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Alikhan & Hocker dermatology > 2 Dermatopharmacology > Flashcards

2 Dermatopharmacology Flashcards

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1
Q

Histamine levels are elevated in the skin of pts with?

A

Chronic urticaria

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2
Q

Itching is largely mediated by which type of histamine receptors?

A

H1 receptors

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3
Q

MoA of H1, H2 antihistamines

A

inverse agonists

(downregulate constitutively activated state of receptor)

or

antagonists at histamine receptors

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4
Q

Location of H1 receptors

A

Periphery of the body

Adrenal medulla

Vascular endothelium

Heart

CNS

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5
Q

H1 receptor functions (5)

A

Ileum contraction

Modulate circadian cycle

Itching

Systemic vasodilation

Bronchoconstriction

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6
Q

Name some H1 receptor antagonists

A

Diphenhydramine

Loratadine

Cetirizine

Fexofenadine

Clemastine

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7
Q

H1 receptor definition

A

Histamine receptors that couple to Cq/11 stimulating phospholipase C

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8
Q

H2 receptor definition

A

Histamine receptors that interact with Gs to activate adenylyl cyclase

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9
Q

Location of H2 receptors

A

CNS

Parietal cells of the stomach

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10
Q

H2 receptor functions

A

Speed up sinus rhythm

Stimulation of gastric acid secretion

Smooth muscle relaxation

Inhibit antibody synthesis

T-cell proliferation, cytokine production

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11
Q

Name some H2 antagonists

A

Ranitidine

Cimetidine

Famotidine

Nizatidine

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12
Q

H1 antihistamines are primarily used in dermatology in?

A

Urticaria

and some cases of eczema

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13
Q

H1 antagonists can be used as monotherapy in urticaria and eczema

T/F?

A

False

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14
Q

H2 antihistamines can be added for chronic urticaria, but evidence is poor

T/F?

A

True

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15
Q

Name 2 H1 antagonists that are safe to use in pregnancy and lactation

A

Diphenhydramine

Chlorpheniramine

(both of them have long safety record)

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16
Q

Antihistamines are primarily used for?

A

Urticaria

Angioedema

(not great option for atopic dermatitis)

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17
Q

Which type of antihistamines is preferred for nocturnal pruritus?

A

first-generation H1 antihistamines

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18
Q

Adverse effects of

first-generation H1 antihistamines

A

sedation

impaired cognitive function

(from lipophilicity; cross blood-brain barrier)

anticholinergic effects

(dry mouth, constipation,dysuria and blurred vision)

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19
Q

Examples of first-generation H1 antihistamines

A

Diphenhydramine

Cyproheptadine

Promethazine

Chlorpheniramine

Hydroxyzine

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20
Q

In which pregnancy drug category belong diphenhydramine and chlorpheniramine?

A

Pregnancy category B

“Adverse effects on animal studies only

Adequate human studies lacking or not shown similar results. Can be used in pregnancy”

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21
Q

Specific side effect of cyproheptadine?

A

interferes with hypothalamic function →

may ↑appetite and retard growth in children

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22
Q

Difference btw 2nd and 1st gen antihistamines

A

2nd gen:

  • Less sedating (↓ability to cross blood-brain barrier)
  • lack anticholinergic effects
  • Appear to be relatively equivalent for dermatologic indications (e.g., chronic urticaria)
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23
Q

Examples of 2nd gen antihistamines

A

Fexofenadine

Loratadine

Cetirizine

Desloratadine

Levocetirizine

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24
Q

Characteristics of Fexofenadine

A
  • active metabolite of the prodrug terfenadine (which was withdrawn because of Q-T elongation and torsades de pointes)
  • not metabolized by the liver and excreted unchanged
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25
Q

Name 2 second gen antihistamines that can be used in pregnancy

A

Loratadine

Cetirizine

↓dose in patients with hepatic or renal impairment

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26
Q

Name the active metabolites of:

  1. Loratadine
  2. Cetirizine
A
  1. Desloratadine: 5× more potent than loratadine in suppressing histamine wheal
  2. Levocetirizine: active metabolite and R-enantiomer of cetirizine
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27
Q

TCA with H1 and H2 antihistamine activity

A

Doxepin

available both orally and topically

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28
Q

Indications of doxepin?

A

effective in urticaria and depressed patients with neurotic excoriations

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29
Q

SE of topical 5% doxepin cream

A

can cause allergic contact dermatitis and drowsiness

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30
Q

Benefits of doxepin vs rest of antihistamines

A
  • Much higher affinity for histamine receptors than
    most antihistamines
  • Therapeutic effect longer lasting than
    diphenhydramine and hydroxyzine because of long
    half-life (thus QHS dosing)
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31
Q

SE of doxepin?

A
  • Sedation (MC SE)
  • anticholinergic SEs
  • orthostatic hypotension
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32
Q

Warnings of doxepin?

A
  • Do not give with other antidepressants, or with severe
    heart disease (risk of heart block)
  • Can ↓seizure threshold
  • Can induce manic episodes in patients with manic-
    depressive disorder
  • Black box warning for suicidality
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33
Q

Definition of retinoids

A

Vitamin A and related natural and synthetic compounds

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34
Q

Name the 3 interconvertible forms of retinoids

A
  • retinol (alcohol)
  • retinal (aldehyde)
  • retinoic acid (acid)
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35
Q

Other characteristics of retinoids?

A
  • Acquired through diet (dairy, fish, meat, eggs, leafy greens, and orange/yellow vegetables)
  • Carotenoids (beta-carotene) are precursors of vitamin A
  • Stored in the liver as retinol
  • Retinol is transported in plasma by binding to a complex of retinol binding protein and transthyretin
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36
Q

MoA of retinoids

A
  • Binds cytosolic retinoid binding protein → transported to the nucleus → binds intracellular nuclear receptors
  • Binds to two families of nuclear receptors: retinoic acid receptors (RARs) and retinoid X receptors (RXRs)

Each receptor family contains 3 isotypes (α, β,
and γ)

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37
Q

Name the major intercellular retinoid nuclear receptors in keratinocytes

A

RXR-α

and

RAR-γ (most abundant in skin)

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38
Q

What is the impact of photoaging in retinoid receptors?

A

↓RXR-α and RAR-γ

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39
Q

MoA of topical retinoids

A

↑stratum corneum thickness,

epidermal hyperplasia,

correction of atypia,

dispersion of melanin granules,

↑dermal collagen I,

↑papillary dermal elastic fibers,

↑hyaluronic acid,

↓matrix metalloproteinases,

↓angiogenesis

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40
Q

What is the impact of retinoids binding to RAR/RXR?

A
  • Inhibits AP1 and NF-IL-6, which are important in proliferation and inflammatory responses
  • Inhibits TLR2, which is important in inflammation
  • ↓tumorigenesis and induces apoptosis
  • Antikeratinization (downregulates K6 and K16)
  • Inhibits ornithine decarboxylase
  • ↑TH1 cytokines and ↓TH2 cytokines (helpful in CTCL)
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41
Q

What is the earliest and most common SE of retinoids?

A

Cheilitis

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42
Q

Name a few mucocutaneous SEs of retinoids

A

Thirst

dry nasal mucosa

epistaxis

xerosis
xerophthalmia

palmoplantar peeling

photosensitivity

exacerbation of eczema

nail fragility

sticky sensation (palms and soles)

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43
Q

What type of alopecia can be triggered by retinoids?

A

telogen effluvium

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44
Q

What is the result of dryness of the nasal mucosa in pts on retinoid treatment?

A

Staphylococcus aureus colonization of the nasal mucosa (75%–90%)

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45
Q

Pt with nodulocystic acne, treated with topical tazarotene, presents with a dome-shaped well demarcated erythematous lesion on the left cheek.

Dx?

A

Pyogenic granuloma-like lesions

(commonly seen in pts on either oral or topical retinoid tx)

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46
Q

Name some systemic SEs of retinoids?

A

Myalgias

arthralgias

anorexia

nausea

diarrhea

abdominal pain

IBD (controversial)

headache

fatigue

reduced night vision

questionable depression/suicidal ideation

hepatitis

pancreatitis secondary to hypertriglyceridemia

calcification of tendons and ligaments

premature epiphyseal closure

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47
Q

MC lab abnormality of pts on retinoids?

Highest risk with?

A

Hyperlipidemia/hypertriglyceridemia

bexarotene

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48
Q

When should you discontinue tx with retinoids and why?

A
  • fasting TGs >800 mg/dL ( ^pancreatitis risk)
  • LFTs greater than 3× the upper limit of normal
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49
Q

Pt on retinoid therapy presents with ^LFTs after 4 weeks of tx.

BNS?

A

Continue tx with the same dose

^ LFTs are usually transient within 2 to 8 weeks of starting treatment, return to normal after another 2 to 4 weeks of treatment

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50
Q

^LFTs are more frequent with?

A

acitretin

(lower risk with isotretinoin or bexarotene)

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51
Q

Current recommendations are to start low-dose
levothyroxine in all patients on retinoids

T/F?

A

True

80% of pts on bexarotene present with reversible central hypothyroidism (Decreased TSH and T4)

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52
Q

Hematologic SEs of bexarotene?

A

Leukopenia (neutropenia) and agranulocytosis

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53
Q

Pt on isotretinoin tx gives birth to a normal appearing baby

How would you interpret this phenomenon?

A

50%–60% of isotretinoin-exposed pregnancies result in “healthy-appearing” births (lack obvious retinoid embryopathy)

↓mental function becomes apparent in
majority of these children over time: 30% have gross mental retardation and 60% have mild-moderate mental deficits

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54
Q

MC adverse results in pregnant patients exposed to isotretinoin?

A
  • Spontaneous abortion (20%)
  • Retinoid embryopathy (18%–28%): craniofacial,
    cardiac, CNS, and thymic abnormalities are most
    common
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55
Q

Features of retinoid embryopathy

A
  • Craniofacial: microtia, cleft palate, mircophthalmia, hypertelorism, dysmorphic facies, and ear abnormalities
  • CNS: microcephaly, hydrocephalus, CN7 palsy, and cortical and cerebellar defects
  • CV: cardiac septal defects, tetralogy of Fallot, transposition of great vessels, and aortic arch hypoplasia
  • Thymic: thymic aplasia/ectopia
  • No risk of retinoid embryopathy reported in male
    partners taking retinoids; however, iPledge requires male registration because pregnancies have been reported where women have “borrowed” their male partner’s medication
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56
Q

Absolute CIs to retinoid therapy

A

pregnancy

women contemplating pregnancy

noncompliance with contraception

breastfeeding

hypersensitivity to parabens

(some capsules may contain parabens)

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57
Q

Relative CIs to retinoid tx

A

leukopenia

moderate/severe hypercholesterolemia or hypertriglyceridemia

significant hepatic or renal dysfunction

hypothyroidism (bexarotene)

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58
Q

Combination of Isotretinoin + tetracyclines can lead to?

A

Pseudotumor cerebri

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59
Q

Combination of alcohol + acitretin can lead to?

A

conversion of acitretin to etretinate

hepatotoxicity

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60
Q

Oral retinoids are lipophilic → fatty meals ↑bioavailability

T/F?

A

True

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61
Q

Combination of Bexarotene + gemfibrozil can lead to?

A

severe hypertriglyceridemia

bexarotene is metabolized by cytochrome P450 3A4; avoid with gemfibrozil as it inhibits 3A4 → ↑plasma levels of bexarotene

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62
Q

Tx of ^LDL in pts on retinoids can be implemented with any statin, except?

A

simvastatin

(interacts with CYP450 3A4)

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63
Q

Treatment of ↑TG in pts on retinoids?

A

fenofibrate and/or omega 3

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64
Q

Drugs to avoid while on retinoid tx?

A
  • Vitamin A supplements ( risk of hypervitaminosis A)
  • MTX (increased liver toxicity)
  • Tetracyclines (^ risk of pseudotumor cerebri)
  • Gemfibrozil (severe hypertriglyceridemia)
  • Simvastatin ( << <<)
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65
Q

Name some topical retinoids

A

Tretinoin (all-trans retinoid acid)

Alitretinoin (9-cis-RA)

Adapalene

Tazarotene

Bexarotene

Retinol

Retinaldehyde

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66
Q

Topical retinoids of pregnancy category X

A

Tazarotene

Bexarotene

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67
Q

Topical retinoid used in the Rx of Kaposi sarcoma?

A

Alitretinoin (9-cis-RA)

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68
Q

Features of topical tretinoin

A

1st gen (non aromatic)

1-2% of dose systemic absorption

Binds to all RAR nuclear receptors

Improvement in 8-12w

Apply at night (inactivated by UV)

Oxidized by benzoyl peroxide

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69
Q

Features of topical Alitretinoin (9-cis-RA)

A

1st gen

Not measurable systemic absorption

Binds to ALL forms of retinoid nuclear receptors(NRs)

(RAR & RXR)

ALLitretinoin binds to ALL forms of NRs

Improvement in 4-8weeks

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70
Q

Features of adapalene

A

3gen polyaromatic

Binds to RAR-β/γ >α

LIGHT STABLE

Used for acne (hyperpigmentation, photoaging)

Improvement in 2-3mo

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71
Q

Features of tazarotene

A

3gen

Binds to RAR-β/γ>α

<5% of dose systemic absorption

Used for acne, plaque psoriasis

(hyperpigmentation,photoaging,disorders of keratinization, AKs)

category X

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72
Q

Features of topical bexarotene

A

3gen

Binds to all RXR nrs

(beXarotene binds to RXR)

Used for cutaneous T-cell lymphoma, hand dermatitis, psoriasis, alopecia areata, lymphomatoid papulosis(LyP)

Category X

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73
Q

Features of topical retinol & retinaldehyde

A

Precursor of RA

Used for photoaging, hyperpigmentation and as cosmeceutical product

Improvement in 2-3 mo

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74
Q

Table of topical retinoids

A
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75
Q

Name the most common systemic retinoids

A
  • Tretinoin
  • Isotretinoin
  • Etretinate
  • Acitretin
  • Bexarotene

All of them pregnancy category X

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76
Q

Name the 1st generation systemic retinoids

and their IUPAC name

A

Tretinoin (ATRA or all-trans- RA)

Isotretinoin (13-cis- RA)

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77
Q

Features of tretinoin

A
  • 1st gen systemic retinoid(nonaromatic)
  • 1hr half-life
  • Binds to al RAR
  • Treats APML
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78
Q

Features of isotretinoin

A
  • 1st gen systemic retinoid
  • 20hr half-life
  • Hepatic metabolism ( to tretinoin)
  • Excretion via bile,urine
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79
Q

Uses and dose treatment of isotretinoin

A
  • Severe acne & other follicular disorders
  • Usual daily dose: 0,5-2mg/kg/d
  • Goal cumulative dose: 120-150mg/kg for severe acne
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80
Q

SIs of isotretinoin in acne tx

A
  • May flare in the first few weeks
  • Lag period of 1-3 months before effect
  • Continued healing after discontinuation
  • 1/3 require 2nd course
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81
Q

Systemic SIs of isotretinoin

A
  • Hyperostosis (long-term use)
  • Pyogenic granulomas
  • Excessive granulation response
  • Telogen effluvium
  • ^ Staph.aureus infections
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82
Q

Which type of drugs should not be administered while on isotretinoin tx?

A

Tetracyclines

^risk of pseudotumor cerebri

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83
Q

Special feature of isotretinoin

A

Only retinoid to affect sebum production
so P. acnes unable to thrive

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84
Q

Features of etretinate

A
  • 2nd gen (monoaromatic)
  • 120 days half-life
  • Hepatic metabolism (to acitretin)
  • Excreted via bile,urine
  • 50 times more lipophilic than acitretin (persists very long)
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85
Q

Features of acitretin(Neotigason)

A
  • 2nd gen
  • 2 days half-life
  • Hepatic metabolism (reesterification to etretinate by alcohol)
  • Excreted via bile,urine
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86
Q

What is a strong recommendation for pts on acitretin?

A

Must avoid concurrent alcohol use

because alcohol converts acitretin->etretinate

–> significantly prolonged effects

87
Q

Uses of acitretin

A

Psoriasis (pustular, erythrodermic, severe & recalcitrant plaque)

88
Q

What is RePUVA or ReUVB therapy?

A

acitretin is given 10–14 days prior to starting PUVA which

  1. accelerates the response
  2. ​decreases the carcinogenic risk of PUVA

Usual dose: 25–50 mg/day

89
Q

Features of bexarotene(Targretin)

A
  • The only 3rd gen (poly-aromatic)
  • 7-9hr half-life
  • Hepatic metabolism
  • Excreted via hepatobiliary sysem
  • Binds to al RXR
90
Q

Uses of bexarotene

A
  • CTCL resistant to at least one systemic therapy
  • Usual starting dose: 75mg/day up to 300mg/day
  • Response to tx takes up to 6 months
91
Q

SIs of bexarotene?

A

Central hypothyroidism

↑↑TGs (severe)

Leukopenia

92
Q

Special recommendations for pts on bexarotene

A

Avoid gemfibrozil (worsens hyper-TG)

“beXarotene - RXR”

93
Q

Contraceptive therapy for female pts on systemic retinoid tx

A
  • Isotretinoin,bexarotene:
  1. 2 negative pregnancy tests prior to initiating
  2. contraception for 1 month before, during, and 1 month after cessation of therapy)
  • Same as above PLUS 3 year contraceptive therapy after cessation of tx
94
Q

Other diseases where systemic retinoids may be used?

A
  • Disorders of keratinization:
  1. ichthyosis
  2. pityriasis rubra pilaris
  3. keratoderma
  4. Darier’s
  • chemoprophylaxis of premalignant and malignant skin cancers:
  1. nevoid basal cell carcinoma syndrome
  2. xeroderma pigmentosum
  3. transplant patients).
95
Q

Basic pharmacological structure of corticosteroids(CS)

A

3 hexane rings and 1 pentane ring

modifications to this structure result in various CS (e.g.addition of 1,2 double bond to hydrocortisone → prednisone)

96
Q

Exogenous corticosteroids are absorbed in?

A

Upper jejunum

(more than 50% of prednisone is absorbed)

97
Q

CS in dermatology achieve their desired effects via?

A

Glucocorticoid activity

mineralocorticoid effects are never desirable (sodium and water retention, HTN) for dermatologic purposes

98
Q

Short-acting (hydrocortisone and cortisone)

A

↓glucocorticoid, ↑mineralocorticoid activity

99
Q

Intermediate-acting (prednisone, prednisolone, methylprednisolone, and triamcinolone)

A

↑glucocorticoid and ↓mineralocorticoid activity

100
Q

Long-acting (dexamethasone and betamethasone)

A

↑↑glucocorticoid, no mineralocorticoid activity

101
Q

Cortisol-binding globulin (CBG) is main carrier protein

steroid that is bound to CBG is inactive and unbound steroid (free fraction) is active

T or F?

A

True

102
Q

Conditions that ↑ Cortisol-binding globulin (CBG)

A

↑CBG:

  • estrogen therapy
  • pregnancy →
  • hyperthyroidism

↓CS free fraction

103
Q

Conditions that ↓ Cortisol-binding globulin (CBG)

A

↓CBG:

  • hypothyroidism
  • liver disease →
  • renal disease
  • obesity

↑CS free fraction

104
Q

Intracellular transport of CS

A

Glucocorticoid receptor (GCR) binds to CS in the cytoplasm

→ translocates to nucleus

→ binds nuclear DNA to act as transcription factor

→ altered gene regulation/transcription

105
Q

Name the hepatic enzyme that converts CS from their inactive to active forms, as wells as some pairs of them

PS: Liver disease can impair conversion → preferable to
give active forms of steroids in this setting
(eg, prednisolone instead of prednisone)

A

11β-hydroxysteroid dehydrogenase

  • Cortisone (inactive form) → cortisol
    (aka hydrocortisone, active form)
  • Prednisone (inactive form) → prednisolone (active
    form)
106
Q

MoA of CS?

A

Via immunosuppressive and antiinflammatory effects, primarily via cytokine alterations (e.g., ↓proinflammatory cytokines and ↑antiinflammatory cytokines

Major effects on cellular immunity (> humoral immunity) and cell trafficking

107
Q

Use of CS cause reduction in?

A
  • NFκB, AP-1,
  • phospholipase A2,
  • eicosanoids (e.g., leukotrienes, prostaglandins, 12-HETE, and 15-HETE),
  • COX-2,
  • activity of all types of WBCs,
  • fibroblast activity
  • prostaglandin production
108
Q

Use of CS cause increase in?

A
  • IL-10 (major downregulator of cell- mediated immunity)
  • antiinflammatory proteins (e.g., vasocortin, lipocortins, and vasoregulin)
  • ↑apoptosis of lymphocytes and eosinophils
109
Q

Distinction btw physiologic & pharmacological CS therapy

A

Physiologic CS therapy = 5 to 7.5 mg/day of prednisone

pharmacologic is anything higher

110
Q

Pharmacology Key Concepts – Systemic Corticosteroids

A
111
Q

Main adverse effects of systemic CS

A

HPA axis suppression

Hypertriglyceridemia

Lipodystrophy

Osteoporosis

Bowel perforation, PUD

Cataracts, glaucoma

Psychosis, hypomania

Pseudotumor cerebri, seizures

112
Q

Features of CS-induced myopathy

A

Proximal lower extremity weakness

NORMAL LAB VALUES(MG & CK)!!!

113
Q

Risk of HPA axis suppression with topical CS does it exist?

A

nearly nonexistent

except in setting of whole-body clobetasol application for autoimmune blistering diseases

114
Q

Layman’s Explanation of Exogenous Adrenal Insufficiency

A

If you keep giving a person systemic steroids with glucocorticoid (cortisol-like) effects, their adrenal glands become “lazy” and stop making endogenous cortisol → over time, the adrenals become shrunken/atrophic, and can no longer produce adequate cortisol; immediately upon cessation of systemic steroid administration → “exogenous adrenal insufficiency” as a result of insufficient cortisol → may appear to be steroid withdrawal syndrome (most common), or very rarely, adrenal (Addisonian*) crisis.

115
Q

Features of HPA axis suppression from CS

A
  • Hypothalamus: first to be suppressed, but quickest to recover
  • Adrenals: last to be suppressed, but slowest to recover
116
Q

True Addisonian crisis w/ severe hypotension and coma is extremely uncommon in pts on CS therapy

True / False?

A

True

RAAS is NOT suppressed by exogenous CS used in dermatology

Mineralocorticoid axis is preserved

117
Q

When is HPA axis suppression typically seen?

A

Pts taking pharmacologic CS doses for ≥3 to 4 weeks

118
Q

Risk Factors of HPA axis suppression

A
  • Abrupt cessation of CS (always taper if CS course is
    >4 weeks)
  • Major stressor (surgery, trauma, or illness)
  • Divided dosing (BID or TID)
  • Daily dose given at any time other than the morning
119
Q

Benefits of QOD (alternate) dosing in CS therapy?

A

↓risk of: HPA axis suppression, growth suppression,
HTN, opportunistic infections, and electrolyte
disturbances

120
Q

QOD dosing in CS therapy reduces the risk of cataracts and osteoporosis

True/ False?

A

False

121
Q

Exogenous adrenal insufficiency can present under 2 clinical forms

A
  • Steroid withdrawal syndrome (SWS)
  • Adrenal (Addisonian) crisis
122
Q

Steroid withdrawal syndrome is ass/w arthralgias, muscle weakness, anorexia, fatigue and ↓cortisol levels

True/ False?

A

SWS presents with normal serum cortisol levels

but rather ↓available intracellular CS

123
Q

Features of Addisonian crisis

A

p/w symptoms of SWS + hypotension, ↓↓↓cortisol levels

124
Q

What SIs do CS with high mineralocorticoid activity cause?

A

HTN, CHF, weight gain, and hypokalemia

125
Q

Considerations on using systemic CS in pediatric population?

A

Growth impairment (as a result of ↓growth hormone and IGF-1 production)

Can be eased with QOD dosing (↓risk)

126
Q

Features of osteoporosis in CS tx

A
  • consider calcium + vitamin D +/- bisphosphonates, teriparatide, nasal calcitonin
  • greatest reduction in bone mass occurs in first 6 months
  • ↑fracture risk in postmenopausal women
  • greatest absolute loss of bone mass occurs in young men (they have highest baseline bone mass)
127
Q

Bone SE of CS tx

A
  • Osteoporosis
  • Osteonecrosis (usually at least 2 to 3 month courses; proximal femur most common)
  • Hypocalcemia
128
Q

Name some opportunistic infections with ^ occurrence in CS tx?

A
  • Tuberculosis reactivation
  • deep fungi
  • prolonged herpes virus infections
  • Pneumocystis jiroveci pneumonia
129
Q

Cutaneous SEs of CS tx

A
  • ↓wound healing
  • striae
  • atrophy
  • telangiectasias
  • steroid acne
  • purpura
  • infections (staphylococcal, herpes virus)
  • telogen effluvium
  • hirsutism
  • pustular psoriasis flare (upon drug withdrawal),
  • perioral dermatitis, contact dermatitis
  • hypopigmentation
130
Q

CIs to systemic CS use

A
  • Systemic fungal infections
  • herpes simplex keratitis
  • hypersensitivity reactions
131
Q

Can systemic CS be used during pregnancy?
If so name two cutaneous diseases

A

Category C, but likely safe for short courses if needed

severe PUPPP or gestational pemphigoid

PUPPP = Pruritic urticarial papules and plaques of pregnancy

132
Q

CS dose in pemphigus

A

start at 1 mg/kg daily in divided doses

^ up to 2 mg/kg daily (if needed) for 4 to 6 weeks,

consolidate dose to once a day & taper quickly to 40 mg daily, and slowly thereafter; a steroid-sparing agent should either be started at the get-go or
before tapering

133
Q

CS in toxicodentron dermatitis tx

A
  • DO not to stop oral CS too early because of the ↑likelihood of flare;
  • best option is a 3 week tapering course starting at about 1 mg/kg daily
134
Q

Effect of CS in herpes zoster tx

A

↓acute pain in herpes zoster, but likely do not prevent postherpetic neuralgia

135
Q

Why do we prefer single dose regimens in CS tx over divided ones?

A

Divided dose regimens are more effective, but have a
higher risk of SEs than single dose regimens (best taken in AM to simulate body’s diurnal variation of cortisol production)

136
Q

Benefits of QOD dosing in CS

A
  • the antiinflammatory effects of CS last longer than the HPA axis suppressive effects
  • QOD dosing helps maintain control of disease activity after course with daily CS
137
Q

Adverse effects of IM CS?

A
  • Cold abscesses (!!!)
  • subcutaneous fat atrophy
  • crystal deposition
  • menstrual irregularities
  • purpura
138
Q

Pulse IV CS dose & SE

A
  • Generally 0.5–1 g of methylprednisolone IV over ≥ 1 h × 5 consecutive days
  • Indications: systemic vasculitis, SLE, pyoderma gangrenosum, and bullous pemphigoid
  • Adverse effects: sudden cardiac death, atrial fibrillation, anaphylaxis, electrolyte shifts, seizures
139
Q

Monitoring tests while on systemic CS tx

A
  • Fasting glucose levels, BP (mild ↑ is ok), triglycerides
  • weight
  • height/weight for children
  • DEXA scans (T score < −2.5 = osteoporosis)
  • MRI if pain in hip/ shoulder/knee (osteonecrosis)
  • slit-lamp examination q6–12 months
  • TB screening and CXR
140
Q

Tests to evaluate adrenal insufficiency

A

■ AM cortisol: primary screening tool, >10 mcg/dL = good basal adrenal function

■ 24 hour urine free cortisol: more accurate test for
basal adrenal function (advantage); main disadvantage
is patient compliance with 24 hour urine collection

■ ACTH stimulation: most commonly used provocative
test for adrenal function; check basal cortisol level → then inject ACTH → check cortisol levels at 30 and 60 minutes

141
Q

Apremilast features

A

PDE-4 inhibitor

Used for psoriasis and PA

MC SEs: Diarrhea, nausea (resolve on
their own within 4 weeks usually)

LC SEs: Depression, weight loss

142
Q

Advantage of Apremilast

A

No laboratory monitoring required

(Dose halved in patients with severe renal impairment)

143
Q

Name 2 JAK inhibitors

A

Tofacitinib

Ruxolitinib

144
Q

Features of Tofacitinib

A

JAK 1 and 3 inhibitor
• FDA approved for moderate to severe RA who have failed MTX
• Topical and oral have been tested in psoriasis; reports of
oral used in alopecia areata
• MC SEs: URI, mild headaches, and nausea
• May have ↓Hb and mean neutrophil count, but
usually normalize on treatment
• May have ↑LDL, HDL, CK, TGs, and LFTs

• Tuberculosis reactivation not reported

145
Q

Features of Ruxolitinib

A
  • JAK 1 and 2 inhibitor
  • FDA approved for treatment of intermediate- or high-risk myelofibrosis
  • Topical version tested in psoriasis; reports of oral used in alopecia areata
  • Mainly local SEs
146
Q

Uses of azathioprine

A

Organ transplantation

Severe RA

Atopic dermatitis

Chronic actinic dermatitis

Oral LP

Behçet disease

Cicatricial/ bullous pemphigoid

Pemphigus

Dermatomyositis

147
Q

MoA of azathioprine

A

Inhibits purine metabolism and cell division

(particularly in fast-growing cells that do not have a salvage pathway, like lymphocytes)

148
Q

How is HGPRT enzyme implicated in the MoA of AZA?

A

Converts AZA to its active metabolite 6TG (thioguanine)

that shares similarities with endogenous purines so it gets incorporated in the DNA,RNA

&

inhibitis purine metabolism & cell division

149
Q

Immunological effects of AZA

A

Diminishes T-cell function and antibody production by B-cells

150
Q

Name two enzymes that convert AZA to inactive metabolites

A

Xanthine oxidase

&

thiopurine methyltransferase

151
Q

What kind of drugs should be avoided while on AZA tx?

A

Drugs that

  • ↓ activity of TPMT (measured by allele activity)
  • ↓ xanthine oxidase (allopurinol, febuxostat)

↑AZA levels

↑risk of life-threatening myelosuppression

152
Q

Other drugs that increase risk of myelosuppression if they are used in concomitance with AZA

A

ACEIs

Sulfadiazine

Folate antagonists (TMP-SMX, MTX)

153
Q

MC SEs of AZA

A

Nausea, diarrhea, vomiting

(present btw 1-10 days of tx)

Transaminase elevation

154
Q

Usage of AZA for dermatologically dosed indications increases risk of cSCC and non-Hodgkin BCL

True / False?

A

False

Squamous cell carcinoma (SCC) and lymphoma (particularly non-Hodgkin’s B-cell lymphoma)

can occur only in pts on high-dose AZA

155
Q

SEs of AZA

A

Leukopenia, thrombocytopenia, immunosuppression

Infection (scabies, HPV, HSV)

Teratogenicity

Hypersensitivity syndrome

Hepatotoxicity (rare)

156
Q

Monitoring tests for pts on AZA

A
  • Baseline pregnancy test & TB skin test
  • Annual complete physical examination with particular attention to possible lymphoma & SCC
  • CBC with differential & LFTs every 2 weeks for the first 2 months & every 2-3 months thereafter
157
Q

The killed HBV vaccine administered to patients on AZA & CS has shown a decreased response

True / False?

A

True

158
Q

Pts on AZA & anti-TNF-a are in increased risk of?

A

Hepatosplenic T-cell lymphoma

159
Q

Indications of cyclosporine

A

Psoriasis

Off-label uses: atopic dermatitis, chronic
idiopathic urticaria, pyoderma gangrenosum, LP, bullous dermatoses, autoimmune connective tissue diseases, neutrophilic dermatoses, PRP

160
Q

MoA of cyclosporine

A

Inhibits calcineurin

Forms complex with cyclophilin ==>

↓ activity of NFAT-1 (nuclear factor of activated T cells)

==> ↓IL-2 production

==> CD4 & CD8 cells

161
Q

Maximum dose of cyclosporine?

A

5mg/kg daily

Can be used continuously for up to 1 year maximum

For obese patients, ideal body weight should be used to
calculate starting dose

162
Q

Cyclosporine SEs

5H 2N mnemonic

A

Hyperplasia gingival

Hepatotoxicity

Hyperglycemia

HTN

Hypertrichosis

Nephrotoxicity

Neuropathy

163
Q

Other SEs of cyclosporine

A

Hyperuricemia (can precipitate gout)

Hypomagnesemia

Hyperkalemia

Hyperlipidemia

164
Q

List the 2 MC dose and duration-dependent cyclosporine’s SE

A

Nephrotoxicity

HTN

165
Q

How can you avoid irreversible kidney damage from cyclosporine?

A
  • Pts receive 2,5-5mg/kg daily
  • Dose-adjustment when Cr rises 30% from baseline
  • Treatment lasts < 1 year
166
Q

Management of cyclosporine-induced HTN

A
  • Thought to be due to renal vasoconstriction
  • NOT a CI to continuing therapy
  • Prescribe CCB (nifedipine, isradipine)

==>vasodilators that do not alter cyclosporine serum levels

167
Q

Psoriasis pts on cyclosporine for > 2 years are at ^risk of?

A

NMSC

168
Q

What percentage of pts is free of cyclosporine SE?

A

56%

169
Q

Management of cyclosporine dosage when Cr >30% baseline value

A
  • Recheck Cr level → if remains elevated >30% ==>
  • ↓dose by at least 1 mg/kg for 4 weeks, then ==>
  • If Cr level drops back down to <30% above
    baseline, can continue therapy
  • If it does not drop, then discontinue therapy; if it
    returns to within 10% of baseline, cyclosporine can be resumed at lower dose
170
Q

When should you discontinue cyclosporine tx?

A

When Cr levels >50% baseline

discontinue therapy until level returns to baseline

171
Q

Monitoring for pts on cyclosporine

A
  • Baseline, BUN, CBC, LFTs, fasting lipid profile,
    magnesium, potassium, and uric acid
  • Obtain two baseline BP at least 1 day apart
    and two baseline Cr values at least 1 day apart
  • Reevaluation of labs & BP every 2 weeks for the first 1-2 months, then every 4-6 weeks with BP checked at every visit
172
Q

Cyclosporine can be used successfully as monotherapy in which diseases?

A

Poststreptococcal pustulosis

Subcutaneous panniculitis-like T-cell lymphoma (SPTCL)

173
Q

MoA of MTX

A

DHF reductase inhibitor

Prevents conversion of DHF to THF

Inhibits purine synthesis

174
Q

Concomitant use of MTX & folic acid or leucovorin(folinic acid) results in?

A

↓MTX-induced adverse effects

↓GI adverse effects by 26% (nausea, vomiting, and
abdominal pain)

↓risk of LFT abnormalities by 76%

↓risk of pancytopenia

↑ability to tolerate MTX (↓MTX discontinuation rate
for any reason)

175
Q

When is testing for MTX-induced hepatic fibrosis recommended?

A

Pts on high cumulative doses ≥ 1.5–4 g

Particularly for pts with preexisting liver disease, alcohol abuse, hepatitis C, psoriasis, or those who did not receive folic acid supplementation

176
Q

Gold standard for testing of MTX-induced liver fibrosis?

A

Liver biopsy

177
Q

Indications of MTX

A
  • extensive, severe, debilitating, or recalcitrant psoriasis
  • Sezary syndrome

Off-label uses:

  • PLEVA, LyP, Pemphigus, Pemphigoid, Sarcoidosis, MF
  • Autoimmune connective tissue diseases, cutaneous vasculitis
178
Q

Absolute CIs to MTX

A

Pregnancy (category X)

Lactation

179
Q

Relative CIs to MTX

A
  • Unreliable patient
  • Compromised renal function
  • Hepatic disease
  • Metabolic disease (obesity or DM)
  • Severe hematologic abnormalities
  • Man or woman contemplating conception (3 months off drug for men, off one ovulatory cycle for women)
  • Immunodeficiency syndrome
  • Active infectious disease or Hx of severe infectious that could reactivate
180
Q

Pt on MTX comes to the office complaining about newly developed bumps in his hands over the last 2 months. Dx?

A

MTX-induced accelerated nodulosis

similar to rheumatoid nodules, but smaller and classically on fingers

Rx: Discontinuance of MTX

181
Q

DD btw MTX-induced accelerated nodulosis & RA

A
  • more rapid onset & growth
  • smaller size of nodules
  • different distribution of nodules

(MTX: hands,feet,ear vs periarticular region in RA)

182
Q

SE of MTX

A

Pulmonary fibrosis

Nausea,anorexia >>diarrhea, vomiting, ulcerative stomatitis

Alopecia

Dizziness

Myelosuppression

183
Q

Which drugs increase MTX risk of myelosuppression?

A
  • Agents that inhibit folic acid metabolism

(TMP, sulfonamides, dapsone)

  • Agents that displace plasma proteins

(tetracyclines, phenytoin, phenothiazines, sulfonamides, NSAIDs, salicylates)

184
Q

Monitoring for pts on MTX

A
  • CBC w/ differential, LFTs, Cr, BUN, viral hepatitis panel at baseline
  • repeat weekly for first month (excluding the viral hepatitis panel), and gradually decrease frequency every 2 weeks × 2 months, every month × 2 months, every 3 months thereafter)
185
Q

Preferable route of administration of MTX in the pediatric population?

A

Injectable form

Pediatric patients may have reduced oral absorption of
MTX when taken with various foods or have underlying diseases

186
Q

What is radiation recall dermatitis?

A

toxic cutaneous reactions reappear on previously irradiated skin

can be seen in pts on MTX

187
Q

Indications of mycophenolate mofetil

A
  • FDA approved for renal, cardiac, and liver allograft rejection prevention
  • Off-label dermatologic uses: psoriasis, atopic dermatitis, pemphigus, pemphigoid, autoimmune connective tissue diseases, vasculitis, lichen planus, and sarcoidosis
188
Q

MoA of Mycophenolate mofetil

A

Binds and inhibits inosine monophosphate dehydrogenase

(key enzyme for the de novo synthesis of purines – which is essential in activated lymphocytes)

189
Q

Absolute and relative CIs of mycophenolate mofetil

A
  • Absolute: Pregnancy, Drug allergy
  • Relative: Lactation, PUD, Hepatic or renal disease, concomitant use of cholestyramine, AZA
190
Q

SE of mycophenolate mofetil

A
  • Risk of carcinogenesis (lymphoma, lymphoproliferative disorders)
  • Diarrhea, abdominal pain, N & V
  • pseudo-Pelger-Huet anomaly (type of neutrophil dysplasia, predictor of neutropenia)
191
Q

Indications of hydroxyurea

A
  • CML, SCC of head & neck, sickle cell anemia, some forms of metastatic melanoma
  • Off-label for: recalcitrant psoriasis, Sweet’s syndrome, erythromelalgia, hypereosinophilic syndrome
192
Q

SE of hydroxyurea

A

Megaloblastic anemia

Dermatomyositis like eruption

Leg ulcers

Hyperpigmentation of skin & nails

Radiation recall

Alopecia

193
Q
A

Hydroxyurea induced leg ulcers and melanonychia

(ass/w prolonged use of hydroxyurea)

Resolve after drug discontinuation

194
Q

Cyclophosphamide MoA

A

Alkylating agent

directly damaging DNA via cross-linking

Nitrogen mustard derivative

195
Q

Indications of cyclophosphamide

A
  • Mycosis fungoides
  • Off-label: severe immunobullous
    disease (e.g., ocular cicatricial pemphigoid), severe systemic vasculitides, neutrophilic dermatoses, and autoimmune connective tissue diseases
196
Q

SE of cyclophosphamide

A
  • Hemorrhagic cystitis (as a result of acrolein)
  • ↑risk of transitional cell carcinoma of the bladder, non-Hodgkin’s lymphoma, leukemia, SCC
  • N & V ( most common)
  • ↑risk infertility: amenorrhea (27%–60%); premature ovarian failure (up to 80%)
197
Q

Cutaneous SE of cyclophosphamide

A
  • permanent pigmented band on the teeth
  • anagen effluvium
  • hyperpigmentation of skin and nails
198
Q

Indications of antimalarials (chloroquine & hydroxychloroquine)

A
  • SLE, malaria, and RA
  • Off-label: particularly useful in disorders with significant lymphocytic infiltrates (polymorphous light eruptions, lymphocytic infiltrate of Jessner, lupus panniculitis, and discoid LE)
199
Q

Absolute & relative CIs to antimalarials

A
  • Absolute: Hypersensitivity to drug, retinopathy, myasthenia gravis (CQ)
  • Relative: Pregnancy, lactation, severe blood dyscrasias, hepatic disfunction, retinal or neurological disorders
200
Q

Mucocutaneous SE of antimalarials

A
  • Yellow pigmentation of the skin (quinacrine)
  • Drug-induced LP
  • Morbilliform hypersensitivity eruption; may also
    present as erythroderma or SJS
  • Psoriasis exacerbation (CQ in particular)
  • Bluish-gray to black hyperpigmentation (typically affecting the shins)
  • Nail hyperpigmentation
201
Q

SE of antimalarials

A
  • Hemolysis in G6PD deficient population
  • GI SEs
  • Keratopathy, retinopathy, ciliary body dysfunction
202
Q

Current eye monitoring recommendations for antimalarials

A
  • Baseline examination including visual field testing
  • Dilated examination and visual acuity testing within first year of starting therapy
  • Dilated examination and visual acuity testing yearly after 5 years of treatment (some patients, such as the elderly, may require more frequent examinations)
203
Q

Is G6PD testing necessary before the commencement of antimalarial agent tx?

A

No, risk of hemolysis for HCQ, CQ, and quinacrine with therapeutic doses il low

Hemolysis risk is mainly a concern for 8-aminoquinoline and primaquine

204
Q

CQ and HCQ should be given together to maximize therapeutic effect

True / False?

A

False

CQ and HCQ should NOT be given simultaneously

Quinacrine may be added to HCQ or CQ for ↑therapeutic effect

205
Q

Use of HCQ in pts with cutaneous lupus…?

A

Delays the time to fulfill criteria for SLE

206
Q

Appropriate dose of antimalarials for porphyria cutanea tarda?

A

Low-dose HCQ or CQ may be used in porphyria cutanea tarda (i.e., 100–200 mg/day of HCQ vs 400 mg/day used for DLE)

207
Q

Indications of dapsone

A
  • dermatitis herpetiformis and leprosy

​

  • Off-label: neutrophilic dermatoses (linear IgA dermatosis, bullous SLE, erythema elevatum diutinum, pyoderma gangrenosum,Sweet’s syndrome,neutrophilic urticaria,subcorneal pustular dermatosis/IgA pemphigus & Behcet’s syndrome), vasculitides
208
Q

MoA of dapsone

A

Inhibits myeloperoxidase

→ ↓oxidative damage to normal tissue in various neutrophilic dermatoses

209
Q

Important pharmacology points

Dapsone

A
  • undergoes significant enterohepatic recirculation, remaining in the circulation 30 days after a single dose
  • Hemolysis has been demonstrated in nursing infants of mothers taking dapsone
210
Q

Important monitoring points

Dapsone

A
  • Baseline G6PD level
  • CBC w/ differential, LFTs, renal function tests, and UA at baseline
  • Must monitor CBC very closely during “high-risk window” for agranulocytosis: CBC weekly for 4 weeks, then every 2 weeks until 3 months into treatment (agranulocytosis is most common in first 12 weeks of treatment)
  • After 3 months, continue checking renal function, LFTs, and UA every 3 to 4 months
  • Methemoglobin levels are needed if there is clinical suspicion of decreased oxygen circulation or anemia
211
Q

Dapsone SE

A
  • Hemolytic anemia and methemoglobinemia
  • Agranulocytosis, the most serious idiosyncratic reaction to dapsone, usually occurs at 7 weeks(manifests as fever, pharyngitis, rarely sepsis)
  • Peripheral neuropathy (predominantly distal motor)
  • Nausea, gastritis, reversible cholestasis and hepatitis, and hypersensitivity syndrome
212
Q

Most patients treated with dapsone for
dermatitis herpetiformis rapidly respond within…?

A

24 to 36 hours

bullous SLE also responds very well to Dapsone

213
Q

Interesting facts for dapsone

A
  • Cimetidine & vitamin E decreases risk of methemoglobinemia without affecting dapsone’s plasma level
  • Methemoglobinemia emergency → use methylene blue
  • Worsening of methemoglobinemia has been shown
    intra- and postoperatively after both local amide and general anesthetic; vitamin C can be used when this occurs
214
Q
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Alikhan & Hocker dermatology (16 decks)

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