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Signs and symptoms of a peptic ulcer can include one or more of the following:
- abdominal pain, classically epigastric strongly correlated to mealtimes. In case of duodenal ulcers the pain appears about three hours after taking a meal;
- bloating and abdominal fullness;
- waterbrash (rush of saliva after an episode of regurgitation to dilute the acid in esophagus - although this is more associated with gastroesophageal reflux disease);
- nausea and copious vomiting;
- loss of appetite and weight loss;
- hematemesis (vomiting of blood); this can occur due to bleeding directly from a gastric ulcer, or from damage to the esophagus from severe/continuing vomiting.
- melena (tarry, foul-smelling feces due to presence of oxidized iron from hemoglobin);
- rarely, an ulcer can lead to a gastric or duodenal perforation, which leads to acute peritonitis, extreme, stabbing pain, and requires immediate surgery.
A history of heartburn, gastroesophageal reflux disease (GERD) and use of certain forms of medication can raise the suspicion for peptic ulcer. Medicines associated with peptic ulcer include NSAIDs (non-steroid anti-inflammatory drugs) that inhibit cyclooxygenase, and most glucocorticoids (e.g. dexamethasone and prednisolone).
In people over the age of 45 with more than two weeks of the above symptoms, the odds for peptic ulceration are high enough to warrant rapid investigation by esophagogastroduodenoscopy.
The timing of the symptoms in relation to the meal may differentiate between gastric and duodenal ulcers: A gastric ulcer would give epigastric pain during the meal, as gastric acid production is increased as food enters the stomach. Symptoms of duodenal ulcers would initially be relieved by a meal, as the pyloric sphincter closes to concentrate the stomach contents, therefore acid is not reaching the duodenum. Duodenal ulcer pain would manifest mostly 2–3 hours after the meal, when the stomach begins to release digested food and acid into the duodenum.
Also, the symptoms of peptic ulcers may vary with the location of the ulcer and the person's age. Furthermore, typical ulcers tend to heal and recur and as a result the pain may occur for few days and weeks and then wane or disappear. Usually, children and the elderly do not develop any symptoms unless complications have arisen.
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.
Peptic ulcer disease (PUD) is a break in the lining of the stomach, first part of the small intestine or occasionally the lower esophagus. An ulcer in the stomach is known as a gastric ulcer while that in the first part of the intestines is known as a duodenal ulcer. The most common symptoms of a duodenal ulcer are waking at night with upper abdominal pain or upper abdominal pain that improves with eating. With a gastric ulcer the pain may worsen with eating. The pain is often described as a burning or dull ache. Other symptoms include belching, vomiting, weight loss, or poor appetite. About a third of older people have no symptoms. Complications may include bleeding, perforation and blockage of the stomach. Bleeding occurs in as many as 15% of people.
Common causes include the bacteria "Helicobacter pylori" and non-steroidal anti-inflammatory drugs (NSAIDs). Other less common causes include tobacco smoking, stress due to serious illness, Behcet disease, Zollinger-Ellison syndrome, Crohn disease and liver cirrhosis, among others. Older people are more sensitive to the ulcer-causing effects of NSAIDs. The diagnosis is typically suspected due to the presenting symptoms with confirmation by either endoscopy or barium swallow. "H. pylori" can be diagnosed by testing the blood for antibodies, a urea breath test, testing the stool for signs of the bacteria, or a biopsy of the stomach. Other conditions that produce similar symptoms include stomach cancer, coronary heart disease, and inflammation of the stomach lining or gallbladder inflammation.
Diet does not play an important role in either causing or preventing ulcers. Treatment includes stopping smoking, stopping NSAIDs, stopping alcohol and giving medications to decrease stomach acid. The medication used to decrease acid is usually either a proton pump inhibitor (PPI) or an H2 blocker with four weeks of treatment initially recommended. Ulcers due to "H. pylori" are treated with a combination of medications such as amoxicillin, clarithromycin and a PPI. Antibiotic resistance is increasing and thus treatment may not always be effective. Bleeding ulcers may be treated by endoscopy, with open surgery typically only used in cases in which it is not successful.
Peptic ulcers are present in around 4% of the population. Newly ulcers were found in around 87.4 million people worldwide during 2015. About 10% of people develop a peptic ulcer at some point in their life. They resulted in 267,500 deaths in 2015 down from 327,000 deaths in 1990. The first description of a perforated peptic ulcer was in 1670 in Princess Henrietta of England. "H. pylori" was first identified as causing peptic ulcers by Barry Marshall and Robin Warren in the late 20th century, a discovery for which they received the Nobel Prize in 2005.
Many people with gastritis experience no symptoms at all. However, upper central abdominal pain is the most common symptom; the pain may be dull, vague, burning, aching, gnawing, sore, or sharp. Pain is usually located in the upper central portion of the abdomen, but it may occur anywhere from the upper left portion of the abdomen around to the back.
Other signs and symptoms may include the following:
- Nausea
- Vomiting (if present, may be clear, green or yellow, blood-streaked, or completely bloody, depending on the severity of the stomach inflammation)
- Belching (if present, usually does not relieve the pain much)
- Bloating
- Early satiety
- Loss of appetite
- Unexplained weight loss
Curling's ulcer (stress ulcer) or a Curling ulcer is an acute gastric erosion resulting as a complication from severe burns when reduced plasma volume leads to ischemia and cell necrosis (sloughing) of the gastric mucosa. The condition was first described in 1823 and named for a doctor, Thomas Blizard Curling, who observed ten such patients in 1842.
These stress ulcers (actually shallow multiple erosions) were once a common complication of serious burns, presenting in over 10% of cases, and especially common in child burn victims. They result in perforation and hemorrhage more often than other forms of intestinal ulceration and had correspondingly high mortality rates (at least 80%).
A similar condition involving elevated intracranial pressure is known as Cushing's ulcer.
Chronic gastritis is a chronic inflammation of the gastric mucosa.
While emergency surgery was once the only treatment, combination therapies including enteral feeding with powerful antacids such as H-receptor antagonists or, more recently, proton pump inhibitors such as omeprazole have made Curling's ulcer a rare complication.
Common causes include "Helicobacter pylori" and NSAIDs. Less common causes include alcohol, cocaine, severe illness and Crohn disease, among others.
Many people who have chronic gastritis do not experience any noticeable symptoms. Those who do, claim to experience one or several of the following: upper abdominal pain, indigestion, bloating, nausea, vomiting, belching, loss of appetite, and weight loss. Stomach bleeding or black stool has been reported in extreme cases.
This is the most common type of aphthous stomatitis, accounting for about 80–85% of all cases. This subtype is termed minor aphthous ulceration (MiAU), or minor recurrent aphthous stomatitis (MiRAS). The lesions themselves may be referred to as minor aphthae or minor aphthous ulcers. These lesions are generally less than 10 mm in diameter (usually about 2–3 mm), and affect non-keratinized mucosal surfaces (i.e. the labial and buccal mucosa, lateral borders of the tongue and the floor of the mouth). Usually several ulcers appear at the same time, but single ulcers are possible. Healing usually takes seven to ten days and leaves no scar. Between episodes of ulceration, there is usually an ulcer-free period of variable length.
This subtype makes up about 10% of all cases of aphthous stomatitis. It is termed major aphthous ulceration (MaAU) or major recurrent aphthous stomatitis (MaRAS). Major aphthous ulcers (major aphthae) are similar to minor aphthous ulcers, but are more than 10 mm in diameter and the ulceration is deeper. Because the lesions are larger, healing takes longer (about twenty to thirty days), and may leave scars. Each episode of ulceration usually produces a greater number of ulcers, and the time between attacks is less than seen in minor aphthous stomatitis. Major aphthous ulceration usually affects non keratinized mucosal surfaces, but less commonly keratinized mucosa may also be involved, such as the dorsum (top surface) of the tongue or the gingiva (gums). The soft palate or the fauces (back of the throat) may also be involved, the latter being part of the oropharynx rather than the oral cavity. Compared to minor aphthous ulceration, major aphthae tend to have an irregular outline.
A Cushing ulcer, named after Harvey Cushing, is a gastric ulcer associated with elevated intracranial pressure. It is also called von Rokitansky-Cushing syndrome. Apart from in the stomach, ulcers may also develop in the proximal duodenum and distal esophagus.
A wide range of other diseases may cause mouth ulcers. Hematological causes include anemia, hematinic deficiencies, neutropenia, hypereosinophilic syndrome, leukemia, myelodysplastic syndromes, other white cell dyscrasias, and gammopathies. Gastrointestinal causes include celiac disease, Crohn's disease (orofacial granulomatosis), and ulcerative colitis. Dermatological causes include chronic ulcerative stomatitis, erythema multiforme (Stevens-Johnson syndrome), angina bullosa haemorrhagica and lichen planus. Other examples of systemic disease capable of causing mouth ulcers include lupus erythematosus, Sweet syndrome, reactive arthritis, Behçet syndrome, granulomatosis with polyangiitis, periarteritis nodosa, giant cell arteritis, diabetes, glucagonoma, sarcoidosis and periodic fever, aphthous stomatitis, pharyngitis and adenitis.
The conditions eosinophilic ulcer and necrotizing sialometaplasia may present as oral ulceration.
Macroglossia, an abnormally large tongue, can be associated with ulceration if the tongue protrudes constantly from the mouth. Caliber persistent artery describes a common vascular anomaly where a main arterial branch extends into superficial submucosal tissues without a reduction of diameter. This commonly occurs in elderly people on the lip and may be associated with ulceration.
A mouth ulcer is an ulcer that occurs on the mucous membrane of the oral cavity. Mouth ulcers are very common, occurring in association with many diseases and by many different mechanisms, but usually there is no serious underlying cause.
The two most common causes of oral ulceration are local trauma (e.g. rubbing from a sharp edge on a broken filling) and aphthous stomatitis ("canker sores"), a condition characterized by recurrent formation of oral ulcers for largely unknown reasons. Mouth ulcers often cause pain and discomfort, and may alter the person's choice of food while healing occurs (e.g. avoiding acidic or spicy foods and beverages).
They may form individually or multiple ulcers may appear at the same time (a "crop" of ulcers). Once formed, the ulcer may be maintained by inflammation and/or secondary infection. Rarely, a mouth ulcer that does not heal may be a sign of oral cancer.
A perforated ulcer, is a condition in which 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.
Most patients who are eventually diagnosed with watermelon stomach come to a physician complaining of anemia and blood loss. Sometimes, a patient may come to the physician because he or she notices blood in the stools—either melena (black and tarry stools) and/or hematochezia (red bloody stools).
Skin ulcers appear as open craters, often round, with layers of skin that have eroded. The skin around the ulcer may be red, swollen, and tender. Patients may feel pain on the skin around the ulcer, and fluid may ooze from the ulcer. In some cases, ulcers can bleed and, rarely, patients experience fever. Ulcers sometimes seem not to heal; healing, if it does occur, tends to be slow. Ulcers that heal within 12 weeks are usually classified as acute, and longer-lasting ones as chronic.
Ulcers develop in stages. In stage 1 the skin is red with soft underlying tissue. In the second stage the redness of the skin becomes more pronounced, swelling appears, and there may be some blisters and loss of outer skin layers. During the next stage, the skin may become necrotic down through the deep layers of skin, and the fat beneath the skin may become exposed and visible. In stage 4, deeper necrosis usually occurs, the fat underneath the skin is completely exposed, and the muscle may also become exposed. In the last two stages the sore may cause a deeper loss of fat and necrosis of the muscle; in severe cases it can extend down to bone level, destruction of the bone may begin, and there may be sepsis of joints.
Chronic ulcers may be painful. Most patients complain of constant pain at night and during the day. Chronic ulcer symptoms usually include increasing pain, friable granulation tissue, foul odour, and wound breakdown instead of healing. Symptoms tend to worsen once the wound has become infected.
Venous skin ulcers that may appear on the lower leg, above the calf or on the lower ankle usually cause achy and swollen legs. If these ulcers become infected they may develop an unpleasant odour, increased tenderness and redness. Before the ulcer establishes definitively, there may be a dark red or purple skin over the affected area as well as a thickening, drying, and itchy skin.
Although skin ulcers do not seem of great concern at a first glance, they are worrying conditions especially in people suffering from diabetes, as they are at risk of developing diabetic neuropathy.
Ulcers may also appear on the cheeks, soft palate, the tongue, and on the inside of the lower lip. These ulcers usually last from 7 to 14 days and can be painful.
The ulcer has punched-out appearance. It is intensely painful. It has gray or yellow fibrotic base and undermining skin margins. Pulses are not palpable. Associated skin changes may be observed, such as thin shiny skin and absence of hair. They are most common on distal ends of limbs. A special type of ischemic ulcer developing in duodenum after severe burns is called Curling's ulcer.
Gastric antral vascular ectasia (GAVE) is an uncommon cause of chronic gastrointestinal bleeding or iron deficiency anemia. The condition is associated with dilated small blood vessels in the antrum, or the last part of the stomach. The dilated vessels result in intestinal bleeding. It is also called watermelon stomach because streaky long red areas that are present in the stomach may resemble the markings on watermelon.
The condition was first discovered in 1952, and reported in the literature in 1953. Watermelon disease was first diagnosed by Wheeler "et al." in 1979, and definitively described in four living patients by Jabbari "et al." only in 1984. As of 2011, the cause and pathogenesis are still not known. However, there are several competing hypotheses as to various causes.
Stercoral ulcer is an ulcer of the colon due to pressure and irritation resulting from severe, prolonged constipation due to large bowel obstruction. It is most commonly located in the rectum. Individuals with this condition are at risk for stercoral perforation.
An ulcer is a sore on the skin or a mucous membrane, accompanied by the disintegration of tissue. Ulcers can result in complete loss of the epidermis and often portions of the dermis and even subcutaneous fat. Ulcers are most common on the skin of the lower extremities and in the gastrointestinal tract. An ulcer that appears on the skin is often visible as an inflamed tissue with an area of reddened skin. A skin ulcer is often visible in the event of exposure to heat or cold, irritation, or a problem with blood circulation. They can also be caused due to a lack of mobility, which causes prolonged pressure on the tissues. This stress in the blood circulation is transformed to a skin ulcer, commonly known as bedsores or decubitus ulcers. Ulcers often become infected, and pus forms.
In about 50-70% of patients with dyspepsia, no definite organic cause can be determined. In this case, dyspepsia is referred to as non-ulcer dyspepsia and its diagnosis is established by the presence of epigastralgia for at least 6 months, in the absence of any other cause explaining the symptoms.
The mechanism of development of Cushing ulcers is thought to be due to direct stimulation of vagal nuclei as a result of increased intracranial pressure. Alternatively, it may also be a direct result of Cushing reaction. Efferent fibers of the vagus nerve then release acetylcholine onto gastric parietal cell M receptors, causing insertion of hydrogen potassium ATPase vesicles into the apical plasma membrane. The end result is increased secretion of gastric acid with eventual ulceration of the gastric mucosa.
Corneal ulcer, or ulcerative keratitis, is an inflammatory or more seriously, infective condition of the cornea involving disruption of its epithelial layer with involvement of the corneal stroma. It is a common condition in humans particularly in the tropics and the agrarian societies. In developing countries, children afflicted by Vitamin A deficiency are at high risk for corneal ulcer and may become blind in both eyes, which may persist lifelong. In ophthalmology, a corneal ulcer usually refers to having an infectious cause while the term corneal abrasion refers more to physical abrasions.
Corneal ulcers are extremely painful due to nerve exposure, and can cause tearing, squinting, and vision loss of the eye. There may also be signs of anterior uveitis, such as miosis (small pupil), aqueous flare (protein in the aqueous humour), and redness of the eye. An axon reflex may be responsible for uveitis formation—stimulation of pain receptors in the cornea results in release inflammatory mediators such as prostaglandins, histamine, and acetylcholine.
Sensitivity to light (photophobia) is also a common symptom of corneal ulcer.
Edema and fibrinous exudate leads to fibrosis of subcutaneous tissues with localized pigment loss and dilation of capillary loops. This is called atrophic blanche. This can occur around ankles and gives an appearance of inverted champagne bottle to legs. Large ulcers may encircle the leg.
Lymphedema results from obliteration of superficial lymphatics. There is hypertrophy of overlying epidermis giving polypoid appearance, known as lipodermatosclerosis.