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19 Skin Pathology > 1.1 Inflammatory Dermatoses > Flashcards

1.1 Inflammatory Dermatoses Flashcards

1
Q

Urticaria

  • most common cause
  • how long can it last?
A
  • most cases idiopathic
  • URI is most common cause
  • also drug, food allergies
  • can last 6 weeks!
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2
Q

What is it?

  • pruritic, planar, polygonal, purple papules
  • wrist, elbows, oral mucosa
A

Lichen planus

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2
Q

Auspitz sign

A
  • psoriasis
  • easy bleeding of skin because thinning of epidermis
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2
Q

Psoriasis–variants (5)

A
  1. plaque (most common–pink scaly patches)
  2. inverse (folds of skin)
  3. guttate (“tear drop”)
  4. pustular
  5. erythrodermic
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3
Q

Psoriasis

-histology findings

A
  • thickened layer of keratin
  • thinning of epidermis above elongated dermal papillae–results in easy bleeding when scale is picked off (Auspitz sign)
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3
Q

seborrheic dermatitis

A

“cradle cap”

  1. babies–crusty cradle cap
  2. adults–yellow-red papules, scaly
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4
Q

psoriasis

-what meds not to use!

A
  • no systemic corticosteroids, as withdrawal of that can worsen symptoms.
  • common mistake
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4
Q

Henoch-schonlein purpura (HSP)

  • clinical presentation
  • most common cause
A
  • subtype of leukocytoclastic vasculitis
  • Classic triad: palpable purpura (legs, butt), joint pain, abdominal pain. wide systemic involvement possible.
  • most common cause: Strep URI. but many infections, drugs, vaccines possible
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5
Q

SPF–measures what UV type?

A

-only measures UVB protection

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6
Q

keratinization:
- what is it
- timeframe

A
  • process of keratinocyte migration and maturation
  • 28 days total
    1. migration from stratum basale to corneum: 14 days
    2. stratum corneum to shedding: 14 days
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7
Q

what is stratum lucidum

A
  • an extra layer found between stratum corneum and stratum granulosum
  • found only in acral parts (eg sole, palms)
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7
Q

Koebner phenomenon

A
  • development of skin lesions at sites of injury
  • characteristic of Psoriasis (b/c easy blistering, Auspitz sign)
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7
Q

Wickham’s striae

A

grayish streaks/lines over surface of papules

-characteristic of lichen planus

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7
Q

Henoch-schonlein purpura (HSP)

-tx

A
  • skin eruption resolves 2-4 weeks
  • but systemic involvement can have permanent effects
  • supportive care for pruritis (antihistamines, topical steroids)
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8
Q

Leukocytoclastic vasculitis (LCV)

  • etiology
  • clinical presentation
A
  • aka hypersensitivity vasculitis
  • inflammation, destruction of vessels by infiltrating neutrophils
  • 50% idiopathic, can be caused by infections, drugs, autoimmune, cancer
  • palpable purpura
  • systemic involvement possible
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9
Q

Epidermis:

  • layers?
  • characteristics of each
A

Epidermis from deep to superficial

  1. Stratum basalis–stem cell layer
  2. Stratum spinosum–connected to each other by desmosomes (which make it cell borders look spinous)
  3. Stratum granulosum–granules inside
  4. strarum corneum–keratin in anuclear cells

Californians like girls in string bikinis

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10
Q

morphea

A
  • known before as ‘localized scleroderma’
  • autoimmune
  • causes sclerosis (thickening of collagen), leading to hardened sclerotic plaques
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11
Q

Lichen planus also has Nail and Mucosal forms.

clinical findings of each?

A
  1. thinning of nail plates, loss of nails
  2. reticulated pattern of papules inside mouth
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13
Q

contact dermatitis

A
  • type 4 HSR
  • eg poison ivy, nickel jewelry, penicillin
15
Q

ichthyosis vulgaris

  • clinical findings
  • etiology
  • associated with what?
A
  • scaly, dry skin
  • mutation in profilaggrin gene, so defective filaggrin–important for keratin formation
  • associated with allergic rhinitis, asthma, etc
15
Q

psoriasis

-what medications can trigger it (5 types)

A
  1. systemic corticosteroid withdrawal
  2. lithium
  3. beta blockers
  4. antimalarials
  5. interferons
16
Q

psoriasis

-tx (3)

A
  1. corticosteroids (topical, not systemic!)
  2. ‘PUVA’ tx: (Psoralen + UV light)–destroy surface keratin. psoralen is a drug to induce UV sensitivity
  3. immune-modulating drugs (psoriasis may be autoimmune)
17
Q

Psoriasis

  • clinical findings
  • common location
  • mech
  • etiology
A
  • salmon-colored plaques with silvery scales, pitting of nails
  • usu extensor surfaces and scalp
  • excessive keratinocyte proliferation
  • possible autoimmune
18
Q

exanthematous drug eruption

  • what does it look like
  • timeframe
A
  • aka Morbilliform drug rash (measles)
  • type 4, delayed reaction, 2-14 days after starting med
20
Q

acne vulgaris

-mech of formation?

A
  1. increase in sebum production (hormone associated)
  2. excess keratin production blocks follicle shaft
  3. sebum backs up, and is infected by P. acnes
  4. P. acnes produces lipases to break down sebum, releasing proinflammatory fatty acids. Pustule formation.
21
Q

Atopic dermatitis

  • what is it
  • where typically located
  • what associated with?
A

aka Eczema

  • pruritic, erythematous, ozzing rash with vesicles and edema
  • often face and flexor surfaces
  • Type 1 HSR, associated with asthma and allergic rhinitis
23
Q

erythema nodosum

  • what is it
  • clinical findings
A
  • reactive panniculitis (inflammation of subQ fat)
  • tender red nodules on the shins, feels like hard lumps
25
Q

UVA vs UVB: which causes what?

A

UVA: penetrates deeper–tanning, wrinkles

UVB: sunburns

(not clear cut though)

26
Q

embryonic origins?

  1. epidermis
  2. dermis
  3. subcutaneous fat
A
  1. ectoderm

2, 3. mesoderm

27
Q

systemic sclerosis (aka scleroderma)

  • what is it
  • clinical features (5)
A
  • autoimmune, widespread sclerosis
  • for limited scleroderma: CREST syndrome
    1. calcinosis
    2. raynaud’s phenomenon
    3. esophageal dysmotility
    4. sclerodactyly
    5. telangiectasia
28
Q

What is it?

  • pruritic, erythematous, ozzing rash with vesicles and edema
  • often face and flexor surfaces
A

Eczema (atopic dermatitis)

29
Q

Acne vulgaris

-tx? (2)

A
  1. benzoyl peroxide–antimicrobial, kills P. acnes
  2. Vitamin A derivatives (retinoids)–reduce keratin overproduction in follicle by cell cycle mechanism
30
Q

What is it?

  • salmon-colored plaques with silvery scales, pitting of nails
  • usu extensor surfaces and scalp
A

Psoriasis

31
Q

DRESS syndrome:

-what can happen in the future after resolution?

A
  • higher risk of autoimmune diseases
  • eg thyroiditis, DM, autoimmune hemolytic anemia
33
Q

where is keratin synthesized?

A

in stratum spinosum

34
Q

DRESS syndrome

  • tx
  • timeframe
A
  • danger! 10% mortality
  • stop drug
  • topical steroids, antihistamines, may need to be hospitalized
  • slow resolution over weeks, months
35
Q

exanthematous drug reaction

-tx

A
  1. discontinue culprit drug
  2. puriritus supportive care:
    - antihistamines, topical steroids
  3. resolves in 1-2 weeks
37
Q

how is keratin assembled?

A

they assemble into tetramers and then into intermediate filaments

39
Q

erythema nodosum

  • triggers (4)
  • which is most common
A

-reactive panniculitis

triggers:

  1. strep throat (most common)
  2. oral contraceptives
  3. IBD
  4. malignancy
40
Q

lichen planus

  • clinical findings
  • common locations
  • histology
  • etiology
A

“P’s”:

  • pruritic, planar, polygonal, purple papules
  • wrist, elbows, oral mucosa
  • inflammation at dermal-epidermal junction with “saw-tooth” appearance
  • etiology unknown, associated with Hep C
41
Q

what disease is lichen planus associated with?

A

Hep C infection

42
Q

DRESS syndrome

  • what happens
  • timeframe
A

‘drug reaction with eosinophilia and systemic systems’

  • type 4 HSR
  • many organs affected: liver, kidney, hematologic, etc
  • later onset, 2-8 weeks after drug
43
Q

what do you see in psoriatic arthritis?

A
  1. sausage digits
  2. pencil-in-cup deformity
  3. nail disruption
44
Q

Dermis:

layers?

A
  1. papillary dermis
  2. reticulated dermis (deeper)
45
Q

atopic dermatitis

-tx (4 categories)

A
  1. topical corticosteroids
  2. topical immunomodulators–calcineurin inhibitors

(eg tacrolimus ointment)

  1. antihistamines to relieve pruritus
  2. Phototherapy

19 Skin Pathology (8 decks)

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