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".

Excoriation disorder is a mental disorder characterized by the repeated urge to pick at one's own skin, often to the extent that damage is caused.

Research has suggested that the urge to pick is similar to a body-focused repetitive behavior but others have argued that for some the condition is more akin to a substance abuse disorder. The two main strategies for treating this condition are pharmacological and behavioral intervention.

Episodes of skin picking are often preceded or accompanied by tension, anxiety, or stress. In some cases, following picking, the affected person may feel depressed. During these moments, there is commonly a compulsive urge to pick, squeeze, or scratch at a surface or region of the body, often at the location of a perceived skin defect. When picking one may feel a sense of relief or satisfaction.

The region most commonly picked is the face, but other frequent locations include the arms, legs, back, gums, neck, shoulders, scalp, abdomen, chest, and extremities such as the fingernails, cuticles, and toenails. Most patients with excoriation disorder report having a primary area of the body that they focus their picking on, but they will often move to other areas of the body to allow their primary picking area to heal. Individuals with excoriation disorder vary in their picking behaviour; some do it briefly multiple times a day while others can do one picking session that can last for hours. The most common way to pick is to use the fingers although a significant minority of people use tools such as tweezers or needles.

Skin picking often occurs as a result of some other triggering cause. Some common triggers are feeling or examining irregularities on the skin and feeling anxious or other negative feelings.

Complications arising from excoriation disorder include: infection at the site of picking, tissue damage, and septicemia. Damage from picking can be so severe as to require skin grafting. Severe picking can cause epidermal abscesses. Severe cases of excoriation disorder can cause life-threatening injuries. For example, in one reported case a female picked a hole through the bridge of her nose, which required surgery to fix, and a 48-year-old female picked through the skin on her neck exposing the carotid artery. Pain in the neck or back can arise due to prolonged bent-over positions while engaging in the behavior. Besides physical injuries, excoriation disorder can cause severe physical scarring and disfigurement.

Excoriation disorder can cause feelings of intense helplessness, guilt, shame, and embarrassment in individuals, and this greatly increases the risk of self-harm. Studies have shown that excoriation disorder presented suicidal ideation in 12% of individuals with this condition, suicide attempts in 11.5% of individuals with this condition, and psychiatric hospitalizations in 15% of individuals with this condition.

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).

Animal lead poisoning (also known as avian plumbism, or avian saturnism for birds) is a veterinary condition and pathology caused by increased levels of the heavy metal lead in animal's body.

Lead interferes with a variety of body and natural processes.

It is toxic to many organs and tissues including the heart, bones, intestines, kidneys, and reproductive and nervous systems. It mainly affects the haematopoietic system. It also affects the sulfhydryl group containing enzymes and also thiol content of erythrocyte. It inhibits the enzyme delta amino levaminic acid dehydrogenase enzyme(ALA) which is present in the rbc.

It is therefore particularly toxic to young animals, mainly dogs and cattle.

As in humans, "animal lead poisoning" may be acute (from intense exposure of short duration) or chronic (from repeat low-level exposure over a prolonged period). Acute intoxication can quickly lead to death.

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).

The rheumatoid nodule, which is sometimes in the skin, is the most common non-joint feature and occurs in 30% of people who have RA. It is a type of inflammatory reaction known to pathologists as a "necrotizing granuloma". The initial pathologic process in nodule formation is unknown but may be essentially the same as the synovitis, since similar structural features occur in both. The nodule has a central area of fibrinoid necrosis that may be fissured and which corresponds to the fibrin-rich necrotic material found in and around an affected synovial space. Surrounding the necrosis is a layer of palisading macrophages and fibroblasts, corresponding to the intimal layer in synovium and a cuff of connective tissue containing clusters of lymphocytes and plasma cells, corresponding to the subintimal zone in synovitis. The typical rheumatoid nodule may be a few millimetres to a few centimetres in diameter and is usually found over bony prominences, such as the elbow, the heel, the knuckles, or other areas that sustain repeated mechanical stress. Nodules are associated with a positive RF (rheumatoid factor) titer, ACPA, and severe erosive arthritis. Rarely, these can occur in internal organs or at diverse sites on the body.

Several forms of vasculitis occur in RA, but are mostly seen with long-standing and untreated disease. The most common presentation is due to involvement of small- and medium-sized vessels. Rheumatoid vasculitis can thus commonly present with skin ulceration and vasculitic nerve infarction known as mononeuritis multiplex.

Other, rather rare, skin associated symptoms include pyoderma gangrenosum, Sweet's syndrome, drug reactions, erythema nodosum, lobe panniculitis, atrophy of finger skin, palmar erythema, and skin fragility (often worsened by corticosteroid use).

Lung fibrosis is a recognized complication of rheumatoid arthritis. It is also a rare but well-recognized consequence of therapy (for example with methotrexate and leflunomide). Caplan's syndrome describes lung nodules in individuals with RA and additional exposure to coal dust. Exudative pleural effusions are also associated with RA.

Swan neck deformity is a deformed position of the finger, in which the joint closest to the fingertip is permanently bent toward the palm while the nearest joint to the palm is bent away from it (DIP flexion with PIP hyperextension). It is commonly caused by injury or inflammatory conditions like rheumatoid arthritis or sometimes familial (congenital, like Ehlers-Danlos syndrome).

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

The symptoms of pulmonary hypertension include the following:

Less common signs/symptoms include non-productive cough and exercise-induced nausea and vomiting. Coughing up of blood may occur in some patients, particularly those with specific subtypes of pulmonary hypertension such as heritable pulmonary arterial hypertension, Eisenmenger syndrome and chronic thromboembolic pulmonary hypertension. Pulmonary venous hypertension typically presents with shortness of breath while lying flat or sleeping (orthopnea or paroxysmal nocturnal dyspnea), while pulmonary arterial hypertension (PAH) typically does not.

Other typical signs of pulmonary hypertension include an accentuated pulmonary component of the second heart sound, a right ventricular third heart sound, and parasternal heave indicating a hypertrophied right atrium. Signs of systemic congestion resulting from right-sided heart failure include jugular venous distension, ascites, and hepatojugular reflux. Evidence of tricuspid insufficiency and pulmonic regurgitation is also sought and, if present, is consistent with the presence of pulmonary hypertension.

Pulmonary hypertension (PH or PHTN) is a condition of increased blood pressure within the arteries of the lungs. Symptoms include shortness of breath, syncope, tiredness, chest pain, swelling of the legs, and a fast heartbeat. The condition may make it difficult to exercise. Onset is typically gradual.

The cause is often unknown. Risk factors include a family history, prior blood clots in the lungs, HIV/AIDS, sickle cell disease, cocaine use, COPD, sleep apnea, living at high altitudes, and problems with the mitral valve. The underlying mechanism typically involves inflammation of the arteries in the lungs. Diagnosis involves first ruling out other potential causes.

There is no cure. Treatment depends on the type of disease. A number of supportive measures such as oxygen therapy, diuretics, and medications to inhibit clotting may be used. Medications specifically for the condition include epoprostenol, treprostinil, iloprost, bosentan, ambrisentan, macitentan, and sildenafil. A lung transplant may be an option in certain cases.

While the exact frequency of the condition is unknown, it is estimated that about 1,000 new cases occur a year in the United States. Females are more often affected than males. Onset is typically between 20 and 60 years of age. It was first identified by Ernst von Romberg in 1891.

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.

Signs and symptoms of mitral stenosis include the following:

- Heart failure symptoms, such as dyspnea on exertion, orthopnea and paroxysmal nocturnal dyspnea (PND)

- Palpitations

- Chest pain

- Hemoptysis

- Thromboembolism in later stages when the left atrial volume is increased (i.e., dilation). The latter leads to increase risk of atrial fibrillation, which increases the risk of blood stasis (motionless). This increases the risk of coagulation.

- Ascites and edema and hepatomegaly (if right-side heart failure develops)

Fatigue and weakness increase with exercise and pregnancy.

An electrocardiogram helps establishing the exact diagnosis and guides treatment, it may reveal:

- Abnormal heart rhythms, such as bradycardia (slowed heart rate)

- myocardial infarction (ST-elevation MI, STEMI, is usually more dangerous than non-STEMIs; MIs that affect the ventricles are usually more dangerous than those that affect the atria; those affecting the left side of the heart, especially the left ventricle, are usually more dangerous than those affecting the right side, unless that side is severely compromised)

- Signs of cardiomyopathy

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.