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Questions Q35.1 What are the four main categories of psychodermatologic disorders? (Pg. 383, Fig. 35.1 ) Q35.2 What are the four major underlying psychopathologic conditions upon which the medication choice is decided (what is the ‘fifth’ nonpsychiatric category of interest)? (Pg. 384, Fig. 35.2 ) Q35.3 What is the basis of the tremendous dosing variation between patients receiving doxepin for depression or for pruritus (and how…

Questions Q34.1 What is the difference between an ‘antiandrogen’ and ‘androgen inhibitor’? (Pg. 367) Q34.2 For which skin disorders are antiandrogens and androgen inhibitors clinically useful from a mechanistic standpoint? (Pgs. 367, 368) Q34.3 What are the key differences in type I versus type II isoenzymes of 5-α reductase, and how do these differences relate to the response to antiandrogen therapies? (Pgs. 368, 376, 378) Q34.4…

Questions Q33.1 What are several of the important nitric oxide releasers involving cutaneous vasculature? (Pg. 359, Table 33.1 ) Q33.2 Which drugs discussed in this chapter have demonstrated efficacy in patients with Raynaud phenomenon? (Pgs. 359, 364×3, 365, Box 33.1 ) Q33.3 Which calcium channel blockers are most appropriate for use in patients with cyclosporine-induced hypertension? (Pg. 361) Q33.4 What are several of the common mucocutaneous adverse…

Questions Q32.1 How do first- and second-generation antihistamines differ regarding lipophilic properties and anticholinergic effects, and what are the resultant clinical differences? (Pgs. 350, 352) Q32.2 What are the advantages of second-generation over first-generation H 1 antihistamines? (Pgs. 350, 352) Q32.3 Concerning chronic urticaria patients, (1) in what percentage are autoantibodies produced, and (2) what two types of autoantibodies are typical of this subgroup? (Pg. 350)…

Questions Q31.1 For which category of patient with atopic dermatitis is dupilumab US Food and Drug Administration (FDA)-approved? (Pg. 339) Q31.2 What are several non-dermatologic conditions for which dupilumab is being considered? (Pg. 340) Q31.3 The exact method of dupilumab clearance is unknown; however, it is thought to mimic endogenous clearance via what mechanism? (Pg. 340) Q31.4 What is the mechanism of action of dupilumab that…

Questions Q30.1 Rituximab is US Food and Drug Administration (FDA) approved for what dermatologic conditions? What are several categories of dermatoses for which off-label use of rituximab has at least some literature support? (Pg. 331×2) Q30.2 How do the half-lives of endogenous IgG 1 and rituximab compare, and what are some factors that may alter the rituximab half-life? (Pg. 331×2) Q30.3 Concerning B-cell depletion with rituximab,…

Questions Q29.1 What are the two subunits that make up interleukin (IL)-23? (Pg. 321) Q29.2 What subunit of IL-23 do IL-23 inhibitors target? (Pg. 321) Q29.3 What interleukin inhibitors are directed against IL-23? (Pg. 321) Q29.4 How does the efficacy of IL-23 inhibition alone compare with IL-12/23 inhibition? (Pg. 321) Q29.5 What conclusions were drawn from the phase III guselkumab trials with regard to efficacy? (Pg.…

Questions Q28.1 What is the rationale strongly supporting the role of interleukin (IL)-17 in the pathogenesis of psoriasis? (Pg. 312) Q28.2 What is the rationale strongly supporting the role of IL-17 in the pathogenesis of psoriatic arthritis? (Pg. 313) Q28.3 What interleukin inhibitors are directed against IL-17? (Pg. 313) Q28.4 Which IL-17 inhibitors are approved for psoriatic arthritis? (Pgs. 313, 316) Q28.5 What is one unique…

Questions Q27.1 Which IL 12/23 inhibitor is currently approved for the treatment of psoriasis and which biologics are in development? (Pg. 303) Q27.2 What cytokines are inhibited by ustekinumab? (Pg. 303) Q27.3 Which recently discovered immunopathogenic model for psoriasis has markedly influenced both research and drug development for psoriasis? (Pg. 303) Q27.4 What conclusions were drawn from the phase III ustekinumab trials with regard to efficacy?…

Questions Q26.1 What is the rationale strongly supporting the role of TNF-α in the pathogenesis of psoriasis? (Pg. 288) Q26.2 How does TNF-α relate to the Th17 and Th22 pathways? ( Fig. 26.1 ) (Pg. 288) Q26.3 Of the four TNF-α inhibitors discussed in this chapter, which are the most immunogenic? (Pgs. 290, 292, 293×3, 294, 295, 296) Q26.4 How do the maximum PASI-75 rates compare…

Questions Q25.1 Which anatomic structure is the limiting factor for aminolevulinic acid (ALA) and methyl aminolevulinate (MAL) percutaneous absorption, and what are several measures, which can improve absorption for these products? (Pg. 280) Q25.2 Concerning biochemistry of ALA/MAL, what (1) is the endpoint of this metabolism, (2) is the photosensitizing porphyrin that accumulates, and (3) what are the differences between ALA and MAL metabolism? (Pg. 281)…

Questions Q24.1 What are the advantages of extracorporeal photopheresis (ECP) systems in which the psoralen is released directly into the treatment mix (vs oral administration)? (Pg. 272) Q24.2 What are the potential cardiovascular and thromboembolic risks of ECP? (Pg. 272) Q24.3 What are the proposed mechanisms by which ECP may benefit patients with cutaneous T-cell lymphoma (CTCL)? (Pg. 273) Q24.4 What are proposed mechanisms by which…

Questions Q23.1 What is the pharmacologic importance of food intake and the hepatic ‘first-pass effect’ on methoxsalen bioavailability? (Pg. 264) Q23.2 In which part of the ultraviolet A (UVA) spectrum does methoxsalen have its maximum absorption? (Pg. 264) Q23.3 What is the risk of squamous cell carcinoma (SCC) from long-term psoralen plus UVA (PUVA) therapy and are these more biologically aggressive than actinically-induced SCC? (Pg. 266)…

Questions Q22.1 What are the various endogenous forms of vitamin A, and what is the physiologic role of each form? (Pg. 247×2) Q22.2 How much time is needed for complete serum elimination of (1) isotretinoin, (2) acitretin, and (3) bexarotene; what is the role of acitretin re-esterification to etretinate in this issue? (Pgs. 248×2, 254) Q22.3 What are the primary retinoid nuclear receptors, and how do…

Questions Q21.1 What are the proposed mechanisms by which antimalarials work in various dermatoses discussed in this chapter? (Pg. 236) Q21.2 In general, concerning responses of lupus erythematosus to antimalarials, (1) which cutaneous subsets respond well, (2) which cutaneous subsets respond less well, and (3) which systemic features/organ systems respond well? (Pg. 237) Q21.3 How strong is the evidence that cigarette smoking impairs the efficacy of…

Questions Q20.1 What is the role of hydroxylamine metabolites in dapsone toxicities, and how does cimetidine alter these effects? (Pg. 224) Q20.2 What is the overall function of the myeloperoxidase system in neutrophils? (Pg. 225) Q20.3 Concerning the myeloperoxidase system, (1) what are several additional cells that use this enzyme, and (2) which dapsone-responsive dermatoses involve these cell types? (Pg. 226) Q20.4 What is a typical…

Questions Q19.1 Concerning cytotoxic drug use in dermatology, what are (1) five to six of the disease categories for which these drugs are used, and (2) the three most important adverse effect categories? (Pg. 209) Q19.2 What are (1) the two major categories of cytotoxic agents, (2) major drug examples of each category, and (3) the mechanism for each category concerning the cell cycle? (Pgs. 210,…

Questions Q18.1 What are the most important differences between small molecule drugs (such as apremilast and tofacitinib) and biologics? (Pg. 200) Q18.2 What is the role of phosphodiesterase 4 in inflammatory diseases? (Pg. 200 ) Q18.3 What drugs inhibit phosphodiesterase 4 and for what diseases are these drugs being used for? (Pgs. 200, 201, 202) Q18.4 What can be expected of apremilast in terms of efficacy…

Questions Q17.1 What are the differences between the Sandimmune and Neoral versions of cyclosporine (CsA) in their (1) formulation, (2) bioavailability, and (3) consistency of absorption? (Pgs. 187, 188, 195) Q17.2 Regarding the mechanism of action for CsA, what is (1) the enzyme inhibited, (2) the transcription factor inhibited, and (3) the resultant cytokine alterations? (Pg. 188 , Table 17.3 , Fig 17.2 ) Q17.3 What…

Questions Q16.1 How do MMF and mycophenolic acid (MPA) relate pharmacologically: (1) prodrug/active drug, or (2) active drug/active metabolite? (Pg. 178) Q16.2 What metabolic process is vital in maintaining MPA and mycophenolic acid glucuronide (MPAG) levels? (Pg. 179) Q16.3 Why are mycophenolate therapeutic benefits and adverse effects commonly localized to the skin and gastrointestinal tract? (Pg. 179) Q16.4 What clinical circumstances may cause an increase in…