Ncm 104 Lecture Notes

NCM 104 dermatological DISORDERS I. REVIEW OF THE INTEGUMENTARY SYSTEM SKIN also known as the integument which means covering largest pipe organ system barrier between external and internal environment FUNCTIONS OF THE SKIN 1) Protection protects from accidental injury (Mechanical, Radiation, Thermal) change whittle on palms and soles provides additional covering against trauma r/t constant use inherent head start prime defense (prevents invasion of microorganisms) secretions(from sebaceous gland) are oily and s murderedly acidic (prevents/limits the mult. of mcgs) 2) concern of Homeostasis prevents excessive redness of water and electrolytes 3) Thermoregulation affected by production of perspiration (dehydration pyrexia) activity constriction (v extravagance of heat) and dilation of blood vessels external BT - consistencys core temperature 4) Reception of stimuli sports stadium in the brain somatosensory CORTEX abundance of dissolve nerve endings and rec eptors * NOCICEPTOR pain * END-ORGAN OF RUFFINI/PACINIAN CORPUSCLE pressure * MECHANORECEPTOR machanical * MEISSNERS CORPUCLES (MERKEL DISCS/CELLS) touch 5) implication of vitamin D helps the uptake of Ca2+ and PO4 in intra boothular level with the aid of sunlight activates Vitamin D to D3 (Cholecalciferol) 6) Immunity/ bring of antigenic substances immunologically mediated defenses against microorganisms Ex. Langerhans mobile phones Keratinocytes 7) Provide an outward come forthance or cosmetic adornment acceptance of the appearance of the throw together, hair, or nail is critical to psychosocial being 8) Excretion unclothe has a vital role in ejection of Na+ and H2O for homeostasis (maintaining balance in the internal environment) STRUCTURES OF THE SKIN LAYERS OF THE SKIN 1) EPIDERMIS avascular in nature Thickness 0. 04 mm (eyelids- hacknest) to 1. mm (palms and soles- thickest) 4 Cell types of the Epidermis a) Keratinocytes 95% engenders Keratin non-water-so luble protein helps create a waterproof barrier function in immunity guard water loss b) Melanocytes laid at the base of the epidermis Produces Melanin responsible for splutter color and absorption of UV light the darker you are, the more protection against cancer acts as an umbrella covering that shields DNA from UV c) Merkels cell It is located at the basal stratum of the epidermis but can usually be located just now with the use of an electron microscope one of the receptors scarcely located in the palms, soles, oral and genital epithelial tissue d) Langerhans cell play a role in cell-mediated immune responses in coordination with T cell originates in the bone marrow and migrates into the epidermis Layers of the Epidermis a) degree Germinativum/Basale innermost cells are columnar in shape where melanin is found in grea foot race amount lies close to the dermis stage cells at the basale layer receives nutrition from the dermis via diffusion and undergo mi tosis every 19 days and senileer cells are festeringhed upward undergoing changes in shape and chemical composition through a process known as keratinization ) Stratum Spinosum cells are maverickly-shaped known as prickle cells (have sharp cytoplasmic projection at the covering) c) Stratum Granulosum 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 * non responsible for water loss in the pores d) Stratum Lucidum thin transparent layer Skin moisture-can only be seen in thick jumble like the palms and soles immunity e) Stratum Corneum composed of dead keratinized cells (contain keratin -acidic in nature) serves as a durable overcoat of the body DESQUAMATION natural process of breaking apart of dead pare down cells for every 35-35 days, an individual will have a rude(a) epidermal skin Epidermal Appendages a) Eccrine glands stew-producing gla nd thermoregulation can be found throughout the skin but with some exemptions numerous on palms, soles, axilla and forehead not found in vermillion border(junction of the pink battlefield of lips surrounding skin) Lips, Ears, Nailbeds, Glans penis,Labia minora b) Apocrine glands function is not clearly known abundant in the axilla, breast, areola, anoogenital knowledge domain, ear canal, and eyelids c) Sebaceous glands release of sebum (has lubricating and bactericidal effect) can be found all throughout the skin overleap on the palms, soles, and axilla d) Hair a non-viable protein end-product found in all skin waxs except palms and soles e) Nails horny scales of the epidermis 2) DERMIS a dense-layer of tissue beneath the epidermis gives the skin most of its substances and structures 14 mm (thickest dermis is found in the back) has characteristics for -WOUND HEALING because it contains fibroblast, macrophages, mast cells, lymphocytes - MAINTENANCE OF EQUILIBRIUM be cause it contains lymphatic, vascular, and nerve write out 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 deepest skin layer contains BV, sweat glands, and deep pressure receptor (Pacinian corpuscles) abundant phagocytes are located as one ages, depleted collagen and malleable fibers -collagen for TOUGHNESS OF EPIDERMIS Elastic fiber for SKIN ELASTICITY 3) SUBCUTANEOUS FAT/ HYPODERMIS AKA adipose layer Functions * Source of energy * Hormone metabolism * Insulation from extreme hot and snappy 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 fetching assess for pre-existing factors 1) Chief complaint (if Derma conditions already exists) Assessment on itchiness, dryness, rashes, lesions, ecchymosis, lumps & mass Changes in skin, hair, and nails Onset of the condition opposite accompanying symptoms with known cause (pain, fever, swelling, redness) Alleviating factor such as frozen weather 2) Past Health write up Hx of previous derma disorder Previous trauma and symptoms interventions Other systemic illnesses relevant to the skin such as immunologic, endocrine, vascular, renal, or hepatic conditions Age of onset special season/month of the year manipulation done Immunization status Recent exposure to insects/ childhood diseases 3) Known exposure to communicable disease (school, neighbourhood) 4) Travel to foreign countries/places assertable environmental factors that the patient is open(a) to Ex. Poison ivy 5) Medications currently being taken/ has recently finished Photosensitivity drugs- causes sunburn-like rashes in areas of exposureEx. Phenothiazides Tetracyclines Diuretics Sulfonamides topical preparations containing derivatives of ingredients which are kno wn as sensitizing Ex. Neomycin Ethylaminobenzoate/ benzocaine Diphenhydramine HCl 6) Occupation and recreational activities exposure to irritants and chemicals either in the home or environment Ex. Prolonged exposure to the sun Unusual cold exposure 7) Allergies medications or foods assess if after ingestion, complains of itchiness, burning, or eruption of rashes substances that cause local, skin angers/lesions with direct clashing Ex. Textile, Metal (Ni), Wool Allergic reception could trigger skin discoloration & eruption of rashes, skin irritation *oral cortico steroids which may cause Acne breakouts, Thinning of the skin, Stretch marks, and Other systemic manifestations if this is used at last dose or routinely 8) Family health history Family lifestyle and living environment Genetically transmittable Derma conditions such as * Alopecia * Psoriasis * Atopic dermatitis Systemic diseases with derma manifestations such as * DM * LE * lineage dyscrasia 9) Habits (the pat ient as an individual) hygiene practices products/cosmetics use changes in clothing or bedding diet (sufficient using up of nutrients like H2O, vitamins and dietary fats) -Exercise -Sleep patterns which affect circulation, nourishment, and repair of the skin B) OBECTIVE DATA appraise the entire skin sur plaque on head-to-toe including oral mucosa appraise thoroughly use INSPECTION, PALPATION, OLFACTION PHYSICAL APPRAISAL 1) tint areas of irregular pigmentation (hypo/hyperpigmentation) Paleness/pallor Cyanosis Jaundice Assess sclera for a very dark person 2) Texture palpation (stroke the patient with the fingertips lightly to assess texture) popular Smooth, Soft, Resilient, No areas of lumps, No unusual hickening/ turn 3) Moisture hydration level of the skin for both wetness(Fluidity) and oiliness(Sebum) assess INTERTRIGINOUS AREAS (parts which have skin-to-skin contact like axilla & groin) NORMAL Well-hydrated but not excessively moist 4) Temperature use the dor sum of the hand compare hypothermia/hyperthermia with the area on the opposite side NORMAL uniformly warm 5) Turgor skins elasticity the prison term it takes for the skin and underlying tissue to return to its original contour after being pinched up (usually on the abdominal area) -older individuals v skin turgor NORMAL 3 sec ) Odor NORMAL free from pungent odors 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 LESIONS first lesions to appear on the skin and has a recognisable structure in response to some changes in the external and internal environment A. Erythema redness and dismission (skin/mucous membrane) result of dilation and congestion of superficial capillaries Ex. Nervous blush, Sunburn B. Macule unelevated change in color flat 1mm-1cm circumscribed Ex. Freckles, measles, petechiae, flat moles PATCHES larger than 1 cm and may have irregular shape Portwine birthmarks, Vitiligo (White Patches) C. Papule small, circumscribed, solid elevation, 1 mm-1cm Ex. Warts, Acne, Pimple, Elevated moles D. Vesicle circumscribed round or oval thin translucent mass change with serous fluid or blood 1mm-1cm Ex. Herpes simplex, Early fearful pox, Small burn blisters E. Bullae Large blisters (larger than vesicle) Ex. 2nd degree burn, Herpes simplex (Big) F. Pustule Vesicle or bullae filled with pus Ex. Acne vulgaris, Impetigo G. Nodule elevated solid hard mass that extends deeper into the dermis than a papule have a circumscribed border 2cm irregular border Ex. Malignant melanoma, Hemangioma I. Wheal reddened localize collection of edema fluid irregular in shape varies in size Ex. Hives, Mosquito bites J. Plaque raised lesion organise from merging of papules and nodules 1cm Ex. Psoriasis, Rubeolla K. Cyst elevated, encapsulated, fluid-filled mass arising from SC tissues 1cm or large r Ex. Sebaceous vesicle, Epidermoid cyst L. Comedo accumulation of sebum and keratin within a hair follicle occurs due to clogging 2 types Open comedo (black head) unkindly comedo (white head) M. Telangiectasia permanent dilation of capillaries in the skin SECONDARY LESIONS develop/occur if changes occur in the primary lesions relate to clients health status, environment, & status of the epidermal layer possible causes Scratching, Rubbing, Medications, infixed disease progression, Process of involution or Healing A. Crust (SCAB) a rough dry area formed by the coagulation of drying plasma or exudates could be a alter sebum, serum, blood, or pus on skin surface producing a temporary barrier to the environment Ex. Impetigo, Eczema, Healing of burns/LesionsB. Scales dried fragments of sloughed epidermal cells irregular in shape and size colors vary from White, Tan, Yellow, to Silver -Ex. Dandruff, change skin, Psoriasis C. ulcer depressed lesion in which entire epider mis and upper layer of dermis are lost could be due to trauma or tissue destruction irregular in shape and exudative Ex. Stasis ulcer D. gap deep linear split through epidermis into dermis Ex. Tinea pedis E. Scar Mark go forth on skin after healing F. Hyperkeratotic Plaque (Callus/ Kalyo) excessive thickness of the epidermal layer caused by chronic friction or pressure ) PRURITUS unpleasant skin sensation that provoke the desire to scratch Skin, Certain MM, Eyes, Perineum, Nostril, External ear canal r/t mechanical stimulation of chemical go-between r/t systemic disease Chicken pox, Severe liver disease, DM , Uremia 3) annoyance stimulation of Nociceptor 4) SWELLING due to release of chemical mediators 5) chromaticNESS due to hyperemia 6) SYSTEMIC ss fever (release of pseudothermoregulators), leucocytosis (WBC) DIAGNOSTIC TESTS 1) LAB TEST a. Tzanck smear Named after Arnault Tzanck Aka Chickenpox riddle/ Herpes skin test A microscopic assessment of fluid and cells from vesicles or bullae Top of vesicle is cut with the use of scalpel so a smear is taken from the base of vesicle using the scalpel Differentiates vesicular disorders may identify a virus (-) reaction vesicle from burns (+) H. unidirectional or Acantholytic cells varicella virus multinucleated giant cells b. KOH test done if the causative agent is suspected to be a fungus the specimen (smear) is treated with 10-20% of KOH before microscopic study Normal or (-) result shows no Fungi (No dermatophytes/yeast) c. Culture done to identify the item microorganisms to determine specific antibiotic treatment 2) SKIN BIOPSY ex. Dermal punch biopsy a sample of skin tissue is removed, processed, & examined under a microscope 4 types 1. Excision Biopsy entire skin area is cut 2. stop up Biopsy a small cylinder of skin is removed 3. Shave biopsy outermost part of a lesion is shave dour with a scalpel 4. Aspiration biopsy indicated for fluid-filled lesion 3) WOODS LIGHT EXAMINATION Skin is viewed under UV light through a special glass (Woods glass ) to identify superficial transmittances of the skin Place the patient in a dark room before examination 4) SKIN examination used to identify substances causing the allergy 3 ways 1. Scratch test aka Puncture/ start test Pricking the skin 2. Intradermal test Similar to Tuberculin test *DURATION OF TEST FOR some(prenominal) SCRATCH AND INTRADERMAL TEST IS 5-10 MINS OR 15 MINS 3. Patch Test the allergen is placed on a patch then placed on the skin Duration 48 hours (2 days) 4 TYPES OF HYPERSENSITIVITY REACTIONS TYPE I (ANAPHYLACTIC/IMMEDIATE HYPERSENSITIVITY) may involve the skin (disorders such as urticarial or eczema), eyes (conjunctivitis), nasopharynx (rhinorrhea/ rhinitis), bronchopulmonary tissues ( asthma attack), GIT (gastroenteritits) rxn may range from minor inconveniences to death (r/t bronchopulmonary constriction-vO2) takes 15 to 30 minutes from the time of exposure hold up onset of type I = 10 to 12 hours mediated by Ig E primary cell components Mast cell and Basophil TYPE II (CYTOTOXIC HYPERSENSITIVITY) may affect variety of organs and tissues reaction time minutes to hour after exposure mediated by Ig G and Ig M ex. Drug-induced haemolytic anemia Granulocytopenia Thrombocytopenia TYPE III (IMMUNE-COMPLEX HYPERSENSITIVITY) the type of reaction is considered as GENERAL ex. Serum sickness may involve individual organ such as the skin (SLE and Arthus reaction), kidneys, lungs, blood vessels and joints reaction time 3 to 10 hours mediated by soluble immune complexes curiously Ig G TYPE IV (CELL-MEDIATED/ DELAYED TYPE) ex. Mantoux test (PTB test), PPV test, tuberculin test 48 to 72 hours (2 to 3 days) II. SKIN DISORDERS A. DERMATITIS/ECZEMA irritation of the epidermal layer Rashes are characterized by itching and redness Types I. touching Dermatitis inflammatory reaction either caused by Allergens or Irritants utilize PATCH TEST to identify the cause 2 TYPES BASED ON ETIOLOGY Irritant Contact Dermatitis Most common There is no sensitised reaction but there is inflammation that occurs because of either a PHYSICAL or CHEMICAL IRRITANTS Manifestations Lesions appear sooner Appear on exposed areas Ex. Mechanical (glass fiber, wool) Chemical (cleaning compounds, perfume) Physical (clothing, stuff toy) * Allergic Contact Dermatitis A Delayed type (TYPE 4) of hypersensitivity rxn from contact with allergens Immune-mediated response by previously sensitized Lymphocytes to specific antigen (allergen) Ex. Drugs (Penicillin, Sulfonylamides) Metals (Nickel)Spandex rubber eraser Bra MANAGEMENT OF CONTACT DERMATITIS 1. Topical corticosteroids use BID for 2 weeks causes thinning of the skin 2. spoken Antibiotics if lesions develop into 2 lesion or if 2 infection sets in 3. Oral Antihistamines, Topical Antipruritic agents, Colloid oatmeal baths to control itching NURSING INTERVENTIONS 1. Avoiding irritants and sens itizing substances 2. Wear appropriate clothing 3. Wear gloves 4. Use mild welt products II. Atopic Dermatitis Genetically-based skin disorder that is both chronic and relapsing ( bec. it involves type 1 rxn) Strongly linked with asthma and hay fever Most common in children Immunologic irregularity (Cytokines and inflammatory mediators) v Vasoconstriction of careless vessel v vProtective barrier function of the skin FOCUS OF NURSING CARE in managing atopic dermatitis is pitch toward addressing the social and emotional disturbances and sleep pattern disturbance EXACERBATING FACTORS * Change in temperature COLD dry out skin HOT Vasodilation Inflammation Itching & Redness * Other irritants * Physiologic try direct stress to the area * Exercise loss of H2O Dryness MANAGEMENT OF ATOPIC DERMATITIS (SYMPTOMATIC ONLY NO CURE) 1. Hydrating the Skin Cornerstone of way Apply moisturizer 3-4x a day to reestablish hydration of the S. corneum 2. Corticosteroid a. Systemic b. Top ical * Educate on * Proper Application (Only apply to area being affected) * Duration of Use (BID X 2 weeks) * grimace effects Thinning of the skin Jeopardizing the immune system Application of WET WRAPPINGS To enhance absorption and Helps change magnitude pruritus 3. Protopic ointment (tacrolimus) pimecrolimus (Elidel) IMMUNOMODULATORS (block T cell activation) Indication Moderate to Severe atopic dermatitis Side effects Itching, Burning, Irritation for fewer days Avoid sunlight/ artificial sunlight for prolonged periods (photosensitivity rxn) 4. Antihistamines for itchiness 5. Antibiotic if petty(a) infection sets in III. Seborrheic Dermatitis Eczematous eruptions typically occur in hairy areas Sebaceous gland in which there is an enlarge amount and alteration in the quality of sebum/serum Usually occurs on Scalp, Eyebrow, Central chest, Face, Genital skin fold PREDISPOSING FACTORS 1. Family history of skin diseases 2. Winter months symptoms usually worsen (dryi ng effect) 3. Over growth of yeast organisms ( secondary to fungal infection) Inflammatory changes Around sebaceous glands and hair follicles) v Red, greasy scales (Characteristic symptom scale) MANAGEMENT 1. diffused Tar, Selenium, Zinc, or Ketoconazole shampoo preparations Have antibacterial effect on the normal flora found at the hair follicles 2. Chronic Topical corticosteroids To flatten thick, scaly plaques (SCALP) Low potency topical steroids/ topical antimycotic agent agents (FACIAL) IV. Stasis Dermatitis Eczematous eruption common in light extremities occurring in older persons 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 2 infection MANAGEMENT (prevention of predisposing factors) 1. Treatment of peripheral vascular conditions 2. Prevent constriction of 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 To address itching and scratches V. Lichen Simplex Chronicus Usually occurs in the Wrist, Ankles, and Back of the skull (Easily reached) A localised, well-circumscribed eczematous eruption caused by repeated rubbing and scratching Aka ITCH-SCRATCH rack PREDISPOSING FACTOR Stress where scratching becomes habitual and worse at NIGHT elephant skin B. ACNE An inflammatory disease of sebaceous follicle marked with comedone, macules, and papules TYPES I. Acne Vulgaris Occurs on the Face, Neck, Upper chest, & Buttocks Common among adolescents (80%) & may occur in adults PREDISPOSING FACTORS 1. Stress (activation of hormone production) 2.Heredity (familial tendency of androgen imbalance) 3. Endocrine (hormonal imbalances) 4. Diet (free fatty a cids) 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) MANAGEMENT 1. Topical Benzoyl Peroxide Retinoids Retinoid-like drugs such as Adapaline, Tretinoids, Azeleic acid Antibiotics such as Clindamycin, Erythromycin, & Sulfa-based agents *Dont self-medicate 2. Systemic Antibiotic indicated for inflammatory acne lesionsIsotretinoin (Accutane) vitamin A analog Side effx Dry lips & conjunctiva, and skin hairloss, muscle ache, photosensitivity, humor disturbance prevents pregnancy, Risk of birth defects 3. Intralesional therapy 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 Characterized as a RED facial rash which mostly affect 30-60 y/o It has both vascular and acne component Chronic, localized eruption with vascular and acne characteristic PREDISPOSITION . Affects women more than men ( S/S is more backbreaking in female) 2. Fair complexion individuals are more inclined 3. Familial predisposition CHARACTERISTICS 1. Red papules (sometimes pustules) usually located on nose, forehead, cheeks, chin, rarely involves trunk and upper limbs 2. Blushing or flushing (Red face) telangiectasia 3. Dry and flaky facial skin 4. Enlarged unshapely nose with sebaceous hyperplasia (the pores will become prominent) and hammer nose (fibrous thickening) 5. Eye symptoms eyelid inflammation/ conjunctivitis *Appearance of Lesion DOME-SHAPED (no black/white heads no deep cyst/lumps) MANAGEMENTS 1. Antibiotics (Tetracycline) including doxycycline and minocycline Duration 6-12 weeks to discredit inflammation (redness, papules, pustules and eye symptoms) 2. Topical metronidazole/ Azeleic acid jactitate or lotion applied 2x a day directly to the affected area 3. Nutraceuticals / clonidine ? -2 recepto agonists reduce vasodilation vflushing/redness in the area 4. Anti-inflammatory drugs (diclofenac) to reduce discomfort and redness on the affected skin 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 A genetically determined, chronic, epidermal, proliferative, not curable dse *control fast cellular proliferation aka PAPULO-SQUAMOUS LESION scaly in characteristic a chronic, recurrent, erythematous inflammatory disorder involving keratin synthesis History 1841 Viennese dermatologist known as Ferdinand von Hebra coined the term psoriasis from Greek word psora which means to itch relative incidenceMen and women are equally affected Occurs in all ages but is less common among children and time-worn Commence at early adulthood (18-24) Increased incidence among Whites Decreased among Japanese, American Indians, West African origin exacerbated by several factors manifestations usually appear between 15 and 35 years old CAUSE unknown But with high link to alteration in cyclic nucleotide and possible immunologic abnormality CONTRIBUTORY FACTORS 1. Immune-mediated condition The condition is believed to be caused by faulty signals in the bodys immune system the body tends to overreact and accelerate the growth of skin cells the T cells abnormally trigger inflammation 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 It has been appreciated by physicians t hat it occurs in families high rates among monozygotic twins known to be linked with inherited genes or other immune-mediated conditions when both parents have psoriasis, a child may have 40% probability of growing the disease