COLA lectures Flashcards by Jack McDonnell

What is the recommended treatment for molluscum contagiosum?

Imiquimod cream (TLR 7 agonist) intralesional candida also helps

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what is the itchy rash people get on their scapulae

notalgia paresthetica

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what commonly misdiagnosed skin rash looks like a combination of eczema and acne

perioral dermatitis

steroids make it worse hugs up against the nares

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erythema multiforme - typical presentation

21 year old M with targetoid lesions on hands

do not treat with oral steroids, can make the HSV relapse

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what distribution does CTCL (mycosis fungiodes) typically present with

bathing suit distribution

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classic drugs for fixed drug eruptions

NSAIDs, antibacterials

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what condition should you consider in older people with hives?

bullous pemphigoid - starts out with urticarial phase

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on IF, what antibodies do you look for with bullous pemphigoid

IgG against BP180 and IgG to BP230

BP stands for “bullous pemphigoid”

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what topical steroid is best to use if patient is sensitized on patch testing to other steroids

desoximetasone (class C in general)

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What level of eosinophils is considered hypereosinophilia

>1500

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what herbal supplement can cause eosinophilia

tryptophan

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What are some good initial labs for HES

CBC/diff

CMP

ESR

IgE

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What is a good mnemonic for eosinophilia causes?

NAACP

neoplastic

allergic disease

adrenal disease

connective tissue problems

parasites

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What key mutation/fusion do folks with chronic eosinophilic leukemia have (know for boards)

FIP1L1-PDGFRa

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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

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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

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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**