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Phase 2a > Rheumatology > Flashcards

Rheumatology Flashcards

1
Q

What’s the function of oestoblasts?

A
  • Synthesis type I collagen rich matrix (osteoid).

- Secrete RANK-ligand.

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2
Q

What’s the function of osteoclasts?

A
  • Responsible for bone resorption.
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3
Q

What’s the function of RANK-ligand? What inhibitors RANK-ligand?

A
  • Binds to osteoclasts + essential for their formation, function + survival.
  • OPG.
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4
Q

What are ESR/CRP?

A

Inflammatory markers.

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5
Q

Briefly describe vitamin D synthesis

A
  • In liver, 25-hydroxylase converts cholecalciferol into calcifediol.
  • In kidneys, 1-alpha-hydroxylase converts calcifediol into calcitriol.
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6
Q

Describe the function of PTH.

A
  • Increases bone resporption + so calcium + phosphate.
  • Increases calcium reabsorption in DCT + decreases phosphate reabsorption in PCT.
  • Stimulates 1-hydroxylase release, increasing calcitriol + so calcium/phosphate absorption in intestine.
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7
Q

Describe uric acid metabolism.

A
  • Purines (A+G) > hypoxanthine > xanthine > uric acid > monosodium urate.
  • Xanthine oxidase converts hypoxanthine > xanthine.
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8
Q

OSTEOARTHRITIS

What is the pathophysiology of OA?

A
  • Non-inflammatory degernative disorder of synovial joints characterised by deterioration of articular cartilage + formation of new bone.
  • Progressive destruction of articular cartilage makes exposed subchondral bone become sclerotic, increases vascularity + subchondral cysts form where repair produces cartilaginous growths from chondrocytes which become calcified (osteophytes)
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9
Q

OSTEOARTHRITIS

What is the aetiology of OA?

A
  • Usually primary with no predisposing factors.

- Secondary OA sometimes occurs to damaged/congenitally abnormal joints.

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10
Q

OSTEOARTHRITIS

What are the risk factors of OA?

A
  • Female.
  • Family Hx.
  • Obesity.
  • Occupation (manual labour).
  • Increasing age (cumulative effect of trauma + decrease in neuromuscular function).
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11
Q

OSTEOARTHRITIS

What are the symptoms of OA?

A
  • Morning stiffness <30m.
  • Joint pain exacerbated by exercise.
  • Joint stiffness after rest (gelling).
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12
Q

OSTEOARTHRITIS

What are the signs of osteoarthritis?

A 
Bony swelling's...
- DIPJs = Herberden's nodes.
- PIPJs = Bouchard's nodes.
- Carpal metacarpal joints affected.
- Medial surface of knee affected.
Joint deformities/tenderness.
Reduced range of movement.
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13
Q

OSTEOARTHRITIS

What are the investigations for OA?

A

Plain X-ray = LOSS…

  • Loss of joint space.
  • Osteophytes.
  • Subarticular sclerosis.
  • Subchondral cysts.
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14
Q

OSTEOARTHRITIS

What is the non-medical treatment of OA?

A
  • Education.
  • Exercise to improve local muscle strength.
  • Weight loss.
  • PT/OT.
  • Walking aids.
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15
Q

OSTEOARTHRITIS

What is the medical treatment for OA?

A
  • Regular paracetamol ± topical NSAIDs.
  • Codeine.
  • Intra-articular steroid injections.
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16
Q

OSTEOARTHRITIS

What is the surgical treatment for OA?

A
  • Arthroscopy for loose bodies (can cause locking, e.g. knee).
  • Osteotomy (change bone length).
  • Arthroplasty (joint replacement).
  • Fusion (ankle + foot often).
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17
Q

OSTEOARTHRITIS

What is a negative to arthroplasty?

A
  • Prosthetic joint infection can be a serious complication, requires exchange arthroplasty.
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18
Q

RHEUMATOID ARTHRITIS

What is the pathophysiology of RA?

A
  • Autoimmune inflammatory synovial joint disease.
  • Chronic inflammation leads to B/T cells + neutrophils to infiltrate the synovium, formation of new synovial blood vessels occur causing synovium to proliferate leading to pannus formation, grows over articular cartilage + destroys it + subchondral bone leading to bony erosions.
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19
Q

RHEUMATOID ARTHRITIS

What is the epidemiology of RA?

A
  • 1% prevalence (increased in smokers).
  • F:M = 2:1.
  • Peak incidence in 40s.
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20
Q

RHEUMATOID ARTHRITIS

What is the aetiology of RA?

A
  • Autoantibodies such as rheumatoid factor (Anti-IgG) + anti-cyclic citrullinated peptide (CCP) lead to defective cell mediated immune response.
  • HLA DR4/DRB1 linked.
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21
Q

RHEUMATOID ARTHRITIS

What are the symptoms are RA?

A
  • Morning stiffness (>30m).
  • Pain eases with use.
  • Swelling.
  • Systemic illness like general fatigue, malaise.
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22
Q

RHEUMATOID ARTHRITIS

What are the extra-articular symptoms of RA?

A
  • Eyes = dry, scleritis.
  • Neuro = neuropathies like carpal tunnel.
  • Haem = lymphadenopathy, anaemia.
  • Resp = pleural effusion, nodules.
  • Cardio = pericardial effusion, IHD.
  • Kidneys = amyloidosis.
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23
Q

RHEUMATOID ARTHRITIS

What are the signs of RA?

A

Symmetrical swollen painful + stiff joints…
- Typically metacarpophalangeal + PIPJ + wrist affected.
Deformities…
- Ulnar deviation (Swelling of metacarpophalangeal + PIPJ joints).
- Boutonierre thumb (Z-thumb).
- Swan-neck deformity.
Polyarthropathy.

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24
Q

RHEUMATOID ARTHRITIS

What are the investigations for RA?

A 
Bloods...
- ESR/CRP raised.
- Anaemia (normochromic/cytic).
Test for serum antibodies...
- Rheumatoid factor (>70% present).
- Anti-CCP (specific, predicts disease progression).
X-ray shows LESS...
- Loss of joint space.
- Erosions.
- Soft tissue swelling.
- Soft bones (osteopenia).
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25
Q

RHEUMATOID ARTHRITIS

What is the treatment for RA?

A
  • Early use of 2x DMARDs = methotrexate + sulfasalazine + biological agents (rituximab) to slow progression + target parts of immune system involved in inflammation.
  • Steroids help rapidly reduce symptoms.
  • NSAIDs/analgesia.
  • PT/OT.
  • Encourage exercise.
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26
Q

GOUT

What is the pathophysiology of gout?

A
  • Inflammatory arthritis caused by hyperuricaemia + intra-articular monosodium urate crystals.
  • Hyperuricaemia results from overproduction of uric acid/renal underexcretion.
  • Urate is derived form breakdown of purines.
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27
Q

GOUT

What is the aetiology + risk factors for gout?

A
  • Hyperuricaemia – idiopathic with impaired renal excretions from CKD, diuretics, HTN.
  • Men >75y/o.
  • RFs = alcohol, red meat + seafood, chemotherapy.
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28
Q

GOUT

What are the mean differentials for gout?

A
  • Septic arthritis.

- Reactive arthritis.

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29
Q

GOUT

What are the symptoms of gout?

A
  • Hot + swollen joints.

- Toes commonly affected (metatarsophalangeal joint of big toe).

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30
Q

GOUT

What are the signs of gout?

A
  • Tophi = aggregates of urate crystals w/ inflammatory cells, proteolytic enzymes are released leading to erosion.
  • Poly-articular inflammatory arthritis.
  • Erythema.
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31
Q

GOUT

What are the complications of gout?

A

Increased risk of developing…

  • HTN.
  • CVD like stroke.
  • Renal disease.
  • T2DM.
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32
Q

GOUT

What are precipitating factors for an acute attack of gout?

A
  • Cold/trauma.
  • Drugs.
  • Dehydration.
  • Sepsis.
  • Sudden overload.
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33
Q

GOUT

What are the investigations for gout?

A

Joint fluid aspiration + microscopy…
- Needle-shaped crystals, negatively birefringent under polarised light.
Serum uric acid raised.
Tophi.

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34
Q

GOUT

What is the treatment for gout?

A

Lifestyle = diet, weight loss, reduce alcohol.
Rest + elevate joint, ice packs.
- NSAIDs like diclofenac, colchicine if NSAIDs C/I.
- Allopurinol.
- Corticosteroids.
- Switching bendroflumethiazide to cosartan.

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35
Q

GOUT

What is the mechanism of action of allopurinol?

A
  • Blocks xanthine oxidase.
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36
Q

PSEUDOGOUT

What is the pathophysiology of pseudogout?

A
  • Deposition of calcium pyrophosphate crystals on joint surfaces + the crystals ellicit an inflammatory response.
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37
Q

PSEUDOGOUT

What diseases is pseudogout associated with?

A
  • Hyperparathyroidism.
  • Haemochromatosis.
  • Hypophosphataemia.
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38
Q

PSEUDOGOUT

What is the clinical presentation of gout?

A
  • Acute, hot + swollen joints.

- Usually knee/wrist.

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39
Q

PSEUDOGOUT

What are the investigations of pseudogout?

A

Joint fluid microscopy…
- Rhomboid-shaped crystals showing positive birefringence in polarised light.
X-ray…
Can show chondrocalcinosis (linear calcification parallel to articular surfaces).

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40
Q

PSEUDOGOUT

What is the treatment for pseudogout?

A
  • Rest + elevate joint, ice packs.
  • Joint aspiration w/ NSAIDs/colchicine.
  • Intra-articular steroids.
  • Methotrexate.
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41
Q

ANKYLOSING SPONDYLITIS

What is the pathophysiology of ankylosing spondylitis?

A
  • Inflammation of spine leads to erosive damage causing repair/new bone formation, resulting in bony spurs (syndesmophytes) that leads to irreversible fusion of the spine (ankylosis).
  • Typically asymmetrical large joints are affected in seronegative spondyloarthropathies.
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42
Q

ANKYLOSING SPONDYLITIS

What is the aetiology of ankylosing spondylitis?

A
  • Unknown, M>F.

- Strong association with HLA-B27 antigen presenting cell.

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43
Q

ANKYLOSING SPONDYLITIS

What are the symptoms of ankylosing spondylitis?

A
  • Typically young man.
  • Increasing pain + prolonged morning stiffness in lower back + buttocks, improves with exercise, not rest.
  • Progressive loss of spinal movement.
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44
Q

ANKYLOSING SPONDYLITIS

What are the signs of ankylosing spondylitis?

A
  • Loss of lumbar lordosis (curve).
  • Increased kyphosis.
  • Limitation of lumbar spine mobility.
  • Enthesitis.
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45
Q

ANKYLOSING SPONDYLITIS

What are the investigations for ankylosing spondylitis?

A

Bloods…
- ESR/CRP often raised.
X-ray…
- Erosion + sclerosis of margins of sarcoiliac joints > sacroilitis.
- Bamboo spine = progressive calficiation of interspinous ligaments + syndesmophytes.
HLA-B27 test, MRI.

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46
Q

ANKYLOSING SPONDYLITIS

What is the treatment for ankylosing spondylitis?

A
  • Morning exercises to maintain posture + spinal mobility.
  • Slow release NSAIDs taken at night to relieve night pain + morning stiffness.
  • Methotrexate for peripheral arthritis.
  • TNF-alpha inhibitors like rituximab.
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47
Q

PSORIATIC ARTHRITIS

What is the pathophysiology + aetiology of psoriatic arthritis?

A
  • Psoriasis occurs commonly at elbow, knees + fingers.

- Occurs in 10–40% of those with psoriasis.

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48
Q

PSORIATIC ARTHRITIS

What is the clinical presentation of psoriatic arthritis?

A 
Skin rash, check behind/in ears + umbilicus...
- Symmetrical distribution.
- Itchy.
- Well-circumscribed margins.
- Deep red colour on extensor srufaces.
DIPJ involvement.
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49
Q

PSORIATIC ARTHRITIS

What are specific psoriatic arthritis features?

A
  • Symmetrical polyarthritis.
  • Dactylitis (inflammation of whole digit).
  • Spinal involvement.
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50
Q

PSORIATIC ARTHRITIS

What are the investigations for psoriatic arthritis?

A

X-rays…
- Pencil in cup deformity in interphalangela joints where bone erosion create pointed appearance + articulating bone is concave.

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51
Q

PSORIATIC ARTHRITIS

What is the treatment for psoriatic arthritis?

A
  • Analgesia + NSAIDs.

- Methotrexate, TNF-alpha inhibitor.

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52
Q

REACTIVE ARTHRITIS

What is the pathophysiology of reactive arthritis?

A
  • Sterile inflammation of the synovial membrane in which arthritis occur as an autoimmune response to infection elsewhere in body, typically GI/GU.
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53
Q

REACTIVE ARTHRITIS

What is the aetiology of reactive arthritis?

A
  • GI infection like Shigella, Salmonella.

- STI like chlamydia trachomatis.

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54
Q

REACTIVE ARTHRITIS

What is the clinical presentation of reactive arthritis?

A

Reiter’s syndrome “can’t see, pee or climb a tree”
- Conjunctivitis.
- Urethritis.
- Arthritis.
Acute onset malaise, fatigue, fever.
Low back pain, asymmetrical, oligoarthritis.

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55
Q

REACTIVE ARTHRITIS

What are the investigations + treatments for reactive arthritis?

A
  • Bloods = CRP/ESR raised.
  • Aspirated synovial fluid sterile with high neutrophil count.
  • NSAIDs + local corticosteroid injections, methotrexate in relapsing cases.
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56
Q

ENTEROPATHIC ARTHRITIS

What is it associated with? How does it improve? Treatment for resistant cases?

A
  • IBD.
  • Improves w/ bowel symptoms.
  • DMARDs like methotrexate.
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57
Q

JIA

What is the diagnostic criteria + aetiology of juvenile idiopathic arthritis (JIA)?

A
  • Joint swelling/stiffness >6w in children <16y/o + no other cause identified.
  • Idiopathic but autoimmune so genetic factors.
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58
Q

JIA

Where should you check especially in JIA + why? Other features of JIA.

A
  • Eyes, lining of eyes + joints very similar so high risk of uveitis.
  • Oligoarthritis affecting ≤4 joints, often antinuclear antibody (ANA) positive.
  • Enthesitis related JIA is similar to adult ankylosing spondylitis + is HLA-B27 positive.
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59
Q

JIA

What is the treatment of JIA?

A 
Non-medical = education, support, physiotherapy.
Medical = steroid joint injections, NSAIDs + methotrexate.
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60
Q

JIA

What are the complications with JIA?

A
  • Damage, deformity, disability.
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61
Q

SEPTIC ARTHRITIS

What is the pathophysiology + aetiology of septic arthritis?

A
  • Acute infection of joint which can cause damaging inflammation + loss of function, can destroy joint in <24h.
  • Mostly S. aureus, Streptococci, Neisseria.
62
Q

SEPTIC ARTHRITIS

What are the risk factors with septic arthritis?

A
  • Pre-existing joint disease (Esp. RA).
  • Prosthetic joints.
  • IVDU.
  • Age >80y/o.
  • DM.
63
Q

SEPTIC ARTHRITIS

What is the clinical presentation of septic arthritis?

A
  • Fever.
  • Red/swollen/hot.
  • Single swollen joint w/ pain on movement (often knee).
64
Q

SEPTIC ARTHRITIS

What are the investigations + treatment for sepetic arthritis?

A
  • Bloods = ESR/CRP raised.
  • Joint aspiration for synovial fluid microscopy + culture prior to antibiotics.
  • Immediate empirical antibiotics (flocloaxicillin), aspiration to drain, rest/splinting.
65
Q

OSTEOMYELITIS

What is osteomyelitis?

A
  • Bone inflammation leading to destruction, secondary to infection of the bone marrow.
66
Q

OSTEOMYELITIS

What are the two easiest routes for pathogens to get into the bone?

A
  • Inoculation of infection into bone (trauma, open wound).

- Continguous spread of infection to bone from adjacent tissues.

67
Q

OSTEOMYELITIS

What is the hardest way for pathogens to get into the bone?

A
  • Haematogenous seeding, often seen in vertebrae in adults + as with age vertebrae become more vascular.
  • Bacterial seeding means bacterial can move from blood to bone e.c. due to cannula infection, IVDU.
68
Q

OSTEOMYELITIS

What are host factors affecting pathogenesis of osteomyelitis?

A
  • Behavioural (risk of trauma).
  • Vascular supply (arterial disease).
  • Pre-existing bone/joint problems (RA).
  • Immune deficiency.
69
Q

OSTEOMYELITIS

What is the aetiology of osteomyelitis?

A

Local infection…

  • S. aureus, H. influenzae, Salmonella.
  • Metastatic haematogenous spread.
  • TB (caseating granuloma).
70
Q

OSTEOMYELITIS

What are the risk factors for osteomyelitis?

A
  • Pre-existing joint disease (Esp. RA).
  • Prosthetic joints.
  • Age >80y/o.
  • DM.
  • Immunosuppression.
71
Q

OSTEOMYELITIS

What is the clinical presentation of osteomyelitis?

A
  • Fever, dull, localised bone pain worse on movement.
  • Tenderness.
  • Erythema.
72
Q

OSTEOMYELITIS

What are the investigations with osteomyelitis?

A 
Bloods...
- Raised ESR/CRP, WCC.
- Cultures.
X-rays first line.
Bone biopsy + cultures = diagnostic.
73
Q

OSTEOMYELITIS

What is the treatment for osteomyelitis?

A
  • Surgical debridement (removal of damage tissue), drainage of abscess.
  • IV Abx (often flucloxacillin).
74
Q

OSTEOPOROSIS

What is the pathophysiology of osteoporosis?

A
  • Systemic skeletal disease characterised by low bone mass + micro-architectural deterioration where the patient is at increased risk of fracture.
75
Q

What are 2 factors important in determining likelihood of osteoporotic fall? What makes bone strength?

A
  • Propensity to fall leading to trauma + bone strength.

- Bone mineral density, size, micro-architecture + mineralisation.

76
Q

OSTEOPOROSIS

Why does the bone become so much weaker in osteoporosis?

A
  • Trabecular thickness decreases meaning there’s fewer connections between trabecular + so overall decrease in strength.
  • Excessive bone resorption + inadequate formation of new bone during remodelling occurs.
77
Q

OSTEOPOROSIS

What are the secondary causes of osteoporosis?

A
  • Steroid use.
  • Hyper/hypothyroid.
  • Alcohol/smoking.
  • Thin (low BMI).
  • Testosterone low.
  • Early menopause.
  • Renal/liver failure.
  • Relatives (FHx).
  • Erosive bone disease (RA).
  • Dietary calcium low.
78
Q

OSTEOPOROSIS

What is the clinical presentation of osteoporosis?

A
  • Develops asymptoamtically.
  • Fracture often first sign…
    Distal radius = Colles’ fracture.
    Thoracic vertebrae > kyphosis (widow’s stoop).
    Proximal femur.
    Lumbar vertebrae.
79
Q

OSTEOPOROSIS

What are the investigations for osteoporosis?

A
  • Bloods normal (no issue with mineralisation).
  • Dual-energy X-ray absorptiometry (DEXA) scan is gold standard.
  • X-ray show fractures.
  • FRAX to assess someone’s risk of osteoporotic fracture.
80
Q

OSTEOPOROSIS

What is the DEXA T score and what does it tell you?

A
  • T score is a standard deviation compared to a gender-matched young adult mean.
  • DEXA-T ≤ –2.5 = osteoporosis.
  • –2.5 < DEXA-T ≤ –1 = osteopenia (low bone mass).
81
Q

OSTEOPOROSIS

What is the lifestyle advice for osteoporosis?

A
  • Quit smoking, reduce alcohol.
  • Calcium + vitamin D supplement (AdCal D3).
  • HRT.
  • Balance exercise to reduce risk of falls.
82
Q

OSTEOPOROSIS

What are the medical therapies for osteoporosis?

A

Anti-resorptive (decrease osteoclast activity + bone turnover)…
- Bisphosphonates (alendronate).
- Denosumab (human monoclonal antibody to RANK-L).
- HRT in early post-menopausal women.
Anabolic (increase osteoblast activity)
- Teriparatide.

83
Q

SLE

What is the pathophysiology of systemic lupus erythematosus?

A
  • Inefficient phagocytosis > cell fragments transferred to lymphoid tissue where they’re taken up by antigen presenting cells where self-antigens are present to T cells.
  • T cells stimulate B cells to produce autoantibodies against self-antigens.
  • Results in complement activation, influx of neutrophils + abnormal cytokine production leads to inflammation + tissue damage.
84
Q

SLE

What are the risk factors + triggers of SLE?

A 
Risk factors...
- 90% young women.
- Commoner in Afro-Caribbeans.
- Genetic association.
Triggers...
- UV light.
- EBV.
85
Q

SLE

What are the symptoms of SLE?

A
  • Weight loss.
  • Migraines.
  • Photosensitivity.
  • Myalgia + arthralgia.
86
Q

SLE

What are the signs of SLE?

A
  • Butterfly rash.
  • Pericarditis.
  • Raynaud’s phenomenon.
  • Anaemia.
87
Q

SLE

What is a major complication of SLE?

A

Antiphospholipid syndrome.

  • There are antiphospholipid antibodies which causes CLOTs…
  • Coagulation defect.
  • Livedo reticularis (mottled rash).
  • Obstetric (recurrent miscarriage).
  • Thrombocytopenia.
88
Q

SLE

What are the investigations for SLE?

A 
Bloods...
- Raised ESR, normal CRP.
- Normochromic/cytic anaemia.
Serum autoantibodies...
- ANA (specific, not sensitive).
- Anti-dsDNA (sensitive, not specific).
89
Q

SLE

What is the treatment for SLE?

A

Education + support, UV protection + smoking cessation, screening for organ involvement.
- Corticosteroids, NSAIDs, DMARDs, monoclonal antibody. (rituximab).

90
Q

PRIMARY BONE TUMOURS

What is a primary bone tumour? Give an example

A
  • Bone tumours that originate in bone or from bone-derived cells + tissues.
  • Sarcoma is rare tumour of mesenchymal origin – malignant connective tissue neoplasm.
91
Q

PRIMARY BONE TUMOURS

Give examples of benign + malignant tumours.

A
  • Osteoid osteoma, osteoblastoma, osteochondroma.

- Osteosarcoma, chondrosarcoma, Ewing’d sarcoma.

92
Q

PRIMARY BONE TUMOURS

What are bony sarcomas?

A

Make up 20% sarcomas.

  • Osteosarcoma (fast growing, aggressive, 15–17y/o).
  • Ewing’s sarcoma (neural crest cells), onion-skin appearance on x-ray, responds well to chemotherapy.
93
Q

PRIMARY BONE TUMOURS

What are red flag symptoms for primary bone tumours?

A
  • Loss of function, non-mechanical bone pain present when still.
  • Weight loss, night pain, swelling.
  • Tiredness, pyrexia.
94
Q

PRIMARY BONE TUMOURS

What are signs of primary bone tumours?

A
  • Lump >5cm.
  • Lump increasing in size + deep to fascia.
  • Rest pain/pain at night.
  • Codman’s triangle + sunburst appearance (osteosarcoma + Ewing’s).
95
Q

PRIMARY BONE TUMOURS

What are the investigations of primary bone tumours?

A
  • Bloods, FBC, U+E, ALP.
  • Plain X-rays.
  • Bone scan.
  • Core needle biopsy.
  • CT/MRI scan.
96
Q

PRIMARY BONE TUMOURS

What is the treatment of primary bone tumours?

A
  • Chemo ± radiotherapy.
  • Surgery.
  • Bisphosphonates.
97
Q

SECONDARY BONE TUMOURS

What are the most common secondary bone tumours?

A
  • Breast.
  • Lung.
  • Prostate.
  • Kidney.
  • Thyroid.
98
Q

SECONDARY BONE TUMOURS

What is the clinical presentation of secondary bone tumours?

A
  • Bone pain.
  • Generally unwell.
  • Pathological fracture.
99
Q

SECONDARY BONE TUMOURS

What are the investigations + treatment for secondary bone tumours?

A
  • Bloods, FBC, U+E, ALP.
  • Plain X-rays, bone scan, core needle biopsy, CT/MRI scan.
  • Treat cause, surgery, correct metabolic abnormalities.
100
Q

FIBROMYALGIA

What is the pathophysiology of fibromyalgia?

A
  • Chronic widespread pain + sensitivity to pressure.
101
Q

FIBROMYALGIA

What can increase/decrease the volume of pain?

A
  • Increase = substance P, glutamate, serotonin.

- Decrease = opioids, GABA + cannabinoids.

102
Q

FIBROMYALGIA

What are the associations + triggers of fibromyalgia?

A

Associations…
- Depression, chronic fatigue, IBS.
Triggers…
- Physical trauma, infections, hormonal alterations.

103
Q

FIBROMYALGIA

What is the clinical presentation of fibromyalgia?

A
  • Morning stiffness.
  • Poor concentration, sleep disturbances.
  • Headaches.
  • Pain worse w/ stress, cold.
104
Q

FIBROMYALGIA

What are the investigations for fibromyalgia?

A
  • Chronic widespread pain lasting >3 months w/ other causes excluded.
  • Pain is at 11/18 tender sites.
105
Q

FIBROMYALGIA

What is the treatment for fibromyalgia?

A
  • Exercise + fitness important.
  • Acupuncture.
  • Low dose amitriptyline (sleep).
  • CBT, acupuncture.
106
Q

MECHANICAL BACK PAIN

What is the pathophysiology of mechanical back pain?

A
  • Back pain as a result of physical wear + tear.
107
Q

MECHANICAL BACK PAIN

What is nerve root pain?

A
  • Nerve root impingement due to herniated discs causes a sharp, well localised pain + can be associated with paraesthesia.
108
Q

MECHANICAL BACK PAIN

What are risk factors with mechanical back pain?

A
  • Manual labour work.
  • Smoking.
  • Low socioeconomic status.
  • Females.
109
Q

MECHANICAL BACK PAIN

What’s the clinical presentation of mechanical back pain?

A
  • Back pain in lumbosacral area.
  • Worse on movement.
  • Systemically well.
110
Q

MECHANICAL BACK PAIN

What are the investigations for mechanical back pain?

A
  • FBC, ESR/CRP.

- Only x-ray if red-flags (IVDU, night sweats, incontinence, fever).

111
Q

MECHANICAL BACK PAIN

What is the treatment for mechanical back pain?

A
  • Resolves after 6w.
  • Education + self-management.
  • Analgesic ladder.
  • Acupuncture, physio.
112
Q

OSTEMOMALACIA

What is the pathophysiology of osteomalacia + rickets?

A
  • Manifestation of profound vitamin D deficiency where inadequate mineralisation of osteoid framework leads to soft bones + produces rickets during bone growth + osteolamalcia following epiphyseal closure.
  • Normal amount of bone but mineral content low.
113
Q

OSTEMOMALACIA

What’s the aetiology of vitamin D deiciency?

A
  • Lack of exposure to sun.
  • Malabsorption/poor diet.
  • Renal disease.
114
Q

OSTEMOMALACIA

What’s the clinical presentation of osteomalacia + rickets?

A
  • Osteomalacia = proximal muscle weakness + pain, fractures (esp. femoral neck).
  • Rickets = bowed legs + knock knees, growth retardation.
115
Q

OSTEMOMALACIA

What are the investigations + treatment for osteomalacia?

A 
Plasma...
- Hypocalcaemia, high PTH, high ALP.
- Low calcitriol + phosphate.
Bone biopsy = incomplete mineralisation.
X-ray = loss of cortical bone.
- Oral calciferol.
116
Q

SJÖGRENS SYNDROME

What is the pathophysiology of Sjögrens syndrome?

A
  • Immunologically mediated destruction of epithelial exocrine glands, especially lacrimal + salivary.
  • Lymphocytic infiltration of exocrine glands.
117
Q

SJÖGRENS SYNDROME

What’s the aetiology of Sjögrens syndrome?

A
  • Primary = idiopathic.

- Secondary = autoimmune related (RA).

118
Q

SJÖGRENS SYNDROME

What is the clinical presentation of Sjögrens syndrome?

A
  • Dry eyes + mouth = sicca complex.

- Arthritis.

119
Q

SJÖGRENS SYNDROME

What are the investigations + treatment for Sjögrens syndrome?

A
  • Schirmer’s test = measure conjunctival dryness.
  • Serum autoantibodies like anti-Ro, rheumatoid factor, ANA.
  • Artifical tear + saliva replacement.
120
Q

POLYMYOSITIS

What is the pathophysiology of polymyositis?

A
  • Rare muscle disorder where there’s autoimmune-mediataed striated muscle inflammation (myositis), mediated by cytotoxic T cells.
121
Q

POLYMYOSITIS

What is the clinical presentation of polymyositis.

A
  • Symmetrical progressive muscle weakness.

- Skin invovlement with scaly erythematous plaques over knucles (dermamyositis).

122
Q

POLYMYOSITIS

What are the investigations + treatment for polymyositis?

A
  • Serum muscle enzymes raised, muscle biopsy diagnostic.

- Oral prednisolone + immunosuppressive therapy.

123
Q

SCLERODERMA

What is the pathophysiology of scleroderma?

A

Multisystem autoimmune connective tissue disorder with involvement of skin, excessive collagen production + deposition, inflammation + autoantibody production.

124
Q

SCLERODERMA

What is the clinical presentation of limited cutaneous?

A 
Face, forearms, lower legs up to knee...
Calcinosis.
Raynaud's phenomenon.
oEsophageal involvement (dysmotility).
Sclerodactyly.
Telangiectasia.
125
Q

SCLERODERMA

What is the clinical presentation of diffuse cutaneous?

A
  • Affects whole body.
  • Pulmonary fibrosis + HTN.
  • Poor prognosis.
126
Q

SCLERODERMA

What are the investigations + treatments for scleroderma?

A 
Serum autoantibodies (antinuclear, anti-Ro).
- Treat symptoms, PPIs for GORD, CCB for Raynaud's, annual echo.
127
Q

VERTEBRAL DISC DEGENERATION

What is the pathophysiology of vertebral disc degeneration?

A
  • Pathological process of degeneration of intervertebral discs where there’s protrusion, spondylosis +/or spinal stenosis.
128
Q

VERTEBRAL DISC DEGENERATION

What is the aetiology of vertebral disc degeneration?

A
  • Disease of ageing, increased fragility of cartilage of disc can lead to pathology.
129
Q

VERTEBRAL DISC DEGENERATION

What is the clinical presentation of vertebral disc degeneration?

A
  • Chronic lower back pain, sometimes radiating to hips _ buttocks.
130
Q

VERTEBRAL DISC DEGENERATION

What are the investigations + treatment for vertebral disc degeneration?

A
  • Physical therapy, NSAIDs, surgery.
131
Q

POLYMYALGIA RHEUMATICA

What is the pathophysiology of polymyalgia rheumatica?

A
  • Pain + stiffness results from inflammatory cells concentrating in tissues surrounding affecting joints, attacking the lining of joints.
  • Especially shoulders, neck + hip.
132
Q

POLYMYALGIA RHEUMATICA

What is the clinical presentation of polymyalgia rheumatica?

A
  • Bilateral aching/tenderness.
  • Morning stiffness in shoulders, hips + proximal limbs.
  • Associated with giant cell arteritis.
133
Q

POLYMYALGIA RHEUMATICA

What are the investigations + treatment for polymyalgia rheumatica?

A
  • Bloods, ESR/CRP raised.

- Corticosteroids.

134
Q

POLYARTERITIS NODOSA

What is the pathophysiology of polyarteritis nodosa?

A
  • Necrotising arteritis that causes aneurysms + thrombosis in medium-sized arteries, leading to infarction in affected organs with severe systemic symptoms.
135
Q

POLYARTERITIS NODOSA

What is the clinical presentation of polyarteritis nodosa?

A
  • Systemic = fever, malaise, weight loss, myalgia.

- Skin can show rash, punched out ulcers, nodules.

136
Q

POLYARTERITIS NODOSA

What are the investigations + treatment for polyarteritis nodosa?

A

Bloods = ESR, CRP, WCC raised.

  • Renal/mesenteric angiography or renal biopsy = diagnostic.
  • Control BP, corticosteroids.
137
Q

WEGENER’S GRANULOMATOSIS

What is the pathophysiology of Wegener’s granulomatosis?

A
  • Necrotising granulomatous inflammation + vasculitis of small + medium vessels, normally affects arterioles + capillaries.
138
Q

WEGENER’S GRANULOMATOSIS

What is the clinical presentation of Wegener’s granulomatosis?

A
  • Upper RT = sinusitis, otitis.
  • Lungs = pulmonary nodules.
  • Kidney = glomerulonephritis.
  • Skin = ulcers.
  • Eyes = uveitis.
139
Q

WEGENER’S GRANULOMATOSIS

What are the investigations + treatment for Wegener’s granulomatosis?

A
  • c-ANCA +ve.
  • Urinalysis for proteinuria/haematuria.
  • CXR nodules.
  • High dose steroids.
140
Q

PAGET’S DISEASE

What is the pathophysiology of Paget’s disease?

A
  • Increased bone turnover associated with increased numbers of osteoblasts + osteoclasts w/ resultant remodelling, bone enlargement, deformity + weakness as new bone is mechanically weaker, more vascularised + poorly organised (pathological fractures).
141
Q

PAGET’S DISEASE

What is the clinical presentation of Paget’s disease?

A
  • Mostly asymptomatic.
  • Deep, boring pain in bone/nearby joint.
  • Deformities like skull enlargement, bowing of tibia (bowed sabre tibia).
142
Q

PAGET’S DISEASE

What are the complications with Paget’s disease?

A
  • Pathological fractures.
  • Nerve compression.
  • OA.
143
Q

PAGET’S DISEASE

What are the investigations + treatment for Paget’s disease?

A
  • Bloods = high serum ALP.
  • X-ray = localised bony enlargement, distortion, sclerotic changes + osteolytic areas.
  • Bisphosphonates + analgesia.
144
Q

NSAIDs

What is the mechanism of action? Give some examples. List some side effects.

A
  • Non-selective inhibitors of cyclo-oxygenase + so inhibit prostaglandins.
  • Naproxen, diclofenac, ibuprofen.
  • Peptic ulcers (co-prescribe PPIs), renal failure (AA vasoconstriction so reduced GFR), increased risk of MI/CVD.
145
Q

STEROIDS

Give an example. What are the side effects of steroids?

A
  • Prednisolone.

- Acne, HTN, osteoporosis, skin atrophy.

146
Q

DMARDS

What is the mechanism? Give examples. Advice for when taking methotrexate?

A
  • Non-specific inhibition of inflammatory cytokine cascade = reduced joint pain, stiffness + swelling.
  • Methotrexate, sulfasalazine.
  • Take once weekly, folic acid co-prescribed, can cause liver problems so regular bloods.
147
Q

TNF-ALPHA BLOCKER

Give an example.

A

Rituximab, adalimumab.

148
Q

BISPHOSPHONATES

Example + mechanism.

A
  • Alendronate.

- Reduces bone tunrover by inhibiting osteoclast mediated bone resorption by targeting HMG-CoA reductase pathway.

149
Q

ANALGESIC LADDER

What are the three steps?What is the additional step?

A 
Non-opioids, mild pain..
- NSAIDs, paracetamol.
Weak-opioids, moderate pain...
- Codeine + derivatives.
Strong opioids, high pain...
- Morphine, oxycodone.
?Nerve blocks.
150
Q

ANALGESIC LADDER

What does NICE recommend at each level of the ladder?

A
  • Adjuvant pharmacological agents like muscle-relaxants, anti-depressants + corticosteroids.
151
Q

OSTEOMYELITIS

What is the difference between acute + chronic osteomyelitis?

A

Acute - dendritic cells, macrophages, oedema = resolution often.
Chronic - necrotic bone (sequestra), new bone formation.

Phase 2a (12 decks)

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