CLINICAL CORRALATION

PEPTIC ULCER

•Is an erosion of the gastro intestinal

mucosa/sub-mucosa resulting from the digestive
action of HCI and pepsin
•A non – malignant ulcer in those parts of the
digestive tract in contact with gastric secretions.
Usually in the lower oesophagus, stomach,
duodenum and margin of gastrojejunal
anastomosis after surgical procedure.
 Classification
• According to location:- gastric or duodenal
• According to degree of mucosal involvement (severity)
• Acute ulcer is associated with superficial erosion and
minimal inflammation. Its of short duration and resolves
quickly when the cause is identified and removed.
• Chronic Ulcer:- Is one of long duration, eroding throuth
the muscular wall with formation of firous tissue.
• Its present continuously for many months or
intermittently through out the person’s life time. Chronic
ulcer is at least 4 times as common as a cute ulcer.
 AETIOLOGY
• Infection by Helicobacter pylori (70% of all
duodenal ulcers and 50% of gastric ulcers). It’s a
gram negative motile organism which sits just
behind the mucous layers of the stomach and
duodenum.
• It produces enzyme urase, which converts urea into
ammonia which is alkaline and combines the
hydrogen ions to ensures that environment is
alkaline and favourable for its survival.
• NH3 + H⁺ NH4⁺
• It also stimulates the gastric cells in the antrum of the
stomach to secrete gastrin which stimulates the parietal cells
to produce histamine which binds to his tamine receptors
and hence stimulate the H⁺K⁺-ATpase pump causing
secretion of H⁺ into the lumen of the stomach in exchange
for K⁺ that are secreted into the parietal cell.H+ later causes
destruction of the mucosa of the stomach
• The H⁺ Pylori also inhibits the D.Cells to release
somatostatin. Somatostatin antagonizes the action of gastrin,
this leads to excessive secretion of H⁺ by the un antagonised
gastrin cells therefore causing excessive destruction of the
mucosa.
K⁺ H⁺

ATP

K⁺ H⁺- K⁺- ATpase Pump

 Drugs
• Nsaids e.g. Aspirin
They prevent production of prostaglandins necessary for
formation of the mucus in the stomach and duodenum and
production of bicarbonates.
Corticosteroids reduce the rate of mucosal renewal
Arachidonic acid
-Lipo-oxygenase
Phospholipids
-Cyclo-oxygenase NSAIDS
inhibit
Prostoglandins
• Stress – Increased amount of stress leads to
decrease in the production of prostaglandins
• Zollinger – Ellison syndrome. Symptoms,
include hypergastrineamia, severe peptic
ulceration from gastrinoma.
• Burns – cause stress e.g. curling uclers.
 PATHOPHY SIOLOGY
• The integrity of the gastric mucosa is maintained when a
balance exists between the acid – secreting functions and
mucosal protective functions of the stomach and duodenum.
• The stomach is normally protected from autodigestion by
gastric mucosal barrier. When the barrier is broken, HCI
freely enters the mucosa and causes injury to the tissues.
This results in cellular destruction and inflammation. His
tamine is released from the damaged mucosa resulting in
vosodilation and increased in vasodilation and increased
capillary permeability.
• The release of histamine is then capable of stimulating
further secretion of acid and pepsin.
 Clinical Presentation
• Gastric ulcer;
• Pain; dull epigastric, located near midline, gets worse on feeding
or relieved by vomiting
• Reflux of gastric, contents into esophagus causes heart burn,
cough from aspiration, expectoration of chyme
• Common in younger individuals others; Anorexia, nansea &
vomiting
• Hematemesis; vomiting of blood, coffee – ground emesis,
reflects slow bleeding; bright –red emesis implies rapid bleeding
• Melena
• Signs of anaemia i.e. Ulcer are bleeding
 Summary
• Tripple therapy
• Omeprazole + Amoxicillin + Metronidazole 20mg od. 500mg 8⁰hly.
400mg 8⁰hly for at least 2 weeks
Diet
• eat 3 balanced meals a day
• eat slowly and chew food thoroughly
• do not over eat
• avoid any foods that increase discomfort e.g. fizzy drinks like soda,
fatty, oily food.
• Avoid bed time snacking because it increases night time acid secretion
• Stress reduction
• Surgical management
Indication
• Intractibility; failure of the ulcer to heal or
recurrence after therapy
• History of haemorrhage during RX
• Multiple ulcers
• Possible existence of malignant ulcer
• Gastric outlet obstruction
• Partial Gastrectomy with removal of the distal
2/3 of the stomach and anastomosis of gastric
stump to the duodenum is called
gastroduodenostomy (Billroth’s Operation)
• Gastro-jejunostomy (Billroth’s II operation)
• Vagotomy
 Duodenal Ulcer
• Pain; epigastric location near midline, may
radiate around costal border to back.
• Pain is described as gnawing, burning, aching,
episodic in nature lasting between 30 mins to
2 hours. Worsened on starvation and relieved
by feedng
• Weight gain
• Common in elderly
 Diagnosis
• History + physical examination
• Fibroptic endoscopy
• Upper GI barium contrast
• H- Pylori testing of blood, stool
• Urine, breath
• CBC, Biopsy, LFYs etc.
 Management
• Medical regimen consists of adequate rest,
dietary modifications, medications,
elimination of smoking and long term follow
up.
 Medication
• Anticids to neutralise free Hcl to prevent irritation
and permit mucosal healing e.g. magnesium
trisilicate either tablets or syrup
• Histamine (H₂) receptor blockers e.g. (cemetidine,
Ranitidine, famotidine.
• Proton pump inhibitor e.g. omeprazole lan soprazole
• Anti biotics e.g. amoxicillin, metrondozole,
clarithromycin
• Mucosal protective agents e.g. misoprosol
 Complications of PUD
• Gastric outlet obstruction (Ulcers heal by
fibrosis) sign and symptoms include; vomiting
after feeds, food vomited even after 24 hours
is easily identified.
• Gastric perforation; common in the lesser
curvature of the stomach
 Dsis: Usually known PUD patient

• Sudden on set of constant, generalised abdominal pain

• Shortness of breath (diaphragmatic irritation)
• Abdominal tenderness, rigidity, guarding
• Signs and symptoms of hypovolaemic shock
• Air under diaphragm on plain erect abdominal x-ray
(80% of cases)
• Positive fluid aspiration
• Gastric tumor; usually formed by chronic ulcers
• Bleeding;hematemesis