? Medications ? Can target the skin by either topical/ intralesional/
systemic routes
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? Intralesional administration ? Additional option for very localized
lesions e.g. IL steroids in keloids, AA etc.
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? Topical application ? Often a very effective therapeutic modality(frequently successful alone) for dermatological disease
? Will be ineffective if physical properties of drug leads to problem with
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passive diffusion from the skin surface
? Systemic medications ? Distributed via the cutaneous vasculature
? Have the potential to exert pharmacological actions on all elements
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of the skin ? therapeutic efficacy? Not only the skin but also most of the other organs are exposed to
the drug
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? Therefore, systemic therapies may have potential for significant
adverse effects
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? Sometimes life-threatening? One of the basic principles of medical ethics
? L. `primum non nocere', i.e. `first, do no harm'
? Before considering systemic options ? The clinician always to consider
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possibility of unwanted consequences of any therapeutic intervention
? Clinician ? To use systemic medications safely
? Also ? Appreciate the patient's perspective
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? Assess the detrimental impact of a skin disorder on the patient'squality of life (QoL; DQLI)
? Assess the risk?benefit balance of a particular medication
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? Best ? A shared & informed decision between patient &dermatologist
Standards of care
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? No perfect medical management plan in all cases
? The competent clinician ? Follow peerdetermined & approved
standards of care, e.g. in evidencebased/ National guidelines etc.
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?The Indian Association of Dermatologists, Venereologists & Leprologists (IADVL)
?The British Association of Dermatologists (BAD)
?The American Academy of Dermatology (AAD)
?The National Institute for Health and Care Excellence (NICE)
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?The European Academy of Dermadology & Venereology (EADV)?For STIs: CDC guidelines etc.
Drug-drug interactions
? Clinicians ? To exclude potential interactions with the patient's
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existing medication
? To provide the patient with a list of drugs that may interact with the
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new drug? To ensure the patient makes the prescribers of any future medication
aware of the medicines they are already taking
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Immunomodulatory/ Immunosuppresive
drugs
? Many (but not all) of the systemic agents ? Immunomodulatory or
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(potent) immunosuppressive
? Require Pretreatment screening & subsequent monitoring
? Prior to initiation ? Patients to be carefully counselled about the risk/
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benefit aspects
? Written information Preferable
? Particular regard ? To infection, systemic & cutaneous malignancy,
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bone marrow suppression & conceptionrelated issues
? Women ? Adequate contraceptive guidance if applicable
? Cervical cytology screening history if applicable
? A h/o malignancy in any organ Seek appropriate specialist advice
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? The entire skin ? Examine to exclude the presence of dysplastic/neoplastic lesions
? Minimize the risk of reactivation of infections ? Screen for latent
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bloodborne viruses (e.g. hepatitis B and C & HIV), latent tuberculosis
? Review vaccinations
? Periodic followup visits ? Regular investigations with regard to
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particular as per guidelines
? Occasional GPE ? With a view to excluding lymphoma & cutaneous
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neoplasiaAntihistamines
? H1 antihistamines Mainstay of treatment for
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?Chronic urticaria & angiooedema?Physical urticarias,
?Urticarial vasculitis,
?Cutaneous mastocytosis,
?Insect bite reactions,
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?Anaphylaxis & allergic reactions to drugs? Effectiveness in atopic eczema ? Sedating H 1antihistamines - a role in
the management of nocturnal pruritus
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? The combination of H1 & H2 antihistamines ? The treatment ofurticaria
Formula and structure
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? H1 antihistamines ? 6 Structural classes:
?Alkylamines
?Ethanolamines
?Ethylenediamines
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?Phenothiazines?Piperidines
?Piperazines
? 1st generation of antihistamines ? Representatives in each structural
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group? Majority of 2nd generation antihistamines ? Piperidines or piperazines
? Doxepin ? Tricyclic antidepressant with antihistamine activity
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Pharmacodynamics? Traditionally, antihistamines ? Considered reversible competitive
inhibitors of histamine
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? However, histamine receptors have an intrinsic level of activity
? H1 and H2 antihistamines are now best regarded as inverse agonists,
? Not just simply block the interaction of histamine with its receptors
? Also induce an opposite pharmacological response by decreasing the
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constitutive activity of the receptors
Dose & regimens
? If recommended dose of individual antihistamines ? Not clinically
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effective May prescribe higher doses i.e. updosing (limited
evidence for the efficacy & safety)
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? Combination of two or more antihistamines ? Can be more effectivethan monotherapy
? The combination of H1 & H2 antihistamines
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Pregnancy
? Limited guidelines for use of H1 antihistamines in pregnancy
? Most ? Classified as Food & Drug Administration (FDA) pregnancy
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category B or C
? Earlier reports ? Link H1 antihistamines to fetal malformations (e.g.
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particularly cleft palate)? Usually avoided in the first trimester of pregnancy
? Newer studies ? (including a meta-analysis of 200,000 first-trimester
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exposures to first-generation antihistamines) ? No increased risk ofcongenital malformations
Breastfeeding
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? No formal studies ? During breastfeeding? Theoretically ? May diminish milk supply via anticholinergic effects
? Many e.g. diphenhydramine, promethazine, cetirizine, loratadine,
? fexofenadine, levocetirizine etc. - Excreted in breastmilk
? However, effects on the nursing infants ? Not studied
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Tricyclic antidepressants
? TCAs ? Bind to both H1 & H2 receptors
? TCA MC used in dermatology ? doxepin ? about 800 times more potent
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than diphenhydramine
? Uses:
?Refractory CSU
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?Physical urticarias?Pruritus associated with systemic conditions
? Sedation is the most common adverse effect - some patients may develop
tolerance with regular use
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? Oral doxepin - FDA as a pregnancy category C
? Use with caution in elderly - May be more susceptible to its anticholinergic
effects, including urinary retention & blurred vision
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Antifungal drugs? The systemic antifungal drugs ? Broadly classified by MoA
vAct on the fungal wall or cell membrane
vAct intracellularly
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? The fungal wall/cell membrane agents Subdivided
?Inhibit ergosterol (integral part of fungal cell membrane) function
?Inhibit glucan synthase
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? The ergosterol inhibitors? Azoles (inhibit lanosterol 14 demethylase, essential for the synthesis of
ergosterol)
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?Imidazoles (5membered aromatic ring with 2 nitrogen & 3 carbon atoms)e.g. ketoconazole
?Triazoles (5membered aromatic ring with 3 nitrogen & 2 carbon atoms)
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e.g. fluconazole, itraconazole, posaconazole, voriconazole
? Allylamines (inhibit squalene epoxidase, essential in ergosterol synthesis)
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e.g. terbinafine? Polyenes (bind to ergosterol & interfere with fungal cell membrane) e.g.
nystatin & amphotericin B
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? glucan synthase inhibitors Interfere with the synthesis of glucan(component of the fungal cell wall) e.g. echinocandin antifungals
caspofungin, micafungin
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? Intracellular MoA
? Flucytosine A pyrimidine analogue, inhibits fungal DNA & RNA
synthesis
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? Griseofulvin ? A spirobenzo[b]furan inhibits fungal mitosis by
binding to tubulin thus disrupting microtubule function
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Thank you