal pain

• Weight loss

• Frequency and urgency of defecation

• Tenesmus

• General malaise

(reproduced with permission, Schiller et al, 1986)

Endoscopic appearance of Crohn’s

disease

Anatomical location of Crohn’s disease

Clinical presentation of Crohn’s

disease

• Diarrhoea

• Abdominal pain

• Bleeding

• Pyrexia

• Weight loss

• Fistulae

• Perianal disease

• General malaise

Intestinal complications of

Crohn’s disease

• Fistulae

• Abscesses

• Adhesions

• Strictures

• Obstruction

Perianal complications of Crohn’s disease

Systemic complications of

Crohn’s disease

• Arthritis

• Gallstones

• Malabsorption

– Lactase deficiency

– Vitamin B12 deficiency

• Renal stone formation

Differences in clinical presentation between ulcerative

colitis and Crohn’s disease

Ulcerative colitis Crohn’s disease

Symptoms

Pain * * * *

General malaise * * * * *

Fever * *

Diarrhoea * * * *

Stools

Blood * * * *

Mucus * * *

Pus * * *

The number of * symbols indicates the frequency with which

each symptom is present

Pathological and anatomical features distinguishing

ulcerative colitis from Crohn’s disease

Ulcerative colitis Crohn’s disease

Localisation Distal Segmental,

proximal

Rectum affected Always 50% of cases

Intestinal wall Normal thickness Thickened

Adhesions Rare Common

Inflammation Superficial layers All layers

Ulcerations Superficial Deep

Mucous membrane Denuded Cobblestones

Granulomas 0–4% 50–70%

Lymphocytic infiltration Rare Always

Fistulae Rare Common

(reproduced with permission, the AGA Teaching Project, 1992)

Geographical distribution of IBD

Etiological theories of IBD

• Genetic

• Smoking

• Dietary

• Infection

• Immunological

• Psychological?

Pharmacological treatment of IBD

• 5-ASA-containing compounds – mesalazine

Pentasa®

Asacol®

Claversal®/Mesasal®/Salofalk®

– sulphasalazine Salazopyrin®

– olsalazine Dipentum®

• Corticosteroids

• Immunosuppressants

Treatment: indications for

surgery

• Perforation

• Toxic dilatation

• Massive haemorrhage

• Chronic ill-health

• Risk of cancer

• Peptic Ulcer Disease.

• Inflammatory Bowel Disease.

• Acute diarrhea.

• Normally 10 liters enter the duodenum daily, of which 1 liter is absorbed by the small intestine.

• Colon resorbs most of the remaining fluid with only 100 ml fluids lose in the stool.

• Medical definition of diarrhea: a stool weight more than 250 g/day.

• Practical definition: increased stool frequency more than 3 times/day or liquidity.

• There are 2 types of diarrhea: acute diarrhea (less than 3 weeks) and chronic diarrhea (more than 3 weeks).

Acute diarrhea

• Acute diarrhea: acute onset of diarrhea

and present for less than 3 weeks

• Mostly caused by infectious agents,

bacterial toxins (ingested preformed in

food or produced in gut) and drugs.

• Similar recent illness in family members

suggests an infectious etiology.

Non-inflammatory diarrhea

• Fever absent.

• Stool without blood or fecal leucocytes.

• Watery stool with peri-umbilical cramps, bloating, nausea and vomiting (small bowel enteritis) caused by either a toxin or other a toxin producing toxin or other agents that disrupt the normal absorption and secretory process in the small intestine.

How do we recognize non-

inflammatory diarrhea?

By examining the absence of the

leucocytes in the stool

What are the causes of Non-

inflammatory diarrhea?

• Viral: Norwalk virus, Rotavirus.

• Protozoa: Giardia lamblia, Cryptosporidium.

• Bacterial:

• Preformed entero-toxins: Staphylococcus aureus, Bacillus cereus, and Clostridium perfringens.

• Intra-intestinal enterotoxin production: E. coli (enteropathogen) and Vibrio cholera.

• New medication.

• Fecal impaction.

Inflammatory diarrhea

• Presence of fever and bloody diarrhea

(dysentery) indicates colonic damage caused by

invasion (shigellosis, salmonellosis, yersinia and

amibiasis) or a toxin (C.difficile, E. coli 0157:H7).

• Colonic diarrhea is a small amount diarrhea in

volume (< 1l/day) and associated with left lower

quadrant cramps, urgency and tenesmus.

• Fecal leucocytes are present in infections with

invasive organisms.

How do we recognize inflammatory

diarrhea?

By examining the presence of the

leucocytes in the stool

What are the causes of

inflammatory diarrhea? • Viral: Cytomegalovirus.

• Bacterial:

1. Cytotoxin production: E. coli 0157:H7 (enterohemorhagic), Vibrio parahemolyticcus and Clostridium difficile.

2. Mucosal invasion: Shigella, Salmonella, enteroinvasive E. coli, aeromonas and Yersinia.

3.Bacterial proctitis: Chlamydia, N. gonorrhea.

• Protozoa: E. histolytica.

• Other: Ischemic colitis, I.B.D. and radiation colitis.