Enlarged adenoids can become nearly the size of a ping pong ball and completely block airflow through the nasal passages. Even if enlarged adenoids are not substantial enough to physically block the back of the nose, they can obstruct airflow enough so that breathing through the nose requires an uncomfortable amount of work, and inhalation occurs instead through an open mouth. Adenoids can also obstruct the nasal airway enough to affect the voice without actually stopping nasal airflow altogether.

Nasal blockage is determined by at least two factors: 1) the size of the adenoids, and 2) the size of the nasal pharynx passageway.

The adenoid usually reaches its greatest size by about age 5 years or so, and then fades away ("atrophies") by late childhood - generally by the age of 7 years. The lymphoid tissue remains under the mucosa of the nasopharynx, and could be seen under a microscope if the area was biopsied, but the mass is so reduced in size that the roof of the nasopharynx becomes flat rather than mounded. Just as the size of the adenoids is variable between individuals, so is the age at which adenoids atrophy.

The symptoms caused by enlarged adenoids are mostly due to "where" this lymphoid tissue is located. The adenoids are in the midline of the nasopharynx, and the Eustachian tubes open from either ear to the right and left of them. In children with excessive middle ear infections and chronic middle ear fluid, there is a high bacterial count in the adenoids as compared to children without problematic otitis media, even if the size of the adenoids is small. The adenoids in these cases provides a reservoir of pathogenic bacteria that cause ear infections and subsequent middle ear effusions (fluid).

The nasopharynx lies right above the throat. Splashes of excessive "drip" from infected adenoids may land directly on the vocal cords. Although the larynx and vocal cords do not ordinarily become infected from adenoiditis, their mucosa does become irritated. The vocal cords are extremely sensitive to touch, and any fluid drops falling on them cause an irresistible urge to cough. Adenoiditis therefore is one of the causes of cough.

Adenoid hypertrophy (or enlarged adenoids) is the unusual growth ("hypertrophy") of the adenoid tonsil first described by the Danish physician Wilhelm Meyer (1824-1895) in Copenhagen in 1868. He described that a long term adenoid hypertrophy will cause an obstruction of the nasal airways. These will lead to a dentofacial growth anomaly that was defined as "adenoid facies" (see long face syndrome).

There is very little lymphoid tissue in the nasopharynx of young babies; humans are born without substantial adenoids. The mat of lymphoid tissue called adenoids starts to get sizable during the first year of life. Just how big the adenoids become is quite variable between individual children.

Rhinoliths present as unilateral nasal obstruction. Foul-smelling, blood-stained discharge is often present. Epistaxis and pain may occur due to the ulceration of surrounding mucosa.

A rhinolith is a calculus present in the nasal cavity. The word is derived from the roots "" and "", literally meaning "nose stone". It is an uncommon medical phenomenon, not to be confused with dried nasal mucus. A rhinolith usually forms around the nucleus of a small exogenous foreign body, blood clot or secretion by slow deposition of calcium and magnesium salts. Over a period of time, they grow into large irregular masses that fill the nasal cavity. They may cause pressure necrosis of the nasal septum or lateral wall of nose. Rhinoliths can cause nasal obstruction, epistaxis, headache, sinusitis and epiphora. They can be diagnosed from the history with unilateral foul smelling blood stained nasal discharge or by anterior rhinoscopy. On probing probe can be passed around all its corners. In both CT and MRI rhinolith will appear like a radiopaque irregular material. Small rhinoliths can be removed by foreign body hook. Whereas large rhinoliths can be removed either by crushing with luc's forceps or by Moore's lateral rhinotomy approach.

Four types have been proposed:

- ENS secondary to inferior turbinate resection

- ENS secondary to middle turbinate resection

- ENS secondary to both inferior and middle turbinate

- ENS after turbinate-sparing procedures

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.

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).

Labial fusion is never present at birth, but rather acquired later in infancy, since it is caused by insufficient estrogen exposure and newborns have been exposed to maternal estrogen "in utero". It typically presents in infants at least 3 months old. Most presentations are asymptomatic and are discovered by a parent or during routine medical examination. In other cases, patients may present with associated symptoms of dysuria, urinary frequency, refusal to urinate, or post-void dribbling. Some patients present with vaginal discharge due to pooling of urine in the vulval vestibule or vagina.

A concha bullosa is a pneumatized (air-filled) cavity within a turbinate in the nose. (Concha is another term for turbinate.) Bullosa refers to the air-filled cavity within the turbinate. It is a normal anatomic variant seen in up to half the population. Occasionally, a large concha bullosa within a turbinate may cause it to bulge sufficiently to obstruct the opening of an adjacent sinus, possibly leading to recurrent sinusitis. In such a case the turbinate can be reduced in size by endoscopic nasal surgery (turbinectomy). The presence of a concha bullosa is often associated with deviation of the nasal septum toward the opposite side of the nasal cavity. Although it is thought that sinusitis or sinus pathology has relation to concha bullosa, no strong statistical correlation has been demonstrated.

The most frequent types of cleft palates are overt, submucous, and occult submucous.

Post-nasal drip (PND, also termed upper airway cough syndrome, UACS, or post nasal drip syndrome, PNDS) occurs when excessive mucus is produced by the nasal mucosa. The excess mucus accumulates in the throat or back of the nose. It is caused by rhinitis, sinusitis, gastroesophageal reflux disease (GERD), or by a disorder of swallowing (such as an esophageal motility disorder). It is frequently caused by an allergy, which may be seasonal or persistent throughout the year.

However, other researchers argue that mucus dripping down the back of the throat from the nasal cavity is a normal physiologic process that occurs in healthy individuals. Post-nasal drip has been challenged as a syndrome due to a lack of an accepted definition, pathologic tissue changes, and available biochemical tests.

It can be unilateral or bilateral.

- Sometimes, a unilateral choanal atresia is not detected until much later in life because the baby manages to get along with only one nostril available for breathing.

- Bilateral choanal atresia is a very serious life-threatening condition because the baby will then be unable to breathe directly after birth as babies are obligate nasal breathers (they mainly use their noses to breathe). In some cases, this may present as cyanosis while the baby is feeding, because the oral air passages are blocked by the tongue, further restricting the airway. The cyanosis may improve when the baby cries, as the oral airway is used at this time. These babies may require airway resuscitation soon after birth.

In teratology, proboscis is a blind-ended, tubelike structure, commonly located in the midface.

Proboscis formation are classified in four general types: holoprosencephalic proboscis, lateral nasal proboscis, supernumerary proboscis, and disruptive proboscis.

- Holoprosencephalic proboscis is found in holoprosencephaly. In cyclopia or ethmocephaly, proboscis is an abnormally formed nose. In cyclopia, a single median eye is associated with arrhinia (absence of the nose) and usually with proboscis formation above the eye. In ethmocephaly, two separate hypoteloric eyes are associated with arrhinia and supraocular proboscis formation. In cebocephaly, no proboscis formation occurs, but a single-nostril nose is present.

- Lateral nasal proboscis (proboscis lateralis) is a tubular proboscis-like structure and represents incomplete formation of one side of the nose; it is found instead of a nostril. The olfactory bulb is usually rudimentary on the involved side. The lacrimal duct (tear duct), nasal bone, nasal cavity, vomer, maxillary sinus, cribriform plate, and ethmoid cells are often missing on the involved side. Ocular hypertelorism may be present. The proboscis lateralis is a rare nasal anomaly.

- Supernumerary proboscis (Accessory proboscis) is found when both nostrils are formed and a proboscis occurs additionally. Accessory proboscis arise from a supernumerary olfactory placode.

- Disruptive proboscis occur if an early embryonic hamartoneoplastic lesion arises in the primitive prosencephalon.

A cleft palate is one of the most common causes of VPI. Cleft palate is an anatomical abnormality that occurs in utero and is present at birth. This malformation can affect the lip and palate, or the palate only. A cleft palate can affect the mobility of the velopharyngeal valve, thereby resulting in VPI.

The condition can be diagnosed based on inspection of the vulva. In patients with labial fusion, a flat plane of tissue with a dense central line of tissue is usually seen when the labia majora are retracted, while an anterior opening is usually present below the clitoris.

Permanent loss of smell and impairment of taste may also be a result of this disease, even after the symptoms are cured.

Chronic atrophic rhinitis is a chronic inflammation of nose characterised by atrophy of nasal mucosa, including the glands, turbinate bones and the nerve elements supplying the nose. Chronic atrophic rhinitis may be primary and secondary. Special forms of chronic atrophic rhinitis are rhinitis sicca anterior and ozaena.

Nasal vestibulitis is the diffuse dermatitis of nasal vestibule. It is often caused by "Staphylococcus aureus." It may be secondary to chronic rhinorrhea, nose picking or viral infections. In acute vestibulitis, the skin is red, swollen and tender. In chronic vestibulitis, induration of vestibular skin and crusting is seen. It is treated by cleaning the nasal vestibule of all crusts with a cotton applicator soaked in hydrogen peroxide. Antibiotic steroid ointment is sometimes helpful. Chronic fissures are treated by cautery.

Although often the terms "erythroplasia" and "erythroplakia" are used synonymously, some sources distinguish them, stating that the latter is maccular (flat) while the former is papular (bumpy).

Erythroplakia of the genital mucosae is often referred to as erythroplasia of Queyrat.

The most common areas in the mouth where erythroplakia is found are the floor of the mouth, buccal vestibule, the tongue, and the soft palate. It appears as a red macule or plaque with well-demarcated borders. The texture is characterized as soft and velvety. An adjacent area of leukoplakia may be found along with the erythroplakia.

Erythroplasia may also occur on the laryngeal mucosa, or the anal mucosa.

Mondini dysplasia, also known as Mondini malformation and Mondini defect, is an abnormality of the inner ear that is associated with sensorineural hearing loss.

This deformity was first described in 1791 by Mondini after examining the inner ear of a deaf boy. The Mondini dysplasia describes a cochlea with incomplete partitioning and a reduced number of turns, an enlarged vestibular aqueduct and a dilated vestibule. A normal cochlea has two and a half turns, a cochlea with Mondini dysplasia has one and a half turns; the basal turns being normally formed with a dilated or cystic apical turn to the cochlear. The hearing loss can deteriorate over time either gradually or in a step-wise fashion, or may be profound from birth.

Hearing loss associated with Mondini dysplasia may first become manifest in childhood or early adult life. Some children may pass newborn hearing screen to lose hearing in infancy but others present with a hearing loss at birth. Hearing loss is often progressive and because of the associated widened vestibular aqueduct may progress in a step-wise fashion associated with minor head trauma. Vestibular function is also often affected. While the hearing loss is sensorineural a conductive element may exist probably because of the third window effect of the widened vestibular aqueduct. The Mondini dysplasia can occur in cases of Pendred Syndrome and Branchio-oto-renal syndrome and in other syndromes, but can occur in non-syndromic deafness.

VVS is characterized by severe pain with attempted penetration of the vaginal orifice and complaints of tenderness with pressure within the vulval vestibule. Usually there are no reports of pain with pressure to other surrounding areas of the vulva. The feelings of irritation and burning can persist for hours or days following sexual activity, engendering a sense of hopelessness and depression. VVS also can often cause dyspareunia.

The pain may be provoked by contact with an object, such as with the insertion of a tampon or penis or with the pressure from sitting on a bicycle seat, "provoked vestibulodynia", or it may be constant, as in the case of unprovoked, generalized vestibulodynia. Some women have had pain since their first penetration (primary vulvar vestibulitis) while some have had it after a period of time with pain-free penetration (secondary vulvar vestibulitis).

Relationship problems often occur as the result of chronic frustration, disappointment, and depression associated with the condition.

The lesion is usually painless. The usual appearance is of two excess tissue folds in alveolar vestibule/buccal sulcus, with the flange of the denture fitting in between the two folds. It may occur in either the maxillary or mandibular sulci, although the latter is more usual. Anterior locations are more common than posterior. Less commonly there may be a single fold, and the lesion may appear on the lingual surface of the mandibular alveolar ridge.

The swelling is firm and fibrous, with a smooth, pink surface. The surface may also show ulceration or erythema. The size of the lesion varies from less than 1 cm to involving the entire length of the sulcus.

Epulis (literally, 'on the gingiva') is a general term for any gingival or alveolar tumor (i.e. lump on the gum). This term describes only the location of a lump and has no implication on the histologic appearance of a lesion. "Epulis" is also sometimes used synonymously with epulis fissuratum, however other conditions are classified as epulides, e.g. giant cell epulis (peripheral giant cell granuloma), ossifying fibroid epulis (peripheral ossifying fibroma), and congenital epulis.

A nasal septal abscess is frequently a result of a secondary bacterial infection of a nasal septal hematoma. Individuals with this condition may also have fever, general malaise and nasal pain, including tenderness over the dorsum of the nose. A bilateral persistent nasal obstruction may also be present.

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.