ch 64 arthritis Flashcards
which primarily affect body joints, tendons, ligaments, muscles, and bones.
rheumatic diseases
inflammation, pain, and loss of function in 1 or more of the body’s connecting or supporting structures.
rheumatic diseases are often marked by
inflammation of a joint or joints
Arthritis involves
is the most common chronic condition of the joints.
Osteoarthritis
rheumatoid arthritis (RA), fibromyalgia, systemic lupus erythematosus (SLE), and gout.
Other forms arthritis include
is a slowly progressive noninflammatory disorder of the diarthrodial (synovial) joints
Osteoarthritis (OA)
gradual loss of articular cartilage with formation of bony outgrowths (spurs or osteophytes) at the joint margins
OA involves the
indomethacin, colchicine, and corticosteroids, can stimulate collagen-digesting enzymes in joint synovium.
Drugs, such as (effects on joint cartilage)
knee OA
People with hand OA are more likely to develop
incidence of OA in aging women.
Decreased estrogen at menopause may contribute to the increased
cartilage deterioration from damage at the level of the chondrocytes
Genetic, metabolic, and local factors interact to cause
The normally smooth, white, translucent articular cartilage becomes dull, yellow, and granular as the disease progresses. Affected cartilage steadily becomes softer and less elastic. It is less able to resist wear with heavy use
change in articular cartilage
pain and stiffness of OA. Pain in later disease occurs when articular cartilage is lost, and bony joint surfaces rub each other.
changes in cartilage/ synovitis cause the early
In early stages of OA, joint pain is relieved by rest. However, the patient with advanced disease may have pain at rest or have trouble sleeping due to increased joint pain. Pain may worsen as the barometric pressure falls before the onset of severe weather.
-OA progresses, increasing pain can contribute greatly to disability and loss of function
pain described with OA in early and advanced disease
pain of OA may be referred to the groin, buttock, or outside of the thigh or knee. Sitting down becomes hard, as does rising from a chair when the hips are lower than the knees. As OA develops in the intervertebral (apophyseal) joints of the spine, local pain and stiffness are common.
sign/symp of OA
OA joint stiffness occurs after periods of rest or an unchanged position. Early morning stiffness is common. It generally resolves within 30 minutes.
-Overactivity can cause a mild joint swelling that temporarily increases stiffness. Crepitation, a grating sensation caused by loose cartilage particles in the joint cavity, can cause stiffness. Crepitation is common in patients with knee OA.
-OA usually affects joints on 1 side of the body (asymmetrically) rather than in pairs
-distal interphalangeal (DIP) and proximal interphalangeal (PIP) joints of the fingers, and the metacarpophalangeal (MCP) joint of the thumb are often affected. Weight-bearing joints (hips, knees)
-metatarsophalangeal (MTP) joint of the foot, and the cervical and lower lumbar vertebrae are often involved
distinguishes OA from inflammatory joint disorders, such as RA.
the DIP joints due to osteophyte formation and loss of joint space
-can appear as early as age 40 and tend to be seen in family members
Heberden’s nodes occur on (deformity with OA)
on the PIP joints indicate similar disease involvement.
Bouchard’s nodes (deformity with OA)
are often red, swollen, and tender.
-usually do not cause significant loss of function, the visible deformity may bother the patient.
Heberden’s and Bouchard’s nodes
obvious joint deformity due to cartilage loss in 1 joint compartment.
-ex: bowlegged (varus deformity) from medial joint arthritis
-Lateral joint arthritis causes a knock-kneed appearance (valgus deformity)
Knee OA often leads to
1 leg may become shorter as the joint space narrows.
advanced hip OA,
Fatigue, fever, and organ involvement are not present in OA. This is an important distinction between OA and inflammatory joint disorders, such as rheumatoid arthritis.
rheumatoid arthritis. has systemic symptoms NOT OA
bone scan, CT scan, or MRI may be used to diagnose OA
-X-rays help confirm disease and stage joint damage. As OA progresses, x-rays often show joint space narrowing and increasingly dense bone. Osteophytes may be visible. However, these changes do not always reflect the degree of pain the patient has. Despite strong x-ray evidence of disease, the patient may be relatively free of symptoms. Another patient may have severe pain with only slight x-ray changes.
-No laboratory tests or biomarkers can be used to diagnose
-Synovial fluid analysis helps distinguish OA from other types of inflammatory arthritis
diagnosis of OA
, the fluid is clear yellow with little or no sign of inflammation.
In OA synovial fluid description
OA has no cure. Interprofessional care focuses on managing pain and inflammation, preventing disability, and maintaining and improving joint function. Nondrug interventions are the basis of OA management
Tx for OA
Ice can be helpful if the patient has acute inflammation. Heat therapy is especially useful for stiffness.
***heat better for OA
-hot packs, whirlpool baths, ultrasound, and paraffin wax baths.
treatment for OA nonpharmacological
Acupuncture, massage, and Tai Chi may reduce arthritis pain and improve joint mobility.
-Some nutritional supplements may have antiinflammatory effects (e.g., fish oil, ginger, SAM-e). BUT not recommended
complemtary and alternative therapies for OA
acetaminophen (Tylenol).
-topical agent, such as capsaicin cream, may be helpful, alone or with acetaminophen. It blocks pain by locally interfering with substance P.
patient with mild to moderate joint pain may get relief from
Creams of 0.025% to 0.075% capsaicin are available over the counter (OTC). OTC products that contain camphor, eucalyptus oil, and menthol (e.g., Bengay, Arthricare) may provide
OTC ointment for OA to reduce pain
a nonsteroidal antiinflammatory drug (NSAID) may be more effective with misoprostol (Cytotec), for GI adverse effect in NSAID
-Arthrotec, a combination of misoprostol and the NSAID diclofenac, is available.
***Diclofenac gel may be applied to the affected joint.
Tx moderate to severe OA pain, or has signs of joint inflammation,
at high risk for bleeding.
Patients taking an anticoagulant (e.g., warfarin [Coumadin]) and an NSAID are
celecoxib (Celebrex) may be considered in selected patients.
Long-term NSAID treatment may affect cartilage metabolism, especially in older patients who may have poor cartilage integrity. As an alternative to traditional NSAIDs, the COX-2 inhibitor
because both inhibit platelet function and prolong bleeding time.
NSAIDs & Aspirin should Not be taken together
local inflammation and swelling. Four or more injections without relief suggest the need for more intervention.
Intraarticular injections of corticosteroids may be needed for those with
has been a common treatment for knee OA.
injection of hyaluronic acid (viscosupplementation)
Drugs thought to slow the progression of OA or support joint healing are known as
disease-modifying osteoarthritis drugs (DMOADs).
arthroscopy to remove loose bodies from the joint.
-However, it does not have any benefit over physical therapy and medical treatment
Patients with knee OA used to undergo (surgery)
Avoid cigarette smoking.
* Promptly treat any joint injury.
* Maintain healthy weight and eat a balanced diet.
* Use safety measures to protect and decrease risk for joint injury.
* Exercise regularly, including strength and endurance training.
Preventing Osteoarthritis
a low-impact form of exercise
therapist may recommend Tai Chi as
rest and stabilize painful or inflamed joints.
Splints may be prescribed to (OA)
removing throw rugs, placing rails at the stairs and bathtub, using night-lights, and wearing well-fitting supportive shoes. Assistive devices, such as canes, walkers, elevated toilet seats, and grab bars, reduce the load on an affected joint and promote safety. Urge the patient to continue all prescribed therapies at home
safety Measures for OA include
is a chronic, systemic autoimmune disease characterized by inflammation of connective tissue in the diarthrodial (synovial) joints.
Rheumatoid arthritis (RA)
one of the most disabling forms of arthritis
RA has long been considered
results from a combination of genetics and environmental triggers. An autoimmune cause is currently the most widely accepted theory.
Cause of RA
RA is marked by autoantibodies to this abnormal IgG. The autoantibodies are known as
rheumatoid factor (RF)
fatigue, anorexia, weight loss, and generalized stiffness, may precede the onset of joint symptoms. Stiffness becomes more localized in the following weeks to months.
Specific joint involvement is marked by pain, stiffness, limited motion, and signs of inflammation (e.g., heat, swelling, tenderness). Joint symptoms occur symmetrically and often affect the small joints of the hands (PIP and MCP) and feet (MTP). Larger peripheral joints such as wrists, elbows, shoulders, knees, hips, ankles, and jaw may be involved. The cervical spine may be affected, but the axial skeleton (spine and bones connected to it) is generally spared.
-Nonspecific manifestations, such as fatigue, anorexia, weight loss, and generalized stiffness, may precede the onset of joint symptoms
s/s of RA
human leukocyte antigens (HLA), especially the HLA-DR4 and HLA-DR1 antigens.
strongest evidence for a genetic influence is the role of
Morning stiffness may last from 60 minutes to several hours or more, depending on disease activity. MCP and PIP joints are typically swollen. In early disease, the fingers may become spindle shaped from synovial hypertrophy and thickening of the joint capsule. Joints are tender, painful, and warm to the touch. Joint pain increases with motion.
RA pt may have joint stiffness after periods of inactivity.
the extensor and flexor tendons around the wrists. This causes symptoms of carpal tunnel syndrome and makes it hard for the patient to grasp objects.
Tenosynovitis often affects (RA)
1 joint surface to slip past the other (subluxation). Metatarsal head dislocation and subluxation in the feet may cause pain and walking disability
Muscle atrophy and tendon destruction cause (RA)
common in the hands
Ulnar drift (“zig-zag deformity”), swan neck, and boutonnière deformities are (RA)
under the skin as firm, nontender masses. They are often found on bony areas exposed to pressure, such as the fingers and elbows. Nodules at the base of the spine and back of the head are common in older adults.
-(these nodules can break down, like pressure injuries. )
Rheumatoid nodules appear
Cataracts and vision loss can result from scleral nodules.
scleral nodules. (RA)
pain like that of vascular insufficiency.
Nodular myositis and muscle fiber degeneration can cause
pleurisy, pleural effusion, pericarditis, pericardial effusion, and cardiomyopathy.
In later disease, nodules in the heart and lungs can cause
by itself or with other arthritic disorders, such as RA and SLE.
-inflammation of RA can damage the tear-producing (lacrimal) glands, making the eyes feel dry and gritty. Affected patients may have photosensitivity.
Sjögren’s syndrome can occur
inflammation of RA can damage the tear-producing (lacrimal) glands, making the eyes feel dry and gritty.11 Affected patients may have photosensitivity.
is rare but can occur in those with long-standing RA. It is characterized by an enlarged spleen and low white blood cell (WBC) count. Patients with Felty syndrome are at increased risk for infection and lymphoma.
Felty syndrome
decreased grasp strength and affect the patient’s ability to perform self-care tasks.
Flexion contractures and hand deformities cause
struggling with chronic pain and disability or if depression is part of the autoimmune disease process.
-Levels of C-reactive protein (CRP), a marker of inflammation, are higher in patients with depression compared to those with no symptoms of depression.
Depression may occur. However, it is unclear if the patient becomes depressed from (RA)
specific than RF for RA
Testing for the antibodies to citrullinated peptide (anti-CCP) is more
indicator of autoimmune reaction.
increase in antinuclear antibody (ANA) titers is an
- At least 1 joint with definite clinical synovitis
- Synovitis not better explained by another disease
Patients should be tested for RA who initially are seen with:
is preferred for early treatment of patients diagnosed with RA
Methotrexate (DRUG Tx FOR RA)
are used to slow disease progression in RA
Biologic response modifiers (BRMs) (also called biologics or immunotherapy)
can be used to treat patients with moderate to severe RA who have not responded to DMARDs. They can be used alone or in combination therapy with a DMARD, such as methotrexate
Biologic response modifiers (BRMs) (also called biologics or immunotherapy) used
etanercept (Enbrel), infliximab (Remicade), adalimumab (Humira), certolizumab (Cimzia), and golimumab (Simponi).
TNF inhibitors include
is a biologically engineered copy of the TNF cell receptor. It binds to TNF in circulation before TNF can bind to the cell surface receptor. Thus it inhibits the inflammatory response. This drug is given as a subcutaneous injection.
Etanercept
monoclonal antibodies that bind to TNF, preventing it from binding to TNF receptors on cells.
-Infliximab is given IV in combination with methotrexate
-Adalimumab is given subcutaneously.
Infliximab and adalimumab are
TNF inhibitors that improve symptoms in patients with moderate to severe RA. Both drugs are given in combination with methotrexate.
Certolizumab and golimumab are
Perform tuberculin test and chest x-ray before starting therapy.
* Monitor for signs of infection. Stop the drug temporarily and notify HCP if acute infection develops.
* Teach patients to avoid live vaccination while taking drug.
* Report bruising, bleeding, or persistent fever and other signs of infection.
Tumor Necrosis Factor Inhibitors
a subcutaneous injection. It is used to reduce pain and swelling of moderate to severe RA. It can be used in combination with DMARDs but not with other TNF inhibitors. Using these agents together can lead to serious infection and neutropenia.
Anakinra is given as
block the action of IL-6, a cytokine that contributes to inflammation.
-used to treat patients with moderate to severe RA who have not responded to or cannot tolerate other drugs for the disease.
Tocilizumab (Actemra) and sarilumab (Kevzara)
blocks T-cell activation. It is recommended for patients who have inadequate response to DMARDs or TNF inhibitors. It is given IV. Like anakinra, it should not be used with TNF inhibitors.
Abatacept (Orencia)
is a monoclonal antibody that targets B cells. It may be used in combination with methotrexate for patients with moderate to severe RA not responding to TNF inhibitors. It is given IV.
Rituximab (Rituxan)
These medications are used less often because they are weak treatments compared to other DMARDs and biologics.
Other DMARDS include immunosuppressants (azathioprine), penicillamine (Cuprimine), and gold preparations.
to manage symptoms during disease flares
Corticosteroid therapy can be used (RA)
temporarily reduce acute pain and inflammation. Low-dose oral corticosteroids may be used for a limited time to decrease disease activity until the effects of DMARDs or biologics are seen
-**they are inadequate as a sole therapy because they do not affect disease progression. Their long-term use should not be a mainstay of RA treatment. Complications include osteoporosis and avascular necrosis.
Intraarticular injections may
used to treat arthritis pain and inflammation
Various NSAIDs and salicylates are
dosages of 3 to 4 g/day in 3 to 4 doses. Blood salicylate levels should be monitored in a patient taking more than 3600 mg daily.
Aspirin may be used in
the patient cannot tolerate aspirin.
NSAIDs may be used when
the only available COX-2 inhibitor, is effective in RA as well as OA. All nonaspirin NSAIDs can increase the risk for blood clots, heart attack, and stroke.
Celecoxib (Celebrex),
a loss of appetite.
Fatigue, pain, and depression may cause (RA)
unwanted weight gain
Corticosteroid therapy and decreased mobility due to pain may cause
Cushing syndrome (e.g., moon face, redistribution of fatty tissue to the trunk) change the physical appearance. Encourage the patient not to change the dose or stop therapy abruptly.
taking corticosteroids may become distressed as signs and symptoms of
Removal of the joint lining (synovectomy) is one type of surgery. Total joint replacement (arthroplasty) can be done for many different joints in the
Surgery options for RA
stiffness, pain, and muscle spasm.
Cold and heat applications can help relieve
during periods of increased disease activity
Ice is especially helpful
(peas or kernel corn) can easily mold around the shoulder, wrists, or knees to be an effective home treatment.
Cold application should not exceed 10 to 15 minutes at a time. Plastic bags of small frozen vegetables
chronic stiffness. However, heat application should not exceed 20 minutes at a time.
Moist heat offers better relief for
stiffness to allow the patient to take part in therapeutic exercise
-avoid using a heat-producing cream (e.g., capsaicin) with an external heat device.
-Heating pads, moist hot packs, paraffin baths, and warm baths or showers can relieve
can worsen the problem of decreased bone density from aging and inactivity. The risk for pathologic fractures is increased, especially vertebral compression fractures.
Osteopenia from corticosteroid use
corticosteroid use can be minimized by an age-appropriate exercise program. An adequate support system for the older adult is critical to the ability to follow a treatment plan
Myopathy related to
is a type of arthritis characterized by elevation of uric acid (hyperuricemia) and the deposit of uric acid crystals in 1 or more joints.
Gout
gout is marked by painful flares lasting days to weeks followed by long periods without symptoms.
Gout sign/symp
