COLA lectures Flashcards

1
Q

What is the recommended treatment for molluscum contagiosum?

A

Imiquimod cream (TLR 7 agonist) intralesional candida also helps

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2
Q

what is the itchy rash people get on their scapulae

A

notalgia paresthetica

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3
Q

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

A

perioral dermatitis

steroids make it worse hugs up against the nares

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4
Q

erythema multiforme - typical presentation

A

21 year old M with targetoid lesions on hands

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

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5
Q

what distribution does CTCL (mycosis fungiodes) typically present with

A

bathing suit distribution

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6
Q

classic drugs for fixed drug eruptions

A

NSAIDs, antibacterials

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7
Q

what condition should you consider in older people with hives?

A

bullous pemphigoid - starts out with urticarial phase

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8
Q

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

A

IgG against BP180 and IgG to BP230

BP stands for “bullous pemphigoid”

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9
Q

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

A

desoximetasone (class C in general)

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10
Q

What level of eosinophils is considered hypereosinophilia

A

>1500

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11
Q

what herbal supplement can cause eosinophilia

A

tryptophan

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12
Q

What are some good initial labs for HES

A

CBC/diff

CMP

ESR

IgE

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13
Q

What is a good mnemonic for eosinophilia causes?

A

NAACP

neoplastic

allergic disease

adrenal disease

connective tissue problems

parasites

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14
Q

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

A

FIP1L1-PDGFRa

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15
Q

what are the pathological features in EGPA (eosinophilic granulomatosis with polyangiitis)?

What did this disease used to be called?

A

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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16
Q

What are the CSS diagnostic criteria for EGPA?

A

4/6 of the following

asthma

eosinophilia

mononeuropathy or polyneuropathy

transient pulmonary opacities

paranasal sinus abnormality

biopsy showing vasculitis

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17
Q

What are the major parasites causing eosinophilia in the US

A

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)

18
Q

For hypereosinophilia - what parasites WON’T show up on O+P

A

strongyloides

trichinella

toxocara

bolded are key titers for the US

wuchereria bancrofti

schistosoma

eichinococcus

19
Q

HES

A

1500 eos - 2 or more readings >1 month part

(DONT WAIT 6 MONTHS ANYMORE)

no identifiable cause

organ involvement

20
Q

For HES, what mutation might persuade you to prescribe what special medication?

A

FIP1L1-PDGFRa

particularly responsive to imatinib (Gleevec)

21
Q

what are omabs derived from

A

mice

22
Q

what are “zimabs” and “zumabs” derived from

A

chimeric and humanized monoclonal antibodies

23
Q

what are “mumabs” derived from

A

human monoclonal antibodies

24
Q

Review the WTF-umabs

A
25
Q

list indications for treatment with omalizumab

A

note: approved for kids >= 6
note: does not actually affect lung function test

26
Q

which biologics (2) bind to IL-5?

which biologic (1) binds to IL-5R

A

mepolizumab (12+, increased risk of zoster), reslizumab (18+, IV only, eos >= 400)

benralizumab (eos should be >= 300)

27
Q

what is the eosinophilia IL?

A

IL-5, hence efficacy of anti-5 biologics for eo-driven processes

28
Q

review summary of targets for biologics, including some that are not FDA approved for use

A
29
Q

which biologic is approved for nasal polyposis

which biologic is approved for atopic dermatitis

A

dupixent

dupixent - may be associated with allergic conjunctivitis when given for this reason

30
Q

which biologic commonly used by allergists is approved for a rheumatologic indication

what other allergic problem might it be used for (compassionate use)

A

Mepolizumab - steroid-sparing option for EGPA (Churg-Strauss)

hyper IgE

31
Q

what is UNC93B important for (innate immunity)

A

endosomal localization of toll-like receptor

32
Q

all TLRs bind to MDY88 except one, what is it? What does it bind to

A

the exception is TLR3. It binds to TRIF

33
Q

what is the major clinical relevance of this slide on TLR

A

because of the nature of the defects, no inflammation even with serious infections

34
Q

what immune problems can NLR2 mutation cause

A

Crohn disease, Blau syndrome

35
Q

ok, I’ll bite. WTF is Blau Syndrome

A

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].

36
Q

what general molecular problem do NLRP (inflammasome) problems lead to

A

too much IL1-Beta

associated with gout, pseudogout, MEF, cryopyrin associated periodic syndromes

generally can be treated with 1L1 beta antagonists

37
Q

What do your cytosolic DNA sensors (CDSs) do

A

fight viruses with STING pathway (stimulator of interferon gamma)

38
Q

what are ILC1 cells and what transcription factor produces them

A

ILC1 cells - innate lymphoid cells that fight virus (interferon gamma). like NK cells

produced by T-Bet

39
Q

What transcription factor brings about IL2 cells

A

GATA-3

produce IL-5, IL-13

40
Q

What transcription factor brings about IL3 cells

A

RORgammat

IL-17

41
Q

what receptor helps NK cells turn on for ADCC

A

CD16/FcGammaRIIIA

42
Q
A