Integumentary System Study Guide PDF

lOMoARcPSD|25656094 Integumentary System Study Guid Pathophysiology 2 (Massachusetts College of Pharmacy and Health Sciences) Scan to open on Studocu Studocu is not sponsored or endorsed by any college or university...

lOMoARcPSD|25656094 Integumentary System Study Guid Pathophysiology 2 (Massachusetts College of Pharmacy and Health Sciences) Scan to open on Studocu Studocu is not sponsored or endorsed by any college or university Downloaded by Daisy Escobar ([email protected])  lOMoARcPSD|25656094 Integumentary System Skin: First line of defense - Largest organ in the body - Surface area of 1.2-2.2m2 & weighs 9-11 lbs. (~7% total body weight) - Varies in thickness from 1.5-4mm o Thickness helps withstand the excess pressure Three major regions: Epidermis, Dermis, Hypodermis Epidermis - outmost layer, made mostly of epithelial cells - Cells of the epidermis and their function: protective shield - Keratinocytes: proteins that exerts water protective effect o Produce keratin, the protein that helps give the skin its protective property § Made by stratum basale § Pushed upward as more cells are made beneath them § The outer most layer is scale like and dead cells § Shed at a rate of millions/day § Melanocytes: produce melanosomes (vesicles containing the pigment) and melanin, that protects cells from UV radiation o Melanin is synthesis from tyrosine via tyrosinase which is activated by UV light § 2 types of melanin: U melanin (tanning) & Feel melanin (found mostly on lips) § The melanin gets exocytosed, the pigments/melanin get picked up by other cells and the melanin help surround the nucleus, essentially creating a shield so the genetic material is not effected by UV radiation § Langerhans’ cells (aka dendritic cells) o Epidermal macrophages, whenever a pathogen penetrates our skin, these cells can phagocytize the pathogens § Made in bone marrow and migrate to the epidermis § The immune system for the skin § Merkel Cells: Found at the epidermal-dermal junction o Function as touch receptors in association with sensory nerve endings o Sensory nerve endings found in the dermis o The merkel cell is found in epidermis side o High amount found in fingertips Layers of the epidermis § Stratum corneum (outer most) § Stratum lucidum (only in thick skin) § Stratum granulosum § Stratum spinosum § Stratum basale (inner most) § Find dividing cells, mitotic cells, as they divide, they get pushed up into the next layer, etc. by the time they reach the stratum corneum, the cells are dead. Dermis: Middle layer, thickest layer § Strong and flexible connective tissue § Full of fibrous connective tissue and additional structures o Blood vessels, lymph vessels, roots of hair, 70% collagen, sebaceous glands (moisturizes the skin and antibacterial properties (no overgrowth of bacterial cells on skin)), Merkel cells/receptors that allow us to feel sensation (touch, temperature) § Richly supplied with nerve fibers & lymph vessels as well § Cell types: Fibroblasts, Mast cells, Immune cells (dendritic cells, macrophages, T cells) § Nociceptors: receptors that allow you to feel dangerous sensations like pain § Thermoreceptors: feel temperature changes § Paninian corpuscles: mechanoreceptors: allow feeling of vibration and pressure § Meissmer corpuscles: tactile receptors: allows feeling of light touch 1 Downloaded by Daisy Escobar ([email protected])  lOMoARcPSD|25656094 Hypodermis: innermost layer, aka superficial fascia or subcutaneous layer § Serves to anchor the skin to the underlying structures § Subcutaneous layer deep to the skin o Subq injections à max volume of ~1mL § Has a lot of adipose tissue and areolar connective tissue. o Helps insulate the body o Help cushion the underlying structures o Storage site for triglycerides, just in case we need additional fuel sources § Deep Fascia (underneath superficial fascia) o Forms a strong, fibrous internal framework o Dense connective tissue o Bound to capsules, tendons, ligaments, etc. § Subserous Fascia o Between serious membranes and deep fascia o Areolar tissue Skin color: three pigments contribute to skin color § Melanin (the only one made in the skin) o Freckles and pigmented moles=local accumulation of melanin o All humans have ~the same # of melanocytes; amount of pigment produced differs § Albinism: Inherited inability to produce melanin o Congenital defect, person is born with a deficient tyrosinase enzyme: the enzyme that converts tyrosine to melanin o Either the enzyme is inactive or don’t make enough; they lack pigment, iris look red/lack color, hair lacks color § Vitiligo: a partial or complete loss of melanocytes from patches of skin o May happen gradually - Carotene: yellow to orange pigment, most obvious in the palms and soles of the feet - Hemoglobin: reddish pigment responsible for the pinkish hue in our skin Skin Lesions: Causes 1. Liver disease: § When the liver has problems, liver failure, hepatitis, you immediately start seeing it in the skin, turns yellow (jaundice). You also get itching due to the bilirubin depositing in the skin, leading to inflammation 2. Systemic infections § Chicken pox (varicella virus) and measles: § Systemic infections that patient gets fevers, etc. virus manifests itself with lesions on skin that are very characteristic. 3. Allergies § Systemic allergic reaction to foods or drugs § Results in: Itching (pruritus), Red rash and/hives, Angioedema (patient’s eyes, lips, tongue, throat swell up) o Can lead to anaphylaxis § So much histamine is being released, causing widespread vasodilation and hypotension § Cardiovascular system can’t be maintained Topical allergic reactions Local skin irritation 4. Local irritants § Poison ivy/poison oak; Itchiness 5. Burns: Types of skin lesions: § Macule: flat but circumcised lesion; Redness in skin and has a circular type look, not raised, completely flat § Nodule: firm raised deep lesion; filled with cells, not fluid; Example: wart § Papule: small solid elevation § Pustule: raised lesion that has a “head”; Inside contains pus § Vesicle (or blister): has a thin membrane/wall; Fluid filled (clear) § Plaque § Ulcer: cavity in tissue § Fissure: crack in tissue § Decubitus Ulcers or Pressure sores: occur to patients who undergo long periods of immobility Pressure of bone against hard surface, pinching off blood vessels, leading to friction of skin against the surface and ulcer formation 2 Downloaded by Daisy Escobar ([email protected])  lOMoARcPSD|25656094 Pruritus: severe itching - Usually a response to exposure to allergens or irritants - Mechanism: not fully understood § Histamine release from mast cells may be a contributing factor § Sensation of itching is carried by small malonated type-C fibers to the dorsal horn of the spinal cord and then the somatosensory cortex for processing - Things that make itching worse: Anything that leads to vasodilationà inflammatory mediators being release, skin being dry and hot - Treatment: Antihistamines (Benadryl), Topical anti-inflammatory agents (glucocorticoids, hydrocortisone), Systemic anti-inflammatory agents if severe (glucocorticoid, prednisone), Topical administration of colloidal oatmeal (aveeno?) Inflammatory disorders of the skin: - Contact Dermatitis: exposure to allergen or irritant o Results in a localized rash & itching o Round, red, flat, macuole - Urticaria (Hives): type I systemic hypersensitivity reaction o Usually spread through the body o Raised, red, and itchy lesions on the skin - Eczema (Atopic Dermatitis): Persistent inflammation of the upper layers of the skin o Type I hypersensitivity reactions § Manifests on skin in patches, appears red and dry, blisters may appear and ooze. Don’t itch the skin, can lead to bacteria entering the skin and causes an infection o Characterized by: itching o Treatment: topical corticosteroids and antihistamines - Psoriasis o Chronic, inflammatory, autoimmune disease o Raised & red epidermal lesions o Covered w/ white silvery scales (plaque) § Itchy, Cracks, Burns, sometimes they bleed & become infected o Treatment: UV light, immune modulators and chemotherapy - Discoid Lupus Erythematosus o Inflammatory & autoimmune condition o Women>men o Typical butterfly pattern appears over nose o Some may develop alopecia (losing hair) - Scleroderma o Unknown cause, causes collagen deposition, inflammation and fibrosis o Skin becomes so tight § Loss of facial expression & movement of mouth and eye Bacterial skin infections: - Acne vulgaris: Inflammation & blockage of sebaceous glands and associated hair folliclesà pimples (pustules or cysts) o Can lead to proliferation of bacteria à staphylococcus aureus o Common in young adults; May persist into adulthood in severe cases o Can be mild or severe; May lead to scarring & stains o Men>womenà sebaceous glands stimulated by androgens § Face, neck and upper trunk are usually affected o Two types of lesions § Comedones (white or blackheads): Non-inflammatory collection of sebum & No scarring § Pustule lesion: SeverE inflammatory response to a bacterial infection & Scarring § May become a cyst in severe cases o Treatment: § Frequent cleansing with non-irritating soaps § Agents with antibacterial properties: § Benzoyl peroxide, Salicylic acid, Tetracycline, minocycline, doxycycline & erythromycin (topical), Aczone (Dapsone) gel: anti-inflammatory effects § Vitamin A derivatives: Retinoid derivatives; Example: Accutane Problem: they may lead to birth defects § Laser treatments § Agents to control hormones (ex. Oral contraceptives): Help balance and control hormonal spikes § Microderm abrasion: Helps unclog the pores 3 Downloaded by Daisy Escobar ([email protected])  lOMoARcPSD|25656094 Cellulitis - Infection of the dermis and subcutaneous tissue - Skin flora like Staph. Aureus (sometimes streptococcus) - Follows trauma and/or break in the skin - Common in lower trunk: In patients with patients with impaired blood supply to their periphery - Common problem in diabetics: have microvascular occlusions - Signs and symptoms: Redness, swelling and pain, **Red streaking across the lymph vessels - Treatment: medical emergency, hospitalization o may require amputation § the bacteria may spread to the blood streamà resulting in sepsis o systemic antibioticsà usually IV § can give a higher dose compared to oral without effected the normal flora like in the gut Impetigo - Infants and children - Staph aureus infection, may also be caused by group A beta hemolytic strep - Usually affects the face, Highly contagious, Can spread systemically and cause glomerulonephritis - Forms lesions that ooze yellow liquid that will crust o Very itchy - Make sure bedding, pillows, towels, stuffed toys are cleaned regularly for it can easily spread - Causes lots of pruritus; Scratching can spread the disease - Treatment: Topical antibiotics at first then systemic antibiotics if it has spread Acute necrotizing fasciitis - Life threatening; “flesh eating bacteria” - mixture of aerobic and anaerobic bacteria present - main culprit: group A beta hemolytic step pyogenes - secrets proteases and penetrates deep into the tissue o invades subcutaneous fascia and the fascia surrounding skeletal muscle (deep into tissue) o very easy for bacteria to hit a ride in the blood and spread systemically - results in edema, necrosis - bacteria produce a toxin and can cause toxic shock if it spreads into the systemic circulation o fever, hypotension, organ failure, death - medical emergency; rapid spreadà may need amputation - increase mortality rate (40-60%), increase rate of disability - risk factors: trauma, compromised immune system, chronic health condition such as diabetes, renal or liver failure, chicken pox infection - treatment: debridement and/or amputation, aggressive systemic antibiotic treatment (IV), fluid replacement, pain management Viral skin infections: - Herpes Simplex (Cold sores) o Herpes simplex virus type 1à fever blisters/cold sores o Herpes simplex virus type 2à genital herpes o Cold sores; Asymptomatic at first § Virus has a latent phase in the trigeminal nerve (sensory neuron) Virus gains access to nerve is via retrograde signaling It enters the nerve terminal and travels back via the axon towards the cell body and hides there Primary infection where the epithelial cells of cells are being infected, cells are dividing, cause the sore to appear o Lesions reoccur which can be trigger by: Common cold, Sun exposure, Stress o Signs and symptoms of reoccurrence: Tingling/Burning sensation § Painful blister àrupturesà forms a crustàheals spontaneous in 2-3 weeks o Virus is spread by: Direct contract with the fluid from the lesions o Treatment: topical antiviral (not a cure) –Abreva - Herpes Zoster (Shingles): Varicella-zoster virus o Reactivation of varicella virus infection (chicken pox) o Can you spread shingles? NO § Someone with shingles can infect someone with chicken pox o Painful blisters develop in a line unilaterally, Burning sensation, Paresthesias o Can result in lasting neuralgia:Nerve damage which causes chronic pain o Treatment: Systemic antivirals (not a cure), Pain medication 4 Downloaded by Daisy Escobar ([email protected])  lOMoARcPSD|25656094 - Verrucae (warts) o Human papilloma viruses (HPV) o Plantar warts: HPV 1-4à painful o Bottom on feet, looks like cauliflower o Treatment: Laser & Freezing w/liquid nitrogen and excising o Common warts: cosmetic o Genital wats: HPV 6+11 o HPV 16+18: can lead to cervical cancer Fungal skin infections - Mycoses of skin or nails o Diagnosed by scraping the skin and observing under a microscope o Superficial infections of keratocytes o May cause pruritus or be asymptomatic o Nail fungal infections require systemic antifungals and months (3-6) of treatment § Topical antifungals cannot penetrate deep enough into the nail bed to eradicate the infection - Tinea (ring worm) o Fungal infection that affect the skin, scalp & nails o Treat with antifungals Other skin infections: - Scabies: Mite infection: sarcoptes scabiei o Female mite burrows into epidermis and lays her eggs o Areas affected are the wrists, fingers, elbows and waist o Transmitted through close contact o Treatment: lindane (pesticide) - Pediculosis (lice) o 3 types: body lice (corporis), Pubic lice (pubis), Head lice (capitis) § Feed off human blood § Female lice lay eggs on hair shaftà called a nit Skin cancers: 3 major types - Basal cell carcinoma o Least malignant and most common o Stratum basale cells proliferate and invade the dermis and hypodermis o Slow growing and do not often metastasize o Can be cured by surgical excision in 99% cases - Squamous cell carcinoma o Arises from keratinocytes of stratum spinosum o Usually on scalp, ears and lower lip o Grows rapidly and metastasizes if not removed o Prognosis is good if treated by radiation therapy or removed surgically - Melanoma o Cancer of melanocytes o Most dangerous type of skin cancer because it is § Highly metastatic § Resistant to chemotherapy o 5% of all skin cancers but incidence increasing o 1/3 of cases appear in pre-existing moles o They have the following characteristics (ABCDE rule) § A: Asymmetry Usually they are asymmetric, if it is, do to doctor § B: Border Mole stays within a border § C: Color (pigmented area) If color goes outside the border Pigment should be uniform, if becomes darker, go to doctor § D: diameter: >6mm (size of a pencil eraser) E: Elevation, is a lesion growing in height? o Treatment: Wide surgical excision, Immunotherapy, Chemotherapy o Chance of survival is poor if the lesion is >4mm thick 5 Downloaded by Daisy Escobar ([email protected])  lOMoARcPSD|25656094 Kaposi’s Sarcoma - Rare form of skin cancer - Associated with HIV and/or immunocompromised - Unknown etiology, but herpes virus is suspected - Malignant cells arise from endothelial cells - Treatment: radiation and chemotherapy Burns - Immediate threat to life from severe burns: loss of body fluids, dehydration and electrolyte imbalance. Can lead to: o Acute renal failure & Circulatory shock - Treatments: o IV fluids: to try to maintain them from having hypotension due to dehydration o Large amounts of calories in the form of proteins and fats: as body starts to heal, need building blocks to create new cells o Prophylactic antibiotics - Classified by severity o First degree burn- only the epidermis is damaged § Redness, Sunburn o Second degree burn- Epidermis and upper regions of dermis damaged § Blisters appear § White colorless fluid, if there’s pus, may be infected § Skin regeneration occurs with little or no scarring within 3-4 weeks § Care must be taken to prevent infection o Third degree burn- All layers affected § Burned area appears gray-white, cherry red, or black; there’s no initial edema or pain (since nerve endings are destroyed) § As the nerve endings regenerate, the pain becomes excruciating § Skin grafting is usually necessary Taking skin from other parts of body § Extensive scar tissue forms Stevens Johnson’s syndrome or Toxic Epidermal Necrosis - Life threatening condition - Some drugs can cause this in some people o Believed to be caused by a hypersensitivity reaction o Genetic component also identified for some drugs - Dermis separates from the epidermis - Treatment: o Immediate discontinuation of the drug o Treat as you would a sever burn: o Fluid replacement o Prophylactic antibiotics o Skin grafts 6 Downloaded by Daisy Escobar ([email protected])