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Skin Treatments

Skin is the largest organ of the body, accounting for about 15% of the total adult body weight. It is not uniformly thick, the average thickness of the skin is about 1 to 2 mm. The skin is continuous, with the mucous membranes lining the body’s surface. The integumentary system is formed by the skin and its derivative structures.

Skin is made up of 3 layers:
I. Outer epidermis
II. Inner dermis.
III. Subcutaneous tissue

EPIDERMIS

Epidermis is the outer layer of skin. It is formed by stratified, squamous epithelium layer that is composed primarily of two types of cells:
⦁ Keratinocytes
⦁ Dendritic cells.

KERATINOCYTE -

At least 80% of cells in the epidermis are the ectodermally derived keratinocytes. The differentiation process that occurs as the cells migrate from the basal layer to the surface of the skin results in keratinization . It consists of a specific constellation of cells known as keratinocytes, which function to synthesize keratin, a long, threadlike protein with a protective role. The keratinocytes differ from the “clear” dendritic cells by possessing intercellular bridges and ample amounts of stainable cytoplasm. Bundles of these keratin filaments converge on and terminate at the plasma membrane forming the intercellular attachment plates known as desmosomes. The epidermis harbors a number of other cell populations, such as Melanocytes - The melanocyte is a dendritic, pigment-synthesizing cell derived from the neural crest and confined in the skin pre- dominantly to the basal layer . Melanocytes are responsible for the production of the pigment melanin and its transfer to keratinocytes.


Melanocytes -

The melanocyte is a dendritic, pigment-synthesizing cell derived from the neural crest and confined in the skin pre- dominantly to the basal layer . Melanocytes are responsible for the production of the pigment melanin and its transfer to keratinocytes.


Langerhans cells –

Langerhans cells are involved in a variety of T-cell responses. Derived from the bone marrow, these cells migrate to a suprabasal position in the epidermis early in embryonic development and continue to circulate and repopulate the epidermis throughout life. Langerhans cells constitute 2%–8% of the total epidermal cell population and maintain nearly constant numbers and distributions in a particular area of the body. hey are found in other squamous epithelia in addition to the epidermis, including the oral cavity, oesophagus, and vagina, as well as in lymphoid organs and in the normal dermis

Merkel cells –

They are oval-shaped, slow-adapting, type I mechanoreceptors located in sites of high tactile sensitivity that are attached to basal keratinocytes by desmosomal junctions. Merkel cells are found in the digits, lips, regions of the oral cavity, and outer root sheath of the hair follicle and are sometimes assembled into specialized structures known as tactile discs or touch domes. They secrete a chemical signal that generates an action potential in the adjoining afferent neuron, which relays the signal to the brain. The high concentration of Merkel cells in certain regions such as the fingertips results in smaller and more densely packed receptive fields and thus higher tactile resolution and sensitivity.

Three Basic Cell Types in the Epidermis

The three basic cell types in the epidermis include keratinocytes (some labelled K ) and Langerhans cells (L) in the Malpighian layer and melanocytes (M ) in the basal layer. Arrows point to the basement membrane zone, which separates the basal layer of the epidermis from the underlying dermis (D).

Layers of Epidermis (according to keratinocyte morphology and position)

1. Stratum corneum (the cornified or horny cell layer)
2. Stratum lucidum
3. Stratum granulosum (the granular cell layer)
4. Stratum spinosum (the squamous cell layer)
5. Stratum germinativum (basal cell layer)

The lower three layers that constitute the living, nucleated cells of the epidermis are sometimes referred to as the stratum malpighii and rete malpighii. The epidermis is a continually renewing layer and gives rise to derivative structures, such as pilosebaceous apparatuses, nails, and sweat glands. The basal cells of the epidermis undergo proliferation cycles that provide for the renewal of the outer epidermis. The epidermis is a dynamic tissue in which cells are constantly in unsynchronized motion, as differing individual cell populations pass not only one another but also melanocytes and Langerhans cells as they move toward the surface of the skin. Important feature of epidermis is that, it does not have blood vessels. Nutrition is provided to the epidermis by the capillaries of dermis.

⦁ STRATUM CORNEUM -

It is the outermost layer and consists of dead cells, which are called corneocytes. These cells lose their nucleus due to pressure and become dead cells. The cytoplasm is flattened with fibrous protein known as keratin. These cells also contain phospholipids and glycogen. The corneocytes, which are rich in protein and low in lipid content, are surrounded by a continuous extracellular lipid matrix.

⦁ STRATUM LUCIDUM –

It is made up of flattened epithelial cells. Many cells have degenerated nucleus and in some cells, the nucleus is absent. As these cells exhibit shiny character, the layer looks like a homogeneous translucent zone. So, this layer is called stratum lucidum (lucid = clear).

⦁ STRATUM GRANULOSUM –

It is the most superficial layer and thin layer of epidermis containing two to five rows of flattened rhomboid cells (living cells). Cytoplasm contains granules of a protein called keratohyalin. Keratohyalin is the precursor of keratin. under thin cornified layer areas, the granular layer may be only 1–3 cell layers in thickness, whereas under the palms of the hands and soles of the feet the granular layer may be 10 times this thickness. A very thin or absent granular layer can lead to extensive parakeratosis in which the nuclei of keratinocytes persist as the cells move into the stratum corneum, resulting in psoriasis. they are necessary in the formation of both the inter fibrillary matrix that holds keratin filaments together and the inner lining of the horny cells.

⦁ STRATUM SPINOSUM –

It is also known as prickle cell layer because, the cells of this layer possess some spinelike protoplasmic projections. By these projections, the cells are connected to one another. It is 5 – 10 cells thick and known as squamous cell layer. The squamous layer is composed of a variety of cells that differ in shape, structure, and subcellular properties depending on their location. Intercellular spaces between spinous cells are bridged by abundant desmosomes that promote mechanical coupling be- tween cells of the epidermis and provide resistance to physical stresses.

⦁ STRATUM GERMINATIVUM -

It is a thick layer made up of polygonal cells, superficially and columnar or cuboidal shaped keratinocytes that attach to the basement membrane zone with their long axis perpendicular to the dermis. Here, new cells are constantly formed by mitotic division. The stem cells, which give rise to new cells, are known as keratinocytes. Another type of cells called melanocytes are scattered between the keratinocytes. Melanocytes produce the pigment called melanin. The color of the skin depends upon melanin. From this layer, some projections called rete ridges extend down up to dermis. These projections provide anchoring and nutritional function.

Epidermal Appendages

They are ectodermally derived appendages.

1. Eccrine and apocrine glands
2. Ducts
3. Pilosebaceous

Features Eccrine glands Apocrine glands
1. Distribution Throughout the body Only in limited areas like axilla, pubis, areola and umbilicus
2. Opening Exterior through sweat pore Into the hair follicle
3. Period of functioning Function throughout life Start functioning only at puberty
4. Secretion Clear and watery Thick and milky
5. Regulation of body temperature Play important role in temperature regulation Do not play any role in temperature regulation
6. Conditions when secretion increases During increased temperature and emotional conditions Only during emotional conditions
7. Control of secretory activity Under nervous control Under hormonal control
8. Nerve supply Sympathetic cholinergic fibers Sympathetic adrenergic fibers

APOECCRINE SWEAT GLANDS –

They develops during puberty from eccrine-like precursors, opening directly unto the skin. The AEG has a secretory rate as much as 10 times that of the eccrine gland and is therefore thought to contribute to axillary hyperhidrosis

HAIR FOLLICLES -

Hair has many valuable biologic functions including protection from the elements and distribution of sweat-gland products. In addition, it has an important psychosocial role in society. The number and distribution of hair follicles over the body and the future phenotype of each hair is established during fetal development; no extra follicles are added after birth. The sebaceous gland forms from a bud in the fetal hair follicle. The arrector pili (AP) are a smooth muscle bundle that attaches to the external root sheath of the follicle. Hair color is determined by the distribution of melanosomes in the hair shaft. The hair bulb contains melanocytes that synthesize melanosomes and transfer them to the keratinocytes of the bulb matrix.

Phases Of Hair Growth

SEBACEOUS GLANDS -

Sebaceous glands are simple or branched alveolar glands, situated in the dermis of skin.

Structure

Sebaceous glands are ovoid or spherical in shape and are situated at the side of the hair follicle. These glands develop from hair follicles. So, the sebaceous glands are absent over the thick skin, which is devoid of hair follicles. Each gland is covered by a connective tissue capsule. Sebaceous glands open into the neck of the hair follicle through a duct. In some areas like face, lips, nipple, glans penis and labia minora, the sebaceous glands open directly into the exterior.

Secretion of Sebaceous Gland – Sebum

Sebaceous glands secrete an oily substance called sebum. Sebum is formed by the liquefaction of the alveolar cells and poured out through the ducts either via the hair follicle or directly into the exterior.

Composition of Sebum

Sebum contains: 1. Free fatty acids
2. Triglycerides
3. Squalene
4. Sterols
5. Waxes
6. Paraffin.

Functions of Sebum

⦁ Free fatty acid content of the sebum has antibacterial and antifungal actions.Thus, it prevents the infection of skin by bacteria or fungi

⦁ Lipid nature of sebum keeps the skin smooth and oily. It protects the skin from unnecessary desquamation and injury caused by dryness

⦁ Lipids of the sebum prevent heat loss from the body. It is particularly useful in cold climate.

Fingernails provide protection to the fingertips, enhance sensation, and allow small objects to be grasped. The underlying nail bed is part of the nail matrix containing blood vessels, nerves, and melanocytes and has parallel rete ridges. The nail plate is formed from matrix keratinocytes. Fingernails grow at an average rate of 0.1 mm per day, two to three times faster than the rate of toenail growth. For example, arsenic poisoning may cause a horizontal hypopigmentation across all nail plates known as Mees lines.

Nail psoriasis

Nail psoriasis can cause nail denting or crumbling.

Causes

People living with psoriasis may develop symptoms. It occurs when psoriasis affects the skin of the nail bed or near the nail beds.

Symptoms

⦁ crumbling nails pitting
⦁ changes in color to yellow or brown
⦁ a build-up of skin under the nails
⦁ blood under the nails
⦁ the nail separates from the bed

Brittle splitting nails

Brittle splitting nails, or onychoschizia, is a common issue that dermatologists see. The condition can cause brittle, soft, splitting, or thin nails.



Causes

Common causes of brittle nails are repeatedly wetting and drying the nails. Though less common, other causes may include iron deficiency or underlying illness.

Symptoms

The most common symptom is that the nails break easily. The American Osteopathic College of Dermatology state people can often tell if the cause is internal, as the condition affects both fingernails and toenails. If there is an external cause, symptoms will typically only affect the fingernails.

Onychogryphosis

Onychogryphosis is a condition where the nail becomes overgrown and thick, often affecting the big toe. It can cause one portion of the nail to grow longer than the other part.

Causes

Potential causes of onychogryphosis include: ⦁ genetics ⦁ injury ⦁ circulation issues ⦁ psoriasis ichthyosis

Symptoms

When a person has onychogryphosis, the nail grows very thick. In other cases, a portion of the nail may grow larger than the other part. The growth can resemble a ram’s horn, so people often refer to it as Ram’s horn nails

Ingrown toenails 

An ingrown toenail can cause pain and swelling, and in some cases, they can become infected.

Causes

According to the American Academy of Orthopaedic Surgeons, genetics may play a role in the development of ingrown toenails. Also, there are other potential causes, including: ⦁ not keeping nails trimmed ⦁ wearing tight socks or shoes ⦁ physical injury

Symptoms

Symptoms can include: ⦁ swelling and tenderness ⦁ redness ⦁ soreness pus

Nail fungal infections

Nail fungal infections are a common condition that causes the nails to become thick, discolored, and easier to break. Nail fungus is more common in the toes than fingers.

Causes

Several different types of molds and fungus can affect nails. They grow when a crack or break traps fungi between the nail and the nail bed. Sweat, athlete’s foot, and salon manicures and pedicures can put people at higher risk of nail fungal infections.

Symptoms

Symptoms include: ⦁ thick nails ⦁ discolored nails that are brown, yellow or white ⦁ fragile or cracked nails Fungus under the nails often is not painful

Onycholysis 

Onycholysis is when the toe or fingernail painlessly separates from the nail bed. It typically occurs slowly over time and could result from an underlying health condition or injury.

Causes

The most common cause is from local injury to the nail. Other triggers include: ⦁ excessive filing ⦁ exposure to chemicals ⦁ allergic ⦁ contact dermatitis ⦁ submersion in water Psoriasis, fungal infections, and reactions to certain medications are also common causes.

Symptoms

The main symptom of onycholysis is the separation of the nail from the nail bed. This can result in discoloration of the nail, turning it green, yellow, or opaque. It can also cause additional skin tissue under the nail, nail pitting, nail thickening, or bending of the nail edges.

Paronychia 

Paronychia is an infection that causes redness and swelling around the edges of a nail bed.

Causes

There are two types of paronychia: acute and chronic. Acute paronychia occurs when there is an infection due to direct or indirect trauma to the cuticle or nail fold. Chronic paronychia is often the result of allergens or irritants.

Symptoms

Acute paronychia symptoms can include:
⦁ swelling
⦁ pain
⦁ redness 
⦁ fever and gland pain in severe cases
⦁ yellow pus
Chronic paronychia often starts on one nail and spreads to others. The nail folds may have the following symptoms:
⦁ redness 
⦁ pain
⦁ swelling
⦁ yellow or green pus
⦁ lifting of the nail from the bed
⦁ tenderness
Dermis is the inner layer of the skin. It is an integrated system of fibrous, filamentous, and amorphous connective tissue that accommodates stimulus induced entry by nerve and vascular networks, epidermally derived appendages, fibroblasts, macrophages, and mast cells. It is a connective tissue layer, made up of dense and stout collagen fiber fibroblasts and histiocytes. Collagen fibers exhibit elastic property and are capable of storing or holding water. Collagen fibers contain the enzyme collagenase, which is responsible for wound healing. The dermis lies on the subcutaneous tissue, or panniculus, which contains small lobes of fat cells known as lipocytes. The thickness of these layers varies considerably, depending on the geographic location on the anatomy of the body. The eyelid, for example, has the thinnest layer of the epidermis, measuring less than 0.1 mm, whereas the palms and soles of the feet have the thickest epidermal layer, measuring approximately 1.5 mm. The dermis is thickest on the back, where it is 30–40 times as thick as the overlying epidermis. The dermis comprises the bulk of the skin and provides its pliability, elasticity, and tensile strength. It protects the body from mechanical injury, binds water, aids in thermal regulation, and includes receptors of sensory stimuli.

LAYERS OF DERMIS

Dermis is made up of two layers: 1. Superficial papillary layer 2. Deeper reticular layer.

SUPERFICIAL PAPILLARY LAYER -

It projects into the epidermis. It contains blood vessels, lymphatics and nerve fibers. This layer also has some pigment containing cells known as chromatophores. Dermal papillae are finger like projections, arising from the superficial papillary dermis. Each papilla contains a plexus of capillaries and lymphatics, which are oriented perpendicular to the skin surface.

RETICULAR LAYER -

It is made up of reticular and elastic fibers. These fibers are found around the hair bulbs, sweat glands and sebaceous glands. The reticular layer also contains mast cells, nerve endings, lymphatics, epidermal appendages and fibroblasts. Immediately below the dermis, subcutaneous tissue is present. It is a loose connective tissue, which connects the skin with the internal structures of the body. It serves as an insulator to protect the body from excessive heat and cold of the environment.



1. PROTECTIVE FUNCTION

2. SENSORY FUNCTION

3. STORAGE FUNCTION

4. SYNTHETIC FUNCTION

5. REGULATION OF BODY TEMPERATURE

6. REGULATION OF WATER AND ELECTROLYTE BALANCE

7. EXCRETORY FUNCTION

8. ABSORPTIVE FUNCTION

9. SECRETORY FUNCTION

PROTECTIVE FUNCTION -

Skin forms the covering of all the organs of the body and protects these organs from the following factors: i. Bacteria and toxic substances ii. Mechanical blow iii. Ultraviolet rays.

SENSORY FUNCTION -

Skin is considered as the largest sense organ in the body. It has many nerve endings, which form the specialized cutaneous receptors These receptors are stimulated by sensations of touch, pain, pressure or temperature sensation and convey these sensations to the brain via afferent nerves. At the brain level, perception of different sensations occurs.

STORAGE FUNCTION -

Skin stores fat, water, chloride and sugar. It can also store blood by the dilatation of the cutaneous blood vessels.

SYNTHETIC FUNCTION -

Vitamin D3 is synthesized in skin by the action of ultraviolet rays from sunlight on cholesterol

REGULATION OF BODY TEMPERATURE -

Skin plays an important role in the regulation of body temperature. Excess heat is lost from the body through skin by radiation, conduction, convection and evaporation. Sweat glands of the skin play an active part in heat loss, by secreting sweat. The lipid content sebum prevents loss of heat from the body in cold environment.

REGULATION OF WATER AND ELECTROLYTE BALANCE -

Skin regulates water balance and electrolyte balance by excreting water and salts through sweat.

EXCRETORY FUNCTION -

Skin excretes small quantities of waste materials like urea, salts and fatty substance.

ABSORPTIVE FUNCTION -

Skin absorbs fat-soluble substances and some ointments.

SECRETORY FUNCTION -

Skin secretes sweat through sweat glands and sebum through sebaceous glands. By secreting sweat, skin regulates body temperature and water balance. Sebum keeps the skin smooth and moist.

SKIN AS A WHOLISM


PSYCHONEUROIMMUNO DERMATOLOGY


SKIN TYPES AS A PERSONALITY REFLECTION

TYPES OF LESION

Basic skin lesions are broadly categorized as :

1. PRIMARY – Basic reaction patterns of skin with a definite morphology.

2. SECONDARY – Develop during the evolutionary process of skin disease or are created by scratching or infection.

3. SPECIAL – Specific for certain disease.

DESCRIPTION OF PRIMARY SKIN LESIONS

1. Macule:

A flat, colored lesion, < 2cm in diameter, not raised above the surface of the surrounding skin. A “freckle” or ephelid is a prototypical pigmented macule.

2. Patch: A large (>2-cm) flat lesion with a color different from the surrounding skin. This differs from a macule only in size.

3. Papule:

A small, solid lesion, < 0.5cm in diameter, raised above the surface of the surrounding skin and thus palpable (e.g., a closed comedone, or whitehead in acne)

4. Plaque:

A large (>1-cm), flat-topped, raised lesion; edges may either be distinct (e.g., in psoriasis) or gradually blend with surrounding skin (e.g., in eczematous dermatitis).

5. Nodule:

A larger (0.5- to 5.0-cm), firm lesion raised above the surface of the surrounding skin. This differs from a papule only in size (e.g., a large dermal nevomelanocytic nevus).

6. Tumor:

A solid, raised growth >5 cm in diameter.

7. Vesicle:

A small, fluid-filled lesion, 0.5 cm in diameter, raised above the plane of surrounding skin. Fluid is often visible, and the lesions are translucent (e.g., vesicles in allergic contact dermatitis caused by Toxicodendron [poison ivy].

8. Bulla:

A fluid-filled, raised, often translucent lesion >0.5 cm in diameter.

9. Pustule:

A vesicle filled with leukocytes. Note: The presence of pustules does not necessarily signify the existence of an infection.

10. Abscess:

It is a localized collection of pus deep in dermis or subcutaneous tissue. Due to deep seated location pus may not be visible on skin surface but would show sign of inflammation.

11. Cyst:

It is a spherical or oval sac or an encapsulated cavity containing fluid or semi solid material. It is lined with true epithelium.

12. Wheal:

It is a transient swelling of skin disappearing within 24hr. A raised, erythematous, edematous papule or plaque, usually representing short-lived vasodilation and vasopermeability.

13. Telangiectasia:

A dilated, superficial blood vessel.

DESCRIPTION OF SECONDARY SKIN LESIONS

1. Lichenification:

A distinctive thickening of the skin that is characterized by accentuated skin-fold markings.

2. Scale:

Excessive accumulation of stratum corneum. They are dead epidermal cells that are produced by abnormal keratinization and shedding.

3. Crust:

Dried exudate of body fluids that may be either yellow

4. Erosion:

Loss of epidermis without an associated loss of dermis. Therefore they heal without scarring.

5. Ulcer:

Loss of epidermis and at least a portion of the underlying dermis. Scarring depends o the depth of ulc

6. Fissure:

It is a linear loss of continuity of skin due to excessive tension.

7. Excoriation:

Linear, angular erosions that may be covered by crust and are caused by scratching.

8. Atrophy:

An acquired loss of substance. In the skin, this may appear as a depression with intact epidermis (i.e., loss of dermal or subcutaneous tissue) or as sites of shiny, delicate, wrinkled lesions (i.e., epidermal atrophy).

9. Keloid –

An area of overgrowth of fibrous tissue that usually. Develops after healing of skin injury and extends beyond the original defect.

10. Scar:

A change in the skin secondary to trauma or inflammation. Sites may be erythematous, hypopigmented, or hyperpigmented depending on their age or character. Sites on hair-bearing areas may be characterized by destruction of hair follicles


SPECIAL LESIONS


1. Burrow:

It is a serpentine tunnel made by scabies mite in stratum corneum. The open end of the tunnel has a papule.

2. Comedones:

It is a tiny plug present at opening of hair follicle formed by keratin and sebum. It is of two types: Open comedone (black head) and Closed comedone (white head).

3. Milia:

It is a tiny superficial cyst with epidermal lining. Milia are seen on face at periorbital. They are small, firm, white papules filled with keratin.

4. Telengiectasia:

It is visible dilatation of capillaries of skin which blanch on pressure.

5. Poikiloderma:

It is a combination of reticulate telangiectasia, pigmentary change and atrophy.

6. Purpura:

Extravasation of red blood cells from cutaneous vessels in skin and mucous membrane.

7. Infarct:

Area of cutaneous necrosis – tender, irregularly shaped dusky red grey macule or firm plague.

Clinical Features Other Notable Features Histologic Features
Psoriasis Sharply demarcated, erythematous plaques with mica-like scale; predominantly on elbows, knees, and scalp; atypical forms may localize to intertriginous areas; eruptive forms may be associated with infection May be aggravated by certain drugs, infection; severe forms seen in association with HIV Acanthosis, vascular proliferation
Lichen planus Purple polygonal papules marked by severe pruritus; lacy white markings, especially associated with mucous membrane lesions Certain drugs may induce: thiazides, antimalarial drugs Interface dermatitis
Pityriasis rosea Rash often preceded by herald patch; oval to round plaques with trailing scale; most often affects trunk; eruption lines up in skinfolds giving a “fir tree–like” appearance; generally spares palms and soles Variable pruritus; self-limited, resolving in 2–8 weeks; may be imitated by secondary syphilis Pathologic features often nonspecific
Dermatophytosis Polymorphous appearance depending on dermatophyte, body site, and host response; sharply defined to ill-demarcated scaly plaques with or without inflammation; may be associated with hair loss KOH preparation may show branching hyphae; culture helpful Hyphae and neutrophils in stratum corneum

1. Alopecia:

Hair loss, partial or complete.

2. Annular:

Ring-shaped

3. Cyst:

A soft, raised, encapsulated lesion filled with semisolid or liquid contents

4. Herpetiform:

In a grouped configuration.

5. Lichenoid eruption:

Violaceous to purple, polygonal lesions that resemble those seen in lichen planus.

6. Morbilliform rash:

Generalized, small erythematous macules and/or papules that resemble lesions seen in measles.

7. Nummular:

Coin-shaped.

8. Polycyclic lesions:

A configuration of skin lesions formed from coalescing rings or incomplete rings.

9. Pruritus:

A sensation that elicits the desire to scratch. Pruritus is often the predominant symptom of inflammatory skin diseases (e.g., atopic dermatitis, allergic contact dermatitis); it is also commonly associated with xerosis and aged skin. Systemic conditions that can be associated with pruritus include chronic renal disease, cholestasis, pregnancy, malignancy, thyroid disease, polycythemia vera, and delusions of parasitosis.
Diagnosis Common Distribution Usual Morphology Diagnosis Common Distribution Usual Morphology
Acne vulgaris Face, upper back, chest Open and closed comedones, erythematous papules, pustules, cysts Seborrheic keratosis Trunk, face Brown plaques with adherent, greasy scale; “stuck on” appearance
Rosacea Blush area of cheeks, nose, forehead, chin Erythema, telangiectases, papules, pustules Folliculitis Impetigo Any hair-bearing area Anywhere Follicular pustules Papules, vesicles, pustules, often with honey-colored crusts
Seborrheic dermatitis Scalp, eyebrows, perinasal areas Erythema with greasy yellow-brown scale Herpes simplex Lips, genitalia Grouped vesicles progressing to crusted erosions
Atopic dermatitis Antecubital and popliteal fossae; may be widespread Patches and plaques of erythema, scaling, and Lichenification; pruritus Herpes zoster Dermatomal, usually trunk but may be anywhere Vesicles limited to a dermatome (often painful)
Stasis dermatitis Ankles, lower legs over medial malleoli Patches of erythema and scaling on background of hyperpigmentation associated with signs of venous insufficiency Varicella Face, trunk, relative sparing of extremities Lesions arise in crops and quickly progress from erythematous macules, to papules, to vesicles, to pustules, to crusted sites.
Dyshidrotic eczema (Pompholyx) Palms, soles, sides of fingers and toes Deep vesicles Pityriasis rosea Trunk (Christmas tree pattern); herald patch followed by multiple smaller lesions Symmetric erythematous patches with a collarette of scale
Allergic contact dermatitis Anywhere Localized erythema, vesicles, scale, and pruritus (e.g., fingers, earlobes—nickel; dorsal aspect of foot—shoe; exposed surfaces—poison ivy) Tinea versicolor Chest, back, abdomen, proximal extremities Scaly hyper- or hypopigmented macules
Psoriasis Elbows, knees, scalp, lower back, fingernails (may be generalized) Papules and plaques covered with silvery scale; nails have pits Candidiasis Groin, beneath breasts, vagina, oral cavity Erythematous macerated areas with satellite pustules; white, friable patches on mucous membranes
Lichen planus Wrists, ankles, mouth (may be widespread) Violaceous flat-topped papules and plaques Dermatophytosis Feet, groin, beard, or scalp Varies with site, (e.g., tinea corporis—scaly annular plaque)
Keratosis pilaris Extensor surfaces of arms and thighs, buttocks Keratotic follicular papules with surrounding erythema Scabies Groin, axillae, between fingers and toes, beneath breasts Excoriated papules, burrows, pruritus
Melasma Forehead, cheeks,temples, upper lip Tan to brown patches Insect bites Anywhere Erythematous papules with central puncta
Vitiligo Periorificial, trunk, extensor surfaces of extremities, flexor wrists, axillae Chalk-white macules Cherry angioma Keloid Dermatofibroma Trunk Anywhere (site of previous injury) Anywhere Red, blood-filled papules Firm tumour, pink, purple, or brown Firm red to brown nodule that shows dimpling of overlying skin with lateral compression
Actinic keratosis Sun-exposed areas Skin-colored or red-brown macule or papule with dry, rough, adherent scale Acrochordons (skin tags) Groin, axilla, neck Fleshy papules
Basal cell carcinoma Face Papule with pearly, telangiectatic border on sun-damaged skin Urticaria Anywhere Wheals, sometimes with surrounding flare; pruritus
Squamous cell carcinoma Face, especially lower lip, ears Indurated and possibly hyperkeratotic lesions often showing ulceration and/or crusting Transient acantholytic dermatosis Xerosis Trunk, especially anterior chest Extensor extremities, especially legs Erythematous papules Dry, erythematous, scaling patches; pruritus


DISEASE OF SKIN



PAPULOSQUAMOUS DISORDERS



Clinical Features Other Notable Features Histologic Features
Psoriasis Sharply demarcated, erythematous plaques with mica-like scale; predominantly on elbows, knees, and scalp; atypical forms may localize to intertriginous areas; eruptive forms may be associated with infection May be aggravated by certain drugs, infection; severe forms seen in association with HIV Acanthosis, vascular proliferation
Lichen planus Purple polygonal papules marked by severe pruritus; lacy white markings, especially associated with mucous membrane lesions Certain drugs may induce: thiazides, antimalarial drugs Interface dermatitis
Pityriasis rosea Rash often preceded by herald patch; oval to round plaques with trailing scale; most often affects trunk; eruption Variable pruritus; self-limited, resolving in 2–8 weeks; may be Pathologic features often nonspecific
lines up in skinfolds giving a “fir tree–like” appearance; generally spares palms and soles imitated by secondary syphilis
Dermatophytosis Polymorphous appearance depending on dermatophyte, body site, and host response; sharply defined to illdemarcated scaly plaques with or without inflammation; may be associated with hair loss KOH preparation may show branching hyphae; culture helpful Hyphae and neutrophils in stratum corneum
one of the most common chronic, noncontagious, dermatologic diseases, affecting up to 2% of the world’s population. It is an immune-mediated disease clinically characterized by an unpredictable course of remissions and relapses and presence at typical sites of well- defined erythematous, sharply demarcated papules and rounded plaques covered by silvery micaceous scale. The skin lesions of psoriasis are variably pruritic. Traumatized areas often develop lesions of psoriasis (the Koebner or isomorphic phenomenon). There is frequent nails and joint involvement.

EPIDEMIOLOGY


1. GENETIC FACTOR- Some HLA markers like HLA-CW6 carries very high risk and HLA -B13 and HLA – B17.
2. DRUGS – Lithium carbonate and Propranolol due to their inhibiting action on adenyl cyclase altering epidermal cell kinetics may cause psoriasis.
3. INFECTION – Psoriatic lesion have been seen in children after sore throat caused by beta – haemolytic streptococci.
4. TRAUMA – Repeated trauma over the elbow and knee may explain the site of psoriasis.
5. MENTAL STRESS
ETIOLOGY

1. Disturbed fat metabolism
2. Hormonal imbalance
3. Septic focus
4. Allergy
5. Anxiety
6. Stress
7. Hereditary influences

TYPE OF PSORIASIS
1. Plaque – The most common form of psoriasis, causes dry, raised, red skin lesions (plaques) covered with silvery scales. The plaques itch or may be painful and can occur anywhere on your body. 

2. Guttate – It is seen in children and young adults where raindrop like lesion develops. It is a type of ⦁ psoriasis that presents as small (0.5–1.5 cm in ⦁ diameter) ⦁ lesions over the ⦁ upper trunk and ⦁ proximal extremities; it is found frequently in young adults.

3. Inverse- It is a form of ⦁ psoriasis that selectively, and often exclusively, involves the folds, recesses, and flexor surfaces such as the ⦁ ears, ⦁ axillae, ⦁ groin folds, ⦁ inframammary folds, ⦁ navel, ⦁ intergluteal cleft, ⦁ penis, lips, and webspaces.
4. Pustular - The term pustular psoriasis is used for a heterogeneous group of diseases that share pustular skin characteristics. It can be localized, commonly to the hands and feet (⦁ localized pustular psoriasis), or generalized with widespread patches appearing randomly on any part of the body (⦁ generalized pustular psoriasis). Scaling is very much prominent and nail changes including thickening and colour changes are very common.

5. Erythrodermic – It represents a form of ⦁ psoriasis that affects all body sites, including the face, hands, feet, nails, trunk, and extremities. This specific form of psoriasis affects 3 percent of persons diagnosed with psoriasis.

SYMPTOMS



1. Initial lesion consists of red spots which vary in sizes and may appear in any part of body.
2. They are popular lesions which are covered with silvery scales which after scraping leave behind a shiny bleeding surface.(Auspitz sign).
3. Itching is usually absent but may be present when lesions are in the body folds and on vulva.
4. Psoriatic lesions may develop in the line of scratch during its active phase known as Koebner’s phenomenon.
5. The nails may also become thickened, pitted and striated.

PSORIASIS MEDICINES
1. GRAPHITES – Complaints from grief and vexation; suppression of skin eruptions; extremes of heat and cold. There is obstinate dryness of the skin. Eruption oozes out thick, sticky, honey like exudation. Unhealthy skin, every little injury suppurates. Severe itching on the surface of skin. Scabby eruption. Worse – warmth, night, during and after menstruation. Better – dark, from wrapping up.

2. SULPHUR – Complaints from alcohol, sun’s heat, suppression of skin diseases, over exertion. Dry, scaly, unhealthy skin, every little injury suppurates. Itching, burning, worse scratching and washing. Exanthema in general on any part of body which is < by heat, warmth at work. Tetters of a greenish yellow colour with itching. Worse – Standing, at rest, washing, warmth of bed and changeable weather. Better – Open air, motion, lying on right side and sweating.

3. CUPRUM ARS – skin is very sensitive to touch, pressure < all symptoms.

4. ANTIMONIUM CRUDDUM – Complaints from disappointed love, cold bathing, alcohol, fat, fruits, suppressed eruptions, extremes of heat and cold. Thick hard honey coloured scabs. Itching when warm in bed. Dry skin, scaly, pustular eruption with burning and itching < night. Concomitant - There are eruption with gastric derangement.
Worse – evening, heat, acids, water, washing
Better – open air, during rest, moist warmth.

5. STAPHISAGRIA - Complaints from onanism, sexual excess, sexual abuse, loss of vital fluids. There is yellowish, acrid moisture oozes out, forming crusts over it. Thick scabs, dry and itch violently scratching changes location of itching. Exanthema on cheeks, face, yellow with a creeping itching.
Worse – mental affection, anger, indignation, grief, onanism.
Better -
The term eczema means “to boil out”, because it seems that the skin is "boiling out" or "oozing out" in eczema.

Eczema is a type of dermatitis. It is a reaction pattern that has two components:

1. Clinical component

2. Histological component

Clinical Component - Eczema, clinically manifests as pruritus, erythema, edema, papule, vesicles, scaling and Lichenification.The feature that predominates depends on the stage – acute eczema is exudative, while chronic eczema is dry, scaly, and often lichenified.

Histological Component - the hallmark of eczema is spongiosis. In the chronic stage, the lesion shows hyperkeratosis and acanthosis. Primary lesions may include erythematous macules, papules, and vesicles, which can coalesce to form patches and plaques. Secondary lesions from infection or excoriation, marked by weeping and crusting, may predominate. In chronic eczematous conditions, Lichenification (cutaneous hypertrophy and accentuation of normal skin markings) may alter the characteristic appearance of eczema.

ETIOLOGICAL CLASSIFICATION

.
ENDOGENOUS EXOGENOUS COMBINED
Seborrheic dermatitis Irritant dermatitis Atopic dermatitis
Nummular dermatitis Allergic dermatitis Pompholyx
Lichen simplex chronicus Photodermatitis
Pityriasis alba Radiation dermatitis
Stasis dermatitis Infective dermatitis

CLASSIFICATION OF ECZEMA

.
ETIOLOGY PATTERN/MOROHOLOGY CHRONICITY
Endogenous Discoid Acute
Exogenous Hyperkeratotic Chronic
Combined Lichenified
seborrheic

The most practical way to classify eczema, according to etiology is:

1. Endogenous eczema: Where constitutional factors predispose the patient to developing an eczema.
2. Exogenous eczema: Where external stimuli trigger development of eczema, e.g., irritant dermatitis.
3. Combined eczema: When a combination of constitutional factors and extrinsic triggers are responsible for the development of eczema e.g. atopic dermatitis.


CLINICAL FEATURES
The clinical features of eczema depend on the stage of the disease :

1. ACUTE
2. CHRONIC

Acute Eczema
– It is characterized by erythematous and oedematous plaque, which is ill – defined and is surmounted by papules, vesicles, pustules and exudate that dries to form crusts

Chronic Eczema - It is characterized by Lichenification, which is a triad of hyperpigmentation, thickening oof skin and increased skin markings. The lesions are less exudative and more scaly.

POINT OF DIAGNOSIS

1. Acute eczema – Itchy exudative plaques, surmounted by papulovesicles.
2. Chronic eczema – Lichenified scaly plaques

1) GRAPHITES- Complaints from grief and vexation; suppression of skin eruptions; extremes of heat and cold. The eruption is crusty, moist, yellow and sticky; especially forming in the folds of joints such as the elbows, knees or groin. The skin can become very dry, cracked, red, itchy and painful. Eczematous and herpetic eruption predominate. Eczema of ears and moist eczema round anus

Worse – warmth, night, during and after menstruation
Better – dark, from wrapping up.

2) CICUTA VIROSA - Complaints from nervous irritation, worms, suppressed eruption, shock and injury. Burning itching over the whole body. Purulent eruption with yellowish and burning scabs. The eczema forms thick yellow scabs (like dried honey) and affects the cheeks, chin and scalp where it is burning and itchy.

Worse – touch, draught, tobacco smoke.
Better – rest, dark room.

3) RHUS TOX – Complaints from spraining and straining, over lifting, from wetting, summer bathing in lake or river, getting wet when heated. Red, swollen, itching intense. Vesicles, herpes, vesicular suppurative forms. Burning eczematous eruptions with tendency to scale formation.

Worse – during sleep, cold, wet rainy weather and after rain, during rest
Better – warmth, dry weather, motion, walking, rubbing, warm application.

4) LYCOPODIUM – Complaints from fright, anger, mortification, or vexation with reserved displeasure. Chronic eczema associated with urinary, gastric and hepatic disorders; bleed easily. Skin becomes thick and indurated. It is used for eczema that is bleeding, moist or discharging; affecting the scalp, armpits, limbs, back and neck.

Worse –4 – 8 p.m., right side, from heat, warm air
Better – warm food and drinks, uncovering the head, open air.

5) BOVISTA – Unhealthy skin. The eczema may be either dry or moist, with thick crust formed by very thick, tough, stringy and tenacious discharges from the eruption.

Worse –on waking up in the morning and after bathing.
Better – after meals.

The word “atopy” means “no (without) place” was first used for a group of hereditary disorders in people who had a tendency to develop an urticarial response to foods and inhaled substances. It is a chronic inflammation of the epidermis and dermis, characterized by a family history of asthma, allergic rhinitis, or eczema.

It is and endogenous eczema triggered by exogenous agents and characterized by :
1) Extremely pruritic, recurrent, symmetric eczematous lesions.
2) Personal and family history of atopic diathesis.
3) Increased ability to form IgE to common environmental allergens


Seborrheic dermatitis is a common, chronic disorder characterized by greasy scales overlying erythematous patches or plaques. Induration and scale are generally less prominent than in psoriasis, but clinical overlap exists between these diseases (“sebopsoriasis”).
ETIOLOGY

1. Microbial etiology – overgrowth of yeast, MALASSEZIA FURFUR may play a part in the development of seborrheic dermatitis.
2. Genetic predisposition
3. Immunodeficiency

EPIDEMIOLOGY
1. Prevalence - fairly common if all the patient with mild dandruff. Incidence of SD is very common in HIV – positive patient.
2.Age – most common in adults.
3.Gender – More common in males.

SITE
1. The most common location is in the scalp, where it may be recognized as severe dandruff (“cradle cap”).
2. On the face, seborrheic dermatitis affects the eyebrows, eyelids, glabella, nasolabial folds, retroauricular aarea, interscapular regions.
3. Scaling of the external auditory canal is common in seborrheic dermatitis.
4. It may also develop in the central chest, axilla, groin, submammary folds, and gluteal cleft
Contact dermatitis is an inflammatory skin process caused by an exogenous agent or agents that directly or indirectly injure the skin. It is the reaction of the skin to the contactants.

TYPES


IRRITANT ALLERGIC
In IRRITANT CONTACT DERMATITIS (ICD), this injury is caused by an inherent characteristic of a compound—for example, a concentrated acid or base.

ETIOLOGY
1. Occupational exposure, either industrial contact or as a household contact.
2. Airborne exposure, costume jewellery, hair dyes, cosmetics, topical antibiotics, local anesthetics.

PREDISPOSING FACTORS
1). Dry skin is more susceptible to irritant dermatitis.
2). Atopic individual are more susceptible.
3). SITE – face, scrotum and back of the hands is more susceptible while skin of palms and soles is resistant.
4. Protective measures reduces the rate of ICD.


CLINICAL FEATURES
1. Little dryness, redness or chapping to various types of eczematous dermatitis to an acute caustic burn.
2. Acute exudative lesions – If the exposure is to a strong irritant.
3. Dry dermatitic lesions – If there is chronic repeated exposure to a weal irritant.
4. The clinical lesions of contact dermatitis may be acute (wet and oedematous) or chronic (dry, thickened, and scaly), depending on the persistence of the insult
ALLERGIC CONTACT DERMATITIS
Agents that cause ACD induce an antigen-specific immune response (e.g., poison ivy dermatitis).

ETIOLOGY Common allergens are plants (parthenium), metals (nickel), cosmetics (hair dyes and fragrances), medicines and rubber.

PATHOGENESIS

Develop due to involvement of immunological pathway, being a type IV reaction to exogenous contact antigens. It does not develop on the first exposure because patients immunological pathway has not been sensitized

It is a papulosquamous disorder that may affect the skin, scalp, nails, and mucous membranes. It is flat topped inflammatory erythematous or purplish papules showing a criss – cross appearance of the surface often seen on the flexor surface of the skin with symmetric distribution along with lacy lesions of buccal mucesa. The skin lesions may occur anywhere but have a predilection for

ETIOLOGY 1). Nervous and Mental tension
2). Trauma


PATHOLOGY
At the epidermo – dermal junction band – like infiltration of melanophage, histiocyte is seen . At the same site immunoglobulin mainly IgM deposits are seen.

SITES –
1. Lesions are most frequently seen on extremities and lower back.
2. Lesions may appear at the sites of trauma.
3. Lesions may appear on wrists, shins and genital


VARIANT CHANGE MORPHOLOGY SITES OF PREDILECTION
ANNULAR Hyperpigmented flat center.
Violaceous elevated periphery.
Face, glans penis.
ACTINIC Annular lesions with thready edge.
Perilesional hypopigmented halo.
Face, dorsal/ dorsolateral aspect of upper extremities.
LINEAR Papules arranged linearly Extremities
FOLLICULAR Perifollicular violaceous papules
leading to cicatricial alopecia.
Scalp, trunk,medial aspect of extremities.
HYPERTROPHIC Central depigmentation.
Verrucous hyperkeratotic
papules and nodules.
Shins
BULLOUS Lesion on LP.
Bulla
Extremities

CLINICAL FEATURES


Age – Young adults and children.
Onset – acute or insidious.
1). The primary cutaneous lesions are pruritic, polygonal, pleomorphic papules which are very small violaceous papules on flexor aspect of upper or lower limbs, over the axillae and on the abdomen, forearms, wrists, legs, genitalia and on face symmetrically.
2). Papule may enlarge with cleaning of the centre called lichen planus annularis .
3). It develop a network of Gray lines (Wickham’s striae) and shiny waxy appearance may also be seen.
4). Mucous membrane is involved with bluish patches are seen.
5). Moderate to severe itching is always present.
6). The triad of diagnosis is typical skin lesions, typical mucosal lesion and typical histopathologic findings.

POINT OF DIAGNOSIS
1). Itchy violaceous, polygonal flat topped papules with characteristic Wickham’s striae on the surface.
2). Typical sites of involvement.
3). Oral lesion – lacy reticulate lesions.
4). Nail changes – Thinning of nail plate and pterygium corroborate diagnosis.


Pityriasis rosea (PR) is a papulosquamous eruption of unknown etiology occurring more commonly in the spring and fall. This is followed in a few days to a few weeks by the appearance of many smaller annular or papular lesions with a predilection to occur on the trunk. Individual lesions may range in color from red to brown and have a trailing scale.
ETIOLOGY
1. Self – limiting condition (2-10 weeks).
2. Caused by virus - HHV - 739 MORE FREQUENTLY
3. It is non – contagious.

EPIDEMIOLOGY
1. Age – usually between ages 10 - 3 5 years.
2. Season - Incidence lowest in summer.

CLINICAL FEATURES
EVOLUTION
HERALD PATCH
MANY SIMILAR LESIONS, WHICH ANLARGE SLOWLY
MILD PIGMENTARY CHANGE


FADES SLOWLY
1. Itching, usually mild.
2. HERALD PATCH – it is the first lesion of pityriasis rosea and is seen in sbout 80% of patients.
3. Oval lesions with wrinkled, salmon pink centre and collarette of scales at the periphery.
4. SECONDARY LESION – begin as scaly papules, which enlarge to form oval annular plaques similar to herald patch.
5. They are arranged characteristically along the long axis of patches run downwards and outwards from the spine, along the lines of ribs.

TYPES

.
1. INVERSE PR.
2. PAPULAR PR.
3. BULLOUS PR

POINT OF DIAGNOSIS
1. Presence of herald patch.
2. Eruption consisting of erythematous, oval annular plaques with a peripheral collarette of scales.
3. Typical distribution on the trunk.

PITYRIASIS ROSEA
1. CALCAREA HYPO –
2. RHUS TOX – Complaints from spraining and straining, over lifting, from wetting, summer bathing in lake or river, getting wet when heated. Red, swollen, itching intense. Erysipelas vesicular eruptions, vesicles are yellow, from left to right, with much swelling, inflammation, burning, itching and stinging erysipelatous and oedematous.
Worse – during sleep, cold, wet rainy weather and after rain, during rest
Better – warmth, dry weather, motion, walking, rubbing, warm application.
3. SEPIA – Complaints from cold, laundry work, alcohol, tobacco, wetting before and during menses, after eating. Itching not relieved by scratching; is apt to change into burning, worse in bends of elbows and knees.
Worse – evening, washing, left side, after sweat.
Better – exercise, pressure, warmth of bed, hot application.
4. ARSENIC ALBUM – Complaints from Chewing tobacco, alcoholism, sea bathing, sausage poisoning, Chill, cold fruit. Itching, dry, rough and scratching of skin. There may be pustules, vesicles, desquamation from head to foot. Burning and itching followed by pain after scratching.
Worse – cold drinks, food, cold air, alcohol.
Better – hot application, warm food and drink, motion, sitting erect.

It is an intraepidermal bullous disorder, which is associated with substantial mortality and morbidity and characterized clinically by presence of cutaneous and mucosal blisters and histologically by acantholysis, which occurs due to the deposition of intercellular autoantibodies.
ETIOLOGY –
1. Idiopathic autoimmune phenomenon – it is an autoimmune disorder characterized by the presence of IgG autoantibodies against desmogleins (Dsg)5 (present in desmosomes),which are involved in keratinocyte-keratinocyte adhesion. Antibodies are deposited in the intercellular area resulting in separation of keratinocytes from each other .
3. Neosplasia-induced autoimmune phenomenon: Thymoma and lymphonma.
4. Drug-induced autoimnmune phenomenon: Penicillamine, rifampicin and captopril.

CLASSIFICATION
Pemphigus is classified ( based on the level of split, clinical features and serological profile) into :

1. Pemphigus vulgaris: Where split is supra basal.
2. Pemphigus vegetans: Where split is supra basal.
3. Pemphigus foliaceus: Where split is either in granular layer or just below the horny layer.
4. Pemphigus erythematosus: Where split either in granular layer or just below the stratum corneum
Warts are cutaneous neoplasms caused by papillomaviruses. More than 100 different human papillomaviruses (HPVs) have been described. A typical wart, verruca vulgaris, is sessile, dome-shaped, and usually about a centimetre in diameter. Its surface is hyperkeratotic, consisting of many small filamentous projections.

ETIOLOGY
1). Human papilloma virus (HPV) is a DNA virus which has not been cultured in vitro.
2). Due to PCR more than 100 type of HPV has been identified.

EPIDEMIOLOGY
1). AGE
. Nongenital warts – Most frequently in children and young adults.
. Anogenital warts – in adolescents and adults, though occasionally may be seen in children.
2. TRANSMISSION
. Nongenital warts – transmitted through direct skin – to – skin contact and by auto – inoculation.
. Anogenital warts – Sexual transmission - both in heterosexual and homosexual.
Vertical transmission – Mother with anogenital warts can transmit infection to the newborn, during vaginal delivery.

Sexual transmission - both in heterosexual and homosexual.
Vertical transmission – Mother with anogenital warts can transmit infection
to the newborn, during vaginal delivery.

Warts present clinically as :
. Verruca vulgaris
. Palmoplantar warts
. Verruca plana
. Filiform warts
. Epidermodysplasia verruciformis.
. Anogenital warts.

Verruca vulgaris (common warts)
Usually asymptomatic

Morphology
Single or multiple, circumscribed, firm papules with verrucous (hyperkeratotic) dry, stippled surface.
About 60% of common warts resolve spontaneously

Palmoplantar warts
Palmoplantar warts are of two types:
⦁ Superficial palmoplantar warts.
⦁ Deep palmoplantar warts.

Superficial palmoplantar warts (mosaic warts)
Usually painless.
Morphology: Hyperkeratotic papules and plaques consisting of multiple, small warts, which are tightly packed.

Sites: Soles and less often palms.
Deep palmoplantar warts (myrmecia)

Painful (sometimes excruciatingly so!).

Morphology: Hyperkeratotic, deep seated papules, surrounded by a horny collar. Presence of black dots, representing thrombosed capillary loops).

Sites – less often on palms and on sides of fingers


Verruca plana (plane warts)

Morphology
*Multiple, slightly elevated, that smooth papules
Skin colored or darker lesions: may have an erythematous halo.
*Lesions may be arranged linearly (pseudo Koebner's phenomenon) due to auto-inoculation.

Site
Face and on dorsal aspects of hands.


Filiform warts

Morphology - Asymptomatic, thin elongated, firm projections arising from a horny base.

Site – Most frequently on face and scalp

Anogenital warts


⦁ Sexually transmitted disease.
⦁ A variety of clinical variants, e.g., condyloma acuminata, papular warts and Bowenoid papulosis.
⦁ Most frequently on the glans, perianal region, vulva, and cervix

COURSE OF WARTS
Spontaneous resolution - In healthy individuals spontaneously (30% in 6 months and 60% in 12 months) as the host mounts an immune response. When wart is spontaneously regressing, punctate area of blackish discoloration appear on surface and the wart resolves with no sequelae.

Persistent warts - Mosaic warts very recalcitrant. In immunocompromised individuals, (on immunosuppressive therapy, with lymphoreticular malignancies or with HIV infection) warts are persistent, extensive, and have an oncogenic potential.

CLINICAL FEATURES 1. Plantar warts are endophytic and are covered by thick keratin.
2. Paring of the wart will generally reveal a central core of keratinized debris and punctate bleeding points.
3. Filiform warts are most commonly seen on the face, neck, and skinfolds and present as papillomatous lesions on a narrow base.
4. Flat warts are only slightly elevated and have a velvety, non-verrucous surface. They have a propensity for the face, arms, and legs and are often spread by shaving.
5. Genital warts begin as small papilloma that may grow to form large, fungating lesions. In women, they may involve the labia, perineum, or perianal skin. In men, the lesions often occur initially in the coronal sulcus but may be seen on the shaft of the penis, the scrotum, or the perianal skin or in the urethra.
6. The risk is higher among patients immunosuppressed after solid organ transplantation and among those infected with HIV.
POINTS FOR DIAGNOSIS
Warts are diagnosed on the basis of :
. Characteristic warty appearance with a rough, dry stippled surface.
. Presence of pseudo Koebner's phenomenon, especially in plane warts.
. Typical histology.

It is a dermatophyte infection caused by 3 different types of fungi called “Microsporum, Epidermophyton and Trichophyton”. They can easily penetrate the keratinised structures and causes skin, hair and nail infection. Dermatophytes are keratinophilic fungi, living on dead keratin so in stratum corneum.
They induce inflammation in skin due to :
Permeation of their metabolic products into deeper layers.
Induction of delayed hypersensitivity.

SOURCE –
1. Zoophilic ( induce significance inflammation ) – Animal to Man
2. Anthropophilic (induce less inflammation) – Man to Man
3 Geophilic ( induce significance inflammation – Soil to Man
ETIOLOGY –
CLINICAL FEATURES ETIOLOGY –

Prototype lesion
Is an annular or arcuate lesion which spreads centrifugally.
Margin is active, showing papulovesiculation, pustulation, and scaling .
Center is relatively clear, though in chronic lesions there may be nodules, hyperpigmentation and even Lichenification in the center.
These features may be modified, depending on:
Site of infection
Strain of fungus
RINGWORM
1. ARSENIC ALBUM – Complaints from Chewing tobacco, alcoholism, sea bathing, sausage poisoning, Chill, cold fruit. Itching, dry, rough and scratching of skin. Eruptions with raised and hard edges, surrounded by a red and shining crown with bottom like lard or of a blackish – blue colour with burning pains or shooting .
Worse – cold drinks, food, cold air, alcohol.
Better – hot application, warm food and drink, motion, sitting erect.
2. BACILLINUM –
3. NATRUM MUR – Complaints from anger, grief, vexation, excessive use of salt, bread, quinine, fright, loss of vital fluid, sexual excess. Dry herpetic eruptions especially around the edges of hair, nape of neck and bends of joints. Greasy skin Worse – music, warm room, lying down, at sea shore, mental exertion, heat, talking. Better – open air, cold bathing, pressure, lying on right side, tight clothing.
4. SEPIA – Complaints from cold, laundry work, alcohol, tobacco, wetting before and during menses, after eating. Herpes circinatus in isolated spots. Itching not relieved by scratching; worse in bends of elbows and knees. Ringworm like eruption every spring.
Worse – evening, washing, left side, after sweat.
Better – exercise, pressure, warmth of bed, hot application.
5. MERCURIUS – Complaints from sugar, fright, suppressed foot sweat, suppressed gonorrhoea. Itching is worse from warmth of bed.
Persistent dryness of the skin contraindicates merc.
Worse – night, wet, damp weather, perspiration.
Better – rest, coition, weeping
6. DULCAMARA – Complaint appear at the end of the summer season when the weather becomes damp and humid. Ringworm lesions on the scalp that bleed on scratching. Eruptions on the hands, face and arms. Skin rashes in women seen just before their periods begin. Red spots and small fluid-filled boils on the skin
Worse - night, from cold or humid weather
Better - warmth.

Age - Invariably a child
Morphology
1. Discoid patch of partial alopecia from which the hair can easily and painlessly be plucked.
2. Degree of inflammation varies, depending on the strain of fungus, being more when tinea capitis is caused by zoophilic or geophilic species than with anthropophilic species.

Tinea capitis (tinea of trunk and limbs)
Morphology
Annular/arcuate lesions with relative clearing in centre and an active periphery.
Site

Infection of the glabrous skin, except palms, soles and groins.

Tinea incognito
Dermatophytic infection of skin modified by steroid therapy.
Atypical lesions, usually asymptomatic, poorly defined edge with minimal scales and papulovesicles.
Tinea cruris (tinea of groin)
Incidence - A very common condition.
Predisposing factors
⦁ Summer’s and rainy season.
⦁ Occlusion; use of synthetic clothes.
⦁ Affects men more often than women and adults more than children.
Site
Groins, genitalia, pubic area, perineal and perianal areas.
Morphology
Seen on the inner aspect of thighs as arcuate, sharply demarcated plaques with peripheral scaling, papulovesiculation, and pustulation.
Lesions expand centrifugally and centre clears.
Chronic lesions may show hyperpigmentation nodulation and Lichenification in center.
Tinea pedis
Predisposing factors
1. Hot moist weather.
2. Occlusive foot wear.
3. Hyperhidrosis of soles.
4. Sharing of wash places.
5. Presence of tinea unguium.
Morphology Three clinical patterns recognized
Interdigital variant : Interdigital scaling seen most frequently in the lateral two interdigital spaces of the feet.
Hyperkeratotic variant : well – defined scaly plaque on the sole, usually unilateral.
Hyperkeratotic variant : Well-defined scaly plaque on the sole, usually unilateral.
Vesicular variant: Recurrent vesiculation of soles.
Tinea manuum (tinea of hands )
Dermatophytic infection of the hands is usually associated with tinea pedis.
Lesions manifest as unilateral, well – defined plaques or as diffuse erythema of the palms with accumulation of fine scales in the creases.
Tinea unguium (tinea of nails)
Tinea unguium is dermatophyte infection of nails.
Incidence
Tinea of toe nails is more frequent than that of finger nails and may be associated with tinea pedis.
Tinea of finger nails is associated with dermatophytic infection of other parts of the body, e.g. tinea cruris.
Morphology
Tinea unguium usually affects only a few nails and is asymmetrical.
Nail involvement begins at the fire edge of the distal part of nail and the nail shows the following changes.
Yellow-brown discoloration and crumbling and tunneling of nail plate.
Collection of friable debris under the nail (subungual hyperkeratosis).
Separation of nail plate from nail bed (onycholysis)


ACNE VULGARIS


It is a disorder of pilosebaceous complex which predominantly affects the peripubertal population and clinically manifests as comedones (open/closed), papules, nodules, pustules and cysts and heals with scars. There is excessive secretion of sebum by which obstructing horny plugs (comedones) develop associated with inflammation of the pilosebaceous duct.

Etiology:
1. Androgenic influence - increased sebum secretion (due to increased end organ sensitivity to androgens)
2. Follicular duct hyper cornification.
3. Abnormal keratinization.
4. Infection – Anaerobic diphtheroid known as “Propionibacterium Acnes”
5. Increased colonization with Propionibacterium acnes and inflammation.

Onset: 12 - 14 years of age.
Morphology:
Polymorphic, eruption consisting of papules, pustules, nodules, cysts, and pathognomonic open and closed comedones on a background of oiliness.
Sites: Face, upper trunk, and deltoid region. Variants:
Acne conglobata, occupational acne, drug induced acne, and acne after massage.
Acne from drug and chemicals – Glucocaticoids when used for a long time as in nephrotic syndrome, rheumatoid arthritis, may produce acne.
Oil acne - Continuous use of lubricating oils, develop acne like lesion on the sites of contact. Cosmetics containing mineral oils may also produce acne.
Excoriated acne – after continuous injury of acne by nails particularly in young women, infection papules, crustification and scarification develop.
CLINICAL FEATURES
1. Skin is very much greasy due to excessive sebum secretion.
2. Comedones are seen on the hair follicles.
3. When pigmentation occurs they are called as black comedones, which are elevated papules.
4. In white comedones there is absence of keratin plugs, these can be extracted by nails.
⦁ MERCURIUS – complaints from sugar, fright, suppressed foot sweat, suppressed gonorrhoea. Pustular, vesicular, purulent eruption.
Small and very itchy pimples, which ulcerate and becomes encrusted. Pimples around the main eruption.
Worse – night, wet, damp weather, perspiration.
Better – rest, coition, weeping
⦁ HEPAR SULPHUR – Complaints from suppressed eruption, quinine, cold in general, gonorrhoea. Eruption of pimples and tubercles, painful to touch, patient cannot bear even the touch of the cloth. Unhealthy skin, every injury tends to suppurates. Acne are prone to suppurates which bleed easily. Acne in the youth. Putrid ulcers surrounded by little pimples.
Worse – cold air, uncovering, eating and drinking cold things, touching affected parts.
Better – warmth in general, from wrapping up and in damp wet weather.
⦁ ANTIMONIUM CRUDDUM – Complaints from disappointed love, cold bathing, alcohol, fat, fruits, suppressed eruptions, extremes of heat and cold. Pimples, vesicles and pustules are well marked. Sensitive to cold bathing. Scaly, pustular eruption with burning and itching < at night.
Worse – evening, heat, acids, water, washing
Better – open air, during rest, moist warmth.
⦁ NITRIC ACID – Complaints from long lasting anxiety, over – exertion of body and mind. Pimples or exanthema in general.
Worse – evening, night, cold climate
Better - riding, carriage.
⦁ SARSAPARILLA –

It is characterized clinically by development of totally white macules, microscopically by complete ansence of melanocytes, and medically by an increased risk of certain diseases, particularly thyroid diseases.
ETIOLOGY ⦁ GENETIC – 20% of petients have a positive family history.
⦁ AUTOIMMUNE HYPOTHESIS – frequent association with other autoimmune disorder like alopecia areata and thyroid disorder. Presence of antibodies to melanocytes.
⦁ NEUROGENIC HYPOTHESIS - Segmental vitiligo is present along a dermatome in distribution of nerves, suggesting a neurogenic origin.
⦁ Race - Appears in all races. The apparently increased prevalence reported in some countries and among darker-skinned people results from a dramatic contrast between white vitiligo macules and dark skin and from marked social stigma in countries such as India.
EPIDEMIOLOGY
INCIDENCE - occur in 1% of population.
AGE - affect all ages; between 10 - 30 years.
Physical Examination
Skin Lesions
TYPE - Macules; 5mm to 5cm or more in diameter.
COLOR - Chalk white. Newly developed macules may be off – white in colour; this represents transitional phase. The disease progresses by gradual enlargement of the old macules or by development of new ones.
SHAPE - Convex margins (as if the pathologic process of depigmentation were flowing into normally pigmented skin). Round, oval, or elongated. Linear or artifactual macules represent the isomorphic or “Koebner phenomenon”.
CLINICAL FEATURES
⦁ Characterized by depigmented macules, which are chalky or milky white. Sometimes, pigment loss is partial and occasionally, three shades are seen in the lesion.
⦁ Macules have a scalloped outline and form geographical patterns on fusion with neighboring lesions.
⦁ Hair in the lesions may remain pigmented, though in the older lesions the hairs may lose their pigment leucotrichia
SITE - lesion can occur in anypart of the body
PATTERN Vitiligo vulgaris- Commonest type, Occurs after-second decade. May be slowly or rapidly progressive.
Segmental vitiligo- Occurs in children. Not associated with autoimmune disease. Depigmentation is dermatomal. Most frequently (50%) seen in distribution of trigeminal nerve (mandibular division). It has a stable course, i.e., lesions increase initially and then remain static.
Generalized vitiligo - . Extensive lesions.

Variants of generalized vitiligo are:
⦁ Acrofacial vitiligo
⦁ Lip -tip vitiligo
⦁ Vitiligo-universalis
Course
Onset usually before age of 20 years. Usually slowly progressive, but sometimes can progress rapidly. Segmental vitiligo progresses initially but stabilizes in about 6 months.
Points for diagnosis
1. Age of onset
2. Depigmented macules (milky white) with scalloped borders.
3. Leucotrichia
4. Koebner’s phenomenon
5. Predilection for sites of trauma

Melasma (Greek: "a black spot") is an acquired light or dark-brown hyperpigmentation that occurs in the exposed areas, most often on the face, and results from exposure to sunlight; may be associated with pregnancy, with ingestion of contraceptive hormones, or possibly with certain medications such as diphenylhydantoin or be idiopathic. Synonyms: Chloasma (Greek: "a green spot"), mask of pregnancy.

ETIOLOGY
⦁ Hormonal factors - Estrogen often appear first during pregnancy or in a patient taking OCP.
⦁ Other factors - Sunlight plays important role, as melasma darkens after sun exposure.
⦁ Melasma has recently been appearing in menopausal women as a result of regimens for prevention of osteoporosis using a combination of oestrogens and progesterone
⦁ Melasma did not appear in those women who were given Estrogen replacement treatment but without progesterone.
⦁ Melasma is still occurring in women given the contraceptive agents that are combinations of estrogen - type compounds and progestational agents.
EPIDEMIOLOGY It is Common, especially among persons with constitutive brown skin color and who are taking contraceptive regimens and who live in sunny areas.
Age –. young adults. Peak incidence 30 - 50 years.
Race – Melasma is more apparent or more frequent in persons with brown or black constitutive skin color (people from Asia, the Middle East, India, South America).
Females are more frequently affected.
Precipitating Factors : Sun exposure plus pregnancy or oral contraceptives, diphenylhydantoin; cosmetics probably do not play a role.
Physical Examination
Skin Lesions TYPE – completely macular hyperpigmentation, the hue and intensity depending largely on the skin phototype of the patient.
Color – Light or dark brown or even black. Color is usually uniform but may be splotchy.
ARRANGEMENT - Most often symmetric
SHAPE AND BORDER OF INDIVIDUAL LESIONS - The pattern follows the areas of exposure, and the lesions have serrated, irregular, and geographic borders.
DISTRIBUTION Two-thirds on central part of the face: cheeks, forehead, nose, upper lip, and chin; a smaller percentage involve the malar or mandibular areas of the face and occasionally the dorsa of the forearms.
CLINICAL FEATURES ⦁ Brown macular pigmentation with well - defined scalloped margins.
⦁ Pigmentation darkens on sun exposure.
⦁ Symmetrically on cheeks, nose, forehead, and chin.
⦁ SEPIA – Complaints from cold, laundry work, alcohol, tobacco, wetting before and during menses, after eating. Itching not relieved by scratching; is apt to change into burning,
Worse – evening, washing, left side, after sweat.
Better – exercise, pressure, warmth of bed, hot application.
⦁ CAULOPHYLLUM – Complaints from
Worse – open air, by coffee
Better – emission of flatus
⦁ CALCAREA CARB – Complaints from defective assimilation, imperfect ossification, suppressed sweat, cold moist wind, over lifting. Unhealthy skin, readily ulcerated.
Worse – cold air, wet weather, cold water, from washing in morning.
Better – lying on painful side

Freckles are clusters of concentrated melaninized cells which are most easily visible on people with a fair complexion. Freckles do not have an increased number of the melanin-producing cells, or melanocytes, but instead have melanocytes that overproduce melanin granules (melanosomes) changing the coloration of the outer skin cells (keratinocytes).
ETIOLOGY
Inheritance - Autosomal dominant genodermatosis, seen in red haired, and fair individual.
The formation of freckles is caused by exposure to sunlight. 
Pathology - Number of melanocytes is normal, but they produce more melanosomes.
CLINICAL FEATURES
1. Lesions are multiple, ill - defined brown macules, which become darker on sun exposure.
2. Individual macule may show variegation in skin color.
3. Photo - exposed area (face, dorsolateral aspect of forearms, hands and V of neck ).

FRECKLE


1. ANT TART – Complaints from anger, vexation, smallpox, vaccination, damp, debility. Reddish itching all over the body.
Worse – damp, cold weather, lying down at night, warmth of room.
Better – cold open air, sitting upright, expectoration, lying on right side.
2 CALCAREA CARB - Complaints from defective assimilation, imperfect ossification, suppressed sweat, cold moist wind, over lifting.
Unhealthy skin, readily ulcerated, warts on face and hands. Nettle rash better on cold air.
Worse – cold air, wet weather, cold water, from washing in morning.
Better – lying on painful side.
3. LYCOPODIUM – Complaints from fright, anger, mortification, or vexation with reserved displeasure Worse – 4 – 8 p.m., right side, from heat, warm air.
Better – warm food and drinks, uncovering the head, open air.
4.SULPHUR – Complaints from alcohol, sun’s heat, suppression of skin diseases, over exertion. Dry, scaly, unhealthy skin, every little injury suppurates. Itching, burning, worse scratching and washing.
Worse – Standing, at rest, washing, warmth of bed and changeable weather.
Better – Open air, motion, lying on right side and sweating.

A corn (or clavus, plural clavi or clavuses) is a distinctively shaped callus of dead skin that usually occurs on thin or glabrous (hairless and smooth) skin surfaces, especially on the dorsal surface of toes or fingers. They can sometimes occur on the thicker skin of the palms or bottom of the feet. The scientific name for a corn is heloma (plural helomata). A hard corn is called a heloma durum, while a soft corn is called a heloma mole. Corns form when the pressure point against the skin traces an elliptical or semi-elliptical path during the rubbing motion, the center of which is at the point of pressure, gradually widening. Signs and symptom
The hard part at the center of the corn resembles a barley seed, that is like a funnel with a broad raised top and a pointed bottom. Because of their shape, corns intensify the pressure at the tip and can cause deep tissue damage and ulceration. Hard corns are especially problematic for people with insensitive skin due to damaged nerves (e.g., in people with diabetes mellitus). The location of soft corns tends to differ from that of hard corns. Hard corns occur on dry, flat surfaces of skin. Soft corns (frequently found between adjacent toes) stay moist, keeping the surrounding skin soft. The corn's center is not soft, however, but indurated.
Diagnosis
A skin biopsy.
Imaging studies to detect any underlying bony abnormalities that causes abnormal pressure on overlying skin.

CORN THERAPEUTICS


⦁ NITRIC ACID – Complaints from long lasting anxiety, overexertion of body and mind. Often useful for growth that have a horny wall surrounding a central depression .  Presence of corns with splinter-like or sticking pains.
Worse – evening, night, cold climate
Better - riding, carriage
⦁ SILICEA – Complaints from vaccination, suppressed foot sweat, exposure to draught air. Soft corns between the toes may be sore and painful. Patients may also feel burning or tearing pain in these corns. Corns between toes that tend to suppurate . Excessive sweat with an offensive odour may be present on the foot where the corn is located.
Worse – new moon, cold, during menses, from washing and uncovering.
Better –warmth, wrapping up the head and in summer.
⦁ ANTIMONIUM CRUDDUM – Complaints from disappointed love, cold bathing, alcohol, fat, fruits, suppressed eruptions, extremes of heat and cold. There is presence of large, horny corns on feet which may or may not be inflamed. Corns are very tender. Pain is felt in the corns while walking.
Worse – evening, heat, acids, water, washing
Better – open air, during rest, moist warmth.
⦁ THUJA OCCIDENTALIS – Complaints from suppressed gonorrhoea, vaccination, tea, coffee, sexual excess, sunstroke. Perspiration sweetish and strong. Dry akin with brown spots. Eruption only on covered parts; worse after scratching. Very sensitive to touch.
Worse – night, 3 p.m. and 3 a.m., from cold, damp air, cold water, fat coffee, vaccination, tobacco, touch.
Better – open air, warmth, movement, pressure, rubbing and scratching.
⦁ ARNICA – complaints from bad effect of mechanical injury, fall, blow, concussion, contusion, fright and anger. Itching, burning of the eruption. Symmetry in distribution.
Worse – least touch, motion, rest in damp cold weather.
Better – lying down

(Nettle rash, Wheals, Hives ) This is a transient localised or generalised eruption with swelling of the skin characterised by formation of wheals or hives due to endogenous or exogenous allergen.These may develop out of various immunologic or non - immunologic stimuli.
In some chronic cases autoantibodies are produced against mast cells epitopes with liberation of histamine.
Aetiology
1. Physical agents : Cold, Trauma, Stings.
2. Drugs : Liver extract, Penicillin, Serum, NSAID and various others.
3. Food : Shellfish, crabs, eggs, milk etc.
4. Parasitic inflammation by :Ascaris, giardia, lice, fleas etc.
5. Complement mediated - Serum sickness, blood transfusion reaction, necrotising vasculitis, etc.
6. Psychogenic causes
7. Idiopathic.
Types Physical urticaria
Clinical Features
The eruptions appear as raised wheals or hives surrounded by a zone or erythema.
The wheals vary in size and may blend together.
The lesions are extremely itchy.
Sometimes there may be involvement of deeper vessels resulting in swelling of the skin which is called angioneurotic edema or Giant urticaria.
This swelling may involve the mucous surface
When urticaria persists for more than 6 months its known as chronic urticaria.
The eruptions appear as raised wheals or hives surrounding a zone or erythema. The wheals by may show eosinophilia, ova, parasite or cyst together. They vary in sizes and may blend morphology varies from minutes to hours formation of various geographic bizarre are extremely patterns.
URTICARIA 1. ARSENIUM ALBUM - complaints get after midnight, in humid and rainy weather, and on consuming cold food and drinks. Excessive itching and swelling on the affected area. Dry and scaly skin eruptions, which worsen on scratching and in cold weather.
Urticaria associated with a lot of burning and restlessness.
Worse – wet weather, after midnight, from cold, seashore.
Better - heat, warm drinks and with warmth in general.
2. BOVISTA - Urticaria on excitement with rheumatic lameness, palpitations and diarrhoea. Urticaria covers nearly the whole body from exertion. Itching on getting warm, intense itching at the tip of coccyx, scratches until it bleeds, still there is no relief. Urticaria on waking up in the morning, worse from bathing.
Worse - on waking up in the morning and after bathing.
Better - after meals.
3. APIS MELLIFICA – Erysipelas, with sensitiveness and swelling, rosy hue.
1. PSORINUM – It is especially used to treat eruptions that have a foul smell. Unbearable itching.
Worse - on drinking coffee, with changes in weather, and from cold.
Better - wearing warm clothing, in summers and with warmth in general.
2. SULPHUR – Complaints from alcohol, sun’s heat, suppression of skin diseases, over exertion. Dry, scaly, unhealthy skin, every little injury suppurates. Itching, burning, worse scratching and washing. Tetters of a greenish yellow colour with itching.
Worse – Standing, at rest, washing, warmth of bed and changeable weather.
Better – Open air, motion, lying on right side and sweating.
3. NITRIC ACID – Complaints from long lasting anxiety, overexertion of body and mind.
Worse – evening, night, cold climate
Better - riding, carriage.
4. RHUS TOX – Complaints from spraining and straining, over lifting, from wetting, summer bathing in lake or river, getting wet when heated. Red, swollen, itching intense. Erysipelas vesicular eruptions, vesicles are yellow, from left to right, with much swelling,
inflammation, burning, itching and stinging erysipelatous and edematous.
Worse – during sleep, cold, wet rainy weather and after rain, during rest
Better – warmth, dry weather, motion, walking, rubbing, warm application.
1. GENETIC PREDISPOSITION - When both parents are affected by AD, >80% of their children manifest the disease. When only one parent is affected, the prevalence drops to slightly over 50%.
2. IMMUNOLOGICAL CHANGES – Patients with AD may display a variety of immunoregulatory abnormalities, including increased IgE synthesis; increased serum IgE levels; and impaired, delayed-type hypersensitivity reactions. Abnormalities of lymphocytes.

EPIDEMIOLOGY

1. Seen in 3% of all infants.
2. Begins between 3 and 6 months of age.
3. Increased exposure to pollutants.
4. Increase exposure to indoor allergens
5. Decline in breast feeling.
Type – I hypersensitivity reaction occurring as a result of the release of vasoactive substance from both mast cells and basophilis. IgE in AD shows that epidermal Langerhans cells possess high affinity IgE receptors through which an eczema – like reaction could be mediated.
The infantile phase begins after the age of 3 months. It is characterized by weeping inflammatory patches and crusted plaques on the face, neck, and extensor surfaces. Intense itchy papules and vesicles, which soon becomes exudative.
The childhood phase characterized by dry, leathery and extremely itchy plaques. Mainly on the elbow and knee flexor.
The adult phase characterized by intensely itchy, lichenified plaques. Cubital and popliteal fossae and sometimes the neck. Many of the cutaneous findings in affected patients, such as Lichenification, are secondary to rubbing and scratching.
Asymptomatic
Begins as cradle cap, usually at birth.
May involve other seborrheic area.
Self – limiting.
1. SCALP – Dandruff usually earliest and only manifestation of SD in most. Some patients develop perifollicular redness and scaling initially localized, then diffuse.
Associatedretroauricular erythema and scaling, sometimes crusted fissures develop.
2. FACE – Erythema and scaling, occur usually in association with involvement of the scalp. It may be triggered by stress and photoexposure.
Distribution – it involves medial part of eyebrows, glabella and nasolabial folds.
Association – usually associated with scalp involvement. Squamous blepharitis is common. Manifests as erythema, scaling and yellow crusts on lid margin.
3. TRUNK - Nonexudative, scaly annular and circinate lesions with follicular papules surmounted with greasy scales.
Petaloid pattern
Pityriasiform pattern.
Seborrheic folliculitis.

POINT OF DIAGNOSIS


1. Folliculocentric papules surmounted with typical yellow, greasy scales.
2. It has a typical distribution.
It is a papulosquamous disorder that may affect the skin, scalp, nails, and mucous membranes. It is flat topped inflammatory erythematous or purplish papules showing a criss – cross appearance of the surface often seen on the flexor surface of the skin with symmetric distribution along with lacy lesions of buccal mucesa. The skin lesions may occur anywhere but have a predilection for

ETIOLOGY


1. Nervous and Mental tension
2. Trauma

PATHOLOGY


At the epidermo – dermal junction band – like infiltration of melanophage, histiocyte is seen . At the same site immunoglobulin mainly IgM deposits are seen.

SITE


1. Lesions are most frequently seen on extremities and lower back.
2. Lesions may appear at the sites of trauma.
3. Lesions may appear on wrists, shins and genitalia.

1. THUJA OCCIDENTALIS – Complaints from suppressed gonorrhea, vaccination, tea, coffee, sexual excess, sunstroke.Flat black warts, large seedy, pedunculated; sometimes oozing moisture and bleeding readily. It is helpful for treating wart arising on any part of body, with a little stalk called fig – warts, tubular warts, flat warts. Dry skin, warts are sensitive to touch. Warts especially on left side of the body and on covered parts only. Unhealthy skin, offensive sweating leaves yellow stain. Patient is very sensitive to cold weather.
Worse – night, 3 p.m. and 3 a.m., from cold, damp air, cold water, fat coffee, vaccination, tobacco, touch.
Better – open air, warmth, movement, pressure, rubbing and scratching.
2. NITRIC ACID – Complaints from long lasting anxiety, overexertion of body and mind. Warts are large, jagged or pedunculated and bleed easily.
Bleeding from warts may arise from touching or washing, warts that are sensitive to touch. It also helps to treat warts that are attended with itching. There may be moist, oozing, offensive and acrid discharge from them with typical pricking splinter like pain. Often useful for growth that have a horny wall surrounding a central depression or the more common plantar wart.
Worse – evening, night, cold climate
Better - riding, carriage.
3. CARBO ANIMALIS – Complaints from loss of fluids, lifting, strain, eating spoiled fish and decayed vegetables. Warts on hand and face of old people with a bluish colour. Of extremities.
Worse – shaving, loss of animal fluid, slightest touch.
Better – laying hand on affected part.
4. NATRUM MUR – Complaints from anger, grief, vexation, excessive use of salt, bread, quinine, fright, loss of vital fluid, sexual excess. Greasy skin . Warts on palms of hands. Chaps of herpetic eruption < flexures or about knuckles.
Worse – music, warm room, lying down, at sea shore, mental exertion, heat, talking.
Better – open air, cold bathing, lying on right side.
5. PHOSPHORIC ACID – Complaints from bad news, grief, chagrin, home sickness, disappointed love, loss of vital fluid, sexual excess.
Worse – mental affections, loss of vital fluid, self-abuse, sexual excess Better – sitting, standing and warmth of bed.
6. SILICEA – Complaints from vaccination, suppressed foot sweat, draught air. Unhealthy skin. Dry finger tips. Eruption itch only during daytime and in the evening.
Worse – cold, during menses, from washing and uncovering.
Better - warmth, wrapping up the head and in summer.
It is a disorder of pilosebaceous complex which predominantly affects the peripubertal population and clinically manifests as comedones (open/closed), papules, nodules, pustules and cysts and heals with scars. There is excessive secretion of sebum by which obstructing horny plugs (comedones) develop associated with inflammation of the pilosebaceous duct.

Etiology:

1. Androgenic influence - increased sebum secretion (due to increased end organ sensitivity to androgens)
2. Oil acne - Continuous use of lubricating oils, develop acne like lesion on the sites of contact. Cosmetics containing mineral oils may also produce acne.
3. Excoriated acne – after continuous injury of acne by nails particularly in young women, infection papules, crustification and scarificationdevelop.

CLINICAL FEATURES

1. Skin is very much greasy due to excessive sebum secretion.
2. Comedones are seen on the hair follicles.
3. When pigmentation occurs they are called as black comedones, which are elevated papules.
4. In white comedones there is absence of keratin plugs, these can be extracted by nails.
1. NITRIC ACID – Complaints from long lasting anxiety, overexertion of body and mind. Often useful for growth that have a horny wall surrounding a central depression . Presence of corns with splinter-like or sticking pains.
Worse – evening, night, cold climate
Better - riding, carriage
2. SILICEA – Complaints from vaccination, suppressed foot sweat, exposure to draught air. Soft corns between the toes may be sore and painful. Patients may also feel burning or tearing pain in these corns. Corns between toes that tend to suppurate . Excessive sweat with an offensive odour may be present on the foot where the corn is located.
Worse – new moon, cold, during menses, from washing and uncovering.
Better –warmth, wrapping up the head and in summer.
3. ANTIMONIUM CRUDDUM – Complaints from disappointed love, cold bathing, alcohol, fat, fruits, suppressed eruptions, extremes of heat and cold. There is presence of large, horny corns on feet which may or may not be inflamed. Corns are very tender. Pain is felt in the corns while walking.
Worse – evening, heat, acids, water, washing
Better – open air, during rest, moist warmth.
4. THUJA OCCIDENTALIS – Complaints from suppressed gonorrhoea, vaccination, tea, coffee, sexual excess, sunstroke. Perspiration sweetish and strong. Dry akin with brown spots. Eruption only on covered parts; worse after scratching. Very sensitive to touch.
Worse – night, 3 p.m. and 3 a.m., from cold, damp air, cold water, fat coffee, vaccination, tobacco, touch.
Better – open air, warmth, movement, pressure, rubbing and scratching.
5. ARNICA – complaints from bad effect of mechanical injury, fall, blow, concussion, contusion, fright and anger. Itching, burning of the eruption. Symmetry in distribution.
Worse – least touch, motion, rest in damp cold weather.
Better – lying down.
1. Burrow - It is a serpentine tunnel made by scabies mite in stratum corneum. The open end of the tunnel has a papule.
2. Comedones – It is a tiny plug present at opening of hair follicle formed by keratin and sebum. It is of two types: Open comedone (black head) and Closed comedone (white head).
3. Milia – It is a tiny superficial cyst with epidermal lining. Milia are seen on face at periorbital. They are small, firm, white papules filled with keratin.
4. Telengiectasia – It is visible dilatation of capillaries of skin which blanch on pressure.
5. Poikiloderma – It is a combination of reticulate telangiectasia, pigmentary change and atrophy.
6. Purpura – Extravasation of red blood cells from cutaneous vessels in skin and mucous membrane.
7. Infarct – Area of cutaneous necrosis – tender, irregularly shaped dusky red grey macule or firm plague.