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Phase 2A revision > RHEUMATOLOGY > Flashcards

RHEUMATOLOGY Flashcards

1
Q

Define rheumatology

A

Medical management of musculoskeletal disease

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2
Q

Give 3 causes of inflammatory joint pain?

A
  1. Autoimmune (RA, connective tissue disease, spondyloarthropathy, vasculitis)
  2. Crystal arthritis
  3. Infection
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3
Q

Give 2 causes of non-inflammatory joint pain?

A
  1. Degenerative (OA)

2. Non-degenerative (fibromyalgia)

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4
Q

What are the 5 main signs of inflammation?

A
  1. Red (rubor)
  2. Heat (calor)
  3. Pain (dolor)
  4. Swelling (tumour)
  5. Loss of function
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5
Q

How does inflammatory pain differ from degenerative non-inflammatory pain?

A

Inflammatory pain eases with use

Degenerative pain increases with use

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6
Q

Are you more likely to see swelling in inflammatory or degenerative pain?

A

In inflammatory pain = synovial swelling

Often no swelling in degenerative

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7
Q

What is bone pain?

A

Pain at rest and at night

Can be due to tumour, infection, fracture

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8
Q

What is inflammatory joint pain?

A

Pain and stiffness in joints in the morning, at rest and with use
Can be inflammatory or infective

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9
Q

Name 2 inflammatory markers that can be detected in blood tests

A
  1. ESR (erythrocyte sedimentation rate)

2. CRP

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10
Q

Explain why ESR levels are raised in someone with inflammatory joint pain

A

Inflammation leads to increased fibrinogen –> RBC’s clump together –> RBC’s fall faster = increased ESR

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11
Q

Explain why CRP levels are raised in someone with inflammatory joint pain

A

Inflammation leads to increased IL-6 levels –> CRP produced in response to IL-6 –> CRP raised

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12
Q

Describe the ESR and CRP levels in someone with lupus

A

ESR raised

CRP low

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13
Q

Other than inflammatory markers, might be seen in blood tests when investigating joint pain?

A

Auto-antibodies = immunoglobulins that bind to self antigens

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14
Q

With what tissue type are all spondyloarthropathies conditions associated?

A

HLA B27 tissue type

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15
Q

Give 5 conditions that fall under the term spondyloarthritis

A
  1. Ankylosing spondylitis
  2. Reactive arthritis
  3. Psoriatic arthritis
  4. Enteropathic arthritis
  5. Juvenile idiopathic arthritis
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16
Q

Give the 3 main clinical features of spondyloarthritis

A
  1. Seronegative and HLAB27 association
  2. Axial arthritis
  3. Asymmetrical large joint arthritis
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17
Q

Give 6 signs of spondyloarthritis

A

SPINE ACHE

  1. Sausage digits = dactylics
  2. Psoriasis
  3. Inflammatory back pain
  4. NSAID responsive
  5. Enthesitis
  6. Arthritis
  7. Crohn’s/UC
  8. HLAB27
  9. Eye - uveitis
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18
Q

What is the general treatment for all spondyloarthritis?

A

Initially DMARDs and then biological agents if DMARDS fail (TNF blockers)

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19
Q

Describe the pathophysiology of ankylosing spondylitis

A

Inflammatory arthritis of spine + rib cage → leads to new bone formation + fusion of joints (syndesmophytes)

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20
Q

what is the epidemiology of ankylosing spondylitis?

A

● More common and severe in men
● Usually presents in young adults – 16-30yrs
● 88% are HLA-B27 positive
● Women present later and are underdiagnosed
● Low incidence in Africa and Japan
● Native North Americans have high incidence

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21
Q

what is the clinical presentation of ankylosing spondylitis

A
  • Lower back pain + stiffness → worse with rest + improves with movement
  • Sacroiliac pain - radiates to hips
  • Flares of worsening symptoms
  • loss of lumbar lordosis and increased kyphosis
  • progressive loss of spinal movement
  • anterior uveitis
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22
Q

What investigations might you do in someone who you suspect to have ankylosing spondylitis?

A

CRP + ESR - raised
HLA B27 genetic test
X-ray of spine + sacrum
- Bamboo spine
- Squaring of vertebral bodies
- Subchondral sclerosis + erosions
- Syndesmophytes
- Ossification of ligaments, discs + joints
- Fusion of facet, SI + costovertebral joints
MRI spine - bone marrow oedema in early disease before x-ray changes

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23
Q

What is the diagnostic criteria for ankylosing spondylitis?

A
  1. > 3 months back pain
  2. Aged <45 at onset
  3. Plus one of the SPINE ACHE symptoms
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24
Q

What is the treatment for ankylosing spondylitis?

A

NSAIDs
corticosteroids
anti-TNF drugs infliximab

Physio, lifestyle advice
Surgery for deformities

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25
Q

Give 3 locations that psoriasis commonly occurs at

A
  1. Elbows
  2. Knees
  3. Fingers
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26
Q

what are the clinical features of psoriatic arthritis

A
  • Asymmetrical oligoarthritis (60%)
  • Large joint arthritis (15%)
  • Enthesitis - inflammation of entheses
  • Dactylitis - inflammation of full finger
  • Nail changes (pitting, onycholysis)
  • inflammatory joint pain
  • plaques of psoriasis
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27
Q

What investigations might you do in someone you suspect to have psoriatic arthritis?

A

X-ray

- Erosion in DIPJ + periarticular new-bone formation  - Osteolysis  - Pencil-in-cup deformity

Bloods

  • ESR + CRP - normal or raised
  • Rheumatoid factor -ve
  • anti-CCP - negative

Joint aspiration - no bacteria or crystals

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28
Q

How do you treat psoriatic arthritis?

A
  • NSAIDs
  • Physio
  • Steroid injection
  • DMARDs - methotrexate
  • TNF alpha inhibitor - infliximab
  • Ustekinumab - last line (MAb that targets IL 12 + 23)
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29
Q

What is reactive arthritis?

A

● A sterile synovitis which occurs following GI infection or STI
● Typically affects lower limb

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30
Q

What GI infections are associated with causing reactive arthritis?

A 
Salmonella
Shigella
Yersinia 
enterocolitica
campylobacter
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31
Q

What GU infections are associated with causing reactive arthritis?

A

Chlamydia
Ureaplasma
urealyticum

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32
Q

What is the classic triad of symptoms for reactive arthritis?

A
  1. Arthritis
  2. Conjunctivitis
  3. Urethritis(can’t see, can’t pee, can’t climb a tree)
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33
Q

What investigations might you do in someone you suspect to have reactive arthritis?

A 
ESR + CRP - raised
ANA - negative
RF - negative
X-ray - sacroiliitis or enthesopathy
Joint aspirate - negative (exclude septic arthritis + gout)
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34
Q

How is reactive arthritis treated?

A

NSAID
Corticosteroids
DMARD - chronic arthritis
infliximab

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35
Q

What type of spondyloarthritis occurs in 20% of patients with IBD?

A

Enteropathic arthritis

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36
Q

Psoriatic arthritis commonly involved swelling of what joint?

A

DIP joint

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37
Q

Describe a psoriatic plaque

A

Pink, scaling lesion

Occurs on extensor surfaces of limbs

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38
Q

Give 3 differences between RA and psoriatic arthritis

A 
Psoriatic = psoriatic lesions, sausage like swelling around DIP joint, pencil in cup erosion on XR, HLAB27 associated.
RA = hands and wrists typically affected, peri-articular erosion on XR, rheumatoid nodules
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39
Q

Define osteoporosis

A

A systemic skeletal disease characterised by low bone mass and micro architectural deterioration of bone tissue

Increase in bone fragility and fracture susceptibility

Defined as bone mineral density more than 2.5 standard deviations below the young adult mean

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40
Q

Describe the epidemiology of osteoporosis

A

50% of women and 20% of men over 50 are affected
● Over 50, females > males as women lose trabeculae with age
● More common in Caucasians and Asians
● Increased risk with age

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41
Q

What 2 factors are important for determining the likelihood of osteoporotic fracture?

A
  1. Propensity to fall –> trauma

2. Bone strength

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42
Q

Give 4 properties of bone that contribute to bone strength

A
  1. Bone mineral density
  2. Bone size
  3. Bone turnover
  4. Bone micro-architecture
  5. Mineralisation
  6. Geometry
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43
Q

Name a hormone that can control osteoclast action and so bone turnover

A

Oestrogen

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44
Q

Why are so many women over 50 affected by osteoporosis?

A

Likely to post-menopausal –> less oestrogen –> osteoclast action isn’t inhibited
High rate of bone turnover –> bone loss and deterioration –> increased fracture risk

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45
Q

What happens to bone micro-architecture as we get older that leads to a reduction intone strength?

A

Trabecular thickness decreases and horizontal connection decrease –> lowers trabecular strength –> increase risk of fracture

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46
Q

Why can RA cause osteoporosis?

A

RA is an inflammatory disease

High levels of IL-6 and TNF –> increase bone resorption

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47
Q

What is the affect of high cortisol levels on bone turnover?

A

Cortisol increases bone turnover –> increase bone resorption and induces osteoblast apoptosis

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48
Q

Give 5 risk factors for osteoporosis

A
  • old age, women, FHx, previous fracture, smoking, alcohol, Asian/Caucasian

‘SHATTERED’

  • Steroid use
  • Hyperthyroidism, hyperparathyroidism, hypercalciuria
  • Alcohol + tobacco use
  • Thin (BMI < 18.5)
  • Testosterone (low)
  • Early menopause
  • Renal or liver failure
  • Erosive/inflammatory bone disease (e.g. myeloma or RA)
  • Dietary low calcium /malabsorption or Diabetes type 1
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49
Q

Name 3 endocrine disease that can be responsible for causing osteoporosis

A
  1. Hyperthyroidism and primary hyperparathyroidism - TH and PTH increase bone turnover
  2. Cushing’s syndrome - cortisol leads to increase bone resorption and osteoblast apoptosis
  3. Early menopause, male hypogonadism - less oestrogen/testosterone to control bone turnover
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50
Q

Name 2 medications that can cause osteoporosis

A
  1. Glucocorticoids (steroids)
  2. Depo-povera (contraceptive injection)
  3. GnRH analogues
  4. Androgen deprivation
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51
Q

Give the clinical presentation of osteoporosis

A
  1. Asymptomatic development
  2. Fragile bones
  3. Pathological fractures (femur neck)
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52
Q

What investigations might you do in someone who you suspect to have osteoporosis

A

DEXA scan = bone mineral density scan - gives you a T score

X-ray - detect fractures

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53
Q

Name 2 areas of the skeleton commonly affected by osteoporosis that the DEXA scan focuses on

A

o Thoracic and lumbar vertebrae
o Proximal femur
o Colles fracture of the wrist (distal radius)

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54
Q

What is a T score?

A

Is a standard deviation that is compared to a gender-matched young adult mean

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55
Q

What is a normal T score?

A

> -1.0

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56
Q

What T score signifies that a patient has osteopenia?

A

-2.5 < t < -1

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57
Q

What T score signifies that a patient has osteoporosis?

A

T < -2.5

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58
Q

What tool can be used to assess someones risk of osteoporotic fracture?

A

FRAX = predicts 10 year fracture chance

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59
Q

Give 2 examples of anti-resorptive treatments used in the management of osteoporosis

A

Decrease osteoclast activity and bone turnover

  1. Bisphosphonates - alendronate, risedronate
  2. HRT - oestrogen
  3. Denosumab - monoclonal Ab that blocks activity of osteoclasts – binds to RANK-ligand
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60
Q

what is the treatment for osteoporosis?

A
  • Lifestyle advice → exercise, maintaining a healthy weight, stop smoking, reduce alcohol
  • Vitamin D + calcium supplementation - 1st line
  • Bisphosphonates e.g. alendronate, risendronate, zolendronic acid - 1st line
    Denosumab - 2nd line
    HRT
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61
Q

Give 3 advantages of HRT

A
  1. Reduces fracture risk
  2. Stops bone loss
  3. Prevent menopausal symptoms
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62
Q

Give 3 disadvantages of HRT

A
  1. Increased risk of breast cancer
  2. Increased risk of stroke and CV disease
  3. Increased risk of thrombo-embolism
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63
Q

How do bisphosphonates work?

A

Inhibit cholesterol formation –> osteoclast apoptosis

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64
Q

Define osteopenia

A

Pre-cursor to osteoporosis characterised by low bone density

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65
Q

What is vasculitis?

A

Inflammation and necrosis of blood vessel walls with subsequent inspired blood flow

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66
Q

What cells might you see on a histological slide taken form someone with vasculitis?

A

Neutrophils

Giant cells

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67
Q

Describe the pathophysiology of of vasculitis

A

Vessel wall destruction –> perforation and haemorrhage

Endothelial injury –> thrombosis and infarction

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68
Q

Give an example of large vessel vasculitis

A

Giant cell arteritis

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69
Q

Give an example of medium/small vessel vasculitis

A

Wegner’s granulomatosis (Granulomatosis polyangitis)

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70
Q

What is Giant cell arteritis?

A

Granulomatous inflammation of large cerebral arteries as well as other large vessels (aorta) which occurs in association with Polymyalgia rheumatica

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71
Q

Describe the epidemiology of giant cell arteritis

A

Affects those > 50 years old

Incidence increases with age

Twice as common in women

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72
Q

Describe the pathophysiology of giant cell arteritis

A

Arteries become inflamed, thicken and can obstruct blood flow

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73
Q

what are is the clinical presentation of giant cell arteritis?

A
  1. Headache, typically unilateral over temporal area
  2. Temporal artery/scalp tenderness
  3. Jaw claudication
  4. Visual symptoms - vision loss (painless)
  5. Systemic symptoms - fever, malaise, lethargy
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74
Q

How does giant cell arteritis present in a medical emergency?

A

Stroke and blindness

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75
Q

What are the investigations for giant cell arteritis?

A
  • ↑ESR and/or CRP (=highly sensitive) ESR >50 mm/hr
  • Halo sign on US of temporal and axillary artery
  • Temporal artery biopsy = gold standard for Dx (show giant cells, granulomatous inflammation)
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76
Q

What is the diagnostic criteria for giant cell arteritis?

A
  1. Age >50
  2. New headache
  3. Temporal artery tenderness
  4. Abnormal artery biopsies
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77
Q

Describe the treatment for giant cell arteritis

A
  1. High dose corticosteroids - prednisolone ASAP
  2. DMARDs - methotrexate (sometimes)
  3. Osteoporosis prophylaxis is important - lansoprazole, alendronate, Ca2+, vit D
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78
Q

Give 2 complications of giant cell arteritis

A
  1. Increased CVA risk

2. Visual loss

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79
Q

What does ANCA stand for?

A

Anti-neutrophil cytoplasmic antibodies

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80
Q

What is the pathophysiology of Wegener’s granulomatosis?

A

Necrotising granulomatous vasculitis affecting arterioles and venules
ANCAs can activate primed circulating neutrophils which leads to fibrin deposition in vessel walls and deposition of destructive inflammatory mediators

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81
Q

What organ systems can be affected Wegener’s granulomatosis?

A
  1. URT
  2. Lungs
  3. Kidneys
  4. Skin
  5. Eyes
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82
Q

What is the affect of Wegener’s granulomatosis on the Upper respiratory tract?

A
  1. Sinusitis
  2. Otitis
  3. Cough
  4. Haemoptysis
  5. Saddle nose deformity
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83
Q

What is the affect of Wegener’s granulomatosis on the lungs?

A
  1. Pulmonary haemorrhage/nodules

2. Inflammatory infiltrates are seen on X-ray

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84
Q

What is the affect of Wegener’s granulomatosis on the Kidney?

A

Glomerulonephritis –> haem/proteinuria

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85
Q

What is the affect of Wegener’s granulomatosis on the skin?

A

Ulcers Pulpura

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86
Q

What is the affect of Wegener’s granulomatosis on the eyes?

A

Uveitits
Scleritis
Episcleritis

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87
Q

What investigations might you do in someone you suspect to have Wegener’s Granulomatosis?

A

ANCA testing - c-ANCA
Tissue biopsy - (renal biopsy best) - shows granulomas
CT - assessment of organ involvement
FBC - high eosinophils

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88
Q

What is the treatment for Wegener’s Granulomatosis?

A
  • Glucocorticoids (prednisolone)
  • Immunosuppresive drugs (cyclophosphamide OR rituximab)
  • plasma exchange for specific complications
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89
Q

Define osteoarthritis

A

A non-inflammatory degenerative disorder of moveable joints characterised by the deterioration of articular cartilage and the formation of new bone

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90
Q

Why does the prevalence of OA increase with age?

A

Due to the cumulative effect of trauma and a decrease in neuromuscular function

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91
Q

Give 5 risk factors for developing OA

A
  1. Genetic predisposition - females, FHx
  2. Trauma
  3. Abnormal biomechanics (e.g. hypermobility)
  4. Occupation (e..g manual labor)
  5. Obesity = pro-inflammatory state
  6. Old age
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92
Q

What are the most important cells responsible for OA?

A

Chondrocytes

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93
Q

Describe the pathophysiology of osteoarthritis

A

Mechanical stress –> progressive destruction and loss of articular cartilage
exposed subchondral bone becomes sclerotic
cytokine mediated TNF/IL/NO involved
deficiency in growth factors

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94
Q

Name the 2 main pathological features of osteoarthritis

A
  1. Cartilage loss

2. Disordered bone repair

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95
Q

Name the 3 joints of the hand that are commonly affected in osteoarthritis

A
  1. Distal interphalangeal joint
  2. Proximal interphalangeal joint
  3. Carpal metacarpal joint
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96
Q

Which surface of the knee is most commonly affected by OA?

A

Medial surface

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97
Q

What are the symptoms of OA?

A

● Joint pain worsened by movement and relieved by rest
● Stiffness after rest – gelling
● Only transient (<30 minute) morning stiffness

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98
Q

What is the primary investigation used to make a diagnosis of OA?

A

X-ray

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99
Q

Give 5 radiological features associated with OA

A

LOSS

  1. Loss of joint space - articular cartilage destruction
  2. Osteophyte formation - calcified cartilaginous destruction
  3. Subchondral sclerosis - exposed
  4. Subchondral cysts
  5. Abnormalities of bone contour
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100
Q

Describe the non-medical management of osteoarthritis

A
  1. Education
  2. Weight loss
  3. Activity and exercise
  4. Physiotherapy and occupational therapy
  5. Walking aids/podiatry
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101
Q

Describe the pharmacological management of OA

A
  1. Pain relief - paracetamol and NSAIDs –> opioids if needed
  2. Intra-articular steroid injections
  3. DMARDs - in inflammatory OA
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102
Q

Describe the surgical management for OA

A

Arthroscopy for loose bodies
Osteotomy (changing bone length)
Arthroplasty (joint replacement)
Fusion (ankle/foot)

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103
Q

Give 3 indications for surgery in OA

A
  1. Significant limitation of function
  2. Uncontrolled pain
  3. Waking at night from pain
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104
Q

A patient complains of ‘locking’, what is the most likely cause?

A

A loose body - bone or cartilage fragment

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105
Q

Nodal osteoarthritis can affect the DIP and PIP joints. What are the 2 terms sued for nodes on these joints?

A
  1. PIP = Bouchard’s nodes

2. DIP = Heberden’s nodes

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106
Q

Give an example of an inherited connective tissue disease

A
  1. Marfan’s syndrome = abnormal fibrillar production

2. Ehlers Danlos syndrome = abnormal collagen production

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107
Q

Give an example of an autoimmune connective tissue disease

A
  1. SLE
  2. Systemic sclerosis (scleroderma)
  3. Sjogren’s syndrome
  4. Dermatomyositis/Polymyositis
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108
Q

What is SLE?

A

Systemic lupus erythematous = inflammatory multi-system disease characterised by the presence of serum anti-nuclear antibodies (ANA)

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109
Q

Describe the epidemiology of SLE

A
  1. 90% of cases are in young women
  2. More common in afro-caribbean
  3. Genetic association
  4. peak onset = 20-40yrs
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110
Q

Describe the pathogenesis of SLE

A

Type 3 hypersensitivity reaction = immune complex mediated

Autoantibodies to a variety of auto antigens result in formation and deposition of immune complexes

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111
Q

What can cause thrombosis in SLE?

A

The presence of antiphospholipid antibodies

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112
Q

What autoantibody is specific to SLE?

A

Anti-double stranded DNA

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113
Q

what are the clinical features of SLE?

A

Symptoms:
butterfly rash, wt loss, fever, fatigue, joint pain, mouth ulcers

Signs: correctable ulnar deviation

  1. Rash - photosensitive vs diced vs malar (butterfly rash)
  2. Mouth ulcers
  3. Raynaud’s phenomenon
  4. General - fever, malaise, fatigue
  5. Depression
  6. Lupus nephritis –> proteinuria, renal failure and renal hypertension
  7. Arthritis - symmetrical
  8. Serositis - pleurisy/pleural effusion
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114
Q

What investigations might you do in someone who you suspect has SLE?

A
  1. Blood tests = anaemia, neutropenia, thrombocytopenia, RAISED ESR and NORMAL CRP
  2. Serum autoantibodies - ANA, anti-dsDNA
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115
Q

Describe the non medical treatment for SLE

A

Patient education and support
UV protection
Screening for end organ damage
Reduce CV risk factors - smoking cessation

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116
Q

Describe the pharmacological treatment for SLE

A 
● Avoid excessive sunlight and reduce CVS risk factors 
● NSAIDs - ibuprofen
● Chloroquine and hydroxychloroquine 
● Corticosteroids - prednisolone
● cyclophosphamide
● methotrexate
● Topical steroids
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117
Q

What is systemic sclerosis (scleroderma)?

A

A multi system disease characterised by excess production and accumulation of collagen –> inflammation and vasculopathy

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118
Q

Describe the pathophysiology of scleroderma

A

Various factors cause endothelial lesion and vasculopathy

Excessive collagen deposition –> inflammation and auto-antibody production

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119
Q

Give 5 signs of limited scleroderma

A

CREST
1. Calcinosis - skin calcium deposits
2. Raynauds
3. Esophageal reflux/stricture
4. Sclerodactyly - thick tight skin on fingers/toes
5. Telangiectasia - dilated facial spider veins
Pulmonary arterial hypertension

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120
Q

Give 4 signs of diffuse scleroderma

A

Skin changes develop more rapidly and are more widespread than inlimited cutaneous scleroderma/CREST

  1. Proximal scleroderma
  2. Pulmonary fibrosis
  3. Bowel involvement
  4. Myositis
  5. Renal crisis
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121
Q

What is a diagnostic test for scleroderma?

A

Limited - ACAs

Diffuse - 
Anti-topoisomerase, 
Anti scl-70
ANAs
ESR (normal)

If renal involvement, there may be anemia

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122
Q

Describe the management of scleroderma

A

avoid smoking, handwarmers

GI - PPIs, Antibiotics
Renal - ACEi
Pulmonary fibrosis - cyclophosphamide

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123
Q

What is the pathophysiology of sjögren’s syndrome?

A

Lymphatic infiltration of exocrine glands - especially lacrimal and salivary

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124
Q

What does sjögren’s syndrome often occur secondary to?

A

Other autoimmune disease –> SLE, RA, scleroderma, primary biliary cirrhosis

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125
Q

Give 5 symptoms of sjögren’s syndrome

A
  1. Dry eyes and dry mouth
  2. dry skin and dry vagina
  3. Inflammatory arthritis
  4. Rash
  5. Neuropathies
  6. Vasculitis
  7. fatigue
  8. salivary and parotid gland enlargement
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126
Q

Why does someone with sjögren’s syndrome have dry eyes and a dry mouth?

A

There is immunologically mediated destruction of epithelial exocrine glands meaning the lacrimal and salivary glands produce fewer secretions

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127
Q

What investigations might you do in someone who you suspect to have sjögren’s syndrome?

A

Serum auto-antibodies –> anti-RO, anti-La, RF, ANA

Raised immunoglobulins and ESR

Schirmer’s test
- ability for eyes to self-hydrate - <10mm in 5 minutes

Rose bengal staining and slit lamp exam

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128
Q

What is the treatment for sjögren’s syndrome?

A
  • Artificial tears, artificial saliva, vaginal lubricants
  • Hydroxychloroquine
  • NSAID
  • M3 agonist - pilocarpine
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129
Q

What is dermatomyositis?

A

A rare disorder of unknown aetiology

Inflammation and necrosis of skeletal muscle fibres and skin

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130
Q

Give 3 symptoms of dermatomyositis

A
  1. Rash
  2. Muscle weakness
  3. Lungs are often affected too (e.g. interstitial lung disease)
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131
Q

What investigations might you do in someone who you suspect has dermatomyositis?

A
  1. Muscle enzymes raised
  2. Electromyography (EMG)
  3. Muscle/skin biopsy
  4. Screen for malignancy
  5. CXR
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132
Q

What is the treatment for dermatomyositis?

A

Steroids - prednisolone

Immunosuppressants

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133
Q

What is the name given to inflammation of an entire digit?

A

Dactylitis

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134
Q

What class of drugs can cause Raynaud’s?

A

Beta blockers

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135
Q

What are the 3 phases of Raynaud’s?

A

White (vasoconstriction) –> Blue (tissue hypoxia) –> red (vasodilation)

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136
Q

What class of drugs does Nifedipine fall into and why can is be used to treat Raynaud’s?

A

Nifedipine - CCB

Relaxes blood vessels and stops vasospasm

137
Q

Describe the pathophysiology of septic arthritis

A

Infection produces inflammation in joints

Knee > Hip > Shoulder

138
Q

what are the causes of septic arthritis?

A
  1. Staphylococcus aureus
  2. Streptococci
  3. Neisseria Gonorrhoea
  4. Gram negative = E. coli, pseudomonas aeruginosa
139
Q

what are the risk factors for septic arthritis?

A 
Pre-existing joint disease (OA or RA)
Joint prostheses
IVDU
Immunosuppression
Alcohol misuse
Diabetes
Intra-articular corticosteroid injection
Recent joint surgery
140
Q

what are the clinical features of septic arthritis

A

Hot, swollen, painful, restricted joint
Onset < 2 weeks
Fever
Commonest → knee

141
Q

What investigation would you do to someone you suspect has septic arthritis?

A

Aspirate joint → MC+S
Blood culture
WCC → may be raised
ESR + CRP → raised

142
Q

Describe the treatment for septic arthritis

A 
Aspirate joint 
Empirical Abx - flucloxacillin 
- if allergic to penicilin = clindamycin
- if MRSA = vancomycin
- if gram negative = cefotaxime
Analgesia - NSAIDS
143
Q

Define osteomyelitis

A

Bone inflammation secondary to infection

144
Q

Describe the epidemiology of osteomyelitis

A

Increasing incidence of chronic OM
Bimodal age distribution (children and elderly)
● Predominantly occurs in children
● Increasing incidence of chronic osteomyelitis
● Adolescents and adults tend to get osteomyelitis due to infection secondary to direct trauma
● Elderly get it due to risk factors
● Majority of haematogenous acute osteomyelitis occurs in children

145
Q

What organisms can cause osteomyelitis?

A
  1. Staph. aureus
  2. Coagulase negative staph (s. epidermidis)
  3. Aerobic gram negate bacilli (salmonella)
  4. haemophilus influenza
  5. Mycobacterium TB
146
Q

Name 2 predisposing conditions for osteomyelitis

A
  1. Diabetes

2. PVD

147
Q

Osteomyelitis: Describe the 3 routes of infection into bone

A
  1. Direct inoculation of infection to bone (trauma, surgery)
  2. Contagious spread of infection from adjacent tissues to bone
  3. Hematogenous seeding (e.g. due to cannula infection)
148
Q

Osteomyelitis: Who is most likely to be effected by contagious spread of infection?

A

Affects older adults, those with DM, chronic ulcers, vascular disease, arthroplasties

149
Q

What bones are likely to be affected by hematogenous seeding in adults?

A

Vertebrae

150
Q

What bones are likely to be affected by hematogenous seeding in children?

A

Long bones

151
Q

Why do vertebrae tend to be affected by hematogenous seeding in adults?

A

With age, the vertebrae become more vascular meaning bacterial seeding is more likely

152
Q

Why do long bones tend to be affected by hematogenous seeding in children?

A

In children the metaphysis of long bones has a high but slow blood flow and basement membrane are absent meaning bacteria can move from the blood to bone

153
Q

Name a group of people who are at risk of hematogenous osteomyelitis

A

IVDU and other groups at risk from bacteraemia

154
Q

Give 4 host factors that affect the pathogenesis of osteomyelitis

A
  1. Behavioural (risk of trauma)
  2. Vascular supply (arterial disease, DM)
  3. Pre-existing bone/joint problems (RA)
  4. Immune deficiency
155
Q

Acute osteomyelitis: what changes to bone might you see histologically?

A
  1. Inflammatory cells
  2. Oedema
  3. Vascular congestion
  4. Small vessel thrombosis
156
Q

Chronic osteomyelitis: what changes to bone might you see histologically?

A
  1. Necrotic bone - ‘squestra’
  2. New bone formation ‘involucrum’
  3. Neutrophil exudates
  4. Lymphocytes and histiocytes
157
Q

Why does chronic osteomyelitis lead to sequestra and new bone formation?

A
  • Inflammation in BM increase intramedullary pressure exudate into bone cortex which rupture through periosteum
  • this causes interruption of periosteum blood supply which results in necrosis and sequestra
  • therefore new bone forms
158
Q

What is acute osteomyelitis associated with?

A

Associated with inflammatory bone changes caused by pathogenic bacteria

159
Q

What is chronic osteomyelitis associated with?

A

Involves bone necrosis

160
Q

what is the clinical presentation of osteomyelitis?

A
  1. Slow onset
  2. Dull pain at OM site, aggravated by movement
  3. Systemic = fever, rigors, sweating, malaise
161
Q

what are the signs of acute osteomyelitis?

A
  1. Tender
  2. Warm
  3. Red swollen area around OM
162
Q

what are the signs of chronic osteomyelitis?

A
  1. Acute OM signs
  2. Draining sinus tract
  3. Non-healing ulcers/fracture
163
Q

What is the differential diagnosis of osteomyelitis?

A
  1. Cellulitis
  2. Charcot’s joints (sensation loss –> degeneration)
  3. Gout
  4. Fracture
  5. Malignancy
  6. Avascular bone necrosis
164
Q

What investigations might you do on someone who you suspect may have osteomyelitis?

A
  1. Bloods - raised inflammatory markers (CRP, ESR) and WCC
  2. X-rays (cortical erosion, sequestra, sclerosis) and MRI (delineates inflammatory layers, marrow oedema)
  3. Bone biopsy - gold standard
  4. Blood cultures
165
Q

Describe the usual treatment for osteomyelitis

A

Large dose IV antibiotics tailored to culture findings (S. aureus = flucloxacillin)
immobilisation
Surgical treatment = debridement +/- arthroplasty of joint involved

166
Q

How is the stopping of antibiotics determined in osteomyelitis?

A

Guided by ESR and CRP

167
Q

Give 4 ways in which TB osteomyelitis is different to other osteomyelitis

A
  1. Slower onset
  2. Epidemiology is different
  3. Biopsy is essential - caseating granuloma
  4. Longer Treatment = 12 months
168
Q

Why is osteomyelitis difficult to treat?

A

Antibiotics struggle to penetrate bone and bone has a poor blood supply

169
Q

What is bacteraemia?

A

Bacteria in the blood

170
Q

What is debridement?

A

The removal of damaged tissue

171
Q

What condition must always be rules out in an acutely inflamed joint?

A

Septic arthritis –> aspirate the joint

172
Q

What is rheumatoid arthritis?

A

An auto-inflammatory synovial joint disease causing symmetrical polyarthritis

173
Q

Name 3 risk factors of RA

A
  1. Smoking
  2. Women
  3. family history
  4. Other AI conditions
  5. genetic factors - HLA-DR4 and HLA-DRB1
174
Q

Describe the pathophysiology of RA

A
  1. Chronic inflammation - B/T cells and neutrophils infiltrate
  2. Proliferation –> pannus formation (synovium grows out and over cartilage)
  3. Pro-inflammatory cytokines –> proteinases –> cartilage destruction
175
Q

what are the symptoms of RA?

A
  1. Early morning stiffness (>60 mins)
  2. Pain eases with use
  3. Swelling
  4. General fatigue, malaise
  5. Extra-articular involvment
176
Q

what are the signs of RA?

A
  1. Symmetrical polyarthorpathy
  2. Deforming –> ulnar deviation, swan neck deformity, boutonniere deformity
  3. Erosion on X-ray
  4. 80% = RF positive
177
Q

RA extra-articular involvement: describe the effect on soft tissues

A

Nodules
Bursitis
Muscle wasting

178
Q

RA extra-articular involvement: describe the effect on the eyes

A

Dry eyes
Scleritis
Episcleritis

179
Q

RA extra-articular involvement: describe the neurological effects

A

Sensory peripheral neuropathy
Entrapment neuropathies (carpal tunnel syndrome)
Instability of cervical spine

180
Q

RA extra-articular involvement: describe the haematological effects

A

Felty’s syndrome (RA + splenomegaly + neutropenia) Anaemia

181
Q

RA extra-articular involvement: describe the pulmonary effects

A

Pleural effusion

Fibrosing alveolitis

182
Q

RA extra-articular involvement: describe the effects on the heart

A

Pericardial rub

Pericardial effusion

183
Q

RA extra-articular involvement: describe the effects on the kidney

A

Amyloidosis

184
Q

RA extra-articular involvement: describe the effects on the skin

A

Vasculitis - infarcts in nail bed

185
Q

What investigations might you do in someone you suspect has rheumatoid arthritis?

A
  • Blood for inflammatory markers
  • ESR and CRP raised
  • RF and Anti-CCP

X-ray- Synovial fluid is sterile with high neutrophil count

186
Q

What is rheumatoid factor?

A

An antibody against the Fc portion of IgG

187
Q

What is seen on an X-ray of someone with RA?

A

LESS:

  • Loss of joint space (due to cartilage loss)
  • Erosion
  • Soft tissue swelling
  • Soft bones = osteopenia
188
Q

Describe the treatment for rheumatoid arthritis

A
  • NSAIDS and paracetamol
  • Corticosteroids
  • intra-articular glucocorticoid injections
  • DMARDs (methotrexate) + folic acid
  • Biological agents (TNF inhibitor - infliximab)
  • Physio and OT
  • Synovectomy
189
Q

What joints tend to be affects in RA?

A

MCP
PIP
Wrist (DIP often spared)

190
Q

What is gout?

A

Crystal arthritis

Inflammatory arthritis caused by hyperuricaemia and intra-articular sodium urate crystals

191
Q

Describe the epidemiology of gout?

A

● 5x more common in men
● Occurs rarely before young adulthood
● Rarely occurs in pre-menopausal females
● Often a family history

192
Q

What joint does gout most commonly affect?

A

Big toe metatarsophalangeal joint

193
Q

Describe the pathophysiology of gout

A

Purine –> (by xanthine oxidase) xanthine –> uric acid –> monosodium rate crystals OR excreted by kidneys

Urate blood/tissue imbalance –> rate crystal formation –> inflammatory response through phagocytic activation

Overproduction/under excretions of uric acid causes build up and precipitated out in joints

194
Q

Give 3 causes of gout

A

= Hyperuricaemia

  1. Impaired excretion - CKD, diuretics, hypertension
  2. Increased production - hyperlipidaemia
  3. Increased intake - high purine diet = red meat, seafood, fructose, alcohol
195
Q

Name 3 common precipitants of a gout attack

A
  1. Aggressive introduction of hypouricaemic therapy
  2. Alcohol or shellfish binges
  3. Sepsis, MI, acute severe illness
  4. Trauma
196
Q

Name 4 diseases that someone with gout might have an increased risk of developing

A
  1. Hypertension
  2. CV disease - e.g. stroke
  3. Renal disease
  4. Type 2 diabetes
197
Q

what is the clinical presentation of gout?

A

SYMPTOMS
inflamed joints - 1st metatarsal and distal interphalangeal often affected.

SIGNS
tophi- lumps of urate salts

198
Q

What are tophi?

A

Onion like aggregates of urate crystals with inflammatory cells.
Proteolytic enzymes are released –> erosion

199
Q

What investigations might you do in a patient you think has gout?

A

first line = bloods

  • U&E and eGFR - renal failure
  • Uric acid levels - 4-6 weeks after to confirm hyperuricaemia
  • gold standard = joint aspiration
200
Q

What is the aim of treatment for gout?

A

To get urate levels < 300 mol/L

201
Q

How would you treat acute gout?

A

1st line = NSAID or colchicine

2nd line = intra-articular steroid injection

lifestyle advice - wt loss, exercise, diet, alcohol and fluid intake

202
Q

what is the management for chronic gout?

A

1st line = allopurinol - inhibits xanthine oxidase

2nd line = febuxostat

consider co-prescribing colchicine with allopurinol for 6 months

203
Q

You see a patient with gout who is taking bendroflumethiazide. What drug might you replace this with to help treat their gout?

A

You would switch bendroflumethiazide to cosartan as bendroflumethiazide is a diuretic and so impairs urate excretion

204
Q

Name 6 factors that can cause an acute attack of gout

A
  1. Sudden overload
  2. Cold
  3. Trauma
  4. Sepsis
  5. Dehydration
  6. Drugs
205
Q

A patient presents with an acute mono-arthropathy of their big toe. What are the two main differential diagnoses?

A
  1. Gout

2. Septic arthritis

206
Q

A patient presents with an acute mono-arthropathy of their big toe. What investigations might you do?

A

Joint aspirate
If septic arthritis - high WCC and neutrophilia and bacteria on gram stain
If gout - urate crystals

207
Q

Describe the pathophysiology of pseudogout

A

Calcium pyrophosphate crystals are deposited on joint surfaces - produces the radiological appearance of chondrocalcinosis
Crystals elicit an acute inflammatory response

208
Q

What can cause pseudogout?

A
  1. Hypo/hyperthyroidism
  2. Haemochromatosis
  3. Diabetes
  4. Magnesium levels
209
Q

what is the clinical presentation of pseudogout?

A

SYMPTOM
hot, swollen, tender joint, usually knees

SIGNS
recent injury to the joint in the history
Typically the wrists and knees

210
Q

What investigations might you do in someone you suspect might have pseudogout?

A

Aspiration –> fluid for crystals and blood cultures = positive birefringent rhomboid crystals

X-rays –> can show chondrocalcinosis

211
Q

What is the most likely differential diagnosis for pseudogout?

A

Infection

212
Q

Describe the treatment for pseudogout

A
  • high dose NSAIDs - ibuprofen
  • Colchicine - anti-gout
  • IM prednisolone
  • Aspiration, intra-articular steroid injections
213
Q

How can you distinguish OA from pseudogout?

A

Pattern of involvement –> Pseudo = wrists, shoulders, ankle, elbows
Marked inflammatory component –> Elevated CRP and ESR Superimposition of acute attacks

214
Q

What kind of crystals do you see in pseudogout?

A

Positive birefringent calcium pyrophosphate rhomboid crystals

215
Q

What kind of crystals do you see in gout?

A

Monosodium urate crystals = negatively birefringent

216
Q

What kind of crystals fo you see in pseudogout?

A

Calcium pyrophosphate crystals = positively birefringent

217
Q

What is the diagnostic criteria for fibromyalgia?

A

Chronic widespread pain lasting for > 3 months with other causes excluded
Pain is at 11/18 tender point sites for 6 months

218
Q

Name 4 diseases that fibromyalgia is commonly associated with

A
  1. Depression
  2. Choric fatigue
  3. IBS
  4. Chronic headache
219
Q

Give 4 symptoms of fibromyalgia

A
  1. Neck and back pain
  2. Pain is aggravated by stress, cold and activity
  3. Generalised morning stiffness
  4. Paraesthesia of hands and feet
  5. Profound fatigue
  6. Unrefreshing sleep
  7. poor concentration, brain fog
220
Q

Give 3 disease that might be included in the differential diagnosis for fibromyalgia

A
  1. Hypothyroidism
  2. SLE
  3. Low vitamin D
221
Q

How is fibromyalgia diagnosed?

A

Everything seems normal 11/18 trigger points

Exclude other diagnoses

222
Q

Describe the management of fibromyalgia

A
  • CBT and exercise programmes
  • Acupuncture
  • opiate = tramadol, codeine
  • anticonvulsants = pregabalin
  • TCA = amitriptyline
223
Q

Why is the ACL so important?

A

Important stabiliser of the knee joint, limits anterior translation of the tibia and also contributes to knee rotational starbility

224
Q

Define sarcoma

A

A rare tumour of mesenchymal origin

A malignant connective tissue neoplasm

225
Q

What are the red flag symptoms for bone malignancy?

A 
Rest pain
Night pain
Loss of function
Neurological problems 
Weight loss
Growing lump 
Deformity
226
Q

Who are primary bone tumours seen in?

A

they are rare - are mainly seen in children and young peoplemore common in males

227
Q

Give 3 primary bone tumours

A
  1. Osteosarcoma
  2. Fibrosarcoma
  3. Chondrosarcomas
  4. Ewings sarcoma
228
Q

What are secondary bone tumours?

A

Metastases from:

  1. Lungs
  2. Breast
  3. Prostate
  4. Thyroid
  5. Kidney
229
Q

What investigations might you do in someone you suspect has bone cancer?

A

1st line → x-ray
Gold standard → biopsy
Bloods → FBC, ESR, ALP, lactate dehydrogenase, Ca, U+E
CT chest/abdo/pelvis

230
Q

What might you seen on an X-ray of someone with bone cancer?

A

Onion skin/sunburst appearance = Ewings

Colman’s triangle = osteosarcoma, Ewings, GCT, Osteomyelitis, metastasis

231
Q

What staging is used for bone cancers?

A

Enneking grading

232
Q

How are malignant bone cancers staged using Enneking grading?

A 
G1 = Histologically benign
G2 = Low grade
G3 = High grade
A = intracompartmental
B = extracompartmental
233
Q

How are benign bone cancers staged using Enneking grading?

A 
G1 = Latent
G2 = Active 
G3 = Aggressive
234
Q

How are bone cancers treated?

A 
MDT management 
Benign 
- NSAIDS
- Bisphosphonates (alendronate) 
- symptomatic help

Malignancy = surgical excision –> limb sparing/amputation
radio/chemotherapy

235
Q

Give 4 local complications with surgery for bone cancers

A
  1. Haematoma
  2. Loss of function
  3. Infection
  4. Local recurrence
236
Q

Where do osteosarcomas usually present?

A

Knee - distal femur, proximal humerus

237
Q

What is an osteosarcoma?

A

Malignant tumour of bone
Spindle cell neoplasm that produce osteoid
rapidly metastases to the lung

238
Q

Give 3 features of osteosarcoma

A
  1. Fast growing
  2. Aggressive - Destroys bone and spreads into surrounding tissues, rapidly metastasises to lung
  3. Typically affects 15-19 year olds
  4. often relatively painless
239
Q

What is a chondrosarcoma?

A

A malignant neoplasm of cartilage

240
Q

Name a boney sarcoma that responds well to chemotherapy

A

Ewings sarcoma

241
Q

Where does Ewings sarcoma arise from?

A

mesenchymal stem cells

242
Q

Boney sarcomas make up what percentage of overall sarcomas?

A 
20% = boney 
80% = soft tissue
243
Q

Name 3 soft tissue sarcomas

A
  1. Liposarcoma = malignant neoplasm of adipose tissue
  2. Leiomyosarcoma = malignant neoplasm of smooth muscle
  3. Rhabdomyosarcoma = malignant neoplasm of skeletal muscle
244
Q

If it not possible to get a wide margin when resecting a sarcoma what might you do?

A

Give adjuvant radiotherapy

245
Q

Name 2 NSAIDs

A
  1. Ibuprofen

2. Naproxen

246
Q

Give 3 side effects of NSAIDs

A
  1. Peptic ulcer disease
  2. Renal failure
  3. Increased risk of MI and CV disease
247
Q

What can you do to reduce the risk of gastric ulcers and bleeding in someone taking NSAIDs?

A
  1. Co-prescribe PPI

2. Prescribe low doses and short courses

248
Q

Give 5 potential side effects of steroids

A
  1. Diabetes
  2. Muscle wasting
  3. Osteoporosis
  4. Fat redistribution
  5. Skin atrophy
  6. Hypertension
  7. Acne
  8. Infection risk
249
Q

How do DMARDs work?

A

Non-specific inhibition of inflammatory cytokines cascade = reduces joint pain, stiffness and swelling

250
Q

Give an example of a DMARD

A

Methotrexate = gold standard
Hydroxychloroquine
Sulfasalazine

251
Q

How often should methotrexate be taken?

A

Once weekly

252
Q

Give 3 potential side effects of methotrexate

A
  1. Bone marrow suppression
  2. Abnormal liver enzymes
  3. Nausea
  4. Diarrhoea
  5. Teratogenic
253
Q

What can be co-prescribed with methotrexate to reduce the risk of side effects?

A

Folic acid

254
Q

What are cytokines?

A

Short acting hormones

255
Q

Name a TNF blocker

A

InfliximabAdalimumab

256
Q

Name a monoclonal antibody that binds to CD20 on B cells

A

Rituximab - binds to CD 20 –> B cell depletion

257
Q

Describe the mechanism of action of infliximab

A

Inhibits T cell activation

258
Q

How does alendronate work?

A

Reduces bone turnover by inhibiting osteoclast mediated bone resorption

259
Q

What class of drug is alendronate?

A

Bisphosphonate

260
Q

Name 2 drugs that act on the HMGcoA pathway

A
  1. Bisphosphonates - alendronate

2. Statins - simvistatin

261
Q

what are the signs of osteoarthritis?

A

● Deformity and bony enlargement of the joints
● Limited joint movement
● Muscle wasting of surrounding muscle groups
● Crepitus (grafting) due to disruption of normally smooth articulating surfaces of joints
● May be joint effusion
● Heberden’s nodes are bony swellings at DIPJs
● Bouchard’s nodes occur at proximal interphalangeal joints

262
Q

what is the epidemiology of osteoarthritis?

A

● Most common form of arthritis & most common condition affecting synovial joint
● Prevalence increases with age
● Most people over 60 have some radiological evidence of it – only a fraction have symptoms
● Women > men
● Familial tendency to develop nodal and generalised OA

263
Q

what are the investigations for osteoarthritis?

A

● FBC and ESR normal
● Rheumatoid factor is negative but positive low titre tests may occur incidentally in elderly
● XRs abnormal in advanced disease

264
Q

what are the complications of rheumatoid arthritis?

A

Cervical spinal cord compression- weakness and loss of sensation
Lung involvement- interstitial lung disease, fibrosis.

265
Q

what is the difference between the presentation of early and late septic arthritis

A

● Early infection presents with inflammation, discharge, joint effusion, loss of function and pain
● Late disease presents with pain or mechanical dysfunction

266
Q

what are the risk factors for gout?

A

Middle age overweight males.
high purine diet,
increased cell turnover

267
Q

what are the complications of gout?

A

Infection in the tophi

Destruction of the joint

268
Q

what are the risk factors for osteomyelitis?

A 
Previous osteomyelitis
Penetrating injury
IVDU
Diabetes
HIV
Recent surgery
Distant or local infection
Sickle cell disease
RACKD
Children → upper resp tract  or varicella infection
269
Q

what is the pathophysiology of osteomyelitis?

A

● Pathogen has to get into bone – many routes
o Direct inoculation of infection via trauma/surgery – easy
o Contagious spread without skin breaking – infection of adjacent tissue spreading into bone, seen in elderly who have DM, chronic ulcers, vascular disease, joint replacements and prostheses
o Haematogenous seeding – infection from skin spreading to bone

270
Q

what are the risk factors for ankylosing spondylitis?

A

HLA-B27

environment - klebsiella, salmonella, shigella

271
Q

what is ankylosing spondylitis?

A

● Chronic inflammatory disorder of the spine, ribs and sacroiliac joints
● Ankylosis is abnormal stiffening and immobility of a joint due to new bone formation

272
Q

what is psoriatic arthritis?

A

Inflammatory arthritis associated with psoriasis

1 in 5 patients with psoriasis have psoriatic arthritis

273
Q

what is arthritis mutilans?

A

Most severe form of psoriatic arthritis
Occurs in phalanxes
Osteolysis of bones around joints in digits → leads to progressive shortening
Skin then folds as digit shortens → telescopic finger

274
Q

what are the different types of psoriatic arthritis?

A

● Distal interphalangeal arthritis – most typical pattern of joint involvement – dactylitis is characteristic
● Mono- or oligoarthiritis
● Symmetrical seronegative polyarthritis – resembling RA
● Arthritis mutilans – a severe form with destruction of the small bones in the hands and feet
● Sacroiliitis – uni- or bilateral

275
Q

what is the clinical presentation of reactive arthritis?

A

Begin 1-4 weeks after onset of infection
Asymmetrical oligoarthritis
Painful, swollen, warm, red + stiff joints
Dactylitis

Classic triad → conjunctivitis, urethritis + arthritis (can’t see, can’t pee, can’t climb a tree)

276
Q

what treatment should be used if reactive arthritis relapses?

A

methotrexate or sulfasalazine

277
Q

what is the epidemiology of reactive arthritis?

A

● Males who are HLA-B27 positive have a 30-50 fold increased risk
● Women less commonly affected

278
Q

what is the pathophysiology of reactive arthritis?

A

● Bacterial antigens or DNA have been found in the inflamed synovium of affected joints – suggests persistent antigenic material is driving the inflammatory response

279
Q

what are the complications for SLE?

A

Cardiac, lung, kidney involvement. Widespread inflammation causing damage.

280
Q

what is the epidemiology of fibromyalgia?

A

women, poor socioeconomic status, 20-50 year old

281
Q

what is the the pathophysiology of fibromyalgia?

A

Unknown, possibly pain perception/hyper excitability of pain fibres

282
Q

what are the complications of fibromyalgia?

A
  • can really affect quality of life
  • anxiety, depression, insomnia
  • opiate addiction
283
Q

what is fibromyalgia?

A

Also known as chronic persistent pain
● Widespread msk pain after other diseases have been excluded
● Symptoms present at least 3 months and other causes have been excluded
● Characterised by central (non-nociceptive) pain
o Due to a central disturbance in pain processing
o Biopsychosocial factors important
● Not easily diagnosed as there is no specific pathology

284
Q

what is rickets?

A

Rickets: inadequate mineralization of the bone and epiphyseal cartilage in the growing skeleton of CHILDREN.

285
Q

what is the difference between primary and secondary sjogren’s syndrome?

A
  • primary = syndrome on it’s own

- secondary = associated with connective tissue disease e.g. RA, SLE

286
Q

what are the complications of Sjogren’s syndrome?

A
  • eye infections- oral problems (dental cavities, candida infections)
  • vaginal problems (candidiasis, sexual dysfunction)

RARE

  • pneumonia and bronchiectasis
  • non-hodgkin’s
  • vasculitis
  • renal impairment
  • peripheral neuropathy
287
Q

which arteries are particularly affected by giant cell arteritis?

A
  • aorta and vertebral arteries
  • Cerebral arteries affected in particular e.g. temporal artery
  • Opthalmic artery can also be affected potentially resulting in permanent ortemporary vision loss
288
Q

what is found on physical examination of giant cell arteritis?

A

temporal arteries may be tender on palpation and thickened. Pulses may be diminished.

289
Q

what is antiphospholipid syndrome?

A
  • Syndrome characterised by thrombosis (arterial or venous) and/or recurrentmiscarriages with positive blood tests for antiphospholipid antibodies (aPL) - hypercoagulable state
290
Q

what is the epidemiology of antiphospholipid syndrome?

A
  • 20-30% are associated with SLE- more common in females- more often primary disease
291
Q

what are the risk factors for antiphospholipid syndrome?

A
  • diabetes
  • hypertension
  • obesity
  • female
  • underlying autoimmune condition
  • smoking
  • oestrogen therapy
292
Q

what is the clinical presentation of antiphospholipid syndrome?

A
  • thrombosis
  • miscarriage
  • livedo reticularis - purple lace rash
  • ischaemic stroke, TIA, MI
  • DVT, budd-chiari syndrome
  • thrombocytopenia
  • valvular heart disease, migraines, epilepsy
293
Q

what is the pathophysiology of antiphospholipid syndrome?

A
  • Antiphospholipid antibodies (aPL) play a role in thrombosis by binding tophospholipid on the surface of cells such as endothelial cells, platelets andmonocytes
  • Once bound, this change alters the functioning of those cells leading tothrombosis and/or miscarriage
  • Antiphospholipid antibodies (aPL) cause CLOTs:
    • Coagulation defect
    • Livedo reticularis - lace-like purplish discolouration of skin
    • Obstetric issues i.e. miscarriage
    • Thrombocytopenia (low platelets)
294
Q

what are the investigations for antiphospholipid syndrome?

A

Hx of thrombosis/ pregnancy complications + Antibody screen with raised:

  - anticardiolipin antibodies
 - lupus anticoagulant
 - anti-beta-2 glycoprotein I antibodies
295
Q

what is the treatment for antiphospholipid syndrome?

A
  • long term warfarin
  • Pregnant women on low molecular weight heparin (e.g. enoxaparin) + aspirin
  • lifestyle - smoking cessation, exercise, healthy diet
296
Q

what are the complications of antiphospholipid syndrome?

A
  • Venous thromboembolisms (e.g. DVT, pulmonary embolism)
  • Arterial thrombosis (stroke, MI, renal thrombosis)
  • Pregnancy complications (recurrent miscarriage, pre-eclampsia,…)
297
Q

what is the clinical presentation of wegener’s granulomatosis?

A

Classic sign on exams: saddle shaped nose

Epistaxis

Crusty nasal/ ear secretions 🡪 hearing loss

Sinusitis

Cough, wheeze, haemoptysis

298
Q

what are the complications of wegener’s granulomatosis?

A

Glomerulonephritis

299
Q

what is the most common primary bone malignancy in children?

A

osteosarcoma

300
Q

what condition is osteosarcoma associated with?

A

Paget’s disease

301
Q

what is the appearance of osteosarcoma on x-rays?

A

bone destruction and formation,

soft tissue calcification produces a sunburst appearance

302
Q

what is the clinical presentation of ewing’s sarcoma?

A

● Presents with mass/swelling, most commonly in long bones of the
o Arms, legs, pelvis, chest
o Occasionally skull and flat bones of the trunk

● Painful swelling, redness in surrounding area, malaise, anorexia, weight loss, fever, paralysis and/or incontinence if affecting the spine, numbness in affected limb

303
Q

what is the epidemiology of Ewing’s sarcoma?

A

● Very rare

● Average age of onset 15

304
Q

where is Ewing’s sarcoma commonly found?

A

Presents with mass/swelling, most commonly in long bones of the
o Arms, legs, pelvis, chest
o Occasionally skull and flat bones of the trunk

305
Q

where does chrondosarcoma commonly present?

A

Common sites are pelvis, femur, humerus, scapula and ribs

306
Q

what is the clinical presentation of chrondrosarcoma?

A

Associated with dull, deep pain and affected area is swollen and tender

307
Q

which is the most common sarcoma in adults?

A

chondrosarcoma

308
Q

which types of malignancy cause bone pain?

A
  • multiple myeloma
  • lymphoma
  • primary bone tumours
  • metastases - secondary bone tumour
309
Q

other than bone pain, what other symptoms can indicate bone tumours?

A
  • Mobility issues → unexplained limp, joint stiffness, reduced ROM
  • Inflammation + tenderness over bone
  • Systemic symptoms
310
Q

what is the prophylactic treatment for antiphospholipid syndrome?

A

aspirin or clopidogrel for people with aPL

311
Q

what is the epidemiology of scleroderma?

A
  • more common in females
  • peak incidence = 30-50yrs
  • rare in children
312
Q

what are the risk factors for scleroderma?

A
  • exposure to vinyl chloride, silica dust, rapeseed oil, trichloroethylene
  • bleomycin
  • genetic
313
Q

what is polymyositis?

A

a rare muscle disorder of unknown aetiology in which there is inflammation and necrosis of skeletal muscle fibres

314
Q

what is dermatomyositis?

A

polymyositis with skin involvement

315
Q

what is the epidemiology of polymyositis/dermatomyositis?

A
  • Very rare
  • Both affect adults and children
  • More common in FEMALES than males
316
Q

what is the clinical presentation of polymyositis?

A
  • symmetrical progressive muscle weakness and wasting - affects proximal muscles of shoulder and pelvic girdle
  • difficulty squatting, going upstairs, rising from chair and raising hands above head
  • involvement of pharyngeal, laryngeal and respiratory muscles = dysphagia, dysphonia and respiratory failure
  • pain and tenderness = uncommon
317
Q

what is the clinical presentation of dermatomyositis?

A
  • heliotrope (purple) discolouration of eyelids
  • scaly erythematous plaques over knuckles (Gotton’s papules)
  • arthralgia, dysphagia and raynauds
318
Q

what are the investigations for polymyositis/dermatomyositis?

A

Muscle Biopsy

Bloods
- serum creatine kinase, aminotransferases, lactate dehydrogenase (LDH) and aldolase all raised

Immunology
ANA, Anti jo1, anti mi2

319
Q

what is the treatment for polymyositis/dermatomyositis?

A
  • bed rest + exercise plan
  • oral prednisolone
  • steroid sparing immunosuppressive - azathioprine, methotrexate, ciclosporin
  • hydroxychloroquine for skin disease
320
Q

what factors are used in the FRAX score calculation?

A
  • age
  • sex
  • height and weight
  • previous fractures
  • smoking
  • parent fractured hip (FHx)
  • steroid (glucocorticoid use)
  • RA
  • secondary osteoporosis
  • alcohol consumption (>3 units)
  • femoral neck bone mineral density
321
Q

what is the diagnostic criteria for RA?

A

RF RISES - >6 weeks and >4 of following:

  • RF positive
  • Finger/hand/wrist involvement
  • Rheumatoid nodules present
  • Involvement of >3 joints
  • Stiffness in morning >1 hr
  • Erosions on x-ray
  • Symmetrical involvement
322
Q

what is the treatment for raynauds phenomenon?

A

Lifestyle - protect the hands, stop smoking

Medications - CCB

323
Q

what is limited scleroderma?

A
  • skin involvement limited to hands, face, feet and forearms
  • characteristic ‘beak’-like nose and small mouth
  • Microstomia - small mouth
324
Q

what is diffuse scleroderma?

A

skin changes develop more rapidly and are more widespread
Raynaud’s phenomenon coincident with skin involvement
GI, Renal, Lung involvement

325
Q

what is paget’s disease?

A

localized disorder of bone remodelling
↑ osteoclastic bone resorption followed by ↑ formation of weaker bone
Leads to structurally disorganized mosaic of bone (woven bone)

326
Q

what is the pathophysiology of paget’s disease?

A

↑ osteoclastic bone resorption followed by ↑ formation of weaker bone
Leads to structurally disorganized mosaic of bone (woven bone)

327
Q

what is the epidemiology of paget’s disease?

A

incidence ↑ with age, rare under 40 y.o

- affects up to 10% of individuals by the age of 90

328
Q

what are the clinical features of paget’s disease?

A

60-80% are asymptomatic

  • bone pain
  • joint pain
  • deformities -> bowed tibia and skull changes
  • neurological complications
  • CN8 compression -> deafness
  • blockage of aqueduct of sylvius causing hydrocephalus
329
Q

what are the investigations for paget’s disease?

A

Bloods - Increased ALP, normal calcium and phosphate
Urinary hydroxyproline increase
X-rays - Findings of osteoarthritis

330
Q

what is the management for paget’s disease?

A

Bisphosphonates, NSAIDS

331
Q

what is osteomalacia?

A

Defective mineralization of newly formed bone matrix or osteoid in adults, due to inadequate phosphate or calcium, or due to ↑ bone resorption (hyperPTH)

332
Q

what are the causes of osteomalacia?

A

malnutrition (most common)
drug induced
defective 1-alpha hydroxylation
Liver disease

333
Q

what is the clincial presentation of osteomalacia?

A 
Osteomalacia
widespread bone pain and tenderness
gradual onset and persistent fatigue
muscle weakness, parasthesia, waddling gait
fractures
334
Q

what is the clincial presentation of rickets?

A

leg-bowing and knock knees
- tender swollen joints
- growth retardation
- bone and joint pain
dental deformities – delayed formation of teeth, enamel hypoplasia
- enlargement of end of ribs (‘rachitic rosary’)

335
Q

what are the investigations for Osteomalacia / rickets?

A

Bloods - U&Es, Serum ALP, Vit D

X-rays - defective mineralisation, rachitic rosary

336
Q

what is the management for osteomalacia/rickets?

A

Lifestyle - nutrition, sunlight
Medications - Vit D replacement
Malabsorption/Renal disease - IM calcitriol

337
Q

what is hyperuricaemia?

A 
men = >420umol/L
female = >360umol/L
338
Q

what is the sepsis 6?

A
  1. administer O2
  2. take blood cultures
  3. give IV antibiotics
  4. give IV fluids
  5. check serial lactates
  6. measure urine output

Phase 2A revision (38 decks)

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