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Causes can be remembered by mnemonic HERNIA:
- Hereditary factors: the disease runs in families
- Endocrine imbalance: the disease tends to start at puberty and mostly involves females
- Racial factors: whites are more susceptible than natives of equatorial Africa
- Nutritional deficiency: vitamins A or D, or iron
- Infection: "Klebsiella ozaenae", diphtheroids, "Proteus vulgaris", "E. coli", etc.
- Autoimmune factors: viral infection or some other unidentified insult may trigger antigenicity of the nasal mucosa.
Specific infections, such as syphilis, lupus, leprosy and rhinoscleroma, may cause destruction of the nasal structures leading to atrophic changes. Atrophic rhinitis can also result from long-standing purulent sinusitis or radiotherapy of the nose, or as a complication of surgery of the turbinates. The United Kingdom National Health Service has stated that "Most cases of atrophic rhinitis in the UK occur when the turbinates are damaged or removed during surgery". Some authors refer to as Atrophic rhinitis secondary to sinus surgery as the empty nose syndrome.
Common issues that lead to overuse of topical decongestants:
- Deviated septum
- Upper respiratory tract infection
- Vasomotor rhinitis
- Cocaine use and other stimulant abuse
- Pregnancy (these products are not considered safe for pregnancy)
- Chronic rhinosinusitis
- Hypertrophy of the inferior turbinates
Rhinorrhea can also occur when individuals with allergies to certain substances, such as pollen, dust, latex, soy, shellfish, or animal dander, are exposed to these allergens. In people with sensitized immune systems, the inhalation of one of these substances triggers the production of the antibody immunoglobulin E (IgE), which binds to mast cells and basophils. IgE bound to mast cells are stimulated by pollen and dust, causing the release of inflammatory mediators such as histamine. In turn, this causes, among other things, inflammation and swelling of the tissue of the nasal cavities as well as increased mucus production. Particulate matter in polluted air and chemicals such as chlorine and detergents, which can normally be tolerated, can make the condition considerably worse.
Nasal mucosa has rich blood supply and has venous sinusoids or "lakes" surrounded by smooth muscle fibers. These smooth muscle fibers act as sphincters and control the filling and emptying of sinusoids. Sympathetic stimulation causes vasoconstriction and shrinkage of mucosa, which leads to decongestion of nose. Parasympathetic stimulation causes not only excessive secretion from the nasal gland but also vasodilatation and engorgement, which lead to rhinorrhoea and congestion of nose. The autonomic nervous system, which supplies the nasal mucosa, is under the control of the hypothalamus. Therefore, emotions play significant role in nonallergic rhinitis.
Rhinorrhea can be a symptom of other diseases, such as the common cold or influenza. During these infections, the nasal mucous membranes produce excess mucus, filling the nasal cavities. This is to prevent infection from spreading to the lungs and respiratory tract, where it could cause far worse damage. It has also been suggested that rhinorrhea is a result of viral evolution, and may be a response that is not useful to the host, but which has evolved by the virus to maximise its own infectivity. Rhinorrhea caused by these infections usually occur on circadian rhythms. Over the course of a viral infection, sinusitis (the inflammation of the nasal tissue) may occur, causing the mucous membranes to release more mucus. Acute sinusitis consists of the nasal passages swelling during a viral infection. Chronic sinusitis occurs when one or more nasal polyps appear. This can be caused by a deviated septum as well as a viral infection.
Rhinitis medicamentosa (or RM) is a condition of rebound nasal congestion brought on by extended use of topical decongestants (e.g., oxymetazoline, phenylephrine, xylometazoline, and naphazoline nasal sprays) and certain oral medications (e.g., sympathomimetic amines and various 2-imidazolines) that constrict blood vessels in the lining of the nose.
Nonallergic rhinitis is inflammation of the inner part of the nose that is not caused by an allergy. Nonallergic rhinitis involves symptoms including chronic sneezing or having a congested, drippy nose without an identified allergic reaction. Other common terms for nonallergic rhinitis are vasomotor rhinitis and perennial rhinitis. The prevalence of nonallergic rhinitis in otolaryngology is 40%. Allergic rhinitis is more common than nonallergic rhinitis; however, both conditions have similar presentation, manifestation and treatment. Nasal itching and paroxysmal sneezing are usually associated with nonallergic rhinitis in comparison to allergic rhinitis.
Nonallergic rhinitis refers to rhinitis that is not due to an allergy. The category was formerly referred to as vasomotor rhinitis, as the first cause discovered was vasodilation due to an overactive parasympathetic nerve response. As additional causes were identified, additional types of nonallergic rhinitis were recognized. Vasomotor rhinitis is now included among these under the more general classification of nonallergic rhinitis. The diagnosis is made upon excluding allergic causes. It is an umbrella term of rhinitis of multiple causes, such as occupational (chemical), smoking, gustatory, hormonal, senile (rhinitis of the elderly), atrophic, medication-induced (including rhinitis medicamentosa), local allergic rhinitis, non-allergic rhinitis with eosinophilia syndrome (NARES) and idiopathic (vasomotor or non-allergic, non-infectious perennial allergic rhinitis (NANIPER), or non-infectious non-allergic rhinitis (NINAR).
In vasomotor rhinitis, certain nonspecific stimuli, including changes in environment (temperature, humidity, barometric pressure, or weather), airborne irritants (odors, fumes), dietary factors (spicy food, alcohol), sexual arousal, exercise, and emotional factors trigger rhinitis. There is still much to be learned about this, but it is thought that these non-allergic triggers cause dilation of the blood vessels in the lining of the nose, which results in swelling and drainage.
Non-allergic rhinitis can co-exist with allergic rhinitis, and is referred to as "mixed rhinitis." The pathology of vasomotor rhinitis appears to involve neurogenic inflammation and is as yet not very well understood. Vasomotor rhinitis appears to be significantly more common in women than men, leading some researchers to believe that hormones play a role. In general, age of onset occurs after 20 years of age, in contrast to allergic rhinitis which can be developed at any age. Individuals with vasomotor rhinitis typically experience symptoms year-round, though symptoms may be exacerbated in the spring and autumn when rapid weather changes are more common. An estimated 17 million United States citizens have vasomotor rhinitis.
Drinking alcohol may cause rhinitis as well as worsen asthma (see alcohol-induced respiratory reactions). In certain populations, particularly those of East Asian countries such as Japan, these reactions have a nonallergic basis. In other populations, particularly those of European descent, a genetic variant in the gene that metabolizes ethanol to acetaldehyde, ADH1B, is associated with alcohol-induced rhinitis. It is suggested that this variant metabolizes ethanol to acetaldehyde too quickly for further processing by ALDH2 and thereby leads to the accumulation of acetaldehyde and rhinitis symptoms. In these cases, alcohol-induced rhinitis may be of the "mixed rhinitis" type and, it seems likely, most cases of alcohol-induced rhinitis in non-Asian populations reflect true allergic response to the non-ethanol and/or contaminants in alcoholic beverages, particularly when these beverages are wines or beers. Alcohol-exacerbated rhinitis is more frequent in individuals with a history of rhinitis exacerbated by aspirin.
Aspirin and other non-steroidal anti-inflammatory drugs (NSAIDs), particularly those that inhibit cyclooxygenase 1 (COX1), can worsen rhinitis and asthma symptoms in individuals with a history of either one of these diseases. These exacerbations most often appear due to NSAID hypersensitivity reactions rather than NSAID-induced allergic reactions.
The antihistamine azelastine, applied as a nasal spray, may be effective for vasomotor rhinitis. Fluticasone propionate or budesonide (both are steroids) in nostril spray form may also be used for symptomatic treatment. The antihistamine cyproheptadine is also effective, probably due to its antiserotonergic effects.
A Cochrane review on non-allergic rhinitis reports improvement of overall function after treatment with capsaicin (the active component of chili peppers). The quality of evidence is low, however.
Chronic rhinitis is a form of atrophy of the mucous membrane and glands of the nose.
This is a rare condition, probably caused by an allergic reaction, in which there is sudden swelling of the salivary glands. It is associated with other allergic conditions such as asthma, urticaria, allergic rhinitis and food allergy.
One way to prevent allergic rhinitis is to wear a respirator or mask when near potential allergens.
Growing up on a farm and having multiple brothers and or sisters decreases the risk.
Allergic rhinitis is the type of allergy that affects the greatest number of people. In Western countries, between 10 and 30 percent of people are affected in a given year. It is most common between the ages of twenty and forty.
Smoking, especially heavy smoking, is an important predisposing factor but the reasons for this relationship are unknown. One hypothesis is that cigarette smoke contains nutritional factors for "C. albicans", or that local epithelial alterations occur that facilitate colonization of candida species.
Sialodochitis (also termed ductal sialadenitis), is inflammation of the duct system of a salivary gland. This is compared to sialadenitis, which is inflammation of the gland parenchyma.
Sialodochitis may be associated with salivary duct strictures and salivary stones.
It is common in both the parotid glands and submandibular glands.
The treatment is as for sialadenitis.
Malnutrition, whether by malabsorption, or poor diet, especially hematinic deficiencies (iron, vitamin B12, folic acid) can predispose to oral candidiasis, by causing diminished host defense and epithelial integrity. For example, iron deficiency anemia is thought to cause depressed cell-mediated immunity. Some sources state that deficiencies of vitamin A or pyridoxine are also linked.
There is limited evidence that a diet high in carbohydrates predisposes to oral candidiasis. "In vitro" and studies show that Candidal growth, adhesion and biofilm formation is enhanced by the presence of carbohydrates such as glucose, galactose and sucrose.
First-generation antihistamine has been suggested as first-line therapy to treat post-nasal drip.
Good oral hygiene (thorough tooth brushing and flossing and regular professional cleaning and examination) may be helpful to prevent these disorders. Drinking plenty of water and the production of enough saliva, aid in the reduction of bacterial growth. Minimizing irritants or injury in the mouth when possible can aid in the prevention of glossitis. Avoiding excessive use of any food or substance that irritates the mouth or tongue may also help.
Many conditions can cause glossitis via malnutrition or malabsorption, which creates the nutritional deficiencies described above, although other mechanisms may be involved in some of those conditions listed.
- Alcoholism
- Sprue (celiac disease, or tropical sprue), secondary to nutritional deficiencies
- Crohn’s disease
- Whipple disease
- Glucagonoma syndrome
- Cowden disease
- Acquired immunodeficiency syndrome (AIDS)
- Carcinoid syndrome
- Kwashiorkor amyloidosis
- Veganism and other specialized diets,
- Poor hydration and low saliva in the mouth, which allows bacteria to grow more readily
- Mechanical irritation or injury from burns, rough edges of teeth or dental appliances, or other trauma
- Tongue piercing Glossitis can be caused by the constant irritation by the ornament and by colonization of Candida albicans in site and on the ornament
- Exposure to irritants such as tobacco, alcohol, hot foods, or spices
- Allergic reaction to toothpaste, mouthwash, breath fresheners, dyes in confectionery, plastic in dentures or retainers, or certain blood-pressure medications (ACE inhibitors)
- Administration of ganglion blockers (e.g., Tubocurarine, Mecamylamine).
- Oral lichen planus, erythema multiforme, aphthous ulcer, pemphigus vulgaris
- Heredity
- Albuterol (bronchodilator medicine)
- Schizophrenia
A painful tongue may be an indication of an underlying serious medical condition and nearly always merits assessment by a physician or dental surgeon.
The treatment of nasal congestion frequently depends on the underlying cause.
Alpha-adrenergic agonists are the first treatment of choice. They relieve congestion by constricting the blood vessels in the nasal cavity, thus resulting in relieved symptoms. Examples include oxymetazoline and phenylephrine.
Both influenza and the common cold are self-limiting conditions that improve with time; however, drugs such as acetaminophen (paracetamol), aspirin, and ibuprofen may help with the discomfort.
A cause of nasal congestion may also be due to an allergic reaction caused by hay fever, so avoiding allergens is a common remedy if this becomes a confirmed diagnosis. Antihistamines and decongestants can provide significant symptom relief although they do not cure hay fever. Antihistamines may be given continuously during pollen season for optimum control of symptoms. Topical decongestants should only be used by patients for a maximum of 3 days in a row, because rebound congestion may occur in the form of rhinitis medicamentosa.
Nasal decongestants target discomfort directly. These come as nasal sprays like naphazoline (Privine), oxymetazoline (Afrin, Dristan, Duramist), as inhalers, or phenylephrine (Neo-Synephrine, Sinex, Rhinall) or as oral pills (Bronkaid, Sudafed, Neo-Synephrine, Sinex, Rhinall). Oral decongestants may be used for up to a week without consulting a doctor, with the exception of Bronkaid and Sudafed, which can be taken as long as needed, but nasal sprays can also cause "rebound" (Rhinitis medicamentosa) and worsen the congestion if taken for more than a few days. Therefore, you should only take nasal sprays when discomfort cannot be remedied by other methods, and never for more than three days.
If an infant is unable to breathe because of a plugged nose, a nasal aspirator may be useful to remove the mucus. The mucus might be thick and sticky, making it difficult to expel from the nostril.
Nasal congestion is the blockage of the nasal passages usually due to membranes lining the nose becoming swollen from inflamed blood vessels.
Nasal decongestants target the discomfort directly. These come as nasal sprays, inhalers, and as oral pills.
Nasal congestion has many causes and can range from a mild annoyance to a life-threatening condition. Most people prefer to breathe through the nose (historically referred to as "obligate nasal breathers"). Nasal congestion in an infant in the first few months of life can interfere with breastfeeding and cause life-threatening respiratory distress; in older children and adolescents it is often just an annoyance but can cause other difficulties.
Nasal congestion can interfere with the hearing and speech. Significant congestion may interfere with sleep, cause snoring, and can be associated with sleep apnea. In children, nasal congestion from enlarged adenoids has caused chronic sleep apnea with insufficient oxygen levels and hypoxia, as well as right-sided heart failure. The problem usually resolves after surgery to remove the adenoids and tonsils, however the problem often relapses later in life due to craniofacial alterations from chronic nasal congestion.
Nasal congestion can also cause mild facial and head pain, and a degree of discomfort, often from allergies or the common cold.
PND is suggested to be a cause of extra-oral halitosis, especially when a sinus infection is also present. Acid reflux or heartburn is believed to aggravate and in some cases cause post-nasal drip. Post-nasal drip can be a cause of laryngeal inflammation and hyperresponsiveness, leading to symptoms of vocal cord dysfunction (VCD).
It is not lethal in nature and is responsive to tetracycline or ciprofloxacin. Surgical treatment include rhinoplasty. However, if left untreated the disease can lead to sepsis, bleeding, or other chronic conditions that can be fatal.
Empty nose syndrome has been observed to affect a small proportion of people who have undergone surgery to the nose or sinuses, particularly those who have undergone turbinectomy (a procedure that removes some of the bones in the nasal passage). The incidence of ENS is variable and has not yet been quantified, but it is considered rare.
Untreated, the condition can cause significant and longterm physical and emotional distress in some people; some of the initial presentations on the condition described people who committed suicide. It is difficult to determine what treatments are safe and effective, and to what extent, in part because the diagnosis itself is unclear.
It is caused by "Klebsiella rhinoscleromatis"—subspecies of
"Klebsiella pneumoniae"— a gram-negative, encapsulated, nonmotile, rod-shaped bacillus (diplobacillus), member of the Enterobacteriaceae family. It is sometimes referred to as the "Frisch bacillus," named for Anton von Frisch who identified the organism in 1882. It is contracted directly by droplets or by contamination of material that is subsequently inhaled.