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 acidpeptic 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
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United Kingdome
Duodenal ulcer
Gastric ulcer( Benign)
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Esophagitis
Mallory-Weiss tear
Gastroesophageal varices
Gastritis or gastric erosions
Tumors
United states
Peptic ulcer disease
Gastroesophageal
varices
Angiomas
Mallory-Weiss tear
Tumors
Erosions
Dieulafoy's lesion
Jordan (Al Bashir Hospital)
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Duodenal ulcer
Esophageal varices
Erosive gastritis/duodenitis
Esophagitis
Gastric ulcer
Gastric and duodenal ulcers
Esophageal ulcer
Anastomotic ulcer
Mallory-Weiss tear
Esophageal tumor
Gastric tumor
Waseem H. et al. Upper G.I Bleeding in Jordan- Retrospective statistical analysis 1996-2000
41.90%
16.07%
14.09%
8.64%
5.87%
3.60%
3.25%
2.26%
1.55%
1.41%
1.27%
• 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
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Fibrosis
Shortening of the colon
Bleeding
Stricture
Bowel perforation
Toxic megacolon
Systemic complications of
ulcerative colitis
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Arthritis
Iritis
Erythema nodosum
Pyoderma gangrenosum
Sclerosing cholangitis
Aphthous stomatitis
Thromboembolic disorders
Clinical presentation of
ulcerative colitis
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Bloody diarrhoea
Fever
Cramping abdominal pain
Weight loss
Frequency and urgency of defecation
Tenesmus
General malaise
Endoscopic appearance of Crohn’s
disease
(reproduced with permission, Schiller et al, 1986)
Anatomical location of Crohn’s disease
Clinical presentation of Crohn’s
disease
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Diarrhoea
Abdominal pain
Bleeding
Pyrexia
Weight loss
Fistulae
Perianal disease
General malaise
Intestinal complications of
Crohn’s disease
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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
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*
*
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*
Blood
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*
Mucus
*
**
Pus
*
**
Symptoms
Pain
General malaise
Fever
Diarrhoea
Stools
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
Distal
Segmental,
proximal
Always
50% of cases
Normal thickness
Thickened
Rare
Common
Superficial layers
All layers
Superficial
Deep
Denuded
Cobblestones
Granulomas
0–4%
50–70%
Lymphocytic infiltration
Rare
Always
Fistulae
Rare
Common
Localisation
Rectum affected
Intestinal wall
Adhesions
Inflammation
Ulcerations
Mucous membrane
Geographical distribution of IBD
(reproduced with permission, the AGA Teaching Project, 1992)
Aetiological theories of IBD
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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
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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 noninflammatory diarrhea?
By examining the absence of the
leucocytes in the stool
What are the causes of Noninflammatory diarrhea?
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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.