Rheumatology & MSK Flashcards
what is the most common arthritis?
osteoarthritis
who gets osteoarthritis?
older females overweight excessive joint use trauma/malalignment etc
how do you end up with bony changes in osteoarthritis?
mechanical forces –> cartilege lost
cartilege loss = cytokines - TNFa, IL-1, NO
cytokines = cartilege cannot repair properly
loss of cartilege = bone rubbing on bone
reactive changes in bone, it is not designed to rub on bone
reactive changes you see in the bone in osteoarthritis?
loss of joint space osteophytes sclerosis subchondral cysts synovial hypertrophy
what is sclerosis in relation to arthritis?
thickening and widening of the bone at the joint
what is an osteophyte?
an area of bone which has been reactively laid down in the wrong place
what joints might be affected in osteoarthritis? (give 5)
those that are used a lot! knees hips sacro ileac cervical spine wrist carpmetacarpal - base of thumb DIP PIP
how is the pain different in osteooarthritis vs inflammatory arthritis?
osteo - morning stiffness only lasting up to 15 mins, generally worsens throughout day
RA - - stiff for 30+ mins, better with use
apart from pain, give 3 other clinical presentations of osteoarthritis?
effusion crepitus pt reports the joint 'gives way' tender to palpation deformity herbedens/bouchards nodes
what are herbedens and bouchards nodes?
soft tissue swellings on the fingers seen in the early stages of osteoarthritis herbedens = DIP bouchards = PIP (HD AND BP)
when would arthroscopy be indicated?
knee ‘locking’ indicates a loose body which can be removed (arthroscopy)
4 x ray changes typical of osteoarthritis?
LOSS L - loss of joint space O - osteophytes S - subchondral sclerosis S - subchondral cysts
some management options of osteoarthritis?
physio weight loss occupational therapy eg footwear, walking aid nsaid opioid amytriptiline topical capsaicin steroid injection hydroxychloroquine
what produces synovial fluid?
the synovial membrane
typical patient with RA?
post menpausal woman
smoker
past infection
what is the pathophysiology of RA?
a reaction to self antigens eg type II collagen, vimentin
= inflammation at the synovial membrane
= damage to soft tissue and cartilege
= damage to bone
what joints are affected in RA?
small joints
symmetrical
hands, wrists & feet
not DIP or spine
if you were examining the hands of someone with RA give 5 things you might expect to see?
DIP not affected hurts to squeeze the joints joints are warm ulnar deviation cannot make a fist z thumb swan neck deformity
are there any systemic features of RA?
myalgia, malaise and low grade fever, if the cytokines go around the body Rheumatoid nodules - skin eye inflammation eg scleritis ihd/pericarditis lung inflam
3 blood tests you could do if you suspect RA?
ESR/CRP
rheumatoid factor - low sensitivity and specificity
anti-CCP (anti- cyclic citrillunated peptide) - good specificity, sensitive enough to highlight the most severe disease
some bony changes you might see on x ray in RA?
you dont see bony changes on x ray immediately!
soft tissue swelling
periarticular ostoepenia (low bone density)
loss of joint space
subluxation
erosion
3 drugs you could give in RA?
Methotrexate sulphasalazine hydroxychloroquine infliximab short term NSAID
who gets gout?
men over 40 - esp diabetes, overweight, hypertension purine rich diet renal impairment IHD diuretics
what enzyme converts hypoxanthine to xanthine and xanthine to uric acid?
xanthine oxidase
what happens when urate crystals are deposited in the joint?
they activate phagocytes –> inflammation –> joint pain (gout)
give 2 causes of too much uric acid production, other than diet?
increased cell turnover, as in:
- myeloproliferative disorders
- psoriasis
- tumour lysis syndrome
what drugs can impair uric acid excretion?
tacrolimus
aspirin
thiazides
which joint is most commonly affected in gout?
1st MTPJ (metatarsalphalyngeal joint) - big toe
how does gout present?
usually monoarticular - big toe/foot/ankle/knee sudden onset 1-3 weeks intense pain esp at night heat, swelling, redness stiffness
what do you see in the joint aspirate in gout?
needle shaped crystals
negatively birefringent
what do you see on an x ray in gout, how can you differentiate it from other arthritis?
joint effusion
punched out lesions
no loss of joint space
no periarticular osteopenia
how do you manage acute gout?
nsaids, colchicine
intrarticular steroid inj
rest and elevate
dont start allopurinol until the acute stage has finished
what drug is first line for maintaining remission of gout?
what is the mechanism of action?
2 side effects?
allopurinol
xanthine oxidase inhibitor, stops the conversion of purines to uric acid
rash, headache, hypersensitivity
what is the second line treatment for gout, when should it not be used?
febuxostat
not for renal or hepatic impairment
what foods have high purines?
meat seafood alcohol beans/lentils mushrooms carbonated drinks / fructose
3 risk factors for pseudogout?
osteoarthritis age haemachromotosis high PTH low phosphate low magnesium hypothyroidism acromegaly illness surgery trauma
pseudogout is caused by crystals of ?
calcium pyrophosphate
what joints does pseudogout affect?
larger - knee/wrist/elbow/shoulder
symmetrical, if chronic
what kind of crystals do you see in the joint aspirate in pseudogout?
rhomboid shaped
positively birefringent
what might you see on the x ray of pseudogout?
chondrocalcinosis
calcification of cartilege
(neither is specific)
what is the management for pseudogout?
aspiration to relieve pain
NSAID/colchicine/prednisolone to relieve pain
hydroxychloroquine/methotrexate may help
some infections that commonly trigger reactive arthritis?
salmonella shigella yersinia enterocolitica chlamydia n. gonorrhoea (but more commonly causes gonococcal arthritis which is different) (STI or GI) e. coli (GI symptoms) EBV - rarely
what is the presentation of reactive arthritis?
‘can’t see, pee or climb a tree’
conjunctivitis
sterile urethritis
arthritis
what is the arthritis like in reactive arthritis?
acute
asymmetrical
lower leg
some other things (apart from conjunctivitis, urethritis and arthritis) associated with reactive arthritis?
iritis keratoderma blenorrhagica - red pustules and brown scaly feet circinate balanitis enthesitis mouth ulcers
4 investigations you would do for ?reactive arthritis?
joint aspiration - to exclude septic arthritis and gout
serology/stool culture/STI swab - to find infectious cause
X ray - enthesitis, periosteal reaction
CRP
Typical exam presentation for ankylosing spondylitis?
young male
what HLA is ankylosing spondylitis associated with?
hla b 27
explain the pathophysiology of ankylosing spondylitis?
inflammation in the anterior corners of the spine
fat is laid down
fat is replaced with bone (syndesmophites)
joint fusion
=stiffness
what joints does ankylosing spondylitis affect?
spine
sacroiliac
1-3 joints
asymetrical
what is the time course of ankylosing spondylitis?
at least 3 months
with flares/remitting
is there morning stiffness in ankylosing spondylitis?
yes
some presentations of ankylosing spondylitis? (4)
lower back or buttock pain vertebral fractures enthesitis dactylitis chest pain - costovertebral/costosternal joints eye inflammation kyphotic posture
what changes would you see on x ray in ankylosing spondylitis? (5)
bamboo spine fusion of facet joints squaring of vertebral bodies ossification syndesmophites subchondral sclerosis erosion
3 extra articular features of ankylosing spondylitis?
anterior uveitis weight loss fatigue anaemia pulmonary fibrosis aortitis
treatment for ankylosing spondylitis?
infliximab
Nsaids
steroids
osteomyelitis is?
infection of the bone
3 risk factors for osteomyelitis?
inflammatory arthritis sickle cell IVDU immunocomp diabetes prosthesis trauma
4 bacteria that commonly cause osteomyelitis?
staph aureus
pseudomonas aeruginosa
salmonella
TB
what bacteria is particularly associated with osteomyelitis in sickle cell?
salmonella
how might contigious spread come about?
from infectious soft tissue, eg an ulcer
what are some features of chronic osteomyelitis, why do they happen?
sequestrum
involcrums
because there is necrosis and the osteoblasts try to remodel
what types of bones are normally affected by haematogenous osteomyelitis?
long bones in children
vertebrae in adults
what is the clinical presentation of osteomyelitis?
rigor, sweats, malaise and fever
vertebral fractures
lesions/fractures take ages to heal
joint exudate - when infection has broken through the cortex
what is the gold standard investigation for osteomyelitis?
open bone biopsy - for culture and histology
what x ray changes would you see in osteomyelitis?
cortical erosion periosteal reaction lucency sclerosis sequestrae, involcrums
what can you see on mri and ct? - relating to rheumatology?
bone marrow inflammation
management for osteomyelitis? (3)
debridement
abx
analgaesia
2 differential diagnoses for osteomyelitis?
cellulitis charcot avascular necrosis gout fracture malignancy
what is septic arthritis?
infection of the joint
what bacteria commonly cause septic arthritis? (give 4)
staph aureus staph epidermis strep A/B/pneumoniae n. gonoorhoea pseudomonas e coli TB
what is the most common bacteria in septic arthritis?
staph aureus
what bacteria is often associated with prosthetics in septic arthritis?
staph epidermis
pseudomonas septic arthritis is usually seen in who?
elderly
immunocomp
IVDU
what joints are most commonly affected by septic arthritis?
knee
hip
shoulder
presentation of septic arthritis?
hot, tender, red, swollen
very painful
limited range of movement
fever
3 investigations for septic arthritis?
arthrocentesis (joint aspiration) –> mc&s
blood culture
plain x ray
what investigation d you do if you suspect TB septic arthritis?
synovial biopsy
3 typical antibiotics for septic arthritis?
flucloxacillin
clindamycin
ciprofloxacin
vancomycin
how does gonococcal arthritis present?
fever, arthritis, tendonitis
multiple joints
maculopapular pustular rash on palms + soles
how would an infected prosthetic joint present?
chronic low grade pain ever since it was done staph aureus/enterococci low esr, crp, normal wcc diagnosis - joint aspirate arthropathy (remove and replace)
the epidemiology of psoriatic arthritis?
10% pts with psoriasis
within 10yrs of getting psoriasis
typically middle aged
3 main patterns of psoriatic arthritis?
symmetrical polyarthritis - hands, wrists, ankles, DIP - women
asymmetrical oligoarthritis - hands + feet
spondyloarthritis - spine - men
is there morning stiffness in psoriatic arthritis?
yes
extra articular features of psoriatic arthritis?
psoriatic skin plaques pitting / onikolysis enthysitis conjuntivitis/uveitis aortitis
3 x ray features of psoriatic arthritis?
pencil in cup - due to central erosion of bone
osteolysis
fusion
soft tissue swelling
periostitis
what is ustekumab?
il-12, il-23 inhibitor biologic - used for inflam arthritis
what is the epidemiology of lupus?
women
15-30
african-carribean or asian
what genetic associations is there in lupus?
HLA DR2
HLA DR 3
complement C4 allele
what are the antibodies against in lupus?
ANA - anti nuclear antibody
anti ds-DNA
also sometimes phospholipids etc
what kind of hypersensitivity reaction is lupus? how is it mediated?
type 3 hypersensitivity
T, B, cells, ytokines and complement
some clinical presentations (5) of lupus?
malar erythromatous rash - ‘butterfly’
muscle & joint pain - arthritis is symmetrical and affects the tendons and ligaments more than the bone
fatigue
fever
discoid/photosensitivity rash/lupus profundus
alopecia
raynauds
nephritis
pericarditis
headache – seizure – mononeuropathy – psychosis
autoimmune haemolytic anaemia
what tests would you do for lupus?
ANA - non specific but negatively predictive
anti DS DNA - more specific
urinalysis for asymptomatic proteinuria
complement (low)
ESR high, CRP normal - in managed lupus. In a flare, CRP is also high
treatment of lupus? (5)
hydroxychloroquine methotrexate rituximab NSAIDs/steroids for short term warfarin - because antiphospholipid syndrome = greater risk of clotting manage triggers eg sunlight
what is osteoporosis?
low bone density
+ architectural deficits in bone
5 risk factors for osteoporosis?
inflam arthritis / connective tissue dis IBD high PTH cushings low oestrogen/testosterone (low bodyweight/athlete/post menopausal) reduced skeletal loading fractures family history smoking/alcohol renal/liver failure
what is bone strength determined by?
bone mineral density (at its peak and the rate of loss)
size
quality - architecture/turnover/mineralisation
how does menopause affect osteoporosis?
oestrogen is supposed to restrict bone turnover
with oestrogen gone there is more bone turnover
cancellous bone is particularly affected
why do bones weaken with age? (what part of the bone is affected?)
there is a reduction in trabecular thickness and the number of trabeculae decrease
what system is used to predict the risk off osteoporotic fracture? what things does it consider?
FRAX
bmi, age, smoking, drugs, medical history
what is a DEXA scan?
dual energy x ray absorptiometry
measures bone mineral density
at most common fracture sites - hip, lumbar spine, distal radius
t score - how different to a young healthy adult it is
what is osteopenia?
weakening of the bone, but not as much as osteoporosis
how does alendronate work?
-onate = bisphosphonate
inhibit farnesyl phosphatase
– > osteoclast apoptosis
some treatments for osteoporosis? (4)
bisphosphonate eg alendronate
HRT
denosumab - RANK-L antibody - prevents osteoclast activation
teriparatide - PTH analogue, decreases bone resorption
raloxifene - stimulates oestrogen receptors on bone
primary bone tumours originate from the _____ tissue
mesenchymal
what is osteochondroma? 3 things to say
forms cartilege
benign
long bones of men under 25
what is osteosarcoma? 4
bone forming (produce osteoid)
malignant
in the young
ALP will be raised, as osteoblast hyperactivity
what is a giant cell bone tumour?
malignant or benign
osteoclasts
after trauma
what is an osteoid osteoma?
benign bone forming osteoblasts disorganised blood vessels and trabeculae pain worse at night
what is a ewing sarcoma?
malignant bone marrow mesenchymal stem cells/neuroectodermal cells very young lamellated bone can compress nerves lytic bone lesions, onion skinning
chondrosarcoma?
forms cartilege
old people
chondrocytes
osteoblastoma?
benign
bone forming
axial skeleton
can compress nerves
what kind of anaemia in myeloma?
microcytic
some presentations of a bone tumour? - 5
constant, non mechanical bone pain
swelling
fracture
b symptoms - fever, night sweats, malaise
avascular necrosis
symptoms of nerve compression - numbness/weakness
serum ____ is high in secondary bone tumours
calcium
____ level is a marker of osteoBLAST activity?
ALP
do sclerotic or lytic lesions mean benign/malignant?
sclerotic = healed or benign lytic = malignant
what does the zone of transition tell you?
wide zone of transition - means there is poor definition of healthy | not healthy - so more likely to be malignant
narrow zone of transmission does not always mean benign, beware of myeloma esp in old people
stages of the periosteal reaction and what they tell you about the tumour?
- callus - slow growing
- lamellated / onion skinning - slow growing but deffo a tumour - ewings
- sunburst spicules, codmans triangle – an aggressive tumour eg osteosarcoma
how to tell on an x ray if something if a tumour of bone or cartilege?
cartilege: popcorn stippling / rings and arcs eg chondrosarcoma
bone: fluffy/trabecular
what other conditions is fibromyalgia associated with?
functional eg IBS, chronic fatigue
inflammatory eg RA, SLE
why may the pain signals be amplified in fibromyalgia?
high substance p
low 5ht
allodynia is ___
pain in response to a non painful stimulus
what is the pain like in fibromyalgia, what pattern of joints are affected?
widespread
symmetrical
above and below the waist
morning stiffness
what do you need to remember to exclude in fibromyalgia?
osteoarthritis - probably not the same presentation
hypothyroidism
anything inflam - esr/crp
lupus
hypercalcaemia - would cause the same parasthesia
management of fibromyalgia?
amitriptyline
duloxetine
lifestyle
what is sjogrens syndrome?
secondary to RA
anti-Ro and anti-La antibodies (anti-La is more specific)
dry mucus membranes - eyes/mouth/vagina
what is osteomalacia?
‘soft bone’ due to defective mineralisation - eg low calcium
why is osteomalacia less common in the UK than it once was
used to be common because we have little sunlight in the UK
no foods are fortified with vit D
3 risk factors for osteomalacia?
lack of exposure to sunlight eg indoors, lots of clothing dark skin malabsorption eg IBD low dietary vit D, eg vegan kidney disease (they activate vit D)
in the skin, ________ (made from ________) is metabolised to vit D3, in the presence of _______
previt D3
cholesterol
UVB
vit D is important for bones because ________
it is needed for the absorption of calcium and phosphate from the GI tract
in the ________, vit D3 is metabolised to _________
liver
calcidiol/25-hydroxyvitamin D
in the _______, _________ is metabolised to __________ (calcitriol)
kidney
25 hydroxyvitamin D
1,25-dihydroxyvitamin D
how does the body respond to low vit D?
there will be low calcium and phosphate (because vit D is needed to absorb them)
so PTH is released
PTH mobilises calcium from bones
= bone weakness –> osteomalacia
what is ricketts?
osteomalacia in children, before the growth plates have fused
4 presentations of osteomalacia?
bone pain - esp hip/rib/pelvis/thigh/foot fractures muscle weakness/pain muscle spasm due to hypocalcaemia fatigue waddling gait - late sign
first line investigation for osteomalacia?
serum 25-hydroxyvit D
gold standard test for osteomalacia?
iliac bone biopsy with double tetracycline labelling
in osteomalacia ALP will be ..
high
what is the supplementary vitamin D (that you would give for osteomalacia) called?
cholecalciferol
what is spondylolithesis & lumbar spondylosis?
spondylolithesis = vertebrae slips out of place
lumbar spondylosis = damage to the intervertebral disk
what is facet joint syndrome?
how does it develop?
what position relieves it?
secondary to lumbar spondylosis
joints become misaligned – secondary osteoarthritis
worse when bending backwards
what is fibrositic nodulosis?
tender nodules in the buttock
when does the pain happen if it is caused by mechanical lower back pain?
sudden onset
worse in evening or on exercise
no morning stiffness
when there is a visible muscle spasm in the lower back, the pain is generally better when..
sitting or lying
when would you do a spinal x ray in lower back pain?
when there is red flags eg nocturnal pain leg pain sphincter disturbance violent trauma
a differential for lower back pain with no obvious cause or red flags?
polymyalgia rheumatica – muscle ache affecting the shoulders, arms, hips, neck
will have a raised ESR
epidemiology of vasculitis?
50 +
associated with polymyalgia & RA
in general rare, GCA is the most common type
aetiology of vasculitis? 3
idiopathic autoimmune secondary to infection secondary to RA drugs
in GCA which layers of the artery are affected? what is the net effect of this?
tunica media + interna
inflammation = narrowing of lumen
what arteries are commonly affected in GCA?
common temporal (splits into frontal + temporal)
linguinal / facial
cilliary (to retina)
4 presentations of cranial GCA?
abrupt temporal unilateral headache
changes to vision - amaurosis faux/diplopia/flashing lights
scalp tenderness
jaw claudication
visible dilation of temporal artery on side of face
presentation of non temporal GCA? 3
polymyalgia
chronic low grade fever/malaise
limb claudication
what is the gold standard investigation for cranial GCA?
what other imaging could you use?
temporal artery biopsy
(you see giant multinucleated cells)
duplex temporal artery ultrasound - halo sign + inflammation
how could you image for systemic / non cranial vasculitis?
PET-CT using a glucose tracer
what blood tests results would you see in vasculitis?
raised ESR
normocytic anaemia
thrombocytosis
raised ALP
treatment for GCA
initially - iv prednisolone
wean off steroids after 1-2 yrs
methotrexate or tocilizumab if steroids not tolerated
what size vessels does ANCA vasculitis affect?
small
what are the two ANCA associated vasculitides?
p-ANCA: microscopic polyangiitis, eosinophillic, UC, primary schlerosing cholangitis
c-ANCA: granulomatosis with polyangiitis (aka wegeners)
some general features of all vasculitis? 4
pain purpura HTN neuropathy fever weight loss
what is an intervertebral disk made up of?
outer fibrous : annulus fibrosis
inner gel like : nucleus propulsus. becomes dehydrated over time
what part of the spine is usually affected by vertebral disk degeneration?
lumbar
how does vertebral disk degeneration present?
shooting pain sudden onset radiates to arms/legs muscle spasm tingling / parasthesia / numbnesss
two types of surgery for prolapsed vertebral disks?
corpectomy
discectomy
what is pagets disease of the bone?
excessive activity of osteoblasts and osteoclasts
what is the epidemiology of pagets?
over 40
triggered by infection
genetic link
3 phases of pagets disease?
- lytic: osteoclasts – low density bone
- lytic + blastic – patchy lysis and sclerosis
- blastic (latent) - osteoblasts lay down weak new bone
clinical presentation of pagets?
generalised bone pain
fracture
deformity
hearing loss
what do you see on x ray in pagets? 3
cotton wool skull
lysis (osteolysis circumscripta) + sclerosis
big bones
v shaped defects in long bones
treatment for pagets?
bisphosphonate eg allendronate
what do you need to give alongside bisphosphonates? how do they need to be taken?
calcium/vit D supplement
once a week
sitting upright
empty stomach
3 drugs that can cause drug induced lupus?
isoniazid
procainamide
hydralazine
what antibiotics interact with methotrexate to cause pancytopenia?
trimethoprim
because they are both anti folate drugs
(they both have meth in)
they also compete for renal excretion
some presentations of granulomatosis with polyangiitis?
upper and lower resp tract - granulomas in lungs - haemoptysis - saddle nose glomerulonephritis weight loss/night sweats coagulopathy PE mitral stenosis pulm hypertension conjunctivitis
what colour are the fingers in raynauds?
white – blue – red
what are some causes of secondary raynauds?
what features distinguish secondary raynauds from primary?
lupus, drugs, trauma
red marks on the nail bed, asymmetrical - suggestive of secondary
what fbc results would you expect in lupus?
low WCC
low platelet
(antiphospholipid syndrome = increased clotting but not because of platelets)
what blood test results would you see in pagets?
raised ALP
normal calcium, phosphate, PTH, etc
what blood test results would you see in pagets?
raised ALP
normal calcium, phosphate, PTH, etc
symptoms of L4 (L3-L4) lesion?
thigh to calf pain
loss of knee jerk
symptoms of L5 (L4-L5) lesion?
weak dorsiflexion
buttock to foot pain
symptoms of L1 lesion?
sciatic pain
buttock to ankle pain
loss of ankle jerk
what is a normal/osteopenic/osteoporotic T score?
osteosclerosis = 2.5 or more normal = 1 - -1 osteopenia = -1 or less osteoporosis = -2.5 severe osteoporosis = -2.5 or less + silly fracture
what does schoberg’s test measure, what diagnosis is a positive result associated with?
spine mobility
ankylosing spondylitis
presentation of antiphospholipid syndrome?
CLOT C - coagulopathy - raised APTT normal PT L - livedo reticularis - red/blue skin O - obstretic problems eg miscarriage T - thrombocytopenia can be primary, or secondar, eg to lupus (also non infective endocarditis)
risk factors for osteoporosis?
S - steroid H - hyperthyroid, hyperparathyroid A - alcohol, smoking T - thin T - testosterone decrease E - early menopause R - renal/liver failure (less vit D activation) E - erosive bone dis D - diet/diabetes
‘hidden’ places where you may find psoriasis?
scalp
behind ears
genitals
which primary cancers are most likely to metastasise to bone?
breast/prostate
lung
kidney (renal cell carcinoma)
thyroid
what blood test is used to monitor lupus?
ESR
what antibodies are there in anti phospholipid syndrome?
anti cardiolipin - also in syphilis
lupus anticoagulant
anti beta 2 Glyco Protein 1
= hypercoagulable state
microscopic polyangiitis affects only the
kidney and lung
eosinophilic granulomatosis presents similarly to
allergy
asthma
Henoch-Schoenlein purpura
rash
abdo pain
glomerulonephritis
arthritis/arthralgia
what is a swan neck deformity?
hyperextension of PIP
hyperflexion of DIP
what is burronaires deformity?
feature of RA
hyperflexion of PIP
hyperextension of DIP
explain how to do Schober’s test?
have the patient stand locate L5 vertebrae mark a point 10cm above and 5cm below as pt to bend over as far s they can measure the new distance less than 20cm is positive for AS
how are asthma attacks categorised according to severity? (for people aged 12+)
moderate = peak flow below 75%
acute severe = peak flow below 50%, resp 25+, pulse 110, accessory muscle use, or unable to complete sentence
life threatening: peak flow below 33%, sats less than 92%, confused, or silent chest
what is acute severe asthma in a child 5-12?
resp rate 30
pulse 125
what is acute severe asthma in child 2-5 yrs?
resp rate 40
pulse 140
