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disease profiles MSK Flashcards

1
Q

what is osteoporosis

A

reduced bone mineral density and increased porosity

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2
Q

what comes as a result of osteoporosis

A

increased fragility and fracture risk

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3
Q

normal quality of bone just not enough of it

A

osteoporosis

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4
Q

risk factors of osteoporosis

A

smoking, poor diet, female, inactivity, increased alcohol intake and lack of sunlight exposure

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5
Q

what is the intermediate stage of osteoporosis

A

osteopenia

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6
Q

what is type 1 osteoporosis

A

post menopausal

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7
Q

what is type 2 osteoporosis

A

osteoporosis of old age

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8
Q

what type of fractures dominate osteoporosis type 2

A

neck and vertebral fractures

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9
Q

how to diagnose osteoporosis

A

DEXA scanning

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10
Q

how to treat (slow process) of osteoporosis

A

calcium and vit D supplements

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11
Q

abnormal softening of bone due to deficient minerilisation of osteoid secondary to inadequate amounts of calcium and phosphorus

A

osteomalacia

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12
Q

what is an osteoid

A

immature bone

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13
Q

what is osteomalacia in children known as

A

rickets

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14
Q

what are the causes of osteomalacia and rickets

A

insufficinet calcium and phosphate deficiency

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15
Q

how can there by a lack of calcium

A

lack of absorption in intestine or resistance to action of vit D

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16
Q

how does phosphate deficiency happen

A

increased renal losses

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17
Q

what is the presentation of osteomalacia and rickets

A

pain, deformities from soft bone, pathological fractures, symptoms of hypocalcaemia

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18
Q

how to treat osteomalacia and rickets

A

vit D therapy with calcium and phosphate supplementation

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19
Q

what is hyperparathyroidism

A

over activity of parathyroid glands with high levels of PTH

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20
Q

what is primary hyperparathyroidism due to

A

benign adenoma, hyperplasia or rarely a malignant neoplasia

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21
Q

labs of someone with primary hyperparathyroidism

A

raised serum PTH, raised Ca, phosphate low or normla

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22
Q

what is secondary hyperparathyroidism due to

A

physiologial overproduction of PTH secondary to hypocalceamia

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23
Q

what is secondary hyperparathyroidism caused by

A

vit D deficincy or chronic kidney disease

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24
Q

what is tertiary hyperparathyroidism due to

A

people with chronic secondary who develop adenoma which continues to produce PTH despite biochemical correction

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25
Q

what is renal dystrophy

A

reduced phosphate excretion and inactive activation of Vitamin D

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26
Q

what does renal dystrophy lead to

A

secondary hyperparathyroidism with subsequent osteomalacia, sclerosis of bone and calcification of soft tissues

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27
Q

what is pagets disease

A

a chronic disorder resulting in thickened britter and misshapen bones

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28
Q

labs of pagets disease

A

serum alk phos is raised whilsy calcium and phsphorus are usually normal

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29
Q

how to treat pagets disease

A

with biphosphonates or calitonin

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30
Q

what is rheumatoid arthritis

A

symmetrical inflammatory polyarthtritis affecting mainly the peripheral joints which if untreated can potentially lead to joint damage and irreversible deformities and increased morbidity and mortality

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31
Q

prevalence of RA in men and women

A

3x more common in women

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32
Q

prevalence of RA in the UK

A

1%

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33
Q

what is RA mediated by

A

HLA -DR4

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34
Q

cause of RA

A

unknown

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35
Q

trigger of RA

A

infections, stress, cigarette smoking

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36
Q

severity of RA depends on

A

genetic factors, presence of auto antibodies

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37
Q

what is the main structure involved in RA

A

synovium

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38
Q

what does the synovium line

A

the inside of the synovial joint capsules and tendon sheaths

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39
Q

what joints in the spine are synovial fluid lined

A

C1/C2

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40
Q

what joints are usually affected by RA

A

hand joints, wrists, elbows, shoulders, TMJs, knees, hips, ankles, feet

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41
Q

difference between osteoarthritis and RA

A

osteoarthritis is when bone ends rub together and RA is when a swollen inflamed synovial membrane causes bone erosion

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42
Q

inflamed synovial is called

A

pannus

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43
Q

what happens when panes is in contact with bone

A

osteoclast is activated causing bone erosion

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44
Q

what is released from macrophage in RA

A

TNFa, IL1 and IL6

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45
Q

what is released from B cells in RA

A

RF and IL 6

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46
Q

what do the activation of pro inflammatory cytokines lead to in RA

A
  • activation of synoviocytes to cause the hypertrophic synovium / pannus
  • activation of osteoclasts
  • inhibition of chondrocytes
  • stimulation of angiogenesis
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47
Q

what drugs inhibit TNFa

A

infliximab, etanercept, adalimumab, certolizumab, golimumab

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48
Q

what drugs inhibit iL1-

A

anakinra

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49
Q

what drugs inhibit the IL6 receptor

A

tocilizumab

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50
Q

presentation of RA

A

pain and swelling in symmetrical fashion affecting peripheral synovial joints, typically small joints of hands and feet, prolonged morning stiffness, monoarthritis (rare), tenosynovitis, trigger finger, carpal tunnel, palindromic, systemic symptoms, poor grip strength

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51
Q

what test can be used of the detection of synovitis in RA

A

squeeze test

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52
Q

what is tenosynovitis

A

inflammation of the tendon sheath

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53
Q

what is trigger finger

A

fingers lock

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54
Q

palindromic

A

episodic RA

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55
Q

lung manifestations of RA

A

Plueral effusion, rheumatoid nodules

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56
Q

heart manifestations of RA

A

pericarditis, pericardial effusions

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57
Q

neurological manifestations of RA

A

peripheral neuropathy, carpal tunnel syndrome

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58
Q

leg ulcers associated with RA

A

arterial

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59
Q

diagnosis of RA

A

mainly clinical, peripheral symmetrical polyarthtritis affecting hands and feet, raised inflammatory markers, antibody testing not always positive, imaging

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60
Q

autoantibodies in RA

A

rheumatoid factor (rheumatoid IgM), antiCCP antibodies

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61
Q

what autoantibody in RA is more specific

A

Anti CCP

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62
Q

what autoantibody has low sensitivity in RA

A

anti CCP

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63
Q

score for disease activity in RA

A

DAS 28

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64
Q

management of RA

A

early diagnosis, disease modifying anti rheumatic drugs, NSAIDs and steroids, education

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65
Q

what is early RA defined as

A

less than 2 years since symptom onset

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66
Q

therapeutic window of opportunity in RA

A

first 3 months

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67
Q

first line for RA

A

education, rest, exercise, social services, salicylates, NSAIDs

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68
Q

second line for RA

A

gold salts, hydroxychloroquine

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69
Q

third line for RA

A

MTX, penicillin amine, AZA

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70
Q

last line for RA

A

cytotoxic agents and experimental drugs

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71
Q

examples of DMARD

A

methotrexate, sufasalazine, hydrochloroquine, leflunomide, steroids

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72
Q

what can methotrexate cause in the lungs

A

pneumonitis

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73
Q

who to avoid methotrexate with

A

people with lung disease

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74
Q

less than 2.6 DAS28 scoring

A

remission

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75
Q

2.6-3.2 DAS28 scoring

A

low disease activity

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76
Q

3.2-5.1 DAS28 scoring

A

moderate disease activity

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77
Q

more than 5.1 DAS28 scoring

A

active disease

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78
Q

what DAS28 score qualifies for biologic therapy

A

3.2 inspite of 2 DMARDs

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79
Q

what is osteoarthritis

A

a chronic disease characterised by cartilage loss and accompanying periarticular damage

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80
Q

what are the most affected joints in osteoarthritis

A

knees, hands and hips

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81
Q

what is the pathophysiology of OA

A

metabolically active dynamic process that involves all joint tissues

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82
Q

what are the key pathological changes in OA

A

localised loss of hyaline cartilage and remodelling of adjacent bone with new bone formation at joint margins

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83
Q

what indicates a repair process of synovial joints

A

combination of tissue loss and new tissue synthesis

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84
Q

risk factors of OA

A

genetic, ageing, female, obesity, biomechanics

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85
Q

features of a OA joint

A

subchondral bone cyst, thickened joint capsule, episodic synovitis, fibrillated cartilage, osteophyte, degenerative cartilage loss, subchondral bone sclerosis

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86
Q

localised OA

A

can effect hips, knees, finger interphalangeal joints, facet joins of lower cervical and lower lumbar spines

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87
Q

generalised OA

A

defined as OA at either the spinal or hand joints and in atleast 2 other joint regions

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88
Q

what does the presence of multiple heberdens nodes indicate

A

a subset of OA involving DIP joints, thumb bases, first MTP joints, lower lumbar and cervical facet joints, knees and hips

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89
Q

joints most affected by OA

A

neck, lower back, hips, base of thumb, finger joints, knee, base of toe

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90
Q

examination features of OA

A

joint line tenderness, crepitus, joint effusion, bony swelling, deformity, limitation of motion

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91
Q

where is heberdens node found

A

top of fingers

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92
Q

where is bouchards node found

A

bottom of fingers

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93
Q

presentation of knee OA

A

osteophytes, effusions, crepitus, restriction in movement, genuflects varies and valgus deformities, bakers cysts

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94
Q

distribution of hip OA

A

pain felt radiating to knee or groin, pain in hip can be radiating from lower back, hip movement restricted

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95
Q

distribution of spine OA

A

cervical - pain and restriction of movement , occipital headaches, osteophytes may impinge on nerve roots
lumbar - osteophytes can cause spinal stenosis if they encroach on the spinal canal q

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96
Q

diagnosis of spinal OA

A

clinical, imaging

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97
Q

what would u see on a OA x ray

A

marginal osteophytes, joint space narrowing, subchondral sclerosis, subchondral cysts

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98
Q

management of OA

A

education, lifestyle, physiotherapy, occupation therapy, analgesia, local intra articular steroid infections

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99
Q

surgical management of OA

A

joint replacements arthroscopic surgery to remove loose bodies

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100
Q

what are crystal arthropathies

A

a diverse group of disorders characterised by the deposition of various minerals in joints and soft tissues leading to inflammation

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101
Q

types of crystal arthropathies

A

gout monosodium urate crystals, pseudogount calcium pyrophosphate crystal deposition, hydroxyapatite - basic calcium phosphate deposition

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102
Q

define gout

A

a potentially disabling and erosive inflammatory arthritis caused by deposition of monosodium urate crystals into joints and soft tissues

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103
Q

prevalence of gout

A

2.49%

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104
Q

prevalence of gout in men vs women

A

more common in men

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105
Q

causes of hyperuricaemia

A

increased urate production and reduced urate excretion

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106
Q

what causes increase urate production

A

inherited enzyme defects, myeloproliferative / lymphoproliferative disorders, psoriasis, alcohol, high dietary purine intake

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107
Q

what causes reduced urate excretion

A

chronic renal impairment, volume depletion, hypothyroidism, diuretics, cytotoxic

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108
Q

how long does acute gout usually last

A

3 days with treatment, 10 days without

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109
Q

what is chronic tophaceous gout associated with

A

diuretics

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110
Q

investigations of gout

A

serum uric acid is raised, raised inflammatory markers, polarised microscopy synovial fluid, renal impairment, x rays

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111
Q

treatment of acute gout

A

NSAIDs, cohcicine, steroids, lifestyle modification

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112
Q

preventative measures for gout

A

Xanthine oxidase inhibitors - allopurinolm febuxostat, uricosuirc drugs - sulfinpyrzone, prodenecid, benzbromarone,

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113
Q

when should you start preventive treatment for gout

A

1 week after acute attack

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114
Q

WHO target for serum uric acid

A

300-360 mol/L

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115
Q

indications for prophylactic treatment of gout

A

one or more attacks of gout in a year inspite of lifestyle modifications, presence of gouty tophi or signs of gouty arthritis, uric acid calculi, chronic renal impairment, heart failure where unable to stop diuretics, chemo therapy patients who develop gout

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116
Q

who is pseudo gout most common in

A

elderly

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117
Q

what is pseudo gout also known as

A

calcium pyrophosphate deposition disease

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118
Q

treatment of pseudo gout

A

NSAIDS, cochincine, steroids rehydration

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119
Q

what is hydroxyapatite

A

crystal deposition in or around the joint

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120
Q

treatment of hyrocyapaitie

A

NSAIDs, intra articular steroid injection, physiotherapy, partial or total arthroplasty

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121
Q

what does hydroxyapatite lead to the release of

A

collagenases, serine proteinases and IL-1

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122
Q

what is soft tissue rheumatism

A

pain that is caused by inflammation/damage to ligaments, tendons, muscles or nerve near a joint rather than bone or cartilage

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123
Q

generalised soft tissue pain

A

fibromyalgia

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124
Q

what is the most common area for soft tissue pain

A

shoulder

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125
Q

investigation of soft tissue rheumatism

A

clinical history and examination, Xray, US, MRI, identify precipitating factors

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126
Q

treatment of soft tissue rheumatism

A

pain control, rest and ice compression, PT, steroid injections surgery

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127
Q

prevalence of joint hyper mobility syndrome in men and women

A

women more than men

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128
Q

genetic syndromes leading to joint hypermobility syndrome

A

marfans, Ehlers danlos syndrome

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129
Q

when does joint hyper mobility syndrome tend to present

A

childhood or 3rd decade

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130
Q

signs and symptoms of jointer hypermobility syndrome

A

joint pains, joint stiffness, foot and ankle pain, neck and backaches frequent sprains and dislocations, thin stretchy skin

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131
Q

what scoring system is used for hypermobility syndrome

A

beighton score

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132
Q

what score on the Brighton score constitutes a diagnosis

A

> 4/9

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133
Q

treatment of joint hypermobility syndrome

A

patient education, physiotherapy, analgesiA

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134
Q

what are connective tissue diseases

A

conditions associated with spontaenous overactivity of the immune system

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135
Q

what is present in connective tissue disease

A

auto antibodies

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136
Q

types of CTD

A

SLE, sjogrens syndrome, systemic scleoriss, dermatomyositis, polymyositis, anti phospholipid syndrome

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137
Q

what is SLE

A

an auto immune condition that can affect most organ systems

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138
Q

pathophysiology of SLE

A

immune system attcks cells causing inflammation and tissue damage

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139
Q

ratio of female to male prevelance of SLE

A

9:1

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140
Q

when does SLE present

A

at child bearing women

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141
Q

pathogenesis of SLE

A

defective apoptosis leading to cell contents float about for longer than normal allowing the immune system to start to develop a reaction against them so the cell contents are seen as antigens (autoantigens), immune cells trigger a response which means over time there are antbodies against these antigens which then start to recognise antigens within normal cells and attack them this causes immune complexes to form and they get deposited in skin, blood vessel walls of kidneys and that deposition activates the complement cascade causing focused inflammation in certain areas causing necrosis and fibrosis causing organ damage

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142
Q

SLE score

A

EULAR/ACR

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143
Q

what must be positive in SLE

A

ANA

144
Q

what score constitutes SLE

A

10

145
Q

skin manidestatins of SLE

A

discoid lupus, cutaneous lupus, alopecia, oral ulceration, buttterly facial rash

146
Q

types of arthritis in SLE

A

synovitis, jaccouds arthropathy

147
Q

x ray of jaccouds athropathy

A

normal

148
Q

neorological manifestations of SLE

A

delirium, psychosis, seizure, headache, cranial nerve disorders

149
Q

serositis in SLE

A

pleurisy, pericarditis, pericardial effusions

150
Q

heamotological manifestations of SLE

A

leukpenia, thrombocytopenia, haemolytic anaemia, lymphadenopathy

151
Q

renal manifestatiosn of SLE

A

proteinuria, biopsy proven nephritus, red cell casts

152
Q

what is specific in SLE

A

dsDNA

153
Q

what is highly specific for lupus

A

anti Sm

154
Q

management of lupus (mild)

A

sun protection, vaccinations, lifestyle, HCQ, short courses of steroids, MTX/AZA

155
Q

treatment for patients with anti phosphilipd syndrome

A

antiplatelets and anti coagulants

156
Q

management of moderate lupus

A

HCQ,MTX/AZA, GC.PO/IV

157
Q

treatment of severe lupus

A

cyclic phosphilide

158
Q

how to monotor lupus

A

SLEDAI score

159
Q

symptoms of sjogrens

A

drye eyes, gritty feeling, dry mouth, dry throat, vagina dryness, bilateral parotid gland enlargement, joint pains, fatigue,, unexplained increase in dental caries

160
Q

immunology of sjogrens

A

anti Ro, anti La

161
Q

what does sjogrens put people at risk of

A

lymphoma

162
Q

what is systemic scleorisis

A

a multisystem autoimmune disease characterised by vasculopathy, autoimmunity and fibrosis

163
Q

sympyoms of systemic scleorisis

A

raynauds, skin thickenng, difficulty swallowing, GORD, telangiectasia, calcinosis, +/- SOB, digital ulcers or ischeamia, skin tightness/loss of dexterity of hands

164
Q

diffuse cutaneous systemic sclerosis

A

skin involvement above and below elbows and knees

165
Q

limited systemic sclerosis

A

skin involvement on extermities below the elbows and knees - sparing the torsu

166
Q

key antibodies in systemic sclerosis

A

anti centromere - limited , anti STL70 - diffuse, anti RNA polymerase 3

167
Q

facial changes in systemic sclerosis

A

small mouth with puckering, beaked nose, tigh skin - no wrinkles and telangiasia

168
Q

GI complications of systemic sclorisis

A

dysphagia, GORD, GAVE, small intestinal bacterial overgrowth, malabsorption, fluctuating bowel habiy, faecal incontinance

169
Q

cardio plmonary complications of systemic sclerosis

A

interstitial lung disease, pulmonary arterial hypertension, myocardial disease

170
Q

renal complications of systemic sclerosis

A

sclerodrma renal crisis, non specific progressive renal dysfunction

171
Q

what is raynauds phenomenon

A

blanching, acrocyanosis, reactive hypereamia

172
Q

how to treat rynauds

A

nifedipine - first line, PDE-5 inhibitor- sildenafil, proyacyclin infisiom - iloprots, endothelin recepyor antagonst - basentan

173
Q

pulmonary hypertension classified by

A

> 25mmhg at rest by right heart catheterisation

174
Q

symtoms of pulmonary hypertension

A

SOB on exertion

175
Q

treatment for pulmonary hypertension

A

PDE5 inhibitor, ERA, eproprotinol infusions, oxgen

176
Q

examples of PDE5 inibitor

A

sildenafil

177
Q

example of ERA

A

bosentan

178
Q

treatment of interstitial lung disease

A

MYCOPHEMOLATE, rarely cyclophosphamide, rituximab, nintedanib

179
Q

what is systemic sclerosis renal disease assoiated with

A

anti RNA polymerase 111 antibody

180
Q

what puts people at risk of enal disease

A

steroids

181
Q

how to treat renal crisis

A

ace inhibitors

182
Q

treatment of skin fibrosis

A

methotrexate, mycophenolate

183
Q

what is spndyloarthropathy

A

family of inflammatory arthritides characterised by involvement of both spine and joints, principally in genetically predisposed individuals

184
Q

genetic predisposition of spondyloarthropathies

A

HLA-B27

185
Q

what is HLA-B27 associated with

A

ankylosing sponylitis, reactive arthritis, crohns disease, uveitis

186
Q

spondyloarthrtitis sub groups

A

ankylosing spondylitis, psoriatic arthritis, reactive arthritis, enteropathic arthritic

187
Q

mechanical back pain

A

worsened by activity, typically worst at end of the day, better with rest

188
Q

inflammatory back pain

A

worse with rest, better with activity, significant early morning stiffness

189
Q

what is enthesitis

A

inflammation at isertion of tendons into bones

190
Q

what is anklylosing sponylitis

A

chronic systemic inflammatory disorder that primarily affects the spine

191
Q

when does ankylosing spondylitis present

A

late adolescence or early childhood

192
Q

who is ankylosing spondylitis more common in

A

men

193
Q

sacrolitis on imaging

A

active acute inflammation on MRI suggestive of sacroilitis associated with SpA

194
Q

clinical features of ankylosing spondylitis

A

back pain, enthesitis, peripheral arthritis, uveitis, cardiovascular involvement, enetric mucosal inflammation, neurological involvement, amyloidosis

195
Q

diagosis of ankylosing spondylitis

A

history, examination, bloods, x ray

196
Q

examination of ankylosing spondylitis

A

tragus/occiput to wall, chest expansion, modified schober test

197
Q

bloods for ankylosing spondylitis

A

inflammatory parameters, HLAB27

198
Q

x rays for ankylosing spondylitis

A

sacroiliitis, syndesmophytes, bamboo spine

199
Q

difference between AS and OS on imaging

A

bone density is normal in early AS but reduced in late disease, shiny corners in AS and bamboo spine but in OA there is normal bne density and reduced joint space

200
Q

what is psoriasitic arthritis

A

inflammatory arthritis asscoated with psoriasis

201
Q

clinical features of psoriasitic arthritis

A

nail pitting, onycholysis, dactylitis, enthesitis, extra articular features

202
Q

bloods of psoriasitic arthtritis

A

raised inflammatory parameters, negative RF

203
Q

xray findings of psoriasitic arthritis

A

marginal erosions and whiskering, pencil in cut deformity, osteolysis, enthesitis

204
Q

what is reactive arthritis

A

infection induced systemic illness characterised primarily by an inflammatory synovitis from which viable microorganisms cannot be cultures

205
Q

when do symptoms of reactive arthritis occur

A

1-4 weeks after infection

206
Q

common infections for reactive arthritis

A

urogenital eg chlamydia, enterogenic eg salmonella, shigella and yersinia

207
Q

who does reactive arthritis typically affect

A

young adults

208
Q

HLA B27 in reactive arthritis

A

positive

209
Q

what is reiters syndrome

A

triad and a form of reactive arthritis

210
Q

what is the triad of reiters syndrome

A

urethritis, conjutivitis, arthritis

211
Q

clinical features of reither syndrome

A

general symptoms, asymmetrical monarthritis or oligoarthritis, enthesitis, mucocutaneous lesions, ocular lesions and visceral manifestations

212
Q

bloods of reiters syndrme

A

inflammatory parameters, FBC, U +Es, HLA B27

213
Q

what is enteropathic arthritis associated with

A

IBS

214
Q

clinical symptoms of enteropathic arthritis

A

loose watery stool with mucous and blood, weeightloos and low grade fever, eveitis, pyoderma gangrenosum, enthesitis and oral apthous ulcers

215
Q

management of spondyloarthropathies

A

NSAIDs, corticosteorids, topical steroid eyedrops, MTX, anti TNF

216
Q

when can you ise secukinumab

A

only for PsA and AS

217
Q

what is secunumab

A

anti IL 17

218
Q

what is SLE

A

a chronic auto immune disease

219
Q

what does SLE incidence increase with

A

high oestrogen exposue

220
Q

pathogenesis of SLE

A

developmemnt of autoantibodies as a result of a defect in apoptosis that causes increased cell death and a disturbance of immine tolerance

221
Q

what does increased apoptosis release

A

nuclear material

222
Q

what produces autoantibodies inSLE

A

B cell adn T cells

223
Q

epidemiology of SLE

A

high prevelance in back people in the uS but not black people in africa

224
Q

prognosis of SLE

A

10 year survival of >90%

225
Q

presentation of SLE

A

fever, fatigue, weight loss, athralgia, myalgia, inflammatory arthrtitis, avascular necrosis, jacouds arthritis

226
Q

what is jaccouds arthritis

A

lateral shift on metacarpal = parangeal joint

227
Q

skin manifestations of SLE

A

malar rash, photosensitiviy, discoid lupus, alopecia, subacute cutaenous lupus, oral/nasal ulceration (painless), reynaids phenomenon

228
Q

what is raynauds phenominon

A

white/blue extremities in cold

229
Q

renal manifestation of SLE

A

lupus nephritis

230
Q

respiratory manifestation of SLE

A

pleurisy, pleural effusion, pnuemonitis, PE, pH and ILD

231
Q

haemolytic manifestations of SLE

A

leukopenia, lymphopenia, anaemia, thrombocytopenia

232
Q

neuropsychiatric manifestations of SLE

A

seizures, psychosis, headache, aseptic meningitis

233
Q

cardiac manifestations of SLE

A

pericarditis, pericardial effusion, PH, sterile endocardiris, and accelerated ischeamic heart disease

234
Q

neurological manifestations of SLE

A

migraines, seizures, cranial or peripheral neuropathy, mononeuritis complex

235
Q

GI manifestations of SLE

A

autoimmune hepatitis, pancreatitis, mesenteric vasculitis

236
Q

serositis

A

inflammation of serous membranes

237
Q

investigations of SLE

A

immunology, FBC, urinalysis, imaging

238
Q

ANA positive in what % of SLE patients

A

> 95%

239
Q

is ANA specific to SLE

A

no also in RA, HIV and hepC

240
Q

what antibody is specific to SLE

A

anti-dsDNA

241
Q

what antibody is spefic to SLE but has low sensitivity

A

anti-sm

242
Q

what is low when SLE is activity

A

C3/4 levels

243
Q

what may FBC of SLE show

A

anaemia, leucopenia, thrombocytopenia

244
Q

what may urinalysis show

A

glomerulonephritis

245
Q

if glomerulonephritis is positive what should you do

A

kidney biopsy

246
Q

management of SLE - non pharmacological

A

Counselling, regular monitoring, avoid sun,

247
Q

what does every lupus get

A

hydrochloroquine

248
Q

how to treat skin disease and arthralgia in SLE

A

hydrochloroquine, topical steroids and NSAIDs

249
Q

how to treat inflammatory arthritis or evidnee of some types of organ involvement in SLE

A

immunosuppresion, moderate corticosteroids

250
Q

how to treat severe organ disease in SLE

A

Iv steroids, cyclophosphamide

251
Q

how to treat unresponsive SLE

A

Iv immunoglobin and rituximab

252
Q

mild SLE management

A

HCQ, topical steroids NSAIDs

253
Q

moderate SLE management

A

oral steroids, azatioprine/methotrexate

254
Q

severe SLE management

A

IV steroids cyclophosphamide rituximab

255
Q

what is sjogrens syndrome

A

autoimmune condition characterised by lymphocyte infiltrates in exocrine organs

256
Q

presentations of sjogrens syndrome

A

dryness of eyes and mouth, arthralgia, fatigue and vagina dryness and parotid gland swelling

257
Q

what does sjorgens syndrome put people at risk of

A

lymphoma

258
Q

what can sjorgens syndrome be secondary to

A

RA or SLE

259
Q

diagnosis of sjorgens syndrome

A

confirmation of ocular dryness (schirmers test)< +anti-ro and anti-la antibodies and typical features on a lip gland biopsy

260
Q

management of sjorgens syndrome

A

symptomatic, lubricating eye drops, saliva replacement, dental care, HCQ for athragia and faatigue, immunosuppression in organ involvement

261
Q

what is systemic sclerosis

A

systemic connective tissue disease

262
Q

what constitutes systemic sclerosis

A

vasomotor disturbances (raynauds), fibrosis and subsequent atrophy of the skin and subcutaneous tissue, excessive collagen deposition causes skin and internal oragn chnages

263
Q

what causes death in systemic sclerosis

A

renal and lung changes

264
Q

what % of petinets with systemic sclerosis have pulmonary hypertesion

A

12%

265
Q

major features of systemic sclerosis

A

centrally located skin sclerosis that affects the arms, face or neck

266
Q

minor features of systemic sclerosis

A

includes sclerodactyl and atrophy of the fingertips and bilateral lung fibrosis

267
Q

diagnosis of systemic sclerosis

A

1 major and 2 minor features

268
Q

organ involvement in systemic sclerosis

A

pulmonary hypertension, pulmonary fibrosis and accelerated hypersion causing renal crisis, gut involvement may cause dysphagia, malabsorption and bacterial overgrowth of small bowel inflammatory arthritus and myositis

269
Q

limited systemic sclerosis

A

skin affected confined ti face, hands, forearms and feet

270
Q

antibody in systemic sclerosis limited

A

anti centromere

271
Q

antibody in diffuse systemic sclerosis

A

anti - acl- 70

272
Q

what is diffuse systemic sclerosis

A

organ involvement, rapid skin changes, may involve trunk

273
Q

investigations of systemic sclerosis

A

anti centromere and anti scl-70, organ screening

274
Q

management of raynauds

A

raynauds - CCB

275
Q

management of renal crisis

A

ACEi

276
Q

management of GI symptoms in systemic sclerosis

A

PPI

277
Q

management of interstitial lung disease

A

immunosuppression, usually cyclophophamide

278
Q

what is MCTD

A

raynauds, arthraligia, myositis, slcerodactyl, PH and ILD

279
Q

what is MCTD associated with

A

anti RNP antibodies

280
Q

managements of MCTD

A

regular echos, screen of ILD

281
Q

whats is anti phosphilipd syndrome

A

recurrent venous or arterial thrombosis and / or fetal loss, may not have associated disease but often occurs in conjunction with SLE

282
Q

presentation of APS

A

increased frequency of stroke or MI, multiorgan infarctions, migraines

283
Q

invesitations of APS

A

thrombocytopenia and prolongaton of APTT, lupus anticoagulant, ant cardioliin antibodies and anti beta 2 glycoprotein may be positive

284
Q

management of APS

A

anticoagulation - LMWH in pregnancy as warfarin is teratogenic

285
Q

acute attack of crystal arthropathies duration

A

upto 2 weeks

286
Q

cause of gout is

A

monosodium urate

287
Q

how many people have gout in the world

A

1-2%

288
Q

what gender is gout more common in

A

men

289
Q

when does prevelance of gout increase

A

with age

290
Q

what is hyperuricemia

A

serum uric acid >7mg/dL

291
Q

diagnosis of gout

A

radiograohic identification of crystals and hyperuricemia

292
Q

when should you meaure serum urate

A

2 weeks after attack

293
Q

how can hyperuricaemia occur

A

renal underxcretion or excessive intake of alcohol, red meat and seafood

294
Q

where can uric acid crytals precipitate

A

in joints which can be triggered by dehydration traima or surgery

295
Q

what can renal underexcretion be exacerbated by

A

diuretics or renal failure

296
Q

most affected joints in gout

A

1st MTP, ankle and knee are most affected joints

297
Q

clinical presentation of gout

A

rapid onset, red, hot joint, severe pain - mimics spetic arthritis symptoms last for 7-10 days

298
Q

what is gouty tophi

A

painless accumulations of uric acid which can occur in soft tissue and occasuonally erput through skin

299
Q

what. ischronic polyarticular gout

A

chronic joint inflammation, usually after having recureent acut attacks >10 years. Often diuretic associated. may get acute attacks can alos cause erosive arthritis

300
Q

investigations of gout

A

inflammatory markers raised, WCC may be raised, X ray, joint aspirate with polarised microscopu

301
Q

what should you see in gout joint aspirate and polarised microscopy

A

needle shaped crystals yellow to blue

302
Q

management of acute gout

A

NSAIDs, colchoncne or corticosterods

303
Q

lifestyle modifications in gout

A

less red meat, beans, shellfish, reduve alcohol,wgt loss, fluids

304
Q

how should you treat people who suffer from recuurent attacks of gout

A

urate lowering therapy - allopurinal

305
Q

when to start allopurinal in gout

A

AFTER FLARE HAS CLEARED

306
Q

what is pseudogot caused by

A

CPPD

307
Q

who mainly gets pseudogout

A

elderly

308
Q

what is pseudogout related to

A

OA

309
Q

what does pseudogout tend to affect

A

knee wrist and ankle

310
Q

crystals seen in pseudogout

A

rhomboid / envelop shaped crystals

311
Q

treatment of pseudogout

A

NSAIDs, colchincine, corticosteroids, rehydration

312
Q

what is hydroxyapatite

A

crystal deposiy in shoulder, acute and rapid deterioration

313
Q

who gets hydroapatite

A

females 50-60 years old

314
Q

what is hydroxyapatite also known as

A

milwaukee shoulder

315
Q

what are inflammatory myopathies

A

polymyositis and dermatomyositis

316
Q

prevelnace of muscle disease by gender

A

2x more common in females

317
Q

peak age for inflammatory myopathies

A

40-50 years

318
Q

what does inflammatory myopathies come with

A

increased incidence of malignancy

319
Q

increase in malignancy in dermatomyositis

A

15%

320
Q

increase in malignancy in polymyositis

A

9%

321
Q

pathophysiology of inflammatory myopathies

A

muscle fibre necrosis, degneration, regeneration, inflammatory cell infitrate

322
Q

clinical features of inflammatory myopathies

A

muscle weakness (neck, shoulder, hips), worsening onset, usually symmetrical and proximal muscles, often difficulty doing specific tasks myalgia

323
Q

signs of demratomyositis

A

gottrons sign, heliostrope rash, shawl sign

324
Q

what is gottrons sign

A

pink rash over MCPJ

325
Q

what is shawl sign

A

rash accross back of shoulders

326
Q

other manifestations of inflammatory myoapthies

A

ILD, resp muscle weakness, dysphagia, myocarditis, also fever weight loss, raynauds, non erosive, polyarthritis

327
Q

what to ask about in patients with inflammatory myopaties

A

diabetes, thyroid disease, steroids, statins, alcohol and illicit drugs

328
Q

diagnosis of inflammatory myopathies

A

confrontational testing, isotonic testing, blood test, auto antibodies, EMG, muscle biopsy, MRI

329
Q

auto antibodies in inflammatory myopathies

A

ANA, anti jo 1

330
Q

treatment of inflammatory myopathies

A

high dose steroid to suppress initially and then decease dose, 20 mg of prednisolone + methotrexate or azathioprine

331
Q

who is body myositis more common in

A

men and older people

332
Q

what muscles does inclusion body myositis effect

A

distal muscles

333
Q

what des polymyalgia rheumatica present as

A

ache in shoulder and hip girdle, morning stiddness, symmetrical, fatigue, anorexia, weight loss, fever, reduced movement, muscle strength is normal

334
Q

who does polymyalgia present in

A

over 50s

335
Q

incidence of polymyalgia

A

1%

336
Q

what is polymyalgia associated iwth

A

temporal arteritis/giant cell arteritis

337
Q

what is termpal arteritis /giant cell arteritis

A

granulomas arteis of large vessels

338
Q

presentation of temporal/giant cell arthritis

A

headaches, scalp tenderness, jaw claudication, visual loss and tender enlarged non pulstile temporal arteries

339
Q

diagnosis of polymyaligia rheumatica

A

exclude other diagnosis, raised ESR, plasma viscosity, CRP, temperoal artery biopsy

340
Q

treatment of polymyalgia rheumatica

A

treat with low dose steroids, gradually reduce over 18 months to 2 years

341
Q

what is fibromyalgia

A

oversensitised pain stimulus

342
Q

prevelance of fibromyalgia

A

2.5%

343
Q

who does fibromyalgia present in

A

women 22-50

344
Q

presentation of fibromyalgia

A

pain in neck, shoulders, lower back, chest wall, pins and needles, ibs, poor concentration and memroy

345
Q

examination of fibromyalgia

A

excessive tenderness on palpation of soft tissues

346
Q

treatment of firbomyalgia

A

pain control - atypical analgesia - amitriptyline, gabapentin, pregbalin, graded excersise programme, cbt

347
Q

what. is vasculitis

A

presence of leukocytes / immune complexes in vessel wall damaging structure

348
Q

how to classify vasculiti

A

by size of vessel or ANCA +

349
Q

example of ANCA + vasculitis

A

wegeners, microscopic polyangitis, churg strauss

350
Q

presentation of vasculitis

A

myalgia, arthralgia, fever, wgt loss, skin infarct, bloody nasal discharge, ulcers, paranasl sinus involvement, gangrene, subglottic stenosis, conductive deafness, sensorineural, hearing loss, pulse loss, valve disease, pericarditis, cardiomyopathy, congestive HF, peritonitis, bloody diarrhoea, ischeamic abdominal pain

351
Q

test for vasculitis

A

ANCA

352
Q

score for vasculitis

A

BVAS

353
Q

untreated vasculitis prognosis

A

fatal

354
Q

prognosis of treated vasculitis

A

5 yr survival is 90%

355
Q

least common small cell

A

microscopic polyangitis

356
Q

what does small cell microscopic polyangitis affect

A

kidneys

MSK (19 decks)

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