msk top tier Flashcards
in what condition is it typical to see DIPJ joint, knee and 1stCMC(carpometocarpal = thumb base) arthritis distribution
OA
is OA more common in men or women
women
- + rises post menopause
race association with OA
less common in black, A-C, asian, malaysian
name 5 conditions that increase one’s risk of OA
obesity - pro inflam (TNF, IL1, adipokines)
– esp knee/hip
local trauma - accelerates damage
inflammatory arthritis
hypermobile joints/ congential hip dysplasia (wear/tear starts earlier)
diabetic neuropathy
where would you expect to see OA in
1 farmers
2 labourers
3 footballers
1 hips
2 small joints/hands
3 knees
OA pathophysiology
progressive degeneration in response to insult/injury (Wear/tear)
loss of articular cartilage
exposed bone–> sclerosis (thickened) + cyst formation (less thick)
disorder bone repair - cartilagenous growths –> calcification –> osteophytes
inflammation present (even though this s degenerative, not inflammatory arthritis)
what is inflammatory OA
- AKA
- features
- treatment
= “erosive OA”
more inflammation than typical OA
no psoriasis (rule out PSA) big knuckle spaces (MCPjoint) joint 'locks' - bone/cartilage fragment (Arthroscopy)
DMARD therapy
name 5 potential signs of OA
gait alteration joint swelling deformity tenderness limited range of movement crepitations joint locking no systemic signs!
name 3 symptoms of OA
painful, tender
swelling
deformity
functional impairement
describe OA joint distribution
often unilateral often one set of joints (but multijoint) often begins at base of thumb -1st CMCj (trouble opening jars/taps) DIP knees spine hip
heberdens node
DIP
bouchards node
PIP
OA of hip pain feels like?
groin pain (rather than lateral hip pain)
if patient complaints of hip pain- usually=back
OA investigations
x ray (LOSS) Loss of joint space Osteophyte Subchondral sclerosis subchondral cysts \+ gull wing appearance (like flat m) on articular joint surface
MRI can see earlier changes but most dont need this
bloods
- normal esr, normal/slightly raised crp
OA management
- non medical
- pharmacological
- surgical
non medical (weight loss, education, physiotherpay, walking aids etc)
pharmacological
- analgesisa (NSAIDS, opioids, steroid injectuions etc)
surgical
- athroscopy (if loose bodies of cartilage/bone - knee locking)
osteotomy (bone cut/shaped/realigned)
athroplasty (replaced)
fusion (ankle/foot – but decreased movement)
what is arthroplasty
- when is it done
- s/e
joint replacement
for uncontolled pain, esp at night
comes with slight decrease in function
what is arthrocopy
Only indication for arthroscopy= for loose bodies- cartilage/bone!
Associated with knee locking
what is osteotomy
bone is cut/ realigned/ shortened
are men or women more affected by RA
women
most common RA age group?
40-60
genetic factors associated with RA
HLA DR4
HLA DRB1
+ associated with other autoimmune conditions
triggers of RA
stress
trauma
RA pathophysiology
inflammation of synovium (synovitis) and joint capsule
B,T cells, neutophils, cytokines
capillaries form within synovium- angiogenesis
synovial villli form - proliferate –> pannus (tumour-like mass). this grows over articular cartilage and destroys it and the subchondral bone! by erosion!
what type of immune reaction is RA
autoimmune
is RA mainly chronic, subacute or acute
chronic
what is the joint distribution typical of RA
symmetrical -bilateral
polyarthritic
mainly smaller joints- hands and feet
DIP sparing!!!
name 3 defromities associated with RA
1 mobile nodules (elbows, back of hands, lungs)
2 ulnar drift (fingers displaced towards ulnar(little finger))
3 swan neck (tendons- DIP arched)
4 z thumb deformity (thumb z shape)
5 boutonniere (DIP thumb opposite of arched)
pallindromic RA=
(A type)
episodic RA. never persistent
does RA have systemic sign/symptoms?
yes- fatigue/malasise
does OA have systemic sign/symptoms?
no
what does antiCCP indicate?
what does it stand for
RA
anti-cyclic citrullinated peptide
RA investigations (7)
bloods
- Anaemia
- High ESR/CRP
- Thrombocytosis (high)
+ rheumatoid factor (antibody against IgG heavy chain)- not specific – also in othe autoimmune
+ anti CCP – highly specific
antinuclear antibody
synovial fluid biopsy – high neutrophil count but sterile (rule out infection)
XRAY - LESS Loss of articualr space Erosion of articular cartilage and bone Soft tissue swelling Soft bones- osteopenia
RA treatment
non-pharm
- smoking cessation
- depression
- occupational therapy/rehab
pharm
- DMARDS (methotrexate)
- bioological DMARDs
- corticosteroids
- NSAIDs
- analgesia
pro and con of corticosteroids for RA
suppress disease, helps pain and swelling
but risks long term toxicity
pro and con of NSAIDs for RA
reduces pain and stiffness
but no effect on disease progression
RA complication- name 5
lung involvement - rheumatoid nodules
heart - pericardial rub/infection/effusion
scleritis/episcleritis
spinal cord compression
anaemia
(plus GI, vasculitis, kidney amyloidosis, muscle wasting, bursitis, sjorgens)
what is the most likely MSK cause of intersitial lung disease
RA
gout age and gender
men
middle aged
pseudogout age and gender
elderly
women
gout race risk factors
chinese
polynesian (pacific islands- somoa, figi, tonga, tom said mauri people)
fillipino
with westernised diet
gout diet
alcohol esp beer
red meat, liver
shellfish
sugar - fructose drinks
all these things are high purines
is hyperuricaemia more commonly due to underexcretion or overproduction
underexcretion
name 5 causes of underexcretion of uric acid (hyperuricaemia)
aspirin renal impairment dehydration diabetes diuretics
hypertension
hypothyroid
hyperparathyroid
obesity
name 3 causes of uric acid overproduction (hyperuricaemia)
high purine intake (diet) increased cell turnover -psoriasis -leukemia -lymphoma hyperlipidemia
triggers for gout attack
alcohol/shellfish binges
sepsis
MI
trauma (can be as minor as toe stubbing, surgery)
dehydration
sudden start/stop or hypouricaemic therapy
triggers for pseudogout attak
trauma illness surgery -esp parathyroid removeal hypothyroid hyperparathyroid T4 replacement blood transfusion -- excess iron most spontaneous
how do crystal arthropathies cause arthritis
urate crystals activate phagocytes – inflamamtion
gout crystal=
monosodium urate
pseudogout crystal substance=
calcium pyrophosphate
purine conversion to uric acid
then uric acid –> ?
purines –> hypoxanthine –> xanthine (may use xanthine oxidase here- sources vary)
xanthine –> uric acid using xanthine oxidase
uric acid
- excreted by kidnyes
- excess –> monosodium urate –> deposited in joints
gout joint distribution
polyarticular
asymmetrical
toes - esp big toe (1st MTPJ)
ankles
feet
(also knees, wrist, finger)
pseudogout joint distrubtion
monoarticular
joint surface
knees = most common wrist shoulder ankle elbow
(MCP (big knuckle))
is gout/pseudogout acute or chronic condition
can be acute or chronic
chronic condition but is episodic with acute flare ups
pseudogout often resolves by self 1-3w but we speed it up :)
tophi =
onion like aggregates of urate crystals with inflammatory cells around the joint
seen in chronic gout. can take long time to resolve. can consider it a gout complication
soft tissue masses, replaced by crystals
crystal arthropathies investigation
joint aspiration –> polarised light microscopy
Xray
bloods
- raised wbc
- raised esr
- serum uric acid
- serum creatinine - check for renal impairment
Examination- check ears for deposits
what does gout look like under polarised light microscopy
negatively birefringent needles of monosodium crystals (N)
what does pseudogout look like under polarised light microscopy
(weakly) positive birefringent rhomboid shaped of calcium pyrophosphate crystals (P)
gout xray
BEST bony hooks (from erosions) erosions (rat bite, punched out erosions) space intact (no joint space lost) tophi
pseudo gout xray
chrondocalcinosis = linear calcification parallel to articular surfaces, in joint gap
differentaites from OA (subcondral sclerosis)
pharmacological management of crystal arthropathies
anti-inflam
- NSAIDs
- colchine (if NSAIDs not tolerated)
- steroids
xanthine oxidase inhibitors - PREVENTATIVE- prevent uric acid production
(gout only)
-allopurinol
(-febuxostat)
what is given for crystal arthropathies if NSAIDs cannot be tolerated
colchine
non pharmacological crystal arthropathies management
diet change
weight loss
physiotherapy
joint aspiration
- esp pseudogout
potential for surgery-
if long term
- synovectomy
- joint replacement
pseudogout = screen for associated conditions
when should you screen for associated conditions of pseudo gout
early onset - <55y
polyarticular (usually mono)
frequent/recurrent episodes
there is a long list of associated conditions for pseudogout. name 3
haemochromatosis (most common)
hyperPTH
hypothyroidism
acromegaly
what is bursitis
where
seen in what conditions
inflammation of fluid sacs that cushion joints
Commonly elbow swelling. Could also be knee, shoulder, ankle
seen in crystal arthropathies, RA
gout complications
kidney disease (uric acid deposits)
bursitis
ear deposits
tophi
is osteoperosis more common in men or women
women
osteoperosis risk factors to do with patient
old age menopause thin/ low BMI family history diet-low ca athlete alcohol smoking
osteroperosis risk facots to do with patient disease
- joint - RA/SLE
- hyperthyroidism /hyperparathyroidism
- cushings (high cortisol)
- low oes/test (hypogonadism, anorexia, menopause)
- renal disease (lower vit d)
- previous fractures
osteoperosis risk factors to do with drugs
corticosteroids hormonal -aromatase inhibitors -GnRH analogues -androgen deprivation -depo provera (contraceptive)
primary osteoperosis causes
menopause (oes protects)
age (bone density naturally lost)
secondary osteoperosis causes
SHATTERED
Steroid use - (osteoclast activation)
Hyperthyroidism, hyperparathyroidism, hypercalciuria (inc turnover)
Alcohol + smoking
Thin (BMI<18.5)
Testosterone decrease (eg prostate cancer, hypogonadism)
Early menopause
Renal / liver failure
Erosive/ inflammatory bone disease (eg RA, myeloma)
Dietary decrease - low calcium, malabsorption, lactose intol, T1DM
osteomalacia vs osteoperosis
In ostoporosis, bone mineralisation is normal but there is reduced amount of bone
In osteomalacia bone mineralisation is reduced but there is normal amount of bone
bone mineral density=
how does it change with age
bone mass
quick rise in childhood/puberty and decline after menopause/old-ness
how do you measure bone density
bone densitometry aka DEXA
inflammatory disease effect on bone
bone turnover increase - increased bone resorption (osteoclast activity)
endocrine disease effect on bone
- thyroid
- parathyroid
- cushings
- oes
- test
thyroid hormone and PTH –> increase in bone turn over
high cortisol (cushing’s syndrome) –> increased bone resorption, increased osteoblast apoptosis
oestrogen and testosterone restrains bone turnover
how does skeletal loading affect bone
decreased skeletal loading increases resorption – strong bones not needed (immobility, low BMI)
microarchitecture of osteoperosis
trabeculae broken away –> big holes –> less strong
trabeculae thickness decreases in thickness
- decrease more in horizontal than vertical (because vertical is used more than horizontal)
alcohol effect on bone
bad for osteoblast
smoking effect on bone
decreases vitD increases bone turnover
dowagers hump
what i have! neck slumpy thing
osteoperosis
symptoms of osetoperosis
asymptomatic until fracture
where do you fall to break neck of femur
fall on side/back
fall on outstretched arm
distal radius (thumb wrist )
kyphosis
stooping
DEXA
dual energy xray absorptiometry (aka bone densitometry)
low raditation dose
t score compares bone density to young adult mean - male /female
0 to -1 = normal
- 1 to -2.5 = osteopenia
- 2.5 beyond= osteoperosis
is X ray useful for osteoperosis
it is insensitive
what is FRAX assessment
- who can take it
predicts risk of fracture in next 10 y by looking at risk factors
only suitable if 40y+
first line osteoperosis treatment
- eg
- how does it work
- take it when?
- bisphophonates (eg alendronic acid)
(oral)
antiresorptive = decrease osteoclast activity , decrease bone turnover and causes osteoclast apoptosis
best taken in morning, empty stomach (no food/med), sat up (prevent reflux)
non first line osteoperosis treatment (3)
(First line= bisphosphonates)]
monoclonal antibody to RANK ligand – denosumab
HRT , oes supplement
teriparatide = PTH analogue . increase osteoblast activity – not only stops decline but rebuilds and restores (v good but expensive)
lifestyle osteoperosis treatment
- stop alcohol/ smoking
- do weight bearing excericese
- calcium and vit d supplement / in diet
what is the genetic component of spondyloartopathies
HLA B27
when is onset for ankylosing spondylitis
teens/20s
ankylosing spondylitis race association
low = african, japanese high = N america
reactive arthritis : male or female
male
ankylosing spondylitis: male or female
male
what is HLA B27
human leukocyte antigen. On all cells except rbc , so they are APC (tissue type)
not = cause, makes more susceptible for ANKYLOSING SPONDYLITIS (different strength of link for each condition)
molecular mimicry theory
HLA B27 looks similar to infectious agents’ peptides to cause a (auto)immune response – autoimmune agonist
mis folding theory
HLA B27antigen trapped in ER. this causes an inflammatory response – IL23 released
Heavy chain homodimer hypothesis
B27 heavy chains form stable dimers (two identical molecules connected) which accumulate in the endoplasmic reticulum and can bind to other factors and so produce pro-inflam mediators
reactive arthritis triggers
usually genital vs GI
Common cause of reactive arthritis = STI –
Chlamydia, gonorrhea
Also GI associated ones
salmonella, shigella, yersinia, campylobacter
This infection may have resolved/ be asymptomatic but still can affect
UTIs, bowel infection
ankylosing spondylitis pathophysiology
- chronic inflammation of spine and sacroiliac joints (SIJ)- destroys them
- erosive damage repaired (joints replaced with fibrin )–> less movement range
new bone formation – ossification makes it immobile. joint/bony fusion
syndesmophytes
bony growth originating inside a ligament, often the spine
when is psoriasis seen with psoriatic arthritis
before/after/never
reactive arthritis pathophysiology
inflammation of synovial membrane, tendons, and fascia –autoimmune response
triggered by an infection at a distant site, normally 2-6w before (often STI)
where does reactive arthriits commonly affect
lower limb
what is enteropathic arthritis associated with
this is a type of spondyloarthropthy
it is associated with IBD
where does enteropathic arthritis affect
lower limbs
asymmetrical
episodic
general spondyloarthopathies feature
SPINE ACHE
Sausage digit -- dactylitis (tendon/joint inflam) Psoriasis Inflam back pain NSAIDs -good response Enthesitis
Arthritis
Crohns/colitis/CRP elevated
HLAB27+
Eye- uveitis/iritis
psoriasis =
ON SKIN
red
itchy
ON NAIL
thickened, flakey, lifting
can hide – scalp, ears, nails, belly button, genital
enthesitis
heel
inflammation of junction between ligament / tendon and bone
uveitis/irits (seen in spondyloathropathies) presents as ?
blurred vision
painful
red eye
children= ASYMPTOMATIC - so screened if have juveniile arthritis
what are juvenile arthrits children scanned for
uveitis/iritis
= asymptomatic in children!!
what condition do you think of with alternating buttock pain
sponfyloarthropathies
what condition do you think of with bamboo spine
what is happening
ankylosing spondylitis
new bone formation and fusion of vertebrae
is ankylosing spondylitis a-/symmetrical?
asymetrical
ankylosing spondylitis symptoms
Weight loss Fever, fatigue buttock/thigh pain neck/back stiffness (thoracic and cervical) Can cause SOB
progressed :
need to turn body to turn head (neck movement poor)
cant see sun/mirrored glasses extreme kyphosis
5 types of psoriatic arthritis
- distal arthritis (DIP only)
- RA-like (symmetrical, polyarth) – most common
- axial (sacroilitis)
- arthritis mutilans (severe hand/feet deformation)
- large joint (asymmetrical oligoarthritis)
reactive arthritis presentation
reiter’s triad
- cant see (conjunctivitis/uveitis)
- cant pee (urethritis)
- cant climb a tree (Arthritis)
also
- skin things: psoriasis/keratoderma
- willy thing : circinate balantis
- mouth/mucosal ulcers
ankylosing spondylitis diagnosis criteria
3+ months back pain sacroilitis (xray/MRI) SPINEACHE features limited back movement age under 45 y
x ray/MRI features of spondyloarthropathies
syndesmophytes sacroilitis sclerosis erosions joint fusion
ankylosing spondylitis treatmnet
non-pharm
- physiotherapy , occupational therapy
- excercise
pharm
- NSAIDs = first line
- DMARDs - if peripheral arthritis)
- antiTNF (biologics) if NSAIDs is insufficient
- local steroid injections
surgery
- straighten spine
hip replacement
psoriatic arthritis treatment
- immunosuppressive DMARDs
- biological drugs is DMARDs insufficent – antiTNF/ IL blockers
reactive arthritis treatment
NSAIDs steroid injections antibiotics if infection persists DMARDs TNF blockers= last resort
what is happening to incidence of osteomyelitis and why
increasing incidence
-PVD and dibaetes
age - osteomyelitis
bimodal: children + old
main cause (route ) of osteomyelitis in children, adults and elderly
children= heamotgenous seeding adults= direct inoculation elderly = contiguous spread
name 5 risk factors for osteomylitis
1 poor vascular supply
- diabetes (foot ulcer–> infection), sickle cell, arterial disease
2 immune deficiecny/suppression
3 high risk behaviour
- high risk of trauma, IVdrug use, alcohol in excess
4 bone/joint problems
- prosthetics/surgery, inflam arthrit
5 risk factors for haemotgenous osteomyelitis
-catheters, dialysis, central lines, UTIs
- most common bacterial cause of osteomyelitis
- why is
- others
staph aureus
- good at adhering,
- can live intracellularly
- can live on skin and invade through skin breaches
also MRSA staph epidermis salmonella pseudomonas
also
steprococci
fungi
TB etc
not haemophilius influenzae (vaccine)
direct innoculation (osteomyelitis)
- causes
- mono or poly microbial
- what age group
exposed bone
- trauma- open wound
- surgery
- mono/poly microbial
most common cause for adults
contiguous spread (osteomyelitis)
- causes
- mono or poly microbial
- what age group
- adjacent soft tissue infection spreads to bone
- cellulitis
mono/polymicrobial
most common cause in elderly
haematogenous seeding (osteomyelitis) -causes -mono or poly microbial - what age group
blood flow
- in children long bones affected> vertabrae
- in adults: vertabrae > long bones
monomicrobial
most common cause for children
why are long bones affected by ostemylitis in children
blood flow is slower over the growth plate so bacteria settle well here
no basement membrane
high blood flow
why are vertebrae affected by osteomylitis in adults
high blood supply to vertebrae
osteomyelitis acute vs chronic
acute = <2w chronic= >6w + chronic, by definition, involves necrosis
osteomyelitis pathophysiology
- infection spread reaches bone (3 routes)
- inflammatory response
- vascular congestion
- small vessel thrombosis
- inflammatory exudate increases pressure so periosteum ruptures
- periosteal blood supply interupted
- necrosis , bone death. sequestra and involucrum
sequestrum and involucrum formation
sequestrum = dead pieces of bone involucrum= new bone that forms outside of this
these are features of CHRONIC osteomyelitis
features of chronic osteomyelitis
non-healing fractures
deep/large ulcers
draining sinus tract – a passage (sinus tract) forms from infection to skin from which pus drains
do you see systemic signs/symptoms with osetomyelitis
yes fevers rigors sweats malaise fatigue
onset of osteomyleitis
days
classic symptoms of ostemyelitis
weakness
dull local pain
– aggrevated by movement
(+ cardinal inflam signs)
what would blood investifations on osteomyelitis show
raised ESR/CRP
raised WBC
blood culture = positive
(chronic bloods may have normal ESR/CRP/WBC)
osteomyeitis investigations
bloods
bone bopsu
x ray - do one, and again in 2w. if no changes –>mri (picks up sooner)
(PET is good but expesive)
what are you looking for with xray osteomyelitis
erosion
periosteal reaction (=formation of new bone)
sclerosis
sequestra (like darker oval/shape– dead bone)
soft tissue swelling
periosteal reaction=
formation of new bone
when is bed rest advised for osteomyelitis
if site is spinal
osteomyelitis pharmaco treatment
- =what
- probelems with this
antibiotics broad spectrum whilst pending culture. often: flucloxacillin (6w) or clindamycin if allergic to penicillin triple therapy is used if cause is TB monitor response with imaging/ ESR+CRP
bacteria virulence factors + penetration of drug to bone is variable, and is worsened by poor vascular supply so antibiotics ned to be taken for longer
surgical treatment for osteomyeltisi
- debridement (removal of dead / damaged/ foreign objects inc bone)
- replacement (prosethis)
- abscess drainage
is septic arthritis more common in men or women
equal
how common is septic arthritis
rare
name 5 risk factors for septic arthritis
1 damaged joint- RA/ prosethis/ surgery 2 immunosuppressed 3 low socio-econmic status 4 IV drug user 5 intra articular injection users 6 osteomyelitis
most common bacterial cause of joint infection
staph aureus
most common bacterial cause of prosthetic cause of joint infection
staph aureus
also staph epidermis
gonococcal arthritis
- commonness
- mono/poly/ same/different to normal
- test for it
this is the minority (majority = staph aureus, non-gonococcal)
polyarthritis (normal mono with infection)
synovial fluid = negative, so need to look at the blood culture
most common septic arthritis distrubtuion
knee hip shoulder but can be any normally just one
do you get systemic features in septic arthritis
yes
fever, tachy, malaise
what does septic arthritis look like in the immunosupressed/elderly
presentation may be muted
septic arthritis triad
impaired range of movement
joint pain
fever
bloods for septic arthritis
CRP rises quickly
ESR rises more slowly
high wbc- neutrophilia
blood culture
septic arthritis investigations
joint aspirate
- need to do OFF antibiotics
- bad if cloudy +pale. should be yellow and transparent
- polarised light microscopy (rules gout/ pseudpgout)
STI screen
x ray
what are you looking for on xray with septic arthrititis
extra bone formation
periosteal changes (fluffy)
lytic areas
do again after 2w
septic arthritis management
antibiotics (flucoxycilin from staph aureus . clindamycin/erythromycin if allergic to pencillin)
joint aspiration!- decompress the joint
analgesia
steroid sick day rules
off load joint (splinter)
stop RA medication
surgical:
- prosethis
- debridement
- excision/exchange arthroplasty of prosthetic joint (depending on how much surgery patient can toleratE)
SLE gender association
f»_space;m
age range for SLE
15-45
high incidence premenopausal
race assocaition SLE
Black af
a-c
asians
hispanic
Genetic associtation
HLAD DR2
is smoking protective or a risk factor for SLE
risk factor
SLE flare up triggers
- sunlight overexposure (B>A UV light)
- oestrogen - preg, contraceptives
- infection
- stress
- sulfasalazine (DMARD
What is important to rule out before treating SLE
Infection
because the treatment is immunosuppressive
SLE pathophysiology
dysfunction of apoptosis
- intracellular material isnot disposed of correctly by pahgocytes –> apoptic remnant (Cells and fragments) transfer to lymphoid tissue.
This is taken up by APC, allowing autoantibody to nuclear material to develop (=antiDsDNA antibodies)
B cell hyperactivity (dysfunction) –> Ab –> immune response (autoimmune)
inflammation –> tissue damage (antiDsDNA antibodies (autoantibodies) attack nuclear matterial in tissues)
why is their an increase in thrombosis with SLE
thrombosis mediated by phospholipid antibodies
do you see systemic signs in SLE
yes
fever, fatigue, weight loss, headache
jaccoud’s arthropathy =
non-deforming /erosive (correctable) arthritis
sometimes seen in SLE
common presentation features of SLE
often non-specific and begins mild
fever mouth ulcers fatigue phtosensitive rash butterfly rash
flare-ups occur - relapsing and remitting
SLE has many other presentations name 5
- Hair loss, alopecia
- Fever,
- fatigue,
- weight loss,
- headache
- Myalgia = muscle pain
- Arthralgia
- Myositis = muscle inflammation
- joint pain/swelling (RA like)
- Raynauds
- Pleuritic chest pain
- Deforming arthritis (Symmetrical, non-erosive, polyarticular)
- Seizures
- Many rash forms, some specific, some not
- -Discoid rash = deep + sensitive
- Pericarditis
- hypertension
- MI
- Psychosis - many inc anxiety, depression
- Proteinuria
- Renal failure eventually
- Vasculitis
SLE investigations
+whether they are specific or not
- ANA+ (antinuclear antibodies)
- not specific, but sensitive
- high ESP, normal CRP
- specific
- antiDsDNA antibodies (double stranded DNA)
- specific but not as sensitive
antiRo/antiLA autoantibodies
–?
- bloods
- low platelets, rbc, nuetophils, lymphocytes
- not specific
- u/e s raised in advanced renal disease
skin/ renal biopsy – IgG and complement depositon
pharmacological SLE management
antimalarials – (hydroxy)chloroquine
steroids (prednisolone) for rashes
NSAIDs/steroids for joints
immunosuppressants
glucocorticoids high dose for complications
cyclophasphamide = what type of drug
immunosuppressant
chloroquine = what type of drug
antimalarials
non pharm SLE management
UV protection manage risk of -atherosclerosis -screen for other organ involvement -look for phospholipid antibodies (they mediate increase in thrombosis)
does SLE complications include the lung?
where else?
no – this is more RA
thrombosis (gangrene, stroke, MI…)
renal failure
cv disease
cerebreal vasculitis
sulfasalazine = what type of drug
DMARD
methotrexate = what type of drug
DMARD
teriparatide = what type of drug
PTH analogue
denosumbad = what type of drug
monoclonal antibody to RANKligand
antiresorpative drug
alendronic acid= what type of drug
bisphosphonate (antiresorpative)
allopurinol= what type of drug
xanthine oxidase inhibitor
what gel and coombs category does SLE fit into
type 3 sensitivity
Deposition of immune complexes in tissue
Complement activation
Neutrophil and cytokine influx
inflammation
sle curable?
no. manageable
age for juvenile arthritis
16 or younger
RA first line
what is taken with this
DMARD- methotrexate
glucocorticoids whilst DMARD kicks in
