A doctor will take a thorough medical history, and may take blood tests as well as examining liver and kidney function. Improvements have also been reported from treating malnutrition associated with zinc deficiency and other minerals. Intracellular (red blood cell) assays are more sensitive than tests for plasma levels.

The diagnostic testing for vasculitis should be guided by the patient's history and physical exam. The clinician should ask about the duration, onset, and presence any associated symptoms such as weight loss or fatigue (that would indicate a systemic cause). It is important to distinguish between IgA and non-IgA vasculitis. IgA vasculitis is more likely to present with abdominal pain, bloody urine, and joint pain. In the case that the cause is not obvious, a reasonable initial workup would include a complete blood count, urinalysis, basic metabolic panel, fecal occult blood testing, erythrocyte sedimentation rate (ESR), and C-reactive protein level. Small vessel cutaneous vasculitis is a diagnosis of exclusion and requires ruling out systemic causes of the skin findings. Skin biopsy (punch or excisional) is the most definitive diagnostic test and should be performed with 48 hours of appearance of the vasculitis. A skin biopsy will be able to determine if the clinical findings are truly due to a vasculitis or due to some other cause.

Purpura hemorrhagica may be prevented by proper management during an outbreak of strangles. This includes isolation of infected horses, disinfection of fomites, and good hygiene by caretakers. Affected horses should be isolated at least one month following infection. Exposed horses should have their temperature taken daily and should be quarantined if it becomes elevated. Prophylactic antimicrobial treatment is not recommended.

Vaccination can reduce the incidence and severity of the disease. However, horses with high SeM antibody titers are more likely to develop purpura hemorrhagica following vaccination and so these horses should not be vaccinated. Titers may be measured by ELISA.

In approximately half of suspected nail fungus cases there is actually no fungal infection, but only some nail dystrophy. Before beginning oral antifungal therapy the health care provider should confirm a fungal infection. Administration of treatment to persons without an infection is unnecessary health care and causes needless exposure to side effects.

Waldenström hyperglobulinemic purpura (also known as "Purpura hyperglobulinemica") is a skin condition that presents with episodic showers of petechiae (small red or purple spots) occurring on all parts of the body, most profusely on the lower extremities.

Purpura is a condition of red or purple discolored spots on the skin that do not blanch on applying pressure. The spots are caused by bleeding underneath the skin usually secondary to vasculitis or dietary deficiency of vitamin C (scurvy). They measure 0.3–1 cm (3–10 mm), whereas petechiae measure less than 3 mm, and ecchymoses greater than 1 cm.

Purpura is common with typhus and can be present with meningitis caused by meningococci or septicaemia. In particular, meningococcus ("Neisseria meningitidis"), a Gram-negative diplococcus organism, releases endotoxin when it lyses. Endotoxin activates the Hageman factor (clotting factor XII), which causes disseminated intravascular coagulation (DIC). The DIC is what appears as a rash on the affected individual.

Prognosis is good with early, aggressive treatment (92% survival in one study).

Solar purpura (also known as "Actinic purpura," and "Senile purpura") is a skin condition characterized by large, sharply outlined, 1- to 5-cm, dark purplish-red ecchymoses appearing on the dorsa of the forearms and less often the hands.

The condition is most common in elderly people of European descent. It is caused by sun-induced damage to the connective tissue of the skin.

No treatment is necessary. The lesions typically fade over a period of up to 3 weeks.

Most instances of onycholysis without a clear cause will heal spontaneously within a few weeks. The most commonly recommended treatment is to keep the nail dry as much as possible and allow the nail to slowly reattach. Trimming away as much loose nail as can be done comfortably will prevent the nail from being pried upwards. Cleaning under the nail is not recommended as this only serves to separate the nail further. Bandages are also to be avoided. When kept dry and away from further trauma, the nail will reattach from the base upward (i.e., from proximal to distal).

If the underlying cause of the condition is not found and the nail continues to detach despite conservative treatment, the nail bed may begin to form a granular layer of abnormal cells on its surface. After six months of detachment, this layer is likely to prevent the adhesion of any new nail tissue, possibly leading to permanent deformity.

Nail inspection can give hints to the internal condition of the body as well.

Nail disease can be very subtle and should be evaluated by a dermatologist with a focus in this particular area of medicine. A nail technician may be the first to note a subtle change in nail health.

Subungual hematomas are treated by either releasing the pressure conservatively when tolerable or by drilling a hole through the nail into the hematoma (trephining), or by removing the entire nail. Trephining is generally accomplished by using a heated instrument to pass through the nail into the blood clot. Removal of the nail is typically done when the nail itself is disrupted, a large laceration requiring suturing is suspected, or a fracture of the tip of the finger occurs. Although general anesthesia is generally not required, a digital nerve block is recommended to be performed if the nail is to be removed.

Subungual hematomas typically heal without incident, though infection or disruption of the nail (onycholysis) may occur.

Multiple standards exist for defining Henoch–Schönlein purpura, including the 1990 American College of Rheumatology (ACR) classification and the 1994 Chapel Hill Consensus Conference (CHCC). Some have reported the ACR criteria to be more sensitive than those of the CHCC.

More recent classifications, the 2006 European League Against Rheumatism (EULAR) and Pediatric Rheumatology Society (PReS) classification, include palpable purpura as a mandatory criterion, together with at least one of the following findings: diffuse abdominal pain, predominant IgA deposition (confirmed on skin biopsy), acute arthritis in any joint, and renal involvement (as evidenced by the presence of blood and/or protein in the urine).

Cryofibrinogenemic purpura is a skin condition that manifests as painful purpura with slow healing ulcerations and edema of both feet during winter months.

Daily use of hand lotion or hand cream may help prevent the formation of hangnails.

For home treatment, the American Academy of Dermatology recommends washing the hands, clipping the loose piece of skin with a clean nail clipper or nail scissors, and applying over-the-counter antibiotic ointment if the area appears inflamed. Persistent hangnails should be evaluated by a physician.

Purpura are a common and nonspecific medical sign; however, the underlying mechanism commonly involves one of:

- Platelet disorders (thrombocytopenic purpura)

- Primary thrombocytopenic purpura

- Secondary thrombocytopenic purpura

- Post-transfusion purpura

- Vascular disorders (nonthrombocytopenic purpura)

- Microvascular injury, as seen in senile (old age) purpura, when blood vessels are more easily damaged

- Hypertensive states

- Deficient vascular support

- Vasculitis, as in the case of Henoch–Schönlein purpura

- Coagulation disorders

- Disseminated intravascular coagulation (DIC)

- Scurvy (vitamin C deficiency) - defect in collagen synthesis due to lack of hydroxylation of procollagen results in weakened capillary walls and cells

- Meningococcemia

- Cocaine use with concomitant use of the one-time chemotherapy drug and now veterinary deworming agent levamisole can cause purpura of the ears, face, trunk, or extremities, sometimes needing reconstructive surgery. Levamisole is purportedly a common cutting agent.

- Decomposition of blood vessels including purpura is a symptom of acute radiation poisoning in excess of 2 Grays of radiation exposure. This is an uncommon cause in general, but is commonly seen in victims of nuclear disaster.

Cases of psychogenic purpura are also described in the medical literature, some claimed to be due to "autoerythrocyte sensitization". Other studies suggest the local (cutaneous) activity of tissue plasminogen activator can be increased in psychogenic purpura, leading to substantial amounts of localized plasmin activity, rapid degradation of fibrin clots, and resultant bleeding. Petechial rash is also characteristic of a rickettsial infection.

Longitudinal leukonychia is far less common and features smaller 1mm white longitudinal lines visible under the nail plate. It may be associated with Darier's disease.

The amount of fresh frozen plasma required to reverse disseminated intravascular coagulation associated with purpura fulminans may lead to complications of fluid overload and death, especially in neonates, such as transfusion-related acute lung injury. Exposure to multiple plasma donors over time increases the cumulative risk for transfusion-associated viral infection and allergic reaction to donor proteins found in fresh frozen plasma.

Allergic reactions and alloantibody formation are also potential complications, as with any protein replacement therapy.

Concomitant warfarin therapy in subjects with congenital protein C deficiency is associated with an increased risk of warfarin skin necrosis.

Henoch–Schönlein purpura may present with an atypical manifestation, which can be confused with papular urticaria, systemic lupus erythematosus, meningococcemia, dermatitis herpetiformis, and acute hemorrhagic edema of infancy.

Hangnails can become infected and cause paronychia, a type of skin infection that occurs around the nails. Treatments for paronychia vary with severity, but may include soaking in hot salty water, the use of oral antibiotic medication, or clinical lancing. Paronychia itself rarely results in further complications but can lead to abscess, permanent changes to the shape of the nail or the spread of infection.

The differential diagnoses are: acrodermatitis enteropathica, erythema infectiosum, erythema multiforme, hand-foot-and-mouth disease, Henoch–Schönlein purpura, Kawasaki disease, lichen planus, papular urticaria, papular purpuric gloves and socks syndrome, and scabies.

The diagnosis of Gianotti–Crosti syndrome is clinical. A validated diagnostic criteria is as follows:

A patient is diagnosed as having Gianotti–Crosti syndrome if:

1. On at least one occasion or clinical encounter, he/she exhibits all the positive clinical features,

2. On all occasions or clinical encounters related to the rash, he/she does not exhibit any of the negative clinical features,

3. None of the differential diagnoses is considered to be more likely than Gianotti–Crosti syndrome on clinical judgment, and

4. If lesional biopsy is performed, the histopathological findings are consistent with Gianotti–Crosti syndrome.

The positive clinical features are:

- Monomorphous, flat-topped, pink-brown papules or papulovesicles 1-10mm in diameter.

- At least three of the following four sites involved – (1) cheeks, (2) buttocks, (3) extensor surfaces of forearms, and (4) extensor surfaces of legs.

- Being symmetrical, and

- Lasting for at least ten days.

The negative clinical features are:

- Extensive truncal lesions, and

- Scaly lesions.

The cardinal features of purpura investigations are the same as those of disseminated intravascular coagulation: prolonged plasma clotting times, thrombocytopenia, reduced plasma fibrinogen concentration, increased plasma fibrin-degradation products and occasionally microangiopathic haemolysis.

There are four classic types of onychomycosis:

- Distal subungual onychomycosis is the most common form of "tinea unguium" and is usually caused by "Trichophyton rubrum", which invades the nail bed and the underside of the nail plate.

- White superficial onychomycosis (WSO) is caused by fungal invasion of the superficial layers of the nail plate to form "white islands" on the plate. It accounts for around 10 percent of onychomycosis cases. In some cases, WSO is a misdiagnosis of "keratin granulations" which are not a fungus, but a reaction to nail polish that can cause the nails to have a chalky white appearance. A laboratory test should be performed to confirm.

- Proximal subungual onychomycosis is fungal penetration of the newly formed nail plate through the proximal nail fold. It is the least common form of "tinea unguium" in healthy people, but is found more commonly when the patient is immunocompromised.

- Candidal onychomycosis is "Candida" species invasion of the fingernails, usually occurring in persons who frequently immerse their hands in water. This normally requires the prior damage of the nail by infection or trauma.

Getting a regular eye exam may play a role in identifying the signs of some systemic diseases. "The eye is composed of many different types of tissue. This unique feature makes the eye susceptible to a wide variety of diseases as well as provides insights into many body systems. Almost any part of the eye can give important clues to the diagnosis of systemic diseases. Signs of a systemic disease may be evident on the outer surface of the eye (eyelids, conjunctiva and cornea), middle of the eye and at the back of the eye (retina)."

Since 500 B.C., some researchers have believed that the physical condition of the fingernails and toenails can indicate various systemic diseases. Careful examination of the fingernails and toenails may provide clues to underlying systemic diseases , since some diseases have been found to cause disruptions in the nail growth process. The nail plate is the hard keratin cover of the nail. The nail plate is generated by the nail matrix located just under the cuticle. As the nail grows, the area closest to becoming exposed to the outside world (distal) produces the deeper layers of the nail plate, while the part of the nail matrix deeper inside the finger (proximal) makes the superficial layers. Any disruption in this growth process can lead to an alteration in the shape and texture.

For example, pitting looks like depressions in the hard part of the nail. Pitting is to be associated with psoriasis, affecting 10% - 50% of patients with that disorder. Pitting also may be caused by a variety of systemic diseases, including reactive arthritis and other connective tissue disorders, sarcoidosis, pemphigus, alopecia areata, and incontinentia pigmenti. Because pitting is caused by defective layering of the superficial nail plate by the proximal nail matrix, any localized dermatitis (e.g., atopic dermatitis or chemical dermatitis) that disrupts orderly growth in that area also can cause pitting.

To avoid misdiagnosis as nail psoriasis, lichen planus, contact dermatitis, nail bed tumors such as melanoma, trauma, or yellow nail syndrome, laboratory confirmation may be necessary. The three main approaches are potassium hydroxide smear, culture and histology. This involves microscopic examination and culture of nail scrapings or clippings. Recent results indicate the most sensitive diagnostic approaches are direct smear combined with histological examination, and nail plate biopsy using periodic acid-Schiff stain. To reliably identify nondermatophyte molds, several samples may be necessary.