By T. Killian. Morehouse College.

Although orthoses cannot correct the rotational deformities lumigan 3ml without a prescription, if functional orthoses are used Knee extension contractures for other reasons lumigan 3 ml with amex, major deviations in the foot position from the direction of walking must be avoided as much 3 Definition as possible proven lumigan 3 ml. A VY-plasty of the quadriceps tendon produces good results if physio- Definition therapeutic stretching exercises fail lumigan 3ml discount. There is best lumigan 3ml, however, a Functional and structural problems of the knee associ- risk of an active extension lag as a consequence of weak- ated with myopathies are limited to flexion deformi- ening, which may finally result in a crouch gait. Muscular dystro- unbalanced muscle forces lead to rotational defects in phy patients tend to suffer flexion contractures as they the lower leg. Both external and internal rotational defor- approach the end of their ability to walk. Although, in purely statistical terms, such opera- orthosis to stabilize the feet. Flexible orthoses are of no tions can postpone the loss of walking and standing func- use since they are unable to prevent talipes calcaneus. We therefore consider the onset ing action more difficult, and therefore require the fitting of contractures as a compromise for the timing of surgical of a rocker to the shoe. If the feet deviate only slightly procedures, even if this potentially involves the loss of the from the direction of walking, every step produces a tor- ability to stand and walk for several months. Muscular sion moment which, even after the age of 5, can lead to a dystrophy patients sit for longer periods and their muscles gradual change in rotation. An external or internal rota- undergo fibrous and fatty changes, thus making stretching tional error can require correction if the feet can no longer more difficult. However, since our treatment regimen al- be positioned in the direction of walking, the efficiency of ready ensures a minimal loss of extension at the hips and the gait is impaired or the patients trip over their feet. Oc- knees, almost no functional surgery has been carried out casionally, cosmetic reasons can play a decisive role. Functional deformities in muscular dystrophies Deformity Functional Functional drawbacks Treatment benefit Knee extensor insufficiency – Standing with flexed knees not possible Full knee extension, prevention of pes calcaneus Knee flexor insufficiency – Deficient momentum (knee extension Passive swinging of the leg during walking contracture) ⊡ Table 3. Structural deformities in muscular dystrophies Deformity Functional Functional drawbacks Treatment benefit Flexion contracture at the knee – Crouch position (loss of walking and standing) Lengthening of knee flexors 329 3 3. Aspden RM, Porter RW (1994) Nerve traction during correction ing, these functions are only possible if the joints can be of knee flexion deformity. Baumann JU, Ruetsch H, Schurmann K (1980) Distal hamstring small contractions. Int the knee flexor lengthening procedure must be performed Orthop 3: 305–9 towards the end of the ability to walk, when the muscles are 3. Baumann JU (1992) Behandlungskonzepte bei Kniefehlstellung increasingly degenerated, and in such a way that sufficient im Rahmen neurologischer Grunderkrankungen. Orthopäde 21: 323–31 length can be obtained directly by the operation without 4. Beals RK (2001) Treatment of knee contracture in cerebral palsy the need for protracted follow-up treatment. For this rea- by hamstring lengthening, posterior capsulotomy, and quadri- son, tendon lengthening procedures are preferable to those ceps mechanism shortening. Brunner R, Döderlein L (1996) Pathological fractures in patients the operation is part of the follow-up management. J Pediatr Orthop B 5: 232–8 In muscular dystrophy patients in particular, the equi- 7. Chambers H, Lauer A, Kaufman K, Cardelia JM, Sutherland D nus foot represents a key stabilizing component in stand- (1998) Prediction of outcome after rectus femoris surgery in ce- ing and walking. The slight equinus foot position locks rebral palsy: the role of cocontraction of the rectus femoris and the upper part of the ankle and prevents dorsiflexion. J Pediatr Orthop 18: 703–11 indirectly extends the knee and the patient is able to hold 8. Dhawlikar SH, Root L, Mann RL (1992) Distal lengthening of the hamstrings in patients who have cerebral palsy. J Bone Joint Surg (Am) 74: 1385–91 surgery is indicated to correct this equinus deformity. Forst R, Forst J (1995) Importance of lower limb surgery in the contrary, the ankles must be stabilized with an ortho- Duchenne muscular dystrophy.

Beunen GP discount lumigan 3ml visa, Malina RM buy lumigan 3 ml, Renson R (1992) Physical activity and growth discount lumigan 3ml fast delivery, maturation and performance: A longitudinal study lumigan 3ml. Dorizas J generic 3ml lumigan mastercard, Stanitski C (2003) Anterior cruciate ligament injury in the skeletally immature. Herman M, Pizzutillo P, Cavalier R (2003) Spondylolysis and spon- dylolisthesis in the child and adolescent athlete. Hasler C, Dick W (2002) Spondylolyse und Spondylolisthesis im Wachstumsalter. Hatton J, Pooran M, Li C, Luzzio C, Hughes-Fulford M (2003) A short pulse of mechanical force induces gene expression and growth in MC3T3-E1 osteoblasts via an ERK 1/2 pathway. Hefti F, Morscher E (1985) Die Belastbarkeit des wachsenden Be- wegungsapparates. Hefti FL, Kress A, Fasel J, Morscher EW (1991) Healing of the tran- sected anterior cruciate ligament in the rabbit. Mankin K, Zaleske D (1998) Response of physeal cartilage to low- level compression and tension in organ culture. Morscher E (1968) Strength and morphology of growth cartilage under hormonal influence of puberty Reconstr. Karger, Basel New York (Surgery and Traumatology, vol 10) 3 Diseases and injuries by site 3. History To ensure that the patient’s back is at eye-level, the examiner himself should not stand but preferably ▬ Trauma history: Has trauma occurred? Inspection from behind – What was the patient doing (sport, playing, normal We observe the position of the shoulders, the height routine)? We look for pigmentation over the ▬ Pain history: spinous processes, especially over the lumbar spine, Where is the pain located (neck, upper thoracic spine, as this can be an indication of (usually pathological) lower thoracic spine, lumbar spine, lumbosacral kyphosis in this area. If so, does the pain occur We assess the sagittal curves and establish a pos- only while changing position, or does the pain cause tural type: normal (physiological) back, hollow back the patient to wake up at night? Does the pain occur (increased thoracic kyphosis and lumbar lordosis), on bending down or straightening up again? Does the fully rounded back (kyphosis extending down to the pain also radiate to the legs? Does the pain occur on lumbar area), hollow-flat back (hyperlordosis of the coughing or sneezing? If Scheuermann disease is suspected backwards or forwards, then postural variants are ask specifically whether the patient is involved in cycle involved rather than (fixed) pathological changes. Are We observe whether a ventral or dorsal overhang is pres- there problems of micturition or defecation? Small children may need to stand on a box so that the iliac crest is at the examiner’s eye level. Girls who have reached puberty should also a be allowed to wear their brassiere. In order to assess posture-related muscle performance, 3 Matthiass has proposed the arm-raising test. The child is asked to stand as straight as possible and raise his arms and keep them in a horizontal position. A child or adoles- cent with normal postural capacity is able to maintain this position, in contrast with a child with postural weakness (⊡ Fig. We now ask the child to bend down as far as pos- sible while keeping the knees perfectly straight. Nor- a b mally, children and adolescents should be able to touch the floor with their fingertips or even place the whole palm of their hand on the floor. Ventral and b dorsal overhang: A vertical line from the cen- measure the distance from the fingertips to the floor in ter of the shoulders falls in front of or behind the center of the ankle a b c d e ⊡ Fig. Pelvic tilt: The forward and downward pelvic tilt in relation back, d hollow-flat back, e flat back to the horizontal is normally approx. Arm-raising test according to Matthiass:The child is asked to maintain this position (a), in the case of a postural weakness this to stand as straight as possible and raise his arms and keep them in a posture is lost (b), while a child with extremely weak muscles cannot horizontal position.

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Boutonnière Deformity Swan Neck Deformity (Calliet buy lumigan 3 ml cheap, 1982) (Figure 3–2) Mechanism Contracture of the intrinsic and deep flexor muscles and tendons of the fingers Result Flexion contracture of the MCP Hyperextension of the PIP Flexion of the DIP Orthotic Swan neck ring splint FIGURE 3–2 3 ml lumigan sale. Swan Neck Deformity 86 RHEUMATOLOGY Ulnar Deviation of the Fingers (Calliet discount 3ml lumigan mastercard, 1982) Mechanism Weakening of the extensor carpi ulnaris (ECU) order 3ml lumigan otc, ulnar and radial collateral ligament Wrist deviates radially Increases the torque of the stronger ulnar finger flexors Flexor/extensor mismatch deviates the fingers in the ulnar direction as the patient tries to extend the joint Result Ulnar deviation is due to the pull of the long finger flexors Orthotic Ulnar deviation splint Tenosynovitis of the Flexor Tendon Sheath One of the most common manifestation of the hands in RA Can be a major cause of hand weakness Result Diffuse swelling of the volar surfaces of the phalanges between the joints with palpable grating of the flexor tendon sheath May be confused with deQuervain’s disease DeQuervain’s disease Tenosynovitis of the extensor pollicis brevis (EPB) and abductor pollicis longus tendon (APL) Thickening of the tendon sheath results in tenosynovitis and inflammation Pain over the tendons on the radial wrist EPB and APL Test: Finkelstein Test (Figure 3–3) Full flexion of the thumb into the palm followed by ulnar deviation of the wrist will produce pain and is diagnostic for deQuervain’s tenosynovitis FIGURE 3–3 order 3 ml lumigan with mastercard. Finkelstein’s Test: Full flexion of the thumb into the palm will produce pain when the wrist is deviated in the ulnar direction. Rosemont, Illinois: American Academy of Orthopaedic Surgeons, 1997, with permission. RHEUMATOLOGY 87 Carpal Bones Rotate in Zig-Zag Pattern Mechanism Ligament laxity Radial deviation of the wrist Ulnar styloid rotates dorsally Carpal bones rotate – Proximal row: volarly – Distal row: dorsally Result Zig-zag pattern Floating Ulnar Head (Piano-Key Sign, Think of the Black Keys) Mechanism Proliferating synovium leads to rupture or destruction of the ulnar collateral ligament Result The ulnar head raises up to the dorsal wrist Easily compressible elevated ulnar styloid Ulnar head floats Resorptive Arthropathy Mechanism Digits are shortened and phalanges appear retracted with skin folds Result Telescoping appearance of the digits Most serious arthritic involvement Pseudobenediction Sign Mechanism Stretched radioulnar ligaments allow the ulna to drift upward Extensor tendons of the fourth and fifth digit are subject to abrasion from rubbing on the sharp elevated ulnar styloid Result Extensor tendon rupture Inability to fully extend the fourth and fifth digit Cervical Spine Atlantoaxial Joint Subluxations → Most Common are Anterior Subluxations Instability – Odontoid or Atlas can erode – With flexion, the Atlantoaxial (AA) space should not increase significantly: any space larger than 2. The MCP is thought to be the primary site of RA and inflammation can lead to weakening of joint supporting structures. Insidious Onset Surgical Options Synovectomy Arthroplasty Arthrodesis Tendon repairs TABLE 3–1. Treatment Options for Rheumatoid Arthritis (Verhoeven, 1998) Poor Prognostic Disease Stage Features Treatment Medications 1. Compliance antirheumatic drug (DMARD) Hydroxychloroquine Sulfasalazine Oral gold Moderately (+) 1. Compliance Weekly oral or parental methotrexate May add a second DMARD 3. Corticosteroids PT = Physical Therapy OT = Occupational Therapy NSAID = non-steroidal anti-inflammatory drugs DMARD = disease modifying anti-rheumatic drug RHEUMATOLOGY 93 TABLE 3–2. Drugs Used in Rheumatoid Arthritis and Common Side Effects (Gerber, Hicks, 1995) DMARDs General (Disease Modifying Degree of Anti-rheumatic Drugs) Toxic Profile Toxicity Hydroxychloroquine Macular damage Safer Sulfasalazine Myelosuppression, gastrointestional (GI) distrubances Safer Auranofin GI disturbances, diarrhea, nausea, vomiting, anorexia, rash pruritus, conjunctivitis, stomatitis, anemia, thrombocytopenia, proteinuria, elevated liver enzymes Safer Methotrexate Stomatitis, myelosuppression, hepatic fibrosis, cirrhosis, pulmonary involvement, worsens rheumatoid nodules More toxic Cyclosporine Renal dysfunction, tremor, hirsutism, hypertension, gum dysplasia More toxic Gold, Intramuscular, Myelosuppression, renal → proteinuria Oral Diarrhea (#1, oral), Rash (#1, Intramuscular) More toxic Azathioprine Myelosuppression, hepatotoxicity, lymphoproliferative disorders More toxic D-Penicillamine Oral ulcers, bone marrow suppression induction of autoimmune disease, proteinuria More toxic Chlorambucil Bone marrow suppression, GI disturbances, nausea, vomiting, diarrhea, oral ulceration, central nervous system (CNS) dis- turbances, tremors, confusion, seizures, skin hypersensitivity, pulmonary fibrosis, hepatotoxicity, drug fever peripheral neuropathy, infertility, leukemia and 2˚ malignancies Very toxic Cyclophosphamide Carcinogenesis, impairment of fertility, mutagenesis, GI disturbances, nausea, vomiting, anorexia, alopecia, leukopenia, thrombocytopenia, anemia, cystitis, urinary bladder fibrosis, interstitial pulmonary fibrosis, anaphylactic reaction Very toxic Other Drugs for the Treatment of Rheumatoid Arthritis Toxic Profile ASA, NSAID GI ulceration and bleeding Therapeutic levels for ASA 15 mg/dl–25 mg/dl Toxic > 30 mg/dl Corticosteroids Hyperglycemia, inhibits immune response, osteoporosis, peptic ulcer disease, emotional liability 94 RHEUMATOLOGY OSTEOARTHRITIS (OA) DEFINITION A noninflammatory progressive disorder of the joints leading to deterioration of the articular cartilage and new bone formation at the joint surfaces and margins Disease of the cartilage initially, not bone PREVALENCE Most common form of arthritis and the second most common form of disability in the United States Prevalence increases with age: approximately 70% population > 65 years old have radio- graphic evidence of osteoarthritis (Lane, 1997) Increase in occupations with repetitive trauma Male:female ratio is equal between the ages of 45–55. Because of this, it is suggested that spondyloarthropathies in children include another syndrome, Seronegative Enthesopathy and Arthropathy (SEA) SEA Syndrome – (–) RF – (–) ANA – Enthesitis and either arthritis or arthralgia RHEUMATOLOGY 101 TABLE 3–4. Key Points of Juvenile Arthritides JUVENILE RHEUMATOID ARTHRITIS SYSTEMIC JUVENILE Multisystemic POLYARTICULAR SPONDYLO- Involvement Many joints PAUCIARTICULAR ARTHROPATHIES RF(–) (~98%) RF(–) (90–95%) RF(–) (> 98%) Ankylosing Still’s Disease No extraarticular 1–4 joint involvement Spondylosis (AS) High fever manifestations of Few systemic effects Reiter’s Rheum. Chronic Iridocyclitis: Psoriatic arthritis Lymphadenopathy Gradual onset of: < 6 yrs. RA Both have synovial inflammation that can lead to destruction of articular cartilage and ankylosis of the joint Ankylosing Spondylitis Rheumatoid Arthritis More common in males More common in females Absence of rheumatoid nodules Presence of rheumatoid nodules RF (–) RF (+) in 85% of cases Prespinous calcification RHEUMATOLOGY 105 Clinical Manifestations Skeletal Involvement Sites of Involvement in AS Insidious onset, back pain or tenderness 1→ SI joint in the bilateral SI joint 2→ Lumbar Vertebrae – First site of involvement is SI joint 3→ Thoracic Vertebrae – Initially asymmetric 4→ Cervical Vertebrae Persistent symptoms of at least three months Lumbar morning stiffness that improves with exercise Lumbar lordosis—decreased and thoracic kyphosis—increased Cervical ankylosis develops in 75% of the patients who have AS for 16 years or more Lumbar spine or lower cervical is the most common site of fracture Enthesitis (An inflammatory process ocurring at the site of insertion of muscle. On forward flexion, the line should increase by greater than 5 cm to a total of 20 cm or more (from 15 cm) – Any increase less than 5 cm is consid- ered a restriction Treatment Education FIGURE 3–4 – Good posture – Firm mattress, sleep straight—Supine or prone – Prevent flexion contractures Physical Therapy – Spine mobility—Extension exercises – Swimming is ideal – Joint protection Pulmonary—Maintain chest expansion – Deep breathing exercises – Cessation of smoking Medications – NSAIDs—Indocin Control pain and inflammation Allow for physical therapy RHEUMATOLOGY 107 – Corticosteroids—Tapering dose, PO and Injections – Sulfasalazine Improves peripheral joint symptoms Modify disease process – Methotrexate – Topical corticosteroid drops—Uveitis REITER’S SYNDROME ~ 3%–10% of Reiter’s Triad of Reiter’s Syndrome progress to AS 1. Nongonococcal urethritis Epidemiology Males >> females Organisms → Chlamydia, Campylobacter, Yersinia, Shigella, Salmonella More common in whites Associated with HIV Clinical Manifestations Arthritis Arthritis appears 2 to 4 weeks after initiating infectious event—GU or GI Asymmetric Oligoarticular—average of four joints – LE involvement >> UE – More common in the knees, ankles, and small joints of the feet – Rare hip involvement – UE → Wrist, elbows, and small joints of the hand Sausage digits (dactylitis) – Swollen tender digits with a dusklike blue discoloration – Pain on ROM Enthesopathies—Achilles tendon – Swelling at the insertion of tendons, ligaments, and fascia attachments Low back pain—Sacroilitis Ocular Conjunctivitis, iritis, uveitis, episcleritis, corneal ulceration Genitourinary Urethritis, meatal erythema, edema Balanitis Circinata—small painless ulcers on the glans penis, urethritis Skin and Nails Keratoderma blennorrhagica—hypertrophic skin lesions on palms and soles of feet Reiter’s Nails—thickened and opacified, crumbling, nonpitting Cardiac Conduction defects 108 RHEUMATOLOGY General Weight loss, fever Amyloidosis Lab Findings Synovial fluid—inflammatory changes Reiter’s Syndrome: Synovial Fluid Turbid Poor viscosity WBC 5-50,000-PMN ↑ protein, normal glucose Increased ESR RF (–) and ANA (–) Anemia–normochromic/normocytic (+) HLA B27 Radiographic Findings “Lover’s Heel”—erosion and periosteal changes at the insertion of the plantar fascia and Achilles tendons Ischial tuberosities and greater trochanter Asymmetric sacroiliac joint involvement Syndesmophytes Pencil in cup deformities of the hands and feet—more common in psoriatic arthritis PSORIATIC ARTHRITIS Prevalence ~5% to 7% of persons with psoriasis will develop some form of inflammatory joint disease Affects 0. Seronegative Spondyloarthropathy Fact Sheet The following are all Seronegative Spondyloarthropathies. Arthritis of Inflammatory Bowel Disease Arthritis of All have the following Ankylosing Reiter’s Psoriatic Inflammatory characteristics: Spondyloarthropathy Syndrome Arthropathy Bowel Disease 1. RF (–) RHEUMATOLOGY 111 CTD (CONNECTIVE TISSUE DISORDERS) AND SYSTEMIC ARTHRITIC DISORDERS MCTD: MIXED CONNECTIVE TISSUE DISORDERS Combination 1. Polymyositis SYSTEMIC LUPUS ERYTHEMATOSUS Diagnosis of SLE Multisystemic disease, autoimmune Any 4 of 11 criteria present Females > > > males Serially and simultaneously Criteria—American Rheumatologic Association (ARA) 1. Arthritis—Nonerosive arthritis involving two or more peripheral joints with tender- ness, swelling and effusion 6. Hematologic disorder—Hemolytic anemia, leukopenia, thrombocytopenia, lymphopenia 10. Immunologic—(+)LE cell preparation or Anti-DNA antibody, or Anti-SM, false positive test for syphilis 11. ANA Clinical Fatigue, fever, weight loss, GI complaints Alopecia Vasculitis Arthritis Jaccoud’s Arthritis – Small joints of the hands, wrist, Nonerosive deforming arthritis and knees Ulnar deviations of the fingers and sublux- – Symmetric ations which are reversible early – Migratory, chronic, nonerosive May become fixed – Soft tissue swelling – Subcutaneous nodules – Synovial analysis—ANA (+) – Jaccoud’s arthritis Arthralgias Muscle pain and weakness 112 RHEUMATOLOGY Labs Depressed complement—C3 and C4 Ds-DNA Anti-SM Treatment NSAIDs, corticosteroids, antimalarials, methotrexate, cyclophosphamide, azathioprine, cyclosporine A PROGRESSIVE SYSTEMIC SCLEROSIS (SCLERODERMA) Progressive Chronic Multisystem Disease Classified by the degree of skin thickening Fibrosis-like changes in the skin and epithelial tissues of affected organs Subsets: – Diffuse Cutaneous Scleroderma Heart, lung, GI, kidney ANA(+) Anticentromere Antibody (–) Rapid onset after Raynaud’s phenomenon Variable course—poor prognosis – Limited cutaneous Scleroderma—CREST Syndrome Crest Syndrome Progression after Raynaud’s phenomenon Calcinosis Anticentromere Antibody (+) Raynaud’s phenomenon Good prognosis Esophageal dysmotility – Overlap syndromes Sclerodactyly Combinations of connective tissue disease Telangiectasia – Undefined CTD No clinical or laboratory findings – Localized scleroderma Morphea, linear scleroderma Clinical Skin thickening—face, trunk, neck Symmetric arthritis with involvement of the fingers, hands, arm, legs Initial symptoms—Raynaud’s phenomenon with fatigue, and musculoskeletal complaints Raynaud’s Phenomenon Vasospasm of the muscular digital Causes of Raynaud’s arteries can lead to ischemia, Collagen vascular disease—PSS, ulceration of the fingertips SLE, RA, Dematomyositis/ Triggered by cold and emotional stresses Polymyositis Reversal of episode occurs after Arterial occlusive disease stimulus has ended—and digits rewarmed Pulmonary HTN Present in 90% of patients with scleroderma Neurologic—SCI, CVA Treatment Blood dyscrasia – Education against triggers—cold, smoking Trauma – Rewarming Drugs—ergots, beta blockers, – Calcium channel blockers—nifedipine cisplatin – EMG and biofeedback—self-regulation (Braunwald, et al. ANA AND RF ANA RF MCTD + + RA + + SLE + – Scleroderma (PSS) + – Polymyositis + – Sjögren’s + + (+) HLA-B27 A S Reiter’s Psoriatic arthritis Enteropathy arthropathy Pauciarticular JRA RHEUMATOLOGY 115 VASCULITIS POLYARTERITIS NODOSA Systemic necrotizing vasculitis Male:female ratio is 2:1 Also seen in: Small, medium artery involvement R Glomerulonephritis—#1 cause of death SLE Lungs spared Sjögren’s Skin—palpable purpura Mononeuritis multiplex, arthritis GIANT CELL ARTERITIS: ALSO KNOWN AS TEMPORAL ARTERITIS (TA) More common in females > 50 years old Large arteries Tenderness of the scalp and in the muscle of mastication Headaches, abrupt visual loss in 15% of patients Diagnosis: Elevated ESR, temporal artery biopsy Treatment: High dose steroids imperative to prevent permanent visual loss Polymyalgia Rheumatica (PMR) In view of clinical similarities between PMR patients with and without signs of arteritis in a temporal artery biopsy, many authors believe that PMR is an expression of giant cell arteritis Fever, weight loss, malaise Proximal muscles—neck, pelvic Shoulder Morning stiffness—muscle tenderness Abrupt myalgias/arthralgia Diagnosis: ↑ ESR > 50 Treatment: steroids WEGENER’S GRANULOMATOSIS Small artery involvement Male, middle aged Necrotizing granulomatous vasculitis involving – Upper/lower respiratory tract – Focal segmental glomerulonephritis “Saddle-nose” deformity Pulmonary, tracheal, ocular, and cutaneous manifestation 116 RHEUMATOLOGY TAKAYASU Elastic large arteries—Aorta Asian females, 40 years old Erythema nodosum on the legs Pulselessness, arm claudication BEHÇET’S Small vessels Oral and genital skin ulcers 20% experience venous thrombosis GOODPASTURE’S Pulmonary and kidney involvement SJÖGREN’S SYNDROME Autoimmune-mediated disorder of the exocrine glands CLINICAL PRESENTATION: (sicca symptoms) Dry eyes Dry mouth Skin lesions Parotid involvement LABS: ANA (+), RF (+) Classification: Primary and secondary forms Primary—Dry eyes and mouth with ANA (+) , RF (+) Secondary—sicca symptoms – Sjögren’s syndrome plus evidence of SLE, RA, PSS, Polymyositis EXTRAGLANDULAR MANIFESTATIONS Arthralgias Raynaud’s phenomenon RHEUMATOLOGY 117 ARTHRITIS AND INFECTIOUS DISORDERS SEPTIC ARTHRITIS Clinical Picture: Septic Arthritis Rapid onset of moderate to severe joint pain, erythema, and decreased ROM Monoarticular, leukocytosis Knee is the most common joint Risk factors—age, prosthetic joints, comorbidities such as anemia, chronic diseases, hemophilia. Coli) Bone scans 118 RHEUMATOLOGY Treatment Antibiotic coverage Frequent needle aspirations with arthroscopic lavage TABLE 3–7. Joint Fluid Analysis Property Normal Noninflammatory Inflammatory Septic Viscosity High High Low Variable Color Colorless Straw Yellow Turbid-Yellow Clarity Transluscent Transluscent Transluscent Opaque WBC < 200 < 5000 1000–75000 > 100,000 PMN% < 25 < 25 > 50 > 85 Culture Negative Negative Negative Positive Mucin clot Good Good Fair Poor Glucose Equal to blood Equal to blood < 50 mg/dl > 50 mg/dl lower than lower than blood blood OTHER INFECTIOUS CAUSES OF ARTHRITIS Viral Infections—Rubella, infectious hepatitis Fungi—Seen in Immunocompromised adults Mycobacterium—tuberculosis of the spine (Pott’s disease) – Thoracic involvement – TB arthritis—Hips and knees Monoarticular Radiologic findings—Phemister’s triad Juxta-articular osteoporosis Marginal erosions Joint space narrowing Lyme Disease – Tick borne—Borrelia burgdorferi – Classic presentation Erythema migrans—bull’s eye rash Cardiac, neurologic, articular manifestations – Intermittent migratory episodes of polyarthritis – Commonly affects the knee – Synovial fluid—Inflammatory – Diagnosis—ELISA, Western blot analysis – Management—First-line antibiotics: Adults: Doxycycline Children: Amoxicillin – Pattern of Onset: Bite Rash Systemic dz. Neurologic involvement RHEUMATOLOGY 119 DEPOSITION AND STORAGE DISEASE HEMOCHROMATOSIS Organ damage and tissue dysfunction secondary to excessive iron stores and the deposi- tion of hemosiderin Organs → Hepatic cirrhosis, cardiomyopathy, DM, pituitary dysfunction Skin pigmentation Chronic progressive arthritis – Occurs commonly in second and third MCP, PIP joints. It may also affect the hip joints Males ~40–50 years old Treatment: Phlebotomy, NSAIDs ALKAPTONURIA (OCHRONOSIS) Autosomal recessive Deficiency in the enzyme homogentisic acid oxidase leads to its increase Alkalinization and oxidation causes darkening of tissue parts termed ochronosis – Blueish discoloration of the urine, cartilage, skin, sclera secondary to the accumulation of homogentisic acid Progressive degenerative arthropathy – Onset—in the fourth decade – Spinal column involvement – Arthritis of the large joints, chondrocalcinosis, effusions, osteochrondral bodies WILSON’S DISEASE Autosomal recessive Deposition of copper leads to destruction: – Liver leading to cirrhosis – Brain – Kidneys – Ocular—Kayser-Fleischer rings OA—wrists, MCP, knees, spine Osteoporosis Treatment: Copper chelation with penicillamine, dietary restriction GAUCHER’S DISEASE Autosomal recessive—Ashkenazi Jews Glucocerebroside accumulates in the reticuloendothelial cells of the spleen, liver, and bone marrow Monoarticular hip and knee degeneration 120 RHEUMATOLOGY OTHER SYSTEMIC DISEASES SARCOIDOSIS Systemic chronic granulomatous disease—can affect any organ system Pathogenesis: disseminated noncaseating granulomatous Eight times more common in blacks, females > males Clinical features: – Pulmonary – Hilar adenopathy – Fever, weight loss, fatigue – Arthritis: polyarthritis, 4-6 joints Knees, PIP, MCP, wrists – Skin—Lofgren’s Syndrome – Arthritis, Hilar adenopathy, Erythema nodosum AMYLOIDOSIS Homogeneous eosinophilic material seen with Congo red dye Deposition of amyloid in the kidneys, liver and spleen Clinical features: – Renal disease is primary clinical feature – Cardiomyopathy – Median neuropathy – Pseudoarthritis—periarticular joint inflammation – Effusions: Arthrocentesis—“Shoulder-pad” sign HEMOPHILIA ARTHROPATHY X-linked recessive disorder, predominately in males—associated with HIV 2° to transfu- sions of factor and blood Blood coagulation disorder caused by Factor VIII deficiency (classic hemophilia A) and Factor IX deficiency (Christmas disease, hemophilia B) Bleeding into bones and soft tissue causes hemarthrosis, necrosis and compartment syn- drome Elbow, knee, wrist are common Arthritis is caused by the remaining blood in the joint depositing hemosiderin into the synovial lining → proliferation of the synovium and pannus formation Radiologic: Joint space narrowing, subchondral sclerosis and cyst formation Treatment: Conservative care (immobilization, rest, ice), Factor VIII replacement, reha- bilitation, joint aspiration as a last resort SICKLE-CELL DISEASE Biconcave RBC changes to an elongated crescent sickle-shape causing obstruction of the microvasculature Musculoskeletal complications: – Painful crisis—Most common event Abdomen, chest, back Pain in the large joints from juxta-articular bone infarcts with synovial ischemia RHEUMATOLOGY 121 – Dactylitis—“Hand-Foot” Syndrome Painful non-pitting swelling of the hands and feet – Osteonecrosis Local hypoxia with occlusion to the venous system by the sickled cells 1/3 femoral heads and 1/4 humeral heads go on to osteonecrosis – Osteomyelitis—most commonly caused by Salmonella NEUROPATHIC ARTHROPATHY (CHARCOT’S JOINT) DEFINITION Chronic progressive degenerative arthropathy, secondary to a sensory neuropathy with loss of proprioception and pain sensation, leading to instability and joint destruction CAUSES → “STD” “SKA” → SHOULDER, KNEE, ANKLE Syringomyelia → Shoulder Tabes dorsalis # 2 → Syphilis → Knee Diabetic Neuropathy → # 1 cause → Ankle CLINICAL Early findings: Painless swelling, effusion and joint destruction Late findings: Crepitation, destruction of cartilage and bones, intra-articular loose bodies Subtle fractures RADIOLOGIC Joint destruction Hypertrophic osteophytes Loose bodies caused by micro fractures Disorganization of the joint—Subluxation and dislocation TREATMENT Immobilization Restriction of weight bearing Charcot Joint vs.

Graphical presentations of steady state and exercise can continue for an extended the domains (moderate cheap lumigan 3ml with mastercard, heavy cheap 3ml lumigan visa, and severe) are pre- period of time purchase lumigan 3ml fast delivery. In panel in VO2 beyond the 3rd min is observed when exercise is one discount lumigan 3ml visa, the lactate threshold (TLac) represents the bound- above the lactate threshold cheap lumigan 3 ml online. The upper boundary of the heavy gradually increases until it reaches a steady state. TLac represents the lactate threshold and Wa represents critical power or work rate where maximal lactate at steady state occurs. This term, O2 debt, was coined lifted, and is expressed as a percent of the maximum by AV Hill in the early 1900s, but is transitioning to weight (1RM). If the 1RM for a particular exercise excess postexercise oxygen consumption (see is 80 kg, then a weight of 40 kg would be a 50% and below). It is The specificity principle states that physiological, neu- highly correlated with exercise intensity, and the fast rological, and psychological adaptations to training are portion may reflect resynthesis of stored PC and specific to the “imposed demand. The slow develop speed, power, and specific metabolic path- component may reflect elevated body temperature, ways, the imposed demand must target those specific catecholamines, accelerated metabolism (conversion areas. Low numbers of repetitions (6–10 RM) are associated with increases in strength and high num- Resistance exercise is used to improve muscular fit- bers (20–100 RM) are associated with increases in ness, which is a combination of strength, endurance, endurance. Strength is the greatest force a muscle can tion from strength to endurance. The primary components to muscle hypertrophy include a neural response, followed by an upregulation WEIGHT TRAINING PARAMETERS of second messenger systems to activate the family of W hen training with weights, the magnitudes of immediate early genes that dictate the responses of increase in muscle strength and endurance depend on contractile protein genes, and message passing down the specific training parameters: repetitions, sets, to alter protein expression. The Repetition maximum: The amount of force a subject new contractile proteins appear to be incorporated can lift a given number of repetitions defines repeti- into existing myofibrils and there may be a limit to tion maximum (RM). For example, 1RM is the maxi- how large a myofibril can become: they may split at mal force a subject can lift with one repetition and some point. Hypertrophy results primarily from 5RM would be the maximal force someone could lift growth of each muscle cell, rather than an increase in five times. For examples, repetitions could be 5, 10, Physiologic adaptations and performance are linked 12, 25, or 50. For BIOMECHANICAL FACTORS IN MUSCLE STRENGTH example, a training session could consist of three sets Neural control, muscle cross-sectional area, arrange- of 12 repetitions. For example, if the ity, strength-to-mass ratio, body size, joint motion session was three sets of 12 repetitions, the volume (joint mobility, dexterity, flexibility, limberness, and would be 3 × 12 or 36 repetitions. Volume indicates range of motion), point of tendon insertion, and the how much work was done: the greater the volume, the interactions of these factors influence muscle greater the total work. CHAPTER 8 BASICS IN EXERCISE PHYSIOLOGY 45 DELAYED-ONSET MUSCLE SORENESS different VO2max values. Tom would be working at Delayed-onset muscle soreness (DOMS) is a term 2. It is usually noted the day after the exercise and may ADAPTATIONS TO TRAINING last 3 to 4 days. The force generated RESISTANCE TRAINING by a lengthening contraction (eccentric) can be Resistance training induces a variety of adaptations, markedly increased if it is followed by a shortening with clear increases in strength. EXERCISE TRAINING Fiber type specific adaptations induced by resistance training depend on volume and intensity, but a PRINCIPLES OF TRAINING common change is an increase in the percentage of Type IIa fibers, at the expense of the Type IId(x/b) FITT: This is an acronym to describe a physical train- fibers. Resistance training is not usually associated ing variable that can be altered to achieve various fit- with increases in VO2max, but may enhance overall car- ness goals. FITT stands for frequency, intensity, time diovascular function by improving strength that (duration), and type of exercise. ESTIMATING STRENGTH Periodization: This is a technique that involves alter- AND ENDURANCE ing training variables (repetitions/set, exercises per- formed, volume, and rest interval between sets) to AEROBIC AND ANAEROBIC POWER achieve well-defined gains in muscular strength, endurance, and overall performance for a specific Simple in-office and field tests can be used to estimate event. These include the 2-mi run, 12-min run, and 2max the body ready for a new activity–about 4 weeks), fol- the 3-min step test. Other tests include submaximal lowed by strength development (4 to 7 weeks) and cycle ergometry. Tests for anaerobic power include then muscular endurance (8 to 12 weeks). Rodriguez LP, Lopez-Rego J, Calbet JA, et al: Effects of training number of push-ups, pull-ups, and/or sit-ups, as well status on fibers of the musculus vastus lateralis in professional as hand grip dynamometry (sustained submaximal road cyclists. Testing and Interpretation: Including Pathophysiology and Clinical Applications, 3rd ed.

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