Pathophys/Path 5 Flashcards

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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
Q

Criterial of Dermatitis

A

-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)

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26
Q

Atopic dermatitis: infantile phase

A

cheeks, forehead, scalp, extensor

  • spares diaper are
  • intense pruritis,erythema, oozing
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27
Q

Atopic Dermatitis: childhood phase

A

favors flexor surfaces, wrists, ankles, neck

-lichenification common

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28
Q

AD complications

A

Infection-staph (90%)

  • eczema herpeticum-explosive eruption of herpes simplex
  • molluscum contagiosum-more in AD
  • behavioral- increased ADHD
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29
Q

AD Management

A

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
Q

other management

A

food allergens-increased AD

  • consider testing moderate to severe AD unresponsive to traditioinal treatment
  • contact dermatitis
  • antihistamines (consider at night)
  • wet wraps
31
Q

Acne Vulgaris

A

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
Q

Acne Pathogenesis

A

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
Q

Contributing factors

A
  • 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
Q

Geriaric Dermatology

A
  • aging population
  • Intrinsic vs extrinsic
  • diabetes, CHF, HIV, athersclerosis (impede vascular efficiency, decrease immune response)
35
Q

Normal Aging

A

(instrinsic)

  • loss of elasticity
  • skin thinning
  • xerosis
  • wrinkling
36
Q

Sucking Blisters

A

blister where they sucked finger in womb

37
Q

Lanugo

A

hair over infant body, goes away

38
Q

Sebaceous Gland Hyperpalsia

A

-spots around nose

39
Q

Milia

A

white spots on hard pallet or gum

40
Q

Mongolion spot

A

grey area on back

41
Q

Salmon patch

A

on forehead

42
Q

Stork Bite

A

on back of neck

43
Q

Hormonal effects of Acne Vulgaris

A
  • sebum production is affected by hormones
  • androgens produced inside sebaceous gland by adrenals and gonads
  • estrogen? local inhibition, gonadal inhibition, gene regulation?
44
Q

Open Comedones

A

black head

45
Q

Closed Comedones

A

white head

46
Q

Acne Conglobata (acne fulminans)

A
  • severe eruptive nodulocystic acne
  • Conglobata- no systemic symptoms
  • Fulminans-systemic, fever, arthralgias, osteolytic bone lesions, hepatosplenomegaly
47
Q

Steroid induced acne

A

all at same stage

48
Q

Acne Excoriee de jeunes filles

A

young females picking acne

49
Q

Acne Vulgaris Treatments

Topical:

A

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
Q

Acne Vulgaris Treatments

Systemic:

A
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
Q

Keloids

A
  • more common in darker skin

- high risk of recurrence with removal

52
Q

Photoaging

A

(extrinsic)

  • actinic keratoses
  • coarse wrinkling
  • elastosis with giant comedones
53
Q

Decubitus Ulcers

A

-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
Q

Dermatitis in Geriatric Patients

A
  • asteatotic eczema
  • nummular eczema
  • stasis dermatitis
  • seborrheic dermatitis
55
Q

Geriatric: Stasis Dermatitis

A
  • due to venous insufficiency and edema
  • can result in venous ulvers
  • treat: exercise, elevation, compression, topical steroids, antibiotics (infection)
56
Q

Scurvy

A

Vit C deficiencies

poor teeth

57
Q

Pellagra

A

Niacin (B3) deficiencies

  • dementa
  • dermatitis
  • diarrhea
58
Q

Geriatric Infection

A

staph, strep, HZV, candida, tinea pedis, tinea cruris, onychomycosis

59
Q

Gianotti-Crosti

A

EBV, HIV

60
Q

Henoch-Schonlein Purpura

A
  • vasculitis

- glomerunephritis

61
Q

Kawasaki disease

A

epidemic
-puffy hands/feet
strawberry tongue
anyuruseums of coronary artery

62
Q

Keratosis pilaris

A

features of atopic dermatitis

kerotitic follicles

63
Q

Pityriasis alba

A

features of atopic dermatitis

hypopigmented areas

64
Q

Nummula Dermatitis

A

features of atopic dermatitis

coin shaped lesions

65
Q

Dyshydrotic eczema

A

features of atopic dermatitis

vesicles along fingers (tapioka pudding)

66
Q

Juvenile plantar dermatosis

A

features of atopic dermatitis

“sweaty sock” dry feet

67
Q

Denny-Morgan pleats

A

features of atopic dermatitis

transverse line under eye

68
Q

Allergic shiners

A

features of atopic dermatitis

dark circles

69
Q

Allergic salute

A

features of atopic dermatitis

crease across nose from wiping

70
Q

Accentuated palmar creases

A

features of atopic dermatitis