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Phase 2a diseases > 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
  • 40 to 60 years old
  • Female
  • Family history
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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 if methotrexate not tolerated (unless pregnant or planning pregnancy).
  • Often low dose oral prednisolone to help help symptoms before the DMARD kicks in.

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 mass 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 MINERAL 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.
  • Symptoms all relate to the increased bone fragility.
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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 risk factors of osteoporosis?

A
  • Female
  • Old
  • Low BMI
  • Low calcium and/or vitamin D
  • Post menopause
  • Smoking
  • Alcohol
  • Corticosteroid use.
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19
Q

What are the causes 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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20
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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21
Q

What treatment is given for osteoporosis?

A

1st line:

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

2nd line:

  • Denosumab. This is a RANK ligand inhibitor.
  • Oestrogen can be given to young post-menopausal women with low oestrogen levels.
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22
Q

What are the main complications of osteoporosis?

A
  • Recurrent fractures (especially hip/rib).

- Chronic pain.

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23
Q

What is osteomalacia?

What is rickets?

A
  • Metabolic bone disease.
  • Incomplete mineralisation of the underlying bone matrix FOLLOWING GROWTH PLATE CLOSURE.
  • Rickets is the same pathophysiology, but occurs prior to growth plate closure.
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24
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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25
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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26
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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27
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.
  • PTH - High in Ca 2+ or Vit D deficiency.
  • Raised ALP.

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

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28
Q

What is the treatment for osteomalacia?

A

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

2nd line:
Swap ergocalciferol (vit. D) for calcitriol (activated form of vitamin D).
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29
Q

What is Systemic Lupus Erythematosus (SLE)?

A
  • A heterogenous and inflammatory muti-system autoimmune disease.
  • It is characterised by the presence of antinuclear antibodies in the patient’s serum.
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30
Q

What is the clinical presentation of SLE?

A

There are a vast number of symptoms due to the systemic nature of the disease:

  • General symptoms (fatigue, fever, weight loss)
  • Arthralgia
  • Malar (butterfly) rash.
  • Photosensitive rash.
  • Alopecia.
  • Renal (GLOMERULONEPHRITIS) due to autoimmune attack.
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31
Q

What is the pathophysiology of SLE?

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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32
Q

What are the risk factors of SLE?

A
  • Female
  • 30-70 YO
  • FH
  • SLE can be drug induced (e.g. sulfasalazine).
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33
Q

What are the potential complications of SLE?

A
  • Thrombocytopenia
  • Leukopenia
  • Anaemia
  • Corticosteroid-induced disorders (such as osteoporosis, due to reduced calcium absorption and increased bone resorption).
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34
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).
  • Urea/creatinine. Raised if there are renal manifestations of SLE.
  • aPPT elongated in certain forms of SLE.
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35
Q

What is the treatment for a patient with SLE?

A

1st line:

  • Avoid sunlight and smoking.
  • Give hydroxychloroquine (DMARD)
  • Naproxen (NSAID) for arthralgia, or celecoxib (COX-2 inhibitor) if high risk of GI ulceration.

2nd line:
- Prednisolone (oral or IV) if the DMARD + NSAID are not adequate. LOWEST POSSIBLE DOSE FOR SHORTEST PERIOD OF TIME.

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36
Q

What is the disease pattern of SLE?

A
  • 70% of patients have a relapsing-remitting form of the disease.
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37
Q

What is SLE short for?

A
  • Systemic Lupus Erythematosus.
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38
Q

What are the two types of crystal arthropathy?

A
  • Gout

- Pseudogout

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39
Q

What is gout?

A

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

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40
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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41
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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42
Q

What are the potential complications of gout?

A
  • Nephropathy (CKD risk increased)

- Nephrolithiasis.

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43
Q

What are the risk factors associated with gout?

A
  • Male
  • Meat/seafood consumption
  • Alcohol
  • Diuretics, ciclosporins, pyrazinamide.
  • Genetic predisposition.
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44
Q

What are the investigations used for gout?

A
  • Arthrocentesis (joint aspiration) + synovial fluid analysis.
  • Will show NEGATIVELY BIFRINGENT NEEDLE CRYSTALS.
  • “N+N”
  • Gout can usually be diagnosed by examination.
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45
Q

How is gout treated?

A

Acute attack:

  • NSAID (naproxen) or steroids (prednisolone injected or oral) or colchicine (guide by patient preference/comorbidity).
  • Aim is to relieve pain and resolve function.

Chronic management: Allopurinol (xanthine oxidase inhibitor).

46
Q

What is pseudogout?

A
  • Deposition of calcium pyrophosphate crystals within the joints.
  • Can be acute or chronic.
47
Q

What is the clinical presentation of pseudogout?

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

- Larger joints typically involved (knee most common).

48
Q

What is the pathophysiology of pseudogout?

A

Excess of calcium in the blood, usually with an identifiable primary cause. Examples are:

  • Hyperparathyroidism
  • Haemochromatosis (deactivates pyrophosphatases that would be breaking down the crystals).
49
Q

What are the risk factors for pseudogout?

A
  • Injury to joint (organic or surgical).
  • Hyperparathyroidism (high calcium)
  • Haemochromatosis.
50
Q

What is the investigation used to diagnose pseudogout definitively?

A
  • Arthrocentesis (joint aspiration) + synovial fluid analysis.
  • Will show positively bifringent, rhomboid shaped crystals.
  • NOT “N+N”
51
Q

What is the treatment for pseudogout?

A

1st line:

  • Paracetamol (simple analgesics).
  • ICS (dexamethasone) if monoarticular.
  • Naproxen if ICS declined, or disease is polyarticular.

Preventative measures:
- Potentially low-dose colchicine.

52
Q

What are the 3 types of spondyloarthropathy?

A
  • Ankylosing spondylitis
  • Psoriatic arthritis
  • Reactive arthritis
53
Q

What is a spondyloarthropathy?

A
  • Joint disease affecting the vertebral column.
54
Q

What are the differentials for ankylosing spondylitis?

A
  • OA. Will be worse at night after use, whereas AS is worse in the mornings.
  • Reactive arthritis. History will reveal a prior infection as the trigger.
55
Q

What is ankylosing spondylitis?

A
  • Chronic progressive inflammatory disorder of the spine.
  • Causes severe spinal pain and stiffness.
  • Radio-graphical changes will usually be present.
56
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.
57
Q

What is the pathophysiology of ankylosing spondylitis?

A
  • Chronic inflammation of the enthesitis of the spine.

- Causes fibrosis and calcification of the enthesitis.

58
Q

What is the epidemiology of ankylosing spondylitis?

A
  • Late teens/early 20’s.
  • Male
  • HLA-B27 +ve
  • Family history.
59
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 and MRI (pelvis) can be used to pick up AS earlier if needed, but not 1st line.
60
Q

What is the treatment given for ankylosing spondylitis?

A

1st line:

  • Physiotherapy
  • Naproxen (+ paracetamol if not sufficient analgesia).
  • Can use hydrocortisone injections into the enthesitis.
  • Sulfasalazine (DMARD) if there is peripheral joint disease too.

If 2 NSAIDS fail to control pain/stiffness, 2nd line is DMARDS, specifically TNF-a inhibitors:

  • Infliximab.
61
Q

What is psoriatic arthritis?

A
  • Chronic inflammatory arthritis associated with psoriasis.
62
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.
63
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).
64
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).
  • Can also do an anti-CCP test. If -ve, helps to rule out RA.
65
Q

What is the treatment for psoriatic arthritis?

A

If disease is limited:

  • NSAIDS (naproxen)
  • Physiotherapy
  • Methylprednisolone acetate injections (as required).

If disease is progressive:

  • SAME AS ABOVE
  • PLUS METHOTREXATE (DMARD)

IF 2 CONVENTIONAL DMARDS ARE INEFFECTIVE:
- Swap methotrexate for infliximab (TNF-a inhibitor).

66
Q

What is reactive arthritis?

A
  • Inflammatory arthritis that occurs following a GI or GU infection.
67
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.
68
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
Rare in practice to see the triad present all at once.

  • Peripheral and/or proximal arthritis.
  • Enthesitis of achilles heel.
69
Q

What is the pathophysiology of reactive arthritis?

A
  • Infection stimulates an autoimmune attack on healthy, normal joint tissues.
70
Q

What are the risk factors associated with reactive arthritis?

A
  • Recent GI/GU infection.
  • HLA-B27 positive.
  • Male.
71
Q

What investigations are used to diagnose reactive arthritis?

A
  • Generally, the history will provide clues that it is reactive arthritis.
  • ESR/CRP raised
  • ANA negative. (rules out SLE, helps rule out RA).
  • RF and anti-CCP negative (rules out rheumatoid arthritis).
  • HLA-B27 +ve (not very specific).

X-ray:

  • Enthesitis of the achilles.
  • Sacroiliitis of the spine.
72
Q

What is the treatment for reactive arthritis?

A

1st line:

  • Naproxen (NSAID’s)
  • Prednisolone (corticosteroid injections) if needed.

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

  • ANTIBIOTICS NOT INDICATED UNLESS THERE IS AN ACTIVE GU OR GI INFECTION STILL.
73
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.

74
Q

What are the two MSK diseases directly caused by infection?

A
  • Septic arthritis

- Osteomyelitis

75
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.

76
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.
77
Q

What is the most common causative organism of septic arthritis?

A

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

78
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).

79
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).
80
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).
  • Presence of microbes in synovial fluid culture can be used to differentiate SA from the other differentials (e.g. OA, RA, PsA).
81
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.) IMMEDIATELY AFTER JOINT ASPIRATION FOR CULTURE HAS BEEN OBTAINED.

  • Change antibiotics to be more targeted to the pathogen when the culture comes back.

If the joint is prosthetic, consider surgery.

Consider paracetamol or NSAIDS (Ibuprofen) to manage the pain.

82
Q

What is osteomyelitis?

A

Acute inflammatory condition due to infection of the bone with a microorganism (usually staph. A)

83
Q

What is the clinical presentation of osteomyelitis?

A
  • Limp/inability to bear weight.
  • Non-specific pain at site of infection.
  • Fever
  • Lethargy
  • Reduced ROM.
  • If disease is chronic, sinus formation may occur (a passage from the infected bone to the skin surface).
84
Q

What is the pathophysiology of osteomyelitis?

A
  • Infection of the bone, usually due to staphylococcus aureus.
  • 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.
85
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
  • Diabetes (diabetic foot disease).
86
Q

What are the potential differentials for osteomyelitis and how are they differentiated?

A
  • ReA and SA. Differentiate using XR.

- If there is effusion in the joints, points more towards joint disease than osteomyelitis.

87
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 culture (may show causative organism).
  • ESR/CRP raised.
88
Q

What is the treatment for osteomyelitis?

A
  • NSAIDS 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.
  • If septic, SEPSIS-6.
89
Q

What is multiple myeloma?

A
  • Malignant disease of the bone marrow plasma cells.
90
Q

What is the clinical presentation of multiple myeloma?

A

KEY SYMPTOMS:

  • Bone pain
  • Anaemia

Also:

  • Fatigue
  • Renal impairment

REMEMBER “CRAB”:

  • hyperCalcaemia
  • Renal impairment
  • Anaemia
  • Bone pain
91
Q

What is the pathophysiology of multiple myeloma?

A
  • Uncontrolled proliferation of plasma cells/B cells, and uncontrolled secretion of antibodies.
  • The production of cytokines (especially IL-6) is responsible for much of the local damage observed in multiple myeloma (such as osteoporosis).
  • The antibodies produced are deposited in more distant organs, causing more distant disease such as AKI (hypercalcaemia and hyperuricaemia).
92
Q

What are the risk factors for MM?

A
  • Abnormal free light-chain ratio.
  • FH
  • Radiation exposure.
93
Q

What is the epidemiology of multiple myeloma?

A
  • Peak presentation at 70 years old.
94
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
  • Serum/urine electrophoresis. Paraprotein spike (raised IgG and/or IgA) will be detected in MM.
  • Whole body CT to find osteolytic lesions/fractures.
95
Q

What is the treatment for multiple myeloma?

A

Chemotherapy (Thalidomide + dexamethasone is 1st line for patients illegible for stem cell transplant).

  • Stem cell transplant (if illegible).
  • Dexamethasone and biphosphonates may be used to treat bone disease/bone pain.
96
Q

What is the mean survival time for patients with multiple myeloma?

A
  • 5 years.
97
Q

What is fibromyalgia?

A
  • Chronic widespread body pain.
98
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.
99
Q

What is the pathophysiology of fibromyalgia?

A
  • Unknown.
100
Q

What are the risk factors associated with fibromyalgia?

A
  • Women
  • 20-60
  • FH
  • Often occurs alongside other rheumatological conditions such as SLE, rheumatoid arthritis and osteoarthritis.
101
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.
102
Q

What is the treatment for fibromyalgia?

A
  • 1st line is amitriptyline (tricyclic antidepressant) + CBT.
103
Q

What is Paget’s disease?

A

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

104
Q

What are the symptoms of Paget’s disease?

A
  • Commonly is asymptomatic.
  • When presents, often with bone pain and bone deformity.
  • Symptoms will be localised to one or a few bones.
  • There will be increased bone fragility, causing pathological fractures.
105
Q

What is the pathophysiology of Paget’s disease?

A
  • Lytic phase. Increased bone resorption with abnormal osteoclast activity.
  • Leads to a rapid increase in bone formation by osteoblasts.
  • Due to speed of bone formation, new bone will be mechanically weaker and less organised.
  • This results in pathological fractures and misshapen bones.
106
Q

What are the risk factors of Paget’s disease?

A
  • FH

- Over 50

107
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 that are already structurally compromised, so is rarely possible for Paget’s disease.
108
Q

What is the treatment for Paget’s disease?

A
  • Alendronic acid (1st line)
  • Inhibit bone resorption by reducing osteoclast activity.
  • Ensure normal calcium and Vit D levels prior to commencing treatment to prevent hypocalcaemia.
  • Calcitonin (2nd line) if biphosphonates not tolerated/unsuccessful.

PRESCRIBING BOTH AT ONCE IS STRONGLY CONTRAINDICATED.

109
Q

What is the main differential for Paget’s disaese, and how is it distinguished?

A
  • Osteomalacia. Will have a low vit. D, whereas in Paget’s vit. D will be normal.
110
Q

What are some common differentials for osteoporosis?

A

Differentials for osteoporosis are almost indistinguishable clinically. Further investigations will be needed if suspected:

  • Osteomalacia (poor mineralisation on biopsy).
  • CKD (High creatinine).
111
Q

What are some common complications of osteomalacia?

A
  • Pseudofractures.
  • Bone pain.
  • Secondary hyperPTH (if Calcium or vit D are chronically low.

Phase 2a diseases (18 decks)

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