Apocrine Glands Structure and Development

Apocrine Glands Development and Structure

• Apocrine units originate from the upper portion of hair follicles, not directly from the epidermis.
• Immature apocrine units are present over the entire surface of the human fetus, regressing before term.
• The straight excretory duct features a double layer of cuboidal epithelial cells and opens into the hair follicle.
• Coiled secretory glands are situated at the dermis-subcutaneous fat junction, lined by a single layer of varying columnar to cuboidal cells surrounded by myoepithelial cells.

Apocrine vs. Eccrine Glands

• Apocrine coils are more widely dilated compared to eccrine coils and exhibit deeper red staining in H&E sections, contrasted with the pale pink of eccrine sweat.
• Columnar cell apices project into the gland lumen, appearing extruded in histological cross-sections, indicative of decapitation secretion.

Secretion Mechanism and Composition

• Controversy exists regarding whether apocrine secretion occurs via merocrine, apocrine, or holocrine mechanisms.
• Apocrine secretions are partially understood, containing proteins, carbohydrates, ammonia, lipids, and iron, and typically appear milky white.
• Rarely, lipofuscin pigment can cause dark shades due to apocrine chromhidrosis.

Apocrine Sweat Characteristics

• Apocrine sweat is odorless until it interacts with skin bacteria, which then generates odor.
• Adrenergic innervation and circulating catecholamines stimulate apocrine secretion, with vasoactive intestinal polypeptide potentially playing a role.
• Although apocrine excretion is episodic, gland secretion itself is continuous.

Function and Distribution

• No known function for apocrine secretion in humans; however, it serves protective, sexual, and thermoregulatory functions in other species.
• Apocrine glands are generally confined to specific body regions: axillae, areolae, anogenital region, external auditory canal (ceruminous glands), and eyelids (glands of Moll).
• Prominent presence noted in the stroma of sebaceous nevus of Jadassohn.
• Apocrine glands become functional at puberty.

Embryogenesis of Hair Follicles

• Mesenchymal cells in the fetal dermis accumulate under the epidermis basal layer, facilitating the formation of hair follicles.
• Epidermal buds penetrate the dermis, leading to the development of follicles at an angle to the skin surface.
• Follicle bases enlarge, forming bulbs around mesenchymal cells, which harbor mesenchymal stem cells with potential hematopoietic capabilities.

Follicle Development and Function

• Upper and lower buds from the fetal follicle differentiate into the sebaceous gland and the attachment for arrector pili muscle, respectively.
• An additional epithelial bud above the sebaceous gland develops into the apocrine gland.
• The infundibular segment of the follicle is linked to the surface epidermis and consists of keratinocytes resembling those of the epidermis.

Hair Cycle Phases

• Hair follicles are structured with an upper infundibulum and isthmus that are permanent, while the inferior segment is replaced each growth cycle.
• Anagen phase (active growth) lasts 3–5 years on the scalp; 85%-90% of scalp hairs are typically in this phase.
• Catagen phase (involution) lasts about 2 weeks; telogen phase (rest) lasts 3–5 months.

Variability in Hair Growth

• Sites across the body show shorter anagen and longer telogen phases, resulting in shorter hairs.
• Anagen phase prolongation can lead to longer eyelashes in patients with AIDS.
• Hair follicles do not undergo synchronized hair shedding, unlike other mammals; follicles independently cycle through varying activity and rest stages.

Factors Influencing Hair Loss and Growth

• Telogen effluvium arises from early anagen release due to illness, surgery, or weight loss.
• Pregnancy often induces longer anagen retention, leading to noticeable hair loss post-delivery, as telogen hairs are released synchronously after childbirth.
• Chemotherapy disrupts hair matrix mitotic activity, predominantly affecting anagen hairs and resulting in sparse telogen hairs.

Hair Structure and Characteristics

• Anagen hair is characterized by a pigmented bulb; catagen hairs show many apoptotic cells in the outer root sheath; telogen club hairs have a shaggy appearance and a nonpigmented bulb.
• Hair shape varies: round hair in white individuals, oval in black, and triangular in uncombable hair due to the trichohyalin gene's influence.

Hair Color and Graying

• Hair color is determined by melanin levels; black hair contains larger melanosomes, while white hair has smaller aggregated melanosomes.
• Red hair is marked by spherical melanosomes; graying is linked to reduced melanocyte numbers and oxidative stress, causing melanocyte apoptosis.
• Genetic factors influence hair graying and polynomials in the androgen receptor gene contribute to male-pattern baldness; female-pattern hair loss genetics remain less understood.

Nail Structure and Function

• Nails aid in gripping small objects and offer protection to the fingertips, also serving a sensory function.
• Pacinian corpuscle-like structures are found in the nail bed of human fetuses but are harder to identify in adults.

Growth Rates

• Fingernails grow approximately 0.1 mm per day, needing around 4-6 months for complete replacement.
• Toenails grow slower, with the great toenail taking 12-18 months for full replacement.

Keratin Composition

• Nails contain a mixture of epidermal and hair-type keratin, with hair types being predominant.
• Nail isthmus keratinization is distinct; it contains keratin 10, which is absent in the nail bed.

Nail Pathology

• Brittle nails show widened intercellular spaces between keratinocytes upon electron microscopy examination.
• The nail bed is characterized by parallel rete ridges, unlike most skin which has rete pegs, leading to splinter hemorrhages from extravasated red blood cells.

Nail Anatomy

• The nail cuticle is comprised of keratinocytes from the proximal nail fold, while the nail plate is created by matrix keratinocytes.
• Endogenous pigments align with the lunula contour, whereas exogenous pigments follow the contour of the cuticle.

Nail Plate Formation

• The dorsal nail plate originates from the proximal matrix, and the ventral nail plate comes from the distal matrix with input from the nail bed.
• The location of a melanocytic lesion within the matrix can be identified by observed pigment in the dorsal or ventral nail plate.

Role and Characteristics of Mast Cells

• Critical in normal immune responses, immediate-type sensitivity, contact allergy, and fibrosis.
• Normal mast cells have a diameter of 6–12 microns, amphophilic cytoplasm, and a small round central nucleus, resembling fried eggs in histological sections.
• In telangiectasia macularis eruptiva perstans (TMEP mastocytosis), mast cells appear spindle-shaped, hyperchromatic, and resemble large, dark fibroblasts.
• Each mast cell contains up to 1000 granules, between 0.6–0.7 micron in diameter.
• Granules include coarse particulate, crystalline forms, and others with scrolls; they stain metachromatically with toluidine blue and methylene blue due to high heparin content.

Surface Markers and Subtypes

• Surface of mast cells hosts 100,000–500,000 glycoprotein receptor sites for immunoglobulin E (IgE).
• Mast cells are heterogeneous: type I (connective tissue mast cells) are located in the dermis and submucosa; type II (mucosal mast cells) are in the bowel and respiratory tract mucosa.

Chemical Components and Mediators

• Mast cell granules contain histamine, neutrophil chemotactic factor, eosinophil chemotactic factor of anaphylaxis, tryptase, kininogenase, and β-glucosaminidase.
• Slow-reacting substances of anaphylaxis (leukotrienes C4 and D4), leukotriene B4, platelet-activating factor, and prostaglandin D2 are generated after IgE-mediated release.

Staining and Detection

• Mast cells reliably stain with the Leder ASD–chloracetase esterase stain, useful even when granules have degranulated.
• In forensic medicine, fluorescent labeling of mast cells with antibodies to enzymes chymase and tryptase helps determine the timing of skin lesions post-death.
• Lesions from living subjects show an initial increase followed by a decline in mast cells, while postmortem lesions have few mast cells.

Environmental Response and Mastocytosis

• Environmental conditions affect cutaneous mast cells; dry environments increase mast cell count and histamine levels.
• In mastocytosis, abnormal proliferation and migration of mast cells lead to their accumulation in skin due to failure of apoptosis.
• The TUNEL method assesses apoptosis, showing decreased staining in mastocytomas, indicating impaired cell death.
• Proliferation of mast cells in mastocytosis is typically moderate.

Macules and Patches

• Macules are nonpalpable skin color changes, varying in size and shape (circular, oval, irregular).
• They may be distinct or fade into surrounding skin and can represent the whole lesion or part of an eruption.
• A patch refers to a macule that is 1 cm or larger, commonly seen in conditions like nevus flammeus and vitiligo.

Papules

• Papules are solid, raised lesions without visible fluid, measuring from pinhead size to 1 cm.
• They can take various shapes: acuminate, rounded, conical, flat-topped, or umbilicated.
• Papules can appear in multiple colors: white (milium), red (eczema), yellowish (xanthoma), black (melanoma).
• Typically located in the dermis, they may cluster around sweat ducts or hair follicles and vary in consistency (soft or firm).

Plaques and Nodules

• Plaques are broad papules or confluences of papules, measuring 1 cm or more, generally flat with possible central depression.
• Nodules are similar to papules but larger than 1 cm, often centered in the dermis or subcutaneous fat.

Tumors

• Tumors are larger masses (greater than 2 cm) that can be soft, firm, movable, or fixed, and can vary in shape.
• They can be elevated or deep-seated, with some being pedunculated, such as neurofibromas.

Wheals (Hives)

• Wheals are temporary, edematous platelet-like elevations that are usually pink to red, often surrounded by macular erythema.
• They can be discrete or merge, develop rapidly, and are the main feature of urticaria.

Vesicles and Bullae

• Vesicles are small, fluid-containing elevations under 1 cm that can be serous or blood-tinged.
• They may appear as distinct, grouped, or linear lesions and can arise from macules or papules.
• Bullae are larger than 1 cm, containing similar fluids as vesicles but present as rounded or irregular-shaped blisters.
• Nikolsky sign tests for blister formation, while Asboe-Hansen sign evaluates blister spreading on pressure.

Pustules

• Pustules are small elevations containing purulent material and can arise from papules or vesicles.
• Typically exhibit a white or yellow center with a red halo if hemorrhagic, indicating underlying inflammation.

Macules and Patches

• Macules are nonpalpable skin color changes, varying in size and shape (circular, oval, irregular).
• They may be distinct or fade into surrounding skin and can represent the whole lesion or part of an eruption.
• A patch refers to a macule that is 1 cm or larger, commonly seen in conditions like nevus flammeus and vitiligo.

Papules

• Papules are solid, raised lesions without visible fluid, measuring from pinhead size to 1 cm.
• They can take various shapes: acuminate, rounded, conical, flat-topped, or umbilicated.
• Papules can appear in multiple colors: white (milium), red (eczema), yellowish (xanthoma), black (melanoma).
• Typically located in the dermis, they may cluster around sweat ducts or hair follicles and vary in consistency (soft or firm).

Plaques and Nodules

• Plaques are broad papules or confluences of papules, measuring 1 cm or more, generally flat with possible central depression.
• Nodules are similar to papules but larger than 1 cm, often centered in the dermis or subcutaneous fat.

Tumors

• Tumors are larger masses (greater than 2 cm) that can be soft, firm, movable, or fixed, and can vary in shape.
• They can be elevated or deep-seated, with some being pedunculated, such as neurofibromas.

Wheals (Hives)

• Wheals are temporary, edematous platelet-like elevations that are usually pink to red, often surrounded by macular erythema.
• They can be discrete or merge, develop rapidly, and are the main feature of urticaria.

Vesicles and Bullae

• Vesicles are small, fluid-containing elevations under 1 cm that can be serous or blood-tinged.
• They may appear as distinct, grouped, or linear lesions and can arise from macules or papules.
• Bullae are larger than 1 cm, containing similar fluids as vesicles but present as rounded or irregular-shaped blisters.
• Nikolsky sign tests for blister formation, while Asboe-Hansen sign evaluates blister spreading on pressure.

Pustules

• Pustules are small elevations containing purulent material and can arise from papules or vesicles.
• Typically exhibit a white or yellow center with a red halo if hemorrhagic, indicating underlying inflammation.

Scales (Exfoliation)

• Scales are dry or greasy masses made of keratin, formed through abnormal epidermal cell shedding.
• Normal skin constantly sheds tiny, imperceptible fragments of stratum corneum.
• Rapid formation of epidermal cells or disturbed keratinization leads to pathological scaling.
• Types of scales:
  • Fine and delicate (branny) scales seen in tinea versicolor.
  • Coarser scales occurring in eczema and ichthyosis.
  • Stratified scales characteristic of psoriasis, often with a silvery sheen due to trapped air (micaceous scales).
• Scale coloration ranges from white-gray to yellow or brown due to dirt or melanin.
• Scaling typically indicates a pathological process in the epidermis, frequently observed with parakeratosis.

Crusts (Scabs)

• Crusts consist of dried serum, pus, or blood mixed with epithelial and sometimes bacterial debris.
• Base of detached crusts may appear dry or red and moist.

Excoriations and Abrasions (Scratch Marks)

• Excoriations are punctate or linear abrasions from mechanical means, usually involving the epidermis.
• Caused by scratching to relieve itching; can reach the papillary dermis layer.
• Abrasions result from mechanical trauma or constant friction.
• Excoriations often have an inflammatory halo and can be covered in dried serum or blood.
• They can provide entry for microorganisms, leading to crusting, pustules, or cellulitis, with potential lymphatic gland enlargement.
• Severity of pruritus correlates with the length and depth of excoriations, except in conditions like lichen planus where pruritus is severe but excoriations are rare.

Fissures (Cracks, Clefts)

• Fissures are linear clefts through the epidermis or into the dermis, ranging in size and shape.
• Commonly occur in thickened, inelastic skin due to inflammation or dryness, especially in areas with frequent movement (e.g., fingers, heels, mouth angles).
• Can be dry or moist and may lead to stinging or burning sensations, particularly in cold or windy conditions.
• Movement often exacerbates pain from fissures.

Erosions

• Erosions represent loss of part or all of the epidermis, such as in impetigo.
• May crust but generally heal without scarring.

Ulcers

• Ulcers are round or irregular excavations resulting from the loss of epidermis plus some dermis.
• Size ranges from a few millimeters to several centimeters and may be shallow or deeply extend into subcutaneous tissues.
• Heal with scarring.

Scars

• Scars form from new connective tissue replacing lost substances in the dermis or deeper, as part of healing.
• Size and shape vary based on prior tissue destruction and can provide diagnostic value in inflammatory processes.
• Conditions like discoid lupus erythematosus cause scarring while lichen planus rarely results in skin scarring.
• Hypertrophic scars and keloids may develop, particularly in individuals prone to scarring in certain body areas.
• Scars initially appear pink or violaceous, eventually fading to white or glistening over time, and can rarely become hyperpigmented.

General Diagnosis in Dermatology

• Clinical interpretation can be challenging due to identical lesions having multiple causes.
• One skin disease can manifest in various ways, e.g., lichen planus presents as hyperpigmented patches, violaceous plaques, and hypertrophic papules.
• Skin lesions are superficial, making them easily observable and palpable; magnification enhances detail visualization.
• Smears and cultures for bacteria and fungi can be simply obtained for diagnostic purposes.
• Biopsy and histologic examination are minor procedures, crucial in dermatologic evaluations; low biopsy threshold is recommended.
• Special attention to biopsy is necessary for inflammatory dermatoses, infectious conditions, and immunosuppressed patients, where lesions may appear atypical.

Patient History

• Gathering the patient’s age, health status, occupation, hobbies, diet, and living conditions is essential.
• Important to document the onset, duration, disease course, and previous treatment responses.
• Family history of similar disorders and related diseases can provide valuable context.
• A comprehensive drug history is critical, including all medications—prescription, over-the-counter, supplements, and topical agents—as drug reactions can mimic various skin diseases.
• It’s important to ask about topical agents used for medicinal or cosmetic purposes due to potential cutaneous or systemic reactions.
• Some skin diseases are connected to other underlying conditions, e.g., cutaneous manifestations in Crohn's disease.
• Travel history, environmental factors, seasonal patterns, and geographical diseases should be considered.
• Sexual orientation and practices may relate to specific conditions like STDs and HIV.

Examination Techniques

• Conduct examinations in a well-lit environment; natural sunlight is ideal for visibility.
• Ultraviolet (UV) light effectively highlights melanin pigmentation disorders, like vitiligo and melasma.
• Wood’s light is useful for diagnosing specific infections such as tinea capitis and erythrasma.
• A magnifying lens aids in the examination of smaller lesions for detailed assessment.
• Palpation is essential to determine firmness or fluctuation of lesions; rubbing or scraping can reveal the characteristics of scales and lesions.
• For pigmented lesions in infants, eliciting Darier sign (whealing) is important for diagnosis.
• Dermoscopy plays a crucial role in examining neoplasms, offering better clarity.
• The complete body eruption should be evaluated from a distance for overall distribution before examining individual lesions for details such as evolution and presence of secondary manifestations.

Distribution of Lesions

• Lesions can be few or numerous, with patterns ranging from discrete to coalescent patches.
• Locations of lesions may cover the whole body or follow specific anatomical lines like cleavage (pityriasis rosea), dermatomes (herpes zoster), or Blaschko's lines (epidermal nevi).
• Groupings or configurations of lesions can include rings, crescents, linear patterns, and bilateral symmetry seen in conditions like dermatitis herpetiformis and psoriasis.

Evolution of Lesions

• Some lesions appear fully formed, while others start as smaller lesions and maintain size (e.g., warts).
• Sequential lesions can arise in stages, resulting in polymorphous eruptions, as observed in varicella and dermatitis herpetiformis.
• Lesion involution may lead to complete disappearance, residual pigmentation, or scarring; residual dyspigmentation is a cosmetic issue but not classified as a scar.

Grouping of Lesions

• Dermatitis herpetiformis and herpes zoster lesions often display a grouped appearance.
• Corymbose arrangement features small lesions surrounding a larger one.
• Concentric annular lesions are indicative of borderline Hansen disease and erythema multiforme, sometimes described as a "cockade" pattern.
• Arthropod bites typically present as grouped, linear lesions, often referred to by the "breakfast-lunch-and-dinner" sign.

Configuration of Lesions

• Different configurations of lesions include linear (confluent or discrete), annular (complete or partial circles), polycyclic (intersecting circles), and serpiginous (wavy lines).
• Lesion sizes may vary, with smaller round lesions termed guttate and larger ones nummular.
• Unusual configurations warrant suspicion of exogenous dermatosis or factitia.

Color of Lesions

• Skin color results from melanin, hemoglobin (both oxy and reduced), lipid, and carotene, with proportions and depths affecting appearance.
• The color observed in lesions is crucial for diagnosis; various shades of pink, red, and purple may indicate specific conditions.
• Lipid-containing lesions appear yellow, while salmon color indicates pityriasis rubra pilaris.
• Depigmenting conditions may range from complete to partial loss of skin color; hypopigmented conditions include tinea versicolor and hypomelanosis of Ito.

Texture and Consistency

• Palpation helps determine lesion characteristics; failure to blanch may indicate purpura.
• Fluctuation suggests presence of free fluid, while nodules may indicate deeper skin involvement or calcification.
• Certain lesions display a firm texture similar to keloids or dermatofibromas.

Sensation Changes

• Variations in sensation (hyperesthesia or anesthesia) can be present in lesions; anesthetic centers are typical of Hansen disease.
• Complex regional pain syndrome is characterized by spontaneous pain and tenderness.
• Conditions like notalgia paresthetica involve pruritus coupled with hyperesthesia, indicating potential nerve involvement.

Thermal Burns Overview

• Thermal burns are injuries caused by excessive heat affecting the skin, classified into four degrees based on severity.

First-Degree Burns

• First-degree burns involve congestion of superficial blood vessels, leading to erythema (redness) and possible epidermal desquamation (peeling).
• Commonly associated with sunburn.
• Symptoms include severe pain and increased surface temperature; larger burns can provoke systemic reactions.

Second-Degree Burns

• Second-degree burns are divided into superficial and deep categories.
• Superficial second-degree burns manifest as serum transudation, edema, and formation of vesicles and bullae, usually healing without scarring.
• Deep second-degree burns are pale and anesthetic, damaging the reticular dermis, prolonging healing beyond one month, and resulting in scarring.

Third-Degree Burns

• Third-degree burns destroy the full thickness of the dermis and possibly some subcutaneous tissue, producing ulcerating wounds.
• Lack of skin appendages impedes regeneration, leading to scarring upon healing.

Fourth-Degree Burns

• Fourth-degree burns extend through the skin, subcutaneous fat, to underlying tendons; these burns necessitate grafting for closure.
• Both third and fourth-degree burns lead to severe systemic symptoms, influenced by burn depth, surface area, and location.

Risk and Prognosis

• High mortality risk for extensive burns, especially over two-thirds of body surface area.
• Women, infants, and toddlers are at a greater risk of death from burns compared to men.
• Excessive scarring can result in keloids or contractures, causing joint dysfunction and chronic ulcers.

Delayed Complications

• Delayed postburn blistering can occur in partial-thickness wounds and donor sites, typically healing on its own.
• Burn scars may have a modest association with squamous cell carcinoma, but modern reconstructive techniques minimize risks.

Treatment Strategies

• Immediate first aid involves cold applications to reduce pain; prolonged use until pain subsides is recommended.
• Do not disrupt vesicles in second-degree burns, preserve them as a barrier to infection, but fluid may be evacuated aseptically if necessary.
• Excision of non-healing full-thickness wounds can reduce infections and promote survival.
• Skin grafting and biologic dressings support healing, while laser treatments are under investigation to treat and improve scarring.

Critical Care Necessities

• Critical care for burns includes fluid resuscitation, managing inhalation injuries, monitoring for sepsis, pain control, and nutritional support.
• Intensive management is essential for significant partial-thickness burns and all full-thickness burns, particularly in vulnerable areas (face, hands, feet, genitalia, joints) or injuries from electrical, chemical, or inhalation sources.

Electrical Burns

• Electrical burns can occur from direct contact or flash exposure; contact burns are small but deep, causing tissue necrosis.
• Low-voltage injuries are common at home and usually heal well; more severe cases may need reconstructive procedures.
• High-voltage burns often have minimal surface changes with significant internal damage; early intervention is crucial.
• Flash burns resemble surface burns in treatment, and lightning strikes can lead to distinct burn patterns and systemic complications.

Specific Burn Types

• Lightning strikes can produce entrance/exit wounds, linear burns, feathery arborescent patterns, punctate lesions, or thermal burns from ignited objects such as metal or electronics.

Hot Tar Burns

• Removal of hot tar can be facilitated using dispersing agents like bacitracin zinc–neomycin–polymyxin B ointment, vitamin E ointment, or sunflower oil.

Thermal Burns Overview

• Thermal burns are injuries caused by excessive heat affecting the skin, classified into four degrees based on severity.

First-Degree Burns

• First-degree burns involve congestion of superficial blood vessels, leading to erythema (redness) and possible epidermal desquamation (peeling).
• Commonly associated with sunburn.
• Symptoms include severe pain and increased surface temperature; larger burns can provoke systemic reactions.

Second-Degree Burns

• Second-degree burns are divided into superficial and deep categories.
• Superficial second-degree burns manifest as serum transudation, edema, and formation of vesicles and bullae, usually healing without scarring.
• Deep second-degree burns are pale and anesthetic, damaging the reticular dermis, prolonging healing beyond one month, and resulting in scarring.

Third-Degree Burns

• Third-degree burns destroy the full thickness of the dermis and possibly some subcutaneous tissue, producing ulcerating wounds.
• Lack of skin appendages impedes regeneration, leading to scarring upon healing.

Fourth-Degree Burns

• Fourth-degree burns extend through the skin, subcutaneous fat, to underlying tendons; these burns necessitate grafting for closure.
• Both third and fourth-degree burns lead to severe systemic symptoms, influenced by burn depth, surface area, and location.

Risk and Prognosis

• High mortality risk for extensive burns, especially over two-thirds of body surface area.
• Women, infants, and toddlers are at a greater risk of death from burns compared to men.
• Excessive scarring can result in keloids or contractures, causing joint dysfunction and chronic ulcers.

Delayed Complications

• Delayed postburn blistering can occur in partial-thickness wounds and donor sites, typically healing on its own.
• Burn scars may have a modest association with squamous cell carcinoma, but modern reconstructive techniques minimize risks.

Treatment Strategies

• Immediate first aid involves cold applications to reduce pain; prolonged use until pain subsides is recommended.
• Do not disrupt vesicles in second-degree burns, preserve them as a barrier to infection, but fluid may be evacuated aseptically if necessary.
• Excision of non-healing full-thickness wounds can reduce infections and promote survival.
• Skin grafting and biologic dressings support healing, while laser treatments are under investigation to treat and improve scarring.

Critical Care Necessities

• Critical care for burns includes fluid resuscitation, managing inhalation injuries, monitoring for sepsis, pain control, and nutritional support.
• Intensive management is essential for significant partial-thickness burns and all full-thickness burns, particularly in vulnerable areas (face, hands, feet, genitalia, joints) or injuries from electrical, chemical, or inhalation sources.

Electrical Burns

• Electrical burns can occur from direct contact or flash exposure; contact burns are small but deep, causing tissue necrosis.
• Low-voltage injuries are common at home and usually heal well; more severe cases may need reconstructive procedures.
• High-voltage burns often have minimal surface changes with significant internal damage; early intervention is crucial.
• Flash burns resemble surface burns in treatment, and lightning strikes can lead to distinct burn patterns and systemic complications.

Specific Burn Types

• Lightning strikes can produce entrance/exit wounds, linear burns, feathery arborescent patterns, punctate lesions, or thermal burns from ignited objects such as metal or electronics.

Hot Tar Burns

• Removal of hot tar can be facilitated using dispersing agents like bacitracin zinc–neomycin–polymyxin B ointment, vitamin E ointment, or sunflower oil.

Overview of Miliaria

• Miliaria results from sweat retention due to occlusion of eccrine sweat ducts, prominent in hot, humid climates.
• Staphylococcus epidermidis can induce miliaria by producing a polysaccharide that obstructs sweat delivery.
• Sweat gland pressure leads to ruptures, causing sweat to escape into adjacent tissues.

Types of Miliaria

Miliaria Crystallina

• Characterized by small, clear vesicles, appearing usually without inflammation.
• Common in bedridden patients, bundled children, or due to hypernatremia without fever.
• Lesions are asymptomatic, brief, and rupture easily with minimal trauma.
• Induced by drugs like isotretinoin and doxorubicin; self-limited with no treatment necessary.

Miliaria Rubra (Prickly Heat)

• Features discrete, itchy erythematous papulovesicles with a prickling or burning sensation.
• Commonly affects areas like the antechubital and popliteal fossae, trunk, inframammary areas, abdomen, and inguinal regions.
• Evaporation is compromised, leading to maceration of the skin.
• Can be triggered by exercise and may resemble atopic dermatitis.
• Occurs in the prickle cell layer with spongiosis indicating sites of sweat escape.

Miliaria Pustulosa

• Preceded by dermatitis that damages or blocks sweat ducts.
• Distinct, superficial pustules unrelated to hair follicles occur primarily in intertriginous areas or on flexural surfaces.
• Associated with conditions like contact dermatitis and lichen simplex chronicus.
• Recurrent episodes may indicate type I pseudohypoaldosteronism, related to salt-losing crises that trigger miliaria.

Miliaria Profunda

• Defined by non-itchy, flesh-colored, deep-seated whitish papules.
• Typically asymptomatic and resolves within 1 hour after overheating.
• Concentrated on trunk and extremities; nonfunctional sweat glands, except in the face, axillae, hands, and feet.
• Occlusion occurs in the upper dermis and is primarily observed in tropical regions, commonly following severe miliaria rubra.

Acrocyanosis

• Persistent blue discoloration of hands or feet exacerbated by cold exposure; hyperhidrosis may also be present.
• Primarily affects young women; severity increases as temperature drops.
• Distinct from Raynaud syndrome due to its persistent nature and absence of tissue damage.
• Smoking is advised against to prevent worsening symptoms.
• Can occur after inhalation of butyl nitrite and due to certain medications (Interferon alpha-2a and beta).
• Repeat narcotic injections may lead to lymphedema and resemble edematous scleroderma.
• Patients with anorexia nervosa might show acrocyanosis alongside other skin conditions, improving with weight gain.
• Common in approximately one-third of patients with skin findings of POEMS syndrome.
• Acrocyanosis can be seen in patients with SAMDH1 mutations and cerebrovascular disease.
• Acral vascular syndromes may indicate malignancy; 47% of cases showed cancer coinciding with acral disease onset.
• Sudden changes in older males without prior vascular conditions may suggest paraneoplastic origin.

Perniosis (Chilblains)

• Localized erythema and swelling due to cold exposure; severe cases may lead to blistering or ulceration.
• Predominantly affects individuals with poor peripheral circulation; cold dampness enhances onset.
• Associated with cryoglobulins, antiphospholipid antibodies, and cold agglutinins; may signify underlying conditions like lupus or leukemia.
• May develop in those using crack cocaine due to its vasoconstrictive effects.
• Common sites include hands, feet, ears, and face, with women being particularly susceptible.
• Can result from prolonged exposure in certain occupations or activities (e.g., equestrians in cold weather).
• Symptoms often manifest as bluish-red areas, which may be cool to touch and show color changes upon pressure.
• New lesions may appear as long as cold exposure continues; investigation needed for recurrent or chronic cases.
• Histology reveals lymphocytic vasculitis and dermal edema.

Treatment for Perniosis

• Protect affected areas from further cold and damp exposure; warm socks recommended during cold months.
• Emphasize appropriate dress despite lack of cold sensation.
• Maintain overall body warmth to prevent peripheral vasoconstriction.
• Judicious use of heating pads advised; smoking cessation strongly recommended.
• Effective medications include Nifedipine, nicotinamide, and phosphodiesterase inhibitors.
• Spontaneous resolution may occur within 1-3 weeks; systemic corticosteroids useful for chilblain lupus.

Frostbite

• Injury from freezing soft tissues, commonly affecting nose, ears, cheeks, fingers, and toes.
• Tissue changes range from erythema to gangrene, depending on temperature and exposure duration.
• Risk factors include race, with higher vulnerability in African Americans.
• Small joint arthritis may develop months or years post-injury.

Treatment for Frostbite

• Immediate covering of the affected area with warmth to maintain circulation.
• Preferred treatment involves rapid rewarming in controlled water baths (37°C to 43°C).
• Delay thawing until refreezing risk is eliminated; analgesics are essential to manage pain.
• Complete thawing is indicated by skin pliability and redness.
• Tissue plasminogen activator can reduce amputation risk if administered early.
• Supportive care includes rest, nutritious diet, wound care, and trauma avoidance.
• Preventive measures against thrombosis may incorporate anticoagulants and adjunctive treatments.
• Recovery time can span several months; prior cold injuries increase risks for recurrence.

Acrocyanosis Overview

• Acrocyanosis presents as a persistent blue discoloration of hands or feet, exacerbated by cold exposure.
• Common in young women; manifesting symptoms may include hyperhidrosis (excessive sweating).

Symptoms and Characteristics

• Cyanosis intensifies in lower temperatures and transitions to erythema (redness) when the affected extremity is elevated.
• Unlike Raynaud syndrome, acrocyanosis is persistent and does not lead to tissue damage (e.g., ulceration or fingertip resorption).

Potential Triggers

• Exposure to butyl nitrite may cause acrocyanosis along with swelling of the nose, ears, and backs of hands.
• Medications, including interferon alpha-2a and beta, can induce acrocyanosis.
• Narcotic drug injections in the dorsal hand may lead to lymphedema, resembling symptoms of scleroderma, referred to as puffy hand syndrome.

Associated Conditions

• Patients with anorexia nervosa often experience acrocyanosis, alongside perniosis, livedo reticularis, and coldness of the limbs; symptoms generally improve with weight gain.
• Approximately one-third of individuals with POEMS syndrome display acrocyanosis as part of their skin manifestations.

Genetic and Disease Links

• Acrocyanosis is frequently observed in patients with a homozygous mutation in SAMDH1 and those suffering from cerebrovascular occlusive disease.
• Acral vascular syndromes, including gangrene and Raynaud phenomenon, may indicate underlying malignancies.

Cancer Connection

• In about 47% of 68 cases studied, the diagnosis of cancer coincided with the onset of acral symptoms.
• Sudden appearance or worsening of symptoms in elderly patients, particularly men, warrants suspicion of a paraneoplastic cause, especially in the absence of known vasoconstrictive drug exposure or previous autoimmune/vascular conditions.

Sunburn and Solar Erythema

• The solar spectrum is divided into regions based on wavelength: UV radiation (<400 nm), visible light (400–760 nm), and infrared radiation (>760 nm).
• UV radiation consists of three bands: UVA (320–400 nm), UVB (280–320 nm), and UVC (200–280 nm). UVC is mostly absorbed by the ozone layer, preventing it from reaching Earth.
• UVA is further divided into UVA I (340–400 nm) and UVA II (320–340 nm).
• The minimal erythema dose (MED) is the smallest amount of UV radiation inducing erythema on skin.
• UVB radiation, although less abundant than UVA, is significantly more erythemogenic, making it responsible for almost all solar erythema.
• The most effective wavelength for inducing sunburn is 308 nm.
• UVA contributes to drug-induced photosensitivity, photoaging, and cutaneous immunosuppression.
• UV exposure increases with altitude, summer months in temperate climates, and in tropical regions.
• UVB is reflected less than UVA by surfaces like sand and snow, while water allows significant UV penetration.
• Midday UVB intensity peaks 2–4 times higher than in the morning or late afternoon.

Clinical Signs and Symptoms of Sunburn

• Sunburn is a normal cutaneous response to excessive sunlight, with UVB erythema becoming noticeable about 6 hours post-exposure, peaking at 12–24 hours.
• Symptoms include tenderness, severe discomfort, blistering, and systemic signs like chills, fever, nausea, tachycardia, and hypotension in severe cases.
• Desquamation typically occurs about a week post-burn, with initial pigment changes being immediate (IPD) and delayed melanogenesis starting 2–3 days after exposure.
• IPD is not protective; delayed melanogenesis can provide limited protection at a cellular damage cost.

Treatment of Sunburn

• Limited effectiveness of treatment once symptoms appear; focus is on pain management using NSAIDs or topical emollients.
• Prostaglandins, particularly E series, are key mediators in the inflammatory response.
• Medium-potency topical steroids may slightly reduce symptoms when applied shortly after exposure.
• Prophylaxis is more effective than treatment, with educational programs to raise awareness of sun hazards.

Prophylactic Measures

• Key messages for sunburn prevention include avoiding midday sun, seeking shade, wearing protective clothing, and applying sunscreen.
• Highest UVB intensity occurs between 9 AM and 3-4 PM, ideal times for sun protection measures.
• Shade can offer substantial protection (equivalent to SPF 4-50) depending on density.
• Clothing effectiveness is measured by UPF, with denser and older, looser-fitting fabrics providing better UVB shielding.
• Sunscreen efficacy is conveyed through SPF, indicating protection levels against UVB.
• Most people apply sunscreen too thinly, resulting in an actual SPF of about half that indicated on the label.
• Broad-spectrum sunscreens protect against both UVB and UVA, crucial for preventing photoaging and skin cancers.

Sunscreen Recommendations

• Daily use of a broad-spectrum sunscreen SPF 30 is advised for individuals with skin types I to III.
• For outdoor activities, SPF 30+ is recommended, with application at least 20 minutes prior to sun exposure and reapplication after swimming or vigorous activity.
• Men often fail to apply sunscreen adequately, leading to increased risk.
• Vitamin D supplementation (600 IU daily for those under 70, 800 IU for older patients) is recommended alongside stringent sun protection.
• Photoaging and immunosuppression require sunscreens that offer excellent UVA protection, denoted by "broad spectrum" on labels.

Pruritus Overview

• Pruritus, or itching, is a skin-exclusive sensation that incites the desire to scratch.
• Keratinocytes respond to pruritogenic stimuli by releasing various mediators, alongside the activation of fine intraepidermal C-neuron filaments.
• Approximately 5% of unmyelinated C neurons are involved in transmitting itch sensations to the brain via the lateral spinothalamic tract.

Mechanism and Neuromediators

• The brain processes itch through various foci that generate both stimulatory and inhibitory responses, influencing the quality and intensity of the sensation.
• Common triggers for itching include light touch, temperature changes, emotional stress, and other chemical, mechanical, and electrical stimuli.
• Key neuromediators implicated in pruritus include:
  • Histamine and H4 receptors
  • Tryptase and proteinase-activated receptor type 2
  • Opioid peptides (μ and κ receptors)
  • Leukotriene B4, prostaglandins (e.g., PGE)
  • Thymic stromal lymphopoietin, acetylcholine, and various cytokines (e.g., IL-31).

Classification of Itch

• Pruritus is classified into four main categories:
  • Pruritoceptive itch: Initiated by skin disorders.
  • Neurogenic itch: Arises from the central nervous system due to systemic disorders.
  • Neuropathic itch: Caused by lesions in the central or peripheral nervous systems.
  • Psychogenic itch: Linked to psychological conditions, such as parasitophobia.
• These categories can overlap in individual cases.

Factors Influencing Itch Severity

• Itching can vary significantly among individuals and may depend on the stimulus.
• Common aggravating factors include:
  • Heat, stress, lack of distractions, anxiety, and fear.
• Itch often worsens when preparing for bed and can be severe enough to wake patients.

Characteristics of Severe Pruritus

• Pruritus can be paroxysmal with sudden onset, potentially inducing bleeding from scratching.
• Eliciting immediate relief from scratching can be hard despite skin damage awareness.

Common Dermatoses Associated with Itch

• Conditions characterized by intense pruritus include:
  • Lichen simplex chronicus, atopic dermatitis, nummular eczema, dermatitis herpetiformis, neurotic excoriations, eosinophilic folliculitis, and prurigo nodularis.

Management Strategies for Itching

• General treatment recommendations:
  • Maintain a cool environment, avoid hot showers/baths, and steer clear of irritants like wool.
  • Limit soap use, pat skin dry, and apply moisturizers to prevent itching.
• Techniques such as "soaking and smearing" may provide significant relief.
• Cold packs can soothe itching, while hot water can exacerbate skin irritation.

Topical Treatments

• Topical anesthetics (e.g., benzocaine, lidocaine, EMLA ointment) can relieve localized itching, but care should be taken to avoid large area application due to toxicity risks.
• Topical antihistamines are generally not recommended, though doxepin cream may help mild pruritus.
• Lotions with menthol or camphor can cool the skin and alleviate discomfort.
• Capascin can be effective by depleting substance P but may cause initial burning.

Phototherapy and Oral Medications

• Phototherapy options, including UVB and PUVA, benefit various pruritic conditions.
• First-generation H1 antihistamines (e.g., hydroxyzine, diphenhydramine) can help with nocturnal itching but are limited in effectiveness for other disorders.
• Doxepin offers benefits for anxiety-related pruritus.
• Opioids can influence itch perception through μ and κ receptor pathways.
• Anticonvulsants (e.g., gabapentin) and specific antidepressants (e.g., mirtazapine, SSRIs) can centralize itch perception reduction.

Additional Treatments

• Thalidomide has applications for its immunomodulatory and sedative effects in select cases.
• Treatment options should be tailored to individual patient needs, considering condition specifics and responses.

Winter Itch Overview

• Also known as asteatotic eczema, eczema craquelé, and xerotic eczema.
• Characterized by intense itching (pruritus), primarily affecting the legs and arms.

Affected Areas

• Extension to other body parts is common; however, the face, scalp, groin, axillae, palms, and soles remain unaffected.
• Pretibial regions are particularly prone to eczema craquelé, showing fine cracks similar to old porcelain.

Causes

• Frequent, prolonged bathing with excessive soap during winter months is a leading cause.
• Older adults experience reduced epidermal water barrier repair and diminished sebaceous gland activity.
• Low indoor humidity in heated rooms during cold weather exacerbates skin dryness.

Epidemiology

• In a study involving 584 elderly individuals, 28.9% presented with asteatosis, making it the second most common skin condition after seborrheic dermatitis.

Treatment Approaches

• Patients should use soap sparingly, limited to axillae and inguinal areas, followed by immediate application of emollients.
• Lactic acid or urea-containing preparations can be used post-bathing but may irritate sensitive skin with erythema or eczema.

Intensive Regimen

• “Soaking and smearing” treatment proves highly effective for severe symptoms:
  • Soak in lukewarm water for 20 minutes before bedtime.
  • On exiting, apply triamcinolone ointment (0.025%–0.1%) directly on wet skin to trap moisture and enhance steroid absorption.
  • Wear old pajamas to maintain moisture overnight.

Long-term Care

• After several nights of soaking treatment, patients may rely on ointment alone for symptom management.
• Maintenance includes restricting soap to axillary and groin areas and moisturizing post-shower.
• Plain petrolatum can serve as a lubricant for simple dryness without inflammation.

Potential Complications

• Treatment may lead to folliculitis as a secondary complication.

Aquagenic Pruritus Overview

• Characterized by itching triggered by any water contact, regardless of temperature.
• Symptoms typically include severe, prickling discomfort emerging within minutes of water exposure.

Patient Groups

• Approximately one third are older males with underlying conditions like polycythemia vera, hypereosinophilic syndrome, or myelodysplastic syndrome.
• About two thirds are younger women who develop symptoms as adults, often with no identified underlying disease; some may have a family history of aquagenic pruritus.

Diagnosis Considerations

• Important to distinguish aquagenic pruritus from xerosis, as dry skin may react adversely to water.
• For xerosis, an initial trial of "soaking and smearing" is recommended to alleviate symptoms.

Treatment Options

• Antihistamines, sodium bicarbonate in bath water, propranolol, atenolol, selective serotonin reuptake inhibitors (SSRIs), acetylsalicylic acid (aspirin), pregabalin, montelukast, and phototherapy (NB UVB or PUVA) are potential treatments.
• One individual reported relief from symptoms by wearing tight-fitting clothing within 5 minutes.

Related Conditions

• "Aquadynia" described by Shelley et al. as a reaction to water exposure leading to widespread burning pain lasting 15-45 minutes; considered a variant of aquagenic pruritus.
• Relief for aquadynia observed with clonidine and propranolol.

Overview of Atopic Dermatitis

• Atopic dermatitis (AD) is a chronic, inflammatory skin condition marked by itching and a cycle of flare-ups and remissions.
• It is commonly associated with other allergic conditions like food allergies, asthma, and allergic rhinoconjunctivitis.

Atopic March

• AD often precedes other atopic diseases, suggesting it could be the initial step in an "atopic march," where skin sensitization leads to allergic reactions in other areas (airways/digestive tract).
• The causal link between AD and the development of other atopic conditions remains unproven, but early treatment of AD may help prevent these outcomes.

Prevalence and Trends

• The prevalence of AD, asthma, and allergic rhinoconjunctivitis rose significantly in the latter half of the 20th century, especially in developed countries.
• Rates of AD are about 30% in highly developed nations and exceed 10% in many other countries, contributing to a global prevalence rate of approximately 20%.
• AD rates stabilized in the 1990s in developed countries while continuing to rise in developing nations.

Geographic and Environmental Factors

• High latitude and low average temperatures are associated with higher AD rates, potentially due to lower sun exposure.
• Studies do not strongly support the role of environmental allergen exposure as a trigger for AD; for example, Iceland shows high AD rates (27%) despite low environmental allergens.

Demographic Risk Factors

• Girls have a slightly higher likelihood of developing AD.
• In the U.S., increased AD risk in infants is linked to African and Asian ethnicities, male gender, higher gestational age, and familial atopy, especially maternal eczema.
• Other early-life risk factors include a Western diet, higher birth order, cesarean delivery, and prenatal antibiotic exposure, influencing the gut microbiome.

Microbiome and Preventive Factors

• A diverse gut microbiome may offer protection against AD, with colonization by Clostridium cluster I being notably beneficial.
• Dog ownership before age one appears to reduce AD risk, while cat ownership does not affect risk levels.
• The hygiene hypothesis indicates that rural farm upbringing lowers AD risk, contrasting with higher risk in modern, cleaner living conditions.

Age of Onset

• Approximately 50% of AD cases emerge within the first year of life, with most cases appearing by age five; remaining cases generally arise before age 30.
• Atopy is prevalent in the population, leading to widespread family histories of the condition.

Adult Atopic Dermatitis Diagnosis

• Elevated immunoglobulin E (IgE) levels are not definitive for diagnosing atopy in adults.
• An adult's new-onset dermatitis, with elevated IgE and family atopy history, alone is insufficient for confirming adult AD.
• Diagnosis of adult AD should occur only if the dermatitis displays characteristic features, and other serious conditions (e.g., allergic contact dermatitis) are ruled out.
• Dermatologists rarely diagnose adult AD for dermatitis presenting after the age of 30.

Explore the origins, structure, and development of apocrine glands in this quiz. Learn about their association with hair follicles and their unique epithelial configurations. This quiz is essential for understanding the histological aspects of skin anatomy.