Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Exam - M - MSK + Rheumatology Pathologies (Meg & Rach) > autoimmune tings > Flashcards

autoimmune tings Flashcards

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what causes SLE

A

genetics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what are risk factors for SLE

A

female

pregnancy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

how can you manage SLE

A 
prevent flare ups  - suncream 
corticosteroids - prednisolone 
hydroxychloroquine 
immunosuppressants - methotrexate 
NSAIDS 
biologic agents in severe disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what is systemic sclerosis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what are the types of sclerosis

A

diffuse cutaneous

limited cutaneous/CREST

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what causes sclerosis

A

environment

genetics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what are risk factors for sclerosis

A

female

30-50

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

how does diffuse sclerosis present

A

fast progression
interstitial lung disease
cardiac and renal involvement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what can cause sjogren’s syndrome

A

usually follows infection
usually women
Anti Lo, Anti La.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
Q

what is wegener’s syndrome/granulomatosis with polyangiitis

A

Small blood vessel vascilutus
ANCA-associated disease
necrotising granulomatous inflammation usually in the lungs (respiratory system and kidneys)

26
Q

how does wegener’s present

A 
haemoptysis - from ulcers in lungs
sinusitis 
epistaxis 
wheeze
bloody mucous
hearing loss
rapidly progressing glomerulonephritis.
27
Q

what are clinical signs of wegeners

A

collapsed nasal bridge

can effect kidneys and cause glomerulonephritis and patient will have oliguria and hypertension

28
Q

what investigation can you do for wegener’s

A

x-ray - look for cavitating lesions in lungs

29
Q

how do you manage wegeners

A

corticosteroids

cyclophosphamide (immunosuppresant)

30
Q

what is churg-strauss syndrome/eosinophilic granulomatosis with polyangiitis

A

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
Q

how does churg-strauss syndrome present

A 
similar to late onset asthma 
nasal polyps 
sinusitis 
GI involvement 
neuro involvement 
lung and kidney damage
32
Q

what investigations could you do for churg-strauss syndrome

A

bloods - WBCs
biopsy
may be anti-MPO +ve

33
Q

how can you manage churg-strauss syndrome

A

no cure

try manage symptoms

34
Q

what is polymyalgia rheumatics

A

inflammatory condition

associated with giant cell arteritis

35
Q

what age group is most likely to have polymyalgia rheumatics

A

50+
caucasian
female

36
Q

how does polymyalgia rheumatics present

A 
symptoms must be > 2 weeks.
shoulder or pelvic girdle most commonly effected - bilateral
stiffness 
muscle ache 
joint pain 
malaise
weight loss 
fever 
anaemia
37
Q

what investigations could you do for polymyalgia rheumatics

A

rule out giant cell arteritis
ESR > 50
DEXA for patients over 65 with osteoporosis risks and all patient under 65

38
Q

how do you manage polymyalgia rheumatica

A

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
Q

What is the key investigation done for GCA?

A

ESR - will be >50mm/hour.
Ultrasound - will show halo sign.
Biopsy - will show multinucleate giant cells.

40
Q

What is the main complication of GCA?

A

painless vision loss - permanent
cerebrovascular stroke

relapses of condition
steroid side effects
aortitis

41
Q

What is elevated in churg Strauss syndrome?

A

raised eosinophils.

42
Q

How is SLE characterised?

A

Anti-nuclear antibodies.

Exam - M - MSK + Rheumatology Pathologies (Meg & Rach) (13 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions