Victoria Booth
Digestive Problems
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I have been sick for two months with alternating diarrhea and constipation. Sometimes there is blood in my stools. I have had both a sigmoidoscopy and a colonoscopy both are normal/healthy. I have been avoiding dairy products. I’m growing fatigued. Any suggestions on possible medical problems? What type of physician should I see to further investigate this? I’ve noticed that when I run, the bleeding is worse. Otherwise, I am a healthy, 33 year old woman with no history of digestive (or other) significant medical problems.
24th October 2025
The presence of blood in your stools is a significant sign and it will be important to determine the source of the bleeding so that the best treatment can be provided. Sometimes the appearance of the blood can give clues about its origin – fresh red blood tends to have come from the last part of the digestive tract, for example from ruptured haemorrhoids or a problem with the rectum, while darker, more tarry’ blood would have arisen from further back along the digestive tract. You mention that the bleeding is worse when you have diarrhoea – this is sometimes an indication of ulcerative colitis or perhaps an intestinal infection such as amoebiasis. Have you travelled overseas in previous months, and perhaps been exposed to unfamiliar micro-organisms? Tests carried out on your stools should be able to eliminate or confirm this possibility. Sigmoidoscopy and colonoscopy are usually very effective at showing up problems with the large intestine and in your case the results have been normal, so perhaps your problem is situated more proximally, for example in the small intestine. About 2% of the population have what is called Meckel’s diverticulum – a vestige of an embryonic structure that normally disappears during development. When it is present, it can be a source of bleeding if it becomes ulcerated. You have already modified your diet to see whether perhaps a food allergy is causing the problem, and may wish to continue investigating that possibility by deleting and adding specific food materials, but at the same time it will be best to continue with the clinical investigations. Physicians who specialise in gastroenterology will be in a good position to help you.
My wife is 40. She was diagnosed with adencarcinoma of the stomach stage IV signet ring features, linitis plastica type. She has not taken any chemo or radiation. She has a blockage that the doctors will not do anything about. Are there any methods open to us to help relieve her?
2nd October 2025
Discuss very carefully with the doctors the outlook for your wife and the treatment options that are available, so that you can both understand the situation fully. Although the finding of signet ring cell histology is generally interpreted as suggesting a poor prognosis, a recent study suggests that it does not influence survival in advanced gastric cancer cases (Theuer et al, 2025). There are mechanical devices (stents) that can be used to open up a part of the digestive tract that has become obstructed by a tumour (Olsen et al, 2025), but the success of this approach will depend on where the tumour is located and its stage of development. Several new treatments for advanced gastric cancer are being tried. One involves the use of antibodies against a growth factor that is used by the tumour to establish its blood supply (Kamiya et al, 2025), and another uses a platinum derivative with antitumour activity (Kim et al, 2025). However, these approaches must be considered as experimental at this stage and are not widely available.
References
Kamiya, K., Konno, H., Tanaka, T., Baba, M., Matsumoto, K., Sakaguchi, T., Yukita, A., Asano, M., Suzuki, H., Arai, T., and Nakamura, S. (2025) Antitumor effect on human gastric cancer and induction of apoptosis by vascular endothelial growth factor neutralizing antibody. Japanese Journal of Cancer Research, 90(7), 794-800 (Jul).
Kim NK, Im SA, Kim DW, Lee MH, Jung CW, Cho EK, Lee JT, Ahn JS, Heo DS, Bang YJ (2025) Phase II clinical trial of SKI-2053R, a new platinum analog, in the treatment of patients with advanced gastric adenocarcinoma. Cancer, 86(7), 1109-1115 (Oct 1).
Olsen, E., Thyregaard, R., and Kill, J. (2025) Esophacoil expanding stent in the management of patients with nonresectable malignant esophageal or cardiac neoplasm: a prospective study. Endoscopy, 31(6), 417-420 (Aug).
Theuer, C.P., Nastanski, F., Brewster, W.R., Butler, J.A., and Anton-Culver, H. (2025) Signet ring cell histology is associated with unique clinical features but does not affect gastric cancer survival. American Surgery, 65(10), 915-921 (Oct).
For one of my GNVQ Advanced Science assignments I have to find out about the effect of acid (production and release), of blockers, antacids, anti-diarrhoea tablets, laxatives and aspirin on the digestive system.
1st March 2024
Hydrochloric acid production and release
Stomach secretions include hydrochloric acid, gastrin, intrinsic factor, pepsinogen, and mucus. Gastric secretion, including the secretion of hydrochloric acid, is controlled by a variety of neural and hormonal factors. For example, the parasympathetic division of the autonomic nervous system supplies the stomach wall via branches of the vagus (10th cranial) nerves. Vagal stimulation brings about contraction of the stomach muscle, release of hydrochloric acid and gastric juices from the tubular gastric glands, and secretion of the hormone gastrin from cells of the gastric mucosa. Gastrin increases the flow of gastric juices. As well as being released in response to neural stimulation, gastrin secretion is also triggered whenever food is present in the stomach.
Acid-Secreting Parietal Cell
< Diagram of acid-secreting parietal cell
The high concentration of hydrochloric acid in the stomach (pH usually between 1 and 3) has several effects: it begins to denature proteins, it activates pepsinogen in the gastric juices to become the digestive enzyme pepsin which further breaks down proteins in the food, and it also kills many of the bacteria ingested with the food.
The lining of the stomach is protected from the corrosive effects of the highly acidic contents by a film of mucus. Peptic ulceration can arise when this protective barrier is breached, perhaps as a result of excess production of hydrochloric acid or due to the presence of the bacterium Helicobacter pylori which is adapted to survive in the hostile environment. When acid and pepsin penetrate the gastric mucosa, histamine (a signalling molecule) is released from the damaged tissues and becomes a potent stimulus to the parietal cells to secrete even more hydrochloric acid, thus accelerating the progression of the ulceration.
H-2 Antagonists
The discovery of the role of Helicobacter pylori in the causation of peptic ulcers was made during the early 1990s. For two decades before that, the leading treatment for ulcers was the antihistamine cemetidine which acted by reducing the amount of hydrochloric acid being secreted in the stomach. Other drugs using the same principle were also introduced: ranitidine, famotidine, and nizatidine. These drugs are known as H-2 receptor antagonists because they block the type of histamine receptors carried on the outer cell membranes of parietal cells. (A different histamine receptor, H-1, is involved in allergic reactions.) Since the discovery of the involvement of Helicobacter pylori, the treatment of peptic ulcers usually includes a course of antibiotics.
Antacids
Antacids are a group of preparations that can be used to raise the pH of gastric contents to about pH 3 to 4. Some antacids contain foaming agents which produce a layer of foam on top of the gastric contents and are thought to reduce oesophageal reflux and consequent heartburn.
Examples of commonly used antacids Antacids
Aluminium salts, for example aluminium hydroxide
Magnesium salts, for example magnesium trisilicate
Sodium salts, for example sodium bicarbonate
Common Additives
Foaming agents, eg: alginates
Anti-foaming agents, eg: dimethicone (simethicone)
Surface (local) anaesthetics, eg: oxethazaine
Common Combinations
Aluminium+magnesium salts
Aluminium+magnesium salts+dimethicone
Sodium+aluminium+magnesium salts+alginic acid
(From: Dalton 1994, Table 25.1 p 319)
Anti-Diarrhoeal Drugs
Anti-diarrhoeal preparations are normally administered to provide symptomatic relief. One of the functions of the large intestine is to store faeces. Absorption of water takes place from both the small and large intestines – of the 1 to 1.5 litres of water entering the large intestine each day only 100-200 ml are lost with the faeces. Faecal matter is propelled through the large bowel by peristaltic activity of the smooth muscle in its wall. When food enters the stomach, peristaltic activity within the large intestine increases – the gastrocolic reflex. This is why the urge to evacuate the bowel commonly occurs following a meal. Drugs that are used in the management of diarrhoea are designed to either modify the amount of water contained in the faeces or to reduce bowel motility, thereby allowing more time for water absorption to take place.
Drugs used in the symptomatic treatment of diarrhoea Drugs which alter gastrointestinal motility Codeine
Diphenoxylate (combined with atropine in Lomotil)
Loperamide
Morphine
Fluid absorbents Kaolin Drugs used in specific circumstances Indomethacin (post-irradiation enteritis)
Cholestyramine (diarrhoea due to excess bile acids)
Pancreatic enzymes (pancreatic malabsorption)
(From Dalton 1994, Table 25.6 p 330)
Laxatives
Laxatives are used to facilitate bowel evacuation. If appropriate, a review of the dietary intake of fibre should be undertaken before a laxative is administered, as attention to the diet will often correct constipation. Laxatives are used to either increase bulk in the stools, to soften the faeces or to stimulate bowel peristalsis. The osmotic laxatives act by reducing water reabsorption.
Commonly used laxatives
Bulk-forming agents Bran
Isaghula husk
Methylcellulose
Sterculia
Faecal softeners and lubricants Arachis oil
*Dioctyl sodium sulphosuccinate
*Glycerol
Gastrointestinal stimulants Frangula
Senna
Anthraquinones
Danthron
Sodium picosulphate
Bisacodyl
Castor oil
Osmotic laxatives Lactulose
Magnesium salts
Sodium salts
*also act as stimulants NB: the bulk forming preparations are not used for patients with underlying intestinal disease such as adhesions, stenosis, and ulceration as they may cause intestinal obstruction.
(From Dalton 1994, Table 25.5 p 328)
It is important to appreciate that like the antacids, anti-diarrhoeal preparations, and laxatives are normally given to provide symptomatic relief. Attempts are usually made to identify, and where possible treat, any underlying cause.
The effects of aspirin on the digestive tract
Aspirin (acetylsalicylic acid) is often used to treat pain (for example: musculoskeletal pain, headache and dysmenorrhea), to counter the effects of inflammation, and to diminish fever. More recently aspirin in low doses has been found to be beneficial in the secondary prevention of thrombotic cerebrovascular and cardiovascular disease. Aspirin is also used to reduce mortality after myocardial infarction (British National Formulary, 2025).
Aspirin has side effects on the gastrointestinal system. Occult blood loss of just a few ml is said to occur whenever aspirin is consumed. The risk of gastric haemorrhage increases significantly in anyone with a history of peptic ulceration. In children under 12 years aspirin is avoided because of the risk of Reye’s syndrome developing.
H-2 antagonists, antacids, anti-diarrhoea preparations, laxatives and aspirin are all drugs that are commonly administered by nurses. It is not only important to be aware of the therapeutic effects of each but also the non-therapeutic side effects. Nurses, being close to patients, are in a good position to observe and report any adverse effects before they become severe.
References
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British National Formulary (2025) A joint publication by the British Medical Association and the Royal Pharmaceutical Society of Great Britain (March, Section 2.9 Antiplatelet drugs p 114).
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Dalton, H.R. (1994) The drug therapy of gastrointestinal, hepatic, and biliary disorders. In: Oxford textbook of pharmacology and drug therapy, edited by D.G. Grahame-Smith and J.K. Aronson. Oxford:Oxford University Press (pp 319-331).
I am a 24year old female and have recently been diagnosed with severe diverticular disease. Doctors have said that it is almost unheard of for someone of my age. Please could you tell me if this is the case and if so, why?
20th February 2024
Diverticulum – literally ‘a wayside house of ill repute,’ is an out-pouching of the colonic mucosa through a defect in the muscle wall of the colon (Cotton 1992).
Yes, it is unusual for the symptoms severe diverticular disease to emerge during the 20s. It tends to be more common in the later years. That is not to say that diverticula suddenly appear in later life, rather that this is a progressive disorder that is initially symptom-free and it is usually only later that it become sufficiently advanced to cause symptoms. An exception to this generalisation about age is provided by Meckel’s diverticulum. This is a developmental disorder affecting the small intestine and present from before birth – it is a blindly-ending pouch that should have disappeared during development, and it can become inflamed and ulcerated because of the presence of ectopic gastric mucosa. Meckel’s diverticulum affects younger people more than older people (Mackey and Dineen, 1983). However, we infer from your question that you are referring to diverticular disease of the large intestine.
Diverticular disease of the colon (large intestine) is actually quite common in the richer countries, present in perhaps two thirds of the elderly population (Wilson and Lester, 1992; Burkitt et al, 1996; Stollman and Raskin, 2025). However, only about 10% of the population are affected by the age of 40 (Nemec, 1988). Most affected people remain entirely without symptoms, and only about 20% will become ill. It used to be believed that diverticular disease at a young age had more serious consequences than later onset diverticulitis, but recent evidence does not support this belief (Spivak et al, 2024).
The condition occurs mainly, but not always, in the sigmoid colon (Wilson and Lester, 1992). Here a pouch (diverticulum) or multiple pouches (diverticula) develop. These are thought to be caused by an increase in intraluminal pressure as a result of consuming a diet low in fibre and high in refined carbohydrates (Cotton 1992; Ozick, Salazar, and Donelson, 1994). It is comparatively rare in tropical countries and in Japan.
Diverticulitis is inflammation of a diverticulum (or diverticula) and is usually triggered by the presence of a hardened faecal mass (faecolith). There is persuasive evidence that diet is linked with diverticular disease (Nowak and Handford, 1994; Kennedy and Zarling, 2023). There should be adequate fibre in the diet to facilitate the passage of food through the digestive tract. The primary prevention of diverticular disease begins with a review of the current intake of dietary fibre followed by appropriate adjustments to intake. Dietary fibre helps to reduce the gastro-intestinal transit time, with the result that less water is absorbed from the stools and the risk of constipation thereby reduced. However, a sudden change to a high-fibre diet can induce rectal gas accumulation and result in frequent diarrhoea, so a gradual change in fibre intake, with the monitoring of any ill effects, is the better course (Nowak and Handford, 1994). Other risk factors for the early development of diverticular disease include obesity (Schauer et al, 1992; Ozick et al, 1994) and smoking (Papagrigoriadis et al, 2025).
Although uncomplicated diverticular disease is usually asymptomatic, diverticula can give rise to serious complications including lower abdominal pain, haemorrhage, intestinal obstruction, and fistula and abscess formation. These complications require antibiotics, intravenous therapy, and sometimes surgery (Thompson and Patel, 1986).
References
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Burkitt, H.G., Quick, R.G., and Gatt, D. (1996) Disorders of large bowel dynamics – diverticular disease. In: Essential Surgery (2nd edition), edited by L. Hunter and S. Beasley. Edinburgh: Churchill Livingstone (Chapter 17, pp 332-333).
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Cotton, R. E. (1992) Diseases of the alimentary system – diverticular disease. In: Lecture notes on pathology. (4th. edition) Oxford: Blackwell Scientific Publications. (Chapter 2, pp 46-47).
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Kennedy, M.V., and Zarling, E.J. (2023) Answers to 10 key questions on diverticular disease of the colon. Comprehensive Therapy, 24(8), 364-369 (Aug).
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Mackey, W.C., and Dineen, P. (1983) A fifty year experience with Meckel’s diverticulum. Surgical Gynecology and Obstetrics, 156(1), 56-64 (Jan).
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Nemec, R. (2023) Diverticular disease of the colon: manual of clinical problems in gastroenterology. Boston: Little, Brown & Co (pp 122-124).
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Nowak, T.J., and Handford, A.G. (1994) Gastrointestinal pathology – diverticulitis. In: Essentials of pathophysiology, concepts and applications for health care professionals, edited by C. H. Wheatly, J. E. DeShaw, C. Ford-Smith, J. Wagner, and R. Deluhery. Dubuque: Wm. C. Brown Publishers (Chapter 13, pp 326-327).
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Ozick, L.A., Salazar, C.O., and Donelson, S.S. (1994) Pathogenesis, diagnosis, and treatment of diverticular disease of the colon. Gastroenterologist, 2(4), 299-310 (Dec).
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Papagrigoriadis, S., Macey, L., Bourantas, N., and Rennie, J.A. (2025) Smoking may be associated with complications in diverticular disease. British Journal of Surgery, 86(7), 923-926 (Jul).
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Schauer, P.R., Ramos, R., Ghiatas, A.A., and Sirinek, K.R. (1992) Virulent diverticular disease in young obese men. American Journal of Surgery, 164(5), 443-446; discussion 446-448 (Nov).
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Spivak, H., Weinrauch, S., Harvey, J.C., Surick, B., Ferstenberg, H., and Friedman, I. (2024) Acute colonic diverticulitis in the young. Diseases of the Colon and Rectum, 40(5), 570-574 (May).
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Stollman, N.H., and Raskin, J.B. (2025) Diverticular disease of the colon. Journal of Clinical Gastroenterology, 29(3), 241-252 (Oct).
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Thompson, W.G., and Patel, D.G. (1986) Clinical picture of diverticular disease of the colon. Clin Gastroenterology, 15(4), 903-916 (Oct).
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Wilson, L. M. & Lester, L. B. (1992) Large intestine – diverticular disease of the colon – pathophysiology. In: Pathophysiology, clinical concepts of disease processes.4th. edition. Edited by D. Ladig. St. Louis Mosby-Year Book, Inc (chapter 26, p 326).
I have been suffering from recurrent GI problems for three years now. I get bouts of severe nausea, run fevers often (about 100-101 F), as well as have diarrhea. I have also had one episode of rectal bleeding, where I passed a large purple blood clot (and had severe abdominal cramping). Recently things have gotten really bad and my stools are quite loose, greasy and floating.
I cannot eat anything with fats. I have been tested for gallbladder disease as well as I have had numerous blood tests a barium swallow and a gastroscopy which have revealed nothing. Otherwise I am pretty healthy, besides having asthma. I am 5’3” and weigh 93 lbs, and have trouble keeping weight on. Do you have any ideas what might be causing this? My doctors are baffled.
22nd January 2024
We are not in a position to diagnose your problem. Clearly your doctors have carried out numerous tests which are capable of detecting a range of problems affecting the gastro-intestinal tract and associated organs such as the liver and so far the results have been reassuringly clear. It will now be worth exploring the possibility that you have developed an allergic response to something in your diet. The fact that you have asthma may indicate that you have a very sensitive and perhaps overactive immune system. You can begin the process of detection yourself: make a complete list of all the foods that make up your diet and then reduce the range of foods down to a reasonable level – the greater the reduction the better the chances of detection. Items previously taken in the diet can then be gradually re-introduced and the response noted. If the symptoms settle and then re-emerge when a factor is returned to the diet, this will be valuable information for you to work from, perhaps with the help of a nutritionist. A wide range of foods can produce the kinds of symptoms you have described in sensitised people, common examples being gluten (in wheat products) and nuts such as peanuts.
