The most prominent symptoms of erythromelalgia are episodes of erythema, swelling, a painful deep-aching of the soft tissue (usually either radiating or shooting) and tenderness, along with a painful burning sensation primarily in the extremities. These symptoms are often symmetric and affect the lower extremities more frequently than the upper extremities. Symptoms may also affect the ears and face. For secondary erythromelalgia, attacks typically precede and are precipitated by the underlying primary condition. For primary erythromelalgia, attacks can last from an hour to months at a time and occur infrequently to frequently with multiple times daily. Common triggers for these episodes are exertion, heating of the affected extremities, and alcohol or caffeine consumption, and any pressure applied to the limbs. In some patients sugar and even melon consumption have also been known to provoke attacks. Many of those with primary erythromelalgia avoid wearing shoes or socks as the heat this generates is known to produce erythromelalgia attacks. Raynaud's phenomenon often coexists in patients with Erythromelalgia. Symptoms may present gradually and incrementally, sometimes taking years to become intense enough for patients to seek medical care. In other cases symptoms emerge full blown with onset.

Erythromelalgia can be found in several billing codes systems and other systems. Erythromelalgia is generally classified as a disease of the circulatory system, falling under the class of "other peripheral vascular disease", as the following two billing code systems will show:

ICD-9-CM

According to the ICD-9-CM database (International Classification of Diseases, Ninth Revision, Clinical Modification), Erythromelalgia is listed under Diseases of the Circulatory System and is identified by number 443.82.

ICD-9-CM Diagnosis Codes > Diseases of the circulatory system (390-459) > Diseases of arteries, arterioles, and capillaries (440-449) > Other peripheral vascular disease (443) > Other specified peripheral vascular disease (443.8) > Erythromelalgia (443.82).

ICD-10-CM

According to the ICD-10-CM database (International Classification of Diseases, Tenth Revision, Clinical Modification), Erythromelalgia is listed under Diseases of the circulatory system and is identified by I73.81.

ICD-10-CM Diagnosis Codes > Diseases of the circulatory system (I00-I99) > Diseases of arteries, arterioles and capillaries (I70-I79) > Other peripheral vascular diseases (173-9) > Erythromelalgia (I73.81)

Mesh

According to the MESH database (Medical Subject Headings), Erythromelalgia is classified under the unique ID number of D004916.

OMIM

According to the OMIM database (NCBI - Online Mendelian Inheritance in Man), Primary Erythromelalgia is listed under the number: 133020.

Livedo reticularis is a common skin finding consisting of a mottled reticulated vascular pattern that appears as a lace-like purplish discoloration of the skin. The discoloration is caused by swelling of the venules owing to obstruction of capillaries by small blood clots. The blood clots in the small blood vessels can be a secondary effect of a condition that increases a person's risk of forming blood clots, including a wide array of pathological and nonpathological conditions . Examples include hyperlipidemia, microvascular hematological or anemia states, nutritional deficiencies, hyper- and autoimmune diseases, and drugs/toxins.

The condition may be normal or related to more severe underlying pathology. Its differential diagnosis is broadly divided into possible blood diseases, autoimmune (rheumatologic) diseases, cardiovascular diseases, cancers, and endocrine disorders. It can usually (in 80% of cases) be diagnosed by biopsy.

It may be aggravated by exposure to cold, and occurs most often in the lower extremities.

The condition's name derives from the Latin "livere" meaning bluish and "reticular" which refers to the net-like appearance.

Basophilia is a condition where the basophil quantity is abnormally elevated (more than 10 basophils per liter of blood). Basophilia is associated with pruritus (itching) due to the release of histamine.

Most people with ET are without symptoms referable to ET at the time of diagnosis, which is usually ultimately made after noting an elevated platelet level on a routine complete blood count (CBC). The most common symptoms are bleeding (due to dysfunctional platelets), blood clots (e.g., deep vein thrombosis or pulmonary embolism), headache, nausea, vomiting, abdominal pain, visual disturbances, dizziness, fainting, and numbness in the extremities; the most common signs are increased white blood cell count, reduced red blood cell count, and an enlarged spleen.

Essential thrombocythemia (ET) is a rare chronic blood condition characterised by the overproduction of platelets by megakaryocytes in the bone marrow. It may, albeit rarely, develop into acute myeloid leukemia or myelofibrosis. It is one of four myeloproliferative neoplasms (blood cancers that occur when the body makes too many white or red blood cells, or platelets).

Budd–Chiari syndrome is a very rare condition, affecting 1 in a million adults. The condition is caused by occlusion of the hepatic veins that drain the liver. It presents with the classical triad of abdominal pain, ascites, and liver enlargement. The formation of a blood clot within the hepatic veins can lead to Budd–Chiari syndrome. The syndrome can be fulminant, acute, chronic, or asymptomatic.

Capillary leak syndrome is characterized by the escape of blood plasma through capillary walls, from the blood circulatory system to surrounding tissues, muscle compartments, organs or body cavities. It is a phenomenon most commonly witnessed in sepsis, and less frequently in autoimmune diseases, differentiation syndrome, engraftment syndrome, hemophagocytic lymphohistiocytosis, the ovarian hyperstimulation syndrome, viral hemorrhagic fevers, and snakebite and ricin poisoning. Pharmaceuticals, including the chemotherapy medication gemcitabine, as well as certain interleukins and monoclonal antibodies, can also cause capillary leaks. These conditions and factors are sources of secondary capillary leak syndrome.

Systemic capillary leak syndrome (SCLS, or Clarkson's disease), or primary capillary leak syndrome, is a rare, grave and episodic medical condition observed largely in otherwise healthy individuals mostly in middle age. It is characterized by self-reversing episodes during which the endothelial cells which line the capillaries, usually of the extremities, separate for one to three days, causing a leakage of plasma mainly into the muscle compartments of the arms and legs. The abdomen, the central nervous system, and the organs (including the lungs) are typically spared, but the extravasation in the extremities is sufficiently massive to cause circulatory shock and compartment syndromes, with a dangerous hypotension (low blood pressure), hemoconcentration(thickening of the blood) and hypoalbuminemia (drop in albumin, a major protein) in the absence of other causes for such abnormalities. SCLS is thus a limb- and life-threatening illness, because each episode has the potential to cause damage to limb muscles and nerves, as well as to vital organs due to limited perfusion. It is often misdiagnosed as polycythemia, polycythemia vera, hyperviscosity syndrome, or sepsis.

A number of conditions may cause the appearance of livedo reticularis:

- Cutis marmorata telangiectatica congenita, a rare congenital condition

- Sneddon syndrome – association of livedoid vasculitis and systemic vascular disorders, such as strokes, due to underlying genetic cause

- Idiopathic livedo reticularis – the most common form of livedo reticularis, completely benign condition of unknown cause affecting mostly young women during the winter: It is a lacy purple appearance of skin in extremities due to sluggish venous blood flow. It may be mild, but ulceration may occur later in the summer.

- Secondary livedo reticularis:

- Vasculitis autoimmune conditions:

- Livedoid vasculitis – with painful ulceration occurring in the lower legs

- Polyarteritis nodosa

- Systemic lupus erythematosus

- Dermatomyositis

- Rheumatoid arthritis

- Lymphoma

- Pancreatitis

- Chronic pancreatitis

- Tuberculosis

- Drug-related:

- Adderall (side effect)

- Amantadine (side effect)

- Bromocriptine (side effect)

- Beta IFN treatment, "i.e." in multiple sclerosis

- Livedo reticularis associated with rasagiline

- Methylphenidate and dextroamphetamine-induced peripheral vasculopathy

- Gefitinib

- Obstruction of capillaries:

- Cryoglobulinaemia – proteins in the blood that clump together in cold conditions

- Antiphospholipid syndrome due to small blood clots

- Hypercalcaemia (raised blood calcium levels which may be deposited in the capillaries)

- Haematological disorders of polycythaemia rubra vera or thrombocytosis (excessive red cells or platelets)

- Infections (syphilis, tuberculosis, Lyme disease)

- Associated with acute renal failure due to cholesterol emboli status after cardiac catheterization

- Arteriosclerosis (cholesterol emboli) and homocystinuria (due to Chromosome 21 autosomal recessive Cystathionine beta synthase deficiency)

- Intra-arterial injection (especially in drug addicts)

- Ehlers-Danlos syndrome – connective tissue disorder, often with many secondary conditions, may be present in all types

- Pheochromocytoma

- Livedoid vasculopathy and its association with factor V Leiden mutation

- FILS syndrome (polymerase ε1 mutation in a human syndrome with facial dysmorphism, immunodeficiency, livedo, and short stature)

- Primary hyperoxaluria, oxalosis (oxalate vasculopathy)

- Cytomegalovirus infection (very rare clinical form, presenting with persistent fever and livedo reticularis on the extremities and cutaneous necrotizing vasculitis of the toes)

- Generalized livedo reticularis induced by silicone implants for soft tissue augmentation

- As a rare skin finding in children with Down syndrome

- Idiopathic livedo reticularis with polyclonal IgM hypergammopathy

- CO angiography (rare, reported case)

- A less common skin lesion of Churg-Strauss syndrome

- Erythema nodosum-like cutaneous lesions of sarcoidosis showing livedoid changes in a patient with sarcoidosis and Sjögren's syndrome

- Livedo vasculopathy associated with IgM antiphosphatidylserine-prothrombin complex antibody

- Livedo vasculopathy associated with plasminogen activator inhibitor-1 promoter homozygosity and prothrombin G20210A heterozygosity

- As a first sign of metastatic breast carcinoma (very rare)

- Livedo reticularis associated with renal cell carcinoma (rare)

- Buerger's disease (as an initial symptom)

- As a rare manifestation of Graves hyperthyroidism

- Associated with pernicious anaemia

- Moyamoya disease (a rare, chronic cerebrovascular occlusive disease of unknown cause, characterized by progressive stenosis of the arteries of the circle of Willis leading to an abnormal capillary network and resultant ischemic strokes or cerebral hemorrhages)

- Associated with the use of a midline catheter

- Familial primary cryofibrinogenemia.

Basophilia as an isolated finding is uncommon. However it is a common feature of myeloproliferative disorders and particularly prominent in chronic myelogenous leukemia.

Conditions Associated with Increased Numbers of Blood Basophils

- Allergy or inflammation

1. Ulcerative colitis

2. Drug, food, inhalant hypersensitivity

3. Erythroderma, urticaria

4. Juvenile rheumatoid arthritis

- Endocrinopathy

1. Diabetes mellitus

2. Estrogen administration

3. Hypothyroidism (myxedema)

- Infection

1. Chicken pox

2. Influenza

3. Smallpox

4. Tuberculosis

- Iron deficiency

- Exposure to ionizing radiation

- Neoplasia

1. "Basophilic leukemia" (see text)

- Myeloproliferative neoplasms (especially chronic myelogenous leukemia; also polycythemia vera, primary myelofibrosis, essential thrombocythemia)

- Carcinoma

Chronic and repetitive scratching, picking, or rubbing of the nodules may result in permanent changes to the skin, including nodular lichenification, hyperkeratosis, hyperpigmentation, and skin thickening. Unhealed, excoriated lesions are often scaly, crusted or scabbed. Many patients report a lack of wound healing even when medications relieve the itching and subsequent scratching.

Patients often:

- seek treatment during middle-age, although PN can occur at any age.

- have a history of chronic severe pruritus.

- have a significant medical history for unrelated conditions.

- suffer from liver or kidney dysfunctions.

- suffer secondary skin infections.

- have a personal or family history of atopic dermatitis.

- have other autoimmune disorders.

- have low vitamin D levels.

The acute syndrome presents with rapidly progressive severe upper abdominal pain, yellow discoloration of the skin and whites of the eyes, liver enlargement, enlargement of the spleen, fluid accumulation within the peritoneal cavity, elevated liver enzymes, and eventually encephalopathy. The fulminant syndrome presents early with encephalopathy and ascites. Liver cell death and severe lactic acidosis may be present as well. Caudate lobe enlargement is often present. The majority of patients have a slower-onset form of Budd–Chiari syndrome. This can be painless. A system of venous collaterals may form around the occlusion which may be seen on imaging as a "spider's web". Patients may progress to cirrhosis and show the signs of liver failure.

On the other hand, incidental finding of a silent, asymptomatic form may not be a cause for concern.

Malar flush is a plum-red discolouration of the high cheeks classically associated with mitral stenosis due to the resulting CO retention and its vasodilatory effects.

It can also be associated with other conditions, such as SLE or polycythemia rubra vera.

Many conditions affect the human integumentary system—the organ system covering the entire surface of the body and composed of skin, hair, nails, and related muscle and glands. The major function of this system is as a barrier against the external environment. The skin weighs an average of four kilograms, covers an area of two square meters, and is made of three distinct layers: the epidermis, dermis, and subcutaneous tissue. The two main types of human skin are: glabrous skin, the hairless skin on the palms and soles (also referred to as the "palmoplantar" surfaces), and hair-bearing skin. Within the latter type, the hairs occur in structures called pilosebaceous units, each with hair follicle, sebaceous gland, and associated arrector pili muscle. In the embryo, the epidermis, hair, and glands form from the ectoderm, which is chemically influenced by the underlying mesoderm that forms the dermis and subcutaneous tissues.

The epidermis is the most superficial layer of skin, a squamous epithelium with several strata: the stratum corneum, stratum lucidum, stratum granulosum, stratum spinosum, and stratum basale. Nourishment is provided to these layers by diffusion from the dermis, since the epidermis is without direct blood supply. The epidermis contains four cell types: keratinocytes, melanocytes, Langerhans cells, and Merkel cells. Of these, keratinocytes are the major component, constituting roughly 95 percent of the epidermis. This stratified squamous epithelium is maintained by cell division within the stratum basale, in which differentiating cells slowly displace outwards through the stratum spinosum to the stratum corneum, where cells are continually shed from the surface. In normal skin, the rate of production equals the rate of loss; about two weeks are needed for a cell to migrate from the basal cell layer to the top of the granular cell layer, and an additional two weeks to cross the stratum corneum.

The dermis is the layer of skin between the epidermis and subcutaneous tissue, and comprises two sections, the papillary dermis and the reticular dermis. The superficial papillary dermis with the overlying rete ridges of the epidermis, between which the two layers interact through the basement membrane zone. Structural components of the dermis are collagen, elastic fibers, and ground substance. Within these components are the pilosebaceous units, arrector pili muscles, and the eccrine and apocrine glands. The dermis contains two vascular networks that run parallel to the skin surface—one superficial and one deep plexus—which are connected by vertical communicating vessels. The function of blood vessels within the dermis is fourfold: to supply nutrition, to regulate temperature, to modulate inflammation, and to participate in wound healing.

The subcutaneous tissue is a layer of fat between the dermis and underlying fascia. This tissue may be further divided into two components, the actual fatty layer, or panniculus adiposus, and a deeper vestigial layer of muscle, the panniculus carnosus. The main cellular component of this tissue is the adipocyte, or fat cell. The structure of this tissue is composed of septal (i.e. linear strands) and lobular compartments, which differ in microscopic appearance. Functionally, the subcutaneous fat insulates the body, absorbs trauma, and serves as a reserve energy source.

Conditions of the human integumentary system constitute a broad spectrum of diseases, also known as dermatoses, as well as many nonpathologic states (like, in certain circumstances, melanonychia and racquet nails). While only a small number of skin diseases account for most visits to the physician, thousands of skin conditions have been described. Classification of these conditions often presents many nosological challenges, since underlying etiologies and pathogenetics are often not known. Therefore, most current textbooks present a classification based on location (for example, conditions of the mucous membrane), morphology (chronic blistering conditions), etiology (skin conditions resulting from physical factors), and so on. Clinically, the diagnosis of any particular skin condition is made by gathering pertinent information regarding the presenting skin lesion(s), including the location (such as arms, head, legs), symptoms (pruritus, pain), duration (acute or chronic), arrangement (solitary, generalized, annular, linear), morphology (macules, papules, vesicles), and color (red, blue, brown, black, white, yellow). Diagnosis of many conditions often also requires a skin biopsy which yields histologic information that can be correlated with the clinical presentation and any laboratory data.

The cause of prurigo nodularis is unknown, although other conditions may induce PN. PN has been linked to Becker's nevus, linear IgA disease, an autoimmune condition, liver disease and T cells. Systemic pruritus has been linked to cholestasis, thyroid disease, polycythaemia rubra vera, uraemia, Hodgkins disease, HIV and other immunodeficiency diseases. Internal malignancies, liver failure, renal failure, and psychiatric illnesses have been considered to induce PN, although more recent research has refuted a psychiatric cause for PN. Patients report an ongoing battle to distinguish themselves from those with psychiatric disorders such as delusions of parasitosis and other psychiatric conditions.

Most SCLS patients report having flu-like symptoms (like a runny nose), or else gastro-intestinal disorders (diarrhea or vomiting), or a general weakness or pain in their limbs, but others get no particular or consistent warning signs ahead of their episodes. They subsequently develop thirst and lightheadedness and the following conditions measurable in a hospital emergency-room setting:

- hemoconcentration (elevated hematocrit or hemoglobin readings, with hematocrit levels >49% in men and >43% in women, not because of an absolute increase in them but because of the leak of plasma);

- very low blood pressure (profound arterial hypotension, with systolic blood pressure levels <90 mm Hg);

- albumin deficiency (hypoalbuminemia measuring <3.0 g/dL);

- partial or generalized edema, and cold extremities;

- a paraprotein in the blood (an MGUS in approximately 80% of cases).

In dentistry, anodontia, also called anodontia vera, is a rare genetic disorder characterized by the congenital absence of all primary or permanent teeth. It is associated with the group of skin and nerve syndromes called the ectodermal dysplasias. Anodontia is usually part of a syndrome and seldom occurs as an isolated entity.

Congenital absence of permanent teeth can present as hypodontia, usually missing 1 or 2 permanent teeth, or oligodontia that is the congenital absence of 6 or more teeth. Congenital absence of all wisdom teeth, or third molars, is relatively common. Anodontia is the congenital absence of teeth and can occur in some or all teeth (partial anodontia or hypodontia), involve two dentitions or only teeth of the permanent dentition (Dorland's 1998). Approximately 1% of the population suffers from oligodontia. Many denominations are attributed to this anomaly: partial anodontia, hypodontia, oligodontia, the congenital absence, anodontia, bilateral aplasia. Anodontia being the term used in controlled vocabulary Medical Subject Headings (MeSH) from MEDLINE which was developed by the United States National Library of Medicine. The congenital absence of at least one permanent tooth is the most common dental anomaly and may contribute to masticator dysfunction, speech impairment, aesthetic problems, and malocclusion (Shapiro and Farrington 1983). Absence of lateral incisors represents a major stereotype. Individuals with this condition are perceived as socially most aggressive compared with people without anodontia (Shaw 1981).

Aphthous stomatitis is a common condition characterized by the repeated formation of benign and non-contagious mouth ulcers (aphthae) in otherwise healthy individuals. The informal term canker sores is also used, mainly in North America, although this may also refer to any mouth ulcer.

The cause is not completely understood, but involves a T cell-mediated immune response triggered by a variety of factors. Different individuals have different triggers, which may include nutritional deficiencies, local trauma, stress, hormonal influences, allergies, or genetic predisposition.

These ulcers occur periodically and heal completely between attacks. In the majority of cases, the individual ulcers last about 7–10 days, and ulceration episodes occur 3–6 times per year. Most appear on the non-keratinizing epithelial surfaces in the mouth (i.e. anywhere except the attached gingiva, the hard palate and the dorsum of the tongue), although the more severe forms, which are less common, may also involve keratinizing epithelial surfaces. Symptoms range from a minor nuisance to interfering with eating and drinking. The severe forms may be debilitating, even causing weight loss due to malnutrition.

The condition is very common, affecting about 20% of the general population to some degree. The onset is often during childhood or adolescence, and the condition usually lasts for several years before gradually disappearing. There is no cure, and treatments aim to manage pain, reduce healing time and reduce the frequency of episodes of ulceration. The term is from meaning "mouth ulcer".

Persons with aphthous stomatitis have no detectable systemic symptoms or signs (i.e., outside the mouth). Generally, symptoms may include prodromal sensations such as burning, itching, or stinging, which may precede the appearance of any lesion by some hours; and pain, which is often out of proportion to the extent of the ulceration and is worsened by physical contact, especially with certain foods and drinks (e.g., if they are acidic). Pain is worst in the days immediately following the initial formation of the ulcer, and then recedes as healing progresses. If there are lesions on the tongue, speaking and chewing can be uncomfortable, and ulcers on the soft palate, back of the throat, or esophagus can cause painful swallowing. Signs are limited to the lesions themselves.

Ulceration episodes usually occur about 3–6 times per year. However, severe disease is characterized by virtually constant ulceration (new lesions developing before old ones have healed) and may cause debilitating chronic pain and interfere with comfortable eating. In severe cases, this prevents adequate nutrient intake leading to malnutrition and weight loss.

Aphthous ulcers typically begin as erythematous macules (reddened, flat area of mucosa) which develop into ulcers that are covered with a yellow-grey fibrinous membrane that can be scraped away. A reddish "halo" surrounds the ulcer. The size, number, location, healing time, and periodicity between episodes of ulcer formation are all dependent upon the subtype of aphthous stomatitis.

Segawa Syndrome (SS) also known as Dopamine-responsive dystonia (DRD), Segawa's disease, Segawa's dystonia and hereditary progressive dystonia with diurnal fluctuation, is a genetic movement disorder which usually manifests itself during early childhood at around ages 5–8 years (variable start age).

Characteristic symptoms are increased muscle tone (dystonia, such as clubfoot) and Parkinsonian features, typically absent in the morning or after rest but worsening during the day and with exertion. Children with SS are often misdiagnosed as having cerebral palsy. The disorder responds well to treatment with levodopa.

Symptoms typically present in the 3rd or 4th decade of life, but have been seen as early as the age of 14. It presents with torsion dystonia, particularly when presenting at a younger age, which then progresses to parkinsonism with or without ongoing dystonia. Often the two symptoms coexist.The parkinsonian features of x-linked dystonia parkinsonism include festinating gait, bradykinesia, blepharospasm, and postural instability. It often lacks a resting tremor, helping to differentiate it from Parkinson's disease.

The disease typically starts in one limb, typically one leg. Progressive dystonia results in clubfoot and tiptoe walking. The symptoms can spread to all four limbs around age 18, after which progression slows and eventually symptoms reach a plateau. There can be regression in developmental milestones (both motor and mental skills) and failure to thrive in the absence of treatment.

In addition, SS is typically characterized by signs of parkinsonism that may be relatively subtle. Such signs may include slowness of movement (bradykinesia), tremors, stiffness and resistance to movement (rigidity), balance difficulties, and postural instability. Approximately 25 percent also have abnormally exaggerated reflex responses (hyperreflexia), particularly in the legs. These symptoms can result in a presentation that is similar in appearance to that of Parkinson's Disease.

Many patients experience improvement with sleep, are relatively free of symptoms in the morning, and develop increasingly severe symptoms as the day progresses (i.e., diurnal fluctuation). Accordingly, this disorder has sometimes been referred to as "progressive hereditary dystonia with diurnal fluctuations." Yet some SS patients do not experience such diurnal fluctuations, causing many researchers to prefer other disease terms.

- Other symptoms - footwear

- excessive wear at toes, but little wear on heels, thus replacement of shoes every college term/semester.

- Other symptoms - handwriting

- near normal handwriting at infants/kindergarten (ages 3–5 school) years.

- poor handwriting at pre-teens (ages 8–11 school) years.

- very poor (worse) handwriting during teen (qv GCSE/A level-public exams) years.

- bad handwriting (worsening) during post-teen (qv university exams) years.

- very bad handwriting (still worsening) during adult (qv post-graduate exams) years.

- worsening pattern of sloppy handwriting best observed by school teachers via termly reports.

- child sufferer displays unhappy childhood facial expressions (depression.?)

Ionizing radiation-induced cutaneous conditions result from exposure to ionizing radiation.

- Acute radiodermatitis

- Chronic radiation keratosis

- Chronic radiodermatitis

- Eosinophilic, polymorphic, and pruritic eruption associated with radiotherapy

- Fluoroscopy burn

- Radiation acne

- Radiation cancer

- Radiation dermatitis (radiodermatitis)

- Radiation recall reaction

- Radiation-induced erythema multiforme

- Radiation-induced hypertrophic scar

- Radiation-induced keloid

- Radiation-induced morphea

Symptoms occur for up to 35 minutes; duration of an attack is typically between 10 and 120 minutes. However, sensitivity varies among sufferers, and since water is always present to some extent in the air (atmospheric humidity), those with greater sensitivity who live in moister regions are symptomatic almost constantly, while perspiration can cause frequent symptoms even in the driest climates.

Hematopoietic ulcers are those occurring with sickle cell anemia, congenital hemolytic anemia, polycythemia vera, thrombocytopenic purpura, macroglobulinemia, and cryoglobulinemia.