Arthritis ? Flashcards
What are the different types of Arthritis ?
0 Rheumatoid Arthritis
0 Septic
0 psoriatic
0 osteoathritis
athro - joint
Iitis - inflammation
2 main types od groups
Degenerative - Osteoathritis
Inflammatory - Rheumatoid , Psoriatic , Reactive , Ankolysing Spondylitis , Juvenile inflammatory arthritis , Septic , Viral (associated with hepatitis or HIV , Para virus ,EPV) , Gout & Pseudo gout (Crystal acute arthritis ) , Arthritis associated with connective tissue diseases (CTD)
What is Psoriatic arthritis ?
What causes it ?
Psoriatic athritis
Psoriasis - autoimmune disease
Arthritis - joint inflammation
Joint inflammation that happens in people with arthritis
0 Chronic & progressive
Type of Seronegative Spondyloarthropathies
Serongative - no auto antibodies linked to them
Spondyloarthropathies- autoimmune conditions that affect joints
CAUSE
0 specific form of HLA - B27 + environmental trigger e.g trauma , infection
Have a particular form of HLA - B27 —————————> which leads to autoimmune process ———————-> self antigens seen as foreign ——————————-> T cells release cytokines stimulating inflammation ———————–> IL 23 , 1L -12 and TNF ( Tubular necrosis factor ) also released —————————-> triggers keratinocytes & fibroblasts to proliferate —————————-> Psoriatic plaque formation
mmune system attacks self antigens in joints )———————————–>
( HLA - B27 - encodes for protein MHC 1 - presents molecules from inside the cell on it surface to Cytotoxic T cells - will determine if it is self or no self )
Common symptoms of PA ?
0 Pain
0 Swelling
0 Stiffness
0 Inflammation - usually warm to the touch.
Types of PA ?
0 Oligoarticular -
o mild
o asymmetric
o affects less
than 5 joints.
0 Polyarticular / Rheumatoid pattern
o resembles RA
o symmetric
o affects more
than 5 joints
( hands, feet , wrist , ankles )
0 Spondyloarthritis,
o distal
o asymmetric
o involves spine
& sacroiliac joint
( causes fusion of vertebral bodies - causes stiffness of neck & sacroiliac joint )
0 Distal interphalangeal predominant
o affects joints at
end of fingers
and toes.
causes : nail abnormalities : o ridging o pitting Dactylitis - severe inflammation of finger and toe joint - look like sausages. -
Over time can develop severe bone erosion. - finger deformities
0 arthritis mutilans
o extensive bone erosion ——————-> deformity - opera glass hand characteristic.
Diagnosis of PA ?
Blood tests for:
o RA factor ,
o Anti
Citrullinated
protein
antibodies
( NORMALLY PRESENT IN RA but absent in Psoriatic arthritis )
X - ray show joint erosion
pencil & cup radiographic sign .
Treatment of PA ?
PAIN
0 NSAIDS
Severe cases
0 Immunomodulatory drugs
- Sulfsalazine
- Methotrexate
0 Biological response modifiers
TNF–inhibitors,
o Infliximab,
o Etanercept
o Adalimumab,
block the actions of tumor necrosis factor alpha
IL-12/IL-23 inhibitor o Ustekinumab
blocks the actions of the interleukins.
Surgery
- repair of damage hip , knee joints.
- spinal surgery - risky - rarely done.
What is Septic arthritis ?
Infectious / septic arthritis
- Arthritis caused by a microbe
- usually caused by bacteria infection in the joint .
from :
previous infection - in bone , or spread through blood.
ex - nail into knee
o synovial membrane infected by bacteria from environment or from skin surface (- shoved into knee when skin pierced)
Bacteria destroy articular cartilage with their toxins e.g enzymes that digest collagen in articular cartilage
PAMPs ———————-> immune response ————–> macrophages release IL - 1 , Tumour necrosis factor released ( pro - inflammatory molecules ) - immune cells recruited
2. Mast cells release histamine ——-> vasodilation (increased vascular permability ) ————————> more blood flow to area ——————–> joint looks red, swollen , red.
PROBLEM
0 fluid is leaking out ———–> too much ————–> increased inter -articular pressure —————–> compressed BV ————–> necrosis of affected joint & bone —————————-> joint destruction
What is Septic arthritis ?
Infectious / septic arthritis
EMERGENCY - Complete destruction of joint - rapid.
- Arthritis caused by a microbe
- usually caused by bacteria infection in the joint .
from :
previous infection - in bone , or spread through blood.
ex - nail into knee
o synovial membrane infected by bacteria from environment or from skin surface (- shoved into knee when skin pierced)
Bacteria destroy articular cartilage with their toxins e.g enzymes that digest collagen in articular cartilage
PAMPs ———————-> immune response ————–> macrophages release IL - 1 , Tumour necrosis factor released ( pro - inflammatory molecules ) - immune cells recruited
2. Mast cells release histamine ——-> vasodilation (increased vascular permability ) ————————> more blood flow to area ——————–> joint looks red, swollen , red.
PROBLEM
0 fluid is leaking out ———–> too much ————–> increased inter -articular pressure —————–> compressed BV ————–> necrosis of affected cartilage & bone —————————-> joint destruction
Types of SA ?
Symptoms of SA ?
Fever
Impaired range of motion
joint pain
(regard hot , swollen , acutely painful joint with restricted movement as septic athritis until proven otherwise)
2 types
Non - gonococcal athritis -
o usually affects 1 joint
o usually caused by S. aureus - can completely destroy joint within days.
Gonococcal athritis - less common (but more common in young adults - sexually active)
o causes - Neisseria gonorrhoeae (usually affects sexually active adolescents.)
- if Gonorrhoeae is present should refer to sexual health clinic for counselling on safe sex & testing for other sexual health disease (HIV , Chalamydia etc.)
o spreads hematogenously - from cervix , urethra , pharynx.
o multiple joints affected.
o multiple skin lesions
o Tenosynovitis - inflammation of muscle tendon.
o spread from bone if osteomyelitis present.
DIAGNOSTIC FACTORS
- Hot , swollen , painful, restricted joint
- Acute presentation - symptoms present for less than 2 weeks.
(delays in presentation can occur with TB or prosthetic infections) - Fever
- Monarticular - one joint - most common
(but some have oligoarticular / polyarticular. ) - Prosthetic joint
(always suspect if have this ) - in patients who have underlying joint pathology e.g RA , OA - look for symptoms which are disproportional to their joints - higher risk of SA - immunosuppressants , ANTI - TNF drugs (biological therapy does seem to increase risk )
Lyme athritis - bacteria from lyme disease can infect joint. - lyme disease - are diseases caught
MOST COMMON JOINTS AFFECTED
- Knee - most common
(can also effect shoulder , ankle , elbow , wrist)
RISK FACTORS
- Sexual activity
- Prostethic joint - refer to orthopedics.
- Underlying joint patholgy
- Immunosupression
- IV drug injection - either IV drug misuse of iatrogenic - (intra - articular steriod injection)
-Recent joint surgery - ## other infection
Diagnosis of SA ?
Test synovial fluid - joint aspiration
usually find ;
- looking for Gram stain (MOST IMPORTANT) -
if present (DBSAT)
o high WBC count
o positive culture
0 Blood culture (DBSAT)
Imaging
- bone erosion
- joint effusions
(Joint particularly painful - level of pain seems usual )
WBC
0 ESR
0 CRP
(however , synovial fluid analysis is more important e.g. absence of raised ESR , CRP does not exclude joint infection)
0 Urea & Electrolytes - sepsis , end organ damage
0 LFTs - used to assess for sepsis and end organ damage.
0 Plain X rays
0 Ultrasound
Treatment of SA ?
SUSPECTED/ CONFIRMED SYSTEMIC INVOLVEMENT - SEPSIS PROTOCOL
SUSPECTED/ INFECTED PROSTHETIC JOINT - refer to orthopaedics for ultrasound guided joint aspiration
antibiotics
Pain medication , consider analgesia
if CONFIRMED - refer for surgery to othropaedics.
SUSPECTED INFECTED JOINT -
inaccessible - referral to orthopaedics
accessible - empirical antibiotics + joint aspiration , consider analgesia.
CONFIRMED INFECTED JOINT - NO SYSTEMIC INVOLVEMENT
1ST LINE
0 Pathogen targeted antibiotics
(2 weeks IV unless patient shows lack of response, then start oral 4 weeks) + Joint aspiration ( relieve pressure & remove infection) , consider analgesia
- check signs of re- emergence of infection - 24hrs - 48hrs after starting oral treatment before discharging.
UNCONFIRMED INFECTION - NO SYSTEMIC INVOLVEMENT & responding to empirical antibiotics - continue + joint aspiration , consider analgesia
if not responding:
1ST LINE
- Senior clinician review + joint aspiration , consider analgesia.
(could be bcc of incorrect diagnosis , causative organism , antibiotic therapy , infection elsewhere etc.)
Athrocentesis ( joint aspiration )& wash out
Surgery - athrotomy
What is reactive arthritis ?
inflammation joint after occurrence of an infection e.g . STI , gastroenteritis .
seronegative spondyloarthropathies.
most have HLA -B27 gene - encodes for MH1
usually start 2 - 3 weeks after initial infection
tissues of the joint spaces, but occasionally, the immune system also attacks tissues like the lining of the urethra and the conjunctiva.
0 Reiter syndrome - if all 3 are affected
cevix , pericardium can be involved.
Osteoathritis vs aging
Articular cartilage
Aging
1. Water - decreased
- Less elastic (stiffness increased)
- Chondrocytes - fewer but increased size.
- Collagen - increased collagen - crosslinking / brittleness.
Osteoarthritis
- Water Increased
- More elastic - stiffness decreased.
- Chondrocytes - cells cluster 9at a late stage)
- Collagen - disorganised - increased collagenase.
What carpal bone gets fractured the most ?
Scaphoid bone - usually caused by falling on an outstretched hand.
SIGNS
0 Pain & tenderness in anatomical snuffbox. (triangular area on radial aspect of carpal bones )
proximal pole fracture - bottom 1/3rd of scaphoid bone
Distal pole fracture - top 1/3rd of the bone. (scaphoid bone has retrograde blood supply e.g BV enters wrist and supplies the bone closest to the fingers then comes back to carpal bones ————————-> distal part (top) supplied first - no direct blood supply to proximal part.
- As a result , risk of avascular necrosis to proximal part - if fracture in middle (waist) of bone.
- if scaphoid fracture is missed - likely to develop osteoarthritis in the future.
Old fashioned terms to describe problems with joint?
- just for knowledge.
Calor - heat in joint Dolor - pain Rubor - redness Tumor - swelling Rigor - stiffness Penuria / Inertia - obstruction of movement.
Main site of osteoarthritis ?
Hips - OA of the hip may cause secondary gluteal muscle weakness (positive Trendelenburg test - The unilateral leg stand orTrendelenburg testis a useful procedure for detecting hip-joint dysfunction - unable to maintain the pelvis horizontal to the floor while standing first on one foot and then on the other foot )
- also cause positive thomas test ( one knee flexed - affected side ( sacrum and lower back lift and dont remain on table/ couch) due to causing fixed flexion deformity.
knees
Pain in the knee - if your overweight or starts without any significant trauma - in one place
Primary -. age , overuse , degeneration
Secondary - caused by other conditions e.g -
- inflammatory arthritis causes damage —————> can lead to osteoathritis development in same joint.
- Gout
- Haemochromotosis - usually get arthritis in fingers if they present with osteoarthritis
- Alkaptonuria
- EDS - ehlos danros - hyper mobile joints - frequent dislocation - so damage to joint.
RA
Worse when resting / night
movement makes pain worse.
extra - articular features - inflammation effects other parts of the body e.g pericarditis , uveitis , etc.
Rheumatoid factor
Anti - CCP
(if you have this high supscisionof RA)
BUT people can have RA but not the antibodies
RA
Worse when resting / night
movement makes pain worse.
extra - articular features - inflammation effects other parts of the body e.g pericarditis , uveitis , etc.
Rheumatoid factor
Anti - CCP
(if you have this high supscision of RA)
BUT people can have RA but not the antibodies
ra - days to weeks (rapid)
pseudogout - within hours to days (very rapid , upon joint aspiration - crystals)
(onset)
What is Osteoathritis ?
Degnenerative joint disorder - degradaton of cartilage , subchondral bone (bone just below the cartilage) , subchondral scleroisis & cysts , osteophyte formation
PRESENTATION
- Joint pain - linked with weight bearing , physical activity (vs RA which is worse with inactivity, OA is better at night / with rest)
- Stiffness - the stiffness in your joints is not there in the mornings, or lasts lessthan 30 minutes
(Shorter duration of symptoms than RA , PA) - Functional limitation/difficulties
o knee locking/giving way.
o limited range of movement
0 Malaligment - OA can cause Knocked knees (Genu valgum) or Bow legs (Genu varum)
0 Creptius - audible, palpable creaking evident on active & passive movements.
JOINTS AFFECTED - USUALLY
o Knee
o Hip
O hand (effects DIP - Distal interphalangeal joint & Proximal interphalangeal (PIP)joint -
not MCP *-metacarpophalangeal joint
0 if PIP affected - Bouchard’s nodes form
0 if DIP affected - Heberden’s nodes form)
*also squaring at the base of the thumb , in advance OA - new bone formation - causes bony swellings around the knee joint)
( SHOULDER , ELBOW , WRIST , ANKLE INVOLVEMENT LESS LIKELY UNLESS UNDERLYING INJURY)
- also usually lacks the swelling , redness and inflammatory signs seen in inflammatory athritis.
o Spine (Lumbar/cervical)
RISK FACTORS
0 Age - above 50 0 Female 0 Fx of OA 0 physically demanding job/sport. 0 Obesity 0 Knee malalignment - e.g. bow legs , knocked legs.
Investigations of Osteoathritis ?
OA is a clinical diagnosis - so X rays not done rountine.
0 X ray of affected joint
TO RULE OUT DIFFERENTIAL DIAGNOSIS
0 Serum CRP - normal
0 Serum ESR - normal
0 Rheumatoid factor (RF)
or Anti - CCP (anti-cyclic citullinated peptide antibody) - NEGATIVE-
- indicates RA but could have a mixed pathology.
MRI - done in complex OA - spine involvement with neurological deficits e.g looking for spinal stenosis , nerve root entrapment.
Treatment of OA?
ATHRALGIA - JOINT PAIN
1st line - Topical analgesia
e.g. NSAIDs topical (particularly for hand & knee invlovement- not sure for rest of body):
- Diclofenac epolamine topical
- Diclofenac topical
- methylsalicylicate
- Ketoprofen
or other topical analgesia:
- Capsacin topical
PLUS - Non pharmological approaches e.g excercise , education (Physical activity & exercise, weight loss -if overweight ) physiotherapy , occupational therapy
ADJUNCT - intra -articular corticosteroid s (but being phased out. ) - IF NSAIDS CONTRAINDICATED/ NOT TOLERATED.
e. g methylprednislone acetate
- Triamcinolone acetonide.
2ND LINE
Topical analgesia + Paracetamol
adjunct - same as 1st line.
3RD LINE - oral NSAID (IBU , Diclofenac sodium or potassium , Celecoxib , meloxicam etc. ) + Paracetamol + Topical C
adjunct - same 1st + additional Viscosupplementation with intra- articular Hyaluronic acid ( e.g Sodium Hyaluronate - hyaluronic acid - thick fluid that improves lubricating properties of synovial fluid. )
GASTROPROTECTION - should be considered for all patients on long term NSAID treatment.
4TH LINE - ADD A OPIOD TO THIRD LINE
adjunct - same as rest + Duloxetine
Duloxetine - SNRI (antidepressant m nerve pain , etc)
PARACETAMOL OFTEN OFFERED WITH T NSAIDS AS FIRST LINE.
PERSISTENT PAIN DESPITE MULTIPLE TREATMENTS OT SEVERE DISABILITY.
1st line - surgery (joint replacement e.g total knee replacement)
adjunct - while awaiting surgery e.g topical & oral analagesia , Duloxetine , gastroprotection , viscosupplementation , intra-articular steriod injections.
What is Rheumatoid athritis ?
Chronic inflammatory condition.
CHARACTERISTICS
- joint pain
- Joint swelling
- morning stiffness (for longer than 1 hour - indicative of inflammatory condition - not RA specific)
(Often multiple & bilateral)
0 extra - articular features - inflammation effects other parts of the body e.g pericarditis, Pleuritis (may cause Pleuritic chest pain) , uveitis & Scleritis , etc. , Vasculitis - Seen in some cases of severe RA.
Uncommon
- May see Rheumatoid nodules
or Ulnar deviation of fingers. - swan neck defomity
(DIP) hyperflexion with proximal interphalangeal (PIP) hyperextension.)
or
Boutonniere’s deformity - opposite of swan neck
- proximal interphalangeal (PIP) flexion with distal interphalangeal (DIP) hyperextension.
Suspect RA - if active symmetrical athritis lasting longer than 6 weeks.
MOST COMMON JOINTS AFFECTED
0 MCP - metacarpalphalangeal
0 PIP - proximal interphalangeal
(usually affects small joints of the hand and feet & elbow , wrist ,ankles vs Osteo - Hips , knees)
RISK FACTORS
- Fx of RA
- Smoking - weak
- Age (mean age of incidence- 50 - 55 years (most common)
e. g most cases seen 40s , 50s - Female - higher risk of autoimmune conditions.
Investiagation of RA?
0 Rheuamtoid factor - autoantibody - seen RA but also chronic infections, rheumatological conditions .
- (30 % of RA patients can be RF negative)
Levels above - 1000U should prompt investigation for other causes -
0 Hepatitis
0 Cryoglobulinaemia ( blood proteins (cyroglobulins) that clump together in the cold & cause & inflammation organ damage - usually accompanied with a rash(purpura - red spots or purple bruises usually over lower legs).
0 Anti CCP antibody
(positive in 70 % of patients) - can be positive in some RF negative patients.
0 Radiographs - erosions
0 Ultrasonography - synovitis of wrist & fingers.
Treatment of RA?
MILD 1ST LINE - conventional DMARD - one of these (methotrexate is preferred) 0 Methotrexate 0 Sulfasalazine 0 Hydroxychloroquine 0 Leflunomide
ADJUCNT - Folic acid supplementation when methotrexate is used)
Hepatitis B & C , FBC , LFTS , PPD - purified protein derivative — need to be checked before starting conventional DMARDS)
ADJUNCT - Corticosteriod
(if giver daily e,g oral vs injection - Vitamin D & Calcium supplementation needed)
ADJUCNT - NSAID
MODERATE
1ST LINE
Methotrexate
ADJUNCT - Biological/ targeted DMARDSs
Subgroups ANTI TNFs- 0 Infliximab 0 adalimumab 0 Certolizumab 0 golimumab 0 eneterocept (mumabs)
0 Rituximab
IL- 6 inhibitors
0 Sarilumab
JAK 2 inhibitors 0 Tofacitinib 0 Baricitinib 0 Upadacitinib (citinibs)
(all biological DMARDS are injections & infusions)
ADJUNCT - same as mild
PREGANT OR PLANNING PREGNACY
1ST LINE - Corticosteriod + Sulfasalzine or Hydrochloroquine
(Metho & Lenfluomide - tetragenic - foetal abnormalities - not used in pregnancy)
FAILURE TO REPRESS DISEASE AFTER 3 MONTHS OF THERAPY - NOT FOR PREGNANCY
1ST LINE
Methotrexate + Biological agent or DMARD
ADJUCNT - steroids, NSAIDS
2ND LINE
Triple therapy with conventional DMARDS
(not used anymore really because of the emergence of biological/ Targeted DMARDS)
