Chapter 34: Inflammatory Rheumatic Disorders – Study Guide

I. Overview of Inflammatory Rheumatic Disorders

 Inflammatory Connective Tissue Diseases: AUTOIMMUNE DISEASES
o RHEUMATOID ARTHRITIS (RA) - The body attacks the lining of your joints, causing pain,
swelling, and joint damage.
o SYSTEMIC LUPUS ERYTHEMATOSUS (SLE) - The immune system goes rogue and can
damage skin, joints, kidneys, and more.
o SCLERODERMA - Causes skin and connective tissue to harden and tighten.
 Metabolic Joint, Bone, and Muscle Disorders: NOT AUTOIMMUNE
o GOUT - Caused by too much uric acid in the body, which forms crystals in the joints (super
painful).
o FIBROMYALGIA - Causes widespread pain, fatigue, and sleep issues. It’s not from
inflammation, but the brain and nerves are more sensitive to pain.
Many of these conditions are chronic systemic disorders characterized by diffuse inflammation and degeneration in
connective tissues, with periods of exacerbation (symptoms suddenly get worse) and remission (symptoms go away
or get much better).
II. Rheumatoid Arthritis (RA): RA is a chronic autoimmune inflammatory disorder affecting primarily the
synovial tissue of joints, leading to inflammation (synovitis) and eventual joint fixation: stiffen or lock up
permanently (ankylosis).
Key Facts & Characteristics:
 Affects 1-2% of the population worldwide.
 "Females 3x > Males."
 Most common onset between ages 30-60s, but can occur at any age.
 Risk factors include family history, environmental influences, nulliparity, smoking, and obesity.
 Typically starts in small peripheral joints (e.g., fingers and wrists) and can progress to proximal (bigger)
joints if untreated.
 "Usually symmetric" pain and swelling are usually on both sides of the body.
Pathophysiology:
1. Your body’s immune system attacks the joint lining (synovial tissue) by mistake, thinking it’s a threat.
2. "WBCs invade synovium," leading to inflammation (synovitis).
3. As the inflammation continues, the body forms an abnormal layer of tissue called pannus.
4. The pannus eats away at the bone and cartilage, damaging the joint structure.
5. As damage builds up, space between the bones shrinks and eventually disappears, leading to ankylosis,
which means the bones fuse together and the joint can no longer move.
 RA can also affect extra-articular sites such as the heart, skin, eyes, mouth, and lungs.
Clinical Manifestations ("The Seven S's of RA"):
 Sunrise stiffness (severe pain): Morning stiffness is a prominent early symptom; it can last MORE than
an hour.
 Soft feeling in joints: joints feel tender and soft.
 Swelling in joints (warm): joints get swollen, warm, and puffy
 Symmetrical joint involvement: same joints on both sides
 Synovium is affected and inflamed: lining of the joint (synovium) is inflamed; the root of the disease.
 Systemic symptoms: "Not just joints! Achy, fatigue, fever, affect lungs/heart."
 Stages: Progression from Synovitis to Pannus formation to Ankylosis.
o Joint deformities can include Boutonnière deformity and Swan-neck deformity of the fingers,
and Hallux valgus and Hammer toe in the feet.
 Rheumatoid nodules are common, appearing on the hands and elbows, rarely in the eyes, vocal cords, and
lungs. Means advanced RA.
Assessment and Diagnostic Findings:
 History and Physical: Presence of rheumatoid nodules, joint inflammation, and bilateral, symmetric
stiffness, tenderness, swelling, and temperature changes in joints.
 Laboratory findings:
o "Rheumatoid factor = POSITIVE" - Seen in ADVANCED RA.
o "Anti-CCP antibodies = POSITIVE"
o "Erythrocyte count = DECREASED" (anemia)
o "ESR = INCREASED" and "CRP = POSITIVE" (indicators of inflammation).
o Arthrocentesis: needle is used to take joint fluid. May show cloudy, milky, or dark yellow
synovial fluid.
 Imaging: Plain x-rays are "most common to track disease progression," along with ultrasound and MRI.
Medical Management:
 NO CURE. The goal is to "decrease joint pain and swelling, achieve remission, decrease likelihood of joint
deformity, [and] minimize disability."
 Prior to medication initiation: Baseline CBC, Tuberculin skin test (TB test), and Hepatitis B and C
evaluation are recommended.
 Pharmacologic Therapy: Medical Management of EARLY RA
o Disease Modifying Antirheumatic Drugs (DMARDs):
 Prevent inflammation and joint damage. Relief typically within 6 weeks.
 Nonbiologic: hydroxychloroquine (Plaquenil).
 Janus Kinase (JAK) inhibitors (Synthetic DMARDs): Decrease immune response.
Examples include methotrexate (Rheumatrex), sulfasalazine (Azulfidine), tofacitinib
(Xeljanz). Methotrexate is often used in combination.
 Biologic DMARDs: adalimumab (Humira) is an example of an immunomodulator.
o NSAIDs: (e.g., ibuprofen, naproxen, celecoxib) for pain and inflammation relief, with caution.
o Corticosteroids: (e.g., prednisone) used as "Bridge” therapy for short-term relief until other
medications become effective, or local injection into a single joint.
 Nonpharmacologic Therapy: Medical Management of ESTABLISHED RA
o Occupational and Physical Therapy (PT/OT): Pacing activities, range of motion (ROM)
exercises, muscle-strengthening exercises.
o Reconstructive surgery: Considered when pain is unrelieved and there is a threat of loss of
independence, typically not performed during exacerbations.
Nursing Considerations:
 Adherence to treatment plan is crucial.
 Patient monitoring: Signs of infection (NO LIVE VACCINES like Flu Mist, Varicella), liver disease.
 Medication-specific precautions: No pregnancy with Methotrexate, avoid alcohol use. DMARDs require
ophthalmic examinations every 6-12 months.
 Pain management: Heat and cold to affected joints, rest during flare-ups, avoid deep massage during
flares, splinting.
 Fatigue management: Warm baths, relaxation techniques, energy conservation (pacing, delegating).
 Mobility: Use of assistive devices, ROM exercises, low-impact activity.
 Education is vital for maintaining independence, safe medication use, and correct use of adaptive devices.
 Assess home environment for ADL difficulty and patient safety.
III. Systemic Lupus Erythematosus (SLE)
Key Facts & Characteristics:
 Pathophysiology involves various factors like genetic, environmental, immunoregulatory, hormonal, and
epigenetic influences leading to immune complexes, antibodies, (cytokines, and T cells: (inflammation
messengers)) that cause "Organ damage" to organs like the kidney, skin, lungs, brain, and heart.
Clinical Manifestations:
 Most common symptoms: Fever, "Fatigue w/ anorexia," skin rashes (classic “butterfly rash” or discoid
lesion (round, scaly patches)), "Joint pain and swelling: morning stiffness."
 Systemic symptoms:
o Cardiac: "pericarditis (inflammation of the heart lining) with tachycardia, HTN, edema."
o Respiratory: "Effusions with dec breath sounds."
o Kidneys: "nephritis."
o Mouth: Ulcerations.
o Neurological: Behavior changes, psychosis, depression, seizures.
 "Symmetrical similar to RA"
Diagnosis:
 Physical Assessment Findings: NO single test. Mix of physical signs, lab tests, and a checklist of
symptoms: Erythematous rashes, cutaneous plaques, hyper/depigmentation, alopecia, mouth ulcerations,
pericardial friction rub, abnormal lung sounds, joint swelling, tenderness, warmth, pain with movement,
stiffness, edema, neurological changes.
 American College of Rheumatology (ACR) Classification Criteria: Diagnosis of SLE if 4 or more of 11
criteria are met (mnemonic: SOAP BRAIN MD).
o Serositis (Inflammation around the heart (pericarditis) or lungs (pleuritis))
o Oral Ulcer
o Arthritis
o Photosensitivity
o Blood disorders (Hemolytic anemia, leukopenia, lymphopenia, thrombocytopenia)
o Renal disorders (Proteinuria, cellular casts)
o Antinuclear Antibody (ANA)
o Immunologic disorders (Anti-native DNA, Anti-SM antibody, antiphospholipid antibody)
o Neurological disorders (Seizures, psychosis)
o Malar rash (butterfly rash)
o Discoid rash (raised, round, scaly rashes that leave scars)
 Laboratory findings:
o "Antinuclear antibody ANA: POSITIVE 95%."
o "Creatinine: Increased with kidney damage 2o to SLE."
o "Urinalysis: may have protein or RBCs if renal issues."
o "Erythrocyte Count: DECREASED."
o "ESR and CRP POSITIVE."
o "CBC: all decreased = pancytopenia (decrease in all three types of blood cells: red blood cells,
white blood cells, and platelets).
Medical Management: SLE can be life-threatening. Goals are to "prevent progression, minimize disability, [and]
prevent complications."
 Pharmacologic Therapy:
o Monoclonal antibodies: belimumab (Benlysta), rituximab (Rituxan). Reduce B cell (part of the
immune system that causes inflammation) activity. "NO LIVE VACCINE for 30 days before
med."
o Corticosteroids: Topical for skin, low-dose oral for minor symptoms, high-dose oral or IV for
major symptoms. Risks include osteoporosis and fractures.
o DMARDs: hydroxychloroquine (Plaquenil) for cutaneous, musculoskeletal, and mild systemic
symptoms; helps long-term control and prevents flare-ups.
o NSAIDs: For minor symptom control. DO NOT stop disease progression, just manage symptoms.
o Immunosuppressive agents: methotrexate (Rheumatrex), Azathioprine, Mycophenolate.
Reserved for serious SLE not responding to other therapies.
Nursing Considerations:
 Common nursing diagnoses: Fatigue, impaired skin integrity, body image disturbance, lack of
knowledge.
 Pregnancy concerns: SLE "must be under control for at least 6 months before conceiving." Pregnancy and
post-partum can cause flare-ups.
 Understanding Flares:
o Triggers: "sunlight, stress, sickness, not taking meds correctly or needing adjustment."
o Prevention ("LESS" Flares):
 L = lower stress
 E = exercise (important for joint stability and weight management)
 S = sleep
 S = sun protection
o Signs of flare-ups ("FLARE"):
 F = fatigue
 L = low grade fever
 A = achy joints
 R = rash
 E = edema of legs and hands
IV. Scleroderma
Scleroderma, meaning "HARD SKIN," is a chronic connective tissue disease characterized by excessive collagen
production leading to thickening and tightening of the skin and potential involvement of internal organs.
Key Facts & Characteristics:
 Affects connective tissue of skin, blood vessel walls, and internal organs.
 Two types: Localized ("hard skin") and Diffuse (systemic).
 "Women 4x > Men."
 Onset typically between ages 25-50 years.
 Usually begins with skin involvement, with "insoluble collagen forms and accumulates excessively in
tissues à loss in skin elasticity and movement à degeneration and tissue loses function."
 Can progress to affect blood vessels, major organs (lungs, GI tract, heart, kidneys), and body systems.
Clinical Manifestations:
 Skin: "Hard skin" that cannot be pinched up; wrinkles and lines are obliterated; skin is dry due to
suppressed sweat secretion.
 Extremities: Stiffen and lose mobility; progression is "SLOW progression over years."
 Face: "masklike, immobile, expressionless."
 Internal Organ Involvement:
o Esophagus hardens: problems swallowing and acid reflux
o Scarring to lungs: breathing issues
o Intestinal mucosa scleroses:
o Vascular involvement of kidneys:
o Cardiac change:
 Limited symptoms (CREST syndrome): if someone has 4 out of 5, they likely have this form.
o Calcinosis: Calcium deposits in the skin.
o Raynaud's phenomenon: Spasms of blood vessels in response to cold or stress (common early
symptom).
o Esophageal dysfunction: Acid reflux and decreased motility of the esophagus.
o Sclerodactyly: Thickening and tightening of the skin on the fingers and hands.
o Telangiectasias: Dilation of capillaries causing red marks on the surface of the skin.
Diagnosis:
 "NO ONE conclusive test for scleroderma."
 Diagnosis relies on physical assessment, and "4 out of 5 CREST symptoms."
 Possible lab findings:
o "Creatinine/BUN: increased if kidney involvement."
o "ESR/CRP: increased."
o "Antinuclear Antibody (ANA): positive."
Management:
 "NO MEDICATION is effective in modifying disease process."
 Treatment focuses on managing symptoms and organ system involvement: "Kidney involvement à
ACE inhibitors."
 Nonpharmacologic and Patient Teaching:
o Counseling and support, setting individualized realistic goals.
o "Moderate exercise to prevent joint contractures."
o "Avoid extreme temperatures."
o "Use lotion to minimize skin dryness."
V. Gout
Gout is the most common form of inflammatory arthritis, caused by hyperuricemia (high URIC ACID levels in the
blood) leading to the deposition of uric acid crystals in joints and other tissues.
Key Facts & Characteristics:
 "Men 3-4x > Women."
 Risk Factors/Increased Incidence: Age, BMI, alcohol consumption, hypertension, diuretic and ASA
(aspirin) use, fructose-rich beverage consumption.
Pathophysiology:
 Cause: "Hyperuricemia (serum > 6.8 mg/dL) Producing too much OR not excreting as normal."
 Uric acid (urate) is a natural waste product of purines, which are high in red meats.
 A genetic defect in purine metabolism can contribute.
 When uric acid levels are high, "Uric acid crystals form in joints."
 "Sharp, needle-like sodium urate crystals form around joints with repeated attacks," which are called
"tophi."
 Tophi "Deposit in peripheral areas of body," causing "Intense inflammation, pain, redness."
Clinical Manifestations:
 Acute gouty arthritis:
o "Recurrent attacks of severe articular and periarticular inflammation."
o "BIG TOE most common," but can also affect ankle, knee, wrists, fingers, and elbow.
o "Abrupt onset, often at night with intense pain."
o Periods of "remission and exacerbation."
 Triggers: Trauma, alcohol, dieting, medications, surgical stress, illness.
 Tophi deposits: Can occur in synovium, tendons, subcutaneous tissues of joints, and also in aortic walls,
heart valves, nasal and ear cartilage, eyelids, cornea, and sclera.
 Gouty nephropathy: Renal impairment and kidney stones.
Diagnosis:
 Synovial fluid analysis: "definitive diagnostic" through the "Presence of uric acid crystals."
 Uric Acid serum blood test:
o During an "Acute flare: levels may be normal."
o "AFTER flare subsided: levels elevated."
o Other diagnostic steps include medical history, physical exam, and imaging tests.
Medical Management:
 Goal: Uric acid level < 6 mg/dL.
 Pharmacologic Therapy:
 Acute attacks:
o NSAIDs (e.g., indomethacin) or corticosteroids to relieve acute attack.
o Colchicine (Colcrys) for pain and swelling; "Can also be used for chronic management."
(Colchicine for "Acute gout attacks")
 Chronic Management (prevents gout attacks):
o Allopurinol (Zyloprim, Aloprim): Xanthine oxidase inhibitor; interrupts purine breakdown.
"CANNOT start or increase dose during active flare (bone marrow depression)." ("AlloPurinol -
Prevents gout.")
o Probenecid (Probalan): Increases urinary excretion of uric acid, used for frequent attacks.
Lifestyle Modifications:
 "Avoiding purine-rich foods" (e.g., organ meats, red meat, seafood).
 "Decreasing alcohol consumption" (especially craft beer).
 "NO ASPIRIN: increases uric acid levels." Take NSAIDs or acetaminophen instead.
 Uric acid deposits can cause kidney stones; fluids help prevent this.
VI. Fibromyalgia:
Fibromyalgia is a chronic pain syndrome characterized by widespread pain, fatigue, and other symptoms, with an
amplified pain response originating from the central nervous system.
Key Facts & Characteristics:
 Chronic pain syndrome with:
 Chronic fatigue.
 Generalized muscle aching.
 Stiffness.
 Sleep disturbances.
 Functional impairments.
 "Women > Men."
 Often co-occurs with another rheumatic condition.
Pathophysiology: "Amplified pain neurogenic in origin." The CNS ascending and descending pathways that
regulate pain function abnormally, leading to "amplified pain" where the "“Volume control setting” for pain always
high."
Clinical Manifestations (Common Symptoms):
 Fatigue
 Brain fog
 Depression
 Chronic widespread pain
 Muscle and joint issues
 Digestive issues
 "Increased response to painful stimuli."
 "Sensitivity to stimuli that is not normally painful."
Diagnosis & Management: "Diffuse syndrome à no useful diagnostic testing." Diagnosis is primarily clinical based
on symptoms.
 Management is symptom-specific:
 Medications:
o NSAIDs.
o Tricyclic antidepressants (e.g., Amitriptyline, nortriptyline).
o Serotonin norepinephrine reuptake inhibitors (e.g., Duloxetine, venlafaxine). Side effects may
include dry mouth, nausea, and dizziness.
o Selective serotonin reuptake inhibitors (e.g., Fluoxetine, paroxetine, sertraline).
o Anticonvulsants (e.g., gabapentin, pregabalin).
o Muscle relaxants (e.g., cyclobenzaprine).
 Additional Lifestyle Modifications:
o Sleep hygiene.
o Cognitive behavioral therapy.
o Acupuncture.
What is the primary difference in joint involvement between Rheumatoid Arthritis (RA) and Gout regarding
symmetry?
Rheumatoid Arthritis typically presents with symmetrical joint involvement, affecting the same joints on
both sides of the body. In contrast, Gout often starts in a single joint, most commonly the big toe, and is not
necessarily symmetrical in its initial or recurrent attacks.
1. Describe the role of Disease-Modifying Antirheumatic Drugs (DMARDs) in the management of
Rheumatoid Arthritis.
DMARDs are a cornerstone of RA treatment designed to prevent inflammation and progressive joint
damage, rather than just alleviating symptoms. They aim to slow the disease progression and achieve
remission, with effects usually seen within about six weeks.
2. What is "pannus" in the context of Rheumatoid Arthritis pathophysiology, and what is its
significance?
Pannus is a layer of vascular fibrous tissue that forms in the inflamed synovial membrane during
Rheumatoid Arthritis. Its significance lies in its destructive nature, as it grows and invades, causing erosion
of bone and cartilage within the joint, eventually leading to joint space disappearance and fusion.
3. List two systemic clinical manifestations of Systemic Lupus Erythematosus (SLE) beyond joint and
skin issues.
Two systemic clinical manifestations of SLE beyond joint and skin issues include cardiac involvement,
such as pericarditis with tachycardia, hypertension, and edema, and renal involvement, leading to
nephritis, which can be identified by protein or red blood cells in the urinalysis.
4. What key diagnostic finding is considered definitive for Gout, and why might serum uric acid levels
be misleading during an acute flare?
The definitive diagnostic finding for Gout is the presence of uric acid crystals in a synovial fluid analysis.
Serum uric acid levels can be misleading during an acute flare because the levels may be normal as the
crystals have deposited in the joint, but they will typically be elevated once the flare subsides.
5. Explain the main pathological event leading to the characteristic skin and organ manifestations in
Scleroderma.
The main pathological event in Scleroderma is the excessive and abnormal accumulation of insoluble
collagen in the connective tissues. This leads to the characteristic thickening and tightening of the skin, and
can also affect internal organs, causing hardening and functional loss.
6. Identify two non-pharmacological nursing interventions that can help alleviate pain and stiffness for
a patient experiencing an RA flare-up.
Two non-pharmacological nursing interventions for RA flare-ups include applying heat or cold to the
affected joints to help alleviate pain and stiffness, and assisting the patient with applying splints to the
affected joints to provide support and rest during acute inflammation.
7. Why are live vaccines contraindicated for patients on certain medications for Rheumatoid Arthritis
or Systemic Lupus Erythematosus?
Live vaccines are contraindicated for patients on certain medications for RA or SLE because these
medications (e.g., DMARDs, monoclonal antibodies, immunosuppressants) suppress the immune system.
Administering a live vaccine to an immunocompromised individual can increase the risk of developing the
full-blown disease from the vaccine itself.
8. Describe the underlying mechanism of pain in Fibromyalgia, distinguishing it from inflammatory
causes.
In Fibromyalgia, the underlying mechanism of pain is neurogenic, meaning the pain is amplified by
abnormal functioning of the central nervous system's pain regulation pathways. Unlike inflammatory
conditions, the pain is not primarily the result of inflammation or structural damage to tissues.
9. What is the distinction between allopurinol and colchicine in the pharmacologic management of
Gout?
Allopurinol is a xanthine oxidase inhibitor used for chronic management of Gout to prevent attacks by
interrupting the breakdown of purines and reducing uric acid formation. Colchicine, on the other hand, is
an antigout agent primarily used for acute gout attacks to relieve pain and swelling, although it can also be
used for chronic management at lower doses.
1. What are Inflammatory Rheumatic Disorders?
Inflammatory rheumatic disorders are chronic systemic conditions characterized by inflammation and degeneration
in the connective tissues. These disorders often involve periods of exacerbation (flare-ups) and remission. While
their exact cause is often unknown, immunological abnormalities are suspected. Examples include Rheumatoid
Arthritis, Systemic Lupus Erythematosus, Scleroderma, Gout, and Fibromyalgia.
2. What is Rheumatoid Arthritis (RA) and how does it progress?
Rheumatoid Arthritis (RA) is an autoimmune reaction primarily affecting the synovial tissue, which is the
membrane lining of joints. It impacts 1-2% of the population worldwide, with females being three times more likely
to be affected, most commonly between ages 30-60. Risk factors include family history, environmental influences,
nulliparity, smoking, and obesity. RA typically starts in small peripheral joints (like fingers and wrists) and can
progress to larger, more proximal joints if untreated. A key characteristic is its usual symmetric presentation. The
disease progresses through stages:
1. Synovitis: Inflammation and thickening of the synovial membrane.
2. Pannus Formation: A layer of vascular fibrous tissue (pannus) forms and invades the joint.
3. Cartilage and Bone Erosion: The pannus grows, damaging bone and cartilage.
4. Ankylosis: The space between joints disappears, leading to fusion of the bones. RA can also affect other
organs, including the heart, skin, eyes, mouth, and lungs.
3. What are the key symptoms and diagnostic methods for Rheumatoid Arthritis?
The clinical manifestations of RA can be remembered by the "Seven S's":
 Sunrise stiffness: Severe pain and stiffness, especially in the morning.
 Soft feeling in joints: Joints may feel boggy or spongy.
 Swelling in joints: Joints are often warm and swollen.
 Symmetrical: Symptoms typically affect the same joints on both sides of the body.
 Synovium: The joint lining is affected and inflamed.
 Systemic: Beyond joints, patients may experience fatigue, fever, and effects on organs like lungs and heart.
 Stages: Progression from synovitis to pannus to ankylosis.
Diagnosis involves:
 History and physical examination: Assessing for rheumatoid nodules, joint inflammation, and symmetric
stiffness, tenderness, swelling, and temperature changes.
 Laboratory findings: Positive Rheumatoid factor, positive Anti-CCP antibodies, increased ESR
(Erythrocyte Sedimentation Rate), positive CRP (C-reactive protein), and decreased erythrocyte count.
Arthrocentesis may show cloudy, milky, or dark yellow synovial fluid.
 Imaging: Plain x-rays are common to track disease progression, along with ultrasound and MRI.
4. How is Rheumatoid Arthritis managed?
There is currently no cure for RA. The primary goals of management are to decrease joint pain and swelling, achieve
remission, reduce the likelihood of joint deformity, and minimize disability. Treatment strategies include:
 Pharmacologic Therapy:
 Disease-Modifying Antirheumatic Drugs (DMARDs): Such as hydroxychloroquine, methotrexate,
sulfasalazine, and Janus Kinase (JAK) inhibitors (e.g., tofacitinib). These prevent inflammation and joint
damage, with relief often seen within 6 weeks. Methotrexate use requires avoiding pregnancy and alcohol,
and certain DMARDs necessitate regular ophthalmic examinations. Live vaccines should be avoided when
on these medications.
 NSAIDs (Nonsteroidal Anti-inflammatory Drugs): Like ibuprofen and naproxen, used for pain and
inflammation relief.
 Corticosteroids: Such as prednisone, used as "bridge" therapy for short-term relief until DMARDs become
effective.
 Immunomodulators: Biologic DMARDs like adalimumab.
 Occupational and Physical Therapy: Focus on pacing activities, range of motion (ROM) exercises, and
muscle-strengthening exercises to maintain independence.
 Reconstructive Surgery: Considered when pain is severe and threatens independence, aiming to repair or
replace joints, but not performed during exacerbations.
 Nursing Considerations: Emphasize adherence to treatment, pain management (heat/cold), fatigue
management (warm baths, relaxation, energy conservation), mobility (assistive devices, ROM, low-impact
activity), and rest during flare-ups. Education is crucial for ADL difficulties, patient safety, and medication
adherence.
5. What is Systemic Lupus Erythematosus (SLE) and its symptoms?
Systemic Lupus Erythematosus (SLE) is a chronic systemic autoimmune disorder characterized by widespread
inflammation and degeneration in connective tissues, with periods of remission and exacerbation. The
pathophysiology involves multiple factors (genetic, environmental, immunoregulatory, hormonal, epigenetic)
leading to immune complexes, antibodies, cytokines, and T cells that cause organ damage in various systems,
including kidneys, skin, lungs, brain, and heart.
Common signs and symptoms include:
 Fever
 Fatigue with anorexia
 Skin rashes, notably the classic "butterfly rash" and discoid lesions.
 Joint pain and swelling, including morning stiffness, often symmetrical, similar to RA.
 Systemic symptoms: pericarditis with tachycardia, hypertension, edema, respiratory effusions, nephritis
(kidney inflammation), behavior changes, psychosis, depression, and seizures. Diagnosis often relies on
fulfilling at least 4 out of 11 criteria, using the mnemonic "SOAP BRAIN MD".
6. How is Systemic Lupus Erythematosus diagnosed and managed?
Diagnosis of SLE involves:
 Physical Assessment: Checking for skin rashes (erythematous, plaques, hyper/depigmentation, alopecia),
mouth ulcerations, cardio/respiratory issues (pericardial friction rub, abnormal lung sounds),
musculoskeletal symptoms (symmetric joint swelling, tenderness, warmth, pain, stiffness, edema), and
neurological changes.
 Laboratory findings: Positive Antinuclear Antibody (ANA) in 95% of cases, increased creatinine (if
kidney damage), protein or RBCs in urinalysis, decreased erythrocyte count, positive ESR and CRP, and
pancytopenia (decreased CBC).
Management goals are to prevent progression, minimize disability, and prevent complications. This includes:
 Pharmacologic Therapy:
 Monoclonal antibodies: belimumab (Benlysta) and rituximab (Rituxan) reduce B cell activity; live
vaccines are avoided 30 days prior.
 Corticosteroids: Topical for skin, low-dose oral for minor symptoms, and high-dose oral/IV for major
symptoms, with risks like osteoporosis and fractures.
 DMARDs: hydroxychloroquine (Plaquenil) for cutaneous, musculoskeletal, and mild systemic symptoms
to control disease long-term.
 NSAIDs: For minor symptom control.
 Immunosuppressive agents: Methotrexate, Azathioprine, Mycophenolate, reserved for serious SLE cases
unresponsive to other therapies.
 Nursing Considerations: Address fatigue, impaired skin integrity, body image disturbance, and lack of
knowledge. Pregnancy requires SLE to be controlled for at least 6 months. Patients are educated on
understanding and preventing flares using "LESS" (Lower stress, Exercise, Sleep, Sun protection) and
recognizing flare signs ("FLARE": Fatigue, Low-grade fever, Achy joints, Rash, Edema).
7. What is Gout, its causes, and its manifestations?
Gout is the most common form of inflammatory arthritis, affecting men 3-4 times more often than women. Risk
factors include age, high BMI, alcohol consumption, hypertension, diuretic and aspirin use, and consumption of
fructose-rich beverages. Cause: Hyperuricemia, which is an elevated level of uric acid (urate) in the blood (serum >
6.8 mg/dL). Uric acid is a natural waste product of purine metabolism. Gout occurs either due to overproduction of
uric acid or inefficient excretion by the kidneys. Pathophysiology: High concentrations of uric acid lead to the
formation of sharp, needle-like sodium urate crystals, which deposit in joints, causing intense inflammation, pain,
and redness. These deposits are called tophi and can occur in the synovium, tendons, subcutaneous tissues, and even
in organs like aortic walls, heart valves, and ear cartilage. Clinical Manifestations:
 Acute gouty arthritis: Recurrent attacks of severe inflammation in and around joints, most commonly
affecting the big toe, but also ankles, knees, wrists, fingers, and elbows. Attacks are often abrupt, occur at
night, and are triggered by trauma, alcohol, dieting, medications, surgical stress, or illness. There are
periods of remission and exacerbation.
 Tophi deposits: Visible and palpable nodules of uric acid crystals.
 Gouty nephropathy: Renal impairment and kidney stones due to uric acid deposits in the kidneys.
8. How is Gout diagnosed and managed?
Diagnosis of Gout involves:
 Synovial fluid analysis: The definitive diagnostic test, revealing the presence of uric acid crystals.
 Uric Acid serum blood test: Levels may be normal during an acute flare but are typically elevated after
the flare subsides.
 Medical history, physical exam, and imaging tests are also part of the diagnostic process.
Management aims to achieve a uric acid level below 6 mg/dL. Pharmacologic Therapy:
 Acute attacks: NSAIDs (e.g., indomethacin) or corticosteroids are used to relieve pain and inflammation.
Colchicine (Colcrys) is also used for pain and swelling during acute attacks and for chronic management.
 Chronic Management:
 Allopurinol (Zyloprim, Aloprim): A xanthine oxidase inhibitor that prevents uric acid formation. It
cannot be started or have its dose increased during an active flare due to potential bone marrow depression.
 Probenecid (Probalan): Increases urinary excretion of uric acid and is used for patients with frequent
attacks.
 Important distinction: Allopurinol prevents gout attacks, while Colchicine is for acute attacks. Neither is
solely for pain relief, but rather to reduce uric acid or inflammation associated with it.
Lifestyle Modifications:
 Avoiding purine-rich foods (e.g., red meats, organ meats, some seafood like sardines).
 Decreasing alcohol consumption (especially craft beer).
 Avoiding aspirin, as it can increase uric acid levels.
 Staying hydrated by drinking at least 2000 mL of fluid per day to prevent uric acid deposits and kidney
stones.
 Weight management.
9. What is Fibromyalgia and how is it characterized and managed?
Fibromyalgia is a chronic pain syndrome characterized by chronic fatigue, generalized muscle aching, stiffness,
sleep disturbances, and functional impairments. It affects women more than men and often co-occurs with other
rheumatic conditions. The underlying mechanism is amplified pain of neurogenic origin, where the central nervous
system's pain regulation pathways function abnormally, essentially keeping the "volume control setting" for pain
consistently high.
Diagnosis of fibromyalgia is diffuse, meaning there is no single conclusive diagnostic test. Management is
symptom-specific and involves:
 Medications:
o NSAIDs for pain.
o Tricyclic antidepressants (e.g., amitriptyline, nortriptyline).
o Serotonin-norepinephrine reuptake inhibitors (e.g., duloxetine, venlafaxine).
o Selective serotonin reuptake inhibitors (e.g., fluoxetine, paroxetine, sertraline).
o Anticonvulsants (e.g., gabapentin, pregabalin).
o Muscle relaxants (e.g., cyclobenzaprine).
 Additional Lifestyle Modifications:
o Practicing good sleep hygiene.
o Engaging in cognitive behavioral therapy (CBT).
o Considering acupuncture.
The pain in fibromyalgia is described as an increased response to painful stimuli and sensitivity to stimuli that are
not normally painful, and it is not the result of inflammation or damage.