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Rheumatology Lecture Flashcards

1
Q

Historical Background

A

a. Four humours (400 BC, Hippocrates)
- Black bile from spleen (melancholic)
- Yellow bile from gallbladder (choleric)
- Blood from liver (sanguine)
- Phlegm from brain/lungs (phlegmatic)

b. Rheuma- “a substance that flows”. First century AD.
c. “Rheumatism” introduced by Dr. G. Baillou in 1642.
d. Rheumatology: a medical science devoted to the study of rheumatic diseases and musculoskeletal disorders.

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2
Q

Arthritis burden

A

a. 60 million people (20% of the U.S. population) have one or more of 120 musculoskeletal or rheumatic disorders
- 45.9 million with doctor dx arthritis
- 50% less than age 65
- 32 million with frequent neck/low back pain
- 28 million with osteoporosis/osteopenia

b. Total cost to society: $127.5 billion (1% of 2005 GNP)
i. Direct medical costs: $80.5 billion
* ii. One out of 5 office visits to a PCP is for a MS disorder
iii. 20% of all hospital stays and 10% of all surgical procedures are for a musculoskeletal disorder.

c. Indirect costs: $47 billion in lost earnings
i. 30% of all workers with doctor dx arthritis have arthritis-associated work limitation.
ii. 25% of all disability payments is to a person with a MS disorder (3rd leading cause of work disability).

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3
Q

Arthritis burden: most common diseases

A

a. Arthritis and autoimmune diseases
1) Osteoarthritis 21 million

2) Crystalline arthritis (gout, CPPD) 3 million

3) Autoimmune dz
i. Rheumatoid arthritis 1.3 million
ii. Juvenile RA 50,000
iii. Spondyloarthropathies(AS,PsA) 700,000
iv. Connective tissue diseases
SLE 322,000
PMR 228,000
Scleroderma 50,000
Others (Sjogren’s, polymyositis, vasculitis)

b. Soft tissue rheumatism (periarticular)
i. Bursitis/tendinitis(periarticular) 5 million
ii. Fibromyalgia (nonarticular) 4 million

c. Osteoporosis/osteomalacia
i. Osteoporosis 10 million
ii. Osteopenia 18 million

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4
Q

Types of Joint pain

A
  1. Within Joint “Arthritis”
    i. Subchondral bone
    ii. Cartilage
    iii. Synovial fluid
    iv. Synovium
  2. Around Joint “Periarticular”
    i. Muscle
    ii. Tendon
    iii. Tenosynovium
    iv. Enthesis
    v. Bursa
    vi. Ligament
  3. Away From Joint “Nonarticular”
    i. Muscle
    ii. Bone
  4. Away from Musculoskeletal System “Referred”
    i. Visceral
    ii. Neurological
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5
Q

“Arthritis”

Musculoskeletal Pain

A

Falls into two categories–> Either Arthritis or Soft tissue rheumatism

1. Arthritis 
cartilage - OA
SF - Crystal
synovium - Rheumatoid Arthritis
sub/bone - AVN
  1. Soft tissue rheumatism
    i. Periarticular
    - Tendonitis
    - Tenosynovitis
    - Enthesopathy
    - Ligament
    - Bursitis
    - Other

ii. Nonarticular
- Muscle
- Bone

iii. Referred
- Visceral
- Neurological

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6
Q

Classification

A

a. Arthritis
Noninflammatory: Osteoarthritis
Inflammatory: Crystalline (gout), autoimmune diseases [RA, CTD (SLE), spondyloarthropathies (AS, reactive, psoriatic)]

b. Soft tissue rheumatism
Periarticular: tendinitis, bursitis
Nonarticular: fibromyalgia, bone (osteomalacia, osteoporosis with fracture)

c. Referred pain and other causes

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7
Q

The Arthritis Classification

A

Will be either Inflammatory or Noninflammatory

a. Inflammatory
1. Crystal
2. Septic
3. RA, CTD
4. Spondylos

b. Noninflammatory
- Osteoarthritis
- Endo/metabolic/other
- Miscellaneous
- Trauma
- AVN
- Neuropathic/Charcot

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8
Q

Arthritis History and Physical

A

a. History
i. Pain in joint or in reference area of joint
ii. Pain in all directions of movement

b. Physical exam
i. Swelling and tenderness of entire joint line
ii. Limited/painful ROM in all directions
iii. Pain with active ROM = passive ROM
iv. Effusion=arthritis

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9
Q

Inflammatory vs Noninflammatory Arthritis

A

Inflammatory:

  1. Soft tissue swelling (tumor) +/- effusion
    i. AM stiffness> 60min
  2. Erythema (rubor)
    i. Crystal or septic
  3. Warmth (calor)
  4. Tenderness (dolor)
    i. Pain with rest, nite, activity
  5. Loss of function (functio laeso)-wax and wane
    i. Fatigue and systemic sxs
    ii. May respond to steroids
Noninflammatory :
1. Bony swelling
  i. Effusion in knee OA
 ii. AM stiffness<30min
2. No erythema
3. Minimal warmth
4. Mild tenderness
    i. Pain with use
5. Variable effect on ADLs
   i. Slowly progressive
   ii. No fatigue or systemic sxs
  iii/ No response to oral steroids
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10
Q

Inflammatory Arthritis

5 signs

A
  1. Soft tissue swelling (tumor) +/- effusion
    i. AM stiffness> 60min
  2. Erythema (rubor)
    i. Crystal or septic
  3. Warmth (calor)
  4. Tenderness (dolor)
    i. Pain with rest, nite, activity
  5. Loss of function (functio laeso)-wax and wane
    i. Fatigue and systemic sxs
    ii. May respond to steroids
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11
Q

Non-inflammatory arthritis signs

A
  1. Bony swelling
    i. Effusion in knee OA
    ii. AM stiffness<30min
  2. No erythema
  3. Minimal warmth
  4. Mild tenderness
    i. Pain with use
  5. Variable effect on ADLs
    i. Slowly progressive
    ii. No fatigue or systemic sxs
    iii. No response to oral steroids
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12
Q

Arthritis anatomy

A
  1. Inflammatory arthritis = synovitis

Synovitis is the medical term for inflammation of the synovial membrane. This membrane lines joints that possess cavities, known as synovial joints. The condition is usually painful, particularly when the joint is moved. The joint usually swells due to synovial fluid collection.

  1. Noninflammatory arthritis = cartilage degeneration
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13
Q

Noninflammatory arthritis

Osteoarthritis

A

a. Pain in joint with use in all directions both passive and active ROM

b. Morning stiffness < 30 minutes
i. shorter morning stiffness

c. Slowly progressive

  • d. Weight-bearing joints, spine, DIPs, PIPs, 1st CMC, 1st MTP
    • knee and hips, not ankles

e. Joint effusion< 2000 cells/mm3
f. Normal lab test results
g. Osteophytes on Xray
h. TX–> NSAIDs, analgesics

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14
Q

Imaging in Osteoarthritis

*good slide

A

*Osteoarthritis- Seagull sign

  1. Will see loss of cartilage, transfer of force to the bone
    i. Will see sclerosis on bone
    ii. Asymmetric joint space narrowing
  2. Osteophytes
    i. Osteophytes form because of the increase in a damaged joint’s surface area. This is most common from the onset of arthritis. Osteophytes usually limit joint movement and typically cause pain.
  3. Will see swelling in PIP and DIP joints
    * i. Heberden nodes
    * ii. Bouchard nodes

*4. Osteoarthritis: Asymmetric joint space narrowing

  1. Clinically for hip osteoarthritis
    i. will see hip contractures, will be stuck in hip flexion
    ii. can see varus formation with kness
  2. Bunyon formation
    i. will see valgus bending of toes
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15
Q

Inflammatory arthritis

A

a. Monoarticular (1 joint)
i. Gout
ii. CPPD/Pseudogout
iii. Infectious

b. Oligoarticular, asymmetric (2-4 joints) +/- spine
i. Spondyloarthropathies

c. Polyarticular, symmetric (>/= 5 joints)
i. Rheumatoid arthritis
ii. CTD: SLE, others

d. Spine predominant
Ankylosing spondylitis

e. Signs
1) Pain in joint with rest and use and with active and passive ROM
2) Morning stiffness > 1 hour
3) Flares of disease
4) Any joint: STS, heat, erythema
* 5)Joint effusion> 2000 cells/mm3
6) Abnormal labs: ESR, CRP, RF, ANA, uric acid
7) Erosions on xrays

TX: NSAIDs, prednisone, DMARDs, biologics, dz specific

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16
Q

Laboratory tests for

A

a. Signs of inflammation
i. Anemia of chronic dz, elevated platelet count, low albumin
ii. Erythrocyte sedimentation rate (ESR): time RBCs fall in 1 hour. Immunoglobulins and large proteins which are produced in excess in response to inflammation cause the RBCs to fall faster.
iii. C-reactive protein(CRP): protein produced by liver in response to inflammation

b. Chemistries/ urinalysis
i. Look for abnormalities indicating other organ involvement
ii. Uric acid: usually elevated in gout

c. Serologies
i. Rheumatoid factor: Immunoglobulin (usually IgM) that reacts with the Fc portion of IgG. Seen in RA and other diseases
ii. Anti-cyclic citrullinated protein(CCP): specific for RA
iii. Antinuclear antibodies(ANA): antibodies that are directed against antigenic epitopes in the nucleus. Seen in SLE (>99%) and other diseases.

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17
Q

Erythrocyte Sedimentation Rate (ESR)

Inflammatory Arthritis

A

Upper limit for normal sed rate:
males= 15mm/hr or age/2
females= 20mm/hr or (age + 10 )/2

ESR increased by large asymmetric molecules: fibrinogen, alpha macroglobulins, and immunoglobulins

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18
Q

Signs/SX of inflammatory arthritis

A

1) Pain in joint with rest and use and with active and passive ROM
2) Morning stiffness > 1 hour
3) Flares of disease
4) Any joint: STS, heat, erythema
* 5)Joint effusion> 2000 cells/mm3
6) Abnormal labs: ESR, CRP, RF, ANA, uric acid
7) Erosions on xrays

TX: NSAIDs, prednisone, DMARDs, biologics, dz specific

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19
Q

Types of Inflammatory Arthritis

A

a. Monoarticular (1 joint)
i. Gout
ii. CPPD/Pseudogout
iii. Infectious

b. Oligoarticular, asymmetric (2-4 joints) +/- spine
i. Spondyloarthropathies

c. Polyarticular, symmetric (>/= 5 joints)
i. Rheumatoid arthritis
ii. CTD: SLE, others

d. Spine predominant
i. Ankylosing spondylitis

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20
Q

Signs of Inflammation in inflammatory Arthritis

A
  1. Anemia of chronic dz, elevated platelet count, low albumin
  2. Erythrocyte sedimentation rate (ESR): time RBCs fall in 1 hour. Immunoglobulins and large proteins which are produced in excess in response to inflammation cause the RBCs to fall faster.
  3. C-reactive protein(CRP): protein produced by liver in response to inflammation
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21
Q

Serology and Lab values for Inflammatory Arthritis

A

Chemistries/ urinalysis

i. Look for abnormalities indicating other organ involvement
ii. Uric acid: usually elevated in gout

Serologies

i. Rheumatoid factor: Immunoglobulin (usually IgM) that reacts with the Fc portion of IgG. Seen in RA and other diseases
ii. Anti-cyclic citrullinated protein(CCP): specific for RA
iii. Antinuclear antibodies(ANA): antibodies that are directed against antigenic epitopes in the nucleus. Seen in SLE (>99%) and other diseases.

22
Q

Rheumatoid factors

A

Rheumatoid factor (RF) is the autoantibody (antibody directed against an organism’s own tissues) that was first found in rheumatoid arthritis. It is defined as an antibody against the Fc portion of IgG (an antibody against an antibody) and different RFs can recognize different parts of the IgG-Fc. RF and IgG join to form immune complexes that contribute to the disease process

23
Q

Anti-cyclic citrullinated protein (Anti-CCP)

Inflammatory Arthritis

A

a. Arginine residues in numerous proteins can be deiminated to form citrulline by the enzyme, peptidylarginine deiminase (PAD).
i. This is a normal process which is accelerated at sites of local inflammation.

b. Patients with rheumatoid arthritis can form antibodies to these citrullinated proteins.

c. Value of anti-CCP in patients suspected to have RA
i. High sensitivity (70%), specificity (95%)
ii. More ikely to develop erosions (10x). Maybe worse prognosis
iii. Approximately 10% of RF negative RA pts are anti-CCP positive.

24
Q

Antinuclear antibodies

A

Antinuclear antibodies (ANAs, also known as antinuclear factor or ANF) are autoantibodies that bind to contents of the cell nucleus. In normal individuals, the immune system produces antibodies to foreign proteins (antigens) but not to human proteins (autoantigens). In some individuals, antibodies to human antigens are produced.

There are many subtypes of ANAs such as anti-Ro antibodies, anti-La antibodies, anti-Sm antibodies, anti-nRNP antibodies, anti-Scl-70 antibodies, anti-dsDNA antibodies, anti-histone antibodies, antibodies to nuclear pore complexes, anti-centromere antibodies and anti-sp100 antibodies. Each of these antibody subtypes binds to different proteins or protein complexes within the nucleus. They are found in many disorders including autoimmunity, cancer and infection, with different prevalences of antibodies depending on the condition. This allows the use of ANAs in the diagnosis of some autoimmune disorders, including systemic lupus erythematosus, Sjögren’s syndrome, scleroderma, mixed connective tissue disease, polymyositis, dermatomyositis, autoimmune hepatitis and drug induced lupus.

25
Q

Inflammatory monoarticular arthritis

A
  1. Gout
  2. Pseudogout
  3. Septic (infectious)

FAILURE TO ASPIRATE, PREPARE TO LITIGATE !
-get that fluid, missing septic arthritis is punishable in court

26
Q

Gout

A

a. Males > females
b. Males>age 30, females are postmenopausal
c. Alcohol, obesity
d. Acute onset, monoarticular
e. First MTP and other peripheral jts, tophi
f. Uric acid and uric acid crystals

g. Treatment
i. Acute attack: prednisone, NSAIDs
ii. Chronic therapy: allopurinol

27
Q

Gout Images

A

a. Negative Birefringent crystals–> In gout, crystals of monosodium urate (MSU) appear as needle-shaped intracellular and extracellular crystals.
b. When examined with a polarizing filter and red compensator filter, they are Yellow when aligned parallel to the slow axis of the red compensator but turn blue when aligned across the direction of polarization (ie, they exhibit negative birefringence). Negatively birefringent urate crystals are seen on polarizing examination in 85% of specimens.
c. First MTP and other peripheral jts, tophi

Treatment

i. Acute attack: prednisone, NSAIDs
ii. Chronic therapy: allopurinol

28
Q

Pseudogout

A

a. Males= females
b. Age> 55-60
c. R/O hyperparathyroidism
d. Acute onset
e. Knee and wrist most common, monoarticular
f. Chondrocalcinosis on xray
g. CPPD crystals in SF
h. Acute Rx: prednisone, NSAIDs

29
Q

Pseudogout Images

A

ABC= Alignment Blue Calcium

Microscopic analysis in pseudogout shows calcium pyrophosphate (CPP) crystals, which appear shorter than MSU crystals and are often rhomboidal. Under a polarizing filter, CPP crystals change color depending upon their alignment relative to the direction of the red compensator. They are positively birefringent, appearing blue when aligned parallel with the slow axis of the compensator and yellow when perpendicular.

30
Q

Septic (infectious) arthritis: non gonococcal

A

Nongonococcal
1. Acute onset, fever

  1. Hot,red, pain
  2. Immunosuppressed, IVDA
    i. concern if patient has week immune system
  3. Wt. bearing joint jt
    i. hip, knee, shoulder
  4. SF WBC> 50,000
31
Q

Septic Arthritis: Gonococcal

A

Gonococcal
1. Young females > males

  1. Prodrome: fever, skin lesions, tenosynovitis
    i. look for these infarcted skin lessions, often on extremities
  2. Joint phase: Knee> other wt bearing> hands. May be >1 jt.
  3. Hx: PID but usually not active
32
Q

Inflammatory asymmetric, oligoarticular arthritis +/- spine involvement

A

Seronegative spondyloarthropathies
1. Psoriatic arthritis

  1. Reactive arthritis (Reiter’s syndrome)
  2. Colitic/enteropathic arthritis

4/ Ankylosing spondylitis

33
Q

Psoriatic arthritis

A

Type of Oligoarticular arthritis

  1. Caucasians
  2. Asymmetric oligoarticular (2-4 jts)
  3. Upper extremity joints (DIPs)
  4. Dactylitis
  5. Psoriasis, nail lesions
  6. RF/ANA neg
  7. Therapy: similar to RA, DMARDs, biologics
34
Q

Psoriatic arthritis Wiki

A

Psoriatic arthritis is a long-term inflammatory arthritis that occurs in people affected by the autoimmune disease psoriasis.

The classic feature of psoriatic arthritis is swelling of entire fingers and toes with a sausage-like appearance.This often happens in association with changes to the nails such as small depressions in the nail (pitting), thickening of the nails, and detachment of the nail from the nailbed. Skin changes consistent with psoriasis (e.g., red, scaly, and itchy plaques) frequently occur before the onset of psoriatic arthritis but psoriatic arthritis can precede the rash in 15% of affected individuals.

  • It is classified as a type of seronegative spondyloarthropathy.

Genetics are thought to be strongly involved in the development of psoriatic arthritis. Obesity and certain forms of psoriasis are thought to increase the risk.[3]

Psoriatic arthritis affects up to 30% of people with psoriasis and occurs in both children and adults.[3] Approximately 40-50% of individuals with psoriatic arthritis have the HLA-B27 genotype. The condition is less common in people of Asian or African descent and affects men and women equally

35
Q

Psoriatic Arthritis

A

Pencil in cup deformity

In psoriatic arthritis, pain can occur in the area of the sacrum (the lower back, above the tailbone), as a result of sacroiliitis or spondylitis, which is present in 40% of cases. Pain can occur in and around the feet and ankles, especially enthesitis in the Achilles tendon (inflammation of the Achilles tendon where it inserts into the bone) or plantar fasciitis in the sole of the foot.

Along with the above-noted pain and inflammation, there is extreme exhaustion that does not go away with adequate rest. The exhaustion may last for days or weeks without abatement. Psoriatic arthritis may remain mild or may progress to more destructive joint disease. Periods of active disease, or flares, will typically alternate with periods of remission. In severe forms, psoriatic arthritis may progress to arthritis mutilans which on X-ray gives a “pencil-in-cup” appearance

36
Q

Inflammatory polyarthritis

A

a. Rheumatoid arthritis

b. Connective tissue diseases (with extraarticular manifestations)
i. Systemic lupus erythematosus (SLE)
ii. Sjogren’s syndrome
iii. Systemic sclerosis (scleroderma)

37
Q

Septic (infectious) arthritis

GC vs non-GC

A

Gonococcal

  1. Young females > males
  2. Prodrome: fever, skin lesions, tenosynovitis
  3. Joint phase: Knee> other wt bearing> hands. May be >1 jt.
  4. Hx PID but usually not active

Nongonococcal

  1. Acute onset, fever
  2. Hot,red, pain
  3. Immunosuppressed, IVDA
  4. Wt. bearing joint jt
  5. SF WBC> 50,000
38
Q

Rheumatoid arthritis

A

a. Females > males
b. Subacute and chronic onset. Spongy synovitis

c. Polyarticular: MCPs, PIPs, wrists, and MTPs.
i. Other joints but not DIPs or back

d. ESR/CRP, RF(85%)
e. Erosions on xray
f. TX: DMARDs, biologics

39
Q

Rheumatoid Arthritis Wiki

A

Rheumatoid arthritis (RA) is a long-term autoimmune disorder that primarily affects joints. It typically results in warm, swollen, and painful joints. Pain and stiffness often worsen following rest. Most commonly, the wrist and hands are involved, with the same joints typically involved on both sides of the body. The disease may also affect other parts of the body. This may result in a low red blood cell count, inflammation around the lungs, and inflammation around the heart. Fever and low energy may also be present. Often, symptoms come on gradually over weeks to months.

While the cause of rheumatoid arthritis is not clear, it is believed to involve a combination of genetic and environmental factors. The underlying mechanism involves the body’s immune system attacking the joints. This results in inflammation and thickening of the joint capsule. It also affects the underlying bone and cartilage. The diagnosis is made mostly on the basis of a person’s signs and symptoms.

X-rays and laboratory testing may support a diagnosis or exclude other diseases with similar symptoms. Other diseases that may present similarly include systemic lupus erythematosus, psoriatic arthritis, and fibromyalgia among others.

The goals of treatment are to reduce pain, decrease inflammation, and improve a person’s overall functioning. This may be helped by balancing rest and exercise, the use of splints and braces, or the use of assistive devices. Pain medications, steroids, and NSAIDs are frequently used to help with symptoms. A group of medications called disease-modifying antirheumatic drugs (DMARDs), such as hydroxychloroquine and methotrexate, may be used to try to slow the progression of disease.[1] Biological DMARDs may be used when disease does not respond to other treatments.[6] However, they may have a greater rate of adverse effects.[7] Surgery to repair, replace, or fuse joints may help in certain situations.[1] Most alternative medicine treatments are not supported by evidence

40
Q

Joint Inflammation in Rheumatoid Arthritis

A

Arthritis of joints involves inflammation of the synovial membrane. Joints become swollen, tender and warm, and stiffness limits their movement. With time, multiple joints are affected (polyarthritis). Most commonly involved are the small joints of the hands, feet and cervical spine, but larger joints like the shoulder and knee can also be involved. Synovitis can lead to tethering of tissue with loss of movement and erosion of the joint surface causing deformity and loss of function.

RA typically manifests with signs of inflammation, with the affected joints being swollen, warm, painful and stiff, particularly early in the morning on waking or following prolonged inactivity. Increased stiffness early in the morning is often a prominent feature of the disease and typically lasts for more than an hour. Gentle movements may relieve symptoms in early stages of the disease. These signs help distinguish rheumatoid from non-inflammatory problems of the joints, such as osteoarthritis. In arthritis of non-inflammatory causes, signs of inflammation and early morning stiffness are less prominent with stiffness typically less than one hour, and movements induce pain caused by mechanical arthritis.

The pain associated with RA is induced at the site of inflammation and classified as nociceptive as opposed to neuropathic.[17] The joints are often affected in a fairly symmetrical fashion, although this is not specific, and the initial presentation may be asymmetrical.[15]:1098

As the pathology progresses the inflammatory activity leads to tendon tethering and erosion and destruction of the joint surface, which impairs range of movement and leads to deformity. The fingers may suffer from almost any deformity depending on which joints are most involved. Specific deformities, which also occur in osteoarthritis, include ulnar deviation, boutonniere deformity (also “buttonhole deformity”, flexion of proximal interphalangeal joint and extension of distal interphalangeal joint), swan neck deformity (hyperextension at proximal interphalangeal joint and flexion at distal interphalangeal joint) and “Z-thumb.” “Z-thumb” or “Z-deformity” consists of hyperextension of the interphalangeal joint, fixed flexion and subluxation of the metacarpophalangeal joint and gives a “Z” appearance to the thumb. The hammer toe deformity may be seen. In the worst case, joints are known as arthritis mutilans due to the mutilating nature of the deformities

41
Q

SLE

A
  1. Females > males
  2. Age 15-45, nonwhite > white
  3. Arthritis, rash, kidney disease, CNS disease, clots
    1. ANA (99%)
      i. look for the anti-nuclear antibody
  1. TX: hydroxychloroquine, prednisone, cytotoxics
42
Q

Inflammatory spine disease

A

a. Ankylosing spondylitis and other spondylos

b. Inflammatory back pain
i. Age < 45
ii. Insidious onset
iii. Chronic(>3 mos)
iv. AM/nitetime stiffness
v. Improves with exercise
vi. No neuro sxs
vii. Global loss of ROM

c. Osteoarthritis, degenerative discs

d. Noninflammatory back pain
i. Any age
ii. Acute or insidious
iii. Usually lasts < 1 month
iv. AM stiffness < 30 min
v. *Worse with use
vi. May have neuro sxs
vii. Loss of flexion ROM

43
Q

Ankylosing spondylitis

A
  1. Males > females
  2. Age < 40, Caucasian > others
  3. Sacroiliitis and low back pain with prolonged morning stiffness
  4. HLA-B27 gene
  5. TX: NSAIDs, biologics
44
Q

Noninflammatory spine disease

A
  1. Osteoarthritis (cervical, lumbar)
  2. Spinal stenosis
    i. Simian gait
    ii. Neurogenic claudication
    iii. Spinal Phalen’s
45
Q

Soft tissue rheumatism

A

a. Periarthritis
i. Pain localized near joint
ii. Pain with some movements. Active > passive ROM
iii. Tenderness over specific tendon or bursa
iv. Normal lab results
v. Xrays usually normal
vi. NSAIDs, PT

b. Fibromyalgia
i. Diffuse nonarticular pain
ii. Pain unrelated to joint ROM
iii. Specific tender points
iv. Normal lab results and xrays
v. NSAIDs, PT, exercise, neuroleptics, tricyclics

46
Q

Periarthritis- two types

A

Bursitis and Tendonitis

a. Bursitis
i. Olecranon bursitis (gout, RA, septic, trauma)
ii. Subacromial bursitis
iii. Trochanteric bursitis
iv. Ischial bursitis
v. Prepatellar bursitis
vi. Pes anserine bursitis
vii. Retrocalcaneal bursitis

b. Tendonitis
i. Bicipital tendinitis
ii. Rotator cuff tendinitiis (impingement)
iii. Lateral/medial epicondylitis
iv. DeQuervain’s tendinitis
v. Achilles tendinitis

47
Q

Osteoporosis

A

a. Females > males
b. Caucasians,Asians > African-Americans
c. Postmenopausal, prednisone, calcium or vitamin D problems
d. Not painful unless fracture
e. Calcium, vitamin D, bisphosphonates, teraparatide

48
Q

Vertebral Fractures

A

Get DEXA on all women>65, all men>75, anyone on prednisone for over 3 months, or hx fragility fracture. Get 25OH vitamin D if osteopenic.

49
Q

Ankylosing spondylitis

wiki

A

Ankylosing spondylitis (AS) is a type of arthritis in which there is long term inflammation of the joints of the spine. Typically the joints where the spine joins the pelvis are also affected. Occasionally other joints such as the shoulders or hips are involved. Eye and bowel problems may also occur. Back pain is a characteristic symptom of AS, and it often comes and goes. Stiffness of the affected joints generally worsens over time.

The cause of ankylosing spondylitis is unknown; however, it is believed to involve a combination of genetic and environmental factors. More than 90% of those affected have a specific human leukocyte antigen known as the HLA-B27 antigen. The underlying mechanism is believed to be autoimmune or autoinflammatory.

Diagnosis is typically based on the symptoms with support from medical imaging and blood tests. AS is a type of seronegative spondyloarthropathy, meaning that tests show no presence of rheumatoid factor (RF) antibodies.[2] It is also within a broader category known as axial spondyloarthritis.

There is no cure for ankylosing spondylitis. Treatments may improve symptoms and prevent worsening. This may include medication, exercise, and surgery. Medications used include NSAIDs, steroids, DMARDs such as sulfasalazine, and biologic agents such as infliximab.

Between 0.1% and 1.8% of people are affected. Onset is typically in young adults. Males are more often affected than females. The condition was first fully described in the late 1600s by Bernard Connor; however, skeletons with ankylosing spondylitis are found in Egyptian mummies.[8] The word is from Greek ankylos meaning stiffening, spondylos meaning vertebra, and -itis meaning inflammation

50
Q

Ankylosing spondylitis

Radiographic features

A

The earliest changes in the sacroiliac joints demonstrable by plain x–ray shows erosions and sclerosis.

Progression of the erosions leads to pseudo-widening of the joint space and bony ankylosis.

X-ray spine can reveal squaring of vertebrae with spine ossification with fibrous band run longitudinally called syndesmophyte while producing bamboo spine appearance.

A drawback of X-ray diagnosis is the signs and symptoms of AS have usually been established as long as 8–10 years prior to X-ray-evident changes occurring on a plain film X-ray, which means a delay of as long as 10 years before adequate therapies can be introduced. Options for earlier diagnosis are tomography and MRI of the sacroiliac joints, but the reliability of these tests is still unclear.

Musculoskeletal (26 decks)

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