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SKIN QUICK REVISION NOTES

DERMATOLOGY BASICS:
Layers of Skin

Stratum Corneum Dead layer, Flat cells, No nuclei

Stratum Lucidum •• Palms & Soles
•• Refractile granules of Eleidin
Stratum Granulosum •• Keratohyalin granules – produce FilaggrinQ
•• Lamellar granules / Odland bodies – Lipids
Stratum Spinosum •• Desmosomes are intercellular structures which help in the attachment of keratinocytes
•• Keratin synthesis
Stratum Basale / St. •• Highly mitotically active (proliferating)
Germinativum

Epidermal Turnover Time (ETT) / Skin Doubling Time

•• Time taken by keratinocytes to move from stratum Basale till shedding off in the environment
•• 8 weeks (42 – 75 days)Q
•• Epidermal turn-over is 4 days in Psoriasis.Q

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Cerebellum Quick Revision Notes

•• Intra Epidermal / Inter cellular K-K bridges

•• Defect in Desmoglein (Dsg) – Pemphigus
•• Row of tomb stone appearance seen in pemphigus
as Hemidesmosomes are uninvolved.Q

Cells Of Epidermis
Keratinocytes Non-Keratinocytes
Desmosomes
•• Ectodermal in •• Langerhans cells
origin •• Melanocytes
•• KIF – Keratin •• Merkel cells
intermediate
filaments

Characters: Langerhans cells Melanocytes Merkel cells

Location Spinosum Basale Basale

Origin Bone marrow (macrophages) Mesoderm Neural crest Ectoderm

Components Birbeck granules tennis racquet appearance on electron Melanosomes Neurosecretory

microscopy granules

Function Antigen Presenting Cells Melanin Mechanoreceptors

pigment (Touch): slow
producing cell adapting low
threshold
receptors. (SALT)

Example Langerhans cell histiocytosis Melanoma Merkel cell

carcinoma

Markers S100, CD1a, CD-207 (Langerin) Most specific markerQ S100, HMB 45 CytoKeratin - 20Q
Melan- AQ

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Skin

Subcutaneous Layer
Aka – PANNICULUS / HYPODERMIS / SUBCUTIS
•• Fat lobules & their Septa form subcutaneous
layer
Panniculitis: Inflammation of subcutaneous layer.
•• There are 2 types of panniculitides
–– Septal Panniculitis – Erythema nodosumQ
–– Lobular Panniculitis – Bazin disease

Dermatopathology:
Basement Membrane Junction / Stratum corneum Stratum spinosum
Dermo-Epidermal Junction •• Hyperkeratosis: •• Ballooning degeneration
•• Specialized zone connecting the epidermis & pathological thickening (intracellular edema)
Dermis inside stratum spinosum
•• Parakeratosis: •• Spongiosis; intercellular
Layers of Dermis - retention of nucleus edema in-between cells.Q
•• Dermis divided into 2 layers
–– Superficially, Papillary dermis – Constitutes C/F Of Acantholytic Cells
1/10th portion of the dermis. 1. Oval shaped cells,
–– Deep, Reticular dermis – Constitutes 2. Have large nucleus,
remaining 9/10 portion of the dermis.
3. Shows perinuclear halo

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Cerebellum Quick Revision Notes

•• To see these cells Tzanck smear is prepared Acantholytic cells seen in

(Giemsa stain)
•• Autoimmune: pemphigus group
•• Infection: bacterial / viral
•• Bacterial: bullous impetigo, Staphylococcal
Scalded Skin Syndrome
•• Viral: HSV infection
•• Genetic: Hailey hailey disease, Darier disease.

Lines in Dermatology:
Blaschko’s lines: Langer lines: RSTL

•• Pathways of epidermal cell migration during •• Collagen fibre orientation in the dermis corresponds to
embryonic development them
•• Do not correspond to arteries/veins/nerves •• Applied: put incision along or parallel to these lines→
•• V shaped on upper spine healing better without scarringQ
•• S shaped on abdomen
•• Spiraled on scalp
•• Linear on lower extremities
•• Ex: Incontinentia pigmenti (X linked dominant
inheritance)Q

Diascopy: Vitro Pression Test

•• Press the lesion with Glass slide
•• Uses of Diascopy:

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Skin

Erythema Purpura Apple jelly nodulesQ

(Extravasation of RBCs)

Redness disappears: blanching •• RBCs degenerate along with Erythema disappears, granulomas become
response staining of blood vessel wall. prominent: apple jelly nodules – Lupus vulgaris
•• Redness persists: non blanching
response

Dermatological Investigations
Woods lamp examination:
•• Wavelength: 360-364nmQ
•• Made of filter: 9% nickel oxide+ barium silicate

Tzanck smear (Cyto-Diagnostic test)

Microsporum Blue green

Trichophyton schonleinii Dull blue

Pityriasis versicolor Yellow

Corynebacterium Coral red fluorescenceQ

minutissimum

Vitiligo Milky white

Pityriasis versicolor: Yellow florescence

•• Fluid filled lesion (Vesicle/ Bulla) →deroof the

lesion → scrapping from floor & roof → Giemsa
stain

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Cerebellum Quick Revision Notes

•• Acantholytic cells: pemphigus group & Herpes •• Multinucleate giant cells: HSV 1,2 & Varicella infections.
infections

Dermatological Therapy
1. Cryotherapy: 2. Phototherapy
•• Agent: liquid nitrogen (-196 Celsius) •• UV rays
•• Mechanism: freeze tissue → Cellular death •• NB-UVB (Narrow band UV B radiation) wavelength 311+-2nm
•• Indication: Warts & keloids •• PUVA: Psoralen (P) (Photosensitizer) + UVA therapy
wavelength 320-400nmQ
•• Psoralen is given prior to UVA for better penetration of
skin.
•• Indications: Psoriasis, Vitiligo, Atopic dermatitis

Classification Of Bullous Disorders:

Intraepidermal blistering Subepidermal blistering
1. Immunobullous disorders disorders (superficial): disorders (deeper):
2. Mechanobullous disorders Pemphigus group of disorders Pemphigoid group
3. Inherited acantholytic disorders & dermatitis
herpetiformis
Immunobullous Disorders
(Immuno=Autoimmune) Pemphigus group of disorders:
•• Level: Intraepidermal
Classification: based on the level of the split
in the skin •• Target proteins: desmosomes (connects
keratinocytes to each other)

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Skin

•• Acantholysis is the process by which Nikolsky Sign:

desmosomes get ruptured/separated
•• What is to be done: apply tangential pressure
Desmosomes over skin
•• What happens: upper layers of epidermis
separate from lower layers
Keratinocytes

Pemphigus Foliaceous Pemphigus Vulgaris

*First

Desmoglein-1 antibody Desmoglein-3>1 antibodies

Expression of Desmoglein 1 & 3 (skin / mucosa)

Desmoglein-1 Desmoglein-3
Bulla Spread Sign:
Skin Upper epidermis Lower epidermis
•• What is to be done: apply lateral pressure over
Oral Low concentration/ High concentration
bulla
mucosa absent
•• What happens: extension of margin of bulla with
P. Foliaceous P. Vulgaris
irregular angulated border in case of pemphigus
(Desmoglein 1 (Desmoglein 3Q vulgaris
antibody) antibody)

Skin split Subcorneal split Suprabasal split

Desmoglein-1 Desmoglein-3>1

Mucosa No oral lesions ++ in 95% cases

How to look for Acantholysis:

Clinical: Lab:
Asboe-Hansen sign
•• Nikolsky sign •• Tzanck smear
•• Asboe Hansen sign •• Histopath
•• Bulla spread sign variation
•• Bulla spread sign •• It applies to smaller, intact, tense bullae where
the pressure is applied to the center of the
blister.
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Cerebellum Quick Revision Notes

–– Suprabasal Split - Few rounded cells in

the blister cavity (Row of tombstones) :
acantholytic cells

Intraepidermal split Subepidermal split

Thin roof Comparatively thick roof

•• Direct immunofluorescence
Flaccid bulla Tense bulla –– IgG & C3 deposited Intraepidermally & in
between the keratin cells (intercellular)
Wrinkling + on surface Absent
–– Shows fishnet/ chicken wire patternQ
Pemphigus vulgaris
•• Primary lesions: Flaccid bullae over the normal
skin →Secondary lesions: erosions (tend to
extend / no tendency to heal)
•• Site: scalp, oral mucosa (DSG-3>1), chest, trunk,
flexures
•• Buccal mucosa & Gingival mucosa can be involvedQ

Treatment of Pemphigus vulgaris:

•• Flaccid bullae with erosion which could show
no tendency to heal and eventually spreading •• Systemic steroids (vigorous) are the main stay
further on the skin treatment modality

Lab: •• Cyclophosphamide: monitor urine routine

•• DCP pulse: Dexamethasone Cyclophosphamide
•• Tzanck smear (Cytodiagnostic test)
Pulse
–– Vesicle Deroofed - Base scraped- Giemsa
•• 3 days admitted DCP given 27 days low dose
Stain
Cyclophosphamide
–– Acantholytic cells/Tzanck cells- Round cell,
•• Moderate to severe Pemphigus vulgaris
prominent nucleus, perinuclear halo
Rituximab (FDA approved in 2018), Anti-CD20
Histopathology of Pemphigus vulgaris (CD20 on B cells)

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Skin

Subepidermal Immuno Bullous Disorders

•• Pemphigoid group
•• Dermatitis herpetiformis
Pemphigoid group defect lies in Basement Membrane
Zone proteins
•• KIF keratin
intermediate filament
•• Hemidesmosome
complex
•• Lamina lucida
•• Lamina densa Sign Bullous Pemphigoid Pemphigus vulgaris
•• Sub Lamina densa
Nikolsky sign Negative Positive
(acantholysis)
Bulla spread Extension with Extension with
Zones Components sign regular border irregular border
KIF keratin intermediate Keratin 5/14, BPAG 2 & 1 Asboe Extension with Extension with
filament Hansen’s sign regular border irregular border
Hemidesmosome complex
Investigations:
Lamina lucida BPAG 2 (Transmembrane
molecule), •• Tzanck smear: Presence of eosinophils, Absence
Laminin of acantholytic cellsQ
Lamina densa Laminin
Histopathology
Collagen 4
Subepidermal Split
Sub Lamina densa Collagen 7 (anchoring fibrils)
*Seven

Bullous Pemphigoid
•• Immunobullous disease with a subepidermal
(deeper) split
•• IgG is the autoantibody deposited
•• Target protein: HemidesmosomesQ
•• Target antigens: BPAG 2 >1 (Bullous Pemphigoid
Antigen) •• Direct ImmunoFluorescence
•• No acantholysis - Nikolsky sign absent –– Autoantibody: IgG, C3 - Site: Basement
Membrane Zone, Linear patternQ
Clinical Features
•• 60 to 80 years of age (males=females)
•• Primary lesions:
–– Tense pruritic bullae on erythematous skin or
normal skinQ

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Cerebellum Quick Revision Notes

Clinical Features •• Autoantibody: IgA

•• Bullae itchy → Erosions due to scratching/ •• Age: children

itching •• Morphology: Annular arrangement of vesicles
•• Tend to heal / No tendency to extend (studded at margins)

•• Very good prognosis •• Cluster of jewels / string of pearls appearance

•• Dapsone Rx
Treatment:
•• Topical steroids
•• Low dose oral steroids

Pemphigoid Gestationis: Aka Herpes

Gestationis
•• Bullous Pemphigoid in pregnancy
•• Target antigen BPAG2

LABD Bullous Pemphigoid

Child – CBDC
Adult - LAD
DIF Linear Linear

Autoantibody IgA IgG

Dermatitis Herpetiformis aka Duhring

•• C/F: Tense bullae & Urticarial plaques disease
•• Periumbilical region: important site to note •• Chronically relapsing, itchy, subepidermal
immunobullous disease
•• Extends to the thighs & abdomen
•• Autoantibody: IgA
•• Treatment: systemic steroids DOC
•• Target antigen: epidermal transglutaminase 3
1. Linear IgA Bullous Dermatosis
•• HLA associations: HLA DQ2 DQ8Q
•• Children: CBDC Chronic Bullous Dermatosis of
childhood, •• Systemic important clue: gluten sensitive
enteropathy (asymptomatic)
•• Adults: LAD Linear IgA Disease
•• Manifestations: malabsorption, diarrhea
Chronic Bullous Dermatosis of abdominal pain
Childhood (CBDC) •• Course: Chronically relapsing, itchy,
subepidermal immunobullous disease
•• 20-40 years of age
•• M>F ratio is 2:1
C/F: Primary lesions: extremely itchy Papulo vesicles

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Skin

Treatment
•• Gluten free diet: Avoid Barley Rye Oats, Wheat
–– BROW should not be consumed
•• DOC: DapsoneQ

Mechanobullous disorders almost

synonymous to Epidermolysis Bullosa
•• Mild mechanical injury →Blisters / bullae
•• Secondary lesions: Grouped excoriations
•• Genetic
•• Sites: extensor & pressure points over the
trunk & extremitiesQ EB Simplex K5 / 14

Investigations: EB junctional laminin in lamina lucida

•• Tzanck smear EB dystrophic Collagen 7Q

–– Neutrophils Clues by examiner:

•• Histopathology •• Consanguineous marriage→ (Genetic)
–– Subepidermal split, Papillary tip microabscess: •• Mom → handling the baby → blisters (Mechanical
neutrophils trauma induces blisters)
•• Ix: DIF Negative

Microabscess
- collection of
neutrophils

•• Direct ImmunoFluorescence:
–– IgA is deposited at the Basement Membrane
Zone & dermal papilla granular patternQ

DIF findings Dermatitis Herpetiformis LAD

aka Duhring disease
Autoantibody: IgA IgA

Location: Basement Membrane Zone & BMZ

dermal papilla
Treatment:
Pattern: granular pattern Linear •• GENE Therapy (definitive)
•• supportive management
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Cerebellum Quick Revision Notes

Inherited acantholytic disorders Alopecia

Dariers disease or Hailey Hailey Loss of hair
Keratosis disease or chronic
Classification: *Cicatrix means scar
follicularis benign familial
pemphigus •• Non scarring (non-cicatricial)
Inheritance AD AD •• Scarring (cicatricial) - Stem cells in Bulge area
Defect Ca +2 ATPase Ca +2 ATPase are damaged
involvement involvement
Gene defect ATP 2A2 ATP 2C1
Chromosome 3 chromosome 12

Non cicatricial alopecia classification:

Patchy Diffuse Patterned Systemic

•• Alopecia areata •• Effluvium •• Androgenetic alopecia •• SLE

•• Trichotillomania •• Anagen (chemo & Radio) •• Thyroid
•• Tinea capitis (non-inflammatory) •• Telogen (Stress, Infections) dysfunction
•• Secondary syphilis

Alopecia Areata Exclamatory Mark Hair Sign

•• Areata: patchy/ spotty areas of alopecia

•• Autoimmune disease which Targets anagen hair Histopathology of Alopecia Areata
bulb •• Peribulbar lymphocytic infiltrates
Clinical Features •• Swarm of bees appearanceQ
•• Circular areas of complete hair loss
Nail pitting
•• No signs of inflammation seen •• Regular
•• Margin of lesions: Exclamation mark hair superficial
(Geometric)
•• Autoimmune disease
•• Distal end broad
•• Proximal end tapering

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Skin

Treatment
Localized disease Extensive Disease

•• Topical steroids: Clobetasol Systemic Steroids

(Most potent) Q

•• ILS (triamcinolone acetonide) Scarring Alopecia

(also used for scabies)
•• Papulosquamous disease: Lichen Plano pilaris
Trichotillomania (LPP)

•• A psychiatric condition (OCD) characterized by •• Granulomatous disorders: Sarcoidosis

pulling out of one’s own hair (mostly in Females) •• Connective tissue diseases: Discoid Lupus
Erythematosus, Systemic Lupus Erythematosus
•• Infections: Tinea capitis (inflammatory): Favus,
Kerion

Classification Of Sweat Glands

Eccrine glands Apocrine glands

Site: Entire body (palms & Axilla, areola,

soles) Groin
Opening: Directly open onto Along Hair follicle
•• Incomplete loss of hair in a given patch skin surface
•• Variable lengths of hair follicles seen Nerve Cholinergic Adrenergic
•• Perifollicular hemorrhage supply: sympathetic sympathetic
Secretion Androgen
Patterned Type / Non Cicatricial depends on dependent (glands
Alopecia / Androgenetic AlopeciaQ present at birth→
active puberty
Function Sweat production → Pheromones
Thermoregulation associated with
Body odour

•• Blockage of Eccrine glands: Miliaria

Male pattern AGA Female pattern AGA

Hamilton Ludwig, Olsen

•• Fronto-temporal •• Frontal hairline maintained

recession •• Loss of hair over the central
•• Balding of vertex portion of scalp

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Cerebellum Quick Revision Notes

Fox Fordyce disease: Due to obstruction of the

Apocrine duct
•• Morphology: multiple skin-colored pruritic
papules
•• Sites: Axilla, Areola of the nipple Eyelids: meibomian glands & glands of Zeis
Ectopic sebaceous glands (no association with hair •• Prepuce: Tyson’s glands
follicle)
•• Upper lip, buccal mucosa: Fordyces spots
•• Presents as yellow micro papules

Acne Vulgaris
•• Chronic inflammatory disease of the
pilosebaceous unit
•• Breast: Montgomery tubercles
•• Polymorphic cutaneous lesions (Comedones =
Specific lesions)
•• Organism: Cutibacterium acnes
(Propionibacterium acnes)
•• 4 Grades

Grade 1 Acne Vulgaris

Open comedones Closed comedones

Black because of oxidation of the sebum by the atmospheric air White

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Skin

Treatment
•• Topical Retinoids: Vitamin A analogue (Tretinoin, Adapalene) (ISOTRETINOINis not topical)

Grade 2 Acne Vulgaris Grade 3 Acne Vulgaris Grade 4 Acne Vulgaris

•• Predominant Red Papular Lesions •• Prominent Pustular Lesions •• (Most Severe form):
Nodulocystic Acne with Scars

Treatment Differential Diagnosis

•• DOC: isotretinoin = 13 Cis Retinoic acid
Acne Rosacea
•• Indication: Nodulocystic acne, resistant Morphology: Comedones Comedones absent
recalcitrant acne (Usually Grade 3)Q
present Papules, nodules &
•• Most common side effect: cheilitis (dryness of Papules, pustules present
lips) nodules
•• Dose: 0.5-1 mg/kg/ body weight daily (TCD: pustules &
120-150 mg/kg body weight). scars
Associations Skin greasy Erythema flushing
–– Investigation when on oral retinoids for acne
background: & telangiectasia
•• Lab monitoring: Fasting lipid profile, LFT as prominentQ
oral retinoids are associated with increased Distribution: Face upper Convexities of
triglycerides & total cholesterolQ
part of trunk face Centro facial
Important Syndromes Associated with Acne chest & lesion, cheeks, nose
shoulders & forehead, spares
SAPHO syndrome SAHA HAIRAN periorificial area
syndrome Syndrome
•• Synovitis •• Hyper Acne Rosacea
•• Acne •• Seborrhoea Androgenism •• Chronic inflammatory facial dermatoses
•• Pustulosis •• Acne •• Insulin
•• Sites: Centro-facial areas (convexities of the
•• Hirsutism Resistance
•• Hyperostosis face)
•• Osteitis •• Androgenic •• Acanthosis
•• Sunlight, spicy food, alcohol, stress
alopecia Nigricans
PAPA syndrome
•• Abnormal vascular reactivity (flushing)Q
•• Pyogenic
Arthritis
•• Pyoderma
gangrenosum
•• Acne

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Cerebellum Quick Revision Notes

Papulopustular stage: papules & pustules present

Phymatous type: aka potato nose

•• Lesion: skin over the nose becomes thick Otophyma - Thickening over the ear

•• Surface of nose: prominent pores, surface

Rosacea SLE
nodularity
Photosensitivity Present Absent
•• Pathology: characterized by hypertrophy &
fibrosis of the sebaceous gland Malar rash
Triggers in Spicy food, Absent
•• CO2 laser excision followed by resurfacing is
history alcohol,
TOC
stress
Papules & Present Absent
pustules
Erythema Transient / Fixed
Fixed
Systemic Absent Fever, arthralgia,
features myalgia, oral ulcers

Leukonychia / White Nails:

True leukonychia Apparent leukonychia

Nail matrix Nail bed

Rhinophyma - Thickening over the nose
Mees lines Muehrcke’s bands
Half & half nails / Lindsay nails
Terrys nails

True Leukonychia
•• Chronic arsenic poisoning
•• Mees lines: horizontal, transverse white bands
on the nail plate

Gnathophyma - thickening over the chin

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Skin

Apparent Leukonychia
•• Muehrcke’s bands - paired transverse white
bands
•• Half & half nails / Lindsay nails
•• Terry’s nails
Muehrcke’s bands: Conditions seen in: Hypoalbuminemia
/ Nephrotic syndrome/ Malnutrition

Half & half nails / Lindsay nails Terry’s Nails

•• Kidney failure •• Liver disease
•• Proximal 50%: white/pale •• proximal (90%): white/pale
•• Distal (50%) brown to pink •• distal (10%): pink to brown

Pigmentary Disorders Freckles/ Lentigines

ephelides
Melasma Sites: Sun exposed Sun exposed &
•• Presentation: Symmetrical hyperpigmented protected
brownish macules -> Nose, malar area, and Melanocyte Normal Increased
mandibular area. number
•• Differential diagnosis: SLE Melanocyte Increased Normal
Activity
Seasonal Summer Constant colour
variation worsening+
Associations: Xeroderma Peutz Jeghers
pigmentosum syndrome

Melasma SLE

Malar rash Present Present

Unique Brown - Black Red

feature
Peutz Jeghers syndrome:
•• Autosomal Dominant Inherited Condition
•• Characterized by mucosal lentigines and Gl
polyps.
•• Most common site for polyp is jejunum.

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Cerebellum Quick Revision Notes

•• Most common type of polyp is Hamartomatous

Nevus of Ota: Nevus of Ito

•• Unilateral •• Follows the

•• Blue to slate grey colour posterior
•• Follows the 1st & 2nd supraclavicular &
division of Trigeminal lateral brachial
nerve (ophthalmic and cutaneous nerves.
Maxillary divisions). •• Site: upper
•• Site: Face. shoulder and back
•• 2/3rd of patients has
Becker’s Nevus scleral involvement.
•• Nevus of HORI = B/L
CMN (Congenital BECKERS NEVUS (Puberty)
Nevus of Ota
Melanocytic Nevi) Acquired nevus, seen during
*>20cm has higher risk puberty
of malignant melanoma
Black Brown
Thick skin Normal
Folds Normal
Uni / Bilateral Unilateral Site: Chest and upper
shoulder.

Becker’s nevus Nevus of ITO

Unilateral, brown patch Blue patch on shoulder, upper

on shoulder, back back
Hypertrichosis + -ve

Onset: Puberty Birth

Dermal Melanocytosis
•• Proliferation of melanocytes in the dermis
→Blue colour.
•• Ceruloderma Cerulo blue, derma skin.
•• Blue to slate grey in colour (due to Tyndall
effect)

Mongolian Spot: Treatment of Nevus of Ota/Ito: Q switched Nd YAG

•• Infants laser.
•• Common site is lumbo-sacral DISORDERS OF HYPO/
•• Resolves spontaneously DEPIGMENTATION
Congenital Disorders Of Hypo
Depigmentation.
Albinism
•• Biochemical Defect: Tyrosinase defective

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Skin

•• 2 types: Nevus depigmentosus / Nevus anemicus (Not

1. Ocular albinism: involvement of only the Eyes, Achromicus a Melanin disorder)
(Pharmacological Defect)
2.Oculocutaneous albinism Involvement of eyes, skin
•• Defect in the Transfer •• Defective Blood vessels
and hair.
of Melanosomes to the → Vasoconstriction
Keratinocytes •• Congenital
•• Onset is at birth •• Pale looking →
•• Presents as Decreased Blood supply
depigmented macule → Decreases colour
with feathery margins.

Acquired disorders of hypo/

depigmentation
Vitiligo
Piebaldism:
•• Most accepted theory: Auto-antibodies destroy
Major characteristic of Piebaldism is a white forelock
the Melanocytes → melanocyte absent from the
(a patch of white hair directly above the forehead).
lesion.
•• Autosomal dominant.
•• Association: Thyroid dysfunction, T1DM,
•• Defect in neural crest function. Pernicious anaemia
•• Clinical features - Depigmented chalky white
macules → Melanocytes are AbsentQ
3 varieties
1. Segmental
2. Non segmental
3. Unclassified/ undetermined

Segmental Vitiligo
•• Starts at early childhood.
•• Unilateral, Segmental, does not cross the
midline
White forelock -> Characteristic lesion. Mainly over
forehead
•• Treatment - Surgical intervention melanocyte
transplanting, skin grafting

Islands of normal skin: Trunk, within the white patch Non-segmental Vitiligo
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Cerebellum Quick Revision Notes

•• Acrofacial vitiligo - Face, head, and distal

extremities
•• Mucosal vitiligo - Involves > 1 site,
•• Vitiligo vulgaris (most common type):
Symmetrically Distributed depigmented
macular lesions
•• Universal vitiligo → 80- 90% body surface area
depigmented

Exaggerated white fluorescence can be seen due to

presence of collagen in the dermis

Treatment
Acrofacial Vitiligo Universal Vitiligo
•• Based on the body surface area (BSA) involved
1. <20% BSA involved: Topical steroids, Topical
tacrolimus (Calcineurin inhibitor)Q
2. >20% BSA involved: Systemic steroids (halt the
progress of disease), Azathioprine. (Chronic
duration therapy)
Mucosal Vitiligo
Vitiligo Vulgaris •• NBUVB (Narrow Band UV B radiation) at 311 nm
Wavelength. (Safer)
Unclassified/ Undetermined Vitiligo:
•• Focal vitiligo Small, isolated depigmented
Chemical Leukoderma
lesions - 1-2 over the body •• Melanocyte destruction due to Chemicals
–– Bindi dermatitis: Para tertiary butyl
phenol (PTBP) glue present destroys the
melanocytes

Koebner’s phenomenon Leucotrichia

True Koebner’s phenomenon: Hair follicle melanocytes
new lesions appear at the are involvedQ
site of trauma
–– Rubber footwear: Contains Mono Benzyl Ether
of Hydroquinone (MBEH) causes destruction
of melanocytesQ

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Skin

•• Alta dye has Crocein scarlet MOO & solvent –– Site: Extensors & Lumbo-sacral (Elbows,
yellow 3 causes the depigmentation knees, Back)Q

Psoriasis
•• Definition: Chronic, T cell mediated
inflammatory disease involving skin & multiple
systems.
Pustular Psoriasis
•• Skin: Erythematous plaques with Silvery white
scaling •• Sterile pustules (tiny pus filled lesions) with
inflammatory cells (not infectious cells)
•• Systems: Joints → Arthritis & Metabolic
syndrome (Hyperlipidemia, Hyperglycemia, •• Trigger: sudden withdrawal of systemic
hypertension, visceral obesity). steroidsQ

•• Triggering Environmental factors •• Clinical features: sheets / lakes of pus

1. Seasons - Exacerbation during winters

2. Infections - HIV, Streptococcal Infection
(Guttate)
3. Drugs
4. Substance abuse - Alcohol, smoking
•• Pathogenesis
•• Epidermis: keratinocyte hyperproliferation
•• Dermis: inflammation
•• Etiopathogenesis Generalized pustular psoriasis

Cellular components Signaling molecules

(Cytokines)

Th1 IL-2, TNF alpha, IFN-gamma Acute form :

Th17 IL-17 Von Zumbusch
Type Pregnancy :
Th22 IL-22

Pro-inflammatory cytokines Pustular psoriasis of

Pregnancy(PPP)
Clinical Types of Psoriasis Or
Chronic plaque psoriasis / Psoriasis Vulgaris Impetigo Herpetiformis
(Misnomer)
•• Clinical features
Impetigo = Bacterial
–– Lesions: Erythematous scaly papules & plaques
Herpes = Viral
–– Scales: micaceous silvery white scales

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Cerebellum Quick Revision Notes

Erythrodermic Psoriasis:(Red Skin) 2. Koebners phenomenon

Exfoliative Dermatitis 3. Wornoff ring
•• It is presentation (not a disease) >90% BSA Auspitz SignQ
showing erythema +- Scaling
•• Glass slide→ Scrape psoriasis lesion (Grattage
•• There are multiple causes of erythroderma ex:
test)
psoriasis
•• Accentuation of silvery white scales
•• Burkeley membrane
•• Pin point bleeding spots

Psoriatic arthritis
Koebners Phenomenon / Isomorphic
Response:
•• Clinical significance: Disease is active, so patient
should be advised to avoid any unnecessary
trauma
•• Appearance of morphologically similar lesions
along the lines of trauma over normal skin
•• Types of Koebners phenomenon.Q
•• Seronegative arthritis (RF factor negative)
True Pseudo Rare causes
•• Erosive arthritis
Immunologic Autoinoculation Kaposi sarcoma,
•• Classical joint involved: DIPQ Darier disease,
Lichen nitidus
•• Worst type: Arthritis mutilans severe
destruction (shortening of digits) Psoriasis Viral infections
lichen planus molluscum
•• Dactylitis: Inflammation of digits
Vitiligo contagiosum
Special Signs Phenomenon features (Depigmented viral wartsQ
lesions)
1. Auspitz sign

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Skin

Wornoff’s Ring •• Subungual hyperkeratosis: Below the nail plate

material is depositedQ
•• Hypopigmented rim around psoriasis lesions
•• Onycholysis: separation of the nail plate from
•• Due to abnormal prostaglandin levels in the
the underlying nail bed
peripheral zone of lesionsQ
•• Oil drop sign = Salmon patch
•• Clinical significance: Pathognomonic of nail
psoriasis
•• Description: Yellow discoloration of nail bed

Nail Psoriasis
Matrix Nail bed
Pitting Oil drop sign (Salmon
Patch)
Leukonychia: white Onycholysis
discoloration of nail plate
Thickening of nail plate with yellow colored discoloration
Subungual hyperkeratosis is also present
Splinter hemorrhages

•• Pitting of nails
•• Lesions: Depressions in nail plate
•• Clinical significance: MC nail change in psoriasis
•• Types: DIC (Deep, Irregular, Coarse) (Opposite
in Alopecia Areata)Q
•• Defect: Proximal nail matrix

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Cerebellum Quick Revision Notes

Psoriasis Alopecia areata Stratum Granulosum

Deep Irregular Coarse Superficial regular
Absent / decreased granular Wedge shaped
pits Geometric
layer: psoriasis vulgaris, Hypergranulosis: lichen
icthyosis vulgarisQ planusQ

Regional Variation Of Psoriasis

Scalp Psoriasis
•• No alopecia present only thick micaceous scales

Micro abscess Cells Disease

Munroe's Neutrophils in Psoriasis

microabscess stratum corneum
Spongiform pustules Neutrophils in Psoriasis
of KogojQ stratum spinosum
Inverse Flexural psoriasis: Scaling absentQ

Stratum Corneum
Parakeratosis Spongiform pustules of Kogoj
•• Hyperkeratosis: pathological thickening
•• Parakeratosis: retention of nucleus

Munros’s microabscess

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Skin

Systemic Therapy
Biological agents: Targeted therapy
•• Ustekinumab: IL-12 & 23
•• Guselkumab, Risankizumab, Tildrakizumab: IL-
23 GRT
•• Infliximab, Etanercept, Adalimumab: TNF-
alpha inhibitors
•• Secukinumab, Ixekizumab: IL-17Q
•• Brodalumab: IL-17 (R)

Psoriasis important negative points:

Supra Papillary Thinning
•• Never involves CNS

Histopathology of Psoriasis •• Never affect Mucosa (Geographic tongue)

•• Parakeratosis: Retention of nucleus in topmost •• No Itching

layer •• No Alopecia
•• Agranulosis: Absence of stratum granulosum •• Auspitz’s sign is negative in Inverse and
•• Acanthosis= Thickening of stratum Spinosum Pustular Psoriasis.

•• Dermal papillae are enlarged resulting in Supra

Lichen Planus
papillary thinning
•• Definition: chronic yet self-limiting (1-2
•• Dermal T-cell infiltration
years) immune mediated inflammatory disease
•• Dilated & Tortuous dermal Vessels (results in affecting the skin, mucosa & hair follicle
pin point bleeding when lesion is Scraped)
•• Provocative factors: - Most important: Dental
•• From tip of these dermal papillae, inflammatory amalgam (Presence of mercury)
Cells Come out & starts collecting in epidermis
–– Infections: Hepatitis C & BQ
known as spongiform pustules of kogoj
generally present in stratum Spinosum + –– Drugs: AntiMalarials, ACE inhibitors, Beta
Stratum Basale i e in Malpighian layer) BlockersQ

•• Munros microabscess (Generally present in

Reticulate Lacy
Stratum Corneum) Pattern

Treatment & Options in Psoriasis

•• Basis: BSA <10% or >10%
Dental Amalgam
1. Topicals: BSA <10% conisting of
Mercury
2. Phototherapy: BSA >10%
3. Systemic agents: BSA >10%
•• Oral involvement: 30-70%
Methotrexate Psoriasis vulgaris, Pso arthritis,
•• Reticulate lacy white pattern (net like pattern)Q
(Teratogenic) Erythrodermic psoriasis
Acitretin Pustular psoriasis & HIV
•• Ulcerative / Erosive LP: premalignant lesion
(chance of developing into malignancy +ve)
(Teratogenic)
Steroids Impetigo herpetiformis, Psoriatic Morphology
erythroderma in pregnancy
•• 6 P’s

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Cerebellum Quick Revision Notes

1. Pruritic Nail Involvement:

2. Purple •• M/C finding: thinning of nail plateQ
3. Polygonal •• Most characteristic finding: pterygiumQ of nail
4. Plain topped wing shaped/ triangular shaped fold extend
from Proximal Nail Fold→ destroys nail plate
5. Papules reaches nail bed
6. Plaques

Hair Involvement:
Wickham’s Striae
•• Patient complains of Hair loss: scarring alopeciaQ
•• Surface of LP seen with magnifying lens with (hair destroyed)
oil on top of lesion: whitish linear streaks
Wickham’s striaeQ

Lichen Plano Pilaris

Activity
•• Perifollicular Lichenoid Papules +
•• Scaling +

Stratum Granulosum

•• Koebners phenomenon will be positiveQ

Saw-toothing rete-ridges
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Skin

Lichen Planus Psoriasis

Genetic - +

Itching Most Not common

common++

Oral & Hair Wickhams -

Striae++
Scarring
Alopecia

Arthropathy - +
Histopathology of L.P
S.C -- ++
•• Hyperkeratosis in SC Parakeratosis
•• Wedge shaped Hypergranulosis in SG S.C Munroe’s -- ++
•• Thickening of SS: Acanthosis Microabscess

•• Saw toothing rete ridges Stratum Hyper.G Hypo.G

Granulosum
•• Band like lymphocytic infiltrate at Dermo
Epidermal JunctionQ Stratum Irregular Regular
Spinosum Acanthosis Acanthosis
•• Basal cell degenerationQ
Rete Saw tooth++ Elongation
•• Necrotic keratinocytes / colloid bodies /
+(Camel foot)
Civatte bodiesQ
S. Basale Interface
•• Artefactual cleft at Dermo Epidermal Junction:
dermatitis++
Max joseph spaceQ
Melanin
P’s in Lichen Planus incontinence++

•• P/Flexors, Purple, Pruritic, Plane topped,

Polygonal, Papules, Plaques, Pterygium, Pup tent Pityriasis Rosea
sign, •• Acute self-limiting (6-12 weeks) disease,
•• Pigmentation (lesions heal with •• Etiology: M/C viral trigger: HHV 7,Q
hyperpigmentation).
Morphology / course:
P’s
in Lichen Planus
NOT POLYHEDRAL


Treatment
•• Limited: topical steroids & ILS for Hypertrophic
LPQ
•• Widespread disease: systemic steroids
•• Phototherapy & Steroid sparing agents like Mtx
& Dapsone. •• 1st lesion: Annular Herald patch/ mother patch
*Chronic Inflammatory Disease, Papulo-squamous 1-2 weeks laterQ
Disorders are common for psoriasis & lichen planus •• Secondary lesion: scaly papules →oval annular
plaques→ mild pigmentary changes → fades
slowly in 6-12weeks.

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Cerebellum Quick Revision Notes

•• Scales: collarette (collar like) → outer edge:

within the active margin of lesion (attached)Q
•• Inner edge: Free

Distribution of lesions
•• Christmas tree pattern
•• Downwards & outwards from the spine-->
along the lines of Langer (lines of skin tension) •• >90% of body surface area gets involved
(parallel to the ribs) (erythroderma)
•• Islands of sparing (some patches of the body
are spared)
•• Palms & soles - thick skin
Palmoplantar keratoderma PRP sandal

Pityriasis Rubra Pilaris:

•• Clinical features: hyperkeratotic perifollicular
papules (Nutmeg Grater appearance)

Eczema
•• Response of skin to Endogenous (internal) or
exogenous (external) Stimuli.
•• All eczema is dermatitis, but NOT ALL
dermatitis is eczema
•• Initially discrete → Progress to form confluent
orange red erythema in cephalo-caudal direction

Etiologic Classification

Exogenous Endogenous

•• Contact Dermatitis •• Seborrheic dermatitis/dandruff

•• Photodermatitis •• Stasis eczema
•• Phytodermatitis •• Asteatotic eczema
•• Pityriasis alba
•• Nummular eczema
•• Pompholyx

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Skin

Morphological classification of eczema:

Acute Eczema SubAcute Eczema Chronic Eczema

•• Erythema. •• Erythema •• LichenificationQ

•• Edema. •• Scaling •• Chronic Itching → Skin → Safety
•• Vesicles. measure
•• Oozing 1. Thick skin

2. Hyperpigmentation

3. Exaggerated skin markings

•• Crusting
•• HPE: Spongiosis intercellular
edema between cellsQ

Contact Dermatitis: 2 types

ICD (Irritant contact dermatitis) ACD (Allergic contact dermatitis)

Affects All who are exposed Affects genetically predisposed (Atopy +ve)

Reason Non-immunologic (direct tissue Immunologic (Type IV hypersensitivity reaction

damage) Sensitization needed

Lesions Restricted to site of contact Tends to disseminate beyond the site of contact

Complaints More burning More itching

Examples Diaper dermatitis: Involves convex Hair dye: PPD (para phenylene diamine)
areas Sparing the folds

Diagnosis Patch Test

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Cerebellum Quick Revision Notes

Important Examples of Allergens causing ACD •• Substance in the air→ settles on the exposed
parts of the skin→ ABCD
•• Hair dye: PPD (para phenylene diamine)Q
•• Plant: Parthenium hysterophorus (congress
•• Metal: Nickel (most common)
grass / communist plant)Q
•• Topical antibiotic: Neomycin.
•• Cement: Potassium dichromate.
•• Bindi: PTBP (para tertiary butyl Phenol)Q.

Seborrheic Dermatitis/Dandruff
•• Feature: Inflammatory response of seborrheic
areas to Malassezia. Yeast
•• Sites: Scalp, face, nasolabial folds, Retro-
auricular region.
•• Scales Greasy yellow
•• Severe disease: Seen in Parkinson’s disease,
HIV infection
Patch test: Principle → Type 4 Hypersensitivity
Reaction.
•• Method: Allergens are applied over the patient’s
back & wait for type 4 / Delayed hypersensitivity

Infantile Seborrheic Dermatitis: Cradle Cap

Stasis Eczema
•• Synonym: Gravitational/ varicose eczema.
•• Association: chronic venous insufficiency

•• Patch test reading

–– Read at: 48 hours/ 2 days
–– Best read at: 96 hours/ 4 days. Lipodermatosclerosis or
inverted champagne bottle
Airborne Contact Dermatitis Sesquiterpene lactone appearance
SQL

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Skin

Atopic Dermatitis
Pityriasis (Scaling) Alba (White) •• Chronic, relapsing, inflammatory skin disease
Child, with facial Pityriasis alba Indeterminate
•• It is classified as an endogenous eczema
Hypopigmented leprosy
triggered by Exogenous factors.
patches
Lesions Multiple Single •• Atopy: Localized form of type 1 hypersensitivity
reaction.
Scaling + -
Atopic triad
Atopy + - •• Recurrent allergic rhinitis (upper respiratory
tract).
Sensation Intact Normal /
•• Atopic asthma/ bronchial asthma (lower
Impaired
respiratory tract)
Skin Atrophy Absent Present
•• Skin allergies

Phases Clinical features Characteristic

features
Nummular Eczema Aka Discoid Eczema
Infantile (3 Extremely itchy Clears in 40% by
•• Lesions: Coin shaped lesions with Well months) exudative lesions age of 18 months
demarcated edges.Q ,60% changes to
Birth - 2 years bilaterally
•• Differential diagnosis: Tinea. symmetrical on childhood pattern
face cheeks &
Pompholyx aka dyshidrotic eczema extensors sparing
•• Lesions: Intensely pruritic & also painful deep- diaper area.
Seated vesicles at Sides of digits having sago Childhood Red oozy papules May start denovo
grain like Appearance 2yrs- puberty plaques in cubital
•• M/C in people with history of atopy & popliteal fossa
(Flexures)
Adult Lichenified Less common
> puberty flexural lesions

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Cerebellum Quick Revision Notes

Infantile Phase: white line Appears due to vasoconstriction.

•• Normal skin: On stroking, Wheal flare response.

•• Headlight Sign shows sparing of Periorbital,

Extensor is involved due to crawling perioral & perinasal areaQ

Childhood & Adult phase

Investigations: Investigation of Choice: Clinical

examination
Diagnostic criteria of atopic dermatitis, proposed •• Ophthalmic manifestations:
By Hanifin and Rajka.Q Conical cornea/keratoconus
•• Pruritus: Hallmark (intermittent & intense,
Termed as itch that rashes)
•• Typical morphology & distribution with 3 Phases.
•• Chronic or chronically relapsing Dermatitis
•• Personal/family history of atopy
Minor Diagnostic criteria:
•• Xerosis: Dry skin.
Allergic shiners & salute - over the nose
•• Ichthyosis: Fish like scales.

Allergic Shiner
Allergic Salute

•• White dermographism: On stroking the skin,

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Skin

Shield cataract/ anterior subcapsular cataract •• Dermographism: writing on skin possible

Angioedema: Quincke edema: C1 esterase deficiency

is seenQ
Infraorbital fold of skin: Dennie-Morgan’s fold
•• Swelling ++,
•• Symptoms: non itchy, but painful,
•• Edema: Deeper location (subcutaneous)

Hereditary Angioedema:
•• No urticaria or itching
Lateral madarosis: Hertoghe’s sign due to continuous •• Familial & sudden
rubbing
•• Subglottic area involvement possible → airway
blockage → life threatening (Immediate Rx)

Cutaneous Mastocytosis: Urticaria Pigmentosa

•• Mast cell proliferationQ
•• Children

Summary Of Ophthalmic Manifestations •• C-Kit gene mutations seen

•• Conical cornea/keratoconus. •• Multiple hyperpigmented macules + over trunk

•• Shield cataract/ anterior subcapsular cataract Darier sign: rubbing dark lesions->histamine release-
>erythema with urticarial haloQ
•• Infraorbital fold of skin: Dennie-Morgan’s foldQ
•• Lateral madarosis: Hertoghe’s sign due to
continuous rubbing

Treatment
•• Topical - Emollients (decreases dry skin),
Topical steroids (anti-inflammatory)

Urticaria
•• IgE-mediated Type 1 hypersensitivity reaction
-->degranulation of mast cells--> histamine
Triple response--> Erythema -->Flare -->WhealQ
•• Transient wheals (<24 hours) dermal edema +ve

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Cerebellum Quick Revision Notes

Genodermatoses / Phacomatoses
Neurofibromatosis

NeuroFibromatosis 1 NeuroFibromatosis 2

AKA Von Reckling Hausen disease MISME (Multiple inherited Schwannomas Meningiomas &
Ependymomas)

Chromosome 17 22

Protein Neurofibromin Merlin / Schwannomin

Neurofibromas Plexiform Cafe-Au-Lait macules Skin fold freckling

Neurofibroma

2 1 6 macules Crowes Sign

Button hole sign Bag of worms feel > 5mm, Post pubertal > 15 mm

•• Lesions: Soft, skin coloured, non-tender, papules or nodules

which are Benign tumours of connective tissue of Peripheral
nerve sheath.

Ocular Manifestation In Nf-I:

Lisch iris nodules: Pigmented iris hamartomas Optic pathway glioma.

Ophthalmology ref: slit lamp Examination. •• Proptosis seen
•• Visual acuity Normal

Diagnosis: 2 or more of 7 of following:

•• 6 or more café au lait macules → 5 mm (prepubertal age) → 15 mm (post pubertal age)
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Skin

•• 2 or more neurofibromas of any type OR 1 •• A first-degree relative (parent, sibling,

plexiform neurofibroma offspring) with NF1 by the above criteria.
•• 2 or more Lisch nodules Tuberous Sclerosis Complex Aka Bourneville’s/
•• Freckling in the axillary or inguinal regions Epiloia / Vogt’s Triad
•• Optic glioma •• Autosomal Dominant Disease.
•• A distinctive osseous lesion such as sphenoid TSC Chromosome
dysplasia or thinning of the long bone cortex
with or without pseudoarthrosis 1 9

2 16

Ash leaf macules Adenoma sebaceum Shagreen patch Koenen’s tumours (KT)

•• Earliest skin lesion •• Facial angiofibroma •• Collagenoma •• Periungual fibroma

•• Lance ovate shape: Oval On •• Characteristic Lesions •• Leathery
one side, Pointed on another –– Proliferation of blood plaque,
side. vessels and fibrous tissue • • Located in
lumbosacral
–– Lesions are symmetrical
region.
–– Reddish-brown papules.

•• Ash leaf macules •• Mental retardation “AASK ME SEGAR”

•• Adenoma sebaceum •• Epilepsy
•• Shagreen patch •• SEGA
•• Koenen’s tumours (KT) •• Rhabdomyoma

Sturge weber /Encephalo Trigeminal

angiomatosisQ
•• Sporadic since Birth
•• Low flow capillary Vascular malformation
1 CNS: Epilepsy
2 Eyes: Glaucoma
3 Cutaneous: Facial PWS (U/L) pink-red overtime
turning to purplish. Ichthyosis classification
•• Prognosis: Permanent skin disease •• Congenital: Discussed in table.

•• Management: PDL •• Acquired: Hypo thyroidism, Leprosy, (autonomic

dysfunction), Hodgkin’s lymphoma, HIV, Drugs

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Cerebellum Quick Revision Notes

Icthyosis Vulgaris X linked Icthyosis Lamellar Icthyosis

(Most common) (I nigra)
Inheritance AD XLR AR

Onset 3-12 months age <3 months Birth (collodion membrane)

parchment like membraneQ
Defect Filaggrin (filament Steroid sulfatase (converts Epidermal transglutaminase 1
aggregating protein)Q cholesterol sulphate →
cholesterol
Scales Fine white Brown – black scales Dark-plate like adherent scales

Associations •• Keratosis pilaris •• Corneal opacities •• Eye ectropion

•• Hyperlinear palms •• Cryptorchidism •• Lip eclabium
(undescended testis)
→testicular malignancy

Pyodermas (PD): Furuncle / Boil:

Definition: purulent bacterial skin infections •• Infection of hair follicle with Perifollicular area

Pyoderma Classification:
1. Follicular PD: hair follicles are involved (Etiology:
staphylococcus aureus)
2. Non-Follicular PD: hair follicles are not involved

1. Follicular PD:

Diseases:
Carbuncle:
Folliculitis:
•• Infection of group of multiple hair follicles with
contagious (adjacent area)
•• Lesion: red indurated, tender plaque with
multiple discharging pus points
•• MC site: nape of neck & upper back
•• Most common association: uncontrolled
Diabetes mellitusQ
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Skin

Non follicular PD:

Special Folliculitis: Hair follicles are not involved
Sycosis Barbae:
Classification:
(Site Specific)
Localized Spreading / Diffuse
Staphylococcus aureus infection Impetigo Erysipelas

•• Chronic infection involving whole depth of Ecthyma Cellulitis

follicle of beard area Impetigo:
•• It is a non-scarring pyogenic infection (hairs
It is the bacterial infection of the epidermis
retained)

Classification: 2 Types
Non bullous impetigo / Impetigo contagiosa: Bullous impetigo: Pemphigus neonatorum
Etiology: GABHS (PSGN) > Staphylococcus aureus Etiology: Always staphylococcus aureus (70,71)
Toxin: exfoliative Toxin A ( DSG-1)
Seen in children Seen in children
Site: Face Site: Face Trunk
Lesion: golden brown or honey coloured crust Q Lesion: Superficial flaccid bullae ruptures to give
varnish coloured thin crust

Bullous Impetigo Hypopyon sign: pus settles in the lower half of the
bulla due to gravityQ.

Topical Antibacterials:
•• Fucidic acid
•• Mupirocin:
•• Retapamulin
•• Ozenoxacin: quinolone drug, Currently available
in India

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Cerebellum Quick Revision Notes

Erysipelas: St Anthony’s fire Cellulitis

Level: upper half of the dermis + lymphatics (superficial) Level: lower half of the dermis + subcutaneous tissue

Etiology: GABHS Etiology: GABHS Staphylococcus aureus (rare)

(Hyaluronidase) Spreading infections Margin: ill defined, diffuse

Margin: well defined, raised margin with clear demarcation

between involved & normal skin
MILIAN EAR SIGN;Q

Staphylococcal Scalded Skin Syndrome Staph aureus → Epidermolytic toxin / Exotoxin →

(SSSS) Blood →Targets skin → Target protein desmosomes
→ Target antigen: DESMOGLEIN-1 upper
RITTERS DISEASE / Pemphigus neonatorumQ epidermis→ Subcorneal split
•• Definition: Acute skin exfoliation secondary •• Lesions: initially, periorificial erythema, skin
to toxin producing strains of staphylococcus tenderness (due to acantholysis)
aureus (scald=burn)
•• If untreated, progresses to epidermolysis
•• Etiology: Staphylococcus aureus Gram +ve (sheet like epidermal peeling)
organism Exotoxins
True Nikolsky sign
•• Pathogenesis:
–– Focus / Source of infection: Distant
staphylococcal infection in ear or conjunctiva
–– Epidermolytic toxin (exotoxin) produced
from the foci spreads through blood &
targets the skin

•• Target protein: Desmosomes in the epidermis

•• Target antigen: Desmoglein -1 in upper
epidermis
•• Disease process: Acantholysis (subcorneal
Mucosa: normal (periorificial crusting+) (because DES-
split)
MOGLEIN-1 is expressed in low concentration in the
•• History of distant infection like conjunctivitis/ Mucosa)
otitis media
•• Constitutional symptoms like fever

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Skin

Differential Diagnosis:
•• Staphylococcal Scalded •• Toxic Epidermal
Skin Syndrome Necrolysis
•• Sheet like epidermal •• Sheet like epidermal
peeling & Constitutional peeling & Constitutional
symptoms symptoms
•• CHILD •• ADULTS with Drug
•• Normal mucosa History
•• Rx → Parenteral •• Mucosal involvement Acute Paronychia
Antibiotics is prominent with •• It is an acute infection of the nail folds
hemorrhagic crusts
•• Etiology: staphylococcus aureus
Reiter’s Syndrome •• Predisposing factors: Thumb sucking/ Nail
It is a reactive arthritis; - biting.
C/F –– Erythema around nail folds → pus collection/
purulent discharge at nail folds
•• Arthritis
•• Complications may include: osteitis, lymphangitis.
•• Conjunctivitis
•• Rx → Without abscess: Topical antibacterials
•• Urethritis
–– Abscess formation: Surgical incision &
•• Balanitis
drainage
•• Infections
•• Keratoderma

Cutaneous Corynebacterial Infections

ErythrasmaQ Trichomycosis axillaris/ Pitted keratolysis
Trichobacteriosis axillaris

•• Etiology: Corynebacterium •• Not a fungal infection •• Etiology: Micrococcus/Kytococcus

minutissimum •• Etiology: Corynebacterium tenuis sedentarius
•• Lesion: asymptomatic •• C/F: yellow concretions/deposits •• C/F: pits or depressions in
Hyperpigmented or over hair shafts stratum corneum (due to
•• Erythematous macules with •• site axilla keratolysis due to serine
Creasing / wrinkling on surface •• Sweat may be yellow, Black or red proteases)Q
•• Sites: axilla, inguinal region, toe → stain clothes •• Also complain of malodour &
web spaces maceration
•• (Predilection to folds) •• Sites: soles & palms (associated
•• Woods lamp: coral red with hyperhidrosis)
fluorescence (due to
coproporphyrin-III)
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Cerebellum Quick Revision Notes

ErythrasmaQ Trichomycosis axillaris/ Pitted keratolysis

Trichobacteriosis axillaris

Scrub Typhus
Infectious disease presenting clinically with Fever
•• Etiology: Orientia tsutsugamushi
•• Vector: trombiculid miteQ
•• Infective form of mite: chiggers (larval form)
•• Clinical presentation: Causality with fever, CNS
symptoms
•• Lesion: Eschar (erythema surrounding black Cutaneous anthrax
scab)Q
•• Etiology: Bacillus anthracis
•• Lesion: malignant pustule (misnomer)
•• 3 types: Cutaneous, Inhalational, GI Anthrax
•• Painless papule→ eschar → rim of vesicles

DOC: Doxycycline

Differential diagnosis for eschar:

•• Cutaneous anthrax
•• Brown recluse spider bite (poisonous spider)
•• Scrub typhus

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Skin

Pseudomonas infections
Ecthyma gangrenosum Hot tub folliculitis Green nail syndrome

•• Pseudomonas septicaemia: •• Bathing/shower in an ill Pyocyanin pigment produced by

Immunocompromised pts → maintained spa pseudomonasQ
haemorrhagic necrosis of the skin •• Sites: bathing area / trunk
•• Necrotic crusted ulcers are seen.

1. Ecthyma gangrenosum Tuberculosis Verrucosa Cutis: Post

•• Ecthyma gangrenosum: Pseudomonas primary form
•• Ecthyma pyogenicum: Staphylococcus •• Anatomists’ / Pathologists wart: verrucous
means rough or uneven surface.
•• Ecthyma contagiosum: Parapox virus (Orf virus
goat sheep handling+)Q •• Seen in anatomists due to handling of dead bodies
as M. Tuberculosis gets inoculated on skin,
Meningococcemia •• Lesion: indurated verrucous plaque
•• Etiology: Neisseria meningitidis
•• Site: on distal or acral extremities
•• Fever + signs of meningitis like neck rigidity
•• Diascopy: petechial / purpuric lesion
•• Angular cutaneous infarctsQ

Features Tuberculosis Common warts

Verrucosa Cutis
Discharge + -
Cutaneous TB Classification: Based on Induration + -
mode of acquisition Scarring + -
•• Exogenous (TB Chancre, TuBerculosis Verrucosa Number Single Multiple
Cutis, Lupus Vulgaris)
•• Endogenous (Scrofuloderma, Orificial TB, Lupus
Vulgaris)
•• Tuberculids (Lichen scrofulosorum,
Papulonecrotic Tuberculid, Bazin disease)

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Cerebellum Quick Revision Notes

Lupus Vulgaris •• One margins EXTENDS, other margin SCARS,

Asymmetrical lesion .
•• Most common form of cutaneous Tuberculosis
in adultsQ
•• Route of spread: Endogenous (Blood spread) >
exogenous
•• Patients CMI (cell mediated immunity) is high,
so, this is paucibacillary (less bacilli) form of
cutaneous TB

Scrofuloderma: AKA (Tubercular

lymphadenitis)
•• MC form of cutaneous Tuberculosis in children
•• CMI is LOW, so Multibacillary status
•• Lesion: red/ violaceous annular infiltrated
plaque •• Mode of spread: Direct extension of infection
to the skin from an underlying Tuberculosis
(Active margins), One margins EXTENDS, other focus (lymph node, bone, joint)
margin SCARS
•• MC focus of infection: Cervical lymph nodes
•• Centre: atrophy & scarring with Peripheral
extension •• MC site: Neck & axilla

•• Sites: face buttocks, & extremities •• C//F: Painless subcutaneous swellings → rupture
into overlying skin → discharging sinuses /
•• Diascopy: test where a glass slide is pressed ulcers / fibrotic scars.
over the lesion
•• Lesion colour changes to Golden brown colour
which are called as apple jelly nodules.

Erythema induratum of Bazin Erythema nodosum

Red & Tender nodules

Lobular panniculitis Septal panniculitis
Posterior aspect of leg Anterior aspect of legQ
Ulcers heal with Scarring No ulcers, Nodules heal without scarring

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Skin

Exogenous Hematogenous spread

Tuberculosis MB Lupus Vulgaris PB
Chancre
TuBerculosis PB Miliary MB
Verrucosa Cutis Tuberculosis &
Gumma
Endogenous Tuberculids –– KOH mount in Pityriasis Versicolor: Short
hyphae + round spores, Giving a Spaghetti &
Scrofuloderma MB Lichen Rarely
Meatball appearanceQ
scrofulosorum seen
Periorificial MB Papulonecrotic
Tuberculosis Bazin disease

Pityriasis versicolor
•• Etiology
–– Malassezia globosa > furfur.
•• Asymptomatic Perifollicular scaly macules seen.
•• Fine/ Branny / Furfuraceous scales
•• Hypopigmented > Hyperpigmented maculesQ
•• Treatment of pityriasis versicolor
Pityriasis versicolor
–– 1st line:
Colour of lesions
–– Azoles like Ketoconazole, Clotrimazole are
the mainstay.Q
–– Terbinafine 1% cream twice daily 2-3 weeks
–– 2nd line: Oral itraconazole 200 mg daily
X 5 days

Hypopigmented macules are seen Mucocutaneous candidiasis

Oral candidiasis
1. White plaques
2. Red plaques

Hyperpigmented lesions

•• Site:
–– Trunk is the most common site.
–– Scaling is not visible -> scratch with nail
results – Scales become prominent.
–– This is Known as Scratch sign/ Besnier sign/ Oral candidiasis white plaques -There are two types
Coup de ongle sign. of Candidiasis
•• Investigations 1. Acute Pseudomembranous Candidiasis (oral thrush)
–– 10% KOH mount →dissolves Keratin →fungal MC
elements seen. •• Lesions can be rubbed off

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Cerebellum Quick Revision Notes

2. Chronic hyperplastic type. Common in smokers

Red Plaques /Atrophic Candidiasis Candidial Balanoposthitis

•• Clinical features:
–– Swelling of glans penis with Burning sensation
–– Prepuce shows multiple Radial fissures.

Acute Chronic
Occurs after taking Denture mouth or Denture
antibiotics hence known as candidiasis
antibiotic sore tongue or
•• Associated with diabetes mellitus
sore mouth

Candidial Intertrigo
•• Intertriginous → Skin fold → sweating / friction →
Candidial ProliferationQ
•• Lesions are red, macerated (soft and wet to touch
plaques & in the vicinity of the plaques there are
satellite pustules.
•• Lesions are red, macerated (soft and wet to touch)
plaques •• Rx → FLUCONAZOLE

Candidial paronychia
•• Wet work / detergents (ICD)
•• Characterized by swelling of nail fold and loss
of cuticle.
•• Treatment: Antifungals + Steroids

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Skin

Dermatophytes Skin Hair Nails Inflammatory / Scarring Alopecia

Trichophyton + + +
Favus
Epidermophyton + NO +
•• Causative organism is T schoenleinii
Microsporum + + NO •• Endemic of Kashmir

Non inflammatory / Non Inflammatory / scarring •• Lesion yellow cup shaped crusts known as scutulaQ
scarring alopecia alopecia
Black dot (Endothrix) Favus
Grey patch (Ectothrix) Kerion

Non inflammatory Tinea capitis

Black dot type Grey patch
•• The fungus goes into •• The fungus is covering
the hair, referred to as the hair (ectothrix).
endothrix & hair shaft •• Lusterless grey hair
breaks with patchy alopecia
Two important species •• Organism causing this Kerion
involved are: Trichophyton is Microsporum canisQ •• Causative organisms are zoophilic fungi
tonsurans, T. Violaceum Q
•• Etiology: T mentagrophytes, verrucosum
•• Lesion: boggy indurated scalp swelling
•• Easily pluckable hair associated with regional
lymphadenopathy
•• Investigation: 10% KOH mount
Rx →Overall drug of choice for T capitis: GriseofulvinQ
•• For T capitis with trichophyton species: Terbinafine

Tinea faciei: Face.

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Cerebellum Quick Revision Notes

Tinea barbae: beard

Tinea Manuum: Involves palmar aspect of the hands Onychomycoses

•• Causes → Dermatophytes / Non dermatophytes
/ Candida
•• Dermatophytes → Tinea Unguium.
•• Can be identified by yellow discoloration of the
nail plate and
•• Presence of subungual hyperkeratosis & Nail
Tinea Corporis: involves glabrous/ non-hairy skin tunnelling
(Annular lesion)
Differential Diagnosis;
•• Etiology
–– T. mentagrophytes & T. rubrum. Onychomycosis Psoriasis
Common features Thick, Yellow nails & subungual
•• Lesion
Hyperkeratosis.
–– Annular plaque with central clearing and Nail pitting Pits absent Present
–– Peripheral red raised scaly margins •• DLSO = Distal Lateral Subungual OM (MC)
–– Associated with itching.Q •• PSO = Proximal SO
•• SWO = Subungual White OM
•• TDO = Total Dystrophic OM

Tinea Cruris: Involves groin / Jock itch/ dhobi itch /

eczema marginatum

T. Incognito Steroid modified Tinea

•• Anti-inflammatory Property of steroids
decreases the itchingQ
•• Active margin of lesion is lost and striae is
formed.
Tinea Pedis Aka Athlete’s foot
•• Leads to extensive atypical disease with diffuse
•• Most common site is 4th toe webspace
scaling.
•• Most common organism is T. rubrumQ

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Skin

•• Amorolfine 5%.
•• Tavaborole -5%
•• Ciclopirox-olamine 8%
•• Efinaconazole 10%

Systemic Treatment Of Dermatophytic

Onychomycosis
•• Terbinafine: 250 mg OD
–– Finger nail: 6 weeks
Treatment of dermatophytosis:
–– Toe nails: 12 weeks
•• Azoles → inhibit 14-alpha demethylase.
•• Itraconazole : 200mg BD / week
•• Allylamines → Terbinafine.
–– Finger nail : 2 months
(Duration: 4-6 weeks)
–– Toe nail : 3 months
Treatment Of Onychomycosis: (CEAT)
•• Nail lacquers

Subcutaneous Mycoses (Implantation Mycoses)

Sporotrichosis aka Rose gardener’s Chromoblastomycosis (verrucous Mycetoma
disease dermatitis)Q

Etiology Pigmented / dematiaceous fungi •• Chronic suppurative

•• Sporothrix schenckii. Q Etiology granulomatous disease which
•• Dimorphic fungus ie. Mold at 25c and •• Fonsecaea Pedrosoi. could be Either fungal or
yeast at 37C. •• Fonsecaea compactum bacterial in origin.

•• Thorn prick→ Nodulo-ulcerative •• Phialophora verrucosum

lesion →Lymphocutaneous •• Agricultural workers → vegetative
Proximal Extension → Linear lesions → Material trauma
Sporotrichoid pattern •• Cauliflower like nodules/masses with
black dots on the surface of the
lesion.

HPE: Asteroid body with central •• - Investigations

basophilic yeast with radiating 10% KOH mount: Brown, round, thick-
eosinophilic material is seen Walled bodies called as Copper penny/
medlar/ sclerotic Bodies, diagnostic of
chromoblastomycosis

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Cerebellum Quick Revision Notes

Sporotrichosis aka Rose gardener’s Chromoblastomycosis (verrucous Mycetoma

disease dermatitis) Q

Treatment → Cutaneous: Itraconazole Treatment → Itraconazole Treatment →

Actinomycetoma: Modified
Welsh regimen
•• C otrimoxazole
•• A mikacin+
•• R ifampicin
Eumycetoma: Antifungals

Actinomycetoma Eumycetoma •• Pleomorphic rash - Different stages of rash

coexist together simultaneously, this is because
Bacteria Fungi
lesions appear as Crops
Actinomadura Madurae, Madurella Mycetomatis,
Nocardia Brasiliensis, Madurella grisea •• Stages → Macules→ papules → vesicles →
pustules → scabbing
Streptomyces Somaliensis
Pale granulesQ Black granulesQ Herpes Zoster (Shingles)
•• Reactivation of VZV: Acute cutaneous
HSV-1 Herpes Simplex Virus segmental eruption
•• Orolabial herpes/ fever blister / cold sores
2. Phases:
•• Lesions: multiple grouped vesicles near lip
1. pre-eruptive phase: fever, malaise, excruciating
margin
burning pain within the dermatome before the
•• Orolabial herpes Rash appears.
•• Treatment: Tab acyclovir 400 mg TDS X 5 days 2. Eruptive phase:
•• Unilateral
•• Dermatomal (thoracic dermatome)
•• Painful grouped vesicles on erythematous base.

Varicella Zoster Virus

•• The primary infection is varicella / chickenpox
•• On reactivation it can cause herpes zoster
•• Incubation Period: 14-17 days
•• Infectious period: 2 days before the rash
develops till all the lesions have crusted Complications;
•• Lesions: Dew drops on rose petal appearance •• Post herpetic neuralgia is most disabling
complication,Q
•• Distribution of lesions: predominantly over
trunk •• patient presents with allodynia

Treatment of Herpes Zoster / Varicella:

•• →Tab Acyclovir 800mg 1-1-1-1-1X 7 days
•• →Tab Valacyclovir 1g I-1-1 x 7 days

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Skin

Herpes zoster Herpes Zoster Oticus/ HHV-5: Cytomegalovirus (CMV)

Opthalmicus Ramsay Hunt syndromeQ •• It produces infectious mononucleosis like illness
Ophthalmic division It involves the Geniculate
•• Owl eye inclusion bodies seen
of Trigeminal Nerve ganglion
(V), usually the Frontal
branch
Hutchinson sign of the 3 important features of
nose: Ramsay Hunt syndrome Are:
Tip or side of nose & Ipsilateral 7th nerve palsy
cornea are Otalgia
Supplied by the Vesicles over the external
Nasociliary nerve. ear.

Infectious Mononucleosis/Glandular fever/

HHV-7
Kissing Disease •• Pityriasis rosea (pityriasis Scaling rosea Rose
like rash).
Triad of infectious mononucleosis: 3 Ps
•• First lesion is called the herald patch.
Post cervical lymphadenopathy, pharyngitis, →collarette of scale
Pyrexia
•• Along the lines of Langer: Christmas tree
•• Pharyngitis → Ampicillin → Ampicillin induced pattern
maculo-papular rash.
HHV-8
•• Kaposi sarcoma.
•• Lymphoproliferative diseases (multicentric
Castleman disease, primary effusion lymphoma)Q
•• Seen associated with immunocompromised
individuals
•• Multifocal vascular tumor (Lymph nodes may be
involved)Q

Oral Hairy Leucoplakia (OHL)

•• In HIV infected patient (with EBV), white
corrugated/ridge-like plaque over lateral
border of tongue that cannot be rubbed off is
called as OHL.Q
•• Patient presents with purplish nodules and
plaques.
•• MC site: Extremities

Parvovirus B19 infections / 5th disease

•• Parvovirus B19 is a DNA virus.

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Cerebellum Quick Revision Notes

2. Sexually active adults

3. Immunosuppressed persons
•• Children: Pearly white, dome shaped umbilicated
papule, generally over the face.Q

•• It causes 5th disease or Erythema infectiosum

•• Face→ malar erythematous rash with relative
sparing of the mouth or circumoral sparing
•• Pseudo Koebner’s phenomenon, defined as
•• Slapped cheek Appearance.Q
the appearance of morphologically similar
•• Bridge of the nose is not involved here (Vs SLE) lesions along line of trauma (scratching) due to
•• Maculopapular rash →reticulated lacy exanthem autoinoculation, is also seen in Viral warts.
→net Like rash on the trunk •• Sexually active adults -Site → anogenital region

Investigations
•• Generally, no investigations required
•• In giant molluscum, HPE will show
•• Eosinophilic intra cytoplasmic Inclusion bodies:
Henderson Paterson Bodies within the cellsQ

Henderson Patterson bodies

Treatment → Usually, it is self-limiting and will

disappear by itself. Thus,
There is no need for treatment
•• Physical methods
Molluscum Contagiosum
–– Curettage
•• Causative agents: Pox virus
–– Cryotherapy: Liquid nitrogen is used at a
•• Virus: Molluscum Contagiosum, Virus (MCV). temperature of -196 C, where the lesion is
•• MCV-l → Children →Face Frozen.

•• MCV-2 → Adults → Genitals •• Topicals

•• Transmission: Skin to skin contact. –– Trichloroacetic acid

•• Disease patterns: (3 important patterns) –– Potassium hydroxide KOH.

1. Children –– Imiquimod → Toll like receptor-7 (TLR-7

agonist).
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Skin

Warts Classification Treatment of HPV Warts

•• Genital/ condyloma Acuminata •• Topicals: Keratolytic agents they act by

removing the stratum corneum eg Salicylic acid,
•• Non genital
•• Physical modalities: Electrocautery,
•• Verruca vulgaris Verruca: Rough or uneven Cryotherapy
surface, vulgaris Most common).
•• Deep plantar wart – HPV1 Enteroviral Infections Classification
•• Superficial plantar wart – HPV2Q •• Hand foot mouth Disease

•• Verruca Plana wart – HPV3 •• Herpangina

Common wart – 4 It is the most common non-genital

wartsQ
•• Epidermo Dysplasia verruciformis – 5, 8
•• Larynx – 6
•• Butcher – 7

•• Hand foot mouth Disease

•• Etiology
•• Etiology: Coxsackie A6, Enterovirus 71Q
•• Cutaneous warts: HPV 2, 4, 27.
•• Lesions: Papulovesicular lesions.
•• Transmission: Skin to skin contact
•• Sites: Present on palms, soles oral cavity and
the buttocks.
Migratory Infective Skin Lesions
Cutaneous larva migrans Larva currens

•• Caninum. •• Produced by Strongyloides stercoralis (racing

•• History of walking barefoot (beach) larva)Q
–– Soil containing active forms of the •• Speed: 5-15cm/hour,
•• Lesions: urticaria like lesions
–– Larva in animal excreta → Enters skin.
•• Lesion: Pruritic, elevated Erythematous serpiginous tract.
•• Speed 1-2cm/dayQ

Treatment: Albendazole, ivermectin. DOC: Ivermectin

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Cerebellum Quick Revision Notes

Ectoparasitic Infestations
•• Scabies
•• Pediculosis

Scabies
•• Etiology: Itch mite → Sarcoptes scabei var
hominis
•• Number of mites in a patient: 10-15 mites
per patient, in a Person with normal immunity
(Norwegian scabies /Crusted scabies)

C/F;
1. History Of nocturnal pruritus.
2. History of similar complaints among the family
members/
•• Close contacts are to be assessed. Distribution Of Scabies:
•• Characteristic features: Circle of Hebra
–– Excoriated papules seen predominantly over •• Face Spared in adults: (due to increased sebum
the web spaces. activity that repels mites)Q
–– Vesicles, Nodules also can occur (infantile
Investigations:
scabies)
KOH mount of skin scrapping-
•• The mite is identified by
–– Two anterior pairs of legs.
–– TWO posterior pairs of legs.
–– Eggs: - Faecal pellets (Scybala

•• Examination findings
–– Web spaces & genitalia: Burrows
Pathognomonic lesions are seen.Q
–– Greyish white Serpiginous tunnels in the
stratum corneum in which mite resides
–– Absent in animal scabies.

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Skin

Specific management →
•• Topical drugs: Permethrin 5% creamQ
•• Systemic drugs: Ivermectin

Special Forms Of Scabies

•• Infantile scabies
•• Norwegian Scabies
•• Nodular scabies
Adult scabies Infantile scabies
Face Spared Involved
Palms & soles Spared Involved
Vesicular lesions Absent Present
on palms & soles
Treatment Below neck Apply over face also
Permethrin
application

Scabies Norwegian/Crusted scabies

Severity: - Most severe form (Erythroderma)Q
Predisposed individuals Infects anyone Immunocompromised: HIV, Malignancy
Sensory loss: Leprosy
Psychiatric patients: No proper personal hygiene
Pruritus: + Pruritus is minimal as the immunity is low/ sensations are
absent
Number of mites 10-15mites/ person MILLIONS

Hyperkeratotic plaques - PresentQ

Erythroderma - Possible

Rx 5% Permethrin or •• Ivermectin: 2 doses, 2 weeks apart + Permethrin 5%

Ivermectin multiple applications
•• Keratolytic agent to remove the crust: salicylic acid Helps
in better drug penetration of permethrin.

Nodular scabies
Norwegian scabies

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Cerebellum Quick Revision Notes

Pediculosis
Head lice / Pediculosis capitis Body lice / Pediculosis corporis / Pubic lice /Pthirus pubis
Vagabonds disease
C/F Girl child presents with regional Scratching results in Morbus Maculae ceruleae (blue macule is seen
LAP errorum (excoriation marks at the site of its bite)Q
Itching+ Morbus errorum STI
H/O contact +

Rx Application of permethrin 1% Disinfection of clothes > Application Shaving of pubic hair

of permethrin 1% Application of permethrin 1%
Contact tracing & treatment

Human Lice Old WORld New world

L. majOr & L. trOpica L. mexicana
Delhi bOil/Oriental sore Gum tree harvester’s
ulcer/Chicler ulcer.
NOdulO ulcerative lesion Ulcer affecting the
with crusting in the center cartilage of the ear.
Ulcer margins are raised:
VOlcanO sign.

Leishmaniasis
•• Transmitted by Sand fly
1. Cutaneous Leishmaniasis: Old world Cutaneous
Leishmaniasis, New world Cutaneous Leishmaniasis
2. Mucocutaneous Leishmaniasis Visceral Leishmaniasis Aka Kala-AzarQ
3. Visceral Leishmaniasis •• Caused by L. donovani.
4. Post kala Azar dermal Leishmaniasis •• Presents with fever and hepatosplenomegaly

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Skin

Post Kala-Azar Dermal Leishmaniasis (Pkdl)

•• Visceral leishmaniasis AKA Kala-azar.
↓
Partially or inadequately treated
•• Common in Bihar.
•• Treatment → For Kala azar: Liposomal
Amphotericin BQ
•• For PKDL: Miltefosine

Leprosy/ Hansen’s disease

•• Chronic infectious granulomatous disorder.
Skin → Macrophages & Nerves → Schwann cells
→Granulomas

Etiology:
•• Mycobacterium leprae
•• Mycobacterium lepromatosis

Nerves
•• First modality to be lost: Sensory
•• First sensory modality to be lost: Temperature
•• History of prolonged fever may indicate past
(hot/cold differentiation)Q.
history of visceral Leishmaniasis.
•• NOT TOUCH
Lesions
•• Mc peripheral nerve involved = Ulnar > Posterior
•• Face: Infiltrated nodules.
tibial
•• Trunk: Hypopigmented macules
•• MC cranial nerve involved = FacialQ
PKDL Lepromatous
•• Blindness in leprosy is due to Exposure keratitis
leprosy
Trunk: Hypopigmented Hypopigmented
Greater auricular nerve -
macules macules
Face: Infiltrated Infiltrated nodules.
nodules.
Past History + Absent
of Prolonged
fever
Nerve - Present
thickening
Slit skin smear Amastigotes in +ve for AFB Clinical spectrum by Ridley Jopling ‘s classification
Giemsa Stain •• Tuberculoid pole = Good CMI and limited disease
Giemsa stain Leishman -
•• TT: Tuberculoid type.
Donovan bodies
LD bodies •• BT: Borderline tuberculoid
•• Lab diagnosis: Culture media for leishmania: •• BB: Borderline Borderline
Novy MacNeal Nicolle
•• BL: Borderline leprosy.

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Cerebellum Quick Revision Notes

•• LL: Lepromatous leprosy. •• I mmunologic CMI, Lepromin test.

•• Lepromatous pole = Poor CMI and disseminated •• C linical Skin lesions, Nerve involvement
disease
•• H istopathologic : Granuloma, Status of
Basis for Ridley Jopling ‘s classificationQ macrophages.
•• B acteriological Acid fast bacilli, Slit skin Clinical features and types of leprosy according to
smear. RJ

Tuberculoid Leprosy (TT): Borderline Mid Borderline Leprosy (BB) Borderline

Tuberculoid (BT) Lepromatous leprosy
BL
•• No of skin lesions: 1- 3. •• No. of skin •• No of skin lesions: 10 – 30. •• Skin lesions:
•• morphology of lesion: lesions: 3 – 10. •• Morphology of lesions: Numerous,
Annular plaque. •• Each lesion has •• Polymorphic skin lesions → bilateral, and
•• Center of lesion: Clearing well defined geographic map Like appearance. almost symmetrical,
•• Periphery: Well, defined and ill defined tending to
raised margin. margins symmetry

•• Satellite lesions •• Margin of lesion: Dimorphous skin •• Nerve involvement:

are also seen. Lesions seen, hence Known as Bilateral
Dimorphous leprosy. asymmetric Nerve
thickening

Lepromatous Leprosy (LL): Systemic disease → Leonine facies/lion like facies.

internal organs involvement.
•• Diffuse infiltration of the face.
•• Skin lesions: Symmetrical bilateral, Consisting
•• Loss of Eyebrows called as MadarosisQ.
of ill-defined macules, Papulo nodules, diffuse
Infiltration and thickening of skin. •• Glove and stocking peripheral Neuropathy

•• Nerve: Symmetrical bilateral nerve thickenings,

•• Respiratory → Earliest feature of LL: Epistaxis,
nasal crusting,
•• Autonomic Failure → Pedal edemaLate Features
of LL:

Deformities in leprosy
Trophic ulcers:
•• Chronic ulceration in an anaesthetic foot.

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Skin

•• more commonly found at the soles. NLEP National Leprosy Eradication

ProgrammeQ
Cardinal features Paucibacillary Multibacillary
Skin: Hypopigmented 1-5 >6
/ Hypoanaesthetic
patches
Nerves thickened +/- No nerve / 1 >1
Tenderness

Eye deformities: SSS AFB Absent Present

•• Lagophthalmos → exposure keratitis, corneal WHO

ulcers → corneal opacities.
WHO Paucibacillary Multibacillary

DRUGS 3 drugs 3 drugs

DURATION 6 months 12 months

Treatment of Hansen’s disease (WHO

Regimen)Q
Drugs PB MB
•• Ulnar involved – partial claw hand / Ulnar &
Rifampicin 600 mg once a month
median – complete claw hand
Dapsone 100 mg daily
Clofazimine 300 mg once a month
50 mg daily
Duration 6 months 12 months

NLEP Paucibacillary Multibacillary

DRUGS 2 drugs 3 drugs

DURATION 6 months 12 months

HPE;- cell free zone – Grenz zone +
→MB MDT (maroon Kit).
•• Day l: Rifampicin 300 mg x 2, Dapsone l00 mg,
Clofazimine 100 mg x 3,
•• Day 2-28 Clofazimine 50 mg & Dapsone l00 mg.

Leprosy
•• Chronic, infectious granulomas, Acute
inflammation: Lepra reaction

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Cerebellum Quick Revision Notes

Types of Lepra reactionsQ

Type 1 Lepra reaction Type 2 Lepra reaction ENL
(Erythema nodosum Leprosum)
Hypersensitivity / Pathogenesis Type IV Type III NEW RED ENL
Leprosy type Borderline BT BB BL Lepromatous pole LL, BL
Clinical features •• Preexisting lesions red swollen tender •• New lesions seen
•• No new lesions •• Red tender & evanescent nodules →
ENL

•• Arthritis
•• Orchitis
•• Iridocyclitis
Nerves Neuritis ++++ +/-
Incision & Drainage
DOC Steroids
Prednisolone
1 mg/kg/wt. → Tapered
Thalidomide Not used Gold standard,
But not DOC, expensive, Teratogenic

Treatment Of Lepra Reactions –– Age >2years

•• General management –– Close contact for >20hrs per week

•• Pregnant or non-pregnant: Continue MDT –– Sharing same clothes, towels

•• 95% cases resolve spontaneously after bacillus
Vaccines In Leprosy:
exposure
MIP strain → mycobacterium indicus pranii.
•• Indeterminate leprosy resolves more
Utility spontaneously than Tuberculoid

•• Administered to the contacts of leprosy patient. Anogenital Warts / Condyloma

•• Given along with MDT (immunotherapy) - Faster Acuminata
Clearance of bacilli. •• HPV induced skin proliferations involving the
anogenital region
Single Dose Rifampicin (Sdr)
•• Etiology: HPV- 6>11 (low risk HPVs)Q
•• Purpose: Chemoprophylaxis for contacts of
leprosy patients. •• High risk HPV 16,18Q
•• Dosage 600 mg (adults) •• Clinical features
ChemoprophylaxisQ –– Asymptomatic pointed, fleshy, pink papules
and plaques
•• Requirements / conditions to be met to
administer: –– Cauliflower like hypertrophic masses
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Skin

Investigations- Histopathology
•• Biopsy → Koilocyte cells (squamous epithelial
cell With central Hyperchromatic nucleus & a
perinuclear halo)Q.

Sites
•• Men: Coronal sulcus, frenulum
•• Women: Posterior fourchette

Treatment
Non pregnant Pregnant woman

•• Imiquimod: lmmune response modifier. •• Cryotherapy (treatment of choice): Liquid nitrogen

•• Toll like receptor 7 agonist → activates immunity •• (-196 degree Celsius) ->Freezes wart -> necrosisQ
of patient → Clearance of warts

•• Podophyllin resin Binds to mitotic spindle

→metaphase Arrest → Necrosis of warts •• Trichloroacetic acid (TCA) 70-80% - Coagulation of
Proteins (chemical cauterization)Q

2 Vaginal discharge.
Genital Discharge Disease
Urethral Discharge Disease Urethritis:
Two types of discharges
1 Urethral discharge. •• Inflammation of urethra Characterized by
urethral Discharge and dysuria
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Cerebellum Quick Revision Notes

Gonococcal urethritis Non gonococcal urethritis

Etiology: Neisseria gonorrhea Chlamydia trachomatis (D-K)
Incubation period: 2-5 days 7-14 days
Constitutional symptoms Very severe Absent
Dysuria: Severe (presents early) Variable (mild)
Discharge: Profuse purulent urethral discharge Scanty, mucoid urethral discharge

Gram stain: Gram negative intra cellular diplococci within Only PMNLs in absence of
PMNL (Polymorpho nuclear leucocytes) organisms

Treatment: CDC 2021 criteria: Doxycycline 100 mg BD x 7 days

Inj: ceftriaxone IM stat or
< 150kg: 500 mg Tab azithromycin 1gm stat
>150 kg: 1gm
(if chlamydia is not excluded)
+
Doxycycline 100 mg BD x 7 days
DUAL Therapy

Urethral discharge / Cervicitis / Anorectal •• Tab cefixime 400 mg/ stat (gonococci)
discharge •• Tab Azithromycin 1gm stat
•• Not Doxycycline 100 mg BD x 7 days, to achieve
COMPLIANCE

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Skin

Vaginal Discharge Syndrome

Candidiasis Trichomoniasis Bacterial vaginosis
Etiology: Candida albicans Trichomonas vaginalis (NG Urethritis) Altered vaginal microflora
Flagellate protozoa (NOT STD)
Imbalance:
1. Lactobacilli reduced
2. Anaerobes (Gardnerella
mobiluncus increased
Discharge Curdy white vaginal Greenish yellow frothy vaginal Homogenous white adherent
discharge discharge discharge

Classical pointers Multiple punctate haemorrhages seen Amsel’s criteria

on cervix→ strawberry cervix (colpitis
macularis

Bacterial Vaginosis Amsel’s Criteria: Vaginal discharge

Candidiasis Trichomoniasis Bacterial •• Tab Fluconazole 150 mg stat (for candidiasis)

vaginosis
•• Tab Secnidazole 1gm 2 stat (for Bacterial vaginosis,
Wet mount Clue cells
Trichomoniasis)
>20%
Treatment Fluconazole Metronidazole Metronidazole

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Cerebellum Quick Revision Notes

Clinical condition Kit to be Drugs included Image

prescribed
Urethral or anorectal or KIT 1 : Grey Tab Azithromycin 1 g (1 tab)
cervical discharge Tab Cefixime 400 mg (1 tab)

Vaginal discharge KIT 2 : Green Tab Secnidazole 2 g (1 tab)

(Vaginitis) Tab Fluconazole 150 mg (1 tab)

Genital ulcer disease KIT 3 : White Inj. Benzathine penicillin 2.4 MU (1 vial) +
(Non-herpitic) Tab Azithromycin 1 g (Kit also contains 10
mL disposable syringe + 21 gauge needle +
1 vial of 10 mL sterile water
Genital ulcer disease KIT 4 : Blue Tab Dixycycline 100 mg (1 tab BD for 14
(nonherpetic) in patient days) Tab
allergic to penicillin Azithromycin 1 g × 1 tab

Genital ulcer disease KIT 5 : Red Tab Acyclovir 400 mg × 1 tab TDS × 7
(Herpetic) days

Lower abdominal pain KIT 6 : Yellow Tab Cefixime 400 mg × 1 tab

(Pelvic inflammatory Tab Metronidazole 400 mg × (1 BD 14
disease) days)

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Skin

Inguinal bubo KIT 6 : Black Tab Doxycycline 100 mg (1 BD × 21 days)

Tab Azithromycin 1 g × 1 tab

Syphilis Early < 2 yrs Late > 2 years

•• Causative agent: Treponema pallidum Hepato-splenomegaly

Trepo: Twist.
Nema: Thread.
•• Congenital Syphilis
•• Acquired Syphilis
Congenital Syphilis
•• Infected Mother →BLOOD → fetus in-vitro
•• Early congenital Syphilis first 2 Years of life.
•• Late congenital Syphilis >2 years. Investigation of Choice

CONG Syphilis (TRIAD) Congenital syphilis

•• VDRL Titres of Infant should be four times
Early < 2 yrs Late > 2 years
more than VDRL Titres of mother.
. Snuffles: persistent Hutchinson’s triadQ
rhinitis 1. Hutchinson’s teeth Acquired Syphilis
2. HSM 2. Interstitial keratitis Mode of acquisition: Sexual transmission / Blood
3. Syphilitic pemphigus: 3. SNHL transfusion.
Vesiculobullous lesions Saddle nose, periostitis
palms & soles Primary Syphilis
Wimberger sign: •• Incubation period: 9 – 90 days
bilateral erosion of
•• Secondary lesion: Genital ulcer/ Hard chancre
medial aspect of upper
tibia (SPECIFIC) Hard Chancre
Snuffles: Persistent •• Single
Rhinitis •• Clean based
•• Indurated
•• Pain LESS

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Cerebellum Quick Revision Notes

Primary Syphilis Chancroid Soft Chancre

Hard Chancre / Sore
•• Single •• Multiple
•• Clean based •• Necrotic based
•• Indurated •• Non indurated ( soft )
•• Non tender •• Tender

•• No bleeding •• Bleeds on touch

Treatment of Syphilis
Inguinal lymph nodes
Early Syphilis Late syphilis
•• Bilaterally enlarged.
Primary Syphilis Late latent Syphilis
•• PainLESS Secondary Syphilis Tertiary Syphilis
•• Rubbery/ Shotty consistency Early latent Syphilis
Single dose 3 doses (once Weekly)
Investigation Of Choice
Except in neurosyphilis

Neurosyphilis
•• Aqueous crystalline penicillin
•• Dosage: 18-24 million units per day.
•• Route: Intravenous
•• Duration: 10-14 days.
•• Dark ground microscopy → corkscrew motility
Allergic to Penicillin
Secondary Syphilis
Non-Pregnant Pregnant
•• Symptoms Constitutional Symptoms: (Fever/
Early Syphilis Doxycycline 100 Desensitisation followed
Arthralgia, myalgia)
mg BD for 2 wks by Penicillin.
•• Generalized Lymphadenopathy. Late Syphilis : Doxycycline 100 We cannot take risk,
•• Characteristic lymph node Enlarged in secondary mg BD for 4 wks penicillin is best to
syphilis →Epitrochlear group of nodesQ prevent transmission of
syp from mom to child

Chancroid
•• Org: Hemophilus ducreyi
•• IP: 2-5 days
•• Both ulcer and Lymphadenopathy are PAINFUL
(Hemophilus DO CRY)
•• Symmetric, Polymorphous, Non pruritic
Primary Syphilis Chancroid Soft Chancre
•• ALL RASHES POSSIBLE (except vesicles and
Hard Chancre / Sore
bullae)Q.
•• Single •• Multiple
•• Examination of Palms & Soles. (Hyper-pigmented •• Clean based •• Necrotic based
macules )
•• Indurated •• Non indurated (soft)
•• Mucosal Lesions •• Non tender •• Tender
•• Condyloma lata •• No bleeding •• Bleeds on touch

–– Lata: means flat topped.

–– Moist papules and plaques,

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Skin

•• Grouped vesicles → Rupture → Ulcers

Lymph Nodes

Lymph Nodes:
•• Bilateral enlarged tender
•• Bubo: enlarged pus filled inguinal lymph node
unilateral •• NO BUBO

•• Tenderness +ve Investigation

•• Concomitant ulcer + •• Tzanck smear: Cytodiagnostic test: Acantholytic

cells & MNGCs
Genital ulcer disease (Herpetic)

Chancroid LGV
Inguinal Bubo + +
Concomitant ulcer + -
•• Tab Acyclovir 400 mg TID for 7 days
Investigation: Gram staining
Lymphogranuloma Venereum
•• Gram negative coccobacilli
•• Org: C Trachomatis (L123)
•• In long parallel strands
•• IP: 3-30 days
•• Railroad track /School of fish
•• 1° Stage: Genital ulcer Painless transient
–– Goes unnoticed by patients
Genital ulcer disease NGU
(non gonococcal ulcer)
C Trachomatis L1 L2 L3 Bubo: Lymph node involved
(LGV) Lymphatics
affinity +ve
Transient genital ulcer -
Treatment +ve
•• T Azithromycin (Macrolides) 1gm statQ Bubo: Lymph node -
involved
Genital Herpes
•• 2° Stage / Inguinal stage
•• Organism: HSV 2 > 1
–– Bubo Enlarged tender
•• PAINFUL Ulcer & LAP (Herpes = PISSED OFF)Q
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Cerebellum Quick Revision Notes

–– LNs U/L→ 2/3rd B/L → 1/3rd

–– No concomitant ulcer
–– Groove sign of Greenblatt
–– Enlarged lymph nodes above & below inguinal
ligament

•• Tab azithromycin 1gm stat (chancroid)

•• Tab Doxycycline 100 mg BD for 3 weeks (LGV)

Donovanosis Granuloma Inguinale /

Venereum
(Not LEISHMANIA DONOVANI)
BUBO Chancroid LGV
Ulcer: Concomitant Absent •• Org: Calymmatobacter / Klebsiella granulomatis
ulcer +ve •• IP: 8-80 days
Inguinal Lymph Unilateral U/L - 2/3rd •• NO pain in Ulcer & NO LAP (do NO vanosis = 2
nodes: B/L - 1/3rd NOs )
•• 3° Stage (Deformities) Genital Ulcer
–– C Trachomatis L1 L2 L3 → obstruction •• Beefy red Hard Painless ulcerQ
& destruction of genital lymphatics →
Deformities •• Exuberant Granulation tissue
•• Bleeds on touch
•• MALE genitalia Female: Esthiomene
Saxophone penis. (Genital elephantiasis +
Chronic ulceration)

Investigation Lymph Nodes: Absent

•• NAAT – Nucleic acid amplification test Q
•• PseuDO Bubo (subcutaneous nodules)
Treatment •• PseuDO Grooves sign
•• Doxycycline 100 mg BD x 3 weeks Q
•• PseuDO Elephantiasis
Inguinal Bubo (enlarged + pus filled lymph node)
Investigation
•• Crush tissue smear: (Giemsa stain) – Pund cell
Mononuclear cell→inside the cell→ intracellular
Donovan bodies (closed safety pin appearance)
bipolar condensation of chromatinQ

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Skin

Treatment →
•• Tab Azithro 1gm per week or
•• CDC 2021 guidelines Tab Azithro 500 mg
daily→3 weeks / till ulcer heals
Approach to a GUD Question

Genital ulcer Inguinal lymph nodes

•• Shuster’s Sign;- Scarring of concha

•• Scarring alopecia
Autoimmune Connective Tissue
Systemic LE
Disorders
•• Malar rash (Acute cutaneous LE)
•• Lupus erythematosus,
•• Erythema over malar area and bridge of nose.
•• Dermatomyositis,
•• Nasolabial folds spared
•• Scleroderma
•• Differential diagnosis: RosaceaQ
Lupus Erythematosus (LE)
•• Spectrum: DLE -------- CLE (Skin involvement)
Discoid LE / /Chronic Cutaneous LE
•• Important sites: Face, scalp, Ears. (Sun exposed
areas)
•• Discoid plaque: Coin shaped Lesion.
•• Central atrophy and scarring
•• Surface → Scaling
Dermatomyositis
•• Peripheral hyperpigmentation
Skin lesions
1. Gottron’s sign: violaceous macular erythema

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Cerebellum Quick Revision Notes

•• Upper back, shoulder: Shawl sign.

2. Gottron’s papules: Violaceous flat top Papules

Scleroderma
Scleroderma classification:
3. Heliotrope Rash
•• Morphoea (localised cutaneous form
Skin & Systems: Systemic sclerosis

•• Localised cutaneous form

Morphoea
4. Mechanic’s hand •• Early : violaceous indurated plaque induration =
•• Hyperkeratotic fissuring, involving tips and thickening
sides of digits: •• Later : Ivory white lesions (healed)
•• En-coup De-sabreQ

Named signs of dermatomyositis

•• Anterior chest: V sign.
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Skin

Limited Diffuse cutaneous

cutaneous SSC SSC
CREST syndrome
Skin thickening Distal to the Distal + Areas
elbow, Knee and Proximal to elbow,
face. Knee and trunk,
involved
Antibodies: Anti centromere Anti Scl 70 or Anti
antibodies Topoisomerase 1
Antibodies

CREST syndrome
•• Perioral radiating furrows
Calcinosis cutis, Raynaud’s phenomenon, Oesophageal
dysmotility, Sclerodactyly, Telangiectasia.

•• Microstomia. (Small aperture of mouth)Q

•• Pigmentation: Depigmentation (white in Colour)

•• Hide bound/ taut skin: unable to Pinch skin
+ Perifollicular pigment retention (black/ brown
in colour) → Salt and pepper Pigmentation

•• Wrinkling reduces + mask like face (Expression

less face)

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Cerebellum Quick Revision Notes

•• Extremities •• Central zone: dusky hue → Intermediate zone:

pale oedema →Peripheral zone: erythema
1 Raynaud’s phenomenon
2. Nail fold capillary telangiectasias Dilated Steven Johnson Syndrome & Toxic Epidermal
blood vessels in Nail bed. Necrolysis = Lyell’s Syndrome
3. Digital ulcers, gangrene Digital scars Definition:
4. Pigmentation: Depigmentation (white in Colour) Acute life threatening severe mucocutaneous adverse
+ Per follicular pigment retention (brown in drug reaction ;SCAR
colour) → Salt and pepper Pigmentation →Drugs implicated: >90%, the Etiology for SJS TEN
Fixed Drug eruption is drugs
•• NSAIDS (oxicam group)
–– Mechanism: Localized Type 4 delayed
hypersensitivity response •• Antiepileptic drugs: Phenytoin, Carbamazepine,
Lamotrigine Sulphonamides
–– Causative Drugs: NSAIDS (MC),
Cotrimoxazole, Tetracyclines •• Allopurinol
–– Always recurs at a fixed location, hence •• Anti retrovirals: Abacavir, Nevirapine
Fixed drug eruption.
→Based on body surface area (BSA):
Morphology Of The Lesion:
•• <10% - Stevens Johnson Syndrome
•• well demarcated circular dusky red plaque with
•• 10-30% -Stevens Johnson Syndrome-Toxic
erythema around margins
Epidermal Necrolysis overlap
•• >30% -Toxic Epidermal Necrolysis

→Cutaneous examination:
•• Skin lesions: atypical target lesion (only 2 zones)
•• Distribution: proximal extremities & trunk
•• Progression: diffuse erythema → bullae →
sheet like epidermal peeling

•• Special feature: lesions always heal with

hyperpigmentation

EMF- Erythema Multiforme

–– Acute immune mediated self-limiting
cytotoxic dermatitis
Etiology:
•• infections: herpes simplex virus I (MC),
•• Special lesion: Target

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Skin

•• Pseudo Nikolsky sign Cutaneous Manifestations of Some

Important Drugs
•• Bleomycin: flagellate dermatitis

•• Minocycline induced pigmentation of acne scars

Nikolsky sign
Type True Pseudo •• Amiodarone induced Facial pigmentation
Mechanism Acantholysis Necrosis of
Keratinocytes
Examples Pemphigus foliaceous SJS & TEN toxic
Pemphigus vulgaris epidermal necrolysis
SSSS

•• Mucosa:
Painful erosions covered by hemorrhagic crusts, which
bleed on peeling

Acanthosis Nigricans
•• Presents as: Hyperpigmented velvety plaques
•• Sites: Neck, axilla.
Treatment: •• Cause Obesity >>Diabetes, drugs & Gl
Adenocarcinoma (rare)Q
•• Identify & stop the offending drug
•• Concept: Obesity → increased insulin Like growth
•• Specific management: cyclosporine
factor→ Stimulate epidermal Keratinocytes.
•• IVIG
•• Life support, Iv Fluids, TPN, Ambience control

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Cerebellum Quick Revision Notes

Necrobiotic Disorders
•• Granuloma annulare.
•• Necrobiosis Lipoidica Diabeticorum

Necrobiotic Granuloma annulare Tinea corporis

disorders
Annular lesions + +
Central clearing Present Present
Complaints Asymptomatic Itchy
Scaling Absent Present

Necrobiosis Lipoidica Diabeticorum Pretibial Myxoedema Aka Thyroid

•• When to suspect: Waxy yellow atrophic plaques
Dermopathy
with Intralesional Telangiectasias & ulceration •• Presentation: Pitting edema -Anterior aspect
over Anterior aspect of leg. of legs
•• Marker: Graves diseaseQ

Hypothyroidism Hyperthyroidism
Skin Dryness warm, moist, sweaty Henoch Schonlein Purpura (HSP) IgA
Generalised myxoedema Pretibial Myxoedema Vasculitis.
Madarosis & Chronic Chronic telogen •• Systemic small vessel vasculitis
telogen effluvium effluvium
–– Skin Palpable purpura seen over legs
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Skin

–– Nephritis, Haematuria. 2.Recurrent Genital Ulcers

–– Arthralgia
–– GI symptoms: Abdominal pain
•• Platelet count: Normal (Non thrombocytopenic
Purpura).

3. EN & Papulopustular lesions

•• Palpable purpura : Symmetrically distributed

Over lower extremities.Q

Behcet’s Disease
•• Multisystem disease
•• HLA-B51Q
•• Variable vessel vasculitis
Minor criteria Major criteria
Recurrent genital Recurrent oral ulcerations
ulcerations (aphthous / herpetiform) 3/
year
Eye lesions (uveitis,
Skin and Nutritional Dermatoses
conjunctivitis, Retinal
vasculitis) Phrynoderma:
Skin lesions (Erythema
•• C/F: Hyperkeratotic Follicular papules.
Nodosum, Acneiform
nodules, Papulopustular •• Site: extensor aspect of knees and elbows
lesions) •• Suspect & Supplement: Essential fatty acids ,
Pathergy test Vit. A, B, C, E (NOT associated with Deficiency)
1. Recurrent oral ulcers

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Cerebellum Quick Revision Notes

Pellagra: Scurvy
•• Deficiency: Niacin (vit B3). Amino acid: •• + Bleeding gums, Corkscrew hair +
Tryptophan precursor
•• Diet Jowar, Maize.
•• Substance abuse: Chronic alcohol intake.
•• Triad:
–– Dermatitis: Photodermatitis (Sun exposed
areas)- Casal’s necklace
–– Diarrhea.
–– Dementia.

Premalignant lesions
Cutaneous horn
•• Hard yellow, brown horn like growth
•• The most common underlying lesions are
seborrheic keratosis Viral warts, actinic
keratosis, Squamous Cell CarcinomaQ.
•• Rx: Excise
Pellagra: Acrodermatitis
enteropathica
Deficiency Niacin (vit B3). Zinc absorption
SLC39A4 AR
Diet Jowar, Maize, Weaning of child
Alcohol from Breast milk
Dermatitis Photodermatitis Periorificial and
Casal’s necklace acral dermatitis
Diarrhea + +
Dementia Alopecia
Treatment lifelong zinc
supplementation Mycosis Fungoides
•• Treatment lifelong zinc supplementation Q
•• Type Non-Hodgkin’s lymphoma.
•• CD4 T cell proliferation under influence of
environmental factors or infection in genetically
predisposed individuals
•• Course: Indolent (slow progression)
•• Stages:
–– Patch (flat lesion)

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Skin

–– Tumour (nodular Lesion)

–– Plaque (elevated lesion) Sezary Syndrome

Triad: (SLE)
1. Circulating Sezary cells (atypical mononuclear cells)
>20% of Total lymphocyte Count or 1000 X 10 power
9/L
2. Generalized lymphadenopathy
3. Erythroderma (4th stage of mycosis fungoides)Q

Basal Cell Carcinoma (Bcc)

–– Erythroderma. (>90% surface area of body •• M/C site: Above the line joining the angle of the
has erythema +- scaling) mouth to Lobule of the ear. (Inner canthi)
•• M/C type: Noduloulcerative type – Translucent
nodule with pearly / beaded edges with surface
telangiectasia → undergoes central necrosis ->
Rodent ulcer with rolled out edgesQ
•• Histology: Palisading granulomaQ

•• Histopathology:
–– Epidermotropism: Migration of Atypical T
lymphocytes present in dermis to epidermisQ
–– Pautrier’s microabscess: Collection of
migrated T cells in epidermisQ
–– Sezary cells: Atypical T lymphocytes with
cerebriform nucleiQ

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Cerebellum Quick Revision Notes

Type
•• Superficial spreading: Most common type & MC
type in pre existing Mole / NevusQ
•• Nodular: Most aggressive type
•• Lentigo malignant: MC in elderly, has Best
prognosis
•• Acral lentiginous: MC type in dark skinned
Malignant Melanoma individuals
•• Etiology: actinic damage in genetically
susceptible individual
•• Risk factors: UV rays, Giant CMN, Xeroderma
PigmentosaQ
•• Pathogenesis: CDKN2A gene (Cyclin Dependent
Kinase inhibitor 2A)

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Skin

•• Prognosis
–– Breslow’s method: distance from granular cell layer deep down up to melanoma cellQ
–– Better indicator compared to Clark’s method.
Sweets syndrome / Pyoderma gangrenosum
Acute Febrile Neutrophilic Dermatoses (AFND)
Etiology •• Infections. •• Rheumatoid arthritis (extra-articular
•• Pregnancy manifestation).
•• Hematologic malignancies •• IBD (extra-intestinal manifestation) :
•• AML UC & Crohn’s Disease.Q
•• Leukaemia’s
Clinical features •• Fever. •• Rapidly progressive, painful, cutaneous
•• Abrupt onset of tender ulcer with an undermined edge &
•• Red papules & plaques & Pseudovesicles seen violaceous hueQ
•• Over Face, chest, trunk.

Cutis marmorata Erythema Ab Igne

Meaning: •• Cutis = skin, Marmorata = Marbling •• Igne = Ignition = HEAT
Clinical •• Physiologic vascular response to cold in Neonates •• Lesions over thigh due to hot air from
features •• Reticular (network-like) symmetric marbling laptop
•• Trunk, extremities •• Red reticulate pattern over skin is seen
under constant exposure to heat
Treatment Warming the child Avoid excess heat exposure

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Cerebellum Quick Revision Notes

Dermatitis Artefacta / Factitial

DermatitisQ
(induced by deliberate human action with or without
intention to produce a lesion or disease)
•• psycho cutaneous disorder
•• Self-inflicted injuries → Bizarre lesions
abruptly & repeatedly (inaccessible areas
spared)
•• Do not fit into any disease pattern
Triad:
•• part of an attention seeking behaviour, also
seen in prisoners & hysteria patients •• Atopic dermatitis
•• Icthyosis linearis circumflexa
•• Trichorrhexis invaginata (“bamboo hair”) (hair
Shaft defect)
•• Distal shaft (“ball”) into proximal shaft
(“socket”)

•• Hollow history i.e. sudden appearance of Wiskott Aldrich Syndrome (XLR)Q

complete lesions without prodrome, lack of (Trick; Wiskott Al Drink Syndrome water)
history of progression of lesions, strenuous
• W Wasp gene mutation
denial by the patient of inflicting the lesions
and patient can forecast the site and timing of • A APCs defective
lesions.
• T Thrombocytopenia
•• Patient appears indifferent towards her disease
• E Eczema/Atopic Dermatitis like
- ‘la belle indifference.
• R Recurrent Infections
•• Thus the visible symptoms of dermatitis
artefacta serve as a non verbal communication
Xeroderma Pigmentosum (XP)
- a ‘cry for attention and help’ from a patient
incapable of meaningful verbal communication. Defect in Nucleotide excision:Q
•• Accumulation of damaged DNA.
Netherton Syndrome
•• Genomic instability
•• SPINK5 gene (encodes serine protease
inhibitor) •• Carcinogenesis (Basal cell carcinoma Squamous
cell carcinoma, MDS, AML ALL)

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 Max Discount Code: CERMEDX990
79
Skin

•• Continuous exposure to sunlight.

•• Sunburn: Photosensitive
•• Photoaging
•• Skin becomes dry and it is called as xeroderma

Incontinentia Pigmenti
•• Genetic ectodermal dysplasia involving skin,
CNS, eyes, teeth
–– X linked dominant.Q Affects females,
Miscarriage of affected male conceptuses
seen
Features
•• Follows Blaschko Lines
Clinical phases
•• Vesicular phase: vesicles along Blaschko lines.
•• Verrucous phase: Rough surface called verrucous Aplasia cutis
•• Hyperpigmented phase •• Congenital absence of skin, with or without the
absence of underlying structures such as bone.
•• Hypo pigmented phase. It most commonly affects the scalp.
•• Due to following drugs -methimazole,
carbimazole and misoprostolQ

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 Max Discount Code: CERMEDX990
80
Cerebellum Quick Revision Notes

Trichothiodystrophy/PIBIDS syndrome •• Ichthyosis

•• Photosensitivity (unlike XP, has NO increased •• Brittle hair (short/sparse on scalp/brows/

skin cancer risk) lashes w/alternating light and dark bands
on polarizing light microscopy (“tiger-tail”
abnormality)
•• Trichoschisis and trichorrhexis nodosa may be
seen
•• Intellectual impairment and ataxia
•• Decreased fertility/hypogonadism
•• Short stature

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