DYSPEPSIA AND GERD

The gastrointestinal (GI) tract is composed of organs and tissues that have diverse forms and functions. It includes the esophagus, stomach, small intestine, large intestine, colon, rectum, biliary tract, gallbladder, liver, and pancreas. Common GI symptoms include heartburn, abdominal pain, dyspepsia, nausea, vomiting, diarrhea, constipation, and gastrointestinal bleeding.

Questions in a GI history
Where is your pain located? Please point to the area where you feel pain. What were you doing when the pain occurred? How rapidly did the pain come on? Is your pain constant or intermittent? What factors exacerbate or alleviate your pain? Does the pain awaken you at night? Have you experienced any nausea or vomiting lately?

 Examination of the abdomen is classically approached by inspection, auscultation, percussion, and palpation. Inspection of the abdomen may reveal scars, hernias, bulges, or peristalsis. Auscultation is mainly focused on analysis of bowel sounds and identification of bruits. Percussion of the abdomen allows for detection of tympany (distention of stomach), measurement of visceral organs, and detection of ascites. Palpation may allow the clinician to identify tenderness, rigidity, masses, and hernias.

Dyspepsia also known as upset stomach or indigestion, refers to a condition of impaired digestion It is a medical condition characterized by chronic or recurrent pain in the upper abdomen, upper abdominal fullness and feeling full earlier than expected when eating. It can be accompanied by bloating, belching, nausea, or heartburn. Dyspepsia is a common problem, and is frequently due togastroesophageal reflux disease (GERD) or gastritis, but in a small minority may be the first symptom of peptic ulcer (an ulcer of the stomach or duodenum) and occasionally cancer

 The characteristic symptoms of dyspepsia are upper abdominal pain, bloating, fullness and tenderness on palpation Pain worsened by exertion and associated with nausea and perspiration may also indicate angina. Occasionally dyspeptic symptoms are caused by medication, such as calcium antagonists (used for angina or high blood pressure), nitrates (used for angina), theophylline (used for chronic lung disease), bisphosphonates, corticosteroids and nonsteroidal anti-inflammatory drugs (NSAIDs, used as painkillers).[3]

The presence of gastrointestinal bleeding (vomit containing blood), difficulty swallowing, loss of appetite, unintentional weight loss, abdominal swelling and persistent vomiting are suggestive of peptic ulcer disease or malignancy and would necessitate urgent investigations. People under 55 years, without alarm symptoms, can be treated without investigation. People over 55 years with recent onset dyspepsia or those with alarm symptoms should be urgently investigated by upper gastrointestinal endoscopy. This will rule out peptic ulcer disease, medication-related ulceration, malignancy and other rarer causes.[3]

People under the age of 55 years with no alarm features do not need endoscopy but are considered for investigation for peptic ulcer disease caused by Helicobacter pylori infection. Investigation for H. pylori infection is usually performed when there is a moderate to high prevalence of this infection in the local community or the person with dyspepsia has other risk factors for H. pylori infection. Medication-related dyspepsia is usually related to non-steroidal anti-inflammatory drugs (NSAIDs) and can be complicated by bleeding or ulceration with perforation of stomach wall.

Gastroesophageal reflux disease (GERD)

GERD refers to any symptomatic clinical condition or histologic alteration that results from episodes of gastroesophageal reflux. Gastroesophageal reflux is the retrograde movement of gastric contents from the stomach into the esophagus. Repeated exposure to refluxed material for prolonged periods of time, causes inflammation of the esophagus (reflux esophagitis) Some cases it can progress to erosion of the squamous epithelium of the esophagus (erosive esophagitis).

 Heartburn is the hallmark symptom of GERD A substernal sensation of warmth or burning rising up from the abdomen that may radiate to the neck.

Patho
Gastroesophageal reflux is associated with defective lower esophageal sphincter (LES) pressure or function. Patients may have decreased gastroesophageal sphincter pressures related to
(a) spontaneous transient LES relaxations, (b) transient increases in intra-abdominal pressure (c) an atonic LES

 GERD may lead to esophageal bleeding. The blood loss is usually chronic and low grade in nature, but can lead to anemia. Some patients, the reparative process leads to the replacement of the squamous epithelial lining of the esophagus by specialized columnar-type epithelium. This condition, known as Barretts esophagus, is more likely to occur in those patients with a long history (years) of symptomatic reflux.

 Within the esophageal mucosa and submucosa there are mucus secreting glands. The mucus secreted by these glands may contribute to the protection of the esophagus. Bicarbonate moving from the blood to the lumen can neutralize acidic refluxate in the esophagus. Saliva is also rich in epidermal growth factor, stimulating cell renewal.

Symptoms
Typical symptoms: May be aggravated by activities that worsen gastroesophageal reflux such as recumbent position, bending over, or eating a meal high in fat. Heartburn Water brash (hypersalivation) Belching Regurgitation

Symptoms
Atypical symptoms: Extraesophageal symptoms may be the only symptoms present, making it more difficult to recognize GERD as the cause, especially when endoscopic studies are normal. Nonallergic asthma Chronic cough Hoarseness Pharyngitis Chest pain Dental erosions

Goal
Alleviate or eliminate the patients symptoms; Decrease the frequency or recurrence and duration of gastroesophageal reflux Promote healing of the injured mucosa Prevent the development of complications.

 Lifestyle changes and patient-directed therapy with antacids, nonprescription H2-receptor antagonists, and/or nonprescription proton pump inhibitors. Pharmacologic intervention primarily with standard or high-dose acid-suppressing agents. Interventional therapies (anti reflux surgery or endoluminal therapies)

NONPHARMACOLOGIC THERAPY
LIFESTYLE MODIFICATIONS
(a) weight loss (b) elevation of the head of the bed (c) eating smaller meals and avoidance of eating 3 hours prior to sleeping (d) avoidance of foods or medications that exacerbate GERD (e) smoking cessation; and (f) avoidance of alcohol

INTERVENTIONAL APPROACHES
Antireflux Surgery
to re-establish the antireflux barrier, Endoluminal Therapies Endoscopic suturing and injection of a biopolymer.

PHARMACOLOGIC THERAPY
ANTACIDS AND ANTACID-ALGINIC ACID PRODUCTS

Maintaining the intragastric pH above 4 decreases the activation of pepsinogen to pepsin, a proteolytic enzyme. Neutralization of gastric fluid leads to increased LES pressure. Antacid or antacid combination products may cause gastrointestinal adverse effects (diarrhea or constipation, depending on the product), alterations in mineral metabolism, and acid-base disturbances.

 Aluminum-containing antacids may bind to phosphate in the gut and lead to bone demineralization. Antacids have clinically significant drug interactions with tetracycline, ferrous sulfate, isoniazid, quinidine, sulfonylureas, and quinolone antibiotics. The have short duration of action, frequent administration throughout the day required to provide continuous neutralization of acid.

 ACID SUPPRESSION WITH H2-RECEPTOR ANTAGONISTS (CIMETIDINE, FAMOTIDINE, NIZATIDINE, AND RANITIDINE)

H2-receptor antagonists in divided doses are effective in treating patients with mild to moderate GERD. Hypersecreters and those with erosive disease, higher doses and/or dosing four times daily provides better acid control, especially after mealtime acid surges.
cimetidine 800 mg twice daily, famotidine 40 mg twice daily, nizatidine 150 mg four times daily, ranitidine 150 mg four times daily

 The most common adverse effects are headache, somnolence, fatigue, dizziness, and either constipation or diarrhea. Cimetidine may inhibit the metabolism of theophylline, warfarin, phenytoin, nifedipine, or propranolol, among others.

ACID SUPPRESSION WITH PROTON PUMP INHIBITORS (ESOMEPRAZOLE, LANSOPRAZOLE, OMEPRAZOLE, PANTOPRAZOLE, AND RABEPRAZOLE)

Proton pump inhibitors are superior to H2receptor antagonists in treating patients with moderate to severe GERD. Comparable doses of proton pump inhibitors are omeprazole 20 mg = esomeprazole 20 mg = lansoprazole 30 mg = rabeprazole 20 mg = pantoprazole 40 mg per day.

 Proton pump inhibitors block gastric acid secretion by inhibiting gastricH+/K+adenosine triphosphatase in gastric parietal cells. Rabeprazole have a faster onset of action after the first dose and maintains the gastric pH >4 for a higher percentage of time during a 24hour period as compared with omeprazole

 Esomeprazole, is the S-isomer of omeprazole and may offer greater acid suppression and improved healing rates as compared with the other proton pump inhibitors.

 The proton pump inhibitors are usually well tolerated. Potential adverse effects include headache, dizziness, somnolence, diarrhea, constipation, and nausea.

PROKINETIC AGENTS
The efficacy of the prokinetic agents cisapride, metoclopramide, and bethanechol has been evaluated in the treatment of GERD. Prokinetic agents havealso been used as adjunctive therapy with an H2-receptor antagonist.

MUCOSAL PROTECTANTS
Sucralfate, a nonabsorbable aluminum salt of sucrose octasulfate, has very limited value in the treatment of GERD. Sucralfate has similar healing rates as H2receptor antagonists for patients with mild esophagitis.

COMBINATION THERAPY
Combination therapy with an acidsuppressing agent and a prokinetic agent or a mucosal protectant agent