An ulcer is defined as disruption of the

mucosal integrity of the stomach or

duodenum leading to a local defect due to
active inflammation.

A PEPTIC ULCER is a break or

ulceration in the protective mucosal lining
of the lower esophagus,stomach or
duodenum.
 or,
The breakage and abrasions that affect the mucosa
of GI tract and it is caused by some
trauma,infection,microbes and by some highly
metabolized medicines is known as peptic ulcer
disease(PUD).
•It is the degeneration and programmed cell death of
GI mucosa that exposed to secretion of peptic acid.
•The enzymes HCl and pepsin which exposed to the
alimentary canal can cause ulcer most commonly in
duodenum and stomach of ratio 4:1.
 EPIDEMIOLOGY
• Acid peptic disorders are very common in the
UNITED STATES.
• The prevalence of [Link] is more common in
developing countries than in industrialized
countries,[Link] prevalence exceeds 80% in
adults.
• The prevalence of [Link] in the united states
is 30% to 40%,but remains higher in ethnic
groups such as African and latin americans.
• As many as 90% of ulcers are
associated with Helicobacter pylori, a
spiral-shaped bacterium that lives in the
acidic environment of the stomach.

• Ulcers can also be caused or worsened

by drugs such as aspirin and other
NSAIDs.

• Although H. pylori infection is usually

contracted in childhood, perhaps
through food, water, or close contact
with an infected individual. usually
doesn't cause problems in childhood, if
left untreated it can cause gastritis (the
irritation and inflammation of the lining
of the stomach), peptic ulcer disease,
and even stomach cancer later in life.
 • More peptic ulcers arise in the duodenum
(first part of the small intestine, just after
the stomach) than in the stomach.
• Duodenal ulcers usually first occur between
the ages of 30-50 years and are more
common in men.
• Stomach (or gastric) ulcers usually occur in
people older than 60 years and are more
common in women.
 CLASSIFICATION
1. Acute Peptic Ulcer
[Link] Ulcer
[Link] Ulcer
[Link] Peptic Ulcer
a. Gastric Ulcer
b. Duodenal Ulcer
c. Esophageal Ulcer
d. Bleeding Ulcer
e. Refractory Ulcer
ACUTE PEPTIC ULCER
[Link] Ulcer:
Gastric,duodenal or esophageal ulcer arising in
patients with intercranial injury or operation.
[Link] ulcer:
Occuring mostly in the proximal duodenum and
associated with severe burns and trauma.
CHRONIC PEPTIC ULCER
[Link] ulcer:A gastric ulcer is a sore that is on the inside
of the stomach
Causes:
[Link] with Helicobacter pylori
[Link](Asprin,Ibuprofen,Diclofenac)
[Link] Ulcer:
The peptic ulcer having a sore on the upper part of small
intestine.
Causes:
[Link]
[Link] of lining of mucosal wall.
[Link] Ulcer:
•Open sores or lesions in the lining of esophagus.
•Mostly occur in the lower end of esophagus.
Causes: Associated with bad case of chronic GERD.
[Link] Ulcer:
•Internal bleeding is caused by a peptic ulcer which has been
left untreated.
•When this happens it is now referred to as bleeding ulcer.
•Most dangerous type of ulcer.
[Link] Ulcer:
•These are simply peptic ulcers that have not healed after
atleast 3 months of treatment.
Features Duodenal Ulcer Gastric Ulcer

Age 30-40 50-60

Sex Male Female

Occupation Stress Job E.g,Manager Same

Pain Epigastric,dscomfort Epigastric pain can radiate

to back
Onset 2-3 hrs after eating Immediately after eating

Relived by Eating Lying down or vomiting

Duration 1-2 months Few WEEKS

Vomiting Uncommon Common

Appetite Good Afraid to eat

Diet Good,eat to relieve the pain Avoid fried food

Weight No weight loss Weight loss

Hematemesis 40% 60%

Melena 60% 40%

 ETIOLOGY

• [Link]
• NSAIDS Induced and other drugs
• Dyspepsia
• Cigarette Smoking
• Alcohol Consumption
• Emotional Stress
• Psychologic Stress
• Zollinger Ellison Syndrome
Etiology of PUD

Normal

Increased Attack
Hyperacidity

Weak defense
Helicobacter pylori*
Stress, drugs, smoking
• Peptic ulceration is strongly associated
with [Link] infection.
• Prevalence of [Link] infection rises
steadily with age.
• Infection occurs in childhood but remains
asymptomatic and only minority people
develop clinical disease.
Helicobacter pylori infection
• Gram Negative Organism
• Spiral or helical shape that lives in the acidic
environment in the stomach.
• Microaerophilic
• Resides in gastric-type epithelium within or
beneath the mucous layer.
• [Link] is a potent producer of urease,which is
capable of splitting urea into ammonia and
bicarbonate,creating an alkaline
microenvironment in the setting of an acidic
gastric milieu.
• Production of toxic products that cause local tissue
injury-infection with [Link] leads to the
disruption of gastric mucous barrier by the
enzymes produced by the organism.
• Induction of a local mucosal immune response.
• Increased gastrin levels with a resultant increase in
a secretion.
• Gastric metaplasia occurring in the
duodenum,then decrease duodenal Ph.
• Allows [Link] to colonize these areas of the
duodenum.
• Some strains of [Link] produce
cytotoxins,notably the Cag A and Vac A
products,and the production of cytotoxins
seems to be associated with the ability of
the organism to cause gastritis,peptic
ulceration and cancer.
NSAIDs Induced:
•Cox 1 and 2 is an enzyme which is responsible for the
production of prostaglandins through the arachidonic acid
synthesis and these prostaglandins are responsible for the
inflammatory response,fever or pain.
•PG’s are also responsible to maintain the alkalinity of
stomach by enhancing the production of bicarbonates.
•NSAIDs are used to treat in these conditions in order to
eradicate the inflammation.
•They irreversibly bind with the cyclooxygenase enzyme
and inhibit the production of prostaglandins thus reducing
inflammation.
• The decreased level of prostaglandins diminishes the
protecting capacity of it towards the gastric mucosal
lining as the blood flow towards the linings is altered due
to the use of NSAIDs.
• The production of bicarbonates also diminishes as the
result of which,the environment of the stomach becomes
acidic.
• The acidic environment,make the NSAIDs to remain in
the stomach for the longer period of time,which disturbs
the permeability of gastric cells.
• Damaged mucosal lining and the gastric environment in
this way make the stomach more prone to induce peptic
ulcer
• Gastrinomas (Zollinger Ellison syndrome), rare
gastrin-secreting tumors, also cause multiple and
difficult to heal ulcers.
• Excessive alcohol consumption Alcohol can irritate
and erode the mucous lining of stomach and increases
the amount of stomach acid that's produced. It's
uncertain, however, whether this alone can progress
into an ulcer or if it just aggravates the symptoms of
an existing ulcer.
• Caffeine

Beverages and foods that contain caffeine can stimulate

acid secretion in the stomach. This can aggravate an
existing ulcer, but the stimulation of stomach acid can't
be attributed solely to caffeine.
 Role of Stress

♫ A study of peptic ulcer patients in a Thai hospital showed that chronic stress
was strongly associated with an increased risk of peptic ulcer, and a combination
of chronic stress and irregular mealtimes was a significant risk factor.

♫ An expert panel convened by the Academy of Behavioral Medicine Research

concluded that ulcers are not purely an infectious disease and that psychological
factors do play a significant role. Researchers are examining how stress might
promote H. pylori infection.
CLINICAL MANIFESTATIONS
• Burning Pain • Bloating
• Nausea • Water brash
• Unexplained Weight loss • Hematemesis
• Appetite changes • Melena
• Vomiting • Stomach pain wakes you
• up at night
Anemia
• An early sense of fullness
• Frequent burping or
with eating
hiccupping
 WARNING SIGNS

vomit blood sudden, severe pain

vomit food eaten hours or ongoing nausea or

repeated vomiting.
days before

feel unusually weak or

feel cold or clammy
dizzy

pain doesn't go away

blood in your stools losing weight
With medication
 Pathogenesis of peptic ulcer:

Peptic ulcers are produced by an imbalance

between the gastro-duodenal mucosal defense
mechanisms and damaging forces of gastric
acid and pepsin, combined with superimposed
injury from environmental or immunologic
agents.
COMPLICATIONS
1. Gastrointestinal bleeding is the most common
complication. Sudden large bleeding can be life-
threatening. It occurs when the ulcer erodes one of the
blood vessels. Bleeding can occur as slow blood loss
that leads to anemia or as severe blood loss that may
require hospitalization or a blood transfusion.

2. Perforation (a hole in the wall) often leads to

catastrophic consequences. Erosion of the gastro-
intestinal wall by the ulcer leads to spillage of stomach
or intestinal content into the abdominal cavity.

3. Scar tissue Scarring and swelling due to ulcers

causes narrowing in the duodenum and gastric outlet
obstruction. Patient often presents with severe vomiting.
TESTS AND DIAGNOSIS
 Noninvasive

Urea Breath Test (UBT) Blood test

Invasive

Histology Biopsy Urease Test

 Culture

Other tests Stool antigen test

Endoscopy

Upper gastrointestinal (upper GI) X-ray

TREATMENT
GOALS OF TREATMENT
[Link] elimination of H. Pylori.
[Link] the amount of acid that stomach makes, neutralizing the
acid .
[Link] the injured area so it can heal
[Link]'s also very important to stop smoking and drinking alcohol
[Link] complications (bleeding, perforation, penetration,
obstruction)
[Link] recurrences
 Non-pharmacological Therapy
• Regular small meals are advisable.
• Smoking and alcohol should be avoided.
• Avoid stress.
• Coffee or tea should be taken only in moderation,because they
are strong stimulants of acid secretion.
• Late snacks are best avoided,because they stimulate nocturnal
gastric secretion.
• Drink water.
• Patients with PUD should discontinue NSAIDs.
PHARMACOLOGICAL THERAPY
1. H2 Receptor antagonists.
e.g. Ranitidine
Famotidine
Nizatidine
Cimetidine
•Suppressing nocturnal acid secretion
•Less potent than PPI but still supress 24hr.
•Drug Formulation: PO,IV,IM
•Frequency: SINGLE NIGHT OR TWICE DAILY
DOSE.
 SPECIAL INSTRUCTION:
There is some evidence that dosing
after the evening meal gives superior
results to bedtime dosage.
Reduce dose of H2 receptor
anatagonists in patients with decreased
creatinine clearance.
ADR:Headache,Tiredness,Constipatio
n,Diarrhoea
2. Proton Pump inhibitors(PPI)
Drugs of first choice
•Prefer either complicated or unresponsive
to treatment with H2- receptor antagonists.
•Prevention of recurrence of NSAID
associated gastric ulcers in patients who
continue NSAID use and for reducing the
risk of duodenal ulcer recurrence associated
with [Link] infections.
OLPER
O-Omeprazole
L-Lansoprazole
P-Pantoprazole
E-Esomeprazole
R-Rabeprazole
[Link] Protectants
Example:Sucralfate
•It is a basic aluminium salt of sulfated sucrose.
•Prophylaxis of stress ulcers.
•Instructions:Take the drug in an empty stomach( 1
hour before the major meals)
•Half life: 2-4 hr
•Precaution:Care should be taken patient with CRF.
•CI: Hypersensitivity to sucralfate or any of its
excipients.
ADR
Common:Constipation
Serious:Hyperglycaemia i.e., DM patients
4. Antacids
•In young patients(under 40 years) and those
with chronic,stable,mild symptoms.
•Sodium bicarbonate effectively neutralizes acid.
CI: Chloride loss by vomiting
Precaution: Renal impairement,sodium restricted
diet.
ADR: Cellulitis,Metabolic alkalosis,Skin
ulcer,Tissue necrosis
 Treatment Plan: H. Pylori
• Medications: Triple therapy for 14 days is
considered the treatment of choice.
Proton Pump Inhibitor + clarithromycin and
amoxicillin.
–Goal: complete elimination of H. Pylori.
Once achieved reinfection rates are low.
THREE DRUG REGIMEN
PLEASE CATCH APPLE(MANGO)
•P-PPI
•C-Clarithromycin
•A-Amoxicillin(Alternative-Metronidazole)
FOUR DRUG REGIMEN
PLEASE MAKE TUMMY BETTER
P-PPI
M-METRONIDAZOLE
T-TETRACYCLINE(alternative-
Amoxicillin,Clarithromycin)
B-BISMUTH SUBSALICYLATE
AMOXICILLIN
•Half life:immediate release-61.3 min
extended release-1.5 hrs
Precaution:
Several renal impairement,Erythematous
skin rash
CI: serious hypersensitivity reactions
steven jhonson syndrome
beta-lactam antibiotics(only in
combination)
ADR:
Rash,Vomiting,Diarrhoea,Anaphylaxis,Anem
ia,AST/ALT elevation.
DI:
Tetracyclines
Warfarin
Methotrexate
Piperine
Venlafaxine
CLARITHROMYCIN

DOSE: 250mg every 12 hours(3 to 4 hours)

500mg every 12 hours (5 to 7 hours)

Precaution: Renal impairement

severe ,with or without hepatic
impairement
CI: 1. Cholestatic Jaundice and hepatic dysfunction
2. Hypersensitivity
3. QT Prolongation
DI:
[Link] derivatives and Macrolide antibiotics( increase
risk of acute ergotism)
[Link] and clarithyromycin(Increased risk of
cardiotoxicity)
[Link] and Simvastatin(increased risk of
myopathy or rhabdomyolysis.
ADR:
Common:(GI)Abdominal pain,Diarrhoea,Disorder of
taste,Indigestion,Nausea,Vomiting.
Neurologic: Headache
Serious(CVS):Death,Prolonged QT-Interval.
Hepatic: Hepatitis
METRONIDAZOLE:
Dose:500mg
Half Life:8 hours
Precaution:
Hepatic disease,Peripheral Neuropathy,Skin
reactions,Renal disease.
CI:
Hypersensitivity to Metronidazole
Pregnancy-1st trimester in patients being treated
for trichomoniasis.
DI:
[Link] and Disulfiram(Result in CNS Toxicity)
[Link] and Ziprasidone(Increased risk of QT-Interval
prolongation).
Metronidazoe and Warfarin(Increased risk of bleeding).
ADR:
[Link]:
GI:- Abdominal discomfort,Metallic taste,Diarrhoea,Nausea.
Immunologic: Jarisch Herxheimer reaction.
Neurologic:Dizziness
[Link]:
Stevens-Jhonson syndrome,Leukopenia,Hepatic
failure,Hepatotoxicity,Ototoxicity.
BISMUTH SUBSALICYLATE
•Cytoprotective agents
•Half life: 2-5hrs
•Precaution:
[Link] or other gastrointestinal mucosa abnormalities
[Link] ,Gout or Diabetic medications.
[Link] hypersensitivity.
CI:
[Link] or teenagers with or recovering from
influenza or varicella.
[Link] to the bismuth subsalicylate or
salicylates.
ADR:
Serious: Neurotoxicity
TETRACYCLINE
Tetracycline works best when taken on an empty
stomach 1 hour before or 2 hours after meals.
Do not lie down for atleast 10 minutes after
taking this medication.
Take this medication 2-3 hour before or after
taking any products containing
magnesium,aluminium or calcium.
ADR:
•Nausea,Vomiting,diarrhoea,dizziness,headac
he.
• Serious: Nail discoloration,muscle
pain,brown/gray tooth
discoloration,numbness/tingling of the
hands/feet,yellowing eyes.
•Tetracycline may rarely cause a serious
increase in pressure inside the
skull(intracranial pressure).
LIFE STYLE AND HOME REMEDIES
Don't smoke Spicy foods

Limit or avoid alcohol

Less Avoid nonsteroidal

Coffee and anti-inflammatory
Carbonated drugs (NSAIDs)
Beverages

Exercise

Fruits Stress Relief