Epidermis, dermis, subQ, and basement membrane zone (BMZ) Flashcards

1
Q

Name the 4 layers of the epidermis from outermost to innermost

A
  1. Stratum corneum (cornified layer)
  2. Stratum lucidum (translucent layer) - **palms and soles only
  3. Stratum granulosum (granular layer)
  4. Stratum spinosum (spinous layer)
  5. Stratum basale (basal layer)
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2
Q

Name the contents of keratohyalin granules

A
  1. Filaggrin
  2. Involucrin
  3. Loricrin
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3
Q

Name the contents of lamellar granules

A

a.k.a. Odland bodies

  1. Ceramides
  2. Cholesterol
  3. Fatty acids
  4. Hydrolytic enzymes - responsible for sloughing of the corneal layer
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4
Q

Anuclear cells found in the uppermost layer of the epidermis are called what?

A

corneocytes

held together by corneodesmosomes

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5
Q

Where is the cornified layer thickest? Thinnest? What about mucosa?

A
  1. Palms, soles
  2. face, genitalia
  3. No cornified layer in oral, genital, and ocular mucosa
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6
Q

The process of keratinization takes on average how long?

A

28 days

Stratum basale to stratum corneum: 14 days

Stratum corneum to shedding: 14 days

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7
Q

The keratinocyte lipid envolope is derived from the contents of what? What about the cornified envelope?

A
  1. Lipid envelope: Lamellar granule (Odland body) -> outermost layer
  2. Cornified envelope: keratohyalin granule
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8
Q

Pemphigus vulgaris: describe

  1. mechanism
  2. presentation
  3. prognosis
  4. treatment
A
  1. Acquired autoimmune disease against Desmoglein 1 and 3 in the epidermis
  2. Fragile, flaccid, easily ruptured bullae (intraepidermal, Nikolsky’s sign positive), oral and mucosal lesions
  3. Poor. Often fatal if untreated
  4. Rx: prednisone, azathioprine, mycophenolate mofetil, rituximab
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9
Q

What is Nikolsky’s sign?

A

rubbing or applying pressure to a bulla increases its size

Seen in pemphigus vulgaris

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10
Q

Ichthyosis vulgaris: describe

  1. mechanism
  2. presentation
A
  1. Autosomal dominant genetic condition featuring defective filaggrin, leading to defective keratohyalin granules and improper formation of the corneal layer of the epidermis
  2. Extremely dry, fish-scale skin (ichtyotic, especially on shins), hyperlinear palms (more creases than usual). Associated with atopic dermatitis (eczema), allergic rhinitis, food allergies, and asthma
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11
Q

What is a physical sunscreen? Give a couple examples.

A

Physical sunscreen reflects or scatters UV light

titanium dioxide, zinc oxide

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12
Q

What is a chemical sunscreen? Give a couple examples.

A

Chemical sunscreen absorbs UV light.

PABA, oxybenzone, avobenzone

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13
Q

What is MED?

A

Minimal erythema dose: minimum amount of UVB that causes skin redness at 24 hours.

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14
Q

Define: SPF

A

Sun protection factor (SPF)

SPF = MEDprotected/MEDunprotected

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15
Q

Does SPF60 provide 2x the protection of SPF30?

A

No, despite what the formula would otherwise imply.

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16
Q

Describe:

  1. UVA
  2. UVB
  3. UVC
A
  1. 320-400nm - mostly responsible for tanning and photoaging
  2. 280-320nm - mostly responsible for ertythema and sunburn
  3. 200-280nm - most is absorbed by the atmosphere
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17
Q

The dermis is embryologically derived from what?

A

mesoderm

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18
Q

Describe in terms of cellularity and collagen content:

  1. Papillary dermis
  2. Reticular dermis
A
  1. higher cellularity, loose collagen
  2. lower cellularity, denser collagen
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19
Q

What is the most abundant collagen type in the dermis?

A

Collagen type I

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20
Q

What is the second most abundant type of collagen, involved in wound healing and embyrogenesis?

A

Collagen type III

21
Q
A
22
Q

Give location and function:

  1. Meissner’s corpuscles
  2. Pacinian corpuscles
A
  1. superficial dermis (papillary), responsible for light touch
  2. deep dermis, found in greater density on weight-bearing surfaces, lips, nipples, penis, clitoris. Responsible for deep pressure sensation.
23
Q

Marfan’s Sydrome:

  1. Etiology
  2. presentation
A
  1. autosomal dominant genetic defect in fibrillin, variable expression
  2. Stria, long limbs and fingers, hyperflexible joints, pectus excavatum, aortic anyeurism, mitral valve prolapse, dislocated lens (ectopia lentis), nearsightedness (myopia), scoliosis
24
Q

Ehlers-Danlos Syndome:

  1. Etiology
  2. Presentation
A
  1. Group of inherited connective tissue disorders with abnormalities in collagen production, processing, or assembly. Variable inheritance and clinical features
  2. Fragile/elastic skin, hyperflexibility of joints, scoliosis, dislocations, arthritis
25
Q

Morphea:

  1. Etiology
  2. Presentation
A

localized scleroderma

  1. Autoimmune disease causing sclerosis (thickening of collagen)
  2. F > M; violaceous plaques, progressing to sclerotic plauqes with scarring. Usually little systemic involvement. May also show limb contractures and atrophy, or neurologic disorders (due to contractures over the head).
26
Q

Systemic sclerosis:

  1. Etiology
  2. Presentation
A

systemic scleroderma - very similar to Morphea, but not localized

  1. Autoimmune disease
  2. Primarily affects middle-aged women. Shows widespread sclerosis, leading to microstomia, sclerodactyly, Raynaud’s phenomenon, telangiectasia, and arthritis. May involve organs: pulmonary fibrosis, renal crisis, esophageal dysmotility.
27
Q

subcutaneous fat is derived from what embryological layer?

A

mesoderm

28
Q

What is panniculitis?

A

Inflammation of subcutaneous fat

29
Q

Erythema nodosum:

  1. Etiology
  2. Presentation
A

Reactive panniculities

  1. panniculitis triggered by streptococcal pharyngitis, oral contraceptives, irritable bowel disease, and malignancy. Affects primarily young women.
  2. Tender red nodules on shins (hard lumps), with active inflammation of the subcutaneous fat (seen histologically)
30
Q

Name the four layers of the BMZ

A
  • hemidesmosome
  • lamina lucida
  • lamina densa
  • sublamina densa
31
Q

Describe BP230

A

a.k.a. bullous pemphigoid antigen 1 (BPA-1)

  • cytoplasmic
  • responsible for organization of the cytoskeletal structure
32
Q

Describe BP180

A

a.k.a. bulloud pemphigoid antigen 2 (BPA-2) a.k.a. collagen XVII

  • transmembrane protein connecting basal keratinocytes through BP230 (BPA-1) to the cytoskeleton
  • Also connects to dermal collagen VII through laminin 332
33
Q

Bullous pemphigoid:

  1. Etiology, epidemiology
  2. Presentation
  3. DIF
  4. IIF
  5. Prognosis
  6. Treatment
A
  1. Antibody against BPA-1 (BP230) and BPA-2 (BP180) resulting in subepidermal blisters. Affects primarily the elderly.
  2. Pruritis urticaria without blisters, progressing to tense, serous (hemorrhagic rare) blisters. Blisters are tense/strong because the blistering involves the entire epidermis (separate at dermis/epidermis interface i.e. at BMZ)
  3. DIF: linear IgG and C3 along BMZ
  4. IIF: epidermal-sided linear stain
  5. better than pemphigus vulgaris (flaccid blisters)
  6. high-potency steroids (caution with elderly patient population)
34
Q

GABEB: Generalized Atrophic Benign Epidermolysis Bullosa

  1. Etiology
  2. Presentation
A
  1. Inherited mutation in BP180 (BPA-2)
  2. Generalized blistering, atrophic scarring, nail dystrophy. Presents at birth.
35
Q

Mucous Membrane Pemphigoid:

  1. Epidemiology/etiology
  2. Presentation
  3. DIF
  4. IIF
    5.
A
  1. Predominantly affects elderly. Antibodies against BP180. Some patients have antibodies targeting BP230, integrin beta-4, and laminin 332 (AECP, associated with malignancy).
  2. Recurrent blistering of the mucous membranes and skin. Develop scars, strictures, synechiae, blindness (20%).
  3. Linear IgG and C3 deposits along BMZ
  4. Linear staining epidermal or epidermal and dermal. Laminin 332 MMP (AECP - anti-epiligrin cicatrical pemphigoid) shows on dermal side only.
36
Q

Herlitz Juntional EB:

  1. Etiology
  2. Prognosis
A
  1. laminin 332 mutation
  2. very high mortality
37
Q

Name the genetic (congenital) and autoimmune (acquired) bulloud disorders associated with each of the following:

  1. Desmoglein 1, 3
  2. Keratins 5, 14
  3. BP230
  4. alpha-6-beta-4 integrins
  5. BP180 (type XVII collagen)
  6. Laminin 332
  7. Type VII collagen
A
  1. striate palmoplanar keratoderma (congenital), pemphigus vulgaris (acquired)
  2. epidermolysis bullosa simplex (congenital)
  3. Bulloud pemphigoid (acquired)
  4. Epidermolysis bullosa with pyloric atresia (congenital), bulloud pemphigoid (acquired)
  5. Non-Herlitz epidermolysis bullosa (congenital), Bullous pemphigoid, mucous membrane pemphigoid, linear IgA disease (acquired)
  6. Herlitz epidermolysis bullosa (congenital), mucous membrane pemphigoid (acquired)
  7. Dominant/recessive dystrophic epidermolysis bullosa (congenital), epidermolysis bullosa acquisata (acquired)
38
Q

Epidermolysis Bullosa Acquisata (EBA):

  1. Epidemiology
  2. Presentation
  3. DIF
  4. IIF
A
  1. Acquired autoimmune disease. Antibody against type VII collagen (in the sublamina densa)
  2. Slight trauma elicits blistering and erosions. Mechanically-stressed areas also show blistering and erosions (hands, feet, elbows, knees, oral mucosa, nails.
  3. Linear staining IgG and C3 in BMZ
  4. Dermal side
39
Q

Epidermolysis Bullosa:

  1. Etiology
  2. Presentation
  3. Types and targets
A
  1. Skin fragility disorders resulting from inherited mutations in genes encoding BMZ proteins.
  2. Blisters and erosions from minimal mechanical trauma. Variable features depending on type
  3. Types:
  • Epidermolysis bullosa simplex: autosomal dominant, targets keratins 5, 14 in basal keratinocytes
  • Junctional EB - autosomal recessive, targeting laminin 332 and BP180
  • Dystrophic EB - autosomal dominant or recessive, targeting type VII collagen
40
Q

Stratum lucidum (of the epidermis) is only found where?

A

acral skin (palms and soles)

41
Q

Where are melanocytes typicall found? How many of them are generally present?

A

Basal layer of epidermis

Typically 1:10 (melanocytes:keratinocytes)

42
Q

What are Langherhans cells?

A

Dendritic APCs in the epidermis

43
Q

The papillary and reticular layers of the dermis are delineated by what? Describe the collagen in each layer.

A
  • Delineated by a vascular plexus
  • Papillar: fine, vertical collagen
  • Reticular: coarse, horizontal collaged
44
Q

What touch sensor type is found in the deep dermis/subQ interface of the palms, soles, digits, genitalia, ligaments, and joints and senses deep pressure/vibration?

A

Pacinian corpuscles

45
Q

Name the (3) parts of the hair follicle and what delineates them

A
  • Infundibulum: follicular orifice to entrance of sebaceous duct
  • Isthmus: sebaceous duct to insertion of arrector pili muscle
  • Lower portion: below insertion of arrector pili muscle
46
Q

Sebaceous glands use what type of secretion? Where can they be found?

A

Holocrine secretion

Eyelids, vermillion border of lips, penis, nipple

47
Q

What type of sweat gland is usually activated at puberty? Describe them.

A

Apocrine glands

Typically opens into the hair follicle at the level of the sebaceous gland.

Found in axillae, anogenital area, external ear canal, eyelid, and areola

Decapitation secretion

48
Q

What sweat gland type is found over virtually the entire body, but is especially concentrated in the plams, soles, axillae, and forehead? Where do they generally empty?

A

Eccrine

Empty directly to the skin surface

49
Q

Describe the unique features of skin found in each of the following locations:

  1. scalp
  2. trunk
  3. eyelid
  4. nose
  5. ear
  6. acral
  7. mucosa
A
  1. scalp: many large terminal hairs, with hair bulbs extending into subQ fat
  2. trunk: very thick with broad parallel collagen fascicles in dermis
  3. eyelids: Very thin, skeletal muscle bundles, hair follicles
  4. nose: conspicuous sebaceous glands that often drain directly onto the skin surface
  5. ear: vellous hair follicles and prominent cartilage
  6. acral skin: thick, compact stratum corneum with prominent rete ridge pattern (fingerprints), stratum lucidum is present
  7. mucosa: No granular layer present. Pale keratinocytes due to glycogen content