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AAD ETAS > photo > Flashcards

photo Flashcards

1
Q

UVA2

A

320-340nm

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2
Q

UVL spectrum

A

10-400 nm

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3
Q

photoallergy spectrum

A

320-425nm

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4
Q

UVC spectrum

A

200-290 nm

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5
Q

UVB thermal isomerisation7 dehydrocholesterol–>

A

previtamin D3

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6
Q

Vitamin D synthesis UV spectrum

A

220-320 nm

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7
Q

what photodermatologic disorder in which you should stop naproxen

A

PCT

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8
Q

medication which causes Lichenoid photodistributed

A

fenofibrate

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9
Q

tetracyclines, nalidixic acid, amiodarone, furosemide, ketoprofen cause

A

Pseudoporphyria – signs of PCT with normal porphyrins;

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10
Q

cutaneous immunosuppression wavelength

A

290-320 nm/311 nm

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11
Q

headache nausea syncope

A

SU

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12
Q

EPP-aw

A

SU

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13
Q

VL, UVA, UVB, 15 min add test

A

SU

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14
Q

quinolone tetracycline psolaren quinine

A

photoonycholysis

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15
Q

thick plaques CTCL NBUVB or PUVA?

A

NBUVB > PUVA

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16
Q

woods lamp

A

365nm

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17
Q

chlorpromazine TCA

A

blue gray

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18
Q

candida thyroid dysfunction abn

A

AIRE

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19
Q

AP persist winter

A

most T.

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20
Q

-quinidine sulphonyurea griseofulvin

A

photosensitvity

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21
Q

254nm vapour

A

me

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22
Q

350-360 nm

A

pUVA

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23
Q

CTCL mastocytosis GVHD generalised Ga

A

pUVA

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24
Q

chelitis conjunctivitis,

A

hediataryy PMLE

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25
Q

VL hi-E

A

blue violet

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26
Q

furocoumarin

A

phototoxic

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27
Q

Photoexacerbated hailey hailey,

A

T

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28
Q

antimalarials, thiazides, demethylchlortetracycline, fenofibrate, enalapril, quinine, quinidine

A

Lichenoid eruption – LP-like lesions (may be confluent) on sun-exposed areas;

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29
Q

reduc MED A/B

A

CAD

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30
Q

incandescent safer

A

CAD

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31
Q

PMLE patients have a reduced tendency to develop skin cancers because

A

lesser degree of cutaneous immunosuppression following UVR exposure (compared to normal individuals) likely results in a persistent ability to mount a DTH response against UVR-altered endogenous cutaneous molecules

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32
Q

PMLE never have systemic symptoms

A

General malaise, headache, fever, nausea and other symptoms rarely occur.

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33
Q

a form of PMLE referred to as juvenile spring eruption affects

A

helices of the ears

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34
Q

In darkly pigmented individuals, the most common morphology of PMLE is

A

grouped, pinhead-sized papules in sun-exposed areas

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35
Q

treatment modalities PMLE

A

hardening NB-UVB, PUVA,prednisone azathioprine or cyclosporine.

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36
Q

efficacy of antimalarials for PMLE

A

inconsistent in controlled trials

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37
Q

Cellular photoreceptors that mediate the signaling that leads to UV-induced immune responses are:

A
  • DNA (via formation of DNA damage [DNA photoproducts])
  • urocanic acid in the stratum corneum (via UV-induced isomerization from the trans- to the cis-isoform),
  • membrane lipids
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38
Q

actinic prurigo strong HLA association

A

HLA-DR4 (DRB10401) and subtype DRB10407

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39
Q

pathogenesis HV

A

chronic EBV infection

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40
Q

which photodermatoses: Most commonly, visible light, with extension into UVA, UVB sensitivity less common

A

solar urticaria

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41
Q

what topical vehicle has been successful in decreasing the development of actinic keratoses and BCCs?

A

bacterial DNA repair enzyme T4 endonuclease V (T4N5)

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42
Q

which XP gene also associated with trichothiodystrophy

A

mutations in the XPB and XPD genes

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43
Q

XP variant, which has normal NER, is due to mutations in which gene

A

DNA polymerase-η

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44
Q

Phototesting action spectrum for inflammatory erythema in XP patients

A

290 to 340 nm

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45
Q

XP variant patients usually have neurologic problems

A

no

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46
Q

which XP group in which deafness, seizures most common

A

groups A and D

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47
Q

solar lentigines, skin cancers, pigmentary retinal degeneration, basal ganglion calcification

A

XP–Cockayne syndrome complex have also been reported (with mutations in XPB, XPD or XPG),

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48
Q

how does pathogenesis of cockayne differ from XP?

A

defective transcription-coupled NER (TC-NER)

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49
Q

cockayne syndrome - carcinogenesis T/F

A

F

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50
Q

CS-A due to mutations in

A

ERCC8 (also known as CSA)

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51
Q

CS-B due to mutations in

A

ERCC6 (also known as CSB);

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52
Q

which CS subset longest lifespan?

A

CS type I: 80% of patients; onset at 2 years of age, progressive; life expectancy: second to third decades

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53
Q

which CS subroup late onset, normal growth and development

A

CS type III:

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54
Q

PIBIDS due to ?

A

Mutations in XPD, XPB, general transcription factor IIH polypeptide 5

55
Q

trichothiodystrophy in PIBIDS due to reduction of

A

cysteine-rich matrix proteins and low sulfur content in hair shafts

56
Q

which photosensitive syndromes do not predispose to increased cutaneous malignancies

A

PIBIDS, cockayne

57
Q

Bloom syndrome increased which types malignancies?

A

Increased frequency of leukemia, lymphoma, GI adenocarcinoma

58
Q

quadriradial configurations of chromosomes in lymphocytes and fibroblasts are a diagnostic feature of

A

Bloom syndrome

59
Q

what mutation causes tenfold increased rate of spontaneous sister chromatid exchanges, chromosomal breakage and rearrangements

A

Bloom syndrome

60
Q

Up to one-third of patients develop osteosarcoma in which photosensitive dermatoses

A

rothmund thompson

61
Q

what protein product unwinds DNA and stabilizes the genome.

A

DNA helicase

62
Q

RECQL4 gene mutations causes

A

Rothmund–Thomson syndrome

63
Q

Phototest results in patients taking isotretinoin or etretinate, or applying topical tretinoin,

A

normal

64
Q

road workers occasionally develop phototoxicity secondary to

A

exposure to tar and concomitant UVA from sunlight

65
Q

phototoxic agent in St John’s wort

A

hypericin,

66
Q

which drug causes phototoxic reactions as well as an increased risk for developing large hypertrophic actinic keratoses, aggressive cutaneous squamous cell carcinomas and perhaps cutaneous melanoma

A

voriconazole

67
Q

which 3 drugs responsible for photosensitivity reactions; NOT associated with UVR-induced activation of the drug.

A

5-Fluorouracil (5-FU), methotrexate and retinoids

68
Q

Smith–Lemli–Opitz syndrome features

A

early onset of photosensitivity to UVA

69
Q

Mutations in DHCR7, which encodes 7-dehydrocholesterol reductase, result in an accumulation of 7-dehydrocholesterol.

A

Smith–Lemli–Opitz syndrome

70
Q

which drugs cause slate-gray hyperpigmentation

A

amiodarone, tricyclic antidepressants and diltiazem

71
Q

which drugs cause photo-onycholysis

A

tetracyclines and psoralens

72
Q

which drugs cause lichenoid eruptions

A

quinine and quinidine

73
Q

porphyrins and demeclocycline mechanism of phototoxicity

A

generation of inflammatory mediators

74
Q

chlorpromazine and tetracyclines mechanism of phototoxicity

A

generation of stable photoproducts

75
Q

psoralens mechanism of phototoxicity

A

formation of photoadducts

76
Q

Which interleukin released by UV causes phototoxicity

A

IL6

77
Q

Which interleukin released by UV causes imune suppressio

A

IL1

78
Q

Therapeutic UvB suppresses whih cytokines

A

Il12, IFNy IL8

79
Q

What subset of T cells downregulated in psoriasis by UVB

A

Th17

80
Q

NBUVB wavelength

A

311-313 nm

81
Q

RE: NBUVB

What is first therapeutic dose?

A

70% MED

82
Q

RE: NBUVB

No erythema, increase by ?

A

40%

83
Q

RE: NBUVB
Minimal erythema
Increae by?

A

20%

84
Q

RE: NBUVB

Persisitent asymptomatic erythema

A

No increase

85
Q

RE: NBUVB

Painful erythema/edema/blister

A

No treatment until synptoms resolve

86
Q

RE: NBUVB

Restarting again after ADR

A

Reduce last dose by 50%, subsequent increae by 10%

87
Q

Location of MED testing

A

Normally non sunexposed butocks, lower back, abdomen

88
Q

Excimer laser wavelength

A

308 nm

89
Q

MOA of PUVA in localised scleroderma

A

Increased collagenase expression

90
Q

What wavelength is used in PUVA ?

A

UVA1, 340- 400 nm

91
Q

More water soluble , increased absorption psolaren is ?

A

8 MOP , c.f 5 MOP

92
Q

UVA dose vs UVB dose measurement

A

J/cm2 vs mJ/cm2

93
Q

Peak of UVA lamp wavelengthn

A

352 nm

94
Q

8MOP doses

A

0.6-0.8mg/kg

95
Q

Dose of UVA for type 3 phototype ?

A

1.5 j/cm2

Rule- start at 0.5 j/cm2, increase by 0.5 for every increase in phototype

96
Q

When is psolaren administered before UVA exposure

A

1-3 hours before

97
Q

Minimal perceptible dose definition

A

Minimal dose of UVA following psolaren ingestion that produces barely perceptble but well defined eyrthema.

98
Q

Which psolaren has a higher MPD?

A

5 MOP, as less water soluble

99
Q

contraindication to oral PUVA

A

Hepatitis, renal impairment

100
Q

Timing of irradiation after bath PUVA application

A

Immediate

101
Q

4th MPD dose is ? Of 1st MPD

A

50 %

102
Q

Systemic photosensitiser e.g.

A

Verteporfin

103
Q

In PDT,

O2 delivery via

A

Erythrocyte circulation

104
Q

In PDT, ALA converted to ? In mitochondria

A

Protoporphyrin IX

105
Q

In PDT, what type photochemical reaction ?

A

Type 2 , convert molecular o2 to singlet o2

106
Q

In PUVA , type photochemical reactions

A

Type 1, generate covalent adducts between psolaren and DNA

107
Q

Blue light wavelength? used with ?

A

ALA , 410-420nm

108
Q

Red light wavelengtg, used with ?

A

M-ALA(Red light). 630 nm

109
Q

Type of light in PDT for treatment of AK

A

Blue, red

110
Q

Type of light in PDT for treatment of NMSC

A

Red light

111
Q

Contraindication to PDT

A

Porphyria , photosensitivity disorderm pregnancy, photosensitiser hypersensitivity

112
Q

Treatment schedule for PDT for NMSC

A

2 x PDT 1 week apart, repeat in 3 months if residua

113
Q

standard residential and commercial windows

block transmission of

A

UVB light.

114
Q

New laminated glass, tinted glass, and films

could offer protection from UVA light up to

A

380 nm

115
Q

natural fern leaf extract with antiinflammatory and antioxidant (AO) properties leading to significant reduction in sensitivity to UVR in high-risk patients with malignant melanoma or atypical mole syndrome

A

Polypodium leucotomos

116
Q

a-MSH analogues reduce UV-induced DNA damage via

A

enhanced repair of DNA photoproducts, such as

removal of cyclobutane pyrimidine dimers

117
Q

Afamelanotide MOA

A

nduces epidermal
melanin formation by binding to melanocortin-1 receptors
on melanocytes, leading to increased melanocyte
proliferation and tyrosinase activity

118
Q

which NSAID may prevent SCC
and BCC in individuals with extensive photodamage
who are at high risk for developing
NMSCs

A

celecoxib

119
Q

types of skin cancer is most

closely related to cumulative sun exposure?

A

Squamous cell carcinoma

120
Q

What procedure is this? performed by exposing the skin either to multiples of MEDs or to suberythemo-genic UVdoses for 3 to4 days followed by evaluation 1 to 2 days later for the development of characteristicPMLE lesions.

A

Photoprovocation

121
Q

Solar urticaria represents a type ? hypersen-sitivity response

A

Solar urticaria represents a type I hypersen-sitivity response

122
Q

Actinic prurigo has a strong association with which human leukocyte antigen

A

DRB1*0407

123
Q

earliest clinical signs of neurologic involvement in XP are

A

diminished or absent deep tendon reflexes and high frequency hearing loss.

124
Q

The Circulating form of vitamin D used to determine vitamin D status and for screening for vitamin deficiency

A

25-hydroxyvitamin D, or 25(OH)D

125
Q

Which type of Vitamin D is obtained onlyby diet

A

Vitamin D2 (ergocalciferol)

126
Q

in typical use conditions, what has been shown to appreciably lower vitamin D levels

A

sun-screen use has not been shown to appreciably lower vitamin D levels unless in controlled use
Frequent shade use and long sleeve use ismore likely to cause lower vitamin D levelsthan sunscreen use

127
Q

uvb causes increased expression of ? Thatcauses cell cycle arrest

A

P53

128
Q

Vitamin D deficiency is defined as serum25(OH)D levels below

A

20 ng/mL.

129
Q
  1. What is the upper limit of vitamin D3 intake recom-mended by the Institute of Medicine?
A

4000 IU

130
Q

How much vitamin D should you recommend taking?

A

600 IU

131
Q

signs can be found in severe cases of HV.

A

. Fever, liver damage, and lymphadenopathy—Correct. All of these signs can be found in severe cases of HV.

132
Q

Patients with erythropoietic protoporphyria may develop

A

Patients with erythropoietic protoporphyria may develop cholestasis. This results from the rapid accumulation of protoporphyrin in the hepatobiliary system, which can result in liver damage and potentially failure.

133
Q

First-line therapy PCT .

A

d. Phlebotomy

134
Q

PCTpatient has higher frequency

A

hemochromatosis than the general population, should be screened for the HFEgene mutation

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