Skin and Musculoskeletal 310

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Terms in this set (109)
the thick layer of living tissue below the epidermis, containing blood capillaries, nerve endings, sweat glands, hair follicles, and other structures. Connective tissue layer (collagen); separated epidermis from subcutaneous fat; provided nutrition for the epidermis. Contain macrophages, T cells, and mast cells
Image: Dermis
LesionEruption of the skin due to pathology or traumaMaculeFlat lesion measuring less than 1 cm in diameter ie frecklePatchFlat lesion greater than 1 cm ie vitiligoPapuleRaised, but solid lesion less than 1cm ie elevated nevus (mole)PlaqueRaised, but solid lesion greater than 1cm, usually a collection of papules ie psoriasisNoduleRaised, but solid lesion 0.5-2m , more firm, less mobile than a papuleTumorRaised, but solid lesion greater than 2cmWhealRaised, and fluid filled lesion localized area of skin edema ie urticaria, mosquito biteurticariaHives is a common skin rash triggered by many things including certain foods, medications, and stress. Symptoms include itchy, raised, red, or skin-colored welts on the skin's surface. Hives usually go away without treatment, but antihistamine medications are often helpful in improving symptomsVesiclesRaised, and fluid filled lesion less than 1cm, filled with serous fluid ie herpes simples or zosterBullaRaised, and fluid filled lesion bigger than 1cm filled with serous fluid ie second degree burn blisterPustuleRaised, and fluid filled lesion filled with pus ie acne, impetigo, small poxVitiligo-Vitiligo occurs when pigment-producing cells die or stop functioning. -Loss of skin color can affect any part of the body, including the mouth, hair, and eyes. -Treatment may improve the appearance of the skin but doesn't cure the disease.Cause of Vitiligocan be due to: genetic predisposition, autoimmune disorder, neural - destroyed chemical released by nerve endings, lack of melanocytes growth factor;AlbinismA group of inherited disorders characterized by little or no melanin production. This condition increases the risk of skin cancer. Most people with albinism have pale skin, eye conditions, and are sensitive to the sun. No cure exists, but skin can be protected and eye conditions can be treated.;TineaFungal infection of a particular part of bodytinea capitisFungal infection of the scalp (ringworm)tinea corporisFungal infection of the bodyTinea pedisFungal infection of the feet (athletes foot)Tinea versicolorFungal infection of the upper chest, back and armsTinea crurisFungal infection of the groinTinea corporis presentationFungal lesion: oval papule with central clearingTinea pedis presentationFungal lesion: varies from mild scaling to inflamed lesion with fissuring and passing and oozingTinea versicolor presentationFungal lesion: skin looks dirty, areas are depigmentedImpetigo-A highly contagious skin infection that causes red sores on the face. Superficial bacterial skin infection, most often due to Staph aureus or Strep pyogenes. -The main symptom is red sores that form around the nose and mouth. The small vesicles or pustules sores rupture, ooze for a few days, then form a yellow-brown crust. -Antibiotics shorten the infection and can help prevent spread to others -Most common in childrenCellulitisthe bacteria enter the skin (breaks in skin may facilitate this) infecting the dermis and the subq, may spread rapidly. Affected skin appears swollen and red and may be hot and tender. Without treatment with an antibiotic, cellulitis can be life-threatening.Cellulitis presentationred swollen, tender plaque; vague border; associated with fever, redness, heat, edema, and painCellulitis infectious agentsGroup A hemolytic Streptococcus and Staphylococcus speciesVerrucae (warts)-Viral skin infection: benign papilloma; small, grey-white/tan, flat or elevated, rough surface -Caused by HPV -Usually resolve spontaneously, can be removed by chemicals or freezing, antiviral medications or duct tapeEtiology HPVDirect contact or autoinoculation. Break in the skin facilitates entryHPVOrganism associated with verrucae and cervical cancerPrimary infection of herpes simplexViral skin infection: infection of skin and mucous membranes - painful vesicles and ulcers of the tongue, palate and lips; -associated with feverSecondary infection of herpes simplexViral skin infection: infection of skin and mucous membranes; recurrence after "hibernation" in trigeminal and dorsal root ganglion,HSV-1Herpes simplex virus that is associated with the oral cavity -spread by respiratory droplets and direct contactHSV-2Herpes simplex virus associated with genital infection, spread by contact when lesion is activeHerpes zosterViral skin infection that is painful, sensitive, dermatomally-distributed vesicular eruption; usually unilateral; -recurrence in times of stress of previously contained chickenpox virus that was hibernating in trigeminal and dorsal root ganglion; -can be transmitted person to person vis airborne dropletsAcne vulgarisDisorder of hair follicle and sebaceous gland, caused by chronic inflammatory response and increase sebum productionTypes of Acne leasions-Non-inflammatory- comedones (whiteheads and blackheads) -Inflammatory- papules, pustules, nodulesPropionibacterium acnescausative agent of acne, a relatively slow-growing, typically aerotolerant anaerobic, Gram-positive bacterium linked to the skin condition of acneRosaceaA inflammatory process that causes redness and often small, red, pus-filled bumps on the face (nose, cheeks, forehead) and can lead to thickening of the nose (which can lead to breathing impairment). Rosacea most commonly affects middle-aged women with fair skin. Key symptoms are facial redness with swollen red bumps and small visible blood vessels. Treatments such as antibiotics or anti-acne medications can control and reduce symptoms. Left untreated, it tends to worsen over time.Allergic contact dermatitistype IV hypersensitivity response secondary to sensitization - presentation ranges from redness to large bullies -bacterial infection can occur;type IV hypersensitivityoften called delayed type hypersensitivity as the reaction takes several days to develop. Unlike the other types, it is not antibody-mediated but rather is a type of cell-mediated responseIrritant contact dermatitisIrritation of skin hypersensitivities, due to reaction to some harmful substance; can occur to soaps, detergents, woolSubjectiveIrritant reaction type hypersensitivity in which no clinical manifestations, but with patient complaintAcuteIrritant reaction type hypersensitivity due to a single exposureChronicIrritant reaction type hypersensitivity occurs due to repeated exposureAtopic dermatitis(eczema) A type I hypersensitivity reaction mediated by IgE with different presentations depending on ageInfantile Eczema presentation:Vesicles formation, oozing, excoriations --begins on cheeks and advances to rest of body -may become milder as child ages - >50% will develop asthma and allergiesAdolescent and adults Eczema presentation:dry, red patches affecting face, neck and upper body seen in bending points of elbows and knees itchiness which creates opening for secondary bacterial infectionUrticariaPink, edematous, prurience wheals; pink or red with pale halo, blanch with pressure; may be associated with angioedema; caused by: histamine released, usually result of IgE mediated reaction, food is common antigen; can be acute or chronic;Psoriasis-Circumscribed red, thickened plaques with overlying silvery scale -lesions tend to occur on knees and elbows -unknown cause, possible genetic link, possible autoimmune disorderPityriasis rosea-Oval macule or papule with erythema that do not blanch with pressure -possible due to infectious agent, highest in winter; herald lesion -> Christmas tree pattern on back -children and young adults most commonly affected; treated palliatively with steroidsHerald patchInitial large lesion indicating start of pityriasis roseaScabies-Small, red to reddish-brown burrow caused by S. scabiei mite; most commonly found in webs of finger, flexor surface of wrists, inner elbow, armpits, beltline, and gluteal crease -causes itchiness from burrows and fecal material; secondary bacterial infection is common;Pediculosis (lice)-grey, grey-brown insects that live off the blood fo humans -pierce the skin and drink up to 1mL of blood very host specific; can infest heady, body, and pubic region;Skin cancer-Skin lesion due to increase UV light exposure. -increases due to lifestyle - lack of sunscreen useMalignant melanomaSkin cancer type: rapidly progressing and metastatic -most dangerous; -may bleed -malignant tumor of melanocytesBasal cell carcinoma-most common (75-80%) and most benign, -translucent, flesh colors or pink nodule-tends to develop on nose, ears -associated with talengiectasis can be flat, and red; increased risk with sun exposure, neoplasm of non-keratinized cells -usually non-metastatic but spreads without treatment -May be treated with MohsMohs Surgeryis a precise surgical technique used to treat skin cancer. During Mohs surgery, thin layers of cancer-containing skin are progressively removed and examined until only cancer-free tissue remains. Mohs surgery is also known as Mohs micrographictalengiectasisa condition in which widened venules (tiny blood vessels) cause threadlike red lines or patterns on the skin. These patterns form gradually and often in clusters. They're sometimes known as "spider veins" because of their fine and weblike appearanceSquamous cell carcinoma-Skin cancer type: "in-between risk"; -red keratotic lesion with irregular border; shallow ulcer (crater forms) -tumor of the outer epidermis -can become invasive, and penetrate the basement membrane -treated with excision and chemotherapyFirst degree burn-superficial partial thickness -outer layer of the epidermis, -red and painfulSecond degree burn-partial or full thickness -epidermis and dermis -painful, moist, red, and blistered -blisters prevent release of body waterThird degree burn-full thickness burn -epidermis, dermis, subcutaneous tissue, muscle, bone; -blood vessel thrombosis white, yellow, tan, black, red with edema -no pain bc nerve ending have been destroyedPressure ulcersIschemia to skin and underlying structures due to pressure causes skin lesions -obstruction of blood vessels and lymph vesselsStage 1 Pressure Ulcerpersistent, non-blanching rednessStage 2 Pressure Ulcerpartial thickness loss of skin; epidermis, dermis or both; abrasion or blister;Stage 3 Pressure Ulcerfull thickness loss of skin; damage and necrosis of subcutaneous tissue;Stage 4 Pressure UlcerPressure ulcer stages: damage or necrosis of subcutaneous tissue; destruction of muscle, bone, ligament, and tendon;OsteomyelitisInfection of the bone penetrating injury, contamination of open fracture or wound; -spread through the blood, spread from nearby infectionCausative Agent-S. aureus is most common cause. Can also be caused by E. Coli, N gonorrhoeae, H. InfluenzaReasons why S. aureus causes Osteromyelitis1. can adhere to connective tissue or bone and 2. can survive in osteoblastsOsteonecrosisDeath of bone usually due to impaired interruption of blood supply;Causes of osteonecrosis1. Mechanical disruption (fracture) 2. Thrombosis/ embolus (sickle cell) 3. Vascular injury ( SLE, RA) 4. CorticosteroidsOsteogenesis imperfectaBrittle bone disease caused by defective genes. -These genes affect how the body makes collagen, a protein that helps strengthen bones. -results in thin, brittle bones, short limbs, multiple fractures, and extremity growth can be affected; -fractures that occur without any apparent cause. Treatments include bone-strengthening medications, physical therapy, and orthopedic surgery.ScoliosisLateral deviation of the spine with or without a deviation of the vertebrae; cause is largely unknown, may be congenital or associated with another disorder;OsteoporisisLoss of mineralized bone with an increased risk of fracture often associate with aging, diet, lack of vitamin D and calcium may contributeOsteomalaciais the softening of the bones caused by impaired bone metabolism primarily due to inadequate levels of available phosphate, calcium, and vitamin D, or because of resorption of calcium. The impairment of bone metabolism causes softening of the bone due inadequate bone mineralizationPaget's diseasePaget's disease of bone most commonly occurs in the pelvis, skull, spine, and legs. Risk factors include increasing age and a family history of the condition. Over time, affected bones may become fragile and misshapen. This condition can be symptomless for a long period of time. When symptoms do occur, they may include bone deformities, broken bones, and pain in the affected area.Process of Pagetscharacterized by local areas of excessive bone turnover and disorganized osteoid formation -1st the disease is marked by regions of rapidly occurring osteoclastic bone resorption, followed by a period of hectic bone formation with increased numbers of osteoblasts rapidly depositing bone in a chaotic fashion such that the newly formed bone is of poor quality and is disorganized. 2nd-The bone marrow adjacent to the bone-forming surface is replaced by loose connective tissue that contains osteoprogenitor cells and numerous blood vessels, which transport blood to and from these metabolically active sites. The lesions may be solitary or may occur in multiple sitesOsteopetrosis"Marble bone disease"; reduced osteoclasts activity amid normal osteoblast activity; bones are brittle and break like a piece of chalk; associated with blockage of RANKL receptor; literally "stone bone", also known as marble bone disease, is an extremely rare inherited disorder whereby the bones harden, becoming denserRANKLis known as a membrane protein and is a member of the tumor necrosis factor (TNF) superfamily. RANKL has been identified to control bone regeneration and remodelingrheumatoid arthritisInflammatory disease, systemic, more common in women; cause is no clear: genetic predisposition, joint inflammation seems to be immune mediated;Rheumatoid factorAutoantibody associated with rheumatoid arthritis; creates immune complexes with IgG present in synovial fluid; lead to tissue injury by type III hypersensitivity reaction;Process of Rheumatoid I1)Initiating event (unknown) causes inflammation in person with genetic predisposition - may be microbial 2)Activation of CD4 T-cells (helper cells) - secrete cytokines 3)B-cells activated by cytokines →become plasma cells →secrete Rheumatoid Factors(RF) which are autoantibodies 4)RF binds to IgG on surface of synovial membrane forming immune complex Lead to tissue injury by Type III hypersensitivity reaction and activate complement (enzyme precursors) which attract neutrophils 5)Neutrophils and macrophages are attracted to the site digest immune complexes release enzymesProcess of Rheumatoid II6)Enzymes released by neutrophils and macrophages cause damage to surrounding tissue 7)Inflammation perpetuates the problem 8)Inflammatory response Vasodilation - warmth and redness Increased capillary permeability - swelling 9)Formation of a pannus 10)Destructive due to inflammatory cells present in pannus - secrete enzymes that destroy cartilage 11)RANKL is expressed in synovial sac by T-cells Activates osteoclasts to digest bone and joint destruction occursRANKL and RheumatoidExpressed by T cells in synovial space; Stimulates osteoclasts to digest and break down bone structures which can lead to joint destruction in rheumatoid arthritisPannus-Network of new blood vessels and synovial membrane associated with rheumatoid arthritis -leads to reduced mobility in fingers, hands and feetOsteoarthritisDegenerative joint disease usually from wear and tear -progressive loss of cartilage in the joint and inflammation of synovial membraneEburnationdescribes a degenerative process of bone It is an ivory-like reaction of bone occurring at the site of cartilage erosion and bone becomes thick and polishedOsteophytesbone spurs associated with increase activity of osteoblast activity in lateral portion of bone, related to osteoarthritisGoutDeposits of urticaria acid crystals in the joints; abnormality in purines metabolism resulting in high levels of using acid may be inborn, or secondary 90% are due to enzyme deficit which causes overproduction of urticaria acid and/or inadequate elimination of ruin acid in kidneyGouty attackMonosodium crystals precipitate in joint; inflammatory response initiated usually occurs in cooler parts of the body crystals attract leukocytes, inflammatory response continuesTophiNodules (associated with gout) containing uric acid crystals seen on ears, toesmuscular dystrophy (MD)Progressive deterioration of skeletal muscle, fat and connective tissue replace muscle increase in size of muscle, but decrease in strength;Duchenne muscular dystrophya severe type of muscular dystrophy. The symptom of muscle weakness usually begins around the age of four in boys and worsens quickly, is an X linked trait so more prominent with males. Females with a single copy of the defective gene may show mild symptoms. It is a defect in a protein synthesis, leading to abnormal protein within the musclesystemic lupus erythematosus stats-Chronic autoimmune inflammatory disease; -10 to 1 female predominance; common in African Americans, Hispanics and Asians; -type III hypersensitivity reaction; -genetic predisposition; -autoantibodies and immune complexes that damage tissue and can attack any part of the bodyLupus-Is an autoimmune disease in which the body's immune system mistakenly attacks healthy tissue in many parts of the body. -Common symptoms include painful and swollen joints, fever, chest pain, hair loss, mouth ulcers, swollen lymph nodes, feeling tired, and a red rash which is most commonly on the face. -Often there are periods of illness, called flares, and periods of remission during which there are few symptomAnti-nuclear antibodiesAttack DNA/RNA, histones, centromeres; serum levels are indicative of presence of autoimmune disease;

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