Inflammation, OA/RA/SLE, Osteoporosis

Describe inflammation

• Inflammation is a nonspecific, generalized response to stress/harmful stimuli to dilute or neutralize the inflammatory agent, remove damaged tissue, and set up a suitable environment for healing and repair

• Think about inflammation like broad-spectrum abx (it kills both good and bad bacteria; inflamnmation can be harmful or helpful)

Does infection alway have inflammation?

Yes, but inflammation does not always mean there is an infection.

• Someone can come in with increased WBC, but no infection (inflammation causes leukocytosis)

Chronic, progressive, metabolic bone disease marked by:

• Low bone mass

• Deterioration of bone tissue

This leads to increased bone fragility and instability to withstand normal mechanical stress

Osteoporosis

4 main things in diet to maintain bone health

• Vitamin D

• Calcium

• Phosphorus

• Protein

Factors that increase risk for osteoporosis

• Hormone imbalances (hyperthyroidism/hyperparathyroidism, low estrogen/menopause)

• Inadequate dietary intake (CPPD)

• Medications (steroids, antiseizure/psych meds, Rolaids)

• SAD

Complications of chronic inflammation

• Tissue damage

• Endothelial damage

• Increased r/o clots

• Immunocompromised

• Exhausted metabolism

Pathophysiology of osteoporosis

Bone resportion exceeds bone formation

• Decreased osteoclast apoptosis

• Increased osteoclast development

• Osteopenia (reduced bone density) comes before osteoporosis

S&S of osteoporosis

• “Silent disease”; can progress and deteriorate bone thoroughly before a fracture occurs

• Spontaneous fractures (fracture when you sit down, or just walking)

  • Increased r/o fractures

• Back pain

• Generalized body pain

• Kyphosis (inward curvature/humpback)

• Loss of height

Modifiable and nonmodifiable risk factors for osteoporosis

• Modifiable

  • Diet (CPPD)

    • Sunlight, food

  • Activity level (weightbearing)

    • Swimming and cycling are NOT weightbearing

  • SAD

  • Meds (Tums are good, Rolaids bad)

  • Low body weight

• Nonmodifiable

  • Age 65+ (post menopausal for women (low estrogen);

  • Caucasian or Asian identiy

  • Family hx

  • Female

  • Estrogen deficiency/low testosterone (post-menopausal)

  • Malabsorption diseases)

  • Hysterectomy

Why are females more at risk for osteoporosis than male patients?

• Pregnancy and/or breastfeeding (decreases calcium levels)

• Have lower bone density

• Bone resorption is more rapid after menopause (decreased estrogen protection)

Why is estrogen important for preventing osteoporosis?

Estrogen inhibits bone resorption

Diagnostics for osteoporosis

• Bone mineral density (BMD) → DEXA

  • T-scores (higher T score = increased r/o osteoporosis or active condition)

• X-rays (if you can see osteoporosis on X-ray, condition is already late stage w/ 25-40% bone density loss)

• Nutrition assessment (calcium and vitamin D)

T-scores (osteoporosis)

• 1 to -0.99 = normal bone density

• -1 to -2.4 = Low bone density

• >-2.5 = osteoporosis

Drug therapy for osteoporosis

• Biphosphonates (the -nates)

  • Alendronate, risedronate, pamidronate)

• Calcium supplements

• Vitamin D supplements

MOA of biphosphonates

• Diminishes and interferes with osteoclast activity (reduce bone resorption)

• Patient education:

  • Take w/ full glass of water and sit up for at least 30 min to an hr after taking

Why take biphosphonates w/ full glass of water (30 mins before other meds and food) and sit up for at least 30 min to an hr after taking

Biphosphonates cause significant esophageal irritation (if you lay down, you will have acid reflux)

Nursing implications for biphosphonates

• Take w/ full glass of water and sit up for 30 min to an hr (med causes severe esophageal irritation)

• Take 30 mins before other meds and food

• Lockjaw necrosis = educate patient to alert nurse if they feel jaw tenderness, clicking, S&S of inection

Key sources of calcium

• Dairy (milk, yogurt, cheese)

• Leafy greens (spinach, collards, kale)

• Legumes

• OJ + fortified cereal

Key sources of vitamin D

• Fatty fish (cod, salmon, carp, seal, mackerel, trout, tuna)

• Fortified dairy

• Eggs

• OJ and cereal

Osteoporosis is a normal part of aging. True or false?

False. It’s normal to have some bone loss, but osteoporosis is porous bones, which is abnormal.

The different types of arthritis

• OA

• RA

• Fibromyalgia (FMS)

• SLE

• Gout

Gradual loss and integrity of articular cartilage (padding that covers bones and joints)

OA

Pathophysiology of OA

1) Loss or damage of articular cartilage (e.g. mechanical stress/injury)

2) New bone formation in joint margins (remodeled bone is more cracked and not as smooth)

3) Narrowing of joint margins & bone spurs (articular cartilage flakes off from frictuion, may leave completely exposed bone; bones rubbing against each other causes uneven grooves and bone spurs)

4) Mild synovitis (bone spurs enter synovial fluid causing inflammation)

5) Thickening of joint capsule (decreased ROM)

Secondary osteoporosis is caused by

Hormone imbalances (hyperparathyroidism, hyperthyroidism, diabetes), medications (heparin, steroids, phenytoin, barbiturates, lithium, aluminum, steroids, phenytoin, barbiturates, lithium, aluminum, antacids [Rolaids], SAD

Degeneration, eventual loss, and then disordered repair of recartilage. Increased remodeling = not as smooth or frictionless; loses glistening appearance and yellows.

OA

Areas at high r/o suffering from OA

• Hips

• Knees

• Shoulders

• Hands

S&S of OA

• Joint stiffness

  • More common after periods of disuse

• Joint pain

  • Pain worsens with joint use

• Swelling (depends on stage)

• Joint effusion

• Crepitus

• Bouchard nodes/Herberden nodes

Modifiable risk factors

• Obesity

• Repetitive movement/mechanical stress

• Injury

• Medications

Non-modifiable risk factors

• Increased age

• Female

• Decreased estrogen

Drug therapy for OA

• NSAIDs

• Topical agents

• Celebrex

• Steroid injections for flare-ups

Alternative medicine

• Acupuncture

• Massage

• Yoga

• Anti-inflammatory supplements

Heat therapy vs cold therapy in OA (heat vs cold compress)

• Do whatever makes patient happy

• Heat for muscle pain and joint stiffness (vasodilation)

• Cold for inflammation and associated swelling (vasoconstriction)

Chronic, systemic, autoimmune disease characterized by inflammation of connective tissue in the synovial joints

• Characterized by periods of remission and exacerbation

RA

Autoimmune diseases are characterized by inflammation, which leads to

Generalized fatigue, lethargy

Pathophysiology of RA

1) Antigen (whatever it may be) triggers IgG and autoantibodies (AKA rheumatoid factor (RF))

2) IgG and autoantibodies combine to create immune complexes

3) Complexes deposit in synovial areas of the body resulting in inflammatory reaction (body attacks joints)

4) Inflammation keeps going on and, on cytokines and enzymes destroy healthy tissue long-term

S&S of rheumatoid arthritis

• Nonspecific manifestations

  • Fatigue, lethargy, body ache

• Joint stiffness (typically smally joints of hands and feet)

  • Pain, stiffness, limited ROM

  • Occur systemically (small joints of hands, PIP, MCP, and feet MTP)

  • Joint stiffness after inactivity

  • Ulnar drift and swan-neck deformity

  • RA nodes

    • Morning stiffness last 60 min+

• Bilateral/symmetrical (if RA on one hand, there will be RA on other hand)

• As it progresses, inflammation and fibrosis cause deformity

• Nonspecific manifestations

  • Fatigue, lethargy, body ache

• Joint stiffness (typically smally joints of hands and feet)

  • Pain, stiffness, limited ROM

  • Occur systemically (small joints of hands, PIP, MCP, and feet MTP)

  • Joint stiffness after inactivity

  • Ulnar drift and swan-neck deformity

  • RA nodes

    • Morning stiffness last 60 min+

• Bilateral/symmetrical (if RA on one hand, there will be RA on other hand)

• As it progresses, inflammation and fibrosis cause deformity

These clinical manifestations appear in what condition?

RA

Extra-articular symptoms of RA

• Cardiac: artherosclerosis, MI, stroke, vascular lesions (rheumatoid nodules), pericarditis, myocarditis, Raynaud’s, peripheral edema

• Respiratory: rheumatoid nodules, fibrosis, pleuritis

• HEENT: Sjorgren’s syndrome, conjunctivitis

• Skin: rheumatoid nodules, butterfly rash (but it’s mostly lupus)

• Immunology: immunocomprimised, Felty syndrome

Modifiable risk factors for RA

• Smoking

• Obesity

Non-modifiable risk factors for RA

• Age 30-60

• Female

• Family hx/genetics

Cardiac symptoms of RA

Artherosclerosis, MI, stroke, vascular lesions (rheumatoid nodules), pericarditis, myocarditis, Raynaud’s, peripheral edema

Respiratory symptoms of RA

Rheumatoid nodules, fibrosis, pleuritis

HEENT symptoms of RA

Sjorgren’s syndrome, conjunctivitis

Skin symptoms of RA

Rheumatoid nodules, butterfly rash (butterfly rash mostly SLE)

Immunologic symptoms of RA

Immunocomprimised, Felty syndrome

A common autoimmune disease that targets moisture-producing exocrine gland (leads to symptoms such as dry eyes and dry mouth)

• Xerostomia and keratoconjunctivitis sicca

• Other glands in the stomach, pancreas, intestines

  • Increase risk for non-Hodgkin’s lymphoma

• Usually diagnosed in ages 40s to 50s

• Most patients are women

Sjogren’s syndrome

Primary Sjogren’s syndrome

No other rheumatic disease

• Occurs in combination with another rheumatic disease (e.g. RA, SLE, scleroderma)

• Autoimmune thyroid disorders are common

• Etiology: genetic and evironmental

  • Genes: Whites, Japanese, Chinese, African Americans

  • Trigger: viral or bacterial infection adversely stimualtes immune system

Secondary Sjogren’s syndrome

Diagnostics for RA

• H&P

• RF (not found in all cases of RA)

• Citrullinated peptide (anti-CCP)

• C-reactive protein

• Synovial fluid analysis

Drug therapy for RA

• Disease-modifying antirheumatic drugs (DMARDs) → slow disease progression

  • Methotrexate

• Antimalarial drugs

  • Hydroxychloroquine

• Biologic response modifiers (BRMs)

  • Slow disease progession and 2nd-line after DMARDs)

• NSAIDs

• Steroid injections

Major AEs of methotrexate

• Bone marrow suppression (monitor CBCs)

• Nephrotoxicity and stomatitis (monitor kidney function and mouth)

Nursing management for RA

• Pain (NSAIDs & steroids)

• Mental health

• R/o infection (immunocompromised)

• R/o multiorgan involvement

• ADLs

Modifiable risk factors for osteoporosis

• Diet (CPPD)

• Sunlight, food

• Activity level (weightbearing)

  • Swimming and cycling are NOT weightbearing

• SAD

• Meds (Tums are good, Rolaids bad)

• Low body weight

Nonmodifiable risk factors for osteoporosis

• Age 65+ (post menopausal for women (low estrogen);

• Caucasian or Asian identiy

• Family hx

• Female

• Estrogen deficiency/low testosterone (post-menopausal)

• Malabsorption diseases)

• Hysterectomy

RA vs OA

• RA = symmetric, morning stiffness > 30 min.

  • Patho: joints in hands more PIP, NOT DIP; expected course of worsening (delay progession but incurable). General symptoms like fever, malaise.

  • Inflammaiton around joint capsule; swollen inflammed synovial membrane

• OA = asymmetric, morning stiffness < 30 min.

  • Patho = joints in hands (DIP & PIP); random exacerbations.

  • Bone on bone violence

What can exacerbate/cause flares of RA?

Triggers such as stress or other precipitating events

Multisystem inflammatory autoimmune disease

• Chronic, unpredicatble course with alternating periods of remission and exacerbation

• Stress (e.g. puberty, pregnancy) can precipitate this disease

• Sunlight can also cause this disease to flare

SLE

Pathophysiology of SLE

1. Trigger

2. Autoantibodies are created against nucleic acids and erythrocytes, coagulation proteins, phospholipids, lymphocytes, platelets, and more

3. Has periods of remission and exacerbation

4. Deposition of circulating immune complexes (esp in organs); body attacks itself with inflammation

   1. These complexes have a tendency to deposit in glomerular basement membrane (cause kidney damage)

5. Complementary and inflammatory activation that is never-ending

What to monitor for SLE

• Triggers (e.g. sun exposure)

• Kidney function, hydration, urine output, I/Os

• Immunocomprimised → CBC

Integumentary symptoms of SLE

• Alopecia

• Photosensitivity

• Butterfly rash

• Discoid erythema

• Palmar erythema

• Mucosal ulcers

Cardiopulmonary symptoms of SLE

• Endocarditis

• Myocarditis

• Pericarditis

• Pleural effusion

• Pneumonitis

• Raynaud’s

Urinary symptoms of SLE

• GN (Good Pasture’s syndrome)

• Hematuria

• Proteinuria

Neurologic symptoms of SLE

• Stroke

• Seizures

• Peripheral neuropathy

• Psychosis

• Cognitive impairment

Hematologic symptoms of SLE

• Anemia

• Leukopenia

• Lymphadoenopathy

• Splenomegaly

• Thrombocytopenia

GI symptoms of SLE

• Abd pain

• NVD

• Dysphagia

Musculoskeletal symptoms of SLE

• Arthritis

• Myositis

• Synovitis

Reproductive symptoms

• Menstrual abnormalities

• Very difficult to get pregnant

General symptoms of SLE

• Respiratory

• CV:

  • Raynuad’s, pericarditis, vascular inflammation

• General:

  • Weight loss

  • Fatigue

  • Fever/immuncomprimised

  • Emotional lability

  • Hematologic disorders (anemia)

  • Neurologic disorders (seizure/stroke)

• Photosensitivty + butterfly rash on cheeks

  • Erythematous rash to areas exposed to sunlight

• Kidneys:

  • Lupus nephritis

  • Proteinuria and hematuria

Modifiable risk factors for SLE

• Smoking

• Stress

• Medicaitons

• Environmental factors

  • Air pollution, pesticides, heavy metal exposure

Non-modifiable risk factors for SLE

• Female

• Family hx/genetics

• 15-45 y/o

• Ethnicity (everyone gets affected more except caucasians)

Diagnostic tests for SLE

• No specific test

• Anti-smith antibody (gold-standard)

• Anti-nuclear antibody (ANA)

• H&P

• Inflammatory markers

Gold-standard test for SLE

Presencen of anti-smith antibody

Nursing management of SLE

• Assess for flare-ups and triggers

• Manage pain

• Assess mental status

• ADLs

• Assess multiorgan involvement (especially kidneys)

• Assess for clotting and bleeding (systemic inflammation can precipitate clots and bleeding_

• Risk for infection

Drug therapy for SLE

• Combination NSAIDs

• Steroids (corticosteroids)

• Immunosuppressants

• Antimalarial drugs

  • Hydroxychloroquine and chloroquine

• Methotrexate

AE of this drug toxicity is stomatitis; high doses (toxic effect/OD) can injure kidneys/nephrotoxicity; high doses cause bone marrow suppression

Methotrexate (used to treat RA)

Gold standard diagnostic test for osteoporosis

Dexa scan (measures bone density)

• Dual energy x-ray absorptiometry

Home safety for osteoporosis and reducing r/o falls

• Remove/tape down rugs

• Grab bars

• Assistive devices (cane)

• Adherence to meds, exercise plan, supplements/diet

• Nonslip socks or slippers

A person is classified as having SLE if 4 or more of the criteria are present, serially or simultaneously, during any interval of observation:

• Antinuclear antibody (ANA): abnormal titer

• Anti-smith

• Discoid rash: raised patches with scaling follicular plugging; scarring in older lesions

• Hematologic disorder: hemolytic anemia, leukopenia, lymphopenia, or thrombocytopenia

• Immunologic disorder: anti-DNA antibody or antibody to Sm (Smith) nuclear antigen or positive antiphospholipid antibodies

• Malar rash: fixed redness, flat or raised (butterfly rash)

• Oral ulcers: usually painless

• Neurologic disorder: seizures or psychosis (in the absence of causative drugs or known metabolic disorders)

• Nonerosive arthritis: 2 or more peripheral joints with tenderness, swelling, effusion

• Pleuritis or pericarditis

• Photosensitivity

• Renal disorder: persistent proteinuria, cellular casts in urine

• Antinuclear antibody (ANA): abnormal titer

• Anti-smith

• Discoid rash: raised patches with scaling follicular plugging; scarring in older lesions

• Hematologic disorder: hemolytic anemia, leukopenia, lymphopenia, or thrombocytopenia

• Immunologic disorder: anti-DNA antibody or antibody to Sm (Smith) nuclear antigen or positive antiphospholipid antibodies

• Malar rash: fixed redness, flat or raised (butterfly rash)

• Oral ulcers: usually painless

• Neurologic disorder: seizures or psychosis (in the absence of causative drugs or known metabolic disorders)

• Nonerosive arthritis: 2 or more peripheral joints with tenderness, swelling, effusion

• Pleuritis or pericarditis

• Photosensitivity

• Renal disorder: persistent proteinuria, cellular casts in urine

Diagnostic criteria for SLE (present serially or simultaneously during any interval of observation)

Nursing management for SLE

• Infection prevention (drugs e.g. corticosteroids makes immune system weaker)

• Rest/activity balance

• Sun protection

• Avoid triggers (stress, sun exposure, meds, infections)

• Medication teaching

• Manage pain

• Control inflammation and protect organs

• Pregnancy (some SLE meds are safe, but some like methotrexate have to be stopped)

• Emotional support + positive coping

Metabolic arthritis caused by uric acid crystal deposition. Involves hyperuricemia from overproduction or underexcretion

• Monosodium urate crystals form in joints

• Crystals trigger inflammatory response → pain, swelling & redness

Gout

Clinical manifestations of gout

• Sudden, severe joint pain that occurs at night

• Redness, swelling, warmth on affected joints

• Very sensitive to touch (guarding; don’t touch it)

• Tophi (chronic gout); hard visible lumps of uric acid deposits

• Commonly only affects one joint at a time (typically big toe)

Diagnostic tests for gout

• Symptoms

• Serum uric acid levels

• Synovial fluid aspiration → gold standard

• Renal function (kidney issues worsen gout)

• Medications (e.g. HCTZ)

Gout drugs

• Colchecine → acute gout attacks

• Allupurinol/Febuxostat → long-term uric acid control (chronic gout; not used for acute attacks)

Nursing implications for xanthine oxidase inhibitors (allupurinol/febuxostat)

• Take with meals

• Stay well hydrated (3L of fluid/day)

• Monitor kidney function and la

• Agranulocytosis/aplastic anemia (bone marrow dysfunction)

• Serious skin conditions (exfoliative dermatitis, SJS)

• N/V

• Dizziness, drowsiness

• Kidney stones

Adverse effects of xanthine oxidase inhibitors

Foods high in purines (avoid in gout)

• Shellfish

• Red meat

• Alcohol

• Organ meats

Nursing management of gout

• Drug therapy

• Dietary changes (limit purine-rich foods)

  • Shellfish, red meat, organ meat, alcohol

• Hydrate (esp if taking XOIs → 2-3 L/day)

• Weight control

Nursing focus for gout

• Hydrate (2-3 water L/day) → flush uric acid

• Avoid (Avoid purine → ETOh, red meat, organ meat, shellfish)

• Relieve (take long-term meds consistently e.g. XOIs allupurinol/feboxustat; take colchicine for acute attacks)