Back Anatomy Flashcards
What is the main age of developing herniated disc
30-50 As you get older the discs desiccate and dry out so are less likely to prolapse in those at retirement age
Non specific low back pain
Pain not due to any specific or underlying disease that can be found
Mechanical low back pain?
worse with movement
better or not present at rest
common causes are muscular tension eg chronic poor posture or weak muscles
acute muscle sprain or spasm
degenerative disc disease
osteoarthirits of facet joints
Nerve root pain (sciatica)?
Pain radiating to the lower limbs
may accompany mechanical back pain
usually due to a disc herniation (slipped disc) contacting the exiting lumbar nerve root
location of pain determined by level of herniated disc
Causes of low back pain serious
tumour-metastatic or myeloma
infection such as discitis.vertebral osteomyletis,paraspinal abcess,or microbiology eg TB,staph,srep
inflammatory spondyloarthropathy eg ankylsoing spondylitis,psoriatic artiritis,IBD associated
fracture eg traumatic or atraumatic
large disc prolapse casuing neurological compromise
referred pain from pancreas kindeys or aortic aneurysm
E What are the indicators for sciatica? (5)
- Unilateral leg pain greater than low back pain
- Pain radiating to foot or toes
- Numbness and paraesthesia in the same distribution
- Straight leg raising test induces more leg pain
- Localised neurology- limited to 1 nerve root
- Low back pain- what are red flag symptoms? (10)
-
pain at night or increased pain when supine
constant or agressive pain
thoracic pain
weight loss
previous malignancy
fever/night sweats
immunosuppressed
bladder or bowel dysfunction (sphincter dysfunction)
leg weakness or sensory loss
age<20 or>55
What do we do if we see or don’t see red flag signs for back pain
If we see red flag sign do imaging
If we don’t we can wait 6-12 weeks to do imaging
if symptoms worsen then reassess 3-4 weeks later
- Inflammatory arthropathy e.g. ankylosing spondylitis- what do we see on Xray and mri?
White area- shiny corner- on heavily T2 weighted on mri- means there’s inflammatory arthropathy affecting insertion of fibres of annulus fibrosis as they go into bone
sacro ilitis (x ray)
mri
spinal enthethisis
bridging causes syndesmophtyes (new bone grwoth between adjacent vertebrea) causes
spinal fusion
Tuberculosis of spine- what do we see on X ray?
- Destruction of vertebral body
- Expansion of vertebrae
- Collapse of vertebrae
- Compression of spinal cord
- Paraplegia
function of spine
locomotor-capable of both rigid and mobile
bony amour protects the spinal chord
neurological spinal chord transmission of signals between brain and periphery
spinal chord structure
7 cervical
12 thoracic
5 lumbar vertebrae
intervertebral discs which are shock absorbers allowing segmentation and multi directional movement
facet joints which are small synovial joints at posterior spinal column
muscles to move spine
when does the spinal chord end
at the level of L2
nerve roots exit the spinal chord bilaterally
movement of spine
flexion vs extension
lateral flexion
rotation
back pain
very common >50% of people experience
acute is usually self limiting
96% better in six weeks
chronic back pain>12 weeks also common due to a sedentery lifestyle
cauda equina syndrome
neurosurgical emergency
if untreated can lead to permanent lower limb paralysis and incontinence
symtoms and signs of CES
saddle anasthesia
bladder or bowel incontinece
loss of anal tone PR
radicular leg pain
ankle jerks may be absent
investiagtions for CES
urgent MRI L spine
causes of CES
disc herniation
bony mets
myeloma
tb
paraspinal abcess
treatment for ces
treat underlying cause
may need surgery
hisotry taking for back pain
SOCRATES
effect of movement and inactivtiy
leg weakness
sensory loss or paraesthisa
lower limb claudication
exakine via look fell move straight leg raise lower limb neurological exame and general exam looking for signs of malignancy and AAA
treatment for lower back pain without red flags
time
analgesia eg NSAIDS paracetmaol codeine ibuprofen
avoid bed rest and keep moving
physiotherapy-soft tissue work and corrective exercises
bloods
ESR-increased in myeloma chronic inflammation and tb
crp-increased in infection of inflammation
fbc-anemia in myeloma or chronic disease, wcc increased in infection
alkaline phosphatase(alp)-increased with bony mets
calcium-may be increased in myeloma or mets
psa-increased in prosate cancer with mets
imagin
radiographs(x rays)-poor sensitivity,expose to radiation bt cheap and widely available
CT-good for bony pathology but has larger radiation dose
mri-best visualisation of soft tissue structures like tendons and ligaments best for spinal imaging as can see spinal chord and exiting nerve roots but is expensive and time consuming
herniated disc treatment
conservative analgesia esp nsaids and oysiotherapy to impove core strength and treat muscle spasms
nerve root injection (local anaesthetic or glucocorticoid)
surgery if neurological compromise or symptoms perisist
spontaneous resoltuon
herniated portio of disc tends to regress with time either partial or complete resoltuion occuring in 2 thirds of cases after 6 months
inflammatory spondyloarthiritis
group of autoimmune inflammatory diseases eg ankylosing spondyloarthritis,psoriatic arthirtis,ibd
primary inflammation of spine (spondylitis) and sacro iliac joints (sacroilitis)
peripheral joints esp joint insertions (entheses) affected
extra articular manifestations of inflammatory spondylarthritis
Anteriour uveitis (ocular inflammation)
Apical lung fibrosis
Aortitis or aortic regurgitation
Amyloidosis due to chronically serum amyloid A depostion in organs
what can occur due to entheses
dactylitis (sausage fingers)
ankylosing spondylitis pathophys
chacaterised by enthesis
polygenic
HLA-B27 strongest genetic risk factor
HLA is a region on chromosome encoding MHC molecules,HLAB27 is a class 1 mhc molcule,cells present peptides to cd8 t cells in association with mhc class 1 molecules
HLAB27 used as a diagnostic marker but postive reulst alone not diagnosis
what cytokines contribute to ankylosing spondyltits
TNF A
IL-17
IL-23
as well as abberant peptide processing pathways(aminopeptidases ) in endoplasmic reticulum
management of as
1) Physiotherapy and a life-long regular exercise programme
2) Pharmacological
1st line: non-steroidal anti-inflammatory drugs (NSAIDs)
-e.g. ibuprofen, naproxen, diclofenac
-Mechanism: NSAIDs inhibit cyclooxygenase 1 and 2 (COX1 and 2)
-Risks: peptic ulcer, renal, asthma exacerbation, ↑ atherothrombosis risk
-Selective COX2 inhibitors (e.g. celecoxib) reduce GI ulcer risk
2nd line: ‘Biological’ therapies
Therapeutic monoclonal antibodies (mAbs) targeting specific molecules
Use if inadequate disease control after trying 2 NSAIDs
Anti-TNF-alpha (e.g. adalimumab, certolizumab, infliximab, golimumab)
Anti-IL17 (e.g. secukinumab)
