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Phase 2 v2 > MSK and Rheumatology > Flashcards

MSK and Rheumatology Flashcards

1
Q

What is osteoarthritis?

A
  • Osteoarthritis (OA) is an age-related, dynamic reaction pattern of a joint in response to insult or injury.
  • All tissues of the joint are involved, but primarily the articular cartilage.
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2
Q

What is the clinical presentation of osteoarthritis?

A
  • Joint pain exacerbated by exercise
  • Joint stiffness after rest (Including short-lived pain in the morning <30 mins)
  • Bony swellings (on the distal interphalangeal are called Herberden’s nodes, on the proximal interphalangeal are called Bouchard’s nodes - both are more common in osteoarthritis).
  • Deformity of joint/ surrounding structure.
  • Crepitus (Describes popping, clicking and crackling sounds within the joint).
  • Asymmetrical
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3
Q

What is the pathophysiology of osteoarthritis?

A
  • Chondrocytes and inflammatory cells in the surrounding tissues release enzymes.
  • These enzymes result in the breakdown of collagen and proteoglycans, subsequently the breakdown of articular cartilage.
  • This exposes the subchondral bone which then becomes sclerosed.
  • Bone is remodelled, resulting in the formation of osteophytes and subchondral cysts.
  • Joint space is lost/narrowed over time.
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4
Q

What are the risk factors of osteoarthritis?

A
  • Older age
  • Female
  • Obese
  • Family history
  • Trauma to joint
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5
Q

What are the diagnostic tests for osteoarthritis?

A
  • DIAGNOSIS IS USUALLY CLINICAL.

- X-ray will show: Osteophytes, subchondral cysts, reduced joint space, subarticular sclerosis.

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6
Q

How is osteoarthritis treated?

A

1st line:

  • Exercise/physio (increases joint lubrication, therefore decreasing pain).
  • Topical analgesics, (NSAID’s such as diclofenac)
  • Paracetamol.

2nd line:
- Corticosteroid injections (if NSAIDS/paracetamol are not sufficient or contraindicated).

If pain persists despite multiple treatment modalities, or patient has severe disability:
- Surgery (joint replacement).

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7
Q

What is rheumatoid arthritis?

A
  • Chronic inflammatory disease.

- Affects the small joints of the hands and feet

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8
Q

What is the clinical presentation of rheumatoid arthritis?

A
  • Tender and swollen joints.
  • Active symmetrical arthritis lasting >6 weeks.
  • Joint pain on touch.
  • > 1 hour of morning stiffness.
  • Characteristic deformities: Swan neck, Boutonnière deformity, ulnar deviation, rheumatoid nodules.
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9
Q

What is the pathophysiology of rheumatoid arthritis?

A
  • Inflammation of the synovium.
  • Angiogenesis, cellular hyperplasia, influx of inflammatory cells (both innate and specific ones), cytokine secretion (TNF-a, IL1 and IL6).
  • Locally invasive synovial tissue forms (called a “pannus”).
  • Pannus causes the the bony erosions typically seen in RA.
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10
Q

What are the risk factors associated with rheumatoid arthritis?

A
  • HLA DR4 and HLA DR1 make a person susceptible to rheumatoid arthritis.
  • Family history.
  • Smoking.
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11
Q

What are the tests used to diagnose rheumatoid arthritis?

A

1st line: RF. If this comes back negative but RA still suspected, use anti-CCP (more accurate).

X-ray: If bony erosions seen, prognosis is significantly worse.

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12
Q

How is rheumatoid arthritis treated?

A

1st line:

  • Methotrexate or hydroxychloroquine (DMARD).
  • Prednisolone (corticosteroid).

2nd line:
- Add a biological agent such as infliximab (TNF-a inhibitor).

For acute flares: Corticosteroid injections such as methylprednisolone acetate, or NSAIDS such as ibuprofen.

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13
Q

What are the complications of rheumatoid arthritis?

A
  • Work disability.
  • Increased mortality
  • CVD risk increased
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14
Q

What are the differential diagnoses for RA? How are they different?

A
  • PA (usually has psoriasis too)
  • SLE (arthritis seen in SLE doesn’t normally cause deformations).
  • OA (Gets WORSE with movement, and is usually asymmetrical).
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15
Q

What is osteoporosis?

A
  • Progressive skeletal disease with reduced bone density and micro-deterioration of the bones.
  • Results in increased susceptibility to fracture and increased bone fragility.

OSTEOMALACIA IS REDUCED MINERALISATION OF BONES DUE TO VIT D DEFICIENCY.

OSTEOPOROSIS IS REDUCED OVERALL BONE DENSITY.

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16
Q

What is the clinical presentation of osteoporosis?

A
  • Often the first sign is fracture, typically of the neck of the femur.
  • Micro-fractures in the thoracic vertebrae over time may lead to kyphosis of the spine, and back pain.
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17
Q

What are all the different pathophysiologies of osteoporosis?

A

Varied and depends on the root cause. For example:

  • Coeliac (impaired calcium absorption in gut).
  • RA (disrupts bone remodelling)
  • Hyperparathyroidism (increases bone resorption).

There are many other causes too…

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18
Q

What are the causes/risk factors of osteoporosis?

A

SHATTERED:

  • Steroid use
  • Hyperthyroidism/parathyroidism
  • Alcohol and tobacco
  • Thin
  • Testosterone LOW
  • Early meopause
  • Renal or liver failure
  • Erosive/inflammatory bone disease
  • Dietary calcium decrease/ DM type 1.
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19
Q

What are the tests used to diagnose osteoporosis?

A
  • Bone mass density assessment (DEXA scan)
  • T score < or = -2.5 indicates osteoporosis
  • -1 > T score > -2.5 indicates osteopenia
  • If there are ALSO micro-fractures present, indicates severe osteoporosis.
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20
Q

What treatment is given for osteoporosis?

A

1st line:

  • Alendronic acid (biphosphonates).
  • Calcium and calciferol (vitamin D) supplementation.

2nd line:

  • Denosumab. This is a RANK ligand inhibitor.
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21
Q

What are the main complications of osteoporosis?

A
  • Recurrent fractures (especially hip/rib).

- Chronic pain.

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22
Q

What is osteomalacia?

What is rickets?

A
  • Metabolic bone disease.
  • Deficient bone mineralisation WITHOUT LOSS OF BONE MATRIX (as seen in osteoporosis).
  • Rickets is the same pathophysiology, but occurs prior to growth plate closure.
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23
Q

What is the clinical presentation of osteomalacia?

A
  • Fractures (especially long bones such as the femur).
  • Bone pain at the typical fracture sites.
  • Signs of vit. D or calcium deficiency.
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24
Q

What is the pathophysiology of osteomalacia/rickets?

A
  • Depends on the causative mechanism.
  • Low vit. D and/or calcium causes growth plate disorganisation (rickets) or deficient mineralisation of the bone (osteomalacia).
  • CKD causes increased FGF-23 release. This stimulates increased calcium excretion, increased phosphate retention, decreased vit. D production.
  • KEY DIFFERENCE: OSTEOPOROSIS WILL SEE OVERALL LOSS OF BONY MATRIX, OSTEOMALACIA IS JUST DEMINERALISATION RATHER THAN LOSS OF BONE MATRIX ITSELF.
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25
Q

What are the risk factors of osteomalacia?

A
  • Calcium/vit D deficiency.
  • Malabsorption disorder (e.g. coeliac).
  • Malnutrition.
  • CKD.
  • Hyperparathyroidism.
  • Low sunlight.
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26
Q

What diagnostic tests are used for osteomalacia?

A
  • Serum calcium. Low or normal.
  • 25-hydroxyvitamin-D. Less than 25 nanomol/L indicates high risk of osteomalacia.
  • Raised ALP.

GOLD STANDARD: Bone X-ray to assess for defective mineralisation.

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27
Q

What is the treatment for osteomalacia?

A

1st line:
- Ergocalciferol (source of vitamin D)
AND
- Calcium carbonate/calcium citrate (source of calcium).

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28
Q

What is Systemic Lupus Erythematosus (SLE)?

A
  • A multi-systemic autoimmune disease.

- It is characterised by the presence of antinuclear antibodies (ANA) in the patient’s serum.

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29
Q

What are key signs/symptoms of SLE?

A

Key symptoms/signs:

  • Malar (butterfly) rash (also photosensitive).
  • Arthralgia.
  • Fatigue.
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30
Q

What is the pathophysiology of SLE?

What type of hypersensitivity reaction?

A
  • Autoimmune disorder. ANA (anti-nuclear antibodies) produced.
  • Cell necrosis increased, and clearance of apoptosed material is decreased.
  • Further stimulates autoimmune processes and production of ANAs.
  • Type III hypersensitivity disorder.
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31
Q

What are the risk factors of SLE?

A
  • Female
  • 30-70 YO
  • FH
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32
Q

What are the potential complications of SLE?

A
  • Thrombocytopenia
  • Leukopenia
  • Anaemia
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33
Q

What are the investigations carried out on a patient with suspected SLE?

A
  • ANA testing. Positive suggests SLE
  • If positive, then an anti dsDNA test is done. If elevated, suggests SLE.
  • ESR/CRP (ESR is raised, CRP normal as SLE is an autoimmune disease).
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34
Q

What is the treatment for a patient with SLE?

A

1st line:

  • Avoid sunlight and smoking.
  • Give hydroxychloroquine (DMARD)
  • Naproxen (NSAID) for arthralgia.
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35
Q

What is SLE short for?

A
  • Systemic Lupus Erythematosus.
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36
Q

What are the two types of crystal arthropathy?

A
  • Gout

- Pseudogout

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37
Q

What is gout?

A

Hyperuricaemia resulting in the deposition of urate crystals in the joints.

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38
Q

What is the clinical presentation of gout?

A
  • A joint becomes swollen, extremely tender and erythematous.
  • Usually affects 4 or less joints.
  • Presence of tophi (uric acid crystal depositions in the skin/joint surfaces).
  • Usually seen in the metatarsalphalangeal joint of the big toe.
  • “One of the most painful acute conditions human beings can experience”.
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39
Q

What is the pathophysiology of gout?

A
  • Purine broken down into urate via xanthine oxidase enzymes.
  • Uric acid is excreted renally. However, if too much is in the blood (hyperuricaemia), it precipitates in the joints causing gout.
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40
Q

What are the potential complications of hyperuricaemia other than gout?

A
  • Nephropathy (CKD risk increased)

- Nephrolithiasis.

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41
Q

What are the risk factors associated with gout?

A
  • Male
  • Meat/seafood consumption
  • Alcohol
  • Genetic predisposition.
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42
Q

What are the investigations used for gout?

A
  • Arthrocentesis (joint aspiration) + synovial fluid analysis.
  • Will show NEGATIVELY BIFRINGENT NEEDLE CRYSTALS.
  • “N+N”
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43
Q

How is gout treated?

A

Acute attack:
Analgesia: naproxen (NSAID), prednisolone injection (corticosteroid) and/or colchicine.

Chronic management: Allopurinol (xanthine oxidase inhibitor).

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44
Q

What is pseudogout?

A
  • Deposition of calcium pyrophosphate crystals within the joints.
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45
Q

What is the clinical presentation of pseudogout?

A
  • Moderate joint pain (not as bad as gout).

- Larger joints typically involved (knee most common).

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46
Q

What is the pathophysiology of pseudogout?

A

Excess of calcium in the blood, which is then deposited as calcium pyrophosphate crystals in the joint.

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47
Q

What are the risk factors for pseudogout?

A
  • Hyperparathyroidism (high calcium)
  • Old age.
  • Joint injury.
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48
Q

What is the investigation used to diagnose pseudogout definitively?

A
  • Arthrocentesis (joint aspiration) + synovial fluid analysis.
  • Will show positively bifringent, rhomboid shaped crystals.
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49
Q

What is the treatment for pseudogout?

A

1st line:
- Dexamethasone injection (corticosteroids)

  • Naproxen (NSAIDs) if systemic polyarticular.

Preventative measures:
- Potentially low-dose colchicine.

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50
Q

What are the 3 types of spondyloarthropathy?

A
  • Ankylosing spondylitis
  • Psoriatic arthritis
  • Reactive arthritis
51
Q

What is a spondyloarthropathy?

A
  • Joint disease affecting the joints in the spine and nearby.
  • HLA B27 association.
52
Q

What is ankylosing spondylitis?

A
  • Chronic progressive inflammatory disorder of the spine.

- Causes severe spinal pain and stiffness.

53
Q

What is the clinical presentation of ankylosing spondylitis?

A
  • Inflammatory back pain (early morning stiffness, insidious onset, lasts >3 months).
  • Iritis/uveitis common.
  • Insidious onset.
  • Late teens/early 20’s male.
54
Q

What is the pathophysiology of ankylosing spondylitis?

A
  • Chronic inflammation of the enthesitis of the spine.

- Causes fibrosis and calcification of the enthesitis.

55
Q

What is the epidemiology of ankylosing spondylitis?

A
  • Late teens/early 20’s.
  • Male
  • HLA-B27 +ve
56
Q

What investigations are used in ankylosing spondylitis?

A
  • X-ray of pelvis. Sacroliitis (inflammation of the sacroiliac joint) suggests ankylosing spondylitis.
  • “bamboo spine” from re-healing of the spinal ligaments.
  • HLA-B27 testing. +ve
57
Q

What is the treatment given for ankylosing spondylitis?

A

Just spinal involvment:

  • Physiotherapy
  • Naproxen (NSAIDS.
  • Can use hydrocortisone injections into the enthesitis.

Peripheral joint involvment:

  • Sulfasalazine (DMARD) .
  • Infliximab (tnf-a inhibitor) if DMARD unsuccessful.
58
Q

What is psoriatic arthritis?

A
  • Chronic inflammatory arthritis associated with psoriasis.
59
Q

What is the clinical presentation of psoriatic arthritis?

A
  • Inflammatory joint pain, meaning:
    >30 mins morning stiffness.
    Better on movement
    Worse on rest
  • DIP involvement.
  • Asymmetrical.
  • Mono/oligoarticular.
  • Dactylitis (swelling of entire finger).
  • History of psoriasis (may only be recognised as nail/scalp difficulties.
60
Q

What are the risk factors for psoriatic arthritis?

A
  • Psoriasis. Most significant risk factor.
  • FH of psoriasis/psoriatic arthritis.
  • HLA-B27 +ve (57% of psoriatic arthritis cases).
61
Q

What investigations are used to diagnose psoriatic arthritis?

A
  • X ray of hands/feet.
  • DIP joint erosion.
  • In later-stage disease, pencil in cup deformity. (end of bone has sharpened into a pencil like shape, and the more proximal bone has been eroded into a cup-like shape).
  • HLA B27 genetic test - +ve
62
Q

What is the treatment for psoriatic arthritis?

A

If disease is limited:
Naproxen (NSAIDS) + prednisolone injections (corticosteroids).
Physiotherapy.

If disease is progressive:

  • Add methotrexate (DMARD).
  • 2nd line is infliximab (tnf-a inhibitor).
63
Q

What is reactive arthritis?

A
  • Inflammatory arthritis that occurs following a GI or GU infection.
64
Q

What are the two types of reactive arthritis and what are the typical causative organisms?

A
  • GI. Usually caused by Campylobacter, Salmonella or Shigella.
  • GU. Usually caused by Chlamydia trachomatis.
65
Q

What is the typical clinical presentation of reactive arthritis?

A
  • 1-4 weeks after a GI or GU infection.

“Can’t see, can’t pee, can’t climb a tree”

  • Conjunctivitis
  • Urethritis
  • Arthritis
  • Enthesitis of achilles heel.
66
Q

What is the pathophysiology of reactive arthritis?

A
  • Infection stimulates an autoimmune attack on healthy, normal joint tissues.
67
Q

What are the risk factors associated with reactive arthritis?

A
  • Recent GI/GU infection.
  • HLA-B27 positive.
  • Male.
68
Q

What investigations are used to diagnose reactive arthritis?

A
  • ESR/CRP raised
  • HLA-B27 +ve (not very specific).

X-ray:

  • Enthesitis of the achilles.
  • Sacroiliitis of the spine.

EXCLUDING OTHER DISEASES:

  • RF and anti-CCP negative (rules out rheumatoid arthritis).
  • ANA negative. (rules out SLE, helps rule out RA).
69
Q

What is the treatment for reactive arthritis?

A

1st line:
- Naproxen (NSAID) + prednisolone injections (corticosteroids).

For persistent or recurrent reactive arthritis:
- Sulfasalazine (conventional DMARD).

  • ANTIBIOTICS NOT INDICATED UNLESS THERE IS AN ACTIVE GU OR GI INFECTION STILL.
70
Q

What are the five main things that all spondyloarthropathies share?

A

1) Asymmetrical peripheral arthritis (different to RA)
2) Absence of rheumatoid factor/ anti-CCP (different to RA)
3) Inflammation of the enthesitis.
4) Strong HLA-B27 association.
5) Commonly associated with axial (spinal) inflammation.

71
Q

What are the two MSK diseases directly caused by infection?

A
  • Septic arthritis

- Osteomyelitis

72
Q

What is septic arthritis?

A

Infection of one (typically) or more joints caused by microbes entering the joint capsule. Can be due to direct infection or haematogenous spread.

73
Q

What is the typical presentation of septic arthritis?

A
  • Hot, swollen, painful joint.
  • Acute presentation.
  • Pain on both active and passive movement.
  • Fever.
  • Most commonly monoarticular and affecting the knee.
74
Q

What is the most common causative organism of septic arthritis and osteomyelitis?

A

Most commonly caused by staphylococcus aureus infection (gram +ve, round, clustered bacteria).

75
Q

What are the potential complications of septic arthritis?

A
  • Osteomyelitis (if the infection spreads to the bone).

- Joint destruction (If the infection is inadequately treated/treated late).

76
Q

What are the risk factors associated with septic arthritis?

A
  • Underlying joint disease (OA, RA etc.)
  • Prosthetic joint
  • Over 80
  • Immunocompromised
  • IV drug use (increases risk of microbes entering the bloodstream).
77
Q

What are the investigations used for septic arthritis?

A
  • Joint aspiration and synovial fluid culture. If possible, do before administering antibiotics.
  • Blood culture (especially useful to establish a haematogenous spread).
78
Q

What is the treatment for septic arthritis?

A

If there is systemic involvement:
- Follow local sepsis guidance (e.g. SEPSIS-6).

If there is no systemic involvement:

  • Amoxicillin (empirical antibiotics)
  • Joint aspiration (to remove infectious fluids.)
  • Ibuprofen (NSAID) for pain.

If the joint is prosthetic, consider surgery.

79
Q

What is osteomyelitis?

A

Acute inflammatory condition due to infection of the bone.

80
Q

What is the clinical presentation of osteomyelitis?

A
  • Limp/inability to bear weight.
  • Non-specific pain at site of infection.
  • Fever
  • Reduced ROM.
  • If disease is chronic, sinus formation may occur (a passage from the infected bone to the skin surface).
81
Q

What is the pathophysiology of osteomyelitis?

A
  • Infection of the bone. Usually Staph. A.
  • Can be due to direct infection, or haematogenous spread.
  • A sequestrum may form due to destruction of bone, and this serves as a site for the infection to cultivate.
82
Q

What are the risk factors for osteomyelitis?

A
  • Most common in children under 5.
  • Previous osteomyelitis.
  • Penetrative injury/surgery.
  • Immunosuppression.
  • IV drug use.
  • CKD
83
Q

What are the investigations used for suspected osteomyelitis?

A
  • X-ray. May take a few days for disease to be visible (bone destruction, osteopenia, sequestrum formation).
  • Blood/bone culture (may show causative organism).
  • ESR/CRP raised.
84
Q

What is the treatment for osteomyelitis?

A

If septic, SEPSIS-6.

  • Ibuprofen and limb immobilisation to relieve pain.
  • Flucloxacillin 1st line.
  • If allergic to penicillin OR high chance of MRSA cause, first line is vancomycin.
  • Consider surgery if bone continues to deteriorate.
85
Q

What is multiple myeloma?

A
  • Malignant disease of the bone marrow plasma cells.
86
Q

What is the clinical presentation of multiple myeloma?

A

REMEMBER “CRAB”:

  • hyperCalcaemia
  • Renal impairment
  • ANAEMIA
  • BONE PAIN
87
Q

What are the risk factors for MM?

A
  • Abnormal free light-chain ratio.
  • FH
  • Radiation exposure.
88
Q

What is the epidemiology of multiple myeloma?

A
  • Peak presentation at 70 years old.
89
Q

What are the investigations used for multiple myeloma?

A
  • Bone marrow biopsy. Will show plasma cell infiltration in the bone marrow (gold standard).
  • FBC: Anaemia
  • Whole body CT to find osteolytic lesions/fractures.
90
Q

What is the treatment for multiple myeloma?

A

Chemotherapy (Thalidomide) + dexamethasone (corticosteroids).

  • Stem cell transplant (if illegible).
91
Q

What is fibromyalgia?

A
  • Chronic widespread body pain.
92
Q

What is the clinical presentation of fibromyalgia?

A
  • Chronic, widespread pain.
  • Unrefreshing sleep and tiredness.
  • Symptoms generally worse in the cold and under stress.
93
Q

What is the pathophysiology of fibromyalgia?

94
Q

What are the risk factors associated with fibromyalgia?

A
  • Women
  • 20-60
  • FH
95
Q

What are the investigations used for fibromyalgia?

A
  • There are none.
  • Diagnosis is clinical.
  • Chronic (>3 months), widespread body pain associated with fatigue and sleep disturbance.
96
Q

What is the treatment for fibromyalgia?

A
  • 1st line is amitriptyline (tricyclic antidepressant) + CBT.
97
Q

What is Paget’s disease?

A

Increased bone turnover, leading to enlarged and disorganised bone structure.

98
Q

What are the symptoms of Paget’s disease?

A
  • Bone pain and deformity.

- Pathological fractures.

99
Q

What is the pathophysiology of Paget’s disease?

A
  • Increased osteoclast activity.
  • In response, increased osteoblast activity.
  • Because the bones are formed faster, they are structurally compromised.
  • This results in pathological fractures and misshapen bones.
100
Q

What are the investigations used in Paget’s disease?

A
  • X-ray. Will show deformity and lytic lesions in the bones (commonly long bones, pelvis and skull).
  • Blood tests. Specific alkaline phosphate will be raised. (ALP).
  • Bone biopsy has highest specificity and sensitivity (gold standard). However, is contraindicated in weight bearing bones.
101
Q

What is the treatment for Paget’s disease?

A
  • Alendronic acid (1st line)

IMPORTANT TO MONITOR CALCIUM LEVELS.

102
Q

What is vasculitis?

A
  • Inflammation of the blood vessels.
103
Q

What are the two types of vasculitis I need to be aware of?

A
  • Giant cell arteritis.

- Granulomatosis with polyangitis (formerly known as Wegener’s granulomatosis).

104
Q

How does giant cell arteritis present?

A
  • Scalp tenderness.
  • Headache.
  • Vision changes (amaurosis fugax).
105
Q

How does granulomatosis with polyangitis present?

A

Classic triad:

  • Upper respiratory tract involvement.
  • Lower respiratory tract involvement.
  • Glomerulonephritis.
106
Q

What is the treatment for giant cell arteritis?

A
  • Prednisolone.
107
Q

What is the treatment for granulomatosis with polyangitis?

A
  • Prednisolone + cyclophosphamide.
108
Q

What is cauda equina syndrome?

A
  • Compression of the cauda equina (a continuation of the spinal cord).
109
Q

What are the symptoms of cauda equina syndrome?

A
  • Bladder dysfunction.
  • Bilateral sciatica (pain in lower back, buttocks and upper thigh).
  • Saddle anaesthesia (numbness in buttocks, perianal area, upper thighs).
110
Q

What are the signs of cauda equina syndrome?

A
  • Lower limb weakness/numbness and reduced anal tone.
111
Q

What is the investigation for cauda equina syndrome?

A
  • MRI lower spine.
112
Q

What is the treatment for cauda equina syndrome?

A
  • Nerosurgical decompression of Cauda equina.
113
Q

What is the presentation of spinal cord compression?

A
  • Back pain.

- Sensory/motor deficit.

114
Q

What are the common causes of spinal cord compression?

A
  • Spine trauma.
  • Vertebral compression fracture.
  • Vertebral disk herniation.
  • Primary/metastatic spinal tumor.
  • Spinal infection.
115
Q

What is the investigation for spinal cord compression?

116
Q

What is the treatment for spinal cord compression?

A
  • Immobilise the patient.

- Neurosurgical decompression of the spinal cord.

117
Q

What is Brown-sequard syndrome?

A
  • Hemisection of the spinal cord.
118
Q

What is the presentation of Brown-sequard syndrome?

A
  • Ipsilateral loss of vibration/proprioception below the level of the lesion (dorsal column).
  • Ipsilateral paralysis below the level of the lesion (corticospinal tract).
  • CONTRALATERAL loss of temperature and pain sensation A FEW SEGMENTS BELOW LEVEL OF LESION (spinothalamic tract).
119
Q

What is the investigation for Brown-sequard syndrome?

A

MRI spine.

120
Q

What is the treatment for Brown-sequard syndrome?

A
  • Normally neurosurgical decompression.
121
Q

What is degenerative disc disease?

A
  • A complex condition associated with degeneration of the spinal discs.
122
Q

What is the investigation for spinal disc degeneration?

What are the findings?

A
  • MRI lumbar spine.

- Disc compression/ tears.

123
Q

What is the treatment for spinal disc degeneration?

A
  • Paracetamol + ibuprofen (analgesia).

- ONLY IF SURE IT IS NOTHING MORE SEVERE.

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