r h e m concise Flashcards
what is OA
degenerative joint disorder where there is progressive loss of hyaline cartilage
what are the rx associated with OA
increasing age
obesity
joint abnormality or trauma
what are the sx seen in OA
pain worse after movement, worse at the end of the day
stiffness - after rest, lasts 30 mins
deformity
reduced ROM around the joint
which joints are affected by OA
knee hip DIPS PIPS CMC of thumb
what are the signs seen in OA
bouchards - PIPs
Herbedens nodules DIPS
thumb CMC squaring
fixed flexion deformity
what are ddx for OA
septic
crystal - gout and pseudo gout
trauma
what are the x ray features of oA
LOSS
loss of joint space/ narrowing
osteophytes
subcondral cysts
subcentral sclerosis
how is OA managed
conservative = weight loss, physio muscle strengthening, walking aids, supportive footwear
medical - analgesia = paracetamol, NSAID’s - diclofenac
joint injections - methyl pred
surgery - arthroscopic washout, athroplasty, osteotomy
what is septic arthritis
acutely red, hot, infected joint
what are the source of infection or SA
haematogenous
local
what organisms cause SA
staph most common - staph aureus
gonococcus most common in young sexually active pts
what are the risk factors for SA
joint disease e.g RA
immuosupression e.g DM
prosthetic joints
what are the sx associated with SA
acutely tender, swollen joint
reduced range of movement
systemically unwell
what Lx are required in SA
joint aspiration for MCS raised acc
raised ESR/CRP, raised WCC, blood cultures
x-ray
how is SA managed
IV abx - vancomycin and cefotaxime
consider joint washout under GA
physiotherapy after infection
what are the ddx for SA
reactive arthritis
crystal arthropathy
what are the complications associated with SA
osteomyelitis
arthritis
ankylosis - fusion
what is RA
chronic, autoimmune inflammatory disease characterised by symmetrical deforming peripheral polyarthritis
describe the pathophysiology behind RA
self antigens are recognised by b and t cells
leading to production of RF and anti CCP antibodies
macrohages and fibroblasts produce TNF a, cascade of inflammation
and proliferation of synoviocytes on cartilage as well as differentiate of osteoclasts which contributes to bone damage
what are the risk factors associated with RA
smoking
female gender
increasing age (5th -6th decade)
genetics - HLA DR4/DR1 linked
what are the features of RA
ANTI CCP Or RF
- arthritis
- nodules
- tenosynovitis
- immune
- cardiac
- carpal tunnel
- pulmonary
- opthalamic
- raynaud’s
- felty’s syndrome
describe the arthritic features seen in RA
symmetrical polyarthris of MCPs. PIPs of hands and feet = pain, swelling and deformity
- swan neck
- boutonniere
- z thumb
- ulnar deviation of the fingers
- dorsal subluxation of ulnar styloid
morning stiffness more than an hour
improves with exercise
what is a swan neck deformity
PIPs hyperextension
what is boutonniere’s deformity
DIPs in hyperextension and PIP’s in flexion
seen in RA
where are nodules in RA seen?
seen in elbows and fingers - firm, non tender mobile or fixed
what cardiac features are seen in RA, which pulmonary features
pericarditis, pericardial effusion
fibrosing alveolitis, exudative pleural effusions
what ophthalmic features are seen in RA
episcleritis
secondary sjogren’s syndrome
what is Felty’s syndrome
RA with splenomegaly and neutropenania
Thrombocytopenia
anaemia
how is the diagnosis of RA made
4/7 of
- Morning stiffness >1h (lasting >6wks)
- Arthritis ≥3 joints
- Arthritis of hand joints
- Symmetrical
- RA nodules
- positive RF
- radiographic changes
what x-ray features are seen in RA
LESS
loss of joint space or narrowing
boney erosions
soft bones - osteopenia
soft tissue swelling
what investigations are requird in RA
bloods =FBC - feltys syndrome - anaemia, thrombocytopenia, neutropenia
CRP/ESR
RF, anti CCP = specific, ANA
X-ray
what ddx for RA
psoariatic arthritis = nail changes and plaques
chronic crystal arthritis
jaccoud’s arthritis
describe the management for RA
conservative = regalar exercise, PT, OT = aids, splints
medical = DAS28 assessment to monitor disease activity, DMARDS and biologicals early
steroids IM PO or intra articular for exacerbations
NSAIDs for sx relied
manage CVS risk = RA accelerates atheresclosis
prevent osteoporosis and gastric ulcers
what are the main DMARD’s used and their SE
cause myelosuppression = pancytopenia
methotrexate = hepatotoxic, pulmonary fibrosis
sulfalazine = hepatotoxic, reduced sperm count
hydrochloroquine = retinopathy, seizures
what is the pathophysiology of gout
deposition of monosodium rate crystals in and around joints
describe the presentation of gout
acute monoarthrits with severe joint inflammation
greater toe MTP = podagra
can also present as asymmetric oligoathrits, deposition of rate in pinna and tendons = tophi
renal disease = radiolucent stones and interstitial nephritis
ddx for gout
SA
pseudogout
haemoarthritis
what are the causes of gout
- hereditary
- drugs = diuretics, NSAIDs
- reduced renal excretion = renal impairment
what investigation are required in gout
polarised light microscopy = negatively birefringent needle shaped crystals
increased serum rate
describe acute rx of gout
NSAID’s - diclofenac
colchicine
use steroids if NSAID’s are contraindicated
describe prevention of gout
conservative = weight loss, avoid EtOH excess
allopurinol = xanthine oxidase inhibitors
what are seronegative sponyloarthropathies
group of inflammatory conditions affecting spine and peripheral joints without production of RFs, associated with HLA B27 allele
AS
psoriatic arhtris
reactive arthritis
what is AS and its sx
chronic disease characterised by stiffening and inflammation of spine and sacroiliac joints
gradual onset back pain
progressive loss of all spinal movements
costocondritis
what test is done for AS, what is the question marker posture
Schober’s test , less than 5cm
some pt with question mark posture = thoracic kyphosis and neck hyperextension
what are the extra articular manifestations of as
osteoporosis
acute iritis or anterior uveitis
apical pulmonary fibrosis
what Lx are required in AS
clinical dx
sacroiliitis - ireegularitis, sclerosis, erosions
bamboo spine - calcification of ligaments and periostea bone calcification
FBC anemia, increased ESR/CRP, HLA B27
DEXA scan and CXR
how is AS managed
conservative - exercise, physio
medical - NSAID’s, anti TNF if severe, local steroid injections, bisphosphonates
hip replacement to reduce pain and increase mobility
what is an x ray features of psoriatic arthritis
pencil in cup deformity = erosion
management for psoriatic arthritis
NSAIDs, sulfasalazine, methotrexate, ciclosporin, anti TNF
what is reactive arthritis
sterile arhtris 1=4 weeks after urethritis or dysentry
Urethritis: chlamydia, ureaplasma
Dysentery: campy, salmonella, shigella, yersinia
what lx are required in reactive arthritis
increased cap, ESR
stool culture if diarrhoea
urine chlamydia PCR
how is reactive arthritis managed
NSAID’s and local steroids
what is GCA/ temporal arteritis
inflammation of medium to large sized vessels, arteries
associated with PMR
what are the features of GCA
systemic = fever, malaise, fatigue headache - unilateral temporal artery and scalp tenderness jaw claudication amarosis fugax prominent temporal arteries, pulsation
management and lx in GCA
do ESR and starrt red 40-69mg/d PO increase ESR, CRP increased ALP reduced Hb, increased Plts temporal artery biopsy
PPI and alendronate cover = steroids risk
what is PMR, how does it present
severe pain and stiffness i shoulders, neck and hips, symmetrical, worse in morning, no weakness
carpal tunnel
systemic sx = fever. fatigue, weight loss
GCA association
what are the Lx and management of PMR
increased ESR, CRP, increased ALP
normal CK
rx = pred tapering course add PPI and alendronate cover
what is fibromyalgia and its associations
condition of central pain processing characterized by chronic widespread pain in all 4 quadrants of the body
sleep deprivation
what are the rx for FM
neurosis = depression, anxiety, stress
low income
divorce
what are the features of FM and Lx
chronic widespread MSK and tenderness
morning stiffness fatigue poor concentration sleep disturbance low mood
Lx all normal
how is FM managed
educate pt
CBT
graded exercise programs
amitriptyline or pregabalin
what is SLE
multi systemic autoimmune inflammatory disease
which autoAbs to a variety of autoantigens result in the formation and deposition of immune complexe
features of SLE
relapsing and remitting history
constitutional sx = fatigue, weight loss, fever and myalgia
SOAP BRAIN
soap brain in SLE
S erositis - Pleurisy, pericarditis
O ral ulcers - usually painless; palate is most
specific
A rthritis – small joints nonerosive
P hotosensitivity – or malar or discoid rash
B lood disorders – low WCC, lymphopenia,
thrombocytopenia, hemolytic anemia
R enal involvement -glomerulonephritis
A utoantibodies (ANA positive in >90%
cases)
I mmunologic tests e.g. low complements
N eurologic disorder - Seizures or psychosis
what lx required in SLE, what results are seen
ANA
Anti Ro, Anti La
Anti dsDNA
Antiphospholipid - increase risk of pregnancy loss and thrombosis
what is the management of SLE
sun protection - SPF
reduce CVS risk
hydrochloroquine = rash and arthralgia
short courses of prednisolone for flares
mycophenolate mofetil, azathioprine commonly used
what is SS
multisystem autoimmune disease
increased fibroblast activity result in abnormal growth of connective tissue leading to vascular damage and fibrosis
limited SS (70%) vs diffuse SS
what syndrome and features are seen in SSc
limited SSc
CREST
calconosis cutis raynaud's oesophageal and gut dismotility scelrodactyly telangiectasia skin involvelemt = beak nose, microstomia pulmonary HTN
How is SSc managed
no cure
pre for acute attacks
Raynaud’s: CCBs, ACEi, IV prostacyclin
Renal: intensive BP control – ACEi 1st line
Oesophageal: PPIs, prokinetics (metoclopramide) PHT: sildenafil,
what lx are required for SSc
FBC - anaemia, UE renal impairment
ANA positive
Abs - centromere in limited,
Scl 70 and RNA polymerase III in diffus e X-ray hands- calcinosis CXR, HRCT, PFT- pulmonary disease ECG & ECHO - PA hypertension, heart failure, myocraditis and arrhythmias,
what is sjogrens syndrome, how does it present
mnemonic –madfred! Myalgia Arthralgia Dry Mouth Fatigue Raynaud’s phenomenon Enlarged parotids Dry eyes
what lx are required in sjogren’s and management
Anti Ro and Anti La Antibodies – 90% of patients RF & anti ds-DNA
salivary gland biopsy may be needed
treatment is symptomatic
Avoid dry or smoky atmospheres
Dry eyes–artificial tears
Dry mouth -artificial saliva, sugar free gum/pastilles Skin emollients, vaginal lubricants
what is Osteoporosis
A skeletal condition characterized by low bone mass, deterioration of bone tissue, and disruption of bone architecture that leads to compromised bone strength and an increased risk of fractur
what are the rx factors modifiable and non
Non-modifiable
- Advanced age (>65 years)
- Female gender
- Caucasian or south Asians
- Family history of osteoporosis-genetic
- History of low trauma fracture (fall from
standing height or less, at walking speed or less.
Modifiable
- Low body weight (58 kg or body mass index
[BMI] <21)
- Premature menopause (age<45)
- Calcium/vitamin D deficiency
- Inadequate physical activity
- Cigarette smoking
- Excessive alcohol intake (>3 drinks/day)
- Iatrogenic: e.g. corticosteroids, aromatase
inhibitors
how is a diagnosis of OP made
DEXA) of the lumbar spine and hip
what is T score and its interpretation
- T-score is the number of SDs from the mean bone density of persons of same gender at age of peak density (25 years)
- T-score minus 2.5 or less = osteoporosis
- Normal BMD = T-score ≥ −1
- Osteopenia = T-score between −1 and −2.
what is a Z score
The Z-score is a comparison of the patient’s BMD with an age- & gender-matched population
-A Z-score
what is the treatment for osteopenia and osteoporosis
osteopenia = weight-bearing exercise, vitamin D3 supplementation (800-2000 IU/day), limiting alcohol, and smoking cessation. Dietary advice regarding calcium intake; supplements if needed.
osteoporosis = Vitamin D ± calcium supplementation plus:
1st line: Oral bisphosphonates, or IV if oral not tolerated.
2nd line: Denosumab or teriparatide
what is raynauds phenomenon, puts and color changes
due to vasospasm of the digits. It is painful and is characterized by a typical sequence of colour changes in response to a cold stimulus. It is often also precipitated by stress.
white- inadequate blood flow blue -venous stasis
red -re-warming hyperaemia.
diseases and causes associated with raynauds
SSc
SLE
Sjogrens syndrome
use of heavy vibrating tools
cervical rib
beta blockers
treatment of raynauds
keep warm
avoid smoking.
Calcium-channel blockers are the first-line. Phosphodiesterase-5 inhibitors, and prostacyclins are usually effective.
complications of raynauds
digital ulcers, severe digital ischaemia and infection.
what is OM
steomalacia describes softening of the bones secondary to low vitamin D levels that in turn lead to decreased bone mineral content.
rickets in children
causes of OM
vitamin D deficiency malabsorption lack of sunlight diet chronic kidney disease drug induced e.g. anticonvulsants inherited: hypophosphatemic rickets (previously called vitamin D-resistant rickets) liver disease: e.g. cirrhosis
features of OM
bone pain
bone/muscle tenderness
fractures: especially femoral neck
proximal myopathy: may lead to a waddling gait
lX IN OM
bloods
low vitamin D levels
low calcium, phosphate (in around 30%)
raised alkaline phosphatase (in 95-100% of patients)
x-ray
translucent bands (Looser’s zones or pseudofractures)
TREATMENT IN OM
vitamin D supplmentation
a loading dose is often needed initially
calcium supplementation if dietary calcium is inadequate
