Dermatology

Layers of skin

Basics

Stratum corneum vs basale

Stratum corneum

Stratum Basale

Protective layer. Strength due to keratin

Function is division

Max keratin in this layer

Least keratin

Non nucleated cells

Division -> hence needs nucleated cells

Horizontal layer to increase the coverage

of protection

Vertical layer -> cells divide and migrate

upwards towards corneum

Transition
Stratum basale to corneum 28 days
Hence, nucleated to non nucleated 28 days
If there is a disease that irritates basale > division speeds up
> transit time is highly shortened and enucleation does not
happen -> nucleated cells in stratum corneum PARAKERATOSIS
Parakeratosis a/w
a) Psoriasis
b) Coronoid lamella (unknown cause annular plaque with
keratotic ridge)
c) Parakeratosis is normal in mucus membranes

Terms in dermatopathology
Scales : visible shedding of skin
Hyperkeratosis : accumulation of cells in and thickening of
stratum corneum (a/w psoriasis)
Hypergranulosis : accumulation of cells in and thickening of
stratum granulosum (a/w lichen planus)
Acanthosis : accumulation of cells in and thickening of stratum
spinosum (stratum malphigi or prickle cell layer) (a/w psoriasis)
AcathoLYSIS : Loss of coherence of keratinocytes (a/w
pemphigus)
Dyskeratosis : Abnormal development of epidermal cells
resulting in rounded cells devoid of their prickles, and having
pyknotic nuclei (a/w premalignant and malignant lesions)

Terms in dermatopathology
Foam cell : lipid laden macrophage
Granuloma :
a chronic proliferative lesion consisting of mononuclear
cells and epithelioid cells / multinucleated giant cells /
both
These cells lie in groups and are surrounded by
lymphoid cells
Naked granulomas have very few of these surrounding
lymphoid cells

Terms in dermatopathology Microabscess

a) Munros microabscess
)Degenerated PMNLs
)Stratum corneum
)Psoriasis, seborrheic dermatitis

c) Spongiform pustules of Kogoj

Multilocular pustules
Spinosum
Sponge like network of flattened keratinocytes

b) Pautrier microabscess
)Collections of 3 or more atypical
mononuclear cells in the
epidermis
)Mycosis fungoides

Psoriasis, Reiters, Geographic tongue

Terms in dermatopathology
Corps grains & Corps ronds:
Acantholytic, dyskeratotic
basophilic cells.
Corps ronds have round nuclei
with a perinuclear halo.
Grains have an elongated
grain shaped nucleus
These cells are seen in
Dariers and Grovers disease,
and in warty dyskeratoma.

Grenz Zone:

A free area of uninvolved dermis between the epidermis and a

dermal infiltrate. (inflammatory or neoplastic)
Grenz = 'border' in German.
CLEAR Grenz zone is seen in LEPROMATOUS leprosy
Grenz zone INVOLVED in TUBERCULOID leprosy

Terms in dermatopathology
Pigment incontinence : Deposition of melanin in the
dermis which is not a/w a pigmented lesion -> implies
prior basal layer damage
Hydropic degeneration/liquefaction degeneration of
basal cells type of degeneration causing vacuolization
of the basal cells seen in SLE, dermatomyositis, early
lichen planus
Spongiosis : inter-cellular edema of the epidermis may
lead to vesicle formation in epidermis
(MC ca a/w diagnosis of dermatomyositis ovarian)

Hair cycle
84% of hair is normally in the anogen
phase
Sign of growing hair : black hair bulb
Hair grows for : 3 years
Then the resting phase comes :
telogen (14%)
Telogen has a white hair bulb, grows
for 3 months
After 3 months, the new anogen
pushes out the old telogen hence
hair loss of 100 hairs per day is normal
In between anogen and telogen :
catagen

Abnormal hair loss : effluvium

Anogen effluvium : even 1 is abnormal

Telogen effluvium : > 100

In acute metabolic insults like malaria/typhoid, or in

conditions like pregnancy, the growth factors to hair are cut
of

This causes the composition to change to 0% anogen and

100% telogen

Effluvium comes out after 3m

Chronic telogen effluvium seen in : hypothyroidism, anemia,

chronic organ disease

Anatomy in relation to disorders

Adnexae

Adnexal basic anatomy and assoc

disorders

Acne
Keratin plugging of pilosebaceous ducts -1st stage
Comedones (black heads) are the 1st lesion in acne
vulgaris

Acne vulgaris - pathophysiology

Acne vulgaris c/f

Acne vulgaris - Rx

Acne vulgaris - Rx
Only comedones (stage 1): adapalene/tretinoin
Comedones + papules (stage 2): adapalene/tretinoin +
topical antibiotic
Stage 2 + pustules (stage 3) : adapalene/tretinoin +
ORAL antibiotic (doxy/mino/azithro)
Stage 3 + nodules (stage 4) : Isotretinoin (keratolytic +
sebolytic action)
Stage 5 : stage 4 + cystic lesions : intralesional steroids
If mentioned nodulocystic : isotretinoin best answer

Adverse efects of retinoids

Topical

Teratogenicity

Hypertriglyceridaemia

Skin rash (MC)

Oral

Teratogenicity

Hypertriglyceridaemia

Dry lips and skin (cheilosis)(MC a/e of isotretinoin)

Depression

Hormonal acne

Hormonal acne

Diferences
Acne

Face

Polymorphic lesions

Acneiform eruptions

Only on CHEST

Monomorphic lesions

Drugs causing acneiform eruptions

1. Hormones and steroids anabolic steroids, oral
steroids
2. Anti-epileptic drugs phenytoin, phenobarbitone
3. Anti-tubercular drugs INH, rifampicin

Hidradentitis suppurativa
Keratin plugging of apocrine duct
3 regions of comedones = regions where apocrine
glands are present axilla, perineum, areola
Pathogenesis, c/f and Rx are the same as acne only
characteristic feature is the distribution

Fox Fordyce disease

Only inflammation of apocrine duct
No blockage -> no comedones

Adnexal basic anatomy and assoc

disorders

Fordyce spots
Ectopic sebum glands
Found on lips, buccal
mucosa, glans penis
No duct -> no blockage ->
no acne -> no Rx required

Classical (shapes of) skin lesions

1. Linear discharging sinuses along lymphatics
2. Circinate balanitis
3. Isomorphic/Koebnoers phenomenon
4. Target lesions / Bulls eye lesions / iris lesions
5. Fixed drug eruptions
6. Purpura

1.Linear discharging sinuses along

lymphatics
Causes
a) Sporotrichosis (sporothrix schenkii)
b) Fish tank/swimming pool granuloma (mycobacterium
marinum)

Linear discharging sinuses along

lymphatics
Upper limb

Lower limb

Occupation is important in diagnosis

a)

Farmer/gardener : sporotrichosis (vegetative matter)

b)

Fish handler : fish tank granuloma

Sporotrichosis

Images
Sporotrichosis

Fish tank granuloma

2.Circinate balanitis
Circinate = multiple half
circles
Circinate balanitis is a
feature of Reiters
syndrome
Uveitis, urethritis, arthritis
(refer more what uveitis,
agent causing urethritis,
what arthritis, which is MC
amongst the 3)
Also seen in Reiters :
spongiform pustules of

Chlamydia MC for urethritis (never gonococcus)

Asymmetric oligoarthritis involving large joints and lower

limbs

Keratoderma blenorrhagica

3.Koebners phenomenon =
isomorphic response
The Koebner phenomenon describes the appearance of new skin
lesions on areas of cutaneous injury in otherwise healthy skin.
Lesions arising through the Koebner phenomenon:
Develop at sites of cutaneous injury (such as a scratch), in
previously healthy skin
Have the same clinical and histological features as lesions of the
patient's original skin disease
Are not due to the seeding of an infectious agent, an allergic
reaction to a contact agent, or skin breakdown.
Role of NGF (nerve growth factor) is being assessed

Types
Boyd and Neldner have classified all reported cases of
Koebner phenomenon into four diferent groups
1. True response
2. Pseudo response
3. Occasionally occurring response
4. Questionable response

Causes expect all except questions

from here
True Koebner response (Q)

Pseudo Koebner response

(Seen in infections
autoinoculation) (Q)

Psoriasis

Lichen planus

Vitiligo

Molluscum contagiosum

Warts

Behcets disease

Pyoderma gangrenosum

Occasionally occurring isomorphic

phenomenon
In this category, diseases occasionally localize to sites of trauma
Cancer (gastric, testicular or mammary)
Darier's disease (option in a/e Q)
Erythema multiforme (option in a/e Q)
Hailey-Hailey disease
Kaposi's sarcoma
Kyrle's disease
Lichen sclerosus et atrophicus (option in Q)
Pellagra, perforating folliculitis, reactive perforating collagenosis,

Questionable isomorphic
phenomenon
There are many conditions that have been associated
with the Koebner phenomenon, many of which are
single case reports
List too extensive and probably needless to remember

Related phenomena
Other phenomena in relation to trauma or skin damage are distinct
from the Koebner phenomenon:
Reverse Koebner phenomenon: the disappearance of a skin
lesion after trauma to the area
Wolf's isotopic response: the emergence of new lesions in the
exact place of previous, healed, lesions not necessarily due to
trauma
Renbok phenomenon: the disappearance of an existing
dermatosis after the onset of a new lesion at the same location
Pathergy: altered tissue reactivity in response to trauma, with
formation of papules or pustules

Causes
Reverse Koebner
Granuloma annulare (Q)
25% of psoriasis

Remote reverse Koebner

Vitiligo (Q)

(Spontaneous repigmentation of
vitiligo patches distant from the
autologous skin graft sites has
been termed as a remote reverse
Koebnerphenomenon)

Pathergy

Behcets
Pyoderma gangrenosum
(Pathergy is development of pustules on sterile penetrating
trauma a feature of neutrophilic dermatoses)

Granuloma annulare
Necrobiotic palisading
granuloma
Central clearing
Association : DM
Reverse Koebners

4.Target lesions /Bulls eye

lesions/Iris lesions
Signature lesions of erythema multiforme
Type III hypersensitivity
Drug/infectious antigen

Erythema multiforme
Commonest cause of recurrent EM in India Herpes
Minor

Major

Target lesions (3 zones)

Targetoid lesions (2 zones)

No mucosal involvement

Mucosal involvement ++

Mucosal involvement
SJS (<10% of body surface area involved) Rx : IV steroids
TEN : (> 30% of body surface area involved) (TEN more common)
Rx : IvIG (giving steroids causes sepsis here)
If EM minor not controlled -> progresses to major

5.Fixed drug eruptions

Same mechanism as lichen planus except antigen is
external (refer LP)
Fixed implies that the lesions occur at the same
location even the second or third time the drug is taken
Pointer words for fixed drug eruptions :
a) Recurrent, single, blisters on genitals
b) Hyperpigmentation of skin around blister
)D/D for the above feature : Herpes genitalis (HSV 2)

Fixed drug eruptions vs herpes

genitalis
FDE

Single blisters

Hyperpigmentation around blister resolves on stopping the

drug

Eg : paracetamol

Herpes Genitalis

Grouped blisters

No hyperpigmentation around blisters

HSV 2

Herpes genitalis vs labialis - Rx of

both is acyclovir
Herpes genitalis

Herpes labialis

HSV 2

Latency in sacral dorsal root ganglion

Latency in cervical dorsal root ganglion

Spontaneous reactivation

Reactivation with fevers fever blisters

HSV 1

Verucca vulgaris
acuminata
Non genital warts
HPV causative
Formed in areas of skin with fluctuating
immunity
Jumping lesions
Rx includes
1. Burning : cautery/lasers
2. Cryotherapy
3. Acids : salicylic acid/trichloroacetic
acid
.Imiquimod and podophyllin are not
used in verucca vulgaris as they need
moisture to act

Condyloma

Genital warts

Rx : 5% imiquimod (which is an immunomodulator)

Genital warts in pregnancy : Trichloroacetic acid or Cyro (cryo better

answer) as imiquimod contraindicated

Purpura (3mm?)
Non palpable
Thrombocytopenia

Palpable

Sign of small vessel vasculitis

Vasculitis -> inflammation -> elevation present -> palpable

Erythema multiforme
Target lesions are characteristic
Central dark area, surrounded by pallor, surrounded by
redness
Target lesions = result of type III hypersensitivity
Type III hypersensitivity -> blood vessel injury ->
purpura -> dark colour

Erythema multiforme
MC cause of recurrent EM in india herpes
EM minor/major
Minor target lesions 3 zones as described above, no
mucosal involvement
Major targetoid lesions 2 zones mucosal
involvement ++
Major with mucosal involvement a) TEN 30% b) SJS
10%
If EM minor is not controlled, it may progress to major.

Lichen Planus
Antigen yet unknown
It is in some part of epidermis
Antigen yet undiscovered, hence condition not curable only suppressible
Antigen stimulates C8T cells which accumulate but cannot pass through
the barrier that is epidermis band of T cells
T cells -> cytokines -> Gaps in dermoepidermal junction (max joseph
spaces) -> more cytokines pass -> Basal layer degeneration /
liquefactive degeneration / hydropic degeneration of dermoepidermal
junction
Hydropic degeneration -> dermal keratinocyte (civatte/colloid body) &
dermal melanocytes -> these cause purple colouration -> color of lesion
is purple

Lichen planus
T cell basal layer interaction leaves saw tooth
appearance
Band of lymphocytes + basal cell degeneration =
interface dermatitis
Gaps in DEJ can lead to pigment incontinence
Pigment incontinence = deposition of melanin in dermis
Civatte bodies dermal keratinocyte in lichen planus
IgM on civatte body gives a bunch of grapes
appearance
Malignant transformation to SCC may occur in oral,
esophageal and genital LP

Lichen planus
Most diagnostic of LP basal cell degeneration
Violaceous lesions
Thinned nail plate
Wickhams striae : Fine network of criss-cross grey white
lines on the lesions believed to be due to
hypergranulosis
Koebners phenomenon seen

Skin LP vs Oral LP
Skin LP

Violaceous

Wickhams striae demonstrated with oil

Oral LP

Whitish

Wickhams striae demonstrated automatically due to saliva

causing a lacy reticular pattern

Treatment of lichen planus

6m to 2y heal spontaneously
Topical corticosteroids DOC
Oral LP more difficult to treat hydroxychloroquine DOC

Lichen planopilaris
Hair bulb
Hair bulge with stem cells
T cells shoot cytokines at these
Permanent destruction of hair bulb
Scarring alopecia

Lichen planopilaris & alopecia

areata
Lichen planopilaris

Lymphocytes around the hair bulb -> shoot cytokines ->

destruction of hair bulb -> scarring alopecia

(DLE is also a cause of scarring alopecia has carpet T scales)

Alopecia areata

Alopecia areata

Alopecia areata similar mechanism to planopilaris, except

that it afects only the upper/lower? part of the hair - the
destruction is not permanent, and that the white hair is
spared since the antigen is melanin

Alopecia areata patchy hair loss, sparing of white hairs are

pointer words in mcqs

Rx topical or intralesional steroids

Usually the hair grows

back, except in
Alopecia totalis
Alopecia universalis
Exclamation mark hair

Mast cells and urticaria

Mast cells deep cells in dermis, very attracted to blood
vessels
Not involved in lewis triple response hence NO
ITCHING in Lewis Triple response NORMALLY
In mast cell weakness, Lewis triple response involves
mast cell activation -> histamine release -> itching
Mast cell rupture -> urticaria
Mast cell if in stratum corneum -> trauma -> histamine
release
Dermographism linear urticaria

Acute and chronic urticarias

Acute : FDI (< 6 wks)

Food

Drugs

Infections

Chronic : PAI

Physical

Autoimmune (anti mast cell Abs)

Idiopathic

Physical urticarias
Scratching
Sun (solar urticaria)
Water (aquagenic urticaria)
Cold exposure (cold urticaria)
Sweat (cholinergic urticaria)
Emotion/stress (adrenergic urticaria)

Mastocytosis urticaria pigmentosa

Usually a disorder of children
Mast cells accumulate at DEJ -> activate basal melanocytes -> release
of melanin -> brown skin
To diferentiate from a melanocyte disorder like melasma, scratch the
brown area
The scratching causes mast cell activation -> redness, itching, edema
of brownish areas -> DARIERs SIGN
Confuser : DARIERs DISEASE : Dyskeratosis follicularis -> Abnormality
in desmosome keratin filament complex. ATP2A2 mutation , AD
inheritance, greasy/warty hyperkeratotic papules, plaques

DARIERs SIGN
Urticaria pigmentosa
Xanthogranuloma
ALL
Histiocytosis

Blister formation mechanisms

1. Disruption of desmosomes
2. Improper synthesis of keratinocytes
3. Weak keratinocytes

Blisters
Epidermal

Dermal

Flaccid

Tense

Burst easily

Dont rupture easily

Heal without scarring

Heal with scarring

Pemphigus
Pemphigus foliaceous
endemic variant : fogo selvageum
erythematous variant : senear usher syndrome
Subcorneal blisters in foliaceous
Suprabasal in vulgaris

Pemphigus foliaceous
Seen in seborrheic areas
Desmoglein 1 absent in mucosa since this is a disorder
of desmoglein 1 - mucosa not involved
Desmoglein 3 present all over means desmoglein 3
afection involves mucosa also, like in vulgaris
Blisters BURST VERY EARLY hardly seen at the time of
presentation
LEAF LIKE scaling hence foliaceous
Pemphigus erythematosus features of PF + SLE ->
rash + scaling

Fogo selvageum
Translates to wild fire
Endemic variant of PF
Due to inoculation of black fly antigen
This antigen has molecular mimicry with desmoglein 1
Immune response results in pemphigus

Pemphigus vulgaris
Commonest pemphigus in India
Desmoglein 3 afected
Ulcerative disease -> very prone to infections
Involves mucosa also (desmoglein 3 is present in
mucosa)
Steroids control the disease, but there is a great risk of
immunosuppression with steroids leading to infections
-> so much so that steroid induced sepsis is the MC
cause of death

P.vegetans
Variant of pemphigus vulgaris
Rarest pemphigus in India
Commonly seen in flexures
Brought about by rubbing of the two parts of the
flexures against each other

Paraneoplastic pemphigus
Molecular mimicry of malignant cell antigen with
desmoglein 1,3
Autoantibodies against desmoglein 1,3
Presentation with a mixture of features of foliaceous and
vulgaris, predominantly vulgaris
Diferentiation from vulgaris : presence of target lesions
+ foliaceous like lesions + vulgaris like lesions points
towards paraneoplastic pemphigus

Paraneoplastic pemphigus
Mc seen in
1. NHL
2. CLL
3. Castlemans
4. Thymoma
5. Retroperitoneal sarcoma
6. Waldenstroms macroglobulinemia

Nikolsky sign
Rotational pressure on a perilesional area of epidermis
-> causes separation of epidermis and makes the
disease clinical
Apart from pemphigus, this is also seen in :
1. TEN
2. SSSS (staphylococcal scalded skin syndrome)

Bullous pemphigoid
Elderly
TENSE, ITCHY blisters
Hemorrhagic blisters

Gestationis and cicatricial

Pemphigoid gestationis (=
herpes gestationis)

BP in pregnancy (BP1 involved)

MC site para umbilical

Fetus is Ag to the mother -> hence definitive Rx is delivery

Steroids to suppress Abs till delivery

Cicatricial pemphigoid

Mucus membrane pemphigoid

Heals with scarring

Dermatitis herpetiformis
Primary pathology is gluten sensitive enteropathy
A/w HLA DR3
Gluten shows molecular mimicry with transglutaminase at
the tip of dermal papilla
Resultant antibody response is against transglutaminase
-> gaps in dermal papillae -> fluid to fill gaps -> dermal
blisters
C/F -> severe itching -> hence intact blisters are not very
common, except for at the elbows -> scratching not very
common here, so tense elbow blisters seen

Dermatitis herpetiformis
Rx : Gluten free diet cereals to be avoided are BROW
barley, rice, oats, wheat
Dapsone antineutrophil agent
Dapsone is used in the THERAPEUTIC DIAGNOSIS of
dermatitis herpetiformis

Linear IgA disease (= chronic

bullous disease of childhood ->
CBDC)
Pointer : string of pearls appearance

Hailey Hailey disease (= benign

familial pemphigus)
2nd mechanism of blister
formation improper
synthesis of keratinocytes
(dyskeratosis)
Congenital
Genetic disorder of
synthesis of keratinocytes
Flexural blisters
Dilapidated brick wall
appearance on HPE

Keratinocyte has an envelope and keratin

Envelope gives major strength, so more important

Keratin also gives strength but less important

No envelope since birth in Hailey Hailey and no compensatory

extra keratin synthesis (compensation seen in Dariers , which
also lacks envelope hence hyperkeratotic plaques)

No keratin since birth in EBS

Flexural afection
1. P.Vegetans
2. Hailey Hailey
3. LP
4. Inverse psoriasis (flexural psoriasis has no scaling)

Epidermolysis bullosa simplex (EBS)

3rd mechanism of blister formation -> weak
keratinocytes
Genetic disorder
Trauma induced blisters
Weak keratinocytes destroyed by trivial trauma

EBD
Continuous scarring
Fingers fuse, thumbs separate -> Mitten hand deformity

EB

DIF detects Abs

DIF +ve

Pemphigus

EBA

Both the above are acquired, autoimmune conditions

DIF -ve

Hailey Hailey
EBS, EBD, EBJ

These are congenital conditions, not autoimmune ones

UV rays

UV rays

UV rays

UV rays

Melanocyte disorders
Congenital

Difuse : albinism

Localised

Piebaldism
Nevus depigmentosus
Nevus achromicus

Acquired

Vitiligo

Leucoderma

Melanocyte disorders : albinism

Melanocytes originate from
neural crest -> go to skin, hair
etc

Hence if tyrosinase is
deficient, no melanin ->
albinism

Congenital
Difuse
risk of SCC, BCC,
Melanoma

Piebaldism
Congenital, localized
Neural crest cell disorder
Autosomal dominant
Mutation of C-kit gene
Areas of normal skin
within white patch
(location of white macules
: forehead)
White forelock

Rx : does not respond to medical Rx or UV light

Piebaldism + deafness +
interpupillary distance -> Waardenburg syndrome

Nevus ?pigmentosus : no areas of normal skin, no white

forelock

Vitiligo

Leucoderma

Xeroderma pigmentosum

Melasma
Pigment disorder
Brownish patches on
cheeks
Etiology
1. Genetic predisposition
2. Sun exposure
3. Hormonal disturbances :
OCPs, pregnancy
) Melasma in pregnancy is
called chloasma

Melasma should be diferentiated from SLE

SLE is not a pigment disorder

Erythema in SLE is due to vasodilatation, and NOT

pigmentation

Wherever pigmentation is mentioned, no disorder causing

erythema can be the answer

Psoriasis
Spectrum : stable -> -> -> unstable
Exacerbating factors
1. Withdrawal of oral steroids
2. Drugs : blockers, lithium, chloroquine, NSAIDs
3. Smoking
4. Alcohol
5. Emotional stress
6. Infections like HIV, strepto
7. Pregnancy

Pathophysiology
Ag (unknown?) -> APC (Langerhans cells) -> presented
to lymphocyte -> stimulation of basal keratinocyte ->
division -> accumulation in epidermis
To remove Langerhans cells : phototherapy
To remove lymphocytes : cyclosporine
Prevent keratinocyte division -> methotrexate
Prevent hyperkeratosis : oral retinoid -> acitretin

Classical psoriasis (psoriasis

vulgaris) Plaque form
Silvery scales
These are seen on the extensor surfaces of the body
Not curable
Steroids are CONTRAINDICATED as rebound is massively
increased

Flexural psoriasis has no scaling

Erythrodermic psoriasis vs
generalized pustular
Erythrodermic

Generalised pustular (=Von

Zumbusch)

1st line : methotrexate

2nd line : acitretin

Sheet of pus/lake of pus

These are pointer words pathognomonic features of pustular

psoriasis

1st line : acitretin

2nd line : methotrexate

Impetigo herpetiformis
Von Zumbusch in pregnancy
Fetus is Ag -> molecular mimicry
Ab cross reacts with skin
Rx
1. If near term : deliver
2. 1st month : DOC -> steroids -> give without tapering
till delivery taper after delivery
.Here no rebound with steroids since antigen disappears
after delivery

Guttate psoriasis
Rain drop psoriasis
Antigen is streptococcal
Treatment is antibiotic
CURABLE PSORIASIS

Psoriatic arthritis
Seen in 5-10% psoriatics
Classical/most characteristic joint involvement is : DIP
Rx : methotrexate
Rare form : arthritis mutilans DOC is etanercept

UV light
UV A
used with psoralen
320 400 nm
Psoralen for 2 hrs, then
UV A (PUVA)
A/e of psoralen : nausea
and vomiting
Psoralen C/I in preg

UV B

no psoralen
290-320 nm
Broad based : 290-320 nm
Narrow based : 311 nm
used in Goeckermans regimen ??

CTCL points
Sezary syndrome :
1. Exfoliative dermatitis
due to erythrodermic
MF
2. Sezary cells in blood
3. Generalised
lymphadenopathy

T helper lymphocyte malignancy

Proliferation of dermal lymphocytes
Cerebriform nucleus
Sezary cells : atypical large monocytoid
lymphocytes
These accumulate in epidermis -> Pautriers
microabscess
Dissemination of sezary cells through blood
can lead to erythroderma (>90% skin
involvement)
Erythrodermic MF -> generalized
lymphadenopathy
New DOC : whole body electron beam therapy

Vasculitis classification
Large vessel

Medium Vessel

Small vessel

Takayasu

Kawasaki

HSP

GCA

PAN

Wegeners
Churg Strauss
Cryoglobulinemic vasculitis
Leucocytoclastic vasculitis

Scabies
Burrow entry point in scabies
mite
Burrow is the 1st lesion gen
seen in finger webs
Adults : papular, face spared
Infants : papulovesicular, face
palms and soles all involved
Rx : 5% permethrine from neck
to toe in all groups including
infants and pregnancy
All contacts are to be treated

Scabies
Transmission is by close physical contact
Indirect contact is not important
MC symptom is itching, which is worse at night
Nodular scabies
characteristically seen on scrotum
Hypersensitivity response to scabies mite
Topical steroids

Scabies
Immunocompetent
individuals

Itching dislodges mites

Hence less mites are seen in adults

On an avg : 10-12 (11)

HIV

No itching -> no dislodgement

Hence, upto a million mites may be found Norwegian

scabies

Rx : Ivermectin 2 doses 14 days apart + topical permethrine

STDs - chancroid
H.ducreyi
IP : 2-5 days (syphilis 9-90
days)
Painful and soft ulcer
Unilateral bubo

Diagnosis

School of fish appearance of H.ducreyi in smear from ulcer

Rx : Tab Azithromycin 1g single dose or ceftriaxone 250mg stat

Donovanosis
Calymmatobacter
granulomatis (=klebseilla
granlomatis)
Ulcer full of granulation
tissue (red) and bleeds on
touch
PSEUDOBUBO
Rx : Azithro 1g preferred
> DOC tab doxycycline
100mg BD x 14d

LGV
C.trachomatis
Ulcer never seen
10 stage : transient
20 stage : B/L bubo
Groove sign : swelling of LN
above and below inguinal
ligament
30 stage : genital
lymphedema, proctocolitis
Rx : Doxy 100mg BD x 21 d

Syphilis
Primary

Secondary

Tertiary (tissue phase)

Painless hard chancre at the

site of entry of the
spirochete

3 months after primary skin

lesion
triad non itchy rash,
lymphadenopathy, mucus
lesions

Gummata (chronic
granulomas)

Heals without scarring

Roseolar/papular rashes

Cardiovascular lesions

If syphilis acquired non

venereally, chancre is
extragenital, usually on
fingers

Mucus patches in
oropharynx

Meningovascular lesions like

tabes dorsalis

If syphilis transmitted by
blood transfusion, chancre
does not occur

Condyloma lata in
mucocutaneous junctions
MC site groin/inner thigh

HIV/immunodeficient patient Condyloma have abundant

: persistent/multiple
number of spirochetes and
chancres
are highly infectious

Latent
Early and late latent
Spirochetes inactive
No symptoms
TPPA is IOC

Dermatological signs of syphilis

Primary syphilis

Secondary syphilis

Congenital syphilis

1. DORY FLAP SIGN : Hard

chancre on inner prepuce
flapping sound when
prepuce retracted

1. Condyloma lata
2. Corona veneris
3. Buschke Ollendorf
sign : deep tenderness
elicited over papules
4. Moth eaten alopecia
5. Lichen syphilliticus
6. Leucoderma colli / collar
of venus
7. Lui maligna or
malignancy syphilis
8. Snail track ulcers

Pemphigus syphiliticus
blisters, only congenital
Stigmata of congenital
syphilis
1. Hot cross bun skull
2. Olympian brow
3. Higoumenakis sign
4. Sabre tibia
5. Hutchinsons teeth
6. Mulberry / Moon
Molars
7. Hutchinsons triad
Hutchinsons teeth,
interstitial keratitis,
8th nerve deafness

Syphilis

Syphilis tests
Most sensitive : TPPA
Most specific : TPPA
Earliest to become +ve : FTA-ABS
Primary syphilis IOC : dark ground illumination
Monitor response to therapy : VDRL

Rx kits
Condition

Kit colour

Identification and organism

Rx

Urethral,
cervical
discharge

GREY

Thick : Gonococcus

Tab Ceftriaxone 400 mg

single dose OR IM
ceftriaxone 250mg
single dose

Thin, mucoid : non

gonococcal includes
1. Chlamydia
2. Trichomonas
3. Mycoplasma
4. Ureaplasma

Tab Azithro 1g single

dose

White discharge : candida

Tab Fluconazole 150mg

Strawberry cervix :
trichomonas
Clue cells : gardnerella

Tab
Tini/metro/ornidazole
2g

Vaginal
discharge

GREEN

Rx kits
Condition

Kit
colour

Identification and organism

Rx

Bubo

BLACK

Chancroid

Tab Azithro 1g single dose

LGV

Doxy 100mg BD x 21 days

Genital
ulcer

RED/WHI Viral blister before ulcer

TE
Bacterial ulcer before blister

Acyclovir

Lower
abdominal
pain/PID

YELLOW

Gonococcus

Cefixime

Anaerobes

Metronidazole

Benzathine/Doxy

Phakomatoses Tuberous sclerosis

Bournevilles disease = tuberous sclerosis
1st sign : ash leaf macule
Adenoma sebaceum : it is actually an angiofibroma
mostly seen on face
Shagreen patch : collagenoma
Periungual fibromas : Koenens tumors

Woods lamp uses and colours

Woods lamp filter made of nickel oxide + barium
silicate
Wavelength
Condition : 365 nm
Colour
Tinea capitis (T.violaceum,
M.canis, never E)

Green

Pityriasis versicolor

Yellow

Burrow of scabies

Green

Ash leaf macule

White

Vitiligo

White

Diferentiation of epidermal from

dermal melanin
Porphyria
Erythrasma

Pink Red
Red

Pigment dilution = leucism =

hypomelanism
PAMPA

Piebaldism

Albinism (oculocutaneous)

Menkes kinky hair disease

Phenylketonuria

Ataxia telangiectasia

WITCH

Incontinentia pigmenti

Waardenburgs

Tuberous sclerosis

Chediak Higashi syndrome

Homocystinuria

Leprosy

TB

Nail diseases
Irregular fine pitting : psoriasis
Regular pitting : alopecia
areata (t shaped pitting)
Dorsal Pterygium :
pathognomonic of lichen
planus
Thickening of nails and
longitudinal ridges also seen
in lichen planus
Salmon patch or oil drop sign :
pathognomonic of psoriasis

Half and half nails : in CRF due to capillary proliferation of

whole blood

Terrys nails : 75% white 25% red seen in liver failure

Misc
Ca pt receiving chemo with transverse lines on the
nails Beaus lines
Dimple sign (=Fitzpatrick sign) : Dermatofibroma
Types of collagen in Keloid : type 1 and 3
Beefy red tongue can be a/w hypothyroidism,
amyloidosis, acromegaly, Downs BUT NOT TURNERS
Pityriasis rosea : one herald patch -> Christmas tree
pattern
Rosacea a/w bacterial overgrowth
Sweet syndrome (acute febrile neutrophilic dermatosis):
a/w AML M2

Misc
Dermatomes

Blaschkos lines

Along nerves

Horizontal on trunk, vertical on extremities

HZV

Developmental

Not along nerves/vessels/lymphatics. Vertical

Vertical on extremities, S shaped on trunk

Incontinentia pigmenti

MCQs
Definitive diagnosis of leprosy is by : skin biopsy
Wavelength of UV B wave : 280 nm
Scabies does not show Koebners
DLE causes scarring alopecia
Childhood atopic eczema persists into adulthood
Cutaneous vasculitis is not pruritic
Icthyosis is a side efect of clofazimine
Goeckerman regimen : coal tar + UV-B

MCQs
Podophyllin is used for the treatment of genital warts
Photosensitive rash : erythropoietic porphyria
Type II lepra reaction : LL > BL
Mepacrine does not produce fixed drug eruptions
Time period b/w emotional psychic stress and hair loss :
3 months
Concentration of hydroquinone for treating
hyperpigmentation : 2-5%
Crocodile skin or sauroderma : icthyosis vulgaris
Daily dose of thalidomide for ENL : 200-300mg

MCQs
Dose of zinc used in acrodermatitis enteropathica :
2mg/kg
CTCL is NOT caused by PUVA
Max no of lepra bacilli : LL
Most infective stage of leprosy : lepromatous
Munros microabscess : no eosinophils
Stratum lucidum between : corneum and granulosum
Zoophilic species of Trichophyton : T.mentagrophytes
Dermatopathic lymphadenopathy : mycosis fungoides

MCQs
Variation in skin color is NOT due to number of
melanocytes it is rather due to number, size and
degradation of melanosomes, synthesis and transport of
melanin by melanocytes. NUMBER SAME IN ALL.
Minocycline causes pigmentation of skin
Molluscum sebaceum is another name for :
keratoacanthoma
Dimple sign = Fitzpatrick sign = dermatofibroma
Follicular hyperkeratosis is related to deficiency of
vitamin A
Carpet tack sign : DLE

MCQs
Paracetamol causes : photosensitivity
MCC
Air borne contact dermatitis and plant dermatitis : parthenium
Allergic contact dermatitis due to metal : nickel
Allergic contact dermatitis in Indian females :
1. Hands : detergent
2. Forehead : para tetra butyl phenol in bindi
3. Ear lobe : nickel
)Allergic contact dermatitis due to cosmetics : Balsam of peru
) Allergic contact dermatitis due to drug : neomycin

MCQs
Bowens disease, xeroderma pigmentosum, actinic
keratosis are premalignant lesions of skin.
Psoriasis is NOT premalignant
Giant cell arteritis, being a large vessel vasculitis, does
NOT show any palpable purpura
Rifampicin, cyclosporine are NOT used in Lepra
reactions
Vitamin D is synthesized by keratinocytes max
production is in stratum basale

MCQs
Acid increased in comedones : palmitic acid
Solar urticarias
4th or 5th decade
lesions subside spontaneously on avoiding exposure
within 24 hrs
some cases may develop severe
urticarial/bronchospasm
almost all cases are idiopathic
Rapid, difuse, excessive hair loss 3m after preg :
telogen effluvium

MCQs
Acrodermatitis enteropathica :
AR
Low zinc levels
Wound healing afected
Zinc sulfate used for Rx
Prolonged Rx into adulthood required

MCQs
Steroids are not C/I in eczema
Linear discontinuation of skin : fissure
Buschke Ollendorf sign : secondary syphilis
Psoriasis does not show pigment dilution
Salt and pepper skin : scleroderma
Apple jelly nodules : lupus vulgaris
SSSS does not show Asboe Hansen sign
Immunocompromise + umbilicated papules + budding yeast :
cryptococcosis
Plantar wart : painful on exertion of lateral pressure

MCQs
Linear deposition of IgG and C3 in lamina lucida : BP
Row of tombstones : PV
Saw tooth rete ridges : lichen planus
Vagabonds disease : pediculus corporis
Wavelength of carbon dioxide laser : 10600 nm
Koenens tumor : tuberous sclerosis
Heavy bacterial colonization of tongue presents as : black
tongue
Child presents with multiple skin colored papules over lips
bedside investigation : tzanck smear

MCQs
Peak wavelength on Woods lamp : 360nm
Erythema marginatum : rheumatic fever
MC skin cancer : BCC > SCC
Calcipotriol is used in psoriasis
Rx for tinea unguim : griseofulvin + ketoconazole
Skin blister resulting from a burn is an example of :
serous inflammation
Ringworm infection afects : stratum corneum

MCQs
Drug induced pemphigus MC caused by : penicillamine
Lesions of cutaneous anthrax are not painful
Intraepidermal bullae : pemphigus
Subcutaneous granulomas : Donovanosis
Urticarial lesions are best described as evanescent

DVT additions

Erythema gyratum repens

Internal malignancy

MC Ca lung

Wood grain pattern