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My Phase 2a > Rheumatology COPY > Flashcards

Rheumatology COPY Flashcards

1
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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2
Q

Give 2 causes of non-inflammatory joint pain.

A
  1. Degenerative e.g. osteoarthritis or OP.
  2. Non-degenerative e.g. fibromyalgia.
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3
Q

What are the 5 cardinal signs of inflammation?

A
  1. Rubor (redness).
  2. Calor (heat).
  3. Dolor (pain).
  4. Tumor (swelling).
  5. Loss of function.
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4
Q

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

A
  • Inflammatory pain tends to ease with use
  • whereas degenerative non-inflammatory pain increases with use.
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5
Q
  • Are you more likely to see swelling in inflammatory or degenerative pain?
  • where will the swelling most likely be seen?
A
  • In inflammatory pain you are likely to see synovial swelling.
  • There is often no swelling in degenerative pain.
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6
Q

Name 2 inflammatory markers that can be detected in blood tests.

A
  1. ESR (erythrocyte sedimentation rate).
  2. CRP.
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7
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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8
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 in inflammation.
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9
Q

Describe the ESR and CRP levels in someone with lupus.

A
  • ESR is raised and CRP is normal.
  • raised CRP suggests underlying infection
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10
Q

What protein are all spondyloarthropathy conditions associated with?

A

HLA B27 which raises an autoimmune response

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11
Q

Give 5 conditions that fall under the umbrella term spondyloarthritis.

A
  1. Ankylosing spondylitis.
  2. Reactive arthritis.
  3. Psoriatic arthritis.
  4. Enteropathic arthritis.
  5. Juvenile idiopathic arthritis.
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12
Q

What is the function of HLAB27?

A

It is an antigen presenting cell.

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13
Q

Describe the ‘molecular mimicry’ theory for explaining why HLAB27 is associated with spondyloarthritis.

A

Infectious agents have peptides very similar to HLAB27. An auto-immune response is triggered against HLAB27.

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14
Q

Name 3 theories that can explain why HLAB27 is associated with spondyloarthritis.

A
  1. Molecular mimicry.
  2. Mis-folding theory.
  3. HLAB27 heavy chain hypothesis.
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15
Q

what is enthesitis

A

inflammation of the entheses = the insertion point of the tendons and ligaments to the bone.

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16
Q

Give 9 signs of spondyloarthritis.

A

SPINEACHE
1. Sausage digit – dactylitis = swelling of a whole digit. Predictor of underlying bone damage
1. Psoriasis
1. Inflammatory back pain + buttock pain
1. NSAID – good response
1. Enthesitis of the heel
1. Arthritis –distal joint involvement = psoriatic arthritis [or OA]
1. Crohn’s / colitis / potentially elevated CRP
1. HLAB27
1. Eye – uveitis. Anterior uveitis = iritis

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17
Q

What is the general treatment for all spondyloarthritis?

A
  • Initially early use of DMARDs
  • biological agents if DMARDs fail e.g. TNF inhibitors: adalimumab, infliximab +etanercept.
  • IL12, IL 17blockers
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18
Q

Describe the pathophysiology of ankylosing spondylitis.
- what areas are most commonly affected

A
  • bone marrow oedema -> Inflammation of bone -> erosive damage -> repair/new bone formation -> irreversible bone fusion.
  • spine and sacroiliac joints most affected
  • can also affect the costovertebral + costosternal joints.
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19
Q

Give 8 symptoms of ankylosing spondylitis.

A
  1. BACK PAIN!
  2. Morning stiffness.
  3. Waking in the second half of the night.
  4. Buttock pain - may radiate to the legs.
  5. reduced spinal flexion - schooner’s test.
  6. Usually <40y/o at onset.
  7. Eye pain
  8. loss of lumbar lordosis
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20
Q

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

A
  1. X-ray -> bamboo spine + ligament ossification.
  2. MRI -> bone marrow oedema.
  3. CRP/ESR: elevated
  4. HLAB27 test.

HLAB27 test NOT diagnostic as 90% of AS pts are +ve and 10% of healthy pts are +ve.
useful for differentiating between other rheumatological conditions though

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21
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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22
Q

Give 3 locations that psoriasis commonly occurs at.

A
  1. Elbows.
  2. Knees.
  3. scalp+ lower back.
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23
Q

What is 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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24
Q

What gut infections are associated with reactive arthritis?

A

Salmonella, shigella, yersinia campylobacter.

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25
Q

What sexually transmitted infections are associated with reactive arthritis?

A
  • Chlamydia.
  • Gonorrhoea
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26
Q

What is the triad of symptoms for reactive arthritis?

A
  1. Arthritis.
  2. Conjunctivitis.
  3. Urethritis.
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27
Q

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

A

Enteropathic arthritis.

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28
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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29
Q

What is the aetiology of JIA?

A

Unknown - idiopathic!

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

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30
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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31
Q

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

A

Oligoarthritis.

High risk of developing uveitis!

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32
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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33
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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34
Q

Describe the medical treatment for JIA.

A
  1. Steroid joint injections.
  2. NSAIDS.
  3. Methotrexate.
  4. Systemic steroids.
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35
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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36
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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37
Q

Give 3 factors that increase the volume of pain.

A
  1. Substance P.
  2. Glutamate.
  3. Serotonin.
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38
Q

Give 3 factors that decrease the volume of pain.

A
  1. Opioids.
  2. GABA.
  3. Cannabanoids.
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39
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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40
Q

Give 5 symptoms of fibromyalgia.

A
  1. Chronic pain.
  2. Tiredness/ fatigue
  3. Headache
  4. Difficulty concentrating
  5. sensitivity to pain
  6. sleep disturbance
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41
Q

Give 5 triggers of fibromyalgia.

A
  1. Physical stress.
  2. emotions stress.
  3. Hormonal imbalances e.g. hypothyroid.
  4. Infections.
  5. weather changes - cold.
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42
Q

Give 3 diseases might be included in the differential diagnosis for fibromyalgia?

A
  1. Hypothyroidism.
  2. SLE.
  3. Low vitamin D.
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43
Q

Describe the management for fibromyalgia.

A
  1. Educate the patient and family.
  2. ‘Resent the pain thermostat’.
  3. CBT or antidepressants for Pain-related depression.
  4. Graded aerobic exercise + physiotherapy.
  5. Severe pain: medications such as duloxetine, pregabalin or amitriptyline.
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44
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.
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45
Q

What is vasculitis?

A

Vasculitis is a group of autoimmune diseases that cause damage + inflammation of the blood vessel walls -> ischaemia, infarction or aneurysms.

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46
Q

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

A
  • giant cells.
  • granulomatous inflammation
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47
Q

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

A

Giant cell arteritis.

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48
Q

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

A

Aortitis in RA.

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49
Q

Chapel Hill classification: give an example of a medium/small artery primary disorder.

A

Wegener’s granulomatosis (GPA).

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50
Q

Chapel Hill classification: give an example of a medium/small artery secondary disorder.

A

Vasculitis secondary to autoimmune disease, malignancy, drugs.

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51
Q

What does ANCA stand for?

A

Anti-neutrophil cytoplasmic antibodies.

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52
Q

Describe the epidemiology of giant cell arteritis.

A
  • Affects those >50y/o.
  • Incidence increases with age.
  • Twice as common in women.
  • associated with polymyalgia rheumatica
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53
Q

Give 5 symptoms of giant cell arteritis.

A
  1. unilateral Headache.
  2. Scalp tenderness.
  3. Jaw claudication.
  4. Acute blindness.
  5. Malaise.
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54
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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55
Q

What is the diagnostic criteria for giant cell arteritis?

A
  1. Age >50.
  2. New headache.
  3. Temporal artery tenderness on palpation or decreased pulsation.
  4. Abnormal artery biopsies.
  5. elevated ESR ≥50
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56
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. Fundoscopy, looking at the optic disc for pallor
  3. Temporal artery biopsy.
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57
Q

Describe the treatment for giant cell arteritis.

A
  • Prompt high dose corticosteroids - prednisolone.
  • analgesia
  • PPIs + Osteoporosis prophylaxis is important e.g. lifestyle advice and vitamin D.
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58
Q

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

A

c-ANCA.

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59
Q

What organ systems can be affected by Wegener’s granulomatosis?

A
  1. ENT.
  2. Lungs.
  3. Kidneys.
    | ELK
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60
Q

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

A

Crusty nasal/ ear secretions
Hearing loss
Cough
Sinusitis
Epistaxis: nose bleeds

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61
Q

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

A
  • Pulmonary haemorrhage/nodules.
  • cough, wheeze, haemoptysis

- Inflammatory infiltrates are seen on X-ray.

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62
Q

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

A

Glomerulonephritis.

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63
Q

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

A

Ulcers.

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64
Q

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

A
  • Uveitis.
  • Scleritis.
  • Episcleritis.
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65
Q

What is the treatment for Wegener’s granulomatosis?

A
  • If severe: high dose steroids.

- If non-end organ threatening: moderate steroids.

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66
Q

What is rheumatoid arthritis?

A

An chronic auto-immune inflammatory synovial joint disease.

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67
Q

Describe the epidemiology of RA.

A
  • 2 to 3 times more common in women.

- Approximately 1% of the population affected.

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68
Q

Describe the aetiology of RA.

A

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

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69
Q

Describe the pathophysiology of RA.

A

The body’s immune system attacks the synovium -> inflammation of the synovial membrane -> loss of synovial fluid -> ↓ joint space, cartilage wear and destruction + bone erosion.

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

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70
Q

Give 5 symptoms of RA.

A
  1. Early morning stiffness (>60 mins).
  2. Pain eases with use.
  3. Swelling of joints - symmetrical
  4. General fatigue, malaise.
  5. Extra-articular involvement - e.g. subcutaneous nodules.
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71
Q

Give 5 signs of RA.

include signs from investigations

A
  1. Symmetrical.
  2. Deformities: swan neck, boutonnieres, Z-thumb, ulnar deviation.
  3. Polyarthropathy.
  4. Erosion on X-ray.
  5. 80% are RF positive.
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72
Q

name 4 deformities caused by RA

A
  1. swan neck
  2. boutonniere’s
  3. ulnar deviation of the fingers
  4. Z-thumb
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73
Q

what does an x-ray show in RA

A
  • Loss of joint space
  • erosion of bone
  • soft tissue swelling
  • soft bones - osteopenia

LESS

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74
Q

which joints are spared in RA

A

DIPJ

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75
Q

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

A
  • Nodules.
  • Bursitis.
  • Muscle wasting.
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76
Q

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

A
  • Dry eyes.
  • Scleritis.
  • Episcleritis.
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77
Q

RA extra-articular involvement: describe the neurological effects.

A
  • Sensory peripheral neuropathy.
  • Entrapment neuropathies e.g. carpal tunnel syndrome.
  • Instability of cervical spine.
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78
Q

RA extra-articular involvement: describe the haematological effects.

A
  • Anaemia of chronic disease.
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79
Q

RA extra-articular involvement: describe the pulmonary effects.

A
  • Pleural effusion.
  • pulmonary nodules
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80
Q

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

A
  • Pericardial rub.

- Pericardial effusion.

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81
Q

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

A

Amyloidosis.

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82
Q

What is rheumatoid factor?

A

An auto-antibody against the Fc portion of IgG.

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83
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.
  • x-ray: LESS
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84
Q

Describe the treatment for rheumatoid arthritis.

A
  • NSAIDS.
  • Corticosteroids.
  • conventional DMARDs: methotrexate,leflunomide orsulfasalazine.
  • Biological DMARDs: infliximab, adalimumab, etanercept. rituximab
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85
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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86
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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87
Q

Give 5 risk factors for developing OA.

A
  1. Genetic predisposition/ family hx.
  2. Trauma.
  3. Abnormal biomechanics e.g. hypermobility.
  4. Occupation e.g. manual labour.
  5. Obesity.
  6. female
  7. increasing age
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88
Q

What are the most important cells responsible for OA?

A

Chrondrocytes.

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89
Q

Give 5 symptoms of OA.

A
  1. Joint swelling and bony enlargement
  2. Pain - aggravated by activity.
  3. Tenderness.
  4. Walking and ADLs affected.
  5. No or little morning joint stiffness (<30 minutes).
  6. Deformities - formation of bony growths = osteophytes.
  7. Crepitus.
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90
Q

Give 4 radiological features associated with OA.

A
  1. Joint space narrowing.
  2. Osteophyte formation.
  3. Sub-chondral sclerosis.
  4. Sub-chondral cysts.
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91
Q

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

A
  1. Distal interphalangeal joint.
  2. Proximal interphalangeal joint.
  3. First carpometacarpal joint - base of the thumb.
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92
Q

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

A

The medial surface.

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93
Q

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

A

X-ray.

Look for asymmetric loss of joint space; sclerosis; cysts and osteophytes.

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94
Q

Describe features of the non-medical management for OA.

A
  • Education.
  • Exercise.
  • Weight loss.
  • Physiotherapy.
  • Occupational therapy.
  • Walking aids.
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95
Q

Describe the pharmacological management for OA.

A
  • NSAIDS (topical better than PO).
  • Paracetamol.
  • Intra-articular steroid injections.
  • DMARDs if there is an inflammatory component.
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96
Q

Describe the surgical management for OA.

A
  • Arthroscopy for loose bodies.
  • Osteotomy (changing bone length).
  • Arthroplasty (joint replacement).
  • Fusion (usually ankle and foot).
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97
Q

Give 3 indications for surgery.

A
  1. Significant limitation of function.
  2. Uncontrolled pain.
  3. Waking at night from pain.
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98
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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99
Q

What is the treatment for loose bodies?

A

Arthroscopy.

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100
Q

Give an example of an inherited connective tissue disease.

A
  1. Marfan’s syndrome.

2. Ehler Danlos syndrome.

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101
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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102
Q

What is SLE?

A

Systemic Lupus Erythematosus is an inflammatory multi-system disease characterised by the presence of serum anti-nuclear antibodies (ANA).

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103
Q

Describe the epidemiology of SLE.

A
  • 90% of cases are in young women.
  • More common in afro-Caribbeans.
  • Genetic association.
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104
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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105
Q

What can cause thrombosis in patients with SLE?

A

The presence of antiphospholipid antibodies.

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106
Q

What autoantibody is specific to SLE?

A

Anti-dsDNA.

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107
Q

Give 5 symptoms of SLE.

A
  1. Butterfly rash.
  2. Mouth ulcers.
  3. Raynaud’s phenomenon/’cold pale fingers’.
  4. Fatigue.
  5. Depression.
  6. Weight loss.
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108
Q

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

A
  1. Blood count may show normocytic anaemia; neutropenia; thrombocytopaenia. Raised ESR, normal CRP.
  2. Serum autoantibodies: ANA, anti-dsDNA.
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109
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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110
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.
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111
Q

What is scleroderma?

A

A multi-system disease characterised by skin hardening and Raynaud’s phenomenon.

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112
Q

Give 5 signs of limited scleroderma.

A
  1. Calcinosis.
  2. Raynaud’s phenomenon.
  3. Oesophageal reflux.
  4. Sclerodactyly (thickening and tightening of the skin).
  5. Telangectasia (visible small red blood vessels).
  6. Pulmonary arterial hypertension.
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113
Q

Give 4 signs of diffuse scleroderma.

A
  1. Proximal scleroderma.
  2. Pulmonary fibrosis.
  3. Bowel involvement.
  4. Myositis.
  5. Renal crisis.
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114
Q

Describe the pathophysiology of scleroderma.

A
  • Various factors cause an endothelial lesion and vasculopathy.
  • There is excessive collagen deposition (skin hardening), inflammation and auto-antibody production.
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115
Q

Describe the management of scleroderma.

A
  1. Raynaud’s: physical protection and vasodilators.
  2. GORD: PPI’s.
  3. Annual Echo and pulmonary function tests to monitor arterial pulmonary pressure.
  4. ACEi to prevent renal crisis.
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116
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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117
Q

What does sjögren’s syndrome often occur secondary to?

A

Other auto-immune disorders e.g. SLE, RA, scleroderma, primary biliary cirrhosis.

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118
Q

Give 5 symptoms of sjögren’s syndrome.

A
  1. Dry eyes and dry mouth.
  2. Inflammatory arthritis.
  3. Rash.
  4. Neuropathies.
  5. Vasculitis.
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119
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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120
Q

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

A

Look for serum auto-antibodies e.g. anti-RO, RF, ANA.

Also, raised immunoglobulins and ESR.

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121
Q

What is the treatment for sjögren’s syndrome?

A
  • Tear and saliva replacement.

- Immunosuppression for systemic complications.

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122
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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123
Q

Give 3 symptoms of dermatomyositis.

A
  1. Rash.
  2. Muscle weakness.
  3. Lungs are often affected too e.g. ILD.
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124
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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125
Q

What is the treatment for dermatomyositis?

A

Steroids and immunosuppressants.

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126
Q

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

A

Dactylitis.

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127
Q

What is the approach used for managing trauma patients?

A

ATLS - treat the greatest threat to life first (ABCDE).

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128
Q

Describe the physiological pathway that leads to monosodium urate formation.

A

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

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129
Q

What enzyme converts hypoxanthine to xanthine?

A

Xanthine oxidase.

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130
Q

Give 5 factors that can lead to increased levels of monosodium urate.

A
  1. Increased intake e.g. alcohol, red meat, seafood.
  2. Cell turnover (increased production).
  3. Cell damage e.g. due to surgery.
  4. Cell death e.g. due to chemotherapy.
  5. Reduced excretion (renal problems).
  6. Drugs e.g. bendroflumethiazide - diuretics impair urate excretion.
  7. High insulin.
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131
Q

Name a drug that can lead to increased monosodium urate.

A

Bendroflumethiazide.

Diuretics impair urate excretion.

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132
Q

Describe the epidemiology of gout.

A

Gout is most common in men over 75 y/o.

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133
Q

Give a symptom of gout.

A

Hot and swollen joints.

The toes are commonly effected.

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134
Q

What are tophi?

A

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

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135
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.
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136
Q

What is the aim of treatment for gout?

A

To get urate levels < 300μmol/L.

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137
Q

Name 5 treatment options for gout.

A
  1. Lifestyle modification e.g. diet, weight loss, reduced alcohol.
  2. Allopurinol (blocks xanthine oxidase).
  3. Colchicine or NSAIDS.
  4. Switch from bendroflumethiazide to cosartan.
  5. Rasburicase - rapid urate reduction.
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138
Q

Name a drug used in the treatment of gout that blocks xanthine oxidase.

A

Allopurinol.

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139
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.

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140
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.
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141
Q

Describe the pathophysiology of pyrophosphate arthropathy (pseudogout).

A

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

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142
Q

What can cause pyrophosphate arthropathy (pseudogout)?

A
  1. Hypo/hyperthyroidism.
  2. Diabetes.
  3. Haemochromatosis.
  4. Magnesium levels.
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143
Q

Give a symptom of pyrophosphate arthropathy (pseudogout).

A

Acute, hot and swollen joints. Typically the wrists and knees.

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144
Q

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

A
  1. Aspiration: fluid for crystals and blood cultures.

2. X-rays: can show chondrocalcinosis.

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145
Q

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

A

Infection.

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146
Q

Describe the treatment for pyrophosphate arthropathy (pseudogout).

A

Treat the underlying cause and use methotrexate for inflammation.

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147
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.

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148
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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149
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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150
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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151
Q

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

A

Oestrogen.

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152
Q

Why are so many women over 50 affected by osteoporosis?

A

Women over 50 are likely to be post-menopausal; they therefore have less oestrogen and so osteoclast action isn’t inhibited. There is a high rate of bone turnover -> bone loss and deterioration -> fracture risk.

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153
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.

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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

Name 3 endocrine diseases that can be responsible for causing osteoporosis.

A
  1. Hyperthyroidism and primary hyperparathyroidism: TH and PTH -> increased bone turnover.
  2. Cushing’s syndrome: cortisol leads to increased bone resorption and osteoblast apoptosis.
  3. Early menopause, male hypogonadism: less oestrogen/testosterone to control bone turnover.
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156
Q

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

A

Cortisol increases bone turnover. It leads to increased bone resorption and it also induces osteoblast apoptosis.

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157
Q

Give 5 risk factors for osteoporosis.

A
  1. Previous fracture.
  2. FHx.
  3. Excessive alcohol.
  4. Smoking.
  5. Medications e.g. steroids, depo provera.
  6. Immobility.
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158
Q

What investigation might you do in someone who you suspect to have osteoporosis?

A

DEXA scan.

A T score will be generated.

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159
Q

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

A
  1. Lumbar spine.

2. Hip.

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160
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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161
Q

What T score signifies that a patient has osteoporosis?

A

T < -2.5

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162
Q

What T score signifies that a patient has osteopenia?

A

-2.5 < T < -1

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163
Q

What is a normal T score?

A

-1

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164
Q

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

A

FRAX.

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165
Q

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

A
  1. Bisphosphonates.
  2. HRT.

Anti-resorptive treatments decrease osteoclast activity.

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166
Q

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

A

Teriparatide.

Anabolic treatments increase osteoblast activity.

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167
Q

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

A

They decrease osteoclast activity.

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168
Q

What cells do anabolic treatments target in people with osteoporosis?

A

They increase osteoblast activity.

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169
Q

Give 3 advantages of HRT.

A
  1. Reduces fracture risk.
  2. Stops bone loss.
  3. Prevents menopausal symptoms.
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170
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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171
Q

Give an example of a bisphosphonate.

A

Alendronate.

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172
Q

What pathway do bisphosphonates target?

A

HMGCoA pathway.

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173
Q

What is the physis?

A

The physis is the growth plate in paediatric bone.

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174
Q

What feature of paediatric bone means it can heal rapidly?

A

The thick periosteum.

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175
Q

Describe the 3 initial steps in the management of fractures.

A
  1. Reduce the fracture e.g. restore the length, alignment, rotation.
  2. Immobilise.
  3. Rehabilitate.
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176
Q

What is often the first line management option for paediatric fractures?

A

Non-operative management e.g. traction, casts, splints. This is because paediatric bone heals quickly due to the thick periosteum.

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177
Q

What can happen if the physis is damaged?

A

Physis damage -> growth arrest -> deformity.

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178
Q

What is the name of the classification used for fractures involving the physis?

A

Salter-Harris Fracture classification.

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179
Q

Salter-Harris Fracture classification: describe a type 1 fracture.

A

Transverse fracture through the growth plate.

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180
Q

Salter-Harris Fracture classification: describe a type 2 fracture.

A

A fracture through the growth plate and metaphysis.

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181
Q

Salter-Harris Fracture classification: describe a type 3 fracture.

A

A fracture through the growth plate and epiphysis.

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182
Q

Salter-Harris Fracture classification: describe a type 4 fracture.

A

A fracture through the metaphysis, physis and epiphysis. These fractures often need fixation.

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183
Q

Salter-Harris Fracture classification: describe a type 5 fracture.

A

Crush injury of growth plate! These fractures have a very poor prognosis and growth arrest is likely.

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184
Q

Give 2 ‘red flag’ signs of non-accidental injury in children.

A
  1. Long bone fracture in a child unable to walk.

2. Multiple bruises and fractures.

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185
Q

Describe the management for non-accidental injury in children.

A
  1. Admit the child!
  2. Skeletal survey.
  3. Referral to paediatric medics and safeguarding services.
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186
Q

What can cause a supracondylar fracture in children?

A

Falling on an outstretched hand.

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187
Q

What nerve might be affected in a supracondylar fracture?

A

The median nerve.

188
Q

What is the treatment for a supracondylar fracture?

A

K-wires.

189
Q

Give 5 potential complications of fractures.

A
  1. Open fractures.
  2. Neurovascular compromise.
  3. Mal union - bone heals with deformity.
  4. Non union - bone fails to heal.
  5. Compartment syndrome.
  6. Cast problems e.g. tightness, compartment syndrome, plaster burns/blisters.
190
Q

Define osteomyelitis.

A

Bone inflammation secondary to infection.

191
Q

Describe the epidemiology of osteomyelitis.

A
  • Increasing incidence of chronic OM.

- Bimodal age distribution.

192
Q

What can cause osteomyelitis.

A
  1. S.aureus!
  2. Coagulase negative staphylococci e.g. s.epidermidis.
  3. Aerobic gram negative bacilli.
  4. Mycobacterium TB.
193
Q

Name 2 predisposing conditions for osteomyelitis.

A
  1. Diabetes.

2. PVD.

194
Q

Pathophysiology of osteomyelitis: describe the 3 ways in which the pathogen can get into bone.

A
  1. Easy: inoculation of infection into the bone e.g. trauma/open wound.
  2. Quite easy: contiguous spread of infection to bone from adjacent tissues.
  3. Difficult: hematogenous seeding e.g. due to cannula infection.
195
Q

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

A

Vertebrae.

196
Q

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

A

Long bones.

197
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.

198
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.

199
Q

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

A

IVDU and other groups at risk from bacteraemia.

200
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.
  3. Pre-existing bone/joint problems e.g. RA.
  4. Immune deficiency.
201
Q

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

A
  1. Inflammatory cells.
  2. Oedema.
  3. Vascular congestion.
202
Q

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

A
  1. Necrotic bone - ‘sequestra’.
  2. New bone formation.
  3. Neutrophil exudates.
203
Q

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

A

Inflammatory exudate ruptures periosteum -> blood supply impaired -> necrosis -> sequestra -> new bone forms.

204
Q

Give 5 signs of osteomyelitis.

A
  1. Fever.
  2. Rigors.
  3. Sweats.
  4. Malaise.
  5. Tenderness.
  6. Warmth.
  7. Swelling.
  8. Erythema.
205
Q

Give a sign specific to chronic osteomyelitis.

A

Sinus formation.

206
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.
207
Q

What is the differential diagnosis for osteomyelitis?

A
  1. Cellulitis.
  2. Avascular necrosis.
  3. Gout.
208
Q

Describe the usual treatment for osteomyelitis.

A
  • Large dose IV antibiotics tailored to culture findings (often flucloxacillin).
  • Surgical treatment: debridement.
209
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.
210
Q

What is the most common cause of septic arthritis?

A

Staphylococcus aureus.

211
Q

Give 3 causes of septic arthritis.

A
  1. Staphylococcus aureus.
  2. Streptococci.
  3. Neisseria.

Consider the clinical context of the patient!

212
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.
  5. Elderly.
213
Q

Give 4 symptoms of septic arthritis.

A
  1. Painful.
  2. Red.
  3. Swollen.
  4. Hot.
  5. Fever.
214
Q

Describe the treatment for septic arthritis.

A
  • Antibiotics guided by aspirate cultures.
  • Joint wash out/repeated aspiration.
  • Rest/splint/physio.
  • Analgesia.
215
Q

What is bacteraemia?

A

Bacteria in the blood.

216
Q

What is debridement?

A

The removal of damaged tissue.

217
Q

What is the most serious complication of arthroplasty surgery?

A

Prosthetic joint infection.

218
Q

Give 2 ways in which prosthetic joint infections can be prevented.

A
  1. Aseptic environment and laminar air flow.

2. Systemic prophylactic antibiotics.

219
Q

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

A
  1. Aspirate -> microbiology.
  2. Bloods for inflammatory markers and FBC.
  3. X-rays.
220
Q

What must you never do before aspirating a joint?

A

Never give antibiotics before aspiration!

221
Q

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

A
  1. Eradicate sepsis.
  2. Relieve pain.
  3. Restore function.
222
Q

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

A

Antibiotic suppression.

223
Q

What is the gold standard treatment for prosthetic joint infections?

A

Exchange arthroplasty.

  • Radical debridement of all infected and dead tissue.
  • Systemic and local antibiotic cover.
  • Sufficient joint and soft tissue reconstruction.
224
Q

Define sarcoma.

A

A rare tumour of mesenchymal origin: a malignant connective tissue neoplasm.

225
Q

Soft tissue sarcomas make up what percentage of overall sarcomas?

A

80%. The remaining 20% are boney.

226
Q

Name 3 soft tissue sarcomas.

A
  1. Liposarcoma.
  2. Leiomyosarcoma.
  3. Rhabdomyosarcoma.
227
Q

What is liposarcoma?

A

A malignant neoplasm of adipose tissue.

228
Q

What is leiomyosarcoma?

A

A malignant neoplasm of smooth muscle.

229
Q

What is rhabdomyoscarcoma?

A

A malignant neoplasm of skeletal muscle.

230
Q

Name 3 boney sarcomas.

A
  1. Osteosarcoma.
  2. Ewing’s sarcoma.
  3. Chondrosarcoma.
231
Q

What is chondrosarcoma?

A

A malignant neoplasm of cartilage.

232
Q

Give 3 features of osteosarcoma.

A
  1. Fast growing.
  2. Aggressive.
  3. Typically affects 15 - 17 y/o.
233
Q

Name a boney sarcoma that responds well to chemotherapy.

A

Ewing’s sarcoma.

234
Q

Give 2 red flag symptoms for sarcoma.

A
  1. Non mechanical pain.

2. Pain at night.

235
Q

Give 4 signs that suggest malignancy and can be used to make a diagnosis of soft tissue sarcoma.

A
  1. Lump > 5cm.
  2. Lump is increasing in size.
  3. Lump is deep to fascia.
  4. Pain.
236
Q

What investigations might you do in someone who you suspect to have a sarcoma?

A
  1. MRI.
  2. Core needle biopsy.
  3. CT scan.
237
Q

What is the treatment for sarcomas?

A
  1. MDT meeting.
  2. Surgery for localised soft tissue sarcomas; ensure a wide margin.
  3. Amputation.
  4. If non resectable, chemotherapy and radiotherapy.
238
Q

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

A

Give adjuvant radiotherapy.

239
Q

Name 2 NSAIDs.

A
  1. Ibuprofen.

2. Naproxen.

240
Q

Give 3 side effects of NSAIDs.

A
  1. Peptic ulcer disease.
  2. Renal failure.
  3. Increased risk of MI and CV disease.
241
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.

242
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.
243
Q

How do DMARDs work?

A

Non-specific inhibition of inflammatory cytokine cascade = reduced joint pain, stiffness and swelling.

244
Q

Give an example of a DMARD.

A

Methotrexate = gold standard.
Hydroxychloroquine.
Sulfasalazine.

245
Q

How often should methotrexate be taken?

A

Once weekly.

246
Q

Give 3 potential side effects of methotrexate.

A
  1. Bone marrow suppression.
  2. Abnormal liver enzymes.
  3. Nausea.
  4. Diarrhoea.
  5. Teratogenic.
247
Q

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

A

Folic acid.

248
Q

What are cytokines?

A

Short acting hormones.

249
Q

Name a TNF blocker.

A

Adalimumab.

250
Q

Name a monoclonal antibody that binds to CD20 on B cells.

A

Rituximab: binds to CD20 -> B cell depletion.

251
Q

Describe the mechanism of action of abatacept?

A

Inhibits T cell activation.

252
Q

Give one reason why osteomyelitis is difficult to treat.

A

The antibiotics struggle to penetrate bone and bone has a poor blood supply.

253
Q

With what disease would you associate the ‘pencil-in-cup erosion’ seen on a plain XR with?

A

Psoriatic arthritis.

254
Q

With what disease would you associate the Schirmer’s test?

A

Sjögren’s syndrome.

255
Q

You do some investigations on a 30 y/o woman who has presented with painful, red and swollen MCP and PIP joints. The XR shows swelling of soft tissues, deformity and loss of joint space. What auto-antibodies would you expect to see in the serum?

A

Anti-CCP and RF positive.

This patient has rheumatoid arthritis.

256
Q

How does alendronate work?

A

Alendronate reduces bone turnover by inhibiting osteoclast mediated bone resorption.

257
Q

What class of drug is alendronate?

A

Bisphosphonate.

258
Q

Name 2 drugs that act on the HMGCoA pathway.

A
  1. Bisphosphonates e.g. alendronate.

2. Statins e.g. simvastatin.

259
Q

Describe the treatment for an acute attack of gout.

A
  1. NSAIDs e.g. diclofenac.
  2. Colchicine if NSAIDs are ineffective.
  3. Corticosteroids - IM or IA.
260
Q

What auto-antibodies are often present in people with RA?

A

RF and anti-CCP.

261
Q

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

A
  1. PIP - Bouchard’s nodes.

2. DIP - Herbeden’s nodes.

262
Q

What joint is commonly affected in gout?

A

The MTP joint of the big toe.

263
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.

264
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.

265
Q

What joints tend to be affected in seronegative spondyloarthropathies?

A

Asymmetrical large joints.

266
Q

What joints tend to be affected in RA?

A
  1. MCP.
  2. PIP.
  3. Wrist.
267
Q

Antiphospholipid syndrome is often characterised by 2 key clinical features. What are they?

A

Recurrent miscarriage (due to blood clots) and thrombosis.

268
Q

What is polymyalgia rheumatica (PMR)?

A

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

269
Q

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

A

PMR will show raised inflammatory markers.

270
Q

What disease is giant cell arteritis associated with?

A

Polymyalgia rheumatica.

271
Q

What class of drugs can cause Raynaud’s?

A

Beta blockers.

272
Q

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

A

Nifedipine - CCB.

It relaxes blood vessels and stops vasospasm.

273
Q

Psoriatic arthritis commonly involves swelling of what joint?

A

DIP joint.

274
Q

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

A

Dactylitis, sausage like swelling.

275
Q

Describe a psoriatic plaque.

A

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

276
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.
277
Q

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

A
  1. Sacroiliitis.

2. Syndesmophytes (bamboo spine).

278
Q

What condition must be always ruled out in a acutely inflamed joint?

A

Septic arthritis.

Aspirate the joint!

279
Q

Give 3 symptoms of osteomlacia.

A
  1. Bone pain and tenderness.
  2. Fractures.
  3. Wadding gait.
280
Q

An elderly man presents with worsening bone pain and is found to have an enlarged and bowed tibia. What is the most likely diagnosis?

A

Paget’s disease of bone.

281
Q

An elderly lady with bone pain is found to have hypocalcaemia, hypophosphataemia and a raised ALP. What is the most likely diagnosis?

A

Osteomalacia.

282
Q

What cells secrete RANK ligand?

A

Osteoblasts.

283
Q

What is the function of RANK ligand?

A

It binds to osteoclasts and is essential for their formation, function and survival.

284
Q

What protein inhibits RANK ligand?

A

OPG.

285
Q

What is the function of OPG?

A

OPG inhibits osteoclast formation, function and survival by binding RANK ligand; it prevents RANK ligand from binding to osteoclasts.

286
Q

What is the affect of unopposed RANK ligand?

A

Unopposed RANK ligand leads to increased bone loss. More osteoclasts are stimulated due to a lack of OPG.

287
Q

What enzyme, expressed by osteoclasts, is responsible for bone resorption?

A

Cathepsin K.

288
Q

What provides the best relief for the symptoms associated with ankylosing spondylitis?

A

Exercise.

289
Q

With which disease would you associate positively birefringent crystals?

A

Pseudogout - pyrophosphate crystals that are rhomboid shaped.

290
Q

With which disease would you associate negatively birefringent crystals?

A

Gout - monosodium urate crystals that are thin and needle shaped.

291
Q

What kind of crystals do you see in gout?

A

Monosodium urate crystals - negatively birefringent.

292
Q

What kind of crystals do you see in pseudogout?

A

Calcium pyrophosphate crystals - positively birefringent.

293
Q

Give 5 signs of SLE.

A
  1. Glomerulonephritis.
  2. Thrombocytopenia.
  3. Photosensitivity.
  4. Vasculitis.
  5. Anaemia.
  6. Deforming arthritis.
  7. Pericarditis.
294
Q

What is osteoporosis?

A

Progressive skeletal disease with reduced bone mass and micro-deteriorations. Bone mineral density more than 2.5 sds below the mean

295
Q

What is osteopenia?

A

Pre-cursor to osteoporosis= Bone mineral density 1-2.5 stds below the mean

296
Q

What is the epidemiology of osteoporosis?

A

More common in females over 50. Caucasian and Asian populations more at risk

297
Q

When does peak bone mass occur?

A

25 years

298
Q

How does osteoporosis occur?

A

Increased breakdown by osteoclasts and decreased formation by osteoblasts, leading to loss of bone mass. When there is decreased oestrogen, there is increased numbers of osteoclasts and premature arrest of osteoblasts, and perforation of trabeculae= more likely fracture

299
Q

What are the risk factors of osteoporosis?

A 
Old age
Women
Family history
Previous fracture
Steroid use
Endocrine disease
Alcohol and tobacco
Low BMI
Low testosterone
Early menopause 
Renal or liver failure
Malabsorption
300
Q

What are some lifestyle treatments for osteoporosis?

A

Quit smoking and alcohol
Calcium and vitamin D rich diet
Weight bearing exercise
Balance exercises

301
Q

What is the clinical presentation of osteoporosis?

A

Only get symptoms from fractures

  • Vertebral crush fracture= sudden pain
  • Thoracic vertebral fracture = Kyphoidosis
302
Q

How is osteoporosis diagnosed?

A

Dual energy x-ray absorptiometry (DEXA)= gold standard. Generates T scores. T score of more than 2.5 below mean= osteoporosis.
Calcium, phosphate and alkaline phosphate in bloods all normal

303
Q

What are some pharmacological treatments for osteoporosis?

A

Anti-resorptives to slow down osteoclasts= Bisphosphonates, strontum renelate, denosumab
Hormone replacement therapy of oestrogen or testosterone
Raloxifene

304
Q

What is osteomalacia?

A

Poor bone mineralisation leading to soft bone due to a lack of calcium (adult form of rickets)

305
Q

What is the pathophysiology of osteomalacia?

A

Normal bone mineralisation depends on adequate calcium and phosphate. Vitamin D promotes calcium absorption in the intestines and promotes bone resorption by increasing osteoclast number

306
Q

What is the aetiology of osteomalacia?

A 
Hyperphosphataemia due to hyperparathyroidism
Vit D deficiency
Poor diet
Lack of sunlight 
Drug induced
Liver or renal disease 
Tumour induced
307
Q

What is the clinical presentation of osteomalacia?

A
  • Muscle weakness
  • Dull bone ache
  • Bone pain and tenderness
  • Fracture especially on femur neck
308
Q

What is the clinical presentation of rickets?

A
  • Growth retardation, hypertonia
  • Knock knees, bowed legs
  • Widened epiphyses at wrists
  • Hypocalcaemic tetany in severe cases
309
Q

How is osteomalacia diagnosed?

A

Bloods: Low calcium and low phosphate, raised alk phosphatase, raised PTH, low vit D
Biopsy shows incomplete mineralisation
X ray shows defective mineralisation

310
Q

How is osteomalacia treated?

A

Vit D replacement

  • In dietary insufficiency= Calcium D3 forte
  • In malabsorption/ hepatic disease= Oral ergocalciferol or IM calcitriol
  • In renal disease= Alfacidol or calcitriol
311
Q

What is fibromyalgia?

A

Widespread MSK pain after other conditions are excluded, characterised by central pain due to a central disturbance in pain processing

312
Q

What are the risk factors for fibromyalgia?

A

Female, middle age, low household income, low education status, depression, IBS, ME

313
Q

What is the epidemiology of fibromyalgia?

A

Often over 60 years. More common in females and those with rheumatoid arthritis

314
Q

What is the clinical presentation of fibromyalgia?

A
  • Chronic pain aggravated by cold, stress and exercise in the specific pain areas
  • General morning stiffness
  • Extreme fatigue after minimal exertion
  • Non restorative sleep
  • Patient is often angry as can’t find a reason for pain
315
Q

What are the pain areas associated with fibromyalgia?

A
  • Lower front of neck
  • Base of skull
  • Upper edge of breast
  • Neck and shoulder
  • Upper inner shoulder
  • Elbow
  • Upper outer buttock
  • Inside of knee
  • Hip
316
Q

How is fibromyalgia diagnosed?

A
  • Pain at 11 of 18 tender sites for more than 6 months

- Rule out differentials

317
Q

How is fibromyalgia treated?

A

Educate patient and family about the symptoms
Reset pain thermostat
Low dose tricyclic antidepressants (oral amitriptyline) and anticonvulsants (Oral pregabalin)

318
Q

What is osteomyelitis?

A

Infection localised to bone

319
Q

What is the epidemiology of osteomyelitis?

A

Children more at risk.

320
Q

What infections cause osteomyelitis?

A

Staphylococcus aureus
Coagulase negative staphylococci
Haemophillius influenzae, salmonella, pseudomonas aeruginosa

321
Q

What are the risk factors for osteomyelitis?

A 
Diabetes, IA, sickle cell, peripheral valvular disease
Malnutrition
Decreased immunity 
Prosthetic material
Trauma
322
Q

What is the pathophysiology of osteomyelitis?

A 
Infammatory exudate (in response to bacteria) in the marrow leads to increased intramedullary pressure, with extension of exudate into the bone cortex. 
This causes rupture through the periosteum and interruption of the periosteal blood supply leading to necrosis. This leaves pieces of dead bone (sequestra) and new bone forms around it
323
Q

What are the three ways that infection can spread to bone during osteomyelitis?

A
  1. Directly into bone via trauma or surgery
  2. Spread into bone via soft tissue
  3. Spread from the skin into the blood and then into the bone
324
Q

What are the acute histopathological changes in osteomyelitis?

A

Oedema, inflammatory cells, vascular congestion

325
Q

What are the chronic histopathological changes in osteomyelitis?

A

Sequestra, New bone formation, Neutrophil exudates

326
Q

What is the clinical presentation of osteomyelitis?

A 
Onset over several days
Dull pain at site
Fever, sweats, rigors, malaise
Warmth, erythmia, swelling
If chronic= Sinus formation
327
Q

How is osteomyelitis diagnosed?

A

X ray may show osteopenia
MRI may show oedema
Blood culture for aetiology, ESR and CRP raised. If acute there will be raised WCC (Not if chronic)
Bone biopsy

328
Q

How is osteomyelitis treated?

A

Immobilistation
Tailored antimicrobial therapy= IV teicoplanin, IV flucloxacillin, Oral fusidic acid
Surgical debridgement and removal of dead bone

329
Q

Where is osteomyelitis normally in children?

A

More likely to go into long bones

330
Q

Where is osteomyelitis normally in adults?

A

More likely to go into vertibrae

331
Q

What is the epidemiology of paget’s disease of bone?

A 
Incidence increases with age
Affects up to 10% of individuals by 90
More common in Europe and Northern England
UK has highest prevalence in world 
More common in females
332
Q

What is the aetiology of Paget’s disease of bone?

A

Unknown aetiology
May result from latent viral infection in osteoclasts in susceptible individuals
Family history

333
Q

What is the pathophysiology of Paget’s disease of bone?

A

There is increased osteoclastic bone resororption followed by formation of weaker new bone, increased local bone blood flow and fibrous tissue. Ultimately formation exceeds resorption but new woven bone is weaker= Deformity and fracture risk

334
Q

What are the clinical features of Paget’s disease of bone?

A

Common fracture sites= Pelvis, lumbar spine, femur, thoracic spine, skull and tibia
Often asymptomatic
Bone pain
Joint pain= Cartilage damage and osteoarthritis
Deformities
Neurological complications such as deafness and hydrocephalus
Osteosarcoma

335
Q

How is Paget’s disease of bone diagnosed?

A

Bloods: Increased alk phosphatase, normal calcium and phosphate
Urine= Urinary hydroxyproline excretion is raised
X ray= Localised bone enlargement and distortion, sclerotic changes, osteolytic areas
Isotope bone scans

336
Q

What are the complications of Paget’s disease of bone?

A

Osteoarthritis

337
Q

How is Paget’s disease of bone treated?

A

Bisphosphonates e.g. IV/oral zolendronate or oral alendronate= inhibits bone resorption
NSAIDs e.g. ibuprofen = Pain relief
Disease management and monitoring= Serum alk phos`

338
Q

What is the epidemiology of gout?

A

Common especially in developed countries
More common in males
Rarely occurs before young adulthood
Most common in IA in the UK

339
Q

What is the aetiology of gout?

A
  • Diet= alcohol (beer), purine rich food, high fructose, high saturated fat diet
  • Drugs such as aspirin
  • IHD
  • Family history
  • Renal causes= defective gene for URAT1 transporter, high insulin, diuretics
  • Increased uric acid production
340
Q

What is the pathophysiology of gout?

A

Purines need to be excreted. In the body they are broken down= Hypoxanthine is converted to xanthine and then to uric acid via xanthine oxidase enzyme. This is then excreted via kidneys, but in hyperuricaemia it is converted to monosodium urate crystals which causes symptomatic gout, and causes an inflammatory response.

341
Q

What causes acute gout?

A

Monosodium crystals form, typically in middle aged men, sudden pain, swelling and redness in the first metatarsal joint

342
Q

What are the types of gout?

A
  • Acute gout
  • Chronic gout
  • Tophaceous gout
343
Q

What is tophaceous gout?

A

Peristant hyperuricaemia, monosodium crystals form smooth white deposits (tophi) in skin around joints. Tophi release local proteolytic enzymes which erode bone

344
Q

How is gout diagnosed?

A

Joint fluid aspiration shows needle shaped crystals
Serum uric acid level is raised - may need to be repeated as uric acid levels fall rapidly after an attack
- Over 420 mmol/l in men
- Over 360 mmol/l in women

Serum urea and creatinine, and eGFR

345
Q

How is gout treated?

A

Aim to lower uric acid to normal levels, lose weightm eat dairy, lower alcohol, avoid purine rich food
In acute gout- High dose NSAIDs or COX inhibitor. If NSAID contraindication, offer colchine (but this is very toxic and can cause diarrhoea)

346
Q

How can gout be prevented?

A

Lifestyle changes- stop diuretics, etc
Allopurinol: Inhibits xanthine oxidase so less uric acid production. Not to be given straight after acute attack
Febuxostat: If allopurinol contraindicated

347
Q

What is the epidemiology of septic arthritis?

A

Increases with age

348
Q

What are the possible causes of septic arthritis?

A
  • Staph Aureus = most common
  • Streptococci
  • N. Gonorrhoea
  • Haemophillius influenzae in children
  • Gram negative bacteria e.g. E coli
349
Q

What are the risk factors for septic arthritis?

A
  • Pre existing joint disease e.g. Rheumatoid Arthritis
  • Diabetes mellitus
  • Immunosuppression
  • Chronic renal failure
  • Recent joint surgery/ Prosthetic limbs
  • IV drug abuse
  • Those over 80 and infants
  • Recent intra-articular steroid injection
  • Direct/ penetrating trauma
350
Q

What is the clinical presentation of septic arthritis?

A
  • Pain, red, swollen, fever
  • Most commonly in knee, hip and shoulder
  • Systemic illness
  • Decreased movement
351
Q

How is septic arthritis diagnosed?

A
  • Urgent joint aspiration= Fluid will be purulent, thick and opaque (instead of clear, thin and yellow)- can be cultured
  • Polarised light microscopy for crystals= exclude gout
  • ESR, CRP, WCC raised
  • X ray= Excludes infections
352
Q

How is septic arthritis treated?

A
  • Stop methotrexate and anti-TNF alpha
  • Double prednisolone dose if on long term prednisolone (don’t give if not already on it)
  • Immobilise joint
  • Early physiotherapy
  • IV antibiotics for two weeks after culture
  • Repeated joint drainage
  • NSAIDs
353
Q

What are the risk factors for pseudogout?

A
  • Old age
  • Diabetes
  • Osteoarthritis
  • Joint trauma/ Injury
  • Metabolic disease: haemochromatosis and hyperparathyroidism
354
Q

What is the epidemiology of pseudogout?

A

Affects women mainly

355
Q

Briefly explain the pathophysiology of pseudogout

A

Deposition of calcium pyrophosphate in articular cartilage and periarticular tissue producing the radiological appearance of chonedrocalcinosis (linear calcification parallel to the articular surfaces)

356
Q

What is the clinical presentation of pseudogout?

A
  • Acute synovitis that resembles acute gout but is more common in elderly women
  • Usually affects knee and wrist
  • Very painful attacks
  • Acute hot swollen wrist or knee
357
Q

How is pseudogout diagnosed?

A
  • Joint fluid aspiration and microscopy= Small rhomboid crystals, positively brifringent crystals under polarised light, joint fluid should look purlent so sent for culture to exclude septic arthritis
  • Bloods: raised WCC
  • X-ray: Shows chonedrocalcinosis- linear calcification parallel to articular surface
358
Q

How is pseudogout treated?

A
  • High dose NSAIDs or cox inhibitors
  • If NSAID not tolerated well, then colchicine
  • IM or intra-articular corticosteroid e.g. predrinosolone
  • Aspiration of joint reduces pain dramatically
359
Q

What are the clinical features of Sjorgen’s syndrome?

A

Dry eyes, dry mouth, enlargement of the parotid glands, Blepharitis

360
Q

Briefly explain the pathophysiology of Sjorgen’s syndrome?

A

Not fully known

Possibly inflammation of the glands prompts autoimmune response

361
Q

What is the aetiology of Sjorgen’s syndrome?

A

Can be idiopathic (Primary), or associated with another autoimmune condition (Secondary), often rheumatoid

362
Q

What is the epidemiology of Sjorgen’s syndrome?

A

Classically a disease of middle aged women

363
Q

How is Sjorgen’s syndrome diagnosed?

A

Serum antibodies

Schirmer’s test = Whether the eye can self hydrate

364
Q

How is Sjorgen’s syndrome treated?

A

Artificial tear and saliva replacement

365
Q

What are some possible complications of Sjorgen’s syndrome?

A

Infections of the eyes/Mouth

366
Q

What is the epidemiology of psoriatic arthritis?

A
  • Occurs in 10-40% with psoriasis, and can present before skin changes
367
Q

What are the risk factors for psoriatic arthritis?

A
  • Family history of psoriasis
368
Q

What are the clinical features of psoriatic arthritis?

A

Asymmetrical oligoarthritis
Pain, swelling, stiffness. Reduced range of movement
Systemic symptoms such as lethargy
Most usually, the distal joints of fingers and toes, and lower back.
‘sausage’ fingers and toes. Pitted nails.
Also affects tendons, skin and eyes

369
Q

How is psoriatic arthritis diagnosed?

A
  • Bloods and ESR are often normal
  • X ray= Psoriatic arthritis is centrally erosive. May be a pencil in cup deformity in interphalangeal joints
  • Skin and nail disease
370
Q

How is psoriatic arthritis treated?

A
  • NSAIDs and/or analgesics to help the pain but can occasionally worsen skin lesions
  • Local synovitis responds to intra-articular corticosteroid injections
  • Ciclosporins (immunosuppressants) for severe disease
  • Early intervention with DMARDs can help skin lesions
  • Anti TNF alpha agents for skin and joint disease
371
Q

What is the epidemiology of reactive arthritis?

A
  • In males who are HLA-B27 +ve they have a 30-50x risk

- Men are more commonly affected

372
Q

What are the causes of reactive arthritis?

A
  • GI= Salmonella, shigella, yersinia enterocolitica

- Sexually acquired= Urethritis from chlamydia trachomatis, ureaplasma urealyricum

373
Q

What is reactive arthritis?

A

Sterile inflammation of the synovial membrane, tendons and fascia due to infection

374
Q

What are the clinical features of reactive arthritis?

A
  • Arthritis is typically acute, asymmetrical, lower limb arthritis, occurring a few to a couple of weeks after infection
  • Acute anterior uveitis
  • Enthesitis= common, causes plantar fascitis, Achilles tendon enthesitis
  • Sterile conjunctivitis can occur
  • If HLA-B27 +ve, sacroiliitis and spondylitis may develop
  • Skin lesions that resemble psoriasis
375
Q

How is reactive arthritis diagnosed?

A
  • ESR and CRP are raised in acute phase
  • Culture stool if diarrhoea
  • Sexual health review
  • Aspirated synovial fluid is sterile with increased neutrophil count, check if joint is hot/swollen
  • X ray may show enthesitis
376
Q

How is reactive arthritis treated?

A
  • Joint inflammation= NSAIDs, corticosteroids
  • Treat persisting infection w antibiotics
  • Screen sexual partners
  • Majority of individuals with reactive arthritis have a single attack that settles
  • Relapsing cases use methotrexate, sulfasalazine or TNF alpha blockers
377
Q

What is ankylosing spondylitis?

A

A chronic inflammatory disorder of the spine, ribs and sacroiliac joints. Ankylosis= abnormal stiffening and immobility of joint due to new bone formation

378
Q

What is the epidemiology of ankylosing spondylitis?

A
  • More common and more severe in men

- Usually presents as a young adult <30yrs

379
Q

What are the causes of ankylosing spondylitis?

A
  • HLA-B27

- Klebsiella, salmonella, shigella

380
Q

Briefly explain the pathophysiology of ankylosing spondylitis

A

Lymphocyte and plasma infiltration occurs with local erosion of bone at the attachments of the intervertebral and other ligaments, which heals with new bone = syndesmophyte

381
Q

What are the clinical features of ankylosing spondylitis?

A
  • Characteristic spinal cord abnormalities= loss of lumbar lordosis and increased kyphosis, and limitation of lumbar spine mobility in both sagittal and frontal planes
  • Bamboo spine
  • Pain in the sacroiliac joints to hips/buttocks
  • Morning stiffness over 30 mins
  • Pain improves with exercise
382
Q

How is ankylosing spondylitis diagnosed?

A
  • Blood= raised ESR, High or normal CRP, Normocytic anaemia
  • X ray= Shows erosion and sclerosis, bony spurs, bamboo spine
  • MRI= Shows sacrolitis
383
Q

How is ankylosing spondylitis treated?

A
  • Morning exercise
  • NSAIDS
  • TNF alpha blocker e.g. infliximab
  • Local steroid injection for temporary relief
  • Surgery ie hip replacement
384
Q

What is osteoarthritis?

A

Inflammation of articular and periarticular structure and alteration in cartilage structure. Cartilage loss with accompanying periarticular bone response. Articular cartilage is the most affected.

385
Q

What are the clinical features of osteoarthritis?

A
  • Joint pain exacerbated by exercise
  • Joint stiffness after rest- morning stiffness doesn’t take long to go
  • Reduced functionality
  • Bony swellings and deformity= Heberden’s and Brouchards
  • Crepitus
  • Sometimes warm
  • Can affect any joint but normally weight bearing joints (not particularly symmetrical and normally affects 1 joint first)
386
Q

What are the main pathological features of osteoarthritis?

A

Loss of cartilage and disordered bone repair

387
Q

What are the risk factors for osteoarthritis?

A
  • Females
  • FH
  • Obesity
  • Smoking
  • DM
  • Increasing age
  • Hypermobility
388
Q

What is the aetiology of osteoarthritis?

A
  • Usually primary

- Sometimes secondary to particular joints that have been damaged/ frequently used

389
Q

What is the epidemiology of osteoarthritis?

A

Prevalence increases with age. More common in women, most common form of arthritis

390
Q

How is osteoarthritis diagnosed?

A
  • Examination: Diagnosed in >45yrs, activity related to joint pain, with either no morning stiffness or <30 mins of it
  • X ray (LOSS)= Loss of joint space, osteophytes, subarticular sclerosis, subchondral cysts
  • CRP may be elevated
  • Rheumatic factor and antinuclear antibodies are -ve
  • Aspiration of synovial fluid if theres painful effusion
391
Q

How is osteoarthritis treated?

A
  • Pain relief= Paracetamol or weak opioids
  • Exercise and weight loss
  • Assistive devices
  • Consider surgery as last resort for debilitating
  • Interarticular corticosteroid injection
392
Q

What is the epidemiology of anti-phospholipid syndrome?

A
  • Associated with SLE in 20-30% of cases
  • More often occurs as a primary disease
  • More common in females
393
Q

What are the clinical features of anti-phospholipid syndrome?

A
  • Thrombosis
  • Miscarriage
  • Ischaemic stroke, TIA, MI
  • DVT, Budd-Chiari syndrome
  • Thrombocytopenia
  • Valvular heart disease, epilepsy
394
Q

How is anti-phospholipid syndrome diagnosed?

A
  • Anticardiolipin test: Detects IgG or IgM antibodies that bind the negatively charged phospholipid
  • Lupus anticoagulant test: detects ability of blood to clot
  • Anti-B2- glycoprotein I test

A persistently positive test in 1 or more of these tests is needed to diagnose

395
Q

How is anti-phospholipid syndrome treated?

A

Long term warfarin

396
Q

Briefly explain the pathophysiology of anti-phospholipid syndrome

A

Antiphospholipid antibodies play a role in thrombosis by binding to phospholipid on the surface of blood cells. This changes the function of the cells leading to thrombosis and/or miscarriage

397
Q

List some types of primary bone tumour

A
  • Osteosarcoma
  • Ewing’s sarcoma
  • Chondrosarcoma
398
Q

What is the most common primary bone malignancy in children?

A

Osteosarcoma

399
Q

Where do secondary bone tumours usually arise from?

A 
Lung (Bronchus)
Breast
Prostate
Thyroid
Kidney
400
Q

How are bone tumours diagnosed?

A
  • Skeletal isotope scan
  • X rays
  • MRI
  • Serum alk phos is usually raised
  • Hypercalcaemia in 10-20% of those with metastatic malignancy
401
Q

How are bone tumours treated?

A
  • Analgesics and anti inflammatory
  • Local radiotherapy to bone metastases relieves pain and reduces the risk of pathological fracture
  • Some tumours respond to chemo or hormonal therapy
  • Bisphosphonates e.g. alendronate to help symptomatically
402
Q

What are the red flag symptoms for mechanical lower back pain?

A
  • Age of onset <22 or >55
  • Violent trauma
  • Constant progressive, non mechanical pain
  • Thoracic pain
  • Systemic steroids, drug abuse or HIV
  • Systemically unwell, weight loss
  • Persisting severe restriction of lumbar flexion
  • Widespread neurology
  • Structural deformity
403
Q

What are the main causes of mechanical lower back pain?

A
  • Lumbar disc prolapse
  • Osteoarthritis
  • Fractures
  • Spondylolisthesis
  • Heavy manual handling
  • Stoop/ twist when lifting
  • Exposure to whole body vibration
404
Q

What are the clinical features of mechanical lower back pain?

A
  • Back is stiff and a scoliosis may be present
  • Muscular spasm is visible and palpable, and causes local pain and tenderness
  • Pain is unilateral and helped by rest
  • Episodes are generally short lived and self limiting
  • Sudden onset and pain worse in evening
  • Exercise aggrevates pain
405
Q

How is mechanical lower back pain diagnosed?

A
  • Spinal x rays for red flag
  • MRI preferable than CT
  • Bone scans (DEXA)
406
Q

How is mechanical lower back pain treated?

A
  • Urgent neurosurgical refferal if any neurological deficit
  • Analgesia
  • Combined physio, back muscle training and manipulation
  • Re-education of lifting and exercises to prevent further attacks
407
Q

What is acute disc disease?

A

Prolapse of the intervertebral disc results in acute back pain

408
Q

What is the epidemiology of acute disc disease?

A
  • Disease of younger people as the discs degenerate with age and in the elderly it no longer able to prolapse
409
Q

What are the clinical features of acute disc disease?

A
  • Sudden onset of severe back pain= Often following strenuous activity
  • Muscle spasm leads to a sideways tilt when standing
  • Pain depends on which disc is affected
410
Q

How is acute disc disease diagnosed?

A
  • X rays are often normal

- MRI in whom surgery is considered

411
Q

How is acute disc disease treated?

A
  • Acute= Bed rest on a firm matress, analgesia and epidural corticosteroids
  • Surgery only for severe or increasing neurological impairment
  • Physio in recovery phase
412
Q

What is rheumatoid arthritis?

A
  • A chronic systemic autoimmune disorder causing a symetrical polyarthritis. Disease of the synovial joints
413
Q

What are the clinical features of rheumatoid arthritis?

A
  • Symmetrical
  • Insidious onset of pain in the distal small joints. Pain worse in the morning and in the cold. Joints usually warm and tender
  • Movement limitation and muscle wasting
  • Systemic symptoms
  • Morning stiffness over 30 mins
  • Deformities; Ulnar deviation of fingers, swan neck and boutonniere
  • Can have extra articular manifestations such as pleural effusions, amyloidosis, pericarditis etc
414
Q

Briefly explain the pathophysiology of rheumatoid arthritis

A

Infiltration of the synovium by inflammatory cells, causes angiogenic cytokines and formation of new synovial blood vessels. Synovium proliferates and grows out over the surface of the cartilage producing a pannus= bony erosions

415
Q

How is rheumatoid arthritis diagnosed?

A
  • Bloods= Normochromic normocytic anaemia, ESR and CRP raised, +ve rheumatoid factor in 80%, +ve anti-ccp in 30%
  • X ray= loss of joint space, erosions, soft tissue swelling, soft bones
  • MRI= Erosions and joint margins
416
Q

How is rheumatoid arthritis treated?

A
  • Smoking cessation, decrease BMI, physio
  • B cell inhibitors (Rituximab)
  • TNF-alpha inhibitor (Infliximab)
  • DMARDS= Methotrexate (gold standard)
  • Pain management= NSAIDs and paracetamol
  • Interarticular corticosteroid injection
417
Q

What is vasculitis?

A

A histological term describing inflammation of the vessel wall. Inflammation and necrosis of blood vessel walls with subsequent impaired blood flow= Vessel wall destruction and endothelial injury

418
Q

What are the clinical features of polymyalgia rheumatica?

A
  • Sudden onset of severe pain and stiffness of the shoulders, neck, hips and lumbar spine
  • Symptoms are worse in the morning, lasting 30 mins-hrs
  • Mild polyarthritis of peripheral joints
  • Fatigue, fever, weight loss, depression
419
Q

How is polymyalgia rheumatica diagnosed?

A
  • Clinical history
  • ESR and CRP raised
  • Serum alk phos raised
420
Q

How is polymyalgia rheumatica treated?

A
  • Corticosteroids produce a dramatic reduction of symptoms within 24-48 hrs
  • Decrease dose slowly
421
Q

What is polymysitis?

A

A rare muscle disorder in which there is inflammation and necrosis of skeletal muscle fibres. If the skin is involved= dermatomyositis

422
Q

What viruses are implicated in polymysitis?

A

Coxsackie, rubella and influenza

423
Q

What are the clinical features of polymysitis?

A
  • Symmetrical progressive muscle weakeness and wasting affecting the proximal muscles of the shoulder and pelvic girdle
  • If pharyngeal or laryngeal muscles are involved, can lead to dysphagia, dysphonia and resp failure
424
Q

What are the clinical features of dermatomyositis?

A
  • Characteristic skin changes; heliotrope discolouration of the eyelids and scaly erythematous plaques over the muscles
  • Arthralgia, dysphagia resulting from oesopheageal muscle involvement and raynauds phenomenom
425
Q

How is polymyositis diagnised?

A
  • Muscle biopsy
  • Muscle enzymes
  • Serum antibodies
426
Q

How is polymyositis treated?

A
  • Bed rest and an exercise programme

- Prednisolone

427
Q

How is SLE diagnosed?

A
  • Bloods= Increased ESR, Leucopenia, lymphopenia, thrombocytopenia, anaemia, +ve ANA in 95%, +ve Anti-dsDNA antibody is SLE specific but only positive in 60%
  • Serum complement= Decreased C3 and C4
  • MRI and CT for brain lesions
428
Q

How is SLE treated?

A
  • Reduce sunlight, sunblock
  • NSAIDs for arthralgia, fever and arteritis
  • Antimalarial drugs for mild skin disease, fatigue and arthralgia
  • Immunosuppressives= oral methotrexate
  • Oral corticosteroids for severe flares
  • Biologicals e.g. rituximab
429
Q

What are the clinical features of SLE?

A
  • General: fatigue, malaise, fever, splenomegaly, headaches, lymphadenopathy
  • Arthralgia= Symmetrical joint and muscle pain
  • Mucocutaneous= Photosensitive butterfly rash, vasculitis
  • CVS= Pericarditis, hypertension, IDH and stroke
  • Pulmonary= Pleurisy, pleural effusion
  • Renal= Nephritis, haematuria, glomerulonephritis
  • Neuro= Anxiety and depression
430
Q

What is the epidemiology of SLE?

A

More common in females, peak age of onset between 20-40yrs

431
Q

What is the aetiology of SLE?

A

Cause unknown, HLA gene, some drugs, UV light

432
Q

Briefly explain the pathophysiology of SLE

A

Apoptotic cells and cell fragments are cleared ineffectively by phagocytes, transferred to lymphoid tissue and taken up by APC. Self antigens including nuclear components are presented to T cells, stimulated B cells to produce autoantibodies.

433
Q

What are the clinical features of gout?

A

Sudden severe pain, redness and swelling

Typically in 1st MTP

434
Q

Give 2 examples of large vessel vasculitis

A
  • Giant Cell arteritis

- Takayasu arteritis

435
Q

Give 3 examples of medium vessel vasculitis

A
  • Kawasaki disease
  • Eosinophilic granulomatosis with polyangitis
  • Polyarteritis Nodosa
436
Q

Give 3 examples of small vessel vasculitis

A
  • granulomatosis with polyangitis
  • Eosinophilic granulomatosis with polyangitis
  • Henoch-Scholein Purpura
437
Q

What are the clinical features of Kawasakis disease?

A
  • Fever over 5 days
  • Non-purulent bilateral conjunctivitis
  • Strawberry tongue
  • Erythema and desquamation of palms and soles
438
Q

Where does Kawasaki disease usually effect?

A
  • Mucocutaneous lymph nodes

- Usually affects coronary arteries

439
Q

How would you diagnose Kawasaki disease?

A
  • Increased ESR and/or CRP

- Echo

440
Q

How is Kawasaki disease treated?

A

Aspirin and IV immunoglobulins

441
Q

What is the major complication of Kawasaki disease?

A

Coronary artery spasm

442
Q

What are the clinical features of eosinophilic granulomatosis with polyangitis?

A

Lung and skin problems but can also effect kidneys

= Presents with severe asthma

443
Q

How is eosinophilic granulomatosis with polyangitis diagnosed?

A
  • High eosinophils on FBC

- p-ANCA (MPO antibodies)

444
Q

How is eosinophilic granulomatosis with polyangitis treated?

A

Inhaled cortico-steroids

445
Q

What is the epidemiology of polyarteritis nodosa?

A
  • Rare in the UK
  • Associated with hep B
  • Usually occurs in middle aged men
446
Q

What are the clinical features of polyarteritis nodosa?

A
  • Fever, malaise, weight loss and myalgia
  • Nuerological; mononeuritis multiplex. Numbness, tingling, abnormal sensation
  • Abdominal; Pain due to arterial involvement of the abdominal viscera, GI haemorrhage
  • Renal; Haematuria and proteinuria. Hypertension and kidney disease
  • MI and heart failure
  • Gangrene
447
Q

How is polyarteritis nodosa diagnosed?

A
  • Anaemia
  • WCC and ESR raised
  • ANCA -ve
  • Biopsy of kidney (diagnostic)
  • Angiography
448
Q

How is polyarteritis nodosa treated?

A
  • Control blood pressure

- Corticosteroids e.g. prednisolone, and immunosuppressive e.g. azathioprine

449
Q

What is Marfan syndrome?

A

An autosomal dominant disease affecting the gene involved in creating fibrillin

450
Q

What are the risk factors for Marfan syndrome?

A

Family history

451
Q

What are the clinical features of Marfan syndrome?

A
  • Hypermobility
  • Pectus carinatum/ pectus excavatum
  • High arch palate
  • Tall stature
  • Long limbs
  • Long fingers
452
Q

How is Marfan syndrome diagnosed?

A
  • Physical exam

- Ghent criteria

453
Q

How is Marfan syndrome treated?

A
  • Lifestyle changes; avoid intense exercise, avoid caffeine
  • Beta blockers
  • Yearly echo/ review by opthamologist
454
Q

What is Ehler’s-Danlos syndrome?

A

Group of inherited connective tissue disorders, caused by faulty collagen

455
Q

What are the clinical features of Ehler’s-Danlos syndrome?

A
  • Joint hypermobility
  • Easily stretched skin
  • Easy bruising
  • Chronic joint pain
  • Re-occuring dislocation
456
Q

What are the risk factors for Ehler’s-Danlos syndrome?

A

Family history

457
Q

How is Ehler’s-Danlos syndrome diagnosed?

A

Use beighton score to assess

458
Q

How is Ehler’s-Danlos syndrome treated?

A
  • Physiotherapy
  • Occupational therapy
  • Psychological support
459
Q

What are the complications of Ehler’s-Danlos syndrome?

A

Prone to hernias, prolapse, aortic root dilation, joint pain, abnormal wound healing

460
Q

What is Henoch-Scholein Purpura?

A

IgA vasculitis- IgA deposits in the blood vessels of affected organs such as skins, kidneys, GI tract.

461
Q

What are the clinical features of henoch-Scholein Purpura?

A
  • Symmetrical purpuric rash affecting lower limbs/ buttocks in children
  • Joint pain
  • Abdominal pain
  • Renal involvement (HTN)
462
Q

How is henoch-Scholein Purpura diagnosed?

A
  • Take BP for hypertension
  • Urinalysis= Can see microscopic haematuria/ proteinuria
  • Perform abdo exam
463
Q

How is henoch-Scholein Purpura treated?

A

Supportive: simple analgesia, rest and plenty of fluid

464
Q

What is granulomatosis with polyangitiis?

A

Small vessel vasculitis affecting resp tracts and kidneys

465
Q

What are the clinical features of granulomatosis with polyangitiis?

A
  • Saddle shaped nose
  • Epixstaxis
  • Crusy nasal/ ear secretions
  • Sinusitis
  • Cough/ Wheeze, hemoptysis
466
Q

How is granulomatosis with polyangitiis diagnosed?

A
  • High eosinophils on FBC
  • Histology= Granulomas
  • Presence of c-ANCA
467
Q

How is granulomatosis with polyangitiis treated?

A

(Nasal) Corticosteroids

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