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Dermatology > Epidermis and Disorders of Kertatinization > Flashcards

Epidermis and Disorders of Kertatinization Flashcards

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Dermatology Board Prep flashcards
1
Q

Layers of the epidermis

A
  1. Stratum basalt
  2. Stratum spinosum
  3. Stratum granulosum
  4. Stratum corneum
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2
Q

Basal layer

A

Stratum basale
Cuboidal cells with proliferative function
Adhere to basement membrane via hemidesmosomes

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3
Q

Spinous layer

A

Stratum spinosum
Bind to neighboring keratinocytes via desmosomes (spiny when histology ally treated)
Cells migrate to surface and lose water and flatten

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4
Q

Desmoglein

A

Transmembrane proteins that connect desmosomes

Antibodies to desmogleins can lead to loss of cellular adhesion and blister formation

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5
Q

Desmoglein 1

A

Localized to entire epidermis but especially in upper layers

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6
Q

Desmoglein 3

A

Localized to basal layer

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7
Q

Langerhans cells

A 
Macrophages in epidermis
Found in spinous layer 
Derived from bone marrow
Immunomodulatory role 
Allergic contact dermatitis, graft-versus-host disease and drug eruptions
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8
Q

Granular layer

A

Stratum granulosum
2-3 cells thick
Keratohyaline and lamellar granules

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9
Q

Keratohyaline granules

A

Contain profilaggrin and keratin filaments

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10
Q

Profilaggrin

A

Associated with intermediate filaments

Made up of filaggrin, which promotes aggregation and stabilization of int. filaments in corneum

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11
Q

Lamellar granules

A 
Aka Odland bodies 
Contains lipids, free sterols, hydrolases and ceramides
-barrier function 
-apoptosis
-desquamation
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12
Q

Cornfield layer

A

Stratum corneum
Anucleate cells no longer mitotically active
Not on mucosal surfaces

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13
Q

Lines of Blaschko

A

Linear and whirled pattern keratinocytes follow as they migrate during embryogenesis from dorsal neural crest to the ant. midline of skin and to extremities

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14
Q

Keratin Structure

A

intermediate filament makes up cytoskeleton

  • alpha helical structures
  • 2 types: type1 (acidic) and type2 (basic)
  • type1 and 2 assemble into heteropolymers, which align to form keratin filaments
  • insert into desmosoems and hemidesmosomes
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15
Q

Keratinization

A

aka cornification (takes 12-14 days)

  • enlarge and flatten keratinocytes as migrate towards surface
  • filaggrin-induced keratin filament parallel assembly and cross-linking of proteins to form cornified envelope
  • release of lamellar granule lipids to form hydrophobic barrier
  • degradation of cellular organelles to form anucleate cells
  • apoptosis
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16
Q

Desquamation

A

Shedding of corneocytes (takes 12-14 days)

  • hydrolases divide proteins linking adjacent cells
  • active when stratun corneum well-hydrated
  • disruption results in xerosis (dry, rough, scaly skin)
17
Q

Xerosis

A

dry, rough, scaly skin

  • due to decrease in intracellular lipids and NMF, failure of adherent bonds of stratum corneum to break down, and dehydration of corneocytes
  • stratum corneum becomes less pliable and more susceptible to small fissures and formation of dry scale
  • may req assessment of medication, renal function and overall nutritional status
18
Q

Natural Moisturizing Factors (NMF)

A

free amino acids, lactic acid, urea and salts

  • hygroscopic
  • accounts for pliability of the epidermis
19
Q

Atrophy

A

decreased cell proliferation

-thinning of skin

20
Q

Hyperplasia

A

increase in thickness of tissues

  • Acanthosis - proliferation of stratum spinosum
  • Hyperkeratosis - thickening of stratum corneum due to increase production of corneocytes or reduced desquamation
  • Lichenification - thickening of stratum spinosum and corneum in response to repeated scratching and rubbing
21
Q

Wound healing

A

intermediate filaments associate with actin and tubulin, allowing the keratinocyte to migrate

  • 12 hrs after wound, epidermal keratinocytes flatten and lose bond with BM and dermis
  • keratinocytes migrate across wound by forming a “train”
  • moist wound environment helps
22
Q

Disorders of Cornification

A
  • defects in keratinocytes
  • disrupted intercellular cohesion
  • abnormal lipid function
23
Q

Icthyosis vulgaris (IV)

A

most common disorder of cornification

  • retention hyperkeratosis
  • failure of cellular signals to trigger corneocyte shedding
  • autosomal dominant with variable expression
  • trunk and extremities favored with fish scale
  • mild itching
  • commonly associated with atopic triad
  • some keratosis pilaris
  • hyperlinear palms
  • exacerbated by cold weather and decreased humidity
24
Q

Keratosis pilaris

A

follicular retention hyperkeratosis overlying hair follicles on extensor upper and lower extremities and buttocks

25
Q

Palmoplantar Keratoderma (PPK)

A

hyperkeratosis of palms and soles

  • autosomal dominant AND recessive inheritance patterns
  • due to keratin mutations, resulting in abnormal type1 and type2 pairings of keratins
  • 3 categories:
    1. diffuse (thick, yellow plaques of entire palm/sole, border may be red and patients may complain of hyperhidrosis)
    2. focal (hyperkeratosis localized over pressure points)
    3. punctate (hyperkeratotic papules and nodules, commonly misdiagnosed as warts)
  • treatment: pare hyperkeratotic areas and using topical moisturizers and humectants
26
Q

Diseases characterized by altered epidermis

A

increased inflammation or exposure to toxin

27
Q

Atopic Dermatits

A

eczema: common rash occurring with atopic triad (asthma, eczema, and allergic rhinitis)
- genetic influence
- due to increased inflammation in the skin
- filaggrin defect: mutation causes loss of function, resulting in cell envelope missing protein and subsequent reduction in amino acids, causing dehydration of corneum
- epidermis loses capacity for maintenance of barrier

28
Q

Psoriasis

A

inflammatory skin disease

  • red plaques, thick and adherent scale and nail changes
  • inflammation stimulates shortened cell turnover time (increased proliferation rate), with 4 day transit time
  • cornified layer unable to compensate, resulting in thick, erythematous plaques with adherent scale
29
Q

Staphylococcal Scalded Skin Syndrome (SSSS)

A

rare, prodome of malaise, irritability, fever and skin pain

  • redness starts with head then spreads
  • flaccid bullae develop over involved sites, followed by widespread desquamation over 3-5 days
  • caused by exotoxin secreted by phage group II s. aureus
  • Exfoliative toxins (ET-A and ET-B) target desmoglein 1 and lead to loss of cell-cell adhesion
  • toxins renally excreted so renal failure and immunosuppression/
30
Q

Treatment of disorders of cornification/xerosis

A
  • avoid hot and prolonged showers (lukewarm water)
  • use mild soaps/soapless cleansers
  • avoid products with fragrances
  • do not scrub skin with washcloth nor loofah
  • pat dry with towel and apply emollients immediately
  • moisturizing creams or ointments preferred over lotions
  • humidifiers ma help minimize xerosis in winter
  • inflammatory skin diseases (eczema and psoriasis) benefit from topical steroid to reduce inflamation and allow healing of cutaneous barrier
31
Q

Emollients

A

moisturizers - topical products that hydrate skin

  • lotions, creams, ointments
  • absorb into epidermis and enhance moisture retention
32
Q

Humectants

A

agents that pull water into cells

  • ammonium lactate, urea creams
  • disorders of cornification require these

Dermatology (11 decks)

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