Rheumatolgy - common diseases

1. Rheumatological diseases

2. Rheumatic Diseases
Common Rheumatic Diseases :
1• Rheumatoid arthritis (RA)
G Osteoarthritis
• Systemic fupus erythematous (SLE)
*a Sjogren syndrome
u^ Dermat0myositis/polymyositis
SclerDderma/systemic sclerosis
G Anl‹ylosing spondylitis.
^a Psoriatic arthrltis

3. The MoH Common Autoimmune Disease
i• 1'›t population or 3per 10,000
'0' 3:1 female to male
^a Highest in 3’d and 4” decades
0' Twopeaks incidence
^
a Morbid/mortal disease
0' Description dates to the17” century -ANew World Disease

4. Itheumatoid arthritis (RA)
'0' Rheumatoid Arthritis (RA) is a chronic inflammatory disorder that may affect
many tissues and organs, but mainly attacks the joints producing an
inflammatory synovitis.
^a RA mainly affects the joints.
6 May also produce inflammation in the lungs, pecicacdium, pleura, and sclera.
x* Rheumatoid Arthritis is a chronic disease who's pain intensity and deterioratiDn
of joint structures progress over time often leading to deformations and
disability.

5. Signs and Symptoms of Rheumatoid Arthritis
•• Tender, warm, swollen joints
Joint stiffness that is usuaIly worse in
the mornings and after inactivity.
'0• Fatigue, fever and weight loss

6. RA Diagnosis & Tests
¢' XRays ofhands and feet are generally performed in people with RA.
4' Magnetic Resonance Imaging (MRI)
6 Ultraseunds
6 BIDod Tests: Rheumatoid Factor

7. ¢’ Surgery
• Removal of inflamed synovium
• Arthroplasty
¢• Physical therapy
¢• Cortisone Therapy
^• Ami-inflammatory Agents
• Aspirin
• Ibuprofen
• Naproxen
* Acetaminophen
• Tylenot
Treatment

8. Osteoarthritis
6 Most common theumatic disease and is characterized
by progressive loss of cartilage and reactive changes
at the margins of the jDint and in the subchondral bone
*a Primarily affects weight-bearing jo‹nts
such as the knees, hips and lumbosacral spine
6 In early disease, pain occurs only after joint use
andis relieved byrest
. ’* •.
6 As the disease progresses, pain occurs with
minimal motion or even at rest

9. Etiology is unknown
• More common than secondary OA
• Common-in elders where there is no
previous pathology
• Its mainly due to wear and tear changes
occurring in old ages mainly in weight
bearing joints
Classification of OA
Secondary OA
Etiology is known
Due to a predisposing cause such as:
1) injury to the joint
2) Previous infectiDn
3) RA
4) CDH
5)Deformity
6)Obesity

10. Clinical features of OA
'6' Pain
6 Stiffness
4' Muscle spasm
6 Restricted movement
x* Deformity
'6' Muscle weakness or wasting
6 Joint enlargement and instability
* Crepitus
6 Joint Effuslon

11. Possible Anatomłc Sites Of Pain Generation in OA
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12. 6 Blood tests: Normal
6 Radiological features-
1) Cartilage IDSS
2) Subchondral sclerosis
3) Cysts
4) Osteophytes
Special Investigations

13. ’¢• Education
6 Physiotherapy
—Exerclse program
—Pain relief modalities
6 Aids and appliances
*a Medical Treatment
6 Surgical Treatment
Treatment

14. Systemic Lupus Erythematous (SLE)
6 A multi-system inRammatory, autoimmune connective
tissue disease that occurs most commonly in women
during their reproductive age.
• The hallmark of SLE is its variety of presentation &
autoantibodles.
6 Essentially any organ system can be affected,
particularly the skin, joints, kidneys, and CNS.

15. Epidemiology
'6' More common in urban than in rural areas
'6' 3 -5 cases per 10,000
6 Female : male= 9
- 1 (adult)
'0' OnsRt age= 6596betweRn 15-25 ys(lath Dnset ?40-55)
'0' Identical twin : 3096
•0' First degree relative : 5%
•'a Child of SLE mother has risk of SLE
(whh posltlve antl —Ro/SSA antlbody) =29â

16. Pathophysiology of SLE
6 Systemic lupus erythematous (SLE) is characterized by a global loss of self-
tolerance with activation of auto reactive T and B cells leading to production of
pathogenic autoantibodies and tissue injury.
6 Autoimmune reactions directed against constltuents of cell nucleus, DNA

17. Clinical Features and Clinical Manifestations
¢' Clinical Features:
• Musculoskeletal disease
• Mucocutaneous involvement
• Renal disease
• Central nervous system disease
• Cardiopulmonary disease
• Hematologlc abnormalities
• Gastrointestinal involvement
6 Oin1caIManlfestation:
• Severe fatigue
• Fever
• Weight loss
• Ac‹orexia
• £ymphadenopathy

18. Treatment of SLE
^a Arthritis, Arthralgias, Myalgias:
NSAIDS, Anti-Malarials (eg. Plaquenil),
steroids-injections, oral methotrexate
•5 Photosensitivity, Dermatitis
Avoid Sun exposure
Topical steroids, Plaquenil
vasculitis
* Weight loss and fatigue
Steroids
4' Abortion, Fetal loss
ASA, lmmunosuppression
6 Thrombosis
Anti-coagulants
Glomerulonephrttis
Steroids
Pulse cytotoxic
Mycophenolate mofetil
CN5 disease
Anti-coagutants for thrombosis
SterDids and cyrotoxic for
Infarction
Steroids
Cytotoxic
Prostacyclin

19. SJogren syndrome
6 Achronic, slowly progressive autoimmune
disease characterized by lymphocytic
infiltration of thRexocrine glands resulting in
xerostomia and dry eyes
6 1/3have systemic manifestations
s* Few develop lymphoma

20. 2 Forms: Sjogren syndrome
¢• Primary sjogren's syndrome
The disease presents alone
•
•
•
•
•
•
•
6 Secondary Sjogren's :
Associated with other autoimmune diseases
RA
SLE
Scleroderma
Mixed CT disease
Primary biliary cirrhosis
Vasculitis
Chronic active hepatitis

21. Sjogren syndrome: Etiopathology
'0' Etiology -not wellunderstood
'0' Findings suggest an on-going interactiDn between
The innate and acquired immune systems
• Lymphocytic (T,B) infiltration of exocrine glands
6 B lymphocyte hyper-reactivity
* Inherited susceptibility+ exo /endogenous antigens
'0' Trigger a self perpetuating Inflammatory response

22. Sjogren's: Clinical Manifestation
t¥iedicatlons that ‹ause sImil»r symptoms
• Antidepressants
• Anticholinergic
• Beta blockers
• Diuretics
• Antihistamines
• WDmen on HRT
• Anxiety
Glandular:
• Xerophthalmia
• Xerostomia
• Bilateral parotid swelling
Extra glandular:
• Arthcagias/arthritis
• Raynaud's phenomenon
• Lymphadenopathy

23. Investigations
• Mild normochcomic, normDcytic anaemia
• ESR rise- in 709a
^a Mouth:
• Sialometry
• Sialography
• Imaging: Ultrasound, MRI or MR sialography of salivary glands.
• Salivary gland Biopsy
4' Eya:
• Schirmer test

24. Sjogren's: Treatment
Artificial tears, Rx -corneal ulcerations
*• Avoid drugs that secretions (Diuretics,
antidepressants)
•i• Xerostomia: Best replacement - water
•
3 Vaginal dryness: Propionic acid gets
6 Secretagogues: Oral PilocarpTne / Cevimeline
•'a Arthralgias : HCQ
anti HTs,antichoIinergic &
x* RTA: Oral Soda bicarb
•f• Systemic vasculitis: Steroids,
•
â
• immungsuppressives, M Abs
6 High-grade lymphomas: Chemo (CHOP) + M Abs

25. Dermatomyositis
6 Dermatomyositis is a disease of the connective-tissue which is defined by
swelling of the skin and muscles.
4• DermatDfTgDSitis affects adults and children however it is more common in
females than males.
4 It mostly affects Fhe skin and muscles, but It may also affect the lungs and
oesophagus

26. Dermatomyositis: Symptoms
x* Skinrash
'6' Symmetric proximal muscle weakness
6 Muscle pain
Temporary paralysis
v* Difficulty in swallowing
4 Scaly skin eruption
6 Flat, erythematous lesion on the shoulders and chest
1• Reddish-purple eruption on the upper eyelid
v* Erythema
G Roriasiform scalpchanges
*a Gastrointestinalinfection
* Lung problems

27. Diagnostic Criterla
Bahan and Peter Criteria: Symmetric proximal muscle weakness
6 Typical rash
* Elevated serum muscle enzymes
•"a Myopathic changes on EMG
<* Characteristic muscle biopsy abnormalities and absence of histopathDlogic signs
of other myopathies

28. Treatment
'0' lmprc›ve muscle strength andavoid development of extra muscular
complications
'0' Glucocorticoidsare the cornerstone Df initial therapy
^a Typically initiate prednisone at 1mg/kg to a maximum dose of 80 mg
¢° Initial treatment with high doses for the first several months to establish
disease control
* Slow taper to thelowest effective dose for total duration of 9-12months
6 First line agents include Azathioprine or methotrexate
• More than 80K of patients will improve with glucocorticoids alone

29. '0• Multisystem disorder
& Unknown Etiology
g' Thickening of skin caused by accumulation of
connective tissue (collagen types I and lit)
¢' Involvement of visceral organs
Sclerosis

30. ¢' UnLnown
¢• Environmental Exposures
• Sillca exposure in men conferred Increased risk
• Silicone breast implants: no definite risk identified
• Aniline laced Contaminated rapseed oil in Spain
° Vinyl chloride exposure increased risk of SSc Sitedisorder: Eosinophilic
Fasciitis
• Bleomycin
• L-tryptophan: Eosinophilia Myalgia syndrome
x* Genetic Factoc
Familial Clustering: 1.5-2.59aof those with 1" degree relative
Sclerosis: Etiology

31. Forms of Systemic Sclerosls
6 Mmltad Scleroderma
• Crest Syndrome
• Calcinosis
• Raynaud's
• Esophageal Dysmotility
• Scterodactyly
• Telanglectaslsa
'6' Diffuse Scleroderma
• Organ Involved
• Skin
• Musculoskeletal
• Pulmonary
• Renal
n

32. Forms of Systemic Sclerosls
6 Mmltad Scleroderma
• Crest Syndrome
• Calcinosis
• Raynaud's
• Esophageal Dysmotility
• Scterodactyly
• Telanglectaslsa
'6' Diffuse Scleroderma
• Organ Involved
• Skin
• Musculoskeletal
• Pulmonary
• Renal
n

33. Treatment: Sclerosis
4' Immunosuppressive Therapy
"v Ar›tispasmodlcs (muscle relaxants)
4' NutritiDnal therapy
'0' High-protein diet with supplementary vitamins

34. Ankylosing Spondylitis
'0• A systemic rheumatic disease and is one of
the seronegative spondyloarthropathies
• The typical patient is young, aged 1&30
* Men are affected mtce than women by
a ratio about of 3:1

35. Signs and Symptoms
6 Mild to severe back and buttock pain that is
often worse in the early morning hours
°a Continued lnflammatizsn of the:
• Ligaments
• Tendens
^ JDint capsules
• joints of the spine
6 Common symptom is generalized fatigue.
Spondylitis
Sympt0tTlS t0
never ignore

36. Diagnosis
' • Ablood test for the HLA-B2Y gene
^a T0mography andmagnetic resonance ‹maging of the secroiliacJoinu

37. •
0
• A¥›ti-inflammatory drugs
• N5AlDs such as Aspirin, Ibuprofen, Phenylbutazone,Indomethacin, Naproxen
and COX-2 Inhibitors.
6 DMARDs
• Such as Cyclosporine, Methotrexate, Sulfasalazine, and Corticosteroids
6 TNFa blockers (antagonists)
• Etanercept, infliximab and Adalimumab
'0' Surgical Management
• Osteotomy formarked deformities of the hip/spine.
• Occasionally, hiporknee Arthroplasty is used
Treatment

38. Psoriatic Arthritis
6 Inflammatory arthritis associated with psoriasis
6 One of the spondyloarthropathies.
0' Males and females are equally affected.
* PSDrİatic Arthritis is chronic, ØFDgressive
inflammatory disorder affecting the joints and skin
characterized by osteolysis and bony proliferation.

39. Signs and Symptoms
¢' Morning stiffness lasting >30 min in 5036of patients
6 Patients may present with less joint tenderness than is usually seen in RA
6 Dacrylitis may be noted in >40% of patients"’
'0' Ridging, pitting ofnails. onycholysls —up 90%of patients vsnall changes in only
40%of psoriasis cases2’

40. Main Features of Psoriatic Arthritis
• Psoriasis of skin and
nails
• Rhe‹anatoid lactor
(RF) g Anti-
chrulllzscted protein
• PecJpherel arthrffs
• Distal Interphalang e
“
• Dactylkis
• Elevated Acute
Phase•‘
mserptionc
• M bone ptoMn R
• 8yndaamophytes •

41. Dactylltls
Clinical Features in Psoriatic Arthritis
Enthesltis

42. '6' NSAIDS
•f• DMARDS
• MTX
• £eflunDmlde
• Sutfasalazlne
• Cyclosporine
• TNF a inhibitor
4' Coordlnate b/w Rheumatology and Dermetology
Treatment