Lyrics · 完整歌詞
Gastric mucosal integrity depends on a balance between injurious factors
and the mechanisms that protect and repair the epithelial surface.
Acid, pepsin, Helicobacter pylori and non-steroidal anti-inflammatory drugs erode the surface,
whereas the mucus-bicarbonate layer, prostaglandins and mucosal blood flow repair it.
An ulcer forms when the balance tips,
and its site tells the story.
Duodenal ulcers wake patients at night and ease with food;
almost all are Helicobacter-driven and rarely become malignant.
Gastric ulcers hurt after meals, follow Helicobacter or NSAID injury,
and must be biopsied to exclude carcinoma.
Bleeding ulcers receive endoscopic therapy and a 72-hour proton pump inhibitor infusion.
On the Forrest scale, active spurting rebleeds in about 55 per cent,
a visible vessel in about 43 per cent,
and a clean base in 2 to 5 per cent.
Eradication is a matter of timing.
A urea breath test performed on acid suppression is falsely negative,
so the proton pump inhibitor is withheld for at least two weeks beforehand.
Cure is confirmed at least four weeks after the antibiotics finish.
Where clarithromycin resistance is common,
bismuth quadruple therapy for fourteen days is preferred.
Reflux, by contrast, is not a Helicobacter disease;
it follows a lax lower oesophageal sphincter,
and Barrett's columnar metaplasia is the precursor of adenocarcinoma.
Sliding hiatus hernias are 95 per cent of the total;
the para-oesophageal type can strangulate.
Gastric mucosal integrity depends on a balance between injurious factors
and the mechanisms that protect and repair the epithelial surface.
Gastric surgery leaves two signatures.
Afferent loop syndrome brings post-prandial fullness relieved by bilious vomiting;
bacteria in the stagnant limb consume B12 yet synthesise folate.
Dumping syndrome reflects the lost pylorus:
early symptoms follow hyperosmolar chyme drawing fluid into the jejunum;
late symptoms are reactive hypoglycaemia one to three hours after carbohydrate.
Type A gastritis is autoimmune,
destroys parietal cells in the body and causes B12 deficiency;
type B is bacterial, antral and linked to ulcer and cancer.
Obstruction is sorted by level first.
Small bowel obstruction is usually adhesive, vomits early and profusely,
and shows stepladder fluid levels with valvulae conniventes crossing the lumen.
Large bowel obstruction is usually carcinoma, vomits late and distends more;
a caecum beyond nine centimetres threatens perforation.
Serum amylase stays normal in simple obstruction,
so a rise signals strangulation or pancreatitis.
Uncomplicated cases receive nil by mouth, nasogastric decompression and intravenous fluid;
persistent pain, fever, leucocytosis, lactate or peritonism mandates surgery.
Appendicitis migrates from the umbilicus to McBurney's point,
and Rovsing's sign is right-sided pain on left-sided pressure.
One bowel hosts two inflammations.
Crohn's disease is transmural, skips segments,
favours the terminal ileum and produces granulomas, fistulae and strictures;
ulcerative colitis is mucosal, continuous from the rectum and bleeds.
Smoking worsens Crohn's disease yet protects against colitis, as does appendicectomy.
Corticosteroids induce remission but never maintain it.
Aminosalicylates maintain colitis, anti-TNF antibodies heal fistulae and spare surgery,
and bowel rest with parenteral nutrition rivals steroids in active Crohn's disease.
Toxic megacolon means a transverse colon wider than six centimetres with systemic toxicity,
and anticholinergics and antidiarrhoeals are forbidden.
Gastric mucosal integrity depends on a balance between injurious factors
and the mechanisms that protect and repair the epithelial surface.
Gastric mucosal integrity depends on a balance between injurious factors
and the mechanisms that protect and repair the epithelial surface.