PEPTIC ULSER

Background History
A 65-year-old African American woman presented to the emergency room complaining of worsening of breath and palpitations for about 1 week. She reports feeling "dizzy" on and off for the past year: the dizziness is associated with weakness that has been worsening for the past month. She was been feeling "too tired" to even walk to her backyard and water her flower bed that she use to do "all the time". She has been so dyspneic walking up the stairs at her home that she move down stairs to the guest room about a week ago. Review of systems is significant for knee pain, for which she frequently takes aspirin or ibuprofen; otherwise the review of systems is negative.
She has no significant medical history and has not been to a doctors in several years. She has a normal well-woman examination and screening colonoscopy about 5 years ago. She occasionally has an alcoholic drink and denies tobacco or drugs use. She is married and is a retired shopkeeper. On examination, her blood pressure is 150/85 mmhg; her pulse is 98 beats/min; her respiratory rate is 20 breaths/min; and O2 saturation in 99% on room air. Her temperature is 98,7° F (37.1°C); siginificants findings on examination include conjungtival pallor, mild tenderness with deep palpation in the epigastric and left upper quadrant (LUQ) region of the abdomen with normal bowel sounds, and no organomegaly but a positive stool guaiac test. The remainder of the examination, including respiratory, cardiovascular, and nervous systems, was normal.







KEYWORDS

A 65 years old woman
Worsening shortness of breath and palpitations for about 1 week
Feeling dizzy for the past year
Feeling too tired
Dyspneic waliking up the stairs and downstairs at home about a week ago
Knee pain
Take aspirin or ibuprofen as pharmacology
An alcoholic and denies tobacco and drugs
She is married
BP: 150/85 mmhg
P: 98 beats/min
Conjungtival pallor and mild tenderness
Deep palpation in the epigastric and left upper quadrant region abdomen
Guaiac test (+)















THEORY


Gastric and duodenal ulcers usually cannot be differentiated based on history alone, although some findings may be suggestive (see Diagnosis). Epigastric pain is the most common symptom of both gastric and duodenal ulcers. It is characterized by a gnawing or burning sensation and occurs after meals—classically, shortly after meals with gastric ulcer and 2-3 hours afterward with duodenal ulcer.
In uncomplicated peptic ulcer disease (PUD), the clinical findings are few and nonspecific. "Alarm features" that warrant prompt gastroenterology referral[1]include bleeding, anemia, early satiety, unexplained weight loss, progressive dysphagia or odynophagia, recurrent vomiting, and family history of GI cancer. Patients with perforated PUD usually present with a sudden onset of severe, sharp abdominal pain. (See Clinical Presentation.)
In most patients with uncomplicated PUD, routine laboratory tests usually are not helpful; instead, documentation of PUD depends on radiographic and endoscopic confirmation. Testing for H pylori infection is essential in all patients with peptic ulcers. Rapid urease tests are considered the endoscopic diagnostic test of choice. Of the noninvasive tests, fecal antigen testing is more accurate than antibody testing and is less expensive than urea breath tests. A fasting serum gastrin level should be obtained in certain cases to screen for Zollinger-Ellison syndrome. (See Workup.)
Upper GI endoscopy is the preferred diagnostic test in the evaluation of patients with suspected PUD. Endoscopy provides an opportunity to visualize the ulcer, to determine the presence and degree of active bleeding, and to attempt hemostasis by direct measures, if required. Perform endoscopy early in patients older than 45-50 years and in patients with associated so-called alarm features.
Most patients with PUD are treated successfully with cure of H pylori infection and/or avoidance of nonsteroidal anti-inflammatory drugs (NSAIDs), along with the appropriate use of antisecretory therapy. In the United States, the recommended primary therapy for H pylori infection is proton pump inhibitor (PPI)–based triple therapy.[1] These regimens result in a cure of infection and ulcer healing in approximately 85-90% of cases.[2] Ulcers can recur in the absence of successful H pylori eradication. (See Treatment and Management.)
In patients with NSAID-associated peptic ulcers, discontinuation of NSAIDs is paramount, if it is clinically feasible. For patients who must continue with their NSAIDs, proton pump inhibitor (PPI) maintenance is recommended to prevent recurrences even after eradication of H pylori.[3, 4] Prophylactic regimens that have been shown to dramatically reduce the risk of NSAID-induced gastric and duodenal ulcers include the use of a prostaglandin analog or a PPI. Maintenance therapy with antisecretory medications (eg, H2 blockers, PPIs) for 1 year is indicated in high-risk patients. (See Medication.)
The indications for urgent surgery include failure to achieve hemostasis endoscopically, recurrent bleeding despite endoscopic attempts at achieving hemostasis (many advocate surgery after 2 failed endoscopic attempts), and perforation.
Patients with gastric ulcers are also at risk of developing gastric malignancy




INVESTIGATION
To diagnose an ulcer, you may need a test called an upper endoscopy (EGD).
This is a test to examine the lining of the esophagus (the tube that connects your throat to your stomach), stomach, and first part of the small intestine.
It is done with a small camera (flexible endoscope) that is inserted down the throat.
This test most often requires sedation given through an IV

Upper endoscopy is done on most people when peptic ulcers are suspected or when you:
Have a low blood count (anemia)
Have trouble swallowing
Are vomiting blood or your stools are blood or dark and tarry looking
Have been losing weight without trying
Testing for H. pylori is also needed.
Other tests you may have include:
Hemoglobin blood test to check for anemia
Stool occult blood test to test for blood in your stool
Sometimes, you may need a test called an upper GI series. A series of x-rays are taken after you drink a thick substance called barium. This does not require sedation.

ETIOLOGY

Peptic ulcer disease (PUD) may be due to any of the following:
H pylori infection
Drugs
Lifestyle factors
Severe physiologic stress
Hypersecretory states (uncommon)
Genetic factors

Additional etiologic factors
Any of the following may be associated with PUD:
Hepatic cirrhosis
Chronic obstructive pulmonary disease
Allergic gastritis and eosinophilic gastritis
Cytomegalovirus infection
Graft versus host disease
Uremic gastropathy
Henoch-Schönlein gastritis
Corrosive gastropathy
Celiac disease
Bile gastropathy
Autoimmune disease
Crohn disease
Other granulomatous gastritides (eg, sarcoidosis, histiocytosis X, tuberculosis)
Phlegmonous gastritis and emphysematous gastritis
Other infections, including Epstein-Barr virus, HIV, Helicobacter heilmannii,herpes simplex, influenza, syphilis, Candida albicans , histoplasmosis,mucormycosis, and anisakiasis
Chemotherapeutic agents, such as 5-fluorouracil (5-FU), methotrexate (MTX), and cyclophosphamide
Local radiation resulting in mucosal damage, which may lead to the development of duodenal ulcers
Use of crack cocaine, which causes localized vasoconstriction, resulting in reduced blood flow and possibly leading to mucosal damage


























SYMPTOMS
Small ulcers may not cause any symptoms. Some ulcers can cause serious bleeding.
Abdominal pain is a common symptom. The pain can differ from person to person, and some people have no pain.

Other symptoms include:
Feeling of fullness and problems drinking as much fluid as usual
Hunger and an empty feeling in the stomach, often 1 to 3 hours after a meal
Mild nausea that may go away with vomiting
Pain or discomfort in the upper abdomen
Pain in the upper abdomen that wakes you up at night
Other possible symptoms include:
Bloody or dark tarry stools
Chest pain
Fatigue
Vomiting, possibly bloody

PATHPHYSIOLOGY

Peptic ulcers are defects in the gastric or duodenal mucosa that extend through the muscularis mucosa. The epithelial cells of the stomach and duodenum secrete mucus in response to irritation of the epithelial lining and as a result of cholinergic stimulation. The superficial portion of the gastric and duodenal mucosa exists in the form of a gel layer, which is impermeable to acid and pepsin. Other gastric and duodenal cells secrete bicarbonate, which aids in buffering acid that lies near the mucosa. Prostaglandins of the E type (PGE) have an important protective role, because PGE increases the production of both bicarbonate and the mucous layer.
In the event of acid and pepsin entering the epithelial cells, additional mechanisms are in place to reduce injury. Within the epithelial cells, ion pumps in the basolateral cell membrane help to regulate intracellular pH by removing excess hydrogen ions. Through the process of restitution, healthy cells migrate to the site of injury. Mucosal blood flow removes acid that diffuses through the injured mucosa and provides bicarbonate to the surface epithelial cells.
Under normal conditions, a physiologic balance exists between gastric acid secretion and gastroduodenal mucosal defense. Mucosal injury and, thus, peptic ulcer occur when the balance between the aggressive factors and the defensive mechanisms is disrupted. Aggressive factors, such as NSAIDs, H pylori infection, alcohol, bile salts, acid, and pepsin, can alter the mucosal defense by allowing back diffusion of hydrogen ions and subsequent epithelial cell injury. The defensive mechanisms include tight intercellular junctions, mucus, mucosal blood flow, cellular restitution, and epithelial renewal.
The gram-negative spirochete H pylori was first linked to gastritis in 1983. Since then, further study of H pylori has revealed that it is a major part of the triad, which includes acid and pepsin, that contributes to primary peptic ulcer disease. The unique microbiologic characteristics of this organism, such as urease production, allows it to alkalinize its microenvironment and survive for years in the hostile acidic environment of the stomach, where it causes mucosal inflammation and, in some individuals, worsens the severity of peptic ulcer disease.
When H pylori colonizes the gastric mucosa, inflammation usually results. The causal association between H pylori gastritis and duodenal ulceration is now well established in the adult and pediatric literature. In patients infected with H pylori,high levels of gastrin and pepsinogen and reduced levels of somatostatin have been measured. In infected patients, exposure of the duodenum to acid is increased. Virulence factors produced by H pylori, including urease, catalase, vacuolating cytotoxin, and lipopolysaccharide, are well described.
Most patients with duodenal ulcers have impaired duodenal bicarbonate secretion, which has also proven to be caused by H pylori because its eradication reverses the defect.[5] The combination of increased gastric acid secretion and reduced duodenal bicarbonate secretion lowers the pH in the duodenum, which promotes the development of gastric metaplasia (ie, the presence of gastric epithelium in the first portion of the duodenum). H pylori infection in areas of gastric metaplasia induces duodenitis and enhances the susceptibility to acid injury, thereby predisposing to duodenal ulcers. Duodenal colonization by H pylori was found to be a highly significant predictor of subsequent development of duodenal ulcers in one study that followed 181 patients with endoscopy-negative, nonulcer dyspepsia.

COMPLICATIONS
Untreated ulcers can become worse over time and lead to other, more serious health complications, such as:
Perforation: A hole develops in the lining of the stomach or small intestine and causes an infection. A sign of a perforated ulcer is sudden, severe abdominal pain.
Internal bleeding: Bleeding ulcers can result in significant blood loss and thus require hospitalization. Signs of a bleeding ulcer include lightheadedness, dizziness, and black stools.
Scar tissue: This is thick tissue that develops after an injury. This tissue makes it difficult for food to pass through your digestive tract. Signs of scar tissue include vomiting and weight loss.
All three complications are medical emergencies that require surgery. Call your doctor if you feel dizzy or if symptoms return. Seek urgent medical attention if you experience the following symptoms:
sudden, sharp abdominal pain
fainting, excessive sweating, or confusion, as these may be signs of shock
blood in vomit or stool
abdomen that's hard to the touch


MEDICAL TREATMENT AND EDUCATIONS

Medical treatment
In order for your ulcer to heal and to reduce the chance it will come back, you will be given medicines to:
Kill the H. pylori bacteria (if present)
Reduce acid levels in the stomach
Take all of your medicines as you have been told. Other changes in your lifestyle can also help.
If you have a peptic ulcer with an H. pylori infection, the standard treatment uses different combinations of the following medicines for 7 to 14 days:
Two different antibiotics to kill H. pylori
Proton pump inhibitors such as omeprazole (Prilosec), lansoprazole (Prevacid), or esomeprazole (Nexium)
Bismuth (the main ingredient in Pepto-Bismol) may be added to help kill the bacteria
If you have an ulcer without an H. pylori infection, or one that is caused by taking aspirin or NSAIDs, you will likely need to take a proton pump inhibitor for 8 weeks.
You may also be prescribed this type of medicine regularly if you must continue taking aspirin or NSAIDs for other health conditions.
Other medicines used for ulcers are:
Misoprostol, a drug that may help prevent ulcers in people who take NSAIDs on a regular basis
Medicines that protect the tissue lining (such as sucralfate)
If a peptic ulcer bleeds a lot, an EGD may be needed to stop the bleeding. Methods used to stop the bleeding include:
Injecting medicine in the ulcer
Applying metal clips to the ulcer
Surgery may be needed if:
Bleeding cannot be stopped with an EGD
The ulcer has caused a tear

Educations
Patients should be warned of known or potentially injurious drugs and agents. Some examples are as follows:
NSAIDs
Aspirin
Alcohol
Tobacco
Caffeine (eg, coffee, tea, colas)
Obesity has been shown to have an association with peptic ulcer disease (PUD), and patients should be counseled regarding benefits of weight loss. Stress reduction counseling might be helpful in individual cases but is not needed routinely.
For patient education resources, see Digestive Disorders Center as well as Peptic Ulcers, Heartburn, and Understanding Heartburn/GERD Medications.
Lifestyle change
Discontinue NSAIDs and use Acetaminophen for pain control if possible.
Acid suppression--Antacids
Smoking cessation
No dietary restrictions unless certain foods are associated with problems.
Alcohol in moderation
Men under 65: 2 drinks/day
Men over 65 and all women: 1 drink/day
Stress reduction

PROGNOSIS

When the underlying cause is addressed, the prognosis is excellent. Most patients are treated successfully with eradication of H pylori infection, avoidance of NSAIDs, and the appropriate use of antisecretory therapy. Eradication of H pylori infection changes the natural history of the disease, with a decrease in the ulcer recurrence rate from 60-90% to approximately 10-20%. However, this is a higher recurrence rate than previously reported, suggesting an increased number of ulcers not caused by H pylori infection.
With regard to NSAID-related ulcers, the incidence of perforation is approximately 0.3% per patient year, and the incidence of obstruction is approximately 0.1% per patient year. Combining both duodenal ulcers and gastric ulcers, the rate of any complication in all age groups combined is approximately 1-2% per ulcer per year.
The mortality rate for PUD, which has decreased modestly in the last few decades, is approximately 1 death per 100,000 cases. If one considers all patients with duodenal ulcers, the mortality rate due to ulcer hemorrhage is approximately 5%. Over the last 20 years, the mortality rate in the setting of ulcer hemorrhage has not changed appreciably despite the advent of histamine-2 receptor antagonists (H2RAs) and proton pump inhibitors (PPIs). However, evidence from meta-analyses and other studies has shown a decreased mortality rate from bleeding peptic ulcers when intravenous PPIs are used after successful endoscopic therapy.[19, 20, 21, 22]
Emergency operations for peptic ulcer perforation carry a mortality risk of 6-30%.[23]Factors associated with higher mortality in this setting include the following:
Shock at the time of admission
Renal insufficiency
Delaying the initiation of surgery for more than 12 hours after presentation
Concurrent medical illness (eg, cardiovascular disease, diabetes mellitus
Age older than 70 years
Cirrhosis
Immunocompromised state
Location of ulcer (mortality associated with perforated gastric ulcer is twice that associated with perforated duodenal ulcer.)





























CONCLUSION
A 65 years old woman has a peptic ulser et causa NSAID
































References

Chan FKL, Lau JYW. Peptic ulcer disease. In: Feldman M, Friedman LS, Brandt LJ, eds.Chan FKL, Lau JYW. Peptic ulcer disease. In: Feldman M, Friedman LS, Brandt LJ, eds. Sleisenger & Fordtran's Gastrointestinal and Liver Disease. 9th ed. Philadelphia, PA: Elsevier Saunders; 2010:chap 53.

Lanza FL, Chan FK, Quigley EM; Practice Parameters Committee of the American College of Gastroenterology. Guidelines for prevention of NSAID-related ulcer complications.Lanza FL, Chan FK, Quigley EM; Practice Parameters Committee of the American College of Gastroenterology. Guidelines for prevention of NSAID-related ulcer complications. Am J Gastroenterol. 2009 Mar;104(3):728-38.

Kuipers EJ, Blaser MJ. Acid peptic disease. In: Goldman L, Schafer AI, eds.Kuipers EJ, Blaser MJ. Acid peptic disease. In: Goldman L, Schafer AI, eds. Goldman's Cecil Medicine. 24th ed. Philadelphia, PA: Elsevier Saunders; 2011:chap 141.

Chey WD, Wong BC. American College of Gastroenterology guideline on the management of Helicobacter pylori infectionChey WD, Wong BC. American College of Gastroenterology guideline on the management of Helicobacter pylori infection. Am J Gastroenterol. 2007;102:1808-25. PMID: 17608775

















MEDICAL ENGLISH CASE

PEPTIC ULCER DESEASE





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ARIES SETIAWAN 09310040
EVAN DWI YANA 12310148
M ANDRE YUDIHARWANTIO 12310269
NOVITA DWI A 12310333
ROLANDO SETIAWAN 12310507 P
PUTRI BETANI ISLAMISTY 12310513


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