I.
FUNDAMENTALS OF DERMATOLOGY
Layers of Skin
? Skin is the largest organ in the body.
? The layers of the skin are
o
Epidermis
o
o
Subcutaneous fat/ hypodermis
EPIDERMIS
? Layers of epidermis:
Stratum corneum (Horny cell layer)
? Outermost layer
? No cell organelles
? Underdeveloped in preterm infants for 2-3 weeks.
Stratum lucidum
? Transparent layer
Stratum granulosum
? Made of intracellular basophilic kerato hyaline granules
? Forms a water impermeable layer
? Contains abundant Odland bodies.
Stratum spinosum or
? Provides mechanical strength to the skin
Prickle cells layer [Malphigian layer]
? Langerhan cells present.
? Single layer of columnar/ cuboidal cells
Stratum germinatum
? Contains mitotically active keratinocytes & melanocytes
? Langerhans cells are found scattered evenly throughout the epidermis.
? Merkel cells are normally located in the basal layer
? Merkel's (Tastzellen) cells ? slow adapting mechanoreceptors found in prickle cell layer.
? Keratin filaments are hallmark of keratinocyte
? Adamson's fringe: beginning of Keratinization
? Abrupt Keratinization: seen in pilomatricoma
? Keratin expressed in basal layer: K5, K14
? 1 epidermal melanocyte unit: 36 keratinocytes
? Epidermal turn over time: 1 month
? Accelerated cell turnover: psoriasis and ichthyosiform erythroderma [2 to 4 days]
? Lichen planus: the granular cell layer is focally increased.
? Nail first develops at: 3 months of intra uterine life
? Scalp hair growth: 0.35 mm/day
? Number of hair normally lost pev day:50-100
? Factors stimulating skin development (Epidermopoiesis): EGF, TGF-a, IL-II & fibroblast growth factor.
? Factors inhibiting skin development: Chalones, TGF-B, a and y interferons, TNF
? The stratum corneum of the palms and soles is about 0.5 mm thick and much thicker than that on the trunk
and limbs.
? Stratum corneum is permeable in preterm infants and becomes similar to the adult and full term infant after
2-3 weeks, postnatal maturation.
? In humans there are two classes, the brown-black eumelanin, and the red-yellow phaeomelanin, both
derived from the substrate tyrosine.
? Most natural melanins are mixtures of eumelanin and phaeomelanin, and phaeomelanic pigments,
trichochromes, occur in red hair.
to differences in frequency or distribution
DERMIS
? Consists of connective tissue, cellular elements, and ground substance.
? Contains pilosebaceous, apocrine and eccrine structures.
Adventitial dermis: consists of thin collagen (Type III/reticulin) fibers located beneath the epidermis
(papillary dermis) and surrounding adnexal structures (periadnexal dermis).
? Type IV collagen is a major constituent of the basal lamina of the dermo-epidermal junction.
SUBCUTANEOUS TISSUE
? Constitutes the largest volume of adipose tissue in the body.
? It provides protection from physical trauma and insulation to temperature changes.
Blaschko's Lines:
? Represent the developmental growth pattern of skin.
? Do not correspond to any known nervous, vascular or lymphatic structures.
BLOOD SUPPLY OF SKIN
? No blood vessels in epidermis
? Necessary oxygen + nutrients diffuse from capillaries in the dermal papillae.
? Each glomus body consists of a venous and arterial segment, called the Sucquet-Hoyer canal.
SKIN GLANDS/APPENDAGES
Sebaceous glands:
? Hair follicle + Sebaceous glands + arrector pill muscle
Pilosebaceous unit
? Present everywhere on the skin, except the palms and the soles.
? In most areas they are associated with hair follicles.
o
Buccal mucosa and vermillion border of the lip
o
Nipple, and areola of the breast, labia minora
Eyelids (Meibomian glands).
? The sebaceous glands are holocrine glands.
? Secretion of sebum is not under any neurologic control but is a continuous outflowing of the material of cell
breakdown.
? The sebum is mildly bacteriostatic and fungistatic and retards water evaporation.
? The scalp and the face may contain as many as 1000 sebaceous glands per square centimetre
Apocrine glands:
? Found in the axillae, genital region, external ear canal (ceruminous glands) and eyelid (Moll's glands).
? Breast (mammary gland) is also modified apocrine gland.
? Do not develop until the time of puberty.
? The secretions may act as pheromones (responsible for the production of body odor).
? Obstruction results in Fox Fordyce's disease
? Hidradenitis suppurativa, an inflammatory process that results from follicular obstruction and
Eccrine sweat (merocrine) glands:
? Distributed everywhere on the skin surface
? Most numerous on sole of foot (620/cm2) and least abundant on the back (64/cm9
? Glands first appear on volar surface of hands & feet in 3.5 month old fetus
? The eccrine sweat glands and the vasculature of the skin maintain stable internal body temperature.
? Their prime stimulus is heat and their activity is under the control of hypothalamus.
? Both adrenergic and cholinergic fibers innervate the glands.
?
? If eccrine glands are congenitally absent, as in anhidrotic ectodermal dysplasia, a life-threatening
hyperpyrexia may develop.
? Fordyce spots are visible sebaceous glands without hair follicles.
? Extremely common, benign condition.
? Tiny white / yellowish focally grouped papules in buccal mucosa and vermilion border of lips, scrotum, shaft
of penis and labia
Epidermal Stem Cells
? Three main locations of epidermal stem cells in the adult skin
o
o
Interfollicular epidermis (IFE)
o
Sebaceous gland
Skin stem cells occur in the basal layer of the epidermis and at the base of hair follicles.
TERMINOLOGIES
? Acantholysis: loss of cohesion between epidermal cells, seen in all types of pemphigus.
? Acanthosis: increased thickness of the prickle cell layer due to stimulation of basal layer.
? Foam cells: lipid-laden macrophages containing dead lepra bacilli.
? Hydropic degeneration of basal cells: vacuolization of basal cells seen in LE, dermatomyositis, early lichen
planus.
? Hyperkeratosis: Increased thickening of stratum corneum.
? Spongiosis: accumulation of fluid between epidermal cells, seen in acute eczema.
Skin Lesions
Flat lesions:
? Patch: > 2 cm, colored.
? Purpura: Extravasation of RBCs in the skin, blanches on pressure.
? Telangiectasia: Permanent dilatation of superficial vessels.
Elevated lesions:
? Nodule: 1-5 cm, solid. Examples: tumors, granuloma annulare
? Tumor: > 5 cm, solid.
? Plaque: > 1 cm, flat topped. Example: psoriasis.
? Vesicle: < 1 cm, fluid-filled. Example: blisters of herpes simplex.
? Pustule: Vesicle filled with leukocytes. Examples: acne, folticulitis.
? Wheal: circumscribed, flat-topped, firm elevation of skin resulting from tense edema of the papillary dermis.
Example: urticaria
Scales
Dry, thin plates of keratinized epidermal cells (stratum corneum) Example: psoriasis,
Lichenification
Induration of skin with exaggerated skin lines and a shiny surface resulting from chronic
Impetiginization Bacterial infection resulting in exudation and golden-yellow crusting
Erosion and
A moist, circumscribed, slightly depressed area representing a blister base with the roof of
oozing
Crusts
Dried exudate of plasma on the surface of the skin following acute dermatitis. Examples:
impetigo, contact dermatitis.
Fissures
cheilitis.
Scars
A flat, raised, or depressed area of fibrotic replacement of dermis or subcutaneous tissue.
Atrophy
Example: lichen sclerosis.
Configuration of lesions
Annular
Annular nodules represent granuloma annulare; annular scaly papules are more apt to be
caused by dermatophyte infections.
Linear (straight
Linear papules represent lichen striatus; linear vesicles, incontinentia pigmenti; linear
lines)
Grouped
Grouped vesicles occur in herpes simplex or zoster.
INTRA-EPIDERMAL BLISTERS:
Granular layer
Supra basal layer
Basal Layer
Friction blister
Eczematous
Lupus erythematosus
Pemphigus foliaceous
dermatitis
Darier's disease
Sub corneal pustular
Herpes virus infection
Epidermolysis bullosa simplex
dermatosis
Staphylococcal skin scald
pemphigus
syndrome / Bullous impetigo
Junctional (at the lamina lucida)
Dermolytic (Below basal lamina)
Bullous Pemphigoid
Erythema multiforme
Epidermolysis bullosa acquisita
Junctional Epidermolysis bullosa
Porphyria cutanea tarda
DIAGNOSTIC TECHNIQUES
Disease
Atopic Dermatitis
Clinical evaluation
Contact Dermatitis
Patch Test
Microscopy (Donovan bodies/Safety pin appearance)
Chancroid
Gram staining(gram negative rods/ school of fish / rails road appearance
? Pethergy test: Behcet's syndrome
? Patch test: Contact dermatitis
? Dermatoscopy (Epiluminescence microscopy, dermoscopy): method of observing superficial layers of skin
using 10-100 X magnification under oil immersion.
? Most commonly used in the diagnosis of herpes virus infection ? shows multinucleated giant cells.
? Also used in pemphigus ? shows acantholysis.
SKIN BIOPSY
? Surgical excision with suturing:
o
Good cosmetic result
o
o
Disadvantage: most time consuming of the three techniques, removal of the sutures.
? Punch biopsy:
o
o
Should be deep enough to include subcutaneous fat if used for diagnosis of panniculitis or
o
tumors in a subcutaneous location.
Pigmented lesions should not be punched unless they can be completely excised.
? Excision with scissors:
o
Useful for certain types of elevated lesions and in areas in which the cosmetic result is not too
o
Advantage of this procedure is the speed and the simplicity with which it can be done.
? Shave biopsy:
o
o
Hemostasis can be accomplished by pressure, light electrosurgery, Monsel solution, or aluminium
chloride solution.
o
margin assessment is required.
WOOD'S LAMP
It is a source of ultra violet light (mainly long wave UV-A, at a wavelength of 360nm), from which virtually all variable
? Fungal infections like:
o Tinea capitis = yellow green fluorescence.
o Pityriasis versicolor = golden yellow / apple green
? Bacterial infections like:
o Pseudomonas pyocyanea = yellow-green
? Pigmentary disorder
o Vitiligo = total white
o Ash-leaf macules in tuberous sclerosis = blue white
? Squamous cell carcinoma of skin = red fluorescence
Type of collagen
I
Bone
II
Cartilage, vitreous tumour, Intervertebral disc
Extensive - skin, lung, hollow organ (vascular system)
IV
Basement membrane, Eye lens
VII
VIII
Endothelium
X
Hypertrophic cartilage
Skin, hemidesmosomes
XVIII
Liver, kidney
XIX
Distributions of Glycosaminoglycans (GAGS):
Synovial fluid, Vitreous humour, Loose connective tissue
Chondroitin sulphate
Cartilage, bone, cornea
Keratan sulphate-I
Keratan sulphate-II
Loose connective tissue
Heparin
Mast cells
Skin, Fibroblasts
Dermatan sulphate
Wide distribution
? The panniculus adiposus is the fatty layer of the subcutaneous tissues, superficial to a deeper vestigial layer
of muscle, the panniculus carnosus.
? It includes structures that are considered fascia by some sources but not by others.
? Eg: Fascia of Camper, superficial cervical fascia.
II.
SOLAR INJURY
? UVR of wavelength 250-400 nm is of major importance as far as skin is concerned.
? Narrow-band UVR is UVR at a wavelength of 311 nm
UV-A
UV-C
(Long-wave UVR)
(Medium-wave UVR)
(Short-wave UVR)
280-320 nm
250-280 nm
? 1000-fold less effective at causing
? UV-B [around 290 nm]: mainly
erythema
responsible for sunburn, suntan and
Out by the
? Penetrate to the dermis
ozone layer
? Play a role in causing the dermal
? UVB penetrates as far as the basal
degeneration known as solar
elastosis, which is responsible for the
death of scattered keratinocytes
appearance of ageing & the cause of
(sunburn cells) & damages others
release cytokines and mediators.
? Responsible for photosensitivity
? 2 days after UVR injury, there is an
reactions
synthesis.
Polymorphic light eruption (PMLE)
? A common disorder, occurring in young and middle-aged women
? The rash develops shortly after sun exposure throughout the spring and summer months
? PMLE is chronic in nature
? The action spectrum of PMLE may also extend into the long ultraviolet wavelengths (UVA; 320-400 nm)
? Patients improve when they avoid sun exposure and use sunscreens blocking UVA
? For severe rashes -- hydroxychloroquine or even azathioprine
Photodermatitis
? Painful or pruritic erythema, edema, or vesiculation on sun-exposed surfaces: the face, neck, hands, and "V"
of the chest.
? Sunscreens with an SPF of 30-60 and broad UVA coverage, containing dicamphor sulfonic acid, avobenzone,
titanium dioxide, and micronized zinc oxide, are useful
? Photosensitivity due to porphyria is not prevented by sunscreens and requires barrier protection (clothing)
to prevent outbreaks.
Dermatoses improved by sun exposure: Psoriasis, Acne
III.
SKIN INFECTIONS
The following organism live in the follicular lumina without normally causing harm
o
Gram-positive cocci (Staphylococcus epidermidis)
o
o
Gram-positive yeast-like organism (Pityrosporum ovale or Malassezia furfur)
Dermatophyte infections are restricted to the stratum corneum, the hair and the nails (i.e. horny structures).
? Caused by yeast-like micro-organism Pityrosporum ovale (orbiculare) or Malessezia furfur
? Becomes pathogenic when its growth is encouraged by increased sebum secretion or depressed immunity
? Pale, scaling hypopigmented macules develop over the skin of the chest and back in young adults (Picture
III-E)
? Central upper trunk the most frequent site.
? Microscopy: grape-like clusters of spores and a meshwork of pseudomycelium in skin scrapings made more
transparent by soaking the scales for 20 minutes in 20 per cent potassium hydroxide.
? Skin surface biopsy
Permanent preparation made using cyanoacrylate adhesive to remove a strip of superficial stratum
corneum from the skin surface on a glass slide
o
The slide is 'rolled off' the skin after 20 seconds and then stained with periodic acid- Schiff reagent
The skin patches often fluoresce an apple green in long-wave UVR (Wood's light).
? Treatment
o
Topical imidazole creams (e.g. miconazole, clotrimazole, econazole) for 6 weeks or
Ketoconazole shampoo to wash the affected areas once daily for 5 days
TINEA INFECTIONS
? Also called Dermatophytoses or Ring worm
? T. rubrum, T. mentagrophytes and E. floccosum are the M/c causes of dermatophyte infection
? Inflammatory ringworm can be caught from cattle (T. verrucosum) and horses (T. equinum).
? Hypersensitivity to fungal antigens ? vesicular lesions - dermatophytids (id reaction)
? Hypersensitivity can be demonstrated by skin testing with fungus antigen ? trichophytin
? Kerion ? scalp infection with marked inflammation producing severe boggy swellings
? The diagnosis is confirmed by microscopy of skin scrapings, hair or nail clippings treated with 20% potassium
hydroxide for 20 minutes and identification of fungal hyphae.
? Use of the cyanoacrylate 'skin surface biopsy technique' makes identification quite easy.
TRICHOPHYTON
MICROSPORUM
EPIDERMOPHYTON
? Infects Hair, nail and skin
? Infects skin and nails but not hair
? Abundant microconidia
? Scanty microconidia
? Microconidia absent
? Abundant macroconidia (spindle
? Macroconidia are pear or club
(pencil shaped)
shaped)
Tinea corporis or Tinea circinata (Body ring worm)
? Pruritic, ring-shaped lesions with an advancing scaly border and central clearing
Tinea cruris or Groin ring worm (Jock itch or Dhobis's itch)
? A disorder of young men
? Marked itching in intertriginous areas, usually sparing the scrotum.
? Peripherally spreading, sharply demarcated, centrally clearing erythematous lesions asymmetrically on the
? These gradually extend down the thigh and on to the scrotum unless treated
Tinea manuum
? One palm is involved which is usually dull red with silvery scales in the palmar creases
? T. rubrum is the usual cause
? Ringworm of the scalp occurs in children exclusively
? Mainly due to M. canis or Trichophyton tonsurans
? It invades the hair cuticle (ectothrix infection), causing pink, scaling patches on the scalp skin
? There is patchy loss of hair (only broken hair) with variable degrees of inflammation (to differentiate from
? It is easily spread by the sharing of hairbrushes.
? Infected areas sometimes fluoresce a light green under long-wave UVR (Wood's light)
? Scalp ringworm caused by T. schoenleini, invades the interior of the hair shaft (endothrix) and causes
intense inflammation on the scalp, with swelling, pus formation and scalp scarring.
? Ringworm infection of the nail plate and the nail bed.
? The fungi responsible are T. rubrum, T. metagrophytes or E. floccosum.
? Onycholysis occurs and subungual debris collects
? More common in the toenails than in the fingernails
? Eextensive ringworm with an atypical appearance
? Due to the inappropriate use of topical corticosteroids.
Tinea barbae
? Also called barber's itch or Tinea Sycosis
Dermatophytoses
Causative agent
Tinea capitis
T corporis
T rubrum
T cruris
E floccosum, T rubrum
E floccosum, T rubrum
Favus
T schoenleinii, T violaceum
? Topical imidazole-containing preparation (miconazole, econazole and clotrimazole) used twice daily for a 3-
4-week period is usually adequate
? When topical treatment fails
o
o
Ketoconazole (200 mg daily) or Itraconazole - active in both yeast and dermatophyte infections.
CANDIDIASIS (MONILIASIS, THRUSH)
? A commensal of oral cavity, lower GIT and vagina
? Inflammatory papules and plaques with satellite pustules, frequently in intertriginous areas
? Treatment with the imidazole preparations, topical and systemic
? Serious Candida infections respond to systemic fluconazole.
Bacterial infection of the skin
Staphylococcus aureus
? Impetigo contagiosa
? Ecthyma
? Botryomycosis
? Superficial folliculitis (follicular or Bockhart impetigo)
? Folliculitis (sycosis barbae)
? Blistering distal dactylitis
? Paronychia
Group A Streptococci
? Impetigo
? Blistering distal dactylitis (in nonintertriginous skin) and intertrigo
? Vulvovaginitis
? Perianal cellulitis
Trichomycosis axillaris & pubis is a bacterial (aerobic corynebacterium) not fungal infection of hair shaft.
Erythrasma is superficial bacterial infection of skin caused by corynebacterium minutissimum.
IMPETIGO (PYODERMA)
? Pyodermas are infection in epidermis, just below the stratum corneum or in hair follicles.
? Two main clinical forms
o
Bullous impetigo caused by S. aureus mostly
Nonbullous impetigo (or impetigo contagiosa or Tilbury Fox) may be caused by Staphylococcus aureus
(most common); by group A-beta haemolytic streptococci (mainly in developing nations) or by both.
? Most commonly affects children
? Most common bacterial infection of children
? Spread by close contact (contagious).
? Bullous impetigo
o
Bullae are less rapidly ruptured
Larger (1-2cm)
o
Persist for 2-3 days
o
? Streptococcal impetigo may lead to
o
Post streptococcal acute glomerulonephritis (AGN)
o
o
Erythema multiforme
? Rheumatic fever is not a complication of streptococcal impetigo
? Caused by Staphylococcus aureus and/or beta hemolytic Streptococci
? It is mostly a disorder of prepubertal children
? Initial lesion is a very thin walled vesicle on an erythematous base which ruptures so rapidly that its seldom
seen
? Lesions are usually not painful, heals without scarring, no fever and patient is not ill
? Characteristic feature
o
Golden or Honey colored crust
Neutrophils beneath stratum corneum
? Face around nose and mouth) and limbs are most commonly affected
Erysipelas
? Caused by the beta-haemolytic Streptococcus
? The inflammation may be very intense and the area may become haemorrhagic and even blister.
? There is usually an accompanying pyrexia and malaise.
Pyoderma faciale
? Occurs mainly in adult women (in 20s)
? Sudden, severe eruption of confluent papules, nodules, pustules, cystic swellings which may be
interconnected by draining sinuses usually confined to face, involving checks, chin, nose, & forehead
? Comedones are usually absent or inconspicuous, as are other features of acne vulgaris or rosacea
hepatitis C)
TOXIC EPIDERMAL NECROLYSIS/ STAPHYLOCOCCAL SCALDED SKIN SYNDROME (SSSS)
Also called LyeII syndrome
? Most common site of infection is extracutaneous
? Wide spread erythematous blisterous eruption with striking desquamation of large areas of skin (Nikolsky
sign positive) as seen in scald or burn.
? Mucosa is not involved.
lived flaccid bullae & slough or exfoliation or peeling of superficial epidermis.
? Treated by IV antibiotics
CUTANEOUS TUBERCULOSIS
? Slowly progressive, granulomatous plaque on the skin
? It slowly increases in size, over one, two or three decades.
? Blanching with a glass microscope slide (diascopy) will reveal grey-green foci (apple jelly nodules)
? Seen on the backs of the hands, knees, elbows and buttocks whenever abrasive contact with the earth and
tubercle bacilli has been made.
? Thickened, warty plaques are present - sometimes misdiagnosed as viral warts
? Lupus vulgaris (Apple-jelly nodules)
? Lupus miliaris disseminate faciei
? Lichen scrofulosoeum
? Scrofuloderma (skin T.B. secondary to underlying structure)
? Papulo necrotic tuberculids
? Erythema nodosum
? Erythema induratum
? Acne agmination
Swimming pool granuloma
? Caused by Mycobacterium marinum
? Causes plaques, abscesses and erosions on the elbows and knees in particular.
? The condition responds to minocycline or a trimethoprimsulphamethoxazole combination.
? Mycobacterium ulcerans is responsible for this disorder
? Surgical removal is currently the best treatment.
SARCOIDOSIS
? Bluish chilblain-likeswellings of the fingers, nose and ears (lupus pernio) ? infiltrated by typical sarcoid tissue
? Histologically of the typical Sarcoid lesion: 'naked' tubercle, which contains foci of macrophages and giant
cells without many surrounding lymphocytes.
LYME DISEASE
? Caused by the Borrelia burgdorfii
? Late stages - skin atrophy (acrodermatitis chronica atrophicans), or fibrosis
Viral infection of the skin
HERPES SIMPLEX
? Type I is responsible for the common herpetic infection of the face and oropharynx
? 20 % suffer from recurrent 'cold sores', precipitated by minor pyrexial disorders or sun exposure.
? Commonly, the lesions occur around the mouth or on the lip.
? Genital herpes affects the glans penis and the shaft of the penis.
? In women, the vulval region or labia minora is usually involved
? Mostly affects those past the age of 50 years
? Also affects immunosuppressed individuals
? Due to the reactivation of a latent virus in a posterior root ganglion of a spinal nerve
? Starts with paraesthesiae or pain in the distribution of one or more dermatomes (Picture III-F)
? Involvement of one of the branches of the trigeminal ganglion, with lesions in the distribution of the
maxillary, mandibular or ophthalmic sensory nerves, is common
? Lesions are confined to the skin innervated by the dorsal primary root (s) infected
VIRAL WARTS
? Epidermodysplasia vericuformis
o
Congenital condition
o
o
Some lesions can transform to squamous cell carcinoma
? Verruca vulgaris (Picture III-G)
? Cryotherapy (tissue freezing with liquid nitrogen or solid carbon dioxide)
? Curettage
? Cautery
? Chemical destruction with topical preparations containing salicylic acid, lactic acid, podophyllin or
? Intracutaneous injections of cytotoxics such as bleomycin and injections of recombinant interferon.
MOLLUSCUM CONTAGIOSUM
? Caused by virus of pox virus group
? Transmitted by skin to skin contact and is a STD.
? Face & genitals are commonly involved
? Face is most commonly involved in children
? Pathology: Cup shaped epidermal thickening with characteristic degenerative change in granular cell layer &
Molluscum bodies on giemsa stain is pathognomic.
? Cutaneous form seen in Mediterranean and North America (Old World leishmaniasis)
o
Ccaused by Leishmania major and L. tropica.
o
o
Later, this breaks down to produce a sloughy ulcer ('oriental sore'), which persists for some
months before healing spontaneously, with scarring and the development of immunity.
? Mucocutaneous forms occur mainly in South America (New World leishmaniasis)
Caused by L. mexicana and L. brasiliensis.
o
Small ulcers develop (Chiclero's ulcer) that seem more destructive than the Old World types
o
about half of the patients
IV.
SKIN INFESTATIONS
Phthirus pubis
Pubic lice infestation
Pediculus humanus
Pediculosis
Scabies
SCABIES
Epidemiology:
? Infestation caused by Acarus hominis/Sarcoptes scabie.
? Itching worse at night is most common symptom.
? Family history of similar itchy eruptions in close contact
? On an average, an adult has 12 mites and an infant 20 mites.
Primary lesions:
? Most common sites involved: Inter digital space, Anterior wrist, Ulnar border of hand
? An imaginary circle intersecting the main sites of involvement--axillae, elbow flexures, wrists and
? hands and groins - 'circle of Hebra'.
? In infants and elderly: Scalp, Face, Neck, Palms & Soles, Penis also involved
? Fine pin head size follicular papules
Secondary lesions:
? Pustules due to 2? infection is one of commonest form of presentation.
? Eczematized crusted lesion, in infants & children are predominant lesions.
Types:
? Crusted or Norwegian scabies
o
Most severe form
The average number of mites in these cases is 2 million
o
Seen in immuno compromised, mentally ill patients, GVDH, leprosy, leukemia
o
o
No burrows
o
Minimal itching
Highly contagious
o
Ivermectin is the treatment of choice
? Scabies incognetio - wrongly treated with steroids.
? Drug of choice : 5% Permethrin (1st ) BHC (2nd ).
? Oral drug (Only): Ivermectin.
? Other drugs : Benzyl benzoate 25%, Crotamiton 10%, Malathion, Monosulfiram.
? Drug safe in pregnancy & infants < 2 months: precipitated sulfur 5-10%.
symptomatic or not.
PEDICULOSIS
? Macula cerulea (bluish stain on the skin d/t louse bite) is a typical lesion of Pediculosis
P. Capitis
? Transmitted by Head louse
? Involves scalp
mobile dandruff
? Common in girls with long hairs
P. Corporis (Vagabond's disease.)
? Transmitted by Body louse
? The body louse transmits
o
o
Trench fever
o
Relapsing fever
? Treatmeot: disinfection of clothes with 10% DDT or 1% BHC + Pediculocide drug application
Pthirus Pubis (Pubic louse):
? Is a STD, can also infest body, axillary, and eyelash hairs
? In children the common areas of involvement are the eyebrows and eyelashes (pediculosis palpebrum)
V.
IMMUNE MEDIATED SKIN DISORDERS
URTICARIA (nettlerash, 'weals' and 'hives')
plaques (wheals) of varying sizes and shapes which are usually pruritic.
? Angioedema is the same process but involves the deep dermis, subcutaneous and submucosal tissues
? Urticaria -- dermal edema
? Angioedema -- subcutaneous, submucosal edema
? Type I hypersensitivity mediated by histamine.
? Lesions are itchy, red papules and plaques of variable size that arise suddenly, often within a few minutes
THE 'PHYSICAL' URTICARIAS
Cold urticaria
? The reaction can be elicited by an ice block.
? There is a familial form.
Pressure urticaria
? Lesions develop some time (up to several hours) after pressure on the skin
Dermographism
? Many patients with urticaria mark easily when their skin is rubbed firmly, for example with a key.
? This is an exaggerated 'triple response' and is quite troublesome to some patients
Solar urticaria
? It is a skin sign of one systemic disease-- erythropoietic protoporphyria
Cholinergic Urticaria
? Irritating, small urticaria spots develop after exercise, hot baths, emotions
? Occurs after stimuli that evoke sweating from the post-ganglionic cholinergically enervated sweat glands.
? Penicillin
? NSAIDs
? Sulphonamides
? Aspirin
? Mastocytosis (urticaria pigmentosa)
? Hypo- or hyperthyroidism
? Systemic-onset juvenile idiopathic arthritis (Still's disease)
ERYTHEMA MULTIFORME (EM)
symmetrically distributed erythematous papular, urticaria and typical iris/target shaped lesions (Picture:V-
A)
o
Cause: Herpes simplex virus ? most common cause of recurrent EM
o
Cause: HSV, Mycoplasma, Drugs (sulfonamides, phenytoin, barbiturates, aminopenicillins, non-
nucleoside reverse transcriptase inhibitors, and carbamazepine)
o
? The term "erythema multiforme major" has been replaced by three terms
o
Stevens-Johnson syndrome (SJS), with < 10% BSA skin loss
o
o
SJS/TEN overlap for cases with between 10% and 30% BSA denudation.
? Skin biopsy is diagnostic.
? Direct immunofluorescence studies are negative
? Painful crops of nodules develop in response to antigenic stimuli mostly in shins & forearms.
? Women are predominantly affected by a ratio of 10:1 over men
Causes of erythema nodosum
? Tuberculosis ? most common
? Leprosy (lepromatous type LL & BL)
? Brucellosis
? Streptococcal infection
? Ulcerative colitis & Crohn's disease
LUPUS ERYTHEMATOSUS
? Skin involvement is the 2nd most common clinical manifestation after joint inflammation and is found in up to
70% of patients
o
Chronic scarring (discoid) lesions (DLE)
o
Erythematous non-scarring red plaques (Subacute cutaneous LE) (SCLE).
? The lesions are most commonly found on face and neck
? Permanent hair loss (scarring alopecia) and loss of pigmentation are common sequelae of discoid lesions.
? There is atrophy, telangiectasia, depigmentation, and follicular plugging by scales
? When the scale is removed, its underside shows small excrescences that correlate with the openings of hair
? The disorder may be aggravated or initiated by exposure to the sun.
? Histology: epidermal degenerative changes are more marked, with scattered cytoid body formation and
patchy epidermal atrophy and thickening
? Sun avoidance and use of sunscreens
? Individual lesions sometimes respond to potent topical corticosteroid
? For unresponsive lesions - hydroxychloroquine (200-400 mg per day) is often helpful.
SYSTEMIC SCLEROSIS
? The disease is mostly seen in young women
? Gradual thickening and stiffening of the skin of the hands and face
? This causes a characteristic beak-like facial appearance, with narrowing of the mouth
? There are pigmentary changes over the face and neck in the form of hyperpigmentation and depigmentation
? Telangiectatic macules appear over the face and deposits of calcium develop in the skin.
? Fingers: sclerodactyly or sausage shaped fingers with taut skin over the fingers and thimble pitted scars over
fingertips
? Raynaud's phenomenon is almost a constant feature
? When there is also dysphagia due to Esophageal involvement - CREST syndrome
Morphoea or Localized Scleroderma.
? Linear scleroderma - involvement of the face and/or forehead manifesting as Parry-Romberg syndrome and
'en coup de sabre (depressed sclerotic groove over the frontal/frontoparietal region of the scalp)
85% of cases of generalised morphea
? These antibodies, in contrast to antitopoisomearsel/scl-70 antibodies have been found in 14% of the patients
with systemic scleroderma.
DERMATOMYOSITIS
? An idiopathic inflammatory myopathy of striated muscles along with characteristic cutaneous findings
? Linked to human leucocyte antigen (HLA) DR3, DRS, DR7
? The pathognomonic cutaneous features
o
o
Gottron's papules (papules having violaceous hue overlying the dorsolateral aspect of interphalangeal
or metacorpophalangeal joints)
? Other cutaneous features are
Malar erythema
o
Poikiloderma (variegated telangiectasia along with atrophy and hyperpigmentation)
o
o
Mechanics hands (fingertip erythema and scaling).
o
Calcinosis cutis - firm yellow or flesh coloured nodules extruding calcium through the skin
Intra-epidermal bullae
Sub-epidermal bullae
? Pemphigus vulgaris
? Pemphigus vegetans
? Cicatricial pemphigoid
? Pemphigus foliaceous
? Dermatitis herpetiformis
? Linear IgA buloous dermatosis
? Drug induced pemphigus
? Pemphigoid gestationis
? Paraneoplastic pemphigus
Clinical
Histology
Immunopathology
Pemphigus
Crusts and shallow
Acantholytic blister
Cell surface deposits
foliaceous
erosions on scalp,
formed in
of IgG on
superficial
keratinocytes
chest and back
layer of epidermis;
Pemphigus
Flaccid blisters,
Acantholytic blister
Cells surface
vulgaris
Painless,
formed in supra
deposits
Picture: V-C
MC site: buccal
basal layer of
of IgG on
mucosa
epidermis
keratinocytes
Nikolsky sign: + ve
Bullous
Large tense blisters,
Blister formed in
Linear band of IgG
Pemphigoid
Painless
sub epidermal
and C3 across the
Picture: V-D
MC site: extremities
region; eosinophil-
basement embrane
(Senile
Nikolsky sign: - ye
rich infiltrate
zone (BMZ)
pemphigoid)
Associated with
Acantholysis: - ye
Linear band of C3 in
Pemphigoid
Lymphoma
Teardrop-shaped,
epidermal BMZ.
gestationis
Pruritic, urticaria
sub epidermal
and BP180 (BPAG 1,
blister in dermal
BPAG 2)
vesicles & bullae on
papillae; eosinophil-
the trunk and
rich infiltrate.
in some patients).
extremities
large tense bullae
Sub epidermal
Linear band of IgA,
LAD
filled with clear or
blister with
in epidermal BMZ
disease or
Chronic
or near genitalia,
dermal papillae
bullous disease
of childhood
cluster of jewels
appearance
Cicatricial
Sub epidermal
Linear band of IgG,
BPAG2
pemphigoid
blister
and /or C3 in
mucous membranes
epidermal BMZ
Epidermolysis
Blisters, erosions,
Sub epidermal
Linear band of IgG,
bullosa
scars, and milia on
blister
and /or C3 in
sites exposed to
epidermal BMZ
trauma;
nflammatory,
initially
Dermatitis
Extremely pruritic
Sub epidermal
Epidermal
herpetiformis
small and vesicles
blister with
transglutaminase
mostly on elbows,
neutrophils in
epidermal junction.
dermal papillae
Pemphigus histology
? The superficial portion of epidermis sloughs off, leaving the bottom layer of cells on the "floor" of the blister
? This bottom layer of cells is said to have a "tombstone appearance".
DERMATITIS HERPETIFORMIS
? Intensely itchy vesicles, papulovesicles and urticaria papules symmetrically distributed over extensor
surfaces (elbows, knees, buttocks, back, scalp, and posterior neck)
? Almost all have an associated, usually subclinical, gluten-sensitive enteropathy
? Biopsy of new lesions - vesicle forms subepidermally and develops from collections of inflammatory cells in
the papillary tips (the papillary tip abscess)
? Direct IF- presence of IgA in the papillary tips in the skin around the lesions
? Treatment
Gluten-free diet
o
Dapsone therapy
? Patients are at increased risk for development of gastrointestinal lymphoma
MASTOCYTOSIS (URTICARIA PIGMENTOSA)
? Systemic mastocytosis is defined by a clonal expansion of mast cells that in most instances is indolent and
nonneoplastic
? Cutaneous mastocytosis (CM)
o
o
Variants: plaque form, nodular form; telangiectasia macularis eruptiva perstans (TMEP); diffuse
cutaneous mastocytosis (DCM)
o
? The cutaneous lesions of urticaria pigmentosa are reddish-brown macules or papules that respond to
trauma with urtication and erythema (Darier's sign).
? Urticaria pigmentosa is the most common manifestation of mastocytosis, both in adults & children.
Diseases with numerous telangiectasias
? Osler-Weber-Rendu disease, which also has mucous membrane involvement,
? lupus erythematosus
? scleroderma,
? dermatomyositis,
? metastatic carcinoid syndrome,
? ataxia telangiectasia,
? angiokeratoma corporis diffusum,
? telangiectasia macularis eruptiva perstans, and
? overlying basal cell cancers
VI.
SEXUALLY TRANSMITTED DISEASES
Bacteria
Virus
? Neisseria gonorrhoeae
? Chlamydia trachomatis (D-K)
? Human papilloma virus
? Chlamydia trachomatis (L1, L2, L3)
? Hepatitis B virus
? Cytomegalovirus
? Haemophilus ducreyi
? Molluscum contagiosum virus
? Calymmatobacterium granulomatis
? Mycoplasma hominis
? Human T-lymphotropic virus
? Ureaplasma urealyticum
? Gardnerella vaginalis
Protozoa
Fungi
Ectoparasites
? Candida albicans
? Phthirus pubis
? Sarcoptes scabiei
DISTINGUISHING FEATURES OF GENITAL ULCERS
Features
Syphilis
Chancroid
Lympho -
Herpes genitalia
(1? chancre)
granuloma
(Granuloma
inguinale)
Organism
Treponema
Haemophilus
Calymmato
Herpes simplex
palladium
ducreyi
bacterium
virus type II (rarely
(L1, L2,L3)
granulomatosis
No. of attacks
Only one (1)
1 or 2
Only one (1)
Recurrent
No. of lesions
Usually 1
Usually
Variable
Multiple, may
multiple may
coalesce
Early 1? lesion
Papule
Pustule
Papule, Pustule Papule
Diameter
5-15 mm
Variable
2-10 mm
1-2 mm
Depth
Superficial or Excavated
Superficial or
Superficial
Edges
deep
Undermined,
Elevated, irregular
Sharply
ragged,
Elevated, round serpiginous
demarcated,
irregular
or oval
elevated,
Base
Smooth, non- Purulent,
Variable
Red & velvety
purulent,
bleeds easily
nonvascular
(beefy red),
non-vascular
bleeds easily,
nonvascular
with exuberant
Features
Syphilis
Chancroid
LGV
Herpes genitalis
(1? chancre)
(Granuloma
inguinale)
Firm
Soft
Occasionally
Firm
firm
Pain
Uncommon
Usually very
Uncommon
Frequently tender
tender
Lymphadenopath
Tender, may
Tender, may
No
Firm, tender often
tender,
suppurate,
suppurate,
lymphadenopathy
shotty,
loculated,
loculated, uni
pseudo buboes
usually
or bilateral
(subcutaneous
unilateral
nodules in
(Bubo)
Nodes enlarge
inguinal region,
may ulcerate)
Poupart's
ligament, -
Groove sign
Diagnosis
-Dark field
-Clinical
-Demonstration -Tissue smear &
Microscopy
features
of LGV as
histopathological
-Serological
-Gram
elementary &
microscopy show
tests
Staining
inclusion bodies 1. Donovan
-Culture is
-Frie's test
bodies
confirmatory
cocco-bacilli
2.Safety pin
with rail road
globulinemia
appearance
-Complement
fixation +ve
Treatment
Penicillins/
Doxycycline
Doxycycline /
Acyclovir
Doxycycline /
Tetracycline
tetracycline
tetracycline
Ceftriaxone
Azithromycin /
Ciprofloxacin
erythromycin (in
pregnancy)
Lymphadenopathy
Ulcer
DONOVANOSIS
Indurated, painless, bleeding
SYPHILIS
Painless lymphadenopathy
Painless, non bleeding, indurated, usually single
Painful, suppurated, matted (BUBO)
Asymptomatic, painless, non bleeding ulcer
CHANCROID
Painful. fluctuant, suppurative nodes
indurated
HERPES
Painful lymph nodes
Multiple, painful. Bleeding, non indurated
? Primary chancre
: 9 to 90 days (21 days)
? Chancroid
: One to several weeks (5 to 8 days)
: 9 to 50 days (17 days)
? Lymphogranuloma venereum
: 5 to 30 days (10 days)
? Herpes genitalis (primary)
? Genital warts
: 1 to 8 months (3 months)
? Gonococcal urethritis
: 1 to 14 days (2 to 5 days)
: 7 to 21 days (10 days)
Esthiomine: vaginal & rectal strictures & elephantiasis of the vulva. (Seen in LGV)
Lipschutz ulceration: Non veneral ulcer of the vulva or lower vagina. (Ulcus Vulvae acutum) seen in Behcet's
disease. Similar to aphthous ulcers
CHANCROID:
? Based on history: sexual exposure with infected person, short incubation period & morphology.
? Confirmed by demonstration of organisms from smears taken from bubo.
? Smears are stained with gram's or Pappenheim's stain.
for life.
? Injection of 0.1ml of suspension of killed organism & inferred as positive if a nodule of > 5mm appears after
24 hours.
? Treatment: erythromycin & Ceftriaxone.
? History of occurrence of herpetiform lesions on the genitals, few days after intercourse, followed by painful
unilateral, multilocular inguinal bubo.
? Culture, Frei's intrademal test, complement fixation test can be done.
? Tetracyclines are the DOC.
? Confirmed by demonstration of Donovan bodies in the tissue smears & also by HPE.
? Giemsa stain.
? Few large cells containing cystic spaces, often with nuclei pushed to one side & darkly staining (cells of
Greenblatt) are conspicuous.
REACTIVE ARTHRITIS (REITER'S SYNDROME)
? 50 ? 80% are HLA B27 positive
? Oligoarthritis, conjunctivitis, urethritis, and mouth ulcers most common features
? Most cases of reactive arthritis develop within 1-4 weeks after either a gastrointestinal infection (with
trachomatis or Ureaplasma urealyticum)
? Psoriasiform skin lesions develop on the soles and toes
? These are often severe, persistent, aggressive and pustular (keratoderma blenorrhagica)
? Inflamed, red, scaling patches may also develop on the glans penis (circinate balanitis)
VII.
ECZEMA AND DERMATITIS
Types of eczema
Endogenous eczema
? Atopic dermatitis
? Irritant contact dermatitis
? Seborrhoeic dermatitis
? Allergic contact dermatitis
? Photodermatitis
? Pompholyx (Dyshidrotic eczema)
? Infectious eczematoid dermatitis
? Asteatotic eczema
? Juvenile plantar dermatitis
? Lichen simplex chronicus
ATOPIC DERMATITIS
? Positive family history of allergic rhinitis, asthma or eczema
? Pruritis is the most common symptom
? Course marked by exacerbations and remissions
? Clinical course lasting longer than 6 weeks
? Infantile pattern: involves face, neck, extensor surfaces and groin.
? Childhood and adolescent pattern: involves flexural skin, particularly in the antecubital fossa and popliteal
fossa.
? Cutaneous stigmata of AD
Perioral pallor
o
Extra fold of skin beneath the lower eyelid (Dennie-Morgan folds)
o
o
Increased incidence of cutaneous infections, particularly Staphylococcus aureus
? Diagnosis: clinically - dry skin, severe itching, flexural lichenification, hand eczema, nipple eczerr and eyelid
eczema in adults, history of atopy in the family/patient, and raised IgE serum levels.
Irritant contact dermatitis
? Synonyms: Occupational dermatitis, Housewive's eczema
? Materials may injure by direct toxic action (irritants)
? Housewife's eczema, diaper dermatitis and industrial dermatitis are examples of cumulative irritant contact
dermatitis.
? Most common site affected is hand.
? Most common cause of contact dermatitis in Indian women ? detergent.
? May induce immunological reaction of delayed hypersensitivity type (allergens) ? Allergic contact dermatitis
? Most common metal causing contact dermatitis is nickel.
? Most common cause of air-borne contact dermatitis? parthenium.
? Barloque dermatitis due to cosmetics.
o
Skin hypersensitivity test (delayed type).
o
Readings are made after 48 hours.
Differences Between Irritant and Allergic Contact Dermatitis
Irritant CD
Allergic CD
Symptoms
Acute
itching
Itching
pain
Chronic
Itching/pain
Lesions
Acute
Erythema
erosion
Erythema
papules
vesicles
crust
scaling
crust
scaling
Papules, plaques, fissures, scaling,
Papules, plaques, scaling, crusts
crusts
Margination
Sharp, strictly confined to site of
Sharp, confined to site of exposure but
and site
exposure
papules; may become generalized
Chronic
III-defined
III-defined, spreads
Acute
Rapid (few hours after exposure)
Not so rapid (12 to 72 h after exposure)
Chronic
Months or longer; exacerbation after every
exposure
reexposure
Causative
Relatively independent of amount applied,
agents
agent and state of skin barrier;
usually very low concentrations sufficient
but depends on degree of sensitization
Incidence
May occur in practically everyone
Occurs only in the sensitized
? Caused by chronic exposure to water and detergent.
? Dryness and cracking of the skin of hands with variable erythema and edema
? Diagnosis: Scratch test with latex extract.
Nummular (Discoid) Eczema
? Most common sites are ? trunk and extensor surfaces of extremities (pretibial skin and dorsum of hands)
? Most commonly affects men in middle age group.
Asteatotic Eczema
? Also called the 'Winter-itch' or Xerotic eczema or Eczema craquelee
? Characterized by fine cracks in the areas of dry skin over the anterior surface of legs.
Venous eczema (Gravitational eczema or Stasis Dermatitis)
? Due to venous incompetence and chronic edema.
? Site ? over the medial aspect of the ankle.
? Most common in infants and very young. Most common location is the scalp.
? Greasy scales overlying erythematous patches or plaques
? Scaling of the external auditory canal is common
? In the first week of life, it typically occurs in the scalp ("cradle cap"), face, or groin
? Leser-Trelat sign: Sudden eruption of multiple seborrheic keratosis lesions in associated internal malignancy
Lichen Simplex Chronicus (Circumscribed neuro dermatitis)
? End stage of various eczematous disorders
? Lichenification (thickening) of skin due to chronic scratching and rubbing.
Pompholyx (Dyshidrotic Eczema)
? Affects young adults
? Characterised by sudden crops of highly pruritic, deep-seated sago-like vesicles on the palms, sides of fingers
and/or soles
? Deficiency disease caused by lack of niacin (nicotinic acid), occurs chiefly in countries where corn (maize), a
poor source of tryptophan is basic food stuff.
? Its clinical presentations is "3-D"
Dementia
Dermatitis
o Most characteristic manifestation
o Occurs in form of pigmented, scaly, sharply demarcated & frequently changing cracked skin on parts
exposed to sunlight
Pellagrous glove [lesion on hand]
Pellagrous boot [lesion on boot]
Casal necklace [lesion around neck]
Deficiency of vitamin A leads to follicular hyperkeratosis and roughening of the skin (phrynoderma).
? Autosomal recessive
? Inherited form of zinc deficiency
? Result of a mutation in a zinc transport protein - decreased ability to absorb zinc from dietary sources
? Triad of
Acral dermatitis (face, hands, feet, anogenital area)
o
Alopecia
o
? Requires lifelong zinc supplementation
? 1-3 mg/kg of zinc gluconate or sulfate is administered orally each day
Acrodermatitis chronica atrophicans: skin atrophy in Lyme's disease
Acrodermatitis continua/ Acrodermatitis pustulosa: form of pustular psoriasis
? Generalized redness and scaling of the skin of >30% BSA.
? A preexisting dermatosis is the cause of exfoliative dermatitis in two-thirds of cases, including
Psoriasis
Atopic dermatitis
Pityriasis rubra pilaris
Seborrheic dermatitis.
? Reactions to topical or systemic drugs account 20-40% of cases
? Cancer (lymphoma, solid tumors and, most commonly, cutaneous T cell lymphoma) for 10-20%.
VIII.
PAPULOSQUAMOUS DISORDERS
PSORIASIS
? Typical lesions are erythematous (red), raised, scaly, well demarcated plaques
? Sites: extensor aspect of trunk & limbs preferentially
? Due to increased cell turn over resulting in marked epidermal skin thickening (acanthosis)
? 50% have positive family history
? Associated with HLA-Cw6 (most common)
susceptibility to psoriasis
? Obesity is another factor associated with psoriasis. Weight loss results in significant improvement
Triggering factors
? Trauma (Koebner phenomenon)
? Emotional stress
? Upper respiratory tract infections
? Drugs like beta-blockers, lithium and chloroquine
? Withdrawal of systemic steroids can lead to precipitation of pustular psoriasis.
Plaque type
? Most common type
? Slow, indolent course
? The most commonly involved areas: elbows, knees and scalp
? Affects the intertriginous regions including the axilla, groin, submammary region, and navel
? May be moist and without scale due to their locations
Guttate psoriasis (eruptive psoriasis)
? Most common in children and young adults
? Patients present with many small erythematous, scaling papules, frequently after upper respiratory tract
infection with -hemolytic streptococci
Pustular psoriasis
? Generalized eruption of sterile pustules
? Intense erythema
? Local irritants, pregnancy, medications, infections, and systemic glucocorticoid withdrawal can precipitate
this form of psoriasis
? Types
Acrodermatitis continua
Pustular bacterids
Generalized pustular (Von Zumbusch disease)
Psoriatic arthritis (PsA)
? Symmetric: resembles rheumatoid arthritis, but is usually milder
? Asymmetric: can involve any joint; present as sausage digits (Pencil in cup or Opera glass deformity)
? Distal interphalangeal predominant (DIP): the classic form
? Spondylitis
Scalp psoriasis: Pityriasis amaintaceae
Rupoid psoriasis: classically present in Reiter's syndrome (HLA-B 27)
Koebner's / Isomorphic phenomenon
? Koebner phenomenon is also seen in
Lichen planus
Vitiligo
Toxic Epidermal Necrolysis
Kaposi sarcoma
Necrobiosis lipoidica
Discoid lupus erythematosus.
? Appears usually 7 to 14 days after injury (i.e. trauma or surgery).
sites of injury)
Reverse Koebner phenomenon (reaction) is clearing of existing psoriasis lesions following injury. It also
obeys an all or none rule, and Koebner and reverse Koebner reactions are mutually exclusive.
Pseudo ? isomorphic phenomenon is due to autoinoculation & is seen in infections like
Molluscum contagiosum
? Auspitz sign -a characteristic finding of psoriasis in which removal of scales leads to pinpoint bleeding
? Removal of scales reveals a glistening red membrane of Berkeley
? Grattage Test -- on scratching scales appear
? Candle grease sign
? In nails
Onycholysis (separation of nail plate from nail bed)
Thimble-pitting of nail plate
Alopecia
Mucosal involvement
CNS involvement
? Histological features
Parakeratosis
Hypogranulosis
Munro's micro abscesses in the horny layer
Spongiform pustules of Kogoj
in normal epidermis
? Itching may or may not present
Key diagnostic points for psoriasis
Erythematous scaly plaques
Scales dry loose and micaceous
Koebner phenomenon seen
Auspitz sign positive
Regular, circular pits on nail plates
Histopathological: Spongiform pustules of Kogoj
Treatment
? Treatment of choice: PUVA therapy
? DOC for psoriatic arthropathy: Methotrexate
? DOC in AIDS with psoriasis & pustular psoriasis: Synthetic retinoid -- acitretin
? Biological agents used in the treatment of psoriasis
Alefacept (anti-CD2)
Etarnacept, Adalimumab, Infliximab (anti-TNF)
Disease
Features
Psoriasis
Well-defined, thickened, scaly plaques, usually multiple
Moderately well-defined edge; slightly scaly, pink patches, limited in number
Ringworm
Annular with central clearing; microscopy and culture of scales will reveal fungal mycelium
Bowen's disease
PHOTO CHEMOTHERAPY (PUVA)
? Photosensitizing drug Psoralen + UV-A (300-400nm)
? The UV-A is supplied by special fluorescent lamps housed in cabinets or special frames over beds
? The main psoralen used is 8-methoxy psoralen
? Decrease DNA synthesis in psoriasis & increase melanin synthesis in Vitiligo
? UV-light therapy is contraindicated in patients receiving cyclosporine
Uses
Side effects
? Long term (Major):
? Vitiligo
Skin cancer
? Cutaneous T Cell Lymphoma (Mycosis fungoides)
? Pityriasis lichenoides chronica
Photo (premature) aging
? Atopic dermatitis
? Minor (Short term): Nausea, Burning, Pruritis,
Xeroderma
LICHEN PLANUS
? Affects the skin, scalp, nails, and mucous membranes
? The primary cutaneous lesions are pruritic, polygonal, flat-topped, violaceous papules.
? The skin lesions but have a predilection for the wrists, shins, lower back, and genitalia
? Buccal mucosa is particularly involved
Variants
? Hypertrophic lichen planus- commonest variant, thickened, mauvish papules or nodules of irregular shape
? Annular lichen planus: ring-type configuration, on the male genitalia and lower abdomen.
? Lichen nitidus: is a rare variant, numerous tiny, pink, flat-topped papules develop.
? Bullous lichen planus: blistering occurs on some lesions.
? Lichen plano-pilaris: predominantly involves the hair follicles. Affected sites lose their terminal hair and
Clinical presentation of Lichen planus
Lesions
Characteristic features
Histology
? Wickham's stria
? Band-like infiltration of lymphocytes
? Polygonal
? Lace-like pattern due to
? Purple (violaceous)
involvement of buccal and
? Formation of saw tooth profile &
? Pruritic
cytoid (civatte) body.
? Papule
? Koebner's phenomenon
? Epidermal thinkening
? Scarring alopecia
? Subepidermal lichenoid band
nails
? Max Joseph histological cleft
Associated with: Squamous cell carcinoma, Hepatitis -- C
Treatment: topical steroids are the mainstay of treatment
PITYRIASIS ROSEA
? The exact aetiology of PR is not known though HHV-6 and 7 have been implicated.
? The centers of the lesions have a crinkled or "cigarette paper" appearance
? Followed by smaller annular or papular lesions, predominantly on the trunk along the cleavage lines.
? The eruption has a characteristic 'bathing suit' distribution (trunk and proximal parts of limbs)
? Lesions on the back are parallel to ribs giving 'Christmas tree' appearance or 'hanging curtain sign'
extremely rare in PR and common in secondary syphilis.
? Course -- usually self-limiting.
PITYRIASIS RUBRA PILARIS
? Reddish orange scaly plaques
? Keratotic follicular papules
? Disease begins on the face and scalp, with pinkness and scaling
? The histological appearance: distinctive accentuation of the dermal papillae and the undulations of the
dermoepidermal junction are much less marked than in psoriasis.
IX.
DISORDERS OF SKIN APPENDAGES
MILIARIA
secretory portion located in the reticular dermis and the subcutaneous fat to the skin surface
? There is secondary leakage of sweat in the epidermis and papillary dermis.
Types
? Miliaria crystalline (sudamina)
Vesicle is subcorneal.
It is common in infants in warm ICU conditions where cholinergic & adrenergic agents are employed.
? Miliaria rubra (prickly heat):
Leakage of sweat into epidermis & upper dermis
Intense itching
Miliaria pustulosa: miliaria rubra becoming pustular
? Miliaria profunda
Obstruction of acrosyringium at deeper level
Papules are non-itchy
ACNE VULGARIS
? A self-limited disorder primarily of teenagers and young adults
? The earliest feature is an increased rate of sebum secretion, making the skin look greasy (seborrhoea)
? Small pseudocysts, called comedones, form in hair follicles due to blockage of the follicular orifice
? The clinical hallmark is the comedone, which may be closed (whitehead) or open (blackhead)
? The activity of bacteria (Propionibacterium acnes) within the comedones releases free fatty acids from
sebum, causes inflammation within the cyst, and results in rupture of the cyst wall
? The first lesions, usually comedones, develop on the forehead (pre-adolescent acne)
? At its peak, acne covers the entire face (adolescent acne)
? In mature adults (25 years plus) it settles on the jaw area and the adjacent neck (adult acne).
? The scars formed after healing are often quite irregular and tend to form 'bridges'
? Even the smaller inflamed papules can cause scars - pock-like or triangular indentations (ice-pick scars).
Lesions quite suddenly become very inflamed
Affected individual is unwell and develops fever and arthralgia.
? Treatment:
Oral tetracycline or erythromycin.
Sebum production is decreased by sebotrophic agents (directly) and antiandrogens (indirectly)
o
Tretinoin (all trans retinoic acid)-1st generation (1G)
o
o
Adapalene -- 3G
o
Tazarotene -- 4th generation
? Common chronic inflammatory acneiform disorder of the facial pilosebaceous units, coupled with an
increased reactivity of capillaries leading to flushing and telangiectasia.
? It is seen almost exclusively in adults, rarely affecting patients <30 years.
? Rosacea is more common in women
? Characterized by the presence of erythema, telangiectases, and superficial pustules
? Comedones are not seen
? Predisposing factors: History of flushing associated with heat, emotional stimuli, alcohol, hot drinks or spicy
foods.
? Complications
Nose ? connective tissue overgrowth (Rhinophyma ? sebaceous gland hypertrophy)
Eye ? keratitis, uveitis, chalazion.
Chloracne- extremely severe form of industrial acne due to exposure to complex chlorinated naphthalenic
PHASES OF HAIR GROWTH
? Anagen: Phase of normal active growth, lasts for 3 years, 90% of hairs are in this phase
? Catagen: Brief transition phase (between anagen and telogen) during which hair growth stops, lasts for 3
weeks
? Exogen: Hair shedding phase (relationship between hair shaft and base of telogen follicle)
? Duration and rate of growth of anagen phase determine the ultimate length of hair in that area.
? Eyebrows, eyelashes, and axillary pubic hair: anagen phase is short; telogen phase prolonged.
? Scalp, beard: relatively long anagen phase.
? Vellus hairs: present over most of the body; genetically predestined to produce hairs that are short, fine,
non-pigmented.
HAIR LOSS (ALOPECIA)
? Shedding of hair is termed effluvium or defluvium
? Most common type
? Autosomal dominant
? Progressive form of alopecia
? Mostly seen in men
on the crown (vertex).
? Loss of hair starts in both temporal regions.
Treatment:
? Chemical castration with anti-androgen-prostagen combination in women by cyproterone acetate &
? Anti hypertensive (Vasodilator) ? Minoxidil & Tretinoin
? 5-alpha-reductase inhibitor ? Finasteride.
ALOPECIA AREATA
? Results from arrest of hair follicles in late anagen phase.
? 10-20% patients give a family history
? Polygenic inheritance
? HLA DR4, DR5, DQ3 are associated with severe alopecia
? 'Exclamation mark' hairs at the margin of the lesions.
? Non scarring & non patterned alopecia
? Particularly common between the ages of 15 and 30 years.
? Alopecia totalis is total or almost total loss of scalp hair.
o
Sites of Predilection: Scalp, eyebrows, eyelashes, pubic hair, beard.
o
Nails: Fine pitting ("hammered brass") of dorsal nail plate, mottled lunula, trachyonychia (rough nails),
? Ophiasis is alopecia along scalp margin. (band-like hair loss in the occipital and temporal scalp),
? Sisaipho (predilection for parietal scalp mimicking androgenetic alopaecia),
? Classical feature is sparing of gray/white hairs.
? Positively associated with autoimmune disorders
? Dense 'bee swarm'-like cluster of lymphocytes can be seen around the follicles in biopsies.
? Treatment: Potent topical steroids or systemic steroids, PUVA, dithranol, allergic sensitization with
diphencyprone and topical minoxidil
TELOGEN EFFLUVIUM
? This may occur spontaneously, may appear at the termination of pregnancy, may be precipitated by crash
dieting, high fever, stress from surgery or shock, malnutrition, or hormonal contraceptives.
? Telogen effluvium usually has a latent period of 2-4 months
? The prognosis is generally good
? Non scarring alopecia
? Mucin deposition in hair follicles & sebaceous glands causing epithelial reticular degeneration
? MC site: face & scalp
? Due to inflammatory process like discoid lupus erythematosus and lichen planus
? Result in permanent loss of hair in the affected area.
? Most common congenital cicatrial alopecia is aplasia cute's congenita (i.e. focal absence of epidermis with
or with or with out other layers).
DISORDERS OF NAILS
Koilonychia (Spoon nail)
Iron deficiency anemia
Lichem planus
Hypothyroidism
Racquet Nail
Premature obliteration of epiphyseal line
Anonychia
Lichen panus
Absence of all or part of one or several nails
With tong. bone anomalies
Any severe systemic illness
Poor nutrition to matrix 1/t a defective band of nail
formation resulting in transverse groove of thin nail
plate.
Longitudinal ridges with beaded and/or Fir tree
Median canaliform dystrophy of Heller
appearance
Trachyonychia (Rough sand paper nail)
External chemical treatment
Leuconychia : White discolouration of nail
Nail matrix dysfunction
Apparent leuconychia
White appearance d/t changes in underlying tissue
Muehrck's paired narrow white band
Onychogryphosis (Ram's horn or Oyster ? Nail)
Pressure from foot wear in elderly
sparaled & with out attachment to nail bed
Hook Nail
Lack of support from short bony phalynx
Pterygium
Ventral pterygium in scleroderma with Raynaud's
phenomenon, causalgia of median nerve,
formaldehyde containing nail cosmetics.
Onycholysis : Detachment of nail plate from its bed
starting at its distal &/or lateral attachment
Reiter's syndrome
Onychorrhexis : Splitting & roughness of nail plate
Lichen planus
Alopecia areata
Component of alopecia
Koenen's Periungal Fibroma
Tuberous sclerosis (50% cases)
Arsenic Poisoning.
Pitting
Deep & irregular pits: psoriasis, atopic dermatitis
Superficial & geometric pits in alopecia areata.
-Single band: nail matric nevus or melanoma
Presence of melanin in nail plate presenting as single /
(deserve biopsy), trauma (usually in 4/5th toe nail)
multiple longitudinal brown -- black band.
nail disorder, Lauiger -- Huntziker syndrome (with
pigmented macules on lip & genitals), AIDS,
Addison syndrome
Muehrck's lines
Brown nail
Arsenic poisoning
Addison's disease
Blue nail
X.
GENODERMATOSES & DISORDERS OF KERATINIZATION
Genodermatoses: diseases which are transmitted genetically from parents to children.
? Autosomal dominant
? Plexiform neurofibroma - soft, doughy, subcutaneous swelling having a bag of worm feeling and run along
nerves
? Tiny specks of brownish macules in the axilla (axillary freckling)
TUBEROUS SCLEROSIS (SYN. BOURNEVILLES DISEASE)
? Two third cases ? sporadic, others - Autosomal dominant,
These are called facial angiofibromas (misnamed as adenoma sebaceum)
? Ungual or subungual fibromas, (Koenen's tumours) are small fleshy tumours that grow around and under
the toenails or fingernails
? Hypomelanotic macules ('ash leaf spots') are white or light coloured patches on skin (only visible sign of
? Shagreen patches are areas of thick leathery skin which is dimpled like an orange peel and is usually found
on the lower back or nape of the neck
? Caf? au lait macules can be seen
ICTHYOSIS
? Characterised by the accumulation of 'fish-like' scales due to abnormal epidermal cell kinetics
? Autosomal dominant Icthyosis
Icthyosis vulgaris ? most common type
X-linked icthyosis (seen in boys only)
Lamellar icthyosis
Icthyosiform erythroderma
Icthyosis vulgaris
? Begins in the first year of life
? The scales are larger over the lower extremities
? Mild keratoderma or (thickening of the skin over the palms and soles)
? The dryness becomes worse during winters and improves in summers and humid weather
? Histologically, the only abnormality detectable is a much diminished granular cell layer.
? Deficiency of steroid sulphatase
? The scales are dirty brown in colour and affect both the extensor and flexural surfaces of the extremities
with prominent involvement of the neck and trunk
? Associated disorders: cryptorchidism, ectropion
Acquired icthyosis: The most important cause underlying malignant disease ? particularly lymphoma ?such
as Hodgkin's disease
Tylosis: Marked thickening of palmar and plantar skin due to localized abnormality of keratinization.
XERODERMA PIGMENTOSUM
? An autosomal recessive disorder of DNA repair
? The most common defect - nucleotide excision repair (NER) enzymes are mutated.
? History - the child cries on exposure to light
? Development of freckles and lentiginosis on the exposed area of the body, such as the extensor aspect of
arms, face and the neck are early signs
? Later by adulthood squamous cell carcinoma, basal cell carcinoma, and malignant melanoma may form
EPIDERMOLYSIS BULLOSA
? Characterised by the formation of multiple blisters on gentle rubbing or on minimal skin trauma especially
over the trauma prone areas of the body
? There may be blisters in the pharynx, larynx, eyes and the genital mucosa.
? There may be contractures and mitten like deformities of hands in the severe variants
PALMOPLANTAR KERATODERMA
? Inherited defects due to mutations in the enzymes involved in the synthesis of keratin
? Skin over palms and soles becomes hard, thick, dry and hyperkeratotic
REFSUM'S SYNDROME (HEREDOPATHIA ATACTICA NEURITIS FORMIS)
? Accumulation of phytanic acid in all the tissues
? Cerebellar ataxia, polyneuritis, retinitis pigmentosa, nerve deafness, generalized ichthyosiform scaling.
DARIER'S DISEASE (KERATOSIS FOLLICULITIS)
? Inherited as an autosomal dominant disorder, but also occurs sporadically.
? Oral cavity shows: Cobble stone appearance
? V shaped nicking of nails seen
? Presence of tiny pits on the palms
? There is a curious loss of cohesion between keratinocytes above the basal layer
XI.
PEDIATRIC DERMATOLOGY
NEONATAL DERMATOLOGY
Transient Neonatal Pustular Melanosis
? Common in darkly pigmented infants
? Smear of sterile pustule shows numerous neutrophils
? Histology: subcorneal pustules with neutrophils
Erythema Toxicum Neonatorum
? Onset typically 24 ? 48 h after birth
? Occurs in half of all full-term infants
? Presents with blotchy erythematous macules, papules, pustules, and wheals
? Smear of sterile vesicle/pustule shows eosinophils
Neonatal Cephalic Pustulosis (Neonatal Acne)
? Onset typically within first 30 days
? Malassezia spp. implicated in pathogenesis
? Histology: follicular pustules with neutrophils
Sclerema Neonatorum
? Onset usually within first week of life
? Presents with diffuse woody hardening of skin
? Spares genitalia, palms, and soles
? Histology: needle-shaped clefts with necrotic adipocytes with little surrounding inflammation
Seborrheic Dermatitis
? Onset typically 1 week after birth; lasts several months, mostly resolves by 1 year of age
? Presents with ill-defined erythematous patches with waxy scale over scalp ("cradle cap"), ? axillae and groin
Aplasia Cutis Congenita (ACC)
? Localized defect in epidermis, dermis and/or fat
? Typically along midline
? Presents with erosion, ulceration, scar, or membranous defect (ovoid lesion covered by an epithelial
membrane)
Cutis Marmorata Telangiectatica Congenita (CMTC)
? Onset at birth
? Typically improves with age
? Associated anomalies in 1/2 of patients (varicosities, nevus flammeus, macrocephaly, ulceration, hypoplasia,
and/or hypertrophy of soft tissue and bone)
Congenital Infections of the Newborn
PAPULOSQUAMOUS AND ECZEMATOUS DERMATOSES
Psoriasis
? 25% patients will have presentation before age 15
? Guttate psoriasis more common in children
Acropustulosis of Infancy
? Onset from 6 months to 2 years; resolves by age 3
? Presents with recurrent crops of pruritic pustules on palms, soles, distal extremities (may mimic scabies
infection so prudent to perform mineral oil scraping)
PIGMENTED LESIONS
Lentigines
? Presents as brown macules with increased number of melanocytes
? No relationship to sunlight
LEOPARD Syndrome
PTPN11 gene mutation
Autosomal dominant
Caf?-noir macules
Hypertelorism
Pulmonary stenosis
Abnormal genitalia
Growth retardation
Carney Complex (LAMB or NAME syndrome)
PRKAR1A gene mutation
Autosomal dominant
Psammomatous melanotic schwannomas,
Blue nevi
Endocrine overactivity
Peutz?Jeghers Syndrome
STK11 gene (serine threonine kinase)
Mucocutaneous (oral/acral) lentigines
ntestinal polyposis, ? intussusception
Various malignancies
Laugier?Hunziker Syndrome
Longitudinal melanonychia
Genital melanosis
Bannayan?Riley-- Ruvalcaba Syndrome
PTEN gene mutation
Penile > vulvar lentigines
Lipomas
Hemangiomas
Ephelides (Freckles)
? More prominent in children with fair skin and during summer time
? Onset typically within first 3 years of age
? Can be a marker for UV-induced damage if acquired
? Histology: normal number of melanocytes, increased pigment in keratinocytes
? Onset at birth or first year typically
? Slight risk of melanoma (highest in large CNs)
? Axial nevi with greatest risk of developing melanoma
? Neurocutaneous melanosis: intracranial pressure, leptomeningeal melanoma, spinal cord compression
? Presents as dome-shaped red-brown or tan-pink smooth surfaced papule
? Typically occurs within first two decades
? Histology: K amino bodies (PAS + globules)
? Characteristic starburst dermoscopic finding in pigmented Spitz nevi
? Acquired unilateral lesion found in males (second or third decade) typically on shoulder, upper chest, or back
? Hyperpigmented hypertrichotic patch or plaque associated with underlying smooth muscle hamartoma
(arrector pili)
? Histology: melanin in epidermis, often smooth muscle hamartoma present in dermis
? Congenital or acquired (typically early childhood)
? Multiple blue nevi associated with Carney complex (LAMB/NAME syndrome)
? Histology: normal epidermis, many elongated dendritic melanocytes within dermis, large amounts of
melanin often seen within melanocytes
? Onset either near birth or during puberty
? Mostly in women
? Caused by the entrapment of melanocytes in the upper third of the dermis
? Presents as unilateral (90%), blue-gray hyperpigmented macules in the face (forehead, temple, malar area,
? Typically involving ophthalmic and maxillary branches of trigeminal nerve
? Most common extracutaneous sites: sclera (increased risk of glaucoma)
? Malignant melanoma develops very rarely
? Mongolian spot - a birthmark caused by entrapment of melanocytes in the dermis but is located in the
Nevus of Ito (Nevus Fuscoceruleus Acromiodeltoideus)
? Similar presentation to nevus of Ota
? Usually unilateral
? Typically occurs in shoulder region (supraclavicular, scapular, and deltoid)
? Onset in late adolescence
? Bilateral nevus of Ota-like macules of the zygomatic region
? May be misdiagnosed as melasma
Nevus achromicus (Nevus depigmentosus)
? Often, smaller hypopigmented macules arise around the edges, resembling a splash of paint
? Achromic naevus is not completely white (differentiates from vitilligo)
? Achromic naevi are usually solitary (in contrast to tuberous sclerosis, where multiple pale patches occur and
are called ash-leaf spots)
Congenital Dermal Melanocytosis (Mongolian Spot)
? Common in infants with pigmented skin
? Presents with blue-gray macules or patches typically over lumbosacral skin or buttocks
TELANGIECTASIAS
Spider Angioma (Spider Nevus)
? Common acquired lesion seen in children and adults
? Comprised of central arteriole with radiating thin walled vessels
? Temporary obliteration seen with compression
XII.
DISORDERS OF PIGMENTATION
Normal human skin colour is primarily related to size and the arrangement of melanosomes in melanocytes.
Melanocytopaenic
Melanopaenic
Non-melanotic
(Melanin decreased or absent)
(No melanin defect)
Piebaldism
Albinism
Vitiligo
Homocystinuria
Woronoff's ring
Vogt-Koyanagi-Harada syndrome
(hypopigmentation
Xeroderma pigmentosum
Nevus depigmentosus
around psoriasis
Tuberous sclerosis
lesions)
Pityriasis lichenoides chronica
Leprosy
Pityriasis alba
Leucoderma acquisitum centrifugum
Pityriasis versicolour
Burns (Ionising, Thermal, UV)
Trauma
inflammatory)
Alopaecia areata
Melanoma
Post-dermabrasion
Post-laser
VITILIGO
? A typical vitiligo macule has a chalk or milky white colour, round to oval in shape often with convex margins
? Associated with various autoimmune diseases, most commonly thyroid disorders
? Localized Vitiligo ? focal, segmental or mucosal
? Generalized Vitiligo is the most common type characterised by few to many to widespread macules
Acrofacial: distal fingers and periorificial areas
Mixed
? Universal Vitiligo indicates almost total involvement of the body with few remaining areas of pigmentation -
associated with various endocrinopathy syndromes.
? In the sharply demarcated, symmetrical macular lesions there is loss of melanocytes and melanin.
? Limited disease: Topical corticosteroids (triamcinolone)are the 1st line treatment
? Topical tacrolimus (0.03% and 0.1%) ointment - safe and effective in childhood vitiligo.
? Generalised Vitiligo: Narrow band UVB
? Topical or oral psoralen (8 methoxy psoralen) with UV-A (320 ? 400nm) radiation (PUVA)
Topical PUVA is used for old lesion involving <20% of body surface area
o
Oral psoralen is used in extensive disease or in patients not responding to topical PUVA
Albinism
? Normal number and structure of melanocytes
? Characteristic albino with white hair, white skin and blue eyes.
Piebaldism
? Autosomal dominant
? Stable leucoderma
? Characterised by chalk or milk-white macules like that of vitiligo
? Typical white forelock.
White patch of skin: differential diagnosis (Mnemonic: "Vitiligo PATCH")
? Pityriasis alba/ Post-inflammatory hypopigmentation
? Age related hypopigmentation
? Tinea versicolor/ Tuberous sclerosis (ash-leaf macule)
? Congenital birthmark
HYPERPIGMENTATION
Melanocytotic
Melanotic
(increase in melanin)
? Lentigines
? Caf?-au-lait macules
? Chronic pruritis
? Freckles
? Post inflammatory
? PUVA therapy
? Naevus spilus
? Lentigo, solar, UV (radiation tanning)
? Hemochromatosis
? Mastocytosis
? Melasma
? Exogenous ACTH
MELASMA
? Dark areas appear symmetrically across the cheeks, around the eyes and over the forehead, giving a mask-
like appearance
? Seen more often in people with dark skin
? The majority of cases appear related to pregnancy or oral contraceptives
? High expression of -MSH in the lesional keratinocytes plays an important role in the melanisation of skin
? Topical hydroquinone (2% to 4%) with retinoids and or steroids is the usual treatment
XIII.
SKIN IN SYSTEMIC DISEASES & MISCELLANEOUS
PARANEOPLASTIC SIGNS OF INTERNAL MALIGNANCY
? Acanthosis nigricans - Brown-back velvety plaques over neck and flexures
? (Sweet's syndrome)
? Acquired Ichthyosis - Dry fish-like skin most commonly in Hodgkin's lymphoma
? Clubbing - Severe grades of clubbing with lung carcinoma
? Dermatomyositis - 10% cases have associated with internal malignancy
? Hypertrophic osteoarthropathy - Subperiosteal new bone formation
? Migratory thrombophlebitis ? Pancreatic cancer
? Myeloma-associated amyloidosis - Skin nodules and purpura
Associated with endocrine neoplasm
? Necrobiosis lipoidica diabeticorum ? Diabetes mellitus
? Addisonian pigmentation - Adrenal corticotropin hormone (ACTH) secreting neoplasms
? Carcinoid tumours - Flushing of face and upper trunk
ACANTHOSIS NIGRICANS
? Primarily involves flexures ? axilla & groin.
? Thickened areas bear skin tags & seborrheic warts
? In majority of patients, it is associated with obesity (pseudo acanthosis nigricans) and insulin resistance
? The skin changes are reversible on weight reduction.
? Also seen in: Endocrine diseases like Cushings syndrome, Acromegaiy, Poiycystic ovarian disease, insulin
resistant DM
? HAIR- AN syndrome: in women, the triad of
Hyperandrogenism
Acanthosis nigricans
NECROBIOSIS LIPOIDICA DIABETICORUM
? A disorder of collagen degeneration with a granulomatous response, thickening of blood vessel walls, and
fat deposition
? Strongly associated with diabetes mellitus
? Usually present with shiny, asymptomatic patches that slowly enlarge over months to years
? The patient's main complaint is the unsightly cosmetic appearance of the lesions.
? Most cases of necrobiosis lipoidica occur on the pretibial area
? Major criteria for diagnosis of rheumatic fever
? Extremely rare in Indians
? Erythematous pink rashes with a clear center and round or serpiginous margin.
? Not raised above the skin
? Most commonly seen on the trunk and proximal parts of extremities, but never on face.
SKIN CANCER
BASAL CELL CARCINOMA, SQUAMOUS CELL CARCINOMA & MALIGNANT MELANOMA
MYCOSIS FUNGOIDES
? Also known as cutaneous T cell lymphoma
? More common in males and in blacks.
? An indolent lymphoma with patients often having several years of eczematous or dermatitic skin lesions
? Pruritus is a frequent complaint
? In advanced stages, the lymphoma can spread to lymph nodes and visceral organs
? Lymph node enlargement may be due to benign expansion of the node (dermatopathic lymphadenopathy)
or by specific involvement with mycosis fungoides.
picture sometimes referred to as L'Homme rouge
? The skin biopsy remains the basis of diagnosis
? Circulating malignant T cells (S?zary cells) can be detected in the blood (T cell gene rearrangement test)
? Ulcerative colitis
? Crohn's disease
? Rheumatoid arthritis
? Monoclonal gammopathy
XANTHOMA & LIPOPROTEIN DISTURBANCES
Xanthoma tendineum
Familial hypercholesterolemia (typella)
Xanthelasma palpebrarum
Familial hypercholesterolemia
Familial dybetalipidemia
Xanthoma eruptivum (or tubero
Familial dybetalipidemia
Familial combined hypertriglyceridemia
Familial lipoprotein lipase deficiency (rare)
Xanthoma striatum palmare
Familial dybetalipidemi (type Ill)
Patients often develop a monoclonal gammopathy associated
with myeloma (type Ill), macroglobulinemia, or lymphoma, and
with normal plasma lipid levels. Less commonly, FHT may be present.
CONDITION
Necrotizing fasciitis
Strep. Pyogenes
Erysipelas
Ecthyma
Erythrasma
Corynebacterium minuttissmus
Erythema migrans
Borrelia burgdorferi
Repetitive exposure to infrared rays
Erythema annulare centifugum
Hypersensitivity [gyrate erythema]
Erythema gyratum repens
Erythema dyschromicum perstans
Ashy dermatosis, idiopathic
Erythema chronicum migrans
Cutaneous manifestation of stage I Lyme disease
Localized fibrosing small vessel vasculitis
Erythema induratum of Bazin
Tuberculosis
Erythema infectiosum
Lesion
Found in
Erythema pernio (chill blain)
Cold
Sarcoidosis
Lupus profundus
SLE
Lupus Vulgaris
Phrynoderma
Vit-A deficiency
Essential fatty acid deficiency
Sauroderma/Crocodile skin
Weldt sores
Desert areas
Black hairy tongue
Broad spectrum antibiotics
AIDS (not candidiasis)
Rain drop pigmentation
Chronic Arsenic Poisoning
Pyoderma Gangrenosa
Slapped Cheek appearance
Erythema infectiosum
Honey Crust
Impetigo
Pseudoxanthoma Elasticum
Axillary freckling & Lisch nodule (Iris hamartoma)
Neurofibromatosis
Cradle cap appearance
Coyenne pepper stippling (d/t hemosiderin)
Plasma cell balenitis of Zoom
NIKOLSKY SIGN: Positive in
? Pemphigus Vulgaris / foliaceous & Epidermolysis bullosa congenita
? Stevens Johnson Syndrome
? Leukemia
? Herpes
The Asboe-Hansen sign ("indirect Nikolsky sign" or "Nikolsky II sign") refers to the extension of a blister to
SIGNS IN DERMATOLOGY
? Antenna sign ? Keratosis Pilaris
? Asboe Hansen sign (Bulla spread sign) ? Pemphigus
? Auspitz sign ? Psoriasis
? Birbeck's granules: Langhan cell histiocytosis
? Chandelier's sign - Gonorrhea in women
? Candle sign & last cuticle sign: Psoriasis
? Carpet tack's sign ? DLE
? Coup'd'ongue sign ?Tinea versicolor
? Crowe's sign ? Axillary freckling in Neurofibromatosis
? Comby sign: Measles
? Russell's sign: Bulimia Nervosa
? Deckchair sign: Papulo erythrodema
? Dimple sign (Fitzpatrick sign ) ? Dermato fibro sarcoma protuberans, differentiates dermatofibroma
? from malignant melanoma
? Dubois sign ? Short little finger in congenital syphilis
? Flag sign ? Kwashiorkor
? Forscheimer sign ? Enanthema on soft palate in Rubella
? Groove sign of Greenblat ? LGV
? Head light sign ? Perinasal and periorbital pallor in Atopic dermatitis
? Higouminaki's sign ? Congenital syphilis; thickened sternal portion of clavicle.
? Leopard sign: Onchocerciasis
? Milian's ear sign ? Erysipelas can spread into the pinna (being cuticular infection), whereas cellulitis cannot
spread to the pinna due to close adhesion of skin to cartilage of ear (without any areolar tissue.)
? Ollendorf sign ? Papule is very tender to touch in secondary syphilis
? Osler's sign ? Alkaptonuria
? Pillow sign ? Netherton's syndrome; hair shaft defect patient sees hair on pillow on getting up in the morning
? Trichrome sign ? Vitiligo
? Shawl sing ? Erythema over the upper back and shoulders in dermatomyositis
? Wrist sign , Thumb sign or Steinberg's thumb ? Marfan syndrome
IMPORTANT PEARLS:
? Spongiform pustule of Kogoj: accumulation of neutrophils in Malphigian layer.
? Tzanck cell: keratinocyte.
? Clue cells: vaginal epithelial cells
? Fordyce spots: ectopic sebaceous glands
? Binkley's spots: Diabetic dermatopathy
? Muehrcke's nail: seen in chronic hypoalbuminemia
? Circle of Hebra: seen in scabies
? Ritter's disease: caused by Staph. aureus
? Anatomist's wart: Tuberculosis verrucosa cutis/Warty TB
? Remote reverse Koebner phenomenon: Vitiligo
? Dermographism: Urticaria
? White dermographism: Atopy
? Dermatomyositis: Helitrope rash/ Gottron sign/ Gottron papule
? Most common form of oral candidiasis: acute pseudo membranous
? M/c dermatophyte producing favus: T. schoenleinii
? M/c photodermatoses: Polymorphic Light Eruptions (PLE)
? M/c manifestation of gonococcal infection in males: Anterior urethritis
? M/c manifestation of acute gonococcal infection in females: endocervicitis
? M/c cause of vaginal discharge in India: Bacterial vaginosis
? M/c cosmetic allergen: fragrances > hair dye
? M/c teeth affected in leprosy: upper incisors
? Black Piedra/ Trichomycosis nodularis: Piedraia hortae.
? White piedra: Trichosporon ovoides
? Copper penny bodies: Chromomycosis
? Profeta's law: fetus maybe born normal but may develop signs of early congenital syphilis during first few
weeks/months
? Colle's law: syphilitic infant may not infect its own mother but is capable of infecting others.
? Truck driver's disease: Hydradenitis suppurative of perianal region in males
Chloasma)
? Thinning of nails : involves nail matrix
? Dilapidated brick walls: Hailey-Hailey disease
? Syringoma: Tadpole like appearance
? Cork screw hair: Scurvy
? Selenium deficiency: Pseudoalbinism
? Louis bar syndrome: Ataxia telangiectasia
? Pseudo-Hutchinson's sign: Bowen's disease
? Keratosis follicularis squamosa: lotus leaves on water appearance
? Jigsaw puzzle appearance: cylindroma
? Trimethylamine: fish odour syndrome
? Urbach Wiethe disease: lipoid proteinosis
? Basal cell carcinoma: Bazex syndrome
? Erythema induratum affecting legs of young women: Bazin's disease
? Mouse ear appearance: X- ray feature of psoriatic arthritis
? Least affected in Atopic dermatitis: Mid chest
? Green nail syndrome with fruity odor: Pseudomonas aeruginosa
? Haverhill fever/ erythema arthriticum: Streptobacillus moniliformis
? Jungle sore: cutaneous diphtheria
? Woody fibrosis: actinomycosis
? Subcutaneous fat necrosis: Carcinoma pancreas
? Cigarette paper scars: Ehler Danlos Syndrome
? Hot tub follicles: Pseudomonas aeruginosa
? Slavic leprosy: Rhinoscleroma
? Alkaptonuria: sweat that stains
? Pseudo-Cushing's disease: chronic alcoholism
? Angel's kiss: Nevus flammeus
? Bath itch: Polycythemia rubra vera
? Effective drug for pruritus due to polycythemia rubra vera: Aspirin
? Mediator of pruritus in Hodgkin's Lymphoma: Leukopeptidase
? Syphilitic gumma: involves left atrium & septum
? Secondary syphilis never involves: bone
? Photopatch testing: patch testing + UV irradiation [to document photoallergy]
? Worm eaten skull: Gummatous osteoperiosteitis of skull bones in syphilis
? Earliest feature of congenital syphilis: nasal discharge
? Pseudo paralysis of parrot in congenital syphilis: due to osteochondritis.
? Olympian brow: Supra orbital thickening in syphilis
? Blaschko's lines: system of lines along which many linear nevus & dermatoses arrange themselves.
? Weber Christian panniculitis: seen in pancreatic disorders
? Shell nail: seen in bronchiectasis
? Foshay test: 48-hour intradermal test that, if positive, indicates tularemia.
? Berloque dermatitis: increased pigmentation due to cosmetics
? Treatment of choice for pruritis due to Uremia: UV light
? Acantholytic cells can be seen in bedside Tzanck test
? Pigmented purpuric dermatoses: shows recent pinpoint cayenne pepper--colored hemorrhages associated
*****END*****
FUNDAMENTALS OF DERMATOLOGY
Layers of Skin
? Skin is the largest organ in the body.
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? Total surface area: 1.7m2.? The layers of the skin are
o
Epidermis
o
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Dermiso
Subcutaneous fat/ hypodermis
EPIDERMIS
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? 0.4 -1.6 mm in thickness? Layers of epidermis:
Stratum corneum (Horny cell layer)
? Outermost layer
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? Made of flat, anucleated cells? No cell organelles
? Underdeveloped in preterm infants for 2-3 weeks.
Stratum lucidum
? Transparent layer
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? Seen only in palm & soleStratum granulosum
? Made of intracellular basophilic kerato hyaline granules
? Forms a water impermeable layer
? Contains abundant Odland bodies.
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? Layer absent in nail bed & matrixStratum spinosum or
? Provides mechanical strength to the skin
Prickle cells layer [Malphigian layer]
? Langerhan cells present.
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Stratum basale or? Single layer of columnar/ cuboidal cells
Stratum germinatum
? Contains mitotically active keratinocytes & melanocytes
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? Langerhans cells ? antigen-presenting cells, derived from bone-marrow and found in the prickle cell layer.? Langerhans cells are found scattered evenly throughout the epidermis.
? Merkel cells are normally located in the basal layer
? Merkel's (Tastzellen) cells ? slow adapting mechanoreceptors found in prickle cell layer.
? Keratin filaments are hallmark of keratinocyte
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? Keratinization: conversion of keratinocyte into keratin (4 weeks)? Adamson's fringe: beginning of Keratinization
? Abrupt Keratinization: seen in pilomatricoma
? Keratin expressed in basal layer: K5, K14
? 1 epidermal melanocyte unit: 36 keratinocytes
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? Skin doubling time: 4 weeks? Epidermal turn over time: 1 month
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? Accelerated cell turnover: psoriasis and ichthyosiform erythroderma [2 to 4 days]
? Lichen planus: the granular cell layer is focally increased.
? Nail first develops at: 3 months of intra uterine life
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? Finger nail growth: 0.1mm/day? Scalp hair growth: 0.35 mm/day
? Number of hair normally lost pev day:50-100
? Factors stimulating skin development (Epidermopoiesis): EGF, TGF-a, IL-II & fibroblast growth factor.
? Factors inhibiting skin development: Chalones, TGF-B, a and y interferons, TNF
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? Grenz zone: narrow clear zone B/W epidermis & dermis.? The stratum corneum of the palms and soles is about 0.5 mm thick and much thicker than that on the trunk
and limbs.
? Stratum corneum is permeable in preterm infants and becomes similar to the adult and full term infant after
2-3 weeks, postnatal maturation.
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? Acantholytic cells are derived from stratum basale in pemphigus vulgaris.? In humans there are two classes, the brown-black eumelanin, and the red-yellow phaeomelanin, both
derived from the substrate tyrosine.
? Most natural melanins are mixtures of eumelanin and phaeomelanin, and phaeomelanic pigments,
trichochromes, occur in red hair.
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? Racial variations in pigmentation are due to differences in melanocyte morphology and activity rather thanto differences in frequency or distribution
DERMIS
? Consists of connective tissue, cellular elements, and ground substance.
? Contains pilosebaceous, apocrine and eccrine structures.
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? Anatomically, it is divided into two compartments.Adventitial dermis: consists of thin collagen (Type III/reticulin) fibers located beneath the epidermis
(papillary dermis) and surrounding adnexal structures (periadnexal dermis).
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Reticular or deep dermis: composed of thick collagen (Type I) bundles & comprises the bulk of the dermis.? Type IV collagen is a major constituent of the basal lamina of the dermo-epidermal junction.
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SUBCUTANEOUS TISSUE
? Constitutes the largest volume of adipose tissue in the body.
? It provides protection from physical trauma and insulation to temperature changes.
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Blaschko's Lines:
? Represent the developmental growth pattern of skin.
? Do not correspond to any known nervous, vascular or lymphatic structures.
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? Blaschko's lines are characteristic of mosaicism and lionization.BLOOD SUPPLY OF SKIN
? No blood vessels in epidermis
? Necessary oxygen + nutrients diffuse from capillaries in the dermal papillae.
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? Glomus body: most commonly seen on the tips of the fingers and the toes, and under the nails.? Each glomus body consists of a venous and arterial segment, called the Sucquet-Hoyer canal.
SKIN GLANDS/APPENDAGES
Sebaceous glands:
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? Small saccular structures lying in the dermis.? Hair follicle + Sebaceous glands + arrector pill muscle
Pilosebaceous unit
? Present everywhere on the skin, except the palms and the soles.
? In most areas they are associated with hair follicles.
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? Sebaceous glands that are not associated with hair follicles:o
Buccal mucosa and vermillion border of the lip
o
Nipple, and areola of the breast, labia minora
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oEyelids (Meibomian glands).
? The sebaceous glands are holocrine glands.
? Secretion of sebum is not under any neurologic control but is a continuous outflowing of the material of cell
breakdown.
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? The sebum is mildly bacteriostatic and fungistatic and retards water evaporation.
? The scalp and the face may contain as many as 1000 sebaceous glands per square centimetre
Apocrine glands:
? Found in the axillae, genital region, external ear canal (ceruminous glands) and eyelid (Moll's glands).
? Breast (mammary gland) is also modified apocrine gland.
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? Apocrine glands are adrenergic; stimulated by epinephrine > nor epinephrine? Do not develop until the time of puberty.
? The secretions may act as pheromones (responsible for the production of body odor).
? Obstruction results in Fox Fordyce's disease
? Hidradenitis suppurativa, an inflammatory process that results from follicular obstruction and
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retention of follicular products, usually occurs in patients with the acne-seborrhea complex.Eccrine sweat (merocrine) glands:
? Distributed everywhere on the skin surface
? Most numerous on sole of foot (620/cm2) and least abundant on the back (64/cm9
? Glands first appear on volar surface of hands & feet in 3.5 month old fetus
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? Develop as a downgrowth from the primitive epidermis.? The eccrine sweat glands and the vasculature of the skin maintain stable internal body temperature.
? Their prime stimulus is heat and their activity is under the control of hypothalamus.
? Both adrenergic and cholinergic fibers innervate the glands.
?
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Blockage of the eccrine ducts results in miliaria (prickly heat).? If eccrine glands are congenitally absent, as in anhidrotic ectodermal dysplasia, a life-threatening
hyperpyrexia may develop.
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Fox Fordyce's Spot (Disease)? Fordyce spots are visible sebaceous glands without hair follicles.
? Extremely common, benign condition.
? Tiny white / yellowish focally grouped papules in buccal mucosa and vermilion border of lips, scrotum, shaft
of penis and labia
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? No treatment is indicated other than reassurance.Epidermal Stem Cells
? Three main locations of epidermal stem cells in the adult skin
o
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Bulge region of the hair follicleo
Interfollicular epidermis (IFE)
o
Sebaceous gland
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Stem cells of small blood vessels: PericytesSkin stem cells occur in the basal layer of the epidermis and at the base of hair follicles.
TERMINOLOGIES
? Acantholysis: loss of cohesion between epidermal cells, seen in all types of pemphigus.
? Acanthosis: increased thickness of the prickle cell layer due to stimulation of basal layer.
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? Dyskeratosis: premature keratinization of epidermal cells.? Foam cells: lipid-laden macrophages containing dead lepra bacilli.
? Hydropic degeneration of basal cells: vacuolization of basal cells seen in LE, dermatomyositis, early lichen
planus.
? Hyperkeratosis: Increased thickening of stratum corneum.
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? Parakeratosis: presence of immature nucleated cells in stratum corneum.? Spongiosis: accumulation of fluid between epidermal cells, seen in acute eczema.
Skin Lesions
Flat lesions:
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? Macule: < 2 cm, colored. Examples: white (vitiligo), brown (caf? au lait spot), purple (petechia).? Patch: > 2 cm, colored.
? Purpura: Extravasation of RBCs in the skin, blanches on pressure.
? Telangiectasia: Permanent dilatation of superficial vessels.
Elevated lesions:
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? Papule: < 1 cm, solid. Examples: acne, warts, small lesions of psoriasis.? Nodule: 1-5 cm, solid. Examples: tumors, granuloma annulare
? Tumor: > 5 cm, solid.
? Plaque: > 1 cm, flat topped. Example: psoriasis.
? Vesicle: < 1 cm, fluid-filled. Example: blisters of herpes simplex.
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? Bullae: > 1 cm, fluid-filled. Example: bullous impetigo.? Pustule: Vesicle filled with leukocytes. Examples: acne, folticulitis.
? Wheal: circumscribed, flat-topped, firm elevation of skin resulting from tense edema of the papillary dermis.
Example: urticaria
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Secondary changesScales
Dry, thin plates of keratinized epidermal cells (stratum corneum) Example: psoriasis,
Lichenification
Induration of skin with exaggerated skin lines and a shiny surface resulting from chronic
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rubbing of the skin. Example: atopic dermatitis.Impetiginization Bacterial infection resulting in exudation and golden-yellow crusting
Erosion and
A moist, circumscribed, slightly depressed area representing a blister base with the roof of
oozing
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the blister removed. Examples: burns, impetigo. Most oral blisters present as erosions.Crusts
Dried exudate of plasma on the surface of the skin following acute dermatitis. Examples:
impetigo, contact dermatitis.
Fissures
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A linear split in the skin extending through the epidermis into the dermis. Example: angularcheilitis.
Scars
A flat, raised, or depressed area of fibrotic replacement of dermis or subcutaneous tissue.
Atrophy
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Depression of the skin surface caused by thinning of one or more layers of skin.Example: lichen sclerosis.
Configuration of lesions
Annular
Annular nodules represent granuloma annulare; annular scaly papules are more apt to be
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(circular)caused by dermatophyte infections.
Linear (straight
Linear papules represent lichen striatus; linear vesicles, incontinentia pigmenti; linear
lines)
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papules with burrows, scabies.Grouped
Grouped vesicles occur in herpes simplex or zoster.
INTRA-EPIDERMAL BLISTERS:
Granular layer
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Spinous layerSupra basal layer
Basal Layer
Friction blister
Eczematous
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Pemphigus vulgarisLupus erythematosus
Pemphigus foliaceous
dermatitis
Darier's disease
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Lichen planusSub corneal pustular
Herpes virus infection
Epidermolysis bullosa simplex
dermatosis
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Familial benignStaphylococcal skin scald
pemphigus
syndrome / Bullous impetigo
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BLISTERS AT DERMAL EPIDERMAL JUNCTIONS:Junctional (at the lamina lucida)
Dermolytic (Below basal lamina)
Bullous Pemphigoid
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Epidermolysis bullosa dystrophicansErythema multiforme
Epidermolysis bullosa acquisita
Junctional Epidermolysis bullosa
Porphyria cutanea tarda
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Dermatitis herpetitiformisDIAGNOSTIC TECHNIQUES
Disease
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Diagnosed byAtopic Dermatitis
Clinical evaluation
Contact Dermatitis
Patch Test
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Donovanosis (GI)Microscopy (Donovan bodies/Safety pin appearance)
Chancroid
Gram staining(gram negative rods/ school of fish / rails road appearance
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? Grattage test: Psoriasis? Pethergy test: Behcet's syndrome
? Patch test: Contact dermatitis
? Dermatoscopy (Epiluminescence microscopy, dermoscopy): method of observing superficial layers of skin
using 10-100 X magnification under oil immersion.
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Tzanck Smear? Most commonly used in the diagnosis of herpes virus infection ? shows multinucleated giant cells.
? Also used in pemphigus ? shows acantholysis.
SKIN BIOPSY
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There are four principal techniques for performing skin biopsies:? Surgical excision with suturing:
o
Good cosmetic result
o
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Entire lesion is removed.o
Disadvantage: most time consuming of the three techniques, removal of the sutures.
? Punch biopsy:
o
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Inadequate for evaluation of vesiculobullous diseaseso
Should be deep enough to include subcutaneous fat if used for diagnosis of panniculitis or
o
tumors in a subcutaneous location.
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oPigmented lesions should not be punched unless they can be completely excised.
? Excision with scissors:
o
Useful for certain types of elevated lesions and in areas in which the cosmetic result is not too
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important.o
Advantage of this procedure is the speed and the simplicity with which it can be done.
? Shave biopsy:
o
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Can be performed superficially or deeply.o
Hemostasis can be accomplished by pressure, light electrosurgery, Monsel solution, or aluminium
chloride solution.
o
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Not recommended for excision of melanocytic lesions or other potentially malignant tumor wheremargin assessment is required.
WOOD'S LAMP
It is a source of ultra violet light (mainly long wave UV-A, at a wavelength of 360nm), from which virtually all variable
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rays have been excluded by filter (made of nickel oxide i.e. Ni02 and Si). It is used in:? Fungal infections like:
o Tinea capitis = yellow green fluorescence.
o Pityriasis versicolor = golden yellow / apple green
? Bacterial infections like:
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o Erythrasma & Acne = Coral red / pinko Pseudomonas pyocyanea = yellow-green
? Pigmentary disorder
o Vitiligo = total white
o Ash-leaf macules in tuberous sclerosis = blue white
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? Urine examination in Porphyria (red / pink urine)? Squamous cell carcinoma of skin = red fluorescence
Type of collagen
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LocationI
Bone
II
Cartilage, vitreous tumour, Intervertebral disc
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IIIExtensive - skin, lung, hollow organ (vascular system)
IV
Basement membrane, Eye lens
VII
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Anchoring fibrils at Dermo-epidermal junctionVIII
Endothelium
X
Hypertrophic cartilage
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XVIISkin, hemidesmosomes
XVIII
Liver, kidney
XIX
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Rhabdomyasarcoma cellsDistributions of Glycosaminoglycans (GAGS):
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Hyaluronic acidSynovial fluid, Vitreous humour, Loose connective tissue
Chondroitin sulphate
Cartilage, bone, cornea
Keratan sulphate-I
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CorneaKeratan sulphate-II
Loose connective tissue
Heparin
Mast cells
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Heparan sulfateSkin, Fibroblasts
Dermatan sulphate
Wide distribution
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PANNICULUS ADIPOSUS? The panniculus adiposus is the fatty layer of the subcutaneous tissues, superficial to a deeper vestigial layer
of muscle, the panniculus carnosus.
? It includes structures that are considered fascia by some sources but not by others.
? Eg: Fascia of Camper, superficial cervical fascia.
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II.
SOLAR INJURY
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ULTRA VIOLET RADIATIONS? UVR of wavelength 250-400 nm is of major importance as far as skin is concerned.
? Narrow-band UVR is UVR at a wavelength of 311 nm
UV-A
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UV-BUV-C
(Long-wave UVR)
(Medium-wave UVR)
(Short-wave UVR)
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320-400 nm280-320 nm
250-280 nm
? 1000-fold less effective at causing
? UV-B [around 290 nm]: mainly
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? Mostly filterederythema
responsible for sunburn, suntan and
Out by the
? Penetrate to the dermis
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? skin cancer.ozone layer
? Play a role in causing the dermal
? UVB penetrates as far as the basal
degeneration known as solar
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layer of the epidermis, but causes theelastosis, which is responsible for the
death of scattered keratinocytes
appearance of ageing & the cause of
(sunburn cells) & damages others
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skin cancerrelease cytokines and mediators.
? Responsible for photosensitivity
? 2 days after UVR injury, there is an
reactions
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increase in the rate of melaninsynthesis.
Polymorphic light eruption (PMLE)
? A common disorder, occurring in young and middle-aged women
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? Itchy papules and papulovesicles on exposed sites -- particularly the forearms? The rash develops shortly after sun exposure throughout the spring and summer months
? PMLE is chronic in nature
? The action spectrum of PMLE may also extend into the long ultraviolet wavelengths (UVA; 320-400 nm)
? Patients improve when they avoid sun exposure and use sunscreens blocking UVA
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? Treatment: Weak topical corticosteroids? For severe rashes -- hydroxychloroquine or even azathioprine
Photodermatitis
? Painful or pruritic erythema, edema, or vesiculation on sun-exposed surfaces: the face, neck, hands, and "V"
of the chest.
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? These eruptions may become generalized with time to involve even photoprotected areas? Sunscreens with an SPF of 30-60 and broad UVA coverage, containing dicamphor sulfonic acid, avobenzone,
titanium dioxide, and micronized zinc oxide, are useful
? Photosensitivity due to porphyria is not prevented by sunscreens and requires barrier protection (clothing)
to prevent outbreaks.
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Dermatoses aggravated by solar exposure: Lupus erythematosus, Rosacea, Atopic dermatitisDermatoses improved by sun exposure: Psoriasis, Acne
III.
SKIN INFECTIONS
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The stratum corneum is an excellent barrier to pathogenic micro-organismsThe following organism live in the follicular lumina without normally causing harm
o
Gram-positive cocci (Staphylococcus epidermidis)
o
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Gram-positive lipophilic microaerophilic rods (Propionibacterium acnes)o
Gram-positive yeast-like organism (Pityrosporum ovale or Malassezia furfur)
Dermatophyte infections are restricted to the stratum corneum, the hair and the nails (i.e. horny structures).
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PITYRIASIS VERSICOLOR? Caused by yeast-like micro-organism Pityrosporum ovale (orbiculare) or Malessezia furfur
? Becomes pathogenic when its growth is encouraged by increased sebum secretion or depressed immunity
? Pale, scaling hypopigmented macules develop over the skin of the chest and back in young adults (Picture
III-E)
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? Fine velvety scales that are not visible but are seen by scraping the lesion.? Central upper trunk the most frequent site.
? Microscopy: grape-like clusters of spores and a meshwork of pseudomycelium in skin scrapings made more
transparent by soaking the scales for 20 minutes in 20 per cent potassium hydroxide.
? Skin surface biopsy
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oPermanent preparation made using cyanoacrylate adhesive to remove a strip of superficial stratum
corneum from the skin surface on a glass slide
o
The slide is 'rolled off' the skin after 20 seconds and then stained with periodic acid- Schiff reagent
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oThe skin patches often fluoresce an apple green in long-wave UVR (Wood's light).
? Treatment
o
Topical imidazole creams (e.g. miconazole, clotrimazole, econazole) for 6 weeks or
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oKetoconazole shampoo to wash the affected areas once daily for 5 days
TINEA INFECTIONS
? Also called Dermatophytoses or Ring worm
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? Trichophyton, Microsporon and Epidermophyton species are responsible for this group of infections.? T. rubrum, T. mentagrophytes and E. floccosum are the M/c causes of dermatophyte infection
? Inflammatory ringworm can be caught from cattle (T. verrucosum) and horses (T. equinum).
? Hypersensitivity to fungal antigens ? vesicular lesions - dermatophytids (id reaction)
? Hypersensitivity can be demonstrated by skin testing with fungus antigen ? trichophytin
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? Favus - chronic type of ring worm which leads to alopecia and scarring? Kerion ? scalp infection with marked inflammation producing severe boggy swellings
? The diagnosis is confirmed by microscopy of skin scrapings, hair or nail clippings treated with 20% potassium
hydroxide for 20 minutes and identification of fungal hyphae.
? Use of the cyanoacrylate 'skin surface biopsy technique' makes identification quite easy.
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TRICHOPHYTON
MICROSPORUM
EPIDERMOPHYTON
? Infects Hair, nail and skin
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? Infect hair and skin but not nails? Infects skin and nails but not hair
? Abundant microconidia
? Scanty microconidia
? Microconidia absent
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? Scanty macroconidia? Abundant macroconidia (spindle
? Macroconidia are pear or club
(pencil shaped)
shaped)
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shapedTinea corporis or Tinea circinata (Body ring worm)
? Pruritic, ring-shaped lesions with an advancing scaly border and central clearing
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? Can be distinguished from eczema or psoriasis by history and the presence of mycelium in the scales.Tinea cruris or Groin ring worm (Jock itch or Dhobis's itch)
? A disorder of young men
? Marked itching in intertriginous areas, usually sparing the scrotum.
? Peripherally spreading, sharply demarcated, centrally clearing erythematous lesions asymmetrically on the
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medial aspects of both groins? These gradually extend down the thigh and on to the scrotum unless treated
Tinea manuum
? One palm is involved which is usually dull red with silvery scales in the palmar creases
? T. rubrum is the usual cause
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Tinea capitis? Ringworm of the scalp occurs in children exclusively
? Mainly due to M. canis or Trichophyton tonsurans
? It invades the hair cuticle (ectothrix infection), causing pink, scaling patches on the scalp skin
? There is patchy loss of hair (only broken hair) with variable degrees of inflammation (to differentiate from
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alopaecia areata - no inflammation and total loss of hair from the root)? It is easily spread by the sharing of hairbrushes.
? Infected areas sometimes fluoresce a light green under long-wave UVR (Wood's light)
? Scalp ringworm caused by T. schoenleini, invades the interior of the hair shaft (endothrix) and causes
intense inflammation on the scalp, with swelling, pus formation and scalp scarring.
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Tinea unguium (Onychomycosis)? Ringworm infection of the nail plate and the nail bed.
? The fungi responsible are T. rubrum, T. metagrophytes or E. floccosum.
? Onycholysis occurs and subungual debris collects
? More common in the toenails than in the fingernails
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Tinea incognito? Eextensive ringworm with an atypical appearance
? Due to the inappropriate use of topical corticosteroids.
Tinea barbae
? Also called barber's itch or Tinea Sycosis
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? Caused by T. Mentagrophytes & T. VerrucosumDermatophytoses
Causative agent
Tinea capitis
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Microsporum, TrichophytonT corporis
T rubrum
T cruris
E floccosum, T rubrum
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T pedis (atheletes foot)E floccosum, T rubrum
Favus
T schoenleinii, T violaceum
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Treatment? Topical imidazole-containing preparation (miconazole, econazole and clotrimazole) used twice daily for a 3-
4-week period is usually adequate
? When topical treatment fails
o
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Griseofulvin (500 mg b.d.) - only active in ringworm infectionso
Ketoconazole (200 mg daily) or Itraconazole - active in both yeast and dermatophyte infections.
CANDIDIASIS (MONILIASIS, THRUSH)
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? Caused by a yeast pathogen - Candida albicans? A commensal of oral cavity, lower GIT and vagina
? Inflammatory papules and plaques with satellite pustules, frequently in intertriginous areas
? Treatment with the imidazole preparations, topical and systemic
? Serious Candida infections respond to systemic fluconazole.
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Bacterial infection of the skin
Staphylococcus aureus
? Impetigo contagiosa
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? Bullous impetigo? Ecthyma
? Botryomycosis
? Superficial folliculitis (follicular or Bockhart impetigo)
? Folliculitis (sycosis barbae)
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? Furncle (boil), carbuncle? Blistering distal dactylitis
? Paronychia
Group A Streptococci
? Impetigo
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? Ecthyma? Blistering distal dactylitis (in nonintertriginous skin) and intertrigo
? Vulvovaginitis
? Perianal cellulitis
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Pyoderma gangrenosum, pyoderma faciale & impetigo herpetiformis are not pyodermas.Trichomycosis axillaris & pubis is a bacterial (aerobic corynebacterium) not fungal infection of hair shaft.
Erythrasma is superficial bacterial infection of skin caused by corynebacterium minutissimum.
IMPETIGO (PYODERMA)
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? It is a contiguous, superficial pyogenic infection of skin? Pyodermas are infection in epidermis, just below the stratum corneum or in hair follicles.
? Two main clinical forms
o
Bullous impetigo caused by S. aureus mostly
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oNonbullous impetigo (or impetigo contagiosa or Tilbury Fox) may be caused by Staphylococcus aureus
(most common); by group A-beta haemolytic streptococci (mainly in developing nations) or by both.
? Most commonly affects children
? Most common bacterial infection of children
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? Occurs in all age including adults and neonates (called pemphigus neonatorum)? Spread by close contact (contagious).
? Bullous impetigo
o
Bullae are less rapidly ruptured
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oLarger (1-2cm)
o
Persist for 2-3 days
o
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After rupture thin, flat brownish crusts are formed.? Streptococcal impetigo may lead to
o
Post streptococcal acute glomerulonephritis (AGN)
o
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Scarlet fevero
Erythema multiforme
? Rheumatic fever is not a complication of streptococcal impetigo
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IMPETIGO CONTAGIOSA? Caused by Staphylococcus aureus and/or beta hemolytic Streptococci
? It is mostly a disorder of prepubertal children
? Initial lesion is a very thin walled vesicle on an erythematous base which ruptures so rapidly that its seldom
seen
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? Gradual, irregular, peripheral extension occurs without central healing? Lesions are usually not painful, heals without scarring, no fever and patient is not ill
? Characteristic feature
o
Golden or Honey colored crust
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oNeutrophils beneath stratum corneum
? Face around nose and mouth) and limbs are most commonly affected
Erysipelas
? Caused by the beta-haemolytic Streptococcus
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? Sudden onset of a well-marginated, painful and swollen erythematous area, on the face or lower limbs.? The inflammation may be very intense and the area may become haemorrhagic and even blister.
? There is usually an accompanying pyrexia and malaise.
Pyoderma faciale
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? Also called rosacea fulminas or rosacea conglobate? Occurs mainly in adult women (in 20s)
? Sudden, severe eruption of confluent papules, nodules, pustules, cystic swellings which may be
interconnected by draining sinuses usually confined to face, involving checks, chin, nose, & forehead
? Comedones are usually absent or inconspicuous, as are other features of acne vulgaris or rosacea
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? Some cases may develop during pregnancy or medication (interferon alpha-2B & ribavirin therapy forhepatitis C)
TOXIC EPIDERMAL NECROLYSIS/ STAPHYLOCOCCAL SCALDED SKIN SYNDROME (SSSS)
Also called LyeII syndrome
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? Caused by ET (Exfoliative / Erythematogenic toxin) producing Staph. aureus (phage group II)? Most common site of infection is extracutaneous
? Wide spread erythematous blisterous eruption with striking desquamation of large areas of skin (Nikolsky
sign positive) as seen in scald or burn.
? Mucosa is not involved.
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? Initial findings are redness & tenderness of central face, neck, truck & interiginous zone followed by shortlived flaccid bullae & slough or exfoliation or peeling of superficial epidermis.
? Treated by IV antibiotics
CUTANEOUS TUBERCULOSIS
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Lupus Vulgaris? Slowly progressive, granulomatous plaque on the skin
? It slowly increases in size, over one, two or three decades.
? Blanching with a glass microscope slide (diascopy) will reveal grey-green foci (apple jelly nodules)
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Tuberculosis Verrucosa Cutis (Warty Tuberculosis)? Seen on the backs of the hands, knees, elbows and buttocks whenever abrasive contact with the earth and
tubercle bacilli has been made.
? Thickened, warty plaques are present - sometimes misdiagnosed as viral warts
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Different types of cutaneous TB? Lupus vulgaris (Apple-jelly nodules)
? Lupus miliaris disseminate faciei
? Lichen scrofulosoeum
? Scrofuloderma (skin T.B. secondary to underlying structure)
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? Tuberculosis cutis orificalis (TB. of orifices - oral, anal, urogenital)? Papulo necrotic tuberculids
? Erythema nodosum
? Erythema induratum
? Acne agmination
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Other Mycobacterial InfectionsSwimming pool granuloma
? Caused by Mycobacterium marinum
? Causes plaques, abscesses and erosions on the elbows and knees in particular.
? The condition responds to minocycline or a trimethoprimsulphamethoxazole combination.
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Buruli ulcer? Mycobacterium ulcerans is responsible for this disorder
? Surgical removal is currently the best treatment.
SARCOIDOSIS
? Bluish chilblain-likeswellings of the fingers, nose and ears (lupus pernio) ? infiltrated by typical sarcoid tissue
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? Erythema nodosum ? not infiltrated by typical sarcoid tissue? Histologically of the typical Sarcoid lesion: 'naked' tubercle, which contains foci of macrophages and giant
cells without many surrounding lymphocytes.
LYME DISEASE
? Caused by the Borrelia burgdorfii
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? Early stages - erythema chronicum migrans? Late stages - skin atrophy (acrodermatitis chronica atrophicans), or fibrosis
Viral infection of the skin
HERPES SIMPLEX
? Type I is responsible for the common herpetic infection of the face and oropharynx
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? Type II herpes simplex infects the genitalia? 20 % suffer from recurrent 'cold sores', precipitated by minor pyrexial disorders or sun exposure.
? Commonly, the lesions occur around the mouth or on the lip.
? Genital herpes affects the glans penis and the shaft of the penis.
? In women, the vulval region or labia minora is usually involved
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HERPES ZOSTER (SHINGLES)? Mostly affects those past the age of 50 years
? Also affects immunosuppressed individuals
? Due to the reactivation of a latent virus in a posterior root ganglion of a spinal nerve
? Starts with paraesthesiae or pain in the distribution of one or more dermatomes (Picture III-F)
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? Dermatome frequently affected - thoracic? Involvement of one of the branches of the trigeminal ganglion, with lesions in the distribution of the
maxillary, mandibular or ophthalmic sensory nerves, is common
? Lesions are confined to the skin innervated by the dorsal primary root (s) infected
VIRAL WARTS
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? Caused by a member of the human papillomavirus family? Epidermodysplasia vericuformis
o
Congenital condition
o
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Plane warts spread extensively on the arms, face, trunk and limbso
Some lesions can transform to squamous cell carcinoma
? Verruca vulgaris (Picture III-G)
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Treatment? Cryotherapy (tissue freezing with liquid nitrogen or solid carbon dioxide)
? Curettage
? Cautery
? Chemical destruction with topical preparations containing salicylic acid, lactic acid, podophyllin or
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glutaraldehyde.? Intracutaneous injections of cytotoxics such as bleomycin and injections of recombinant interferon.
MOLLUSCUM CONTAGIOSUM
? Caused by virus of pox virus group
? Transmitted by skin to skin contact and is a STD.
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? Typical lesion is pink or skin colored, umbilicated papule containing a grayish central plug? Face & genitals are commonly involved
? Face is most commonly involved in children
? Pathology: Cup shaped epidermal thickening with characteristic degenerative change in granular cell layer &
Molluscum bodies on giemsa stain is pathognomic.
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LEISHMANIASIS? Cutaneous form seen in Mediterranean and North America (Old World leishmaniasis)
o
Ccaused by Leishmania major and L. tropica.
o
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A boil-like lesion appears, usually on an exposed site ('Baghdad boil')o
Later, this breaks down to produce a sloughy ulcer ('oriental sore'), which persists for some
months before healing spontaneously, with scarring and the development of immunity.
? Mucocutaneous forms occur mainly in South America (New World leishmaniasis)
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oCaused by L. mexicana and L. brasiliensis.
o
Small ulcers develop (Chiclero's ulcer) that seem more destructive than the Old World types
o
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Also more persistent, and later in the disease destructive lesions appear, affecting nasal mucosa inabout half of the patients
IV.
SKIN INFESTATIONS
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ECTOPARASITESPhthirus pubis
Pubic lice infestation
Pediculus humanus
Pediculosis
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Sarcoptes scabieiScabies
SCABIES
Epidemiology:
? Infestation caused by Acarus hominis/Sarcoptes scabie.
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? Incubation period is 2-4 weeks.? Itching worse at night is most common symptom.
? Family history of similar itchy eruptions in close contact
? On an average, an adult has 12 mites and an infant 20 mites.
Primary lesions:
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? Serpentine (S-shaped) burrows traversed by parasite in stratum corneum (pathognomic lesion)? Most common sites involved: Inter digital space, Anterior wrist, Ulnar border of hand
? An imaginary circle intersecting the main sites of involvement--axillae, elbow flexures, wrists and
? hands and groins - 'circle of Hebra'.
? In infants and elderly: Scalp, Face, Neck, Palms & Soles, Penis also involved
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? Papules & papulo-vesicles: due to hypersensitivity to the mite.? Fine pin head size follicular papules
Secondary lesions:
? Pustules due to 2? infection is one of commonest form of presentation.
? Eczematized crusted lesion, in infants & children are predominant lesions.
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? Nodular lesions are seen on scrotum (most common), groin, and anterior axillary fold (Nodular scabies).Types:
? Crusted or Norwegian scabies
o
Most severe form
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oThe average number of mites in these cases is 2 million
o
Seen in immuno compromised, mentally ill patients, GVDH, leprosy, leukemia
o
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Psoriatiform or warty lesions accompanied by nail hyperkeratosiso
No burrows
o
Minimal itching
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oHighly contagious
o
Ivermectin is the treatment of choice
? Scabies incognetio - wrongly treated with steroids.
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Treatment? Drug of choice : 5% Permethrin (1st ) BHC (2nd ).
? Oral drug (Only): Ivermectin.
? Other drugs : Benzyl benzoate 25%, Crotamiton 10%, Malathion, Monosulfiram.
? Drug safe in pregnancy & infants < 2 months: precipitated sulfur 5-10%.
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? Scabicides should be applied to the whole body (below jaw line in adults) to all members of family whethersymptomatic or not.
PEDICULOSIS
? Macula cerulea (bluish stain on the skin d/t louse bite) is a typical lesion of Pediculosis
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P. Capitis
? Transmitted by Head louse
? Involves scalp
mobile dandruff
? Common in girls with long hairs
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? The diagnosis is made by seeing the lice in the scalp or more often, nits glued to the hair shaftP. Corporis (Vagabond's disease.)
? Transmitted by Body louse
? The body louse transmits
o
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Epidemic typhuso
Trench fever
o
Relapsing fever
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? The diagnos s is positively established by finding the lice or nits in the seams of clothing? Treatmeot: disinfection of clothes with 10% DDT or 1% BHC + Pediculocide drug application
Pthirus Pubis (Pubic louse):
? Is a STD, can also infest body, axillary, and eyelash hairs
? In children the common areas of involvement are the eyebrows and eyelashes (pediculosis palpebrum)
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? Diagnosis is made on seeing black speck like bodies attached to the root of hair at an angle--t.,e crab liceV.
IMMUNE MEDIATED SKIN DISORDERS
URTICARIA (nettlerash, 'weals' and 'hives')
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? Urticaria is a vascular reaction pattern characterised by transient, erythematous, oedematous papules orplaques (wheals) of varying sizes and shapes which are usually pruritic.
? Angioedema is the same process but involves the deep dermis, subcutaneous and submucosal tissues
? Urticaria -- dermal edema
? Angioedema -- subcutaneous, submucosal edema
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? Result of histamine release from mast cells in the skin.? Type I hypersensitivity mediated by histamine.
? Lesions are itchy, red papules and plaques of variable size that arise suddenly, often within a few minutes
THE 'PHYSICAL' URTICARIAS
Cold urticaria
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? Occur after exposure to the cold.? The reaction can be elicited by an ice block.
? There is a familial form.
Pressure urticaria
? Lesions develop some time (up to several hours) after pressure on the skin
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? For example from belts or other tight clothing, or from the rungs of a ladder.Dermographism
? Many patients with urticaria mark easily when their skin is rubbed firmly, for example with a key.
? This is an exaggerated 'triple response' and is quite troublesome to some patients
Solar urticaria
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? Urticaria spots develop on exposed skin a few minutes after exposure to the sun.? It is a skin sign of one systemic disease-- erythropoietic protoporphyria
Cholinergic Urticaria
? Irritating, small urticaria spots develop after exercise, hot baths, emotions
? Occurs after stimuli that evoke sweating from the post-ganglionic cholinergically enervated sweat glands.
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DRUG-INDUCED URTICARIA? Penicillin
? NSAIDs
? Sulphonamides
? Aspirin
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Urticaria lesions are seen in patients with? Mastocytosis (urticaria pigmentosa)
? Hypo- or hyperthyroidism
? Systemic-onset juvenile idiopathic arthritis (Still's disease)
ERYTHEMA MULTIFORME (EM)
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? EM minor: an acute, self-limiting, usually mild, often recurrent inflammatory syndrome characterised bysymmetrically distributed erythematous papular, urticaria and typical iris/target shaped lesions (Picture:V-
A)
o
Cause: Herpes simplex virus ? most common cause of recurrent EM
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? EM major: more severe variant with extensive mucous membrane involvement and constitutional symptomso
Cause: HSV, Mycoplasma, Drugs (sulfonamides, phenytoin, barbiturates, aminopenicillins, non-
nucleoside reverse transcriptase inhibitors, and carbamazepine)
o
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Hemorrhagic crusts of lips? The term "erythema multiforme major" has been replaced by three terms
o
Stevens-Johnson syndrome (SJS), with < 10% BSA skin loss
o
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Toxic epidermal necrolysis (TEN) when there is > 30% BSA skin losso
SJS/TEN overlap for cases with between 10% and 30% BSA denudation.
? Skin biopsy is diagnostic.
? Direct immunofluorescence studies are negative
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ERYTHEMA NODOSUM? Painful crops of nodules develop in response to antigenic stimuli mostly in shins & forearms.
? Women are predominantly affected by a ratio of 10:1 over men
Causes of erythema nodosum
? Tuberculosis ? most common
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? Sarcoidosis? Leprosy (lepromatous type LL & BL)
? Brucellosis
? Streptococcal infection
? Ulcerative colitis & Crohn's disease
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? Oral contraceptivesLUPUS ERYTHEMATOSUS
? Skin involvement is the 2nd most common clinical manifestation after joint inflammation and is found in up to
70% of patients
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? The two most common forms of chronic cutaneous lupus erythematosus (CCLE) areo
Chronic scarring (discoid) lesions (DLE)
o
Erythematous non-scarring red plaques (Subacute cutaneous LE) (SCLE).
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? Discoid LE (DLE) or Chronic cutaneous LE? The lesions are most commonly found on face and neck
? Permanent hair loss (scarring alopecia) and loss of pigmentation are common sequelae of discoid lesions.
? There is atrophy, telangiectasia, depigmentation, and follicular plugging by scales
? When the scale is removed, its underside shows small excrescences that correlate with the openings of hair
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follicles (carpet tacking or thumbtack like)? The disorder may be aggravated or initiated by exposure to the sun.
? Histology: epidermal degenerative changes are more marked, with scattered cytoid body formation and
patchy epidermal atrophy and thickening
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Treatment? Sun avoidance and use of sunscreens
? Individual lesions sometimes respond to potent topical corticosteroid
? For unresponsive lesions - hydroxychloroquine (200-400 mg per day) is often helpful.
SYSTEMIC SCLEROSIS
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Progressive systemic sclerosis? The disease is mostly seen in young women
? Gradual thickening and stiffening of the skin of the hands and face
? This causes a characteristic beak-like facial appearance, with narrowing of the mouth
? There are pigmentary changes over the face and neck in the form of hyperpigmentation and depigmentation
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(pepper-salt pigmentation) (Picture V-B)? Telangiectatic macules appear over the face and deposits of calcium develop in the skin.
? Fingers: sclerodactyly or sausage shaped fingers with taut skin over the fingers and thimble pitted scars over
fingertips
? Raynaud's phenomenon is almost a constant feature
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? CRST syndrome (Calcinosis cutis, Raynaud phenomenon, Sclerodactyly, and Telangiectasia)? When there is also dysphagia due to Esophageal involvement - CREST syndrome
Morphoea or Localized Scleroderma.
? Linear scleroderma - involvement of the face and/or forehead manifesting as Parry-Romberg syndrome and
'en coup de sabre (depressed sclerotic groove over the frontal/frontoparietal region of the scalp)
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? Anti-topoisomerase II antibodies have been detected in 76% of patients with localised scleroderma and in85% of cases of generalised morphea
? These antibodies, in contrast to antitopoisomearsel/scl-70 antibodies have been found in 14% of the patients
with systemic scleroderma.
DERMATOMYOSITIS
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? An idiopathic inflammatory myopathy of striated muscles along with characteristic cutaneous findings
? Linked to human leucocyte antigen (HLA) DR3, DRS, DR7
? The pathognomonic cutaneous features
o
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Heliotrope rash (periorbital confluent macular mauve or violaceous erythema)o
Gottron's papules (papules having violaceous hue overlying the dorsolateral aspect of interphalangeal
or metacorpophalangeal joints)
? Other cutaneous features are
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oMalar erythema
o
Poikiloderma (variegated telangiectasia along with atrophy and hyperpigmentation)
o
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Periungual and cuticular changes (cuticular hypertrophy with haemorrhagic infarcts)o
Mechanics hands (fingertip erythema and scaling).
o
Calcinosis cutis - firm yellow or flesh coloured nodules extruding calcium through the skin
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IMMUNE MEDIATED BULLOUS DISORDERS:Intra-epidermal bullae
Sub-epidermal bullae
? Pemphigus vulgaris
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? Bullous pemphigoid? Pemphigus vegetans
? Cicatricial pemphigoid
? Pemphigus foliaceous
? Dermatitis herpetiformis
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? Pemphigus erythematosus? Linear IgA buloous dermatosis
? Drug induced pemphigus
? Pemphigoid gestationis
? Paraneoplastic pemphigus
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? Epidermolysis bullosa aquisitaClinical
Histology
Immunopathology
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Auto antigensPemphigus
Crusts and shallow
Acantholytic blister
Cell surface deposits
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Desmogleins (Dsg1)foliaceous
erosions on scalp,
formed in
of IgG on
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central face, uppersuperficial
keratinocytes
chest and back
layer of epidermis;
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(epidermis)Pemphigus
Flaccid blisters,
Acantholytic blister
Cells surface
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Dsg 3 (+ Dsg 1 invulgaris
Painless,
formed in supra
deposits
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patient with skinPicture: V-C
MC site: buccal
basal layer of
of IgG on
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involvement)mucosa
epidermis
keratinocytes
Nikolsky sign: + ve
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(epidermis)Bullous
Large tense blisters,
Blister formed in
Linear band of IgG
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Proteins in basalPemphigoid
Painless
sub epidermal
and C3 across the
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keratinocytesPicture: V-D
MC site: extremities
region; eosinophil-
basement embrane
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Bullous Pemphigoid(Senile
Nikolsky sign: - ye
rich infiltrate
zone (BMZ)
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AntiGen. Twopemphigoid)
Associated with
Acantholysis: - ye
Linear band of C3 in
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important BPPemphigoid
Lymphoma
Teardrop-shaped,
epidermal BMZ.
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antigens: BP 230gestationis
Pruritic, urticaria
sub epidermal
and BP180 (BPAG 1,
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plaques, rimmed byblister in dermal
BPAG 2)
vesicles & bullae on
papillae; eosinophil-
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BPAG2 (plus BPAG1the trunk and
rich infiltrate.
in some patients).
extremities
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Linear IgAlarge tense bullae
Sub epidermal
Linear band of IgA,
LAD
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bullousfilled with clear or
blister with
in epidermal BMZ
disease or
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haemorrhagic fluid on neutrophils inChronic
or near genitalia,
dermal papillae
bullous disease
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arciform blister,of childhood
cluster of jewels
appearance
Cicatricial
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Erosive and / orSub epidermal
Linear band of IgG,
BPAG2
pemphigoid
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blistering lesions ofblister
and /or C3 in
mucous membranes
epidermal BMZ
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and possibly the skin;Epidermolysis
Blisters, erosions,
Sub epidermal
Linear band of IgG,
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Type VII collagen.bullosa
scars, and milia on
blister
and /or C3 in
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acquisitasites exposed to
epidermal BMZ
trauma;
nflammatory,
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tense blisters seeninitially
Dermatitis
Extremely pruritic
Sub epidermal
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Granular deposits ofEpidermal
herpetiformis
small and vesicles
blister with
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IgA in dermo-transglutaminase
mostly on elbows,
neutrophils in
epidermal junction.
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knees, buttocksdermal papillae
Pemphigus histology
? The superficial portion of epidermis sloughs off, leaving the bottom layer of cells on the "floor" of the blister
? This bottom layer of cells is said to have a "tombstone appearance".
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The Asboe-Hansen sign (bullae spread sign) -- characteristic of pemphigusDERMATITIS HERPETIFORMIS
? Intensely itchy vesicles, papulovesicles and urticaria papules symmetrically distributed over extensor
surfaces (elbows, knees, buttocks, back, scalp, and posterior neck)
? Almost all have an associated, usually subclinical, gluten-sensitive enteropathy
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? >90% express the HLA-B8/DRw3 and HLA-DQw2 haplotypes? Biopsy of new lesions - vesicle forms subepidermally and develops from collections of inflammatory cells in
the papillary tips (the papillary tip abscess)
? Direct IF- presence of IgA in the papillary tips in the skin around the lesions
? Treatment
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oGluten-free diet
o
Dapsone therapy
? Patients are at increased risk for development of gastrointestinal lymphoma
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MASTOCYTOSIS (URTICARIA PIGMENTOSA)
? Systemic mastocytosis is defined by a clonal expansion of mast cells that in most instances is indolent and
nonneoplastic
? Cutaneous mastocytosis (CM)
o
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Urticaria pigmentosa (UP)/maculopapularcutaneous mastocytosis (MPCM)o
Variants: plaque form, nodular form; telangiectasia macularis eruptiva perstans (TMEP); diffuse
cutaneous mastocytosis (DCM)
o
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Solitary mastocytoma of skin? The cutaneous lesions of urticaria pigmentosa are reddish-brown macules or papules that respond to
trauma with urtication and erythema (Darier's sign).
? Urticaria pigmentosa is the most common manifestation of mastocytosis, both in adults & children.
Diseases with numerous telangiectasias
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? cirrhosis of the liver,? Osler-Weber-Rendu disease, which also has mucous membrane involvement,
? lupus erythematosus
? scleroderma,
? dermatomyositis,
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? cutaneous polyarteritis,? metastatic carcinoid syndrome,
? ataxia telangiectasia,
? angiokeratoma corporis diffusum,
? telangiectasia macularis eruptiva perstans, and
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? rosacea.? overlying basal cell cancers
VI.
SEXUALLY TRANSMITTED DISEASES
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Sexually transmitted agentsBacteria
Virus
? Neisseria gonorrhoeae
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? Herpes simplex virus 1, 2? Chlamydia trachomatis (D-K)
? Human papilloma virus
? Chlamydia trachomatis (L1, L2, L3)
? Hepatitis B virus
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? Treponema pallidum? Cytomegalovirus
? Haemophilus ducreyi
? Molluscum contagiosum virus
? Calymmatobacterium granulomatis
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? Human immunodeficiency virus? Mycoplasma hominis
? Human T-lymphotropic virus
? Ureaplasma urealyticum
? Gardnerella vaginalis
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? Group B -haemolytic StreptococcusProtozoa
Fungi
Ectoparasites
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? Trichomonas vaginalis? Candida albicans
? Phthirus pubis
? Sarcoptes scabiei
DISTINGUISHING FEATURES OF GENITAL ULCERS
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Features
Syphilis
Chancroid
Lympho -
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DonovanosisHerpes genitalia
(1? chancre)
granuloma
(Granuloma
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venereuminguinale)
Organism
Treponema
Haemophilus
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ChlamydiaCalymmato
Herpes simplex
palladium
ducreyi
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trachomatisbacterium
virus type II (rarely
(L1, L2,L3)
granulomatosis
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type I)No. of attacks
Only one (1)
1 or 2
Only one (1)
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Only one (1)Recurrent
No. of lesions
Usually 1
Usually
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Usually 1Variable
Multiple, may
multiple may
coalesce
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coalesceEarly 1? lesion
Papule
Pustule
Papule, Pustule Papule
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VesicleDiameter
5-15 mm
Variable
2-10 mm
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Variable1-2 mm
Depth
Superficial or Excavated
Superficial or
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ElevatedSuperficial
Edges
deep
Undermined,
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deepElevated, irregular
Sharply
ragged,
Elevated, round serpiginous
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Erythematousdemarcated,
irregular
or oval
elevated,
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round / ovalBase
Smooth, non- Purulent,
Variable
Red & velvety
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Serous,purulent,
bleeds easily
nonvascular
(beefy red),
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Erythematous,non-vascular
bleeds easily,
nonvascular
with exuberant
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granulation tissueFeatures
Syphilis
Chancroid
LGV
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DonovanosisHerpes genitalis
(1? chancre)
(Granuloma
inguinale)
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IndurationFirm
Soft
Occasionally
Firm
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Nonefirm
Pain
Uncommon
Usually very
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VariableUncommon
Frequently tender
tender
Lymphadenopath
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Firm, nonTender, may
Tender, may
No
Firm, tender often
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Ytender,
suppurate,
suppurate,
lymphadenopathy
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bilateralshotty,
loculated,
loculated, uni
pseudo buboes
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bilateralusually
or bilateral
(subcutaneous
unilateral
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(Bubo)nodules in
(Bubo)
Nodes enlarge
inguinal region,
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above & belowmay ulcerate)
Poupart's
ligament, -
Groove sign
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(Pic: VI-A)Diagnosis
-Dark field
-Clinical
-Demonstration -Tissue smear &
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-MultinucleatedMicroscopy
features
of LGV as
histopathological
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giant cell on-Serological
-Gram
elementary &
microscopy show
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Tzanck smeartests
Staining
inclusion bodies 1. Donovan
-Culture is
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(gram-ye-Frie's test
bodies
confirmatory
cocco-bacilli
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-Hyper gamma-2.Safety pin
with rail road
globulinemia
appearance
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appearance)-Complement
fixation +ve
Treatment
Penicillins/
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AzithromycinDoxycycline
Doxycycline /
Acyclovir
Doxycycline /
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ErythromycinTetracycline
tetracycline
tetracycline
Ceftriaxone
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ErythromycinAzithromycin /
Ciprofloxacin
erythromycin (in
pregnancy)
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PIC: Groove sign in LGVLymphadenopathy
Ulcer
DONOVANOSIS
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NilIndurated, painless, bleeding
SYPHILIS
Painless lymphadenopathy
Painless, non bleeding, indurated, usually single
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LGVPainful, suppurated, matted (BUBO)
Asymptomatic, painless, non bleeding ulcer
CHANCROID
Painful. fluctuant, suppurative nodes
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Multiple, painful, bleeding, r,indurated
HERPES
Painful lymph nodes
Multiple, painful. Bleeding, non indurated
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STDs & Incubation Period (mean)? Primary chancre
: 9 to 90 days (21 days)
? Chancroid
: One to several weeks (5 to 8 days)
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? Donovanosis: 9 to 50 days (17 days)
? Lymphogranuloma venereum
: 5 to 30 days (10 days)
? Herpes genitalis (primary)
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: 5 to 7 days (5 days)? Genital warts
: 1 to 8 months (3 months)
? Gonococcal urethritis
: 1 to 14 days (2 to 5 days)
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? Non-gonococcal urethritis: 7 to 21 days (10 days)
Esthiomine: vaginal & rectal strictures & elephantiasis of the vulva. (Seen in LGV)
Lipschutz ulceration: Non veneral ulcer of the vulva or lower vagina. (Ulcus Vulvae acutum) seen in Behcet's
disease. Similar to aphthous ulcers
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MANAGEMENT OF STD'sCHANCROID:
? Based on history: sexual exposure with infected person, short incubation period & morphology.
? Confirmed by demonstration of organisms from smears taken from bubo.
? Smears are stained with gram's or Pappenheim's stain.
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? Ito-Reenstierna intradermal test: becomes positive 1 or 2 weeks after appearance of sore & persists positivefor life.
? Injection of 0.1ml of suspension of killed organism & inferred as positive if a nodule of > 5mm appears after
24 hours.
? Treatment: erythromycin & Ceftriaxone.
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LGV:? History of occurrence of herpetiform lesions on the genitals, few days after intercourse, followed by painful
unilateral, multilocular inguinal bubo.
? Culture, Frei's intrademal test, complement fixation test can be done.
? Tetracyclines are the DOC.
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GRANULOMA INGUINALE:? Confirmed by demonstration of Donovan bodies in the tissue smears & also by HPE.
? Giemsa stain.
? Few large cells containing cystic spaces, often with nuclei pushed to one side & darkly staining (cells of
Greenblatt) are conspicuous.
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? Rx: streptomycin, tetracyclines & cotrimoxazole.REACTIVE ARTHRITIS (REITER'S SYNDROME)
? 50 ? 80% are HLA B27 positive
? Oligoarthritis, conjunctivitis, urethritis, and mouth ulcers most common features
? Most cases of reactive arthritis develop within 1-4 weeks after either a gastrointestinal infection (with
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Shigella, Salmonella, Yersinia, Campylobacter) or a sexually transmitted infection (with Chlamydiatrachomatis or Ureaplasma urealyticum)
? Psoriasiform skin lesions develop on the soles and toes
? These are often severe, persistent, aggressive and pustular (keratoderma blenorrhagica)
? Inflamed, red, scaling patches may also develop on the glans penis (circinate balanitis)
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VII.
ECZEMA AND DERMATITIS
Types of eczema
Endogenous eczema
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Exogenous eczema? Atopic dermatitis
? Irritant contact dermatitis
? Seborrhoeic dermatitis
? Allergic contact dermatitis
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? Nummular eczema? Photodermatitis
? Pompholyx (Dyshidrotic eczema)
? Infectious eczematoid dermatitis
? Asteatotic eczema
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? Stasis dermatitis? Juvenile plantar dermatitis
? Lichen simplex chronicus
ATOPIC DERMATITIS
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? Synonyms: Neurodermatitis, Besnier's prurigo, Infantile eczema? Positive family history of allergic rhinitis, asthma or eczema
? Pruritis is the most common symptom
? Course marked by exacerbations and remissions
? Clinical course lasting longer than 6 weeks
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? Lichenification of skin? Infantile pattern: involves face, neck, extensor surfaces and groin.
? Childhood and adolescent pattern: involves flexural skin, particularly in the antecubital fossa and popliteal
fossa.
? Cutaneous stigmata of AD
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oPerioral pallor
o
Extra fold of skin beneath the lower eyelid (Dennie-Morgan folds)
o
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Increased palmar skin markingso
Increased incidence of cutaneous infections, particularly Staphylococcus aureus
? Diagnosis: clinically - dry skin, severe itching, flexural lichenification, hand eczema, nipple eczerr and eyelid
eczema in adults, history of atopy in the family/patient, and raised IgE serum levels.
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CONTACT DERMATITISIrritant contact dermatitis
? Synonyms: Occupational dermatitis, Housewive's eczema
? Materials may injure by direct toxic action (irritants)
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? Due to contact with irritants like detergents, acids, alkaline chemicals, oils, organic solvents etc? Housewife's eczema, diaper dermatitis and industrial dermatitis are examples of cumulative irritant contact
dermatitis.
? Most common site affected is hand.
? Most common cause of contact dermatitis in Indian women ? detergent.
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Allergic contact dermatitis? May induce immunological reaction of delayed hypersensitivity type (allergens) ? Allergic contact dermatitis
? Most common metal causing contact dermatitis is nickel.
? Most common cause of air-borne contact dermatitis? parthenium.
? Barloque dermatitis due to cosmetics.
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? Diagnosis: Patch test.o
Skin hypersensitivity test (delayed type).
o
Readings are made after 48 hours.
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Differences Between Irritant and Allergic Contact Dermatitis
Irritant CD
Allergic CD
Symptoms
Acute
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Stinging, smartingitching
Itching
pain
Chronic
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Itching/painItching/pain
Lesions
Acute
Erythema
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vesicleerosion
Erythema
papules
vesicles
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erosionscrust
scaling
crust
scaling
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ChronicPapules, plaques, fissures, scaling,
Papules, plaques, scaling, crusts
crusts
Margination
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AcuteSharp, strictly confined to site of
Sharp, confined to site of exposure but
and site
exposure
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spreading in the periphery; usually tinypapules; may become generalized
Chronic
III-defined
III-defined, spreads
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EvolutionAcute
Rapid (few hours after exposure)
Not so rapid (12 to 72 h after exposure)
Chronic
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Months to years of repeatedMonths or longer; exacerbation after every
exposure
reexposure
Causative
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Dependent on concentration ofRelatively independent of amount applied,
agents
agent and state of skin barrier;
usually very low concentrations sufficient
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occurs only above threshold levelbut depends on degree of sensitization
Incidence
May occur in practically everyone
Occurs only in the sensitized
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Hand Eczema? Caused by chronic exposure to water and detergent.
? Dryness and cracking of the skin of hands with variable erythema and edema
? Diagnosis: Scratch test with latex extract.
Nummular (Discoid) Eczema
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? Characterized by circular or oval 'coin-like' lesion.? Most common sites are ? trunk and extensor surfaces of extremities (pretibial skin and dorsum of hands)
? Most commonly affects men in middle age group.
Asteatotic Eczema
? Also called the 'Winter-itch' or Xerotic eczema or Eczema craquelee
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? Seen in elderly people in dry season.? Characterized by fine cracks in the areas of dry skin over the anterior surface of legs.
Venous eczema (Gravitational eczema or Stasis Dermatitis)
? Due to venous incompetence and chronic edema.
? Site ? over the medial aspect of the ankle.
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Seborrheic Dermatitis? Most common in infants and very young. Most common location is the scalp.
? Greasy scales overlying erythematous patches or plaques
? Scaling of the external auditory canal is common
? In the first week of life, it typically occurs in the scalp ("cradle cap"), face, or groin
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? In adults, it is seen in patients with Parkinson's disease, CVA and HIV infection? Leser-Trelat sign: Sudden eruption of multiple seborrheic keratosis lesions in associated internal malignancy
Lichen Simplex Chronicus (Circumscribed neuro dermatitis)
? End stage of various eczematous disorders
? Lichenification (thickening) of skin due to chronic scratching and rubbing.
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? Most common sites ? nuchal region, dorsum of feet and anklesPompholyx (Dyshidrotic Eczema)
? Affects young adults
? Characterised by sudden crops of highly pruritic, deep-seated sago-like vesicles on the palms, sides of fingers
and/or soles
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PELLAGRA? Deficiency disease caused by lack of niacin (nicotinic acid), occurs chiefly in countries where corn (maize), a
poor source of tryptophan is basic food stuff.
? Its clinical presentations is "3-D"
Dementia
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DiarrheaDermatitis
o Most characteristic manifestation
o Occurs in form of pigmented, scaly, sharply demarcated & frequently changing cracked skin on parts
exposed to sunlight
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o Various types on locationPellagrous glove [lesion on hand]
Pellagrous boot [lesion on boot]
Casal necklace [lesion around neck]
Deficiency of vitamin A leads to follicular hyperkeratosis and roughening of the skin (phrynoderma).
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ACRODERMATITIS ENTEROPATHICA? Autosomal recessive
? Inherited form of zinc deficiency
? Result of a mutation in a zinc transport protein - decreased ability to absorb zinc from dietary sources
? Triad of
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oAcral dermatitis (face, hands, feet, anogenital area)
o
Alopecia
o
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Diarrhea? Requires lifelong zinc supplementation
? 1-3 mg/kg of zinc gluconate or sulfate is administered orally each day
Acrodermatitis chronica atrophicans: skin atrophy in Lyme's disease
Acrodermatitis continua/ Acrodermatitis pustulosa: form of pustular psoriasis
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EXFOLIATIVE DERMATITIS (EXFOLIATIVE ERYTHRODERMA)? Generalized redness and scaling of the skin of >30% BSA.
? A preexisting dermatosis is the cause of exfoliative dermatitis in two-thirds of cases, including
Psoriasis
Atopic dermatitis
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Contact dermatitisPityriasis rubra pilaris
Seborrheic dermatitis.
? Reactions to topical or systemic drugs account 20-40% of cases
? Cancer (lymphoma, solid tumors and, most commonly, cutaneous T cell lymphoma) for 10-20%.
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VIII.
PAPULOSQUAMOUS DISORDERS
PSORIASIS
? Typical lesions are erythematous (red), raised, scaly, well demarcated plaques
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? Characteristically presents with silvery mica scales.? Sites: extensor aspect of trunk & limbs preferentially
? Due to increased cell turn over resulting in marked epidermal skin thickening (acanthosis)
? 50% have positive family history
? Associated with HLA-Cw6 (most common)
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? Deletion of 2 late cornified envelope (LCE) genes, LCE3C and LCE3B, is a common genetic factor forsusceptibility to psoriasis
? Obesity is another factor associated with psoriasis. Weight loss results in significant improvement
Triggering factors
? Trauma (Koebner phenomenon)
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? Season (worsens in winter)? Emotional stress
? Upper respiratory tract infections
? Drugs like beta-blockers, lithium and chloroquine
? Withdrawal of systemic steroids can lead to precipitation of pustular psoriasis.
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VariantsPlaque type
? Most common type
? Slow, indolent course
? The most commonly involved areas: elbows, knees and scalp
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Inverse psoriasis? Affects the intertriginous regions including the axilla, groin, submammary region, and navel
? May be moist and without scale due to their locations
Guttate psoriasis (eruptive psoriasis)
? Most common in children and young adults
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? It develops acutely in individuals without psoriasis or in those with chronic plaque psoriasis? Patients present with many small erythematous, scaling papules, frequently after upper respiratory tract
infection with -hemolytic streptococci
Pustular psoriasis
? Generalized eruption of sterile pustules
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? Fever? Intense erythema
? Local irritants, pregnancy, medications, infections, and systemic glucocorticoid withdrawal can precipitate
this form of psoriasis
? Types
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Palmo plantarAcrodermatitis continua
Pustular bacterids
Generalized pustular (Von Zumbusch disease)
Psoriatic arthritis (PsA)
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Occurs in 5 ? 10% of patients with psoriasis. There are five subtypes? Symmetric: resembles rheumatoid arthritis, but is usually milder
? Asymmetric: can involve any joint; present as sausage digits (Pencil in cup or Opera glass deformity)
? Distal interphalangeal predominant (DIP): the classic form
? Spondylitis
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? Arthritis mutilans: severe and deforming, affects primarily the small joints of the hands and feet.Scalp psoriasis: Pityriasis amaintaceae
Rupoid psoriasis: classically present in Reiter's syndrome (HLA-B 27)
Koebner's / Isomorphic phenomenon
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? Psoriasis appears at the site of minor injury such as scratch or graze.? Koebner phenomenon is also seen in
Lichen planus
Vitiligo
Toxic Epidermal Necrolysis
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Molluscum contagiosumKaposi sarcoma
Necrobiosis lipoidica
Discoid lupus erythematosus.
? Appears usually 7 to 14 days after injury (i.e. trauma or surgery).
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? It is an all or none phenomenon (i.e. if psoriasis occurs at one site of injury it does so means will occur at allsites of injury)
Reverse Koebner phenomenon (reaction) is clearing of existing psoriasis lesions following injury. It also
obeys an all or none rule, and Koebner and reverse Koebner reactions are mutually exclusive.
Pseudo ? isomorphic phenomenon is due to autoinoculation & is seen in infections like
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Plane wartsMolluscum contagiosum
? Auspitz sign -a characteristic finding of psoriasis in which removal of scales leads to pinpoint bleeding
? Removal of scales reveals a glistening red membrane of Berkeley
? Grattage Test -- on scratching scales appear
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? Wornoff Ring -- White halo around lesion? Candle grease sign
? In nails
Onycholysis (separation of nail plate from nail bed)
Thimble-pitting of nail plate
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? Not seen in psoriasisAlopecia
Mucosal involvement
CNS involvement
? Histological features
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Elongation of rete-ridgesParakeratosis
Hypogranulosis
Munro's micro abscesses in the horny layer
Spongiform pustules of Kogoj
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? The psoriatic epidermis shows rapid transition of epidermal cells in as fast as 2 days as compared to 13 daysin normal epidermis
? Itching may or may not present
Key diagnostic points for psoriasis
Erythematous scaly plaques
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Well-defined borderScales dry loose and micaceous
Koebner phenomenon seen
Auspitz sign positive
Regular, circular pits on nail plates
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Involvement of DIP joints of fingers and toesHistopathological: Spongiform pustules of Kogoj
Treatment
? Treatment of choice: PUVA therapy
? DOC for psoriatic arthropathy: Methotrexate
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? Tar preparations, Vit-D3 analogs like calcipotriol, Anthralin etc... can be used locally? DOC in AIDS with psoriasis & pustular psoriasis: Synthetic retinoid -- acitretin
? Biological agents used in the treatment of psoriasis
Alefacept (anti-CD2)
Etarnacept, Adalimumab, Infliximab (anti-TNF)
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Differential diagnosis of round, red, scaling patchesDisease
Features
Psoriasis
Well-defined, thickened, scaly plaques, usually multiple
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Discoid eczemaModerately well-defined edge; slightly scaly, pink patches, limited in number
Ringworm
Annular with central clearing; microscopy and culture of scales will reveal fungal mycelium
Bowen's disease
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Often slightly irregular in shape; edge is well defined; biopsy is decisivePHOTO CHEMOTHERAPY (PUVA)
? Photosensitizing drug Psoralen + UV-A (300-400nm)
? The UV-A is supplied by special fluorescent lamps housed in cabinets or special frames over beds
? The main psoralen used is 8-methoxy psoralen
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? Psoralen is given orally 2 hours before exposure & the dose 0.6 mg/kg? Decrease DNA synthesis in psoriasis & increase melanin synthesis in Vitiligo
? UV-light therapy is contraindicated in patients receiving cyclosporine
Uses
Side effects
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? Psoriasis? Long term (Major):
? Vitiligo
Skin cancer
? Cutaneous T Cell Lymphoma (Mycosis fungoides)
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Cataract? Pityriasis lichenoides chronica
Photo (premature) aging
? Atopic dermatitis
? Minor (Short term): Nausea, Burning, Pruritis,
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? PompholyxXeroderma
LICHEN PLANUS
? Affects the skin, scalp, nails, and mucous membranes
? The primary cutaneous lesions are pruritic, polygonal, flat-topped, violaceous papules.
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? Close examination of the surface of these papules reveals a network of gray lines (Wickham's striae)? The skin lesions but have a predilection for the wrists, shins, lower back, and genitalia
? Buccal mucosa is particularly involved
Variants
? Hypertrophic lichen planus- commonest variant, thickened, mauvish papules or nodules of irregular shape
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with a warty or scaling surface.? Annular lichen planus: ring-type configuration, on the male genitalia and lower abdomen.
? Lichen nitidus: is a rare variant, numerous tiny, pink, flat-topped papules develop.
? Bullous lichen planus: blistering occurs on some lesions.
? Lichen plano-pilaris: predominantly involves the hair follicles. Affected sites lose their terminal hair and
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develop horny spines. Involvement of scalp results in scarring alopeciaClinical presentation of Lichen planus
Lesions
Characteristic features
Histology
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? Plain (flat) topped? Wickham's stria
? Band-like infiltration of lymphocytes
? Polygonal
? Lace-like pattern due to
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in the upper dermis? Purple (violaceous)
involvement of buccal and
? Formation of saw tooth profile &
? Pruritic
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vaginal mucosacytoid (civatte) body.
? Papule
? Koebner's phenomenon
? Epidermal thinkening
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? Pterygium (thinning) of? Scarring alopecia
? Subepidermal lichenoid band
nails
? Max Joseph histological cleft
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? Pigmentation on healingAssociated with: Squamous cell carcinoma, Hepatitis -- C
Treatment: topical steroids are the mainstay of treatment
PITYRIASIS ROSEA
? The exact aetiology of PR is not known though HHV-6 and 7 have been implicated.
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? First manifestation is an annular lesions of 2-6 cm diameter (the herald patch)? The centers of the lesions have a crinkled or "cigarette paper" appearance
? Followed by smaller annular or papular lesions, predominantly on the trunk along the cleavage lines.
? The eruption has a characteristic 'bathing suit' distribution (trunk and proximal parts of limbs)
? Lesions on the back are parallel to ribs giving 'Christmas tree' appearance or 'hanging curtain sign'
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? PR shares many clinical features with the eruption of secondary syphilis, but palm and sole lesions areextremely rare in PR and common in secondary syphilis.
? Course -- usually self-limiting.
PITYRIASIS RUBRA PILARIS
? Reddish orange scaly plaques
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? Palmoplantar keratoderma? Keratotic follicular papules
? Disease begins on the face and scalp, with pinkness and scaling
? The histological appearance: distinctive accentuation of the dermal papillae and the undulations of the
dermoepidermal junction are much less marked than in psoriasis.
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IX.
DISORDERS OF SKIN APPENDAGES
MILIARIA
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? Results from blockage of the acrosyringium, the long thin duct that carries sweat from the coiledsecretory portion located in the reticular dermis and the subcutaneous fat to the skin surface
? There is secondary leakage of sweat in the epidermis and papillary dermis.
Types
? Miliaria crystalline (sudamina)
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Obstruction is superficial in stratum corneumVesicle is subcorneal.
It is common in infants in warm ICU conditions where cholinergic & adrenergic agents are employed.
? Miliaria rubra (prickly heat):
Leakage of sweat into epidermis & upper dermis
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Papules around sweat poresIntense itching
Miliaria pustulosa: miliaria rubra becoming pustular
? Miliaria profunda
Obstruction of acrosyringium at deeper level
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Sweat leaking into deeper dermisPapules are non-itchy
ACNE VULGARIS
? A self-limited disorder primarily of teenagers and young adults
? The earliest feature is an increased rate of sebum secretion, making the skin look greasy (seborrhoea)
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? A disorder in which hair follicles develop obstructing horny plugs (comedones).? Small pseudocysts, called comedones, form in hair follicles due to blockage of the follicular orifice
? The clinical hallmark is the comedone, which may be closed (whitehead) or open (blackhead)
? The activity of bacteria (Propionibacterium acnes) within the comedones releases free fatty acids from
sebum, causes inflammation within the cyst, and results in rupture of the cyst wall
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? The first lesions, usually comedones, develop on the forehead (pre-adolescent acne)
? At its peak, acne covers the entire face (adolescent acne)
? In mature adults (25 years plus) it settles on the jaw area and the adjacent neck (adult acne).
? The scars formed after healing are often quite irregular and tend to form 'bridges'
? Even the smaller inflamed papules can cause scars - pock-like or triangular indentations (ice-pick scars).
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? Acne fulminansLesions quite suddenly become very inflamed
Affected individual is unwell and develops fever and arthralgia.
? Treatment:
Oral tetracycline or erythromycin.
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Topical -- retinoic acid (for nodulocystic acne), benzoyl peroxide, salicylic acid.Sebum production is decreased by sebotrophic agents (directly) and antiandrogens (indirectly)
o
Tretinoin (all trans retinoic acid)-1st generation (1G)
o
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Isotretinoin (13-cis isomer of tretinoin)-2Go
Adapalene -- 3G
o
Tazarotene -- 4th generation
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ROSACEA (ACNE ROSACEA)? Common chronic inflammatory acneiform disorder of the facial pilosebaceous units, coupled with an
increased reactivity of capillaries leading to flushing and telangiectasia.
? It is seen almost exclusively in adults, rarely affecting patients <30 years.
? Rosacea is more common in women
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? But those most severely affected are men? Characterized by the presence of erythema, telangiectases, and superficial pustules
? Comedones are not seen
? Predisposing factors: History of flushing associated with heat, emotional stimuli, alcohol, hot drinks or spicy
foods.
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? Site: typically involves the central face. This does not affect the trunk.? Complications
Nose ? connective tissue overgrowth (Rhinophyma ? sebaceous gland hypertrophy)
Eye ? keratitis, uveitis, chalazion.
Chloracne- extremely severe form of industrial acne due to exposure to complex chlorinated naphthalenic
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compounds and dioxin.PHASES OF HAIR GROWTH
? Anagen: Phase of normal active growth, lasts for 3 years, 90% of hairs are in this phase
? Catagen: Brief transition phase (between anagen and telogen) during which hair growth stops, lasts for 3
weeks
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? Telogen: Resting phase, lasts for 3 months? Exogen: Hair shedding phase (relationship between hair shaft and base of telogen follicle)
? Duration and rate of growth of anagen phase determine the ultimate length of hair in that area.
? Eyebrows, eyelashes, and axillary pubic hair: anagen phase is short; telogen phase prolonged.
? Scalp, beard: relatively long anagen phase.
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? Terminal scalp hair follicles: 100,000 at birth; genetically determined to produce long, thick pigmented hairs.? Vellus hairs: present over most of the body; genetically predestined to produce hairs that are short, fine,
non-pigmented.
HAIR LOSS (ALOPECIA)
? Shedding of hair is termed effluvium or defluvium
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PATTERN ALOPECIA or MALE ALOPECIA or ANDROGENIC ALOPECIA? Most common type
? Autosomal dominant
? Progressive form of alopecia
? Mostly seen in men
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? The earliest changes occur at the anterior portions of the calvarium on either side of the "widow's peak" andon the crown (vertex).
? Loss of hair starts in both temporal regions.
Treatment:
? Chemical castration with anti-androgen-prostagen combination in women by cyproterone acetate &
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ethinylestranol ? Dianette.? Anti hypertensive (Vasodilator) ? Minoxidil & Tretinoin
? 5-alpha-reductase inhibitor ? Finasteride.
ALOPECIA AREATA
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? Autoimmune disorder of hair follicles causing loss of hair in sharply defined areas of skin? Results from arrest of hair follicles in late anagen phase.
? 10-20% patients give a family history
? Polygenic inheritance
? HLA DR4, DR5, DQ3 are associated with severe alopecia
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? HLA DQ3 and DR11 ? associated with alopecia totalis & universalis? 'Exclamation mark' hairs at the margin of the lesions.
? Non scarring & non patterned alopecia
? Particularly common between the ages of 15 and 30 years.
? Alopecia totalis is total or almost total loss of scalp hair.
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? Alopecia universalis is loss of all body hair.o
Sites of Predilection: Scalp, eyebrows, eyelashes, pubic hair, beard.
o
Nails: Fine pitting ("hammered brass") of dorsal nail plate, mottled lunula, trachyonychia (rough nails),
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onychomadesis (separation of nail from matrix).? Ophiasis is alopecia along scalp margin. (band-like hair loss in the occipital and temporal scalp),
? Sisaipho (predilection for parietal scalp mimicking androgenetic alopaecia),
? Classical feature is sparing of gray/white hairs.
? Positively associated with autoimmune disorders
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? Alopecia Aerata + Vitiligo + Uveitis Vogt Koyanagi syndrome? Dense 'bee swarm'-like cluster of lymphocytes can be seen around the follicles in biopsies.
? Treatment: Potent topical steroids or systemic steroids, PUVA, dithranol, allergic sensitization with
diphencyprone and topical minoxidil
TELOGEN EFFLUVIUM
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? Transitory increase in the number of hairs in the telogen (resting) phase of the hair growth cycle.? This may occur spontaneously, may appear at the termination of pregnancy, may be precipitated by crash
dieting, high fever, stress from surgery or shock, malnutrition, or hormonal contraceptives.
? Telogen effluvium usually has a latent period of 2-4 months
? The prognosis is generally good
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ALOPECIA MUCINOSA? Non scarring alopecia
? Mucin deposition in hair follicles & sebaceous glands causing epithelial reticular degeneration
? MC site: face & scalp
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SCARRING/CICATRICAL ALOPECIA? Due to inflammatory process like discoid lupus erythematosus and lichen planus
? Result in permanent loss of hair in the affected area.
? Most common congenital cicatrial alopecia is aplasia cute's congenita (i.e. focal absence of epidermis with
or with or with out other layers).
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? Pseudopelade - small, rounded patches of scarring alopecia without any inflammation.DISORDERS OF NAILS
Koilonychia (Spoon nail)
Iron deficiency anemia
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The nail is concave with raised edgesLichem planus
Hypothyroidism
Racquet Nail
Premature obliteration of epiphyseal line
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Width of nail bed & nail plate is greater than their lengthAnonychia
Lichen panus
Absence of all or part of one or several nails
With tong. bone anomalies
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Beau's LineAny severe systemic illness
Poor nutrition to matrix 1/t a defective band of nail
formation resulting in transverse groove of thin nail
plate.
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Onychomadesis : Separation of nail from matrixLongitudinal ridges with beaded and/or Fir tree
Median canaliform dystrophy of Heller
appearance
Trachyonychia (Rough sand paper nail)
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20 nail dystrophy (alopecia areata)External chemical treatment
Leuconychia : White discolouration of nail
Nail matrix dysfunction
Apparent leuconychia
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Tery's nail, half & half nailWhite appearance d/t changes in underlying tissue
Muehrck's paired narrow white band
Onychogryphosis (Ram's horn or Oyster ? Nail)
Pressure from foot wear in elderly
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Nail is severly distorted, thickened, opaque, brownish,sparaled & with out attachment to nail bed
Hook Nail
Lack of support from short bony phalynx
Pterygium
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Dorsal pterygium in lichen planusVentral pterygium in scleroderma with Raynaud's
phenomenon, causalgia of median nerve,
formaldehyde containing nail cosmetics.
Onycholysis : Detachment of nail plate from its bed
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Psoriasisstarting at its distal &/or lateral attachment
Reiter's syndrome
Onychorrhexis : Splitting & roughness of nail plate
Lichen planus
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Onychoptosis defluvium (Alopecia unguim)Alopecia areata
Component of alopecia
Koenen's Periungal Fibroma
Tuberous sclerosis (50% cases)
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Mee's LineArsenic Poisoning.
Pitting
Deep & irregular pits: psoriasis, atopic dermatitis
Superficial & geometric pits in alopecia areata.
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Melanonychia-Single band: nail matric nevus or melanoma
Presence of melanin in nail plate presenting as single /
(deserve biopsy), trauma (usually in 4/5th toe nail)
multiple longitudinal brown -- black band.
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-Multiple band: dark race, pregnancy, inflmatorynail disorder, Lauiger -- Huntziker syndrome (with
pigmented macules on lip & genitals), AIDS,
Addison syndrome
Muehrck's lines
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HypoalbuminemiaBrown nail
Arsenic poisoning
Addison's disease
Blue nail
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Wilson's diseaseX.
GENODERMATOSES & DISORDERS OF KERATINIZATION
Genodermatoses: diseases which are transmitted genetically from parents to children.
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NEUROFIBROMATOSIS (VON RECKLINGHAUSEN'S DISEASE)? Autosomal dominant
? Plexiform neurofibroma - soft, doughy, subcutaneous swelling having a bag of worm feeling and run along
nerves
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? Multiple, brownish macules (Caf? au lait macules)? Tiny specks of brownish macules in the axilla (axillary freckling)
TUBEROUS SCLEROSIS (SYN. BOURNEVILLES DISEASE)
? Two third cases ? sporadic, others - Autosomal dominant,
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? Multiple, brown, soft, grouped papules present in the perinasal area and cheeks in a butterfly distributionThese are called facial angiofibromas (misnamed as adenoma sebaceum)
? Ungual or subungual fibromas, (Koenen's tumours) are small fleshy tumours that grow around and under
the toenails or fingernails
? Hypomelanotic macules ('ash leaf spots') are white or light coloured patches on skin (only visible sign of
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tuberous sclerosis at birth)? Shagreen patches are areas of thick leathery skin which is dimpled like an orange peel and is usually found
on the lower back or nape of the neck
? Caf? au lait macules can be seen
ICTHYOSIS
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? Characterised by the accumulation of 'fish-like' scales due to abnormal epidermal cell kinetics
? Autosomal dominant Icthyosis
Icthyosis vulgaris ? most common type
X-linked icthyosis (seen in boys only)
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? Autosomal recessive Icthyosis ? more severe than the dominant formLamellar icthyosis
Icthyosiform erythroderma
Icthyosis vulgaris
? Begins in the first year of life
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? Dry, scaly skin over the extensor aspects of the arms and legs? The scales are larger over the lower extremities
? Mild keratoderma or (thickening of the skin over the palms and soles)
? The dryness becomes worse during winters and improves in summers and humid weather
? Histologically, the only abnormality detectable is a much diminished granular cell layer.
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X-linked ichthyosis? Deficiency of steroid sulphatase
? The scales are dirty brown in colour and affect both the extensor and flexural surfaces of the extremities
with prominent involvement of the neck and trunk
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? These male children are often the products of postmature pregnancies and difficult labours.? Associated disorders: cryptorchidism, ectropion
Acquired icthyosis: The most important cause underlying malignant disease ? particularly lymphoma ?such
as Hodgkin's disease
Tylosis: Marked thickening of palmar and plantar skin due to localized abnormality of keratinization.
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XERODERMA PIGMENTOSUM
? An autosomal recessive disorder of DNA repair
? The most common defect - nucleotide excision repair (NER) enzymes are mutated.
? History - the child cries on exposure to light
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? Skin turns erythematous on exposure to sun? Development of freckles and lentiginosis on the exposed area of the body, such as the extensor aspect of
arms, face and the neck are early signs
? Later by adulthood squamous cell carcinoma, basal cell carcinoma, and malignant melanoma may form
EPIDERMOLYSIS BULLOSA
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? An inherited defect in the keratin formation? Characterised by the formation of multiple blisters on gentle rubbing or on minimal skin trauma especially
over the trauma prone areas of the body
? There may be blisters in the pharynx, larynx, eyes and the genital mucosa.
? There may be contractures and mitten like deformities of hands in the severe variants
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? Pyloric stenosis and squamous cell carcinoma are other complicationsPALMOPLANTAR KERATODERMA
? Inherited defects due to mutations in the enzymes involved in the synthesis of keratin
? Skin over palms and soles becomes hard, thick, dry and hyperkeratotic
REFSUM'S SYNDROME (HEREDOPATHIA ATACTICA NEURITIS FORMIS)
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? Autosomal recessive,? Accumulation of phytanic acid in all the tissues
? Cerebellar ataxia, polyneuritis, retinitis pigmentosa, nerve deafness, generalized ichthyosiform scaling.
DARIER'S DISEASE (KERATOSIS FOLLICULITIS)
? Inherited as an autosomal dominant disorder, but also occurs sporadically.
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? Appearance of groups of brownish, horny papules over the central trunk, shoulders, face and elsewhere? Oral cavity shows: Cobble stone appearance
? V shaped nicking of nails seen
? Presence of tiny pits on the palms
? There is a curious loss of cohesion between keratinocytes above the basal layer
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XI.
PEDIATRIC DERMATOLOGY
NEONATAL DERMATOLOGY
Transient Neonatal Pustular Melanosis
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? Onset at birth? Common in darkly pigmented infants
? Smear of sterile pustule shows numerous neutrophils
? Histology: subcorneal pustules with neutrophils
Erythema Toxicum Neonatorum
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? Onset typically 24 ? 48 h after birth
? Occurs in half of all full-term infants
? Presents with blotchy erythematous macules, papules, pustules, and wheals
? Smear of sterile vesicle/pustule shows eosinophils
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? Histology: subcorneal pustules with eosinophils, associated with pilosebaceous unitNeonatal Cephalic Pustulosis (Neonatal Acne)
? Onset typically within first 30 days
? Malassezia spp. implicated in pathogenesis
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? Presents with erythematous follicular comedones, papules, and pustules on face? Histology: follicular pustules with neutrophils
Sclerema Neonatorum
? Onset usually within first week of life
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? Form of panniculitis in severely ill, premature infants; often fatal? Presents with diffuse woody hardening of skin
? Spares genitalia, palms, and soles
? Histology: needle-shaped clefts with necrotic adipocytes with little surrounding inflammation
Seborrheic Dermatitis
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? Onset typically 1 week after birth; lasts several months, mostly resolves by 1 year of age
? Presents with ill-defined erythematous patches with waxy scale over scalp ("cradle cap"), ? axillae and groin
Aplasia Cutis Congenita (ACC)
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? Onset before birth? Localized defect in epidermis, dermis and/or fat
? Typically along midline
? Presents with erosion, ulceration, scar, or membranous defect (ovoid lesion covered by an epithelial
membrane)
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? Hair collar sign: ring of dark long hair encircling lesion; ? marker of underlying neural tube defectCutis Marmorata Telangiectatica Congenita (CMTC)
? Onset at birth
? Typically improves with age
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? Presents with blanching reticulated vascular pattern on trunk/extremities with segmental distribution? Associated anomalies in 1/2 of patients (varicosities, nevus flammeus, macrocephaly, ulceration, hypoplasia,
and/or hypertrophy of soft tissue and bone)
Congenital Infections of the Newborn
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PAPULOSQUAMOUS AND ECZEMATOUS DERMATOSES
Psoriasis
? 25% patients will have presentation before age 15
? Guttate psoriasis more common in children
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? Presents with raindrop-like papules in an eruptive patternAcropustulosis of Infancy
? Onset from 6 months to 2 years; resolves by age 3
? Presents with recurrent crops of pruritic pustules on palms, soles, distal extremities (may mimic scabies
infection so prudent to perform mineral oil scraping)
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? Treatment: topical corticosteroidPIGMENTED LESIONS
Lentigines
? Presents as brown macules with increased number of melanocytes
? No relationship to sunlight
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? Multiple lentigines may be associated with the following:LEOPARD Syndrome
PTPN11 gene mutation
Autosomal dominant
Caf?-noir macules
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ECG changesHypertelorism
Pulmonary stenosis
Abnormal genitalia
Growth retardation
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DeafnessCarney Complex (LAMB or NAME syndrome)
PRKAR1A gene mutation
Autosomal dominant
Psammomatous melanotic schwannomas,
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Cardiac/cutaneous myxomasBlue nevi
Endocrine overactivity
Peutz?Jeghers Syndrome
STK11 gene (serine threonine kinase)
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Autosomal dominantMucocutaneous (oral/acral) lentigines
ntestinal polyposis, ? intussusception
Various malignancies
Laugier?Hunziker Syndrome
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Mucocutaneous lentiginesLongitudinal melanonychia
Genital melanosis
Bannayan?Riley-- Ruvalcaba Syndrome
PTEN gene mutation
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Autosomal dominantPenile > vulvar lentigines
Lipomas
Hemangiomas
Ephelides (Freckles)
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? Light brown macules in sun-exposed areas? More prominent in children with fair skin and during summer time
? Onset typically within first 3 years of age
? Can be a marker for UV-induced damage if acquired
? Histology: normal number of melanocytes, increased pigment in keratinocytes
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Congenital Nevus (CN)? Onset at birth or first year typically
? Slight risk of melanoma (highest in large CNs)
? Axial nevi with greatest risk of developing melanoma
? Neurocutaneous melanosis: intracranial pressure, leptomeningeal melanoma, spinal cord compression
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Spitz Nevus (Epithelioid or Spindle Cell Nevus)? Presents as dome-shaped red-brown or tan-pink smooth surfaced papule
? Typically occurs within first two decades
? Histology: K amino bodies (PAS + globules)
? Characteristic starburst dermoscopic finding in pigmented Spitz nevi
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Becker's Nevus (Becker's Melanosis)? Acquired unilateral lesion found in males (second or third decade) typically on shoulder, upper chest, or back
? Hyperpigmented hypertrichotic patch or plaque associated with underlying smooth muscle hamartoma
(arrector pili)
? Histology: melanin in epidermis, often smooth muscle hamartoma present in dermis
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Blue Nevus? Congenital or acquired (typically early childhood)
? Multiple blue nevi associated with Carney complex (LAMB/NAME syndrome)
? Histology: normal epidermis, many elongated dendritic melanocytes within dermis, large amounts of
melanin often seen within melanocytes
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Nevus of Ota (Nevus Fuscoceruleus Ophthalmomaxillaris, Oculodermal Melanocytosis, Congenital melanosis bulbi)? Onset either near birth or during puberty
? Mostly in women
? Caused by the entrapment of melanocytes in the upper third of the dermis
? Presents as unilateral (90%), blue-gray hyperpigmented macules in the face (forehead, temple, malar area,
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or periorbital skin)? Typically involving ophthalmic and maxillary branches of trigeminal nerve
? Most common extracutaneous sites: sclera (increased risk of glaucoma)
? Malignant melanoma develops very rarely
? Mongolian spot - a birthmark caused by entrapment of melanocytes in the dermis but is located in the
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lumbosacral region.Nevus of Ito (Nevus Fuscoceruleus Acromiodeltoideus)
? Similar presentation to nevus of Ota
? Usually unilateral
? Typically occurs in shoulder region (supraclavicular, scapular, and deltoid)
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Hori's Nevus (Acquired Nevus of Ota-like Macules)? Onset in late adolescence
? Bilateral nevus of Ota-like macules of the zygomatic region
? May be misdiagnosed as melasma
Nevus achromicus (Nevus depigmentosus)
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? An uncommon birthmark characterised by a well-defined pale patch.? Often, smaller hypopigmented macules arise around the edges, resembling a splash of paint
? Achromic naevus is not completely white (differentiates from vitilligo)
? Achromic naevi are usually solitary (in contrast to tuberous sclerosis, where multiple pale patches occur and
are called ash-leaf spots)
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? Most commonly seen on the upper chest, but may also arise on the limbsCongenital Dermal Melanocytosis (Mongolian Spot)
? Common in infants with pigmented skin
? Presents with blue-gray macules or patches typically over lumbosacral skin or buttocks
TELANGIECTASIAS
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Spider Angioma (Spider Nevus)
? Common acquired lesion seen in children and adults
? Comprised of central arteriole with radiating thin walled vessels
? Temporary obliteration seen with compression
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? Multiple lesions associated with liver disease, pregnancy, and estrogen therapyXII.
DISORDERS OF PIGMENTATION
Normal human skin colour is primarily related to size and the arrangement of melanosomes in melanocytes.
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HYPO PIGMENTATIONMelanocytopaenic
Melanopaenic
Non-melanotic
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(Melanocytes decreased or absent)(Melanin decreased or absent)
(No melanin defect)
Piebaldism
Albinism
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Nevus anemicusVitiligo
Homocystinuria
Woronoff's ring
Vogt-Koyanagi-Harada syndrome
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Nevus of Ito(hypopigmentation
Xeroderma pigmentosum
Nevus depigmentosus
around psoriasis
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Mycosis fungoidesTuberous sclerosis
lesions)
Pityriasis lichenoides chronica
Leprosy
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Halo naevusPityriasis alba
Leucoderma acquisitum centrifugum
Pityriasis versicolour
Burns (Ionising, Thermal, UV)
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Discoid lupus (Post-Trauma
inflammatory)
Alopaecia areata
Melanoma
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SclerodermaPost-dermabrasion
Post-laser
VITILIGO
? A typical vitiligo macule has a chalk or milky white colour, round to oval in shape often with convex margins
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which are usually well defined? Associated with various autoimmune diseases, most commonly thyroid disorders
? Localized Vitiligo ? focal, segmental or mucosal
? Generalized Vitiligo is the most common type characterised by few to many to widespread macules
Acrofacial: distal fingers and periorificial areas
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Vulgaris: scattered patches that are widely distributedMixed
? Universal Vitiligo indicates almost total involvement of the body with few remaining areas of pigmentation -
associated with various endocrinopathy syndromes.
? In the sharply demarcated, symmetrical macular lesions there is loss of melanocytes and melanin.
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Treatment? Limited disease: Topical corticosteroids (triamcinolone)are the 1st line treatment
? Topical tacrolimus (0.03% and 0.1%) ointment - safe and effective in childhood vitiligo.
? Generalised Vitiligo: Narrow band UVB
? Topical or oral psoralen (8 methoxy psoralen) with UV-A (320 ? 400nm) radiation (PUVA)
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oTopical PUVA is used for old lesion involving <20% of body surface area
o
Oral psoralen is used in extensive disease or in patients not responding to topical PUVA
Albinism
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? Genetic abnormalities of melanin synthesis (in hair, skin and eye)? Normal number and structure of melanocytes
? Characteristic albino with white hair, white skin and blue eyes.
Piebaldism
? Autosomal dominant
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? Congenital? Stable leucoderma
? Characterised by chalk or milk-white macules like that of vitiligo
? Typical white forelock.
White patch of skin: differential diagnosis (Mnemonic: "Vitiligo PATCH")
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? Vitiligo? Pityriasis alba/ Post-inflammatory hypopigmentation
? Age related hypopigmentation
? Tinea versicolor/ Tuberous sclerosis (ash-leaf macule)
? Congenital birthmark
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? Hansen's (leprosy)HYPERPIGMENTATION
Melanocytotic
Melanotic
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(increase in number of melanocytes)(increase in melanin)
? Lentigines
? Caf?-au-lait macules
? Chronic pruritis
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? Peutz-Jegher syndrome? Freckles
? Post inflammatory
? PUVA therapy
? Naevus spilus
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? Melanoma,? Lentigo, solar, UV (radiation tanning)
? Hemochromatosis
? Mastocytosis
? Melasma
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? Acanthosis nigricans? Exogenous ACTH
MELASMA
? Dark areas appear symmetrically across the cheeks, around the eyes and over the forehead, giving a mask-
like appearance
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? It is much more common in women? Seen more often in people with dark skin
? The majority of cases appear related to pregnancy or oral contraceptives
? High expression of -MSH in the lesional keratinocytes plays an important role in the melanisation of skin
? Topical hydroquinone (2% to 4%) with retinoids and or steroids is the usual treatment
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XIII.
SKIN IN SYSTEMIC DISEASES & MISCELLANEOUS
PARANEOPLASTIC SIGNS OF INTERNAL MALIGNANCY
? Acanthosis nigricans - Brown-back velvety plaques over neck and flexures
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? Acute febrile neutrophilic dermatosis - Tender, red plaques over limbs and face in a middle-aged lady? (Sweet's syndrome)
? Acquired Ichthyosis - Dry fish-like skin most commonly in Hodgkin's lymphoma
? Clubbing - Severe grades of clubbing with lung carcinoma
? Dermatomyositis - 10% cases have associated with internal malignancy
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? Erythema gyratum repens - Concentric rings of erythema and scaling over trunk (Ca bronchus)? Hypertrophic osteoarthropathy - Subperiosteal new bone formation
? Migratory thrombophlebitis ? Pancreatic cancer
? Myeloma-associated amyloidosis - Skin nodules and purpura
Associated with endocrine neoplasm
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? Necrolytic migratory Erythema ? Glucagonoma? Necrobiosis lipoidica diabeticorum ? Diabetes mellitus
? Addisonian pigmentation - Adrenal corticotropin hormone (ACTH) secreting neoplasms
? Carcinoid tumours - Flushing of face and upper trunk
ACANTHOSIS NIGRICANS
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? It is a velvety hyperpigmentation, thickening & increased rugosity of skin? Primarily involves flexures ? axilla & groin.
? Thickened areas bear skin tags & seborrheic warts
? In majority of patients, it is associated with obesity (pseudo acanthosis nigricans) and insulin resistance
? The skin changes are reversible on weight reduction.
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? It can reflect internal malignancy ? most commonly gastrointestinal malignancy? Also seen in: Endocrine diseases like Cushings syndrome, Acromegaiy, Poiycystic ovarian disease, insulin
resistant DM
? HAIR- AN syndrome: in women, the triad of
Hyperandrogenism
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Insulin-resistanceAcanthosis nigricans
NECROBIOSIS LIPOIDICA DIABETICORUM
? A disorder of collagen degeneration with a granulomatous response, thickening of blood vessel walls, and
fat deposition
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? The main complication of the disease is ulceration, usually occurring after trauma? Strongly associated with diabetes mellitus
? Usually present with shiny, asymptomatic patches that slowly enlarge over months to years
? The patient's main complaint is the unsightly cosmetic appearance of the lesions.
? Most cases of necrobiosis lipoidica occur on the pretibial area
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ERYTHEMA MARGINATUM? Major criteria for diagnosis of rheumatic fever
? Extremely rare in Indians
? Erythematous pink rashes with a clear center and round or serpiginous margin.
? Not raised above the skin
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? They are brought on by application of heat? Most commonly seen on the trunk and proximal parts of extremities, but never on face.
SKIN CANCER
BASAL CELL CARCINOMA, SQUAMOUS CELL CARCINOMA & MALIGNANT MELANOMA
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Refer SPEED VISION-- PATHOLOGY SECTIONMYCOSIS FUNGOIDES
? Also known as cutaneous T cell lymphoma
? More common in males and in blacks.
? An indolent lymphoma with patients often having several years of eczematous or dermatitic skin lesions
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before the diagnosis is finally established? Pruritus is a frequent complaint
? In advanced stages, the lymphoma can spread to lymph nodes and visceral organs
? Lymph node enlargement may be due to benign expansion of the node (dermatopathic lymphadenopathy)
or by specific involvement with mycosis fungoides.
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? Patients may develop generalized erythroderma and circulating tumor cells, called Sezary's syndrome, apicture sometimes referred to as L'Homme rouge
? The skin biopsy remains the basis of diagnosis
? Circulating malignant T cells (S?zary cells) can be detected in the blood (T cell gene rearrangement test)
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Diseases that pyoderma gangrenosum may occur with? Ulcerative colitis
? Crohn's disease
? Rheumatoid arthritis
? Monoclonal gammopathy
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? LeukaemiaXANTHOMA & LIPOPROTEIN DISTURBANCES
Xanthoma tendineum
Familial hypercholesterolemia (typella)
Xanthelasma palpebrarum
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Normolipemic (50%)Familial hypercholesterolemia
Familial dybetalipidemia
Xanthoma eruptivum (or tubero
Familial dybetalipidemia
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eruptivum)Familial combined hypertriglyceridemia
Familial lipoprotein lipase deficiency (rare)
Xanthoma striatum palmare
Familial dybetalipidemi (type Ill)
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Xanthoma planum (generalized)Patients often develop a monoclonal gammopathy associated
with myeloma (type Ill), macroglobulinemia, or lymphoma, and
with normal plasma lipid levels. Less commonly, FHT may be present.
CONDITION
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CAUSENecrotizing fasciitis
Strep. Pyogenes
Erysipelas
Ecthyma
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PseudomonasErythrasma
Corynebacterium minuttissmus
Erythema migrans
Borrelia burgdorferi
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Erythema Ab IgneRepetitive exposure to infrared rays
Erythema annulare centifugum
Hypersensitivity [gyrate erythema]
Erythema gyratum repens
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Associated with malignancy [M/C: lung, esophagus, breast]Erythema dyschromicum perstans
Ashy dermatosis, idiopathic
Erythema chronicum migrans
Cutaneous manifestation of stage I Lyme disease
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Erythema elevatum diutinumLocalized fibrosing small vessel vasculitis
Erythema induratum of Bazin
Tuberculosis
Erythema infectiosum
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Parvovirus B 19Lesion
Found in
Erythema pernio (chill blain)
Cold
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Lupus pernio & Epitheloid granulomaSarcoidosis
Lupus profundus
SLE
Lupus Vulgaris
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Cutaneous TBPhrynoderma
Vit-A deficiency
Essential fatty acid deficiency
Sauroderma/Crocodile skin
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Icthyosis VulgarisWeldt sores
Desert areas
Black hairy tongue
Broad spectrum antibiotics
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Oral Hairy LeukoplakiaAIDS (not candidiasis)
Rain drop pigmentation
Chronic Arsenic Poisoning
Pyoderma Gangrenosa
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Ulcerative ColitisSlapped Cheek appearance
Erythema infectiosum
Honey Crust
Impetigo
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Angioid StreakPseudoxanthoma Elasticum
Axillary freckling & Lisch nodule (Iris hamartoma)
Neurofibromatosis
Cradle cap appearance
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Seborrheic Dermatitis (Pityriasis capitis)Coyenne pepper stippling (d/t hemosiderin)
Plasma cell balenitis of Zoom
NIKOLSKY SIGN: Positive in
? Pemphigus Vulgaris / foliaceous & Epidermolysis bullosa congenita
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? Staphylococcal Skin Scald Syndrome (SSSS) & Toxic Epidermal Necrolysis (TEN)? Stevens Johnson Syndrome
? Leukemia
? Herpes
The Asboe-Hansen sign ("indirect Nikolsky sign" or "Nikolsky II sign") refers to the extension of a blister to
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adjacent unblistered skin when pressure is put on the top of the bullaSIGNS IN DERMATOLOGY
? Antenna sign ? Keratosis Pilaris
? Asboe Hansen sign (Bulla spread sign) ? Pemphigus
? Auspitz sign ? Psoriasis
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? Button hole sign ? Neurofibromatosis.? Birbeck's granules: Langhan cell histiocytosis
? Chandelier's sign - Gonorrhea in women
? Candle sign & last cuticle sign: Psoriasis
? Carpet tack's sign ? DLE
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? Cerebriform tongue sign ? Pemphigus vegetans? Coup'd'ongue sign ?Tinea versicolor
? Crowe's sign ? Axillary freckling in Neurofibromatosis
? Comby sign: Measles
? Russell's sign: Bulimia Nervosa
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? Premalatha Sign: Pemphigus Vulgaris? Deckchair sign: Papulo erythrodema
? Dimple sign (Fitzpatrick sign ) ? Dermato fibro sarcoma protuberans, differentiates dermatofibroma
? from malignant melanoma
? Dubois sign ? Short little finger in congenital syphilis
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? Dory flap sign: Primary chancre? Flag sign ? Kwashiorkor
? Forscheimer sign ? Enanthema on soft palate in Rubella
? Groove sign of Greenblat ? LGV
? Head light sign ? Perinasal and periorbital pallor in Atopic dermatitis
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? Hertoghe's sign ? Loss of lateral third of eyebrow in Atopic dermatitis? Higouminaki's sign ? Congenital syphilis; thickened sternal portion of clavicle.
? Leopard sign: Onchocerciasis
? Milian's ear sign ? Erysipelas can spread into the pinna (being cuticular infection), whereas cellulitis cannot
spread to the pinna due to close adhesion of skin to cartilage of ear (without any areolar tissue.)
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? Oil drop sign ? Discoloration of nail bed in Psoriasis.? Ollendorf sign ? Papule is very tender to touch in secondary syphilis
? Osler's sign ? Alkaptonuria
? Pillow sign ? Netherton's syndrome; hair shaft defect patient sees hair on pillow on getting up in the morning
? Trichrome sign ? Vitiligo
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? Romana's sign -T.Cruzi; Chaga's disease? Shawl sing ? Erythema over the upper back and shoulders in dermatomyositis
? Wrist sign , Thumb sign or Steinberg's thumb ? Marfan syndrome
IMPORTANT PEARLS:
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? Area of skin: 1.7m2, constitutes 4kg of body weight in adult man.? Spongiform pustule of Kogoj: accumulation of neutrophils in Malphigian layer.
? Tzanck cell: keratinocyte.
? Clue cells: vaginal epithelial cells
? Fordyce spots: ectopic sebaceous glands
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? Target lesions: Erythema multiforme? Binkley's spots: Diabetic dermatopathy
? Muehrcke's nail: seen in chronic hypoalbuminemia
? Circle of Hebra: seen in scabies
? Ritter's disease: caused by Staph. aureus
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? Lichen nitidus: claw clutching a ball appearance? Anatomist's wart: Tuberculosis verrucosa cutis/Warty TB
? Remote reverse Koebner phenomenon: Vitiligo
? Dermographism: Urticaria
? White dermographism: Atopy
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? Myrmecia warts: Plantar warts? Dermatomyositis: Helitrope rash/ Gottron sign/ Gottron papule
? Most common form of oral candidiasis: acute pseudo membranous
? M/c dermatophyte producing favus: T. schoenleinii
? M/c photodermatoses: Polymorphic Light Eruptions (PLE)
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? M/c form of cutaneous TB: Lupus Vulgaris? M/c manifestation of gonococcal infection in males: Anterior urethritis
? M/c manifestation of acute gonococcal infection in females: endocervicitis
? M/c cause of vaginal discharge in India: Bacterial vaginosis
? M/c cosmetic allergen: fragrances > hair dye
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? M/c site of trophic ulcer: ball of great toe? M/c teeth affected in leprosy: upper incisors
? Black Piedra/ Trichomycosis nodularis: Piedraia hortae.
? White piedra: Trichosporon ovoides
? Copper penny bodies: Chromomycosis
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? Endothrix dermatophytosis in India is due to: T. Violaceum? Profeta's law: fetus maybe born normal but may develop signs of early congenital syphilis during first few
weeks/months
? Colle's law: syphilitic infant may not infect its own mother but is capable of infecting others.
? Truck driver's disease: Hydradenitis suppurative of perianal region in males
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? Kligman's formula/ Triluma cream: 5% hydroxyquinone, 0.1% dexamethasone, 0.1% Tretinoin (ForChloasma)
? Thinning of nails : involves nail matrix
? Dilapidated brick walls: Hailey-Hailey disease
? Syringoma: Tadpole like appearance
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? Miescher's granuloma: Erythema nodosum? Cork screw hair: Scurvy
? Selenium deficiency: Pseudoalbinism
? Louis bar syndrome: Ataxia telangiectasia
? Pseudo-Hutchinson's sign: Bowen's disease
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? Hutchinson's sign: Melanoma in nail matrix? Keratosis follicularis squamosa: lotus leaves on water appearance
? Jigsaw puzzle appearance: cylindroma
? Trimethylamine: fish odour syndrome
? Urbach Wiethe disease: lipoid proteinosis
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? Mauserung phenomenon: icthyosis bullosa of Siemens? Basal cell carcinoma: Bazex syndrome
? Erythema induratum affecting legs of young women: Bazin's disease
? Mouse ear appearance: X- ray feature of psoriatic arthritis
? Least affected in Atopic dermatitis: Mid chest
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? Pharyngeal dysmotility: seen in polymyositis? Green nail syndrome with fruity odor: Pseudomonas aeruginosa
? Haverhill fever/ erythema arthriticum: Streptobacillus moniliformis
? Jungle sore: cutaneous diphtheria
? Woody fibrosis: actinomycosis
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? Mickey mouse ears: Cockayne syndrome? Subcutaneous fat necrosis: Carcinoma pancreas
? Cigarette paper scars: Ehler Danlos Syndrome
? Hot tub follicles: Pseudomonas aeruginosa
? Slavic leprosy: Rhinoscleroma
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? Pretibial fever: leptospirosis? Alkaptonuria: sweat that stains
? Pseudo-Cushing's disease: chronic alcoholism
? Angel's kiss: Nevus flammeus
? Bath itch: Polycythemia rubra vera
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? Nostalgia parasthetica: itch in interscapular region? Effective drug for pruritus due to polycythemia rubra vera: Aspirin
? Mediator of pruritus in Hodgkin's Lymphoma: Leukopeptidase
? Syphilitic gumma: involves left atrium & septum
? Secondary syphilis never involves: bone
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? Photopatch testing: patch testing + UV irradiation [to document photoallergy]
? Worm eaten skull: Gummatous osteoperiosteitis of skull bones in syphilis
? Earliest feature of congenital syphilis: nasal discharge
? Pseudo paralysis of parrot in congenital syphilis: due to osteochondritis.
? Olympian brow: Supra orbital thickening in syphilis
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? Wooly headedness: adverse effect of Dapsone? Blaschko's lines: system of lines along which many linear nevus & dermatoses arrange themselves.
? Weber Christian panniculitis: seen in pancreatic disorders
? Shell nail: seen in bronchiectasis
? Foshay test: 48-hour intradermal test that, if positive, indicates tularemia.
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? The intradermal reaction (sporotriquin test) - confirm the diagnosis for sporotrichosis.? Berloque dermatitis: increased pigmentation due to cosmetics
? Treatment of choice for pruritis due to Uremia: UV light
? Acantholytic cells can be seen in bedside Tzanck test
? Pigmented purpuric dermatoses: shows recent pinpoint cayenne pepper--colored hemorrhages associated
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with older hemorrhages and hemosiderin deposition.*****END*****