CONTENT

NO TITLE PAGE

1 Acknowledgement

2 Overview

3 Aetiology

Pathophysiology

4 Stages of rheumatoid arthritis

5 Case

1) Real case

2) Reference A

3) Reference B

6 Discussion

7 Conclusion

8 Reference
 ACKNOWLEGEMENT

The internship opportunity I had at emergency department, Hospital slim river was a great
chance for learning and professional development. Therefore, I consider myself as a very
lucky individual as I was provided with an opportunity to be part of it. I am also grateful for
having a chance to meet so many wonderful people who led me though this internship period.

Bearing in mind previous I am using this opportunity to express my deepest gratitude and
special thanks to our coordinator instructor Encik Mahidzir Bin Hassan, Encik Wahyudin
Bin Ahmad and our lecturer who in spite of being extraordinary busy with their duties, took
time out to hear, guide and keep me on the correct path and allowing me to carry out my
project at their esteemed organization, extending during the training and giving necessary
advices and guidance and arranged all facilities to make life easier.

It is my radiant sentiment to place on record my best regards, deepest sense of gratitude to

Hospital Slim River and all the Medical staff at Surgical (Ward 9) for their careful and
precious guidance which were extremely valuable for my study both theoretically and
practically.

I express my deepest thanks to Bathumini A/P Raman and her family to giving me correct
information about the patient and help me to carry out my project.

Last but not least, I would like to thank my batch mates who guide me on the correct path and
giving advices during carry out my project.

I perceive as this opportunity as a big milestone in my career development. I will strive to use
gained skills and knowledge in the best possible way, and I will continue to work on their
improvement, in order to attain desired career objectives. Hope to continue cooperation with
all of you in the future.
 OVERVIEW OF RHEUMATOID ARTHRITIS

Rheumatoid arthritis (RA) is a chronic systemic inflammatory disease of unknown cause. The
hallmark feature of this condition is persistent symmetric polyarthritis (synovitis) that affects
the hands and feet, though any joint lined by a synovial membrane may be involved. Extra-
articular involvement of organs such as the skin, heart, lungs, and eyes can be significant.
No laboratory test results are pathognomonic for RA, but the presence of anti-cyclic
citrullinated protein antibody (ACPA) and rheumatoid factor (RF) is highly specific for this
condition.
Optimal care of patients with RA requires an integrated approach that includes
nonpharmacologic therapies and pharmacologic agents such as nonbiologic and biologic
disease-modifying antirheumatic drugs (DMARDs), nonsteroidal anti-inflammatory drugs
(NSAIDs), analgesics, and corticosteroids.
Early therapy with DMARDs has become the standard of care; it not only can more
efficiently retard disease progression than later treatment but also may induce more
remissions. Many of the newer DMARD therapies, however, are immunosuppressive in
nature, leading to a higher risk for infections.
Macrophage activation syndrome is a life-threatening complication of juvenile idiopathic
arthritis (JIA) that necessitates immediate treatment with high-dose steroids and cyclosporine.
(See Complications.)
The following guidelines on treating RA to therapeutic target were issued in 2015 by an
international task force of rheumatologists, patient representatives, and a rheumatology nurse:
 The primary target for treatment of RA should be a state of clinical remission.
Clinical remission is defined as the absence of signs and symptoms of significant
inflammatory disease activity.
 While remission should be a clear target, low-disease activity may be an acceptable
alternative therapeutic goal, particularly in long-standing disease.
 The use of validated composite measures of disease activity, which include joint
assessments, is needed in routine clinical practice to guide treatment decisions.
 The choice of the (composite) measure of disease activity and the target value should
be influenced by comorbidities, patient factors, and drug-related risks.
 Measures of disease activity must be obtained and documented regularly: as
frequently as monthly for patients with high/moderate disease activity or less frequently
(such as every 6 months) for patients in sustained low-disease activity or remission.
 Structural changes and functional impairment and comorbidity should be considered
when making clinical decisions, in addition to assessing composite measures of disease
activity.
 Until the desired treatment target is reached, drug therapy should be adjusted at least
every 3 months.
 The desired treatment target should be maintained throughout the remaining course of
the disease.
 The rheumatologist should involve the patient in setting the treatment target and the
strategy to reach this target.
 ETIOLOGY OF RHEUMATOID ARTHRITIS

The cause of RA is unknown. Genetic, environmental, hormonal, immunologic, and

infectious factors may play significant roles. Socioeconomic, psychological, and lifestyle
factors (eg, tobacco use, the main environmental risk) may influence disease development and
outcome.

Genetic factors

Genetic factors account for 50% of the risk for developing RA. About 60% of RA patients in
the United States carry a shared epitope of the human leukocyte antigen (HLA)-DR4 cluster,
which constitutes one of the peptide-binding sites of certain HLA-DR molecules associated
with RA (example, HLA-DR beta *0401, 0404, or 0405). HLA-DR1 (HLA-DR beta *0101)
also carries this shared epitope and confers risk, particularly in certain southern European
areas. Other HLA-DR4 molecules (example, HLA-DR beta *0402) lack this epitope and do
not confer this risk.
Genes other than those of the major histocompatibility complex (MHC) are also involved.
Results from sequencing genes of families with RA suggest the presence of several resistance
and susceptibility genes, including PTPN22 and TRAF5. 
Juvenile idiopathic arthritis (JIA), also known as juvenile rheumatoid arthritis (JRA), is a
heterogeneous group of diseases that differs markedly from adult RA. JIA is known to have
genetically complex traits in which multiple genes are important for disease onset and
manifestations, and it is characterized by arthritis that begins before the age of 16 years,
persists for more than 6 weeks, and is of unknown origin.  The IL2RA/CD25 gene has been
implicated as a JIA susceptibility locus, as has the VTCN1 gene. 
Some investigators suggest that the future of treatment and understanding of RA may be
based on imprinting and epigenetics. RA is significantly more prevalent in women than in
men, which suggests that genomic imprinting from parents participates in its expression.
Imprinting is characterized by differential methylation of chromosomes by the parent of
origin, resulting in differential expression of maternal over paternal genes. 
Epigenetics is the change in DNA expression that is due to environmentally induced
methylation and not to a change in DNA structure. Clearly, the research focus will be on
environmental factors in combination with immune genetics.

Infectious agents

For many decades, numerous infectious agents have been suggested as potential causes of
RA, including Mycoplasma organisms, Epstein-Barr virus (EBV), and rubella virus. This
suggestion is indirectly supported by the following evidence:
 Occasional reports of flulike disorders preceding the start of arthritis
 The inducibility of arthritis in experimental animals with different bacteria or
bacterial products (example, streptococcal cell walls)
 The presence of bacterial products, including bacterial RNA, in patients’ joints
 The disease-modifying activity of several agents that have antimicrobial effects
(example, gold salts, antimalarial agents, minocycline)
Emerging evidence also points to an association between RA and periodontopathic bacteria.
For example, the synovial fluid of RA patients has been found to contain high levels of
antibodies to anaerobic bacteria that commonly cause periodontal infection,
including Porphyromonas gingivalis. 

Hormonal factors

Sex hormones may play a role in RA, as evidenced by the disproportionate number of
females with this disease, its amelioration during pregnancy, its recurrence in the early
postpartum period, and its reduced incidence in women using oral
contraceptives. Hyperprolactinemia may be a risk factor for RA.
Immunologic factors

All of the major immunologic elements play fundamental roles in initiating, propagating, and
maintaining the autoimmune process of RA. The exact orchestration of the cellular and
cytokine events that lead to pathologic consequences (example, synovial proliferation and
subsequent joint destruction) is complex, involving T and B cells, antigen-presenting cells
(example, B cells, macrophages, and dendritic cells), and various cytokines. Aberrant
production and regulation of both pro inflammatory and anti-inflammatory cytokines and
cytokine pathways are found in RA.
T cells are assumed to play a pivotal role in the initiation of RA, and the key player in this
respect is assumed to be the T helper 1 (Th1) CD4 cells. (Th1 cells produce IL-2 and
interferon [IFN] gamma.) These cells may subsequently activate macrophages and other cell
populations, including synovial fibroblasts. Macrophages and synovial fibroblasts are the
main producers of TNF-a and IL-1. Experimental models suggest that synovial macrophages
and fibroblasts may become autonomous and thus lose responsiveness to T-cell activities in
the course of RA.
B cells are important in the pathologic process and may serve as antigen-presenting cells. B
cells also produce numerous autoantibodies (example, RF and ACPA) and secrete cytokines.
The hyperactive and hyperplastic synovial membrane is ultimately transformed into pannus
tissue and invades cartilage and bone, with the latter being degraded by activated osteoclasts.
The major difference between RA and other forms of inflammatory arthritis, such as psoriatic
arthritis, lies not in their respective cytokine patterns but, rather, in the highly destructive
potential of the RA synovial membrane and in the local and systemic autoimmunity.
Whether these 2 events are linked is unclear; however, the autoimmune response conceivably
leads to the formation of immune complexes that activate the inflammatory process to a much
higher degree than normal. This theory is supported by the much worse prognosis of RA
among patients with positive RF results.
 PATHOPHYSIOLOGY OF RHEUMATOID ARTHRITIS

The pathogenesis of RA is not completely understood. An external trigger (example, cigarette

smoking, infection, or trauma) that sets off an autoimmune reaction, leading to synovial
hypertrophy and chronic joint inflammation along with the potential for extra-articular
manifestations, is theorized to occur in genetically susceptible individuals.
Synovial cell hyperplasia and endothelial cell activation are early events in the pathologic
process that progresses to uncontrolled inflammation and consequent cartilage and bone
destruction. Genetic factors and immune system abnormalities contribute to disease
propagation.
CD4 T cells, mononuclear phagocytes, fibroblasts, osteoclasts, and neutrophils play major
cellular roles in the pathophysiology of RA, whereas B cells produce autoantibodies (ie,
rheumatoid factors). Abnormal production of numerous cytokines, chemokines, and other
inflammatory mediators has been demonstrated in patients with RA, including the following:
 Tumor necrosis factor alpha (TNF-α)
 Interleukin (IL)-1
 IL-6
 IL-8
  Transforming growth factor beta (TGF-ß)
 Fibroblast growth factor (FGF)
 Platelet-derived growth factor (PDGF)
Ultimately, inflammation and exuberant proliferation of the synovium (example, pannus)
leads to destruction of various tissues, including cartilage (see the image below), bone,
tendons, ligaments, and blood vessels. Although the articular structures are the primary sites
involved by RA, other tissues are also affected.

This gross photo shows destruction of the cartilage and erosion of the underlying bone with
pannus from a patient with rheumatoid arthritis
 STAGES OF RHEUMATOID ARTHRITIS

The American College of Rheumatology has developed a system for classifying rheumatoid

arthritis that is primarily based upon the X-ray appearance of the joints. This system helps
medical professionals classify the severity of your rheumatoid arthritis with respect to
cartilage, ligaments, and bone.

Stage I

 No damage seen on X-rays, although there may be signs of bone thinning

Stage II

 On X-ray, evidence of bone thinning around a joint with or without slight bone
damage
 Slight cartilage damage possible
 Joint mobility may be limited; no joint deformities observed
 Atrophy of adjacent muscle
 Abnormalities of soft tissue around joint possible
Stage III

 On X-ray, evidence of cartilage and bone damage and bone thinning around the joint
 Joint deformity without permanent stiffening or fixation of the joint
 Extensive muscle atrophy
 Abnormalities of soft tissue around joint possible

Stage IV

 On X-ray, evidence of cartilage and bone damage and osteoporosis around joint

 Joint deformity with permanent fixation of the joint (referred to as ankylosis)
 Extensive muscle atrophy
 Abnormalities of soft tissue around joint possible

Rheumatologists also classify the functional status of people with rheumatoid arthritis as
follows:

 Class I: completely able to perform usual activities of daily living

 Class II: able to perform usual self-care and work activities but limited in activities
outside of work (such as playing sports, household chores)
 Class III: able to perform usual self-care activities but limited in work and other
activities
 Class IV: limited in ability to perform usual self-care, work, and other activities
 COMPLICATIONS OF RHEUMATOID ARTHRITIS

RA itself is not fatal, but complications of the disease may shorten survival by years in some
individuals. In general, RA is progressive and cannot be cured, but in some patients, the
disease gradually becomes less aggressive, and symptoms may even improve. However, if
bone and ligament destruction and any deformities have occurred, the effects are permanent.
Joint disability and pain with daily life are common. Affected joints can become deformed,
and the performance of even ordinary tasks may be very difficult or impossible; these factors
can severely affect patients’ quality of life. In addition, RA is a systemic disease that can
affect other parts of the body in addition to joints. These effects include the following:
 Anemia
 Infections – Patients with RA are at greater risk for infections; immunosuppressive
drugs further increase that risk
 GI problems – Patients with RA may experience stomach and intestinal distress;
however, lower rates of stomach and colorectal cancers have been reported in RA
patients
 Osteoporosis – This condition is more common than average in postmenopausal
women with RA; the hip is particularly affected; the risk of osteoporosis appears to be
higher than average in men with RA who are older than 60 years
 Lung disease – A small study found a high prevalence of pulmonary inflammation
and fibrosis in patients with newly diagnosed RA, but this finding may be associated
with smoking
 Heart disease – RA can affect blood vessels and increase the risk of coronary
ischemic heart disease
 Sjögren syndrome – Keratoconjunctivitis sicca is a common complication of RA; oral
sicca and salivary gland enlargement are less common
 Felty syndrome – This condition is characterized by splenomegaly, leukopenia, and
recurrent bacterial infections; it may respond to disease-modifying antirheumatic drugs
(DMARDs)
  Lymphoma and other cancers – RA-associated immune system alterations may play a
role; aggressive treatments for RA may help prevent such cancers

CASES
REAL CASE

A) Patient History
Real case I studied is rheumatoid arthritis (RA). Patient name, Bathumini A/P Raman (RN
6358), aged 35 years old, came to Emergency department of Hospital Slim River
accompanied by her sister with the chief complaint of bilateral leg pain since 2 weeks. The
history of presenting complaint made by the patient is bilateral leg pain since 2 weeks with
limited range of movement, bilateral finger and elbow pain, swelling at right leg, fever on and
off, loose stool about 2 times and unable to walk. This patient have past medical history of
goitre since 2016, not on treatment and given follow up at Klinik Pakar Medikal, Hospital
slim River and do not have any surgical history.

FAMILY TREE

Husband Patient

-36 years old -35 years old

-No medical and surgical -Goitre

history available

Son
th
st
1 daughter 2nd
daughter rd
3 daughter 4 daughter
-Nil
-Nil -Asthma -Nil -Nil

Based on patient’s family history, we know that this patient is a single mother and have 5
children. This patient do not have any drug allergic. While according to social history, we get
to know this patient is non-alcoholic and smoking person and last time work as cleaner but
have been stopped since having leg pain.

B) Physical examination

During general examinations, this patient is look alert, have good pulse volume, pink, CRT<
2sec, conscious which achieve 15/15 Glasgow coma scale (GCS), and have a good hydration.
His vital sign are observe and recorded.

The vital sign of this patient is,

Vital Sign On arrival Current

Blood pressure (BP) 102/53 mmHg 117/70 mmHg
Pulse rate (PR) 85 bpm 84 bpm
Respiration rate (RR) 21/min 21/min
Body temperature (BT) 37.2 degree Celsius 36.8 degree Celsius
Spo2 100% under room air 98% under room air
Pain score 2/10 4/10

Cardiovascular system is shown dual rhythm no murmur (DRNM). When auscultate the
lungs, air entry show clear and bilaterally equal. While during palpitation, stomach show soft,
non-tender, no mass condition and bowel sound active also found in stomach.

Other physical examination found in her body is swelling at right leg and bilateral elbow and
finger pain.
 Bilateral
elbow and
finger pain

Leg pain

C) Differential diagnosis

- Rheumatoid arthritis

- Thyroid disease

- Osteoarthritis

- Psoriatic arthritis

Systemic lupus erythematous (SLE)

D) Investigation

After undergo the history of patient, physical examination and finding differential diagnosis,
next doctor carry out some laboratory and radiology investigation. For laboratory test, full
blood count (FBC) were taken. The result is as shown below:

Full blood count Result Normal range

White blood count (WBC) 14.60x10^3/UL 4.0-10.0
Total red cells 4.51 x10^6/UL 4.5-5.5
Haemoglobin 13.2 g/dl 13-18
Platelet count 351 x 10^3/UL 150-450

While the result for renal profile (RP) is as shown below:

Renal profile Result Normal range
Blood urea nitrogen 5.4 mmol/L 1.7-8.3
Sodium 138.3 mmol/L 135-154
Potassium 4.5 mmol/L 3.6-5.4
Chloride 106.1 mmol/L 93-108
Creatinine 46 umol/L 48-95

Beside this laboratory investigations, doctor carry out other radiology tests like
electrocardiogram (ECG) shows sinus rhythm and no ischemic discharge, chest x-ray shows
nothing abnormal detected and knee x-ray shows the view of anteroposterior (AP) and lateral
view of both knee.

E) Diagnosis

Rheumatoid arthritis

F) Treatment and management

Initial Management

Patient came to emergency department accompanied by her sister due to leg pain since 2
weeks and bilateral elbow and finger pain. Patient is refereed from Klinik Kesihatan Slim
River. Next, assistant medical officer was checking for the patients vital sign and monitoring
electrocardiogram. Next initial management done in emergency department is taking patient
history, including family, drug and social history and triage this patient at green zone,

Treatment

Pharmacological treatment

Drugs Generic name Trade name Dose Indication

IV Ranitidine Ranitidine 25mg/ml ZANTAC 1.ADULT: Slow 1.Benign
50 mg stat injection Injection IV injection of 50 gastric/
mg diluted to 20 duodenal
ml and given ulceration,
over at least 2 reflux
 minutes. May be oesophagitis
repeated every 6-
8 hours or IV
infusion at rate of
25 mh/hour for 2
hours, may be
repeated at 6-8
hours intervals or
IM. CHILD: 1
mg/kg/dose 6-8
hourly.
2.Initial slow IV
injection of 50
mg, then
continuous
infusion of 125-
250mcg/ kg/hour
IV Maxolon Metoclopramide MAXOLON 1. ADULT: Over 1. Dyspepsia,
10mg Stat HCL 5mg/ml Injection 20 years; 10mg 3 peptic
injection times daily. ulceration,
Maximum daily duodenitis,
dose is 30 mg or nausea,
0.5m/kg vomiting,
2.Single dose 5- choleliathiasis
10 minutes 2. Promote
before bowel transit
examination; during
Adult and Child diagnostic
over 15 years: procedures
10-20mg; CHILD
over 15 years:
10-20mg; Child
less than 15 years
: 0/12mg/kg/dose
 6-12 hourly
ORS Oral Rehydration ORS ADULT: 200- Replacement
Salt 400ml (1-2 of fluid and
sachets) for every electrolyte
loose motion. loss in
CHILD: 200ml diarrhoea
(1 sachet) for
every loose
motion. In severe
dehydration
100ml/kg for 3-4
hours.
INFANTS: 1-1.5
times their usual
feed volume (50
ml per stool for
small infants
T.Paracetamol Paracetamol 500 PANADOL ADULT: 500- Mild to
1g QID mg Tablet Tablet 1000mg every 4- moderate pain
6 hours, and pyrexia
maximum of 4g
daily

G) Advice
- Eat medications followed by the dosage that had been prescribed by doctor

-Eat healthy and vitamin rich diet

-Drink plenty of water

-Take care personal hygiene to avoid from infection

-Do simple exercise

- Ask patient to follow up at Klinik Pakar Orthopedic, Hospital Slim River

-Take plenty of rest

-Avoid harmful environment factor such as smoke or dust and chemical

-Do not lift any heavy objects

REFERENCE A

DEFINITION OF RHEUMATOID ARTHRITIS

According to author named Brenda B.Spriggs from the article Healthline (22 Septembr 2017)
said rheumatoid arthritis (RA) is an autoimmune disease that can cause joint pain and damage
throughout body. The joint damage that RA causes usually happens on both sides of body. So
if a joint is affected in one of the arms or legs, the same joint in the other arm or leg will
probably be affected, too. This is one way that doctors distinguish RA from other forms of
arthritis, such as osteoarthritis (OA).

TYPES OF RHEUMATOID ARTHRITIS

There are several different types of RA. Knowing which type a patient have may help doctor
provide the best type of treatment for you. Types of RA include:

 Seropositive RA: If the patient have seropositive RA, patient have a positive
rheumatoid factor blood test result. This means they have the antibodies that cause
immune system to attack their joints.

 Seronegative RA: If patinet have a negative rheumatoid factor blood test result and a
negative anti-CCP blood test result, but they still have RA symptoms, they may have
seronegative RA. Patient may eventually develop antibodies, changing diagnosis to
seropositive RA.

 JIA (juvenile idiopathic arthritis): Juvenile idiopathic arthritis refers to RA in

people younger than 17 years of age. The condition was previously known as JRA
(juvenile rheumatoid arthritis). The symptoms are the same as those of other types of RA,
but they may also include eye inflammation and issues with physical development.

CAUSES OF RHEUMATOID ARTHRITIS

The cause of RA isn’t known. However, certain factors seem to have a role in increasing the
risk of developing RA or triggering its onset. Factors that increase risk of RA include:

 being a woman

 having a family history of RA

Factors that may trigger onset of RA include:

 exposure to certain types of bacteria, such as those associated with periodontal disease

 having a history of viral infections like infection with the Epstein-Barr virus, which
causes mononucleosis

 trauma or injury, such as bone breakage or fracture, dislocation of a joint, and

ligament damage

 smoking cigarettes

 obesity

SIGN AND SYMPTOMS

RA is a long-term or chronic disease marked by symptoms of inflammation and pain in the

joints. These symptoms and signs occur during periods known as flares. Other times are
known as periods of remission, this is when symptoms dissipate completely.

RA symptoms, which can occur throughout the body, include:

 joint pain

 joint swelling

 joint stiffness

 loss of joint function

Symptoms can vary from mild to severe. It’s important not to ignore your symptoms, even if
they come and go. Knowing the early signs of RA will help the patient and doctor to better
treat it.

INVESTIGATION OF RHEUMATOID ARTHRITIS

Diagnosing RA can take time and may require multiple lab tests to confirm clinical
examination findings. Doctor will use several tools to diagnose RA.

First doctor will ask about the symptoms and medical history. They’ll also perform a physical
exam of joints. This will include looking for swelling and redness, and testing reflexes and
muscle strength. Doctor will also touch the affected joints to check for warmth and
tenderness. If they suspect RA, they’ll most likely refer patient to a specialist called a
rheumatologist.

Since no single test can confirm a diagnosis of RA, doctor or rheumatologist may use several
different types of tests. They may test blood for certain substances like antibodies, or check
the level of certain substances like acute phase reactants that are elevated during
inflammatory conditions. These can be a sign of RA and help support the diagnosis.

They may also request certain imaging tests. Tests such as ultrasonography, x-ray exams, and
magnetic resonance imaging (MRI) not only show if damage from RA has been done to the
joints but also how severe the damage is. A complete evaluation and monitoring of other
organ systems might be in order for some people with RA, too. 

Blood test for rheumatoid arthritis

There are several types of blood tests that help doctor or rheumatologist determine whether
patient have RA. These tests include:

 Rheumatoid factor test: This blood test checks for a protein called rheumatoid
factor. High levels of rheumatoid factor are associated with autoimmune diseases,
especially RA.
 Anticitrullinated protein antibody test (anti-CCP): This test looks for an antibody
that’s associated with RA. People who have this antibody usually have the disease.
However, not everyone with RA tests positive for this antibody.

 Antinuclear antibody test: This tests the immune system to see if it’s producing
antibodies. The body may make antibodies as a response to many different types of
conditions, including RA.

 Erythrocyte sedimentation rate: This test helps determine the degree of

inflammation in body. The result tells doctor whether inflammation is present. However,
it doesn’t indicate the cause of the inflammation.

 C-reactive protein test: A severe infection or significant inflammation anywhere in

body can trigger your liver to make C-reactive protein. High levels of this inflammatory

marker are associated with RA.

TREATMENT OF RHEUMATOID ARTHRITIS

There’s no cure for RA, but there are treatments that can help to manage it. Treatments for
RA help to manage the pain and control the inflammatory response which can in many cases
result in remission. Decreasing the inflammation can also help to prevent further joint and
organ damage.

Treatments may include:

 medications

 alternative or home remedies

 dietary changes

 specific types of exercise

Doctor will work with patient to determine the best types of treatments for you. For many
people, these treatments can help them live an active life and reduce the risk of long-term
complications. 

Rheumatoid arthritis medications

There are many types of medication for RA. Some of these medications help to reduce the
pain and inflammation of RA. Some help to reduce flares and limit the damage that RA does
to your joints. The following medications help reduce the pain and inflammation during RA
flares:

 nonsteroidal anti-inflammatory drugs (NSAIDs)

 corticosteroids

 acetaminophen

The following drugs work to slow the damage that RA can cause to our body:

 Disease-modifying antirheumatic drugs (DMARDs): DMARDs work by blocking

body’s immune system response. This helps to slow down RA’s progression.

 Biologics: These new generation DMARDs provide a targeted response to

inflammation rather than blocking body’s entire immune system response. They may be
an effective treatment for people who don’t respond to treatment with more traditional
DMARDs.

 Janus kinase (JAK) inhibitors: These are a new subcategory of DMARDs that block
certain immune responses. These are drugs that your doctor may use to help prevent
inflammation and stop damage to your joints when DMARDs and biologics don’t work
for you.

Home remedies for rheumatoid arthritis

Certain home remedies and lifestyle adjustments may help to improve your quality of life
when living with RA.
 1. Exercise

Low-impact exercises can help to improve the range of motion in joints and increase our
mobility. Exercise can also strengthen muscles, which can help to relieve some of the
pressure from the joints. We can also try gentle yoga, which will help to regain strength and
flexibility.

2. Get enough rest

We may need more rest during flare-ups and less during remission. Getting enough sleep will
help to reduce inflammation and pain as well as fatigue.

3. Apply heat or cold

Ice packs can help to reduce inflammation and pain. They may also be effective against
muscle spasms. You can alternate cold with hot treatments such as warm showers and hot
compresses. These treatments may help to reduce stiffness.

4. Try assistive devices

Certain devices such as splints and braces can hold joints in a resting position. This may help
to reduce inflammation. Canes and crutches can help you maintain mobility, even during
flares. We can also install household devices, such as grab bars and handrails in bathrooms
and along staircases.

Rheumatoid arthritis diet

Doctor or dietitian may recommend an anti-inflammatory diet for patient to help with
symptoms. This type of diet includes foods that have lots of omega-3 fatty acids.

Foods high in omega-3 fatty acids include:

 fatty fishes, including salmon, tuna, herring, and mackerel

 chia seeds

 flax seeds

 walnuts

Antioxidants, such as vitamins A, C, and E, and selenium, may also help reduce
inflammation. Foods high in antioxidants include:

 berries, such as blueberries, cranberries, goji berries, and strawberries

 dark chocolate

 spinach

 kidney beans

 pecans

 artichokes

Eating lots of fiber is also important, because according to some researchers, fiber may help
reduce inflammatory responses which can be seen as a decrease in C-reactive protein levels.
Choose whole grain foods, fresh vegetables, and fresh fruit. Strawberries may be particularly
beneficial.

Foods containing flavonoids can also help to counter inflammation in the body. They include:

 soy products, such as tofu and miso

 berries

 green tea

 broccoli

 grapes
What we don’t eat is just as important as what we do eat. Make sure to avoid trigger foods.
These include processed carbohydrates and saturated or trans fats. Avoiding trigger foods and
choosing the right foods to follow an anti-inflammatory diet may help to manage our RA.

REFERENCE B

DEFINITION OF RHEUMATOID ARTHRITIS

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. Joint deformity also can occur. Joint damage cannot be
reversed, and because it can occur early, doctors recommend early diagnosis and aggressive
treatment to control RA.

Rheumatoid arthritis most commonly affects the joints of the hands, feet, wrists, elbows,
knees and ankles. The joint effect is usually symmetrical. That means if one knee or hand if
affected, usually the other one is, too. Because RA also can affect body systems, such as the
cardiovascular or respiratory systems, it is called a systemic disease. Systemic means “entire
body.” 
CAUSES OF RHEUMATOID ARTHRITIS

The cause of RA is not yet fully understood, although doctors do know that an abnormal
response of the immune system plays a leading role in the inflammation and joint damage
that occurs. No one knows for sure why the immune system goes awry, but there is scientific
evidence that genes, hormones and environmental factors are involved.

Researchers have shown that people with a specific genetic marker called the HLA shared
epitope have a fivefold greater chance of developing rheumatoid arthritis than do people
without the marker. The HLA genetic site controls immune responses. Other genes connected
to RA include: STAT4, a gene that plays important roles in the regulation and activation of
the immune system; TRAF1 and C5, two genes relevant to chronic inflammation; and
PTPN22, a gene associated with both the development and progression of rheumatoid
arthritis. Yet not all people with these genes develop RA and not all people with the condition
have these genes.

Researchers continue to investigate other factors that may play a role. These factors include
infectious agents such as bacteria or viruses, which may trigger development of the disease in
a person whose genes make them more likely to get it; female hormones (70 percent of
people with RA are women); obesity; and the body’s response to stressful events such as
physical or emotional trauma. Research also has indicated that environmental factors may
play a role in one's risk for rheumatoid arthritis. Some include exposure to cigarette smoke,
air pollution, insecticides and occupational exposures to mineral oil and silica

SIGN AND SYMPTOMS RHEUMATOID ARTHRITIS

In the early stages, people with RA may not initially see redness or swelling in the joints, but
they may experience tenderness and pain.

These following joint symptoms are clues to RA:

 Joint pain, tenderness, swelling or stiffness for six weeks or longer

 Morning stiffness for 30 minutes or longer

 More than one joint is affected

 Small joints (wrists, certain joints of the hands and feet) are affected

 The same joints on both sides of the body are affected

Along with pain, many people experience fatigue, loss of appetite and a low-grade fever.

The symptoms and effects of RA may come and go. A period of high disease activity
(increases in inflammation and other symptoms) is called a flare. A flare can last for days or
months.
Ongoing high levels of inflammation can cause problems throughout the body. Here of some
ways RA can affect organs and body systems:
 Eyes. Dryness, pain, redness, sensitivity to light and impaired vision
 Mouth. Dryness and gum irritation or infection
 Skin. Rheumatoid nodules – small lumps under the skin over bony areas
 Lungs. Inflammation and scarring that can lead to shortness of breath
 Blood Vessels. Inflammation of blood vessels that can lead to damage in the nerves,
skin and other organs
 Blood. Anaemia, a lower than normal number of red blood cell

INVESTIGATION OF RHEUMATOID ARTHRITIS

A primary care physician may suspect RA based in part on a person's signs and symptoms. If
so, the patient will be referred to a rheumatologist – a specialist with specific training and
skills to diagnose and treat RA. In its early stages, RA may resemble other forms of
inflammatory arthritis. No single test can confirm RA. To make a proper diagnosis, the
rheumatologist will ask questions about personal and family medical history, perform a
physical exam and order diagnostic tests.

Medical History

The doctor will ask about personal and family medical history as well as recent and current
symptoms (pain, tenderness, stiffness, difficulty moving).

Physical Exam

The doctor will examine each joint, looking for tenderness, swelling, warmth and painful or
limited movement. The number and pattern of joints affected can also indicate RA. For
example, RA tends to affect joints on both sides of the body. The physical exam may reveal
other signs, such as rheumatoid nodules or a low-grade fever.

Blood Tests

The blood tests will measure inflammation levels and look for biomarkers such as antibodies
(blood proteins) linked with RA.

Inflammation

Erythrocyte sedimentation rate (ESR, or “sed rate”) and C-reactive protein (CRP) level are
markers of inflammation. A high ESR or CRP is not specific to RA, but when combined with
other clues, such as antibodies, helps make the RA diagnosis.

Antibodies

Rheumatoid factor (RF) is an antibody found in about 80 percent of people with RA during
the course of their disease. Because RF can occur in other inflammatory diseases, it’s not a
sure sign of having RA. But a different antibody – anti-cyclic citrullinated peptide (anti-CCP)
– occurs primarily in patients with RA. That makes a positive anti-CCP test a stronger clue to
RA. But anti-CCP antibodies are found in only 60 to 70 percent of people with RA and can
exist even before symptoms start.

Imaging Tests

An X-ray, ultrasound or magnetic resonance imaging scan may be done to look for joint
damage, such as erosions – a loss of bone within the joint – and narrowing of joint space. But
if the imaging tests don’t show joint damage that doesn’t rule out RA. It may mean that the
disease is in an early stage and hasn’t yet damaged the joints.

TREATMENT FOR RHEUMATOID ARTHRITIS

The goals of rheumatoid arthritis (RA) treatment are to:

 Stop inflammation (put disease in remission)

 Relieve symptoms

 Prevent joint and organ damage

 Improve physical function and overall well-being

 Reduce long-term complications

To meet these goals, the doctor will follow these strategies:

Early, aggressive treatment. The first strategy is to reduce or stop inflammation as quickly

as possible – the earlier, the better.
Targeting remission. Doctors refer to inflammation in RA as disease activity. The ultimate
goal is to stop it and achieve remission, meaning minimal or no signs or symptoms of active
inflammation. One strategy to achieve this goal is called “treat to target.”
Tight control. Getting disease activity to a low level and keeping it there is what is called
having “tight control of RA.” Research shows that tight control can prevent or slow the pace
of joint damage.

Medications for RA

There are different drugs used in the treatment of rheumatoid arthritis. Some are used
primarily to ease the symptoms of RA; others are used to slow or stop the course of the
disease and to inhibit structural damage.

Drugs That Ease Symptoms

Nonsteroidal anti-inflammatory drugs (NSAIDs) are available over-the-counter and by

prescription. They are used to help ease arthritis pain and inflammation. NSAIDs include
such drugs as ibuprofen, ketoprofen and naproxen sodium, among others. For people who
have had or are at risk of stomach ulcers, the doctor may prescribe celecoxib, a type of
NSAID called a COX-2 inhibitor, which is designed to be safer for the stomach. These
medicines can be taken by mouth or applied to the skin (as a patch or cream) directly to a
swollen joint.

Drugs That Slow Disease Activity

Corticosteroids. Corticosteroid medications, including prednisone, prednisolone and

methyprednisolone, are potent and quick-acting anti-inflammatory medications. They may be
used in RA to get potentially damaging inflammation under control, while waiting for
NSAIDs and DMARDs (below) to take effect. Because of the risk of side effects with these
drugs, doctors prefer to use them for as short a time as possible and in doses as low as
possible.
DMARDs. An acronym for disease-modifying antirheumatic drugs, DMARDs are drugs that
work to modify the course of the disease. Traditional DMARDs include methotrexate,
hydroxycholorquine, sulfasalazine, leflunomide, cyclophosphamide and azathioprine. These
medicines can be taken by mouth, be self-injected or given as an infusion in a doctor’s office.
Biologics. These drugs are a subset of DMARDs. Biologics may work more quickly than
traditional DMARDs, and are injected or given by infusion in a doctor’s office. Because they
target specific steps in the inflammatory process, they don’t wipe out the entire immune
response as some other RA treatments do. In many people with RA, a biologic can slow,
modify or stop the disease even when other treatments haven’t helped much.
JAK inhibitors. A new subcategory of DMARDs known as “JAK inhibitors” block the Janus
kinase, or JAK, pathways, which are involved in the body’s immune response. Tofacitinib
belongs to this class. Unlike biologics, it can be taken by mouth.

Surgery

Surgery for RA may never be needed, but it can be an important option for people with
permanent damage that limits daily function, mobility and independence. Joint replacement
surgery can relieve pain and restore function in joints badly damaged by RA. The procedure
involves replacing damaged parts of a joint with metal and plastic parts. Hip and knee
replacements are most common. However, ankles, shoulders, wrists, elbows, and other joints
may be considered for replacement.
SELF-CARE OF RHEUMATOID ARTHRITIS

Self-care, or self-management, means taking a proactive role in treatment and maintaining a

good quality of life. Here are some ways you can manage RA symptoms (along with
recommended medication) and promote overall health.

Anti-inflammatory Diet and Healthy Eating

While there is no specific “diet” for RA, researchers have identified certain foods that are rich
in antioxidants and can help control and reduce inflammation. Many of them are part of the
so-called Mediterranean diet, which emphasizes fish, vegetables, fruits and olive oil, among
other healthy foods. It’s also important to eliminate or significantly reduce processed and fast
foods that fuel inflammation.

Balancing Activity with Rest

Rest is important when RA is active and joints feel painful, swollen or stiff. Rest helps reduce
inflammation and fatigue that can come with a flare. Taking breaks throughout the day
conserves energy and protects joints.

Physical Activity

For people with RA, exercise is so beneficial it’s considered a main part of RA treatment.
The exercise program should emphasize low-impact aerobics, muscle strengthening and
flexibility. The program should be tailored to fitness level and capabilities, and take into
account any joint damage that exists. A physical therapist can help to design an exercise
program.
Heat and Cold Therapies
Heat treatments, such as heat pads or warm baths, tend to work best for soothing stiff joints
and tired muscles. Cold is best for acute pain. It can numb painful areas and reduce
inflammation.

Topical Treatments
These treatments are applied directly to the skin over the painful muscle or joint. They may
be creams or patches. Depending on the type used, it may contain nonsteroidal anti-
inflammatory drugs (NSAIDs), salicylates or capsaicin, which help reduce pain.

Natural and Alternative Therapies

Relaxation techniques, such as deep breathing, guided imagery and visualization can help
train painful muscles to relax. Research shows massage can help reduce arthritis pain,
improve joint function and ease stress and anxiety. Acupuncture may also be helpful. This
involves inserting fine needles into the body along special points called “meridians” to
relieve pain. Those who fear needles might consider acupressure, which involves applying
pressure, instead of needles, at those points.

Supplements

Studies have shown that turmeric and omega-3 fish oil supplements may help with
rheumatoid arthritis pain and morning stiffness. However, talk with a doctor before taking
any supplement to discuss side effects and potential interactions.

Positive Attitude and Support System

Many studies have demonstrated that resilience, an ability to “bounce back, “encourages a
positive outlook. Having a network of friends, family members and co-workers can help
provide emotional support. It can help a patient with RA cope with life changes and pain.

DISCUSSION

SIMLARITIES
Real case, Reference A and Reference B

Based on my case study, there have a few similarity I found in real case, Reference A and B.
First similarity want to discuss is the sign and symptoms of rheumatoid arthritis. These three
cases said rheumatoid arthritis started by having joint pain, swelling and tenderness,
especially in leg, knee, elbow and fingers, more than one joint is affected, same joints on both
sides of the body are affected like in real case and loss of joint function or range of movement
is limited. Not only that, sometimes patient also can get on off fever.

Next similarity from these cases is the investigation of rheumatoid arthritis. Real case,
reference A and B used medical history for their investigation. The doctor will ask about
patient’s personal and family medical history as well as recent and current symptoms, for
example doctor will ask the pain, tenderness, difficulty of movement and stiffness of affected
body parts. Next same investigation used by these three cases is the physical exam. Doctor
will perform a physical examination of each joint, looking for tenderness, swelling, warmth
and painful or limited movement. During the physical examination, doctor also will check the
number and pattern of joint affected that also can indicate rheumatoid arthritis. For example,
rheumatoid arthritis tends to affect joints on both sides of the body. The physical exam may
reveal other signs, such as rheumatoid nodules or a low-grade fever.

x-ray of affected body parts

.

DIFFERENCES
Real case, Reference A and Reference B

Based on my case study, there also have a few differences found in real case, reference A and
B. First difference I found from these cases is the investigation of rheumatoid arthritis. For
example, according to laboratory and radiology test, real case used full blood count (FBC) for
the investigation. Complete blood count is one of the test used to evaluate overall health and
detect a wide range of disorders, including anaemia, infection and leukaemia. This test also
help to measures several components and features of blood. Next different test used in real
case is renal profile (RP) test that evaluate kidney function.

Other different investigation used by real case is an electrocardiogram (ECG) which help for
heart’s electrical activity and chest x-ray which used by doctor to view the inside of body
without having to make an incision and this also help them to diagnose, monitor and treat
many medical conditions. Even real case only used full blood count (FBC), chest x-ray, renal
profile (RP) and electrocardiogram, but author named from reference A and B respectively do
not mentioned about this investigations in their article.
 CONCLUSION
As a conclusion we get know that rheumatoid arthritis (RA) is an autoimmune in which the
normal immune response is directed against an individual’s own tissue, including the joints,
tendons and bone, resulting an inflammation and destruction of these tissues. Rheumatoid
arthritis also usually affects joint symmetrically may initially begin in a couple of joints only
and most frequently attacks the wrist, hands, elbows, shoulders, knees and ankles. The cause
of rheumatoid arthritis is unknown. This disease affects approximately 0.5-1 percent of the
general population worldwide and 2 to 3 times more common in women than in men and can
start at any age, but most commonly starts in middle adult life.

According to World Health Organization, rheumatoid arthritis result in more the 9 million
physician visits and more than 250,000 hospitalizations per year in the developed country.
The outcome in rheumatoid arthritis is compromised when diagnosis and treatment are
delayed. The clinical course of RA is generally one of exacerbations and remissions.
Approximately 40% of patients with this disease become disabled after 10 years, but
outcomes are highly variable. Some patients experience a relatively self-limited disease,
whereas others have a chronic progressive illness.

Not only that, beside learned about rheumatoid arthritis, during posting in Emergency
department, I got chance to do case study about rheumatoid arthritis. I gained knowledge in
depth by comparing the care with patient, I collected information from internet, doctors, ward
sisters, nurses, lab, radiology and record section and compared it with patient in real situation.
During my duty period in emergency department, I provided her a holistic care, diversional
therapy in very aspects like physical, emotional, economical and socio-cultural view.

I also gained the knowledge about the Medical Assistant theory and application in real
situation. So this case, not only gives the cognitive domain but also provides us the
opportunity to develop psychomotor domain, which is very important in Medical Assistant
course, so the patient is the main source of conveying knowledge in practice.

REFERENCE
https://emedicine.medscape.com/article/331715-overview#a5
https://www.medicalnewstoday.com/articles/323095.php

https://www.healthline.com/health/rheumatoid-arthritis/effects-on-body#8

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

https://www.healthline.com/health/rheumatoid-arthritis

https://www.mayoclinic.org/diseases-conditions/rheumatoid-arthritis/diagnosis-treatment/drc-
20353653

https://www.webmd.com/rheumatoid-arthritis/rheumatoid-arthritis-medications

https://www.aafp.org/afp/2005/0915/p1037.pdf