PEPTIC ULCER

DISEASE

By
Mrs. Sharmila P. Ghodke
Tutor, INE, Mumbai
MSc. Nursing (Med-Surg Nursing - CVTN)
 INTRODUCTION
Peptic ulcer is a condition in which a person experience
severe abdominal pain, especially around the inner part
of the stomach. In this disease, mucous membrane
around the digestive organs gets weakens.

This is most common in those who suffer from acidity

or have some stomach infection.
 QUICK
REVIEW OF
ANATOMY
• Mucous cells in the gastric pits secrete
mucus

• Parietal cells secrete hydrochloric acid

• G cells, which are present

predominantly only in the antrum of the
stomach, secrete gastrin

• ECL cells secrete histamine

• Chief cells secrete Pepsinogen.

 DEFINITION

• Peptic ulcer disease is a condition characterized by

erosion of the GI mucosa resulting from the
digestive action of HCl acid & pepsin.

• Peptic ulcer disease is also called as acid pepsin

ulcer disease or ulcer pepticum.
 INCIDENCE & PREVALENCE
Incidence
• PUD occurs in approximately 10% of the population.
• Gastric ulcers are more likely to occur during 5th & 6th decades of life.
• Duodenal ulcers more commonly occur during the 4th & 5th decades in men. For
women, the occurrence is about 10 years later in life.
• Men - gastric & duodenal ulcers.
• Female - gastric

Prevalence
• 4-10/1000 population in India
• Higher prevalence in developing countries
– H. Pylori is sometimes associated with socioeconomic status and poor hygiene
 TYPES

BASED ON DURATION OF
MUCOSAL INVOLVEMENT BASED ON LOCATION

– Acute • Type I: Ulcer along the lesser curve of

– Chronic stomach
• Type II: Two ulcers present - one
gastric, one duodenal
• Based on location
• Type III: Prepyloric ulcer
– Gastric
• Type IV: Proximal gastroesophageal
– Duodenal ulcer
• Type V: Anywhere along gastric body,
NSAID induced
 CONT…

ACUTE CHRONIC
• Superficial erosion • Long duration
• Minimal inflammation • Eroding through the muscular
• Short duration wall with the formation of
• Resolve quickly when cause is fibrous tissue
identified & removed. • More common than acute
erosion
 COMPARISON OF GASTRIC & DUODENAL ULCERS
Assessment data Gastric ulcer Duodenal ulcer
Lesion Superficial, smooth margins, round, oval or Penetrating
cone shaped
Location Predominantly antrum, also in body & fundus First 1-2 cm of duodenum
Acid secretion Normal to decreased Increased
Sr. pepsinogen Normal Increased
Incidence  Greater in women  Greater in men, but increasing in women
 Peak age- 50-60 yrs (postmenopausal)
 More common in low socio-economic status  Peak age- 35-yrs
 Increases with smoking, drug use (aspirin,  Associated with psychological stress
NSAIDs) & alcohol  Increases with smoking, drug use (aspirin, NSAIDs)
 Increases with incompetent pyloric sphincter & alcohol
& bile reflux  Associated with other diseases (COPD,
Hyperparathyroidism, pancreatic disease, Zollinger-
Ellison syndrome, CRF)
Clinical  Burning or gaseous pressure in high left  Burning, cramping, pressure like pain across
manifestations epigastrium, back & upper abdomen midepigastrium & upper abdomen. Back pain with
 Pain 1-2 hour after meal. If penetrating ulcer, posterior ulcers
aggravation of discomfort with food.  Pain 2-4 hours after meal & midmorning,
 Occasional nausea & vomiting. midafternoon & midnight. Periodic & episodic.
 Weight loss.  Relief with antacid & food.
 Occasional nausea & vomiting.
Recurrence rate High High
Blood group No difference Most frequently type o
Associated gastritis Common and Increased None
Nutritional status Probably Malnourished Usually well Nourished
Malignancy potential Occurs in approximately 10% of clients Rare, no increase in incidence

Bleeding Pattern Hematemesis more common than Melena Melena more common than hematemesis
PEPTIC ULCERS: GASTRIC &
DUODENAL
 ETIOLOGY

• A bacterium: 60% of gastric and up to 90% of duodenal

ulcer is the chronic inflammation due to Helicobactor
pylori.
• Medication induced injury: ulcerogenic drugs (aspirin,
NSAIDs)
• Lifestyle factors
– High alcohol intake
– Coffee
– Psychologic distress (stress & depression)
– Smoking
 ETIOLOGY CONT…
Stress related mucosal disease (SRMD)
 Shock
 Severe burns, severe trauma or major illness
Malignant tumor (4%)
Dietetic indiscretion like overeating, taking of heavy
meals or highly spicy food.
Head injury, or intracranial disease (cushing ulcer)
Gastro esophageal reflux disease.
Zollinger Ellison syndrome (gastrin secreting tumor).
PATHOPHYSIOLOGY
CLINICAL MANIFESTATIONS
GASTRIC ULCER
• Discomfort high in epigastrium &
occurs about 1-2 hrs after meal.
• Burning or gaseous pain.
• If ulcer has eroded through gastric
mucosa, food tend to aggravate the
pain.
DUODENAL ULCER
• Burning or cramplike pain.
• Symptoms: 2-5 hrs after meal
• Pain in midgastric region beneath
the xiphoid process.
• Back pain.
• Antacid, H2 receptor blocker, food
neutralize the acid to provide relief.
• Silent peptic ulcer: common in older
adults & those taking NSAIDs
DIFFERENTIAL DIAGNOSIS
• Neoplasm of the stomach
• Pancreatitis
• Pancreatic cancer
• Diverticulitis
• Nonulcer dyspepsia (also called functional dyspepsia)
• Cholecystitis
• Gastritis
• GERD
• MI—not to be missed if having chest pain
 DIAGNOSIS ENDOSCOPY

• History & PE
• Upper GI endoscopy with biopsy
• H. pylori testing of breath, urine, blood & tissue
• CBC
• Sr. electrolytes
• Liver enzymes
• Sr. amylase
• GI tract x-ray: shows presence of air or gas in peritoneal
cavity in case of ulcer perforation.
• Stool for occult blood
 COMPLICATIONS
• Hemorrhage
• Perforation
• Gastric outlet obstruction
• Perforation & Penetration—into pancreas, liver and retroperitoneal
space
• Peritonitis
• Bowel obstruction
• Bleeding--occurs in 25% to 33% of cases and accounts for 25% of
ulcer deaths.
• Gastric CA
MANAGEMENT
 TREATMENT PLAN: H. PYLORI
• Medications: Triple therapy for 14 days is considered the treatment of
choice.
– Proton Pump Inhibitor + clarithromycin and amoxicillin
• Omeprazole (Prilosec): 20 mg PO bid for 14 d or
Rabeprazole (Aciphex): 20 mg PO bid for 14 d plus
Clarithromycin (Biaxin): 500 mg PO bid for 14 and
Amoxicillin (Amoxil): 1 g PO bid for 14 d
– In the setting of an active ulcer, continue proton pump inhibitor
therapy qds for additional 2 weeks.
• Goal: complete elimination of H. Pylori. Once achieved reinfection rates
are low.
TREATMENT PLAN: NOT H.
PYLORI
• Medications—treat with Proton Pump Inhibitors or H2 receptor
antagonists to assist ulcer healing

– H2: Tagament, Pepcid, or Zantac for up to 8 weeks

– PPI: Prilosec, Prevacid, Nexium, Protonix, or Aciphex for 4-8

weeks.
LIFESTYLE CHANGES
• Discontinue NSAIDs and use Acetaminophen for pain control if
possible.
• Acid suppression--Antacids
• Smoking cessation
• No dietary restrictions unless certain foods are associated with
problems.
• Alcohol in moderation
– Men under 65: 2 drinks/day
– Men over 65 and all women: 1 drink/day
• Stress reduction
 PREVENTION
• Consider prophylactic therapy for the following patients:
– Patients with NSAID-induced ulcers who require daily NSAID therapy
– Patients older than 60 years
– Patients with a history of PUD or a complication such as GI bleeding
– Patients taking steroids or anticoagulants or patients with significant
comorbid medical illnesses

• Prophylactic regimens- prostaglandin analogue or a proton pump inhibitor.

– Misoprostol (Cytotec) 100-200 mcg PO 4 times per day
– Omeprazole (Prilosec) 20-40 mg PO every day
– Lansoprazole (Prevacid) 15-30 mg PO every day
EVALUATION/FOLLOW-UP/
REFERRALS
• H. Pylori Positive: retesting for tx efficacy
• Urea breath test—no sooner than 4 weeks after therapy
to avoid false negative results
• Stool antigen test—an 8 week interval must be allowed
after therapy.

• H. Pylori Negative: evaluate symptoms after one month.

Patients who are controlled should cont. 2-4 more weeks.

• If symptoms persist then refer to specialist for additional

diagnostic testing.
 CONSERVATIVE THERAPY

• Adequate rest

• Cessation of smoking

• Drugs

• Nutritional therapy

• Stress management
 CONSERVATIVE THERAPY
CONT…
• Drugs:
– H2 receptor blockers
• Promote ulcer healing
• Reduce amount of stomach acid secretion into digestive tract

– Proton pump inhibitors

• Block the gastric H, K-ATPase
• Inhibit gastric acid secretion
 CONSERVATIVE THERAPY
CONT…
• Drugs:
– Antibiotics
• Triple drug therapy: (PPI, Amoxicillin, clarithromycin; 7-14 days; eradication
rate- 70-85%)
• Quadruple therapy: (PPI, Bismuth, Tetracycline, Metronidazole; 10-14 days;
85% eradication rate)

– Antacids
• Increase gastric pH by neutralizing the HCl acid
• Aluminum hydroxide: bind the bile salts, thus decreasing damage to gastric
mucosa
 CONSERVATIVE THERAPY
CONT…
• Drugs:
– Cytoprotective drug therapy
• Sucralfate: provides cytoprotection
• Misoprostol: protective & antisecretory effect, given in gastric ulcer
caused by NSAIDs & Aspirin

– Other drugs
• Tricyclic antidepressants: reduces acid secretion & pain
• Anticholinergics: chlorpromazine, antipsychotics
 CONSERVATIVE THERAPY
CONT…
• Nutritional therapy:
– No specific recommendations
– Eat & drink foods & fluids that do not cause any distressing
symptoms.
– Avoid caffeine containing beverages
– Eliminate alcohol
– Avoid hot, spicy foods, pepper, carbonated beverages & broth
(meat extract)
 THERAPEUTIC DIET
NAME OF DIET INGREDIENTS
1.Sippy`s diet and its Hourly feeds of milk, cream and olive
modification by hurst. oil with antacids medication.

1. Lenhartz diet. Fluid diet based on milk and eggs.

1. Meulengracht diet. A mixed bland diet containing milk,

egg. meat and fish(minced and
strained)- Given once in 2 hrs.
SURGICAL MANAGEMENT
• Indications
– Patients with complications
– Unresponsive to medical management

• Surgical procedures
– Billroth I (Gastroduodenostomy)
– Billroth II (Gastrojejunostomy)
– Total gastrectomy
– Vagotomy (Truncal or selective)
– Pyloroplasty
Antrectomy - remove the
lower part of the stomach
(antrum), which produces a
hormone that stimulates the
stomach to secrete
digestive juices. A
vagotomy is usually done
in conjunction with an
antrectomy.
Pyloroplasty - the opening into
the duodenum and small
intestine (pylorus) are enlarged,
enabling contents to pass more
freely from the stomach. May
be performed along with a
vagotomy.
 VAGOTOMY

Vagotomy - cutting the vagus nerve to

interrupt messages sent from the brain
to the stomach to reducing acid
secretion.
 COMPLICATION OF
GASTRIC SURGERIES
COMPLICATION OF GASTRIC
SURGERIES
ACUTE
• Bleeding at surgical site
LONG TERM
• Dumping syndrome
• Postprandial hypoglycemia
• Bile reflux gastritis
TREATMENT OF HAMORRAGE
 Assess bleeding.
 Prevent shock
 Administer vasopressin.
 Maintain rest
 Maintain high gastric PH-
 Stop bleeding surgically.-Perform multipolar
electro coagulation or heater probe therapy- to
cauterizes bleeding lesion
Photocoagulation( Laser)
Electrocoagulation( heat is generated
by high frequency electrical current)
Injection therapy ( Adrenalin or saline)
Angiographic therapy
DUMPING SYNDROME
POSTPRANDIAL HYPOGLYCEMIA

Bolus of concentrated CHO

Hyperglycemia

Release of excessive insulin

Reflex hypoglycemia
 BILE REFLUX GASTRITIS

Reconstruction or removal of pylorus

Reflux of bile into stomach

Prolong contact damages gastric mucosa

Chronic gastritis

Recurrence of PUD
 NURSING DIAGNOSIS

– Acute pain or chronic pain related to effect of gastric acid secretion

on damaged tissue.
– Imbalanced nutrition less than body required related to decrease
nutrient absorption. secondary to dumping syndrome.
– Ineffective therapeutic regimen management related to lack of
knowledge of cause of ulcer and measures to prevent recurrence.
– Risk for injury related to bleeding & distention.
 NURSING DIAGNOSIS
1.Acute pain or chronic pain related to effect of
gastric acid secretion on damaged tissue.
Intervention:-

a) Assess the general condition of patient.

b) Assess the onset, duration, location and severity of
pain.
c) Administer prescribe medication and avoid steroids.
d) Promote rest and relaxation.- It helps in decreasing
gastric secretion and peristalsis.
e) Modify diet.- Advise the patient to eat small amount
at frequent, regular intervals.
2.Risk for injury related to bleeding, distention .and
atelectasis.

INTERVENTION:-
Maintain NG tube
Monitor for complication
Promote comfort
Monitor the sign and symptoms hemorrhage such as
haematemesis and melena
Monitor vitals signs.
Monitor hematocrit and hemoglobin level as ordered
3.Imbalanced nutrition less than body required related to
decrease nutrient absorption. secondary to dumping syndrome.

INTERVENTION:-

Assess the general condition of patient.

Maintain intake/output chart.

Clamp NG tube as healing occurred. As per doctors order.

And initiate clear water 30 ml at a time.

Ask patient to take regular diet of 5to 6 small meals a day.

Maintain daily weight recording.

4.Ineffective therapeutic regimen management related
to lack of knowledge of cause of ulcer and measures to
prevent recurrence.

INTERVENTION:-

• Educate client regarding pathogenesis of ulcer.

• Educate client regarding importance of continuing medication.

• Help client to realize that healing takes place rapidly when irritating
effect is removed.

• Provide psychological support to client and discuss about coping

and relaxation technique.
THANK YOU