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Flashcards in MSK Deck (420):
1

What is Raynaud's phenomenon?

peripheral digital ischemia due to paroxysmal vasospasm affecting arteries supplying fingers and toes

2

What precipitates Raynaud's syndrome?

cold

3

What relieves Raynaud's syndrome?

heat

4

What are the symptoms of Raynaud's syndrome?

numbness, burning sensation, severe pain when warmed up

5

Who is mainly affected by Raynaud's syndrome?

young women

6

What happens in Raynaud's syndrome?

initial pallor from vasoconstriction, followed by cyanosis due to sluggish blood flow, then redness from hyperamia

7

DD of Raynaud's syndrome?

autoimmune rheumatic disease, bb therapy, raynauds disease

8

What is the treatment of Raynaud's syndrome?

stop smoking, keep hands and feet warm, oral nefdipine, prostacyclin infusions, lumbar symphathectomy, evening primrose oil, sildenafil, prostsacyclin, vasodilators, avoid vibrating tools

9

What are the causes of gout?

hereditary, increased dietary purines, alcohol excess, diuretics, leukaemia, cytotoxics

10

Where do we acquire purines from?

from the break down of food or break down inown tissues in pathway

11

What are purines broken down into?

hypoxanthine, xanthine and then uric acid to be carried around in the bloodstream

12

What are the two outcomes for uric acid in humans?

be removed by the kidney or into monosodium urate crystals

13

What happens if there us a build up on uric acid?

overflows in the kidneys and becomes crystals in the joints and tissues

14

What can cause a increase of urate?

increased urate in diet, increase in cell death and turnover, increased cell damage, decreased excetion, drugs, fructose, genetics, increase in insulin levels, red meat, seafood

15

What 4 conditions can hyperuricaemia and deposition of sodium urate crystals result in?

acute gout, chronic polyarticular gout, chronic tophaceous gout, urate renal stone formation

16

What conditions can gout be a marker for?

CV disease, hypertension, diabetes, chronic renal failure

17

How common is gout?

prevalence is around 1%

18

Is gout more common in males or females?

Male, rare before adulthood

19

How many people with hyperuricaemia develop gout?

20%

20

What foods help against gout?

dairy, cherries, vit C, carbohydrate, smaller meals, 2000 calories

21

What is the saturation point of uric acid compared to the normal range?

Normal = 200-430umol/L
Saturation = 380umol/L

22

What is acute gout?

inflammatory arthritis caused by hyperuricaemia and intra articular sodium urate crystals

23

What causes acute gout?

A sudden change in blood:tissue urate balance, either sudden overload or sudden reduction (ULT), cold, trauma, sepsis, dehydration, drugs

24

What symptoms does acute gout cause?

urate crystals trigger intracellular inflammation, causes severe pain, swelling, redness, commonly on metatarsophalangeal joint of big toe

25

What is the treatment of acute gout?

colchicine 500ug max tds, NSAIDs, steroids, ice, cherries, vit C, coxib

26

How does chronic trophaceous gout present?

large, smooth, white deposits (tophi) in the skin and around the joints, particularly on ear, fingers and Achilles tendon

27

What investigations can be used for gout?

polarised light microscopy of joint synovial fluid shows negatively birefringent urate crystal, raised serum urate (but can be normal in acute attack), radiographs show tissue swelling, serum urea and creatinine show renal impairment, well defined punched out erosions in juxta articular bone, no sclerotic reaction, joint spaces preserved till late

28

What is the long term treatment of gout?

stop diuretics and use losartan or fenofibrate instead, reduce weight, stop smoking, change diet, reduce alcohol, allopurinol 100mg/day, colchicine, NSAIDs, steroids

29

What should the starting dose for allopurinol be and how much should it be increased by if serum urate is not below 300 - WITH NO RENAL IMPAIRMENT??

100mg/day, increased by 100mg

30

What should the starting dose for allopurinol be and how much should it be increased by if serum urate is not below 300 - WITH RENAL IMPAIRMENT??

1.5mg/unit eGFR/day and increase by 1.5mg/unit eGFR/day

31

What are side effects of allopurinol?

rash, headache, myalgia

32

What value of eGFR can allopurinol be used down to in gout treatmeant?

30 eGFR

33

What should be monitored in allopurinol gout treatment and what can it rarely cause?

LFTs and U and Es, hypersensitivity syndrome

34

What mediations can be problematic in renal impairment for out?

NSAIDs and colchicine

35

What kind of medication Is Febuxostat for gout and how does it work?

It is a non purine Xanthine Oxidase inhibitor causing a decrease in uric acid

36

When should Febuxostat be used in gout treatment?

If Allopurinol is contraindicated , and it is more effective at decreasing serum urate

37

What is a side effect of Febuxostat?

increased LFTs

38

How do uricosuric drugs work in gout treatment?

increase urate excretion by inhibiting renal absorption of urate

39

What kind of drug is Benzbromarone in gout treatment?

a uricosuric drugs

40

What is the effect of Rasburicase in gout treatment?

rapid urate reduction

41

What is a risk of using Rasburicase in gout treatment?

high incidence of drug reactions

42

How is pegloticase used in gout treatment?

It is pegylated uricase

43

How is Tophi used in gout treatment?

It releases local protolytic enzymes causing erosisons of urate crystal

44

What is pyrophosphate arthropathy?

pseudogout from deposition of calcium pyrophosphate crystals on joint

45

Where on the body is pyrophosphate arthropathy commonly seen?

MCPs, wrists, knees, ankles

46

How does pyrophosphate arthropathy present?

as a hot or OA type joint, condrocalcinosis seen on x-ray

47

What is the treatment of pyrophosphate arthropathy?

IA steroids, orals steroids, colchicine, NSAIDs, coxibs, corticosteroids, correct metabolic abnormalities

48

How can you prevent future attack of pyrophosphate arthropathy?

decrease serum uric acid levels, lose weight, reduce alcohol, stop thiazides and salicylate, reduce calorie intake, avoid purine rich foods, allopurinol

49

What is pseudogout?

The deposition of calcium pyrophosphate dehydrate in articular cartilage and periarticular tissue producing chondroclacinosis

50

What is another word for pseudogout?

acute calcium pyrophosphate crystal arthritis

51

What can pesudogout be provoked by?

illness , surgery, trauma,

52

What kind of joints does pseudogout commonly affect?

larger joints

53

Who is most likely to get pseudogout?

elderly women

54

What conditions are associated with pesudogout in the young?

haemochromatosis, hyperparathyroidism, Wilson's disease, acaptomina

55

What investigations should you do for pseudogout?

fluid joint microscopy - small brick shaped pyrophosphate crystals which are positively birefringent, increased WBC

56

What is the difference in appearance of gout and pseudogout fluid microscopy?

gout - negatively birefringent
pseudogout - positively birefringent

57

What is the treatment for pseudogout?

NSAIDs or colchicine, corticosteroid injection, methotrexate and hydroxycholorquine if chronic

58

What is fibromyalgia?

chronic widespread pain for >3 months below waist

59

What is the pain like in fibromyalgia?

widespread, unremitting, aching discomfort, sleep disturbances, poor concentration and awake unrefreshed

60

How many tender sites must be painful to be classified as fibromyalgia?

11/18

61

What are the symptoms of fibromyalgia?

Pain, sleep disturbance, poor concentration, IBS, tension headache, dysmenorrhoea, atypical facial or chest pain

62

Who is mainly affected by fibromyalgia?

middle ages women, with low income, divorce and low eductation

63

What causes pain amplication syndrome?

changes in descending inhibitory pathways in the spinal cord, causing maladaptive pain response

64

What is the treatment for fibromyalgia?

psychosocial, MDT, exercise, CBT, treat depression, analgesics, antidepressants, low dose amitriptyline, dosulepin, trigger point injections with local anaesthetics, acupuncture, avoid unnecessary investigations

65

how do low dose amitriptyline or dosulpin help in firbromyalgia?

increase serotonin level in CNS, and increase descending sensory inhibition

66

What do investigations show in fibromyalgia?

They are normal, but appear agitated tender points, wincing, skin fold tenderness, tearful

67

What conditions are closely related to fibromyalgia?

depression, chronic headache, IBS, chronic fatigue, myofascial pain syndrome

68

What causes peripheral (nociceptive) pain?

stress, genes, cognitive and behavioural adaption

69

In what kind of pain are behavioural factors important?

central (non nociceptive) pain

70

What is the pain mechanism behind central (non nociceptive) pain?

There is a central disturbance in pain processing

71

Examples of peripheral (nociceptive) pain?

OA, RA, cancer

72

Examples of central (non nociceptive) pain?

fibromyalgia, IBS, tension migraine

73

What is the pain mechanism behind nociceptive pain?

due to inflammation or damage in periphery

74

How do analgesic affect central pain?

They have no effect

75

What can increase your pain volume and therefore increase pain?

substance P, glutamate, EAA, serotonin, neurotensin, nerve growth factor

76

What can decrease your pain volume and therefore decrease pain?

descending analgesic pathways, GABA, cannabanoids, adenosine

77

What can aggravate and trigger fibromyalgia pain?

stress, cold, activity, peripheral pain sundromes, infections, physical trauma, psychological stress, hormones alterations, vaccines

78

What kind of pain is experienced in fibromyalgia?

frequent wakng, waking unrefreshedm poor concentration, forgetful, low mood

79

DD for fibromyalgia?

hypothyroidism, SLE, PMR, inflammatory myopathy, increase calcium, lower vitamin D

80

What is hypermobility?

joints that move easily beyond expected range

81

Who is hypermobility common in?

children, decreases with age

82

Are there any symptoms to hypermobility?

mainly asymptomatic but can cause widespread joint pain

83

In the Brighton criteria, what is the diagnosis of hypermobility?

5 or more /9 joint hypermobile

84

What does benign joint hypermobility syndrome increase the tendency of?

recurrent sprains or dislocation

85

What is spondyloarthritis?

a group of conditions affecting the spine and peripheral joints

86

What are the common features that all spondyloarthritis conditions share?

predilection for axial inflammation, asymmetrical peripheral arthritis, sero negative, inflammation of the enthesis, associated with HLA-B27

87

What does seronegative mean?

absence of rheumatoid factor

88

what is ankylosing spondylits?

chronic inflammatory disease of spine and sacroiliac joints, unknown aietiology

89

What is the prevalence anykylosing spondylitis and in who is it most likely?

0.25-1%, in males aged 16 or 30

90

What are the clinical features of ankylosing spondylitis?

increasing pain and prolonged morning stiffness in lower back, limitation of lumbar spine mobility in saggital and frontal planes, anterior mechanical chest pain, acute intis, Achilles tendernitis, plantar fasciitis, tender chest wall,

91

How does ankylosing spondylitis affect movement?

progressive loss of spinal movement, decreased thoracic expansion, loss of lumbar lodosis, increased kyphosis, limitation of lumbar spine mobility in saggital and frontal planes

92

What causes anterior mechanical chest pain in anylosing spondylitis?

costochondritis and fatigue

93

What conditions are associated with ankylosing spondylitis?

osteoporosis, aortic valve incompetence, pulmonary apical fibrosis

94

What will investigations show in akylosing spondylitis?

increased ESR and CRP, X-ray shows erosion and sclerosis of sacroiliac joint margins with blurring of upper and lower vertebral rims at thoracolumbar junction, bony spurs when bone heals, progressive calcification of interspinous ligaments leading to bamboo spine, MRI shows sacroillitis, normocytic anaemia

95

What is the treatment of ankylosing spondylitis?

morning exercise, slow release NSAID s at night, methotrexate, TNF a blocking drugs for active inflammatory disease, physiotherapist, surgery of hip replacement, spinal osteotomy

96

how does morning exercise help in akylosing spondylitis?

maintains posture and spinal mobility

97

how do TNF a blockin drugs help in ankylosing spondylitis?

improve spinal and peripheral joint inflammation

98

What factors lead to a poorer prognosis in ankylosing spondylitis?

early hip involvement, poor response to NSAIDs, ESR

99

How many of those with psoriasis develop psoriatic arthritis?

10-40%, particularly with nail disease, can precede skin disease

100

Where does psoriatic arthritis usually affect?

the distal interphalangeal joints

101

What is arthritis mutilans?

destruction of small bones in hands and feet

102

What symptoms and other conditions are seen in psoriatic arthritis?

arthritis of distal interphalengeal joints, arthritis muilans, sacroilitis, nail changes, synovitis, acneiform rashes, palmoplantar pustulosis

103

What is the treatment of psoriatic arthritis?

analgesics, NSAIDs, anti TNF agents

104

What is reactive arthritis?

sterile arthritis affecting lower limbs

105

When does reactive arthritis usually occur?

1-4 weeks after GI infection or STI

106

How does an infection cause reactive arthritis?

persistent bacterial antigen in the inflamed synovium of affected joints cause inflammation

107

Where is reactive arthritis usually seen?

knees, ankles, feet

108

What is reites syndrome and in what disease is it usually seen?

the triad of urethritis, arthritis and conjunctivitis - seen in reactive arthritis

109

What can circinate balanitis lead to and in what disease is it usually seen?

causes superficial ulcers around penis and can harden and crust, seen in circumcised males

110

What do investigations show in reactive arthritis?

increased ESR, sterile synovial aspirate, increase neutrophils

111

What other conditions are usually seen in reactive arthritis?

circinate balanitis, keratoderma blenorrhagica, nail dystrophy, acute anterior ureitis, reites syndrome, sacroiliitus, spondylitis

112

What is the management of reactive arthritis?

STI check, NSAIDs, local corticosteroid injections, antibiotics for persistant infection, TNF a blocking drugs

113

What is enteropathic arthritis?

large joint mono or asymmetrical oligoarthritis

114

In what disease is enteropathic arthritis usually seen?

10-15% of IBD and 5% of IBS

115

What is the treatment of enteropathic arthritis?

DMARDS

116

In who is septic arthritis usually seen?

those over 65 and in prosthetic joint infection

117

What organisms commonly cause septic arthritis?

Staph. aureus, streptococci A or B or pnumoniae, Neisseria gonorrhoea, e. coli, pseudomonas aeruginoas, clostridium, bacterioides, mycobacterium, fungi

118

If not treated immediately, what does septic arthritis cause?

destroyed joint in U24hrs, long term disability

119

What is the most common joint affected by septic arthritis?

the knee in >50% of cases

120

What are risk factors for septic arthritis?

prosthetic joints, pre existing joint disease, recent intra-articular steroid injection, diabetes mellitus, immunosuppression, chronic renal failure, recent joint surgery, IV drug abuse, over 80

121

how does septic arthritis present?

hot, painful, swollen, red joint developing acutely, fever and evidence of infection

122

How does infection in septic arthritis present?

wound inflammation, discharge, joint effusion, loss of function, pain

123

What investigations should be done in septic arthritis?

joint aspiration with gram satin, culture, WBC count, polarised light microscopy, bloods, leucocytosis, swabs

124

What would the WBC count appear to be in septic arthritis?

opaque, with up to 75,000 (inflammation is >3000 and normal is

125

What is a sign of septic arthritis in children?

They just won't use the joint

126

What is the management of septic arthritis?

antibiotics depend on organism, joint drainage, aspiration, arthroscopy, open drainage, prosthetic joint, NSAIDs, splint, analgesics, physio, immobilise joint

127

What antibiotic should be used in immunocompromised patients for septic arthritis?

gentamicin

128

What are the main antibiotics used in septic arthritis?

flucolaxacillin IV and oral fusidic acid

129

What are the negatives in using excision arthroplasty in septic arthritis?

high risk if co morbidities or frail, low functional demand, uncontrolled with antibiotic suppression, re infection, poor functional outcome

130

What are the exchange arhroplasty principles for septic arthritis?

know the organism, debridgement of all infected and dead tissue, confirmatory intraoperative microsamples, appropriate antibiotic cover, sufficient soft tissue cover, stable joint reconstruction

131

What happen in a one stage exchange arthroplastly?

radical debridment, implant new prosthesis, cemented, symstemic and local antibiotics, avoid bone graft

132

What happen in a two stage exchange arthroplastly?

radical debridement, local antibiotic spacer, systemic antibiotics, interval stage, implant new prosthesis with tissue samples for culture, cemented or cementless with or without bone graft, routine antibiotic prophylaxis

133

What is osteomyelitis?

infection localised to bone

134

What makes you more susceptible to osteomyelitis?

malnutrition, diabetes, PVD, debilitating disease, decreased immunity

135

What are the main microorganisms in osteomyelitis?

Staphylococci is 90%, H.influenzae and salmonella, s.aureus, fungi, mycobacteria

136

How does osteomyelitis present?

fever, bone pain, with overlying tenderness and erythema, rigors, sweats, malaise

137

What do investigations show in osteomyelitis?

osteopenia, marrow oedema, blood cultures show infection, bone biopsy, foot swab

138

What is the treatment of osteomyelitis?

IV teicoplanin or flucoxacillin or ceftriaxone, oral fusidic acid after, surgical drainage, remove dead bone

139

What are some complications of osteomyelitis?

sinus and abscess formation, TB osteomyelitis, septic arthritis

140

What causes osteomyelitis?

trauma, surgery, spread of infection to bone, haematogenous seeding

141

What are the acute changes in osteomyelitis?

inflammatory cells, oedema, vascular congestion, small vessel thrombosis

142

What are the chronic changes in osteomyelitis?

necrotic bone, new bone formation, neutrophil exudates, lymphocytes and histocytes

143

How does inflammation cause necrosis in osteomyelitis?

Inflammatory exudate in the marrow increases intramedullary pressure and extension of exudate in the bone cortex causing rupture through periosteum, interruption of periosteal bone supply causes necrosis, leaving separated dead bone

144

Where does osteomyelitis usually occur?

hip, vertebrae, pelvis

145

Where is the most common place in the vertebrae to get osteomyelitis?

lumbar > thoracic > cervical

146

What is the difference on movement affecting the pain in osteomyelitis and septic arthritis?

septic is painful on movement and rest, osteomyelitis pain is localised and painful on movement

147

Is swelling more likely in osteomyelitis or septic arthritis?

septic arthritis

148

is fever more likely in osteomyelitis or septic arthritis?

osteomyelitis

149

What will investigations show in osteomyelitis?

increased WCC (acute only), increased ESR and CR, x-ray shows cortical erosion, periosteal reaction, mixed luceney, sclerosis, sequestra, soft tissue swelling, MRI shows marrow oedema, bone biopsy and culture (2 specimens)

150

What will blood cultures show in osteomyelitis?

positive in 50%, most useful in haematogenous OM

151

In who and where about is haematogenous OM most commonly seen?

adults over 50 in vertebra > clavicle/pelvis > long bones
children (85%) in long bones > vertebra

152

What are risk factors for haematogenous OM?

central lines, dialysis, sickle cell disease, urethral catheterisation, UTI, CF endocarditis

153

DD for osteomyelitis?

soft tissue infection, charcot joint, avascular necrosis of bone, gout, fracture, bursitis, maligancy

154

What is the treatment of osteomyelitis?

debridement , hardware placement or removal, antimicrobial therapy depending on organism , stop treatment based on ESR and CRP, failure to respond requires reimaging

155

How does biopsy differ in TB osteomyelitis?

prolonged culture, caeseating granulomatrix, induced sputum

156

What are the causes of mechanical lower back pain?

lumbar disc prolapse, osteoarthritis, fractures, spondyolsthesis, spinal stenosis

157

When is pain worse in mechanical lower back pain?

evening, absent in the morning, aggravated by exercise

158

What are risk factors for mechanical lower back pain?

female, age, pr existin widespread pain, psychological distress, poor health

159

What do bone scans show in mechanical lower back pain?

increased uptake with infection or malignancy

160

What investigations should you do in lower back pain?

Ct, MRI, bone scan, FBC, ESR, spinal x-ray

161

Red flags in back pain?

acute onset in elderly, nocturnal pain, younger than 22, older than 55, fever, night sweats, weight loss, morning stiffness, malignancy history, abdominal mass thoracic back pain, infection, immunosuppressed

162

What is the treatment of mechanical lower back pain?

treat underlying cause, analgesics, brief rest, physio, stay active, long term exercise programme

163

What does back pain in 15-30 years suggest of cause?

prolapsed disc, trauma, fractures, akylosing spondylitis, pregnancy

164

What does back pain in 30-50 years suggest of cause?

degenerative spinal disease, prolapsed disc, malignancy

165

What does back pain over 50 years suggest of cause?

degenerative, osteoporotic vertebral collapse, pagets malignancy, myeloma, spinal stenosis

166

What should you do in a back pain examination?

lumbar flexion and extension, test for sacroiliitis, check for neurological defects, digital rectal examination for perianal tone and sensation

167

What is spinal stenosis?

a narrowing of lower spinal canal, compresses the cauda equine causing back and butlock pain

168

What is the treatment of spinal stenosis?

surgical decompression

169

What is spondylolisthesis?

a slipping forward of one vertebra on another, mainly at L4/5

170

When should you treat with antibiotic suppression in infection?

if patient is unfit for surgery, multiple prosthetic joint infections, poor distal skin/soft tissues, low virulence infecting organisms, available oral antibiotics, prosthesis not loose,

171

How long must a patient be off antibiotics to do a diagnostic aspiration?

2 weeks

172

What is osteoporosis?

a systemic skeletal disease with low bone mass and micro-architectural detection of bone tissue with increase in bone fragility and susceptible to fracture

173

What is the bone density in osteoporosis?

less than -2.5 standard deviation

174

What is the condition called when bone density is between -1 and -2.5 sd?

osteopaenia

175

How common is osteoporosis?

50% of women and 20% of men over 50 have an osteoporotic fracture

176

Bone mineral density dependent risk factors for osteoporosis?

female, Caucasian, Asian, hypogonadism, immobilisation, low calcium, drugs, chronic liver or renal disease, copd, Gi disease, vit D insufficiency, endocrine disease

177

Bone mineral density independent risk factors for osteoporosis?

age, previous fracture, family history of hip fracture, glucocorticoid herapy, increased falling risk, low BMi, smoking, alcohol abuse, high bone turnover, RA

178

When do you achieve your peak bone mass?

in early adult life, depends on genetic factors, nutrition, sex hormones and exercise

179

What are potential consequences of a hip fracture?

death, permanent disability, unable to walk independently, unable to carry outa daily living activity

180

When is age related bone loss accelerated in women?

Starting at menopause

181

What happens in women post menopause in the bones?

remodelling imbalance causing a net loss of bone due to the loss of restraining effect of oestrogen on bone turnover

182

how can bone turnover be reduced in women?

oestrogen replacement therapy

183

What are the clinical features of osteoporosis?

fractures, sudden onset of severe pain radiating to front , pain from mechanical derangement, increasing kyphosis, height loss, abdominal prohiberase follows enished vertebra

184

What does a DEXA scan detect in osteoporosis?

measures bone density on important fracture sites, precise, accurate and low radiation dose, spine values may be elevated due to osteophytes, deformity or fractures

185

What investigations are done is osteoporosis?

dexa sscan, quantitive US of calcaneium, quantitive CT scan for volumetric assessment shows destruction between trabecular and cortical bone, bloods, normal biochemistry, X-ray shows fractures

186

Indications for a DEXA scan?

radiographic osteopenia, previous fragility fracture

187

What kind of changes occur in trabecular architecture with aging?

decrease in trabecular thickness, decrease in connections between horizontal trabecular, decrease in trabecular strength and increased susceptibility to fracture

188

How does inflammatory disease cause osteoporosis?

inflammatory cytokines increase bone resorption

189

How does endocrine disease cause osteoporosis?

thyroid and parathyroid hormone increase bone turnover
cortical increases bone resorption and osteoblast apoptosis
oestrogen/testosterone control bone turnover

190

How does reduced skeletal loading affect osteoporosis?

It increases resorption

191

What types of drugs can cause osteoporosis?

glucocorticoids, depoprovera, aromatase inhibitors, GnRH analogues, androgen deprivatia

192

What is the treatment of osteoporosis?

best rest, strong analgesics, muscle relaxants, physio, IV pamidronate for pain, orthopaedics, calcium and vit D supplements, anti-resorptive or anabolic drugs, weight bearing exercise, reduce fall risks, avoid alcohol and smoking, bisphosphonates, strontium renelate, raloxifene, teriparatide, recombinant human parathyroid peptide 1-34 and 1-84, hormone replacement therapy, testosterone, denosumab

193

How do bisphosphonates treat osteoporosis?

e.g. alendronate - inhibit osteoclast activity to inhibit bone resorption which increases bone mass at hip and spine to reduce fractures

194

What are the side effects of bisphosphonates?

oesophagitis, osteonecrosis

195

What are the advantages of bisphosphonates?

cheap, effective

196

How does strontium renelate treat osteoporosis?

reduces bone absorption but maintains bone formation

197

What are the advantages of strontium renelate?

alternative to bisphosphonates, good in elderly with poor compiance

198

What are the side effects of strontium renelate?

nausea, diarrhoea, headaches, thromboembolism

199

How does Raloxifene treat osteoporosis?

It is a selective oestrogen receptor modulator (SERM) which activates oestrogen receptors on bone with no stimulatory effect on the endometrium and reduces BMD loss at the spine and hip, reduces fractures

200

What are the side effects of Raloxifene?

leg cramps, flushing, thromboembolism

201

How does Teriparatide treat osteoporosis?

Reduces fracture risk by increasing bone density, improves trabecular structure, increases osteoblast activity and bone formation. It is a 1st anabolic treatment. PTH analogue (1-34)

202

How does recombinant human parathyroid peptide and hormone treat osteoporosis?

Stimulates bone formation with a daily injection

203

What is the main complication of recombinant human parathyroid peptide and hormone treatment ?

hypercalcaemia

204

How does hormone replacement therapy treat osteoporosis?

decreases osteoclast activity and bone turnover, reduces fractures, stops bone loss, prevents hot flushes, reduces colon cancer risk,

205

What are the side effects of hormone replacement therapy?

breast cancer, increased CV risk, vaginal bleeds, stroke

206

How does Denosumab treat osteoporosis?

a human monoclonal antibody to RANKL, sc 6 monthly injection, reduces resorption, increases BMD, reduces spine fractures, decreases osteoclast activity and bone turnover

207

What is a side effect of Denosumab?

affects the immune system and can cause eczema

208

How do you treat glucocorticoid induced osteoporosis?

reduce corticosteroids, give alternative immunosuppressive agents, calcium and vit d

209

What is osteonecrosis?

deat of bone and marrow cells due to a reduced blood supply

210

What can cause osteonecrosis?

medication, alcohol abuse, sickle cell disease, trauma, radiation, HIV infection

211

Where does osteonecrosis mainly affect?

femoral neck

212

What is large vessel vasculitis?

inflammatory disorder of blood vessel walls causing destruction or stenosis

213

What are the 3 types of large vessel vasculitis?

Giant cell arthritis, polymyalgia rheumatic, takayasis arteritis

214

How does polymyalgia rheumatic present?

sudden severe pain and stiffness of shoulders, neck, hips, lumbar spine in a limb griddle pattern

215

In who is polymyalgia rheumatic and giant cell arthritis most common?

over 50s, women twice as likely

216

When is pain in polymyalgia rheumatic worst?

in the morning

217

What symptoms can accompany polymyalgia rheumatic ?

tiredness, fever, wight loss, depression, nocturnal sweats, tenderness over temple and claudication of jaw when eating

218

What do investigations show in polymyalgia rheumatic ?

increased ESR ad CRP, increased alkaline phosphate, mild normochromic normocytic anaemia, angiography and increased creatinine if renal failure

219

What is giant cell arthritis?

inflammatory granulomatous arteritis of large cerebral arteries with PMR

220

How does giant cell arthritis present?

severe headache, tenderness of scalp, claudication of jaw when eating, swelling and tenderness of temporal or occipital arteries, painless temporary or permanent loss of vision due to ophthalmic artery involvement

221

What do investigations show in giant cell arthritis?

normochromic normocytic anaemia, increased ESR ad CRP, low albumin, increased alkaline phosphate, temporal artery biopsy is diagnostic

222

What does histology show in giant cell arthritis?

CD4+ T lymphocyte, macrophages and giant cell infiltration in vessel walls, granulomatous inflammation of intima and media, breaking up of internal elastic lamina, giant cell and lymphocytes and plasma cells in internal elastic lamina

223

How many oh polymyalgia rheumatic cases have giant cell arthritis in biopsy?

10-30%

224

What is the treatment of PMR and GCA?

high dose corticosteroids (higher in GCA and reduce if visual loss), prednislone (high in GCA and gradually reduce), steroid sparing immunosuppressant, calcium and vit D supplements, bisphosphonates,

225

What is Takayasus arteritis?

granulomatous inflammation of aortic arch and major branches

226

Where does Takayasus arteritis mainly occur?

in japan

227

What does Takayasus arteritis cause?

hypertension, absent peripheral pulses, strokes, cardiac failure

228

What is the treatment of Takayasus arteritis?

corticosteroids

229

What is the main type of medium sized vessel vasculitis?

Polyarteritis nodosa (PAN)

230

In who is Polyarteritis nodosa (PAN) mainly seen?

rare, in middle aged men with severe systemic manifestations

231

What disease is Polyarteritis nodosa (PAN) associated with?

hepatitis B anigenaemia

232

What is Polyarteritis nodosa (PAN)?

fibrinoid necrosis of vessel walls with micro-aneurysm formation, thrombosis and infarction

233

What will tests show in Polyarteritis nodosa (PAN)?

increase WCC, ESR and CRP, mild eoisinophilia, anaemia, ANCA positive, angiography and diagnosis on biopsy

234

What are the clinical features of Polyarteritis nodosa (PAN)?

fever, malaise, weight loss, myalgia, mononeuritis multiplex, strokes, abdominal pain, pancreatitis, haematuria, proteinuria, hypertension, MI, HF, gangrene, lungs are rarely involved

235

What is the treatment of Polyarteritis nodosa (PAN)?

corticosteroids, immunosuppressive drugs e.g. azathioprine, cyclophosphamide, control BP

236

What are the main 3 ANCA positive small vessel vasculitis?

Wegeners granulomatosis, Churd Strauss granulomatosis, microscopic polyangitis

237

What are the main 3 ANCA negative small vessel vasculitis?

Henoch-Schonlein purpura, cryoglobulinaemic vasculitis, ctaenous leucocytoclastic

238

Wjat is the triad of symptoms in Churg Strauss syndrome?

asthma, eosinophilia and a systemic vasculitis affecting the peripheral nerves and skin

239

What is the treat of Churg Strauss syndrome?

corticosteroids, and immunosuppressive drugs

240

How does Henoch Schonelein purpura present?

purpuric rash on legs and buttocks

241

in who is Henoch Schonelein purpura mainly seen?

children

242

What symptoms can accompany Henoch Schonelein purpura?

abdominal pain, arthritis, haematuria and nephritis

243

What is the cause of Henoch Schonelein purpura

IgA dominant immune complexes

244

When does Henoch Schonelein purpura normally occur?

Post acute upper respiratory tract infection

245

What is the treatment of Henoch Schonelein purpura?

recovery is spontaneous

246

What is cryoglobulinaemia vasculitis?

cryoglobulins are immunogolublins and complement components that precipitate reversibly in the cold, involves the sin, kidneys ad polyneuropathy

247

What are the 3 types of cryoglobulinaemia vasculitis?

essential cryoglobulinaemia, associated with infection or autoimmune

248

What is Behcet's disease?

recurrent oral ulceration

249

What is the treatment of Behcet's disease?

immunosuppressive therapy or thalidomide

250

What is the treatment of small vessel vasculitis?

high dose corticosteroids, immunosuppression, plasma exchange, rituximab for B cell depletion

251

What are the two types of anti neutrophillic cytoplasmic antibodies?

pANCA and cANCA

252

What does histology of vasculitis show?

vessel wall infiltration, fibrinoid necrosis

253

3/5 of what are used in the diagnosis of large vessel vasculitis?

over 50, new headache, temporal artery tenderness or decreased pulsation, ESR >50mm/G and CRP, abdominal artery biopsy shows necrotising arteries

254

How does anterior ischaemic optic neuropathy present?

sudden painless monocular and severe vision loss, transient visual loss, optic disc becomes pale and swollen with flame shaped haemorrhages at margin

255

What is the treatment of anterior ischaemic optic neuropathy present?

corticosteroids, prednisolone, steroid sparing agents, prophylaxis of osteoporosis

256

How does granulomatosis with polyangitis present?

Depends of which vasculature of which organ it affects, treat with high dose corticosteroids

257

What is antiphospholipid syndrome?

Thrombosis and/or recurrant miscarriages and persistently positive blood tests for antiphospholipid antibodies detected by the anticardiolipin, lupus anticoagulant or antiB2 glycol protein 1 test - caused by the antibodies reacting with the plasma proteins and phospholipids affecting platelet membranes, endothelial cells and clotting compounds causing thrombosis

258

How many cases of SLE have antiphospholipid syndrome?

20-30%

259

What are the causes of antiphospholipid syndrome?

coagulation defect, livedo reticularis, recurrent miscarriage, thrombocytopenia, DVT, Budd Chaiari syndrome, Stroke, MI

260

What are the 3 tests that can detect antiphospholipid syndrome?

anticardiolipin test, lupus anticoagulant test, anti B2 glycoprotein test

261

How many tests need to be positive for antiphospholipid syndrome?

2 on separate occasions, 12 weeks apart

262

What is the management of antiphospholipid syndrome?

long term warfarin if thrombosis, aspirin and heparin in pregnant, aspiring and clopidogrel for prophylaxis if ALS but no thrombosis

263

What is systemic sclerosis also called?

scleroderma

264

What is systemic sclerosis?

multisystem disease with involvement of skin and Raynaud's phenomenom

265

In who is systemic sclerosis mainly seen?

women aged 30-50

266

What are risk factors for systemic sclerosis?

exposure to vinyl chloride, silica dust, adulterated rapeseed oil, trichloroethylene, drugs, higher concordance in myozygotic pairs

267

What is the pathophysiology behind systemic sclerosis?

increased vascular permeability and activation of endothelial cells result in up regulation of adhesion molecules, cell adhesion and migration through the leaky endothelium into the extracellular matrix, causing cytokine and growth factor production causing proliferation and activation or vascular and connective tissue cells, mainly fibroblasts. Can cause uncontrolled and irreversible proliferation with narrowing of vessel lumen

268

How is fibrosis caused in systemic sclerosis?

proliferation and activation of fibroblasts, increase collagen types 1 and 2 and fibronetin and glyosaminoglycans, leading to fibrosis in lower dermis of skin and internal organs

269

What are the clinical features of limited cutaneous scleroderma?

RAYNAUD'S PHENOMENOM can precede by years, tight skin, beak nose, small mouth, painful digital ulcers, telangiectasia with dilated nail fold capillary loop but no drop out, digital ischemia and gangrene, pulmonary hypertension

270

What parts of the body have skin involvement in limited cutaneous scleroderma?

hands, feet, face, forearms

271

How common is limited cutaneous scleroderma compared to diffuse in systemic sclerosis cases?

70% - lcssc
30% - dcssc

272

What parts of the body have skin involvement in diffuse cutaneous scleroderma?

face, trunk, proximal extremities

273

What are the clinical features of diffuse cutaneous scleroderma?

Raynauds phenomenom within 1 year precede, extensive skin thickening, dilatation and drop out of nail fold capillaries, oedematous, rapid skin sclerosis, pulmonary, renal, hypertensive and GI involvement.

274

How will investigations differ between DcSSc and LcSSc?

D -antitopoisomerase 1 and anti RNA polymerase
L - anticentromere

275

What will investigations show in all systemic sclerosis?

normochromic, normocytic anaemia, increased urea and creatinine if renal disease, ANA positive in 95%, RhF positive in 30%. proteiinuris, ACR, CXR shoes cardac size, deposits of calcium around fingers, barium swallow confirms oesophageal motility, CT show fibrotic lung involvement, oesophageal manometry shoes peristalsis failure and reduced oesophageal sphincter pressure

276

What is the management of systemic sclerosis?

symptomatic, based on organ involvement, no cure, educate, counselling, regular exercise, skin lubricants, hand warmers, oral vasodilators, lumbar symphatectomy, radical miroarteriolysis, PPIs for oesophageal symptoms, nutritional supplements, ACE-I, immunosuppression for pulmonary fibrosis

277

What is the prognosis for LcSSc and DcSSc?

L - 70% 10 yr survival
D - 35% 10 yr survival

278

What are the major causes of death from systemic sclerosis?

pulmonary fibrosis and pulmonary hypertension

279

What does CREST stand for in systemic sclerosis?

calcinosis, raynauds, oesophageal reflux, sclerodactyly, pulmonary arterial hypertension, antibodies centromere

280

What is sjogran's syndrome?

an immunologically mediated destruction of epithelial exocrine gland , caused by cell hyperplasia and obstruction, then atrophy, fibrosis and hyalinisation leading to destruction.

281

What are the main exocrine glands involved in sjogran's syndrome?

lacrimal and salivary

282

Who si mostly affected in sjogran's syndrome?

women ages 40-50

283

What are the causes of sjogran's syndrome?

primary or RA, SLE, systemic sclerosis

284

What is the prognosis of sjogran's syndrome?

5% mortality

285

What are the 3 types of salivary gland?

sublingual, submandibular and parotid

286

What is a major complication of sjogran's syndrome?

non hodgkins lymphoma

287

What are the main symptoms of sjogran's syndrome?

alopecia, dry skin eyes and nose and respiratory tract, cough, dry vagina, dyspareunia, poor vision, photosensitivity, enlarged parotid galnds arthritis, raynauds phenomenon

288

What is the treatment of sjogran's syndrome?

lubricants, drink more water, sugar free gum, corticosteroids, saliva replacement, hydroxycholoroquine, good oral hygiene, immunosuppression

289

DD of dry eyes?

steven Johnson syndrome
pemphigoid
chronic conjunctivitis
chronic belpharitis
trauama
vit A deficiency

290

What investigation should you do for dry eyey in sjogran's syndrome?

Schirmers test - filter paper placed on inside of lower eyelip and wetting of

291

What is the treatment of dry eyes?

artificial tears, cAMP, cyclosporine 2% olive solution, plugs in tear duct, avoid anithcolingenics and antipressants,

292

DD of dry mouth?

viral infections, antihistamine, anticholinergic, antidepressants, irradiation, DM, trauma

293

What tests are used for dry mouth in sjogran's syndrome?

salivary flow is

294

What investigations are needed in sjogran's syndrome?

blood test, anaemia, leukopenia, increased sedimentation rate, SS-a and SS -ro antibodies and, RhF positive, biopsy

295

What does a biopsy show in sjogran's syndrome?

lymphocyte infiltration and destruction of acinar tissue

296

What is polymyositis?

Inflammation and necrosis of skeletal muscle fibres?

297

What is dermatomyositis?

polymyositis with skin involvement

298

Who does polymoyositis and dermatomyositis most commonly affect?

women

299

What are the clinical features of polymoyositis?

symmetrical proximal muscle weakness and autoimmune mediated striated mucle inflammation, myalgia, arthralgia, pain and tendernes

300

What clinical features occur is dermatomyositis in addition to polymyositis?

heliotrope (purple) discolouration of eyelids and scaly erythematous plaques over knuckles (Gottrons papules), nailfold erythema, subcutaneous calcifications

301

What can muscle weakness in polymoyositis and dermatomyositis lead to?

dysphagia, dysphonia, respiratory weakness, difficulty squatting, going upstairs, rising from a chair and raising hands above head

302

What will biopsy of polymoyositis and dermatomyositis show?

inflammatory cell infiltration, necrosis of muscle cells

303

What will investigations show in polymoyositis and dermatomyositis ?

increased serum muscle enzymes (ALT, AST, LDH, CK, aldolase), positive anti JO antibodies, ESR is normal, EMG shows characteritis fibrillation potentials, MRI shows inflammation and muscle oedema

304

What is the treatment for polymoyositis and dermatomyositis ?

screen systemically for malignancy, prednisolone, immunosuppressant and cytotoxics in early resistant cases, hydroxycloroquine, topical tacrolimus, rituximab

305

What is systemic lupus erythromatosis?

autoimmune inflammatory inflammatory disorder which makes autoantibodies against autoantigens (ANA)

306

In who is systemic lupus erythromatosis most commonly seen?

African American women aged 20-40, 1/1000 people

307

What are the risk factors for systemic lupus erythromatosis?

premenopausal, male XXY, UV trigger flares in skin, exposure to Epstein Barr virus triggers, drugs e.g. hydralazine, isoniazid, procainamide, 20 genes linked, deficiencies of C1q, C2 and C4, have type 2 and 3 hypersensitivity, high concordance rate in monozygotic (25%) and dizygotic twins (3%) due to MHC-DQ and DR genetic factors causing defect in rulatory T cells

308

What is the pathophysiology behind systemic lupus erythromatosis?

cells die of apoptosis and the remnants carry self antigens which appear on the surface which include nuclear constituents normally hidden from the immune system, but are not in SLE.

These remnants are transferred to lymphoid tissues and taken up by antigen presenting cells, presented to T cells and stimulate B cells to produce autoantibodies against the antigen.

This leads to development of autoantibodies, completement activation and influx of neutrophils causing inflammation with abnormal cytokine production of IL-10 and IFN-a

309

What can complications of systemic lupus erythromatosis lead to?

MI, stroke, atherosclerosis, lupus nephritis, depression, osteoporosis

310

What are the clinical features of systemic lupus erythromatosis?

fatigue, myalgia, fever, depression, butterfly rash, discoid, epilepsy, migraine, cerebellar ataxia, raynauds, thrombosis, Mi, pericaridits, glomerulonephritis, haemolytic anaemia, thrombocytopaenia, photosensitivity, oral ulcers, immunological, RA

311

What is used as a diagnostic in systemic lupus erythromatosis?

Anti dsDNA positive (ANA is positive in 95% of cases)

312

What do investigations show in systemic lupus erythromatosis?

increase in ESR and CRP, decreased serum albumin, normochromic normocytic anaemia , anti dsDNA, ANA positive, deposition of IgG and complement, sjogrens in 15-20%, brain infarcts, GFR, pulmonary function tests, anti smith and anti Ro and anti La antibodies

313

You need 4 or more out of 11 of what criteria for systemic lupus erythromatosis?

(I AM PORNN HSD)
immunological, ana positive, malar rash, photosensitivity, oral ulcer, renal disorder, non erosive arthritis, neurological disorder, haematological disorder serositus, discoid rash

314

What is the management for systemic lupus erythromatosis?

educate, avoid sun and smoking, assess psychological impact, NSAIDs for mild and arthralgia, topical steroids for discoid lupus, immunosuppressive therapy, monoclonal antibodies, chloroquine and hydrochloroquine for mild, corticosteroids for overall treatment

315

What is the prognosis for systemic lupus erythromatosis?

80% at 15years, but increased risk of cv disease and osteoporosis, decreased survival if major organ involved

316

What is Ehler Danlos syndrome?

hypermobile joints

317

What is Marfans syndrome?

tall, long, arms fingers and toes, faulty collagen

318

What is osteoarthritis?

degenerative arthritis affecting synovial joint with cartilage degeneration and pain worse at the end of the day

319

What are the causes of osteoarthritis?

wear and tear of joint, age, genetics (mutation in gene for collagen II), loss of articular cartilage with peri-articular bone response, trauma to joint, hemochromatosis, Ehlers Danlos syndrome, obesity, birth deformity,

320

What is the pathology behind osteoarthritis?

articular cartilage failure with chondrocytes secreting metalloproteases that degrade collagen and proteoglyces. Il-1 and TNF a stimulate metalloproteases production and inhibit collagen II production. Deficiency in ILGF and TGF b cause impairment in matrix repair, causing inflammation and exposed subchondrol bone becomes sclerotic with increased vascularity and cyst formation which can later become calcified.

321

DD for osteoarthritis?

RA, gout, osteonecrosis, neuropathic joint

322

Complications of osteoarthritis?

gout risk and chondro calcinosis

323

What are the symptoms of osteoarthritis?

pain, stiffness and joint tenderness, swelling, muscle wasting, deformity, decreased range of movement, crepitus, osteophytes palpable, joint instability, Heberdens nodes ar DIP joints, Bouchards nodes at PIP joints, continuous capsular thickening, insidious pain over years, intermittent swelling and effusion

324

What joints does osteoarthritis mainly affect?

DIP joints, thumb, carpometacarpal joint, knees

325

What do the radiographs for osteoarthritis show? (loss)

Loss of joint spaces
osteophytes
subchondral cysts
subarticular sclerosis

326

What do investigations for osteoarthritis show?

RhF is negative, normal FBC and ESR, increased vascularity due to new bone formation, joint aspiration, MRI, BMI

327

What is the most common joint disease?

osteoarthritis

328

Who is most likely to get osteoarthritis?

100% are >65

329

What aggravates and relieves osteoarthritis?

aggravated by exercise and relived by rest so it becomes background pain

330

What does crepitus mean?

grating of joint due to disruption of smooth articulating surfaces

331

What does osteoarthritis management depend on?

age, functional needs, stage of disorder, joint involved

332

What is the treatment of osteoarthritis?

topical capsaicin, joint replacement, steroid injection, surgery, drugs, splints, exercise, physio, NSAIDs, analgesics, weight loss, walking stick, soft shoe soles, heel raises, visco supplementation action

333

Where are Bouchards nodes found in osteoarthritis?

proximal inter phalangeal joints

334

Where are Heberdens nodes found in osteoarthritis?

distal inter phalangeal joints

335

What questions should you ask about joint pain?

location, exacerbating factors, reliving factors, night pain, associated clicks

336

What can cause foot deformity?

poor shoeswear, congenital, trauma, previous surgery,

337

What should be done in a foot and ankle examination?

look, feel, move, special test, standing and sitting examination, shoes, flexibility

338

What is the classification called joint fractures?

Salter Harris Classification 1-5

339

In the Salter Harris Classification for paediatric fractures, what is the most common on?

2 -

340

In the Salter Harris Classification, which one crosses the plate line which can cause problems?

4

341

In the Salter Harris Classification, which one can cause malalignment?

3

342

What is a fracture?

a break in continuity of a surface or substructure of bone with a soft tissue injury

343

What bones are commonly broken in neonates?

humerus and clavicle

344

What bones are commonly broken in infants?

radius

345

What bones are commonly broken in toddlers

tibia

346

What bones are commonly broken in children?

fibula, radius and femur

347

What bones are commonly broken in adolescents?

tibia

348

What investigations are need in a fracture?

90 degree x-ray, and see joint top and bottom

349

What is pethase disease?

In young boys, affecting the subchondral

350

What is an elastic intramedullary nailing?

It is prebent to a curve to hold a fracture and is passed up inside a bone

351

What are the four stages of bone formation?

haematoma formation, callus formation, callus ossification, bone remodelling

352

What is the main cause of arthritis in the young?

trauma

353

How does arthritis present in children?

joint swelling, stiffness and limitation of use

354

What are the 7 types of juvenile arthritis?

RhF +, RhF -, psoriatic, exthestitis related HLAB27+, extended oligoarticular, persistent oligoarthritis, systemic onset

355

How many joints are involved in an oligoarthritis?

1-4 (50% only have 1 joint affected)

356

What is a major complication of oligoarthritis?

uveitis

357

Treatment of oligoarthritis?

grow out of it

358

What do investigations show in oligoarthritis?

ANA +

359

How old are people with oligoarthritis?

360

How many joints does extended oligoarthritis affect?

1-4 in first 6 months, then more after

361

Who is most likely to get extended oligoarthritis?

girls aged 2-4

362

How many with extended oligoarthritis carry it on into adulthood?

50%

363

What should you always screen for in extended oligoarthritis?

uveitis

364

How many joints are involved in juvenile polyarticular arthritis?

5 or more, usually symmetrical

365

What other symptoms could be seen in polyarticular arthritis?

malaise, fever, anaemia, uveitis

366

Which juvenile arthritis is most similar to adult RA?

RhF+

367

What is a difference between adult and juvenile RA?

juvenile is CCP Ab negative, and could be related to smoking habit

368

In who is enthesitis JIA normally seen in?

young males of >6 years

369

How does enthersitis JIA present?

HLAB27+, inflammatory back or sacroiliac pain

370

What is psoriatic type JIA?

JIA in children with or with a FH of psoriasis

371

At what age will you normally acquite systemic onset JIA?

4-6 years

372

How do you present with systemic onset JIA?

systemic illness, with fever rash and arthritis, anaemia, high platelets and high ferritin, lymphadenopathy, hepatosplenomegaly and serositis

373

What is the treatment of JIA?

steroid joint injections, e.g. GA, entonox, topical, NSAIDs, methotrexate, systemic steroids, biologic drugs, indo and educate, support, liase with school, physio, occupational therapy, psychology

374

What complications can occur it JIA is untreated

joint damage, psychological impact, bony overgrowth, unequal leg length, anaemia, weight loss, failure to grow, uveitis

375

What investigations should be done in JIA?

FBC, anaemia, thrombocytosis, U and E, ER and CRP, ferritin, US, MRI, X-ray

376

What should doctors be aware of in transitional medicine? (HEADS)

physical maturation, developing autonomy, risky behaviours, intimate relationships, education, vocation

home, education, activities, alcohol, drugs, sexual health, suicide, spiritual

377

What is rheumatoid arthritis?

a chronic, autoimmune type 3 hypersensitivity reaction affecting joints and other organs, has symmetrical deformation with pain worse in the morning

378

What complications can rheumatoid arthritis cause?

carpal tunnel syndrome, pericarditis, tendon rupture, cervical myopathy, depression, sjogren syndrome

379

Who are most likely to get rheumatoid arthritis?

women more than men, until after menopause

380

What are makers for rheumatoid arthritis?

HLA DR4 and HLA DR1

381

What are risk factors for rheumatoid arthritis?

female, smoking, high concordance in monozygotic (15-30%) and dizygotic twins

382

What is the function of rheumatoid factor in rheumatoid arthritis?

chronically maintains synovial inflammation caused by activated inflammatory cells

383

What the is pathogenesis behind rheumatoid arthritis?

activated T cell, macrophages, mast cells and firbroblasts produce factors causing synovial fluid which is chronically maintained by RF and immune complex formation and complement activation caused by B cells, so continuous inflammation and thickening of the synovial linging with inflammatory cell infiltration. There is extravasation of leucocytes into synovium causing it to proliferate and grow out over the cartilage surface producing a pannus, destroying the articular cartilage and sub chondral bone, causing bone erosions.

384

What is the purpose of angiogenic cytokines in rheumatoid arthritis?

produce new synovial blood vessels

385

What is the purpose of endothelial cells in rheumatoid arthritis?

produce adhesion molecules to cause extravasation of leucocytes into synovium

386

What are the symptoms of rheumatoid arthritis?

hands - z deformity, boutonmere and swan neck deformity, ulnar deviation, subluxation of fingers, Raynaud's
Wrist - carpal tunnel syndrome
Feet - subluxation of toes and hammer toe deformity
Skin - rheumatoid nodule and vasculitis
CV - atherosclerosis
Respiratory - pulmonary fibrosis
Bones - osteoporosis
Pain and stiffness

387

What would investigations show in rheumatoid arthritis?

RhF+, increased ESR and CRP, CCP antibodies (can suggest erosive)

388

How is CCP produced in rheumatoid arthritis?

produced when arginine residues in proteins are enzymatically converted into cetruline ones which are seen as antigens to the immune system causing an immune response, radiology

389

What does the radiology show on rheumatoid arthritis?

bony erosisons, sublaxation, carpal instability, joint involvement, periarticular osteoporosis

390

What must you assess symptoms on in rheumatoid arthritis?

occupation, hobbies, lifestyle expectations, family duties

391

What is the management of rheumatoid arthritis?

treat predisposing factors, educate, exercise, weight loss, physio, analgesics, corticosteroids, surgery, topical gels e.g. capsaicin, splints, orthotics, walking stick, MDT, DMARDS

392

How do analgesics treat rheumatoid arthritis?

relieve joint pain but do not slow progression

393

How do corticosteroids treat rheumatoid arthritis?

suppress disease activity, reduce pain and synovitis and effusion and inflammation

394

What is a risk of using corticosteroids in rheumatoid arthritis?

It is a high dose so risk of long term toxicity

395

What kind of surgery is used in rheumatoid arthritis and how can it help?

excision arthroplasty and joint replacement, helps to relieve and improve pain and prevent deformity

396

how does a DMARD treat rheumatoid arthritis?

inhibits inflammatory cytokines to reduce inflammation and slow development of joint erosions, irreversible damage and CV risk

397

What DMARD is mainly used in mild rheumatoid arthritis?

sulfasalazine

398

What are the side effects of sulfasalazine?

mouth ulcers, hepatitis, reversible male infertility

399

Which is better for young women in rheumatoid arthritis, sulfasalazine or methotrexate?

sulfasalazine

400

What DMARD is mainly used in severe rheumatoid arthritis?

methotrexate

401

When is methotrexate contraindicated?

in pregnant or trying to conceive

402

What are the side effects of What DMARD is mainly used in mild rheumatoid arthritis?

mouth ulcers, diarrhoea, liver fibrosis, pulmonary fibrosis, renal impairment

403

How does leflunomide treat rheumatoid arthritis?

blocks T cell proliferation

404

What are the side effects of leflunomide?

diarrhoea, hepatitis, hypertension and alopecia

405

How does infliximab treat rheumatoid arthritis?

It is a TNF a inhibitor to prevent interactions with TNF receptors, rapid onset

406

How often is infliximab given for rheumatoid arthritis?

every 8 weeks

407

How does entanercept treat rheumatoid arthritis?

binds to TNF a so is a TNF a inhibitor to slow/hault erosion

408

What is an advantage of using entanercept as treatment for rheumatoid arthritis?

It is self administered subcutaneously

409

What are the side effects of etanercept?

infusion reactions, infections, demyelinating disease, heart failure, injection site reactions, lupus like syndrome

410

How is rituximab used in the treatment of rheumatoid arthritis?

It is a B cell inhibitor as it causes B cell lysis and mature B cell depletion. Does this by containing IgG-1 constant regions and immune variable regions that recognise CD20 and binds Fc receptors

411

How often and how is rituximab given in rheumatoid arthritis?

Iv 2x a month

412

How abatacept treat rheumatoid arthritis?

blocks T cell activation by selectively targeting the costimulation of T cell upstream without depleting level, inhibits proliferation of T cells in vitro and in vivo, reduces adhesion and migratory capacity of monocytes and inflammatory response of synovial macrophages

413

What are the side effects of abatacept?

nausea, vomiting and headaches

414

How does Tocilizumab treat rheumatoid arthritis?

Il-6 receptor antibody, inhibiting cell to cell communication to prevent further T and B cell production

415

How often is Tocilizumab used to treat rheumatoid arthritis?

Iv once a month

416

What are the side effects of Tocilizumab?

TB, decreased platelets and hypertension

417

How does anakenra treat rheumatoid arthritis?

Il-1 receptor blocker.

418

When should you use the criteria for diagnosis of rheumatoid arthritis?

test if 1 or more joint with definite swelling which is not explained by another disease

419

What are the 4 parts of the criteria for rheumatoid arthritis diagnosis?

joint involvement, serology, acute phase reactants, duration of symptoms

420

What score is needed for diagnosis of rheumatoid arthritis in the criteria?

6 or more