G disease.docx

Gastroesophageal Reflux Disease (GERD)  GERD is caused by gastric contents that enters the esophagus primarily due to the relaxation of the lower esophageal sphincter (LES).  The influx of chyme from the stomach into the esophagus results in inflammation leading to reflux esophagitis. It is typical...

Gastroesophageal Reflux Disease (GERD)  GERD is caused by gastric contents that enters the esophagus primarily due to the relaxation of the lower esophageal sphincter (LES).  The influx of chyme from the stomach into the esophagus results in inflammation leading to reflux esophagitis. It is typically caused by an incompetent LES, hiatal hernia, gastroparesis, and obesity. The LES plays a critical role in the development of GERD symptoms. In an LES defect, the decreased tone of the LES allows acid to flow from the stomach into the esophagus, which results in the burning sensation that patients report.  The worse the LES tone, the more reflux the patient will have. In examining the diagram below, the LES is not a true anatomical sphincter because there is no connection.  Instead it is composed of smooth muscles in the distal esophageal area that causes it to close and open during swallowing. When the LES opens repeatedly over a long period of time, stomach contents can enter the esophageal area leading to the symptomatic burning.  From the diagram to the right, you can see that LES sphincter is never fully closed with GERD. When evaluating a patient with GERD, the NP must consider the types of presenting symptoms. It is easy to evaluate typical GERD symptoms. But, with atypical and associated symptoms, the patient may not realize that these also reflect GERD.  The typical, atypical and associated symptoms are listed below.  Whether the symptoms are atypical or associated, all have heartburn and reflux in common.  **Typical Symptoms** Atypical symptoms:Hoarseness,Chronic sore throat,Chronic cough,Wheezing/asthma-can exacerbate asthma symptoms ,Dental erosions, Non-cardiac chest pain GERD Risk Factors and Warning Signs Some individuals have risk factors for the development of GERD. Obesity is a risk factor that worsens not only the symptoms of GERD, but also its complications (i.e. Barrett's Esophagus; esophageal cancer). A hiatal hernia can trap gastric contents above the diaphragm which can also worsen GERD symptoms. Additionally, some medications can worsen GERD symptoms, such as calcium channel blockers, antibiotics and bisphosphonates. Finally, pregnancy is also a condition that can worsen GERD symptoms due to pressure that pushes the stomach above the diaphragm.    Helicobacter pylori (H. pylori) is a gram-negative bacterium that is associated with GERD. Most individuals world-wide have been exposed to H. pylori at some time. Although most individuals never develop symptoms, some do. Complications of H. pylori include dyspepsia and adenocarcinoma.   With an understanding of the typical, atypical and associated symptoms of reflux and its risk factors, it is extremely important to consider the patient's history when he or she presents to the office. The patient will often report burning or reflux that occurs 30-90 minutes following a meal; the symptoms are worse in a reclining position, but symptoms improve with sitting or standing or when an antacid is taken.  Sour taste, lump in the throat, cough, hoarseness, worsening asthma episodes, epigastric pain and chest pain may also be reported.   As providers, we are always concerned about any patient that presents with chest pain.  In these patients, a cardiac cause should be ruled out first, especially in older individuals who have cardiac risk factors and co-morbidities such as diabetes.  Warning signs for GERD should also be explored and include:  [Transcript Link](https://items.adtalem.edapt.ai/student-activity.html?cId=45d809bd-30b4-4754-ae90-a97c9dd3553c&classroomId=4fb298d3-e60c-4056-8de2-67efca758132&previewStep=1&stepIndex=1) ✖ **Warning signs for GERD should also be explored and include: ** Symptoms over the age of 50.  Dysphagia (difficulty with swallowing food).  Odynophagia (pain on swallowing).  Nausea and vomiting.  Weight loss.  Melena.   Early satiety (feeling full after eating very little food).  During collection of the social, diet and medication history, the NP should explore if the patient smokes or drinks alcohol, ingests foods that triggers reflux (i.e. peppermint and chocolate) or takes medications which may be predispose the patient to GERD by relaxing the LES allowing for the reflux of acid. A diagnosis of GERD can often be made on patient history alone, especially when the patient presents with the typical symptoms of heart burn and regurgitation and have no warning signs. Additional diagnostic tests may be performed when it is unclear if the patient's symptoms are due to acid reflux. These tests require a referral to a gastroenterologist and may be used to establish the diagnosis:  - Upper GI series  - Endoscopy  - Esophageal manometry  - Esophageal pH   Treatment Treatment goals include:  - Eliminating symptoms  - Healing esophagitis  - Preventing the relapse or development of complications    - Decreasing the amount of acid that refluxes from the stomach back to the esophagus     Management In many patients, GERD is a chronic, relapsing disease and long-term treatment may be needed to control symptoms and prevent complications. Maintenance therapy will vary in individuals and may include simple lifestyle modifications, over the counter antacids or prescription medication. Proton-pump inhibitors (PPI) are the gold standard for treating GERD when it's required. All PPIs are considered effective for treating reflux. The NP must be mindful of the dosage and length of therapy recommendations when prescribing a PPI as well as each patient's severity of symptoms.  For example, in mild, intermittent GERD (\  - Elevating the head of bed  - Avoiding food 2-3 hours prior to bedtime  - Eliminating trigger foods.  Although trigger foods can vary for individuals, some of the universal trigger foods include chocolate, caffeine, alcohol or spicy and acidic food.   © 2022 Chamberlain University LLC. All rights reserved. Hiatal Hernia  A hiatal hernia is a diaphragmatic hernia that protrudes (herniates) through the upper part of the stomach through the diaphragm and into the thorax due to dilation of the gastroesophageal junction (GJ).   There are four types of hiatal hernias:   1. Sliding hiatal hernia. This is where the junction of the esophagus slides up past the GE junction.  2. Paraesophageal hernia. In a paraesophageal hernia, the contents of the abdomen slide up around the esophagus and into the chest. The GE junction in the type 2 hernia does not go up into the chest.  3. Mixed hiatal hernia. This is a combination of both Type 1 and Type 2 hernias. The GE junction slides up into the chest and the fundus of the stomach slides up and around.   4. The type 4 hernia is an aggravated Type 3 where other organs other than the stomach slide up into the chest including the colon and small bowel and spleen.  Patients who present with a hernia are often asymptomatic. When symptoms do develop, it is usually later in life and associated with other gastrointestinal disorders including GERD symptoms such as heartburn, regurgitation, dysphagia and epigastric pain. Hernia strangulation is a complication of the hernia and results in ischemia. Symptoms include acute, severe chest of epigastric pain, nausea, vomiting and GI bleeding.    Bowel Obstruction  In a bowel obstruction, the patient presents with nausea, vomiting, cramping abdominal pain, constipation, diarrhea, distended abdomen, fever, tachycardia. It can be of the small intestine or the large intestine. In an obstruction, the food "piles up". Normally in the intestine, we find bacteria but when the bacteria are exposed to food stuck in the stomach, it will begin to grow.   Bowel obstruction can be categorized into mechanical and pseudo-obstructions:  Mechanical Obstructions There are 5 types of mechanical obstructions:   1. Adhesion: in an adhesion, two parts of the bowel are connected to one another by a fibrous band to create the obstruction; It is the most common type and can occur post-surgically if scar tissue forms. The fibrous adhesions between the bowel segments results in extrinsic compression of the bowel that can lead to an obstruction.  2. Tumor: A tumor is growth in the bowel as in the case of colorectal cancer; The risk factors for the development of a bowel tumor includes age, family, obesity, inflammatory bowel disease and diet. As the tumor enlarges, the it can lead to an obstruction.   3. Intussusception:  this is a condition where part of the bowel invaginates itself. Intussusception occurs when part of the bowel goes into the other part of the bowel.  The part of the bowel that is located on the outside is the intussusception. The most common site of obstruction is the ileocecal valve. Bowel obstruction due to intussusception is rare in adults.   4. Hernia: A hernia occurs when an organ or tissue protrudes through a weak spot in the muscle or connective tissue. Common sites include the cecum and sigmoid area of the colon into the inguinal canal.  5. Volvulus:  A volvulus is the twisting of the bowel. Common sites include the cecum and sigmoid area of the colon. A small bowel adhesion can lead to a Volvulus.   Pseudo Obstruction Pseudo obstructions are false obstructions due to myopathy or neuropathy. These result in false obstructions because there is no actual structural factor involved or no contents within the bowel that leads to the obstruction.   1. Myopathy: In myopathy, the bowel muscle does not function. This can result in the patient having no bowel movement that leads to an obstruction.    2. Neuropathy: Neuropathy is an issue of nerve innervation within the bowel. Decreased innervation or no innervation of the bowel's smooth muscle results in abnormal movement of contents through the bowel. Hirschsprung's disease, for example, is a congenital condition where the nerves are missing at the distal end of the colon that results in no muscle innervation or peristaltic contractions. This can be corrected by surgery. The types of bowel obstructions are depicted below.   3. Peptic Ulcer Disease (PUD)  4. Peptic ulcer disease (PUD) is defined as a break or ulceration in the protective mucosal lining of the lower esophagus, stomach, or duodenum. As a result, severe inflammation occurs that can penetrate the submucosa. The diagram below compares the lesions of PUD. An erosion does not penetrate the mucosa as deeply as an ulcer, which extends well into submucosa.    5. 6. ulcers are distinguished according to their location in the GI tract. The two most common types of peptic ulcers that are seen in clinical practice are duodenal and gastric ulcers. Risk factors highly associated with peptic ulcers include Nonsteroidal Anti-inflammatory Drug (NSAID) use and H. pylori infections.  7. NSAIDS suppress mucosal prostaglandin synthesis which results in decreased bicarbonate and mucin secretion and the production and increased secretion of hydrochloric acid.  H. pylori is a gram-negative bacterium that is only found in the gastric epithelium. It produces NH3 (urease) to decrease acid production. H. pylori does not favor an acid environment. Therefore, its production of urease neutralizes stomach acid.  Protease production promotes the movement of H. pylori into the gastric mucosa. Duodenal and Gastric Ulcers --------------------------- Duodenal Ulcer  --------------- Duodenal ulcers occur in the lining of the upper most part of the small intestine just after the stomach most commonly due to a H. pylori infection which results in inflammation and ulceration of the gastric mucosa.  Hypersecretion of stomach acid and pepsin occur primarily due to NSAID use and smoking. Symptoms of duodenal ulcers include GI bleeding and stomach pain that decreases after a meal. There is no risk to the progression of cancer with a duodenal ulcer.  Gastric Ulcer  -------------- Gastric ulcers are commonly located in the antral region of the stomach. There is increased permeability to hydrogen ion in the stomach mucosa that increases the amount of acid, whereas a H. Pylori infection causes direct effects on the mucosa. Symptoms include GI bleeding, GI discomfort and pain that increases after a meal. Long-standing inflammation can lead to stomach cancer. Patients with gastric ulcers are monitored with serial esophagogastroduodenoscopies (EGD) and biopsy. Gastric ulcers that progress to gastric cancer may be asymptomatic which is why serial monitoring is important. If symptoms are present, they are usually non-specific: weight loss, abdominal pain, dysphagia, indigestion, heartburn, anemia, or hematemesis. Once symptoms occur, the cancer is often advanced and incurable.  Inflammatory bowel disease is chronic and relapsing. Although the origin is unknown, it is associated with genetics, alterations of the epithelial barrier functions, immune reactions to the intestinal flora and abnormal T-cell responses.  A predisposition for developing IBD seems to be triggered by some unknown mechanism possibly related to the result of an infections (campylobacter or salmonella) within the large and/or small intestine. It seems to be a combination of a genetic predisposition and environmental factors that lead to the immune system to attacking the GI tract.  The two most common IBD diseases are Ulcerative Colitis and Crohn Disease.  There is also similarity and overlap of the symptoms as well as the associated risk factors. Risk factors for Ulcerative Colitis and Crohn's Disease:   1\. Age-diagnosed highest between the ages of 15-45 and between the ages of 60-80  2\. Family history-especially someone with an immediate family member with the disease  3\. History of smoking, especially in Crohn's Disease  4\. High fat diet, especially in Ulcerative Colitis  5\. History of salmonella or campylobacter infection that often cause infections of the GI tract  Crohn's disease Crohn disease is an inflammatory bowel disease (IBD) that presents with an array of signs and symptoms. It has an insidious onset that is characterized by intermittent low-grade fever, diarrhea and right lower quadrant (RLQ) pain and tenderness. On occasion, a right lower quadrant (RLQ) mass can be palpated. Chronic inflammation associated with Crohn's disease can eventually lead to perianal disease with abscess and fistulas.   The NP must rely on excellent history taking skills to gain a comprehensive understanding of the patient's signs and symptoms. When collecting the patient's history, the NP should ask about any low-grade fevers, weight loss, fatigue, presence of abdominal pain and the number and consistency of bowel movements per day. Patients with Crohn's disease will typically describe the bowel movements as diarrhea, usually non-bloody with fecal urgency. Cramping or persistent RLQ or periumbilical pain is also characteristic. Any past abdominal surgeries should also be obtained.   On physical exam, the NP should focus on obtaining the patient's temperature, weight and nutritional status. A thorough abdominal exam should be performed, especially assessing for abdominal tenderness or mass, and a rectal exam should be performed to assess for blood. The NP should also assess extra-intestinal manifestations including arthralgias, arthritis, iritis or uveitis, aphthous skin lesions, or gallstones.   For diagnosis, the NP will obtain a complete blood count (CBC) and serum albumin. The presence of anemia will alert the NP that the inflammation is chronic. If anemic, the patient may have mucosal blood loss or vitamin B12 malabsorption. If leukocytosis is present, the NP may suspect inflammation or abscess formation.  The albumin level may be low (hypoalbuminemia) due to loss of protein, chronic inflammation and malabsorption. A sedimentation rate and C-reactive protein may be elevated which reflects active inflammation.  One very helpful non-invasive test is fecal calprotectin. Elevation of fecal calprotectin reflects active inflammation. Finally, stool samples may be obtained to identify clostridium difficile colitis. Endoscopy and colonoscopy may be performed throughout the disease process for monitoring.   Pharmacological management may include the use of aminosalicylic acid (5-ASA), corticosteroids, immunomodulating drugs, biologic therapies, and Janus kinase inhibitors.  Fortunately, most patients usually have a non-progressive disease course of Crohn disease or ulcerative colitis.  Remember that the goal of patient management is to reduce inflammation, improve quality of life, and reduce the risk of surgery and hospitalization.   Location of inflammation - exact mechanism and cause of inflammation unknown. Lesion: occur anywhere from the mouth to the anus proceeding in a discontinuous and skip lesion pattern. Gaps between inflamed areas are normal. Most common area of inflammation is the terminal ileum of the small intestine; the second most common area of inflammation is the large intestine. Pathology: Macrophages and neutrophils attack the intestinal wall causing damage due to inflammation. This results in lesions that extend through all three layers of the intestinal wall (transmural inflammation) -- it is one of the most important pathological distinction between Crohn's disease and ulcerative colitis. T-cell lymphocytes infiltrate to cause transmural inflammation which overtime, forms another type of lesions (non-caseating granuloma), that indicates chronic inflammation 1. Complications: Crypt abscesses, in which the epithelium of the crypt breaks down and the lumen fills with polymorphonuclear cells, occur as inflammation progresses which may result in mild fever. Abscesses can rupture leading to peritonitis. Identification of an abscess prompts treatment with intravenous antibiotic therapy and drainage to prevent rupture.  2. Fistula formation occurs when worsening inflammation results in tunneling between two structures with the lumen of one section of bowel in communication with a different section of bowel. A fistula location can be anywhere a lesion is adjacent to an area (i.e. fistula between a segment of bowel and the bladder). Fistulas are associated with pain and severe infection which usually requires surgical intervention.  3. Obstruction.  4. Malabsorption of vitamins A, D, B12 if there have been multiple surgical procedures.  5. Colon cancer.  Ulcerative colitis Ulcerative colitis is an inflammatory bowel disease (IBD) that involves the mucosal surface of the colon. Chronic inflammation results in erosion and bleeding. There is potential for the entire colon to be affected. However, involvement may only include the distal portion of the colon or extend into the colon proximal to the distal colon, even to the point where the total colon is involved (total colitis). The disease is characterized by periods of flare-up and remission. Patients are usually classified according to the severity of the disease as mild, moderate, or severe. On collection of the patient's history, the NP should ask, about the frequency of stools and the presence of rectal bleeding. Bloody diarrhea is the hallmark sign of ulcerative colitis. Patients will also complain of abdominal cramping, fecal urgency and tenesmus (a continual or recurrent inclination to evacuate the bowels). Extra-intestinal symptoms may also be present such as arthralgias, arthritis, iritis or uveitis, aphthous skin lesions, or gallstones.   On physical exam, the NP should focus on the patient's volume status by checking orthostatic blood pressure, pulse and nutritional state. Signs of dehydration should be identified as well.  A thorough abdominal exam should be performed to identify abdominal tenderness along with a rectal exam to identify blood.   For diagnosis, the NP will obtain a complete blood count (CBC), serum albumin and inflammatory markers (erythrocyte sedimentation rate and C-reactive protein).  The state of the disease is reflected in the degree of abnormality of the results. A sigmoidoscopy is the key to diagnosing the disease. The mucosa will be edematous with mucopus and erosions. In more severe disease, there will be deep ulceration and spontaneous bleeding. A colonoscopy should not be performed in more severe disease due to the risk of perforation. Once the patient is treated and has improved, a colonoscopy can be performed to determine the extent of the disease.   The goals of treatment for ulcerative colitis are to alleviate acute symptoms and prevent their reoccurrence. Pharmacological management may include the use of aminosalicylic acid (5-ASA), corticosteroids, immunomodulating drugs, biologic therapies, and Janus kinase inhibitors.  Exact mechanism and cause of inflammation unknown.  Lesion: Begins in the rectum and moves backward to the sigmoid colon in a continuous fashion (subtotal colitis). Inflammation can extend beyond the rectum and sigmoid colon to include the entire colon (total colitis). Inflammation completely contained within the large intestine. Macrophages and neutrophils attack the intestinal wall causing damage due to inflammation.  Lesions do not extend all the way through the intestinal wall (only through the mucosa and submucosa) it is one of the most important pathological distinction between Crohn's disease and ulcerative colitis. T-cell lymphocytes infiltrate to cause mucosal and submucosal inflammation and overtime, forms another type of lesions (non-caseating granuloma) that indicates chronic inflammation.   Complications : 1. Crypt abscesses, in which the epithelium of the crypt breaks down and the lumen fills with polymorphonuclear cells, occur as inflammation progresses which may result in mild fever. Abscesses can rupture leading to peritonitis. Identification of an abscess prompts treatment with intravenous antibiotic therapy and drainage to prevent rupture.  2. Pseudo-polyp formation occurs with worsening inflammation causing thinning of the mucosal and submucosal layers in an uneven pattern. Has the appearance of a polyp protruding out of the intestinal wall, but not an actual growth. \*\*  3. Colon cancer