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Switch to non-opioid analgesics and antipyretics

Exp:

Paracetamol (e.g. 1g TID PRN)

First-line for OA pain, much safer on GI tract.

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Initial dose: 5 to 60 mg orally per day; may be give once a day or in divided doses
Maintenance dose: Adjust or maintain initial dose until a satisfactory response is obtained; then, gradually in small decrements at appropriate intervals decrease to the lowest dose that maintains an adequate clinical response

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Initial dose: 4 mg orally once a day
Maintenance dose: 4 to 8 mg orally per day in 1 or 2 divided doses
Maximum dose: 16 mg/day

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10 - 80 mg depending on patient condition once daily taken during nighttime. Lipid profile should be analyzed within 2 to 4 weeks, and adjust the dosage.

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Using prednisoLONE together with naproxen may increase the risk of side effects in the gastrointestinal tract such as inflammation, bleeding, ulceration, and rarely, perforation. Gastrointestinal perforation is a potentially fatal condition and medical emergency where a hole forms all the way through the stomach or intestine. You should take these medications with food to lessen the risk. Talk to your doctor if you have any questions or concerns. Your doctor may be able to prescribe alternatives that do not interact, or you may need a dose adjustment or more frequent monitoring to safely use both medications. Your doctor may also be able to recommend medications to help protect the stomach and intestine if you are at high risk for developing serious gastrointestinal complications. You should seek immediate medical attention if you experience any unusual bleeding or bruising, or have other signs and symptoms of bleeding such as dizziness; lightheadedness; red or black, tarry stools; coughing up or vomiting fresh or dried blood that looks like coffee grounds; severe headache; and weakness. It is important to tell your doctor about all other medications you use, including vitamins and herbs. Do not stop using any medications without first talking to your doctor.

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Coadministration with antacids may decrease the oral bioavailability of captopril and other angiotensin converting enzyme (ACE) inhibitors due to delayed gastric emptying and/or elevated gastric pH. In 10 healthy volunteers, 50 mL of an antacid suspension decreased the mean peak plasma concentration (Cmax) and area under the concentration-time curve (AUC) of captopril (50 mg single oral dose) by 50% and 42%, respectively, compared to administration after fasting. The relative bioavailability of captopril was 0.66 with antacid, although its hypotensive activity did not seem to be affected. Based on available data, the clinical significance of this interaction appears to be minor. As a precaution, patients may want to consider separating the administration times of ACE inhibitors and antacids or oral medications that contain antacids (e.g., didanosine buffered tablets or pediatric oral solution) by 1 to 2 hours.

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Antacids and some oral aluminum, calcium, or magnesium containing preparations may decrease the gastrointestinal absorption of enteric-coated naproxen, which requires an acidic environment for dissolution. The proposed mechanism is an increase in gastric pH (i.e. decreased gastric acidity) produced by antacids. In patients treated with antacids, the possibility of a reduced or subtherapeutic response to enteric-coated naproxen should be considered. Concomitant use of these drugs is generally not recommended. Aluminum hydroxide and some magnesium-containing antacids have also been reported to reduce the absorption of regular naproxen. The interaction may be minimized by separating the times of administration by at least 2 hours.

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MONITOR: Nonsteroidal anti-inflammatory drugs (NSAIDs) may attenuate the antihypertensive effects of ACE inhibitors. The proposed mechanism is NSAID-induced inhibition of renal prostaglandin synthesis, which results in unopposed pressor activity producing hypertension. In addition, NSAIDs can cause fluid retention, which also affects blood pressure. Some NSAIDs may also alter the pharmacokinetics of certain ACE inhibitors. For example, oxaprozin has been shown to reduce the systemic exposure (AUC) of enalapril and its active metabolite, enalaprilat.

MONITOR: Concomitant use of NSAIDs and ACE inhibitors may cause deterioration in renal function, particularly in patients who are elderly or volume-depleted (including those on diuretic therapy) or have compromised renal function. Acute renal failure may occur, although effects are usually reversible. Chronic use of NSAIDs alone may be associated with renal toxicities, including elevations in serum creatinine and BUN, tubular necrosis, glomerulitis, renal papillary necrosis, acute interstitial nephritis, nephrotic syndrome, and renal failure. Additionally, in patients with prerenal conditions whose renal perfusion may be dependent on the function of prostaglandins, NSAIDs may precipitate overt renal decompensation via a dose-related inhibition of prostaglandin synthesis. ACE inhibitors can further worsen renal function by blocking the effect of angiotensin II-mediated efferent arteriolar vasoconstriction, thereby decreasing glomerular filtration.

MANAGEMENT: Patients receiving ACE inhibitors who require prolonged (greater than 1 week) concomitant therapy with an NSAID should have blood pressure monitored more closely following initiation, discontinuation, or change of dosage of the NSAID. Renal function should also be evaluated periodically during prolonged coadministration. The interaction is not expected to occur with low doses (e.g., low-dose aspirin) or intermittent short-term administration of NSAIDs.

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a) Definition

NSAIDs are a common cause of peptic ulcer disease in the stomach and duodenum, and dyspeptic symptoms occur commonly in the absence of peptic ulcer disease

b) Pathophysiology - refer to the pic

c) Diagnosis

Detailed medical history and physical examination

Upper endoscopy

H.pylori test

Lab test

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ACG-H.-pylori-Guideline-Summary.pdf

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Overview of Peptic Ulcer Disease

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also known as Blumberg's sign

It occurs when the tissue that lines the abdominal cavity (the peritoneum) is irritated, inflamed, or infected. This is called peritonitis.

Peritonitis is an inflammation (irritation) of the peritoneum. This is the thin tissue that lines the inner wall of the abdomen and covers most of the abdominal organs.

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Using perindopril together with celecoxib. (moderate in mims)

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Using perindopril together with celecoxib. (moderate in mims)

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Combining these medications may reduce the effects of perindopril in lowering blood pressure. In addition, these medications may affect your kidney function, especially when they are used together frequently or chronically.

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NSAIDs

corticosteroids

bisphosphonates

potassium chloride

fluorouracil

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Lifestyle Changes

Balanced Diet:

Avoid spicy, sour, fatty foods, and alcohol.

Increase intake of vegetables, fruits, and fiber.

Quit Smoking:

Smoking damages the stomach lining and increases acid production.

Stress Management: (Stress does not directly cause peptic ulcers, but it can worsen symptoms, delay healing, and increase the risk of recurrence by: i) Increasing stomach acid production ii) Reducing blood flow to the stomach lining, iii) Weakening the immune system, making it harder to fight H. pylori infections)

Use relaxation techniques, meditation, and exercise to reduce stress.

Deep Breathing Exercises

Yoga & Tai Chi: Combines movement, breathing, and meditation to reduce stress.

Moderate exercise: walking, swimming (helps regulate stress hormones)

Adequate Sleep & Rest: Poor sleep increases cortisol (stress hormone), worsening ulcer symptoms. At the same time, tiredness will weaken our immune system

Maintain Healthy Weight:

Obesity increases ulcer recurrence risk; diet and exercise help prevention.

Dietary Changes

Eat slowly, chew food well, and consume smaller portions to reduce stomach pressure.

Irregular eating patterns can trigger excessive acid production, damaging the stomach lining.

Prolonged hunger causes strong stomach contractions, worsening irritation.

Warm Water Compress

Reduces pain by:

Relaxing muscle spasms.

Improving blood flow (vasodilation).

Triggering endorphin release (natural pain relief).

Helps divert attention from pain and promotes relaxation.

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https://pmc.ncbi.nlm.nih.gov/articles/PMC10063898/

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https://pmc.ncbi.nlm.nih.gov/articles/PMC4848239/table/T1/

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Chronic and concomitant use of NSAIDs and PPIs increase the risk of microscopic colitis.

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Medication Counseling & Adherence

Educate patients on correct use of medications such as proton pump inhibitors (PPIs), H2-receptor antagonists, and antibiotics for H. pylori eradication.

Emphasize importance of completing full antibiotic courses to prevent resistance and recurrence.

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1.     Stool tests

·       Stool antigen test. This is the most common stool test to detect H. pylori. The test looks for proteins (antigens) associated with H. pylori infection in the stool.

·       Stool PCR test. A lab test called a stool polymerase chain reaction (PCR) test can detect H. pylori infection in stool. The test can also identify mutations that may be resistant to antibiotics used to treat H. pylori. However, this test is more expensive than a stool antigen test and may not be available at all medical centers.

2.     Urea Breath Test

·       Patients will swallow a pill, liquid or pudding that contains tagged carbon molecules. If patients have H. pylori infection, carbon is released when the solution comes in contact with H. pylori in your stomach. Because your body absorbs the carbon, it is released when you breathe out. To measure the release of carbon, you blow into a bag. A special device detects the carbon molecules. This test can be used for adults and for children over 6 years old who are able to cooperate with the test.

3.     Rapid Urease Test

·       This test involves taking a tissue sample from the stomach during endoscopy and placing it on a substrate that contains urea. If H. pylori is present, the bacteria's urease enzyme will break down the urea, producing ammonia which will increase the pH of the medium and change the color of an indicator on the test strip from yellow to red (positive).

Upper endoscopy (esophagogastroduodenoscopy)

An upper endoscopy is the most accurate at detecting H. pylori. Healthcare providers may perform this test if they’re looking for other issues (like signs of cancer) in addition to H. pylori infection. This test involves using a scope to remove tissue from your stomach or duodenum and testing the sample for H. pylori.

H. pylori blood test

An H. pylori blood test detects antibodies associated with an H. pylori infection. Antibodies are proteins your immune system makes if it detects a harmful antigen. The antibodies circulate in your bloodstream to find and destroy the offending germ (like H. pylori). Antibodies can still circulate in your bloodstream after an infection is gone. For this reason, healthcare providers mostly use blood tests to screen for H. pylori infections in populations where the bacteria are more common. H. pylori are more widespread in Africa, South America and western Asia.

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Using prednisolone together with naproxen may increase the risk of side effects in the gastrointestinal tract such as inflammation, bleeding, ulceration, and rarely, perforation.

Prednisolone may reduce the effects of perindopril in lowering blood pressure. The interaction is most likely to occur when prednisolone is used for more than a week, since prolonged use can cause sodium and water retention.

COX-2 inhibitors (esp. Etoricoxib > Celecoxib) are associated with increased risk of heart attack and stroke. Caution in hypertensive or dyslipidaemic patients like RB. Use lowest effective dose for shortest duration.

perindopril + naproxen.

Combining these medications may reduce the effects of perindopril in lowering blood pressure. In addition, these medications may affect your kidney function, especially when they are used together frequently or chronically.

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Definition of H.pylori-induced peptic ulcer disease

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Definition of H.pylori-induced peptic ulcer disease

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Helicobacter pylori-induced peptic ulcer disease is a condition where ulcers develop in the lining of the stomach or the upper part of the small intestine (duodenum) due to infection with Helicobacter pylori (H. pylori), a spiral-shaped, gram-negative bacterium, that resides between the mucus layer and surface epithelial cells in the stomach.

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Except PPI, any other drugs? H2 inhibitor? Which one better? Why? 

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Except PPI, any other drugs? H2 inhibitor? Which one better? Why? 

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High dose of H2 antagonist, sucralfate and E-prostaglandin (PGE) analogue such as misoprostol and enprostil can be used to treat and prevent NSAID-induced peptic ulcer disease.

The PGE analogues misoprostol, arbaprostil and enprostil have shown efficacy in healing NSAID-induced ulcers if NSAIDs are continued while GI damage is present.

Neither H2 antagonists, sucralfate and sulglycotide (a cytoprotective drug) have shown efficacy in preventing NSAID-induced gastric ulcers. However, H2 antagonists have shown efficacy in preventing NSAID-induced duodenal ulcers.

In contrast, only misoprostol prevents the development of NSAID-induced peptic and duodenal ulcer.

PPIs are more preferred to be given to RB, because of more rapid symptom’s relief and ulcer healing.

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History of ulcer of ulcer complications

Patients with more than 65 years old

Use of high dose of NSAIDs or multiple NSAIDs

Selection of NSAIDs (COX1 vs COX2 inhibition

Concomitant use of NSAIDs, corticosteroids, aspirin or anticoagulants

H pylori infection.

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Managements of NSAIDs-induced peptic ulcer disease

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Managements of NSAIDs-induced peptic ulcer disease

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Discontinue NSAIDs (if possible):

Stop the NSAID to allow mucosal healing.

If NSAID therapy must continue, use the lowest effective dose or switch to a safer alternative (e.g., selective COX-2 inhibitor).

2. Proton Pump Inhibitors (PPIs):

First-line therapy for healing and symptom relief.

Examples: omeprazole, pantoprazole, esomeprazole.

Typically given for 4–8 weeks.

H. pylori Testing and Eradication (if positive):

If present, treat with an appropriate eradication regimen (e.g., PPI + clarithromycin + amoxicillin/metronidazole for 14 days).

Confirm eradication after treatment.

Use of Gastroprotective Agents:

PPIs: Preferred for prevention and treatment.

Misoprostol: Can be used but may cause diarrhea and cramping.

H2-receptor antagonists: Less effective than PPIs.

Switch to a COX-2 Selective NSAID (if anti-inflammatory therapy is still needed):

e.g., celecoxib – less GI toxicity but still requires PPI co-therapy in high-risk patients.

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It found that selective COX-2 inhibitors in combination with proton pump inhibitors were associated with the lowest absolute event probability for ulcer complications (0.07; 95% confidence interval 0.02–0.18).

https://pmc.ncbi.nlm.nih.gov/articles/PMC5478398/

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Proton pump inhibitors reduce the secretion of gastric acid by inhibiting H+/K+-ATPase. They are widely used to induce healing of gastric and duodenal ulcers. In a double-blind randomised trial, a standard dose of proton pump inhibitor therapy was efficacious in ulcer healing and preventing recurrence of gastroduodenal injury in patients taking NSAIDs.

Proton pump inhibitor

Proton pump inhibitors are usually well-tolerated.

Potential adverse effects include headache, dizziness, constipation, nausea and Vit B12 deficiency.

Concern of using proton pump inhibitor is it may play in acquisition of Clostridium difficile infection during acid suppression. Acid suppression may result in loss of host defense against ingested spores and bacteria.

Although there are potential adverse events related to long-term PPI therapy, the beneficial effect of co-administration of PPIs is greater than the potential risks in high-risk patients for NSAID-induced PU. Taken together, we recommend that high-risk patients who are taking long-term NSAID medications receive low-dose PPIs to prevent PU and its complications.

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For the treatment in trigger 1,

for the treatment for NSAIDs induced PUD patients on taking NSAIDs(especially cox-1 and non-selective)

substitution of selective COX-2 inhibitor for non-selective NSAID.

medical co-therapy with PPI, H2RA, or misoprostol. (PPI are preferred because of more rapid symptom relief and ulcer healing. )

Thus, the naproxen used for osteoarthritis should be stopped and switch to selective cox-2 inhibitor for his osteoarthritis.

celecoxib 200mg daily in 1-2 divided dose, max.400mg daily. use the lowest effective dose for the shortest possible duration.

Etodolac 300mg bid or tid, 400mg bd, or 500mg bd.

Etoricoxib 30mg od, max 60mg od.

Valdecoxib 10mg OD.

The strategy of using selective COX-2 inhibitor to lower the risk of PU development is advantageous compared to co-administration of PPIs or misoprostol because it can reduce the risk without additional medication. Although unspecific abdominal pain, diarrhea, and dyspepsia were reported as common adverse events of selective COX-2 inhibitor, they were mild and the adverse event-related discontinuation rate of selective COX-2 inhibitor was significantly lower than that of nonselective COX inhibitor.

start with PPI, pantoprazole(lesser drug interaction) 40mg OD for 2 weeks is rationale.

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✅ Methods to Confirm Recovery from Peptic Ulcers

1. Surveillance Endoscopy

Duodenal Ulcers:

Not routinely needed if symptoms resolve after treatment (acid suppression + H. pylori eradication + NSAID discontinuation).

Recommended only if symptoms persist despite appropriate therapy — to check for refractory ulcers or other causes.

Gastric Ulcers:

Surveillance endoscopy is more commonly practiced due to:

Risk of false-negative biopsies (2–5% of malignant ulcers may initially appear benign).

Potential for occult malignancy.

Recommended if:

Ulcer looks suspicious or was not biopsied initially.

Symptoms persist after treatment.

No clear cause was identified (e.g., NSAID or H. pylori).

Follow-up endoscopy is typically done after 8–12 weeks of medical therapy.

2. Biopsy at Follow-up Endoscopy

If a gastric ulcer is unhealed at follow-up, repeat biopsies should be performed to rule out malignancy.

Multiple specimens should be taken from the edges and base of the ulcer.

3. Symptomatic Improvement

Resolution of symptoms after treatment is a clinical marker of recovery, especially in duodenal ulcers.

Persistent or atypical symptoms warrant further endoscopic evaluation.

4. H. pylori Testing and Eradication Confirmation

For H. pylori-positive ulcers, confirmation of eradication (usually via urea breath test or stool antigen test) is essential to prevent recurrence.

Should be done at least 4 weeks after antibiotic therapy ends and after stopping PPIs for 1–2 weeks.

5. Imaging (If Endoscopy Contraindicated)

In rare cases where endoscopy can't be performed, radiologic imaging might be used to assess healing — though it's less accurate than endoscopy.

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Pharmacological prevention for recurrence of peptic ulcer

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Pharmacological prevention for recurrence of peptic ulcer

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🔑 Pharmacologic Strategies to Prevent Peptic Ulcer Recurrence

1. Proton Pump Inhibitors (PPIs)

Mainstay for prevention of recurrence.

Examples: omeprazole, esomeprazole, pantoprazole.

Often used in long-term maintenance therapy in high-risk patients or those who must continue NSAIDs.

Dose: Typically 20–40 mg daily.

2. Misoprostol

Prostaglandin analog that protects gastric mucosa.

Reduces ulcer recurrence and NSAID-induced complications.

Limitation: GI side effects like diarrhea and cramping.

Dose: 200 mcg 2–4 times daily.

3. H2-Receptor Antagonists

Less effective than PPIs but still used in some cases.

Examples: ranitidine (withdrawn in many countries), famotidine, nizatidine.

High doses needed to match PPI efficacy for NSAID ulcers.

4. Eradication of Helicobacter pylori

In patients with H. pylori, eradication therapy significantly lowers recurrence risk.

Usually a combo of PPI + 2 antibiotics (e.g., clarithromycin + amoxicillin/metronidazole) for 10–14 days.

5. COX-2 Selective NSAIDs

If NSAIDs must be continued, switching to a COX-2 selective inhibitor (e.g., celecoxib) plus a PPI can reduce risk.

Still not without risk, especially at high doses or in high-risk patients

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As for H.Pylori PUD. the treatment goal is to eradicate the h.pylori bacteria, heal the ulcer, and cure the disease.

Successful eradication heals ulcers and reduces the risk of recurrence to less than 10% at 1 year.

When possible, most cost-effective drug regimen should be utilized.

reference: Dipiro, pharmacotherapy handbook sixth edition. Online book.

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Overall treatment for peptic ulcer disease is aimed at relieving ulcer pain, healing the ulcer, preventing ulcer recurrence, and reducing ulcer related complications.

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📌 Key Risk Factors That Worsen Outcomes:

Advanced age

History of ulcers or GI bleeding

Concurrent steroid or anticoagulant use

High NSAID dosage or long-term use

Presence of H. pylori infection

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Complications of untreated NSAIDs induced peptic ulcer 

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Complications of untreated NSAIDs induced peptic ulcer 

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🔥 Major Complications if NSAID-Induced Peptic Ulcers Are Not Treated:

1. Gastrointestinal Bleeding

One of the most serious and common complications.

Caused by NSAID-induced ulcers due to inhibition of COX-1 which can help with production of gastroprotective or exacerbated by NSAID effects on platelet dysfunction (which impairs blood clotting).

Can lead to:

Anemia (chronic blood loss)

Hematemesis (vomiting blood)

Melena (black tarry stools)

Life-threatening hemorrhage requiring hospitalization

2. Perforation

A full-thickness hole in the GI tract wall, often in the stomach or duodenum.

Leads to leakage of stomach contents into the abdominal cavity ➝ peritonitis (severe infection).

A surgical emergency.

3. Gastric Outlet Obstruction

Scar tissue and inflammation from chronic ulceration can narrow the pyloric channel.

Causes vomiting, bloating, early satiety, and weight loss.

Though less common, it can be disabling if untreated.

4. Delayed Healing and Chronic Ulcers

Continued NSAID use impairs healing, especially in large, fibrosed, or deep ulcers.

Risk of recurrence remains high without adequate treatment or cessation of NSAIDs.

Fibrotic ulcer beds may resist full healing even after NSAID withdrawal.

5. Increased Risk with Comorbidities and Drug Interactions

Elderly, those with cardiovascular disease, or taking corticosteroids or anticoagulants face dramatically increased risk.

Combining NSAIDs with steroids or anticoagulants increases GI bleeding risk up to 12-fold.

6. Exacerbation of Pre-existing Peptic Ulcers

NSAIDs can convert subclinical or inactive ulcers (often due to H. pylori) into active bleeding ulcers.

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Initial dose: 5 to 60 mg orally per day; may be give once a day or in divided doses
Maintenance dose: Adjust or maintain initial dose until a satisfactory response is obtained; then, gradually in small decrements at appropriate intervals decrease to the lowest dose that maintains an adequate clinical response

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Prednisolone, a corticosteroid with primarily glucocorticoid activity, reduces inflammation by reversing increased capillary permeability and suppressing polymorphonuclear leucocyte migration. It also affects the lymphatic system by reducing its activity and volume resulting in the suppression of the immune system.

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immunosuppression; acute myopathy, insomnia, electrolyte imbalance, fluid retention, hypertension; altered glucose tolerance, increased risk of gastrointestinal perforation (particularly in patients with certain gastrointestinal disorder).

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Absorption: Rapidly and well absorbed from the gastrointestinal tract. Time to peak plasma concentration is 1-2 hours. *Initial absorption is affected by food, but does not affect overall bioavailability.

Distribution: Crosses the placenta; enters breast milk (small amount). Volume of distribution is 0.22-0.7L/kg. Plasma protein binding is 70-90%. Mainly to albumin, and corticosteroid-binding globulin.

Metabolism: Metabolised mainly in the liver into a biologically inactive compound.

Excretion: Via urine (as glucuronide and sulfate conjugates; small amounts as unchanged drug). Elimination half-life is 2-4 hours

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What is FOBT?

The Fecal Occult Blood Test (FOBT) is a non-invasive test used to detect hidden (occult) blood in the stool, which is not visible to the naked eye.

Purpose:

It helps screen for colorectal cancer or other causes of gastrointestinal bleeding, such as ulcers, polyps, or hemorrhoids.

Types of FOBT:

Guaiac-based FOBT (gFOBT):

Uses a chemical reaction with guaiac to detect blood.

Requires dietary restrictions to avoid false positives (e.g. avoiding red meat, some raw vegetables, and certain medications).

Fecal Immunochemical Test (FIT or iFOBT):

Uses antibodies to detect human hemoglobin (blood) in stool.

More specific to lower GI bleeding.

Does not require dietary restrictions.

How it’s done:

A small stool sample is collected using a test kit.

The sample is then analyzed for the presence of blood.

Significance:

Positive FOBT results warrant further diagnostic testing, usually a colonoscopy.

It's often part of routine colorectal cancer screening, especially in individuals over 50 years old.

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H.pylori:

Helicobacter pylori is a gram-negative bacterium that live in low-oxygen environments. It commonly infects the human stomach, leading to inflammation and the development of ulcers.

Monitoring for Efficacy

Symptom resolution (e.g. epigastric pain, bloating, nausea)

Test of eradication (usually done ≥4 weeks after therapy)

Urea Breath Test (preferred)

Stool antigen test

Endoscopy with biopsy (if clinically indicated)

Avoid PPI and antibiotics for at least 2 weeks before testing to avoid false-negative.

Monitoring for Side Effects

Common side effects by drug class:

1. Proton Pump Inhibitors (PPIs)

Headache

Diarrhea or constipation

Long-term use: hypomagnesemia, B12 deficiency, increased fracture risk

2. Amoxicillin

GI upset (nausea, diarrhea)

Rash (monitor for allergic reaction)

3. Clarithromycin

Metallic taste

QT prolongation (rare, ECG if needed in high-risk patients)

Drug interactions (CYP3A4 inhibitor)

4. Metronidazole

Metallic taste

GI upset

Disulfiram-like reaction with alcohol

Peripheral neuropathy (if prolonged use)

5. Tetracycline

Photosensitivity

GI irritation

Contraindicated in pregnancy and children <8 years

6. Levofloxacin (Fluoroquinolone)

Tendonitis, tendon rupture

QT prolongation

CNS effects (confusion, dizziness in elderly)

Risk of aortic aneurysm/dissection (rare but serious)

7. Bismuth compounds

Black stools or tongue (harmless)

Nausea, constipation

Source:

https://sites.google.com/moh.gov.my/nag/contents/section-a-adult/a4-gastrointestinal-infections#h.g1wrutmgw5z9

MIMS Malaysia

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• Track symptoms -> Keep a diary of when symptoms occur (e.g., after eating, after taking certain meds).

• Follow up -> Check if symptoms improve with lifestyle changes or OTC meds.

• Watch for red flags -> If there is weight loss, persistent vomiting, or worsening dysphagia → urgent referral.

• Monitor adherence -> Ensure the patient follows the recommended regimen -> how?

1. Clear Education

• Explain purpose, timing, and how to take meds in simple terms.

• Highlight what happens if they skip doses.

2. Address Concerns

• Ask if they have any doubts or side effect worries.

• Reassure and clarify when needed.

4. Simplify the Regimen

• Adjust dosing schedule if possible

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MOA:

Neutralise the gastric acid and raise pH of gastric content and it is a Reflux suppressant.

(best for mild+ short term relief)

Dose:

Liquid:

Adults and Children 12 Years and Over:

One to two sachets or doses (10–20 mL) after meals and at bedtime, up to four times per day.

CI:

Should not be used in patients with moderate or severe renal insufficiency.

SE:

Hypersensitivity reactions (including anaphylaxis and urticaria) and respiratory effects (including bronchospasm) have been reported very rarely.

According to NCBI

The presence of calcium carbonate may cause acid rebound and constipation

DDI:

Due to the presence of calcium and carbonates, a time-interval of 2 hours should be considered between intake of this product and the administration of other medicinal products — especially:

Tetracyclines

Fluoroquinolones

Iron salts

Thyroid hormones

Chloroquine

Bisphosphonates

Estramustine

Source: https://www.mims.com/malaysia/drug/info/gaviscon-advance?type=full

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Relief of heartburn and acid indigestion (also known as dyspepsia).
Heartburn and acid indigestion are common and experienced by most people at some time. They may be felt as a burning sensation across the lower part of the chest, a pain spreading from the stomach towards the throat or regurgitation of a sour-tasting liquid. Heartburn and acid indigestion often occur during pregnancy or if you have a medical condition called hiatus hernia. Heartburn and acid indigestion can be made worse if the patient eats fatty or very spicy foods, drinks too much alcohol, smokes, wears very tight clothing, is overweight or when the patient bends forward or lies down.
Relief of symptoms of conditions eg, hiatus hernia and reflux oesophagitis (inflamed food pipe), including symptoms of laryngopharyngeal reflux such as hoarseness and other voice disorders, sore throats and cough. It can also be used to treat the symptoms of gastrooesophageal reflux during concomitant treatment with or following withdrawal of acid suppressing therapy.

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Gaviscon Advance prescribing information for healthcare professionals. Discover details, users, dosages, indications and special precautions etc. Get the insights now!

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d) Management

1st line treatment : PPI , Clarithromycin, either Amoxicillin or Metronidazole (PPI based triple therapy) : 10-14 days

Preferred regimen : PPI-based triple therapy amoxicillin containing regimen

In penicillin allergic patients : Substiute metronizadole for amoxcillin in the PPI-based triple therapy regimen

Alternative initial strategy : PPI, H2RA, Bismuth salt, Tetracycline, Metronidazole : 10-14 days

e) Risk factor

People often get H. pylori infection during childhood. Risk factors for H. pylori infection are related to living conditions in childhood, such as:

Living in crowded conditions. Living in a home with many other people can increase your risk of H. pylori infection.

Living without a reliable supply of clean water. Having a reliable supply of clean, running water helps reduce the risk of H. pylori.

Living in a developing country. People living in developing countries have a higher risk of H. pylori infection. This may be because crowded and unsanitary living conditions may be more common in developing countries.

Living with someone who has an H. pylori infection. You're more likely to have H. pylori infection if you live with someone who has H. pylori infection.

Other factors :

Too much alcohol intake

Regular use of aspirin, ibuprofen, naproxen or other NSAIDs

Smoking cigarettes or chewing tobacco

Radiation treatments

Stress

f) Complication if it is not treated?

Upper gastrointestinal bleeding

Gastric outlet obstruction

Gastric cancer

Perforation

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The test is performed at the time of gastroscopy

[ a medical procedure where a thin, flexible tube with a camera and light (endoscope) is inserted into the esophagus, stomach, and upper part of the small intestine to examine the upper digestive tract ]

A biopsy of mucosa is taken from the antrum of the stomach, and is placed into a medium containing urea and an indicator such as phenol red.

The urease produced by H. pylori hydrolyzes urea to ammonia, which raises the pH of the medium, and changes the color of the specimen from yellow (NEGATIVE) to red (POSITIVE)

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Dose: (RB is taking T.Naproxen 500mg BD)

According to Mims, Naproxen can give to acute musculoskeletal disorder, dysmenorrhea, acute gout, fever, and mild to moderate pain with respective dosage regimen

Based on RB condition:

Ankylosing spondylitis, Osteoarthritis, Rheumatoid arthritis

Adult:
Doses are expressed in terms of naproxen base (each 200 mg naproxen base is equivalent to 220 mg naproxen Na).

RB is under this category

Conventional tab/oral suspension:
500–1,000 mg daily as a single or in 2 divided do

SE:

Gastrointestinal disorders:

Nausea, vomiting, dyspepsia, constipation, diarrhoea, flatulence, abdominal pain or discomfort, epigastric distress, heartburn.

Musculoskeletal and connective tissue disorders:

Muscle weakness, myalgia, arthralgia.

Respiratory, thoracic and mediastinal disorders:

Dyspnoea, eosinophilic pneumonitis, pulmonary oedema, asthma.

Monitor the SE:

Observe the s/sx of the RB for example: the respiratory function, gastrointestinal ulceration or bleeding

DDI:

May reduce the therapeutic efficacy of antihypertensive agents, such as:

ACE inhibitors

β-blockers
Angiotensin II receptor blockers

Diuretics (e.g. furosemide, thiazide diuretics)

Antacids, colestyramine, and sucralfate may delay naproxen absorption.

Potentially Fatal:
Increased risk of gastrointestinal toxicity or bleeding when used together with:

Other NSAIDs

Corticosteroids

Anticoagulants (e.g. warfarin)

SSRIs

Antiplatelet agents (e.g. aspirin)

Food drug interaction:

Increase risk of gastrointestinal bleeding with alcohol

Source: https://www.mims.com/malaysia/drug/info/naproxen?mtype=generic

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Patient Counseling

Educate on:

Symptom recognition (e.g., tarry stools, severe epigastric pain)

Proper medication use (timing of PPI, completing antibiotics)

Importance of follow-up tests and appointments

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Dose:

Acute bronchospasm

Adult:

Treatment and prevention in patients with reversible obstructive airway disease.

As metered-dose aerosol or dry powder inhaler (90 or 100 mcg/actuation):

1 or 2 inhalations every 4–6 hours.

Max: 800 mcg daily.

Prophylaxis of exercise-induced bronchospasm

Adult:
As metered-dose aerosol or dry powder inhaler (90 or 100 mcg/actuation):
2 inhalations 15–30 minutes prior to exercise.

Chronic bronchospasm

Adult:
Via nebuliser: 2.5–5 mg up to 3–4 times daily.

SE:

Significant:

Hypersensitivity reactions (e.g. urticaria, angioedema, rash, bronchospasm, oropharyngeal oedema), hypokalaemia (high doses).

Gastrointestinal disorders:

Nausea, vomiting, mouth and throat irritation (inhalation).

DDI:

Increased risk of hypokalaemia with:

Corticosteroids

Diuretics (e.g. loop, thiazide)

Xanthines (e.g. theophylline)

Increased vascular effects with:

MAOIs

Tricyclic antidepressants (TCAs)

May cause severe bronchospasm when used with β-blockers (e.g. propranolol)

May decrease serum concentrations of digoxin

Source: https://www.mims.com/malaysia/drug/info/salbutamol?mtype=generic

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Non-invasive

HOW ? ->

Urease is not present in mammalian cells, and its presence indicates urease-containing microbes.

1. You drink a solution containing urea.

The urea has a special carbon atom in it (either ¹³C or ¹⁴C).

2. If H. pylori is present, it will break down the urea using urease.

3. This produces CO₂ with the special carbon atom.

4. That CO₂ travels through your blood and is breathed out through your

5. The test then measures the special CO₂ in your breath.

Withholding PPIs, H2 antagonists, bismuth, and antibiotics before a urea breath test is crucial to prevent false negative results. These medications can:

Reduce H. pylori bacteria: Antibiotics and bismuth directly kill or suppress the bacteria.

Suppress urease activity: PPIs and H2 antagonists reduce stomach acid, which can inhibit the activity of the H. pylori urease enzyme.

A reduced bacterial load or suppressed urease activity leads to less labeled CO2 production, indicating a negative result even if H. pylori is still present. Withholding these medications ensures the test accurately reflects the presence or absence of active H. pylori infection.

*The sensitivity and specificity range from 88% to 95% and 95% to 100% respectively

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Celecoxib was given to patient to manage osteoarthritis as an alternative to naproxen.

Naproxen is a non-selective COX inhibitor which inhibit both COX-1 and COX-2. Inhibition of COX-1 prevents the prostaglandin secretion that protects the stomach lining, increasing risk of peptic ulcer.

Celecoxib is a selective COX-2 inhibitor which mainly acts on the COX-2 pathway, which causes the synthesis of prostaglandin that causes inflammation and pain. This allows celecoxib to exert anti-inflammatory, analgesics and anti-inflammatory effects.

Dosage regimen

Osteoarthritis

200 mg daily in 1-2 divided dose. Increase to 200 mg BD if necessary. Discontinue if no improvement after 2 weeks using maximum dose. (BNF88)

Monitoring

Celecoxib is less likely to cause GI complication compared to non-selective NSAIDs. However, since it is also an NSAID, it is advisable to monitor for sign and symptoms for GI bleeding, especially with long-term usage. (melena stool)

Use of anti-ulcer therapy is recommended.

Prescribers need to monitor patients for adverse drug reactions due to the risk of celecoxib causing new or worsening hypertension. (cautious use, BNF 88)

Drug-drug Interaction

Combination of celecoxib and corticosteroids which is prednisolone, increase risk of GI toxicity, including inflammation, bleeding, ulcer and perforation. (categorised as severe, BNF 88)

Caution is advised when both celecoxib and prednisolone are being used, especially patient with history of peptic ulcer disease, GI bleeding and elderly. Advise patient to report any signs and symptoms of GI ulceration and bleeding. Use of anti-ulcer therapy is recommended

Appropriateness

Based on study, combination of celecoxib and PPI (eg. pantoprazole) is the preferred treatment to reduce the risk of recurrent upper gastrointestinal bleeding in patients at high risk of both cardiovascular and gastrointestinal events who require aspirin and NSAID for cardiovascular and anti-inflammatory therapies.

References:

Drug Interaction Report: Celebrex, prednisolone

Sci-Hub | Gastrointestinal safety of celecoxib versus naproxen in patients with cardiothrombotic diseases and arthritis after upper gastrointestinal bleeding (CONCERN): an industry-independent, double-blind, double-dummy, randomised trial. The Lancet, 389(10087), 2375–2382 | 10.1016/s0140-6736(17)30981-9

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Sci-Hub | Gastrointestinal safety of celecoxib versus naproxen in patients with cardiothrombotic diseases and arthritis after upper gastrointestinal bleeding (CONCERN): an industry-independent, double-blind, double-dummy, randomised trial. The Lancet, 389(10087), 2375–2382 | 10.1016/s0140-6736(17)30981-9

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Most frequent adverse events reported in clinical trials and observed with perindopril are: dizziness, headache, paraesthesia, vertigo, visual disturbances, tinnitus, hypotension, cough, dyspnoea, nausea, vomiting, prurit, rash, muscle cramp, and asthenia.

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a) NSAID

NSAID inhibit cyclooxygenase (COX-1 and COX-2). Inhibition of COX-1 affects the conversion of arachidonic acid to prostaglandins that protects the GI layer. This increases the risk of ulceration and damage to stomach lining.

b) Dual antiplatelet therapy (MI) (aspirin,

clopidogrel)

Dual antiplatelet therapy provides therapeutic benefits in high-risk vascular disease patients. However, it would increase the risk of gastrointestinal (GI) complications. -

Major complications include gastroduodenal ulcerations would cause GI haemorrhage, perforation, and death. Minor complications include dyspepsia, pill esophagitis, subepithelial haemorrhages, erosions, and ulcerations in the stomach and duodenum.

Elderly, patient with a history of gastroduodenal ulcers, gastroesophageal reflux disease, esophagitis, untreated Helicobacter pylori infection, intestinal polyps, or cancer, and those using concomitant anticoagulants, steroids, or nonsteroidal anti-inflammatory drugs are at high risk of GI complications.

c) Potassium supplement

The potassium pumps can activate the H/K ATPase which can leads to the increase secretion of hydrochloric acid into the parietal cell, increasing the risk for ulcers. Study has shown that patients taking potassium supplementation medications, especially for the treatment of hypokalaemia, often experience gastric ulcers as a side effect.

References:

Gastrointestinal Complications of Dual Antiplatelet Therapy | Circulation

Aspirin vs Clopidogrel: Antiplatelet Agent of Choice for Those With Recent Bleeding or at Risk for Gastrointestinal Bleed - PMC

Non-steroidal Anti-inflammatory Drug (NSAID)-, Potassium Supplement-, Bisphosphonate-, and Doxycycline-Mediated Peptic Ulcer Effects: A Narrative Review - PMC

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Esophagogastroduodenoscopy(EGD)

Barium swallow

Complete blood, liver function, levels of amylase and lipase

Computerized tomography of the abdomen

Helicobacter pylori testing

Serologic testing

Urea breath test

Stool antigen test

Urine based ELISA and rapid urine test

Endoscopic biopsy

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Age: 65 years old

Smoking (12-pack-year)

Alcohol consumption

NSAID use (Naproxen)

Corticosteroid use (Prednisolone)

Comorbidities: Asthma, Osteoarthritis

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All segments of the GI tract are divided into four layers: the mucosa (epithelium, lamina propria, and muscular mucosae), the submucosa, the muscularis propria (inner circular muscle layer, intermuscular space, and outer longitudinal muscle layer), and the serosa.

The major functions of the muscularis propria are to propel food through the gut by contractile peristaltic waves initiated and regulated by various neural and hormonal events. Flow is regulated by peristaltic mechanisms and by sphincters located in the upper oesophagus, in the distal portions of the oesophagus, stomach, and ileum and in the anus.

Reference

Intestinal Architecture and Development - Regulation of Gastrointestinal Mucosal Growth - NCBI Bookshelf

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Absorption: Rapid and reaches the peak concentration within 1 hour.  The half-life of perindopril is equal to 1 hour.

Metabolism: Perindopril is a prodrug and it is extensively metabolized, with only 4-12% of the dose recovered in urine following oral administration. 27% of the administered perindopril dose reaches the bloodstream as the active metabolite perindoprilat. The peak plasma concentration of perindoprilat is achieved within 3 to 4 hours. However, ingestion of food decreases conversion to perindoprilat (active metabolite). Hence it should be given orally in a single daily dose in the morning before a meal.

*Six metabolites have been identified: perindoprilat, perindopril glucuronide, perindoprilat glucuronide, a perindopril lactam, and two perindoprilat lactams. Only perindoprilat is pharmacologically active. Perindoprilat and perindoprilat glucuronide are the two main circulating metabolites.

Distribution: The volume of distribution is approximately 0.2L/kg for unbound perindoprilat. Protein binding of perindoprilat to plasma proteins is 20%, principally to angiotensin converting enzyme, but is concentration-dependent.

Elimination: Perindoprilat is eliminated in the urine and the terminal half-life of the unbound fraction is approximately 17 hours, resulting in steady-state within 4 days.

Special elimination: Decreased elimination in the elderly, and also in patients with heart or renal failure. Dosage adjustment in renal insufficiency is desirable depending on the degree of impairment (creatinine clearance).

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Definition

Peptic ulcer is characterised by the breaking of the inner linking of the GI tract, caused by the GI secretion such as gastric acid or pepsin.

Peptic ulcer is different from erosion as it would extends deeper into the muscularis propria layer of the gastric epithelium stimulate more inflammatory reaction at the infected tissue and occasionally accompany with scarring.

Peptic ulcer also referred as peptic ulcer disease (PUD). Commonly caused by heavy use of NSAIDS and H.pylori infection.

Types of Peptic Ulcer

Gastric Ulcer

Duodenal Ulcer

References

Peptic Ulcer Disease - StatPearls - NCBI Bookshelf

Duodenal Ulcer - StatPearls - NCBI Bookshelf

Sci-Hub | 7 Helicobacter pylori in duodenal and gastric ulcer disease. Baillière’s Clinical Gastroenterology, 9(3), 529–547 | 10.1016/0950-3528(95)90047-0

Peptic Ulcer Types, Causes, Symptoms, Stomach Pain, Treatment

Peptic Ulcer - Gastric vs Duodenal - GP Exams

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a.

* Past two days symptoms worsened and is not relieved by maximum dose of gaviscon

Complication = Intermittent heartburn that is disrupting his sleep

EXPLANATION =

- Epigastric pain

- Nausea

- Fatigue

- Dysphagia

- Pain during swallowing

- Nausea,loss of appetite and burning sensation in his chest and throat after meals

Gastroesophageal reflux disease (GERD), where stomach acid backs up into the esophagus, causing irritation and the characteristic burning sensation.

Over the past two days his symptoms worsening suggesting the escalation of his condition or even a development of complication especially with the condition disrupting his sleep

-Pale during examination and dark tarry stools

Dark tarry stools indicate bleeding internally [esophagus, stomach or first part of small intestine ] * sometimes iron/activated charcoal supplements

Most likely, anemia

*From the 32 patients with anemia, 23 were associated with GERD, a higher number than those without GERD

[https://pmc.ncbi.nlm.nih.gov/articles/PMC9818737/#:~:text=From%20the%2032%20patients%20with,%2C%2095%25%20confidence%20interval)]

b.Tenderness of upper abdominal

It indicates the presence of localized pain in the upper region of the abdomen, which houses organs such as the stomach, duodenum, and parts of the esophagus, liver, gallbladder, and pancreas.

This tenderness suggests underlying inflammation, irritation, or another pathological process affecting one or more of these structures.

Due to the worsening of reflux systems likely indicates peptic ulcer disease

[ NOT liver inflammation -> liver inflammation is upper right quadrant of abdomen, just below ribcage ]

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Pharmacotherapeutic group ACE inhibitor.

An inhibitor of the enzyme that converts angiotensin I into angiotensin II (Angiotensin Converting Enzyme). The converting enzyme is an exopeptidase that allows conversion of angiotensin I into angiotensin II which cause vasoconstriction, and degradation of the vasodilator bradykinin into an inactive heptapeptide. Inhibition of ACE results in a reduction of angiotensin II in the plasma, which leads to increased plasma renin activity (by inhibition of the negative feedback of renin release) and reduced secretion of aldosterone. Since ACE inactivates bradykinin, inhibition of ACE also results in an increased activity of circulating and local kallikrein-kinin systems (and thus also activate prostaglandin system).

Discontinuation of treatment does not lead to a rebound hypertension effect.

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Generally, well tolerated. Adverse reactions have usually been mild and transient. Most frequent adverse effects associated with atorvastatin therapy:

Metabolism and nutritional disorders: hyperglycaemia.

Respiratory, thoracic, and mediastinal disorders: pharyngolaryngeal pain, epistaxis.

Gastrointestinal disorders: nausea, diarrhea, dyspepsia, flatulence.

Musculoskeletal and connective tissue disorders: arthralgia, pain in extremity, musculoskeletal pain, muscle spasms, myalgia, joint swelling.

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Pharmacokinetics:

Absorption: Atorvastatin is rapidly absorbed after oral administration and achieve maximum plasma concentration within one to two hours.

Distribution: Atorvastatin is ≥ 98% bound to plasma proteins. A red blood cell/plasma ratio of 0.25 indicates a poor drug penetration into RBC.

Metabolism: Atorvastatin is extensively metabolised in the liver by the enzyme Cytochrome P450 3A4, into ortho- and para-hydroxylated derivatives. Therefore, adjustment may be needed if concurrently used with enzyme inhibitor of CYP450 3A4. Example drug Erythromycin.

Excretion: Atorvastatin and its metabolites are eliminated primarily in bile following hepatic and/or extrahepatic metabolism. However, the drug does not appear to undergo enterohepatic recirculation. Mean plasma elimination half-life of atorvastatin in human is14 hours, but the half-life of inhibitory activity for HMG-CoA reductase is 20-30 hours due to the contribution of active metabolites. Less than 2% is excreted in urine.

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3-hydroxy-3-methylglutaryl coenzyme-A (HMG-CoA) reductase. The enzyme catalyzes the conversion of HMG-CoA to mevalonate, an early and rate-limiting step in cholesterol biosynthesis.

Atorvastatin is a selective, competitive inhibitor of HMG-CoA reductase. Thus, inhibiting the synthesis of cholesterol in the liver and increased in number of hepatic LDL receptors on the cell surface for an enhanced uptake and catabolism of LDL.