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Phase 2a > MSK > Flashcards

MSK Flashcards

1
Q

What is Raynaud’s phenomenon?

A

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

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2
Q

What precipitates Raynaud’s syndrome?

A

cold

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3
Q

What relieves Raynaud’s syndrome?

A

heat

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4
Q

What are the symptoms of Raynaud’s syndrome?

A

numbness, burning sensation, severe pain when warmed up

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5
Q

Who is mainly affected by Raynaud’s syndrome?

A

young women

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6
Q

What happens in Raynaud’s syndrome?

A

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

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7
Q

DD of Raynaud’s syndrome?

A

autoimmune rheumatic disease, bb therapy, raynauds disease

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8
Q

What is the treatment of Raynaud’s syndrome?

A

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

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9
Q

What are the causes of gout?

A

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

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10
Q

Where do we acquire purines from?

A

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

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11
Q

What are purines broken down into?

A

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

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12
Q

What are the two outcomes for uric acid in humans?

A

be removed by the kidney or into monosodium urate crystals

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13
Q

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

A

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

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14
Q

What can cause a increase of urate?

A

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

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15
Q

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

A

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

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16
Q

What conditions can gout be a marker for?

A

CV disease, hypertension, diabetes, chronic renal failure

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17
Q

How common is gout?

A

prevalence is around 1%

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18
Q

Is gout more common in males or females?

A

Male, rare before adulthood

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19
Q

How many people with hyperuricaemia develop gout?

A

20%

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20
Q

What foods help against gout?

A

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

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21
Q

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

A 
Normal = 200-430umol/L
Saturation = 380umol/L
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22
Q

What is acute gout?

A

inflammatory arthritis caused by hyperuricaemia and intra articular sodium urate crystals

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23
Q

What causes acute gout?

A

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

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24
Q

What symptoms does acute gout cause?

A

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

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25
Q

What is the treatment of acute gout?

A

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

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26
Q

How does chronic trophaceous gout present?

A

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

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27
Q

What investigations can be used for gout?

A

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

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28
Q

What is the long term treatment of gout?

A

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

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29
Q

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??

A

100mg/day, increased by 100mg

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30
Q

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??

A

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

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31
Q

What are side effects of allopurinol?

A

rash, headache, myalgia

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32
Q

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

A

30 eGFR

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33
Q

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

A

LFTs and U and Es, hypersensitivity syndrome

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34
Q

What mediations can be problematic in renal impairment for out?

A

NSAIDs and colchicine

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35
Q

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

A

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

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36
Q

When should Febuxostat be used in gout treatment?

A

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

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37
Q

What is a side effect of Febuxostat?

A

increased LFTs

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38
Q

How do uricosuric drugs work in gout treatment?

A

increase urate excretion by inhibiting renal absorption of urate

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39
Q

What kind of drug is Benzbromarone in gout treatment?

A

a uricosuric drugs

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40
Q

What is the effect of Rasburicase in gout treatment?

A

rapid urate reduction

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41
Q

What is a risk of using Rasburicase in gout treatment?

A

high incidence of drug reactions

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42
Q

How is pegloticase used in gout treatment?

A

It is pegylated uricase

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43
Q

How is Tophi used in gout treatment?

A

It releases local protolytic enzymes causing erosisons of urate crystal

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44
Q

What is pyrophosphate arthropathy?

A

pseudogout from deposition of calcium pyrophosphate crystals on joint

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45
Q

Where on the body is pyrophosphate arthropathy commonly seen?

A

MCPs, wrists, knees, ankles

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46
Q

How does pyrophosphate arthropathy present?

A

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

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47
Q

What is the treatment of pyrophosphate arthropathy?

A

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

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48
Q

How can you prevent future attack of pyrophosphate arthropathy?

A

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

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49
Q

What is pseudogout?

A

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

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50
Q

What is another word for pseudogout?

A

acute calcium pyrophosphate crystal arthritis

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51
Q

What can pesudogout be provoked by?

A

illness , surgery, trauma,

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52
Q

What kind of joints does pseudogout commonly affect?

A

larger joints

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53
Q

Who is most likely to get pseudogout?

A

elderly women

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54
Q

What conditions are associated with pesudogout in the young?

A

haemochromatosis, hyperparathyroidism, Wilson’s disease, acaptomina

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55
Q

What investigations should you do for pseudogout?

A

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

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56
Q

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

A

gout - negatively birefringent

pseudogout - positively birefringent

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57
Q

What is the treatment for pseudogout?

A

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

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58
Q

What is fibromyalgia?

A

chronic widespread pain for >3 months below waist

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59
Q

What is the pain like in fibromyalgia?

A

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

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60
Q

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

A

11/18

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61
Q

What are the symptoms of fibromyalgia?

A

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

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62
Q

Who is mainly affected by fibromyalgia?

A

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

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63
Q

What causes pain amplication syndrome?

A

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

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64
Q

What is the treatment for fibromyalgia?

A

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

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65
Q

how do low dose amitriptyline or dosulpin help in firbromyalgia?

A

increase serotonin level in CNS, and increase descending sensory inhibition

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66
Q

What do investigations show in fibromyalgia?

A

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

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67
Q

What conditions are closely related to fibromyalgia?

A

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

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68
Q

What causes peripheral (nociceptive) pain?

A

stress, genes, cognitive and behavioural adaption

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69
Q

In what kind of pain are behavioural factors important?

A

central (non nociceptive) pain

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70
Q

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

A

There is a central disturbance in pain processing

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71
Q

Examples of peripheral (nociceptive) pain?

A

OA, RA, cancer

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72
Q

Examples of central (non nociceptive) pain?

A

fibromyalgia, IBS, tension migraine

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73
Q

What is the pain mechanism behind nociceptive pain?

A

due to inflammation or damage in periphery

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74
Q

How do analgesic affect central pain?

A

They have no effect

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75
Q

What can increase your pain volume and therefore increase pain?

A

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

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76
Q

What can decrease your pain volume and therefore decrease pain?

A

descending analgesic pathways, GABA, cannabanoids, adenosine

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77
Q

What can aggravate and trigger fibromyalgia pain?

A

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

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78
Q

What kind of pain is experienced in fibromyalgia?

A

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

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79
Q

DD for fibromyalgia?

A

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

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80
Q

What is hypermobility?

A

joints that move easily beyond expected range

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81
Q

Who is hypermobility common in?

A

children, decreases with age

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82
Q

Are there any symptoms to hypermobility?

A

mainly asymptomatic but can cause widespread joint pain

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83
Q

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

A

5 or more /9 joint hypermobile

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84
Q

What does benign joint hypermobility syndrome increase the tendency of?

A

recurrent sprains or dislocation

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85
Q

What is spondyloarthritis?

A

a group of conditions affecting the spine and peripheral joints

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86
Q

What are the common features that all spondyloarthritis conditions share?

A

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

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87
Q

What does seronegative mean?

A

absence of rheumatoid factor

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88
Q

what is ankylosing spondylits?

A

chronic inflammatory disease of spine and sacroiliac joints, unknown aietiology

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89
Q

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

A

0.25-1%, in males aged 16 or 30

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90
Q

What are the clinical features of ankylosing spondylitis?

A

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,

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91
Q

How does ankylosing spondylitis affect movement?

A

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

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92
Q

What causes anterior mechanical chest pain in anylosing spondylitis?

A

costochondritis and fatigue

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93
Q

What conditions are associated with ankylosing spondylitis?

A

osteoporosis, aortic valve incompetence, pulmonary apical fibrosis

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94
Q

What will investigations show in akylosing spondylitis?

A

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

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95
Q

What is the treatment of ankylosing spondylitis?

A

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

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96
Q

how does morning exercise help in akylosing spondylitis?

A

maintains posture and spinal mobility

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97
Q

how do TNF a blockin drugs help in ankylosing spondylitis?

A

improve spinal and peripheral joint inflammation

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98
Q

What factors lead to a poorer prognosis in ankylosing spondylitis?

A

early hip involvement, poor response to NSAIDs, ESR

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99
Q

How many of those with psoriasis develop psoriatic arthritis?

A

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

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100
Q

Where does psoriatic arthritis usually affect?

A

the distal interphalangeal joints

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101
Q

What is arthritis mutilans?

A

destruction of small bones in hands and feet

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102
Q

What symptoms and other conditions are seen in psoriatic arthritis?

A

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

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103
Q

What is the treatment of psoriatic arthritis?

A

analgesics, NSAIDs, anti TNF agents

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104
Q

What is reactive arthritis?

A

sterile arthritis affecting lower limbs

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105
Q

When does reactive arthritis usually occur?

A

1-4 weeks after GI infection or STI

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106
Q

How does an infection cause reactive arthritis?

A

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

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107
Q

Where is reactive arthritis usually seen?

A

knees, ankles, feet

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108
Q

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

A

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

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109
Q

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

A

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

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110
Q

What do investigations show in reactive arthritis?

A

increased ESR, sterile synovial aspirate, increase neutrophils

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111
Q

What other conditions are usually seen in reactive arthritis?

A

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

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112
Q

What is the management of reactive arthritis?

A

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

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113
Q

What is enteropathic arthritis?

A

large joint mono or asymmetrical oligoarthritis

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114
Q

In what disease is enteropathic arthritis usually seen?

A

10-15% of IBD and 5% of IBS

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115
Q

What is the treatment of enteropathic arthritis?

A

DMARDS

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116
Q

In who is septic arthritis usually seen?

A

those over 65 and in prosthetic joint infection

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117
Q

What organisms commonly cause septic arthritis?

A

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

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118
Q

If not treated immediately, what does septic arthritis cause?

A

destroyed joint in U24hrs, long term disability

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119
Q

What is the most common joint affected by septic arthritis?

A

the knee in >50% of cases

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120
Q

What are risk factors for septic arthritis?

A

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

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121
Q

how does septic arthritis present?

A

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

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122
Q

How does infection in septic arthritis present?

A

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

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123
Q

What investigations should be done in septic arthritis?

A

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

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124
Q

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

A

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

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125
Q

What is a sign of septic arthritis in children?

A

They just won’t use the joint

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126
Q

What is the management of septic arthritis?

A

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

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127
Q

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

A

gentamicin

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128
Q

What are the main antibiotics used in septic arthritis?

A

flucolaxacillin IV and oral fusidic acid

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129
Q

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

A

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

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130
Q

What are the exchange arhroplasty principles for septic arthritis?

A

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

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131
Q

What happen in a one stage exchange arthroplastly?

A

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

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132
Q

What happen in a two stage exchange arthroplastly?

A

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

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133
Q

What is osteomyelitis?

A

infection localised to bone

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134
Q

What makes you more susceptible to osteomyelitis?

A

malnutrition, diabetes, PVD, debilitating disease, decreased immunity

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135
Q

What are the main microorganisms in osteomyelitis?

A

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

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136
Q

How does osteomyelitis present?

A

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

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137
Q

What do investigations show in osteomyelitis?

A

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

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138
Q

What is the treatment of osteomyelitis?

A

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

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139
Q

What are some complications of osteomyelitis?

A

sinus and abscess formation, TB osteomyelitis, septic arthritis

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140
Q

What causes osteomyelitis?

A

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

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141
Q

What are the acute changes in osteomyelitis?

A

inflammatory cells, oedema, vascular congestion, small vessel thrombosis

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142
Q

What are the chronic changes in osteomyelitis?

A

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

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143
Q

How does inflammation cause necrosis in osteomyelitis?

A

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

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144
Q

Where does osteomyelitis usually occur?

A

hip, vertebrae, pelvis

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145
Q

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

A

lumbar > thoracic > cervical

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146
Q

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

A

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

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147
Q

Is swelling more likely in osteomyelitis or septic arthritis?

A

septic arthritis

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148
Q

is fever more likely in osteomyelitis or septic arthritis?

A

osteomyelitis

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149
Q

What will investigations show in osteomyelitis?

A

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)

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150
Q

What will blood cultures show in osteomyelitis?

A

positive in 50%, most useful in haematogenous OM

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151
Q

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

A

adults over 50 in vertebra > clavicle/pelvis > long bones

children (85%) in long bones > vertebra

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152
Q

What are risk factors for haematogenous OM?

A

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

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153
Q

DD for osteomyelitis?

A

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

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154
Q

What is the treatment of osteomyelitis?

A

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

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155
Q

How does biopsy differ in TB osteomyelitis?

A

prolonged culture, caeseating granulomatrix, induced sputum

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156
Q

What are the causes of mechanical lower back pain?

A

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

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157
Q

When is pain worse in mechanical lower back pain?

A

evening, absent in the morning, aggravated by exercise

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158
Q

What are risk factors for mechanical lower back pain?

A

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

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159
Q

What do bone scans show in mechanical lower back pain?

A

increased uptake with infection or malignancy

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160
Q

What investigations should you do in lower back pain?

A

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

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161
Q

Red flags in back pain?

A

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

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162
Q

What is the treatment of mechanical lower back pain?

A

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

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163
Q

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

A

prolapsed disc, trauma, fractures, akylosing spondylitis, pregnancy

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164
Q

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

A

degenerative spinal disease, prolapsed disc, malignancy

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165
Q

What does back pain over 50 years suggest of cause?

A

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

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166
Q

What should you do in a back pain examination?

A

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

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167
Q

What is spinal stenosis?

A

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

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168
Q

What is the treatment of spinal stenosis?

A

surgical decompression

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169
Q

What is spondylolisthesis?

A

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

170
Q

When should you treat with antibiotic suppression in infection?

A

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
Q

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

A

2 weeks

172
Q

What is osteoporosis?

A

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
Q

What is the bone density in osteoporosis?

A

less than -2.5 standard deviation

174
Q

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

A

osteopaenia

175
Q

How common is osteoporosis?

A

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

176
Q

Bone mineral density dependent risk factors for osteoporosis?

A

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

177
Q

Bone mineral density independent risk factors for osteoporosis?

A

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

178
Q

When do you achieve your peak bone mass?

A

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

179
Q

What are potential consequences of a hip fracture?

A

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

180
Q

When is age related bone loss accelerated in women?

A

Starting at menopause

181
Q

What happens in women post menopause in the bones?

A

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

182
Q

how can bone turnover be reduced in women?

A

oestrogen replacement therapy

183
Q

What are the clinical features of osteoporosis?

A

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

184
Q

What does a DEXA scan detect in osteoporosis?

A

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
Q

What investigations are done is osteoporosis?

A

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
Q

Indications for a DEXA scan?

A

radiographic osteopenia, previous fragility fracture

187
Q

What kind of changes occur in trabecular architecture with aging?

A

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

188
Q

How does inflammatory disease cause osteoporosis?

A

inflammatory cytokines increase bone resorption

189
Q

How does endocrine disease cause osteoporosis?

A

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

190
Q

How does reduced skeletal loading affect osteoporosis?

A

It increases resorption

191
Q

What types of drugs can cause osteoporosis?

A

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

192
Q

What is the treatment of osteoporosis?

A

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
Q

How do bisphosphonates treat osteoporosis?

A

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

194
Q

What are the side effects of bisphosphonates?

A

oesophagitis, osteonecrosis

195
Q

What are the advantages of bisphosphonates?

A

cheap, effective

196
Q

How does strontium renelate treat osteoporosis?

A

reduces bone absorption but maintains bone formation

197
Q

What are the advantages of strontium renelate?

A

alternative to bisphosphonates, good in elderly with poor compiance

198
Q

What are the side effects of strontium renelate?

A

nausea, diarrhoea, headaches, thromboembolism

199
Q

How does Raloxifene treat osteoporosis?

A

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
Q

What are the side effects of Raloxifene?

A

leg cramps, flushing, thromboembolism

201
Q

How does Teriparatide treat osteoporosis?

A

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
Q

How does recombinant human parathyroid peptide and hormone treat osteoporosis?

A

Stimulates bone formation with a daily injection

203
Q

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

A

hypercalcaemia

204
Q

How does hormone replacement therapy treat osteoporosis?

A

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

205
Q

What are the side effects of hormone replacement therapy?

A

breast cancer, increased CV risk, vaginal bleeds, stroke

206
Q

How does Denosumab treat osteoporosis?

A

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

207
Q

What is a side effect of Denosumab?

A

affects the immune system and can cause eczema

208
Q

How do you treat glucocorticoid induced osteoporosis?

A

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

209
Q

What is osteonecrosis?

A

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

210
Q

What can cause osteonecrosis?

A

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

211
Q

Where does osteonecrosis mainly affect?

A

femoral neck

212
Q

What is large vessel vasculitis?

A

inflammatory disorder of blood vessel walls causing destruction or stenosis

213
Q

What are the 3 types of large vessel vasculitis?

A

Giant cell arthritis, polymyalgia rheumatic, takayasis arteritis

214
Q

How does polymyalgia rheumatic present?

A

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

215
Q

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

A

over 50s, women twice as likely

216
Q

When is pain in polymyalgia rheumatic worst?

A

in the morning

217
Q

What symptoms can accompany polymyalgia rheumatic ?

A

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

218
Q

What do investigations show in polymyalgia rheumatic ?

A

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

219
Q

What is giant cell arthritis?

A

inflammatory granulomatous arteritis of large cerebral arteries with PMR

220
Q

How does giant cell arthritis present?

A

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
Q

What do investigations show in giant cell arthritis?

A

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

222
Q

What does histology show in giant cell arthritis?

A

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
Q

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

A

10-30%

224
Q

What is the treatment of PMR and GCA?

A

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
Q

What is Takayasus arteritis?

A

granulomatous inflammation of aortic arch and major branches

226
Q

Where does Takayasus arteritis mainly occur?

A

in japan

227
Q

What does Takayasus arteritis cause?

A

hypertension, absent peripheral pulses, strokes, cardiac failure

228
Q

What is the treatment of Takayasus arteritis?

A

corticosteroids

229
Q

What is the main type of medium sized vessel vasculitis?

A

Polyarteritis nodosa (PAN)

230
Q

In who is Polyarteritis nodosa (PAN) mainly seen?

A

rare, in middle aged men with severe systemic manifestations

231
Q

What disease is Polyarteritis nodosa (PAN) associated with?

A

hepatitis B anigenaemia

232
Q

What is Polyarteritis nodosa (PAN)?

A

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

233
Q

What will tests show in Polyarteritis nodosa (PAN)?

A

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

234
Q

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

A

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

235
Q

What is the treatment of Polyarteritis nodosa (PAN)?

A

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

236
Q

What are the main 3 ANCA positive small vessel vasculitis?

A

Wegeners granulomatosis, Churd Strauss granulomatosis, microscopic polyangitis

237
Q

What are the main 3 ANCA negative small vessel vasculitis?

A

Henoch-Schonlein purpura, cryoglobulinaemic vasculitis, ctaenous leucocytoclastic

238
Q

Wjat is the triad of symptoms in Churg Strauss syndrome?

A

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

239
Q

What is the treat of Churg Strauss syndrome?

A

corticosteroids, and immunosuppressive drugs

240
Q

How does Henoch Schonelein purpura present?

A

purpuric rash on legs and buttocks

241
Q

in who is Henoch Schonelein purpura mainly seen?

A

children

242
Q

What symptoms can accompany Henoch Schonelein purpura?

A

abdominal pain, arthritis, haematuria and nephritis

243
Q

What is the cause of Henoch Schonelein purpura

A

IgA dominant immune complexes

244
Q

When does Henoch Schonelein purpura normally occur?

A

Post acute upper respiratory tract infection

245
Q

What is the treatment of Henoch Schonelein purpura?

A

recovery is spontaneous

246
Q

What is cryoglobulinaemia vasculitis?

A

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

247
Q

What are the 3 types of cryoglobulinaemia vasculitis?

A

essential cryoglobulinaemia, associated with infection or autoimmune

248
Q

What is Behcet’s disease?

A

recurrent oral ulceration

249
Q

What is the treatment of Behcet’s disease?

A

immunosuppressive therapy or thalidomide

250
Q

What is the treatment of small vessel vasculitis?

A

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

251
Q

What are the two types of anti neutrophillic cytoplasmic antibodies?

A

pANCA and cANCA

252
Q

What does histology of vasculitis show?

A

vessel wall infiltration, fibrinoid necrosis

253
Q

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

A

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

254
Q

How does anterior ischaemic optic neuropathy present?

A

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

255
Q

What is the treatment of anterior ischaemic optic neuropathy present?

A

corticosteroids, prednisolone, steroid sparing agents, prophylaxis of osteoporosis

256
Q

How does granulomatosis with polyangitis present?

A

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

257
Q

What is antiphospholipid syndrome?

A

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
Q

How many cases of SLE have antiphospholipid syndrome?

A

20-30%

259
Q

What are the causes of antiphospholipid syndrome?

A

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

260
Q

What are the 3 tests that can detect antiphospholipid syndrome?

A

anticardiolipin test, lupus anticoagulant test, anti B2 glycoprotein test

261
Q

How many tests need to be positive for antiphospholipid syndrome?

A

2 on separate occasions, 12 weeks apart

262
Q

What is the management of antiphospholipid syndrome?

A

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

263
Q

What is systemic sclerosis also called?

A

scleroderma

264
Q

What is systemic sclerosis?

A

multisystem disease with involvement of skin and Raynaud’s phenomenom

265
Q

In who is systemic sclerosis mainly seen?

A

women aged 30-50

266
Q

What are risk factors for systemic sclerosis?

A

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

267
Q

What is the pathophysiology behind systemic sclerosis?

A

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
Q

How is fibrosis caused in systemic sclerosis?

A

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
Q

What are the clinical features of limited cutaneous scleroderma?

A

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
Q

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

A

hands, feet, face, forearms

271
Q

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

A

70% - lcssc

30% - dcssc

272
Q

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

A

face, trunk, proximal extremities

273
Q

What are the clinical features of diffuse cutaneous scleroderma?

A

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
Q

How will investigations differ between DcSSc and LcSSc?

A

D -antitopoisomerase 1 and anti RNA polymerase

L - anticentromere

275
Q

What will investigations show in all systemic sclerosis?

A

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
Q

What is the management of systemic sclerosis?

A

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
Q

What is the prognosis for LcSSc and DcSSc?

A

L - 70% 10 yr survival

D - 35% 10 yr survival

278
Q

What are the major causes of death from systemic sclerosis?

A

pulmonary fibrosis and pulmonary hypertension

279
Q

What does CREST stand for in systemic sclerosis?

A

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

280
Q

What is sjogran’s syndrome?

A

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

281
Q

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

A

lacrimal and salivary

282
Q

Who si mostly affected in sjogran’s syndrome?

A

women ages 40-50

283
Q

What are the causes of sjogran’s syndrome?

A

primary or RA, SLE, systemic sclerosis

284
Q

What is the prognosis of sjogran’s syndrome?

A

5% mortality

285
Q

What are the 3 types of salivary gland?

A

sublingual, submandibular and parotid

286
Q

What is a major complication of sjogran’s syndrome?

A

non hodgkins lymphoma

287
Q

What are the main symptoms of sjogran’s syndrome?

A

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

288
Q

What is the treatment of sjogran’s syndrome?

A

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

289
Q

DD of dry eyes?

A 
steven Johnson syndrome
pemphigoid
chronic conjunctivitis
chronic belpharitis
trauama
vit A deficiency
290
Q

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

A

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

291
Q

What is the treatment of dry eyes?

A

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

292
Q

DD of dry mouth?

A

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

293
Q

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

A

salivary flow is

294
Q

What investigations are needed in sjogran’s syndrome?

A

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

295
Q

What does a biopsy show in sjogran’s syndrome?

A

lymphocyte infiltration and destruction of acinar tissue

296
Q

What is polymyositis?

A

Inflammation and necrosis of skeletal muscle fibres?

297
Q

What is dermatomyositis?

A

polymyositis with skin involvement

298
Q

Who does polymoyositis and dermatomyositis most commonly affect?

A

women

299
Q

What are the clinical features of polymoyositis?

A

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

300
Q

What clinical features occur is dermatomyositis in addition to polymyositis?

A

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

301
Q

What can muscle weakness in polymoyositis and dermatomyositis lead to?

A

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

302
Q

What will biopsy of polymoyositis and dermatomyositis show?

A

inflammatory cell infiltration, necrosis of muscle cells

303
Q

What will investigations show in polymoyositis and dermatomyositis ?

A

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
Q

What is the treatment for polymoyositis and dermatomyositis ?

A

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

305
Q

What is systemic lupus erythromatosis?

A

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

306
Q

In who is systemic lupus erythromatosis most commonly seen?

A

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

307
Q

What are the risk factors for systemic lupus erythromatosis?

A

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
Q

What is the pathophysiology behind systemic lupus erythromatosis?

A

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
Q

What can complications of systemic lupus erythromatosis lead to?

A

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

310
Q

What are the clinical features of systemic lupus erythromatosis?

A

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
Q

What is used as a diagnostic in systemic lupus erythromatosis?

A

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

312
Q

What do investigations show in systemic lupus erythromatosis?

A

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
Q

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

A

(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
Q

What is the management for systemic lupus erythromatosis?

A

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
Q

What is the prognosis for systemic lupus erythromatosis?

A

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

316
Q

What is Ehler Danlos syndrome?

A

hypermobile joints

317
Q

What is Marfans syndrome?

A

tall, long, arms fingers and toes, faulty collagen

318
Q

What is osteoarthritis?

A

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

319
Q

What are the causes of osteoarthritis?

A

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
Q

What is the pathology behind osteoarthritis?

A

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
Q

DD for osteoarthritis?

A

RA, gout, osteonecrosis, neuropathic joint

322
Q

Complications of osteoarthritis?

A

gout risk and chondro calcinosis

323
Q

What are the symptoms of osteoarthritis?

A

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
Q

What joints does osteoarthritis mainly affect?

A

DIP joints, thumb, carpometacarpal joint, knees

325
Q

What do the radiographs for osteoarthritis show? (loss)

A

Loss of joint spaces
osteophytes
subchondral cysts
subarticular sclerosis

326
Q

What do investigations for osteoarthritis show?

A

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

327
Q

What is the most common joint disease?

A

osteoarthritis

328
Q

Who is most likely to get osteoarthritis?

A

100% are >65

329
Q

What aggravates and relieves osteoarthritis?

A

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

330
Q

What does crepitus mean?

A

grating of joint due to disruption of smooth articulating surfaces

331
Q

What does osteoarthritis management depend on?

A

age, functional needs, stage of disorder, joint involved

332
Q

What is the treatment of osteoarthritis?

A

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
Q

Where are Bouchards nodes found in osteoarthritis?

A

proximal inter phalangeal joints

334
Q

Where are Heberdens nodes found in osteoarthritis?

A

distal inter phalangeal joints

335
Q

What questions should you ask about joint pain?

A

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

336
Q

What can cause foot deformity?

A

poor shoeswear, congenital, trauma, previous surgery,

337
Q

What should be done in a foot and ankle examination?

A

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

338
Q

What is the classification called joint fractures?

A

Salter Harris Classification 1-5

339
Q

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

A

2 -

340
Q

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

A

4

341
Q

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

A

3

342
Q

What is a fracture?

A

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

343
Q

What bones are commonly broken in neonates?

A

humerus and clavicle

344
Q

What bones are commonly broken in infants?

A

radius

345
Q

What bones are commonly broken in toddlers

A

tibia

346
Q

What bones are commonly broken in children?

A

fibula, radius and femur

347
Q

What bones are commonly broken in adolescents?

A

tibia

348
Q

What investigations are need in a fracture?

A

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

349
Q

What is pethase disease?

A

In young boys, affecting the subchondral

350
Q

What is an elastic intramedullary nailing?

A

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

351
Q

What are the four stages of bone formation?

A

haematoma formation, callus formation, callus ossification, bone remodelling

352
Q

What is the main cause of arthritis in the young?

A

trauma

353
Q

How does arthritis present in children?

A

joint swelling, stiffness and limitation of use

354
Q

What are the 7 types of juvenile arthritis?

A

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

355
Q

How many joints are involved in an oligoarthritis?

A

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

356
Q

What is a major complication of oligoarthritis?

A

uveitis

357
Q

Treatment of oligoarthritis?

A

grow out of it

358
Q

What do investigations show in oligoarthritis?

A

ANA +

359
Q

How old are people with oligoarthritis?

A
360
Q

How many joints does extended oligoarthritis affect?

A

1-4 in first 6 months, then more after

361
Q

Who is most likely to get extended oligoarthritis?

A

girls aged 2-4

362
Q

How many with extended oligoarthritis carry it on into adulthood?

A

50%

363
Q

What should you always screen for in extended oligoarthritis?

A

uveitis

364
Q

How many joints are involved in juvenile polyarticular arthritis?

A

5 or more, usually symmetrical

365
Q

What other symptoms could be seen in polyarticular arthritis?

A

malaise, fever, anaemia, uveitis

366
Q

Which juvenile arthritis is most similar to adult RA?

A

RhF+

367
Q

What is a difference between adult and juvenile RA?

A

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

368
Q

In who is enthesitis JIA normally seen in?

A

young males of >6 years

369
Q

How does enthersitis JIA present?

A

HLAB27+, inflammatory back or sacroiliac pain

370
Q

What is psoriatic type JIA?

A

JIA in children with or with a FH of psoriasis

371
Q

At what age will you normally acquite systemic onset JIA?

A

4-6 years

372
Q

How do you present with systemic onset JIA?

A

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

373
Q

What is the treatment of JIA?

A

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
Q

What complications can occur it JIA is untreated

A

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

375
Q

What investigations should be done in JIA?

A

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

376
Q

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

A

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

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

377
Q

What is rheumatoid arthritis?

A

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

378
Q

What complications can rheumatoid arthritis cause?

A

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

379
Q

Who are most likely to get rheumatoid arthritis?

A

women more than men, until after menopause

380
Q

What are makers for rheumatoid arthritis?

A

HLA DR4 and HLA DR1

381
Q

What are risk factors for rheumatoid arthritis?

A

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

382
Q

What is the function of rheumatoid factor in rheumatoid arthritis?

A

chronically maintains synovial inflammation caused by activated inflammatory cells

383
Q

What the is pathogenesis behind rheumatoid arthritis?

A

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
Q

What is the purpose of angiogenic cytokines in rheumatoid arthritis?

A

produce new synovial blood vessels

385
Q

What is the purpose of endothelial cells in rheumatoid arthritis?

A

produce adhesion molecules to cause extravasation of leucocytes into synovium

386
Q

What are the symptoms of rheumatoid arthritis?

A 
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
Q

What would investigations show in rheumatoid arthritis?

A

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

388
Q

How is CCP produced in rheumatoid arthritis?

A

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
Q

What does the radiology show on rheumatoid arthritis?

A

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

390
Q

What must you assess symptoms on in rheumatoid arthritis?

A

occupation, hobbies, lifestyle expectations, family duties

391
Q

What is the management of rheumatoid arthritis?

A

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

392
Q

How do analgesics treat rheumatoid arthritis?

A

relieve joint pain but do not slow progression

393
Q

How do corticosteroids treat rheumatoid arthritis?

A

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

394
Q

What is a risk of using corticosteroids in rheumatoid arthritis?

A

It is a high dose so risk of long term toxicity

395
Q

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

A

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

396
Q

how does a DMARD treat rheumatoid arthritis?

A

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

397
Q

What DMARD is mainly used in mild rheumatoid arthritis?

A

sulfasalazine

398
Q

What are the side effects of sulfasalazine?

A

mouth ulcers, hepatitis, reversible male infertility

399
Q

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

A

sulfasalazine

400
Q

What DMARD is mainly used in severe rheumatoid arthritis?

A

methotrexate

401
Q

When is methotrexate contraindicated?

A

in pregnant or trying to conceive

402
Q

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

A

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

403
Q

How does leflunomide treat rheumatoid arthritis?

A

blocks T cell proliferation

404
Q

What are the side effects of leflunomide?

A

diarrhoea, hepatitis, hypertension and alopecia

405
Q

How does infliximab treat rheumatoid arthritis?

A

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

406
Q

How often is infliximab given for rheumatoid arthritis?

A

every 8 weeks

407
Q

How does entanercept treat rheumatoid arthritis?

A

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

408
Q

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

A

It is self administered subcutaneously

409
Q

What are the side effects of etanercept?

A

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

410
Q

How is rituximab used in the treatment of rheumatoid arthritis?

A

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
Q

How often and how is rituximab given in rheumatoid arthritis?

A

Iv 2x a month

412
Q

How abatacept treat rheumatoid arthritis?

A

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
Q

What are the side effects of abatacept?

A

nausea, vomiting and headaches

414
Q

How does Tocilizumab treat rheumatoid arthritis?

A

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

415
Q

How often is Tocilizumab used to treat rheumatoid arthritis?

A

Iv once a month

416
Q

What are the side effects of Tocilizumab?

A

TB, decreased platelets and hypertension

417
Q

How does anakenra treat rheumatoid arthritis?

A

Il-1 receptor blocker.

418
Q

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

A

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

419
Q

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

A

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

420
Q

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

A

6 or more

Phase 2a (15 decks)

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