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
what joints are not affect in RA
DIPs
26
how can RA cause cervical chord compression
cervical spine affected- atlanto-axial subluxation
27
antibodies used to diagnose RA, which is more specific
RF and anti-CCP (more specific)
28
what investigations to diagnose RA
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)
29
when do you aim to start DMARDs
within 3 months of symptom onset
30
what is the treatment for RA
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
31
what are the four components of DAS28 scores
tender joint count, swollen joint count, CRP/ESR, visual analogue score
32
what are the perimeters of DAS28 scores
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
33
patients with seronegative inflammatory arthropathies usually have what gene
HLA-B27
34
who gets AS
males (3:1), typically between 20-40
35
what is the presentation of AS
spinal pain, stiffness, may also develop knee and hip arthritis
36
describe the posture in AS
question mark- loss of lumbar lordosis and increased thoracic kyphosis
37
what test measures lumbar spine flexion
schobers test (measuring 5cm below posterior superior iliac crests and 10 cm above- when bending forward should extend beyond 20cm)
38
what conditions are associated with AS
anterior uveitis, aortitis, pulmonary fibrosis, amyloidosis
39
what might x rays show in AS
slcerosis, fusion of sacroiliac joints, syndesmophytes (bony spurs which can bridge the intervertebral disc resulting in fusion= bamboo spine)
40
what early features of AS can MRI detect
bone marrow oedema, enthesitis of spinal ligaments
41
what is the treatment for AS
physio, exercise, NSAIDs, anti TNF DMARDS HAVE NO EFFECT on spinal disease but may help peripheral joint inflammation
42
what pattern is psoriatic arthritis
asymmetrical oligoarthritis
43
what symptoms do PA patients usually have
nail changes- pitting, onycholysis
44
what is arthitis mutlians
aggressive form of PA
45
what is the treatment for PA
similar to RA, with DMARDs, usually methotrexate. Anti-TNF therapy is available for those who do not respond to standard treatment
46
what is enteropathic arthritis
inflammatory arthritis involving the peripheral joints and sometimes spine, occurring in patients with inflammatory bowel disease
47
what pattern in enteropathic arthritis
large joint asymmetrical oligoarthritis
48
what infections most commonly cause reactive arthritis
gentiourinary (chlamydia, neisseria) and GI (salmonella and campylobacter)
49
what is reiters syndrome
traid of symptoms in reactive arthritis- urethritis, uveitis/ conjunctivitis and arthritis
50
what is the treatment for reactive arthritis
underlying infection treated, symptomatic relief (IA or IM steroids) occasionally DMARDs in chronic cases
51
what is the pathogenesis of SLE
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
52
what renal symptoms in SLE
lupus nephritis
53
what resp symptoms in SLE
pleurisy, pleural effusion, pneumonitis, PE, PHT, ILD
54
what haematological symptoms in SLE
leukopenia, lymphopenia, anaemia, thrombocytopenia
55
what neuropsychiatric symptoms in SLE
seizures, psychosis, headache, aseptic meningitis
56
what cardio symptoms in SLE
pericarditis, pericardial effusion, PHT, sterile endocarditis, accelerated ischemic heart disease
57
what immunology for SLE
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
what is urinalysis for in SLE
evidence of glomerulonephritis
59
what imaging for SLE
to look for evidence of organ involvement eg CT chest for interstitial lung disease, MRI brain for cerebral vasculitis, echo for pericardial effusion
60
management for SLE skin disease and arthralgia
hydroxychloroquine, topical steroids and NSAIDs
61
management for SLE with inflammatory arthritis/ organ involvement
immunosuppression, corticosteroids
62
what is sjogrens characterised by
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
what can sjogrens occur secondary to
RA and SLE
64
what complications can occure in sjogrens
ILD, peripheral neuropathy, increased risk of lymphoma
65
how do you diagnose sjogrens
confirmation of ocular dryness (schirmers test), positive anti-ro and anti-la antibodies, typical features on a lip gland biopsy
66
what is the treatment for sjogrens
symptomatic (lubricants) regular dental care Hydroxychloroquine - arthralgia and fatigue immunosuppresion in organ involvement
67
what are characteristics of systemic sclerosis
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
what are the phases of cutaneous involvment in systemic sclerosis
1. oedematous 2. indurative 3. atrophic skin becomes thickened and tight
69
what are signs of systemic sclerosis on the face
beaking of nose tightening of skin around mouth telangiectasia
70
describe organ involvement in systemic sclerosis
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
describe diffuse ans limited systemic sclerosis
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
what conditions comprised the symptoms seen in MCTD
Raynauds phenomenon Arthralgia/arthritis Myositis Sclerodactyly Pulmonary hypertension Interstitial lung disease (ILD)
73
what antibody in MCTD
anti-RNP
74
what management for MCTD
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
what is the treatment for systemic sclerosis
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
what can anti-phospholipid syndrome occur in association with
SLE/ rheumatic/ autoimmune disorder
77
what is libman sacks
sterile lesions in endocarditis (seen in APS)
78
what is a common cutaneous finding of APS
livedo reticularis
79
what investigations into APS
may be thrombocytopenia and prolongation of APTT. Lupus anticoagulant, anti-cardiolipin antibodies and anti-beta 2 glycoprotein may be positive.
80
what treatment for APS
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
what is uric acid
the final compound in the breakdown of purines in DNA metabolism
82
what can cause hyperuricaemia
renal underexcretion (which can be exacerbated by diuretics or renal failure) or due to excessive intake of alcohol, red meat and seafood
83
what can cause the precipitation of urate crystals
dehydration, trauma or surgery
84
what is podagra
classic site of gout- 1st MTP
85
how does gout present
intensely painful, red, hot, swollen joint- lasts 7-10 days in untreated
86
what are gouty trophi
painless white accumulations of uric acid
87
what can chronic gout result in
destructive erosive arthritis
88
what is seen in gout in polarised microscopy
negative birefringence
89
what is the treatment for gout
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
what crystals in pseudogout
calcium pyrophosphate
91
what is chondrocalcinosis
when calcium pyrophosphate deposition occurs in cartilage and other soft tissues in the absence of acute inflammation
92
what is CPPD
Calcium Pyrophosphate Deposition disease (pseudogout and chondrocalcinosis)
93
what joints does CPPD affect
knee, wrist, ankle
94
what is the treatment for CPPD
Treatment of acute attacks includes NSAIDs, corticosteroids (systemic and intra‐articular) and occasionally colchicine nothing for prophylaxis
95
who does Polymyalgia rheumatica affect
over 50s
96
what is Polymyalgia rheumatica characterised by
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
what biochem signs is Polymyalgia rheumatica always associated with
raised CRP, PV, ESR
98
what treatment can be used as a diagnostic tool for Polymyalgia rheumatica
Symptoms respond very dramatically to low dose steroids (prednisolone 15mg daily)
99
what is the most common form of systemic vascultitis in adults
giant cell arteritis
100
describe GCA histologically
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
what are the symptoms of GCA
visual disturbances, headache, jaw claudication and scalp tenderness. Constitutional manifestations, such as fatigue, malaise, and fever
102
describe the headache in GCA and the clinical signs of this
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
what is the definitive test for GCA
arterial biopsy
104
what do biopsys find in GCA
mononuclear infiltration or granulomatous inflammation, usually with multinucleated giant cells.
105
what is the treatment for GCA
40mg prednisolone, 60mg if vision impaired ASAP | tapered over 18 months-2 years
106
what is polymyositis
idiopathic inflammatory myopathy that causes symmetrical, proximal muscle weakness in upper and lower extremities
107
who gets Polymyositis and dermatomyositis
women 2:1 | over 20s, peak 45-60
108
what is the pathogenesis of Polymyositis
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
what antibodies in Polymyositis and dermatomyositis
ANA, anti-RNP antibody (shred with other autoimmune) unique- anti-Jo-1, anti-SRP antibodies
110
what are the complications of polymositis
Dysphagia secondary to oropharyngeal and esophageal involvement ILD
111
what investigations into PM
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
what is the management for PM and DM
prednisolone (initially around 40mg) combined with immunosuppressive drugs such as methotrexate or azathioprine.
113
what are the cutaneous features of DM
V shaped rash over chest gottrons papules heliotrope rash
114
describe large vessel vasculitis
primary vasculitis that causes chronic granulomatous inflammation predominantly of the aorta and its major branches
115
what are the two types of large vessel vasculitis
temporal (giant cell) arteritis and Takayasu arteritis (TA)
116
what happens if larger vessel vasculitis is left untreated
vascular stenosis and aneurysms- reduced pulses and bruits
117
what investigations in vasculitis
raised ESR, PV, CRP MR angiography good for stenosis/ thickened vessels
118
what is the treatment for large vessel vasculitis
corticosteroids, starting at 40-60mg prednisolone and gradually reducing. Steroid sparing agents such as methotrexate and azathioprine may be added
119
what are common features of small vessel vasculitis
Fever and weight loss A raised, non blanching purpuric rash Arthralgia/arthritis Mononeuritis multiplex Glomerulonephritis Lung opacities on x-ray
120
what are the four types of ANCA associated vasculitis
Granulomatosis with polyangiitis (GPA) or Wegeners Eosinophilic granulomatosis with polyangiitis (EGPA) Microscopic polyangiitis churg strauss syndrome
121
what symptoms are common in GPA
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
what antibodies are associated with GPA
cANCA and PR£
123
what symptoms are associated with EGPA
late onset asthma, rhinitis and a raised peripheral blood eosinophil count. Neurological symptoms such as mono neuritis multiplex are common
124
what is the most common complication in microscopic polyangitis
glomerulonephritis, which occurs in up to 90% of patients.
125
what investigations in AAV
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
treatment for AAV
IV steroids and cyclophosphamide due to their aggressive disease course
127
what is henloch-schonlein purpura
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
who does Henoch-Schönlein purpura affect and how
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
what is the treatment form Henoch schonlein purpura
self limiting condition not requiring specific treatment. It usually settles over the course of weeks to months.
130
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
pneumothorax
131
what antibody is most specific to SLE
anti-DNA binding, anti dsDNA
132
cane sacrolitis be a feature of crohns related arthritis
yes
133
is aortic valve incompetence a common manifestation of the spondyloarthritides
yes
134
should allopurinol be stopped during acute flares of gout
no