Dermatology Atf
Dermatology Atf
com
1
BASIC OF DERMATOLOGY - /
Functions of skin
• Protection ( Barrier )
• Vitamin P protection: S .basaleQ® >>> S .Spinosum
• Sensation
• Thermoregulation
• Excretion
Cutaneous membranes
• Epidermis
• Permis
• Subcutaneous structure
Basic of Dermatology - I
Layers of skin
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
Basic of Dermatology - I
4
S .spinosum
Pesmosomes
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
Basic of Dermatology - I
[Link]
5
Granules
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 ,
}
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
Basic of Dermatology - I
[Link]
7
Changes in keratinocytes
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
Melanocytes
• Immigrant cell
• Origin: Neural crest
• Location : S .basale
• Shape : Dendritic
• Content : Melanosomes ( granules ) -> contain melanin
Basic of Dermatology - !
10
Merkel cells
Fig : 1-0
• Origin : Ectoderm
[Link]
• Location: S .basale
• Shape : Disc shaped
• Content : Neurosecretory granules
• Function: Mechano receptor fine / light touch
j
Basic of Dermatology - I
[Link]
11
Langerhans cells
Basic of Dermatology - l
12
Rete ridges & dermal papillae
Projections
• Epidermis — ^ Dermis ( Rete ridges )
[Link]
Projections
• Epidermis < Dermis ( Dermal papillae )
Basic of Dermatology - I
[Link]
13
Basement membrane zone : Interface/ PEJ
Damage
• Hemidesmosomes Bullous
Damage
pemphigoid
Basic of Dermatology - I
14
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
Basic of Dermatology - I
16
Subcutaneous tissue
Dennis
Fig : 17
[Link]
• Fatty layer/ pannicutus
Panniculitis
( Inflammation of fatty layer )
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
Basic of Dermatology - I
18
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.
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
[Link]
v. Wheal: urticaria
• ErythematouSj Edematous j Evanescent skin lesion
sU sU
Blanchable central pallor <2-4-hours
Peripheral erythema
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
,
EROSION ULCE R
?CA7
\
1 o
iv. Excoriations
• Linear scratch marks on skin
[Link]
v. Lichenification
vu . Scars
• Burrows
• Comedones
• Target lesions
i. Burrows
• Seen in: Scabies
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
[Link]
Fig : 17
Serpiginous
• Example : Cutaneous larva migrans ( C L M )
VJWorled
• Streaks
• BlascWkoicL
• Example : Incontinetia pigmenti
Reticular
• Example :
• Diseases
- Incontinentia pigmentiQ
- Epidermal nevi ®
- Linear psoriasis & LP
- Licinen striatus
- Hypometanosis of I to $
- 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
• Diascopy :
- Synonym : vitropression
- Glass slide -> Press on lesion
i. Erythema vs purpura :
- Erythema blanchable
- Purpura -> non blanchable
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
• Nikolsky sign
- Acantlnolysis : breakdown of desmosomes
Basic Dermatology Part - II
[Link]
15
*keratinocytes
Separation of
Tangential pressure on skin
- 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
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
• Vitiligo :
• Melasma: Exaggerated
Accentuation of dermal
lesion fluorescence
Ivory white
Porphyria :
Fig : 2.4
Dermoscopy
• Surface microscopy
• Epiluminiscence microscopy
- N o n invasive
- Surface features : magnified , clearly
i. Lichen planopilaris : perifollicular scale
[Link]
Hi. Trichotillomania:
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
Hair:
• Isthmus: bulge -> Stem cells
-> Damage = permanent loss of hair
Cross section
Cuticle
Iff
fjy
hip I
. Huxley layer
Henley layer .
IRS
1 <3/
f @ w
3
Glassy mevnbrane
KeratinisecL '
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
Fig : 5
Phases
Anayen Catayen Teloyen teloyen
Growth Involution Restiny Shed off
lony
2 (o % of hair 1% %0 -% 5%
Anagen : telogen = S :2 /
^ :2 N
Growth rate - 0.3 Smm / d
2 cm / month.
Non scarring
Scarring (cicatricial alopecia )
•Temporary • Permanent loss
•Regrowtla + • No regrovstin
• 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
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
- CovicL
• Surgical stress
• Accident
Triggers 3 -4 m
Meek : Anagen > Telogen sWed off
History : ZO - l S % 30 % tt taiV ( oss no balding
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
?
• HPB: Peribulbar lymphocytic infiltrate = swarm of
bees appearance
[Link]
• Alopecia totalis : entire scalp Inair
• Alopecia universalis : entire body hair
• Other sites: eye brow , beard area
Nail involvement :
• Ml feature = pitting
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
Tinea capitis :
• Causes: fungi
• Clinical features:
- Non scarring alopecia
- Irregular margin
- Partial alopecia
- Easy pluckability of hair
- Skin -> scaling , redness, vesicles, pustules
• Non inflammatory
- Qrey patch
~ Non scarring alopecia
- Slack dot
• Inflammatory
- Favusl
scarring alopecia
- Kerion
Neutrophilic :
• Folliculitis decalvans and
tufted folliculitis
Lichen planopilaris:
• Lupus hair
• 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 :
Traction alopecia :
Morphea :
Tinea capitis:
Favus:
• Endemic : Kashmir / Africa
• Etiology : T schoenleinii
Appendageal Disorders. Part I
[Link]
18
Kerion:
• Etiology: T. Mentagroptnytes
• Clinical features: Red , Boggy swelling on scalp
- Studded with pustules
- Easy pluck ability of Wair
- Occipital lyvnpWadenopatlny
Eccrine
Apocrine
-<0
I I
SprtH IppM E Skj)
Chord
2 .H y p o / Hyperhidrosis
3 .Neutrophilic eccrine hidradenitis
*
In cancer chemotherapy
Miliaria
s]/
[Link]
Blockage of
• Stratum corneum - Miliaria crystalline
• Stratum spinosum -> miliaria Rubra
• Dermoepidermo junction -> miliaria Profunda
• 2° staple assesus lesion -> M . Pustulosa
Miliaria crystalline
• Seen in neonates
• Cause : over warding
• Clinical features : Multiple superficial clean
Vesicles which may rupture
• 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]
J
• Synonym: - apocrine miliaria
• Onset: - After puberty
Hidradenitis suppurative
M
• SLst stage : - Only black comedones
• 2 nd stage : - nodules and abscesses
Sebaceous glands
-
• Ectopic sebaceous glands
• Not an disease but an ectopic presence
• Yellow pinbead papules -> lips oral mucosa, benitalia
• No treatment is needed
Acne vulgaris
Vi , ; • to**octal*?
of Aid
h
Stood*
Hprlcfldl
f
r tettMdMfe
wartcrr*
if
I wjfltortrtofcmi
'
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
Other factors
1) Diet -> high glycemic index ( Sugary )
Dairy products
Hormones
• 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 ]
Prug induced
• Most common cause of acneiform eruption
steroids
• Most common ATT isoniazid
Acne excorier
Acne : Treatment
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
• Adverse effects : -
- Most common cheilitis ( inflammation of lips )
s|/
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
- Acne scars
J i
I I
- Treatment
• Micro needling
• Loses resurfacing of skin by Co% laser
Hr YAP laser
Rosacea
- 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
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 )
Fig : 1
• Nail Anatomy
Lunula (Visible
Nail plate (White colour )
Nail Matrix
Mai’ f bed
Hyponychium
Terminal phalanx
Fig : 2
Diagnosis
Fixed erythema telangiectatic changes
Phyma
Major
Papules
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
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
Pitting
© No
i l
Psoriasis onycholysis
[Link]
Types: Tinea unguim
Investigation:
• KOH mount :
•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
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
• Importance : Me finding
• Cause : Parakeratosis in proximal nail matrix
• Characteristics:
- C : Coarse
- I: Irregular
- P : Peep
• Characteristics:
- S : Superficial
- F: Fine
- R: Regular
• Called as : Geometric nail pittingj sandpaper nail
TV
i \
damages N . matrix / nail bed
/
/
'\
/
/ \
\
Permanent nail loss
/
/ \
/
/
V
\
Anonychia
/ \
/ \
/ \
/
[Link]
Ventral Pterygium : 00 :Z 3 : S4
Leuconychia :
• White discoloration of N . plate
• True : defect in N . matrix
Press nail -> white
• Apparent : N . Bed
Press -> Changes
• Findings:
- Proximal - white ( opaque )
- Distal ( Z 07o ) - Normal | brown
• Seen in : Chronic liver disease
CCF
Beau' s Line
[Link]
• Triad :
- Lgmplnoedema
- Pleural Effusion
- Yellow discoloration + N . thickening .
Permatomyositis: Nail
• Periungual Telangiectasia’ s
BACTERIAL INFECTIONS OF S K I N
• Propionibacterium acnes
• Corynebacterium sps
• Staphylococcus epidermidis
• Candida albicans ( yeast )
• Many others
Pyoderma :
• Bacterial infections of skin
• Classification:
- Non - Fotticular
[Link]
- Follicular
Impetigo:
• Superficial bacterial infection of skin
• Classification:
- Non bullous
- Bullous
Bacterial Infections
[Link]
Bacterial Infections
Bullous impetigo:
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 :
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
• Subcutaneous fat
• Diffuse swelling
- Painful
- Warm to touch
• No clear margins
Bacterial Infections
[Link]
• 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
}
\ '
o
\ \
\ v * < \
[Link]
/ /
/ i
1
M ' /?
> f
i
\
/
/
\
s
* A /
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
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
Strawberry tongue
• Staphylococcus aureus :
- ssss [Link]
- Toxic shock syndrome -> tamponSj multisystemic
disease
Bacterial Infections
[Link]
10
Pathogenesis :
- t •
(
(
ri- (
r
r Blood
V ^ /
Bacterial Infections
11
• Signs :
- Skin tenderness ©
- Nikolsky sign ©
• Mucosa : no
• Treatment : antibiotics
[Link]
Other staphylococcal infections : 00 : 32 : 3 <b
i. Sycosis barbae :
Bacterial Infections
[Link]
12
/7. Paronychia :
Botryomycosis : Misnomer
2 .ecthyma
3. erysipelas
[Link]
[Link] fasciitis
• toxin -> scarlet fever
[Link]
2 .Ecthyma
3 .Folliculitis
4. Furunculosis
[Link]
[Link] barbae
7 .Botryomycosis
• Toxin mediated
2 .Staphylococcal scalded skin syndrome
X .erytlnrasma
2 . pitted keratolysis
3 .tricbomycosis axillaris
Erythrasma :
Bacterial Infections
15
Trichomycosis axillaris ( Misnomer )
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
Bacterial Infections
17
Ecthyma gangrenosum:
Fig : 22
Bacterial Infections
[Link]
18
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
Bacterial Infections
19
Expanding annular erythematous rash
ECM ( Erythema chronicum migrans )
• DOC = DOXY
3 .Cutaneous anthrax:
Bacterial Infections
[Link]
20
• T/T: doxy
S. Erysipeloid :
Bacterial Infections
21
Bacterial Infections
[Link]
1
MYCOBACTERIA S K I N INFECTION
Cutaneous TB 00 :00 : 50
Exogenous TB
- Bacteria come directly to skin from outside
NAIVE -> TB chancre
- Host
GOOD -> TBVC ( tuberculosis verrucosa cutis )
Route
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
Warty Viral
TB warts
i. No. of Lesions Single Multiple
ii. Induration
Hi. Discharge
Lupus vulgaris
Centre Periphery
Lupus vulgaris Scarring Activity
Leishmaniosis Activity Scarring
Scrofuloderma 00 : 37 :11
[Link]
On' fical T 8 00 : 37 : 32
infection
[Link]
Tuberculids - Classification
i. True
- 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
VI v Fig : 7
Erythema Nodosum
Treatment of TB
- ATT
Conditions (4 m) HRE
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]
M. Ulcerans
- Ubiquitous
- Seen in soil
- Surgical equipment
- Salon equipment
[Link]
LEPROSY PART -/
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 - %
• Site : 3 sites
i. Lesion
ii . Eyebrow
Hi. Ear lobule
[Link]
LEPROSY I
[Link]
3
Bacteriological inderx :
• Total density of bacterial load ( HPE)
Morphological index:
% Live bacillij monitoring of disease response to t / E
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
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
LEPROSYi
6
PP:
Pityriasis alba:
• Endogenous eczema
Hypopigmented macules , Pace , child
- Multiple
- Fine scaling
- Episodic recurrence
[Link]
- Atopic dermatitis
- HPE : Spongiosis
Determinate leprosy :
LEPROSY I
[Link]
7
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 )
( SSS ) <£> +
•
LL
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
LEPROSY I
[Link]
9
Borderline tuberculoid leprosy : Most common type of
leprosy ( India )
• Number of lesions : up to 1-0
Borderline leprosy:
Rarest most unstable
BT + * BL
• Number of lesions ; up to 20
LEPROSY I
10
• SSS: 3+ to 44-
• Appearance :
LEPROSY I
[Link]
11
Lepromatous leprosy
• Number of lesions : multiple , symmetrical diffuse is
filtration of skin +
systemic involvement
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
— •«*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
[Link]
Lepra Bonita
LEPROSY I
[Link]
15
LEPROSY I
16
Ocular Involvement
[Link]
LEPROSY I
[Link]
17
Sanctuary sites
• Spared in leprosy
LEPROSY I
1
LEPROSY - II
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
T / t:
Multidrug therapy : MPT
2 .Rifampicin -> most potent / cidal
2 .Clofazimine
3 .P apsone
• 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
Leprosy reactions:
• Immune dysregulation
H .Type - H
2 .Type -2
LEPROSY II
[Link]
4
• MB - MPTContinue MB - MPT
• Mild -UNSAID' S
• Mod -Severe -> systemic steroids( prednisolone )
• Other drugs : negative
• No role : clofazimine / Thalidomide
LEPROSY II
5
- Type a : 3 (3 +2 = 5)
[Link]
S'
T/t
• MP - MPT : Continue
• Mild : NASAIPS
• Mod - severe : prednisolone $
LEPROSY II
[Link]
• Other Prugs :
- Clofazimine
- Thalidomide
- Methotrexate
- Pentoxifylline
LUCRO PHENOMENA:
• Ischemia
• Ulcerative fatal
Deformities in leprosy :
i. Primary
ii . Secondary
[Link]
• Madarosis
• Saddle Nose
• Buddha Bar
ii . Secondary deformities :
LEPROSY II
[Link]
8
• Trophic Ulcer
• Claw island
LEPROSY II
Deformity Due to Ulnar Nerve paralysis :
• Partial claw Wand
[Link]
LEPROSY II
[Link]
10
LEPROSY II
1
Classification
• Superficial
• Subcutaneous
• Deep / systemic
• Superficial fungal infections
• 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
Fungal Infection’ s
Part — l
3
• 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
PIEDRA -
00 : l 2.:2.2
- 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
Diabetes
Z . Pregnancy
3 . Immunesuppression - Organ transplantation,
chemotherapy , HIV - A / PS
Fungal Infection’ s
Part — l
4. Long term antibiotics
Candidiasis : Types
2.0 ra!
2 . Intertrigo
3. Paronychia
4 .Vulvo -vaginal
[Link] - posthitis
X .Oral
• VJhite -4 Hyperplastic
• Red -> [Link]
Angular chelilitis
Fungal Infection’ s
Part — l
7
• Clinical features : -
i. Damage to cuticles — Dagged / absent
ii. Redness and swelling of nail folds
Investigations of candidiasis
• KOH mount : - budding spores and pseudo hyphae
Fig : 12.
Candidiasis treatment
• Azoles
• Precipitating factors treated
Fungal Infection’ s
Part — l
1
Dermatophytes : Genera
y y
Nail X
Dermatophytosis (Tinea )
(tinea facieii
[Link]
Ringworm of the face Ringworm of the scalp
(tinea capitisi
Fungal Infection’s
Part - l
[Link]
2
isle"
:
'
m
V
Fig : 3
Tinea Cruris
Fungal Infection’ s
Part - l
3
Tinea Pedis
Tinea Manuum
[Link]
Fungal Infection’ s
Part - l
[Link]
4
Tinea Faciei
• Affects face
Tinea barbae
• affects beard
Tinea Incognito
Fungal Infection’s
Part - l
- Decrease Redness
- Decrease Scaling
- Decrease Itching
- Hyper pigmented lesions,
^ itching
On Stopping these creams -> sudden rebound
• Onychomycosis —caused by
- DM
- Non - DM
- Yeasts
[Link]
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
of the surface
Fig : 13
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 )
Fungal Infection’ s
Part - l
[Link]
8
• Favus
- Endemic : - Africa, Kashmir
- Etiology : - Trichophyton schoenleinii
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
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 :
Antifungals - MOA
Squalon «
, Squalen epoxidase
*
«
1 i -
X
CT)
2.3*oxidosqualene
La nosterol synthetase
Lenosterol X
-
Lanoftterol ( C 14 ) a demethyldse
V
- —
Zymosterol
IW KoteAx^
~
A
f
^ Ergosterol
j * Fig -- 21
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
[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
Subcutaneous mycoses
T .Sporotrichosis
Fungal Infection’ s
Part - l
[Link]
12
2..Chromoblastomycosis
3 .Mycetoma
Sporotrichosis 00 : 34 :50
Sporotrichosis : Investigations
• KOH Mount
Fungal Infection’ s
Part - l
13
Cl
M
• Histopathology
••
•
/
-
•
•
I
#
H
9
s
*• -
%
>#
»
v .+ <
-
I
4 t
lJK % 1 •
1
a >* > <
%
t
•4 .. «
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
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 )
• Triad :
3- . Painless subcutaneous swelling (Tumefaction ) -
earliest clinical sign
2 Sinuses
3 .Cj rain
Mycetoma - Investigations
Fungal Infection’ s
Part - l
[Link]
16
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
Slav }
* - CiAclf
I
wvluAXfl- (WJ
*
Fig : 30
Fungal Infection’ s
Part - l
17
Mycetoma. - Treatment
• Eumycetoma -> Long term antifungals + Surgical
debridement
• DOC - Itraconazole
[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
HlSTOPATHOLOdY Fig : 33
Fungal Infection’ s
Part - l
VIRAL INFECTIONS
• 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
Viral Infections
[Link]
2
Fig : 2.
Viral Infections
3
• Triggers :
- Fever
- Menstruation
- Sun exposure
- Stress
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
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
- Qiemsa stain
Viml Infections
7
- Multinucleated giant cells -> characteristic of viral
vesicular disorder
• PCR : dold standard
T/T:
• 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
•% , , Ulcer
#
¥
V
«1
/•
/
Blister
Papule
\ * * *:
Fig : lO
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
fever
• T/ t: IV acyclovir
• 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 :
[Link]
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
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 )
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
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
[Link]
HHV - 8:
• Kaposi saroma
Viral Infections
[Link]
18
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
Warts causes:
Verruca vulgaris :
Pseudokoebers phenomenon
Viral Infections
[Link]
22
Plantar warts :
• Soles
- Deep plantar : HPV = 2 ( Myrmecia )
- Superficial plantar : HPV 2 ( mosaic wart )
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
Viral Infections
[Link]
24
T/t:
Enteroviral infection 0 2 :0 2 : 3 8
• Lesions :
- Multiple elliptical vesicles
- Hand and feet
- VesicleSj erosions -> oraf mucosa ( painful)
- Fe /er ±
' children
Z .Herpangina :
Viml Infections
1
[ l
Ectoparasites Eiectoparasite
Skin surface inside
Scabies 00 :00 : 50
[Link]
Pathogenesis:
• Hypersensitivity : Delayed Type HS Response
- Saliva
- Faeces
History :
2 .Nocturnal pruritus
2 .Family members / Siblings — Similar ItcW
Clinical Features :
Distribution of lesions :
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)
Treatment :
• General Measures
[Link] treatment
2 .Systemic
[Link]
Topical :
• DOC : Permethrin 5% cream
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
Infantile scabies:
I
Maternal VDRL/ Syplnilis
Other findings
• Infantile scabies :
Family H / O similar complaints
Itchy
Norwegian scabies:
[Link]
1
Mites ttt ( millions)
Nodular scabies
Animal scabies
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
Pediculosis capitals:
Clinical features :
i
Body -> iteking
• Clinical features : Extensive excoriation : Morbus
errorum
Pediculosis pubis:
• Synonym : ptkiriasis Q
Treatment :
• General measures
Pemodicosis:
• Mite : demodex folliculorum Q
Pemodex brevis
• Lives in : commensals
Pilosebaceous unit Q
Fig : 11
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
Rapid migration
Pruritic + urticarial lesions ( Intradermal
migration)
• T / t : ivermectin
Calabar swelling :
• Lesions :
- migrate subcutaneously
- pruritic, erythematous swelling ( Calabar swellings )
- eosinophilia
• Treatment : DEC ( Diethyl Carbazine )
Trypanosomiasis 00 : 44 : ZS
phase )
i
Sleeping sickness
- Most common: posterior cervical LN
i
Winter bottom sign
• American trypanosomiasis :
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
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
• Etiology : L. donovani
• History : endemic - Bihar , Jharkhand
Parasitic Infections of Skin
21
Clinical features :
• Hypopiymented macules
• Plaques
• Nodules -> diffuse nodules entire body
Investigations :
[Link]
Treatment :
PD:
LL Hansen’ s PKDL
Nerves Enlarged No nerve
enlargement
Sensory Glove stock No sensory loss
anestlnesia
SSS 6 -H AF3 LP bodies
Classification [Link]. XC
[Link] ulcer disease
2 .Genitaldischarge
3 .Anogenital warts
[Link]
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
Round
Well defined
Clean base, moist ( Serum )
Indurated
Painless
• Heals : No scarring
• Dory flop sign
Sexually Transmitted
Disease Part l
3
Button ulcer
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
Mucosal lesions :
• Condyloma lata
Sexually Transmitted
Disease Part l
• Mucous patch: Flat erosions , tongue , oral cavity
• Snail track ulcers : Coalesce ,Oral cavity
Hair.
Sexually Transmitted
Disease Part l
[Link]
6
Syphilis d’ emblee :
m
V AV \ \ \ Fig : 8
Latent syphilis :
Classification
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
Early RS Late RS
2 .CVS :
[Link]
Cardiovascular syphilis
Incidence : 10 %
Onset : lO - AOyrs
Lesion : Aneurysm of ascending aorta
aortic regurgitation
3 .CVS : Neurovascular syphilis
Syphilis investigation:
si
Fig ,- to
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
}
x 22 days ( 4 wks )
• Pregnancy +- Allergic : TOC = Desensitization
2 nd TOC :
Erythromycin/ Azithromycin
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
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
Other feature :
Sexually Transmitted
Disease Part l
1
Chancroid 00 :00 : ZS
[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
Investigations :
• VPRL titre ( Baby ) > » > Mother ( 4-times )
• IgM FTA - ABS
Treatment:
• Inj . Crystalline penicillin
Sexually Transmitted
Disease Part l
2
Unilateral
Painful
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
Viral STI
Etiology : Herpes simplex virus { HSV 2 »1- ( most
common)}
- IP: 3 -12 d
- Most common STI
- Most common viral STI
Clinical features:
Sexually Transmitted
Disease Part - II
4
i'
iW
Jks* s
M
*hr , Mil
'
i t*
i Fig - s
Investigation
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
Sexually Transmitted
Disease Part -ll
[Link]
7
- Painful LN ®
- Suppurative - BUBO
- Skin -> Red , swelling
OOP
OOP
AS /S PS
Inguinal BUBO
I
r l
% »•
Sexually Transmitted
Disease Part - ll
Tertiary stage
Investigation
• Specific : NAAT ( gold standard )
• Non -specific : CFT > i : 64
> > 1.:2 S (o ( diagnostic )
Treatment
Donovanosis 00 : 25: 34
• Bacterial STf
• Etiology : Klebsiella granulomatis
Sexually Transmitted
Disease Part -ll
[Link]
9
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
Treatment
[Link]
• DOC : Azithromycin Hgm , weekly x 3weeks ( or ) till
ulcer heals
Approach to QUP
1
r i
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
Genital Discharge
\
Gonococcal N on -Gonococcal
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
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 :
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
}
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
• Risk factors :
i. Pregnancy
ii. Diabetes
iii. Immunosuppression
iv. Long term antibiotics
Sexually Transmitted
Disease Part III
4
Clinical features
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
Sexually Transmitted
Disease Part III
6
l investigation:
. %2r
Fig : (o
Bacterial vaginosis
[Link]
&
(
Vf
Fig : 7
Sexually Transmitted
Disease Part III
[Link]
Sexually Transmitted
Disease Part III
8
Treatment : Tab. Metronidazole 400 mg TPS x 7 d
Anogenital VJarts
• Etiology : Human papilloma virus
[Link]
Giant warts :
• Synonym: Buschke - Lowestein tumour
• Risk : SCC
• HPE :
Sexually Transmitted
Disease Part III
[Link]
9
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 :
[Link]
Genital Molluscum Contagiosum
Sexually Transmitted
Disease Part III
1
PAPULO SQUAMOUS DISORDERS
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
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
Papulosquamous
Disorders Part I
[Link]
Dermal inflammation: 4
IL 22 IL2 , TNF o(
IL 23 -XTHZ 7 IL 27 , IL 22
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
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)
True : Pseudo :
Endogenous new Endogenous in origin
lesions -viral wart
- psoriasis - molluscum
- Lichen planus
• 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
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 .
• Axilla, groin
• Red plaque
• Minimal scaling
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?
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
trimester )
Pustules : initially : Flexures
i
Spread over entire body
- risk of foetal damage
4
Red skin
> PO% skin -> red and scaly = erythroderma / exfoliative
dermatitis
HPE : Spongiosis [ Intraepidermal , intracellular edema ]
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]
onycholysis
Separate -
Nail broken
Psoriatic arthritis :
1
Increase long standing psoriasis
Increase severity
^
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 :
[Link]
keratinization
iv . Topical retinoids
v . Coal tar derivatives cytotoxic
vi . Antitrain decrease proliferation
vii . Salicylic acid * keratolytic , decrease
scaling .
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
Cyclosporine :
• Rapid benefit and clearances
• Impetigo herpetiformis ( Pregnancy category fc* )
IV . Systemic steroids :
• impetigo Herpetiformis
Doc for severe
Therefore severe impetigo herpetiformis :
2 . cyclosporine : ( Category eC )
Papulosquamous
Disorders Part I
Side, effects 13
3) Biologies :
[Link]
Cytokine Drug
TNF Btanercept
Infliximab
Adalimumab
IL 22 / 23 ustekinumab
IL 27 A Seaikinumab
Ixekinumab
brodaliumab
PPE -4 apremilast
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
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
- 1313
- C£ Z3
- Diuretics
3 .Mercury amalyam
• Clinical features
Papulosquamous
disorders - II
2
- Hair
- Nail
- Sites> [Link]
-
-> P - Polygonal
> P - Planar
-
Papulosquamous
disorders - II
[Link]
3
- At surface of lens
i
Wickham' s Striae
Papulosquamous
disorders - II
4
Reticular oral LP
• Importance Most —
[Link]
common type OLP
—
• Symptoms Asymptomatic
• Risk - No risk of malignancy
Erosive Oral LP
Papulosquamous
disorders - II
[Link]
5
tea / coffee
Genital LP
Nail LP
+’
Fig : 8
Papulosquamous
disorders - II
[Link]
7
Hair - lichen Plano pilaris
Histopathology
• •M l I
• |II lI|l
Fig : ii
• SC - Hyperkeratosis
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
LP : Histopathology
<9 <S
fot( c\ c8 feodum
[Link]
Fig : 12
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
2 .Infections - HHV7
3 .Drugs - Metronidazole, NS AIDS
Clinical feature
Fig : 13
Papulosquamous
disorders - II
10
L ; i 4 Fig : IS
PR -Typical lesion 00 : 31 : SO
[Link]
Fig : 3- 6
Papulosquamous
disorders - II
[Link]
11
Treatment
1 .No
- treatment needed ( <6 - 2 weeks )
2 .Emollients
3 .Topical steroids & Anti Inistamines
4 . Plnoto therapy ( N 3 UVB )
i I 1
Means red Inair
Scale
• Clnronic immune -mediated inflammation of tine skin
Papulosquamous
disorders - II
12
PRP - Erythroderma -
00 : 32 :1 0
[Link]
Treatment
• MetWotrexate
• Acit retin
• PWototWerapy
Papulosquamous
disorders - II
1
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
Basics : pemphigus :
• Level : intra epidermal
• Disease : immune bullous ( Ab mediated )
• Target : desmosomes
V ©
AI 0
•p
i
Vesiculobullous - £
Pemphigus : classification
• P. vulgaris
• P. foliaceous
• Paraneoplastic p.
• Drug induced p.
• Ig A pemphigus
Pemphigus vulgaris :
Skin
[Link]
Mucosa
Fig : 3
Pemphigus foliaceus:
• Disease : immune bullous
• Level : intra -epidermal
• Target structure : Desmosomes
• Clinical features:
Nikolsky sign:
• 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 :
PF - Histopathology :
[Link]
>
if A i •r
v
\#
%>
Iwx 4
Fig : 12
Pemphigus : treatment :
l- .Steroids ( Prednisolone methylpred )
}
[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
- 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
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]
Epidermis
Hemi - desmosome
— Lamina lucida
BM 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
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
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
• Cicatricial Pemphigoid
• Involvement : Mucous membrane only
- Oral
- Ocular
- Cenital
• Risk : Scarring
• 21 to bullous pemphigoid
B\o Aa M 0 l. VJt
i. BP Agi 230 KD
ii. Bp Ag 2 120 KP
f t
Fig : S-
Fig : 7
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
HPE
• Subepidermal cleft r
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
X molar saline
Normal skin
Cleft formed
si/
IF
fYY^)
Roof = Hemidesmosomes : BP
(
n5 serrated ^
Floor = Anchoring fibrils : EBA
'U ’ serrated
Cleft/ Bulla
s|/
EB acquisita
• EB Congenital EB
Congenital EB
• Defect :
Laminin: L3 - EB junctional
Anchoring
~ filaments = Dystrophic EB
( Collagen 7)
Clinical features
[Link]
• Aye : Early onset ( child )
• History : Consanyuinity ± ( ARj AD )
Family members +
• Mucosa : ±
• Trauma Contractures -> Syndactyly
*
k / A mitten Hands & Feet
Diagnosis
• DIF : Neyative
• IOC : Electron microscopy
HHP & PP
• Inheritance : Autosomal dominant
• Defect : Caz ATPase enzyme
+
i
• Process : r 1
Keratinization P esmosomes
s|/ si/
Dyskeratosis Acantho lysis
• Onset : 3 rd decade
• Lesions : Vesicles -> erosions
drey colored macerated plaque
with overlying erosion
• Site : Intertriginous/ flexures
-> neckj groin, gluteal fold
Parriers disease
[Link]
• Nails
Vesiculo Bullous Part II
[Link]
14
ECZEMA - l
Eczema
• Inflammation of skin
4 /
• reaction pattern
• means to boil
Tl
*
Fig .- 1
Acute Eczema
Eczema - I
[Link]
2
- %
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
• Long duration
• Chronic itching Lichenification
• lesions : - T color ( Hyper pigmented )
T lines
T thickness
• HPB : - Acanthosis
[Link]
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
Necrosis apoptosis
cellular activation
Cytokines
Chemokmes
,
Inflammatory
infiltrate
Eczema - I
5
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
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
Diaper dermatitis ( I C D )
Paedrous dermatitis
X .BlackDermographism
1
Seen only with Nickle dermatitis
Z . Red Dermographism - physical urticaria
3 .White Dermographism - Atopic Dermatitis
Eczema - I
[Link]
8
Cement Dermatitis
Bindi Dermatitis
Phytodermatitis
[Link]
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-
Eczema - I
[Link]
ENDOGENOUS ECZEMA - ll
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
\
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
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
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
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
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
Eczew\a - II
[Link]
• Antenna sign
• VJhite Dermographism
- Stroke skin
- Delayed blanching
- Happens because of exaggerated vasoconstriction
Eczema - II
• Hyperlinear palms
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 )
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
Pompholyx OO : 34:i 9
a Fig : ZZ
Fig : 25
Antigen - presenting
»
* %
l.l
Mast cell ••
degranulation •••• •.
Y
Y V' Y
& B cell
antibodies
Urticaria
2
• Antibody : ly E
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]
Cholinergic urticaria :
• Trigger :
- Exercise
_
- Sun ( 2.0 -(SO mins ) increase core body temperature
- Hot / spicy food
Urticaria
6
Urticarial Vasculitis
[Link]
• Causes
- Drugs , infections
- Connective tissue diseases
Urticaria
[Link]
7
Urticarial pigmentosa :
Fig : 2
I
Observation: wheal on the lesion &c around it
Urticaria
8
.
Angioedema 00 :22 :1- 8
im- ,r
4- Fig : q
Classification of angioedema
[Link]
Allergic angioedema Drugs Hereditary
i
Associated with
urticarial
Hereditary angioedema :
Urticaria
[Link]
9
Pre kallikrien
Trauma
Factor xii a
Plasmin
Cl Esterase inhibitor
Kallikrein
High molecular weight kininogen
I > bradykinin
• 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
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
Anaphylaxis :
• Urticaria | Angioedema + Multisystemic Involvement
RT Cl CVS CNS
Urticaria
[Link]
11
o
coc- y
. \ H
HHCOCH
ptnicillin
J -OH ,
OR
OR ,
cephalosporin ,
^
f r» %
CELLS
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
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 )
i. Urticarial Vasculitis
ii. Urticarial pigmentosa
Urticaria
[Link]
1
- Cotrimoxazole ( Genital )
- Tetracycline
• Rash
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
Clinical features :
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 %
• etiology : [Link]
- Drugs : > 90%
2 .Anticonvulsants : phenytoin, Carbamezepine,
lamotrigine
2 .Antibiotics : Sulphonamides , cotrimoxazole,
penicilUn quinolones
}
3 .Allopurinol
• HLA predisposition:
Oral / mucosal
h
“
Skin rash
• SJS :
• TEN
i
Pseudo nikolsky sign
- Skin tenderness present
Neoplasia 2
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
a. MINOCYCLINE :
• Treatment of Acne
• Blue black pigmentation of acne scars
• Iron clnelates +- minocycline -> deposited in skin
[Link] :
Ichthyosis
Fig : ZO
d . BLEOMYCINE :
• Metabolised by hydrolase
[Link]
h. Exogenous Ochronotic :
GENODERMATOSES
Inheritance AD
Classification NF ® NF ©
Genetics Chr ® 7 Chr © 2
Protein Neurofibril Q
Merlin Q
Skin:
- Cafe -are -lait macules
• Size : prepubertal O. S cm
Post pubertal l .S cm
- Axillary freckling
[Link]
- Neurofibroma
[Link] .atoses
[Link]
Qeno dermatoses - 2
Plexiform neurofibroma :
Cfenodenwatoses
• Lesion: bigger in size
Extends along length of nerve
• Pathology : multiple nerve bundles 4- profit of
varicocele )
[Link]
Cfenodenwatoses
[Link]
Lisch nodules :
NF 1 other features :
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
NF 2
• Chr 22 merlin
j
i
Mis me
Multiple inherited tumors
- Schwannomas
- Meningiomas
- Ependymomas
Most characteristic : B / L acoustic
schwannoma
Tuberous sclerosis:
• Synonym : Bourneville' s disease Q
• Inheritance : AD
• Qenetics :
- TSC 1
• Ha mart in
• Chr <?
- TSC 2
• Tuber in
• Chr -LG ?
- Epilepsy
- Low intelligence ( Mental retardation )
- Adenoma sebaceum
1. Skin
Fig : 9
[Link]
Cfenodenwatoses
[Link]
10
• Lesion : collagenomas
Skin colored plaque , orangish ( due to
dermal
Infiltration )
Leathery surface
• Site : lower back
Koenon tumours :
Cfenodenwatoses
2.. Systemic features :
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
Clinical features :
w
/;
t &
Fig : 13
Skin malignancy :
• 3CC
• SCC
• 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
• AD
• Q [ Hamarotomatous polyp
Cfenodenwatoses
15
h
"
increase Q\ malignancy
4-
Cowden syndrome : AP
• Ql polyp + increase breast / thyroid
malignancy
• Skin: trichilemmomas
Acral keratoses
[Link]
Gardners syndrome :
• AP
• Familial colorectal polyposis
• Q\ polyps 4-
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
Skin Tumor
2
- Normal
- Nevi
• Embryonal mutation -> tumors
• Blaschkoid lines distribution
[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 :
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]
Skin Tumor
[Link]
IV . Dermatofibroma
V . Acrochordon
Axillae, groins
Skin Tumor
6
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 : <?
sand paper
Skin Tumor
[Link]
7
Increases scaling, redness
• HPE: Dyskeratosis
Nuclear atypia
Parakeratosis
• Treatment: 5 - FU
*
Imiguimod
Cryotherapy
PDT ( PWotodynamic tWerapy )
Skin T u m o r
III . Bowens disease :
— [Link]
Imiquimoid
Cryotlnerapy
• Pre -malignant : M . Melanoma
i. diant CMN
ii. Dysplastic nevi
Skin Tumor
[Link]
9
ii . Dysplastic nevi
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
• Clinical features :
Skin Tumor
[Link]
11
- Tel eng iectasias
- 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
Skin Tumor
[Link]
13
Treatment
• Wide local excision with T -Z cm margin
• Radiation
• Chemotherapy
• 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
[Link]
fHutcbinsons sign”
Fig : 2.2.
Skin Tumor
[Link]
15
Management
Patient with, lesion
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
IV . Mycosis fungoides
Clinical stages:
i. Patch: flat
[Link]
Skin Tumor
[Link]
17
HPE 00 :40 : 42
Skin Tumor
18
Treatment
- TOC — Electron beam therapy
- Patch stage : PUVA, Topical Nz mustard
- Tumor/ spread : systemic chemotherapy
Congenital LCH
[Link]
Fig : ZS
Skin Tumor
[Link]
19
/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
Skin lesions
Synonym : Hand schuller Christian disease
Skin Tumor
[Link]
21
- Single lesion
- Young adults
- Eosinophilic granuloma: most common — Temporo
parietal region
- 3rd / 4-th decade of life -> pulmonary LCH
i. Acanthosis nigricans
[Link] palms
Hi. Erythema gyratum repens
iv. Necrolytic migratory erythema
v. Migratory thrombophlebitis
vi. Paraneoplastic pemphigus
Skin Tumor
—
22
M Fid : 33
• HPE : Hyperkeratosis
Triple Palms
[Link]
Skin T u m o r
[Link]
23
• Associated : Ca lung
• Lesion : Red rash
Roundj circlesj >Tcm/ day
Skin Tumor
24
: 36
[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
LB - skin involvement :
Skin in CTD' s
[Link]
Other features :
• Photosensitivity
• Oral ulcers -> painless
• Lupus hair:
- Hair -> unrulyj dry short hair
}
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]
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
Skin in CTD' s
c . Mechanic' s hand :
• Lesion : hyperkeratotic papules with fissures and
plaques
[Link]
Skin in CTD' s
[Link]
8
• Photosensitivity
• HCQS : Hydroxychloroquine = systemic sunscreen
Classification :
i. Localized
• morphea
- pathology : fibrosis
- lesion : violaceous indurated plaque
i
Sclerotic plaque ( depressed )
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
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 } >
Skin in CTD' s
11
- Telangiectasia
• Hands : thin, tapered fingers -> sclerodactyly pitted
scarring
• Whitish deposition on joints = calcinosis cuties
[Link]
Skin in CTD' s
[Link]
12
A B
wu’
Fig : 12
• Sclerodactyly
• Digital pitted scarring
• Bilateral basal pulmonary fibrosis .
Skin in CTD' s
1
• Disease : Pellagra
• Triad :
- Diarrhea ( first symptom)
- D - Dermatitis
-P - Dementia
- 4 tW D - Death
• Photosensitivity rash
[Link]
• Hair loss
d .Vitamin C deficiency : survey :
• Bleeding gums
• Deficiency : Vitamin A, D , E
• Lesion : Follicular papules on d r y j rouyln, skin
• Site : Extensors ( Elbow, knee )
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
[Link]
• 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
• Granuloma annulare :
I
DM and vaccines , insect bite -> no association with
malignancy
Skin and Systems
[Link]
• Atrophy
ti
• Tel eng iectasias on
Fig :
- Site : shin
- HPB : Collagen degeneration
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
SHORT TOPICS
Ichthyosis : 00 :00 : 30
• Disorder : keratinization
• Typical features : fish like scales
• Classification:
[Link] : birth
i . Ichthyosis vulgaris
7. X linked recessive ichthyosis
/
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
• 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
• 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
[Link]
• Associated features :
2 . Difficult labor
3 .Corneal opacities
Short topics
[Link]
4
• Inheritance : AR
• Defect : Transglutaminase enzyme
Short topics
5
• 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
-
l .Sweet syndrome :
Acute febrile neutrophilic dermatoses ®
• Etiology :
- Malignancies hemolympho proliferative
- Drugs
- Pregnancy
- Infections
- II3 D UC , CD
[Link]
- Painful
Short topics
[Link]
• 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
Short topics
[Link]
10
BV
DIF : IgA, C 3 deposits in vessel wall
Short topics
11
rV.. %
%
*
.rv
%
.- A U
ISA ' •
F% : 15
[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
Short topics
13
[Link]
Short topics
[Link]
14
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
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 )
symmetrical
Short topics
17
Short topics
[Link]
18
Short topics
19
[Link]
<? years
^
-> 90 % regression
• T/t:
- Rapid growth ulcerative
- Cosmetically disfiguring - TOC : oral propranolol
- Functional defect
Short topics