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Year 4 > Rheumatology > Flashcards

Rheumatology Flashcards

1
Q

What features in the history would you expect to see in a patient with gout?

A 
Severe pain in a single joint (usually big toe)
Acute onset (typically <24 hours, often overnight) with episodes lasting 1-2 weeks
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2
Q

What features would you expect to see on examination of a patient with gout?

A

Tender, red, hot, swollen joint
Tophi (chalky deposits) typically in the digits or over the elbow
Marked swelling with red, shiny skin

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3
Q

What investigations would you carry out in a patient with suspected gout?

A 
Baseline LFT and renal function
Serum rate levels
X-ray of symptomatic joints
Screen patients for cardiovascular risk factors
Synovial aspirate (in secondary care)
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4
Q

What criteria scoring system is used to diagnose gout?

A

The Nijmegen criteria (score >7 = 80% chance of gout)

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5
Q

Describe the factors and scores used in the Nijmegen criteria

A

Male sex: 2
Previous reported arthritis attack: 2
Onset within 1 day: 0.5
Joint redness: 1
First metatarsophalangeal joint involvement: 2.5
Hypertension/>1 cardiovascular risk factor: 1.5
Serum uric acid >0.35mmol: 3.5

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6
Q

How is a definitive diagnosis of gout made?

A

Identification of urate crystals in synovial fluid or tophi aspirate

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7
Q

Name 3 key differential diagnoses for gout

A 
Septic arthritis
Pseudo-gout (secondary to chondrocalcinosis)
Psoriatic arthritis (severe psoriasis can cause elevated urate).
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8
Q

When would you refer a patient with suspected gout?

A

You are unsure if they have septic arthritis/other differential
Patient is resistant to treatment

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9
Q

Mechanism of action of allopurinol

A

Xanthine oxidase inhibitor (XO prolongs activity of 6-mercptopurine)

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10
Q

When is urate lowering therapy indicated?

A

Patients with tophi, erosions or recurrent gout attacks (>2/year), renal impairment, nephrolithiasis or on diuretics

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11
Q

Which patients should allopurinol doses be reduced in?

A

Elderly patients
Patients with impaired renal function
Patients with impaired hepatic function

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12
Q

Mechanism of action of Benzbromarone

A

Uricosuric - urate excretion therapy

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13
Q

Why can benzbromarone only be used in hospital?

A

Rare side effect of hepatotoxicity

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14
Q

Guidelines state that serum urate levels should be ?? to achieve rapid clearance of urate crystals and ?? to achieve adequate maintenance

A

<0.3mmol/L

<0.36mmol/L

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15
Q

How long should you wait after starting urate lowering therapy to recheck serum urate levels, and why?

A

2 weeks, as 50% of gout patients will have normal urate levels during an attach due to the effect of inflammation on urate excretion

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16
Q

What is the prophylactic treatment used to prevent gout flares?

A

Allopurinol 100mg daily increased by 100mg every 4 weeks until target serum uric acid reached, side effects occur or maximum dose is reached

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17
Q

What are the side effects of colchicine?

A

Diarrhoea, colic

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18
Q

What patients is colchicine contra-inidicated in?

A

Patients with renal or hepatic impairment who are taking a P-glycoprotein inhibitor or a strong CYP34A inhibitor

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19
Q

What medication should be used to treat gout in patients intolerant of colchicine?

A

Low dose NSAIDs

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20
Q

What lifestyle changes can be made to prevent gout attacks?

A

Reduce/remove diuretics
Reduce alcohol intake to within recommended limits
Gradual weight loss to ideal body weight
Avoid sweetened, sugary beverages and rich foods

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21
Q

What features would you expect to see in the history of someone with a connective tissue disorder?

A 
Photosensitive skin rash
Polyarthritis/polyarthralgia affecting small joints
Pleurisy 
Pericarditis
Muscle pain/weakness
Dyspnoea
Severe Raynaud's
Seizures/focal neurological defects
Psychosis
Mouth ulcers
Dry mouth, dry eyes
Hair loss
Recurrent miscariage
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22
Q

What features would you expect to see on examination a patient with a connective tissue disorder?

A 
Skin rash
Synovitis
Mouth ulcers
Scarring alopecia
Sclerodactyly
Raynaud's (with digital ulceration)
Telangiectasia
Pleural or pericardial effusion
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23
Q

What investigations would you perform in a patient with suspected connective tissue disease?

A

FBC & ESR (will show raised ESR, anaemia, leukopenia and thrombocytopenia)
Immunology (will show ANA +++, anti dsDNA +, extricable nuclear antigen (ENA) +

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24
Q

When should you consider referral of a patient with suspected connective tissue disorder

A

Patient with several (<4) symptoms

Patient with signs and have a + ANA and sDNA antibody

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25
Q

What features would you expect to see in the history of a patient with fibromyalgia?

A 
Generalised musculoskeletal pain
Fatiguability
Disability
Constant fatigue, poor sleep
Poor concentration
Irritability
Associated facial pain, IBS, irritable bladder, allodynia, chemical sensitivity and tension headaches
History of stressful events often dating back to childhood
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26
Q

What features would you expect to see on examination in a patient with fibromyalgia

A

Multiple tender spots on the back and anterior trunk with moderate digital pressure

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27
Q

What investigations would you perform in a patient with suspected fibromyalgia?

A 
Routine bloods (should be normal)
Inflammatory markers
TFTs
Bone profile (calcium, vit D, etc)
Anti-CCP antibodies (to rule out RA, should be negative)
Imaging (to exclude other disease)
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28
Q

How would you manage a patient with fibromyalgia?

A

Education
Pain control - gabapentin, amitryptilline, nortriptylline, fluoxetine
Sleep disturbance - guidance on getting a good night’s sleep
Physiotherapy
CBT

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29
Q

What features would you expect to see in the history of a patient with ankylosing spondylitis?

A

Low back pain and stiffness in sacroiliac region, sometimes radiating to buttocks
Marked early morning stiffness, improving as day goes on
Onset in the late teens/early 20s
Associated iritis and IBD

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30
Q

What features would you expect to find on examination of a patient with ankylosing spondylitis?

A

Reduced range of spinal movements

Reduced chest expansion

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31
Q

What investigations would you carry out in a patient with suspected ankylosing spondylitis?

A

ESR & CRP (often raised but may be normal)

Pelvic and lumbar spine X-rays (sacroileitis and possible syndesmophytes)

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32
Q

What differential diagnoses would you consider in a patient with suspected ankylosing spondylitis?

A

Prolapsed intervertebral disc (pain will follow nerve root distribution)
Mechanical back pain (worse on movement, relieved by rest)

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33
Q

What features would you expect to see in the history of a patient with giant cell arteritis and polymyalgia rheumatica?

A 
New onset headache (usually unilateral in the temporal or occipital area)
Jaw claudication
Scalp tenderness/pain
Visual disturbances
Neurological involvement (rare)

Symmetrical pain and stiffness affecting shoulder and pelvic girdle
Difficulty raising from chair unaided and brushing hair
General malaise
Age >50

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34
Q

What features would you expect to see on examination in a patient with giant cell arteritis?

A

Usually unremarkable on examination
Occasionally focal tenderness or thickening over temporal artery
Visual field defects or reduced visual acuity

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35
Q

What investigations would you perform in a patient with suspected giant cell arteritis/PMR?

A 
Routine bloods (will show mild anaemia, elevated ESR &amp; CRP)
Temporal artery biopsy (can be negative)
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36
Q

What are the indications for referral of a patient with GCA?

A

Unusual presentation (suggestive symptoms but normal ESR, age <50)
Patient fails to respond adequately to corticosteroid treatment (suggests diagnosis is wrong)
Symptoms cannot be controlled with <10mg daily prednisolone (may need to consider immunosuppressive therapy)

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37
Q

Describe the management plan for a patient diagnosed with GCA

A
  1. Check FBC & ESR before commencing treatment
  2. 40-60mg daily prednisolone (>0.75mg/kg/day)
  3. Review after a week of treatment and recheck FBC & ESR - symptoms should dramatically improve and ESR should fall in 2-3 days
  4. Continue high-dose steroid therapy for 4 weeks
  5. Step-down steroid therapy by 10mg every 2 weeks until 20mg daily dose is reached
  6. Step-down steroid therapy by 2.5mg every 2 weeks until 10mg daily dose is reached
  7. Step-down steroid therapy by 1mg every month until the steroids can be completely withdrawn
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38
Q

In a patient with GCA, you should treat an asymptomatic patient with steroids if their ESR is high (true/false)

A

False - steroid dose should be titrated against ESR and symptom presence

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39
Q

What should you do if symptoms reoccur during the steroid step-down process in a patient with GCA?

A

Increase the prednisolone dose to the one which was last controlling symptoms and recommence the program of reduction.

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40
Q

What two medications should all patients undergoing GCA treatment receive?

A

Calcium and Vitamin D supplements.
Additional bone protection (bisphosphonates) should be considered in all patients >65 or patients <65 with a T-score of <1.5.

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41
Q

What features would you expect to see in the history of a patient with Hypermobility syndromes?

A

Generalised joint pain
Increased joint laxity
Back pain
Dislocations (uncommon)

Fibromyalgia-like syndromes
Easy bruising 
Abdominal symptoms 
Mitral valve prolapse
Postural tachycardia symptoms
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42
Q

Describe the test and scores used to calculate a modified Beighton score for patients with suspected hyper mobility?

A

Extend 5th finger by 90o: 1 point for each side
Extend thumb back to touch forearm or lie parallel to forearm: 1 point for each side
Extend elbow by >10o: 1 point for each side
Extend knee by >10o: 1 point for each side
Bend over and tough floor with flat of hands with legs straight: 1 point

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43
Q

How would a diagnosis of hyper mobility be made?

A

A score >3 on the modified Beighton test alongside pain for >3 months in >3 joints.

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44
Q

How is hypermobility managed?

A

Patient education
Pain relief - analgesics, NSAIDs, gabapentin, amitryptilline, fluoxetine
Physiotherapy - muscle strengthening to improve joint stability

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45
Q

Describe the management algorithm for a patient with OA?

A

1) Disease education, weigh loss and physiotherapy
2) Topical NSAIDs, paracetamol
3) Oral NSAIDs
4) Substitute compound analgesic for paracetamol
5) Add gabapentin or low dose amitryptilline
6) Consider tramadol
7) Consider strong opiate

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46
Q

What features would you expect to see in the history of a patient with polymyalgia rheumatica?

A 
Symmetrical pain and stiffness affecting shoulder and pelvic girdle
Difficulty rising from chair unaided
Difficulty combing hair
General malaise
Age >50
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47
Q

What features would you expect to see on examination of a patient with polymyalgia rheumatica?

A

Nothing (trick question lol)

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48
Q

What investigations would you perform in a patient with suspected polymyalgia rheumatica?

A

Routine bloods (normally normal except raised ESR)

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49
Q

When would you consider referring a patient with polymyalgia rheumatica to rheumatology?

A

When the patient fails to respond adequately to corticosteroid treatment
When symptoms can not be controlled with <10mg prednisolone daily (consider immunosuppressive treatment)

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50
Q

Describe the management plan of a patient with polymyalgia rheumatica

A
  1. Check FBC and ESR
  2. Prescribe 15-20mg prednisolone daily
  3. Review after 1 week - assess symptomatic response and recheck ESR - symptoms should improve dramatically and ESR should have fallen
  4. Reduce steroid dose by 2.5mg/month until daily dose is 10mg
  5. Reduce steroid dose by 1mg/month until treatment can be withdrawn (usually 1-2 years)
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51
Q

What should you do if a patient symptoms recur during treatment for polymyalgia rheumatica?

A

Increase prednisolone dose by 5mg daily then resume dose reduction at 1mg/month

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52
Q

What additional medications should you consider in patients on steroid therapy for polymyalgia rheumatica?

A

Bisphosphonates in patients >65 taking >7.5mg prednisolone for >3 months, or patients <65 with a DEXA scan T-score <1.5.

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53
Q

What features would you expect to see in the history of a patient with psoriatic arthritis?

A

Joint pain, stiffness and swelling in an asymmetrical distribution affecting the PIP and DIP joints of the hands, feet and large joints
Early morning joint stiffness (typically <30 mins)
Inactivity gelling
History of psoriasis

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54
Q

What features would you expect to see on examination of a patient with psoriatic arthritis?

A

Soft tissue swelling, tenderness of affected joints
Nail pitting and nail dystrophy
Skin rash

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55
Q

What investigations would you perform in a patient with suspected psoriatic arthritis?

A

FBC & ESR (ESR raised)
Anti-CCP antibodies (typically negative)
X-ray of affected joints

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56
Q

What is the main differential diagnosis to consider in a patient with suspected psoriatic arthritis?

A

Osteoarthritis in a patient with concurrent psoriasis.

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57
Q

How would you differentiate between a patient with psoriatic arthritis and a patient with osteoarthritis and concurrent psoriasis?

A

Patients with OA and psoriasis will have bony swelling of the DIP, PIP and MCPJs rather than synovitis, and stiffness will not be limited to the morning. OA will show joint changes and no erosions on X-ray.

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58
Q

What features would you expect to see in the history of a patient with rheumatoid arthritis?

A

Joint pain, stiffness and swelling in a symmetrical distribution affecting wrists, MCPJ/MTPJ and PIPs in the hands and feet. Large joints may also be affected.
Early morning stiffness (typically >30 mins)
Inactivity gelling

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59
Q

What features would you expect to see on examination of a patient with rheumatoid arthritis

A

Soft tissue swelling and tenderness of affected joints

Painful squeeze test

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60
Q

What investigations would you carry out in a patient with suspected rheumatoid arthritis?

A

FBC, ESR, LFTs
Anti-CCP antibodies
X-ray of affected joints

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61
Q

How is the severity of rheumatoid arthritis assessed?

A

Das28 score

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62
Q

Describe the factors and scores considered in the DAS28 test

A 
Joints affected:
1 large joint - 0
2-10 large joints - 1
1-3 small joints - 2
4-10 small joints - 3

ESR & CRP
Normal - 0
Raised - 1

Duration of symptoms:
<6 wks - 0
>6 wk - 1

Immunology:
Negative CCP - 0
Low positive CCP - 2
High positive CCP - 3

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63
Q

A DAS28 score of >? is definitive of rheumatoid arthritis

A

> 6
Score <4 - consider other diagnosis
Score 4-5 - potential RA

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64
Q

What are the differential diagnoses which should be considered in a patient with suspected rheumatoid arthritis?

A

Viral arthritis
Osteoarthritis
Psoriatic arthritis

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65
Q

What features would you expect to see in the history of a patient with Osteogenesis Imperfecta?

A 
Multiple low trauma fractures during childhood/adolescence continued into adult life
Back pain
Height loss
Deafness
Soft tissue injury
Family history
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66
Q

What features would you expect to find on examination of a patient with Osteogenesis Imperfecta?

A

Blue sclera
Hypermobility
Bone deformity (in severe cases)

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67
Q

What investigations would you carry out in a patient with suspected Osteogenesis Imperfecta?

A

Routine bloods and Vitamin D levels
X-ray of thoracic and lumbar spine
DEXA scan (unless already done in last 5 years)

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68
Q

What features would you expect to see in the history of a patient with Paget’s Disease of the Bone

A 
Bone pain
Pathological fracture
Bone deformity
Deafness
Osteoarthritis
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69
Q

What features would you expect to see on examination of a patient with Paget’s disease of the bone

A 
No abnormalities
Bone deformities (usually affecting the tibia, skull and fibula)
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70
Q

What investigations would you perform in a patient with suspected Paget’s disease of the bone?

A 
Routine bloods (Raised ALP)
X-ray lumbar spine and pelvis (Abnormal in 70% of patients)
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71
Q

What treatment would you recommend in a patient with symptomatic Paget’s disease which is not controlled by simple analgesics?

A

IV bisphosphonates (single IV zolendronate infusion) to suppress bone turnover and reduce pain.

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72
Q

What is the prevalence of RA?

A

1%

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73
Q

What is the female: male ratio of RA?

A

3:1

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74
Q

How much does RA decrease life expectancy by in males and females

A

Males - 4 years

Females - 10 years

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75
Q

How many loci have been associated with RA, and which ones show the strongest association?

A

~100 loci

HLA-DRB1, HLA-B and HLA-DPB1

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76
Q

What is the main risk factor for RA?

A

Smoking

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77
Q

What is the main protective factor for RA?

A

Pregnancy - many people enter remission due to immunosuppression and hormonal changes

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78
Q

What cells invade the synovial membrane in RA?

A

Lymphocytes
Plasma cells
Dendritic cells
Macrophages

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79
Q

What is the role of lymphoid follicles in RA?

A

Lymphoid follicles form in the synovial membrane and activate T-cells to produce cytokines, and B-cells to produce antibodies (RF and ACPA).

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80
Q

Describe the role of T-cells in RA

A

T-cells produce TNFa and INF-y which activate synovial macrophages which activate synovial fibroblasts to produce further cytokines

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81
Q

Describe the role of synovial fibroblasts in RA

A

Synovial fibroblasts proliferate, causing synovial hypertrophy and produce matrix metalloproteinases which degrade soft tissue and cartilage. The inflamed synonym produces PGs and NO which causes vasodilation resulting in swelling and pain.

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82
Q

Systemic release of … triggers production of the acute phase response proteins by the liver in RA?

A

IL6

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83
Q

What are the pathological features of RA?

A

Inflamed synovial membrane
T-lymphohyctes, macrophages and fibroblasts in the panes
Neutrophils in the synovial fluid

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84
Q

Describe the typical presentation of a patient with undiagnosed RA

A

Symptoms >6 weeks duration
Symmetrical polyarticular joint pain, swelling
Morning stiffness lasting >1 hour
Systemic symptoms (weight loss, fatigue, fever, susceptibility to infection)
Extra-articular symptoms

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85
Q

Describe the MSK features of RA

A

Muscle wasting
Tenosynovitis
Bursitis
Osteoporosis

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86
Q

Describe the haematological features of RA

A

Anaemia
Thrombocytosis
Eosinophilia

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87
Q

Describe the lymphatic features of RA

A

Felty’s syndrome

Splenomegaly

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88
Q

What is Felty’s syndrome?

A

Presence of RA, splenomegaly and a low WCC

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89
Q

Describe the ocular features of RA

A

Episcleritis/scleritis
Scleromalacia
Keratoconjuctivis sicca

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90
Q

Describe the vascular features of RA

A 
Digital arteritis
Ulcers
Pyoderma gangrenosum
Mononeuritis multiplex
Visceral arteritis
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91
Q

Describe the cardiac features of RA

A

Pericarditis/myocarditis/endocarditis
Conduction defects
Coronary vasculitis
Granulomatous aortitis

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92
Q

Describe the pulmonary features of RA

A

Nodules/Caplan syndrome
Pleural effusion
Fibrosing alveolitis
Bronchiolitis

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93
Q

Describe the neurological features of RA

A

Cervical cord compression
Compression neuropathies
Peripheral neuropathies
Mononeuritis multiplex

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94
Q

Name some deformities characteristic of RA

A

Ulnar deviation
Swan neck
Boutonniere
Z-thumb

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95
Q

What is the main indication for X-ray in RA patients?

A

Assess for structural damage

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96
Q

What is the DAS28 score used to assess, and how is it calculated?

A

Used to assess disease activity, response to treatment and need for biologic therapy.
Calculated by counting the number of involved joints, the ESR and the patient global health.

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97
Q

What tests could you do to help you establish a diagnosis of RA?

A 
Clinical picture
CRP
ACPA
RF
Ultrasound/MRI
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98
Q

What tests could you do to help you monitor disease activity/drug efficacy in RA?

A

DAS28 score

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99
Q

What tests could you do to help you monitor drug safety in RA?

A 
Urinalysis
FBC
Chest X-ray
U&amp;Es
LFTs
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100
Q

Describe the typical management plan in RA patients

A

1) Initiate steroid step down therapy (30mg, reduce by 5mg every 2 weeks)
2) Initiate methotrexate (15mg weekly) and folic acid (5 mg weekly) - can escalate to 25mg depending on response
3) Commence additional DMARD - usually triple therapy
4) Commence additional/subsitute DMARD or glucocorticoids
5) Commence biologic - reduce dose after 12 months of remission

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101
Q

What is the triple therapy used for RA?

A

Methotrexate
Hydroxychloroquine
Sulfasalazine

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102
Q

What could you use to treat a transient RA flare?

A

Intra-articular glucocorticoid injections OR a short course of oral glucocorticoids

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103
Q

Mechanism of action of methotrexate

A

Dihydrofolate reductase inhibitor

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104
Q

Side effects of methotrexate

A 
Hair loss
GI upset
Pneumonitis
Hepatotoxicity
Reduced WCC/platelets
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105
Q

What advice would you give to a woman of reproductive age on methotrexate?

A

Discontinue >3 months before conception

Don’t use during breast-feeding

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106
Q

Side effects of sulfasalazine

A 
Skin rashes
GI upset
Reversible azoospermia
Anaphylaxis
Reduced folic acid levels
Abnormal LFTs
Reduced WCC/platelets
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107
Q

What monitoring would you do in an RA patient on methotrexate?

A

Regular FBC, LFTs and U&Es

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108
Q

What advice would you give to an RA patient on sulfasalazine?

A

Get regular FBC and LFTs

Report unexplained bleeding/bruising/purpura/sore throat or fever

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109
Q

Side effects of leflunomide

A

Hepatotoxicity

Reduced WCC/platelets

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110
Q

What advice would you give to an RA patient on leflunomide?

A

Get regular FBC, LFTs and U&Es
Discontinue >24 months before conception
Don’t use in breast-feeding

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111
Q

Side effects of azathioprine

A 
Myelosuppression
GI symptoms
Skin eruptions
Hepatotoxicity
Reduced WCC/platelets
Increased cancer risk with long term use
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112
Q

Mechanism of action of azathioprine

A

Purine analogue which inhibits DNA synthesis

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113
Q

Mechanism of action of Infliximab

A

TNFa inhibitor

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114
Q

Side effects of Infliximab

A 
Hypotension
Chest pain
SOB
Rash/itching
Fever/chills
TB/Hep B reactivation
Hepatosplenic T-cell lymphoma
Drug-induced lymphoma
Demyelinating CNS disorders
Vitiligo
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115
Q

Mechanism of action of tocilizumab

A

Anti-IL6

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116
Q

Mechanism of action of abatercept

A

Prevents T-cell activation

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117
Q

Mechanism of action of Rituximab

A

B-cell inhibitor

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118
Q

What could you consider in patients who fail to respond to biologics or intra-articular injections?

A

Synovectomy
Joint replacement
Metatarsal head excision
Fusion of wrist/ankle

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119
Q

List the potential complications of RA

A

Osteoporosis
Amyloidosis
Microcytic anaemia - caused by NSAID-induced GI bleed
Normochromic normocytic anaemia/thrombocytosis
Felty’s syndrome
Lymphadenopathy

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120
Q

Mechanism of action of hydroxychloroquine

A

Decreases TLR signalling (by increasing lysosomal pH in antigen-presenting cells)

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121
Q

Side effects of hydroxychloroquine

A 
Eye problems
GI upset
Acne
Blisters
Blood disorders
Convulsions
Vision difficulties
Diminished reflexes
Emotional changes
Pigmentation changes
Hepatotoxicity
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122
Q

Mechanism of action of leflunomide

A

Dihydroorotate inhibitor - inhibits synthesis of pyrimidines

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123
Q

When is leflunomide contra-indicated?

A

Pregnancy/breast-feeding
Liver disease
Hepatitis B/C infection
Serious infection

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124
Q

What monitoring would you do regularly in patients on DMARDs for RA?

A

Monthly FBC
Regular LFTs
Regular U&Es
Regular CRP

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125
Q

What monitoring would you do regularly in patients on biologics for RA?

A

Regular FBC, LFTs, lipid panel
Annual skin examination
TB/Hep B monitoring
Blood pressure and heart monitoring

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126
Q

Side effects of Tocilizumab

A 
Hepatotoxicity
Reduced WCC
Upper respiratory tract infections
Headache
Hypertension
Hypercholesterolaemia
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127
Q

Side effects of Abatercept

A

Infection
Anaphylaxis
Increased progression of slow growing cancer
URTIs

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128
Q

Side effects of Rituximab

A 
Infection
Rash/itching
Hypotension
SOB
Hep B reactivation
Leukoencephalopathy 
Toxic epidermal necrosis
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129
Q

Side effects of Baricitinib

A

URTIs

Hypercholesterolaemia

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130
Q

Mechanism of action of Baricitinib

A

JAK Kinase inhibitor

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131
Q

Mechanism of action of cyclophosphamide

A

Alkylating agent - interferes with DNA duplication

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132
Q

Side effects of cyclophosphamide

A 
GI upset
Bone marrow suppression
Hemorrhagic cystitis
Pigmentation changes
Hair loss/changes
Lethargy
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133
Q

When is cyclophosphamide contra-indicated?

A

Pregnancy/breast-feeding
Active infection
Neutropenia
Bladder toxicity

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134
Q

Side effects of glucocorticoids

A 
Immunodefifiency 
Hyperglycaemia
Easy bruising
Thin skin
Reduced calcium absorption and OP
Weight gain
Impaired memory/attention span
Muscle/tendon breakdown
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135
Q

Side effects of paracetamol

A

Hepatotoxicity

Rash

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136
Q

Side effects of NSAIDs

A

GI upset/ulcers
Kidney disease
Adverse cardiovascular events
Asthma

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137
Q

When are NSAIDs contra-indicated?

A 
>50s
GI upset
Uncontrolled hypertension
Kidney disease
IBD
Past TIA/stroke
Asthma
3rd trimester of pregnancy
138
Q

??? is the most common inflammatory arthritis in men and older women

139
Q

Prevalence of gout

140
Q

Gout shows a ?:1 male:female ratio

141
Q

Risk factors for gout

A 
Obesity
Metabolic syndrome
High alcohol intake
Generalised OA
Diet high in game/offal/seafood, low in Vit C
Age
Male
Ethnicity (Pacific and Maoris islanders)
High serum uric acid levels
Lead poisoning
142
Q

Describe the pathophysiology of gout

A

Gout is caused by deposition of monosodium urate monohydrate crystals in the synovial joint. The body’s uric acid concentration depends on the balance between purine synthesis (2/3) and dietary intake (1/3) and elimination by the kidney and gut. Purine synthesis is regulated by xanthine oxidase.

143
Q

in 90% of gout patients, the main abnormality is …?

A

Renal uric acid excretion, which is genetically determined

144
Q

List some causes of diminished renal uric acid excretion

A 
Increased renal tubular absorption
Renal failure
Lead toxicity
Lactic acidosis
Alcohol
Drugs (thiazides, aspirin, cyclosporin, pyrazinamide)
145
Q

List some causes of increased uric acid production

A 
Myeloproliferative disease
Lymphoproliferative disease
Psoriasis
High fructose intake
Glycogen storage disease
Inherited disorders (Lesch-Nyhan syndrome, Phosphoribosyl pyrophosphate synthetase 1 mutations)
146
Q

First line treatment for an acute flare up of gout

A

Colchicine

147
Q

Mechanism of action of colchicine

A

Inhibits microtubule assembly in neutrophils

148
Q

Side effects and contra-indications of colchicine

A

GI upset

CI in renal impairment, hepatic impairment and patients taking P-glycoprotein inhibitors or CYP34A inhibitors

149
Q

2nd line treatment for a gout flare up

150
Q

1st line treatment for gout prophylaxis

A

Allopurinol

151
Q

2nd line treatment for gout prophylaxis

A

Febuxostat

152
Q

Mechanism of action of Febuxostat

A

Xanthine oxidase inhibitor

153
Q

List 3 uricosurics which can be used to prevent gout

A

Probenecid
Sulfinpyrazone
Benzbromarone

154
Q

List some considerations that have to be taken into account with uricosurics

A

CI in over-producers of uric acid
CI in renal impairment or urolithiasis
Require patients to maintain high fluid intake
Can only be initiated in hospital due to high toxicity

155
Q

Mechanism of action of pegloticase

A

Enhance uric acid breakdown

156
Q

When is pegloticase indicated?

A

Tophaceous gout reistant to standard therapy

157
Q

What lifestyle measures should be recommended to a gout patient?

A

Weight loss
Reduce alcohol intake
Avoid seafood and offal
Substitute anti-hypertensives for losartan if possible

158
Q

Prevalence of fibromyalgia

A

2-3%, reaches a peak of 7% in women >70

159
Q

Fibromyalgia shows a ??:1 female: male ratio

160
Q

Risk factors for fibromyalgia

A

Female sex

Life events causing psychosocial distress

161
Q

Two interrelated abnormalities in fibromyalgia

A

1) Non-restorative sleep

2) Pain sensitisation

162
Q

Average age of onset of PMR and GCA

163
Q

GCA and PMR affect females and males in a ?:1 ratio

164
Q

What is the overall prevalence of GCA and PMR in >50s?

A

~2 in 10,000 people affected

165
Q

What may you see on a fundoscopy in a patient with GCA?

A

Pale/swollen optic disc 24-36 hours after event

166
Q

What 3 tests could you do to definitively diagnose GCA?

A

1) Temporal artery biopsy
2) Temporal artery ultrasound
3) Fluorodeoxyglucose PET scan

167
Q

What would you see on a temporal artery biopsy in a patient with GCA?

A

Fragmentation of the internal elastic lamina, with necrosis of the media, in combination with mixed inflammatory cell infiltrate

168
Q

What would you see on a temporal artery ultrasound in a patient with GCA?

A

‘Halo’ sign around affected arteries

169
Q

What would you see on a Fluorodeoxyglucose PET Scan in a patient with GCA?

A

Strongly positive result

170
Q

1st line management of GCA/PMR?

A

Prednisolone (with oral bisphosphonate, calcium and vitamin D supplementation)

171
Q

When should symptoms resolve after starting steroid treatment in a PMR/GCA patient?

A

48-72 hours after starting treatment

172
Q

Higher doses of prednisolone are required in PMR compared to GCA (true/false)

173
Q

What rate of reduction is suggested in steroid step down therapy in patients with GCA/PMR?

A

1mg per month

174
Q

Prevalence of pseudogout in 65-75 year olds, and >585s

A

10-15% of 65-75 year olds

30-60% of >85s

175
Q

Risk factors for pseudogout

A 
Age
OA
Primary hyperparathyroidism
Familial factors
Haemochromotosis
hypophosphatasia
Hypomagnesemia
Wilson's disease
176
Q

Triggers for an attack of pseudogout

A

Trauma
Intercurrent illness
Dehydration
Surgery

177
Q

Describe the pathophysiology of pseudogout

A

Condition associated with deposition of calcium pyrophosphate dihydrate crystals within the articular and hyaline cartilage. The underlying mechanisms are poorly understood.

178
Q

Clinical features of pseudogout

A 
Can be asymptomatic 
Swollen, tender joint
Large joint effusion (warm, erythematous)
Fever
Confusion/Malaise
179
Q

Clinical features of chronic arthropathy caused by pseudogout

A 
Chronic joint pain
Early morning stiffness
Inactivity gelling
Functional impairment
OA features with varying degrees of synovitis
180
Q

What is the 1st line investigation in pseudogout? And what other investigations would you consider?

A

1st line: join aspiration and synovial fluid examination (to demonstrate CPPD crystals and differentiate from gout)
Gram stain and culture of fluid to rule out co-existing sepsis

X-rays - may show calcification in the cartilage
Screening for secondary causes of pseudogout

181
Q

What does synovial joint aspirate look like in patients with pseudogout?

A

Turbid and blood-stained

182
Q

List the potential treatment options for a patient with pseudogout

A

1) Joint aspiration = may provide symptomatic relief
2) Intra-articular glucocorticoids injections, colchicine or NSAIDs
3) Early active mobilisation

183
Q

Most common form of arthritis

184
Q

What percentage of people develop knee and hip OA?

A

45% develop knee OA

25% develop hip OA

185
Q

Risk factors for OA

A 
Family history 
- Multiple epiphyseal dysplasia
- Polygenic inheritance
Developmental abnormalities
- SUFE
-DDH
Limb deformities
Repetitive loading 
- Famers - hip OA
- Miners - knee OA
- Athletes - knee/ankle OA
Destabilising injuries
- Cruciate ligament tear
- Meniscectomy
Obesity
Trauma
Hormonal
- Oestrogen deficiency
- Aromatase inhibitors
186
Q

List the 4 characteristic pathological features of OA

A

1) Focal loss of cartilage
2) Subchondral osteosclerosis
3) Osteophyte formation
4) Remodelling of joint contour

Also see increased bone mineral density, capsule thickening and surrounding muscle wasting.

187
Q

Describe the pathophysiology of OA

A

Chondrocytes start to divide and produce nests of metabolically active cells - these increase production of matrix components but also accelerate the breakdown of major structural components of the collagen matrix. This makes the cartilage vulnerable to load-bearing injury. Fissuring occurs and deep vertical clefts develop, localised chondrocyte death and decreased cartilage thickness occurs.

188
Q

Clinical features of OA

A

Characteristic joint involvement - PIPs, DIPs, knees, hips, neck, lumbar spine
Painful and functional joint restriction
Pain
- insidious onset
- intermittent nature
- mainly related to movement/weight-bearing
-only brief (<15 min) morning stiffness and inactivity gelling

Examination shows:
Restricted movement
Palpable crepitus
Bony swelling
Deformities
Joint line/peri-articular tenderness
Muscle weakness/wasting
Mild/absent synovitis
189
Q

Generalised nodal OA has a weak genetic predisposition (true/false)

A

False - strong genetic predisposition

190
Q

Generalised nodal OA shows a marked female preponderance (true/false)

191
Q

Describe the characteristic features of generalised nodal OA

A 
Polyarticular DIP and PIP joint involvement
Heberden's/Bouchard's nodes
Good functional outcome for hands
Lateral deviation
Predisposition to OA at other joints
192
Q

Which 2 joints does knee OA typically originate in?

A

1) patellofemoral

2) medial tibiofemoral

193
Q

What is an important risk factor which can lead to unilateral OA in men?

194
Q

Describe the characteristic features of knee OA

A

Bilateral and symmetrical knee involvement
Pain localised to anterior or medial aspects of knee and upper tibia
Pain usually worse on stairs/inclines
Difficulty with prolonged walking, rising from a chair, bending over

Examination:
Jerky, antalgic gait
Varus or fixed flexion deformity 
Joint line/peri-articular tenderness
Quadriceps weakness/wasting
Restricted movements with crepitus
Bony swelling
195
Q

Which part of the hip does hip OA commonly affect?

A

The superior aspect of the joint - it is often unilateral and frequently progresses with superolateral migration of the femoral head, which has a poor prognosis.

196
Q

Which part of the hip does hip OA less commonly affect?

A

Medial OA - this shows more central cartilage loss and is largely confined to women. It is often bilateral at presentation but has a better prognosis as axial migration of the femoral head is uncommon.

197
Q

Obesity is associated with a more rapid progression of hip OA (true/false)

198
Q

List the characteristic features of hip OA

A

Anterior groin pain
Functional difficulties

Examination:
Antalgic gait
Quadriceps/gluteal wasting and weakness
Pain and restriction of internal rotation with hip flexed
Fixed flexion, external rotation deformity
Ipsilateral leg deformity

199
Q

Which parts of the spine are most commonly affected by OA?

A

Cervical and lumbar spine

200
Q

List the characteristic features of spine OA

A 
Pain localised to lower back or neck
Pain relieved by rest and worsened by movement
Limited range of movement
Loss of lumbar lordosis
Positive straight leg raise test
201
Q

Describe the typical features of early-onset OA

A

Onset before 45 years old
Monoarthritic
Clear history of previous trauma

202
Q

List the causes of early-onset OA

A 
Previous trauma
Localised instability
Juvenile idiopathic arthritis
Haemochromotosis
Ochronosis
Acromegaly
Spondyloepiphyseal dysplasia
Late avascular necrosis
Neuropathic joint
Kashin-Beck disease
203
Q

Describe erosive OA

A

A group of patients with hand OA who have a more prolonged inflammatory response, more overt inflammation, more disability and worse outcome than nodal OA

204
Q

List the distinguishing features of erosive OA

A

Preferential targeting of PIP joints
Subchondral erosions on X-ray
Occasional ankylosis of affected joints
Lack of association with OA in other joints

205
Q

What investigations would you perform in a patient with suspected OA?

A

1) Plain x-ray of affected joints
- hip = non-weightbearing posteroanterior
- knee = weight-bearing anteroposterior & flexed skyline
- spine = weight-bearing anteroposterior
2) Routine biochemistry, haematology, auto-antibodies (moderate acute phase response seen)
3) Synovial fluid aspirate (viscous with low cell count)
4) Additional investigations in early-onset OA to determine cause

206
Q

List the management options for OA patients

A 
Education
Lifestyle advice
- Weight loss
- Strengthening and aerobic exercise
- Pacing of activities
- Walking aids
Non-pharmalogical measures
- Acupuncture
- TENS
- Heat/cold compress
Pharmalogical measures
- Paracetamol
- Topical NSAID
- Topical Capsaicin
- Oral NSAID
- Antineuropthic drug
Intra-articular glucocorticoid injections
Nutraceuticals

Surgery
Total joint replacement
Osteotomy
Cartilage repair

207
Q

What is the most rapid and destructive joint disease?

A

Septic arthritis

208
Q

Prevalence of septic arthritis

A

2-10 per 100,000 in the general population

30-70 per 100,000 in those with pre-existing joint disease or joint replacement

209
Q

Morality of septic arthritis

210
Q

Risk factors for septic arthritis

A 
Age
Pre-existing joint disease
Diabetes
Immunosuppression
IVDU
211
Q

Most common route of spread of infection in septic arthritis

A

Haematogenous spread from skin infections or upper respiratory tract infections

212
Q

What organisms would you suspect in an adult with septic arthritis?

A

Staphylococcus Aureus

213
Q

What organism would you suspect in a young, sexually active adult with septic arthritis?

A 
Gonococcus (from untreated gonorrhoea). Presents with:
Migratory arthralgia
Low-grade fever
Tenosynovitis
Painful pustular skin lesions
214
Q

Which organisms would you suspect in an elderly patient with septic arthritis?

A

Gram negative bacilli

Group B/C/G streptococci

215
Q

Which organisms would you suspect in an IVDU with septic arthritis?

A

Gram negative bacilli

Group B/C/G streptococci

216
Q

Name 4 less common organisms which can cause septic arthritis

A

Group A streptococci
Pneumococci
Meningococci
Haemophilus Influenzae

217
Q

Describe the clinical features of septic arthritis

A

Acute/sub-acute mono arthritis
Fever
Swollen, hot, red joint
Pain on rest and movement

218
Q

What investigations would you perform in a patient with suspected septic arthritis?

A

1) Joint aspiration –> send for Gram stain and culture (synovial fluid usually turbid and blood-stained)
2) Blood cultures
3) CRP –> may not be raised in elderly or immunocompromised patients or early in disease course

219
Q

Describe the management protocol for a patient with suspected septic arthritis

A

1) Joint aspirate –> Gram stain and culture
Blood cultures
Routine biochemistry and haematology
(Consider other cultures to determine primary source of infection)

2) Commence IV antibiotics –> usually IV Flucloxacillin (covers most Staph and Streps). Use IV Vancomycin if MRSA suspected or IV Gentamicin if you suspect a gram- sepsis.
3) Pain relief
4) Daily joint aspiration
5) Early physiotherapy

220
Q

Which conditions does the term ‘Juvenile Idiopathic Arthritis’ encompass?

A 
Systemic JIA (5%)
Oligoarthritis (60%)
Polyarthritis (20%)
Anthesis-Related arthritis (5%)
RF+ arthritis (5%)
Psoriatic arthritis (5%)
221
Q

Prevalence of JIA

A

1 in 1000 <16s

222
Q

Incidence of JIA

A

1 in 10,000 people a year

223
Q

Immunology of JIA

A 
Systemic JIA - autoantibody -
Oligoarthritis/polyarthritis - ANA+
Anthesis-Related arthritis - HLAB27+
RF+ arthritis - RF+, ACPA+
Psoriatic arthritis - autoantibody negative
224
Q

Describe the clinical features of systemic JIA

A 
Fever
Rash
Arthralgia
Hepatosplenomegaly
Haemophagocytic syndrome
225
Q

What is the investigation of choice to confirm synovitis or tenosynovitis in children with JIA?

A

Ultrasound

226
Q

1st line treatment for JIA?

A

Methotrexate

227
Q

Name 2 treatments which could be considered in JIA patients with uveitis?

A

Azathioprine

Cyclosporin

228
Q

Name the 5 conditions which are considered spondyloarthropathies

A

1) Axial spondyloarthritis
2) Ankylosing spondylitis
3) Reactive arthritis
4) Psoriatic arthritis
5) Enteropathic spondyloarthritis

229
Q

Define spondyloarthropathies

A

A group of related inflammatory MSK diseases that show overlap in their clinical features and have a share immunogenic associated with HLA-B27

230
Q

Describe the clinical features common to spondyloarthropathies

A 
Asymmetrical inflammatory oligoarthritis (more common in lower limb)
History of inflammatory back pain
Sacroileitis and spinal osteitis
Enthesitis
Tendency for familial aggregation
HLA-B27 association
Psoriasis
Uveitis
Sterile urethritis or prostatitis
IBD
Aortic root lesions
231
Q

Prevalence of spondyloarthropathies

232
Q

Describe the suggested pathophysiology of spondyloarthropathies

A

Aberrant host response to infection and abnormal mucosal immunity mediated through changes in IL12, IL23 and Th17

233
Q

Ankylosing spondylitis affects males: females in a ?:1 ratio

234
Q

Prevalence of ankylosing spondylitis

235
Q

Describe the suspected pathophysiology of axial spondyloarthropathies

A

Abnormal host response to intestinal microbiota with Th17 cell involvement - this leads to production of inflammatory cytokines. HLA-B27 is also involved - it can activate leucocytes, and misfiled to cause inflammatory response.

236
Q

List the clinical features of axial spondyloarthropathies

A

Inflammatory back pain, radiating to buttocks and posterior thighs
Early morning stiffness
Symptoms exacerbated by rest and received by movement
Often have history of IBD and psoriasis
Reduced lumbar spine range of movement in all directions
Pain on sacroiliac stressing
High enthesitis index

237
Q

Extra-articular features of axial spondyloarthropathy

A 
Fatigue, anaemia
Anterior uveitis
Prostatitis, sterile urethritis
IBD
Osteoporosis
CVD
Amyloidosis (rare)
Atypical upper lobe pulmonary fibrosis
238
Q

What investigation would you perform in someone with suspected axial spondyloarthropathy?

A

MRI/Ultrasound

239
Q

What is the diagnostic criteria for Axial Spondyloarthritis

A

1) Sacroilitis on MRI AND 1 other feature in history, clinical examination or investigation

OR

2) HLA-B27+ patients with one other clinical feature

240
Q

What is the diagnostic criteria for Ankylosing Spondylitis?

A

X-ray evidence of sacroileitis AND 1 other feature on clinical history, exam or investigation

241
Q

Describe the management of a patient with axial spondyloarthropathy

A

1) Patient education
2) NSAID (can progress to TNF inhibitor or Secukinumab)
3) Physical therapy
4) Consider Sulfasalazine/Methotrexate for severe/persistent MSK features
5) Consider local glucocorticoid injections for persistent plantar fascitits, peripheral arthritis and other enthesopathies

242
Q

Sexually acquired reactive arthritis shows a male: female predominance of ??:1?

243
Q

??% of patients attending a sexual health clinic with non-specific urethritis have sexually acquired reactive arthritis?

244
Q

List the common bacterial causes of reactive arthritis

A 
Chlamydia 
Campylobacter
Salmonella
Shigella
Yersinia
245
Q

List the common causes of non-spondylo- reactive arthritis

A 
Many viruses
Mycoplasma
Borrelia
Streptococci
Mycobacter
246
Q

Describe the clinical features of non-spondylo- reactive arthritis

A

Acute monoarthalgia not associated with HLA-B27

247
Q

Describe the typical features of reactive arthritis

A

Acute onset
Inflammatory enthesitis, oligoarthritis, and/or spinal inflammation
Lower limbs predominantly affected
Systemic features

248
Q

Describe the extra-articular features of reactive arthritis

A 
Circinate balanitis
Keratoderma blennorrhagica
Pustular psoriasis
Nail dystrophy
Mouth ulcers
Conjunctivitis
Uveitis
249
Q

??% of patients still have active disease 20 years after initial presentation with reactive arthritis

250
Q

List some rare complications of reactive arthritis

A 
Aortic incompetence
Conduction defects
Pleuropericarditis
Peripheral neuropathy
Seizures
Meningoencephalitis
251
Q

What investigations would you consider doing in a patient with suspected reactive arthritis?

A

1) Joint aspiration –> exclude gout, sept arthritis
2) ESR –> raised
3) ‘two glass’ test –> demonstration of mucoid threads in first void specimen that clear in the second to confirm urethritis
4) High vaginal swabs –> test for chlamydia
5) Stool culture –> usually negative except in Salmonella, but may show previous dysentery
6) RF, ACPA, ANA –> negative

252
Q

What features would you see on the X-ray of a patient with chronic or recurrent reactive arthritis?

A

1) Periarticular osteoporosis
2) Proliferative erosions
3) Periostitis
4) Large ‘fluffy’ calcaneal spurs
5) Asymmetrical and often unilateral sacroiliitis
6) Coarse and asymmetrical syndesmophytes

253
Q

1st line treatment for reactive arthritis

A

Rest
NSAIDs
Analgesia

254
Q

What treatments could you consider in a reactive arthritis patient when 1st line options have been exhausted?

A

1) Intra-articular or systemic glucocorticoids
2) DMARDs - in patients with marked persistent symptoms or chronic/recurrent disease
3) Anti-TNF therapy in DMARD resistance
4) Treat cause e.g. doxycycline or azithromycin for chlamydia

255
Q

Prevalence of psoriatic arthritis in general population

256
Q

Prevalence of psoriatic arthritis in patients with psoriasis

257
Q

What age does psoriatic arthritis usually onset?

A

25-40 years

258
Q

Studies suggest that heritability of psoriatic arthritis may exceed ??%?

259
Q

What two gene variants are the strongest genetic risk factors for psoriatic arthritis?

A

HLA-B

HLA-C

260
Q

Where do the genetic variants involved in psoriatic arthritis tend to lie?

A

Within or close to IL12, IL23 and NFkB signalling pathways

261
Q

Describe the typical clinical features of psoriatic arthritis

A

Pain and stiffness affecting joints, spine, tendons and enthesis without synovitis

262
Q

List the 6 patterns of psoriatic arthritis

A

1) Asymmetrical inflammatory mono/oligoarthritis –> typically in hands and feet, ‘sausage digits’
2) Symmetrical polyarthritis –> mainly in women, resembles pattern of RA
3) DIPJ arthritis –> similar to generalised nodal OA, associated with psoriatic nail disease
4) Psoriatic spondylitis –> back/neck pain and stiffness
5) Arthritis Mutilans –> targets fingers and toes, ‘telescoping’
6) Enthesitis-predominant –> enthesitis and nail changes

263
Q

What is the CASPAR criteria used to diagnose?

A

Psoriatic arthritis - inflammatory articular disease with 3 or more points

264
Q

What criteria does the CASPAR grading system include?

A 
Current psoriasis (2 points)
History of psoriasis in 1st/2nd degree relative
Psoriatic nail dystrophy
Negative RF IgM
Current dactylitis
History of dactylitis
Juxta-articular new bone
265
Q

How is a diagnosis of psoriatic arthritis made?

A

Clinical features
(Antibodies usually negative)

X-rays may be normal or show erosive changes - features that favour psoriatic arthritis over RA include:

  • Characteristic distribution of proliferative erosions
  • New bone formation
  • Absence of periarticular osteoporosis and osteosclerosis

MRI and Doppler US are increasingly used to detect synovial and enthesis inflammation

266
Q

Describe the management protocol for psoriatic arthritis

A

1) NSAIDs
Analgesia

2) Intra-articular glucocorticoid injections

3) DMARDs - usually methotrexate
(Can also use sulfasalazine, cyclosporin or leflunomide) - pay attention to LFTs as abnormalities are common in psoriatic arthritis

4) Anti-TNF therapy OR Secukinumab (IL17 inhibitor)
Ustekinumab (IL12/23 inhibitor) can be used to improve joint, dactylitis and enthesitis

OR

Apremilast (PDE4 inhibitor) but not as effective as biologics

267
Q

What treatments are contra-indicated in psoriatic arthritis and why?

A

1) Splints and prolonged rest –> tendency to fibrous and bony ankylosis
2) Hydroxychloroquine –> can cause exfoliative skin reactions

268
Q

Side effects of Apremilast

A

Weight loss
Depression
Suicidal thoughts

269
Q

Prevalence of SLE

A

0.02 - 0.3%

270
Q

??% of SLE patients are male?

271
Q

SLE is associated with a ?x increased mortality

A

5x, mainly due to increased risk of premature CVD

272
Q

Describe the pathophysiology of SLE

A

Main pathophysiology is autoantibody production, mainly directed against antigens within the cell or nucleus - this leads to defects in apoptosis or apoptotic cell clearance which leads to inappropriate exposure of intracellular antigens on the cell surface and polyclonal T and B-cell activation

273
Q

List the typical features of SLE

A 
Systemic symptoms - fever, weight loss, lymphadenopathy, fatigue
Arthralgia and early-morning stiffness
Secondary Raynauds
Rash
Proliferative glomerulonephritis
Pericarditis
Increased risk of CVD
Pleurtic pain
Pleual effusion
Pneumonitis
Atelactasis
Reduced lung volume
Pulmonary fiborosis
Headache
Poor concentration
Visual hallucinations
Chorea
Organic psychosis
Transverse myelitis
Lymphocytic meningitis
Blood abnormalities
Mouth ulcers
Perionteal serositis
274
Q

? out of 11 criteria have to be met to be diagnosed with SLE

275
Q

List the 11 criteria used to diagnose SLE

A

1) Malar rash
2) Discoid rash
3) Photosensitivity
4) Oral ulcers
5) Arthritis
6) Serositis
7) Renal disorder
8) Neurological disorder
9) Haematological disorder
10) Immunological evidence
11) ANA

276
Q

What are the 3 mandatory tests needed in a SLE diagnosis?

A

1) ANA –> +
2) ENAs and complement antibodies
3) Routine haematology, biochemistry and urinalysis

277
Q

Describe the management of mild-moderate SLE

A

1) Analgesics
NSAIDs
Hydroxychloroquine

2) Glucocorticoids
Methotrexate/Azathioprine/Mycophenolate mofetil

3) Belimumab

278
Q

Describe the management of severe-life-threatening SLE

A

High dose glucocorticoids e.g. methylprednisolone

High dose immunosuppression e.g. cyclophosphamide

279
Q

Describe the maintenance protocol for SLE

A

Oral prednisolone
Azathioprine/Methotrexate/Mycophenolate mofetil
Control CVD risk factors
Smoking cessation
Warfarin (if antiphospholipid antibodies present)

280
Q

Peak age of onset of systemic sclerosis

A

40-50 year olds

281
Q

Prevalence of systemic sclerosis

A

10-20 per 100,000

282
Q

Systemic sclerosis affects females: males in a ?:1 ratio

283
Q

Name the two types of systemic sclerosis

A

1) Diffuse cutaneous systemic sclerosis (30%)

2) Limited cutaneous systemic sclerosis (70%)

284
Q

List the factors associated with poor prognosis in diffuse systemic sclerosis

A 
Older age
Diffuse skin disease
Proteinuria
High ESR
Low gas transfer for carbon monoxide
Pulmonary hypertension
285
Q

Describe the pathophysiology of systemic sclerosis

A

Autoimmune disorder of connective tissue which results in fibrosis of skin, internal organs and vasculature. T-lymphocytes infiltrate the skin and lead to abnormal fibroblast activation, which leads to excess production of ECM in the dermis. This causes symmetrical thickening, tightening and induration of the skin, arterial narrowing and endothelial injury.

286
Q

List the typical features of systemic sclerosis

A 
Non-pitting oedema of fingers and flexor tendon sheather
Thinning lips
Raynauds
Digital ischaemia
Sclerodactyly
Calcinosis
Telangiectasia

Arthralgia
Flexor tenosynovitis
Muscle weakness/wasting

Erosive oesophagitis
Dysphagia
Odynophagia
Early satiety
Outlet obstruction
'Watermelon' stomach
Bacterial overgrowth
Pseudo-obstruction

Pulmonary hypertension
Interstitial lung disease

Hypertensive renal crisis

287
Q

What investigations would you perform in a patient with suspected systemic sclerosis?

A

1) Routine haematology, renal, liver and bone function tests
Urinalysis

2) Chest X-ray, trans-thoracic echocardiography and lung function tests –> assess for interstitial lung disease and pulmonary hypertension
High-resolution CT –> ?interstitial lung disease
Right heart catheter measurements –> ?pulmonary hypertension

3) Barium swallow –> assess oesophageal involvement
Hydrogen breath test –> indicate bacterial overgrowth

288
Q

Describe the management of systemic sclerosis

A

Raynauds/digital ulcers:

  • Avoidance of cold exposure, thermal insulation
  • Calcium channel blockers/losartan/fluoxetine/sildenafil
  • IV prostacyclin –> severe disease/critical ischaemia
  • Bosentan –> ischaemic digital ulcers
  • Fucidin-hydrocortisone cream –> digital tip health

GI complications:

  • PPIs/anti-reflux agents
  • Rifaximin/tetracycline/metronidazole –> bacterial overgrowth
  • Metroclopramide/domperidone –> dysmotility/pseudo-obstruction

Hypertension
- ACE inhibitors

Joint involvement:

  • Analgesics
  • NSAIDS
  • Methotrexate

Pulmonary hypertension:
- Bosentan

Interstitial lung disease:
- Glucocorticoids and IV cyclophosphamide

289
Q

Which 3 conditions make up a mixed connective tissue disorder?

A

1) Systemic sclerosis
2) Myositis
3) SLE

290
Q

List the 3 typical features of a mixed connective tissue disorder

A

1) Indolent finger puffiness
2) Raynaud’s
3) Myalgia

291
Q

Which antibody is present in most patients with mixed connective tissue disorder?

A

Anti-RNP antibodies

292
Q

Primary Sjogren’s typically onsets between ??-?? years?

293
Q

Primary Sjogren’s affects females: males in a ?:1 ratio

294
Q

Describe the pathophysiology of Sjogren’s syndrome

A

Lymphocytic infiltration of the salivary and lacrimal glands, leading to glandular fibrosis and exocrine failure.

295
Q

Describe the typical features of Sjogren’s

A 
Dry eyes
Conjunctivitis
Blepharitis
Filamentary keratitis
Xerostomia
Dental caries
Salivary gland enlargement
Rashes
Non-erosive arthralgia
Generalised OA
Raynauds
Fatigue
296
Q

Which autoimmune conditions is Sjogren’s commonly associated with?

A 
SLE
Systemic sclerosis
Coeliac disease
Primary biliary cholangitis
Chronic active hepatits
Myasthenia Gravis
297
Q

What test would you do to initially establish a diagnosis of Sjogren’s syndrome?

A

Schirmer tear test - measure tear flow over 5 minutes using absorbent paper strips placed on lower eye lid (>6mm is normal).

298
Q

What test would you do if the diagnosis of Sjogren’s remained in doubt after initial tests?

A

Minor salivary gland biopsy - to demonstrate lymphocytic infiltrate

299
Q

What blood test results would be present in a patient with Sjogren’s?

A 
Raised ESR
Hypergammagobulinaemia
One or more antibodies:
- RF
- ANA
- SS-A (anti-Ro)
- SS-B (anti-La)
- Gastric parietal cell antibody
- Thyroid antibody
300
Q

What two complications do Sjogren’s patients need to be screened for?

A

1) Interstitial lung disease (chest x-ray and lung function tests)
2) Interstitial nephritis

301
Q

Describe the symptomatic management of Sjogren’s

A

Dry eyes –> lacrimal substitutes
Filamentary keratitis –> soft contact lenses, lacrimal duct occlusion
Xerostomia –> chewing gum, artificial salvia
Dental caries –> post-prandial oral hygiene, prompt treatment of oral candidiasis
Vaginal dryness –> lubricants

302
Q

Name the treatment which can be considered in early Sjogren’s disease

A

Systemic pilocarpine - to amplify disease activity

303
Q

What can be used to treat skin and MSK features of Sjogrens?

A

Hydroxychloroquine

304
Q

When would you consider immunosuppressant use in Sjogren’s?

A

Interstitial lung disease (glucocorticoids and cyclophosphamide) and interstitial nephritis (if Hydroxychloroquine alone is not sufficient)

305
Q

What test would you do in a patient with Sjogren’s who had non-resolving lymphadenopathy or salivary gland enlargement, and why?

A

Biopsy to exclude malignancy

306
Q

Incidence of polymyositis and dermatomyositis

A

2-10 per million/year

307
Q

Typical age of onset of Polymyositis and dermatomyositis

308
Q

Pathophysiology of polymyositis and dermatomyositis

A

Skeletal, cardiac and gut smooth muscle inflammation

309
Q

Typical features of polymyositis and dermatomyositis

A

Symmetrical proximal muscle weakness affecting mainly lower limbs and occurring over a few weeks
Difficulty rising from chair/climbing stairs/lifting
Muscle pain
Systemic symptoms
Skin lesions
- Gottron’s papules
- Heliotrope rash
- Periorbital oedema
- ‘Shawl’ rash
- Enlarged, tortuous periungal nail-fold capillaries

310
Q

Interstitial lung disease occurs in ??% of polymyositis and dermatomyositis patients, and is strongly associated with the ??? antibody

A

30%

Antisynthetase

311
Q

What is the pivotal investigation in polymyositis/dermatomyositis and what does it show?

A

Muscle biopsy - shows fibre necrosis, regneration and inflammatory cell infiltrate.

MRI should be used to identify abnormal muscle for biopsy

312
Q

What blood test is a good marker of disease activity in polymyositis/dermatomyositis?

A

Serum CK - should be raised

313
Q

What is the initial management of polymyositis/dermatomyositis?

A

Oral glucocorticoids (or IV in respiratory/pharyngeal weakness), then reduced by 25% each month to a maintenance dose

Can consider immunosuppressive therapy (methotrexate or MMF)

Can consider IV Ig therapy in refractory disease

Mepacrine or Hydroxychloroquine can be used in skin-predominant disease

314
Q

Main risk of glucocorticoid treatment in polymyositis/dermatomyositis?

A

Glucocorticoid-induced myopathy - biopsy shows type II fibre atrophy and treatment response is poor.

315
Q

Most common inflammatory arthropathy in children

A

Juvenile dermatomyositis

316
Q

Incidence of juvenile dermatomyositis

A

2-4 per million

317
Q

Median age of onset of juvenile dermatomyositis

318
Q

Management of juvenile dermatomyositis

A

1) IV methylprednisolone
2) Oral glucocorticoids and methotrexate
3) Cyclophosphamide for lesional ulceration
IV immunoglobulins in resistant disease

319
Q

Clinical features of Adult-onset Still’s disease

A 
Intermittent fever
Rash
Arthlagia
Splenomegaly
Hepatomegaly
Lymphadenopathy
320
Q

What would investigations reveal in a patient with adult-onset Still’s disease?

A

1) Acute phase response
2) Elevated serum ferritin
3) Negative RF and ANA

321
Q

Management protocol for adult-onset Still’s disease

A

1) Glucocorticoids
2) Azathioprine or MMF
3) Canakinumab or anakinra

322
Q

What is the most common bone disease?

A

Osteoporosis

323
Q

Risk factors for osteoporosis

A 
Genetics - LRP5 mutations, oestrogen receptor mutations
Hypogonadism
Hyperthyroidism
Hyperparathyroidism
Cushing's
IBD
Ankylosing spondylitits
Rheumatoid arthritis
Drug
Malabsorption
Chronic liver disease
COPD
CF
Myeloma
Low BMI
HIV
Immobilisation
Heavy smoking
324
Q

What does and duration of glucocorticoid treatment substantially increases osteoporosis risk?

A

> 7.5mg daily for >3 months

325
Q

Symptoms of osteoporosis

A

Osteoporosis is asymptomatic until a fracture occurs. Fracture symptoms:

  • Pain
  • Local tenderness
  • Deformity
326
Q

List 4 common osteoporotic fractures

A

1) Vertebral fracture
2) Colle’s fracture
3) Hip
4) Humerus

327
Q

Define a fragility fracture

A

‘A fracture which occurs from a fall of standing height or less’

328
Q

What investigation would you carry out in a patient with suspected osteoporosis?

A

Hip and lumbar spine DEXA scan

329
Q

Indications for DEXA scan

A 
Fragility fracture in patient >50
Clinical risk factors
Increased fracture risk assessment score
Glucocorticoid therapy
Assessment of response to treatment
Assessment of progression from osteopenia to osteoporosis
Age <50 but strong risk factors
330
Q

Management of osteoporosis

A

Non-pharmalogical

  • Smoking cessation
  • Alcohol reduction
  • Adequate dietary calcium
  • Exercise

Pharmacological

1) Allendronic acid
2) IV zolendronate

331
Q

What advice would you give to someone taking an oral bisphosphonate?

A

Take on an empty stomach with water, sitting upright

Side effects include: GI upset, worsening of GORD, jaw osteonecrosis

Report any dysphagia - oesophageal ulceration and perforation can occur

332
Q

What would you do after a patient with osteoporosis had been on an oral bisphosphonate for 3 years?

A

Review with a DEXA scan

1) Stop treatment
2) Continue treatment for 5 more years
3) Switch to IV bisphosphonate

333
Q

Causes of osteomalacia/rickets

A 
Vitamin D deficiency
Chronic renal failure
Vitamin-D resistance
Vitamin D receptor defects
Hyophosphatemia
Bisphosphonate therapy
Aluminium
Fluoride
334
Q

Clinical features of osteomalacia

A 
Fractures
Bone pain
Generalised malaise
Proximal muscle weakness
Bone/muscle tenderness on pressure
335
Q

What investigations would you do in a patient with suspected osteomalacia?

A

Serum vitamin D
Serum PTH, calcium, phosphate, ALP
X-rays
Bone biopsy

336
Q

How would you manage a patient with osteomalacia?

A

Cholecalciferol - high doses for 2-4 weeks then reduce to maintenance dose

337
Q

Prevalence of Paget’s disease

A

1% of >55s, but prevalence doubles each decade so affects 8% of >85s

338
Q

Clinical features of Paget’s

A 
Axial skeleton involvement
Bone pain
Bone deformity or expansion
Increased warmth over affected bone
Neurological problems
- Deafness
- Cranial nerve defects
- Nerve root problem
- Spinal cord compression/spinal stenosis
339
Q

What investigations would you do if you suspected Pagets? What would they show?

A

Isolated rise in ALP
X-ray - bone expansion with alternating radiolucucenfcy and osteosclerosis.
Radionucleotide bone scan - used to identify affected sites
Bone biopsy (rare) - exclude bony metastasis

340
Q

Management of Paget’s

A

Bisphosphonates - pamidronate, risedronate or zolendronic acid

Year 4 (11 decks)

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