CASE STUDY

Rheumatoid
Arthritis
Submitted To: Mrs. Michelle Suguitan, RN

Submitted By: Group Two

1. Garcia, Cyrrus Inorey P.

2. Hassan, Faduma M.

3. Ibikunle, Eniola O.

4. Liwanag, Ruben Jr. A.

5. Lunzaga, Berna Jean

6. Mallo, Jessy F.

7. Marjolino, Emilyn

8. Mohamed Adem, Amda N.

9. Omotara Okunlule
Patient Profile

N.M. is a 36-year-old overweight white woman who has RA. When her symptoms began to
interfere with her daily activities, she sought medical help.

Subjective Data

• Has painful, stiff hands and feet

• Feels tired all of the time

• Reports an intermittent low-grade fever

• Takes naproxen (Aleve) 220 mg twice daily

• Wears a copper bracelet on the advice of a neighbor

Objective Data

• Hands show mild ulnar drift and puffiness

• Temp: 100°F (37.8°C)

• Admitted to the hospital for examination and comprehensive treatment plan

• Methotrexate (Rheumatrex) therapy to be initiated

Discussion Questions

Using a separate sheet of paper, answer the following questions:

1. How should the nurse explain the pathophysiology of rheumatoid arthritis to N.M.?
The exact reason for rheumatoid arthritis is not yet identified; but it well known that
when this happens, the body's immune system all of a sudden turns against itself -
articularly the tissues found at the joints. This is why the symptoms of this disease
include extreme pain at the joints (usually in pairs, for example - both elbows, both
knees, etc). It is believed that genetics also play a very important role here.

2. What manifestations does N.M. have that suggest the diagnosis of RA?
N.M complains of painful and stiff hands and upon assessment her hands shows mild
ulnar drift with puffiness which indicates Rheumatoid Arthritis.

3. What diagnostic studies will confirm the diagnosis of RA?

The diagnosis is done by identifying the rheumatoid factor which is actually an antibody
that indicates the presence of this dreadful disease. The presence of this antibody (in the
blood) as well as the typical symptoms such as pain, inflammation and movement
limitation can confirm the diagnosis. An X-ray of the affected joints can further confirm
the presence of the disease.

4. What results may be expected from methotrexate therapy? What are the nursing
responsibilities related to methotrexate therapy?
MTX can be administered orally or subcutaneously and is take once a week. MTX
(particularly in its oral preparation) can cause nausea and this side effect is often reduced
by the co-administration of folic acid 5-10mg the day after MTX. MTX can cause blood-
test abnormalities including cytopenias and raised liver function tests. Patient’s bloods
are checked regularly to monitor for these abnormalities and may necessitate a temporary
cessation of the drug.

5. What are some suggestions that may be offered to N.M. concerning home
management and joint protection?
NM can take steps to care for their body if they have rheumatoid arthritis. These self-care
measures, when used along with their rheumatoid arthritis medications, can help them
manage their signs and symptoms:
- Exercise regularly. Gentle exercise can help strengthen the muscles around the
joints, and it can help fight fatigue they might feel. Check with the doctor before they
start exercising. If they're just getting started, begin by taking a walk. Try swimming
or gentle water aerobics. Avoid exercising tender, injured or severely inflamed joints.
 - Apply heat or cold. Heat can help ease the pain and relax tense, painful muscles.
Cold may dull the sensation of pain. Cold also has a numbing effect and decreases
muscle spasms.
- Relax. Find ways to cope with pain by reducing stress in your life. Techniques such
as guided imagery, distraction and muscle relaxation can all be used to control pain.

6. How can the nurse help N.M. to recognize ineffective, unproven methods of
treatment?
It’s important as a nurse to properly explain to N.M that using unproven methods of
treatment has their own risks and can worsen the condition of her Rheumatoid Arthritis
and encourage and teach her the proper management of rheumatoid arthritis so they
won’t have to consider using other methods.

7. What other sources of information regarding arthritis might the nurse suggest to
N.M.?
If the patient plans to know more about rheumatoid arthritis it’s important to refer her to
her doctor so he could properly discuss the matter that is solely for her condition and can
focus on what she needs anf what she has to know.

8. Priority Decision: Based on the assessment data presented, what are the priority
nursing diagnoses? Are there any collaborative problems?
The priority nursing diagnosis would be Impaired physical mobility related to decreased
range of motion. There would be no collaborative problem because it is highly
recommended that the patient would be sent to a physical or occupational therapist who
can teach them exercises to help keep their joints flexible. The therapist may also suggest
new ways to do daily tasks, which will be easier on their joints.
 I. Objectives of the Study.
1. To understand what Rheumatoid Arthritis is.
2. To know about its Pathophysiology and its related causative factors.
3. Formulate a Nursing care plan for the client and its management.

II. Introduction
A. Definition of Case

-Rheumatoid arthritis (RA) is an autoimmune disease in which the body’s immune system –
which normally protects its health by attacking foreign substances like bacteria and viruses –
mistakenly attacks the joints. This creates inflammation that causes the tissue that lines the inside
of joints (the synovium) to thicken, resulting in swelling and pain in and around the joints. The
synovium makes a fluid that lubricates joints and helps them move smoothly.

-If inflammation goes unchecked, it can damage cartilage, the elastic tissue that covers the ends
of bones in a joint, as well as the bones themselves. Over time, there is loss of cartilage, and the
joint spacing between bones can become smaller. Joints can become loose, unstable, painful and
lose their mobility.

B. Etiology

-Cause is unknown

-May be autoimmune process/may be genetic

-Predisposing factors include fatigue, cold, emotional, stress, infection.

C. Incidence

-About 1.5 million people in the United States have rheumatoid arthritis (RA). Nearly three times
as many women have the disease as men. In women, RA most commonly begins between ages
30 and 60. In men, it often occurs later in life. Having a family member with RA increases the
odds of having RA; however, the majority of people with RA have no family history of the
disease.

D. General signs and symptoms

 Tender, warm, swollen joints

 Joint stiffness that is usually worse in the mornings and after inactivity

 Fatigue, fever and weight loss

Early rheumatoid arthritis tends to affect your smaller joints first — particularly the joints that
attach your fingers to your hands and your toes to your feet.

As the disease progresses, symptoms often spread to the wrists, knees, ankles, elbows, hips and
shoulders. In most cases, symptoms occur in the same joints on both sides of your body.

About 40 percent of the people who have rheumatoid arthritis also experience signs and
symptoms that don't involve the joints. Rheumatoid arthritis can affect many non-joint structures,
including:

 Skin

 Eyes

 Lungs

 Heart

 Kidneys

 Salivary glands

 Nerve tissue

 Bone marrow

 Blood vessels
III. Patient’s Data

A. Patient Data

Name: N.M.

Age: 36 years old

Nutritional Status: Over weight

B. Nursing History

Present history:

Subjective Data:

• Has painful, stiff hands and feet

• Feels tired all of the time

• Reports an intermittent low-grade fever

• Takes naproxen (Aleve) 220 mg twice daily

• Wears a copper bracelet on the advice of a neighbor

Objective Data:

• Hands show mild ulnar drift and puffiness

• Temp: 100°F (37.8°C)

• Admitted to the hospital for examination and comprehensive treatment plan

• Methotrexate (Rheumatrex) therapy to be initiated

Past history:

Repeated symptom’s interfere with daily activity

 C. Course in the Ward

Example of Examination and Therapy done with RA

Blood tests

People with rheumatoid arthritis often have an elevated erythrocyte sedimentation rate (ESR, or
sed rate) or C-reactive protein (CRP), which may indicate the presence of an inflammatory
process in the body. Other common blood tests look for rheumatoid factor and anti-cyclic
citrullinated peptide (anti-CCP) antibodies.

Imaging tests

Your doctor may recommend X-rays to help track the progression of rheumatoid arthritis in your
joints over time. MRI and ultrasound tests can help your doctor judge the severity of the disease
in your body.

Treatment

There is no cure for rheumatoid arthritis. But recent discoveries indicate that remission of
symptoms is more likely when treatment begins early with strong medications known as disease-
modifying antirheumatic drugs (DMARDs).

Medications

The types of medications recommended by your doctor will depend on the severity of your
symptoms and how long you've had rheumatoid arthritis.

 NSAIDs. Nonsteroidal anti-inflammatory drugs (NSAIDs) can relieve pain and reduce
inflammation. Over-the-counter NSAIDs include ibuprofen (Advil, Motrin IB) and
naproxen sodium (Aleve). Stronger NSAIDs are available by prescription. Side effects may
include ringing in your ears, stomach irritation, heart problems, and liver and kidney
damage.
 Steroids. Corticosteroid medications, such as prednisone, reduce inflammation and pain
and slow joint damage. Side effects may include thinning of bones, weight gain and
diabetes. Doctors often prescribe a corticosteroid to relieve acute symptoms, with the goal
of gradually tapering off the medication.
Disease-modifying antirheumatic drugs (DMARDs). These drugs can slow the progression of
rheumatoid arthritis and save the joints and other tissues from permanent damage. Common
DMARDs include methotrexate (Trexall, Otrexup, Rasuvo), leflunomide (Arava),
hydroxychloroquine (Plaquenil) and sulfasalazine (Azulfidine).

Side effects vary but may include liver damage, bone marrow suppression and severe lung
infections.

Biologic agents. Also known as biologic response modifiers, this newer class of DMARDs
includes abatacept (Orencia), adalimumab (Humira), anakinra (Kineret), certolizumab (Cimzia),
etanercept (Enbrel), golimumab (Simponi), infliximab (Remicade), rituximab (Rituxan),
tocilizumab (Actemra) and tofacitinib (Xeljanz).

These drugs can target parts of the immune system that trigger inflammation that causes joint
and tissue damage. These types of drugs also increase the risk of infections.

Biologic DMARDs are usually most effective when paired with a nonbiologic DMARD, such as
methotrexate.
Therapy

Your doctor may send you to a physical or occupational therapist who can teach you exercises to
help keep your joints flexible. The therapist may also suggest new ways to do daily tasks, which
will be easier on your joints. For example, if your fingers are sore, you may want to pick up an
object using your forearms.

Assistive devices can make it easier to avoid stressing your painful joints. For instance, a kitchen
knife equipped with a saw handle helps protect your finger and wrist joints. Certain tools, such as
buttonhooks, can make it easier to get dressed. Catalogs and medical supply stores are good
places to look for ideas.

Surgery

If medications fail to prevent or slow joint damage, you and your doctor may consider surgery to
repair damaged joints. Surgery may help restore your ability to use your joint. It can also reduce
pain and correct deformities.

Rheumatoid arthritis surgery may involve one or more of the following procedures:

 Synovectomy. Surgery to remove the inflamed synovium (lining of the joint).

Synovectomy can be performed on knees, elbows, wrists, fingers and hips.
  Tendon repair. Inflammation and joint damage may cause tendons around your joint to
loosen or rupture. Your surgeon may be able to repair the tendons around your joint.
 Joint fusion. Surgically fusing a joint may be recommended to stabilize or realign a joint
and for pain relief when a joint replacement isn't an option.
 Total joint replacement. During joint replacement surgery, your surgeon removes the
damaged parts of your joint and inserts a prosthesis made of metal and plastic.

IV. Anatomy and Physiology

There are over 100 forms of arthritis affecting Americans today and one of the most
known, but not necessarily the most common, is Rheumatoid Arthritis. Rheumatoid arthritis or
RA, is a form of inflammatory arthritis and an autoimmune disease, meaning the body's immune
system mistakenly attacks healthy tissue. This form of arthritis can not be cured, making it a
chronic disease. In some people the disease is continuously active and gets worse over time while
others enjoy long periods of remission were they experience no disease activity or symptoms at
all. No one fully understands why in rheumatoid arthritis the immune system – which is designed
to protect our health by attacking foreign cells like viruses and bacteria – instead attacks the body’s
own tissues. It specifically attacks the synovium, a thin membrane that lines the joints. As a result
of the attack, fluid builds up in the joints, causing pain in the joints and inflammation that can
occur throughout the body. Many would love to know how this form of arthritis forms so they can
stop it but what causes RA are unknown. Doctors and researchers have said it had something to
do with ones genes but not everyone with these specific genes have RA.

What is astonishing about Rheumatoid arthritis is the common people who get it. An
estimated 1.3 million people in the United States have RA. People of every race and ethnic group,
men, women, and children get RA. There are of course some people who are more likely to get it
than others like, females, Native Americans, smokers, people between the age of 30 and 50, and
people related to people with RA. Researchers have also found many other possibilities like
obesity, a history of blood transfusions, a short fertile period in women, and making to much or
too little of certain hormones. Although RA is not curable, treatment is still necessary. The reason
for treatment is to reduce joint inflammation and pain, maximize joint function, and prevent
destruction and deformity. It is necessary to get treatment because it improves function, it stops
damage at the joints and most importantly prevents work disability. Treatment for this RA involves
a combination of medications, rest, joint-strengthening exercises, joint protection, and patient
education. All treatments are different because it goes according to many factors like, disease
activity, the types of joint involved, general health, age, and patient’s occupation. There are two
classes of medications: fast acting "first-line drugs" and slow acting "second-line drugs". RA can
be destructive but it varies among affected individuals. Some can manage it with rest plus pain
control and anti-inflammatory medications alone and in some cases with severe joint deformity,
surgery may be necessary.

V. Pathophysiology

The synovitis, swelling, and joint damage that characterize active RA are the end results
of complex autoimmune and inflammatory processes that involve components of both the innate
and adaptive immune systems.In a susceptible individual, the interaction of environment and genes
results in a loss of tolerance of self-proteins that contain a citrulline residue. These proteins are
generated via post translational modification of arginine residues to citrulline residues by the
enzyme peptidylarginine deiminase.9 Patients with shared epitopes generate citrullinated peptides
that are no longer recognized as “self” by the immune system, which consequently develops
ACPAs against them.16 Comparison of magnetic resonance imaging (MRI) and synovial biopsy
data from healthy individuals with MRI and biopsy data from patients positive for RF and/or
ACPA demonstrate that systemic autoantibody production precedes inflammation and adhesion
molecule formation in the synovium, indicating that perhaps some secondary event is required to
initiate involvement of the synovium in RA.17 In a study of 79 patients with RA, the initial
appearance of RF and ACPA preceded the development of clinical RA involving the synovium by
a median of 4.5 years.

Synovitis occurs as a consequence of leukocyte infiltration into the synovium. The

accumulation of leukocytes in the synovium does not result from local cellular proliferation but
rather from migration of leukocytes from distant sites of formation in response to expression of
adhesion molecules and chemokines by activated endothelial cells of synovial microvessels.9The
interior of the inflamed synovium is hypoxic,19 presumably as a result of the proliferation of
synovial cells and reduction in synovial capillary flow as a consequence of increased fluid volume
in the synovium.20 Hypoxia, in turn, stimulates angiogenesis in the synovium, perhaps by
inducing the formation of factors that stimulate vessel formation such as vascular endothelial
growth Factors. Immune activation and RA disease progression is a complex process that involves
interactions between components of both the adaptive and innate immune pathways. The nature of
these interactions is greatly affected by the local cytokine and chemokine environment of the
synovium in which they take place. In established RA, the synovial membrane is populated by a
variety of inflammatory cell types that work together to cause joint destruction.9

The importance of the adaptive immune pathway in RA is suggested by the presence of

dendritic cells, a major class of antigen-presenting cells that expresses a variety of cytokines, HLA
class II molecules, and costimulatory molecules in close proximity to clusters of T cells in the
synovium. Dendritic cells present antigens to T cells that are present in the synovium and also
serve as one component of the T-cell activation process.22 Activation of T cells requires 2 signals.
The first signal is antigen presentation to the T-cell receptor. The second signal, the costimulatory
signal, requires interaction of the cell surface protein CD80/86 on the antigen-presenting
(dendritic) cell with the CD28 protein on the T cell.23 Blockade of the costimulatory signal through
competitive inhibition of CD80/86 interferes with T-cell activation and downstream events. The
effectiveness of CD80/86 blockade as a treatment for RA validates the concept that T cells play
an active role in the pathophysiology of RA.

When T-cell activation does occur, naïve T helper (Th) cells differentiate into 3 major
subpopulations (Th1, Th2, and Th17) with distinct cytokine production profiles and functions.
Although RA has long been considered to be a disease that is mediated by Th1 cells, recent interest
has been focused on the Th17 subpopulation. Dendritic cells and macrophages both secrete
transforming growth factor β, interleukin (IL)-1β, IL-6, IL-21, and IL-23, cytokines that support
Th17 differentiation and suppress production of regulatory T cells, thus shifting the homeostatic
balance in the synovium toward inflammation. In turn, Th17 cells produce IL-17A, IL-17F, IL-22,
IL-26, interferon-g, the chemokine CCL20, and the transcription factor ROR-g. Production of IL-
17A stimulates fibroblast-like synoviocytes (FLSs) and macrophage-like synoviocytes to up
regulate production of IL-26, which induces production of the inflammatory cytokines IL-1β, IL-
6, and TNF-α by monocytes; these cytokines stimulate further differentiation of Th17 cells. In
addition to antigen-driven inflammatory pathways, inflammation can be mediated through
antigen-nonspecific pathways initiated by cell-to-cell contact between activated T cells and
macrophages and fibroblasts.

Humoral adaptive immunity also plays an integral role in the pathogenesis of RA. The
contribution of B cells to autoimmune disease can be mediated through several potential
mechanisms. Defects in B-cell tolerance checkpoints can result in auto reactive B cells that act as
antigen-presenting cells that are capable of activating T cells. B cells can also produce both pro-
and anti-inflammatory cytokines. Finally, B cells can function as antibody-producing cells.
Separately or in combination, these mechanisms can contribute to RA pathogenesis.30 Additional
support for the involvement of B cells in RA is provided by the successful use of agents that deplete
specific B-cell populations for the management of RA. Rituximab, a monoclonal antibody directed
against CD20-positive B cells, has demonstrated success in RA clinical trials and is currently
approved for use in patients with RA who are refractory to TNF inhibitors.

Cells of the innate immune system, including macrophages, mast cells, and natural killer
cells, are located in the synovial membrane, whereas neutrophils are typically found in the synovial
Intracellular signaling pathways are also involved in the pathogenesis of RA. All of the various
cytokines, chemokines, antibodies, and antigens that contribute to inflammation bind to receptors
on the cell surface of specific target cells. Receptor binding typically results in a cascade of
intracellular signaling events that ultimately converges upon the nucleus of the cell and alters gene
expression in ways that can affect cell function. In particular, changes in gene expression in
immune cells are frequently associated with production and secretion of inflammatory mediators
in response to a particular stimulus. Secretion of these mediators into the extracellular milieu
results in further amplification and/or modification of the original signal. Examples of intracellular
signaling pathways include the mitogen-activated protein kinase (MAPK) pathway, the Janus
kinases (JAK) pathway, the signal transducers and activators of transcription (STAT) pathway,
spleen tyrosine kinase (Syk) signaling, and the nuclear factor κ-light-chain enhancer of activated
B cells (NF-κB) pathway. Cross communication between pathways has been reported.

Intracellular signaling pathways are essential for a normal immune response, and
aberrations in these pathways may contribute to autoimmune disease. The first generation of small
molecules directed against intracellular targets is now being used for the treatment of RA. Further
understanding of these pathways will likely lead to the identification of additional therapeutic
targets. The inflammation of RA is also associated with characteristic changes in mesenchymal
tissue. FLSs, which are normally resident in the synovium, proliferate and change their phenotype
in the setting of RA.9 In the inflamed synovium, cell contact between FLSs and T cells results in
the induction of a variety of inflammatory mediators and adhesion molecules, including IL-6, TNF,
interferon-g, intracellular adhesion molecule-1, and vascular cell adhesion molecule-1. Altered
FLSs invade the cartilage of the joint and produce a variety of proteases that contribute to joint
destruction.

Macrophages, in particular, are important effectors of synovitis that act through

phagocytosis; antigen presentation; and the release of pro-inflammatory cytokines, reactive
oxygen intermediates, prostanoids, and matrix-degrading enzymes. Toll like receptors (TLRs) on
monocytes, macrophages, and dendritic cells serve to initiate the inflammatory and immune
response upon exposure to an immunogenic stimulus, such as a microbial pathogen. Activation of
TLRs results in the rapid expression of proinflammatory cytokines that mediate an immune
response that recruits neutrophils, monocytes, and lymphocytes. Macrophages and dendritic cells
accumulate processed antigen and migrate to peripheral lymphoid tissue where antigen is
presented to cells of the adaptive immune system with resultant activation of cellular immunity
and production of antibodies. In most cases, the combination of innate and adaptive immune
system responses will eliminate the pathogen, leading to cessation of the immune response. In the
setting of RA, however, the inflammatory response is not terminated following clearance of the
pathogen but rather remains chronically activated.

VIII. Discharge Planning

 Disorder education. The patient and family must be able to explain the nature of the
disease and principles of disease management.

 Medications. The patient must be able to describe the medication regimen (name of
medications, dosage, schedule of administration, precautions, potential side effects, and
desired affects.

 Pain Management. The patient must be able to describe and demonstrate use of pain
management technique such as:
a. Getting Regular Exercise. Exercise is important because it promotes both
muscle strength and joint flexibility. Swimming is an excellent choice because
it places minimal stress on joints.
b. Applying hot and cold compress. Stiffness affects rheumatoid arthritis,
particularly in the morning.

 Independence. The patient must be able to describe and demonstrate ability to perform
self-care activities independently.
-Eating a healthy diet. A healthy diet can maintain an appropriate body
weight. Adequate calcium in the body to prevent developing of weak bones.

 Follow-up care. The patient must go to all appointments, and call the doctor or nurse if
having problems. It’s also a good idea to know the test results.

IX. Implications of case study in the following areas

 Nursing research
The most common issues that should be address in the case study for the patient with rheumatoid
arthritis (RA) include pain, sleep disturbance, fatigue, altered mood, and limited mobility. The
patient with newly diagnosed RA needs information about the disease to make daily self-
management decisions and to cope with having a chronic disease.
Nursing intervention with related rationale example

 Nursing intervention

Recommend or provide firm mattress or bedboard, small pillow. Elevate linens with bed cradle as
needed.

Rationale

Soft and sagging mattress, large pillows prevent maintenance of proper body alignment, placing
stress on affected joints. Elevation of bed linens reduces pressure on inflamed or painful joints.

 Nursing education

Explaining to them how to prevent and avoid the re occurrence of RA

Informing them about the importance of complete medication

Educating the watcher about comfortable position while in bed and advantage of firm mattress

And also health teachings to avoid exposure to so much cold

 Nursing practice

Medication should be given at the right time.

Observe the patient and also ask question about the pain observe for altered mood and limited
mobility .

The patient must also be informed about the disease condition to make daily self management
decision and to cope with having the disease.

X. References

https://www.ajmc.com/journals/supplement/2014/ace017_may14_ra-ce/ace017_may14_ra-
ce_gibofsky1_s128?p=2

https://www.arthritis.org/about-arthritis/types/rheumatoid-arthritis/what-is-rheumatoid-
arthritis.php

https://nurseslabs.com/rheumatoid-arthritis/?fbclid=IwAR0jN4-2AMp6ALGu9XwF2w2Unswm-
kFSycbvROC2TgToWyIIvycacgZFtmQ
https://www.medicinenet.com/naproxen/article.htm

https://www.mayoclinic.org/diseases-conditions/rheumatoid-arthritis/symptoms-causes/syc-
20353648

https://myhealth.alberta.ca/?fbclid=IwAR0GZh5zcB4gXTK1lcMxMJ3-
mnw105VQIrPECjUti0F4zO1A8p7w17xnSos

https://www.spineuniverse.com/conditions/spinal-arthritis/rheumatoid-arthritis/anatomy-
rheumatoid-arthritis