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77 Cards in this Set
- Front
- Back
1. WHAT ARE THE CHARACTERISTICS OF GOUT?
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a. Asymptomatic, acute, intercritical, chronic (developes in four stages)
b. Joints: hot, inflamed, tender, dusky red, cyanotic, fever c. common in feet (starts @ metatarsophalangeal) and legs d. MBD: increased urate deposits on joints |
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2. WHAT IS THE BASIC PATHOS OF GOUT?
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a. purine (protein) metabolism is altered & the by-product uric acid accumulates
b. increased uric acid leads to tophi deposits on joints which triggers an immune response which leads to necrosis or fibrosis |
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3. WHAT IS PRIMARY GOUT?
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a. Inherited defect: increased or decreased renal excretion
b. It’s caused by a genetic defect in purine metabolism causing hypercemia or retention of uric acid |
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4. WHICH POPULATION IS AT RISK FOR PRIMARY GOUT?
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a. 30 yrs to 40yrs
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5. WHAT IS SECONDARY GOUT?
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a. developes during the course of other diseases: obesity, type 2 diabetes, hypertension, renal failure, cancer
b. hematopoeitic, starvation, radiation, chemo, meds: ASA, diueretics, anti-tb |
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6. WHERE DOES SECONDARY GOUT ACCUMALATE?
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a. myocardium, blood, synovial fluid, ears, kidney
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7. WHAT IS TOPHI AND WHERE IS IT DEPOSITED?
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a. uric acid crystals deposited in connective tissue
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8. HOW DO YOU DIAGNOSE GOUT?
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a. persistent hyperuricemia, arthrocentesisi: tophi in synovial fluid
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9. WHAT ARE 3 THINGS A NURSE MANAGES FOR GOUT?
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a. pain control
b. bed rest c. assistive devices for ambulation |
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10. WHAT ARE THE PHARMACOLOGICAL TREATMENTS USED TO MANAGE GOUT?
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a. pain: NSAIDS
b. inflammation: colchine, corticosteroids injections c. decrease acid levels: allopurinol, probenecide, indomethicin |
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11. WHICH MEDICATIONS ARE USED TO LOWER URIC ACID?
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a. decrease formation: allopurinol, no for renal failure
b. increase reabsorption and excretion: probenecide, sulfinpyrazone |
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12. WHAT IS THE MAIN PHARMACOLOGICAL TREATMENT USED TO MANAGE AN ACUTE ATTACK OF GOUT?
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a. colchicine: prevents recurrent acute attacks until uric acid is back to normal level
b. q 8 hrs PO/IV |
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13. WHAT MUST YOU REMEMBER ABOUT COLCHICINE?
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a. toxic dose close to therapuetic
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14. WHAT ARE THE SIGNS AND SYMPTOMS OF COLCHICINE TOXICITY?
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a. nausea, vomiting, diarrhea
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15. WHAT ARE THE NON-PHARMACOLOGICAL TREATMENTS USED TO HELP MANAGE GOUT?
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a. hot/cold application
b. diet low in purine c. weight loss |
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1. WHAT ARE THE CHARACTERISTICS OF GOUT?
|
a. Asymptomatic, acute, intercritical, chronic (developes in four stages)
b. Joints: hot, inflamed, tender, dusky red, cyanotic, fever c. common in feet (starts @ metatarsophalangeal) and legs d. MBD: increased urate deposits on joints |
|
2. WHAT IS THE BASIC PATHOS OF GOUT?
|
a. purine (protein) metabolism is altered & the by-product uric acid accumulates
b. increased uric acid leads to tophi deposits on joints which triggers an immune response which leads to necrosis or fibrosis |
|
3. WHAT IS PRIMARY GOUT?
|
a. Inherited defect: increased or decreased renal excretion
b. It’s caused by a genetic defect in purine metabolism causing hypercemia or retention of uric acid |
|
4. WHICH POPULATION IS AT RISK FOR PRIMARY GOUT?
|
a. 30 yrs to 40yrs
|
|
5. WHAT IS SECONDARY GOUT?
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a. developes during the course of other diseases: obesity, type 2 diabetes, hypertension, renal failure, cancer
b. hematopoeitic, starvation, radiation, chemo, meds: ASA, diueretics, anti-tb |
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6. WHERE DOES SECONDARY GOUT ACCUMALATE?
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a. myocardium, blood, synovial fluid, ears, kidney
|
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7. WHAT IS TOPHI AND WHERE IS IT DEPOSITED?
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a. uric acid crystals deposited in connective tissue
|
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8. HOW DO YOU DIAGNOSE GOUT?
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a. persistent hyperuricemia, arthrocentesisi: tophi in synovial fluid
|
|
9. WHAT ARE 3 THINGS A NURSE MANAGES FOR GOUT?
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a. pain control
b. bed rest c. assistive devices for ambulation |
|
10. WHAT ARE THE PHARMACOLOGICAL TREATMENTS USED TO MANAGE GOUT?
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a. pain: NSAIDS
b. inflammation: colchine, corticosteroids injections c. decrease acid levels: allopurinol, probenecide, indomethicin |
|
11. WHICH MEDICATIONS ARE USED TO LOWER URIC ACID?
|
a. decrease formation: allopurinol, no for renal failure
b. increase reabsorption and excretion: probenecide, sulfinpyrazone |
|
12. WHAT IS THE MAIN PHARMACOLOGICAL TREATMENT USED TO MANAGE AN ACUTE ATTACK OF GOUT?
|
a. colchicine: prevents recurrent acute attacks until uric acid is back to normal level
b. q 8 hrs PO/IV |
|
13. WHAT MUST YOU REMEMBER ABOUT COLCHICINE?
|
a. toxic dose close to therapuetic
|
|
14. WHAT ARE THE SIGNS AND SYMPTOMS OF COLCHICINE TOXICITY?
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a. nausea, vomiting, diarrhea
|
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15. WHAT ARE THE NON-PHARMACOLOGICAL TREATMENTS USED TO HELP MANAGE GOUT?
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a. hot/cold application
b. diet low in purine c. weight loss |
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16. WHAT ARE SOME LONG-TERM INTERVENTIONS USED TO MANAGE GOUT?
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a. meds
b. avoid alcohol c. diet low in purines (anchovies, lentils, alcohol) d. oral fluid |
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17. WHAT ARE THE LONG-TERM AFFECTS OF INDOCIN AND COLCHICINE?
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a. bone marrow suppression
b. alopecia c. hepatic damage |
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18. WHAT IS ARTHROPLASTY?
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a. replacement of a joint with a prosthetic
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19. WHAT IS OSTEOPLASTY?
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a. scraping off degenerative bone (OA
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20. WHAT WOULD YOU ASSESS THE NEUROVASCULAR SYSTEM FOR WHEN CONSIDERING THE MUSCULOSKELETAL SYSTEM
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a. pain
b. pallor c. temperature d. pulses e. capillary refill f. paresthesia g. mobility of affected joints: crepitation, muscle shotening, ankylosis h. sensation and motor function of peripheral nerves: strength aagainst resistence, posture, natural directional movement, balance, coordination, picking things up |
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21. WHAT ARE THE DIAGNOSTIC/LAB TESTS FOR OA?
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a. x-ray: shows narrowing joint space by erosion of cartilage, osteophytes
b. Synovial fluid analysis: rules out inflammatory arthritis (rheumatoid arthritis) |
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22. WHAT ARE THE LAB TESTS FOR OP?
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a. usually made after a fracture, vertebral compression fracture
b. x-ray: vatebral bodies appear flattened, collapsed, wedged |
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23. WHAT IS ARTHROSCOPY?
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a. evaluate the knee by visuliaztion
b. biopsy lg scope can remove articular debris, repair torn meniscus |
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24. WHAT ARE THE LAB TESTS FOR RA?
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a. +RF
b. x-ray: demineralization, soft tissue swelling c. synovial fluid analysis: increased complement, volume, turbidity d. –lyme titer e. ESR elevated |
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25. WHAT IS OSTEOMYELITIS?
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a. bone infection: caused by virus, staph
b. breakdown and decalcification c. acute, chronic, usually localized |
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26. IN WHAT PART OF THE BODY DOES OSTEOMYELITIS OCCUR?
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a. femur, tibia, sacrum, heels
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27. WHICH POPULATIONS ARE AFFECTED BY OSTEOMYELITIS?
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a. males
b. rapidly growing boys |
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28. WHAT ARE THE GENERAL RISK FACTORS FOR SUSCEPTIBILITY OF OSTEOMYELITIS?
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a. IV use
b. Diabetes c. Immunocompramised d. History of blood stream infection e. Pressure ulcer, chronic wounds |
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29. WHAT ARE THE LAB TESTS USED TO ASSESS OSTEOMYELITIS?
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elevated WBC, ESR
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30. WHAT ARE THE DIAGNOSTIC TESTS FOR OSTEOMYELITIS?
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. x-ray
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31. WHAT ARE THE WAYS OF MANAGING OSTEOMYELITIS?
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surgery, ABs
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32. WHAT IS SEPTIC ARTHRITIS?
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a. bone infection
b. pyrogenic in synovial membrane: neissra gonorrhea, staph |
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33. WHAT ARE THE 10 CLINICAL MANIFESTATIONS OF A FRACTURE?
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a. deformity
b. swelling c. bruising d. muscle spasm e. pain f. tenderness g. loss of function h. abnormal mobility, crepitus i. neurovascular changes j. shock |
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WHAT ARE THE TREATMENTS FOR MANAGEMENT OF FRACTURES?
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a. Assessment, monitor complications
b. reduction, stabilization, immobilization of fracture c. remobilization, rehabilitation d. restore alignment: open reduction & internal fixation, casts, splints, traction |
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35. WHAT ARE THE11 MAJOR COMPLICATIONS AFTER A FRACTURE?
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a. nerve injury
b. compartment syndrome c. volkman’s contracture d. fat embolism syndrome e. DVT f. Infection g. Cast syndrome h. Long term: joint stiffness, post-traumatic arthritis i. Avascular necrosis j. Unions: non-functional union, malunion, delayed union, non-union, fibrous union k. Complex regional pain syndrome |
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40. WHAT ARE THE MAJOR NURSING ASSESSMENTS OF A CLIENT IN A CAST?
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a. assessment: neurovascular, pain, cast, complications
b. drying a cast |
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41. WHAT IS THE LEADING CAUSE OF MORBIDITY/MORTALITY FOR THE OLDER POPULATION?
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hip fractures
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42. WHAT FACTORS PREDISPOSE ONE TO A HIP FRACTURE?
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a.low bone mass
b. increasing age |
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43. DECREASED BLOOD FLOW TO THE HIP PUTS A PATIENT AT RISK FOR WHAT?
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a. necrosis to the hip area
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44. WHAT ARE THE DIAGNOSTIC TESTS USED FOR HIP FRACTURES?
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a. history
b. x-ray c. ct d. mr i |
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45. WHAT ARE THE DIFINING CHARACTERSITICS OF OSTEOARTHRITIS?
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common, not systemic, chronic
b. stiffness, morning, after exercise c. achieness weather d. crepitus, motion e. narrowed joint space f. pain/stiffness inc w/activity dec w/rest g. mild tenderness joint area h. dec ROM i. joint enlrg |
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46. WHICH POPULATIONS ARE AFFECTED BY OSTEOARTHRITIS?
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a. symp middle age, progress with age
b. 65yrs < c. obesity (knees) disability in lower extremities due to effects on lg wt bearing joints d. PT no hist. of joint inj or disease, nor systemic ill assoc w/arthritis |
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47. WHAT ARE THE TWO TYPES OF OSTEOARTHRITIS AND WHICH POPULATIONS ARE AFFECTED BY THEM?
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a. Primary: (idiopathic) norm aging, mostly women, genetic
b. Secondary: mostly men, pre-disposing event ex. trauma, Paget’s leads to degenerative changes |
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49. WHAT IS A COMMON REGIMEN USED TO TREAT OA?
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a. Exercise-regular, stimulates cartilage growth, protects joints, weight bearing creates support
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50. WHAT IS USED TO MANAGE OA AND RHEUMATOID ARTHRITIS?
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a. Pain and Inflamation relief
b. Dec joint stress c. low impact exercise d. independent ADL e. Maintain quality of life f. cane, brace, neoprene, collar, corset g. apply Heat Cold |
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51. WHAT MEDICATIONS ARE USED TO HELP MANAGE OA AND RHEUMATOID ARTHRITIS?
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a. TYLENOL oa
b. NSAIDS rheumatoid c. worse oa nsaids w/ misoprostol(cytotec), celebrex(cox2) d. viscosupplementation (hyaluronan) injection-OA, glucosamine + chrondroitin, sam-e |
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53. WHAT ARE 4 SURGICAL INTERVENTIONS USED TO HELP MANAGE OA?
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a. Osteotomy: bone excision
b. Arthrodesis: bone fusion, laminectomy c. Arthroplasty: prosthetic, knee hip |
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54. WHAT ARE THE OA POST-OPERATIVE NURSING RESPOSIBILITIES?
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a. pain
b. mobility c. peripheral neurovascar care d. prevent: injury, infection, skin breakdown, DVT e. promote: self care |
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55. WHAT IS RHEUMATOID ARTHRITIS?
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a. degenerative, chronic, progressive, acute episodes of exacerbations
b. similar pathos to OA but SYSTEMIC auto-immune: complement and attacks muscle/ligaments too c. synovial effusion common |
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56. WHICH AREAS OF THE BODY DOES IT AFFECT?
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a. small joints PIP, MCP
b. knees, wrists |
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57. WHAT ARE THE CLINICAL MANIFESTATIONS OF RHEUMATOID ARTHRITIS?
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a. edema, tenderness, pain@rest, red, warmth, fatigue, nodules, inc esr, anemia, muscle ache, + RF test
b. affects lung heart skin |
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58. WHICH POPULATIONS ARE AFFECTED BY RHEUMATOID ARTHRITIS?
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a. avg/below wt
b. young/mid age c. women more d. family history |
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59. WHAT TREATMENTS ARE USED TO MANAGE RHEUMATOID ARTHRITIS?
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a. inflammation reduction, NSAIDs
b. diet exercise c. hot/cold app d. sugery |
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60. WHAT ARE THE CHARACTERISTICS OF OSTEOPOROSIS?
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a. bones loose CA+ and PO and become susceptible to fractures
b. diagnoses after fracture, or xray c. metabolic bone disorder |
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61. WHAT ARE THE COMPONENTS OF BONE STRENGHT CONSIDERED WITH CONCERNS TO OP?
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a. bone density and quality
b. Porous and brittle, re-absorption inc as formation dec |
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62. WHAT IS OSTEOPENIA?
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a. thinning of bone, low density porous and brittle
b. may lead to/first symptoms of osteoporosis |
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63. THE WHO DEVELOPED 4 LEVELS OF CATEGORIES THAT DETERMINE WHAT?
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a. WHO
b. risk of fracture |
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64. WHICH POPULATIONS ARE AFFECTED BY OP?
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a. postmenses white women, US
b. reduction of estrogen |
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65. WHAT ARE THE RISK FACTORS FOR OP?
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a. previous adult fracture, fragile bones, low weight (128), smoking, oral contraceptives
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66. WHAT ARE SOME MANIFESTATIONS OF OP?
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a. shortened stature
b. kyphosis c. ab distension d. bloating e. restricted RR by rest. Lung expanse f. chronic pain g. func. diasbility |
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67. WHAT ARE THREE MAJOR OP PREVENTIONS AND/OR TREATMENTS?
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a. prevent bone loss and fragility fractures:
i. CA+, vit D, reg Weight Bearing exercise, avoid tobacco, alcohol ii. back brace, exercise iii. meds: estrogen: hormone replacment therapy aledronate, raloxifene, risedronate, calcitonin, teriparatide |
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68. WHAT ARE 6 MAJOR NURSING RESPONSIBILITIES USED TO PROMOTE HEALING AFTER A FRACTURE?
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a. manage pain
b. regain mobility and strength c. promote healing d. reduce bone loss e. prevent further fracture f. limit the disability |