GORD Aetiology and pathopjysiology
Reflux if gastric contents into the oesophagus most commonly due to an incompetent lower oesophageal sphincter (which under normal conditions acts as an anti-reflux barrier), decreased gastric motility or increased intra-abdominal pressure
VVV
Gastric HCl and pepsin secretions that reflux cause oesophageal irritation and inflammation
Contributing risk factors for GORD
- lifestyle behaviours such as smoking, alcohol consumption, over eating and stress
- ingestion of caffeine, chocolate or peppermint which all decreases LOS pressure
- ingestion of anticholinergics which decrease LOS pressure
- positioning such as bending over and lying down
- hiatus hernia
GORD signs and symptoms
- heartburn (pyrosis): a burning, tight sensation felt intermittently beneath the lower sternum upward the throat. Heartburn that occurs more than twice a week is rated as severe.
- dyspepsia: a pain or discomfort centred in the upper abdomen
- regurgitation of hot, bitter, or sour liquid from throat to mouth
- hypersalivation
- respiratory symptoms such as wheezing, coughing and dyspnea
- Otolaryngological symptoms including hoarseness, sore throat, a globus sensation and choking
Complications of GORD
- oesophagitis-inflammation and irritation of the oesophageal mucosa
- oesophageal ulcer
- oesophageal scar tissue formation
- peptic stricture which can lead to dysphasia
- hemorrhage
- Barrett’s oesophagus, also known as oesophageal metaplasia, is when a flat epithelial cells of the oesophagus change to columnar epithelial cells
- respiratory complications due to irritation of upper airway by gastric secretions
- oesophageal cancer
Diagnostic tests GORD
- barium swallow
- upper endoscopy
- 24 hour ambulatory pHonitoring
- oesophageal manometry
Nursing management GORD
- eat small meals to avoid over filling the stomach
- avoid eating 3 hours before bedtime
- for 2-3 hours after meals the patient should be in fowlers position
- follow dietary restrictions and avoid foods that are gas forming (choc, peppermint and fatty foods)
- avoid alcohol and smoking
- avoid acidic beverages
- raising the head of the bed by 30 degrees
Pharmacological management of GORD
Antacids
An alkaline solution that combines with HCl to form a viscous jelly that floats on the surface of the mucosal membranes to prevent the movement of gastric contents into the oesophagus.
Pharmacological management of GORD
H2 receptor antagonists
Acid secretion is stimulated by the binding of histamine to the H2 receptor. Antagonists bond to this receptor and because the receptor is not activated the portion of histamine induced acid secretion is inhibited.
Pharmacological management of GORD
PPI’s
The proton pump is responsible for the transport of H+ ions into the stomach. PPIS bind proton pump and deactivate it permanently therefore stopping gastric secretion until a new pump is manufactured in 24-48 hours.
Pharmacological management of GORD
Prostaglandins
Prostaglandin E stimulates production of mucous in the stomach and inhibits the secretion of gastric acid. Misoprostol bonds to the receptor and elicits the response of naturally occurring prostaglandins.
Pharmacological management of GORD
Sucralfate
A complex of sugar and aluminium which in the presence of acid forms a thick paste in that adheres to the gastric mucosa to protect it from damage. Works better in an acidic environment and therefore better taken on an empty stomach stomach
Pharmacological management of GORD
Helicobacter pylori eradication
Triple therapy; PPI and two different class antibiotics to inhibit resistance developing
PUD aetiology and pathophysiology
Peptic ulcer disease is characterised by erosion of the gastrointestinal mucosa resulting from the digestive action of HCl and pepsin. Peptic ulcers can be acute (superficial erosion with quick resolution ) or chronic (muscular wall erosion and fibrosis with long duration). With this in mind, proposed mechanism for development include both breakdown of “protective mucosal barrier” and excessive chronic exposure to acid and pepsin.
PUD aetiology and pathophysiology
Peptic ulcer disease is characterised by erosion of the gastrointestinal mucosa resulting from the digestive action of HCl and pepsin. Peptic ulcers can be acute (superficial erosion with quick resolution ) or chronic (muscular wall erosion and fibrosis with long duration). With this in mind, proposed mechanism for development include both breakdown of “protective mucosal barrier” and excessive chronic exposure to acid and pepsin.
