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Haroon Phase 2A > MSK & Rheumatology > Flashcards

MSK & Rheumatology Flashcards

1
Q

What is bone structure made up of?

A

1) Cortical bone outside (arranged in osteon functional units) 2) Trabecular bone inside

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2
Q

Structure of osteons?

A

Made up of concentric lemellae (like a tree trunk) and central Haversian canal - Haversian canal supplies a single longitudinal osteon - horizontal communication between osteons = volkmann canals

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3
Q

Component of bone? (Inorganic and organic)

A

Inorganic component = hydroxyapatite (Ca2(PO4)3) - stiffness Origanum component = collagen T1 - elasticity

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4
Q

Purpose of trabecular bone?

A

Bone marrow structural meshwork Low in mass but high in strength

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5
Q

Three types of joints?

A

1) Fibrous (synarthrosis, unmovable) - skull sutures 2) Cartilaginous (amphiarthrosis, partially moveable) - IV disc, pubic symphysis 4) Synovial (diarthrosis, freely moveable) - most joints of body (knee, hip, shoulder etc)

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6
Q

Synovial joint components?

A
  • articular cartilage - joint capsule (inner lining = synovial membrane) - synovial cavity filled with little synovial fluid
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7
Q

Attachment from bone to bone?

A

Ligaments

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8
Q

Attachment from muscle to bone?

A

Tendons

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9
Q

Most common type of arthritis?

A

Osteoarthritis

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10
Q

What is osteoarthritis?

A
  • Traditionally a “non-inflammatory” age-related “degenerative” joint disorder characterised by joint pain and functional limitation. - No longer thought to be the case as it is shown to be inflammatory too. - Metabolically active and dynamic process that is mediated by cytokines. - Often symmetrical and bilateral
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11
Q

What joints does osteoarthritis typically affect?

A

Knees Hips Hands Spine (cervical and lumbar) Base of thumb pain pain almost ALWAYS osteoarthritis

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12
Q

Non modifiable risk factors for osteoarthritis?

A
  • Age (50+) - uncommon in those under 45 - Females (hip OA is twice as common in women than men) - Genetics (COL2A1= predisposition) - more common when it presents bilaterally - High bone density - but actually protective against osteoporosis - abnormal biomechanics - joint hypermobility or congenital hip dysplasia
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13
Q

Modifiable risk factors for osteoarthritis?

A
  • obesity (3x increased risk) as it is a low grade inflammatory state with release of cytokines - joint injury and damage (history of inflammation can increase risk) - Exercise stresses (occupation with lots of standing or professional athletes) footballers more likely to have osteoarthritis of knees and those with lots of manual labour more likely to have osteoarthritis in the hands
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14
Q

Aetiology of osteoarthritis?

A

Imbalance between extracellular matrix synthesis vs degradation regulated by chondrocytes within the cartilage => loss of cartilage, remodelling of adjacent bone and subsequent inflammation

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15
Q

Pathophysiology of osteoarthritis?

A

Increased metalloproteinase secretion by chrondocytes which degrades T2 collagen and causes cysts - bone attempts to overcome this with T1 collagen leading to abnormal bony growths (osteophytes) + remodelling

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16
Q

Symptoms of osteoarthritis?

A
  • Transient morning pain (<30min) - joint pain exacerbated by movement and gets worse as the day goes on - swelling - joint locking (particularly common at the knee) - functional impairment such as walking or activities of daily living
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17
Q

Signs of osteoarthritis in the hands?

A

Haberden’s nodes: asymmetrical bony swelling at the distal interphalangeal joint -Bouchard’s nodes: asymmetrical bony swelling at proximal interpharangeal joint (also seen in RA) -Thenar wasting -First carpometacarpal joint: most typically affected as most stressed

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18
Q

Sign of osteoarthritis in the knee?

A

Crepitus: crackeling or grating sensation when moving a joint

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19
Q

Signs of osteoarthritis in the hips?

A

Antalgic gait: patients may walk with a limp Restricted internal rotation: when hip flexed

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20
Q

Investigations to diagnose osteoarthritis?

A

joint x-rays: LOSS LOSS of joint space osteophytes Subchondral cysts Subchondral sclerosis -bloods will be normal with no inflammatory markers

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21
Q

Treatment of osteoarthritis?

A

img

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22
Q

Complications of Osteoarthritis?

A

Biopsychosocial: NSAID complications Low mood Chronic pain Fictional decline in activities of daily living

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23
Q

What is rheumatoid arthritis?

A

Chronic, systemic inflammatory disease => deforming, symmetrical inflammatory arthritis of the small joints and progresses to involve larger joints and other organs

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24
Q

Genetic risk factors for rheumatoid arthritis?

A

HLA-DR1 and DR4 are crucial in activating t-cells -PTPN22 also implicated

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25
Q

Environmental triggers for rheumatoid arthritis

A

Smoking

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26
Q

Epidemiology of rheumatoid arthritis?

A

Age- peak onset = 30-50 years of age Females (2-4x more common) Prevalence is 1% in the UK

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27
Q

Pathophysiology of rheumatoid arthritis?

A
  • arginine -> citrulune mutation in T2 collagen causes anti - CCP (cyclic citrulinated peptide) formation - IFN -a catses further pro inflammatory recruitment to synovium - synovial lining expands and tumour like mass “pannus” grows past joint margins - pannus destroys Subchondral bone and articulatar cartilage
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28
Q

Symptoms of rheumatoid arthritis?

A

Often worse in the morning (~30mins) eases as day goes on - often struggle to make a tight fist

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29
Q

Signs of rheumatoid arthritis?

A

1) Boutonnière deformity (PIP flexion and DIP hyperextension) 3) swan-kneck deformity (PIP hypertension and DIP flexion) 4) z-thumb deformity (hypertensions of the thumb IP joint with flexion of MCP joint) 5) ulnar deviation of fingers - usually symmetrical and DIPs are spared

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30
Q

How to differentiate psoriatic arthritis from rheumatoid arthritis?

A

DIP joints often spared in rheumatoid arthritis but affected in psoriatic arthritis

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31
Q

What is felty syndrome?

A

Triad of: 1) rheumatoid arthritis 2) granulocytopejia 4) splenomegaly = life threatening risk of infection

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32
Q

Extra-articular complications for rheumatoid arthritis?

A

Lungs - Pericardial effusion, pulmonary fibrosis - Heart - Increased IHD risk - Eyes - episcleritis, keratoconjuctivitis sicca (dry Eyes) - spinal cord compression - kidney (CKD) - rheumatoid skin nodules (often at elbows) - peripheral sensory neuropathy

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33
Q

Investigations to diagnose rheumatoid arthritis?

A

BLOODS: Increased ESR/CRP (used to monitor disease progression), normocytic normochromic anaemia (mc) SEROLOGY: +ve anti CCP (80% specific), +ve RF (70% non specific) X-RAY: LESS - Loss of joint space - Eroded bone - Soft tissue swelling - Soft bones (osteopenia)

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34
Q

Treatment for rheumatoid arthritis?

A

1) DMARD- methotrexate (CI in pregnancy as it is a folate inhibitor) => DNA synthesis affected - gold standard and often give with biologic 2) BIOLOGICS (v good but expensive) -1st line (given with methotrexate) = TNF-d inhibitor INFLIXIMAB or ETANERCEPT -2nd line = b cell inhibitor (CD20 target) - RITUXIMAB Referral to physio, OT, podiatry as indicated

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35
Q

What is gout caused by?

A

Hyperuricemia which results in sodium urate crystal deposition along joints + intrarticularly (inside entry to joint)

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36
Q

Most common inflammatory arthritis in the uk?

A

Gout

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37
Q

What is an arthroplasty?

A

surgical reconstruction or replacement of joint

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38
Q

What are crystalline arthropathies?

A

Group of joint disorders caused by deposits of crystals in joints and the soft tissues around them

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39
Q

How does gout typically present?

A

Middle aged overweight men who drink a lot of BEER

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40
Q

Risk factors for Gout?

A

Purine rich foods i.e meat, seafood, beer - CKD - Diuretics

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41
Q

Food group that can be anti-gout?

A

Dairy

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42
Q

Pathophysiology of gout?

A

Underlying hyperuricaemia Uricase not found in humans so uric acid is insoluble Hence USIC acid deposits in joints causing symptoms

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43
Q

Symptoms of Gout?

A

Monoarthritis; -Typically BIG TOE (metatarsophalangeal joint) PODAGRA -Sudden onset -Severe swollen red toe -Can’t put weight on it -Low grade fever Onset is typically at night

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44
Q

Differential diagnosis for gout?

A

Septic arthritis but this typically affects the knee rather than big toe Trauma Rheumatoid arthritis

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45
Q

Does hyperuricemia guarantee gout?

A

No it increases gout risk

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46
Q

Investigations to diagnose gout?

A
  • measure serum urate level to see if there’s hyperuricemia - if not high but still suspected, repeat in 2-4 weeks Gold standard: (if still unsure) - Joint aspiration and light microscopy of synovial fluid
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47
Q

Treatment for acute gout?

A

-Change diet: decrease purines and increase dairy intake -NSAIDs -> colchine -> prednisolone Don’t use nsaids if they have renal failure, peptic ulcer disease or some pts with asthma and reduce colchine dose for patients with renal failure

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48
Q

Prophylactic/long term treatment for gout?

A

PREVENTION: (after several attacks) Allopurinol as part of Urate Lowering Therapy (ULT) = xanthine oxidase inhibitor - decreases uric acid production - target uric acid <360 mmol/l If that doesn’t work due to intolerance or inefficacy can use febuxostat Plus colchicine 500 micrograms OD for up to 6 months for gout prophylaxis

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49
Q

What is Pseudogout?

A

Calcium pyrophosphate (not sodium urate) crystals deposit along joint capsule

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50
Q

Typical presentation of pseudogout?

A

Elderly female, 70+

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51
Q

Risk factors for pseudogout?

A

Diabetes -Metabolic diseases -Osteoarthritis

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52
Q

Symptoms of pseudogout?

A

Often polyarticular with knee commonly involved = Swollen, hot, red joint

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53
Q

Differential diagnosis of pseudogout?

A

Sceptic arthritis as both effect the knee

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54
Q

Investigations to diagnose Pseudogout?

A

Aspirate joint and analyse sample with polarised light microscopy = gold standard - chrondocalcinosis on x ray

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55
Q

Light microscopy results with pseudogout?

A

Positively birefringent, rhomboid shaped crystals

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56
Q

Light microscopy results of gout?

A

Negatively birefringent needle shaped crystals

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57
Q

Treatment for pseudogout?

A

Only acute management: NSAIDS –> colchicine–>steroid injections

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58
Q

What is osteoporosis?

A

Decreased bone density by 2.5+ SDs below young adult mean value (T<2.5) Systemic skeletal disease characterised by low bone mass and micro architectural deterioration of bone tissue, with a consequent increase in bone fragility and susceptibility to fracture.

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59
Q

What is a decrease in bone mineralisation known as?

A

Osteomalacia

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60
Q

Typical patient presentation of osteoporosis?

A

50+ postmenopausal Caucasian women

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61
Q

Risk factors for osteoporosis

A

SHATTERED -Steroids -Hyperthyroid/Hyperparathyroid -Alcohol+smoking -Thin (decreased BMI) -Testerone (decreased) -Early menopause (decreased oestrogen) -Renal / liver failure -Erosive + inflammatory disease -DMT1 or malabsorption

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62
Q

What is T-Score?

A

Standard deviations from gender-matched young adult mean > -1 Normal -1 to -2.5 Osteopenia (precursor) < -2.5 Osteoporosis < -2.5 plus fracture is severe osteoporosis

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63
Q

Symptoms of Osteoporosis?

A

Only Fractures: 1) Proximal femur (falls) 2) Collles’ (forked wrist - fall on outstretched wrist) 3) Compression vertebral crush (may cause kyphosis “widows stoop”)

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64
Q

Investigations to diagnose osteoporosis?

A

Dexa scan (gold standard) = Dual energy XR absorptiometry; yields T score by comparing patient BMD to reference Also use FRAX score (fracture risk assessment tool in osteoporotic patients)

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65
Q

Treatment for osteoporosis?

A

1) FIRST LINE: = bisphosphonates (osteoclast inhibitors) eg. aldrenoate, risedronate which inhibits RANK-L signalling =CHEAP + EFFECTIVE 2) SECOND LINE: -mAB denosumab (inhibits RANK L) -HRT (testosterone, oestrogen) -Recombinant PTH - Teriparatide -Oestrogen receptor modulator - raloxifene

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66
Q

What is systemic lupus erythmatosus? (SLE)

A

Hypersensitivity T3 reaction (A-A complex depositon) = autoimmune systemic inflammation

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67
Q

Who does SLE typically effect?

A

-Females -Afro Caribbean -20-40 (premenopausal)

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68
Q

Risk factors for SLE?

A

-Female (12x more than males) (90% are women) -HLAB8/DR2/DR3 + low C4 (null allele) -drugs (isoniazid)

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69
Q

Pathophysiology of SLE?

A

Impaired apoptotic debris presented to TH cells -> B cell activation -> antigen-antibody complexes

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70
Q

Symptoms of SLE?

A

-butterfly rash -photosensitivity -glomerulonephritis -seizures + psychosis -mouth ulcers -anamia -joint pain -raynauds -pyrexia -serositis (pleural/pericardial inflammation of lungs) -pericarditis

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71
Q

Investigations to diagnose SLE?

A

-Bloods -> anaemia -Increase ESR + normal CRP -Urine dipstick -> haematuria++++ proteinuria++ (NephrItic syndrome) -Serology: -ANA Abs (99% of cases) -Anti ds DNA Ab’s (to monitor progression) -Decreased C3+C4

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72
Q

Which combination of v. specific and v. sensitive tests are used as essentially diagnostic for SLE?

A

img

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73
Q

Treatment of SLE?

A

-Lifestyle changes (less sunlight or UV protection + stop the triggering drugs) - Drugs: 1) Corticosteroids (main) 2) + hydroxychloroquinine 3) + NSAIDS (+ azathioprine, mycophenolate if severe (cytotoxic)) - even biologically like rituximab if they don’t work - if patient exhausts all treatment options they can be considered for stem cell transplant

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74
Q

Treatment for SLE once stable?

A

Aim to taper off other drugs leaving only hydroxychloroquine

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75
Q

What is antiphospholipid syndrome characterised by?

A

Thrombosis -Recurrent miscarriage -aPL Abs

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76
Q

Presentation of antiphospholipid syndrome?

A

Can be primary (idiopathic) or secondary (to other diseases, especially SLE) -Higher risk in Females

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77
Q

Symptoms of antiphospholipid syndrome?

A

CLOTS Coagulopathy Livedo reticularis (purple discolouration of skin, lace-like) Obstetric issues - miscarriages Thrombocytopenia + Higher risk of arterial (stroke, MI) + venous thrombosis (DVT)

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78
Q

Investigations to diagnose antiphospholipid syndrome?

A

1) lupus anticoagulant 2) Anti cardiolipin antibodies (IgG/M) +ve 3) Anti beta-2 glycoprotein-1 antibodies

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79
Q

Treatment for antiphospholipid syndrome?

A

1st line = warfarin long term if have had a thrombosis * if pregnant give aspirin + heparin

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80
Q

Prophylactic treatment for antiphospholipid syndrome?

A

If not had a thrombosis = ASPIRIN

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81
Q

What is sjogrens syndrome?

A

An autoimmune exocrine dysfunction DRY!!!

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82
Q

Typical presentation and risk factors of Sjogren syndrome?

A

-Can be primary or secondary to other autoimmune diseases - Females (40-50) - fHx - HLAB8/DR3

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83
Q

Symptoms of Sjogren syndrome?

A

1) Dry eyes (keatoconjuctivitis sicca) 2) Dry mouth (xerostoma) 3) Dry vagina

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84
Q

Complication/association of Sjogrens?

A

Directly confers an increase risk of lymphomas

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85
Q

Investigations to diagnose Sjogren syndrome?

A

Serology = anti-RO + anti LA Ab’s (ANA often +ve) Schrimer test = induce tears + place filter paper under eyes-tears travel <10mm (should be 20mm+)

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86
Q

Treatment of Sjogren’s?

A

Artificial tears, saliva + lubricant for sexual activity *Sometimes hydroxychloroquine given for fatigue, myalgia and rashes (up to dr)

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87
Q

What is scleroderma?

A

Systemic condition also known as systemic sclerosis, is a group of rare diseases that involve the hardening and tightening of the skin.

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88
Q

Most common type of scleroderma?

A

CREST- limited cutaneous scleroderma

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89
Q

Conditions CREST is made up of?

A

Calcinosis Raynauds Esophageal dysmotility/strictures Sclerodactyly Telenagiectaria

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90
Q

What is Calcinosis and what does it lead to?

A

Ca deposits in SC tissue -> renal failure Look like bright white deposits on x-ray

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91
Q

What is Raynaud’s?

A

Digit ischemia due to sudden vasospasm, often precipitated by the cold and relieved with heat Classic patient has white fingers

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92
Q

what is Sclerodactyly and what dose it lead to?

A

Local skin thickening or tightening on fingers/toes -> movement restriction

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93
Q

What is Telangiectasia and what does it lead too?

A

Spider veins -> risk of pulmonary htn

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94
Q

Investigations to diagnose scleroderma (CREST)?

A

Anti centromere antibodies (ACAs) - 70% ANA often +ve

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95
Q

Treatment for scleroderma (CREST)?

A

No Cure Treat Sx (e.g raynauds = handwarmers, GI Sx = PPI etc) Annual echo’s and pulmonary function tests Prevent renal crisis using ACEi

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96
Q

What is polymyositis/dermatomyositis?

A

Inflammation + necrosis of skeletal muscle Where skin is involved it is called dermatomyositis

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97
Q

Risk factors for polymyositis/dermatomyositis?

A

Females -HLA B8/DR3 genetic link

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98
Q

Symptoms of polymyositis/dermatomyositis?

A

Symmetrical wasting of muscles of shoulders + pelvic girdle - Hard to stand from sitting, to squat - Hard to put hands on top of head Dermatomyositis = + skin changes - Gottron papules- scales on knuckles - Heliotrope - purple eyelid

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99
Q

Investigations to diagnose polymyositis/dermatomyositis?

A

Muscle enzymes (CK)Muscle fibre biopsy, necrosis = diagnostic LDH + CK raised Anti Jo1 + Anti Mi2 Ab’s –> dermatomyositis only

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100
Q

Treatment for polymyositis/dermatomyositis?

A

Bed rest + prednisolone (1 month then taper dose down) => Steroids and then immunosuppressive drugs

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101
Q

What is fibromyalgia?

A

MSK equivalent of IBS = chronic widespread pain (MSK) for 3months+ with all other causes ruled out *Affects non nociceptive pain pathway

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102
Q

What is nociceptive pain compared to non-nociceptive pain?

A

img

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103
Q

Typical patient presentation of fibromyalgia?

A

-Females -Depression + stress -Poor -60+

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104
Q

Symptoms of Fibromyalgia?

A

-Stressed depressed female 60+ -Fatigue -Sleep disturbance + morning stiffness (esp back, neck stiff) -Pain

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105
Q

Investigations to diagnose Fibromyalgia?

A

-No serological markers -No increased ESR/CRP -Pain in 11+ / 18 regions palpated on body => DIAGNOSIS CLINICALLY MADE

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106
Q

Treatment of fibromyalgia?

A
  • Educate what it is to patient - Physiotherapy - Antidepressants for severe neuropathic pain (eg. TCAs, -Amitriptyline) - CBT
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107
Q

Differential diagnosis for fibromyalgia?

A

Polymyalgia Rheumatica (PMR)

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108
Q

What is PMR?

A

Large cell vasculitis presenting as chronic pain syndrome - affects muscles and joints (similar to fibromyalgia)

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109
Q

Who does PMR effect?

A

Females always 50+

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110
Q

Investigations to diagnose PMR?

A

Increase ESR + CRP = diagnostic - Temporal artery biopsy may show GCA, and may have anaemia of normocytic/chronic disease

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111
Q

Treatment of PMR

A

Oral prednisolone

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112
Q

What is Vasculitis and where can it occur?

A

Inflammation of vessels -> large/medium/small vessels

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113
Q

What conditions occur in large vessels?

A

GCA (giant cell arteritis) -Takayatsu (asian women, affects aortic arch, otherwise same as GCA)

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114
Q

What conditions occur in medium vessels?

A
  • Polyarteritis nodosa - Buerger’s disease (male smokers 20-40, peripheral skin necrosis) - Kawasaki disease (children, causes coronary artery aneurysms)
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115
Q

What conditions occur in small vessels?

A
  • Eosinophilic granulomatosis w/polyangitis (EGPA) (“Churg strauss disease” pANCA +ve) - Granulomatosis w/polyangitis (Wegener disease (cANCA +ve) causes glomerulonephritis + pulmonary symptoms and saddle shaped nose) - Henloch schonlein purpura
116
Q

What is Henloch schonlein purpura? (HSP)

A

IgA vasculitis and a differential diagnosis for IgA nephropathy *both present as IgA deposition in GBM in kidney biopsy BUT HSP has a purpuric rash on shins + affects other organs (joints, abdo, renal)

117
Q

General treatment for Vasculitis?

A

Corticosteroids

118
Q

What to consider when steroids given long-ish term?

A

GI and bone protection - PPI - Bisphosphonate

119
Q

Typical patient presentation of giant cell arteritis (GCA)?

A

50+ Caucasian female presenting with: - unilateral temple headache - jaw claudication - +/- vision changes - temporal scalp tenderness Particularly prevalent in Scandinavians

120
Q

Symptoms of GCA?

A

Affects external carotid branches: - temporal branch=scalp tenderness - ophthalmic branch=vision (blurring, Diplopoda, photopsia, loss) - facial branch=jaw and tongue claudication

121
Q

Investigations to diagnose GCA?

A

Increased ESR +/- CRP = 1st line Temporal artery biopsy = granulomatous inflammation of media + intima = diagnostic Or Temporal artery ultrasound Or both * often patchy skip lesions so take a big sample

122
Q

Treatment of GCA?

A

Corticosteroids (prednisolone) 40- 60 mg with no delay, higher doses of 60 for those patients with a history of ischaemia symptoms including visual loss, limb or jaw claudication IV methylprednisolone for those with visual loss Aim to taper prednisolone to zero over 12-18 months provided no return in symptoms

123
Q

Complication of GCA?

A

Sudden painless vision loss in one eye (optic neuropathy): - temporary = amaurosis fugax (typically seen in TIA) - may be permanent if not dealt with asap with high dose IV Methylprednisolone - overall visual outcomes are poor

124
Q

What is polyarteritis nodosa?

A

Blood vessel inflammation that causes injury to multiple organ systems

125
Q

What sex is more affected with polyarteritis nodosa?

A

males

126
Q

What condition is associated with polyarteritis nodosa?

A

Hep B

127
Q

Symptoms of polyarteritis nodosa?

A

Severe systemic symptoms: - mononeuritis multiplex (ischaemia of vasa nervosum) - GI bleeds (mesenteric artery) - CKD/AKI (renal artery)- causing pre renal AKI - skin nodules + haemorrhage

128
Q

Investigations to diagnose polyarteritis nodosa?

A

CT angiogram = looks like ‘beads on string’ (microaneurysms) Biopsy (kidney) = necrotising vasculitis due to e.g htn

129
Q

Treatment for polyarteritis nodosa?

A

1) Corticosteroids (prednisolone) 2) Control hypertension with ACE-inhbitors 3) Hep B treatment given after corticosteroids

130
Q

What are Spondylarthropathies?

A

Asymmetrical seronegative (rheumatoid factor -ve) arthritis - associated w/HLAB27 - an MHC-I serotype (interacts with T cells) - Inflammatory

131
Q

General features of Spondylarthropathies?

A

SPINEACHE - Sausage fingers (dactylitis) - Psoriasis - Inflammatory back pain - NSAIDS good response - Enthesitis (plantar fasciitis, inflamed heel tendon) - Arthritis - Crohn’s or Colitis = IBD - HLAB27 - Eyes -> Uveitis

132
Q

Types of Spondylarthropathies?

A

Ankylosing Spondylitis Psoriatic Arthritis Reactive Arthritis + IBD associated arthritis

133
Q

What is ankylosing spondylitis?

A

Abnormal stiffening of joints (sacroiliac + vertebral) due to new bony formation

134
Q

Risk factors for ankylosing spondylitis?

A

young males HLAB27 +ve

135
Q

Pathophysiology of ankylosing spondylitis?

A

Syndesmophytes (vertical abnormal bony growth) replace spinal bone damaged by inflammation + makes spine much less mobile - also causes inflamed tendons, eye, fingers

136
Q

Typical patient presentation of Ankylosing spondylitis?

A

Young male with progressively worsening back stiffness - Worse in morning/night - Better with exercise

137
Q

Symptoms of Ankylosing Spondylitis?

A
  • anterior uveitis - ertheritis - dactylitis - Lumbar pathology: - decreased in natural lumbar lordosis - Schober test shows decreased lumbar flexion (<20cm)
138
Q

Investigations to diagnose ankylosing spondylitis?

A

X-Ray = bamboo spine + sacroiliitis + squared vertebral bodies + syndesmphytes (fusion of vertebral bodies MRI -> can show sacroiliitis before X-ray therefore better screening tool ESR and CRP will be raised and can be HLA-B27 +ve

139
Q

Treatment for Ankylosing Spondylitis?

A

Symptoms can be treated with exercise and/or NSAIDS (steroid injection if severe) Biologics: DMARD (improve disease) = TNF alpha blockers: - Infliximab (mAB) - Etanercept

140
Q

Last resort for ankylosing spondylitis?

A

Surgery

141
Q

What % of people who have psoriasis develop psoriatic arthritis?

A

10-40% within 10 years

142
Q

Moderate symptoms of psoriatic arthritis?

A
  • Inflamed DIP joints - Nail dystrophy (onycholysis) - Dactylitis - Enthesitis - Psoriatic rash on skin on hidden sites -> behind ears, scalp, under nails, penile
143
Q

Severe symptom/complication of psoriatic arthritis?

A

Arthritis mutilans (5%) = pencil in cup deformity: - osteolysis of bone = progressive shortening - fingers telescope in on themselves

144
Q

Treatment of psoriatic arthritis?

A

Symptoms = NSAIDS DMARD = methotrexate most commonly if it occurs outside the spine = > treatment is similar to rheumatoid arthritis - if that fails = anti TNF (infliximab, etanercept) - if that fails IL 12+23 inhibitors (ustekinumab) - IL 17 blockers (secukinumab)

145
Q

What is reactive arthritis?

A

sterile inflammation of synovial membranes + tendons and fascia - usually reacting to a distant infection - eg. GI or STI

146
Q

Causes of reactive arthritis?

A

Gastroenteritis = C.jejuni, salmonella, shigella, Yersinia - STI = C.trachomatis, N.Gonorrhoea, Urea urealyticum

147
Q

Most common cause of reactive arthritis?

A

C.trachomatis

148
Q

Symptoms of reactive arthritis?

A

Can’t see, can’t pee, can’t climb a tree -> uveitis/conjunctivitis, urethritis/balanitis, arthritis + Enthesitis *may have keratoderma blennorrhagicum (browny discoloured rash and soles of foot) - or circinate balantitis (small sores/lesions of the head of the penis)

149
Q

Main differential diagnosis of reactive arthritis?

A

Septic arthritis: - painful hot swollen joint - red - signs or history of infection

150
Q

Investigations to diagnose reactive arthritis?

A

joint aspirate (remove fluid from space around a joint) = MC + S shows no organism - Plane polarised light microscopy = -ve for crystalarthropathy - sexual health review - stool culture - ESR/CRP increases and may be HLAb27 +ve

151
Q

Treatment of reactive arthritis?

A

Symptoms = NSAIDS (+ steroid injection) Mostly single attack -> if have 6+ months of recurrence = CHRONIC -> methotrexate

152
Q

What is septic arthritis?

A

Direct bacterial infection of joint (either direct access, or haematogenous spread)

153
Q

Why is septic arthiritis a medical emergency?

A

Acutely inflamed joint with fever, typically knee, is extremely painful => Can destroy knee in ≤24hrs

154
Q

What organisms can cause septic arthiritis and which are most common?

A

S.aureus = most common H.influenza (historically in children- but now rare due to immunisation) N.gonorrhea E.coli/pseudomonas

155
Q

Risk factors for septic arthritis?

A

IVDU - Immunosuppression - Recent surgery - Trauma - Prosthetic joints - inflammatory joint disease (RA)

156
Q

Investigations to diagnose septic arthritis?

A

Urgent joint aspirate with MC+S & polarised light microscopy - normal joint aspirate is clear and yellow but infected is cloudy and turgid - Check for Increased ESR/CRP - Consider blood culture - sexual health review (due to potential gonorrheareal cause)

157
Q

Differential diagnosis of joint pain using aspirate and culture + light microscopy?

A

1) Septic arthritis = ID causative organism 2) Reactive arthritis = sterile and crystal free joint 3) Gout = sterile and -ve birefringent needle crystals 4) Pseudogout = sterile and +ve birefringent rhomboid crystals

158
Q

Treatment of Septic arthritis?

A

Joint aspiration (drainage) ALWAYS then empirial Antibiotics: - flucoxacillin + rifampicin (gram -ve eg e.coli) - vancomycin (MRSA) - IM ceftriaxone + azithromycin (gonorrhoea) - joint washout until no recurrent effusion * if on methotrexate/anti-TNFa then STOP THESE + Use NSAIDs for pain relief - rest/ splint/ physio - stop any immunosuppression temporarily if you can

159
Q

Treatment for septic arthritis if on steroids?

A

Double prednisolone dose (increased stress response)

160
Q

What are prosthetic joints commonly infected with?

A

Cuagulase -ve Staphs eg. S. epidermis

161
Q

What is osteomyelitis?

A

Acutely inflamed, infected bone marrow via haematogenous or local spread (eg from infected joint/trauma)

162
Q

What age group does oesteomyelitis commonly occur in?

A

Mainly in children (85%) - long bones > vertebrae In adults they’re usually >50yrs - vertebrae > clavicle/pelvis»long bones

163
Q

What is the most common type of spread of osteomyelitis in children + adults?

A

Children = haematogenmous Adults = local

164
Q

What organsisms can cause osteomyelitis?

A
  • S.aureus (90%) - Salmonella in sickle cell patients
165
Q

Risk factors of Osteomyelitis?

A

IVDU - Immunosuppression - PVD - DM - Sickle cell anaemia - inflammatory arthritis - UTI, urethral catheterisation - central lines, on dialysis - Trauma

166
Q

Cause and spread of osteomyelitis?

A

Direct innoculation organism - due to Trauma or surgery and Can be any bacteria - Contiguous spread- from adjacent soft tissues and joints (repaired joints or Prosthetic) RF- Diabetes - Haematogenous - children (long bones) > adults (vertebrae) (monomicrobial)

167
Q

Acute bone changes in osteomyelitis?

A

inflammation and bone oedema

168
Q

Chronic bone changes and complications of osteomyelitis?

A

1) Sequestra (necrotic bone embedded in pus) 2) Involucrum (thick sclerotic bone placed around sequestra to compensate for support = abnormal)

169
Q

Acute Symptoms of osteomyelitis?

A

Dull bony pain + hot swollen area (+/- joint) - Worse with movement

170
Q

Chronic symptoms of osteomyelitis?

A

Also have deep ulcers (sequestrae)

171
Q

Differential diagnosis for Osteomyelitis?

A

Charcot joint = (damage to sensory nerve due to diabetic neuropathy) - causes progrssive degeneration of weight bearing joint + bony destruction - Often presents with “diabetic feet” Soft tissue infection Avascular necrosis of bone Gout

172
Q

Investigations to diagnose osteomylitis?

A

Bone marrow biopsy + culture + blood mc+s -> IDs causative organism X-Ray for osteopenia MRI (after XR) = bone marrow oedema Check for increased ESR/CRP

173
Q

Treatment for Osteomylitis?

A

Immobilise + Abx: - vancomycin or teicoplanin (MRSA + s.aureus) - fusidic acid (s.aureus) - flucoxacillin (salmonella) Start with a broad antibiotic and then focus according to culture findings Surgical= debridement or hardware placement or removal

174
Q

Vancomycin vs teicoplanin?

A

Teicoplanin is longer lasting than vancomycin but increased side effects: - GI upset - pruritus - rash

175
Q

What is important when considering osteomyelitis patients?

A

Rule out tuberculosis osteomyelitis with bone marrow biopsy (caseating granuloma +ve on histology) - may be slower onset - longer treatment of 6 months

176
Q

4 primary bone tumours?

A

Osteosarcoma - Ewing sarcoma - Fibrosarcoma - Chondrosarcoma

177
Q

Prevalence of bone tumours?

A

1° are rarer and seen mostly in children 2° are most common

178
Q

Most common types of cancer that can resut in secondary bone metastases?

A

BLT KP - Breast - Lung - Thyroid - Kidney - Renal cell cancer - Prostate *myeloma can also cause bone pain

179
Q

Of secondary bone cancers, which are osteolytic and osteosclerotic?

A

Osteolytic (softened bone, due to loss of calcium) = breast + lung Osteosclerotic (Abnormal bone hardening) = prostate

180
Q

What is the most common primary bone tumour?

A

Osteosarcoma

181
Q

Which organ does osteosarcoma metastisise to?

A

Lungs

182
Q

What is osteosarcoma associated with?

A

Pagets and 15-19 yr old patients

183
Q

Investigation to diagnose osteosarcoma and results?

A

X-ray= “sunburst” appearing bone

184
Q

What cells does ewing sarcoma originate from?

A

Mesenchymal (multipotent stem cells found in bone marrow) stem cells

185
Q

Prevalence of Ewing sarcoma?

A

Very rare and mostly in teens (15yr olds)

186
Q

What is Chondrosarcoma?

A

Cartilage cancer

187
Q

General local symptoms of bone tumours?

A

Severe pain = worst at night (wake up in middle of night) Decreased ROM of long bone and/or verterbrae Lump - pressure effect on local structures, snapping of tendons etc

188
Q

General systemic symptoms of bone tumours?

A

Weight LOSS - Fatigue - Fever - Malaise

189
Q

Investigations to diagnose bone tumours?

A

Skeletal isotope scan (shows changes before XR) - XR = shows osteolysis or osteosclerosis - Increased ALP, ESR/CRP - Hypercalcemia (of malignancy) - Biopsy - percutaneous, excisional, incisional = definitive diagnostic test

190
Q

General treatment of bone tumours?

A

Chemo or radiotherapy - Bisphosphates - surgery eg. Tumour excision or angioembolization

191
Q

What is osteomalacia and it’s cause?

A

Defective bone mineralisation - due to vitamin D deficiency => decreased Ca2+ + PO43- (hydroxyapatite mineral of bone)

192
Q

Osteomalacia vs Rickets?

A

Osteomalacia = After epiphyseal fusion Rickets = Before epiphyseal fusion

193
Q

What are the 5 causes of osteomalacia?

A

1) HyperPTH 2) Vit D deficiency 3) CKD/Renal failure 4) Liver Failure 5) Anticonvulsant drugs

194
Q

Draw out the Vitamin D pathway

A

img

195
Q

How does hyperPTH cause osteomalacia?

A

CA2+ released from bone so less available for mineral formation - Seconadary reason is due to vit D deficiency

196
Q

How does Vitamin D deficiency cause osteomalacia?

A

most common cause - due to malabsorption/reduced intake/Poor sunlight - Results in decreased absorption of calcium from gut and decreased reabsorption in renal pct

197
Q

How does CKD/renal disease cause osteomalacia?

A

Reduced activation of vitamin D (1-alpha-hydroxylation)

198
Q

How does liver dysfunction cause osteomalacia?

A

Reduced activation of vitamin D (25-hydroxylation)

199
Q

How can anticonvulsive drugs cause osteomalacia?

A

Increase CYP450 metabolism of vitamin D

200
Q

Symptoms of osteomalacia?

A

Fractures - proximal weakness - Difficulty Weight bearing

201
Q

Symotoms of Rickets?

A

Skeletal deformities: - knocked knees - bow legs - wide epiphyses

202
Q

Investigations to diagnose osteomalacia?

A
  • BM biopsy = incomplete mineralisation - Bloods: hypocalcemia Increased PTH Decreased serum Ca2+ Decreased 25-hydroxyvit D (best marker) X ray = Looser’s zones (defective mineralisation)
203
Q

Treatment for Osteomalacia?

A
  • Vit D replacement (calcitriol) - Increase dietary intake (D3 tablets + eggs)
204
Q

What is Paget’s disease?

A

Focal disorder of bone remodelling (areas of patchy bone due to improper osteoblast/clast function) Typicall idiopathic and presents in females 40+

205
Q

Symptoms of Paget’s?

A
  • Bone pain - Bone changes: - bowed tibia - skull changes - Neurological Sx: - nerve compression of CN8 (deafness) - hydrocephalus (sylvian aquaduct blockage)
206
Q

Investigations to diagnose Paget’s?

A

X-Ray: - osteoporosis circumscripta - cotton wool skull (skull changes; lysis + sclerosis) Urinary hydroxyproline: protein constituent of bone collagen = good marker of progression Also may have increased ALP

207
Q

Treatment for Paget’s?

A

Give bisphosphonates + NSAIDS for pain relief

208
Q

What is marfans syndrome?

A

Connective tissue disorder = inherited - due to auto dominant FB1 mutation => decreased connective tissue tensile strength

209
Q

What are the symptoms of marfans syndrome?

A

1) “Marfans body habitus”: - tall + thin - long fingers (arachnodactyly) - pectus excavatum/carinatum (sternum pressed in/puffed out) 2) Aortic complications: - aortic regurgitation murmur - AAA - aortic dissection

210
Q

Investigations to diagnose marfans?

A

Clinical diagnosis + FBN-1 mutation positive test

211
Q

What is Ehlers-Danos?

A

Connective tissue disorder: - auto dominant mutations affecting collagen proteins with 13ish subtypes

212
Q

Symptoms of Ehler’s danos?

A

joint hypermobility - CV complications: mitral regurg + AAA

213
Q

Investigations to diagnose Ehlers danos?

A

Clinical Diagnosis - look for collagen mutations (beighton score?) - Echo

214
Q

What will connective tissue disorders result in?

A

1) Weak valves 2) Weak vessels Key complications to monitor: - regurgitation murmurs - aortic aneurysm ruptures/aortic dissection

215
Q

What is mechanical lower back pain?

A
  • Common patient complain in community - Very common and often self-limiting - May be normal, especially people 20-55yrs old - Can be trauma or work related
216
Q

Signs for serious pathology in mechanical lower back pain?

A

Elderly (e.g myeloma) - neuropathic pain (spinal cord compression)

217
Q

What is lumbar spondyloisis?

A

Degeneration of IV disc acuses it to lose its compliance + thin over time More common in older patients

218
Q

Symptoms for lumbar spondylosis?

A

Initally asymptomatic -> progressively worsens

219
Q

What spinal levels are most commonly affected by lumbar spondylosis?

A

L4/5 or L5/S1

220
Q

Investigations to diagnose Lumbar spondylosis?

A

X-Ray + MRI if a serious pathology is suspected eg. neurological pain

221
Q

Treatment of lumbar spondylosis?

A

Main treatment is analgesia and physiotherapy if this is simple mechanical pain

222
Q

Can you see bone inflammation on x-ray?

A

No but it is obvious on MRI

223
Q

Main bacterial cause of osteomyelitis?

A

STAPH AUREUS

224
Q

When do you stop osteomyelitis treatment?

A

It’s very variable but 6 weeks of IV Abx is considered minimum - switch to oral may work in some circumstances - stop treatment guided by CRP response - failure to respond requires re-imaging

225
Q

Why is treatment so long for osteomyelitis?

A

Vascular supply and microbial virulence factors make antimicrobial treatment complex and long

226
Q

What is gonococcal arthritis?

A

Occurs with disseminated gonococcal infection. - causes Fever, arthritis, tenosynovitis - maculopapular- pastular rash - painful before visible

227
Q

What is debridement?

A

Removal of all infected tissue and bone and thorough cleaning of wounds

228
Q

What would you suspect in a young patients presenting with single acutely swollen joint?

A

Gonococcus septic arthritis until proven otherwise - this infection is common and delaying treatment puts joint in danger - if the patient has urinary or genital symptoms, exclude gonococcal septic arthritis first before considering reactive arthritis

229
Q

Joints affected typically by gout?

A

Feet Ankles Knees Elbows Hands

230
Q

Joints typically affected by pseudo gout?

A

Wrist Knees Hands

231
Q

Age of onset in Inflammatory arthritis vs osteoarthritis?

A

Inflammatory: can happen at any age Osteoarthritis: usually later in life

232
Q

Speed of onset Inflammatory arthritis vs osteoarthritis?

A

Inflammatory arthritis: rapid, weeks to months Osteoarthritis: slow, over years

233
Q

Distributed of Inflammatory arthritis vs osteoarthritis?

A

Inflammatory arthritis: symmetrical polyarthritis Osteoarthritis: initially asymmetrical mono arthritis —> polyarthritis

234
Q

Joints affected with Inflammatory arthritis vs osteoarthritis?

A

Inflammatory arthritis: small joints of hands and feet Osteoarthritis: weight bearing joints- knees, hips, thumb base, big toe

235
Q

Duration of morning stiffness Inflammatory arthritis vs osteoarthritis?

A

Inflammatory arthritis: Stiffness worse in the morning >1 hr Osteoarthritis: Stiffness <1hr and worse at the end of the day

236
Q

Areas of the body affected with psoriatic arthritis?

A

Spine - asymmetrical big joints - isolates fingers and toes

237
Q

Why might uric acid levels be low in gout?

A

Going through an attack so uric acid goes to the joint

238
Q

Aim of gout treatment?

A

To reduce uric acid below <300umol/1 Start at 100mg allopurinol and increase every 2-4 weeks until target met

239
Q

Complications of gout?

A
  • disability and misery - Tophi - Renal disease: - calculus 10-15% - chronic update nephropathy -acute rate nephropathy (cytoxics)
240
Q

Why is a normal x ray not conclusive when dismissing rheumatoid arthritis?

A

Takes up to 6 months of disease to show up on x ray

241
Q

Why do we want to catch rheumatoid arthritis earlier?

A

Lots of evidence that early diagnosis and treatment makes a huge difference to prognosis Inflammation is reversible but damage is not “Window of opportunity” where DMARDs can settle disease very quickly

242
Q

Anti- CCP vs Rheumatoid factor in diagnosing RA?

A
  • rheumatoid factor is falsely positive in 10-15% of patients - anti- ccp is almost never falsely positive
243
Q

Types of connective tissue diseases?

A

Inherited Auto immune (inflammatory)

244
Q

How many people inherit Marfans?

A

3/4 and the rest develop it with no family history

245
Q

Joint deformations in SLE?

A

Can look very similar to rheumatoid arthritis but non erosive and less proliferative

246
Q

How to diagnose lupus nephritis?

A

Crescent formation in histology

247
Q

Haematological features of SLE?

A

Anaemia (haemolytic, Coombs positive) Thrombocytopenia Neutropenia Lymphopenia

248
Q

Auto antibodies with SLE?

A

Double stranded DNA antibody is specific to lupus

249
Q

What is anterior Uveitis?

A

Also called iritis and it is inflammation of the iris and/or the ciliary body and is a frequent extra-articulate manifestation of axial spondyloarthritis

250
Q

Why is HLA b27 allele special?

A

It’s presence alone can cause spondyloarthritis

251
Q

How might HLAb27 cause spondyloarthritis?

A
  • “molecular mimicry” infection —> immune response—> infectious agent has peptides very similar to HLAB27 molecule - > autoimmune response triggered against HLA B27 - misfolding theory - HLA b27 heavy chain homodimer hypothesis
252
Q

Symptoms for inflammatory back pain in ankylosing spondyloarthritis?

A

Inflammatory back pain which: - starts under 40yrs of age - wake up at night with back pain that improves with movement - improvement with exercise - insidious onset

253
Q

Types of bone tumour

A

Primary Secondary/metastatic

254
Q

Types of primary bone tumour

A

Based on biological behaviour: - Benign - slow and don’t spread - Intermediate - Malignant - grow fast and spread to distant sites

255
Q

Differential diagnosis for bone tumours?

A

Infection - Hyperparathyroidism (Brown’s Tumour)

256
Q

Staging of Bone tumours?

A

Enneking staging - AJCC TNM staging system

257
Q

What is benign osteochondroma?

A

Exostois that is most common around the knee = aberrant growth of fragment of epiphyseal plate Treatment is excision

258
Q

Most common sites for bone metastases in order

A
  1. Lung 2. Liver 3. Bone
259
Q

Aims of fracture treatment?

A

Relieve pain + disability, to improve function

260
Q

Fracture treatment?

A

4Rs: (Deal with catastrophic bleeding) - Resuscitate - Reduce the fracture to correct alignment - Retain the position of the fracture (using splint, pins, rods etc) - Rehab

261
Q

How to present an Orthopedic x-ray?

A

ALWAYS USE TWO ORIENTATIONS/VIEWS (fracture might not be visible at both) Intro : who, what, when ABCs Alignment - dislocation Bones- fractures= pattern/position of fracture, condition and displacement Cartilage - widened joint Soft tissues - swelling, effusion

262
Q

Patterns of fractures

A

Transverse - common in younger fitter patients Oblique Spiral

263
Q

Conditions of fracture?

A

Comminuted - greater soft tissue involvement Segmental -usually only one fracture will heal out of the two Impacted - inherent stability so might not have to do anything

264
Q

How to describe displacement of bones?

A
  • length eg shortened - alignment eg translation or angulation - rotation ?
265
Q

Types of soft tissue swelling?

A

Intra articular Extra articular

266
Q

Types of bone healing?

A

Direct: absolute stability and compression with gap healing => no callus can only be done with a gap of <1mm Indirect: relative stability => movement causes callus formation if gap is larger than 1mm

267
Q

Bone remodelling cycle?

A

img

268
Q

Callus formation in bone?

A

img

269
Q

Stages of osteoarthritis

A

1-4 1 is doubtful with minimum disruption but 10% cartilage loss 4 is severe with joint space largely reduced and 60% cartilage loss

270
Q

Radiological features of osteoarthritis

A

joint space narrowing - osteophyte formation - Subchondral sclerosis - suchondral cysts - abnormalities of bone contour

271
Q

Controversial subset of osteoarthritis?

A

Inflammatory/erosive arthritis with a strong inflammatory component - some radiologist don’t believe it exist - in addition to standard to standard management , DMARD therapy (usually milder agents) often used

272
Q

Lifestyle treatments for chronic gout?

A

Dietary modifications: - alcohol (reduce, beer to cider) - Lose weight - Reduced red meat, offal, shellfish, fructose containing drinks

273
Q

Pathophysiology of vasculitis?

A

activated immune cells infiltrate vessel walls and lead to Direct damage and stimulate vascular smooth muscle cell remodelling - vessel wall infiltration, proliferation and damage causes weakening and occlusion of blood vessel - leads to ischaemia, infarction, aneurysm - Results in clinical manifestations

274
Q

How to classify vasculitis?

A
  1. By vessel size 2. Consensus classification (Chapel-Hill 2012) - hybrid classification of vessel size, pathophysiology and underlying cause
275
Q

Important negative features of GCA?

A

Features of a serious headache but not of GCA - Vomiting ( raised intercranial pressure) - Any acute localising clinical signs ( acute intracerebral bleeding, encephalitis, meningitis) - Fever (infection)

276
Q

New persistent headache in an elderly patient?

A

Must be treated seriously and is GCA until proven otherwise - Dont delay treatment with steroids and refer to rheumatology

277
Q

What proportion of women and men over age 50 will have a fracture due to osteoporosis?

A

50% of women 1 in 5 men

278
Q

Three classic fractures of osteoporosis?

A

Hip fracture Wrist fracture Vertebrae fractures

279
Q

Morbidity of hip fractures?

A

20% of patients will die in the next year

280
Q

Factors that play a role in fracture?

A

Combination of trauma and bone strength

281
Q

Factors that effect bone strength?

A

Peak bone mass/rate of bone loss Bone size Bone turnover Bone architecture Bone mineralisation

282
Q

Post menopausal osteoporosis?

A

Loss of restraint effects of oestrogen on the burn turnover Characterised by: - high bone turnover (resorption>formation) - predominantly cancellous bone loss - microarchitectural disruption

283
Q

Changes in trabecular architecture with ageing?

A

decrease in trabecular thickness, more pronounced for non-load bearding horizontal trabeculae - decrease in connections between horizontal trabeculae - decrease in trabecular strength and Increased susceptibility to fracture

284
Q

What is bone densitometry for?

A

For risk assessment and for diagnosis, the characteristic of major importance is the ability of a technique to predict fractures

285
Q

Two types of treatments for osteoporosis?

A

1) Anti-resorptive - decrease osteoclast activity and bone turnover - Bisphosphonate = 1st line - HRT - Denosumab 2) Anabolic - Increase osteoblast activity and bone formation - Teriparatide

286
Q

Denosumab?

A

Rapid acting and very potent anti-resorptive Good fracture risk reduction BUT rebound increase of bone turnover when stopped

Haroon Phase 2A (14 decks)

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