P. Kolala presented on peptic ulcer disease. PUD is caused by an imbalance between gastric acid production and mucosal defenses, resulting in ulcers in the esophagus, stomach, or duodenum. Risk factors include H. pylori infection, NSAID use, smoking, and stress. Symptoms include epigastric pain relieved by food or antacids. Treatment involves eradicating H. pylori with antibiotics, reducing acid with PPIs, and surgery if complications occur or medications fail. Nursing care focuses on pain management, diet, medication administration and monitoring for complications.

1. SURGERY AND SURGICAL NURSING
Topic: PEPTIC ULCER DISEASE
Presenter: P . KOLALA
Bsc Nursing Student, DNS, Ridgeway Campus,
UNZA

2. General Objective
At the end of this lecture/discussion, students should
be able to demonstrate knowledge on Peptic Ulcer
Disease and how to manage it.
Specific Objectives
• At the end of the lecture/discussion students
should be able to:
• Define Peptic Ulcer Disease
• State predisposing Factors of PUD.
• Describe the pathophysiology of PUD.
• State the S/S of PUD
• Discuss Medical MNGT of PUD.
• Outline the Nursing Care of PUD.
• Elaborate the I.E.C of PUD.
• State the complications of PUD

3. Anatomy Review

4. Definition of Peptic Ulcer
• A peptic ulcer is also known as ulcus pepticum.
1) It is a break in the continuity of the GIT that may
involve the mucosa, submucosa or muscular layer
of oesophagus, stomach, duodenum.
2) This is a result of an imbalance between the
digesting power of acid secretion and the ability of the
mucosa to resist these digestive action leading to
ulceration of the intestinal walls of the oesophagus,
stomach and duodenum (Dossey, M.B. 2002)

5. 3) Peptic ulcer disease is a condition
characterized by erosion of the gastro-intestinal
mucosa resulting from the digestive action of
hydrochloric acid and pepsin (Lewis et al 2004)
4) A peptic ulcer is a well-defined round or oval
sore where the lining of the oesophagus,
stomach or duodenum has been eaten away by
stomach acid and digestive juices (Berkow et al
1997)

6. TYPES OF PEPTIC ULCERS IN RELATION TO ANATOMICAL
LOCATION
• Oesophageal Ulcers – lower part of oesophagus
• Gastric Ulcers – are found in any part of the stomach but
most common on the lesser curvature.
• Duodenal Ulcers – in the duodenum but most of them are
found in the duodenal cap.
• Marginal Ulcers – where the remaining stomach is
connected to the intestines.
• Merkel’s Diverticulum ulcer- a small, naturally occurring,
outward protrusion (sac or pouch) of the inner lining of the
small intestine through the muscular wall.
• Stress (curlings) Ulcers- occur under stress of severe illness,
burns or trauma. They don’t have have a specific location.

9. INCIDENCE:.
• It is a common condition in males
aged between 40 – 55.
• Duodenal Ulcers are 2-3 times more
common than Gastric Ulcers.
• Gastric Ulcers are more common in
women.
• Duodenal Ulcers is about 5-10 times
more common in men than women.
• Perforation is 20 times more in men
than women.

10. • Acute Ulcers – there is superficial erosion &
minimal inflammation. They are of short duration &
resolves quickly if cause is known & removed. Acute
ulcers are often multiple and are usually located in
the fundus of the stomach. These ulcers are thought
to be stress related, superficial, and self-limiting.
Occasionally, they penetrate a blood vessel causing
haemorrhage of varying degrees of severity.
• Chronic Ulcers – of long duration eroding through
muscular wall with the formation of the fibrous
tissue. It is present continuously for many months
or intermittently throughout the person’s age.
Chronic ulcers are more common than acute ulcers.
These ulcers usually occur as a single lesion with
margins that are thickened, hyperaemic, and
oedematous. Chronic ulcers tend to recur
frequently, causing extensive scarring.

11. • The cause is not fully understood, however, there
are PREDISPOSING FACTORS;
• Emotional Factors: emotional tension, anxiety,
frustration and stress may cause an imbalance in
the autonomic nervous system, resulting in
increased vagal stimulation of gastric secretion.
• Inflammation: gastritis and trauma of the mucosa
reduces the resistance of the membrane to
digestion.
• Hereditary: gastric ulcers are common in people
with type A blood while duodenal ulcers are
common in people with type O blood.

12. • Trauma and serious illness: critical illnesses
especially if it is characterized by hypotension or
respiratory insufficiency may complicate into peptic
ulcer. Conditions such as severe burns or shock may
lead to peptic ulceration.
.
• Exposure to irritants: Chronic use of Non Steroidal
Anti Inflammatory Drugs( NSAIDs) such as
Acetylsalicylic acid and Indomethacin inhibit
prostaglandin production which helps the gut lining
resist corrosive acidic damage.
• Other Drugs like some steroids, phenylbutazone are
ulcerogenic.
• Alcohol also inhibits prostaglandin secretion.

13. Cigarette smoking:
Nicotine in cigarette smoke inhibits pancreatic secretion of
bicarbonate, it also may accelerate the emptying of gastric acid
into the duodenum and promote mucosal breakdown.
Nicotine also increase parasympathetic nerve activity to the
GIT thus increasing the amount of histamine and gastrin
secreted which lead to increased acidity of the gastric juice.
Tar also found in cigarette smoke causes vasoconstriction and
vasospasms leading to vascular insufficiency and promoting the
development of ulcers through ischaemia. This delays wound
healing.
Bile reflux:
the reflux of bile and pancreatic enzymes into the stomach due
to an incompetent pyrolic sphincter may lead to a gastric ulcer.
The bile salts damage the gastric mucosa, predisposing it to
ulceration. Normal aging may also wear down the pyloric
sphincter, which in turn, permits the reflux of bile into the
stomach.

14. Helicobacter Pylori bacteria found in the acidic media
of the human stomach burrow into the mucus that
coats and protects the lining of the stomach and
duodenum leading to ulcers. This bacteria interferes
with normal defences against stomach acid, or give a
toxin that contribute to ulcer formation.
Zollinger Ellison syndrome : A rare condition in which
a pancreatic tumour or Gastrinoma produces
excessive gastrin hormone and excessive outpouring
of Gastric juice leading to mucosal ulceration.
Age; More common in adults & rare in children.
Low socio-economic status may play a role.
Poor eating habits; hurriedly & irregularly.

15. PATHOPHYSIOLOGY
The GIT is normally protected from auto digestion by
the gastric mucosal barrier.
• The mechanisms of mucosal injury in PUD are
brought about by an imbalance in Gastric acid
production and defensive factors such as mucous
production, bicarbonate and blood flow.
• Gastric acid is secreted in the parietal cells of the
fundus of the stomach, as a result of stimulation of
the vagus nerve.
• The Histamine (H2) receptors are found in the cells
of the stomach walls mediate secretion of
hydrochloric acid.

16. • In PUD, the changes in the mucosa occur as a
result of the following:
• Back diffusion of H+ ions into the epithelium,
which causes a release of histamine and
stimulates the production of more
Hydrochloric acid (HCl).
• The erosion of the gastric mucosa is caused
by the digestive action of hydrochloric acid
and pepsin.
• This results in cellular destruction,
inflammation and impairement of mucus
secretion leading to mucosal ulceration.

17. • Histamine is released from the damaged mucosa
resulting in vasodilatation and increased capillary
permeability.
• The released histamine is then capable of
stimulating further secretion of acid and pepsin.
The mucosa lining necrotises with continuous
exposure to gastric acid. The area sloughs off and
the ulcer develops.
• Narrowing of the mucosa causes dysfunction of the
pyloric sphincter leading to reflux of bile from the
duodenum into the stomach which causes further
ulceration.

18. • The bacteria, Helicobacter pylori, causes a
chronic active gastritis resulting in an
increased production of gastrin hormone.
Gastrin stimulates the production of gastric
acid (HCl) and the increase in acid can
contribute to the erosion of the mucosa and
therefore ulcer formation.
• NSAIDs such as aspirin also interfere with the
protective mucus layer by inhibiting mucosal
activity, reducing mucosal prostaglandins
which cause abnormal permeability of the
mucus layer.

19. • If the ulcer erodes through all the layers of the
stomach or duodenum wall, perforation occurs.
Erosion of a blood vessel causes haemorrhage.
• Large ulcers often penetrate into adjacent tissues
such as Liver or Pancreas causing fistula formation.
• Regenerative changes may give rise to malignant
changes of the Gastric mucosa.
• Oedema, spasms or contraction of scar tissue
formed during healing process may cause pyloric
stenosis or obstruction. #

20. CHARACTERISTIC GASTRIC ULCER DUODENAL ULCER
Site Of Pain Left Epigastrium Epigastrium
Type of pain Patient describes the pain as heartburn or
indigestion accompanied by a feeling of abdominal
fullness.
Patient describes the pain as being sharp, burning,
aching and poorly defined.
Pain Aggravation Food Intake: because acid secretion increases at
meal time.
Hunger : when the stomach is empty, the pyloric
sphincter allows passage of gastric fluids into the
Duodenum.
Timing and duration of Pain Pain occurs half to 1 hour after ingestion of food.
No pain at hours of sleep because of reduction in
HCl Production.
Pain occurs 90 minutes to 3 hours after eating. Usually
occurs at night disrupting his sleep because gastric
emptying continues in sleep.
Relief of Pain Relieved by an empty stomach hence, Weight Loss. Relieved by food intake, hence, Weight Gain
Vomiting Relieved by Vomiting because acid is expelled Not relieved by vomiting.
DISTINCT CHARACTERISTICS BETWEEN GASTRIC AND PEPTIC ULCERS

21. Signs and Symptoms of Peptic Ulcers
• Epigastric pain which is burning and relieved
by food or antacid. (Duodenal ulcers) or dull
pain and not usually relieved by food or
antacid (gastric ulcer).
• Persistent vomiting due to pyloric stenosis
and acid regurgitation.
• Nausea, vomiting and anorexia – common in
gastric ulcers due to vagus nerve which
stimulate the hypothalamus and
consequently the vomiting centre.
• Dyspepsia (Indigestion) and HeartBurn due to
regurgitation of Gastric contents.

22. • Occult Blood in stool due to bleeding
from a perforated ulcer.
• Weight loss due to painful gastric ulcers
which occurs soon after eating food. But
there is weight gain in duodenal ulcers
because pain is relieved by food intake.
• Haematemesis and Malaena
• Anaemia – may be present in chronic
peptic ulcer cases due to haemorrhage
from perforated ulcers & poor Nutrition.
• Leucocytosis – common when
perforation or penetration has occurred.

23. INVESTIGATIONS
History:
• pain relieved with food or
aggravated by food intake.
• Blood in Stool or Vomitus.
• Persistent epigastric pain
Physical Examinations:
• Pain on epigastric palpation.
• Blood in vomitus or stool.

24. Clinical Tests:
• Endoscopy to visualize the stomach and the
duodenum since an ulcer is usually visible through
an endoscope and this is a first diagnostic
procedure done by the doctor.
Endoscopy (confirms the presence of an ulcer and
permits cytologic studies to rule out H. pylori and
cancer.
• Exfoliative cytology – secretory cells scrapped off
the membrane to distinguish malignant from
benign ulcers.

25. • Barium Contrast X-Rays of the stomach
and the duodenum (Barium Meal) are
useful when endoscopy doesn’t reveal
an ulcer.
• Gastric analysis done to measure the
acidic levels.
In Zollinger Ellison Syndrome there will be
hyperacidity.
• Tissue biopsy from the stomach lining to
test for Helicobacter pylori infection and
also to exclude cancer.

26. • Stool for microscopic to rule out
occult blood.
• Stool test for qualitative detection
of H. Pylori
• Haemogloblin level estimation to
rule out anemia as a result of
bleeding.
• FBC: White cell count will be
elevated if infection is present

27. TREATMENT
Conservative management:
AIMS
• To provide pain relief
• To eradicate H. pylori infection
• To heal ulcerations by reducing gastric secretions and
protecting the mucosa from further damage,
• To prevent recurrence
• To relieve symptoms
• prevention of complications
EMPHASIS MUST BE PUT ON;
• Diet – non irritating foods
• Rest and stress reduction
• Avoidance of Smoking

28. Drug Therapy
Eradication therapy
• Current recommendations are that all
patients with duodenal ulcers and gastric
ulcers should have H. pylori eradication
therapy (triple therapy) for 14 days using a
proton pump inhibitor, and a combination of
two antibiotics :
• Omeprazole,
• Clarithromycin,
• Tinidazole.

29. Omeprazole 20mg orally twice daily for 4 to 8
weeks
• Action: inhibits the activity of the proton
pump and blocks the formation of gastric
acid (HCl).
• Side effects: headache, dizziness, diarrhea,
abdominal pain, nausea, vomiting,
constipation, flatulence, rash, cough, upper
respiratory infection
• Nursing Implications: caution patient not to
perform hazardous activities if dizziness
occurs; tell patient to swallow capsules
whole and not to open or crush them

30. Clarithromycin 500mg orally tds
• Action: blocks bacterial protein synthesis
• Side effects: headache, diarrhea, nausea, abdominal pain or
discomfort
• Nursing Implications: use cautiously in patients with hepatic
or renal impairment.
Tinidazole 500mg orally bd
Also helps in alleviating bacteria.
• Side effects: vertigo, headache, ataxia, syncope, abdominal
cramps, nausea and vomiting, anorexia, seizures
• Nursing Implications: instruct patient to take drug with
food; tell patient to avoid alcohol while taking the drug and
for at least 48 hrs after completing therapy; tell patient that
he will experience metallic taste and dark or red-brown
urine.
• Where Tinidazole is absent: GIVE
• Metronidazole 400mg (orally) or 500mg (intravenously) TDS
OR
• Amoxicillin 500mg TDS

31. Other Drugs
ANTIACIDS
• To reduce the total acid load in GIT,
elevate gastric PH to reduce pepsin
activity, strengthens the gastric mucosal
barrier and increases oesophageal
sphincter tone:
• Magnesium Triscilicate 250mg-500mg
chewed as required.
• Aluminum Hydroxide 500mg chewed as
required.

32. HISTAMINE (H2) RECEPTOR ANTAGONISTS
• Ranitidine 150mg -300mg P.O
• 25mg-50mg intramuscularly or
intravenously QID.
Ranitidine reduce gastric secretion for
short term therapy up to 8 weeks.
• Cimetidine; 200mg daily per oral to
reduce the risk of bleeding from stress
ulcers. Depending on the condition,
400mg -800mg BD can be given.

33. MUCOSAL BARRIER FORTIFIERS:
• sucralfate 1g PO qid or 2g BD 1hr before and 2hrs
after meals, and at bed time; do not give within
30min of giving antacids or other drugs.
• adheres to and protects the ulcer’s by forming a
barrier so that hydrochloric acid does not gain
access onto the ulcer.
ANTICHOLINERGICS
• Propantheline Bromide 15-30mg, to inhibit the
vagus nerve effect on the parietal cells by blocking
Acetylcholine (a neurotransmitter) thereby reducing
gastrin production and excessive gastric activity.

34. SURGERY
• The aim of surgery is to reduce acid and
pepsin secretion and this is achieved by
interrupting the vagus nerve by Surgical
intervention.
Indications:
• failure of medical treatment.
• Complications like perforation, pyloric
stenosis & haemorrhage.
• Potential malignant lesions.
• Chronic recurring ulcers.

35. TYPES OF SURGERY
• .Partial gastrectomy (Billroth I) – part of the stomach
affected by an ulcer is removed with part of the pylorus and
the stomach connected to the duodenum.
• Gastro-jejunostomy (Billroth II) – pyloric area, duodenum
and part of the stomach are removed with the remaining
stomach being connected to the jejunum.
• Total gastrectomy – complete removal of the stomach with
anastomosis of oesophagus to the jejunum in multiple
ulcers.
• Vigotomy – dissecting the vagus nerve in order to reduce the
secretion of acid.
• Pyloroplasty – repairing or widening pyloric area.
• Antrectomy – removal of cells that secrete gastrin thus
reducing the amount of Gastric acid production..

36. NURSING CARE
Hospitalization is not always
necessary, however, if patient can not
adhere to treatment regimen or
home situation is not conducive, the
patient may be hospitalized until
symptoms are relieved and patient
and relatives appreciate treatment
plan. Treatment and care is
individualized for all patients.

37. PRE-OPERATIVE CARE
Surgery is generally classified as elective or emergency.
ELECTIVE SURGERY
Psychological Care
• The condition is explained to the patient that surgical
intervention is the only treatment for example in the case of
pyloric stenosis. . All questions should be answered to allay
anxiety.
Relief of Pain and Discomfort
• Administer analgesics such as Paracetamol.
• Ensure quiet environment
• Do related procedures at same time to avoid disturbing the
patient.
• Limit visitation since sometimes they can be distressing.

38. Nutrition
• Prior surgery, the patient should fast for
4hours for fluids and 6 -8hours for food. Keep
him on IV Fluids
Hygiene
• The patient is asked to shower several hours
prior to theatre. Dress him in a clean theatre
gown to reduce post-operative infections and
exposure to nosocomial infections.
• Shave or trim hair on the abdominal surface.
Identification Band
• A name band is written bearing patients
name, age, sex, type of procedure and ward.
This is important for identification and
avoiding performing a different operation.

39. Informed Consent
• Ensure the patient signs a consent form. In case the
patient does not know how to write, a thumb print
is legal and the nurse may finish off filling the
consent form.
Specimens
• Venous blood for haemoglobin estimation, grouping
and cross match is collected and taken to the lab
before surgery. Blood for transfusion is collected in
advance from the laboratory in case of severe
bleeding during surgery.
Elimination
• The patient is catheterized prior surgery with a
urethral indwelling catheter.

40. Observations
• The general condition of patient is
reviewed and vital signs checked.
The general condition should be
good before surgery and vital signs
should be within normal range.
• Document the findings.
Pre Medication
• Administer premedication such as
Atropine, An Antibiotic or
Diazepam.

41. POST OPERATIVE CARE
Position
• Position patient comfortably and change
position 2 hourly promote comfort.
Environment
• The environment should be quite to promote
rest and clean to prevent infections. All the
necessary accessories such as oxygen
concentrator, suction machine and drip stand
should be available.
Psychological Care
• Patient may be anxious and restless due to
the effects of surgery and pain. Answer his
questions to allay anxiety. Explain every
therapeutic intervention done. Let the loved
ones visit the patient at appropriate times.

42. Observations
• Vital Signs
• Airway obstruction
• The nasogastric aspirate
• Bleeding and drainage from the
wound
• Skin colour
• The intravenous infusion and site
• Urinary out put

43. Exercises
• Patient is encouraged to mobilize in bed
and walking around as the condition
allows to prevent Deep Vein Thrombosis
and deep breathing frequently to
prevent hypostatic pneumonia.
Encourage early ambulation.
Medication
• Strong analgesia such as Pethidine 50-
100mg QID intramuscularly is given to
relieve pain. Antibiotics are given to
combat infection and other drugs are
given as prescribed and documented.

44. Hygiene
• Bed bath is done in the first 48hours thereafter as condition
allows an assisted bath in the bathroom is done. Oral care
2hourly is done for the patient in the first 24hours
thereafter, patient can do it on his/her own.
• Wound dressing is changed as ordered, suture line swabbed
with spirit, dressing changed and sutures removed as
ordered.
Nutrition
• The patient will be nil orally until bowel sounds are heard or
until he is able to pass flatus. Initially, the patients will be on
IVF 3litres in 24hours or as per prescription. When bowels
sounds return, sips of water will be given first, free fluids,
soups, porridge, semi-solid foods and later normal diet.

45. Elimination
• The patient will have a urethral indwelling
catheter.
• Catheter toilet is done once or twice a day.
• Monitor Elimination closely and update a
fluid balance chart.
• Urine output is recorded taking note of the
amount and colour before discarding.
• By third day post operatively, the indwelling
catheter is removed to prevent ascending
infections.

46. I.E.C
• Teach the patient about the disease.
• Encourage the patient to stop smoking and avoid
disturbing /stressful activities.
• Encourage the patient to eat at regular intervals.
• Teach on stress management especially at work e.g.
taking leaves, work delegation.
• Keep review dates and adhere to treatment.
• Offer regular meals, small in amount and easily
digestable.
• Encourage proper chewing.
• Avoid very hot, cold and highly seasoned food –
these stimulate secretion of HCL
• Diet: Substances which stimulate gastric secretions
such as coffee, strong tea, highly seasoned food,
citrus fruit and alcohol should be avoided.

47. • Bed time snacks should be avoided
because they stimulate gastric acid
secretion.
• Avoidance of irritating agents e.g.
smoking and alcohol, drugs such as
aspirin and medications that are not
prescribed.
• Complications: any pain, vomiting,
abdominal distention or gastric distress
should be reported promptly to the
health facility so that early treatment
may be instituted.

48. COMPLICATIONS
HAEMORRAGE
• This is due to erosion of blood vessels and this may lead to
haematemesis and melaena. If haemorrage is severe, signs
of shock are present such as cold clammy skin, hypotension,
tachycardia and restless.
PERFORATION
• perforation result from progressive erosion of the mucosa,
submucosa and muscular layers of the gastrointestinal wall.
• A peptic ulcer may perforate through into the peritoneal
cavity and cause acute abdomen.
• Perforation complicates to bacterial septicaemia,
hypovolaemic shock, and paralytic ileus.
Perforated peptic ulcer is a surgical emergency and requires
surgical repair.

49. PENETRATION:
• An ulcer located along the posterior wall of the
duodenum or stomach may perforate into
contiguous structures such as the pancreas, liver, or
biliary tree.
• Patient complain of a change in the intensity and
rhythmicity of the ulcer symptoms.
PYLORIC STENOSIS
• this may be caused by inflammation, oedema and
spasms when the ulcer is in the acute stage or by
scar tissue which is formed as the ulcer heals
• The constriction causes Gastric outlet obstruction
leading to gastric retention.

50. MALIGNANT CHANGE
• Gastric ulcers undergo malignant changes as a result of
chronic gastritis.
ANAEMIA
Due to haemorrhage resulting from perforated peptic ulcers.
PERITONITIS
When the peritoneum is penetrated, some of the stomach or
duodenal contents escapes into the peritoneal cavity and
causes generalized peritonitis by chemical irritation and
infection.
DUMPING SYNDROME
• This occurs as a result of surgical removal of a large
portion of the stomach and the pyloric sphincter.
• One of the contributing factors is rapid entry of food
directly into the upper small intestine without first
undergoing the usual break down and dilution in the
stomach.
• It presents with abdominal fullness and discomfort,
nausea, diarrhoea, weakness and dizziness

51. Keep the FOCUS as You
Stay FOCUSED.
‘’Unless you keep Changing
the goal posts, you will not
score GOALs.’’