Saturday, August 31, 2019
Ncm 104 Lecture Notes
NCM 104 DERMATOLOGIC DISORDERS I. REVIEW OF THE INTEGUMENTARY SYSTEM SKIN ââ¬â also known as the integument which means covering ââ¬â largest organ system ââ¬â barrier between external and internal environment FUNCTIONS OF THE SKIN 1) Protection ââ¬â protects from trauma (Mechanical, Radiation, Thermal) ââ¬â thickened skin on palms and soles provides additional covering against trauma r/t constant use ââ¬â Intact skin ââ¬â primary defense (prevents invasion of microorganisms) ââ¬â secretions(from sebaceous gland) are oily and slightly acidic (prevents/limits the mult. of mcgs) 2) Maintenance of Homeostasis prevents excessive loss of water and electrolytes 3) Thermoregulation ââ¬â affected by: > production of perspiration (dehydration fever) > activity > constriction (v dissipation of heat) and dilation of blood vessels > external BT -bodyââ¬â¢s core temperature 4) Reception of stimuli ââ¬â area in the brain ââ¬â SOMATOSENSORY CORTEX â⠬â abundance of free nerve endings and receptors * NOCICEPTOR ââ¬â pain * END-ORGAN OF RUFFINI/PACINIAN CORPUSCLE ââ¬â pressure * MECHANORECEPTOR ââ¬â machanical * MEISSNERââ¬â¢S CORPUCLES (MERKEL DISCS/CELLS) ââ¬â touch 5) Synthesis of vitamin D ââ¬â helps the uptake of Ca2+ and PO4 in intracellular level with the aid of sunlight activates Vitamin D to D3 (Cholecalciferol) 6) Immunity/processing of antigenic substances ââ¬â immunologically mediated defenses against microorganisms Ex. Langerhans cells Keratinocytes 7) Provide an outward appearance or cosmetic adornment ââ¬â acceptance of the appearance of the skin, hair, or nail is critical to psychosocial being 8) Excretion ââ¬â skin has a vital role in elimination of Na+ and H2O for homeostasis (maintaining balance in the internal environment) STRUCTURES OF THE SKIN LAYERS OF THE SKIN 1) EPIDERMIS ââ¬â avascular in nature ââ¬â Thickness: 0. 04 mm (eyelids- thinnest) to 1. mm (palms and soles- thickest) 4 Cell types of the Epidermis a) Keratinocytes ââ¬â 95% ââ¬â Produces Keratin ââ¬â insoluble protein ââ¬â helps create a waterproof barrier ââ¬â function in immunity ââ¬â control water loss b) Melanocytes ââ¬â located at the base of the epidermis ââ¬â Produces Melanin ââ¬â responsible for skin color and absorption of UV light ââ¬â the darker you are, the more protection against cancer ââ¬â acts as an umbrella covering that shields DNA from UV c) Merkelââ¬â¢s cell ââ¬â It is located at the basal layer of the epidermis but can usually be located only with the use of an electron microscope ââ¬â one of the receptors scarcely located in the palms, soles, oral and genital epithelium d) Langerhanââ¬â¢s cell ââ¬â play a role in cell-mediated immune responses in coordination with T cell ââ¬â originates in the bone marrow and migrates into the epidermis Layers of the Epidermis a) Stratum Germinativum/Basale â⠬â innermost ââ¬â cells are columnar in shape ââ¬â where melanin is found in greatest amount ââ¬â lies close to the dermis layer ââ¬â cells at the basale layer receives nutrition from the dermis via diffusion and undergo mitosis every 19 days and older cells are pushed upward undergoing changes in shape and chemical composition through a process known as keratinization ) Stratum Spinosum ââ¬â cells are irregularly-shaped known as prickle cells (have sharp cytoplasmic projection at the covering) c) Stratum Granulosum ââ¬â cells are nucleated granular cells which contain keratohyalin granules (contain lipids with desmosomal connections which helps to form waterproof barrier) water loss from the body *not responsible for water loss in the pores d) Stratum Lucidum ââ¬â thin transparent layer Skin moisture-can only be seen in thick skin like the palms and soles immunity e) Stratum Corneum ââ¬â composed of dead keratinized cells (contain keratin -acidic in nature) ââ¬â serves as a durable overcoat of the body DESQUAMATION ââ¬â natural process of breaking apart of dead skin cells; for every 35-35 days, an individual will have a new epidermal skin Epidermal Appendages a) Eccrine glands ââ¬â sweat-producing gland ââ¬â thermoregulation ââ¬â can be found throughout the skin but with some exemptions ââ¬â numerous on palms, soles, axilla and forehead ââ¬â not found in: Vermillion border(junction of the pink area of lips surrounding skin) Lips, Ears, Nailbeds, Glans penis,Labia minora b) Apocrine glands ââ¬â function is not clearly known ââ¬â abundant in the axilla, breast, areola, anoogenital area, ear canal, and eyelids c) Sebaceous glands release of sebum (has lubricating and bactericidal effect) ââ¬â can be found all throughout the skin except on the palms, soles, and axilla d) Hair ââ¬â a non-viable protein end-product ââ¬â found in all skin surfaces except palms and soles e) Nails â⬠â horny scales of the epidermis 2) DERMIS ââ¬â a dense-layer of tissue beneath the epidermis ââ¬â gives the skin most of its substances and structures ââ¬â 1ââ¬â4 mm (thickest dermis is found in the back) ââ¬â has characteristics for: ->WOUND HEALING: because it contains fibroblast, macrophages, mast cells, lymphocytes -> MAINTENANCE OF EQUILIBRIUM: because it contains lymphatic, vascular, and nerve supply Layers of the Dermis a) Papillary Layer -upper dermal region with finger-like projections -contains: >papillary loops (provide nutrients to the epidermis) >Pain receptors b) Reticular Layer ââ¬â deepest skin layer ââ¬â contains BV, sweat glands, and deep pressure receptor (Pacinian corpuscles) ââ¬â abundant phagocytes are located ââ¬â as one ages, depleted collagen and elastic fibers -collagen for TOUGHNESS OF EPIDERMIS ââ¬â Elastic fiber for SKIN ELASTICITY 3) SUBCUTANEOUS FAT/ HYPODERMIS ââ¬â AKA adipose layer ââ¬â Functions: * S ource of energy * Hormone metabolism * Insulation from extreme hot and cold Cushion to trauma -specialized layer of connective tissue -absent in the: eyelids, scrotum, areola, tibia ASSESSMENT OF CLIENTS WITH INTEGUMENTARY DISORDERS A) SUBECTIVE DATA HISTORY TAKING ââ¬â assess for pre-existing factors 1) Chief complaint (if Derma conditions already exists) ââ¬â Assessment on itchiness, dryness, rashes, lesions, ecchymosis, lumps & mass ââ¬â Changes in skin, hair, and nails ââ¬â Onset of the condition ââ¬â Other accompanying symptoms with known cause (pain, fever, swelling, redness) ââ¬â Alleviating factor such as cold weather 2) Past Health History ââ¬â Hx of previous derma disease Previous trauma and symptoms; interventions ââ¬â Other systemic illnesses relevant to the skin such as immunologic, endocrine, vascular, renal, or hepatic conditions ââ¬â Age of onset ââ¬â Particular season/month of the year ââ¬â Treatment done ââ¬â Immuniza tion status ââ¬â Recent exposure to insects/childhood diseases 3) Known exposure to communicable disease (school, neighbourhood) 4) Travel to foreign countries/places ââ¬â possible environmental factors that the patient is exposed to Ex. Poison ivy 5) Medications currently being taken/ has recently finished ââ¬â Photosensitivity drugs- causes sunburn-like rashes in areas of exposureEx. Phenothiazides Tetracyclines Diuretics Sulfonamides ââ¬â topical preparations containing derivatives of ingredients which are known as sensitizing Ex. Neomycin Ethylaminobenzoate/ benzocaine Diphenhydramine HCl 6) Occupation and recreational activities ââ¬â exposure to irritants and chemicals either in the home or environment Ex. Prolonged exposure to the sun Unusual cold exposure 7) Allergies ââ¬â medications or foods ââ¬â assess if after ingestion, complains of itchiness, burning, or eruption of rashes ââ¬â substances that cause local, skin irritations/lesions with di rect contact Ex. Textile, Metal (Ni), Wool Allergic reaction could trigger skin discoloration & eruption of rashes, skin irritation *oral corticosteroids which may cause Acne breakouts, Thinning of the skin, Stretch marks, and Other systemic manifestations if this is used at high dose or routinely 8) Family health history ââ¬â Family lifestyle and living environment ââ¬â Genetically transmitted Derma conditions such as: * Alopecia * Psoriasis * Atopic dermatitis ââ¬â Systemic diseases with derma manifestations such as: * DM * LE * Blood dyscrasia 9) Habits (the patient as an individual) ââ¬â hygiene practices ââ¬â products/cosmetics use ââ¬â changes in clothing or bedding diet (sufficient intake of nutrients like H2O, vitamins and dietary fats) -Exercise -Sleep patterns which affect circulation, nourishment, and repair of the skin B) OBECTIVE DATA ââ¬â appraise the entire skin surface on head-to-toe including oral mucosa ââ¬â appraise thoroughly â⬠â use INSPECTION, PALPATION, OLFACTION PHYSICAL APPRAISAL 1) Color ââ¬â areas of irregular pigmentation (hypo/hyperpigmentation) ââ¬â Paleness/pallor ââ¬â Cyanosis ââ¬â Jaundice ââ¬â Assess sclera for a very dark person 2) Texture ââ¬â palpation (stroke the patient with the fingertips lightly to assess texture) ââ¬â NORMAL: Smooth, Soft, Resilient, No areas of lumps, No unusual hickening/thinning 3) Moisture ââ¬â hydration level of the skin for both wetness(Fluidity) and oiliness(Sebum) ââ¬â assess INTERTRIGINOUS AREAS (parts which have skin-to-skin contact like axilla & groin) ââ¬â NORMAL: Well-hydrated but not excessively moist 4) Temperature ââ¬â use the dorsum of the hand ââ¬â compare hypothermia/hyperthermia with the area on the opposite side ââ¬â NORMAL: uniformly warm 5) Turgor ââ¬â skinââ¬â¢s elasticity ââ¬â the time it takes for the skin and underlying tissue to return to its original contour after being pinch ed up (usually on the abdominal area) -older individuals: v skin turgor ââ¬â NORMAL: 3 sec ) Odor ââ¬â NORMAL: free from pungent odors ââ¬â usually present in the axilla, skin folds, open wounds related to presence of bacteria in the skin 7) Presence and characteristics of Lesions MANIFESTATIONS OF SKIN DISORDERS 1) LESIONS PRIMARY LESIONSââ¬â first lesions to appear on the skin and has a recognizable structure in response to some changes in the external and internal environment A. Erythema ââ¬â redness and inflammation (skin/mucous membrane) ââ¬â result of dilation and congestion of superficial capillaries ââ¬â Ex. Nervous blush, Sunburn B. Macule ââ¬â unelevated change in color ââ¬â flat ââ¬â 1mm-1cm ââ¬â circumscribed Ex. Freckles, measles, petechiae, flat moles PATCHES ââ¬â larger than 1 cm and may have irregular shape ââ¬â Portwine birthmarks, Vitiligo (White Patches) C. Papule ââ¬â small, circumscribed, solid elevation, 1 mm-1cm ââ¬â Ex. Warts, Acne, Pimple, Elevated moles D. Vesicle ââ¬â circumscribed round or oval ââ¬â thin translucent mass ââ¬â filled with serous fluid or blood ââ¬â 1mm-1cm ââ¬â Ex. Herpes simplex, Early chicken pox, Small burn blisters E. Bullae ââ¬â Large blisters (larger than vesicle) ââ¬â Ex. 2nd degree burn, Herpes simplex (Big) F. Pustule ââ¬â Vesicle or bullae filled with pus ââ¬â Ex. Acne vulgaris, Impetigo G. Nodule elevated solid hard mass that extends deeper into the dermis than a papule ââ¬â have a circumscribed border ââ¬â 2cm ââ¬â irregular border ââ¬â Ex. Malignant melanoma, Hemangioma I. Wheal ââ¬â reddened localize collection of edema fluid ââ¬â irregular in shape ââ¬â varies in size ââ¬â Ex. Hives, Mosquito bites J. Plaque ââ¬â raised lesion formed from merging of papules and nodules ââ¬â >1cm ââ¬â Ex. Psoriasis, Rubeolla K. Cyst ââ¬â elevated, encapsulated, fluid-filled mass arising from SC tissues ââ¬â 1cm or larger ââ¬â Ex. Sebaceous cyst, Epidermoid cyst L. Comedo ââ¬â accumulation of sebum and keratin within a hair follicle ââ¬â occurs due to clogging 2 types: Open comedo (black head) Closed comedo (white head) M. Telangiectasia ââ¬â permanent dilation of capillaries in the skin SECONDARY LESIONS ââ¬â develop/occur if changes occur in the primary lesions ââ¬â relate to clientââ¬â¢s health status, environment, & status of the epidermal layer ââ¬â possible causes: Scratching, Rubbing, Medications, Natural disease progression, Process of involution or Healing A. Crust (SCAB) ââ¬â a rough dry area formed by the coagulation of drying plasma or exudates ââ¬â could be a dried sebum, serum, blood, or pus on skin surface producing a temporary barrier to the environment ââ¬â Ex. Impetigo, Eczema, Healing of burns/LesionsB. Scales ââ¬â dried fragments of sloughed epidermal cells ââ¬â irregular in shape an d size ââ¬â colors vary from White, Tan, Yellow, to Silver -Ex. Dandruff, Dry skin, Psoriasis C. Ulcer ââ¬â depressed lesion in which entire epidermis and upper layer of dermis are lost ââ¬â could be due to trauma or tissue destruction ââ¬â irregular in shape and exudative ââ¬â Ex. Stasis ulcer D. Fissure ââ¬â deep linear split through epidermis into dermis ââ¬â Ex. Tinea pedis E. Scar ââ¬â Mark left on skin after healing F. Hyperkeratotic Plaque (Callus/ ââ¬Å"Kalyoâ⬠) ââ¬â excessive thickness of the epidermal layer caused by chronic friction or pressure ) PRURITUS ââ¬â unpleasant skin sensation that provoke the desire to scratch ââ¬â Skin, Certain MM, Eyes, Perineum, Nostril, External ear canal ââ¬â r/t mechanical stimulation of chemical mediator ââ¬â r/t systemic disease ââ¬â Chicken pox, Severe liver disease, DM , Uremia 3) PAIN ââ¬â stimulation of Nociceptor 4) SWELLING ââ¬â due to release of chemical mediato rs 5) REDNESS ââ¬â due to hyperemia 6) SYSTEMIC ss ââ¬â fever (release of pseudothermoregulators), leucocytosis (^WBC) DIAGNOSTIC TESTS 1) LAB TEST a. Tzanck smear ââ¬â Named after Arnault Tzanck ââ¬â Aka Chickenpox test/ Herpes skin test A microscopic assessment of fluid and cells from vesicles or bullae ââ¬â Top of vesicle is cut with the use of scalpel then a smear is taken from the base of vesicle using the scalpel ââ¬â Differentiates vesicular disorders ââ¬â may identify a virus (-) reaction ââ¬â vesicle from burns (+) H. Simplex or Acantholytic cells; varicella virus; multinucleated giant cells b. KOH test ââ¬â done if the causative agent is suspected to be a fungus ââ¬â the specimen (smear) is treated with 10-20% of KOH before microscopic study Normal or (-) result shows no Fungi (No dermatophytes/yeast) c. Culture ââ¬â done to identify the specific microorganisms to determine specific antibiotic treatment 2) SKIN BIOPSY ââ¬â ex . Dermal punch biopsy ââ¬â a sample of skin tissue is removed, processed, & examined under a microscope ââ¬â 4 types: 1. Excision Biopsy ââ¬â entire skin area is cut 2. Punch Biopsy ââ¬â a small cylinder of skin is removed 3. Shave biopsy ââ¬â outermost part of a lesion is shaved off with a scalpel 4. Aspiration biopsy ââ¬â indicated for fluid-filled lesion 3) WOODââ¬â¢S LIGHT EXAMINATION ââ¬â Skin is viewed under UV light through a special glass (Woodââ¬â¢s glass ) to identify superficial infections of the skin ââ¬â Place the patient in a dark room before examination 4) SKIN TESTING used to identify substances causing the allergy ââ¬â 3 ways: 1. Scratch test ââ¬â aka Puncture/Prick test ââ¬â Pricking the skin 2. Intradermal test ââ¬â Similar to Tuberculin test *DURATION OF TEST FOR BOTH SCRATCH AND INTRADERMAL TEST IS 5-10 MINS OR 15 MINS 3. Patch Test ââ¬â the allergen is placed on a patch then placed on the skin ââ¬â D uration: 48 hours (2 days) 4 TYPES OF HYPERSENSITIVITY REACTIONS TYPE I (ANAPHYLACTIC/IMMEDIATE HYPERSENSITIVITY) ââ¬â may involve the skin (disorders such as urticarial or eczema), eyes (conjunctivitis), nasopharynx (rhinorrhea/ rhinitis), bronchopulmonary tissues (asthma), GIT (gastroenteritits) rxn may range from minor inconveniences to death (r/t bronchopulmonary constriction-vO2) ââ¬â takes 15 to 30 minutes from the time of exposure ââ¬â delayed onset of type I = 10 to 12 hours ââ¬â mediated by Ig E ââ¬â primary cell components : Mast cell and Basophil TYPE II (CYTOTOXIC HYPERSENSITIVITY) ââ¬â may affect variety of organs and tissues ââ¬â reaction time: minutes to hour after exposure ââ¬â mediated by Ig G and Ig M ââ¬â ex. Drug-induced haemolytic anemia Granulocytopenia Thrombocytopenia TYPE III (IMMUNE-COMPLEX HYPERSENSITIVITY) ââ¬â the type of reaction is considered as GENERAL ââ¬â ex. Serum sickness may involve individual organ suc h as the skin (SLE and Arthus reaction), kidneys, lungs, blood vessels and joints ââ¬â reaction time: 3 to 10 hours ââ¬â mediated by soluble immune complexes particularly Ig G TYPE IV (CELL-MEDIATED/ DELAYED TYPE) ââ¬â ex. Mantoux test (PTB test), PPV test, tuberculin test ââ¬â 48 to 72 hours (2 to 3 days) II. SKIN DISORDERS A. DERMATITIS/ECZEMA ââ¬â Inflammation of the epidermal layer ââ¬â Rashes are characterized by itching and redness Types: I. Contact Dermatitis ââ¬â Inflammatory reaction either caused by Allergens or Irritants ââ¬â utilize PATCH TEST to identify the cause ââ¬â 2 TYPES BASED ON ETIOLOGY: Irritant Contact Dermatitis ââ¬â Most common ââ¬â There is no allergic reaction but there is inflammation that occurs because of either a PHYSICAL or CHEMICAL IRRITANTS ââ¬â Manifestations: > Lesions appear sooner > Appear on exposed areas ââ¬â Ex. Mechanical (glass fiber, wool) Chemical (cleaning compounds, perfume) Physical ( clothing, stuff toy) * Allergic Contact Dermatitis ââ¬â A Delayed type (TYPE 4) of hypersensitivity rxn from contact with allergens ââ¬â Immune-mediated response by previously sensitized Lymphocytes to specific antigen (allergen) ââ¬â Ex. Drugs (Penicillin, Sulfonylamides) Metals (Nickel)Spandex Rubber Bra ââ¬â MANAGEMENT OF CONTACT DERMATITIS: 1. Topical corticosteroids ââ¬â use BID for 2 weeks ââ¬â causes thinning of the skin 2. Oral Antibiotics ââ¬â if lesions develop into 2ââ¬â¢ lesion or if 2ââ¬â¢ infection sets in 3. Oral Antihistamines, Topical Antipruritic agents, Colloid oatmeal baths ââ¬â to control itching ââ¬â NURSING INTERVENTIONS 1. Avoiding irritants and sensitizing substances 2. Wear appropriate clothing 3. Wear gloves 4. Use mild soap products II. Atopic Dermatitis ââ¬â Genetically-based skin disorder that is both chronic and relapsing ( bec. it involves type 1 rxn) ââ¬â Strongly linked with asthma and hay fever Most common in children Immunologic irregularity (Cytokines and inflammatory mediators) v Vasoconstriction of Superficial vessel v vProtective barrier function of the skin ââ¬â FOCUS OF NURSING CARE in managing atopic dermatitis is geared toward addressing the social and emotional disturbances and sleep pattern disturbance ââ¬â EXACERBATING FACTORS: * Change in temperature COLD ââ¬â Dry skin HOT ââ¬â Vasodilation > Inflammation> Itching & Redness * Other irritants * Physiologic Stress ââ¬â direct stress to the area * Exercise ââ¬â loss of H2O > Dryness ââ¬â MANAGEMENT OF ATOPIC DERMATITIS (SYMPTOMATIC ONLY; NO CURE): 1. Hydrating the Skin Cornerstone of management ââ¬â Apply moisturizer 3-4x a day to reestablish hydration of the S. corneum 2. Corticosteroid a. Systemic b. Topical * ââ¬â Educate on: * Proper Application (Only apply to area being affected) * Duration of Use (BID X 2 weeks) * Side effects: Thinning of the skin Jeopardizing the immune sys tem ââ¬â Application of WET WRAPPINGS ââ¬â To enhance absorption and ââ¬â Helps decrease pruritus 3. Protopic ointment (tacrolimus); pimecrolimus (Elidel) ââ¬â IMMUNOMODULATORS (block T cell activation) ââ¬â Indication: Moderate to Severe atopic dermatitis ââ¬â Side effects: Itching, Burning, Irritation for few days Avoid sunlight/ artificial sunlight for prolonged periods (photosensitivity rxn) 4. Antihistamines ââ¬â for itchiness 5. Antibiotic ââ¬â if secondary infection sets in III. Seborrheic Dermatitis ââ¬â Eczematous eruptions typically occur in hairy areas ââ¬â Sebaceous gland in which there is an increase amount and alteration in the quality of sebum/serum ââ¬â Usually occurs on Scalp, Eyebrow, Central chest, Face, Genital skin fold ââ¬â PREDISPOSING FACTORS: 1. Family history of skin diseases 2. Winter months ââ¬â symptoms usually worsen (drying effect) 3. Over growth of yeast organisms ( secondary to fungal infection) Inf lammatory changes Around sebaceous glands and hair follicles) v Red, greasy scales (Characteristic symptom > scale) ââ¬â MANAGEMENT: 1. Mild ââ¬â Tar, Selenium, Zinc, or Ketoconazole shampoo preparations > Have antibacterial effect on the normal flora found at the hair follicles 2. Chronic ââ¬â Topical corticosteroids > To flatten thick, scaly plaques (SCALP) ââ¬â Low potency topical steroids/ topical antifungal agents (FACIAL) IV. Stasis Dermatitis ââ¬â Eczematous eruption common in lower extremities occurring in older persons ââ¬â PREDISPOSING FACTORS: 1. Varicosities (venous insufficiency) 2. Poor circulation vVenous return (From legs) Substances remain in the tissues v Irritation, brawny colored skin associated with edema v Itching (May or May not occur) v Scratches v Break in the epidermis (Stasis ulcer) v 2ââ¬â¢ infection ââ¬â MANAGEMENT (prevention of predisposing factors): 1. Treatment of peripheral vascular conditions 2. Prevent constriction o f the circulation 3. Treat lower extremity edema * Elevate lower extremity (CI: Cardio/Pulmonary problems) * Compression stockings * Unna boots (bandage application on the lower extremities) 4. Topical corticosteroids ââ¬â To address itching and scratches V. Lichen Simplex Chronicus Usually occurs in the Wrist, Ankles, and Back of the skull (Easily reached) ââ¬â A localized, well-circumscribed eczematous eruption caused by repeated rubbing and scratching ââ¬â Aka ITCH-SCRATCH CYCLE ââ¬â PREDISPOSING FACTOR: Stress where scratching becomes habitual and worse at NIGHT ââ¬â elephant skin B. ACNE ââ¬â An inflammatory disease of sebaceous follicle marked with comedone, macules, and papules TYPES: I. Acne Vulgaris ââ¬â Occurs on the Face, Neck, Upper chest, & Buttocks ââ¬â Common among adolescents (80%) & may occur in adults ââ¬â PREDISPOSING FACTORS: 1. Stress (activation of hormone production) 2.Heredity (familial tendency of androgen imbalance) 3. En docrine (hormonal imbalances) 4. Diet (free fatty acids) Puberty [^Androgen] (Sebaceous glands undergo enlargement) v Produce sebum v Binds with debris (Keratin, Bacteria, Cell fragments) v Plug hair follicle v Comedo (open/close) v Inflammation (Papules, Pustules, Nodules, Cyst) ââ¬â MANAGEMENT: 1. Topical Benzoyl Peroxide Retinoids Retinoid-like drugs such as Adapaline, Tretinoids, Azeleic acid Antibiotics such as Clindamycin, Erythromycin, & Sulfa-based agents *Donââ¬â¢t self-medicate 2. Systemic Antibiotic ââ¬â indicated for inflammatory acne lesionsIsotretinoin (Accutane) ââ¬â vitamin A analog ââ¬â Side effx: Dry lips & conjunctiva, and skin hairloss, muscle ache, photosensitivity, mood disturbance ââ¬â prevents pregnancy, ^Risk of birth defects 3. Intralesional therapy ââ¬â NURSING CARE: 1. Keep hands and hair away from face 2. Avoid exposure to oil and greases a. Eat well-balanced diet b. Wash face 2 or 3X a day with mild cleanser c. Use only water- based cosmetics II. Acne Rosacea ââ¬â Characterized as a RED facial rash which mostly affect 30-60 y/o ââ¬â It has both vascular and acne component ââ¬â Chronic, localized eruption with vascular and acne characteristic ââ¬â PREDISPOSITION: . Affects women more than men ( S/S is more severe in female) 2. Fair complexion individuals are more inclined 3. Familial predisposition ââ¬â CHARACTERISTICS: 1. Red papules (sometimes pustules) ââ¬â usually located on nose, forehead, cheeks, chin, rarely involves trunk and upper limbs 2. Blushing or flushing (ââ¬Å"Red faceâ⬠) ââ¬â telangiectasia 3. Dry and flaky facial skin 4. Enlarged unshapely nose with sebaceous hyperplasia (the pores will become prominent) and rhinophyma (fibrous thickening) 5. Eye symptoms ââ¬â eyelid inflammation/ conjunctivitis *Appearance of Lesion: DOME-SHAPED (no black/white heads; no deep cyst/lumps) MANAGEMENTS: 1. Antibiotics (Tetracycline) including doxycycline and minocycline ââ¬â Duration : 6-12 weeks ââ¬â to reduce inflammation (redness, papules, pustules and eye symptoms) 2. Topical: metronidazole/ Azeleic acid cream or lotion ââ¬â applied 2x a day directly to the affected area 3. Nutraceuticals / clonidine ââ¬â ? -2 recepto agonists > reduce vasodilation > vflushing/redness in the area 4. Anti-inflammatory drugs (diclofenac) ââ¬â to reduce discomfort and redness on the affected skin ââ¬â NURSING INTERVENTIONS: 1. Avoid oil-based facial creams 2. Use water-based make-up 3. Never apply a topical steroid (to the rosacea) . Protect yourself from the sun. (Use light oil-free facial sunscreens) 5. Keep your face cool: minimize your exposure to hot or spicy foods, alcohol, hot showers and baths and warm rooms. C. PSORIASIS ââ¬â A genetically determined, chronic, epidermal, proliferative, not curable dse *control fast cellular proliferation ââ¬â aka PAPULO-SQUAMOUS LESION > scaly in characteristic ââ¬â a chronic, recurren t, erythematous inflammatory disorder involving keratin synthesis ââ¬â History: 1841 ââ¬â Viennese dermatologist known as Ferdinand von Hebra coined the term psoriasis from Greek word ââ¬Å"psoraâ⬠which means ââ¬Å"to itchâ⬠ââ¬â INCIDENCE:Men and women are equally affected Occurs in all ages but is less common among children and elderly Commence at early adulthood (18-24) Increased incidence among Whites Decreased among Japanese, American Indians, West African origin ââ¬â exacerbated by several factors ââ¬â manifestations usually appear between 15 and 35 years old ââ¬â CAUSE: unknown But with high link to alteration in cyclic nucleotide and possible immunologic abnormality ââ¬â CONTRIBUTORY FACTORS: 1. Immune-mediated condition ââ¬â The condition is believed to be caused by faulty signals in the bodyââ¬â¢s immune system ââ¬â the body tends to overreact and accelerate the growth of skin cells the T cells abnormally trigger inflamma tion in the skin (accelerates skin cells to grow faster and to pile up on the outer surface of the skin> the skin does not desquamate but piles up) *Normally, skin cells mature and sheds off every 28-30 days Cytokines (Lymphokines) v ^Platelet, Neutrophils, Basophils v Release of Histamine v Inflammation 2. Genetic ââ¬â It has been appreciated by physicians that it occurs in families ââ¬â high rates among monozygotic twins ââ¬â known to be linked with inherited genes or other immune-mediated conditions ââ¬â when both parents have psoriasis, a child may have 40% probability of developing the disease
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