Inflammation Of Mucous Membrane Is Called

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Inflammation Of Mucous Membrane Is Called
Can mucositis be prevented? – There’s not much in our toolbox yet to prevent mucositis from cancer treatment, but healthcare providers are working on it. Several medications are being tested that may help reduce the length and severity of the condition for certain people. Options include:

Cryotherapy, Sucking on ice chips before and during chemotherapy treatments can help protect against oral mucositis. Palifermin, This drug is a synthetic version of keratinocyte growth factor (KGF), a substance your body produces to help protect and repair the cells that line your mouth and GI tract. It’s been shown to reduce the length and severity of mucositis in people with blood cancer undergoing bone marrow or stem cell transplants. Topical agents, Two topical gels, Gelclair® and Zilactin®, have been shown to reduce oral mucositis by coating and protecting the mucosa before radiation treatments. Amifostine, This drug may lessen the severity of oral mucositis in people receiving radiation therapy to their head and neck when taken in advance. It may cause nausea as a side effect.

What is another name for mucous membrane called?

(MYOO-kus MEM-brayn) The moist, inner lining of some organs and body cavities (such as the nose, mouth, lungs, and stomach). Glands in the mucous membrane make mucus (a thick, slippery fluid). Also called mucosa.

What causes mucosal inflammation?

Proctitis and anusitis – If either issue results from an infection, the symptoms should go away after the infection is treated. If proctitis or anusitis results from an IBD, the symptoms may reoccur, requiring treatment. Complications of proctitis and anusitis include:

abscessesbleeding that leads to anemiafistulasnarrowing of the rectumulcers

Some people with erythematous mucosa have no symptoms. If a person experiences any symptoms of a health issue that causes this inflammation, they should contact a healthcare provider. Some symptoms require immediate medical attention. Examples include:

stomach cramps or painsevere abdominal pain fatigue, shortness of breath, or becoming lightheadedmucus or pus discharged from the rectumstool that is black or tarry, or contains dark red bloodvomiting red blood or what looks like coffee groundsbleeding from the rectum

Erythematous mucosa is inflammation of the mucosal lining of the digestive tract. It can be a sign of gastritis, colitis, proctitis, or anusitis. Environmental factors or an infection may be causing the underlying issue, and treating this issue will resolve the inflammation.

How do you treat inflamed mucous membranes?

Standard Therapies – Treatment The treatment of MMP is directed toward the specific symptoms that are apparent in each individual. Treatment depends upon the specific area(s) of the body affected, the severity of the disease, and its rate of progression.

  • Treatment may require the combined efforts of a team of specialists.
  • Dental specialists (oral pathologists), specialists who assess and treat skin problems (dermatologists), specialists who assess and treat eye problems (ophthalmologists), specialists who assess and treat ear and throat problems (otolaryngologists), and other healthcare professionals may need to systematically and comprehensively plan an affected individual’s treatment.

If the patient has not seen an ophthalmologist, then an appointment should be made right away to have the eyes evaluated because treatment often depends on whether or not there is eye involvement. The earliest changes of scarring just underneath the lining of the eye (subepithelial fibrosis) are often asymptomatic and can only be detected by slit-lamp microscopic evaluation by an ophthalmologist.

  1. Such scarring interferes with the glands that produce the tears, and this results in dryness of the eye.
  2. Affected patients may need to use artificial tears frequently to reduce damage to the eye.
  3. No large-scale, multi-center studies have been done regarding the treatment of MMP.
  4. The usual treatment for MMP is certain drugs, used either singly or in various combinations.

Corticosteroid drugs are often prescribed for affected individuals. Topical corticosteroids such as fluocinonide can relieve inflammation and itching in mild cases such as those that affect oral cavity only or the oral cavity and the skin. Other, more potent, gel preparations such as betamethasone dipropionate or clobetasol may also be used.

When pemphigoid affects the gums, keeping the teeth clean by tooth-brushing will help reduce the sores, especially when topical corticosteroids are used at the same time. Some antibiotic drugs can affect the inflammatory process. One such drug is dapsone, a sulfa-type medication that may be used to treat mild cases of MMP.

Special blood tests are needed before this drug is used, however. A combination of the antibiotic drug tetracycline and nicotinamide (vitamin B3) can also be helpful in some cases of MMP. Individuals with widespread or severe MMP may be treated with systemic corticosteroids such as prednisone and/or immunosuppressive drugs such as mycophenolate mofetil, cyclophosphamide or azathioprine.

  1. Individuals with eye involvement, severe or rapidly progressing MMP may be treated with prednisone combined with cyclophosphamide, mycophenolate mofetil, or azathioprine.
  2. Patients who are taking the above mentioned drugs must be carefully monitored by a dermatologist or physician familiar with their use because of potentially significant side effects.

If these drugs are not helping, or if the pemphigoid seems to be getting worse, then other treatments that can be tried include rituximab and IV-IG (intravenous immunoglobulin G). Rituximab is an antibody that destroys the cells that produce antibodies.

  1. IV-IG is produced by purifying and concentrating antibody molecules from hundreds of blood donors.
  2. Both rituximab and IV-IG can have very serious side effects, so they usually are not given unless the patient has pemphigoid that is not getting better with other treatments.
  3. In rare cases, surgical procedures such as a tracheostomy may become necessary if scarring narrows the airway and breathing becomes difficult.

A tracheostomy is a procedure in which a tube is inserted through a surgical opening in the windpipe (trachea) to assist breathing. A procedure to widen (dilate) a narrowed or obstructed esophagus may also be necessary if the esophagus is involved. Surgical removal (ablation) of ingrown eyelashes may be performed if the eyes are affected.

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What is a mucosal inflammation?

Definition : An INFLAMMATION of the MUCOSA with burning or tingling sensation. It is characterized by atrophy of the squamous EPITHELIUM, vascular damage, inflammatory infiltration, and ulceration. It usually occurs at the mucous lining of the MOUTH, the GASTROINTESTINAL TRACT or the airway due to chemical irritations, CHEMOTHERAPY, or radiation therapy (RADIOTHERAPY).

What are the 4 mucous membranes?

Mucosae of the Digestive System – The mouth, tongue, esophagus, stomach, and intestines are all lined with mucous membranes. These membranes are referred to as the oral mucosa, esophageal mucosa, gastric mucosa, and intestinal mucosa. Oral mucosa is found in the mouth, and changes in its condition can be signs of vitamin deficiencies, diabetes, or a result of long-term use of tobacco or alcohol.

There are three types of oral mucosa: lining, masticatory, and specialized. Lining mucosa lines surfaces such as the soft palate and the floor of the mouth. The masticatory mucosa provides a firmer surface for chewing, while the specialized mucosa is found on the tongue and contains the taste buds. The esophageal mucosa secretes mucus that protects the esophagus from abrasion by food.

The gastric mucosa, found in the stomach, produces mucus, digestive enzymes, and cells that stimulate acid production in order to break down food. The intestines are lined with intestinal mucosa, which absorbs nutrients from food and also absorbs water. This is a microscope image of the gastric mucosa.

What are the symptoms of a mucous membrane damage?

Mucous membrane pemphigoid is an autoimmune disorder that causes blisters to form in the mucous membranes of the body. The mucous membranes most often affected are the mouth and eyes.

Mucous membrane pemphigoid occurs when the immune system attacks the mucus membranes and causes blisters and sores. People have blistering in the mouth and on other areas of the body. Doctors diagnose mucous membrane pemphigoid by examining tissue samples under a microscope. Treatment usually involves corticosteroids or drugs that suppress the immune system.

The body’s immune system Overview of the Immune System The immune system is designed to defend the body against foreign or dangerous invaders. Such invaders include Microorganisms (commonly called germs, such as bacteria, viruses, and fungi) Parasites.

  1. Read more makes special cells that protect the body against harmful foreign invaders such as bacteria and viruses.
  2. Some of these cells respond to invaders by producing proteins called antibodies.
  3. Antibodies Antibodies One of the body’s lines of defense ( immune system) involves white blood cells (leukocytes) that travel through the bloodstream and into tissues, searching for and attacking microorganisms and.
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read more target and attach to the invaders and attract other cells in the immune system to destroy them. In an autoimmune disorder Autoimmune Disorders An autoimmune disorder is a malfunction of the body’s immune system that causes the body to attack its own tissues.

What triggers an autoimmune disorder is not known. Symptoms vary depending. read more, the body’s immune system mistakenly attacks the body’s own tissues—in this case, the skin. The antibodies that are produced mistakenly target the tissues as invaders, which makes them susceptible to destruction. In mucous membrane pemphigoid, the antibodies react with the mucous membranes of the mouth (or other mucous membranes), which blister and break down, forming open sores (ulcers).

The major symptom of mucous membrane pemphigoid is the development of painful blistering that causes redness, swelling, and breakdown of the mucous membranes, eventually forming open sores (ulcers). As they heal, these ulcers may cause scars to form in the affected area.

People rarely see actual blisters, and typically see only the raw, worn away areas. In the mouth, blistering typically involves the gums and anywhere along the lining of the mouth. The inside of the cheeks, the gums, and roof of the mouth are red and sore. Wearing down of the mucous membranes causes ulcers that burn or sting.

In other mucous membranes, such as in the nose, down the throat, or on the surface of the genitals and anus, the ulcers heal, often with scarring. Scarring can cause the lining of the esophagus (the tube that connects the throat to the stomach) to become narrow, which makes swallowing difficult.

  1. In some people with mucous membrane pemphigoid, actual blisters form on the skin.
  2. They tend to appear on the scalp, face, trunk, or limbs.
  3. The skin typically scars once the blisters heal.
  4. Doctors usually recognize mucous membrane pemphigoid by its characteristic appearance.
  5. The disorder is diagnosed with certainty by examining a sample of tissue under a microscope (biopsy).

Sometimes doctors use special chemical stains that allow antibody deposits to be seen under the microscope (called an immunofluorescence assay). Mucous membrane pemphigoid progresses slowly, rarely goes away without treatment, and often does not go away completely with treatment.

Corticosteroids and doxycycline plus nicotinamide Sometimes other drugs, including immunosuppressants for people with severe disease

Treatment of mucous membrane pemphigoid includes corticosteroids and a combination of doxycycline and nicotinamide taken by mouth. The corticosteroids may be applied directly to the affected area or may be injected into the sores. People who have severe mucous membrane pemphigoid may need drugs that suppress the immune system (immunosuppressants), so dapsone or prednisone may be given.

Generic Name Select Brand Names
doxycycline Acticlate, Adoxa, Adoxa Pak, Avidoxy, Doryx, Doxal, Doxy 100, LYMEPAK, Mondoxyne NL, Monodox, Morgidox 1x, Morgidox 2x, Okebo, Oracea, Oraxyl, Periostat, TARGADOX, Vibramycin, Vibra-Tabs
dapsone Aczone
prednisone Deltasone, Predone, RAYOS, Sterapred, Sterapred DS
azathioprine Azasan, Imuran
mycophenolate CellCept, Myfortic
cyclophosphamide Cyclophosphamide, Cytoxan, Neosar

NOTE: This is the Consumer Version. DOCTORS: VIEW PROFESSIONAL VERSION VIEW PROFESSIONAL VERSION Copyright © 2023 Merck & Co., Inc., Rahway, NJ, USA and its affiliates. All rights reserved.

What are the symptoms of mucosal inflammation?

How does mucositis affect my body? – Therapies designed to treat cancer will attack any cells that rapidly divide. Unfortunately, that includes any mucosa in the area — these therapies can’t discriminate between the two. Mucous membranes line your entire GI tract, including your mouth, throat, esophagus, stomach and small and large intestines,

  • Ordinarily, rapid cell turnover is part of what makes your mucosa the protective barrier that it is.
  • It allows the mucous membrane to regularly refresh itself, clearing out abrasive particles and pathogens and healing quickly from injuries.
  • Mucositis not only damages the existing cells in your mucosa, but also their ability to replicate themselves and heal.

This means that parts of your body that normally require that protective barrier are now exposed to irritation from their everyday functions. In your digestive system, that’s eating. These parts are also more vulnerable to infection. Mucositis most commonly affects your mouth and the inner lining of your cheeks (buccal mucosa).

These mucous membranes are particularly sensitive. Oral mucositis makes the inside of your mouth inflamed — red, shiny, swollen, raw and painful. It often leads to mouth sores or white patches of pus in your mouth. Oral mucositis can be mild or severe. Healthcare providers have a grading system for pain levels, with grades 1 and 2 being relatively mild and grades 3 and 4 being severe.

Severe cases can interfere with eating and can cause people with cancer to reduce their treatment. Some people also get gastrointestinal mucositis. This may manifest as abdominal pain and nausea if the inflammation is closer to your stomach, or as diarrhea or painful bowel movements if the inflammation is in your colon.

What are the symptoms of mucosal infection?

Enhancing Healthcare Team Outcomes – Patients with oral mucosal infections frequently present with symptoms of pain, inflammation, and odynophagia to the emergency department or dental office. Oral manifestations of bacterial infections are common, and most importantly, they tend to be one of their first clinical signs.

Dentists have a unique opportunity to identify these infectious diseases at early stages and make the appropriate referral for further testing and treatment. The described conditions require an interprofessional team effort and management, including dentists, primary care physicians, nurses, pharmacists, pathologists, and other specialists.

Pharmacists should emphasize compliance with the antibiotic regimen and alert patients about antibacterial resistance. The healthcare professionals team should stress any delay in treatment can worsen the disease, increase the risk of transmission and lead to irreversible complications.

Is mucosa life threatening?

What can I expect if I have this condition? – Mucosal melanoma is life-threatening. Healthcare providers use surgery and other treatments to remove tumors and eliminate cancer cells. But mucosal melanoma tumors often come back (recur). If you have mucosal melanoma, you may need additional surgery or other treatment.

What foods irritate mucous membranes?

Preventing irritation of mucous membranes

Irritants Substitutes
Cola-type soft drinks Carbonated fruit juices
Citrus fruit and their juice All other fruits
Spices Fresh herbs
Tomato and tomato juice Beet juice

What vitamins are good for mucous membranes?

Retinol Vitamin A is a fat-soluble vitamin that has several important functions in the body.

It helps cells reproduce normally, a process called cellular differentiation.It is essential for good vision. The first sign of a vitamin A deficiency is often poor sight at night.It is needed for the proper development of an embryo and fetus.

Vitamin A helps keep skin and mucous membranes that line the nose, sinuses, and mouth healthy. It also plays a role in:

Immune system functionGrowthBone formationReproductionWound healing

Vitamin A comes from two sources. One group, called retinoids, comes from animal sources and includes retinol. The other group, called carotenoids, comes from plants and includes beta-carotene. The body converts beta-carotene to vitamin A. Major carotenoids, including lycopene, lutein, and zeaxantuin, have important biological properties, including antioxidant and photoprotective activities.

Dry eyesNight blindnessDiarrheaSkin problems

While vitamin A is essential for good health, it can be toxic in high doses. Never take more than the recommended daily allowance without first talking to your doctor.

How do mucous membranes become infected?

Abstract – Skin infections are more frequent in immunodeficient patients, seniors and infants than in healthy individuals with an intact immune system. The severity of infections ranges from localized, self-limiting cutaneous infections to widespread necrosis of the skin, muscle, and fascia.

What is an example of mucosal infection?

Overview – Mucosal disorders are diseases of the mucous membranes of the mouth and genitals caused by yeast, viruses and bacteria. Mucosal disorders include:

Candidiasis (yeast infection): Candidiasis is an infection caused by excess yeast on the skin or mucus membranes. Yeast infections can occur in skin folds, genitals, mouth and corners of the mouth and nail beds. Canker sores: Canker sores are small sores on the lips, cheeks and tongue. Canker sores usually have a yellow center surrounded by redness that heals in 10 to 14 days. Herpes: The herpes simplex virus causes blisters around the mouth (HSV-1) and genitals (HSV-2) that break and form scabs. HSV is spread through skin-to-skin contact such as kissing and sexual intercourse. HSV can also be contagious even when no lesions are present.

What causes mucosal damage?

Causes and Diagnoses – The causes of mucosal disorders are generally bacteria, viruses or fungi, such as yeast. A weakened immune system, stress or dietary deficiencies can make you more prone to a mucosal disorder. Mucosal disorders can develop in a variety of ways:

Candidiasis is often caused by humid conditions, damaged skin or a depressed immune system. Canker sores are the result of a condition called aphthous stomatitis, and brought on by a weakened immune system, food allergies, viruses, bacteria and poor nutrition. Herpes is spread through skin-to-skin contact such as kissing and sexual intercourse. It can also be passed via a glass or lip balm of someone who has the herpes simplex virus. It can be contagious even when no lesions are present.

What is the difference between mucus and mucous membranes?

Simply put, mucus is a noun and mucous is an adjective. So, the actual fluid that comes out of your nose when you are congested is mucus and the linings in your body that secrete mucus are mucous membranes.

What do mucous membranes indicate?

What is mucosa? – Mucosa is another name for mucous membrane. Mucosa lines the insides of organs and cavities throughout your body that are exposed to particles from the outside. The mucous membrane lubricates and protects these organs and cavities from abrasive particles and bodily fluids, as well as invasive pathogens.

What is inflammation of the mucous membrane lining the sinuses?

Sinusitis is inflammation of the mucous membrane lining the sinuses. It is also known as rhinosinusitis (“rhino” means nose) because inflammation in the sinuses is usually accompanied by nasal inflammation. When the mucous membrane around the sinus openings (ostia) become obstructed, the sinuses fill with fluid creating a moist environment in which bacteria can grow.

How do you test for mucous membranes?

Abstract – Background: Mucous membrane pemphigoid (MMP) is an uncommon bullous disease typically involving the oral cavity. The most commonly used laboratory test for the diagnosis of MMP is direct immunofluorescence (DIF) on fresh perilesional tissue; however, the sensitivity of this test may be hampered by technical difficulties.

Immune-serological investigations can also be employed to render a diagnosis. The purpose of this paper was to present an evaluation of diagnostic testing for MMP within an Oral Medicine Unit in UK. Methods: A retrospective analysis of the medical records was undertaken for patients who had undergone biopsy and DIF testing from January 2016 to December 2018.

Parameters analysed included clinical presentation, histopathological features, DIF, salt-split skin indirect immunofluorescence, ELISA anti-BP180 and BP 230 and HLA-DQB1*03:01 findings. Results: Thirty patients (23 females and 7 males, mean age 66.8 years old) were diagnosed with MMP through a combination of histopathology and serological testing.

  1. Sixteen patients (53%) were DIF positive, whereas in 14 (47%), MMP diagnosis was achieved using immune-serologic tests.
  2. HLA DQB1*03:01 status was undertaken in 15 DIF-positive and 12 DIF-negative patients, and HLA DQB1*03:01 was found in 73% and 58% of the cases, respectively.
  3. Conclusions: This service evaluation has shown that when DIF is informative, it remains the gold standard technique for diagnosis of MMP.

However, we have also highlighted the value of serological testing for increasing diagnostic yield for patients with suspected MMP and the potential for HLA DQB1*03:01 as an adjunctive test for the evaluation of MMP. Keywords: ELISA; HLA; diagnosis; immunofluorescence; mucous membrane pemphigoid.

Can a damaged mucosa be repaired?

The canine and feline stomach suffers from a wide spectrum of primary and secondary disease. Most, if not all of these can cause vomiting and abdominal pain and are associated with some degree of damage to the gastric mucosa. The purpose of this paper is to review the mechanisms that facilitate or impair gastric mucosal protection in order to permit better understanding and treatment of gastric disease.

Why doesn’t the stomach digest itself? Physicians, physiologists and many others have been puzzled by this question since René Antonoine Ferchault de Réamur, the 18th century man of many sciences, showed that juice secreted by the stomach could digest meat. One answer of course is that it sometimes does.

Under some circumstances gastric juice can produce ulcers and even destroy most of the stomach lining. Normally, however, the stomach wall staunchly resists attack; as Claude Bernard observed, it behaves as if it was made of porcelain. Gastric juice contains hydrochloric acid, one of the most corrosive acids known.

  • At the concentration secreted by the gastric mucosa this acid is capable of dissolving zinc and is deadly to cells.
  • Yet in the stomach it ordinarily acts only to perform the useful actions of killing ingested bacteria, softening fibrous foods and promoting pepsin formation.
  • In the normal stomach this corrosive juice is prevented from contacting and damaging the stomach wall by a complex and interrelated series of physical and chemical processes that are only now beginning to be fully understood.

Collectively these processes are called the gastric mucosal barrier and comprise the structural and functional protection of the stomach against its own secreted acid and pepsin as well as against the ravages of refluxed bile and pancreatic enzymes and ingested abrasive or toxic materials.

  • There are five interrelated components: 1) the gastricepithelial cells; 2) gastric mucosal blood flow and local acid base balance; 3) gastric mucus; 4) mucosal prostaglandins and associated cytoprotection; and 5) the epithelial cell basement membrane.
  • The Gastric Epithelial Cells The epithelial cells of the gastric mucosa form a formidable barrier against penetration by luminal contents, including hydrogen ions.

The cells have very tight junctions, a lipid-rich, hydrophobic, acid-repelling mucosal surface, and secrete bicarbonate and mucus. The gastric mucosa is routinely exposed to trauma, indeed, focal destruction of the mucosal barrier is a normal physiologic event, occurring for example, during intragastric digestion of a meal, after thermal, mechanical or osmolar damage and after ingestion of several different types of drug.

Normally, however, the mucosa can repair or minimize this damage almost as soon as it occurs by a process of epithelial cell migration called restitution. This is a physiological event in which the epithelial cells at the mouth of the gastric glands adjacent to a damaged area flatten themselves and project finger like processes called lamellipodia.

These extend over the underlying basal membrane and eventually fuse to form a new intact epithelial barrier. Gastric Mucosal Blood Flow The gastric mucosal blood supply has been called the mainstay of the gastric mucosal defense mechanisms that sustain a healthy gastric mucosa.

Mucosal blood flow is achieved in a variety of ways, foremost of which is a unique vascular supply that maximizes mucosal oxygenation, bicarbonate delivery and buffering. Bicarbonate, a byproduct of acid production, is carried up to the mucosal surface by capillaries that surround each gastric gland.

This bicarbonate escapes from the capillaries into the submucosa underneath the mucosa from where it is taken up by the epithelial cells and secreted into the surface mucus layer. The bicarbonate is trapped here and neutralizes any hydrogen ions that may diffuse into the mucus layer.

  • As a result, the surface of the mucosa is maintained at a pH of about 7.2 while the pH of the lumen may be as low as 1.5.
  • The bicarbonate-rich mucosal blood flow also maintains intramucosal acid base neutrality such that any hydrogen ions that may leak into the submucosa through a damaged epithelium are quickly neutralised.

A decrease in mucosal blood flow however, will result in an increase in mucosal hydrogen ion concentration with subsequent tissue damage. Mucus Secretion Mucus neck cells produce the bulk of gastric mucus. This forms a viscid unstirred protective layer of varying thickness over the surface mucosa that traps secreted bicarbonate and lubricates the lining of the stomach.

  • When damaged the epithelial cells themselves rupture and release copious quantities of protective mucus that forms a bicarbonate-rich protective mucus cap over the denuded area.
  • Surrounding epithelial cells can migrate over the basal membrane and under this protective mucus cap.
  • Prostaglandin Secretion and Cytoprotection Cytoprotection refers to the ability of certain substances to maintain tissue or cellular integrity in the face of mucosal damage.

The term was originally coined to describe the ability of prostaglandins to reduce or eliminate hemorrhagic damage in mucosa exposed to injury. The term has been extended however, to describe a similar protective ability for a large number of endogenous and exogenously administered substances with anti-ulcerogenic effects.

Cytoprotection is based upon the ability of these substances to inhibit acid secretion, stimulate mucus and bicarbonate secretion, and increase mucosal cell turnover and blood flow. Prostaglandins PGE 2 and PGF 2a are perhaps the best known examples of cytoprotectants. However, IL-1 and TNF released during inflammation increase mucosal blood flow and cytoprotection, as do exogenously administered sulfhydryl compounds such as acetylcysteine, glutathione and penicillamine.

Epidermal growth factor which is found in saliva as well as in the gastric mucosa plays an important role in maintaining and stimulating mucosal cell turnover. The Basal Membrane This, the last defensive barrier is important for the process of restitution.

  • The basal membrane is permeable to fluid and electrolytes and when disrupted allows an inrush of hydrogen ions and proteases from the gastric lumen.
  • These invoke an inflammatory response and mark the changeover from physiologic to pathologic (i.e., inflammatory) repair of the mucosa.
  • BARRIER DISRUPTION Pathologic and inflammatory barrier disruption occurs in virtually every type of gastric disease as well as in a variety of less well appreciated circumstances such as stress, brain and spinal cord injury, hypotension, hypoadrenocorticism, sepsis, uremia, liver disease, hypoproteinemia and protein-calorie malnutrition (Table 1).

Most instances of barrier disruption associated with this diverse group of disorders can be attributed to a decrease in gastric mucosal blood flow, except for the hypoproteinemic or cachectic patient in which decreased cell turnover also plays a role. Gastric Disease Hypoadrenocorticism Liver disease Acidosis Sepsis (esp. peritonitis) Shock (septic > hypovolemic > traumatic) “Stress” Protein-calorie malnutrition Hypoproteinemia Enteritis (with vomiting) Uremia Hypoxemia NSAID therapy CNS and spinal cord injury In humans and some other species, infection with the Gram negative gastric bacteria Helicobacter is associated with gastric and duodenal injury. Mucosal damage from infection with H. pylori in humans is associated with the cytotoxic effects of a number of bacterial metabolites including ammonia, endotoxin, and a variety of inflammatory peptides.

  1. The organism also inhibits somatostatin secretion allowing an increase in acid secretion.
  2. Strangely, these properties do not appear to be present in the Helicobacter species (e.g., H. felis, H.
  3. Bizzozeroni) that infect the dog and cat.
  4. Gastric structure and function for example, are no different between infected and uninfected dogs.

The exact role of Helicobacter infection, if any, in the genesis of gastric lesions in the dog and cat therefore remains to be elucidated. Virtually every critically ill patient has some degree of gastric mucosal damage that is evidenced by gastric erosions or ulceration with associated hemorrhage.

This sometimes “hidden” injury very often prolongs patient morbidity, and if unappreciated or untreated may progress to a serious or life-threatening condition. An appreciation of the processes of barrier disruption and repair, together with an understanding of current methods for facilitating or enhancing the repair process are therefore important for most clinicians.

THE RESPONSE TO INJURY A break in the gastric mucosal barrier allows hydrogen ions and pepsin to diffuse into the mucosa from the lumen and sodium ions to diffuse in the opposite direction. Back-diffusion of acid and pepsin into the tissues stimulates further acid and pepsin secretion, decreases mucosal blood flow and decreases gastric motility.

  • The acid also damages connective tissue and submucosal capillaries to cause focal mucosal hemorrhage and microulceration.
  • If sufficiently severe and prolonged overt gastric ulceration may occur.
  • Mucosal integrity, however, is rapidly reestablished if the inciting cause is removed or if appropriate and prompt treatment is given.

Of concern to the clinician are factors that may delay or impair epithelial cell restitution and the repair process, such as hypoxia, sepsis or concomitant drug therapy. Corticosteroids for example, decrease gastric epithelial cell renewal and while relatively harmless in the healthy animal may delay repair or exacerbate mucosal injury in the sick one.

  • It should be noted however that methyl prednisolone sodium succinate at a dose of 30mg/kg/day for two days induced gastric hemorrhage in 100% of healthy normal dogs and that the synthetic prostaglandin misoprostol did not prevent the hemorrhage.
  • Nonsteroidal anti-inflammatory drugs (NSAIDs) are another group of compounds that exacerbate underlying disease and delay repair, primarily through their inhibition of cyclooxygenase and a decrease in mucosal prostaglandin concentration.

Recent attention has focused on the fact that there are two types of cyclooxygenase (cyclooxygenase 1 and 2 or COX-1 and COX-2). COX-1 is constitutively expressed in most cells and tissues, notably platelets, endothelial cells, stomach and kidney. COX-1 plays a key role in the synthesis of prostaglandins responsible for mucosal cytoprotection.

  • COX-2 on the other hand is typically undetectable in normal tissue but is induced in inflammatory conditions by cytokines or lipopolysaccharides.
  • NSAIDs exert their antiinflammatory effect through the inhibition of COX-2 whereas many of their adverse effects are due primarily to the inhibition of COX-1.

Several COX-2 specific antiinflammatory drugs have recently been introduced and purportedly reduce inflammation while sparing the gastric mucosa. Aspirin inhibits both cyclooxygenases but in addition, when the intragastric pH is less than 4.0, it undergoes a change in lipid permeability and is absorbed directly into the gastric epithelial cell where it disrupts cellular function.

  1. The drug is also purported to facilitate bile reflux in the dog.
  2. The canine stomach is particularly sensitive to NSAIDs and none of these drugs should be considered “safe” in this species.
  3. FACILITATION OF MUCOSAL REPAIR The most important concept in dealing with the disrupted mucosal barrier is to recognize that disruption is widespread and that it can occur in such a wide variety of diseases (Table 1).

Barrier disruption occurs routinely for example in hypoadrenocorticism, peritonitis, pyometra, pneumonia, liver disease, hypoproteinemia, severe trauma, uremia and in most if not all primary gastric diseases. The most important remedy in all these disorders is to treat the underlying disease.

Antisecretory Cytoprotectants
Cimetidine 5mg/kg q8h Misoprostol 3-4μg/kg q12h
Ranitidine 2mg/kg q12h Sucralfate 0.25-1.0g/patient q8-12h
Famotidine 1mg/kg q24h Aluminum ions to effect
Omeprazole 0.7mg/kg q24h Bismuth subsalts to effect

Antisecretory Drugs A variety of compounds have been used to reduce acid secretion but most widely used are the H2 receptor antagonists such as cimetidine, ranitidine and famotidine. Cimetidine interferes with the cytochrome p450 system in the liver and can influence the action of some drugs (e.g., ketoconazole, theophylline, propranolol, quinidine and metronidazole) and the absorption or effect of others (e.g., metoclopramide and sucralfate). Cimetidine, however, is ineffective against aspirin-induced mucosal injury in dogs. Ranitidine binds much more strongly to the H2 receptor on the parietal cell and therefore requires a lower frequency of administration as well as indirectly increasing gastric motility. Cimetidine also has additional protective effects on the mucosal barrier (increased cell turnover, mucus production, mucosal blood flow, bicarbonate secretion and cellular integrity). Famotidine inhibits stress-induced decreases in gastric mucosal blood flow and has the benefit of once daily dosage which makes it attractive to many clients. The prophylactic use of H2 receptor antagonists should therefore be routine in critically ill patients. Omeprazole, is another very effective antisecretory drug. Cimetidine, famotidine and ranitidine block only histamine-induced acid secretion but omeprazole blocks all acid secretion by inhibiting H+K+ATP’ase at the luminal surface of the parietal cell. While a major portion of the therapeutic efficacy of omeprazole involves inhibition of gastric acid secretion, some of its cytoprotective properties are probably associated with its action on the mucosal vasculature. Oral omeprazole for example, maintains mucosal blood flow in the face of mucosal damage and decreases mucosal production of the vasoconstrictor phospholipid platelet activating factor (PAF). Cytoprotective Drugs These include synthetic prostaglandins, sucralfate, antacids containing aluminum, and the bismuth sub-salts. Sucralfate is a complex polymer of sucrose with multiple substitutions of sulfate and aluminum salts. At a pH <4.0 it undergoes a change in chemical configuration, developing a positive charge which binds electrochemically with the negative charge in serum protein to form a protective layer over ulcerated areas which protects the mucosa against further injury by acid, pepsin and bile salts. The drug also stimulates the synthesis and release of prostaglandins, epidermal growth factor and nitric oxide as well as augmenting other aspects of the mucosal barrier such as gastric mucosal blood flow, bicarbonate secretion and mucus production. Sucralfate also stimulates angiogenesis in injured gastric mucosa. The bismuth subsalts and aluminum containing antacids at doses less than those required to neutralize acid also exert beneficial effects on the mucosal barrier through augmented prostaglandin synthesis. CONCLUSION Gastric mucosal damage and repair are ongoing processes in the normal stomach with repair, primarily through epithelial cell restitution, rapidly restoring the ravages of normal wear and tear. The repair process however, may be impaired in gastric disease as well as in a variety of other diseases that weaken gastric defenses. If unrecognized and untreated this will increase patient morbidity with the likelihood of overt ulceration. Treatment with H2 receptor antagonists and cytoprotective drugs is critical to patient well being.

What is the name of one mucus membrane?

Function – One of its functions is to keep the tissue moist (for example in the respiratory tract, including the mouth and nose). : 480  It also plays a role in absorbing and transforming nutrients, : 5, 813  Mucous membranes also protect the body from itself.

What are other names for mucosa?

Also called mucous membrane.

What is the medical term for mucus?

Listen to pronunciation. (flem) A more than normal amount of thick mucus made by the cells lining the upper airways and lungs. A buildup of phlegm may be caused by infection, irritation, or chronic lung disease, and can cause discomfort in the chest and coughing.