Inflammatory

Dermatoses
Definition of Terms

DERMATOSES = Entire spectrum of

skin disorders
(inflammatory, congenital,
neoplastic, etc.)

DERMATITIS = Inflammatory diseases

of the skin

ECZEMA = Inflammatory diseases

asstd with intraepidermal
edema (spongiosis)
vesiculation
ECZEMA
(Greek eksein = to boil out)

cute! subacute!
chronic

" G#$%&'(
I. topic dermatitis
II. )ontact dermatitis
III. $ther Ec*emas
)lassification( Ec*ema
I. +$&I) ,E#-+I+I'
II. )$.+)+ ,E#-+I+I'
a. llergic ),
b. Irritant ),
III. $+/E# E)0E-'
a. .ummular! discoid dermatitis
b. 'eborrheic dermatitis
c. 'tasis dermatitis
d. /and and foot dermatitis (palmoplantar
pompholy1)
+$&I) ,E#-+I+I'

chronic, relapsing inflammatory skin disease affecting

up to 234 of the population

multigenic disorder = the genetics of atopy are

comple1

/as a serious impact on the 5uality of life of patients

and their families

Increasing prevalence worldwide noted due to

6. environmental factors ( house dust mites, airborne
allergens, poor air 5uality, poorly7ventilated homes
2. 89estern lifestyle: factors( Increased urbani*ation,
increasing industriali*ation in dev. countries stress,
dietary changes, travel to new environments, new
microbial environment, most time spent indoors, more
pets
+$&I) ,E#-+I+I'

Diagnosis is arrived at by history taking

and clinical criteria based on Clinical
criteria as g!idelines for d" of AD by Ra#ka
and $anifin%&
A' Ma#or criteria ( or more%&
6. &ruritus
2. +ypical morphology and distribution
7 dults( ;le1ural lichenification
7 )hildren( ;acial and E1tensor involvement
". )hronic or chronically relapsing dermatitis
<. &ersonal!;amily /1 of +$&= (asthma, allergic
rhinitis aka 8hay fever:, atopic dermatitis,
allergic con>unctivitis, GI allergy)
+$&I) ,E#-+I+I'
)' Minor feat!res ( or more%
6. ?erosis (dry skin)
2. Ichthosis!palmar hyperlinearity! keratosis pilaris
". Immediate(type I) skin test reactivity
<. Elevated serum IgE
@. Early age of onset
A. +endency towards skin infections(esp. '.aureus B /erpes simple1) ! impaired cell7
mediated immunity
C. +endency towards nonspecific hand or foot dermatitis
D. .ipple ec*ema
E. )heilitis
63. #ecurrent con>unctivitis
66. ,ennie7-organ infraorbital folds
62. Feratoconus
6". nterior subcapsular cataracts
6<. $rbital darkening
6@. ;acial pallor!erythema
6A. &ityriasis alba
6C. nterior neck fold
6D. Itch when sweating
6E. Intolerance to wool and lipid solvents
23. &erifollicular accentuation
26. ;ood intolerance
22. )ourse influenced by environemental and emotional factors
2". 9hite dermographism
I##I+.+ )$.+)+
,E#-+I+I'
nonallergic inflammatory reaction
7
-ay be induced in any person if sufficiently high
concentration of the irritating substance is used
7
.o previous e1posure to a substance necessary
7
Effect is evident within minutes or a few hours at most
7
E1amples of irritating substances(
7
A' A*+A*IS& Dissolve keratin penetrate B destroy
deeply (Eg.soaps, detergents,
bleaches)
+1( pply weak acids like vinegar, lemon >uice
)' ACIDS & E"' /ydrochloric acid= blisters
.itric B sulfuric acids =corrosive! can cause deep
burns
+1( #inse with copious amounts of water and
alkalini*ation with sodium bicarbonate! )a$/
(lime)!soap solutions
GGE#GI) )$.+)+
,E#-+I+I'

#esults when an allergen comes into

contact with previously sensiti*ed skin

#esults from a specific ac55uired

hypersensitivity of the delayed type H
a.k.a. cell7mediated immunity or cell7
mediated hypersensitivity

-ay be induced upon a sensiti*ed area

of skin when an allergen is taken
internally

&atient may have e1posure to an

allergen for years before developing
hypersensitivity e.g. hair dyes, rubber,
cosmetics, insecticides
+#E+-E.+
. +opical #egimen
6. 'teroids H hydrocortisone, de1amethasone,
mometasone, methylprednisolone, triamcinolone,
betamethasone, clobetasol, fluocinolone
2. ntibiotics H gram7positive coverage, broad7
spectrum
". Immunomodulatory drugs H tacrolimus
<. Emollients ! -oisturi*ers !hypoallergenic cleansers
. 'ystemic ,rugs
6. ntihistamines H sedating! nonsedating
2. ntibiotics
". 'teroids H prednisone, methylprednisolone,
hydrocortisone
<. Immunomodulatory drugs H cyclosporine,
methotre1ate, a*athioprine
). &hototherapy
%se of ultraviolet light(
6. %I76 atopic dermatitis
2. .arrow7band %IJ
,. Intralesional in>ections of
corticosteroids
+#E+-E.+
,SORIASIS
7
chronic, relapsing disease
characteri*ed by red, scaling skin
lesions of variable forms(
-',SORIASIS ./*0ARIS
1v!lgaris2 3 common% = circular
pla5ues predominantly on scalp
(particularly) retroauricular areas ,
elbows B knees, lower back (lumbar
area)
= 8chronic stationary psoriasis: H
months!yrs.
,SORIASIS& Clinical
forms
4' I5.ERSE ,SORIASIS = lesions
located on fle1ures a1illary vaults,
antecubital fossae, popliteal vaults,
inguinal!crural creases,
inframammary areas
(' 0/TTATE ,SORIASIS (guttate =
droplike)
=a.k.a.8eruptive: psoriasis
(sudden!acute onset)
= +runk and pro1imal e1tremities
most affected
,SORIASIS& Clinical
forms
6' ,/ST/*AR ,SORIASIS = lesions
are sterile pustules
Iariant forms of pustular psoriasis(
a.Gocali*ed( &ustular palmoplantar
psoriasis, crodermatitis continua of
/allopeau
b.Generali*ed( Ion 0umbusch
pustular psoriasis
,SORIASIS& Clinical
forms
@. 0enerali7ed psoriasis
A. 0eogra8hic psoriasis (map7like)
psoriasis coalesced pla5ues form
irregularly7shaped 8islands:
C. Ann!lar psoriasis (ring7shaped)
D. 9ollic!lar psoriasis
,SORIASIS&
E8idemiology

ffects about 24 of population

(K) Genetic predisposition

6!" of patients have (K)family history

$ccurs at .= GE

&EF' at 2 age groups(

6A722 y!o and @@7A3 y!o
,SORIASIS& ,athogenesis

-' :%$y8er8roliferation of
keratinocytes& epidermal cell cycle
shortened from "66 hrs to "A hours
= )ells mature more 5uickly
accumulation of scales
,SORIASIS& ,athogenesis
4' Role of imm!ne system mechanisms&
Th-;driven disorder T;cell mediated imm!ne
res8onse%
A' 5onc!taneo!s trigger factors&
eg. Infection ('treptococci, /II),
e.g.,rugs (lithium, J7adrenergic blockers, )E inhibitors)
generate 8autoantigens:
)' S!sce8tibility genes activated & -ost fre5uently /G7b6", 7J6C, 7Jw@C, 7)wA
C' Th-;Th4 imbalance cytokines, IG76 ;gf, IG7A Egf, IG7D +.; generatedlack
of downregulation influ1 of neutrophils and macrophages!monocytes
amplified immune response
D' E"8ression of 8soriasis 8henoty8e&
= tortuous dilated capillaries (seen clinically as erythema)
= presence of microabscesses filled with neutrophils (-unro microabsecesses) (
hallmark of psoriasis
&'$#I'I'( +reatment
-' TO,ICA* Treatment 3 a88lied to
skin

Glucocotricosteroids

Iitamin ," analogues( calcipotriol

+opical retinoid( +a*arotene

+ar

nthralin

Emollients! -oisturi*ers( eg. &etroleum

>elly commonly used because cheap but
greasiness is uncomfortable
&'$#I'I'( +reatment

4' S<STEMIC Treatment oral=IM=

I.%

-ethotre1ate

)yclosporine

#etinoids (Iit derivatives)=

etretinate, acitretin

Jiologicals ( genetically engineered

medication from a living organism
(e.g. virus), gene or protein
in>ected or infused intravenously =
e.g. etanercept , infli1imab
&'$#I'I'( +reatment

". &/$+$+/E#&=
+reatment with ultraviolet (%I) light
6.&hotochemotherapy ( &%I = a
photosensiti*er (metho1ypsoralen) is
ingested and the patient is sub>ected
to %I light
2.%IJ light = broad band %IJ
= narrowband %IJ
E?;$GI+IIE ,ermatitis

a.k.a. Erythroderma

Inflammatory skin disease in which

erythema and scaling is
widespread!generali*ed(8GE,: =
generali*ed e1foliative dermatitis)

,ue to a preceding skin or systemic

dse

,rugs implicated

-ay occur as an idiopathic entity w!o

preceding dermatitis or systemic
disease
E?;$GI+IIE ,ermatitis

S+I5 Dses= Ec*ematous dermatitis,

&soriasis, superficial fungal infections
(dermatophytosis), scabies

S<STEMIC Dses = )ancers (leukemia,

lymphoma, rectal ), lung)), /II
infection

DR/0S = allopurinol, .'I,',

anticonvulsants! psychotropic
drugs()arbame*apine, &henytoin,
Githium), antibiotics (penicillin,
trimethoprim, sulfonamides,
sulfonyureas, I./!#ifampicin, etc.)