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skin through the ages Flashcards

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Dermatology Board Prep flashcards
1
Q

At gastrulation, cells divide into 3 layers: what are they?

A

Ectoderm

Mesoderm

Endoderm

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2
Q

ectoderm then divides into_________(2 layers)

A

Ectoderm

Neuroectoderm (neural crest and neural tube)

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3
Q

epidermis is derived from________

A

Formed from Ectoderm

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4
Q

what are the five layers of the skin?

A

Stratum Basale

Stratum Spinulosum

Stratum Granulosum

Stratum Lucidum

Stratum Corneum

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5
Q

at week 6, what is developed in the epidermis?

A

Week 6

Bilayered Epidermis

Periderm

Basal Layer

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6
Q

at week 8, what is happening in the development of the epidermis?

A

Week 8

Stratification begins

Intermediate layer and Basal layer

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7
Q

defects at week 8 of skin development lead to which condition?

A

Defects at this point lead to Ectodermal Dysplasia

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8
Q

what defects are seen in ectodermal dysplasia?

A

Defects in hair, teeth, bone, skin

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9
Q

by mid-third trimester, describe development of the skin. which protein is expressed and what about the cell formation of the cell envelope? what do defects at mid 3rd trimester lead to?

A

By Mid 3rd Trimester: Terminally differentiated epidermal layers similar to adult skin

Filaggrin expressed and the cornified cell envelope formed

Defects at this point lead to some of the ichthyoses

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10
Q

which conditoin? mutation in what causes this?

A

ichythosis vulgaris

filaggrin mutation

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11
Q

what are the three specialized cells in the epidermis?

A

melanocytes (produce and distribute melanin)

langerhan cells (

merkle cells (specialized cell, neural type)

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12
Q

know: where do melanocytes originate?

A

neural crest

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13
Q

where do melanocytes migrate to?

A

ear(cochlear)

eye(choroid, iris, ciliary body, retnia)

skin(epdiermeis and hair follicles)

leptomeninges

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14
Q

KNOW: Origin/migration/survival- defect leads to _________________

A

Origin/migration/survival- defect leads to **patches of depigmentation where no migration took place (eg **Waardenburg Syndrome, Piebaldism) **

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15
Q

KNOW: melanin synthesis defects lead to _____________

A

Melanin synthesis- defect leads to **defective production of melanin (albinism) **

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16
Q

KNOW:Melanosome formation and movement- defect leads to ___________

A

Melanosome formation and movement- defect leads to pigment dilution
Chediak-Higashi, Hermansky Pudlak Syndrome

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17
Q

which condition?

cause?

A
  • *disorder: Piebaldism**
  • *cause: Defective melanocyte mutation leads to patches of depigmentation**
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18
Q

condition?

what causes it?

A

MOSAICISM

cause: Different gene populations in one individual

Melanocytes develop along lines of Blaschko

Pigmentary mosaicism seen as linear streaks or whorls

X-linked conditions often follow lines of blaschko due to lyonization(x-incactivation)

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19
Q

conditoin?

what causes it

A

cause: Waardenberg Syndrome
Defective survival of melanocytes leads to patches of depigmentation
Enteric ganglion cells also affected (also from neural crest)

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20
Q

condition?

what causes it?

A

Albinism
cause: Due to ineffective production of melanin
Melanocytes are present, but there is no melanin
Different genes lead to different phenotypes

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21
Q

conditoin?

cause?

A

condition: Hermansky Pudlak and Chediak Higashi Syndrome
cause: Ineffective transfer of melanosomes to keratinocytes lead to pigmentary dilution (silver hue).
what is affected: May affect other cells where lysosomal trafficking is important (Neutrophils, Neurons, Platelets)

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22
Q

which condtion?

mode of inheritance?

progression of disease?

which three defects are present?

which gender is it fatal in utero in?

A

condition: incontientia pigmenti

XLD: x-linked dominant

progression of disease: blaschkoid vesicles–>verrucous–>hyperpigmented–>hypopigmented lesions

defects: ocular, dental, CNS

FATAL in utero in males (females can survie b/c of lyonization)

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23
Q

______ lines

A

blaschko lines

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24
Q

KNOW: dermis is dervied from _________

A

Derived from both ectoderm and **mesoderm **

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25
Q

dermis: By 12 weeks EGA, _____________is fully functional

___________function of skin not fully developed until 3 weeks after birth

A

By 12 weeks EGA, dermal-epidermal junction is fully functional

Barrier function of skin not fully developed until 3 weeks after birth

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26
Q

Body surface area to weight ratio is ________ times that of adults

infants have increase ___________of topical medicines

Premature infants have increased_________loss

A

Infant Body surface area to weight ratio is five times that of adults

Increased percutaneous absorption of topical medicines

Premature infants have increased transepidermal water loss (TEWL)

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27
Q

considerations in prematurity:

  1. stratum cornenum of premature babies compared to adults and full term infants?
  2. How long does it take premature babies to have competent barrier function?
  3. increased ________ loss compared to full-term infants
  4. 3 ways premature infants differ from regular infants
A
  1. thinner stratum corneum than adults and full-term infants
  2. can take longer than 3 weeks for competent barrier function
  3. increased Transepidermal water loss compared to full-term infants
  4. increased risk of infections, increased percutaneous absorption of topical medicines, and decreased temp and fluid regulation
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28
Q

what is it?

what is its function?

what is it composed of?(3)

A

Vernix Caseosa
Protective membrane present at birth
Mechanical barrier in utero
Composed of epithelial cells, sebaceous secretions, and shed lanugo hair

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29
Q

physiologic changes in new born:

what is it?

what is it accentuated with?

how does it resolve?

A

Cutis Marmorata
Accentuated with temperature decrease
Resolves with re-warming

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30
Q

neonatal desquamation, sucking blisters, lanugo, sebaceous gland hyperplasia, and milia are all _______

A

physiologic changes in newborn

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31
Q

which condition?

A

milia

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32
Q

what is it?

A

salmon patch: physiologic change

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33
Q

what is it?

A

mongolian spot: physiological changes in newborn

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34
Q

what is it?

A

stork bite: physiologic changes in newborn

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35
Q

condition?

benign or malignant?

prevalence?

how does it resolve?

A

Erythema Toxicum Neonatorum
Benign
Up to 50% of infants
Resolves spontaneously

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36
Q

conditin?

what causes it?

what are two types?

A

Miliaria
cause: Due to occlusion of eccrine glands at different levels(wrapped baby up too tight)
subtypes: Miliaria Crystallina - pinpoint clear vesciles; sweat in occluded seat glands
Miliaria Rubra- prickly heat, erthematous papulovesciles; both miliaria respond to cooling

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37
Q

condition?

possible cause?

which yeast may play a role?

how does it resolve?

A

NEONATAL ACNE =“Neonatal Cephalic Pustulosis”

Possibly due to maternal hormones

  • *Mallessezia** may also play a roles
  • *Resolves spontaneously**
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38
Q

condiiton?

who is it most common in?

how does it resolve?

A

Transient Neonatal Pustular Melanosis
More common in African American infants
Resolves spontaneously

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39
Q

condition?

cause?

A

Seborrheic Dermatitis
called Cradle Cap in newborns

caused by Malassezia furfur
Self-limited

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40
Q

condition?

causes

A

Diaper Dermatitis (in image due to candida b/c of satellite pustules)

Wide Differential
Several common causes:
Irritant
Candida

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41
Q

differential diagnosis for diaper dermatitis

A

Differential Diagnosis
Seborrheic Dermatitis
Psoriasis
Allergic Contact Dermatitis
Nutritional Deficiencies (zinc)
Langerhans cell histiocytosis
Jacquet’s Dermatitis(severe irritant, sign of neglect)

42
Q

common viral infections in kids(8)? think: MMR SlapRoseHand MonoVar

A

Viral Infections
Measles
Mumps
Rubella
Erythema Infectiosum
Roseola
Hand Foot and Mouth Diease
Mononucleosis
Varicella

43
Q

Common bacterial infections in kids? (5)

A

Bacterial Infections
Staph Scalded Skin Syndrome
Toxic Shock Syndrome
Scarlet Fever
Impetigo
Bacterial meningitis

44
Q

childhood infections:

a rash in response to lots of different viruses esp HepB and EBV

A

Gianotti- Crosti

45
Q

childhood infections: vasculitis usually caused by strep and can lead to glomerulonephritis. need to check kidney function

A

Henoch-Schonlein Purpura

46
Q

childhood infections: vasculitis associated with desquamation of the hands and feet, strawberry tongue, anuersysms of coronary artery leading to permanent heart problems and possibly stroke

A

kawaski’s disease

47
Q

which condition?

Up to 20% prevalence in the US
60% of affected individuals will present within first year of life
85% by 5 years of age
Often associated with asthma and allergic rhinitis

A

Atopic Dermatitis

48
Q

KNOW: what is the atopic march?

A
  1. atopic dermatitis = eczyma as a kid
  2. asthma as they get a little older
  3. allergic rhinitis as adult
49
Q

how are fillagrin mutations associated with atopic dermatitis?

A

Filaggrin mutations
Known to cause ichthyosis vulgaris
Strongly assoicated with AD
Linked with early onset of AD

50
Q

what is the pathogenesis of atopic dermatitis?

A

Pathogenesis
Barrier dysfunction leads to exposure to allergens
Secondary immune dysregulation due to increased allergen exposure

51
Q

what is the clinical criteria for atopic dermatitis?

A

Pruritus in past 12 months

  • *PLUS at least 3 of the following:**
    1. History of generally dry skin in the last year
    2. Personal history of allergic rhinitis or asthma (or family history in first degree relative if <4 years of age)
    3. Onset before 2 years of age
    4. History of skin crease involvement
    5. Visible flexural dermatitis (if <4 years, include cheeks, forehead, extensor surface of limbs)
52
Q

describe the infantile phase of atopic dermatitis

A

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

53
Q

describe the childhood phase of atopic dermatitis

A

Favors flexor surfaces, wrists, ankles, neck
Lichenification common

54
Q

condition?

A

atopic dermatitis

55
Q

FYI: associated features of atopic dermatitis

A

Associated features
Keratosis pilaris-keratotic follicles on back of arms
Pityriasis alba – light hypopigemented area(on face)
Nummular Dermatitis- more coin shaped lesions
Dyshydrotic eczema- vesicles along lateral fingers(tapioca pudding)
Juvenile plantar dermatosis –sweaty sock dermatosis(dry, fissured feet)
Denny-Morgan pleats-transverse line under eye
Allergic shiners- look like haven’t slept, dark circles under eye
Allergic salute- crease across the nose, constantly wiping nose
Accentuated palmar creases -

56
Q

condition?

A

atopic dermatitis

can see denny-morgan pleats(transverse lines under the eye)

milia (superficial epidermal inclusion cysts)

57
Q

atopic dermatitis

  1. what type of hypersensivity reaction?
  2. appearance on kids
A
  1. type I IgE mediated hypersensitivity rxn
  2. dry skin and eczema on cheeks and extensor and flexural surfaces
58
Q
A
59
Q

condition?

A

lichenification in older kid with atopic dermatitis

60
Q

condition

association

A

nummular dermatisis

atopic dermatitis

61
Q

which condition?

association

A

keratosis pilaris

atopic dermatis

62
Q

three infectious complications of atopic dermatitis.

KNOW: Which one is an emergency? how do you treat?

A
  • *Infections**
  • *Staph. Aureus-**90% of AD lesions colonized with S. aureus (causes impetigo)

**Eczema Herpeticum- **Explosive eruption of Herpes simplex (EMERGENCY: admit and give IV acyclovir

Molluscum Contagiosum-More extensive in AD

63
Q

condition?

which association?

A

pityriasis alba

atopic dermatitis

64
Q

t/f. kids with atopic dermatitis also have increased risk of ADHD

A

true

65
Q

what is the basic managemet of atopic dermatitis?

A

1 = moisturize!!!!

Emollients
Daily bathing with mild soaps (Dove, Cetaphil)
Dilute bleach baths
Avoidance of skin irritation (heat, wool clothes, etc.)
Topical steroids
Topical calcineurin inhibitors (Tacrolimus)
Treatment of secondary infections

66
Q

what are 4 other alteranate management considerations in AD?

A

Food Allergens
Increased incidence in AD
Consider testing in moderate to severe AD unresponsive to traditional treatment

  • *Contact Dermatitis**
  • *Antihistamines**-Consider at night time
  • *Wet wraps**
67
Q

define acne

where is it most dense?

primarily it is a disease of ____ with greatest frequency btw ages ______

involution at which age?

A
  1. A multifactorial disorder of the pilosebaceous unit.
  2. Acne occurs where the densest population of sebaceous follicles are located: face, upper chest and back.
  3. Primarily a disease of adolescents with greatest frequency between ages 15-18.
  4. Involution usually by age 25, however around 5-12% of people still with acne at age 45.
68
Q

first step in acne pathogenesis

A
  1. Hyperproliferation and abnormal differentiation of keratinocytes leading to plugging of the follicular infundibulum.
69
Q

second step in acne pathogenesis

A
  1. Excess sebum production due to hormonal stimulation
70
Q

what is the third step in acne pathogenesis

A
  1. Presence of Propionibacterium acnes
    A gram + rod present deep within the follicle that breaks down sebum and produces inflammatory mediators.
71
Q

how do hormones affect acne vulgaris pathogenesis?

what is the role of androgens?

how is estrogen invovled?

A

Hormonal effects
Sebum production is affected by hormonal input

Androgens are produced inside the sebaceous gland, by the adrenals and the gonads

How is estrogen involved?
Local inhibition?
Gonadal inhibition?
Gene regulation?

72
Q

what is the fourth step in acte vulgaris pathogenesis?

A
  1. Inflammation
    After continued dilation, comedo rupture leads to spilling of its immunogenic contents (sebum, keratin, bacteria) into the dermis and neutrophil-rich inflammation.
73
Q

4 steps of acne pathogenesis

A
    1. Hyperproliferation and abnormal differentiation of keratinocytes leading to plugging of the follicular infundibulum
  2. Excess sebum production due to hormonal stimulation
  3. Presence of Propionibacterium acnes - A gram + rod present deep within the follicle that breaks down sebum and produces inflammatory mediators.
  4. Inflammation-After continued dilation, comedo rupture leads to spilling of its immunogenic contents (sebum, keratin, bacteria) into the dermis and neutrophil-rich inflammation.
74
Q

difference btw white and black head

A

black head - open comedo

white head- closed comedo

75
Q

what are 4 additional contributing factors to acne?

A

Additional contributing factors:
Comedogenic greasy or occlusive products

Mechanical irritation: overzealous washing, chin straps, hats, etc.

Medications: corticosteroids, lithium, etc.

Hyperandrogenic states
Polycystic ovarian syndrome
Virilizing tumors
Congenital adrenal hyperplasia

76
Q

what is it?

A

Histology of an Inflamed Comedo

77
Q

what is it?

A

open comedo = black head

78
Q

KNOW: what are the two subtypes of severe nodulocystic acne?

KNOW: which subtype has systemic symtoms?

A

1. Acne conglobata does not have systemic symptoms

  1. Acne fulminans has systemic manifestations including fever, arthralgias, osteolytic bone lesions, hepatosplenomegaly
79
Q

which condition?

A

Clinical Features: Acne fulminans

80
Q

which condition?

A

Clinical Features: Steroid-induced Acne = monomorphic. lesions look like they developed at same time

81
Q

which condition?

A

Clinical Features: Pityrosporum Acne

treat like seborrheic dermatitis(malassezia furfur caused)

82
Q

which condtion?

A

acne excoriee de juenes filles - of young females who keep on scratching face

83
Q

acne caused by chin strap

A

acne mechanica (would appear around chin)

84
Q

acne caused by occupation (eg cutting oil production, solar damage)?

A

Clinical Features: Occuptional acne/Chloracne

85
Q

KNOW: what is the follicular occlusion tetrad?

A
  1. acne conglobata
  2. hidradenitis supparativa
  3. pilonidal cyst
  4. dissecting cellulitis
86
Q

what is the mainstay TOPICAL treatment for acne?

A

TOPICAL RETINOIDS

  • *Topical retinoids:** promote normal desquamation of the follicular epithelium, reducing comedones; some anti-inflammatory effect
    e. g. adapalene, tretinoin, tazarotene
87
Q

what are three topical tx for acne vulgaris?

A

Benzoyl peroxide: bactericidal to P. acnes and bacterial resistance does not occur. OTC and Rx.

  • *Topical antibiotics:** effective against P. acnes. Can develop resistance if used alone, often combine with BPO.
    e. g. clindamycin, erythromycin
    e. g. ketoconazole shampoo, ZNP soap

Topical retinoids: promote normal desquamation of the follicular epithelium, reducing comedones; some anti-inflammatory effect e.g. adapalene, tretinoin, tazarotene

88
Q

what are three systemic tx for acne?

KNOW: which one is teratogenic?

A

Antibiotics: Anti-inflammatory properties and effective against P. acnes. Resistance common.e.g. tetracyclines, erythromycin

  • *Hormonal therapies**: Decrease effective androgens
    e. g. some OCP’s, spironolactone

Oral retinoids: normalize epidermal differentiation, decrease sebum production, and have anti-inflammatory properties. Teratogenic! Must avoid in pregnant women (category X).

e. g. isotretinoin
* *Use with systemic corticosteroids in treatment of acne fulminans**

89
Q

condition?

risk of reccurence?

A

KELOIDS

More common in darker skin types
High risk of recurrence with removal

90
Q

effects of Diabetes, congestive heart failure, HIV, athersclerosis, etc. on aging?

A

Impede vascular efficiency
Decrease immune responses

91
Q

4 characteristcis of normal aging?

is it extrinsic or intrinsic?

A

Normal Aging(instrinsic):

Loss of elasticity
Thinning of skin
Xerosis- skin drying
Wrinkling

92
Q

condition?

is it extrinsic or intrinsic?

what are three aspects of it?

A

Photoaging (extrinsic):
Actinic keratoses
Coarse wrinkling
Elastosis with giant comedones

93
Q

condition?

what causes it?

how is it graded?

A

Decubitus Ulcers
Caused by pressure over bony prominences for extended periods of time
Graded by stage:
I- nonblanchable erythema, intact skin
II- necrosis with superficial to partial-thickness involvement of epidermis +/- dermis
III- deep necrosis with full-thickness skin loss down to but not through fascia
IV- extensive necrosis into fascia +/- muscle, bone, supporting structures

94
Q

condition?

what causes it?

what can it result in?

KNOW two treatments that must be employed?

A

Stasis Dermatitis
Due to venous insufficiency and edema

Can result in venous ulcers

Treatment:
Exercise
_Elevation
Compression hose every day!!!_
Topical steroids
Antibiotics (if secondarily infected

95
Q

6 common infections in older ppl.

just keep in mind that weak immune system –> infections can be workse

A

Infections

Staph and Strep infections

  • *Herpes Zoster - reactivation of VSV, if suspect Hutchinson’s sign=ocular involvement=see eye doc immediately**
  • *Candida - **Perleche, Intertrigo, Anogenital

Tinea pedis
Tinea cruris
Onychomycosis- (nail fungal infection)

96
Q

which nutrtional deficiency in old ppl

A

Scurvy

pic 1 –notice the hemorrhage btw teeth b/c vit C is needed for formation of clotting factors

97
Q

which condition?

what are the classic three D’s associated with conditon?

A

pellagra

pellagra = niacin deficiency. niacin = vit B3

three D’s: dementia, dermatitis, diarrhea

98
Q

hand-foot-mouth disease caused by ____ virus

A

coxsackie

99
Q

condition?

A

molluscum contagioisum: no inflammatory reaction around

also key words: umbilicated, central core or depression, Henderson-Paterson bodies, poxvirus

100
Q

condition?

A

gionatti-crosti

Rash that comes after viral infection. eg EBV. can last for at least a month.

Dermatology (18 decks)

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