Dermatology Class Notes

Dermatological Pathology Leslie Solomonian, BSc., ND BAS 206 – Pathology Module 2

Review of Normal Physiology  Diagram of normal skin Skin Functions: Protection – barrier from UV Absorption Temp regulation/thermoregulation Antibacterial properties IgA Sensation

Review of Normal Physiology 

Layers from the TOP 1) Epidermis  Basal cell layer – from bottom they multiply and migrate up  Keratinocytes – top – dead layer 2) Dermis  Active skin function  Sweat glands, hair follicles, sebaceous glands (appendages)  Nerve endings, blood vessels  Damage more serious to dermis 3) Adipose  Insulation/padding

Naturopathic Concepts of Dermatology  Skin is the manifestation of other conditions, for example gut function Asian med: LI/LU manifests on skin & Wei Qi Herings Law: cure starts from the inside and moves out If skin is unhealthy: elimination backed up OR skin is taking on too much Look at DIET – 1st thing to do for lesions is elimination diet

Terminology

– Papule – less than 5mm

• Change because of initial lesion (e.g. scratching) • Scale – imperfect cornification

– Nodule – greater than 5mm

• Lichenification –

• Flat lesions – Macule – colour e.g. freckle

• Elevated solid lesions bump

domed

– Plaque – elevated, flat top

• Elevated fluid-filled lesions – Vesicle – fluid filled blister

skin

markings (due to scratching usually)

• Excoriation –

breakage in

epidermis

less than 5mm

– Bulla – fluid filled blister greater than 5mm

– Pustule – pus instead of fluid

• Hyperkeratosis/Acan thosis – hyperkeratosis increased keratin in s. corneum and acanthosis=spinosum.

Disorders of Hair Follicles • Acne vulgaris • Acne rosacea • Folliculitis – inflammation of the follicle. Evolves to boils, cysts, cellulitis. Usually staph aureus. • See the next few slides for summaries

Acne vulgaris • There is a danger zone on the face: drains into the sinuses  bloodstream. Usually not harmful • Open comedomes: blackheads – sebum is oxidized and turns black – Non-inflammatory – Follicular papules with black keratin plug

• Closed comedomes: whiteheads – Inflammatory – Trapped keratin plug  inflammation  erythema, papules, nodules, pustules

Acne vulgaris If you damage the follicle it has the tendency to be affected again (why squeezing is bad) Naturopathic Diet: Vitamin A very important (watch toxicity & pregnancy), topical antimicrobials (tee tree oil), EFA’s (anti-inflamm), Se (free radical scavenging) Stress Decreases the immune system & digestive function

Summary: •Acne vulgaris is a common skin disorder •Chronic disease of sebaceous follicle, primarily affecting face, chest, and back •Onset typically occurs at puberty because of increased sebum production triggered by increased androgen levels •Inflammation is due in part to over-proliferation of Propionibacterium acnes, an anaerobic Gram-positive organism that resides in follicles •Classified on basis of type of lesions (comedonal noninflammatory vs inflammatory) and number of lesions present

Acne vulgaris Androgens Increased sebum production

Hyperkeratinization of follicular canal

Propionibacterium acnes

Keratin plug formation Follicular obstruction

FFA release Inflammation Closed comedome

Open comedome

Acne Rosacea •Chronic facial skin disorder most commonly seen in individuals between the ages of 30 and 60 years •More common in women than men, but often more severe in men •Features include erythema, telangiectasia, papules, pustules, ocular lesions (conjunctivitis), and edema of midfacial skin •Frequently causes significant psychologic distress •Disease is progressive, commonly with periods of exacerbation and remission •Originally termed 'acne rosacea' because of the similarity in appearance to acne vulgaris •Often associated with easy flushing and blushing •Eye involvement is common •Rhinophyma Common causes •Cause is largely unknown •Theories suggest underlying vasomotor instability, or infestation with the skin mite Demodex follicularum, but there is little evidence for either Contributory or predisposing factors •Genetic predisposition: 40% of sufferers have a family member with the disease •In sensitive individuals: sun exposure, stress, hot and cold weather, alcohol, spicy foods, exercise, wind, hot baths, hot drinks, skin care products, certain drugs •Topical or oral steroid treatment

Folliculitis • • • • • • •

Inflammation of a hair follicle caused by bacterial and viral infections, chemical irritation, or physical injury Lesions generally consist of asymptomatic erythematous perifolicular papules or pustules, but may be painful or itchy pustules surrounded by erythema with a central hair present The scalp, face, legs (thighs), inguinal area, axilla, and trunk are most often affected May be superficial or deep in the hair follicle; if deep may cause scarring Usually asymptomatic, but may be itchy Postinflammatory hyper- or hypopigmentation may occur around resolving lesions Scarring may result from scratching

Bullous Diseases • Pemphigus vulgaris • Bullous pemphigoid

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Pemphigus vulgaris Autoimmune – – – – –

IgG to intercellular adhesion molecules Desmosomes – connect epithelial cells FRAGILE blisters. Risk of infection Middle age and older Involves mucosa and skin on scalp, face, axilla, groin, trunk and points of pressure.

Lysis of epithelial intercellular adhesions Fragile suprabasal blister Rupture of blisters Erosions and crusting

Bullous Pemphigoid • Elderly • Autoimmune – IgG to basement membrane (hemidesmosomes – connect basement mem & basal cells). Basal cells lift off dermis. More tesnse bullous – less fragile – Occur on inner aspects of the thighs, flexor surfaces of the forearms, axillae, groin, and lower abdomen Destruction of connection between dermis and epidermis Tense subepidermal blister

Urticaria (hives)  IgE associated with allergic reactions (hypersensitivity) Mast cells (high # near small blood vessels in skin) contain histamines – creates itchiness Spongiosis (WHEAL) is primary lesion

Antigen sensitization (IgE) Mast cell degranulation – releases histamines Dermal vascular hyperpermeability Dermal edema and pruritis Papules  Plaques (Wheals)

Urticaria • • • • • • •

Urticaria is due to localized capillary vasodilatation, followed by extravasation of protein-rich fluid into the surrounding tissues It is characterized by the appearance of a transient, migratory pruritic rash with raised, round, oval, or serpiginous patches that blanch on pressure (wheals) Lesions often have a pale center and are surrounded by an area of erythema Lesions may vary in diameter from a few millimeters to the size of a hand or more and may be confluent Most common on trunk and limbs, but may affect any epidermal or mucosal surface May be most prominent in areas of chafing (e.g. waistband or bra strap area) Angioedema is due to the same process occurring at deeper levels. It presents as a poorly-defined swelling that may be painful rather than pruritic and often occurs on the face

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GUT

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FOOD

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STRESS

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TCM  wind-heat; wind-damp; ST/SI-heat

Inflammatory Conditions • • • •

Dermatitis (eczema) Psoriasis Pityriasis rosea Lichen Planus

Eczematous Dermatitis

atopic eczema

Atopic is IgE related – priming immune system (hygiene hypothesis). Cascades and dehydrates. Associated with allergies, Middle ear infections, asthma • • • • •

Allergic contact Atopic Drug-related Photoeczematous Primary irritant (immediate)

•Atopic dermatitis is an inflammatory skin disorder •Characterized by erythema, edema, intense pruritus, exudation, crusting, xerosis, and lichenification •Many patients have a family history of allergy or a personal history of asthma, hay fever, or allergic rhinitis •This is the first of the allergic diathesis to present. The child with atopic dermatitis may go on to develop allergic asthma and allergic rhinitis

Antigen stimulation Inflammatory infiltrate into dermis and epidermis Fluid separates keratinocytes Dermal edema and vesicle formation Hyperkeratosis and acanthosis Possible lichenification and excoriation

Atopic Dermatitis • Viewed as a hypersensitivity reaction • Skin tends to be dry, hyperkeratotic and easily lichenified • Risk factors: – – – – – – –

Not breastfed Urban environment Hygiene Diet Poor digestive health Histamine release* “Emotional tension”

• Multifactorial

Psoriasis

• intrinsic (genetics) and extrinsic (environment) factors associated with it

T-cell infiltrate into epidermis

Secretion of cytokines and growth factors Increased keratinocyte replication Higher than squamas cell carcinoma! (except no mutations, no dysplasia/anaplasia)

Acanthosis and extensive hyperkeratosis

Thinned stratum granulosum Stratum cornium – dead top layer Granulosum is next – if thin, you expose dermis more readily = PINPOINT bleeding = Auspitz sign

“Auspitz sign”

*Silvery scales on extensor surfaces. Plaques of dead skin cells

Psoriasis • What stimulates the T-cells???? • ALWAYS ASK WHY!!! – find etiology! •Autoimmune condition – some sort of Ag attracting T-cells •Associated with gut conditions and chrone’s – when reacting to one part of the body they may also react to other parts of the body •Pathogenic bacteria in the gut – tend to break down proteins and produce toxic byproducts •These toxic metabolites may leave, go into bloodstream and INC cyclic GMP •Cyclic GMP (self proliferation) to AMP (maturation and proliferaction decrease) ratio increases = increased proliferation (may want to down reg cyclic GMP) •Also people with psoriasis have decrease in vitamin D – sunlight helps with tx

Pityriasis Rosea • Initial lesion is “herald patch”, which is pink-salmon coloured patch/plaque with slightly raised margin (on trunk, neck, proximal extremeties) •Cause unknown, resolves spontaneously in 6-8 weeks •Eruptions last hours/days/weeks of oval – annular lesions •Up to 100 lesions, 4-5 mm in diameter •Symmetrical lesions •Puritis occasionally •Symptoms mimicking viral infection

Lichen Planus • "Pruritic, purple, polygonal papules" •resolves spontaneously 1 to 2 years after onset, often leaving zones of postinflammatory hyperpigmentation •Oral lesions may persist for years. Malignant degeneration has been noted to occur in chronic mucosal and paramucosal lesions •Cutaneous lesions consist of itchy, violaceous, flattopped papules that may coalesce focally to form plaques. These papules are often highlighted by white dots or lines called Wickham striae, representing the clinical correlates of zones of hypergranulosis that typify lesions histologically. •Multiple lesions are characteristic and are symmetrically distributed, particularly on the extremities, often about the wrists and elbows, and on the glans penis •In 70% of cases, oral lesions are present as white, reticulated, or netlike areas involving the mucosa •It is plausible that lesions are caused by cell-mediated immune reactions secondary to release of antigens at the levels of the basal cell layer and the dermoepidermal junction. •characterized histologically by a dense, continuous infiltrate of lymphocytes along the dermoepidermal junction

Inflammatory Reactions •

Drug eruptions – adverse reactions (Common). Hypersensitivity. Unintended

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Erythema multiforme – hypersensitivity rxn

response to meds

– Many forms – can be pustular, macular, bullous – Tends to have characteristic “target lesions” – Target lesions caused by the centrifugal spread of red maculopapules with a purpuric, vesicular, or papular center – Symmetric lesions – 1-3cm in diameter – Mainly on hands, feet, and extensor surface of forearms and legs – In severe form, can be on the trunk, in the oral cavity, nasopharynx, conjunctiva, and urethra – Urticarial papules, vesicles, and bullae in severe disease – Individual lesions heal without scarring in 1-2 weeks – Due to CD8 cytotoxic T cells reacting with antigens near basal cell layer of skin or mucosa

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Erythema nodosum (next slide)

Erythema nodosum • • • • • • • • •

Acute tender, erythematous, nodular skin eruptions Fever, arthralgia, and malaise usually precede the tender nodules Nodules erupt without ulceration normally on anterior aspects of legs Other sites include the backs of legs, thighs, neck, face, and forearms Usually between five and 10 nodules, each up to 4 inches (101.6mm) in diameter Nodules may become fluctuant, but they never suppurate Slow regression over several weeks to resemble contusions The nodules usually disappear within 6 weeks, but they may recur Signs of the underlying disease may be present, e.g. respiratory or gastrointestinal illness

• inflammatory reaction in the subcutaneous fat

Pigmentary Conditions Moles and freckles are different. Moles – increase in prolif of melanocyte. Freckle – increase melanin

• Vitiligo – autoimmune – melanocytes destroyed by the body in epidermis. Common

disorder characterized by partial or complete loss of pigment-producing melanocytes within the epidermis – – – –

Can be developed at the site of trauma (koebnerization). Asymptomatic, flat, well-demarcated macules and patches of pigment loss; their size varies from few to many centimeters. Vitiligo often involves the hands and wrists; axillae; and perioral, periorbital, and anogenital skin Albinisim is different – enzyme missing in melanocyte (all over the body) – melanocytes present but not working = NO MELANIN Associated with other autoimmune conitions More frequent in darker individuals. May show up in lighter individuals after tanning

• Lentigo – one long flat line along basement membrane. Melanocytes proliferate move along this membrane. Forms macule. The essential histologic feature of the lentigo is linear (non-nested) melanocytic hyperplasia (hyperplasia restricted to the cell layer immediately above the basement membrane) that produces a hyperpigmented basal cell layer*** – – – – –

benign localized hyperplasia of melanocytes occurring at all ages but often in infancy and childhood Unlike freckles, lentigines do not darken when they are exposed to sunlight Associated with age – solar lentigo (due to skin damage) – this is lentigo in older individuals after prolonged sun exposure Different than freckles due to increased proliferation of melanocytes small (5 to 10 mm across), oval, tan-brown patches (macule)

• Melasma – look up (next slide)

Melasma •

Melasma produces dark brown patches of pigmentation on sun-exposed areas, usually the face.

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Melasma tends to appear during pregnancy (mask of pregnancy) and in women who take oral contraceptives, although it can occur in anyone. The disorder is most common in sunny climates and in people of Latin or Asian origin.

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poorly defined, blotchy, tan-brown macules and patches involving the cheeks, temples, and forehead bilaterally. Sometimes people have the patches only

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on the sides of the face. Rarely, melasma appears on the forearms. The patches do not itch or hurt and are only of cosmetic significance. Melasma usually fades after pregnancy or when an oral contraceptive is discontinued. People with melasma can use sunscreens on the dark patches and avoid sun exposure to prevent the condition from getting worse. Skin-bleaching creams containing hydroquinone and retinoic acid can help lighten the dark patches. The pathogenesis of melasma appears to relate to functional alterations in melanocytes resulting in enhanced pigment transfer to basal keratinocytes or to dermal macrophages

Benign and Premalignant Lesions •

Common – usually not clinically relevant but psychological. Confused with malignancies.

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Seborrheic Keratosis Keratoacanthoma Verrucae – wart! Melanocytic Nevi Actinic Keratosis

Seborrheic Keratosis • •

Middle-age to older Spontaneous; trunk

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Exophytic neoplasm (exophytic = goes outward – large and dark) – Proliferation of basal cells – Hyperkeratosis  keratin-filled cysts and invaginations – may extend down into the dermis – Large and unsightly – Sometimes in people who have a neoplasma somewhere else in the body. Screen for cancer elsewhere

– Lesions may give the impression that they are "stuck on" and may be easily peeled off. Inspection with a hand lens will usually reveal small, round, porelike ostia impacted with keratin, a feature helpful in differentiating these pigmented lesions from melanomas. – round, flat, coinlike, waxy plaques that vary in diameter from millimeters to several centimeters – uniformly tan to dark brown and usually show a velvety to granular surface

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Keratoacanthoma

a rapidly developing neoplasm that clinically and histologically may mimic well-differentiated squamous cell carcinoma. Often it will heal spontaneously, without treatment! Men are more often affected than women, and lesions most frequently affect sun-exposed skin of whites older than age 50 years Originate in pilosebacious glands flesh-colored, dome-shaped nodules with a central, keratin-filled plug, imparting a craterlike topography predilection for facial skin, including the cheeks, nose, and ears, and the dorsa of the hands (sunlight exposed areas) There is growing belief that keratoacanthomas may represent a form of squamous cell carcinoma that regresses as a consequence of interactions with host tissues that fail to support inexorable growth Like most squamous cell carcinomas, the majority of keratoacanthomas have mutations in the p53 gene Pathophysiology: Both sunlight and chemical carcinogens have been implicated as pathologic factors in growth of the tumor. Trauma, human papilloma virus, genetic factors, and immunocompromised status also have been implicated as etiologic factors.

Verrucae • • • • • • •

caused by human papillomaviruses (60 types) – epithelial tumors HPV 16 linked to cancer May be single or multiple. May be malignant. Exist in outer epithelium, not deep enough to serve as antigens. Many types. Verruca vulgaris is the most common and is characterized by gray-white to tan, flat to convex, 0.1- to 1-cm papules with a rough, pebble-like surface Transmission of disease usually involves direct contact between individuals or autoinoculation. Verrucae are generally self-limited, regressing spontaneously within 6 months to 2 years Histologic features common to verrucae include epidermal hyperplasia that is often undulant (wave-like) in character (so-called verrucous or papillomatous epidermal hyperplasia) and cytoplasmic vacuolization (koilocytosis) that preferentially involves the more superficial epidermal layers, producing halos of pallor surrounding infected nuclei.

Melanocytic Nevi = MOLES • Benign melanocytic neoplasm – Congenital – Blue – Spitz – Halo – Dysplastic

Aggregation of melanocytes at dermoepidermal junction Growth into dermis “Maturation”

Elevation above epidermis Distinguises between malignancy. Hair = functional (mature) cells

All similar in that there is an aggregation of melanocytes – different shapes/configurations. It is CONTROLLED growth – just hyperplastic Some people have sporatic nevi or Familial nevi (this group is more predisposed to dysplasia). Increased vulnerability to UV (both types)

Melanocytic Nevi •

tan to brown, uniformly pigmented, small (usually <6 mm across), solid regions of relatively flat (macules) to elevated skin (papules) with well-defined, rounded borders • Melanocytic nevi are initially formed by melanocytes that have been transformed from highly dendritic single cells normally interspersed among basal keratinocytes to round cells that grow in aggregates, or "nests," along the dermoepidermal junction • Progressive growth of nevus cells from the dermoepidermal junction into the underlying dermis is accompanied by a process termed maturation. Whereas less mature, more superficial nevus cells are larger, tend to produce melanin, and grow in nests, more mature, deeper nevus cells are smaller, produce little or no pigment, and grow in cords. • This sequence of maturation of individual nevus cells is of diagnostic importance in distinguishing some benign nevi from melanomas, which usually show little or no maturation.

Actinic Keratosis • • • •

Premalignant dysplasia – excessive sun exposure. Actinic = solar usually less than 1 cm in diameter; are tan-brown, red, or skin-colored; and have a rough, sandpaper-like consistency. lesions may produce so much keratin that a "cutaneous horn" develops Generally referred. Nuclei of keratinocytes retained (abnormal)

Excessive sun exposure Basal cell hyperplasia

Fibroblast damage (dermal layer)

Parakeratosis (abnormal formation of horn cells, Persistance of nuclei, incomplete formation of keratin = observed as scaling)

Atypia and dyskeratosis Abnormal fiber synthesis

Thickened stratum corneum (keratin layer of the skin)

Thickened dermis

Actinic Keratosis

Leukoplakia • “White plaque” – Atypia of squamous cells, hyperkeratosis

– WHO definition: a white patch or plaque that cannot be scraped off and cannot be characterized clinically or pathologically as any other disease – Considered precancerous until proven otherwise – Risks  men 40-70yoa; tobacco use

Malignant Lesions •

Skin is a common place for cancers. It’s what we face the world with. 1st and foremost interaction!

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Squamous cell carcinoma Basal cell carcinoma Malignant melanoma Kaposi’s sarcoma

Squamous Cell Carcinoma •

Generally small and removable; low invasive potential

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Dysplasia/anaplasia Lack of control – irregular relplication Lack of differentiation of cells Grows quickly. Asymmetrical. Caused by: sun, industrial chemicals, old scars and trauma, tobacco (in the mouth) COMPARE THIS WITH BASAL CARCINOMA – cells, where??

In situ (in one place – contained) carcinoma In epidermal layer and not invading dermis Hyperkeratosis and ulceration Invasion through basement membrane

Squamous cell carcinoma • The age-adjusted incidence among Caucasians is 1-1.5/1000 per year in the US • Clinical presentation varies from scaly erythematous plaques or cutaneous horn to crusted ulcerated lesions • Unlike basal cell carcinomas, squamous cell carcinomas are associated with a substantial risk of metastasis • Second most common type of skin cancer • Chronic sun exposure is the strongest environmental risk factor • Precancerous lesions associated with sun damage are strong risk factors • Histology shows full-thickness pleomorphic, atypical keratinocytes in the epidermis. Invasive squamous cell carcinomas also show dermal invasion Basal cell carcinoma • Most common malignant skin tumor arising from the basal cells of the epidermis • There are four main subtypes: nodular, superficial, pigmented, and aggressive growth type (morpheaform, infiltrative, or sclerosing) • These subtypes vary with respect to macroscopic appearance (and thus presentation), histology, and biologic aggressiveness • Most common presentation is the nodular type, with a papule that has a pearly, shiny border, and surface telangiectasia. The lesion may ulcerate in the center, thus causing the characteristic bleeding and scabbing lesion that heals and recurs • Morpheaform basal cell carcinoma is the most biologically aggressive • They rarely metastasize: their malignant potential lies in their ability to invade and destroy local tissues, such as bone and brain • Main causative factor is accumulative exposure to sunlight • 85% occur on the face and neck, as these areas are most exposed to the sun • Treatment depends on the site and size of the tumor, tumor margins, and histology

Malignant Melanoma

Malignant Melanoma • • • • •

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SUN! Prevalence is increasing Nevi are predisposing. most important clinical sign of the disease is change in color, size, or shape in a pigmented lesion. Usually greater than 10mm variations in pigmentation, appearing in shades of black, brown, red, dark blue, and gray clinical warning signs of melanoma are (1) enlargement of a pre-existing mole, (2) itching or pain in a pre-existing mole, (3) development of a new pigmented lesion during adult life, (4) irregularity of the borders of a pigmented lesion, and (5) variegation of color within a pigmented lesion. Radial growth (horizontal)  vertical growth (into deeper layers) – no maturation  metastasis (increases with vertical growth due to blood vessels and movement throughout the body) The nature and extent of the vertical growth phase determine the biologic behavior of malignant melanoma Increased mitoses

Kaposi’s Sarcoma • Cancer that causes multiple flat, pink, brown or purple patches or bumps on the skin • three stages can be identified: patch, plaque, and nodule • Caused by human herpes virus (HHV) type 8 • Occurs in several distinct groups of pepople, acts differently in each group – – – – –

Older men Mediterranean Jewish People with AIDS Immunosuppressants after transplants Childern and young men from Africa

Vasculitis • Manifest on skin. Covered in CV system (inflammation of blood vessels) • Not tested here – familiarize yourself

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Hemangioma Spider angioma Telangiectasis Cherry angioma

Infectious Conditions • Viruses – needs a host & machinery – Herpes Zoster / Pox •

Acute infection with VZV (varicella zostar virus) causes chickenpox; reactivation of latent VZV causes shingles

• VZV infects neurons and/or satellite cells around neurons in the dorsal root ganglia and may recur many years after the primary infection, causing shingles • vesicular lesions, pruritis and PAIN in shingles •

Painful, unilateral dermatomal erupation, common in thoracic region

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HPV Type 16 and 18 – best known and mostly studied Involved in cervical dysplasia So associated that HPV should be tested in pap smear! Looking at vaccinating all girls for this

– Human Papillomae (verrucae) – warts (epidermal hyperplasia). Manifests differently

• Bacteria – Impetigo, folliculitis, boils, cellulitis

• Fungi

– Ringworm (tinea), Candidiasis – yeast affects mucous membranes (ubuqitous, seen in HIV, diaper rash – likes warm, moist environment), tinea versicolour – due to a yeast, manifests differently –

Confined to stratum corneum

– Dermatophyte – all “tinea” (fingi that are skin loving – defined by where it occurs on the body) – Bacteria gets in and infects the area – leads to inflammation – Name based on area (e.g. capitis, pedis)

Herpes Simplex • •

80% have it! Manifest differently Viral infection of epithelium  inflammatory reaction of the epithelium (vesicles on an erythematous (inflammation - hyperemia) base)  dormancy in a nerve ganglion (moves to spine and can be transmitted by touch) If activated they are transmissible. • Herpes 1 AND 2 – can be transferred

• Aggravating factors: stress, sunlight, temperature changes, acidic foods, illness, lack of sleep, menses • •

Lysine controls the infection, Arginine increases infection (used in naturopathic tx – high lysine and low arg foods) Oregano – antiviral

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Treat the predisposition!

Herpes Simplex • 30-100% carrier rate; 20-40% recurrence rate • WHY THE DISCREPANCY? – Dormancy – Individual susceptibility (cancer, HIV positive) – Decreased immunitiy

Impetigo – superficial bacterial inflammation of the skin • Organism: staph aur. • Transmission: pus is infectious. Contains the bacteria, neutrophils and dead cells.

Neutrophilic infiltrate Superficial dermal inflammation

Pustule formation – goes to epidermis here Rupture of pustules Boils & folliculitis – affect hair follicle. Impetigo is the actual epidermis Homeopathic remedy: graphities – strongly associated with impetigo

Wet erosions “Honey-coloured crust”