Syndrome Without A Name (SWAN) is the name given to any pathological set of symptoms that does not represent any of the known diseases. In other terms, SWAN simply means "an unknown disease".

It has been estimated that up to 40% of all disabled children in the UK, or 6,000 per year, do not have a diagnosis and their condition is thus termed "SWAN".

The prevalence of excoriation disorder is not well understood.

Estimates of prevalence of the condition range from 1.4 to 5.4% in the general population. One U.S. telephone survey found that 16.6% of respondents "picked their skin to the point of noticeable tissue damage" and that 1.4% would qualify as meeting the requirements of excoriation disorder. Another community survey found a rate of 5.4% had excoriation disorder. A survey of college students found a rate of 4%. One study found that among non-disabled adults, 63% of individuals engaged in some form of skin picking and 5.4% engaged in serious skin picking. Lastly, a survey of dermatology patients found that 2% suffered from excoriation disorder.

In some patients excoriation disorder begins with the onset of acne in adolescence, but the compulsion continues even after the acne has gone away. Skin conditions such as keratosis pilaris, psoriasis, and eczema can also provoke the behavior. In patients with acne, the grooming of the skin is disproportionate to the severity of the acne. Certain stressful events including marital conflicts, deaths of friends or family, and unwanted pregnancies have been linked to the onset of the condition. If excoriation disorder does not occur during adolescence another common age of onset is between the ages of 30 to 45. Additionally, many cases of excoriation disorder have been documented to begin in children under the age of 10. One small survey of patients with excoriation disorder found that 47.5% of them had an early onset of excoriation disorder that began before age 10. Traumatic childhood events may initiate the behavior.

Excoriation disorder is statistically more common in females than in males.

Excoriation disorder has a high rate of comorbidity with other psychiatric conditions, especially with mood and anxiety disorders . One survey of patients with excoriation disorder found that 56.7% also had a DSM-IV Axis-I disorder and 38% had alcohol- or drug-abuse problems. Studies have shown the following rates of psychiatric conditions found in patients with excoriation disorder: trichotillomania (38.3%), substance abuse (38%), major depressive disorder (approximately 31.7% to 58.1%), anxiety disorders (approximately 23% to 56%), obsessive-compulsive disorder (approximately 16.7% to 68%), and body dysmorphic disorder (approximately 26.8% to 44.9%). There are also higher rates of excoriation disorder in patients in psychiatric facilities; a study of adolescent psychiatric inpatients found that excoriation disorder was present in 11.8% of patients. It is also present at high rates with some other conditions: 44.9% of patients with body dysmorphic disorder also have excoriation disorder; 8.9% of patients with OCD have excoriation disorder; and 8.3% of patients with trichotillomania have excoriation disorder.

Skin picking is also common in those with certain developmental disabilities; for example, Prader–Willi syndrome and Smith–Magenis syndrome. Studies have shown that 85% of people with Prader–Willi syndrome also engage in skin-picking. Children with developmental disabilities are also at an increased risk for excoriation disorder.

Excoriation disorder also correlates with "social, occupational, and academic impairments, increased medical and mental health concerns (including anxiety, depression, obsessive–compulsive disorder) ... and financial burden". Excoriation disorder also has a high degree of comorbidity with occupational and marital difficulties.

Substance abuse is often present, and individuals with excoriation disorder are twice as likely to have first-degree relatives who have substance abuse disorders than those without the condition.

Some cases of body-focused repetitive behaviors also suggest a hereditary factor.

There have been many different theories regarding the causes of excoriation disorder including biological and environmental factors.

A common hypothesis is that excoriation disorder is often a coping mechanism to deal with elevated levels of turmoil, arousal or stress within the individual, and that the individual has an impaired stress response. A review of behavioral studies found support in this hypothesis in that skin-picking appears to be maintained by automatic reinforcement within the individual.

In contrast to neurological theories, there are some psychologists who believe that picking behavior can be a result of repressed rage felt toward authoritarian parents. A similar theory holds that overbearing parents can cause the behavior to develop in their children.

There are established epigenetic and environmental risk factors for RA. Smoking is an established risk factor for RA in Caucasian populations, increasing the risk three times compared to non-smokers, particularly in men, heavy smokers, and those who are rheumatoid factor positive. Modest alcohol consumption may be protective.

Silica exposure has been linked to RA.

Those routes include contaminated air, water, soil, and food, and also, for birds ingestion of grit (lead shots, lead bullets).ingestion of paints,materials that are left out from the factories like batteries etc.

Lead is now a common environmental pollutant. For the birds, a commons source is lead shot, eaten as grit.

RA reduces lifespan on average from three to twelve years. According to the UK's National Rheumatoid Arthritis Society, Young age at onset, long disease duration, the concurrent presence of other health problems (called co-morbidity), and characteristics of severe RA—such as poor functional ability or overall health status, a lot of joint damage on x-rays, the need for hospitalisation or involvement of organs other than the joints—have been shown to associate with higher mortality". Positive responses to treatment may indicate a better prognosis. A 2005 study by the Mayo Clinic noted that RA sufferers suffer a doubled risk of heart disease, independent of other risk factors such as diabetes, alcohol abuse, and elevated cholesterol, blood pressure and body mass index. The mechanism by which RA causes this increased risk remains unknown; the presence of chronic inflammation has been proposed as a contributing factor. It is possible that the use of new biologic drug therapies extend the lifespan of people with RA and reduce the risk and progression of atherosclerosis. This is based on cohort and registry studies, and still remains hypothetical. It is still uncertain whether biologics improve vascular function in RA or not. There was an increase in total cholesterol and HDLc levels and no improvement of the atherogenic index.

PCNA and Ki67 immunoreactivity happens in case of fibroma and peripheral granuloma.

Giant-cell fibroma is a type of fibroma not associated with trauma or irritation. It can occur at any age and on a mucous membrane surface. The most common oral locations are on the gingiva of the mandible, tongue, and palate. It is a localized reactive proliferation of fibrous connective tissue.

Giant-cell fibroma (GCF) is a benign non-neoplastic lesion first described by Weathers and Callihan (1974). It occurs in the first three decades of life and predominates in females (Houston, 1982; Bakos, 1992). Clinically, the GCF presents as an asymptomatic, papillary and pedunculated lesion. The most predominant location is the mandibular gingiva (Houston, 1982; Bakos, 1992). Histologically, the GCF is distinctive, consisting of fibrous connective tissue without inflammation and covered with stratified squamous hyperplastic epithelium. The most characteristic histological feature is the presence of large spindle-shaped and stellate-shaped mononuclear cells and multinucleated cells. These cells occur in a variety of lesions, such as the fibrous papule of the nose, ungual fibroma, acral fibrokeratoma, acral angiofibroma and desmoplastic fibroblastoma (Swan, 1988; Pitt et al., 1993; Karabela-Bouropoulou et al., 1999; Jang et al., 1999).

Despite many studies, the nature of the stellated multinucleate and mononuclear cell is not clear (Weathers and Campbell, 1974; Regezi et al., 1987; Odell et al., 1994; Magnusson and Rasmusson, 1995).

Swan neck deformity has many possible causes arising from the DIP, PIP, or even the MCP joints. In all cases, there is a stretching of the volar plate at the PIP joint to allow hyperextension, plus some damage to the attachment of the extensor tendon to the base of the distal phalanx that produces a hyperflexed mallet finger. Duck bill deformity is a similar condition affecting the thumb (which cannot have true swan neck deformity because it does not have enough joints).

Splinting for fingers.

Passive stretching and clearing the deformity.

The epidemiology of IPAH is about 125–150 deaths per year in the U.S., and worldwide the incidence is similar to the U.S. at 4 cases per million. However, in parts of Europe (France) indications are 6 cases per million of IPAH. Females have a higher incidence rate than males (2–9:1).

Other forms of PH are far more common. In systemic scleroderma, the incidence has been estimated to be 8 to 12% of all patients; in rheumatoid arthritis it is rare. However, in systemic lupus erythematosus it is 4 to 14%, and in sickle cell disease, it ranges from 20 to 40%. Up to 4% of people who suffer a pulmonary embolism go on to develop chronic thromboembolic disease including pulmonary hypertension. A small percentage of patients with COPD develop pulmonary hypertension with no other disease to explain the high pressure. On the other hand, obesity-hypoventilation syndrome is very commonly associated with right heart failure due to pulmonary hypertension.

The prognosis of pulmonary arterial hypertension (WHO Group I) has an "untreated" median survival of 2–3 years from time of diagnosis, with the cause of death usually being right ventricular failure (cor pulmonale). A recent outcome study of those patients who had started treatment with bosentan (Tracleer) showed that 89% patients were alive at 2 years. With new therapies, survival rates are increasing. For 2,635 patients enrolled in The Registry to Evaluate Early and Long-term Pulmonary Arterial Hypertension Disease Management (REVEAL Registry) from March 2006 to December 2009, 1-, 3-, 5-, and 7-year survival rates were 85%, 68%, 57%, and 49%, respectively. For patients with idiopathic/familial PAH, survival rates were 91%, 74%, 65%, and 59%. Levels of mortality are very high in pregnant women with severe pulmonary arterial hypertension (WHO Group I). Pregnancy is sometimes described as contraindicated in these women.

Cardiogenic shock is a life-threatening medical condition resulting from an inadequate circulation of blood due to primary failure of the ventricles of the heart to function effectively. Signs of inadequate blood flow to the body's organs include low urine production (<30 mL/hour), cool arms and legs, and altered level of consciousness. It may lead to cardiac arrest, which is an abrupt stopping of cardiac pump function.

As this is a type of circulatory shock, there is insufficient blood flow and oxygen supply for biological tissues to meet the metabolic demands for oxygen and nutrients. Cardiogenic shock is defined by sustained low blood pressure with tissue hypoperfusion despite adequate left ventricular filling pressure.

Treatment of cardiogenic shock depends on the cause. If cardiogenic shock is due to a heart attack, attempts to open the heart's arteries may help. An intra-aortic balloon pump or left ventricular assist device may improve matters until this can be done. Medications that improve the heart's ability to contract (positive inotropes) may help; however, it is unclear which is best. Norepinephrine may be better if the blood pressure is very low whereas dopamine or dobutamine may be more useful if only slightly low. Cardiogenic shock is a condition that is difficult to fully reverse even with an early diagnosis. With that being said, early initiation of mechanical circulatory support, early percutaneous coronary intervention, inotropes, and heart transplantation may improved outcomes.

Almost all cases of mitral stenosis are due to disease in the heart secondary to rheumatic fever and the consequent rheumatic heart disease. Uncommon causes of mitral stenosis are calcification of the mitral valve leaflets, and as a form of congenital heart disease. However, there are primary causes of mitral stenosis that emanate from a cleft mitral valve. It is the most common valvular heart disease in pregnancy.

Other causes include infective endocarditis where the vegetations may favor increase risk of stenosis. Other rare causes include mitral annular calcification, endomyocardial fibroelastosis, malignant carcinoid syndrome, systemic lupus erythematosus, whipple disease, fabry disease, and rheumatoid arthritis. hurler' disease, hunter's disease, amyloidosis.

Cardiogenic shock is caused by the failure of the heart to pump effectively. It can be due to damage to the heart muscle, most often from a large myocardial infarction. Other causes include abnormal heart rhythms, cardiomyopathy, heart valve problems, ventricular outflow obstruction (i.e. aortic valve stenosis, aortic dissection, cardiac tamponade, constrictive pericarditis, systolic anterior motion (SAM) in hypertrophic cardiomyopathy), or ventriculoseptal defects.

It can also be caused by a sudden decompressurization (e.g. in an aircraft), where air bubbles are released into the bloodstream (Henry's Law), causing heart failure.

The natural history of mitral stenosis secondary to rheumatic fever (the most common cause) is an asymptomatic latent phase following the initial episode of rheumatic fever. This latent period lasts an average of 16.3 ± 5.2 years. Once symptoms of mitral stenosis begin to develop, progression to severe disability takes 9.2 ± 4.3 years.

In individuals having been offered mitral valve surgery but refused, "survival" with medical therapy alone was 44 ± 6% at 5 years, and 32 ± 8% at 10 years after they were offered correction.