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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
Pathogenisis of psoriasis
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
26
Which is more common, seborrheic dermatitis or psoriasis
Seborrheic dermatitis
27
Involves regions with high densities of sebaceous glands (but nit diseases of them)
Seborrheic dermatitis | -scalp ,forehead
28
Most common clinical expression of seborrheic dermatitis
Dandruff | Cradle cap
29
Morphology of seborrheic dermatitis in early stage
Similar to eczema
30
Seborrheic dermatitis morphology in late stage
Similar to psoriasis
31
Follicular lipping
In seborrheic dermatitis | -mounds of parakeratosis containg neutrophils and serum present at Ostia of hair follicles
32
Etiology of seborrheic dermatitis
Unknown
33
Pruritic, purple, polygonal papules often highlighted by wickham striae (zones of hypergranules)
Lichen planus
34
Resolution of lichen planus
Resolve spontaneously after 1-2 years - may leave behind hyperpigmentation - may progress to malignancy
35
Lots of ____ in lichen planus
lymphocytes - epidermal cell turnover causing thickening as well as lymphocytic cell killing - has a saw tooth pattern under microscope
36
Rare, autoimmune blistering disorder, usually >40yo, no sex predilection
Pemphigus
37
Pemphigus vulgaris
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
What kind of blistering disease is present in pre schoolers?
Impetigo
39
What kind of blistering disease more prevalent in 50 years old
Pemphigus
40
4 types of pemphigus
Pemphigus vulgaris Pemphigus vegetables Pemphigus fallacious Pemphigus erythematosus
41
Why do pemphigus vulgaris bullae rupture so easily
Skin lifts about the stratum basal
42
How do you detec pemphigus vulgaris
Sera from patients contain IgG Ab to desmoglein of skin and mucous membranes -immunoflourescence shoes IgG deposited in fish net pattern
43
Bullous pemphigoid
elderly range of presentations - localized: generalized -cutaneous: mucous membrane involvement Tense bullae filled with clear fluid -do not rupture easily, heal without scarring
44
Bullae in bullous pemphigoid
Do not rupture easily
45
Where do you see bullous pemphigoid
Inner thighs, flexor surfaces or forearm, axial, groin | 30% have mouth leasions
46
Pathogenisis of bullous pemphigoid
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
Pathogenisis of bullous pemphigoid
- 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
Blackheads are caused by dirt
False
49
Acne is caused or worsened by certain foods, such as chocolate, sweets, and greasy junk food
False
50
Scrubbing the face daily will help clear up acne
False
51
Acne should disappear after your teens or 20s
False
52
Stress exacerbates acne
False
53
Disorder of sebaceous follicles beginning in adolescence, androgenic homrons cause abnormal keratinization of follicles, sebaceous duct blocked, microcomedo, comedome, tendency to be hereditary
Acne vulgaris (adolescent acne)
54
Pathognomonic for acne vulgaris
Comedome
55
What is a blackhead
Sebum, keratin, oxidized melanin | Open comedome
56
Closed comedome
Whiteheads | -bacteria, inflammatory cells
57
Bacteria responsible for acne
Prorpionibacterium acnes | -bacterial lipases convert lipids in sebum to pro-inflammatory fatty acids
58
Papules and pustules in acne.
A little larger than the comedome. Pustules are more severe
59
Mild acne
Comedome | Occasional papules and pustules
60
Moderate acne
More inflammatory | Lesions may heal with scars
61
Cystic acne
- 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
Seqeulae of acne
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
Keloids
Raised lesion as it is healed
64
Frequently mistaken for acne, conditions look alike, respond to same treatments, and can coexist in samepatient, lacks comedome
Rosacea | NOT ROSACEA ACNE
65
Difference between acne and rosacea
NOT COMEDOMES
66
Lesions of rosacea
Usually on flushareas, nose cheeks, forehead, and chin
67
Cause of rosacea
Idiopathic, not inheritance patterns
68
Ocular involvement of rosacea
-blepharoconjunctivis Usually just cosmetic otherwise
69
Precipitating factors of rosacea
- sun exposure - excessive face washing - irritating cosmetics - MYTHS: excess alcohol, stress, foods, smoking, caffeine
70
Clinical variants of rosacea
Rhinophyma | Prerosacea
71
Rhinophyma
Rosacea - disfiguring sebaceous hyperplasia - usually middle-aged men that have rosacea
72
Prerosacea
- 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
Loss of melanocytes in affected skin, tanning of surrounding skin makes areas more prominent
Vitiligo
74
Loss of pigmentation may be caused by ___ in vitiligo
- infection - dermatitis - chemical irritation - idopathic
75
Enhanced pigment transfer from melanocytes, associated with pregnancy, oral contraceptives, hydantoins, idiopathic
Melasma | -estrogen can stimulate
76
Morphology of melasma
Sunlight can accentuate; usually resolved spontaeously or after hormone administration is discontinued
77
Localized hyperplasia of melanocytes
Lentigines
78
When does lentigines occur most
In infancy and childhood
79
Oval, tan-brown macules or patches-cafe au laitspots
Lentigines
80
Cause of lentigines
Unknown
81
Key difference of lentigines and freckles
Lentigo does not darken in sunlight | Rate ridges commonly elongate and thin
82
Too many cafe au lait spots (lentigo)
Singlan neurofibromatosis type I
83
So alt lentigines
Develop with age (liver spots) and sun exposure
84
What are the bacterial dermatoses
``` Impetigo Folliculitis Furuncle Carbuncle Erysipelas ```
85
What are the chronic inflammatory dermatoses
Psoriasis Seborrheic dermatitis Lichen planus
86
Blistering (bullous) diseases of the skin
Pemphigus | Bullous pemphigoid
87
Diseases of epidermal appendages
Acne vulgaris | Rosacea
88
Disorders of pigmentation and melanocytes
Vitiligo Melasma Lentigines Solar lentigines

Pathology Block 10 (8 decks)

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