In the name of Allah, the Most Gracious, the Most Merciful

ZI MY RHEUMATOLOGY NOTEBOOK - MPR

2019 | ZI
 In the name of Allah, the Most Gracious, the Most Merciful

PROGRAMME :

RHEUMATO:
1. PR
2. SPA
3. Post-infectious rheumatism: post-streptococcal in adults
4. Septic arthritis, OMA, Spondylodiscitis
5. Metabolic rheumatism: Gout, Chondrocalcinosis CCA
6. Arthrose : coxarthrose, Gonarthrose
7. Diffuse demineralizing osteopathies:
Osteoporosis
Osteomalacia
Multiple myeloma
8. Connectivities: LED, SAPL, sec Sd, Scleroderma, Raynaud
9. Vasculitis: Behcet's disease, nodular periarteritis
10. Algoneurodystrophy
11. Painful shoulder
Sciatica

MPR :
Scoliosis
Amputation
3. Complications of bedsores
4. Articular and muscular assessment
 RHEUMATOID ARTHRITIS
Generalities:
The most common inflammatory rheumatism (AS 2th )
Tendance destructrice et déformante, touchant en particulier les poignets, les mains et les avant-pieds.
Middle-aged woman (3F/1H), more serious in men

Pathogenesis: multifactorial
Autoimmune disease: anti-citrullinated peptide antibodies (ACPA), rheumatoid factor
Environmental factors: tobacco, silica, Porphyromonas gingivalis, EBV, E. coli
Genetic factors: HLA DR1, DR4
Hormonal factors: Prolactin, Testosterone, perimenopause +++

Clinic:
Modes of start
Distal oligoarthritis (70%):
-Wrists +++ MCP: especially the 2 thor the 3thor IPP, sometimes the toes, knees, or elbows

Fixed, bilateral, symmetrical involvement

Inflammatory pain: nocturnal, waking up patients, maximum in the morning upon waking, morning stiffness > 30 minute
Aspect of the fingers with a very evocative spindle shape
-General signs frequency: discreet AEG, fever at 38°, weight loss and especially asthenia

2. Acute febrile polyarthritis (20%)

3. Rarer:
Rhizomelic involvement in the elderly subject: affecting the hips and shoulders
Monoarthritis (especially wrists or knees)
Persistent polyarthralgias for several months.
-Start after a trauma: begin with the traumatized joints.
Isolated extra-articular manifestations: vasculitis, pleuropulmonary involvement, rheumatoid nodules

State phase:
Bilateral and symmetrical polyarthritis
Most affected: MCP and IPP of 2emeand 3thfingers
Never reaches: the spine (except cervical), sacroiliac, IPD

2. Synovial pannus: thickening of the synovial membrane osteo-cartilaginous and tendon lesions
►Main dishes (90% of cases):
ulnar deviation of the fingers 'in a gust of wind'
Swan neck deformity: index and middle finger (rupture of the extensor of the first phalanx)
buttonhole deformity (rupture of the extensor of the second phalanx)
finger deformation in 'hammer' or more rarely in 'mallet'.
thumb in "Z": metacarpophalangeal arthritis
thumb adductus: trapeziometacarpal arthritis.
Wrists:
Piano touch: Injury to the ulnar styloid may cause a rupture of the extensor of the V finger.
Tenosynovitis: characteristic creaking during tendon mobilization.
►Feet: flat foot, then round, subluxations, plantar dislocations of the metatarsals.
Shoulders: Frequent 40%, often overlooked involvement
Elbows: irreducible flexion
Cervical spineC1-C2: pain, subluxation or dislocation
Coxofemoral: 15% of patients, poor functional prognosis.
3. Extra-articular lesions:
Frequent:
Rheumatoid nodules: 10 to 20% of patients, after several years of progression, on the extension surfaces.
2. Carpal tunnel syndrome (median nerve)
3. Gougerot-Sjögren syndrome: xerophthalmia and xerostomia
4. Raynaud's phenomenon: 10% of patients
5. Lymphadenopathy: 30% of patients
6. Felty's Syndrome: PR+ SMG+ leukopenia
[Link]: dilatation of the bronchi

Severe:
1. Rheumatoid vasculitis: digital infarcts periungual, purpura, deep punch-like ulcers,
and digital/toe necrosis
2. Cardiovascular: dyslipidemia, hypertension, stroke, myocardial infarction: favored by corticosteroid therapy.

3. Cardiac: pericarditis, myocarditis.

4. Pulmonary: rheumatoid pleurisy, diffuse interstitial fibrosis, pulmonary rheumatoid nodules and
obstructive bronchopneumopathies, Caplan-Colinet syndrome (pulmonary nodules in a silicosis patient)
5. Ocular: scleritis and episcleritis are uncommon.
6. Hematology: Inflammatory anemia, Felty's syndrome (SMG, granulopenia, lymphocytic abnormalities).
7. Renal: secondary amyloidosis type AA
8. Spinal compressions: secondary to atlantoaxial dislocation

rheumatoid nodules
Subcutaneous, mobile, firm, painless
Central zone of fibrinoid necrosis
Extension faces (elbow, forearm, fingers)
RADIO :
Diffuse narrowing of the interline
Geodes
Demineralization in the epiphyseal band
Epiphyseal erosions, early erosion of the 5thmetatarsal
Opacification of soft tissues

BIOLOGY :
FNS: Inflammatory anemia, Hyperleukocytosis, rarely leukopenia (Felty's syndrome), Thrombocytosis
Elevation of the VS, CRP, fibrinogen
EPS : 2 and gammaglobulins
Normal or elevated serum complement (if complement is low vasculitis

PUNCTURE:
Inflammatory fluid, lemon yellow, viscous, rich in cells > 2000 elements/mm350% PNet in prot (> 30 g/l)
Lower complement ++++
Presence of macrophages: nonspecific degenerating cells but frequently found in RA
FR may be present

SYNOVIAL BIOPSY: no indication, except to eliminate differential diagnoses

Hypertrophy of the synovial fringes and the bordering layer
Neo-vascularization
Lymphoplasmatic infiltration
Fibrinoid necrosis
IMMUNOLOGY:
Anti-citrullinated cyclic peptides: ACPA = anti-CCP
Early, sensitive, and specific for RA
AC anti-peptides that have undergone citrullination (arginine converted to citrulline). Citrullination is a
usual phenomenon in inflammatory sites
Same family: antinuclear antibodies, anti-keratin, anti-filaggrin
FR
IgM (sometimes IgG or IgA, exceptional IgE) anti Fc fragment of IgG (always anti-IgG)
Negative at the beginning Positive in 80% of cases after one year
ELISA detects (IgG, IgM, IgA)
Remains negative in 20% of cases
Agglutination Tests (Latex, Waaler
Her presence at the beginning is a bad omen.
rose) only detects IgM
Seropositive if both tests are positive: latex 1/80, Waler-Rose 1/64
LeFR is not specific: LED, Sjögren's syndrome, endocarditis, elderly subject...

ACR-EULAR 2010 Criteria: RA + 6

1 average or large articulation 0
2-10 medium or large joints 1
Type of joint involvement (0-5) 1-3 small joints 2
4-10 small joints 3
>10 articulations (at least 1 small joint) 5
Serology (0-3) Neither FR nor ACPA 0
At least one weakly positive test ≤ 3N 2
At least one test is forcibly positive > 3N 3
Duration of the synovitis (0-1) > 6 weeks 0
6 weeks 1
Inflammation markers (0-1) Both CRP and VS are elevated 0
Elevated CRP or VS 1

Factors of poor prognosis:

young age < 35 years
2. elevated synovitis name
3. importance of the initial inflammatory syndrome: CRP ++
4. Presence (and high levels) of rheumatoid factors and/or anti-CCP antibodies (ACPA)
[Link] DR B4
6. early presence (and rapid progression) of radiographic signs
7. The importance of the diagnostic delay and the delay in the initiation of the first disease-modifying treatment
8. the non-response to the first line treatment

TREATMENT :
Symptomatic treatment:
Rest, AINS +++, analgesics, low-dose corticosteroids (0.1 mg/kg/day)
Corticosteroid infiltrations, synoviorrhaphy, tenosynovectomies or synovectomies if infiltrations fail

Background processing:
Immunomodulators
Methotrexate +++ (purine synthesis inhibitor): reference treatment
Improves disability, prevents destruction, allows for remission and survival
Small doses: 0.3 mg/kg/week (10 to 20 mg/week) orally
Systematic folic acid, 48 to 72 hours after MTX, 10mg orally/week
In case of digestive intolerance, the subcutaneous or intramuscular route can be suggested.
The association with auxAINS is allowed, but Bactrim is contraindicated (anti DNA synthesis)
Effective contraception in young women
 Frequent side effects:
Digestifs: nausées, douleurs abdominales
Hepatic cytolysis dose-depletion: transaminases/15 days the first 3 months, then every month
Effect II rare airs:
Pancytopenia: CBC every month
Severe hypoxemic interstitial pneumonia (immunoallergic): 2 to 8%, definitive stop
Leflunomide (ARAVA): pyrimidine synthesis inhibitor:
Same effectiveness as methotrexate
Effects on blood lines + provider of hypertension.
Biological monitoring is the same as that of methotrexate.

Pregnant woman: the PR during pregnancy and 2 months postpartum, allowed medications:
Sulfasalazine
Synthetic antimalarial: Hydroxychloroquine (Plaquenil)
Azathioprine

2) Targeted treatments (biotherapies): anti-TNF, anti CD20

Expensive, reserved for active PR, after failure of MTX (3 months), in association with it or not.
Major risk: tuberculous reactivation. If TBK: anti-TNF is formally contraindicated.

Abandoned medications: Thiol derivatives, D-penicillamine, Gold salt (Proteinuria+++ + hematotoxicity)

Disease monitoring:
DAS28 :VS, CRP, number of painful joints, number of synovitis, overall assessment of the patient
THE < 2.6 2.6 ≤ DAS ≤ 3.2 3.2 ≤ DAS ≤ 5.1 DAS > 5.1
Status remission low activity moderate activity strong activity

Flat File
PR: bilateral, symmetrical, fixed, small joints
Treatment symptoms: analgesics, NSAIDs, low-dose corticosteroids
Background treatment: MTX, Leflunomide (ARAVA), Sulfasalazine, Synthetic antimalarial (Plaquenil), Azathioprine
CTCs are not a long-term treatment.
Abandoned salt: causes proteinuria + leukopenia
Contraindications for gold salts: proteinuria, anemia, leukopenia, thrombocytopenia, anti-native DNA antibodies
Medications that may negatively impact serology: gold salt, penicillamine (both discontinued)
Felty's syndrome: PR+ SMG+ leukopenia
Waaler rose: passive hemagglutination, IgM berk
FNS : Anémie inflammatoire, Hyperleucocytose, Thrombocytose
supplement (if low) vasculitis
Puncture: Inflammatory fluid (exudate), fluid (non-viscous), Base complement ++++
ACPA = anti-CCP: Early and specific
IgM anti Fc fragment of IgG: delayed and non-specific
Synovial biopsy: lympho-plasmacytic infiltration, not eosinophilic
Non-destructive PR in young women: NSAIDs (symptomatic) + MTX (maintenance)
Early prescription to request: ¼ before foot
Rheumatoid nodules: Subcutaneous, mobile, firm, painless, central area of fibrinoid necrosis, faces
extension (elbow, forearm, fingers)
Anti-malarial: ophthalmological monitoring (corneal deposits)
PR more frequent in silicosis
 2. SPONDYLARTHROPATHIES

DEFINITION :
Set of inflammatory rheumatisms sharing in common:
Genetic factors: HLA B27 (presentation of bacterial peptides to CD8 T cells)
Environmental factors: infections, tobacco
Axial involvement: pelvic-spinal and/or peripheral (arthritis, enthesitis, dactylitis)
Privileged access tothe enthesis(anchorage zone in the bone of tendons, ligaments, or capsules)
Extra-articular manifestations
Tendency to bone ankylosis
Absence of autoantibodies, mainly rheumatoid factor
Young man (3M/1F)

This family includes:

1. Axial spondyloarthritis: Ankylosing spondylitis: leader
2. Peripheral predominant spondyloarthritis:
Psoriatic arthritis
2) Reactive arthritis: Fiessinger Leroy Reiter syndrome
3) Rheumatism of enterocolopathies: Crohn's disease, ulcerative colitis

4) Undifferentiated spondyloarthritis
5) SAPHO (Synovitis –Acne–Palmoplantar Pustulosis –Hyperostosis–Osteitis)

BASIC CRITERIA
Axial spondyloarthritis: Peripheral spondyloarthritis
patients with back pain ≥ 3 months and onset < 45 years
Sacroiliitis imaging + ≥1 manifestation of SpA Arthritis or enthesitis or dactylitis
HLA B27 associated with ≥ 2 manifestations of SpA
1.HLAB27 Associated with ≥ 1 of the symptoms below:
Psoriasis Sacroiliitis in imaging
3. Crohn's or UC 2. HLAB27
4. Uveitis Psoriasis
5. Inflammatory rachialgia 4. Crohn or UC
6. Arthritis Uveitis
7. Enthesitis (heel) 6. Recent infection
[Link] Or at least 2 of the following events
[Link] response to NSAIDs Inflammatory rachialgias
10. Family history of SpA Arthritis
11. Elevated CRP 3. Enthesitis (heel)
Dactylite
5. History of inflammatory back pain
6. Family history of SpA
 ANKYLOSING SPONDYLITIS

Chronic inflammatory rheumatism, primarily affecting the axial structures (spine and sacro-)
iliac), with ankylosing tendency due to sub-ligamentous ossification and entheses

Epidémio: homme entre 20 et 30 ans, rare après 40 ans

Clinic:
1-Pelvic-lumbar syndrome: inaugural 75%
a) Sacroiliac injury:
Superior-inner gluteal pain, unilateral or bilateral or shifting
Sign of the tripod, spreading-closing of the Iliac wings, Mennel's maneuver
b) Spinal pain: ascending evolution
Lumbar spine+++, lumbosacral pain (pseudo-sciatica with tilt)
c) Lumbar stiffness: the most constant sign, Anteflexion: finger-to-floor distance and Schöber index < 4 cm
d) Thoracic wall: Early, thoracic expansion: Hirtz index < 5 cm

2. Enthesopathy syndrome:
Calcaneal injury: the most frequent and the most evocative bilateral post or inferior talalgies +++
3. Peripheral joint syndrome:
Asymmetric arthritis, lower limbs+++ Hip: the most common, early and bilateral
Can affect the IPD: 3 joints of the same radius "fingers and toes in sausage shape"

4. Extra-articular injury:
1. Anterior uveitis: most frequent complication +++++
2. SG: moderate, asthenia, weight loss accompanying inflammatory flare-ups
3. Cardio: BAV, aortic insufficiency, pericarditis
4. Respiratory:
Restrictive syndrome: sternoclavicular and costovertebral ankylosis
More rarely: apical bullous fibrosis characteristic of AS
5. Renal: amyloidosis AA+++, IgA nephropathy
6. Neuro: C1-C2 dislocation, spinal cord compression, Cauda equina (the most specific CPC for AS)
7. Bone: Hypertransparency with the possibility of vertebral compressions.
RADIO:
The first radiological signs appear at the dorso-lumbar junction.

X-rays to request:
Frontal basin +++, dorsal-lumbar spine from the front and side, thorax
If talalgias: X-ray of both feet in profile
1. Spine :
Ankylosing spondylitis SAR: erosion of the anterior corners of the vertebrae Square aspect 'squarring'
Syndesmophytes (≠ osteophytes): the most characteristic lesion: bony bridges between the vertebrae.
When they extend to the entire spine bamboo column
Ossification of the ligaments: image of tramway tracks
C1-C2 diastasis: vital prognosis
Spinal demineralization: related to ankylosis, may be complicated by vertebral crush fractures.

2. Sacroiliitis: Constant, bilateral, and roughly symmetrical involvement

Stage 1: pseudo-expanded aspect of the interline: subchondral demineralization
Stage 2: bank erosion 'postage stamp'
Stage 3: Bank condensation
Stage 4: Ankylosis by fusion of the margins
3. Enthesopathies: calcaneus +++
erosions, geodes and irregular ossification, calcaneal shielding
4. Coxite: erosive+++, enclosing, synostosing

BIOLOGY
VS low
HLA B27: present in 90% of AS, its absence does not eliminate the diagnosis.
-Puncture: lemon yellow, fluid, runny, >3000 elements (GB), few PNN, sterile

Positive diagnosis: New York/Van Der Linden criteria 1984

Clinical criteria:
Lower back pain with stiffness for more than 3 months, improved with effort, but not relieved by rest.
Limitation of movements of the lumbar spine in the frontal and sagittal planes.
Limitation of thoracic expansion.
Radiological criterion: Bilateral sacroiliitis of grade ≥2 or unilateral grade ≥3
SPA defined: radiological criterion + at least 1 clinical criterion.
SPA likely if: 3 clinical criteria or radiological criteria without clinical criteria

Assessment indices: BASDAI, BASFI, ASDAS (disease is active from 1.3)

TREATMENT
Treatment of the burst
NSAID high dose: Diclofenac: 100 to 150mg/day Indomethacin: 150 to 200mg
Painkillers: paracetamol 2 to 4 g/day Risks of Arctic infiltrations
from CTC:
Local: corticosteroid infiltration, Synoviorthesis: if infiltration fails
- Infections
Background processing - Aseptic necrosis
NSAIDs: minimum effective dose
Sulfasalazine (Salazopyrine) ++++
Methotrexate (Cytotrex): SPA with peripheral involvement
Anti-TNFα (Enbrel, Humira): indicated if
- Active disease
- Axial SPA: failure of at least 2 NSAIDs
- Peripheral SPA: failure of at least one background process
Other treatments: Gold salt, synthetic antimalarials
No corticosteroids ++++++
Surgical treatment: Hip ankylosis Total prosthesis
Rehabilitation: respiratory and anti-cyphotic
Flat file:
No fracture, no erythema nodosum
Square vertebra and not blind vertebra (the blind vertebra is malignant)
Osteophytes are present in osteoarthritis, absent in arthritis (RA and AS)
SPA = AINS+++ in crisis treatment (high dose) and maintenance (minimum effective dose)
Background treatment: NSAIDs, if peripheral involvement (coxitis, ankle, knee..): Sulfasalazine (Salazopyrine)
In front of peripheral arthritis and suspicion of AS: do an X-ray of the pelvis and not of the joint in question.
Respiratory CPC: bullous fibrosis (the diffuse interstitial pneumonia CPC of RA)
Lumbar stiffness Schober < 4 cm, thoracic compliance Hirtz < 5cm
Frozen hip: THA
Arthritis fluid ++++ characteristics: Citrine yellow, fluid, stringy, >3000 elements (WBC), few neutrophils, sterile
UAA : CTC + Mydriatic (Atropine)
Ophthalmology extension report ++++ + ECG (AV block +++)
 PR SPA
Terrain Average age of perimenopausal women Young man 20-30 years old
Bilateral, symmetric, fixed polyarthritis of 1-Pelvic-lumbar syndrome:
small articles MCP and IPP of 2thand 3emefingers Sacroiliac involvement + Lumbar spine +++
Never reaches: the spine (except cervical), lumbar-gluteal pain (pseudo-sciatica with a tilt)
sacroiliac, IPD Lumbar stiffness: Schöber < 4 cm
Clinic 2. Synovial pannus: thoracic expansion: < 5 cm
►Main (90% of cases): deformities 2. Enthesopathy syndrome:
Wrists: Piano touch - Achilles tendon injury: talalgias
Feet: flat foot, then round, subluxations, 3. Peripheral joint syndrome:
metatarsal plantar dislocations. Asymmetric arthritis of large joint: Hip
Cervical spineC1-C2: subluxation or luxation Peut toucher les IPD: 3 articulations du même
Coxo-femoral: 15% detrimental rayon "finger and toes in sausage"
Extra-articular 1. Rheumatoid nodules: extension faces Anterior uveitis
2. Carpal tunnel syndrome (median nerve) 2. Cardio: BAV, aortic insufficiency
3. Gougerot-Sjögren, Raynaud, vasculitis 3. Pulmonary: apical bullous fibrosis
4. Lymphadenopathy 4. Renal: AA amylose
5. Felty's syndrome: PR+ SMG+ leukopenia 5. Neuro: C1-C2 dislocation, compression
6. Bronchiectasis: dilations of the bronchi medullary, Ponytail++
7. Cardiac: pericarditis, myocarditis.
8. Pulmonary: rheumatoid pleurisy
9. Ocular: scleritis and episcleritis
10. Renal: AA amyloidosis
11. Spinal compressions: secondary to
atlantoaxial dislocation
RX Diffuse pinching of the interline 1. Vertebral column :

Geodes Square aspect 'squaring'

Demineralization in the epiphyseal band Syndesmophytes bamboo column
Epiphyseal erosions, early erosion of Ossification of ligaments: tram rails
5thmetatarsal Diastasis C1-C2
Opacification of the soft tissues Spinal demineralization
2. Sacroiliitis: bilateral symmetrical, 4 stages rx
3. Enthesopathies: erosions, geodes and ossification
Punchtime Lemon yellow, fluid, runny, >3000 elements (GB), few PNN, sterile
Auto-AC Anti CPP and FR Absents
VS Elevated Low
Trt de AINS +++ NSAIDs: High dose
push Analgesics 2. Analgesics: paracetamol 2 to 4 g/day
Low-dose corticosteroids (0.1 mg/kg/day) 3. Local: corticosteroid infiltration, Synoviorthesis:
Local: corticosteroid infiltration, if infiltrations fail
Synoviorthesis: if injection therapy fails
Methotrexate +++ 10 to 20 mg orally/week AINS: minimum effective dose
Leflunomide (ARAVA) Sulfasalazine (Salazopyrine) ++++
Pregnant woman, CI MTX: MTX: SPA+ peripheral involvement (coxitis…)
Background TRT Sulfasalazine Anti-TNFα (Enbrel, Humira): indicated if
Antipalu : Hydroxychloroquine - Active disease
Plaquenil - Axial SPA: failure with at least 2 NSAIDs
Azathioprine - SPA with peripheral involvement: failure to
anti-TNFα, anti CD20: PR active, after failure at least one background treatment
the MTX (3 months) Others: Gold salt, synthetic antimalarials
Abandoned medications: Thiol derivatives, No corticosteroids ++++++
D-penicillamine, Gold salt
Follow-up THE 28 BASDAI, BASFI, ASDAS (active disease from 1.3)
 REACTIVE ARTHRITIS

Peripheral arthritis, sterile (aseptic) occurring 3 weeks after an infection:

- Venereal ++++ (Chlamydia +++ Ureaplasma)
- Digestive (Campylobacter–Yersinia–Shigella–Salmonella)

FIESSINGER-LEROY-REITER SYNDROME (Urethro-conjunctive-synovial syndrome)

• The most complete form of reactive arthritis: Urethritis, conjunctivitis, and arthritis.
• HLA B27: 50 to 90%

CLINIC:
General signs: slight fever, mild AEG
Joint manifestations: oligo or mono arthritis of the MI (ankle+++)
Extra-articular manifestations: Urethritis or cervicitis, Bilateral conjunctivitis+++, Diarrhea
Rare signs:
Psoriasis-like skin lesions
Vidal and Jacquet's blennorrhagic keratoderma (palmo-plantar keratoderma)
Erythematous oral erosions and circinate erosive balanitis: Painless

BIOLOGY: Inconsistent inflammatory syndrome

BACTERIOLOGY: Serology, Stool Culture
PUNCTURE: Sterile inflammatory fluid
EVOLUTION :
- Permanent healing in 3 to 6 months+++, Recurrence, chronicity
- 1/3 evolution towards ankylosing spondylitis (especially in HLA B27 subjects)

TREATMENT
AINS
Local treatment: corticosteroid injections, synoviorthesis if unsuccessful
Bi-ATB: often extended 6 months!!!
Treatment of venereal or digestive infection, ineffective on joint manifestations
Background treatment: After 3 months of progress: Sulfasalazine

PSORIATIC ARTHRITIS
• Occurs in 0.5 to 25% of patients with psoriasis.
• HLA B27 in 60-70% of cases when the involvement is axial and 24% in peripheral forms.
• Joint pain after psoriasis, sometimes simultaneously and rarely before psoriasis.
• Five clinical pictures: Moll and Wright classification
Polyarticular involvement
2. Oligo-polyarticular involvement
3. Predominant involvement of the distal interphalangeal joint
4. Predominant axial involvement
5. Mutilating arthritis.
 3. POST-INFECTIOUS RHEUMATISMS

Definition: sterile arthritis occurring following a bacterial infection (most often), to be differentiated from
septic arthritis where the germ is found at the joint.
Group together:
Reactive arthritis (HLA B27): FLR syndrome
Post-streptococcal rheumatism

SUBACUTE CURABLE RHEUMATISM IN ADULTS

Post-streptococcal rheumatism

Other germs may be involved: staphylococcus, pneumococcus, meningococcus

Occurs 15 to 20 days after an infection: rhinitis, otitis ...

Post-streptococcal rheumatism ≠ RHD

EPIDEMIOLOGY:
Young adult 30 to 50 years old
Devenu très rare: diagnostic d’élimination

CLINIC:
General signs absent +++
Arthritis
Fixes, asymmetric
Especially in the lower limbs
Non-eroding and non-deforming
Nodular erythema: indicative of the diagnosis

Chorea and subcutaneous nodules are never observed in adults.

BIOLOGY:
Hyperleukocytosis, accelerated ESR, elevation of gammaglobulins
Elevated ASLO (if streptococcal infection)

PUNCTURE: Inflammatory fluid, sterile

EVOLUTION: Favorable, without carditis and without sequelae +++++

TREATMENT :
AINS
2. Corticosteroids: if NSAIDs are not effective
3. Penicillin:
-Attack phase: Penicillin for 15 days
Phase of treatment: Extencillin every 15 days for 3 months
 4. SEPTIC ARTHRITIS

Septica arthritis Acute hematogenous osteomyelitis

purulent effusion in a joint primitive metaphysical infection, by way of
following a bacteremia or direct (wound/surgery) hematogenous from an infectious focus at
with the presence of germs in the joint distance most often
far from the elbow, near the knee, child +++
Fever 40° + inflammatory signs + pain and weakness Fever 40° + inflammatory signs + pain and weakness
Dlr on metaphysical palpation+++
Absolute urgency: hospitalization + drainage puncture + dual antibiotic therapy IV
Strict rest, discharge of the member + preventive HBPM
Plaster immobilization ++++ (analgesic)
Golden staph++++ Staph endowed +++ strepto
Gonococcus is the primary cause in young women.
Strepto, brucella, BK

SPONDYLODISCITIS: infectious spinal involvement

Clinic High fever + pain and spinal stiffness (Shober < 4cm)
Spinal cord: pain upon palpation of the vertebrae
RX Disc herniation, destruction of vertebral plates, erosions and geodes,
aspect nibbled in side mirror
Complete exams DISCOVERTEBRAL BIOPSY PUNCTURE: purulent, septic fluid
3 blood cultures
Spinal MRI +++
Germs Banal germs Brucellosis BK (pot disease)
Destruction + ++ +++
Reconstruction fast Lens Very slow
(healing)
Others multivertebral: staph+ Breeding areas, milk Paravertebral area (psoas abscess)
Exams Blood culture+++ Séro Wright IDR with tuberculin
Trt Fluoro + RMP Cycline + RMP Anti-TBK 18 months
Immobilization by plaster cast

Flat file:
First intention examination: Lumbar spine X-ray + TLT (TBK)
Spondylodiscitis: perform FNS+ Wright's serology + BK IDR (if psoas abscess only FNS + IDR)
Easy diagnosis: DISCOVERTEBRAL PUNCTURE-BIOPSY
Medical treatment (ATB) and orthopedic (immobilization by plaster cast)
Spondylolisthesis (slipping of a vertebra) spondylodiscitis (spinal infection)
Curare paralysis: compression by the psoas abscess surgical decompressive drainage
Multivertebral involvement: staph+++
Psoas abscess: Pott's disease thoracolumbar pain
Spinal fever in a young subject + weight loss = spondylodiscitis or metastases
 5. METABOLIC RHUMATISM: MICROCRYSTALLINE ARTHROPATHY

THE DROP
GENERALITIES :
Especially affects men (20H/1F), over 60 years old
Normal uricemia: < 70 mg/L (< 360 micromol/L)
Gout = 100% hyperuricemia, but hyperuricemia accounts for 10% of gout

PATHOPHYSIOLOGY :
Gouty access
Chronic hyperuricemia > 70 mg/l Intra-articular urate crystals Phagocytosed by neutrophils
Macrophages secrete pro-inflammatory cytokines Synovitis
2. Chronic arthritis: Intra-osseous deposits of urate
Tophus: Tissue deposits of urate

ETIOLOGIES :
Primitive drop
Idiopathic +++
Enzymatic: PRPP hyperactivity, HGPRT deficiency (Lesch-Nyhan), Von Gierke
Secondary drop
Excess food intake (purines +++)
Hematology: chronic myeloid hematopathies, chronic hemolytic anemias, acute leukemias, Multiple Myeloma
Psoriasis
Renal failure, dehydration
Hyperuricemic drugs: competitive inhibition of tubular secretion
Cytolytic treatments, Anti-mitotic chemotherapy, Cyclosporine
Aspirin, corticosteroids, thiazide diuretics, and loop diuretics
Anti-TBK: Ethambutol–Pyrazinamide

sharp drop
Clinic:
Typical form
Triggering factor: - Excess food (proteins+++), excess alcohol
Hyper or hypo-uricemic treatment
Trauma, surgery, prolonged effort (walking...)
Prodromes :fièvre, céphalée, malaise général, colique néphrétique
Inflammatory pain, intense, starts at night at the base of the big toe (1MTP)
Aspect: inflamed big toe (red, swollen, warm)
In front of this clinical picture: no additional examination is necessary.
Colchicine: TRT and therapeutic test (Pain disappears in 24 to 48 hours)

2. Atypical forms:
Monoarthritis (Gneou..), oligo or polyarthritis, tendonitis
Uveitis, pharyngitis, orchitis, phlebitis
Biology: Hyperleukocytosis, VS and CRP. Hyperuricemia: not constant
Radio: normal or epiphyseal demineralization
Puncture: inflammatory fluid: rich in cells (> 2000 elements/mm)3in PNN) and in proteins (> 30g/l)+
urate crystals
CHRONIC GOUT:
Clinic:
1. Oligo or polyarthritis chronic asymmetrical
2. Tophus: White-yellowish, hard, painless swellings.
Helix Pavilion +++
Dorsal sides of the hands and feet
Olecranian and patellar bursae
Achilles tendon
Biology: Hyperuricemia
Radio: POGO (like osteoarthritis) + Notch:
. Line spacing adjustment
. Osteo-condensation
. Cookie-cutter geodes
. Osteophytes Bristling aspect
. Epiphyseal notches Aspect in halberd
EVOLUTION :
Renal manifestations indicate the severity of the disease: uric stones, chronic renal failure.

TREATMENT :
Gouty access
Repos
Colchicine: inhibits the mitosis of neutrophils
-Durée : 6 à 10jr
Contraindications: Pregnancy, severe renal or hepatic insufficiency
AINS: If failure or intolerance to colchicine
Corticosteroids: Not recommended, except in cases of severe crisis
2. Hypouricemic treatment:
1. Inhibitors of urico-synthesis:
Allopurinol (Zyloric) +++ inhibits xanthine oxidase (prevents the transformation of xanthine urate
Indications: symptomatic hyperuricemia > 3 attacks, tophus
Started at a distance from the gouty access: 1 month
Association with colchicine in the first 3 months (risk of triggering a gout attack)
-100 to 300 mg/day, for life
Side effects: leukopenia
2. Uricosurics:
["Benzbromarone (Desuric)","Benziodarone (Amplivix)","Indomethacin"]
Contraindicated in chronic renal failure
Flat file
Hyperuricemia > 70mg/l (crystallization rate)
Tophus: Chronic gout, ear cartilage +++
Crisis treatment: colchicine (therapeutic test for pain control in 24-48 hours), NSAIDs.
Background treatment: Allopurinol (during the crisis)
Allopurinol prevents the conversion of xanthine urate
Normal radiography of acute gout or demineralization.
Chronic gout: POGO + notches
Chronic hyperuricemia: hypertension, digestive disorders, impotence.. no pulmonary fibrosis.
Oligoarthritis in a patient treated for 10 years with diuretics = Gout
Cpc to fear f the drop: renal
 CHONDROCALCINOSIS
EPIDEMIOLOGY: postmenopausal woman over 50 years
PHYSIOPATHOLOGY :
Acute access: Intra-articular diphosphate crystals Synovitis
Chronic arthritis: degradation of cartilage infiltrated with crystals
ETIOLOGIES :
CCA primitive
Aging
Inhibition of alkaline phosphatase (which degrades crystals): Magnesium deficiency, excess iron
secondary CCA
Hyperparathyroidism+++ Hypothyroidism, Hemochromatosis, Hypomagnesemia

CLINIC:
1. Polymorphic articular table: pseudo-gouty, pseudo-arthritic, pseudo-rheumatoid, pseudo-
septic
2. Osteoarthritis Localizations : +++
3. Rapid destructive osteoarthritis Knee - Wrist - Pelvis - Shoulder
4. Calcification of fibrocartilages: knee menisci, intervertebral discs

RADIO: Calcifications+++: of the encroaching cartilage, fibrocartilages

PUNCTURE:
Inflammatory fluid if arthritis, mechanical if osteoarthritis
Presence of calcium diphosphate crystals
TREATMENT :
Repos + AINS +++
Colchicine: less spectacular effect than in gout.
Local treatment: corticosteroid infiltration, synoviorthesis

Drop Chondocalcinosis CCA

Male predominance Female predominance
Urate crystals Calcium pyrophosphate
. Fine, long, tapered crystals . Short crystals with square ends
. Intra and extra-leukocytic . Intra and extra-leukocytic
. Uricase: sensitive . Uricase: resistant
. EDTA: resistant . EDTA: sensitive
. Refringent to polarized light . Slightly refractive to polarized light

Metabolic rheumatism (gout, CCA) is sometimes febrile, differential diagnosis with septic arthritis.
 6. ARTHROSIS
Definition:
Chronic joint affection characterized by cartilage degradation associated with bone remodeling.
subchondral and limited phenomena of synovial inflammation

Epidemiology
Woman+++
In order of frequency: Digital osteoarthritis Gonarthrosis Osteoarthritis of the hip: 5% Rachis

Physiopath: 3 phases
Degradation of the cartilage matrix
2. Inflammatory reaction of the synovial membrane + joint effusion
[Link] of the subchondral bone: proliferation of newly formed bone osteophyte (hypertrophic formation)

Osteoarthritis Arthritis
Def Alteration of the cartilage of the joint Inflammation of the synovial membrane
Pain Mechanics: diurnal, effort repos Inflammatory: nocturnal, movements
not calmed at rest
ClinicSometimes irregular swelling Diffuse swelling (effusion), redness, heat
POGO Diffuse pinching of the spacing
Localized narrowing of the interline Epiphyseal demineralization
PrescriptionSubchondral osteocondensation (sclerosis) Microgeodes or diffuse erosions
Subchondral geodes: advanced stage
Osteophytes
Absence of demineralization+++
Bio VS normal Sd inflammation: high VS, positive CRP
Liquid Viscous Fluid
Citrine (transparent) Trouble or clear
Poor in protein (transudative) rich in protein: exudative
Poor in cell < 1000 /mm3) rich in cells > 1000

Arthrosis: POGO
Absence of demineralization in osteoarthritis
Localized pinching+++
 Gonarthrosis
Clinic:
Instability, cracking, theft
Stiffness in walking, evasive limping
Progressive reduction of the walking perimeter

Femoral-tibial gonarthrosis Femoro-patellar gonarthrosis (the most common one)

Seat pain Side pain Anterior pain
Signs Walk on flat or uneven ground Climbing and especially descending stairs
functional Knee dislocation Prolonged standing, prolonged sitting (sign of Cinema)
Crouched position
Pain on palpation of the joint line Patellar syndrome:
femoral-tibial (internal or external) Pain upon palpation of the patella
Signs Look for a static disorder: Pain with opposed extension
physiques Bow legs (o) favor knee osteoarthritis Sign of the plane
internal femoro-tibial (most common)
Genu valgum ( x ) favors the
external femoro-tibial gonarthrosis
Radio Cliché of face in charge ++++++ Femoro-patellar clichés 30°, 60°, 90°
Cliché of the Schuss Cliché de profil, Cliché axial

Inter-malleolar distance > 8 cm Knock-knees

II. Intercondylar distance > 3 cm Genu-varum

Etiologies:
1) Primary gonarthrosis (50% of cases): Woman aged 50-60, obese +++ bilateral but asymmetrical,
frequently associating femorotibial osteoarthritis and femoropatellar osteoarthritis.
2) Secondary gonarthrosis (50% of cases):
Anomalies of the leg axes in varus, valgus, recurvatum or flexum.
Infectious, inflammatory, or microcrystalline arthritis.
Meniscal lesion, meniscectomy, osteochondromatosis
Osteonecrosis of the internal condyle, osteochondritis.
Occupational or sports trauma: fracture or dislocation.

Flat File
Varus tibia: the most common cause of Gonarthrosis perform valgus osteotomy
Preoperative assessment (valgus osteotomy): CT scan + Telemetry + forced varus X-ray
Gonarthrosis: genu varum, the cold is internal, internal tibial
Corrective osteotomy (varus, valgus, dysplasia) in young subjects, early osteoarthritis
Intercondylar distance > 3 cm: Genu-varum
Inter-malleolar distance > 8 cm: Genu-valgum
Gonarthrosis: standing front X-ray + femoro-patellar
No anterior drawer in the femoropatellar compartment (ACL injury: anterior cruciate ligament)
 COXARTHROSIS
Clinic:
Mechanical pain:
Brief morning loosening, calmed by rest
irradiant from the groin to the knee
Prolonged standing position, prolonged sitting, squatting
Climbing and descending stairs, lifting a low seat, tying one's shoes
Sometimes: isolated knee pain ++++++ (deceptive form Rx of the pelvis
Limitation of hip mobility:
Limitation of extension, abduction, and internal rotation
The bending and the amplitude of movements remain preserved for a long time.
Market:
Stiffness, evocative limping.
Advanced coxarthrosis: plunging gait +++++, reduction of walking perimeter
Frequent quadriceps and gluteal muscular atrophy

Biology: VS normal
Radio: Front basin in load + false profile of Lequesne (but true profile of hip) + Coxometry

Super-external coxarthrosis +++ internal polar coxarthrosis

Hip joint dysplasia Acetabular protrusion
The pinch is superior The pinch is posterior-internal or axial
Cotyloid deficiency: Lack of coverage Excess external coverage > 25°
external < 25° Coxa vara < 120°
Coxa-valga > 135° Often well tolerated
Often poorly tolerated

Positive diagnosis:
ACR criteria: 3 out of 4 criteria:
Subject > 50 years, Mechanical hip pain, Osteophytes or joint space narrowing, VS < 20 mm

Etiology:
1) Primitive coxarthrosis (40% of cases): Unilateral or bilateral, 60-70 years old, women > men, overweight
2) Secondary coxarthrosis (60% of cases): younger woman, history of:
Congenital dysplasia
Traumatic coxopathy, infectious, inflammatory or microcrystalline coxitis
Aseptic osteonecrosis of the femoral head
Osteochondritis in children (Legg Perthes Calvé disease = flat hip)
Epiphysiolysis in children (reversed coxa and coxa vara)
Paget's disease of bone, Forestier's disease
Synovial osteochondromatosis; villonodular synovitis

Evolution:
Frequent bilateralization, especially if in secondary form
Frequent aggravation with the need for total hip replacement within 10 years: 90% of cases
RAPIDLY DESTRUCTIVE GONARTHROSIS AND COXARTHROSIS
Définition :Perte de la totalité du cartilage en seulementquelques mois,unilatérale ++ femme > 50 ans
Clinic:
- Inflammatory type pain
- Functional impotence, limitation of movements
- Absence of general signs
Biology: VS slightly increased
Radio: may be normal, pinching without osteophytes or geodes
MRI: joint effusion, subchondral edema
Puncture: Mechanical fluid ++++

TREATMENT
Lifestyle hygiene:
Resting the limb in severe flare-ups: joint economy
Physical exercise outside of pushes
Use of the cane on the healthy side
Push treatment:
Analgesics: preferable to NSAIDs
AINS: severe, inflammatory flare-up, or with effusion
Background treatment:
Slow-acting anti-arthritics: Chondroitin sulfate, glucosamine sulfate, avocado unsaponifiables and
of soy
Recommended at a poorly evolved stage of osteoarthritis for 3 to 6 months. Good tolerance.
Local treatment:
Infiltration of corticosteroids:
In inflammatory flare-ups, or with effusion
Hip infiltrations
Their number should not exceed 3 per year, planned in the short and medium term (<6 months)
Washing: in gonarthrosis
Visco-supplementation: hyaluronic acid
thermal cure

Surgical treatment:
Preventive: Correction of a dysplasia, a genu varum or a genu valgum...
Should be proposed at a less advanced stage (localized pinching)
Total hip or knee prosthesis
The indication for the prosthesis is based on clinical criteria and not on radiological ones, an index of
lequesne > 12, PM < 500m is a good indication for surgery
Flat file:
The prolonged use of CTC does not promote arthritis, but it does encourage aseptic necrosis of the head.
femoral (cause of secondary Coxarthrosis)
The CTC however is not a treatment for arthritis.
No cortisone infiltration in coxarthrosis
Isolated gonalgia, think of coxarthrosis!
La douleur au niveau de l’aine est très évocatrice de l’atteinte coxo-fémorale (hanche)
Coxarthrosis: flexion is maintained for a long time
Algodystrophy does not cause either gonarthrosis or coxarthrosis.
Hip dislocation is not a cause of coxarthrosis.
In a patient with hip osteoarthritis: Activate the gluteus medius++++ (to avoid muscle atrophy)
 7. OSTEOPOROSIS
GENERALITIES :
The most common of the debilitating osteopathies
Bone mineral density
Must be mentioned in the occurrence of fractures for minor trauma
DMO = g /cm2
Decrease in bone mass and alteration of bone microarchitecture
DMO : T score < -2.5

RISK FACTORS :
White and Asian race
Underweight: BMI < 19
Calcium and vitamin D deficiency
Smoking, alcohol, caffeine, sedentary lifestyle
Chronic kidney failure (hypocalcemia)
Malabsorption: inflammatory bowel diseases, gastric surgery
Estrogen deficiency menopause++++, hypogonadism (testosterone for men)
Endocrinopathies : Hyperthyroïdie, hyperparathyroïdie, hypercorticisme
Genetics: Lobstein, Marfan, Ehlers-Danlos, Homocystinuria, Gaucher's disease
Iatrogenic: CTC > 3 months, long-term heparin therapy

CLINIC:
1. Vertebral compressions: Mechanical type back pain (relieved by rest)
The cervical spine and the first 3 thoracic vertebrae are always respected: never above D5.
Do not touch the back wall and the back arch
Never spinal or radicular compression
2. Fractures
Vertebral fracture: the most common: 50%, asymptomatic+++, risk of recurrences
The peripherals: Wrists, Hips
Consolidate within the usual timeframes ++++

Osteoporotic vertebral fracture Metastatic vertebral fracture

symmetric, homogeneous, respects the cortical, neither asymmetric, cortical lysis, osteolysis and geodes, wall and arch
osteolysis nor geode, wall and arch post spared post reached (blind or sightless vertebra)

3. Physical signs:
Pain on palpation and pressure of the spinous processes.
Spinal stiffness + segmental muscular contracture (acute)
↓ size (3cm → sensitive sign).
Respiratory restriction
Static issues ( dorsal kyphosis, lumbar lordosis, iliac space, abdominal protrusion
Oblique thoraco-lumbar skin folds: Christmas tree sign

RADIOLOGY:
1. Homogeneous bone hyper-transparency
- Rarefied bony trabeculae
2. Deformation of the vertebral bodies:
- Biconcave, cup-shaped, wedge-shaped, in a cake
- Aspect in 'glass', uninhabited, outlined in pencil (mourning border).
3. Thinning of the cortices of long bones

BIOLOGY: Normal ++++ (no dyscalcemia unlike other differential diagnoses)

eliminate multiple myeloma ++++ : VS PIC monoclonal to EPS, PMO: Plasma cell count >10%
 OSTEODENSITOMETRY :
►T score :DMO subject - average DMO of young subjects of the same sex, at the same bone site → serves to
diagnostic
►Z score DMO
: subject - average DMO of subjects of the same age: not useful for diagnosis

Normal Osteopenia Osteoporosis Severe osteoporosis

DS -1 -1 to -2.5 < -2.5 < -2.5 + fracture

HISTOMORPHOMETRY (Bone Biopsy)

Decrease in trabecular volume and trabecular calcium

DMO= Dual-energy X-ray absorptiometry (DEXA or DXA):

Reference technique: estimates bone strength by measuring bone mineral content (BMC)
Non-invasive, early diagnosis

TYPES :
TYPE 1 TYPE 2 : Senile TYPE 3: Juvenile
Terrain Postmenopausal woman over 55 After 70 years (2F/1H) Subject young < 50 years
and 65 years old (6F/1H) Child
Cause Hypoestrogenism Calcium deficiency2 Idiopathic hypercalciuria
Based on intestinal absorption of Ca2+
OS Trabecular+++ Cortical and trabecular
Clinic Vertebral fractures and external frc Vertebral fractures and long bone fractures
inf of radius (Pouteau-Colles)

TREATMENT :
Biphosphonates :
in 1eraintention inhibits osteoclastic activity
Fosamax (alendronate), Actonel (risedronate)
Effects IIairmyalgias, episcleritis, esophagitis, GERD, mandibular osteonecrosis, flu syndrome, hypocalcemia
SERMs (Raloxifene): selective estrogen receptor modulators
Estrogen antagonists at the level of the breast and endometrium: used for breast cancer, the endometrium
Agonists on bone (inhibit resorption) and lipid metabolism
Protective effect on the cardiovascular level
Contraindicated if history of thromboembolic events
Cannot be prescribed for humans (logic)
- Others: Parathormone (teriparatide) 1 SC injection/day, calcitonin (inhibits resorption), Strontium ranelate,
Denosumab: Humanized monoclonal anti-RANKL antibody
Hormone replacement therapy, Tibolone: it is the HRT for men

Indications: treatment is not systematic

Post-menopause: Calcium + Vit D, Bisphosphonates, Hormone replacement therapy or SERMs (SERMs+++)
Osteoporosis due to corticosteroids: Calcium + Vit D, Bisphosphonates
Treatment of vertebral compressions: Rest in a lying position, Analgesics +++ ± NSAIDs
Flat File
Never above D5 (if cervical = malignant)
Normal phosphocalcium balance
Mechanical-type back pain (relieved by rest)
Vertebral collapse and long bone fractures
Respect of the post-arc, no lysis of the spines, the disc is not pinched, no neuro signs
FDR: CTC and prolonged heparin therapy (not AVK)
Diffuse homogeneous demineralization, histo: decrease of trabecular calcium
Bisphosphonate (anti-osteoclast) orally gives epigastric pain, replace with IV form.
 8. OSTEOMALACIA: MY BONE
GENERALITIES:
Insufficient mineralization of the bone trabeculae: osteoid tissue
No decrease in bone mass
It pertains to the spongy (trabecular) bone and the cortical bone.
It is the equivalent of rickets in children.

ETIOLOGIES: 02 etiologies
Vitamin D deficiency +++: malabsorption +++ (celiac disease), lack of intake or sun exposure,
deficiency of hepatic or renal hydroxylation
Hypophosphatemia: phosphoric diabetes

CLINIC:
Bone pain: pelvic-crural region, groin, buttock +++
Muscle weakness and myalgias: waddling gait like a duck
Vertebral compressions and fractures: rare
Deformations:
the size
Dorsal kyphosis
Bell-shaped thorax, in keel
Flared basin, Coxa-vara
Lower limbs in parentheses

RADIOLOGY:
Demineralization: blurred, washed-out aspect of the bone framework 'blurry image'
2. Looser-Milkman fissures: Pathognomonic
De-mineralization bands of 2 to 3 mm
Surrounded by osteo-condensation
Perpendicular to the mechanical axis of the bone
In the scintigraphy: hyperfixation
3. Deformations:
Bell-shaped thorax
Biconcave vertebrae known as fish vertebrae
Heart-shaped pool in a playing card
Acetabular protrusion, Coxa-vara

BIOLOGY :
Collapsed Vitamin D levels
Hypocalcemia, constant hypocalciuria
Secondary hyperparathyroidism due to hypocalcemia
Hypophosphatemia, Hyperphosphaturia

Hypocalcemia PTH Hyperphosphaturia Hypophosphoremia

BONE DENSITOMETRY: no interest

HISTOMOROPHOMETRY
Increase in osteoid tissue
The calcification front is greatly reduced.
Hyperosteoclastosis Due to secondary hyperparathyroidism
The total bone volume is normal.

TRAITEMENT :Vitamine D à vie,Calcium,Phosphore

 Calcium level: 80 - 100 mg/l (calciuria follows calcium level)
Phosphoremia: 40-60 mg/l
Osteoporosis normal
Osteomalacia The two diminished
Classification Fraser :
Rickets I :Ca Normal phosphoremia
(enf) II: Ca normal, Ph
III: the two
Hyperparathyroidism PTH Calcemia Phosphoremia
MM, bone metastasis, Vitamin D intoxication The two

Diffuse demineralizing osteopathies

Osteoporosis Osteomalacia
Def DMO: T score < -2.5 Insufficient mineralization of the bone trabeculae:
osteoid tissue
Mass Diminution No reduction
bony
Etiologies Menopause ++++ hypoestrogenism Hypovitaminosis D, Hypophosphoremia
Vertebral fractures++++ Bone pains: pelvic-crural, inguinal, gluteal +++
Clinic Assessments: Mechanical back pain Muscle weakness and myalgias: Walk
↓ size (3cm → sensitive sign) dancing in 'duck'
Compression and rare fractures
1. Homogeneous hypertransparency of bone 1. Heterogeneous blurry hyper-osseous transparency
2. Deformation of the vertebral bodies: 2. Looser-Milkman fractures: Pathognomonic
Rx - Biconcave, cup-shaped aspect, Demineralization bands of 2 to 3 mm
cuneiform, in tablet Surrounded by osteo-condensation
- Aspect in 'glass', uninhabited, Perpendicular to the mechanical axis of the bone
outlined in pencil (mourning border). Scintigraphy: hyperfixation
3. Thinning of the cortical bones 3. Deformations:
longs size
Bell-shaped thorax
Biconcave vertebrae known as fish vertebrae
Heart-shaped pond on a playing card
Acetabular protrusion, Coxa vara
Bio Normal Collapsed Vitamin D levels
Hypocalcemia PTH Hyperphosphaturia
Hypophosphoremia
Histomorphology - Diminution of trabecular volume Increase
and of osteoid tissue
trabecular calcium phometry HyperosteoClastosis, Rate of calcification

Flat file osteomalacia:

02 etiologies
Vitamin D deficiency +++ :malabsorption +++ (celiac disease), lack of intake
Hypophosphatemia: phosphorous diabetes
Hypocalcemia PTH Hyperphosphaturia Hypophosphatemia
Pelvic pain and walking disorders (waddling gait)
Looser-Milkmann fissures
VS normal
osteoid tissue (hyperosteoidosis), normal bone mass
Heterogeneous diffuse demineralization
Trt: calcium + Vit D
Hydroxylated derivatives of vitamin D: renal insufficiency, hepatic insufficiency (cirrhosis), deficiency in 1 alpha hydroxylase
Calcitonin: hypocalcemic hormone, inhibits bone resorption
Vitamin D is hydroxylated to 25 in the liver and then to 1 in the kidney.
 9. MULTIPLE MYELOMA: KAHLER'S DISEASE
Generalities:
Malignant hemopathy: predominantly bone-localized plasma cell monoclonal proliferation.
Median age: 65 years, rare before 40 years, slight male predominance

Pathophysiology: plasma cell proliferation leads to

- Osteoclastic resorption: bone manifestations + hypercalcemia, mediated by: IL1-beta, IL6, TNF
- Suppression of hematopoiesis: anemia, thrombocytopenia, neutropenia
- Inhibition of normal B lymphopoiesis Ig polyclonals susceptibility to bacterial infections

Clinic:
Bone pain +++ present 70% in the initial phase
- Seat: spine, ribs, pelvis
- Do not yield to rest or painkillers.
- In relation to bone lysis or swellings (sternal, costal, clavicular).
Spontaneous bone fractures:lumbar spine++++, thoracic spine, humerus, femur, ribs and sternum
Hypercalcemia syndrome:
- Anorexia, nausea, abdominal pain, constipation
- Polyuric-polydipsic syndrome, dehydration, consciousness disorders
- ECG: hyper-excitability: extrasystole, short QT
RX :
- Diffuse demineralization
- Multiple punch-out lesions: well-defined osteolytic lesions without peripheral reaction
- Osteocondensing lesions: 3%, POEMS
- Cortical destruction with tumor mass in the soft tissues, vertebral compressions
- Normal: 20% of cases
*** MRI if there is spinal cord compression !!
*** Bone scintigraphy: unremarkable, myelomatous lesions are rarely hyperfixing.

Biology:
- FNS: anemia, pancytopenia in advanced forms
- VS with 3 digits
- Hyperproteinemia > 100g, hypercalcemia
- 24-hour proteinuria: Bence-Jones proteinuria
Precipitation at 56-60°C, dissolution at boiling: 100° and reappearance after cooling.
Quantification of light chains in urine.
- β2-microglobulin: its dosage should be systematic as it reflects the importance of tumor mass.
Immuno:
- EPS :
Narrow pic migrant in the gamma zone +++ or beta, exceptionally alpha 2
Hypogammaglobulinemia if MM with light chains
- Immunofixation of blood proteins: IgG +++ IgA (GALDEM)
- Weight dosage: of the other classes of Ig
- Immunoelectrophoresis of concentrated urine: kappa or lambda light chain
- Bone marrow test: > 20% normal plasma cells or > 10% dysplastic plasma cells
- Bone marrow biopsy: if the myelogram is not contributory

Positive diagnosis:
2 critères majeurs :Ig monoclonale dans le sérum ou les urines,Plasmocytose médullaire 10%
And at least one of the CRAB criteria: hypercalcemia, renal insufficiency, anemia, and bone lesions

Complications
- Recurrent infections: ENT and pulmonary+++primary cause of death
- Spinal or radicular compression: cauda equina syndrome, carpal tunnel syndrome
- Renal failure: hypercalcemia and tubulopathy, amyloidosis +++
- Hyperviscosity syndrome: rare
 Clinical forms
1- Immunochemical forms: in descending order of frequency: GALDEM
- IgG (55 %), IgA (20 %) , chaine légère 14%
- Light chain myeloma: low or slightly elevated VS, no monoclonal peak but hypogammaglobulinemia.
very often complicated by renal insufficiency
- IgD myeloma: rare and severe. lambda light chain +++ renal insufficiency and amyloidosis
- MM non-excreting: no monoclonal peak, detection of monoclonal protein by immunofluorescence
- MM biclonal
2- Indolent MM: does not require treatment
3- MM to normal VS: MM with light chains, non-excreting myeloma, MM with cryoglobulinemia.
4- Solitary plasmacytoma: Single plasmacytic tumor either bone or extra-bone. In some cases cured.
after surgery and/or RT. The progression to myeloma is possible.
5- Plasma cell leukemia:
- Acute leukemia table: bone marrow failure+++, hepatosplenomegaly, fever
- Circulating plasmocytosis > 20%
6- POEMS syndrome:
- Sensitive-motor polyneuropathy (P) organomegaly (O) endocrinopathy (E) plasma cell dyscrasia
(Myeloma or solitary plasmacytoma) skin anomalies
- Bone involvement is often sclerosing.
- Light lambda chain

Prognostic factors:
A. Salmon-Durie classification: guide for therapeutic choice
Stage I Stage II Stage III
Tumor mass < 0,6.1012cells/m2 Intermediate > 0.6.1012 Strong > 1.2 x 1012
All the criteria At least one of the criteria
Hb 10 g/dL < 8.5 g/dL
Prescription normal or single lesion you I you III 3 lytic bone lesions
Calcemia <2.60 mmol/l > 3mmol : > 12 mg/dl
IgG < 50g/l > 70g/L
IgA < 30g/l 50 g/L
Light urinary chain < 4 g/24 hr 12 g/24 hr

Stage A: Absence of kidney involvement

Stage B: kidney damage: creatinine level > 150umol/l

B. International classification (ISS): prognosis based on Beta 2-microglobulin and Alb levels.
Stage I Stage II Stage III
2-microglobulin < 3.5 mg/L < 3.5 mg/L 5.5 mg/L
Albumin 3.5 g/dL < 3.5 g/dL
Median survival 62 months 45 months 29 months

Specific treatment: Chemotherapy

Before 65 years: Bortezomib (Velcade*) then Melphalan with hematopoietic stem cell transplant.
After 65 years: Melphalan, prednisone, Thalidomide or Bortezomib Association
Radiotherapy: if spinal compression or persistent bone pain: Lytic lesions, vertebral fractures
Flat file:
Gaps: clear boundaries and not blurred
Absence of osteocondensation at the limits
Diffuse demineralization and not banded
Geodes: areas of preference: skull+++ and pelvis
More serious if IgD, more serious in the young
Score ISS (B2m, Alb), Salmon Durie (tumor mass: 6 radio-biological criteria)
Renal insufficiency in MM is due to a tubulopathy resulting from hypercalcemia.
 10. CONNECTIVITY OR SYSTEMIC DISEASES

DISSEMINATED LUPUS ERYTHEMATOSUS

EPIDEMIOLOGY: Young woman (20–25 years), black race, HLA DR2, DR3

PATHOPHYSIOLOGY: Apoptosis anomalies persistence of apoptotic bodies expressing antigens

nuclear presentation to LT: immune response Circulating Immune Complexes (CIC): deposition
in the VX vasculitis in various organs

CLINIC:
► General signs: fever, asthenia, anorexia, weight loss: 80% of cases
► Joint signs: 80 to 90%, most frequent revealing manifestation
migratory arthralgias
Acute polyarthritis: bilateral, symmetrical, non-destructive, without synovial pannus: the most frequent
Jaccoud's rheumatism: rare, deformities related to subluxation of the finger tendons, non-erosive
Septic arthritis :1eracause of mortality, joint weakened by a synovitis or CTC, Knee +++

► Musculoskeletal: Myalgias, aseptic osteonecrosis favored by corticosteroids

► Cutaneous monkeys:
Vespertilio: erythematous-squamous facial eruption in butterfly wing shape (not periorbital)
Alopecia, Nails: striation or cup-shaped depression.
Discoid lupus, Urticaria, Photosensitivity
Ulcerations: skin, oral mucous membranes and genital
Vascular: Raynaud's, livedo reticularis, leg ulcer, telangiectasia, vascular purpura
► Hematological signs: ADP, SPM
► Renal signs: 2thcause of mortality from SLE: highlights the severity of DLE
Glomerular involvement +++ nephrotic syndrome, nephritic syndrome, proteinuria, hematuria, renal insufficiency
Mécanismes de l’atteinte rénale:
- Deposit of immune complexes
- Antibodies that recognize renal antigens or antigens fixed on the glomeruli
- Microthrombosis (APS)
► Cadiac: Pericarditis (frequent), Myocarditis, Liebmann–Sacks verrucous endocarditis
► Respiratory: Pleurisy, Fibrosis
► Neurological: aseptic meningitis, convulsion, stroke (anti-phospholipid antibodies)
► Psychological troubles: depression, psychosis, hallucinatory syndrome, delirious, confusional, early, sometimes revealing.

BIOLOGY:
Pancytopenia: Anemia (inflammatory, autoimmune), leukopenia: Mainly lymphopenia, thrombocytopenia
Elevation: VS, fibrinogen, gammaglobulins. Normal CRP, if increased: infection
Complement: - Decrease during acute episodes: By activation of the classical pathway ++++
Normal outside of outbreaks (unless there is a congenital deficiency in C1, C2, C4)
Immunology:
Anti-nuclear antibodies (ANA): Always present at a high rate
Searched byIFI, positive 1/80
Anti-DNA :
Native anti-DNA (double strand): Very specific, increased during exacerbations
Anti-denatured DNA (single strand): Non-specific, LED induced (medicinal)
2) Soluble nuclear anti-Ag antibodies (nucleoprotein):
According to the type of fluorescence
Anti-Sm: pathognomonic+++ but inconsistent
Homogeneous: anti-DNA, anti-Histones
Anti SSA and anti SSB
Peripheral reinforcement: anti-DNA
Anti RNP Spotted: soluble anti-nucleoproteins
Sm, RNP, SSA, SSB, Scl70
 3) Antihistone antibodies: drug-induced lupus

AC anti-phospholipids Drug-induced lupus:

Anti C1q antibodies: 100% of patients, low specificity: positive in other pathologies Penicillin, sulfonamides, Aldomet,
["Sectral","Isoniazid","Tegretol"]

Biopsy: Interest if performed on healthy, unexposed skin. Dihydralazine (Népressol)

Procainamide, D-penicillamine
11 Diagnostic criteria ARA: 4 simultaneous or successive criteria
Butterfly wing malaria eruption
Specific LED antibodies:
2. Eruption of discoid lupus
Native anti-DNA antibodies
3. Photosensitivity
4. Oral or nasopharyngeal ulcers Anti-Sm
5. Non-erosive polyarthritis Push markers:
6. Pleurisy or pericarditis Anti-native DNA antibodies

7. Renal: proteinuria > 0.5g/24h or urinary casts The supplement

8. Neuro: convulsions or psychosis
9. Hematology: hemolytic anemia or leukopenia < 4000 or lymphopenia < 4500 or thrombocytopenia < 100
10. Immuno: presence of LE cells, anti-native DNA antibodies, anti-Sm antibodies, false syphilitic serology
11. Antinuclear antibodies at abnormal levels (in the absence of inducing medications): in immunofluorescence

Treatment :
- NSAIDs, Corticosteroids, immunosuppressants (synthetic antimalarials, cyclophosphamide, not MTX)
- More recently: Anti CD20, Anti TLR.
Follow-up:
Req !! Contraception :
- Complement: CH50, C3, C4
- Renal function: urea, creatinine, 24-hour proteinuria, urine culture pure progestogens,
- Anti-nuclear (title, aspect), Anti-native DNA. contradicted estrogens

Flat File
The most revealing involvement of the LED: joint
PR of the LED: sharp, symmetric bilateral without destruction or deformation = without erosions on the X-ray
Specific LED Auto-AC: Native Anti-DNA (double strand), Anti-Sm
Push markers: Anti-native DNA antibodies supplement bas (activation of the classical pathway)
LED anemia: inflammatory++++ and autoimmune
Contraception with pure progestins (OP Contraindicated)
Monitoring: supplement + kidney function + AC
Clinical case: young woman, arthritis + weight loss, but leukopenia and positive ANA = systemic lupus erythematosus.
Typical clinic of PR in young women and other signs (Auto-Ab, butterfly wing) = LED
Immunosuppressants of lupus erythematosus (synthetic anti-malarials (hydroxychloroquine) +++, cyclophosphamide..)
no MTX
Hydroxychloroquine (anti-malarial): causes retinopathy ophthalmic surveillance
No eye damage f'LED
LED: hypergammaglobulinemia
LED mortality: 1theseptic arthritis, 2threnal impairment
Jacoud's rheumatism (LED): deformation of the hands+++ or feet, non-erosive
Phlebitis during a systemic lupus erythematosus: look for anti-phospholipid antibodies (circulating anticoagulants, anti-cardiolipin...)
Anti-phospholipid in SLE: sign of severity (phlebitis, stroke, embolism..)
 ANTIPHOSPHOLIPID ANTIBODY SYNDROME: APS
CAUSES: Primary, or secondary to another disease, often lupus.
CLINIC:
Thromboses, vascular issues, especially venous (stroke, pulmonary embolism)
Repeated abortions
Livedo reticularis
No joint involvement
Catastrophic Antiphospholipid Syndrome:
simultaneous multiple thromboses: multivisceral failure
BIOLOGY :
FNS :anémie hémolytique,thrombopénie
Livedo reticularis
Elevation of the ESR and gammaglobulins
Immunology:
AC anti-phospholipids (IgG or IgM):
1. Anti-cardiolipin antibody: ACL
2. Anti-beta2 glycoprotein 1 (Aβ2GP1) (not beta2 microglobulin)
3. Circulating anticoagulants (anti-prothrombinase) Prolonged APTT not corrected by normal plasma
4. False syphilitic serology: VDRL positive, TPHA negative
Note: only one of the ACs is sufficient for the diagnosis.
Many false positives: at least 2 tests with a 12-week interval.
Antibodies must persist for more than 12 weeks but not more than 5 years.
TREATMENT :
Thrombosis: Heparin
Preventive: AVK
Pregnancy: Aspirin, Heparin

SJÖGREN'S SYNDROME: DRY SYNDROME

The most common connectivity
Mainly non-specific organ involvement but preferentially affecting exocrine glands (lacrimal and salivary).
Maybe: Primitive or secondary to a PR+++ or a connectivity

PHYSIOPATH: Infiltration LT4 at the level of the affected organs with Th1 type immune response
CLINIC:
Dry syndrome:
Xerophthalmia (tear dryness) Eye burning, photophobia, kerato-conjunctivitis
Xerostomia (dry mouth) Difficult swallowing
Vaginal, nasal, tracheal (cough), cutaneous dryness
2. Systemic manifestations:
General symptoms: Asthenia
Articular signs: Arthralgias or non-destructive chronic polyarthritis
Neurological, pulmonary, renal damage
3. Complication: lymphomas 10%

DIAGNOSTIC :
B is more specific than A, but both
Anti-SSA antibodiesprimitive SGJ
are not specific to this pathology
Anti-SSB antibody SGJ secondary
Other auto-AC: FR, anti-nuclear AC, cryoglobulin

►Biopsy of the salivary glands in difficult cases: Lymphoplasmacytic infiltrate

TREATMENT :
Symptoms: artificial tears, artificial saliva, secretory stimulants
From the background: CTC, Synthetic antimalarials, immunosuppressants
 SCLERODERMA
Accumulation of collagen: affection of connective tissue, arterioles, and micro-vessels leading to fibrosis
The most specific disease is hepatitis C.

CLINIC:
Systemic form: Preferentially affects the skin, digestive tract, lungs, and kidneys.
Skin lesion:
Cutaneous fibrosis: Atrophic, indurated, retracted skin, difficult to pinch QCM: no ENT affection
-Face: wrinkle removal, limitation of mouth opening
-Hands: sclerodactyly: bulbous appearance of the fingers
Hyperpigmentation or depigmentation
Calcinosis: small very hard painful subcutaneous nodules that may ulcerate
Telangiectasias: abnormal proliferation of capillaries localized in the hands, lips, and oral cavity.
- Raynaud's phenomenon: Constant (90%), usually the 1ersign of the ScS
Joint signs: arthralgias or chronic polyarthritis, asymmetrical, non-destructive
Frequent tendon injury: audible crackling
-Signes digestifs :Œsophage: dysphagie, RGO Fréquent +++, Grêle et colon: malabsorption, trbl du transit
Cardiac arrest:myocardium+++
Pulmonary fibrosis
**CREST syndrome: Calcifications cutanées, Raynaud, Œsophage,Sclérodactylie, Télangiectasie
Immuno:
Anti-scl70 antibodies: Systematic form
Anti-centromere: CREST
Others: Anti-nuclear, Cryoglobulin: abnormal Ig, precipitates when cold, Redissolves at 37°, Not specific
Skin biopsy: in difficult cases

RAYNAUD'S PHENOMENON
It is a paroxysmal, vascular, localized acrosyndrome, triggered by the cold, affecting the extremities.
(fingers, toes, nose and ears)
EPIDEMIOLOGY: Common, Women +++, winters (cold++)
CLINIC:
1. Syncopal white phase: White, cold hands
2. Asphyxiating blue phase: Bluish, painful hands
3. Red recovery phase: Swollen, red, painful hands
Complications
Very painful fissures cupuliform scar (Pitting scar)
Digital ischemias distal gangrene or a false finger infection abusive amputations
Raynaud's phenomenon Raynaud's disease
Unilateral Bilateral Idiopathic
Regional cause Secondary to the connectivities, Before 40 years
Thrombosis vasculitis Bilateral and symmetrical
Tumor compression Often after 40 years Never complicate yourself
Carpal tunnel syndrome Bilateral and asymmetrical Absence of others
-Sd of vibrations Rapid evolution manifestations
jackhammer Other events
Capillaroscopy Abnormal Normal (healthy arteries)

TREATMENT:
RHD: Stopping tobacco, caffeine, protection against cold and humidity, avoidance of inducing medications.
Medical treatment: Syndrome de Sharp = connectivité mixte
First-line calcium channel blockers: nifedipine, amlodipine Overlap syndrome:
Alpha-blockers (and not BB: residency multiple choice questions) Anti-nuclear antibodies and anti-ribonuclear antibodies

Prostanoid IV (Iloprost) protein (anti RNP antibodies)

 10. VASCULITIS

Vasculitis of large trunks Giant cell arteritistrt CTC

Takayasu arteritisthe woman without a pulse
Vasculitis of the arteries of Nodular periarteritisPAN
medium caliber Kawasaki diseasechild
Micropolyangitis
Associated with Granulomatose de Wegener
Vasculitis ANCA Churg and Strauss granulomatosis:
small ones atopy + corticosteroid-dependent asthma + eosinophilia
vessels : Rheumatoid purpurahyper-IgA
Without ANCA Cryoglobulinemic vasculitis(essential mix)
Antibody-mediated glomerular vasculitisti-MBG
Behçet's disease
*ANCAanti-cytoplasm antibodies of neutrophils

Horton’s disease

Granulomatous inflammatory arteritis

Woman > 60 years old, headache + fever + inflammatory syndrome++++

Temporal artery +++ (external carotid)

Touch the cephalic arteries and the major trunks but never the aorta or the pulmonary artery.
Emergency CTC 1mg/kg/day orally until biological normalization, then DME for 12 to 18 months.
Risk of permanent blindness
 Polyarteritis nodosa (PAN)

Systemic necrotizing vasculitis of medium caliber arteries that can affect any vessels
of the organism except for the pulmonary arteries

Epidemiology: rare, 40-60 years, 3H / 1F

Pathogenesis: VHBS + 30 to 50%, immune complexes

General condition Neuro: 70% Cardiovascular: 40%

Fever, sweats SNP : Multiple Neuritis SPE+++ SPI, Distal arterial thromboses
Asthenia, pallor muscle atrophy mainly in the lower limbs Myocarditis progressing to IVG
Weight loss > 4kg CNS: rare meningeal hemorrhage +++) Pericarditis, Endocarditis

Rheumatoid Renal impairment: 50% Pneumonia

Conditions the vital prognosis
Severe hypertension, malignant hypertension Asthmerebelle [15%] aux
Myalgias
usual treatments
Inflammatory arthralgias renal failure, HUS
Bone: bone infarction Glomerulopathies, Nephrotic syndrome
Pleuisy and infiltrate [25%]
Vascular nephropathies (20%)
Skin signs: 40% Orchid Eye Digestif
Nodules dermo- Febrile orchitis
fleeting hypodermics, perineal hematomas Abdominal pain (40%) and nausea
No erythema nodosum ureter in a chain Acute pain tablet
Livedo, Purpura,Urticaire, Ocular: uveitis, DR, exudate, Perforation(HD)
Raynaud hypertensive retinopathy Mesenteric infarction
NECROSIS OF THE EXTREMITIES

HBV-related PAN: are more often associated with hypertension, orchitis, digestive signs, and less often with asthma.

Never mention PBR when talking about the CEO of PAN because of the risk of an aneurysm rupture = catastrophic hemorrhage.

Biology
Inflammatory disease: ESR, CRP, Hypergammaglobulinemia and leukocytosis
thrombocytosis > thrombopenia
Sometimes hyperEo > 5,000 mm3 (30%).
Immuno :
- ANCA (peripheral fixation in IFID) 20%: their negativity is more indicative of PAN
- AANegative
Angiography: abdominal and renal arteries: micro-aneurysms+++, stenosis, renal infarcts
Pathological study +++ (necessary for diagnosis)
Biopsies in diseased area: muscle, nerve +++, skin, kidney
only after arteriography, PBR contraindicated if micro-aneurysm
Results:
Necrotizing vasculitis: Inflammatory granuloma with fibrinoid necrosis of the media
No giant cells.
Immune complex deposits containing HBV antigens
TREATMENT
Oral cortico therapy
- prednisone 1 mg/kg/day for 4 to 6 weeks then gradual decrease
- certain severe forms: Methylprednisolone bolus
Immunosuppresseurs :Cyclophosphamide : ENDOXAN,Azathioprime,Antiviraux : pour l’hépatiteB
Evolution
Unpredictable and variable with close bursts affecting multiple organs
Severe prognosis even under treatment: 50% mortality at 5 years
 Churg-Strauss Syndrome
Clinic:
Atopic terrain, chronic rhinitis evolving into severe corticosteroid-dependent asthma.
A few years later, a hyperEo appears
extrapulmonary signs associated with Loeffler syndrome and systemic vasculitis.
Histology: Periarterial granulomas with necrosis, epithelioid cells, and giant cells.
Type P ANCA: more common during Churg-Strauss angitis than in PAN (60%)
the treatment, the response to the treatment, the prognostic criteria, and long-term survival are the same as with PAN
Relapses are more frequent in this syndrome, asthma persists.

Behçet's disease
Terrain: Man 15-40 years old, Mediterranean terrain. HLA B51
CLINIC:
Bipolar recurrent aphthae: oral +++++ and genital
Skin signs: Pseudofolliculitis, erythema nodosum
Articular signs: Arthralgia, monoarthritis, symmetrical polyarthritis. Erosive involvement is rare.
Venous affections: Superficial and deep thrombophlebitis
Arterial injuries: Thrombosis, aneurysms
NeuroBehcet: aseptic lymphocytic meningitis, meningoencephalitis, stroke
Ocular damage: Posterior uveitis ++++ Anterior uveitis: Risk of blindness
All parts of the eye can be affected
Cardiac injury: Pericarditis, myocarditis, endocarditis, coronaryitis
Respiratory signs: Pleurisy, pulmonary embolism, arterial aneurysm Hemoptysis
Renal signs: Subacute glomerulopathy
BIOLOGY :
Hyperleukocytosis with neutrophils, Inflammatory syndrome (ESR, CRP): inconsistent

Pathergic test
Treatment
Thrust:Colchicine: effective against aphthae and arthritis
From the background:Corticosteroids, immunosuppressants: if corticosteroid therapy fails
 11. PAINFUL SHOULDER

PAINFUL SHOULDER Sharp Shoulder FAUX EPAULE GELLED SHOULDER

SIMPLE HYPERALGIC PARALYTIC
Degenerative lesion of a Migration of Tendon rupture Frozen shoulder
Tendon mechanism: tendinitis calcification Crystals - Degenerative (Moderate Dlr) idiopathic
hydroxyapatite or traumatic (Sharp pain)
Bursitis Transfixing (all)
the thickness) or not
Moderate pain, General signs Active movements Intense pain
spontaneous or Dlr intense reduced permanent
Clinic provoked permanent Passive movements Limitation of
Active movements and Signs of inflammation: preserved movements
possible passive tum, heat, Jump: Contact assets and liabilities
redness, pain humerus-acromion
Total impotence
Maybe normal Disappearance or Head ascent Radiological signs
Radio Calcification of migration of a humeral delayed / clinic.
tendon known calcification Diminution de l’espace Demineralization
Restructuring of acromio-humeral heterogeneous of the
insertion zones Break of the hanger humeral head
Ultrasound: useless if the Ultrasound and MRI :
Others VS and CRP Rupture is visible on the x-ray. Thickening of the
exams Show the breaks capsule
transfixing agents Arthrography:
Arthroscanner: Examination of Retraction of the
choice capsule
Don't show the breaks.
non piercing surfaces
IRM: Shows the breaks
transfix and non-transfixing
90%: Favorable Favorable in a few Complete healing
Evolution : 10 % : Complications : days in 12 to 30 months
Rupture With treatment: 3 to 4 months
Migration of
calcification = épaule
hyperalgesic
Adhesive capsulitis
Medical: analgesics, Immobilization Medical: Analgesics, NSAIDs Analgesics, NSAIDs
AINS Medical: Analgesics, Corticosteroid infiltration Local: Infil CTC
Local: infiltration CTC AINS Contraindicated +++++++ Kiné: Passive then
Trt Aspiration of the Infiltration of Physiotherapy: Active active
calcification corticosteroids Repair: Arthrodistention :
calcification > 5 mm and Drainage If partial rupture Injection into
refractory pain at Arthroscopy (acromioplasty) the articulation of:
treatment Total break Surgery serum, anesthesia,
Kinéactive (repair + acromioplasty) corticosteroids
Surgery in case of failure Rehabilitation
intensive
Forced mobilization
under AG
 Muscles Movement Maneuver
30° flexion
Sus-spinous Abduction JOBE Abduction of 80°
Thumbs down
Subscapular Rotation LIFT-OFF Hands behind the back Detached by the examiner
internal (GERBER test) - The patient must keep it detached
Long biceps Flexion ou PALM-UP Palm up Flexion of the arm
antepulsion (SPEED test)
Under spiny and Rotation PAW Elbow glued to the body or in anterior elevation of 90°
little round external The patient must resist external rotation pressure.

MCQ:
Microcrystalline bursitis of the shoulder: Pain + weakness + significant inflammatory syndrome
 12. SCIATICA
CLINIC:
1. Lumbar syndrome:
Low back pain: mechanical type
Antalgic posture: disappearance of lumbar lordosis, inflection of the spine
Segmental stiffness: decreased Schöber, sign of the fracture
2. Radicular syndrome:
Pain follows the path of L5 or S1
Bell sign: palpation of the lumbosacral region Pain identical to spontaneous pain

S1 : SPI L5: SPE

Butt Front of the thigh butt Posterior-external part of the thigh
Popliteal fossa External part of the knee
Front of the leg Front or antero-external face of the leg
Route of the Achilles tendon or retro-groove Lateral malleolus or pre-malleolar groove
external malleolus Back of the foot
pain
Heel, external edge of the foot Big toe
Last toe Pain in a bracelet around the ankle
Can radiate to the inner part of the groin Can radiate to the outer part of the groin
Motor deficit muscles of the posterior compartment muscles of the anterior and lateral compartments of the leg
Loss of plantar flexion in the foot Loss of dorsiflexion of the foot
Market Walking on tiptoe is impossible: Steppage = drop foot = Walking on heels
Trendelenburg impossible
Hypoesthesia outer edge of the foot + sole + heel two of the foot

ROT Achilles reflex impairment Absence of impairment

Attention: stepping is often the first sign of ALS

Exacerbated pain: Coughing, exertion, defecation, Lasègue: Homolateral and contralateral
Diminished pain: DL in a shooting dog position, DD with a cushion under the knees.

IMAGERY:
Radio :
- Direct signs: Lateral or posterior disc yawning
- Indirect signs (POC): Disc narrowing, Osteophytes, Condensation of the plates
TDM: first intention examination
Radiculography: useful in dynamic hernias (which only appear when standing)
BIOLOGY: Sometimes moderate hyperalbuminorachia

SERIOUS FORMS: Emergency surgical treatment

Hyperalgesic sciatica, debilitating sciatica, cauda equina (genitourinary and sphincter disorders)

TREATMENT :
Relative rest (not strict) for 8 to 10 days, lying down on a firm surface
Lombostatrigide for 4 to 6 weeks Then a more flexible lombostat
Medical treatment: NSAIDs +++, analgesics, and muscle relaxants. If failure: Corticosteroids
Local treatment: epidural or intrathecal corticosteroid injections
Surgery: If medical treatment fails after 6 to 8 weeks
Chimionucleolysis: disc herniation not excluded (if excluded, it is contraindicated)
Rehabilitation: after the acute phase
Flat file
L5: anterolateral face of the leg anterior machi
5 > 1 therefore L5 big toe, S1 small toe. S1, 1 as I, S1 = SPI
En5thLegros year external steppeura lost sadorsi-flexiondu foot and let the heels fall on the
Luckily, his roots are not affected.
Disc hernia: disc bulge posterior
 13. ALGONEURODYSTROPHY
DEFINITION
Local vasomotor disturbance
Touch the entire joint area: skin, bone, tendons... except for the cartilage (avascular).
Poorly known physiopathology
Topography:
- MI 60%: foot or ankle ++++, knee, hip (pregnant woman)
- MS: 40%: main++++, frozen shoulder, shoulder-hand syndrome (rarely the elbow)
ETIOLOGIES
Primitive : 25%
- Metabolic disorders: diabetes, hypertriglyceridemia, hyperuricemia...
- Psychological troubles: anxious profile
Secondary: 75%
- Trauma 50%: trauma, surgery, plaster, no correlation between trauma and algodystrophy.
- Medical: neuro, cardio-pulmonary, cancers, Phenobarbital, Isoniazid...
- Pregnancy: hip algodystrophy at T3 or after childbirth

Hot phase (pseudo-inflammation) Cold phase (ischemic) Phased inversion

Duration A few weeks to 2 months A few weeks in Plz months Healing in 3 to 18 months
Absence of general signs and ADP: important for diagnosis
- Vascular disorders: edema, May be inaugural Remineralization
hypersudation, erythrocyanosis ... Pain and edema complete
Pain: regress Aftermath:
Clinic Mixed (inflation and mechanical) Trophic disorders +++: skin persistence of the
Touch a segment of a limb thin, pale, hairless pain and some
Permanent–Insomniac Capsular retraction and trophic troubles
- Trouble sensitivity: hyperesthesia, allodynia ligamentous: joint stiffness Recidivism
Decreased active and passive mobility Disuse atrophy
Balance Normal +++ : No inflammatory syndrome, normal calcium-phosphate balance
Puncture Mechanical fluid: low in cells <1000 and in proteins, sterile
Important: Negative signs POGO of osteoarthritis (Sometimes micro-geodes)
Heterogeneous locoregional demineralization (not diffuse):
Radio blurred hypertransparency, mottled or speckled at the epiphyseal pre Remineralization
Respect for line spacing takes several months
Thickening of the soft tissues (edema)
These signs are sometimes absent in phase 1, but evident in phase 2
IRM Edema (T1: hypointense, T2: hyperintense) The signs regress early.
Scintillation Tc99 Early and late hyperfixation Persistence of late hyperfixation Hyperfixation
Discharge, analgesics, tricyclic antidepressants
NSAIDs and CTCs peros: not recommended
TRT Background treatment (efficacy not demonstrated): Calcitonin ++, BB, Bisphosphonates
Not indicated in the ischemic phase
Gentle rehabilitation: Hydrotherapy
Flat File
Focal hypertransparency, mottled or spotted with predilection for the epiphysis
The line spacing is respected++++
RX standard: May be normal in the hot phase, the RX signs are delayed compared to the clinical findings.
The X-rays must be bilateral and comparative and especially repeated.
Early images: MRI and Scintigraphy
In the ischemic phase: it is the normality of the Doppler that guides the diagnosis.
Healing is faster in the lower limb (3 to 12 months) compared to the upper limb (2 to 3 years)
Sensitive trouble: hyperesthesia and not hypoesthesia or anesthesia
More frequent after FrPouteau-Colles
Trt: antidepressant 3C. NSAIDs and corticosteroids not recommended
 FLAT FISH

Mechanical pains Inflammatory pains

Arthrosis Arthritis: PR, SPA, associated with connective tissues
Osteoporosis Metabolic rheumatism: Gout, CCA
Sciatica Multiple myeloma
Algodystrophy Nodular periarteritis
Algodystrophy

Nodular periarteritis, ironically, no erythema nodosum

Square vertebra (squaring): SPA

Biconcave vertebra in small plate: MM
Ivory vertebra: TBK
Vertebra in frame: Paget
Blind vertebra: metastasis

Articular pinching Demineralization

Osteoarthritis localized Absent
Arthritis (PR) Diffuse In the epiphyseal band
Osteoporosis Absent Diffused man
Osteomalacia Diffuse hetero +
in a gang (Loser-milkman)
Algoneurodystrophy Respect line spacing local, dimpled or
spotted at metaphysis
MM Diffused
OMA Diffuse
Tuberculous spondylodiscitis Diffused

Patho Specific Auto-AC

PR FR, ACAPA = anti CCP
LED Native anti-DNA antibodies
Ac anti-Sm
SAPL
Sd sec (Gougerot) Anti-SSA: Primary Sjögren's Syndrome
connectivity the + frq Anti-SSB: Secondary Sjögren's (more specific)
Scleroderma Anti-scl70 antibodies: Systematic form
Anti-centromere: CREST (Cutaneous calcifications, Raynaud,
Œsophage,Sclérodactylie, Télangiectasie
 IDIOPATHIC SCOLIOSIS
Generalities:

- 80% Idiopathic, female predominance (little girl)

- Diagnosis + : clinical-radiological
- Vertebral deformation in the 3 planes (3D):
Horizontal : spinal rotation
Frontal: S inclination
Sagittal: kyphoscoliosis
- Spinal rotation is clinically manifested as:
Dorsal gibbus
Lumbar support

Anapath:

The vertebra is deformed: cuneiform, lateralization, rotation

Differential diagnosis: Scoliotic attitude (Functional scoliosis)

Vicious attitude, spinal deviation without vertebral rotation (no kyphosis)

Reducible in a lying position
No passage between scoliotic attitude true scoliosis
Causes :inégalité de longueur des membres, asymétrie du bassin, position antalgique

Classifications based on the age of appearance: the earlier the age, the more severe it is.

-nourrisson : 90% résolutives

infantile: < 3 years severe
-juvénile : j1 (4-7ans), j2 (7-11ans), j3 (11-puberté)
pubertal scoliosis: 12 years in girls, 14 years in boys

Radiology: spinal assessment + assessment of bone maturity

Spinal assessment:
total front standing column
upper and lower limiting vertebrae: vertebrae that limit scoliosis
apical vertebra: the most rosette-shaped
Angle of scoliosis: from the upper edge of the upper limit vertebra lower edge of the vertebral limit
(Cobb angle, Moe angle)
Rotation of the vertebra: takes place on the vertebra at the top
total standing column from the side: appreciates frontal balance
total column lying face down: allows to see the reducibility of scoliosis
2) Assessment of bone maturity:
left wrist radio: the thumb sesamoid signals puberty
elbow radio: elbow closure announces the end of rapid growth
Risser index (spinal maturation): ossification of the iliac wings
Risser 0: no ossification
Risser 1: 1/3 superficial external of the cartilage
Risser 2: 2/3 external
Risser 3: 3/3 external (bony growth of the iliac wing)
Risser 4 :1eradeep half
Risser 5: fusion = adult

Evolution:

Evolves mainly during growth, accelerates during puberty and slows down at bone maturity

Treatment:

1) Orthopedic: must be early

a. elongation devices: spinal traction at night
plastered corsets:
EDF: elongation, derotation, flexion
Donaldson plaster: stagnant
c. orthoses +++
Milwaukee corset: child+++active, dynamic corset
Lyonnais corset: teenager+++, passive corset
Boston corset: dynamic corset for kyphosis, indicated for lumbar scoliosis

Rehabilitation: at all stages of scoliosis aims to reduce its progression.

3) Surgery: after softening plaster
scoliosis that escaped orthopedic treatment
after the rapid growth
arthrodesis of the spine affected by scoliosis
material: Harrington, Dubousset cortel
Indications :
Cobb angle < 20°: RHD and monitoring
20°: plaster or corset do not remove the cast
50°: surgery

Fich Flach
Gravity without scalability (puberty push+++)
Cardio-respiratory CPC
Scoliotic attitude = spinal deviation and not vertebral (no rotation)
Cortical classification: etiological (80% idiopathic, 20% secondary)
Milwaukee corset: child+++active, dynamic corset
 AMPUTATIONS
Etiologies
Arteritis 70%: diabetics+++, senile (arteriosclerosis), juvenile (Buerger's disease)
Traumas 25%
Malignant tumors of the bones and soft tissues, malformations, infections
The level of amputation depends on:
Age: in the child, the diaphyseal-epiphyseal growth zone must be preserved
Extent of injuries
Type of intervention: emergency or cold

Cold surgery: osteo-myoplasty in 5 stages

Classification of stumps:

Ideal stump: obtained by osteomyoplasty

level of amputation 1/3 middle
cylindro-conical shape
slightly posterior frontal scar
normal color and heat
good muscle strength
no exostosis or neuroma or orthopedic disorders (flexion/abduction)

Defective stump: occurs after

severe trauma: unsightly scar, fragile, underlying fracture, nerve damage
arteritis: thin, cold stump, deformity, and site of ulcerations
infection: infected open fracture complicated by osteitis with permanent fistulas

Painful stump: 100%

sensation of painful phantom limb
causalgias: increasing burning sensations, hyperesthesia, red and shiny skin that is sweating
scar neuroma
TRT: infiltration of lidocaine

PEC :

preparation of the stump:

fighting against edema: drainage, elastic bandage, elevation of the limb
fight against vicious attitudes
fight against muscular atrophy: isometric contractions + globulization of the stump
2) preparation of the patient for standing: walking between parallel bars
3) equipment phase: 15 to 21 days after the operation
temporary appliance: made of plaster on a healed but not yet stabilized stump
semi-permanent prosthesis: stump is stabilized
definitive prosthesis = socket + underlying segment
 COMPLICATIONS OF DECUBITUS

1) Cutaneous-trophic complications:
Evolving stages: World center of pressure sores
stage 0: venous and lymphatic stasis (clinically not apparent)
Stage 1: Erythematous plaque: inflammation of the epidermis and superficial dermis
stage 2: blister: the dermis is separated by serous fluid
stage 3: black necrotic plaque: gangrene of all dermal layers
stage 4: ulceration of necrosis
stage 5: multiple sores
Complications :
Sepsis is the most common and the most fearsome complication.
hemorrhage, extension of the sore, carcinization (squamous cell carcinoma)
Treatment:
the treatment is essentially preventive:
- returned the patient every 3 hours
- special lights: water, air, fluidized, foam
- good hygiene of the patient and their bedding
- examination of support areas after each turnover
- massage of pressure points, icing and friction with alcohol on erythematous areas
curative treatment
- pressure ulcer discharge
- surgical flattening in advanced cases
2) metabolic complications: phosphocalcic: phosphoremia calcemia and calciuria lithiases
3) osteo-articular complications: muscle atrophy, retraction of soft tissues, malunions, osteomas,
ankylosis
4) respiratory complications:
- decrease in thoracic expansion hypoventilation stasis
congestion, bronchopulmonary infections
atelectasis, pulmonary edema due to fluid overload, pulmonary embolism
advanced stage respiratory failure
5) urinary complications: urinary stasis infections, retention and urinary stones IR
prevention
good daily diuresis 2l/day
acidification of urine by vitamin C
6) digestive complications: stasis constipation, fecal impaction, intestinal obstruction, gastric dilation with
formation of a third sector (collapse)
prevention:
- fiber-rich diet and olive oil
- massage of the colonic frame in the direction of its progression
- stimulation of defecation by nasogastric tube, rectal examination
7) cardiovascular complications: thromboembolic +++, maladaptation: orthostatic hypotension
8) nervous complications: compression of a nerve trunk
9) complications psychiques :tristesse, insomnie, dépression, agressivité, angoisse

Do not change positions for the spinal cord injured person!!!

 ARTICULAR AND MUSCLE ASSESSMENT
I. Articular assessment
It is the measurement of the amplitudes of each joint with a goniometer. highlighting of stiffnesses

Classification of joints:
1) Synarthroses (immobile):
- syndesmoses: sutures of the skull bones, union by collagen and elastic fibers
- symphysis: union of 2 bones by hyaline cartilage (adolescence)
- symphysis: between 2 pubic bones
- synostosis: the strongest bony union between the different portions of the ilium

2) Diarthroses (mobile)
- arthrodial: 2 almost flat surfaces (acromioclavicular)
- trochlear: convex-concave in pulley, 1 degree of freedom (humeroulnar, knee)
- condylar: concave-convex, circular movements (radio-carpal)
- saddle: 2 saddle-shaped surfaces, 2 degrees of freedom and multiaxial (ankle)
- enarthrosis: 2 segments of spheres (concave-convex): coxofemoral, glenohumeral

Reference position = position 0 = position of the soldier at attention

- standing, heels together, knees straight, feet slightly apart,
- elbows extended, little finger on the seam of the pants

II. Muscle assessment

►Concept of main root: if it is reached, the corresponding muscle is severely affected: e.g. C5 for
the deltoid
►Concept of muscle group: a movement is ensured by several muscles
►Static muscle contraction: does not allow movement, useful under plaster
►Dynamic muscle contraction: allows movement, useful after plaster removal
►Biarticular muscle: has insertions on 2 joints => 2 actions (e.g., anterior rectus => flexion of
the hip and knee extension

Muscle testing: 0 to 5

0. No contraction
Contraction without movement
2. Movement in weightlessness
3. Movement against gravity
4. Movement against resistance
5. Nrml

0-3: cannot walk

4: walking with a walker
5: walks normally
 Paraplegia

Classification FRANKLE: paralysis starts with recovery

Group A: complete impairment, no motor or sensory function below the level of the injury.
Group B: complete motor impairment, preservation of sensory function including perineal.
group C: motor conservation but muscular strength not usable
group D: sufficient muscular motor strength to walk
Group E: no neurological impairment, no muscle weakness, no sensory disturbances, nor sphincter disorders.