Pearls

1889. Colour of Skin and Fitzpatrick Classification of Skin types

Dermatology
 The color of the skin is a property of the pigment melanin synthesized by Melanocytes.
 Melanocytes are dendritic cells derived from neural crest cells and are present
in Stratum Basale of Epidermis.
 Each melanocyte synthesizes melanin and packs it in cell organelles to
form melanosomes. These melanosomes are transferred through dendritic processes to
36 keratinocytes forming the ‘Epidermal melanin’ unit.

 The main function of Melanin is to impart uniform color to the skin. It also protects

cells from UV light.
 Colour of skin depends on the following:
o Amount of melanin inside melanocytes
o Number and size of melanosomes
o Degree of transfer of melanin into keratinocytes
 It does NOT depend on the number of melanocytes.
  This is because all individuals contain the same number of melanocytes /cm2 of skin
area.

Different shades of skin color in humans is due to 2 factors:

 Difference in number, size and distribution of melanosomes.
 Difference in proportion of Eumelanin and Pheomelanin. 

The two types of melanin are as follows: 

 Eumelanin – true melanin, brown or black pigment present in dark skinned individuals
 Pheomelanin – false melanin, yellow-red pigment present in fair skinned individuals

The different shades have been classified in the Fitzpatrick Classification of Skin type
scale and it is based on tan ability and burn ability of skin.
Type 1 Type 6

Excess Pheomelanin Excess Eumelanin

Always burns Never burns

Never tans Always tans

Maximum Malignant Potential Least malignant potential

Pearls
1880. Cells of the epidermis
Dermatology, Anatomy
Cells of the
Origin and location Characteristic features
epidermis

Present in- All

Layers of
Epidermis (90-95% Rich in the intermediate
Keratino- of all epidermal cells) filaments called keratin that provides mechanical
cytes Derived from- strength to the cell. The keratinocytes in basal layer
Ectoderm divide and generate the upper layers. 

Differentiated in situ

Present in- Stratum

basale Synthesize melanin in granules
called melanosomes that is transferred to
Derived from- keratinocytes of epidermis through elongated
Melano-cytes Neural Crest processes called dendrites. Each melanocyte
Migrate to the transfers melanosomes to 36 keratinocytes. This is
epidermis called as Epidermal melanin unit (36K:1M)   

Present in-Stratum
basale (RETE
RIDGES)
Also known as Touch cells or Haascheiban
Merkel   cells Derived from- cells. They are Type 1 slow adapting touch
Ectoderm/ Neural receptors.  
Crest
Differentiates in-situ

Present in-Stratum They are dendritic Antigen Presenting Cells

spinosum (APCs).   Characterized by presence of rod shaped or
Langerhans Derived from- Bone Tennis Racket shaped granules called Birbeck
cells Marrow granules which are seen on electron microscopy.  
Immunohistochemical Markers
Migrate to Epidermis are CD1a, CD207(Langerin) and S100.   

 
Pearls
1875. Dermoepidermal Junction/Basement Membrane Zone
Dermatology
 The junction between epidermis and dermis is called the basement membrane
zone or dermoepidermal junction and consists of a number of extracellular
macromolecules.
 As many of these components are glycoproteins, the BMZ can be recognized
histologically by staining with PAS stain.
 Ultrastructural examination by electron microscopy shows 2 different layers with
different optical densities
o Lamina Lucida - upper, less electron dense layer
o Lamina Densa - lower, more electron dense layer
 This zone is composed of 3 components : 1. Hemidesmosome 2. Anchoring Filaments
3. Anchoring Fibrils.

1.HEMIDESMOSOME
 Hemidesmosomes are multiprotein complexes that facilitate the stable adhesion of basal
epithelial cells to the underlying basement membrane.
 The intermediate keratin filaments K5/K14 present within the basal keratinocytes attach
to the hemidesmosomes at the base of the cell.
 The major hemidesmosomal Protein is Bullous Pemphigoid Antigen-1 (BPAg1 or
BP230) and this attaches to the transmembrane component protein BPAg2
(BP180) below.
 The other hemidesmosomal protein Plectin is attached to the transmembrane component
protein called as α6β4 integrin below.

2.ANCHORING FILAMENTS/Lamina Lucida and Lamina Densa

 The anchoring filaments form the Lamina Lucida layer.
 Anchoring filaments consist of Laminin5/332 proteins that connect BPAg2 and α6β4
integrin above to Lamina Densa below.
 Lamina Densa consists mainly of type IV Collagen and other proteins like Nidogen.  

3.ANCHORING FIBRILS
 These are ultrastructurally U shaped structures that attach the Lamina Densa above to
the underlying connective tissue below in dermis.
 Type VII Collagen is the major protein in anchoring fibrils.
Blistering disorders in the DEJ/BMZ arise due to defects or antibodies against any of the above
mentioned proteins.
Image: Gene/protein systems within the cutaneous basement membrane zone that can harbour
mutations and result in blistering of the skin in different forms of epidermolysis bullosa (EB).
BP, bullous pemphigoid
Pearls
2213. Benign findings in a newborn
Dermatology, Paediatrics
Erythema toxicum – small white papules on an erythematous base which is usually present on
the face, trunk and extremities. They contain eosinophils and may persist for a week. 

 
Mongolian spots – Slate-blue, demarcated areas of pigmentation seen over the buttocks and
back.
 
Pustular melanosis – Benign lesions seen predominantly in black neonates, contains
neutrophils and is present at birth as vesiculopustular eruption around the chin, neck, back,
extremities, palms and soles.
 
Sebaceous Hyperplasia - White-Yellow papules on nose of a newborn due to hyperplastic
sebaceous glands
 
Milia - Pearly opalescent white, epidermal inclusion cysts usually over the face.

 
Epstein Pearls - nests of epithelial cells, that appear as whitish/yellowish spots on hard palate.
Usually, resolve by 3 months.
 
Cutis Marmorata - Transient lacy reticular vascular pattern of skin caused due to exaggerated
physiologic vasomotor response on exposure to low environmental temperature.
 
Sucking Blisters - Solitary or scattered superficial bullae present at birth on the upper limbs of
infants, which are caused by vigorous sucking on the affected part in-utero.
 
Vaginal bleeding in the newborn at 2–3 days of age and enlargement and secretion of the
breasts in both sexes.
Hymenal tags
Physiological phimosis
Conjunctival hemorrhage
Peeling of skin (especially in post terms)
Pearls
1962. Flowchart for Quick Diagnosis using Tzanck Smear
Results
Dermatology
Pearls
1961. Tzanck Smear in Dermatology
Dermatology
The Tzanck smear, introduced by the Frenchman Tzanck, is a simple to perform, inexpensive
bed side cytological test that aids in the diagnosis of vesicular, pustular and bullous diseases,
in particular herpes.
The sensitivity of the Tzanck smear exceeds 80%, and the specificity 90% when the
investigators are experienced.
Preparation of Tzanck smear:
 Viral infections and Blistering disorders - fresh vesicle or intact blister is de-roofed
and base is scraped 
 Suspected tumors - any crust should be removed from ulcerated tumors, and non-
ulcerated tumors should be incised with a sharp, pointed scalpel and sample is then
obtained with either a blunt scalpel or a small curette
 The smear should preferably be fixed immediately using Formol-Zenker solution since
significant artifacts can result from drying.
 Tzanck smear can be stained by a variety of methods, most commonly by Giemsa
stain. Other stains used are hematoxylin and eosin, Wright, methylene blue,
Papanicolaou and toluidine blue. 

Results in Tzanck Smear:

A typical Tzanck cell is a large round keratinocyte with a hypertrophic nucleus, hazy or absent
nucleoli, and abundant basophilic cytoplasm. The basophilic staining is deeper peripherally on
the cell membrane ("mourning edged" cells) due to the cytoplasm's tendency to get condensed
at the periphery, leading to a perinuclear halo.
Immunobullous Disorders 

Pemphigus Vulgaris Multiple acantholytic cells (Tzanck cells)

Staphylococcal Scalded Skin Syndrome Dyskeratotic acantholytic cells with very

(SSSS) few inflammatory cells

Necrotizing or degenerating basal

Toxic Epidermal Necrolysis(TEN) cells with scattered inflammatory cells and
fibroblasts 

Bullous pemphigoid (BP), Stevens-Johnson

No acantholytic cells ; Many leucocytes
syndrome (SJS) and erosive lichen planus

Cutaneous Infections 
 Herpes simplex, Ballooning degeneration and multinucleated giant cells are
varicella, herpes zoster seen

Diagnostic intracytoplasmic molluscum bodies (Henderson-

Molluscum contagiosum Patterson bodies), the largest known inclusion bodies (30-35
microns)

Vaccinia, orf, milker's Acantholytic squamous keratinocytes , eosinophilic cytoplasmic

nodules and variola inclusion called a "Guarnieri body"

Leishman-Donovan (LD) bodiesgrouped together in a

 Leishmaniasis typical "swarm of bees" fashion, within large macrophages
(Wright's cells)

Dyskeratotic acantholytic cells with abundant neutrophils

Bullous Impetigo
and clusters of coccoid bacteria

Genodermatoses 

Hailey-
Hailey Multiple acantholytic cells; Direct Immunofluorescence Negative
disease

"Corps ronds" are isolated keratinocytes with a round shape and an

Darier's
acidophilic cytoplasm. The corps grains are seen as small, hyaline,
Disease
acidophilic ovoid bodies resembling pomegranate seeds.

Cutaneous Tumours 

Squamous Cell Carcinoma Atypical Squamous Cells

Basal Cell Carcinoma Clusters of Basaloid cells

 
Image : Tzanck smear , showing three multinucleated giant cells in center.
Pearls
366. Difference between classic and neonatal scabies
Dermatology, Community Medicine
  Classic scabies Neonatal scabies

Interdigital webs, trunk, genitals, flexors,

Site of
sparing of palms and soles, and skin above Face, scalp, palm, and soles
involvement
neck

Morphology of Papules, pustules, excoriation, Vesicles, pustules, bullae,

Lesion eczematization, burrow erosions, and ulcerations

Burrows Present Usually absent

Pearls
260. Wood's lamp examination
Dermatology
Wood's Lamp Examination
Wood's lamp examination is a diagnostic test wherein the skin or hair is examined under
exposure to the black light emitted by the Wood lamp. Black light is invisible to the naked eye
because it is in the ultraviolet spectrum, with wavelength just shorter than the color violet. The
lamp glows violet in a dark environment because it also emits some light in the violet part of the
electromagnetic spectrum.
A traditional Wood lamp is a low-output mercury arc covered by
a Wood filter (barium silicate and 9% nickel oxide) and emits light at wavelength 320–
450 nm (peak 365 nm).
Table: Various diseases and their color on Wood’s lamp examination

Disease Colour on Wood’s Light

Microsporum species: blue-green (M. canis, M. audouinii, M.

ferrugineum, M. distortum); 
Tinea capitis Trichophyton schoenleinii: dull blue.
  Most Trichophyton species, with the exception of T. schoenleinii,
are non-fluorescent
 

Erythrasma Coral pink

Pityriasis
Faint yellow
versicolor

Pseudomonas Green

Scabies Fluorescein solution fills the burrows and fluoresces on Wood’s light.

Porphyria Urine, feces, blister fluid fluoresce red or pink

Vitiligo Ivory or milky white

Pearls
258. Mnemonic for Secondary Lesions of Skin
Dermatology
Mnemonic for Secondary Lesions of Skin
"LEAF SUCKS water"
 L — Lichenification
 E — Erosion / Excoriation
 A — Atrophy
 F — Fissure
 S — Scale
 U — Ulcer
 C — Crust
 K — Kind-of-hard to feel (Induration)
 S — Scar
Pearls
257. Primary Lesions of Skin
Dermatology
Primary lesions of the skin include:
 Papule
 Plaque
 Wheal
 Vesicle
 Bulla
 Nodule
 Macule
 Patch
 Purpura
 Pustule

For mnemonic lovers, the following mnemonic might help!

"Predatory Poisonous Wasps Viciously Bit on the Nose of My Patient causing Purulent Pus"
 
Secondary lesions of the skin include:
Mnemonic- "LEAF SUCKS water"
 L — Lichenification
 E — Erosion / Excoriation
 A — Atrophy
 F — Fissure
 S — Scale
 U — Ulcer
 C — Crust
 K — Kind-of-hard to feel (Induration)
 S — Scar
Pearls
256. Shapes of skin lesions
Dermatology
Shapes of Skin Lesions

Shape Description Examples

Discoid
A filled circle Discoid eczema, Psoriasis
(nummular)

Discoid lesions which have merged

Petaloid Seborrhoeic dermatitis on the trunk
together

Arcuate Incomplete circles Urticaria

Open circles with different central

Annular Tinea corporis, granuloma annulare
skin compared with the rim

Polycyclic Circles which have merged together Psoriasis

Erythema ab igne, polyarteritis

Livedo Chicken‐wire criss‐cross pattern
nodosa

Reticulate Fine lace‐like pattern Oral lichen planus

Target Multiple concentric rings Erythema multiforme

Lesions of meningococcal
Stellate Star‐shaped
septicaemia

Koebner reaction to a scratch in

Linear Straight line
lichen planus or psoriasis

Serpiginous Snake‐like Cutaneous larva migrans

Epidermal naevi, late‐stage

Whorled Swirling pattern
incontinentia pigmenti
Pearls
255. Glossary of important skin lesions
Dermatology
Glossary of Important Skin Lesions

Lesion Description

Alopecia Absence of hair from a normally hairy area

Aphtha A small ulcer of the mucosa

Loss of tissue from one or more of the epidermis, dermis or subcutaneous

Atrophy
tissues

Burrow A small tunnel in the skin that houses a parasite, such as the scabies acarus

Callus A localized hyperplasia of the stratum corneum

An inflammation of cellular tissue, particularly purulent inflammation of

Cellulitis
the deep dermis and subcutaneous tissue

Comedo A plug of keratin and sebum in a dilated pilosebaceous orifice

Crusts (scabs) Crusts consist of dried serum and other exudates

Any closed cavity or sac (normal or abnormal) with an epithelial,

Cyst endothelial or membranous lining and containing fluid or semi‐solid
material

Ecchymosis A macular area of hemorrhage more than 1 cm (bruise) in diameter

A loss of epidermis, which heals without scarring. It commonly follows a

Erosion
blister.

Redness of the skin produced by vascular congestion or increased

Erythema
perfusion

Excoriation Loss of skin substance, specifically produced by scratching

Exfoliation The splitting off of the epidermal keratin in scales or sheets

Fibrosis The formation of excessive fibrous tissue

Fissure Any linear gap or slit in the skin surface

An abnormal passage from a deep structure, such as a hollow viscus, to the

Fistula
skin surface or between two structures

Gangrene Death of tissue, usually due to loss of blood supply

Small round or oval lesions distributed as a ‘shower’ of droplets. Usually

Guttate lesions
applied to a form of psoriasis

Haematoma A localized tumour‐like collection of blood

Keratoderma A horny thickening of the skin

Thickening of the epidermis (and to some extent also of the dermis) in

Lichenification
response to prolonged rubbing

A flat circumscribed, non‐palpable lesion that differs in colour from the

Macule surrounding skin. It can be of any colour or shape. A macule is <1 cm in
diameter, larger lesions are a patch.

Maculopapular Rash consisting of both macules and papules

Milium A tiny white cyst containing lamellated keratin

A solid palpable lesion in the dermis or subcutis, which can be observed as

Nodule*
an elevation or can be palpated. It is >0.5 cm in diameter.

Papule An elevated solid lesion that is < 1cm in diameter.

Petechia A punctate haemorrhagic spot, approximately 1–2 mm in diameter.

An elevated circumscribed lesion > 1 cm diameter; its surface is usually

Plaque
flat. Plaques may form from coalesced papules.

Poikiloderma The association of cutaneous pigmentation, and telangiectasia.

Pustule A circumscribed lesion that contains purulent material. 

Pyoderma Any purulent skin disease

Scale Scale is a flat plate or flake-like lesion desquamated of stratum corneum.

Replacement by fibrous tissue of another tissue that has been destroyed by

injury or disease
Scar
An atrophic scar is thin and wrinkled.
A hypertrophic scar is elevated, with excessive growth of fibrous tissue.

Diffuse or circumscribed induration of the subcutaneous tissues. It may

Sclerosis also involve the dermis, when the overlying epidermis may be atrophic. It
is characteristically seen in scleroderma.

Sinus A cavity or track with a blind ending

These are <3 cm in diameter and have three or more zones, usually a
Target lesions central area of dusky erythema or purpura, a middle paler zone of oedema,
and an outer ring of erythema with a well‐defined edge.

Literally a swelling; the term is used to imply enlargement of the tissues by

Tumour
normal or pathological material, or cells that form a mass. 

Ulcer (of skin) A loss of dermis and epidermis, often with loss of the underlying tissues

 A vesicle is a circumscribed elevation <0.5cm in diameter that contains

Vesicles and fluid
Bullae
Bullae are >0.5 cm in diameter 

 A transient elevation of the skin due to dermal and hypodermal, often pale
Wheal centrally with an erythematous rim; it is the characteristic lesion of
urticaria.
 *While Rook's textbook of Dermatology,9th edition mention nodule as >0.5cm. Some authors
define nodules as >1cm.
Pearls
248. Key Chart to help differentiate lesions on face
Dermatology
Key Chart to help Differentiate Lesions on face
Pearls
1917. Fox-Fordyce disease
Dermatology
Fox Fordyce disease, also known as Apocrine Miliaria, is characterized by intensely pruritic,
white pearly papules in apocrine areas. It most commonly involves axilla, then areolae. It is
commonly seen in women (90%).
The condition occurs as a result of apocrine sweat duct occlusion by aggregates of epithelial
cells of the apocrine or apoeccrine secretory cells. The earliest pathological sign is a small
vesicle in the apocrine duct.
Later, the apocrine glands are seen to be enlarged, and as a consequence of repeated
inflammatory events, perifollicular xanthomatosis with perifollicular foam cells expressing
CD68 may develop.
Treatment:
First-line
 Topical or intralesional steroids
 Topical clindamycin lotion
 Topical retinoids

Second line
 Ultraviolet light
 Oral retinoids

Third line
 Surgery

This should not be confused with Fordyce spots or Fordyce disease which is due to ectopic
sebaceous glands.
Image: Fox-Fordyce disease of the axilla
Pearls
1914. Different types of miliaria
Dermatology
Miliaria is a common acute or subacute skin condition that arises due to
the occlusion or disruption of eccrine sweat ducts in hot humid conditions.
Based on the level of blockade it is differentiated into
 Miliaria Crystallina- Stratum corneum
 Miliaria Rubra - Malpighian Layer
 Miliaria profunda - Dermoepidermal junction

Pathophysiology:
 The first event may be an increase in the skin flora, perhaps with Staphylococcus
epidermidis being responsible for producing an extracellular polysaccharide substance or
slime that blocks the lumen of the sweat duct.
 The parakeratotic plugs, a notable feature of the later stages of the disease, are not the
primary cause of the obstruction but arise in the repair process, and further aggravate the
obstruction.
 Leakage of sweat into the epidermis is responsible for the final production of the
lesions, and for their further aggravation.
 Miliaria crystallina occurs commonly in infants due to a delay in the development of
patency in the sweat ducts.

Clinical features:
 Miliaria crystallina: Clear, thin‐walled vesicles, 1–2 mm in diameter without an
inflammatory areola, are usually symptomless and develop in crops, mainly on the
trunk. In persistent febrile illnesses, recurrent crops may occur. The vesicles soon rupture
and are followed by superficial, branny desquamation.
 
 Miliaria rubra: Typical lesions develop on the body, especially in areas of friction with
clothing, and in flexures. The lesions are uniformly minute erythematous papules,
which may be present in very large numbers. Characteristically, the lesions produce
intense discomfort in the form of an unbearable pricking sensation. Relief is often
instantaneous when the stimulus to sweating is abolished by a cool shower. In infants,
lesions commonly appear on the occluded skin of the neck, groins and axillae, but also
occur elsewhere.

 
 
 Miliaria profunda: This nearly always follows repeated attacks of miliaria rubra, and
is common only in the tropics. The lesions are easily missed. The affected skin is
covered with pale, firm papules 1–3 mm across, especially on the body, but sometimes
also on the limbs. There is no itching or discomfort from the lesions.

 
Treatment:
 First line
• Control local environment (remove excess bedding, fans, air
conditioning)
• Cool the skin (damp compresses, cool showers)
• Avoid tight or excessive clothing
 Second line
• Menthol (e.g. 0.5% menthol in aqueous cream)
• Topical antibiotics if there is secondary infection
• Mild topical steroids
 Third line
• Removal to cooler climate
• Prophylactic oral vitamin C
Pearls
1913. Fordyce Spots
Dermatology
Fordyce spots/Fordyce granules:
 The Fordyce spots are heterotopic sebaceous glands wherein the duct is
connected directly to the overlying skin or mucosal surface unlike other sebum glands
which open into the follicle.
 They are called ectopic/free-lying sebaceous glands.
 They occur commonly on the vermilion border of upper lip(m/c), buccal mucosa, skin
over penile shaft and areolar of the breast.
 They are commonly multiple and appear as symmetrical discrete yellow papules.
 Fordyce spots on penis are called Tyson glands.
 They are asymptomatic.
 Treatment ladder
o First line: Reassurance
o Second line
 Local destruction with superficial cautery or electrodessication
 Topical trichloracetic acid 

Image: Fordyce spots on the vermilion border of both lips in A, upper lip in B, and buccal
mucosa in  C.
Pearls
243. Global Alliance Algorithm for Acne Treatment
Dermatology
Global Alliance Algorithm for Acne Treatment
Image: Global Alliance Algorithm for Improving Outcomes in acne

BPO - Benzoyl peroxide

Pearls
240. Important Syndromes Related to Acne
Dermatology
Important Syndromes Related to Acne
I. SAPHO syndrome
1. Synovitis
2. Acne
3. Pustulosis
4. Hyperostosis
5. Osteitis

II. HAIR-AN syndrome

1. Hyperandrogenism (HA)
2. Insulin Resistance (IR)
3. Acanthosis Nigricans(AN)

III. SAHA syndrome

1. Seborrhoea
2. Acne
3. Hirsutism
4. Androgenetic alopecia

IV. PAPA syndrome

1. Pyogenic Arthritis (PA)
2. Pyoderma gangrenosum (P)
3. Acne(A)
Pearls
1897. Causes of scarring and non-scarring alopecia- Mnemonic
Dermatology
Alopecia or hair loss can be classified as :
1. Non-Scarring/Non-Cicatricial alopecia
2. Scarring/Cicatricial alopecia 

Mnemonic for causes of non-scarring alopecia: THATS STD!

 Tinea capitis(Non-Inflammatory Type  - grey patch and black dot types )
 Hormonal - Hypothyroidism, Androgenetic alopecia
 Anagen effluvium, Alopecia areata
 Trichotillomania
 Secondary syphilis (moth-eaten alopecia)
 SLE(predominantly causes non-scarring alopecia but also can cause scarring alopecia)
 Telogen effluvium
 Deficiency of Zinc, Iron 

Mnemonic for causes of scarring alopecia: SF2L3

 Scleroderma - Linear scalp morphea (en coup de sabre)
 Favus and Kerion (Inflammatory Type of Tinea capitis)
 Folliculitis decalvans
 Lichen planopilaris
 Lupus vulgaris
 Lupus erythematosis - discoid (DLE)
 Pseudopelade of Brocq
Pearls
295. Features of Nail Psoriasis
Dermatology
Features of Nail Psoriasis – Mnemonic
“Nail – POLISH”
 P – Pitting
 O – Oil drop sign, Onycholysis
 L – Leuconychia
 I – Irregular pitting pattern
 S – Splinter Hemorrhage
 H – Hyperkeratosis (Subungual)
Pearls
182. Hair Cycle
Dermatology
Hair follicles undergo a repetitive sequence of growth and the rest is known as the hair cycle.
Hair Cycle is usually described under three phases: Anagen, Catagen, and Telogen.

1. Anagen
 The period of active hair growth is known as anagen and the duration of this phase is
responsible for determining the final length of the hair.
 The entry of a resting hair follicle into anagen is heralded by the onset of mitotic activity
in epithelial cells overlying the dermal papilla at the base of the follicle (the secondary
epithelial germ).
 Under normal circumstances, 80–90% of hair follicles on the human scalp are in anagen
at any one time.
 Anagen can continue for several years.

Fig 1. Scalp hair follicle in the anagen II stage of development

Fig 2.  Anagen hair bulb. Co, hair cortex; Cu, hair cuticle; DP, dermal papilla; DS, dermal
sheath; He, Henle layer; HM, hair matrix; Hu, Huxley layer; IRSCu, inner root sheath
cuticle; Me, melanocyte; ORS, outer root sheath
2. Catagen
 At the end of anagen, epithelial cell division declines and ceases, and the follicle enters
an involutionary phase known as catagen.
 During catagen, the proximal end of the hair shaft keratinizes to form a club-shaped
structure and the lower part of the follicle involutes by apoptosis.
 The basement membrane surrounding the follicle becomes thickened and corrugated to
form the ‘glassy membrane’.
 It lasts for about 10 days.

Fig 3.  Human hair follicle in mid-catagen. There is a prominent glassy membrane surrounding
the regressing epithelial column. The dermal papilla is rounded and condensed. 
3. Telogen
 It is the time period between catagen and the next anagen.
 It lasts for about 3 months.
 Club hair is eventually shed through an active process called exogen.
 In the human scalp, hair follicles may remain in a state of latency, also known
as kenogen, for a prolonged period after the club hair is shed.
Pearls
180. Nail findings and associated systemic conditions
Dermatology, Medicine
Nail finding Associated systemic condition

 Inflammatory bowel disease

 Lung cancer
 Idiopathic pulmonary fibrosis
 Complicated tuberculosis
Clubbing  Suppurative lung disease (lung abscess, empyema, bronchiectasis,
cystic fibrosis)
 Mesothelioma
 Cirrhosis

 Congenital heart disease, Endocarditis

Koilonychia Iron-deficiency anemia, hemochromatosis, Raynaud’s disease

Onycholysis Psoriasis, onychomycosis, hyperthyroidism, sarcoidosis, trauma, amyloidosis

Pitting Psoriasis, Reiter’s syndrome, Alopecia areata

Any severe systemic illness that disrupts nail growth, Raynaud’s disease,
Beau’s lines
pemphigus, trauma

Lymphedema, pleural effusion, immunodeficiency, bronchiectasis, sinusitis,

Yellow nail rheumatoid arthritis, nephrotic syndrome, thyroiditis, tuberculosis, Raynaud’s
disease

Dorsal: Lichen Planus

Nail
Pterygium Ventral: trauma, systemic sclerosis, Raynaud phenomenon, lupus
erythematosus

 
Nail finding Associated systemic condition

Terry’s (white) Hepatic failure, cirrhosis, diabetes mellitus, CHF, hyperthyroidism,

nails malnutrition

Hepatolenticular degeneration (Wilson’s disease), silver poisoning,

Azure lunula
quinacrine therapy
Half-and-half
Specific for renal failure
nails

Muehrcke’s lines Specific for hypoalbuminemia

Arsenic poisoning, Hodgkin’s disease, CHF, leprosy, malaria,

Mees’ lines
chemotherapy, carbon monoxide poisoning, other systemic insults

Dark longitudinal Melanoma, benign nevus, chemical staining, normal variant in darkly
streaks pigmented people

Subacute bacterial endocarditis, SLE, rheumatoid arthritis,

Splinter
antiphospholipid syndrome, peptic ulcer disease, malignancies, oral
hemorrhage
contraceptive use, pregnancy, psoriasis, trauma

Telangiectasia Rheumatoid arthritis, SLE, dermatomyositis, scleroderma

Pearls
2299. Variant forms of melanocytic nevi
Pathology, Dermatology
Nevus
Diagnostic Features Cytologic Features Clinical Significance
Variant

Deep dermal and sometimes

subcutaneous growth around Present at birth; large
Congenital Identical to ordinary
adnexa, neurovascular variants have increased
nevus acquired nevi
bundles, and blood vessel melanoma risk
walls

Non-nested dermal Highly Black-blue nodule;

Blue nevus infiltration, often with dendritic, heavily often confused with
associated fibrosis pigmented nevus cells melanoma clinically

Large, plump cells Common in children; red-

Spitz with pink-blue pink nodule;
Fascicular growth
nevus cytoplasm; spindle to often confused with
epithelioid cells hemangioma clinically

Host immune response

Lymphocytic
Identical to ordinary against nevus cells and
Halo nevus infiltration surrounding
acquired nevi surrounding normal
nevus cells
melanocytes

Potential marker
Dysplastic Coalescent intraepidermal
Cytologic atypia or precursor of
nevus nests
melanoma
Pearls
1911. Algorithm for the differential diagnosis of
Hypomelanosis
Dermatology
Pearls
1948. Erythema multiforme vs. Stevens-Johnson
syndrome/Toxic epidermal necrolysis
Dermatology
Earlier, erythema multiforme (EM), Stevens–Johnson syndrome (SJS), toxic epidermal
necrolysis (TEN or Lyell syndrome) were considered to form a spectrum from mild to
fulminatingly severe cases. Now, this has been revised to separate Erythema multiforme as part
of a different spectrum.
Erythema Multiforme is regarded as a self‐limiting cytotoxic dermatitis resulting from cell‐
mediated hypersensitivity most commonly to infection or drugs.

Stevens–Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are severe

mucocutaneous reactions, usually to drugs, characterized by blistering and epithelial sloughing.
The two terms describe phenotypes within a severity spectrum, in which SJS is the less extensive
form and TEN is the more extensive.

Erythema Stevens-Johnsons Toxic Epidermal

 
multiforme major Syndrome Necrolysis

% Body
<10% <10% >30%
Surface-area

Herpes simplex> Drug induced e.g. Drug induced e.g.

Causes Mycoplasma cephalosporins, sulfa drugs, cephalosporins, sulfa drugs,
infection allopurinol allopurinol

Less fever and other

Associated Fever, malaise and Fever, malaise and
constitutional
Symptoms headache headache
symptoms

Mucosal Milder mucosal Severe mucosal Severe mucosal

Lesions lesions involvement involvement

Lesions Erythematous Vesicles on erythematous Diffuse, generalized

papules, Target base, erosions, purpuric epidermal detachment
lesions, raised macules, Flat atypical
atypical target lesions TEN with spots - with
target lesions, widespread purpuric
occasional bullous Nikolsky Sign Positive macules and flat atypical
lesions target lesions
TEN without spots- loss
of large epidermal sheets
without purpuric macules
or target lesions
  Nikolsky Sign Positive

Acral – distal
Distribution Variable distribution Extensive distribution
extremities

Interface
Epidermal necrosis,
dermatitis – Basal Dermo-epidermal
Dermo-epidermal
cell vacuolization, separation, Intense
Histo- separation, minimal dermal
apoptotic bodies and inflammatory cell infiltrates
pathology inflammatory cell infiltrate,
inflammatory cells in dermis, some areas of
large areas of epidermal
at Dermo-epidermal epidermal detachment 
detachment.
junction

Common, related to
Recurrence Uncommon, drug-related Uncommon, drug-related
Herpes infections

Rare – recovery in 1
Mortality Elevated mortality Highest mortality
to 4 weeks
 
Note: Overlap SJS-TEN: There is detachment of 10–30% body surface area, plus widespread
purpuric macules or flat atypical targets.
Pearls
232. Characteristic features of various types of Angioedema
Dermatology
Characteristic Features of Various Types of Angioedema
Clinical Presentation C4 Level C1-INH C1-INH C1q Level
Function by Level
Chromogenic
Assay  
 
Hereditary Inherited defect in the gene for C1-esterase inhibitor. Autosomal dominant: patients have one
Angioedema normal, one abnormal gene
(HAE)
Type I Recurrent episodic angioedema and Usually LOW NORMAL
abdominal attacks without urticaria.
Type II Onset in childhood or young Usually LOW NORMAL
adulthood. 75% have family history. or HIGH
Note that attacks may be oestrogen
dependent in this group as well as
the Type III form.
Type III Family history present in most cases, NORMAL
onset after childhood. Female
patients predominate and attacks
often appear to be estrogen-
dependent.
Acquired Condition not inherited but due to other underlying disease. C1-esterase inhibitor is low due
Angioedema to consumption
(AAE)
Type I Onset age variable; symptoms same Usually LOW LOW Usually
as HAE. No family history, may be LOW, May
associated with underlying be
lymphoproliferative disease. NORMAL
 
Type II Onset at variable age; symptoms NORMAL
indistinguishable from HAE. No
family history, often associated with
an autoantibody that binds to C1-
INH.
Drug-induced Angioedema occurs through allergic mechanism and does not involve C1-INH.
Angioedema
ACE Inhibitors Pseudoallergic (NSAID) or non- NORMAL NORMAL
NSAIDs allergic (ACE) inhibitors
Angioedema may start at first use.
Acute onset of well-demarcated
subcutaneous non-pitting edema of
the face or hands
Angioedema with Angioedema is accompanied by urticaria. Does not usually involve C1-INH.
Urticaria
Allergic AE Exposure to food, venom, latex, May be LOW NORMAL NORMAL
drug, or environmental allergen. or NORMAL OR LOW
May include anaphylaxis  

AE with Vasculitis Long-lasting urticaria with

tenderness. Vascular Damage. With
Hypocomplementemic Urticarial
Vasculitis, the CH5O is usually
LOW and so are classical pathway
components.
Idiopathic AE Frequently chronic and relapsing, NORMAL
often occurs with urticarial.
Consider test for chronic urticarial
(CD203c)
Pearls
206. UK refinement of Hanifin & Rajka’s diagnostic criteria of
atopic dermatitis (eczema)
Dermatology
In order to qualify as a case of atopic dermatitis (eczema) with the UK  diagnostic criteria, the
child must have an itchy skin condition (or parental report of scratching or rubbing in a child).
Plus three or more of the following:
 Onset below age of 2 years (not used if child is under 4 years)
 History of skin crease involvement (including cheeks in children under 10 years)
 History of a generally dry skin
 Personal history of other atopic disease (or history of any atopic disease in a first-degree
relative in children under 4 years)
 Visible flexural dermatitis (or dermatitis of cheeks/forehead and outer limbs in children
under 4 years)
Pearls
1956. Koebner phenomenon
Dermatology
Koebner or isomorphic Phenomenon is the development of new lesions along the line of
trauma in a previously normal skin. The new lesions have 'iso' (same) and 'morphic'
(morphology) as the existing lesions.
The trauma may include mechanical trauma, thermal trauma, allergic or irritant reactants or any
treatment procedures.

Psoriasis
True Koebner's Vitiligo
In immune-mediated conditions
phenomenon
Lichen planus

Viral warts
False Koebner's
In infectious diseases Molluscum
phenomenon
contagiosum

Reverse Koebner Area of psoriasis clears and heals following Psoriasis

phenomenon injury(trauma)

Spontaneous repigmentation of vitiligo

patches distant from the autologous skin graft
Remote reverse Koebner sites (trauma) Vitiligo
phenomenon
Generalized granuloma annulare

Some rare causes of True Koebner Phenomenon are : Darier's disease, Hailey-Hailey disease,
Erythema multiforme, Kaposi's Sarcoma and Lichen sclerosus.
Image: Koebner phenomenon with linear psoriasis patch on the abdomen
Pearls
1954. Drug of choice for different types of psoriasis
Dermatology
Type Drug of choice

Chronic Plaque Psoriasis Methotrexate

Erythrodermic Psoriasis Methotrexate 

Psoriatic Arthritis Methotrexate / Apremilast

Pustular Psoriasis Acitretin

Psoriasis in HIV patients Acitretin

1. Systemic Corticosteroids
Impetigo Herpetiformis
2. Cyclosporine

Erythrodermic Psoriasis in Pregnancy Systemic Corticosteroids 

Pearls
296. Treatment Ladder for Psoriasis
Dermatology, Pharmacology
Treatment Ladder for Psoriasis
I. In Mild Psoriasis Without Arthritis
First line
 Coal tar
 Dithranol
 Potent topical steroid
 Vitamin D analogue

Second line
 Local NB-UVB or PUVA
 Excimer laser

II. In Moderate or Severe Psoriasis Without Arthritis

First line
 NB-UVB or PUVA

Second line
 Acitretin
 Apremilast
 Ciclosporin
 Fumaric acid esters (where available)
 Methotrexate

Third line
 Adalimumab
 Etanercept
 Infliximab
 Secukinumab
 Ustekinumab

III. In Moderate or Severe Psoriasis with Psoriatic Arthritis

First line
 Apremilast
 Methotrexate
Second line
 Adalimumab
 Etanercept
 Infliximab
 Ustekinumab

Third line
 Combination therapy
Pearls
294. Drugs Inducing or Exacerbating Psoriasis
Dermatology
Drugs Inducing or Exacerbating Psoriasis
The following drugs are implicated in the exacerbation of psoriasis:
 Beta blockers
 Synthetic antimalarials
 NSAIDS
 Lithium
 ACE inhibitors & angiotensin receptor blockers

 Interferon alpha
 Tetracycline
 Terbinafine
 Gemfibrozil
Pearls
292. Papulosquamous Disorders
Dermatology
 Lichen planus
 Psoriasis
 Parapsoriasis
 Pityriasis rubra pilaris
 Pityriasis rosea
 Seborrheic dermatitis
 Secondary Syphilis
 Drug Reactions
 Reiter’s disease
 Eczema
 Neoplasms (Mycosis fungoides, Squamous cell carcinoma,  Bowen’s disease)
 Tinea infections
Pearls
259. Types of scales associated with dermatological
conditions
Dermatology
Types of Scales and Associated Diseases

Type of Scale Associated Disease

Its is a fine, peripherally attached and centrally detached scale at the edge
Collarette scale
of an inflammatory lesion. It is seen in Pityriasis rosea.

They are seen in Ichthyosis Vulgaris (Ichthyos = Fish). Ichthyotic scales

Fish-like scales
are large and polygonal.

They are characteristic of processes involving parakeratosis,

Silvery/mica-like
especially psoriasis. The silvery color is due to reflection of light at
scales
several air–keratin interfaces.

Yellow/Greasy
Seborrheic dermatitis
scale

Leaf-like scale Pemphigus foliaceous

Powdery, branny,
Pityriasis Versicolor
fine scales

 
Images:
Fine, peripherally attached and centrally detached Collarette scales of Pityriasis Rosea
 
Large and Polygonal Fish like scales of Ichthyosis Vulgaris
 
Silvery/mica-like scales of Psoriasis

 
Yellow/Greasy scale of Seborrheic dermatitis

 
Leaf-like scale of Pemphigus foliaceus
 
Powdery, branny, fine scales of Pityriasis Versicolor
Pearls
2085. Differences between pemphigus vulgaris and bullous
pemphigoid
Dermatology
  Pemphigus vulgaris Bullous pemphigoid

Age 30-40 years 70-80 years

Antibody Anti-desmoglein Anti-hemidesmosome

Location of target antigens Intraepidermal Subepidermal

Immuno-fluorescence Fish-net pattern Linear, shoreline pattern

Bullae Thin and fragile Deep and tense

Mouth involved Yes No

Nikolsky’s sign Positive Negative

Symptom Painful Pruritic

Severity Life threatening Resolves

Pearls
363. Classification of vesiculobullous disorders
Dermatology
Classification of Vesiculobullous Disorders
1. According to Pathology
1. Immunobullous disorders (Primary blistering disease): Due to autoimmunity

A) Intraepidermal B) Subepidermal

Pemphigus
1. Pemphigus vulgaris  Bullous pemphigoid
2. Pemphigus foliaceous  Dermatitis herpetiformis
3. Pemphigus vegetans
 Epidermolysis bullous acquisita
4. Pemphigus erythematosus

2. Mechanobullous disorders: Due to defect in structure of epidermis

 Epidermolysis bullosa

 Bullous ichthyosiform erythroderma

3. Other disorders

1. Infections:               VZV, HSV, Bullous Impetigo, SSSS

2. Metabolic:               Porphyria, Diabetes, Hemodialysis

3. Drug eruptions:       Fixed drug eruption, Steven Johnson Syndrome, Erythema

Multiforme
2. According to Site
Intraepidermal Sub-epidermal (Dermo-epidermal)

1. Subcorneal (granular layer) 1. Junctional (at basal lamina)

 Pemphigus foliaceous & erythematosus  Junctional epidermolysis bullosa
 Staphylococcal scalded skin syndrome  Bullous pemphigoid
 Miliaria crystalina  Toxic epidermal necrolysis
 Bullous impetigo
 Friction blister 2. Dermolytic (below basal lamina)
 Subcorneal pustular dermatosis
 Epidermolysis bullosa acquisita
2. Spinous layer  Epidermolysis bullosa
dystrophicans
  Eczematous (atopic) dermatitis
 HSV/VZV infection
 Molluscum contagiosum
 Familial benign pemphigus (Hailey-hailey
disease)

3. Suprabasal  Deep burns

 Pemphigus vulgaris
 Darrier’s disease  Porphyria cutanea tarda

4. Basal layer
 Erythema multiforme

 Epidermolysis bullosa simplex

Pearls
224. Vesiculobullous Disorders
Dermatology, Pathology
Clinical Immuno-
Disease Histology Autoantigens
Manifestations pathology

Flaccid blisters, Cell surface Dsg3, Dsg1 in

Acantholytic blister
Pemphigus denuded deposits of IgG on patients with
formed in suprabasal
vulgaris       skin,oro-mucosal keratinocytes- fish skin
layer of epidermis 
lesions net pattern involvement

Crusts and
shallow erosions
Acantholytic blister Cell surface
Pemphigus on the scalp,
formed in superficial deposits of IgG Dsg1
foliaceus       central face,
layer of epidermis  onkeratinocytes
upper chest, and
back

Large tense
Subepidermal blister Linear band of IgG
Bullous blisters on flexor BPAG1,
with eosinophil-rich infiltand/or C3 in
pemphigoid     surfaces and BPAG2
rate epidermal BMZ 
trunk 

Extremely
pruritic small
papules and Subepidermal blister Granular deposits Epidermal
Dermatitis
vesicles on with neutrophils in of IgA at the tips of trans-
herpetiformis     
elbows, knees, dermal papillae  dermal papillae glutaminase
buttocks, and
posterior neck

Pruritic small
papules on
extensor Subepidermal blister
Linear IgA Linear band of IgA
surfaces; with neutrophil-rich BPAG2
disease     in epidermalBMZ
occasionally infiltrate 
larger, arciform
blisters 

IgG and C3 DEJ –

Epidermo-lysis Tense bullae and Type VII
Subepidermal blister  Continous and
bullosa acquisita erosions  collagen
linear 
Pearls
2455. Skin and soft tissue lesions caused by Staphylococcus
Dermatology, Microbiology
Staphylococcus causes a variety of skin and soft tissue infections. These include:
a. Furuncle/boil- Infection of the hair follicle.
The given image shows a furuncle:

 
b. Carbuncle: A cluster of several furuncles:
The given image shows a carbuncle:
 
c. Bullous impetigo: Results in large blisters called bullae, usually seen in areas with skin folds
such as armpits, groin, buttocks, etc.
The given image shows ruptured bullous impetigo:
 
d. Cellulitis: It is a rapidly spreading infection of the skin and subcutaneous tissue, usually
associated with wounds, incisions, burns, etc.
The given image shows cellulitis following an abrasion. The red streaks indicate the involvement
of the lymphatics:

 
e. Staphylococcal scalded skin syndrome: Caused by exfoliating toxin that causes peeling of
the skin.
The given image shows SSSS:
 
Note: The conditions shown above are most commonly caused by Staphylococcus. It is
important to remember that they may also be caused by other bacteria. Cellulitis is more
commonly caused by Streptococcus.
Pearls
2454. Skin and soft tissue lesions caused by Streptococcus
Dermatology, Microbiology
Streptococcus causes a variety of skin and soft tissue infections. These include:
a. Impetigo- Infection of superficial layers of the skin. It presents as superficial vesicles which
break down and are then encrusted by honey-colored scab. It usually occurs in children.
The given image shows impetigo:

 
b. Erysipelas- Infection of the superficial epidermis. It presents as an erythematous raised lesion
with sharply demarcated edges that differentiate it from the surrounding skin. 
The given image shows erysipelas- note the clear demarcation at the nasolabial folds seen in
facial erysipelas.
 
c. Cellulitis- Infection of the skin and subcutaneous tissue. It presents with erythema and edema.
It can be differentiated from erysipelas by - i. Erysipelas is a raised lesion whereas cellulitis is
not, ii. Cellulitis is poorly demarcated from the surrounding skin whereas erysipelas is clearly
demarcated.
The given image shows cellulitis:
 
d. Necrotizing fasciitis- Infection involving the fascial planes. It presents with dark areas of
necrosis, erythema, and edema.
The given image shows necrotizing fasciitis with areas of erythema and necrosis:
 
d. Myositis and myonecrosis- Infection of the muscle.
The given image shows necrotizing myositis:
Pearls
1995. Nail changes in lichen planus
Dermatology
Nail involvement in lichen planus occurs in up to 10% of the cases but is usually a minor
feature of the disease.
Dorsal Nail Pterygium is the most specific nail change in Lichen planus. The fusion of dorsal
nail fold and nail bed leads to pterygium.
The most frequent nail change is the exaggeration of longitudinal lines and linear depressions
due to a slight thinning of the nail plate.
Pup-tent sign - elevation of nail in shape of tent
Trachonychia - 20 nail dystrophy
Subungual Hyperkeratosis and Onycholysis
Longitudinal Melanonychia in Lichen Planus of the nail bed
Permanent destruction of several toenails with ulceration of soles (rare variant)

Image shows  Nails in Lichen planus presented with irregular longitudinal grooves and ridges .
Image : Dorsal Nail Pterygium
Image : Pup-tent sign 

Image : Trachonychia

Pearls
1994. Nail changes in psoriasis
Dermatology
Nail changes in psoriasis are present in about 40% of the cases at any point in time. Nail
psoriasis is associated with more extensive psoriasis, longer disease duration, family history of
psoriasis, and the presence of psoriatic arthritis.
Subungal oil drop sign or Salmon Patch is a highly specific pathognomonic sign seen in Nail
psoriasis. It is a yellow-red discoloration in the nail bed resembling a drop of oil.
Nail pitting however is the most frequent sign. Individual pits are uniformly sized, deep and
irregular in nature. These nail pits are also known as Thimble pits and are due to the
involvement of the proximal nail matrix.
Nail Bed disease also causes subungual hyperkeratosis, splinter hemorrhages, and distal
onycholysis.
Leuconychia may also be present.
Trachonychia or Twenty Nail dystrophy may be present in severe cases.

Image :  Pitting is the commonest manifestation of nail psoriasis.

Image: oil drops visible in the nail bed.

Image: pitting and salmon patches in fingernails.

Image: Leukonychia in a patient with psoriasis.
 
Features of Nail Psoriasis – Mnemonic
“Nail – POLISH”
 P – Pitting
 O – Oil drop sign, Onycholysis
 L – Leuconychia
 I – Irregular pitting pattern
 S – Splinter Hemorrhage
 H – Hyperkeratosis (Subungual)
Pearls
1971. Classification of cutaneous tuberculosis
Dermatology
The classification of cutaneous tuberculosis is based on the mode of acquisition.

Tuberculous chancre - Primary skin TB

Inoculation from Exogenous Tuberculosis verrucosa cutis (Anatomist's

source wart/Pathologist's wart)
Lupus vulgaris

Scrofuloderma
Endogenous source
Periorificial tuberculosis

Acute Cutaneous Miliary Tuberculosis

Hematogenous spread Lupus vulgaris

Tuberculous gumma

Micropapular- Lichen scrofulosorum

Tuberculids
Papulonecrotic Tuberculid
(Hyper-sensitivity phenomenon)
Nodular- Erythema induratum of Bazin
Pearls
1967. Characteristics of Ridley Jopling Classification in
Leprosy
Dermatology
TT (Tuberculoid BT (Borderline LL (Lepromatous
  BB (Borderline) BL(Borderline Lepromatous)
Leprosy) Tuberculoid) Leprosy)

Hypopigmented
1-3 well macules or Hypopigmented macules Numerous hypopigmented Hypopigmented
defined hypopigmented plaques, variable in or plaques with annular, macules, papules, plaques, and macules, plaques,
macule(s) or plaque(s) number, up to 10. ‘swiss cheese’ /inverted some nodules, lesions and nodular lesions
Number and with elevated sloping saucer/punched out with swiss cheese’ /inverted
Occasionally appearance saucer/punched out Innumerable lesions
Type of lesions borders  -'saucer right
showing fingerlike appearance almost showing perfect 
side up' lesion.
extensions Variable in number symmetrical in symmetrical distributio
Asymmetrical
(pseudopodia) (10–30) distribution n
distribution.
or satellite lesions

Variable size,
Variable size,usually
Size of Lesion some lesions are Variable Variable, usually small Small
large
large

Dry, scaly
Surface of Dry, scaly and Dry, scaly and slightly
infiltrated (but less Shiny (less than LL) Shiny
Lesion infiltrated shiny
than TT)

Markedly
Sensations Absent.  Moderately diminished Slightly diminished May be normal
diminished

Symmetrical
involvement of
Asymmetrical, single nerve trunks with
nerve ‘glove and stocking
enlargement. Asymmetrical Increasingly anesthesia’.
Peripheral Asymmetrical involvement
enlargement of few symmetric enlargement of
Nerves of several nerves
Nerve to patch may nerves nerves Nerves may feel normal
be palpable on
palpation or may be
thickened.

Markedly Almost normal

Hair Absent Moderately diminished Slightly diminished
diminished (initially)
Bacteriology on Negative or Scanty Moderate number of AFB Plenty of AFB
Negative Large number of AFB 
Split Skin Smear Bacilli present including Globi are seen

Typical Lepra
Type 1 Type 1 Type 1/Type 2 Type 1/Type 2 Type 2
Reaction

Strongly Positive Weakly Positive

Lepromin
Negative/ Weakly positive Negative Negative
Reactivity (+++) (+ or ++)

Most prominent Grenz

Fewer Tuberculoid zone
granulomas
Expansive and loose
Grenz clear Prominent foam cells granulomas
zone in upper Tuberculoid granulomas
less prominent Prominent Grenz zone Plenty of macrophages
papillary
Dermal Tuberculoid loaded with
dermis starts to Grenz zone is more Nerves show concentric
granulomas (arranged AFB- Virchow cells or
form prominent perineural cell infiltration
Histopathology around nerves) Lepra cells
and more conspicuous cut
Nerves are Transverse section of the
No bacilli are seen onion appearance. AFB are seen in
replaced by nerve shows cut onion
granulomas AFB are plentiful, including endothelial cells and
appearance
small globi Schwann cells as clumps
Fragmented - globi
bacilli are seen
with AFB stain Nerves are minimally
involved.
Pearls
1966. Lepra Reactions
Dermatology, Community Medicine, Pharmacology
Lepra Reactions:

Type 1 Reaction Type 2 Reaction

(Reversal/Upgrading) (Erythema Nodosum Leprosum)

Mainly seen in Borderline spectrum

(BT,BB,BL)
Mainly seen in LL(50%)>BL(15%)
Most severe in Bordeline Lepromatous(BL)
leprosy

Usually seen within 12 months of initiation of Unrelated to Multidrug therapy. May occur

Multidrug Therapy before, during or after treatment

Type 3 Hypersensitivity
Type 4 Hypersensitivity
Primarily Humoral
Due to enhanced Cell mediated
(Immune complex Deposition in tissues and
response increased destruction of bacilli
vessels)
following treatment in reversal
Cytokine involved - TNF-α

Inflammation of existing skin lesions (red,

painful edematous skin lesions) that New, erythematous and tender,
may ulcerate subcutaneous and dermal nodules that are
New lesions may occur (rare) widely distributed over extremities and face

Neuritis and Nerve abscesses (red, painful Existing lesions do not change

inflamed nerves)

Systemic symptoms present - fever,

myalgias, arthralgias, anorexia, keratitis,
No systemic involvement
iritis, nephritis, synovitis, orchitis,
lymphadenopathy

Treatment: Treatment:
Supportive therapy for mild reactions Oral Corticosteroids - First line drug
with NSAIDs
Clofazimine (Steroid dependent ENL)
In case of severe reactions with neuritis and eye
lesions- Oral corticosteroids Thalidomide -most effective but not used
(Drug of Choice) first due to various side effects

Nerve Abscess - Additional surgical drainage  

Other drugs: Clofazimine, Cyclosporine  

Pearls
618. Skin rashes: 1st to 6th diseases
Dermatology, Paediatrics, Microbiology
1st disease Measles

2nd disease Scarlet fever

3rd disease Rubella

4th disease Duke’s disease

5th disease Erythema infectiosum

6th disease Roseola infantum

Pearls
615. Clinical manifestations of Herpes simplex virus
Dermatology, Microbiology
1. Cutaneous lesions: Fever blister, herpetic whitlow, herpetic gladiatorum, eczema
herpeticum. Eczema herpeticum is a generalised eruption caused by Herpes infections in
children suffering from eczema
2. Mucosal: most common site involved is buccal mucosa. It may cause Gingivostomatitis
& Pharyngitis, Recurrent herpes labialis.
3. Ophthalmic: Follicular conjunctivitis and acute keratoconjunctivitis also occur. 
4. Nervous System: HSV encephalitis, HSV meningitis. 
Pearls
360. Cutaneous Infections/Diseases caused by Staphylococcus
aureus
Dermatology, Microbiology
Cutaneous Infections/Diseases caused by Staphylococcus aureus
A. Direct infection of skin and adjacent tissues
 Carbuncle
 Ecthyma
 Folliculitis
 Furunculosis
 Impetigo
 Sycosis

B. Secondary infection
 Eczema, infestations, ulcers, etc.

C. Cutaneous disease due to effect of bacterial toxin

 Staphylococcal scalded skin syndrome (SSSS)
 Toxic shock syndrome
 Staphylococcal scarlatina
 Recurrent toxin‐mediated perineal erythema
Pearls
359. Cutaneous Infections/Diseases caused by Streptococcus
pyogenes
Dermatology, Microbiology
Cutaneous infections/diseases caused by Streptococcus pyogenes
Direct infections of skin or subcutaneous tissue
 Cellulitis
 Impetigo
 Ecthyma, Erysipelas
 Vulvovaginitis
 Perianal infection
 Streptococcal ulcers
 Blistering distal dactylitis
 Necrotizing fasciitis

Secondary infection
 Eczema, infestations, ulcers, etc.

Tissue damage from circulating toxin

 Scarlet fever
 Toxic‐shock‐like syndrome
 Recurrent toxin‐mediated perineal erythema

Skin lesions due to allergic hypersensitivity to Streptococcal antigens

 Erythema nodosum
 Vasculitis

Skin disease provoked or influenced by Streptococcal infection (mechanism uncertain)

 Psoriasis, especially guttate forms
 Kawasaki disease
Pearls
342. Differentiating features between Tuberculoid Leprosy
(TT) and Lepromatous Leprosy (LL)
Dermatology
Differentiating features between Tuberculoid Leprosy (TT) and Lepromatous Leprosy
(LL)

  Tuberculoid Lepromatous

Number of lesions 1 -10 Hundreds, confluent

Symmetrical, avoiding
Distribution Asymmetrical, anywhere
‘soared’ areas

Defined edge, markedly Vague edge, slight

Definition and clarity
hypopigmented hypopigmented

Early, marked, defined, Late, initially slight, ill-

Anaesthesia localized to skin lesions or defined, but extensive, over
major peripheral nerve ‘cool’ areas of body

Late, extensive as for

Autonomic loss Early in skin and nerve lesions
anesthesia

Nerve enlargement Marked, in a few nerves Slight but widespread

Common, severe during type

Mucosal and systemic Absent
2 reactions

Number of Mycobacterium Numerous in all affected

Not detectable
leprae tissue
Pearls
341. WHO proposed Multi Drug Therapy (MDT) for the
treatment of Leprosy
Dermatology, Community Medicine
WHO proposed Multi-Drug Therapy (MDT) for the treatment of Leprosy

Age group Drug Duration of Treatment

Rifampicin 600 mg once a month

+
12
Clofazimine 300 mg once a month and 50 months(Multibacillary)
Adult
mg daily
6 months(Paucibacillary)
+
Dapsone 100 mg daily

Rifampicin 450 mg once a month

+  
Clofazimine 150 mg once a month and 50 12
Children (10–14 years) months(Multibacillary)
mg alternate days.
+ 6 months(Paucibacillary)

Dapsone 50 mg daily 

Rifampicin 10 mg/kg once a month

+ 12
months(Multibacillary)
Children <10 years old Clofazimine 100mg once a month, 50mg
or <40 kg twice weekly 6 months(Paucibacillary)
+  
Dapsone 2 mg/kg daily
Pearls
2456. Sexually transmitted infections
Dermatology, Microbiology, Community Medicine
Genital herpes- caused by herpes simplex virus (human herpesvirus 1 and 2).
 It appears as blisters (usually multiple) that lead to ulcer formation on breaking.
 The ulcers are painful.
 
Granuloma inguinale / Donovanosis- caused by Klebsiella granulomatis (formerly known as
Calymmatobacterium granulomatis).
 It usually causes beefy red genital ulcers that may bleed on touch.
  The ulcers are usually painless.
 Lymphadenopathy is usually absent but subcutaneous granulomas cause pseudo buboes. 
 Microscopy shows Donovan bodies with closed safety pin appearance

The given images show genital ulcer in granuloma inguinale:

 
Chancroid/ Soft chancre- caused by Haemophilus ducreyi.
 Causes genital ulcers that are non indurated with undermined edges.
 The ulcer is painful.
 Multiple/ Kissing ulcers develop due to autoinoculation from the primary ulcer.
 It usually causes tender unilateral inguinal buboes. 
 Microscopy- School of fish/Railroad track appearance
 
Syphilitic chancre/ Hard chancre- caused by Treponema pallidum.
 It presents as a small, button-like, indurated ulcer that is usually round/oval.
 The ulcer is painless.
 Causes painless lymphadenopathy.
 Microscopy- Spirochetes seen on dark ground illumination.

 
Lymphogranuloma venereum- caused by Chlamydia trachomatis.
 It usually presents with a transient single shallow ulcer that heals rapidly and usually
goes unnoticed.
 The secondary stage presents with tender inguinal buboes.
  Groove sign is seen when the lymph nodes above and below the inguinal ligament are
enlarged leading to the appearance of a groove.

The given images show the ulcer and the groove sign seen in LGV:
 
Gonorrhea- caused by Neisseria gonorrhoeae.
 It leads to purulent inflammation of the genital mucous membranes.
 It may present as urethritis, cervicitis, epididymo‐orchitis, or pelvic inflammatory
disease.
 The usual presentation is acute urethritis with complaints of burning dysuria and
purulent discharge.

The given image shows purulent genital inflammation due to gonorrhea:

Pearls
2340. Stages of syphilis
Dermatology, Microbiology
 Primary Syphilis:

Chancre- Painless, indurated, usually single

Lymphadenopathy- Painless, unilateral or bilateral, shotty and rubbery inguinal nodes
Dory flop sign- As the chancre is too hard to fold, it will flip over once the prepuce is retracted
back.
The chancre self heals in 1-4 months.
 
Secondary Syphilis:
A & B: Generalized rash(non-itchy, no vesicles, and palm and sole involvement).
This is the most common lesion.
C & D: Condyloma lata.
E: Moth-eaten alopecia (Non-scarring)
F: Mucous patches(Flat erosions on the tongue which can coalesce and form snail track
ulcers).These are the most infectious lesions.
G: Pigmentary plaques
H: Psoriasiform syphilitic lesions
Generalized diffuse non-tender lymphadenopathy
 
Tertiary Syphilis:
Gummatous syphilis(deep punched-out ulcers, with gum-like secretions on the floor)
Pseudo-chancre redux is a gumma occurring at the site of a previously healed ulcer  
CVS-Aortitis and aneurysm of the ascending aorta
CNS-General paresis of the insane and tabes dorsalis 
 
Latent Syphilis-Period between secondary and tertiary syphilis, when the patient is
asymptomatic clinically, and only serological evidence of infection is present.
 Early latent- Within 1 year of infection
 Late latent- After 1 year of infection
Pearls
2069. Vaginal infections
Dermatology, Obstetrics & Gynaecology, Microbiology

  Bacterial vaginosis Trichomonas vaginalis Candida albicans

Altered vaginal flora- increased

Causative Trichomas vaginalis-
concentration of Gardnerella Fungal infection
organism  parasitic infection
vaginalis

Etiology Increased vaginal pH Sexually transmitted Decreased immunity

Sexual trans-
No Yes No
mission

Discharge Fishy, thin, yellow Frothy, green Curdy, white

Symptoms Fishy odor, no itching Itching and burning Itching, burning

pH >4.5 >4.5 <4.5

No vaginal epithelium
Speculum Strawberry cervix Inflamed-epithelium
inflammation

KOH Positive Whiff test Whiff test can be positive. Pseudohyphae seen.

Motile trichomaonads,
Wet mount Clue cells. No WBCs seen WBCs seen
WBCs seen

Metronidazole, treat partner Oral or vaginal azole, no

Treatment Metronidazole or Clindamycin
also need to treat partner.

Pearls
2036. Partner management in sexually transmitted infections
Dermatology, Community Medicine
Partner Management when asymptomatic is not required for Gardenella vaginalis, Candida
and Herpes infections. 

Syndrome Kit used for Partner Treatment

 Treatment

Urethral Discharge Grey kit Treat all recent partners

Cervical discharge Grey kit Treat partners when symptomatic

Painful scrotal swelling Grey kit Treat all recent partners

Vaginal Discharge Green kit Treat partners when symptomatic

Genital ulcer disease- Non- Treat all sexual partners for past 3

White kit/Blue kit
herpetic months

Genital Ulcer disease

Red kit No partner treatment
-Herpetic

Treat male partners with Grey

Lower Abdominal Pain Yellow kit
kit (kit 1)

Treat all sexual partners for past 3

Inguinal Bubo Black kit
weeks
Pearls
1710. Important sexually transmitted pathogens and the
diseases caused by them
Dermatology, Community Medicine
Pathogen Disease or syndrome

Gonorrhea, urethritis, cervicitis, epididymitis,

Neisseria gonorrhoeae
salpingitis, PID, neonatal conjunctivitis

Treponema pallidum Syphillis

Haemophilus ducreyi Chancroid

LGV, urethritis, cervicitis, proctitis, epididymis, infant

Chlamydia trachomatis pneumonia, Reiter's syndrome, PID, neonatal
conjunctivitis

Klebsiella granulomatis (prev called

Donovanosis (granuloma inguinale)
Calymmatobacterium)

Herpes simplex virus Genital herpes

Hepatitis B virus Acute and chronic hepatitis 

Human papillomaviruses  Genital and anal warts

HIV AIDS

Molluscum contagiosum Genital molluscum contagiosum

Candida albicans Vaginitis

Trichomonas vaginalis Vaginitis

Pearls
8. Comparison of Genital Ulcers
Dermatology, Microbiology
 Syphilitic chancre Donovanosis or
  Genital herpes Chancroid (soft chancre) LGV
(Hard) granuloma inguinale

9-90 days 
Incubation
2-7 days 1-12 weeks 1-14 days 3 days - 6 weeks
period Average: 21days

Chlamydia
Causative Klebsiella
HSV-2>HSV-1 T.pallidum Hemophilus ducreyi trachomatis serovar
agent granulomatis
L1,L2,L3

Painless papule or
nodule erodes into
Cluster of vesicles on Single painless ulcer with Painless genital
beefy red Painful ulcer (ducreyi makes
Clinical erythematous base. clean base and raised, ulcer; painful
granulomatous ulcer you cry), painful inguinal
presentation Painful and pruritic firm, border, painless inguinal
with rolled edges. No lymphadenopathy
lymphadenopathy lymphadenopathy lymphadenopathy
lymphadenopathy,
pseudobubos are seen

Tzanck preparation
Donovan bodies on Nucleic acid
Diagnosis  multinucleated giant Clinical diagnosis Clinical diagnosis
biopsy amplification tests
cells, PCR

Azithromycin/
Acyclovir/famcyclovir
Treatment Penicillin/Ceftriaxone Azithromycin/ceftriaxone  Doxycycline
or valacyclovir Doxycycline
Pearls
368. Important DNA Repair Disorders Associated with
Cutaneous Features
Dermatology, Biochemistry
Disorder DNA Repair Defect

Xeroderma pigmentosum Nucleotide excision repair

Cockayne syndrome Nucleotide excision repair

Trichothiodystrophy Nucleotide excision repair

Rothmund–Thomson syndrome Recombination Q helicase

Bloom syndrome Recombination Q helicase

Werner syndrome Recombination Q helicase

Ataxia telangiectasia Double strand break repair

Fanconi anaemia Interstrand cross‐link repair

Muir–Torre syndrome Mismatch repair

Pearls
185. Antibodies in Dermatomyositis
Pathology, Medicine, Dermatology
 Anti-Mi2 antibodies (directed against a helicase implicated in nucleosome remodeling)
show a strong association with prominent Gottron papules and heliotrope rash.
 Anti-Jo1 antibodies (directed against the enzyme histidyl t-RNA synthetase) are
associated with interstitial lung disease, nonerosive arthritis, and a skin rash described as
“mechanic’s hands.”
 Anti-P155/P140 antibodies (directed against several transcriptional regulators) are
associated with paraneoplastic and juvenile cases of dermatomyositis.
Pearls
2060. Paraneoplastic dermatoses
Dermatology, Medicine, Pathology, Surgery
Cutaneous markers and their commonly associated internal malignancy:

Skin condition Most commonly associated malignancy

Acanthosis nigricans Gastric adenocarcinoma

Acanthosis palmaris Bronchial carcinoma

Sign of LeserTrélat Gastrointestinal adenocarcinoma

Acquired-ichthyosis Hodgkin disease

Pityriasis rotunda Hepatocellular carcinoma

Paraneoplastic pigmentation Small cell bronchial carcinoma

Squamous cell carcinoma of the upper respiratory or

Acrokeratosis paraneoplastica gastrointestinal
tracts

Erythema gyratum-repens Lung cancer

Glucagon secreting
Necrolytic migratory erythema
pancreatic islet cell adenoma

Lung cancer in men, breast and gynaecological tumours in

Dermatomyositis
women and colorectal cancers in both sexes

Scleroderma‐like skin changes Carcinoid syndrome

B‐cell proliferations and thymoma or thymoma‐like

Paraneoplastic pemphigus
neoplasms; specifically Non Hodgkin's lymphoma (42%)

Dermatitis herpetiformis Lymphoma

Porphyria cutanea- tarda and

Hepatocellular Carcinoma
variegate porphyrias

Erythroderma and exfoliative

Mycosis fungoides or Sézary syndrome
dermatitis

Pyoderma gangrenosum Hematological malignancy

Sweet syndrome Hematological malignancy

Migratory thrombo-phlebitis
Carcinoma Pancreas
(Trousseau's syndrome)
Pearls
391. Clinical findings suggestive of melanoma
Dermatology, Pathology, Surgery
The ABCDE of Melanoma consists of the rules for the examination of a nevus to assess its
malignant potential:

A : Asymmetry
 Melanoma lesions are irregular, or not symmetrical, in shape.

B : Border irregular
 Melanoma lesions usually have irregular borders that are ill defined.

C : Color variegation
 The presence of multiple colors (blue, black, brown, tan, etc.) or the uneven distribution
of color.

D : Diameter >6 mm
  Melanoma lesions are often greater than 6 millimeters in diameter (approximately the
size of a pencil eraser).

E : Evolution
 There is a change in the size, shape, symptoms (such as itching or tenderness), surface
(especially bleeding), or color of a mole.
Pearls
390. Main Prognostic Factors for Primary Melanoma
Dermatology, Pathology, Surgery
The following are the prognostic factors for primary melanoma (predictive value from *** high
to * low):
 Thickness (Breslow index)***
 Sentinel node status***
 Ulceration**
 Mitotic rate** (negative value especially in thin tumours)
 Regression* (underestimation of Breslow)
 Age* (negative for older age)
 Sex* (negative for males)
 Location* (negative for head and neck)
Pearls
297. Types of Psoriatic Arthritis
Dermatology, Medicine
Types of Psoriatic Arthritis - Mnemonic
“SODA”
S  —  Symmentrical Polyarthritis
         Spondylitis/Sacroiliits
O —  Oligoarticular Asymmetrical 
D —  DIP(Distal Interphalangeal/Classic Type)
A —  Arthritis Mutilans
 STI/RTI SYNDROMIC CASE MANAGEMENT
Urethral Discharge Cervical Discharge Painful Scrotal Swelling Vaginal Discharge Genital Ulcer-Non Herpetic Genital Ulcer - Herpetic Lower Abdominal Pain (LAP) Inguinal Bubo (IB)

 Urethral Discharge (Pus or  Nature and type of discharge  Swelling and pain in the  Nature and type of discharge  Genital ulcer, single or multiple, painful or painless  Genital ulcer or vesicles,  Lower Abdominal Pain  Swelling in inguinal region
muco-purulent) (quantity, color and odor) scrotal region (quantity, color and odor) single or multiple, painful,  Fever which may be painful
 Pain or burning while passing  Burning while passing urine,  Pain or burning while passing  Burning while passing urine,  Burning sensation in the genital area recurrent  Vaginal Discharge

urine increased frequency urine increased frequency  Menstrual irregularities like heavy,
 Preceding history of genital
 Increased frequency of  Genital complaints by sexual  Systemic symptoms like  Genital complaints by sexual  Enlarged lymph nodes  Burning sensation in the irregular vaginal bleeding ulcer or discharge
urination partners malaise, fever partners genital area  Dysmenorrhoea, dysparenunia,

 Systemic symptoms like  Low backache  History of urethral discharge  Low backache dysuria, tenesmus
malaise, fever (Take menstrual history to rule out (Take menstrual history to rule out  Systemic symptoms like
 Lower backache
pregnancy) pregnancy) malaise, fever etc
 Cervical motion tenderness

Tab. Azithromycin 1 gm OD Tab. Azithromycin 1 gm OD Tab. Azithromycin 1 gm OD Tab. Secnidazole 2 g OD Inj. Benzathine penicillin If allergic to Inj. Penicillin: Tab. Cefixime 400 mg OD stat + Tab. Tab. Azithromycin 1 gm
Stat + Stat + Stat + Stat + (2.4 MU) - 1 vial Doxycycline 100 MG Tab. Acyclovir 400 mg Metronidazole 400 mg OD Stat +
Tab. Cefixime 400 mg OD Tab. Cefixime 400 mg OD Tab. Cefixime 400 mg OD Cap. Fluconazole 150 mg Tab. Azithromycin (1 gm) - (Bid for 15 days) BD X 14 days + Tab. Doxycycline 100 mg
Stat Stat Stat OD Stat Single dose Azithromycin 1GM (Single dose) TDS for 7 days Doxycycline 100 mg BD X 14 days BD for 21 days
KIT 1/Grey KIT 1/Grey KIT 1/Grey KIT 2/Green KIT 3/White KIT 4/Blue KIT 5/Red Kit 6/Yellow Kit 7/Black

Treat all recent partners Treat partners when symptomatic Treat all recent partners No partner treatment Treat all sexual partners for past 3 weeks
Treat partners when symptomatic Treat all sexual partners for past 3 months Treat male partners with Kit 1

IMPORTANT CONSIDERATIONS FOR MANAGEMENT OF ALL STI/RTI


Educate and counsel client and sexual partner/s regarding STI/RTI, safer sex practices and importance of taking complete treatment

Treat partner/s India’s voice against AIDS

Advise sexual abstinence or condom use during the course of treatment

Provide condoms, educate about correct and consistent use

Refer all patients to ICTC

Follow up after 7 days for all STI, 3 , 7 , and 14 day for LAP and 7 , 14 , and 21 day for IB
rd th th th th st


If symptoms persist, assess whether it is due to re-infection and advise prompt referral

Consider immunization against Hepatitis B