patho final pt 4- MS & Integ
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| Musculoskeletal System- Functional units | joints
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| Musculoskeletal System- Function | Movement, Protection, Support, Blood Cell Formation, Mineral Homeostasis
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| Musculoskeletal System- Elements | Bone, Joints, Tendons, Ligaments, Cartilage, Muscle
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| Bone cells | osteoblasts, osteoclasts, osteocytes
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| 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”
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| 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)
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| Mineralization- minerals involved | crystallization = final step in bone formation; mainly calcium phosphate
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| Compact bone | highly organized, solid and strong w/ complex concentric layers of matrix; organized spaces; channels throughout; main central canal- Haversian canal
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| 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
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| Red Marrow | in space of spongy bone
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| Yellow Marrow | in medullary cavity
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| Articular cartilage (joints) | Covers end of each bone; Reduces friction, distributes forces of weight-bearing; Water + proteins + collagen
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| Synovial fluid (joints) | Filtrated plasma: lubricates/nourishes/covers/protects; Hyaluronic acid, synovial cells, leukocytes
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| Ligament | bone to bone
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| Tendon | muscle to bone
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| Muscles | Sensory info from muscle to spinal cord (about stretch and change in muscle) → causes motor response
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| 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
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| 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
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| Aerobic | requires oxygen for oxidation of glycogen
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| Anaerobic | does not require oxygen
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| Excitation of the muscle | Electrical impulse movement
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| Troponin | tropomyosin in thin actin filaments → Ca binds to these → change in shape and movement so actin-myosin binding sites are exposed
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| Myosin/Actin binding | pulls actin inward and to myosin head (thin filament to thick filament) → shortening which is contraction
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| Calcium | into cytoplasm with actin and myosin filaments; also combines with troponin
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| Fracture | break in the continuity of a bone
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| Complete | broken all the way through
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| Incomplete | bone damaged but in one piece
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| Comminuted | broken into 2 or more pieces
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| Linear | parallel to axis of the bone
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| Oblique | 45° angle to the shaft
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| Spiral | encircles the bone
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| Transverse | straight complete brake
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| 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)
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| Bowing fx | extreme stress to bow-unable to reduce
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| Stress | fatigue or insufficiency fx due to other dz
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| 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)
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| 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
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| Tendonitis | inflammation causes thickening → limits movement, causes pain; if tears, bleeding w/ inflame continue; ↓ calcium
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| Bursitis | (tendon/joint padding): overuse of joint causes inflammation → increased fluid; pain, one sided tenderness w/ joint movement; impairs movement
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| Rhabdomylosis | Life threatening complication from severe muscle trauma & ischemia; crush injuries; compartment syndrome; crush syndrome; post viral infections; prolonged unresponsiveness & immobility
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| 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
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| 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
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| 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
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| 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
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| 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
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| Osteomyelitis- sxs | piece of bone that has separated from the surrounding living bone
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| noninflammatory joint disorders | DJD/OA
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| inflammatory | RA, Gout
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| 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
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| RA | Cause- systemic autoimmune disease w/ chronic inflammation of the connective tissue → joint involvement
Major signs and symptoms- fever, leukocytosis, malaise, anorexia
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| Epidermis | keratinocytes, melanocytes, 30 days, 5 layers
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| Dermis | deeper “true skin”; 2 layers, blood vessels, nerves, lymph, glands, appendages
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| Hypodermis | SQ, connective tissue; contains macrophages, fibroblasts, fat cells
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| Appendages | nails, hair, sebaceous & sweat glands
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| Pediatrics- skin | loose, thin, elastic more susceptible to bacterial infection
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| 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
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| Primary | initial reaction to an underlying problem
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| Secondary | changes in appearance of the primary lesion
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| Dermatitis | Link with IgE, asthma, and allergy
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| Acute Dermatitis | blisters, subacute dermatitis has scaling and crusting
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| Chronic Dermatitis | leathery hyperpigmented skin, Irritation & scratching, Lichenification, Risk of secondary skin infections
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| 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
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| 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
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| 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
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| Pemphigous | Autoimmune blistering (no adhesion secondary destruction of adhesion molecules)
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| What is folliculitis? BACTERIAL | hair follicles; staph aureus: causes pustules
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| What is cellulitis? BACTERIAL | dermal & SQ tissue; staph aureus often
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| What is impetigo? BACTERIAL | Often staph aureus or b-hemolytic strep; Honey-crusted lesions; More common in children
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| What is MRSA? BACTERIAL | Methicillin Resistant Staphylococcus Aureus
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| HSV1 vs. HSV2- VIRUS | Herpes Simplex Virus- Oral- cold sores
Genital
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| 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
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| Herpes Zoster- VIRUS | What lesions typically? Know run along dermatome/nerve route.
Latent/dormant varicella infection
Know immunization available for elderly- shingles vaccine
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| Genital Warts- VIRUS | HPV; increased risk of cancer associated with these
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| 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
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| Fifth Disease- VIRUS | Parvovirus B19
“slapped cheek” and typical rash appearance
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| Roseola- VIRUS | High fever 2 days prior and child well otherwise
Most common infantile infection/rash
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| Measles & Rubella (German Measles)- VIRUS | Transmission- Resp tract secretions, blood, infected urine
Contagious- 24 hrs before rash and 4-5 days after rash appears
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| Hand Foot and Mouth- VIRUS | Know strain of coxsackie virus – A virus
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| Smallpox- VIRUS | Know “eradicated”
Know intense and contagious → systemic effects and pox appearance
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| Tinea- FUNGUS | “ringworm”, “athlete’s foot”, etc
Dx: Skin scraping, culture, clinical appearance
Tx: Topical & systemic antifungals
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| Candida Albicans- FUNGUS | “millia”- yeast-like
Mucus membranes affected mostly
Increased in immunosuppression and destruction of normal flora
Diaper dermatitis, etc
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| Acne Vulgaris | Testosterone driven
Sebaceous glands
Comedones and bacteria involved
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| 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
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| Rocky Mtn Spotted Fever | tick bite; Rickettsia ricketti pathogen respond in blood if tick attached 4-6 hrs
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| 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
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| SK | Seborrheic Keratosis ; age spots; Basal cells take on waxy warty appearance; crusty brown, “stuck-on” patches
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| AK | Actinic keratosis; Premalignant lesion@ UV areas
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| Nevi | Congenital hyperpigmentation of the skin; Average person has 20 nevi; 4 /100,000 develop malignant melanoma
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| SCC- Squamous Cell Carcinoma | 75% occur on head & neck, exposed sun areas; malignant tumors of the middle epidermis
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| SCC- type 2 | invasive squamous cell carcinoma: develops from intraepidermal carcinoma or from a premalignant tumor; may be slow or fast growing w/ metastasis
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| 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
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| 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
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| 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
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| 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)
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| 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
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| Malignant Melanoma | “ABCDE”- A- Assymmetry; B- Borders; C- Color; D- Diameter; E- Elevation
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| 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
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