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75 Cards in this Set
- Front
- Back
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WHAT IS ARTICULAR CARTILAGE COMPOSED OF?
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CHONDROCYTES, WATER, COLLAGEN, AND PROTEOGLYCANS
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WHAT IS THE MOST IMPORTANT COMPONENT OF PROTEOGLYCANS?
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GLYCOSAMINGLYCANS WHICH IS WHY WE USE GLUCOSAMINE AND CHONDROITIN SULFATE IN OA; IN OA THERE IS A BREAKDOWN OF THE PROTEOGLYCANS RESULTING IN INCREASED WATER PERMEABILITY AND DETERIORATION OF THE CARTILAGE
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WHAT IS THE PURPOSE OF CORTICOSTEROID INJECTIONS IN THE TREATMENT OF ACUTE AND CHRONIC INFLAMMATORY DISEASES?
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DECREASE INFLAMMATION AND IMPROVE FUNCTION; CAN CAUSE SIGNIFICANT ADVERSE REACTIONS
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WHAT ARE THE GENERAL RULES FOR STEROID INJECTIONS?
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MAX OF 3 (3 PER YR OR 3 IN A LIFETIME DEPENDING ON LOCATION); AT LEAST 6 WEEKS BETWEEN INJECTIONS, RISKS INCLUDE HYPERGLYCEMIA IN DM, POSSIBLE INFECTION, HYPOPIGMENTATION AND LIPODYSTROPHY OR DIVETS IN THE BUTT
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WHAT IS THE PURPOSE OF HYALURONIC ACID IN THE TREATMENT OF OA?
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OA PATIENTS HAVE A DIMINISHED CONCENTRATION WHICH IS A KEY BIOCHEMICAL FOR JOINT MOTION, VISCOELASCTICITY, AND BOUNDARY LUBRICATION
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ONCE CONSERVATIVE MEASURES HAVE FAILED IN OA, WHAT DO WE DO?
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ARTHROSCOPY OR DEBRIDEMENT; JOINT REALIGNMENT PROCEDURE OR INTERPOSITIONAL ARTHROPLASTY; TOTAL OR PARTIAL JOINT REPLACEMENT WHEN THERE IS PAIN AT REST, PAIN AT NIGHT, OR UNACCEPTABLE LOSS OF JOINT FUNCTION; FUSION AS LAST RESORT
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WHAT IS MOSAICPLASTY OR OATS PROCUDURE FOR OA?
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TAKE A CHUCK OUT OF FEMUR AND PLACE IN KNEE; CALLED PLUGS- SLOWS PROGRESSION OF OA
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AT WHAT AGE IS JOINT REALIGNMENT DONE IN OA?
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IN THE 40S B/C PATIENTS ARE STILL TOO YOUNG FOR TOTAL REPLACEMENT; VERY INVASIVE- LASTS ONLY 2 TO 3 YEARS
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HOW LONG DOES A KNEE ARTHROPLASTY LAST?
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10-15 YRS THAT IS WHY WE WAIT UNTIL PT IS 60 TO DO ONE IF POSSIBLE; IF YOU HAVE TO DO MORE THAN 2 THERE IS NO BONE LEFT TO CUT
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REFERRAL DECISIONS/ RED FLAGS FOR OA
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PATIENTS WHO HAVE PAIN AT REST, AT NIGHT, OR UNACCEPTABLE LOSS OF JOINT FUNCTION
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BONE INFECTION CAUSED BY PYOGENIC ORGANISMS, TB, SYPHILIS, AND VIRAL OR FUNGAL ELEMENTS THAT CREATES AN INFLAMMATORY RESPONSE THAT PROGRESSES TO AN ABSCESS THAT DESTROYS THE BONE
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OSTEOMYELITIS
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HOW DOES OSTEOMYELITIS SPREAD?
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HEMATOGENOUS SPREAD, BY DIRECT SPREAD OF A SOFT TISSUE OR BY A PENETRATING WOUND
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MOST COMMON CAUSATIVE AGENT OF OSTEOMYELITIS
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STAPH AUREUS, WITH HEMOLYTIC STREPTOCOCCI NEXT
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CLINICAL SYMPTOMS OF OSTEOMYELITIS
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UNRELENTING PAIN IS FIRST SYMPTOMS, HISTORY OF TRAUMA OR INJURY IN MANY, FEVER, LOCALIZED TENDERNESS, AND FLUSHED APPEARANCE
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EXAMINATION OF OSTEOMYELITIS
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FOCAL BONE TENDERNESS; MORE ESTABLISHED LESIONS WILL HAVE SWELLING, ERYTHEMA, AND INCREASED LOCALIZED WARMTH
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BASIC WORK UP FOR OSTEOMYELITIS
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WBC, ESR, CRP, X RAY, BLOOD CULTURE, AND ASPIRATION AT FOCAL BONE TENDERNESS POINT
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WHAT WILL XRAYS OF OSTEOMYELITIS SHOW EARLY
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WILL BE NEGATIVE OR WILL SHOW ONLY SOFT TISSUE SWELLING; XRAYS 10 DAYS LATER WILL SHOW PERIOSTEAL ELEVATION (DESTRUCTION OF BONE0
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WHAT IS THE MOST IMPORTANT DIAGNOSTIC STEP IN OSTEOMYELITIS?
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ASPIRATION OF THE SUSPECTED SITE
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TREATMENT FOR OSTEOMYELITIS
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IV ANTIBIOTICS ASAP, EMPIRIC THERAPY EVEN BEFORE CONCLUSIVE RESULTS OF CULTURE, IF TEMP AND PAIN DO NOT DRAMATICALLY DECREASE WITHIN 36 HOURS, CONSIDER SURGICAL DECOMPRESSION
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REFERRAL DECISIONS/ RED FLAGS IN OSTEOMYELITIS
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SHOULD BE HOSPITALIZED, ASPIRATION OR SURGICAL DECOMPRESSION USUALLY BE SPECIALIST, INFECTIOUS DISEASE CONSULT IF CULTURE SHOWS AN UNUSUAL ORGANISM
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WHAT IS OSTEOPOROSIS?
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A DISEASE CHARACTERIZED BY LOW BONE MASS LEADING TO MICROARCHITECTURAL DETERIORATION WHICH RESULTS IN AN INCREASED FRAGILITY OF THE BONE AND AN INCREASED RISK OF FRACTURE
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WHAT IS THE CAUSE OF PRIMARY TYPE I OSTEOPOROSIS?
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ESTROGEN/TESTOSTERONE
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WHAT IS THE CAUSE OF PRIMARY TYPE II OSTEOPOROSIS?
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CA METABOLISM (70 PLUS YEARS OLD)
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SECONDARY OSTEOPOROSIS
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DUE TO HORMONE, METABOLIC, OR NEOPLASTIC ABNORMALITIES
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ANOTHER NAME FOR POSTMENOPAUSAL OSTEOPOROSIS
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PRIMARY TYPE I
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WHAT DOES ESTROGEN DEFICIENCY LEAD TO?
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TRABECULAR BONE LOSS
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HOW DO PRIMARY TYPE I OSTEOPOROSIS PATIENTS PRESENT?
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WITH VERTEBRAL COMPRESSION FRACTURES OR FRACTURES OF THE DISTAL RADIUS
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ANOTHER NAME FOR SENILE OSTEOPOROSIS
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PRIMARY TYPE II
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WHAT DOES ALTERED CA METABOLISM AND INTRINSIC PROBLEMS WITH BONE FORMATION LEAD TO IN PRIMARY TYPE II OSTEOPOROSIS?
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A DECREASE IN FORMATION OF NEW BONE
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WHAT ARE THE CLINICAL SYMPTOMS OF OSTEOPOROSIS?
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NORMALLY PT. PRESENTS WITH BACK PAIN, FRACTURE, LOSS OF HEIGHT, OR SPINAL DEFORMITY
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IN ADVANCED OSTEOPOROSIS, WHAT ARE THE FINDINGS?
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TENDERNESS OVER AN AREA OF A FRACTURE, SPINAL DEFORMITY OR LOSS OF HEIGHT, LAX ABDOMINAL MUSCULATURE
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DIAGNOSTIC TESTS FOR OSTEOPOROSIS
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BONE MINERAL DENITY, DUAL ENERGY X-RAY ABSORPTIOMETRY IS THE GOLD STANDARD
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BONE MINERAL DENSITY TESTING IS RECOMMENDED FOR WHO?
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POSTMENOPAUSAL WOMEN UNDER 65 WITH RISK FACTORS BESIDES MENOPAUSE; ALL WOEMN 65 OR OLDER REGARDLESS OF RISK FACTORS; ALL POSTMENOPAUSAL WOMEN WITH FRACTURES, WOMEN ON LONG TERM HORMONE THERAPY
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WHAT TESTS ARE USED TO RULE OUT BONE MARROW DISORDER AS A SECONDARY CAUSE OF OSTEOPOROSIS?
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CBC, ESR, SERUM PROTEIN LEVEL, AND IMMUNOELECTROPHORESIS
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WHAT TEST RULE OUT OSTEOMALACIA AS A SECONDARY CAUSE OF OSTEOPOROSIS?
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SERUM CALCIUM, PHOSPHOROUS, ALK PHOS, VIT D, AND PARATHYROID HORMONE
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PREVENTION OF OSTEOPOROSIS
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ADEQUATE CALCIUM AND VIT D, REGULAR WEIGHT BEARING EXERCISE, AVOID TOBACCO AND ALCOHOL, MAINTAIN BODY WEIGHT AND REDUCE RISK FACTORS FOR FALLS
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PHARMACOLOGIC INTERVENTION FOR OSTEOPOROSIS UNDER WHAT TWO CONDITIONS?
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WOMEN WHOSE BMD SCORE IS 2 STANDARD DEVIATIONS BELOW NORMAL ADULT, WOMEN WHOSE BMD SCORE IS 1.5 SD BELOW NORMAL WHEN RISK FACTORS ARE PRESENT
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WHAT WOMEN OVER 70 SHOULD GET DRUGS FOR OSTEOPOROSIS WITH NO BMD TESTING?
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WHITE WOMEN WITH MULTIPLE RISK FACTORS
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WHAT ARE OVERUSE INJURIES?
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INJURIES CAUSED OR AGGRAVATED BY REPETITIVE MOTION OR SUSTAINED EXERTION OF A PARTICULAR BODY PART, RESULTING IN MICROTRAUMA TO A MUSCULOTENDINOUS UNIT
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THESE INJURIES ARE BLANKETED UDNER WHAT CONDITION OR TERM?---CARPAL TUNNEL, TENNIS ELBOW, ACHILLES TENDINITIS, STRESS FRACTURES, SHN SPLINTS, EXERTIONAL COMPARTMENT SYNDROME
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OVERUSE SYNDROMES
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CONTRIBUTING FACTORS TO OVERUSE SYNDROMES
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REPETITIVE TASKS, VIBRATION OR COLD TEMPS, AWKWARD POSTURES AT WORK, LACK OF JOB SATISFACTION, BOREDOM
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CLINICAL SYMPTOMS OF OVERUSE SYNDROME
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PAIN, FATIGUE, NUMBNESS; MAY REPORT PAIN IN NONANATOMIC DISTRIBUTION
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WHAT MAY BE NECESSARY DIAGNOSTIC TO IDENTIFY A STRESS FRACTURE?
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A BONE SCAN
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DIAGNOSTIC TEST FOR CARPAL TUNNEL
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NERVE CONDUCTION VELOCITY STUDIES
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INITIAL TREATMENT OF OVERUSE INJURIES
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ICE AND EST, PROGRESSIVE EXERCISE PROGRAM TO STRENGTHEN; MODIFY WORK TASKS; OT OR PT; NSAIDS, ANTIDEPRESSANTS IF DEPRESSION IS CONTRIBUTING
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THIS IS A SPECTRUM OF CONDITIONS THAT HAVE IN COMMON DYSFUNCTION AND PAIN THAT IS OUT OF PROPORTION TO WHAT SHOULD BE EXPECTED FROM THE ORIGINAL INJURY
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COMPLEX REGIONAL PAIN SYNDROME
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WHEN YOU HEAR "PAIN OUT OF PROPORTION TO INJURY" WHAT DIAGNOSIS SHOULD COME TO MIND?
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COMPLEX REGIONAL PAIN SYNDROME
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TWO TYPES OF CRPS?
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TYPE I (REFLEX SYMPATHETIC DYSTOPHY)- RDS SYNDROME- PAIN THAT EXTENDS BEYOND AREA SERVED BY PERIPHERAL NERVE WITH PAIN OUT OF PROPORTION TO INCITING EVENT AND TYPE II- CASUALGIA; FOLLOWS A NERVE INJURY BUT SIMILAR TO TYPE I OTEHRWISE
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MOST COMMON INJURY THAT PRECIPITATES RSD
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DISTAL RADIUS FRACTURE
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PATIENTS AT MOST RISK FOR CRPS
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PTS BETW 30 AND 50 YEARS OLD ARE MOST AT RISK; WOMEN MORE LIKEL TO BE AFFECTED; SMOKERS
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DESCRIBE STAGE I OF CRPS
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3 MONTHS W/ PAIN OUT OF PROPORTION- BURNING, THROBBING, OR CUTTING; ANS DYSFUNCTION TO INCLUDE SWELLING, INCREASED SWEATING, SKIN COLOR CHANGE FROM RED TO CYANOTIC, TEMP CHANGES, HAIR GROWTH, EXCESSIVE NAIL GROWTH
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STAGE 2 CRPS
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AFTER 3 TO 4 MONTHS, LOSS OF SKIN LINES, SKIN LOOKS WAXY AND PALE, JOINT STIFFNESS, BRITTLE NAILS, MUSCLE SPASMS, PERSISTENT PAIN
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STAGE 3 CRPS
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LOSS OF MUSCLE AND SKIN, PERMANENT JOINT CONTRACTURES, LOSS OF MOTION, PERSISTENT SEVERE PAIN
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DIAGNOSTIC TESTS FOR STAGE 3 CRPS
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PLAIN FILSM MAY SHOW SPOTTY OSTEOPENIA OR DEMINERALIZATION (SUDEK'S ATROPHY)
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TREATMENT FOR CRPS IS MOST SUCCESSFUL WHEN....
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IT IS TREATED WITHIN THE FIRST YEAR; IF LEFT UNTREATED FOR ONE YEAR OR MORE, THERE WILL BE SIGN. DISABILITY ON 50%
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ADVERSE OUTCOMES OF CRPS
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CHRONIC DEBILITATING PAIN, JOINT CONTRACTURES, LOSS OF FUNCTION, SKIN AND MUSCLE ATROPHY, PSYCH PROBLEMS
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SYSTEMIC AUTOIMMUNE DISORDER CHARACTERIZED BY AN INFLAMMTORY SYNOVITIS THAT CAN ERODE AND DESTROY ARTICULAR CARTILAGE; UNKNOWN ETIOLOGY
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RHEUMATOID ARTHRITIS
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WHAT POPULATION IS MOST COMMONLY AFFECTED BY RA/
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WOEM, PREVALENCE INCREASED WITH AGE WITH PEAK ONSET IN LATE 40S AND EARLY 50S
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THIS TYPE OF ARTHRITIS IS USUALLY BILATERAL SYMMETRICAL AND MOST OFTEN INVOLVES HANDS, WRIST, ANKLES, AND FEET
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RA
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DIAGNOSIS FOR RA DEPENDS ON WHAT
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HAVING 4 OUT OF 7 OF TEH DIAGNOSIS CRITERIA- MORNING STIFFNESS THAT LASTS AT LEAST AN HOUR, ARTHRITIS IN 3 OR MORE JOINTS FOR MORE THAN 6 WEEKS, ARTHRITIS OF HANDS FOR MORE THAN 6 WEEKS, SYMMETRIC ARTHRITIS FOR 6 WEEKS, RHEUMATOID NODULES, POSITIVE SERUM RHEUMATOID FACTOR, RADIOLOGIC CHANGES
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CORRELATE BROUSSARD NODES WITH WHAT CONDITION
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RA
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WHAT WILL EXAMINATION IN RA SHOW?
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JOINT CONTRACTURE, JOINT EFFUSIONS, PAINFUL MOTION, INCREASED WARMTH OR BOGGINESS AT JOINTS; LESS FLUID THAN EXPECTED UPON ASPIRATION, RHEUMATOID NODULES ESP. ALONG EXTENSOR SURFACE OF FOREARMS
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DIAGNOSTIC TESTS FOR RA
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RHEUMATOID FACTOR ELEVATED, ESR AND CRP ELEVATED
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THIS CONDITION WILL ULTIMATE LEAD TO EROSION OF ARTICULAR CARTILAGE AND LIGAMENTOUS CHANGES---CLAW TOE AND ULNAR DRIFTING
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RA
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IF A PATIENT IS ANTICIPATING SURGERY THAT INVOLVES THE NECK, WHAT FINDINGS ARE VERY IMPORTANT
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OFTEN IN RA THERE IS C1-2 INSTABILITY SECONDARY TO EROSION OF THE LIGAMENTS THAT HOLD THE ODONTOID IN PLACE; IF SX IS DONE AND THIS RA FINDING IS PRESENT, PARALYSIS OR DEATH MAY OCCUR
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TREATMENT FOR RA
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ASPIRIN, NSAIDS, TYLENOL, SPLINTING, ORAL AND INTRA-ARTICULAR CORTICOSTEROIDS; CUSTOM SHOES; PT; TOTAL JOINT REPLACEMENT IN END STAGE
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SERONEGATIVE SPONDYLOARTHROPATHIES HAVE THESE FOUR CHARACTERISTICS COMMON
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1. INFLAMMATION OF TENDON, FASCIA, OR JOINT CAPSULE INSERTIONS 2. PAUCIARTICULAR ARTHRITIS IN LOWER EXTRIMITY NORMALLY 3. EXTRA ARTICULAR INFLAMMATION- EYE, SKIN, MUCOUS MEMBRANES, HEART, BOWEL 4. ASSOCIATION WITH HLA-B27 ANTIGEN
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IMPINGEMENT SYNDROME IS AN UMBRELLA TERM FOR (5)
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SUPRASPINATUS TENDONITIS, SUB ACROMIAL BURSITIS, BICIPITAL TENDONITIS, A-C ARTHRITIS
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ESSENTIALLY IMPINGEMENT SYNDROME IS WHAT?
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ROTATOR CUFF ARTHROPATHY
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IMPINGEMENT SYNDROME IS COMMON IN WHAT POPULATION
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MIDDLE AGED PEOPLE
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INVOLVES INFLAMMATION OF THE SUBACROMIAL BURSA AND UNDERLYING ROTATOR CUFF TENDONS
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IMPINGEMENT SYNDROME
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WHAT IS THE MOST COMMON CAUSE OF SHOULDER BURSITIS(SUBACROMIAL BURSITIS) ?
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IMPINGEMENT SYNDROME
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IMPINGEMENT SYNDROME IS USUALLY ASSOCIATED WITH PINCHING OF WHAT?
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PINCHING OR IMPINGEMENT OF THE ROTATOR CUFF TENDONS (ESP. SUPRASPINATUS) BY A SUBACROMIAL SPUR
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WHAT IS THE END RESULT OF IMPINGEMENT SYNDROME?
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ROTATOR CUFF TEAR (ARTHROPATHY)
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TYPE III (HOOKED) ACROMION AND LARGE SUBACROMIAL SPURS ARE COMMON IN PATIENTS WITH WHAT CONDITION
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IMPINGEMENT SYNDROME/ ROTATOR CUFF DISEASE
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