WELCOME

1. WELCOME Disorders of skin eye,ear Presented by Mrs.Benazeera, AsstProfessor Department of Child Health Nursing

2. Disorders of skin

3. SCABIES It is an endemic infestation caused by the scabies mite (sarcoptesscabie)

4. Clinical manifestations • Inflammatory response and intense itching occurs within 48 hours after exposure • Pruritis • Eczematous eruption Treatment Application of scabicide • 5% permethrin cream • 1% lindane cream

5. Dermatitis • Is a clinical and histological pattern of inflammation of the skin seen in a variety of dermatoses with widely diverse aetiologies • ‘Dermatitis’ and ‘Eczema’ are generally regarded as synonymous, although some authors still use the term ‘dermatitis

6. Atopic Dermatitis Is an itchy, chronic or chronically relapsing inflammatory skin disease that occurs most commonly during early infancy & childhood which frequently associated with: • Abnormalities in Skin Barrier Function & • Allergen sensitization

7. ETIOPATHOGENESIS - MULTI FACTORIAL SKIN BARRIER DEFECT ENVIRONMENTAL FACTORS GENETIC FACTORS IMMUNOLOGIC RESPONSE

8. CLINICAL FINDINGS • Intense Pruritus and Cutaneous Reactivity are cardinal features of AD. • Pruritus may be intermittent throughout the day but is usually worse in the early evening and night. • Its consequences are Scratching, Papules, and eczematous skin lesions FIGURE 14-1 papules in a patient with Atopic Dermatitis. FIGURE 14-2 Eczematous lesions

9. STAGES OF ATOPIC DERMATITIS

11. INFANTILE PHASE(2 months_2 years) • DISTRIBUTION • Cheeks, Face and Scalp, Extensor Surfaces of Extremities & Trunk (due to friction from crawling) • Anywhere on the skin surface • Often, Napkin area is spared

12. AD IN INFANT

13. AD IN INFANTS

14. Involvement of the hands, often with exudativelesions, and sometimes with nail changes, is common CHILD HOOD sometimes nail change.

15. TREATMENT Supportive Care • A reduction of trigger factors, including harsh chemicals, alkaline soaps and dust mites, as well as the avoidance (if possible) of occupational triggers (e.g. chemicals used in hair dressing or frequent handwashing)

16. The frequent use of emollients represents a mainstay of AD treatment.

17. Topical Pharmacologic Agents • Topical corticosteroids are frequently the first line of pharmacologic therapy for AD • Topical calcineurin inhibitors (TCls)

18. AcneVulgaris

19. Introduction Acne vulgaris is a common follicular disorder affecting susceptible hair follicles, most commonly found on the face, neck, andupper trunk.

20. Incidence • Acne is the most commonly encountered skin condition in adolescents and young adultsbetween ages 12 and35. • Both genders are affected equally, although onsetis slightly earlier forgirls. • Acne becomes more marked at puberty and during adolescence because the endocrine glands that influence the secretions of the sebaceous glandsare functioning at peakactivity

21. Etiology • Genetic • Hormonal • Bacterialfactors • Family history ofacne

22. Pathophysiology • During puberty, androgens stimulate the sebaceous glands, causing them to enlarge and secrete a natural oil, sebum, which rises to the top of the hair follicle and flows outinto the skinsurface. • In adolescents who develop acne, androgenic stimulation produces a heightened response in the sebaceous glandsso that acne occurs when accumulated sebum plugs the pilosebaceousducts. • This accumulated material formscomedones.

23. PilosebaceousUnit

24. c/m Manifestations: • Polymorphic eruptions • Initially found as white or black heads • Greasy scalp, dandruff, seborrhea, increased production of sebum due to hormonal response

25. WhiteHeads

26. BlackHeads

27. Diagnosticstudies • HistoryCollection • PhysicalExamination • Biopsy OfLesions

28. MedicalManagement • The goals of managementare: • To reduce bacterialcolonies • To Decrease sebaceous glandactivity • To Prevent the follicles from becomingplugged • To Reduceinflammation • To Combat secondaryinfection • To Minimizescarring • To Eliminate factors that predispose the person toacne

29. There is no predictable cure for thedisease, but combinations of therapies are available that can effectively control itsactivity. • Topical treatment may be all that is neededto treat mild to moderate lesions and superficial inflammatorylesions • Systemic treatment may be necessaryfor severe and extensiveacne

30. NUTRITION AND HYGIENETHERAPY • Diet is not believed to play a major rolein therapy. • Avoid chocolate, cola, fried foods, or milk products which are considered to increasethe acnedevelopment. • Maintain good nutrition to equip the immune system for effective action against bacteria and infection.

31. NUTRITION AND HYGIENETHERAPY • For mild cases of acne, wash the face twicewith a cleansing soap. These soaps can remove the excessive skin oil and the comedo in mostcases. • Acne medications contain salicylic acid and benzoylperoxide, which are effective at removing the sebaceous follicularplugs.

32. NUTRITION AND HYGIENETHERAPY • The patient should be instructed to discontinue their use if severe irritationoccurs. • Oil-free cosmetics and creams should bechosen.

33. TOPICAL PHARMACOLOGICTHERAPY • Benzoyl Peroxide. Benzoyl peroxide preparations are widely used because they produce a rapid and sustained reduction of inflammatorylesions. • They depress sebum production and promote breakdown of comedoplugs. • They also produce an antibacterial effectby suppressing P.acnes.

34. Benzoyl peroxide, benzoyl erythromycin, and benzoyl sulfur combinations are availableover the counter and byprescription. • Vitamin A acid (Tretinoin) applied topically is used to clear the keratin plugs from the pilosebaceous ducts. • Vitamin A acid speeds the cellular turnover, forces out the comedones, and preventsnew comedones.

35. TopicalAntibiotics: • Topical antibiotic treatment for acne iscommon. • Topical antibiotics suppress the growth of • P. acnes; reduce superficial free fatty acid levels; decrease comedones, papules, and pustules. • Common topical preparations include tetracycline, clindamycin, anderythromycin.

36. SYSTEMIC PHARMACOLOGICTHERAPY • Antibiotics • Oral antibiotics, such as tetracycline, doxycycline, and minocycline, administered in small doses over a long period are veryeffective in treating moderate and severe acne,especially when the acne is inflammatory and results in pustules, abscesses, andscarring.

37. OralRetinoids: • Synthetic vitamin A compounds (ie, Retinoids) are used in patients who are unresponsive to conventionaltherapy. • Isotretinoinis used for active inflammatorypapular pustular acne that has a tendency toscar. • Isotretinoin reduces sebaceous gland size andinhibits sebumproduction. • It also causes the epidermis to shed, thereby unseatingand expelling existingcomedones.

38. HormoneTherapy • Estrogen therapy (includingprogesterone– estrogen preparations) suppresses sebum production and reduces skinoiliness. • Estrogen in the form of estrogen-dominantoral contraceptive compounds may be administered on a prescribed cyclicregimen. • Estrogen is not administered to male patients because of undesirable sideeffects.

39. SURGICALMANAGEMENT • Extraction Of ComedoContents • Drainage Of Pustules AndCysts • Excision Of Sinus Tracts AndCysts • Intralesional Corticosteroids For Antiinflammatory Action • Cryotherapy • Dermabrasion ForScars • Laser Resurfacing OfScars

40. NursingManagement • Major nursing activities include patient education, particularly in proper skin care techniques, and managing potentialproblems related to the skin disorder ortherapy.

41. PREVENTINGSCARRING • Patients should be warned that discontinuing these medications can exacerbate acne, leadto more flare-ups(sudden out burst), and increase the chance of deepscarring. • Manipulation of the comedones, papules,and pustules increases the potential forscarring

42. PREVENTINGINFECTION • Female patients receiving long-termantibiotic therapy with tetracycline should be advisedto watch for and report signs and symptoms of oral or vaginal candidiasis, a yeastlike fungal infection

43. Teaching PatientsSelf-Care. • Taking prescribed medications, patients are instructed to wash the face and other affected areas with mild soap and water twice each day to remove surface oils and prevent obstruction of the oilglands. • Cautionthepatient to avoid scrubbing theface. • Patients are instructed to avoid manipulationof pimples orblackheads.

44. IMPETIGO

45. DEINITION: • Impetigo is a superficial skin infection that is seen most commonly in children and is transmittedeasily from person toperson. • Based on clinicalpresentations: • BULLOUS • TYPES NON- BULLOUS

46. BULLOUS IMPETIGO(BLISTERS) • This form is caused by staph bacteria that produce a toxin that causes a break between the top layer (epidermis) and the lower levels of skin forming a blister.

47. NON -BULLOUSIMPETIGO This is the common form, caused by both staphand strep bacteria. It appears as small blisters or scabs, which then form yellow or honey-coloredcrusts.

50. There are two ways an initial infection canoccur: • primary impetigo - is when the bacteria invadesthe skin through a cut , insect bite, or other injury,and • secondary impetigo - is where the bacteria invades the skin because the skin barrier has been disrupted by another skin infection, such as scabies oreczema.