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Year 3 > MedEd AI and vasculitides > Flashcards

MedEd AI and vasculitides Flashcards

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1
Q

what is sarcoidosis?

A

chronic multisystem granulamatous disorder of unknown cause

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2
Q

who is more likely to get sarcoidosis?

A

afro caribbeans

20-40 y/o females

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3
Q

what cells are present in sarcoidosis and what do they form?

A

T lymphocytes and macrophages which form non caseating granulomas

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4
Q

what granulmoas do you get in sarcoidosis? why

A

non caseating

there is no necrosis

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5
Q

how do granulomas differ between tb and sarcoidosis and explain why

A 
tb= caseating because theres necrosis
sarcoidosis= caseating because there is no necrosis
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6
Q

how does acute sarcoidosis present?

A 
fever
erythema nodosum
polyarthralgia
bilat hilar lymphadenopathy
dry cough with prgressive dyspnoea
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7
Q

what type of cough do you get in sarcoidosis?

A

dry cough with progressive dyspnoea

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8
Q

what are extrapulmonary features of sarcoidosis?

A 
organomegaly 
uveitis
lupus pernio
subcut nodules 
arrhythmia 
symptoms of hypercalcaemia
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9
Q

what colour is lupus pernio and where is it found?

A

violet macular rash found on the face

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10
Q

in what resp condition is lupus pernio seen?

A

sarcoidosis

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11
Q

out of lupus pernio and lupus vulgaris which is present in tb and which in sarcoidosis?

A

lupus pernio= sarcoidosis

lupus vulgaris= tb

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12
Q

what ix are done for sarcoidosis and what will you see? which ix is diagnostic

A

bloods- high esr, lymphopenia, hypercalcaemia, raised ACE
cxr- bilateral hilar lymohadenopathy
diagnostic- bronchoscopy with biopsy

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13
Q

what are the cxr stages of sarcoidosis?

A

stage 1= BHL
stage 2= BHL with infiltrates
stage 3= only infiltrates
stage 4= extensive fibrosis

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14
Q

how is sarcoidosis managed?

A

conservation- most patients with stage 1 will spontaneously resolve
may give steroids- indications inc parenchymal lung disease, uveitis, hypercalcaemia, neurologic or cardiac involvement

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15
Q

what are some indication for giving steroids in sarcoidosis?

A

parenchymal lung involvement
uveitis
hypercalcaemia
neurologic or cradiac involvement

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16
Q

what tb abx induces lupus?

A

isoniazid

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17
Q

what is sle? describe what happens

A

a multisystemic relapsing remitting AI disease where a wrongful response to host antigens leads to immune complex formation. a lack of clearance of these complexes then causes tissue damage and inflammation

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18
Q

what is formed in SLE?

A

immune complexes

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19
Q

what type of hypersensitivity reaction is present in SLE?

A

type 3

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20
Q

what genes are associated with SLE?

A

HLA DR3

also HLA B8/DR2

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21
Q

what is the the trigger for formation of autoimmune complexes in SLE?

A

host antigens

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22
Q

how does SLE present?

A 
malar rash
discoid rash
oral ulcers
arthritis 
serositis
renal disorder
hematologic disorders
immunological disorders 
antinuclear disoders
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23
Q

what drugs cause SLE?

A 
sulfalazine
hydralazine 
isoniazid 
procainamide
penicillamine
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24
Q

what ix are done for SLE and what will you see?

A

bloods- anaemia, lymphopenia, thrombocytopenia
ESR high
CRP normal
autoantibodies: ANA, anti ds-DNA, anti histone
there may be lupus nephritis on renal biopsy

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25
what are ESR and CRP levels in SLE?
``` ESR= raised CRP= normal ```
26
how is SLE managed?
maintanence= NSAIDs and hydrocychloroquine for joint and skin symptoms mild flare= low dose steroids moderate flaer= DMARDs or mycophenolate severe flare= high dose steroids, mycophenolate, cyclophosphamide, rituximab
27
what is the difference between CRP and ESR and therefore when will either of them be raised?
``` CRP= rises when there is acute inflammation, ischaemia or thromboembolism ESR= increases in a slower manner and then remains raised so with be high in chronic conditions ```
28
what does high CRP normal ESR indicate?
acute infection, inflammation or ischaemia
29
what does high ESR normal CRP mean?
chronic systemic inflammatory or autoimmune process
30
what autoantibodies are associated with SLE?
ANA | anti dsDNA
31
what is sjogrens syndrome?
chronic inflammatory disorder where lymphocytic infiltration destroys exocrine gland and causes extensive fibrosis
32
what glands are affected in sjogrens syndrome?
exocrine- mainly lacrimal and salivary
33
who is more likely to get sjogrens syndrome?
middle aged women
34
how does sjogrens syndrome present?
``` dry eyes- keratoconjucntivis sicca dry mouth- xerostomia parotid swelling polyarthritis raynauds phenomenon vasculitis peripheral neuropthy ```
35
what is keratoconjunctivits sicca? what condition is it seen in
dry eyes | seen in sjogrens syndrome
36
what is xeroztomia? what condition is it seen in
dry mouth | seen in sjogrens syndrome
37
what ix are done for sjogrens syndrome? describe how they are carried out and what is positive
schrimers test- place a piece of paper under the eyelid for 5 mins and if less than 5mm of paper is wet in less than 5 mins this is positive autoantibodies- anti ro and anto la (are not specific enough) can do salivary gland biopsy
38
what is schrimmers test? how is it carried out and which condition is it used for?
place a piece of paper under the eyelid for 5 mins and if less than 5mm of paper is wet in less than 5 mins this is positive for sjogrens syndrome
39
how is sjogrens syndrome managed?
dry eyes= hypromellose (fake tears) and eye drops dry mouth= salivary substitutes (sugar free gum) severe disease= immunosupressants (steroids)
40
what is systemic sclerosis? describe what happens
multisystemic autoimmune disease where there are functional and structural abnormalities of non inflammatory blood vessels, fibrosis of the skin and internal organs
41
what is limited systemic sclerosis and how does it present?
systemic sclerosis that is limited to the hands, face and feet presents with calcinosis cutis, raynauds, oesophageal dysmotility, sclerdactyly and telangiectasia
42
what is diffuse systemic sclerosis and how does it present?
systemic sclerosis with widespread organ involvement | there is rapid progression and early visceral involvement and BP needs to be meticulously monitored
43
how does systemic sclerosis present?
puffy taut skin with no wrinkles and finger tip pitting renal- scleroderma hypertensive crisis pulmonary- interstitial fibrosis, PH GI- dysmotility, reflux and watermelon stomach cardio- pericarditis or effusion
44
what autoantibodies are associated with systemic sclerosis?
anti centromere in limited type | anti scl 70 and anti RNA polymerase III in diffuse type
45
what type of systemic sclerosis are anti centromere antibodies associated with?
limited
46
what type of systemic sclerosis are anti scl 70 and anti RNA polymerase III antibodies associated with?
diffuse
47
how is systemic sclerosis managed?
immunosupression and treat individual symptoms | in renal crisis ACE-I or ARB with agressive hydration
48
what are poly/dermatomyositis?
insidious onset progressive symmetrical proximal muscle weakness (quads, triceps, biceps) due to autoimmune mediated inflammation of straited muscle
49
what muscles are weakened in poly/dermatomyositis?
proximal muscles like quads, biceps, triceps etc
50
what cancer is dermatomyositis associated with?
ovarian
51
what type of inflammation is present in polymyositis?
endomysial inflammation
52
what type of inflammation is present in dermatomyositis?
perimysial
53
what cells are involved with polymyositis?
CD8+ T cells
54
what cells are involved with dermatomyositis?
CD4+ T cells
55
what muscle group does polymyositis often affect?
shoulder girdle
56
how does polymyolitis present?
progressive symmetrical muscle weakness
57
how does dermatomyositis present?
``` progressive symmetrical muscle weakness grottons papules facial erythema shawl rash mechanics hands ```
58
what are grottons papules?
rough red papules across knuckles, knees and elbows
59
what is shawl rash?
shoulders and chest darkening
60
what are mechanics hands in medicine?
dark and thick irregular patches
61
what ix are done for poly/dermatomyositis and what will you see?
CK and adolase enzymes are elevated due to muscle breakdown EMG shows fibrillation potentials msucle biopsy to confirm diagnosis and visualise inflammation autoantibodies; anti srp, anti mi2, anti jo1
62
how are poly/dermatomyositis managed?
corticosteroids
63
what is giant cell arteritis?
Large vessel granulomatous vasculitis
64
what is polymyalgia rheumatica?
inflammatory condition which manifests as pain and morning stiffness in the neck, shoulder and hip girdle
65
what vessel is commonly affected in giant cell arteritis?
external carotid
66
who usually gets giant cell arteritis?
elderly females
67
how does giant cell arteritis present?
``` unilateral headache sclap tendrness tongue/jaw claudication amaurosis fugax unilateral blidness ```
68
what is amaurosis fugax?
vision gradually going away
69
how does polymyalgia rheumatica present?
``` weakness is not a feature subacute onset (2 weeks) of bilateral aching, tenderness and morning stiffness fever weight loss anorexia ```
70
what is not a feature of polymyalgia rheumatica and helps distinguish it from other conditions?
weakness
71
what ix are done for giant cell arteritis and what do you see/
raised ESR raised CRP normocytic anaemia temporal artery biopsy but only after management- will show focal granulomtous inflammation
72
what ix are done for polymyalgia rheumatica and what will you see?
raised ESR | raised CRP
73
in giant cell arteritis what do you do first and second?
first give steroids | second do ix like bloods
74
how is giant cell arteritis managed?
high dose methylprednisolone if blindness is starting | prednisolone if suspected
75
how is polymyalgia rheumatic managed?
give steroids immediately and there should be a response within a week also give bone protection as steroids will be needed for at least 2 years
76
in giant cell arteritis when is methyprednisolone given and when is normal prednisolone given?
methylprednisolone= given if blindness has started | normal prednisolone= give if disease is suspected
77
what is bechets disease?
systemic inflammatory vasculitis
78
what gene is bechets disease associated with?
B51
79
where is bechets disease found and who is most likely to have it?
old silk road along mediterrean to china | most likely a turkish male
80
how does bechets disease present?
``` recurrent oral ulcers genital ulcerations erythema nodosum thrombophlebitis uveitis ```
81
what ix are done for bechets disease and what will you see?
usually diagnosis is clinical | can also perform pathology testing by sticking a needle into their arm and a papule will form in 48 hrs
82
how is bechets disease managed?
topical steroids for orogenital ulceration | prednisolone plus immunosupressant (azathioprine) if there is organ involvement
83
what is polyarteritis nodosa?
necrotising inflammation of medium sized arteries | aneurysms lead to thrombosis and infarction
84
what virus can cause polyarteritis nodosa?
HBV
85
how does polyarteritis nodosa present?
systemic features skin- rash, punched out ulcers, nodules renal- artery narrowing, ischaemia and hypertension livedo reticularis
86
what is livedo reticularis? what does it look like? in what condition is it seen?
a skin symptom where there is mottled appearance of blood vessels often on the leg can be seen in polyarteritis nodosa
87
what ix are done for polyarteritis nodosa and what is seen?
FBC- high WCC HBV serology ESR and CRP high MRA- shows string of pearls appearance due to micoraneurysms and spasm renal biopdy might show transmural inflammation and necrosis
88
how is polyarteritis nodosa managed?
prednisolone and if its severe then a DMARD

Year 3 (104 decks)

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