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Derm > Skin Throughout the Ages > Flashcards

Skin Throughout the Ages Flashcards

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Dermatology Board Prep flashcards
1
Q

The epidermis is derived from what germ layer

A

ectoderm

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2
Q

What is the added layer of the epidermis on the palms and soles?

A

stratum lucidum

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3
Q

defects in hair, teeth, bone, and skin

A

ectodermal dysplasia

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4
Q
  1. defects in fillagrin lead to
  2. During what trimester of preganncy does this occur?
A
  1. Ischythosis vulgaris (*pictured*)

atopic dematitis (eczema)

  1. third timester
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5
Q

What are the specialized cells in the epidermis?

A

Melanocytes

Merkle Cells

Langerhans Cells

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6
Q

Melanocytes originate in the ____

where do they migrate to?

A

neural crest

ear, eye, skin, leptomeninges

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7
Q

patches of depigmentation is due to ….

A

defect in melanocyte migration, survival, or origin

here is another pic of it:

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8
Q

Waardenberg Syndrome

A

patches of depigmentation = defect in melanocyte survival

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9
Q

defect in production of melanin

A

albansim

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10
Q

pigment dilution is due to …

A

defect in melanosome = cannot transfer melanin to keratinocyes

ex: chediak-higashi, hermansky pudlack syndrome

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11
Q

linear streats or whorls (as picuted below)

A

Pigemntary Mosaicsm

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12
Q

lines of Blaschko

A

where melanocytes develop

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13
Q

What is this?

A

lines of blaschko

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14
Q

What germ layer is the dermis derived from?

A

ectoderm and mesoderm

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15
Q

Barrier function of skin is fully developed 3 weeks (before or after) birth

A

after

*dermal-epidermal junction is fully developed by 12 weeks gestation

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16
Q

neonates have (increased or decreased) topical absorption of medicine

A

increased

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17
Q

premature infants have (increased or decreaed) transepidermal water loss

A

increased

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18
Q

protective membrnae present at birth, in utero it was the mechanical barrier to prevent breakdown of skin since babies are living in a water environment in utero

What is this composed of?

A

Vernix Caseosa

epithelial cells, sebaceous fluid, and shed lanugo hair

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19
Q

What is this and what causes it?

Is this physiologic or pathologic?

A

cutis marmorate

baby gets cold

*physiologic

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20
Q

What is it?

Is this physiologic or pathologic?

A

lanugo

physiologic

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21
Q

What is it?

Is this physiologic or pathologic?

A

sebaceous gland hyperplasia

phsyiologic

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22
Q

What is it?

Is this physiologic or pathologic?

A

Sucking Blister

phys

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23
Q

What is it?

Is this physiologic or pathologic?

A

mongolian spot

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24
Q

What is it?

Is this physiologic or pathologic?

A

salmon patch

phys

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25
Q

What is it?

Is this physiologic or pathologic?

A

stork bite (same thing as a salmon patch)

phys

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26
Q

What is it?

Is this physiologic or pathologic?

A

Erythema Toxicum Neonatorum

**up to 50% of infants have this, resolves spontaneously

she has it under disorders, but it is benign

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27
Q

What is this?

What causes it?

A

Miliaria

due to occlusion of eccrine glands

another picture:

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28
Q

aka neonatal cephalic pustulosis

A

neonatal acne

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29
Q

What is it?

A

transient neonatal pustular melanosis

*more common in AA

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30
Q

What is it?

A

Seborrheic Dermatitis

aka cradle cap

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31
Q

What is this?

A

Diaper Dermatitis due to Candida (the dots tell you candida)

Below is diaper dermatitis due to an irritant. Note the lack of the dots

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32
Q

often assc with asthma and allergic rhinitis

A

atopic dermatitis

33
Q

pathogeneis of atopic dermatitis

A

cycle of immune dysreguation, barrier dysfunction, and environmental allergens

34
Q

What is the clinical criteria for atopic dermatitis?

A

PURITIS in the past 12 months

plus at least 3 of the following

  1. dry skin
  2. Hx of allergic rhinitis or asthma (or FHx)
  3. onset before 2 yo
  4. Hx of skin crease involvement
  5. visible flexural dermatitis
35
Q

Favors cheeks, forehead, scalp and extensor surfaces
Spares diaper area
Intense pruritus, erythema, oozing

A

infantile phate of atopic dermatitis

36
Q

Favors flexor surfaces, wrists, ankles, neck
Lichenification common

A

childhood phase of atopic dermatitis

37
Q

What is it?

A

atopic dermatitis

38
Q

What is it?

A

??

39
Q

What is it?

A

??

40
Q

Complication of atopic dermatitis

A

Staph Aureus infeciton

Eczema Herpeticum

Molluscum Contagiosum

41
Q
A

Eczema Herpeticum

42
Q

Multifactorial disorder of pilosebaceous unit

A

acne vulgaris

43
Q

Where does acne occur?

A

denses population of sebaceous follicles:

face, upper chest, back

44
Q

Pathogenesis of acne vulgaris

A
  1. hyperprolif and anb differentiation of keratinocytes = plugging of follicular infundibulum
  2. excess sebum production (hormones)
  3. propionibacterium acnes
  4. inflammation
45
Q

How do androgens (produced inside sebaceous gland) affect acne?

A

increases sebum production, leading to acne vulgaris

46
Q

Why does P. acnes suck so much?

A

G+ rod which breaks down sebum, produces inflammatory mediatiors

47
Q

What causes acne inflammation?

A
  1. comedo rupture
  2. spilling of immunogenic contents (sebum, keratin, bacteria)
  3. neutrophil-rich inflammation
48
Q

Hyperandrogenic states which cause acne:

A

polycystic ovarian syndrome

virilizng tumors

cong. adrenal hyperplasia

49
Q

Histology of an inflammed comedo:

A
  1. fibrin
  2. neutrophils, especially at site of rupture
  3. keratin plug
50
Q

Severe eruptive nodulocystic acne that does NOT have systemic symptoms

A

Acne conglobata

51
Q

Severe eruptive nodulocystic acne that has systemic symptoms (fever, osteolytic bone lesions, hepatosplenomegaly)

A

Acne fulminans

52
Q

Topical Acne vulgaris treatment

A

benzoyl peroxide

topical abx (combine with BPO to vaoid resistance)

topical retinoids (reduce comedones)

53
Q

Systemic acne vulgaris treatments

A

abx (resistance)

hormonal therapy to decrease effective androgens

oral retinoids

54
Q

How do oral retinoids work?

A

normalize epidermal differentiation, decrease sebum production, anti-inflmm

(teratogenic; combined w corticosteroids for acne fulminans)

55
Q

Skin lesion more common with darker skin; high risk of recurrance with removal

A

keloids

56
Q

Normal aging?

“Loss of elasticity”

A

yes

57
Q

Normal aging?

“actinic keratosis”

A

nope- photoaging (extrinsic)

58
Q

Normal aging?

“elastosis with giant comedones”

A

no: photoaging, extrinsic

59
Q

Normal aging?

“thinning, wrinkling skin”

A

yes

60
Q

Caused by pressure of bony prominences for extended periods of time

A

decubitus ulcers

61
Q

How are decub ulcers graded?

A

I through IV

(with I nonblanching/intact; II superficial necrosis; III deep necrosis; IV necrosis into fascia +/- bone/muscle/etc)

62
Q

4 types of geriatric dermatits

A

asteatotic eczema

nummular eczema

stasis dermatitis

seborrheic dermatitis

63
Q

Due to venous insufficiency and edema, can result in venous ulcers

A

stasis dermatitis

64
Q

Dermatitis treated with exercise, elevation, compression and steroids

A

stasis dermatitis

65
Q

Diseases caused by nutritional deficiencies in geriatric patients

A

scurvy (vit C)

pellagra (niacin)

66
Q

3 D’s of niacin deficiency

A

(*Pellagra)

Diarrhea, dermatitis, dementia

67
Q

Kid with a fever, trouble eating

A

hand-foot-mouth

68
Q
A

atopic dermatitis

69
Q
A

erytheoma toxicum neonatorum

70
Q
A

eczema herpeticum

71
Q
A

shingles

72
Q

itchy

A

scabies

73
Q

kid

A

erythema infectiousum (parvo)

74
Q
A

molluscum

75
Q
A

ringworm

76
Q
A

herpes simplex

77
Q
A

perleche

(candida)

78
Q
A

gianotti-crosti

Derm (12 decks)

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