Derm Pharm Cards Part 2 Flashcards

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1
Q

Aldesleukin MAO and use and major AE

A

Bind to cell surface IL-2 receptor
Induces proliferation and differentiation of B/T cells, monocytes, macrophages and CTLs

Clinical use: melanoma

Renal failure insufficiency caused by capillary leak syndrome

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2
Q

Carmustin MAO and use

A

Alkylation and carbamoylation of amino acids

Clinical use: melanoma

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3
Q

Cisplatin MAO, AE, use?

A

Forms DNA intrastrand crosslinks and adducts

severe nephrotoxicity, myelosuppression, and N/V. Significant ototoxicity (tinnitus and occasionally deafness) reported in children

basal cell carcinoma and squamous cell carcinoma

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4
Q

Cyclophosphamide MAO, AE, use?

A

Pro-drug of active alkylating moiety

Renal compromise, hemorrhagic cystitis (MESNA is protective), N/V, rashes. Amenorrhea / infertility. Monitor for 2° malignancies. Pulmonary fibrosis.

basal cell carcinoma

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5
Q

Dacarbazine MAO, use?

A

Pro-drug of active alkylating moiety

Clinical use: melanoma

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6
Q

Imiquimod MAO, use?

A

Small molecule tumor-directed immune response initiator:

  • Direct activation of TLR7 and/or TLR8  activation of NFB  upregulation of proinflammatory cytokines
  • Adenosine receptor blockade  blocks AC  cAMP
  • Bcl-2/Bax shift & caspase activation  apoptosis (at high concentrations)

Clinical use: basal cell carcinoma, actinic keratosis and HPV

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7
Q

Interferon- 2b MAO, use?

A

Binding to receptor causes signaling through JAK/STAT/IRF-9 and results in increased transcription of >300 genes that inhibit cancer growth, collectively called ISGs

Clinical use: melanoma
Cautiously used in autoimmune diseases, cardiac disease and depression (associated with increased risk of suicidal ideation)

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8
Q
What do the following have in common? 
Carmustine
cisplatin 
cyclophosphamide 
dactinomycin 
doxorubicin
lomustine 
methotrexate
A

increase risk of secondary malignancy

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9
Q

Sorafenib MAO, use?

A

Multi-kinase inhibitor:
VEGF, PDGFR, KIT and RAF kinase

Inhibits tumor cell proliferation by targeting the RAF/MEK/ERK pathway at the level of RAF kinase

Exerts an anti-angiogenic effect by targeting the receptor tyrosine kinases VEGFR-2 and PDGFR and their associated signaling
Clinical use: melanoma

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10
Q

Trametinib MAO, use?

A

Reversible MEK inhibitor for patients with BRAF V6ooE or V600K mutations
Melanoma

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11
Q

Trichloroacetic acid MAO, use?

A

Rapidly penetrates and cauterizes skin, keratin and other tissues
“Chemical peel”
Clinical use: actinic keratosis

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12
Q

Vismodegib MAO, use?

A

Oral SMO inhibitor
Lipophilic agent with extensive metabolism

Clinical use: basal cell carcinoma
AE-intrauterine fetal death, male mediated teratogenicity

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13
Q

Vemurafenib

A

Inhibitor of mutated BRAF, including mutated BRAFV600E
(CONFIRMED by genotyping)
Resistance can occur via alternative pathway activation
Hepatic metabolism, PGP & CYP interactions possible, elevated serum creatinine, elevated liver enzymes, QT prolongation/TP, increased photosensitivity, cutaneous SCC in 1/4th patients and severe dermatologic reactions (SJS) possible

Serious ophthalmologic issues: uveitis, iritis, retinal vein occlusion
Clinical use: melanoma

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14
Q

3 best cytotoxic agents for melanoma

A

Dacarbazine
Lomustine
Carmustine

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15
Q

3 immunotherapies for melanoma

A

Aldesleikin (IL-2R agonist)
INF-alpha
Ipilimumab

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16
Q

Ipilimumab

A

Recombinant antibody that binds to cytotoxic T-lymphocyte-associated antigen 4 (CTLA-4) receptor on Tcells and activates them

Bolsters antitumor response of the immune system
Dermatitis including toxic epidermal necrolysis caused by Tcell activation and proliferation
BBW:
Adrenal insufficiency, diarrhea, Guillain-Barre syndrome, hepatitis, hyperthyroidism, hypopituitarism, hypothyroidism, myasthenia gravis, peripheral neuropathy, pregnancy, serious rash
Pregnancy category C

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17
Q

3 signal transduction inhibitors for melanoma

A

Sorafinib
Vemurafenib
Trametinib

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18
Q

UVA1

A

340-400nm

increases photo-aging, cancer risk

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19
Q

UVA2

A

320-340nm

increases photo-aging cancer risk

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20
Q

UVB

A

290-320 nm

burns

21
Q

Only ovicidal therapy available for head lice

A

Malathion

22
Q

Malathion MAO

A

Organophosphate insecticide that louse metabolize to malaoxon  inhibits acetyl-cholinesterase  neuronal hyperstimulation and paralysis

23
Q

If accidental consumption of Malathion? AE and Antidote?

A

SLUDGEBBB
Salivation, Lacrimation, Urination, Defecation, GI, Emesis, Bronchospasm, Bronchorrhea, Bradycardia
Give: Pralidoxime or Atropine

24
Q

Term: kills lice vs. kills eggs

A

Padicuicidal vs. ovicidal

25
Q

Head lice tx 2 methods

A

chemical: paralyze & dehydrate
physical: suffocate

26
Q

Permethrin MAO & rare AE, resistance

A

Synthetic pyrethrin that binds to voltage-gated Na+ channels and causes hyperexcitability and paralysis

Asthma exacerbation in patients allergic to ragweed

Efficacy has waned due to knock-down resistance mutations of louse Na+ channels

27
Q

Lindane AE

A

Headlice tx in pts who have failed first line
(works by blocking GABA - a CNS stimulant)

disfavored because of neurotoxicity & persistence in environment

BBW: skin disease, premies, seizure

28
Q

Compare Trametinib and Vemurafenib for Melanoma

A

Both: genotyping necessary, Melanoma tx, CV effects, eye effects

29
Q

Ivemectin

A

Headlice tx
Binds selectively and with high affinity to glutamate-gated Cl- ion channels present in invertebrate nerve and muscle cells and causes hyperexcitability and paralysis

30
Q

2 chemotherapies - photosensitivity

A

Ipilimumab and Vemurafenib

31
Q

Eflornithine

A

Decreases ornithine decarboxylase  decrease cell division and differentiation of the hair follicle  reduce unwanted facial hair

32
Q

Finasteride

A

Testosterone analog that blocks 5-reductase activity  decreases scalp and serum [DHT], AE-possible to have decreased sex drive even after discontinuing drug

33
Q

Minoxidil

A

May activate the hair follicle directly or stimulated follicular microcirculation
May alter local androgen metabolism
Topical agent for hair growth in male-patterned baldness
Drug treatment must continued for effects to be maintained

34
Q

Methoxsalen

A

Oral and topical pigmenting agent used in the treatment of vitiligo, symptomatic reliefof psoriasis, treatment of cutaneous Tcell lymphoma, alopecia areata, inflammatory dermatoses, eczema and lichen planus

Activated by UV-A radiation  conjugation and cross-linkning of DNA  cell death

Delayed erythema followed over several weeks by increased epidermal melanization and thickening of the stratum corneum

35
Q

Dactinomycin MAO, use?

A

DNA intercalator

Clinical use: melanoma

36
Q

Diclofenac MAO, use?

A

Inhibitor of inflammatory mediator, including PGE2

actinic keratosis

37
Q

Docetaxel MAO, use?

A

Microtubule stabilizer; inhibits depolymerization

Clinical use: melanoma

38
Q

Doxorubicin MAO, use?

A

Intercalator, free radical generator, topo II inhibitor

Clinical use: basal cell carcinoma

39
Q

Fluorouracil MAO, use?

A

Thymidylate synthase (TS) inhibitor; interferes with RNA & RNA synthesis/function

Clinical use: basal cell carcinoma and actinic keratosis

40
Q

Vinblastine use

A

Clinical use: basal cell carcinoma and melanoma

41
Q

Cinoxate

A

Organic UVB filter (290-320nm)

42
Q

Para-aminobenzoic Acid

A

Organic UVB filter (290-320nm)

43
Q

Trolamine

A

Organic UVB filter (290-320nm)

44
Q

Dioxybenzone

A
Organic UVB filter (290-320nm) AND 
UVA2 filter (320-340)
45
Q

Oxybenzone

A
Organic UVB filter (290-320nm) AND 
UVA2 filter (320-340)
46
Q

Avobenzone

A

Only FDA-approved organic sunscreen that protects against UV-A1 radiation
(340-400nm)

47
Q

Titanium dioxide and zinc oxide

A

UVA and UVB protection
Physically reflect and scatters light
Thick consistency & tendency to clump

48
Q

Tri-Luma=use?
Hydroquinone?
Fluocinolone?
Tretinoin?

A

Temporary relief of facial skin darkening by hormonal changes, pregnancy, OCs or HRT

Hydroquinone? inhibits melanin formation by blocking melanocyte enzymatic oxidation of tyrosine to DOPA

Fluocinolone? : anti-inflammatory corticosteroid
Tretinoin?modulates skin growth and pigmentation. Also increased keratinocyte shedding from the retinoid-treated

epidermis, which results in decreased epidermal melanin content