The peptic ulcer disease (PUD) which predominantly embraces both the duodenal and gastric ulcers, has been a major global health concern for many decades, with significant cases of morbidity and mortality. However, evidence-based research points that these cases of morbidity and mortality have substantially fallen, thanks to the discovery of the Helicobacter pylori bacteria, and of potent and effective acid-production suppressants. With the coining of the H. pylori micro-organisms, its causes, and pathogenicity, scientists have not only effectively come up with therapeutic drugs against the PUD disease but also other ways of controlling possible re-manifestation of these micro-organisms through dietary restrictions. Apart, from H. pylori, scientists have deduced that the PUD disease can also clinically manifests in one’s body as a result of continuous use of non-steroidal anti-inflammatory drugs (NSAIDs) such as aspirin. In sum, this paper evaluates James’s PUD case which is a classical representation of the clinical manifestation of duodenal ulcers. It further provides insight on the symptoms exhibited by James, the reasons behind the vulnerability of the duodenum to ulceration as compared to the fundus, the difference in the management of James’s PUD with respect to other GI disorders, the probable dietary advice for the management of PUD, and the mode of action of the drugs prescribed to James.
Which aspects of the patient’s history made peptic ulcer disease the likely diagnosis? Explain your answer.
Presenting symptoms: The patient complained of dull, burning pain in the upper abdomen, and described episodes of recurrent periods of nausea, vomiting, heartburn, loss of appetite every two weeks and general fatigue. These are some of the clinical manifestations of the peptic ulcer disease. The dull burning pain is caused by the potential ulcers in the stomach and sometimes aggravated by the gastric juice (specifically the stomach acid). Likewise, the symptoms of increased pain whenever the stomach is empty, pre-empts such a prognosis because excessive stomach acid production characterizes an empty stomach. Nausea and general fatigue were a clear sign of low blood count in the patient probably because of continuous bleeding from the open ulcers. Also, the reporting of heartburn without reporting any case of oesophagitis pointed to possible stomach ulceration. Lastly, vomiting and lack of appetite is a common symptom for PUD patients because of probable obstruction of the stomach outlets resulting from the swelling of the ulcerated tissue.
Drug history: The patient also attests to using anti-acids in a bid to reduce the pain. Anti-acids are regarded as the first-line medications against peptic ulcers. This is because these drugs neutralize the gastric acid, and reduce the delivery of the acid to the duodenum. In addition, this drugs are also essential in inhibiting the pepsin activity and are capable of binding bile acids (Garrigues-Gil 1988: p.74). Thus, reducing the irritation of the ulcers which is caused by the hypersecretion of the gastric acid.
Social History: The patient was a heavy drinker and smoker. These two etiological factors are closely related with the PUD (peptic ulcer diseases). Excessive alcohol consumption is associated with chronic gastritis. And at times the resultant inflammatory reactions are likely give room for concurrent Helicobacter pylori infection. In other words, chronic alcoholism has been experimentally and clinically proven to alter the histology of the gastric mucosal defense systems. On the other hand, cigarette smoking is associated with initiating and prolonging peptic ulcer diseases. Cigarette smoking has been proven to reduce the circulation of the epidermal growth factor, elevation of in-tissue free radical production, and the reduction of mucosal nitric oxide synthase activity (Ko & Cho 2000: p. 850). In addition, the differentiation of the gastric mucosal blood circulation, the inhibition of cell proliferation, and angiogenesis significantly contribute to poor ulcer healing among smokers. Therefore, having attested to be a smoker and heavy drinker, the patient was largely predisposed to the development of the peptic ulcer disease.
Likewise, the patient was a regular consumer of spicy food. Studies do not directly link spices to causing ulcers; instead, scientists argue that spices are just benefactors of gastric mucosal deterioration (Satyanarayana 2006: p. 290). They are known to cause irritation to open wounds (ulcers).
The GP told James that the location of his ulcer was “typical” for someone with hypersecretion of acid. Explain why the proximal duodenum is particularly vulnerable to ulceration compared to the fundus or body of the stomach.
The duodenum is largely vulnerable to ulceration because of its derailed acid buffering capability. The following duodenal features hamper this capability: Being on the rear end of the stomach, the duodenum receives a large amount of the gastric acid. This increased duodenal acid load paves the way for the formation of gastric metaplasia which is the prerequisite for the colonization of H pylori organisms. Scholarly postulates highlight gastric metaplasia as the major cause of the easy ulceration of the duodenum bulb as compared to the fundus.
Likewise, unlike the fundus whose mucosal barrier uniformly protects the gastric wall, the duodenal Brunner’s glands which secrete protective alkaline mucus unevenly protects the duodenum against ulceration. Studies show that Brunner’s glands near the ulcer are thinner than those that are adjacent or opposite to the ulcer. This is because the presence of a duodenal ulcer results in hyperplastic alterations in the Brunner’s glands. The hyper-plasticity of the Brunner’s glands impair their ability to secrete neutralizing agents which are essential in neutralizing the acidic chime.
James was concerned that he was not advised to take any vitamin or mineral supplements to correct his low haemoglobin. He recalled his friend, Bob who needs regular vitamin injections to “correct his blood” due to a chronic stomach disorder. Do you share his concern? Use your knowledge of pathophysiology of GI disorders, to explain the difference in the management of Bob and James.
Different GI disorders require different types of treatment and management. Unlike Bob’s chronic stomach disorder, James’s stomach disorder (PUD) was acute as a result of initial manifestation of the ulcers, hence first-line medication and dietary advice was essential in combating the disease and controlling further ulceration. Therefore, despite the detection traces of blood in the James’s faecal matter, a 4-8-week prescription of ranitidine a H2 inhibitor and omeprazole a proton pump inhibitor, and antibiotics was enough to normalize gastric production (which is the main cause of ulceration), and hasten the healing process of PUD (Gandy 2014; pp 401-413). In addition, the antibiotic prescription was also meant to ease the eradication of H. pylori micro-organisms. Also, dietary advice, and lifestyle changes such as putting a halt on smoking and drinking tendencies (which exacerbate the ulceration) was enough to minimise the probability of recurrence or chronic manifestation of James’s disease. In short, James did not require vitamin supplements because the above prescriptions were enough to stop the haemorrhage of the ulcers which might have led to the detection of blood in the patient’s stool.
On the other hand, Bob might have been suffering from a wide range of stomach disorders which would have led to the regular vitamin injections to correct his blood. These blood correcting vitamins were meant to correct vitamin B12 deficiency which might have resulted from probable repeated bleeding and inhibited generation of intrinsic factor (which is produced by the fundus parietal cells) (Gandy 2014; pp 401-413). . Some of the probable disorders which might have led to anaemic symptoms include chronic gastritis, chronic PUD, consequences of gastrectomy, and gastroparesis. All these conditions require strict dietary advice such as the elimination of high fibre foods, reduction of fatty foods, among other important nutritive foods. As such, patients require special supplement prescriptions to make up for the absent nutrients.
Outline the dietary advice given to patients with PUD in the past and discuss the basis for it.
For a very long time patients of peptic ulcer diseases have been put on diet therapy which is used to prevent the hypersecretion of peptic chloride, so as to limit the pain and soreness in the duodenal and gastric mucosa. Likewise, this therapy is given to patients in a bid to promote ulcer healing. According to Vomero and Colpo (2014), the distribution of calories among the peptic ulcers patients should be balanced, with 50-60% of carbohydrates consumption, 20-30% of lipids, and 10-16% of proteins (p. 299). Also, calories should be adjusted to fit each and every patients’ needs to normalize their nutritional status. The protein intake levels should be about 1.2g/kg/day in acute cases, and about 1.5g/kg/day in the recovery stage. The PUD patients should also consume carbohydrates which are low in disaccharides concentration in order to avoid fermentation and lipids with minimal concentrations of saturated fats. To speed up the healing of ulcers, PUD patients are also advised to consume specific micronutrients like zinc, which boosts the immune system, in response to possible oxidative stress, and promote the healing of wounds. Selenium is also important for healing purposes because it reduces the complications of infections. Similarly, PUD patients are also advised to use vitamin A supplements in moderate amounts to avoid toxicity.
Also, PUD patients are advised to consume diets with ample amounts of fibres and antioxidants, most preferably 20-30g/day. This is because fibres (soluble-apple, pear, and oatmeal; insoluble-granola, flax seeds, and whole grains) play a role as a buffers to the gastric activities, by reducing the bile acids concentrations in the stomach and intestines, hence reducing abdominal bloating, pain, and discomfort in the GIT (gastrointestinal tract). In addition, the use of probiotics (food supplements which contain live microorganisms) effectively combats the H pylori organisms. These supplements are proving to be the best alternatives in the treatment of many GI disorders, especially the most adaptive and mutative pathogenic bacteria. Therefore, despite not being curative agents, studies shows that probiotics have the ability to reduce the H pylori load from the human system. As such, PUD patients are advised to take substances which contain probiotics, such as the regular intake of yogurt which contains L. acidophilus, and Bifidobacterium animalis to suppress the proliferation of H pylori (Vomero & Colpo 2014: p. 301).
Another diet therapy way of eradicating H. pylori is the use of anti-oxidants. Studies show that the use of antioxidants such vitamin C products aids in the bacterial elimination among the PUD patients. However, experts advise that patients should consume moderate doses of these products, approximately 500-2000mg/day for a period of 3-4 months to initiate a more effective response (Vomero & Colpo 2014: p. 302). Another antioxidant which can be used in eradicating the H. pylori organisms is capsaicin. Capsaicin is largely found in pepper and chilli products. However, researchers reiterate that capsaicin is more effective in combating aspirin or NSAIDs-induced PUD lesions. Therefore, it is essential to note that sometimes pepper might cause irritations in the gastric and duodenal mucosa, but provide no gastro-protective influence on PUD patients.
Lastly, apart from advising people to desist from dangerous lifestyle habits such as smoking and alcohol consumption, researchers also advise people against coffee consumption (Vomero & Colpo 2014: p. 302). This is because coffee (either caffeinated or not) induces increased gastric acid production, which leads to the irritation of the mucosal lining. Similarly, people are advised against soft drinks which not only raises acid production but also results in gastric distension and dyspepsia-related conditions.
Explain the rationale for the pharmacological treatment of James’s ulcer giving a description of the mode of action of each drug.
Ranitidine, the first drug given to James was a Histamine H2 blocker has a 70-80% probability of healing the duodenal ulcer within four weeks, and 87-94% probability of healing after 7-8 weeks (Ramakrishnan and Salinas 2007: pp. 1005-1112). Ranitidine (Zantac) prescription is 300mg once at night, or 150mg twice during the day. Researchers, however, point that this drug is more potent when taken as a single dose during the night.
Pharmacodynamics properties. Studies show that ranitidine specifically inhibits histamine H2-receptors which mediate the last common pathway in the secretion of gastric acid. The above dosage decreases the pH of the stomach in 24 hours. The dosage highlighted above also reduces hydrogen ion action by suppressing the nocturnal acid production. Ranitidine suppresses the basal acid secretion, and the acid which is experimentally secreted, however, the usual dosage does not inhibit the normal acid produced during the meal time. Ranitidine is also known to inhibit pepsin production which, jointly with the reduced amount of gastric acid generation, decreases the pepsin activity in the stomach (Labenz et al. 1993: pp. 1167-1170). As a result, the inhibition of the pepsin and gastric acid activity, which is achieved by the ranitidine therapy, does not give room for microbial colonisation in the stomach, except when the drug is used in high dosage.
Pharmacokinetic properties. Proximal ranitidine concentration in the blood is reached after 1-3 hours of oral administration. A dose of 150mg of ranitidine induces a proximal plasma concentration of approximately 0.4mg/L (Labenz et al. 1993: pp. 1167-1170). The drug is more potent when used intravenously than orally, despite many people preferring the latter. Ranitidine roughly binds over 15 percent of the plasma proteins. Some studies suggest that people suffering from duodenal ulcers might recover from efficient ranitidine therapy.
Pharmacological properties of omeprazole. Omeprazole is widely known for its role in controlling stomach acid secretion by inhibiting the gastric H+, K+-ATPase (proton pump); an enzyme which is responsible for the last step in the production and secretion of stomach hydrochloric acid by the fundus’ parietal cells. Being a weak base, the drug is converted to its active form sulphonamide derivative in the acidic milieu of the secretory canaliculi. In the sulphonamide derivative form, omeprazole is incapable of crossing the cell membrane; hence it is held at the action site. As such, the drug effectively controls the secretion of stomach acid irrespective of the type of stimulatory stimulus and essentially inhibits the secretion of stimulated and basal gastric acid. The activities of the antral G cells (releasing gastrin) proceed after the gastric acid production is inhibited, thus, just like many acid inhibitors, omeprazole use leads to increased levels of gastrin. Therapeutically, omeprazole is supposed to be a short-term treatment measure for duodenal ulcers, Zollinger-Ellison syndrome, and developing gastric ulcers. The drug is also known to provide rapid responses when consumed in 20mg/day dosages. It presents higher healing rates of about 80-100 percent, better than ranitidine. In other words, omeprazole is the best solution for non-responsive to ranitidine or histamine antagonist therapy. (McTavish et al. 1990: pp. 138-170)
Finally, the antibiotics. These drugs were prescribed to lower the H. pylori bacterial load, in assistance with the omeprazole drug. Antibiotics serve to curb the proliferation of the bacteria by inhibiting the formation of their cell walls (Walsh and Peterson 1995: pp. 984-991). This is because the omeprazole monotherapy significantly suppresses bacterial colonisation, more so in the antral region, and at times eliminated the bacteria in some cases. The inhibition of hypersecretion of the gastric acid by omeprazole provides a good environment (neutral pH) which facilitates the action of antibiotics.
- Gandy, J., 2014. Manual of Dietetic Practice. John Wiley & Sons.
- Garrigues-Gil, V., 1988. Antacids in the treatment of peptic ulcer disease. Methods and findings in experimental and clinical pharmacology, 11, pp.73-77.
- Grant, S.M., Langtry, H.D. and Brogden, R.N., 1989. Ranitidine. Drugs, 37(6), pp.801-870.
- Ko, J.K. and Cho, C.H., 2000. Alcohol drinking and cigarette smoking: a” partner” for gastric ulceration. Zhonghua yi xue za zhi= Chinese medical journal; Free China ed, 63(12), pp.845-854.
- Labenz, J., Gyenes, E., Rühl, G.H. and Börsch, G., 1993. Amoxicillin plus omeprazole versus triple therapy for eradication of Helicobacter pylori in duodenal ulcer disease: a prospective, randomized, and controlled study. Gut, 34(9), pp.1167-1170.
- McTavish, D., Buckley, M.M.T. and Heel, R.C., 1991. Omeprazole. Drugs, 42(1), pp.138-170.
- Ramakrishnan, K. and Salinas, R.C., 2007. Peptic ulcer disease. Am Fam Physician, 76(7), pp.1005-1012.
- Satyanarayana, M.N., 2006. Capsaicin and gastric ulcers. Critical reviews in food science and nutrition, 46(4), pp.275-328.
- VOMERO, N.D. and COLPO, E., 2014. Nutritional care in peptic ulcer. ABCD. Arquivos Brasileiros de Cirurgia Digestiva (São Paulo), 27(4), pp.298-302.
- Walsh, J.H. and Peterson, W.L., 1995. The treatment of Helicobacter pylori infection in the management of peptic ulcer disease. New England Journal of Medicine, 333(15), pp.984-991.