Module 4 - Chapter 6 - Rheumatoid Arthritis Flashcards
1
Q
What is Rheumatoid Arthritis (RA)?
A
Rheumatoid Arthritis (RA) is a chronic autoimmune disease characterized by joint inflammation and damage.
2
Q
What is the primary tissue affected in RA?
A
The primary tissue affected in RA is the synovial membrane, which lines the joint cavity.
3
Q
What are the two main types of synovial cells involved in RA?
A
The two main types of synovial cells involved in RA are fibroblastlike synovial cells (SFs) and macrophagelike synovial cells.
4
Q
What triggers the progression of RA, and what happens to SFs as a result?
A
The trigger for RA progression is still unknown, but once activated, SFs undergo significant changes and develop an exaggerated immune response.
5
Q
What do activated SFs in RA produce, and what is the consequence of this production?
A
Activated SFs in RA produce proinflammatory cytokines, enzymes, and prostaglandins, leading to increased inflammation and thickening of the synovial tissue (pannus).
6
Q
What does the thickened synovial tissue (pannus) in RA do to the bone?
A
The thickened synovial tissue (pannus) in RA invades the bone and acts like a localized tumor, causing bone destruction.
7
Q
How do altered signaling pathways in RA affect immune reactions?
A
Altered signaling pathways in RA cause SFs to attach to articular cartilage, attack it, release enzymes, inflammatory chemokines, and cytokines, and promote blood vessel growth.
8
Q
Altered signaling pathways in RA cause SFs to attach to articular cartilage, attack it, release enzymes, inflammatory chemokines, and cytokines, and promote blood vessel growth.
A
Increased blood vessel formation in RA allows activated SFs to enter the bloodstream, affecting other joints in the body.
9
Q
What are the consequences of RA inflammation spreading to the joint capsule, ligaments, and tendons?
A
When inflammation spreads to the joint capsule, ligaments, and tendons in RA, it causes pain, joint deformity, and loss of function.
10
Q
Which parts of the body are commonly affected by RA, aside from joints?
A
RA commonly affects joints in the fingers, feet, wrists, elbows, ankles, and knees. It can also involve other tissues such as the shoulders, hips, cervical spine, as well as the lungs, heart, kidneys, and skin.
11
Q
Break this down into detailed flashcards in question format with answers.
A
RA now affects around 1% of adults in developed countries.
12
Q
Does the risk of developing RA change with age?
A
Yes, the risk of RA increases as people get older.
13
Q
Besides joints, what other symptoms can RA cause?
A
RA can cause fever, general discomfort, skin rashes, enlarged lymph nodes or spleen, and Raynaud’s phenomenon, which affects blood circulation in fingers and toes.
14
Q
What is the exact cause of RA?
A
The exact cause of RA remains unknown but is likely a combination of genetic and inflammatory factors.
15
Q
How do genetic factors contribute to RA?
A
Genetic factors, particularly genes in the human leukocyte antigen (HLA) areas, play a significant role in the development of RA.
16
Q
What recent discovery has been made regarding T-cells and RA?
A
Recent research has suggested that T-cell abnormalities may lead to faster aging of telomeres and affect the immune system in people with RA
17
Q
What are rheumatoid factors (RFs) in the context of RA?
A
In RA, normal antibodies can transform into autoantibodies called rheumatoid factors (RFs) that attack the body’s own tissues.
18
Q
How do environmental factors influence the risk of RA?
A
Environmental factors like birthplace, diet, socio-economic status, and smoking can increase the risk of developing RA and make it more severe.
19
Q
Is RA more common in men or women?
A
RA and other autoimmune diseases are more prevalent among women.
20
Q
How do hormonal changes during pregnancy relate to RA?
A
Hormonal changes during pregnancy can impact the severity of RA symptoms, with symptoms often improving during pregnancy and worsening in the postpartum period.
21
Q
What is citrullination, and how does it relate to RA?
A
Citrullination is a process where arginine is modified into citrulline during inflammation. Citrullinated proteins are recognized as antigens by the immune system in RA.
22
Q
What role do T cells and B cells play in the autoimmune response in RA?
A
Both T cells and B cells (B lymphocytes) are involved in the autoimmune response in RA. T cells express RANKL, promoting osteoclast formation and bone erosion.
23
Q
What are the three main processes that contribute to cartilage damage in RA?
A
Cartilage damage in RA results from (1) activation of cells in synovial fluid, (2) breakdown of cartilage and bone by inflammatory cytokines, and (3) the conversion of synovium into abnormal granulation tissue known as pannus.
24
Q
Which inflammatory cytokines are particularly involved in the breakdown of cartilage and bone in RA?
A
Inflammatory cytokines like tumor necrosis factor-alpha (TNF-α), interleukin-1beta (IL-1β), IL-6, IL-7, and IL-21 induce the enzymatic breakdown of cartilage and bone in RA.
25
What happens when T cells interact with synovial fibroblasts (SFs) in RA?
T cells, through TNF-α interaction with SFs, convert synovium into an abnormal thick layer of granulation tissue called pannus.
26
What role do macrophages play in the pathophysiology of RA?
Macrophages are components of pannus and stimulate the release of inflammatory substances like IL-1, PDGF, and fibronectin in RA.
27
How does the production of rheumatoid factors (RFs) by B cells relate to RA?
In RA, B cells are stimulated to produce more RFs. These RFs target self-antigens (Igs) and perpetuate inflammation and the formation of immune complexes.
28
What are the damaging effects of inflammatory and immune processes on the synovial membrane in RA?
Inflammatory processes in RA cause swelling due to leukocyte infiltration and abnormal thickening as synovial cells proliferate and enlarge.
29
How does inflammation affect blood vessels in the synovial membrane?
Inflammation in the synovial membrane can block small venules with hypertrophied endothelial cells, fibrin, platelets, and inflammatory cells.
30
What are the consequences of reduced blood flow in the synovial membrane?
Reduced blood flow in the synovial membrane, combined with increased metabolic demands, leads to hypoxia (lack of oxygen) and metabolic acidosis.
31
What happens when acidosis occurs in the synovial membrane?
Acidosis triggers the release of hydrolytic enzymes from synovial cells into the surrounding tissue.
32
How do hydrolytic enzymes affect the joint in RA?
Hydrolytic enzymes initiated by acidosis erode the articular cartilage and cause inflammation in supporting ligaments and tendons.
33
What is pannus formation, and what does it lead to in the joint?
Pannus formation is the thickening of the synovial tissue, but it does not lead to synovial or articular regeneration. Instead, it results in the formation of scar tissue that immobilizes the joint.
34
What is the typical onset of RA, and how common is an acute onset?
The onset of RA is usually gradual (insidious), with only about 10% of cases having an acute onset.
35
What are the initial systemic symptoms of RA?
RA starts with systemic symptoms like fever, fatigue, weakness, loss of appetite, weight loss, generalized aching, and stiffness.
36
How do local manifestations of RA develop?
Local manifestations in RA gradually appear over weeks or months, with joints becoming painful, tender, and stiff.
37
What causes pain early in RA, and what causes pain later in the disease?
Early pain in RA results from pressure due to joint swelling. Later in the disease, pain is caused by sclerosis of subchondral bone and new bone formation.
38
What are the main reasons people seek medical help for RA?
Pain and the inability to perform normal functions are the primary reasons people seek medical help for RA.
39
How long does morning stiffness typically last in RA, and what is it related to?
Morning stiffness in RA usually lasts for about 1 hour after waking and is believed to be related to synovitis (inflammation of the synovial membrane).
40
Which joints are commonly involved initially in RA, and which joints may be affected later?
Initially, the joints most commonly involved in RA are the MCP joints (knuckles), proximal interphalangeal joints (finger joints), and wrists. Larger weight-bearing joints may be affected later.
41
What causes widespread, symmetric joint swelling in RA, and how does it feel on palpation?
Widespread, symmetric joint swelling in RA is caused by an increase in inflammatory substances in the synovial membrane, hyperplasia of inflamed tissues, and new bone formation. On palpation, swollen joints feel warm, and the synovial membrane feels boggy.
42
How does the skin over a swollen joint appear in RA?
The skin over a swollen joint in RA may have a ruddy, cyanotic hue and may look thin and shiny.
43
How does joint inflammation affect mobility in RA?
Inflammation in a joint can reduce its mobility. Even mild synovitis (joint inflammation) can lead to a decreased range of motion, which becomes more noticeable once the inflammation subsides.
44
What happens to joint extension in RA?
Extension of a joint can become limited in RA and may be lost if flexion contractures develop.
45
What are some permanent joint deformities that can occur in RA?
RA can lead to permanent deformities in the fingers, toes, and limbs, including ulnar deviation of the hands, boutonnière and swan neck deformities of finger joints, plantar subluxation of metatarsal heads in the foot, and hallux valgus (angulation of the big toe toward other toes).
46
What are flexion contractures, and are they common in RA?
Flexion contractures are joint deformities where the joint is stuck in a bent position. They are common in RA, affecting the knees and hips, among other joints.
47
How do joint deformities affect muscle around the joint?
Loss of joint motion in RA leads to secondary atrophy of the surrounding muscles. This muscle atrophy makes the joint less stable, worsening joint problems.
48
What complications can result from excessive inflammatory exudate in the synovial cavity?
Excessive inflammatory exudate in the synovial cavity can lead to two complications in chronic RA.
Formation of cysts in the articular cartilage or subchondral bone, which can sometimes communicate with the skin surface and drain through passages called fistulae.
Rupture of a cyst or the synovial joint itself, often due to strenuous physical activity, which releases inflammatory exudate into adjacent tissues, spreading inflammation.
49
What are extrasynovial rheumatoid nodules, and how common are they in individuals with RA?
Extrasynovial rheumatoid nodules are collections of inflammatory cells surrounding a central core of fibrinoid and cellular debris. They are the most common extra-articular (outside the joints) manifestations of RA and can be seen in up to 30% of individuals with RA.
50
What types of cells are found in these nodules?
T cells are the predominant type of white blood cells (leukocytes) found within the nodules. B cells, plasma cells, and phagocytes are also present around the periphery.
51
Where are these nodules most commonly found on the body?
Rheumatoid nodules are most often found in subcutaneous (under the skin) tissue over the extensor surfaces of elbows and fingers. Less common sites include the scalp, back, feet, hands, buttocks, and knees.
52
Besides the skin, where else can rheumatoid nodules invade in the body?
Rheumatoid nodules can also invade the skin, cardiac valves, pericardium (the sac around the heart), pleura (lining of the lungs), lung parenchyma (lung tissue), and spleen.
53
What characterizes these nodules when they invade other tissues?
When rheumatoid nodules invade other tissues, they are characterized by central tissue necrosis surrounded by proliferating connective tissue. Large numbers of lymphocytes and occasional plasma cells are also observed.
54
What are some specific complications associated with these nodules?
In some cases, these nodules can lead to acute glaucoma when they form on the sclera (the white part of the eye). Pulmonary involvement can result in conditions like diffuse pleuritis, multiple intraparenchymal (inside lung tissue) nodules, and the development of Caplan's syndrome when combined with pneumoconiosis (lung inflammation from dust inhalation). Diffuse pulmonary fibrosis can also occur due to immune complex deposition.
55
What can rheumatoid nodules within the heart cause?
Rheumatoid nodules within the heart can lead to valvular deformities, particularly affecting the aortic valve leaflets, and can cause pericarditis (inflammation of the sac around the heart).
56
What is lymphadenopathy, and how does it relate to RA?
Lymphadenopathy refers to enlarged lymph nodes. In RA, lymph nodes close to affected joints may become enlarged.
57
What happens when rheumatoid nodules form in the spleen?
Rheumatoid nodules in the spleen can result in splenomegaly, which means an enlargement of the spleen.
58
How can blood vessels be affected by rheumatoid nodules?
Rheumatoid nodules can involve blood vessels and lead to acute necrotizing vasculitis, which is characteristic of inflammatory states. Thromboses (blood clots) in these involved vessels can result in conditions like heart attacks (myocardial infarctions), cerebrovascular blockages, mesenteric infarction (intestinal blood supply blockage), kidney damage, and vascular problems in the hands and fingers (Raynaud's phenomenon).
59
Is there any positive news regarding vascular changes and RA?
Fortunately, the development of vascular changes, particularly systemic vasculitis, is decreasing in frequency as more effective treatments for RA are becoming available.
60
Are there any changes noted in skeletal muscles due to RA?
Yes, changes in skeletal muscles are often seen in the form of nonspecific atrophy, which occurs as a secondary effect of joint dysfunction in RA.
61
How is RA diagnosed, and what are the challenges in early diagnosis?
RA is diagnosed based on clinical evaluation of joint swelling. However, in the early stages, pain and limited movement can make it challenging to identify individuals who would benefit from treatment. Early treatment is crucial to prevent the long-term effects of RA.
62
What are autoantibodies, and how do they relate to RA diagnosis?
Autoantibodies are antibodies produced by the immune system that target the body's own tissues. In RA, two important autoantibodies are RF (rheumatoid factor) and ACPA (anticitrullinated protein antibody). These autoantibodies can be present in the blood for many years before symptoms or visible joint damage occur.
63
What is the significance of ACPA compared to RF in RA diagnosis?
ACPA is a much more specific blood marker for RA compared to RF. It provides a higher level of certainty when diagnosing RA.
64
Have there been updates to the criteria for diagnosing RA?
Yes, in 2010, the American College of Rheumatology and the European League Against Rheumatism revised their RA classification criteria to better identify early-stage RA. These criteria continue to be used for diagnosis.
65
What did the Canadian Rheumatology Association update in 2012?
In 2012, the Canadian Rheumatology Association revised its clinical guidelines for managing RA to reflect recent research on effective methods for achieving remission from the condition.
66
What are the main methods for diagnosing RA?
Clinical examination and medical history are the primary tools for diagnosing RA. However, new imaging techniques are showing promise for earlier diagnosis, which can lead to more timely treatment and a better chance of avoiding disability and joint damage.
67
What is the first step in treating RA?
Early treatment of RA typically begins with disease-modifying antirheumatic drugs (DMARDs), which are medications aimed at slowing down the progression of the disease.
68
Can you provide examples of DMARDs?
Some common DMARDs include methotrexate, azathioprine (Imuran), sulfasalazine (Salazopyrin), hydroxychloroquine (Plaquenil), leflunomide (Arava), and cyclosporine (Sandimmune).
69
What is the primary purpose of DMARDs in RA treatment?
DMARDs not only slow down RA progression but also have the potential to prevent complications such as joint deformities and extra-articular (outside the joints) complications.
70
What are biological DMARDs (bDMARDs), and how do they differ from traditional DMARDs?
bDMARDs are a newer class of medications for RA that target specific processes in the development of the disease. They include TNF inhibitors like etanercept (Enbrel), adalimumab (Humira), and infliximab (Remicade), as well as newer monoclonal antibodies like golimumab (Simponi) and certolizumab (Cimzia). Other bDMARDs interfere with cytokine function (anakinra [Kineret] targets IL-1) or inhibit T-cell activation (abatacept [Orencia]) or deplete B cells (rituximab [Rituxan]).
71
What role does education play in RA treatment?
Education is fundamental in managing RA. Patients need to understand the disease, treatment options, and how to manage their condition effectively.
72
Apart from DMARDs and bDMARDs, what other treatments are available for RA?
Additional treatments and therapies for RA include nonsteroidal anti-inflammatory drugs (NSAIDs), glucocorticoids, intra-articular steroid injections, physical and occupational therapy with therapeutic exercises, and the use of assistive devices.
73
When is surgery considered for RA treatment?
Surgery is an option when there are deformities or mechanical issues with joints. Procedures like synovectomy (removal of inflamed synovial tissue) or joint replacement surgery may be performed.
74
What is rheumatoid arthritis (RA)?
Rheumatoid arthritis (RA) is an autoimmune inflammatory disorder that primarily affects the joints and can lead to joint deformities, functional limitations, and systemic manifestations.
75
When do initial symptoms of RA typically appear?
Initial symptoms of RA usually appear during the third and fourth decades of life.
76
How does the incidence of RA vary between genders?
Among younger patients, RA is more common in females, with three times greater incidence than in males. However, among patients older than 60 years, the incidence becomes equal between men and women.
77
What are some of the symptoms and signs of RA?
RA is characterized by symmetric joint stiffness and pain, most intense in the morning and improving throughout the day. Affected joints become swollen, tender, and warm. It can also have systemic manifestations such as fever, weakness, fatigue, weight loss, and more.
78
What is the typical progression of joint deterioration in RA?
Joint deterioration in RA begins with inflammation in the synovium (joint membrane), leading to synovial membrane thickening (pannus) that envelops the articular cartilage. Enzymes from the pannus and inflammatory chemicals damage the cartilage, eventually leading to complete destruction and direct bone-to-bone contact. This is followed by joint fusion and a reduction in inflammation.
79
What is the initial site of inflammation in rheumatoid arthritis (RA)?
The initial site of inflammation in RA is the synovium, the membrane that encloses the joint cavity.
80
What happens as RA inflammation intensifies in the synovium?
As inflammation intensifies, the synovial membrane thickens and begins to envelop the articular cartilage, a process known as pannus formation.
81
How does pannus formation contribute to joint damage in RA?
Pannus formation in RA leads to the release of enzymes and inflammatory chemicals that damage the articular cartilage, eventually resulting in complete cartilage destruction.
82
What occurs once the articular cartilage in an affected joint is completely destroyed?
Once the cartilage is destroyed, direct bone-to-bone contact between the joint's bones occurs, leading to joint fusion.
83
What happens to inflammation as the RA disease progresses through these stages of joint deterioration?
Inflammation tends to reduce after joint fusion occurs, although the joint structure and function may be severely compromised at this stage.
84
What are the main goals of therapy for the condition described?
The main goals of therapy for this condition are (1) relieving symptoms such as pain, inflammation, and stiffness, (2) maintaining joint function and range of motion, (3) minimizing systemic involvement, and (4) delaying disease progression.
85
What approaches are used to achieve the treatment goals for this condition?
To achieve the treatment goals for this condition, a combination of pharmacologic and nonpharmacologic measures is employed.
86
**Flashcard 1: What are some examples of nondrug measures used to manage rheumatoid arthritis (RA)?**
*Answer:* Nondrug measures for managing RA include physical therapy, exercise, and surgery.
87
**Flashcard 2: How can physical therapy benefit individuals with RA?**
*Answer:* Physical therapy for RA may include techniques such as massage, warm baths, and heat application to affected joints. These methods aim to enhance mobility and reduce inflammation.
88
**Flashcard 3: Why is it important to strike a balance between rest and exercise when managing RA?**
*Answer:* Striking a balance between rest and exercise is essential because excessive rest can lead to joint stiffness, while excessive exercise can worsen inflammation in individuals with RA.
89
**Flashcard 4: What are the advances in orthopedic surgery for RA patients with severe joint involvement?**
*Answer:* For RA patients with severe hip or knee disease, total joint replacement surgery is an option. Additionally, in cases of severely damaged hand or wrist joints, surgery can involve the removal of diseased synovium and repair of ruptured tendons. Plastic implants can be used to correct deformities.
90
**Flashcard 5: What is the role of patient education in RA management?**
*Answer:* Patient education is crucial in RA management. It involves informing the patient about the nature of RA, potential consequences of joint degeneration, management strategies, and the benefits and limitations of drug therapy.
91
**Flashcard 6: When might consultation with a social worker, occupational therapist, or vocational rehabilitation specialist be appropriate for someone with RA?**
*Answer:* Consultation with these professionals may be appropriate when the loss of mobility due to RA limits the individual's ability to function effectively at home, work, or school. These specialists can help improve overall function and quality of life.
92
What are the primary objectives of drug therapy for arthritis?
The primary objectives of drug therapy for arthritis are to provide symptomatic relief and, in some cases, induce protracted remission when started early in the disease process.
93
Is complete remission common in arthritis, and why is drug therapy typically lifelong?
Complete remission is rare in arthritis, and drug therapy is usually lifelong because the disease tends to progress steadily, requiring ongoing management.
94
What are the three major classes of antiarthritic drugs?
The three major classes of antiarthritic drugs are:
Nonsteroidal anti-inflammatory drugs (NSAIDs)
Glucocorticoids
Disease-modifying antirheumatic drugs (DMARDs)
95
How do the major groups of arthritis drugs differ in terms of their effects on RA progression, toxicity, and time course of action?
The major groups of arthritis drugs differ in their effects on RA progression, toxicity, and time course of action.
96
What is the primary benefit of NSAIDs in arthritis treatment, and do they slow disease progression or prevent joint damage?
NSAIDs provide rapid relief of symptoms but do not slow disease progression or prevent joint damage. They primarily offer symptomatic relief.
97
How do glucocorticoids differ from NSAIDs in their effects on RA progression and toxicity, and what limits their long-term use?
Glucocorticoids provide rapid relief of symptoms and can slow disease progression. However, they can cause serious toxicity with long-term use, which limits their duration of treatment to short courses.
98
What is the primary mechanism of action for DMARDs, and how are they categorized?
DMARDs (Disease-Modifying Antirheumatic Drugs) reduce joint destruction and slow disease progression by interfering with immune and inflammatory responses. They are categorized into three groups: conventional DMARDs, biologic DMARDs, and targeted DMARDs.
99
How do conventional DMARDs differ from biologic and targeted DMARDs in terms of their development and mode of action?
Conventional DMARDs are small molecules synthesized using conventional chemical techniques and have extensive effects on the immune system. In contrast, biologic DMARDs are large molecules produced through recombinant DNA technology and work on cytokines. Targeted DMARDs are synthetically developed small molecules that block specific pathways inside immune system cells.
100
Why is close monitoring necessary for patients taking DMARDs?
Close monitoring is required for patients taking DMARDs because all DMARDs have significant adverse effects, and monitoring helps manage and minimize these potential side effects.
101
What are the considerations or concerns regarding the use of Biologic DMARDs in children?
Children and adolescents taking TNF antagonists (Biologic DMARDs) have developed lymphoma and other malignancies.
102
What are the considerations or concerns for pregnant women regarding DMARDs?
For pregnant women:
TNF antagonists (Biologic DMARDs) are categorized as US Food and Drug Administration (FDA) Pregnancy Risk Category B.
Rituximab and abatacept are Pregnancy Risk Category C.
Azathioprine is teratogenic.
Leflunomide and methotrexate can cause fetal death and congenital abnormalities.
Hydroxychloroquine may cause fetal ocular toxicity but is used in some conditions like maternal lupus or malaria when the benefits outweigh the risks.
Sulfasalazine is Pregnancy Risk Category B.
103
What is the recommendation for breastfeeding women taking DMARDs?
Breastfeeding is not recommended for mothers taking DMARDs.
104
What are the concerns for older adults taking DMARDs?
Elderly patients may be at a greater risk for infection due to the immunosuppressive effects of DMARDs.
105
Why are NSAIDs often given alongside DMARDs in the treatment of rheumatoid arthritis (RA)?
NSAIDs are given alongside DMARDs in RA treatment because the effects of DMARDs take weeks or months to develop, while NSAIDs provide immediate relief. The NSAID is continued until the DMARD has had time to take effect.
106
What is the typical use of glucocorticoids in RA management?
Glucocorticoids are generally reserved for short-course management of symptom flare-ups and to control symptoms until the DMARD takes effect.
107
What is the recommended approach if joint injury continues to progress despite initial DMARD treatment?
If joint injury continues to progress despite treatment with an initial DMARD (typically methotrexate), another DMARD can be added or substituted.
108
What is the therapeutic role of NSAIDs in the context of RA treatment?
NSAIDs are prescribed for their anti-inflammatory and analgesic actions in RA. These actions result from inhibiting cyclooxygenase (COX). NSAIDs provide symptomatic relief but do not slow disease progression, so they are often combined with a DMARD.
109
How are NSAIDs classified into two main categories, and what distinguishes them?
NSAIDs are classified into two main categories:
First-generation NSAIDs, which inhibit COX-1 and COX-2.
Second-generation NSAIDs (coxibs), which selectively inhibit COX-2. The anti-inflammatory and analgesic effects come from inhibiting COX-2, while major adverse effects, like gastroduodenal ulceration, come from inhibiting COX-1. Second-generation NSAIDs have less gastrointestinal (GI) ulceration risk while providing similar therapeutic effects.
110
What factors guide the selection of an NSAID for RA treatment?
Selection of an NSAID is based on efficacy, safety, and cost. Efficacy can vary among individual patients. Safety considerations include the risk of thrombotic events, GI ulceration, and bleeding. Cost is also a consideration.
111
What is the therapeutic role of glucocorticoids in the treatment of severe RA?
Glucocorticoids have a therapeutic role in the treatment of severe RA as powerful anti-inflammatory drugs that can relieve symptoms and potentially delay disease progression.
112
In what situations are oral glucocorticoids typically indicated for RA patients?
Oral glucocorticoids are indicated for RA patients with generalized symptoms. They are especially useful when patients experience severe symptoms affecting multiple joints.
113
How are glucocorticoids administered for RA patients with one or two affected joints?
For RA patients with only one or two affected joints, intra-articular injections of glucocorticoids may be employed.
114
Why is short-term therapy preferred when using oral glucocorticoids for RA treatment?
Short-term therapy is preferred when using oral glucocorticoids for RA treatment because long-term use can lead to serious toxicity, including osteoporosis, gastric ulceration, and adrenal suppression.
115
What precautions should be taken when prescribing both NSAIDs and glucocorticoids to a patient for RA treatment?
When prescribing both NSAIDs and glucocorticoids to a patient for RA treatment, it's essential to consider the increased risk of adverse GI effects. The risk for GI ulceration and GI bleeding may be increased fourfold when these drugs are used together. Therefore, NSAID therapy is usually discontinued when the patient is taking glucocorticoids.
