rheumatology + ortho Flashcards

1
Q

osteoarthritis- overview

A

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

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2
Q

risk factors, investigation of osteoarthritis.

A

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.

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3
Q

management of OA

A

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.

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4
Q

principles of cauda equina

A

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

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5
Q

degenerative disc disease overview + diagnostic factors

A

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.

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6
Q

risk factors for DDD + Ix + Mx

A

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)

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7
Q

nerve route entrapment/ sciatica aetiology

A

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.

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8
Q

investigation and management of nerve route entrapment/ radiculopathy

A

X-ray
MRI gold standard

Rx:
nsaids, paracetamol, physiotherapy
amitriptyline
decompression (discectomy, laminectomy)

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9
Q

discuss polymyalgia rheumatica - definition and risk factors

A

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)

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10
Q

how to diagnose PMR + Rx

A

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.

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11
Q

Ix of PMR

A

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.

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12
Q

what guidance do you give to patients whom have been put on steroids

A

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.

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13
Q

discuss osteoporosis + the types available

A

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

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14
Q

risk factors for osteoporosis

A

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+.

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15
Q

diagnosis management of osteoporosis

A

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.

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16
Q

what is osteomalaicia, how does it compare to osteoporosis

A

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.

17
Q

investigation and treatment of osteomalacia

A

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

18
Q

how does rickets differ from osteomalacia

A

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

19
Q

rheumatoid arthritis overview.

A

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.

20
Q

pathophysiology of RA + signs and symptoms

A

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!

21
Q

investigations and management of rheumatoid arthritis

A

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.