rheumatology + ortho Flashcards
osteoarthritis- overview
result of mechanical and biological events that disrupt the bodys ability to synthesize and repair cartilage. affects the whole joint- not just the articular surfaces.
can be primary- not caused by any event or external cause
2’ - brought about by either congenital abnormalities or trauma
risk factors, investigation of osteoarthritis.
RF: over 50, female, obesity, genetic factors, joint abnormality/ misalignment, physically demanding occupation/ sport, trauma/ injury.
Ix: history + physical- generally a clinical diagnosis
X-ray (sclerosis, osteophyte, narrowing, subchondral cysts)
can do bloods- but mostly to R/O inflammatory processes.
management of OA
topical analgesia, lifestyle modification, IA steds,
2nd line- paracetamol + topical
joint replacement surgery.
generally a poor prognosis as will not get better on its own.
principles of cauda equina
Cauda equina
Compression of nerve roots below the end of the spinal cord (L1/L2)
A clinical diagnosis
Occurs acutely
Causes => central massive disc prolapse/ herniation, tumours, abscess, TB, haematoma, trauma
Symptoms => urinary incontinence/ retention, faecal incontinence, bilateral weakness + pain, reduced saddle sensation, reduced anal tone, bilateral ankle reflexes lost, decreased anal tone, LMN signs in the lower limbs
Sudden onset => this is an emergency
Rapid MRI (but can be CT)
Management => Urgent surgical decompression
Important to catheterise
If you do not intervene, these patients can become paralysed permanently
degenerative disc disease overview + diagnostic factors
majority of degenerative discs are asymptomatic
but can cause pain- longstanding with/out concurrent lower limb neuro symptoms.
can be exacerbated by activity- but also positional
can progress leading to loss of height, facet joint OA, herniation, hypertrophic changes, nerve route irritation.
DF:
persistent low back pain +/- radicular pain.
aggravation with activity and relived by rest.
risk factors for DDD + Ix + Mx
age, genetics, occupation, tobacco, facet joint arthitis, abnormal pelvic morphology. obesity, DM.
errect L spine/ MRI.
2nd line- discography.
Rx:
physio
paracetamol/ nsaid
topical analgesia
muscle relaxant ( diazepam)
facet joint blocks, nerve block or epidural.
consider decompression.
longer than 3/12
consider pain clinic + amitriptyline
+ surgery (decompression, fusion)
nerve route entrapment/ sciatica aetiology
due to disc prolapse (pulposus spills out) - contacts the nerve
or spial stenosis (flavum hypertrophy, pedicle damage, osteophytes)
causes unilateral leg pain > back pain. radiates to below knee- can also affect buttocks
can have nerve route motor, sensory or reflex changes.
generally improve after 6-12 weeks.
can get claudication - neurological cause as opposed to vascular- try different spinal positions and see if it is brought on.
investigation and management of nerve route entrapment/ radiculopathy
X-ray
MRI gold standard
Rx:
nsaids, paracetamol, physiotherapy
amitriptyline
decompression (discectomy, laminectomy)
discuss polymyalgia rheumatica - definition and risk factors
an inflammatory condition causing pain and stiffness in the hsoulders, pelvic girdle and neck.
strong association with giant cell arteritis.
RF: older age
female, northern european ancestry
infection (clamydia, mycoplasma, parvovirus)
how to diagnose PMR + Rx
Dx:
core features needed for at least 2/52
bilateral shoulder pain radiating to elbow
bilateral pelvic girdle pain
worsens with movement
interferes with sleep
morning stiffness >45 mins.
R/o other conditions e.g RA.
Rx: should be a response to oral corticosteroids within a week. - normalisation of blood inflam markers by 4 weeks.
15 mg pred per day. reassess in a week.
Ix of PMR
Ix is generally to rule out other conditions
FBC, U+E, LFT.
Ca2+, raised in hpyer PTH, low in osteomalacia
protein electrophoresis- exclude myositis
RF factor + anti CCP
urine dipstick
ANA- exclude SLE
urine bence jones- myeloma
CXR- mediasteinal abnormalitites.
what guidance do you give to patients whom have been put on steroids
DONT STOP
DONT- make them aware after 3 weeks they will be dependant and not to stop taking them
S- sick day rles- increace the dose if theey are more unwell
T- treatment card to alert other med professionals
O- osteoperiosis cover
P- PPI cover for stomach.
discuss osteoporosis + the types available
decreaced bony density- increaced fracture risk
asymptomatic untill #
classification
primary type 1- increaced osteoclast activity, less formation than reabsorbtion. female post menopause- loss of trabecular bone
primary type 2- nutrition
+ decreaced physical acticity related, cortical and trabecular bone lost.
econdary- RARE- assoc with endocrine disease, loss of cortical and trabecular bone
risk factors for osteoporosis
RF:
age
women
post menopause
vit D deficiency
CKD, hypothyroid, coeliac disease, myeloma, HIV, depression
drugs
causes of 2’ osteoporosis:
SHATTERED
Steroids (>5mg a day pred)
hyper (lots)
alcohol + tobacco
Thin
testosterone
early menopause
renal/liver faliure
erosive inflam bone disease
dietary Ca2+.
diagnosis management of osteoporosis
bone densitomotry T score less than 2.5 (each 1SD is 2.6x risk for hip#)
fragility #
Ix: DEXA – gold standard
Rx: 1st line- bisphosphonates + calcium & vit D supplimentation
2nd line- raloxifene OR denosumab + clcium & vitamin D.
what is osteomalaicia, how does it compare to osteoporosis
malacia is the reduced mineralisation of bone, porosis is the reduction in amount of bone.
- definition- a metabolic boen disease characterised by incomplete mineralisation of underlying bone matrix (osteoid) following growth plate closure.
occurs at any age.
pathophysiology - (same a rickets) deficiency in vitamin D or calcium- less mineralisation of bone
secondary hyper PTH- reabsorbing more bone worsening the problem.
S+S- may be asymptomatic- fatigue, bone pain, tenderness.
proximal weakness, hypocalcaemia symptoms.
deformities
abnormal fractures.
investigation and treatment of osteomalacia
Ix:
serum 25 hydroxyvitamin D - less than 25mm is deficient
X-ray- ? more luency
serum calcium and phosphate
serum ALP-high
PTH - high
FBC+ ferratin to exclude Fe deficiency anaemia
ESR + CRP- exclude infections
Rx:
cholecalciferol
how does rickets differ from osteomalacia
largley simalar processes- affecting growth plate of long bones- soft deformed bones
affects growing children before fusion of epiphyses- affects wrists knees and costochondral junctions
presents with knock knee, bow leg, growth retardation
rachitic rosary (rib expansion at costochondral junctions)
Mx:
vitamin D suppliment 400iu
ergocalciferol
rheumatoid arthritis overview.
an autoimmune inflammatory polyarthropathy
causing deformity and restriction in function. - progressive with no sudden onset.
RF: smoking, female, infections, stress
HLA DR1 + 4 are associated.
pathophysiology of RA + signs and symptoms
rheumatoid factor is a IgM vs an IgG. - form an immune complex–> activating compliment and triggering infection.
joint inflammation occurs when white cells, cytokines, and metalloproteinase prroliferation occurs in the synovium - overall joint destruction.
S+S: MCP and PIP joints in hand symmetrically
ulnar deviation
deformities in the hand
rheumatoid nodules on extensor surfaces
morning stiffness lasting over 1 hour in the morning.
more systemic- dry eyes, scletiris, uveitis, cardioresp symptoms
Ischaemic heart disease can also present!
investigations and management of rheumatoid arthritis
American college of rheum criteria, need at least 4, symptoms for 6 weeks.
morning stiffness 1hr or more
>3 joints involved
hand + wrist movement
symmetrical
nodules
positive RF
radiological changes.
Rheumatoid factor and anti-CCP are very specific.
x-ray bony erosions.
check for C spine subluxation with X ray
Rx:
paracetamol + NSAIDS
1st line- DMARDS (meth+ folate) + short term glucocorticoids.
2nd - DMARD + another DMARD
3rd- consider biologics infliximab, adalimumab, (monoclonal against tnf)
must refer to Ra clinic within 3 days (from GP) and be seen in 3 weeks.
