Peptic Ulcer

 

Acute

Acute ulcers are often multiple and may be due to

 

Shock            especially burns - local ischaemia

increased histamine release increases gastric juice secretion

 

Drugs            eg. aspirin                  NSAIDS

 

Uraemia        Acute ulcers usually heal rapidly

 

Chronic

Up to 15% of individuals may have DU at some time in their life.

Ulceration extends through the lining mucosa into the muscle layer of the gut.

Craters up to 5 cm in diameter occur.

A sharply "punched out" edge with a smooth clean floor.

Often local thickening occurs due to fibrous tissue.

Fibrous tissue often contract causing folding of the gut wall.

 

Aetiology

HP (helicobacter pylori)

DU are 10 times more common than gastric

Gastric juices contain hydrochloric acid and digestive enzymes.

Acidity of stomach (HCl) may be as low as pH 1

Peptic ulcers occur at sites where there are peptic juices,

Psychological stress raises acid levels

Familial tendency

More in blood group O, (for DU)

Gastric -  Men : women  2.5 : 1

DU,     -  Men : women  4   : 1

More common in elderly

Drugs, including tobacco

Alteration in mucus production

Duodenogastric reflux, (bile damage to gastric mucosa)

Mucosal ischaemia

Prostaglandins, (are cytoprotective)

Intake of methylxanthines, eg tea coffee, cola, chocolate

 

Sites

Stomach                                                         Oesophagus

Duodenum (most common)                         Meckel`s diverticulum, (ectopic gastric mucosa)

Jejunum (after anastomosis)

 

Signs and Symptoms

Exacerbations of several days or weeks

Remissions may last for months or years

Pain or tenderness in the epigastrium

Pointing sign

Pain is burning or gnawing

Usually worse at night

Pain is relieved by vomiting and antacids

Nausea is not uncommon

Vomiting occurs in 10 -20% of cases

Indigestion symptoms

Weight loss

Flatulence

Heartburn

 

Complications

Haemorrhage - coffee grounds                   melaena                                 haematemesis

Perforation -  peritonitis

Stenosis, pyloric or gastric

Perforation of the pancreas

Deficiencies, haemorrhage and poor diet.

? Malignant changes

 

Investigations

Gastroscopy                                                  Biopsy

Barium meal                                                  Blood profiling

FOBs                                                              Gastric function tests, (pentagastrin)

 

Treatment

Decreasing the amount of acid present

H2 receptor antagonists

Combination of bismuth and tetracycline kills HP

Giving alkali tablets

Vagotomy

Stop smoking

No bed rest

No special diets

Surgical, partial gastrectomy and vagotomy

 

Nursing assessment

History

Locality of pain

How pain is relieved, eating antacids, vomiting etc

Time of day of pain

Foods which increase symptoms

Psychological profiling

Type A personality

Neurotic illness

Intake of drugs or other gastric irritants

Smoker

Vomit/ stool specimen

Level of patient anxiety about the condition

Sleep disturbances

Patients understanding of the condition

Potential for the development of complications

Situation of significant others

 

Patient Education

Adequate rest                                                            Relaxation advice

Smoking                                                                     Adequate balanced diet

Drug education to improve compliance

Alert to possible gastric irritants, eg aspirin

Avoid cola etc.

Observation for haemorrhage, anaemia etc.

Chew food thoroughly, eat in a leisurely manner

Ovoid over large meals