A reviewer by a nursing student

1. Rheumatoid, Osteoarthritis,
Gouty Arthritis
Jerard Lloyd B. Domingo
BSN 3A
THIS ONLY SERVES AS A COMPILATION OF REVIEWER
OF THE AUTHOR. ANY ERRORS YOU MAY SEE ARE
SUBJECT FOR CHANGES.

2. Category Rheumatoid Osteoarthritis (Misnomer) Gouty Arthritis
Mechanism Autoimmune, synovial inflammation Degenerative, wear and tear of articular
cartilage
Hyperuricemia causes Monosodium
Urate to accumulate and triggers joint
inflammation.
Characteristic Symmetrical, bilateral, systemic Asymmetrical, unilateral, non-systemic,
with crepittation
Asymmetric, “FEELS LIKE SAND INSIDE
THE JOINT”
Duration Morning stiffness >30 mins Morning stiffness <30 mins Severe pain @acute gout attacks
Inflammation With cardinal s+s of inflammation. Without cardinal s+s of inflammation.
Local joint inflammation only.
With cardinal s+s of inflammation.
Demographics Women 30-55 y/o (common), genetics
(abnormal recognition) and environment that
caused citrullination.
(+40 y/o) Elderly, obese, trauma (any
form of wear and tear.
Male, obesity, HTN, DM, Diet high in
Purine, less excretion of uric acid, meds,
genes, etc.
Joint involvement Polyarticular (>5), small joints Monoarticular (1) to oligoarticular (2-4),
weight bearing joints
Monoarticular, Common @ 1st MTP
joint/Great Toe and Knee
Diagnosis (+) Rheumatoid Factor, (+) Anti-CCP, High CRP
and ESR, X-ray (narrowed joint spaces)
X-ray only (+) osteophytes Arthrocentesis (+) urate crystals
Medications DMARD’s, Biological Response Modifiers,
NSAIDs, Corticosteroids
Acetaminophen, opioids, NSAIDS, NSAIDS except aspirin, Colchicine,
allopurinol, probenecid.
Deformities Swan neck, Butonniere, Ulnar Deviation,
Atlanto-occipital subluxation, Baker’s Cyst.
Heberden’s Node (DIP), Bouchard’s
Node (PIP), (+) Spurs, (+) synovial cysts
@bone.
Podagra, Tophi

3. Rheumatoid Arthritis
Chronic (>6 weeks), autoimmune,
recurrent, systemic (multi-organ),
symmetric/bilateral inflammation of
synovium.
Etiology
Genetic: HLA DR1 and HLA DR4
Environmental: Smoking, Stress,
pathogen.
Predisposing: Being a woman
with age of 30-55.
Trivia: Autoimmune diseases are common to women and
immunodeficiency disorders are common to men.
Pathophysiology
1. Abnormal Genes (HLA Mutation) causes diminished recognition of Antigen
Presenting cells and Helper T-cells.
2. APC phagocytizes all by-products of citrullination (such as Type 2 collagen,
vimentin and IgG).
3. Antigen presenting cells (macro or mast cell) presents it to a CD4 cells, and CD4
cells travel to the spleen and activate the B-cells.
Note: CD4 cells or Helper T-cells is the bridge of humoral and cell mediated immunity.
4. Activated B-cells transforms into Plasma B-cells and Memory b cells. Whereas
Plasma B-cells creates 2 types of antibodies which are; Rheumatoid Factor and Anti-
Cyclic Citrullinated Peptide or Anti-CCP antibodies.
5. First Phase: Joint Inflammation (SYMMETRIC!!!)
- HTC and APC causes cytokine storm, and release of lysosomal enzymes
causing inflammation and damage to the synovial lining.
6. 2nd Phase: Synovium evolves into a PANNUS made up of granulation and synovial
tissue that secretes inflammatory enzymes, exacerbating the inflammation.
7. Pannus secretes PROTEASES that destroys articular cartilage. RANKL was also
produced by HTC to increase osteoclastic activity = Breakdown of bone.
8. Progressive bone breakdown and articular cartilage.
9. Also, Rheumatoid Factor (an IgM antibody that attacks FC portion of a citrullinated
IgG) and Anti-CCP migrates in the joint, and activates complement system causing
more inflammation.
Smoking and pathogen may
cause citrullination of TII
collagen, Vimentin and IgG
antibodies. Citrullination
refers to change of protein
structure from arginine into
citrulline.

4. Rheumatoid Arthritis
Chronic (>6 weeks), autoimmune,
recurrent, systemic (multi-organ),
symmetric/bilateral inflammation of
synovial lining of joints.
Etiology
Genetic: HLA DR1 and HLA DR4
Environmental: Smoking, Stress,
pathogen.
Predisposing: Being a woman
with age of 30-55.
Trivia: Autoimmune diseases are common to women and
immunodeficiency disorders are common to men.
Pathophysiology
6. Due to chronic joint inflammation, angiogenesis occurs, causing antigen-antibody
complexes to travel to the systemic circulation causing systemic inflammation as they
adhere to prgans with citrullinated factors. .
The following are the effects of systemic inflammation;
a) Brain: Interleukins and TNF-alpha acts as pyrogens in the hypothalamus causing
fever and anorexia (can cause weight loss).
b) Blood vessels: since blood vessels have collagen properties, some antibodies and
antigen-antibody complexes adheres to BV wall causing vasculitis, which later
may cause fatty deposits or atheromatous formation @BV wall = High Risk for
CVA and Heart Attack.
c) Lungs: inflammation of lung interstitium occurs causing pleural effusion or
accumulation of water to the pleural space. Also fibroblasts became activated at
the lungs causing lung fibrosis or scarring of lungs that causes thickening of the
basement membrane and altered gas exchange.
d) Liver: releases hepcidin, that inhibits absorption of iron from the intestines
causing anemia (can cause fatigue and weakness). Because liver thinks that
there’s a pathogen causing the systemic inflammation and iron is essential for
pathogens.
e) Skin - formation of rheumatoid nodules, which are composed of Ag-Ab
complexes, macrophage, and lymphocytes with a central area of necrosis.
f) Skeletal Muscle: increased protein breakdown (proteolysis).
Smoking and pathogen may
cause citrullination of TII
collagen, Vimentin and IgG
antibodies. Citrullination
refers to change of protein
structure from arginine into
citrulline.

5. Signs and Symptoms
1. Pain
2. Redness
3. Warmth (heat)
4. Swelling
5. Loss of function
Cardinal Signs
of
Inflammation
6. Stiffness – SYMMETRICAL! : (early sign) feeling that motion of a joint is limited or difficult. (Parang mahirap igalaw
ang joint).
Usually occurs due to prolonged immobility *wala pa kasing enough synovial fluid (morning stiffness for about >30
mins.) As inflammation debris accumulates in the joints. It subsides with movement as warm-up or mild exercise
increases synovial fluid production and wash away inflammatory debris, reducing stiffness.
7. Deformities:
• Swan Neck Deformity – flexion of Distal Interphalangeal Joint and Hyperextension of Proximal Interphalangeal
Joint.
• Boutonnière's Deformity – flexion of Proximal Interphalangeal Joint and Hyperextension of Distal Interphalangeal
Joint.
• Ulnar deviation – deviation of Metacarpophalangeal joint towards the direction of ulna. Ulnar drift occurs as
knuckle bones or MCP bend abnormally toward the little (pinky) finger.
• Popliteal Cyst or Baker’s Cyst : herniation of synovial membrane into the popliteal bursa.
• Zeta Thumb – “z-thumb”
8. Rheumatoid Nodules – firm lumps under the skin, size of pea to a walnut. Common @ pressure points such as
elbows, hands, knuckles. Rare cases: lungs, spleen, heart, vocal cords.
d/t inflammatory cascade, activation of
complement system, cytokine storm,
release of lysosomal enzymes and
phagocytosis.

6. Diagnosis
1. X-ray - shows narrowed joint spaces, soft tissue swelling and bony erosions sometimes ankylosis.
2. Blood Studies: shows (+) Rheumatoid Factor and Anti-CCP antibodies. (Most diagnostic!))
3. (+) elevation of Acute Phase Reactants (correlates on disease activity) such as;
a. C-reactive protein – NV: 0.8 – 3 mg/L.
TRIVIA: called as C-RP because it first react with C-polysaccharide of streptococcus pneumoniae. It is a protein
synthesized by the liver in response to IL-6 released by WBC, adipocytes, and Malignant cell.
CRP was released to bind with phosphocholine receptors found in bacteria so that phagocytes can identify
them.
b. Erythrocyte Sedimentation Rate (ESR) - rate at which erythrocyte sediments. When blood is left
alone, it sediments.
NV for <50 year old client: Male – 15 mm/hour, female – < or equal to 20 mm/hour.
NV for >50 year old client: Male – 20 mm/hour, and female – < or equal to 30 mm/hour.
Note: ESR and CRP are markers of inflammation .
Can correlate with disease activity, response to therapy, and has no diagnostic value!!! Because it is not
specific, it only indicates an ongoing inflammation inside the body.
4. Hemoglobin Level: below normal.
NV: 13.5 – 17.5 g/dl (male), 12.0 – 15.5 g/dl (female)

7. Management Pearls
*Importance of Early R.A. Diagnosis prevents irreversible joint damage.
*Impaired Physical Mobility for Prolonged Period of Time may cause low self-esteem and depression.
Pain
• Rest if inflamed. Ice packs for pain and
inflammation. Hot compress for
stiffness.
• Mild exercise when not inflamed.
• NSAIDS: Ibuprofen (taken with meals to
prevent GI bleeding.
• Use of assistive Devices (crutch, walkers,
canes)
• Joint support: Splints
• Note: Important to have low-impact
exercise, decrease fatigue, enhance
muscle strength. Don’t overexert, must
have periods of rest between intervals.
MEDS
DMARD’S – Disease Modifying Anti-Rheumatic Drugs
“SHaLoM”
Long term
• Sulfasalazine
• Hydroxychloroquine (*vision changes)
• Leflunomide
• Methotrexate (immunocompromised and risk for bleeding,
d/t bone marrow suppression +Low PLT, RBC, WBC)
Mechanism: Suppresses immune system responses
(inflammation) and slow down progression of joint and tissue
destruction.

8. Biological Response Modifiers “BRiM’s”
• Abatacept – T cell suppressor
• Rituximab – B-cell suppressor
• Adalimumab, etanercept, infliximab – blocks TNF alpha
• Anakinra: Blocks IL-1
• Tocilizumab – blocks IL-6
Mechanism: Inhibits TNF and IL secretion “cytokine storm”
Avoid crowd, sick people, live vaccines because client has a
weak immune system.
Note: If client has TB treat TB first before administering BRiMs.
For Acute Flares:
-NSAIDS (assess for GI bleeding)
-Corticosteroids (short term only)
• Prednisone
• Dexamethasone
• Methylprednisolone

9. Surgical Management:
1. Synovectomy
Synovectomy involves the removal of part of the lining of the joint, called the synovium. During synovectomy, part of the
synovium is left intact so that it can still perform its function of releasing synovial fluid, which serves as a lubricant in the
joint.
2. Tendon repair
Swelling and inflammation of joints and related changes to bones and other structures in RA can often result in tendon
rupture. Ruptures are particularly common in tendons located in the wrist and hand. Surgical repairs, including end-to-end
and end-to-side reconstructions, involve the use of tendons from other areas in the body.
3. Osteotomy - involves the removal of a section of bone and the use of screws or other hardware (plates are often used)
to reconnect the bone so that it can grow together. The goal of osteotomy is to restore correct joint alignment and relieve
symptoms and functional problems related to misalignment. The procedure is often used in conjunction with synovectomy.
4. Arthrodesis- Arthrodesis is a surgical procedure that involves fusion of bones to achieve permanent immobilization of a
joint. During the procedure, cartilage and the surface layer of bone is removed from the ends of the bones that are to be
joined. The joint is then positioned in an alignment that is most functional and locked into place using rods, pins, and
screws. Arthrodesis is most useful in cases where joint stability has been lost and joint movement causes pain. It provides
relief of pain and even preserves some limited joint function.
5. Arthroplasty - replacement of damaged joints can both relieve pain and restore joint function. Arthroplasty can involve
use of different combinations of artificial (prosthetic) and natural components, depending on joint location and the nature
of damage to joints and related structures.