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Give at least 5 disorders with definition, etiology, epidemiology, risk factors, pathophysiology and treatment.
Vitiligo
Definition: Acquired pigmentary condition of the skin known as vitiligo is characterized by concentric, depigmented macules and patches. Thyroid problems are the most common autoimmune disorders with which the condition is usually connected. Etiology: Lack of melanin, a skin pigment, is what causes vitiligo. Melanin, which gives your skin its color, is produced by skin cells called melanocytes. Lack of functioning melanocytes prevents your skin from producing enough melanin when you have vitiligo. Your skin or hair may start to develop white patches as a result. The actual cause of the melanocytes' disappearance from the skin's afflicted regions is unknown. Epidemiology: There has been a reported female preponderance for vitiligo, however this is not statistically significant, and the discrepancy has been linked to a rise in female patients' reporting of cosmetic concerns. Although vitiligo may arise at any moment from birth to senescence, onset is most typically found in adults aged 10-30 years. The average age at which vitiligo first appears is 20 years. It is doubtful that the age of onset will differ between the sexes. Risk factors: Skin trauma or damage- According to research, vitiligo may occur more frequently in regions where there has been a lot of sun exposure and severe sunburns (commonly on the face, neck, and hands). Stress- Studies have indicated that stressful situations or long-term emotional and physical stress can cause vitiligo to develop and grow, especially in patients who are genetically prone to the condition. Substance Exposure- Another environmental risk factor for getting vitiligo may be contact with or exposure to specific substances. According to a theory put out by some professionals, the chemicals speed up stress pathways that are already present in melanocytes and cause autoimmune inflammation. Pathophysiology: A multifactorial polygenic condition with a convoluted pathophysiology is vitiligo. Both hereditary and nongenetic variables are involved. Although numerous hypotheses on the pathophysiology of vitiligo have been put forth, the exact cause is still unknown. It is generally accepted that vitiligo skin lacks functional melanocytes and has lost histochemically visible melanocytes due to their death. However, the devastation is probably a gradual process leading to a declining number of melanocytes. Incomplete penetrance, many susceptibility sites, and genetic heterogeneity are characteristics of vitiligo. Inheritance is complicated and probably involves both genetic and environmental variables, according to studies of families and twins. Furthermore, it is thought that genetic factors may affect the age at which vitiligo first appears. Vitiligo may be passed on through genes involved in melanin manufacture, oxidative stress defense, and autoimmune control. Treatment: Although there are treatments available to lessen their appearance, the white spots brought on by vitiligo are typically permanent. Skin camouflage lotion can be used to conceal tiny spots if necessary. To restore some color, steroid creams can also be applied to the skin; however, prolonged use might result in stretch marks and skin thinning. If steroid creams are ineffective, phototherapy (light therapy) may be employed. Although the procedure might help your skin regain color, the impact typically does not endure. The spread of the illness cannot be halted by treatment.
Dyshidrotic Eczema
Definition: A pruritic vesicular eruption (bullae, or blisters) commonly appears on the edges of fingers, toes, palms, and soles of feet. Dyshidrotic eczema is a kind of eczema (dermatitis) that is characterized by this severely unpleasant blistering. Etiology : The lack of evidence linking vesicles to sweat ducts has disproved the theory that the sweat glands are dysfunctional. A case study from 2009 offered conclusive histopathologic proof that sweat glands are not responsible for dyshidrosis. However, in 40% of people with dyshidrotic eczema, hyperhidrosis is a contributing element in the ailment. After receiving an injection of onabotulinumtoxinA, pruritus, erythema, vesicles, and hand dermatitis improved with fewer or no recurrence symptoms. According to reports, dyshidrosis is apparently made worse by emotional stress and environmental factors such seasonal changes, extreme heat or cold, and humidity. Some people may develop palmar pompholyx as an id response to a distant fungal infection. One study found that following tinea pedis therapy, one-third of pompholyx cases on the palms disappeared. Epidemiology : In 5-20% of people with hand eczema, dyshidrotic eczema develops more frequently in warmer climes and in the spring and summer (seasonal or summer pompholyx). Risk factors : significant amounts of stress. allergens that are seasonal, like hay fever. lingering too long in the water. excessive foot or hand perspiration having atopic dermatitis or another type of eczema. utilizing cement or metal. Pathophysiology : A sudden outbreak of tiny, itchy blisters on your palms and the sides of your fingers is a sign of dyshidrotic eczema. Blisters may also appear on the toes or soles of your feet as a result of this skin ailment. These blisters will appear and go over time because there is no cure. However, you may control them with medication, creams, and excellent cleanliness. Once you reach middle age, they may begin to diminish. Additionally, if your condition is minor, it can go away on its own. The severity of dyshidrotic eczema might vary. Blisters can make it difficult to move around if you have a severe case that affects your feet. A severely damaged epidermal barrier causes dry skin because of a significant trans epidermal water loss on the one hand, and makes it easier for irritants and allergens to penetrate the skin on the other. Genetic changes, such as null mutations in the gene filaggrin that are highly predisposed to the development of E or ichthyosis, may be responsible for the rupture of the epidermal barrier. Filaggrin is encoded by the epidermal differentiation complex and expressed in the stratum corneum's top layers (EDC). Additionally, additional EDC genes like hornerin may also contribute to the development of E. The immune system plays a role in the epidermal barrier function in addition to genetics. It has been shown that Th2 cytokines like IL- suppress the production of the S100 and filaggrin proteins, weakening the epidermal barrier. The epidermal barrier becomes even more vulnerable to mechanical (scratching) or physical irritation (hot water, UV exposure, sweating). Treatment : To reduce swelling and aid in the removal of the blisters, your doctor may prescribe an ointment or cream containing steroids. If you apply a damp compress to your skin after applying the cream, your skin will absorb the medication more effectively. You might need to take a steroid medication in a pill form, such as prednisone, if you experience a severe flare-up. The itch may also be relieved by an antihistamine such as loratadine (Alavert, Claritin) or diphenhydramine (Benadryl). Alternately, use a cold, damp compress for 15 minutes at a time to the blisters numerous times during the day. You could try one of these if these remedies don't seem to be effective for you: light treatment This clears your skin using ultraviolet (UV) radiation. You might first receive medication to improve how well your skin reacts to light. Toxin from botulinum. These shots prevent perspiration in your hands and feet, which can lead to blisters. removing the blisters' pus. The fluid from the blisters can be removed by your dermatologist. Don't try to complete this by yourself. You can aggravate the eczema.
solution. Frequently, the acyclovir cream is administered five times each day for four days. It is possible to utilize calamine lotion, a zinc oxide and iron (III) oxide mixture, as an antipruritic. Additionally, it can be used as a mild antiseptic to stop infections from spreading to the affected area and as an astringent to stop weeping or leaking blisters. However, there is no proof that calamine lotion actually relieves rashes and itching. With minimal, if any, side effects, topical ozone therapy may be helpful in reducing discomfort and shortening the course.
Actinic keratosis
Definition : Skin cancer known as invasive squamous cell carcinoma can develop from the UV light- induced skin condition known as actinic keratosis (AK). It is by far the most frequent lesion on the skin that has the potential to become cancerous. On skin areas that have been exposed to the sun for an extended period of time, fair-skinned people develop actinic keratosis. Etiology : UV light causes actinic keratoses. According to epidemiological findings and molecular biological traits of the tumor cells, UV light alone is sufficient to cause actinic keratosis. Actinic keratoses are more common among fair, redheaded, or blonde patients who burn easily and tan unfavorably because UV light sensitivity is inherited. Actinic keratosis formation is more likely with increased and more intense sun exposure. Actinic keratoses do not form in the absence of sun exposure, but the chance of acquiring them is significantly increased by immunosuppression after organ transplantation. Epidemiology : Australia has the highest frequency due to its high rate of light-skinned residents and popularity of outdoor sports. According to estimates, 40–60% of Australians over 40 are thought to have actinic keratosis. Actinic keratosis is more common in those with fair skin and blue eyes, and less common in people with darker skin tones. Black skin has a comparatively low incidence of actinic keratosis. Actinic keratosis is more common in men than in women. Theoretically, this is because men are more likely to work outdoors, increasing their cumulative UV exposure. Age is one of the most significant predictors of the development of actinic keratosis, especially when combined with other significant factors such cumulative sun exposure, place of birth, occupation, and skin type. Those 20 to 30 years old can develop actinic keratoses, although patients 50 and older are more likely to do so. Risk factors : History of unprotected sun or indoor tanning exposure to ultraviolet (UV) radiation. This includes persons who work outside in the sunlight, those who have thinning hair or a bald head, and those who have sunburns. Age over 40: People over 40 are most likely to develop AKs. Immune system that has been compromised by a disease or treatment. Anyone can acquire AKs, but those with fair skin experience them much more frequently. Pathophysiology : The formation of actinic keratoses has a complicated etiology. The disruption of regulatory mechanisms involved in cell development and differentiation caused by excessive and cumulative sun exposure can result in a variety of pathologic alterations to the epidermal keratinocyte. Dysplastic keratinocytes proliferate intra epidermally as a result of the ensuing inflammation and immunosuppression, giving birth to AKs. Treatment : The characteristics and symptoms of AK, the patient's expectations, the availability of treatments, the patient's capacity to adhere to treatment regimens, the tolerability of side effects, and the cost of treatments should all be taken into account when developing a treatment strategy. When lesions are many, bleeding, painful, and/or expanding quickly in size, it is a sign of urgency. It's important to understand how long blistering, erosion, crusting, burning, discomfort, pain, pruritus, erythema, and edema are expected to last as well as how to take care of the skin as it recovers from the treatment and heals. One popular lesion-directed therapeutic option for AKs is cryotherapy. Through the topical administration of liquid nitrogen using a spray or cotton tip applicator, skin lesions are frozen. It is an effective therapy choice for patients with just a few AKs or isolated lesions because to its outstanding response rates. The length of liquid nitrogen treatment and the quantity of freeze-thaw cycles will determine how quickly an injury will heal.
Acne Vulgaris
Definition : Acne vulgaris is a common chronic skin condition characterized by pilosebaceous unit obstruction and/or irritation (hair follicles and their accompanying sebaceous gland). Acne typically affects the face, but it can also affect the back and chest. It can appear as non-inflammatory lesions, inflammatory lesions, or a combination of both. Etiology : Acne is primarily caused by a hereditary predisposition. Other exacerbating variables are also acknowledged. The use of hair products and cosmetics may make acne worse. Steroid, lithium, certain antiepileptics, and iodides are medications that can encourage the development of acne. Acne vulgaris may occur as a result of excess androgens in the body, including polycystic ovarian syndrome, congenital adrenal hyperplasia, and other endocrine conditions. Even being pregnant can set off an attack. Headbands, shoulder pads, backpacks, and under-wire bras can all cause mechanical occlusion, which can be painful. Overexposure to the sun may help acne or make it worse. In any event, skin ages as a result of UV exposure. Epidemiology : Some racial groups are impacted more than others. From Iran to Spain, the Mediterranean region has a high prevalence of cystic acne. Whites in North America typically have acne. Pomade acne is more common among African Americans, which is probably related to their usage of hair pomades. Post inflammatory hyperpigmentation is also more common in racial groups with darker skin. Males have acne vulgaris during adolescence more frequently than girls do. Women experience acne vulgaris more frequently than males do as adults. The onset of puberty, when the gonads start to manufacture and release more androgen hormone, is typically when adolescent acne first appears. Numerous teenagers and young adults are impacted by it. Risk factors : Age. Acne can affect anyone of any age, although teenagers are the most likely to get it. Hormonal adjustments. These alterations frequently occur during puberty or pregnancy. Family background. Acne is genetically influenced. Oily or greasy substances. Pressure or friction against your skin. Pathophysiology : Acne vulgaris has a complicated pathophysiology. Genetics is the main element. The following four elements interact to cause acne to form: the skin's release of inflammatory mediators. Hyper keratinization of the follicles, followed by follicle clogging. Follicular colonization and excessive sebum production of Cuti-bacterium acnes (formerly Propionibacterium acnes). Another important element in the development of acne vulgaris is excess sebum. Numerous hormones and mediators control the production and excretion of sebum. In particular, androgen hormones encourage the release and production of sebum. Growth hormone, insulin like growth factor, peroxisome proliferator-activated receptors, and a host of other mediators and receptors all regulate the sebaceous gland and may play a role in acne development. Additionally, the sebaceous gland operates as a neuroendocrine-inflammatory organ that is triggered by corticotrophin-releasing hormones in reaction to stress and in the course of regular bodily processes. Treatment : Almost all acne patients should start their treatment with a mix of topical retinoid and antibacterial medication, according to current agreement. When compared to either monotherapy, this combination's better efficacy is the result of complimentary modes of action that target several pathogenic causes. While benzoyl peroxide is an antibacterial with some keratolytic effects and antibiotics have both anti-inflammatory and anti-microbial actions, retinoids prevent aberrant desquamation, are comedolytic, and have some anti-inflammatory benefits. The mainstay of care for moderate-to-severe inflammatory acne vulgaris is systemic antibiotics. These medications are efficient against C acnes and have anti-inflammatory qualities (formerly P acnes). Sarecycline is a brand-new, first-in-class antibiotic produced from tetracyclines that is prescribed for people with non- nodular, moderate-to-severe acne vulgaris who are at least 9 years old. The treatment of acne vulgaris may be helped by some hormone treatments. Sebum production can be reduced by estrogen.
