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Phase 2 > Rheumatology > Flashcards

Rheumatology Flashcards

1
Q

Define rheumatology

A

Medical management of musculoskeletal disease

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2
Q

Define inflammation

A

Reaction of the micro-circulation that results in the movement of fluid and WBC’s into the extra-vascular tissue which causes the release of pro-inflammatory cytokines

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3
Q

What are the 4 pillars of inflammation

A

Red (rubor)
Pain (Dolor)
Hot (Calor)
Swollen (Tumor)

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4
Q

How might inflammation present in the joints

A

Hot, painful red and swollen joint
Stiffness
Poor mobility and function
Deformity

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5
Q

What are the characteristics of an inflammatory rheumatological disease

A

Pain eases with use
Stiffness (Significant >60mins and early morning and at rest)
Swelling
Hot and red
Young, people with psoriasis and family history commonly affected
Joint distribution is commonly in hands and feet
Responds to NSAIDs

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6
Q

What are the characteristics of a degenerative rheumatological disease

A

Pain increases with use
Stiffness that is not prolonged <30 mins and occurs in morning and evening
Swelling
Not clinically inflamed
Older patients with prior occupation or sport affected
less convincing response to NSAIDs

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7
Q

Where does rheumatoid arthritis most commonly affect

A

Synovial joints

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8
Q

What are the some of the characteristic signs of rheumatoid arthritis

A

Ulnar drift
Polyarthritis
Swan neck deformity
Erosion on X-ray

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9
Q

Where does nodal oestoarthritis commonly affect

A

begins at the base of the tumblebug and affects the distal interphalangeal joints

Proximal interphalangeal joints = Bouchards nodes

Distal interphalangeal joints = Hebedens nodes

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10
Q

What is Raynaud’s

A

White areas in the fingers due to a change in temperature, particularly cold which causes the clamping down of capillaries and subsequent hypoxia

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11
Q

What are the enthesitis

A

where the muscle joins the bone

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12
Q

What is dactylitis

A

Inflammation of all joints and tendon sheaths of toe or finger = sausage digits

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13
Q

What investigations might you do insomene with a suspected rheumatological condition

A 
Erythrocyte sedimentation rate 
CRP 
Autoantibodies 
 - Rheumatoid factor 
 - Anti-cycluc citrullinated peptide
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14
Q

What antibody might you see in someone with lupus

A

ANA

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15
Q

Give 3 causes of inflammatory joint pain.

A
  1. Autoimmune disease e.g. RA, vasculitis, connective tissue disease.
  2. Crystal arthritis.
  3. Infection.
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16
Q

Give 2 causes of non-inflammatory joint pain.

A
  1. Degenerative e.g. osteoarthritis.

2. Non-degenerative e.g. fibromyalgia.

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17
Q

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

A

Inflammatory pain tends to ease with use whereas degenerative pain increased with use.

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18
Q

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

A

In inflammatory pain you are likely to see synovial swelling. There is often no swelling in degenerative pain.

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19
Q

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

A

Inflammation leads to increased fibrinogen which means the RBC’s clump together. The RBC’s therefore fall faster and so you have an increased ESR.

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20
Q

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

A

Inflammation leads to increased levels of IL-6. CRP is produced by the liver in response to IL-6 and therefore is raised.

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21
Q

What are seronegative spondyloarthropathies

A

Group of inflammatory arthritides affecting the spine and peripheral joints without the production of rheumatoid factor and associated with HLA-B27

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22
Q

What is HLA-B27

A

Class 1 surface antigen involved with MHC and function as an APC

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23
Q

What conditions are involved in seronegative spondyloarthopathies

A 
Ankylosing Spondylitis 
Psoriatic Arthritis 
Reactive arthritis 
Enteropathic arthritis
Juvenile Idiopathic arthritis
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24
Q

What are the common features of seronegative spondyloarthropathies

A 
Axial arthritis and sacroilitis 
Asymmetrical large joint oligoarthritis/monoarthritis 
Enthesitis 
Dactylitis 
Iritis 
Psoriaform rashes 
Oral ulcers 
Aortic regurgitation
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25
Q

Why is B27 linked with disease

A

Molecular mimicry
Misfolding theory
HLA-B27 heavy chain homodimer hypothesis

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26
Q

Describe the molecular mimicry theory

A

Infection leads to an immunee response - infectious agent has similar peptides to HLA-B27 molecule leading to an autoimmune response against HLA-B27

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27
Q

Describe the misfolding theory

A

Unfolded HLA-B27 proteins accumulate in the endoplasmic reticulum and trigger the ER unfolded protein response which causes IL-23 release and triggers proinfllamtoy response via interleukin 17+ T-lymphocytes

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28
Q

Describe the HLA-B27 heavy chain homodimer hypothesis

A

B27 chains form stable dimers and dimerise and accumulate in the ER which stimulates the ER unfolded protein response
Heavy chains bind immune regulators such as NK receptors causing expression and survival of leukocytes

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29
Q

What is the pneumonic for clinical features of seronegative spondyloarthropathies

A

SPINEACHE

Sausage digit = dactylics 
Psoriasis 
Inflammaotory back pain 
NSAID good response 
Enthesitis (Heel) 
Arthritis 
Crohns/Ulcerative colitis 
HLA-B27
Eye - uveitis
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30
Q

What is ankylosing spondylitis

A

Chronic disease of unknown aetiology characterised by stiffening and inflammation of the spine and the sacroiliac joints leading to joint fusion

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31
Q

Describe the epidemiology of ankylosing spondylitis

A

It is more common in men that women and presents in men earlier around their late teens and early 20’s

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32
Q

Describe the genetic basis of ankylosing spondylitis

A

95% of people who have the condition re HLA-B27+ve

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33
Q

Describe the presentation ankylosing spondylitis

A

Gradual onset back pain that radiates from the sacro-iliac joints (Sacrolitis) to the hips and the buttocks - pain is often worse @ night with morning stiffness and is relieved by exercise

Progressive loss of all spinal movements
Development of kyphosis and neck hyperextension
Enthesitis
Costochondritis

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34
Q

What are the extra-articular manifestations of ankylosing spondylitis

A

Osteoporosis
Acute iritis/anterior uveitis
Aortic valve incompetence
Apical pulmonary fibrosis

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35
Q

What are the investigations for someone with suspected ankylosing spondylitis

A

Radiological Changes (X-ray and MRI)

  • Sacroilitis = irregularities, sclerosis and erosions
  • Vertebra = Corner erosions, syndesmophwytes
  • Bamboo spone

DEXA scan and CXR

HLA-B27 Test

FBC (Anaemia, Increased ESR, CRP and HLA-B27 +ve)

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36
Q

What is the management of ankylosing spondylitis

A 
Exercise 
Physio
Medical 
 - NSAIDs 
 - Anti-TNF = Infiliximab
 - Local steroid injections 
 - Bisphosphonates 
 - IL-17 blockers 
Surgical = hip replacement to decrease pain and increase mobility
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37
Q

Describe some of the clinical features of psoriatic arthritis

A 
Asymmetrical oligoarthritis 
Distal arthritis of the DIP joints 
Symmetrical polyarthritis 
Arthritis mutilans 
Dactylitis 
Psoriatic plaques 
Nail changes 
 - Pitting 
 - Subungual hyperkeratosis 
 - onchyolysis 
Enthesitis (Achilles Tendon and plantar fasciitis)
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38
Q

What changes of X-ray might you see in psoriatic arthritis

A

Erosion leading to pencil in cup deformity of the nails

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39
Q

What is the treatment of psoriatic arthritis

A

NSAIDs - ibuprofen
DMARD = Sulfasalazine, methotrexate and cyclosporin
Anti-TNF - Infiliximab
IL-12/23 blockers - ustekinumab

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40
Q

With what tissue type are all spondyloarthritis conditions associated?

A

They are all associated with tissue type HLAB27

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41
Q

What is the general treatment for all spondyloarthritis?

A

Initially DMARDs and then biological agents if DMARDs fail e.g. TNF blockers.

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42
Q

Describe the pathophysiology of ankylosing spondylitis.

A

Inflammation of spine -> erosive damage -> repair/new bone formation -> irreversible fusion of spine.

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43
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 SPINEACHE symptoms.
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44
Q

Give 3 locations that psoriasis commonly occurs at.

A
  1. Elbows.
  2. Knees.
  3. Fingers.
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45
Q

Define reactive arthritis

A

Sterile inflammation of the synovial membrane, tendons and fascia triggered by an infection at a distant site, usually GI or genital.

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46
Q

What gut infections are associated with reactive arthritis?

A

Campylobacter
Salmonella
Shigella
Yersinia

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47
Q

What STIs are associated with reactive arthritis

A

Chlamydia
Ureaplasma
HIV

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48
Q

Describe the clinical presentation of reactive arthritis

A 
Asymmetrical lower limb oligoarthritis - esp knee 
Iritis and conjunctivitis 
Keratoderma blenorrhagica 
Circinate balanitis 
Enthesitis 
Mouth ulcers 
Sterile urethritis
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49
Q

What are the investigations for someone with reactive arthritis

A

Increased CRP and ESR

Stool culture if diarrhoea

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50
Q

What is the management of reactive arthritis

A

NSAIDs and steroids
Relapse may require sulfsalazine and methotrexate
Antibiotics to treat infection

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51
Q

Enteropathic arthritis is associated with patients of what other disease

A

IBD - Crohns or UC

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52
Q

What is the presentation of enteropathic arthritis

A

Asymmetrical Large joint oligoarthritis mainly affecting lower limbs
Sacroilitis may occur

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53
Q

What is the treatment of enteropathic arthritis

A

Treat the IBD
NSAIDs and articular steroids for arthritis
Colectomy for remission in UC

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54
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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55
Q

What is the aetiology of JIA?

A

Unknown - idiopathic!

However, it is autoimmune so there are genetic factors associated.

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56
Q

Why is it important to check the eyes in JIA?

A

The lining of the eyes and the joints is very similar. Children with JIA are at a high risk of developing uveitis!

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57
Q

What type of JIA affects <4 joints and is usually ANA positive?

A

Oligoarthritis.

High risk of developing uveitis!

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58
Q

What JIA is similar to adult ankylosing spondylitis?

A

Enthesitis related JIA - inflammation of where the tendon joins a bone. HLAB27 positive.

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59
Q

Describe the non-medical treatment for JIA.

A
  1. Information.
  2. Education.
  3. Support.
  4. Liaison with school.
  5. Physiotherapy.
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60
Q

Describe the medical treatment for JIA.

A
  1. Steroid joint injections.
  2. NSAIDS.
  3. Methotrexate.
  4. Systemic steroids.
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61
Q

Give 5 potential consequences that can occur if you fail to treat JIA.

A
  1. Damage.
  2. Deformity.
  3. Disability.
  4. Pain.
  5. Bony overgrowth.
  6. Uveitis.
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62
Q

What is vasculitis?

A

Inflammation and necrosis of blood vessel walls with subsequent impaired blood flow.

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63
Q

What are the consequences of vasculitis

A

Vessel wall destruction = haemorrhage

Endothelial injury = thrombosis and infarction

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64
Q

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

A

Neutrophils and giant cells.

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65
Q

What are the two different systems used for classifying vasculitis

A

Chapel Hill

By vessel size

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66
Q

Chapel Hill classification: give an example of a large artery primary disorder.

A

Giant cell arteritis

Takayasu’s Arteritis

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67
Q

Chapel Hill classification: Give an example of a medium vessel disorder

A

Polyarteritis nodosa

Kawasakis Disease

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68
Q

Chapel hill classification: Give an example of a small vessel disorder

A

Churg-strauss
Wegners granulomatosis
Goodpasture’s disease

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69
Q

How are the small vessel vasculitis’s categorised

A

By the presence of certain anti-neutrophil cytoplasmic antibodies (ANCA)

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70
Q

Define giant cell arteritis

A

Granulomatous inflammation of aorta, external carotid branches

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71
Q

What are the two types of giant cell arteritis

A

Cranial GCA

Large vessel GCA

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72
Q

Describe the epidemiology of giant cell arteritis

A

Affects those over 50 more commonly
Incidence increases with age
Twice as common in women

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73
Q

What are the features of Giant cell arteritis

A 
Systemic signs (Fever, malaise, fatigue)
Visual loss - diplopia 
Headache (Abrupt, temporal, unilateral)
Temporal artery and scalp tenderness 
Jaw and tongue claudication 
Amaurosis fugax
Prominent temporal artery pulsation 
Polymyalgia 
Limb claudication
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74
Q

What might you find on clinical investigation in someone with giant cell arteritis?

A
  1. Palpable and tender temporal arteries with reduced pulsation.
  2. Sudden monocular visual loss, the optic disc is pale and swollen.
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75
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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76
Q

What investigations might you do in someone who you suspect has giant cell arteritis?

A
  1. Bloods for inflammatory markers e.g. CRP, ESR.

2. Temporal artery biopsy.

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77
Q

What is the management for giant cell arteritis

A

Prompt corticosteroids - prednisolone.

  • Methotrexate is sometimes adeed.
  • Osteoporosis prophylaxis is important e.g. lifestyle advice and vitamin D.
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78
Q

What is the pathophysiology of Giant cell arteritis

A
  1. Activation of dendritic cells in adventitia
  2. Recruitment and activation of T cells
  3. Recruitment of CD8+ and monocytes
  4. Vascular damage and remodelling
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79
Q

Define Wegner’s Granulomatosis

A

Rare, life threatening multi system necrotising granulomatous disease causing damage to predominantly small arteries

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80
Q

Is Wegener’s granulomatosis associated with c-ANCA or p-ANCA?

A

c-ANCA.

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81
Q

What organ systems can be affected by 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 URT?

A
  • Sinusitis.
  • Otitis.
  • Epistaxis
  • Saddle nose deformity
  • Nasal crusting.
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83
Q

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

A 
Cough
Haemoptysis 
PLeuritis 
- Pulmonary haemorrhage/nodules.
- 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.
Haematuria
Proteinuria

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85
Q

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

A

Palpable purpura

Vasculitic rash

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86
Q

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

A
  • Uveitis.
  • Scleritis.
  • Episcleritis.
  • ocular keratitis
  • Conjunctivitis
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87
Q

What is the investigations for Wagner’s granulomatosis

A

cANCA
Dipstick for haematuria and proteinuria
CXR = Bilateral nodular and cavity infiltrates

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88
Q

What is the management of Wagner’s granulomatosis

A

Steroids, methotrexate and cyclophosphamide
Induction of remission = cyclophosphamide/rituximab/ glucocorticoids and plasma exchange

Maintenance of remission = DMARDS, Rituximab, glucocorticoid taper

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89
Q

What is the pathophysiology of the ANCA positive Vasculidities (Wegners and Churg strauss

A

Necrotising granulomatous vasculitis affecting the arterioles and venules
- ANCA’s can activate primed circulating neutrophils which lead to fibrin deposition in vessel wall and deposition of destructive inflammatory mediators

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90
Q

Define osteoarthritis

A

Non-inflammatory degenerative joint disorder characterised by progressive loss of hyaline articular cartilage and formation of new bone

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91
Q

What are the risk factors for the development of osteoarthritis

A
  1. Old age
  2. Obesity - pro inflammatory state
  3. Predisposing joint abnormality
  4. Family history
  5. Trauma
  6. Occupation
  7. Abnormal biomechanics (Hypermobility)
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92
Q

Where is osteoarthritis most common

A

In the synovial joints

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93
Q

What are the two classifications of osteoarthritis

A

Primary - no underlying causes

Secondary - known underlying cause suc as obesity

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94
Q

Name a few locations where osteoarthritis is common

A 
Knees
Hips 
DIPs 
PIPs
Thumb carpometacarpal joint
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95
Q

What are the most important cells responsible for OA?

A

Chrondrocytes.

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96
Q

Name 5 symptoms of osteoarthritis

A
  1. Morning stiffness (<30 minutes).
  2. Pain - aggravated by activity and worse at night and with rest
  3. Tenderness.
  4. Walking and ADLs affected.
  5. Joint swelling and bony enlargement.
  6. Deformities.
  7. Crepitus.
  8. Decreased range of movement and functional impairment
  9. Asymmetrical
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97
Q

What are the signs of osteoarthritis

A

Bouchards nodes at PIPJ
Heberdens nodes at DIPJ
Thumb CMC squaring
Fixed flexion deformity

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98
Q

What is the diagnostic investigation for OA

A

X-ray

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99
Q

Give 5 radiological features associated with OA.

A
  1. Joint space narrowing.
  2. Osteophyte formation.
  3. Sub-chondral sclerosis.
  4. Sub-chondral cysts.
  5. Abnormalities of bone contour.
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100
Q

What is the non-medical management for OA

A 
Education 
Decrease Exercise, increase rest 
Weight loss
Physio
Walking aids, supportive footwear
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101
Q

What is the pharmacological management of OA

A
  • NSAIDS (topical better than PO).
  • Paracetamol.
  • Intra-articular steroid injections.
  • DMARDs if there is an inflammatory component.
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102
Q

Describe the surgical management of OA

A
  • Arthroscopy for loose bodies.
  • Osteotomy (changing bone length).
  • Arthroplasty (joint replacement).
  • Fusion (usually ankle and 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 of this?

A

This is probably due to a loose body e.g. a bone or cartilage fragment.

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105
Q

What is the treatment for loose bodies?

A

Arthroscopy.

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106
Q

Give an example of an inherited connective tissue disease.

A
  1. Marfan’s syndrome.

2. Ehler Danlos syndrome.

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107
Q

Give an example of an autoimmune connective tissue disease.

A
  1. SLE.
  2. Systemic sclerosis.
  3. Sjögren’s syndrome.
  4. Dermatomyositis.
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108
Q

Describe the pathophysiology and common features of marfan’s syndrome

A

Abnormal fibrillar production

  • long limbs
  • pectus excavatum
  • aortic root enlargement
  • arachnodactyly
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109
Q

Describe the pathophysiology and common features of Ehlers danlos syndrome

A

Abnormal collagen production

  • stretchy skin
  • joint hyper-mobility
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110
Q

Define SLE

A

Systemic lupus erythamatosus is an autoimmune multi system inflammatory disease in which auto-antibodies to a variety of auto-antigens result in the formation and desposition of immune complexes

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111
Q

What are the causes of lupus

A

Interplay between EBV and genetics
Drugs (Isoniazid, hydralazine and anti-TNF)
Genetic association with HLA DR2, DR3 and C4 A null gene

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112
Q

What is the epidemiology of SLE

A

More prevalent in females
most common around child bearing age
More common in afro-caribbeans and asians

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113
Q

What are the symptoms of lupus

A
  1. Arthritis that is symmetrical, non-erosive and affects the peripheral joints
  2. Renal - proteinuria and BP increase due to lupus nephritis
  3. ANA +ve in 95%
  4. Serositis
    - Pericarditis
    - Pleuritis
  5. Haematological
    - Neutro and lymphocytopaenia
    - Thrombocytopenia
  6. Reynauld’s
  7. Mouth ulcers
  8. Malar Butterfly rash
  9. Neurological
    - Seizures
    - Psychosis
  10. Constitutional = Fatigue, weight loss, fever and myalgia
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114
Q

Describe the pathogenesis of SLE.

A
  • Inefficient phagocytosis means cell fragments are transferred to lymphoid tissue where they are taken up by APC. T cells stimulate B cells to produce antibodies against self-antigens.
  • Immune complex deposition -> neutrophil and cytokine influx -> inflammation and tissue damage.
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115
Q

What can cause thrombosis in patients with SLE?

A

The presence of antiphospholipid antibodies.

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116
Q

What autoantibody is specific to SLE?

A

Anti-dsDNA.

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117
Q

Describe the immunology of lupus

A

95% are ANA+ve
dsDNA is very specific
Anticardiolipin +ve

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118
Q

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

A

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

  1. Blood count may show normocytic anaemia; neutropenia; thrombocytopaenia. Raised ESR, normal CRP.
  2. Serum autoantibodies: ANA, anti-dsDNA.
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119
Q

Describe the non-medical treatment for SLE.

A
  • Education and support.
  • UV protection.
  • Screening for organ involvement.
  • Reduce CV risk factors e.g. smoking cessation
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120
Q

Describe the pharmacological treatment for SLE.

A
  • Corticosteroids.
  • NSAIDS.
  • Anti-malarials (DMARDs).
  • Anticoagulants (for those with antiphospholipid antibodies).
  • Biological therapy targeting B cells e.g. rituximab.
    Treat the proteinuria with ACEi
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121
Q

What is systemic sclerosis

A

Excess collagen production leading to inflammation, vasculopathy and autoantibody production

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122
Q

Describe the epidemiology of systemic sclerosis

A

Females affected more than males

30-50 years most common

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123
Q

What are the two types of systemic sclerosis

A

Limited (70%)

Diffuse (30%)

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124
Q

What are the symptoms of limited systemic sclerosis (CREST)

A

Calcinosis
Raynaud’s
Oesophageal and gut dysmotility
Sclerodactyly (Tightening and thick skin on fingers and toes
Telangiectasia - dilated facial spider veins
Skin involvement is limited to the face, hands and feet

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125
Q

What are the symptoms of diffuse systemic sclerosis

A 
Diffuse skin involvement 
Organ fibrosis 
 - GOR, aspiration, dysphagia 
 - lung fibrosis and pulmonary hypertension 
Cardiac arrthymias 
Renal = acute hypertensive crisis 
Short reynaulds history
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126
Q

What are the ivestigations for someone with systemic sclerosis

A

FBC (anaemia) U+E (renal impairment
Urine = dipstick’
Imaging
- CXR (Cardiomegaly, bibasal fibrosis)
- Hands = calcinosis
- Ba swallow shows impaired oesophageal motility
ECG and Echo show evidence of pulmonary hypertension

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127
Q

What is the conservative management of systemic sclerosis

A

Exercise and skin lubricants

Hand warmers

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128
Q

What is the medical management of systemic sclerosis

A
  1. Immunosuppression
  2. Reynauld’s needs vasodilators = CCb’s ACEis and IV prostacyclin
  3. Renal = ACEi
  4. Oesophageal = PPIs
  5. Pulmonary fibrosis needs cyclophosphamide
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129
Q

What is dermatomyositis

A

A rare disorder of unknown aetiology. There is inflammation and necrosis of skeletal muscle fibres and skin.

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130
Q

Give 3 symptoms of dermatomyositis.

A
  1. Rash.
  2. Symmetrical proximal Muscle weakness.
  3. Lungs are often affected too e.g. ILD.
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131
Q

What are the extra-muscular features of dermatomyositis

A

Fever
Arthritis
Pulmonary fibrosis
Reynauld’s

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132
Q

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

A
  1. Muscle enzymes - raised.
  2. EMG.
  3. Muscle/skin biopsy.
  4. Screen for malignancy.
  5. CXR.
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133
Q

What is the treatment for dermatomyositis?

A

Immunosuppression

  • steroids
  • Cytotoxic (Azathioprine and methotrexate)
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134
Q

What is the pathophysiology of sjögren’s syndrome?

A

Immunologically mediated destruction of epithelial exocrine glands, especially lacrimal and salivary glands.

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135
Q

What are the two types of sjorgens syndrome

A

Primary
- female more common and in 4th to 5th decade of life

Secondary
- second to RA, SLE, Systemic sclerosis and primary biliary cirrhosis

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136
Q

What are the features of Sjorgens

A

Decreased tear production = dry eyes
decreased salvation = xerostomia
Bilateral parotid swelling
Vaginal dryness = dyspareunia

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137
Q

What other autoimmune conditions of sjorgens associated with

A

Thyroid disease
PBC
MALT lymphoma

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138
Q

What is the investigations for sjorgens syndrome

A

Look for serum antibodies
- ANA and RF
Schimmer tear test - ability for eyes to self hydrate
Parotid biopsy

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139
Q

What is the treatment for sjorgens syndrome

A
  • Tear and saliva replacement.
  • Immunosuppression for systemic complications
  • NSAIDs ans hydroxychloroquine for arthralgie, rashes and fever .
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140
Q

What is Reynaulds

A

Peripheral digital ischaemia precipitated by cold or emotion

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141
Q

What is the classification of Reynauld’s

A

Primary = Idiopathic
Secondary = second to systemic sclerosis, SLE, RA, sjorgens, Thrombocytosis, B-blockers, Atherosclerosis, frost bite,
Vibrating tools cause vascular damage

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142
Q

What is the presentation of Reynauld’s

A

Digit pain with triphasic colour change from white to blue to crimson

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143
Q

What is the treatment of Reynauld’s

A

Wear gloves
CCb’s (nifedipine)
ACEi
IV prostacyclin

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144
Q

Define osteoporosis.

A

A systemic skeletal disease characterised by low bone mass and micro-architectural deterioration. The patient is at increased risk of fracture and bone fragility

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145
Q

Describe the epidemiology of osteoporosis.

A

50% of women and 20% of men over 50 are affected. The incidence increases with age.

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146
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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147
Q

What is post menopause osteoporosis

A

Loss of the restraining effects of oestrogen on bone turnover characterised by

  1. high bone turnover
  2. Predominantly cancellous bone formation
  3. Microarchitectural disruption
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148
Q

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

A

Trabecular thickness decreases; especially in the horizontal plane. There are fewer connections between trabecular and so an overall decrease in trabecular strength -> increased risk of fracture.

Remodelling due to increased osteoclast and decreased osteoblast activity

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149
Q

What are the causes of osteoporosis

A
  1. AI conditions because inflammatory cytokines increase resorption
    - RA and IBD
  2. Cushing’s disease (Induces osteoblast apoptosis)
    3 Post menopause
  3. Hyperthyroidism and primary hyperparathyroidism as TH and PTH increase bone turnover
  4. Steroids (Testosterone and oestrogen control bone turnover
  5. Reduced skeletal loading increases resorption
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150
Q

What medications can increase osteoporosis risk

A 
Glucocorticoids 
Depo-provera contraception 
Aromatase inhibitors 
GnRH analogues 
Androgen deprivation
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151
Q

What are the other risk factors for osteoporosis

A 
Previous fracture 
Family history 
Alcohol 
Smoking 
Medications 
immobility
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152
Q

What are the signs and symptoms of osteoporosis

A

asymptomatic development with fragile bone and pathological fractures

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153
Q

Give 4 properties of bone that contribute to bone strength

A
  1. Bone mineral density
  2. Bone size
  3. Bone micro-architecture
  4. Mineralisation
  5. Bone turnover
  6. Geometry
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154
Q

Why can RA cause osteoporosis?

A

RA is an Inflammatory disease. There are high levels of IL-6 and TNF; these are responsible for increased bone resorption.

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155
Q

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

A

DEXA scan to produce a T score

FRAX (10yr fracture risk)

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156
Q

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

A
  1. Lumbar spine.
  2. Hip.
  3. Proximal femur
  4. Distal radius
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157
Q

What is a T score?

A

A T score is a standard deviation that is compared to a gender-matched young adult mean.

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158
Q

What is a FRAX score

A

predicts 10 year fracture chance but cannot be used in people under 40

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159
Q

What T score signifies that a patient has osteoporosis?

A

T >-2.5

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160
Q

What T score signifies that a patient has osteopenia?

A

-2.5 < T < -1

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161
Q

What is a normal T score?

A

-1

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162
Q

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

A
  1. Bisphosphonates (Alendronate, risedronate)
    - inhibit cholesterol formation leading to osteoclast apoptosis
  2. HRT.
    Anti-resorptive treatments decrease osteoclast activity.
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163
Q

Give an example of an anabolic treatment used in the management of osteoporosis.

A

Teriparatide.
- analogue of PTH
Anabolic treatments increase osteoblast activity.

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164
Q

What cells do anti-resorptive treatments target in people with osteoporosis?

A

They decrease osteoclast activity.

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165
Q

What cells do anabolic treatments target in people with osteoporosis?

A

They increase osteoblast activity.

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166
Q

Give 3 advantages of HRT.

A
  1. Reduces fracture risk.
  2. Stops bone loss.
  3. Prevents menopausal symptoms.
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167
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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168
Q

Give an example of a bisphosphonate.

A

Alendronate.

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169
Q

What pathway do bisphosphonates target?

A

HMGCoA pathway.

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170
Q

What is the diagnostic criteria for fibromyalgia?

A

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

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171
Q

Give 3 factors that increase the volume of pain.

A
  1. Substance P.
  2. Glutamate.
  3. Serotonin.
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172
Q

Give 3 factors that decrease the volume of pain.

A
  1. Opioids.
  2. GABA.
  3. Cannabanoids.
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173
Q

Name 4 diseases that fibromyalgia is commonly associated with.

A
  1. Depression.
  2. Chronic fatigue.
  3. Chronic headache.
  4. IBS.
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174
Q

What are the risk factors for fibromyalgia

A 
Neurosis
 - Depression, anxiety and stress 
Disatisfaction at work 
Overprotective family or lack of support 
Middle age 
Low income 
Divorced 
Low educational status
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175
Q

Give 5 symptoms of fibromyalgia.

A
  1. Neck and back pain.
  2. Pain is aggravated by stress, cold and activity.
  3. Generalised morning stiffness.
  4. Subjective swelling of extremities.
  5. Frequent waking during the night.
  6. Waking unrefreshed.
  7. Low mood, irritable, weepy.
  8. Headache and IBS common.
176
Q

Give 5 triggers of fibromyalgia.

A
  1. Physical trauma.
  2. Distress.
  3. Hormonal alterations e.g. hypothyroid.
  4. Infections.
  5. Certain catastrophic events e.g. wars.
177
Q

Describe the management for fibromyalgia.

A
  1. Educate the patient and family.
  2. ‘Resent the pain thermostat’.
  3. Low does amitriptyline can help with sleep.
  4. Graded aerobic exercise.
  5. Acupuncture.
178
Q

What 2 things are essential in the management of fibromyalgia?

A
  1. Explaining that sleep disturbance is central to what they’re feeling.
  2. Emphasising the importance of exercise and fitness.
179
Q

Define rheumatoid arthritis

A

Chronic systemic auto-immune inflammatory disease of the joints characterised by a symmetrical, deforming, peripheral polyarthritis

180
Q

Describe the epidemiology of RA

A

More common in females

occurs in 5th to 6th decade of life

181
Q

Which genes are associated with RA

A

HLA-DR4 and DR1

182
Q

What are the risk factors for RA

A

HLA-DR4/DR1
Smoker
Female
Having other auto-immune conditions

183
Q

Describe the aetiology of RA.

A

Auto-antibodies e.g. RF and anti-CCP lead to a defective cell mediated immune response.

184
Q

Describe the pathophysiology of RA.

A
  1. Chronic inflammation. B/T cells and neutrophils infiltrate.
  2. Proliferation -> pannus formation.
  3. Pro-inflammatory cytokines -> proteinases -> cartilage destruction.
185
Q

Give 5 symptoms of RA

A
  1. Early morning stiffness (>60 mins).
  2. Pain eases with use.
  3. Swelling/deformity
  4. General fatigue, malaise.
  5. Extra-articular involvement.
186
Q

Which joints are commonly affected in RA

A

MCP’s

PIPs of the hand and feet

187
Q

Which joint is sparred in rheumatoid arthritis

188
Q

What are some of the characteristic features of arthritis in rheumatoid arthritis

A

Swan neck = hyperextended PIP and flexed DIP

Boutonniere = Hyperextended DIP and flexed PIP

Z-thumb

Ulnar deviation of the fingers

189
Q

Give 5 signs of RA.

A
  1. Symmetrical.
  2. Deforming.
  3. Polyarthropathy.
  4. Erosion on X-ray.
  5. 80% are RF positive.
190
Q

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

A
  • Nodules on the elbows, fingers, feet, heal and lungs
  • Bursitis.
  • Muscle wasting.
    Atlanto-axial sublimation
191
Q

Describe the composition of RA nodule

A

Palisading ring of macrophages and fibroblasts with a central fibrinoid necrosis

192
Q

What is Atlanta-axial sublimation

A

Axis and odontoid peg shift with the atlas due to synovitis and ligament damage around the peg leading to spinal cord compression

193
Q

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

A
  • Dry eyes (Secondary sjogrens syndrome)
  • Scleritis.
  • Episcleritis.
  • Sicca complex
194
Q

RA extra-articular involvement: describe the neurological effects.

A
  • Sensory peripheral neuropathy.
  • Entrapment neuropathies e.g. carpal tunnel syndrome.
  • Instability of cervical spine.
195
Q

RA extra-articular involvement: describe the haematological effects.

A
  • Palpable lymph nodes.
  • Splenomegaly.
  • Anaemia.
196
Q

Felty’s syndrome is a sign of RA, What is felty’s syndrome

A

RA + Splenomegaly + neutropaenia

197
Q

RA extra-articular involvement: describe the pulmonary effects.

A
  • Pleural effusion.
  • Fibrosing alveolitis
  • Caplan’s syndrome
  • Interstitial lung disease
198
Q

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

A
  • Pericardial rub.
  • Pericardial effusion
  • Pericarditis .
199
Q

RA extra-articular involvement: describe the effect on the kidneys.

A

Amyloidosis

Analgesic nephropathy

200
Q

Is reynauld’s a common presentation of RA?

201
Q

What is rheumatoid factor?

A

An antibody against the Fc portion of IgG.

202
Q

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

A

Bloods for inflammatory markers; ESR and CRP will be raised.

  • Test for anaemia.
  • Test for RF and anti-CCP.
  • US and MRI
203
Q

What might you see in radiography of RA

A

Decreased joint space
Soft tissue swells
Erosion
Soft bones = osteopenia

204
Q

What is the conservative treatment for RA

A

Refer to rheumatology
Regular exercise
PT
Aids and splints

205
Q

What is the medical management of RA

A

NSAIDSs for flare ups
Steroids
Disease modifying anti-rheumatic drugs (DMARDs)
Biologics (Anti-TNF)

206
Q

How do DMARDs work

A

Interferre with folate metabolism

207
Q

Which antibiotic cannot be prescribed with DMARDs

A

Trimethoprim

208
Q

Name the three main DMARDs

A

Methotrexate
Sulfsalazine
Hydroxychloroquine

209
Q

What are the SE of methotrexate

A

Hepatotoxic

Pulmonary fibrosis

210
Q

What are the SE of hydroxychloroquine

A

Retinopathy and seizures

211
Q

When would a patient be given biologics for RA

A

If their RA was severe and they were unresponsive to DMARDs

212
Q

What are the main biologics (Anti-TNF) drugs

A 
Infliximab = Anti-TNF ab 
Etanercept = TNF-receptor 
Adalimumab = Anti TNF ab
213
Q

What are the side effects of anti-TNF

A

increased infection risk (Sepsis and Tb)

Increased AI disease

214
Q

Name some other classes and drug names of biologics for RA

A

Anti-IL1 = Anakira
Anti-IL6 = Toclizumab
JAK inhibitors = Taclifinib

215
Q

What might you give to an RA patient who is unresponsive to DMARDs and anti-TNF therapy

A

Rituximab = anti-CD20 mab

216
Q

When are crystals pathological

A

When they are deposited in abnormal sites leading to local inflammation and tissue damage

217
Q

What is crystal arthropathy

A

Arthritis caused by calcium deposits in the joint lining
Urate = gout
Pyrophosphate = pseudo gout

218
Q

How can you determine between gout and pseudo gout using light microscopy

A

Gout = -ve birefringent needles

Pseudogout = +ve birefringent needles

219
Q

Define gout

A

deposition of monosodium rate crystals in and around the joints = erosive arthritis

220
Q

Describe the pathological pathway that leads to gout

A

Purines -> hypoxanthine -> xanthine -> uric acid -> monosodium urate.

221
Q

What enzyme converts hypoxanthine to xanthine?

A

Xanthine oxidase.

222
Q

Describe the epidemiology of gout

A

More common in males mainly over 75

223
Q

What is the cause of gout

A

Hyperuricaemia due to either impaired excretion, increased production or increased intake

224
Q

What are the causes of impaired excretion of urate

A 
CKD
Diuretics 
Hypertension 
Hypothyroid 
Hyperparathyroid 
Obesity 
DM
Low dose aspirin 
Cyclosporin 
Lead poisoning
225
Q

What are the causes of increased production of urate

A 
Metabolic syndrome
Myeloproliferative disease 
Cytotoxic drugs 
Lesch-nyhan syndrome 
Alcohol 
Excess meat, shellfish, offal, gravy, yeast extract and fructose sweetened drinks
226
Q

What things might contribute to increased purine intake

A

High purine diet = red meat, seafood and fructose

227
Q

What can precipitate a gout attack

A

Anything that suddenly causes an alteration in uric acid concentration

  • Aggressive introduction of hypouricaemic therapy
  • Alcohol and shellfish
  • Sepsis, MI and actue severe illness
  • Sudden cessation of hypouricaemic therapy
  • Trauma surgery and dehydration
228
Q

What are the symptoms of gout

A

Hot and swollen joint
Acute mono arthritis
Tophi

229
Q

What are tophi

A

Urate deposits in the pinna and tendons

230
Q

Which joints are commonly affected by gout

A

Big toe MTP

but also ankle, foot, hand joints, wrist, elbow and knee

231
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.
232
Q

What might investigations for someone with suspected gout show

A

Polarised light microscopy produces negatively birefringent needle-shaped crystals

Joint fluid aspirate and microscopy

X-ray changes produces punched out erosions in junta-articular bone (Rat bites)

233
Q

What is the aim of treatment for gout?

A

To get urate levels < 300μmol/L.

234
Q

What are the treatment options for gout

A
  1. Conservative = Wt loss, avoid fasting and EtOH excess
  2. Xanthine oxidase inhibitor (Allopurinol)
  3. Colchicine and NSAIDs
  4. Uricosuric drugs
235
Q

Name 2 NSAIDs used in management of gout

A

Diclofenac and indomethacin

236
Q

What are the SE of colchicine

237
Q

In renal impaired gout patients where NSAIDs and colchicine are CI, what is given

238
Q

What are the side effects of allopurinol

A

Rash
Fever
Decreased WCC

239
Q

When might the xanthine oxidase inhibitor febuxostat be used

A

If patient has hypersensitivity or renal impairment

240
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.

241
Q

Name a drug that can lead to increased monosodium urate.

A

Bendroflumethiazide.

Diuretics impair urate excretion.

242
Q

Pseudogout is otherwise known as

A

Pyrophosphate arthropathy

243
Q

Describe the pathophysiology of pyrophosphate arthropathy (pseudogout).

A

Calcium pyrophosphate crystals are deposited on joint surfaces. The crystals elicit an acute inflammatory response.

244
Q

What are the causes of pseudogout

A 
Dehydration
Hypo/hyperthyroidism 
Diabetes 
Haemochromatosis 
hypomagnesia 
Hyperparathyroidism
245
Q

Give a symptom of pyrophosphate arthropathy (pseudogout).

A 
Can be asymptomatic 
Acute mono arthritis 
Pain, stiffness, swelling, hot 
Marked synovitis 
Fever 
resolution within 1-3 weeks
246
Q

Which joints does pseudo gout commonly effect

A

Knee>wrist>Shoulder>Ankle>elbow

247
Q

What investigations might you do in someone who you suspect might have pyrophosphate arthropathy (pseudogout)?

A

Chondrocalcinosis on X-ray
Joint fluid aspirate and microscopy
+ve birefingent rhomboid crystals

248
Q

What is the most likely differential diagnosis for pyrophosphate arthropathy (pseudogout)?

249
Q

What might trigger an acute attack of pseudo gout

A 
Direct trauma to the joint 
Intercurrent illness 
Surgery - esp parathyroidesctomy 
Blood transfusion, IV fluid 
T4 replacement 
Joint lavage
250
Q

What is the treatment of pseudo gout

A

Intra-articular steroid injections and colchicine and NSAIDs

If continued inflammatory changes then trial of anti-rheumatic treatment such as methotrexate and hydroxychloroquine

Surgery

251
Q

Define fracture

A

A soft tissue injury with discontinuity of the bone

252
Q

What is the management of a fracture

A
  1. Reduce the fracture (Restore length, align, rotate)
  2. Immobilise
  3. Rehabilitate
253
Q

Describe the physiology of fracture healing

A

Blood rushes to the site forming a haematoma and brings fibroblasts that begin granulation forming a soft callus
Osteoblasts come along and form woven bone which makes the bone stable
Woven bone gets remodelled into lamellae bone

254
Q

Name the 7 different types of fractures

A
  1. Transverse
  2. Linear
  3. Oblique-non displaced
  4. Oblique-displaced
  5. Spiral
  6. Greenstick
  7. Communicated
255
Q

What are the potential complications of fractures

A

Damage to surrounding structures such as vascular, nerve and soft tissue and organs

Contamination –> infection

Compartment syndrome

256
Q

What is compartment syndrome

A

Where there is damage to the blood supply and build up of pressure in the compartment as there is nowhere for the fluid to go leading to restrictions in blood flow to the limb

  • Increase in intra-compartmental pressure due to fluid increase (Blood) puts pressure on the viens causing collapse then collapse the nerves and puts pressure on arteries (Pain, pallor, perishingly cold, paralysis and pulselessness and parathesia)
257
Q

What are the early systemic complications of fractures

A

Fat embolus - fat droplets escape bone marrow and form emboli which hit the lungs causing rash and dyspnoea

Shock - vessel injury causing harm-dynamic instability and shock

Crush syndrome - crush causes muscle to die and release myohaemoglobin which blocks kidneys and causes renal failure

Pneumonia

258
Q

What are the late complications of fractures

A

Delayed union, non-union and Mal union (Bone heals with deformity)

Avascular necrosis
Stiffness
Arthritis
Osteomyelitis

259
Q

What are the different classifications of neck of femur fractures

A

Intracapsular

Extracapsular

260
Q

What are the different types of extracapsular neck of femur fracture

A

Interochanteric

Extratrochanteric

261
Q

What is the presentation of a neck of femur fracture

A 
Fall 
Shorter leg on side of fracture 
Groin pain 
Inability to weight bear 
Externally rotated 
Pain on axial loading
262
Q

What is the management of intracapsular neck of femur fractures

A

Analgesia with morphine or nerve block

Need to replace

  1. Total hip replacement
  2. Hemiarthroplasty
263
Q

What is the management of extra capsular neck of femur fractures

A

Cannulated hip screws

DHS - compression screw

264
Q

What is the classification method for ankle fractures

A

Weber classification
A = below the syndesmosis
B = at the level of the syndesmosis
C = Above the level of the syndesmosis

265
Q

What are the Ottawa rules for who gets an x-ray

A

Bone tenderness at the posterior edge of the lateral malleolus, medial malleolus or inability to weight bear immediately or after 4 steps

266
Q

What is the management of ankle sprains

A

Analgesia
Ice
Elevation
Early mobilisation

267
Q

What is the treatment of open fractures

A

Get antibiotics and tetanus
Splint and align the foot
Stabilise
Debridement

268
Q

What is the treatment for compartment syndrome

A

Fasciotomy after 24 hours so the dead tissue can be removed

269
Q

What is the function of the ACL

A

Important stabiliser of the knee joint, limits anterior translation of the tibia and also contributes to knee rotation stability

270
Q

What is the presentation of an ACL tear

A

Swelling, pain and the knee giving way

271
Q

What are the investigations for ACL injuries

A

Postive lachmanns
Anterior draw test
MRI

272
Q

What is the management of ACL injury

A

Physiotherapy
Surgery
Tendon repair
Artificial graft

273
Q

What is cauda equina

A

Progressive bilateral neurological deficit of the legs leading to major motor weaknesses with knee extension, ankle eversion or foot dorsiflexion

274
Q

What are the symptoms of cauda equina

A

Difficult in initiating micturition or impaired sensation of urinary flow - urinary retention with overflow urinary incontinence

Loss of sensation of rectal fullness - faecal incontinence

Perianal or genital sensory loss

Laxity of the anal sphincter

275
Q

What is the management of cauda equina

A

Urgent decompression and discectomy

276
Q

Shoulder dislocation can cause damage to what nerve

A

Axillary nerve damage which supplies the deltoid

277
Q

What is the management of shoulder dislocation

A

Popping the joint back in and trying to get early mobilisation

278
Q

What are the rotator cuff muscles

A

Supraspinatus
Infraspinatus
Subscapularis
Teres minor

279
Q

What are the investigations for rotator cuff injuries

A

Jobes test for supraspinatus
Put hand behind back and ask to push away
Push hands outwards from forward position - theres minor

280
Q

What is the management of rotator cuff injuries

A 
analgesia 
Physio
Activity modification 
Corticosteroid injections 
Surgery ie. arthroplasty
281
Q

Define osteomyelitis

A

Infection localised to the bone

282
Q

Describe the epidemiology of osteomyelitis.

A
  • Increasing incidence of chronic OM.

- Bimodal age distribution.

283
Q

What are the two predisposing factors for osteomyelitis

A

Diabetes

Peripheral vascular disease

284
Q

What are 2 methods of classifying osteomyelitis

A
  1. Acute = inflammatory bone changes caused by pathogenic bacteria with symptom presentation within 2 weeks
  2. Chronic = bone necrosis with symptom onset after 6 weeks
285
Q

Describe three ways in which pathogens can get into bone

A
  1. Direct inoculation of infection into bone via trauma/surgery
  2. Contiguous spread of infection from adjacent soft tissues and joints to the bone
  3. Haematogenous seeding
286
Q

Contiguous spread of infection from soft tissue to joints is more common in what individuals

A

Older patients and those with DM, chronic ulcers, vascular disease and arthoplasties

287
Q

Haematogenous seeding occurs in which individuals

A

IVDU

Those with central lines, dialysis, sickle cell disease, self catheterisation, UTIs

288
Q

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

A

Vertebrae.

289
Q

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

A

Long bones.

290
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.

291
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 blood flow and BM are absent meaning bacteria can move from the blood to bone.

292
Q

Give 4 host factors that affect the pathogenesis of osteomyelitis.

A
  1. Behavioural e.g. risk of trauma.
  2. Vascular supply e.g. arterial disease, DM, sickle cell disease
  3. Pre-existing bone/joint problems e.g. RA, prosthetic material
  4. Immune deficiency ie. immunosuppressive drugs
293
Q

What is the histopathology of osteomyelitis

A
  1. Inflammatory exudate in marrow
  2. Increased intramedullary pressure
  3. Extension of exudate into bone cortex
  4. Rupture through periosteum
  5. Interruption of periosteal blood supply causing necrosis
  6. Leaves pieces of separated dead bone = Sequestra
  7. New bone forms here = involcrum
294
Q

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

A
  1. Inflammatory cells.
  2. Oedema.
  3. Vascular congestion.
  4. Small vessel thromboses
295
Q

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

A
  1. Necrotic bone - ‘sequestra’.
  2. New bone formation = involcrum
  3. Neutrophil exudates.
  4. Lymphocytes and histiocytes
296
Q

What can cause osteomyelitis.

A
  1. Gram +ve = S.aureus, streptococcus, enterococci
  2. Coagulase negative staphylococci e.g. s.epidermidis.
  3. Aerobic gram negative bacilli.
  4. Mycobacterium TB in immunocompromised
  5. Salmonella in sickle cell disease
  6. Pseudomonas auerginoase and serratia marcescens in IVDU
297
Q

What is the presentation of osteomyelitis

A

Local slow onset dull pain @ osteomyelitis site aggregated by movement with systemic fever, riggers, sweats and malaise

298
Q

What are the acute signs of osteomyelitis

A

Tender, warm and red and swollen at the osteomyelitis site

299
Q

What are the chronic signs of osteomyelitis

A

Non healing ulcers

Draining sinus tract if sequestra is draining to surface

300
Q

What is the differential diagnosis for osteomyelitis

A

Cellulitis
Charcots joint
Gout
Avascular necrosis

301
Q

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

A
  1. Bloods: raised inflammatory markers and WCC.
  2. Plain radiographs and MRI.
  3. Bone biopsy.
  4. Blood cultures.
302
Q

What things might you see on X-ray for someone with osteomyelitis

A

Cortical erosion
Sequestra
Sclerosis
Periosteal reaction

303
Q

Describe the usual treatment for osteomyelitis.

A
  • Large dose IV antibiotics tailored to culture findings (often flucloxacillin).
  • Surgical treatment: debridement +/- arthroplasty
304
Q

What are the potential complications of osteomyelitis

A

Vertebral OM which can lead to abscess formation and meningitis

305
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.
306
Q

What is septic arthritis

A

Infection producing inflammation in the joints

307
Q

What is the most common cause of septic arthritis?

A

Staphylococcus aureus.

308
Q

Give 3 causes of septic arthritis.

A
  1. Staphylococcus aureus (RA/DM)
  2. Streptococci.
  3. Neisseria.
  4. Gonococcus (In sexually active)
  5. Haemophilus influenza in children
  6. Gram -ve bacilli (E.coli and pseudomonas)
309
Q

Give 5 risk factors for septic arthritis.

A
  1. Any cause of bacteraemia e.g. cannula, UTI.
  2. Local skin breaks/ulcers.
  3. Damaged/prosthetic joints.
  4. RA (Joint disease)
  5. Elderly.
  6. IVDU
  7. Immunosuppressed
  8. Chronic renal failure
310
Q

Give 4 symptoms of septic arthritis.

A
  1. Painful.
  2. Red.
  3. Swollen.
  4. Hot.
  5. Fever.
  6. Decreased range of movement
311
Q

Which joints are more commonly affected by septic arthritis

A

Knee>hip>shoulder

312
Q

What are the investigations for someone with septic arthritis

A

Joint aspiration but needs to occur before giving antibiotics
Increased WCC, ESR and CRP
X-ray
Blood culture and microbiology

313
Q

What Is the management for septic arthritis

A

IV Abx: Vanc + cefotaxime
Consider joint washout
Splint joint
Physiotherapy after infection resolved
Prosthetic joint needs to be debridement and arthroplasty
Stop methotrexate and give prednisolone
Flucoxicillin for S.aureus and IV cefotaxime for gram -ve/gonococcal

314
Q

What is the differential for septic arthritis

A

Crystal arthropathy

Reactive arthritis

315
Q

What is bacteraemia?

A

Bacteria in the blood.

316
Q

What is debridement?

A

The removal of damaged tissue.

317
Q

What is the most serious complication of arthroplasty surgery?

A

Prosthetic joint infection.

318
Q

Why is the incidence of prosthetic joint infections increasing

A

Due to increasing incidence of old age, DM and obesity

319
Q

What are the causative agents of prosthetic joint infections

A 
S.aureus 
MRSA 
Anaerobes 
Enterobacter 
Pseudomonas 
Diptheroides 
Haem strep 
Enterococcus 
Coagulase -ve staph
320
Q

What is the presentation of a prosthetic joint infection

A

Pus, redness, hot and swelling of scar

321
Q

What is the history of someone with prosthetic joint infection likely to contain

A

History of UTIs

322
Q

What investigations might you do on someone who you suspect might have a prosthetic

A
  1. Aspirate (Must be done with patient off antibiotics for 2 weeks) -> microbiology.
  2. Bloods for inflammatory markers and FBC.
  3. X-rays.
  4. Microbiology culture
323
Q

What must you never do before aspirating a joint?

A

Never give antibiotics before aspiration!

324
Q

What are the three aims of treatment for prosthetic joint infections?

A
  1. Eradicate sepsis.
  2. Relieve pain.
  3. Restore function.
325
Q

Prosthetic joint infections: what treatment might you choose for a patient that is unfit for surgery?

A

Antibiotic suppression.

326
Q

Prosthetic joint infections: Which patients might you choose for debridements and retention of prosthesis

A

Early postoperative infections and acute haematogenous infections

NOT FOR CHRONIC

327
Q

What is the gold standard treatment for prosthetic joint infections?

A

Exchange arthroplasty.

  • Know the organisms and their sensitivities
  • Radical debridement of all infected and dead tissue.
  • Systemic and local antibiotic cover.
  • Sufficient joint and soft tissue reconstruction.
328
Q

What is excisions arthroplasty

A

Removal of the prosthetic -

Effective in removing the infection but poor at restoring function

329
Q

What is one stage exchange arthroplasty

A

‘Take something out and put a replacement in’

  • radical debridement
  • Implantation of new prosthetic
  • Systemic and local antibiotics
330
Q

What is a two stage exchange arthroplasty

A

‘Take something out, leave it a while and then replace

  • radical debridement
  • Local antibiotic spacer
  • Interval stage
  • Implantation of new prosthesis as per aseptic reconstruction
331
Q

Define good musculoskeletal health

A

Healthy/disease free joints and bones

Ability to carry out a wide range of physical activities both effectively and symptom free

332
Q

What is the Wilson and Junger screening criteria for secondary prevention

A
  1. Condition should be an important health problem
  2. Should be an accepted treatment for patients with recognised disease
  3. Facilities for diagnosis and treatment should be available
  4. Should be a recognisable latent or early symptomatic stage
  5. Should be a suitable test or examination
  6. Test should be acceptable to the population
  7. Natural history of the condition including development from latent to declared disease should be adequately understood
  8. There should be an agreed policy on whom to treat as patients
  9. Cost of case finding should be economically balanced in relation to possible expenditure on medical care as a whole
  10. Case finding should be a continuing process and not a one and for all project
333
Q

Is developmental dysplasia of the hip screened for

A

Yes as part of the 6-8 week baby check as early detection can reduce the need for surgery

334
Q

Why is ultrasound not offered to all babies when screening for developmental dysplasia of the hip

A

can lead to over diagnosis and treatment of causes that would have otherwise resolved without treatment

335
Q

When are individuals routinely tested for vitamin D deficiency

A

If they have deficiency symptoms
Are considered as high risk of deficiency
There is clinical reason to do so

336
Q

What are the benefits of working

A 
Lower mortality 
Social relationships 
Structure to life 
Improved fitness + mental health 
Reduced state benefits
337
Q

What are the high risk activities for MSK problems

A 
Heavy manual handling 
Lifting above shoulder heights 
Lifting below the knee 
Incorrect manual handling techniques 
Forceful repetitive work 
Poor posture
338
Q

When is an illness due to work

A

Symptoms improve away from work
Characteristic distribution of rash ie. contact dermatitis
Clusters of cases at workplace
Exposure to hazard linked to disease

339
Q

What are the epidemiological principles of causality according to Bradford Hill

A 
Strength of association 
Consistency in association 
Exposure-response relationship
Specificity 
Temporal relationship 
Coherence of evidence 
Biological plausible
340
Q

What are the work related conditions associated with the neck

A

Tension neck
thoracic outlet syndrome
Cervical spondylosis

341
Q

What are the work related conditions associated with the shoulder

A

Rotator cuff tendonitis
Shoulder tendonitis
Bicipital tendonitis
Shoulder capsulitis

342
Q

What are the work related conditions associated with the elbow

A

Lateral and medial epicondylitis

343
Q

What are the work related conditions associated with the wrist and the forearm m

A

Carpal tunnel syndrome
Tensosynovitis of wrist
De quervain’s disease of the wrist

344
Q

What is tension neck

A

2nd most common condition after back pain

May be due to whiplash

345
Q

What is thoracic outlet syndrome

A

Pinching of the brachial plexus nerves leading to tingling and wasting of the hands
Associated with poor posture and loading of the shoulders by working at keyboard

346
Q

What is the management of thoracic outlet syndrome

347
Q

What is rotator cuff tendonitis

A

rotator cuff tears leading to swelling

348
Q

What is the test for rotator cuff tears

A

Elevate extended arm against resistance

349
Q

What is carpal tunnel syndrome

A

Pain/tingling and numbness due to compression of the median nerve by flexor tendons

350
Q

Who is at risk of carpal tunnel syndrome

A

Pregnancy, obesity, occupation with repetitive wrist movement

351
Q

What is tenosynovitis

A

Local tenderness and swelling of tendon sheaths and crepitus at the wrist

352
Q

What is the treatment for tenosynovitis

A

NSAIDs and steroid injections and rest

353
Q

When does mechanical back pain first present

A

between 20-55

354
Q

What are the red flags for serious spinal pathology

A 
Age of onset 20/55
violent trauma 
Systemically unwell 
Persisting severe restriction of lumbar flexion 
Widespread neurology
355
Q

What are the markers for chronic conditions

A 
Reduced activity levels 
Low mood patients 
Expectation that passive treatment will help 
Dissatisfaction at work 
Lack of support
356
Q

Causes of MSK injury

A

Single excessive force
Static loading
Repetitive wear and tear

357
Q

What are important questions to ask during history taking for bone tumours

A 
Presenting complaint (Mass, pain, loss of function) 
social history (current level of function)
Past medical history
358
Q

What are the red flag symptoms for bone tumours

A

Rest pain, LOF, Neuro problems, weight loss, growing lump deep to fascia, night pain, deformity, gross loss of movement

359
Q

When examining the joint in bone tumours what should be done

A

Look feel and move the joint and assess function, range of movement and neuromuscular status
If any masses are present, size, shape, pain, smooth/irregular, skin or deep tissue

360
Q

What is the zone of transition

A

Area between normal and abnormal bone

361
Q

What does a wide zone of transition indicate

A

ill-defined border
Cardinal sign of malignancy
Can be mimicked by infection and eosinophilic granuloma

362
Q

What does a narrow zone of transition indicate

A

Well defined border
In young almost certainly benign
In >40 consider plasacytoma, myeloma and metastases

363
Q

If the patient is > 30 then what bone tumour are they likely to have

A

Metatasis or myeloma

364
Q

If the patient is <30 then what bone tumours are they likely to have

A

primary bone tumour

365
Q

What is a periosteal reaction

A

Reaction caused by any irritation to periosteum, trauma and infection

366
Q

Sunburnt spicules are indicative of which bone tumours

A

Osteosarcoma and Ewing’s

367
Q

Onion skinning periosteal reaction is indicative of which bone tumour

368
Q

Codmanns triangle perisoteal reaction is indicative of what bone tumour

A

osteosarcoma, Ewing’s, osteomyelitis an metastasis

369
Q

What investigations would you carry out in someone with suspected primary bone tumour

A

XR - look for bone lesions interactions (Onion skin, sunburnt spicules)
CT scan for assessing bone quality and solid tumours
MRI reactive changes in soft tissue an bone marrow
Bone scan

370
Q

Describe the Enneking grading system for malignant primary bone tumours

A

G1 (Benign history - well differentiated, resembles cell of origin with low mitotic count)

G2 (Low grade malignant - moderate differentiations with few mitosis and local spread)

G3 (high grade malignant, poorly differentiated with frequent mitoses)

371
Q

What are the common primary bone tumours

A

Osteosarcoma of the knee
Chondrosarcoma of the pelvis
Giant cell tumours of the knee
Chondroma of the sacrum

372
Q

Tumours from where metastases to the bone

A

Thyroid, prostate, breast, kidney and lung

373
Q

What is the management of primary bone tumours

A

Benign - NSAIDs

Malignant - Surgical excision with radio/chemotherapy

374
Q

What is a chondroid bone tumour and what is its appearance

A

Cartilaginous tumour which is popcorn stippling, rings and arcs

375
Q

What is an osteoid bone tumour and what is its appearance

A

Bone forming tumour with cloud like or trabecular appearance

376
Q

Most common bone tumours are metastases from where

A

Bronchus
Breast
Prostate

377
Q

X-ray shows metastases as what

A

Osteolytic areas with bony destruction

378
Q

What must have happened for a lytic tumour to be visible on X-ray

A

Must have lost greater than 60% bone density

379
Q

Where in the bone does osteosarcoma occur

A

Metaphyses of long bones

380
Q

What is the most common primary bone malignancy in children

A

Osteosarcoma

381
Q

Ewing’s sarcoma arises from which cell type

A

Mesenchymal stem cells

382
Q

Where does Ewings sarcoma present

A

In the long bones

383
Q

What are the symptoms of Ewing’s sarcoma

A

Painful, swelling, redness in the area surrounding the tumour
Malaise, anorexia, Wt loss, fever, paralysis

384
Q

What is a chondrosarcoma

A

Cancer of the cartilage

385
Q

What are the symptoms of a chondrosarcoma

A

Dull deep pain and affected area is swollen and tender

386
Q

What are the common sites of chondrosarcoma

A

Pelvis, femur, humerus, scapula and ribs

387
Q

What is an osteoid osteoma

A

Benign bone lesion in young patients that causes localised pain and is self limiting

388
Q

Where is an osteoid osteoma found

A

In the proximal femur, tibial diaphysis and spine

389
Q

What are the investigations for osteoid osteoma

A

CT and X-ray

390
Q

What is the treatment for osteoid osteoma

A

NSAIDs

Surgery –> Radiofrequency ablation

391
Q

What is an osteoblastoma

A

Bone producing tumour that presents with non self limiting pain

392
Q

Where are osteoblastomas found

A

Spine, proximal humerus and the sacrum

393
Q

What is the treatment for osteoblastoma

394
Q

What is osteochondroma

A

Metaphyseal lesion covered by cartilage that grows away from the growth plate and stops growing after puberty

395
Q

How does an osteochondroma present

A

Painless lump

396
Q

What is the management of an osteochondroma

A

Surgical excision

397
Q

Define osteosarcoma

A

Spindle cell neoplasm that produce osteoid

398
Q

What is the most common osteosarcoma

A

Intramedullarly osteosarcoma found in the knee, proximal humerus and proximal femur

399
Q

Osteosarcoma occurs secondary to

A

Paget’s disease
Post radiation
Fibrous dysplasia

400
Q

What is the treatment for osteosarcoma

A

Multi agent chemotherapy

401
Q

What are endochondromas

A

Benign lesions in the small bones that produce metaphysical popcorn on X-ray

402
Q

What is a chondroblastoma

A

Rare epiphyseal tumour arising from chondral precursor cells located at the distal femur and proximal humerus

403
Q

What is fibrous dysplasia

A

A developmental abnormality of the bone leading to a failure to produce lamellar bone

404
Q

What is the treatment for fibrous dysplasia

A 
Bisphosphonates 
Surgical (Curettage and cortical autograph)
405
Q

What class of drug is alendronate?

A

Bisphosphonate.

406
Q

How does alendronate work?

A

Alendronate reduces bone turnover by inhibiting osteoclast mediated bone resorption.

407
Q

What is polymyalgia rheumatica (PMR)?

A

A condition that causes pain, stiffness and inflammation in the muscles around the shoulders, neck and hips

408
Q

How can you differentiate between polymyalgia rheumatica (PMR) and fibromyalgia?

A

PMR will show raised inflammatory markers.

409
Q

What disease is giant cell arteritis associated with?

A

Polymyalgia rheumatica.

410
Q

Psoriatic arthritis commonly involves swelling of what joint?

A

DIP joint.

411
Q

How would describe the swelling of fingers seen in psoriatic arthritis?

A

Dactylitis, sausage like swelling.

412
Q

Describe a psoriatic plaque.

A

Pink, scaling lesions. Occur on extensor surfaces of the limbs.

413
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.
414
Q

What 2 features would be seen on an X-ray taken from someone with ankylosing spondylitis.

A
  1. Sacroiliitis.

2. Syndesmophytes (bamboo spine).

415
Q
  1. Which of the following is a clinical feature of osteoarthritis?
    a. 60 minutes of early morning stiffness
    b. Painful swelling across MCP and PIP
    c. Pain in the 1st carpo-metacarpal
    d. Mobile subcutaneous nodules and points of pressure
    e. Alternating buttock pain
A

c. Pain in the 1st carpo-metacarpal

OA is common in the carpo-metacarpal joint, DIP and Knee

416
Q
  1. Which of the following is an extra-articular feature of RA?
    a. Subcutaneous nodules
    b. Episcleritis
    c. Peripheral sensory neuropathy
    d. Pericardial effusion
    e. All of the above
A

All of the above

417
Q

Which of the following is a classical feature of RA 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

418
Q
  1. 53yr old patient presents with 3 day history of lower back pain. Pain started a work and has been unable to work for the past three days and is keen to have a sick note. Physical exam shows lightly overweight with BMI of 29 but no neurological deficit or spinal deformity and pain is not easily located. Which is best management
    a. Given his age he should be referred to a specialist
    b. He should be sent for X-ray to look for pathological changes in 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 a simple analgesic and return to normal activity as soon as he can manage
    e. He should advised to seek other employment
A

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

419
Q
  1. 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

420
Q
  1. 57yr old man presents with 3-day history of painful first MTP joint. On examination there are 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 episodes?
    a. A diet with high red meat content
    b. A diet rich in dairy products
    c. Drinking >5 cans of non-diet fizzy drink per day
    d. A diet rich in sugary food stuffs
    e. Switching from drinking beer to drinking lager
A

b. A diet rich in dairy products

421
Q
  1. Which of the following is not an autoimmune connective tissue disorder?
    a. SLE
    b. Ehler danlos
    c. Primary Sjogren’s
    d. Systemic sclerosis
    e. Dermatomyositis
A

b. Ehler danlos

422
Q
  1. 23yr old woman presents with mouth ulcers, fever, painful white fingers and pleuritic chest pain. She is ANA positive, her ESR is 52 and her white cell count is low. Which of the following features would you not expect with her illness?
    a. Deforming arthritis
    b. Photosensitive rash
    c. Seizures
    d. PE
    e. Thrombocytosis
A

e. Thrombocytosis

423
Q

In lupus, what happens to the ESR and CRP

A

ESR is high but the CRP is NORMAL

424
Q
  1. Which of the following is used in the treatment of SLE?
    a. Anti-TNF
    b. Anti-malarials - Hydroxychloroquine
    c. Ustekinuab
    d. Sulfsalazine
    e. Allopurinol
A

b. Anti-malarials - Hydroxychloroquine

425
Q
  1. Adult male presents with a 6 week right sided headache, general malaise, early morning stiffness and pain in his jaw when eating. His CRP is 63, ESR 78. Which of the following is true regarding his underlying disease?
    a. It is associated with ANCA positivity
    b. It typically affects those between 50 and 60
    c. It can present with acute sight loss
    d. It rarely responds to corticosteroids
    e. It is vasculitis affecting the small blood vessels
A

c. It can present with acute sight loss

426
Q
  1. Which of the following is now a rare cause for joint infection in infants due to standard childhood immunisation schedule in the UK?
    a. Staph.Aureus
    b. Gp A strep
    c. Varicella zoster
    d. Rubella
    e. Haemophilus Influenza
A

e. Haemophilus Influenza

427
Q
  1. 64 yr old woman with T2 DM has been struggling with cellulitis in her right forefoot for 4 weeks. After making no progress with oral antibiotic she has now had IV flucloxacillin and co-amoxiclavulanic acid but the pain and erythema persist and her CRP has only fallen to 47 from its peak of 91. What is the next appropriate investigation?
    a. Blood cultures
    b. MRI right forefoot
    c. Plain X-ray right forefoot
    d. Skin biopsy of right forefoot
    e. Ultrasound scan of right forefoot
A

c. Plain X-ray right forefoot

428
Q
  1. Which of the following is a. non-inflammatory cause of joint pain?
    a. Rheumatoid
    b. Septic arthritis
    c. Spondylarthritis
    d. Fibromyalgia
    e. Gout
A

d. Fibromyalgia

429
Q
  1. Which of these is not a feature of rheumatoid arthritis?
    a. NSAIDs help
    b. Pain eases with use
    c. Effects the DIP
    d. Pain lasts for an hour or so in the morning
    e. Ulnar deviation
A

c. Effects the DIP

430
Q
  1. Alendronic acid is a bisphosphate used in osteoporosis. Which describes the method of action of bisphosphates?
    a. Cause increase bone deposition
    b. Cause reactivation of metaphysis and epiphysis
    c. Inhibit osteoclast and cause osteoclast apoptosis
    d. Reduce the signalling pathway between osteoblasts, clasts by increasing RANK ligand
    e. Increased removal of calcium into the haversian canal within bone
A

c. Inhibit osteoclast and cause osteoclast apoptosis

431
Q
  1. Gout – What is the investigative result from microscopy
    a. Tophi
    b. Needle +ve birefringent
    c. Needle -ve birefringent
    d. Rhomboid shaped +ve birefringent
    e. Rhomboid shaped -ve birefringent
A

c. Needle -ve birefringent

432
Q
  1. What is the most likely causative organism for urethritis, conjunctivitis, arthritis? – reactive arthritis
    a. S. Aureus
    b. E. coli
    c. Strep pneumonia
    d. Hemophilus Influenza
    e. Chlamydia
A

e. Chlamydia

433
Q
  1. Pins and needles in thumb, index and middle fingers, Carpal tunnel syndrome is caused by what
    a. Cervical spine fracture
    b. Compression of median nerve
    c. Compression of radial nerve
    d. CC8-T1 lesion
    e. Compression of ulnar nerve
A

b. Compression of median nerve

434
Q
  1. Ankylosing spondylitis is associated with what genetics
A

a. HLA B27

435
Q
  1. Which of the following is the most common cause of osteomyelitis?
A

a. Staph aureus

436
Q
  1. DXA score of -1.6 means what
A

a. Osteopenia

Phase 2 (16 decks)

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