Rr-Symptoms-Joint Pain

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-Algia

Back 1

Pain

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Arthralgia

Back 2

Pain without objective joint finding (thousand of causes)

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Arthritis

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Diagnosis of arthritis demands an objective finding.
Most commonly a physical finding.
Sometimes a radiographical finding.
Sometime it's a joint fluid abnormality

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Exam for arthritis

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Look for:
Swelling (tumor)
Warmth
Erythema
Tenderness accentuated over joint
Decreased range of motion

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Eliciting Tenderness

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Sufficient to blanch end of thumbnail

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Feeling for warmth with joints

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Use back of hand. Compare to adjacent and contralateral structures.

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Physical exam hints for joint pain

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- A normal control might be the opposite side or adjacent similar joint
- Another normal control is you
- intra-articular problems often restrict passive and active ROM (use joint during any ROM)
- extra- articular problems restrict active or resisted and relative spare passive ROM (use muscles and tendons)

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Non-Inflammatory arthritis (osteoarthritis)

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Tender, swelling often bony rather than soft

Joint fluid WBC > 200 but < 2000

Usually normal acute phase reactants
sclerosis, narrowing, or normal on x-ray

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Inflammatory (rheumatoid arthritis)

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Prominent inflammation
Soft tissue swelling
Joint fluid WBC > 2000/MM3
Usually elevated acute phase reactants
Porosis, narrowing, and/or erosions on x-ray

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Symptoms suggesting an "inflammatory arthritis"

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Pain is similar in severity to "non-inflammatory"
Pain improves with activity, better late in day (non-inflammatory worsens)
Morning stiffness > 30 min
Subjective swelling usually more prominent in inflammatory

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2 Common Arthritis Presentations

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Acute Monoarthritis (one joint)
Chronic polyarthritis

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Acute inflammatory monoarthritis

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Three common causes:

- Inflammatory causes:
.. crystal induced ( gout or pseudogout)
.. septic
... acute non-inflammatory cause (trauma)

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Crystals associated with gout

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Monosodium urate crystals

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Calcium pyrophosphate dihydrate crystals

- pseudogout

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Aspirate Joint Fluid

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- Categorizes inflammatory vs. Non-inflammatory (WBC 2,000)

- Only way to confidently diagnose crystal-induced arthritis

- Can't afford to miss a septic joint due to potential for rapid destruction w/o early intervention

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Chronic Inflammatory polyarthritis

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- Rheumatoid Arthritis
-- mostly peripheral joints
-- some systemic features (fatigue, anemia)

- Connective Tissue Disease
-- prominent extra-articular features (skin, renal, lung, etc.) e.g. - lupus, scleroderma

- Spondyloarthropathies
-- often spine and attachment structures inflamed (ligament, tendon, capsule, periosteum) as well as joint

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Arthritis

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An objective finding by physical exam, direct visualization (surgery or arthroscopy), or by radiographic demonstration of joint damage

- Not merely subjective joint pain
- Not an abnormal blood test
- Is suggested by some typical symptoms, especially prolonged morning stiffness, history of swelling, loss of motion

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Acute Monoarthritis

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Think crystals (inflammatory), infection (inflammatory), or trauma

Aspirate fluid if suspect inflammatory

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Chronic Inflammatory Polyarthritis

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Think RA, Connective Tissue Disease, Enthesopathy

- Consider if primarily joints (RA), joints + other organs (CTD), joints + entheses or spine findings (enthesopathy, spondyloarthritis)

Many clues in extra-articular symptoms and signs, clues in lab, and clues in x-ray indicate specific diagnosis

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Juvenile Idiopathic Arthritis

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Systemic:
- 1-2x daily fever spike
- ecanescent rash

Psoriatic

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Polyarticular

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- more than 4 joints at presentation
- RF+
- RF-

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Oligoarticular

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4 or fewer joints at presentation

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Juvenile Idiopathic Arthritis - Enthesitis-related arthritis

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Inflammation at tendinous inertions "enthesitis" or tendon sheaths
- axial involvement (spine, SI joints)
- larger peripheral joints
- acute anterior uveitis

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NSAIDs

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Inhibit Cox1/2

Cox1- housekeeping
Cox2- inflammation

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COX1

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"housekeeping"
GI protection (gastritis)
Renal blood flow (renal insufficiency)
Platelet aggregation
Vasoconstriction

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COX2

Back 29

Inflammatory
Central mediation of pain/fever
Vasodilation

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NASIDS and CV Risk

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ASA irreversibly inhibits COX
- platelets cannot regenerate
- other nucleated cells (including endothelial cells and vascular smooth muscle can)
- Net effects, platelets permanently inhibited, endothelium transiently inhibited

COX2 Inhibitors
- COX2 more active in endothelial cells but not as much as in platelets

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Glucocorticoids

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Effects on gene transcription - hours
- binds to steroid receptor allowing translocation to nucleus to either activate or repress transcription of genes

"nongenomic effects" - direct effects on
-- signaling molecules
-- ion channels
-- can happen in minutes

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Immunosuppressive Effects of Glucocorticoiuds

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Decreases expression of COX2
Decreases circulating lymphocytes by 70%
-- especially CD4's but also CD8's and B cells
-- likely by sequestration in bone marrow
-- decreased proliferative responses

90% decrease in circulating monocytes

Reduces chemotaxis of neutrophils to inflammatory sites
-- may raise blood neutrophil count ("demargination") --paradoxical increase in neutrophils

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Side Effects of Steroids

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- Immune suppression
- HTN (steroids increase absorption of salt)
- Osteoporosis, poor growth
- Increased hunger, centripetal obesity, buffalo hump, moon facies
- Striae
- Psychiatric (mania, depression, psychosis, sleep disturbance)
- Reversible adrenal insufficiency (need to wean steroids gradually)

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Methotrexate

Back 34

Inhibition of DNA Synthesis
-- inhibits recycling of dihydrofolate reductase which is necessary for recycling of DHF to THF
-- THF is necessary for purine and pyrimidine synthesis
-- This is major action in high dose uses for cancer

Increases levels of immunomodulatory adenosine
-- this is likely the major action for low dose uses for autoimmune diseases

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Methotrexate Effects

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Effects are dependent on polyglutamation
- prevents efflux of MTX from cells

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Indications for Methotrexate

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- Leukemia/lymphoma
- Rheumatoid arthritis
- Inflammatory bowel disease
- Psoriasis

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Side Effects of Methotrexate

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GI mucosa- nausea, mucositis
Bone marrow - anemia, other cytopenias
Liver - hepatitis
Lungs - hypersenstivity pneumonitis
Renal - 90% renal clearance, high dose can cause renal insufficiency

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Tumor Necrosis Factor

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Initially synthesized as membrane bound trimer
Released in soluble form by TNF-alpha converting enzyme
Important role in control of granulomatous infections

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TNF sites of action

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Produced largely by macrophages and CD4 T cells
Important role in control of granulomatous infections

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Patient complains of abdominal pain when using naproxen. What mediation do you use instead?

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Celecoxib. It is a selective Cox-2 inhibitor.

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Anti-TNF : Mechanism

Back 41

Inhibits signaling through TNF-receptor
Antibody dependent cell cytotoxicity of tmTNF expressing cells (less so with etanercept)
Potentially reverse signaling through thTNF itself

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Anti-TNF: Indications

Back 42

Inflammatory bowel disease
RA/JIA
Psoriasis

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Anti-TNF : Side Effects

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- Infection - particularly infections controlled by granulomas (TB, histoplasma)
- Controversial increase in malignancies
- Can develop antibodies to mouse portions of drug
-- infusion reactions
-- reduced efficacy
- Neuropathies
- Autoantibodies/autoimmunity

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NSAIDs block?

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Cox1/Cox2

Includes: aspirin, ibuprofen and naproxen

(acetaminophen) is not considered an NSAID because it has little anti-inflammatory activity


selective cox-2 inhibitor is celecoxib

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