Can you die from an ulcer?
10770742#0
A perforated ulcer is a condition in which an untreated ulcer can burn through the wall of the stomach (or other areas of the gastrointestinal tract), allowing digestive juices and food to leak into the abdominal cavity. Treatment generally requires immediate surgery. The ulcer is known initially as a peptic ulcer before the ulcer burns through the full thickness of the stomach or duodenal wall. A diagnosis is made by taking an erect abdominal/chest X-ray (seeking air under the diaphragm). This is in fact one of the very few occasions in modern times where surgery is undertaken to treat an ulcer. Many perforated ulcers have been attributed to the bacterium "Helicobacter pylori". The incidence of perforated ulcer is steadily declining, though there are still incidents where it occurs. Causes include smoking and nonsteroidal anti-inflammatory drugs (NSAIDs). A perforated ulcer can be grouped into a stercoral perforation which involves a number of different things that causes perforation of the intestine wall. The first symptom of a perforated peptic ulcer is usually sudden, severe, sharp pain in the abdomen. The experience is typically so intense that most people precisely recall the exact moment the pain began. The pain is typically at its maximum immediately and persists. It is characteristically made worse by any movement, and greatly intensifies with coughing or sneezing.
Perforated ulcer
49097223#25
Syrian hamsters are used to study how NSAIDs can cause reactive gastropathy. One way to study is to inject hamsters with indometacin, which causes an ulcer within 1–5 hours depending on the dose. If repeatedly given doses, hamsters get severe lesions and die within 5 days from peptic ulcers in their pyloric antrum. A model for creating a chronically ill hamster which will not die from the ulcers is to give naproxen by gavage. When the hamster is chronically ill, it can be used to test anti-ulcer drugs.
Laboratory Syrian hamster
43153251#5
Both the esophagus and duodenum are also at risk for ulceration. Esophageal ulceration is partially prevented by the tone of the cardia sphincter to prevent reflux, as well as by saliva, which both washes the esophagus and contains mucins that can help protect its surface. The duodenum is protected by its motility which removes HCl, glands in its surface that produce mucins, and products from the pancreas, including bicarbonate, to help neutralize the acidity. Most duodenal ulcers occur in foals, and there appears to be an association between duodenal ulcers and enteritis in these animals. Duodenal ulcers may result in inflammation of the duodenum so profound it blocks gastric emptying, which can cause severe gastric ulcers and occasionally esophageal ulcers. Often this must be treated with a gastrojejunostomy, which is a risky procedure.Horses used for competitive activities, such as showing or racing are at greatest risk of gastric ulceration, with up to 60% of show horses, 60–70% of endurance horses, 75% of event horses, and 80-90% of race horses having ulcers. These horses have stressful lives compared to non-competitive animals, which includes travel, frequent change of environment, and high workload. Additionally, their diet often consists of a higher proportion of grain relative to roughage, to account for their increased caloric requirements.
Equine gastric ulcer syndrome
245969#8
The wounds from which ulcers arise can be caused by a wide variety of factors, but the main cause is impaired blood circulation. Especially, chronic wounds and ulcers are caused by poor circulation, either through cardiovascular issues or external pressure from a bed or a wheelchair. A very common and dangerous type of skin ulcers are caused by what are called pressure-sensitive sores, more commonly called bed sores and which are frequent in people who are bedridden or who use wheelchairs for long periods. Other causes producing skin ulcers include bacterial or viral infections, fungal infections and cancers. Blood disorders and chronic wounds can result in skin ulcers as well. Venous leg ulcers due to impaired circulation or a blood flow disorder are more common in the elderly.
Ulcer (dermatology)
245973#38
Treatment is cause-related, but also symptomatic if the underlying cause is unknown or not correctable. It is also important to note that most ulcers will heal completely without any intervention. Treatment can range from simply smoothing or removing a local cause of trauma, to address underlying factors such as dry mouth or substituting a problem medication. Maintaining good oral hygiene and use of an antiseptic mouthwash or spray (e.g. chlorhexidine) can prevent secondary infection and therefore hasten healing. A topical analgesic (e.g. benzydamine mouthwash) may reduce pain. Topical (gels, creams or inhalers) or systemic steroids may be used to reduce inflammation. An antifungal drug may be used to prevent oral candidiasis developing in those who use prolonged steroids. People with mouth ulcers may prefer to avoid hot or spicy foods, which can increase the pain. Self-inflicted ulceration can be difficult to manage, and psychiatric input may be required in some people. For recurrent ulcers, vitamin B12 has been shown to be effective.
Mouth ulcer
902762#1
Pressure ulcers can trigger other ailments, cause considerable suffering, and can be expensive to treat. Some complications include autonomic dysreflexia, bladder distension, bone infection, pyarthroses, sepsis, amyloidosis, anemia, urethral fistula, gangrene and very rarely malignant transformation (Marjolin's ulcer - secondary carcinomas in chronic wounds). Sores may recur if those with pressure ulcers do not follow recommended treatment or may instead develop seromas, hematomas, infections, or wound dehiscence. Paralyzed individuals are the most likely to have pressure sores recur. In some cases, complications from pressure sores can be life-threatening. The most common causes of fatality stem from kidney failure and amyloidosis.
Pressure ulcers are also painful, with individuals of all ages and all stages of pressure ulcers reporting pain.
Pressure ulcer
63791#5
Burning or gnawing feeling in the stomach area lasting between 30 minutes and 3 hours commonly accompanies ulcers. This pain can be misinterpreted as hunger, indigestion or heartburn. Pain is usually caused by the ulcer but it may be aggravated by the stomach acid when it comes into contact with the ulcerated area. The pain caused by peptic ulcers can be felt anywhere from the navel up to the sternum, it may last from few minutes to several hours and it may be worse when the stomach is empty. Also, sometimes the pain may flare at night and it can commonly be temporarily relieved by eating foods that buffer stomach acid or by taking anti-acid medication. However, peptic ulcer disease symptoms may be different for every sufferer."Helicobacter pylori" is one of the major causative factors of peptic ulcer disease. It secretes urease to create an alkaline environment which is suitable for its survival. It expresses blood group antigen adhesin (BabA) and outer inflammatory protein adhesin (OipA) which enables it to attach to the gastric epithelium. The bacterium also expresses virulence factors such as "CagA" and "PicB" which cause stomach mucosal inflammation. The VacA gene encodes for vacuolating cytotoxin, but its mechanism of causing peptic ulcers is unclear. Such stomach mucosal inflammation can be associated with hyperchlorhydria (increased stomach acid secretion) or hypochlorhydria (reduced stomach acid secretion). Inflammatory cytokines inhibit the parietal cell acid secretion. "H. pylori" also secretes certain products that inhibit hydrogen potassium ATPase, activate calcitonin gene-related peptide sensory neurons which increases somatostatin secretion to inhibit acid production by parietal cells, and inhibit gastrin secretion. This reduction in acid production causes gastric ulcers. On the other hand, increased acid production at the pyloric antrum is associated with duodenal ulcers in 10 to 15% of the "H. pylori" infection cases. In this case, somatostatin production is reduced and gastrin production is increased, leading to increased histamine secretion from the enterochromaffin cells, thus increasing acid production. An acidic environment at the antrum causes metaplasia of the duodenal cells, causing duodenal ulcers.
Peptic ulcer disease
17843917#27
Ulcers of the shell may be superficial or deep, and may be termed "shell rot". Ulcers are generally a result of poor husbandry. Turtles with ulcerative shell lesions should be examined and treated by a veterinarian, as the ulcers may become infected and penetrate through the shell. The shell will need to be cleaned daily, and dead tissue removed. Topical and/or injectable antibiotics are required in the case of bacterial infections. Deep ulcers may need to be repaired through surgery and the application of acrylic or fiberglass material. In a disease called "septicemic cutaneous ulcerative disease", or SCUD, ulcers may be seen on both the shell and legs. This condition is often associated with the bacteria, "Citrobacter freundii".
"Pyramiding" is a shell deformity commonly found in captive turtles, in which the shell grows unevenly resulting in a "pyramid" shape underlying each scute. This deformity can vary in severity from barely noticeable to life-threatening. Indian star tortoises and some other species display this morphology naturally.
Turtle shell
20767375#4
Adequate footwear is important to prevent trauma. General good health and nutrition also reduce ulcer risk. Adequate and prompt cleansing and treatment of ankle and leg skin breaks is also important. Improving hygiene and nutrition may help to prevent tropical ulcers.Tropical ulcer has been described as a disease of the 'poor and hungry'; it may be that slowly improving socioeconomic conditions and nutrition account for its decline. Urbanization of populations could be another factor, as tropical ulcer is usually a rural problem. More widespread use of shoes and socks also provides protection from initiating trauma. Despite this, susceptible individuals still develop tropical ulcers. Sometimes outbreaks can occur; one was recorded in Tanzania in sugarcane workers cutting the crops while barefoot. Tropical ulcers can also occur to the visitors of tropics. The disease is most common in native laborers and in schoolchildren of the tropics and subtropics during the rainy season and is caused in many instances by the bites of insects, poor hygiene, and pyogenic infections. Males are more commonly infected than females.
Tropical ulcer
63791#7
Taking nonsteroidal anti-inflammatory drugs (NSAID) and aspirin can increase the risk of getting peptic ulcer disease by four times when compared to non-users. The risk of getting peptic ulcer is two times for aspirin users. Risk of bleeding increases if NSAIDs are combined with selective serotonin reuptake inhibitor (SSRI), corticosteroids, antimineralocorticoids, and anticoagulants. The gastric mucosa protects itself from gastric acid with a layer of mucus, the secretion of which is stimulated by certain prostaglandins. NSAIDs block the function of cyclooxygenase 1 ("COX-1"), which is essential for the production of these prostaglandins. Besides, NSAIDs also inhibits stomach mucosa cells proliferation and mucosal blood flow, reducing bicarbonate and mucus secretion, which reduces the integrity of the mucosa. Another type of NSAIDs, called COX-2 selective anti-inflammatory drugs (such as celecoxib), preferentially inhibit "COX-2", which is less essential in the gastric mucosa. This reduces the probability of getting peptic ulcers; however, it can still delay ulcer healing for those who already have a peptic ulcer.
Peptic ulcer disease