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Dermatology Atf

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0% found this document useful (0 votes)
241 views438 pages

Dermatology Atf

Uploaded by

najeeblecture1
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PDF, TXT or read online on Scribd

AfraTafreeh.

com
1

BASIC OF DERMATOLOGY - /

The integumentary system ( skin )


• Weight : 4 -Sky
• 7o age BW : 15 -16% ofTBW ^
• Size : 1.7m2 ( BSA )

Functions of skin
• Protection ( Barrier )
• Vitamin P protection: S .basaleQ® >>> S .Spinosum
• Sensation
• Thermoregulation
• Excretion

Structure of skin [Link] 38

Cutaneous membranes
• Epidermis
• Permis
• Subcutaneous structure

Accessory structures / appendages


• Hair
• Nail
• Exocrine glands

Basic of Dermatology - I
Layers of skin

• Epidermis -> avascular


• Vermis -> vascular
O2. to epidermis
[Link]
• Subcutaneous layer -> Deepest
a/ k / a pannicuius

Layers of epidermis

Basic of Dermatology - I
[Link]

• Origin: Ectoderm
• Stratified squamous epithelium
• 4 layers -> Skin on body ( thin skin )
• 5 layers -> Palms &c soles ( thick skin )

Layers
• S .corneum ( outermost )
• S .lucidum -> j^ reseKt oia / y in palms &c soles
• S .yranulosum
• S .spinosum
• S .basale ( deepest )

S .basale
• Deepest/ innermost layer of epidermis
• Synonym: Stratum Qerminativum
• Cells : single layer, columnar cells

Fig : 3

• Function : S .basale has stem cettSj continuously divide


by mitosis.

Basic of Dermatology - I
4
S .spinosum

• Synonym : Prickle cell layer $

Pesmosomes

Spine like processes


Fig : 4

Cells :
- Polyhedral
- multiple layer
- Thickest layer of epidermis
- Intercellular connections : Desmosomes® ( maximum
concentration in [Link]
SS)
- Intraepidermalj intercellular adhesions
- Damage of desmosomes -> Pemphigus

S .granulosm

c-*~-EZQr-IZ
gJT ' -n •

rO
— ZcPT
^ Qranules

Flattened squamous cells Fig : 5

Basic of Dermatology - I
[Link]
5

Granules

Keratohyaline granules Lamellar granules


*
Contain : Profillagrin ->
a / k / a: membrane coating
granules/ Odland
Fillagrin bodies/ cementosomes
( Filament aggregating
protein ) Contain : Lipids/ oils
4,
Function:
2 . Compact
4.
Sterols

Glue / cement
2. Keratinization Between cells
3. Barrier 4,
Barrier
Fillagrin deficiency
2 . Ichthyosis vulgaris
2 . Atopic dermatitis

S .lucidum
• Location: Palms &c soleSj thick skin
• Sandwiched between: S .granulosum &c S .corneum
• Granules: Eleidengranules - Translucent

S .corneum
• Development: Last layer to develop, outermost layer
*
absent in preterm / VLBVJ babies
• Protein: Keratin -> compactness/ barrier
• Importance : Dead cells anucleated ,
}

compacted - Impermeable : barrier


Basic of Dermatology - I
6

Keratinisation

[Link]

• Epidermopoesis
Definition: maturation Sc migration of cells form
S3 -» Sr -> off
Ti'me fine: SB > SC off
4 weeks 4 weeks
L j
T

8 weeks / s belays

• Epidermal turn over time / = 2 weeks / 5todays >>>


4-weeks
Skin doubling time

Basic of Dermatology - I
[Link]
7
Changes in keratinocytes

• Cell shape : flattening ®


• Cell size : increases®
• Nucleus size : Decreasing -> absent ( S .C )
• Hydration: Reducej progressive dehydration
• Metabolism : Reduces
• Keratin: Ks/ i4 ® ( S 3 ) -> K1/ 10® ( S S )

Basic of Dermatology - I
Cells of epidermis 00 : 2.0 : 50

[Link]

Principal cells
• Keratinocytes

Other cells
• Melanocytes
• Merkel cells
• Lanyerhans cells

Keratinocytes
• Origin : ectoderm

Basic of Dermatology - I
[Link]
9

• Principal cells : > c\5°7o of cells


• Hallmark filament : Keratin intermediate filaments

Melanocytes
• Immigrant cell
• Origin: Neural crest
• Location : S .basale
• Shape : Dendritic
• Content : Melanosomes ( granules ) -> contain melanin

Function : Production <k transfer of melanin from


Melanocyte -> keratinocytes
Sunprotection
Markers : S lOOj HM 84?; MELAN A

Basic of Dermatology - !
10

Epidermal melanin unit 00 :24- : S S

2 melanocyte -> 36 keratinocytes

Merkel cells

Fig : 1-0

• Origin : Ectoderm
[Link]
• Location: S .basale
• Shape : Disc shaped
• Content : Neurosecretory granules
• Function: Mechano receptor fine / light touch
j

• Slow adapting , low threshold Mechanoreceptor


• Markers: Cytokeratin 20

Basic of Dermatology - I
[Link]
11

Langerhans cells

• Origin: Mesoderm ( Bone marrow, RES )


• Location: S .spinosum
• Shape : Dendritic
• Content : Birbeckgranules ( tennis racquet
appearance )
• Function : First line of defence
• Innate immunity ARC j

• Markers : S I O O J CD laj CDZ07 -> Langerin ( M . specific


marker )

Basic of Dermatology - l
12
Rete ridges & dermal papillae

Projections
• Epidermis — ^ Dermis ( Rete ridges )
[Link]
Projections
• Epidermis < Dermis ( Dermal papillae )

Function of rete ridges


• Increase surface area of contact : Increase O Z J
increase nutrient
• Increase adhesion

Basic of Dermatology - I
[Link]
13
Basement membrane zone : Interface/ PEJ

Damage
• Hemidesmosomes Bullous
Damage
pemphigoid

Basic of Dermatology - I
14

• Anchoring fibrils Epidermolysis bullosa


acquisita

Per mis

[Link]

• Vascular ( B V j lymphatics )
• Cells.
• ECM
• Appendages
• Nerves
- Upper l- / 1lOtW : papillary dermis ( loose connective
tissue )
- Lower F / SLOth : reticular dermis ( dense connective
tissue )
• Most important cells in dermis = Fibroblast
• Dermis : composition

Basic of Dermatology - I
[Link]
15

STRUCTURE OF DERMIS

Epidermis

Collagen

L Fibroblasts
Dermis
Hyaluronic acid
*
L Elastin

Fig : 16

- Collagen -> Tensile strength


- Elastin -> Elasticity
• Most common collagen : Type2 ( 85 - <? £>%)
• 2 nd most common collagen : Type 3 ( 20 -25% )
• Ratio of type 2 : 3 collagen = 8 :2 1< : 2
}

• Absent in skin : Type 2 collagen (Type2 = only found


in cartilage )
• Most important glycosaminoglycan in skin =
Hyaluronic acid (Turgor )® = Hydration

Basic of Dermatology - I
16
Subcutaneous tissue

Dennis

Fig : 17

[Link]
• Fatty layer/ pannicutus
Panniculitis
( Inflammation of fatty layer )

Lobular panniculitis Septal panniculitis

Histopatlnoloyy of skin 00 : 42:36

S .corneum
• Increased tlnickness : Hyperkeratosis
• Nucleated keratinocytes: Parakeratosis

Basic of Dermatology - I
[Link]
17
Parakeratosis

Normal Ab normal
Oral &c
vaginal
mucosa

Benign Malignant

Psoriasis
*
Actinic
Seborrheic keratosis
dermatitis Bowens ds
SCC

S .grasulosum
• Thickness :
- Increased -> Hypergranulosis : Lichen planus
- Decreased -> Hypogranulosis : Psoriasis
ichthyosis vulgaris

S .spinosum
Increased thickness = Acanthosis
• Stratum Malpighi/ malpighian layer/ = SB+ SS
living layer of epidermis:
• Increase thickness of S .Malpighi = Acanthosis

Acantholysis: Separation of keratinocytes from one


another

Basic of Dermatology - I
18

• Acantholytic cells/ tzanck cells


Round
Large nucleus
Peripheral condensation of cytoplasm
Tzanck smear = shows tzanck cells ( keratinocytes )

Acantholysis : Causes

Primary Secondary
Damage to [Link]
Damage to
desmosomes directly to
2 . Auto immune : keratinocytes
Pemphigus • Ballooning
2 . Inherited : degeneration of
Hailey - Hailey keratinocytes
d/s Ex :
Darriers d / s H .labial is
3 . Infections: H .zoster
Bullous Varicella
impetigo
ssss

Basic of Dermatology - I
[Link]
19
Dyskeratosis
Definition : Abnormal keratinization
Causes

Benign Malignant
Hailey bailey Actinic
d/s keratosis
Darrier d / s Arsenical
P. foliaceus keratosis
Bowens ds
SCC

Microabcessess
Definition : Small , localised collections of immune cells
in skin
Types :
i. Neutrophilic microabscesses
a. Munros microabscesses . .
Psoriasis
j
b. Kogoj spongiform pustules
c . Papillary tip = Dermatitis herpetiformis
ii. Lymphocytic microabscesses: Pautriers abscess -
Mycosis fungoides
Hi. Eosinophilic : Pemphigus vegetans

Basic of Dermatology - l
20
Rete ridges

Normal

i.

• Regular elongation of rete ridges


• camel toe Appearance -> Psoriasis

f f

II .

Pointed tip
[Link]
Saw toothing of rete ridges

*
Lichen planes

Basic of Dermatology - I
[Link]

SASIC DERMATOLOGY - II

• Skin lesions
i. Primary
ii. Secondary
Hi. Special

Primary skin lesions 00 :00:34

• Initial lesions to appear in a disease

i. Plat , non - palpable


• Change in color of skin
<SLcm -> macule
> Hcm -> patch

ii. Circumscribed, solid, raised


<SLcm -> papule
>SLcm -> plaque
Depth > width -> nodule

Basic Dermatology Part - II


2

Hi. Clear, fluid filled


Ccm
^ vesicle
> Hcvn -> bulla

[Link]

iv. Pus filled lesions


• Pin point sized pus - filled blister -> pustule
• Larger collection of pus -> abscess

Basic Dermatology Part - II


[Link]
3

v. Wheal: urticaria
• ErythematouSj Edematous j Evanescent skin lesion
sU sU
Blanchable central pallor <2-4-hours
Peripheral erythema

vi. RBC e>ctravasation


• Non blanchable red lesions
<[Link] : petechiae
2- -5mm\ purpura - palpable purpura: Raised
Basic Dermatology Part - II
Ex : cutaneous vasculitis
>5M M - ecchymosis

vii. Cyst [Link]


• Epithelium lined cavity
• Ex: sebaceous cyst -> central black punctum

Secondary skin lesions 00 :08 : 3<o

• Overlying change to primary skin lesion

Basic Dermatology Part - II


[Link]
5
/. Scale
• Visible desquamation of corneocytes ( SC )
• Composed of keratinocytes Q

m
*>
&
FSHasa SH
tSsmsm §
V

Fif : 8

ii. Crust
• Dried up exudate
• Example : Impetigo : Honey coloured crust

•••
in .
Erosion Ulcer Fissu re
- Partial loss Full thickness loss of - Linear toss
of epidermis of
epidermis
BM : not intact
- BM intact Reaches dermis epidermis
- No scarring - Heals with scanring
,

Basic Dermatology Part - II


6

EROSION ULCE R

?CA7
\
1 o

iv. Excoriations
• Linear scratch marks on skin

[Link]

v. Lichenification

• Chronicj long -term itching


• 3 components
- Increase colour ( dark )
- Increase thickness
- Increase lines
• HPE : Acanthosis ( increase stratum spinosum )

Basic Dermatology Part - II


[Link]
7
vi. Atrophy
• Loss of substance
- Epidermis: Lusterless, wrinkled skin
- Dermis : Depressed

vu . Scars

• Deposition of fibrous tissue ( healing )

Special lesions [Link]

• Burrows
• Comedones
• Target lesions

i. Burrows
• Seen in: Scabies

Basic Dermatology Part - II


8

• Lesion : wavy , linear , serpiginous tunnel ( mite ) in


skin
• Level : S . corneum
• Importance : pathognomic lesion
• Most common : finger webs

ii. Comedones
• Seen in: Acne : primary , pathognomic
[Link]
• Lesion : Dilated pilosebaceous units
- Plugged with sebum &c keratin
• Types
- Open comedone : black heads , oxidation of exposed
keratin
- Closed comedone: white heads

Basic Dermatology Part - II


[Link]
9

iii. Target lesion


• Seen in : erythema multiforme

• Lesion : Round lesion } 3 concentric rings


- Centre : Dusky
- Middle : Pallor
- Periphery : Red
• HPB : Interface dermatitis

Basic Dermatology Part - II


10
Configuration of lesions
Annular
• Ring shaped lesion
- Inner margin
- Outer margin
- Centre clear
• Example :
- Qranuloma annulare
- Tinea corporis
- Erythema annulare centrifugum
- 38 hansens

[Link]

Fig : 17

Round / nu mmular / discoid


• Ex : Discoid eczema -> middle aged men on legs

Basic Dermatology Part - ll


[Link]
11
Linear
• Example : Koebner’ s phenomenon and excoriations

Serpiginous
• Example : Cutaneous larva migrans ( C L M )

VJWorled
• Streaks
• BlascWkoicL
• Example : Incontinetia pigmenti

Reticular
• Example :

Basic Dermatology Part - II


12
- Cutis marmorata = Red , garbling of skin
- Vasculitis

Lines in dermatology 00.2- S :00


i. Blase hko lines
• Represent : direction of embryonal migrations of
keratinocytes
• Shape :
- Midline demarcation
[Link]
- Shape varies with site
• Scalp : Spiral
• Trunk : VJhorled
• Chest: V shaped
• Limbs : Linear
- Don' t correspond to
a rte ries/ ve ins/ ne rves/ ly mphatics

Dermatoses along blaschkoid lines


• Represent : Cutaneous mosaicism
- 2 genetic clones
a. Normal
b. Disease

Basic Dermatology Part - II


[Link]
13

• Diseases
- Incontinentia pigmentiQ

- Epidermal nevi ®
- Linear psoriasis & LP
- Licinen striatus
- Hypometanosis of I to $

ii. Lange rs lines


• Synonym : Relaxed skin tension lines ( RSTL )
• Represent :
- Along the collagen fibres ( parallel )

- perpendicular to muscle
- change throughout lifetime , not constant
• Shape :
- Surgical importance
- Incision: parallel to langer line -> best healing
- If given perpendicular to langer lines -> Gaping
Irregular scarring

Diagnosis in dermatology 00 : 35.00

• Diascopy :
- Synonym : vitropression
- Glass slide -> Press on lesion
i. Erythema vs purpura :
- Erythema blanchable
- Purpura -> non blanchable

Basic Dermatology Part - II


14

ND vs NA
- Nevus anemic us: margin merges wit In surrounding
skin and no clear skin
- Nevus depigmentosus : clear demarcation of nevus

[Link]
Hi. Lupus vulgaris
Golden yellow nodules

Apple jelly nodules

• Nikolsky sign
- Acantlnolysis : breakdown of desmosomes
Basic Dermatology Part - II
[Link]
15

*keratinocytes
Separation of
Tangential pressure on skin

Peeling of upper layers of epidermis -> erosions.

- Example : Pemphigus
SSSS ( desmoglein n targeted )
• Pseudonikolsky sign: come off in sheet
TEN -> sheet like peeling
Due to extensive keratinocyte necrosis
Epidermis separates from dermis

VJood’ s lamp examination

Basic Dermatology Part - II


16

• Light source : UV lights


• VJave length: 3 <aO -3 o5nm
(

• Class : Barium silicate with <? % nickel oxide


• Done in dark room

Infections

i. Tinea capitis
- Bctothrix
- Microsporum
- Blue green F

[Link]
ii. Pityriasis
versicolor ( PV )
PV = PY ( pale
yellow F)

Hi. Brythrasma
- coral red
- Coproporphyrin 3
- Corynehacterium

Basic Dermatology Part - II


[Link]
17
Pigmentation

• Vitiligo :
• Melasma: Exaggerated
Accentuation of dermal
lesion fluorescence

Ivory white

Porphyria :

- Urine : Coral red

Fig : 2.4

Basic Dermatology Part - II


18

- Congenital erythropoeltic porphyria : red teeth-


Erythrodontia

Dermoscopy
• Surface microscopy
• Epiluminiscence microscopy
- N o n invasive
- Surface features : magnified , clearly
i. Lichen planopilaris : perifollicular scale

[Link]

ii. Alopecia areata:

a. Exclamation mark hair

Basic Dermatology Part - II


[Link]
19
[Link] dots ( Empty hair follicles )

Hi. Trichotillomania:

- hair of different length

- Longitudinal splitting of hair

Basic Dermatology Part - II


1

APPENDAGEAL DISORDERS PART - /

Hair OO .OO .H 5

• Origin : Ectoderm
• Structure :

Superficial ~

Infundibulum 5 • .
Upper Segment :
• y-
•• •
/
/ pore to
follicular
/
f /
/
insertion of arrector pili
s.

Isthmus m s
s.
.s. *
s
A
s

'V. /-/-'ife/

r
Bulge : Stem cells [ in
s
ISTHMUS ] -» Damage
Supra bulbar *
A ri
'
'/# -- /r
( stem ) ;•
Permanent hair loss

(Mi' lHair bulb / Lower segment

Dermal papilla : Dermis Invaginating into hair . Fig : 1


[Link]

Hair:
• Isthmus: bulge -> Stem cells
-> Damage = permanent loss of hair

Cross section

Appendageal Disorders Part I


[Link]
2

2 .Medulla ( Inner most )


2 .Cortex
3 .Cuticle

4. Inner root slneatln ( IRS )


S .Outer root slneatW ( ORS )
[Link] sWeatW ( outermost )
Human : Ml : <0.33 ( 2 : 3 )
Hair
/
\
Animal : Ml : >0.50 ( 2 :2 )

Medullary Index : Via of medulla


Total Pi a of laair

Inner root sheatW. IRS


i. Cuticle ( Innermost )
if . Huxley layer
. Henley layer ( outermost )
fii

Cuticle

Iff
fjy

hip I
. Huxley layer
Henley layer .
IRS

1 <3/
f @ w
3
Glassy mevnbrane
KeratinisecL '

/ A Connective tissue sWeatW


zone
Adamson' s fringe : divide
Non - suprabulbar &c bulbar area
Keratinised zone -> Fungal inf (Tinea capitis )
si /

always above adavnsons fringe

fungal inf : Affects keratinized area of hair


Fig : 3

Appendageal Disorders Part l


3

Types of Hair 00 :09 :00

Types of Hair
I
I 1
Intrauterine hair Extrauterine hair
• Lanugo hair -> soft
- Unmedullated vellus hair Terminal hair
- Shed s ^h / qth - Soft - Coarse
month in uterus - Unmedullated - Medullated
- +nt in preterm - Non pigmented - Pigmented
- Short ( <Zcm ) - Long

[Link]
Hair cycle: Maturation of hair

ANAdEN CATAdEN TELOdEN

Fig : 5

Phases
Anayen Catayen Teloyen teloyen
Growth Involution Restiny Shed off
lony
2 (o % of hair 1% %0 -% 5%

3 years 3 weeks 3 months

Appendageal Disorders. Part I


[Link]
4

Anagen : telogen = S :2 /
^ :2 N
Growth rate - 0.3 Smm / d

2 cm / month.

Disorders Of Hair 00 :1S:16


Alopecia:
Loss of hair

Non scarring
Scarring (cicatricial alopecia )
•Temporary • Permanent loss
•Regrowtla + • No regrovstin

Non scarring alopecia :


3- .Patterned -> androgenetic alopecia
2 .Patchy

• Alopecia areata
• Trichotillomania
• Tinea capitis
• Moth eaten alopecia (2° Syphilis )
[Link] -> effluvium

Androgenetic alopecia:
• Most common of alopecia in world
- Cause : hormonal hair loos
Testosterone dermal papilla 5 PHT
S' cx reductase
H .Anagen telogen
2 .M iniatu rizatio n

Appendageal Disorders. Part I


5
( Thinner and smaller hair )
• ACiA: patterned hair loss ( PHL )
FPHL
AQA

MPHL
• A Q A: M E N :
Initial -> Pronto temporal area = Pronto temporal
recession
Vertex involvement
Qrading : Norwood Hamilton grading I -VII

f) ( 1
[Link]
yFig : 6

• AQA: Women:
- Initial : central parting
- Hair line : maintained
- Hair loss progress Prom center to outside :
Christmas tree pattern
Ludwig scaling : I - III

* Fig : 7

Appendageal Disorders Part l


[Link]
6
Treatment :
[Link] :
'
Minoxidil ( arteriodilator ): increase BS
j (X+ channel opener ) decrease
miniaturization
57o in men and 2% in women
Z .Oral : ScX reductase inhibitors
i
finasteride : SLmy daily
Dutasteride: 0.5my daily

Diffuse alopecia : effluvium


Effluvium are divided into two types
• anayen effluvium and teloyen effluvium
Anayen Effluvium :
- Cause : cancer - chemotherapy / radiotherapy
- Mech :
• Arrest in anayen
• Dystrophic
• Fall off
- 3 -4 weeks of ckeiwo / radiotherapy -> f t Hair fall ( 20 - 8 5% )
i
Bald
• Teloyen effluvium : acute
- Cause :
• Delivery of body
• Major illness :
- Typhoid

Appendageal Disorders. Part I


7
- Dengue
- Chikungunya

- CovicL
• Surgical stress
• Accident

Triggers 3 -4 m
Meek : Anagen > Telogen sWed off
History : ZO - l S % 30 % tt taiV ( oss no balding

• Anagen: telogen is <7 :1-

Treatment :
• Self -limited disorder
• No t/ t required
[Link]
Chronic telogen effluvium:
• long term tt fall / hair thinning
anagen -> telogen -> off

Causes :
i. iron deficiency anemia
ii. thyroid dysfunction

Patchy : non scarring alopecia


Alopecia areata :
• disease : auto immune disease , THU-
• target : black anagen bulb
• clinical feature :
Appendageal Disorders. Part I
[Link]
8
- well defined
- round - oval shape
- complete loss of hair with in patch.
- smooth and bald
• sparing : prey hair
• Phenomenon : going grey overnight syndrome
canites subita
hairwhite

Broad ( distal ) Location : margins / peripWery of


patcW
Calles as : exclamation mark Wair
|j
Importance : active disease
^ severe
Tapering ( proximal)

?
• HPB: Peribulbar lymphocytic infiltrate = swarm of
bees appearance

Appendageal Disorders. Part I


9
Pattern:
• Ophiasis : affecting occipital margin

[Link]
• Alopecia totalis : entire scalp Inair
• Alopecia universalis : entire body hair
• Other sites: eye brow , beard area

Nail involvement :
• Ml feature = pitting

Appendageal Disorders. Part I


[Link]
10

• Types- Superficial Fine Regular


• Called as: geometric pitting
Sand paper nail

• Other : trachyonychia ( roughening )


AA : Most common acquired cause of
traclngongclnia

Prognostic factors : poor prognosis in


• Onset : early
• Pattern: ophiasis, totalis, universalis
• Nail changes : positive
• Association: family H / O alopecia areata
Concomitant At disorders
Atopy
r/ t :
• Self -limiting
• Toe : intra -lesional triamcinolone ( steroid ) injection
• Systemic steroids

Appendageal Disorders. Part I


11

Trichotillomania :


• Disease : psycho cutaneous disorder
OCD ( obsessive compulsive disorder )
Recurrent pulling out of own hair
• Clinical feature : Bizarre shaped lesion
[Link]
Hair - broken
Varying length
Perifollicular hemorrhage

• MC Site : temporo - parietal area


• Sign : hair gone from top
Narrow rim + nt
Friar tuck sign / Robbin hood sign
• Card test : card kept under hair = hair of varying
length seen
• HPB: Broken hair shaft
Irregular hair shaft r~ trichomalacia
HemorrhageQ

Appendageal Disorders. Part I


[Link]
12
T/t:

• TOC : cognitive behavioral therapy


• Medical management. SSRI

Tinea capitis :
• Causes: fungi
• Clinical features:
- Non scarring alopecia
- Irregular margin
- Partial alopecia
- Easy pluckability of hair
- Skin -> scaling , redness, vesicles, pustules

Types of tinea capitis:

• Non inflammatory
- Qrey patch
~ Non scarring alopecia
- Slack dot
• Inflammatory
- Favusl
scarring alopecia
- Kerion

Appendageal Disorders. Part I


13
Cirey patch. QMC
• In' / oh ectotWrix
• Etiology: Microsporum
• Clinical features: grey colored scaling

Black dot : BNT


• Involvement : endotWrix
• Etiology: trichophyton
• Clinical feature : black dots ( broken hair )
Cicatricial alopecia
I
1
2° ( Primary )
2° ( secondary )
l
l
Lymphocytic :
• Morphea
• Lichen planopilaris •Traction alopecia
• Discoid lupus erythematosus
• Pseudopelade of brocq
[Link]
• Burns
• Kerion, favus
• Alopecia mucinosa
• Sarcoidosis

Neutrophilic :
• Folliculitis decalvans and
tufted folliculitis

• Dissecting cellulitis of scalp

Lichen planopilaris:

Appendageal Disorders. Part I


[Link]
14

• Initial : perifollicular violaceous papules/ change in


color and scales
I
Violaceous / hgperpigmented scarring alopecia
Lichenoid infiltrate -> damage bulge area ( loss of
stem cells)

Discoid lupus erythematosus: CCLE ( Chronic cut LE)

• Carpet tack sign / Tin tack sign


LE
1
i l
SLB PLE
I i
Non scaring alopecia Scarring alopecia
•Chronic telogen effluvium.

• Lupus hair

Appendageal Disorders Part l


15
Pseudo pelade of brocq :

• Cause : idiopathic
• Clinical feature : svnalh scattered patches of scarring
hair loss - non -inflavnvnatorg / svnooth
• Sign : “ foot prints in SKOW”
• HPE : Perifollicular , concentric lamellar fibrosis
[Link]
Folliculitis decalvans and tufted folliculitis :

• Clinical feature : staph aureus


• Sign : Dolls hair sign = seen in tufted folliculitis

Appendageal Disorders. Part I


[Link]
16
Dissecting cellulitis of scalp:

• Causes: blockage of Fair follicle

Follicular occlusion tetrad :


- Dissecting cellulitis of scalp
- Hidradenitis suppurativa
- Acne conglobata
- Pilonidal sinus

Traction alopecia :

• Causes: pulling of Fair -> Fair loss


( ponytails / braiding )
• Site : temporal area.

Appendageal Disorders. Part I


17

Morphea :

• Disease : Localised scleroderma ( Al )


*
Scarring alopecia ( Forehead -> Scalp ) Linear patch
• Synonym : Linear morphea/ Bn coup de sabre
[Link]

Tinea capitis:

• Inflammatory -> Favus & Kerion

Favus:
• Endemic : Kashmir / Africa
• Etiology : T schoenleinii
Appendageal Disorders. Part I
[Link]
18

• Clinical features : Scutula ( Crust )

Kerion:
• Etiology: T. Mentagroptnytes
• Clinical features: Red , Boggy swelling on scalp
- Studded with pustules
- Easy pluck ability of Wair
- Occipital lyvnpWadenopatlny

Appendageal Disorders Part l


APPENDEGEAL DISORDERS

Sweat glands : Types

Eccrine
Apocrine

Eccrine sweat glands

• Sites : all over body , max on soles > palms


• Opening -> directly on skin
• Development : Present and active since birth
• Control : preoptic nucleus of hypothalamus
• Nerve supply -> Cholinergic sympathetic
• [Link]
Secretion -> sweat , merocrine
• Function thermoregulation

Spmal Sympathetic Nerve Sweat Gland | Sweat |

-<0
I I
SprtH IppM E Skj)
Chord

• Eccrine sweat glands : - structure

Appendegeal Disorders Part II


[Link]

• Apocrine sweat glands


• Site -> Axilla , nipple, georn. areofa
• Opening -> into hair follicle
• Development
- Present since birth
- Active only at puberty
- Haemone / androgen dependent
• Nerve supply -> sympathetic adrenergic
• Trigger -> emotional
• Function
- Secretion -> unknown
- No sweating / No vole in thermoregulation
- Pheromones ( 2° sexual activity )

Apocrine glands : - Modified


H .Ma — Mammary Glands
2 .Mo - Moll' s Glands ( eye )
[Link] — Ceruminous Glands ear ( )

Appendegeal Disorders Part II


Eccrine glands : - Disorders
2 .Miliaria

2 .H y p o / Hyperhidrosis
3 .Neutrophilic eccrine hidradenitis
*
In cancer chemotherapy

Miliaria
s]/

Blockage of eccrine sweat glands


*
'M' Sweating

[Link]

Blockage of
• Stratum corneum - Miliaria crystalline
• Stratum spinosum -> miliaria Rubra
• Dermoepidermo junction -> miliaria Profunda
• 2° staple assesus lesion -> M . Pustulosa

Appendegeal Disorders Part II


[Link]

Miliaria crystalline

• Seen in neonates
• Cause : over warding
• Clinical features : Multiple superficial clean
Vesicles which may rupture

Miliaria rubra / Prickly heat / Heat rash

• Cause : - increase in sweating


• Clinical features : - Multiple, itchy, red papules most
}

commonly on face and hunk

Appendegeal Disorders Part II


5
Miliaria Profunda

• Biquodules
• Non itcWy
Apocrine Gland disorders
1) Fox Fordyce disease
Hidradenitis suppulative
3) CWeom Widrosis -> coloured sweat due to
bacteria , lipofuscin , medicine
4) Offensive sweat order
Brom [Link]

Fox Fordyce disease

J
• Synonym: - apocrine miliaria
• Onset: - After puberty

• Gender : - Females > males


• Sites : - Axilla , Nipple , geoin

Appendegeal Disorders Part II


[Link]

• Lesion: - Multiple skin -coloured papules in axilla ,


nipplej groin
• Treatment: - No treatment
Sometimes OCP’ s can help because they reduce
androgens

Hidradenitis suppurative

• Synoym: - Inverse acni


• Pathology : - hail follicle and apocrine glands is
involved , which are blocked
• Onset : - middle age
• Site : - Axilla, Nipple, geoin
• HS : - Clinical features

M
• SLst stage : - Only black comedones
• 2 nd stage : - nodules and abscesses

Appendegeal Disorders Part II


• 3 rd stage : - Bridging scars

Sebaceous glands

• Site : Associated with Inair follicle, absent in palms


and soles
• Opening into [Link]
follicle

• Development : Present prime birtln but active only at


puberty candrogen dependent )
• Function: - sebum production
• Type of secretion ( = ) dolocrine
• Sebaceous glands : - Modified
SL . M -> Montgomery Qlands

Z .M -> Meibomian glands


3 .T -> Tyson glands

Appendegeal Disorders Part II


[Link]
8
Fordyce spots

-
• Ectopic sebaceous glands
• Not an disease but an ectopic presence
• Yellow pinbead papules -> lips oral mucosa, benitalia
• No treatment is needed

Acne vulgaris

• Multi factorial inflammation of pilo


Sebaceous unit
• Onset - after / at puberty
Etiopatbogenesis
SL .Occlusion of pilo sebaceous duct

Vi , ; • to**octal*?
of Aid

h
Stood*

Hprlcfldl
f
r tettMdMfe
wartcrr*

if
I wjfltortrtofcmi
'

Appendegeal Disorders Part ll


9

2 . Increase size and secretion of sebaceous gland ->


seboulnoea
3 . Increase bacterial proliferation
( Propionibacterium acnes )
4 . Increased inflammation mainly by I L - Z

Acne clinical features

A B C

boenra /

ah/t

fotcuw -
/

o
WHITEHEAD PAPULE PUSTULE NODULE

[Link]
• Grade - I comedones -> kav'e Hack cbt on surface
si/
Open comedones
Have white dot on surface
si/
Closed comedones

Appendegeal Disorders Part II


[Link]
10

Comedones are primary lesions of acne


• Grade - 2- -> Papillary lesions
• Grade - 3 -> Pustule

• Grade - 4 Nodulo cystic acne


Most severe form
Polymorphic lesion - Lesions of multiple morphology
present at same time

Other factors
1) Diet -> high glycemic index ( Sugary )
Dairy products
Hormones

Appendegeat Disorders Part II


11

• Growth harmone
• Insulin
3) Premenstrual excerebration ( Progesterone )
Hormonal acne

[Link]
• Increased androgens [Congenital adrenal
hyperplasia, adrenal tumorj PCOD ]
• Increased sensitivity in skin seen in [ PCOD ]

Types androgenism features like


• Infertility
• Hirsutism
• Acne
• Female pattern hairloss
• Hoarseness of yrice
• Clitoromegaly

Appendegeal Disorders Part II


[Link]
12
Acneiform eruption

Prug induced
• Most common cause of acneiform eruption
steroids
• Most common ATT isoniazid

Monomorplnic , reddisln papules , trunk , face ,

plnenytoin, ciclosporin, exposure to yaloyens iodides


and bromides

Acne excorier

• Psyclno cutaneous disorder


• Patient suffers from stress/ anxiety / depression

Appendegeal Disorders Part II


13
- Excoliations / Scratching
- Scarring / marks

Acne : Treatment

• Topical - topical retinoids


- Tretinoin
- Adapalene
• Salicylic acid
• Topical antibiotics clindamycin, dapsone
• Benzyl peroxide ( Antibiotic + Keratolytic )

Oral
• Oral antibiotic Tetracycline ( Doxycycline ,
minocycline , Iymecycline )
[Link]
• Oral retinoids -> Isoprenoids

Grade lesions
2 .Comedonal -> T . Retinoids , salicyclic acid
2 . Popular -> Topical retinoids r Topical antibiotics
3. Pustular Topical retinoids + Oral antibiotics
4 . Nodulo - cystic - oral retinoids

Oral isotretinoin in acne



• Dose — 0.5 2 mg / kg / day
• Total cumulative dose - 220 - 250 mg / kg
• Precautions : - urinary pregnancy fest - , double
contraceptives , extensively teratogenic drugs
Appendegeal Disorders Part II
[Link]
14

• Adverse effects : -
- Most common cheilitis ( inflammation of lips )
s|/

Dry , chapped lips


- Most important -> Teratogenicity
- Others -> increase liver function test
Increase triglycerides
- Qap between stoppage of drug and pregnancy - %

month
- Topical retinoids ->
Includes side effect -> Irritation / dermatitis
- Doxycydine Q -( - Disturbance
- Minocycline pigmentation
- Antibiotic resistance -> T .O .C Benzylperoxide
- Adverse effect - minocycline
• Blue black pigmentation of acne scars

• Iron chelation in skin


- T .O .C for harmonal acne -> Cyproterone

- Acne scars

J i

I I

Rolling Scars Boxed Scars Icepick Scars Hypertrophic Scars

Rolling Scar Boxcar Scar Keloid (Hypedhroplc)

Appendegeal Disorders Part II


15

- Treatment
• Micro needling
• Loses resurfacing of skin by Co% laser
Hr YAP laser

Rosacea

• Disease due to disorder of sebaceous glands


• Dysregulation of vasculature ( Neuropeptides)
• Mites involvement ( Demodex )
• Triggers
- S u n exposure
- Hot / spicy food
- Alcohol [Link]
• Rosacea: - clinical features
• Age : - middle aged women > Men
}

• Siyus and symptoms : - burning sensation on face

associated with redness ( flushing )


• Triggers : -
- Hot spicy food

- Alcohol intake
- Emotional anxiety
- Cause increased redness
• Rosacea : - clinical features

• Lesions : -
- Fixed erythema
- Papules, pustules
Appendegeal Disorders Part II
[Link]
16
- Telangiectasia

• Sites : - convexities
• Sparing : - Creases
• Not seen: - comedones

Rosacea treatment
• GeneraI measures
- S u n protection
- Avoid triggers
• Mild : - Topical metronidazole' s
Topical clindamycin ,
• Moderate : - capsule doxycycline
• Severe : - Oral retinoids
To decrease redness
o( adrenergic agonist
- Xylometazolines
- Brimonidines
• RtninopWyma: -
- Long standing in Inamatory
4/ Rosacea

Appendegeal Disorders Part II


1

APPEND ACEAL DISORDERS PART - III

Nail 00.00.05

• Origin : Ectoderm
• Site : Tips of fingers and toes
• Growth rate :
- finger nail : 3m m / month Q
- toe nail : 1- mm/ monthQ
• Nail Structure :

Nail Plate
Lateral nail fold '4 Cuticle

[Link]
> Lunula ( Half - moon )

> Thoximal nail fold

Fig : 1

• Nail Anatomy

Lunula (Visible
Nail plate (White colour )

Nail Matrix
Mai’ f bed

Hyponychium
Terminal phalanx
Fig : 2

Appendegeal Disorders Part III


[Link]
17

dland hypertrophy / fibrosis

Potato like nose

- Treatment -> Resurfacing of nose


Coz laser
Surgical technique
2.02- 6 -> New diagnostic criteria

Diagnosis
Fixed erythema telangiectatic changes
Phyma

Major
Papules

Appendegeal Disorders Part II


2

Paronychia : Infection of nail fold 00 :04 : SO

• Paronychia : Infection of nail fold


i I
Acute chronic

Acute Paronychia :

[Link]
• Etiology: Staph aureus QQ
• C / E: Pus + Red / swelling + Pain
• T / t : I &C P
• Antibiotics

Chronic Paronychia :
• Etiology : Infection + Irritation / Inflammation
4 i
• Predisposed : Candida wet work +- Detergents
Housewife

• C / E: Ragged / Absent cuticle


Red / swollen Nail Folds
Roughening / thickening of nail plate
Appendegeal Disorders Part III
[Link]

• T / t : Ainti - fungal + steroids ( Topi cal )

Onychomycosis:

/. Nail
ii. Fungal
• Etiology :
- Dermatophytes : Me ; me -> Trichophyton
ruhrum; synonym: tinea unguim
- Non - Dermatophytes: fusarium, Aspergilli
- Yeast ( Candida )
• Clinical Features :
- Nail plate : Yellow/ brown discoloration $
Thick / rough nail plate
Tunnels

Appendegeal Disorders Part III


4

- Nail bed : Subungual hyperkeratosis ( fungal debris )


Onycholysis ( white )

Pitting

© No

i l
Psoriasis onycholysis

[Link]
Types: Tinea unguim

Z .Distal lateral subungual OM : MC Type Q


Z . Proximal subungual OM
- H I V positive

Appendegeal Disorders Part III


[Link]

3 .Superficial white Onychomycosis


- Dorsal N . plate
[Link] dystrophic Onychomycosis

Investigation:
• KOH mount :

Sample : Nail clipping


i
Overnight KOH dip
Findings : Hyphae

•T / t :
- Topical
- Systemic
i . Nail Lacquers : Topical
Formulation:
a . Amorolfine 5%
b. Ciclopirox 2%

c . Terbinafine HO %
d . Efinaconazole & Tabavirol
ii. Systemic T / t

Appendegeal Disorders Part III


6

Drug Dose Finger Toe

nail nail
Terbinafine 250 mg (o 22
OP weeks weeks
Itraconazole 200 mg (a 22
OP weeks weeks
Qriseotulvin 25 - (b 3

20 mg \ kg \d months months
Q

Pulse Therapy :
• Prug : Itraconazole
• Pose : 200 mg BIP
every month -> single pulse
• Puration : 7 days,[Link]
• Finger nail : 2 pulses Q
• Toe nail : 3 pulses $

Nail Pitting :
• Pepression on nail plate
• Pefect : Keratinization in proximal N . matrix

Nail Psoriasis : 00 : 23 :20

Appendegeal Disorders Part III


[Link]
7

• Importance : Me finding
• Cause : Parakeratosis in proximal nail matrix
• Characteristics:
- C : Coarse

- I: Irregular
- P : Peep

Alopecia aerates : Nail 00 :22 :25

• Characteristics:
- S : Superficial
- F: Fine
- R: Regular
• Called as : Geometric nail pittingj sandpaper nail

Appendegeal Disorders Part III


8
Nail Pterygium:

TV
i \
damages N . matrix / nail bed
/
/
'\
/
/ \
\
Permanent nail loss
/
/ \
/
/
V
\
Anonychia
/ \
/ \
/ \
/

Nail lichen planus: Pterygium

[Link]

• Importance : Patlngnomic finding Q


Permanent / Irreversible loss of nail

Ventral Pterygium : 00 :Z 3 : S4

Appendegeal Disorders Part III


[Link]

• Seen in: Trauma


Systemic sclerosis ^

Leuconychia :
• White discoloration of N . plate
• True : defect in N . matrix
Press nail -> white
• Apparent : N . Bed
Press -> Changes

True Leuconychia : Mee' s lines 00 : 26 :24

• Finding : Transverse white lines


parallel to Lunula
• Seen in: Chronic arsenic Poisoning QQ

Appendegeal Disorders Part III


10

Apparent Leuconychia : muehrcke lines

• Finding : Double bands


parallel to eacln other
• Seen in: Nail bed swelling due to
Hypoalbuminemia
\
< 2gm dl

Terry Nails : [Link] 00:Z 8 : 30

• Findings:
- Proximal - white ( opaque )
- Distal ( Z 07o ) - Normal | brown
• Seen in : Chronic liver disease
CCF

Appendegeal Disorders Part III


[Link]
11

Lindsay Nails : Half & Half nail 00 : 22 : 55

• Finding : Proximal '/2. -> white


Distal '/2. -> brown
• Seen in: chronic kidney disease

Beau' s Line

• Seen in: Transverse depression of nail


- Sever systemic illness
- Nutritional status
• Cause : sudden arrest in Proliferation
• Importance : Qap between illness &c non illness

Appendegeal Disorders Part III


12
Koilonychia :

• Spoon shaped nails


• Iron deficiency Anemia

Trachyonychia : Twenty nail dystrophy Q

[Link]

• C / F: Roughening of nail surface children


• Seen in: MC -> Idiopathic
Next MC -> Alopecia areate Q &c Atopic
Eczema &c Psorasis

Appendegeal Disorders Part III


[Link]
13
Yellow nail Syndrome :

• Triad :
- Lgmplnoedema
- Pleural Effusion
- Yellow discoloration + N . thickening .

Permatomyositis: Nail

• Periungual Telangiectasia’ s

Appendegeal Disorders Part III


1

BACTERIAL INFECTIONS OF S K I N

Normal skin flora : 00 :00 :12

• Propionibacterium acnes
• Corynebacterium sps
• Staphylococcus epidermidis
• Candida albicans ( yeast )
• Many others

Pyoderma :
• Bacterial infections of skin
• Classification:
- Non - Fotticular
[Link]
- Follicular

Non follicular pyodermas :


Types
Localized spreading
• Impetigo • erysipelas
• ecthyma •cellulitis

Impetigo:
• Superficial bacterial infection of skin
• Classification:
- Non bullous
- Bullous

Bacterial Infections
[Link]

Non - Bullous impetigo:

• Most common type of impetigo


• MC cutaneous bacterial infection
• Synonym : impetigo contagiosa
• Etiology : streptococcus pyogenes ( Most common,
India , developing countries)
Stapln aureus ( most common, western, developing )
• Most common age group : children
• Most common site : face perinasal and peri oral
}

• Clinical features : erosion covered with golden yellow


honey -colored crust
• Healing : no scarring
• Complication: M 43 strain ( Nephritogenic )
i
Post streptococcal glomerulonephritis ( P S Q N )

• Risk not altered by use of antibiotics


• Not lead to rheumatic fever

Bacterial Infections
Bullous impetigo:

• Etiology : staph aureus -> toxin


• Most common site : lower legs
• Clinical feature : pus filled bullae, varnish crust
Hypopyon sign
• Healing : no scarring
• Toxin: exfotiatin ( Epidermolytic toxin)
• Target : Psg i
[Link]
• Process : Acantholysis -> separation of cells of
epidermis
• Level of split : sub corneal cleft -> bullae.

Treatment:
• Topical :
- Fusidic acid -> most common
- Retapamulin -> active against resistant bacteria
- Mupirocin -> nasal colonization with SA twice
daily x 7 days
- Bacitracin/ colistin
1
nasal colonization

Bacterial Infections
[Link]
4

• Oral :
- Picloxacillin ( DOC )
- Flucloxacillin

Ecthyma :

• Synonym : Ulcerative impetigo ( deeper dermis )


• Etiology : staphj strep
• Most common site : lower leg
• Clinical feature : ulcer, covered with blackish crust
• Healing : scaifrh ng +
'

Erysipelas :

Bacterial Infections
• Cause : streptococcus
• Level : lymphatics ( Dermal )
• Clinical feature :
- Erythematous indurated lesion
- Bright red
• Margins : clear demarcation between involved and
uninvolved skin
• St. Anthony' s fire
• Most common site : lower leg

Cellulitis

[Link]

Fig : S

• Staph, strep many }

• Subcutaneous fat
• Diffuse swelling
- Painful

- Warm to touch
• No clear margins

Bacterial Infections
[Link]

Non follicular pyoderma :

• Epidermis : impetigo
• Epidermis and dermis : ecthyma
• Dermis : erysipelas ( Lymphatic)
• SC fat : cellulitis
• Fascia + muscle : necrotizing fasciitis

Necrotizing fasciitis :

Bacterial Infections
7

• Etiology : polymicrobial
• Clinical feature : deep entire tissue
}

• Treatment : emergency surgical debridement


-f-

13 road spectrum antibiotics


• Fournier’ s gangrene - perineum

Follicular pyoderma : hair follicle


• Etiology : staph aureus ( most common)
• Types :

\ '
o
\ \
\ v * < \
[Link]
/ /
/ i
1
M ' /?
> f
i
\
/
/
\
s
* A /

Folliculilis Furuncle Carbuncle


Fig : 2

Folliculitis :

• Involvement : infundibulum
• Pustule centered around hair
Bacterial Infections
[Link]
8

• Surrounded by erytkema
• Most common site = face
• Superficial folliculitis -> Bockkart’ s impetigo
• dram negative folliculitis -> Acne,
• pseudomonas ( Hot tub folliculitis )

Fulruncle:

Fig -, to

• Involvement : Hair follicle -t- surrounding area

Peep seated pain full red nodule pus


point us
Most common skin infection caused by
MRS A

Carbuncle:

Bacterial Infections
• Multiple contiguous hair follicle involvement
• MC site : Nape of neck
• Most common association: Diabetics
• Clinical feature : painful indurated plaque, pustules
• TOC : Vancomycin

Toxin mediated diseases : ( Systemic )


• Streptococcus pyogenes : scarlet fever

Exudative pharyngitis -> fever + rash


( orange red )

Strawberry tongue
• Staphylococcus aureus :
- ssss [Link]
- Toxic shock syndrome -> tamponSj multisystemic
disease

Staphylococcal scalded skin syndrome : Ritters disease


• Etiology : staph aureus
• Toxin : exfoliatin ( Epidermolytic toxin )
• Target : Dsg H
• Mechanism: acantholysis
• Level of split : sub corneal level

Bacterial Infections
[Link]
10
Pathogenesis :

Localized Dissemination Skin


infection

Otitis Hematogenous Sub corneal


externa level
Furuncle

- t •
(
(
ri- (
r
r Blood

V ^ /

• History of local infection


• Clinical feature : fever 4- constitutional S / S and skin
rash

Bacterial Infections
11

• Skin lesions : initial = periorificial erythema +-

generalized peeling of skin

• Signs :
- Skin tenderness ©
- Nikolsky sign ©
• Mucosa : no
• Treatment : antibiotics

Generalized peeling of skin

ssss Drug reaction


i i
No SJS / TEN
Always mucosal involvement

[Link]
Other staphylococcal infections : 00 : 32 : 3 <b

i. Sycosis barbae :

• Sycosis barbae : staph aureus


• Site : Deep seated follicular infection of beard area
• Clinical feature : multiple pustules, plaques with
induration
• Healing : scarring

Bacterial Infections
[Link]
12
/7. Paronychia :

• Staph aureus : most common cause of acute


paronychia
• Site : nail fold
• Clinical feature : redness , swelling , pus
• Chronic paronychia:
- low grade , long duration infection Candida
albicans
predisposing factors : frequent wetting , detergents ,
damages cuticle

Botryomycosis : Misnomer

• Etiology : staph aureus ( most common )


• Other : e coli, klebsiella, proteus
Bacterial Infections
13

• Disease : chronic suppurative granulomatous infection


• Site : foot
• Clinical features : chronic diffuse swelling + nodules +

sinus +- pus discharge


( hotryo : means hunch of grapes )

Streptococcus pyogenes : Skin infections :


• direct infection of skin and subcutaneous tissue
2 .impetigo ( Non bullous )

2 .ecthyma

3. erysipelas
[Link]
[Link] fasciitis
• toxin -> scarlet fever
[Link]

Skin infection: Staph aureus


• Direct infection of skin and adjacent tissues
2 .Impetigo ( bullous and non - bullous )

2 .Ecthyma
3 .Folliculitis

4. Furunculosis
[Link]

[Link] barbae
7 .Botryomycosis

• Toxin mediated
2 .Staphylococcal scalded skin syndrome

2 .Toxic shock syndrome


Bacterial Infections
[Link]
14
Corynebacterium infections : commensals 4 Disease

X .erytlnrasma

2 . pitted keratolysis
3 .tricbomycosis axillaris

Erythrasma :

• Etiology: corynebacterium minutissimum


• MC association: PM
• Most common sites :
- Toe webs
- Axilla
• Clinical feature :

- Reddisln brown scaly lesion


- Asymptomatic
• Woods lamp : coral red fluorescence ( CopropWyrin III )

• T/T: Topical clindamycin / oral macro!ides

Bacterial Infections
15
Trichomycosis axillaris ( Misnomer )

• Etiology : Corynebacterium tenuis


• Site : axillae ( most common)
• Clinical : yellowish discoloration of hair
Due to digestion of keratin
• T / T : shave / macro I ides
[Link]
Pitted keratolysis :

• Etiology : micrococcus sedentarius


• Seen in : sweat, wet work ( farmers )
• Site : palms and soles
• Clinical features : crateriform pits + Sweating

Bacterial Infections
[Link]
16

i
Digestion of keratin
• T/T: Avoid sweat/ water
• Whitfield ointment: 3% salicylic acid +- 6 % Benzoic
acid

Pseudomonal infection:
jt . Hot tub folliculitis

2 . Ecthyma gangrenosum
[Link] nail syndrome

Hot tub folliculitis :

• Seen in : community bath/ spas


• Site : bathing trunk area
• Lesions : folliculitis

Bacterial Infections
17
Ecthyma gangrenosum:

• Seen in: ICU with pseudomonal septicemia


• Lesions : Hemorrhagic necrosis -> multiple ulcers
• Ecthyma -> staph and strep
• E . gangrenosum -> pseudomonas
• E . Contagiosum parapox virus

Qreen nail syndrome :[Link]

Fig : 22

• Pyoverdin and pyocyanin

Bacterial Infections
[Link]
18

Other bacterial skin infections : 00 : 58 :00

X . meningococcemia :

• Etiology : N . Meningitides
• Clinical : child + fever + s / o meningitis +- skin rash :
Petechiae , purple patches with irregular angulated
edges
i
Acute purpura fulminans

Z . Lyme disease :

CO
I' Fig : 24

• Causative organism : Borrelia burgdorferi


• Vector : Ixodes tick
• Pash: fever / f l u + Rash -+- local LN © ± systemic s / s

Bacterial Infections
19
Expanding annular erythematous rash
ECM ( Erythema chronicum migrans )
• DOC = DOXY

3 .Cutaneous anthrax:

• Etiology : bacillus anthracis


• Synonym : malignant pustule ( Misnomer )
[Link]
black eschar, surrounded
• Lesion : painless papules
by rim of vesicles
O O
c o
© o
o ©
o
4- Scrub typhus :

• Etiology : orientia tsutsugamushi


• Vector : trombiculid mites -> chiggers ( Larvae )

Bacterial Infections
[Link]
20

• Clinical feature : fever + Rash 4- CNS ( headache )


• Skin : erythematous with central black eschar
,

• T/T: doxy

S. Erysipeloid :

• Etiology : erysipelothrix rhusiopathiae


• Disease : zoonosis , cattle
• Occupation: fish/ meat handlers -> hand
• Lesion : purplish / red erythema and swelling painful
• TOC : Penicillin

[Link] skin infection

• Etiology : Vibrio vulnificus

Bacterial Infections
21

• Seen in : person sea beacln


• Lesion : purplisln erytlnema/ necrosis of skin .

7 . Blistering distal dactylitis

• Etiology : stapIn/ strep


• Seen in: volar fat pad of toes / fingers
• Lesion : [Link]
of skin - blister

• Felon -stapln - pulp of finger

Bacterial Infections
[Link]
1
MYCOBACTERIA S K I N INFECTION

Cutaneous TB 00 :00 : 50

- Cause : Mycobacterium tuberculosis it is an acid - fast


bacterium, decolorized by 207» H 2 S 04
- Manifestation of Infection depends on the route of

entry and host immunity


Naive -> No previous exposure
Host
'
- Qood - Previous 3CQ , Previous Infection
Immune ~ ( or ) healthy Individual
- Poor — Immunocompromised , child , elderly

Classification of cut TB 00 :03 : 5 5


* *

Exogenous TB
- Bacteria come directly to skin from outside
NAIVE -> TB chancre

- Host
GOOD -> TBVC ( tuberculosis verrucosa cutis )

Mycro bade rial Skin Infections


2
Endogenous TB
- Source is within the body

Route

Direct Hematogenous Auto


contiguous lupus vulgaris Inoculation
Scrofuloderma ( good orificial TB
( Immunity immunity ) ( Poor
poor ) Miliary TB immunity )
( Poor
immunity )
TB Gumma
[Link]
( Poor
immunity )

Good -> AF8 Negative -> Panel bacillary TB


Immunity -
L Poor AFB Positive -> Multibacillary TB

Mycrobacterial Skin Infections


[Link]

TB Chancre ( ULCER)

- Host; Naive
- Its primary TB so called Primary Inoculation TB
- When Primary TB Infects -> Lung Tissue 4- LN called
GHON' S FOCUS
- TB chancre in skin is analogous to Qhon' s focus of
lung

Clinical features
- Non tender ulcer with undermined edges bluish
margins occurring on extremities and face in mainly
children following a penetrating Injury associated
with regional Lymph node enlargement

Undermined edges in Dermatology


- TB chancre
- Chancroid
- Pyoderma gangrenosum
Mycrobacterial Skin Infections
- Rodent ulcer

Tuberculosis Verrucosa cutis (TBVC )


- tuberculosis
Post primary
- Syn: Prosecutor' s wart
Anatomist wart
- Paucibacillary TB
- Most common site are bands & feet ( trauma prone
areas )
- Most common pt : Farmer , anatomist
- Solitary , dry , rough, warty surface Verrucous,

brown — Red plaque with rough homey surface and


deep clefts and with crusting and purulent
fissures
[Link]
discharge

Warty Viral
TB warts
i. No. of Lesions Single Multiple
ii. Induration
Hi. Discharge

Mycrobacterial Skin Infections


[Link]

Lupus vulgaris

- Endogenous TBj Qood Immunity , Inost ,


Paucibacillary T 13
- Hematogenous route
- Most common type of cutaneous TJ3 in Adults in
India
- Most common site: buttocks also on extremities
- Usually solitary asymptomatic well defined fleslny
j

red brown plaque which increase in size and got


infiltrated and extends peripherally with central
atrophy and scaring and an advancing and a
receding edge
- Serpiginous margins seen
- Margins may have nodules
- Aka plaque type TB

Centre Periphery
Lupus vulgaris Scarring Activity
Leishmaniosis Activity Scarring

Mycro bade rial Skin Infections


Piascopy

- Press the plaque with clear glass slide


- Erythema decrease ( Blanching nodules)
- Qolden yellow nodules noticed called Apple Jelly
nodules

Scrofuloderma 00 : 37 :11
[Link]

- Endogenous TB , Poor Immunity


- m/ c pt - children
- m/ c type of cutaneous TB in children in India
- Direct contiguous spread from Internal foci which
include Lymph nodes , joints , Bones to skin
Mycrobacterial Skin Infections
[Link]
7
- m/ c source is lymphoma
- m/ c site neck
- m/ c source : cervical LN
- TB sinus : -> 3 tusk, margins
-> Pus discharge APB positive
-> Underlying LN adherent
-> Heals with puckered ( or ) cord like slurs
- Synonymj TB colliguative cutis

On' fical T 8 00 : 37 : 32

- Endogenous TB, Poor Immunity


- Spread : Auto Inoculation
- Pulmonary TB -> Cough sputum. ora / cavity
r Vomit -4 i
6 / TB
- Defecate -> Anaf opening

- Presents as painful ulcers at the skin near mouth }

anus and urethral meatus

Mycrobaderial Skin Infedions


Tuberculids 00 :42:2 S
- Id -> Hypersensitivity
- Hypersensitivity reaction to presence of bacilli in tine
body but organism is never seen in tine lesions , tlnougln
tlney wax & wane with tine condition of focus of

infection

- Person with good Immunity , Monteux test : Highly


positive
- Internal visceral focus of TB
- AFB negative in skin
- Skin lesions resolve with ATT

[Link]
Tuberculids - Classification
i. True

• Lichen scrofulosorum ( micropapular tuberculid )


- Qrouped lichenoid papules with perifollicular
pattern over the trunk
- Children and young adults

Mycro bade rial Skin Infections


[Link]

- m/ c site Trunk
• multiple skin coloured papuler present in a grouped
distribution
- Symmetrical crops of papules tlnat proceed to
central depressed scar
- m/ c affecting limbs ( extensor aspects )
- HPE : Cased ting granulomas
- HPE of lidnen scrofulosorum : perifollicular and
periappendiceal granulomas ( Non caseating
granulomas )

Papulonecrotic tuberculid
• Seen in adults
• Site : Extensors of extremities
• Clinical features : Papule -> necrotic

Ulcer

Heal vJitW scarring

VI v Fig : 7

Mycro bade rial Skin Infections


10
Erythema Induratum
ii. Facultative -

Erythema Nodosum

Erythema Erythema Nodosum


Induratum
Site - Posterior Site - Anterior leys
leys ( c a l f ) ( Shin )
Lesion - Lesion - Erythematous
Erythematous tender nodules ( do not
tender ulcerate )
no du ( es( u [ cerate )
Heal - scariny Heal - No scariny heal
[Link]
with dark piy mentation

Mycrobacterial Skin Infections


[Link]
11
Hi. False Tuberculids

- Lupus Miliaris disseminate faciei


- Site : Face
- Multiple reddish -brown papules and nodules on
central face around orifices
}

- HPE : granulomas, NO AFB

Treatment of TB
- ATT

r Intensive (7- m ) HRZE daily


- HRZE 6 months ~

Conditions (4 m) HRE

Atypical mycobacterial infections


Runyon classification
i. Slow growing
- Photo chromogen -> M. Kansasii
Mycrobacterial Skin Infections
12
M . Marinum
- Scotochromogen -> M . Scrofulaceum

M . Qordonae
- Non chromogen -> M . Avium — Intercellular
M . Xenopi
M . Terrae
ii. Rapid growers -> M . Fortuitism
M . Abscesses
M . Clnelonae

M . Marinum 4 water

[Link]

- Source’. Swimming pools/ fish tanks so called


swimming pool ( or ) fish tank granuloma
- They inoculate in the skin & form multiple nodules
along the lymphatics ( called sporotrichoid pattern)

Mycrobaderial Skin Infedions


[Link]
13

M. Ulcerans

- Tine bacterium releases a my cotoxin resulting in


necrosis of skin & muscle leading to ulcer -> BURULI
ULCER
- It’ s a painless ulcer

Mycobacterium obsesses / Cbelonae : ( Rapid growers)

- Ubiquitous
- Seen in soil
- Surgical equipment
- Salon equipment

Mycrobacterial Skin Infections


14
- Nodules & ulcers & abscess at the site of surgery /
treatment / procedure
- Occurs within 1- month - 3 months

Treatment of Atypical mycobacterial infections


- Antibiotics

[Link]

Mycrobacterial Skin Infections


[Link]
1

LEPROSY PART -/

• Chronic granulomatous infection.


• Etiology : Mycobacterium leprae, M . lepromatis .
• Incubation period : 7.-5 years

Mycobacterium leprae 00 :00 : 57

• Obligate intracellular bacteria

• Doubling time : 72 - rZ- 3 days


• Virulence factor: PQL -7 ( phosphogycolipid -7 ) - in cell
wall

Detection of M . leprae :
7- .Siit skin smear
2 .Culture : Not cultivatable in vitro grow in animal
models
a. Mouse
b. Nine banded armadillos

LEPROSY I
2

3 .Serology : PQL - %

Slit skin smear (SSS)


,

• Site : 3 sites
i. Lesion
ii . Eyebrow
Hi. Ear lobule

[Link]

• Stain: modified ZN stain


S% H 2.SO4

• > SL04 bacteria / ym of skin

LEPROSY I
[Link]
3
Bacteriological inderx :
• Total density of bacterial load ( HPE)

- 2 : 2 - 20 bacilli/ 200 HPF


- 2 : 2 -20 bacilli/ 20 HPF
- 3: 2 - 20 bacilli/ HPF
- 4: 20 -200 bacilli/ HPF
- 5: 200 -2000 bacilli/ HPF
- 6: > 203 bacilli/ HPF.

Morphological index:
% Live bacillij monitoring of disease response to t / E

Solid M . leprae Live , solid uniform staining


j

Fragmented
”~ Dead

dranular

LEPROSY I
Infection
, spread :
• Source of infection: HumanSj only known reservoir
• Portal of entry : Nose ( droplet )
• Mode of Entry : Respiratory tract
• Primary Target : Nerves ( HOO'Vo )

Pathogenesis :
• Bacilli discharged from nose
i
Inhaled by susceptible person
i
Taken up by alveolar macrophages
i
Disseminated through blood
[Link]
I
Spreads to nerves &c skin
i
Bacilli proliferate especially by Schwann cell
( primary tract )

LEPROSY I
[Link]
5

Types of disease 00 :1-0 :1-0

Depend on Lost immunity ( sp. To M . Leprae )


1
1
Excellent Not decided
> 9 (9%
i
i Indeterminate disease
No disease
I 1

Resolve Persist Progress ->


Determinate

Indeterminate leprosy :

• CM I : not decided
• History : R / o endemic area
a. Bilnar
b. JLarkLand
c . CLLattisgarb

• Age : child
• Lesions : single, ill defined , Lypopigmented macule,
No scaling „ No loss of sensation

• HPE : perineural , peri appendageal lymphocytic


infiltration

LEPROSYi
6
PP:
Pityriasis alba:

• Endogenous eczema
Hypopigmented macules , Pace , child
- Multiple
- Fine scaling
- Episodic recurrence
[Link]
- Atopic dermatitis
- HPE : Spongiosis

Determinate leprosy :

Good Fair Poor


I
If i 1
Tuberculoid Borderline Lepromatous
leprosy leprosy
l BT BB BL i
Best prognosis Severe

LEPROSY I
[Link]
7

Ridley jopling classifications : Determinate Hansen' s


Q O : Z 8 : SO

i. Immunological
ii. Bacteriological
Hi. Clinical
iv . Histo pathological
v .TTj BTj BBj BL , LL

Immunological :

BT 88 BL LL
CMl : excellent (tt ) Poor(\ft )

Lepromin test : ++ - negative


Bacteriological :
AF8 : Nil / negative - +++++++

( SSS ) <£> +

LL

Number H - 3( few ) Increase, all over body


Symmetry : Symmetrical
Sensation Anaesthetic No lesional anaesthesia
Nerves Nerve to Symmetrical nerve
patch enlargement
HPB Qranuloma Macrophage collection
( well
defined )

LEPROSY I
8

Tuberculoid leprosy :

• Good CMl
• Number of lesions : i- 3 lesions
• Lesion : well , defined , by pop lamented plaque.
• Appearance :
Sloping inner margin
[Link]
Outer margin

Well defined

Saucer > rigWt way up .

• Sensations : Nerves -> anaesthesia.


Sweat glands Anbidrotic .
Hair follicle-^ No bair
• Nerve : Nerve to patch
• SSS : Negative

LEPROSY I
[Link]
9
Borderline tuberculoid leprosy : Most common type of
leprosy ( India )
• Number of lesions : up to 1-0

• Lesion: well - ill -defined margins


• Special features : satellite lesions
• Sensations : lost 70 - 80%
• Nerve : Regional hUrves
• SSS : 1+ to 2+

Borderline leprosy:
Rarest most unstable
BT + * BL
• Number of lesions ; up to 20

• Lesions : polymorphic , Annular lesions , TARGET


LESIONS ( I N I C E T J u l y 2 2 )

• Sensations : 1-0 -20%

LEPROSY I
10

• Nerves: multiple nerves

• SSS: 3+ to 44-
• Appearance :

Sloping outer margin

inner margin : produced out


Inverted saucer appearance / SWSS cWeese
[Link]
appearance

Borderline lepromatous leprosy :


• Number of lesions : multiple tending to symmetry .
}

• Lesions : Will defined plaques


• Sensation: 1-0 -2.0 % lost

LEPROSY I
[Link]
11

• Nerve : multiple nerves , asymmetric


• SSS : 4 -H to 5 +

Lepromatous leprosy
• Number of lesions : multiple , symmetrical diffuse is
filtration of skin +

systemic involvement

• Lesions : plaques , modules


• Nerve : glove & stocking anaesthesia , multiple ,
symmetrical nerves
• SSS : 6+

• Early features : nasal stuffiness , epistaxis , pedal


edema ( autonomic neuropathy )

LEPROSY I
12

Fig : 13

• Later features :
- Madarosis : loss of outer 1- / 3 eyebrows
- Saddle nose
- Buddlaa ears
- Leonine facies

[Link]
Histopatlnology [Link] .S9

Ho

\^ A -* & ;

-

f *
JZr • •
Qo
i
/

•» 5• • • J•fiSl
ZM

.m - O
*
* twc •
• .• • 1

•w *
•t
-
vSDv *
• •

•I

Fig : 14

LEPROSY /
[Link]
13

LL
• Well defined • Macroplnage
granuloma collection
• Nerve damage • Foamy
• Gaint cells macrophages
• Abutting tine ( Virchow cells )
epidermis • Clear space
( GRENZ ZONE )
*

Pi ^

- : v v; v
A ;
- ^

* • i
**: . * i

. > n /*^ >


- .- --v
i

/*

— •«*fh K/
A * •At
«ry
% J
* Cl :‘ K
.-
«/ > • j» ;
v C? ’ S, * *
A *- 7«f t •* /# A <
V .

•' *
^ V '

'
imHief
Pure neuritic leprosy : (7AL - Indian)
^
• Involvement : only nerves
• C / F : thickeningj sensori motor deficit
• Skin : No skin lesions
• SSS : negative
• Diagnosis : Nerve biopsy -> Radial cutaneous nerveQ

/ sural nerve

LEPROSY I
14
Histoid hansens
• Seen in : Papsone monotherapy

• Lesion: Pome shaped papules & nodules


• Normal skin
• SSS : (o +-

[Link]
Lepra Bonita

• Synonym : Beautiful leprosy / lucio leprosy


• C / F: severe, type of LL harness

Nerve involvement in leprosy

• First function to he affected : Sensory modality QQ

LEPROSY I
[Link]
15

• First sensation to go : Thermal > light touch > pain >


deep touch ( hot & cold differentiated )

• Sensation to nerve go : vibration & proprioception


• MC nerve involved : ulnar nerve Q
• MC cranial nerve : facial nerve
• Nerves : closest to skin coldest

• High ulnarj low median

LEPROSY I
16

Ocular Involvement

[Link]

• Involved : Anterior clnamber


• Not involved : posterior chamber
• C / F: keratitis , conjunctivitis , uveitis , corneal ulcer ,
corneal scarring
• Me lesion: lagophthalmos $

• Most specific lesion: Iris pearl Q

• Me cause blindness : cataract $

LEPROSY I
[Link]
17

Sanctuary sites
• Spared in leprosy

LEPROSY I
1

LEPROSY - II

Cardinal Features : Any one diagnosis 00 :00 :7-0

i. SKIN : Hypopigmented / Erythematous , hypo aesthetic


plaque
ii . Nerve : Enlarged / thickening of nerves + sensory motor
deficit
Hi. Bacteria : SSS -H

Investigations :
[Link]

Z .Lepromin test
3 .Biopsy
[Link]

Lepromin Test :
Intradermal sensitivity testQ
Biphasic
48 hours 3 -4 weeks
• Burly • Lute
• FERNANDEZ Reaction • MITSUDA Reaction

Uses :

[Link] nos is

7 .Classify disease
3 .Monitoring T / t

Not Diagnostic

LEPROSY II
[Link]
2
Leprosy : basis o f T / t :

Paucibacillary Multibacillary
Skin lesions s >6

Nerves <2 >2

SSS Negative Positive

T / t:
Multidrug therapy : MPT
2 .Rifampicin -> most potent / cidal

2 .Clofazimine
3 .P apsone

• Rifampicin: (LOOmg - single one a month

• Clofazimine -
- 300 mg — once a month
- SOmg - daily
• Papsone - 200 mg daily
• 2 kit = 4 weeks

LEPROSY II
3
MPT in paediatric age group ( HO - T4 gears )
• Rifampicin :4 SOmg - once / month
• Clofazimine
- HSOmg — once / month

- SOmg alternate day

- flrMSTF

9> n
*“
re * e
® n "
e
f- e
$

Fi'fl : 2

• Papsone - SOmg [Link]


daily
• QQPB : 6 months
• ^ MB : H 2 Months

Leprosy reactions:
• Immune dysregulation
H .Type - H

2 .Type -2

H .TYPE - H : Leprosy Reaction


• Type of hypersensitivity : type 4 HS
• Seen in:
- Borderline
- BT B 8 , BL
}

LEPROSY II
[Link]
4

• Leprosy lesion : Erythema and Edema in pre -


existing lessons
Hyperaesthesia
• Nerves : Neuritis : Sensori motor deficit
• Others Symptoms : facial Edema
• New lesions: No
• Others Organs : No
T/ t

• MB - MPTContinue MB - MPT
• Mild -UNSAID' S
• Mod -Severe -> systemic steroids( prednisolone )
• Other drugs : negative
• No role : clofazimine / Thalidomide

2 .Type 2 : Leprosy Reaction


• Type of hypersensitivity : Type 3 HS ( immune
complex )

LEPROSY II
5

• Seen in : Lepromatous leprosy


- Type 1: 4 (2+4 = 5)

- Type a : 3 (3 +2 = 5)

• Leprosy lesions : No change


MV
*

[Link]

S'

• New lesions : BNL ( Erythema Nodosum leprosum )


Multiple Redj Tenderj Nodules
• Nerves : Neuritis

• Other Organs : uveitis, HepatitiSj Orchitis Q

• Other symptoms : Fever , Arthralgia

T/t

• MP - MPT : Continue
• Mild : NASAIPS
• Mod - severe : prednisolone $

LEPROSY II
[Link]

• Other Prugs :
- Clofazimine
- Thalidomide
- Methotrexate
- Pentoxifylline

Thalidomide: Type Z reaction


• Importance : Most effective drug , Not POC

• Used in : Not responding , resistant


• Mech : Anti TNF - o(
• Pose : ZOO - AOOmg / d Q
• A/ E : Sedation and constipation
Neuropathy : SNAP ( Sensory Nerve Action Potential )
Teratogenicity ( category eX ’)
• Negative UPT
• Pouble Contraception

LUCRO PHENOMENA:

• Seen in : Lucio Leprosy

• Type of Reaction: Type Z Reaction


LEPROSY II
7

• Pathology : bacteria vessel wall


• Necrosis Bndothelitis

• Ischemia
• Ulcerative fatal

Deformities in leprosy :
i. Primary
ii . Secondary

i. Primary Deformities : Direct tissue damage by


bacteria

[Link]

• Madarosis
• Saddle Nose
• Buddha Bar
ii . Secondary deformities :

LEPROSY II
[Link]
8

• Trophic Ulcer
• Claw island

WHO Grading of Deformities OO .ZO. XC

Grade, Hands and Feet Byes

Grade O No loss of sensations No eye problem due to


No visible deformity / damage leprosy
No evidence of visual
impairment
Grade i Loss of sensation is present Bye problem due to
No visible deformity / damage leprosy positive
Vision (d / (bO or better
Finger counting at 6 m (J)
Lagophthalmos ,
Iridocyclitis , Corneal
opacities
Grade 2 Visible deformity / damage Severe visual impairment
wounds , ulcer , deformity A/ t
muscle weakness , loss of tissue
vision — cannot count
fingers at 6 m
such as foot drop , claw hand ,
loss / partial resorption of
finger / toes

LEPROSY II
Deformity Due to Ulnar Nerve paralysis :
• Partial claw Wand

Deformity Due to Ulnar + Median Nerve Damage :


• Complete claw Wand

[Link]

Only Median Nerve Palsy : TWenar atropWy , Ape TWumb


• Radical Nerve Palsy : VJaist Drop

LEPROSY II
[Link]
10

• Common Personal Nerve : Foot drop

LEPROSY II
1

FUNGAL INFECTION' S PART - /

Classification
• Superficial
• Subcutaneous
• Deep / systemic
• Superficial fungal infections

Pityriasis versicolor 00 :00 : 3 S

• (generally , happens in hot and humid climate


• Etiology : - Malassezia globosa > M . furfur

- Lipophilic fungus , exists in dimorphic form


- It is a normal Commensal
[Link]
• Localization : - Initial lesions -> Perifollicular scales

• Pityriasis - scales
Versicolor - various colours
• Clinical features
- Multiple hypopigmented scaly macules
- On Upper back / upper chest
- Asymptomatic

Fungal Infection’ s
Part — l
[Link]
2
- Polycyclic margin

• Hypopigmented macule is due to azelaic acid


• Hyperpigmentation is due to larger melanosomes
• When extremities are involved sparing trunk - Inverse
pityriasis

• Fine branny scales ( or ) furfuraceous scaling


• Scaling becomes prominent on scratching

SCRATCH SICN / COUP PE ONLCjLE / BESNIER' S


SICN

Fungal Infection’ s
Part — l
3

l investigations 00 :02 :05

• KOH mount
- Exist as botln yeast & hyphae form. Spaghetti and
meat bad appearance or banana and grapes
appearance
- On Wood' s lamp - Pale yellow color
• Treatment
- Azoles - Topically - creams / lotions / shampoos
and oral
- Selenium sulphide lotion — antifungals and
cytostatic
- Ciclopirox olamine
• Not used
- Terbinafine [Link]
- Griseofulvin

Tinea Nigra 00 : ZZ :45

• Caused by fungi - Hortaea werneckii

• Lesion: - Asymptomatic hyper pigmented macules


• Site : - palms ( most common) , soles
• Treatment : - azoles
Fungal Infection’ s
Part — l
[Link]
4

PIEDRA -
00 : l 2.:2.2

• Synonym: - Trichomycosis nodularis


• Site : - Superficial funyal infection of hair shaft
*
Nodular lesions
• Clinical features

- Black Piedra
Etiology : - Piedraia hortae
Nodules : - Black , hard , tightly adherent

- White piedra
Etiology : - Trichosporon heigelii
Nodules : - white , softj loosely attached
• Treatment : - Shave / Clip the hair, azoles

Candidiasis 00 :114 : 50

• Etiology : - Candida albicans ( most common)

Commensal in normal person


• Precipitating factor

Diabetes
Z . Pregnancy
3 . Immunesuppression - Organ transplantation,
chemotherapy , HIV - A / PS
Fungal Infection’ s
Part — l
4. Long term antibiotics

^ - Autoimmune - thyroid diseases j chronic


mucocutaneous candidiasis

Candidiasis : Types
2.0 ra!
2 . Intertrigo
3. Paronychia

4 .Vulvo -vaginal
[Link] - posthitis

X .Oral

• VJhite -4 Hyperplastic
• Red -> [Link]

Hyperplastic oral candidiasis

• Synonym : Oral thrush or pseudomembranous


candidiasis VJhen pseudomembrane is rubbed o f f ,
red raw areas are seen
• 2 types
- Acute
- Chronic Premalignant
Fungal Infection’ s
Part — l
[Link]
6

Atrophic candidiasis ( red )


• Types
- Acute Antibiotic sore mouth
- Chronic -> Denture mouth

Angular chelilitis

• Redness and fissuring in angle of mouth


• Also called as Perleche
• Also seen with riboflavin ( 3 z ) deficiency

Z .Candidial intertrigo ( Folds )

Fungal Infection’ s
Part — l
7

• Hot and humid conditions


• Site : - Inter mammary, neck , axillae , groin, finger
webs
• Lesion: -
SL .Redj maceration
Z .Satellite lesions
3 . Peripheral scaling

3 .Candidial balanoposthitis ( Not a STl )


[Link]

• Associated with MEN with diabetes me ! I it us


• Clinical features : Erythema and swelling of prepuce
radial fissures

4 .Vulvo vaginal candidiasis ( Not a STl )

• Association: - Pregnancy , antibiotics , DM


• Discharge : - Curdy white adherent to vaginal walls
associated with itching
Fungal Infection’ s
Part — l
[Link]
8
[Link] paronychia / chronic paronychia
• Site : - Nail folds
• Association: - wetting of hands -> Dhobi and
housewife

• Clinical features : -
i. Damage to cuticles — Dagged / absent
ii. Redness and swelling of nail folds

Hi. Thickening and rough nail plate

Investigations of candidiasis
• KOH mount : - budding spores and pseudo hyphae

Fig : 12.

Candidiasis treatment
• Azoles
• Precipitating factors treated

Fungal Infection’ s
Part — l
1

FUNGAL INFECTION' S PART - II

Superficial fungal infections - Permatophytosis


[Link]: - Affects non - living skin
Z .Target : - S . corneum ( Keratinophilic )

Dermatophytes : Genera

Trichophyton Epidermopinyton Microsporuvn


y y y
Skin
y y
Hair X

y y
Nail X

Dermatophytosis (Tinea )

(tinea facieii
[Link]
Ringworm of the face Ringworm of the scalp
(tinea capitisi

Ringworm of the beard


(tinea barbae )

Ringworm of the hand


(tinea manus)
Ringworm of the body
(tinea corporis)

Ringworm of the groin


(tinea crunsi

Ringworm of the nails


(tinea unguium)

Ringworm of the foot


(tinea pedis)
Fig : 1

Tinea : - Typical lesion

Fungal Infection’s
Part - l
[Link]
2

• Lesion : - ErythematouSj annular plaque


• Centre: - Central clearing
• Periphery : - Vesicles and pustules at the margin
• Surface : - Scaling
• Symptom: - Itching
• Tinea Corporis ( body )

isle"
:
'

m
V

Fig : 3

• Site : - Non -glahrous skin

Tinea Cruris

• Site : - Qroin folds QQ


• Synonym: - Dhobi Itch
Jock Itch

Fungal Infection’ s
Part - l
3
Tinea Pedis

• Synonym: - Athlete' s foot Q


• Most common Site : - me -> 4tK interdigital / toe
web
• Vesicular T. Pedis T .mentagrophytes var.
interdig itale

Tinea Manuum
[Link]

• Manuum means hands


• Site : - Hands ( palms )
• Association: - Feet + Hands
-Two feet, one hand syndrome Q
- nails
s|/
Caused by T. rubrum Q

Fungal Infection’ s
Part - l
[Link]
4

Tinea Faciei
• Affects face

Tinea barbae
• affects beard

Tinea Incognito

• Disease : - Steroid - modified Tinea QQ


• Cause: - Applied OTC creams ( steroids )
• Lesions : -

Fungal Infection’s
Part - l
- Decrease Redness
- Decrease Scaling
- Decrease Itching
- Hyper pigmented lesions,
^ itching
On Stopping these creams -> sudden rebound

Tinea Unguim ( Nail )

• Onychomycosis —caused by
- DM
- Non - DM
- Yeasts
[Link]

• Site : - Nail plate and Nail bed


• Clinical features

r
L
• Nail plate
T
• Nail Bed : -
- Thickening Subungual
- Brown - Yellow Hyperkeratosis Q
discoloration
- Tunnels

- Roughing /

crumbling
Fungal Infection’s
Part - l
[Link]
6

* -> Onycholysis

Distal lateral subungual onychomycosis

m Proximal subungual OM -Common in HIV

Superficial white onychomycosis


• Superficial infection of NP -> Looks White , crumbling
Fig : 12

of the surface

Superficial white onychomycosis

Fig : 13

Total dystrophic onychomycosis


• Complete involvement of the nail

Total Dystrophic Onychomycosis

Fungal Infection’ s
Part - l
Tinea Capitis

tc MLAcWvvtC
'
^ 'V f

Nt
Fig - is

Adamson' s fringe
• Site : - Hair shaft - above Adamson' s fringe
• Age group : - child ( due to less sebum in prepuberty )
- Partial Hair loss QQ
- Broken hair / easy pluckability
- Inflammation ( scaling , vesicles / pustules )

Non - Inflammatory Inflammatory


• No scarring • Heals with Scarring
I .Qrey [Link]
T .Pavus
Z .Black dot Z .Kerion

• Grey Patch ( GMC )


- Involvement : - Ectothrix -> fungal spores will be
outside the hair shaft
- Aetiology : - Microsporum
- Clinical features : - Pry , lustreless , grey -coloured
scaling

Fungal Infection’ s
Part - l
[Link]
8

• Black dot ( BNT )


,

- Involvement : - Endothrix - fungal spores inside


the Inair slnaft
- Etiology : - Triclnoplnyton
- Clinical : - Black dots on tine surface

• Favus
- Endemic : - Africa, Kashmir
- Etiology : - Trichophyton schoenleinii

- Clinical features : - \ / -> scutula QQ - C


shaped crust

Kerion
- Etiology -> Zoophilic
- Clinical features -
• Red boggy swelling
• Studded with pustules
• Easy pluckability of hair
• Regional lymphadenopathy ( occipital / cervical )
Fungal Infection’ s
Part - l
9

• Non -painful - differentiate it from bacterial


infection

Tinea: - Epidemiology
• Most common organism : - Triclnoplnyton
• Tinea corporis / cruris / pedis / unguim - T.
rubrum
• Tinea capitis
- India: - T. violaceum
[Link]
- VJestern : - T. Tonsurans
- Global : - M . canis
- KOH mount :

• Sample : - In 10 -30% KOH


• Skin : - Scale
• Nail : - Nail plate clipping / subungual debris
• Hair : - Broken Inair scale
• Finding : - Hyplnae
Fungal Infection’s
Part - l
[Link]
10
Treatment (Topical , systemic )
• Azoles : -
• Ally ! amines : - Terbinafine
• driseofulvin : - Oral
• Morpholines : - Amorolfine ( topically )

Antifungals - MOA
Squalon «
, Squalen epoxidase
*
«
1 i -
X
CT)
2.3*oxidosqualene
La nosterol synthetase
Lenosterol X
-
Lanoftterol ( C 14 ) a demethyldse
V

- —
Zymosterol

C -24 sterol reductase


* =,
^
Pecosterol
(Ww -
I C -8 sterol isomerase
Eptsterol

IW KoteAx^
~
A
f
^ Ergosterol
j * Fig -- 21

• Drug of choice : - Terbinafine


• Duration : - ZSOmg OD x 4 -6 weeks
• Itraconazole, driseofulin also used .

Tinea ungium : -Treatment


• Nail lacquers : - single nail / cannot be given oral
( HepatitiSj polypharmacy )

Formulation
• Amorolfine 5%
• Ciclopirox 2 %
• Terbinafine XO % ( Q NBBT 7-07-0 )
• Bfinaconazole & Tavaborole

Fungal Infection’ s
Part - l
11
Tinea Unguim: Systemic Treatment

Pose Duration
Fingernail Toenail
Terbinafine ZSOmg OP 6 weeks TZ weeks
Itraconazole TOO mg BP 6 weeks TZ weeks
Criseofulvin T 5 -ZOmg / kg / d 6 months P months

Tinea Unguim: Pulse therapy


• Prug : Itraconazole
• Pose : ZOOmg BP
• Puration : 7 daySj every month -> T pulse
• Fingernail : Z Pulses
• Toenail : 3 Pulses

[Link]
Tinea capitis : Treatment
• POC ( Overall ) : Ciriseofulvin
• Pose : T 5 -ZO mg / kg / d
• Puration: 4 -6 weeks
• Specific POC
- Qrey patch : Qriseofulvin
- Black Pot : Terbinafine

Subcutaneous mycoses 00 : 33 : 38

• Involves subcutaneous tissue


• Occurs due to penetrating trauma
• Also known as implantation mycosis

Subcutaneous mycoses
T .Sporotrichosis

Fungal Infection’ s
Part - l
[Link]
12
2..Chromoblastomycosis
3 .Mycetoma

Sporotrichosis 00 : 34 :50

• Etiology : Sporothrix schenckii -> dimorphic fungus


• Inoculation : present in soil / plant matterj through
rose thorn prick
• Target : lymphatics
• Synonym : Rose gardener' s diseases

Sporotrichosis: Clinical features


• Lesions : multiple Nodulo ulcerative lesions
• Site : legs/ Arms
• Pattern: linear

• Distribution : Lymphoid / sporotrichoid ascending
lymphangitis
D / D : - Fish tank granuloma caused by mycobacterium
marinum

Sporotrichosis : Investigations
• KOH Mount

Fungal Infection’ s
Part - l
13
Cl
M

Cigar shaped yeast Fig : 2.3

• Histopathology

••

/

-


I
#

H
9
s

*• -
%
>#
»
v .+ <
-
I
4 t
lJK % 1 •
1
a >* > <
%
t

•4 .. «

Asteroid body Fig : 24


[Link]
Sporotrichosis: Treatment
• Itraconazole
• Saturated solution of potassium iodide
- Sporotrichosis
- Sweets syndrome

Chromoblastomycosis - pigmented fungi 00 :40:04

Fungal Infection’ s
Part - l
[Link]
14

• Etiology :
T .Fonsacea pedrosoii
2 .F. compacta
3 . Plnialoplnora

• Lesion :
Multiple nodules, rougln verrucous surface " verrucous
dermatitis”
• Site : Hand and feet

Chromob lasto mycos is - 1 nvestigations

• Brown colourj tlnick -walled spores


• Copper penny bodies
• Medlar bodies
• Sclerotic bodies
• Muriform bodies
• Treatment : Itraconazole
Mycetoma
• Disease : dnronic granulomatous, suppurative
}

infection

• involves -
Z .Skin
2 Subcutaneous tissue
3 .Muscle / bone
• Types
Fungal Infection’ s
Part - l
15
3- . Fungi- Eumycetoma
2 . Bacteria - A cti no mycetoma

Entry of organism

l
ff Trauma ( Thom , wood splinter )

I
Swollen
N .
Drammu sinuses
Pus
Contains
discolored

( imnules
yellow,
( White,
brown, black and Fig : 7 1
red )

• Most common in rural / farmers Q


• Most common site : - Feet
Involves Wand also
[Link]
Eumycetoma

• Triad :
3- . Painless subcutaneous swelling (Tumefaction ) -
earliest clinical sign
2 Sinuses
3 .Cj rain

Mycetoma - Investigations

Fungal Infection’ s
Part - l
[Link]
16

• On examination : black grains are seen wlnicln are


aggregates of fungi
• On microscopy : gram negative fungi

MUAAJ

-
•arf 1 tr Fig : 29

• H P E : - Granulomatous inflammation
• Stain: Qomori metlnenamine silver stain
• Causative organism -> Madurella mycetomatis
( m / c -707o )
-> M . grisea
• Radiology - X Ray -irregular cortex/ cortical reaction
-osteolytic lesions

• Radiology ( MR! ) - Dot -in -circle sign

Slav }
* - CiAclf
I

wvluAXfl- (WJ
*
Fig : 30

Fungal Infection’ s
Part - l
17

Mycetoma. - Treatment
• Eumycetoma -> Long term antifungals + Surgical
debridement
• DOC - Itraconazole

Actinomycetoma 4 Filamentous bacteria

[Link]
• Etiology :
- Actinomadura Madura
- Nocardia brasiliensis
- Streptomyces somaliensis
• Site : Feet / bands
• Clinical features : Rural / farmer
Same as eumycetoma
• Colour of tine granules -red / wlnite / yellow

Actinomycetoma - Investigations
• Cram staining - gram positive filamentous bacteria -
sun ray appearance

Fungal Infection’ s
Part - l
[Link]
18

St ** - -
V* fcj
Central blue area

"TIM *
_ ^ Peripheral pink material

Dense neutrophilic infiltrate


mt

HlSTOPATHOLOdY Fig : 33

• Investigations are same


• Treatment
- Long term Antibiotics -Oral / injectable
• Cotrimoxazole +- Amikacin -> VJeisW Regimen
• Cotrimoxazoie + Streptomycin
• Dapsone

Fungal Infection’ s
Part - l
VIRAL INFECTIONS

Herpes simplex virus : HSV 00 :00 : 2.0

• HHV - (X family
• Virus : PNA
• Replication : nucleus
Primary infection
• Property : latency
Secondary infection
• Primary lesion: vesicle
• Due to : ballooning degeneration of keratinocyte
• HSV -i infection :

[Link]
Cutaneous Non cutaneous

Herpetic gingivostomatitis Meningitis


Oro labial herpes Ocular herpes
Herpetic whitlow Neonatal herpes
Herpes gladiatorum Bell' s palsy
Eczema herpeticum
Erythema multiforme
Qenital herps

Herpetic gingiva stomatitis:


• Most common age : children, primary infection of
oral mucosa
• Site : mucosa of oral cavity gums , tongue, lips

Viral Infections
[Link]
2

• Clinical feature : vesicles, ulcerative lesion painful


fever

Herpes labialis : NBBT ZOZO


• Synonym : fever sores, cold blisters
• Site : lipSj vermilion border
• Clinical features : grouped vesicles on erythematous
base

Fig : 2.

Viral Infections
3

• Triggers :
- Fever

- Menstruation
- Sun exposure
- Stress

• Latency : trigeminal ganglion

Herpetic whitlow :
• Contact infection

[Link]

• Association: dentists
• Site : distal pulp of finger
• Clinical features : grouped painful vesicles

Eczema herpeticum :
• Synonym : Kaposi varicelliform eruption
• Disease : disseminated HSV H infection
• Predisposing dermatoses : atopic eczema most
common

Viral Infections
[Link]
4

Sezary syndrome

Darner ds

P . folia cells

• Clinical features : fever 4- widespread vesicles,


erosions -> umbilicated
• T/T: IV acyclovir

Viml Infections
Erythema multiforme:

• Hypersensitivity rash
• Most common infectious cause : HSV H
• Lesions : taryet rash/ hulls eye lesion
- Centre = purple / blister
- Middle = pallor
- Periphery = erythematous
3 zonesj 3 [Link]
concentric rings
• Sites : acral - hands and feet mucosa
• HPE : interface dermatitis

Meningitis :
HSV rZ- >2
Mollaret meningitis / recurrent benign lymphocytic
mening itis

HSV - Z :
• Genital herpes = most common cause
• Meningitis
• Oro facial herpes

Viral Infections
[Link]

Herpes genitalis :
• Site : genitalia
• Lesion : multiple grouped vesicles red base painful
;

I
Erosions polycyclic margins

• LympW node : tenderj 3 / L inguinal LN

HSV infection - investigations :


• Tzanck smear : cytology test

- Qiemsa stain

Viml Infections
7
- Multinucleated giant cells -> characteristic of viral
vesicular disorder
• PCR : dold standard

T/T:

• Drug of choice : acyclovir


• Dose: 4-OOOmg TDS
• Duration: Primary -> 7 - SCO days
Secondary -> 5"
^ays
• Suppressive therapy : > <S / year acyclovir 400 mg
BD x i-2. year

• Other drugs : valacicloviVj famciclovir


• Resistant cases : ganciclovir, foscarnet
[Link]
Varicella zoster virus : HHV - 3

• V/Vus: PNA
• Primary : varicella / chicken pox
• Latent : dorsal root ganglion
• Secondary : herpes zoster
• Clinical feature
• IP : 7 -i4
^ays
• Lesion : vesicle + fe^er -> re
^ base

ViVaf Infections
[Link]
8

• Name sign: dew drops on rose petals


• Distribution: lines of Langer centripetal

•% , , Ulcer
#

¥
V
«1

/•
/
Blister

Papule
\ * * *:
Fig : lO

• Rash : macule -> papule -> vesicle pustule -> ulcer


-> scabs
• Polymorphic rash
Varicella in pregnancy :

Viral Infections
9

• Mortality :£ 4%
• Severe disease
• Pneumonia
• Risk of fetal transmission

Congenital Varicella:
• Time line : mateernal varicella <20 weeks of
gestation
• Lesion : 2° reactivation in utero
• Skin : cutaneous scaring along dermatome , limb
atrophy
• CNS : microcephaly , MR
• Bye : [Link]

Neonatal Varicella :
• Time tine : S days maternal varicella ( Delivery ) 2
days

Viral Infections
[Link]
10

• Lesions : disseminated vesicles over entire body +

fever

• T/ t: IV acyclovir

Herpes zoster 00 : 24 :50

• 2° reactivation
• Synonym : slninyles
• Lesions : multiple , grouped vesicles on erythematous
base painful
• Pattern: dermatomal

Viral Infections
11

• Distribution: U / L
• Most common site : thoracic
• Triggers : old age, DM , immunosuppression

HZ ophthalmicus :

• Nerve : Vi of trigeminal nerve

• Sign: Tip of nose -> vesicles


• Nasociliary increase risk of ocular involvement
" Hutchinson Sign”

[Link]

• Dendritic ulcer on cornea

HZ oticus :
• Qanglion: geniculate ganglion
• Synonym : Ramsay hunt syndrome

Viml Infections
[Link]
12

• Triad :
- Ear pain ( otalgia )
- Vesicles in EAM
- I/ L facial nerve palsy
• Investigations : Herpes zoster/ varicella zoster
• Tzank smear : mult nucleated giant cells
'
{

- HSV H , X
• Drug : acyclovir
• Dose : sOOmg 5 times a day
• Duration: 7 - HO days

Post herpetic neuralgia :


• Definition: pain persisting > H month after resolution
• Type of pain: Allodynia ( non painful stimuli -> pain )
• T/T:
• Topical : capsaicin, cold compresses , calamine
• Oral : pregahalin, gahapentin , amitriptyline

EBSTEIN BARR virus :


• Virus : DNA, latency

Viral Infections
13

• Diseases :
2. Infectious mononucleosis
2 . Oral hairy leukoplakia
3. Malignancies

Infectious mononucleosis
• Synonym : kissing disease polyglandular
}
fever

[Link]

• Triad :
- Fever
- Sore tinroat
- Cervical lymphadenopathy
• [Link] : atypical lymphocytes
Downy lymphocytes
((

Ampicillin rash:
• Fever + sore throat infectious mononuclear
1
Treatment : ampicillin
i

Vi ml Infections
[Link]
14
Morbilliform red rash
( Entire body )

Oral hairy leucoplakia : OHL


• Association: HIV Aids
• Lesion : white corrugated plaque
Feathery margin

• Site : lateral wall / side of tongue


• P/ P: candidiasis -> rub off the lesion
OHL -> cannot be rubbed
• T / T : HAART -> self -resolve
Viral Infections
15
BBV : malignancies
• Hodgkin' s ( ympWoma
• Burkitt lympWogram ( African endemic ) ^ Jaw lesion
• Nasoplnaryngeal Ca -> most common site = fossa of
rossenmuller
• Qastric malignancy

Cytomegalovirus: ( HIV - 5 )
• Disease : IM like illness ( Fever + sore tlnroat )
Immunocompetent
Immune — compromised ( H I V ) -> severe
systemic infection

• T / t : ganciclovir
• Inclusion bodies : owls eye IB nov anms
[Link]

ft W

* 0
i fl

HHV - <b:
• Disease : disease
• Synonym : roseola infantum
Exantbem subitem

Viral Infections
[Link]
16

• Clinical feature : fever + rash


• Oral lesions :
- Lesion : papules on soft palate ( Posterior palate )
- Name : Nagayama spots

HHV - 7 :

• Association: P. Rosea
• P. rosea : dress syndromes
• SLst lesion: mother' s patch/ herald patch
Single, trunk
I
H -7. weeks
Viral Infections
17

i
Multiple lesions on trunk , Christmas tree pattern

Fig : 23

• Lesion -> annular erythematous plaque peripheral


collarette scales

[Link]
HHV - 8:
• Kaposi saroma

- Association : HIV - AIDS


- Lesion : purple raised lesion ( Papules, nodules)
violaceous
- Sites : skinj mucosa, LN, viscera

Viral Infections
[Link]
18

• Lower body ( Multifocal vascular tumor )


- HPE : proliferating spindle shaped endothelial cells
- T / t: HAART , chemotherapy
• Multicentric Castleman disease
• Primary effusion lymphoma

Molluscum cont agio sum: OOA5 A7


• Virus : mollusci pox virus
• Family : pox viridae
• Types :
- MCV i -> face , children ( Most common )
- MCV 2. -> genitalia, adults (STf )
• Clinical feature :
• Lesions :
- Pearly white
- Dome shaped papules

Fig : 25

- Central umbilication
• Sign:
- Pseudo isomorphic phenomenon/ pseudo koebner' s
phenomenon

Vi ml Infections
19
- Autoinoculation
• HPE : lobular invagination of epidemics

• Inclusion bodies :
- Eosinophilic inclusion bodies
- Intracytoplasmic
- Henderson Paterson bodies
- Largest viral inclusion bodies
[Link]
• T/ t:
- Self -limiting disorder (6 - 9 months )
- Topical -> imiquimod :
• Increase cytoplasmic response
• Immune response modifier
• Immunomodulator
- Physical :
• TCA application
• Cryotherapy with liquid N 2. ( -3- 9 6>° c )

• Curettage

Viral Infections
[Link]
20

Paradox virus:
• Zoonosis
• Based on primary Inost
- Cow : pseudo cowpox virus -> Milker’ s nodule
- SWeep : orf virus -> ectWyma contayiosum
• EctWyma infectiosum / ectWyma : strep / staple
• BctWyma yanyreonosum : pseudomonas
• EctWyma contayiosum : orf virus

Human papilloma virus:

• Virus : DNA virus


• Tropism : squamous epitWelium -> papilloma’ s
• Disease : warts / vascular
• Classification : warts
>7-00 subtypes
2.0 - skin

Non venereal Venereal

• Close contact • Sexual transmission


• Skinj mucosa • Genitalia
HPV 6,

Warts causes:

• V - deep plantar wart


• S - supf plantar wart
• P - planar wartj HPV = 3, 3-0
• C - common wavt HPV 2- > 4
}

• B - epidermodysplasia verruca formis ( HPV = s g)


^
Viral Infections
21

• L - laryngeal wart, anogenital warts, HPV = 6,3- 3-

• B - butcher' s wart, HPV = 7


Heck’s ds = HPV 3-3,32

Verruca vulgaris :

• Most common wart


• HPV 2, 4
[Link]
• Clinical feature : Multiple papules, rough Vaucluse
surface

Pseudokoebers phenomenon

Verruca plana : plane wart / flat wart


• Multiple, shiny, flat -topped papules
• Most common face

Viral Infections
[Link]
22
Plantar warts :
• Soles
- Deep plantar : HPV = 2 ( Myrmecia )
- Superficial plantar : HPV 2 ( mosaic wart )

• Black dots on surface = stippled vascular ( vessels )

Genital warts:
• HPV (S . 22 , - low riskj 2 G , 22 - WiyW risk

• Condyloma acuminata
Most common site : men - coronal sulcus francium
Female = posterior fourdnette

Vi ml Infections
23

Epidermodysplasia verruciformis:

.

'

* .

JS

• Etiology : HPV 5 } 2

• Inheritance AR
• Lesions : multiple warts
- Seborrheic keratosis like warts
- P. versicolor like warts

• Risk : disseminated
1
[Link]
High risk of SCC
• Prevention: No t / t

Sun avoidance = prevent malignancy


• Tree man syndrome
• HPE : vacuolization of keratinocytes koilocytosis

Viral Infections
[Link]
24
T/t:

• Self - limiting ( 2 -3 years )


• Top drugs : imiquimod , S fluoro uracil
'

• Physical modalities: T£Aj cryotherapy, RF ablation


• Surgical excision
• Laser -> Co2 laser

Enteroviral infection 0 2 :0 2 : 3 8

Z .Handj foot and mouth disease


• Etiology : coxsackie A2 b = most common
- Enterovirus 72

• Lesions :
- Multiple elliptical vesicles
- Hand and feet
- VesicleSj erosions -> oraf mucosa ( painful)
- Fe /er ±
' children
Z .Herpangina :

• Etiology : coxsackie A2 - 20, enterovirus 72

Viml Infections
1

PARASITIC INFECTIONS OF SKIN

Parasitic infection of skin 00 :00 :16

Parasitic Infections of Skin:

[ l

Ectoparasites Eiectoparasite
Skin surface inside

Scabies 00 :00 : 50

[Link]

• Mite : Sarcoptes scabiei var hominis


• No of mites : 10 -12. mites
• Spread : close personal contact / fomites
• Type of disease : water washed disease
( Decreased personal hygiene )

Pathogenesis:
• Hypersensitivity : Delayed Type HS Response
- Saliva

Parasitic Infections of Skin


[Link]

- Faeces

• IP : 4 -S weeks ( SLst contact )


i
Memory T cells
• Reinfection : 2 -3 days

History :

2 .Nocturnal pruritus
2 .Family members / Siblings — Similar ItcW

Clinical Features :

• Lesions : Papules , nodules, Excoriations


• Sites : FingerVJebs Q
Folds / flexures
Parasitic Infections of Skin
3
- Below neck $

- Spares palms & soles

Distribution of lesions :

• Circle of tnebra : finger webs


1
[Link]
VJrist
1
Cubical fossa
1
Axillary fossa
1
Nipple
1
Periumbilical area
1
Qroin

• Pathognomic lesion : Burrow

Parasitic Infections of Skin


[Link]
4

Lesion : Burrow
Linear, wavy serpiginous grey tunnel
}

Mite lives
Level : S . Corneum
Site : Finger webs

Diagnosis :

Clinical diagnosis
Scrape burrow -> ZO% KOH Examination
Mite
Eggs
Faecal pellets ( Scybala)

Parasitic Infections of Skin


Mite : Round , ovoid body
4 pairs of ley
- 2 pair ant
-2 pair posterior

Treatment :
• General Measures
[Link] treatment

2 .Laundry used last 3 days -> washed


3 .Pruritus -> antihistamines
• Medical management
2 .Topical

2 .Systemic

[Link]
Topical :
• DOC : Permethrin 5% cream

• MOA: Na+ blocker > paralysis -> death


-

Kills adults
Kills eggs
• Application : 2 applicationSj 2 week apart
Below neck
Full tubej entire body in 2 application
Wash after 2 - 22 hrs
• Others :
- Lindane
- Crotamiton
- Precipitated sulfur

Parasitic Infections of Skin


[Link]
6
- Benzyl benzoate
• Systemic
- Drug : ivermectin
- Doses : 2 doses , Do, Dio 2-OOmcg / kg
- MO A: binds to glutamate gated chloride channels
Increase chloride influx
i
Hyperpolarisation
i
Spastic death

Special forms of scabies :


• Infantile scabies
• Norwegian scabies
• QenitaI scabies
• Animal scabies

Infantile scabies:

Parasitic Infections of Skin


• Distribution: full body, palms and soles
• Lesions : vesiculopustular lesions
Palms and soles
• DP : congenital syplnilis

I
Maternal VDRL/ Syplnilis
Other findings

• Infantile scabies :
Family H / O similar complaints
Itchy

Norwegian scabies:

[Link]

• Most severe type of scabies Q


- Synonym : Crusted scabies Q

- Seen in : AIDS, Immunosuppression


- Pathology : decrease immune response
i
Decrease itching

1
Mites ttt ( millions)

Parasitic Infections of Skin


[Link]
8
- Rash Wyperkeratotic crusted lesions
- Mites : million
- Itching : no
- Treatment : permetinrin + ivermectin +

Decrease scaling ( Salicylic acid preparation)

Nodular scabies

• Path f t Inypersensitivity response


,

• Lesions : Nodules, itcbyj persistent


• T / t : topical steroids

Animal scabies

Parasitic Infections of Skin


9

• Transmission : animal -> humans


• Not seen: burrows .

PEDICULOSIS 00 :21: 48

Ectoparasite
louse
Classification

Louse Disease
Pediculosis Inumanus capitis p. capitis
( Head louse )
Pediculosis humanus corporis p . Corporis
( Body louse )
Ptlnirus pubis ( [Link]
louse ) Ptkiriasis Q

/ pubic fo

Structure of louse :
• Long , do rsovent rally flattened 3 pairs of legs

Parasitic Infections of Skin


[Link]
10
Pubic louse:
• Shorter and broad
• Claws
known as crab louse

Pediculosis capitals:

• Louse : Pediculus humanus capitus/ head louse


• Spread : close personal contact/ fomites
• Type of disease : water washed disease ( decrease
personal hygiene )
• Hypersensitivity : saliva -> CMl : Delayed type HS (Type
4) -> itching .

• IF: first infection =4 -5 weeks


"

• Reinfection: SL- -Z days


• Nits stuck to hair
< icm scalp = active infestation
Parasitic Infections of Skin
11

Clinical features :

• Most common patients : school going girls


• History : pruritus / itching on scalp contact
• Clinical features : Q recurrent scalp pyoderma
Regina! lympWadenopatWy
[Link]
( Occipital / cervical )

• 0/ E: Adult louse / nits - excoriations

Pediculosis corporis : body louse

• Synonym : vagabond' s disease $

• Louse : Pediculus humanus corporis

Parasitic Infections of Skin


[Link]
12

• Live in : clotkes ( seams ) Q

i
Body -> iteking
• Clinical features : Extensive excoriation : Morbus
errorum

Pediculosis pubis:

• Synonym : ptkiriasis Q

• Louse : crab louse


• Transmission: sexual transmission $
• Clinical : lesions -> blue -colored macules = “ Maculae
cerulae”

Treatment :
• General measures

Parasitic Infections of Skin


13
- Treat patient and contacts
- Antihistamines
- Antibiotics
- Laundry
• Medical management
- Topical
- Systemic
• Topical :
- Doc : permethrin 2 % lotion
- Application: 2 application, 2 weeks apart
Apply for 25 minutes -> rinse -> nit combing
- P. corporis : Treat clothes $
• Wash with hot water
• Incinerate [Link]
- Other drugs : malathionj ivermectin
• Systemic :
- Drug : ivermectin
- Dose : ZOOmcg / kgj 2 doses - 0 / 20

- Other : cotrimoxazole -> kill the symbiotic bacteria


in dIT of louse

Pemodicosis:
• Mite : demodex folliculorum Q

Pemodex brevis
• Lives in : commensals
Pilosebaceous unit Q

Long , thin body S pairs of legs


Fig :

Parasitic Infections of Skin


[Link]
14

Fig : 11

• Clinical feature : reddish + papules / pustules on face


• Role in certain PS :
- Rosacea

- Peri oral dermatitis


- Atopic dermatitis
T/t: Topical metronidazole

Migratory infective skin lesions <9(9:3 7:2- 7

• Cutaneous larva migrans


• Larva currens
• Calabar swellings

Cutaneous larva migrans :


• Etiology : Ancylostoma braziliense ( dog hook worm)

• History : H / O barefoot in soil / sandy areas

Parasitic Infections of Skin


15

Humans > accidental Inost


-

Larva -> cannot penetrate BM

Limited to epidermis
• Lesions : Pruritic, erythematous
Linear serpiginous tract skin
Most common site -> foot
• T/t:
- Self - limiting [Link]
- Oral albendazole / ivermectin

Larva currens :

Fig : 21

• Etiology : strongyloides stercoralis


• Synonym : racing larva

Parasitic Infections of Skin


[Link]
16

• Lesion : perianal area

Rapid migration
Pruritic + urticarial lesions ( Intradermal
migration)
• T / t : ivermectin

Calabar swelling :

• Etiology : loa - loa ( African areas )


i
Veer fly ( Chyrsops )

• Lesions :
- migrate subcutaneously
- pruritic, erythematous swelling ( Calabar swellings )
- eosinophilia
• Treatment : DEC ( Diethyl Carbazine )

Parasitic Infections of Skin


17

Trypanosomiasis 00 : 44 : ZS

• It is divided into two types :


• African trypanosomiasis
- Etiology : Trypanosoma brucei
- Vector : tsetse fly
- Synonym : sleeping sickness
- Types : east African and west African
West African trypanosomiasis
[Link]
- Early / acute -> blood / lymph
( Hemolymphocytic phase )
- Late / chronic 4 CNS ( Meningoencephalitic

phase )
i
Sleeping sickness
- Most common: posterior cervical LN
i
Winter bottom sign
• American trypanosomiasis :

Parasitic Infections of Skin


[Link]
18

R 1
Fig: 2.4

- Etiology : T. cruz /
- Vector : reduviid bug
- Synonym : chagas disease
- Acute disease :
• Acute -> blood / tissues; flu like symptoms
• Chronic -> cardiac conduction defect
Mega esophagus, achalasia.
In acute phase : unilateral painless periorbital and
}

palpebral edema
i
Romana sign

Leishmaniasis 00 : 4 P

Vector : sand fly


Classification
l- .Cutaneous leishmaniasis
• Old world leishmaniasis
• New world
Z .Muco cutaneous leishmaniasis
3 .Visceral leishmaniasis
4 . PKPL

Parasitic Infections of Skin


19
Cutaneous leishmaniasis : old world

• Synonym : Delhi boil / oriental sore


• Etiology : L. major/ L. tropica
• Lesion: painless papule -> nodule -> ulcer - black
hard crust
VOLCANO SICiN : scarringQ with crateriform ulcer
[Link]
• T / t : self -limiting

Cutaneous leishmaniasis : new world

• Synonym : gum tree harvesters' ulcer/ chicl ero ulcer


• Etiology : L. Mexicana

Parasitic Infections of Skin


[Link]
20

• Lesion : ear cartilage

Mucocutaneous leishmaniasis :

*
>


;
4
v

Fig : 27

• Etiology : L. Brazilienses
• Lesions : invade mucosa -> nasopharynx -> damage
- Mutilating disease
- Scarring
- known as mucocutaneous leishmaniasis espunctia
• TOC : liposomal amphotericin

Post kala azar dermal leishmaniasis : PKPL

• Etiology : L. donovani
• History : endemic - Bihar , Jharkhand
Parasitic Infections of Skin
21

• H / 0 : fever -H HSM -> ± T/t

Clinical features :
• Hypopiymented macules
• Plaques
• Nodules -> diffuse nodules entire body

Investigations :

[Link]

• Qiemsa stain ( slit skin smear ) : intracellular


amastiyote forms
i
LP bodies

Treatment :

• TOC : Oral miltefosine

PD:

• Bibar + diffuse nodules

Parasitic Infections of Skin


[Link]
22

LL Hansen’ s PKDL
Nerves Enlarged No nerve

enlargement
Sensory Glove stock No sensory loss

anestlnesia
SSS 6 -H AF3 LP bodies

Parasitic Infections of Skin


1

SEXUALLY TRANSMITTED DISEASE PART - /

Classification [Link]. XC
[Link] ulcer disease
2 .Genitaldischarge
3 .Anogenital warts

[Link]

Qenital Ulcer disease:


3- .Syphilis
2 .Chancroid
3 .Genitalherpes
4 .Donovanosis
[Link] Venerum

Syphilis : [Link]
Classification :
Contact > Primary syphilis
-

4/
k / a : Early syphilis
Secondary syphilis
sU
Early latent syphilis
within 1-year of
acquiring ds Late latent syphilis
( CPC : lyr )
( WHO : Zyrs) Late syphilis :
2 / 3 rd ptS l / 3 rd ptS Non infectious
Ft is infectious resolves tertiary
Early syphilis syphilis

Sexually Transmitted
Disease Part I
[Link]
2
Primary syphilis : bacterial STI

Fig : 1

• Synonym: Hard chancre / ulcus durum/ hunter / an


chancre
• Etiology : Treponema pallidum pallidum
• IP : 9 -todays
• Clinical features : Macule -> Papule -> Ulcer ( H° lesion)
Ulcer : Single

Round
Well defined
Clean base, moist ( Serum )
Indurated
Painless
• Heals : No scarring
• Dory flop sign
Sexually Transmitted
Disease Part l
3
Button ulcer

• Lymph nodes: B / L Painless


inguinal LN (V)
Firm consistency

= Shotty LN

Rubbery texture
• Extra genital chancre ( EdC ): Most common site of
EQC - oral cavity
[Link]
M S M : Peno anal contact: peri anal area

Secondary syphilis:
• Dissemination:
- Hematogenous
- Vasculitis
- Obliterative end arteritis
Sexually Transmitted
Disease Part l
[Link]
4

• Clinical features :
- Constitutional : fever , malaise , joint pains
- Skin + Mucosa + Hair
- Lymph nodes : Generalized , Painless , shotty LN
most characteristic = Epitrochlear LN
- Systemic : Any / Every system Inv
- k / a great imitator

Rash:
• Various type / Morphologies of rash
- Asymptomatic
- Non - Pruritic
- Generalized
• Most common: Maculopapular
• Not seen: Vesiculohullous lesions not seen
Site : Palms & Soles

• Lesions : Coppery brown scaly papules/ plaques/ macules


• Sign : Press with blunt / Pin Wead structure

Pain/ winces ( end arteritis ischemia )


DEEP PERMAL TENDERNESS
BUSCHKE -OLLENDORF SION

Mucosal lesions :
• Condyloma lata
Sexually Transmitted
Disease Part l
• Mucous patch: Flat erosions , tongue , oral cavity
• Snail track ulcers : Coalesce ,Oral cavity

Condyloma lata : ( I at a- flat )

• Site : Genitalia , Intertriyinous


• Lesions : Greyish, flat topped papules & plagues
[Link]
shiny , moist ( Serum )
• Importance : Most infectious lesions of 2° syphilis
( The serum is full of treponemes )
• Condyloma acuminate : Genital warts - HPV
l
\ = Pointed
/

Hair.

Sexually Transmitted
Disease Part l
[Link]
6

• Patchy, non -scarring alopecia = Moth eaten alopecia

Syphilis d’ emblee :

m
V AV \ \ \ Fig : 8

• Transmission: Non venereal , transfusion

• Not seen: Primary chancre


• Clinical features : Secondary syphilis

Non venereal transmission of syphilis :


• Syphilis d' emblee
• Congenital syphilis

Latent syphilis :
Classification

Early latent Late latent


( < 1 year ) ( > 1 year)
- Infections - Non - Infections
i I
c / f : Asymptomatic
Serology : Positive serology

Tertiary syphilis :
• SL / 3 rd ptSj delayed type HSj No treponemes
-
l 0 -40 yrs after acquiring ds
l- .Skin
- Qummatous syphilis : Cumma
Sexually Transmitted
Disease Part l
7

- Lesion : Rubbery nodule


i
- .
Sign : Ulcer Pain! ess washed leather slough
- Healing : scarring / disfigurement
- Relapsing syphilis ( RS): Reappreance of ulcer

Early RS Late RS

• Reappearance of primary • Reappearance of ulcer


chance at site of previous ds (gumma ) at site of previous

• k / a Monorecidiv syphilis ulcer


• PSEUDO CHANCRE REDUX

2 .CVS :
[Link]
Cardiovascular syphilis
Incidence : 10 %
Onset : lO - AOyrs
Lesion : Aneurysm of ascending aorta
aortic regurgitation
3 .CVS : Neurovascular syphilis

- It can develop at any point during ds


Late NS
Early NS
2. Generalized paresis of Insane ( Dementia paralytica)
• Meningits
- neuropsychiatric manifestation
Dementia
Psychiatric NEET 201?
2 . Tabes dorsalis
Damage to posterior column of spinal cord
Proprioception, vibration — lost
i
GAIT Ataxia ( Sensory )

Bladder bowel dysfunction


Sexually Transmitted
Disease Part l
[Link]

Syphilis investigation:

si

Fig ,- to

• Park ground microscopy : IOC in primary chancre


• Culture : Not cultivable in vitroj rabbits ( animal
model )
• Serology
• Earliest test to become positive : IgM FTA - Abs
( 3 wks )
• Most specific test : Dark ground microscopy
• Most specific bold test : FTA -ASS, TPPA
• Most sensitive test : FTA -ABS
• Test used for monitoring disease activity : VPRL
• Test used for field -based screening : RPR ( card
based )
• Most common for screening : El A

Syphilis IOC :
• Primary syphilis : Dark ground microscopy
• Secondary syphilis : FTA -ABS
• Latent syphilis : EIA
• Tertiary syphilis : FTA -ABS
• Neurosyphilis : CSF -VDRL

Sexually Transmitted
Disease Part l
Reverse algorithm for screening :
• When patient presents : El A

Positive Negative

VDRL
i
No further testing

Treatment :
• DOC : inj . benzathine penicillin
• Dose : ZAmillion IU T .2 in each buttock IM
}

• Early syphilis: 2° ,2° , early latent -> Single injection


• Late syphilis : Late latent , 3° , unknown duration ->
3 inj . Weekly ( 3 doses )
• Neurosyphilis : Crystalline aqueous penicillin
( penetrate 131313 )
• In penicillin allergy : AST - positive ( Antibiotic
sensitivity test ) DOC : Doxycycline
[Link]
• Primaryj secondary , early latent : ZOOmg doxy 3 D x
24- dsys ( 2 wks )
• Late latent tertiary , unknown duration: 2-OOmg 3 D
j

x 22 days ( 4 wks )
• Pregnancy +- Allergic : TOC = Desensitization
2 nd TOC :
Erythromycin/ Azithromycin

Jarisch herxheimer reaction:


• Seen in secondary syphilis
• 'M' bacteria -> Inj . benzathine penicillin
1s TT Antigens released + Ab •

Circulating Ag - Ab complexes
Type 3 HS response
• Constitutional S / S : fever
Sexually Transmitted
Disease Part l
[Link]
10
- 'M' skin lesions
4

• Rx : Symptomatic treatment
• Pregnant 4- Secondary syphilis 4- JHR= fetal damage

Congenital syphilis:
• Transplacental ( M -> F)
• stage
• > ZOwks POQ ( max )
• Early : <Zyrs of birth
Like secondary syphilis, infections
• Late : >Zyrs more of stigmata , non -infections

Early congenital syphilis :

• Rhinitis ( Syphilitic snuffles )


• Vesiculo bullous rash on skin = Syphilitic pemphigus
• H S M : Flint stone liver
• Periostitis ( Pain ) = Pseudoparalysis of parrot

Sexually Transmitted
Disease Part l
11
Baby + Vesiculobullous lesions
Congenital syphilis Infectious scabies
• Vesiculo bullous • Itchy
• Mother = we test • Vesiculo pustular
& we c/ f • Family H / O (V )

Radiology :

[Link]
• B / L erosion: Upper tibia VJimberger sign
Medial side <
Most specific radiologic finding”
f

Late congenital syphilis :

• > ZyrSj remaining scars


• Hutchinson triad :
1. Interstitial keratitis ( most common finding )
Sexually Transmitted
Disease Part l
[Link]
12
Z .Sensori neural deafness
3 .Hutchinson teeth: Central notching in upper
incisors

Other feature :

Mulberry molars : Vasculitis -> Root


i
III formed cusps
• Periostitis : Frontal bossing / Olympian brow
Saddle nose

Sexually Transmitted
Disease Part l
1

SEXUALLY TRANSMITTED DISEASE PART- / /

Chancroid 00 :00 : ZS

• Etiology : Haemophilus ducrei ( Craw negative


,

facultative anaerobic coco bacilli )


• IP: 3 - 7 days

• Clinical features : Papule -> Pustule -> Ulcer

[Link]
Multiple
Irregular margins with
undermined edges ( ragged )
Yellow necrotic slough
Non indurated -Soft
chancre / ulcus mole
Painful

• Lymph node :

Sexually Transmitted
Disease Part -ll
[Link]
13

• Clavicle : Thickening of sternal end = Higoumenaki


sign
• Bending of long bone = SABRE TIBIA
most common: tibia

Investigations :
• VPRL titre ( Baby ) > » > Mother ( 4-times )
• IgM FTA - ABS

Treatment:
• Inj . Crystalline penicillin

Sexually Transmitted
Disease Part l
2

Unilateral
Painful

Overlying skin -> red


Pus : suppurative -> rupture -> sinus
Concomitant LN +- Ulcer

Investigation [Link]

/1 /
^
*•/ * *
\m *

SL .Gram stain :
• Gram negative coco bacilli arranged in rows
parallel to mucous thread
School of fish/ Q
Rail road track appearanceQ
Z .Culture : MH agar + 5% chocolate blood agar
3 .Other : NAAt

Sexually Transmitted
Disease Part -ll
[Link]
3
Treatment
• Tab azithromycin Hgm stat ( single dose )
• Ceftriaxone

Herpes genitals 00 :08 :21-

Viral STI
Etiology : Herpes simplex virus { HSV 2 »1- ( most
common)}
- IP: 3 -12 d
- Most common STI
- Most common viral STI

Clinical features:

- Vesicle : Multiple, grouped vesicle, painful , red base


*
Erosions
Polycyclic erosions , painful
Poly cy cl it
Erosions
Macules .
4
4, Herpes
Pityriasis versicolor

Sexually Transmitted
Disease Part - II
4

• LN : Bilateral , painful , inguinal LN


- N o n suppurative
• Herpes genitalis : latency ( Sensory ganglion = Sacral
ganglion)
*
Secondary Werpes

i'

iW

Jks* s
M

*hr , Mil
'

i t*

i Fig - s

• Pregnancy : 36 weeks -> Start acyclovir to suppress


secondary episode
[Link]

Investigation

• Qiema stain : Tzank smear


i. Multinucleated giant cells ( M N G' s )
ii. AcantWolytic cells
• Gold standard : PCR
Sexually Transmitted
Disease Part -ll
[Link]
5
Treatment
• DOC : Acyclovir 4-OOmg TPS
- T ° - Vdays
- 2° - Sdays
• Suppressive therapy : xhepisodes/ year
- Acyclovir 4-00 mg BDj 1-2- years
• Other : Famciclovir, valaciclovir

Lymphogranuloma venerum 00 :T (b :4-Z

• Etiology : Chlamydia trachomatis ( L (m o s t


common), L3 )
• IP: 3 -30d
• Stages

Z .Ulcer stage
Z .Inguinal stage
3 .Qenito anorectal syndrome

Sexually Transmitted
Disease Part -ll
6
Primary stage

• Genital ulcer
- Painless
- Transient
- 7 days ( self -resolve )
[Link]
Secondary stage

• Stage of inguinal bubo


• Unilateral lymplnadenopatlny (2/ 3)
• Bilateral lympbadenopatby ( SL / 3 )

Sexually Transmitted
Disease Part -ll
[Link]
7
- Painful LN ®

- Suppurative - BUBO
- Skin -> Red , swelling

OOP
OOP
AS /S PS

= " £Jroo \/e Sign of Green 131at*

Inguinal BUBO
I
r l

Chancroid bubo LdV bubo

% »•

Concomitant genital ulcer No ulcer


-f- Only bubo
LN Qroove sign

Sexually Transmitted
Disease Part - ll
Tertiary stage

• LN © -> damages LN + perinodal tissues


A,
Genital lymphedema
'l'
Genital elephantiasis
( Enlargement &c disfigurement )
Male : Saxophone penis
Female
[Link]
: Esthiomene

Investigation
• Specific : NAAT ( gold standard )
• Non -specific : CFT > i : 64
> > 1.:2 S (o ( diagnostic )

Treatment

• DOC : Poxgcgcline HOOmg BD x 2 ^- days

Donovanosis 00 : 25: 34

• Bacterial STf
• Etiology : Klebsiella granulomatis

Sexually Transmitted
Disease Part -ll
[Link]
9

• Old name : Calymmobacter granulomatis


• IP: rL -36 Sd
• Synonym : granuloma inguinale
• Clinical features : Ulcer

Solitary
Beefy red / velvety red
Exuberant granulation tissue
Bleeds o touch
Painless
• LN : no lymph node involvement

/S\
Cmodule }
Pseudo bubo

Sexually Transmitted
Disease Part -ll
10
Investigation

- Crushed smear : Qiemsa stain


• Intracellular bacteria
• Bipolar staining : Closed safety pin appearance
Also known as : Donovan bodies

Treatment
[Link]
• DOC : Azithromycin Hgm , weekly x 3weeks ( or ) till
ulcer heals

Approach to QUP
1
r i

Painless ulcer Painful ulcer


1 1
r l r l

LN ® LNQ LN ® LNQ

4 . 4, Unilateral Bilateral
Syphilis Ponovanosis suppurative Painful
4' Non -
Chancroid suppurative
4 .
Herpes

LGV :
• Buboj suppurative LN
• GROOVE SIGN
Sexually Transmitted
Disease Part - ll
[Link]
1

SEXUALLY TRANSMITTED DISEASE PART - III

Genital discharge 00.0016

Genital Discharge
\

Urethral / Cervical Vaginal discharge


discharge

Gonococcal N on -Gonococcal

Etiology — N. Gonorrhoea Etiology :


i. Chlamydia trachomatis [ P - K :
me ]
- Most common bacterial STI in

the world
ii . Ureoplasma
Hi. Mycoplasma
iv .Trichomonas vaginalis
v. Herpes genitalis
IP : 2 -5
*
days IP : 3 -12 days
S / S : fever / malaise S / S : Urethral discharge / Cervical
discharge
Urethral / cervical discharge

Dysuria

Mild dysuria
Urethral discharge : profuse Urethral discharge : scanty , mucoid
Purulent
Mild dysuria

Sexually Transmitted
Disease Part III
2

Peri urethral erythema

Severe dysuria
Cervical discharge : profuse Cervical discharge : mild mucoid
Purulent
Pysuria / dyspareunia

Dysuria / dyspareunia
Erythema -> friable
Investigation: Investigation :
i. IOC = NAAT
n c> - Urethral swab
.
i ii - First void urine
i. Gram stain of pus
- Intracellular
[Link]
- Q . negative diplococci
( biconcave = kidney shaped )
ii. Culture : modified Thayer martin
medium
Vancomycin, Nystatin, cofist/ n &:
trimethoprim
Gold standard
Treatment : Treatment :

• Puaf therapy T. Azithromycin 1 gm stat


- Inj . ceftriaxone 2 SO mg IM stat (TOC )
( Or )
- T . cefixime 400 mg stat Others : Doxy 200 mg BDX 7d

T. Azithromycin Igm stat


Complications : i. P / d &c secondary infertility :
i . Ascending infections most common cause of 2°
ii. PID & 2° infertility infertility
Hi . Fitz hugh Curtis syndrome ii . Reactive arthritis : SARA

Sexually Transmitted
Disease Part III
[Link]
3
Non -Cjonococcal urethral
rem ntvrrrnu discharge + conjunctivitis
YiOUv £ TfiJh/ q <\PhTVOh>
^ Arthritis

inf
Hi . Ophthalmia neonatorum
iv. Disseminated gonococcal
I
- Alcoholicsj preg immune f 1
}

Gonococcal Non -Gonococcal


compromised
Skin ( pustules) -h Arthritis ( synovitis )
h Tenosynoritis

Vaginal discharge
• Most common cause : physiological
• Most common of altered vaginal discharge : Bacterial
vaginosis
• Main causes :
i. Candidiasis
[Link]
Hi. Bacterial vaginosis

Candidiasis OO . X 5: 36

• Etiology : Condida albicans ( 20 - 25% )


Non albican species

• Risk factors :
i. Pregnancy
ii. Diabetes
iii. Immunosuppression
iv. Long term antibiotics

Sexually Transmitted
Disease Part III
4
Clinical features

• Typical discharge : curdy white discharge


( Adherent to vaginal walls )
~h

Itching
KOH mount : budding yeast

[Link]
•«
:u
V

~ -A •• Z

A 4»

Pseudohyphae Fig : 2

Treatment
• Tab fluconazole 3- SOmg stat
• Pregnancy : clotrimazole pessary x 7 nights

Sexually Transmitted
Disease Part III
[Link]
5

Trichomoniasis 00 : 18 :2

Fig -. 3

• Etiology : Trichomonas vaginalis


• Clinical features : Typical discharge : greenishj frothy
disease

Cervix : Strawberry cervix/ Colpitis macularis

Sexually Transmitted
Disease Part III
6
l investigation:

. %2r
Fig : (o

• Wet mount -4 motile, flagellate protozoa


Treatment : tab. metronidazole 400 mg TDSx 7 d

Bacterial vaginosis

[Link]
&
(

Vf

Lactobacillus 95% Gardnerella vaginalis

Fig : 7

• Alteration in flora of vagina


Normally : Lactobacilli -4
dardenella vaginalis
Mobilincus — 57o ( dram negative bacilli )
Prevotella
• Lactobacilli
dram negative bacilli 'M'

Sexually Transmitted
Disease Part III
[Link]

Amsel’ s criteria : V* positive


SL .Vaginal discharge : Homogenous , watery , foul -

smelling vaginal discharge

2 .Vaginal Ph: > 4.5 "

3 .W h i f f test : discharge + 20% KOH =


Fishy / ammoniacal odour
A- .Clue cells : >20 %

• Clue cells : vaginal squamous cells


Studded with gardened a

" Stippled Border


>20 % cells -> Criteria

Sexually Transmitted
Disease Part III
8
Treatment : Tab. Metronidazole 400 mg TPS x 7 d

Anogenital VJarts
• Etiology : Human papilloma virus

HPV HPV 31, 33

• Most common • Least common


• Low risk of malig • High risk of
( SCC ) malig ( SCC )

• Clinical features : Synonym - condyloma accuminata


Pointed tip

[Link]

• Lesions : Pink , fleshy , papules


rough surface , pointed tip
Male -> coronal sulcus & frenulum
• Sites : most common .: /
\Female -
> post fourchette

Giant warts :
• Synonym: Buschke - Lowestein tumour
• Risk : SCC
• HPE :

Sexually Transmitted
Disease Part III
[Link]
9

Cells ( Keratinocytes): Central nucleus


Perinuclear halo
Peripheral condensation of cytoplasm
*
K / a : KOILOCYTES

Treatment
• Self - resolving
Podophyllin: Tubulin inhibitor , metaphase arrest
Medical
1 modifier , TLR 7
Imiquimod : Immune response agonist
Chemicals : TCA
- Ablative
Cryotherapy , RFA , C0% laser
Surgical : Excision •A In buschke lowenstein tumors

Treatment in pregnancy :
i. Cryotherapy (TOC ) :
liquid Nz - H 3 (S°C
Preeze cells -> death
[Link]: 70 - 30 %

Sexually Transmitted
Disease Part III
10

Genital scabies :

• Synonym : Nodular scabies


• Transmission: Close - contact
Sexual / venereal mode

[Link]
Genital Molluscum Contagiosum

• Pearly wW\te dome shaped papule with central


}

umbilication in genital area.

Syndrome management of STD ( NACO )


• Syndrome : constellation of S / S : group / syndrome
Sexually Transmitted
Disease Part III
[Link]
11

National AIDS Control Organisation


India ' s Voice against AIDS
Ministry of Health & Family Welfare, Government of India
[Link] . [Link]

Syndromic ma^ageme^t of STD ( NACO )


Color Indication DRUG
KIT 1 Grey Urethral / Cervical / Anorectal discharge 1ab . Cefixime 4-00 my
\ +
Gonococcal NonGonococcal
Tab. Azithromycin Igm

KIT2 Green Vaginal discharge Tab. Fluconazole ZsOmg


- Candidiasis Tab. Secnidazole Tgi-vi ( 2 tab )
- Trjcho mo n 'j as iS
- Bacterial vaginosis
KIT 3 White GUP : Non Herpetic Inj. Benzathine penicillin 2 ,4 MIU
GUP - Syphilis - most common
- ChanOfd _ T. Azithromycin Igm stat
LGV
Donovaniosis
KIT 4 Blue GUP : iNon herpetic , allergic to penicillin .
T Poxy TOOmg BP X is d

GUP T. Azithromycin > gm stat


KIT S Red GUP : herpetic , Vesicles T . Aciclovir 400 mg TPS x 7 days
GUP
KIT 6 Yellow PIP / Lower abdominal pain T . Poxy lOOmg BP
- Chlamydia T . Cefixime 400 mg single dose
- Gonococcal T . Metronidazole 400 mg BIP x T 4 d
- G neagtlve bact / anaerobes
KIT 7 Black Inguinal bubo .
T Azithromycin 1 gm stat
- Chancroid T . Poxy 1-00 mg BIP x 2Td
LGV
Syndrome : Constellation of S / S : Group or syndrome

Sexually Transmitted
Disease Part III
1
PAPULO SQUAMOUS DISORDERS

Basics : PAPULO SQUAMOUS DISORDERS


Papules scales
/ \
Primary Secondary
Solidj Raised Scale : shedding stratum
circumscribed lesion corneum cells
Size : < lcm= papule i
> lcm= plaque Known as Desquamation
Therefore scale is visible
desquamation
i
Contain $$ keratinocytes

PSORIASIS :
• Chronic , T cell mediated inflammation of skin
[Link]
Autoimmune
• Antigen: unknown

Etiology
Genetic : QQHLA - CW6
Type 1: HLA -CW6 ©
Family history ©
early onset
More severe
Increase psoriatic arthritis
• Type 2 :
HLA - CW6 ©
Family history ©
Late onset
Less severe Papulosquamous
Disorders Part I
[Link]
• HLA /327: psoriatic arthritis 2

2) Drugs :
P : Painkillers ( NSAID' S )
L : Lithium

A : Ant / malarias ( Chloroquine' s )


3 : 3 blockers
S: Systemic steroids : pustular psoriasis
Brythrodermic psoriasis
drugs Increase CAMP' S = Increase psoriasis

3) Others :
a ) Infections : group A 3 hemolytic streptococci
Pharyngitis
Increase guttate psoriasis
b ) Alcohol
c ) Smoking

Associations :
l) Other autoimmune diseases : T cell mediated
Example : vitiligo , alopecia areata, Hashimoto
2- ) Cardio vascular diseases :
Psoriasis : inflammation of skin, systemic
Increase inflammation mediators increase
Atherosclerosis
Increase cardiovascular ds

Papulosquamous
Disorders Part I
Increase blood sugars
Increase ITTN
QQ metabolic syndrome
ALLMS , November 29
Lipids

pathogenesis :
epidemic : 0 hyperproliferation increase number of cells
increase thickness
dermic : Q inflammation __ increase speed

epidermal hyperproliferation:
• Time taken for cell to move from stratum basale to
stratum corneum is 4 weeks ( Epidermal transit

time )
• In psoriatic skin, epidermal transit time is 3 -S' days
[Link]
( average 4 days )

(fdjskin : 4 weeks
Psoriatic skin : 4 days

• Cell cycle time : In stratum Basale, time taken for 1


cell to divide into 2 cells
SB : ® ®

(Ny> 322 Hours


Psoriasis -> 36 hours ( y of n )

Papulosquamous
Disorders Part I
[Link]
Dermal inflammation: 4

T cell mediators : TH 2 and TH 27

IL 22 IL2 , TNF o(
IL 23 -XTHZ 7 IL 27 , IL 22

Naive T cell in lymph node


Enzyme : PDE 4

Clinical features :
Sites : extensors , trauma prone areas
i
Knees , elbow , back , buttocks , scalp .
• Bilaterally symmetrical
• Skin, scalp , palms and soles , nails affected
No mucosal involvement

Lesion : well defined


Erytlnematous plaque
Silvery white scale
Pallor around psoriatic lesion = $$ WORNOFF’ S RING

Psoriasis : $ non pruritic , $ asymptomatic

Clinical signs :
With glass slide, scratch the lesion : fGRATTAGE
TEST
i
• Exacerbation of scaring : Grattage sign / candle wax
sign

Papulosquamous
Disorders Part I
• Thin, translucent white membrane : Bulkeley' s 5

membrane
• Pin point bleeding : QQ Auspit3 sign
2) Koebner’ s phenomenon ( Isomorphic
phenomenon)

New psoriatic lesions


Injury to skin Scratching
Trauma developing at those sites
bites i
Koerner ’s phenomenon.

• New lesionsdevelop 7 - 3- 4 days after trauma QQQ


all or none phenomenon.
• Koebner' s phenomenon is indicator of activity of
disease
[Link]
Koebner’ s

True : Pseudo :
Endogenous new Endogenous in origin
lesions -viral wart
- psoriasis - molluscum
- Lichen planus

Rare causes : Erythema multi forme

• PLE

Histopathology :
• S . corneum increase : Q parakeratotiCj hyperkeratosis,
“ QQMUNRO MICROBSCERSJ > ( Neutrophils )
• S. granulosum decreases : Q hypogranulosis Papulosquamous
Disorders Part I
[Link]
• S. spinosum increases : acanthosis
Kogoj pustules ( Q Neutrophilic )
Q " Kogoj spongiform pustules 3 >

Rete : $
Regular Elongation
Dermis : lymphocytic inflammation
Capillaries : $ Dilated and ® tortuous

And Auspitz sign


Supra papillary thinning

Psoriasis ( PS )
Clinical types :
2) Chronic plaque psoriasis ( Psoriasis vulgaris )
• Me type

• Extensors
2) Flexural psoriasis
3) Quttate psoriasis
4) Scalp psoriasis
5) Erythrodermic and pustule psoriasis .

Flexural psoriasis : QQ Inverse psoriasis

• Axilla, groin
• Red plaque
• Minimal scaling

Quttate psoriasis: guttate = drops.


• 3 hemolytic streptococci
• Children

Papulosquamous
Disorders Part I
• Pharyngitis ( Sorethroast ) -> followed by skin
eruption.
• Multiple, small , red scaly papules and plaques
• Back region
• Like rain drops
IX : ASLO titers , throat swab
Qood prognosis
Treatment : QQ Antibiotics

Scalp psoriasis :
• Red , scaly plaques
How to differentiate from seborrheic dermatitis?

• Psoriatic lesions extend beyond the hairline


• No alopecia / hair loss
[Link]
• Pityriasis amiantacea : when scaling increases on

scalp looks as thick , white, scales on scalp Asbestos


sheet
Pityriasis means scales
Amiantacea means asbestos like.

Papulosquamous
Disorders Part I
[Link]
8
pustular psoriasis :
• Primary lesion - pustule -> sterile
• Multiple pus filled lesions ( Pustules )
• Lakes of pus
• Fever , malaise, sick
• Increase VJBC -> Increase ANC

Types of pustular psoriasis :


r
localized
Generalized
i
i
Cieneralized pustular ps of
Acute pustular ps
pregnancy ( CjPPP)
i
i
VON ZOM BUSCH d / s
IMPETIGO HERPETIFORMIS
-6 tK / 7 th month. ( Last

trimester )
Pustules : initially : Flexures
i
Spread over entire body
- risk of foetal damage

ERY THRPPERMIC PSORIASIS :

4
Red skin
> PO% skin -> red and scaly = erythroderma / exfoliative
dermatitis
HPE : Spongiosis [ Intraepidermal , intracellular edema ]

Clinically : Sheets of erythema 3 )

Papulosquamous
Disorders Part I
triggers :
pustular ' lakes of pus*
/
psoriasis
\ erythrodermic " Sheets of erythema 3)

T ) Systemic steroids :
• At sudden withdrawal of high dose steroids
i
Rebound ftt inflammation
• Take high dose steroids
2 ) Topical application of irritants :
• Ayurvedic herbal paste
• Large amount of coal tar

N A I L psoriasis :
[Link]
< Nail matrix: PITTING - NIC Sign of nail psoriasis
Nail bed : Oil drop sign ( Salmon patch ) - most
specific
• Pin point depressions/ crates in nail plate -> pitting
• Defective keratinization in nail matrix ->
parakeratosis
• Oil drop sign/ salmon patch : translucent area under
nail plate
i
Most specific sign of nail psoriasis
• Accumulation of scales under nail plate : Subungual
hyperkeratosis

Papulosquamous
Disorders Part I
[Link]

. Separate, nail plate and lifts up.


10

onycholysis
Separate -
Nail broken

Psoriatic arthritis :
1
Increase long standing psoriasis
Increase severity

Server nail psoriasis


• HLA 27

• Sero negative arthritis


Clinical features :
St ) Joint pain, swelling and redness
X ) Morning stiffness
3) Sausage digits ( Dactylitis )
Classification: Moll and wright
St ) Poly articular : small joints; > 9 joints
X ) Dligo articular : large joints; < 9 joints
3) Arthritis mutilans : Severe type of arthritis
Extensives erosions in joints
Extreme disfigurement

^
Classic joint : DIP
Me joint : knee joint
• Diagnostic arteria: CASPAR Criteria
• X ray : osteolysis -> PENCIL IN CUP
APPEARANCE .

Papulosquamous
Disorders Part I
11
Treatment:
X) Topical therapy
2) Systemic
3) Biologies
4) Photo therapy
How decide? -> OK SSA
CZ- <9% /3SA Involved : Topical therapy
> 20 % BSA lnv6W&® 2 3 4

i) Topical therapy :

i . Emollients : moisturizes, decrease scaling


ii .Topical steroids : Immunosuppressant decrease }

inflammation, decrease redness .


in . Topical vitamin B analogues -> normalize
f f f

[Link]
keratinization
iv . Topical retinoids
v . Coal tar derivatives cytotoxic
vi . Antitrain decrease proliferation
vii . Salicylic acid * keratolytic , decrease
scaling .

i . Emollients : Vaseline jelly , coconut oil , creams


ii .Topical steroid : very good therapy , me used
QQ Potency : Ointment > creams Q

Hi. Topical vitamin D 3 analogues : calcipotriol $ and


Tocalcitol Q

iv . Topical retinoids : Tazarotene QQ

Papulosquamous
Disorders Part I
[Link]
12
2 ) Systemic therapy
i. Methotrexate : immunosuppressive
DHFR inhibitor, 'S’ phase specific
inhibitor
ii . Cyclosporine : oral calcineurin inhibitor , decrease
immunity
Hi. Acitretin: Oral retinoid , normalize keratinization
iv. Hydroxy urea : cytotoxic , decrease epidermal
proliferation
v. Systemic steroids : decrease inflammation
I
Always contraindicated in psoriasis

1. Methotrexate : Doc in ( Category V)


• Chronic plaque psoriasis > 1-0 %
• Erythrodermic psoriasis
• Psoriatic arthritis
ii . Acitretin: Doc in ( Category V)
• Pustular psoriasis
• Psoriasis with HIV
in .
f t #

Cyclosporine :
• Rapid benefit and clearances
• Impetigo herpetiformis ( Pregnancy category fc* )

IV . Systemic steroids :
• impetigo Herpetiformis
Doc for severe
Therefore severe impetigo herpetiformis :

%. Steroids : ( Category 13’ )


(

2 . cyclosporine : ( Category eC )
Papulosquamous
Disorders Part I
Side, effects 13

i . Methotrexate : category V teratogenic


• Bone narrow suppression
• Hep atotoxicity
• Pulmonary fibrosis
ii . Cyclosporine :
• Increase H = hypertension ( increase BP -> renal
damage )
• Increase H = hypertension ( increase cholesterol )
• Increase H = hypertension

i n. Acitretin: increase hep atotoxicity


t t t

“ X’ h Teratogenic increase TQ Levels

3) Biologies :
[Link]

Cytokine Drug
TNF Btanercept
Infliximab
Adalimumab
IL 22 / 23 ustekinumab
IL 27 A Seaikinumab
Ixekinumab
brodaliumab
PPE -4 apremilast

Indications : failure of achieving adequate response


with 2 first line therapies psoriasis
Psoriatic arthritic
Papulosquamous
Disorders Part I
[Link]
Apremilast : mod - severe psoriasis psoriatic arthritis 14

oral drug .

4) Photo therapy :
Use of light in therapeutics
Chamber with multiple tube lights
I
Emit specific wavelength (A) -> treatment.
Ultraviolet ( Useful) -4 UVC : ZOO -Z ^ Onm ( Cermicidal )
-
UVB 29 <9 -32<9h.m
'

UVA: 3Z 0 -400 nm
1
UVA2: 320 -340nm
UVAi: 340 -400nm
UVP -4 2.9 (9 -32.(9 = Brand band UVB
i --
31 3 nm : Narrow band UVB
Best wavelength to use
Best results, least side effects
UVA + Psoralins ( Photo semitising drugt )

Increase proliferation
Kill DNA Decrease T cells

Psoralen Blind to
applied DNA
on skin

Papulosquamous
Disorders Part I
15
Psoralens :
Extensive : orally ( Tab ) -> blood -> lesion
I
Expose to sun after 2 Inour after
intake
ORAL PUVA Therapy
Localized : Topically ( solution ); Expose to sun after

20 -ZOminutes

Example : psoralens : 2 methoxy psoralen


Trimet boxy psoralen
Regimes : ( Photo therapy + Topical treatment )
• Gockerman' s ( GO CA): photo therapy + coal tar
• Ingram regimen ( INA): photo therapy +
anthracites
[Link]
Targeted photo therapy :
• Few lesions on hands and feet

• Some resistant lesions

Machine : Excimer laser


A - 308 nm

Papulosquamous
Disorders Part I
[Link]
1

PAPULOSQUAMOUS DISORDERS - ll

Lichen planus
• Chronic ; Immune mediated ; inflammation of skin
si/
TH 3- CDS T cells
;

si/
Keratinocytes apoptosis
• Antiyen — unknown
• Triyyer

Z . Infections - Hepatitis C Virus


Z .Druys - Anti malaria’ st Anti hypertensives
sP
- ACL

- 1313
- C£ Z3

- Diuretics
3 .Mercury amalyam
• Clinical features

Papulosquamous
disorders - II
2

• Lesions -> purple / violaceous lesions


• involves
- Skin
- Mucosa

- Hair
- Nail
- Sites> [Link]
-

- Symptoms Itclainpj rubbing , No excoriations


• Clinical

- SP’ s -> P - Purple


> P - Pruritic
-

-> P - Polygonal
> P - Planar
-

-> P - Papules / Plaques

Papulosquamous
disorders - II
[Link]
3
- At surface of lens
i
Wickham' s Striae

• True Koebner' s phenomena


- LP
- Psoriasis vulgaris
- Vitiligo
• Lichen planus - other sites
- Mucosa
- Nail
- Hair

Mucosal lichen planus

Papulosquamous
disorders - II
4

• Lesions -Violaceous patches over mucosa with white


lacyj reticulate striae
• Skin - Wickham' s striae
• Types - Reticular Oral LP and Erosive Oral LP

Reticular oral LP

• Importance Most —
[Link]
common type OLP

• Symptoms Asymptomatic
• Risk - No risk of malignancy

Erosive Oral LP

• Lesion - Erosion in OLP lesion

Papulosquamous
disorders - II
[Link]
5

• Symptoms - Burning sensation on Inot / spicy food }

tea / coffee

• Risk. - 0.1% Risk of oral SCC - Premalignant oral


mucosal lesions

Genital LP

• Annular - ring -shaped

Nail LP

• Most common finding


- thinning of the nail
- longitudinal ridging
• Most Pathognomonic finding - PTERYGIUM
Papulosquamous
disorders - II
6

+’

Fig : 8

• Pterygium - Wing shaped fold , from proximal nail


fold to nail bed , it damages matrix

• Importance - leads to permanent , irreversible loss of


the nail
• Anonychia -an absence of nail
[Link]

• Pup -tent appearance

Papulosquamous
disorders - II
[Link]
7
Hair - lichen Plano pilaris

• Lesions - Initial Bluish grey / VJhite perifollicular lesion


i
• Violaceous / hyperpigmented lesion on scalp
• Important -scarring alopecia

Histopathology

• •M l I
• |II lI|l

Fig : ii

• SC - Hyperkeratosis

• SC - Hypergranulosis ( wedge shaped )


• SS -Acanthosis

• SB - Vacuolization, keratinocyte Apoptosis -Colloid


bodies / Civatte bodies

Papulosquamous
disorders - II
8

• BM - Liquefactive degeneration
• Dermis - Band like Iymphocytic infiltrate
• During processing damaged area looks empty -max
Joseph cleft - it is an artifact
• RR -Saw toothed rete

• SBj BMj Dermis damaged Together - Interface


dermatitis
• VJhen basement membrane damaged - pigment
incontinence

LP : Histopathology

<9 <S

fot( c\ c8 feodum
[Link]

Fig : 12

• Wedge -shaped hyper granulosis corresponds to


Wickham striae

Treatment

• self - limiting
• Heals with pigmentation
• TOC -> steroids - For limited lesions -topical
-for extensive lesions -systemic
• Topical -> tacrolimus -> For oral lesions
Papulosquamous
disorders - II
[Link]
9

(TCI )

• Phototherapy — NB UVB

Pityriasis Rosea 00 :27 :22

• Self - limiting hypersensitivity rash on the skin


Trigger
% .Idiopathic - most common

2 .Infections - HHV7
3 .Drugs - Metronidazole, NS AIDS

Clinical feature

Fig : 13

• First lesion : single solitary lesion on trunk


i
Herald patch/ mother' s patch

Papulosquamous
disorders - II
10

• Timeline - after 1 -7- weeks


• Lesions - Multiple similar lesions on tine trunk along
tine lines of cleavage ( RSTL)
• Distribution - Clnristmas tree pattern ( or ) Fir tree
pattern

L ; i 4 Fig : IS

PR -Typical lesion 00 : 31 : SO
[Link]

Fig : 3- 6

• Morplnology - ErythematouSj ova! -shaped , annular


plaque
• Scale - Peripheral collarette of scale

• Symptoms Asymptomatic

Papulosquamous
disorders - II
[Link]
11

• Scale - Hanging curtain sign


- Outer margin - attacked
- Inner margin - free
• Scale folds along tine line of stretcln

Treatment
1 .No
- treatment needed ( <6 - 2 weeks )
2 .Emollients
3 .Topical steroids & Anti Inistamines
4 . Plnoto therapy ( N 3 UVB )

Pityarisis Rubra pilaris 00 : 36 :20

i I 1
Means red Inair
Scale
• Clnronic immune -mediated inflammation of tine skin

Papulosquamous
disorders - II
12

• perifollicular Red , scaly papules


• Initial site - scalp
•|spread (f /Vi size , number )
• Body
• Progress - Cephalo caudal spread

PRP - Erythroderma -
00 : 32 :1 0

[Link]

• Redness on > 90 % BSA


• Color - Reddish orange
• Lesions are well demarcated
i
Islands of sparing / skip areas
Papulosquamous
disorders - II
[Link]
13

. Red follicular Papules - Nutmeg grater papulesj


prominent on tWe dorsum of tine Wand

. On palms and Soles - Waxy keratoderma


i
TWickening of skin
• AKA sandal keratoderma

Treatment
• MetWotrexate
• Acit retin
• PWototWerapy

Papulosquamous
disorders - II
1

VESICULO BULLOUS DISORDERS - I

Lesions in vesiculo bullous d / o (VSP ) 00 :00 :18

Lesions is vesiculo bullous d / o (VI3 P )


I

V
%

Ffr 1

Primary Secondary
• Clear fluid filled lesions •Raw areas,, partial loss
<O .Scm = vesicle W
>0.5cvn - bullae Erosions
Crust

Classification: [Link]
• Immuiao bullous : auto immune
• Meccano bullous : trauma induced
• Inherited acantlnolytic : genetic

Immune bullous disorders :


Basis of level of split

Intra epidermal Sub epidermal


• Within epidermis • Beneath epidermal
Pemphigus Pemphigoid
Superficial Deeper

Vesiculo Bullous Disorders I


[Link]

Basics : pemphigus :
• Level : intra epidermal
• Disease : immune bullous ( Ab mediated )
• Target : desmosomes

• Hypersensitivity : type 2 hypersensitivity


• Mechanism : acantholysis

V ©
AI 0
•p
i

Vesiculobullous - £

Pemphigus : classification
• P. vulgaris
• P. foliaceous
• Paraneoplastic p.
• Drug induced p.
• Ig A pemphigus

Vesiculo Bullous Disorders I


Pemphigus : target
• Target structure : desmosomes
• Target antigen:
• Desmoglein: P.F and P.V ( II 3)
• Desmocoltin: Ig A p .
• Plakins ( Envo peri ) paraneoplastic P

Pemphigus vulgaris :

Skin

[Link]
Mucosa

Fig : 3

• Disease : immune bullous


• Level : intra epidermal
• Target structure : desmosome
• Target antigen: Psg 3, 1 ( Psg 3> X )
• Clinical feature : age : ArO -GO years

Vesiculo Bullous Disorders I


[Link]

s/ s : painful bullae erosions + oral ulcers


• Bulla : flaccid bullae , ruptues easily ( SL -3 d )
• Erosions : red , oozy , tendency to extend at periphery
non healing
• Site : upper body
• Skin and mucosa involved

• Mucosa : oral erosions ( painful ) , ulcers


Eyes , nasal , genital

Pemphigus foliaceus:
• Disease : immune bullous
• Level : intra -epidermal
• Target structure : Desmosomes

Vesiculo Bullous Disorders I


5

• Target antigen: Psg 1

• Clinical features:

- Age : 40 - (SO years


- s/ s : painful bullae, erosions
- Bulla : flaccidt may not find intact bullae
- Erosions : crusted erosions
- Site : [Link]
areas
- Mucosa : not involved

Pemphigus: clinical signs


• Nikolsky sign
• Bulla spread sign
• Asboe - hansen sign

Nikolsky sign:

Vesiculo Bullous Disorders I


[Link]

• Tangential pressure on intact skin


- Upper layers of epidermis separate -> new erosion
• Signify activity of disease
Severity of ds

Bulla spread sign: mark bulla with pen

• On intact bulla
1
Qive pressure from side
I
Bulla spreads

Pemphigus : investigations :
• Tzanck smear: cytology smear
• Skin biopsy :
• Lesional : histopathology
• Peri -lesional : direct immune fluorescence :

Vesiculo Bullous Disorders I


PV : Histopathology

• Suprabasal split + acantlnolytic cells

PF - Histopathology :

[Link]

• Subcorneal split + acantlnolytic cells


- PV : suprabasal
- PF : Subcorneal
• Source of acantlnolytic cells :
- PV : S . spinosum
- PF : S . yranulosum

Vesiculo Bullous Disorders I


[Link]
8
PF :

>
if A i •r
v
\#
%>
Iwx 4

Fig : 12

• Direct immune fluorescence = common in both P.V


and P.F cannot differentiate

• Intra -epidermal Ig 0 deposition


• Fish net appearance

Pemphigus : treatment :
l- .Steroids ( Prednisolone methylpred )
}

Oral ( High dose 2 -2 mg / kg / d )


Injectable ( Pulse therapy )3 days, 2 monthly* till
remission
2 Steroid sparing agents :
• Azathioprine
• Mycophenolate mofetil
• Cyclophosphamide acrolein hemorrhagic cystitis
i
Hydration
-h
Mesna
Transitional cell CA ( Bladder )

Vesiculo Bullous Disorders I


3 .Biologies :

- Mod - severe diseases , not responding


- Rituximab ( Anti CD 20 ) -> B cells
• RA protocol -> 2000 mg of rituximab 2 weekly
• Lymplnoma protocol — 375 mg / mz -> week x 4
weeks
• Other CD 20 -> veltuzumab
A. IVIQ : Intravenous Ig Q ( pooled Ig plasma )
Very effective

Paraneoplastic pemphigus : periplakin, envoplakin’ s Psg


2 ,3

[Link]

• Associations :
- NHL ( Non Hodgkins Lymphoma ) - most common
- CLL
- Castleman d / s
- Thymoma
• Clinical feature : severe stomatitis ( Non stratified
epithelium = respiratory ) polymorphic skin lesions
Vesiculo Bullous Disorders I
[Link]
10

• Most common cause of death: Boop - bronchiolitis


obliterans

Drug induced pemphigus :


• Most common drugs :
- P : penicillamine ( most common)
- C : captopril
- R: rifampicin
• Clinical feature :

- 75 % "
PF like ( only skin )
- 2 S% P.V
Resolve on stopping the drug

Pemphigus : variants
• Pemphigus vegetans :
Flexures exophytic granulating erosions
- Rarest type of pemphigus
• Pemphigus erythematosus : of P. folacious
- FF + LB - PF : Bullae and malar rash
= senear usher syndrome

Vesiculo Bullous Disorders I


1

VESICULO BULLOUS PART - ll

Subepiderma ! Immonobullous Disorders 00 :00 :18

i. Pemphigoid
- Bullous pemphigoid
- Mucous membrane pemphigoid
- Pemphigoid gestationis
- Linear IgA disease
ii. Dermatitis herpetiformis
Hi. Epidermolysis bullosa acquisita
• Defect in BMZ / DEJ -> Sub epidermal cleft / bulla.

BMZ
[Link]

KIF ( Kertain Intermediate Filaments)

Epidermis
Hemi - desmosome
— Lamina lucida

BM Lamina densa

Sub lamina densa

[
Penal's
Anchoring fibrils

BMZ : Components
i. KIF : Keratin 5 / 14-
ii . Hemi desmosomes : Bp Ag ISZZ
iii . Lamina lucida : Lamininj BP Ag ISZZ

Vesiculo Bullous Part 11


[Link]
2
iv. Lamina densa: Laminin , collagen IV
v. Sublamina densa Collagen VII
vi. Anchoring fibril

BMZ : Defects
i. BP Ag 1/ -A Bullous pemphigoid
~
BP Z 50 Bullous pemphigoid
ii. BP AgZ / pemphigus gestationis
BP iso -> Linear IgA ds
Hi. Collagen * -> E3 acquisita

Bullous Pemphigoid 00\0 S :3Z


• Most common autoimmune blistering ds in adult .
• Disease : subepidermal immunobullous disorder
• Level : Subepidermal
• Target structure : Hemidesmosome ( K -> BM )
• Target antigen: Bp AgZ , Bp Agl-
• Process : No acantholysis
• Age : > 6<9 years elderly
}

• S/ S: Intense itching / urticaria

f/ b bullous lesions
• Bullae : "Tense Bullae” on red base + Itching
Vesiculo Bullous Part 11
• Site : Lower body - umbilicus , groin , LL
• Mucosa : inv in X / 3rd of patient
• Bullae -> Erosions : Do not Wave peripWeral extension
Heal rapidly

Bedside tests:
X .Nikolsky sign: negative
2 . Bulla spread sign:

p^
- npKtgiu ;
-
5 ng uicx Lj
^
[Link]
3 .Tzank smear : Negative for acantWolytic cells

EosinopWils
4 .Skin biopsy : HPE -> Subepidermal deft

EosinopWilis
[Link]: Perilesional Normal skin
- Deposited : IgQ & C3
Veslculo Bullous Part 11
[Link]
4
- Site : BMZ / DEJ
- Pattern : Linear

Treatment
i. Steroids : Low dose (0.5 - 0.75 mg / kg / d )
ii. Azat In io p rine, MM F

Mucous Membrane Pemphigoid

• Cicatricial Pemphigoid
• Involvement : Mucous membrane only
- Oral
- Ocular
- Cenital
• Risk : Scarring
• 21 to bullous pemphigoid

Veslculo Bullous Part 11


5
Pemphigoid Gestations : Pregnancy

B\o Aa M 0 l. VJt
i. BP Agi 230 KD
ii. Bp Ag 2 120 KP

• Synonym : Herpes gestations


• Target Ag : BP AgZ [Link]
• Onset : Late pregnancy ( < tW / 7 tW months )
&

• Clinical features : Itching + grouped vesicles / bullae


Initial site = periumbilical

f t

Fig : S-

• Risk : Fetal damage


• Treatment : steroids
• Recurrence : present
Veslculo Bullous Part 11
[Link]
6

Linear IgA disease 0 0 :22 :36

• Clinical features : LAD / CBDC


• Site -> children : Perioral &: perineal
• Bulla -> Tense bullae on normal base / skin
+ Itching

• Mucosa -> HO -50% pts


'

• Sign -> circumferential arrangement of bullae


" String of Pearl sign / Cluster of Jewel 31

Fig : 7

• D / P -> Deposited : IgA

Veslculo Bullous Part 11


7
Site : DEJ / BMZ
Pattern : Linear

• Treatment -> TOC : Papsone


Steroid

Dermatitis Herpetiformis :
• Synonym : Duhring’ s disease
• Level : sub epidermal IB / Deep
• Target Ag : Epidermal Transglutaminase 3
• Genetics : HLA D D Q s , BS
• Systemic Ass : Gluten sensitive enteropathy
• Clinical features : Age -> middle age

f
' 1
•jf
[Link]

I
Fig : 2

S/ S Intense itching
Vesicle -> papulo vesicular lesion + Excoriations
Site B / L symmetrical , extensors -> Shoulders
Arms
Back
Buttocks
Knees

P. foliaceus
No mucosal inv ~

P. Herpetiformis

Vesiculo Bullous Part 11


[Link]
8

HPE

• Subepidermal cleft r

Inflammatory cells = neutrophilic infiltrate


si/
Papillary Tip Abscesses
Increases IL - 2 ( Neutrophil chemotaxis factor)

HPE

• Deposited : IgA
• Site : BMZ / DEJ
• Pattern : Granular

Treatment
i. Gluten cessation
ii . Dapsone ( DOC ) : Decreases IL - 2
Vesiculo Bullous Part 11
9

• Avoid : B - Barley
R — Rye
O - Oats
W - VJheats
• Consume : Rice
Corn
Pulses

Epidermolysis Bullosa Acquisita :


• Disease : Immunobullous disorder
• Level : subepidermal
• Target structure : Anchoring fibrils ( S in sublamina
densal / dermis )
• Target Antigen: Collagen 7
[Link]
• Clinical features : elderly population
Tense bullae
prone sites / - Mechanobullous d / o
Q Trauma
Friction prone sites .
• HPE, P I F L ~ to bullous pemphigoid

Salt split technique of IF:

Vesiculo Bullous Part 11


[Link]
10

X molar saline

Normal skin
Cleft formed
si/
IF
fYY^)
Roof = Hemidesmosomes : BP
(
n5 serrated ^
Floor = Anchoring fibrils : EBA
'U ’ serrated
Cleft/ Bulla

Meccano bullous disease 00 : 44 :16

• Mechanical trauma bullae


Epidermolysis Bullosa
I
I 1
Congenital Acquired
• QenetiCj birth • Autoimmune Elderly }

s|/

EB acquisita

• EB Congenital EB

Congenital EB
• Defect :

>- KIF -> <s / < x4 = EB simplex

Laminin: L3 - EB junctional

Anchoring
~ filaments = Dystrophic EB
( Collagen 7)

Vesiculo Bullous Part II


11
2 .EB simplex -> intraepidermal , superficial bulla
2 . EB junctional - Subepidermal bullae
3 . Dystrophic EB

Clinical features

[Link]
• Aye : Early onset ( child )
• History : Consanyuinity ± ( ARj AD )
Family members +

Trauma/ friction -> bullae Sz erosions


• Site : occiput, shoulders , sacral , hands Sz feet .

• Mucosa : ±
• Trauma Contractures -> Syndactyly
*
k / A mitten Hands & Feet

Diagnosis
• DIF : Neyative
• IOC : Electron microscopy

Vesiculo Bullous Part 11


[Link]
12
Treatment
• No treatment
• Symptomatic mx
• dene therapy

Inherited Acantholytic disorders 00 : S 3 : XX

• Qenetic defect -> Acantholysis -> vesicles, bullae


formation.

H . Hailey - Hailey disease


Z . Darrier disease
3 :Transient acantholytic disorders / drovers disease

HHP & PP
• Inheritance : Autosomal dominant
• Defect : Caz ATPase enzyme
+

i
• Process : r 1
Keratinization P esmosomes
s|/ si/
Dyskeratosis Acantho lysis

Hailey - Hailey Pisease

• Familial benign pemphigus


• Defect : Caz ATPase ZcH
+

Vesiculo Bullous Part 11


13

• Onset : 3 rd decade
• Lesions : Vesicles -> erosions
drey colored macerated plaque
with overlying erosion
• Site : Intertriginous/ flexures
-> neckj groin, gluteal fold

Parriers disease

[Link]

• Parriers disease : Keratosis follicularis

• Defect : Caz+ ATPase 2 A2

• Onset : Second decade


• Lesions : Dirty , Hyperpigmented , warty papules
• Site : Seborrheic areas
- Face PACH
PA: Parriers Az
- Neck CH : HHP 2C 1
- Scalp
- Chest
• Follicular papules: K / a = Keratosis follicularis

• Nails
Vesiculo Bullous Part II
[Link]
14

- V shaped notching on distal free end of nail


Alternating erythronychia & leukonychia
• Oral mucosa : Small papules on hard palate

cobble stone appearance 3 )

• HPE : Dyskeratosis +- Acantholysis


i H H D : Dyskeratosis + Suprabasal c l e f t = “ Dilapidated
brick wall appearance ’ 3

if . DP : Corps Ronds + Crop grains = Dyskeratotic kerati no cysts

HHD & DD : Primary acantholysis


• Treatment
H H D : Topical steroids
DD : Oral retinoids
Veslculo Bullous Part 11
1

ECZEMA - l

Eczema
• Inflammation of skin
4 /

• reaction pattern
• means to boil

Tl
*
Fig .- 1

Morphology classification 00 :00 : SZ

• 3 types -> Acute lesions are of short duration


Subacute
Chronic
[Link]

Acute Eczema

Eczema - I
[Link]
2

• All signs of inflammation are seen


• lesions : - Erythema
- Edema
- Vesicles
- Oozing ->look like weeping rash
- Crusting
• HPE : - changes in stratum spinosum
• Intra - epidermal edema ( within epidermis )
• Inter - cellular ( B / W cells ) edema - spongiosis

- %
r
m

0 0
•• #
0

m
%
V .
m

.
0 % 0 0 4 0
4 00 I
*

- - .V> v..
»*
*s
*
v
» & * • • 40••,T
#
*]
w I*
&* • *
r m *

f %
#
#
1
' *
*
»0 ••
%
r • # ;' • %o vf
7A/
r :
#

• jv
4
4
*
% »; %
4

- s
Ivr- - '
•*• ) i * •
/ •v --
« V
Vi > -

o o
0 O
/

o «0
0 o \J 4

Subacute eczema

• lesions : - Reddish - brownj (ess vesiclesj more


Scaling
• H P E : - Papillomatosis
Eczema - I
3
Chronic eczema

• Long duration
• Chronic itching Lichenification
• lesions : - T color ( Hyper pigmented )
T lines
T thickness
• HPB : - Acanthosis

[Link]

Ethological classification 00 :06 :22

Exogenous Endogenous
si/
External cause ( within the body )

Exogenous eczema
2 .Contact Dermatitis -> Touch
2 . Phyto dermatitis -> Plant
3 . Photo dermatitis -> Sun

Eczema - I
[Link]
4

Contact dermatitis
• Definition: - reaction due to physical contact with
chemicals / trigger
• Classification
I

Irritant Allergic

Irritant CD Allergic CD
Tendency Everyone exposed Qenetic predisposition
Pathogenesis Nonspecific Specific Immune
immune ( Innate ) response (Type IV
Direct toxicity / HSN )
injury
Site Restricted to area Disseminate
of contact
Symptoms Sudden onset Develops on / after 2 nd
Pain, burningj contact .
itching predominantly Itchy

Irritant CD Allergic CD

Irritation
Non specific immunity Allergy
Innate immunity Specific immunity
Adaptive immunity
Chemical

Chemical toxoty and celular Activation of cytotoxic CD8+ T


activation of the akin innate cells against keratmocytes
immunity
\ / (Fast perfonne)

Necrosis apoptosis
cellular activation

Cytokines
Chemokmes
,
Inflammatory
infiltrate

Inflammation induced by the toxicity of Inflammation induced by the


the chemical (nature , dose skin type) activated chemicai-6 pecific T cells

Eczema - I
5

Allergic Contact Dermatitis 00 : 22 : S5

ACD
Antigen 2 nd Exposure Antigen
Senvit i /at ion Elicitation
©Allergen
IL - 1 or
IL - 1 « i

m - 1|t 4
©
fuititw
ttimuUtkM
c4 < %
KCs

' Cellular Recruitment


.
< Lymph
5)nw^v
^
Infill r at ton 4)

Node \
^ fieri
^ "TNT*
N

11 - 17
11 - 22

x
t 1

ipetifK T cell
piolifeution
-- ^
TNf
A IO
TGf |l

NnUffww

TNf tg

ESE2&SEB& ^ Fi' : 8

• Mechanism : - Type IV HSN


contact : - Langerlnans cells
• First cell to come [Link]
• First exposure : - Sensitization
• Subsequent exposure : - Elicitation
• Cell responsible : - T cells ( memory T cells)

Some important causes


• Irritant Contact Dermatitis

- Most common causes ( India ): - Detergents


- Synonym : - House wife eczema
- 2nd most common cause - industrial -Alkalis
Eczema - I
[Link]
6

Diaper dermatitis ( I C D )

• Cause : - Stool and urine


• Involves : - Convexities
• Spares : - creases

Paedrous dermatitis

• Synonym: - Blister Beetle, insect bite reaction


• Season: - Rainy
• Cause : - Paedrin ( vesicant )
• Lesions linear and kissing lesion
Eczema - I
7
Allergic Contact Dermatitis

• Most common metal cause : - Nickel


• Sites : - Neck , Jeans buckle region
ACD : - metals
[Link]

X .BlackDermographism
1
Seen only with Nickle dermatitis
Z . Red Dermographism - physical urticaria
3 .White Dermographism - Atopic Dermatitis

Eczema - I
[Link]
8
Cement Dermatitis

• Occupation: - laborers , masons


• Cause : - Potassium [Link]
• Sites : - Hands <k Feet, disseminate to other areas

Hair dye dermatitis

• Can happen in salon workers rash in hand


in who dye hair -> scalp / face
• Cause : - PPD - Para phenyl diamine can cause
ICD & ACD
• Can be present over scalp, Kead Keck
Eczema - I
9

Bindi Dermatitis

• Cause : - PTBP Paratertiary butyl phenol


i
Present in adhesive of Bindi
ACD

Phytodermatitis

[Link]

• Phyto means plant


• Plant :
- Parthenium hysterophorus ( congress grass )
- Most common plant
- Most common overall cause of ACD in
India
• Allergen: - SQL ( Sesquiterpene lactones )
• Synonym : - Air borne contact dermatitis ( ABCD )
• Mechanism : - Type IV HSN
Eczema - I
[Link]
10

ABCD -> phytophoto dermatitis

• Occupation : - Ruralj farmers


• Lesions : - Exposed areas - face v area of neck
}

• Classical itchy rash

Diagnosis of contact Dermatitis 00 :27 : 30


Patch test

• Indication : - Diagnosis of ACD


Confirmation of cause
Differentiate B / VJ ACD & ( CD
• Principle : - Type IV HSN
• Method : - Finn Chambers
• Site : - Upper back

• Reading : - Most common at 42 hours ( 2 days )


• Q ( Best read at 2 nd visit at <? 6 hours (4 days )
Eczema - I
11
Photo patch test
• Diagnosis of photo allergic dermatitis

r
on a o
oa afl o
« y a cLi'n c
a C DO
n n ao
a
a n o aa
n n ao
a

Fig .- 21-

• Method : - Duplicate sets on either side of hack


• UV : - at 48 hrs -expose one side to UV -A
• Readings : - at 9 [Link]
hours
- Positive on both side
• No photo allergic Dermatitis
• only ACD
- Positive on only UV - A exposed site -* photo
- allergic contact
- dermatitis

Contact Dermatitis - Treatment 00 : 33 :14

• (general : - Avoid contact


Emollients
• Topical : - steroids
• Oral : - Steroids
• DM / HTN : - Azathioprine, ABCD

Eczema - I
[Link]

ENDOGENOUS ECZEMA - ll

• Trigger within the body

Atopic Dermatitis 00 :00:36

• Most common Endogenous eczema


• Chronic , relapsing - remitting inflammation of skin.

Etio pathogenesis
Z .Genetic predisposition
2 .Defective skin barrier
3 .Immune dysregulation
[Link] trigger

Genetic factors
• Most important -> mutation in fillagrin
si/
- Present in Keratohyaline granules
- Filament aggregating Q protein
- Gene in chromosome Z
- Loss on function mutation.
Eczew\a - II
• Atopic penes -> / L -4 / ( L - rZ- 3
£? a /Vv in function ^nutation

— - - I f-

• W

• In a normal skin Impermeable skin barrier


sP
Present in brick & mortar pattern
s i/
Cells Lipids
[Link]
/ sU
sl/ s|/ Filaprin Sterods s|/ s|/

M.*» rv» l imotl


CCNCTIC
BACKGftOUfcD Cipaurt

\
ATOPY
I
& ACMfs
Mr
** unrciu a
:
i t u* U I P N H I

I hi

IL -4 I
IL - 5 Cofl recnjtmnnt
*
-
IL 13 INFLAMMATION

Fig : 3

• TH2. dominant immune response


• Increase IL 4/ i 3
• Increase IpE
• Increase Eosinophils

Eczew\a - II
[Link]

Environmental factor
• House : dust mites ( Per matopWag olds )
• Infection — Staph aureus
• Common allergies

Stages
2 .Infantile AP

l .
r5 a

Fig : 4

• Onset : - < 2 years (2 m - 2 yr )


• Rash : - Acute, red , weepy , oozy rash
• Sites : - Face &c scalp extensors

2 .Childhood AP

Fig : S'

Eczew\a - II
• Onset : - Until puberty
• Rasln : - Subacute — Less oozing and more scaling
• Sites: - Flexural ( cubital fossa ) most common site
[Link] AD

• Onset : - After puberty


• Rash : - [Link]
lichenified eczema
• Sites : - Flexural
Flexural eczema QQ
• Nummular eczema Q

Diagnosis
• CLINICAL : No role of blood tests
HANIFINS Sz RAJKA CRITERIA

• Major criteria
- Early onset rash
- Typical morphology & distribution
- Chronicj relapsing remittins
- Personal / family H / o atopy
3 out of 4 criteria are sufficient to make diagnosis

Eczew\a - II
[Link]

Pruritis

• Importance :
- Hallmark, essential Q
- Itcln that rashes Q

- Itch is a disease

• Characteristics - Intense, episodic / intermittent


• Mediator - Histamine

Atopy
• Personal or family H / o atopic disease

ATOPIC
TRIAD
Asthm . i Hay Fever
A
Fig : 8

- Tendency to allergy
- AR, AC, sinusitis

- Chronic urticaria

Eczew\a - II
- Asthma
- Food Allergy
• Sequence it progresses is Atopic March Q

Other Clinical features

• Lip rick cheilitis


• Red lips
• Perioral sparing -> Headlight sign QQ
[Link]

• Xerosis -> decrease Lipids IV ( Ichthyosis Vulgaris )


si/
Fit a smur

Eczew\a - II
[Link]

• Keratosis pilaris - coiled corkscrew hair


• Extensors

• Antenna sign

• VJhite Dermographism
- Stroke skin
- Delayed blanching
- Happens because of exaggerated vasoconstriction

Eczema - II
• Hyperlinear palms

Pennie - moryan fold QQ


• Multiple Infra orbital folds
[Link]
Hertoyhe’ s Siyn
• Loss of outer X/3 eyebrows QQ

• Anterior subcapsular cataract -> Shield cataract


• Posterior subcapsular cataract -> S / E of liny term
steroids
• Keratoconjunctivitis -> Papillary conjunctivitis

Eczew\a - II
[Link]

Treatment
• General measures : - Avoid contact with triggers
generous use of emollients & moisturizers. QQ
• Topical
- Steroids
- TCI ( Tacrolimus )
- Crisabarole ( PDE - 4 inhibitor ) in moderate to
Severe AD

• Systemic
- Steroids
- Azathioprine
- Cyclosporine
• Biologicals - Dupilumab Q ( IL - 4 / T 3 inhibitor )
Mod - sever AD
• Photo therapy - NB UVB therapy

Complications
• Infections -> m/ c -> staph aureus Q
• Viral ( HSV -T ) -4 Kaposi varicelliform eruptions
eczema herpetiform
• Erythroderma - Eczema -> AP, SD > ABCD
*
Most common of ED in world

Eczew\a - II
Seborrlnoeic Dermatitis ( 0 0 :2 7 :4 2 )

• Exaggerated immune response to Malassezia yeast Q


[Link]
• Site : - Seborrlnoeic areas

• Rasln : - Yellow greasy scales QQ

Eczew\a - II
[Link]

Sites

• Glabellar complex
• Ala of Nose
• Nasolabial folds
• meat at area
• Post auricular / pre auricular

Severe SP

• Elderly
• AIDS
• Parkinson’ s disease

Infantile SP
• Common in first 6 months of life
• Yellow greasy scales on scalp
• Also called as cradle cap

Eczew\a - II
Pity nans alba OO :

• Pityriaris - scales
• Alba - white
• Endogenous eczema Q
• Age group : - children
• Rash : - multiplej hypopigmentedj scaly macules on

face, episodicj recurrent


[Link]
Differential diagnosis - child with hypo pigmented
macule on face

Pityriasis alba Indeterminate Hansen

• No. of lesions • Single face


• Location • No . scaling
• Scaling • Normal sensation
Eczew\a - II
[Link]

• Sensation • Periappendegeal and perineural


• HPH -> Spongiosis lymph node infiltration
• Natural course • 75 % spontaneous regression
*

Pompholyx OO : 34:i 9

• Synonym : - Dyshidrotic eczema Q


• Site: - Palms & soles
• Lesions : - Multiple deep -seated vesicles itchy QQ
• Appearance : - Sogo -grain appearance / Tapioca
grain appearance

Nummular eczema 00 : '5 H : HH

a Fig : ZZ

• Synonym: - Discoid eczema


• Age group : - Middle aged men
• M .C site : - Lower limbs
• Appearance : - Coin like
Eczew\a - II
Varicose eczema OO : 36:2- 7

• Synonym : - Stasis dermatitis


• Cause: - Ckronic venous insufficiency ( varicose veins )
• Site : - Lower :!-/ 3 rd leys

Dark constricted skin


si/
Lipodermatosclerosis ( Inverted
Fig : 24 [Link]
ckampayne ylass appearance)

Asteatotic eczema 00 : 32 :1-1.

Fig : 25

• Synonym : - Eczema crac\ uele winter itck


}

• Age yroup : - Elderly


• Site : - Leys
• Appearance : - Crazy pavement appearance.
Eczew\a - II
[Link]
1

URTICARIA & ANOIODEMA

Mechanism of allergy 00 :00 :2-7-

• Type of Hs: Type H- HS

Antigen - presenting
»
* %
l.l

Mast cell ••
degranulation •••• •.

Mast cell • * ••\


sp
O

Y
Y V' Y
& B cell
antibodies

Urticaria
2

• Antibody : ly E

• Cell : mast cells


• Mediators : Histamine
[Link]
-> dyspnea
• Bronclno constriction
• Bowel peristalsis increase -> abdominal pain
• Vasodilation, permeability increase
,
Edema,
Erythema
CVS -> Hypotension

Clinical spectrum:

/. Urticarial : Dermal Edema Wheal
ii. Anyioedema: subcutaneous/ submucosal Non pittiny
swelliny / edema
Hi. Anaphylaxis : Urticarial / Anyioedema +- Multisystem

Urticaria
[Link]
3
Urticaria :
• Dermal Edema
• Histamine
• Primary lesion : wheal

Classification of urticarial :

Duration
\ l
< 6 weeks > 6 weeks
1 1
Acute chronic

Acute urticarial :
Triggers :
i. Injection: Viral , Parasitic
ii. Ingestion: Drug , Peanuts , sea food
Hi. Inhalation: Pollens , Chemicals

Urticaria
4

Chronic urticarial :
Classification

Spontaneous Inducible
i. Idiopathic physical
ii. Auto immune

Physical Urticarial :
Types :
i . Stroking Symptomatic Demography
ii . Exercise Cholinergic Urticarial
Hi. Sun -> Solar
iv. Heat
v . Cold
vi . Pressure [Link]
[Link] -> Aqua genic Urticaria : differential from
A qua genic pruritus
viii . Contract

Symptomatic Dermographism :

Urticaria
[Link]

• Me type of physical urticarial


• Trigger : blunt instruments -> stroke -> wheal
• Synonym: red demographist
- VJhite demographism -> Atopic dermatitis
- Black dermographism -> Nickel dermatitis

Cholinergic urticaria :
• Trigger :
- Exercise
_
- Sun ( 2.0 -(SO mins ) increase core body temperature
- Hot / spicy food

• Mech: increase eccrine sweat gland Ach increase ->


wheal
• Clinical features : punctate wheals

• T / t : TOC — second generation, non -sedating


antihistamines
- 4- increase dose
- 4- first generation AH

Urticaria
6

• Second : systemic steroid, cyclosporin, methotrexate


• Third : omalizumab ( anti lyB )

Other disorders with urticaria:


i . Urticarial vasculitis
ii . Urticarial pimentos

Urticarial Vasculitis

[Link]

• Causes
- Drugs , infections
- Connective tissue diseases

• lesions : Urticarial wheals -H purple / dusky color in


Centre
- R 2.4 hrs .

- Heal with pigmentation

• HPE : Wheal Vasculitis

Urticaria
[Link]
7
Urticarial pigmentosa :

• Disease : cutaneous masto cytosis


• Aye : children

• Lesions : multiple, hyper piymented skin lesions


trunk
• Darier siyn: method : stroke the lesion

Fig : 2

I
Observation: wheal on the lesion &c around it

• Also seen in: conyenital smooth muscle hamartoma


Juvenile xantho yranuloma

Urticaria
8

.
Angioedema 00 :22 :1- 8

im- ,r
4- Fig : q

• Pathology : subcutaneous / submucosal edema


• Clinical features : non pitting swelling
not itchy

• Most common sites : perioral & peri orbital

Classification of angioedema
[Link]
Allergic angioedema Drugs Hereditary
i
Associated with
urticarial

Hereditary angioedema :

• Synonym : Quinckes disease


• Inheritance : AD
• Defect : Cl- Esterase inhibitor
i
Mechanism : cl- cl- y

Complement pathway kallikrein FXll ( Hageman factor )

Urticaria
[Link]
9
Pre kallikrien
Trauma

Factor xii a
Plasmin

Cl Esterase inhibitor

Kallikrein
High molecular weight kininogen
I > bradykinin

Increase edema vasodilation smooth muscle contraction RTCfl

• Mediator : Bradykinin

HAS : Classification:
i. Cl Esterase - Deficient
[Link] Esterase - dysfunctional
Hi. Factor XII a - tt Cain in function mutation

Clinical Features :
• Repeated attacks of swelling on skin
• Cl -> abdominal pain Sz cramps
• RT: larynx : stridor & Dyspnea
I
Life threatening

Urticaria
10
Investigation:
• Complement levels : low levels of Cu4 Cz
i
Screening testQ

• decrease Cz Esterase Inhibitor


• Normal Cz

Treatment :
Acute Management :

• Airway
• Cz esterase inhibitor aggregates
• FFP
Maintenance :
• Anabolic steroids :[Link]
Panazol
• Tissue plasminogen inhibitors : Tranexanemic acid
• Kallikrein inhibitors: Eccalantide
• Bradykinin Bz receptor antagonist : icatibant

Drug Induced Angioedema :


• Drugs : ACE inhibitors
• C / E: Cough + Angioedema Q
• Mech & Mediator: t Bradykinin QQ

Anaphylaxis :
• Urticaria | Angioedema + Multisystemic Involvement

RT Cl CVS CNS

Urticaria
[Link]
11

• Acute anaphylaxis : 2 nd phase


Therefore, Observe for 42 -72 hrs

MECHANISMS AND TRIGGERS


IMMUNO LOGIC : IgE / Fc Rl IMMUNOLOGIC: OTHER NON - IMMUNOLOGIC
^
• Foods • IgG - antigen complexs • Exersice
• Medications •Complement system activation • Cold air or water
eg. j} - lactam antibiotics •Coagulation system activation • MedicationSj eg. opioids
• Insect stings / bites •Other
• Natural rubber latex heparin OSCS contaminant
.
oifie
• Other
°A.; JX

o
coc- y
. \ H
HHCOCH
ptnicillin
J -OH ,
OR

OR ,

cephalosporin ,
^
f r» %
CELLS

MAST CELLS BASOPHILS


IX MEDIATORS T
PREFORMED NEWLY GENERATED OTHER
HISTAMINE LEUKOTRINES CYTOKINES
TRYPTASE PROSTAGLANDINS CHEMOKINES
CARBOXYPEPTIDASE A PLATELET - ACTIVATING FACTOR
CHYMASE

ORGAN SYSTEMS
T T
SKIN RESPIRATORY GASTROINTESTINAL CARDIOVASCULAR

MUCOSA

S. tryptase Q

Anaphylaxis cause
• Food Peanut, Sea foo^
• Drugs : Penicillin
• Insect bites
• Rubber / Latex
• Vaccinations
• Others

Treatment :

• TOC : Epinephrine
ABC .

Urticaria
12
A core body tamp

Hot / spicy food

Mech: increase Bccrine sweat Gland -> Ach increases ->


wheal

C / F: punctate wheals
[Link]
T / t : TPC - 2 nd generation, no sedating Antihistamines

h increases dose
2 st generation AH
2 nd : systemic steroids cyclosporine , methotrexate
}

3 rd : qmalizum ab ( Anti Ig B )

Other disorders with urticarial :

i. Urticarial Vasculitis
ii. Urticarial pigmentosa

Urticaria
[Link]
1

CUTANEOUS DRUG REACTION

Fixed Drug Eruption 00 :00 : :IP

• Pathology : CML delayed type HS ( type 4)


• History : Drug -> RasK, intake of drug -> same rash
same site repeats.

• Mediated by : memory T Cells


• Drugs :
- NS AID' S

- Cotrimoxazole ( Genital )
- Tetracycline
• Rash

• Lesion : well defined round - oval lesion central dusky


/ violaceous colour peripheral erythema
• Site : Most common site -> mucosa ( Lips
• genitalia) -> erosion on glans
• Time line : Drug 7 - HO days RasW
^
• Re intake : 8 hrs Rash
^
• Heals with hyperpigmentation
Cutaneous Drug Reaction
Treatment :
• Self -limiting
• Topical steroids
• Stop drug

Erythema multiforme : EM
• Self -limiting hypersensitivity response on skin
[Link]

Triggers :
X . Idiopathic = Most common cause
2 . Infections - Most common infection: Herpes labialis
2 nd most common: mycoplasma ( Atypical
pneumonia )
3 . Prugs : NSAIDS

Antimalarials NEET 2022


Antibiotics
4 .CTD' S : SLE
5. Malig : Leukaemias
(o .Food additives

Cutaneous Drug Reaction


[Link]
3
Typical lesion:
Target lesion: 3 concentric rings
i Centre - Dusky / purple
Aka : Bulls eye lesions middle — pallor
Periphery -erythema

Clinical features :

Rash : Bilateral , symmetrical , burning sensation


Site :
a. acral ( Extremities )
b. face
c . mucosa
Types :
a. EM major : Skin 4- mucosa
b. EM minor : Skin
c . mucosal EM mucosa

Treatment :
l .Self -limiting
-
Cutaneous Drug Reaction
2 .Underlying cause
3 .HSV -> Acyclovir
Mycoplasma Azithromycin / clarithromycin
HSV : H / O grouped vehicles painful +- Target lesions
Mycoplasma: H / O coughj fever, dyspnoea + CXR -
atypical pneumonia

SJS - TEN
• Acute mucocutaneous eruption systemic s/ s
a ) Steven Johnson syndrome : < 20 % BSA involved
Overlap : 20 -30 %

b )Toxic Epidermal necrolysis : >30 % BSA involved

• etiology : [Link]
- Drugs : > 90%
2 .Anticonvulsants : phenytoin, Carbamezepine,
lamotrigine
2 .Antibiotics : Sulphonamides , cotrimoxazole,
penicilUn quinolones
}

3 .Allopurinol

[Link] - Abacavir , Nevirapine


[Link] AIDS - Oxicam
- Other : Infection

• HLA predisposition:

Cutaneous Drug Reaction


[Link]
5

Drug HLA- Related


Abacavir HLA 5701-
AKopurinol HLA 5201-
C13 Z / phenytoin HLA 1- 502.

• SJS - TEN pathogenesis :


Drug ( Hapten )
4
CDs T cells
Cell medicated Cytotoxicity
l- .FasI -> cell death receptor -> apoptosis
Z .Cranulysin -> apoptosis
5 .TNF alpha, IL 8 , IL -25 -> ft inflammation
Cell death: keratinocytes
- Timeline : Cap : 4 days 4 weeks
- Clinical features : constitutional S / s ( fever , malaise )
+

Oral / mucosal
h

Skin rash

• SJS :

Cutaneous Drug Reaction


Skin -> Targetold lesions
7- zones Central - dusky
Peripheral - Red
< 10 % BSA

• TEN

• Aka - Lyell' s Syndrome


• Clinical features : [Link]
30 % BSA

Initial -> purple macules


1
Blister
I
Sheet like peeling of skin
• Sign:
- Rub thumb tangentially
Epidermis ( dead ) -> peel off

i
Pseudo nikolsky sign
- Skin tenderness present

Cutaneous Drug Reaction


[Link]
7
SJS / TEN MUCOSA:

• SJS / TEN : Mucocutaneous eruption


2 mucosae involved ( oral / ocular / nasal / genital )
• Haemorrhagic crusting on lips
Erosions — Tonguej mucosa gums }

• SCORTEN score : Severity of disease


Predict mortality

Prognostic factors Points


Age > 40 years 2

Taclnycardia > 220 bpm 2

Neoplasia 2

Initial detachment > 20 % 2

Serum urea > 20

• Prognostic factors : age ( > 4-Oyrs )


Malignancy
> 20 % BSA inv
Increase B urea B } glucose^ HR
( > 220 bmp )
Cutaneous Drug Reaction
8
Decrease HC03 ~
Scoring : 2 st -> admission
2 nd after 24 hrs

Treatment :
l- .Stop drug
2 .Symptomatic ( Acute skin failure )
3 .Cyclosporine / TNF alpha inhibitors / IVIQ

H P E:
2 .FDE

2 .EM
3 .SJS
— 1° pathologies : Interface dermatitis

4 .TEN [Link]

PRESS syndrome :
Drug reaction with Eosinophilia & Systemic symptoms
• Timeline : Long latency , up to 3 months
• Drugs : Anticonvulsants ( Phenytoin &
Carbamazepine )
• Associations : Aromatase deficiency ( Aromatase :
metabolise phenytoin & C 3Z ) HHV 6 infection

• Clinical features : fever +- Rash + Eosinophilia +

deranged LFTS + LN positive


• Treatment : Steroids

Cutaneous Drug Reaction


[Link]
9

Drug Induced Pigmentary Alteration OO : 33:2- 6

a. MINOCYCLINE :

• Treatment of Acne
• Blue black pigmentation of acne scars
• Iron clnelates +- minocycline -> deposited in skin
[Link] :

• Anti -leprosy drug


• Reddish brown discolouration of skin
h
~

Ichthyosis

Cutaneous Prug Reaction


10
c . AMIODARONE :

Fig : ZO

• Anti -arrhythmic drug


• 20 months
> 260 gm ( cumulative dose )
- increase risk of pigmentation

• Slue — grey pigmentation photo / sun exposed arras ( face )


t
• Due to Lip of use [Link]
deposition in macrophages in skin
( Amiodarone decrease lysozyme -> increase
lipofuscin )

d . BLEOMYCINE :

• Metabolised by hydrolase

Cutaneous Drug Reaction


[Link]
11
Decrease hydrolase enzyme -> increase toxicity
- Luny
- Skin
• Flay ell ate erythema
Linear red lines on skin
U
Flayellate piymentation
e . Serpentine Supra venous Hyperpiymentation

• Linear hyperpiymented rash followiny venous


network
IV chemotherapy
- 5 FU
- Docetaxel
• Patho :
- Druy -> cause damaye to vein -> Bxtravasate
Heal with piymentation
- Thrombophlebitis piymentation

Cutaneous Drug Reaction


12
f . Cyclophosphamide :

• Generalised pigmentation : Blue grey


g . Antiretrovirals : Zidovudine -> blackish pigmentation of
nails & mucosa

[Link]

h. Exogenous Ochronotic :

Cutaneous Drug Reaction


[Link]
13

• Hydroquinone : skin lightening ; Tyrosinase inhibitor


i
Prolonged usage
i
Deposition of altered protein in skin
• Clinical features : Rippled blackish pigment on skin
• Deferential Diagnosis : melasma -> Bilateral,
Symmetrical , Brownish pigmentation.

Cutaneous Drug Reaction


1

GENODERMATOSES

• Geno dermatoses and phacomatoses


- Ectoderm
• Skin
• Systemic
-CNS
- Eye
- Musculo skeletal

Neuro fib ro matosis 00 :00 : 55

• Most common Qeno dermatoses


[Link]

Inheritance AD
Classification NF ® NF ©
Genetics Chr ® 7 Chr © 2
Protein Neurofibril Q
Merlin Q

O & node ^ matos&s


[Link]
2
Neurofibromatosis type H:

• Synonym : von reckling Wausesn ds


• Inheritance : AD
• Defect : chr HI , neurofibrin

Skin:
- Cafe -are -lait macules

O & node ^ matos&s


• Lesion: c o f f e e brown macules
• Importance : earliest manifestation Q ( Hence
birth )
• Diagnosis : number > 6

• Size : prepubertal O. S cm
Post pubertal l .S cm
- Axillary freckling

[Link]

• Lesion: pinhead 2 -3mm, brown macules


«

• Importance : most pathognomic sign Q


• Site : axillae, inguinal
• Sign: crowe sign Q

- Neurofibroma

[Link] .atoses
[Link]

• Lesion: multiple , skin colored papulonodular


• Pathology : schwannomas
• Diagnosis: number 2 NF
• Sign - buttonhole sign

Qeno dermatoses - 2

Plexiform neurofibroma :

Cfenodenwatoses
• Lesion: bigger in size
Extends along length of nerve
• Pathology : multiple nerve bundles 4- profit of

connective tissue and skin


• Diagnosis : number -> > SL plexi form NF
• Sign: “ Bag of worm ’ feeling ( also seen in
1

varicocele )

[Link]

Neurofibromatosis type X: eye


• Lisch nodules
• Optic glioma

Cfenodenwatoses
[Link]

Lisch nodules :

• Pathology : pigmented hamartomas of iris ,


• Examine : not visible to naked eye slip lamp
examination
• Visual acuity : do not affect
• Diagnosis : 2

NF 1 other features :

• Bony : sphenoid wing dysplasia


• Phaeochromocytoma Q
• Malignant -> MPNS tumors Q ( Malignant
peripheral nerve sheath tumours )

NF X diagnostic criteria : 12

• Calms
• Axillary freckling

Cfenodermatoses
7

• NF
• Lisch nodules
• Optic glioma
• Sphenoid wing dgsplasia
• Family H / O NFSL in 2 generations

NF 1 treatment :
• Monitor
- MPNS tumours
- HTN
- Bone defects

• Farsenyl transferase inhibitors


[Link]

NF 2
• Chr 22 merlin
j

i
Mis me
Multiple inherited tumors
- Schwannomas
- Meningiomas
- Ependymomas
Most characteristic : B / L acoustic
schwannoma

O & node ^ matos&s


[Link]
8

Tuberous sclerosis:
• Synonym : Bourneville' s disease Q
• Inheritance : AD
• Qenetics :
- TSC 1

• Ha mart in
• Chr <?

- TSC 2

• Tuber in
• Chr -LG ?

•Triad : Vogt' s triad = EPl LO A

- Epilepsy
- Low intelligence ( Mental retardation )
- Adenoma sebaceum

Clinical features 00 :1£ : S1

1. Skin

1. Ash leaf macule : hypomelanotic macule

Fig : 9

O & node^ matos&s


• Lesion: hypopigmented macules
• Site : trunk
• Importance : earliest feature ( Skin )
On woods lamp examination: accentuates

• Baby 4- seizures -> wood' s lamp


2. Adenoma sebaceoum : misnomer

[Link]

• Lesion: facial angiofibroma' s


Latej puberty
• Site : multiplej reddish brown papules
central face
3. Shagreen patch:

Cfenodenwatoses
[Link]
10

• Lesion : collagenomas
Skin colored plaque , orangish ( due to
dermal
Infiltration )
Leathery surface
• Site : lower back

Koenon tumours :

• Synonym : peri ungual fibromas


• Lesion : skin -colored growths
• Site : nail folds

Other skin features:


• Fibrotic plaques on forehead
• Dental enamel pits confetti macules

Cfenodenwatoses
2.. Systemic features :

• Kidney : AML - AnyiomyolipomaSj PCKD


• Lunys: lymphanioleiomyomatosis - cystic
lesions in lunys
• Heart : rhabdomyomas
• CNS"
- Cortical tubers
- Ependymomas
- Seya : subependymal yiant cell astrocytomas

Manayement :
• Monitoriny [Link]
• Anti -epileptics : viyabatrin
• M TOR inhibitor: Rapamycin ( sirolimus )
- Orally - kidney everolimius
- Topical - adenoma sebaceum

Xeroderma piymentosum:
• Inheritance : AR
• Defect : NER -> DNA repair
NER defect -> mutation
i
Maliy nancy

O & node ^ matos&s


[Link]
12

Clinical features :

w
/;

t &

Fig : 13

Xero - dry skin Pigmentosum - piyvnent


• Photosensitivity
• Dry skin
• Freckles

Skin malignancy :

• 3CC
• SCC

O & node ^ matos&s


13

• Melanoma
• MC Cause of death.

Management :
• Sun protection
• Oral Retinoids -> chemop revent ion ( prevent
malignancy)

Incontinentia pigmenti:
• Inheritance : x dominant ^
• Patient : always female
• Male : die in utero
[Link]
• Defect : NEMO gene defect

Clinical stages :
• V - vesicular ( birth )
• V - verrucous papules and plaques
• H - hyperpigmentation
• H - hypopigmentation and atrophy
Distribution: blaschkoid

[Link] nM .atoses
,
[Link]
14

Skin manifestation + polyposis :


• Peutz jeyhers syndrome
• Covjden syndrome
• Gardner' s syndrome

Peutz jeykers syndrome :

• AD
• Q [ Hamarotomatous polyp
Cfenodenwatoses
15

h
"

Lentigines ( lip and mucosa )


4-

increase Q\ malignancy
4-

Thyroid , breast , pancreas

Cowden syndrome : AP
• Ql polyp + increase breast / thyroid
malignancy
• Skin: trichilemmomas
Acral keratoses
[Link]

Gardners syndrome :
• AP
• Familial colorectal polyposis
• Q\ polyps 4-

• Skin: Epidermoid and sebaceous s cyst


Osteomas
Desmoid tumours
Muir - torre syndrome
Sebaceous adenoma .

O & node ^ matos&s


[Link]
1

SKIN TUMORS

i. Benign
ii. Pre malignant
Hi. Malignant

Benign 00 :00 : 3 S

I . Epidermal naevi
It . Seborrheic keratoses
III . Aeroclnordon
IV . Syringoma
V . Permato fibroma
VI . Lipoma

l. Epidermal naevi

• Cutaneous mosaicism: 2 gene clones

Skin Tumor
2
- Normal

- Nevi
• Embryonal mutation -> tumors
• Blaschkoid lines distribution

a. Linear epidermal nevus :

[Link]
Onset : birtln
Clinical features : midline demarcation o / c
Hyper pigmented ; Wyperkeratotic
papules, plaques
Verrucous / rough surface .
b. Inflammatory linear verrucous epidermal nevus -
ILVEN

Skin Tumor
[Link]

- Upto 5 years
- Reddish, scaly appearance, linear , blaschkoid

c . Nevus sebaceous

- Sebaceous glands
Onset : birth -> flat patch ( skin )
Localized alopecia ( scalp )
Clinical features : raised orange yellow papules &
nodules

II . Seborrheic keratoses :

• Origin : Keratinocytes ( Benign tumor )


- Elderly
Skin Tumor
- 'M" sun exposure
• Clinical features : Brown , dry Just ret ess j

papules / plaques
• Site : exposure -> face , dorsum of Wand &
Sun feet

Stuck on appearance
• Sign: Rapid increase in SK all over body
Gastric adeno carcinoma
Lesser Trelat sign

III . Syringomas :

[Link]

• Origin: tumor of " Syrinyx”


Duct of eccrine sweat glands
• Clinical features : skin colored , planar, polygonal
papules
• Site : Periorbital areas

Skin Tumor
[Link]

IV . Dermatofibroma

• Synonym : Beniyn fibrous histiocytoma


• Origin:
• Clinical features : painful nodule on skin
• Sign: Dimple sign
• Site : most common site -> Lower legs

V . Acrochordon

• Path : Benign neoplasms of skin


• Clinical features : skin colored , pedunculated ,
outpouching / growth of skin
• Sites : most common - neck

Axillae, groins
Skin Tumor
6

• Association: Idiopathic, obesity, metabolic syndrome


Increases IGF - PM

Premalfgnant - squamous CC OO .mAO

X .Actinic keratosis
2 .Arsenical keratosis
3 .Kerato -acanthoma

d- .Bowen' s disease
[Link] pagets disease
[Link] : PLE
Burns
Lupus vulgaris
Chronic OM
[Link]
l . Actinic keratosis

/*

\ J

Fig : <?

• Most common premalignant tumor on skin


• Early , sun exposure
• Clinical features : initial -> flat , scaly A better felt

sand paper

Skin Tumor
[Link]
7
Increases scaling, redness

• Site: Headj face, arms, Wands & feet

• HPE: Dyskeratosis
Nuclear atypia
Parakeratosis
• Treatment: 5 - FU
*

Imiguimod
Cryotherapy
PDT ( PWotodynamic tWerapy )

II. Kerat oacanthoma

• Tumor of pilosebaceous unit


• Premalignant , SCC
• Clinical features: Shiny, skin colored , ^ ome shaped
nodule central creater -> keratin debris
• Site: face , hands,
,
( ( f
• MPE: Irregular lobulation —' /

Invagination -> dyskeratosis


Centre : pink colored homogenous keratin
Self - resolving

Skin T u m o r
III . Bowens disease :

• Clinical features : Solitary, red scaly / crusted plaque


well defined margins
• Site : lower legs
• HPE : Squamous cell carcinoma in -situ
• Treatment : S FU'

— [Link]
Imiquimoid
Cryotlnerapy
• Pre -malignant : M . Melanoma
i. diant CMN
ii. Dysplastic nevi

i. diant CMN > 70 cm

Skin Tumor
[Link]
9

ii . Dysplastic nevi

ABODE of melanoma : 00 :7-0 :110

A B C D E

<
«2
J
m Demeter smaler Not evolvrg
5ymetrtcal Even borders One colour
than 1/ 4 nch no changes

•>
5
a
§y
n
I
U4
5 n
19K7

Asymetncal
i
Uneven borders
vI
Multple colour
Dameter larger
than 1/ 4 nch
-
Evolvng changes
in colour shape and
see
Fig :

- A: Asymetncal
- B : Border uneven
- C : Color ( multiple color / variable color )
- P : Diameter larger than 'A inch (> 6mm)
- E : Evolving : Changes in color, shape &c size

Skin T u m o r
10

Malignant 00 :21: 42

X .Basal cell carcinoma


2 .Squamous cell carcinoma
3 . Malignant melanoma
4 . Mycosis fungoidis
[Link] cell histiocytosis

I . Basal cell carcinoma

• Importance : most common skin tumor


• Etiopath: UV rays ( UV - B )
• Premalignant lesion : No
• Course : chronic , slow growing , years
• Metastasis : locally aggressive , not metastasis ( <T % )
-> lymph nodes [Link]

• Clinical features :

- Most common site - face

• Above the line drawn from angle of mouth to ear.


- Shiny , skin colored plaque / nodules
- Rolled up borders

Skin Tumor
[Link]
11
- Tel eng iectasias

- Erosions -> Bleeds


• Pigmented BCC : rolled up margins

• Ulcerative BCC : Rodent ulcer

- Undermined edges

Treatment
• Medical
- SFUj Imiquiniod
- Multiple : Sonic Inedgelnog of pathway inhibitors
Vismedogib

Skin Tumor
12
Sonidogib
• Surgical : Cryotherapy
Wide local excision
MMS - Mohs Micrographic surgery

BCC - Syndromes
i. Gorlin syndrome : PTCH gene
Multiple BCC

II . Squamous cell carcinoma

• Importance : 2nd most common skin malignancyj


most common -> organ transplant
• Etiopath: UV exposure
• Premalignant lesions : Yes
[Link]
• Course : Aggressive, lymphatic
• Metastasis : Yes
• Clinical features : ulcerative lesion with elevated
margins
Nodules / exophytic

Skin Tumor
[Link]
13

Marjolins ulcer. 00 : 21: 55

- Development of SCC in burn scar non - healing chronic


ulcer

Treatment
• Wide local excision with T -Z cm margin
• Radiation
• Chemotherapy

III . Malignant melanoma :

• Cells : Melanocytes
• Premalignant lesion: Yes
- Q iant CMN
- Dysplastic nevi
• Course : Rapidly
• Metastasis : lymphatics
• Clinical features : Blackish, erythema

Skin Tumor
14

I
V}

*c

Fig - 20

• Acral lentiginous melanoma

[Link]

- Acral / extremities black


• Subungual melanoma
- Black color extending into nail fold
(

fHutcbinsons sign”

Fig : 2.2.

• Most common type: superficial spreading

Skin Tumor
[Link]
15

• Most common type in south east - asia : Acral


lentiginous melanoma
• Best prognosis : Lentigo maligna melanoma ( in sites )
• Worst prognosis : Amelanotic melanoma

Management
Patient with, lesion

Biopsy-> confirm diagnosis

Staging
1
Treatment

Staging 00 : 35: 10

Breslow thickness
< Or7 <b mm
0.76 -3- .4 c? mm

-
1 . 5 XAP mm

X .50 -4.00 mm

> 4 mm

- < 0.75mm 4 Breslow thickness ( limited to epidermis )

IV . Mycosis fungoides

• Synonym : (TCL 4 Cutaneous T cell lymphoma)


• Importance : Most common primary lymphoma of
skin
Skin Tumor
16

• Premalignant lesions : parapsoriasis


• Course : Chronic, indolent, fatal ( no cure)
• Metastasis : Regional LN

Clinical stages:
i. Patch: flat

ii. Plaque : raised


Hi. Nodules ( tumor ) : depth systemic spread
iv. Sezary syndrome

[Link]

• Sezary syndrome : Tumor cells spread into blood

i. Erythroderma ( > 90% skin)

Skin Tumor
[Link]
17

ii. Generalised lymphadenopathy


Hi . Sezary cells > X 03 / mm3

• Peripheral smear : atypical lymphocytes with


cerehriform nucleus

" Sezary cell” Fig :

HPE 00 :40 : 42

- Localized collection of tumor lymphocytes in epidermis


k / a PautriePs micro abscess”
C(

Skin Tumor
18
Treatment
- TOC — Electron beam therapy
- Patch stage : PUVA, Topical Nz mustard
- Tumor/ spread : systemic chemotherapy

Langerhans cells histiocytosis : 00 : 42 : 4 3

• Abnormal clonal proliferation of Langerhans cells


• Derived from bone marrow
• Markers : CD ^ a , CDXOl langerinj sTOO
Birbeck granules Tennis racquet appearance

Congenital LCH

[Link]

Fig : ZS

- Lesions are present at birth


- Reddish - brown papules
- Trunk
- Cood prognosis , self healing
- a/ k / a : Hashimoto Pritzker PS

Skin Tumor
[Link]
19

LCH < 2 yrs : 00 : 46 :1- 7

/H
V
i
f

Fig : 30

- Acute disseminated d / s
- Severe, bad prognosis
- " LETTERER SIVJE DISEASE"
- Feverpancytopenia + infection
80 % -> skin lesions ( seborrheic areas )
SO - 80 % -> Bone defects : lytic lesions
30 % -> Visceral : HSM

Skin Tumor
20

LCH < S y r s : ( S - l S y r s ) 00 : 48 :41

- Chronic multifocal disease


- Calvarial bone defects ( Recurrent otitis media )
h

Diabetes Insipidus ( polyuria , polydipsia )


4 "
[Link]
Exophthalmos
+

Skin lesions
Synonym : Hand schuller Christian disease

LCH < 2 yrs : (S-1S yrs)

Skin Tumor
[Link]
21

- Single lesion
- Young adults
- Eosinophilic granuloma: most common — Temporo
parietal region
- 3rd / 4-th decade of life -> pulmonary LCH

Paraneoplastic skin disease


-
00 : 52 : 1 0

i. Acanthosis nigricans
[Link] palms
Hi. Erythema gyratum repens
iv. Necrolytic migratory erythema
v. Migratory thrombophlebitis
vi. Paraneoplastic pemphigus

Acanthosis nigricans : Misnomer

Skin Tumor

22

M Fid : 33

• Associated : Gastric adenocarcinoma


• Lesion : Hyperpigmentedj velvety rash
• Site : Neck , Axillae, Groin Cubital fossa
}

• HPE : Hyperkeratosis

Triple Palms

[Link]

• Associated : Gastric adeno CA


• Lesion : thickening of skin
Accentuation of dermatoglyphics
• Site : palms

Skin T u m o r
[Link]
23

Erythema gyratum repens

• Associated : Ca lung
• Lesion : Red rash
Roundj circlesj >Tcm/ day

• Scale : Trailing scale


• Appearance : wood grain appearance
• Site : Trunk

Necrolytic migratory erythema :

Skin Tumor
24

: 36

• Associated : Qlucagonoma ( o( cells )


• Lesions : NecrotiCj Red Erosive rash
}

7<9% precedes malignancy


• Site : Buttocks

[Link]
Migratory thrombophlebitis

• Associated : Ca pancreas
• Synonym: Trousseau syndrome
• Lesion Painfullumps
- Superficial thrombotic
- Peep

Skin Tumor
[Link]
25

Cutaneous metastasis:


- 13 Breast ( most common in women )

- L Lung ( most common in men )
- O - Ovary ( sister mary Joseph nodules )

- C Colon
- K - Kidney ( vascular, scalp )

Skin Tumor
1

SKIN. IN CTV ' S

Systemic lupus erythematosus : 00 :00 :1-7.

• Alj THZ cells


• Self -nucleic acids
r
Skin * visceral

LB - skin involvement :

• Acute cutaneous LB : Acute rash skin + visceral inv


( wide spread )

• Subacute cutaneous LB : subacute rash + visceral


( limited )
[Link]
• Chronic cutaneous LB : only skin later visceral

Acute cutaneous LB:

• Rash : malar rash, butterfly rash


• Involves : 13 / Lj symmetrical red rash -> malar nose

• Spares : nasolabial folds

Skin in CTD' s
[Link]

Other features :
• Photosensitivity
• Oral ulcers -> painless
• Lupus hair:
- Hair -> unrulyj dry short hair
}

- Site -> frontal hair


- Acute flare -> anayen dystrophic
Teloyen increase; Non scarriny

Subacute cutaneous LB : 00 :04 : 5 6


*

• Antibody : anti Rho/ La


• Rash: photosensitivity
- Annular lesion
- Papule squamous

Chronic cutaneous LB:


• Synonym : P / E ( Discoid LE )

Skin in CTD' s
• Clinical feature : photosensitivity
Rash -> scalp , face , hands
• 3 zones : discoid
- Centre -> erythematous - depigmented scarring
- Middle -> scaling : white , adherent
Telangiectasia: dilated capillaries follicular

[Link]
- Margin -> hyperpigmented

• Sign:
- Tin tack sign
- Carpet tack sign
- Cat tongue sign

Skin in CTD' s
[Link]

- Follicular plugging on concha - Shuster sign


• Scalp : scarring alopecia

• Mucosa : violaceous plaques

Neonatal lupus : 00 :11 : 30

• Path : transplacental transfer of Ah ( m -> f )


• Antibody : Rho / La

• Clinical feature : Raccoon eyes

Cardiac conduction defects : complete heart block.

Skin in CTD' s
Dermatomyositis : 00 \ H7- \ 5(D

l .S kin:

a. Photosensitivity
h. Violaceous macular erythema
• Qottrons papules :
- Lesions : multi, flat topped violaceous papules
- Site : IP and MCP joints

[Link]

• Heliotrope rash :
- Lesion : violaceous macular erythema
- Site : periorbital area

Xi

* 0# Fig : 2

• Qottrons erythema:
- Lesions : violaceous macular erythema, linearly
- Site : interphalanyeal and dorsum of hand

Skin in CTD' s
[Link]
6

• Ant clnest V area = V sign


• Back = slnawl s /gn
• Upper tlnigW = bolster sign

Skin in CTD' s
c . Mechanic' s hand :
• Lesion : hyperkeratotic papules with fissures and
plaques

[Link]

• Site : index finger and thumb


• Nails : ragged cuticle = samitz sign
Nail fold tel angiectasias / peri ungual
tel angiectasias
Z . Muscle ds :

• LNV : proximal myopathyj 3/ L symmetrical


• Serology : anti JoZ

Skin in CTD' s
[Link]
8

PLE and PM treatment : 00 : 24 : S0

• Photosensitivity
• HCQS : Hydroxychloroquine = systemic sunscreen

Scleroderma : fibrosis of skin 00 :20 : 4-2

Classification :
i. Localized
• morphea
- pathology : fibrosis
- lesion : violaceous indurated plaque
i
Sclerotic plaque ( depressed )

- Linear morphea : En coup de sabre ( on scalp )

Skin in CTD' s
ii. Diffuse [Link]
• systemic sclerosis
- involvement : skin 4- visceral
• lungs
• air
• Kidney
- Pathology :
• Fibrosis (TQF ! )
• Vascular defect / dysfunction
• Al -> immune dysfunction

Skin in CTD' s
[Link]
10

Systemic sclerosis ( S S ) 00 :23 : 26


Classification:

X .Limited cutaneous SS :
• Sclerosis : upto elbows + face

• Crest syndrome :
- C : calcinosis cutis
- R: Raynaud' s phenomenon
- E : esophageal dysmotility
- S : sclerodactyly
- T: tel angiectasias
• Serology : Anti centromere Ah
Z . Diffuse cutaneous SS :
• Sclerosis > elbow
• Visceral - pulmonary fibrosis ( I L P )


• Ab anti SCL 70

Clinical features :
• Skin :
- smooth , stretched , wrinkled free “ mask like
facies } >

- punched / beaked nose


- pursing of lips
- peri oral rhagades

Skin in CTD' s
11

- Telangiectasia
• Hands : thin, tapered fingers -> sclerodactyly pitted
scarring
• Whitish deposition on joints = calcinosis cuties

[Link]

Raynaud ' s phenomenon: 00:24 : 4 S

• vasoconstriction in fingers and toes


• Cold exposure
pallor 4 cyanosis 4 red

Skin in CTD' s
[Link]
12

• Limited ss : Raynaud' s phenomenon - for years dev


s/s

• Diffuse ss : Raynaud' s phenomenon for 3. years -> dev


s/ s

A B

wu’
Fig : 12

Nail fold capillaroscopy :


• Nail fold capillary infarcts
• Drop outs
• Diagnosis :
• Major criteria : scleroderma proximal to the digitSj
affecting limbs, face, neck

Minor criteria: ( At least two )

• Sclerodactyly
• Digital pitted scarring
• Bilateral basal pulmonary fibrosis .

Mixed connective tissue disease:


• Mix of : RA + SLE + SS £ +- PM

• Serology : anti Ui RNP QQ

Skin in CTD' s
1

SKIN AND SYSTEM

Skin and Nutrition : 00 :00 :12

[Link] 83 deficiency ( Niacin )

• Disease : Pellagra
• Triad :
- Diarrhea ( first symptom)
- D - Dermatitis
-P - Dementia
- 4 tW D - Death

• Photosensitivity rash

[Link]

Hyperpigmented chronic rash


Neck -> Casal Necklace Q

Hand Cjauntlet sign Q


[Link] Bz deficiency ( Riboflavin )
• / Skin : i Angular cheilitis / Angular stomatitis
\ 7 Magenta colored tongue ( Glossitis)
/

• Eyes : Hi Seborrheic dermatitis ( Nasolabial area)


i
Corneal Revascularization
Skin and Systems
[Link]

c .Vitamin Biz deficiency : ( Cobalamin)


• Glossitis ( B e e f y red tongue)
• B / C , Symmetrical , Hyperpiymentation knuckles ,
palmar creases , mucosa.

• Hair loss
d .Vitamin C deficiency : survey :
• Bleeding gums

Skin and Systems


• Peteckiae
• Perifollicular Inypercitraturia - Corkscrew Inair
[Link]
e . Plnrynoderma :
Froy like skin

• Deficiency : Vitamin A, D , E
• Lesion : Follicular papules on d r y j rouyln, skin
• Site : Extensors ( Elbow, knee )

Skin and Systems


[Link]
4

f . Acrodermatitis enteropathica :
• Deficiency : Zinc
• Inheritance : AR
• Defect : intestinal Zinc receptor -> Zn uptake ->
deficiency
• Onset : after 6 months of aye
H / 0 diarrhea

• Triad :
- D - Diarrhoea
- A - Alopecia
- D - Dermatitis

• Rash :
- Initial -> vesiculohullous rash ( Erosive)
- Chronic -> scaly rash
- Site perioral Q and perineal rash Q

Skin and Systems


g . Iron deficiency anemia: Koilonychia

h. Protein energy malnutrition:


• Kwashiorkor
- Alternating light and dark color hands of hair
Flag sign Q

[Link]

- Dry flaky skin


Crazy flaky skin
Flaky paint sign
• Marasmus
- Monkey facies

Skin and Systems


[Link]

Skin and endocrine system : OO : :L 6:37

• Thyroid
• Diabetes
• Adrenal -> Cushing disease -> Obesity
Moon facies
Striae
Delayed wound
a . Skin and thyroid gland
Hyperthyroidism hypothyroidism
• Skin and hyperthyroidism
- Increase sweating
- Onycholysis ( distal) -> plummers nail
- Pretibial myxedema: seen in - grave ds
Deposition of : If DAGS in dermis
Lesion : Shiny, thickened ,
indurated skin lesion
Site : Shins

Skin and Systems


7

b. Skin and diabetes


• Diabetic dermopathy Necrobiotic disorder
l
• Granuloma annulare Collagen degeneration
• Necrobiosis lipoidica diabeticorum
• Increase infections
• Diabetic dermopathy :
- Lesion: Hyperpigmented , atrophic macules
[Link]
- Site : shins

- Indicator of : lony term disease


Increase vascular , neural , retinal , renal changes

• Granuloma annulare :
I
DM and vaccines , insect bite -> no association with
malignancy
Skin and Systems
[Link]

- Lesion : Annular skin lesions

Skin colored, beaded papules on skin


asymptomatic

- Site : most common -> dorsum of band


- HPB : collagen degeneration and palisading
granulomatosis
• Necrobiosis lipoidica diabeticorum :
- Lesion : waxy yellow plaques on skin

• Atrophy
ti
• Tel eng iectasias on
Fig :

surface erosions and ulcer


13

- Site : shin
- HPB : Collagen degeneration

Skin and Systems


Skin and metabolic syndrome 00:2-6 :4!

i. Acanthosis nigricans
ii. Skin tags ( Acrochordon )
Hi. Psoriasis , lichen planus
iv. Acne , Rosacea, Hidradenitis suppuritiva , AQA
v. Atopic dermatitis

Sarcoidosis :
• Multisystem ds
• dranuloma
• Lofgren syndrome :

[Link]

• Triad
1.3/ L hilar Ln
2 . Erythema nodosum
3 .arthralgia

• Lupus pernio : face , nose

Skin and Systems


[Link]
10
Violaceous ^ indurated plaque
Telangiectasia
Scarring
• Pulmonary sarcoidosis. Q

Skin and Systems


1

SHORT TOPICS

Ichthyosis : 00 :00 : 30

• Disorder : keratinization
• Typical features : fish like scales
• Classification:
[Link] : birth

i . Ichthyosis vulgaris
7. X linked recessive ichthyosis
/

Hi. Lamellar ichthyosis


Z .Acquired : adult onset

Ichthyosis vulyaris : 00 :0 Z : 35
[Link]
• Most type of congenital ichthyosis
• Inheritance : AD
• Defect : filaggrin Q : maintain integrity and barrier
Filament aggregating protein
I
Defect

Atopic Dermatitis Ichthyosis vulgaris

• Clinical features :

Short topics
[Link]
2

- A birth, normal
- Onset : 3m — 12m
QQ
- Scale : fine branny scales
- Involves : entire body
- Spares : Flexures and face

• Associated features :
SL .Atopic dermatitis

Z .Keratosis pilaris
3 . Palman' s by per linearity

X linked recessive ichthyosis: <9<9:<94:S 4


*

• Inheritance : XLR
• Defect : Enzyme : steroid sulphatase -> breakdown
choleaterol
• Clinical features :
- At birth - normal
- Onset : < 3m

Short topics
- Scale : Park brov/ n, polygonal scale
- synonym icbtlnyosis nigra
- distribution: involves - entire body face and flexures

spares - palms and soles

[Link]

• Associated features :

X .Cryptorchidism ( undescended testis ) Q

2 . Difficult labor
3 .Corneal opacities

Short topics
[Link]
4

Lamellar Ichthyosis 00 :08 : 5 3


*

• Inheritance : AR
• Defect : Transglutaminase enzyme

• Onset : collodion baby


• Clinical features : shay > parchment like membrane over
entire body
Over 2 -3 weeks : scales

Short topics
5

• Thick plate like scales


,

• Dark brown in color


• Ectropion Q
• Eclabium Q

Harlequin Ichthyosis : 00 : 11: 42

• Most severe
• Defect : ABC All gene , lipid

[Link]

• Onset : birth
• Scale : multiple , large , geometric / diamond shaped
scales

Acquired ichthyosis :
• Onset : adult , onset
• Associations :
[Link] : MC , N H C , Hematological
Z . Medications : statins , Nicotinic acid , clofazimine
3 . Infections -> Hansen' s , HIV
4. Endocrine 4 Hypothyroidism
5. Autoimmune / inflammatory
6. Metabolic

Short topics
[Link]
6

Neutrophilic dermatosis: 00 : 3-5:00

• Dense neutrophilic infiltrate in dermis

-
l .Sweet syndrome :
Acute febrile neutrophilic dermatoses ®

• Etiology :
- Malignancies hemolympho proliferative
- Drugs
- Pregnancy

- Infections
- II3 D UC , CD

• Clinical feature : fever + rash


Erythematous, edematous papules and plaque
Tender
Short topics
• Site : face , trunk.
2 . Pyoderma yanyrenosum :
Misnomer , not a bacterial infection
• Etioloyy :
- Lymphomas and leukemias
- IBP ( UC and CP )
- R. Arthritis
• Clinical features : lesion : Ulcer:

[Link]

- Painful

- Rapidly spreadiny ( > 2cm / d )


- Violaceous maryins
- Undermined edyes
All cultures are neyative
• Site : shins
CP -> stoma : peristomal
• T / t : pyoderma yanyrenosum and sweet syndrome :
system steroids

Short topics
[Link]

Panniculitis 00 \ 2JD .S0

Inflammation of panni cuius / subcutaneous fat

• Lobular panniculitis
• Septal panniculitis
[Link] nodosum :
• Type : Septal panniculitis
• Triggers :
- Idiopathic ( most common)
- Infections -> streptococcal pharyngitis Q

TB ( facultative TBid )
- Drugs OOP' s , Sulphonamides
- Behcets syndrome, sarcoidosis
• Clinical : lesions : red , painful , nodules

Short topics
9

• Site : skin
• Healing : no ulceration and no scarring

Vasculitis :
• Pathology : inflammation of vessel wall
• Classification :
- Small
[Link]
- Medium
- Large

Cutaneous vasculitis : palpable purpura OO .ZS .OG

• Lesion: Raised red , papules

Short topics
[Link]
10

• Diascopy : non blanchable


• Sitej dependent areas
B / L symmetrical

Henoch scholein purpura


• Synonym: \y A vasculitis
• Classification : small vessel
• Antibody : Ig A
• Most common age : children
• Involvement : skin -h CUT -t- Renal + Joint
• Clinical features: H / O URI
- Skin - palpable purpura over legs / buttocks

- C IT - abd pain/ melena


- Joint - arthralgia
- Renal - glomerulonephritis
• Investigations :
- Skin biopsy : HPE : vasculitis, fibrinoid necrosis of

BV
DIF : IgA, C 3 deposits in vessel wall
Short topics
11

rV.. %
%

*
.rv
%

.- A U
ISA ' •

F% : 15

- Kidney biopsy : HPB : Mesangial proliferative


glomerulonephritis
DIF : IgA, C3

[Link]

• T/t:
- NSAIDS
- Systemic steroids
- IVICi
• Complications :
- RPGN
- Delayed CKD

Short topics
[Link]
12

Behcet’ s disease : 00 : 30 : 28

• Pathology : vasculitis
- Small
- Medium
- large
• HLA: 35 «
• Clinical features : Mucosal + skin + Eye + Multisystemic
• Mucosa :
- Lesion: recurrent oro -genital aphthae
- Aphthae : well defined ulcers
Yellow necrotic slough - painful
Peripheral erythema

- Site : oral and genital


• Skin:
- Classic lesion: Erythema nodosum
- Site : shin
- Other lesions : acneiform lesion pustules

Short topics
13

- Pathergy test: Exaggerated hypersensitivity response


to an
i intradermal saline injection
Bechet' s
PG

[Link]

Short topics
[Link]
14

After 48 days -> inflammatory pustule


• Bye : involvement - uveitis
Lesion : red eye

Eye redness, pain, and blurred vision

Inflamed layer

Fig : 14

•T / t :
- NSAID’ S
- Colclnicine
- Thalidomide

Arthritides : 00 : 35 : 54-

• Reactive arthritis
• Rheumatoid arthritis -4 rheumatoid nodule
1
Skin colored nodules
ft with methotrexate
• Psoriatic arthritis
i
Psoriasis + PSA

Short topics
15

Reactive arthritis: 9([Link]


(
*

• Synonym : Reiters syndrome


• HLA: 327
• Triggers : Bacterial infection
- Q\ : Salmonella / shigella Campylobacter
- QU : Chlamydia trachomatis
mycoplasma/ ureoplasma
- Within 3O days
• SARA: Triad
- Urethritis
- Conjunctivitis
- Arthritis : Asymmetrical
Oligoarthritis ( Knee / ankle )
[Link]
+- tendonitis / enthesis’ s
• Skin:
- Crusted / scaly plaque
- Keratoderma blenorhagiucum: palms and soles
hyperkeratotiCj scaly plaques
- Circinate balanitis: round , inflammatory , red
plaques on glans asymptomatic

Short topics
[Link]
16
Vascular lesions:
[Link] marmorata :
• PatK: physiological response to cold temperature
• Seen in : neonates
• Clinical feature : B / L symmetrical, reticular
}

mottling ( Marbling )

• Site : trunk extremities


;

Warm -> disappear


Z .Salmon patch: most common vascular birth marks

• Synonym : Nevus simplex


• Path: Ectasia/ dilatation of venous capillaries in
skin
• Onset : birth
• Lesion: red macule blanchable midlinet B / L
;

symmetrical

Short topics
17

• Site : most common -> glabella ( Angel' s kiss )


Nape of neck -> stork bite
• Natural course : resolve, KO t /t
3. Portwine stain:

• Synonym : nevus flammeus


• Pat In: Capillary malformation Q® , most common
capillary malformation
[Link]
• Onset: birtln
• Lesion:
- U/ L
- deep red , non -blanclnable Q
- telangiectasia , bumps/ nodules
• Site : face vZ , vZ

Short topics
[Link]
18

• Natural course : persistent


• T / t : pulse dye laser 00 ( PPL )
- Syndromes :

• Sturye weber syndrome


• Klfppel tenancy syndrome: port wine stain
varicose veins limb hypertrophy
- Sturye weber syndrome :
• Any ioma / cap ill ary malformations
• Skin : PWS (vX and vX )
• Bye : Glaucoma
• CNS : Leptomeninyes seizures ( infantile spasm)

• CT : tram track siyn


[Link] hemanyioma : VLBVJ , Preterm, Girl,
Hypoxia
• Path: vascular tumor
• Onset : birth - normal

Short topics
19

• Lesion : grows red nodule


ft /Vv size till 3- -2 t/ ears
• Natural course : U after 5 ears
"

[Link]
<? years
^
-> 90 % regression
• T/t:
- Rapid growth ulcerative
- Cosmetically disfiguring - TOC : oral propranolol
- Functional defect

Short topics

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