Instruct: Given a question, retrieve documents that answer the question.
Query: Can you die from an ulcer?
Richard Pankhurst (1834–1897) had a perforated ulcer and died in 1897. Thomas Preston (1860–1900) had a perforated ulcer and died in 1900.[5] Rudolph Valentino (1895–1926, aged 31) had a perforated ulcer and died on August 23, 1926. Rudyard Kipling (1865–1936, aged 70) died of perforated duodenal ulcer on 18 January 1936. James Joyce (1882–1941, aged 58) had a perforated ulcer and died on January 13, 1941, in Zürich. Charlie Parker (1920–1955, aged 34) had a perforated ulcer, and died on March 12, 1955. Albert Blithe (1923–1967, aged 44) had a perforated ulcer and died on December 17, 1967. Gene Vincent (1935–1971, aged 36) had a ruptured stomach ulcer and died on October 12, 1971. [6] J. R. R. Tolkien (1892–1973, aged 81) had a perforated ulcer and died on September 2, 1973. Count Dante (1939-1975, aged 36) died of internal hemorrhaging caused by a bleeding ulcer, on May 25, 1975. Ian Hendry (1931—1984, aged 53) died of a stomach haemorrhage in London, aged 53. Gene Clark (1944-1991, aged 46) had perforated ulcer and died on May 24, 1991. Doug Hepburn (1926–2000, aged 74) had a perforated ulcer and died on November 22, 2000. Philip Agee (1935–2008, aged 72) had a perforated ulcer and died on January 7, 2008. Barbara Bush (1925-2018) was treated for a perforated ulcer in November 2008.[7] Tara Palmer-Tomkinson (1971 – 2017, aged 45) had a perforated ulcer and died on February 8, 2017.[8]
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.
A venous ulcer tends to occur on the medial side of the leg, typically around the medial malleolus in the 'gaiter area' whereas arterial ulcer tends to occur on lateral side of the leg and over bony prominences. A venous ulcer is typically shallow with irregular sloping edges whereas an arterial ulcer can be deep and has a 'punched out' appearance. Venous ulcers are typically 'wet' with a moderate to heavy exudate, whereas arterial ulcers are typically 'dry' and scabbed. The skin surrounding a venous ulcer may be edematous (swollen) and there may be evidence of varicose veins; the skin surrounding an arterial ulcer may be pale, cold, shiny and hairless. Both venous and arterial ulcers may be painful, however arterial ulcers tend to be more painful, especially with elevation of the leg, for example when in bed.
Pressure ulcers may be caused by inadequate blood supply and resulting reperfusion injury when blood re-enters tissue. A simple example of a mild pressure sore may be experienced by healthy individuals while sitting in the same position for extended periods of time: the dull ache experienced is indicative of impeded blood flow to affected areas. Within 2 hours, this shortage of blood supply, called ischemia, may lead to tissue damage and cell death. The sore will initially start as a red, painful area. The other process of pressure ulcer development is seen when pressure is high enough to damage the cell membrane of muscle cells. The muscle cells die as a result and skin fed through blood vessels coming through the muscle die. This is the deep tissue injury form of pressure ulcers and begins as purple intact skin.
Many micro-organisms cause infective corneal ulcer. Among them are bacteria, fungi, viruses, protozoa, and chlamydia:Superficial ulcers involve a loss of part of the epithelium. Deep ulcers extend into or through the stroma and can result in severe scarring and corneal perforation. Descemetoceles occur when the ulcer extends through the stroma. This type of ulcer is especially dangerous and can rapidly result in corneal perforation, if not treated in time.
Superficial IHs are situated higher in the skin and have a bright red, erythematous to reddish-purple appearance. Superficial lesions can be flat and telangiectatic, composed of a macule or patch of small, varied branching, capillary blood vessels. They can also be raised and elevated from the skin, forming papules and confluent bright-red plaques like raised islands. Infantile hemangiomas have historically been referred to “strawberry hemangiomas” in the past, as raised superficial hemangiomas can look like the side of a strawberry without seeds.
Superficial IHs in certain locations, such as the posterior scalp, neck folds, and groin/perianal areas, are at potential risk of ulceration. Ulcerated hemangiomas can present as black crusted papules or plaques, or painful erosions or ulcers. Ulcerations are prone to secondary bacterial infections, which can present with yellow crusting, drainage, pain, or odor. Ulcerations are also at risk for bleeding, particularly deep lesions or in areas of friction. Multiple superficial hemangiomas, more than five, can be associated with extracutaneous hemangiomas, the most common being a liver (hepatic) hemangioma, and these infants warrant ultrasound examination.
Venous leg ulcers are commonly associated with chronic wound pain. The pain prevalence rate for venous leg ulcers is 50-87%. The pain experienced with venous leg ulcers may be constant, or intermittent varying in intensity. Venous leg ulcers may cause nociceptive and neuropathic pain, and ultimately be expressed as persistent background pain. Venous leg ulceration is due to poor venous return and venous hypertension as resulting from venous reflux or obstruction.1 Consequences of venous leg ulcers are infection, cellulitis, and infection. Venous leg ulcers can affect mobility and ultimately quality of life.
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.
Pressure ulcers, also known as pressure sores, decubitus ulcers, and bedsores, and now referred to as pressure injuries are localized damage to the skin and/or underlying tissue that usually occur over a bony prominence as a result of pressure or pressure in combination with shear and/or friction. The most common sites are the skin overlying the sacrum, coccyx, heels or the hips, but other sites such as the elbows, knees, ankles, back of shoulders, or the back of the cranium can be affected.
Pressure ulcers occur due to pressure applied to soft tissue resulting in completely or partially obstructed blood flow to the soft tissue. Shear is also a cause, as it can pull on blood vessels that feed the skin. Pressure ulcers most commonly develop in individuals who are not moving about, such as those being bedridden or confined to a wheelchair. It is widely believed that other factors can influence the tolerance of skin for pressure and shear, thereby increasing the risk of pressure ulcer development. These factors are protein-calorie malnutrition, microclimate (skin wetness caused by sweating or incontinence), diseases that reduce blood flow to the skin, such as arteriosclerosis, or diseases that reduce the sensation in the skin, such as paralysis or neuropathy. The healing of pressure ulcers may be slowed by the age of the person, medical conditions (such as arteriosclerosis, diabetes or infection), smoking or medications such as anti-inflammatory drugs.
Although often prevented and treatable if detected early, pressure ulcers can be very difficult to prevent in critically ill people, frail elders and individuals with impaired mobility such as wheelchair users (especially where spinal injury is involved). Primary prevention is to redistribute pressure by regularly turning the person. The benefit of turning to avoid further sores is well documented since at least the 19th century. In addition to turning and re-positioning the person in the bed or wheelchair, eating a balanced diet with adequate protein and keeping the skin free from exposure to urine and stool is very important.
The rate of pressure ulcers in hospital settings is high; the prevalence in European hospitals ranges from 8.3% to 23%, and the prevalence is 26% in Canadian healthcare settings. In 2013, there were 29,000 documented deaths from pressure ulcers globally, up from 14,000 deaths in 1990.
Foals start secreting hydrochloric acid at two days of age. Nursing has been shown to increase pH, while gastric pH decreases in foals that are recumbent and not sucking regularly. Up to 50% of all foals and 90% of foals in the ICU have ulcers. This may be due to decreased feedings and recumbency. Ulcers in foals are often "silent", producing no clinical signs, and usually occur in the squamous portion of the stomach in animals four months old and younger. Glandular ulcers in foals are thought to be caused by stress, and are often seen in foals four months old and younger that are also sick or debilitated. Clinical ulcers in foals primarily occur in animals < 270 days old, and are usually found on the squamous epithelium of the stomach. Pyloric or duodenal ulcers are rare, and most often seen in animals three to five months of age. Ulcers in these regions are usually asymptomatic, but can cause stricture, leading to gastric outflow obstruction. Perforation secondary to ulcers, although rare, can occur both in the stomach and the duodenum, producing peritonitis. Rupture can not be predicted by ulcer severity as seen on endoscopic examination, and clinical signs are often not present until just prior to the event.
When fighting a monster or another player, you can either use a standard attack, a skill, or an item. If you use a standard attack, you must randomly select a DC Die from the dice bag. After retrieving the die, the opposing player must roll a die of the same kind. Rolling the die determines the attack strength of both characters. The lowest roll wins and the winning character inflicts the amount of damage as the die reads. If the attacking player loses, the attack has no effect whatsoever. If a skill is used, an absolute damage is inflicted to the opponent, no matter the outcome of a dice roll. Skills, however, take up action points (AP). Items can also be used in combat. If you are fighting a nightmare, a nightmare will deal absolute damage automatically. A restorative item, such as a potion, can be used to restore health points (HP). An offensive item, such as a grenade, can be used to deal an absolute damage to the opponent.
Superficial ulcers involve a loss of part of the epithelium. Deep ulcers extend into or through the stroma and can result in severe scarring and corneal perforation. Descemetoceles occur when the ulcer extends through the stroma, exposing Descemet's membrane. This type of ulcer is especially dangerous and can result in perforation.
Abbott is the inventor of a style of maze called logic mazes. A logic maze has a set of rules, ranging from the basic (such as "you cannot make left turns") to the extremely complicated. These mazes are also called "Multi-State mazes". The reason for this name is that sometimes you can return to a position you were in before, but be traveling in a different direction. That change in direction can put you in a different state and open up different choices for you. One example, from the book "SuperMazes", would be a rolling-die maze. Where you can move from a particular square depends on what number is facing up on the die. If you return to that same square, the die may be in a different state, with a different number on top. Thus, you would have different options than the first time.
"With all his good qualities, Gandhi did not bring the people forward from foolish and evil ways. His murderer was an educated man. Therefore nobody can say this is a time of high culture. If you eat poison, you will die. If electricity hits the body, you will die. If you oppose the Brahmin, you will die. Gandhi did not advocate the eradication of Varnasrama "Dharma" structure, but sees in it a task for the humanisation of society and social change possible within its structure. The consequence of this would be continued high-caste leadership. Gandhi adapted Brahmins to social change without depriving them of their leadership".
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.
Upper Endoscopy often reveals ulcers throughout the esophagus with intervening normal-appearing mucosa. In severe cases the ulcers can coalesce and on rare occasions have a black appearance known as black esophagus. While the diagnosis of herpes esophagitis can be inferred clinically it can only be accurately diagnosed through endoscopically obtained biopsies with microscopic evaluation by a pathologist finding the appropriate inclusion bodies and diagnostic immunochemical staining. False negative findings may occur if biopsies are taken from the ulcer rather than from the margin of the ulcer as the inclusion particles are to be found in viable epithelial cells. Viral tissue culture represents the most accurate means of diagnosing the precise cause.
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 ulcers can be removed through fulguration (burned off with the use of electricity or a laser) or resection (cutting around the ulcer, removing both the ulcer and the surrounding inflamed tissue). Some ulcers may recur in the same location.
Erosions, which involve the epithelial layer, are red in appearance since the underlying lamina propria shows through. When the full thickness of the epithelium is penetrated (ulceration), the lesion becomes covered with a fibrinous exudate and takes on a yellow-grey color. Because an ulcer is a breach of the normal lining, when seen in cross section, the lesion is a crater. A "halo" may be present, which is a reddening of the surrounding mucosa and is caused by inflammation. There may also be edema (swelling) around the ulcer. Chronic trauma may produce an ulcer with a keratotic (white, thickened mucosa) margin. Malignant lesions may ulcerate either because the tumor infiltrates the mucosa from adjacent tissues, or because the lesion originates within the mucosa itself, and the disorganized growth leads to a break in the normal architecture of the lining tissues. Repeat episodes of mouth ulcers can be indicative of an immunodeficiency, signaling low levels of immunoglobulin in the oral mucous membranes. Chemotherapy, HIV, and mononucleosis are all causes of immunodeficiency/immunosuppression with which oral ulcers may become a common manifestation. Autoimmunity is also a cause of oral ulceration. Mucous membrane pemphigoid, an autoimmune reaction to the epithelial basement membrane, causes desquamation/ulceration of the oral mucosa.
Numerous aphthous ulcers could be indicative of an inflammatory autoimmune disease called Behçet's disease. This can later involve skin lesions and uveitis in the eyes. Vitamin C deficiency may lead to scurvy which impairs wound healing, which can contribute to ulcer formation. For a detailed discussion of the pathophysiology of aphthous stomatitis, see Aphthous stomatitis#Causes.
An esophagogastroduodenoscopy (EGD), a form of endoscopy, also known as a gastroscopy, is carried out on people in whom a peptic ulcer is suspected. It is also the gold standard of diagnosis for peptic ulcer disease. By direct visual identification, the location and severity of an ulcer can be described. Moreover, if no ulcer is present, EGD can often provide an alternative diagnosis.
The location of the ulcer depends somewhat on the cause. Central ulcers are typically caused by trauma, dry eye, or exposure from facial nerve paralysis or exophthalmos. Entropion, severe dry eye and trichiasis (inturning of eyelashes) may cause ulceration of the peripheral cornea. Immune-mediated eye disease can cause ulcers at the border of the cornea and sclera. These include Rheumatoid arthritis, rosacea, systemic sclerosis which lead to a special type of corneal ulcer called Mooren's ulcer. It has a circumferential crater like depression of the cornea, just inside the limbus, usually with an overhanging edge.
The location of the ulcer depends somewhat on the cause. Central ulcers are typically caused by trauma, dry eye, or exposure from facial nerve paralysis or exophthalmos. Ulcers in the inferior nasal cornea may be caused by foreign material trapped under the third eyelid. Entropion or distichiae may cause ulceration of the peripheral cornea. Immune-mediated eye disease can cause ulcers at the border of the cornea and sclera.
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.
Refractory corneal ulcers are superficial ulcers that heal poorly and tend to recur. They are also known as indolent ulcers or Boxer ulcers. They are believed to be caused by a defect in the basement membrane and a lack of hemidesmosomal attachments. They are recognized by undermined epithelium that surrounds the ulcer and easily peels back. Refractory corneal ulcers are most commonly seen in diabetics and often occur in the other eye later. They are similar to Cogan's cystic dystrophy.
Melting ulcers are a type of corneal ulcer involving progressive loss of stroma in a dissolving fashion. This is most commonly seen in "Pseudomonas" infection, but it can be caused by other types of bacteria or fungi. These infectious agents produce proteases and collagenases which break down the corneal stroma. Complete loss of the stroma can occur within 24 hours. Treatment includes antibiotics and collagenase inhibitors such as acetylcysteine. Surgery in the form of corneal transplantation (penetrating keratoplasty) is usually necessary to save the eye.
The gameplay of "Art of Murder 3", just like its predecessor, is linear, its in 3-D and have a third-person perspective. The player moves the character by clicking on locations shown in the main display; the scene will only crossfade when a character is finished with all the actions on the screen. Players can interact with specific objects on screens by clicking or dragging them, and NPCs. The player can use an in-game hint system, which is located on the bottom left corner of a screen (in a shape of question mark). The items are carried by the player, and can be combined with other items, when its possible. Unlike the previous version of the game, you can rotate an object inside your inventory. The items return to their original position when dropped. The game have interactive cutcenes which will show up after a player will be done with the location, and before moving to a next one. To complete the game, the player must explore real life locations, such as; Bronx, and Manhattan. The game is non-violent, however, you can die in it. Before you die, the game saves your progress automatically, which means that if you die, you can start from your last save. Some game stages have a time limit as well, which, if you won't complete, is punishable by the death of your character.