autoimmune tings Flashcards

(42 cards)

1
Q

what is systemic lupus erythematous

A

cells become damaged usually from UV
cells die and release DNA and histones, nuclear antigens, immune cells recognise these and B cells create anti-nuclear antibodies forming immune complexes that can deposit anywhere in the body causing local inflammation and reducing self tolerance

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2
Q

what causes SLE

A

genetics

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3
Q

what are risk factors for SLE

A

female

pregnancy

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4
Q

how can SLE present

A
fever 
rash 
joint pain 
serotitis 
ulcers 
photosensitivity rash 
discoid rash 
renal disease 
raynaud's 
butterfly rash 
neurological symptoms 
anaemia 
alopecia 
arthritis 
autoantigens, ANA
ANA 
Anti-smith
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5
Q

what investigations would you do for SLE

A

urine dipstick - check for renal impairment
renal biopsy
C3 and C4 levels
FBC
CRP and ESR
antibody tests -antinuclear-antibodies, anti-dsDNA antibodies

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6
Q

how can you manage SLE

A
prevent flare ups  - suncream 
corticosteroids - prednisolone 
hydroxychloroquine 
immunosuppressants - methotrexate 
NSAIDS 
biologic agents in severe disease
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7
Q

what is systemic sclerosis

A

connective tissue disease
fibrosis of skin and internal organs
changes in microvasculature

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8
Q

what are the types of sclerosis

A

diffuse cutaneous

limited cutaneous/CREST

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9
Q

what causes sclerosis

A

environment

genetics

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10
Q

what are risk factors for sclerosis

A

female

30-50

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11
Q

how does localised sclerosis present

A
only skin distal to the elbows and knees is involved
CREST
calcinosis 
raynaud's 
oesophageal dysmotility 
sclerodactyly 
telangiectasias
should plateau in 5 years
Positive ANA
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12
Q

how does diffuse sclerosis present

A

fast progression
interstitial lung disease
cardiac and renal involvement

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13
Q

how can you manage sclerosis

A

no cure
try and slow progression with immunosuppressants
manage symptoms
for localised reassure patient it won’t progress to systemic and refer to dermatology

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14
Q

what is sjogren’s syndrome

A

autoimmune infiltration of salivary and lacrimal glands

glandular tissue is replaced by lymphocytes so the glands can no longer secrete as much saliva/tears

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15
Q

what can cause sjogren’s syndrome

A

usually follows infection
usually women
Anti Lo, Anti La.

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16
Q

what are the symptoms of sjogrens

A
dry mouth 
dysphagia 
dry eyes 
sore red eyes 
feeling of sand in eyes 
difficulty tasting 
dryness of skin and vagina 
neuro symptoms 
ILD 
arthralgia
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17
Q

what are the two types of sjogren’s disease

A

primary - occurs in isolation

secondary - related to SLE or RA

18
Q

what investigations would you do for sjogrens

A

saliva test - should produce 15ml/min
sjogrens/schirmir test (tears) - less than 10mm is significant 15mm is normal
biopsy
need occular and oral dryness for at least three months for diagnosis

19
Q

how would you manage sjogrens

A

no treatment
manage with eye drops and moisturiser etc
hydroxychloroquine - slows progress

20
Q

what is giant cell arteritis

A

autoimmune infiltration of arteries usually temporal arteries
systemic vasculitis
causes hyperplasia and occlusion

21
Q

what are risk factors for GCA

A

female
white
70+
polymyalgia rheumatica

22
Q

how does GCA present

A
sudden onset painful headache 
scalp tenderness
jaw claudication 
blurred or double vision 
painless blindness 
fatigue 
muscle ache 
peripheral oedema 
tongue necrosis
23
Q

what investigations could you do for GCA

A

temporal artery biopsy
doppler
CT or MRI angiogram
ESR blood test

24
Q

how do you manage GSA

A

immediate high dose prednisolone 40-60mg
aspirin
PPI to protect stomach from steroids
bisphosphonate to protect bone

25
what is wegener's syndrome/granulomatosis with polyangiitis
Small blood vessel vascilutus ANCA-associated disease necrotising granulomatous inflammation usually in the lungs (respiratory system and kidneys)
26
how does wegener's present
``` haemoptysis - from ulcers in lungs sinusitis epistaxis wheeze bloody mucous hearing loss rapidly progressing glomerulonephritis. ```
27
what are clinical signs of wegeners
collapsed nasal bridge | can effect kidneys and cause glomerulonephritis and patient will have oliguria and hypertension
28
what investigation can you do for wegener's
x-ray - look for cavitating lesions in lungs
29
how do you manage wegeners
corticosteroids | cyclophosphamide (immunosuppresant)
30
what is churg-strauss syndrome/eosinophilic granulomatosis with polyangiitis
Small and medium vessel vasculitis. ANCA-associated inflammation of blood vessels with white blood cells and necrotising granulomas usually in respiratory tract it can affect lungs, skin or kidneys
31
how does churg-strauss syndrome present
``` similar to late onset asthma nasal polyps sinusitis GI involvement neuro involvement lung and kidney damage ```
32
what investigations could you do for churg-strauss syndrome
bloods - WBCs biopsy may be anti-MPO +ve
33
how can you manage churg-strauss syndrome
no cure | try manage symptoms
34
what is polymyalgia rheumatics
inflammatory condition | associated with giant cell arteritis
35
what age group is most likely to have polymyalgia rheumatics
50+ caucasian female
36
how does polymyalgia rheumatics present
``` symptoms must be > 2 weeks. shoulder or pelvic girdle most commonly effected - bilateral stiffness muscle ache joint pain malaise weight loss fever anaemia ```
37
what investigations could you do for polymyalgia rheumatics
rule out giant cell arteritis ESR > 50 DEXA for patients over 65 with osteoporosis risks and all patient under 65
38
how do you manage polymyalgia rheumatica
be aware of GCA give steroids - prednisolone bone protection with bisphosphonates if over 65 with risk factors IF its polymyalgia rheumatica - there will be a good response to steroids. should be reduced gradually.
39
What is the key investigation done for GCA?
ESR - will be >50mm/hour. Ultrasound - will show halo sign. Biopsy - will show multinucleate giant cells.
40
What is the main complication of GCA?
painless vision loss - permanent cerebrovascular stroke relapses of condition steroid side effects aortitis
41
What is elevated in churg Strauss syndrome?
raised eosinophils.
42
How is SLE characterised?
Anti-nuclear antibodies.