21.2 — Digestive and Liver Disease

For most of the twentieth century, stomach ulcers were understood as a disease of stress and acid, treated with bland diets, antacids and sometimes surgery that removed part of the stomach.

Then in 1984, an Australian doctor named Barry Marshall drank a flask of bacteria to prove they caused gastritis. He developed it within days, and cured himself with antibiotics.

Peptic ulcer disease turned out to be an infection, and Marshall and Robin Warren received a Nobel Prize for it in 2005.

Which is worth remembering whenever a condition is confidently attributed to lifestyle without a mechanism.

Reflux and heartburn

Stomach contents moving up into the oesophagus.

The barrier is the lower oesophageal sphincter, a ring of muscle at the junction (Chapter 9.2), supported by the diaphragm around it. Reflux happens when that barrier relaxes inappropriately or is weakened.

Symptoms: burning behind the breastbone, worse lying flat or bending over, an acid or bitter taste, and sometimes a chronic cough, hoarseness or a sensation of a lump in the throat.

Contributors: obesity, which raises abdominal pressure; hiatus hernia, where part of the stomach slides up through the diaphragm; large or late meals; alcohol; smoking; and pregnancy.

And a point worth stating: chest pain from reflux and chest pain from the heart can feel identical, including the response to nitrates. New chest pain is not assumed to be reflux without consideration of the heart (Chapter 18.3).

Treatment: weight loss where relevant, which has the best evidence of any lifestyle measure; raising the head of the bed; not eating within three hours of lying down; and reducing alcohol and smoking.

Antacids and alginates for immediate relief — alginates form a raft on top of the stomach contents.

Proton pump inhibitors — omeprazole, lansoprazole, esomeprazole. They block the final step of acid production and are very effective.

On their safety, a balanced view: long-term use has been associated with reduced B12 and magnesium absorption, a modest increase in some gut infections, and possible effects on bone density. The associations are mostly weak and observational. The sensible position is to use the lowest effective dose and to review whether it is still needed, rather than either taking them indefinitely without thought or stopping a drug that is genuinely preventing complications.

The red flags requiring investigation: difficulty swallowing, food sticking, unintentional weight loss, vomiting blood or passing black tarry stools, persistent vomiting, anaemia, or new symptoms over 55.

Barrett's oesophagus — the lining changing to an intestine-like type after years of reflux. It is a precursor to oesophageal cancer, though the annual risk of progression in any individual is low, and it is monitored by endoscopy.

Peptic ulcer disease

Ulcers in the stomach or duodenum.

Two causes account for nearly all of them:

Helicobacter pylori — a bacterium that survives in stomach acid by producing urease, which splits urea into ammonia and neutralises the acid immediately around it. It infects a large fraction of the world's population and causes ulcers in a minority of those it infects.

NSAIDs — ibuprofen, naproxen, aspirin and others. They block prostaglandins, which are needed for the protective mucus and bicarbonate layer (Chapter 22.3). So the stomach's own defence is removed.

Symptoms: burning upper abdominal pain, classically relieved by food in duodenal ulcers and worsened by food in gastric ones, though the distinction is unreliable in practice. Bloating and nausea.

The complications are what matter:

Bleeding — vomiting blood or material like coffee grounds, or black tarry stools. An emergency.

Perforation — sudden severe abdominal pain with a rigid, board-like abdomen. A surgical emergency.

Obstruction from scarring.

Treatment: test for H. pylori by breath test, stool antigen or biopsy, and if positive, eradicate it with a combination of two antibiotics plus a proton pump inhibitor for 7 to 14 days. Confirm eradication afterwards.

Stop the NSAID where possible, or add gastric protection.

And H. pylori eradication also reduces the risk of stomach cancer, which is why it is treated even when the ulcer has healed.

Inflammatory bowel disease

Crohn's disease and ulcerative colitis — chronic immune-mediated inflammation of the gut (Chapter 13.6).

They are not the same as irritable bowel syndrome, and confusing them is common and consequential.

	Crohn's	Ulcerative colitis
Where	Mouth to anus, patchy	Colon only, continuous
Depth	Full thickness of wall	Lining only
From	Any segment	Rectum upward
Typical	Pain, weight loss	Bloody diarrhoea
Smoking	Makes it worse	Oddly protective
Surgery	Not curative	Removing colon cures it

Symptoms: diarrhoea, often with blood in colitis; abdominal pain; weight loss; fatigue; and fever.

Crohn's complications: strictures causing obstruction, fistulas connecting the bowel to other structures, and abscesses.

Ulcerative colitis complications: severe acute colitis, which is a medical emergency, and increased colon cancer risk with long-standing extensive disease, which is why surveillance colonoscopy is offered.

And symptoms outside the gut are common — joints, eyes, skin and liver — which is a reminder that these are systemic immune conditions rather than local gut problems.

Treatment: aminosalicylates for ulcerative colitis; steroids for flares but not for maintenance; immunomodulators such as azathioprine; and biologic therapies — anti-TNF agents and newer targeted drugs — which have substantially changed outcomes.

Nutrition matters, and exclusive enteral nutrition is genuinely effective for inducing remission in paediatric Crohn's disease, which is unusual for a dietary treatment with real trial evidence.

Surgery — for complications in Crohn's, and removing the colon is curative in ulcerative colitis, though it is a major decision with lasting consequences.

And the outlook has improved considerably. Most people with well-treated inflammatory bowel disease work, travel and live normally, which was less true a generation ago.

Irritable bowel syndrome

Very common, genuinely disabling for some, and frequently dismissed.

Abdominal pain related to defecation, with a change in stool frequency or form, without structural disease.

And it is not psychological, and it is not "nothing". The mechanisms identified include visceral hypersensitivity — the gut nerves signal pain at normal levels of stretch — altered gut motility, changes in the gut microbiome, low-grade immune activation, and disturbed communication along the gut–brain axis (Chapter 9.6).

Around 10 percent of people follow an episode of gastroenteritis, which points clearly at a physical trigger.

Red flags that mean it is not IBS: onset over 50, weight loss, blood in the stool, anaemia, a family history of bowel cancer or inflammatory bowel disease, and waking at night with symptoms.

Coeliac disease is tested for, because it presents identically and is treatable (Chapter 9.3).

Treatment: the low FODMAP diet, which has good evidence and should be done with a dietitian because it is restrictive and is meant to be followed by systematic reintroduction rather than permanent avoidance; soluble fibre; antispasmodics and peppermint oil; low-dose tricyclics or SSRIs, used for their effect on gut nerve signalling rather than on mood; and gut-directed hypnotherapy and CBT, both of which have real trial evidence.

Gallstones

Around 10 to 15 percent of adults have them, and most never know.

They form when bile becomes supersaturated with cholesterol (Chapter 9.5).

Biliary colic — severe pain in the upper right abdomen, frequently after a fatty meal, lasting from 30 minutes to a few hours, sometimes radiating to the right shoulder blade. It occurs when a stone temporarily blocks the outlet.

Cholecystitis — the stone stays stuck, the gallbladder becomes inflamed and infected. Constant pain, fever, and tenderness. Needs antibiotics and usually surgery.

Obstruction of the common bile duct — jaundice, dark urine, pale stools, and ascending cholangitis if infected, which is a serious emergency with fever, jaundice and pain together.

Gallstone pancreatitis — a stone obstructing where the pancreatic duct joins.

Treatment: removing the gallbladder laparoscopically, which is one of the commonest operations performed. You can live entirely normally without a gallbladder — bile simply flows continuously rather than being stored and released in a bolus, and some people notice looser stools after fatty meals for a while.

Pancreatitis

Acute pancreatitis — the pancreas digesting itself when its own enzymes activate prematurely inside it (Chapter 9.5).

Two causes account for most cases: gallstones and alcohol.

Severe upper abdominal pain radiating through to the back, frequently relieved slightly by leaning forward, with vomiting.

Diagnosed by raised amylase or lipase plus the clinical picture.

Most cases are mild and settle with fluids, pain relief and treating the cause. A minority become severe, with organ failure and mortality of 15 to 30 percent, which is why it is taken seriously from the outset.

Chronic pancreatitis — repeated damage leading to permanent loss of function. Chronic pain, malabsorption with pale greasy stools, and diabetes as the insulin-producing cells are lost. Treated with enzyme supplements, pain management and alcohol cessation.

Liver disease

And the defining feature is silence. The liver has enormous reserve and few nerve endings, so serious disease frequently produces no symptoms until function is substantially lost.

Fatty liver disease

Now the commonest liver disease in the world, affecting perhaps a quarter to a third of adults.

Fat accumulating in liver cells, associated with obesity, type 2 diabetes and metabolic syndrome (Chapter 18.2).

Most people have simple fat accumulation, which does little. A minority develop inflammation, then fibrosis, then cirrhosis.

And it is frequently found incidentally on a scan or from mildly abnormal blood tests.

Treatment is weight loss — around 7 to 10 percent of body weight produces measurable improvement, including reversal of inflammation — plus controlling diabetes and lipids, exercise independent of weight loss, and avoiding alcohol. Drug treatments are now emerging, and weight loss remains the foundation.

Alcohol-related liver disease

Three overlapping stages: fatty liver, which is reversible; alcoholic hepatitis, which can be severe and life-threatening; and cirrhosis.

And the encouraging part: the first two improve substantially with abstinence, and even established cirrhosis stabilises and sometimes improves.

Viral hepatitis

Hepatitis A — spread by contaminated food and water, acute only, does not become chronic, preventable by vaccine.

Hepatitis B — blood and body fluids, and mother to child. Can become chronic, particularly when acquired in infancy. Preventable by vaccine, and the vaccine is one of the most effective cancer-prevention tools that exists, because chronic hepatitis B causes liver cancer.

Hepatitis C — blood-borne.

And this is one of the great successes of modern medicine. Direct-acting antivirals cure over 95 percent with 8 to 12 weeks of well-tolerated tablets. A disease that meant decades of progressive liver damage and a liver transplant is now curable in three months.

The remaining problem is finding people, since most have no symptoms and do not know they are infected.

Hepatitis E — usually self-limiting, and dangerous in pregnancy, with substantial mortality.

Cirrhosis

Scarring replacing functional liver tissue, distorting the architecture and obstructing blood flow through the organ.

Two sets of consequences:

From loss of function: jaundice; easy bruising and bleeding, because clotting factors are made in the liver (Chapter 7.1); low albumin causing swelling; and hepatic encephalopathy — confusion and drowsiness from toxins, particularly ammonia, that the liver would normally clear (Chapter 9.4).

From obstructed blood flow — portal hypertension: varices, which are enlarged veins in the oesophagus that can bleed catastrophically; ascites, fluid in the abdomen; and an enlarged spleen.

Management: treating the cause, which matters at every stage; beta blockers or banding to prevent variceal bleeding; diuretics and salt restriction for ascites; lactulose and rifaximin for encephalopathy; surveillance for liver cancer, which cirrhosis substantially increases the risk of; and transplantation, which has excellent outcomes.

And the honest hopeful note: the liver is the only internal organ that regenerates substantially, and treating the cause early — stopping alcohol, curing hepatitis C, losing weight — prevents most of this.

What the next page fixes

Chapter 21.3 covers kidney disease — silent, common, and the one where routine blood tests genuinely change outcomes.