The role of Antacids in acid reflux relief

What about Tums for acid reflux relief?
Acid produced in the stomach is the main injurious factor inducing inflammation of the esophagus in acid reflux disease. Since Antacids are medicines that neutralize stomach acid, the refluxed contents would thus be free of the heartburn initiating component. Antacids have a rapid onset and short duration of action, and are most appropriate for rapid acid reflux relief for a short period of time. In contrast to H-2 receptor blockers and proton pump inhibitors which reduce acid production by the stomach, Antacids have no direct effect upon acid producing mechanisms. There are two types of Antacids: the first is sodium bicarbonate which chemically neutralizes the acid and is absorbable, accordingly its use is limited because of the associated systemic side effects. The second type is non-absorbable and acts by attracting acid molecules to its surface, consequently preventing their action, a process called adsorption. Calcium and magnesium salts are examples of the second group and are commonly used.
Acid rebound is a phenomenon encountered during the usage of antacids in which acid returns in greater concentration after the drug effect has stopped.
Another disadvantage of Antacids is that they interact with certain drugs and limit their simultaneous usage. They may also be associted with diarrhea and constipation.
Additional components of some formulations include dimethicone which reduces pain resulting from gaseous distention and alginic acid which, in combination with antacids, may help manage acid reflux.
Additional uses of non-absorbable Antacids include prevention of osteoporosis as the calcium salts would act as dietary supplement. Aluminum carbonate is also useful for binding phosphate, preventing the formation of urinary phosphate stones.
Antacids should be taken when gastric acidity is most likely to be increasing — namely, between one and three hours after each meal and at bedtime.
Examples of Antacids include:
* Aluminum hydroxide (Amphojel®, AlternaGEL®)
* Magnesium hydroxide (Phillips’® Milk of Magnesia)
* Aluminum hydroxide and magnesium hydroxide (Maalox®, Mylanta®)
* Aluminum carbonate gel (Basaljel®)
* Calcium carbonate (Alcalak®, Calcium Rich Rolaids®, Quick-Eze®, Rennie®, Titralac®, Tums®)
* Sodium bicarbonate (Bicarbonate of soda, Alka-Seltzer®)
* Hydrotalcite (Mg6Al2(CO3)(OH)16 · 4(H2O); Talcid®)
* Bismuth subsalicylate (Pepto-Bismol)
* Magaldrate + Simethicone (Pepsil)
Reduced stomach acidity may result in an impaired ability to digest and absorb certain nutrients, such as iron and the B vitamins. Since the normal acidity of the stomach normally kills ingested bacteria, Antacids increase the vulnerability to infection.

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The role of H2 receptor blockers in acid reflux relief

Reflux of stomach contents into the esophagus is known to produce inflammatory changes in the esophageal lining. There are two components in that content responsible for such a damage. These are the hydrochloric acid and a biologically active substance called pepsin, an enzyme which digests protein. Both of acid and pepsin contribute to esophagitis. Inside the stomach acid is mainly produced to activate pepsin from a precursor known as pepsinogen. That reveals the dual effect of the stomach acid in relation to esophageal damage. The first effect being direct and the second indirect through the activation of pepsin which in turn irritates the esophagus.
It is well evident from the previous facts that reduction of acid production prevents damage of the esophageal lining. Acid is produced by cells lining the stomach known as parietal cells. These cells have chemical pumps called proton pumps which moves hydrogen ion from the inside of the parietal cell into the stomach lumen against a concentration gradient. Before this pumping activity the cell responds to signals initiating the process. These signals are: 1- Acetylcholine, a chemical substance released at the nerve endings supplying stomach glands, 2- Gastrin: a local hormone released from capillaries adjacent to stomach glands, and 3- Histamine: a biologically active chemical produced by specialized local cells in the stomach wall. These signals act upon specific sites in the membrane enclosing each parietal cell called receptors and each receptor is named after the name of stimulus which acts upon. Accordingly there are Aceylcholine, Gastrin and histamine receptors.
Acetylcholine is released through the various neurological mechanisms which follow food intake and its digestion. Gastrin is a local hormone produced by G cells located in the wall of the distal part of the stomach called the antrum in response to the chemical effect of digested proteins. Histamine is released mechanically by distention of the stomach and chemically by products of protein breakdown.
Theoretically speaking, we can block acid production by preventing the stimulatory effect of Acetylcholine, Gastrin and Histamine upon the parietal cells. Acetylcholine has well known antagonists but they have generalized effects as Acetylcholine is a universal neuro-transmitter. So far no Gastrin blocker is yet available. In 1964 the role of histamine as a parietal cell stimulant was discovered, however the use of traditional antihhistamine did not reduce acid secretion. That led scientists to postulate the existence of two histamine receptors, the one acted upon by traditional antihistamines (H1) and the other residing in parietal cell wall (H2).

H2-receptor antagonists have some similarity in structure to histamine, consequently they compete with its molecules and combine with receptors instead, of course they don't have the functional activity of histamine. Fortunately, this binding effect is simultaneously accompanied by a reduced stimulating effect of both Acetylcholine and Gastrin upon the parietal cell.
Examples of H2 receptor blockers include: Cimitedine (Tagamet),Ranitidine (Zantac), Nizatidine (Axid) and Famotidine (Pepcid).
They are equally effective, and the standard dose for mild to moderate acid reflux is: 400mg, 150mg, 150mg and 20mg respectively. This dosage is given twice daily for 6-12 weeks. Approximately 50% of patients with esophagitis heal on this regimen. However a high relapse rate of 50% has been reported within two months. Maintenance treatment is indicated in severe esophagitis associated with complications and if symptoms are relapsing immediately after treatment stops. The dosage may be given three times daily in some cases for proper relief of symptoms and healing of complications.
Generally speaking they are more effective than antacids but less effective than proton pump inhibitors.
Together with other measures for acid reflux relieve such as dietary control and lifestyle modifications, they have proven efficacy in mild to moderate symptoms. They are available as over the counter and prescription forms and have relatively lower cost.

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Rule out heart disease even if acid reflux is diagnosed

There are two types of pain related to acid reflux:
1- The classical heartburn characteristic of acid reflux resulting from irritation of the esophageal surface lining.
2- The chest pain which is similar to that associated with coronary artery disease (coronary arteries are blood vessels supplying the heart with its essential requirements of oxygen and nutrients). This pain is due to spasm of the esophageal wall muscles.
It is evident that acid as a pain stimulus acts on surface receptors in case of heartburn. On the other hand it stimulates deeper receptors when causing chest pain and that suggests the pre-existence of breaks in the esophageal surface lining in the form of erosions or ulcers or an increase in the distance of spaces between cells lining the esophageal surface. Both of these mechanisms favor further acid diffusion deeper into the wall of the esophagus.
At times differentiation between esophageal and cardiac causes is very difficult.
In this situation the priority is for considering causes related to the heart first, simply because heart disease is serious and the chest pain may be a symptom of myocardial infarction which is an emergency condition following obstruction of coronary blood supply to the heart and resulting in impending death of a localized area of the musculture of the heart. That is why exclusion of heart disease is important to save life.
Needless to say that this rule applies especially to older patients with hypertension or diabetes or known heart disease.
Actually, both acid reflux and ischemic heart disease may co-exist as they are common health problems and that complicates the decision making process.
Out of all cases, having chest pain similar to typical heart attack, though their coronary arteries are normal, acid reflux contributes to 40-60% of the causes. This finding is documented by ambulatory esophageal acid monitoring.
To recall chest pain associated with heart disease (called angina) is a sense of fullness or tightness, dull aching or crushing in nature, in the middle of the chest. That pain may spread into the neck, shoulder or arm and is associated with difficulty in breathing and a cold sweat. On the other hand, chest pain of esophageal origin spreads more frequently to the back, is initiated by the same factors that trigger heartburn like fatty foods, lying down immediately after meals and is lasting for minutes or hours. Esophageal pain may also be associated with other symptoms of acid reflux such as heartburn, regurgitation and difficult swallowing. It is characteristically relieved with antacids. Diagnosis is confirmed with esophageal manometry which detects abnormalities in esophageal motility.
Chest pain of cardiac origin usually follows exertion and is relieved by rest. Nitrates and calcium channel blockers which are known to alleviate angina, aggravates pain of esophageal origin at the same time as they relaxes the lower esophageal sphincter.

How serious is Barrett's esophagus?

What do you mean by Barrett's esophagus?
Norman Barrett (1903–1979), a British surgeon at St Thomas' Hospital, first described specified changes in the appearance of the esophageal lining of patients with acid reflux disease in 1950. These changes are in the form of abnormal pink projections extending upwards into the esophagus from the stomach. They represent replacement of the normal cells lining the esophagus with another type of cells peculiar to the stomach or the intestine.

When the stomach contents reflux into the esophagus, its cellular lining is eroded. This damage mainly affects the superficial cells and the deep or basal germinative cells (stem cells) usually survive. In these cells a genetic switch causes them to generate new cells of specialized characteristics that differ from native esophageal cells. The new cells produce mucus and are more resistant to acid. They also differ in shape, being columnar instead of the spindle shaped esophageal cells. They also have some cells which are goblet shaped and are stuffed with mucus. This cellular pattern is similar to intestinal cells and is diagnostic of Barrett's esophagus.

About 10% of patients with acid reflux disease have Barrett's esophagus. It's usually diagnosed during endoscopy and has specific features.

The pink projections characteristic of Barrett's esophagus vary in length, some are short (less than 3cm) and others long (more than 3cm) having higher risk of developing intestinal metaplasia . Proper diagnosis is confirmed by taking a specimen of this abnormal tissue and examining it under the microscope.
The process of replacement of esophageal cells with intestinal tissue (transformation of native cellular pattern with normal tissue of another organ) is called Metaplasia.
Metaplasia usually progresses into Dysplasia, a change in individual cellular features. Abnormalities involve cellular architecture, intracellular infrastructure and nuclei. Cells usually vary in size and shape and their nuclei reveal profound changes. Dysplasia may be low-grade or high-grade and this variety is pre-cancerous, usually complicated with a type of cancer called Adenocarcinoma of the esophagus. About 10% of patients with Metaplasia change into Dysplasia, and 1% of patients with Barrett's esophagus will have the risk of developing cancer.
As Barrett-type intestinal metaplastic cells are under-developed, they don't have normal sensory nerve supply and patients used to suffer from heartburn may not experience it any more. Accordingly, sufferers reporting spontaneous relief of symptoms after a long standing heartburn should be managed with a high index of suspicion.
In Barrett's esophagus It's mandatory to monitor cellular changes frequently. If no Dysplasia is associated endoscopy should be performed every year. When Dysplasia is detected, the opinion of an experienced pathologist is essential to confirm the diagnosis and differentiate between low-grade and high-grade types. In low-grade Dysplasia endoscopy should be repeated every six months to detect any progression. In high-grade Dysplasia, if the patient is at high risk for surgery, endoscopic ablative procedures should be considered. In fit patients surgical excision of the esophagus is the preferred approach, the operation is called esophagectomy.
Photo-dynamic therapy is an endoscopic ablative procedure which involves injecting a photo-sensitizing material followed by delivering red laser light to sensitized cells. Consequently, cells containing the drug are destroyed.
Endoscopic mucosal resection is safer than surgery and involves excision of dysplastic tissue, it also has a diagnostic role as it submits an adequate specimen for proper diagnosis and determining the depth of invasion.

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Extra-esophageal symptoms of acid reflux

There are two types of symptoms in acid reflux disease: esophageal and extra-esophageal (also called typical and atypical). We all know about heartburn the typical symptom of acid reflux, which is initiated by the direct injurious effect of acid upon the esophageal lining. Heartburn has been linked to the esophageal entity because it represents a characteristic subjective sensation resulting specifically from esophageal irritation.
So, what about extra-esophageal symptoms?
The term extra-esophageal sounds anatomically; meaning sites other than the esophagus.
Extra-esophageal sites include the larynx, the trachea, the bronchi and both lungs.
The pharynx is a common compartment, at which portals of entry into the esophageal tube and the respiratory tract are located.
At the junction between the esophagus and the pharynx there is a sphincter, the upper esophageal sphincter which opens only during swallowing to allow ingested food pass from the mouth into esophagus. That means it's contracted most of the time and by this function it serves two important actions, first it prevents swallowing of air in one direction and second prevents the incidentally refluxed acid from entering the pharynx in the other direction.
Whenever a disturbance in this activity is encountered due to a motility disorder for example; acid being refluxed into the pharynx, would be aspirated into the larynx.
The effects of pharyngeal irritation are usually experienced as sore throat. The situation is quite different in case of laryngeal irritation because the surface lining of the larynx is very sensitive. Such a characteristic feature of the larynx is meant to protect the respiratory tract from the inhalation of any foreign material. The immediate response is severe cough to expel any aspirated substance. This cough mechanism as a line of defense is endorsed by the contraction of the upper esophageal sphincter on one hand and the esophageal acid clearance mechanisms on the other hand. Repeated exposure of the larynx to chemical irritation associated with acid reflux results in inflammation of the larynx (laryngitis) with symptoms as hoarseness of voice, vocal fatigue and voice breaks. These direct effects would also be encountered when the trachea and bronchi are affected with similar inflammatory changes as they are in continuity with the larynx and are usually complained of as chronic cough. Sometimes the reflux is aspirated in small amounts into the lung (micro-aspirations) and is complicated with inflammation (pneumonia) which may progress to lung fibrosis. These serious complications usually cause difficulty in breathing (dyspnea).
That is all about how acid reflux causes extra-esophageal symptoms by a direct effect upon the respiratory tract, and as we have noticed is associated with evidence of direct chemical irritation in the form of inflammation. That does not conclude the effects as some well known extra-esophageal presentations such as bronchial spasm is not associated with any organic changes; neither irritation nor inflammation?.
Well, that is the other side of the story; acid reflux causes extra-esophageal symptoms by reflex actions. A reflex action is an automatic (involuntary) neuromuscular action elicited by a defined stimulus. To simplify, a reflex action includes: a receptor; a specialized sense organ located in a surface and an effector; muscle fibers located in a wall which automatically respond to an electric impulse generated by stimulation of the receptor and transmitted through nerve fibers to the effector's site. For example, a person stepping on a sharp object would initiate the reflex action through the creation of a stimulus, within receptors located in the skin tissue of the foot. The resulting stimulus would be transmitted through sensory neurons to the spinal cord. This stimulus is usually processed to create an immediate response by initiating a muscular response which is acted upon by muscles of the leg, retracting the foot away from the object. In our case the acid replaces the sharp object (stimulus), the esophageal surface lining replaces the skin tissue of the foot (receptor) and muscle fibers in the wall of the bronchi instead of muscles of the leg (effector). Accordingly asthma like symptoms in the form of wheezing and difficulty in breathing are scenarios of broncho-constriction, a reflex action induced by acid reflux.
Anatomically related sites which show other manifestations of reflux include: para-nasal sinuses and the middle ear, both of them are communicating with the pharynx either directly or indirectly. The effects are mostly related to direct irritation followed by inflammation in the form of sinusitis and otitis media respectively.
Dental changes are due to enamel erosion and a bad breath is a reflection of infection on top of upper respiratory tract inflammation.
Inflammatory changes just enumerated may also be complicated by ulcers, polyps or even cancer and these implicate frequent endoscopies.
Another fact is that acid reflux may present only with these extra-esophageal symptoms without the classical heartburn.
A therapeutic trial of proton pump inhibitors should be attempted twice daily and if no relief within 4-6 weeks acid monitoring should be considered along with the treatment.
Frequent aspirations and recurrent lung inflammations are indications for surgery.

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