Sinusitis (or rhinosinusitis) is defined as an inflammation of the mucous membrane that lines the paranasal sinuses and is classified chronologically into several categories:

- Acute rhinosinusitis – A new infection that may last up to four weeks and can be subdivided symptomatically into severe and non-severe. Some use definitions up to 12 weeks.

- Recurrent acute rhinosinusitis – Four or more full episodes of acute sinusitis that occur within one year

- Subacute rhinosinusitis – An infection that lasts between four and 12 weeks, and represents a transition between acute and chronic infection

- Chronic rhinosinusitis – When the signs and symptoms last for more than 12 weeks.

- Acute exacerbation of chronic rhinosinusitis – When the signs and symptoms of chronic rhinosinusitis exacerbate, but return to baseline after treatment

All these types of sinusitis have similar symptoms, and are thus often difficult to distinguish. Acute sinusitis is very common. Roughly ninety percent of adults have had sinusitis at some point in their life.

Headache/facial pain or pressure of a dull, constant, or aching sort over the affected sinuses is common with both acute and chronic stages of sinusitis. This pain is typically localized to the involved sinus and may worsen when the affected person bends over or when lying down. Pain often starts on one side of the head and progresses to both sides.

Acute sinusitis may be accompanied by thick nasal discharge that is usually green in color and may contain pus (purulent) and/or blood. Often a localized headache or toothache is present, and it is these symptoms that distinguish a sinus-related headache from other types of headaches, such as tension and migraine headaches. Another way to distinguish between toothache and sinusitis is that the pain in sinusitis is usually worsened by tilting the head forwards and with valsalva maneuvers.

Infection of the eye socket is possible, which may result in the loss of sight and is accompanied by fever and severe illness. Another possible complication is the infection of the bones (osteomyelitis) of the forehead and other facial bones – Pott's puffy tumor.

Sinus infections can also cause middle ear problems due to the congestion of the nasal passages. This can be demonstrated by dizziness, "a pressurized or heavy head", or vibrating sensations in the head. Post-nasal drip is also a symptom of chronic rhinosinusitis.

Halitosis (bad breath) is often stated to be a symptom of chronic rhinosinusitis; however, gold standard breath analysis techniques have not been applied. Theoretically, there are several possible mechanisms of both objective and subjective halitosis that may be involved.

A 2004 study suggested that up to 90% of "sinus headaches" are actually migraines. The confusion occurs in part because migraine involves activation of the trigeminal nerves, which innervate both the sinus region and the meninges surrounding the brain. As a result, it is difficult to accurately determine the site from which the pain originates. People with migraines do not typically have the thick nasal discharge that is a common symptom of a sinus infection.

A URI may be classified by the area inflamed.

Rhinitis affects the nasal mucosa, while rhinosinusitis or sinusitis affects the nose and paranasal sinuses, including frontal, ethmoid, maxillary, and sphenoid sinuses. Nasopharyngitis (rhinopharyngitis or the common cold) affects the nares, pharynx, hypopharynx, uvula, and tonsils generally. Without involving the nose, pharyngitis inflames the pharynx, hypopharynx, uvula, and tonsils. Similarly, epiglottitis (supraglottitis) inflames the superior portion of the larynx and supraglottic area; laryngitis is in the larynx; laryngotracheitis is in the larynx, trachea, and subglottic area; and tracheitis is in the trachea and subglottic area.

In uncomplicated colds, cough and nasal discharge may persist for 14 days or more even after other symptoms have resolved.

Acute upper respiratory tract infections include rhinitis, pharyngitis/tonsillitis and laryngitis often referred to as a common cold, and their complications: sinusitis, ear infection and sometimes bronchitis (though bronchi are generally classified as part of the lower respiratory tract.) Symptoms of URTIs commonly include cough, sore throat, runny nose, nasal congestion, headache, low-grade fever, facial pressure and sneezing.

Symptoms of rhinovirus in children usually begin 1–3 days after exposure. The illness usually lasts 7–10 more days.

Color or consistency changes in mucous discharge to yellow, thick, or green are the natural course of viral upper respiratory tract infection and not an indication for antibiotics.

Group A beta hemolytic streptococcal pharyngitis/tonsillitis (strep throat) typically presents with a sudden onset of sore throat, pain with swallowing and fever. Strep throat does not usually cause runny nose, voice changes, or cough.

Pain and pressure of the ear caused by a middle ear infection (otitis media) and the reddening of the eye caused by viral conjunctivitis are often associated with upper respiratory infections.

The characteristic presentation of RM involves nasal congestion without rhinorrhea, postnasal drip, or sneezing following several days of decongestant use. This condition typically occurs after 5–7 days of use of topical decongestants. Patients often try increasing both the dose and the frequency of nasal sprays upon the onset of RM, worsening the condition. The swelling of the nasal passages caused by rebound congestion may eventually result in permanent turbinate hyperplasia, which may block nasal breathing until surgically removed.

Asthma is characterized by recurrent episodes of wheezing, shortness of breath, chest tightness, and coughing. Sputum may be produced from the lung by coughing but is often hard to bring up. During recovery from an attack, it may appear pus-like due to high levels of white blood cells called eosinophils. Symptoms are usually worse at night and in the early morning or in response to exercise or cold air. Some people with asthma rarely experience symptoms, usually in response to triggers, whereas others may have marked and persistent symptoms.

Alcohol may worsen asthmatic symptoms in up to a third of people. This may be even more common in some ethnic groups such as the Japanese and those with aspirin-induced asthma. Other studies have found improvement in asthmatic symptoms from alcohol.

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

Symptoms of polyps include nasal congestion, sinusitis, loss of smell, thick nasal discharge, facial pressure, nasal speech, and mouth breathing. Recurrent sinusitis can result from polyps. Long-term, nasal polyps can cause destruction of the nasal bones and widening of the nose.

As polyps grow larger, they eventually prolapse into the nasal cavity resulting in symptoms. The most prominent symptoms of nasal polyps result blockage of the nasal passage.

People with nasal polyps due to aspirin intolerance often have symptoms known as Samter's triad, which consists of asthma worse with aspirin, a skin rash caused by aspirin, and chronic nasal polyps.

There are no objective physical examination findings that definitely diagnose ENS. Generally, one or more turbinates may be reduced or absent when viewed in medical imaging or via endoscope with no sign of physical obstruction, the mucosa will be dry and pale, and there may be signs of secondary infection.

Symptoms of ENS include a sensation of being unable to breathe, a feeling of nasal obstruction and dryness, and crusting, oozing, and foul smells inside the nose from infections. A person with ENS may complain of pain in their nose or face, an inability to sleep and fatigue, and of feeling irritated, depressed, or anxious; they may be constantly distracted by the sense that they are not getting enough air.

Empty nose syndrome (ENS), one form of secondary atrophic rhinitis, is a rare clinical syndrome in which people who have clear nasal passages experience a range of symptoms, most commonly feelings of nasal obstruction, nasal dryness and crusting, and a sensation of being unable to breathe. People who experience ENS have usually undergone a turbinectomy (removal or reduction of turbinates, structures inside the nose) or other surgical procedures that interfere with turbinates; the overall incidence is unknown but it appears to occur in a small percentage of those who undergo nasosinal procedures. It appears to be a health care caused condition but its existence as a medical condition, cause, diagnosis and management are controversial.

All aspects have been subject to debate, including whether it should be considered solely rhinologic, or may have neurological or psychosomatic aspects. As of 2015 many ear, nose, and throat doctors do not recognize the condition.

The exact cause of VCD is not known, and it is unlikely that a single underlying cause exists. Several contributing factors have been identified, which vary widely among VCD patients with different medical histories. Physical exercise (including, but not limited to, competitive athletics) is one of the major triggers for VCD episodes, leading to its frequent misdiagnosis as exercise-induced asthma. Other triggers include airborne pollutants and irritants such as smoke, dust, gases, soldering fumes, cleaning chemicals such as ammonia, perfumes, and other odours. Gastroesophageal reflux disease (GERD) and rhinosinusitis (inflammation of the paranasal sinuses and nasal cavity) may also play a role in inflaming the airway and leading to symptoms of VCD as discussed below.

Laryngeal hyperresponsiveness is considered the most likely physiologic cause of VCD, brought on by a range of different triggers that cause inflammation and/or irritation of the larynx (voice box). The glottic closure reflex (or laryngeal adductor reflex) serves to protect the airway, and it is possible that this reflex becomes hyperactive in some individuals, resulting in the paradoxical vocal fold closure seen in VCD. Two major causes of laryngeal inflammation and hyperresponsiveness are gastroesophageal reflux disease (GERD) and postnasal drip (associated with rhinosinusitis, allergic or nonallergic rhinitis, or a viral upper respiratory tract infection (URI)). Rhinosinusitis is very common among patients with VCD and for many patients, VCD symptoms are ameliorated when the rhinosinusitis is treated. GERD is also common among VCD patients, but only some experience an improvement in VCD symptoms when GERD is treated. Other causes of laryngeal hyperresponsiveness include inhalation of toxins and irritants, cold and dry air, episodic croup and laryngopharyngeal reflux (LPR).

VCD has long been strongly associated with a variety of psychological or psychogenic factors, including conversion disorder, major depression, obsessive-compulsive disorder, anxiety (especially in adolescents), stress (particularly stress relating to competitive sports), physical and sexual abuse, post-traumatic stress disorder, panic attacks, factitious disorder and adjustment disorder. It is important to note that anxiety and depression may occur in certain patients as a "result" of having VCD, rather than being the cause of it. Psychological factors are important precipitating factors for many patients with VCD; although exercise is also a major trigger for episodes of VCD, some patients experience VCD co-occurring with anxiety regardless of whether or not they are physically active at the time of the VCD/anxiety episode. Experiencing or witnessing a traumatic event related to breathing (such as a near-drowning or life-threatening asthma attack, for example), has also been identified as a risk factor for VCD.

VCD has also been associated with certain neurologic diseases including Arnold-Chiari malformation, cerebral aqueduct stenosis, cortical or upper motor neuron injury (such as that resulting from stroke), amyotrophic lateral sclerosis (ALS), parkinsonism syndromes and other movement disorders. However, this association occurs only rarely.

The symptoms of VCD are often inaccurately attributed to asthma, which in turn results in the unnecessary and futile intake of corticosteroids, bronchodilators and leukotriene modifiers, although there are instances of comorbidity of asthma and VCD.

The differential diagnosis for vocal cord dysfunction includes vocal fold swelling from allergy, asthma, or some obstruction of the vocal folds or throat. Anyone suspected of this condition should be evaluated and the vocal folds (voice box) visualized. In individuals who experience a persistent difficulty with inhaling, consideration should be given to a neurological cause such as brain stem compression, cerebral palsy, etc.

The main difference between VCD and asthma is the audible stridor or wheezing that occurs at different stages of the breath cycle: VCD usually causes stridor on the inhalation, while asthma results in wheezing during exhalation. Patients with asthma usually respond to the usual medication and see their symptoms resolve. Clinical measures that can be done to differentiate VCD from asthma include:

- rhinolaryngoscopy: A patient with asthma will have normal vocal cord movement, while one with VCD will display vocal cord abduction during inhalation

- spirometry: A change in the measure following the administration of a bronchodilator is suggestive of asthma rather than VCD

- chest radiography: The presence of hyperinflation and peribronchial thickening are indicative of asthma, as patients with VCD will show normal results.

Other disorders can mimic the appearance of nasal polyps and should be considered if a mass is seen on exam. Examples include encephalocele, glioma, inverted papilloma, and cancer. Early biopsy is recommended for unilateral nasal polyps to rule out more serious conditions such as cancer, inverted papilloma, or fungal sinusitis.

NSAID or nonsteroidal anti-inflammatory drug hypersensitivity reactions encompasses a broad range of allergic or allergic-like symptoms that occur within minutes to hours after ingesting aspirin or other NSAID nonsteroidal anti-inflammatory drugs. Hypersensitivity drug reactions differ from drug toxicity reactions in that drug toxicity reactions result from the pharmacological action of a drug, are dose-related, and can occur in any treated individual (see nonsteroidal anti-inflammatory drugs section on adverse reactions for NSAID-induced toxic reactions); hypersensitivity reactions are idiosyncratic reactions to a drug. Although the term NSAID was introduced to signal a comparatively low risk of adverse effects, NSAIDs do evoke a broad range of hypersensitivity syndromes. These syndromes have recently been classified by the European Academy of Allergy and Clinical Immunology Task Force on NSAIDs Hypersensitivity. The classification organizes the hypersensitivity reactions to NSAIDs into the following five categories:

- 1) NSAIDs-exacerbated respiratory disease (NERD) is an acute (immediate to several hours) exacerbation of bronchoconstriction and other symptoms of asthma (see aspirin-induced asthma) in individuals with a history of asthma and/or nasal congestion, rhinorrhea or other symptoms of rhinitis and sinusitis in individuals with a history of rhinosinusitis after ingestion of various NSAIDs, particularly those that act by inhibiting the COX-1 enzyme. NERD does not appear to be due to a true allergic reaction to NSAIDs but rather at least in part to the more direct effects of these drugs to promote the production and/or release of certain mediators of allergy. That is, inhibition of cellular COX activity deprives tissues of its anti-inflammatory product(s), particularly prostaglandin E2 while concurrently shuttling its substrate, arachidonic acid, into other metabolizing enzymes, particularly 5-lipoxygenase (ALOX5) to overproduce pro-inflammatory leukotriene and 5-Hydroxyicosatetraenoic acid metabolites and 15-lipoxygenase (ALOX15) to overproduce pro-inflammatory 15-Hydroxyicosatetraenoic acid metabolites, including eoxins; the condition is also associated with a reduction in the anti-inflammatory metabolite, lipoxin A4, and increases in certain pro-allergic chemokines such as eotaxin-2 and CCL7.

- 2) NSAIDs-exacerbated cutaneous disease (NECD) is an acute exacerbation of wheals and/or angioedema in individuals with a history of chronic urticaria. NECD also appears due to the non-allergic action of NSAIDs in inhibiting the production of COX anti-inflammatory metabolites while promoting the production 5-lipoxygenase and 15-lipoxygenase pro-inflammatory metabolites and the overproduction of certain pro-allergic chemokines, e.g. eotaxin-1, eotaxin-2, RANTES, and interleukin-5.

- 3) NSAIDs-induced urticarial disease (NEUD) is the acute development of wheals and/or angioedema in individuals with no history of chronic NSAIDs-induced urticaria or related diseases. The mechanism behind NEUD is unknown but may be due to the non-allergic action of NSAIDs in promoting the production and/or release of allergy mediators.

- 4) Single NSAID-induced urticarial/angioedema or anaphylaxis (SNIUAA) is the acute development of urticarial, angioedema, or anaphylaxis in response to a single type of NSAID and/or a single group of NSAIDs with a similar structure but not to other structurally unrelated NSAIDs in individuals with no history of underlying relevant chronic diseases. SNIUAA is due to a true IgE-mediated allergy reaction.

- 5 Single NSAID-induced delayed reactions (SNIDR) are a set of delayed onset (usually more than 24 hour) reactions to NSAIDs. SNIDR are most commonly skin reactions that may be relatively mild moderately severe such as maculopapular rash, fixed drug eruptions, photosensitivity reactions, delayed urticaria, and contact dermatitis or extremely severe such as the DRESS syndrome, acute generalized exanthematous pustulosis, the Stevens–Johnson syndrome, and toxic epidermal necrolysis (also termed Lyell's syndrome). SNIDR result from the drug-specific stimulation of CD4+ T lymphocytes and CD8+ cytotoxic T cells to elicit a delayed type hypersensitivity reaction.

Drug intolerance or drug sensitivity refers to an inability to tolerate the adverse effects of a medication, generally at therapeutic or subtherapeutic doses. Conversely, a patient is said to be "tolerating" a drug when they can tolerate its adverse effects. It is not to be confused with a drug allergy, which is a form of drug intolerance, but requires an immune-mediated component. It is also not to be confused with drug tolerance ("drug resistance," or tachyphylaxis) which refers to a "lack" of adverse effects even at higher than average doses. Some instances of drug intolerance are known to result from genetic variations in drug metabolism.

Oroantral fistula (OAF) is an abnormal condition of the face where the maxillary sinus is exposed to the oral cavity through an epithelialised fistula. This term signifies pathology and it is not to be confused with oroantral communication (OAC). OAC if left untreated can either heal spontaneously or progress into OAF. The fistulous opening may be situated on the alveolus.

Clinical examination and x rays can help diagnose the condition. For examples :

- Valsalva test (nose blowing test): Ask the patient to pinch the nostrils together and open the mouth, then blow gently through the nose. Observe if there is passage of air or bubbling of blood in the post extraction alveolus as the trapped air from closed nostrils is forced into the mouth through any oroantral communication. Gentle suction applied to the socket often produces a characteristic hollow sound.

- Perform a complete extra- and intra-oral examination using a dental mirror under good lighting, look for granulation tissue in the socket and openings into the antrum.

- Panoramic radiograph or paranasal computed tomography can help to locate the fistula, the size of it and to determine the presence of sinusitis and other foreign bodies. Other methods like radiographs (occipitomental, OPG and periapical views) can also be used to confirm the presence of any oroantral fistulas.

- To test the patency of communication the patient is asked to rinse the mouth or water is flushed in the tooth socket.

- Unilateral epistaxis is seen in case of collection of blood in the sinus cavity.

- Do not probe or irrigate the site, because it may lead to sinusitis or push foreign bodies, such as contaminated fragments, or oral flora further into the antrum. Hence, leading to the formation of a new fistula or widen an existing one.

Intolerance to analgesics, particularly NSAIDs, is relatively common. It is thought that a variation in the metabolism of arachidonic acid is responsible for the intolerance. Symptoms include chronic rhinosinusitis with nasal polyps, asthma, gastrointestinal ulcers, angioedema, and urticaria.

Young's syndrome, also known as azoospermia sinopulmonary infections, sinusitis-infertility syndrome and Barry-Perkins-Young syndrome, is a rare condition that encompasses a combination of syndromes such as bronchiectasis, rhinosinusitis and reduced fertility. In individuals with this syndrome, the functioning of the lungs is usually normal but the mucus is abnormally viscous. The reduced fertility (azoospermia) is due to functional obstruction of sperm transport down the genital tract at the epididymis where the sperms are found in viscous, lipid-rich fluid. The syndrome was named after Donald Young, the urologist who first made observations of the clinical signs of the syndrome in 1972. There have been several studies undertaken suggesting that contact with mercury might cause the syndrome.

A variant of Young's syndrome has been observed in an individual, showing slightly different signs and symptoms.

Patients come to clinical attention early in life (usually at birth or within the first few months), with a firm subcutaneous nodule at bridge of nose, or as a polypoid mass within the nasal cavity, or somewhere along the upper border of the nasal bow. If the patient presents with an intranasal mass, there may be obstruction, chronic rhinosinusitis, or nasal drainage. If there is a concurrent cerebrospinal fluid (CSF) leak, then an encephalocele is much more likely.

This lesion is separated into two types based on the anatomic site of presentation:

1. Extranasal (60%): Subcutaneous bridge of nose

2. Intranasal (30%): Superior nasal cavity

3. Mixed (10%): Subcutaneous tissues and nasal cavity (larger lesions)

Nasal glial heterotopia refers to congenital malformations of displaced normal, mature glial tissue, which are no longer in continuity with an intracranial component. This is distinctly different from an encephalocele, which is a herniation of brain tissue and/or leptomeninges, that develops through a defect in the skull, where there is a continuity with the cranial cavity.

Mold health issues are potentially harmful effects of molds.

Molds (US usage; British English "moulds") are ubiquitous in the biosphere, and mold spores are a common component of household and workplace dust. The United States Centers for Disease Control and Prevention reported in its June 2006 report, 'Mold Prevention Strategies and Possible Health Effects in the Aftermath of Hurricanes and Major Floods,' that "excessive exposure to mold-contaminated materials can cause adverse health effects in susceptible persons regardless of the type of mold or the extent of contamination." When mold spores are present in abnormally high quantities, they can present especially hazardous health risks to humans after prolonged exposure, including allergic reactions or poisoning by mycotoxins, or causing fungal infection (mycosis).

Symptoms of mold exposure can include:

- Nasal and sinus congestion, runny nose

- Respiratory problems, such as wheezing and difficulty breathing, chest tightness

- Cough

- Throat irritation

- Sneezing / Sneezing fits