autoimmune_arthritis_collegendiseases_20.ppt

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Unformatted text preview: Autoimmune Disorders /Arthritis Janet Czermak –Russell APRNBC TYPES: ARTHRITIS Pyrogenic -(Septic, Infective) Psoriatic Rheumatoid (Rheumatoid Polyarthritis) Tuberculosis Osteoarthritis Gouty SEPTIC ARTHRITIS Bacterial Infection In The Synovium And Joint Space Causing Inflammation,> Leukocytes,> Release Of Proteolytic Enzymes PREDISPOSING FACTORS : Trauma, Rheumatoid Arthritis, Diabetes, Steroid Administration, Renal Failure, Malignancy, Drug Abuse, Vascular Insufficiency, Orthopedic Surgery MOST COMMON SITES : Knee 53 % Hip 20 % Elbow 17 % Shoulder 11 % Wrist 9 % Ankle 8 % Common Bacteria Found : Staph Aureus, 50% Streptococcus 20 % Pneumococcal 10% Gonorrheal < 5 % Hemophilus Influenza esp.in children 15% SIGNS /SYMPTOMS Severe Pain, Constant Awaken Out of Sound Sleep Loss of Motion Joint Effusion Swollen, Hot Joint Fever LABORATORY VALUES WBC COUNT 50,000 -100,000 80% POLYMORPHONUCLEAR CELLS, < GLUCOSE LEVEL, > SEDIMENTATION RATE MEDICAL MANAGEMENT Bed Rest Antibiotic (Triple) Aspiration of The Fluid. Elevation of Extremity Ice Pack. Psoriatic Arthritis Inflammatory process associated with psoriasis etiology unknown Psoriatic arthritis- spondyloarthropathies. strong genetic influences increased risk of psoriasis (30% to 50%) or psoriatic arthritis (15%) in first-degree relatives. HLA-C allele Cw0606 is the strongest genetic marker for psoriasis and contributes to the type 1 phenotype (early onset before age 40) of severe psoriasis but delayed appearance of arthritis. Elevated serum immunoglobulins, fibroblast activity Affects tendons, ligaments, fascia and joints Clinical Manifestations cellular immune system with CD8+ T cells both the skin / synovium. Psoriatic synovium- characterized hypervascularity/ and tortuous vessels. Angiogenic growth factors- vascular endothelial growth factor (VEGF)/transforming growth factor (TGF) beta are over-expressed osteoclast proliferation and activation, contributing –erosions/osteolysis. radiologic changes - arthritis mutilans, including pencil-in-cup deformities and newbone formation of periostitis distal interphalangeal (DIP) joint involvement and dactylitis uniquely distinguish psoriatic arthritis from rheumatoid arthritis. extensor tendon enthesitis at the nail bed and flexor tenosynovitis of the entire digit. joint synovitis. Pain Stiffness – worse with immobility Polyarthritis Dactylis –swelling meta and interphalanges Medical Management NSAIDS/COX-2 DMARDS Anti-tumor necrosis factorEtanercept/Infliximab Physical therapy helps improve range of motion and pain as well as muscle strengthening of joints with associated periarticular muscle atrophy. Emerging treatments Alefacept -is a lymphocyte function-associated antigen3/immunoglobulin G fusion protein. Ustekinumab- is a human monoclonal antibody that inhibits the receptor binding of interleukins 23 and 12 (proinflammatory cytokines increasing production of Th17 lymphocytes). Rheumatoid arthritis affected 1,292,000 adults in 2005 1990 estimate of 2.1 million adults average age at diagnosis has increased steadily over time from 63.3 years in 1965 to 66.8 years in 1995. PATIENT PROFILE Peaks 4th-6th Decade of Life Female ( 2-3 X More Than Men) All Racial/Ethnic Groups Reduced Life Expectancy Genetic Factors • Identical Twins 32 % Incidence • Hla-dr4 Short Arm Chromosome #6 (Caucasians) • Hla-dr10 –5 study in South Africa found (Hindus/Tamils Rheumatoid Arthritis: Key Features (cont’d) • • May have nodules: subcutaneous or periosteal at pressure points Rheumatoid factor • • • • 45% positive in first 6 months 85% positive with established disease Not specific for RA, high titer early is a bad sign Marginal erosions and joint space narrowing on x-ray Adapted from Arnett, et al. Arth Rheum. 1988;31:315–324. Rheumatoid Arthritis: Key Features • • • Symptoms >6 weeks’ duration • Often lasts the remainder of the patient’s life Inflammatory synovitis • Palpable synovial swelling • Morning stiffness >1 hour, fatigue Symmetrical and polyarticular (>3 joints) • Typically involves wrists, MCP, and PIP joints • Typically spares certain joints Thoracolumbar spine DIPs of the fingers and IPs of the toes SEVEN DIAGNOSTIC CRITERIA FOR RHEUMATOID ARTHRITIS (RA) 1. Morning stiffness for > one hour 2. Arthritis of at least 3 areas at one time lasting > 6 weeks 3. Arthritis of hand joints lasting > 6 weeks 4. Symmetrical arthritis lasting 6 weeks 5. Rheumatoid nodules 6. Serum Rheumatoid Factor (RA) - Positive, • > Sed Rate, > C-Reactive Protein 7. Radiographic Changes- bony erosion, or juntaarticular osteopenia * Individual has 4 or more of the criteria, diagnosis of RA is made AUTOANTIBODY AGAINST IMMUNOGLOBIN G, ANTI-KEARATIN AND ANTI- PERINUCLEAR FACTOR- PREDICTIVE MARKERS IN THE DEVELOPMENT OF RA Rheumatoid Arthritis: PIP Swelling is Swelling confined to the area of the joint capsule Synovial thickening feels like a firm sponge CLINICAL MANIFESTATIONS Boutonniere Deformity of the finger, with Hyperextension of the distal phalangeal joint and flexion of proximal joint interphalangeal joint Swan –Neck deformity of the finger, with hyperextension at the proximal interphalageal joint and flexion of the distal interphalageal joint Ulnar deviation of the metacarpophalangeal joints Compression of the carpal bones Subluxation of the wrist Critical Elements of a Treatment Plan: Assessment • • • • Assess current activity • Morning stiffness, synovitis, fatigue, ESR Document the degree of damage • ROM and deformities • Joint space narrowing and erosions on x-ray • Functional status Document extra-articular manifestations • Nodules, pulmonary fibrosis, vasculitis Assess prior Rx responses and side effects Rheumatoid Arthritis is Systemic Inflammatory Disease Critical Elements of a Treatment Plan: Assessment • Assess current activity • • Document the degree of damage • • • • ROM and deformities Joint space narrowing and erosions on x-ray Functional status Document extra-articular manifestations • • Morning stiffness, synovitis, fatigue, ESR Nodules, pulmonary fibrosis, vasculitis Assess prior Rx responses and side effects Critical Elements of a Treatment Plan: Assessment • • • • Assess current activity • Morning stiffness, synovitis, fatigue, ESR Document the degree of damage • ROM and deformities • Joint space narrowing and erosions on x-ray • Functional status Document extra-articular manifestations • Nodules, pulmonary fibrosis, vasculitis Assess prior Rx responses and side effects Pathologies with RA Carpal Tunnel Syndrome Rheumatoid nodules Rheumatoid vasculities Peripheral neuropathy Mild pulmonary obstructive disease Pericarditis Increased liver enzymes, Alkaline Phosphate Ketoconjuctivitis Sjogren syndrome MEDICATIONS : NSAIDS & COX 2 INHIBITORS METHOTREXATE CORTICOSTEROIDS NARCOTICS GOLD CYTOXAN Immunosuppressant therapy • Cyclosphosphamide • Azathioprine MEDICAL MANAGEMENT Rest Splints Physiotherapy(Heat) ADL Activity Sjogren Syndrome -Triad 1.Ketoconjunctivitis sicca 2.Xerostomia 3.Connective tissue disease Characterized by CD4 lymphocytes and destruction of lacrimal salivary glands Results: dry eyes, dry mouth, and waxing and waning poly arthritis Schrimer test-tear production; parotid gland flow; lip biopsy Other features are cardiovascular and neurovascular Lyme Disease Bacteria infectionBorrelia burgdorferi Black-legged ticksdeer ticks • Ixodes scapularisnortheast/north central US • Ixodes pacificuswestern part of US Outdoor activities • Gardening, hiking, camping, forestry Pathophysiology Infected tick-attaches to human-suck’s the blood and transmits the disease Three stages • Early localized disease • Early disseminated disease • Late or chronic disease Stages Early localized disease Erythema –where bite occurred Fatigue, malaise, stiff neck, lymphadenopathy Early disseminated disease • Carditis - cardiomyopathy • Neurological- meningitis, peripheral neuropathy , myelitis • Musculoskeletal – polyarthritis • Skin- erythema nodosum • Liver – hepatitis • Kidney – Treatment • Antibiotic therapy Osteoarthritis most common type of arthritis affecting 67 million Americans. Increasing with age affects the hands and knees of women more frequently than men African-Americans more frequently than whites. Osteoarthritis chronic degenerative wear and tear process noninflammatory disorder of movable joints degeneration of articular cartilage formation of new bone at joint surfaces/margins also known as degenerative joint disease RISK FACTORS FOR QA Age Major joint disease trauma Mechanical nature - Previous orthopedic injury, fracture, torn meniscus, or mal-alignment • Repetitive stress and joint overload Obesity Race Genetic factors Female gender Congenital and Developmental defects Quadriceps weakness knee QA) Metabolic /Endocrine disorders Diabetes, Acromegaly Gout, Paget’s disease Osteoarthritis- Pathology Articular surfaces of cartilage with bony formation of the weight bearing joints Early degeneration or disruption of bone called flaking, fibrillation Bone becomes- hard and glossyeburnation Outgrowths of ossified cartilage Osteophytes Thickening /Fibrosis of synovial joint OsteoarthritisClinical Manifestations Morning stiffness, pain on motion-overuse of joint, localized tenderness, crepitation, joint deformity Heberden’s Nodes : detectable bony enlargements- (DIP) distal interphangeal joints of the hand Bouchard’s Node’s Bony enlargement in the proximal interphangeal joints (PIP) WEIGHT BEARING JOINTS :Knees, hips, cervical and lumbar vertebrae, proximal and distant joints of hands and joints of the feet Assessment Data OBJECTIVE Joint crepitation • Audible popping, cracking, grinding with motion • Limited ROM INCREASES • AFFECTED JOINTS UNSTABLE,”give way” with weight bearing, fear of falling increases • Enlarged joints form spurs • Loss of articulation • Instability Assessment Data SUBJECTIVE Deep, aching localized joint pain Early disease- pain with use Late disease- pain at rest, affects sleep pattern Pain on joint palpation Joints stiffen with inactivity and changes in the weather Morning pain <less than 30 minutes DIAGNOSTIC DATA History/Physical ( most important) CBC RHEUMATOID FACTOR ESR X-RAYS- BONE REMODELING MRI OCT-OPTICAL COHERENCE TOMOGRAPHYarticular changes Synovial fluid analysis-differ OA from other forms of arthritis Osteoarthritis Complications Angulation of affected extremity (Loss of joint space) Deformity Subluxation • esp. carpometacarpal joint Ankylosis or Complete Body fusion of the joint esp. greater toe Osteoarthritis- Treatment Physiotherapy - muscle strengthening exercises Application of heat/cold Analgesics Hydrocortisone injections Supportive Bandages and devices Nutrition Stress Management Osteotomy (Realignment of the joint) Arthroplasty ( Construction of a new joint) Complementary/Alternative Therapies Acupuncture Tai Chi- low Impact exercise Ginger Turmeric Red cayenne pepper Kwai garlic Echinacea Ginkgo St John’s Wort Copper/Magnetic Bracelets Bee stings ASPIRIN - SALICYLATE Analgesic Anti-inflammatory Anti-pyretic Anti-platelet Rapidly absorbed Blood Salicylate Level 150 - 300 ug/ml Half-life 15- 20 Minutes Albumin Dependent SIDE EFFECTS • Tinnitus, Vertigo, Hearing Loss, Hyperventilation, Anaphylaxis, Renal Failure, Albuminuria ,Proteinuria Complementary/Alternative Therapies Ginger Anti-inflammatory Large doses-bleeding Cayenne Releases endorphins Interferes with substance Ptransmission of pain impulses Turmeric Cur cumin-inhibits prostaglandins and stimulate cortisol production 400 mg capsules TID Nursing Diagnosis Pain Impaired Physical Mobility Activity Intolerance Sleep-Pattern Disturbance Ineffective Coping Self Care Deficit Alteration in SelfConcept Alteration in Sexuality Alteration nutrition Altered role performance ACETAMINOPHEN TYLENOL Uses : Mild To Moderate Pain First Line For Osteoarthritis Oral - Parenteral Not Available Most Effective With Opioids HEPATOTOXICITY ( 10 Grams or More) Equal Analgesic Effect As Ibupropen Dosage Up To 4,000 Mg/Day Toxicity Tumor Necrosis Factor Inhibitors Etanercept (Enbrel) Infliximab (Remicade) Action: Reduces inflammation by preventing TNF medicated cellular responses Side Effects: N/V/A • Blood dyscrasia, sepsis, hypertension Antimalarials Hydroxychloroquine (Plaquenil) Chloroquine (Aralen) Action : exerts anti-inflammatory effect by inhibiting prostaglandin synthesis Side effects: • • • • Hypotension, N/V/diarrhea Liver and kidney monitoring Retinal damage GI protection CAUSES OF HYPERURICEMIA) Overproduction-uric acid • Cancers, psorasis, sickle cell anemia Under excretion of uric acid • Chronic renal insufficiency, alcohol, thiazide diuretics, nicotinic acid, cyclosporine, diabetic ketoacidosis • Definition-serum urate level exceeding either 6.8 or 7.0 mg/dL PREDISPOSING FACTORS TO A GOUT ATTACK Trauma 3 days after a major operation Major medical illness • • • • • • • Myocardial infarction Stroke Pulmonary embolus Fasting Alcohol use (binging) Infection Acidosis Co-Morbidities Obesity, dietary factors Excessive alcohol intake History of urolithiasis Chronic kidney disease (CKD) Potential genetic or acquired causes of uric acid overproduction (inborn error of purine metabolism, psoriasis, myeloproliferative or lymphoproliferative disease) Lead intoxication CLINICAL MANIFESTATIONS OF GOUT Meta-tarso-phalangeal joint of great toe Rapid joint swelling Uric crystals-needle shaped Usually mono-articular Pain, swelling, redness, tenderness Joint fluid show 50,000 /mm³neutrophils TREATMENT OF ACUTE GOUTY ATTACK NSAIDs or Indomethacin (Indocin) Course 7-10 days Contra indicated in patients with : • CHF, Peptic Ulcer, Renal Insufficiency • Patient with Nasal polps& ASA sensitivity will induce bronchospasm • Oral steroids later if necessary TREATMENT INTERCRITICAL PERIOD Drug therapy includes • Oral colchicine 0.6 bid • Probenecid or allopurinal 6-12 months Colchicine • inhibits leukocyte infiltration • Does not influence production or excretion of uric acid Probenecid • Acts on the renal tubules to inhibit reabsorption of uric acid Allopurinol • reduces uric acid by inhibiting its production Allopurinol-300 mg febuxostat-first line drug • Target goal- lower than 6 mg/dl, preferred < 5 mg/dl First-line treatment for acute gout • Nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids, or oral colchicine are the recommended, ALLOPURINOL ZYLOPRIM Xanthine Oxidase Inhibitor Decreases Uric Acid Synthesis Lowest Dose- 100 Mg/Day Contra - Acute Gouty Attacks Skin Reaction- With Penicillin Monitor Creatinine Levels Force Fluids Drug Of Choice In Patient With Histories Of Renal Calculi, Tophi, Or Renal Insufficiency PROBENECID - BENEMID Uric Acid Excreter Equal To Allopurinol Renal Calculi Formation Force Fluids Avoid ASA Used To Prolong Antibiotic Levels LOWER BACK PAIN -ETIOLOGY Biomechanical And Destructive • Compression,torsion, Occupational Destructive Origins • Infection,tumors,rheumatoid Disorders Degenerative Problems • Osteoporosis, Spinal Stenosis SPINAL STENOSIS Compression Of The Annular Fibers Clinical Manifestations • • • Aching Pain With Standing And Walking Paresthesias Heaviness In The Legs Diagnostic Findings • • • • Mri Myelography With Ct Diskography Somatosensory Evoked Potentials An Algorithmic approach to back pain Phase 1- initial 4-6 weeks of acute low back pain Phase 2 – HNP,stenosis and unremitting low back pain • Treatment: MRI, CT, bone scan, injections and psychological profile Reference: AAOS and NASS An Algorithmic approach to back pain Unremitting pain Non-operative treatment Exercise, physical therapy, NSAIDS, injection program Traction Surgical approaches • Nucleoplasty • HNP • Disc replacement Alternative treatment SURGICAL MANAGEMENT Percutaneous Diskectomy • Removal Of Disk Materials With Trocar Microdiskectomy • Microsurgery, Root Retraction, Preservation Of An Intact Joint Capsule Decompressive Laminectomy • Removal Of Posterior Vertebrae Arch Artificial Disk Replacement • Spinal Fusion – Bone Grafting MEDICAL MANAGEMENT Control Pain And Spasm • NSAID’s, TENS, MANIPULATION Improve Mobility • Body Mechanics, Exercise, Back Brace Lifestyles Changes COMPLICATIONS Paralysis Hemorrhage Recurrent Pain Paralytic Ileus Collagen Diseases What is a collagen disease? A collagen disease is any disorder affecting the collagen (connective tissue), with "rheumatic" symptoms including muscle stiffness, soreness and pain in the joints and associated structures. Produce widespread changes in collagenous connective tissue. Cause problems involving almost every organ May be autoimmune in nature Are difficult to diagnose Have no cure Cannot be prevented TYPES OF COLLAGEN DISEASES Rheumatoid Arthritis Crest Syndrome Poly-arteritis Systemic Lupus Erythematosus Scleroderma Sarcoidosis CREST SYNDROME Is An Acronym For The Cardinal Clinical Features Of The Syndrome In A Given Patient: Calcinosis Raynaud Phenomenon Esophageal Dysmotility Sclerodactyly Telangiectasia CALCINOSIS Abnormal Deposits Of Calcium Salts In Various Tissues Deposits Appear-Nodules or Plaques Found In Skin, Connective Tissue, Muscle Intravertebral Disks Disease Scleroderma, Neoplastic Dermatosis, Inflammatory Degeneratative Disease RAYNAUD PHENOMENON Defined In 1862. Intermittent Attacks Of Ischemia Pallor, Cyanosis, And/Or Rubor On The Hands Bilaterally,toes, Ears, Nose In Response To Cold /Emotional Stimuli Numbness, Tingling, Burning, Pain Normal Color Return With Heat Normal Proximal Arterial Pulsations, And Without Gangrene. RAYNAUD PHENOMENON SCLERODACTYLY Musculoskeletal Deformity • Thickening Of The Skin Affecting The Digits Of The Hands And Feet. Fingers Semi-flexed Subcutanous Calcification Tightened Skin To The Wrist SCLERODACTYLY Three Phases Of Skin Changes Edematous Phase • Puffy Edema In The Fingers Indurative Phase Flexed, Morning Stiffness Atrophic Phase. SCLERODACTYLY SCLER0DERMA-INITIAL/8 YRS LATER TELANGIECTASIA Polyarteritis nodosa: BLOOD VESSEL DISEASE OF SMALL/ MEDIUM-SIZED ARTERIES UNKNOWN CAUSE TYPICALLY STRIKES ADULTS, NOT CH. ILDREN POLYARTERITIS NODOSA: SIGN/SYMPTOMS Generalized Symptoms Include Fever, Fatigue, Weakness, Loss Of Appetite, Weight Loss. Muscle Aches (Myalgia) And Joint Aches(arthralgia) Are Common. Rashes, Swelling, Ulcers, And Lumps (Nodular Lesions). Scleroderma- Progressive Systemic Sclerosis Cause – Unknown- autoimmune? Affects 30 To 50 Years Old Women (4 X> Men) Local or Systemic Symptoms Fibrotic changes in connective tissue Severity Varies Tests-LE Prep; elevated gamma globulin levels;Anti-SCL70 antibody (antipoisomere I antibody) Skin- Ulceration, Calcification, Pigmentation Changes Systemic Features- Fibrosis / Degeneration of Heart, Lungs, Kidneys, GI Tract Treatment: corticosteroids, NSAIDS, Vasodilators; Prilosec; penicillamine; azathioprine,methotrexate; cyclosphosphamide (cytoxan) Sarcoidosis Cause- Unknown Inflammation –Granulomas Of Lymph Nodes Areas- Lungs, Liver, Eyes, Skin, Or Other Tissues. Theory-Hypersensitivity Response, A Genetic Predisposition, Infection, Or Chemicals. Occupational Exposure To Silica Dust And Polyvinyl Chloride SYSTEMIC LUPUS ERYTHEMATOSUS Chronic Autoimmune Diseases Antibodies Are Produced Against Its Own Cells Cause -Not Fully Known Multi-system Involment Affects 9 Times As Many Women As Men May Occur At Any Age, But 10 And 50 Years Sle May Be Caused By Certain Drugs • Drug-induced Lupus Erythematosus And Is Usually Reversible When The Medication Is Stopped. SYSTEMIC LUPUS ERYTHEMATOSUS Musculoskeletal • Joint Pain And Most Develop Arthritis • Fingers, Hands, Wrists, And Knees. • Death Of Bone Tissue Can Occur In The Hips And Shoulders And Is Frequently A Cause Of Pain In Those Areas. • Skin "Butterfly" Rash Over The Cheeks And Bridge Of The Nose • Rash Worsened By Sunlight. • Kidney Only 50% Have Lupus Nephritis As Defined By Persistent Inflammation In The Kidney. SYSTEMIC LUPUS ERYTHEMATOSUS • Kidney Renal Failure ...
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