3. Peptic ulcer is a hole or open sore in the
lining of the stomach, duodenum
(beginning of the small intestine) or
oesophagus.
Edited by :-MR . ROMAN BAJRANG
4. "peptic" refers to pepsin: a stomach
enzyme that breaks down protein.
An ulcer occurs when the lining ofthese
organs is corroded by acidic digestive
juices secreted by the stomach cells.
5. Ulcer may be found :
I n oesophagus
stomach
duodenum,
jejunum at multiple levels
(Zollinger Ellison syndrome).
6. Abdominal discomfort usually occurs in epigastric area
(upper middle part of the abdomen) radiating to the
back described as:
1. A dull gnawing ache comes and goes for several
days.
2. A pain may increase when the stomach is empty at
night or half to three hours after meal.
3. A Pain is relieved by eating & antacid
medication.
11. Other symptoms
Vomiting (relieves episodes of severe
pain due to evacuation of gastric acid
content).
Edited by :-MR . ROMAN BAJRANG
12. Less common symptoms:
1-Constipation and 5% of the patients
with chronic duodenal ulcers has
predominantly colonic symptoms.
2-Heartburn and eructation are also
commonly associated with ulcer activity.
13. While acid is still considered significant in
ulcer formation, the leading cause of ulcer
disease is currently believed to be
infection of the stomach by bacteria called
"Helicobacter pyloridus" (H. pylori).
15. Chronic use of anti-inflammatory medications, commonly referred to as
NSAIDs (Nonsteroidal anti- inflammatory drugs).
16. The H. pyloribacteria
excretes the enzyme urease, which
converts urea into ammonia and
bicarbonate. The release of
ammonia ‘neutralize’ the acidic
environment in the stomach, which
explains the difficulty in destroying .
The H. pylori bacterium.! Ammonia
is toxic to the epithelial cells and
damages them; hence the
beginning of a stomach ulcer
takes its course.
17. H. pylori is diagnosed through:
blood,
breath,
stool,
and tissue tests.
18. Blood tests are
most common. They
detect antibodies to
H. pylori bacteria.
Blood is taken at the
doctor's office
through a finger stick.
19. Ureabreath tests are an effective
diagnostic method for H. pylori.
They are also used after treatment
to see whether it worked. In the
doctor's office, the patient drinks a
urea solution that contains a
special carbon atom. If H. pylori is
present, it breaks down the urea,
releasing the carbon. The blood
carries the carbon to the lungs,
where the patient exhales it. The
breath is accurate.
Edited by :-MR . ROMAN BAJRANG
20. Stool tests detect H.
pylori infection in the
patient's fecal matter.
Helicobacter pylori
stool antigen (HPSA)
test is accurate for
diagnosing H. pylori .
Tissue tests are
usually done using the
biopsy sample that is
removed with the
endoscope.
24. Duodenal ulcer Gastric ulcer
-Incidence
Age 30-60 Usually 50 years and
above
2-3:1 ♀:♂ ♂:♀ 1:1
80% of peptic ulcers
are duodenal
15% of peptic ulcers
are gastric
25. -Signs and
Symptoms
Hyposecretion of
HCl
Weight gain Weight loss
Pain 2-3 hrs after meal;
often awakened btw 1-2
AM; ingestion of food
relieves pain
Pain occurs 12-1 hr
after meal; rarely
occurs at night; may
be relieved by
vomiting; ingestion of
food does not help,
sometimes increases
pain
Vomiting uncommon
It perforates more than
gastric ulcer
Vomiting common
Hemorrhage more
likely to occur than
with duodenal ulcer.
27. Anesophageal ulcer is a hole in the lining of
the esophagus corroded by the acidic digestive
juices secreted by the stomach cells.
Anesophageal ulcer is usually located in the
lower section of esophagus. Esophageal ulcers
are not contagious.
Esophageal ulcers may be a symptom of another
disease or condition.. Bleeding from esophageal
ulcers may cause iron deficiency anemia.
Itis often associated with chronic GERD.
28. A large amount of excess
acid is produced in
response to the
overproduction of the
hormone gastrin, which in
turn is caused by tumors on
the pancreas or duodenum.
These tumors are usually
malignant, must be
removed and acid
production suppressed to
relieve the recurrence of the
ulcers.
29. Curling's ulcer is an acute peptic ulcer of
the duodenum resulting as a complication
from severe burns when reduced plasma
volume leads to sloughing of the gastric
mucosa.
These stress ulcers were once a common
complication of serious burns, especially
common in child burn victims. They result in
perforation and hemorrhage and had
correspondingly high mortality rates.
30. Bleeding:
As an ulcer erodes the muscles
of stomach, or duodenal wall,
blood vessels may also be damaged,
which causes the bleeding.
Over a period of time, the patient
becomes anemic.
Can be treated endoscopically by
Locating the ulcer &cauterizing the BV
With heating device
or injected with material
to stop bleeding.
Perforation:
Sometimes,
ulcer eats a hole
in wall of the stomach, or duodenum.
Bacteria & partially digested food
can spill through the opening
into the sterile abdominal Cavity(paritonium).
This causes paritonitis,an inflammation of the
abdominal cavity & wall.
Immediate hospitalization
and surgery is usually required.
31.
32. Barium X-ray examination (less
expensive method of diagnosing
peptic ulcer).
But X-ray examination does have
some limitations:
I t is unable to definemucosal
disease ex: gastritis.
I t is not definitive in
differentiating benign from
malignant gastric ulcer.
I t cannot delineatesuperficial,
subacute gastric or duodenal
erosions.
I t cannot define completehealing of an
ulcer.
Furthermore, as an ulcer heals, the
surrounding tissue, especially in the
duodenum, becomes scarred and
deformed and radiologic assessment of
activity of the ulcer becomes more
difficult.
33. M 1 Receptors:
stimulated by acetylcholine secreted from the para-sympathetic
nerve endings (vagus nerve).
Gastrin Receptors:
stimulated by gastrin hormone from mucosa of stomach and
duodenum into the blood.
presence of food causes distention of the stomach this will
cause stimulation of mucosa so gastrin hormone increases in blood
and parietal cells increase the secretion of HCl.
H 2 Receptors:
stimulated by histamine secreted from mast cells in stomach.
35. To relieve the
symptoms
(pain, vomiting,
blood loss).
To eliminate
the source
of problem.
Aims
of
treatment
To promote
healing
of ulcer.
To prevent
complications
of ulcer.
To prevent
recurrence of
ulcer by
maintenance
therapy.
36. Anti secretory
Drugs:
they reduce
gastric
acid secretion
Cytoprotective
drugs having
mucosal
Protective
properties
H2 blocker:
first line
of treatment
of
peptic ulcer
Anti-
muscarinic
drugs
Proton
pump
inhibitors
Sucralfates Bi-chelates
Misoprostol Antacids
Antibiotics:
To kill H. Pylori
38. Mode of action:
These are competitive
antagonists with histamine on H2
receptors found on the parietal
cells of the stomach so they can
reduce gastric acid secretion.
They are given as firstline of
treatment for 4 weeks then the
patient is examined to see if ulcer
healed.
I f ulcer is healed so the
patient moves to lower
dosage regimen such as
maintenance therapy.
I f ulcer is not healed so shift
to another line of treatment.
Side effects:
constipation, diarrhea,
H2
antihistaminics
Ranitidine Cimetidene
Nazitidine Famotidine
Axid
(amp+cap)
Apo-famotidine
Apo-cimetidine CimetrilApo-ranitidine Ranicux
Rantag Zantac
Gastrodomina Pepcid
Famodar
Neutronorm
41. Mode ofaction:
They irreversibly inhibit H+
pump or H+/K+ ATPase which is
an enzyme in the cell membrane
of oxyntic or parietal cells, they
block the final step for HCl
secretion.
Regular use of these can
cause achlorohydria because
they act on HCl formation not on
receptors that increase HCl
secretion. They are the most
potent anti-secretory drugs.
Side effects:-
constipation, diarrhea, colic,
nausea.
P.pump
inhibitor
Rabeprazole Pantoprazole
Omeprazole lansoprazol
Gastrimut Risek
Epirazole Gastrazole
Omepral Oprazole
Pariet Inipomp
Takepron Lanzor
Ulstop Zimor
Esomeprazole
Nexium
Rabec
Lanzomide
Omedar Omizec
Omiz
44. Mechanism of action:
they are selective M1 antagonists.
They are used in combination withH2
blocker because histamine is the main
mediator for HCl secretion.
46. Mode of action:
they have mucosal protective activity
1.increase prostaglandins
2.increase bicarbonate
3.increase mucus production
They have toxic effect on Helicobacter pylori (bactericidal)
can be used as first line treatment with H2 blocker if
helicobacter infection is positive.
Side effects:blackening of the tongue, teeth, and
stools.
47. Mechanism of action:
It causes mucosal protection by:
•Increasing mucus and bicarbonate production.
•Decreasing gastric HCl secretion
Uses:
It is only used for prevention of NSAID_induced ulceration in patients
with high risk
•Elderly
•Smokers
•Patients with history of gastric bleeding.
When NSAIDs are stopped, discontinue misoprostol.
Side effects:
•Gastro intestinal disturbances (vomiting, diarrhea, colic) due to
prostaglandin induced smooth muscle contraction.
•Gynecological disturbances (spotting,dysmennorhea).
•Uterine contractions (contra-indicated in pregnancy because they cause
abortion).
48. Mode of action: used for symptomatic relief.
They act via neutralization of the gastric HCl.
Antacid
Al hydroxide
Mg(hydroxide
or trisilicate)
Adverse rxn
constipation
diarrhea
So a mixture of aluminum and magnesium is used
in combination with H2 blocker and to relieve the
symptoms of hyperacidity.
49. H. pylori can be very difficult to completely
eradicate. Treatment requires a combination of
several antibiotics, sometimes in combination with a
proton-pump inhibitor, H2 blockers or Bi-chelate.
Without such treatment there is an eighty percent
chance the ulcer will reoccur within one year.
Eradication of H. pylori prevents the return of ulcers
(a major problem with all other ulcer treatment
options) Elimination of this bacteria may also
decrease the risk of developing gastric cancer in the
future.
An effective combination would be Amoxicillin +
Metronidazole + Pantoprazole.
50. Fiber slows the movement of food and acidic
fluid from the stomach to the intestines, which
should help those with duodenal ulcer.
51. i. Aspirin and related drugs
(NSAID), alcohol, coffee, and
tea can interfere with the
healing of peptic ulcers.
Smoking is also known to
slow ulcer healing.
ii. Whether or not an ulcer is
caused by infection, people
with peptic ulcer should avoid
use of these substances.
52. 1.Vitamin A is needed to heal
the linings (m.m) of the stomach
and intestines.
2.High dose should not be taken by
a pregnant woman, by a woman who
could become pregnant, or by
anyone else without careful
supervision from a doctor.
3.The effect of lower amounts of
vitamin A has not been studied in
people with peptic ulcer.
53. Zinc is also needed for the repair of
damaged tissue and has protected against
stomach ulceration in animal studies.
Copper must be taken to avoid copper
deficiency that would be induced by the
zinc supplementation.
54. Glutamine, an amino acid, is the
principal source of energy for cells that
line the small intestine and stomach.
Glutamine has also prevented stress
ulcers triggered by severe burns in
another preliminary study.
55. Little is known about the effects of
Vitamin C in peptic ulcer cases.
Vitamin C may also help eradicate
H. pylori in people with gastritis.
Vitamin C may one day prove to
have a therapeutic effect for people
with peptic ulcer; however, further
research in this area is needed.
56. Licorice root has a long history of use
for soothing inflamed and injured
mucous membranes in the digestive
tract. Licorice may protect the stomach
and duodenum by increasing
production of mucin.
Flavonoids in licorice may also
inhibit growth of H. pylori.
57. Chamomile has a soothing effect on inflamed and
irritated mucous membranes. It is also high in the flavonoid
apigenin, another flavonoid that has inhibited growth of H.
pylori.
Chamomile is also available in capsules.
Calendula is another plant with anti- inflammatory and
healing activities that can be used as part of a traditional
medicine approach to peptic ulcers.
The same amount as chamomile can
be used.
59. To decrease risk of ulcer from H.
pylori infection:
Wash your hands after using the
bathroom and before eating or
preparing food.
Drink water from a safe source.
Don’t smoke. Cigarette, smoking
increases the chances of getting an
ulcer.
60. To decrease the risk of ulcer from
NSAIDs:
1.Use other drugs when possible for
managing pain.
2.Take the lowest possible dose.
3.Donot take longer thanneeded.
4.Donot drink alcohol while taking
the drugs.
