PEPTIC ULCER

by Yen Express


Mar 19, 2020


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Peptic ulcer is a frequent cause of physician visits worldwide. It leads to treatment of over 3 million people,190000 hospitalization and 5000 deaths each year (USA). In Africa, it Is closely associated with Helicobacter pylori.

Introduction

Ulcers are generally breach in continuity of the epithelium. Peptic ulcer is the breach of mucosa of the stomach and duodenum; sometimes involving the lower oesophagus, jejunum, anastomotic stomas, and Meckel’s diverticulum due to hydrochloric acid. It is one of a syndrome of acid peptic disorders. Duodenal ulcers are very common and has a prevalence of 15%. It is 2-3times commoner than gastric ulcers.. They can be associated with much discomfort in some cases, peptic ulcers can cause serious clinical complications, even though in some cases, there can be spontaneous resolution. They occur most commonly in the first part of the duodenum (immediately after pyloric sphincter), antrum of the stomach and rarely terminal portion of the oesophagus- due to gastro esophegeal reflux disease (GERD).

Epidemiology

Peptic ulcer is a frequent cause of physician visits worldwide. It leads to treatment of over 3 million people,190000 hospitalization and 5000 deaths each year (USA). In Africa, it Is closely associated with Helicobacter pylori. In most western communities, it is not commonly associated with H. pylori infection, and it is more common in the elderly because of chronic NSAID usage. Life time risk for developing  peptic ulcer is 5:2 in Males and females .  The prevalence of ulcer is low among young people and high among the elderly. Deudenal ulcer is more commoner than  gastric ulcer.

Aetiology

  • Helicobacter pylori
  • D rugs e.g NSAIDS
  • Zollinger-Ellison syndrome( gastrinoma)
  • Associations: hyperparathyroidism, cirrhosis, COPD,
  • Genetic: Blood group O, non-secretors of blood group substances==DU, hyperpepsinogenaemia type 1.

Others  are Smoking, stress…

Pathogenesis

Central to the development of PUD is excessive HCL secretion . Basically, due to an imbalance between the aggressive factors; hydrochloric acid, pepsin and protective factors; mucus , bicarbonate, prostaglandins. A balance exist between these two factors. All these etiological agents implicated in PUD disrupt this balance leading to chronic gastritis. H. pylori is implicated in most ulcers, it is a gram negative flagellate, urease producing spiral bacilli. It consists of the following virulent factors; flagella, urease, adherins, toxins( cag-A). The hyperacidity associated with H. pylori infection, zollinger ellison syndrome etc. irritates the epithelial surface causing inflammation and subsequent sloughing of the epithelium.

Clinical manifestation

  • Epigastric pain: high discriminatory value of “pointing sign” for diagnosis.
  • Nocturnal awakening, weight loss or gain, tenderness at the epigastrium and old age
  • Nausea, vomiting, heartburn, anorexia are other symptoms
  • Evidence of complications: heamatemesis, anaemia etc
  • Symptomless in 50%

 

 

 Investigation

  • Routine: FBC to detect Fe deficiency anaemia due to chronic blood loss, Gauiac test for occult blood determination. Serum calcium, blood group.
  • H pylori detection: UBT, CLO , Histology, Faecal Ag test, serology (not relevant in diagnosis).
  • Barium meal (double contrast), less commonly used than endoscopy: ulcers may show as ulcer craters, trefoil deformities.
  • Endoscopy: best investigation as it has added advantage of obtaining tissues for diagnosis, therapeutic interventions.

Treatment

  • Eradication of H. pylori with antibiotics
  • Protein pump inhibitors like omeprazole
  • H2 blockers like ranitidine.
  • Administration of antacid e.g magnesium hydroxide.
  • Prostaglandin analogue -misoprostol

 

Complications

  • Haemorrhage
  • Perforation
  • Pyloric stenosis or obstruction
  • Iron deficiency anemia
  • Perforation
  • Malignant transformation

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