COLA lectures Flashcards
What is the recommended treatment for molluscum contagiosum?
Imiquimod cream (TLR 7 agonist) intralesional candida also helps
what is the itchy rash people get on their scapulae
notalgia paresthetica
what commonly misdiagnosed skin rash looks like a combination of eczema and acne
perioral dermatitis
steroids make it worse hugs up against the nares
erythema multiforme - typical presentation
21 year old M with targetoid lesions on hands
do not treat with oral steroids, can make the HSV relapse
what distribution does CTCL (mycosis fungiodes) typically present with
bathing suit distribution
classic drugs for fixed drug eruptions
NSAIDs, antibacterials
what condition should you consider in older people with hives?
bullous pemphigoid - starts out with urticarial phase
on IF, what antibodies do you look for with bullous pemphigoid
IgG against BP180 and IgG to BP230
BP stands for “bullous pemphigoid”
what topical steroid is best to use if patient is sensitized on patch testing to other steroids
desoximetasone (class C in general)
What level of eosinophils is considered hypereosinophilia
>1500
what herbal supplement can cause eosinophilia
tryptophan
What are some good initial labs for HES
CBC/diff
CMP
ESR
IgE
What is a good mnemonic for eosinophilia causes?
NAACP
neoplastic
allergic disease
adrenal disease
connective tissue problems
parasites
What key mutation/fusion do folks with chronic eosinophilic leukemia have (know for boards)
FIP1L1-PDGFRa
what are the pathological features in EGPA (eosinophilic granulomatosis with polyangiitis)?
What did this disease used to be called?
formerly known as Churg-Strauss
systemic small vessel vasculitis
granulomatosis
eosinophilia
positive ANCA (40-60% of cases)
other organ involvement - lung, skin, sinus, CV, GI, renal, CNS
ASTHMA IS ALMOST ALWAYS SEEN
What are the CSS diagnostic criteria for EGPA?
4/6 of the following
asthma
eosinophilia
mononeuropathy or polyneuropathy
transient pulmonary opacities
paranasal sinus abnormality
biopsy showing vasculitis
What are the major parasites causing eosinophilia in the US
strongyloides (southern states, hot/humid) - bad reaction with systemic steroids
toxocara (can also be in cat and dog feces) - visceral larva migrans
ascaris (SE US)
hookworm (rare)
trichinella (hunting, eating wild meats)
For hypereosinophilia - what parasites WON’T show up on O+P
strongyloides
trichinella
toxocara
bolded are key titers for the US
wuchereria bancrofti
schistosoma
eichinococcus
HES
1500 eos - 2 or more readings >1 month part
(DONT WAIT 6 MONTHS ANYMORE)
no identifiable cause
organ involvement
For HES, what mutation might persuade you to prescribe what special medication?
FIP1L1-PDGFRa
particularly responsive to imatinib (Gleevec)
what are omabs derived from
mice
what are “zimabs” and “zumabs” derived from
chimeric and humanized monoclonal antibodies
what are “mumabs” derived from
human monoclonal antibodies
Review the WTF-umabs
list indications for treatment with omalizumab
note: approved for kids >= 6
note: does not actually affect lung function test
which biologics (2) bind to IL-5?
which biologic (1) binds to IL-5R
mepolizumab (12+, increased risk of zoster), reslizumab (18+, IV only, eos >= 400)
benralizumab (eos should be >= 300)
what is the eosinophilia IL?
IL-5, hence efficacy of anti-5 biologics for eo-driven processes
review summary of targets for biologics, including some that are not FDA approved for use
which biologic is approved for nasal polyposis
which biologic is approved for atopic dermatitis
dupixent
dupixent - may be associated with allergic conjunctivitis when given for this reason
which biologic commonly used by allergists is approved for a rheumatologic indication
what other allergic problem might it be used for (compassionate use)
Mepolizumab - steroid-sparing option for EGPA (Churg-Strauss)
hyper IgE
what is UNC93B important for (innate immunity)
endosomal localization of toll-like receptor
all TLRs bind to MDY88 except one, what is it? What does it bind to
the exception is TLR3. It binds to TRIF
what is the major clinical relevance of this slide on TLR
because of the nature of the defects, no inflammation even with serious infections
what immune problems can NLR2 mutation cause
Crohn disease, Blau syndrome
ok, I’ll bite. WTF is Blau Syndrome
Blau syndrome — Blau syndrome (MIM #186580, also called juvenile systemic granulomatosis) is an autosomal dominant condition characterized by granulomatous inflammation of the skin, eye, and joints [29,30]. Patients exhibit a papular erythematous rash, sometimes only transiently. Arthritis develops in the first decade of life, often as minimally symptomatic swelling in wrists, ankles, knees, and/or elbows with progressive flexion contractures of the fingers (camptodactyly). Biopsy usually reveals synovial granulomas. Granulomatous uveitis may also occur and can lead to glaucoma and blindness. Atypical manifestations include fever, cranial neuropathies, arteritis, and granulomatous involvement of visceral organs [31].
Blau syndrome is due to mutations in NOD2 (nucleotide-binding oligomerization domain protein 2, also called caspase recruitment domain-containing protein 15 [CARD15] or inflammatory bowel disease 1 [IBD1]). These mutations in NOD2 are distinct from those in the same gene seen in some cases of Crohn disease, another disease of granulomatous inflammation, and appear to promote spontaneous activation of the protein [32,33]. NOD2 has several potential functions, including mediating responsiveness to the bacterial cell wall component muramyl dipeptide, activating nuclear factor (NF) kappa B, and regulating apoptosis. The role of interleukin-1 beta (IL-1beta) overproduction is controversial [34,35]. Mutations in NOD2 underlie most case of what was previously termed early-onset sarcoidosis [36,37]. At least four asymptomatic carriers of the disease-related mutation have been reported [38].
An international registry of patients with pediatric granulomatous arthritis, including Blau syndrome and early-onset sarcoidosis, has been established to advance the study of this syndrome [39].
what general molecular problem do NLRP (inflammasome) problems lead to
too much IL1-Beta
associated with gout, pseudogout, MEF, cryopyrin associated periodic syndromes
generally can be treated with 1L1 beta antagonists
What do your cytosolic DNA sensors (CDSs) do
fight viruses with STING pathway (stimulator of interferon gamma)
what are ILC1 cells and what transcription factor produces them
ILC1 cells - innate lymphoid cells that fight virus (interferon gamma). like NK cells
produced by T-Bet
What transcription factor brings about IL2 cells
GATA-3
produce IL-5, IL-13
What transcription factor brings about IL3 cells
RORgammat
IL-17
what receptor helps NK cells turn on for ADCC
CD16/FcGammaRIIIA
