PEPTIC ULCER DISEASE

PRESENTED BY LAYTON
KYOTALIMYE

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 OBJECTIVES
Definition of PUD

Classify of pud

Etiology and risk factors for PUD

clinical features of PUD

Medical and nursing management

Nursing diagnosis

complications

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 Review of anatomy
The wall of the gastro intestinal tract is formed by
walls ;mucus layer, submucous layer, muscular
layer which Consists of a break in the superficial
epithelial cells penetrating down to the muscularis
mucosa

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 Stomach Defense Systems against HCL
destruction
Mucous layer
Coats and lines the stomach
First line of defense
Bicarbonate
Neutralizes acid
Prostaglandins
Hormone-like substances that keep blood
vessels dilated for good blood flow
Also stimulate mucus and bicarbonate
production
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 PUD Refers to ulceration in the mucosa of the
lower oesophagus , stomach or duodenum by
disruption of normal balance of corrosive effect of
gastric juice and the protective effect of the mucus
on the gastric epithelial cells.
It is called peptic ulcer because any portion that
comes into contact with the gastric contents
(pepsin /HCL) maybe affected.
The most common sites for ulcers are Stomach,
the 1st few cms of the duodenum. And in the lower
2/3 of the Oesophagus following reflux of gastric
juice in GERD.
LAYTONK@MEDICINE
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 Peptic Ulcer Disease sites

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 Etiology and risk factors for PUD
if factors associated with the maintenance of the
health mucosa are impaired the acidic gastric juice
gains access to the epithelium causing initial
damage that leads to ulceration with repeated.
The main factors that are impaired include ,.
 Normal blood supply.
 Mucosa secretion.
 Cell replacement and bicarbonate ions
secretion.

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 Pud: pathogenesis

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 Risk Factors
 Lifestyle
 Smoking
 Acidic/spiced foods
 Medications eg
NSAIDS(aspirin,diclofenac)
 H. Pylori infection
 90% have this bacterium
 Passed from person to person
(fecal-oral route or oral-oral
route)
 Age
 Duodenal 30-50 years
 Gastric over 60 years
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 Gender
 Duodenal: are increasing in
older women
 Genetic factors
 More likely if family member
has Hx
 Other factors:
- stress related to
physiological conditions
which lead to release of
adrenaline and cortisol
causing vasoconstiction
-zolliger ellison syndrome leads
to hypersecretion of gastric
juice causing chronic gastritis
10/10/2022
 Classification of PUD
According to site; Gastric and duodenal ulcer are the
commonest, Both are associated with an imbalance
between protective and aggressive factors to the
gastrointestinal tract
According to onset; Can be acute; associated with
superficial erosion and minimal inflammation of mucosa,
having a short course duration and easily resolve with
treatment and lifestyle modification
Chronic PUD has a long duration lasting for months
presenting with complications.
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 Gastric and Duodenal Ulcers

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 Gastric Ulcers
• Pain occurs 1-2 hours after meals

• Pain usually does not wake patient

• Increased by ingestion of food

• Risk for malignancy/chronicity

• Deep and penetrating and usually occur on the lesser

curvature of the stomach

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 Duodenal Ulcers
Pain occurs 2-4 hours after meals

Pain wakes up patient

Pain relieved by food

Very little risk for malignancy and it’s the commonest

form of PUD

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 clinical features

Patients may remain asymptomatic for

sometime because the mucosa is poorly
innervated
Recurrent epigastic pain; its sharp, burning,
aching,gnawing
Persistent severe pain may suggest
penetration into other viscera
Back pain may indicate penetrating
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 Anorexia
 weight loss/Gain may occur in Gus
Dyspepsia
Nausea may be accompanied and/or
relieved by vomiting
belching
Heart burn
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 investigation and diagnosis
For helicobacter pylori. Serological tests: Test for
IgG
Sensitivity (90%); specificity (83%)
Urea breath Test
endoscopy (and biopsy of ulcers) to rule out
gastric cancer for all patients with ALARM
symptoms (, weight loss, vomiting, anorexia,
hematemesis/melana)
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Barium meal and contrast studies
LAYTONK@MEDICINE 10/10/2022
 Drug Therapy and Goals of management
• Provide pain relief
– Antacids and mucosa protectors
• Eradicate H. pylori infection
– Two antibiotics and one acid suppressor
• Heal ulcer
– Eradicate infection
– Protect until ulcer heals
• Prevent recurrence
– Decrease high acid stimulating foods in susceptible people
– Avoid use of potential ulcer causing drugs
– Stop smoking
• Prevent complications
- (bleeding, perforation, penetration, obstruction)
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 Proton Pump Inhibitors
 E.g omeprazole, rabeprazole, lansoprazole, esomeprazole

Suppress acid production

Omeprazole 20-40mg od 4-8weeks,before food as a whole

capsule

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 H2-Receptor Antagonists
 E.g Ranitidine, cimetidine, famotidine,nizatidine

Block histamine-stimulated gastric secretions ie reduce gastric

acid secretion by blocking the action of histamine at the H2

recepors in the pariental cells of the stomach.
Cimetidine 400mg bdnocte 4-6 weeks

Ranitidine 150mg bd 4-8weeks or iv 50mg diluted with 20ml

ns 6hrly

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 Prostaglandin Analogs

Eg misoprostol; tabs 200mcg

Reduce gastric acid, enhances mucosal resistance to injury

and promote secretion of bicarbonate ions and mucus.

Contraindicated in pregnancy, and lactating mothers

Adult dose is 800mcg in 2-4 divided doses with food for 4-8

weeks
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 Drugs cont’d
ANTACIDS.
- An antacid may be taken in addition to aPPIor H2receptor agnoist..
Instead of reducing acid secretion, antacids neutralize existing
stomach acid and can provide rapid pain relief for short period of
time.
- Examples; Magnessium hydroxide, Aluminium
Hydroxide,magnesium trisillicate.
Nb.other igredients may be added into the antiacids to counteract
the effects eg dyspesia and flatulence like simethicone
Mg antiacids tend to cause diarrhea where as aluminium based
antiacids cause constipation, so they be given in combination to
relieve effects of each.
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 CYTOPROTECTIVE AGENTS./mucosal
protective drugs
- These medications help protect the mucosal lining of the
stomach and small intestine by forming abarrier which coats
the ulcer. They should not be combined with
antiacids,because the work in an acidic environment.
-They include; Sucralfate, and Bismuth subsalicylate tbs
120mg.

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 Eradication of H.pylori (tripple therapy)

Examples of Regimens (7 – 14 days of Rx)

Omeprazole (20mg) +clarithromycin (500mg) +
amoxicillin (1g) twice daily.
Omeprazole (20mg) + Metronidazole (400mg)
+clarithromycin (500mg) twice daily.
Eradication failure regimen:
Bismuth chelates (120mg X 4 daily) + Metro (400mg
X 3 daily) + Tetracycline (500mg X 4 daily) + PPI (20-
40mg X 2 daily)
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 Surgical intervention
• Required if ulcer in one of these states

– Perforated and overflowed into the abdomen

– Scarred or swelled so that there is obstruction

– Acute bleeding

– Non-responsive to medications

– Interventions include; gastroenterostomy, vagotomy,

pyloroplasty ,subtotal gastrectomy

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 Nursing diagnosis for PUD
Acute pain related to increased gastric secretions,
decreased mucosal protection as evidenced by
burning sensation in the epigastric region and
abdomen

Ineffective therapeutic regime management related

to lack of knowledge about PUD therapy,
unwillingness to adjust lifestyle modifications
manifested by non compliance to treatment and
reoccurrence of painful episodes
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 Nursing care
Admission; PUD patients are managed in out patient
department, they are only admitted during severe acute
episodes of pain and PUD complications like
perforation and hemorrhage, for close monitoring
During admission; pain management is very important,
vital observations
Patient education about treatments and lifestyle
modification
All other nursing care is given like for all admitted
patients And manage patient according to presentation

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 PUD: prevention
Dietary modification; decrease intake of acid
stimulating foods
Avoid drugs that have corrosive effect on the
GUT
Educate and counsel about drug compliance
Avoid alcoholism and smoking
Co-administration of PPIs in patients on chronic
NSAID use reduces risk of PUD
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 Complications of Peptic Ulcers
 Hemorrhage
Blood vessels damaged as ulcer erodes into the muscles of
stomach or duodenal wall
Coffee ground vomitus (haematemesis) or occult blood in stools
 Perforation
An ulcer can erode through the entire wall
Bacteria and partially digested food spill into peritoneum
leading to peritonitis.
 Narrowing and obstruction (pylorus)
Scarring can cause obstruction of food leaving stomach due to
pyloric stenosis. Will manifest as repeated vomiting
Reoccurance of ulcers
Gastric cancer

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