BINAY PALAI-
BENGAL SCHOOL OF TECHNOLOGY
( A COLLEGE OF PHARMACY )
INTRODUCTION:-
Dyspepsia is a Greek word meaning ―duis‖ (bad or difficult) and ―peptin‖ (to digest). Dyspepsia also called Indigestion is a term that describes discomfort or pain in the upper abdomen that means stomach or chest . It is not a disease. In the majority of cases, indigestion is linked to eating or drinking. It can also be caused by infections or the use of certain medications (NSAIDs).
Patients and doctors interpret this in different ways. Many patients mean heartburn or acid regurgitation, the classic symptoms of gastro-oesophageal reflux disease. Some describe belching, abdominal rumblings, or even bad breath as indigestion. Others mean pain localised to the epigastrium or a non-painful discomfort in the upper abdomen which may be described as fullness, bloating, or an inability to finish a normal meal (early satiety)
Dyspepsia is a symptom and not a diagnosis. Symptoms may last for decades (even lifetime) and remissions and relapses are common. It is one of the commonest gastrointestinal malady affecting at least 25% of the population during a year. Its prevalence varies in different countries, depending upon the prevalence of Helicobacter pylori (H. pylori) infection, obesity, drug- alcohol- tobacco intake and spices in diet; furthermore, a significant and varying number of subjects do not seek medical treatment .
Dyspepsia is an umbrella term used to enclose a number of symptoms thought to originate from the upper gastrointestinal tract. These symptoms are relatively nonspecific; not surprisingly, therefore, a myriad of conditions may present with any one or a combination of these symptoms. Therein make the clinician’s first challenge: detecting the minority who may have a potentially life-threatening disorder, such as gastric cancer, from a population whose symptoms are, for the most part, considered functional in origin. The second challenge lies in the definition and management of those individuals with functional dyspepsia (FD); the major focus of this review. The Rome process has addressed the issue of FD definition and a look back at the evolution of Rome criteria for this dis- order illustrates the complexities that have so frustrated us. There has been no shortage of hypotheses to explain symptom pathogenesis in FD; initially focused on gastric sensorimotor dysfunction, these have now strayed well into the duodenum and have come to entertain such factors as immune responses and the microbes. Functional dyspepsia (FD) has proven to be an equally challenging area for therapeutics; while the staple approaches of acid suppression and eradication of Helicobacter pylori have some limited efficacy in select populations, strategies to ameliorate symptoms in the majority of sufferers based on presumed pathophysiology have largely foundered. Lacking a validated biomarker(s) FD continues to be an elusive target and is likely to remain so until we can better define the various phenotypes that it must surely contain.
Defining dyspepsia allows for more accurate study of the problem and the problem is considerable. Studies from the United States, Great Britain and other parts of the world have shown the prevalence of dyspepsia to be between 26% and 41% [4,5]. While only 20% to 25% of these individuals seek medical care, dyspepsia accounts for 2% to 5% of all consultations in primary care [6]. For gastroenterologists, dyspepsia accounts for between 20% and 40% of consultations [7]. It appears that as primary care physicians have grown more comfortable with proton pump inhibitors and Helicobacter pylori eradication, the percentage of attendees in gastroenterology clinics with functional dyspepsia is steadily increasing.
The burden of illness with respect to quality of life and economic consequences of dyspepsia is considerable. Recent data from a large cross sectional survey in the UK suggest dyspepsia may be costing society approximately £1 billion ($1.46 billion) annually [8]. Similar estimates exist for the costs of diagnosis and management of dyspepsia in the United States [9]. A Swedish study estimated direct costs of dyspepsia to be approximately £26 million annually for 8 million people [10]. When indirect costs were included, total costs increased almost 10-fold. This was largely attributable to the average of 26 more days of lost productivity by dyspeptics. Indirect health costs are parallelled by decreased quality of life, which can be profound.
CLASSIFICATION OF DYSPEPSIA:-
Mainly four types of Dyspepsia have been found, that may be classified as :
1. Organic dyspepsia:
oesophagitis, gastric erosions, acute or chronic gastritis, gastric ulcer, duodenal ulcer, duodenitis, malignancy (carcinoma, lymphoma).
Evidence of an organic disease is observed on upper gastrointestinal endoscopy (and gastric biopsy), or barium meal.
It is suspected in erosive presence of alarm symptoms (weight loss, anaemia, bleeding or occult blood positive, and loss of appetite) or symptoms occurring at night .
2. Functional or non-ulcer dyspepsia:
A patient with anxiety, worry over serious illness (cancer) and/or experiencing adverse events recently, is likely to suffer from dyspepsia.
No organic lesion is detected on investigations.
For patients unresponsive to acid suppressive therapy or H pylori eradication, mechanisms of symptom generation are largely speculative.
3. Drug related:-
aspirin, non-steroidal anti-inflammatory drugs (NSAID), antibiotics, bisphosphonates (alendronate), oestrogens, steroids, digoxin, chloroquine, potassium supplements, iron, etc.
Detailed history of drug intake (present and recent past) should be recorded and rechecked.
4. Extra intestinal systemic diseases such as diabetes mellitus, hypothyroid, hyperparathyroid, Addison’s disease, uraemia. Symptoms of endocrine diseases, are looked for after organic dyspepsia is excluded.
CAUSES :-
Indigestion is usually caused by the lifestyle of an individual and the foods they eat. It can also be related to an infection or other digestive conditions.
The symptoms are normally triggered by stomach acid coming into contact with the mucosa membrane result in break down the mucosa, causing irritation and inflammation. This triggers the uncomfortable symptoms of indigestion. Common causes of indigestion are include-
A. GASTRO-OESOFSGEAL REFLAX DISEASE(GERD) :-
It is very important and practical to distinguish gastro-oesophageal reflux disease (GORD or GERD) from dyspepsia. Frequent heartburn is a cardinal symptom of GORD; acid reflux causes a retrosternal or epigastric burning feeling that characteristically radiates up towards the throat, is relieved transiently by antacids, and is precipitated by taking food or by lying down.
Often 60% of people with upper gastrointestinal symptoms report both heartburn and epigastric pain or discomfort. This overlap can be confusing, but it is not the presence of a symptom but its predominance that is most helpful clinically. For example, if the main complaint is a burning epigastric pain that radiates up towards the throat then this is highly predictive of GERD (as can be objectively demonstrated by abnormal results from 24 hour oesophageal pH monitoring).
Reflux oesophagitis can be detected at endoscopy, but over half of patients with true GORD will not have evidence of mucosal breaks (erosions). Oesophageal erythema or the presence of a hiatal hernia are unreliable signs that cannot be used to determine if a patient has reflux disease. Although some patients are unable to adequately describe their symptoms or decide which is their predominant complaint, if a detailed history is taken a clinical diagnosis of GORD can be made in most cases, including those in whom endoscopy is normal.
Uncommon causes of upper abdominal pain or discomfort that may be confused with dyspepsia
Aerophagy (repetitive belching from air swallowing).
Biliary colic from gall stone.
Abdominal wall pain.
Chronic pancreatitis (episodic dull steady upper abdominal pain that may be aggravated by meals and radiate through to the back).
Malignancy (such as of pancreas or colon).
Mesenteric vascular insufficiency (postprandial pain, weight loss, and a fear of eating).
Metabolic disease (such as-diabetes, renal failure, hypercalcaemia).
Angina
Conditions to be recognised from a patient's history
Symptomatic gastro-oesophageal reflux disease
Burning retrosternal or epigastric pain or discomfort radiating upwards towards the throat and relieved, albeit transiently, by antacids
Regurgitation of acid
Irritable bowel syndrome
Abdominal pain plus an erratic disturbance of defecation linked to the pain (such as pain relief with defecation, looser or harder stools with pain onset, or more frequent or less frequent stools with pain onset)
Biliary tract disease
Biliary-type pain
Peptic ulcer Classic ulcer symptoms do not distinguish peptic ulcer disease from functional dyspepsia .
B. GALL STONE :-
Ultrasonography will detect gall stones in a minority of patients with apparently unexplained dyspepsia. However, gall stones are common and often incidental in the absence of biliary symptoms. Biliary colic is characteristically severe, episodic, and constant (rather than colicky) pain in the epigastrium or right upper quadrant typically lasting one to several hours [15]. This can usually be easily distinguished from the pain or discomfort of functional dyspepsia.
While many patients with gall stones also complain of bloating, nausea, and other vague upper abdominal symptoms. These complaints are just common in patients without gall stones. Moreover, cholecystectomy does not reliably result in long term relief of any of these vague complaints and cannot be recommended. Cholecystectomy in a patient with non-biliary type pain is likely to result in the patient at a later date being labelled as having the postcholecystectomy syndrome.
C. PEPTIC ULCER :-
Many textbooks continue to propagate the myth that symptoms can accurately identify peptic ulcer disease. Unfortunately, classic ulcer symptoms (such as postprandial epigastric pain or night pain) often occur in patients with functional dyspepsia, and many patients with an ulcer have curious complaints.
Endoscopy remains the test of choice to chronic peptic ulceration, but its presence can now be deduced by indirect testing. Helicobacter pylori causes 90% of duodenal ulcers and 70% of gastric ulcers; aspirin and non-steroidal anti-inflammatory drugs (NSAIDs) account for most of the remainder. Patients who are not infected with H. pylori and not taking NSAIDs have very low probability of ulcer disease .
D. GASTRIC CANCER:-
Fear of gastric cancer is one of the main reasons why patients with dyspepsia present to their general practitioner. Gastric cancer is found in less than 2% of all cases referred for endoscopy. Early gastric cancer comprises only 10% of cancer cases, but it is important to diagnose because it is curable and 60-90% of patients initially present with dyspepsia.
Alarm symtoms:-
Anaemia due to iron deficiency
Anorexia Loss of weight
Recent onset of persistent symptoms
Melaena,
haematemesis
Dysphagia.
However, the risk of gastric cancer is extremely low in patients under the age of 55 years presenting with the new onset of dyspepsia in most Western countries including Britain. Furthermore, ―alarm‖ symptoms such as weight loss, dysphagia, or anaemia help to identify those who need to be investigated in order to exclude malignancy, although between 15% and 50% of dyspeptic patients with gastric cancer do not have these symptoms. Endoscopic evaluation is therefore recommended in older patients presenting with new symptoms and in all patients with alarm symptoms [14,16].
E. eating too much or too rapidly
F. eating fatty, greasy, or spicy foods
G. drinking too much caffeine or alcohol
H. consuming too much chocolate or soda
I. emotional trauma
J. infection, especially with a bacteria called Helicobacter pylori (H. pylori)
K. nervousness
L. obesity
M. pancreatitis, or inflammation of the pancreas
N. smoking
O. Certain medications, such as antibiotics and non-steroidal anti-inflammatory drugs (NSAIDs) etc
SYMPTOMS :-
Symptoms of dyspepsia are divided into reflux-type (retrosternal burning, regurgitation), ulcertype (epigastric pain on empty stomach relieved with bland food, antacids or acid suppression drugs), dysmotility-type (postprandial fullness, distension, early satiety, nausea). Rome II criteria excluded symptoms of reflux-type, irritable bowel syndrome (pain relieved with defecation, with diarrhoea or constipation) and hepatobiliary diseases (biliary dyskinesia); chronicity of symptoms for 12 weeks at least (not continuous) during 12 months was emphasised. Rome III criteria divided functional dyspepsia in 2 groups : (i) predominant epigastric pain or burning (the epigastric pain syndrome) and (ii) early satiety or fullness following a meal (the postprandial distress syndrome).
Rome I, Rome II, Rome III criteria described by renowned gastroenterologists indicate that dyspepsia (difficult to digest) is in fact difficult to define. Are ―Rome IV‖ criteria required, to exclude chronic gastritis (gastric biopsy), giardia lamblia (duodenal fluid or biopsy), lactase deficiency (milk intolerance history)?
The following symptoms of dyspepsia are also common
Nausea
belching
pain
a feeling of fullness, or satiety
feeling bloated
In very rare cases, indigestion may be a symptom of stomach cancer.
Mild dyspepsia rarely needs further investigation, and should not be a cause for concern. A visit to a doctor is only needed if symptoms continue for more than 2 weeks.
Seek emergency treatment if the pain is severe and any of the following also occurs:
loss of appetite or weight loss
vomiting
inability to swallow
black stools
yellow coloring in the eyes and skin
chest pain during exertion
shortness of breath
sweating
chest pain that spreads to the jaw, arm, or neck
Heartburn and dyspepsia are often confused for one another, but they are two separate conditions despite regularly occurring at the same time. Heartburn is a symptom of acid reflux, described as a burning feeling behind the breastbone that usually occurs after eating [18].
DYSPEPSIA DIET:-
A high fiber diet is a good way to manage digestive health. It has the effect of clearing out the intestine and making digestion a smoother, cleaner process.
Fruits, nuts, legumes, and wholegrain foods are packed with fiber and an excellent choice for protecting against indigestion. Many yogurts and cereals have also been fortified with fiber.
Eating a balanced diet that excludes spicy or greasy foods is key. Be sure to consume fluids with every meal, as this helps to move food through the digestive tract.
Consuming four or five smaller meals in a day as opposed to three larger ones can also help the digestive system.
DIAGNOSIS:-
Dyspepsia is mild and infrequent for most people with symptoms. In such cases, no treatment is needed. People who experience regular indigestion or severe abdominal pain should see a primary care physician.
A doctor will ask the person experiencing dyspepsia about their symptoms. They will also find out about their medical and family histories and examine the chest and stomach. This may involve pressing down on different areas of the abdomen to find out whether any are sensitive, tender, or painful under pressure.
If the doctor suspects an underlying cause, they can use the following diagnostic tests to identify any underlying health problems:----
a. Blood test:
If the person with indigestion also has any symptoms of anemia, the doctor may order a blood test.
b. Endoscopy:
People who have not responded to previous treatment for dyspepsia may be referred for a more detailed examination of the upper gastrointestinal (GI) tract. A long thin tube with a camera at the end is inserted through the mouth and into the stomach. This produces clear images of the mucosa. The doctor can also perform a biopsy during this procedure to test for cancer.
Tests to diagnose H. pylori infection: These may include a urea breath test, a stool antigen test, and a blood test. An endoscopy would also identify H. pylori as well as any peptic ulcers that are present. Peptic ulcers are often caused by H. pylori.
c. Liver function test:
If the doctor suspects a problem with the bile ducts in the liver, they may request a blood test to assess how the liver is working.
d. X-rays:
X-ray images are taken of the esophagus, stomach, and small intestine.
e. Abdominal ultrasound:
High-frequency sound waves make images showing movement, structure, and blood flow in the abdomen. A gel is applied to the abdomen and a hand-held device pressed against the skin. The device gives off sound waves, and the doctor can see a detailed picture of the inside of the abdomen on a monitor.
f. Abdominal CT scan:
This may involve injecting a dye into the veins. The dye shows up on the monitor. The CT scan takes a series of X-ray images to produce a 3D image of the inside of the abdomen.
TREATMENT:-
Treatment for indigestion depends on the cause and severity of symptoms. If symptoms are mild and infrequent, lifestyle changes will probably ease them. This usually involves consuming fewer fatty and spicy foods and less caffeine, alcohol, and chocolate. Sleeping for at least 7 hours every night may also help to ease mild indigestion [23].
Exercising regularly and quitting smoking are also important lifestyle changes in treating indigestion. Some medication are used to treat dyspepsia, such as----
Digestants:-
These arc substances intended to promote digestion of food. A number of proteolytic, amylolytic and lipolytic are marketed in combination formulations. They are occasionally beneficial, only when their elaboration in g.i.t. s deficient.
Hydrochloric acid :-
It may be used in achlorhydria; 5-10 ml of dilute HCl (10%) should be further diluted to 100-200 ml with water and sipped with a straw (to prevent contact with teeth) during meals.
Pepsin :-
It may be used along with HCl in gastric achylia due to atrophic gastritis, gastric carcinoma, pernicious anaemia, etc.
Papain :-
It is proteolytic enzyme obtained from raw papaya. Its efficacy after oral ingestion is doubtful.
Pancreatin :-
It is mixture of pancreatic enzymes obtained from hog and pig pancreas. It contains amylase, trypsin and lipase and indicated in chronic pancreatitis and other exocrine pancreatic deficiency states. Fat and nitrogen content of stools may be reduced and diarrhoea may be prevented. It has to be used as enteric coated tablets or capsules to protect the enzymes from being themselves digested in stomach by pepsin. Nausea, diarrhoea are the occasional side effects
Methyl polysiloxane (Dimethyl polysiloxane, Simethicone, Dimethicone) It is a silicone polymer, a viscous amphiphilic liquid-reduces surface tension and collapses froth, 'antifoaming agent'. It is not absorbed from g.i.t. and is pharmacologically inert. Added to antacid, digestant and antireflux preparations (see above), it is claimed to relieve flatulence, to coat and protect ulcer surface, to aid dispersion of antacids in gastric contents, and to prevent gastroesophageal reflux. However, clinical efficacy is equivocal.
Dose: 40-120 mg 3 to 4 times a day.
GALLSTONE
1. Regulation of gastric acid secretion:-
Gastric acid secretion by parietal cells of the gastric mucosa is stimulated by acetylcholine, histamine, and gastrin. The receptor-mediated binding of acetylcholine, histamine, or gastrin results in the activation of protein kinases, which in turn stimulates the H+/K+ ―adenosine triphosphatase (ATPase) proton pump to secrete hydrogen ions in exchange for K+ into the lumen of the stomach. A Cl- channel couples chloride efflux to the release of H+. In contrast, receptor binding of prostaglandin E2 and somatostatin diminish gastric acid production. [Note: Histamine binding causes activation of adenylyl cyclase, whereas binding of prostaglandin E2 inhibits this enzyme. Gastrin and acetylcholine act by inducing an increase in intracellular calcium levels.]
2. Antacid:-
These counter the effects of stomach acid. These are over-the-counter (OTC) medicines that do not need a prescription. A doctor will usually recommend an antacid medication as one of the first treatments for dyspepsia [23].
Antacid are weak bases that react with gastric acid to form water and salt to diminish gastric acidity. Because pepsin (a proteolytic enzyme) is inactive at a pH greater than 4, antacid also reduce pepsin activity.
Example:-Aluminum hydroxide and magnecium hydroxide and calcium carbonate etc.
Chemistry:-
Antacid products vary widely in their composition, acid neutralizing capacity, sodium content, palatability and price. The efficacy of an antacid depends on its capacity to neutralize gastric HCl and on whether the stomach is full or empty (food delay stomach emptying allowing more time for antacid to react). Commonly used antacids are combination of salt of aluminium, magnesium, such as aluminium hydroxide, magnesium hydroxide. Calcium carbonate reacts with HCl to form carbondioxide (Co2) and calcium chloride.
Therapeutic uses:-
Antacid are used for symptomatic relief of peptic ulcer disease and GERD, they may also promote healing of duodenal ulcers. They should be administered after meal for maximum effectiveness.
3. H2 receptor antagonist:-
These reduce stomach acid levels and last longer than antacids. However, antacids act more quickly. Gastric acid secretion is stimulated by acetylcholine, histamine and gastrin. The receptor mediated binding of acetylcholine, gastrin, histamine result in activation of protein kinases, which in turn stimulates the H+/K+ adenosine triphosphatease (ATPase) proton pump to secrete hydrogen ions in exchange for K+ into the lumen of the stomach. A Cl- channel couples chloride efflux to the release of H+. In contrast, receptor binding of prostaglandin E2 and somatostatin diminish gastric acid production. [Note: Histamine binding causes activation of adenylyl cyclase, whereas binding of prostaglandin E2 inhibits this enzyme. Gastrin and acetylcholine act by inducing an increase in intracellular calcium levels.]
Example: Ranitidine, Famotidine, cimetidine, Nizatidine are used to peptic ulcer, Acute tress ulcer and GERD etc. Some people may experience nausea, vomiting, constipation, diarrhoea, and headaches after taking these. Other side effects may include bruising or bleeding .
Ranitidine:-
Ranitidine belongs to a group of drugs called histamine-2 blockers. It works by reducing the amount of acid your stomach produces. Ranitidine also treats gastroesophageal reflux disease (GERD) and other conditions in which acid backs up from the stomach into the esophagus, causing heartburn.
Use -
It is used to treat ulcers of the stomach and intestines and prevent them from coming back after they have healed.
This medication is also used to treat certain stomach and throat (esophagus) problems (such as erosive esophagitis, gastroesophageal reflux disease-GERD, Zollinger-Ellison syndrome).
Relief of heartburn
Ranitidine can also be given with nonsteroidal anti-inflammatory drugs (NSAIDs) to reduce the risk of ulceration
Side effect :-
A very serious allergic reaction to this drug is rare, such as swelling (especially of the face/tongue/throat), severe dizziness, trouble breathing and rash.
Head ach, constipation etc.
Dose :-
For ulcer healing 300 mg at bed time or 150 mg BD; for maintenance 150 mg at bed time. Parenteral dose—50 mg i.m. or slow i.v. inj. every 6–8 hrs (rapid i.v. injection can cause hypotension), 0.1–0.25 mg/kg/hr by i.v. infusion has been used for prophylaxis of stress ulcers. For gastrinom300 mg 3–4 times a day.
4. Proton pump inhibitors:-
The PPIs bind to the H+ /K+ ATPase enzyme system with suppress the secretion of h+ ions from gastric lumen. The available PPIs is includes esomeprazole, omeprazole, pantoprazole, rabeprazole, lansoprazole etc. Omeprazole, lansoprazole, esomeprazole are available over the counter foe sort term treatment of GERD.
Actions:-
These agents are prodrugs with acid resistant enteric coating which help to protect them from premature degradation by gastric acid. This coating is remove in alkaline duodenum and absorbed base and transported to the parietal cell. There, it is converted to the active drug with form a covalent bond with h+/k+ ATPase enzyme.
Therapeutic uses:-
The PPIs is the superior to the h2 antagonist in suppressing acid production with healing ulcer. Thus they are preferred drug for stress ulcer treatment and for the treatment of GERD, erosive esophagitis, active duodenum ulcer. If an H2 receptor antagonist is needed, it should be taken after taking PPI. PPI also reduce the bleeding from ulcer located place, caused by aspirin and NSAID drug.
Omeprazole :-
Omeprazole It is the prototype member of substituted benzimidazoles which inhibit the final common step in gastric acid secretion. The only significant pharmacological action of omeprazole is dose dependent suppression of gastric acid secretion; without anticholinergic or H2 blocking action. It is a powerful inhibitor of gastric acid: can totally abolish HCl secretion, both resting as well as that stimulated by food or any of the secretagogues, without much effect on pepsin, intrinsic factor, juice volume and gastric motility.
MOA:-
Omeprazole is inactive at neutral pH, but at pH < 5 it rearranges to two charged cationic forms (a sulphenic acid and a sulphenamide configurations) that react covalently with SH groups
of the H+K+ATPase enzyme and inactivate it irreversibly, especially when two molecules of omeprazole react with one molecule of the enzyme. After absorption into bloodstream and subsequent diffusion into the parietal cell, it gets concentrated in the acidic pH of the canaliculi because the charged forms generated there are unable to diffuse back. Moreover, it gets tightly bound to the enzyme by covalent bonds. These features and the specific localization of H+K+ATPase to the apical membrane of the parietal cells confer high degree of selectivity of action to omeprazole. Acid secretion resumes only when new H+K+ATPase molecules are synthesized (reactivation half time 18 hours). It also inhibits gastric mucosal carbonic anhydrase.
Pharmacokinetics :-
The e.c. tablet or granules filled in capsules should not be broken or crushed before swallowing. Oral bioavailability of omeprazole is ~50% due to acid lability. Bioavailability of all PPIs is reduced by food; they should be taken in empty stomach, followed 1 hour later by a meal to activate the H+K+ ATPase and make it more susceptible to the PPI. Omeprazole is highly plasma protein bound, rapidly metabolised in liver by CYP2C19 and CYP3A4 (plasma t½ ~1 hr). The metabolites are excreted in urine. As such, inhibition of HCl secretion occurs within 1 hr, reaches maximum at 2 hr, is still half maximal at 24 hr and lasts for 2–3 days.
Use-
Peptic ulcer: Omeprazole 20 mg OD is equally or more effective than H2 blockers. Relief of pain is rapid and excellent. Faster healing has been demonstrated with 40 mg/day:
Gastroesophageal reflux disease (GERD): Omeprazole produces more complete round-the-clock inhibition of gastric acid resulting in rapid symptom relief and is more effective than H2 blockers in promoting healing of esophageal lesions. Higher doses than for peptic ulcer or twice daily administration is generally needed.
Aspiration pneumonia: PPIs are an alternative to H2 blockers for prophylaxis of aspiration pneumonia due to prolonged anaesthesia.
Adverse effect:-
PPIs produce minimal adverse effects. Nausea, loose stools, headache, abdominal pain, muscle and joint pain, dizziness are complained by 3–5%. Rashes (1.5% incidence), leucopenia and hepatic dysfunction are infrequent. On prolonged treatment atrophic gastritis has been reported occasionally. No harmful effects of PPIs during pregnancy are known. Though manufacturers advise to avoid, PPIs have often been used for GERD during pregnancy [26].
5. Prokinetics:-
This medication is helpful for stomach that empty slowly. One example of a prokinetic drug is Reglan, propulsid. The Side effects of this drug are include tiredness, depression, sleepiness, anxiety, and muscle spasms.
6. Antibiotics:-
If H. pylori is causing peptic ulcers, result in indigestion, for that an antibiotic will be prescribed. Side effects may include an upset stomach, looseness, and fungal infections.
7. Antidepressants:-
If the doctor finds no causes for indigestion after investigation on patient, and the person with dyspepsia has not responded to treatments, the doctor may prescribe low-dose antidepressants.
Antidepressants sometimes ease discomfort by reducing the sensation of pain. Side effects may include nausea, headaches, agitation, constipation, and night sweats etc.
8. Psychological therapy: -
For people with functional dyspepsia, psychological therapy can help manage the cognitive aspects of indigestion. Cognitive behavioral therapy, hypnotherapy, and relaxation therapy may be recommended.
The doctor may also recommend making changes to a person's current medication schedule if they suspect that it could be causing indigestion. A course of aspirin or ibuprofen may sometimes be stopped and alternative medications advised. It is important to change medications only under the supervision of a doctor.
BENGAL SCHOOL OF TECHNOLOGY
( A COLLEGE OF PHARMACY )
INTRODUCTION:-
Dyspepsia is a Greek word meaning ―duis‖ (bad or difficult) and ―peptin‖ (to digest). Dyspepsia also called Indigestion is a term that describes discomfort or pain in the upper abdomen that means stomach or chest . It is not a disease. In the majority of cases, indigestion is linked to eating or drinking. It can also be caused by infections or the use of certain medications (NSAIDs).
Patients and doctors interpret this in different ways. Many patients mean heartburn or acid regurgitation, the classic symptoms of gastro-oesophageal reflux disease. Some describe belching, abdominal rumblings, or even bad breath as indigestion. Others mean pain localised to the epigastrium or a non-painful discomfort in the upper abdomen which may be described as fullness, bloating, or an inability to finish a normal meal (early satiety)
Dyspepsia is an umbrella term used to enclose a number of symptoms thought to originate from the upper gastrointestinal tract. These symptoms are relatively nonspecific; not surprisingly, therefore, a myriad of conditions may present with any one or a combination of these symptoms. Therein make the clinician’s first challenge: detecting the minority who may have a potentially life-threatening disorder, such as gastric cancer, from a population whose symptoms are, for the most part, considered functional in origin. The second challenge lies in the definition and management of those individuals with functional dyspepsia (FD); the major focus of this review. The Rome process has addressed the issue of FD definition and a look back at the evolution of Rome criteria for this dis- order illustrates the complexities that have so frustrated us. There has been no shortage of hypotheses to explain symptom pathogenesis in FD; initially focused on gastric sensorimotor dysfunction, these have now strayed well into the duodenum and have come to entertain such factors as immune responses and the microbes. Functional dyspepsia (FD) has proven to be an equally challenging area for therapeutics; while the staple approaches of acid suppression and eradication of Helicobacter pylori have some limited efficacy in select populations, strategies to ameliorate symptoms in the majority of sufferers based on presumed pathophysiology have largely foundered. Lacking a validated biomarker(s) FD continues to be an elusive target and is likely to remain so until we can better define the various phenotypes that it must surely contain.
Defining dyspepsia allows for more accurate study of the problem and the problem is considerable. Studies from the United States, Great Britain and other parts of the world have shown the prevalence of dyspepsia to be between 26% and 41% [4,5]. While only 20% to 25% of these individuals seek medical care, dyspepsia accounts for 2% to 5% of all consultations in primary care [6]. For gastroenterologists, dyspepsia accounts for between 20% and 40% of consultations [7]. It appears that as primary care physicians have grown more comfortable with proton pump inhibitors and Helicobacter pylori eradication, the percentage of attendees in gastroenterology clinics with functional dyspepsia is steadily increasing.
The burden of illness with respect to quality of life and economic consequences of dyspepsia is considerable. Recent data from a large cross sectional survey in the UK suggest dyspepsia may be costing society approximately £1 billion ($1.46 billion) annually [8]. Similar estimates exist for the costs of diagnosis and management of dyspepsia in the United States [9]. A Swedish study estimated direct costs of dyspepsia to be approximately £26 million annually for 8 million people [10]. When indirect costs were included, total costs increased almost 10-fold. This was largely attributable to the average of 26 more days of lost productivity by dyspeptics. Indirect health costs are parallelled by decreased quality of life, which can be profound.
CLASSIFICATION OF DYSPEPSIA:-
Mainly four types of Dyspepsia have been found, that may be classified as :
1. Organic dyspepsia:
oesophagitis, gastric erosions, acute or chronic gastritis, gastric ulcer, duodenal ulcer, duodenitis, malignancy (carcinoma, lymphoma).
Evidence of an organic disease is observed on upper gastrointestinal endoscopy (and gastric biopsy), or barium meal.
It is suspected in erosive presence of alarm symptoms (weight loss, anaemia, bleeding or occult blood positive, and loss of appetite) or symptoms occurring at night .
2. Functional or non-ulcer dyspepsia:
A patient with anxiety, worry over serious illness (cancer) and/or experiencing adverse events recently, is likely to suffer from dyspepsia.
No organic lesion is detected on investigations.
For patients unresponsive to acid suppressive therapy or H pylori eradication, mechanisms of symptom generation are largely speculative.
3. Drug related:-
aspirin, non-steroidal anti-inflammatory drugs (NSAID), antibiotics, bisphosphonates (alendronate), oestrogens, steroids, digoxin, chloroquine, potassium supplements, iron, etc.
Detailed history of drug intake (present and recent past) should be recorded and rechecked.
4. Extra intestinal systemic diseases such as diabetes mellitus, hypothyroid, hyperparathyroid, Addison’s disease, uraemia. Symptoms of endocrine diseases, are looked for after organic dyspepsia is excluded.
CAUSES :-
Indigestion is usually caused by the lifestyle of an individual and the foods they eat. It can also be related to an infection or other digestive conditions.
The symptoms are normally triggered by stomach acid coming into contact with the mucosa membrane result in break down the mucosa, causing irritation and inflammation. This triggers the uncomfortable symptoms of indigestion. Common causes of indigestion are include-
A. GASTRO-OESOFSGEAL REFLAX DISEASE(GERD) :-
It is very important and practical to distinguish gastro-oesophageal reflux disease (GORD or GERD) from dyspepsia. Frequent heartburn is a cardinal symptom of GORD; acid reflux causes a retrosternal or epigastric burning feeling that characteristically radiates up towards the throat, is relieved transiently by antacids, and is precipitated by taking food or by lying down.
Reflux oesophagitis can be detected at endoscopy, but over half of patients with true GORD will not have evidence of mucosal breaks (erosions). Oesophageal erythema or the presence of a hiatal hernia are unreliable signs that cannot be used to determine if a patient has reflux disease. Although some patients are unable to adequately describe their symptoms or decide which is their predominant complaint, if a detailed history is taken a clinical diagnosis of GORD can be made in most cases, including those in whom endoscopy is normal.
Uncommon causes of upper abdominal pain or discomfort that may be confused with dyspepsia
Aerophagy (repetitive belching from air swallowing).
Biliary colic from gall stone.
Abdominal wall pain.
Chronic pancreatitis (episodic dull steady upper abdominal pain that may be aggravated by meals and radiate through to the back).
Malignancy (such as of pancreas or colon).
Mesenteric vascular insufficiency (postprandial pain, weight loss, and a fear of eating).
Metabolic disease (such as-diabetes, renal failure, hypercalcaemia).
Angina
Conditions to be recognised from a patient's history
Symptomatic gastro-oesophageal reflux disease
Burning retrosternal or epigastric pain or discomfort radiating upwards towards the throat and relieved, albeit transiently, by antacids
Regurgitation of acid
Irritable bowel syndrome
Abdominal pain plus an erratic disturbance of defecation linked to the pain (such as pain relief with defecation, looser or harder stools with pain onset, or more frequent or less frequent stools with pain onset)
Biliary tract disease
Biliary-type pain
Peptic ulcer Classic ulcer symptoms do not distinguish peptic ulcer disease from functional dyspepsia .
B. GALL STONE :-
Ultrasonography will detect gall stones in a minority of patients with apparently unexplained dyspepsia. However, gall stones are common and often incidental in the absence of biliary symptoms. Biliary colic is characteristically severe, episodic, and constant (rather than colicky) pain in the epigastrium or right upper quadrant typically lasting one to several hours [15]. This can usually be easily distinguished from the pain or discomfort of functional dyspepsia.
While many patients with gall stones also complain of bloating, nausea, and other vague upper abdominal symptoms. These complaints are just common in patients without gall stones. Moreover, cholecystectomy does not reliably result in long term relief of any of these vague complaints and cannot be recommended. Cholecystectomy in a patient with non-biliary type pain is likely to result in the patient at a later date being labelled as having the postcholecystectomy syndrome.
C. PEPTIC ULCER :-
Many textbooks continue to propagate the myth that symptoms can accurately identify peptic ulcer disease. Unfortunately, classic ulcer symptoms (such as postprandial epigastric pain or night pain) often occur in patients with functional dyspepsia, and many patients with an ulcer have curious complaints.
Endoscopy remains the test of choice to chronic peptic ulceration, but its presence can now be deduced by indirect testing. Helicobacter pylori causes 90% of duodenal ulcers and 70% of gastric ulcers; aspirin and non-steroidal anti-inflammatory drugs (NSAIDs) account for most of the remainder. Patients who are not infected with H. pylori and not taking NSAIDs have very low probability of ulcer disease .
Fear of gastric cancer is one of the main reasons why patients with dyspepsia present to their general practitioner. Gastric cancer is found in less than 2% of all cases referred for endoscopy. Early gastric cancer comprises only 10% of cancer cases, but it is important to diagnose because it is curable and 60-90% of patients initially present with dyspepsia.
Alarm symtoms:-
Anaemia due to iron deficiency
Anorexia Loss of weight
Recent onset of persistent symptoms
Melaena,
haematemesis
Dysphagia.
However, the risk of gastric cancer is extremely low in patients under the age of 55 years presenting with the new onset of dyspepsia in most Western countries including Britain. Furthermore, ―alarm‖ symptoms such as weight loss, dysphagia, or anaemia help to identify those who need to be investigated in order to exclude malignancy, although between 15% and 50% of dyspeptic patients with gastric cancer do not have these symptoms. Endoscopic evaluation is therefore recommended in older patients presenting with new symptoms and in all patients with alarm symptoms [14,16].
E. eating too much or too rapidly
F. eating fatty, greasy, or spicy foods
G. drinking too much caffeine or alcohol
H. consuming too much chocolate or soda
I. emotional trauma
J. infection, especially with a bacteria called Helicobacter pylori (H. pylori)
K. nervousness
L. obesity
M. pancreatitis, or inflammation of the pancreas
N. smoking
O. Certain medications, such as antibiotics and non-steroidal anti-inflammatory drugs (NSAIDs) etc
SYMPTOMS :-
Symptoms of dyspepsia are divided into reflux-type (retrosternal burning, regurgitation), ulcertype (epigastric pain on empty stomach relieved with bland food, antacids or acid suppression drugs), dysmotility-type (postprandial fullness, distension, early satiety, nausea). Rome II criteria excluded symptoms of reflux-type, irritable bowel syndrome (pain relieved with defecation, with diarrhoea or constipation) and hepatobiliary diseases (biliary dyskinesia); chronicity of symptoms for 12 weeks at least (not continuous) during 12 months was emphasised. Rome III criteria divided functional dyspepsia in 2 groups : (i) predominant epigastric pain or burning (the epigastric pain syndrome) and (ii) early satiety or fullness following a meal (the postprandial distress syndrome).
Rome I, Rome II, Rome III criteria described by renowned gastroenterologists indicate that dyspepsia (difficult to digest) is in fact difficult to define. Are ―Rome IV‖ criteria required, to exclude chronic gastritis (gastric biopsy), giardia lamblia (duodenal fluid or biopsy), lactase deficiency (milk intolerance history)?
The following symptoms of dyspepsia are also common
Nausea
belching
pain
a feeling of fullness, or satiety
feeling bloated
In very rare cases, indigestion may be a symptom of stomach cancer.
Mild dyspepsia rarely needs further investigation, and should not be a cause for concern. A visit to a doctor is only needed if symptoms continue for more than 2 weeks.
Seek emergency treatment if the pain is severe and any of the following also occurs:
loss of appetite or weight loss
vomiting
inability to swallow
black stools
yellow coloring in the eyes and skin
chest pain during exertion
shortness of breath
sweating
chest pain that spreads to the jaw, arm, or neck
Heartburn and dyspepsia are often confused for one another, but they are two separate conditions despite regularly occurring at the same time. Heartburn is a symptom of acid reflux, described as a burning feeling behind the breastbone that usually occurs after eating [18].
DYSPEPSIA DIET:-
A high fiber diet is a good way to manage digestive health. It has the effect of clearing out the intestine and making digestion a smoother, cleaner process.
Fruits, nuts, legumes, and wholegrain foods are packed with fiber and an excellent choice for protecting against indigestion. Many yogurts and cereals have also been fortified with fiber.
Eating a balanced diet that excludes spicy or greasy foods is key. Be sure to consume fluids with every meal, as this helps to move food through the digestive tract.
Consuming four or five smaller meals in a day as opposed to three larger ones can also help the digestive system.
DIAGNOSIS:-
Dyspepsia is mild and infrequent for most people with symptoms. In such cases, no treatment is needed. People who experience regular indigestion or severe abdominal pain should see a primary care physician.
A doctor will ask the person experiencing dyspepsia about their symptoms. They will also find out about their medical and family histories and examine the chest and stomach. This may involve pressing down on different areas of the abdomen to find out whether any are sensitive, tender, or painful under pressure.
If the doctor suspects an underlying cause, they can use the following diagnostic tests to identify any underlying health problems:----
a. Blood test:
If the person with indigestion also has any symptoms of anemia, the doctor may order a blood test.
b. Endoscopy:
People who have not responded to previous treatment for dyspepsia may be referred for a more detailed examination of the upper gastrointestinal (GI) tract. A long thin tube with a camera at the end is inserted through the mouth and into the stomach. This produces clear images of the mucosa. The doctor can also perform a biopsy during this procedure to test for cancer.
Tests to diagnose H. pylori infection: These may include a urea breath test, a stool antigen test, and a blood test. An endoscopy would also identify H. pylori as well as any peptic ulcers that are present. Peptic ulcers are often caused by H. pylori.
c. Liver function test:
If the doctor suspects a problem with the bile ducts in the liver, they may request a blood test to assess how the liver is working.
d. X-rays:
X-ray images are taken of the esophagus, stomach, and small intestine.
e. Abdominal ultrasound:
High-frequency sound waves make images showing movement, structure, and blood flow in the abdomen. A gel is applied to the abdomen and a hand-held device pressed against the skin. The device gives off sound waves, and the doctor can see a detailed picture of the inside of the abdomen on a monitor.
f. Abdominal CT scan:
This may involve injecting a dye into the veins. The dye shows up on the monitor. The CT scan takes a series of X-ray images to produce a 3D image of the inside of the abdomen.
TREATMENT:-
Treatment for indigestion depends on the cause and severity of symptoms. If symptoms are mild and infrequent, lifestyle changes will probably ease them. This usually involves consuming fewer fatty and spicy foods and less caffeine, alcohol, and chocolate. Sleeping for at least 7 hours every night may also help to ease mild indigestion [23].
Exercising regularly and quitting smoking are also important lifestyle changes in treating indigestion. Some medication are used to treat dyspepsia, such as----
Digestants:-
These arc substances intended to promote digestion of food. A number of proteolytic, amylolytic and lipolytic are marketed in combination formulations. They are occasionally beneficial, only when their elaboration in g.i.t. s deficient.
Hydrochloric acid :-
It may be used in achlorhydria; 5-10 ml of dilute HCl (10%) should be further diluted to 100-200 ml with water and sipped with a straw (to prevent contact with teeth) during meals.
Pepsin :-
It may be used along with HCl in gastric achylia due to atrophic gastritis, gastric carcinoma, pernicious anaemia, etc.
Papain :-
It is proteolytic enzyme obtained from raw papaya. Its efficacy after oral ingestion is doubtful.
Pancreatin :-
It is mixture of pancreatic enzymes obtained from hog and pig pancreas. It contains amylase, trypsin and lipase and indicated in chronic pancreatitis and other exocrine pancreatic deficiency states. Fat and nitrogen content of stools may be reduced and diarrhoea may be prevented. It has to be used as enteric coated tablets or capsules to protect the enzymes from being themselves digested in stomach by pepsin. Nausea, diarrhoea are the occasional side effects
Methyl polysiloxane (Dimethyl polysiloxane, Simethicone, Dimethicone) It is a silicone polymer, a viscous amphiphilic liquid-reduces surface tension and collapses froth, 'antifoaming agent'. It is not absorbed from g.i.t. and is pharmacologically inert. Added to antacid, digestant and antireflux preparations (see above), it is claimed to relieve flatulence, to coat and protect ulcer surface, to aid dispersion of antacids in gastric contents, and to prevent gastroesophageal reflux. However, clinical efficacy is equivocal.
Dose: 40-120 mg 3 to 4 times a day.
GALLSTONE
1. Regulation of gastric acid secretion:-
Gastric acid secretion by parietal cells of the gastric mucosa is stimulated by acetylcholine, histamine, and gastrin. The receptor-mediated binding of acetylcholine, histamine, or gastrin results in the activation of protein kinases, which in turn stimulates the H+/K+ ―adenosine triphosphatase (ATPase) proton pump to secrete hydrogen ions in exchange for K+ into the lumen of the stomach. A Cl- channel couples chloride efflux to the release of H+. In contrast, receptor binding of prostaglandin E2 and somatostatin diminish gastric acid production. [Note: Histamine binding causes activation of adenylyl cyclase, whereas binding of prostaglandin E2 inhibits this enzyme. Gastrin and acetylcholine act by inducing an increase in intracellular calcium levels.]
2. Antacid:-
These counter the effects of stomach acid. These are over-the-counter (OTC) medicines that do not need a prescription. A doctor will usually recommend an antacid medication as one of the first treatments for dyspepsia [23].
Antacid are weak bases that react with gastric acid to form water and salt to diminish gastric acidity. Because pepsin (a proteolytic enzyme) is inactive at a pH greater than 4, antacid also reduce pepsin activity.
Example:-Aluminum hydroxide and magnecium hydroxide and calcium carbonate etc.
Chemistry:-
Antacid products vary widely in their composition, acid neutralizing capacity, sodium content, palatability and price. The efficacy of an antacid depends on its capacity to neutralize gastric HCl and on whether the stomach is full or empty (food delay stomach emptying allowing more time for antacid to react). Commonly used antacids are combination of salt of aluminium, magnesium, such as aluminium hydroxide, magnesium hydroxide. Calcium carbonate reacts with HCl to form carbondioxide (Co2) and calcium chloride.
Therapeutic uses:-
Antacid are used for symptomatic relief of peptic ulcer disease and GERD, they may also promote healing of duodenal ulcers. They should be administered after meal for maximum effectiveness.
3. H2 receptor antagonist:-
These reduce stomach acid levels and last longer than antacids. However, antacids act more quickly. Gastric acid secretion is stimulated by acetylcholine, histamine and gastrin. The receptor mediated binding of acetylcholine, gastrin, histamine result in activation of protein kinases, which in turn stimulates the H+/K+ adenosine triphosphatease (ATPase) proton pump to secrete hydrogen ions in exchange for K+ into the lumen of the stomach. A Cl- channel couples chloride efflux to the release of H+. In contrast, receptor binding of prostaglandin E2 and somatostatin diminish gastric acid production. [Note: Histamine binding causes activation of adenylyl cyclase, whereas binding of prostaglandin E2 inhibits this enzyme. Gastrin and acetylcholine act by inducing an increase in intracellular calcium levels.]
Example: Ranitidine, Famotidine, cimetidine, Nizatidine are used to peptic ulcer, Acute tress ulcer and GERD etc. Some people may experience nausea, vomiting, constipation, diarrhoea, and headaches after taking these. Other side effects may include bruising or bleeding .
Ranitidine:-
Ranitidine belongs to a group of drugs called histamine-2 blockers. It works by reducing the amount of acid your stomach produces. Ranitidine also treats gastroesophageal reflux disease (GERD) and other conditions in which acid backs up from the stomach into the esophagus, causing heartburn.
Use -
It is used to treat ulcers of the stomach and intestines and prevent them from coming back after they have healed.
This medication is also used to treat certain stomach and throat (esophagus) problems (such as erosive esophagitis, gastroesophageal reflux disease-GERD, Zollinger-Ellison syndrome).
Relief of heartburn
Ranitidine can also be given with nonsteroidal anti-inflammatory drugs (NSAIDs) to reduce the risk of ulceration
Side effect :-
A very serious allergic reaction to this drug is rare, such as swelling (especially of the face/tongue/throat), severe dizziness, trouble breathing and rash.
Head ach, constipation etc.
Dose :-
For ulcer healing 300 mg at bed time or 150 mg BD; for maintenance 150 mg at bed time. Parenteral dose—50 mg i.m. or slow i.v. inj. every 6–8 hrs (rapid i.v. injection can cause hypotension), 0.1–0.25 mg/kg/hr by i.v. infusion has been used for prophylaxis of stress ulcers. For gastrinom300 mg 3–4 times a day.
4. Proton pump inhibitors:-
The PPIs bind to the H+ /K+ ATPase enzyme system with suppress the secretion of h+ ions from gastric lumen. The available PPIs is includes esomeprazole, omeprazole, pantoprazole, rabeprazole, lansoprazole etc. Omeprazole, lansoprazole, esomeprazole are available over the counter foe sort term treatment of GERD.
Actions:-
These agents are prodrugs with acid resistant enteric coating which help to protect them from premature degradation by gastric acid. This coating is remove in alkaline duodenum and absorbed base and transported to the parietal cell. There, it is converted to the active drug with form a covalent bond with h+/k+ ATPase enzyme.
Therapeutic uses:-
The PPIs is the superior to the h2 antagonist in suppressing acid production with healing ulcer. Thus they are preferred drug for stress ulcer treatment and for the treatment of GERD, erosive esophagitis, active duodenum ulcer. If an H2 receptor antagonist is needed, it should be taken after taking PPI. PPI also reduce the bleeding from ulcer located place, caused by aspirin and NSAID drug.
Omeprazole :-
Omeprazole It is the prototype member of substituted benzimidazoles which inhibit the final common step in gastric acid secretion. The only significant pharmacological action of omeprazole is dose dependent suppression of gastric acid secretion; without anticholinergic or H2 blocking action. It is a powerful inhibitor of gastric acid: can totally abolish HCl secretion, both resting as well as that stimulated by food or any of the secretagogues, without much effect on pepsin, intrinsic factor, juice volume and gastric motility.
MOA:-
Omeprazole is inactive at neutral pH, but at pH < 5 it rearranges to two charged cationic forms (a sulphenic acid and a sulphenamide configurations) that react covalently with SH groups
of the H+K+ATPase enzyme and inactivate it irreversibly, especially when two molecules of omeprazole react with one molecule of the enzyme. After absorption into bloodstream and subsequent diffusion into the parietal cell, it gets concentrated in the acidic pH of the canaliculi because the charged forms generated there are unable to diffuse back. Moreover, it gets tightly bound to the enzyme by covalent bonds. These features and the specific localization of H+K+ATPase to the apical membrane of the parietal cells confer high degree of selectivity of action to omeprazole. Acid secretion resumes only when new H+K+ATPase molecules are synthesized (reactivation half time 18 hours). It also inhibits gastric mucosal carbonic anhydrase.
Pharmacokinetics :-
The e.c. tablet or granules filled in capsules should not be broken or crushed before swallowing. Oral bioavailability of omeprazole is ~50% due to acid lability. Bioavailability of all PPIs is reduced by food; they should be taken in empty stomach, followed 1 hour later by a meal to activate the H+K+ ATPase and make it more susceptible to the PPI. Omeprazole is highly plasma protein bound, rapidly metabolised in liver by CYP2C19 and CYP3A4 (plasma t½ ~1 hr). The metabolites are excreted in urine. As such, inhibition of HCl secretion occurs within 1 hr, reaches maximum at 2 hr, is still half maximal at 24 hr and lasts for 2–3 days.
Use-
Peptic ulcer: Omeprazole 20 mg OD is equally or more effective than H2 blockers. Relief of pain is rapid and excellent. Faster healing has been demonstrated with 40 mg/day:
Gastroesophageal reflux disease (GERD): Omeprazole produces more complete round-the-clock inhibition of gastric acid resulting in rapid symptom relief and is more effective than H2 blockers in promoting healing of esophageal lesions. Higher doses than for peptic ulcer or twice daily administration is generally needed.
Aspiration pneumonia: PPIs are an alternative to H2 blockers for prophylaxis of aspiration pneumonia due to prolonged anaesthesia.
Adverse effect:-
PPIs produce minimal adverse effects. Nausea, loose stools, headache, abdominal pain, muscle and joint pain, dizziness are complained by 3–5%. Rashes (1.5% incidence), leucopenia and hepatic dysfunction are infrequent. On prolonged treatment atrophic gastritis has been reported occasionally. No harmful effects of PPIs during pregnancy are known. Though manufacturers advise to avoid, PPIs have often been used for GERD during pregnancy [26].
5. Prokinetics:-
This medication is helpful for stomach that empty slowly. One example of a prokinetic drug is Reglan, propulsid. The Side effects of this drug are include tiredness, depression, sleepiness, anxiety, and muscle spasms.
6. Antibiotics:-
If H. pylori is causing peptic ulcers, result in indigestion, for that an antibiotic will be prescribed. Side effects may include an upset stomach, looseness, and fungal infections.
7. Antidepressants:-
If the doctor finds no causes for indigestion after investigation on patient, and the person with dyspepsia has not responded to treatments, the doctor may prescribe low-dose antidepressants.
Antidepressants sometimes ease discomfort by reducing the sensation of pain. Side effects may include nausea, headaches, agitation, constipation, and night sweats etc.
8. Psychological therapy: -
For people with functional dyspepsia, psychological therapy can help manage the cognitive aspects of indigestion. Cognitive behavioral therapy, hypnotherapy, and relaxation therapy may be recommended.
The doctor may also recommend making changes to a person's current medication schedule if they suspect that it could be causing indigestion. A course of aspirin or ibuprofen may sometimes be stopped and alternative medications advised. It is important to change medications only under the supervision of a doctor.
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