ch 64 arthritis Flashcards
(238 cards)
1
Q
which primarily affect body joints, tendons, ligaments, muscles, and bones.
A
rheumatic diseases
2
Q
inflammation, pain, and loss of function in 1 or more of the body’s connecting or supporting structures.
A
rheumatic diseases are often marked by
3
Q
inflammation of a joint or joints
A
Arthritis involves
4
Q
is the most common chronic condition of the joints.
A
Osteoarthritis
5
Q
rheumatoid arthritis (RA), fibromyalgia, systemic lupus erythematosus (SLE), and gout.
A
Other forms arthritis include
6
Q
is a slowly progressive noninflammatory disorder of the diarthrodial (synovial) joints
A
Osteoarthritis (OA)
7
Q
gradual loss of articular cartilage with formation of bony outgrowths (spurs or osteophytes) at the joint margins
A
OA involves the
8
Q
indomethacin, colchicine, and corticosteroids, can stimulate collagen-digesting enzymes in joint synovium.
A
Drugs, such as (effects on joint cartilage)
9
Q
knee OA
A
People with hand OA are more likely to develop
10
Q
incidence of OA in aging women.
A
Decreased estrogen at menopause may contribute to the increased
11
Q
cartilage deterioration from damage at the level of the chondrocytes
A
Genetic, metabolic, and local factors interact to cause
12
Q
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
A
change in articular cartilage
13
Q
pain and stiffness of OA. Pain in later disease occurs when articular cartilage is lost, and bony joint surfaces rub each other.
A
changes in cartilage/ synovitis cause the early
14
Q
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
A
pain described with OA in early and advanced disease
15
Q
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.
A
sign/symp of OA
16
Q
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
A
distinguishes OA from inflammatory joint disorders, such as RA.
17
Q
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
A
Heberden’s nodes occur on (deformity with OA)
18
Q
on the PIP joints indicate similar disease involvement.
A
Bouchard’s nodes (deformity with OA)
19
Q
are often red, swollen, and tender.
-usually do not cause significant loss of function, the visible deformity may bother the patient.
A
Heberden’s and Bouchard’s nodes
20
Q
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)
A
Knee OA often leads to
21
Q
1 leg may become shorter as the joint space narrows.
A
advanced hip OA,
22
Q
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.
A
rheumatoid arthritis. has systemic symptoms NOT OA
23
Q
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
A
diagnosis of OA
24
Q
, the fluid is clear yellow with little or no sign of inflammation.
A
In OA synovial fluid description
25
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
26
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
27
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
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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
29
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
30
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,
31
at high risk for bleeding.
Patients taking an anticoagulant (e.g., warfarin [Coumadin]) and an NSAID are
32
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
33
because both inhibit platelet function and prolong bleeding time.
NSAIDs & Aspirin should Not be taken together
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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
35
has been a common treatment for knee OA.
injection of hyaluronic acid (viscosupplementation)
36
Drugs thought to slow the progression of OA or support joint healing are known as
disease-modifying osteoarthritis drugs (DMOADs).
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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)
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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
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a low-impact form of exercise
therapist may recommend Tai Chi as
40
rest and stabilize painful or inflamed joints.
Splints may be prescribed to (OA)
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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
42
is a chronic, systemic autoimmune disease characterized by inflammation of connective tissue in the diarthrodial (synovial) joints.
Rheumatoid arthritis (RA)
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one of the most disabling forms of arthritis
RA has long been considered
44
results from a combination of genetics and environmental triggers. An autoimmune cause is currently the most widely accepted theory.
Cause of RA
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RA is marked by autoantibodies to this abnormal IgG. The autoantibodies are known as
rheumatoid factor (RF)
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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
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human leukocyte antigens (HLA), especially the HLA-DR4 and HLA-DR1 antigens.
strongest evidence for a genetic influence is the role of
48
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.
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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)
50
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)
51
common in the hands
Ulnar drift (“zig-zag deformity”), swan neck, and boutonnière deformities are (RA)
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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
53
Cataracts and vision loss can result from scleral nodules.
scleral nodules. (RA)
54
pain like that of vascular insufficiency.
Nodular myositis and muscle fiber degeneration can cause
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pleurisy, pleural effusion, pericarditis, pericardial effusion, and cardiomyopathy.
In later disease, nodules in the heart and lungs can cause
56
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
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inflammation of RA can damage the tear-producing (lacrimal) glands, making the eyes feel dry and gritty.11 Affected patients may have photosensitivity.
58
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
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decreased grasp strength and affect the patient’s ability to perform self-care tasks.
Flexion contractures and hand deformities cause
60
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)
61
specific than RF for RA
Testing for the antibodies to citrullinated peptide (anti-CCP) is more
62
indicator of autoimmune reaction.
increase in antinuclear antibody (ANA) titers is an
63
* 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:
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is preferred for early treatment of patients diagnosed with RA
Methotrexate (DRUG Tx FOR RA)
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are used to slow disease progression in RA
Biologic response modifiers (BRMs) (also called biologics or immunotherapy)
66
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
67
etanercept (Enbrel), infliximab (Remicade), adalimumab (Humira), certolizumab (Cimzia), and golimumab (Simponi).
TNF inhibitors include
68
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
69
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
70
TNF inhibitors that improve symptoms in patients with moderate to severe RA. Both drugs are given in combination with methotrexate.
Certolizumab and golimumab are
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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
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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
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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)
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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)
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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)
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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.
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to manage symptoms during disease flares
Corticosteroid therapy can be used (RA)
78
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
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used to treat arthritis pain and inflammation
Various NSAIDs and salicylates are
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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
81
the patient cannot tolerate aspirin.
NSAIDs may be used when
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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),
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a loss of appetite.
Fatigue, pain, and depression may cause (RA)
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unwanted weight gain
Corticosteroid therapy and decreased mobility due to pain may cause
85
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
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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
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stiffness, pain, and muscle spasm.
Cold and heat applications can help relieve
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during periods of increased disease activity
Ice is especially helpful
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(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
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chronic stiffness. However, heat application should not exceed 20 minutes at a time.
Moist heat offers better relief for
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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
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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
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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
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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
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gout is marked by painful flares lasting days to weeks followed by long periods without symptoms.
Gout sign/symp
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the major end product of purine catabolism. It is primarily excreted by the kidneys. Gout occurs when either the kidneys cannot excrete enough uric acid or there is too much being made for the kidneys to handle effectively.
Uric acid is
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primary or secondary
classify hyperuricemia as
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genetic. A hereditary error of purine metabolism leads to the overproduction or retention of uric acid.
Primary hyperuricemia is
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conditions that increase uric acid production or decrease uric acid excretion or drugs that inhibit uric acid excretion (e.g., loop diuretics, β-blockers)
-Organ transplant recipients receiving immunosuppressive agents are at risk for hyperuricemia
Secondary hyperuricemia may be caused by
100
(obesity, insulin resistance, hypertension, hyperlipidemia)
most important is metabolic syndrome (Gout is likely caused by the interaction of several factors)
101
(e.g., red and organ meat, shellfish, fructose drinks) can trigger gout
Increased intake of foods containing purines trigger gout
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prolonged fasting or excessive alcohol use because they increase the production of keto acids, which inhibit uric acid excretion.
High uric acid may result from
103
crystallization and inflammation.
Two processes are essential for a person to develop gout:
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in 1 or more joints (usually less than 4)
Gout may occur acutely
105
Other affected joints may include wrists, knees, ankles, and the midfoot.
-Olecranon bursae may be involved.
Inflammation of the great toe (podagra) is the most common initial problem. (gout)
106
Affected joints may appear dusky or cyanotic and are extremely tender.
sign/symp of gout
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events such as trauma, surgery, alcohol use, or systemic infection.
Acute gout arthritis is usually triggered by
108
at night with sudden swelling and severe pain peaking within several hours. The painful area is highly sensitive to light touch. Low-grade fever is common.
-An attack usually ends in 2 to 10 days with or without treatment.
Symptom onset typically occurs (gout)
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multiple joint involvement and visible deposits of sodium urate crystals called tophi. Tophi are hard white nodules. They are typically seen in subcutaneous tissue, synovial membranes, tendons, and soft tissues
-Tophi generally occur many years after the onset of disease.
-clinical course may involve infrequent mild attacks or multiple severe episodes (up to 12 per year) marked by slowly progressive disability
Chronic gout is characterized by
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joint deformity, and cartilage destruction may lead to secondary OA.
-Large urate crystal deposits may pierce overlying skin, producing draining sinuses that often become infected.
Chronic inflammation may cause
111
stone formation in the kidneys or urinary tract.
Excessive uric acid excretion may lead to
112
and obstruction contributes to kidney disease.
Pyelonephritis related to sodium urate deposits
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increased above 6 mg/dL.
gout, serum uric acid is usually
114
to various drugs or an asymptomatic abnormality in the general population A 24-hour urine uric acid can determine if the disease is caused by decreased renal excretion or overproduction of uric acid.
Increased uric acid may be related
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synovial fluid aspiration. Affected fluid contains needle-like monosodium urate crystals
gold standard for diagnosis of gout is
116
it is the only reliable way to tell gout from septic arthritis or pseudogout (calcium phosphate crystal formation).
synovial fluid aspiration
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oral colchicine (Colcrys, Mitigare) and NSAIDs. Because colchicine has antiinflammatory effects but is not an analgesic, an NSAID is added for pain management.
Acute gout is treated with
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dramatic pain relief when given within 12 hours of an attack.
Colchicine generally produces
119
dose of a xanthine oxidase inhibitor.
-Allopurinol is the most commonly used drug and the first choice for therapy.
Future attacks of gout are prevented in part by a maintenance
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* May cause heart-related death and liver failure.
* Encourage patient with cardiovascular disease to take low-dose aspirin therapy.
* Monitor liver function tests before starting therapy and during treatment.
* Teach patient to notify HCP if symptoms of liver or heart problems occur.
Febuxostat
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allopurinol or febuxostat are contraindicated or the patient has intolerance to either
-Probenecid is a uricosuric, increasing uric acid excretion in the urine. Aspirin inactivates its effect, resulting in urate retention, and must be avoided during treatment.
-Acetaminophen can be used safely if analgesia is needed.
ACR recommends therapy with probenecid if
122
, a new uricosuric agent, can be taken with a xanthine oxidase inhibitor for those with persistent, increased uric acid levels. Duzallo, a fixed-dose combination of lesinurad and allopurinol, is taken once daily.
Lesinurad (Zurampic)
123
taken in the morning with food and water.
--Uricosurics can cause renal impairment
-Teach patients to stay well hydrated and to drink about 2 L of liquid a day when taking the drug.
Uricosurics
124
Patients who cannot take or do not respond to drugs that lower serum uric acid may be given
-enzyme that metabolizes uric acid into a harmless chemical excreted in the urine. It is given IV, usually for at least 6 months. Life-threatening anaphylactic and infusion reactions can occur.
pegloticase (Krystexxa)
125
angiotensin II receptor antagonist losartan (Cozaar) may be effective for treating older patients with gout and hypertension. Losartan promotes urate excretion and may normalize serum urate. Combination therapy with losartan and allopurinol may be used.
Losartan
126
is an infection caused by the spirochete Borrelia burgdorferi.
Lyme disease
127
It is transmitted by the bite of an infected deer tick
-most common vector-borne disease in the United States
-Person-to-person transmission does not occur
Lyme disease
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Symptoms mimic those of other diseases, such as multiple sclerosis, mononucleosis, and meningitis
symptoms mimic other diseases
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most characteristic clinical symptom of early localized disease is erythema migrans (EM)., “bull’s-eye rash”
-appears at the site of the tick bite within 1 month after exposure
-warm to the touch but is not itchy or painful.
main symp lyme disease
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(1) low-grade fever, (2) headache, (3) neck stiffness, (4) fatigue, (5) loss of appetite, and (6) migratory joint and muscle pain. Flu-like symptoms generally resolve over weeks or months, even if untreated.
-if not treated, the spirochete can spread within several weeks or months to the heart, joints, heart, and central nervous system (CNS).
-Cardiac symptoms, such as heart block and pericarditis,
-Bell’s palsy is the most common neurologic effect. Other problems include short-term memory loss, cognitive impairment, shooting pains, and numbness and tingling in the feet.
rash often occurs with acute flu-like symptoms:
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Arthritis is the
-mainly the knee.
second most common manifestation of Lyme disease.
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The first step is the enzyme immunoassay (EIA). It will be positive for most people with Lyme disease. If the EIA is positive or inconclusive, then a Western blot test is done. Results are diagnostic of Lyme disease only if both tests are positive.
CDC recommends a 2-step laboratory testing process to confirm the diagnosis.
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Active lesions are treated with oral antibiotics. Doxycycline (Vibramycin), cefuroxime, and amoxicillin are often effective in treating early-stage infection and preventing later stages of the disease.
Tx for lyme disease in active lesions
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Short-term therapy of 10 to 21 days of doxycycline is preferred. It treats both Lyme disease and human granulocytic anaplasmosis, which can be transmitted as a co-infection with a single tick bite.
doxycycline is preferred. Tx of lyme disease
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(infectious or bacterial arthritis) is caused by microorganisms invading the joint cavity
-Bacteria can travel through the bloodstream from another site of active infection, resulting in seeding of the joint. Organisms also can be introduced directly through trauma or surgical incision.
Septic arthritis
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(bacteria, viruses, mycobacteria, fungi), especially in the immunocompromised patient
-Staphylococcus aureus is the most common causative organism.
Any infectious agent can cause septic arthritis
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(1) diseases with decreased host resistance (e.g., RA, SLE), (2) treatment with corticosteroids or immunosuppressive drugs, and (3) debilitating chronic illness (e.g., diabetes).
Factors that increase the risk for infection include
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the knee and hip, are most often affected.
Large joints, such as (septic arthiritis)
139
inflammation of the joint cavity causes severe pain, redness, and swelling
- Septic arthritis of the hip can cause avascular necrosis. Because infection has often spread from a primary site elsewhere in the body, fever or shaking chills often accompany joint problems.
sign/symp of septic arthritis
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may be made by joint aspiration (arthrocentesis) and synovial fluid culture.
-WBC count may be low early in the infectious process, especially in those who are immunosuppressed, so diagnosis is not possible solely based on WBC count.
-Blood cultures for aerobic and anaerobic organisms should be obtained.
-Irreversible joint damage can occur without rapid, appropriate treatment of septic arthritis.
Diagnosis of septic arthiritis
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Broad-spectrum antibiotics are typically started before culture results have been received. Once the organism is identified, more specific treatment can be determined. IV antibiotics are typically transitioned to oral antibiotics, with total treatment of 4 to 6 weeks.
Tx of septic arthritis
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are a group of multisystem inflammatory disorders that affect the spine, peripheral joints, and periarticular structures.
spondyloarthropathies
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disorders include ankylosing spondylitis, psoriatic arthritis, and reactive arthritis. They are all negative for RF so we call them
seronegative arthropathies.
144
inheritance of human leukocyte antigen (HLA) B27 is strongly associated with these diseases. Both genetic and environmental factors play a role in their development.
play key role to spondyloarthropathies
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include absence of antibodies in the serum, peripheral joint involvement (mainly of the lower extremities), low back pain (sacroiliitis), pain and redness of the eyes (uveitis), intestinal inflammation, and psoriasis.
sign/symp of spondyloarthropathies
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is a chronic inflammatory disease that primarily affects the axial skeleton, including the sacroiliac joints, intervertebral disc spaces, and costovertebral articulations.
Ankylosing spondylitis (AS)
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Inflammation in the joints and adjacent tissue causes the formation of granulation tissue (pannus) and dense fibrous scars that can cause joint fusion. Inflammation can affect the eyes, lungs, heart, kidneys, and peripheral nervous system.
cause of Ankylosing spondylitis (AS)
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AS is characterized by symmetric sacroiliitis and progressive inflammatory arthritis of the axial skeleton. Symptoms of inflammatory spine pain are the first clues to AS. The patient often has low back pain, stiffness, and limitation of motion that is worse during the night and in the morning but improves with mild activity. In women, early symptoms may include pain and stiffness in the neck rather than the lower back. Uveitis is the most common nonskeletal symptom. It can appear as an initial presentation of the disease years before arthritic symptoms develop. Patients with AS may have distressing chest pain and sternal/costal cartilage tenderness.
-Severe postural abnormalities and deformity can cause significant disability (Fig. 64.8). Impaired spinal ROM and fusion, along with vision problems, raise concerns about safe ambulation. Aortic insufficiency and pulmonary fibrosis are common complications. Cauda equina syndrome (compression of the nerves at the end of the spinal cord) can occur. This contributes to lower extremity weakness and bladder dysfunction. The patient is at risk for spinal fracture from associated osteoporosis.
sign/ symp of Ankylosing spondylitis (AS)
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X-rays are the most important radiographic technique for the diagnosis and follow up of AS
-MRI is useful in assessing early cartilage abnormalities. CT scan is appropriate in specific situations (e.g., cases with subtle x-ray changes). Changes on later spinal films include the appearance of “bamboo spine,” the result of calcifications (syndesmophytes) that bridge from one vertebra to another. An increased ESR and mild anemia may be seen.
-presence of the HLA-B27 antigen i
diagnosis of Ankylosing spondylitis (AS)
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AS is aimed at maintaining maximal skeletal mobility while decreasing pain and inflammation. Heat applications can help relieve local symptoms. NSAIDs and salicylates are often prescribed. DMARDs, such as sulfasalazine or methotrexate, have little effect on spinal disease but help with peripheral joint disease. Local corticosteroid injections may be helpful in relieving symptoms.
-TNF, which promotes inflammation, is increased in the blood and certain tissues of patients with AS. Etanercept, a BRM, binds TNF and inhibits its action. Etanercept reduces active inflammation and improves spinal mobility. Other anti-TNF inhibitors (infliximab, adalimumab, golimumab) may be effective.
Tx for Ankylosing spondylitis (AS)
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back, neck, and chest stretches. Hydrotherapy (e.g., sauna, steam bath) can decrease pain and facilitate spinal extension.
exercise plan should include for Ankylosing spondylitis (AS)
152
Surgery may be needed for severe deformity and mobility impairment. Spinal osteotomy and total joint replacement are the most common procedures (
surgery for Ankylosing spondylitis (AS)
153
inflammation, is increased in the blood and certain tissues of patients with AS
TNF, which promotes
154
is a progressive inflammatory disease that affects about 30% of people with psoriasis
Psoriatic arthritis (PsA)
155
a common, benign, inflammatory skin disorder characterized by red, irritated, and scaly patches. Both PsA and psoriasis appear to have a genetic link with HLA antigens in many patients.
Psoriasis is
156
is unknown, we suspect a combination of immune, genetic, and environmental factors.
exact cause of PsA
157
-Distal arthritis
-Asymmetric arthritis
-Symmetric psoriatic arthritis resembles RA
-Psoriatic spondylitis
-Arthritis mutilans
PsA can occur in different forms
158
the ends of the fingers and toes, with pitting and color changes in the fingernails and toenails.
Distal arthritis mainly involves (form of PsA )
159
different joints on each side of the body
Asymmetric arthritis involves (form of PsA )
160
joints on both sides of the body at the same time.
-accounts for about 50% of cases
Symmetric psoriatic arthritis resembles RA. It affects (form of PsA )
161
pain and stiffness in the spine and neck.
Psoriatic spondylitis is marked by (form of PsA )
162
only 5% of people with PsA. It is the most severe form of the disease, causing complete destruction of small joints.21
Arthritis mutilans affects (form of PsA )
163
On x-ray, the cartilage loss and erosion are similar to RA. Advanced cases often show widened joint spaces. A “pencil in cup” deformity is common in the DIP joints due to thinning, weakened bone. In this deformity, the narrowed ends of the metacarpals or phalanges insert into the expanded end of the other bone sharing the joint. Increased ESR, mild anemia, and increased serum uric acid can be seen in some patients. Thus the diagnosis of gout must be excluded.
diagnosis of Psoriatic arthritis (PsA)
164
splinting, joint protection, and PT. NSAIDs given early in the course of the disease may help with inflammation. Drug therapy includes the DMARDs, such as methotrexate, which is effective for both articular and cutaneous manifestations. Sulfasalazine, cyclosporine, and BRMs (e.g., etanercept, golimumab, adalimumab, infliximab) may be used. Apremilast (Otezla), an inhibitor of the enzyme phosphodiesterase-4, can treat adults with active PsA.
treatment of Psoriatic arthritis (PsA)
165
occurs more often in young men. It is associated with a symptom complex that includes urethritis, conjunctivitis, and mucocutaneous lesions.
Reactive arthritis (Reiter’s syndrome)
166
reaction triggered in the body after exposure to specific genitourinary or GI tract infections. Chlamydia trachomatis spreads by sexual contact. Reactive arthritis is associated with GI infections from Shigella, Salmonella, Campylobacter, or Yersinia species and other pathogens.
-positive for HLA-B27 are at increased risk for developing reactive arthritis after sexual contact or exposure to certain GI pathogens.
causes Reactive arthritis (Reiter’s syndrome)
167
Urethritis develops within 1 to 2 weeks after sexual contact or GI infection. In women, symptoms include cervicitis. Low-grade fever, conjunctivitis, and arthritis may occur over the next several weeks. This type of arthritis tends to be asymmetric. It often involves the toes and the large joints of the lower extremities. Lower back pain may occur with severe disease. Lesions involving the skin and mucous membranes often occur as small, painless, superficial ulcerations on the tongue, oral mucosa, and glans penis. Soft tissue manifestations include Achilles tendinitis or plantar fasciitis.
sign/ symp of Reactive arthritis (Reiter’s syndrome)
168
doxycycline is widely recommended for patients and their sexual partners.
Because reactive arthritis is often associated with C. trachomatis infection, treatment with
169
Topical ophthalmic corticosteroids may be prescribed for treatment of uveitis. Conjunctivitis and lesions generally do not need treatment. NSAIDs and DMARDs may be used if joint symptoms do not resolve.
-Most patients have complete remission with return of full joint function.
Tx for Reactive arthritis (Reiter’s syndrome)
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X-ray changes in chronic reactive arthritis closely resemble those of AS
diagnosis of Reactive arthritis (Reiter’s syndrome)
171
is a multisystem inflammatory autoimmune disease.
Systemic lupus erythematosus (SLE)
172
It is a complex disorder of multifactorial origin resulting from interactions among genetic, hormonal, environmental, and immunologic factors
cause Systemic lupus erythematosus (SLE)
173
the skin, joints, and serous membranes (pleura, pericardium). Renal, hematologic, and neurologic systems are also affected.
SLE typically affects
174
Multiple genes from the HLA complex, including HLA-DR2 and HLA-DR3, are associated with SLE.
cause SLE
175
Hormones are known to play a role in SLE. Onset or worsening of disease symptoms may occur after the start of menses, with the use of oral contraceptives, and during and after pregnancy. The disease tends to become worse in the immediate postpartum period.
symtoms gets severe during (SLE)
176
sun or ultraviolet light exposure, stress, and exposure to some chemicals and toxins. Infectious agents, such as viruses, may stimulate immune hyperactivity. More than 45 drugs currently in use may trigger SLE. Most cases have been related to procainamide, hydralazine, and quinidine.
environmental factors cause SLE
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No characteristic pattern occurs in the progression of SLE. The circulating immune complexes can affect any organ. The most commonly involved tissues are the skin and muscle, lining of the lungs, heart, nervous tissue, and kidneys. General complaints, such as fever, weight loss, joint pain, and excessive fatigue, may precede worsened disease activity.
sign/ symp of SLE
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Severe skin reactions can occur in people who are sensitive to sunlight (photosensitivity). The classic butterfly rash over the cheeks and bridge of the nose occurs
-skin disease can occur in people who do not have full-blown SLE
-chronic cutaneous lupus (CCLE) with discoid (round, coin-shaped) lesions.
-subacute cutaneous lupus (SCLE). Lesions in SCLE usually do not scar or itch and are not thick and scaly.
-Oral or nasopharyngeal ulcers
-Alopecia is common, with or without related scalp lesions.
-scalp becomes dry, scaly, and atrophied.
dermatologic problems (SLE)
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multiple joints (polyarthralgia) with morning stiffness is often the first complaint. It may precede the onset of multisystem disease by many years. Diffuse swelling occurs with joint and muscle pain and some stiffness. SLE-related arthritis is generally nonerosive but may cause deformities (e.g., swan neck deformity of the fingers, ulnar deviation, subluxation with joint laxity). Patients have increased risk for bone loss and fracture.
arthiritis in SLE
180
Tachypnea and cough suggest the presence of lung disease. Pleurisy is possible. Cardiac involvement may include dysrhythmias due to fibrosis of the sinoatrial and atrioventricular nodes
-Inflammation can lead to pericarditis, myocarditis, and endocarditis. Hypertension and hypercholesterolemia from steroid use need aggressive treatment and careful monitoring
-risk for secondary antiphospholipid syndrome. This coagulation disorder causes clots in the arteries and veins. It increases the risk for stroke, gangrene, and heart attack.
heart problems SLE
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. This coagulation disorder causes clots in the arteries and veins. It increases the risk for stroke, gangrene, and heart attack.
secondary antiphospholipid syndrome (SLE)
182
Renal involvement is usually present within the first 5 years after diagnosis.26 Manifestations vary from mild proteinuria to rapidly progressive glomerulonephritis. Scarring and permanent damage can lead to end-stage renal disease (ESRD).
renal problems with SLE
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corticosteroids, cytotoxic agents (cyclophosphamide), and immunosuppressive agents (azathioprine, cyclosporine, mycophenolate mofetil [CellCept]). Oral prednisone or pulsed IV methylprednisolone may be used, especially in the initial treatment period when cytotoxic agents have not yet taken effect.
-high-intensity treatment with warfarin.(blood problem)
-Vaccinations are generally safe for patients with SLE. Patients receiving corticosteroids or cytotoxic drugs must avoid live virus vaccines. (infections)
Tx for SLE
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SLE have generalized-onset or focal-onset seizures. Seizures are generally controlled by corticosteroids or antiseizure drugs. Peripheral neuropathy can occur, leading to sensory and motor deficits.
Cognitive problems may result from the deposit of immune complexes within the brain. There may be disordered thinking, disorientation, and memory deficits. Various psychiatric problems may occur, including depression, mood disorders, anxiety, and psychosis.
- stroke or aseptic meningitis. Headaches are common
Neurologic SLE
185
due to formation of antibodies against blood cells. Anemia, leukopenia, thrombocytopenia, and coagulation disorders (excess bleeding or clotting)
-high-intensity treatment with warfarin.
Blood problems are common (SLE)
186
. Risk may be due to impaired ability to eliminate invading bacteria, deficient antibody production, and immunosuppressive effects of many antiinflammatory drugs.
-***Pneumonia is the most common infection
-Vaccinations are generally safe for patients with SLE. Patients receiving corticosteroids or cytotoxic drugs must avoid live virus vaccines.
infection for SLE
187
SLE is marked by the presence of ANA in 97% of persons with the disease.
-Anti-DNA antibodies are found in half the persons with SLE.
-Anti-Smith (Sm) antibodies are found in 30% to 40% of persons with SLE and are almost always considered diagnostic.
-Nearly 30% of people with SLE will have antiphospholipid antibodies.
-Antibodies to histone are most often seen in people with drug-induced SLE.
diagnosis for SLE
188
-NSAIDs -mild joint pain
**Monitor the patient on long-term NSAID therapy for GI and renal effects.
-Antimalarial agents, such as hydroxychloroquine and chloroquine, are often used to treat fatigue and skin & and joint problems& reduce occurrence of flares. (repress the immune system but do not cause immunosuppression.)
****hydroxychloroquine should have eye examinations by an ophthalmologist every 6 to 12 months. Retinopathy can develop with high doses of these drugs.
-if cannot tolerate an antimalarial agent, an antileprosy drug, such as dapsone, may be used.
-Use of corticosteroids should be limited to the lowest dose for the shortest possible time. For example, steroids can be used for a few weeks until a slower acting medication becomes effective. Taper the patient’s dose of steroid slowly rather than stopping the medication abruptly.
---High doses of corticosteroids may be especially appropriate for the patient with severe cutaneous SLE.
-Belimumab (Benlysta) is a B-lymphocyte stimulator that inhibits the inflammation of SLE.
-Immunosuppressive drugs, such as azathioprine and cyclophosphamide, may be used to suppress the immune system and reduce end-organ damage.
-Topical immunomodulators can be used instead of corticosteroids to treat serious skin conditions. Tacrolimus (Protopic, Prograf) and pimecrolimus (Elidel) suppress immune activity in the skin, affecting the butterfly rash and discoid lesions.
Tx for SLE (drug)
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is a disorder of connective tissue characterized by fibrotic, degenerative, and, sometimes, inflammatory changes in the skin, blood vessels, synovium, skeletal muscle, and internal organs.
Scleroderma (systemic sclerosis)
190
localized scleroderma, which is the more common form, and systemic scleroderma.
Two types of disease exist:
191
skin changes of localized disease are usually limited to a few places on the skin or muscle without involvement of the trunk or internal organs. The prognosis of patients with limited disease is better than for those with systemic disease.
localized Scleroderma
192
Skin and connective tissue changes progress rapidly during the first months of systemic scleroderma, which is associated with internal organ involvement.
systemic disease. Scleroderma
193
immunologic and vascular abnormalities play a role in the development of systemic disease
cause systemic disease Scleroderma
194
environmental or occupational exposure to coal, plastics, and silica dust.
Risk factors Scleroderma include
195
(protein that gives normal skin its strength and elasticity)
collagen
196
body makes too much collagen (protein that gives normal skin its strength and elasticity). this leads to progressive tissue fibrosis and occlusion of blood vessels. Collagen overproduction also disrupts normal function of internal organs, such as the lungs, kidney, heart, and GI tract.
-Vascular problems, which mainly involve the small arteries and arterioles, are almost always present. These changes are some of the earliest changes in scleroderma.
systemic Scleroderma pathology
197
range from benign limited skin disease to diffuse skin thickening with rapidly progressive and widespread organ involvement.
manifestation of Scleroderma
198
Calcinosis: painful deposits of calcium in skin of fingers, forearms, pressure points
Raynaud’s phenomenon: intermittent vasospasm of fingertips in response to cold or stress
Esophageal dysfunction: difficulty swallowing due to internal scarring
Sclerodactyly: tightening of skin on fingers and toes
Telangiectasia: red spots on hands, forearms, palms, face, and lips from capillary dilation
-(Raynaud’s phenomenon (sudden vasospasm of the digits) is the most common first complaint in localized scleroderma.)
-skin thickening generally does not extend above the elbow or knee, although the face may be affected.
-fingers may stay in a semiflexed position (sclerodactyly), with tightened skin to the wrist (Fig. 64.12). Reduced peripheral joint function may be an early symptom of arthritis.
Localized disease is often marked by the CREST syndrome
199
Symmetric painless swelling or thickening of the skin of the fingers and hands may progress to diffuse scleroderma of the trunk.
-skin loses elasticity and becomes taut and shiny.
-causes the typical expressionless face with tightly pursed lips. Skin changes in the face may contribute to reduced ROM in the temporomandibular joint
systemic symp skin and joint changes
200
develop secondary Sjögren’s syndrome, a condition associated with dry eyes and dry mouth. Dysphagia, gum disease, and dental decay can result. Frequent reflux of gastric acid can occur due to esophageal fibrosis. If swallowing becomes difficult, the patient is likely to decrease food intake and lose weight. GI effects include constipation from colonic hypomotility and diarrhea due to malabsorption from bacterial overgrowth.
-Lung problems include pleural thickening, pulmonary fibrosis, and abnormal pulmonary function. The patient develops a cough and dyspnea. Pulmonary arterial hypertension and interstitial lung disease may occur. Lung disease is the main cause of death in scleroderma.
-Heart disease includes pericarditis, pericardial effusion, and dysrhythmias. Heart failure from myocardial fibrosis occurs most often in patients with systemic disease.
-renal disease bc malignant hypertension associated with rapidly progressive, irreversible renal insufficiency can occur, early recognition of renal involvement (angiotensin-converting enzyme (ACE) inhibitors (e.g., lisinopril [Prinivil]) has had a marked effect on the ability to treat renal disease.)
internal organ involvement with Scleroderma
201
* History and physical examination
* Antibodies to topoisomerase-1
* Anticentromere antibody
* Nail bed capillary microscopy
* Chest x-ray
* Skin or organ biopsy
* Urinalysis (proteinuria, hematuria, casts)
* Pulmonary function tests
* ECG
diagnosis of Scleroderma
202
(Vasoactive agents are often prescribed in early disease ex:reserpine, bosentan, epoprostenol) Calcium channel blockers (nifedipine [Procardia], diltiazem [Cardizem]) and the angiotensin II blocker losartan are common treatments for Raynaud’s phenomenon
-Reserpine, an α-adrenergic blocking agent, increases blood flow to the fingers.
-Bosentan (Tracleer), an endothelin-receptor antagonist, and the vasodilator epoprostenol (Flolan) may improve blood flow to the lung.
-NSAIDs and topical agents may give some relief from joint pain
-Capsaicin cream may be useful, not only as a local analgesic but also as a vasodilator
-Other therapies prescribed to treat specific systemic problems include (1) tetracycline for diarrhea caused by bacterial overgrowth, (2) histamine (H2) receptor blockers (e.g., cimetidine) and proton pump inhibitors (e.g., omeprazole) for esophageal symptoms, and (3) antihypertensive agent (e.g., captopril, propranolol, methyldopa) for hypertension with renal involvement. Immunosuppressive drugs (e.g., cyclophosphamide, mycophenolate mofetil) are used in severe cases.
-
Tx of Scleroderma
203
is diffuse, idiopathic, inflammatory myopathy of striated muscle. It causes bilateral weakness, usually most severe in the proximal or limb girdle muscles.
Polymyositis (PM) (more severe than DM)
204
When muscle changes associated with PM are accompanied by distinctive skin changes, the disorder is called
dermatomyositis (DM).
205
origin with T cell–mediated destruction of unidentified muscle antigens. Environmental factors are likely, including viral and bacterial infection, certain drugs, supplements, vaccines, medical implants, and occupational exposure.
cause Polymyositis (PM) dermatomyositis (DM).
206
weight loss and increasing fatigue, with gradually developing muscle weakness that causes difficulty in performing ADLs.
-most commonly affected muscles are in the shoulders, legs, arms, and pelvic girdle
-Repetitive movements are more likely to cause trouble than a single strength exercise.
-unable to raise the head from a pillow as neck muscles weaken.
- Muscle discomfort or tenderness is uncommon.
-Muscle examination shows an inability to move against resistance or even gravity.
****Weak pharyngeal muscles may cause dysphagia and dysphonia (nasal or hoarse voice).
PM and DM muscular sign/symp
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DM symp:
-Rashes are typical with DM (early recognition)
-classic red or purple symmetric rash (heliotrope) with edema around the eyelids
-scaly, smooth, or raised rash may be seen on the knuckles and sides of the hands (Gottron’s papules)
-Reddened, smooth, or scaly patches appear with the same symmetric distribution but sparing the interphalangeal spaces (Gottron’s sign).
- rash can be confused with psoriasis or seborrheic dermatitis
-red, scaling rash (poikiloderma) may develop as a late finding on the back, buttocks, and a V-shaped area of the anterior neck and chest.
-Hyperemia and telangiectasia are often present at the nail beds.
-Calcium nodules (calcinosis cutis) can develop throughout the skin and are especially common in long-standing DM.
-DM have increased risk for cancer and should receive age- and gender-appropriate screenings.
-PM Symp:
has no rashes
sign/symp with dermal (PM&DM)
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Joint redness, pain, and inflammation often occur. They contribute to limited joint ROM in PM and DM. Contractures and muscle atrophy may occur with advanced disease. Weakened pharyngeal muscles can lead to poor cough effort, difficulty swallowing, and increased risk for aspiration pneumonia. Interstitial lung disease is a common complication.
-associated with other connective tissue disorders (e.g., scleroderma).
other signs/ symp with (PM&DM)
209
Biopsy is the gold standard for diagnosis of PM or DM after other neuromuscular diseases are excluded.
-Muscle biopsy shows necrosis, degeneration, regeneration, and fibrosis with pathologic findings distinct for DM or PM.
gold standard for diagnosis of PM or DM
210
MRI can identify areas of inflammation and guide the biopsy site selection.
-Increased muscle enzymes (e.g., creatine kinase, myoglobin) reflect muscle damage but will decrease to normal or near normal with treatment.
- EMG suggestive of PM shows bizarre high-frequency discharges and spontaneous fibrillation, with positive spikes at rest.
-Increased ESR or CRP occurs with active disease.
Diagnosis of PM or DM
211
high-dose oral corticosteroids, with the dose tapered based on patient response. Most patients respond well to treatment. Long-term corticosteroid therapy may be needed because relapses are common when the drug is withdrawn.
Immunosuppressive drugs (methotrexate, azathioprine, tacrolimus, cyclophosphamide) may be used in combination with steroids or as a second-line therapy if the patient does not respond to steroids. IV immunoglobulin (IVIG) may be given with corticosteroids or immunosuppressants, but it is not a first-line treatment.
Tx for PM or DM
212
* Give by slow infusion to decrease risk for thromboembolic complications.
* Hydrate patient well during infusion to decrease risk for renal failure.
* Treat transient adverse effects, such as headache.
IV Immunoglobulin (IVIG) (TX for PM, DM)
213
-Injection of synthetic ACTH (repository corticotropin injection [Acthar]) helps with muscle spasms.
(TX for PM, DM)
214
combination of clinical features of several rheumatic diseases are described as having
-SLE, scleroderma, and PM
mixed connective tissue disease
215
connective tissue disease develop another related disease over the course of several years, which is known as
overlap syndrome
216
is a relatively common autoimmune disease that targets the moisture-producing exocrine glands
Sjögren’s syndrome
217
leads to xerostomia (dry mouth) and keratoconjunctivitis sicca (dry eyes).
-nose, throat, airways, and skin can become dry. The disease may affect other glands, including those in the stomach, pancreas, and intestines (extraglandular involvement).
Sjögren’s syndrome
218
, problems occur with lacrimal and salivary glands.
- extended disease affecting the lungs, liver, kidneys, and skin= occurrence increases the risk for non-Hodgkin’s lymphoma.
primary Sjögren’s syndrome
219
genetic and environmental factors
-trigger may be a viral or bacterial infection that adversely stimulates the immune system.
Sjögren’s syndrome appears to be caused by
220
lymphocytes attack and damage the lacrimal and salivary glands.
Sjögren’s syndrome,
221
common with Sjögren’s syndrome.
Autoimmune thyroid disorders, including Graves’ disease and Hashimoto’s thyroiditis, are
222
the lymph nodes, bone marrow, and visceral organs (pseudolymphoma).
Sjögren’s syndrome, may become more generalized and involve
223
Ophthalmologic examination (Schirmer’s test for tear production), measures of salivary gland function, and lower lip biopsy of minor salivary glands aid in diagnosis.
diagnosis for Sjögren’s syndrome,
224
(1) instillation of preservative-free artificial tears or ophthalmic antiinflammatory drops (e.g., cyclosporine [Restasis]) as needed for adequate hydration and lubrication, (2) surgical punctal occlusion, and (3) increased fluids with meals. Dental hygiene is important.
Treatment is symptomatic, including (Sjögren’s syndrome,)
225
Pilocarpine (Salagen) and cevimeline (Evoxac) can ease the dry mouth. Increased humidity at home may reduce respiratory tract infections. Vaginal lubrication with a water-soluble product, such as K-Y Jelly, may increase comfort during intercourse.
Tx for Sjögren’s syndrome,
226
is a chronic form of muscle pain and tenderness, typically in the chest, neck, shoulders, hips, and lower back. Referred pain from these muscle groups can travel to the buttocks, hands, and head, causing severe headaches.
-Temporomandibular joint pain may originate in myofascial pain
-Regions of pain are often within the connective tissue (fascia) that covers skeletal muscles
Myofascial pain syndrome
227
deep, aching pain with a sensation of burning, stinging, and stiffness.
sign/symp of Myofascial pain
228
PT treatment is the “spray and stretch” method. The painful area is iced or sprayed with a coolant, such as ethyl chloride and then stretched. Positive results have been seen with topical patches and injection of the trigger points with a local anesthetic (e.g., 1% lidocaine). Massage, dry needling, and ultrasound therapy have helped some patients.35
Tx for Myofascial pain
229
is a chronic central pain syndrome marked by widespread, nonarticular musculoskeletal pain and fatigue with multiple tender points
Fibromyalgia
230
share many common features
Fibromyalgia and systemic exertion intolerance disease (SEID) (formerly called chronic fatigue syndrome)
231
include (1) increased levels of substance P in the spinal fluid, (2) low blood flow to the thalamus, (3) dysfunction of the hypothalamic-pituitary-adrenal (HPA) axis, (4) low serotonin and tryptophan, and (5) abnormal cytokine function.
pain occurs bc (Fibromyalgia)
232
Head or facial pain often results from stiff or painful neck and shoulder muscles. The pain can accompany temporomandibular joint dysfunction, which affects about one third of patients with fibromyalgia.
-widespread burning pain that fluctuates through the course of a day.
-tenderness at 11 or more of 18 identified sites
-palpation of all sites may cause pain.
-migraine headaches. Depression and anxiety
-Stiffness, nonrefreshing sleep, fatigue, and numbness or tingling in the hands or feet often accompany fibromyalgia. Restless legs syndrome is typical. Some describe an irresistible urge to move the legs when at rest or lying down.
-Irritable bowel syndrome with constipation and/or diarrhea, abdominal pain, and bloating is common. Patients may have difficulty swallowing, perhaps because of problems in esophageal smooth muscle function. Increased frequency of urination and urinary urgency, in the absence of a bladder infection, may occur. Women with fibromyalgia may have more difficult menstruation, with disease symptoms worse during this time.
symp of Fibromyalgia
233
pain in response to a stimulus that does not typically cause pain
(allodynia)
234
(1) pain is experienced in 11 of the 18 tender points on palpation (Fig. 64.14) and (2) a history of widespread pain is noted for at least 3 months.37 Widespread pain is defined as pain that occurs on both sides of the body and above and below the waist
ACR classifies a person as having fibromyalgia if 2 criteria are met: ( Fibromyalgia)
235
an alternative method of diagnosis. A symptom severity scale and a widespread pain index are used to identify disease characteristics
ACR classification uses non–tender point diagnostic criteria as ( Fibromyalgia)
236
pregabalin (Lyrica), duloxetine (Cymbalta), and milnacipran (Savella). Low-dose tricyclic antidepressants, selective serotonin reuptake inhibitors (SSRIs), or benzodiazepines (e.g., diazepam) may be prescribed. SSRI antidepressants (e.g., sertraline [Zoloft], paroxetine [Paxil]) tend to be reserved for patients who also have depression. SSRIs may have to be prescribed at higher doses than when used to treat depression. Antidepressants and muscle relaxants (e.g., baclofen) have sedative effects that can improve nighttime rest for the patient with fibromyalgia.
-Long-acting opioids are not recommended unless other therapies are not successful. In some patients, pain may be managed with OTC analgesics, such as acetaminophen, ibuprofen, or naproxen (Aleve). Nonopioids, such as tramadol (Ultram), may be used. Zolpidem (Ambien) or trazodone is sometimes given for short-term intervention in patients with severe sleep problems
Tx Fibromyalgia
237
is a serious, complex, multisystem disease in which exertion of any sort (physical, emotional, cognitive) is impaired and accompanied by profound fatigue
Systemic exertion intolerance disease (SEID), formerly called chronic fatigue syndrome,
238
Neuroendocrine abnormalities have been implicated involving a hypofunction of the HPA axis and hypothalamic-pituitary-gonadal (HPG) axis, which together regulate the stress response and reproductive hormone levels. Several microorganisms have been investigated as causative agents, including herpes viruses (e.g., Epstein-Barr virus [EBV], cytomegalovirus [CMV]), retroviruses, enteroviruses, Candida albicans, and mycoplasma. Because many patients have cognitive deficits (e.g., decreased memory, attention, concentration), changes in the CNS have been suggested as the cause of SEID.
possible cause of Systemic exertion intolerance disease (SEID)
