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Dermatology > Pathophys/Path 5 > Flashcards

Pathophys/Path 5 Flashcards

1
Q

Embryology of Skin

A

gastrulation: divide into 3 layers
- ectoderm goes to ectoderm and neuroectoderm
- mesoderm
- endoderm

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2
Q

Epidermis

A

formed by epidermis

-stratum baslaem
-stratum spinulosum
-stratum granulosum
stratum lucidum
stratum corneum

  • defect lead to ectodermal dysplasias
    week 6-bilayered epidermis (periderm, basal layer)
    week 8-stratification begins (intermediate, basal)
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3
Q

Ectodermal Dysplasias

A

defects in hair, teeth, bone, skin

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4
Q

Skin by mid Trimester

A
  • terminally differentiated epidermal layers similar to adult skin
  • filaggrin expressed and cornified cell envelope formed
  • defects lead to ichthyoses
  • Ichythosis vulgaris due to filaggrin mutation
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5
Q

Cell lines in epidermis

A
  • melanocytes
  • langerhans
  • merkle
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6
Q

Melanocyte embryology

A

Originate in the neural crest

  • migrate to ear,eye,skin,leptomeninges
  • origin/migration/survival defect leads to patches lead depigmentation where no migration took place
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7
Q

Piebaldism

A

-defective melanocyte mutation leads to patches of depigmentation

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8
Q

Waardenberg syndrome

A
  • defective survival of melanocytes leads to patches of depigmentation
  • enteric ganglion cells also effected (heart/other problems)
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9
Q

Hermansky Pudlak and Chediak Higashi Syndrome

A
  • ineffective transfer of melanosomes to keratinocytes lead to pifmentary dilution (silver hue)
  • may affect other cells where lysosomal trafficking is important (neutrophils, neurons, platelets)
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10
Q

Alminism

A
  • ineffective melanin production
  • melanocytes are present, but no melanin
  • genes lead to diff phenotypes
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11
Q

Mosaicism

A
  • 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 lyonizatioin
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12
Q

Dermis embryology

A
  • derived from both ectoderm and mesoderm
  • by 12 weeks, fully functional EGA (dermal-epidermal junction)
  • barrier function of skin not fully developed until 3 weeks after birth
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13
Q

Neonatal Dermatology

A
  • surface area to weight ratio is 5 times that of adults
  • increased percutaneous absorption of topical medicines
  • premature infants have increased transepidermal water loss (TEWL)
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14
Q

Vernix Caseosa

A
  • protective membrane present at birth
  • mechanical barrier in utero
  • composed of epithelial cells, sebaceous secretions, and shed lanugo hair
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15
Q

Cutis Marmorata

A
  • accentuated with temperature decrease

- resolves with re-warming

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16
Q

Erythema Toxicum Neonatorum

A
  • tiny pustules with wheel, evervescent
  • benign
  • up to 50% of infants
  • resolve spontaneously
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17
Q

Miliaria

A
  • due to occlusion of eccrine glands at different levels
  • miliaria cystallina
  • miliaria rubra
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18
Q

Neonatal Acne

A

“Neonatla Cephalic Pustulosis”

  • primary lesion is pustule not comodone
  • due to maternal hormones
  • Maallessezia may also play role
  • resolves spontaniously
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19
Q

Transient Neonatla Pustular Melanosis

A

-leaves darker spots
-more common in AA infants
-resolves spontaneously
-

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20
Q

Seborrheic Dermatitis

A

cradle cap

self-limited

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21
Q

Diaper Dermatitis

A
  • wide differentiation
  • several common causes: irritant, candidia
    other: seborrhic
    or: seborrheic dermatitis, psoriasis, allergic contact, nutritional deficiencies, langerhans cell histiocytosis, jacquet’s dermatitis
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22
Q

Atopic Dermatitis

A

-up to 20% in US
-60% will present within first year of life
-85% by age 5
-can be associated with asthma and allergic rhinitis
“atopic march”-eczema, asthma, rhinitis

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23
Q

Cause of atopic dermatitis

A

filaggrin mutatuins -know to cause ichthyosis vulgaris

-strongly associated with AD, linked with early onset

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24
Q

Pathogenesis of Atopic Dermatits

A
  • barrier dysfunction leads to exposure to allergens

- secondary immune dysregulation due to increased allergen exposure

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25
Criterial of Dermatitis
-Pruritus in past 12 months plus 3 of following: *history of dry skin in last year *personal/family allergic rhinitis history *onset before 2 *history of skin crease involvement *visible flexural dermatitis (<4 cheeks, forehead, extensor)
26
Atopic dermatitis: infantile phase
cheeks, forehead, scalp, extensor - spares diaper are - intense pruritis,erythema, oozing
27
Atopic Dermatitis: childhood phase
favors flexor surfaces, wrists, ankles, neck | -lichenification common
28
AD complications
Infection-staph (90%) - eczema herpeticum-explosive eruption of herpes simplex - molluscum contagiosum-more in AD - behavioral- increased ADHD
29
AD Management
Moisture:vasiline, seromides,etc. Daily bathing with mild soaps (dove, cetaphil) dilute bleach baths avoidance of heat, wool clothes, etc. topical steroids topical calcineurin inhibitors (tacrolimus) treatment of secondary infections
30
other management
food allergens-increased AD - consider testing moderate to severe AD unresponsive to traditioinal treatment - contact dermatitis - antihistamines (consider at night) - wet wraps
31
Acne Vulgaris
multifactorial disorder of pilosebaceous unit - densest population of sebaceous follicles: face, upper chest, back - disease of adolesents (15-18) - involution by 25, 5-12% still have it at 45y/o
32
Acne Pathogenesis
1) hyperproliferation & abnormal differentiation of keratinocytes leading to plugging of follicular infundibulum 2) excess sebum production due to hormonal stimulation 3) presence of propinoibacterium acnes, gram + rod present deep within follicle that breaks down sebum & produces inflammatory mediators 4) INFLAMMATION - comedo rupture leads to spilling of immunogenic contents (bacteria, keratin, seebum, neutrophil)
33
Contributing factors
- comedogenic greasy or occlussive products - mechanical irritation: overzealous washing, chin straps, hats, etc - medications: corticosteroids, lithium, etc. - Hyperandrogenic states (polycystic ovarian syndrome, virilzing tumors, congenital adrenal hyperplasia)
34
Geriaric Dermatology
- aging population - Intrinsic vs extrinsic - diabetes, CHF, HIV, athersclerosis (impede vascular efficiency, decrease immune response)
35
Normal Aging
(instrinsic) - loss of elasticity - skin thinning - xerosis - wrinkling
36
Sucking Blisters
blister where they sucked finger in womb
37
Lanugo
hair over infant body, goes away
38
Sebaceous Gland Hyperpalsia
-spots around nose
39
Milia
white spots on hard pallet or gum
40
Mongolion spot
grey area on back
41
Salmon patch
on forehead
42
Stork Bite
on back of neck
43
Hormonal effects of Acne Vulgaris
- sebum production is affected by hormones - androgens produced inside sebaceous gland by adrenals and gonads - estrogen? local inhibition, gonadal inhibition, gene regulation?
44
Open Comedones
black head
45
Closed Comedones
white head
46
Acne Conglobata (acne fulminans)
- severe eruptive nodulocystic acne - Conglobata- no systemic symptoms - Fulminans-systemic, fever, arthralgias, osteolytic bone lesions, hepatosplenomegaly
47
Steroid induced acne
all at same stage
48
Acne Excoriee de jeunes filles
young females picking acne
49
Acne Vulgaris Treatments | Topical:
1) benzoyl peroxide: bactericidal , no resistance 2) abx: agianst P. acnes, combine or resistant 3) retinoids: desqumation of follicular epithelium decrease comedones and anti-inflammatory
50
Acne Vulgaris Treatments | Systemic:
``` Abx: anti-inflammatory P. acnes Hormonal decrease androgens Oral retinoids: normalize epidermal differentiation, decrease sebum production , anti-inflammatroy ***teratogenic - "I pledge" -give with steroids ```
51
Keloids
- more common in darker skin | - high risk of recurrence with removal
52
Photoaging
(extrinsic) - actinic keratoses - coarse wrinkling - elastosis with giant comedones
53
Decubitus Ulcers
-caused by pressure over bony prominences for extended periods of time -Stage I-nonblanchable erythema, intact skin II-necrosis with superficial/partial thickness can have dermis involvement III-deep necrosis with loss of skin to fascia IV- extensive necrosis into fascia/bone/muscle
54
Dermatitis in Geriatric Patients
- asteatotic eczema - nummular eczema - stasis dermatitis - seborrheic dermatitis
55
Geriatric: Stasis Dermatitis
- due to venous insufficiency and edema - can result in venous ulvers - treat: exercise, elevation, compression, topical steroids, antibiotics (infection)
56
Scurvy
Vit C deficiencies | poor teeth
57
Pellagra
Niacin (B3) deficiencies - dementa - dermatitis - diarrhea
58
Geriatric Infection
staph, strep, HZV, candida, tinea pedis, tinea cruris, onychomycosis
59
Gianotti-Crosti
EBV, HIV
60
Henoch-Schonlein Purpura
- vasculitis | - glomerunephritis
61
Kawasaki disease
epidemic -puffy hands/feet strawberry tongue anyuruseums of coronary artery
62
Keratosis pilaris
features of atopic dermatitis | kerotitic follicles
63
Pityriasis alba
features of atopic dermatitis | hypopigmented areas
64
Nummula Dermatitis
features of atopic dermatitis | coin shaped lesions
65
Dyshydrotic eczema
features of atopic dermatitis | vesicles along fingers (tapioka pudding)
66
Juvenile plantar dermatosis
features of atopic dermatitis | "sweaty sock" dry feet
67
Denny-Morgan pleats
features of atopic dermatitis | transverse line under eye
68
Allergic shiners
features of atopic dermatitis | dark circles
69
Allergic salute
features of atopic dermatitis | crease across nose from wiping
70
Accentuated palmar creases
features of atopic dermatitis

Dermatology (9 decks)

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