Gastroesophageal reflux disease (GERD) affects approximately 40% of adults. Strictures occur in 7 to 23% of patients with GERD who are untreated.

GERD may lead to Barrett's esophagus, a type of intestinal metaplasia, which is in turn a precursor condition for esophageal cancer. The risk of progression from Barrett's to dysplasia is uncertain, but is estimated at about 20% of cases. Due to the risk of chronic heartburn progressing to Barrett's, EGD every five years is recommended for people with chronic heartburn, or who take drugs for chronic GERD.

GERD is caused by a failure of the lower esophageal sphincter. In healthy patients, the "Angle of His"—the angle at which the esophagus enters the stomach—creates a valve that prevents duodenal bile, enzymes, and stomach acid from traveling back into the esophagus where they can cause burning and inflammation of sensitive esophageal tissue.

Factors that can contribute to GERD:

- Hiatal hernia, which increases the likelihood of GERD due to mechanical and motility factors.

- Obesity: increasing body mass index is associated with more severe GERD. In a large series of 2,000 patients with symptomatic reflux disease, it has been shown that 13% of changes in esophageal acid exposure is attributable to changes in body mass index.

- Zollinger-Ellison syndrome, which can be present with increased gastric acidity due to gastrin production.

- A high blood calcium level, which can increase gastrin production, leading to increased acidity.

- Scleroderma and systemic sclerosis, which can feature esophageal dysmotility.

- The use of medicines such as prednisolone.

- Visceroptosis or Glénard syndrome, in which the stomach has sunk in the abdomen upsetting the motility and acid secretion of the stomach.

GERD has been linked to a variety of respiratory and laryngeal complaints such as laryngitis, chronic cough, pulmonary fibrosis, earache, and asthma, even when not clinically apparent. These atypical manifestations of GERD are commonly referred to as laryngopharyngeal reflux (LPR) or as extraesophageal reflux disease (EERD).

Factors that have been linked with GERD, but not conclusively:

- Obstructive sleep apnea

- Gallstones, which can impede the flow of bile into the duodenum, which can affect the ability to neutralize gastric acid

In 1999, a review of existing studies found that, on average, 40% of GERD patients also had "H. pylori" infection. The eradication of "H. pylori" can lead to an increase in acid secretion, leading to the question of whether "H. pylori"-infected GERD patients are any different than non-infected GERD patients. A double-blind study, reported in 2004, found no clinically significant difference between these two types of patients with regard to the subjective or objective measures of disease severity.

Most damage to the pyloric valve occurs as a complication of gastric surgery. Other causes of biliary reflux may be:

- Peptic ulcer

- Gallbladder surgery (cholecystectomy)

A significant fraction of cases are idiopathic, with no identified specific etiology.

Barrett's esophagus is a premalignant condition. Its malignant sequela, oesophagogastric junctional adenocarcinoma, has a mortality rate of over 85%. The risk of developing esophageal adenocarcinoma in people who have Barrett's esophagus has been estimated to be 6–7 per 1000 person-years, however a cohort study of 11,028 patients from Denmark published in 2011 showed an incidence of only 1.2 per 1000 person-years (5.1 per 1000 person-years in patients with dysplasia, 1.0 per 1000 person-years in patients without dysplasia). The relative risk of esophageal adenocarcinoma is approximately 10 in those with Barret's esophagus, compared to the general population. Most patients with esophageal carcinoma survive less than one year.

Causes

Esophagitis cannot be spread. However, infections can be spread by those who have infectious esophagitis. Esophagitis can develop due to many causes. GERD is the most common cause of esophagitis because of the backflow of acid from the stomach, which can irritate the lining of the esophagus.

Other causes include:

- Medicines- Can cause esophageal damage that can lead to esophageal ulcers

- Nonsteroidal anti-inflammatory drugs (NSAIDS)-aspirin, naproxen sodium, and ibuprofen. Known to irritate the GI tract.

- Antibiotics- doxycycline and tetracycline

- Quinidine

- Biphosphonates- used to treat osteoporosis

- Steroids

- Potassium chloride

- Chemical injury by alkaline or acid solutions

- Physical injury resulting from nasogastric tubes.

- Alcohol abuse- Can wear down the lining of the esophagus.

- Crohn's disease – a type of IBD and an autoimmune disease that can cause esophagitis if it attacks the esophagus.

- Stress- Can cause higher levels of acid reflux

- Radiation therapy-Can affect the immune system.

- Allergies (food, inhalants)- Allergies can stimulate eosinophilic esophagitis.

- Infection-People with an immunodeficiencies have a higher chance of developing esophagitis.

- Vitamins and supplements (iron, Vitamin C, and potassium)-Supplements and minerals can be hard on the GI tract.

- Vomiting- Acid can irritate esophagus.

- Hernias-A hernia can poke through the diaphragm muscle and can inhibit the stomach acid and food from draining quickly.

- Surgery

Prevention

Since there can be many causes underlying esophagitis, it is important to try to find the cause to help to prevent esophagitis. To prevent reflux esophagitis, avoid acidic foods, caffeine, eating before going to bed, alcohol, fatty meals, and smoking. To prevent drug-induced esophagitis, drink plenty of liquids when taking medicines, take an alternative drug, and do not take medicines while lying down, before sleeping, or too many at one time. Esophagitis is more prevalent in adults and does not discriminate.

The treatment for bile reflux is the same as the treatment for acidic reflux. In general, everything that can

reduce acidic reflux can reduce bile reflux. Examples include lifestyle modification, weight reduction, and the avoidance of eating immediately before sleep or being in the supine position immediately after meals. In addition, smoking has been found to be a factor in the development of acidic reflux. Thus, all of these factors should be applied to bile reflux as well.

Likewise, drugs that reduce the secretion of gastric acid (e.g., proton pump inhibitors)

or that reduce gastric contents or volume can be used to treat acidic bile reflux. Because prokinetic drugs increase the motility of the stomach and accelerate gastric emptying, they can also reduce bile reflux. Other drugs that reduce the relaxations of the lower esophageal sphincter, such as baclofen, have also proven to reduce bile reflux, particularly in patients who are refractory to (medically unresponsive to) proton pump inhibitor therapy.

Medications used in managing biliary reflux include bile acid sequestrants, particularly cholestyramine, which disrupt the circulation of bile in the digestive tract and sequester bile that would otherwise cause symptoms when refluxed; and prokinetic agents, to move material from the stomach to the small bowel more rapidly and prevent reflux.

Biliary reflux may also be treated surgically, if medications are ineffective or if precancerous tissue is present in the esophagus.

It can be caused by or associated with gastroesophageal reflux disease, esophagitis, a dysfunctional lower esophageal sphincter, disordered motility, lye ingestion, or a hiatal hernia. Strictures can form after esophageal surgery and other treatments such as laser therapy or photodynamic therapy. While the area heals, a scar forms, causing the tissue to pull and tighten, leading to difficulty in swallowing.

Dietary factors such as spice consumption, were hypothesized to cause ulcers until late in the 20th century, but have been shown to be of relatively minor importance. Caffeine and coffee, also commonly thought to cause or exacerbate ulcers, appear to have little effect. Similarly, while studies have found that alcohol consumption increases risk when associated with "H. pylori" infection, it does not seem to independently increase risk. Even when coupled with "H. pylori" infection, the increase is modest in comparison to the primary risk factor.

Incidence of achalasia has risen to approximately 1.6 per 100,000 in some populations. Disease affects mostly adults between ages 30s and 50s.

Ileus is a cause of colic in horses due to functional obstruction of the intestines. It most commonly seen in horses postoperatively, especially following colic surgery. Horses experiencing ileus are at risk for gastric rupture due to rapid reflux build-up, and require intense medical management with frequent nasogastric intubation. Ileus may increase adhesion formation, because intestinal segments have more prolonged contact and intestinal distention causes serosal injury and ischemia. It is usually treated with aggressive fluid support, prokinetics, and anti-inflammatories.

Stress due to serious health problems such as those requiring treatment in an intensive care unit is well described as a cause of peptic ulcers, which are termed stress ulcers.

While chronic life stress was once believed to be the main cause of ulcers, this is no longer the case. It is, however, still occasionally believed to play a role. This may be by increasing the risk in those with other causes such as "H. pylori" or NSAID use.

The incidence in the United States among Caucasian men is eight times the rate among Caucasian women and five times greater than African American men. Overall, the male to female ratio of Barrett's esophagus is 10:1. Several studies have estimated the prevalence of Barrett's esophagus in the general population to be 1.3% to 1.6% in two European populations (Italian and Swedish), and 3.6% in a Korean population.

The causes are divided into benign or malignant.

- Benign

- Peptic ulcer disease

- Infections, such as tuberculosis; and infiltrative diseases, such as amyloidosis.

- A rare cause of gastric outlet obstruction is blockage with a gallstone, also termed "Bouveret's syndrome".

- In children congenital pyloric stenosis / congenital hypertrophic pyloric stenosis may be a cause.

- A pancreatic pseudocyst can cause gastric compression.

- Pyloric mucosal diaphragm could be a rare cause.

- Malignant

- Tumours of the stomach, including adenocarcinoma (and its linitis plastica variant), lymphoma, and gastrointestinal stromal tumours

In a peptic ulcer it is believed to be a result of edema and scarring of the ulcer, followed by healing and fibrosis, which leads to obstruction of the gastroduodenal junction (usually an ulcer in the first part of the duodenum).

Immediate treatment is the most important factor in a favorable prognosis. A delay in treatment greater than six hours or the presence of peritonitis, sepsis, hypotension, or disseminated intravascular coagulation are negative prognostic indicators.

Historically, GDV has held a guarded prognosis. Although "early studies showed mortality rates between 33% and 68% for dogs with GDV," studies from 2007 to 2012 "reported mortality rates between 10% and 26.8%". Mortality rates approach 10% to 40% even with treatment. A study determined that with prompt treatment and good preoperative stabilization of the patient, mortality is significantly lessened to 10% overall (in a referral setting). Negative prognostic indicators following surgical intervention include postoperative cardiac arrhythmia, splenectomy, or splenectomy with partial gastric resection. Interestingly, a longer time from presentation to surgery was associated with a lower mortality, presumably because these dogs had received more complete preoperative fluid resuscitation and were thus better cardiovascularly stabilized prior to the procedure.

Treatments for esophagitis include medications to block acid production, to manage pain, and to reduce inflammation. Other treatments include antibiotics and intravenous nutrition.

To treat reflux esophagitis, over the counter antacids, medications that reduce acid production (H-2 receptor blockers), and proton pump inhibitors are recommended to help block acid production and to let the esophagus heal. Some prescription medications to treat reflux esophagitis include higher dose H-2 receptor blockers, proton pump inhibitors, and prokinetics, which help with the emptying of the stomach.

To treat eosinophilic esophagitis, avoiding any allergens that may be stimulating the eosinophils is recommended. As for medications, proton pump inhibitors and steroids can be prescribed. Steroids that are used to treat asthma can be swallowed to treat eosinophil esophagitis due to nonfood allergens. The removal of food allergens from the diet is included to help treat eosinophilic esophagitis.

For infectious esophagitis, a medicine is prescribed based on what type of infection is causing the esophagitis. These medicines are prescribed to treat bacterial, fungal, viral, and/or parasitic infections.

An endoscopy can be used to remove ill fragments. Surgery can be done to remove the damaged part of the esophagus. For reflux esophagitis, a fundooplication can be done to help strengthen the lower esophageal sphincter from allowing backflow of the stomach into the esophagus. As for patients that have a narrowing esophagus, a gastroenterologist can perform a procedure to dilate the esophagus.

Some home remedies and lifestyle changes to help with esophagitis include losing weight, stop smoking, lowering stress, avoid sleeping/lying down after eating, raise your head while laying down, taking medicines correctly, avoiding certain medications, and avoiding foods that cause the reflux that might be causing the esophagitis.

If the disease remains untreated, it can cause scarring and discomfort in the esophagus. If the irritation is not allowed to heal, esophagitis can result in esophageal ulcers. Esophagitis can develop into Barrett's esophagus and can increase the risk of esophageal cancer.

The prognosis for a person with esophagitis depends on the underlying causes and conditions. If a patient has a more serious underlying cause such as a digestive system or immune system issue, it may be more difficult to treat. Normally, the prognosis would be good with no serious illnesses. If there are more causes than one, the prognosis could move to fair.

As a general rule, GDV is of greatest risk to deep-chested dogs. The five breeds at greatest risk are Great Danes, Weimaraners, St. Bernards, Gordon Setters, and Irish Setters. In fact, the lifetime risk for a Great Dane to develop GDV has been estimated to be close to 37 percent. Standard Poodles are also at risk for this health problem, as are Irish Wolfhound, Doberman Pinschers, Rottweilers, German Shorthaired Pointer, German Shepherds, Rhodesian Ridgebacks. Basset Hounds and Dachshunds have the greatest risk for dogs less than .

The role of "Helicobacter pylori" in functional dyspepsia is controversial, and no clear causal relationship has been established. This is true for both the symptom profile and pathophysiology of functional dyspepsia. Although some epidemiologic studies have suggested an association between "H. pylori" infection and functional dyspepsia, others have not. The discrepancy may stem in part from differences in methodology and lack of adequate consideration of confounding factors such as past history of peptic ulcer disease and socioeconomic status. Controlled trials disagree about whether or not "H. pylori" eradication is beneficial in functional dyspepsia, with roughly half of the trials showing improvement and the other half no improvement. In a recent multicenter U.S. trial that randomized 240 patients to treatment or placebo, and followed patients for 12 months, 28% of treated patients versus 23% of those receiving placebo reported relief of symptoms at the 12-month follow-up. Similarly, recent European trials have not shown significant differences in symptoms after "H. pylori" eradication as compared with controls. Systematic reviews of eradication have been conducted, with varying results. A systematic review in the Annals of Internal Medicine suggested no statistically significant effect, with an odds ratio (OR) for treatment success versus control of 1.29 (95% CI, 0.89–1.89; P = 0.18). Still, no effect was seen after adjusting for heterogeneity and for cure of "H. pylori". In contrast, a Cochrane review found a small but statistically significant effect in curing symptoms ("H. pylori" cure vs placebo, 36% vs 30%, respectively).

Acute, self-limited "dyspepsia" may be caused by overeating, eating too quickly, eating high-fat foods, eating during stressful situations, or drinking too much alcohol or coffee. Many medications cause dyspepsia, including aspirin, nonsteroidal anti-inflammatory drugs (NSAIDs), antibiotics (metronidazole, macrolides), diabetes drugs (metformin, Alpha-glucosidase inhibitor, amylin analogs, GLP-1 receptor antagonists), antihypertensive medications (angiotensin converting enzyme [ACE] inhibitors, Angiotensin II receptor antagonist), cholesterol-lowering agents (niacin, fibrates), neuropsychiatric medications (cholinesterase inhibitors [donepezil, rivastigmine]), SSRIs (fluoxetine, sertraline), serotonin-norepinephrine-reuptake inhibitors (venlafaxine, duloxetine), Parkinson drugs (Dopamine agonist, monoamine oxidase [MAO]-B inhibitors), corticosteroids, estrogens, digoxin, iron, and opioids.

Nutcracker esophagus, or hypertensive peristalsis, is a disorder of the movement of the esophagus characterized by contractions in the smooth muscle of the esophagus in a normal sequence but at an excessive amplitude or duration. Nutcracker esophagus is one of several motility disorders of the esophagus, including achalasia and diffuse esophageal spasm. It causes difficulty swallowing, or dysphagia, to both solid and liquid foods, and can cause significant chest pain; it may also be asymptomatic. Nutcracker esophagus can affect people of any age, but is more common in the sixth and seventh decades of life. The diagnosis is made by an esophageal motility study (esophageal manometry), which evaluates the pressure of the esophagus at various points along its length. The term "nutcracker esophagus" comes from the finding of increased pressures during peristalsis, with a diagnosis made when pressures exceed 180 mmHg; this has been likened to the pressure of a mechanical nutcracker. The disorder does not progress, and is not associated with any complications; as a result, treatment of nutcracker esophagus targets control of symptoms only.

Nutcracker esophagus is a benign, nonprogressive condition, meaning it is not associated with significant complications. Patients are usually reassured by their physicians that the disease is unlikely to worsen. However, the symptoms of chest pain and dysphagia may be severe enough to require treatment with medications, and rarely, surgery.

The initial step of treatment focuses on reducing risk factors. While weight reduction may be useful in reducing symptoms, the role of acid suppression therapy to reduce esophageal reflux is still uncertain. Very cold and very hot beverages may trigger esophageal spasms.

Medical therapy for nutcracker esophagus includes the use of calcium-channel blockers, which relax the lower esophageal sphincter (LES) and palliate the dysphagia symptoms. Diltiazem, a calcium-channel blocker, has been used in randomized control studies with good effect. Nitrate medications, including isosorbide dinitrate, given before meals, may also help relax the LES and improve symptoms. The inexpensive generic combination of belladonna and phenobarbital (Donnatal and other brands) may be taken three times daily as a tablet to prevent attacks or, for patients with only occasional episodes, as an elixir at the onset of symptoms. Phosphodiesterase inhibitors, such as sildenafil, can be given to reduce symptoms, particularly pain, but small trials have not been able to demonstrate clinical improvement. Finally, trazodone, an antidepressant that reduces visceral sensitivity, has also been shown to reduce chest pain symptoms in patients with nutcracker esophagus.

Endoscopic therapy with botulinum toxin, known also as Botox, can also be used to improve dysphagia which stabilizes unintentional weight loss, but the effect has limited effect on other symptoms, including pain, while also being a temporary treatment lasting a few weeks. Finally, pneumatic dilatation of the esophagus, which is an endoscopic technique where a high-pressure balloon is used to stretch the muscles of the LES, can be performed to improve symptoms, but again no clinical improvement is seen in regards to motility.

Incidence of hiatal hernias increases with age; approximately 60% of individuals aged 50 or older have a hiatal hernia. Of these, 9% are symptomatic, depending on the competence of the lower esophageal sphincter (LES). 95% of these are "sliding" hiatus hernias, in which the LES protrudes above the diaphragm along with the stomach, and only 5% are the "rolling" type (paraesophageal), in which the LES remains stationary, but the stomach protrudes above the diaphragm.

Hiatus hernia are most common in North America and Western Europe and rare in rural African communities. Some have proposed that insufficient dietary fiber and the use of a high sitting position for defecation may increase the risk.

Even after successful treatment of achalasia, swallowing may still deteriorate over time. The esophagus should be checked every year or two with a timed barium swallow because some may need pneumatic dilatations, a repeat myotomy, or even esophagectomy after many years. In addition, some physicians recommend pH testing and endoscopy to check for reflux damage, which may lead to a premalignant condition known as Barrett's esophagus or a stricture if untreated.

Paralysis of the intestine is often termed paralytic ileus, in which the intestinal paralysis need not be complete, but it must be sufficient to prohibit the passage of food through the intestine and lead to intestinal blockage. Paralytic ileus is a common side effect of some types of surgery, commonly called postsurgical ileus. It can also result from certain drugs and from various injuries and illnesses, such as acute pancreatitis. Paralytic ileus causes constipation and bloating. On listening to the abdomen with a stethoscope, no bowel sounds are heard because the bowel is inactive.

A temporary paralysis of a portion of the intestines occurs typically after abdominal surgery. Since the intestinal content of this portion is unable to move forward, food or drink should be avoided until peristaltic sound is heard, by auscultation (use of a stethoscope) of the area where this portion lies. Intestinal atony or paralysis may be caused by inhibitory neural reflexes, inflammation or other implication of neurohumoral peptides.