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Patho final pt 4
patho final pt 4- MS & Integ
| Question | Answer |
|---|---|
| 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
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