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GP block (Y3) > Week 2: MSK conditions > Flashcards

Week 2: MSK conditions Flashcards

1
Q

causes of back pain

A
  • Herniated discs e.g. sciatica
  • Muscle strain (overuse or poor posture)
  • Muscle injury
  • Vertebral fracture
  • Osteoporosis
  • Metastases
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2
Q

types of back pain

A

axial

referred

radicular

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3
Q

axial pain

A
  • ‘mechanical pain’
    • Confused to one spot or region
    • Sharp or dull, comes and goes, constant or throbbing
    • E.g. muscle strain
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4
Q

referred pain

A
  • Dull and achey, pain moves around and varies in intensity
  • E.g. degenerative disc disease may cause referred pain to the hips and posterior thighs
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5
Q

radicular pain

A
  • Electric shock-like or searing
  • Pain follows path of the spinal nerve as it exits the spinal canal
  • Caused by compression or inflammation of the spinal nerve root
  • May be accompanied by weakness/ numbness
  • E.g. sciatica
    • Herniated discs
    • Spinal stenosis
    • Spondylolisthesis
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6
Q

red flags of MSK presentation

A
  • Back pain
    • Cauda equina
    • Bone cancer
  • Joint pain
    • Septic arthritis
  • Bone pain
    • Bone malignancy
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7
Q

Inflammatory joint disease

A

Joint inflammation caused by an overactive immune system affects many joints at the same time.

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8
Q

major types of inflammatory joint disease

A
  • RA
  • Psoriatic arthritis
  • Ankylosing spondylitis
  • Gout
  • Lupus
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9
Q

Difference between OA and inflammatory

A
  • OA- caused by physical use i.e. wear and tear of joint over time
    • >50yo
  • Inflammatory arthritis is a chronic autoimmune disease
    • Affects people of all ages
    • F>M
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10
Q

presentation of inflammatory joint disease

A
  • Morning joint stiffness
  • Swelling, redness, warmth in affected joints
  • ‘flare’ periods
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11
Q

treatment of inflammatory joint disease

A
  • Early use of DMARD
  • Steroids
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12
Q

rheumatoid arthritis background

A
  • Autoantibodies RF and anti-ccp cause destruction of bone
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13
Q

RF for rheumatoid arthritis

A
  • 3:1 female
  • 30-50 years old
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14
Q

presentations of rheumatoid arthritis

A
  • Progressive, peripheral and symmetrical polyarthritis
  • Commonly affected joints: MCP/ PIP/ MTPs (typically spares DIP (OA)). May effect any joint inc hip/knees/shoulders/c-spine
  • Hx .6 weeks
  • Morning stiffness >30 min duration
  • Fatigue/ malaise
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15
Q

examination for rheumatoid arthritis

A
  • Soft tissue swelling and tenderness first
  • Ulnar deviation/palmar subluxation of MCP
  • Swan-neck and boutonniere deformity to digits
  • Rheumatoid nodules- most common on elbows
  • Median nerve- carpal tunnel association
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16
Q

investigations for RA

A
  • Auto antibodies: RF and anti-CCP
  • FBC- normocytic anaemia (chronic disease)
  • WCC (septic arthritis)
  • Inflammatory markers (CRP and ESR)- elevates
  • X-ray changes apparent in established disease- USSS/MRI more sensitive in early disease
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17
Q

treatment of RA

A
  • Initially DMARD monotherapy (methotrexate), Consider combination DMARDs (leflunomide, hydroxychloroquine, sulfasalazine)
  • Steroids (acutely)= PO/IM or intra-articular
  • Symptoms control with NSAID (PPI cover)
  • If disease still severe add biologic- anti-TNFs – etanercepts
  • Non-drug- OT/PT, podiatry, psychological
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18
Q

OA background

A
  • Commonest arthritis- progressive loss of articular cartilage due to wear and tear
19
Q

RF for OA

A
  • age
  • women
  • obesity
  • trauma
  • hereditary
20
Q

presentation of OA

A
  • hip knee and spine most commonly affected
  • pain is provoked by movement and weight-bearing
  • at first intermittent, but later constant
  • at the knee- a feeling that the joint will give way are common
21
Q

Investigation for OA X-ray

A

LOSS

 Loss of Joint

 Osteophytes

 Subarticular sclerosis

 Subchondral cysts

22
Q

Treatment of OA

A

Aim to reduce pain and disability

  • Non-drug
    • Strengthening and range of movement exercises
    • Weight loss to reduce joint loading
    • Laterally wedged insoles/ walking stick
  • Drug
    • Paracetamol regularly
    • NSAIDs short-term
    • Topical NSAIDs
    • Intraarticular corticosteroids (evidence of benefit from glucosamine or chondroitin sulphate supplements not convincing
  • Surgery
    • If pharmacological and physical modalities of treatment don’t work
    • Younger patients have higher chance of revision surgery int eh future
23
Q

osteoporosis background

A

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 fracture

24
Q

non-modifiable RF for osteoporosis

A
  • 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.
25
Q

modifiable risk factors for osteoporosis

A
  • 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
26
Q

presentation of osteoporosis

A
  • Back pain, caused by a fractured or collapsed vertebra
  • Loss of height over time
  • A stooped posture
  • A bone that breaks much more easily than expected
27
Q

investigations for osteoprosois

A
  • Dual energy x-ray absorptiometry (DEXA) of the lumbar spine and hip is considered the gold standard for the diagnosis of osteoporosis.
    • T-score is the number of SDs from the mean bone density of persons of same gender at age of peak density (25 years)
28
Q

T-score suggestive of osteoporosis (DEXA)

A

>-2.5

29
Q

normal T-score

A

>-1

30
Q

T-score suggestive of osteopenia(DEXA)

A

between −1 and −2.5

31
Q

treatment of osteopenia

A
  • Risk modification: weight-bearing exercise, VitD3 supplementation (800-20000 IU/day), limiting alcohol and smoking cessation. Dietary advice regarding calcium intake
32
Q

treatment of osteoporosis

A
  • VitD +- calcium supplementation
  • Oral bisphosphonates or IV if oral not tolerated
    • Always take on an empty stomach with a full glass of water. Stand or sit upright for 30 mins after taking them. Wait between 30 mins and 2 hours before eating or drinking
    • 2nd line: `Denosumab or teriparatide’
33
Q

prevention of osteoporosis

A

Regular weight-bearing exercise prevents osteoporosis

34
Q

bursitis background

A

Inflammation of a bursa (a closed, fluid- filled sac that works as a cushion and gliding surface to reduce friction between tissues of the body). Major bursae are located next to the tendons near large joints such as in shoulder, elbows, hips and knees.

35
Q

bursitis RF

A
  • Injury
  • Overuse
  • Infection
36
Q

bursitis presentation

A
  • Pain
  • Localised tenderness
  • Limited motion
  • Swelling and redness
37
Q

diagnosis of bursitis

A
  • X-ray
  • MR
  • US
  • Aspiration
38
Q

treatment of bursitis

A
  • Treat underlying cause
  • NSAID and pain meds
  • Injection of steroids
  • Antibiotics
  • Surgical drainage
39
Q

types of bursitis

A
  • Retromalleolar tendon bursitis. This type of bursitis is also called Albert disease. It’s caused by things like injury, disease, or shoes with rigid back support. These put extra strain on the lower part of the Achilles tendon. This attaches the calf muscle to the back of the heel. This can lead to inflammation of the bursa located where the tendon attaches to the heel.
  • Posterior Achilles tendon bursitis. This type of bursitis, also called Haglund deformity, is in the bursa located between the skin of the heel and the Achilles tendon. This attaches the calf muscles to the heel. It is aggravated by a type of walking that presses the soft heel tissue into the hard back support of a shoe.
  • Hip bursitis. Also called trochanteric bursitis, hip bursitis is often the result of injury, overuse, spinal abnormalities, arthritis, or surgery. This type of bursitis is more common in women and middle-aged and older people.
  • Elbow bursitis. Elbow bursitis is caused by the inflammation of the bursa located between the skin and bones of the elbow (the olecranon bursa). Elbow bursitis can be caused by injury or constant pressure on the elbow (for example, when leaning on a hard surface).
  • Knee bursitis. Bursitis in the knee is also called goosefoot bursitis or Pes Anserine bursitis. The Pes Anserine bursa is located between the shin bone and the three tendons of the hamstring muscles, on the inside of the knee. This type of bursitis may be caused by lack of stretching before exercise, tight hamstring muscles, being overweight, arthritis, or out-turning of the knee or lower leg.
  • Kneecap bursitis. Also called prepatellar bursitis, this type of bursitis is common in people who are on their knees a lot, such as carpet layers and plumbers.
40
Q

gout background

A
  • Inflammatory arthritis related to a hyperuricemia- causes deposition of monosodium urate crystal which accumulate in joints and soft tissue
  • Big toe (hallux) most commonly affected
41
Q

risk factors for gout

A
  • Increased purine (meats and seafood)
  • Alcohol intake (esp beer)
  • High fructose intake
  • Obesity
  • CHF
  • CAD
  • Dyslipidaemia
  • Renal disease
  • Organ transplant
  • Hypertension
  • Smoking
  • DM
  • Urate-elevating medications e.g. diuretics
42
Q

presentations of gout

A
  • severe pain in one or more joints
  • the joint feeling hot and very tender
  • swelling in and around the affected joint
  • red, shiny skin over the affected joint
43
Q

investigations for gout

A
  • Joint aspiration (MSU crystals)
  • Blood tests for uric acid
  • X-ray
  • Urate crystals are negatively birefringent through polarised light (microscope)
44
Q

treatments of gout

A
  • General prevention: lose weight, exercise, reduced purine in diet, reduce alcohol consumption, smoking cessation, avoid dehydration
  • First line treatment NSAIDs
  • Long terms oral/IM steroids or colchicine
  • Chronic cases: commence urate lowering therapy (ULT) after acute attack
    • E.g. allopurinal and febuxostat (xanthine oxidase inhibitors and reduce urate formation)
    • Aim to reduce SUA to <360 micromol/L

GP block (Y3) (39 decks)

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