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RHEUMATOID ARTHRITIS
INTRODUCTION
 A chronic inflammatory disease
 Unknown aetiology
 Symmetrical polyarthritis
 Chronic inflammation resulting in joint damage
and physical disability
 Systemic involvement is common
 Fatigue/Anemia
Extra Articular features
 Sub cutaneous nodules(on knuckles)
 Pleural nodules
 Pericarditis
 Peripheral neuropathy
 Vasculitis
 Kerato conjunctivitis sicca
 Episcleritis
 Xerostomia
CLINICAL FEATURES
 Age : 25 to 55 years
 Sex : Female predominance
 Early morning joint stiffness lasts for half to one
hour, gets eased with activity
 Earliest joints involved :
 Small joints of hand and feet
 Usually monoarticular
 Oligoarticular
 Polyarticular
 Usually symmetrical
 Results in inflammation of joints tendons and
bursae
 Frequently involved joints
 MCP
 DIP
 PIP
 Flexor tendon synovitis(Hallmark of RA)
 Decreased ROM
 Decreased grip strength
 Trigger finger
 Irreversible deformities with destruction of joints and
soft tissue
 Ulnar deviation
 Subluxation of MCP joints
 Subluxation of proximal phalynx
 Subluxation of volar side
 Z line deformity
 Piano key movement
 Flat feet(Pes Plano valgus)
 Main target of RA are 14 joint groups
 PIP
 MCP
 Wrist
 Elbow
 Knees
 Ankle
 MTP
 Does not affect thoracic, lumbar spine and rarely temporo-
mandibular joint.
 Constitutional
 Loss of body weight
 Malaise
 Fever
 Fatigue
 Cachexia
 Depression
 Temperature >101*F
Nodules
 30-40%
 Benign subcutaneous nodules
 Common sites
 Forearm, sacral prominence, achilles tendon
 Lung, Pleura
 Pericardium
 Peritoneum
 Firm, non tender
 Adherent to periosteum, tendon, bursae
 Sign of increased disease activity
 Associated with infection, ulceration and gangrene
COMPLICATIONS
 Sjogren’s syndrome: 10% of RA patients
 Kerratoconjunctivitis sicca
 Xerostomia
 Pulmonary
 Pleuritic chest pain
 Friction rub
 Effusion-exudative
 Nodules
 Interstitial lung disease
 Symptoms: cough, SOB,
 Diagnosis:HRCT, Restrictive pattern in PFT
 Very poor prognosis
 Bronchiolitis
 bronchiectasis
 Cardiac
 Pericarditis
 Cardiomyopathy
 Myocarditis
 CAD
 Amyloid infiltration
 Vasculitis
 Rare <1%
 Long standing disease
 RA positive
 Cutaneous signs
 Petechiae
 Purpura
 Digital infarcts
 Gangrene
 Livedo reticularis
 Painful ulcerations
 Heamotological
 Anaemia
 Correlates well with increased CRP/ESR
 Increased platelets(APR)
 Thrombocytopaenia
 Felty’s
 Neutopenia
 Spleenomaegaly
 Nodular RA
 T-LGL with enlarged spleen and neutopenia
 Lymphoma: 2-4% incidence
 Most common- large B Cell lymphoma
 Cardiovascular
 Common cause of death
 Atherosclerosis/CAD
 Higher in RA, even after risk factors
 CHF- 2 fold higher
 Osteoporosis
 20-30% incidence
 Generalized bone lossimmobility
 Fracture hip common
 Treatmnert with cortisone
 Androgrenism
 Old aged male – decreased testosterone
 Post menospausal
 Note-increased testosterone levels offer protection from RA in
younger males.
Epidemiology
 RA seen in 0.5 to 1% of population
 Varies based on geographical location
 0.2-0.4% in africa/asia
 7% in native americans tribes in america
 Female:male ratio 2-3:1
 Incidence more in latin america
 Possible role of estrogens in its pathogenesisin
enhancing immune response
 As this stimulates TNF-a a major cytokine in RA
pathogenesis
 Genetic considerations
 First degree relatives share RA 2-10 times
 Twins upto 60%
 Alleles in RA located in MHC
 1/3rd genetic risk rests in this locus
 In HLA-DRB1 gene
 Encodes the MHC-II B chain
 Groups of alleles collectively identified as Shared
epitopes
 Include HLA-DR4(DRB1:0401, DRB1: 0101)
 Genetic susceptibilty in indians to RA with highest risk
with DRB1 0405 DRB1 0401
 DQB1:0302-DR4 haplotypes
 Certain HLA-DR alleles are protective for RA. Eg:
DRB1:1502, DRB1: 0403
 Environmental factors
 Cigarette smoking: risk increases 1.5-3.5 times,
higher risk in twins
 Increased anti CCP antibodies in RA
 Recurrent insult to mucosa of airways leads to low
grade inflammation activating innate immune system
 Infective: EB virus, parvovirus
 Women: 2-4 times higher risk
 Role of hormones, pregnancy
PATHOLOGY
 Synovium-primary site of inflammation
 Hypertrophied intima layer(seen as 10 cell layer)
 Increase in number of synoviocytes
 Microvascular injury/thromvbosis of sub intimal
region
 Neovascularization
 Hyperplasia and increased cellularity
 Pannus
 Consists of edema of synovium
 Overgrowth
 Villious projections
 Protruding into joint cavity
 Cytokines
 TNF-a from macrophages of synovium
 Triggers inflammation cascade
 Inbalance between pro and anti inflammatory cytokines
 Chronic inflammatory synovitis
 RH Synovitis
 Variable number of B-cells
 Polyclonal increase in immunoglobulins
 Auto antibodies production
 Lymphoid aggregates coupled with CD4+Th1, Th17 and t-helper,
memory cells
CLASSIFICATION OF RA
LAB INVESTIGATIONS
• ESR
• CRP
• Reversal of alb/globulin ratio
• Raised serum alkaline phosphartase
• Hepatic enzymes
• RBS
• Renal parameters
• RA factor
• Anti-CCP
• Imaging
• MRI : Periarticular osteopenia
• Narrowing of joint space
• Loss of cartilage of joint
TREATMENT OF RA
 Damage, disability seen during first few months to
two years
 Delay of 3-4 years is disastrous
 Plan for early and aggressive treatment
programme
 To combine medical, surgical and rehabilitative
procedures.
Goals of Treatment
 To suppress joint inflammation
 To maintain joint function
 To prevent deformities
 To repair damage
 To relieve pain
 To improve function/mobility of joint
Basic principles
 Early diagnosis for better outcome
 Accurate objectified assessment of disease
activity
 Aggressive treatment with disease modifying
drugs
 As monotherapy or in combination
 Step-up, step-down, saw tooth strategy
 Methotrexate is the anchor drug which prevents
damage to joints or any other complications
 Judicious use of corticosteroids is better
Methotrexate
 Initial choice of DMARD
 Indicated in RA with
 Synovitis
 Myositis
 Felty’s with leukopenia
 Evidence of increased disease activity
 A purine inhibitor and folic acid antagonist
 Clinical response in 4-8 weeks
 Start with 7.5 mg to 10mg weekly once and increment of 2.5-5mg every month to
be followed
 Contraindicated in pregnancy, hepatic and renal impairment
 1-2mg folic acid to reduce toxicity
 Side effects
 GI intolerance
 Stomatitis/Headache
 Rash/Alopecia
 BM suppresion with higher doses
 Cirrhosis of liver
OTHER DRUGS
NSAIDS SULFASALAZINE HCQ
•Non selective
•Acetic acid deriviative
•Indomethican
•Etodolac
•Anthranilic acid
•Mefanemic acid
•Aryl propionic acid
•Ibuprofen
•Naproxen
•Ketoprofen
•Enolic acid
•Piroxicam
•Meloxicam
•Good in seronegative
•500mg orally
•Weekly increments by
500mg upto 2-3 months
•Response in 6-10
weeks
•Avoid in sulpha allergy,
G6PD defeciency
•High toxicity
•Nausea
•Frequent monitoring of
CBP and LFT required
•Anti malarial used in
RA, SLE
•4-6mg/kg/daily
•Response in 4-8
weeks i.e 200-400mg
once daily
•Safe in pregnancy
LEFLUNOMIDE TNF-A INHIBITORS INTERLEUKIN
INHIBITORS
•Pyrimidine inhibitor
•Used in RA treatment
•10-20 mg daily
•Response in 4-8 weeks
•Contraindicated in
pregnancy and hepatic
dysfunction
•GI side effects common
•Diarrhoea in 20% cases
•Loperamide or dose
reduction
•Expensive
•Good in seronegative RA
•In those with poor
response to DMARD’s
•Reduces joint damage
•Monoclonal antibodies with
suffix MAB
•Fusion proteins with suffix
CEPT
•Etenarcept – 50 mg/ week
SC
•Infliximab- 3mg/kg initially
at 2 month/ 6th or 8th weekly
therafter, IV infusin with
methotrexate
•Adalimumab- 40 mg SC
every other week, specific
to TNF-a
•Gulimumab-once a month
•Certolimab- pegylated
humanized FAB fragment of
TNF-a, monthly once
•Anakinra
•Recombinant IL-1
receptor antagonist
•Immunomodulation of
IL-1, inhibits pro-
inflammation
•100mg SC daily
•Not for sepsis
•Tocilizumab
•IL-6 receptor
antagonist
•IV infusion
CONTRAINDICATIONS
 Serious infections/Sepsis
 In active/latent tuberculosis
 CHF or LVEF<30%
 Those for elective surgery
 Local infection site reactions
 Common with SC administration
 Generally self limited
 Serious systemic effects rare
 Other side effects
 Lupin like illness
 Demylienating disorder
 Exacerbations of pre existing multiple sclerosis
 Lymphoma
 Combine therapy
 DMARD’s with two biological agents
 Contraindicated in view of increased infective complications
 NSAID’s selective COX-2 inhibitors as adjunct to DMARD
 Glucocorticoids
 Not curative
 Delays erosions of joints
 Uses
 Patients with constitutional symptoms
 Weight ;loss
 Extra articular features
 Vasculitis
 Episcleritis
 Pleurisy
 Persistent synovitis
 Dose
 5-20 mg daily – prednisolone
 If severe- 1mg/kg body weight
NON PHARMACOLOGICAL
 Acute care of inflamed joint
 Pain relief
 Joint protection
 Keep joint in proper position
 SplintinG if necessary
 Local heat application
 Subacute
 Passive and active joint movement
 Chronic
 Adaptive equipment
 Splints
 Orthoptics
 Mobility aids
 Specific exercises
 Overall cardiac conditioning
SURGICAL
 Synovectomy
 Total joint replacement
 Joint fusion
 Thank you

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Rheumatoid arthritis

  • 2. INTRODUCTION  A chronic inflammatory disease  Unknown aetiology  Symmetrical polyarthritis  Chronic inflammation resulting in joint damage and physical disability  Systemic involvement is common  Fatigue/Anemia
  • 3. Extra Articular features  Sub cutaneous nodules(on knuckles)  Pleural nodules  Pericarditis  Peripheral neuropathy  Vasculitis  Kerato conjunctivitis sicca  Episcleritis  Xerostomia
  • 4. CLINICAL FEATURES  Age : 25 to 55 years  Sex : Female predominance  Early morning joint stiffness lasts for half to one hour, gets eased with activity  Earliest joints involved :  Small joints of hand and feet  Usually monoarticular  Oligoarticular  Polyarticular  Usually symmetrical  Results in inflammation of joints tendons and bursae
  • 5.  Frequently involved joints  MCP  DIP  PIP  Flexor tendon synovitis(Hallmark of RA)  Decreased ROM  Decreased grip strength  Trigger finger  Irreversible deformities with destruction of joints and soft tissue
  • 6.  Ulnar deviation  Subluxation of MCP joints  Subluxation of proximal phalynx  Subluxation of volar side  Z line deformity  Piano key movement  Flat feet(Pes Plano valgus)  Main target of RA are 14 joint groups  PIP  MCP  Wrist  Elbow  Knees  Ankle  MTP  Does not affect thoracic, lumbar spine and rarely temporo- mandibular joint.
  • 7.  Constitutional  Loss of body weight  Malaise  Fever  Fatigue  Cachexia  Depression  Temperature >101*F
  • 8. Nodules  30-40%  Benign subcutaneous nodules  Common sites  Forearm, sacral prominence, achilles tendon  Lung, Pleura  Pericardium  Peritoneum  Firm, non tender  Adherent to periosteum, tendon, bursae  Sign of increased disease activity  Associated with infection, ulceration and gangrene
  • 9. COMPLICATIONS  Sjogren’s syndrome: 10% of RA patients  Kerratoconjunctivitis sicca  Xerostomia  Pulmonary  Pleuritic chest pain  Friction rub  Effusion-exudative  Nodules  Interstitial lung disease  Symptoms: cough, SOB,  Diagnosis:HRCT, Restrictive pattern in PFT  Very poor prognosis  Bronchiolitis  bronchiectasis
  • 10.  Cardiac  Pericarditis  Cardiomyopathy  Myocarditis  CAD  Amyloid infiltration  Vasculitis  Rare <1%  Long standing disease  RA positive  Cutaneous signs  Petechiae  Purpura  Digital infarcts  Gangrene  Livedo reticularis  Painful ulcerations
  • 11.  Heamotological  Anaemia  Correlates well with increased CRP/ESR  Increased platelets(APR)  Thrombocytopaenia  Felty’s  Neutopenia  Spleenomaegaly  Nodular RA  T-LGL with enlarged spleen and neutopenia  Lymphoma: 2-4% incidence  Most common- large B Cell lymphoma
  • 12.  Cardiovascular  Common cause of death  Atherosclerosis/CAD  Higher in RA, even after risk factors  CHF- 2 fold higher  Osteoporosis  20-30% incidence  Generalized bone lossimmobility  Fracture hip common  Treatmnert with cortisone  Androgrenism  Old aged male – decreased testosterone  Post menospausal  Note-increased testosterone levels offer protection from RA in younger males.
  • 13. Epidemiology  RA seen in 0.5 to 1% of population  Varies based on geographical location  0.2-0.4% in africa/asia  7% in native americans tribes in america  Female:male ratio 2-3:1  Incidence more in latin america  Possible role of estrogens in its pathogenesisin enhancing immune response  As this stimulates TNF-a a major cytokine in RA pathogenesis
  • 14.  Genetic considerations  First degree relatives share RA 2-10 times  Twins upto 60%  Alleles in RA located in MHC  1/3rd genetic risk rests in this locus  In HLA-DRB1 gene  Encodes the MHC-II B chain  Groups of alleles collectively identified as Shared epitopes  Include HLA-DR4(DRB1:0401, DRB1: 0101)  Genetic susceptibilty in indians to RA with highest risk with DRB1 0405 DRB1 0401  DQB1:0302-DR4 haplotypes  Certain HLA-DR alleles are protective for RA. Eg: DRB1:1502, DRB1: 0403
  • 15.  Environmental factors  Cigarette smoking: risk increases 1.5-3.5 times, higher risk in twins  Increased anti CCP antibodies in RA  Recurrent insult to mucosa of airways leads to low grade inflammation activating innate immune system  Infective: EB virus, parvovirus  Women: 2-4 times higher risk  Role of hormones, pregnancy
  • 16. PATHOLOGY  Synovium-primary site of inflammation  Hypertrophied intima layer(seen as 10 cell layer)  Increase in number of synoviocytes  Microvascular injury/thromvbosis of sub intimal region  Neovascularization  Hyperplasia and increased cellularity
  • 17.  Pannus  Consists of edema of synovium  Overgrowth  Villious projections  Protruding into joint cavity  Cytokines  TNF-a from macrophages of synovium  Triggers inflammation cascade  Inbalance between pro and anti inflammatory cytokines  Chronic inflammatory synovitis  RH Synovitis  Variable number of B-cells  Polyclonal increase in immunoglobulins  Auto antibodies production  Lymphoid aggregates coupled with CD4+Th1, Th17 and t-helper, memory cells
  • 19. LAB INVESTIGATIONS • ESR • CRP • Reversal of alb/globulin ratio • Raised serum alkaline phosphartase • Hepatic enzymes • RBS • Renal parameters • RA factor • Anti-CCP • Imaging • MRI : Periarticular osteopenia • Narrowing of joint space • Loss of cartilage of joint
  • 20. TREATMENT OF RA  Damage, disability seen during first few months to two years  Delay of 3-4 years is disastrous  Plan for early and aggressive treatment programme  To combine medical, surgical and rehabilitative procedures.
  • 21. Goals of Treatment  To suppress joint inflammation  To maintain joint function  To prevent deformities  To repair damage  To relieve pain  To improve function/mobility of joint
  • 22. Basic principles  Early diagnosis for better outcome  Accurate objectified assessment of disease activity  Aggressive treatment with disease modifying drugs  As monotherapy or in combination  Step-up, step-down, saw tooth strategy  Methotrexate is the anchor drug which prevents damage to joints or any other complications  Judicious use of corticosteroids is better
  • 23. Methotrexate  Initial choice of DMARD  Indicated in RA with  Synovitis  Myositis  Felty’s with leukopenia  Evidence of increased disease activity  A purine inhibitor and folic acid antagonist  Clinical response in 4-8 weeks  Start with 7.5 mg to 10mg weekly once and increment of 2.5-5mg every month to be followed  Contraindicated in pregnancy, hepatic and renal impairment  1-2mg folic acid to reduce toxicity  Side effects  GI intolerance  Stomatitis/Headache  Rash/Alopecia  BM suppresion with higher doses  Cirrhosis of liver
  • 24. OTHER DRUGS NSAIDS SULFASALAZINE HCQ •Non selective •Acetic acid deriviative •Indomethican •Etodolac •Anthranilic acid •Mefanemic acid •Aryl propionic acid •Ibuprofen •Naproxen •Ketoprofen •Enolic acid •Piroxicam •Meloxicam •Good in seronegative •500mg orally •Weekly increments by 500mg upto 2-3 months •Response in 6-10 weeks •Avoid in sulpha allergy, G6PD defeciency •High toxicity •Nausea •Frequent monitoring of CBP and LFT required •Anti malarial used in RA, SLE •4-6mg/kg/daily •Response in 4-8 weeks i.e 200-400mg once daily •Safe in pregnancy
  • 25. LEFLUNOMIDE TNF-A INHIBITORS INTERLEUKIN INHIBITORS •Pyrimidine inhibitor •Used in RA treatment •10-20 mg daily •Response in 4-8 weeks •Contraindicated in pregnancy and hepatic dysfunction •GI side effects common •Diarrhoea in 20% cases •Loperamide or dose reduction •Expensive •Good in seronegative RA •In those with poor response to DMARD’s •Reduces joint damage •Monoclonal antibodies with suffix MAB •Fusion proteins with suffix CEPT •Etenarcept – 50 mg/ week SC •Infliximab- 3mg/kg initially at 2 month/ 6th or 8th weekly therafter, IV infusin with methotrexate •Adalimumab- 40 mg SC every other week, specific to TNF-a •Gulimumab-once a month •Certolimab- pegylated humanized FAB fragment of TNF-a, monthly once •Anakinra •Recombinant IL-1 receptor antagonist •Immunomodulation of IL-1, inhibits pro- inflammation •100mg SC daily •Not for sepsis •Tocilizumab •IL-6 receptor antagonist •IV infusion
  • 26. CONTRAINDICATIONS  Serious infections/Sepsis  In active/latent tuberculosis  CHF or LVEF<30%  Those for elective surgery  Local infection site reactions  Common with SC administration  Generally self limited  Serious systemic effects rare  Other side effects  Lupin like illness  Demylienating disorder  Exacerbations of pre existing multiple sclerosis  Lymphoma
  • 27.  Combine therapy  DMARD’s with two biological agents  Contraindicated in view of increased infective complications  NSAID’s selective COX-2 inhibitors as adjunct to DMARD  Glucocorticoids  Not curative  Delays erosions of joints  Uses  Patients with constitutional symptoms  Weight ;loss  Extra articular features  Vasculitis  Episcleritis  Pleurisy  Persistent synovitis  Dose  5-20 mg daily – prednisolone  If severe- 1mg/kg body weight
  • 28. NON PHARMACOLOGICAL  Acute care of inflamed joint  Pain relief  Joint protection  Keep joint in proper position  SplintinG if necessary  Local heat application  Subacute  Passive and active joint movement  Chronic  Adaptive equipment  Splints  Orthoptics  Mobility aids  Specific exercises  Overall cardiac conditioning
  • 29. SURGICAL  Synovectomy  Total joint replacement  Joint fusion