Rheumatological

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    Rheumatological

    What meds will someone take for

    low bone density?

    Fosamax

    Non Steroidal anti-inflammatories

    Rheumatoid Arthritis

    What is it? Chronic, inflammatory disorder which mainly attacks synovial

    joints (but may affect many tissues a& organs)

    F to M 3:1

    Age Range 20-70

    Typical Age 40 - 50 years

    S&S morning stiffness for more than 30 min

    malaise

    arthritis in 3+ joints and soft tissue swelling

    arthritis in hand joints rheumatoid nodules (found at elbow or wrist)

    symmetrical arthritis

    fever

    What kind of investigations to

    confirm

    positive RF

    Increased ESR

    Increased WBC count

    Increased CRP

    X ray changes with erosions esp. in wrist hands and feet

    Which joints does initially RA affect? 75% at the joints of the hands, wrist and feet

    30% at the large joints

    Red= more common

    Cause / aetiology unknown, considered multi-factorial, with genetic,

    environmental and hormonal factor

    What is Pannus? Vascularised granulation tissue (rich in fibroblasts,lymphocytes & macrophages) derived from synovial tissue,which overgrows the surface of joint

    What is the pathology of RA? Auto-immune response triggered (normal tissue targeted)

    Inflammatory reaction in the synovium (& subsequent joint

    damage)

    Synovium then develops a PANNUS (associated with the

    breakdown of the articular surface)

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    Effusion distends the capsule & stretches ligaments

    Laxity, joint deformity and rheumatoid nodules

    Describe what happens to the joint

    In brief terms what can happen to

    hands with RA?

    Differential Diagnosis for RA Gout, OA, SLE ,Psoriatic Arthritis ,Reactive Arthritis

    Ankylosis SPondilitisWhat are the TTT goals for RA? Relieve pain

    Reduce inflammation

    Slow down or haltjoint damage

    Improve sense of well being & ability to function

    Sjogrens Syndrome

    What is it? Autoimmune disease; characterised by inflammation of

    exocrine glands that produce tears and saliva

    What is its aetiology? Unknown, possible link with HLA DR3?

    How prevalent is it in the

    population?

    Prevalence 1-3%

    What is the male to female ratio? Female-Male ratio 9:1

    What is the typical age group? 5060

    What are the classifications? Primarya disease in its own right

    Secondaryas a result of another disease

    What other diseases may cause

    secondary?

    Association with RA, SLE, systemic sclerosis, chronic

    acute hepatitis,

    What are the symptoms? Dry Mouth - difficulty swallowing or talking for long

    periods, tongue fissures, dental caries, oral candidiasis

    Dry Eyes - less tears, dry, gritty, reddened

    RA - episodic arthritisVaginal Dryness

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    Systemic: fever, weight loss, fatigue, Raynauds

    Sarcoidosis

    What is sarcoidosis? An autoimmune disease in which abnormal collections of chronicinflammatory cells (granulomas) form in multiple organs.

    What is its Aetiology? Unknown; environmental, genetic factors link with HLAB8 DR3

    AGE 10-40years

    S&S May be assymptomatic

    Common symptoms are:

    Fatigue unchanged by sleep

    Lack of energy

    Weight loss

    Aches & pains

    Arthritis

    Dry eyes SOB

    Blurry vision

    Rashes and noduli

    Diagnosis Chest x-ray or CT scann

    Whatd a hand xray look like? Hand x-ray reveals osseous erosions bilaterally.

    Swollen fingersArrows: granulomous erosion

    OA

    What is it? A degenerative condition of synovial joints affecting the

    articular cartilage and subchondral bone.

    S&S Joint pain, tenderness, stiffness, locking and effusionCauses Hereditary, mechanical, metabolic, developmental

    http://en.wikipedia.org/wiki/Granulomashttp://en.wikipedia.org/wiki/Granulomashttp://en.wikipedia.org/wiki/Granulomashttp://en.wikipedia.org/wiki/Granulomas
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    Progression Slow

    Explain the process?

    BS RED

    1. Breakdown of articular surface cartilage becomes

    fissured. Small particles of cartilage of break of down

    2. Synovial Irritation

    Friction from cartilage particles causes the release ofinflammatory mediators

    3. Remodelling

    Cartilage is slow to repair due to its poor bloods supply. The

    increased pressure on the bone causes excessive subchondral

    activity causes increase in bone cells and density giving rise

    to osteophytes.

    4. Eburnation of bone & cyst formation:

    Eventually cartilage layer may be completely eroded. This

    causes bone on bone contact pain & the exposed bonebecoming polished & eburnated. This causes changes in

    structure & overloads certain parts of the joint causing micro-

    fracture in the cancellous (spongy/less dense bone). Healing

    via callus formation leading to increased rigidity, increased

    density & reduced resilience, in turn there are more micro

    fracture

    5. Disorganisation

    Cells grow back in a disorganised

    What is the common demographic

    for O/A?

    The 4 Fs:

    Female Fat

    Forty

    Fair (Caucasian)

    What different physiological

    stages/events may occur?

    How is O/A classified? Primary O/A(no specific underlying cause)

    Secondary O/A(secondary to an identifiable cause) Metabolic: calcium crystal deposition, acromegal

    Inflammatory: A/S, septic arthritis

    Congenital / Developmental: Perthes disease, slippedupper femoral epiphysis, CDH

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    Traumatic:joint trauma, surgery, chronic injury,

    neuropathic

    What are the risk factors? increasing age, gender, obesity

    trauma, repetitive occupational trauma

    genetic factors, history of inflammatory arthritis, metabolic

    disorderneuromuscular disorder, infection

    Which joints are normally involved? Typically the weight bearing joints & hands

    How is the patients general health? Systemically well

    What is the character of their pain? Often burning or aching in character

    What is their pain pattern like? Worse after activity or at the end of the day

    What is causing the pain? Inflammatory mediators, intra-articular hypertension,

    bursitis, enthesis pain (tendinous attachment to bone), muscle

    weakness, lack of use

    Relieved by? Relieved by rest

    What is the joints quality of motion

    like?

    Joints feel stiff to move, patients occasionally mention

    clicking or crepitus

    Is their any weakness? Weakness is usually a secondary issue due to lack of muscle

    activity

    What are Herbedens Nodes? Heberdens nodes often affects the base of thumb & DIP

    joints. Initially are red, swollen & tender, over time swellings

    become firm & painless. Despite the nodes function is usuall

    good, however the thumb may be a persistent problem.

    Typical of OA

    What should you observe for? Observation look for altered weight bearing, joint deformity

    muscular wasting (secondary to disuse) swelling of whole

    joint often with effusion

    What should you palpate? Palpate for swelling often with effusion, crepitus on

    movement and ROM or joint deformity

    What is the aim of osteopathic OA

    TTT?

    Given that there is no cure for osteoarthritis

    Aim of treatment: reducing pain levels

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    maintain function

    develop muscle strength (OA knees)

    Hip OA