Ncm 104 Lecture Notes

NCM 104 DERMATOLOGIC DISORDERS I. REVIEW OF THE INTEGUMENTARY SYSTEM SKIN – also known as the integument which means covering – largest organ system – barrier between external and internal environment FUNCTIONS OF THE SKIN 1) Protection – protects from trauma (Mechanical, Radiation, Thermal) – thickened skin on palms and soles provides additional covering against trauma r/t constant use – Intact skin – primary defense (prevents invasion of microorganisms) – 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 – affected by: > production of perspiration (dehydration fever) > activity > constriction (v dissipation of heat) and dilation of blood vessels > external BT -body’s core temperature 4) Reception of stimuli – area in the brain – SOMATOSENSORY CORTEX â₠¬â€œ abundance of free nerve endings and receptors * NOCICEPTOR – pain * END-ORGAN OF RUFFINI/PACINIAN CORPUSCLE – pressure * MECHANORECEPTOR – machanical * MEISSNER’S CORPUCLES (MERKEL DISCS/CELLS) – touch 5) Synthesis of vitamin D – 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 – immunologically mediated defenses against microorganisms Ex. Langerhans cells Keratinocytes 7) Provide an outward appearance or cosmetic adornment – acceptance of the appearance of the skin, hair, or nail is critical to psychosocial being 8) Excretion – 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 – avascular in nature – Thickness: 0. 04 mm (eyelids- thinnest) to 1. mm (palms and soles- thickest) 4 Cell types of the Epidermis a) Keratinocytes – 95% – Produces Keratin – insoluble protein – helps create a waterproof barrier – function in immunity – control water loss b) Melanocytes – located at the base of the epidermis – Produces Melanin – responsible for skin 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) Merkel’s cell – It is located at the basal layer of the epidermis but can usually be located only with the use of an electron microscope – one of the receptors scarcely located in the palms, soles, oral and genital epithelium d) Langerhan’s 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) Stratum Germinativum/Basale â⠂¬â€œ innermost – cells are columnar in shape – where melanin is found in greatest amount – lies close to the dermis layer – 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 – cells are irregularly-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 *not responsible for water loss in the pores d) Stratum Lucidum – thin transparent layer Skin moisture-can only be seen in thick skin 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 skin cells; for every 35-35 days, an individual will have a new epidermal skin Epidermal Appendages a) Eccrine glands – sweat-producing gland – 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 area 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 area, ear canal, and eyelids c) Sebaceous glands release of sebum (has lubricating and bactericidal effect) – can be found all throughout the skin except on the palms, soles, and axilla d) Hair – a non-viable protein end-product – found in all skin surfaces 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 – 1—4 mm (thickest dermis is found in the back) – 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 – deepest skin layer – contains BV, sweat glands, and deep pressure receptor (Pacinian corpuscles) – abundant phagocytes are located – as one ages, depleted collagen and elastic fibers -collagen for TOUGHNESS OF EPIDERMIS – Elastic fiber for SKIN ELASTICITY 3) SUBCUTANEOUS FAT/ HYPODERMIS – AKA adipose layer – 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 – 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 – Other accompanying symptoms with known cause (pain, fever, swelling, redness) – Alleviating factor such as cold weather 2) Past Health History – Hx of previous derma disease Previous trauma and symptoms; interventions – Other systemic illnesses relevant to the skin such as immunologic, endocrine, vascular, renal, or hepatic conditions – Age of onset – Particular season/month of the year – Treatment done – Immuniza tion status – Recent exposure to insects/childhood diseases 3) Known exposure to communicable disease (school, neighbourhood) 4) Travel to foreign countries/places – possible environmental factors that the patient is exposed 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 known 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 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 – Family lifestyle and living environment – Genetically transmitted Derma conditions such as: * Alopecia * Psoriasis * Atopic dermatitis – Systemic diseases with derma manifestations such as: * DM * LE * Blood dyscrasia 9) Habits (the patient as an individual) – hygiene practices – products/cosmetics use – 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 – appraise the entire skin surface on head-to-toe including oral mucosa – appraise thoroughly †“ use INSPECTION, PALPATION, OLFACTION PHYSICAL APPRAISAL 1) Color – 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) – NORMAL: Smooth, Soft, Resilient, No areas of lumps, No unusual hickening/thinning 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 dorsum of the hand – compare hypothermia/hyperthermia with the area on the opposite side – NORMAL: uniformly warm 5) Turgor – skin’s elasticity – 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 – 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 recognizable structure in response to some changes in the external and internal environment A. Erythema – redness and inflammation (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 – filled with serous fluid or blood – 1mm-1cm – Ex. Herpes simplex, Early chicken 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 formed from merging of papules and nodules – >1cm – Ex. Psoriasis, Rubeolla K. Cyst – elevated, encapsulated, fluid-filled mass arising from SC tissues – 1cm or larger – Ex. Sebaceous cyst, Epidermoid cyst L. Comedo – accumulation of sebum and keratin within a hair follicle – occurs due to clogging 2 types: Open comedo (black head) Closed 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 client’s health status, environment, & status of the epidermal layer – possible causes: Scratching, Rubbing, Medications, Natural 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 dried 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 an d size – colors vary from White, Tan, Yellow, to Silver -Ex. Dandruff, Dry skin, Psoriasis C. Ulcer – depressed lesion in which entire epidermis and upper layer of dermis are lost – could be due to trauma or tissue destruction – irregular in shape and exudative – Ex. Stasis ulcer D. Fissure – deep linear split through epidermis into dermis – Ex. Tinea pedis E. Scar – Mark left on skin after healing F. Hyperkeratotic Plaque (Callus/ â€Å"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 mediator – r/t systemic disease – Chicken pox, Severe liver disease, DM , Uremia 3) PAIN – stimulation of Nociceptor 4) SWELLING – due to release of chemical mediato rs 5) REDNESS – 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 test/ Herpes skin test A microscopic assessment of fluid and cells from vesicles or bullae – Top of vesicle is cut with the use of scalpel then a smear is taken from the base of vesicle using the scalpel – Differentiates vesicular disorders – may identify a virus (-) reaction – vesicle from burns (+) H. Simplex 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 specific 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. Punch Biopsy – a small cylinder of skin is removed 3. Shave biopsy – outermost part of a lesion is shaved off with a scalpel 4. Aspiration biopsy – indicated for fluid-filled lesion 3) WOOD’S LIGHT EXAMINATION – Skin is viewed under UV light through a special glass (Wood’s glass ) to identify superficial infections of the skin – Place the patient in a dark room before examination 4) SKIN TESTING used to identify substances causing the allergy – 3 ways: 1. Scratch test – aka Puncture/Prick test – Pricking the skin 2. Intradermal test – Similar to Tuberculin test *DURATION OF TEST FOR BOTH 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 – D uration: 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), 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 – delayed 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 suc h as the skin (SLE and Arthus reaction), kidneys, lungs, blood vessels and joints – reaction time: 3 to 10 hours – mediated by soluble immune complexes particularly 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 – Inflammation of the epidermal layer – Rashes are characterized by itching and redness Types: I. Contact 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 allergic 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 Bra – MANAGEMENT OF CONTACT DERMATITIS: 1. Topical corticosteroids – use BID for 2 weeks – causes thinning of the skin 2. Oral 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 sensitizing substances 2. Wear appropriate clothing 3. Wear gloves 4. Use mild soap 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 Superficial vessel v vProtective barrier function of the skin – FOCUS OF NURSING CARE in managing atopic dermatitis is geared toward addressing the social and emotional disturbances and sleep pattern disturbance – EXACERBATING FACTORS: * Change in temperature COLD – Dry skin HOT – Vasodilation > Inflammation> Itching & Redness * Other irritants * Physiologic Stress – direct stress to the area * Exercise – loss of H2O > Dryness – MANAGEMENT OF ATOPIC DERMATITIS (SYMPTOMATIC ONLY; NO CURE): 1. Hydrating the Skin Cornerstone of management – Apply moisturizer 3-4x a day to reestablish hydration of the S. corneum 2. Corticosteroid a. Systemic b. Topical * – 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 – Application of WET WRAPPINGS – To enhance absorption and – Helps decrease pruritus 3. Protopic ointment (tacrolimus); pimecrolimus (Elidel) – IMMUNOMODULATORS (block T cell activation) – Indication: Moderate to Severe atopic dermatitis – Side effects: Itching, Burning, Irritation for few days Avoid sunlight/ artificial sunlight for prolonged periods (photosensitivity rxn) 4. Antihistamines – for itchiness 5. Antibiotic – if secondary infection sets in III. Seborrheic Dermatitis – Eczematous eruptions typically occur in hairy areas – Sebaceous gland in which there is an increase 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 (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) – MANAGEMENT: 1. Mild – 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 antifungal agents (FACIAL) IV. Stasis Dermatitis – Eczematous eruption common in lower 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 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 – To address itching and scratches V. Lichen Simplex Chronicus Usually occurs in the Wrist, Ankles, and Back of the skull (Easily reached) – A localized, well-circumscribed eczematous eruption caused by repeated rubbing and scratching – Aka ITCH-SCRATCH CYCLE – 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. 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) – MANAGEMENT: 1. Topical Benzoyl Peroxide Retinoids Retinoid-like drugs such as Adapaline, Tretinoids, Azeleic acid Antibiotics such as Clindamycin, Erythromycin, & Sulfa-based agents *Don’t 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, mood 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 severe 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 (â€Å"Red face†) – 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 – 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 reduce inflammation (redness, papules, pustules and eye symptoms) 2. Topical: metronidazole/ Azeleic acid cream 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, recurren t, erythematous inflammatory disorder involving keratin synthesis – History: 1841 – Viennese dermatologist known as Ferdinand von Hebra coined the term psoriasis from Greek word â€Å"psora† which means â€Å"to itch† – 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 – 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 body’s immune system – 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 – It has been appreciated by physicians that 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 developing the disease