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MSK > Cortex- Rheumatology > Flashcards

Cortex- Rheumatology Flashcards

1
Q

what are the 4 sub chatagories of inflammatory arthritis

A

seropistive, seronegative, infectious and crystal induced

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2
Q

what are the seropositive arthrides

A

RA, lupus, scleroderma, vasculitis, srogrens

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3
Q

what are the seronegative arthrides

A

AS, psoriatic arthritis, reactive arthritis, IBD arthritis

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4
Q

name the conditions associated with this antigen:

anti-ccp

A

RA

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5
Q

name the conditions associated with this antigen:

ANA

A

SLE, sjogrens, systemic sclerosis, MCTD, autoimmune liver disease

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6
Q

name the conditions associated with this antigen:

anti-dsDNA

A

SLE

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7
Q

name the conditions associated with this antigen:

anti-sm

A

SLE

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8
Q

name the conditions associated with this antigen:

anti-ro

A

SLE, sjogrens

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9
Q

name the conditions associated with this antigen:

anti-la

A

sjogrens

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10
Q

name the conditions associated with this antigen:

anti-centromere

A

systemic sclerosis (limited)

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11
Q

name the conditions associated with this antigen:

anti-scl-70

A

systemic sclerosis (diffuse)

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12
Q

name the conditions associated with this antigen:

anti-rnp

A

SLE, MCTD

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13
Q

name the conditions associated with this antigen:

anti-jo-1

A

myositis

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14
Q

name the conditions associated with this antigen:

anti-cardiolipin antibody and lupus anti- coagulant

A

anti-phopholipid syndrome

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15
Q

name the conditions associated with this antigen:

ANCA

A

small vessel vasculitis (GPA, EGPA, MPA)

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16
Q

what mutation in OA

A

none found, no pattern of madelian inheritance

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17
Q

what can cause secondary osteoarhritis

A

injury dislocation, perthes disease, crystal arthropathy, inflammatory arthritis, genu varum or valum

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18
Q

what does LOSS on x ray if OA mean

A

Loss of joint space
Osteophytes
Sclerosis
Subchondral cysts

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19
Q

what is the main treatment for osteoarthritis

A

analgesia, mild opiates, physiotherapy, weight loss and exercise, joint replacement

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20
Q

what are the antiflammatory treatments

A

steroids and NSAIDs

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21
Q

what is the joint involvement pattern of RA

A

symmetric polyarthopathy, mostly small joints of hands and feet- larger joints as disease progresses

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22
Q

who gets RA

A

women 2x more likely

peak age 35-50

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23
Q

what is the pathogenesis of RA

A

immune response against synovium initiated by e.g smoking, infection or trauma

inflammatory pannus forms which then attacks and denudes articular cartilage

=joint destruction, tendon ruptures, joint instability, subluxation

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24
Q

what are the clinical features of RA

A

symmetrical synovitis (doughy swelling), pain and morning stiffness

rheumatoid nodules

lung involvement- pleural effusions, interstitial fibrosis, pulmonary nodules

cardio morbidity and mortality increased

occular- keratoconjunctivitis, sicca, episcleritis, uveitis, nodular scleritis

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25
Q

what joints are not affect in RA

A

DIPs

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26
Q

how can RA cause cervical chord compression

A

cervical spine affected- atlanto-axial subluxation

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27
Q

antibodies used to diagnose RA, which is more specific

A

RF and anti-CCP (more specific)

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28
Q

what investigations to diagnose RA

A

antibodies (RF, anti-CCP)
CRP and ESR raised

ultrasound for synovial inflammation

x rays might show peri-articular osteopenia, soft tissue swelling (more helpful in late disease)

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29
Q

when do you aim to start DMARDs

A

within 3 months of symptom onset

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30
Q

what is the treatment for RA

A

short term- analgesia, NSAIDs, steroids (IM, IA, oral)

DMARDs- methotrexate first line (also have sulphasalazine, hydroxycholorquine and lefunomide) (regular blood tests required for immune suppression)

last line biologics- anti TNF (all given by injection) (screen for TB)

physio, occupational therapy, podiatrists, orthotists

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31
Q

what are the four components of DAS28 scores

A

tender joint count, swollen joint count, CRP/ESR, visual analogue score

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32
Q

what are the perimeters of DAS28 scores

A

DAS 28 < 2.6 Remission

DAS 28 2.7-3.2 Low disease activity

DAS 28 3.3-5.1 Moderate disease activity

DAS 28 >5.1 High disease activity

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33
Q

patients with seronegative inflammatory arthropathies usually have what gene

A

HLA-B27

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34
Q

who gets AS

A

males (3:1), typically between 20-40

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35
Q

what is the presentation of AS

A

spinal pain, stiffness, may also develop knee and hip arthritis

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36
Q

describe the posture in AS

A

question mark- loss of lumbar lordosis and increased thoracic kyphosis

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37
Q

what test measures lumbar spine flexion

A

schobers test (measuring 5cm below posterior superior iliac crests and 10 cm above- when bending forward should extend beyond 20cm)

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38
Q

what conditions are associated with AS

A

anterior uveitis, aortitis, pulmonary fibrosis, amyloidosis

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39
Q

what might x rays show in AS

A

slcerosis, fusion of sacroiliac joints, syndesmophytes (bony spurs which can bridge the intervertebral disc resulting in fusion= bamboo spine)

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40
Q

what early features of AS can MRI detect

A

bone marrow oedema, enthesitis of spinal ligaments

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41
Q

what is the treatment for AS

A

physio, exercise, NSAIDs, anti TNF

DMARDS HAVE NO EFFECT on spinal disease but may help peripheral joint inflammation

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42
Q

what pattern is psoriatic arthritis

A

asymmetrical oligoarthritis

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43
Q

what symptoms do PA patients usually have

A

nail changes- pitting, onycholysis

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44
Q

what is arthitis mutlians

A

aggressive form of PA

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45
Q

what is the treatment for PA

A

similar to RA, with DMARDs, usually methotrexate. Anti-TNF therapy is available for those who do not respond to standard treatment

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46
Q

what is enteropathic arthritis

A

inflammatory arthritis involving the peripheral joints and sometimes spine, occurring in patients with inflammatory bowel disease

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47
Q

what pattern in enteropathic arthritis

A

large joint asymmetrical oligoarthritis

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48
Q

what infections most commonly cause reactive arthritis

A

gentiourinary (chlamydia, neisseria) and GI (salmonella and campylobacter)

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49
Q

what is reiters syndrome

A

traid of symptoms in reactive arthritis- urethritis, uveitis/ conjunctivitis and arthritis

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50
Q

what is the treatment for reactive arthritis

A

underlying infection treated, symptomatic relief (IA or IM steroids)

occasionally DMARDs in chronic cases

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51
Q

what is the pathogenesis of SLE

A

mediated by circulating immune complexes that are formed in the small blood vessels and lead to complement activation and inflammation

antibody-antigen complexes are deposited on the basement membranes of the skin and kidney

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52
Q

what renal symptoms in SLE

A

lupus nephritis

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53
Q

what resp symptoms in SLE

A

pleurisy, pleural effusion, pneumonitis, PE, PHT, ILD

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54
Q

what haematological symptoms in SLE

A

leukopenia, lymphopenia, anaemia, thrombocytopenia

55
Q

what neuropsychiatric symptoms in SLE

A

seizures, psychosis, headache, aseptic meningitis

56
Q

what cardio symptoms in SLE

A

pericarditis, pericardial effusion, PHT, sterile endocarditis, accelerated ischemic heart disease

57
Q

what immunology for SLE

A

ANA- not specific
anti dsDNA- specific, varies with disease activity
Anti-sm specific, low sensitivity
Anti-ro, anti- RNP- seen in other conditions
C3/C4 level- low when disease activity high

58
Q

what is urinalysis for in SLE

A

evidence of glomerulonephritis

59
Q

what imaging for SLE

A

to look for evidence of organ involvement eg CT chest for interstitial lung disease, MRI brain for cerebral vasculitis, echo for pericardial effusion

60
Q

management for SLE skin disease and arthralgia

A

hydroxychloroquine, topical steroids and NSAIDs

61
Q

management for SLE with inflammatory arthritis/ organ involvement

A

immunosuppression, corticosteroids

62
Q

what is sjogrens characterised by

A

lymphocytic infiltrates in exocrine organs- typically causes dryness of the eyes, mouth (sicca symptoms)

other symptoms include arthralgia, fatigue, vaginal dryness, parotid gland swelling

63
Q

what can sjogrens occur secondary to

A

RA and SLE

64
Q

what complications can occure in sjogrens

A

ILD, peripheral neuropathy, increased risk of lymphoma

65
Q

how do you diagnose sjogrens

A

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

66
Q

what is the treatment for sjogrens

A

symptomatic (lubricants)
regular dental care
Hydroxychloroquine - arthralgia and fatigue
immunosuppresion in organ involvement

67
Q

what are characteristics of systemic sclerosis

A

vasomotor disturbances (raynauds)
fibrosis
subsequent atrophy of skin and subcutaneous tissue
excessive collagen deposition causes skin and internal organ changes
calcinosis (subcutaneous calcium deposits in digits)
sclerodactyly

68
Q

what are the phases of cutaneous involvment in systemic sclerosis

A
  1. oedematous
  2. indurative
  3. atrophic

skin becomes thickened and tight

69
Q

what are signs of systemic sclerosis on the face

A

beaking of nose
tightening of skin around mouth
telangiectasia

70
Q

describe organ involvement in systemic sclerosis

A

Pulmonary hypertension, pulmonary fibrosis and accelerated hypertension leading to renal crisis are important organ manifestations.

Gut involvement may lead to dysphagia, malabsorption and bacterial overgrowth of the small bowel.

Inflammatory arthritis and myositis may be seen.

71
Q

describe diffuse ans limited systemic sclerosis

A

Limited: skin involved tends to be confined to face, hands and forearms and feet. Organ involvement tends to occur later. Anti-centromere antibody association.

Diffuse: skin changes develop more rapidly and can involve the trunk. Early significant organ involvement. Anti-Scl-70 antibody association.

72
Q

what conditions comprised the symptoms seen in MCTD

A

Raynauds phenomenon

Arthralgia/arthritis

Myositis

Sclerodactyly

Pulmonary hypertension

Interstitial lung disease (ILD)

73
Q

what antibody in MCTD

A

anti-RNP

74
Q

what management for MCTD

A

risk of pulmonary hypertension, regular echocardiograms (annually) are suggested. Screening for ILD with pulmonary function tests should also take place

Calcium channel blockers may be helpful for Raynauds.

If there is significant muscle or lung disease then immunosuppression may be required

75
Q

what is the treatment for systemic sclerosis

A

Raynauds/digital ulcers: calcium channel blockers, Iloprost, bosentan

Renal involvement: ACE inhibitors

GI involvement: proton pump inhibitors for reflux

Interstitial lung disease: immunosuppression, usually with cyclophosphamide

76
Q

what can anti-phospholipid syndrome occur in association with

A

SLE/ rheumatic/ autoimmune disorder

77
Q

what is libman sacks

A

sterile lesions in endocarditis (seen in APS)

78
Q

what is a common cutaneous finding of APS

A

livedo reticularis

79
Q

what investigations into APS

A

may be thrombocytopenia and prolongation of APTT.

Lupus anticoagulant, anti-cardiolipin antibodies and anti-beta 2 glycoprotein may be positive.

80
Q

what treatment for APS

A

anti-coagulation for those with an episode of thrombosis. In patients with recurrent pregnancy loss low molecular weight heparin is used during pregnancy (warfarin is teratogenic).

Patients who are found to have positive antibodies but who have never had had an episode of thrombosis do not require anti-coagulation.

81
Q

what is uric acid

A

the final compound in the breakdown of purines in DNA metabolism

82
Q

what can cause hyperuricaemia

A

renal underexcretion (which can be exacerbated by diuretics or renal failure) or due to excessive intake of alcohol, red meat and seafood

83
Q

what can cause the precipitation of urate crystals

A

dehydration, trauma or surgery

84
Q

what is podagra

A

classic site of gout- 1st MTP

85
Q

how does gout present

A

intensely painful, red, hot, swollen joint- lasts 7-10 days in untreated

86
Q

what are gouty trophi

A

painless white accumulations of uric acid

87
Q

what can chronic gout result in

A

destructive erosive arthritis

88
Q

what is seen in gout in polarised microscopy

A

negative birefringence

89
Q

what is the treatment for gout

A

acute attacks;
NSAIDs,
corticosteroids,
opioid analgesics and colchicine for patients who cannot tolerate NSAIDs.

For sufferers of recurrent attacks or those with joint destruction or tophi, allopurinol or other urate lowering therapies can prevent attacks but they should not be started until an acute attack has settled as they can potentiate a further flare

90
Q

what crystals in pseudogout

A

calcium pyrophosphate

91
Q

what is chondrocalcinosis

A

when calcium pyrophosphate deposition occurs in cartilage and other soft tissues in the absence of acute inflammation

92
Q

what is CPPD

A

Calcium Pyrophosphate Deposition disease (pseudogout and chondrocalcinosis)

93
Q

what joints does CPPD affect

A

knee, wrist, ankle

94
Q

what is the treatment for CPPD

A

Treatment of acute attacks includes NSAIDs, corticosteroids (systemic and intra‐articular) and occasionally colchicine

nothing for prophylaxis

95
Q

who does Polymyalgia rheumatica affect

A

over 50s

96
Q

what is Polymyalgia rheumatica characterised by

A

proximal myalgia of the hip and shoulder girdles with accompanying morning stiffness that lasts for more than 1 hour. Symptoms tend to improve as the day goes on and with movement.

97
Q

what biochem signs is Polymyalgia rheumatica always associated with

A

raised CRP, PV, ESR

98
Q

what treatment can be used as a diagnostic tool for Polymyalgia rheumatica

A

Symptoms respond very dramatically to low dose steroids (prednisolone 15mg daily)

99
Q

what is the most common form of systemic vascultitis in adults

A

giant cell arteritis

100
Q

describe GCA histologically

A

transmural inflammation of the intima, media, and adventitia of affected arteries, as well as patchy infiltration by lymphocytes, macrophages, and multinucleated giant cells. Vessel wall thickening can result in arterial luminal narrowing, resulting in subsequent distal ischemia

101
Q

what are the symptoms of GCA

A

visual disturbances, headache, jaw claudication and scalp tenderness. Constitutional manifestations, such as fatigue, malaise, and fever

102
Q

describe the headache in GCA and the clinical signs of this

A

continuous and located in the temporal or occipital areas. Focal tenderness on direct palpation is typically present. The patient may note scalp tenderness with hair combing.

The temporal artery may be thickened and prominent and tender to touch.

103
Q

what is the definitive test for GCA

A

arterial biopsy

104
Q

what do biopsys find in GCA

A

mononuclear infiltration or granulomatous inflammation, usually with multinucleated giant cells.

105
Q

what is the treatment for GCA

A

40mg prednisolone, 60mg if vision impaired ASAP

tapered over 18 months-2 years

106
Q

what is polymyositis

A

idiopathic inflammatory myopathy that causes symmetrical, proximal muscle weakness in upper and lower extremities

107
Q

who gets Polymyositis and dermatomyositis

A

women 2:1

over 20s, peak 45-60

108
Q

what is the pathogenesis of Polymyositis

A

T-cell–mediated cytotoxic process directed against unidentified muscle antigens. CD8 T cells, along with macrophages, initially surround healthy nonnecrotic muscle fibers and eventually invade and destroy them

109
Q

what antibodies in Polymyositis and dermatomyositis

A

ANA, anti-RNP antibody (shred with other autoimmune)

unique- anti-Jo-1, anti-SRP antibodies

110
Q

what are the complications of polymositis

A

Dysphagia secondary to oropharyngeal and esophageal involvement

ILD

111
Q

what investigations into PM

A

Inflammatory markers are often raised.

Serum creatine kinase (CK) level is usually raised, often more than 10 times the normal level.

Autoantibodies include ANA, anti-Jo-1 and anti-SRP.

MRI may be useful to localize the extent of muscle involvement.

electromicrograph

muscle biopsy- fibres in stages of inflammation, necrosis, and regeneration.

112
Q

what is the management for PM and DM

A

prednisolone (initially around 40mg) combined with immunosuppressive drugs such as methotrexate or azathioprine.

113
Q

what are the cutaneous features of DM

A

V shaped rash over chest
gottrons papules
heliotrope rash

114
Q

describe large vessel vasculitis

A

primary vasculitis that causes chronic granulomatous inflammation predominantly of the aorta and its major branches

115
Q

what are the two types of large vessel vasculitis

A

temporal (giant cell) arteritis and Takayasu arteritis (TA)

116
Q

what happens if larger vessel vasculitis is left untreated

A

vascular stenosis and aneurysms- reduced pulses and bruits

117
Q

what investigations in vasculitis

A

raised ESR, PV, CRP

MR angiography good for stenosis/ thickened vessels

118
Q

what is the treatment for large vessel vasculitis

A

corticosteroids, starting at 40-60mg prednisolone and gradually reducing. Steroid sparing agents such as methotrexate and azathioprine may be added

119
Q

what are common features of small vessel vasculitis

A

Fever and weight loss

A raised, non blanching purpuric rash

Arthralgia/arthritis

Mononeuritis multiplex

Glomerulonephritis

Lung opacities on x-ray

120
Q

what are the four types of ANCA associated vasculitis

A

Granulomatosis with polyangiitis (GPA) or Wegeners

Eosinophilic granulomatosis with polyangiitis (EGPA)

Microscopic polyangiitis

churg strauss syndrome

121
Q

what symptoms are common in GPA

A

ENT symptoms are common in GPA and include nose bleeds, deafness, recurrent sinusitis and nasal crusting (over time there can be collapse of the nose). Respiratory symptoms such as haemoptysis and cavitating lesions on x-ray

122
Q

what antibodies are associated with GPA

A

cANCA and PR£

123
Q

what symptoms are associated with EGPA

A

late onset asthma, rhinitis and a raised peripheral blood eosinophil count.

Neurological symptoms such as mono neuritis multiplex are common

124
Q

what is the most common complication in microscopic polyangitis

A

glomerulonephritis, which occurs in up to 90% of patients.

125
Q

what investigations in AAV

A

ESR, PV and CRP and raised

Anaemia of chronic disease is common.

U+E looking for renal involvement

Anti-neutrophil cytoplasmic antibody (ANCA)

Urinalysis (looking for renal vasculitis)

CXR

Biopsy of an affected area e.g. skin or kidney

126
Q

treatment for AAV

A

IV steroids and cyclophosphamide due to their aggressive disease course

127
Q

what is henloch-schonlein purpura

A

acute immunoglobulin A (IgA)–mediated disorder characterized by a generalised vasculitis involving the small vessels of the skin, the gastrointestinal (GI) tract, the kidneys, the joints, and, rarely, the lungs and the central nervous system

128
Q

who does Henoch-Schönlein purpura affect and how

A

children. Commonly a history of an upper respiratory tract infection predates the symptoms by a few weeks.

purpuric rash over the buttocks and lower limbs, abdominal pain and vomiting and joint pain

129
Q

what is the treatment form Henoch schonlein purpura

A

self limiting condition not requiring specific treatment. It usually settles over the course of weeks to months.

130
Q

what is the least likely cause of chest pain in SLE out of ;

a. Pleurisy
b. Pulmonary embolus
c. Pneumothorax
d. Pericarditis
e. Myocardial infarction

A

pneumothorax

131
Q

what antibody is most specific to SLE

A

anti-DNA binding, anti dsDNA

132
Q

cane sacrolitis be a feature of crohns related arthritis

A

yes

133
Q

is aortic valve incompetence a common manifestation of the spondyloarthritides

A

yes

134
Q

should allopurinol be stopped during acute flares of gout

A

no

MSK (71 decks)

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