When accompanied by the combination of situs inversus (reversal of the internal organs), chronic sinusitis, and bronchiectasis, it is known as Kartagener syndrome (only 50% of primary ciliary dyskinesia cases include situs inversus).

Several diagnostic tests for this condition have been proposed. These include nasal nitric oxide levels, light microscopy of biopsies for ciliary beat pattern and frequency and electron microscopic examination of dynein arms. Genetic testing has also been proposed but this is difficult given that there are multiple genes involved.

Lip pits are harmless and do not usually require any treatment, although in some reported cases surgical excision has been used.

The features of this condition include

- Facial dysmorphism

- Short stature

- Mild motor control and learning difficulties

- Mild ataxia

- Microcephaly

- Normal intelligence

- Conjunctival telangiectasia

- Recurrent sinus infections

- Decreased serum IgA

- Late onset of pulmonary fibrosis

- Increased alpha-fetoprotein

- Increased radiosensitivity

THS is usually diagnosed via exclusion, and as such a vast amount of laboratory tests are required to rule out other causes of the patient's symptoms. These tests include a complete blood count, thyroid function tests and serum protein electrophoresis. Studies of cerebrospinal fluid may also be beneficial in distinguishing between THS and conditions with similar signs and symptoms.

MRI scans of the brain and orbit with and without contrast, magnetic resonance angiography or digital subtraction angiography and a CT scan of the brain and orbit with and without contrast may all be useful in detecting inflammatory changes in the cavernous sinus, superior orbital fissure and/or orbital apex. Inflammatory change of the orbit on cross sectional imaging in the absence of cranial nerve palsy is described by the more benign and general nomenclature of orbital pseudotumor.

Sometimes a biopsy may need to be obtained to confirm the diagnosis, as it is useful in ruling out a neoplasm.

Differentials to consider when diagnosing THS include craniopharyngioma, migraine and meningioma.

Studies have shown that patients with Pacemaker syndrome and/or with sick sinus syndrome are at higher risk of developing fatal complications that calls for the patients to be carefully monitored in the ICU. Complications include atrial fibrillation, thrombo-embolic events, and heart failure.

Courses of treatment typically include the following:

- Draining the pus once awhile as it can build up a strong odor

- Antibiotics when infection occurs.

- Surgical excision is indicated with recurrent fistular infections, preferably after significant healing of the infection. In case of a persistent infection, infection drainage is performed during the excision operation. The operation is generally performed by an appropriately trained specialist surgeon e.g. an otolaryngologist or a specialist General Surgeon.

- The fistula can be excised as a cosmetic operation even though no infection appeared. The procedure is considered an elective operation in the absence of any associated complications.

This condition is rare. Only four cases have been described up to 2017.

At the time of pacemaker implantation, AV synchrony should be optimized to prevent the occurrence of pacemaker syndrome. Where patients with optimized AV synchrony have shown great results of implantation and very low incidence of pacemaker syndrome than those with suboptimal AV synchronization.

Studies have shown that sinusitis is found in about 60% of the cases on the fourth day after the manifestation of sinus. Moreover, patient may be afflicted with an acute sinus disease if OAC is not treated promptly upon detecting clear signs of sinusitis. So, early diagnosis of OAC must be conducted in order to prevent OAF from setting in.

Spontaneous healing of small perforation is expected to begin about 48 hours after tooth extraction and it remains possible during the following two weeks. Patient must consult the dentist as early as possible should a large defect of more than 7mm in diameter or a dogged opening that requires closure is discovered so that appropriate and suitable treatment can be swiftly arranged or referral to Oral Maxillofacial Surgery (OMFS) be made at the local hospital, if required.

A comprehensive preoperative radiographic evaluation is a must as the risk of OAC can increase due to one or more of the following situations :-

- Close relationship between the roots of the maxillary posterior teeth and the sinus floor

- Increased divergence or dilaceration of the roots of the tooth

- Marked pneumatization of the sinus leading to a larger size

- Peri-radicular lesions involving teeth or roots in close association with the sinus floor

Hence, in such cases:

- Avoid using too much of apical pressure during tooth extraction

- Perform surgical extraction with roots sectioning

- Consider referral to OMFS at local hospital

The prognosis of THS is usually considered good. Patients usually respond to corticosteroids, and spontaneous remission can occur, although movement of ocular muscles may remain damaged. Roughly 30–40% of patients who are treated for THS experience a relapse.

No formal diagnostic criteria exist. A diagnosis of Inappropriate sinus tachycardia is primarily one of exclusion and the following may be observed:

- Exclusion of all other causes of sinus tachycardia

- Common forms of supraventricular tachycardia (SVT) must be excluded

- Normal P wave morphology

- A resting sinus tachycardia is usually (but not always) present

- Nocturnal dip in heart rate

- Inappropriate heart rate response on exertion

- Mean heart rate in 24hrs >95 bpm

- Symptoms are documented to be due to tachycardia

- Hypotension is occasionally observed

- Syncope (fainting) is occasionally reported

Affected males develop generalized reticular hyper pigmentation in early childhood.

Hair often looks bedraggled or brushed backwards, hanging low on the forehead.

Among the associated extracutaneous manifestations are described:

- Respiratory infections

- Dyskeratosis corneal photophobia

- Hypohidrosis with large deficit of thermoregulation

- Growth retardation

- Gastrointestinal disorders

- Kidney disease

- Kidney stones

- Urinary infections

- Webbed feet or hands

- Electrolyte imbalance

- Retinitis pigmentosa

- Lymphoedema

- Thyroid abnormalities

Each patient shows some of the symptoms listed above. Not every sick person will show all of the listed symptoms.

In females the disease is characterized by skin rashes linear hyper pigmentation following the Blaschko's lines, morphologically similar to stage 3 pigment incontinence. There are no systemic manifestations associated with XLPDR in females.

1)positive tuberclin test

2)chest radiograph

3)CT scan

4)cytology/biopsy (FNAC)

5)AFB staining

6)mycobacterial culture

X-linked reticulate pigmentary disorder (also known as "familial cutaneous amyloidosis", "Partington amyloidosis", "Partington cutaneous amyloidosis", "Partington syndrome type II", "reticulate pigmentary disorder", and "X-linked reticulate pigmentary disorder with systemic manifestations") is a cutaneous condition that has been described in adult women that had linear streaks of hyperpigmentation and in which male patients manifested a reticulated mottled brown pigmentation of the skin, which, on biopsy, demonstrated dermal deposits of amyloid.

The syndrome is also referred with the acronym X-Linked-PDR or even XLPRD.It's a very rare disease, genetically determined, with a chronic course.

It was characterized in 1981. Mutation of the "POLA1" gene leads to loss of expression of the catalytic subunit of DNA polymerase-α and is responsible for XLPDR. Loss of POLA1 expression results in reduced levels of RNA:DNA hybrids in the cytosol and unexpectedly triggers aberrant immune responses (e.g. type I interferon production) which at least in part can account for the symptoms associated with XLPDR.

They are divided into three types based on their location:

- commissural pits, which are small pits near the labial commissure of the mouth,

- a pit in the upper lip, in which case it may be called a midline sinus of the upper lip, and

- pits in the lower lip, in which case it may be called a congenital sinus of the lower lip.

In some cases commissural pits have been reported in combination with preauricaluar pits, which are near the ear.

The primary aim of treatment of a newly formed oroantral communication is to prevent the development of an oroantral fistula as well as chronic sinusitis. The decision on how to treat OAC/OAF depends on various factors. Small size communications between 1 and 2 mm in diameter, if uninfected, are likely to form a clot and heal by itself later. Communications larger than this require treatments to close the defect and these interventions can be categorised into 3 types: surgical, non-surgical and pharmacological.

Silent sinus syndrome is a spontaneous, asymptomatic collapse of the maxillary sinus and orbital floor associated with negative sinus pressures. It can cause painless facial asymmetry, diplopia and enophthalmos. Usually the diagnosis is suspected clinically, and it can be confirmed radiologically by characteristic imaging features that include maxillary sinus outlet obstruction, sinus opacification, and sinus volume loss caused by inward retraction of the sinus walls. Treatment is surgical involving making an outlet for mucous drainage from the obstructed sinus.

Binder's Syndrome/Binder Syndrome (Maxillo-Nasal Dysplasia) is a developmental disorder primarily affecting the anterior part of the maxilla and nasal complex (nose and jaw). It is a rare disorder and the causes are unclear.

The characteristics of the syndrome are typically visible. The syndrome involves hypoplasia of variable severity of cartilaginous nasal septum and premaxilla. It includes complete total absence of the anterior nasal spine. There are also associated anomalies of muscle insertions of the upper lip and the nasal floor and of the cervical spine. Affected individuals typically have an unusually flat, underdeveloped midface (midfacial hypoplasia), with an abnormally short nose and flat nasal bridge. They have an underdeveloped upper jaw, relatively protruding lower jaw with anterior mandibular vertical excess and a Class III skeletal and dental (reverse overjet) profile. They have a small frontal sinus and global facial imbalance.

Treatment is encouraged as early as possible with posteroanterior traction on the maxilla and, at about age 8, reinsertion of the nasolabial muscles onto the anterior border of the cartilaginous system. Many who have a severe case of the disorder undergo plastic surgery or orthodontic treatment for cosmetic reasons.

First-generation antihistamine has been suggested as first-line therapy to treat post-nasal drip.

While sick building syndrome (SBS) encompasses a multitude of non-specific symptoms, building-related illness (BRI) comprises specific, diagnosable symptoms caused by certain agents (chemicals, bacteria, fungi, etc.). These can typically be identified, measured, and quantified. There are usually 4 causal agents in BRI; 1.) Immunologic, 2.) Infectious, 3.) toxic, and 4.) irritant. For instance, Legionnaire's disease, usually caused by "Legionella pneumophila", involves a specific organism which could be ascertained through clinical findings as the source of contamination within a building. SBS does not have any known cure; alleviation consists of removing the affected person from the building associated with non-specific symptoms. BRI, on the other hand, utilizes treatment appropriate for the contaminant identified within the building (e.g., antibiotics for Legionnaire's disease). In most cases, simply improving the indoor air quality (IAQ) of a particular building will attenuate, or even eliminate, the acute symptoms of SBS, while removal of the source contaminant would prove more effective for a specific illness, as in the case of BRI. Building-Related Illness is vital to the overall understanding of Sick Building Syndrome because BRI illustrates a causal path to infection, theoretically. Office BRI may more likely than not be explained by three events: “Wide range in the threshold of response in any population (susceptibility), a spectrum of response to any given agent, or variability in exposure within large office buildings." Isolating any one of the three aspects of office BRI can be a great challenge, which is why those who find themselves with BRI should take three steps, history, examinations, and interventions. History describes the action of continually monitoring and recording the health of workers experiencing BRI, as well as obtaining records of previous building alterations or related activity. Examinations go hand in hand with monitoring employee health. This step is done by physically examining the entire workspace and evaluating possible threats to health status among employees. Interventions follow accordingly based off the results of the Examination and History report.

Occasionally a preauricular sinus or cyst can become infected.

Most preauricular sinuses are asymptomatic, and remain untreated unless they become infected too often. Preauricular sinuses can be excised with surgery which, because of their close proximity to the facial nerve, is performed by an appropriately trained, experienced surgeon (e.g. a specialist General Surgeon, a Plastic Surgeon, an otolaryngologist (Ear, Nose, Throat surgeon) or an Oral and Maxillofacial Surgeon).

The condition is suspected in an elderly person, especially male, presenting with symptoms of heart failure such as shortness of breath or swollen legs, and or disease of the electrical system of the heart with ensuing slow heart rate, dizziness or fainting spells. The diagnosis is confirmed on the basis of a biopsy, which can be treated with a special stain called Congo Red that will be positive in this condition, and immunohistochemistry.

Ambulatory monitoring of the electrocardiogram (ECG) may be necessary because arrhythmias are transient. The ECG may show any of the following:

- Inappropriate sinus bradycardia

- Sinus arrest

- Sinoatrial block

- Tachy-Brady Syndrome

- Atrial fibrillation with slow ventricular response

- A prolonged asystolic period after a period of tachycardias

- Atrial flutter

- Ectopic atrial tachycardia

- Sinus node reentrant tachycardia

- Wolff-Parkinson-White syndrome

Electrophysiologic tests are no longer used for diagnostic purposes because of their low specificity and sensitivity. Cardioinhibitory and vasodepressor forms of sick sinus syndrome may be revealed by tilt table testing.

Athlete's heart is not dangerous for athletes (though if a nonathlete has symptoms of bradycardia, cardiomegaly, and cardiac hypertrophy, another illness may be present). Athlete's heart is not the cause of sudden cardiac death during or shortly after a workout, which mainly occurs due to hypertrophic cardiomyopathy, a genetic disorder.

No treatment is required for people with athletic heart syndrome; it does not pose any physical threats to the athlete, and despite some theoretical concerns that the ventricular remodeling might conceivably predispose for serious arrhythmias, no evidence has been found of any increased risk of long-term events. Athletes should see a physician and receive a clearance to be sure their symptoms are due to athlete’s heart and not another heart disease, such as cardiomyopathy. If the athlete is uncomfortable with having athlete's heart or if a differential diagnosis is difficult, deconditioning from exercise for a period of three months allows the heart to return to its regular size. However, one long-term study of elite-trained athletes found that dilation of the left ventricle was only partially reversible after a long period of deconditioning. This deconditioning is often met with resistance to the accompanying lifestyle changes. The real risk attached to athlete's heart is if athletes or nonathletes simply assume they have the condition, instead of making sure they do not have a life-threatening heart illness.