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MY REVISION - ALL PHASES > 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

What else might be seen in blood tests for 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

Inflammation of spine –> erosive damage –> repair/new bone formation –> irreversible fusion of spine (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
Steroids during flares
anti-TNF drugs - etanercept
MAb against TNF - infliximab or adalimumab 
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

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, sulfasalazine
  • TNF inhibitor or MAb - etanercept, infliximab or adalimumab
  • 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
o A GI infection with Shigella, Salmonella, Yersinia or Campylobacter
o Sexually acquired infection
● 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

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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

What is the criteria for making a clinical diagnosis of juvenile idiopathic arthritis?

A

Joint swelling/stiffness >6 weeks in children <16 and no other cause is identified

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37
Q

What is the aetiology of JIA?

A

Unknown - idiopathic

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38
Q

Why is it important to check the eyes in JIA?

A

Children with JIA are at high risk of developing uveitis

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39
Q

Describe the treatment for JIA

A
  1. Steroid joint injections
  2. NSAIDs
  3. Methotrexate
  4. Systemic steroids
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40
Q

Psoriatic arthritis commonly involved swelling of what joint?

A

DIP joint

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41
Q

Describe a psoriatic plaque

A

Pink, scaling lesion

Occurs on extensor surfaces of limbs

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42
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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43
Q

Defne 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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44
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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45
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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46
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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47
Q

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

A

Oestrogen

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48
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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49
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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50
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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51
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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52
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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53
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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54
Q

Name 2 medications that can cause osteoporosis

A
  1. Glucocorticoids
  2. Depo-povera
  3. GnRH analogues
  4. Androgen deprivation
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55
Q

Give the clinical presentation of osteoporosis

A
  1. Asymptomatic development
  2. Fragile bones
  3. Pathological fractures (femur neck)
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56
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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57
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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58
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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59
Q

What is a normal T score?

A

> -1.0

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60
Q

What T score signifies that a patient has osteopenia?

A

-2.5 < t < -1

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61
Q

What T score signifies that a patient has osteoporosis?

A

T < -2.5

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62
Q

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

A

FRAX = predicts 10 year fracture chance

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63
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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64
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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65
Q

Give 3 advantages of HRT

A
  1. Reduces fracture risk
  2. Stops bone loss
  3. Prevent menopausal symptoms
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66
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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67
Q

How do bisphosphonates work?

A

Inhibit cholesterol formation –> osteoclast apoptosis

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68
Q

Define osteopenia

A

Pre-cursor to osteoporosis characterised by low bone density

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69
Q

Define osteomalacia

A

Poor bone mineralisation leading to soft bone due to lack of Ca2+ in adults

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70
Q

What is vasculitis?

A

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

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71
Q

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

A

Neutrophils

Giant cells

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72
Q

Describe the pathophysiology of of vasculitis

A

Vessel wall destruction –> perforation and haemorrhage

Endothelial injury –> thrombosis and infarction

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73
Q

Give an example of large vessel vasculitis

A

Giant cell arteritis

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74
Q

Give an example of medium/small vessel vasculitis

A

Wegner’s granulomatosis (Granulomatosis polyangitis)

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75
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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76
Q

Describe the epidemiology of giant cell arteritis

A

Affects those > 50 years old
Incidence increase age
Twice as common in women

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77
Q

Describe the pathophysiology of giant cell arteritis

A

Arteries become inflamed, thicken and can obstruct blood flow

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78
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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79
Q

How does giant cell arteritis present in a medical emergency?

A

Stroke and blindness

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80
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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81
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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82
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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83
Q

Give 2 complications of giant cell arteritis

A
  1. Increased CVA risk

2. Visual loss

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84
Q

What does ANCA stand for?

A

Anti-neutrophil cytoplasmic antibodies

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85
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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86
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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87
Q

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

A
  1. Sinusitis
  2. Otitis
  3. Cough
  4. Haemoptysis
  5. Saddle nose deformity
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88
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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89
Q

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

A

Glomerulonephritis –> haem/proteinuria

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90
Q

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

A

Ulcers

Pulpura

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91
Q

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

A

Uveitits
Scleritis
Episcleritis

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92
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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93
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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94
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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95
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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96
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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97
Q

What are the most important cells responsible for OA?

A

Chondrocytes

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98
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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99
Q

Name the 2 main pathological features of osteoarthritis

A
  1. Cartilage loss

2. Disordered bone repair

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100
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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101
Q

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

A

Medial surface

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102
Q

Give 5 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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103
Q

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

A

X-ray

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104
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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105
Q

Describe the non-medical management of osteoarthritis

A
  1. Eduction
  2. Weight loss
  3. Activity and exercise
  4. Physiotherapy and occupational therapy
  5. Walking aids/podiatry
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106
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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107
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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108
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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109
Q

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

A

A loose body - bone or cartilage fragment

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110
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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111
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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112
Q

Give 3 features of Marfan’s syndrome

A
  1. Long limbs
  2. Lens dislocation
  3. Abnormal sternum (pectus excavatum)
  4. Aortic root enlargement
  5. Arachnodactyly - long fingers
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113
Q

Give 2 features of Ehler Danlos syndrome

A
  1. Stretchy skin

2. Joint hypermobility

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114
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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115
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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116
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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117
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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118
Q

What can cause thrombosis in SLE?

A

The presence of antiphospholipid antibodies

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119
Q

What autoantibody is specific to SLE?

A

Anti-double stranded DNA

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120
Q

Give 5 symptoms 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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121
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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122
Q

Describe the non medical treatment for SLE

A

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

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123
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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124
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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125
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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126
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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127
Q

Give 4 signs of diffuse scleroderma

A

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

  1. Proximal scleroderma
  2. Pulmonary fibrosis
  3. Bowel involvement
  4. Myositis
  5. Renal crisis
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128
Q

What is a diagnostic test for scleroderma?

A

Centromere autoantibody = diagnostic

  • ANA, RF
  • anti-centromere antibodies
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129
Q

Describe the management of scleroderma

A
  1. Raynauds = physical protection and vasodilators (nifedipine -CCB)
  2. GORD = PPI (lansoprazole) for life
  3. Annual echo and pulmonary function tests to monitor arterial pulmonary pressure
  4. ACEi (ramipril) to prevent renal crisis
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130
Q

What is the pathophysiology of sjögren’s syndrome?

A

Lymphatic infiltration of exocrine glands - especially lacrimal and salivary

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131
Q

What does sjögren’s syndrome often occur secondary to?

A

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

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132
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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133
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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134
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

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135
Q

What is the treatment for sjögren’s syndrome?

A
  • Artificial tears, artificial saliva, vaginal lubricants

- Hydroxychloroquine used to halt progression

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136
Q

What is dermatomyositis?

A

A rare disorder of unknown aetiology

Inflammation and necrosis of skeletal muscle fibres and skin

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137
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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138
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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139
Q

What is the treatment for dermatomyositis?

A

Steroids - prednisolone

Immunosuppressants

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140
Q

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

A

Dactylitis

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141
Q

What class of drugs can cause Raynaud’s?

A

Beta blockers

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142
Q

What are the 3 phases of Raynaud’s?

A

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

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143
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

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144
Q

Describe the pathophysiology of septic arthritis

A

Infection produces inflammation in joints

Knee > Hip > Shoulder

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145
Q

what are the causes of septic arthritis?

A
  1. Staphylococcus aureus
  2. Streptococci
  3. Neisseria Gonorrhoea
  4. Gram negative = E. coli, pseudomonas aeruginosa
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146
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
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147
Q

what are the clinical features of septic arthritis

A

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

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148
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

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149
Q

Describe the treatment for septic arthritis

A

Aspirate joint
Empirical Abx - flucloxacillin IV and oral fusidic acid
Pathogen-directed Abx
Analgesia - NSAIDS

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150
Q

Define osteomyelitis

A

Bone inflammation secondary to infection

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151
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

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152
Q

What 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
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153
Q

Name 2 predisposing conditions for osteomyelitis

A
  1. Diabetes

2. PVD

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154
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)
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155
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

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156
Q

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

A

Vertebrae

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157
Q

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

A

Long bones

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158
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

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159
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

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160
Q

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

A

IVDU and other groups at risk from bacteraemia

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161
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
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162
Q

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

A
  1. Inflammatory cells
  2. Oedema
  3. Vascular congestion
  4. Small vessel thrombosis
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163
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
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164
Q

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

A

Inflammation in BM increase intramedullary pressure –> exudate into bone cortex –> rupture through periosteum –> interruption of periosteum blood supply –> necrosis –> sequestra –> new bone forms

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165
Q

What is acute osteomyelitis associated with?

A

Associated with inflammatory bone changes caused by pathogenic bacteria

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166
Q

What is chronic osteomyelitis associated with?

A

Involves bone necrosis

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167
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
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168
Q

what are the signs of acute osteomyelitis?

A
  1. Tender
  2. Warm
  3. Red swollen area around OM
169
Q

what are the signs of chronic osteomyelitis?

A
  1. Acute OM signs
  2. Draining sinus tract
  3. Non-healing ulcers/fracture
170
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
171
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
  4. Blood cultures
172
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

173
Q

How is the stopping of antibiotics determined in osteomyelitis?

A

Guided by ESR and CRP

174
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
175
Q

Why is osteomyelitis difficult to treat?

A

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

176
Q

What is bacteraemia?

A

Bacteria in the blood

177
Q

What is debridement?

A

The removal of damaged tissue

178
Q

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

A

Septic arthritis –> aspirate the joint

179
Q

What is rheumatoid arthritis?

A

An auto-inflammatory synovial joint disease causing symmetrical polyarthritis

180
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
181
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
182
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
183
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
184
Q

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

A

Nodules
Bursitis
Muscle wasting

185
Q

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

A

Dry eyes
Scleritis
Episcleritis

186
Q

RA extra-articular involvement: describe the neurological effects

A

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

187
Q

RA extra-articular involvement: describe the haematological effects

A

Felty’s syndrome (RA + splenomegaly + neutropenia)

Anaemia

188
Q

RA extra-articular involvement: describe the pulmonary effects

A

Pleural effusion

Fibrosing alveolitis

189
Q

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

A

Pericardial rub

Pericardial effusion

190
Q

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

A

Amyloidosis

191
Q

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

A

Vasculitis - infarcts in nail bed

192
Q

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

A
  • Blood for inflammatory markers - ESR and CRP raised
  • Test for anaemia - normochromic normocytic anaemia
  • Test for RF and Anti-CCP
    X-ray
  • Synovial fluid is sterile with high neutrophil count
193
Q

What is rheumatoid factor?

A

An antibody against the Fc portion of IgG

194
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
195
Q

Describe the treatment for rheumatoid arthritis

A
  • NSAIDS and paracetamol
  • Corticosteroids - intra-articular glucocorticoid injections
  • DMARDs (methotrexate)
  • Biological agents (TNF inhibitor - infliximab)
  • Physio and OT
  • Synovectomy
196
Q

What joints tend to be affects in RA?

A

MCP
PIP
Wrist
(DIP often spared)

197
Q

What is gout?

A

Crystal arthritis

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

198
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

199
Q

What joint does gout most commonly affect?

A

Big toe metatarsophalangeal joint

200
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

201
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
202
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
203
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
204
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

205
Q

What are tophi?

A

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

206
Q

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

A

Joint aspiration & polarised light microscopy (needle like negative birefringent crystals),
Increased Urate on blood test
X-ray = rat bite erosions

207
Q

What is the aim of treatment for gout?

A

To get urate levels < 300 mol/L

208
Q

How would you treat acute gout?

A

Ice packs and rest
NSAIDS
Colchicine = anti-gout medication
Corticosteroids - IM or IA

209
Q

Name 3 treatment options for gout

A
  1. Lifestyle modifications - diet, weight loss, reduce alcohol
  2. Allopurinol (xanthine oxidase inhibitor)
  3. NSAIDs or colchicine
    IM prednisolone
210
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

211
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
212
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

213
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

214
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

215
Q

What can cause pseudogout?

A
  1. Hypo/hyperthyroidism
  2. Haemochromatosis
  3. Diabetes
  4. Magnesium levels
216
Q

what is the clinical presentation of pseudogout?

A

SYMPTOMS
hot, swollen, tender joint, usually knees

SIGNS
recent injury to the joint in the history

Typically the wrists and knees

217
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

218
Q

What is the most likely differential diagnosis for pseudogout?

A

Infection

219
Q

Describe the treatment for pseudogout

A
  • high dose NSAIDs - ibuprofen
  • Colchicine - anti-gout
  • IM prednisolone
  • Aspiration, intra-articular steroid injections
220
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

221
Q

What kind of crystals do you see in pseudogout?

A

Positive birefringent calcium pyrophosphate rhomboid crystals

222
Q

What kind of crystals do you see in gout?

A

Monosodium urate crystals = negatively birefringent

223
Q

What kind of crystals fo you see in pseudogout?

A

Calcium pyrophosphate crystals = positively birefringent

224
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

225
Q

Name 4 diseases that fibromyalgia is commonly associated with

A
  1. Depression
  2. Choric fatigue
  3. IBS
  4. Chronic headache
226
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
227
Q

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

A
  1. Hypothyroidism
  2. SLE
  3. Low vitamin D
228
Q

How is fibromyalgia diagnosed?

A

Everything seems normal
11/18 trigger points
Exclude other diagnoses

229
Q

Describe the management of fibromyalgia

A
  • Educate the patient and family
  • CBT and exercise programmes - reset pain thermostat
  • Acupuncture
  • Analgesics - tramadol, codeine
  • Low dose antidepressants (amitriptyline) and anticonvulsants (pregabalin)
230
Q

What is mechanical back pain?

A

Back pain resulting from physical wear and tear

231
Q

Name 3 causes of mechanical back pain

A
  • lumbar disc prolapse
  • osteoarthritis
  • fractures
  • spondylolisthesis
  • heavy manual handling
  • stooping and twisting whilst lifting
  • exposure to whole body vibration
232
Q

Name 3 risk factors of mechanical back pain

A
  1. Psychological distress
  2. Smoking
  3. Dissatisfaction with work
233
Q

Give 3 symptoms of mechanical back pain

A
  • stiff back and scoliosis
  • muscular spasm visible and palpable - lessens when sitting/lying
  • unilateral pain, helped by rest
  • episodes are short-lived/self-limiting
  • sudden onset
  • pain worse in evening
  • exercise aggravates pain
234
Q

Describe the management of mechanical back pain

A

Prevention = education, exercise
Analgesic ladder = paracetamol –> NSAIDS –> codeine –> low dose amitriptyline
Adjuvant procedures –> physio, acupuncture, CBT

235
Q

Define fracture

A

Soft tissue injury with discontinuity of the bone

236
Q

Describe the 3 initial steps in the management of fractures

A
  1. Reduce the fracture –> restore length, alignment and rotation
  2. Immobilisation
  3. Rehabilitation
237
Q

What are the 4 main stages of fractures healing?

A
  1. Haematoma formation
  2. Fibrocatilaganeous callus formation
  3. Bony callus formation
  4. Bone remodelling
238
Q

what are the different types of fracture?

A
  1. Transverse
  2. Linear
  3. Oblique, non-displaced
  4. Oblique, displaced
  5. Spiral
  6. Greenstick (specific to children)
  7. Comminuted
239
Q

Give 5 potential complications of fractures

A
  1. Contamination (infection)
  2. Compartment syndrome
  3. Damage to surrounding structures
  4. Mal union = bone heals wit deformity
  5. Non union = bone fails to heal
  6. Avascular necrosis
  7. Crush syndrome
  8. Cast problems
240
Q

Why is a neck of femur fracture considered so bad?

A

Cuts off the blood supply to the head of the femur = avascular necrosis of head of femur

241
Q

How does a NOF fracture present?

A

Fall
Groin pain
Inability to weight bare
Externally rotated and short leg (on side of fracture)

242
Q

What is the treatment for a NOF fracture?

A 
ANALGESIA = morphine and regional nerve block 
Intracapsular = Total hip replacement or hemi arthroplasty 
Extracapsular = DHS or cannulated hip screws
243
Q

How are ankle fracture classified?

A

By Weber classification
A = fracture below syndesmosis
B = fracture at level of syndesmosis
C = fracture above level of syndesmosis (worst)

244
Q

How do you treat an open fracture?

A 
Tetanus vaccination 
Antibiotics
Cover with saline soaked gauge 
Stabilise 
Debridement 
Surgery as soon as X-ray has been done
245
Q

What is compartment syndrome?

A

Increase in intra-compartmental pressure due to build up of fluid –> pressure on veins causing collapse –> collapse of nerves –> pressure on arteries

246
Q

How does compartment syndrome present?

A

Tense compartment with pain disproportionate to injury and the 5 P’s

  1. Pain
  2. Pallor
  3. Perishingly cold
  4. Pulselessness
  5. Paraesthesia
247
Q

What is the treatment of compartment syndrome?

A

Fasciotomy = relieves pressure

248
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

249
Q

Define sarcoma

A

A rare tumour of mesenchymal origin

A malignant connective tissue neoplasm

250
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
251
Q

Who are primary bone tumours seen in?

A

they are rare - are mainly seen in children and young people

more common in males

252
Q

Give 3 primary bone tumours

A
  1. Osteosarcoma
  2. Fibrosarcoma
  3. Chondrosarcomas
  4. Ewings sarcoma
253
Q

What are secondary bone tumours?

A

Metastases from:

  1. Lungs
  2. Breast
  3. Prostate
  4. Thyroid
  5. Kidney
254
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

255
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

256
Q

What staging is used for bone cancers?

A

Enneking grading

257
Q

How are malignant bone cancers staged using Enneking grading?

A 
G1 = Histologically benign
G2 = Low grade
G3 = High grade
A = intracompartmental
B = extracompartmental
258
Q

How are benign bone cancers staged using Enneking grading?

A 
G1 = Latent
G2 = Active 
G3 = Agressive
259
Q

How are bone cancers treated?

A

MDT management

Benign

  • NSAIDS
  • Bisphosphonates (alendronate) - symptomatic help

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

260
Q

Give 4 local complications with surgery for bone cancers

A
  1. Haematoma
  2. Loss of function
  3. Infection
  4. Local recurrence
261
Q

Where do osteosarcomas usually present?

A

Knee - distal femur, proximal humerus

262
Q

What is an osteosarcoma?

A

Malignant tumour of bone
Spindle cell neoplasm that produce osteoid

rapidly metastases to the lung

263
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
264
Q

What is a chondrosarcoma?

A

A malignant neoplasm of cartilage

265
Q

Name a boney sarcoma that responds well to chemotherapy

A

Ewings sarcoma

266
Q

Where does Ewings sarcoma arise from?

A

mesenchymal stem cells

267
Q

Boney sarcomas make up what percentage of overall sarcomas?

A 
20% = boney 
80% = soft tissue
268
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
269
Q

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

A

Give adjuvant radiotherapy

270
Q

Name 2 NSAIDs

A
  1. Ibuprofen

2. Naproxen

271
Q

Give 3 side effects of NSAIDs

A
  1. Peptic ulcer disease
  2. Renal failure
  3. Increased risk of MI and CV disease
272
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

273
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
274
Q

How do DMARDs work?

A

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

275
Q

Give an example of a DMARD

A

Methotrexate = gold standard
Hydroxycholoquine
Sulfasalazine

276
Q

How often should methotrexate be taken?

A

Once weekly

277
Q

Give 3 potential side effects of methotrexate

A
  1. Bone marrow suppression
  2. Abnormal liver enzymes
  3. Nausea
  4. Diarrhoea
  5. Teratogenic
278
Q

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

A

Folic acid

279
Q

What are cytokines?

A

Short acting hormones

280
Q

Name a TNF blocker

A

Infliximab

Adalimumab

281
Q

Name a monoclonal antibody that binds to CD20 on B cells

A

Rituximab - binds to CD 20 –> B cell depletion

282
Q

Describe the mechanism of action of infliximab

A

Inhibits T cell activation

283
Q

How does alendronate work?

A

Reduces bone turnover by inhibiting osteoclast mediated bone resorption

284
Q

What class of drug is alendronate?

A

Bisphosphonate

285
Q

Name 2 drugs that act on the HMGcoA pathway

A
  1. Bisphosphonates - alendronate

2. Statins - simvistatin

286
Q

Which of the following is a typical clinical feature of osteoarthritis?

a. 60 minutes of early morning stiffness
b. Painful, swelling across the metacarpophalangeal joints and PIP joints
c. Pain in 1st carpometacarpal joints
d. Mobile subcutaneous nodules and points of pressure
e. Alternating buttock pain

A

c. Pain in 1st carpometacarpal joints

Morning stiffness is only 15 mins ish in OA
OA = CMC and DIP joints

287
Q

Which of the following is an extra-articular manifestation of rheumatoid arthritis?

a. Subcutaneous nodules
b. Episcleritis
c. Peripheral sensory neuropathy
d. Pericardial effusion
e. All of the above

A

e. All of the above

288
Q

Which of the following is a classical feature of rheumatoid arthritis on X-ray?

a. Peri-articular sclerosis
b. Sub-chondral cysts
c. Osteophytes
d. Peri-articular erosions
e. New bone formation

A

d. Peri-articular erosions Inflammatory cytokines causing lysis of bone causing joint damage

Peri-articular sclerosis = OA
Sub-chondral cysts = OA
Osteophytes = OA
New bone formation = SpAs)

289
Q

A 53-year-old man presents to you with a 3-day history of pain in his lower ache. The pain started spontaneously, and he first noticed it at work. He works as a builder and has been unable to go to work for the last 3 days and is keen to have a sick note. Physical examination reveals him to be slightly overweight with a BMI of 29, but there are no neurological deficits or spinal deformity and the pain is not easily localised on examination. Which of the following describe the best management?

a. Given his age, he should be referred to a specialist
b. He should be sent for an x-ray to look for any pathological changes in his spine
c. He should not be given a sick note, and advised to return to work straight away
d. He should be reassured and advised to take simple analgesics and return to normal activity as soon as he can manage
e. He should be advised to seek other employment

A

d. He should be reassured and advised to take simple analgesics and return to normal activity as soon as he can manage

290
Q

For a lytic tumour to be visible on X-ray, it must have lost:

a. Greater than 6% bone density
b. Greater than 16% bone density
c. Greater than 60% bone density
d. Greater than 90% bone density
e. 100% bone density

A

c. Greater than 60% bone density

291
Q

A 57-year-old man presents with a 3-day history of a painful 1st MTP joint. ON examination the area is red and very warm. He has a BMI of 32 and hypertension and has had identical episodes before. Which of the following dietary changes would reduce his risk of future similar episodes?

a. Diet with a high red meat content
b. A diet rich in dairy products
c. Drinking >5 cans of non-diet fizzy drinks per day
d. A diet rich in sugary foodstuffs
e. Switching form drinking beer to drinking larger

A

b. A diet rich in dairy products

= GOUT

292
Q

Which of the following is not an autoimmune connective tissue disease?

a. Systemic lupus erythematosus
b. Ehler Danlos syndrome
c. Primary Sjogren’s syndrome
d. Systemic sclerosis
e. Dermatomyositis

A

b. Ehler Danlos syndrome (inherited connective tissue disease)

293
Q

A 23-year-old woman presents with mouth ulcers, fever, painful white fingers and pleuritic chest pain. She is antinuclear antibody (ANA) positive, her ESR is 52 (0-15), and her WCC is low (leucopenic). Which of the following features would you not expect to be associate with her illness?

a. Deforming arthritis
b. Photosensitive rash
c. Seizures
d. Pulmonary embolism
e. Thrombocytosis

A

e. Thrombocytosis

= SLE so would be thrombocytopenia

294
Q

Which of the following is used in the treatment of SLE?

a. Anti-TNF
b. Anti-malarials
c. Ustekinumab (IL12/23 blocker)
d. Sulfasalazine
e. Allopurinol

A

b. Anti-malarials (hydroxycloroquinine)

Others
Ustekinumab (IL12/23 blocker) = SpAs
Sulfasalazine = RA
Allopurinol = Gout

295
Q

An adult male present with a 6-week history of right sided headache. General malaise, early morning stiffness, and pain in his jaw when eating. His CRP is 63 (0-5), ESR 78 (0-15). Which of the following is true about his underlying disease?

a. It is associated with ANCA positivity
b. It typically affects those between 50 and 60 years old
c. It can present with acute sight loss
d. It rarely responds to corticosteroids
e. It is a vasculitis affecting small blood vessels

A

c. It can present with acute sight loss

GIANT CELL ARTERITIS (VASCULITIS)

ANCA = small vessel vasculitis
Giant cell arteritis = patients 70-75 years old

296
Q

Which of the following is now a rare cause for joint infections in infants, due to the standard childhood immunisation schedule in the UK?

a. Staphylococcus Aureus
b. Gp A (B haemolytic) streptococcus
c. Varicella Zoster
d. Rubella
e. Haemophilus Influenzae

A

e. Haemophilus Influenzae

297
Q

A 64-year-old women with T2DM has been struggling with cellulitis of her right forefoot for 4 weeks. After making no progress with oral antibiotics, she has now had 14 days of IV flucloxacillin and co-amoxiclavulanic acid but then pain and erythema persist, and her CRP has only fallen to 47 from its peak of 91. What is the next most appropriate investigation?

a. Blood cultures
b. MRI right forefoot
c. Plain x-ray right forefoot
d. Skin biopsy of right forefoot
e. USS of right forefoot

A

c. Plain x-ray right forefoot

298
Q

Which of the following is a non-inflammatory cause of joint pain?

a. RA
b. Septic arthritis
c. SpAs
d. Fibromyalgia
e. Gout

A

d. Fibromyalgia

299
Q

Which of these is not a feature of RA?

a. NSAIDs help
b. Pain eases with use
c. Effects the DIP joints
d. Pain lasts for an hour or so in the morning
e. Ulnar deviation

A

c. Effects the DIP joints

Symptom of OA

300
Q

Alendronic acid is a bisphosphate used in treatment of osteoporosis. What is the MOA?

a. Cause increased bone deposition
b. Cause reactivation of the metaphysis and epiphysis
c. Inhibit osteoclast activity and cause osteoclast apoptosis
d. Reduce the signalling pathway between osteoblasts and clasts by increasing RANK ligand
e. Increase removal of calcium into the haversian canal within bone

A

c. Inhibit osteoclast activity and cause osteoclast apoptosis

301
Q

Pain big toe = gout. Joint aspiration – what is seen to confirm diagnosis?

a. Tophi
b. Needle shaped crystals which are +ve birefringent
c. Needle shaped crystals which are -ve birefringent
d. Rhomboid shaped crystals which are +ve birefringent
e. Rhomboid shaped crystals which are -ve birefringent

A

c. Needle shaped crystals which are -ve birefringent = Gout

PSEUDOGOUT = Rhomboid shaped crystals which are +ve birefringent

302
Q

3 weeks stiff and painful knee, urethritis and conjunctivitis. What is the most likely cause?

a. Staphylococcus aureus
b. E. coli
c. Streptococcus pneumonia
d. Haemophilus influenzae
e. Chlamydia

A

e. Chlamydia

Reactive arthritis symptoms –> often caused by STI

303
Q

Aching hand arm and pins and needles in thumb, index and middle fingers. Shaking his hand seems to help. What is it?

a. Cervical spine fracture
b. Compression of median
c. Compression of radial
d. C8-T1 lesion
e. Compression of ulnar

A

b. Compression of median = Carpal tunnel syndrome

304
Q

Ankylosing spondylitis, what tissue type is associate with this condition?

a. HLA DQ2
b. HLA B27
c. HLA DR3
d. HLA DR2
e. HLA AD6

A

b. HLA B27

305
Q

Which is most common cause of osteomyelitis?

a. Strep pneumonia
b. Staph aureus
c. Strep pyogens
d. Mycobacterium TB
e. Haemophilus influenzae

A

b. Staph aureus

306
Q

Lupus –> blood test reveal what?

a. Anti-DsRNA positive
b. Raised ESR and CRP
c. Raised ESR but normal CRP
d. ANCA positive
e. ANA negative

A

c. Raised ESR but normal CRP

307
Q

DEXA scan with T score -1.6, what does this mean?

a. Normal
b. Osteopenia
c. Osteoporosis
d. Severe osteoporosis
e. Paget’s disease

A

b. Osteopenia

308
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

309
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

310
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

311
Q

what are the complications of rheumatoid arthritis?

A

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

312
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

313
Q

what are the risk factors for gout?

A

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

314
Q

what are the complications of gout?

A

Infection in the tophi

Destruction of the joint

315
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
RA
CKD
Children → upper resp tract  or varicella infection
316
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

317
Q

what are the risk factors for ankylosing spondylitis?

A

HLA-B27

environment - klebsiella, salmonella, shigella

318
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

319
Q

what is psoriatic arthritis?

A

Inflammatory arthritis associated with psoriasis

1 in 5 patients with psoriasis have psoriatic arthritis

320
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

321
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

322
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)

323
Q

what treatment should be used if reactive arthritis relapses?

A

methotrexate or sulfasalazine

324
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

325
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

326
Q

what are the complications for SLE?

A

Cardiac, lung, kidney involvement.

Widespread inflammation causing damage.

327
Q

what is the epidemiology of fibromyalgia?

A

women,

poor socioeconomic status, 20-50 year old

328
Q

what is the the pathophysiology of fibromyalgia?

A

Unknown, possibly pain perception/hyper excitability of pain fibres

329
Q

what are the complications of fibromyalgia?

A
  • can really affect quality of life
  • anxiety, depression, insomnia
  • opiate addiction
330
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

331
Q

what is rickets?

A

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

332
Q

what is the pathophysiology of osteomalacia?

A

Calcium deficiency is usually due to vitamin D deficiency

333
Q

what is the clinical presentation of osteomalacia?

A
  • Bone pain and tenderness. Dull ache that is worse on weight-bearing exercises
  • Fractures – esp NOF
  • Muscle weakness - waddling gait, difficulty with stairs
334
Q

what is the clinical presentation of rickets?

A

Growth retardation
Hypotonia
Knock-kneed, bow-legged

335
Q

what are the investigations for osteomalacia?

A

X-ray → loss of cortical bone – defective mineralisation
Bloods → Low calcium and phosphate
Bone biopsies → incomplete mineralization

336
Q

what is the management of osteomalacia?

A

Vitamin D supplements – rapid mineralization of bone and resolution of symptoms
If dietary insufficiency – calcium D3 forte
If due to malabsorption, give IM calcitriol
If due to renal disease give alfacalcidol

337
Q

what are the causes of osteomalacia?

A

● Hypophosphatemia due to hyperparathyroidism secondary to Vit D deficiency ● Vit D deficiency due to malabsorption, poor diet, lack of sunlight
● Renal disease means there’s inadequate conversion of 25-hydroxy-Vitamin D to 1,24-hydroxy vitamin D
● Drug induced – increased vitamin D breakdown
● Liver disease – reduced hydroxylation of vitamin D
● Tumour induced

338
Q

what is paget’s disease?

A

● Focal disorder of bone remodelling - disorder of bone turnover
● Also known as osteitis deformans

339
Q

what is the pathophysiology of paget’s disease?

A

Excessive bone turnover (formation + resorption) due to excessive osteoblast + osteoclast activity
Leads to patchy areas high density (sclerosis) + low density (lysis)
Enlarged + misshapen bones → risk of fracture

340
Q

what is the clinical presentation of paget’s disease?

A

Bone pain
Bone deformity
Fractures
Hearing loss (if bones of ear affected)

341
Q

what is the epidemiology of paget’s disease?

A

● Incidence increases with age – rare under 40yrs
● Affects up to 10% of those over 90
● Females > males

342
Q

what are the risk factors for paget’s disease?

A

latent viral infection (e.g. measles) in genetically susceptible people
family history

343
Q

what are the investigations for paget’s disease?

A

X-ray

   - Bone enlargement + deformity
   - Osteoporosis circumscripta (well defined osteolytic lesions)
   - Cotton wool appearance of skull (poorly defined areas of sclerosis + lysis) 
   - V-shaped defects in long bones

Bloods

   - Raised ALP
   - Normal calcium + phosphate
344
Q

what is the management for paget’s disease?

A

Bisphosphonates
NSAIDs for bone pain
Calcium + Vit D supplements

345
Q

what are the complications of paget’s disease?

A

Osteosarcoma
Spinal stenosis + cord compression
hydrocephalus

346
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

347
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
348
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 or
    temporary vision loss
349
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.

350
Q

what is the pathophysiology of Marfan syndrome?

A

Autosomal dominant condition
Affects gene involved in creating fibrillin
fibrillin is an important component of connective tissue therefore people with Marfan have features resulting from abnormal connective tissue

351
Q

what are the risk factors for Marfan syndrome?

A

Family history

352
Q

what is the clinical presentation of Marfan syndrome?

A
  • tall stature
  • long limbs
  • long fingers
  • hypermobility
  • pectus carinatum/pectus excavatum
  • high arch palate
353
Q

what are the investigations for Marfan syndrome?

A

Physical exam (e.g. S&S above, heart murmur,..)
Can do echo to check heart, valves and aorta conditions
MRI
Eye exam

Ghent criteria

354
Q

what is the management for Marfan syndrome?

A

Lifestyle changes: avoid intense exercise, avoid caffeine
Beta-blockers / ARBs
Yearly echo / review by ophthalmologist

355
Q

what are the complications for Marfan syndrome?

A
  • Mitral/ aortic valve prolapse (with regurgitation)
  • Aortic aneurysms
  • Lens dislocation
  • Pneumothorax
  • GORD
  • scoliosis
356
Q

what is the Ghent criteria for Marfan syndrome?

A

Major: enlarged aorta, lens dislocation, Fx, at least 4 skeletal problems

Minor: myopia, loose joints, high arched palate

357
Q

what is ehler’s danlos syndrome?

A

EDS is an umbrella term used for a group of genetic conditions that cause defects in collagen, resulting in hypermobility of joints and abnormalities in connective tissue such as the skin, bones, blood vessels and organs

358
Q

how many types of EDS are there? which is most common?

A

13 types

hypermobile EDS = most common

359
Q

which is the most dangerous type of EDS?

A

vascular EDS - need monitoring for vascular abnormalities, very prone to rupture

360
Q

what are the risk factors for EDS?

A

family history

361
Q

what is the clinical presentation of EDS?

A

Varies between types but generally:

  • Joint hypermobility
  • Easily stretched skin (hyperextensibility)
  • Easy bruising
  • Chronic joint pain
  • Re-occurring dislocations
362
Q

what are the investigations for EDS?

A

beighton score - assess hypermobility

363
Q

what is the management for EDS?

A

Physiotherapy
Occupational therapy
Psychological support (chronic condition+pain)

364
Q

what is antiphospholipid syndrome?

A
  • Syndrome characterised by thrombosis (arterial or venous) and/or recurrent
    miscarriages with positive blood tests for antiphospholipid antibodies (aPL) - hypercoagulable state
365
Q

what is the epidemiology of antiphospholipid syndrome?

A
  • 20-30% are associated with SLE
  • more common in females
  • more often primary disease
366
Q

what are the risk factors for antiphospholipid syndrome?

A
  • diabetes
  • hypertension
  • obesity
  • female
  • underlying autoimmune condition
  • smoking
  • oestrogen therapy
367
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
368
Q

what is the pathophysiology of antiphospholipid syndrome?

A
  • Antiphospholipid antibodies (aPL) play a role in thrombosis by binding to
    phospholipid on the surface of cells such as endothelial cells, platelets and
    monocytes
  • Once bound, this change alters the functioning of those cells leading to
    thrombosis 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)
369
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
370
Q

what is the treatment for antiphospholipid syndrome?

A
  • long term warfarin

- Pregnant women on low molecular weight heparin (e.g. enoxaparin) + aspirin

371
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,…)
372
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

373
Q

what are the complications of wegener’s granulomatosis?

A

Glomerulonephritis

374
Q

what is the most common primary bone malignancy in children?

A

osteosarcoma

375
Q

what condition is osteosarcoma associated with?

A

Paget’s disease

376
Q

what is the appearance of osteosarcoma on x-rays?

A

bone destruction and formation, soft tissue calcification produces a sunburst appearance

377
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

378
Q

what is the epidemiology of Ewing’s sarcoma?

A

● Very rare

● Average age of onset 15

379
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

380
Q

where does chrondosarcoma commonly present?

A

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

381
Q

what is the clinical presentation of chrondrosarcoma?

A

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

382
Q

which is the most common sarcoma in adults?

A

chondrosarcoma

383
Q

which types of malignancy cause bone pain?

A
  • multiple myeloma
  • lymphoma
  • primary bone tumours
  • metastases - secondary bone tumour
384
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
385
Q

what is the prophylactic treatment for antiphospholipid syndrome?

A

aspirin or clopidogrel for people with aPL

386
Q

what is the epidemiology of polymyalgia rheumatica?

A
  • systemic disease of elderly
  • affects those over 50 years
  • more common in females
387
Q

what are the risk factors for polymyalgia rheumatica?

A
  • SLE

- polymyositis/dermatomyositis

388
Q

what is the clinical presentation of polymyalgia rheumatica?

A
  • sudden onset severe pain and stiffness of shoulders and neck, hips and lumbar spine
  • symptoms are worse in morning -> last 30 mins to several hours
  • mild polyarthritis of peripheral joints
  • 1/3 experience fever, fatigue, weight loss, depression
389
Q

what are the investigations for polymyalgia rheumatica?

A
  • Clinical history is usually diagnostic and the patient is ALWAYS OVER 50
  • BOTH ESR & CRP RAISED - diagnostic
  • ANCA negative
  • Serum alkaline phosphatase raised
  • Mild normochromic, normocytic anaemia may be present
  • Temporal artery biopsy:
    • Shows giant cell arteritis in 10-30% cases
390
Q

what is the treatment for polymyalgia rheumatica?

A

corticosteroids - ORAL PREDNISOLONE

LANSOPRAZOLE, ALENDRONATE and Ca2+ and vitamin D - GI and bone protection

391
Q

which type of fracture is specific to children?

A

greenstick fracture

392
Q

what is the epidemiology of scleroderma?

A
  • more common in females
  • peak incidence = 30-50yrs
  • rare in children
393
Q

what are the risk factors for scleroderma?

A
  • exposure to vinyl chloride, silica dust, rapeseed oil, trichloroethylene
  • bleomycin
  • genetic
394
Q

what is polymyositis?

A

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

395
Q

what is dermatomyositis?

A

polymyositis with skin involvement

396
Q

what is the epidemiology of polymyositis/dermatomyositis?

A
  • Very rare
  • Both affect adults and children
  • More common in FEMALES than males
397
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
398
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
399
Q

what are the investigations for polymyositis/dermatomyositis?

A
  • muscle biopsy - fibre necrosis and inflammatory cell infiltrate (diagnostic)
  • serum creatine kinase, LDH, aldolase raised
  • ESR not raised
  • ANA positive
400
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
401
Q

how many different types of juvenile idiopathic arthritis are there?

A

7

  • synovitis
  • persistent oligoarthritis
  • extended oligoarthritis
  • RF negative polyarthritis
  • RF positive polyarthritis
  • enthesitis related JIA
  • stills disease
402
Q

what is the treatment for juvenile idiopathic athritis?

A
  • non medical - info and education, physio, psychology
  • medical
    • steroid injections
    • NSAIDs - ibuprofen
    • methotrexate
    • TNF-alpha inhibitors - IV infliximab
403
Q

what are children with juvenile idiopathic arthritis at risk of developing?

A
  • uveitis
  • inflammation of the lining of the eye
  • can result in blindness - need ophthalmic screening every 3 months
404
Q

what are the red flags for serious spinal pathology?

A
  • <20 or >50
  • violent trauma
  • constant, progressive, non-mechanical pain
  • thoracic pain
  • systemic steroid, drug abuse, HIV
  • systemically unwell, weight loss
  • persisting severe restriction of lumbar flexion
  • widespread neurology
  • structural deformity
405
Q

what is vertebral disc degeneration

A

Prolapse of the intervertebral disc results in acute back pain (LUMBAGO)

406
Q

what is the epidemiology of vertebral disc degeneration

A

Disease of younger people (20-40 yrs) since the disc degenerates with age
and in the elderly it is NO LONGER ABLE TO PROLAPSE

407
Q

what is the clinical presentation of vertbral disc degeneration?

A
  • sudden onset severe back pain - following strenuous activity
  • pain is related to position and aggravated by movement
  • muscle spasm leads to sideways tilt when standing
408
Q

how does an S1 root lesion present (vertebral disc degeneration)?

A
  • pain in buttock, back of thigh to ankle/foot
  • lost ankle jerk reflex
  • diminished straight leg raising
409
Q

how does an L5 root lesion present (vertebral disc degeneration)?

A
  • pain in buttock to lateral aspect of leg and top of foot

- diminished straight leg raising

410
Q

how does an L4 root lesion present (vertebral disc degeneration)?

A
  • pain in lateral aspect of thigh to medial side of calf
  • loss of knee jerk reflex
  • positive femoral stretch test
411
Q

what is the treatment for vertebral disc degeneration?

A
  • bed rest on firm mattress, analgesia and epidural corticosteroid
  • surgery if severe
  • physiotherapy
  • weight reduction
412
Q

what is polyarteritis nodosa?

A

medium vessel vasculitis

413
Q

what is the epidemiology of polyarteritis nodosa?

A
  • rare in UK
  • usually occurs in middle-aged men
  • male>female
  • associated with hep B
414
Q

what are the risk factors for polyarteritis nodosa?

A
  • male
  • hep B
  • RA, SLE, scleroderma
415
Q

what is the pathophysiology of polyarteritis nodosa?

A
  • Necrotising vasculitis that causes aneurysms and thrombosis in medium
    sized arteries, leading to infarction in affected organs
  • Has severe systemic symptoms
416
Q

what is the clinical presentation of polyarteritis nodosa?

A
  • Peripheral neuropathy – mononeuritis multiplex
  • Cutaenous/subcut nodules (hallmark feature)
  • Abdo pain
  • Unilateral orchitis - testicle inflammation (characteristic feature)
  • Livedo reticularis
  • HTN
417
Q

what are the investigations for polyarteritis nodosa?

A
  • ↑ESR and/or CRP
  • HBsAg
    Biopsy: shows transmural fibrinoid necrosis
418
Q

what is the treatment for polyarteritis nodosa?

A

If Hep B negative – corticosteroids + cyclophosphamide

If Hep B positive – antiviral agent, plasma exchange and corticosteroids

419
Q

what are the complications of polyarteritis nodosa?

A 
GI perforation & haemorrhages
Arthritis
Renal infarcts
Strokes 
MI

MY REVISION - ALL PHASES (26 decks)

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