photo Flashcards
1
Q
UVA2
A
320-340nm
2
Q
UVL spectrum
A
10-400 nm
3
Q
photoallergy spectrum
A
320-425nm
4
Q
UVC spectrum
A
200-290 nm
5
Q
UVB thermal isomerisation7 dehydrocholesterol–>
A
previtamin D3
6
Q
Vitamin D synthesis UV spectrum
A
220-320 nm
7
Q
what photodermatologic disorder in which you should stop naproxen
A
PCT
8
Q
medication which causes Lichenoid photodistributed
A
fenofibrate
9
Q
tetracyclines, nalidixic acid, amiodarone, furosemide, ketoprofen cause
A
Pseudoporphyria – signs of PCT with normal porphyrins;
10
Q
cutaneous immunosuppression wavelength
A
290-320 nm/311 nm
11
Q
headache nausea syncope
A
SU
12
Q
EPP-aw
A
SU
13
Q
VL, UVA, UVB, 15 min add test
A
SU
14
Q
quinolone tetracycline psolaren quinine
A
photoonycholysis
15
Q
thick plaques CTCL NBUVB or PUVA?
A
NBUVB > PUVA
16
Q
woods lamp
A
365nm
17
Q
chlorpromazine TCA
A
blue gray
18
Q
candida thyroid dysfunction abn
A
AIRE
19
Q
AP persist winter
A
most T.
20
Q
-quinidine sulphonyurea griseofulvin
A
photosensitvity
21
Q
254nm vapour
A
me
22
Q
350-360 nm
A
pUVA
23
Q
CTCL mastocytosis GVHD generalised Ga
A
pUVA
24
Q
chelitis conjunctivitis,
A
hediataryy PMLE
25
VL hi-E
blue violet
26
furocoumarin
phototoxic
27
Photoexacerbated hailey hailey,
T
28
antimalarials, thiazides, demethylchlortetracycline, fenofibrate, enalapril, quinine, quinidine
Lichenoid eruption – LP-like lesions (may be confluent) on sun-exposed areas;
29
reduc MED A/B
CAD
30
incandescent safer
CAD
31
PMLE patients have a reduced tendency to develop skin cancers because
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
32
PMLE never have systemic symptoms
General malaise, headache, fever, nausea and other symptoms rarely occur.
33
a form of PMLE referred to as juvenile spring eruption affects
helices of the ears
34
In darkly pigmented individuals, the most common morphology of PMLE is
grouped, pinhead-sized papules in sun-exposed areas
35
treatment modalities PMLE
hardening NB-UVB, PUVA,prednisone azathioprine or cyclosporine.
36
efficacy of antimalarials for PMLE
inconsistent in controlled trials
37
Cellular photoreceptors that mediate the signaling that leads to UV-induced immune responses are:
- 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
38
actinic prurigo strong HLA association
HLA-DR4 (DRB1*0401) and subtype DRB1*0407
39
pathogenesis HV
chronic EBV infection
40
which photodermatoses: Most commonly, visible light, with extension into UVA, UVB sensitivity less common
solar urticaria
41
what topical vehicle has been successful in decreasing the development of actinic keratoses and BCCs?
bacterial DNA repair enzyme T4 endonuclease V (T4N5)
42
which XP gene also associated with trichothiodystrophy
mutations in the XPB and XPD genes
43
XP variant, which has normal NER, is due to mutations in which gene
DNA polymerase-η
44
Phototesting action spectrum for inflammatory erythema in XP patients
290 to 340 nm
45
XP variant patients usually have neurologic problems
no
46
which XP group in which deafness, seizures most common
groups A and D
47
solar lentigines, skin cancers, pigmentary retinal degeneration, basal ganglion calcification
XP–Cockayne syndrome complex have also been reported (with mutations in XPB, XPD or XPG),
48
how does pathogenesis of cockayne differ from XP?
defective transcription-coupled NER (TC-NER)
49
cockayne syndrome - carcinogenesis T/F
F
50
CS-A due to mutations in
ERCC8 (also known as CSA)
51
CS-B due to mutations in
ERCC6 (also known as CSB);
52
which CS subset longest lifespan?
CS type I: 80% of patients; onset at 2 years of age, progressive; life expectancy: second to third decades
53
which CS subroup late onset, normal growth and development
CS type III:
54
PIBIDS due to ?
Mutations in XPD, XPB, general transcription factor IIH polypeptide 5
55
trichothiodystrophy in PIBIDS due to reduction of
cysteine-rich matrix proteins and low sulfur content in hair shafts
56
which photosensitive syndromes do not predispose to increased cutaneous malignancies
PIBIDS, cockayne
57
Bloom syndrome increased which types malignancies?
Increased frequency of leukemia, lymphoma, GI adenocarcinoma
58
quadriradial configurations of chromosomes in lymphocytes and fibroblasts are a diagnostic feature of
Bloom syndrome
59
what mutation causes tenfold increased rate of spontaneous sister chromatid exchanges, chromosomal breakage and rearrangements
Bloom syndrome
60
Up to one-third of patients develop osteosarcoma in which photosensitive dermatoses
rothmund thompson
61
what protein product unwinds DNA and stabilizes the genome.
DNA helicase
62
RECQL4 gene mutations causes
Rothmund–Thomson syndrome
63
Phototest results in patients taking isotretinoin or etretinate, or applying topical tretinoin,
normal
64
road workers occasionally develop phototoxicity secondary to
exposure to tar and concomitant UVA from sunlight
65
phototoxic agent in St John’s wort
hypericin,
66
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
voriconazole
67
which 3 drugs responsible for photosensitivity reactions; NOT associated with UVR-induced activation of the drug.
5-Fluorouracil (5-FU), methotrexate and retinoids
68
Smith–Lemli–Opitz syndrome features
early onset of photosensitivity to UVA
69
Mutations in DHCR7, which encodes 7-dehydrocholesterol reductase, result in an accumulation of 7-dehydrocholesterol.
Smith–Lemli–Opitz syndrome
70
which drugs cause slate-gray hyperpigmentation
amiodarone, tricyclic antidepressants and diltiazem
71
which drugs cause photo-onycholysis
tetracyclines and psoralens
72
which drugs cause lichenoid eruptions
quinine and quinidine
73
porphyrins and demeclocycline mechanism of phototoxicity
generation of inflammatory mediators
74
chlorpromazine and tetracyclines mechanism of phototoxicity
generation of stable photoproducts
75
psoralens mechanism of phototoxicity
formation of photoadducts
76
Which interleukin released by UV causes phototoxicity
IL6
77
Which interleukin released by UV causes imune suppressio
IL1
78
Therapeutic UvB suppresses whih cytokines
Il12, IFNy IL8
79
What subset of T cells downregulated in psoriasis by UVB
Th17
80
NBUVB wavelength
311-313 nm
81
RE: NBUVB
| What is first therapeutic dose?
70% MED
82
RE: NBUVB
| No erythema, increase by ?
40%
83
RE: NBUVB
Minimal erythema
Increae by?
20%
84
RE: NBUVB
| Persisitent asymptomatic erythema
No increase
85
RE: NBUVB
| Painful erythema/edema/blister
No treatment until synptoms resolve
86
RE: NBUVB
| Restarting again after ADR
Reduce last dose by 50%, subsequent increae by 10%
87
Location of MED testing
Normally non sunexposed butocks, lower back, abdomen
88
Excimer laser wavelength
308 nm
89
MOA of PUVA in localised scleroderma
Increased collagenase expression
90
What wavelength is used in PUVA ?
UVA1, 340- 400 nm
91
More water soluble , increased absorption psolaren is ?
8 MOP , c.f 5 MOP
92
UVA dose vs UVB dose measurement
J/cm2 vs mJ/cm2
93
Peak of UVA lamp wavelengthn
352 nm
94
8MOP doses
0.6-0.8mg/kg
95
Dose of UVA for type 3 phototype ?
1.5 j/cm2
| Rule- start at 0.5 j/cm2, increase by 0.5 for every increase in phototype
96
When is psolaren administered before UVA exposure
1-3 hours before
97
Minimal perceptible dose definition
Minimal dose of UVA following psolaren ingestion that produces barely perceptble but well defined eyrthema.
98
Which psolaren has a higher MPD?
5 MOP, as less water soluble
99
contraindication to oral PUVA
Hepatitis, renal impairment
100
Timing of irradiation after bath PUVA application
Immediate
101
4th MPD dose is ? Of 1st MPD
50 %
102
Systemic photosensitiser e.g.
Verteporfin
103
In PDT,
| O2 delivery via
Erythrocyte circulation
104
In PDT, ALA converted to ? In mitochondria
Protoporphyrin IX
105
In PDT, what type photochemical reaction ?
Type 2 , convert molecular o2 to singlet o2
106
In PUVA , type photochemical reactions
Type 1, generate covalent adducts between psolaren and DNA
107
Blue light wavelength? used with ?
ALA , 410-420nm
108
Red light wavelengtg, used with ?
M-ALA(Red light). 630 nm
109
Type of light in PDT for treatment of AK
Blue, red
110
Type of light in PDT for treatment of NMSC
Red light
111
Contraindication to PDT
Porphyria , photosensitivity disorderm pregnancy, photosensitiser hypersensitivity
112
Treatment schedule for PDT for NMSC
2 x PDT 1 week apart, repeat in 3 months if residua
113
standard residential and commercial windows
| block transmission of
UVB light.
114
New laminated glass, tinted glass, and films
| could offer protection from UVA light up to
380 nm
115
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
Polypodium leucotomos
116
a-MSH analogues reduce UV-induced DNA damage via
enhanced repair of DNA photoproducts, such as
| removal of cyclobutane pyrimidine dimers
117
Afamelanotide MOA
nduces epidermal
melanin formation by binding to melanocortin-1 receptors
on melanocytes, leading to increased melanocyte
proliferation and tyrosinase activity
118
which NSAID may prevent SCC
and BCC in individuals with extensive photodamage
who are at high risk for developing
NMSCs
celecoxib
119
types of skin cancer is most
| closely related to cumulative sun exposure?
Squamous cell carcinoma
120
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.
Photoprovocation
121
Solar urticaria represents a type ? hypersen-sitivity response
Solar urticaria represents a type I hypersen-sitivity response
122
Actinic prurigo has a strong association with which human leukocyte antigen
DRB1*0407
123
earliest clinical signs of neurologic involvement in XP are
diminished or absent deep tendon reflexes and high frequency hearing loss.
124
The Circulating form of vitamin D used to determine vitamin D status and for screening for vitamin deficiency
25-hydroxyvitamin D, or 25(OH)D
125
Which type of Vitamin D is obtained onlyby diet
Vitamin D2 (ergocalciferol)
126
in typical use conditions, what has been shown to appreciably lower vitamin D levels
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
uvb causes increased expression of ? Thatcauses cell cycle arrest
P53
128
Vitamin D deficiency is defined as serum25(OH)D levels below
20 ng/mL.
129
3. What is the upper limit of vitamin D3 intake recom-mended by the Institute of Medicine?
4000 IU
130
How much vitamin D should you recommend taking?
600 IU
131
signs can be found in severe cases of HV.
. Fever, liver damage, and lymphadenopathy—Correct. All of these signs can be found in severe cases of HV.
132
Patients with erythropoietic protoporphyria may develop
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
First-line therapy PCT .
d. Phlebotomy
134
PCTpatient has higher frequency
hemochromatosis than the general population, should be screened for the HFEgene mutation
