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Core Conditions > locomotor > Flashcards

locomotor Flashcards

1
Q

Osteoarthritis definition

A
  • Result of mechanical and biological events that destabilise the normal process of degradation and synthesis of articular cartilage chondrocytes, extracellular matrix and subchondral
  • Involves the entire joint, including the articular cartilage, subchondral bone, pericapsular muscles, capsule and synovium
  • Condition leads to loss of cartilage, sclerosis and eburnation of subchondral bone, osteophytes and subchrondral cysts
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2
Q

how common is Osteoarthritis

A

• 8.5 million people in the UK have OA

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3
Q

causes of Osteoarthritis

A
  • In the affected joint, there is a failure in maintaining the homeostatic balance of the cartilage matrix synthesis and degradation, resulting from reduced formation or increased catabolism
  • Focal strss, trauma and eventual cartilage loss – this canfurther alter the joint anatomy, to predispose it even more to the potential detrimental effects of mechanical factors and physical activities, by redistributing and increasing the focal laoding in the joint
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4
Q

risk factors for Osteoarthritis

A
  • Age >50 years
  • Female
  • Obesity
  • Genetic factors
  • Physical/manual occupation
  • Knee malalignment
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5
Q

symptoms/signs of Osteoarthritis

A
  • Presence of risk factors
  • Pain
  • Functional difficulties – knee giving away or locking, can be present
  • Knee, hip, hand or spine involvement
  • Bony deformities – MCPJs and involves the PIPJs and DIPJs – helps to distinguish it from RA
  • Limited range of motion - both active and passive range of joint movement is reduced in moderate to advanced OA and this is usually associated with pain
  • Malalignment – particularly in the knee where OA causes both gene valgum (knock-knees) and genu varum (bow-legs)
  • Tenderness
  • Crepitus
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6
Q

DDx of Osteoarthritis

A
  • Gout
  • Pseudogout
  • RA
  • Psoriaric arthritis
  • Avascular necrosis (AVN)
  • Internal derangements (e.g. meniscal tears)
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7
Q

Investigations of Osteoarthritis

A

• 1ST LINE:

  • XR OF AFFECTED JOINTS: new bone formation (osteophytes), joint space narrowing, and subchondral sclerosis and cysts
  • SERUM CRP: normal
  • SERUM ESR: normal
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8
Q

Management of Osteoarthritis

A

• ACUTE:
- 1ST LINE: local analgesia e.g. capsaicin topical – apply to the affected areas three to four times daily
- 2nd LINE: paracetamol + local analgesia e.g. paracetamol + capsaicin topical
- 3rd LINE: NSAIDs + paracetamol + local analgesia e.g. paracetamol + naproxen + capsaicin
- 4th LINE: opioids + NSAIDs + paracetamol + local analgesia e.g. paracetamol + capasaicin + naproxen + oxycodone
• ONGOING:
- 1ST LINE: surgery

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9
Q

Prognosis and complications of Osteoarthritis

A

prognosis - Chronic slowly progressive disease and is almost ubiquitous with advancing age – no cure

complications - • Functional decline and inability to perform activities of daily living, spinal stenosis in cervical and lumbar OA, NSAID-related GI bleeding, effusion, NSAID-renal dysfunction

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10
Q

Gout definition

A
  • Gout is a syndrome characterised hy: hyperuricaemia and deposition of urate crystals causing attacks of acute inflammatory arthritis, tophi around the joints and possible joint destruction, renal glomerular, tubular and interstitial disease and uric acid urolithiasis
  • Most commonly affects the first toe, foot, ankle, knlee, fingers, wrist and elbow but can affect any joint
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11
Q

how common is Gout

A
  • 1.6 per 1000 men and 0.3 per 1000 in owmen

* Mainly adults

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12
Q

causes of gout

A
  • Uric acid is the end-product of the breakdown of purines (adenine and guanine), and exists as sodium urate in extracellular fluid
  • Two-thirds of urate is excreted by the kidneys and a third by the GI tract. Hyperuricaemia is the single most important risk factor for developing gout
  • The duration and magnitude of hyperuricaemia is directly correlated with the likelihood of subsequent development of gouty arthritis, uric acid kidney stones, and age of onset of clinical gouty manifestations
  • However, gout can occur in people with normal plasma urate levels. Hyperuricaemia is usually due to impaired renal excretion of urate
  • About 90% of people with hyperuricaemia are under excretors of urate, about 10% are over-producers, and some can be both
  • Gout tends to attack joints in the extremities because temperatures in the feet and hands can be low enough to precipitate urate from plasma
  • Thus tophi typically form in the helix of the ear, finger tips, olecranon bursae, and other cool anatomical sites
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13
Q

risk factors of gout

A
  • Older age
  • Male
  • Menopausal status
  • Consumption of meat, seafood, alcohol
  • Use of diuretics, ciclosporin or tacrolimus, pyrazinamide and aspirin
  • Genetic susceptibility
  • High cell turnover state
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14
Q

symptoms of gout

A
  • Presence of risk factors
  • Rapid-onset severe pain
  • Foot joint distribution
  • Few affected joints
  • Swelling and joint effusion
  • Tenderness
  • Tophi
  • Erythema and warmth
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15
Q

DDx of gout

A
  • Pseudogout (calcium pyrophosphate deposition disease)
  • Septic arthritis
  • Trauma
  • RA
  • Reactive arthritis and psoriatic arthritis
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16
Q

Investigations of gout

A
  • 1st LINE: arthrocentesis with synovial fluid analysis  WWC count >2/0 x10^9/L; strongly negative birefringent needle-shaped crystals under polarised light
  • CONSIDER: uric acid level, x-ray of affected joint, ultrasound
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17
Q

Management of gout

A

• ACUTE:
- 1ST LINE – NSAID: naproxen
- 2nd LINE – colchicine  used when NSAIDs and COX-2 inhibitors are contraindicated because of a Hx of GI bleeding or comorbidities e.g. asthma
- 3rd LINE – corticosteroid: prednisolone  when 1st line and nd line are contraindicated e.g. in patients with renal insufficiency
• RECURRENT (2-3 WEEKS POST-ACUTE EPISODE):
- 1ST LINE: allopurinol (xanthine oxidase inhibitor)
- 2nd LINE: febuxostat (nonpurine selective xanthine oxidase inhibitor that reduces the production of uric acid)
- 3rd LINE: probenecid – if patient cannot tolerate allopurinol or febuxostat  not effective in pts with renal insufficiency and could be used in combination with allopurinol

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18
Q

Prognosis and complications of gout

A

prognosis - good prognosis if managed well

complications - acute uric and nephropathy, nephrolithiasis

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19
Q

Septic arthritis definition

A
  • Infection of 1 or more joints caused by pathogenic inoculation of microbes
  • Occurs either by direct inoculation or via haematogenous spread
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20
Q

how common is septic arthritis

A
  • 6 cases per 100,000

- mainly adults

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21
Q

causes of septic arthritis

A
  • It results from the infection of the joint with pyogenic organisms, most commonly staphylococcus aureus
  • In sexually active patients, gonococcal arthritis may be suspected
  • Gram-negative organisms are more common in the elderly or immunosuppressed e.g. TB
  • Joints become infected by direct injury or by blood borne infection from an infected skin lesion or other site
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22
Q

risk factors of septic arthritis

A
  • Underlying joint disease
  • Joint prostheses
  • IV drug abuse
  • Diabetes
  • Presence of cutaneous ulcers
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23
Q

symptoms/signs of septic arthritis

A
  • Hot, swollen, tender, restricted joint
  • Low-SES
  • Hx of IV drug abuse, diabetes, cutaneous ulcers, RA, OA
  • Prosethtic joint
  • Short Hx of symptoms
  • Fever
24
Q

DDx of septic arthritis

A
  • OA
  • PA
  • RA
  • Gout
  • Pseudogout
  • Haemarthrosis
  • Trauma
25
Q

Investigations of septic arthritis

A

• 1st LINE:

  • Blood culture  1st to build a systemic picture
  • Synovial fluid gram stain and culture: drawn before abx therapy  presence of micro-organisms; subsequent culture revealing organism type and sensitivities to abx therapy
  • Synovial fluid WCC  quantity of WCs
  • WCC  may be elevated
  • ESR and CRP  raised
  • Plain radiograph  may reveal degenerative changes or chondrocalcinosis
  • USS  if hip sepsis is suspected, it is recommended that aspiration be performed under US guidance, may show the presence of an effusion to guide aspiraton
26
Q

management of septic arthritis

A

• GRAM-POSITIVE OR NEGATIVE GRAM STAIN:
- 1ST LINE: vancomycin plus joint aspiration IV
- 2ND LINE: clindamycin or cephalosporin plus joint aspiration IV
• SUSPECTED GRAM-NEGATIVE INFECTION:
- 1ST LINE: 3rd gen cephalosporin e.g. ceftriaxone IV
- 2nd LINE: IV ciprofloxacin plus joint aspiration e.g. ciprofloxacin IV

27
Q

prognosis of septic arthritis

A

prognosis:
- Delayed or inadequate treatment can lead to irreversible joint destruction and subsequent disability
• Estoimated case fatality rate of 11%

28
Q

complications of septic arthritis

A

• Antibiotic-associated allergic reaction, osteomyelitis, joint destruction

29
Q

prolapsed disc definition

A

• Disorders affecting intervertebral discs include:
- Disc herniation (prolapsed intervertebral disc)
- Degenerative disc disease
- infection (discitis)
• Spinal disc problems can lead to symptoms of back pain and/or sciatica
• There are many other causes of back pain and/or sciatica but they do not primarily originate from the intervertebral discs

30
Q

how common is a prolapsed disc

A

• Back pain without sciatica is extremely common

31
Q

causes of prolapsed disc

A
  • The spinal cord is shorter than the spinal canal and ends between the L1 and L2 vertebrae in adults
  • Below the termination of the cord, the nerve roots form the cauda equina which has a horse-tail like appearance containing nerve roots L1-L5 and S1-S5
  • Spinal pathology below L1 of the vertebral column produces mostly lower motor neurone signs
  • The intervertebral discs lie between adjacent vertebrae - they consist of a peripheral fibrocartilaginous part called the annulus fibrosus and a central semifluid/gelatinous part - the nucleus pulposus
  • The nucleus pulposus of the disc is usually contained by the annulus fibrosus - if the nucleus herniates, it can irritate and/or compress the adjacent nerve root, causing symptoms of sciatica
  • Traumatic disc herniation can occur - disc herniation can also occur secondary to degenerative disc disease
  • A herniated nucleus pulposus is most common in those aged below 40 years, whilst degeneration of discs tends to affect those aged over 40 years, with the prevalence increasing with advancing age
  • Disc lesions of the lumbar spine are more common than the cervical spine and disc lesions of the thoracic spine are rare
  • The term sciatica is used for the pain, tingling, and numbness that arise due to nerve root entrapment in the lumbosacral spine. The symptoms may be felt in one or more of the lumbar nerve roots
  • About 90% of cases of sciatica are caused by a herniated intervertebral disc. This most commonly occurs at the L5/S1 level
32
Q

risk factors for prolapsed disc

A
  • Risk factors for any of the causes

* Lorry drivers

33
Q

symptoms/signs of prolapsed disc

A

• Lumbosacral disc herniation:
- If there is nerve entrapment in the lumbosacral spine, this leads to symptoms of sciatica which include  unilateral leg pain, radiates below the knee to the foot/toes, leg pain more severe than back pain, relieved by lying down and exervated by long walks and prolonged sitting, numbness, paraesthesia, weakness, loss of tendon reflexes, found in the same distribution and only in one nerve root distribution, positive straight leg raise, large herniations can compress the cauda equine leading to symptoms/signs of saddle anaeasthesia, urinary retention and incontinence
• Thoracic disc herniation:
- Nerve root irritation or cord compression, thoracic spine lesions can present with symptoms similar to lumbar disc lesions, in nerve root irritation, there may be shooting pain down the legs, there may be pain, paraestehisa or dysaestehsia in a dermatomal distribution, a thoracoabdominal sensory examination can help to determine the level of the lesion, testing of the abdominal and cremasteric reflexes can help to identify myelopathy and cord compression
• Cord compression:
- This is a neurosurgical emergency, cord compression in the thoracic spine can produce paraplega, there may be clonus or a positive Babinski reflex, there may be bladder/bowel dysfunction
• Herniation of T2-T5 can mimic cervical disc disease

34
Q

DDx of prolapsed disc

A
  • Degenerative disc disease

* Discitis

35
Q

Investigations for prolapsed disc

A
  • No investigation may be needed if symptoms settle within six weeks
  • 1st LINE: MRI is very sensitive in showing disc herniations, CT myelography may also be used
  • 2nd LINE: plain x-rays are sometimes usefl, as they can show misalignments, instabilities and congenital abnormalities as well
36
Q

management for prolapsed disc.

A
  • 1ST LINE: analgesia e.g. paracetamol or NSAIDs – may be used in combination ADJUNCT: codeine or tramadol may be added if pain is still present
  • If muscle pain is present  benzodiazepine
  • Persistent sciatica  trial of tricyclic antidepressant or gabapentin if there is persistent sciatica
37
Q

prognosis and com0plications of prolapsed disc

A

prognosis - favourable

complications - permanent nerve damage with sensory deficits and/or permanent motor weakness

38
Q

rheumatoid arthritis definition

A
  • Chronic inflammatory condition which primarily affects the small joints of the hands and feet and if not tx aggressively can be a mjor cause of work loss, decreased QOL, need for joint replacement surgery and mortality
  • It is a clinical diagnosis
39
Q

how common is rheumatoid arthritis

A

• Affects 1% of the population

40
Q

causes of rheumatoid arthritis

A
  • Inflamed synovium is central to the pathogenesis
  • The synovium shows increased angiogenesis, cellular hyperplasia, influx of inflammatory cells, changes in the expression of cell surface adhesion molecules and many cytokines
  • The synovial lining becomes hyperplastic, with infiltration of the sublining with mononuclear cells including T cells, B cells and macrophages and plasma cells
  • This formation of locally invasive synovial tissue is characteristic and it is involved in causing the erosions seen in RA
  • Leads to a very inflammatory setting that, when not tx, leads to the eventual destruction of the involved joint
41
Q

risk factors for rheumatoid arthritis

A
  • Genetic predisposition

* Smoking

42
Q

symptoms of rheumatoid arthritis

A
  • Active symmetrical arthritis lasting >6 wks
  • Age 50-55
  • Female
  • Joint pain and swelling – most commonly bilateral MCP, proximal IP and MTP joints are involved, they are painful to touch and when range of motion exercises are performed, wrists, elbows, and ankles are also affected
43
Q

signs of rheumatoid arthritis

A
  • Swan neck deformity – seen in advanced RA with damage to ligaments and joints, DIP hyperflexion and PIP hyperextension
  • Boutonniere’s deformity – PIP flexion with DIP hyperextension
  • Ulnar deviation – due to inflammation of the MCP joints causes the fingers to become dislocated
  • Rheumatoid nodules – nodules over the extensor surfaces of tendons
  • Skin rashes
  • Pleuritc chest pain
  • Scleritis and/or uveitis – inflammatory eye disease may be seen in severe RA
44
Q

DDx of rheumatoid arthritis

A
  • Psoriatic arthritis
  • Infectious arthritis
  • Gout
  • SLE
  • OA
45
Q

Investigations for rheumatoid arthritis

A

• 1ST LINE:

  • RHEUMATOID FACTOR: positive (in 60-70% of pts), can also be seen in chronic infections, hep C and other rheumatological conditions
  • ANTI-CCP Ab: positive (70% of pts)
  • RADIOGRAPHS: erosions at the margings of the joint, affecting the subchondral bone first and later progress to cause joint space narrowing  PRESENCE OF EROSIONS
  • ULTRASONOGRAPHY: may be useful at initial presentation to detect synovitis of the wrist and fingers  synovitis of the wrist and fingers
46
Q

management of rheumatoid arthritis

A

• 1ST LINE:

  • NOT PREGNANT/PLANNING PREGNANCY: methotrexate
  • PREGNANT: corticosteroid (prednisolone) or sulfasalazine or hydroxychloroquine
47
Q

prognosis and complications of rheumatoid arthritis

A

prognosis - RA pts tx aggressively and early have a good prognosis with most pts achieving good disease control

complications - Work disability, increased joint replacement surgery, increased CAD

48
Q

Osteoporosis definition

A

• Complex skeletal disease characterised by low bone density and micro-architectural defects in bone tissue, resulting in increased bone fragility and susceptibility to fracture

49
Q

how common is osteoporosis

A
  • Predominantly affects white menopausal women
  • Affects 10 million people in the US
  • Affects 1 in 2 women and 1 in 5 men
50
Q

risk factors for osteoporosis

A
  • Prior fragility fracture
  • Female sex
  • White ancestry
  • Older age (>50 years for women and >65yrs for men)
  • Low BMI
  • Fx of maternal hip fracture
  • Loss of height
  • Smoking
  • Low calcium/vit D
51
Q

symptoms/signs for osteoporosis

A
  • Presence of risk factors
  • Back pain – may be due to vertebral facture
  • Kyphosis – may be evidence of vertebral fractures
  • Impaired vision – may result in an increased risk of falling and thus increased risk of fracture
  • Impaired gait, imbalance and lower-extremity weakness
  • Vertebral tenderness
52
Q

DDx for osteoporosis

A
  • Multiple myeloma
  • Osteomalacia
  • CKD
  • Primary hyperparathyroidism
53
Q

Investigations for osteoporosis

A

• 1ST LINE:

  • DXA SCAN: T-score <2.5 indicates osteoporosis, same score but with fragility fracture indicates severe or established OP
  • QUS OF THE HEEL
  • X-RAY OF WRIST, HEEL, SPINE AND HIP: not diagnostic of OP, may reveal osteopenia and/or fractures
  • SERUM ALKALINE PHOSPHATASE: if elevated could indicate osteomalacia  normal
54
Q

management of osteoporosis

A

• 1ST LINE:
- ORAL BISPHOSPHONATES: aledronic acid
• 2nd LINE: if oral bisphosphonates not tolerated
- DENOSUMAB

55
Q

prognosis and complications of osteoporosis

A

prognosis - with preventative tx, fractures can be avoided

complications - Hip factures, rib fractures, wrist fractures, chronic pain syndrome, jaw necrosis associated with bisphosphonates tx

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