skin through the ages Flashcards

(100 cards)

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
dermis: By 12 weeks EGA, \_\_\_\_\_\_\_\_\_\_\_\_\_is fully functional \_\_\_\_\_\_\_\_\_\_\_function of skin not fully developed until 3 weeks after birth
By 12 weeks EGA, **dermal-epidermal junction** is fully functional **Barrier function** of skin not fully developed until 3 weeks after birth
26
Body surface area to weight ratio is ________ times that of adults infants have increase \_\_\_\_\_\_\_\_\_\_\_of topical medicines Premature infants have increased\_\_\_\_\_\_\_\_\_loss
Infant Body surface area to weight ratio is **five** times that of adults Increased **percutaneous absorption** of topical medicines Premature infants have increased t**ransepidermal water loss (TEWL)**
27
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
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
28
what is it? what is its function? what is it composed of?(3)
**Vernix Caseosa** **Protective membrane present at birth Mechanical barrier in utero Composed of epithelial cells, sebaceous secretions, and shed lanugo hair**
29
physiologic changes in new born: what is it? what is it accentuated with? how does it resolve?
**Cutis Marmorata** **Accentuated with temperature decrease Resolves with re-warming**
30
neonatal desquamation, sucking blisters, lanugo, sebaceous gland hyperplasia, and milia are all \_\_\_\_\_\_\_
physiologic changes in newborn
31
which condition?
milia
32
what is it?
salmon patch: physiologic change
33
what is it?
mongolian spot: physiological changes in newborn
34
what is it?
stork bite: physiologic changes in newborn
35
condition? benign or malignant? prevalence? how does it resolve?
**Erythema Toxicum Neonatorum** **Benign Up to 50% of infants Resolves spontaneously**
36
conditin? what causes it? what are two types?
**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
37
condition? possible cause? which yeast may play a role? how does it resolve?
**NEONATAL ACNE =“Neonatal Cephalic Pustulosis”** Possibly due to **maternal hormones** * *Mallessezia** may also play a roles * *Resolves spontaneously**
38
condiiton? who is it most common in? how does it resolve?
**Transient Neonatal Pustular Melanosis** More common in **African American** infants **Resolves spontaneously**
39
condition? cause?
Seborrheic Dermatitis called Cradle Cap in newborns caused by Malassezia furfur Self-limited
40
condition? causes
Diaper Dermatitis (in image due to candida b/c of satellite pustules) Wide Differential Several common causes: Irritant Candida
41
differential diagnosis for diaper dermatitis
**_Differential Diagnosis_** Seborrheic Dermatitis Psoriasis Allergic Contact Dermatitis Nutritional Deficiencies (zinc) Langerhans cell histiocytosis Jacquet’s Dermatitis(severe irritant, sign of neglect)
42
common viral infections in kids(8)? think: MMR SlapRoseHand MonoVar
**_Viral Infections_** Measles Mumps Rubella Erythema Infectiosum Roseola Hand Foot and Mouth Diease Mononucleosis Varicella
43
Common bacterial infections in kids? (5)
**_Bacterial Infections_** Staph Scalded Skin Syndrome Toxic Shock Syndrome Scarlet Fever Impetigo Bacterial meningitis
44
childhood infections: a rash in response to lots of different viruses esp HepB and EBV
Gianotti- Crosti
45
childhood infections: vasculitis usually caused by strep and can lead to glomerulonephritis. need to check kidney function
Henoch-Schonlein Purpura
46
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
kawaski's disease
47
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
Atopic Dermatitis
48
KNOW: what is the atopic march?
1. atopic dermatitis = eczyma as a kid 2. asthma as they get a little older 3. allergic rhinitis as adult
49
how are fillagrin mutations associated with atopic dermatitis?
**Filaggrin mutations** Known to cause ichthyosis vulgaris Strongly assoicated with AD Linked with early onset of AD
50
what is the pathogenesis of atopic dermatitis?
**Pathogenesis** Barrier dysfunction leads to exposure to allergens Secondary immune dysregulation due to increased allergen exposure
51
what is the clinical criteria for atopic dermatitis?
**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
describe the infantile phase of atopic dermatitis
**_Infantile phase:_** Favors cheeks, forehead, scalp and **extensor surfaces** **Spares diaper area** Intense pruritus, erythema, oozing
53
describe the childhood phase of atopic dermatitis
**Favors flexor surfaces,** wrists, ankles, neck Lichenification common
54
condition?
atopic dermatitis
55
FYI: associated features of atopic dermatitis
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
condition?
atopic dermatitis can see denny-morgan pleats(transverse lines under the eye) milia (superficial epidermal inclusion cysts)
57
atopic dermatitis 1. what type of hypersensivity reaction? 2. appearance on kids
1. type I IgE mediated hypersensitivity rxn 2. dry skin and eczema on cheeks and extensor and flexural surfaces
58
59
condition?
lichenification in older kid with atopic dermatitis
60
condition association
nummular dermatisis atopic dermatitis
61
which condition? association
keratosis pilaris atopic dermatis
62
three infectious complications of atopic dermatitis. KNOW: Which one is an emergency? how do you treat?
* *_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
condition? which association?
pityriasis alba atopic dermatitis
64
t/f. kids with atopic dermatitis also have increased risk of ADHD
true
65
what is the basic managemet of atopic dermatitis?
#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
what are 4 other alteranate management considerations in AD?
**_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
# define acne where is it most dense? primarily it is a disease of ____ with greatest frequency btw ages \_\_\_\_\_\_ involution at which age?
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
first step in acne pathogenesis
1. Hyperproliferation and abnormal differentiation of keratinocytes leading to plugging of the follicular infundibulum.
69
second step in acne pathogenesis
2. Excess sebum production due to hormonal stimulation
70
what is the third step in acne pathogenesis
3. Presence of Propionibacterium acnes A gram + rod present deep within the follicle that breaks down sebum and produces inflammatory mediators.
71
how do hormones affect acne vulgaris pathogenesis? what is the role of androgens? how is estrogen invovled?
**_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
what is the fourth step in acte vulgaris pathogenesis?
4. Inflammation After continued dilation, comedo rupture leads to spilling of its immunogenic contents (sebum, keratin, bacteria) into the dermis and neutrophil-rich inflammation.
73
4 steps of acne pathogenesis
1. 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
difference btw white and black head
black head - open comedo white head- closed comedo
75
what are 4 additional contributing factors to acne?
**_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
what is it?
Histology of an Inflamed Comedo
77
what is it?
open comedo = black head
78
KNOW: what are the two subtypes of severe nodulocystic acne? KNOW: which subtype has systemic symtoms?
**1. Acne conglobata does not have systemic symptoms** 2. **Acne fulminans has systemic manifestations** including fever, arthralgias, osteolytic bone lesions, hepatosplenomegaly
79
which condition?
Clinical Features: Acne fulminans
80
which condition?
Clinical Features: Steroid-induced Acne = monomorphic. lesions look like they developed at same time
81
which condition?
Clinical Features: Pityrosporum Acne treat like seborrheic dermatitis(malassezia furfur caused)
82
which condtion?
acne excoriee de juenes filles - of young females who keep on scratching face
83
acne caused by chin strap
acne mechanica (would appear around chin)
84
acne caused by occupation (eg cutting oil production, solar damage)?
Clinical Features: Occuptional acne/Chloracne
85
KNOW: what is the follicular occlusion tetrad?
1. acne conglobata 2. hidradenitis supparativa 3. pilonidal cyst 4. dissecting cellulitis
86
what is the mainstay TOPICAL treatment for acne?
**_TOPICAL RETINOIDS_** * *_Topical retinoids:_** promote normal desquamation of the follicular epithelium, reducing comedones; some anti-inflammatory effect e. g. adapalene, tretinoin, tazarotene
87
what are three topical tx for acne vulgaris?
**_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
what are three systemic tx for acne? KNOW: which one is teratogenic?
**_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
condition? risk of reccurence?
**_KELOIDS_** More common in darker skin types High risk of recurrence with removal
90
effects of Diabetes, congestive heart failure, HIV, athersclerosis, etc. on aging?
Impede vascular efficiency Decrease immune responses
91
4 characteristcis of normal aging? is it extrinsic or intrinsic?
**Normal Aging(instrinsic):** Loss of elasticity Thinning of skin Xerosis- skin drying Wrinkling
92
condition? is it extrinsic or intrinsic? what are three aspects of it?
**_Photoaging (extrinsic):_** Actinic keratoses Coarse wrinkling Elastosis with giant comedones
93
condition? what causes it? how is it graded?
**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
condition? what causes it? what can it result in? KNOW two treatments that must be employed?
**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
6 common infections in older ppl. just keep in mind that weak immune system --\> infections can be workse
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
which nutrtional deficiency in old ppl
Scurvy pic 1 --notice the hemorrhage btw teeth b/c vit C is needed for formation of clotting factors
97
which condition? what are the classic three D's associated with conditon?
pellagra pellagra = niacin deficiency. niacin = vit B3 three D's: dementia, dermatitis, diarrhea
98
hand-foot-mouth disease caused by ____ virus
coxsackie
99
condition?
**_molluscum contagioisum:_** no inflammatory reaction around also key words: umbilicated, central core or depression, Henderson-Paterson bodies, poxvirus
100
condition?
gionatti-crosti Rash that comes after viral infection. eg EBV. can last for at least a month.