Presentation on Problems Associated With Skin

B pharm Final year review article topic.
Prblem associated with skin.
Skin diseases

1. Cosmetic science GUIDED BY - Prof . Rajashree V. Lode M.Pharm (Assistant Professor) PRESENTED BY: NAME- Mr . Mukesh V. Kapse CLASS- B.PHARM (IV YEAR) SEMESTER- 8 th SEM Roll No - 32 HI-TECH COLLEGE OF PHARMACY Padoli phata , Nagpur Highway, Morwa , Chandrapur 2021-2022 SEMINAR ON “ A Review on Problems Associated with Skin "

2. CONTENTS Introduction Literature Review Problems Associated with Skin Argyria Psoriasis Atopic Dermatitis Sleroderma Vitiligo 3. References

3. 1. Introduction Skin is the outer covering of the body. In human, it is the largest organ of the integumentary system. The skin compose of three layers, Epidermis, Dermis, Hypodermis and Subcutis . Skin diseases are a major health problem affecting a high proportion of the population in India. Skin diseases are conditions that affect your skin. These diseases may cause rashes, inflammation, itchiness or other skin changes. Some skin conditions may be genetic, while lifestyle factors may cause others. Problems Associated with Skin Such as, Argyria : Skin may start to turn slate-gray, metallic, or blue-gray Psoriasis: Scaly skin that may swell or feel hot Atopic Dermstities (eczema): Dry, itchy skin that leads to swelling, cracking or scaliness . Sleroderma (systemic sclerosis): Tightening of the skin, joint pain, exaggerated response to cold and heartburn. Vitiligo : Patches of skin that lose pigment .

4. 2. LITERATURE REVIEW Raharja A, et al . (2021) In this review the treatment for psoriasis is given. The aim of this chapter is to provide an overview of basic and tailored topical moisturisers and discuss how and why they form the backbone for the management of psoriasis. Rendon A, (2019). In the present review the introduction and the two distinct localized phenotype have been described. This review discusses the mechanisms involved in the initiation and development of the disease, as well as the therapeutic options that have arisen from the dissection of the inflammatory psoriatic pathways. Kapur S , (2018). In this review the epidemiology of atopic dermatitis is described briefly, it is a common, chronic skin disorder that can significantly impact the quality of life of affected individuals as well as their families. Nuten S , (2015) It represents the natural history of atopic manifestation, characterized by a typical sequence of atopic disease in childhood preceding the development of other allergic disorders later in Life. Atopic dermatitis (AD) is a chronic inflammatory skin disease posing a significant burden on health-care resources and patients' quality of life. Joseph, N et al . (2014). In this review, we introduce the general introduction of skin diseases. Skin diseases are a common problem among young adults. There is paucity of data about it among medical students. This study aimed to find out the pattern of skin disorders and to describe their association with various socio-demographic factors among medical students.

5. Argyria Introduction Argyria is an acquired condition caused by the exposure to or ingestion of silver, and it presents with the insidious onset of gray or blue mucocutaneous discoloration.  Argyria is an extremely rare condition first detailed by Hill and Pillsbury in 1939, that is thought to have disappeared due to the suspension of the use of silver in drugs orally, However, silver is in local antiseptics such as nitrate and sulfadiazine, nasal drops, powders used in jewellery, acupuncture needles, and supplements, therefore, may also penetrate through the skin or respiratory tract. Colloidal silver dietary supplements – marketed widely as a treatment for arthritis, diabetes, cancer. Surgical and dental procedures – silver sutures used in abdominal surgery and silver dental fillings.

6. Subtypes Of Argyria Generalized argyria: This is due to systemic exposure to silver followed by its uptake by the dermis, leading to a gray/blue saltish or metallic diffuse hue to the skin. This color difference becomes evident predominantly in sun-exposed areas . 2.   Localized argyria: This is due to local silver deposition through skin incisions or percutaneous absorption via sweat gland pores. The resultant macular spots or clusters of spots tend to be darker, sometimes almost black. 3. Argyrosis:  This is due to the deposition of silver in the eye. The lesions have a predilection for the corneal Descemet membrane and appear small, darker lesions with greenish and brownish tones.

7. Symptoms Chronic or overexposure to products containing silver can cause an irreversible color change to the skin. The skin becomes a blue/ gray color , also affecting the lips, gums, nail beds, nasal passages, internal organs, and membranes of the eyes. Once the skin has changed color , it is permanent. There is no known way of removing the silver deposits from the affected tissues.

8. Treatment There is no cure for Argyria, but some treatment options are available for those with the disorder .   To help lessen the skin pigmentation, using a 5% hydroquinone treatment could help reduce the amount of silver in the skin, making it look less blue or gray . Laser therapy has also been explored as a viable option for the treatment of the disease . Diagnosis The doctor assesses the levels of silver present in the body by collecting samples of the patient’s urine, stool and blood. To accurately diagnose argyria, the doctor will usually take a biopsy (a small sample of tissue) of the skin that will be evaluated and analyzed under a microscope by a trained pathologist. A confirmation of the diagnosis of argyria usually requires the patient to take certain precautions at avoiding further exposure to the harmful metal.

9. Psoriasis Introduction Psoriasis is a common chronic inflammatory skin disease with a spectrum of clinical phenotypes and results from the interplay of genetic, environmental, and immunological factors. Psoriasis is a lifelong immune-mediated inflammatory skin disease, associated with morbidities such as psoriatic arthropathy , psychological, cardiovascular and hepatic diseases. In 2014, the World Health Organization recognised psoriasis as a serious non-communicable disease and highlighted the distress related to misdiagnosis, inadequate treatment and stigmatisation of this disease. The Global Burden of Disease Study estimated that psoriasis accounted for 5.6 million all-age disability-adjusted life-years (DALYs) in 2016; at least three-fold that of inflammatory bowel disease .

10. Clinical Classification of Psorisis 1.Plaque Psoriasis It characterized by dry scaly patches. About 90% of psoriasis cases correspond to chronic plaque-type psoriasis. Common locations include the trunk, the extensor surfaces of the limbs, and the scalp. 2.Pustular Psoriasis Pustular psoriasis contains pus like fluid mainly infiltrated with white blood cells is characterized by multiple, coalescing sterile pustules. It affect's the hands and feet. 3.Erythrodermic Psoriasis Characterized by exfoliation of fine scaly skin with pain and itching, is an acute condition in which over 90% of the total body surface is erythematous and inflamed. 4.Guttate psoriasis Characterized by drop like dots, is a variant with an acute onset of small erythematous plaques. 5. Psoriatic arthritis Characterized by enthesitis. 6. Psoriatic nail disease Fingernails are more commonly affected than toe nails. The commonest finding is small pits in the nail plate, resulting from defective nail formation in the proximal portion of the nail matrix.

11. Treatment of Psorisis Drugs Description Corticosteroids Topical It is the most commonly prescribed treatment available in ointment, cream, lotion and solution forms Topical steroids are classified as low-, medium-, high-and super-high potency agents. Apremilast Apremilast is a drug you take by mouth that's approved to treat psoriatic arthritis and plaque psoriasis in adults. It curbs phosphodiesterase-4 (PDE-4), an enzyme that controls inflammation. Side effects include diarrhea, nausea, and headache. Vitamin D3 Analogue Calcipotriol, calcitriol and tacalcitol are analogues of vitamin D3. inhibit cell proliferation and stimulate differentiation of keratinocytes. Cream formulation are available. Cyclosporine Cyclosporine is a T cell-inhibiting immunosuppressant from the group of the calcineurin inhibitors. The dosage is 2.5 to 5.0 mg/kg of body weight for up to 10 to 16 weeks. Methotrexate MTX is a folic acid analogue that inhibits DNA synthesis by blocking thymidine and purine biosynthesis. The initial recommended dose of 7.5-10 mg/weekly may be increased to a maximum of 25 mg/weekly Anti TNF-A Agents Etanercept (Enbrel®), Adalimumab (Humira®), Certolizumab Pegol (Cimzia®), Infliximab (Remicade®) 2.Ultraviolet B (UVB) Phototherapy It is also called broadband UVB, can be used to treatsingle patches, widespread psoriasis and psoriasis that resist topical treatments.

12. Atopic Dermatitis Introduction Atopic dermatitis (AD), also called atopic eczema. It is a common chronic or recurrent inflammatory skin disease and affects 15–20% of children and 1–3% of adults worldwide. It is characterized by acute flare-ups of eczematous pruritic lesions over dry skin. AD usually starts in early childhood and may represent the initial step of the so-called ‘atopic march’. Which represents the natural history of atopic manifestations, characterized by a typical sequence of atopic diseases in childhood preceding the development of other Allergic disorders later in life. Atopy is defined as an inherited tendency to produce immunoglobulin E (IgE) antibodies in response to minute amounts of common environmental proteins such as pollen,house dust mites and food allergens.

13. Fig 1: -Atopic dermatitis on flexual surface of the arm/Acute Atopic Dermatitis in its weeping, blistering form/ Subacute Atopic dermatitis in its dry, scaly, popular form.  

14. Clinical Manifestations Table: Clinical sign and symptoms of Atopic Dermatitis Clinical Signs Discription Pruritus The unpleasant sensation of the skin that provokes the urge to scratch; it is the primary hallmark of atopic dermatitis. Scratching the skin can aggravate existing dermatitis, causing excoriations that are either linear or punctate. Skin becomes leathered, rough, hard, and thickened upon scratching. 2. Xerosis Dry skin in areas without clinically apparent inflammation. More common during periods of low humidity (eg, winter) and primarily affects the legs. Dysfunctional epidermal barrier function leads to dehydration of the stratum corneum layer that should have a 10% moisture content. 3. Follicular prominence Follicles have a goose-bump appearance. Most commonly seen on the trunks of children and in darker-skinned individuals of any age.

15. 4. Ichthyosis vulgaris Fish like dry scales that can often look extremely thick and dry. Affected patients may alternately have excessively thin, whitish to brown scaling that classically affects the lower legs and shins while sparing the flexures. It is inherited in an autosomal semidominant manner. 5. Keratosis pilaris Patients will have thick scale and redness around the hair follicles that may be surrounded by a patchy erythema. This condition most frequently affects the lateral cheeks, extensor (outer) aspect of the upper arms, and anterior thighs. The onset is typically during childhood and can persist into adulthood. 6. Palmar and plantar hyperlinearity Patients more often have exaggerated palmar hand creases than plantar creases. 7. Periorbital darkening (“allergic shiners”) Refers to gray to violet-brown discoloration and swelling around the eyes because of intermittent edema and rubbing of the region.

16. Diagnosis In the differential diagnosis, combination forms with components of atopic, contact, and irritative eczema are important. Atopic eczema of the hands and the feet must be differentiated from Psoriasis, from keratodermas in the palms and soles and from tinea. The differential diagnosis of acute AD with intense erythema of the skin, together with exudation or blistering, for example, differs from differential diagnosis of the chronic lichenified form.

17. Treatment Emollients Topical Corticosteroids Topical Calcineurin Inhibitors Systematic Immunosuppressant Treatment Systemic antihistamines Antibiotics Other Therapies Phototherapy Cyclosporine A Mycophenolate mofetil (MPA) Azothioprine Methotrexate

18. Scleroderma Introduction Scleroderma originates from the Greek words skleros , meaning “hard,” and derma, meaning “skin.” Scleroderma is the initial manifestation of a disease process better described as progressive systemic sclerosis (PSS), which was named by Goetz in 1945. It is autoimmune disorder, Chronic hardening and tightening of the skin and connective tissues. Scleroderma is a group of rare diseases that more often affects women. It commonly occurs between the ages of 30 and 50.

19. Pathogenesis PSS is Systematic disease that affects many organs. The symptoms result from inflammation and progressive tissue fibrosis and occlusion of the microvasculature by excessive production and deposition of types and III collagens. On skin, Skin tightness and induration Skin pigmentary changes ( hyperpigmentation or hypopigmentation) Figure :swelling of the thumb and flexion contractures of fingers. Figure : Hypopigmantation of skin

20. Classification system for scleroderma Localized scleroderma: Often affects only the skin and not major organs. MORPHEAA rare skin condition that causes reddish or purplish patches on your skin. Tends to affect only the outermost layers of your skin-the dermis and the fatty tissue just beneath the dermis.
Location – Abdomen, chest and back Face, Arms and legs Systemic scleroderma: affects the skin and may affect the tissues under it, including blood vessels and major organs, such as the gastrointestinal tract, heart, lungs or kidneys.

21. Treatment Raynaud’s phenomenon and ischemia Avoid cold exposure (layers of warm, loose-fitting clothing)
Quit smoking
Vasodilator therapy- Calcium channel blocker ( nifedipine ), prazosin , ACE
Finger/toe necrosis- Intravenous prostaglandin (PGE, PGI) amputation A wide spectrum of clinical manifestations and severity – spontaneous improvement occurs frequently Disease modifying interventions - Penicillamine - Methotrexate
- Immunosuppressive agent: cyclosporin , IFN-Y - Recombinant human relaxin Symptomatic (organ-specific) treatment

22. Vitiligo Vitiligo, a depigmenting skin disorder, is characterized by the selective loss of melanocytes, which in turn leads to pigment dilution in the affected areas of the skin. The characteristic lesion is a totally amelanotic, nonscaly, chalky-white macule with distinct margins. Considerable recent progress has been made in our understanding of the pathogenesis of vitiligo, and it is now clearly classified as autoimmune disease, associated with genetic and environmental factors together with metabolic, oxidative stress and cell detachment abnormalities.

23. Diagnosis The diagnosis of vitiligo is generally straight forward, made clinically based upon the finding of acquired, amelanotic, nonscaly, chalky-white macules with distinct margins in a typical distribution: periorificial, lips and tips of distal extremities, penis, segmental and areas of friction. The diagnosis of vitiligo does not usually require confirmatory laboratory tests. The absence of melanocytes in a lesion can be assessed non invasively by in vivo confocal microscopy or by a skin biopsy. The diagnosis of vitiligo may be facilitated by the use of a Wood’s lamp, a hand-held ultraviolet (UV) irradiation device that emits UVA. It helps identify focal melanocyte loss and detect areas of depigmentation that may not be visible to the naked eye, particularly in pale skin. Under the Wood’s light, the vitiligo lesions emit a bright blue-white fluorescence and appear sharply demarcated .

24. Treatment These treatments include phototherapy, topical and systemic immunosuppressants , and surgical techniques, which together may help in halting the disease, stabilizing depigmented lesions and stimulating repigmentation . First-line treatments consist of topical treatments (corticosteroids and calcineurin inhibitors). Second-line treatments consist of phototherapy (NB-UVB and psoralen and UVA [PUVA]) and systemic steroid treatment. Third-line treatments consist of surgical grafting techniques and fourth-line of depigmenting treatments.

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