Gastroenterology

[Virtual Presenter] The importance of objective diagnosis and treatment in medicine cannot be overstated. As healthcare professionals, it is essential that we approach each patient encounter with an open mind, unencumbered by preconceived notions and biases. By doing so, we can ensure that we are providing the most effective care possible. This involves actively listening to and evaluating patients' symptoms, rather than relying on assumptions or prior knowledge..

[Audio] The esophagus is a membrane-bound organ, varying in length between 18-26 centimeters depending on the height of individuals. It can be classified into two types: anatomical distinction and functional distinction. The upper esophageal sphincter, cervical esophagus, esophageal body, thoracic esophagus, and lower esophageal sphincter are all parts of the esophagus. The lower esophageal sphincter is particularly significant, as 90% of esophageal pathologies are related to its dysfunction. Anatomically, the upper esophagus consists of voluntary striated musculature, the middle is mixed, and the lower half is composed entirely of smooth muscle. The mucosa, submucosa, and muscularis layers are also present in the esophagus. These layers contain various tissues such as stratified epithelium, connective tissue, and esophageal glands. The adventitia, a connective tissue rich in elastic fibers and vessels, surrounds the esophagus..

[Audio] The esophagus has its own nervous network, which is similar to the one found throughout the gastrointestinal tract. This extrinsic nervous network includes both afferent and efferent fibers, originating from the sympathetic and parasympathetic systems. The process begins with pharyngeal receptors informing the brain that we are about to ingest material. This information then reaches the swallowing center, where 26 different muscles and six cranial nerves are activated within 0.8 seconds to perform the swallowing motion. Many patients experience neurological issues related to this process, known as dysphagia. The afferent nerve fibers originate from the vagus nerves, controlling the majority of the gastrointestinal tract from the esophagus to the colon transversum. Typical neurotransmitters involved include acetylcholine, noradrenaline, and others such as nitric oxide, serotonin, VIP, enkephalin, and gamma-aminobutyric acid. Additionally, there is an intrinsic nervous network located within the thickness of the organ, comprising the mucosa, submucosa, and muscularis layers. This network forms plexuses, including the myenteric plexus (Auerbach), which only modulates the motility of the organ, and the submucosal plexus (Meissner)..

[Audio] The esophagus contains sensitive fibers that can stimulate glandular secretion. These fibers also play a role in detecting incompletely translated boluses and toxic substances, provoking the sensation of retrosternal pain. Peristalis is defined as the movement that allows progression of transiting material along the digestive tract. It is an intrinsic property of any tubular organ with a layer of syncytial smooth muscle cells. The movement is controlled by the oesophageal myenteric plexus and vagal activity. A wave of proximal contraction and distal relaxation follows the contraction of the circular and longitudinal fibers. The lower esophageal sphincter remains contracted until the bolus reaches the end of the esophagus, then it relaxes and allows passage into the stomach. When this mechanism does not work properly, we see two types of diseases: achalasia, characterized by too much contraction or incomplete relaxation, and reflux, resulting from absence or reduced capacity of contraction..

[Audio] The Lower Esophageal Sphincter plays a crucial role in maintaining the integrity of the esophageal lining and preventing gastroesophageal reflux disease. Its functions include receptive relaxation, allowing food to enter the stomach, and anti-reflux barrier, preventing gastric juices from flowing back up into the esophagus. Factors such as age, sex, and certain medical conditions can affect the pressure of the LES, leading to various esophageal symptoms. These symptoms can be categorized into typical and atypical presentations. Typical symptoms include dysphagia, odynophagia, heartburn, and regurgitation, while atypical symptoms may manifest as rumination, mastication of food, or return of chewed material from the stomach to the mouth..

[Audio] Regurgitation is a type of reflux that occurs due to a decreased tone of the lower esophageal sphincter. Food, usually liquids, comes up spontaneously and passively when the patient is lying down, bending over, or even experiencing hiccups. On the other hand, vomiting is a coordinated action involving the brain, contraction of striated muscles, and anti-peristaltic activity. Atypical chest pain may also occur, which is characterized by angina-like pain with radiation to the back, not associated with swallowing or reflux. This type of pain is caused by abnormal contraction of the circular fibers, which may be irritated by acid or irritant solutions. It's essential to differentiate between true angina and angina-like pain, as they have distinct characteristics. True angina is sudden and has a short duration, whereas angina-like pain is experienced while eating and has a longer duration. Both types of pain can have similar radiations because they receive sensitive fibers from the phrenic nerve. Additionally, patients may experience sensations such as globus sensation, which is a feeling of a lump in the throat, commonly found in individuals with psychiatric disorders and women. Other symptoms include belching, emission of air of gastric origin, hiccups, and diaphragmatic reflex in response to a stimulus of the region of the cardia, suggesting involvement of the diaphragm through the phrenic nerves..

[Audio] When recognizing oropharyngeal dysphagia, we look for certain signs and symptoms. A rapid onset of difficulty swallowing, typically within two seconds after swallowing, is a key indicator. Patients often point to the affected area, indicating discomfort or pain. They may also exhibit difficulties in positioning the bolus on the tongue, leading to fractionated swallowing. Other common signs include drooling, bronchial aspiration, masticatory deficits, and nasopharyngeal regurgitation. In some cases, organic causes such as stenosis of the esophageal lumen, neoplasm, or stenotic scar secondary to GERD or corrosive esophagitis may be present. Functional causes like functional diseases of the esophagus, achalasia, diffuse esophageal spasm, and Allgrove syndrome should also be considered. Rare causes include extrinsic compression, esophageal varices, cardiomegaly, and DES. By being aware of these signs and symptoms, healthcare professionals can better diagnose and treat patients suffering from oropharyngeal dysphagia..

[Audio] Esophageal dysphagia is recognized by several signs and symptoms. The slow onset of symptoms takes more than two seconds after swallowing, stopping below the sternum. The lack of peristalsis in the esophageal body is another characteristic, causing chest pain, heartburn, regurgitation, and hiccup. As the disease progresses, symptoms become more severe, involving different types of food, starting with solid food, then semi-solid, and eventually liquids. In some cases, paradoxical esophageal dysphagia may occur, where the patient experiences difficulty swallowing liquids first, followed by solids, which is particularly common in patients with achalasia. Chest pain is a non-specific symptom that can arise from various sources, including the heart, lungs, pleura, osteoarticular structures, muscles, tendons, and nerves..

[Audio] When performing clinical-instrumental diagnosis of chest pain, we proceed with X-ray with barium contrast after excluding cardiovascular causes. This non-invasive and low-radiation examination provides valuable information about possible tumors, stenosis, and lack of relaxation of the lower esophageal sphincter. We can perform it in the Trendelenburg position to observe whether the barium enters the esophagus. It's essential to conduct this test before using probes, as direct probing might cause damage and hemorrhage if there's a tumor protruding into the lumen. Additionally, this examination enables us to locate and measure the distance from the pharynx, allowing us to obtain precise measurements when using a probe later on..

[Audio] Achalasia is a primary disorder of esophageal motility, characterized by incomplete or absent relaxation of the lower esophageal sphincter, accompanied by a reduction or absence of normal peristaltic activity in the esophageal body. This condition can affect individuals of all ages, with a higher prevalence observed among those between 30 and 60 years old. The incidence rate is approximately 0.6 cases per 100000 people per year. The etiology of achalasia is multifactorial, with idiopathic, neurotoxicity caused by autoimmune activity, and Chagas disease being identified as potential causes. The pathophysiological mechanisms underlying this condition involve abnormalities in the relaxation of the lower esophageal sphincter and the peristaltic activity of the esophageal body. Clinically, achalasia presents with paradoxical dysphagia, regurgitation, substernal chest pain, and heartburn. These symptoms often worsen over time, with patients initially experiencing difficulty with solid foods, followed by semisolids, and eventually liquids..

[Audio] The esophagus gradually worsens over time, initially experiencing intermittent dysphagia caused by stress or rapid consumption of liquids and foods, resulting in moderate dilation of the esophagus. As the disease progresses, dysphagia becomes nearly constant, accompanied by increasing dilation of the esophagus and decompensated megaoesophagus, leading to declining nutritional status. Eventually, severe dysphagia develops, marked by significant impairment of nutritional status and substantial expansion of the esophagus. Various diagnostic tools are used to diagnose this condition, including x-ray and barium contrast studies, which reveal a characteristic "mouse tail" appearance, manometry, which assesses motility and identifies impairments in LES relaxation, and esophagogastroduodenoscopy and biopsy, which provide a comprehensive diagnosis, excluding neoplastic stenosis and confirming the presence of megaoesophagus. High-resolution manometry also detects subtle changes in pressure and relaxation patterns, allowing for accurate diagnosis and management of this complex condition..

[Audio] Complications may arise from the failure to relax the lower esophageal sphincter, including lung infections due to aspiration pneumonia, esophageal perforation caused by constant dilation, esophagitis, and even esophageal cancer, which is less common. The choice of therapy depends on the stage of the disease and the patient's overall condition. Medical therapy using nitrates or calcium channel blockers before meals can help relax the muscles, whereas botulinum toxin injection through upper endoscopy provides intermediate-term relief. However, balloon dilation is an invasive procedure that carries risks of mucosal fracture, hemorrhage, and stenosis. Extramucosal myotomy and antireflux therapy are considered the most definitive treatments, but these procedures are typically performed in specialized centers and require careful consideration due to potential complications..

[Audio] Chagas disease, caused by the parasitic infection with T. cruzi, is a significant public health problem in central and south America, affecting millions of people. The parasite can invade various tissues, including the reticuloendothelial system, striated muscles, myocardium, and autonomic and central nervous system. The clinical symptoms of this disease are diverse and can include acute manifestations such as fever, myalgia, lymphadenopathy, hepatosplenomegaly, skin rash, insomnia, dyspnea, gastrointestinal disorders, and respiratory disorders. In chronic cases, patients may develop Chagas heart diseases and chronic digestive disease. Furthermore, immunosuppressed patients may experience more severe complications, including acute diffuse meningoencephalitis, brain abscess lesions, and inflammatory digestive forms..

[Audio] The destruction of the ganglia of the autonomic nervous system leads to various gastrointestinal manifestations, including megaesophagus, megacolon, and megaureter. Patients who have received blood transfusions and exhibit symptoms such as fever attacks, lymphadenopathy, and myocarditis of uncertain etiology should be suspected of having this condition. Infectious causes like mononucleosis, idiopathic achalasia, Crohn's disease, leukemia, leishmaniasis, post-stenotic ulcers, ulcerative colitis, lymphoma, tuberculosis, Hirschsprung's disease, rheumatoid arthritis, toxoplasmosis, rheumatic heart disease, typhoid fever, and salmonellosis must be considered when diagnosing these cases. This helps us understand the integrity of contraction in these patients..

[Audio] The most important comorbidity related to GERD is obesity. This has been confirmed with epidemiological studies. Generally, the risk is independent from BMI because it does not take into consideration fat distribution. The circumference of the abdomen is much more specific when talking about obesity and risk to develop GERD. Obesity favors GERD in two main ways: 1. Gastroesophageal dysmotility, and 2. Higher incidence of hiatal hernias. Non-Erosive Reflux Disease (NERD) is a type of GERD where we have clinical symptoms but no endoscopic findings of erosions in the esophagus. With a prevalence of 40% of all cases. Although the epithelium seems macroscopically normal, microscopically we have an alteration of intercellular spaces. There is an increased interaction between the lumen and neurological sensors, explaining why the patient refers symptoms. Gastroesophageal reflux disease (GERD) is a syndrome characterized by the passage of acid, neutral, or alkaline secretions from the stomach to the esophagus for more than 60 minutes within 24 hours, usually associated with endoscopically documented esophagitis and/or other complications. We have alkaline secretions when we have duodenal GER, where the material is coming from the gallbladder. We have to check the pH to verify the origin. Epidemiology shows that GERD is the most frequent cause of outpatient gastroenterology visits, represents up to 17% of all diagnoses in the digestive tract, and causes 23% of all hospital admissions for digestive diseases. Classification is based on pathological forms, including non-erosive esophagitis (NERD). Oropharyngeal dysphagia is recognized by rapid onset, patient pointing in that area, patient keeping chewing and attempting to swallow many times, drooling, fractionated swallowing, difficulties in positioning the bolus on the tongue, bronchial aspiration, masticatory deficits, nasopharyngeal regurgitation, and esophageal dysphagia. Organic causes include stenosis of the esophageal lumen, neoplasm, or stenotic scar secondary to GERD or corrosive esophagitis. Functional causes include functional diseases of the esophagus, achalasia, diffuse esophageal spasm, and Allgrove syndrome. Rare causes include extrinsic compression, esophageal varices, and cardiomegaly. Sucralfate represents a complex of sucrose and aluminum hydroxide octasulfate capable of binding to gastric mucosa and acting as a barrier. Adhesion molecules, hyaluronic acid and chondroitin sulfate carried by carrier Poloxamer 407, act like saliva. They coat the esophageal mucosa, especially if damaged, and protect it against the action of the reflux. Baclofen is not approved, was used in a few studies. Surgical therapy is usually reserved for younger patients where medical therapy would last decades. Surgical therapy allows for long-term treatment of GER.

[Audio] The progression of these diseases is influenced by both protective and aggressive factors. Protective factors include mechanisms that prevent the damage of the esophageal mucosa, while aggressive factors contribute to its irritation. Gastric and duodenal juices contain substances like hydrochloric acid and lytic enzymes that can damage the mucosa. Additionally, conditions like Zollinger-Ellison syndrome, where there is an overproduction of gastrin, can lead to the formation of multiple ulcers throughout the gastrointestinal tract. Furthermore, functional factors such as hypotonia and transient relaxation of the lower esophageal sphincter can also contribute to the development of these diseases..

[Audio] In many cases of ERD, a decrease in esophageal clearance occurs due to abnormal primary peristalsis. Slowed gastric emptying is also common, particularly in patients with GERD. This slowing is typically observed two hours after a meal, as the stomach adapts to the new content, leading to altered fundus contraction and reduced contractile activity. These alterations in fundus contraction ultimately result in slower gastric emptying. Anatomical factors, including diaphragmatic columns, phrenoesophageal ligament, gastric muscle ring, and intra-abdominal pressure, also play a role in preventing and reducing reflux, and compromise of these structures can contribute to reflux..

[Audio] The esophageal mucosal barrier is composed of mucosa, which is lubricated by the secretion of glands that protect it against the action of reflexes, including salivary reflexes. This lubrication also serves as a protective coating, containing bicarbonate ions. The loss of these components can lead to the penetration of acids and enzymes, resulting in the development of diseases. One comorbidity associated with this condition is hiatal hernia, which occurs when part of the stomach slides up into the chest cavity through the diaphragmatic esophageal hiatus. There are different types of hiatal hernias, including sliding hiatal hernia, paraesophageal hiatal hernia, and mixed-type hiatal hernia. Sliding hiatal hernia is the most common type, observed in 80-90% of cases, and is often associated with gastroesophageal reflux disease (GERD). In contrast, paraesophageal hiatal hernia is less common but more serious, as food can penetrate into the hernia or lead to infarction. Mixed-type hiatal hernia is very rare..

[Audio] Obesity plays a crucial role in the development of gastroesophageal reflux disease, or GERD. Studies have consistently shown that obesity is the most significant comorbidity associated with GERD. Waist circumference is a better indicator than body mass index, or BMI, as fat distribution can significantly impact the likelihood of experiencing GERD symptoms. Two primary mechanisms contribute to the association between obesity and GERD. Firstly, obesity can lead to gastroesophageal dysmotility, including reduced lower esophageal sphincter pressure, increased transient relaxation of the sphincter, and elevated intragastric pressure. These changes can facilitate the flow of stomach contents back up into the esophagus, leading to symptoms such as heartburn and regurgitation. Secondly, obesity is linked to a higher incidence of hiatal hernias, which can further compromise the integrity of the lower esophageal sphincter and increase the risk of GERD. Additionally, non-erosive reflux disease, or NERD, accounts for approximately 40% of all GERD cases. In this condition, patients experience typical GERD symptoms despite the absence of visible esophageal erosion. Microscopic examination reveals alterations in intercellular spaces, which can explain why patients continue to experience symptoms despite the lack of visible damage..

[Audio] The classification of GERD from a clinical perspective focuses on the "Acid Pocket" concept, where ingested food acts as a buffer against the acidic pH and enzymes secreted by the stomach, meaning symptoms should not appear after food intake. However, some patients experience symptoms shortly after eating, which can be attributed to altered peristaltic activity in the upper part of the stomach, resulting in the accumulation of peptic acid secretions. The characteristics of the acid pocket include a fasting pH of 1.4, postprandial pH of 4.4, and an acid pocket pH of 1.6, suggesting an alteration in the mixing of ingested material with gastric secretions and a failure to adapt the fundus to the food eaten, accompanied by a transient, inappropriate relaxation of the lower esophageal sphincter. The goals of treatment for GERD aim to improve the quality of life of the patient, particularly during nighttime episodes, involving controlling symptoms, healing esophageal mucosal damage, and preventing complications..

[Audio] Weight loss, elevation of head in bed, avoidance of eating before sleeping, eating meals at least three hours before bedtime, elimination of smoke and alcohol, elimination of chocolate, coffee, carbonated drinks, and acidic foods, and elimination of food if the patient experiences a subjective improvement are some interventions that can improve symptoms and esophageal pH. Medical therapy using proton pump inhibitors is also recommended, particularly for patients with erosive esophagitis or Barrett's esophagitis. The treatment should be taken once a day, thirty minutes before breakfast, and the duration should not exceed eight weeks. On-demand treatment may be preferred over continuous treatment, especially for patients who experience partial responses..

[Audio] Short-term side effects of proton pump inhibitors include headaches, nausea, abdominal pain, diarrhea, constipation, and hypocalcemia. Long-term side effects may lead to small intestine bacterial overgrowth, ion absorption deficiency, and pneumonia caused by microaspiration. H2 antagonists are less effective and less potent than proton pump inhibitors, but still useful in patients who do not respond well to proton pump inhibitors. Prokinetics work on the motility of the stomach and increase the tone of the lower esophageal sphincter, making them useful in cases where the mechanism of disease is related to altered emptying of the stomach. Antacids and alginates are also used to treat gastroesophageal reflux disease, with antacids providing quick relief and alginates suppressing reflux. However, prokinetics have side effects such as tremors, restlessness, dizziness, hyperprolactinemia, especially in young women, and QT prolongation..

[Audio] Sucralfate represents a complex of sucrose and aluminium hydroxide octasulfate capable of binding to gastric mucosa and acting as a barrier. It is not as effective as an antacid and has no anti-reflux function. Adhesion molecules, including hyaluronic acid and chondroitin sulphate carried by the carrier Poloxamer 407, act like saliva in the body, coating the esophageal mucosa, especially if damaged, and protecting it against the action of reflux. Baclofen is not approved and has only been used in a few studies. Surgical therapy is usually reserved for younger patients where medical therapy would last for decades. It allows for long-term treatment of GERD. Fundoplication is one type of surgery, where part of the fundus is bent to reduce the possibility of reflux into the esophagus. However, it is not recommended for obese patients who have undergone bariatric surgery. The indications for surgical therapy include the desire to stop medical therapy, side effects due to medical therapy, presence of a large hiatal hernia, presence of esophagitis, and recurrent or persistent symptoms. Contraindications for surgery include patients who do not respond to PPI, as their symptoms are likely not due to GERD, and surgery would not provide relief for those symptoms..

[Audio] Gastritis is a type of gastroduodenal disorder characterized by gastric mucosal damage associated with the presence of an inflammatory infiltrate. The degree of damage and distribution depend on the underlying etiology, typically involving the fundus. The diagnosis can only be confirmed through histological examination. There are two types of gastritis: acute and chronic. Acute gastritis is caused by viral infections, which accelerate cellular turnover, leading to cell damage, alteration of the gastric mucosal barrier, and acute inflammation. Non-steroidal anti-inflammatory drugs, such as NSAIDs, can also induce acute gastritis by inhibiting prostaglandins, which regulate mucus production. Other factors, like anticoagulants, age, oral route, smoking, and acetylsalicylic acid, can synergize the side effects of NSAIDs. Chronic gastritis, on the other hand, is characterized by an inflammatory infiltrate of lymphocytes and monocytes. Its causes include H. pylori infection, autoimmune disorders, stress, infectious agents, and other diseases..

[Audio] Gastritis is a condition characterized by inflammation of the stomach lining. Various causes of gastritis include Helicobacter pylori infection, drug-induced reactions, autoimmune disorders, stress, infectious agents, and exposure to external factors such as alcohol, radiation, and chemicals. Additionally, gastritis can also be caused by underlying diseases like Crohn's disease, sarcoidosis, vasculitis, and others. In some cases, the cause of gastritis may remain unknown. The histopathological classification of gastritis includes superficial, acute hemorrhagic, and chronic atrophic types..

[Audio] Body-Fundus Gastritis affects the oxyntic mucosa, resulting in an increase in gastric pH and a decrease in intrinsic factor. This type of gastritis is often associated with gastric ulcers and may lead to cancer. On the other hand, Antral Gastritis is limited to the distal part of the stomach, the antrum, and is characterized by an increased release of gastrin, leading to gastric secretions and association with duodenal ulcers. Pangastritis, meanwhile, affects the entire stomach and is typically linked to autoimmune diseases, with the production of antibodies reactive to the gastric mucosa. It may also result from a H. pylori infection with extended inflammation. When examining histological parameters for chronic gastritis, we need to consider various factors, including epithelial damage, foveolar hyperplasia, hyperemia and edema of the lamina propria, cellular infiltration, glandular atrophy, and epithelial metaplasia..

[Audio] Erosive-hemorrhagic gastropathy is a condition that results from the damage of the gastric mucosa due to various factors such as nonsteroidal anti-inflammatory drugs, alcohol consumption, and severe physical stress. These factors can reduce blood flow to the mucosa, making it fragile and susceptible to damage by gastric secretions. The condition is characterized by occult or overt bleeding in the gastrointestinal tract, which may manifest as melena or hematemesis. The bleeding can irritate the mucosa, leading to increased peristaltic activity and decreased digestion. Diagnosis is typically made through endoscopy, where erosions or subepithelial hemorrhages may be observed. In contrast, Helicobacter pylori gastritis is an inflammatory condition caused by the infection of the stomach lining with this specific bacterium. The bacterium's ability to survive in acidic environments and penetrate the mucosal layer allows it to colonize the gastric epithelium, leading to characteristic changes in the stomach lining..

[Audio] Helicobacter pylori, one of the most widespread infections worldwide, infects approximately half of the global population. The transmission route primarily involves family members through oral-oral and fecal-oral routes. Risk factors include poor socioeconomic conditions, poor hygiene, overcrowding, and infections in early childhood, which often persist throughout life. As the pathogen resides in the mucosal layer, sometimes even between epithelial cells, it triggers the production of inflammatory cytokines such as IL-1, TNF, and gastric acid, accompanied by a reduction in somatostatin..

[Audio] H. pylori's ability to penetrate the mucosa layer and release toxins, including urease, initiates a series of events that can ultimately lead to the development of an ulcer. The bacteria's presence triggers the production of inflammatory cytokines, such as IL-1 and TNF, which contribute to the erosion of the mucosa. Furthermore, H. pylori's ability to produce toxins, such as nitro compounds, antioxidant reduction, excessive dietary salts, environmental toxins, and drugs, facilitates the progression to a carcinoma. The host-related factors, including the individual's genetic predisposition and lifestyle choices, also play a crucial role in determining the severity of the condition. Ultimately, the interaction between H. pylori and the host's immune system determines the outcome of the infection, ranging from asymptomatic carriage to severe disease..

[Audio] In most cases, the symptoms of H. pylori infections are absent. However, they can present with various symptoms and signs. These may include dyspeptic symptoms, delayed gastric emptying, epigastralgia, and iron deficiency and megaloblastic anaemia, which occurs only if there is mucosal atrophy..

[Audio] Therapy for Helicobacter pylori infection is challenging because the bacteria can develop resistance to single or dual classes of antibiotics, making it difficult to achieve a 100% cure rate with a single regimen. To overcome this challenge, a combination therapy approach is often employed, which typically involves the use of proton pump inhibitors and at least two antibiotics from different classes. These antibiotics include penicillin, macrolides, imidazoles, tetracyclines, and fluoroquinolones. The rationale behind using proton pump inhibitors is to enable the mechanisms of action of the antibiotics to occur through the lumen, thereby ensuring that the bacteria are exposed to the therapeutic agents. Without proton pump inhibitors, the effectiveness of the antibiotics would be compromised. Additionally, Helicobacter pylori-related pathologies, such as primitive gastric lymphoma and peptic ulcer, require careful consideration during treatment..

[Audio] Autoimmune gastritis, also known as Type A gastritis, is a type of gastritis that is characterized by autoimmune disorders of the gastric mucosa, leading to atrophy and intestinal metaplasia. It is not rare, but less common than H. pylori gastritis, and it usually does not respond to PPI treatment. In 50% of cases, it's possible to detect antibodies against the proton pumps, resulting in a reduction of the intraluminal secretion of HCl and a decrease in the absorption of vitamin B12. This leads to the clinical picture known as Biermer disease, which involves a triad of pernicious anemia, constipation, and neurological disorders. Another type of gastritis is lymphocytic gastritis, which is characterized by the presence of inflammatory infiltrate with CD8+ T cells. The signs of gastritis can be unspecific, making it essential to take a biopsy to differentiate between different forms of gastritis. Lymphocytic gastritis often occurs in patients with celiac disease, and 80% of patients will show varioliform endoscopic lesions, resembling blisters. The diagnosis of lymphocytic gastritis is confirmed by counting more than 25 intraepithelial CD8+ lymphocytes per 100 epithelial cells. Finally, there is granulomatous gastritis, which is characterized by the presence of granulomas in the gastric mucosa. The etiology can be due to infections, sarcoidosis, or Crohn's disease, and the diagnosis is confirmed histologically..

[Audio] The Menetrier Syndrome is a rare disease of unknown etiology, characterized by the abnormal secretion or leakage of proteins into the gastric lumen, leading to symptoms such as excessive protein loss, protein loss in diarrhea, weight loss, and edema. As a gastropathy, there is no inflammation present; instead, we see hypersecretion by the stomach glands, causing the appearance of giant folds along with symptoms like pain, vomiting, and lack of appetite. Laboratory tests would show decreased total protein and albumin levels, hypochlorhydria, and endoscopy would reveal thickened folds, erosions, and ulcerations. Histological examination would confirm foveolar hyperplasia and atrophy. It's essential to differentiate Menetrier Syndrome from neoplasia and Zollinger-Ellison syndrome. Treatment options include proton pump inhibitors, and in severe cases, total gastrectomy may be necessary. Additionally, a high-protein diet can help combat protein loss..

[Audio] In Zollinger-Ellison Syndrome, there is an excessive production of gastric acid, resulting in the formation of multiple ulcers throughout the gastrointestinal tract. The condition is typically seen in individuals between 30 and 50 years old, with a male-to-female ratio of 2:1. Apart from the direct effects of hyperacidity on the mucosa, another significant symptom is pancreatic insufficiency. The acidic environment in the lumen inactivates pancreatic enzymes, leading to malabsorption, diarrhea, steatorrhea, and colitis. To diagnose this condition, doctors assess gastric acid secretions using the basic acid output (BAO) test, measuring the output of a fasting, unstimulated stomach. Additionally, gastrin serum levels and the secretin test may be used to confirm the diagnosis..

[Audio] Calcium infusion test is used to evaluate the response of gastrin-producing cells to calcium infusion in patients with Zollinger-Ellison syndrome. This test helps to confirm the diagnosis of Zollinger-Ellison syndrome, which is characterized by excessive gastrin production. The test involves infusing calcium into the patient's bloodstream, which stimulates the release of gastrin from the gastrin-producing cells. In patients with Zollinger-Ellison syndrome, this results in an exaggerated response, indicating the presence of the condition. The standard meal administration test is similar, but instead of using secretin, a meal is given to stimulate secretin production and create a constant hyperacidic state in patients with ZES. Both tests help to identify the underlying cause of the patient's symptoms and guide treatment decisions..

[Audio] Eosinophilic gastroenteritis is a condition where the body's immune system reacts abnormally to certain foods, leading to inflammation and damage in various parts of the gastrointestinal tract. This condition can affect anyone, regardless of age, but it tends to occur more frequently in children. The severity of the symptoms depends on which layer of the gut wall is affected. For example, if the mucosa is involved, patients may experience stomach pain, nausea, and vomiting. On the other hand, if the muscular layer is affected, they may suffer from abdominal pain, diarrhea, and occult bleeding. The serosa can also be involved, leading to similar symptoms..

[Audio] Muscular involvement can cause a pseudo-obstruction, which is not a true obstruction because symptoms can rapidly normalize and disappear once the disease is treated. This condition arises from a thickening of the mucosa and reduced functioning of the muscular layer. Patients may experience late vomiting, abdominal pain, serosa involvement, ascites, and the presence of numerous eosinophils..

[Audio] The patency capsule test is a safe method to determine if an object the size of a capsule used for capsule endoscopy can pass through the intestine. The test involves swallowing a capsule made of dissolvable material surrounding a tiny RFID tag. If the capsule leaves the body before it dissolves, it confirms that the intestine is suitable or 'patent' for an object of that size. If the capsule remains inside the body after 30 hours, it will dissolve into small pieces that can pass naturally through the intestine. This information is crucial for diagnosing and treating patients with gastrointestinal issues..

[Audio] Diarrhea is a common symptom characterized by an increase in the water content of the feces, resulting in increased fluidity and volume of stools. This condition is often accompanied by an increase in stool weight, frequency of bowel movements, and an urgent feeling to evacuate. In some cases, proctitis may occur, where the individual is unable to accumulate feces in the rectum. Infectious agents account for approximately 70% of acute diarrhea cases, with causes including invasive bacteria, non-invasive bacteria, viruses, and protozoa. Non-infectious causes of diarrhea include food poisoning, heavy metals, certain medications, and stress..

[Audio] Chronic gastrointestinal symptoms lasting more than four weeks affect approximately five percent of the population in Western countries. These symptoms can result from various causes, including infections such as giardiasis caused by Giardia lamblia, amebiasis caused by Entamoeba histolytica, and mycobacterial infections. Other possible causes include inflammatory bowel disease, celiac disease, microscopic colitis, autoimmune enteritis, eosinophilic enteritis, and diverticulitis. Additionally, chronic gastrointestinal symptoms may be triggered by exposure to certain drugs and toxic substances, such as antibiotics, laxatives, antacids, nonsteroidal anti-inflammatory drugs, and opioids. Furthermore, malabsorption, often resulting from maldigestion, can also lead to chronic gastrointestinal symptoms. This includes cases where the small intestine is shortened due to bowel resection, gallbladder resection, or absence of bile, as well as those with pancreatic insufficiency or gluten-sensitive enteropathy. Autoimmune disorders, ischemic enteritis, and radiation enteritis can also contribute to chronic gastrointestinal symptoms. Finally, small intestine bacterial overgrowth, often caused by excessive use of proton pump inhibitors or diabetes, can also lead to these symptoms..

[Audio] Diabetes mellitus can cause a decrease in peristalsis, resulting in constipation. On the other hand, some hormone-secreting pancreatic tumors can induce a hypersecretion of VIP, leading to a secretory diarrhea syndrome similar to cholera. The villous adenoma of the rectum can also cause a secretory diarrhea syndrome. Moreover, colon cancer can lead to paradoxical diarrhea, where patients may experience a sudden change from constipation to diarrhea due to the use of laxatives to overcome the obstacle caused by the tumor's stenosis. Additionally, irritable bowel syndrome can manifest with both diarrhea and constipation in mixed forms..

[Audio] When you ingest food and water, your body requires three times more endogenous secretions to mix the food and create a liquid environment that enables proper digestion and absorption. Only about 1.5 liters of suspension reaches the colon, mostly consisting of water and electrolytes. Ultimately, only 200 milliliters of stool form. A crucial point to note is that dietary fibers are indigestible carbohydrates. Normally, they reach the colon where they're broken down by colonic bacteria into short-chain fatty acids, particularly butyric acid. This fatty acid serves as the primary energy source for the intestinal colonic mucosa, much like glucose is essential for the brain. However, in patients without a colon, consuming fiber becomes ineffective..

[Audio] Osmotic diarrhea commences when the intraluminal osmolarity surpasses 100 mOs/Kg relative to plasma, leading to the elimination of watery stools ranging from 500 to 1000 milliliters per 24 hours. This mechanism underlies the action of laxatives, which are non-absorbable and induce an osmotic effect. Osmotic diarrhea is characterized by a positive fasting test and the absence of electrolyte and acid-base balance abnormalities. In contrast, inflammatory diarrhea is marked by watery or unformed stools exceeding 500 milliliters per day, accompanied by the presence of blood, mucus, or pus. Furthermore, additional symptoms may include tenesmus, hypokalemia, and hypochloremia, as well as metabolic alkalosis and systemic effects of the underlying disease. Weight loss is typically not observed in inflammatory diarrhea confined to the colon, except in instances where patients deliberately restrict their food intake to alleviate diarrhea. Dysmotility-induced diarrhea arises due to various diseases, encompassing reduced intestinal transit time, increased intestinal transit time, diminished intestinal motility, and systemic sclerosis. These findings underscore the significance of considering multiple factors when diagnosing and treating patients with diarrhea..

[Audio] When evaluating a patient with traveller's diarrhea, we need to consider the clinical characteristics, including the onset of symptoms within 14 days of travel and the frequency of bowel movements, which can reach up to 10 discharges per day. The etiology of this condition is typically infectious, caused by enterotoxigenic Escherichia coli, Cryptosporidium, Salmonella, Shigella, Staphylococcus aureus, or Giardia. We should look for signs of steatorrhea, characterized by pale, abundant, greasy, and shiny stools that may adhere to the toilet bowl and have a malodorous smell. To diagnose traveller's diarrhea, we must collect a complete anamnesis of the patient, including physical examination, looking for signs of pain upon palpation and performing a digital rectal examination to rule out tumours or faecalomas. Dehydration is another important aspect to assess, checking for dry mucous membranes, lifting the skin of the back of the hands, and hypotension. Blood tests can help identify inflammatory markers, while stool examination can reveal the characteristics of the faeces, including dosage of faecal fat, presence of food residues, pH, electrolytes, organic anions, bile salts, and osmolarity..

[Audio] When diagnosing and treating patients with diarrhea, microbiological examinations play a crucial role in completing the diagnosis. These examinations help identify the underlying cause of the diarrhea, whether it's a bacterial or protozoan infection. By analyzing the patient's symptoms, such as onset, duration, and stool volume, we can narrow down the list of potential pathogens. Additionally, clinical history plays a significant part in our evaluation process, as we ask the patient about their associated symptoms, including fever, pain, weight loss, and blood in their stool. Furthermore, laboratory tests can provide valuable information, especially if we're brave enough to remember some key findings. Therapy options include fluid intake, correction of electrolytic balance, and artificial nutrition, if necessary. Prescribed medications may include antibiotics, biological drugs for irritable bowel syndrome, hormones to reduce secretion, probiotics in specific situations, and antiperistaltic drugs. However, it's essential to note that inflammatory diarrhea can increase the risk of microbial invasion, leading to complications such as bacteremia and sepsis..

[Audio] Constipation is a condition in which a person has a decreased frequency of bowel movements, less than three times a week, along with at least two of the following symptoms for a minimum of three months. These symptoms include passing hard stools in 25% of cases, feeling like the bowels were not fully emptied in 25% of cases, and needing to forcefully evacuate. Epidemiological data shows that constipation is a prevalent issue in developed countries, affecting approximately 2% of the population in the United States. Women are more commonly affected, with a four times higher rate than men, which is primarily due to the effects of progesterone on bowel movement. The elderly and hospitalized individuals are also at a higher risk of experiencing constipation. There are two main types of constipation - organic and functional. Organic constipation is a result of an underlying intestinal disease, such as tumors, narrowing of the intestines, or damage to the muscles, leading to a large colon or rectum. Functional constipation, on the other hand, is caused by diet, irritable bowel syndrome, or external factors..

[Audio] Constipation is a common issue in pediatric patients, especially those with Hirschsprung disease. This condition is characterized by an underdeveloped nervous system, leading to abnormal muscle activity and an enlarged colon. A thorough evaluation of the patient's symptoms is necessary for diagnosing constipation, including the presence of rectocele, rectal prolapse, and stenotic mechanisms. These conditions may cause changes in stool consistency, such as normal or hard stools becoming watery due to laxative use. The diagnosis of constipation involves endoscopy, radiological, and physical examinations, as well as assessing dyssynergy, rectocele, and megacolon. Intestinal factors, descending perineum, and hypertonia of the internal anal sphincter are common causes of abdominal and pelvic dyssynergia..

[Audio] The rectum has a significant role in the process of defecation. It starts below the S2 vertebra and extends for 15 centimeters. It follows the curve of the coccyx and then enters the anus, forming a reservoir called the ampulla with a maximum diameter of six centimeters for storing feces. The ampulla opens into the anus at a right angle. When it is stretched, it triggers the urge to defecate. The internal anal sphincter, which is not under voluntary control, relaxes to allow the feces to enter the rectum. The puborectalis muscle also relaxes, helping to straighten the rectum. Hyperperistaltic activity in the sigmoid colon aids in moving the feces towards the rectum. The abdominal muscles compress to discharge the feces, while the voluntary relaxation of the external anal sphincter enables the patient to control the release of stool during defecation..

[Audio] Functional constipation is a condition that is widespread and affects individuals all around the world. As healthcare professionals, it is critical to be knowledgeable about the different causes of this condition, as they can significantly impact the effectiveness of treatment. There are three main categories of functional constipation: those related to diet, irritable bowel syndrome (IBS), and extraintestinal causes. Diet-related constipation usually begins in childhood and is often connected to low fiber intake, irritable bowel, and changes in periods of diarrhea. This type of constipation may not respond well to traditional treatments like fiber supplements or laxatives. On the other hand, IBS-related constipation is typically characterized by a mixed pattern of alternating constipation and diarrhea. In these situations, constipation may persist even with a sufficient intake of fiber, and alternative treatment methods may be necessary. Extraintestinal causes of functional constipation include endocrine disorders like Addison's disease, hypothyroidism, hyperparathyroidism, pheochromocytoma, pregnancy, and certain medications. These medical conditions can disrupt normal bowel function and lead to constipation. It is essential for healthcare providers to thoroughly evaluate each patient's medical history, including any potential extraintestinal causes, to develop effective treatment plans. By understanding the underlying causes of functional constipation, healthcare professionals can provide targeted interventions and improve patient outcomes..

[Audio] When conducting the first medical visit for constipation, our objective is multifaceted. Recognizing the type of constipation, taking into account the patient's symptoms and definitions of constipation, is essential. This involves understanding the patient's experience and identifying any underlying conditions that may be contributing to their symptoms. We also establish a relationship with the patient, building trust and rapport through open communication. Determining the honest and subsequent developments, gathering information about the patient's history, including any previous treatments or medications they have taken, is crucial. Furthermore, we determine the purpose of the visit since the onset of the condition, clarifying the patient's expectations and goals for treatment. Additionally, we assess the environmental, psychological, dietary factors and comorbidities, examining how these factors may be impacting the patient's symptoms. Finally, we search for faecal impaction and anorectal disorders, using various diagnostic tests such as barium enema, study of transit time, ano-rectal or colonic manometry, defecography, and anal US. These tests help us identify any structural abnormalities or functional issues that may be contributing to the patient's constipation. By taking a comprehensive approach to diagnosing and treating constipation, we can provide effective care and improve the patient's quality of life..