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Pathology Block 10 > Dermopathology II > Flashcards

Dermopathology II Flashcards

1
Q

Superficial gram + infection of staph aureus and group A beta hemolytic streptococci

A

Impetigo

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2
Q

Honey colored lesions

A

Impetigo

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3
Q

2 forms of impetigo

A
  • impetigo contagiosa=crusty pustules

- impetigo bullish=bulla (usually staph aureus)

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4
Q

Most common sites of impetigo

A
  • Nose

- Secondary infection of other dermatomes, breaks in skin, wounds, etc

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5
Q

What gives the impetigo its appearance

A

Accumulation of neutrophils beneath the stratum corneum

-often leads to subcorneal pustules-rupture leads to crust

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6
Q

Pathoigensis of blisterformation of impetigo

A

Bacteria produce toxin that cleaves desmoglein

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7
Q

Desmoglein

A

Skin glue

  • epithelial cells attach to one another
  • impetigo has a bacterial toxin that breaks that down
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8
Q

Ecthyma in impetigo

A

Deeper infection, resulting in erosion of dermis

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9
Q

Impetigo treatment

A

Oral Ab
AB ointment

Easy to treat

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10
Q

Staphylococcal infection of hair follicle, leading to itching and burning

A

Folliculiits

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11
Q

What areas of the body are most susceptible to folliculitis

A

Any region with hair, but most common in Willa, face, and legs

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12
Q

Frequently occurs in setting of staphylococcal folliculits, initially a firm nodule that develops an abscess, sometimes with a central pustule

A

Furuncule

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13
Q

Composed of multiple, coalescing furuncles. Contains subcutaneous abscesses, superficial pustules, and openings draining pus

A

Carbuncle

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14
Q

What causes the abscess in furunrcle

A

Bacterial and neutrophil produces leading to abscess

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15
Q

Beat-hemolytic strep colonize skin and spread along superficial lymphatic vessels, erythematous expanding plaque

A

Erysipelas

Common on face and butt

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16
Q

How common is psoriasis

A

Common; affects 1-2% of people in US

In all ages

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17
Q

Not itchy, associated with psoriatic arthritis, myopathy, eneropathy, and AIDS

A

Psoriasis

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18
Q

Where does psoriasis frequency affect

A

Elbow, knees, scalp, lumbosacral, intergluteal cleft, glans penis

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19
Q

Lesions of psoriasis

A

Well demarcated
Pink to salmon colored
Covered with silver white loose scales

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20
Q

Psoriasis and face

A

Usually not on the face, if you see it there usually indicates AIDS

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21
Q

Nail involvement of psoriasis

A

~30%

Pitting, yellow-brown discoloration

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22
Q

“Salmon colored” lesions

A

Psoriasis

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23
Q

Pathogenisis of psoriasis

A

Increased epidermal cell turnover-acanthosis (epidermal thickening)
-in stratum corneum, they don’t have nuclei
-in psoriasis they still have their nuclei
-because very high epidermal cell turnover
elongated rete ridges
Superficial dermal infiltrate (inflammation)

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24
Q

Acanthosis

A

Epidermal thickening

-seen in psoriasis

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25
Q

Pathogenisis of psoriasis

A

T cell mediated

  • strong associated with HLA-C
  • CD4+ T cells interact with antigen presenting cells in skin-CD8+ T cells activated-cytokines (TNF)
  • lymphocytes produce keratinocytes growth factors
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26
Q

Which is more common, seborrheic dermatitis or psoriasis

A

Seborrheic dermatitis

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27
Q

Involves regions with high densities of sebaceous glands (but nit diseases of them)

A

Seborrheic dermatitis

-scalp ,forehead

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28
Q

Most common clinical expression of seborrheic dermatitis

A

Dandruff

Cradle cap

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29
Q

Morphology of seborrheic dermatitis in early stage

A

Similar to eczema

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30
Q

Seborrheic dermatitis morphology in late stage

A

Similar to psoriasis

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31
Q

Follicular lipping

A

In seborrheic dermatitis

-mounds of parakeratosis containg neutrophils and serum present at Ostia of hair follicles

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32
Q

Etiology of seborrheic dermatitis

A

Unknown

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33
Q

Pruritic, purple, polygonal papules often highlighted by wickham striae (zones of hypergranules)

A

Lichen planus

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34
Q

Resolution of lichen planus

A

Resolve spontaneously after 1-2 years

  • may leave behind hyperpigmentation
  • may progress to malignancy
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35
Q

Lots of ____ in lichen planus

A

lymphocytes

  • epidermal cell turnover causing thickening as well as lymphocytic cell killing
  • has a saw tooth pattern under microscope
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36
Q

Rare, autoimmune blistering disorder, usually >40yo, no sex predilection

A

Pemphigus

37
Q

Pemphigus vulgaris

A

Most common type

  • Involves mucosa and skin (scalp, Avila, groin, trunk, other pressure points)
  • superficial vesicles and bull are that rupture easily–dried serum, crust
38
Q

What kind of blistering disease is present in pre schoolers?

A

Impetigo

39
Q

What kind of blistering disease more prevalent in 50 years old

A

Pemphigus

40
Q

4 types of pemphigus

A

Pemphigus vulgaris
Pemphigus vegetables
Pemphigus fallacious
Pemphigus erythematosus

41
Q

Why do pemphigus vulgaris bullae rupture so easily

A

Skin lifts about the stratum basal

42
Q

How do you detec pemphigus vulgaris

A

Sera from patients contain IgG Ab to desmoglein of skin and mucous membranes
-immunoflourescence shoes IgG deposited in fish net pattern

43
Q

Bullous pemphigoid

A

elderly
range of presentations
- localized: generalized
-cutaneous: mucous membrane involvement
Tense bullae filled with clear fluid
-do not rupture easily, heal without scarring

44
Q

Bullae in bullous pemphigoid

A

Do not rupture easily

45
Q

Where do you see bullous pemphigoid

A

Inner thighs, flexor surfaces or forearm, axial, groin

30% have mouth leasions

46
Q

Pathogenisis of bullous pemphigoid

A

Entire epidermis lifted up

  • this causes it to be stronger so the blister wont rupture
  • subepidermal nonacantholyitc blister (cells in epidermis are not target to lyse, happening to the dermis)
47
Q

Pathogenisis of bullous pemphigoid

A
  • Ag are proteins in hemidesmosomes that attach basal cells to BM
  • immunoflourescence showas linear deposits of Ab along the BM
  • no attack of epidermis
48
Q

Blackheads are caused by dirt

A

False

49
Q

Acne is caused or worsened by certain foods, such as chocolate, sweets, and greasy junk food

A

False

50
Q

Scrubbing the face daily will help clear up acne

A

False

51
Q

Acne should disappear after your teens or 20s

A

False

52
Q

Stress exacerbates acne

A

False

53
Q

Disorder of sebaceous follicles beginning in adolescence, androgenic homrons cause abnormal keratinization of follicles, sebaceous duct blocked, microcomedo, comedome, tendency to be hereditary

A

Acne vulgaris (adolescent acne)

54
Q

Pathognomonic for acne vulgaris

A

Comedome

55
Q

What is a blackhead

A

Sebum, keratin, oxidized melanin

Open comedome

56
Q

Closed comedome

A

Whiteheads

-bacteria, inflammatory cells

57
Q

Bacteria responsible for acne

A

Prorpionibacterium acnes

-bacterial lipases convert lipids in sebum to pro-inflammatory fatty acids

58
Q

Papules and pustules in acne.

A

A little larger than the comedome. Pustules are more severe

59
Q

Mild acne

A

Comedome

Occasional papules and pustules

60
Q

Moderate acne

A

More inflammatory

Lesions may heal with scars

61
Q

Cystic acne

A
  • larger, deeper, more numerous papules or pustules
  • lesions tend to occur on trunk
  • not true cysts

If seeing them on trunk, usually indicative of cystic acne

62
Q

Seqeulae of acne

A

Trunk involvement is porgnostic of treatment difficulty

  • more severe forms prone to heal with strophic or pitted scars on face; hypertrophic scars of keloids on back
  • postinflammtory hyperigmentation
63
Q

Keloids

A

Raised lesion as it is healed

64
Q

Frequently mistaken for acne, conditions look alike, respond to same treatments, and can coexist in samepatient, lacks comedome

A

Rosacea

NOT ROSACEA ACNE

65
Q

Difference between acne and rosacea

A

NOT COMEDOMES

66
Q

Lesions of rosacea

A

Usually on flushareas, nose cheeks, forehead, and chin

67
Q

Cause of rosacea

A

Idiopathic, not inheritance patterns

68
Q

Ocular involvement of rosacea

A

-blepharoconjunctivis

Usually just cosmetic otherwise

69
Q

Precipitating factors of rosacea

A
  • sun exposure
  • excessive face washing
  • irritating cosmetics
  • MYTHS: excess alcohol, stress, foods, smoking, caffeine
70
Q

Clinical variants of rosacea

A

Rhinophyma

Prerosacea

71
Q

Rhinophyma

A

Rosacea

  • disfiguring sebaceous hyperplasia
  • usually middle-aged men that have rosacea
72
Q

Prerosacea

A
  • facial erythema and terlangiestasias (tiny dilated BV)
  • rosy cheeked complexion
  • although called prerosacea, they never go on to develop inflammatory lesions typical of rosacea
73
Q

Loss of melanocytes in affected skin, tanning of surrounding skin makes areas more prominent

A

Vitiligo

74
Q

Loss of pigmentation may be caused by ___ in vitiligo

A
  • infection
  • dermatitis
  • chemical irritation
  • idopathic
75
Q

Enhanced pigment transfer from melanocytes, associated with pregnancy, oral contraceptives, hydantoins, idiopathic

A

Melasma

-estrogen can stimulate

76
Q

Morphology of melasma

A

Sunlight can accentuate; usually resolved spontaeously or after hormone administration is discontinued

77
Q

Localized hyperplasia of melanocytes

A

Lentigines

78
Q

When does lentigines occur most

A

In infancy and childhood

79
Q

Oval, tan-brown macules or patches-cafe au laitspots

A

Lentigines

80
Q

Cause of lentigines

A

Unknown

81
Q

Key difference of lentigines and freckles

A

Lentigo does not darken in sunlight

Rate ridges commonly elongate and thin

82
Q

Too many cafe au lait spots (lentigo)

A

Singlan neurofibromatosis type I

83
Q

So alt lentigines

A

Develop with age (liver spots) and sun exposure

84
Q

What are the bacterial dermatoses

A 
Impetigo 
Folliculitis 
Furuncle 
Carbuncle 
Erysipelas
85
Q

What are the chronic inflammatory dermatoses

A

Psoriasis
Seborrheic dermatitis
Lichen planus

86
Q

Blistering (bullous) diseases of the skin

A

Pemphigus

Bullous pemphigoid

87
Q

Diseases of epidermal appendages

A

Acne vulgaris

Rosacea

88
Q

Disorders of pigmentation and melanocytes

A

Vitiligo
Melasma
Lentigines
Solar lentigines

Pathology Block 10 (8 decks)

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