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MyDermatology-Bolognia > Ch. 9-Other papulosquamous > Flashcards

Ch. 9-Other papulosquamous Flashcards

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1
Q

Typical onset of PRP?

A

2 peaks
1st/2nd decade

6th decade

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2
Q

Gender differences PRP?

A

Equally affected

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3
Q

What gene is involved in familial PRP

A

CARD14

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4
Q

Name 4 hypothesized triggers for PRP

A

Infection
Trauma
UV exposure
Drugs-imatinib
Malignant-renal and hepatocellular carcinoma
Autoimmune-celiac, MG and hypothyroid have been associated

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5
Q

Name 6 classic findings in PRP

A

Orange-red hyperkeratotic follicular papules nutmegrater papules

Coalescing orange-red plaques with islands of sparing

Erythroderma

Orange-red waxy keratoderma

Erythema with fine diffuse scaling to scalp

Spreads caudally

*Nails change-thickened plate with a yellow–brown discoloration and subungual debris.

*The mucous membranes are rarely involved, but they may show features similar to oral lichen planus.

*Can show photo aggravation

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6
Q

According to the Griffith classification, what are the 5 variants of pityriasis rubra? What is the 6th additional variant?

A

Type I-Classic adult PRP
Type II-Atypical adult PRP
Type III-Circumscribed juvenile PRP
Type IV- Classic juvenile PRP
Type V- Atypical juvenile PRP
Type VI-HIV associated PRP

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7
Q

What is prognosis of:
classic adult PRP
Classic juvenile
Atypical adult
Atypical juvenile
Circumscribed/localized juvenile
HIV

A

Classic adult - 80% clear in 3 years
Classic juvenile-same
Atypical adult-Chronic course, 20% clear in 3 yrs
Atypical juvenile-chronic course
Circumscribed-variable
HIV-variable

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8
Q

What % of PRP does Type I-VI make up?

A

Type I- 55%
Type II-5%
Type III-circumscribed-25%
Type IV-classic juvenile 10%
Type V-Atypical juvenile 5%
Type VI-<1%

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9
Q

Describe 3-4 differences each from classic PRP in:
-adult atypical
-juvenile atypical

A

Adult:
1. Coarse, lamellar keratoderma
2. eczematous dermatitis
3. Icthyosiform scaling to legs
4. occasional alopecia

Juvenile:
1. itchyosiform scaling
2. sclerodermoid changes to hands and feet
3. If familial with CARD14 gene, typically present-with atypical juvenile

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10
Q

What is Kaposi varicelliform eruption

A

Eczema herpeticum

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11
Q

NAme 3 features circumscribed PRP

A
  1. Prepubertal onset
  2. Ertyhematous well demarcated plaques over knees, elbows, knuckles and dorsal fingers
    3.Follicular keratotic papules
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12
Q

Name 4 features HIV associated PRP that are unique

A
  1. Erythematous follicular papules w/ Keratotic spines
  2. HS
  3. Acne conglobata
  4. May improved with anti-retrovirals, often fails to respond to typical therapy

*Can also get coalescing plaques

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13
Q

Name 4 features HIV associated PRP that are unique

A
  1. Erythematous follicular papules w/ Keratotic spines
  2. HS
  3. Acne conglobata
  4. May improved with anti-retrovirals, often fails to respond to typical therapy

*Can also get coalescing plaques

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14
Q

5 histopathological features of PRP

A
  1. Alternating vertical and horizontal ortho and parakeratosis “checkerboard pattern”
  2. Dilated hair follicles with follicular plug
  3. Parakeratosis on the shoulder of a dilated follicle
  4. Hypergranulosis
  5. Shortened, thick, rete pegs
    6.Sparse perivascular lymphohistiocytic infiltrate
  6. acantholysis with focal dyskeratosis can be seen
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15
Q

What is the 7th proposed form fruste of PRP

A

Facial discoid dermatosis

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16
Q

Name 3 classes/ exampled ofsystemic treatments for PRP

A

Retinoids–> isotretinoin or acitretin
MTX
TNF-alpha inhibitors, secukinumab ustekinumab

Others:
-other immunosuppresives
-anabolic steroids

*TCS, TCIs, tar, vitamin D3 can be used as adjuncts
*UV therapy can exacerbate but some case series nbUVB or PUVA + retinoid show improvement

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17
Q

Who gets pityriasis rosea

A

10-35 years on average, slight female predominance, peak adolescence

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18
Q

How long does PR last?

A

6-8 weeks, up to 5 months

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19
Q

What are the two proposed causes of PR

A

HHV-6
HHV-7*-predominant

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20
Q

Name the classic cutaneous findings of PR

A

Herald patch, solitary on trunk, 2-4 cm (1-10 cm descibred), pink-salmon or pink-brown scaly plaque, enlarges over days with a advancing border, trailing scale, in-toeing, branny scale

followed days later by multiple smaller scaly papules and plaques, round to oval, often following langers lines, trunk and extremities. Similar central fine scaling or sometimes collarette scale, a advancing border

Face, palms, soles typically spared

Minute pustules sometimes may be seen

Priuritus in 25%

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21
Q

2 differences in darker skin types in PR

A

More papular and hyper pigmented, sometimes follicular

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21
Q

What are 6 morphological variants of Pityriasis Rosea?

A

Purpuric
Vesicular
Pustular
Inverse
Gigantea
EM-like
Atypical
Urticarial

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22
Q

What are 5 features seen on pathology for Pityriasis Rosea?

A

Mounds of parakeratosis
Lymphohistiocytic perivascular and interstitial infiltrate
Mild RBC extravasation
Spongiosis
Papillary dermal edema
Diminution granular layer
Rarely epidermal pustules

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23
Q

Number 1 ddx for PR

24
What are 5 medications known to cause drug induced PR?
o Ketotifen o Flagyl o Clonidine o Bismuth, beta-blocker, barbituates, BCG vaccine o Arsenic, Ace-Inhibitors (#1), Accutane o Gold o Salvarsan Additionally: TNF inhibitors, HCTZ, omeprazole
25
5 possible tx's for PR
None-self resolves UVB Sunlight Erythromycin PO x 14 days Acyclovir PO-800 mg 5x daily x 1 week Antihistamines Rarely oral steroids
26
3 variants pityriasis lichenoides
Pityriasis lichenoides et variolofirmis acute Pityriasis lichenoides chronica Febrile ulceronecrotic Mucha–Habermann disease (FUMHD)
27
Name 3 possible triggers for PLEVA/PLC
DRugs-tnfs inhibitors, statins, estrogen-progesterone Radiocontrast dye Infection: HIV, parvo ?maternal GVHD
28
What is the main infiltrate in PLEVA? PLC?
Clonal T-cell proliferation thus seen as T-cell lymphoproliferative disase PLEVA=CD8 PLC=CD4
29
What are the clinical manifestations of PLEVA
Recurrent and spontaneously regressing crops of erythematous to purpuric papules and papulovesicles, can develop crust and ulcerations. May have varioliform scarring Asymptomatic, resolve most often with out scarring
30
What is febrile ulceronecrotic Mucha–Habermann disease (FUMHD)
Develop large coalescing ulcerative-necrotic lesions Can have mucosal, gastrointestinal, and pulmonary involvement can be observed May have malaise, fever, lymphadenopathy, arthritis, and/or bacteremi
31
What are the clinical features of PLC
Red-brown scaly papules More indolent course, regress over weeks to months--> result in hypo pigmented macules
32
What is the prognosis of PLEVA? PLC?
PLC-may regress over several months, often relapsing and remitting with long periods remissions
33
What is a predictor of length of disease course?
Distribution of lesions: generalized-short course(11 months) Peripheral distribution had the longest average clinical course (33 months). The central distribution variant was intermediate.
34
Name 6 histopath findings of pityriasis lichenoides
1. superficial perivascular interface dermatitis in all cases 2. Lymphocytic infiltrate, may be neutrophils 3. Focal parakeratosis 4. Epidermal edema 5. Fun thickness epidermal necrosis 6. RBC extravasation 7. Lymphocytic vasculitis is sometimes described, but true fibrinoid necrosis of blood vessels is not seen 8. necrotic keratinocytes
35
Name 4 ddx for PLEVA
lymphomatoid papulosis, arthropod reactions, cutaneous small vessel vasculitis, varicella drug eruption EM
36
Name 4 ddc for PLC
Small plaque parapsoriasis Guttate psoriasis Exnathematous LP PR Syph Papular dermatitis Lichenoid drug
37
Name 4 clonal T-cell related dermatitides
PArapsoriasis PLEVA/PLC LYP
38
Which type of parapsoriasis is associated with MF
LArge plaque
39
Who gets parapsoriasis
5th decade peak, sl. male predominance
40
What are the clinical features of small plaque parapsoriasis
Round-oval PATCHES, variably erythematous, fine scale, <5 cm, some with yellow hue Asymptomatic or mildly pruritic Widespread on trunk and extremities OR localized on sun protected sites
41
Name a variant of small plaque parapsoriasis and describe the clinical features
Digitate dermatosis 1-10 cm patches Elongated, finger-like patches symmetrically distributed on the flanks Risk MF is LOW
42
What is the name of the yellow hue small plaque parapsoriasis
xanthoerythrodermia perstan
43
Name 3 histopath findings of parapsoriasis
-mild, nonspecific spongiotic dermatitis - focal parakeratosis - Exocytosis of lymphocytes is variable but usually present. CD4+
44
Name 5 possible tx option small plaque parapsoriasis
TCS TCIs Topical tar Topical baxarotene Imiquimod UVA/PUVA/nbUVB
45
What is risk of progression from LPP to MF?
10% to 35% over a period of 6–10 years * Some think this is patch stage MF
46
Predominant cell infiltrate in large plaque psoriasis
CD4+ T cells
47
Describe the clinical features of Large plaque parapsoriasis
Variably erythematous to red brown, round to irregularly shaped, slightly scaly patches > 5 cm May show poikiloderma
48
What is the variant of Large plaque parapsoriasis? What is the risk of MF progression?
Retiform parapsoriasis widespread, ill-defined patches in a net-like or zebra-stripe pattern Almost all progress to MF
49
Name 5 features LPP on path
parakeratosis a mild, nonspecific spongiotic dermatitis or an interface lymphocytic infiltrate with a variable degree of lichenoid features may contain atypical lymphoid cells epidermal atrophy, telangiectasia, and pigment incontinence if poikiloderma
50
Contrast the two types of pityriasis rotunda
Type I-occurs mostly in black and asian, associated with internal malignancy, no family history, hyperpigmented plaques Type II- multiple plaques (>30), family gig story, but no internal malignancy association
51
What are the two main theories on the pathogenesis of pityriasis rotunda
1. Associated with malnutrition (common final pathway for malignancy or infection like TB or leprosy, infection) 2. Minor acquired ichthyosis that can be familial
52
Who gets pityriasis rotunda
Far East (Japan, china), Middle East (Morocco, Italy, Israel), African americans 25-45
53
Describe the clinical features pityriasis rotunda
large circular and polycyclic lesions that are often 10 cm (but may be up to 30 cm) fine scale and are moderately hyperpigmented with a sharp margin and no inflammation. The trunk and extremities are favored. A hypopigmented halo has been described in some patients, and sometimes the entire lesion can be hypopigmented.
54
Name 4 histopathological features pityriasis rotunda
Hyperkeratosis without parakeratosis Diminished granular cell layer Epidermal atrophy Pigment incontinence perivascular lymphohistiocytic infiltrate, and occasional follicular plugging increased pigmentation basal cellnlayer
55
What is a treatment that has moderate evidence in pityriasis rotunda
topical lactic acid, urea, tars, emollients, and corticosteroids have provided little benefit. Topical tretinoin cream 0.1% can result in modest improvement and systemic retinoids warrant consideration for patients with more extensive disease. However, reversal of any underlying disorder – in particular, malnutrition, infection, or malignancy – should be addressed first.
56
Who gets granular parakeratosis
Middle age to older adult women
57
What is the underylgin pathogenesis in granular parakeratosis
Underlying profillagrin to fillagrin processing defect with retention of keratohyaline granules with resulting aggregate keratin filaments during cornification.
58
Describe the clinical features of granular parakeratosis
Keratotic brown-red papules with conical shape Occurs in intertriginous areas May coalesce into larger plaques, may become macerated Often quite pruritic

MyDermatology-Bolognia (31 decks)

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