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Patho final pt 4

patho final pt 4- MS & Integ

QuestionAnswer
Musculoskeletal System- Functional units joints
Musculoskeletal System- Function Movement, Protection, Support, Blood Cell Formation, Mineral Homeostasis
Musculoskeletal System- Elements Bone, Joints, Tendons, Ligaments, Cartilage, Muscle
Bone cells osteoblasts, osteoclasts, osteocytes
Remodeling (of bone) Existing bone resorbed and new bone replaces; Ongoing- bone turnover every 7-10 yrs Basic Multicellular units → osteoblasts and clasts; Stimulated by hormone, drug, vitamin, physical stressor, etc. Activation → reabsorption → formation “secondary bone”
Repair (of bone) new bone formation (NOT SCAR); Remodeling but initiated by inflammation/hematoma → osteoblasts form callus, then multicellular units as above (months to yrs)
Mineralization- minerals involved crystallization = final step in bone formation; mainly calcium phosphate
Compact bone highly organized, solid and strong w/ complex concentric layers of matrix; organized spaces; channels throughout; main central canal- Haversian canal
Spongy bone less organized and complex; lacks central canal; the organization is in bars of irregular meshwork. These bars are organized in different directions with particular layout depending on stress on that bone
Red Marrow in space of spongy bone
Yellow Marrow in medullary cavity
Articular cartilage (joints) Covers end of each bone; Reduces friction, distributes forces of weight-bearing; Water + proteins + collagen
Synovial fluid (joints) Filtrated plasma: lubricates/nourishes/covers/protects; Hyaluronic acid, synovial cells, leukocytes
Ligament bone to bone
Tendon muscle to bone
Muscles Sensory info from muscle to spinal cord (about stretch and change in muscle) → causes motor response
Motor Unit of muscles; increase contrax? Anterior horn of spinal cord →axon lower motor neuron →muscle fibers You CANNOT increase # of fibers but increase diameter and length of fibers
Metabolism/ energy ATP and Phosphocreatine Lactic acid production (what is this a byproduct of? Why? Causes pain! Requires oxygen to remove from muscle!)- byproduct of metabolizing glucose for energy
Aerobic requires oxygen for oxidation of glycogen
Anaerobic does not require oxygen
Excitation of the muscle Electrical impulse movement
Troponin tropomyosin in thin actin filaments → Ca binds to these → change in shape and movement so actin-myosin binding sites are exposed
Myosin/Actin binding pulls actin inward and to myosin head (thin filament to thick filament) → shortening which is contraction
Calcium into cytoplasm with actin and myosin filaments; also combines with troponin
Fracture break in the continuity of a bone
Complete broken all the way through
Incomplete bone damaged but in one piece
Comminuted broken into 2 or more pieces
Linear parallel to axis of the bone
Oblique 45° angle to the shaft
Spiral encircles the bone
Transverse straight complete brake
Greenstick perforates one cortex & splinters the spongy bone: proximal metaphysis/diaphysis (in young, soft bone, bone bends and partially breaks) aka torus/buckling fx (most common in kids)
Bowing fx extreme stress to bow-unable to reduce
Stress fatigue or insufficiency fx due to other dz
Subluxation partial dislocation in which the bone ends w/in the joint are still in partial contact with each other (i.e., child’s elbow)
Dislocation loss of articulation of the bone ends with the joint capsule caused by displacement or separation (temporary)- congenital, traumatic, or pathologic causes; potentially threatens use of limbs 2° nerve supply & blood supply compromise
Tendonitis inflammation causes thickening → limits movement, causes pain; if tears, bleeding w/ inflame continue; ↓ calcium
Bursitis (tendon/joint padding): overuse of joint causes inflammation → increased fluid; pain, one sided tenderness w/ joint movement; impairs movement
Rhabdomylosis Life threatening complication from severe muscle trauma & ischemia; crush injuries; compartment syndrome; crush syndrome; post viral infections; prolonged unresponsiveness & immobility
Osteoporosis Density of bone or mass of bone is diminished (mineralization = ok); Imbalance btw bone reabsorption & bone formation; Trabeculae become thin & sparse, compact bone is porous: brittle/weak & collapse-deform easily; pain & bone deformity; fractures
Osteoporosis- risk factors concurrent illness/drugs: loss of absorptive GI surface, RA, hyperthyroidism, Parkinson, Cushing’s/corticosteriods, heparin; genetic: white women; small boned life-style: reduction in activity reduces bone stress & increases calcium loss
Osteoporosis- risk factors hormonal: post-menopausal: w/ loss of estrogen - PTH overstimulates osteoclasts to initiate remodeling & resorb dietary deficiencies & malabsorptions- calcium; vitamins: C, D; others
Osteomyelitis- risk factors long, difficult, expensive ordeal caused by bacteria & microbes; The bone’s microscopic channels are inaccessible to the body’s own natural defenses- if bacteria enter- able to proliferate unhindered
Osteomyelitis- risk factors Bone’s microcirculation is vulnerable to damage & destruction by bacterial toxins→vessel damage & local thrombosis & ischemia; Bone cells have limited capacity to replace bone destroyed by infection → lags & incomplete remodeling and repair
Osteomyelitis- sxs piece of bone that has separated from the surrounding living bone
noninflammatory joint disorders DJD/OA
inflammatory RA, Gout
Gout Related to purine metabolism & kidney function; Over production of uric acid- greater than 7.0 mg/dL; Under excretion by kidney; Do not have to manifest the disease w/ increased levels Major signs and symptoms- fever, leukocytosis, malaise, anorexia
RA Cause- systemic autoimmune disease w/ chronic inflammation of the connective tissue → joint involvement Major signs and symptoms- fever, leukocytosis, malaise, anorexia
Epidermis keratinocytes, melanocytes, 30 days, 5 layers
Dermis deeper “true skin”; 2 layers, blood vessels, nerves, lymph, glands, appendages
Hypodermis SQ, connective tissue; contains macrophages, fibroblasts, fat cells
Appendages nails, hair, sebaceous & sweat glands
Pediatrics- skin loose, thin, elastic more susceptible to bacterial infection
Geriatrics- skin aging seen everywhere, thinner, drier, wrinkled, color changes; ↓melanocytes: ↑d susceptibility to UV ↓ # of immune cells (Langerhans cells); ↓ in vasculature contributes to atrophy of glands; Loss of melanocytes in hair bulb → graying
Primary initial reaction to an underlying problem
Secondary changes in appearance of the primary lesion
Dermatitis Link with IgE, asthma, and allergy
Acute Dermatitis blisters, subacute dermatitis has scaling and crusting
Chronic Dermatitis leathery hyperpigmented skin, Irritation & scratching, Lichenification, Risk of secondary skin infections
Psoriasis Systemic disease, arthritis & immunologic link Typical appearance of lesions- white, scaling patches of various sizes on skin Classic locations of lesions- Extensor surfaces; Face, scalp, elbows, knees, at site of trauma
Rosacea Typical appearance- redness, bumps, vesicles, thickened skin on the nose; hypertrophic sebacceous glands Locations- Face; neck & upper chest exacerbate- heat/strenuous exercise, sun, wind, cold, hot drinks, spicy foods, emotional stress, & coughing
DLE Altered immune response- –IgM deposits in ski; Autoimmune papulosquamous disorder May be subset of SLE appearance- red plaque w/ brown scale; lesions stay for months Classic locations of lesions- face, ears, and scalp- Butterfly malar facial rash
Pemphigous Autoimmune blistering (no adhesion secondary destruction of adhesion molecules)
What is folliculitis? BACTERIAL hair follicles; staph aureus: causes pustules
What is cellulitis? BACTERIAL dermal & SQ tissue; staph aureus often
What is impetigo? BACTERIAL Often staph aureus or b-hemolytic strep; Honey-crusted lesions; More common in children
What is MRSA? BACTERIAL Methicillin Resistant Staphylococcus Aureus
HSV1 vs. HSV2- VIRUS Herpes Simplex Virus- Oral- cold sores Genital
Varicella- VIRUS immunization-Varicella Zoster- VZV, chicken pox, Herpes 3 What lesions?- macule/papule/vesicle rash; very pruritic; all 3 present with crusting How spread?- Mainly nasopharyngeal secretions (airborne droplet); direct contact Complication- Shingles
Herpes Zoster- VIRUS What lesions typically? Know run along dermatome/nerve route. Latent/dormant varicella infection Know immunization available for elderly- shingles vaccine
Genital Warts- VIRUS HPV; increased risk of cancer associated with these
Mulluscum Contagiosum- VIRUS Know typical lesion appearance- slightly umbilicated, dome-shaped papules viral etiology; usually childhood disease and increased contagious, self-limiting- 6-9 months to resolve
Fifth Disease- VIRUS Parvovirus B19 “slapped cheek” and typical rash appearance
Roseola- VIRUS High fever 2 days prior and child well otherwise Most common infantile infection/rash
Measles & Rubella (German Measles)- VIRUS Transmission- Resp tract secretions, blood, infected urine Contagious- 24 hrs before rash and 4-5 days after rash appears
Hand Foot and Mouth- VIRUS Know strain of coxsackie virus – A virus
Smallpox- VIRUS Know “eradicated” Know intense and contagious → systemic effects and pox appearance
Tinea- FUNGUS “ringworm”, “athlete’s foot”, etc Dx: Skin scraping, culture, clinical appearance Tx: Topical & systemic antifungals
Candida Albicans- FUNGUS “millia”- yeast-like Mucus membranes affected mostly Increased in immunosuppression and destruction of normal flora Diaper dermatitis, etc
Acne Vulgaris Testosterone driven Sebaceous glands Comedones and bacteria involved
When is tick dz a risk? Where? What ticks especially? How do we avoid? 5-9 yrs old; Apr-Sept; coastal Atlantic (NC and OK)- full body checks
Rocky Mtn Spotted Fever tick bite; Rickettsia ricketti pathogen respond in blood if tick attached 4-6 hrs
Lyme Disease (VECTOR)- Risks? Appearance of EM? cardiac and neurologic manifestations that present weeks to months later; arthritis: develops wks - yrs later in 60% of cases “Bull’s eye” appearance
SK Seborrheic Keratosis ; age spots; Basal cells take on waxy warty appearance; crusty brown, “stuck-on” patches
AK Actinic keratosis; Premalignant lesion@ UV areas
Nevi Congenital hyperpigmentation of the skin; Average person has 20 nevi; 4 /100,000 develop malignant melanoma
SCC- Squamous Cell Carcinoma 75% occur on head & neck, exposed sun areas; malignant tumors of the middle epidermis
SCC- type 2 invasive squamous cell carcinoma: develops from intraepidermal carcinoma or from a premalignant tumor; may be slow or fast growing w/ metastasis
SCC- type 1 in situ intraepidermal squamous cell carcinoma- remains confined to the epidermis for a long time but at an unpredictable moment penetrates the basement membrane to the dermis & metastasizes to the regional lymph nodes
BCC Light-skinned people are more susceptible; exposed sun areas of face, arms, hands; interfollicular basal cells, follicles, or sebaceous gland – deeper than squamous cell CA
BCC- cont'd begins as a small flesh-colored smooth pink transparent nodule that enlarges over time What is major risk factor? UV rays, X-rays, Gamma rays
Malignant Melanoma rapidly progressing, metastatic form of cancer that accounts for 2.5% of all cancers; result of malignant degeneration of melanocytes; proto-oncogenes are identified (increased growth)
Malignant Melanoma- risks white, higher S.E.S; severe, blistering sunburns in early childhood & intermittent intense sun exposures (trips to sunny climates); immigration to sunny locations; people who burn easily and tan minimally; use of tanning salons/beds
Malignant Melanoma “ABCDE”- A- Assymmetry; B- Borders; C- Color; D- Diameter; E- Elevation
KS- Kaposi Sarcoma What is it?- Vascular malignancy; proliferation depends on presence of platelet-derived growth factors What populations at greatest risk?- HIV, herpes, & CMV viruses may be cofactors and herpes virus may promote AIDS-KS
Created by: sccrgrl159 on 2010-11-29



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