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)
What are lytic lesions?
Lytic lesions — spots where bone tissue has been destroyed — can be seen in other cancers, including breast cancer, lung cancer and kidney cancer. They can also be seen with infections of bone and even in some benign conditions. Taking a biopsy of one of the lytic lesions may help with your diagnosis.
Appear as a hole on x ray due to decreased bone density.
What are the differential diagnoses for acute mono articular athritis ?
INFLAMMATORY CAUSES
- Infection (Septic Athritis)
- Reactive Athritis (Reiters syndrome)
- Pseudogout/gout (Crystal induced)
- RA
- Connective tissue disease , seronegative spondyloarpathy
NON- INFLAMMATORY CAUSES
- Trauma (haemarthrosis, effusion)
- (Haemarthrosis -Bleeding into joint cavity - if secondary to injury occurs within minutes—– if occurs spontaneously suggests underlying coagulation disorder e.g haemophilla - Non-traumatic haemarthrosis (coagulopathy)
(HAEM - BLOOD , ATHROSIS - JOINT ARTICULATION) - Sickle cell crisis Gout & pseudogout
( common causes in the older population, and usually have some underlying reason to have an elevated serum urate or calcium.)
- Sickle cell crisis should be considered in any Afro - Caribbean patient with acute bone or joint pain
(SICKLE CELL CRISIS - Painful episodes that can last up to a week on average - abnormal shape of RBC can block BV leading to pain) - main symptom of sickle cell (also increasd risk of infection & anaemia)
What is Perthes’s disease?
CHARACTERISTICS
- RISK FACTORS
- DIAGNOSIS
(Legg - Calve- Perthes disease)
Uncommon & Self limiting
Interruption to blood supply femoral head causes bone to deterioration.
(Avascular necrosis of femoral head)
CHARCTERISTICS
0 Pain
0 Limp
0 Limited range of movement at Hip joint.
RISK FACTORS
0 Age - young (4-8 most common ) (2-12) - the older the onset , the more likely to be severe.
0 Male - more common
DIAGNOSIS
- Bilateral hip X rays.
can do:
ESR , FBC , CRP etc.
(Self - limiting - bcc revalsculation occurs (new BV) and reossification (new bone in affected area)
Treatment of Perthes disease?
ACUTE PAIN
1ST LINE
- Pain relief (PARA , IBUPRO)
0 ONGOING
UNDER 5
1ST LINE
Mobilizing therapy + monitoring (M+M)
if lateral extrusion (bulge etc) - then non surgical containment with brace , cast, splint etc.)
5 TO 7
0 epiphyseal involvement less than 50%
1ST LINE
(M + M)
0 Greater than 50%
1ST LINE
Surgical containment (SC)
7 TO 12
0 Stage 1-2
(1st line - SC)
0 Stage 3-4 ( 1st line - Salvage procedure - SP)(SC is contraindicated in this group)
OVER 12
No Athritis
(1st line - SP)
Athritis
(Hip replacement - after sketetal maturaity)
Treatment get more serious as age increases as younger people’s bone repairs better.
What is Gout ?
Common type of inflammatory arthritis
Hyperuricemia ( too much uric acid in the blood ————-> Uric acids crystals form and deposit in joints & Tissues—————-> joint pain , swelling , effusion ,warmth , erythema (redding of skin), tenderness.
MOST COMMONLY FOUND IN BIG TOE. (and foot in general)
- mostly mono-articular or oligoarticular but can be poly
DIAGNOSTIC FACTORS
- Rapid onset - severe pain
(Can pin point when severe pain occurred - ACUTE ATTACK) - Joint stiffness
- (Limited movement of affected joint)
- Swelling , effusion
- Tenderness
- Tophi (Large visible bumps made uric acid crystals)
RISK FACTORS
- Age - Older (risk increases with age )
- Male sex
- Consumption of red meat , seafood, alcohol
SOME MEDICATIONS
- Use of diuretics
- Ciclosporin (Cyclosporin) or Tarcolimus
- Pyrazinamide (Tuberclosis medication)- CONTRAINACTED IN GOUT
- Aspirin
Diagnosis of Gout ?
Athrocentesis with synovial fluid analysis .
(Will find negative bifringement crystals on microscopy)
CAN CONSIDER
- Serum uric acid level
- Ultrasound
- X ray
(Liver function test - if Hyperuricaemia - high uric acids can cause renal stones & failure)
Treatment of Gout?
Acute gout
1ST LINE
0 NSAIDS
or
Colchicine
( also used to treat FMF - Familial Mediterranean fever - inherited inflammatory condition
If these not tolerated;
Corticosteriods (Pred , methylpred ,etc) oral or single IM injection(if oligoartic ) intra articular (if mono)
2ND LINE
IL - 1 inhibitors
e.g. Anakinra , Canakinumab
ONGOING - Recurrent gout - 2-3 weeks after acute episode
ALL ARE URATE LOWERING DRUGS
1ST LINE
0 Allopuriol
(urate lowering drug)
2ND LINE
0 Febuxostat
3RD LINE
0 Probenecid or Sulfinpyrazone
4TH LINE
0 Pegloticase (associated with anaphylaxisis and serious hypersentivity reactions)
PLUS - Suppressive agent (needed during initiation & tapering of urate lowering drug( NSAIDS , Colchicine (Low dose)
(FOR ALL LINES TREATMENT)
In particular it is important to advise the use of urate-lowering therapy to people with:
Two or more attacks of acute gout in 12 months.
Tophi.
Chronic gouty arthritis.
Joint damage.
Renal impairment (eGFR less than 60 ml/min).
A history of urinary stones.
Diuretic use.
Young age of onset of primary gout.
What is Pseudogout ?
OTHER NAMES ` calcium Pyrophosphate disease (CPPD)
CPPD crystals build up in joints
DIAGNOSTIC FACTORS
Present similar to Gout often can only be differentiated with analysis of crystals.
- Painful , tender , red & swollen joints
- Joint effusion
(symptoms may look like osteoarthritis - difference is they happen in joints where OA is common at all e.g SHOULDER , WRIST)
RISK FACTORS
- Advanced age
- Injury / joint surgeries especially involving menicus of knee
- Hyperparathyroidism ( linked to hypercalcemia ) (calcification)
- Haemochromatosis (Iron levels slowly build - inherited ) - athritis - complication of serious cases.
- Family Hx of CPPD
- Hypomagnesemia
(Mg needed to produce co factor to enzyme that degrades Pyrophosphate) - Hypophosphatasi a (lack of Phosphatase enzyme which degrades pyrophosphate.)
CAN BE MONO , OLIGO, POLYARTICULAR!!
Diagnosis of Pseudogout ?
Arthrocentesis with synovial fluid analysis
(Positive birefringent rhomboid crystals)
- X ray of affected ( cartilage calcinosis )
- Serum : Calcium PTH Mg Alkaline Phosphatase ( Enzyme )
- Iron studies?
CAN DO:
0 Ultrasound / CT scan- to confirm CPPD diagnosis
Treatment of Pseudogout ?
Mono / oligo articular
0 JOINT ACCESIBLE TO INJECTION
1ST LINE
- Intra- articular Corticosteriods (IAC)
0 INACCESSIBLE / INJECTION REJECTED
1ST LINE
- NSAIDS
2ND LINE
- Colchicine (C)
0 Treatment failure /contraindication
1ST LINE
- Systemic Corticosteriods (SA)
2ND LINE
- Combination of analgesics ( para , codeine , oxycodone ) + Joint aspiration + splinting (CAJAS)
POLYARTICULAR DISEASE
1ST LINE & 2ND LINE
( same as first line for inacessible/ injection not tolerated - mono/oligo)
TREATMENT FAILURE ETC
1ST LINE
- SA
2ND LINE - IAC
- CAJAS
- ONGOING
CHRONIC RECURRENT - SEVERE DEGENERATION (KNEE , HIP, SHOULDER)
1ST LINE
- Joint replacement surgery
WITH OSTEOARTHRITIS / RA - like disease
1ST LINE
- maintenance with Colchicine
All of the lines of treatment all the way to the top have Paracetamol as ADJUNCTS.
What is felty syndrome?
Extra articular manifestation of ra
Presence if ra , splenomegaly & neutropina
Neutropina mean repeated infections are common
Sulfasalzine and infertility?
Can cause reversible male infertility
Causes oligospermia - reduce sperms molitlity and an increase in abnormal forms
Stopping it can reverse infertility.
Side effects of ciclosporin?
Givingal hypertrophy ( overgrowth of the gums )
Hypertension
Tremors
Can also cause nausea, vomiting , diarrhoea, headache, change in blood sugar .
Side effects of anti tnf drugs ? - severe ones
Blocking tnf and immune response
So development of opportunistic effective especially tb and lymphoma
What is retroperitoneal fibrosis?
Fibrosis occurs in the membranes of the peritoneum can cause blockage and symptoms will depend on location of blockage.
Can obstruct ureters ( unilateral or bilateral obstructive uropathy) ——》 leads to hydronephoris ( swelling of renal pelvis & duct ) and hypertension & renal failure.
Symtoms - are unrelenting back pajn( may be a dull ache , difficult to localise) , can also be in abdomen.
Can also have nausea and vomiting , anaemia , loss of appetite, jaundice , unilateral leg swelling, sometimes that can be hemorrhaging into the stomach.
Usually idiopathic but can be caused by methsergide ( used to treat migranes ) & cancers.
What is alkaptonuria?
Basically build up of a chemical causes black staining of urine —–》 if missed when young chemical continues to build up in body and joints ——》 pre dispose patient to osteoathritis ‐——–》 will also get discoloration of the ear cartilage , blue bock spots on skin bcc of discoloration of sweat , blue black nails , breathing difficulties- bones & muscles around the lungs can become stiff so chest cant expand.
Alkaptonuria, or “black urine disease”, is a very rare inherited disorder that prevents the body fully breaking down two protein building blocks (amino acids) called tyrosine and phenylalanine.
It results in a build-up of a chemical called homogentisic acid in the body.
Thiscan turn urine and parts of the body a dark colour andlead to a range of problems over time.
Amino acids are usually broken down in a series of chemical reactions. But in alkaptonuria, a substance produced along the way, homogentisic acid, cannot be broken down any further.
This is becausethe enzyme that normally breaks it down does not work properly. Enzymes are proteins thatmake chemical reactions happen.
One of the earliest signs of the condition is dark-stained nappies, as homogentisic acid causes urine to turn black when exposed to air for a few hours.
If this sign is missed or overlooked, the disorder may go unnoticed until adulthood, as there are usually no other noticeable symptoms until the person reaches their late 20s to early 30s.
Signs and symptoms in adults
Over the course of many years, homogentisic acidslowly builds up in tissues throughout the body.
Itcan build up in almost any area of the body, including the cartilage, tendons,bones, nails, ears and heart. It stains the tissues dark and causes a wide range of problems.
Joints and bones
When a person with alkaptonuria reaches their 20s or 30s, they may start to experience joint problems.
Typically, they’ll have lower back pain and stiffness, followed by knee, hip and shoulder pain. These are theearly symptoms ofosteoarthritis.
Eventually, cartilage– a tough, flexible tissue found throughout the body – may become brittle annd break, leading to joint and spinal damage. Joint replacement operations are often needed.
Ears and eyes
An obvious sign of alkaptonuria in adults is thickening and blue-black discolouration of ear cartilage. This is called ochronosis.
The earwax may also be black or reddish-brown.
Many people develop brown or grey spots on the whites of their eyes as well.
