question: when we get a sunburn, why does it take 1-2 weeks for the skin to start peeling?
comment: The radiation from the sun damages cell DNA. This by itself does not automatically kill the cell. Cells go through phases during its reproduction. Several phases include checkpoints where it checks everything to make sure it's ready to divide. If things aren't in order like the dna is damaged then the cell kills itself. So the period it takes for cells to die can be a while. The dead cells then act as a layer of protection for new cells to grow underneath. The new cells push the dead cells up and the dead cells flake off the top. When there's s mass cell die off then you get peeling.
passages: After the exposure, skin may turn red in as little as 30 minutes but most often takes 2 to 6 hours. Pain is usually strongest 6 to 48 hours after exposure. The burn continues to develop for 1 to 3 days, occasionally followed by peeling skin in 3 to 8 days. Some peeling and itching may continue for several weeks.
  
  Section::::Signs and symptoms.:Skin cancer.
   Though environmental causes are not well understood, it seems clear that factors like sun exposure, wind and air conditioning add to the degree of skin inflammation that sets the start of a new cycle.
  
  Section::::Diagnosis.
  
  Section::::Diagnosis.:Differential diagnosis.
  
  This includes erythrokeratodermia variabilis and loricrin keratoderma
  
  Section::::Treatment.
  
  Definitive treatment does not exist at the moment. Palliative treatment are intended to alleviate the itching that often accompanies the skin inflammation and to moisture the dry skin to prevent excessive dryness and scaling of the plaques.
  
  Section::::History.
   Normal, nonpathologic desquamation of the skin occurs when keratinocytes, after moving typically over about 14 days, are individually shed unnoticeably. Obvious but nonpathologic visible desquamation can be observed after immersion of the skin in warm or hot water, encouraging the topmost layer of dead skin cells to shed and, as such, is a common result from the use of a hot shower or bath. In pathologic desquamation, such as that seen in X-linked ichthyosis, the stratum corneum becomes thicker (hyperkeratosis), imparting a "dry" or scaly appearance to the skin, and instead of detaching as single cells, corneocytes are shed in clusters, forming visible scales. Desquamation of the epidermis may result from disease or injury of the skin. For example, once the rash of measles fades, there is desquamation. Skin peeling typically follows healing of a first degree burn or sunburn. Toxic shock syndrome, a potentially fatal immune system reaction to a bacterial infection such as "Staphylococcus aureus", can cause severe desquamation; so can mercury poisoning. Other serious skin diseases involving extreme desquamation include Stevens–Johnson syndrome and toxic epidermal necrolysis (TEN). Radiation can cause dry or moist desquamation.
   When peeling of skin occurs, the newly exposed layer of skin underneath is moist, raw and very sensitive. While this may result in minor discomfort and inconvenience, in severe cases of KWE where large areas of raw skin are present, it is often life-altering and debilitating.
  
  KWE is inherited in an autosomal dominant manner. This means that the defective gene responsible for the disorder is located on an autosome (chromosome 8 is an autosome), and one copy of the defective gene is sufficient to cause the disorder when inherited from a parent who also has the disorder.
   Skin plaques start to appear as reddened areas of inflammation, thus often leading to the mistaken diagnosis of Atopic Dermatitis. Following inflammation, the red areas start keratinization, eventually forming the definitive plaques that appear brownish, dry and scaled. Following quite a precise temporal pattern of evolution, the keratinized plaques last for weeks or months, eventually leading to periods of desquamation that leads to the uncovering of "normal" skin. Then, a new cycle usually begins, leaving a variable number of days of delay between the cycles.
   Though people with keratosis pilaris experience the condition year-round, the problem can become exacerbated and the bumps are likely to look and feel more pronounced in color and texture during the colder months when moisture levels in the air are lower. The symptoms may also worsen during pregnancy or after childbirth. It is speculated that increased sun exposure can mitigate the symptoms of KP.
  
  Section::::Pathophysiology.
   BULLET::::- Phytophotodermatitis: UV radiation induces inflammation of the skin after contact with certain plants (including limes, celery, and meadow grass). Causes pain, redness, and blistering of the skin in the distribution of plant exposure.
  
  BULLET::::- Polymorphic light eruption: Recurrent abnormal reaction to UVR. It can present in various ways including pink-to-red bumps, blisters, plaques and urticaria.
  
  BULLET::::- Solar urticaria: UVR-induced wheals that occurs within minutes of exposure and fades within hours.
   Photoprovocation tests are usually not required but may be undertaken by specialised centres in winter. When a decision to undertake this is made, a small area of the frequently affected skin is exposed to varying doses of UVA and minimal erythema dose (MED) (amount of UV radiation that will produce minimal redness of skin within a few hours following exposure) of broadband UVB for three consecutive days. An examination of the skin to detect the rash is made, however, up to 40% have false negative responses.
  
  Section::::Diagnosis.:Biopsy findings.
   Sunburn is an inflammatory response in the skin triggered by direct DNA damage by UV radiation. When the skin cells' DNA is overly damaged by UV radiation, type I cell-death is triggered and the skin is replaced.
  
  Sun protective measures including sunscreen and sun protective clothing are widely accepted to prevent sunburn and some types of skin cancer. Special populations including children are especially susceptible to sunburn and protective measures should be used.
  
  Section::::Signs and symptoms.
  
  Typically, there is initial redness, followed by varying degrees of pain, proportional in severity to both the duration and intensity of exposure.
   Treatments include prevention with sun avoidance and supervised light therapy, and symptom control with topical steroids. 
  
  Section::::Signs and symptoms.
  
  Typically, the first episode develops in the spring following the first exposure to intense sun. Further episodes of the irritable rash occur several hours to days following subsequent sun exposure. 
   The rash begins 12 days following the onset of symptoms caused by the strep pharyngitis (sore throat, fever, fatigue). This characteristic rash has been denoted as "scarlatiniform" and it appears as a diffuse redness of the skin with small papules, or bumps, which resemble goose pimples. These bumps are what give the characteristic sandpaper texture to the rash. The reddened skin will blanch when you apply pressure to it. It is possible for the skin to be itchy, but it will not be painful. It usually first appears on the trunk and then gradually spreads out to the arms and legs. The palms, soles and face are usually left uninvolved by the rash. The face, however, is usually flushed, most prominently in the cheeks, with a ring of paleness around the mouth. After the rash spreads, it becomes more pronounced in creases in the skin, such as the skin folds in the inguinal and axillary regions of the body. Also in those areas it is possible for there to be Pastia’s Lines which are petechiae arranged in a linear pattern. Within 1 week of onset the rash begins to fade followed by a longer process of desquamation, or shedding of the outer layer of skin, which lasts several weeks. The desquamation process usually begins on the face and progresses downward on the body. After the desquamation the skin will be left with a sunburned appearance.
   Once affected, the symptoms may not show for several days. The symptoms can be severe burning, itching, swelling and pain in the affected areas. The areas exposed to sunlight may have the appearance of a sunburn - where clothing is worn the skin is protected. There is no known reaction to moonlight, but reflections from windows and mirrors of sunlight can still cause damage.
  
  Section::::Diagnosis.
   Wound healing is a complex and fragile process in which the skin repairs itself after injury. It is susceptible to interruption or failure that creates non-healing chronic wounds.
  
  Section::::Nutrition.
  
  Add from
  
  BULLET::::- 2001 American Society for Clinical Nutrition Nutritional skin care: health effects of micronutrients and fatty acids Esther Boelsma, Henk FJ Hendriks, and Len Roza.
  
  Section::::Radiation.
   There are certain genetic conditions, for example xeroderma pigmentosum, that increase a person's susceptibility to sunburn and subsequent skin cancers. These conditions involve defects in DNA repair mechanisms which in turn decreases the ability to repair DNA that has been damaged by UV radiation.
  
  Section::::Causes.:Medications.
  
  The risk of a sunburn can be increased by pharmaceutical products that sensitize users to UV radiation. Certain antibiotics, oral contraceptives, and tranquillizers have this effect.
  
  Section::::Causes.:UV intensity.
  
  The UV Index indicates the risk of getting a sunburn at a given time and location. Contributing factors include:
   Treatment typically takes place in hospital such as in a burn unit or intensive care unit. Efforts include stopping the cause, pain medication, and antihistamines. Antibiotics, intravenous immunoglobulins, and corticosteroids may also be used. Treatments do not typically change the course of the underlying disease. Together with SJS it affects 1 to 2 persons per million per year. It is more common in females than males. Typical onset is over the age of 40. Skin usually regrows over two to three weeks; however, recovery can take months and most are left with chronic problems.
  
  Section::::Signs and symptoms.
  
  Section::::Signs and symptoms.:Prodrome.
   Desquamation
  
  Desquamation, commonly called skin peeling, is the shedding of the outermost membrane or layer of a tissue, such as the skin. The term is .
  
  Section::::Skin.
   BULLET::::- History of sunburn: Studies show that even a single episode of painful sunburn as a child can increase an individual's risk of developing AK as an adult. Six or more painful sunburns over the course of a lifetime was found to be significantly associated with the likelihood of developing AK.
  
  Section::::Risk factors.
  
  Section::::Risk factors.:Skin pigmentation.
   In pretreatment samples, the zone of collagen shows a dense accumulation of elastin, but in posttreatment samples, this zone contains less dense elastin with significant, interlocking new collagen. Repeated low-energy PSR treatment is an effective modality for improving dyspigmentation, smoothness, and skin laxity associated with photoaging. Histologic analysis of posttreatment samples confirms the production of new collagen and remodeling of dermal architecture. Changes consist of erythema and superficial epidermal peeling without complete removal, generally complete by 4 to 5 days.
  
  Section::::Plasma medicine.
  
  Section::::Plasma medicine.:Dental treatments.
   BULLET::::- Immediate photosensitivity. This is typical of XLDPP and EPP. Following a variable period of sun exposure—typically about 30 minutes—patients complain of severe pain, burning, and discomfort in exposed areas. Typically, the effects are not visible, though occasionally there may be some redness and swelling of the skin.
   The rash caused by dermatitis herpetiformis forms and disappears in three stages. In the first stage, the patient may notice a slight discoloration of the skin at the site where the lesions appear. In the next stage, the skin lesions transform into obvious vesicles and papules that are likely to occur in groups. Healing of the lesions is the last stage of the development of the symptoms, usually characterized by a change in the skin color. This may result in areas of the skin turning darker or lighter than the color of the skin on the rest of the body. Because of the intense itching, patients usually scratch, which may lead to the formation of crusts.
   Other symptoms can include blistering, swelling (edema), pruritus (itching), peeling skin, rash, nausea, fever, chills, and fainting (syncope). Also, a small amount of heat is given off from the burn, caused by the concentration of blood in the healing process, giving a warm feeling to the affected area. Sunburns may be classified as superficial, or partial thickness burns. Blistering is a sign of second degree sunburn.
  
  Section::::Signs and symptoms.:Variations.
   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 via 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% 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.
   Early and effective treatment of acne scarring can prevent severe acne and the scarring that often follows. no prescription drugs for the treatment or prevention of scars were available.
  
  Section::::Treatment.:Chemical peels.
  
  Chemical peels are chemicals which destroy the epidermis in a controlled manner, leading to exfoliation and the alleviation of certain skin conditions, including superficial acne scars. Various chemicals can be used depending upon the depth of the peel, and caution should be used, particularly for dark-skinned individuals and those individuals susceptible to keloid formation or with active infections.
  
  Section::::Treatment.:Filler injections.
   PLE can be provoked by UVA or UVB (chief cause of sunburn) rays, meaning it can be triggered even by sunlight through glass. UV-A is a major constituent of sunlight, can pass through glass, is relatively resistant to sunscreen and can cause light eruption without sunburn.
  
  Artificial UV light sources from tanning units and phototherapy treatment units can also trigger PLE. About three-quarters of sufferers acquire PLE after UV-A exposure only, one-tenth after UV-B exposure only, and the rest after a combination of UV-A and UV-B exposure.
  
  People vary in the amount of sun exposure needed to trigger the rash.
   Sun protection is an important aspect of skin care. Though the sun is beneficial in order for the human body to get its daily dose of vitamin D, unprotected excessive sunlight can cause extreme damage to the skin. Ultraviolet (UVA and UVB) radiation in the sun's rays can cause sunburn in varying degrees, early ageing and increased risk of skin cancer. UV exposure can cause patches of uneven skin tone and dry out the skin.
  
raw_presuppositions: Sunburn burns the skin so it should instantly start peeling.
raw_corrections: Sunburn damages cell DNA, which does not automatically kill the cell.