DERMATOLOGY

I.INTRODUCTION TO DERMATOLOGY
 
Skin is the largest organ of the body composed of epidermis, dermis and subcutaneous layer. Skin is derived from ectoderm.

EPIDERMIS
1) Stratum basale consists of tall columnar cells with high mitotic activity. It is the dividing layer of the epidermis also called as
stratum germinatum. These cells contain many housekeeping organelles (RER, golgicomplex, mitochondria, lysosomes and
ribosomes).Vitamin D is synthesized from basal layer  
2) Stratum spinosum is thickest layer of skin consisting of polyhedral cells with large nuclei. Also called as prickle cell layer. The
spines are abundant desmosomes and cell surface modifications. Malpighian layer includes stratum basal and stratum spinosum
 
3) Stratum granulosum consists of flattened cells with keratohyaline granules and membrane coating granules (Odland Bodies) which
help in the formation of a water impermeable barrier.
 
4) Stratum corneum(Horny Layer) is flat anucleated dead cell layer. It shows basket weave appearance on Hematoxylin and eosin
staining,prevents water loss
 
5) Stratum lucidum is present between stratum corneum and granulosum,in the skin of palms and soles. The cells in this zone are in
transitional zone and degenerate as they move towards stratum corneum
 
• Mucous membranes lack stratum corneum and stratum granulosum
• The normal turnover rate of epidermis is 28 days

Cells in the Skin

 
• 80-90% of epidermal cells are Keratinocytes.
• Melanocytes are derived from neural crest cells and are present in stratum basale.. They synthesize Melanin & transfer it
to keratinocytes.
• For every 10 stratum basale cells there is one melanocyte.
• Each melanocyte provides melanin to about 36 keratinocytes.
• Stain for melanocyte-- silver nitrate stain
• Variation in skin color is not due to number of melanocytes but due to the number of melanosomes, production of
melanin and break down of melanosomes. (activity and distribution)
• Albinism is due to decreased production of melanin by melanocytes.
• Vitiligo is due to decreased number of melanocytes.
• Langerhans cells are derived from bone marrow, they are antigen presenting (APC) cells in the epidermis. These cells are
present in stratum spinosum. CD marker for Langerhans cell is CD 1. Langerhans cells have Bier beck granules (tennis
racket shaped granules). Tumor of Langerhans cells is Histiocytosis X
• Merkel cells are also derived from neural crest and acts as Mechanoreceptors. They are present in stratum basale.

DERMIS
• It is Mesodermal in origin
• The major type of collagen is Type I collagen(70%) and about 20% is Type III collagen.
• Dermis is further divided into superficial papillary dermis and deep Reticular dermis.
• Scarring occurs when reticular dermis is disrupted.
• Loosely arranged elastic fibers give elasticity to skin.
• Dermis contains lymphocytes, fibroblasts, mast cells.

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 • Stain for mast cells (Toulidine blue).
• The Nourishment to the Epidermis is provided by the Dermis.
• Basement membrane is present between the epidermis and dermis
• Electron microscopically it contains basal cell membrane, lamina lucida, lamina densa and sublamina densa with
anchoring filaments and fibers.
 
SUBCUTANEOUS LAYER
• It consists of abundant adipose cells, blood vessels and lymphatics.
• Absent in the eyelids and male genitalia, abundant in the abdomen.
 
SWEAT GLANDS
• They are ectodermal in origin
• Coiled tubular glands residing in the dermis.
• There are 2 main types of sweat glands i.e., Eccrine and Apocrine sweat glands.
• Eccrine sweat glands are present all over the skin particularly in the palms and soles. They secrete watery hypotonic
secretions onto the skin.
• Eccrine glands are innervated by sympathetic cholinergic system
• Blockade of eccrine sweat glands is k/a Miliria.
• Blockade of superficial opening is called miliria crystalline
• Blockade of eccrine gland ducts is called as miliria rubra
• Blockade of complete eccrine gland is called miliria profunda
 
• Apocrine sweat glands open into hair follicle. They are present in the Axilla, Anogenital region, scalp and near nipples. They
start functioning at the time of puberty. Secretions of apocrine glands are sterile. Bacterial action gives these secretions odor.
• Apocrine secretions are under Sympathetic Adrenergic nerve supply.
 

Fox Fordyce disease

Modified apocrine sweat glands

• Mammary Glands, Mohl glands of eye, cerumen glands (ear wax) of ear are modified apocrine glands.
•
• Blockade of apocrine sweat glands is called as Fox Fordyce disease
• Pus containing infection of apocrine sweat glands is called as hidradenitis
 
 
SEBACEOUS GLANDS
• They are present all over the body except palms and soles
• They produce sebum made of fatty acids, cholesterol esters and wax.
• The major areas of sebaceous glands are scalp, face, interscapular and sternal areas.
• They are holocrine glands that act as a pilo sebaceous unit.
• Enlarge and become active during puberty due to their androgen sensitivity.
 
Ectopic sebaceous Glands:-.
• They are not associated with hair follicles.
• Fox – Fordyce spots are ectopic sebaceous glands on the lips, can be seen in normal healthy people.

• Tyson glands are ectopic sebaceous glands on penis

• Meibomian glands are ectopic sebaceous glands of eyes
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 • Montgomery tubercles are ectopic sebaceous glands of breasts
 
Types of Hair
1. Lanugo Hair– These are long fine silky hair present in Embryonic life (only on babies)
2. Vellus hair are short, fine hair present mainly over malar region of face, Non-pigmented hair.
3. Terminal hair are pigmented, long and coarse hair
 
Stages of Hair Cycle
1. Anagen phase – it is actively growing phase of the hair that constitutes 90% of total hair. Duration of anagen is 3-5 years. It grows at
rate of 0.4 mm / day.
2. Catagen phase – it is transitional phase of hair constituting 1-3% of total hair, duration is for 3 weeks.
3. Telogen phase – It’s a resting phase of the hair, constitutes 8-9% and has a depigmented
narrow club. Duration is upto 3 months.
 
Nails
• It’s a hard plate of keratin with high sulphur content
• Finger nails grows 0.1 mm/day(1cm/3 months) Toe nails grow at a rate of 0.03 mm/day.(1cm/9 months)
• Mees line are seen in arsenic poisoning
• Beau’s line occurs when nail growth stops and then regrows producing transverse ridges, seen in patients with infections
and soon after recovery.
• Half and Half nail is seen in chronic renal failure.
• Terry Nails are seen in cirrhosis
• Periungual Fibroma is seen in tuberous sclerosis
 
Skin Lesions and Terminology
• linear skin lesions are seen in contact dermatitis and koebner phenomenon.
• Koebner phenomenon is development of isomorphic skin lesions on uninvolved skin after trauma, seen in psoriasis, lichen
planus and vitiligo
• Pseudokoebner phenomenon is seen in warts, molluscum contagiosum and pyoderma gangrenosum

ERYTHEMAS
Erythema multiformis Target lesions/iris lesions/bulls eye lesion Drugs/Herpes
infection/Mycoplasma
Erythema Migrans Gradually enlarging annular lesion with central clearing Lymes Disease
Erythema Marginatum Transient-annular erythematous plaques on trunk and Rheumatic Carditis
extremities.
Erythema Gyratum Repens Wood Grain Pattern Marker of malignancy
Most common-Lung cancer
Most characteristic-Breast ca.
Necrolytic Migratory Erythema with superficial pustules and erosions on face Glucaganoma
Erythema extremities
Erythema Infectiosum Slapped Cheek Appearance Parvo virus B 19
 
• Herald patch / circinate patch also k/a mother patch is seen pytyriasis Rosea.
• Morbilliform rash is seen in Measles.
• Sheet line rash called as scalariform rash is seen in scarlet fever.
 
MacroscopicTerminology

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• Macule Change in colour of skin less than 0.5cm

• Patch Change in colour of skin more than 0.5cm

• Papule Elevated solid lesion less than 0.5cm

• Plaque Elevated lesion more than 0.5cm

• Vesicle Fluid filled raised lesion less than 0.5cm

• Bullae Fluid filled raised lesion more than 0.5cm

• Nodule Solid raised dome shaped circumscribed lesion more than 0.5cm

• Petechia Pin sized bleeding points less than 3mm

• Purpura Extravasation of blood beneath the skin 3mm-1cm

• Ecchymoses Extravasation of blood beneath the skin more than 1 cm

• Telangectasia Visible Dilatation of Blood Vessels

• Pustule Pus filled vesicle

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 • Lichenification Thickened rough skin with hyperpigmentation and prominent skin markings

• Erythroderma Inflammation involving more than 90 % of Body surface area, Dermatological Emergency

• Onycholysis Separation of nail plate from Nail bed

• Excoriation Traumatic break in epidermis causing raw linear area

. 
Technical microscopic terms:
• Acanthosis is increased thickening of stratum spinosum
• Acantholysis is loss of cell adhesions between keratinocytes producing rounded cells, called Tzanck cells. Tzanck test is
demonstration of Tzanck cells (acantholytic cells) using Giemsa stain. These cells are seen in Herpes zoster, chicken Pox and
Pemphigus.
• Parakeratosis is presence of nuclei in stratum corneum, seen in psoriasis and actinic keratosis.

• Hyperkeratosis is proliferation of stratum corneum

• Dyskeratosis is faulty premature keratinization,within cells below stratum granulosum seen in dariers disease.
• Spongiosis is intra epidermal intercellular edema
• Epidermotropism is the extravasation of blood cells into the epidermis.

• Munro-Micro abscess is seen in Psoriasis consisting of neutrophils in the stratum corneum of epidermis.

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 • Pautrier’s abscess is seen in Mycosis fungoides (cutaneous T cell Lymphoma) Papillary tip abscess is seen in Dermatitis
Herpetiformis.
• Hypergranulosis is increase in stratum granulosum
• Papillomatosis is hyperplasia and enlargement of dermal papilla producing surface elevation.
• Lentiginous –Linear pattern of melanocyte proliferation within the epidermal basal cell layer
 
Clinical Testing
• Diascopy(Vitropression) is visualizing the skin through glass slides, useful in differentiating erythema(blanches) from
purpura(doesnot blanch)

• Wood lamp examination uses 360 nanometers (UV vays). It has Nickeloxide and barium silicate filter. It produces
fluorescence of objects under it.

 
On Wood Lamp Examination
Tinea capitis(hair) Light Yellow green
Pseudomonas Apple green/golden yellow
Tuberous sclerosis Blue White
Vitiligo White
Erythrasma(corynebacterium minutissimum) Coral Red/Pink
Porphyria cutanea tarda(urine) Red/pink
Pityriasis versicolor Golden Yellow/apple Green

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Nikolsky’s sign is shearing of skin on application of lateral pressure, seen in Pemphigus Vulgaris, Staphylococcal Scalded Skin
Syndrome(SSSS) And Toxic Epidermal Necrosis(TEN)
Nikolskys sign is absent in bullous pemphigoid

• Bulla spread sign also called as Asboe-Hansen sign, is +ve in pemphigus vulgaris and bullous pemphigoid,
• Auspitz sign is fine pinpoint bleeding points after removal of scales seen in Psoriasis.

• Darrier sign is seen in urticaria Pigmentosa. There is itching, Erythema and edema
• Dermographism /Triple response of Lewis consists of Redness due to vasodilation, Axonal flare and wheal due to
extravasation of fluid (RAW)
• White dermatographism is seen in atopic dermatitis.

• Dimple sign is seen in Dermatofibroma, dermatofibrosarcoma protuberans

• Apple Jelly nodules are seen in lupus vulgaris (cutaneous TB) and Sarcoidosis

• Patch test is done for contact allergic Dermatitis.

• KOH examination with 10-20% KOH is used for all fungal infections.
• Aceto whitening test – subclinical penile warts(condyloma acuminata)
• Carpet Tack Sign-Removal of scales in DLE shows downward projecting follicular plugs
• Button hole sign-Neurofibromatosis
 
II.Blistering Disease of Skin / Vesiculobullous lesions
• Immune mediated
• Pemphigus
• Bullous pemphigoid
• Dermatitis Herpetiformis
• CBDC (Chronic bullous dermatoses of childhood)
• Epidermolysis bullosa acquisita Genetic
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 • Epidermolysis bullosa
 
Pemphigus Vulgaris
• It is the most common type of pemphigus.
• It is an Intra epidermal break
• It is a supra basal break (occurs in stratum spinosum i.e. above stratum basale)
• It is auto immune disorder with production of IgG antibodies directed against Desmoglein 3 that are cell adhesion molecules.
• There is destruction of intracellular cementing substance with loss o
• f cell adhesion molecules producing Acantholysis.
• It is a type II hypersensitivity reaction

Clinical Features
• Seen in 4th – 6th decade. The initial lesion are painful oral mucosal lesions
• Involvement of skin is in the form of non – itchy bullae over the face, scalp, axilla and trunk
• Bulla spread sign also k/aAsboe. Hansen sign is positive and Nikolsky’s sign is +ve.
• The bullae ruptures to produce painful eruptions Tzanck smear shows Tzanck cells (Acantholytic cells), smear taken from
floor of blister

• The basal keratinocytes remain attached to basement membrane & form Row of tombstone appearance.
• Immunofluoroscence shows fish net pattern with deposition of intercellular IgG throughout the epidermis.
• Pemphigus may be associated with other autoimmune diseases like myasthenia gravis and malignancies like non hodgkins
lymphoma,CLL, thymoma, lymphoma etc. (Paraneoplastic Pemphigus)
Pemphigus Vegetans
• It is a variant of pemphigus vulgaris effecting mainly the flexor areas
Pemphigus Foliaceous
• It is a sub-corneal break characterized by IgG antibodies directed against Desmoglein -1
• It is usually seen in seborrheic areas like scalp, face etc.
• It does not have oral lesions.
• Nikolsky’s sign is +ve, but bulla formation is rare only superficial vesicles and crusting.
• Tzanck smear shows Tzanck cells.
• Immunofluorescence is similar to Pemphigus vulgaris.

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Pemphigus Erythematosis
• It’s a variant of pemphigus foliaceous having features of pemphigus and lupus Erythematosus. Erythematous rash over the
cheek and lesions on trunk IgG, C3 antibodies in epidermis and ANA antibodies.
Rx of Pemphigus:
• High Dose Systemic Steroids,Pulse Steroid therapy (dexamethasone cyclophosphamide pulse) are main stay and
antibiotics to prevent secondary infections.
• Drug induced pemphigus: it usually presents as pemphigus foliaceous. Commonly associated drugs are captopril,
penicillamine, Rifampicin, penicillin etc.
Bullus Pemphigoid
• Autoimmune disease with Antibodies (IgG) directed against the basement membrane hemidesmosomes (BPAGs – Bullous
pemphigoid antigen)
• It produces sub-epidermal break.

Clinical Features
Onset usually after 60 years of age. Intense Itching with dense intact bullae especially on the flexor aspects, axilla, abdomen and groin
• Facial skin and scalp are usually spared,Mucosal lesions are less common
• The lesions rupture producing erosions and post inflammatory hyperpigmentation.
• Nikolsky’s sign is usually negative and Bulla spread sign is positive.
• It is commonly associated with gastric carcinoma, diabetes, Rheumatoid arthritis and psoriasis.
• Tzanck cells are not seen. Tzanck smear shows eosinophils.
• Immunofluorescence shows linear IgG and c3 deposits on basement membrane
• Prognosis of Bullus pemphigoid is better than pemphigus. Chronic self limiting course.
Rx: Topical or Systemic steroids,Based on severity,pulse dexamethasone cyclophoshamide,self limiting course.
 
Cicatricial Pemphigoid

• Variant of Bullous Pemphigoid,involving mucosa and skin producing severe scarring

• Not self limiting ,chronic debilitating course with oropharyngeal adhesions, esophageal strictures
Dermatitis Herpetiformis
• It is intensely pruritic chronic, recurrent, papulovesicular lesions with underlying gluten sensitive enteropathy
• This is the only condition of vesiculo bullus disease where papules can be seen.

• Usually occurs b/w 25-55 yrs,More common in males than females

• symmetrical involvement with erythematous papules vesicles. involving mainly extensors of limbs (elbows and knees), more
common in males, between 20 – 55 years HLA – B8.
• Oral lesions are common and Assymptomatic.
• Oral lesions are worsened with oral iodides or by iodide patch testing (provocative testing)
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 • Histological examination shows neutrophilic collection at tip of dermal papillae k/a Papillary Tip Abcess.
• Immunofluorescence is diagnostic and performed on normal skin preferably buttocks, shows granular IgA deposits in dermal
papillae
• Anti basement antibodies are –ve but anti thyroid, Epidermal transglutaminase and anti gliadin antibodies are present
Rx: Dapsone and gluten free diet
Herpes Gestationalis
• It is a non – viral autoimmune blistering disease of young women occurring during 21 – 28 weeks of gestation
characterized by pruritis and blisters around Periumbilical area.
• Immunofluorescence shows mainly linear C3 and sometimes IgG deposits along the basement membrane.
Rx:Steroids

III.Scaling Disorders/Papulo squamous Skin Diseases

Psoriasis
• It is a scaling disorder of skin, affecting 1-2% of the population, mc in whites
• a chronic relapsing inflammatory disorder with presence of erythema, papules and plaques covered by silvery micaceous
scales
• They commonly involve extensors of elbows and Knees.
• Lesions tend to be symmetrical.
• Koebners phenomenon is development of isomorphic lesions after trauma or itching at the uninvolved site.
• Psoriasis have variable pruritis.
• No known causative agent, multifactorial. Has a strong association with HLA CW6
Precipitating factors of Psoriasis:
• Beta hemolytic streptococcal infection,HIV, Trauma
• Drugs like Li, B-Blockers, NSAIDS, Iodides, and antimalarials.
• HLA – B27 +ve is seen in 70% of patients with Psoriatic arthritis.
• There is rapid epidermal turnover within 3-4 days faster cell cycle.
• Intracellular C-GMP levels are and c-AMP levels are¯.
 
Types of Psoriasis:
• Chronic plaque psoriasis is Mc type of Psoriasis
 
Guttate Psoriasis:
• Also called as Rain drop Psoriasis. It is seen in children and is precipitated by B-hemolytic streptococcal infections.
 

Pustular Psoriasis:
Acute widespread lakes of pus
• It is precipitated by steroidal withdrawal.
• Von Zumbusch reaction is a very severe generalized pustular psoriasis.
Treatment-DOC are Retinoids(Acitretin)

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 Impetigo Herpetiformis
• It is pustular Psoriasis in Pregnancy and is treated by giving steroids.
Erythro dermic Psoriasis:
• In this 90% of skin is involved with erythema, edema and scaling and is a dermatological emergency.
• Treatment-Methotrexate (DOC)
• Rupioid Psoriasis: limpet like cone shaped hyperkeratotic lesions of psoriasis
• Ostraceous Psoriasis: very thick scaled ring like areas resembling oyster shell
Inverse Psoriasis:
• It is the one involving flexor surfaces. It usually does not producing scaling.

 
Nail changes in Psoriasis: upto 50% Of psoriasis patients
• MC and characteristic change is nail pitting.
• Earliest change is nail discolouration.
• Hyperkeratosis and nail dystrophy are present.
• onycholysis is breaking up of nails
• Oil drop sign present under nail plate is pathognomic.

• Acrodermatitis Continua- Type of pustular involving tips of fingers and toes with nail dystrophy. also called Dermatitis
Repens.
 

Psoriatic Arthritis:5-10% of cases

• It is a sero –ve arthritis, oligo articular involving the DIP joints, also associated with sacroiliitis asymmetric.
• It is erosive arthritis producing pencil in cup deformity/opera glass deformity(arthritis mutilans)

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 • HLA B 27 positive
• Telescopic sign of DIP is +ve.
• Sausage shaped fingers and toes
• There is involvement of Achilles tendon usually asymmetrical
• Only about 5-10% of Psoriasis patients develop Psoriatic arthritis
Treatment-Methotrexate(DOC),Etanernacept  
Diagnosis
• It is made by clinical characteristics and skin biopsy of the lesion site.
• Histopathology shows parakeratosis, hyperkeratosis, there is elongation of rete ridges, loss of granular cell layer
k/aAgranulosis and suprapapillary thinning of epithelium.
• There is intra epidermal presence of neutrophils k/a munro – microabcess(stratum corneum) and pustule of
kogoj(stratum spinosum)
• There is Acanthosis
• Dilated capillaries are seen in the dermis that are responsible for Auspitzsign.
• The scales are easily removed in the form of white shining membrane,k/a grattage test (candle grease sign). Followed by
red bulkeleys membrane,which when removed produces pin point bleeding points.(Auspitz sign)
Rx :
Emollients +,treat precipitating causes
Localised Plaque psoriasis-Topical steroids ,Calcipotriol,Tazarotene,Tar +salicylic acid,excimer laser
systemic Steroids are C/I in Psoriasis
• Coal tar has anti inflammatory and anti – mitotic activity and is used in Psoriasis.
• Goeckerman regimen is UV light + coal tar.
• Ingram regimen is UV light + Anthralin
• PUVA therapy is psoralen + UV A light.
• Immunosuppressants like methotrexate, cyclosporine, mycophenolate
• Tacrolimus also k/a FK-506 is a T cell modulator
• Other agents used are Infliximab, Etanercept
• Retinoids are used in Rx of Pustular Psoriasis.
• Topical Vit-D3 – calcipotriol, tacalcitol
Indications for Methotrexate therapy in Psoriasis
• Psoriatic arthritis, Erythrodermic Psoriasis and chronic plaque Psoriasis not responding to R x
Lichen Planus
• Idiopathic Chronic inflammatory dermatosis involving skin, mucosa, nails and hair.
• It’s a papillosquamous scaling disorder characterized by pruritic, polygonal, purple, plane topped papules . MC-30-60 yrs

• Koebner phenomenon is most characteristic (more than in psoriasis)

• Etiology is not known, strong association with Hep C virus.
• ?CMI,?Autoimmune, chronic liver diseases,Hep B and Hep C
• HLA B8 in oral LP and HLA Bw-35 with cutaneous lichen planus.
• Oral LP associated with gold and mercury in dental amalgams.

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 • It commonly involves flexor areas of the wrist, lower back,penis,shins(hypertrophic LP)and oral mucosa
• Mucosal Lesions are present as net like white reticular laces or erosive stomatitis.
• Wickham’s Striae is a network of greyish lines along the papules seen due to hypergranulosis characteristic of Lichen
planus.

• Nail changes are seen in 10% of patients, it consists of Pterygium formation, longitudinal ridges, splitting of nail
plate and onychodystrophy.
• Involvement of hair prod Cicatricial Alopecia (Scarring Alopecia)
• Diagnosis is made by clinical features i.e. Hyperkeratosis, Hypergranulosis, Acanthosis, Basal cell degeneration
prod Civattebodies and Max Joseph Space. There is a band like infiltration of Lymphocytes at dermo-epidermal
junction.
• There is saw toothing of Rete – Ridges.

• Cutaneous eruptions resembling lichen planus can occur after administration of drugs like thiazide diuretics, gold,
antimalarials, pencillamine, phenothiazines, and in chronic graft versus host disease.
• Lichen planus erosive stomatitis of mucosa and hypertrophic LP can increase risk of SCC
• Lichen planus can be associated with Hep C.
Rx:
• It undergoes spontaneous remission. Topical steroids are mainstay of R x
• PUVA
• Topical soothing agents, Vit A derivative, Anti histaminics are also used.
• Oral Dapsone is used for oral Lichen Planus.
Lichen Nitidus:-lesions are similar to lichen planus,smaller size 1-2 mm,grouped lesions over elbows,abdomen,dorsum of hand and
penis.Histology shows characteristic BALL in Clutch appearance .Treatment:-Antihistaminics and topical steroids
Lichen Actinicus:-lesions on sun exposed areas,deeply hyperpigmented centre surrounded by hypopigmented zone.treatment:-topical
steroids and sunscreens.
 
Pityriasis Rosea
• It is a acute symmetrical self limiting papulosquamous disorder seen especially on trunk in children and young adults
common during spring and fall.
• The first manifestation is a 2-6 cm. annular lesion called a Herald patch (mother patch, circinate patch) with fine scaling,
fine cigarette paper like collaret of scales.
• They have truncal predilection (Christmas tree pattern)/fir tree pattern.
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 • Pityriasis Rosea Resembles lesion of secondary syphilis but palm and sole lesions are rare
• Hanging curtain sign is seen
  Rx:
• No Rx required, it is self limiting
• Doesnot produce erythroderma
• Moderately pruritic so antihistaminics and topical steroids and UV – B phototherapy can be used.
IV.Keratinization Disorders Ichthyosis
• It’s a Keratinization disorder which can be hereditary or acquired characterized by excessive scaling.
Hereditary Ichthyosis
• Ichthyiosis vulgaris
autosomal dominant condition involving Extensor surfaces while flexor surfaces like cubital fossa and popliteal fossa are spared,with
decreased granular layer.
• X linked recessive Ichthyiosis is common in males and is due to deficiency of sterol sulfatase
• Lamellar ichthyosis is present at birth and is called colloidon baby. or Alligator Boy .AR ,baby is encased in a taut
membrane later develops large thick scales covering the entire body including flexures

Refsums Disease
• AR, It is due to deficiency of Phytanic acid oxidase, characterized by cutaneous and neurologic manifestations due to
accumulation of phytanic acid.
Skin lesions are similar to Ichthyiosis and neurological symptoms include cerebellar Ataxia, Progressive Polyneuropathy, Retinitis
Pigmentosa and sensorineural deafness.
 
Sjogren Larsson Syndrome
• AR, It is due to deficiency of enzyme fatty alcohol:nicotinamide adenine dinucleotide oxidoreductase, characterized by
cutaneous and neurologic manifestations
• Skin lesions are similar to Ichthyiosis scaling over the body and hyperkeratosis of palms and soles and neurological
symptoms include spastic diplegia or tetraplegia with mental retardation

Pityriasis Rubra Pilaris

• It is characterized by epidermal over activity near hair follicles.
• There is erythematous rash similar to seborrheic dermatitis. progressing cephalo caudally with follicular hyper
keratosis,follicular plugging and Palmo – plantar keratoderma.
• Salmon coloured patch over trunk and extremities with areas of uninvolved skin in between
Rx: Retinoid, Steroids and Methotrexate.

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DARIER'S DISEASE (KERATOSIS FOLLICULARIS) '

• It is dyskeratosis with dirty, greasy, wart-like malodorous papules in the sebborheic areas.
• Autosomal dominant inheritance (chromosome 12)
• There is V shape splitting of nails,palmar pits,cobble stone appearance of mucosa,dome shaped papular lesions
on acral areas called acrokeratosis verruciformis of Hopf
• Exacerbation occurs after sun exposure.
2. Presence of corps and Ronds on histology.
3. Corps ronds (in stratum spinosum) and grains (stratum corneum) on histology which are dyskeratotic keratinocytes
• Histopathology shows dyskeratosis and acantholysis.
Rx : Retinoids(Acitretin) are the drug of choice.

Acanthosis Nigricans:-charecterised by hyperpigmented,velvety,verrucous symmetrical lesions involving body folds and

mucocutaneous junctions.
There is thickening of palm with accentuated dermatoglyphics with deep sulci of fingertips called Tripe Palms.
Acanthosis Nigricans
• Benign or Insulin resistance variety (HAIR-AN syndrome: associated with Hyper Androgenism, Insulin Resistance and AN.):
Acromegaly, Cushing's Disease, PCOD
• Pseudoacanthosis nigricans: associated with obesity
• Drug induced AN: Nicotinic Acid, Fusidic Acid, diethylstilbestrol, nicotinic acid, glucocorticoids, growth hormones
• Malignant AN: usually associated with adenocarcinomas (MC stomach) and other GIT tumors.
• Tripe Palms is a variety more strongly associated with malignancy

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V.Disorders of Hair Aloplecia
• Physiological hair loss is 100/day.
• Scarring Alopecia
Cutaneous disorders Systemic disorders
- Discoid lupus Erythematosis(DLE) Chemicals,radiation,burns,Mechanical trauma
- Lichen Planus - Sarcoidosis
- Folliculitis decalvans - Cutaneous metastases
- Linear scleroderma (morphea)  
- Kerion, Favus,herpes zoster Congenital and developmental
Pseudopelade -Nevus sebaceous and Epidermal Nevus
Malignancies-BCC,SCC -Aplasia Congenital Epidermolysis Bullosa
 
2. Non Scarring alopecia
a. Androgenetic alopecia
b. Telogen Effluvium
c. Anagen Effluvium
d. Trichotillo mania
e. Alopecia areata.
Androgenetic alopecia
• physiological process not a disease
• Seen in genetically predisposed. The terminal hair are transformed into vellus hair, this is k/a miniaturization.
• Bitemporal and Frontal Recession with preservation of hair on occiput and sides(male pattern androgenic alopecia)
• Rx –Topical Minoxidil, Oral Finasteride, wigs and Hair Transplant
• Central thinning of hair with diffuse hair loss with preservation of anterior hair line (female pattern)
• Rx- Cyproterone Acetate, Spironolactone, Minoxidil 2%,wigs
• Surgical correction
  Alopecia Areata
• an auto Immune disease occurs due to genetic factors, viral infection or emotional stress, commonest cause of patchy
alopecia.
• Associated with Atopic Dermatitis, AutoImmune diseases (vitiligo, myasthenia, hashimoto) and Downs syndrome. M=F
• There is smooth discrete bald patch with no scarring over eyebrows, scalp or beard. Exclamation mark(Broken hairs with
tapering shafts) is present in Alopecia areata.
• Hair follicles enter telogen phase prematurely. Histology shows perifollicular T lymphocytic Infiltration in a pattern called
swarm of bees.
• Presence of nail pitting,beaus line may be present
• Alopecia Totalis is total loss of scalp hair
• Alopecia Universalis-All scalp as well as body hair is lost
• Ophiasis-Hair loss involving occipital and sides of scalp.
• Rx-75% of patients undergo spontaneous remission.
• Topical and intralesional Steroids,Topical Minoxidil,PUVA/UVB/prednisolone-wigs.
• Signs Of Poor Prognosis-
• Underlying Atopy
• Presence of autoimmune diseases
• Family history
• Nail involvement
• Multiple extensive patches-Eyebrows and eyelashes involvement,Alopecia Totalis/Universalis
• Ophiasis,
• Young Age
• Recurrent Frequent Attacks,
• Downs Syndrome.  
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Trichotillomania
• occurs in psychologically disturbed females usually in age group 11-17 yrs. The patient twists the hair and pulls it deliberately.
• Irregular asymmetric patches with many broken hairs.
• The alopecia covers the entire scalp except the margins. It is also called tonsure alopecia / orentrich sign.
• Rx-psychological treatment
 Telogen Effluvium
• shedding of hair > 100 per day seen in patient undergoing surgeries anemias, acute febrile illness, endocrine
disorders or Drugs.
• Hair loss usually occurs 2-3 months after the trigger (Anagen hairs all simultaneously shift to telogen phase) and
there is usually recovery after 6 months.
• Drugs –ACEI,B-blockers,OCPS,Bromocriptine,Cimetidine,Retinoids,Lithium,levodopa and Antithyroid
drugs,Anticoagulants,Colchicine.
• Rx : Assurance and Minoxidil,Removal of drug.
 Anagen effluvium
loss of hair even in Anagen phase seen in patient undergoing cancer therapy.
 Traction Alopecia is seen in females keeping tight pony tail.
 Alopecia Steatoidis is non-scarring occurring due to dandruff.
• Tinea capitis usually Non cicatricial(except Kerion and Favus)associated with redness and scaling.  
• Pseudopelade-destructive inflammatory process in the scalp,characteristically involving the vertex with crab like
extensions,producing scarring alopecia.
• Systemic Causes –
Secondary Syphilis-Moth Eaten Alopecia
Systemic Lupus Erythematous(Lupus Hair-Frontal Hair is Thin and craggy)
Hiv
ACNE
• Acne patient secretes more sebum than normal people.
• Its primarily disease of sebaceous follicles. Occurs mc in adolescents,starts earlier in females
• Trauma, friction, cosmetics, industrial exposure, steroids, OCPs, lithium, INH, phenytoin and Phenobarbital may produce
acneiform eruptions genetics and PCOD also play a role.
• Its consists of polymorphic lesion like pustules, comedones, papules.
Pathogenesis of Acne:
• Sebum production,hypercornification of sebaceous duct,microbial infection and inflammation.
• Most cases of acne have pleomorphic lesions,papules,pustules,comedones and nodules
• Two types of lesions
✓ Noninflammatory(comedones)
✓ Inflammatory(Nodulocystic)
• Comedones are pathognomic for Acne.,they are conical raised lesions with broad base
• Open comedones are k/a Blackheads
• Closed comedones are k/a white heads.
• Comedones represent hyper proliferating ductal Keratinocytes.
• Acne is not infectious, however Propionobacter, Malasezzia furfur and staph epidermidis are sometimes isolated
• predominantly occurs over the face(mc)back and chest.
• Infra orbital area is usually spared.
• Acne Conglobata is highly inflammatory acne with comedones,nodules,abscesses and draining sinuses which heal with
severe scarring.occurs in adults Rx-Oral isotretinoin.
• Acne Fulminans-sudden appearance of severe acne with systemic signs and symptoms like fever
polyarthralgia,polymyalgia,leucocytosis.occurs in teenage boys,face is often not involved.Rx-High dose steroids to reduce
the severe inflammation and then retinoids.
• Acne Tetrad-Acne Conglobata,Hidradenitis suppurativa,dissecting cellulitis of scalp and Pilonidal sinus.more common in
men,also called Follicular Occlusion Tetrad.
• SAPHO Syndrome-Synovitis
✓ Acne(conglobata,fulminans)
✓ Pustulosis(pustular psoriasis,palmoplantar pustulosis)
✓ Hyperostosis
✓ Osteitis

Acneiform Drug eruptions

-Hormones and Steroids -Antiepileptic Drugs
Gonadotropins Phenytoin
Androgens Phenobarbitone
Anabolic steroids -Antitubercular Drugs
Oral/topical steroids Isoniazid

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 -Halogens Rifampicin
Bromides -Other Drugs
Iodides Lithium
Halothane Cyclosporine.
Acne can occur in diseases with excess androgen synthesis(PCOD,Adrenogenital syndrome,Hormone producing tumors)
  Rx:
• Comedolytic agents like Tretinoin (Retinoids), Adapalene,Azelaic Acid
• Anti-microbial creams like Benzoyl Peroxidase, Erythromycin, and clindamycin.
• Systemic antibiotics like oral Minocycline, Doxycycline and Erythromycin are used for moderate-severe acne.
• Adapalene has good anti-inflammatory activity.
• Isotretinoin affects all four etiological mechanisms,is preferred for nodulocystic acne,acne Conglobata,Acne
Fulminans,unresponsive acne,acne causing psychosocial and physical scarring.It is very Teratogenic,avoided in pregnancy
and lactating women. Adequate contraceptive is essential during and one month after therapy.
• Acne surgeries:- comedo extraction, aspiration of cyst, incision and drainage, intrasterioid injections with Triamcinolone
• Latest techniques include laser abrasion and Derma abrasion and laser peeling.
Rosacea
• It’s a chronic Centro facial disease papulopustular lesions on an erythematous background with telangiectasia preceded
by episodes of flushing,related to intake of hot spicy foods.
• There is hyperplasia and enlargement of sebaceous glands esp. of nose k/a Rhinopyma
• Women more often affected than men,3-4th decade
• Opthalmological complications like conjunctivitis,keratitis,episcleritis,blepharitis are common(50% of cases)
• Demodex folliculorum,tiny mites that live in the hair follicle on facial skin especially the forehead, cheeks, sides of the
nose, eyelashes and external ears is found to be associated in the etiology
• Rx-Topical Metronidazole cream(DOC)
✓ Oral Doxycycline
✓ Isotretinoin
✓ Rhinophyma-Surgical correction.

Urticaria/Hives
It is appearance of sudden transient, varying erythematous,pruritic, edematous vascular eruptions of Dermis,with elevated itchy
wheals.
Mc site -trunk
• Usually associated with Itching.
• Main chemical mediator is histamine.
• Urticaria is transient (less than 24hrs), vasculitis persists
• Acute Urticaria-Duration less than 6 weeks-insect bites,drugs like pencillin,shell fish.
• Chronic urticaria-Duration more than 6 weeks-idiopathic,autoimmune( Functional IgG autoantibodies binding IgE
receptors)
Types
• Idiopathic(mc)
• Dermographism
• Cholinergic Urticaria occurs after exercise and exposure to sun,heat
• Cold Urticaria
• Solar Urticaria
• Acquagenic
• Adrenergic due to stress
Treatment
• Symptomatic- Antihistaminics,H1 blockers
▪ Corticosteroids-prednisolone
▪ Adrenaline in Anaphylaxis
• Eliminate underlying cause
• Propanolol for adrenergic stress related urticaria
 
Angio edema / Quinke’s Edema
• It caused due to deficiency of c1 esterase inhibitor(Hereditary)or Acquired.
• Urticaria involving subcutaneous tissues, involving genitalia, lips, eyelids. Involvement of tongue and larynx gives acute
onset.
• Itching is absent.
 
Urticaria Pigmentosa
• It is cutaneous mastocytosis presenting as itchy skin lesions with Erythema and Edema k/a Darriers Sign.
• Histological exam shows mast cell infiltration in dermis.

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Nutritional Disorders Affecting Skin

Pellagra.
• Its due to deficiency of Niacin or Tryptophan
• Four D”s of Pellagra are Dermatitis, Dementia, Diarrhea, and Death if untreated.
• Skin lesions in pellagra are symmetrical photosensitive skin eruptions.
• An erythematous rash involving dorsum of hand.
K/a glove / gauntlet of pellagra.
• On the face it produces lesions similar to LE (lupus)-butterfly rash
• Eruption on neck appears like a necklace k/a casal necklace. Also k/a cravat.
• Rx-Oral Niacin or Nicotinamide 100-300mg/day in three divided doses.
 

Acrodermatitis Enteropathica
• AR disorder due to defective gut absorption of Zinc.manifests between 3 weeks-18 months
• It presents with Dermatitis, Alopecia and Diarrhea esp. when baby is shifted from Breast milk to cow’s milk.
• There is perioriphyseal acral dermatitis, alopecia and diarrhea
Rx : Zinc sulphate/gluconate(1-2mg/kg/day)

Ariboflavinosis(ORO-OCULO-GENITAL syndrome)
• Occurs due to Vitamin B2 (Riboflavin)deficiency
• Angular stomatitis,cheilosis,glossitis ---increased corneal vascularity----scrotal and vulvar dermatitis
Rx-Riboflavin
 

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Vitamin A deficiency
Xerosis of skin and eye

Keratomalcia

Phrynoderma-Toad skin,a type of follicular hyperkeratosis on elbows,knees and thigh(can also occur with essential fatty acid
deficiency)

Rx-Oral Vitamin A 1 lakh IU/day for 2-3 days

Kwashiorkor
• Depigmentation Including circumoral pallor
• Desquamative Dermatitis-Crazy Pavement/Flaky paint dermatoses
• Flag Sign-Hair Depigmentation
• Unruly hair-staring hair on scalp,broomstick on eyelashes
• Orofacial gangrene(cancrum oris)in severe PEM.
• (Marasmus has dry wrinkled skin with loss of subcutaneous fat but no classical skin changes as in Kwashiorkor)
Eczematous Lesions of skin :
• Eczema(Dermatitis) is inflammatory response of the skin characterized by Erythema,Vesiculation,crusting occur during
acute episode.
• Scaling and lichenification in chronic stages
• Vesiculation is an important feature of Eczema
• Histologically Eczema shows spongiosis, Acanthosis, perivascular lymphocytic infiltration.
Classification of Eczema
• Exogenous : Contact irritant dermatitis, contact allergic dermatitis ; Infective Eczema
• Endogenous: Atopic dermatitis, Seborrheic dermatitis.
• Nummular Dermatitis, stasis eczema,
• Asteatotic eczema (xerotic eczema), Discoid
• Eczema, Hand eczema, Pityriasis Alba
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Contact Irritant Dermatitis:
• Its char by burning sensation limited to area of contact.
• The 1st step is Vesiculations.
• Common irritants include water(mc), detergents(housewives eczema), alkalis, acids, soaps,thermal burns,frost
bites.urine(napkin dermatitis)
• Common in people working in printing, painting, hair dressing, agricultural, medicinal professions.
• No Memory T cell or antibodies involved.short latent period
  Clinical Features :
• There is erythema, vesicular bullous lesions, crustations in acute cases.
• Lichenification (thickening of epithelium) and scaling in chronic cases.
Contact Allergic Dermatitis
• Occurs after a long contact with Allergen.
• Type IV hypersensitivity,occurs in sensitized individuals after a latent period of 8-16 hrs.
• There is severe itching going beyond the area of contact.
• Common allergens include rubber, dyes, and cosmetics.
ClinicalFeatures :
• Erythema, Swelling, Lichenification with constant Itching.
• MC recognized form is Phytodermatitis(Parthenium/congress weed)-mc cause of air borne allergic contact dermatitits
• Other causes Photodermatitis,Nickel(mc allergen),latex,fragnance,cosmetics(berloque dermatitis)
Atopic Dermatitis:
• Type I hypersensitivity reaction
Patient has predisposition to develop asthma, allergic rhinitis along with Atopic dermatitis
• 70% of patients have a positive family history.
• There is eosinophilia and elevated Ig E.
• It usually manifests in 1st year of life and 90% of time within 5 years.
Major Criteria:
1. Itching -Pruritis is Hall mark of Atopic Dermatitis,severe at night. Itch-scratch-itch cycle
2. Typical Morphology and distribution –extensors and cheek in children,flexural in adults
3. Chronic and relapsing
4. Positive family history of Atopy.
Other Clinical Features:
• Dry Skin (xerosis)
• Eczematous lesion
• Lichenification involving cubital,popliteal and neck areas
• Double infra orbital fold k/a ‘Dennie Morgan fold’.
• Hertoghe sign –lateral thinning of eyebrows
• Headlight sign-perioral,perinasal and periorbital pallor
• Allergic shiners-periorbital darkness
• Allergic salute-Horizontal groove on dorsum of nasal bridge
• Keratosis pilaris
• Susceptibility to cutaneous infection of staph Aureus and HSV
• Association with staph aureus superantigen
• White dermatographism is seen with Atopic Dermatitis.
• Wool and synthetic fibers can exaggerate the lesions.
• Diagnosis is mainly clinical with a history of asthma.
Rx :
• Tacrolimus / pimecrolimus which is a T cell modifier
• Antibiotics for secondary infections
• Topical steroids for inflammatory aspect,Systemic steroids in acute flare ups.
• Emollients decrease dryness and are mainstay.
Seborrheic Dermatitis :
• It is chronic erythematous condition with sharply marginated lesions covered by yellowish greasy scales.
• The area of distribution is distinctive, involving scalp, face near the foreheads, eyebrows at upper trunk (sternum and
scapula)
• Etiology –seborrhea(oily skin)colonization by Malassezia (pityrosporum)
• Dandruff is earliest manifestation of seborrheic Dermatitis. Also k/a Pityriasis capitis
• In the infant it could form a cradle cap.
Rx :
• Selenium Sulphide
• Topical steroids
• Oral Ketoconazole / Itraconazole.
Nummular Eczema / Discoid Eczema:
• In these there is single circular Eczema Plague with clearly demarcated edge (coin like lesions):
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 • Mainly present on trunks and extensor surface of limbs.
 

Stasis Eczema:
• Occurs in patients with venous incompetence / chronic Edema
• Primarily involving lower limbs in patients of Varicose veins
• Hyperpigmentation of lesion due to Extravasation of blood and Hemosiderin pigment.
Rx:
• Elevation of leg.
• Compression stockings.
• Steroids should be cautiously used ,as they delay healing.

Asteatotic Eczema
• Also k/a Xerotic Eczema / Winter Itch/Eczema craquele
• Lack of skin surface lipids ,dry scaly skin with crazy paving reticulate pattern with minimal inflammation.
Lower leg is commonly inv and MC in elderly.

Lichen Simplex(Circumscribed Neurodermatitis)

• Circumscribed area of lichenification due to repeated rubbing and scratching occurring on easily reachable sites without
any known predisposing skin disorder
• Treatment-topical steroids,reduce anxiety and psychological stress.

Hand Eczema
• It’s confined to the hands.
• Pompholyx(Dishydrotic eczema) is crops of clear vesicles with itching developing in palms and soles.
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Pityriasis Alba
• Nonspecific superficial dermatitis of unknown origin and can be associated with Atopic dermatitis
• Initially presents with round plaques over the face which on healing produce hypo pigmented scaly patch.

Naevi :
• They are congenital lesions / birth marks.
• Melanocytic Naevi are benign tumors derived from melanocyte. They are further classified into junctional naevi, compound
naevi and dermal naevi.
• Junctional Naevi are proliferative nevus cells at derma-epidermal junc.
• If the Junctional nevus extends into dermis we call it compound naevi.
• If Junctional component resolves leaving a initial Dermal part its k/a Intradermal Nevus.
Rx: Surgical excision.
  Nevus of Ota
• It is a type of oculodermal melanocytosis,a blue grey hyper pigmentation  that occurs on the face.
• Nevus of Ota is caused by the entrapment of melanocytes in the upper third of the dermis. It is found on the face unilaterally
and involves the first two branches of the trigeminal nerve.
• The sclera is involved in two-thirds of cases (causing an increased risk of glaucoma)
• . Women are nearly five times more likely to be affected than men
Nevus of Ito
• Dermal melanocytosis involving the Acromio-clavicular region
Nevus achromicus
• Nevus achromicus/nevus depigmentosus.– strictly unilateral hypopigmented patch.
Nevus anemicus
• Hypopigmented macule occurring due to sustained local vasoconstriction.
Mongolian Spot
Mongolian spots are dermal nevus that produce blue greyish macular pigmentation usually seen on sacral region at birth They resolve
spontaneously on 1st decade of life no Rx required.

Port Wine Stain ( NEVUS FLAMMEUS)

• Capillary vascular malformation consisting of increased numbers of dilated dermal vessels.
• Present at birth
• No spontaneous resolution
• Macular in infancy- grow with patient and become darker in color.
Treatment: Q switched Pulsed Dye Laser(585 nm) treatment is most preferred 

Sturge-Weber syndrome / Encephalotrigeminal syndrome

characterized by :
• unilateral cutaneous angioma (port-wine stain)
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 • Associated with Ipsilateral Leptomeningial vascular abnormalities, epilepsy, hemiplegia and ipsilateral choroidal lesions.
• Focal seizures typically occurs opposite to the side of lesion
• Adrenal pheochromocytoma
• Cerebral angiomas lead to cortical atrophy
• Angiomas are visible radiologically as Tram-track or rail track calcification mainly in occipital region.
 CAPILLARY HEMANGIOMA OF INFANCY ("STRAWBERRY HEMANGIOMA")
• Benign neoplasm
• dome shaped raised, circumscribed bright red nodule (cutaneous hemangioma),
• subcutaneous Hemangioma= cavernous hemangioma.(pink/blue)
• Appear within the first month of life, grows rapidly in first few years of life, begin to regress slowly
• complete involution by age 6-8 yr in majority.
• Emptying sign ie, collapse of swelling with pressure is seen.
• Head and neck are commonest site
• Treatment: Spontaneous regression is the rule

Vascular Anomalies
Port-wine Stain
• vascular malformation
• Present at birth
• Grows along with the child
• Do not regress
Face involvement in areas supplied by
5th cranial nerve
Strawberry Angiomas Salmon Patch
• Type of capillary hemangioma • Also known as Macular stain or
stork bite
• Baby is normal at birth
• Appears at the age of 1-3 weeks • Present at birth
• Grows with the child upto 1 year of age
and then cease to grow • Seen over forehead in the midline
• By the age of 9 years, 90% demonstrate and over the occiput
complete involution
• Disappears by the age 1 year
• Emptying sign is demonstrable

Salmon patch
Keratoacanthoma
• Keratoacanthoma is self healing nodular lesion with central ulceration
• More common in men
• usually found on the face of 50-70 years old.
• typically resolve spontaneously over the subsequent 6 months.
• Classically a cup-shaped growth 1-3 cms
• Central crater is filled with a plug of keratin.
• Unclear etiology
• Associated with HPV,smoking and chemical carcinogen exposure.
• Treatment :
• Removal of central keratin plug may speed resolution
• Excision is recommended for persistent lesions
• Excision scar is often better than that which remains after resolution.

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Pyoderma Gangrenosum
uncommon destructive cutaneous lesion.
Rapidly enlarging, necrotic lesion with surrounding erythema
Commonly associated with IBD, rheumatoid arthritis, hematologic malignancy and monoclonal immunoglobulin A gammopathy.
  Treatment :
First-line therapy : Systemic treatment by corticosteroids and cyclosporine.
If ineffective, corticosteroids and mycophenolate mofetil; mycophenolate mofetil and cyclosporine.

• PYOGENIC GRANULOMA
• misnomer as it is not infective or granulomatous.
• common vascular lesion of skin and mucosa
• Most are small, raised, pedunculated, soft, red nodular lesions showing superficial ulceration and a tendency to
bleed after trivial trauma.
• Fingers, lips, mouth, trunk, toes and other trauma-prone areas are classic sites.
• It is usually seen in children and young adults
• Pregnancy may cause PG on gums,
• Retinoid therapy may induce multiple PGs
• Typically lesions do not spontaneously disappear
• Treatment : Local excision

CHERRY ANGIOMA ("SENILE ANGIOMA")

• Almost universal with aging presenting as small, punctate, discrete bright red to purple soft papules
• Trunk and proximal extremities are common sites.
• Completely benign in nature and no treatment is needed.
 

Seborrheic Keratosis
• Stuck on appearance.
• Benign epidermal tumors occurring in middle age and elderly over face scalp trunk and shoulder with distinctive horn pearls
seen on dermatoscopy.

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 • Present as superficial flesh coloured tan,brown or black small papules with verrucous surface,greasy crust and typical stuck on
appearance.
• Sudden appearance of numerous lesions may be a marker of underlying cancer(Sign of Leser Trelat)
• Treatment-nil or destruction by electrodessication,cryotherapy,curettage,excision.

SKIN TAGS
(Acrochordons or pedunculated fibromas)
• Develop in neck and axillae of obese middle-aged adults
• Present as flesh-colored, pedunculated, soft outgrowths sometimes with a central vessel.
• Treatment is usually surgical snipping,or Electrocautery.

DERMATOFIBROMA
• Common dark brown, red, or skin colored nodules fixed to the skin surface but freely moveable over the subcutaneous tissue.
• Legs most common site
• Lateral compression produces the characteristic dimple sign.
• Classical histology with whorled spindle shaped cells.
• No treatment is usually necessary.
• Malignant form dermatofibrosarcoma protuberans
(DFSP) is histologically charecterised by "storiform" or "cart wheel" arrangement of spindle cells.

Looks like a mole but when you press it forms a dimple- DF

Glomus Tumor
• Its neuromyo arterial receptor (glomus body tumor)
• These tumors are common on fingers and toes and beneath the nail plates.
• These receptors detect temp changes and regulate Arterial blood flow.
• Isolated nodule on nail bed with Paroxysmal pain elicited by changes in temp
Rx : Simple excision is Rx of choice.

Pre Malignant Conditions of Skin 

- Actinic Keratosis (Solar Keratosis)-Most common premalignant skin condition.
Irregular keratotic papules surrounded by erythema,involving back of hands,forearm and face.Treatment –Topical 5-FU

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Squamous Cell Carcinoma
• It is a carcinoma of the cells of epidermis
• Originate from prickle cell layer
• Seen in > 40 years of age.
• MC skin cancer in darkly pigmented races
• 2nd MC skin cancer in light skinned races
• MC causative factor : Sunlight
• MC site : Ears, cheeks, lower lip and back of hands
• Predisposing Factors for SCC
✓ Senile or actinic keratosis
✓ Contact with tars and hydrocarbons
✓ Chronic skin lesions
✓ Erythroplasia of Queyrat (lupus vulgaris, cutaneous TB)
✓ Sunlight or Irradiation
✓ Immunosuppression
✓ Chronic irritation; HIV, HPV – 16
✓ Psoralens, Arsenic exposure
Pathology :
• Microscopically mass of keratin is surrounded by normal looking squamous cells, presenting with characteristic prickle cell
appearance, which are arranged in concentric manner as seen in ‘onion skin’. This whole appearance is called “cell nest or
epithelial pearl”.
• MC type of SCC: Ulcerative type
Clinical Features :
MC symptom : Nodule or ulcer
Edge of ulcer : Raised and everted with indurated base (pathognomonic)
 

Diagnosis :
Diagnosis is made by wedge biopsy (taken from edge of ulcer)
Treatment :
Small (<1cm) or non-invasive SCC : Excision with 1 cm margin
Large, aggressive, located at vital areas or recurrent : Moh’s micrographic surgery
Basal Cell Carcinoma (Rodent Ulcer)
• Locally invasive carcinoma, arises from the basal layer of the epidermis
• MC type of skin cancer
• The commonest human cancer found mostly on sun-exposed areas in fair-skinned individuals.
• 90% of BCC are seen in the face, above a line from the corner of mouth to lobule of ear.
• MC site : Inner canthus of the eye, also known as Tear cancer .

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Types of BCC :
• Nodular : MC type of BCC, characterized by small slow growing pearly nodules, often with telengiectatic vessels on its surface.
Central depression with umbilication is a classic sign.
• Pigmented : Mimic malignant melanoma
• Cystic
• Superficial  
• Characteristic Features of BCC
✓ Low grade malignancy
✓ Exposure to sunlight is an important etiological factor
✓ More common in fair and dry skinned people
✓ Has been seen following prolonged administration of Arsenic
• Nuclear palisading on histology
• Histology: Proliferation of atypical basal cells with "peripheral palisading".
Spread :
• BCC usually spreads by local invasion
• Rodent ulcer : It gradually destroys the tissues, it comes in contact with.
• Lymphatic spread is not seen (Regional lymph nodes are not enlarged)
• Blood spread is extremely rare.  
Diagnosis :
Diagnostic procedure for BCC is wedge biopsy.  
Treatment :
Non-aggressive tumor on trunk or extremities : Excision or Electrodissection and curettage
Large, aggressive, located at vital areas or recurrent : Moh’s micrographic surgery
Malignant Melanoma
• Melanoma is neoplastic disorder produced by Malignant transformation of normal melanocytes
• Site most commonly associated with melanocytic transformation in the skin, where melanocytes reside at the dermo-
epidermal junction (Junctional melanocytes)
• MC site of MM in men : Back and trunk
• MC site of MM in women: Lower extremity
• Most susceptible individuals : Fair complexions, red or blonde hair, blue eyes and freckles and who tan poorly and
sunburn easily.

Risk factors for Malignant Melanoma

• Xeroderma pigmentosum Giant congenital melanocytic nevus
• Actinic damage (UVR) Increased number of ordinary melanocytic naevi
• Family history of melanoma History of sunburn
• Presence of dysplastic naevus
Characteristic Features :
• Classic appearance of melanoma: ABCD (Asymmetry, Border Irregularity, Color variation, Diameter > 6 mm)
• MC route of metastasis : Through Lymphatics
• MC site of systemic metastasis : Liver

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 • Microsatellites : Discrete tumor nests > 0.05 mm in diameter, separated from main body of tumor by normal dermal collagen
or subcutaneous fat.
• Microsatellites are associated with increased risk of regional LN metastasis.
Diagnosis :
• Confirmed by full thickness excisional biopsy’
Incisional biopsy for large lesions and lesions in proximity to important structures (eye, nose, ear)  
Treatment :
Treatment : Surgical excision with sentinel LN biopsy (Margin: 1cm for <1 mm thickness, 2 cm for 1-4 mm thickness, 2-3 cm for >4 mm
thickness)
LN dissection if LN is palpable or positive on sentinel LN biopsy
MM is radioresistant tumor; Chemotherapy : IFN – alpha
Clark’s levels(on the basis of depth of invasion) : EPIRS
I Melanoma restricting to Epidermis and appendages
II Invading Papillary dermis without filling it
III Reach Interface of papillary and reticular dermis
IV Invading reticular dermis
V Invading subcutaneous tissue
• MM is sub-classified into 5 Clark levels, to indicate their depth of invasion and prognosis.
• Breslow’s depth of invasion : Actual measurement of the deepest invasion from the granular layer.
Breslow’s Thickness
Stage I <0.75 mm
Stage II 0.75-1.5 mm
Stage III 1.6-4.0 mm
Stage IV >4.0 mm
Prognostic Factors (Depends most importantly on staging)
• Depth of invasion (most important Lymph node status
prognostic factor)
Satellite lesion
• Ulceration(presence of ulceration Distant metastasis
carries worst prognosis)
MYCOSIS FUNGOIDES (CUTANEOUS T-CELL LYMPHOMA):
• Non-Hodgkin’s type lymphoma presenting with skin infiltration; T cell origin;
• MC in middle aged males and blacks.
• This CTCL involves the skin only
• (rarely in terminal stages invade the lymph nodes and the visceral organs may be involved).
• Mycosis fungoides is a T-helper cell lymphocyte malignancy.
• Associations with HTLV I and II and Epstein-Barr virus
Mycosis fungoides present with pruritic localised erythmatous plaques in the skin
C/F: disease is classically divided into three stages:
• Erythematous stage: Scaly,.red, well defined, intensely itchy patches resembling atopic dermatitis or psoriasis.
• Plaque stage: The patches of 1st stage develop thickening and elevation and lymphadenopathy occurs.
• Tumor stage: This last stage is characterized by nodular and tumorous growths of the plaques.
• Histology shows Pleomorphic atypical lymphocytes in clusters within the epidermis called pautrier’s microabscesses.
• Once the tumor stage is reached Prognosis is poor.

SEZARY'S SYNDROME:
• This rare form of CTCL presents as a triad of
• 1. Exfoliative dermatitis (erythroderma)
• 2. Lymphadenopathy
• 3. Sezary cells: Atypical large monocytoid T lymphocytes with cereberiform nuclei in the blood (> 15% is very suggestive) and
in the skin.
Treatment of Mycosis Fungoides
• Localized disease : topical corticosteroids; topical nitrogen mustard, bexarotene gel; PUVA;
• Advanced disease: PUVA + oral retinoids; electron beam therapy; interferon alpha, IL-12 and denileukin;
• extracorporeal photopheresis (first line for sezary cells in blood); alemtuzumab (anti-CD52 IgG antibody).

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REACTIVE SKIN DIS  
Erythema Multiformis
• Its caused by circulating immune complexes (Type III Hypersensitivity reaction).
• Herpes viruses are strongly associated.
• Other causes include Mycoplasma, Isoniazid, Anti Epileptic drugs,pencillins,sulfonamides and Malignancies.
• Its common in young adults and presents as vesicles, bullae and target lesions,symmetrically involving extensor surface of
limbs.Mucous membranes not involved
• Typical Target Lesions symmetrically over acral areas
• Target lesion / Bull’s eye / Iris Lesion has 3 zones a) A central dark zone surrounded by edematous zone and peripheral
surrounding edema. It has a centrifugal spread.
• No prodromal symptoms
• Nikolsky negative
Rx :Symptomatic.
Acyclovir if Herpes is suspected
Topical steroids ,antibiotics
 
Steven – Johnson Syndrome
They are acute mucocutaneus intolerance reactions,more common in children and young adults.
Caused mainly by drugs,and rarely infections

• In SJs the mucosal erosions are < 10%

• In TEN the mucosal erosions are > 30%
• Drugs associated c SJS are sulfonamides, Phenytoin Penicillin, NSAID’s and phenobarbitone etc.
• Ulcerative stomatitis and hemorrhagic crusting are the most characteristic features.
Fever,myalgia,mucocutaneous lesions.
Rx :
Withdraw the drug
Supportive care
Steroids
IVIG
 
Toxic Epidermal Necrosis(TEN,Lyell syndrome)
It’s a life threatening mucocutaneous reaction charecterised by sheets of Erythema, necrosis and epidermal bullae.
Nickolsky’s sign +ve
• Mucosal and conjunctival erosions are common.
• Drugs causing TEN –Antiepileptics,sulfonamides,thiaacetazone,isoniazid,ampicillin and NSAIDS
• Septicemia is mcc of death in TEN.
• There is sub-epidermal break in TEN.
• In staphylococcal scalded skin syndrome, there is sub corneal break.
• The skin lesions in TEN are erythematous, necrotic with wetness.
• In SSSS skin lesions are dry and parchment like with absence of mucosal lesion.
Rx :Intensive care management c fluid maintenance and electrolyte balance.
i.v.Immunoglobulius (DOC) but steroids are CI
  Erythroderma

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 • It’s also k/a Exfoliative dermatitis.
• Its inflammatory skin disorder affecting > 90% of body surface area. There is generalized edema with scaling and scarring
• causes are Eczema, Psoriasis ,lichen planus,pityriasis rrubra pilaris,pemphigus foliaceous,dermatomyositis
• drugs like phenytoin,carbamazepine, gold, mercury, lithium,arsenic, chloroquine,thiazides,Rifampicin and Isoniazid.
• It can be seen with cancers like Leukemias and Lymphomas,Sezary Syndrome(can be a marker of malignancy)
• Chronic prolonged erythroderma of unknown origin in eldery is called Red Man Syndrome
Rx :
• ICU management
• Electrolyte and fluid balance
• Methotrexate is started in erythrodermic Psoriasis.
  Henoch-Scholein Purpura
-occurs in children and young adults after upper respiratory infection
-purpuric skin eruptions on extensor surface of lower limbs and buttocks,arthritis,abdominal pain and glomerulonephritis
with haematuria
-Raised Serum Ig A and Ig A immune deposits found on affected vessel walls.
-Platelet count is normal ,No Thrombocytopaenia.

 
Fixed Drug Eruptions  
• They occur at fixed sites. They are single or multiple with burning sensation.
• Present as well demarcated reddish brown macule recurring periodically and resolves slowly with some persisting
hyperpigmentation.
• Most common site is genitalia.
• Usually unilateral and heal by greyish pigmentation
• Mucocutaneous junctions are often involved.
• FDE can be seen by sulfonamides, Dapsone, captopril, Tetracycline and Phenopthelin, many over the counter drugs like
laxatives and ibuprofen.
• The drug started within one week of onset of eruption is most important suspect.
• In Vivo testing for drug allergies include patch testing and challenge re challenge test.
• In vitro testing is done by radio allergo sorbent assay (RAST), ELISSA etc.
 

Chancroid (soft Chancre)

• Its caused by Haemophilus Ducreyi, they are multiple painful ulcers with deep ulceration 3-4 weeks after exposure.
• The ulcer is soft, non-indurated.
• Produces painful, inguinal lymphadenitis k/a Inflammatory Bubo.
Diagnosis:
• H. ducreyi forms pool school of fish of gram –ve cocobacilli in the smear taken from ulcer or from the pus from the bubo.
• Rx: Ceftriaxone i.m or Azithromycin 1 gm single oral dose.or alternative is Doxycycline if chlamydia is suspected.
 

Granuloma Inguinale (Donovanosis) :

• Its caused by calymmatobacterium granulomatosis a gram –ve obligate intracellular bacillus.
• It prod multiple, painless, beefy red ulcerations with distinct raised rolled up margins after an incubation period of 8-12 days
weeks.
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 • There is enlargement in inguinal region due to subcutaneous granulomas that arise superficially k/a PseudoBubo’s
• The Beefy red ulcer bleeds on touch.
• Diagnosis: There is presence of intracytoplasmic inclusion bodies k/a Donovan/safetypin bodies inhistiocytes
  Rx : Doxycycline / cotrimoxazole.

Herpes Genitalis
• HSV is mcc of genital ulcerations
• Incubation period is 3-4 days. There is prod of small grouped vesicles that progress and break to ulcerative lesion.
• Painful inguinal lymphadenopathy can occur
• Rx : Acyclovir

Miscellaneous topics
Epidermoid Cyst (Sebaceous or Epidermal Cyst)

• Epidermoid cyst results from proliferation of epidermal cells within a circumscribed space of dermis (which had got implanted
within the dermis)
• Sebaceous cyst is a misnomer as the cysts are not of sebaceous origin and the white creamy material filled within is not sebum,
but is keratin (desquamated epithelial cells
• Cyst wall consist of a layer of epidermis oriented with the basal layer superficial and more matured layers are deep.
• Desquamated cells (keratin) collect in the centre and form creamy substance of the cyst.
Clinical Features :
• Usually asymptomatic,
• Firm, round, flesh colored or yellow white subcutaneous nodules of variable size.
• Central punctum from which the white creamy material can be expressed.
• Rarely malignancies (BCC, SCC) can develop in epidermoid cyst.
• No punctum in scrotal and scalp sebaceous cyst.
Treatment :
• Excision with the wall is treatment of choice
• Infected cyst : Incision and drainage (After resolution of the abscess, cyst wall must be excised to prevent recurrence)
Lipoma
• MC subcutaneous neoplasm : Lipomas
• Also known as universal tumor
• MC site: Trunk (may appear anywhere)
• Can be encapsulated or diffuse  

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Pathology :
• Lobulated tumor composed of normal fat cells  
Clinical Features :
• Typical soft and fleshy on palpation
• May grow to a large size  
• Bracket calcification is seen in lipoma of corpus callosum
Treatment :
• Surgical excision is required for tumor removal.    
Sweet’s Syndrome
(Acute Febrile Neutrophilic Dermatosis)
Etiology
• Idiopathic (MC in women following resp. tract infection,streptococcal infection).
• Malignancy ( MC AMLQ; Solid tumors (of genitourinary tract);
• Drugs (all-trans-retinoic acid, granulocyte stimulating factors);
• SS is often associated with hematologic disease (including leukemia), and immunologic disease rheumatoid
arthritis, inflammatory bowel disease, behcet syndrome. An underlying condition streptococcal infection, inflammatory bowel
disease, nonlymphocytic leukemia and other hematologic malignancies, solid tumors, pregnancy

Clinically
• Affects F>M ,
Four features
• Red to red-brown plaques and nodules, painful and occur on the head, neck, and upper extremities.
• Fever,
• neutrophilia,(leucocytosis)
• and a dense papillary dermal infiltrate of neutrophils in the lesions.
Extracutaneous sites of involvement = Joints, muscles, eye, kidney (proteinuria, occasionally glomerulonephritis), and lung (neutrophilic
infiltrates)
 Systemic corticosteroids such as (prednisone) can produce rapid improvement and are the “gold standard” for treatment
Important hyperpigmentation disorders
Melasma(chloasma) is hyperpigmentation involving cheeks occurring due to pregnancy,ocp,phenytoin and sun exposure.
 

 
Freckles(Ephelides)
• These are small areas of brown hyperpigmentation usually less than 3 mm occurring due to functionally overactive
melanocytes,though the number of melanocytes are normal.
• Seen in fair skinned people only,stimulated by UV radiation
• Histology shows excess melanin in basal layer.  

Lentigo/Lentigines
• Sharply demarcated circular brown hyperpigmented macule appearing as a result of increased number of melanocytes in the
basal layer.Histology shows linear increase of melanocytes in basal layer.They are not affected by sun exposure/UV radiation

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DERMATOMYOSITIS (DRM)
Presentation
• Bilateral progressive symmetrical proximal muscle weakness.
• DRM is usually associated polymyositis as a symptom complex
• Unknown etiology,autoimmune,Associated with internal malignancy.
• Heliotrope rash : Purple red discolouration of upper eyelids,MC manifestation.

• Gottrons papules : violaceous flat-topped papules over bony prominences of hands, particularly the MCP joints and PIP
joints.

• Poikiloderma may occur on exposed skin such as the extensor surfaces of the arm, the “V” of the neck or the upper
back (Shawl sign).

• “mechanic’s hands” -hyperkeratosis along the radial and palmar aspects of the fingers

XERODERMA PIGMENTOSUM (XP)

Etiology
• AR; defective DNA repair,DNA excision repair damaged by ultraviolet radiation ; there is abnormal response of polymerase to
UV light exposure.
Presentation
• XP is characterised by photosensitivity, pigmentary changes, multiple freckles,premature skin aging and development of
malignant tumors in sun-exposed areas of the body due to defective DNA repair.
• The skin is normal at birth;dryness and freckling appear between 6 months-3 years,skin becomes dry parchment like
progressing to poikilodermatous stage with atrophy,telangiectasia superadded to freckles and hyperpigmentation.

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 • Ocular problems (seen in 80%): consist of dry eye, photophobia, conjunctivitis, ectropion, symblepharon, corneal
ulceration; .
• Actinic keratosis,Keratoacanthomas occur
• 1000 fold increased risk of developing squamous cell carcinoma,basal cell carcinoma or melanoma at a median age of 8 years.
• Increased risk of internal malignancies
• 20% have neurological complications –ataxia,spasticity,mental retardation
• 2/3 of cases die by 20 years
De Sanctis-Cacchione Syndrome-XP with microcephaly,mental deficiency,ataxia,choreoathetosis ,dwarfism and
hypogonadism.  
Treatment
• Maximum photoprotection ,Sunscreens; Oral retinoids,topical 5FU

Skin Changes in Diabetes Mellitus :

 
NECROBIOSIS LIPOIDICA DIABETORIUM (NLD)
• More common in young female patients
• It usually presents as symmetrical, well defined, irregular, brown-red plaques on both shins and feet.
• The epidermis is atrophic and delicate vessels occur over the surface. Chronic stage may present as ulcers.
• Treatment is very unsatisfactory. Intralesional steroids are sometimes useful
• Does not correlate with normalization of hyperglycemia

GRANULOMA ANNULARE :
• Well defined, annular lesions with the margin made up of multiple discrete flat topped yellowish to skin-colored papules
usually in childhood and juvenile diabetics. [GA is not seen in internal malignancies]
• These lesions are commonly found over the dorsal hands, feet, ankle and limbs
• It responds well to intralesional steroids but recurs.
• Histologically characterized by Necrobiosis (Granulomatous inflammation around collagen bundles).
• Other Necrobiotic dermatoses Include NLD and Rheumatoid nodules

Acanthosis Nigricans
• Benign or Insulin resistance variety (HAIR-AN syndrome: associated with Hyper Androgenism, Insulin Resistance and AN.):
Acromegaly, Cushing's Disease, PCOD
• Pseudoacanthosis nigricans: associated with obesity
• Drug induced AN: Nicotinic Acid, FusidicAcid, OCP etc
• Malignant AN: usually associated with adenocarcinomas (MC stomach) and other GIT tumors.
• Tripe Palms is a variety more strongly associated with malignancy
 

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NEUROFIBROMATOSIS (NF)

Characterized by neurofibromas and are of two types:

a. Neurofibromatosis-l (NF-l): Von Recklinghausen disease
b. Neurofibomatosis-2 (NF-2): Bilateral acoustic neurofibromatosis
ETIO-PATHOGENESIS:
Mutations in suppressor genes leading to multiple tumors. The implicated genes are at chromosome 17q in NF1 & chromosome 22q in
NF2
 
CLINICAL FEATURES:
NF-1: NF2:
Multiple anomalies are seen and 2 of the Patients classically presents bilateral acoustic neuromas and uncommonly with skin
following 7 criteria need to be fulfilled for findings of NF-1. Criteria for diagnosis require at least one of the following: Bilateral
diagnosing NF-1. Acoustic Neuromas or
1. Family history; First degree relative with' First degree relative with NF-2 and either
NF-1. ' 1. Unilateral VIII,h nerve mass or
2. Axillary freckling [Crowe's sign] 2. Two or more of the following:
3. Neurofibromas: 2 or more 1. Neurofibromas
neurofibromas or one or more 2. Meningioma
plexifcrm neurofibromas. 3. Glioma
4. Cafe au la it macules (CALMs): 6 or 4. Schwannomas
more over 1.5 cm in adults-and > 0.5
cm in prepubertal children. [CALMs
are earliest but NOT pathognomonic
sign of NF-1 and appear within first
year and have a smooth margin called
"Coast of California"]
5. Optic glioma
6. Osseous lesions: cortical thinning of
long bones, sphenoid dysplasia.
1. Lisch nodules: pigmented iris
hamartomas
 
TUBEROUS SCLEROSIS OR TS COMPLEX (TSC) of children and other autistic or learning disabilities may be present.
Classically described by Vogt's triad of EPILOIA i.e. EPilepsy, 13. Gliomas and gingival fibromas: Subependymal giant cell
LOw Intelligence (mental retardation) and Adenoma Sebaceum. astrocytomas (SEGAs) and other glial nodules may appear
  as can fibromas on the gum.
AD inheritance with linkage to chromosome 9(hamartin gene) 14. Hamartomas: presenting as multiple retinal nodular
and 16(tuberin gene). hamartomas and rectal polyps
The clinical picture includes following 15. Tubers: Classical CNS. lesions which are small areas in the
changes: cortex (the outer layer of the brain) that do not develop
1) Hypomelanotic macules: (Ash-leaf macules (most normally.
distinctive) which become more visible under woods 16. Shagreen patches: These are connective tissue (collagenous)
lamp light, Thumb-print macules and Confetti (Small nevi. typically seen in lumbosacral area.
lentil like) macules) 17. Most cases are sporadic ,about 1/3 are AD.
2) Cardiac rhabdomyomas: the most common primary  
cardiac tumor of TSC  
3) Teeth: enamel pits  
VON-Hippel Lindau Disease(VHL)
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4) Renal angiomyolipomas (AML): Renal AD,VHL gene on Chromosome 3p,
angiomyolipomas—made up of vascular tissue (angio), Retinal Haemangiomas
smooth muscle (myo),.and fat (lipoma)—are benign Cerebellar Haemangiomas
hamartomas occurring in Bilateral RCC
70 - 80 percent of adults and older children. Cystic lesions in kidney,liver,pancreas
5) Angiofibromas (Adenoma Sebaceum): they are Cutaneous findings-Portwine stain
neither adenomas nor sebaceous but are angiofibromas Café Au lait macules
occurring on face and sebaceous areas.
6) Convulsions: Epilepsy occurs in 60 -90 percent of
individuals diagnosed with TSC.
7) Koenen's tumor: are periungual and subungual
fibromas.
8) forehead plaques: fibromatous plaques on forehead.
9) Lymphangioleiomyomatosis (LAM): of lungs
commonly in women.
10) Intelligence is low (mental retardation): Seen in
majority

   

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