Dermatology Flashcards

1
Q

What embryonic layer do skin cells come from?

A

The skin comes from the ectoderm.

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2
Q

At what week gestation does the stratification of the epidermis start? When does it end

A
  • Stratification of the epidermis begins at week 8 and ends at week 24
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3
Q

What is ectoderm dysplasia and name some defomrities that occur as a result?

A
  • Ectodermo-dysplasia: abnormality of ectoderm development during gestation
    • Deformities: no sweat glands, abnormal teeth, hair, and skin formation
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4
Q

What are the 5 main functions of the skin?

A
  • Mechanical support
  • Homeostasis
  • Physical barrier
  • Interacting with the environment
  • Social interactions (cosmesis)
    • Skin defects can result in considerable psychological distress
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5
Q

List the three cells that are involved in the epidermis.

A

Keratinocytes, Langerhans Cells, Melanocytes

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6
Q

What are the four layers of the keratinocytes and what is the function of each?

A
  • Layers (from top to bottom) - LABELED PIC ATTACHED
    • Stratum Corneum (SC): anuclear, dead cells that shed; barrier/immune defense (1)
    • Stratum Granulosum (SG): the glue; keratin protein and lipid accumulation (2)
    • Stratum Spinosum (SS): contains desmosomal junctions; integrity/barrier (3)
    • Basal: the basement; cell division (4)
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7
Q

What proteins are secreted by keratinocytes? Two types of proteins, but three total.

A
  • Proteins secreted
    • Keratin Type I: acidic
    • Keratin Type II: basic
    • Filaggrin: “filament aggregation protein
      • Helps assemble keratins into KIFs
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8
Q

When there are mutations in keratin, what disease occurs and what is its manifestation?

A
  • Keratin mutations
    • Epidermolysis Bullosa Simplex: blistering due to lack of stable keratin in the epidermis
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9
Q

What is the function of the Langerhans Cells in the Epidermis? What can dysfunction of them lead to?

A
  • Langerhans Cells (dendritic cells of the skin/mucosa)
    • Resident immune cells used for antigen recognition and presentation to T-cells, initiating immune response
      • Reaches all layers except for stratum corneum
    • Dysfunction of dendritic cells can lead to skin conditions like eczema and allergies
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10
Q

What is the function of melanocytes and what layer of the epidermis are they found in? What can their dysfunction lead to?

A

Basal layer, protect from UV damage

Dysfunction: can lead to DNA damage and therefore XP

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11
Q

What is the general function of the dermis and what are the main cells in this layer (what is then function of these cells)?

A
  • Provides pliability, elasticity, and tensile strength to skin
  • Main cell: fibroblast, which produces collagen
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12
Q

What are the two layers of the dermis and how do they appear?

A
  • Two layers
    • Papillary dermis (closest to epidermis) - top black line
      • Lighter, thinner, more diffuse collagen fibrils
    • Reticular dermis (deep down dermis) - bottom black line
      • Large diameter collagen fibrils
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13
Q

What three diseases can result from dysfunction of the dermis? Discuss the defects in these three diseases.

A
  • Dysfunction
    • Ehlers Danlos: defect in type III collagen where joints dislocate and skin stretches
    • Marfans Syndrome: defect in fibrillin1 affecting elastic fibers where individuals are very tall, lanky, and have long fingers
    • Senile Purpura: aging causes fibroblasts to produce fewer dermal fibers, causing bruising
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14
Q

What occurs in the subcutis (hypodermis)?

A

Subcutis (Hypodermis)

  • Contains subcutaneous fat
  • Adipocytes and adipokines (leptin and ghrelin) are here
  • Dysfunction
    • Lipodystrophy: redistribution of fat
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15
Q

List the appendages of the skin.

A
  • Hair follicles
  • Nails
  • Sebaceous glands
  • Vascular plexi
  • Nerves
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16
Q

List the function and dysfunction (what condition) of hair follicles?

A
  • Hair follicles
    • Function: to produce hair shaft
    • Hair cycle is regulated by Wnt signaling pathway
    • Dysfunction: alopecia – immune system attacks hair
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17
Q

What is the anatomy of nails and what is a condition that is caused by the dysfunction of nails?

A
  • Dysfunction: nail psoriasis – inflammation of nail causes separation
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18
Q

What do sebaceous glands do, where do they attach, and what can dysfunction cause?

A
  • Sebaceous glands
    • Oil glands that produce sebum
    • Attached to hair follicles
    • Dysfunction: acne vulgaris
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19
Q

Where are the two places where the vascular plexi is located? What is the function and what can be caused by dysfunction?

A
  • Vascular plexi
    • Superficial (epidermis/dermis border)
    • Deep (dermis/subcutis border)
    • Function: nutrient supply and theroregulation
    • Dysfunction: Raynaud phenomenon – digital ischemia provoked by cold
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20
Q

What is caused by the dysfunction of nerves?

A
  • Nerves (sensory receptors)
    • Dysfunction: pruritis (itch), dysesthesia (abnormal sensation), loss of feeling
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21
Q

What are the phases of injury and regneration of the skin? 4 phases.

A

Injury Repair and Regeneration

  • Phases
    • Coagulation
    • Inflammatory phase
    • Proliferative-migratory phase (tissue formation)
    • Remodeling phase
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22
Q

What is the morphology and general distribution of psoriasis vulgaris?

A
  • Morphology: Pink-red with silvery scales, Dry, Raised, Definitive Borders
  • Distribution: Scalp, Elbows, Knees, Gluteal Cleft, Nails, Umbilicus
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23
Q

What is the morphology, distribution, and what is a similar skin condition of psoriasis inverse?

A
  • Morphology: Very pink, Definitive borders, Very little plaque
  • Distribution: Folds of the skin: under arm, under breast, belly
  • ***Hard to distinguish from seborrhea
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24
Q

What is the morphology or psoriasis guttate?

A

1000s of small scaly drops

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25
Q

What is the morphology of psorias erythrodermic?

A

all over red (like a bad sunburn)

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26
Q

What is the morphology and distribution of eczema?

A

Morphology

Acute = wet and blistering

Chronic = pink lichenified with no edges

Both have no scale

Distribution

Popliteal fossa and antecubital

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27
Q

What is the morphology and distribution of seborrhea?

A

Morphology

Faint pink, greasy look to skin

Neurological conditions

Distribution

Scalp, brows, ears, nose, chest, armpits

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28
Q

What is the morphology, distribution, and general diagnostic criteria of pityriasis rosea?

A

​Morphology

Light pink, annular, raised patches

Distribution

Back, abdomen

Herald patch: first lesion that is mistaken for tinea

“Christmas tree” pattern

Diagnostic Criteria

KOH

***Hard to differentiate from guttate psoriasis

**Rule out syphilis (syphillis can be found on hand and palms)

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29
Q

What is the morphology, distribution, and diagnostic criteria of Lichen planus?

A

Morphology

Leathery, pink-purple, Variable scale, itchy

Distribution

Wrists/arms, Ankles/legs, Mouth, Nails

Diagnostic Criteria

Hepatitis screening

***Psoriasis never occurs on the wrist

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30
Q

In terms of dermatologic appearance, what is the morphology, distribution, and diagnostic criteria of lupus?

A

Morphology

Pink-Red-Brown

Annular

Variable scale

Variable Scarring

Distribution

Discoid LE: regions exposed to sun

Subacute LE: Chest, back

Systemic LE: elbows

Diagnostic Criteria

Biopsy

ANA, etc

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31
Q

For tinea, what is the morphology, distribution, and diagnostic criteria?

A

Morphology

Pink annular,

patches with advancing scale on edge

Not raised

Not continuous

Distribution

Anywhere with stratified squamous epitheium

Diagnostic Criteria

KOH

***DO NOT treat with steroids because it will spread fungus

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32
Q

What is this?

A

Onycholysis – lifting below nail

This is often found in psoriasis vulgaris.

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33
Q

What is this?

A

pitting of nail, often found in psoriasis vulgaris

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34
Q

What is this?

A

Psoriasis Vulgaris.

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35
Q

What is this?

A

Psoriasis Guttate

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36
Q

What is this?

A

Psorias Erythrodermic

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37
Q

What is this?

A

Acute Eczema

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38
Q

What is this?

A

Chronic Eczema

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39
Q

What is this?

A

Seborrhea

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40
Q

What is this?

A

Pitysiasis rosea

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41
Q

What is this?

A

Lichen Planus

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42
Q

What is this?

A

Discoid LE rash

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43
Q

What is this?

A

General Lupus rash

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44
Q

What is this?

A

Tinea

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45
Q

What is the pathophysiology of psoriasis (know the cytokines involved)?

A
  • Pathophysiology: environmental stimuli → activation of dendritic cells → stimulation of T-helper cells via release of TNF-alpha → release of IL-17 and IL-22 → cytokines cause premature maturation of keratinocytes → characteristic psoriatic lesion
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46
Q

What drugs are generally used to treat psoriasis?

A
  • Topical steroids as a more affordable and baseline drug for all dermatoses except tinea
  • Since there are cytokine specificity in the immune response of psoriasis, specific cytokines can be targeted for therapy to not block entire immune system
    • TNF-alpha inhibitors
    • IL-17, IL-12, and IL-23 targets
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47
Q

Is there a genetic component to psoriasis?

A
  • Genetic component and environmental stimuli play role
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48
Q

Is this normal histology of the skin or abnormal?

A

NORMAL

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49
Q

Is this normal histology of the skin or abnormal?

A

Abnormal. The histology shows dermatoses (psoriasis/eczema). The thickened epidermis with the fingerlike projections is especially characteristic.

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50
Q

Stevens-Johnson Syndrome

Clinical Features?

Distrubution?

Etiology?

A

C: Sloughing of epidermis with blistering and 2 or more mucosal membranes affected

D:<10% of BSA

E: Immediate medication reaction

51
Q

Toxic Epidermal Necrolysis

Clinical Features?

Distrubution?

Etiology?

A

C: Sloughing of epidermis with blistering and 2 or more mucosal membranes affected

D:>30% of BSA

E: Immediate medication reaction

52
Q

Erythema Multiforme

Clinical Features?

Distrubution?

Etiology?

A

C:Typical 3-zoned target of purple, red, and white and 1 mucosal membrane affected

D:Extremities

E: Infections

53
Q

Simple Drug Exanthem

Clinical Features?

Distrubution?

Etiology?

A

C: Itchy rash

**Not an emergency (otherwise healthy)

D:Spares face and mucosal membranes

E: Medication reaction occurring 4-14 days after drug initiation

54
Q

DRESS (Drug Reaction with Eosinophilia and Systemic Symptoms)

Clinical Features?

Distrubution?

Etiology?

A

C: Polymorphous rash, facial edema, fever, and eosinophilia

D:Everywhere

E: Medication reaction occurring 2-6 weeks after start of medication

55
Q

Acute Generalized Exanthematous Pustulosis (AGEP)

Clinical Features?

Distrubution?

Etiology?

A

C: Erythroderma with tiny pustules all over

D: Everywhere

E: Medication reaction, especially IV antibiotic

56
Q

Medically induced Psoriasis

Clinical Features?

Distrubution?

Etiology?

A

C:Black scaling all over skin, Corpse-looking

D: Everywhere

E: Prednisone tapering

57
Q

Kawasaki Disease

Clinical Features?

Distrubution?

Etiology?

A

C: Red eyes, Strawberry tongue, Cervical adenopathy, Acral edema (puffy feet and hands),Polymorphous rash, 4 out of 5 + high fever and rash

**Requires aspirin and echocardiogram as treatment

D: Everywhere

E: Vasculitis

58
Q

Purpura fulminans

Clinical Features?

Distrubution?

Etiology?

A

C: Non-blanching purpura

D: Everywhere

E: Sepsis, Disseminated Intravascular Coagulation, Shock

59
Q

Necrotizing Fasciitis

Clinical Features?

Distrubution?

Etiology?

A

C: Pain out of proportion, necrotic tissue, subcutaneous crepitus, purple and black purpura

D: Site of infection

E: Bacterial infection

60
Q

Pemphigus Vulgaris

Clinical Features?

Distrubution?

Etiology?

A

C: Erosions – very rarely see blister formation, No fever

D: Always involves oral mucosa (Dsg 3), May involve skin (with Dsg 1)

E: Autoantibodies against keratinocytes desmosomes in epidermal layer of skin

61
Q

Pemphigus Foliaceous

Clinical Features?

Distrubution?

Etiology?

A

C: Crusting and scaling in sebaceous areas (corn flake skin) with no intact blisters

D: Only skin (only Dsg 1) with no oral involvement

E: Autoantibodies against keratinocyte desmosomes in epidermal layer of skin

62
Q

Bullous Pemphigoid

Clinical Features?

Distrubution?

Etiology?

A

C: Multicolored blisters

D: Skin at juncture between epidermis and dermis

E: Autoantibodies to BP antigen 1 and 2 (hemidesmosomes)

63
Q
A

Stevens-Johnson Syndrome

64
Q
A

Toxic Epidermal Necrolysis

65
Q
A

Erythema Multiforme

66
Q
A

Simple Drug Exanthem

67
Q
A

DRESS (Drug Reaction with Eosinophilia and Systemic Symptoms)

68
Q
A

Acute Generalized Exanthematous Pustulosis (AGEP)

69
Q
A

Medically induced Psoriasis

70
Q
A

Kawasaki Disease

71
Q
A

Purpura fulminans

72
Q
A

Necrotizing Fasciitis

73
Q
A

Rocky Mountain Spotted Fever

74
Q
A

Pemphigus Vulgaris

75
Q
A

Pemphigus Foliaceous

76
Q
A

Bullous Pemphigoid

77
Q

Risk Factors for Melanoma (6)

A
  • Skin phototype – lighter phototypes are more at risk
  • Family history/genetics
    • Familial – CDKN2A (most common) > BRAF
    • De novo – BRAF
  • Dysplastic/atypical nevi
  • Greater than 25 common acquired nevi
  • Immunosuppression
  • UV exposure
    • Intermittent, intense sun exposure
    • Sunburns, especially blistering
    • Tanning bed
78
Q

Diagnosis for melanoma

A
  • A – Asymmetry
  • B – Border
  • C – Color
  • D – Diameter
  • E – Evolving
    • the “Ugly Duckling” sign – one atypical nevi compared to rest
  • Gold standard for diagnosis is histology
79
Q

Melanoma Subtype: Superficial Spreading Melanoma

A
  • Most common
  • Horizontal growth
80
Q

Melanoma Subtype: Nodular Melanoma

A
  • Vertical growth (measured by Breslow’s Depth)
  • Rapid growth
81
Q

Melanoma Subtype: Lentigo Meligna Melanoma

A
  • Occurs in elderly in sun-exposed areas
  • Horizontal growth
82
Q

Melanoma Subtype: Acral Lentiginous Melanoma

A
  • Common in darker skin types
  • Palms, soles, nail plate
83
Q

Management for Melanoma

A
  • Initial: surgical
  • Adjuvant therapy
    • Dabrafenib (blocks BRAF) + Vemurafenib
    • Anti-PDL1
84
Q

Prognosis for melanoma

A
  • Tumor depth is predictor of survival
85
Q

Junctional Nevus

A
  • Junctional Nevus – cells limited to dermal-epidermal junction
    • Horizontal growth
86
Q

Compound Nevus

A
  • Compound Nevus – cells in dermal-epidermal junction and dermis
    • Vertical growth
87
Q

Intradermal Nevus

A
  • Intradermal Nevus – cells limited to dermis
    • Vertical growth
88
Q

Melasma

A

Mask of pregnancy – polymorphous dots on face of women

89
Q

Freckles

A

Occurs in children of fair complexion on sun-exposed areas

90
Q

Solar Lentigines

A
  • Age spots occurring in elderly population on sun-exposed areas
  • Must differentiate from lentigo maligna melanoma
91
Q

Vitiligo

A
  • Acquired disorder of melanocytes
  • White, sharply demarcated macules and patches without scales
  • Pathogenesis suspected to be autoimmune related
  • Systemic diseases
    • DATA: diabetes, Addison’s disease, thyroid disease, pernicious anemia
92
Q
  • “Pasted-on” dry and waxy plaque
  • Uniform in color: brown, black, pink, tan, white
  • Can be confused with melanoma
A

Seborrheic keratosis

93
Q
  • Vascular lesion that is very red due to increase in capillaries
  • Never turns into cancer
A

Angioma

94
Q
  • Growth of epidermis and dermis
  • Must be differentiated with melanoma by pinching around it
    • Dimples inward
A

Dermatofibroma

95
Q
  • Protuberant scar tissue that extends beyond site of injury
  • Excess collagen production causes excessive scarring
A

Keloid scar

96
Q
  • Hyperplasia of keratinocytes creating non-harmful appendages of skin
  • Genetic
A

Skin Tags

97
Q
  • Pocket of epidermis with keratin and bacteria
    • Bacteria feeds on keratin
    • Hole on surface of skin allows for cheesy-material to come out when squeezed
A

Epidermal inclusion cyst

98
Q

Soft, squishy cyst due to proliferation of adipocytes

A

Lipoma

99
Q
  • Rough, braille-like scaling patches
  • Pink-tan color
  • Pre-malignant for squamous cell carcinoma
A

Actinic Keratoses

100
Q
  • Most common skin cancer
  • Arises from the basal cell layer of the epidermis
  • Can also appear as non-healing ulcers with slight erosion/scabbing
  • Arborizing vessels
  • Presents as a pink pearly growth on sun-exposed skin
  • Local invasion with almost no metastasis
A

Basal Cell Carcinoma

101
Q

Treatment for basal cell carcinoma (2)

A
  • Excision
  • Vismodegib: binds SMO (usually bound by PTCH1/2) to prevent downstream activation of TFs
102
Q

Etiology for squamous cell carcinoma

A

Etiology beyond UV exposure: XR radiation, HPV, chronic inflammation, ulcer, immunosuppression

103
Q
  • Ulcerated scaling papule, plaque, or nodule
  • Rarely metastasis
A

Squamous Cell Carcinoma

104
Q

dome-shaped nodule with rapid growth

A

Keratoacanthoma

105
Q
A

Basal Cell Carncinoma – basal cells extend into dermis

106
Q
A
  • Squamous Cell Carcinoma – more differentiated epidermal cells are pleomorphic and have large nucleoli
    • Have keratinic pearls
107
Q
A
  • Squamous Cell Carcinoma – more differentiated epidermal cells are pleomorphic and have large nucleoli
    • Have keratinic pearls
108
Q

Actopic dermatitis (eczema)

Patho? Genetic?

A
  • Family history of atopy (predisposition to allergies like asthma)
  • Triggered by allergens or irritants (foods, pets, heat, cold, etc.)
    • Fillagrin defect causes loose keratin cables, allowing allergens to enter into epidermis layers and react with Langerhans Cells
109
Q

Actopic dermatitis (eczema)

Presentation?

A

Clinical features: pruritus (itching) + eczematous rash (red and scaly) + early onset

110
Q

Actopic dermatitis (eczema)

Tx? Complication?

A
  • Treatment: avoidance of triggers, moisturization, hydrocortisone cream
  • Secondary infections
    • Molluscum contagiosum: viral infection
111
Q

Measles

Presentation?

Etiology?

A

Clinical features: rash that begins on face behind ears and spreads downwards

Etiologic agent: paramyxovirus

112
Q

Scarlet Fever

Presentation?

Etiology?

A

Clinical features: sudden fever with sandpaper rash, especially under skin folds, and strawberry tongue

Etiologic agent: Group A Streptococcus

113
Q

Erythema Infectiosum

Presentation?

Etiology?

A

Clinical features: “slapped cheeks” and lacy, reticulated rash on extremities

Etiologic agent: parvovirus B19

114
Q

Roseola

Presentation?

Etiology?

A

Clinical features: fever, fever, fever, fever, rash!

Etiologic agent: HHV6

115
Q

Hand, Foot, and Mouth Disease

Presentation?

Etiology?

A

Clinical features: flu like symptoms with grey oval vesicles on hands, feet, and mouth

Etiologic agent: Coxsackie virus A16

116
Q

Infantile hemangioma

Stages?

A
  • Gradual onset in first weeks of life
  • Proliferates for first year of life
  • Gradual resolution – does not have to go away completely
117
Q

Infantile hemangioma

Features, complications?

A
  • Clinical features: deep red, undefined edges, raised body on face
  • Complications: hemorrhage and ulcerations
118
Q

Subglottic IH

A

Subglottic IH: beard formation of hemangioma and can be deadly

119
Q

Capillary malformation (“port wine stain”)

stages, features?

A
  • Stages
    • Present at birth
    • Affects fixed proportion of face
  • Clinical features: pink color that lies flat on face
120
Q

Diaper dermatitis irritant

A

Irritant: spotted rash due to urine and feces, sparing creases of body

121
Q

Diaper Dermatities Candidal

A

Candidal: beefy-red freckled rash due to growth of Candidia

122
Q
A

Hand, foot, mouth disease

123
Q
A

Irritant diaper rash

124
Q
A

Candidal diaper rash