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Allergy and Immunology > skin > Flashcards

skin Flashcards

1
Q

diagnostic criteria for eczema

A

evidence pruritic skin

PLUS 3 of

  1. Crease involvement
  2. Dry skin
  3. Visible dermatitis
  4. asthma or seasonal AR of fmhx (if <4yo)
  5. less then 2yo
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2
Q

acute vs chronic findings in AD

A

acute - pruritic erythematous papulovesicular excoration serous exudate

CD - lichenification, fibrotic ppaule and excoraite

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3
Q

name 6 genetic changes inc risk of AD

A 
spink5,
flg
stat3
dock 8
was
foxp3
loss of fxn of tlr9, myd88
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4
Q

list 4 functions of filaggrin

Filaggrin levels are diminished in AD due to:
• Mutations in the FLG gene
• Th2 cytokines down-regulating FLG expression

A

1) prevent transepidermal water loss
2) natural moisterizing factor
3) anti staph activity
4) UV protection
5) acidification

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5
Q

cytokines in acute vs chronic AD

A

Il4,13

chronic il512 and intfergon gamma

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6
Q

all slit therapy prescriptions and age

A

grasstek 5-65
2800 BAU

oralair 5-50
100IU, 200IU and 300IU

ragwitech
18-50, 12 amb aa IU

acarizax
18-65 12 SQ HDM

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7
Q

five immunoregulatoary abnormalities in AD

A

inc IGE
inc in food allergen

inc CD23 in B cell
inc expression of FcepR1
inc CTACK and TARC (bring t cell to skin)

inc il4,13,5 and decreased inferferon gamma by Th1

dec T reg after superantigen stimulation
dec antimicrobial peptide by keratinocyte
inc level cAMP with inc IL10 and pge2

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8
Q

name 7 trigger of AD

A

irritant (disinfectant, wool)
contact and aero allergen (pollem animal nickel dust mite

micornbial agent (staph viral infxn yeast

other: food, stress, climate, hormone and vaccine

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9
Q

name 5 bugs assoc with AD

A 
staph aurues
eczema herpticum
mollsucum contagioisum
HPV 
coxsackie

fungal: malassezia furfur

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10
Q

how much does 1g cover of steroids

A 
10 x 10cm
group 1-7
mild HC1%
mld med hydroval
med bethamesone valerate 0.05
med high betamethasone velaerte .1%
high lyderm, mometasone
very high clobetasol or betamethasone diproprionate
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11
Q

ddx for AD

A 
DDx
Other dermatitis: seborrheic, nummular, ICD, lichen simplex, asteatotic (scaly fissuered pathces on lower leg)
ID: dermatohpyte, impetigo, scabies
Congeintal: HIES, WAS, Omenn, IPEX, PGM3
Keratinization: ichthyosis, netherton
Nutrition: zinc
Neoplastic CTCL
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12
Q

skin indviduals with AD are deficient in:

A

ceramides (lipid molecule)

microbial antipeptides - cathelicidins

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13
Q

what are some pretanal things showed to reduced asthma

A

Prenatla RF for easly asthma is aternal smoking, use of abx and c/s
Pretnal diet: higher fish intake during pregnnacy and prenatal vit E and zinc
The il4,5, 9 and 13 with IgE → histamine and cytesinyl leukotriene

Later RF is sensitiziation, tobacco smoke, breastfeeding, dec lung function in infancy, abx and infxn and gend

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14
Q

5 phenotypes (SARP - severe asthma research program) differ in lung fxn, age of asthma onset and duration, atopy and sex?

A

5 phenotypes (SARP - severe asthma research program) differ in lung fxn, age of asthma onset and duration, atopy and sex (CLUSTER 1-5, where 3-5 are severe)
Cluster 1: Transiet early wheeze: 3-5y of life, not fmhx or allergy, usu matenral smoke, sibs or children day care
Cluster 2: Non atopic wheeze: upto adolescence wiht no atopy - RSV link in first 3 years of life - mold asthma
IgE mediated wheeze: wheeze with atopy, allergic sens, long fxn dec and airway hyperrresonsiveness (can be ADULT or peds)
In realisty they have the 3-5
Cluster 3: peds and adult (are the obesity, GERD< sinus disease htn)
Cluster 4: is peds and adult with sensiztation and classic allergic asthma
Cluster 5: only adult: COPD pneumonia and obestiy and pulm HTN

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15
Q

treatment of CSU cold induced

A

cyprohepatadine
h2
epi pen

r/o
cryoglobinemia
cold agglutinin disease
cryofibronogemia
paroxysmal cold hemoglobinura 
cold hemolysis

PLAID (phosphiolipase assoc ab deficienc and immundysregu
AD mtation in PLCG2 - cold urticaria at young age
ice cube NEG test - can also be FCAS (c1as1 mutation)

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16
Q

five diff btwn cholinergic urt and EIB

A

1) trigger with body temp elevation
2) smaller wheal size (1-3mm)
3) occlusive body suit test - drop in lung fxn with CIU
4) positive hot water test in CIU
5) intramdermal methcolinc halenge causes hive
6) responve to hyrdoxizine

17
Q

6 causes of acute and chronic urtricaria

A

acute - spontaneous infection food meds, venom latex and contact

chronic
spontanoeus
demratographoc
cholinergic
water, 
pressure
vibration
cholinergic
exercise
delayed pressure
18
Q

urticaria ddx

A

DDX: urticarial vasculitis, mastocyotiss, AD, bullous pemphigoid, EM, FCAS, drug eruption, SLE, pruritic papule of pregnancy, Muckle wells, schinztler

19
Q

what does c1 inhb block

A

ROLE: inhibits c1 proteases and c1r and c1s, MASPS, factor 11a and factor 12a and kallikrein

20
Q

what is ID reaction

A

A more generalized dermatitis, termed autoeczematization, may develop distal to the original site of contact one or more weeks after the appearance of the initial localized dermatitis. This secondary dermatitis is also called autosensitization dermatitis or an “id” reaction. Autoeczematization is particularly common among children with nickel dermatitis who have subacute dermatitis at the initial site for several weeks before appearance of a more widespread dermatitis [36]. Autoeczematization is treated in the same manner as widespread ACD. (

21
Q

ddx eczema

A

CZEMATOUS ERUPTION
•INFECTION (would add scabies)

•CANCER

◦CTCL/MF

•PID-associated

◦WAS

◦IPEX

◦HIGE

◦Acrodermatitis enteropathica

◦GVHD

◦SCID

◦Omenn

•METABOLIC/NUTRITIONAL

◦Celiac

◦Zn deficiency

◦Niacin deficiency

•INFLAMMATORY SKIN Dz

◦Atopic

◦ACD

◦Irritant

◦Psoriasis

◦Etc

22
Q

eyelid contact dermatitis ddx

A
  • Eye drops-neomycin/bacitracin, topical anesthetic
  • Cosmetics

◦Preservatives

◦Fragances, Balsam of peru

  • Nails-formaldehyde, acrylates
  • Hair-PPD
  • Sunscreen-PABA
  • Eyeglass frames-nickel
  • Ix: Patch
  • Rx: Avoid, low potency steroid or topical CnI
23
Q

optical complications of AD

A
  • Allergic Keratoconjunctivitis
  • Vernal Keratoconjunctivitis

VKC: Atopic families, boys 3-20, flares in spring exacerbations, eosinophilic infiltrate,

cobblestoning, stringy discharge (ropy discharge), shield ulcer, resolves after puberty

AKC: Sight-threatening! Patients with AD and periocular dermatitis and conjunctivitis – not seasonal – 20-50 years, Male>F. Skin and ocular changes:
•Skin: Scaling, flaking dermatitis, leather-like lid with keratinization, Cicatricial ectropion (turning outward of the lid from skin scarring), Lagophthalmos (incomplete closure of eyelids), Cracking as well as lash loss (madarosis), ulceration

•Ocular changes:Subepithelial fibrosis, Horner-Trantas dots (whitish aggregates of degenerated epithelial and eosinophils on surface of the limbus), Significant vision loss (Epithelial keratopathy, epithelial defects, scarring, ulceration, and neovascularization), Corneal transplantation may be needed, Herpetic keratitis 14% to 17.8%, Cataract is increased, because steroids, The lens opacity typically associated with AKC is an anterior or subcapsular cataract. This cataract often has the configuration of a multilobed opacity resembling a “milk splash”, Retinal detachment been reported

Management:
1. General eye care:

  • Patients should not rub their eyes (mechanical mast cell degranulation)
  • Cool compresses —> reduce eyelid and periorbital edema
  • Frequent use of refrigerated artificial tears to dilute and remove allergens
  • Stop use of contact lenses during symptomatic periods

2.Allergen avoidance (stay home, windows closed, shower, air filters, mite mx)

The treatment of choice: Topical application of dual-acting ocular medication (patanol and pataday)

  1. Topical administration of steroids such as prednisolone acetate four times per day for 7 to 10 days (NB risks of increased IOP, cataracts, cornea thinning)
  2. Topical mast cell stabilizers one to four times daily
  3. Uncontrolled dermatitis with vision-threatening complications: oral steroids, cyclosporine or plasmapheresis.
  4. Infection control (staphylococcal blepharitis, HSV keratitis)
  5. Oral antihistamines may help to relieve eye itch (first generation

drugs also may decrease tear production, causing more ocular symptoms)

  1. CONSULT OPHTHALMOLOGY!
24
Q

pathophys of AD

A

Pathophys
Deficient in lipids (ceramides) and antimicrbial peptides (cathelicidins LL37) and HBD
Fillgarin on 1q21 - produced by keratinocytes and filament agreggating protein to form skin barrier. S100 respinsible to INCREASE keratinocyte and fillagrin
Matrix protein and promote aggregation and DISULFIDE bonding btwn keratin filament to form protein lipid cornfied envelope of epidermeis to help with water permability and block allergen and microbe entry
Ag to langerhan cells and dermal DC, go to LN and present to T0 which become Th2/17 andth22, these are then in the blood, the T cell is activated
TH22 and Th17 release IL22 and 17 which reduce the S100 protein (which inc keratinocyte and fillagrin) - now this is a disrupted barrier
Danger signal TSLP IL33 and IL25 is sent which further activates Th2 cells which produces Il31 to ITCH and scratch and lichenify
IL4 and 13 also INHIBIT AMP

25
Q

what is substance P

A

In the airways of numerous animal species, including humans, neuronal C fibers containing the neurotransmitters substance P (SP), neurokinin A (NKA), and calcitonin gene–related peptide (CGRP) form a sensory neural system with a motor function termed sensory efferent nerves
The sensory neuropeptides have a variety of biologic activity, including effects on secretion. The tachykinins SP and NKA increase plasma exudation, an effect potentiated by the potent vasodilator activity of CGRP, and also increase mucin secretion. The secretory effects are mediated through interaction with tachykinin NK1 receptors.
Activation of sensory nerves therefore might contribute to the pathophysiology of airway hypersecretion in allergic rhinitis and asthma.
The secretory effects of sensory nerve activation can be blocked through
(1) inhibition of nerve activation
(2) inhibition of release of sensory neuropeptides
3) inhibition of neurokinin activity by tachykinin receptor antagonists

Allergy and Immunology (10 decks)

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