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Block 7 Week 2 > Dermatology 1 > Flashcards

Dermatology 1 Flashcards

1
Q

What part of the skin is involved in shock absorbance and thermoregulation?

A

subcutaneous layer

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2
Q

Where do you find anexal structures (aka hair follicles and sebacous glands)?

A

dermis

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3
Q

the epidermis is a layer of (blank) cells that produces keritan.

A

stratified squamos cells

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4
Q

What is the lowest layer of the epithelium, this layer is responsible for regenerating keritinocytes.

A

stratus basale

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5
Q

What layer of the epidermis produces cytokeratins that form tonofibrils that make desmosomes (intercellular bridges)?

A

stratum spinosum

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6
Q

What layer of the epidermis is darker blue because of Keratohyaline granules?

A

stratum granulosum

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7
Q

WHen keratohyaine granules and tonofibrils combine they produce (blank) and as they mature they are manifested in the stratum (Blank) where they lose their nuclei and cytoplasm

A

keratin

stratum corneum

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8
Q

(blank) function in protecting the skin from UV injury

A

Melanocytes

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9
Q

(blank) function in antigen recognition in the immune system

A

Langerhann cells

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10
Q

What do you find under the epidermis that connects it to the dermis?

A

the basement membrane

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11
Q

The skin is the largest organ and undergoes (blank) forces. To combat these forces the epidermis has (blank).

A

sheering

ridges

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12
Q

What are the 2 layers to the dermis?

A

Papillary

Reticular layer

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13
Q

the (blank) is partially water-soluble.

A

epidermis

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14
Q

What layer is this: loose collagen, capillaries, Meissner’s corpuscles.

A

Papillary dermis

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15
Q

What is below the papillary layer of the dermis?

A

reticular dermis

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16
Q

What layer is this:

densely packed collagen, elastic fibers

A

reticular dermis

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17
Q

What is the function of the reticular dermis?

A

to provide strength and extensibility

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18
Q

Which layer of the dermis has the adenexal structures?

A

reticular dermis

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19
Q

Where do you find apocrine sweat glands?

A

axilla, groin

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20
Q

Where do you find eccrine glands?

A

sweats

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21
Q

soles and palms dont have (blank) structures. they have thicker layers of (blank)

A

adnexal

keratin (stratum lucidum)

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22
Q

What is this:

circumscribed, flat lesions <5mm distinguished from surrounding skin by color

A

Macule

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23
Q

What is this:

circumscribed flat lesion >5mm distinguished from surrounding skin by color

A

patch

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24
Q

What is this:

elevated dome-shaped or flat-topped lesion <5mm

A

Papular

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25
Q

What is this:

elevated dome-shaped or flat topped lesion >5mm

A

Nodule

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26
Q

What is this:

elevated flat-topped lesion >5mm

A

plaque

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27
Q

What is this:

Discrete, pus-filled, raised lesion

A

pustule

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28
Q

What is this:

Dry, horny, platelike excrescence; usually the resut of imperfect cornification

A

Scale

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29
Q

What is this:

fluid filled raised lesions <5mm, also called a blister

A

Vesicle

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30
Q

What is this:

fluid filled raised lesion > 5mm, also called a blister.

A

Bulla

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31
Q

What is this:

Itchy, transient, elevated lesion with variable blanching and erythema formed as the result of dermal edema.

A

wheal

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32
Q

Which kind of skin things are sharply demarcated?

A

macule

patch

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33
Q

If your skin thing is fluid, then what is it?

A

vesicle/bulla

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34
Q

If your skin thing is pus, then what is it?

A

pustule

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35
Q

What do you call diffuse epidermal hyperplasia?

A

acanthosis

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36
Q

What do you call abnormal, premature keratinization within cells below the stratum granuosum?

A

Dyskeratosis

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37
Q

What do you call hyperplasia of the stratum granulosum?

A

hypergranulosis

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38
Q

What do you call a thickening of the stratum corneum?

A

hyperkeratosis

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39
Q

What do you call a linear pattern of maloncyte proliferation within the epidermal basal cell layer?

A

Lentiginuous

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40
Q

What do you call a surface elevation caused by hyperplasia and enlarement of contiguous dermal papillae?

A

papillomatosis (papilla fragmentation)

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41
Q

What do you call keritinization with retained nuclei in the stratum corneum?

A

parakeratosis

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42
Q

What do you call intercellular edema of the epidermis?

A

spongiosis

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43
Q

Thickening of stratum corneum but with retained nuclei is (blank)

A

parakeratosis

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44
Q

What is this:

surface elevation, caused by hyperplasia and fragmentation of dermal papilla.

A

papillomatosis

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45
Q

What is this:

edema that pushes apart stratum spinosum; intracellular bridges become very prominant

A

spongiosis

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46
Q

What is this:

radial growth pattern of pigmentation along the stratum basale.

A

Lentiginous

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47
Q

What is this:

abnormal keratinization due to malignant change; cells keratinize prematurely below the granulosom.

A

Dyskeratosis

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48
Q

What are the 2 types of inflammatory dermatoses?

A

acute

chronic

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49
Q

Acute inflammatory dermatoses is characterized by (blank)

A

lymphocytic and macrophage inflammatory infitrate and edema

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50
Q

How long does acute inflammatory dermatoses last?

A

days to weeks

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51
Q

How long does chronic inflammatory dermatoses last?

A

persist for months to years

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52
Q

Chronic inflammatory dermatoses is characterized by (blank)

A

changes in epidermal growth (atrophy or hyperplasia) or dermal fibrosis
the skn is roughened due to excess or abnormal

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53
Q

What is this:
common disorder characterized by localized mast cell degranulation and dermal microvascular hypermeability.
-patients present with pruiritic edamtous plaques (wheals)
-Angioedema is a related condition with edema of the deeper dermis and subcutaneous fat

A

Urticaria (hives)

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54
Q

How long does urticaria (hives) last?

A

can be acute (less than 6 weeks) or chronic

55
Q

if you have urticaria, what will the histo slide show?

A

edema in the papillary dermis

56
Q

What are the causes of urticaria?

A 
immunologic mechanisms
non-immunologic mechanisms
physical stimuli
skin contact
small vessel vasculitis
57
Q

What is the treatment for urticaria?

A

avoidance of specific allergense
oral H1 antagonists
epinephrine

58
Q

What is the most common acute inflammatory dermatoses?

A

acute eczematous dermatitis

59
Q

Acute eczematous dermatitis can be subdivided into 5 categories, what are they?

A

-Allergic contact dermatitis
-Atopic dermatitis
-drug-related eczematous dermatitis
-photoeczematous dermatitis
Primary irridant dermatitis

60
Q

What kind of reaction is atopic dermatitis?

A

type 1 hypersensitivity reaction

61
Q

Drug related ecematous dermatitis, photoeczematous dermatitis, and primary irritant dermatitis are all types of (blank) dermatitis

A

contact

62
Q

Acute eczematous dermatitis results from (blank) which is a type IV hypersensitivity reaction

A

T-cell mediated inflammatory reactions

63
Q

What are the causes of acute eczematous dermatitis?

A

inside: reaction to an internal circulating antigen
outside: reaction from external application of an antigen

64
Q

What is the treatment of acute eczematous dermatitis?

A

removal of the offending substance and topical steroids

65
Q

What is this:
self-limited hypersensitivity reaction that is associatd with infections from virus (herpes simplex), bacteria (mycoplasma, leprosy, typhoid), fungus (histoplasma, coccidioides)

A

Erythema mulitforme

66
Q

Exposure to which drugs can cause erythema multiforme?

A

sulfonamides, penicillin, barbiturates, salicylate, antimalarias.

67
Q

What are the four causes of erythema multiforme?

A

Infections
Drugs
Cancer
Collagen vascular disease

68
Q

What are targetoid lesions and where are they found?

A

Central epidermal necrosis surrounded by erythema

Erythema Muliforme

69
Q

What are the 2 types of Erythema multiforme?

A

Stevens Johnson Syndrome

Toxic Epidermal Necrolysis

70
Q

What is this:

  • a febrile form with extensive skin involvement
  • also involves oral mucosa, conjunctiva, urethra, genital and perinanal areas,
  • may lead to spesis
  • often seen in children
A

Erythema Multiforme-Stevens Johnson Syndrome

71
Q

What is this:

  • characterized by diffuse necrosis and sloughing of cutaneous and mucosal epithelial surfaces
  • clinical pictures similiar to that of burn atients
A

Erythema multiforme-toxic epidermal necrosis

72
Q

What is this:

  • a common disorder affecting 1-2% of the US population
  • results from interaxn’s of genetic (HLA-C) and environmental factors (trauma)
  • Activated T cells in skin stimulate cytokine and grow
A

Psoriasis

73
Q

In Psoriasis patients, 15% of them have (blank) associated with it.

A

arthritis

74
Q

What does psoriasis happen?

A

activated T cells in the skin stimulating the secretion of cytokines and growth factors that induce keratinocyte proiferation

75
Q

What is the genetic element associated with psoriasis?

A

HLA-C

76
Q

Where do you typically find psoriasis?

A

on exterior surfaces and scalp

77
Q

What all can you see in psoriasis?

A
  • acanthosis
  • parakeratosis
  • Munro microabscesses
  • elongated dermal papillae
78
Q

What do you call a collection of neutrophils in the stratum corneum?

A

munro microabscesses

79
Q

What does elongated dermal papilae result in?

A

pinopoint bleeding when scale is picked off “Auspitz sign”

80
Q

What are the treatments for psoriasis?

A

-topical steroids***
-intralesional steroid injection
-UVB and tar**
-methotrexate
-cyclosporino
-soriatane
(UVB and Psoralen)

81
Q

What is this:

  • common chronic inflammatory dermatosis that affects up to 5% of the general pop.
  • Involves regions with high density of sebacous glands
A

Seborrheic dermatitis

82
Q

Where do you often find seborrheic dermatitis?

A 
scalp
foreheard
external auditory canal
retroauricular canal
retroauricular area
nasolabial folds
presternal area
83
Q

What disease is “cradle cap” associated with?

A

seborrheic dermatitis

84
Q

What are the causes of sebhorreic dermatitis?

A

increased sebum production

colonization of the skin by malassezia

85
Q

When do you see the severe form of sebhorreic dermatitis?

A

in HIV + patients with low CD4 counts

86
Q

What is increased sebum production due to?

A

hormones

87
Q

The appearance of sebhorreic dermatitis is seen on skin as (blank)

A

erythematous plaques

88
Q

What is the treatment of sebhorreic dermatitis?

A
  • frequent washing of the affected area with antisebhoreic soaps
  • topical steroids
  • anti-yeast medications
  • oral antifungals
89
Q

What is this:
self-limitd condition most commonly resolving spontaneously 1-2 years after onset.
Involves the 6 Ps.

A

Lichen planus.

90
Q

What are the 6 Ps of Lichen planus?

A

Pruritic, purple, polygonal, planar, papules, and plaques

91
Q

Resolution of lesions of lichen planus results in (blank)

A

postinflammatory hyperpigmentation

92
Q

In lichen planus, (blank) may develop in oral lesions

A

squamos cell carcinoma

93
Q

Oral involvement in lichen planus manifests as (blank)

A

Wickham striae

94
Q

What is wickham striae?

A

white areas within purple plaques caused by hypergranulosis

95
Q

What type of disease is this:

inflammation of the dermal-epidermal junction with a saw-tooth appearance.

A

Lichen planu

96
Q

What is the treatment of lichen planus?

A
  • topical steroids
  • intralesional steroids
  • systemic steroids
  • azathioprine
  • cyclosporine
  • light therapy (PUVA & UVB)
97
Q

Many conditions exist in which blisters are a feature of the condition…. what are the four?

A

Herpes virus
Spongiotic dermatitis
Erythema multiforme
thermal burns

98
Q

(blank) disorders are a group of diseases in which blisters are the primary and most distinctive feature.

A

bullous (bistering)

99
Q

Blistering disorders are due to (inflammatory/non-inflammatory) causes

A

Both!!

100
Q

Where do you find pemphigus foliaceus? What protein is affected in this case?

A

submucosal blistering disorders

Desmoglein I

101
Q

Where do you find pemphigus vulgaris? What protein is affected in this case?

A

suprabasal

desmoglein III

102
Q

Where do you find bullous pemphigoid? What protein is affected in this case?

A

Subepidermal

Hemidesmosome

103
Q

What will you find within the desmosome of the stratum spinosum?

A

desmoglein (pemphigus), plakophilin, plakogloblin, desmoplakin, desmocolin

104
Q

What will you find within the hemidesmosome of the basement membrane?

A

BPAG1, BPAG2 (pemphigoid), intermediate fibers

105
Q

(blank) is an inflammatory blistering disorder caused by autoantibodies that result in the dissolution of intercellular attachments within the epidermis and mucosal epithelium

A

Pemphigus

106
Q

Why do you get pemphigus?

A

IgG autoantibodies to desmoglein 1 and 3 disrupt intercellular adhesions of desmosomes

107
Q

What are the varients of pemphigus?

A
  • pemphigus vulgaris
  • pemphigus vegetans
  • pemphigus foliaceus
  • pemphigus erythematosus
  • paraneoplastic pemphigus
108
Q

What is the most common pemphigus (80%) and it is found on the oral mucosa?

A

pemphigus vulgaris

109
Q

What is a rare pemphigus that shows up as plaques around groin?

A

pemphigus vegetans

110
Q

What type of pemphigus shows up as subcorneal blisters?

A

pemphigus foliaceus

111
Q

What type of pemphigus is this, it is a form of foliaceus bt less severe?

A

pemphigus erythematosus

112
Q

What type of pemphigus is this; associated with cancer

A

paraneoplastic pemphigus

113
Q

If you see a tombstone row, what are you looking at?

A

pemphigus

114
Q

If you see a swiss cheese partern then what are you looking at?

A

pemphigus foliaceus

115
Q

How do you treat pemphigus?

A

immunosuppressive agents to decrease the titers of the pathogenic antibodies

116
Q

(blank) is a blistering disorder caused by autoantibodies directed to the proteins that bind basal keratinocytes to the basement mebrane. Antibody deposition occurs in a (blank) pattern at the dermoepidermal junction.

A

Bullous pemphigoid

linear

117
Q

The proteins (blank) are part of the hemidesosomes that link basal keratinocytes to the basement membrane.

A

BPAGs

118
Q

If you see linear IgG on root of blister on a histo slide, what are you looking at?

A

bullous pemphigoid

119
Q

What is the treatment for bullous pemphigoid?

A

topical steroids
systemic steroids
methotrexate
azathioprine

120
Q

What is this:

rare disorder characterized by urticaria and grouped vesicles. Strong association with HLA-B8, HLA-DR3 and HLA-DQw2

A

Dermatitis herpetiformis

121
Q

In dermatitis herpetiformis, genetically predisposed individuals develop (blank) antibodies to dietary gluten.

A

IgA

122
Q

Why do you get subepidermal blisters in dermatitis herpetiformis?

A

IgA antibodies to dietary gluten, these antibodies cross react with reticulin which is a component of the anchoring fibrils that attaches the epidermal basement membrane to the superifical papillary dermis.

123
Q

If you see a subepidermal blister , what are you looking at?

A

dermatitis herpetiformis

124
Q

What is the treatment for dermatitis herpetiformis?

A

dapsone

sulfapyridine

125
Q

What is this:
inherited defect in structural proteins that cause mechanical instability to the skin. Clinical manifestations soon after birth with blister formation at sites of pressure, rubbing or trauma.

A

Epidermolysis bullosa

126
Q

What are the 4 types of epidermolysis bullosa?

A

simplex
junctional
dystrophic
mixed

127
Q

What type of epidermolysis bullosa is this:
autosomal dominant inheritance of defects in keratin 14 or keratin 5 resulting in defects in the basal cell layer of the epidermis.

A

Simplex type

128
Q

What type of epidermolysis bullosa is this:
autosomal recessive inheritance of defects in laminin, a protein at the lamina lucida. Blisters are seen at the level of the lamina lucida.

A

Junctional type of epidermolysis bullosa

129
Q

What does the lamina lucida do?

A

binds to both hemidesmosomes and anchoring filaments

130
Q

What makes up the basement membrane?

A

lamina lucida +lamina densa

131
Q

What type of epidermolysis bullosa is this:
autosomal dominant or recessive inheritance of defects in type VII collagen (a major component of the basement membrane anchoring fibrils)
Defects causes blisters at the level of lamina densa.
This is a scarring disorder.

A

Epidermolysis bullosa

132
Q

Why does epidermolysis bullosa cause scarring?

A

cuz its a collagen defect

133
Q

Dystrophic type of epidermolysis bullosa can be inherited autosomal dominant or recessive due to defects in (blank)

A

type VII collagen

134
Q

(blank) is a mjor component of the basement membrane anchoring fibrils.

A

type VII collagen

Block 7 Week 2 (10 decks)

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