psoriasis

Question 1

is psoriasis involving the entire skin

Answer 1

paoriasis erythroderma

Question 2

ps arthritis occurs in how many % pxs

Answer 2

Psoriatic arthritis occurs in 10 to 25% o patients

Question 3

age peak incidence

Answer 3

Allages.Early:Peakincidence occursat22.5yearso age(inchildren,the meanageo onsetis8years).Late:Presents around age 55. Early onset predicts a more severe and long-lasting disease, and there is usuallyapositive amilyhistoryo psoriasis.

Question 4

gender gender

Answer 4

equal

Question 5

how many percent will children have ps if 1 or 2 parents have psoriasis

Answer 5

HEREDITY Polygenic trait. When one parent has psoriasis,8%o hisorhero springdevelop psoriasis; when both parents have psoriasis, 41% o their children develop psoriasis

Question 6

HLA for ps

Answer 6

HLA- B13, B37, -B57, and, most impor- tantly,HLA-Cw6,whichisacandidate or
unctional involvement

Question 7

infection that triggers acute guttate ps

Answer 7

Acute streptococcal in ection precipitates gut- tate psoriasis. Stress is a actor in ares o pso- riasis and is said to be as high as 40% in adults and even higher in children. Drugs: Systemic glucocorticoids, oral lithium, antimalarial drugs, inter eron, and β-adrenergic blockers can cause ares and cause a psoriasi orm drug eruption. Alcohol ingestion is a putative trigger
actor

Question 8

Psoriasis is a cell–drivendiseaseandthecytokinespectrum is that o a H1 response. Maintenance o psori- atic lesions is considered an ongoing autoreac- tiveimmuneresponsedrivenby….

Answer 8

TNFα,IL-17 and IL-23

Question 9

dist and pred sites for acute guttat and chronic stable ps

Answer 9

AcuteGuttate. Disseminated,generalized, mainlytrunk.
Chronic Stable. Single lesion or lesions local- ized to one or more predilection sites: elbows
knees, sacral gluteal region, scalp, and palm/ soles (Fig. 3-5). Sometimes only regional involvement(scalp),o engeneralized. Pattern. Bilateral,o ensymmetric(predilec- tionsites,Fig.3-5);o ensparesexposedareas.

Question 10

pathognomonic

Answer 10

oil spot (pathognomonic)

Question 11

nail lesiosn

Answer 11

Fingernailsandtoenails requently(25%) involved, especially with concomitant arthri- tis (Fig. 3-10). Nail changes include pitting, subungual hyperkeratosis, onycholysis, and yellowish-brown spots under the nail plate— the oil spot (pathognomonic)

Question 12

DP

Answer 12

Markedoverallthickeningo theepidermis (acanthosis)andthinningo epidermisover elongated dermal papillae. Increased mitosis o keratinocytes, broblasts, and endothelial cells. Parakeratotic hyperkeratosis (nuclei retained
 FIGURE3-5 Predilection sites o psoriasis. in the stratum corneum). In ammatory cells in

Question 13

why do an aso titer and culture for what organism

Answer 13

SERUM Increased antistreptolysin titer in acute guttate psoriasis with antecedent streptococcal inection

T roat culture or group A β -hemolytic streptococcus in ection.

Question 14

tx localized psoriasis

Answer 14

LOCALIZED PSORIASIS (Fig. 3-3)
MANAGEMENT OF PSORIASIS
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opical uorinated glucocorticoid covered with plastic wrap. Glucocorticoid- impregnated tape also use ul. Beware o glucocosteroidsidee ects.
Hydrocolloid dressing, le on or 24 to 48 h, is e ectiveandpreventsscratching.
For small plaques (≤ 4 cm), triamcinolone acetonideaqueoussuspension3mg/mL

topical anthralin
vit d

opicalpimecrolimus,1%,ise ectivein inverse psoriasis and seborrheic dermatitis- likepsoriasiso the aceandearcanals.
azarotene (a topical retinoid, 0.05 and 0.1% gel) has similar ef cacy, best combined with class II topical glucocorticoids.
All these topical treatments can be combined with 311-nm UVB phototherapy or PUVA

Question 15

tx scalp psoriasis

Answer 15

SCALP Super cialscalingandlackingthick plaques: ar or ketoconazole shampoos ollowed bybetamethasonevalerate,1%lotion;i rerac- tory,clobetasolpropionate,0.05%scalpapplica- tion. In thick, adherent plaques (Fig. 3-7): scales have to be removed by 10% salicylic acid in mineral oil, covered with a plastic cap and
le on overnight be ore embarking on topical therapy.I thisisunsuccessul,considersys- temic treatment

Question 16

palm and sole ps tx

Answer 16

PALMS AND SOLES (Fig. 3-6) Occlusive dressings with class I topical glucocorticoids

Question 17

tx for inverse ps and nail lesions

Answer 17

Inverse Psoriasis (Fig. 3-9). opical glucocorti- coids (caution: these are atrophy-prone regions; steroidsshouldbeapplied oronlylimited periodso time);switchtotopicalvitaminD derivatives such as tazarotene, topical tacroli- mus, or pimecrolimus. I resistant or recurrent, consider systemic therapy.
NAILS (Fig. 3-10) opical treatments o the
ngernails are unsatis actory. Systemic M andCStherapyaree ectivebuttaketimeand arethuspronetosidee ects.

Question 18

tx acute guttatE

Answer 18

ACUTE, GUTTATEPSORIASIS (Fig. 3-2) reat streptococcal in ection with antibiotics. Narrowband (311 nm) UVB irradiation most e ective.

Question 19

tx generalized plaque type ps

Answer 19

GENERALIZEDPLAQUE-TYPEPSORIASIS (Fig.3-4) PUVA or systemic treatments that are given as either mono—or combined—or rotational therapy

Question 20

uv tx in generalized ps

Answer 20

NARROWBAND UVB PHOTOTHERAPY (311 nm)
E ectiveonlyinthinplaques;e ectivenessis increased by combination with topical gluco- corticoids, vitamin D analogues, tazarotene, or topical tacrolimus/pimecrolimus.
ORALPUVA reatment consists o oral inges- tion o 8-methoxypsoralen (8-MOP) (0.6 mg 8-MOP per kilogram body weight) or, in some European countries, 5-MOP (1.2 mg/kg body weight)andexposuretodoseso UVAthatare adjustedtothesensitivityo thepatient.Most patients clear a er 19 to 25 treatments, and the amount o UVA needed ranges rom 100 to 245 J/cm2. Long- erm Side Ef ects PUVA kerato- ses and squamous cell carcinomas in some patients who receive an excessive number o treatments.

Question 21

what do you call the triple dose tx of methotrexate in ps

Answer 21

METHOTREXATETHERAPY Oral M X is one o the most e ective treatments but response is slow and long-term treatment is required. Hepatic toxicity may occur a ter cumula- tive doses in normal persons (≥ 1.5 g). he
riple-Dose (Weinstein) Regimen Pre erred by most over the single-dose M X once weekly, 5 mg is given every 12 h or a total
o three doses, i.e., 15 mg/week. Achieves an 80% improvement but total clearing only in some, and higher doses increase the risk o toxicity

Question 22

cyclosporine toxicity

Answer 22

CYCLOSPORINE1 CS treatment is highly e ective atadoseo 3to5mg/kgperday.I thepatient responds, the dose is tapered to the lowest
e ectivemaintenancedose.Monitoringblood pressure and serum creatinine is mandatory becauseo theknownnephrotoxicityo

Question 23

monoclonal tx

Answer 23

Alefacept isahumanlymphocyte unction- associated antigen (LFA)-3-IgG1 usion protein that prevents interaction o LFA-3 and CD2. Given intramuscularly once weekly

Tumor Necrosis Factor-Alpha (TNF-α ) antagoniststhataree ectiveinpsoriasisare in iximab,adalimumab,andetanercept.In- liximab is a chimeric monoclonal antibody to
NF-α . Administered intravenously at weeks 0,2,and6,itishighlye ectiveinpsoriasis andpsoriaticarthritis.Adalimumabisa ully human recombinant monoclonal antibody that speci cally targets NF-α. It is administered subcutaneously every other week andissimilarlye ectiveasin iximab.Etaner- cept is a human recombinant, soluble NF-α receptor that neutralizes NF-α activity. Administered subcutaneously twice weekly and islesse ectivethanin iximabandadalim- umabbutishighlye ectiveinpsoriatic arthritis.
Ustekinumab (Anti-Interleukin (IL) 12/Inter- leukin23p40) isahumanIgG1κmonoclo- nal antibody that binds to the common p40 subunit o human IL-12 and IL-23, preventing its interaction with its receptor. Given every 4monthssubcutaneously,itishighlye ective. Sekinumab is an anti-IL-17 recombinant ully human monocloncal antibody that neutralizes theproin ammatorycytokineIL-17A.Itis

delivered subcutaneously at weeks 0, 1, 2, and 3 ollowed by monthly maintenance doses
o 300 mg. It is rapidly e ective, even more
e ective than Ustekinumab, and is approved by EMA or the treatment o plaque psoriasis in adults.
Apremilast is a “small molecule”, phosphodiesterase-4 inhibitor which can be administered orally and leads to a reduction
o proin ammatorycytokines( NFα,IL-23, IL-17) and thus to a down regulation o the
in ammatory process. Doses start with 10 mg POdaily,whichisgraduallyincreasedto 300mgbid.APASI75responseat16weeksis 33%,whichmeansasigni cantimprovement.
Allthesebiologicalsandotherscurrently developedinclinicaltrialshavesidee ects, and there are long-term sa ety concerns. Also, currently they are extremely expensive, which limits their use in clinical practice. For doses, see warnings and side e ects

Question 24

tx general pustular ps

Answer 24

GENERALIZED PUSTULAR PSORIASIS (see Fig. 3-12)
Ill patients with generalized rash should be hospitalized and treated in the same manner as patients with extensive burns, toxic epidermal necrolysis, or ex oliative erythroderma—in a specialized unit. Isolation, uid replacement, and repeated blood cultures are necessary. Rapid suppression and resolution o lesions is achieved by oral retinoids (acitretin, 50 mg/ day). Supportive measures should include uid intake, IV antibiotics to prevent septicemia, cardiac support, temperature control, topi-
cal lubricants, and antiseptic baths. Systemic glucocorticoids to be used only as a rescue intervention as rapid tachyphylaxis occurs. OralPUVAise ective,butlogisticso treat- ment are usually prohibitive in a toxic patient with ever.

Question 25

ACRODERMATITIS CONTINUA HALLOPEAU tx

Answer 25

Oral retinoids as in von Zumbusch pustular psoriasis; M X, once-a-week schedule, is the second-line choice