ulcer(redirected from pemphigoid aphthous ulcer)
Also found in: Dictionary, Thesaurus, Encyclopedia.
ulcer/ul·cer/ (ul´ser) a local defect, or excavation of the surface, of an organ or tissue, produced by sloughing of necrotic inflammatory tissue.
ulcerDermatology A defect in a mucocutaneous surface. See Bairnesdale ulcer, Buruli ulcer, Esophageal ulcer, Kissing ulcer, Pressure ulcer, Rodent ulcer ENT Mouth ulcer, see there. See Aphthous ulcer GI disease Duodenal ulcer, see there. See Cushing's ulcer, Dieulafoy ulcer, Peptic ulcer, Stercoral ulcer, Stress ulcer Ophthalmology A defect on the epithelium of the eye. See Corneal ulcer, Corneal neurotrophic ulcer, Geographic ulcer, Peptic ulcer, Serpiginous ulcer.
ulcer(ul'ser) [L. ulcus, sore, ulcer]
Aphthous ulcers are found in stomatitis, Behçet syndrome, Crohn disease, acquired immunodeficiency syndrome, and some cancers.
For patients with oral ulcers, application of a topical anesthetic or a protective paste provides symptomatic relief and makes it possible to eat without pain.
arterial ulcerIschemic ulcer.
Cameron ulcerSee: Cameron ulcer
chronic leg ulcer
Curling ulcerSee: Curling ulcer
Cushing ulcerSee: Cushing, Harvey
decubitus ulcerPressure ulcer
To prevent irritation and ulceration of the mucous membranes of the mouth, denture wearers should clean dentures daily and remove them while sleeping. Poorly fitting dentures should be reconstructed or padded by a denturist.
diabetic foot ulcerDiabetic foot infection.
Common causes are NSAIDs, use of alcohol or tobacco, and infection with H. pylori.
Hunner ulcerInterstitial cystitis.
Marjolin ulcerSee: Marjolin ulcer
Meleney ulcerSee: Meleney ulcer
Mooren ulcerSee: Mooren ulcer
Common causes of peptic ulcer are factors that increase gastric acid production or impair mucosal barrier protection, e.g., salicylates and NSAIDs, smoking, H. pylori infection of the upper gastrointestinal tract, pathological hypersecretory disorders, consumption of alcohol and coffee, and severe physiological stress. Ulcers occur in men and women and occur most frequently in patients over age 65, with about 1.6 million cases diagnosed annually in the U.S. The relationship between peptic ulcer and emotional stress is not completely understood.
Patients with peptic ulcers may be asymptomatic or have gnawing epigastric pain, esp. in the middle of the night or when no food has been eaten for several hours. At times, heartburn, nausea, vomiting, hematemesis, melena, or unexplained weight loss may signify peptic disease. Food intake often relieves the discomfort. Peptic ulcers that perforate the upper gastrointestinal tract may penetrate the pancreas, causing symptoms of pancreatitis (severe back pain) and chemical peritonitis followed by bacterial peritonitis or an acute abdomen as irritating gastrointestinal (GI) contents and bacteria enter the abdominal cavity. Bacterial peritonitis can lead to sepsis, shock, and death.
Endoscopy (esophagogastroduodenoscopy) provides the single best test to diagnose peptic ulcers because it allows direct visualization of the mucosa and permits carbon–13 urea breath testing, cytological studies, and biopsy to diagnose H. pylori and rule out cancer. During endoscopy, tissue can be excised, vessels ligated, or sclerosants injected. Barium swallow or upper GI x-ray series may also be used to provide images for diagnosis or follow-up and may be the initial test for patients whose symptoms are not severe.
H. pylori causes most peptic ulcers in the duodenum; antibiotics (clarithromycin and amoxicillin) are prescribed to treat H. pylori, and antisecretory (proton pump inhibitor) drugs like lansoprazole or omeprazole should be given to all patients with duodenal ulcers. Bismuth or other coating agents may be used as a barrier to protect the duodenal mucosa. Peptic ulceration of the stomach may be treated with the same medications if biopsies or breath tests reveal H. pylori. When patients have ulcers caused by the use of NSAIDs or tobacco, withholding these agents and treating with an H2 blocker, e.g., ranitidine, provides an effective cure. The prostaglandin analogue misoprostol may also be used to suppress or prevent peptic ulcer caused by use of NSAIDs. GI bleeding is managed initially with passage of a nasogastric tube and iced saline lavage, possibly with norepinephrine added. Gastroscopy then allows visualization of the bleeding site and laser or cautery coagulation. When conservative medical treatment is ineffective, vagotomy and pyloroplasty may be used to reduce hydrochloric acid secretion and enlarge the pylorus to enhance gastric emptying. More extreme surgical therapy (including subtotal gastric resection) may be needed in rare instances of uncontrollable hemorrhage or perforation occurring as a result of peptic ulcer disease.
The ambulatory patient is educated about agents that increase the risk for peptic ulceration and given specific instructions to avoid them. Instruction should include the importance of adhering to prescription drug therapies, adverse reactions to H2-receptor antagonists and omeprazole (dizziness, fatigue, rash, diarrhea), and the need for follow-up examination and care.
For the hospitalized patient with ulcer-related bleeding, careful monitoring of vital signs, fluid balance, hemoglobin levels, and blood losses may enhance early recognition of worsening disease. Intravenous (IV) access is established, and IV opiates are administered as prescribed for pain control. The patient is kept nil per os (NPO). Electrolytes and fluids are replaced as needed. Endoscopic or other diagnostic and treatment procedures are explained to the patient, and the effects of prescribed therapies or transfusions are carefully assessed. All patient care concerns apply after major surgery. The patient is assessed for possible complications: hemorrhage, shock, malabsorption problems (iron, folate, or vitamin B12 deficiency anemias), and dumping syndrome. To avoid these problems, the patient is advised to drink fluids between meals rather than with meals, eat 4 to 6 small, high-protein, low-carbohydrate meals daily, and lie down after eating. Before and after discharge, health care professionals should help the patient to develop coping mechanisms to relieve anxiety. Patients are taught to recognize signs and symptoms of disease recurrence (e.g., coffee-ground emesis, the passage of black or tarry stools, or epigastric pain). Patients who use antacids and have a history of cardiac disease or whose sodium intake is restricted for any reason are warned to take only those antacids that have low amounts of sodium. The need for ongoing medical care is stressed.
phagedenic ulcerTropical ulcer.
The most common sites of skin breakdown are over bony prominences (the sacrum and the trochanters, the heels, the lateral malleoli and also the shoulder blades, ischial tuberosities, occiput, ear lobes, elbows, and iliac crests). The combination of pressure, shearing forces, friction, and moisture leads to tissue injury and occasionally necrosis. If the ulcer is not treated vigorously, it will progress from a simple red patch of skin to erosion into the subcutaneous tissues, eventually extending to muscle or bone. Deep ulcers often become infected with bacteria and develop gangrene. See: illustration
Treatment and Prevention
The most important principle is to prevent the initial skin damage that promotes ulceration. In patients at risk, aggressive nursing practices, such as frequent turning of immobile patients and the application of skin protection to bony body parts, are frequently effective. Gel flotation pads, alternating pressure mattresses, convoluted foam mattresses and sheepskins or imitation sheepskins may be employed. Specialized air-fluid beds, waterbeds, or beds with polystyrene beads provide expensive but effective prophylaxis. If the patient develops an ulcer, topical treatments with occlusive hydrocolloid dressings, polyurethane films, absorbable gelatin sponges, collagen dressings, wound-filter dressings, water-vapor permeable dressings, and antibiotic ointments aid the healing of partial-thickness sores. Deeper lesions may need surgical débridement. Skin-damaging agents such as harsh alkaline soaps, alcohol-based products, tincture of benzoin, hexachlorophene, and petroleum gauze should be avoided. Consultation with a wound care specialist is advantageous.
The skin is thoroughly cleansed, rinsed, and dried, and emollients are gently applied by minimizing the force and friction used, esp. over bony prominences. Patients who are not able to position themselves are repositioned every 1–2 hr to prevent tissue hypoxia resulting from compression. A turning sheet or pad is used to turn patients with minimal skin friction. Care providers should avoid elevating the head of the bed higher than 30° (except for short periods) to reduce shearing forces on the skin and subcutaneous tissues overlying the sacrum. Range-of-motion exercises are provided, early ambulation is encouraged, and nutritious high-protein meals are offered. Low-pressure mattresses and special beds are kept in proper working order. Doughnut-type cushions should not be used because they decrease blood flow to tissues resting in the center of the doughnut.
Ulcers are cleansed and débrided, and other therapeutic measures are instituted according to institutional protocol or prescription. Consultation with a nutritionist may be needed to assess and optimize the patient's nutritional status, and to provide high-protein meals with added vitamin C to promote healing, protein and calorie-rich supplements, or enteral feedings. Weak or debilitated patients should be assisted to eat, with care taken to prevent swallowing difficulties.
Saemisch ulcerSee: Saemisch ulcer
venous stasis ulcer
Assessment includes a detailed medical and surgical history and physical examination. When the lower extremities are examined, characteristic markers of venous ulceration include ankle flare (distention of small veins on the medial aspect of the foot due to chronic venous hypertension); dermatitis; pigmentation changes on the skin surface, usually appearing as brown discolorations affecting the medial part of the leg; woody induration of the leg; and varicosities. The health care professional should examine the leg for lesions superior to the medial malleolus and should carefully measure the size, shape, and margins of wounds; drainage or exudates; surrounding skin; and pain or tenderness. The patient should be advised to elevate the legs 7 in (18 cm) above the heart for 2 to 4 hr during the day and at night. Compression devices (such as graduated pressure stockings, Unna boot) are used to help reduce edema, improve venous blood flow, and aid healing. Before applying any compression device or wrap, the health care professional should measure the patient’s leg circumference at the wound and the wound size of the ulcer. The wound should be cleansed regularly, and aggressive debridement employed as needed. Wounds with light to moderate drainage benefit from a moisture-retentive dressing (such as hydrocolloid, transparent film, some foams), whereas wounds with moderate to heavy drainage do better with an absorbent dressing (such as foams, alginates, special absorptive dressings). Underlying problems such as obesity, deep venous thrombosis, diabetes, and cardiovascular disease must be assessed and managed as part of the wound care protocol.
ulcerA local loss of surface covering (EPITHELIUM).and sometimes deeper tissue in skin or MUCOUS MEMBRANE. An open sore. Loss of surface leads to infection and further tissue damage. Ulcers may be caused by physical or chemical damage, by loss of blood supply or by local infection. Ulcers of the STOMACH or DUODENUM are called peptic ulcers. See also BEDSORES, VARICOSE ULCERS and TROPICAL ULCERS.
corneal ulcer A superficial loss of corneal tissue as a result of infection that has led to necrosis. It may be caused by a bacterium (e.g. Pseudomonas aeruginosa, Streptococcus pneumoniae), by a virus (e.g. herpesvirus), or by a fungus (e.g. Candida, Aspergillus, Penicillium). It causes pain and usually reduced visual acuity, especially if the ulcer occurs in the centre of the cornea. Corneal ulcers usually look dirty grey or white and are opaque areas of various sizes and a mucopurulent discharge may be present. If induced by contact lenses, especially extended wear lenses, patients must cease wearing their lenses immediately, and the appropriate therapy instituted: antibacterial, antifungal or antiviral agent. See corneal facet; herpes simplex keratitis; hypopyon keratitis; rosacea keratitis; ulcerative keratitis; keratocele; keratomycosis; leukoma.
dendritic ulcer See herpes simplex keratitis.
von Hippel's internal ulcer A depression noted in the posterior surface of the cornea. This lesion resembles posterior lenticonus, except that it is thought to be due to an infection or inflammation. The lesion can be differentiated from Peter's anomaly by the presence of endothelium and Descemet's membrane in the former. Due to its posterior location, the lesion does not usually disturb visual function. See Peter's anomaly.
marginal corneal ulcer Benign condition due to a hypersensitivity reaction to bacterial conjunctivitis, particularly staphylococcal blepharoconjunctivitis. It is characterized by infiltration of the peripheral cornea by white cells and by ocular irritation. The condition is usually self-limiting but painful. Treatment includes frequent cleaning of the eyelid margin with a cotton-tipped applicator or face cloth or cotton ball with baby shampoo, warm compresses, antibiotic ointment and occasionally topical corticosteroids.
Mooren's ulcer A rare, superficial ulcer of the cornea of unknown origin. It starts near the limbus as an overhanging advancing edge that in severe cases spreads over the entire cornea and may even invade the sclera. The patient complains of pain and blurred vision. There are two types: a self-limiting form, usually unilateral, affecting old people, and a progressive form, bilateral, affecting young people. The condition is difficult to treat and this may include topical and systemic steroids, immunosuppressants, or conjunctival excision. See peripheral ulcerative keratitis.
serpiginous ulcer See hypopyon keratitis.
shield ulcer A localized corneal ulcer noted in severe cases of vernal conjunctivitis. The lesion is usually oval or pentagonal resembling a warrior's shield. It is located in the upper portion of the cornea as a result of irritation from the large papillae on the palpebral surface of the overlying eyelid.
Patient discussion about ulcer
Q. Is it an ulcer? I am worried! Hi friend, I'm 35 year old male and recently I started to suffer from some strange symptoms I have never experienced. The first symptom was sharp pain in my upper abdomen that starts two of three hours after eating. In the beginning I thought it could be connected with some food intolerance but then I started to get this pain early in the morning, before any eating what so ever and all this was accompanied with nausea, frequent burping and weight loss. I have read some stuff about stomach ulcer and I could say that I poses almost every major symptom. Is there any way for me to be sure that I have developed disease of ulcer?
Q. What are the symptoms of Ulcerative Colitis? I am 40 years old and suffer from a lot of stomach aches and diarrhea. Do I have Ulcerative Colitis? What are its symptoms?
Q. What is the difference between duodenal ulcer and stomach ulcer? I was diagnosed recently with duodenal ulcer. I heard the term stomach ulcer but not duodenal. What causes duodenal and what cause stomach ulcer? And how do they treat duodenal ulcer?