Logan Class of December 2013 - Home



Lecture 1

Wednesday, May 14, 2008

9:31 AM

 

Key to colors/notations

Green highlighted words and phrases represent definitions

Yellow highlighted words and phrases represent things Dr. Kuhn emphasized or which seem key to learning

A small pen to the left of something (typically a chart) indicates the information is important

 

Pre test

1. Provide a definition for CT

A computerized imaging modality utilizing attenuating X-rays and simultaneous motion of the tube and scintillator to produce a 3-dimensional, variable slice, image of the part imaged

a. Examples of proper use

Trauma situations, measurements of anatomical size, enhanced soft tissue resolution over plain film

a. Examples of weaknesses of the tool

Starburst artifact of occipital bone, difficulty with imaging near metal implants, high radiation dose, doesn't demonstrate physiology

1. Provide a definition for MRi

A computerized imaging modality utilizing induced precession and radio frequency output to produce a 3-dimensional, variable slice, image of the part imaged

a. Examples of proper use

Soft tissue imaging, central canal imaging, neural imaging, skeletal survey for tumors, physiology

a. Examples of weaknesses of the tool

Claustrophobia, metal implants, expenses, time of exposure

1. List several other imaging tools

Diagnostic ultrasound

Bone scan (SPECT)

MRA

FMRi

Myelogram

Tomogram

1. Define the following and give examples:

a. Congenital anomaly=a lesion that an individual is born with

Straight back syndrome, Os Odontoidium (now thought as non-union fracture)

a. Normal variant=a different than 'normal' presentation but with no clinical significance

a. Dysplasia=congenital anomaly with multiple systems involved, typically has similar risk profile

1. What is the classification system used for soft tissue calcification

 

| |  |

| |Physiological |

| |Dystrophic |

| |Metastatic |

| | |

| |Serum calcium |

| |Normal |

| |Normal |

| |Abnormal (high) |

| | |

| |Tissue calcium |

| |Normal |

| |Abnormal |

| |Normal |

| | |

| |Examples |

| |Thyroid cartilage |

| |Stylohyoid ligament |

| |Arcuate Foramen |

| |Calcific tendonitis |

| |Calcific bursitis |

| |Myositis Officans |

| |Hyperparathyroidism |

| |Lytic Metastasis |

| |Multiple Myeloma |

| | |

 

 

 

 

 

Lecture 2

Monday, May 19, 2008

10:16 AM

 

Arthritis

 

4 categories of arthritis

Degenerative-DJD

Inflammatory-RA

Metabolic-Gout

Septic joint/Septic arthritide

 

Terms

Enthesis= musculotendonous attachment of Sharpe's fibers

Monoarticular=1 joint

Polyarticular=4+ joints

Pauciarticular=2-3 joints

Osteophyte=accessory boney growth adjacent to the joint (periarticular)

Syndesmophyte=calcification of outer annular fibers

Seronegative=no chemical marker within the blood

 

Poster children

Degenerative-DJD/OA

Clinical features

Local inflammation is present

Morning stiffness in affected joints

Reduced range of motion

Swelling of afflicted joint

Osteophytic change

Monoarticular

Changes in soft tissue contour

Lab findings

No prominent findings (seronegative)

No change in ESR (Eosinophil Sedimentation Rate)

Biopsy abnormality

Thinner cortices

Lowered MMP (methylmetalo protease)

Activation of cytokines (pathologic)]

Radiographic findings

Decreased joint space in asymmetric patter(medial worst) owing from decreased articular cartilage

Subchondral sclerosis=whitening/thickening of cortical bone underneath articular cartilage

(due to increased stress input from decreased articular cartilage)

Osteophytes

Geode/subchondral cyst formation (can be synovial fluid or blood or both)

Most commonly seen in large joints (hips, knee, shoulders)

Inflammatory-RA

System inflammation is present

Metabolic-Gout

Septic joint/Septic arthritide

 

 

 

Lecture 3

Wednesday, May 21, 2008

9:19 AM

 

Continued from last lecture

 

DJD=gradual loss of articular cartilage, combined w/ thickening of the subchondral bone; bony outgrowths at the joint margins, and nonspecific synovial inflammation

 

Poster children

Degenerative-DJD/OA

Clinical features

Local inflammation is present

Morning stiffness in affected joints

Reduced range of motion

Swelling of afflicted joint

Osteophytic change

Monoarticular

Changes in soft tissue contour

Lab findings

No prominent findings (seronegative)

No change in ESR (Eosinophil Sedimentation Rate)

Biopsy abnormality

Thinner cortices

Lowered MMP (methylmetalo protease)

Activation of cytokines (pathologic)]

Radiographic findings

Decreased joint space in asymmetric patter(medial worst) owing from decreased articular cartilage

Subchondral sclerosis=whitening/thickening of cortical bone underneath articular cartilage

(due to increased stress input from decreased articular cartilage)

Osteophytes

Geode/subchondral cyst formation (can be synovial fluid or blood or both)

Most commonly seen in large joints (hips, knee, shoulders)

 

Inflammatory-Rheumatoid Arthritis

Clinical presentation

System inflammation is present

Ulnar deviation of MP joints of hands

Decreased and painful movements

Lots of soft tissue swelling

Polyarticular process

Also present in the C-spine, hips, knees, elbows

Pannus formation

Destruction of the soft tissue surfaces leading to ulnar deviation

Usually bilateral

Symmetrical joint space narrowing (w/in same joint)

Don't mess with when flared up

RA Produces highest number of ankylosis in the hands

ALL Inflammatory arthritides present danger of ADI instability

Ankylosis may produce lack of joint motion in all inflammatory arthritides

Hyperemia (increased periarticular blood flow) may erode bone and produce osteopenia

Lab findings

Positive rheumatoid factor (usually present)

Increased ESR

C-reactive protein

Radiographic findings

Ulnar deviation

1st thing seen: Decreased joint space (symmetrically)

Swelling of MP, PIP joints (Bouchard's nodes)

No swelling of DIP!!!

Periarticular soft tissue swelling

Periarticular osteoporosis

Rat bite lesions (produced by pressure erosion and pannus formation)

Metabolic-Gout (will be CPPD)

Clinical presentation

Older men predominantly

Predominance of the heels, big toe, thumb

Abnormal soft tissue (sticking out), pannus

Changes made to the underlying bone

No initial changes in joint spacing/bone makeup

Pain and redness in area of swelling

Lab findings

Tissue/suction biopsy

Increased ESR

Blood/urine may be normal or abnormal

Radiographic findings

No bone changes seen but adjacent soft tissue may calcify (dystrophic)

 

Septic joint/Septic arthritide

Clinical presentation

Lots of swelling/pain

If younger person they got sick quickly

If older person they took a while to develop

Destruction of both joint surfaces will occur in chronic conditions

Hot, red, swollen, tender joints

Previous URTI, recent UTI, or recent skin infection

Lab findings

WBC elevation

ESR elevation when large joints are involved

Core of ESR measures stability of blood pool

If sampled infectious organism may be present

Radiographic findings

Symmetrical destruction of joint space

Cortical damage

Watch what separates from arthritide

 

Degenerative category

DJD=gradual loss of articular cartilage, combined w/ thickening of the subchondral bone; bony outgrowths at the joint margins, and nonspecific synovial inflammation

Generals

Most common joint disorder in the world

Striking age correlation

1/3 of all 65 year olds affected

More common in men vs women younger than 50 (post traumatic/wear and tear)

More common in women vs men older than 50 (hormonal changes)

Predilection for weight bearing joins of the lower extremity, cervical and lumbar spine, and some joints of the hand

Etiology

Known local factors associated with secondary DJD

Weight

Injury

Occupational

Recreational

Skeletal anomalies

Quadriceps strength

Known systemic factors

Reduction in estrogen levels

Genetic susceptibility

Low vitamin D and C intake

Crystal deposition diseases

Hemophilia

Paget's

Most sero - and sero + arthritides

Stages (3)

Phase I: Edema and microcracks (enchondral tissue)

Edema of the extracellular matrix, cartilage loses its smooth aspect, and microcracks appear

There is focal loss of chondrocytes, alternating with areas of chondrocytes proliferation

Phase II: Fissuring and pitting

The microcracks deepen in the direction of the forces of tangential cutting and along fibrils of collagen

Clusters of chondrocytes appear around these clefts and at the surface

Phase III: Erosion

Fissures cause fragmentation of cartilage to detach

These loose fragments cause the local inflammation

This form of inflammation is much more limited than the typical RA

Subchondral microcysts form (may develop into geodes later)

Pathogenesis

The physiologic homeostasis of normal articular cartilage is driven by chondrocytes, which synthesize collagens, proteoglycans, and proteinases

DJD results from failure by chondrocytes to synthesize good quality matrix

This abnormal chondrocytes synthesis is the result of tissue activation by cytokines, lipid mediators (mainly prostaglandins) free radicals (NO, H2O2) and constituents of the matrix itself, such as fibronectin fragments

Activated chondrocytes become capable of producing proinflammatory mediators

 

Certain proteinases are involved in the destruction of cartilage

Matrix metalloprotienases (MMPs) are the most potent

The MMPs are held in check by Tissue Inhibitor MetalloProteinases (TIMPs)

As long as the MMPs and TIMPs are in balance no degradation occurs

The enzyme, aggrecanase, plays a major role in the degradation of the matrix

 

Although DJD is classified as non-inflammatory arthritis, inflammatory cytokines may stimulate chondrocytes to release cartilage-degrading enzymes

Lipid mediators, eicosanoids, can activate chondrocytes to increase synthesis of MMPs ,tipping the balance towards degradation

 

Nitric Oxide plays an uncertain role in DJD

Some studies suggest an ability to induce "DJD, while other studies suggest some protection of the cartilage"

Degenerative

[pic]

Inflammatory-RA

[pic]

 

Metabolic-Gout

[pic]

Septic

[pic]

 

 

 

DJD

[pic]

[pic]

 

 

Lecture 4

Wednesday, May 28, 2008

9:14 AM

 

Frequency of Arthritis on radiographs (how often you will see stuff on films)

|Weekly |Monthly |Yearly |

|DJD |Ankylosing spondylitis |Gout infection |

| |CPPD |Lupus |

| |DISH |Reiter's syndrome |

| |Osteitis Condensans Ilii (OCI) |Scleroderma |

| |Psoriatic arthritis | |

| |RA | |

| |Synoviochondrometaplasia | |

 

Age of onset Arthritis

|0-20 years |20-40 year old |40+ years |

|JRA (Juvenile Rheumatoid Arthritis)/JCA (Juvenile|Ankylosing spondylitis |DJD |

|Chronic Arthritis) |Osteitis Condensans Ilii (OCI) |DISH |

|May be seropositive or seronegative |Lupus |Gout |

| |Reiter's syndrome/Reactive arthritis |Hypertrophic osteoarthropathy |

| |Psoriatic arthritis |Pseudogout (CPPD) |

| |Scleroderma | |

| |Synoviochondrometaplasia | |

 

Arthopathies associated with distinct sex predilection

|Male |Female |

|Ankylosing spondylitis |JRA/JCA |

|Gout |Lupus |

|Hypertrophic osteoarthropathy |OCI |

|Reiter's syndrome/Reactive arthritis |Primary OA |

|Secondary OA |Rheumatoid Arthritis |

| |Scleroderma |

 

Reminders of Categories of joints

Fibrous

Stressed Syndesmosis found in Running sports, martial arts, springboard divers

Cartilage joint (disc)

Not compartmentalized like always depicted

Discogram does show NP in disc

Synovial joints

Variety of arthritides

|FIBROUS |CARTILAGINOUS |SYNOVIAL |

|Cranial sutures |Symphysis pubis |Fingers |

|Syndesmosis |IVD |Toes |

|(tib/fib, radius/ulna) |Sternal Angle of Lewis |Knees |

| |Sternoclavicular |Hips |

| |Acromioclavicular |Apophyseal joints |

| |Joint Capsules |SI joints |

 

 

DJD

Predominates in the spine and in large weight bearing joints

Incomplete understanding of DJD

Appears to be an end point

Need to de-emphasize the -itis (as in arthritis)

Local inflammatory reactions

 

Film: Lower Cervical AP

Common radiographic findings

Decreased disc space

Subchondral sclerosis should be seen

Sharpening/thickening of uncovertebral joints (1st stage of degenerative stage of Uncovertebral Arthrosis)

Remodeling of lateral margin due to altered alignment

  

Film: Oblique Cervical

Common radiographic findings

Shows anterior-lateral osteophytes

Watch for

Abnormal IVF (oval with concave edges)

Uncovertebral encroachment

Positioning is very important (may appear to have smaller IVFs but may not)

 

Film: Lateral Cervical

Common radiographic findings

Look at disc spacing (should be even posterior and anterior)

Watch posterior elements for sclerosis/thickening

Examine the anterior body and posterior elements for osteophytes

 

 

Pt asks "How did my neck get like that?"

Improper wear and tear

The body's process of stabilization of a joint not moving/functioning properly

 

Couch potato story

Large group of patients split in half (homogenized except for activity level)

People that are less active get more DJD and wear faster than active group

Rat Study

Genetically identical rats at different ages

Older versions have synovial fluid removed and stuck into younger versions

Controls and young versions dissected and experimental rats had local subchondral sclerosis and osteophyte growth after short periods of time

Film: Lower Cervical

Typically not symmetrical

This particular film shows uncovertebral hypertrophy (previous "T-bone" style accident)

Film: Proton Density MR image

Posterior vertebral bodies have osteophytic growths

  

Film: CT Bone window

Shows osteophytes in posterolateral margin of the vertebral body

Film: Lateral Cervical

Routinely we will see major changes and alterations in osteophytic growth and/or alterations in lordosis/motion planes

Film: Lateral Thoracic

True retrolisthesis

Facet degeneration definitely present

Loss of disc space

Huge osteophytes

Limited segmental motion

 Film: AP Lumbar

Massive osteophytes on left connecting L5-S1 on left

None to little segmental motion (can't claim fusion unless we see trabecular fibers bridging the former joint space)

May have hook shaped osteophytes between segments

Film: Lateral Lumbar

Vacuum phenomenon=tearing of annular fibers leading to opening of space and pulling of gas out of solution after the NP dissolves

Vacuum cleft=marginal disruption of outer annular fibers (may be trauma related or related to degenerative changes)

Hahn's fissure=midline artery supply and vein drain for vertebral body (shows up on MR)

Lower Cervical AP (DJD)

[pic]

Oblique Cervical (DJD)

[pic]

Lateral Cervical (DJD)

[pic]

 

 

Proton Density MR vs T1 MR (DJD)

[pic]

Lateral Thoracic (DJD)

[pic]

AP Lumbar (DJD)

[pic]

Vacuum Cleft

[pic]

 

Lecture 5

Monday, June 02, 2008

10:16 AM

 

DJD

Spondylolisthesis

Anterolisthesis

Spondylolysis=fracture acting as causative agent for anterolisthesis

Spect or MR scans become indicated if modified Stork Test is positive (localizes pain to one area)

Stork Test/Modified Stork Test=Gillet's Test

Facet degeneration=alternative causative agent for anterolisthesis

Oblique film will allow classification easily (check for pars break)

Examine the cortical lines to evaluate for fracture

Subchondral sclerosis will compromise the joint space

 

Film: CT Myelogram-demonstrating neuritis (shown in class)

Shows bone window but cord appears as white dot and cauda equina appears as black dot w/ white border (nerve root inflammation will appear as blurriness)

The nerve root sitting against a facet osteophyte is the likely cause of the neuritis (nerve root inflammation) and would benefit quite nicely from adjustment

Film: Plain film showing L-T scoliosis

Only able to offer relief care

Do not try to correct the curve because it isn't going anywhere (in DJD patients)

Wolf's law and other models show this to be the case

Special features

Directly posterior jetting of annular fibers of disc

Herniation=NP stays connected to AF but pushes out on Annulus Fibrosus

Sequestration=a free floating fragment of NP not attached to Annulus Fibrosus 

Hemispherical Spondylosclerosis=half circle of lucency at anterior margin of vertebral body

Shows the body's response to the increase in anterior stress

Most commonly seen on lateral view

SI DJD

Will have consistent cortical margin vs a tumor which would not

Sacro-Coccygeal joint

DJD may show up here as well

 

DISH=Diffuse Idiopathic SkeletalHyperostosis

May occur at same time as DJD

Anterolisthesis (DJD)

[pic]

CT Myelogram Bone window-not showing neuritis!

[pic]

L-T Scoliosis (DJD)

[pic]

What comes up when Google Image Searching Hemispherical Spondylosclerosis?

[pic]

Dr. Kettner and nothing else!

 

Lecture 6

Wednesday, June 04, 2008

9:17 AM

 

DJD

 

Film: AP Shoulder plain film

Typically onset is predicated by trauma and related irregular contour (thru avascular necrosis or frank damage)

Acromio-humeral space is supposed to be non-articular (but supraspinatus lives here)

Point of opposition of rotator cuff group and deltoid

Prior avascular necrosis plays an important role in progression (person will feel better prior to actual bone remodeling)

Ball and socket joints (especially hip) socket joint surface shapes the 'ball' surface

Incremental loading is better than jumping up and walking after non load bearing period of recovery

If person is less than 60 years old and has DJD present then you can't assume 'normal use' was the cause

 

 

 

Film: CT of chest showing Sternoclavicular DJD

May project over lung on plain film

Film: plain film AP Pelvis

Hip is #1 site of DJD in weight bearing joints

Knee is #2 site of DJD in weight bearing joints

Decreased joint space

Subchondral sclerosis

Osteophytic change occurs after the decreased joint space

Subchondral cyst is more likely to be seen in the acetabulum than the femoral head

Frog leg view may show more osteophytes that are not available on the AP view

Osteophytes may appear as a single hook but because we are only seeing along one angle we may actually be viewing a rounded ridge

Film: Lateral Knee plain film

May show exaggerated superior pole of patella (owing from increased traction forces)

Dystrophic calcification w/in patellar bursa, calcific bursitis (not shown but would be

in the superior tendon of the patella)

Film: Tunnel view

May show wasting of the tibial eminence (which could lead to lateral translation during ambulation)

May have bones appearing osteopenic

Film: Sunrise view

Hook (osteophyte) may encroach upon cartilage surfaces

Dystrophic calcific tendonitis may involve calcification of Sharpe's fibers leading to an irregular border of the anterior surface of the patella 

DISH=Diffuse Idiopathic Skeletal Hyperostosis (aka Forestier's Disease)

If present in the Cervical spine may present w/ difficulty swallowing

Dysphasia occurs in 1/5 of those w/ DISH

While there is calcification of the ALL it doesn't always alter ROM

Hypertrophy does not become a problem unless the PLL is involved

40% incidence of co-presence of Diabetes Mellitus patients

4 continuous segments with smooth and flowing ligamentous hypertrophy and ossification required for DISH diagnosis

Will not get a cavitation (adjusting will feel boggy)

Predominates T6-11, mid cervicals to CT junction, L3-S1

 

Film: Cervical Lateral plain film

Major hypertrophy and calcification of the ALL

Disc space remains preserved

No subchondral sclerosis present 

Flam shaped Syndesmophyte

Has 3 differentials

DISH (Dx by eliminating other disorders)

Twin pair=different conditions but look THE SAME on film

Reactive arthritis (Reiter's)

Psoriatic arthropathy (must have psoriasis lesions)

Reiter's disease pneumonic

Can't see=Conjunctivitis

Can 't pee=Urethritis

Can't dance w/ me

Osteophyte on calcaneus (lover's heel)

Polyarticular arthritis

Fluid filled pustules on soles of feet

Beuboitis/balanitis=inflammation of glans penis (a classical feature of Reiter's)

 

Types of osteophytes/Diff Dx

| |Osteophyte |

| |Features |

| |Disorder/Diff Dx |

| | |

| |Claw osteophytes |

| |Associated w/ disc degeneration |

| |DJD |

| | |

| |Traction spurs |

| |Parallel endplate |

| |DJD |

| | |

| |Flowing exuberant ossification |

| |Along ALL, PLL |

| |DISH |

| | |

| |Syndesmophytes |

| |Ossification of the annulus fibrosus. Pencil thin Paravertebral ossification (Marginal) |

| |Ankylosing spondylitis, Enteropathic arthritis |

| | |

| |Paravertebral ossification |

| |Ossification of connective tissue separated from edge of the vertebral body (C shaped, comma shaped, stuck on, non marginal) |

| |Reiter's Syndrome, Psoriatic Arthropathy |

| | |

AP Shoulder plain film

[pic]

CT Sternoclavicular DJD

[pic]

AP Pelvis plain film

[pic]

Lateral Knee plain film

[pic]

Cervical Lateral plain film

[pic]

Lecture 7

Monday, June 09, 2008

10:15 AM

 

DISH

Diff Dx tree (MUCHO IMPORTANO!!!)

Osteophyte?

Yes->

Hands?

Yes->Erosive Arthritis (Gullwing deformity DIP/PIP)

No->DJD. Now claw or traction?

No->

Flowing/exuberant->DISH

Conform to ALL pathway->DISH

Maintenance of disc space->DISH

 

Pencil thin marginal->Enteropathic Arthritis (GI issues w/ spinal arthopathies as a secondary component) or Ankylosing Spondylitis

GI Issues?

Yes->Enteropathic Arthritis

No->Ankylosing Spondylitis

 

C-shaped non marginal->Reiter's, psoriatic arthropathy

Skin Lesions (past/present)?

Yes->Psoriatic

No->Reiter's

Urethritis, Conjunctivitis, Polyarthritis?

Yes->Reiter's

No->Psoriatic

Flamed shape Syndesmophyte->DISH, Psoriatic, or Reiter's

HLA 8 may be elevated in some DISH patients

Half of DISH patients may have PLL thickening (C and T spine predominate) with some portion having calcification of the PLL also

 

Discogenic spondylosis (aka spondylosis)=DJD of the spine

Check Sign=visible sign of endplate fracture (looks like V entering into the vertebra from above)

Calcification of ligaments may also show up more in DISH patients

 

Film: Bone Window CT of C-spine

Soft tissue window of CT of C-spine

Showing ossification of PLL and the location of the cord is altered

A surgeon should be consulted if the cord is impacted by the PLL hypertrophy 

Erosive Osteoarthritis (EOA)=inflammatory variant of DJD involving the IP joints of the hands

Sometimes thought like an RA presentation (but not)

Typically B/L presentation

Swelling of the digits (DIP/PIP)

Classically a hand disease w/ priority given to the DIP (Distal InterPhalangeal joints)

Gullwing Deformity=classic sign of EOA where a down sweep and up sweep down sweep appears across the DIPs

1st metacarpal-carpal joint is decreased w/ osteophytic growth (just like DJD) is not needed to confirm diagnosis but will aid as a sign (2nd most common finding)

PLL Hypertrophy

Plain Film (DISH)

[pic]

CT Bone Window (DISH)

PLL hypertrophy/ossification

[pic]

Erosive Osteoarthritis (Gullwing Deformity)

[pic]

 

Lecture 8

Wednesday, June 11, 2008

9:14 AM

 

Table 10.24 diagnostic criteria for RA

Physical

1. Morning stiffness

1. Pain on motion or tenderness in at least 1 joint

1. Soft tissue swelling or joint effusion in at least 1 joint

1. Swelling of at least 1 other joint (w/in 3 months)

1. Bilateral, symmetrical, and simultaneous joint swelling (except DIP)

1. Subcutaneous nodules-boney protuberances (extensor surfaces), justaarticular

Laboratory

1. Positive sheep agglutination test (Rh Factor)

1. Poor mucin precipitate from synovial fluid (have to aspirate from joint)

1. Synovium-at least three of (have to open joint to perform)

a. Marked villous hypertrophy

a. Superficial synovial cell proliferation

a. Marked inflammatory cell infiltrate fibrin deposition

a. Foci of cell necrosis

1. Nodules-granulomas with central necrosis, proliferated fixed cells, peripheral fibrosis, and chronic inflammatory cell infiltrate

1. Typical changes-uniform joint space loss, marginal erosions, etc. (radiographic)

Classification

Classic >7 criteria (w/ swelling for > 6 months)

Definite >5 criteria (w/ continuous joint symptoms >6 weeks)

Probable >3 criteria (w/ continuous joint symptoms) (4-6 weeks)

Possible at least 2 of stiffness, pain, welling, nodules, elevated ESR or CRP, or iritis, with joint symptoms for at least 3 weeks

 

Drawings of joints

[pic]

 

[pic]

 

Early pathologic change includes proliferation of pannus

Bone erosion is a later change (predominately occurring at 'bare area' distal to joint but near the articular cartilage)

 

Table 10.26 pathologic-radiologic correlation in RA

|Pathologic features (physical stuff) |Radiologic features (seen on film) |

|Synovial edema and effusion |Periarticular soft tissue swelling |

|Rheumatoid nodule |Subcutaneous soft tissue mass |

|Cartilage destruction by pannus |Uniform loss of joint space |

|Pannus eroding in the "bare area" |Marginal erosion |

|Intra-osseous pannus and synovial fluid intrusions |Subchondral bone cysts |

|Inflammatory hyperemia |Juxta-articular osteoporosis |

|Periostitis |Juxta-articular periosteal new bone (linear) |

|Fibrous tissue metaplasia |Ankylosis |

|Capsule and ligamentous laxity, tendon rupture |Deformity |

 

Film: Left hand showing RA hand with cylastic implant (appears like soft tissue mass)

Implant requires 8-10 hours to apply

Implant appears w/ soft tissue contrast and level

Film: B/l hands showing MCP joint and Carpal coalition

Carpal coalition=fusion of the carpal bones (ankylosis)

Pencil in cup appearance=head of metacarpal gets thinned and pushes into the phalanx

Film: lateral cervical spine (zoomed to atlantodental interspace)

1/5 of all RA patients develop ADI instability

Pannus formation and granulation tissue decreases the integrity of the Cruciate ligament

Safe to x-ray yearly to check progress

May actively translate during flexion/extension views

LHermitte's sign=electric shocks down both arms (think central canal stenosis)

If patient has this then do NOT manipulate

Film: AP pelvis

Bilateral involvement at the acetabulum (symmetric involvement)

Left femur head representing Protrusio Acetabuli (no teardrop space)

Both spaces show no joint space

Decreased bone density is seen also

Can't be DJD because it is B/l symmetrical and there are NO osteophytes present

Film: B/l knees

Symmetrical decreased joint space seen on both lateral and medial surfaces

Reduced cortical space (almost 0) vs medullary portion

 

 

Film: lateral knee Arthrogram

Contrast has leaked into Baker's Cyst

Baker's Cyst=represents defect in the capsule allowing herniation of synovial lining beyond its normal chamber (usually contains synovial fluid). Commonly seen w/ RA but may be caused by other conditions

Film: PA chest

Pleural Interstitial fibrosis-associated finding w/ RA due to it being a systemic condition

[pic]

 

 

 

 

 

Film: Left hand showing ulnar deviation (RA)

[pic]

Carpal Coalition (RA)

[pic]

Film: lateral cervical spine (increased ADI)

[pic]

AP Pelvis (RA)

[pic]

Baker's Cyst (RA)

Lateral Knee Plain film

[pic]

Lecture 9

Monday, June 16, 2008

10:14 AM

 

Juvenile Chronic Arthritis

Formerly Juvenile Rheumatoid Arthritis

Film: Lateral Cervical

Fusion of posterior elements w/ no facet joint seen b/t 2,3,4

Anomalous IVFs (shouldn't be seen here)

Thin/tall vertebral bodies

ADI instability present

Dx: sero + JCA

Inflammatory arthritides most common type to produce ankylosis

Premature maturation=early closure of the growth plates

Typical cutoff age is 14 y/o but may occur as late as 20 y/o

Film: bilateral AP foot view

Dx: Seronegative JCA (Still's disease)

Bilateral but not symmetrical

Always do flexion/extension views on JCA patients to document stability/instability

Film: AP Pelvis

Joint replacement of hip on right side w/ slipped capitis femoral epiphysis on left

Enlarged obturator foramen bilaterally due to reduced growth inferior and superior pubic rami

Film: 2 views of left hand

Showing severe ulnar deviation

Degradation of carpals is nearly complete w/ no spacing seen

Dx: seronegative JCA

Pencil in a cup appearance of metacarpals and proximal end of phalanx

Ankylosing Spondylitis

Railroad track sign=Vertically oriented white lines overlying the pedicle area

Ossification of interpedicle ligaments and ligamentum flavum

Pencil thin ossification of outer annular fibers

Ghost joint=No spacing seen of the SI joint (but present on CT)

Disuse osteoporosis of vertebral bodies leading to carrying of weight on calcified soft tissues

Associated w/ HLA-B27 genetic profile

Film: AP Pelvis

Dagger Sign=ossification of interspinous and supraspinatus ligament

SI joints are visualized better but with greater degree of osteoporosis

Progression typically

SI

TL

Lumbar

CT

Thoracic

Cervicals

Equal distribution in men and women

More prone to fracture (also in unusual locations)

Midvertebral fracture

Disc space fracture

Carrot stick fracture=unusual fracture seen in Ankylosing Spondylitis

Very common to see dystrophic calcification of ligaments

Syndesmophyte=Calcification of outer annular fibers

Will end up carrying the weight instead of the bodies/posterior elements

 

Dagger Sign

[pic]

AP Pelvis w/ replaced right femoral head (JCA)

[pic]

Slipped Femoral Capitis Epiphysis (JCA)

[pic]

 

Ankylosing Spondylitis

Railroad Track Sign

[pic]

 

 

Ghost Joint

[pic]

 

Lecture 10

Wednesday, June 18, 2008

9:20 AM

 

Ankylosing Spondylitis

Trolley Track Sign=a combination of Railroad sign and Dagger Sign

Star Sign=pattern made by ossification of soft tissues at top of SI joint in AS

#1 cause of death in AS=Suicide

Disc ballooning=unrestricted imbibition of NP w/ water increasing its dimension (leading to weakening of cortical margin of vertebral body and deep depressions into the vertebral body possibly both superior and inferior)

May lead to disc calcification

Disc calcification=dystrophic calcification of the disc starting w/ the outer annular fibers

In patients w/ involvement of any sort flexion/extension views are needed to rule in ADI stability

Order of progression of AS

Romanus lesion=next step after sacroiliits (then shiny corner sign consisting of focal sclerosis)

Shiny corner sign (Romanus lesion)=vertebral body “squaring” with anterior vertebral body corner reactive Osteitis seen on lateral radiographs

Bridging syndesmophyte (calcification of outer annular fibers)

Classic presentation

B/l sacroiliits

TL junction

40% more problematic inflammatory bowel disease

HLA B27 from lab tests

If no HLA B27 then check ESR (for Enteropathic Arthritis)

Psoriatic Arthritis

Pictures of surface lesions of psoriasis

10-30% of those with surface lesions will get joint problems

Produces highest percentage of ankylosis in hands

Film: B/l hands

Pencil in cup deformity seen

DIP joint is affected=Psoriatic Arthritis

Carpal coalition present

Will be Seronegative

Bilateral and symmetrical=inflammatory

Mutilating

Distribution (complete=Ray's Sign)

Ray's Sign=complete distribution to all 5 rays (fingers)

Tends to produce normal density

Greater mutilating ability than RA

Greater percentage will have ankylosis

If present in hands (or other small joints) Reiter's must be left out

Preservation of bone density (vs RA which does not preserve bone density)

Degree of involvement of surface lesions on body does not correlate w/ psoriatic arthropathy

100% of people w/ psoriatic arthropathy does have history of skin lesions

May produce sacroilitis

Film: AP Pelvis

Right Femur has moved superior thru softened bone

Pubic symphysis is bridged along superior portion

Film: Lumbar AP view

Stuck on, non-marginal density seen

Radiologic changes in the SI joints w/ Ankylosing spondylitis

General

Bilateral, symmetric

Iliac side is more extensively involved

Initially involves lower 2/3 of joint

Early "sacroiliitis"

Articular erosions (Rosary bead)

Diminished joint space

Loss of articular cortex definition (pseudowidening)

Patchy reactive sclerosis

Subchondral osteoporosis

Late

Bony ankylosis

Generalized osteoporosis-disappearance of reactive sclerosis

"Ghost" joint margin

"Star" sign

 

Reactive Arthritis (formerly Reiter's Syndrome)

Produces pustule like surface lesions on the soles of the feet or palms of the hands

Will be different types of lesion than psoriasis

Spine and big joints

Urethritis, conjunctivitis, balanitis, calcaneal spur (also at Achilles' insertion spur)

Will have non-osteophyte

No disc problem

Non C-shaped but marginal

Film: AP pelvis

Pubic symphysis narrowed w/ adjacent osteophyte like bone

Erosion of inferior margin of pubic bones

 

Table from Yochum and Rowe

Radiologic Diff Dx of SI disease

| |Disease |

| |Bilateral symmetric |

| |Bilateral asymmetric |

| |Uni-lateral |

| | |

| |Ankylosing Spondylitis |

| |+++ |

| |+ (early) |

| |+(early) |

| | |

| |DISH |

| |+ |

| |(upper joint) |

| |  |

| | |

| |Enteropathic sacroilitis |

| |+++ |

| |  |

| |  |

| | |

| |Gouty arthritis |

| |+ |

| |+ |

| |+ |

| | |

| |Hyperparathyroidism |

| |+++ |

| |  |

| |  |

| | |

| |Infection |

| |  |

| |  |

| |+++ |

| | |

| |Osteitis Condensans ilii |

| |(Pregnant female) |

| |+++ |

| |+ |

| |+ |

| | |

| |Osteoarthritis (DJD) |

| |  |

| |+ |

| |+++ |

| | |

| |Psoriatic spondylitis |

| |+ |

| |+++ |

| |++ |

| | |

| |Reiter's Syndrome |

| |++ |

| |++ |

| |+++ |

| | |

| |Rheumatoid arthritis |

| |  |

| |+ |

| |+++ |

| | |

 

SI Disease Diff Dx

Bilateral Symmetrical

Ankylosing Spondylitis

Increasing stiffness w/ aging

Dagger Sign

Railroad/Trolley sign

Star sign

Osteopenia of vertebral bodies

Bridging syndesmophytes

Enteropathic Arthritis

GI disturbances (past/present)

Hyperparathyroidism

Low levels of Parathormone in circulation

Osteopenia

Osteitis Condensans Ilii

Post-multi parity female

Bilateral Asymmetrical

Psoriatic Arthritis

Focal/global skin lesions (past/present)

Unilateral

DJD

Osteophytes

Subchondral sclerosis

Subchondral cysts

Asymmetrical (across joint) space loss

Asymmetrical distribution

Sero -

Reiter's

Conjunctivitis

Urethritis

Calcaneal spur

Often asymptomatic

Sero -

Rheumatoid

Sero +

Likely hand involvement

Uniform joint space loss

Morning stiffness

Pannus formation

Lots of soft tissue swelling

Infection

Infective agent within joint capsule

Ankylosing spondylitis

Dagger Sign

[pic]

Star Sign

[pic]

Shiny Corner Sign

[pic]

 

B/L hand view w/ Psoriatic Arthritis

[pic]

Reactive Arthritis

[pic] 

Lecture 11

Monday, June 23, 2008

10:18 AM

Table 10.53 Diff Dx of Psoriatic arthritis

| |Feature |

| |Psoriatic Arthritis |

| |Reiter's Syndrome |

| |Rheumatoid Arthritis |

| |Ankylosing Spondylitis |

| | |

| |Distribution |

| |  |

| |  |

| |  |

| |  |

| | |

| |Upper extremity hand |

| |+++ |

| |DIP/PIP |

| |- |

| |- |

| |+++ |

| |MCP/Wrist |

| |+ |

| | |

| |Lower extremity |

| |+++ |

| |+++ |

| |+++ |

| |- |

| | |

| |SI |

| |++ |

| |++ |

| |+ |

| |+++ |

| | |

| |B/l |

| |++ |

| |++ (asymmetric) |

| |+ |

| |+++ |

| | |

| |U/l |

| |++ |

| |+++ |

| |+++ |

| |+ |

| | |

| |Spine |

| |++ |

| |+ |

| |+++ (cervical) |

| |+++ |

| | |

| |Key Signs |

| |  |

| |  |

| |  |

| |  |

| | |

| |Osteoporosis |

| |  |

| |+ |

| |+++ |

| |+++ |

| | |

| |Joint space |

| |+++ (widening) |

| |+ (narrowing) |

| |+++ (narrowing) |

| |++ (narrowing) |

| | |

| |Ankylosis |

| |++ |

| |- |

| |+ |

| |+++ |

| | |

| |Periostitis |

| |+++ (fluffy) |

| |+++ (fluffy) |

| |+ (linear) |

| |+++ (fluffy) |

| | |

| |Tuft resorption |

| |+++ |

| |- |

| |- |

| |- |

| | |

| |Soft tissue swelling |

| |++ |

| |++ |

| |+++ |

| |+ |

| | |

| |Laboratory |

| |  |

| |  |

| |  |

| |  |

| | |

| |ESR |

| |+ |

| |++ |

| |+++ |

| |+++ |

| | |

| |RA Factor |

| |  |

| |- |

| |+++ |

| |- |

| | |

| |HLA-B27 |

| |60% |

| |75% |

| |8% (normal) |

| |90% |

| | |

Scale

Rare -

Occurs +

More common++

Very common +++

Dystrophic calcification

Calcific tendonitis/HADD (Hydroxy-Apatite Deposition Disease)

Film: AP and oblique foot (unilateral)

Concretion of Peroneus longus tendon (dystrophic calcification)

Will occur due to change in pH and may lead to spontaneous rupture

Likely suffered several inversion injuries

Looks similar to Os Peronei but won't be palpable

Composed of HAD

Tx: ultrasound

Film: AP Shoulder

Showing calcific tendonitis of the supraspinatus where it attaches to the greater tubercle of the humerus

Changes in pH due to blood-flow changes w/in the bursa cause precipitation to occur

Metabolic arthritide

Gout

Tophi=uric acid crystal accumulation on the pinna of the ear

Sodium monourate=uric acid crystals

Big toe is major spot where Gout shows up

Bone changes created due to pannus formation began under deposition of uric acid crystals

Overhang sign=overhanging of one bone upon an adjacent bone

Typically not seen on radiographs now due to early treatment

Calcific Tendonitis (Shoulder)

[pic]

Tophi of ear (Gout)

[pic]

Overhang sign

[pic]

Lecture 12

Wednesday, June 25, 2008

9:18 AM

 

Continuing metabolic arthritide

Gout

Metabolic arthritide

Aberration of purine pathway->uremia->(Uric acid crystal deposition)

Transient process

Deposition occurs in smaller vessels w/ slower flow

Break in lesion=classic radiographic sign of Gout producing Overhang Sign

Avascular necrosis due to blood vessel impaction

Not a tremendous risk to the kidneys

Film: B/l foot AP film

Overhang sign present

Mucho soft tissue swelling (may make you think infection)

Film: B/l hand AP film

Lots of small depositions in the phalanges

Dystrophic soft tissue calcification

Tophaceous Gout=metabolic arthritic disorder producing soft tissue calcification after uric acid deposition

No organization

Film: Lateral knee

Lucency seen in proximal tibial shaft

Initial Diff Dx: cyst, enchondroma, Giant Cell tumor

CT of same patient shows very sclerotic margin (slow onset)

Biopsy shows uric acid crystals

Dx: Intraosseous Gout 

CPPD (Calcium PyroPhosphate Dihydrate Deposition)

Will likely become the poster-child for metabolic disorders later

Joint space is NOT black

Some Calcium pyrophosphate deposition in the joint space

Film: AP knee

Lines or triangles seen b/t articular cartilages

Film: AP shoulder

What appears to be thickened cortical margin but upon closer inspection is not connected to cortical margin

Homogentisic acid (aka: Alkaptonuria/ochronosis)

Dermatology Slide: Ear

Darkening skin in superior pinna of ear

Darkened skin on cheek

Blackening due to oxidized homogentisic acid

Pt is missing enzyme: homogentisic acid oxidase

Takes long time to develop in the body (genetic disorder)

Onset around age 30

Lab finding: urine will turn black if left exposed to air

No osteophytes normal cortices

No bony hypertrophy, no subchondral sclerosis

Film: AP lumbar

Multi-level degeneration and major sclerosis (S1-L4)

DJD in wrong age and wrong distribution

Film: Lateral Thoracic

Normal cortices but calcification of disc spaces

HADD (Calcific tendonitis)

Film: AP and oblique foot (unilateral)

Concretion of Peroneus longus tendon

Dystrophic calcification=occurs due to change in pH and may lead to spontaneous rupture

Likely suffered several inversion injuries

Looks similar to Os Peronei but won't be palpable

Composed of HADD (Hydroxy-Apatite Deposition Disease)

Tx: ultrasound

Film: AP Shoulder

Showing calcific tendonitis of the supraspinatus where it attaches to the greater tubercle of the humerus

Changes in pH due to blood-flow changes w/in the bursa

 

OCI (Osteitis Condensans Ilii)

10:1 Women: men

Brought on by multiple full term pregnancies

Bright triangle of sclerosis along iliac margin of SI joint

Film: AP Pelvis

Classic bright triangle of sclerosis in ilii

 Hypertrophic Pulmonary OsteoArthropathy (HPOA)

Looking at the trabecular bone, then cortico-trabecular interaction, cortical bone then we see some of the periosteal tissue (periosteal reaction)

Typically due to either reduction of lung function or metastatic bone disease

Solid periosteal reaction is present

If no lung disease present HOA (Hypertrophic OsteoArthropathy)is present

Clubbing will be present

Misc

Scleroderma

CREST Syndrome

Calcinosis (calcium deposits, usually on fingers)

Raynaud phenomenon (Red, White, Blue fingers)

Esophageal dysmotility (inability to swallow)

Sclerodactyly (tapering deformity of bones, seen on X-ray)

Telangiectasia (red spots seen on fingers/mouth)

Difficulty protruding tongue

Difficulty opening mouth

Truncated=retraction of skin at fingertips

Reduction of blood flow to and from the distal extremities due to aberrant connective tissue deposition

Acroosteolysis=consumption of distal portion bones w/in extremities

Systemic Lupus Erythematosus (SLE)

Changes soft tissues not bone

Small joint disease

Appears like RA but pt will be able to flatten hand to film (Reversible Subluxation)

Break in=something breaking into the bone (pannus). Will carry a solid cortical margin

Osteopoikilosis=polka dots w/in bone

Synoviochondrometaplasia=metaplasia of synovial cells into cartilage (and later bone) within the joint capsule but outside the cortical bone

Typically affects only 1 joint at a time

Appears as polka dots (joint mice) outside the cortical bone and within the synovial capsule

Intracapsular and extra cortical

Joint will 'lock' (due to 'joint mice)

Tunnel view is best to view joint mice

Loose chondral bodies w/in joint at to predispose to DJD

Pressure erosion of nearby bones may occur (may produce Apple Core Deformity)

Dystrophic calcification of the glenoid labrum

Pigmented Villonodular Synovitis=villous tissue hypertrophies to produce synovial fluid they attract hemosiderin

Apple Core Deformity=pressure erosion of bone

Break In Lesion (Gout)

[pic]

Tophaceous Gout

[pic]

CPPD AP Knee

[pic]

Alkaptonuria

 

[pic]

 

 

HADD (Calcific Tendonitis)

[pic]

Osteitis Condensans Ilii

[pic]

Hypertrophic Pulmonary OsteoArthropathy

[pic]

[pic]

Scleroderma

[pic]

Systemic Lupus Erythematous (SLE)

[pic]

Osteopoikilosis

[pic]

Synoviochondrometaplasia

[pic]

Pigmented Villonodular Synovitis

[pic]

 

Lecture 13

Monday, June 30, 2008

10:17 AM

 

Arthritides of the Axial and Appendicular Skeleton

Dr. Bonic DC RT®

 

25 cases w/ arthritides then normal w/ abnormal

 

Case 1

DISH

Dish space/Z joint preserved

Exuberant hyperostosis on 4 continuous levels

PLL may ossify

Case 2

RhA

ADI enlarged (3 mm+)

Disruption of spinolaminar line

Osteopenia

B/l symmetrical

Typically shows

Uniform joint space narrowing

Marginal erosions

Deformities

Atlantodental instability

Protrusio acetabuli

Osteopenia

Rotator cuff tears

Case 3

DJD

IVD narrowing

Osteophytes

Uncovertebral and Z joint arthrosis/sclerosis (may narrow IVF)

Case 4

JRA

Atlantodental instability

Apophyseal ankylosis

Hypoplasia of vertebral bodies and discs

Osteopenia

Case 5

Ossification of PLL (DISH)

May compromise spinal canal

Case 6

Ankylosing Spondylitis

Thin, marginal syndesmophyte

Ankylosis of apophyseal joints

Decreased lordosis and marked anterior head carriage often seen

ADI instability likely

Carrot stick pathologic fractures

Spinous process erosion

Case 7

Infectious discitis

Widened retropharyngeal and retrotracheal soft tissues

Cortical destruction

IVD narrowing

Case 8

Ankylosing spondylitis

Thin, marginal syndesmophytes

'Bamboo spine'

'Trolley track spine'

IVD calcification

Dagger sign=interspinous calcification

Case 9

Reiter's

Non-marginal syndesmophytes

Can't pee, can't see, can't climb a tree

Polyarthritis

Lover's heel

Non marginal syndesmophytes

B/l sacroiliitis

Urethritis

Conjunctivitis

Case 10

Apophyseal Joint Arthrosis

Hypertrophy and arthrosis of Z-joints

May change in pedicle-facet angle leading to non Lytic/fracture Spondylolisthesis

Case 11

Discogenic spondylosis (DJD)

IVD narrowing

Osteophytosis

Discovaccum phenomenon

Case 12

Villonodular

B/l sacroiliitis

May fuse SI joints

Will then ascend into lumbar spine

Case 13

Psoriatic arthritis

Psoriatic skin lesions

Non-symmetrical

Erosive changes, widening of SI

Common=SI, hands (DIP), feet (DIP), spine

Case 14

Rheumatoid arthritis

Carpal fusion

B/l symmetrical

MCP deviation to ulnar side

Swan neck deformity (Boutonniere deformity)=flexion deformity of PIP, extension deformity of DIP

[pic]

Marginal erosion

Case 15

Psoriatic arthritis

MCP intact (rules out RhA)

Fusiform swelling

Predominately affects DIP

Pencil in cup deformity

Case 16

Gout

Sodium monourate (uric acid) crystal deposition

Metabolic

Marginal erosions, Intraosseous

Overhang sign

Unilateral

Distribution is definitive

Tophi, bone erosions (long standing only), normal bone density seen

Case 17

Scleroderma

Soft tissue changes

Tapered conical fingertips, retraction of tip (truncation), soft tissue calcification

Resorption of distal tufts (Acroosteolysis)

Normal joints

Case 18

Synoviochondrometaplasia

Benign arthropathy

3-5th decade

Calcific loose bodies outside joint capsule (joint mice)

May produce erosions on the bone

Case 19

Neuropathic Arthropathy (Joint Disease)

6 D's "Bens lot", "De, De, De, Dis, Dis, Dis"

Debris

Density

Destruction

Dislocation

Disorganization

Distension

Case 20

Pigmented villonodular synovitis

Usually affects 1 joint

Effusion

'Apple core deformity' secondary to extrinsic erosions

Case 21

HADD (calcific bursitis/tendonitis)

Calcification of tendons, bursas, capsules

HydroxyAppatite Deposition disease

Shoulder, hip, spine

Case 22

CPPD

Calcium PyroPhosphate Dihydrate deposition

Hot tender swollen joints

Knee, wrist

Pyrophosphate arthropathy may be seen

Atypical location

Subchondral cysts

Destruction changes in list

Slac risk (scapholunate advance collapse)

Case 23

Juvenile Chronic Arthritis (formerly Juvenile Rheumatoid Arthritis)

Hyperemia seen

Accelerated growth in epiphysis leads to ballooning

Osteopenia seen

Soft tissue swelling

Uniformed joint space narrowing

Ankylosis possible

Linear Periostitis

Case 24

Systemic Lupus Erythematosus

Deforming arthropathy w/out permanent changes (Reversible Subluxation)

Swann neck deformity

Affects many system

Rash, Arthralgia

Case 25

Primary OsteoArthritis

Peripheral erosions of distal phalanx 'Gull wing Sign'

Osteophytosis

Non-uniform joint space loss

Ankylosis

Subchondral sclerosis

 

 

Lecture 14

Wednesday, July 02, 2008

9:16 AM

 

Neurotrophic joint disease

Not only do we have the kind we normally think about but there is finer proprioception within joints (keeping the cartilage from banging together)

Damage results from loss of proprioception function

May be associated w/ diabetic neuropathy

Hypertrophic joint disease

Characterized by 6 Ds/(BNSLOT)

Debris (from destruction)

Density (subchondral intensity increase)

Destruction

Dislocation (or feels like it/to much motion)

Disorganization

Distension

Occurs in weight bearing joints

Case: 52 year old woman w/ diabetic neuropathy

Calcaneus is pretty destroyed

Talus is almost totally missing

This patient walked in, felt the joint was unstable

Atrophic Joint Disease

Small non-weight bearing joints

Surgically amputed appearance or Candy lick appearance

Candy lick appearance=smooth cortical bone and worn down to a fine point 

3 causes

Diabetes Mellitus

Tabes dorsalis=a slow degeneration of the nerve cells and nerve fibers that carry sensory information to the brain

Syringomyelia

Typically occurs in the shoulder

C-spine surgery

Due to formation of Syrinx w/in cord

Syrinx=CSF cyst w/in spinal cord

Enteropathic Arthritis

Acts as a complication to Chron's or Ulcerative Colitis

Radiographic twin for Ankylosing Spondylitis

Distinguish by history (will have GI issues) and HLA B27 (will not be present in EA but will be in AS)

Predict as male

Atrophic Neurotrophic Joint Disease

[pic]

Syrinx/Syringomyelia

[pic]

Enteropathic Arthritis

[pic]

 

Lecture 15

Monday, July 07, 2008

10:15 AM

 

Video of Dr. Gross (guy w/ Ankylosing Spondylitis)

Defect on 6th chromosome creating an abnormal charge potential in collagen strands

This happens all over the body

Signs of collage disruption=idiopathic sore throats, recurrent bladder infections, eye irritation

Onset of signs occur in the twenties

HLA-B27 is positive only after puberty

Gait=shuffle w/ arms extended posteriorly as balance/pain relief

Primary causes of death

Suicide

Congestive heart failure

Hypertension->stroke

Fracture, dislocation of C/S following MVA

Renal failure typically liked to medical complications

Acute liver failure

Secondary leukemia associated w/ radiation therapy

Surgical complications

Traditional medical treatments

NSAIDs

Muscle relaxants

Anti-depressants-you still feel the pain but don't give a damn

Blood thinners

Pain killers

Joint replacements as indicated

Alternative therapy options

Regularly scheduled chiropractic care

Nutritional support

Strength and mobility exercises (pain can't hit a moving target)

Emotional support groups and professional counseling

Lifestyle assistance devices and options

Massage therapy for pain control and flexibility

Dr. Stan's Nutritional program

Ascorbic acid: 10-15 grams/day (gradual delivery)

Beta glucans: yeast derived immune support 600 mg daily

A high quality multivitamin/multimineral base

Hyaluronic acid: 150 mg natural anti-inflammatory

Extremely limited refined carbohydrates-raw fruits and vegetables preferred-avoidance of processed foods

Moderately limited meat and animal products

1-2 gallons of water per day (80% compliance is acceptable)

Fiber, fiber, more fiber

Dr. Stan's Lifestyle Modifications

Dressing successfully (simple modifications to make getting dressed a little easier

Gadgets galore (walking sticks, arm extenders)

Make list of things that you would do if you didn't have AS (then show them how they can do these things)

Exercise for the unique physique (swimming and aerobic workouts)

Not accepting limitations (find out goals and help them accomplish those goals)

Staying motivated (realize that AS isn't the end of the world)

Other problems to consider

Number of joints replaced

Age of onset (often mis-diagnosed)

The support system

The level of progression

The emotional support

Other health complications

Complications from medications

 

DrStan@

 

 

 

Lists

Sunday, July 06, 2008

3:55 PM

 

Degenerative Arthritides

DJD

Erosive Arthritis

DISH

OPLL

Neurotrophic Arthropathy

Synoviochondrometaplasia

Inflammatory

Rheumatoid Arthritis

Juvenile Chronic Arthritis (Juvenile Rheumatoid Arthritis)

Reactive Arthritis (Reiter's)

Ankylosing Spondylitis

Psoriatic

Enteropathic Arthritis

Systemic Lupus Erythematosus

Scleroderma

Osteitis Condensans Ilii

Hypertrophic Osteoarthropathy

Metabolic

Gout

CPPDD

HADD

Ochronosis

Pigmented Villonodular Synovitis

 

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