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key points AI diseases Flashcards

1
Q

SS primary

A

no CT disease

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2
Q

SS triad

A

exocrinopathy - dryness mouth and eyes
fatigue
joint pain

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3
Q

SS epidemiology

A

usually 40-60yrs

F

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4
Q

SS aetiology

A

infections
biological factors
chemical
genetic - HLA association

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5
Q

SS proposed immunopathogenic mechanisms

A 
microbial trigger
destroys SG epithelium
autoantigens
differentiation of B cells into plasma cells
auto-ABs form complex with auto Ags
captured by DCs - T1 interferon
activation of cytotoxic CD8

innate and adaptive

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6
Q

oral S+S SS

A 
salivary hypofct
caries
fungal infections
oral trauma
lip dryness
orofacial pain
dysphagia
dysgeusia
swollen SGs
GORD
oral lesions of AI aetiology
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7
Q

SS systemic manifestations

A 
30-40%
constitutional
LNs
renal - interstitial nephritis
articular - arthralgias
cutaneous
peripheral neuropathy
muscular - myositis
pulmonary
glandular
CNS
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8
Q

SS ESSDAI

A

clinical index to measure disease activity in pts w primary SS
each has a weighting - give score depending on severity

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9
Q

SS salivary hypofct/dysfct

A

diminished secretions on palpation
thicker/opaque/viscous secretions
recurrent SG infection
enlarged SGs in 30% (parotid)

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10
Q

SS caries

A

hyposalivation - reduced IgA secretion
- AB responsible for oral mucosal immunity that prevents caries
saliva in pSS not effective buffer
cervical and other atypical sites e.g. lingual surface, incisal edge and cusps

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11
Q

what fungal infection is prevalent in SS?

A

candidiasis

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12
Q

SS AI/immunomediated lesions

A

oral LP/lichenoid lesions
RAS
MMP
PV

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13
Q

secondary SS

A 
when pt already has another AI disease then presents with extreme dryness of the eyes and mouth
CT disease (SLE, RA, systemic sclerosis)
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14
Q

SS eye

A 
dry eye
extraglandular ocular complications
 - corneal inflammation
 - conjunctival inflammation
 - uveitis
 - scleritis/episcleritis
 - optic neuritis
 - retinal vasculitis
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15
Q

SS autoABs

A

anti-SSA ABs - antiRo
anti-SSB ABs - antiLa
present in 2/3 pts

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16
Q

SWSF >0.7ml/min

A

normal/mild dysfct
non-pharmacological stimulation
(saliva subs/pharmacological stimulation)

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17
Q

SWSF 0.1-0.7ml/min

A

mod dysfct
non-pharmacological/pharmacological stimulation
(saliva substitutes)

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18
Q

SWSF <0.1ml/min

A

severe dysfct

saliva substitutes

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19
Q

SS classification criteria - American College of Rheumatology/European League against Rheumatism
inclusion criteria

A

≥1
daily, persistent, troublesome dry eyes >3m?
recurrent sensation sand/gravel in eyes?
use tear substitutes ≥3 times daily?
daily feeling of dry mouth for >3m?
freq drink liquids to aid swallowing dry food?

or when suspicion of SS from EULAR SS DAI (≥1 positive)

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20
Q

SS classification criteria - American College of Rheumatology/European League against Rheumatism exclusion criteria

A 
history of H+N radio
active Hep C
AIDS
sarcoidosis
amyloidosis
GvHD
IgG4-related disease
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21
Q

SS classification criteria - American College of Rheumatology/European League against Rheumatism - what do you need to score?

A

meet inclusion criteria
no exclusion criteria
score ≥4

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22
Q

SS classification criteria - American College of Rheumatology/European League against Rheumatism - scoring

A 
biopsy - 3
antiSSA/Ro + - 3
ocular staining score ≥5 - 1
schirmer's test ≤5mm/min - 1
UWSF ≤0.1ml/min - 1
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23
Q

biopsy requirements SS

A

labial SG with focal lymphatic sialadenitis and focus score of ≥1 foci/4mm2
- ≥1 dense aggregates of ≥50 lymphocytes usually located in perivascular or periductal locations

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24
Q

biopsy technique SS

A

≥5 minor glands, L lip in paramedian region, incision parallel to labial frenum, identify minor gland, lift, remove, suture

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25
Q

SS non-pharmacological stimulation

A

gustatory stimulants: SF acidic candies, lozenges

mechanical stimulants: SF chewing gum

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26
Q

SS caries prevention

A 
freq recall 4-6m
OH
F
non-F remineralising agents
salivary stimulation
AM agents e.g. CHX
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27
Q

why is pilocarpine not always possible?

A

salivary residual secretory capacity needed - still need fct parenchyma

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28
Q

pilocarpine dose

A

5mg lozenges

3-6 daily

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29
Q

pilocarpine contraindications

A 
uncontrolled asthma/COPD
uncontrolled cardiorenal disease
narrow-angle closure glaucoma
gall bladder stones
acute iritis
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30
Q

main primary sites of lymphoma in primary SS

A 
SALIVARY GLANDS (parotid)
lungs, gastric, ocular, oral/ENT, spleen
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31
Q

lymphoma risk in SS

A 
risk of haematological malignancy
most B-cell origin
3 subtypes
 - MALT lymphoma
 - DLBCL
 - MZL
small number get non-B-cell haematological cancers - myeloid leukaemia, Hodgkin disease or T/NK cell lymphoma

test regularly (1-2yrs, high risk 6m)

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32
Q

SS risk factors for lymphoma

A 
recurrent swelling of parotid glands
splenomegaly/lymphadenopathy
purpura
> on ESSDAI
RF
cryoglobulinaemia
low C4 level
CD4 T-cell lymphocytopenia
presence of ectopic germinal centres
focus score of >3
germinal mutations in TNF AIP3
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33
Q

SS tx

A

inhibit proinflammatory cytokines - infliximab
interfere w T1 interferon production - hydroxychloroquine
immunobiologics - rituximab, infliximab

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34
Q

sicca syndrome

A

partial SS findings

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35
Q

American European Consensus Group Revised International Criteria SS

A 
1 - dry eyes subjective
2 - dry eyes objective
3 - dry mouth subjective
4 - dry mouth objective
5 - autoAB findings
6 - histopathology

≥4 positive criteria (must inc 5 and/or 6)

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36
Q

T1 hypersensitivity

A

IgE - anaphylaxis

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37
Q

T2 hypersensitivity

A

IgG/M - cytotoxic - AgAB

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38
Q

T3 hypersensitivity

A

IgG/M - immune complex deposition (Ag-Ab)

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39
Q

T4 hypersensitivity

A

T cell mediated (delayed type)

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40
Q

what type of blister is pemphigus?

A

intraepithelial

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41
Q

what hypersensitivity reaction is pemphigus?

A

T2 - cytotoxic
Ag-Ab reaction - destruction of desmoglein
damage to LP
IgG Abs form

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42
Q

pemphigus HP

A

take perilesional biopsy of area not ulcerated/blistered - as won’t have epithelium in ulcer
acantholysis
suprabasal split
tzank cells
basal cells still fully attached by hemidesmosomes

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43
Q

acantholysis

A

spaces between spinous cells

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44
Q

tzank cells

A

in pemphigus

epithelial cells fall off into blister/bullae

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45
Q

DIF

A

tissue biopsy
usually for diagnosis
AB and fluorophore

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46
Q

IIF

A

serum
usually to measure ABs but can be used for diagnosis
can monitor progress and response to therapies
unlabelled Ab (primary) and supporting Ab with fluorophore (secondary)

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47
Q

positive DIF pemphigus

A

basket weave pattern
reflect where you get Ag-Ab reaction
grey areas - intraepithelial split/cleft
desmosomes

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48
Q

positive DIF pemphigoid

A

linear pattern

in hemidesmosomes - basal cell layer

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49
Q

what type of blister is pemphigoid?

A

subepithelial

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50
Q

what type of hypersensitivity reaction is pemphigoid?

A

T2

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51
Q

pemphigoid HP

A

sub basal split
no acantholysis or tzank cells
LP shows inflammation - inflammatory cells
eosinophils characteristic of bullous pemphigoid not so obvious in MMP

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52
Q

why do many diseases affect both skin and oral/genital mucosa?

A

they share many common antigens and epitopes
antigens - provoke immune response but epitope binds
epitopes - part of Ag that binds to Ab

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53
Q

general pathogenesis of AMBDs

A 
auto-AB attack on skin components causing loss of cell-cell adhesion
 - desmosomes
 - hemidesmosomes (basal cell layer)
split/cleft forms in skin
 - fills with inflammatory exudate
 - vesicle (<5mm)/bulla (>5mm)
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54
Q

SS histology minor gland

A 
focal lymphocytic sialadenitis
acinar loss
fibrosis
focal collections of lymphocytes (50+)
 - ≥1 collection per 4mm2
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55
Q

SS histology major gland

A

lymphocytic infiltrate, extends to whole lobules
epithelial hyperplasia of duct (myoepithelial islands) eventually occludes
atrophy of acini

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56
Q

pemphigus pathogenesis

A 
autoABs against desmoglein
intraepithelial blister
acantholysis
autoABs deposited in epithelium
anti-Dsg3 IgF
complement activated and plasmin
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57
Q

pemphigus classification

A 
vulgaris
foliaceous
drug-induced
paraneoplastic
IgA
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58
Q

age pemphigus

A

40-60s

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59
Q

pemphigus foliaceous

A

superficial form - skin
lacks mucosal involvement
anti-Dsg1
oral lesions rare

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60
Q

pemphigus prognosis

A

untxed often fatal - metabolic consequences, dehydration/infection
mucosal lesions may persist after skin controlled
- topical CS/tacrolimus
now often complications of tx major cause of death - CS, MAbs

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61
Q

pemphigus mucosal features

A

progressive - typically begins oral cavity, can spread to skin
oral cavity
- anywhere
- non-healing erosions/ulcers, rarely see intact blisters
- desquamative gingivitis
- yellow fibrinous slough
- painful, plaque irritates lesions
- easily peel off - haemorrhagic erosion
- spongiosis
- no scarring

62
Q

pemphigus diagnosis

A

DIF - basket weave/fishnet like pattern in epithelium
- IgG, C3, IgM, IgA (variant)
IIF - high % positive
- IgG, C3, IgM, IgA
histopathology - intraepithelial blisters

63
Q

pemphigus tx

A

CS
adjuvant CS sparing agents
CHX 0.12% alcohol free rinse

anti-mycotic agents
triamcinolone injections

advanced therapeutic options

  • IVIgG
  • rituximab (anti-CD20)
  • anti-TNFa
  • plasmapheresis
  • immunoadsorption
64
Q

pemphigoid epidemiology

A

> 75s

rare

65
Q

pemphigoid pathogenesis

A

autoABs against hemidesmosomes
complement, leukocytes, BM damage
subepithelial blister

66
Q

pemphigoid clinical

A 
bullae/vesicles
 - often blood filled
erosions/ulcers
 - yellow fibrinous slough
desquamative gingivitis
67
Q

MM pemphigoid

A

mostly mucosae
20% skin
HP/SP, uvula, gingivae

68
Q

bullous pemphigoid

A

skin (flexor)

oral 20%

69
Q

cicatritial pemphigoid

A

scarring

70
Q

pemphigoid diagnosis

A 
DIF - linear pattern - u or n serrated
 - deposition along BMZ
 - IgG, C3, IgA
IIF salt split (NaCl scissors at lamina lucida)
 - IgG
HP - subepithelial blister
71
Q

pemphigoid tx

A

low risk - oral +/- limited skin - topical CS
high risk - diffuse and progressive oral mucosa, ocular, genital, oesophageal, laryngeal
CS +/- azathioprine etc
IVIgG/rituximab (partial response/progressive)

72
Q

diagnosis of AMBDs

A 
Nikolsky sign
biopsy
need immunologic signal to confirm
DIF
IIF
ELISA
73
Q

Nikolsky sign

A

marginal - next to blister
direct - healthy skin
induce erosion by rubbing on skin

74
Q

DIF

A

oral mucosa, detect tissue bound immunodeposits

75
Q

IIF

A

pts sera

detect circulating IgG autoABs

76
Q

ELISA

A

detect anti-Dsg ABs

77
Q

why is early diagnosis of AMBDs essential?

A 
may not be AMBDs
prevent mucosal spread
prevent MC spread
mucosal scarring phenotype of MMP
 - oesophageal stricture
 - eye scarring - blindness
78
Q

PAMS

A 
MC syndrome
heterogeneous S+S
 - desquamative stomatitis
 - polymorphous cutaneous eruption
 - progressive resp failure
underlying malignancy
79
Q

pathogenesis of PAMS

A

cancer cells activate wide number of immune cells - activated autoreactive T cells induce both humoral and cell mediated immunity

80
Q

PAMS spectrum

A

humoral immunity —– cell mediated immunity

acantholysis, bronchiolitis obliterans, lichenoid dermatitis

81
Q

PAMS spectrum similar to oral diseases

A

humoral immunity —- cell mediated immunity

pemphigus, bullous pemphigoid, EM like, GvHD like, lichenoid/LP like

82
Q

what is the major antigenic target in PAMS?

A

plakins

- desmoplakin 1 and 2, envoplakin, periplakin, plectin, BP230

83
Q

lesions in PAMS?

A

ocular
lip
oral

84
Q

what is the key thing to do in PAMS?

A

detect a neoplasm

tx of malignancy essential but not always sufficient to tx PAMS

85
Q

AMBDs

A

Ig-mediated diseases with autoantibodies against desmosomal or BM zone molecules

86
Q

PAMS suggested criteria

A

clinical signs
- severe stomatitis, blisters, LP like plaques, bronchiolitis obliterans
HP
DIF
IIF
detection of circulating auto-ABs - envoplakin/periplakin
detection of a neoplasm

87
Q

what BPs are the target in pemphigoid?

A

BP180

BP230

88
Q

Behcet disease triad

A

oral ulcers
genital ulcers
uveitis

89
Q

Behcet disease - what is now recognised along with the triad?

A

involvement of most organ systems recognised
systemic vasculitis
often delayed diagnosis

90
Q

what is Behcet disease known as and why?

A

silk road disease

more common in people of this bloodline

91
Q

Behcet disease pathogenesis

A

disruption of innate immunity
disruption of adaptive immunity
AB dependent cellular cytotoxicity to oral epithelium
hypercoagulability
autoABs deposited around blood vessel walls

92
Q

Behcet disease aetiology

A 
genetic predisposition - HLA B51 association
env factors
 - HSV
 - s sanguis
 - pollutants
93
Q

Behcet disease clinical manifestations

A 
oral aphthous ulcers
genital lesions
ocular lesions
skin lesions - palpable purpura, SC nodules
vasculitis

can be more extensive

94
Q

Behcet disease pathargy test

A

needle prick (SC puncture)
24-48hrs
exaggerated inflammatory reaction
- pustule/nodule forms

95
Q

Behcet disease diagnosis

A

difficult
no lab test
mostly clinical
history key

96
Q

Behcet disease - consensus classification of paediatric Behcet disease

A

recurrent oral aphthosis ≥3 a
genital ulceration and aphthosis
skin - necrotic folliculitis, acneform lesions, erythema nodosum
ocular - uveitis, retinal vasculitis
neurological signs (not isolated headaches)
vascular signs - venous thrombosis, arterial thrombosis/aneurysm

score ≥3

97
Q

Behect disease tx

A 
CS
topical
colchicine
azathioprine
biologic therapies
98
Q

what is the most common manifestation of Behcets?

A

oral aphthous ulcers 90-100%

99
Q

Behcet disease differential diagnoses

A 
RAS
infections
skin diseases
Crohns
SJS
pemphigoid
pemphigus
SLE
IBD
sarcoidosis
100
Q

SLE what is it?

A

AI multisystem disorder
CT disease
almost all tissues and organs
systemic inflammation and tissue damage

101
Q

SLE antibody

A

ANA+

102
Q

SLE epidemiology

A

more F

103
Q

SLE contributing factors

A 
genetic predisposition
env
 - smoking, UV, EBV, exposure to silica dust, petroleum, organic solvents and mineral oils
hormonal
epigenetic
immunoregulatory factors
104
Q

SLE manifestations

A 
constitutional - fatigue and fever
renal - lupus nephritis
CV - pericarditis
MS - arthritis/arthropathy
neuropsychiatric
pulmonary
GI
ocular
cutaneous
105
Q

types of cutaneous lupus

A

chronic/discoid cutaneous
subacute cutaneous
acute cutaneous

106
Q

discoid/chronic cutaneous lupus

A

most common clinical manifestation of cutaneous lupus
disk lesions - plaques, scar
scarring alopecia
dsDNA+
oral mucosa - OLLs 25% (mainly HP)
oral DLE is an OPMD but malignant transformation is extremely rare

107
Q

subacute cutaneous lupus

A

erythematous macules/papules, evolve into either
- scaly papulosquamous psoriasiform lesions
- annular patches and plaque
oral lesions rare, similar to discoid
healing - post-inflammatory hyper and/or hypopigmentation, greyish atrophic scarring and telangiectasias

108
Q

acute cutaneous lupus

A 
can be 1st sign of SLE - preceding onset of systemic disease by weeks/months
malar/butterfly rash - erythematous
oral lesions - ulcerations
 - mainly HP
 - intense erythema +/- petechiae
also when your systemic lupus is active
109
Q

SLE lab testing

A

+ANA
mandatory entry criterion - 99% cases present
v high sensitivity but limited specificity (occur in other CT diseases)
anti-SM and anti-dsDNA highly specific, less sensitive

110
Q

SLE oral manifestations

A 
oral mucosa
 - ulcerations
 - LLs
 - erythematous lesions
 - leukoplakias
 - petechiae
 - cheilitis with erythema
salivary gland
 - low flow rate (associated with SS)
caries
TMJ involvement
PDDs
111
Q

SLE classification criteria (not diagnostic)

A

entry criterion ANA titre ≥1:80
additive criteria
- don’t count if more likely explanation than SLE
- one occasion sufficient
- don’t need to occur simultaneously
- need ≥1 clinical criterion and ≥10 points
- in each domain count only highest criterion

112
Q

SLE pharmacological tx

A 
based on pt manifestations
CS - prednisolone
hydroxychloroquine
immunosuppressive e.g. azathioprine
NSAIDs for MS pain
drugs targeting B cells: rituximab
113
Q

SLE and cancer

A 
slight increase in cancer risk overall
haematologic (lymphoma, leukaemia, MM), NHL, H+N cancer
possible factors mediating risk
 - lupus-related meds e.g. cyclophosphamide
 - inherent immune system abnormalities
 - overlap with SS
 - viral infections e.g. HPV/EBV
 - traditional cancer RFs e.g. smoking
114
Q

what oral effect can hydroxychloroquine cause?

A

oral pigmentation

115
Q

SLE and lichenoid oral reactions

A

central atrophic/shallow erosions with white striae at margins
often patchy and unilateral
may be on HP (usually spared by OLP)

116
Q

EM - what is it?

A

vasculitic AI disease
acute immune-mediated inflammatory MC disease
triggered by hypersensitivity reactions to various antigens with a tendency to recur
can affect MM and skin

117
Q

EM epidemiology

A

usually young adults

118
Q

EM pathogenesis

A

T3 hypersensitivity reaction

  • form Ag-Ab complex in circulation
  • deposit of immune complex in bv’s
  • appearance of inflammatory reaction with subsequent vasculitis
119
Q

EM causes

A

INFECTIONS and DRUGS

120
Q

EM - what is the most commonly identified cause?

A

HSV infection

121
Q

what is the most common cause of EM in kids?

A

mycoplasma pneumoniae infection

122
Q

EM - drugs that can cause it

A 
ABs
sulfonamides
antiepileptics
barbituates
NSAIDs
123
Q

other conditions that can cause EM

A

IBD
malignancy
menstruation

124
Q

DIEM immunology

A

no IFNy but have TNFa
produced by macrophages, which along with perforin and granzyme B, will induce keratinocytes apoptosis with subsequent epithelial destruction

125
Q

EM subtypes

A

isolated
recurrent
persistent

126
Q

HAEM

A

7-21 days after primary or recurrent viral infection
- HSV DNA engulfed
- migrate to epidermis to transfer these antigens to keratinocytes
- expression leads to activation of HSV specific CD41 Th1 cells, which produce IFNy
epithelial damage

127
Q

isolated EM

A

occurs just once

- infections, drugs

128
Q

recurrent EM

A

freq occurrence of EM over a period of years, usually >6 episodes p.a.
- infections, menstruation

129
Q

persistent EM

A

continuous occurrence of typical and atypical lesions without interruption
- IBD, infections, malignancy

130
Q

clinical forms of EM

A

minor

major

131
Q

minor EM

A

skin <10% BSA
mucosa uncommon, 1 site only, usually oral
usually target lesions/bullae

132
Q

major EM

A

skin <10% BSA
mucosa ≥2 sites
usually begins with starting a new drug or HSV
myalgias, sore head, throat and fever
spreads to mouth, upper resp tract, GIT, then kidneys and joints

133
Q

HAEM cause

A

HSV 1 or 2

134
Q

HAEM course

A

no/mild prodromal S+S
acute
self-limiting
recurrent

135
Q

HAEM site

A

skin

minimal mucosal

136
Q

HAEM histology

A

focal keratinocyte necrosis, edema, predominant mononuclear infiltration CD4+

137
Q

HAEM cytokine

A

IFNy

138
Q

DIEM cause

A

drugs

139
Q

DIEM course

A

flu-like prodrome
acute
self-limiting
not recurrent

140
Q

DIEM site

A

skin and mucosa

141
Q

DIEM histology

A

extensive keratinocyte necrosis, less edema, prominent mononuclear infiltration CD4+

142
Q

DIEM cytokine

A

TNFa

143
Q

typical target lesion EM

A

central blister
edematous ring
erythematous border

144
Q

atypical target lesion EM

A

raised, edematous lesion with two zones of colour change and a poorly defined border

145
Q

oral lesions EM

A

small ulcers to widespread huge erosive lesions
can lead to pts not being able to eat, speak or open mouths
precede lesions in other SSE
diffuse and widespread macules - blisters - ulceration
lips swollen, cracked/crusted
usually lips and anterior mouth

146
Q

EM skin lesions

A

commonly distal extremities of extensor surfaces (arms, legs, elbows, knees, dorsum of hands and feet)
lesions symmetric, round, slightly pruritic, may evolve into papules
some lesions may form the large annular (ring shaped) target lesions, the dark centre of it being a necrotic ulcer

147
Q

EM diagnosis

A 
no standardised criteria
clinical history
clinical exam
biopsy (skin) - HandE, DIF
lab studies - test for ESR, WCC, LFT, electrolytes
 - IIF to rule out AI blistering disease
148
Q

EM diagnosis - clinical history

A

acute, episodic, self-limiting
symptoms of HSV, mycoplasma pneumoniae and other infections
thorough meds history (often started 2-3 days prior)

149
Q

EM diagnosis - clinical exam

A

skin lesions: typical, atypical

morphology: pleomorphic appearance of oral lesions
location: lips and anterior mouth
- erythematous, erosions, fibrin, haemorrhagic

150
Q

EM tx

A

tx underlying infection/medication
symptomatic tx - clinical severity
- prevent infections and local symptom control
mild: topical antiseptics, antihistamines, analgesics, topical CS
MM: high potency CS gel, oral anaesthetic solutions, topical ophthalmic preparations
severe mucosal: 40-60mg prednisolone, taper 2-4wks
recurrent: 6m trial of continuous antiviral therapy

Oral medicine (14 decks)

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