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General Medicine sara > Rheumatology > Flashcards

Rheumatology Flashcards

1
Q

How are the negative arthropathies characterised?

A

Group of diseases negative for RF and ANA and involve the axial skeleton

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2
Q

What conditions belong to the seronegative spondyloarthropathies?

A 
Ankylosing spondylosis  
Reactive arthritis 
Psoriatic arthritis 
Enteropathic arthritis 
Juvenile enthesitis related arthritis 
Undifferentiated spondylosis
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3
Q

What are the common clinical characteristics amongst the seronegative spondyloarthropathies?

What else sometimes is seen?

A

Inflammatory back pain
Sacroilitis
Enthesitis

Peripheral arthritis - mainly in lower limb
Anterior uveitis - mainly in AS
Other extra articular disease

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4
Q

Which of the seronegative spondyloarthropathies do not have an equal male: female ratio?

A

Ankylosing spondylosis
- 3 times more common in men

The others are equal amongst men and women

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5
Q

Which allele is psoratic arthritis associated with ?

A

HLA B27

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6
Q

What allele is Ankylosing Spondylosis associated with ?

A

HLAB27

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7
Q

What cell mediates psoratic arthritis ?

A

T cells

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8
Q

What are the 5 types of psoratic arthritis ?

A 
Rheumatoid like polyarthritis ( most common) 
Asymmetric olgioarthritis 
Sacroilitis 
DIPJ 
Arthritis mutilans
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9
Q

What are the clinical signs / symptoms of psoratic arthritis ?

A

Psoriasis skin changes (however the arthritis may come first)

Assymetric oligoarthritis or symmetric polyarthritis

DIPJ arthritis and nail changes (pitting and yellow)

Back pain - spondylosis

Arthritis mutilans

Dactylitis - inflammation of digit

Enthesitis - especially Achilles

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10
Q

What is arthritis mutilans ?

A

A clinical feature of psoratic arthritis

There is bone resorption and soft tissue collapses into the space leading to deformity of fingers = telescoping fingers

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11
Q

Is psoratic arthritis benign or progressive?

A

Usually benign

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12
Q

What is the treatment for psoratic arthritis?

A

Similar to rheumatoid arthritis treatment but better prognosis

DMARDs and steroids 
Anti TNF 
Collaborate with dermatologist 
Physiotherapy
IL12 and 23 antagonist are the new therapies
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13
Q

What is ankylosing spondylosis ?

A

Chronic inflammatory arthritis which affects the joints in the spine and sacroilium causing eventual fusion of the spine

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14
Q

Give 10 symptoms of ankylosing spondylosis.

A

Back pain and stiffness especially in the morning
Pain improves with exercise and not with rest
Pain referred to buttocks and thigh
Weight loss
Low grade fever
Fatigue
Onycholysis - nail bed detaches
Pain where tendons insert - inc plantar fasciitis, Achilles tendinitis
Eye pain
Breathing issues
U

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15
Q

What is the pathophysiology of ankylosing spondylosis ?

A

Autoimmune inflammation of spinal column leading to fusion of vertebrae
Involves HLA B27, TNFa and IL1

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16
Q

Which age range does ankylosing spondylosis commonly affect?

A

18 to 30

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17
Q

What are the clinical examination findings in someone with AS?

A 
Spine: 
- reduced lateral flexion 
- reduced forward flexion - schobers test 
Sacroiliac stress test is positive 
Head: 
- wall Tragus distance is increased
- wall occiput distance is increased 
Chest: 
- reduced chest expansion (due to costovertebral involvement )

Stooped posture, hyperextension of neck, flexion at hips and knees)

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18
Q

List the clinical features of ankylosing spondylosis (remember 7As and 3 more)

A
  1. Achilles tendositis - enthesitis esp Achilles, SIJ and discs but also forearm flexor , plantar fascia and intercostal muscles
  2. Arthritis ( peripheral) - esp hips and knees
  3. Anterior uveitis - includes iritis - usually unilateral
  4. Apical fibrosis - upper lobe bilateral lung fibrosis
    - other lung features : pleuritis, fusion of thoracic wall leads to reduced chest expansion and rigidity
  5. Amyloidosis (renal )
  6. Aortic valve incompetence - regurgitation.
  7. AV node block
    - another heart defect = cardiomegaly

Others:

  • cauda equina syndrome
  • spine fuses and micro fractures - severe pain
  • loss of lumbar lordosis
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19
Q

What is the modified New York criteria for AS?

A

Clinical:

  • back pain and stiffness > 6 months which improves with exercise and not rest
  • limitation of chest expansion
  • limitation of movement of lumbar spine

Radiological:

  • > or = grade 2 bilateral sacroilitis
  • > grade 3 or 4 unilateral sacroiliitis

Either all 3 clinical criteria or 1 radiological criteria for probable AS
Or
All clinical and one radiological = definitive AS

Also consider HLAB27

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20
Q

Which investigations could you carry out if you suspect AS?

A

ESR and CRP - if not raised can’t exclude AS
- levels do not correlate with symptoms

HLA B27 allele

X-ray changes
CT
MRI - more sensitive
Spirometry - restrictive lung pattern

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21
Q

What is the treatment for AS ?

A

Conservative = physiology , exercise, stop smoking, hydrotherapy
Pharm:
- NSAIDs - first line
- DMARDs - only for peripheral synovitis
- anti TNF for severe axial disease
- analgesia

Steroids for plantar fasciitis and uveitis

Surgery : joint replacement, spine osteotomy for severe deformity , treat any spine fracture (more common in AS)

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22
Q

State 2 anti TNF agents

A

Infliximab

Etanercept

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23
Q

What is reiters syndrome?

A

Clinical syndrome associated with reactive arthritis which consists of the triad: arthropathy, urethritis and conjunctivitis following dysenteric illness

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24
Q

What is reactive arthritis ?

A

Sterile inflammatory arthritis precipitated by distant infection
Seronegative spondyloarthropathies associated with HLA B27

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25
Q

What is the typical presentation of someone with reactive arthritis ?

A

Young patient (usually male 15-40) with recent history of infection
Occurs up to 1 month following distant infection
The arthritis can last up to 4-6 months

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26
Q

What are the causes of reactive arthritis ?

A

Prostatitis, urethritis, cervicitis:

  • clamidyia trachomatis
  • neisseria gonorrhoea

Acute diarrhoea:

  • salmonella
  • campylobacter
  • shigella
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27
Q

What are the symptoms of reactive arthritis ?

A

Acute onset of arthritis - usually lower limb
Can last 4-6 months
Can be accompanied by fever, malaise, weight loss
Dactylitis
Extra-articular:
- urethritis , prostatitis, cervicitis
- conjunctivitis / uveitis
- colitis, ilitis
- mucocutaneous: circinate balanitis (painless ulcers on penis) , keratoderma blenorrhagia (waxy yellow papules on hands and feet) and painless oral ulcers

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28
Q

What investigations can be carried out if reactive arthritis is expected ?

A

Raised ESR and CRP. raised WCC

Aspirated joint to rule out septic arthritis and gout (I.e. No white cells or crystals) - Reactive arthritis will be a sterile cloudy fluid with low viscosity and raised WCC with giant reiter cells (macrophages) may be seen

Vaginal swab, urine and stool sample and culture

No radiological signs in early stage

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29
Q

What is the outcome of reactive arthritis ?

A

More than 80% are resolved

Some develop into relapsing disease

Less than 10% can become spondyloarthropathies

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30
Q

What is the treatment for reactive arthritis ?

A

No cure
NSAIDs / steroid injections
- steroids only when infection is excluded can give injections or oral steroids.
If symptoms > 6 months and evidence of joint destruction can start DMARDs - methotrexate/sulphasalazine
Abx to clear underlying infection (no effect on joint )
- tetracyclines for clamidyia

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31
Q

What is enteric arthropathy?

A

A disease belonging to the seronegative spondyloarthropathies associated with crohns and UC

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32
Q

What is the pathophysiology of enteric arthropathy?

A

Unknown but it is thought that there is impairment of gut mediated immunity and increased permeability allowing microbes into the circulation

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33
Q

What type of arthritis is seen in enteric arthropathy I.e. Poly, Oligio , mono etc ?

A

Mono

Or assymetric oligioarthritis

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34
Q

Which joint problems coincide with IBD flares

A

Peripheral arthritis coincides with onset and severity of IBD and disappears if affected bowel is removed

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35
Q

What joint problems do not coincide with the IBD status

A

Sacroilitis is seen in IBD but is not clearly correlated with flares and onset.
In fact sacroilitis can be present many years before IBD

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36
Q

What are the non articular symptoms associated with enteric arthropathy

A

Erythema nodusum
Pyoderma gangrenous
Aphthous stomatosis
Uveitis

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37
Q

How do we treat enteric arthropathy?

A

Treat the bowel symptoms and usually arthritis improves

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38
Q

What is the name of the crystal that is responsible for causing gout ?

A

Monosodium urate monohydrate

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39
Q

What is the pathophysiology of gout?

A

MSU crystal deposit in joints
Innate immunity recognise and phagocytose crystals
NALP3 inflammasome is activated and IL1b is released
IL1b receptor is activated and cytokines are released
Neutrophils recruited
Inflammation (synovitis) results in joint destruction and pain

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40
Q

What are the clinical features of an acute attack of gout

A

Rapid onset of severe pain in joint (burning pain)
Tender, swelling and redness
Usually monoarthritis in 1st MTPJs
Can last 2 days to 2 weeks

bursitis, tendonitis or cellulitis

more common in men.

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41
Q

How does chronic gout present clinically?

A

Acute attacks fail to completely resolves and the period between acute attacks is shortened

Polyarticular and polyarthritis due to bone and cartilage degradation.
Bony ankyloses - union of bones due to inflammation

Top hi seen

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42
Q

What are the main joints that gout attacks ?

A 
MTPJ (called the Podagra) 
Mid foot 
Ankles 
Knees 
Olecranon bursa
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43
Q

What are tophi?

A

Clinical feature associated with gout
The MSU crystals become embedded in lipid, protein and calcific matrix
Commonly found on pinna, dorsum of MCPJ, Achilles’ tendon and elbow/knee bursae
Rarely can be found in eyes and bones

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44
Q

Are tophi seen in gout dangerous?

A

No usualky painless

However can ulcerate and become infected

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45
Q

What are the other problems associated with gout other than arthropathy?

A

Tophi
Uris acid nephrolithiasis
Gouty nephropathy

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46
Q

How is gout diagnosed ?

A

2 of the following:

  • typical history
  • raised serum urate
  • crystals found in joint aspirate during attack

investigations:
- bloods: raised ESR/ CRP and WCC, raised urea (normal urea doesn’t rule out gout), abnormal U&Es if renal disease.
- joint aspiration.
- Xray

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47
Q

Describe the crystals found in gout

A

Needle shaped crystals with strong negative debridement in polarised light

(sterile cloudy aspirate with raised WCC and low viscosity)

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48
Q

Does a normal serum urate exclude gout?

A

No.
High levels with symptoms are highly suggestive of gout

Some people have high levels and no symptoms

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49
Q

What X-ray changes are associated with gout?

A

Swelling
Opacities - tophi
Good joint space / loss of joint space and osteophytes
Punched out erosions, sclerotic margins and overhanging edges
No periarticular osteopenia

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50
Q

What are the causes / risk factors of gout

(11 points )

A
  • Family history
  • Obesity
  • Hypertension
  • Male
  • > 40yrs
  • Purine rich diet (esp if renal impairment)
  • Alcohol - metabolism result in adenosine monophosphate which is a precursor of uric acid
  • Genetic condition - Von gierke , lesch Nyhan
  • Uric acid over production - tumour lysis ( chemo), haemolytic anaemia, myeloproliferative disease
  • uric acid under excretion - renal disease,
  • drugs : tacrolimus, cyclosporin, diuretic (thiazides), levodopa, laxatives, warfarin
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51
Q

What level of uric acid is classed as hyperuricaemia?

A

> 450uM

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52
Q

How is an acute attack of gout managed ?

A

NSAIDs (however contraindicated in renal insufficiency)
Colchicine - slower onset and often given alongside NSAIDs
Corticosteroids injection can be considered

Oral prednisolone if NSAIDs and colchicine are contraindicated

long term advice: reduce alcohol, keep hydrated, reduce weight,

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53
Q

How does colchicine work?

A

Reduces neutrophil chemotaxis

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54
Q

What are the ADRs of colchicine ?

A

Mostly safe however can cause diarrhoea after about 3 days so need to warn patient

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55
Q

What is given as prophylaxis treatment for gout ?

A

Mainly allopurinol

But others include febuxostat and sulphinpyrazone pr Probenecid (increase uric acid excretion)

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56
Q

How does allopurinol work?

A

Xanthase oxidase inhibitor

- the enzyme responsible for converting purines to uric acid

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57
Q

How does sulphinpyrazone work?

A

Prophylaxis for gout

Increases uric acid excretion

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58
Q

What EGFR is allopurinol safe at?

A

Anything above 30ml/min

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59
Q

What advice/ guidance should be given when taking allopurinol?

A

Never start during acute attack, only 2 weeks after otherwise can precipitate attack

If already on it, do not stop during attack

When starting use NSAIDs / colchicine to cover

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60
Q

How do you decide how much allopurinol is given?

A

Start with 100mg od and then titrate until uric acid levels are less than 300uM

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61
Q

When is allopurinol indicated?

A

Recurrent attacks of gout

If increased risk e.g. Von gierkes, lesch nyhan syndrome, renal impairment

Tophi

Uric acid renal stones

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62
Q

What are the ADRs of allopurinol?

A

Steven johnsons
Hypersensitivity
Pancytopenia - when taken with azothioprine

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63
Q

What should be used if allopurinol is contraindicated ?

A

Febuxostat

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64
Q

What is the conservative treatment/ prevention for gout?

A 
Well hydrated
Avoid purine rich food- liver , kidney, oily fish 
Reduce alcohol 
Loose weight 
Control Bo
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65
Q

What crystal causes pseudogout?

A

Calcium pyrophosphate dehydrate

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66
Q

What joints does pseudogout target?

A

Wrists, shoulders, hips and knees

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67
Q

how does pseudogout present clinically?

What is a clinical sign of pseudogout that is also seen in OA?

A

acute onset red, swollen, hot and tender joint.

Heberdens nodes

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68
Q

What are the risk factors/ associations with pseudogout?

A 
Elderly - mainly affects 60-80yrs
genetic
OA
Hyperparathyroid
Haemochromatosis
Wilsons 
Hypo mg /phosphate 
surgery / trauma 
dehydration 
infection
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69
Q

What are the X-ray features associated with pseudogout?

A

OA changes

Chondrocalcinosis - calcification of cartilage - hyaline,fibrocartilage (menisci) or ligaments.

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70
Q

How can pseudogout be distinguished from OA?

A

In pseudogout you see:

  • axial involvement
  • sacroiliac erosion
  • cortical erosion of femur
  • osteonecrosis of medial femoral condolences
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71
Q

Describe the aspirate fluid seen in pseudogout

A

Rhomboid shaped crystals with slight positive debridement

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72
Q

What are the triggers of acute pseudogout?

A 
Infection 
Direct trauma to joint
Blood transfusion 
Thyroxine 
Dehydration 
Surgery esp. parathyroidectomy
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73
Q

What is the treatment for pseudogout?

A 
NSAIDs 
Aspirate and corticosteroids injection 
Colchicine - low dose to reduce frequency of attacks 
Splinting and rest
Eventually joint replacement
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74
Q

Which antibodies are associated with SLE?

A

Anti do DNA and anti smith
These are known as anti nuclear antibodies
Positive in 98% of patients

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75
Q

Which antibodies are mainly associated with rheumatoid arthritis ?

A

Rheumatoid factor

Anti CCP

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76
Q

Which antibodies are mainly associated with sjrogens ?

A

Anti Ro and anti La

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77
Q

What antibodies are associated with vasculitis ?

A

ANCA

Wegeners:

   - P- ANCA: perinuclear which binds myeloperoxidase
   - C- ANCA: cytoplasmic which binds proteinase 3 (very strong association with wegeners)
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78
Q

What antibody is associated with inflammatory myopathy?

A

Anti jo

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79
Q

Which antibodies are associated with scleroderma?

A

Systemic sclerosis - anti topoisomerase - anti scl70

CREST - anti centromere

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80
Q

What vessels does wegeners granulomatous affect?

A

Small and medium vessels of a variety of different organs

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81
Q

Are the relapse rates in wegeners granulomatosis high or low?

A

High

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82
Q

What are the symptoms of wegeners granulomatosis? (Start from eyes and work way down)

A

Eyes: scleritis, conjunctivitis, uveitis, proptosis, cranial nerve palsy
Nose: epistaxis, septal perforation, saddle deformity, rhinitis and pain
Ears: otitis media, sensorineural and conductive hearing loss
Facial pain
Trachea: subglottal stenosis
Lungs:
- CT scan shows nodules and cavities
- biopsy shows necrosis and multinucleated giant cells
- pulmonary haemorrhage and haemoptysis
Kidneys: rapidly progressive Glomerulonephritis that leads to CKD
Arthritis
Skin: nodules

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83
Q

How is remission induced in wegeners granulomatosis?

A

High dose steroids + cyclophosphamide / methotrexate

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84
Q

How is remission in wegeners maintained ?

A

Low dose steroid + methotrexate/ azothioprine

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85
Q

What vessels does takayasu arteritis affect?

A

Large vessels and aorta

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86
Q

What is the main problem in takayasu arteritis?

A

Congestive heart failure and systemic hypertension

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87
Q

What is giant cell arteritis also known as ?

A

Temporal arteritis

Hortons disease

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88
Q

What vessels does giant cell arteritis affect?

A

Aorta and large vessels esp extra cranial branches of carotid e.g. Temporal artery

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89
Q

Who does giant cell arteritis mainly affect?

A

More common in women above the age of 50

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90
Q

What are the symptoms of giant cell arteritis ?

A 
Headache 
Malaise
Morning stiffness
Jaw claudication 
Tongue claudication 
Temporal artery tenderness and raised
Visual disturbances
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91
Q

What is the ARA criteria for giant cell arteritis diagnosis ?

A

3 or more of :

  • age onset > 50
  • new headache
  • temporal artery tenderness/ decreased pulsation
  • ESR > 50mm/hr
  • abnormal artery biopsy
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92
Q

How would you describe the artery biopsy in giant cell arteritis ?

A

Necrotising arteritis with mononuclear infiltrate or granulomatous inflammation (giant cells)

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93
Q

What is the treatment for giant cell arteritis ?

A

Prompt treatment to prevent blindness :
40-60mg prednisolone for 1 month atleast
If visual disturbances already experienced then IV methyl prednisolone

Osteoporosis prophylaxis
Methotrexate and aspirin for 2 years after

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94
Q

What type of autoimmune disease is SLE?

A

Type 3

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95
Q

Who is SLE more likely to affect?

A

10-20x more likely in women
Afrocaribean
15-40 yrs

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96
Q

What is the pathophysiology of SLE

A

An innate susceptibility + environmental triggers leads to autoimmune hyperactive b and T cells and autoantibody production.

Innate susceptibility includes: complement levels, hormonal levels, HLA DR3/2
Environmental stimulus: UV exposure , microbial response, drugs

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97
Q

Which drugs cause SLE?

A 
Isoniazid 
Methyl dopa 
Sulphasalazine 
Anti TNF 
Quinidine
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98
Q

What are the musculoskeletal symptoms of SLE?

A

Morning stiffness due to polyarticular arthralgia (non erosive )
Osteoporosis
Reversible subluxation of joints
Jaccouds deformity - due to ligament laxity
Myalgia is common but myositis is rare

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99
Q

What skin symptoms do people with SLE experience ?

A 
Alopecia 
Butterfly rash - malar rash 
Discoid rash 
Photosensitive rash 
Ulcers
Raynauds
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100
Q

What are the cardiovascular problems in SLE?

A 
Pericarditis and pericardial thickening 
Myocarditis 
Systolic murmurs 
Dyslipidaemia, hypertension and atherosclerosis 
Increased risk of MI
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101
Q

What are the pulmonary complications in SLE?

A 
Shrinking lung syndrome - SoB and restrictive lung function test
Pleuritic check pain 
Pleural effusions 
Pulmonary hypertension 
Interstitial fibrosis 
Pneumonitis
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102
Q

What are the renal complications in SLE?

A

AKI, CKD
Glomerulonephritis –> hypertension and haematuria
Nephrotic syndrome –> hyperlipidaemia and prothombosis, oedema and weight gain

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103
Q

What is the haemopoietic problems in SLE?

A 
Increased ESR
Normochromic normocytic anaemia
Thrombocytopenia 
Leucopenia/ lymphopenia
Lymphoma
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104
Q

What are the neural complications in SLE?

A 
Headaches
Seizures 
Cognitive impairment 
Asceptic meningitis 
Anxiety and depression 
Sensory peripheral neuropathy
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105
Q

What are the GI complications in SLE?

A 
Diarrhoea
Abdo pain 
N&V 
Diabetes
Hepatomegaly and splenomegaly
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106
Q

What is antiphospholipid syndrome?

A 
Antiphospholipid autoantibodies are Presents in 1/3 of patients with SLE
This leads to a hypercoaguable state: 
- thrombosis 
- thrombocytopenia 
- cerebral disease 
- recurrent foetal loss
- pulmonary hypertension

Some people develop renal impairment from multiple mini thrombi

107
Q

What is the ARA criteria for SLE diagnosis

A

4 or more of the following:

  • scerositis
  • oral ulcers
  • Arthritis
  • photosensitive rash
  • blood - anaemia, thrombocytopenia, lymphopenia, leucopenia
  • renal disease
  • ANA positive
  • immunology - anti ds DNA, anti smith, antiphospholipid
  • neurology- seizures etc
  • malar rash
  • discoid rash
108
Q

What monitoring can be done in SLE?

A

Low C3/4
Raised ESR (normal CRP)
Increased anti ds DNA

109
Q

What investigations can be carried out in SLE?

A

Bloods:

  • FBC: anaemia, leucopenia, thrombocytopenia
  • ESR raised , normal CRP
  • u&es
  • anti ds DNA, anti smith : very specific
  • raised APTT if anti phospholipid syndrome
Urinalysis : haematuria and protienuria 
CXR: pleural effusion and cardiomegaky 
Joint X-ray: non erosive 
USS kidneys 
ECG
Echo
110
Q

What risks are there of SLE in pregnancy ?

A 
Gestational diabetes
Pre eclampsia 
Pulmonary hypertension 
Thrombosis 
Miscarriage and preterm
111
Q

What treatment is given in SLE?

A

Hydroxychloroquine for skin and joint problems
Other organs involvement: methotrexate, azothioprine, prednisolone and ciclosporin
Severe renal, cardiac or neurological : high dose steroid and cyclophosphamide

Low dose steroids and azothioprine for maintainance

NSAIDs for arthritis

Vit D and bisphosphonates for long term steroids

112
Q

What medication should be avoided by SLE?

A

COCP: increased risk of thrombosis

113
Q

What advice can be given to SLE patients

A

Control cardiovascular risk factors e.g. Stop smoking
Plan pregnancy and have SLE well controlled prior
UV sun block
Prompt treatment of any infections

114
Q

What is sjogrens ?

A

Chronic autoimmune condition with lymphocyte infiltration into exocrine glands. Leads to fibrosis and destruction of exocrine glands. It particularly affects salivary and lacrimal glands

115
Q

Who does sjogrens most commonly affect?

A

9x more common in women

Aged 40-50yrs

116
Q

What is the difference between primary and secondary sjogrens?

A

Secondary sjogrens is symptoms of sjogrens associated with other autoimmune conditions e.g. SLE, systemic sclerosis and RA

117
Q

What is the pathophysiology of sjogrens

A

Interaction between genetic predisposition and environmental factors (HCV,HIV, EBV, CMV, HTLV)
This leads to polyclonal B cell hyperactivity and immunoglobulin production.

118
Q

Which cancer is sjogrens linked to and why?

A

Hodgekins B cell lymphoma

- because it involves B cell hyperactivity and thus proliferation

119
Q

What is the criteria for diagnosing sjogrens?

A

4 out of 6 of the following and 1 must include the * criteria

  • anti Ro and anti La
  • abnormal lower lip biopsy
  • dry mouth >3 months, swollen glands
  • dry eyes > 3 months
  • positive schirmers test
  • low unstimulated salivary flow
120
Q

What are the clinical features of sjogrens? (7 points + 3)

A
  • Xerophthalmia- and associated complications e.g. Ulcers
  • Xerostomia - dysphagia and coughing
  • Parotid swelling
  • Joint pain- not erosive arthritis
  • Raynauds
  • Alopecia and hypopigmentation
  • Malaise, low grade fever , myalgia

Also associated with autoimmune cholangitis, peripheral sensory neuropathy and renal disease

121
Q

What investigations may you do if you suspected sjogrens?

A

Bloods:

  • raised ESR
  • anaemia
  • thrombocytopenia, leucopenia

Abs:

  • 74% ANA positive
  • some RF
  • anti Ro and la are specific

Other:

  • schrimers test - less than 5 mm of tears in 5 mins on 30mm paper
  • sailometry - salivary flow
122
Q

What treatment is available for sjogrens ?

A

Dry eyes: topical cyclosporin, artificial tears
Dry mouth: artificial saliva , lose gets
Dry vagina: propanoic acid gel
Treat vagina and salivary gland infections
Hydrocloroquine for arthralgia
Interstitial lung disease and vasculitis - prednisolone

123
Q

What are the causes of dry mouth/ eyes other than sjorgens?

A

Age
Infection
Drugs: parasympathetic drugs and diuretics

124
Q

What are the two types of chronic widespread pain syndromes? And how are these characterised?

A

Fibromyalgia and joint hyper mobility syndrome
Chronic pain in absence of any degenerative or inflammatory disease. Pain for more than 6 months in 2 or more sites above and below the pelvis

125
Q

Who does fibromyalgia affect?

A

Much more common in women
Quite a common problem
40-50yrs
May develop in patients with RA/SLE

126
Q

What is fibromyalgia

A

Condition of widespread muscle and connective tissue pain and allodynia (due to central sensitisation) . also fatigue and sleep disruption

127
Q

What is the pathogenesis of fibromyalgia

A

Unknown
Genetic predisposition and stress affects the hippocampus and HPA axis. There is lack of serotonin / dopamine
Pain centres are overacitvated due to central sensitisation and it is found that substance p is raised in CSF
Chronic but not always progressive

128
Q

What are the symptoms of fibromyalgia

A 
Widespread pain 
Joint/ muscle stiffness 
Profound tiredness 
Numbness 
IBS 
Depression/anxiety 
Poor concentration / memory
129
Q

What is the criteria for fibromyalgia

A
  1. History of widespread pain
    - only if all of the following:
    - pain left and right side of body
    - pain below and above pelvis
    - axial skeletal pain
  2. > 3months
  3. Pain in atleast 11 of 18 tender points
130
Q

What are the tender points in fibromyalgia?

A
  1. Occipitut
  2. Low cervical
  3. Trapezius
  4. Supraspinatus
  5. 2nd rib
  6. Lateral humeral epicondyles
  7. Gluteal
  8. Greater trochanter
  9. Knees
131
Q

What are the findings on clinical examination in fibromyalgia

A

Normal range of movement
Normal strength
Absence of swelling
Normal reflexes

132
Q

What is the treatment for fibromyalgia

A

Multidisciplinary approach

  • CBT
  • drugs: tramadol, amytriptiline, gabapentin , opioids and antidepressants
  • exercise and massages
  • education
133
Q

What is a typical presentation of someone with joint hypermobility syndrome ?

A

Pain in multiple joints
Dislocations
Tiredness

134
Q

Which genetic conditions are associated with joint hypermobility syndrome?

A

Marfans and Ehlers Danlos

135
Q

What is the pathogenesis of marfans?

A

Fibrillin 1 defect leads to reduced integrity of ECM

136
Q

What are the signs/ symptoms of marfans ?

A 
Long arm span 
Pectus 
High arched palate 
Flat feet 
Scoliosis
Long hands and feet
137
Q

What are the complications of marfans

A

Lens dislocation
Aortic root dissection
Aortic aneurysm
Spontaneous pneumothorax

138
Q

What are the different types of ehlers danlos?

A

Hypermobility type
Classical type
Vascular type

139
Q

Which type of ehlers danlos does not have a genetic cause?

A

The hypermobility type

140
Q

What gene is responsible for causing the classical and vascular type of ehlers danlos

A

Classical type : collagen V

Vascular type: collagen III

141
Q

What are the symptoms of classical ehlers danlos?

A

Smooth, hyperelastic skin
Hypermobility since childhood
Severe bruising

142
Q

What are the symptoms of vascular ehlers danlos?

A

Thin skin, easily bruised (not stretchy )
Protruding eyes
Thin nose and lips
Hypermobility in small joints
Fragile blood vessels, gut wall and uterus

143
Q

What is the Brighton scoring system?

A

Touch floor with hands , knees straight - 1 point
Touch thumb with back of forearm -1 point each side
Little finger bent back to 90 degrees - 1 point each side
Hyperextended elbows - 1 point each side
Hyperextend knees - 1 point each side

144
Q

What is the Beighton criteria for hypermobility syndrome

A

Major criteria :

  • beighton score > or = 4
  • arthralgia >3months in >/=4 joints

Minor criteria:

  • beighton score 1-3
  • arthralgia in 1-3 joints
  • dislocation
  • soft tissue rheumatism
  • marfanoid habitus
  • abnormal skin
  • drooping eyelids
  • varicose veins / hernia

For diagnosis:

  • 2 major ones or
  • 1 major and 2 minor
  • 4 minor
145
Q

Which joints are affected in reactive arthritis and what pattern?

A

Larger joints in a symmetrical pattern

146
Q

Who is reactive arthritis most likely to affect?

A

Men aged 15-40

147
Q

What will the joint aspirate in reactive arthritis be?

A

Sterile
Raised white cells - cloudy
Low viscosity
Giant macrophages - reciter cells

148
Q

Someone presents with reactive arthritis. After investigations they are found to be positive for clamidyia. What is the best treatment?

A

Antibiotic- tetracycline

149
Q

Is gout more common in men or women?

A

Men

150
Q

What is probenecid?

A

Another drug like sulphinpyrazone that increases uric acid excretion to help reduce likelihood of gout

151
Q

Apart from crystals seen in gout and pseudogout, what else can be said about the joint aspirate?

A

Sterile, cloudy, raised wcc, low viscosity

152
Q

What is osteoporosis?

A

most common metabolic bone disease where there is a reduced bone mass and increased bone fragility. The remaining bone components are normal just there is less of it. It is defined as a BMD of less than 2.5 Standard deviations below normal (by DEXA)

153
Q

Who does osteoporosis mostly affect?

A

Post menopausal women

154
Q

What are the different types of osteoporosis?

A 
Primary- 
     - type 1 : caused by menopause 
     - type 2: caused by age 
Secondary: 
    Caused by other diseases  - hyperthyroid, hyperparathyroid , steroids , CPRS
155
Q

What is the pathogenesis of osteoporosis?

A

Osteoblasts activity decreases which doesn’t match osteoclasts activity

156
Q

What are the causes of osteoporosis (pneumonic =fractures, blem)

A 
F =fractures, FHx, female
R = rheumatoid arthritis
A= age
C = cigarettes 
T = thin
U = u/C crohns
R= reduced mobility
E = endocrinopathy- hyperparathyroid , hyperthyroid, Cushing's, T1D
S = steroids 
B= blood - multiple myeloma, sickle cell and thalaessemia
L = liver disease
E= eating = coeliacs and eating disorders
M = menopause

. Hyperthyroid, hyperparathyroid, Cushing’s, T1D, sickle cell, thalaesmia , multiple myeloma, eating disorders, coeliacs, liver disease. Steroids and nutrition

157
Q

What can cause localised osteoporosis and what causes diffuse osteoporosis?

A

Localised: previous fracture, inflammatory arthritis, tumour, infection and reflex sympathetic dystrophy

Diffuse - menopause and age

158
Q

What are the clinical features associated with osteoporosis ?

A

Fractures - common sites inc wrist, hip, spine

Deformity due to fracture e.g. Kyphosis and loss of height due to vertebral fractures

159
Q

What are the pattern of fractures seen in osteoporosis

A

Colles fracture - 50yrs +
Vertebral fracture -60 yrs +
Hip fracture - 70 yrs +

160
Q

What are the risk fractures to fractures other than osteoporosis?

A

Age - loss of balance, loss of eye sight, muscle weakness, gait problems
Medication
Previous fracture

161
Q

What investigations would you carry out if osteoporosis is suspected?

A

Blood test - find cause, I.e. If primary cause then bloods should be normal however may find abnormal TFT, PTH, ALP (pagets),ESR (inflammatory cause). Vit D (rule out osteomalacia). ca/Po4 is abnormal in secondary osteoporosis

X-ray - osteopenia, cortical thining, fish vertebrae
DXA bone scan
FRAX tool

162
Q

What is the DXA scan

Including the t and z scores

A

Scans bone for bone density allowing diagnosis of osteoporosis/osteopenia and allows us to monitor therapy

T score is given which is the number of standard deviations below the average young person of same age and ethnicity

Z score is the number of sd below the average person of the SAME age, gender and ethnicity -if abnormal it’s due to factors other than age for example steroid use

163
Q

What do different t scores correspond to when diagnosing osteoporosis

A

> -1.5 is normal
-1.5 to - 2.5 is osteopenia
less than -2.5 = osteoporosis

164
Q

What are the limitations to the DXA scan?

A

It doesn’t assess the quality of the bone just the quantity

It can’t predict future fracture risk because this depends on other risk factors e.g. Balance

165
Q

What is the FRAX tool

A

Takes into a account a number of different risk factors to predict the risk of future fracture
Risk factors include: age, gender, height, weight, smoking, RA, steroids, smoking alcohol
If the risk is high the patient is treated with bisphosphonates etc

166
Q

Name another tool similar to the FRAX tool

A

Q fracture

167
Q

What is the treatment regime for osteoporosis ?

A

Lifestyle advice: stop smoking, improve diet, increase BMI, exercise, reduce alcohol
Drugs:
- stimulate bone formation: PTH analogue (teriparatide)
- prevent bone resorption : HRT, raloifene, bisphosphonates
- dual action : strontium ranelate
Also give 1g calcium and 400u vit D once daily (ADCAL-D3)

can also give calcitonin

168
Q

Name 3 oral bisphosphonates

A

Alendronate , risendronate and etidronate

169
Q

How do bisphosphonates work?

A

They are taken up by osteoclasts and cause apoptosis

170
Q

Which is the most commonly used bisphosphonate and what advice is given when taking this?

A

Alendronate / alendronic acid
Take on empty stomach and sitting up right
Avoid in pregnancy
Caution in renal impairment

171
Q

Can bisphosphonates be given IV, give examples? What is the advantage of this?

A

Ibandronate. - IV 3 monthly
Zoledronate - IV annually

More potent than orally

172
Q

How does teriparatide work?

How is it given ?

A

PTH analogue but only contains the first 33 amino acids so works differently.
It causes bone formation
Given once daily as a subcutaneous injection

Note continuous PTH - catabolic
Period PTH - anabolic

173
Q

What is denosumab?

How is it given

A

Monoclonal Ab against RANKL
Inhibits binding of RANKL on osteoblasts with RANK on osteoclasts to reduce osteoclasts activation and proliferation

6 monthly subcut injection

174
Q

How does strontium ranelate work? How is it given? What is the ADR?

A

Dual action - bone formation and inhibits resorption.
Add sachet to water
Diarrhoea

175
Q

If someone is on steroids when is bone protection medication indicated?

A

If prednisolone >5mg for > 3 months then use bone protection if
> 65 yrs
Or <65 yrs and T score of less than 1.5

176
Q

What is the risk of HRT

A

Breast cancer
P.E/ DVT
Stroke

177
Q

What are SERMs and when can they be used

A

Selective oestrogen receptor modulator
Raloxifene
does not allievate menopause symptoms
Risk of DVT /p.e

178
Q

What is osteomalacia ?

A

Low bone mass density due to impaired bone metabolism causing inadequate mineralisation - low density and abnormal bone consistency

179
Q

What are the causes of osteomalacia

A

Calcium vitamin D deficiency - dietary, lack of UV and malabsorption

Defective hydroxylation - cirrhosis and renal failure

Increased 25 hydroxy vit D breakdown - anticonvulsants (phenytoin)

Defective organ response to catciterol- hereditary vitamin D resistance rickets

Glucocorticoids
Tumours

180
Q

What is the clinical presentation of osteomalacia ?

A 
Bone pain - spine , pelvis and ribs 
Muscle pain 
Skeletal deformity - rickets 
Proximal weakness - waddling gait 
Fatigue / malaise
Fractures
181
Q

What is the treatment for osteomalacia

A

Vitamin D suplements - cholecalciferol
- calcitriol or 1-OH vit d (alfacalcidol ) if renal failure
Dietary advice - salmon and dairy
Sunlight exposure

182
Q

From X-ray when do you expect to find with someone with osteomalacia?

A

Osteopenia

Looser zone : small fractures at edge of bones - distinguishes osteomalacia from osteoporosis

183
Q

What blood result do you expect to find in someone with osteomalacia?

A

High PTH, and ALP

Low calcium, phosphate and vitamin D

184
Q

What investigations can be carried out in osteomalacia?

A

X-rays
Bloods
Bone biopsy - more bone but uncalcified

185
Q

Describe the pathogenesis behind osteomalacia

A

Lack of vitamin D means calcium cannot be absorbed from the gut
Serum calcium levels drop
This stimulates release of PTH
PTH stimulate bone resorption to help raise serum calcium
Results in poor bone mineralisation

186
Q

What joints does osteoarthritis mainly affect?

A 
Knees
Hips
Spine 
Feet
If a lot of manual work then hands too
187
Q

What are the risk factors for osteoarthritis?

A

Overuse: age, repetitive use, injury, obesity

Genes: female, family history, haemochromatosis, Wilson, pagets

Congenital : perthes, DDH

Pathology: gout, neuropathy, infection, surgery, acromegaly

188
Q

Describe the pathogenesis behind osteoarthritis

A
  1. Breakdown of cartilage at the joint surface- released fragments set up an inflammatory response. The surface becomes frayed and roughened. Therefore joint space is reduced leading to further irritation
  2. Synovial irritation leads to huge production of cytokines - inflammation and alters Chondrocyte activity
  3. Remodelling: osteophytes form induced by friction at free edges of joint - further restricts joint movement
  4. Sclerosis - microfractures and healing with callus lead to sclerosis
  5. Cyst formation- synovial fluid enters bone under high pressure to produce cavity/cyst
189
Q

What is the typical presentation of someone with osteoarthritis

A

Gradual onset of pain
Start up pain which reduces with gentle mobilisation but worsens with increasing activity
Stiffness and swelling

Specific:

  • knee: locking (osteophytes),giving way (due to pain) , crepitus (bone on bone)
  • hip: may radiate to knee. Pain may be in thigh , groin or buttocks
  • hand: difficulty writing, holding things

In late stages heberdens nodes and Bouchards nodes

190
Q

What investigations can be carried out in OA?

A

Bloods - to rule out other causes because in OA bloods and biochem/immunology should be Normal
Aspirate joint to rule out septic and gout
X-ray (LOSS): loss of joint space, osteophyts, sclerosis, subchondral cysts
MRI can determine cartilage involvement , tendon involvement and meniscal involvement

191
Q

What is the management of OA?

A

Conservative: physiotherapist , weight loss, walking aids
First line pharm: paracetamol or topical NSAIDs
Second line : oral NSAIDs
Follow WHO ladder (e.g. Fentanyl patches )
Steroid injections

Surgical

192
Q

What are the different surgical options for osteoarthritis

A

Joint replacement
Arthrodesis
Specific surgery to tidy joint e.g. Osteotomy

193
Q

What determines whether a patient with OA has a joint replacement or arthrodesis

A

Joint replacement requires patient to be medically fit

Arthodesis is usually first line option for the ankle because limited movement at ankle is not very disabling and arthrodesis works a lot better than a replacement t in this case

Arthrodesis is indicated in very badly damaged knees in young adult as they will out live their joint replacement

194
Q

When is an ankle replacement indicated

A

Normally arthrodesis
However replacement only if there is good alignment, little load, RA>OA because in RA more joints are affected so by fusing one, there is more pressure on others

195
Q

In OA of a shoulder what are the 2 surgical options?

A

Total shoulder replacement

Reverse shoulder replacement: glenoid fossa is replaced by artificial ball and humeral head becomes a socket

196
Q

When is a reverse shoulder replacement indicated?

A

When rotator cuff muscles are damaged

197
Q

What is the average life expectancy for a knee replacement ? Hip?

A

20years for knee

15-20 for hip

198
Q

Is OA progressive

A

Yes

199
Q

Who is scleroderma most likely to affect?

A

4 x more common in women

Aged 30-50

200
Q

What is scleroderma?

A

A spectrum of rare disorders where there is an abnormal overproduction of collage in skin, microvasculature and eventually other organs leading to fibrosis /hardening

201
Q

Apart from ANA antibodies what antibody is associated with scleroderma?

A

RF in 30 % of patients

202
Q

Describe the pathophysiology of scleroderma

A

Autoimmune condition where there is abnormal collagen laid down in skin and blood vessels leading to scleroderma and raynauds

Eventual fibrosis of internal organs and organ failure

Caused by endothelial cell damage, T cell infiltration and activation of fibroblasts

203
Q

How is scleroderma diagnosed?

A

As a minimum patients must have raynauds and be ANA positive

204
Q

What are the different signs of scleroderma?

A

Microstomia
Telangiectasia
Skin changes - thickening and pigmentation
Puffy hands - with ulcerations on knuckles
Signs of raynauds

205
Q

What are the two forms of scleroderma ?

A

Diffuse cutaneous - systemic sclerosis

Limited cutaneous - CREST

206
Q

What does CREST stand for

A 
Calcinosis 
Raynauds
Eosphageal dysmotilty 
Sclerodactly
Telangiectasia
207
Q

In limited cutaneous scleroderma where does the scleroderma affect compared to the diffuse type

A

Limited: affects distal limbs (below knees and elbows) and face

Diffuse : affects trunk and proximal limbs

208
Q

What is the difference in progression between the diffuse and limited scleroderma

A

Limited: much slower progression (10 to 15 years after presentation)
Diffuse: more rapid(5 years after presentation)

209
Q

What usually is the cause of death in scleroderma

A

Pulmonary hypertension

Scleroderma renal crisis

210
Q

List the skin and vascular features of scleroderma

A

Hardening and scarring of skin - tight , red and scaly
Morphoea- itchy hypo/hyperpigmented skin
Gluttate morphoea
Non pitting oedema
Sclerodactly
Raynauds- along with thickened skin this leads to ulcers and necrosis

211
Q

What are the GI complications of scleroderma

A

Reduces intestinal motility
Malabsorption
Constipation
Reflux oesophagitis

212
Q

What pulmonary disease is associated with scleroderma

A

Pulmonary fibrosis
Pulmonary hypertension - 80% even in CREST type
Oedema

213
Q

What cardiac disease is associated with scleroderma

A

Pericardial effusion
Arrhythmia
Myocardial fibrosis

214
Q

What renal disease is associated with scleroderma

A

Scleroderma renal crisis although rare

215
Q

What musculoskeletal complications are associated with scleroderma

A

Myalgia
Tendon pain
Carpal tunnel syndrome

216
Q

What is the treatment for scleroderma

A

NSAIDs for pain symptoms
Immunosuppression for lung fibrosis and extensive skin involvement : steroids and DMARDs
ACEi for renal failure
New treatment : phosphoritesterase inhibitors and endothelium 1 antagonist for pulmonary hypertension and severe raynauds

217
Q

Is polymyositis/ dermatomyositis more likely to affect men or women?

A

2 x more likely in women

218
Q

What is polymyositis and dermatomyositis characterised by?

A

Proximal muscle weakness and evidence of autoimmune mediated muscle breakdown

219
Q

What are the features of

a) polymyositis
b) dermatomyositis

A

a and b) muscle weakness, aching, fatigue easily. Usually symmetrical and diffuse affecting proximal muscle or the neck, shoulder, trunk, hips and thigh. General: extreme tiredness and feeling unwell

Just b) photosensitive rash , heliotroph rash, gottrons papules. Increased risk of malignancy

220
Q

What patterns of disease are found in polymyositis and dermatomyositis

A

Severe and acute
Chronic
Relapsing

221
Q

What is the criteria for diagnosis of polymyositis

A
  1. Proximal muscle weakness
  2. Raised serum muscle enzymes (CK and Aldose)
  3. Abnormal muscle biopsy
  4. Abnormal muscle EMG - low amplitude , short duration
  5. Dermatology findings - gottrons papules, heliotrope rash and photosensitive rash
222
Q

What investigations can we do for polymyositis and dermatomyositis

A

Muscle enzyme serum levels - CK and aldose
Abnormal muscle biopsy
Anti Jo - ANA
Abnormal EMG

223
Q

What are the biopsy results of someone with dermatomyositis

A

Ischaemic infarction at the periphery of the fascicles

224
Q

What are biopsy results in polymyositis

A

Endomysial cell infiltrate and fibre necrosis

225
Q

What is the treatment for polymyositis and dermatomyositis

A

Start promptly
High dose corticosteroids
Exercise and physio
Immune suppression- methotrexate, azothioprine, cyclophosphamide

For rash hydroxychloroquine or steroid cream

226
Q

Who does poymyalgia rheumatica more commonly affect?

A

Women

Over the age of 60

227
Q

What other autoimmune condition is polymyalgia rheumatica strongly associated with?

A

Temporal arteritis

228
Q

What is polymyalgia rheumatica

A

Inflammatory condition of the muscles

229
Q

What are the signs and symptoms of polymyalgia rheumatica?

A

Sudden onset < 1month
Pain and stiffness in shoulder, hips and neck - bilateral and symmetric
Fatigue, weight loss, low grade fever and depression
Normal muscle strength
Be aware to look for signs of temperol arteritis too

230
Q

What blood results are found in someone with polymyalgia rheumatica?

A

Raised ESR and CRP
Normocytic normochromic anaemia
Reduced CD8 T cells

231
Q

What investigations should be carried out in polymyalgia rheumatica

A

Bloods
Muscle biopsy is normal
Artery biopsy to see if coexistent temporal arteritis

232
Q

What is the treatment for polymyalgia rheumatica

A

Dramatic response to steroids (prednisolone)

NSAIDS, exercise and diet

233
Q

Who is rheumatoid arthritis most common in

A

Women aged 30-50

234
Q

What is RA

A

Multi system inflammatory disease primarily affecting joints

235
Q

What is the pathophysiology of rheumatoid arthritis

A

Innate susceptibility + environmental trigger (virus or smoking) leads to cross reactivity with endogenous antigen

Mediated by T cell responses to autoantigen in synovium

T cells produce TNFa and IL6

Macrophages and B cells also play a role - B cells produce RF and anti CCP

Inflammation of synovium - joints tender, stiff, deformed and loss of function

236
Q

What investigations are needed for rheumatoid arthritis

A

Bloods - raised ESR / CRP and abnormal LFTs in active disease

Joint aspirate -sterile, cloudy (white cells) and low viscosity

Serology- RF and antiCCP

X-ray
Ultrasound- look at tendons

237
Q

What is RF

A

An IgM
Associated with nodules and vasculitis seen in RF
Higher titres indicate more severe disease
Also seen in SLE and sjogrens

238
Q

What is anti CCP

A

An anti- citrullinated protein antibody seen in RF
It is rarely positive in patients without RF- therefore very specific to the disease
Has a pathogenic role within the synovium
Titres are associated with severity

239
Q

Which antibody is most specific to RA

A

Anti CCP

240
Q

What are the symptoms/clinical features associated with RA

A

Swollen, warm, tender and stiff joints
Symmetrical polyarthritis affecting small joints
Early morning stiffness >30mins
Deformity - swan neck, ulnar deviation etc
Rheumatoid nodules
Systemic features- fever fatigue, weight loss, vasculitis, sjogrens, breathing difficulties

241
Q

What is the ARA criteria for RA

A

4 of 7 are needed

  1. Arthritis >3/14 joints for atleast 6 months
  2. Arthritis of hands for atleast 6 weeks
  3. Symmetric arthritis for atleast 6 weeks
  4. Subcut nodules in specific places
  5. RF present
  6. X-ray changes associate with RF
  7. Morning stiffness >1 hour
242
Q

What is the problem with the ARA criteria for RA ? What’s the newest criteria called

A

Only sensitive in progressed disease

EULAR - takes into account CCP and number of joints

243
Q

How can we assess severity of rheumatoid arthritis ?

A 
Degree of joint pain 
Duration of morning stiffness 
Level of fatigue 
Deformity
CRP 
Progression of X-ray changes
244
Q

What are the complications of rheumatoid arthritis ?

A 
MSK:
  - carpal tunnel
  - Atlanta-axial subluxation which can cause cervical cord compression
  - osteoporosis
  - tenosynovitis 
Lungs: 
    - lung fibrosis , nodules and pleural effusion 
    - bronchiolitis obliterans 
    - methotrexate pneumonitis 
 Eyes: 
    - sjogrens 
    - scleritis 
CVS:
    - pericarditis 
    - IHD - increased risk of MI
    - anaemia 
    - atherosclerosis  - increased risk of stroke
Kidneys:
   - amyloidosis

Other: increased risk of infection , lymphoma, ankle oedema, sensorimotor neuropathy, leg ulcers

245
Q

What is the treatment for rheumatoid arthritis ?

A

Conservative:

  • advice: stop smoking (smoking is associated with severity)
  • splinting: so that the joint is under less stress, but don’t wear too much or muscle atrophy
  • physiotherapist

Pharmacological:

  • DMARDs
  • corticosteroids injections
  • oral steroids for flare ups
  • biologics - anti TNF
  • NSAIDs
  • NICE guidelines say newly diagnosed RA should be given combination of DMARDs and low dose steroids (short course)

Surgery:

  • joint replacement
  • arthrodesis - pain relief but reduced movement
  • proximal row carpectomy- remove 3 carpal bones for more space
  • tendon repair
246
Q

What is the difference between seropositive and seronegative RA?

A

Seropositive: either RF or anti-CCP present
Seronegative: neither of the above, unknown ab is the cause

247
Q

What is raynauds?

A

Episodic vasoconstriction resulting in cold extremities and colour changes. Mainly affects fingers but can also affect toes and rarely ears, nose and tongue

Can also be associated with pain and tingling

In response to cold and sometimes emotion

Can be idiopathic or associated with a number of autoimmune diseases e.g scleroderma and SLE

248
Q

Who does idiopathic raynauds mainly affect?

A

Females <25yrs

249
Q

What is raynauds caused by ?

A

Imbalances between endothelium vasodilator (NO and prostacyclin) and vasoconstrictors
Also parasympathetic involvement

Connective tissue disease.
Obstructive disease - thoracic outlet syndrome
Drugs: b blockers, chemotherapy
Occupation: vibrating tools

250
Q

What is the treatment of raynauds?

A

Conservative : hand warmers, stop smoking
Pharmacological:
- oral vasodilator : nifedipine, amylodipine and diltiazem
- parenteral vasodilator: nifedipine, amylodipine, losartan, prostacyclin ( for severe attacks e.g. Gangrene of a digit)

Surgery : digital sympathetectomy , amputation

251
Q

What scoring system tells you about a ankylosing spondylosis patients functional limitation ?

A

BASFI

252
Q

What scoring system in AS tells you about disease activity ?

A

BASDAI

- asks about degree of morning stiffness, fatigue, pain etc

253
Q

What type of hypersensitivity reaction are the autoimmune diseases including rheumatoid arthritis ?

A

Type 3

254
Q

Name / describe some of the deformities seen in the hand of a rheumatoid arthritis patient

A 
Fixed flexion: boutonnière 
Fixed hyperextension : swan neck 
Ulnar deviation 
Subluxation of ulnar styloid- can lead to subluxation of extensor tendon and sudden drop of 4th/ 5th digit 
Z thumb
255
Q

what is the CASPAR score used for?

A

a scoring system to assess likelihood of psoriatic arthritis with 3 or more being likely.

256
Q

how can you tell the difference between osteomalacia and osteoporosis clinically?

A

both have bone pain and fractures.
osteomalacia mayalso have muscle pain and fatigue due to lack of vit D
also clue in cause - old women more likely osteoporosis , dark skin osteomalacia

257
Q

which diseases show osteopenia?

A

osteoporosis, osteomalacia, hyperparathyroid, multiple myeloma

258
Q

How can we measure bone resorption?

A

urinary hydroxyproline excretion

high if there is increased bone turnover - pagets

259
Q

what investigations should be carried out for pseudogout?

A

raised WCC and ESR and CRP in acute attack
joint aspiration
imaging

260
Q

what should you look for when aspirating a joint?

A 
Crystals 
gram staining 
white cells
clear/ cloudy
viscosity
261
Q

what is henoch- schonlein purpura? include symptoms and treatment

A

IgA mediated vasculitis (often this is preceeded by throat infection)
purpuric rash - small vessels of skin inflamed and bleed
also joint pain, abdominal pain and haematuria (can affect kidneys - glomerulonephritis)

high spontaneous recovery - so no treatment just analgesia. however if kidneys involved steroids/azathioprine can be used

262
Q

what vitamin/mineral supplements can be given to protect cartilage?

A

glucosamine and chrondroitin

often used in OA

263
Q

What is heridary vit D resistant rickets also known as ?

A

Hypophosphataemic rickets

264
Q

how does systemic sclerosis/ CREST cause dysphagia?

A

As well as oesophageal dysmotility the lower oesophageal sphincter (LES) pressure is decreased.

General Medicine sara (4 decks)

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