skin Flashcards
diagnostic criteria for eczema
evidence pruritic skin
PLUS 3 of
- Crease involvement
- Dry skin
- Visible dermatitis
- asthma or seasonal AR of fmhx (if <4yo)
- less then 2yo
acute vs chronic findings in AD
acute - pruritic erythematous papulovesicular excoration serous exudate
CD - lichenification, fibrotic ppaule and excoraite
name 6 genetic changes inc risk of AD
spink5, flg stat3 dock 8 was foxp3 loss of fxn of tlr9, myd88
list 4 functions of filaggrin
Filaggrin levels are diminished in AD due to:
• Mutations in the FLG gene
• Th2 cytokines down-regulating FLG expression
1) prevent transepidermal water loss
2) natural moisterizing factor
3) anti staph activity
4) UV protection
5) acidification
cytokines in acute vs chronic AD
Il4,13
chronic il512 and intfergon gamma
all slit therapy prescriptions and age
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
five immunoregulatoary abnormalities in AD
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
name 7 trigger of AD
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
name 5 bugs assoc with AD
staph aurues eczema herpticum mollsucum contagioisum HPV coxsackie
fungal: malassezia furfur
how much does 1g cover of steroids
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
ddx for AD
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
skin indviduals with AD are deficient in:
ceramides (lipid molecule)
microbial antipeptides - cathelicidins
what are some pretanal things showed to reduced asthma
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
5 phenotypes (SARP - severe asthma research program) differ in lung fxn, age of asthma onset and duration, atopy and sex?
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
treatment of CSU cold induced
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)
five diff btwn cholinergic urt and EIB
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
6 causes of acute and chronic urtricaria
acute - spontaneous infection food meds, venom latex and contact
chronic spontanoeus demratographoc cholinergic water, pressure vibration cholinergic exercise delayed pressure
urticaria ddx
DDX: urticarial vasculitis, mastocyotiss, AD, bullous pemphigoid, EM, FCAS, drug eruption, SLE, pruritic papule of pregnancy, Muckle wells, schinztler
what does c1 inhb block
ROLE: inhibits c1 proteases and c1r and c1s, MASPS, factor 11a and factor 12a and kallikrein
what is ID reaction
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. (
ddx eczema
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
eyelid contact dermatitis ddx
- 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
optical complications of AD
- 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)
- 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)
- Topical mast cell stabilizers one to four times daily
- Uncontrolled dermatitis with vision-threatening complications: oral steroids, cyclosporine or plasmapheresis.
- Infection control (staphylococcal blepharitis, HSV keratitis)
- Oral antihistamines may help to relieve eye itch (first generation
drugs also may decrease tear production, causing more ocular symptoms)
- CONSULT OPHTHALMOLOGY!
pathophys of AD
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
what is substance P
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
