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92 Cards in this Set
- Front
- Back
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Rheumatology
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-study of rheumatic disease
-any disease or condition that involves the musculoskeletal system -connective tissue disease (CTD) is a mojor focus of rheumatology -most CTD's are autoimmune disorders |
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Arthritis
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-inflammation of one or more joints
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Osteoarthritis
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-non-inflammatory arthritis
-not systemic -not autoimmune diseas -majority of people over 65 have osteoarthritis -more that 2/3 of those affected are women -most common type -involves joint pain and less function due to deterioration and loss of cartilage in the joints |
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Pathophysiology of osteoarthritis
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-erosion of cartilage and bone
-joint space narrows |
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What does joint space norrowing cause?
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-osteophytes (bone spurs)
-cartilage cont. to thin -bone cysts and synovitis -subluxation (partial joint dislocation) and joint deformities |
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What does osteoarthritis lead to?
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-immobility
-pain -muscle spasm -local inflammation |
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What are causes and risk factors to osteoarthritis
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-age
-genetic changes -obesity -smoking -repetitive motion -joint injury |
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Who are at greater risk for osteoarthritis?
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-people >60 y/o
-women > 50 y/o |
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Physical findings of osteoarthritis
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-joint involvement
-Heberden's nodes -Bouchard's nodes -joint effusion (fluid in joint) -atrophy of skeletal muscle |
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Symptoms of osteoarthritis
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-chronic joint pain and stiffness
associated with exercise and relieved by rest -inflammation may be present, but is usually minimal -aching in the joints during weather changes -crepitus -limited movement -joint is enlarged |
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Heberden's nodes
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distal interphalangeal joint enlargement (first digit)
-tend to appear oon both hands -nodes may be painful and red |
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Bouchards nodes
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-proximal interphalangeal joint enlargement, knuckles
-tend to appear oon both hands -nodes may be painful and red |
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Areas where osteoarthritis occurs
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-neck
-lower back -knees -hips -ends of fingers -thumbs |
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How do you diagnosis osteoarthritis?
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-psychosocial assessment
-history and physical exam -x-ray, MRI's, CT scans that show narrowing of joint spaces -joint deformity -bony growth |
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What labs are looked at for diagnostic reason with OA
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-C-reactive protein and erythrocyte sedimentation rate (ESR), can be elevated with synovitis
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Treatment of OA
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-prevention
-relieve pain -maintain or improve mobility -minimize disability |
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Analgesics for OA and their purpose
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-decrease pain and secondary joint inflammation
-acetaminophen-do not exceed >4000mg/daily -topical drugs-Lidocaine 5% patch every 12 hrs. -aspercreme -NSAIDS-Celebrex & Ibuprophen -Opioids-Tylenol #3, Vicodin -Intra-articular injections -synthetic joint fluid implants -muscle relaxants-Flexeril |
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Non pharmacologic management
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-rest
-joint positioning -heat/cold application -weight control |
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Dietary supplements
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-Gamma-linolenic acid (GLA)
-glucosamine -chondroitin |
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Surgical treatment for OA
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-total joint arthroplasty (TJA)
-total joint replacement (TJR) |
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Postoperative care for total hip arthroplasty
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-prevent dislocation, infection and throboembolic complications
-assess bleeding -manage of anemia -manage pain -incisional care -regular postoperative care |
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Diffuse connective tissue disease
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-chronic in nature
-have inflammation and degeneation in the connective tissues -due to immunological abnormalities -usually include exacerbations and remissions |
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Examples of connective tissue disease
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-rheumatoid arthritis
-systemic lupus erythematosus -scleroderma |
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What is rheumatoid arthritis?
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-a chronic systemic inflammator disease
-attacks joints and surrounding muscles, tendons, ligaments -can also attack organs -requires life long treatment |
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Who is most affected by rheumatoid arthritis and what ages are onset of symptoms?
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-strikes women 3x more often than men
-peak onset for women is between ages 35-50 |
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What is rheumatoid factor?
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-IgM antibody develops against the body's naturally occurring antibody IgG
-unkown trigger |
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What happens to IgG when IgM is developed in the body?
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-IgG becomes antigen
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What is formed when IgG (rheumatoid factor) and IgM are combined in the body, what is produced?
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-antigen-antibody complexes
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What happens when antigen-antibody complexes are deposited in the synovium
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-stimulate immune cells (T-cells) and macrophages to enter the synovial fluid and
TNF and interleukin-1 are released. |
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What do TNF and Interleukin-1 cause?
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Inflammation
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What is the path of the body when the immune system attacks itself?
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-unknown triggers cause rheumatoid factor (IgM) to develop against the body's naturally occurring antibody IgG
-IgG then becomes an antigen -Rheumatoid factor antibodies (IgM) then combine with these IgG antigens and make antigen antibody complexes. -These antigen antibody complexes are deposited into the synovium -The complexes stimulate immune cells (T-cells) and macrophages to enter the synovial fluid -The T-cells and macrophages cause TNF and Interleukin-1 to be released. -TNF and Interleukin-1 cause inflammation |
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When the body attacks intself how does the body react?
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-causes synovitis (inflammation)
-warmth -redness -swelling -pain |
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What is "pannus"
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-as the cells in the synovium grow and divide abnormally they form a mass, also similair to scar tissue
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What are some clinical manifestations of rheumatoid arthritis, which ones differentiate from OA
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-joint pain
-swelling -warmth -erythema -lack of function -joint stiffness, especially in the morning, lasting longer than 30 min.****opposite of OA |
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What patterns of joint involvement are involved in rheumatoid arthritis
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-begins in small joints in hands, wrists, feet
-as it progresses knees, shoulders, hips, elbows, ankles, cervical spine |
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Are symptoms of rheumatoid arthritis acute or chronic?
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Acute
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Are S/S of rheumatoid and OA bilateral and symmetrical or does it attack one joint with no pattern?
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Rheumatoid is bilateral and symmetrical, deformities of feet and hands are common
OA-attacks one joint and is not bilateral/symmetrical |
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What are some common hand and foot deformities associated with rheumatoid arthritis
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-ulnar drift-hands face outward
-RA joint involvement -swan neck deformity -double jointed finger -boutonniere deformity - knuckle up reversed of swan neck -foot deformities - |
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RA systemic complications
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-weight loss, fever, and extreme fatigue
-exacerbations -subcutaneous nodules -pulmonary complications -vasculitis -periungual lesions -paresthesias -cardiac complications |
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what is Sjogren's syndrome and what is it associated with?
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-dry eys and dry mucous membranes, enlarged parotid gland
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What is Raynaud's phenomenon and what is it associated with?
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-color changes of the fingers and toes due to vasospasms from cold or stress
-associated with RA |
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Who are affected by Raynauds
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-10-15% of healthy women (15-45y/o
-RA |
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Assessment and diagnostic findings for RA
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-bilateral joint pain
-joint inflammation -Labs rheumatoid factor, ESR, RBC, C4, ANA |
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Lab test associated with RA
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-rheumatoid factor-present in >80% of people with RA
-ESR-erythrocyte sedimentation rate is increased -RBC-decreased -C4 complement -decreased -antinuclear antibody (ANA) is positive. |
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Diagnostic tests for RA
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-arthrocentesis-synovial fluid is cloudy, milky, yellow and has increase inflammatory cells such as leukocytes
-x-ray -CT -bone scan |
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What do disease-modifying antirheumatic drugs (DMARDs) do?
Examples? |
-reduce inflammation associated with RA
-suppress the immune systme -some decrease progression of RA examples include-Rheumatrox, Plaquenifl, sulfasalazine |
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Common side effects of DMARDS?
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-renal-protein, WBC, RBC in urine
-skin-rash -GI-N/V/D, abd. cramping, mouth sores -lung-fibrosis -liver-fibrosis -immune-susceptible to infection |
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What are NSAIDs and what are they used for?
Example? |
-Non steroidal anti-inflammatory drug
-used for shor-term therapy of RA -antiinflammatory -analgesic -Cox-2 inhibitor -if no change in 6-8 weeks change drugs Example-Celebrex |
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What are Biologic Response Modifiers drugs and what are they used for?
Examples? Major side effects? |
-newer treatment, used for RA
-neutralize biological activity of tumor necrosis factor (TNF) Examples-Enatercept (Enbrel) -Infliximab (Remicade) -Adalimumab (Humira) SE-serious infection |
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Glucocorticoids (steroids) can be used with RA but have SE what are they?
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-short duration therapy or low chronic dose
-SE over time include DM, infection, F/E imbalances, HTN, osteoporosis, glaucoma |
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Systemic Lupus Erythematosus (SLE)
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-autoimmune (inflammatory) condition in which the immune system loses its ability to tell the difference between foreign harmful invaders from the outside and "self".
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Characteristics of Lupus
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-young black, hispanic women (9:1)
-automimmune, inflammation, and tissue damage of organs -mild inflammation of joints, hands -major systemic involvement -genetic predisposition (viruses), drug induced |
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signs/symptoms of Lupus
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-fever, weakness, fatigue, weight loss
-skin has rash, butterfly blush, made worse with sunlight -musculoskeletal has joint tenderness, swelling, stiffnes, pain |
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What other organs can be involved with lupus
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-kidney 50%
-oral ulcers -pericarditis 30% -lung involvement 40-50% -vasculitis-lesions on fingers, elbows, toes, forearms -depression -lymphadenopathy |
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Medical treatment of Lupus
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-depends on which organs are involved
-NSAIDS with corticosteroids -tylenol -immunosuppresants -plaquenil |
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What are some other characteristics of Lupus
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-hair loss
-stay out of sun -fatigue -facial rash -lupus support groups |
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What should Lupus patients know about the sun and their skin?
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-avoid prolong exposure to sun and other UV lights
-wear long sleeves and hats -use sun-block -clean skin w/ mild soap -avoid perfumed soaps -rinse and dry skin well, apply lotion- -avoid powder -mild protein shampoos for hair, avoid permanents |
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Systemic sclerosis (Scleroderma)
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"sclerosis" or hardening of the skin
-can effect the viscera w/ symptoms occurring in one or more organs -occurs in women more then in me -not always progressive |
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Pathophysiology of scleroderma
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-usually begins with skin involvement-immune system causes deposits of collagen in the tissues.
-initially causes edema which results in taunt, smooth and shiny skin. -eventually tissue degenerates and becomes nonfunctional -the changes also occur in blood vessels, organs, and body system-can lead to death |
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clinical signs of scleroderma
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-starts with raynaud's and swelling in the hands
-skin and subcutaneous tissues become increasingly hard and rigid -extremitites stiffen, lose mobility -condition spreads slowly -face appears mask like -hands, appear waxy and like a manikin |
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What changes occur inside the body with scleroderma
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-heart-left ventricle hardens->heart failure
-esophagus hardens -lungs-scarring -digestive problems-hardening of intestines -kidney problems |
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CREST
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C-calcinosis (calcium deposits in the tissue)
R-Raynaud's phenomenon E-esophageal hardening S-sclerodactyly (scleroderma of the digits) T-telangiectasis (capillary dilation that forms a vascular lesion) |
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Diagnosis of scleroderma
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-usually on assessment of findings
-no one conclusive test; testing according to system's involvement |
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Treatment of scleroderma
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-get disease into remission (steroids, immunosuppressants)
-warmth to hands -avoid trauma to hands -treat symptoms as they appear in each organ -lotions for dry skin -good nutrition |
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Medication for scleroderma
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-systemic steroids
-immunosuppressants |
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Ankylosing spondylitis
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-stiffening of the spine
-attacks cartilage, ligaments and tendons of the spine, becomes inflamed -back becomes stiff, inflamed and sore -disease progresses, ligaments and tendons become more like bone tissue |
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Lumbar flattening
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-comes on gradually
-pain/stiffness settles in lower back or joints -may be worse at night or upon rising -usually gets better as the person moves around -a systemic disease |
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Since lumbar flattening is a systemic disease what symptoms will you see
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-can cause skin and eye problems
-loss of appetite -fatigue -fever |
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Pharmacologic therapy for lumbar flattening
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-NSAIDS
-DMARD's-methotrexate, sulfasalazine |
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What is a metabolic disease associated with rheumatic disorder
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-Gout
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What is gout?
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crystal-induced arthritis caused by deposit of sodium urate in joint tissues. Due to uric acid overproduction or underexcretion
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Who suffer from gout?
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-2 million americans
-mostly males |
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Stage 1 of gout, what is it and how do you diagnosis it.
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-Asymtomatic hyperuricemia
-the only sign is a serum uric acid level of over 7 mg/dl |
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Stage 2 of gout, what is it?
How long does it last? what triggers it? |
-acute gouty arthritis
-inflammatory reaction in a single joint -onset is sudden, usually at night -usually subsides 3-10 days -triggered by: -trauma -alcohol -surgery -illness |
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Sumptoms of Stage 2
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-joint is stiff and warm to touch
-swollen which causes skin to look shiny, tight, reddish or purplish and streatched over the area -very sensitive to touch -fever -chills -rapid heart rate -general "blah" feeling |
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Stage 3 of Gout
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-intercritical stage
-followed by a symptom -free period until the next attack -may not come for months or years -over time attacks are more frequent, involve more joints, last longer |
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Stage 4 of Gout
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-chronic gout
-repeated attacks cause sodium urate crystals to accumulate (tophi) in other parts of body such as: toe, hands, ear, kidneys |
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What is Tophi
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-tophi is due to repeated attacks cause sodium urate crystals to accumulate
-takes about 10 years -genetic 6-18% have gout in family |
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What foods stimulate production of uric acid?
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-food with purines which stimulate production of uric acid
-organ meats or meat -gravies -peas -anchovies -dried peas -beans |
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Other causes of production of uric acid?
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-some drugs can lead to a increase
-certain diseases, kidneys |
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Treatment for ACUTE Gout?
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-colchicine-decreases inflammation by inhibiting production and relase of phagocytic leukocytes
-NSAIDS |
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Treatment of Chronic Gout?
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-uricosuric agent (probenecid)-promote excretion of uric acid by inhibiting renal tubular reabsorption
-zanthine oxidase inhibitor-zanthinoxidase is the enzyme that breaks down protein into uric acid -allopurinol-limited use due to toxicity; however is the treatment of choice for patients |
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Plan of care for Gout
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-protect affected areas from trauma, including weight of bed linens
-cold applications and joint immobilization -medications as discussed |
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Osteoporosis
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-Metabolic bone disorder in which the:
-the rate of bone resorption increases -rate of bone formation decreases -overall effect-decreases bone mass - |
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What do bones affected by osteoporosis lose?
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-calcium and phosphate
-become porous, brittle, and are prone to fractures |
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Who are at risk for primary osteoporosis
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-occurs in 90% of cases
-occurs between age 51-70 -6x more common in women -may be due to lack of estrogen |
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Risk factors of osteoporosis?
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-female, caucasian, non-hispanic or asian
-increased age -estrogen deficiency /menopause -inadequate calcium intake -lack of weight-bearing exercise -tobacco use -alcohol use |
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Secondary osteoporosis causes
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-due to some other causes such as malabsorption of ood, prolonged heparin therapy, diabetes, steroids, etc.
-occurs in 10% of cases |
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Diagnosis of osteoporosis
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-x-ray shows changes in bone
-person may have height changes and old fractures on x-ray -significant fractures occur with little trauma |
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Dowager's hump
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-outward hump in the back of people with osteoporosis
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Prevention for osteoporosis
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-to achieve peak bone mass
-maintain adequate dietary calciym and vit. D intake -perform weight bearing exercises -do not smoke -caffeine and alcohol in moderation -maintain optimal body weight |
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Medications used for osteoporosis
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-estrogen replacement
-estrogen receptor modulators (Evista) -alendronate (fosamax)-increases bone mass -calcitonin (miacalcin)-supresses bone loss -maintain adequate dietary calciym and vi. D intake |
