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Dermatology Board Review > Dermatopharmacology > Flashcards

Dermatopharmacology Flashcards

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1
Q

MOA: H1 and H2 antihistamines

A

Inverse agonists (downregulate constitutively activated state of receptor) or antagonists at histamine receptors

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2
Q

T/F: Histamine levels are elevated in the skin of chronic urticaria

A

True

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3
Q

H1 antihistamines with Pregnancy category A

A

None

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4
Q

Adverse effects: 1st gen H1 antihistamines

A 
Sedation
Impaired cognitive function 
Anticholinergic effects (dry mouth, constipation, dysuria, and blurred vision)
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5
Q

T/F: 1st gen H1 antihistamines are not metabolized by cytochrome P-450 system

A

False

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6
Q

Pregnancy category B 1st gen H1 antihistamines

A

Diphenhydramine

Chlorpheniramine

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7
Q

Pregnancy category B 2nd gen H1 antihistamines

A

Loratadine

Cetirizine

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8
Q

Carboxylic acid metabolite of hydroxyzine, mainly excreted unchanged; >10% get drowsiness (most sedating of second-generation antihistamines

A

Cetirizine

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9
Q

Tricyclic antidepressant with H1 and H2 antihistamine activity; effective in urticaria and depressed patients with neurotic excoriations; available orally and topically

A

Doxepin

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10
Q

Black box warning: Doxepin

A

Suicidality

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11
Q

Three interconvertible forms of vitamin A

A

Retinol (alcohol)
Retinal (aldehyde)
Retinoic acid (acid)

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12
Q

Precursors of vitamin A

A

Carotenoids

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13
Q

Storage form of Vitamin A

A

Retinol (in the liver)

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14
Q

MOA: Retinoids

A

Binds cytosolic retinoid binding protein → transported to the nucleus → binds intracellular nuclear receptors

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15
Q

Vitamin A and related natural and synthetic compounds are known as

A

Retinoids

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16
Q

Major retinoid receptors in keratinocytes

A

RXR-α and RAR-γ (most abundant in skin)

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17
Q

Effect of photoaging on retinoid receptors

A

Decreased RXR-α and RAR-γ

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18
Q

Effects of binding to RAR/RXR

A

Inhibits AP1 and NF-IL6 - important in proliferation and inflammatory responses
Inhibits TLR2 - important in inflammation
Decrease tumorigenesis and induces apoptosis
Antikeratinization (downregulates K6 and K16)
Inhibits ornithine decarboxylase
Increase TH1 cytokines and Decrease TH2 cytokines (helpful in CTCL)

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19
Q

Earliest and most common SE of systemic retinoids

A

Cheilitis

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20
Q

Seen in 75%–90% of isotretinoin patients as a result of dryness of the nasal mucosa

A

Staphylococcus aureus colonization

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21
Q

SE of retinoid used in conjunction w/ tetracyclines

A

Pseudotumor cerebri

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22
Q

Bone toxicity in retinoids more common in acitretin

A

Diffuse idiopathic skeletal hyperostosis (DISH)

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23
Q

Most common laboratory abnormality, highest risk w/ bexarotene

A

Hyperlipidemia/hypertriglyceridemia

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24
Q

T/F: Discontinue retinoid if fasting TGs >800 mg/dL because of a pancreatitis risk

A

True

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25
Q

T/F: If LFT elevations are greater than 3× the upper limit of normal, should discontinue retinoid

A

True

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26
Q

Occurs in 80% on bexarotene

A

Central hypothyroidism

Decreased TSH and T4

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27
Q

Leukopenia (neutropenia) and agranulocytosis are most common with which retinoid

A

Bexarotene

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28
Q

Most common adverse results in pregnant patients exposed to isotretinoin

A 
Spontaneous abortion (20%)
Retinoid embryopathy (18-28%)
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29
Q

Specific features of Retinoid embryopathy - Craniofacial:

A 
Microtia
Cleft palate
Microphthalmia
Hypertelorism
Dysmorphic facies
Ear abnormalities
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30
Q

Specific features of Retinoid embryopathy - CNS

A

Microcephaly
Hydrocephalus
CN7 palsy
Cortical and cerebellar defects

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31
Q

Specific features of Retinoid embryopathy - CV

A

Cardiac septal defects
Tetralogy of Fallot
Transposition of great vessels
Aortic arch hypoplasia

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32
Q

Specific features of Retinoid embryopathy - Thymus

A

Thymic aplasia/ectopia

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33
Q

Interaction: Bexarotene + Gemfibrozil

A

Bexarotene is metabolized by cytochrome P450 3A4; avoid with gemfibrozil as it inhibits 3A4 → Increased plasma levels of bexarotene → severe hypertriglyceridemia

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34
Q

Basic structure of corticosteroids

A

3 hexane rings and 1 pentane ring

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35
Q

Exogenous Corticosteroids absorbed in

A

Upper jejunum

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36
Q

Short-acting Corticosteroids

A

Hydrocortisone and cortisone: ↓glucocorticoid, ↑mineralocorticoid activity
Half life: 8–12 hours

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37
Q

Intermediate-acting Corticosteroids

A

Prednisone, prednisolone, methylprednisolone, and triamcinolone: ↑glucocorticoid and ↓mineralocorticoid activity
Half life: 24–36 hours

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38
Q

Long-acting Corticosteroids

A

Dexamethasone and betamethasone: ↑↑glucocorticoid, no mineralocorticoid activity
Half life: 36–54 hours

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39
Q

T/F Glucocorticoid receptor (GCR) binds to CS in the cytoplasm then translocates to nucleus

A

True

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40
Q

Increased Cortisol-binding globulin

A

Estrogen therapy
Pregnancy
Hyperthyroidism

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41
Q

Decreased Cortisol-binding globulin

A

Hypothyroidism
Liver disease
Renal disease
Obesity

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42
Q

Converts steroids to active forms in the liver

A

11β-hydroxysteroid dehydrogenase

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43
Q

Major downregulator of cell-mediated immunity

A

IL-10

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44
Q

Physiologic CS therapy dose

A

5 to 7.5 mg/day day of Prednisone

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45
Q

Risk factors for 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
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46
Q

T/F Alternate day dosing lowers risk of cataracts or osteoporosis

A

False

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47
Q

Two clinical presentations of exogenous adrenal insufficiency

A
  1. Steroid withdrawal syndrome (SWS): most common presentation; presents with (p/w) arthralgias, myalgias, mood changes, headache, fatigue, and anorexia/nausea/vomiting; no change in serum cortisol level, but rather ↓available intracellular CS
  2. Adrenal (Addisonian) crisis: extremely uncommon; life-threatening; p/w symptoms of SWS + hypotension, ↓↓↓cortisol levels
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48
Q

Glucocorticoid effects: CS

A

Hyperglycemia

Increased appetite/weight gain

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49
Q

Mineralocorticoid effects: CS

A

HTN
CHF
Weight gain
Hypokalemia

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50
Q

Lipid effects: CS

A

Hypertriglyceridemia (may result in acute pancreatitis)
Cushingoid changes
Menstrual irregularity
Lipodystrophy (moon face, buffalo hump, and central obesity)

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51
Q

Cutaneous effects: CS

A 
Decrease 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
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52
Q

Unique adverse effects of Intramuscular CS

A 
Cold abscesses
Subcutaneous fat atrophy
Crystal deposition
Menstrual irregularities
Purpura
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53
Q

Most commonly used provocative test for adrenal function

A

ACTH stimulation

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54
Q

More accurate test for basal adrenal function (advantage); main disadvantage is patient compliance

A

24 hour urine free cortisol

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55
Q

Primary screening tool to evaluate adrenal insufficiency

A

AM cortisol

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56
Q 
First generation (nonaromatic) topical retinoid
1-2% skin absorption in normal skin
Improvement in 8-12 weeks
Pregnancy Category C
All RAR Nuclear receptors
For acne and photoaging
SE include irritation, erythema, peeling, pruritus, photosensitivity, and temporary worsening of acne
Inactivated by UV (apply at night)
Oxidized by benzoyl peroxide
A

Tretinoin (all-trans-RA)

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57
Q 
First generation topical retinoid
Improvement in 4-8 weeks
Pregnancy Category D
All RAR and RXR Nuclear receptors
Used for Kaposi sarcoma
SE include irritation, erythema, and pruritus
A

Alitretinoin

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58
Q 
Third generation topical retinoid
Improvement in 8-12 weeks
Pregnancy Category C
RAR-β/γ > α Nuclear receptors
For acne
SE include irritation, erythema, peeling, and pruritus
Light stable
A

Adapalene

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59
Q 
Third generation topical retinoid
<5% systemic absorption in normal skin
Improvement in 8-12 weeks
Pregnancy Category X
RAR-β/γ > α Nuclear receptors
For acne and plaque psoriasis 
SE include irritation, erythema, peeling, and pruritus
A

Tazarotene

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60
Q 
Third generation topical retinoid
Improvement in 20 weeks
Pregnancy Category X
All RXR Nuclear receptors
For CTCL
SE include irritation, and erythema
A

Bexarotene

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61
Q 
First generation (nonaromatic) systemic retinoid
Half life of 1 hour
Metabolism: Hepatic	
Excretion: Bile, urine	
Pregnancy Category X
All RAR Nuclear receptors
For Acute promyelocytic leukemia
A

Tretinoin (ATRA or all-trans-Retinoic Acid)

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62
Q

First generation systemic retinoid
Half life of 20 hours
Metabolism: Hepatic
Excretion: Bile, urine
Pregnancy Category X (women must have 2 negative pregnancy tests prior to initiating; requires contraception for 1 month before, during, and 1 month after cessation of therapy)
For Severe acne and other follicular disorders

A

Isotretinoin (13-cis-Retinoic Acid)

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63
Q

Isotretioin dose for acne

A

Usual daily dose: 0.5–1 mg/kg per day

Goal cumulative dose: 120–150 mg/kg for severe acne

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64
Q

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

A

Isotretinoin

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65
Q

Second generation (monoaromatic) systemic retinoid
Half life of 120 days
Metabolism: Hepatic (to acitretin)
Excretion: Bile, urine
50 times more lipophilic than acitretin → persists very long
No longer available

A

Etretinate

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66
Q

Second generation systemic retinoid
Half life of 2 days
Metabolism: Hepatic
Excretion: Bile, urine
Pregnancy Category X (requires contraception for 1 month before, during, and 3 years after cessation of therapy)
For Psoriasis (pustular, erythrodermic, severe and recalcitrant plaque)

A

Acitretin

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67
Q

Why should concurrent alcohol use avoided in Acitretin intake?

A

Because alcohol → acitretin conversion to etretinate → significantly prolonged effects

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68
Q

Dose of Acitretin

A

Usual dose: 25–50 mg/day
Can be combined with PUVA (Re-PUVA); acitretin is given 10-14 days prior to starting PUVA, which accelerates the response

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69
Q

Third generation (polyaromatic) systemic retinoid
Half life of 7–9 hours
Metabolism: Hepatic
Excretion: Hepato-biliary
Pregnancy Category X (requires contraception for 1 month before, during, and 1 month after cessation of therapy)
All RXR Nuclear receptors
For CTCL resistant to at least one systemic therapy

A

Bexarotene

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70
Q

Dose of Bexarotene

A

Usual starting dose is 75 mg/day up to 300 mg/day

Response to treatment takes up to 6 months

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71
Q

Why should Gemfibrozil be avoided with use of Bexarotene?

A

Worsens the hypertriglyceridemia

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72
Q

Phosphodiesterase-4 (PDE-4) inhibitor used for psoriasis and psoriatic arthritis

A

Apremilast

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73
Q

MC SE of Apremilast

A

Diarrhea and nausea which resolve on their own within 4 weeks usually

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74
Q

JAK 1 and 3 inhibitor FDA approved for moderate to severe rheumatoid arthritis (RA) patients who have failed MTX
Topical and oral have been tested in psoriasis; reports of oral used in alopecia areata

A

Tofacitinib

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75
Q

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

A

Ruxolitinib

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76
Q

MOA: Azathioprine

A

Azathioprine’s active metabolite, 6-TG (thioguanine), is produced by the hypoxanthine guanine phosphoribosyltransferase (HGPRT) pathway and shares similarities with endogenous purines → therefore, it gets incorporated into DNA and RNA → inhibits purine metabolism and cell division (particularly in fast-growing cells that do not have a salvage pathway, like lymphocytes)

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77
Q

Convert azathioprine into inactive metabolites

A 
Xanthine oxidase
Thiopurine methyltransferase (TPMT)
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78
Q

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

A

Azathioprine

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79
Q

Concomitant use with Azathioprine increases risk of myelosuppression

A

ACE inhibitors
Sulfasalazine
Folate antagonists

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80
Q

Decreases activity of xanthine oxidase which may lead to myelosuppressino with use of Azathioprine

A

Allopurinol or Febuxostat

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81
Q

FDA approved indications of Azathioprine

A

Organ transplantation and severe RA

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82
Q

Monitoring: Azathioprine

A

Baseline pregnancy test
Tuberculin skin test
Annual complete physical examination with particular attention to possible lymphoma and squamous cell carcinoma
CBC with differential and liver function tests every 2 weeks for the first 2 months and every 2 to 3 months thereafter

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83
Q

Increased risk of hepatosplenic T-cell lymphoma with Azathioprine use

A

TNF-α inhibitor

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84
Q

MOA: Cyclosporine

A

Forms a complex with cyclophilin, which inhibits calcineurin – an intracellular enzyme – which in turn reduces the activity of NFAT-1 (transcribes various cytokines, such as IL-2)
↓IL-2 production leads to decreased numbers of CD4 and CD8 cells.

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85
Q

Dermatologic dose of Cyclosporine

A

5 mg/kg daily and can be used continuously for up to 1 year according to the FDA (2 years for worldwide consensus data)
Cyclosporine lipid nanoparticles formulation maximum dermatolyte dose = 4 mg/kg
Obese patients - ideal body weight should be used

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86
Q

FDA approved dermatologic indications of Cyclosporine

A

Psoriasis

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87
Q

Two most notable SEs of Cyclosporine, which are dose- and duration-dependent

A

Nephrotoxicity (Irreversible kidney damage is avoided if patients receive dermatologic doses (2.5–5 mg/kg daily), have dose adjusted when creatinine increases by 30% from baseline, and use cyclosporine for no longer than 1 year)
Hypertension (occurs in 27% of psoriasis patients and is thought to be secondary to renal vasoconstriction; Prescription of choice = CCBs, because they do not alter cyclosporine serum levels)

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88
Q

T/F: There is risk of NMSC in psoriasis patients taking Cyclosporine treated for >2 years

A

True

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89
Q

Other SE of Cyclosporine

A 
Hypertrichosis
Gingival hyperplasia
Myalgia, paresthesia, tremors
Malaise
Hyperuricemia (can precipitate gout), hypomagnesemia, and hyperkalemia
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90
Q

Monitoring of Creatinine in Cyclosporine

A

Recheck creatinine level if ↑ by >30% from baseline → if remains elevated above 30%, ↓dose by at least 1 mg/kg for 4 weeks, then:
- If the creatinine 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
If at any time creatinine increases by ≥50% above baseline, discontinue therapy until level returns to baseline

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91
Q

Monitoring: Cyclosporine

A

Two baseline blood pressures at least 1 day apart and two baseline creatinine values at least 1 day apart
Baseline BUN, CBC, LFTs, fasting lipid profile, magnesium, potassium, and uric acid
Reevaluation of labs and blood pressure every 2 weeks for the first 1 to 2 months, then every 4 to 6 weeks with blood pressure checked at every visit

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92
Q

MOA: Methotrexate

A

Binds dihydrofolate reductase with greater affinity than folic acid → prevents conversion of dihydrofolate to tetrahydrofolate (a necessary cofactor of purine synthesis) → inhibition of cell division

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93
Q

The inhibition of dihydrofolate reductase may be bypassed by

A

Leucovorin (folinic acid) or Thymidine

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94
Q

An active, naturally occurring version of folate (vitamin B9); most commonly used medication for rescue of high-dose MTX adverse effects/overdose

A

Leucovorin (folinic acid)
↓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)

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95
Q

FDA approved dermatologic indications of Methotrexate

A

For extensive, severe, debilitating, or recalcitrant psoriasis and Sezary syndrome

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96
Q

Absolute contraindications to Methotrexate use

A

Pregnancy (category X)

Lactation

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97
Q

Testing indicated for high cumulative doses (≥ 1.5–4 g) of Methotrexate

A

Liver biopsy (gold standard)

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98
Q

Monitoring: Methotrexate

A

CBC w/ differential, LFTs, creatinine, BUN, and viral hepatitis panel at baseline, then repeat weekly for first month (excluding the viral hepatitis panel), and gradually decrease frequency to every 3 to 4 months (e.g., every 2 weeks × 2 months, every month × 2 months, every 3 months thereafter)

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99
Q

Causes UV and radiation recall (toxic cutaneous reactions reappear on previously irradiated skin)

A

Methotrexate

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100
Q

MOA: Mycophenolate mofetil

A

Binds and inhibits inosine monophosphate dehydrogenase - a key enzyme for the de novo synthesis of purines, which is essential in activated lymphocytes

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101
Q

Dermatologic doses of Mycophenolate mofetil

A

From 2 to 3 g divided in twice daily doses

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102
Q

Antacids and proton pump inhibitors decreases its serum levels

A

Mycophenolate mofetil

Requires gastric acidity for cleavage into its active state

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103
Q

Most common SEs of Mycophenolate mofetil

A

Diarrhea, abdominal pain, nausea, and vomiting

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104
Q

Mycophenolate mofetil is associated with a form of neutrophil dysplasia which is characterized by nuclear hypolobulation with a left shift (may predict the development of neutropenia) called

A

Pseudo-Pelger-Huet anomaly

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105
Q

MOA: Hydroxyurea

A

Impairs DNA synthesis through inhibition of ribonucleotide diphosphate reductase; hypomethylates DNA resulting in altered gene expression

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106
Q

Most common adverse effect of Hydroxyurea

A

Megaloblastic anemia (myelosuppression)

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107
Q

Can cause dermatomyositis-like eruption, lichenoid drug eruption resembling graft-versus-host disease, leg ulcers, alopecia, photosensitivity, radiation recall, and hyperpigmentation of the skin and nails

A

Hydroxyurea

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108
Q

MOA: Cyclophosphamide

A

An alkylating agent (exerts its effect by directly damaging DNA via cross-linking)

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109
Q

Metabolite of Cyclophosphamide which is cleaved intracellularly into acrolein and enhances cellular damage by depleting glutathione store

A

Aldophosphamide

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110
Q

Occurs in 5% to 41% as a result of acrolein (prevented by adequate hydration as well as mesna, which binds acrolein in the bladder and reduces irritation) associated with increased risk of transitional cell carcinoma of the bladder

A

Hemorrhagic cystitis

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111
Q

Cutaneous SE of Cyclophosphamide

A

Permanent pigmented band on the teeth
Anagen effluvium
Hyperpigmentation of skin and nails

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112
Q

MOA: Chlorambucil

A

Alkylating agent that directly damages DNA via cross-linking

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113
Q

MOA: Antimalarial agents

A

Inhibit ultraviolet-induced cutaneous reactions by binding to DNA and inhibiting superoxide production
Raise intracytoplasmic pH and stabilize the microsomal membrane → ↓ability of macrophages to express MHC complex antigens on cell surface
Reduce lysosomal size and impair chemotaxis
Inhibit platelet aggregation and adhesion

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114
Q

Steady-state concentration of antimalarial agents is attained at

A

3 to 4 months, which explains the long treatment duration required to achieve clinical benefit

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115
Q

FDA approved dermatologic indications of antimalarial agents

A

SLE
Malaria
RA

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116
Q

Contraindicated in patients who have myasthenia gravis

A

Chloroquine

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117
Q

T/F: Continued use of CQ and HCQ is contraindicated in patients who develop retinopathy

A

True

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118
Q

Mucocutaneous drug reactions of antimalarial agents

A

Yellow pigmentation of the skin (quinacrine)
Drug-induced LP
Morbilliform hypersensitivity eruption; may also present as erythroderma or SJS - Risk is much greater in dermatomyositis (31%) than lupus (3%)
Psoriasis exacerbation (CQ in particular)
Bluish-gray to black hyperpigmentation in 10-30% of patients treated for ≥4 months typically affecting the shins (clinically indistinguishable from type II minocycline hyperpigmentation), face, and palate
Nail hyperpigmentation

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119
Q

Ophthalmologic toxicity with CQ and HCQ

A 
Corneal deposits (keratopathy)
Neuromuscular eye toxicity (ciliary body dysfunction)
Retinopathy (maculopathy) - Irreversible
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120
Q

Eye monitoring recommendations with CQ and HCQ

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

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121
Q

MOA: Dapsone

A

Inhibits myeloperoxidase → ↓oxidative damage to normal tissue in various neutrophilic dermatoses (affects eosinophils and monocytes to a lesser extent)
Decreases hydrogen peroxide and hydroxyl radical levels
Inhibits chemotaxis of neutrophils, although this has not been demonstrated in therapeutic doses

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122
Q

Dapsone undergoes significant enterohepatic recirculation, thus remaining in the circulation for how many days

A

30 days

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123
Q

FDA approved indications for Dapsone

A

Dermatitis herpetiformis

Leprosy

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124
Q

Dose-related AE and occurs in ALL individuals to some degree (related to oxidative stress from N-hydroxy metabolites of Dapsone)

A

Hemolytic anemia

Methemoglobinemia

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125
Q

Most serious idiosyncratic reaction to dapsone, usually occurs at 7 weeks (3–12 weeks) and may manifest as fever, pharyngitis, and occasionally sepsis

A

Agranulocytosis

Most recover quickly after cessation of dapsone; may consider giving G-CSF

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126
Q

Peripheral neuropathy with Dapsone is seen predominantly in

A

Distal motor

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127
Q

Decreases risk of methemoglobinemia without affecting dapsone’s plasma level

A

Cimetidine

Vitamin E - may also provide small amount of protection

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128
Q

Monitoring: Dapsone

A

Baseline G6PD level, CBC w/ differential, LFTs, renal function tests, and UA
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 - needed if there is clinical suspicion of decreased oxygen circulation or anemia

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129
Q

T/F: Most patients treated with dapsone for dermatitis herpetiformis rapidly respond within 24 to 36 hours

A

True

130
Q

Fully human dimeric fusion protein (TNF-receptor linked to Fc portion of IgG) that binds both TNF-α (soluble and membrane-bound) and TNF-β
Given subcutaneously

A

Etanercept

131
Q

Chimeric monoclonal IgG antibody binding TNF-α only (targets soluble and transmembrane TNF-receptor)
Given intravenously

A

Infliximab

132
Q

Fully human monoclonal IgG antibody against transmembrane TNF-receptor
Given subcutaneously

A

Adalimumab

133
Q

FDA approved indications for TNF-α inhibitors

A

Plaque psoriasis

Psoriatic arthritis

134
Q

Fully human monoclonal IgG1 antibody directed against the common p40 subunit of IL-12 and IL-23; FDA approved for adults with psoriasis and psoriatic arthritis; some evidence for efficacy in hidradenitis suppurativa

A

Ustekinumab

135
Q

Possible association with reversible Posterior leukoencephalopathy syndrome

A

Ustekinumab

136
Q

Chimeric IgG monoclonal antibody targeting the B-cell surface antigen (CD20) used in pemphigus vulgaris and severe bullous pemphigoid

A

Rituximab

137
Q

IL-1 inhibitors

A

Canakinumab
Anakinra
Rilonacept
Gevokizumab

138
Q

Most commonly reported SE of IL-17 inhibitors

A

Nasopharyngitis

139
Q

MOA: neutralizes IL-17A

A

Secukinumab

Ixekizumab

140
Q

MOA: antagonizes the IL-17 receptor

A

Brodalumab

141
Q

Monoclonal anti-IgE antibody → ↓IgE levels and ↓IgE receptors on mast cells and basophils; FDA approved for allergic asthma and chronic idiopathic urticaria

A

Odalimumab

142
Q

MOA: Vismodegib

A

Targets sonic hedgehog pathway by inhibiting smoothened receptor → GLI1/2 transcription factors stay inactive → inhibition of transcription of target genes

143
Q

SE of Vismodegib

A 
Muscle spasms (MC)
Alopecia
Dysgeusia
Fatigue 
Nausea, anorexia, and diarrhea
144
Q

Used for metastatic and locally advanced basal cell carcinoma, as well as those unamenable to surgery/radiation; may be used in patients with nevoid basal cell carcinoma syndrome

A

Vismodegib

145
Q

MOA: Vemurafenib and Dabrafenib

A

Inhibition of BRAF

BRAF: serine/threonine signal transduction kinase important to the MAPK pathway, which regulates cell division

146
Q

MOA: Imatinib mesylate

A

Tyrosine kinase inhibitor
Binds to the kinase domain of various tyrosine kinases (e.g., Bcr-Abl, c-Kit receptor [CD117], and platelet-derived growth factor receptor [PDGFR])

147
Q

Used in melanoma, myeloproliferative hypereosinophilic syndrome, and dermatofibrosarcoma protuberans

A

Imatinib mesylate

148
Q

Most common cutaneous reaction with Imatinib mesylate

A

Superficial edema (periorbital edema mainly)

149
Q

A nitrogen mustard alkylating agent, is used for patch/plaque MF; contact dermatitis is the most common SE, but anaphylaxis and SCC development are the most concerning

A

Mechlorethamine hydrochloride

150
Q

MOA: 5-Fluorouracil

A

Antimetabolite/pyrimidine analog which binds to thymidylate synthase (normally converts deoxyuridine → thymidine), and results in ↓DNA synthesis

151
Q

MOA: Imiquimod

A

Activator of Toll-like receptors 7 and 8 → activation of NF-κB transcription factor → Increase cytokines/chemokines (e.g., TNF α and IFN γ) → innate/acquired immune pathway stimulation → antitumor and antiviral activity
Also antiangiogenic, proapoptotic, and increased lymphatic transport of immune cells/factors → tumor destruction

152
Q

Bactericidal agent made by Bacillus subtilis with activity against Neisseria and gram positives (GP)

A

Bacitracin

153
Q

MOA: Bacitracin

A

Binds to C55-prenol pyrophosphatase → disruption of bacterial cell wall peptidoglycan synthesis

154
Q

Antibacterial agents commonly causing allergic contact dermatitis (especially common in patients with stasis dermatitis/ulcers)

A

Bacitracin

Neomycin

155
Q

Bactericidal agent made by Bacillus polymyxa and B. subtilis with activity against GN (e.g., Pseudomonas)
Pregnancy category B

A

Polymixin B

156
Q

MOA: Polymixin B

A

↑cell membrane permeability via detergent-like phospholipid interaction

157
Q

Aminoglycoside made by Streptomyces fradiae with activity against GP and GN; possibility of ototoxicity/nephrotoxicity but very rare
Pregnancy category D

A

Neomycin

158
Q

MOA: Neomycin

A

Binds 30s subunit of bacterial ribosomal RNA → ↓protein synthesis

159
Q

Made by Pseudomonas fluorescens with activity against MRSA (can ↓nasal carriage) and S. pyogenes but resistance has been reported; not effective against Pseudomonas (made by Pseudomonas)
Pregnancy category B

A

Mupirocin

160
Q

MOA: Mupirocin

A

Binds to bacterial isoleucyl tRNA synthetase → ↓RNA/protein synthesis

161
Q

Pleuromutilin made by Clitopilus scyhpoides with activity against MRSA, S. pyogenes, and anaerobes; FDA approved for impetigo to MSSA and S. pyogenes

A

Retapamulin

162
Q

MOA: Retapamulin

A

Binds to L3 protein on 50s subunit of bacterial ribosome → ↓protein synthesis

163
Q

Aminoglycoside made by M. purpurea with activity against GP and GN (e.g., Pseudomonas)

A

Gentamicin

164
Q

MOA: Gentamicin

A

Binds to bacterial 30s ribosomal subunit →↓protein synthesis

165
Q

MOA: Silver Sulfadiazine

A

Binds bacterial DNA → ↓DNA synthesis; also disrupts cell walls and membranes

166
Q

Sulfa drug Activity against GP and GN, including MRSA and P. aeruginosa which may cross-react with sulfonamides; Used extensively for burn wounds
Pregnancy category B

A

Silver Sulfadiazine

167
Q

SE: Silver Sulfadiazine

A 
Hemolysis (in G6PD patients)
Methemoglobinemia
Renal insufficiency
Argyria
Leukopenia
Unmasking porphyria
168
Q

Quinolone-derivative with high iodine concentration with activity against GP and GN and dermatophytes/yeasts

A

Iodoquinol

169
Q

Broad-spectrum antibacterial agent that functions via strong oxidizing properties (good vs P. acnes) – no bacterial resistance reported to date; Used for acne and has keratolytic properties

A

Benzoyl peroxide

170
Q

Nitroimidazole that disrupts DNA synthesis with activity against protozoa and anaerobes; not active against P. acnes, staphylococcus, streptococcus, fungi, or Demodex
Pregnancy category B

A

Metronidazole

171
Q

Dicarboxylic acid that activity against P. acnes thus used in acne and rosacea (including perioral dermatitis); also competitively inhibits tyrosinase → ↓pigmentation so used in hyperpigmentation disorders

A

Azelaic acid

172
Q

MOA: Azelaic acid

A

Disrupts mitochondrial respiration, ↓DNA synthesis (especially in abnormal melanocytes), and ↓ROS production by PMNs

173
Q

MOA: Sodium sulfacetamide

A

Inhibits bacterial dihydropteroate synthetase (prevents conversion of PABA → folic acid) → ↓nucleic acid/protein

174
Q

MOA: Penicillins

A

β-Lactam ring binds to bacterial enzyme DD-transpeptidase → inhibits formation of peptidoglycan cross-links in the bacterial cell wall → cell wall breakdown

175
Q

Peniciliins which are good for GP cocci, like MSSA

A

First generation:
Dicloxacillin
Oxacillin

176
Q

Ampicillin + mononucleosis/allopurinol/lymphocytic leukemia

A

Generalized morbilliform itchy eruption starting 1 week after antibiotic initiation

177
Q

Peniciliins with antipseudomonal activity

A

Third and Fourth generation:
Carboxypenicillins (carbenicillin)
Ureidopenicillins (piperacillin)

178
Q

Treatment of choice for animal or human bites

A

Amoxicillin-clavulanate

179
Q

Prolongs renal excretion → ↑penicillin levels (also can ↑cephalosporin levels)

A

Probenicid

180
Q

How many % of cephalosporin-allergic patients are penicillin-allergic

A

2%

181
Q

Structure of cephalosporins

A

β-lactam ring + 6-membered dihydrothiazine ring

182
Q

Cephalosporins that are best for GP cocci, but not good for MRSA or penicillin-resistant S. pneumonia

A

First generation:
Cefadroxil
Cephalexin

183
Q

Cephalosporins that have more GN activity and less GP activity; good for H. influenzae, M. catarrhalis, N. meningitides, and N. gonorrhoeae

A

Second generation:
Cefaclor
Cefuroxime

184
Q

Cephalosporins with good GN activity, but not GP activity; some good for P. aeruginosa (i.e., ceftazidime); good for soft tissue abscesses and diabetic foot ulcers

A 
Third generation:
Cefixime
Cefdinir
Cefotaxime
Ceftazidime
Cefpodoxime
Ceftriaxone
185
Q

Cephalosporins with broad coverage – MSSA, nonenterococcal streptococci, and GNs (including P. aeruginosa)

A

Fourth generation:

Cefepime

186
Q

How many of of penicillin-allergic patients have cross reactivity with cephalosporins?

A

5-10%

187
Q

Why should cephalosporins not be given aminoglycosides?

A

↑risk of nephrotoxicity

188
Q

MOA: Vancomycin

A

Tricyclic glycopeptide that inhibits bacterial cell wall synthesis

189
Q

Most common cause of drug-induced Linear IgA Bullous Disease as a result of IgA antibodies to LAD285 and IgA/IgG to BP180

A

Vancomycin

190
Q

Only works for GP organisms – most important use in dermatology is against MRSA skin and soft tissue infections

A

Vancomycin

191
Q

MOA: Macrolides

A

Bind to 50s subunit of bacterial ribosome → ↓protein synthesis; also has antiinflammatory properties

192
Q

Not used as commonly these days because of ↑resistance (particularly S. aureus) and GI SEs; Used for Lyme disease, erythrasma/pitted keratolysis, anthrax, erysipeloid, chancroid, and LGV; may be used for acne, rosacea, and pityriasis rosea; potent CYP3A4 inhibitor (e.g., monitor use of warfarin, mexiletine, theophylline, and statins [↑ rhabdomyolysis])

A

Erythromycin

193
Q

Better than erythromycin for GPs; often used as second line prophylactic antibiotic in dermatology surgery for PCN/CSN-allergic patients; has some GN activity (E. coli, N. gonorrhoeae, H. ducreyi, and C. trachomatis)

A

Azithromycin

194
Q

Erythromycin estolate in pregnancy

A

Hepatotoxicity (intrahepatic cholestasis) in mother

Possible association of cardiovascular malformation and pyloric stenosis if fetus exposed in utero

195
Q

Better than erythromycin for GPs; CYP3A4 inhibitor (less potent than erythromycin); Has activity against some GNs, atypical mycobacteria (good activity against M. leprae), T. pallidum, B. burgdorferi, and T. gondii

A

Clarithromycin

196
Q

MOA: Fluoroquinolones

A

Inhibits DNA gyrase (bacterial topoisomerase II) +/− topoisomerase IV → DNA fragmentation
DNA gyrase - target in GN
topoisomerase IV - target in GP

197
Q

Target of 1st and 2nd generation Fluoroquinolones

A

(ciprofloxacin, ofloxacin, and nalidixic acid)

only target DNA gyrase (topoisomerase II) → only effective against GN

198
Q

Target of 3rd and 4th generation Fluoroquinolones

A

(levofloxacin, moxifloxacin, sparfloxacin, and gatifloxacin): target both topoisomerase forms (IV > II) → ↑GP coverage and ↓bacterial resistance; slightly ↓efficacy against GN

199
Q

Treatment of choice for cutaneous anthrax (B. anthrax)

A

Ciprofloxacin

200
Q

Has good activity for GNs, like P. aeruginosa

A

Ciprofloxacin

201
Q

Fluoroquinolone NOT associated with photosensitivity

A

Levofloxacin

202
Q

SE: Quinolones

A 
GI symptoms (#1)
CNS SEs (headache, dizziness, seizures, psychosis, and depression)
Tendinitis/tendon rupture
Hypersensitivity
Photosensitivity/photo-onycholysis
203
Q

T/F: Quinolones are CYP1A2 inhibitors

A

True

204
Q

Decreases absorption of Quinolones

A

Administration with divalent cations (calcium, magnesium, aluminum, and zinc)

205
Q

MOA: Tetracyclines

A

binds 30s subunit of bacterial ribosome → ↓protein synthesis; antiinflammatory properties (e.g., inhibits multiple matrix metalloproteinases, neutrophil migration, and ↓innate cytokines)

206
Q

Treatment of choice in LGV

A

Doxycycline

207
Q

Treatment of choice for rickettsial and rickettsial-like infections

A

Doxycycline

208
Q

Treatment of choice in early stage of Lyme disease

A

Doxycycline

209
Q

Minocycline hyperpigmentation types

A

Type 1: Blue-gray in sites of facial scarring – stains for iron and melanin
Type 2: Blue-gray on shins and/or forearms – stains for iron and melanin
Type 3: Diffuse muddy brown on sun-exposed skin – stains melanin only; represents a low-grade phototoxic eruption with PIH

210
Q

SE: Tetracyclines

A 
GI symptoms 
Acute vestibular SEs 
Benign intracranial hypertension/pseudotumor cerebri (↑risk if given w/ isotretinoin)
Photosensitivity/photo-onycholysis
Vaginal candidiasis
GN acne/folliculitis
211
Q

SE: Minocycline

A

Hyperpigmentation of skin/nail beds/teeth/ mucous membranes/bone
Serum sickness-like reactions
Drug-induced Sweet’s syndrome
Autoimmune hepatitis
DRESS/DHS
Llupus-like syndrome (usually ANA+ and antihistone AB+ )
Cutaneous PAN/vasculitis (pANCA+)

212
Q

Produces tooth discoloration in patients below 8 years old

A

Tetracyclines

213
Q

Tetracyclines are excreted except for this which can be used in renal disease

A

Doxycycline (mainly GI)

214
Q

MOA: Rifampin

A

binds β-subunit of bacterial DNA-dependent RNA polymerase → ↓RNA/protein synthesis

215
Q

Major CYP450 inducer

A

Rifampin

↑drug clearance/↓efficacy (e.g., OCPs, warfarin, azoles, CCBs, statins, and cyclosporine)

216
Q

Should NOT be given as monotherapy, because of rapid development of resistance

A

Rifampin

217
Q

SE: Rifampin

A 
Orange-red discoloration of body fluid
CNS (headache and drowsiness)
GI symptoms
Development of rifampin-dependent antibodies (can → anaphylaxis, flu-like symptoms, renal failure, and hemolytic anemia)
Hepatotoxicity (especially w/ isoniazid)
DVTs
Pulmonary fibrosis
Ocular SEs
Worsening of porphyria (induces δ-ALA synthetase), Possible hemorrhagic disease of the newborn and mother in pregnancy
218
Q

MOA: Trimethoprim-sulfamethoxazole (or cotrimoxazole)

A

Dihydrofolate reductase inhibitor (trimethoprim) + dihydropteroate synthetase inhibitor (sulfamethoxazole) → ↓tetrahydrofolic acid → ↓bacterial nucleic acid/protein synthesis

219
Q

This can:
↑dapsone levels
↑hematologic toxicity in patients taking MTX (both ↓THF)
↑renal toxicity in patients taking cyclosporine
↑K+ in patients on ACEIs/ARBs

A

Trimethoprim-sulfamethoxazole (or cotrimoxazole)

220
Q

Accounts for 30% of SJS/TEN cases

A

Trimethoprim-sulfamethoxazole (or cotrimoxazole)

221
Q

MOA: Clindamycin

A

Lincosamide that binds to 50S subunit of bacterial ribosomal RNA → ↓ribosomal translocation/protein synthesis

222
Q

Helps determine whether inducible resistance is present in an erythromycin-resistant, clindamycin-sensitive organism (bacteria with erm gene)

A

“D zone” test

223
Q

May produce an antibiotic-associated colitis

A

Clindamycin

224
Q

MOA: Linezolid

A

Binds 23S portion of 50S ribosomal subunit of bacteria

225
Q

SEs: Linezolid

A

Myelosuppression in 2%
Serotonin syndrome (if given with serotonergic drugs)
Optic/peripheral neuropathy

226
Q

MOA: Quinupristin and dalfopristin

A

Diffuses through bacterial cell wall and binds 50s ribosomal subunit sites → ↓protein synthesis

227
Q

MOA: Daptomycin

A

Depolarizes bacterial cell membrane → cell death

228
Q

Guanosine analog that requires phosphorylation

A

Acyclovir

229
Q

Initial phosphorylation of Acyclovir by:

A

Acyclovir monophosphate

230
Q

Subsequent phosphorylation of Acyclovir by:

A

Acyclovir triphosphate

231
Q

MOA: Acyclovir

A

After phosphorylation, competes with deoxyguanosine triphosphate as a substrate for viral DNA polymerase → incorporates into viral DNA → chain terminates and ↓viral duplication

232
Q

Dermatologic indications of Acyclovir

A

Herpes simplex infections
Varicella zoster
Recurrent EM 2° to HSV (>6 outbreaks per year)

233
Q

Prodrug of acyclovir with great bioavailability; with oral and topical forms and has the same uses as acyclovir with excellent SE profile (Rarely can cause TTP/HUS in HIV patients)

A

Valacyclovir

234
Q

More effective at ↓VZV pain than acyclovir

A

Famciclovir and valacyclovir

235
Q

Indication of Penciclovir (topical only)

A

Herpes labialise

236
Q

Nucleoside phosphate analog of deoxycytidine monophosphate effective in HPV, HSV, CMV retinitis, orf, and molluscum; does not require viral thymidine kinase

A

Cidofovir

237
Q

MOA: Cidofovir

A

Acts as a competitive inhibitor and alternate substrate for viral DNA polymerases → incorporates into DNA strand → blockage/termination of DNA synthesis

238
Q

MOA: Foscarnet

A

An intravenous pyrophosphate analog that binds to pyrophosphate-binding site on viral DNA polymerase → inhibition of pyrophosphate cleavage from deoxyadenosine triphosphate → disruption of DNA elongation

239
Q

Treatment of choice for acyclovir-resistant HSV

A

Foscarnet

240
Q

SE: Foscarnet

A 
Penile erosions
Thrombophlebitis
Nephrotoxicity
Seizures
Electrolyte disturbances
241
Q

MOA: Bleomycin

A

Binds DNA → single strand breaks → ↓protein synthesis → ↑apoptosis/necrosis of keratinocytes

242
Q

Chemotherapeutic agent that can be used intralesionally for warts

A

Bleomycin

243
Q

SE: Bleomycin

A

Injection pain
Raynaud’s phenomenon
Loss of nail plate/nail dystrophy
Flagellate hyperpigmentation

244
Q

MOA: Podophyllin

A

Antimitotic agent that binds tubulin → cell cycle arrest in metaphase

245
Q

Blistering agent (comes from blister beetle/Spanish fly, Lytta vesicatoria) which is applied in office under occlusion for warts/molluscum then washed off at home 4 hours later

A

Cantharidin

246
Q

MOA: Cantharidin

A

Disrupts desmosomes → intraepidermal acantholysis → bullae

247
Q

Green tea (Camellia sinensis)–derived polyphenol epigallocatechin gallate → apoptosis, inhibition of telomerase, and an antioxidant effect on cells; approved for genital/perianal warts

A

Sinecatechins

248
Q

MOA: Azoles

A

inhibit 14α demethylase (catalyzes conversion of lanosterol to ergosterol) → ↓ergosterol → ↓cell membrane synthesis, ↑ membrane rigidity/permeability, growth inhibition, and cell death

249
Q

Metabolized mainly in liver (CYP3A4); absorption enhanced in an acidic environment; FDA approved for dermatophyte onychomycosis, oropharyngeal/esophageal candidiasis, blastomycosis, histoplasmosis, and aspergillosis refractory to amphotericin B

A

Itraconazole

250
Q

Itraconazole dosage for Onychomycosis

A

200 mg/day for 12 weeks course for toenails

251
Q

Contraindications: Itraconazole

A

Ventricular dysfunction and CHF
Active liver disease or h/o liver toxicity with other drugs
Concurrent use of certain drugs metabolized via CYP3A4 as it is a CYP3A4 inhibitor
Concurrent use with levomethadyl, dofetilide, statins, midazolam, triazolam, nisoldipine, and ergot alkaloids

252
Q

FDA approved for vaginal/oropharyngeal/esophageal candidiasis and cryptococcal meningitis

A

Fluconazole

253
Q

Contraindications: Fluconazole

A

Potent CYP2C9 inhibitor – Do NOT administer with pimozide, quinidine, cisapride, erythromycin, terfenadine, astemizole, voriconazole, or statins

254
Q

Systemic form not commonly used today because of the associated high rate of hepatic toxicity; If used, typically <10 days; FDA approved for tinea corporis/cruris/pedis/capitis, chronic mucocutaneous candidiasis, vaginal and cutaneous candidiasis, chromoblastomycosis, blastomycosis, histoplasmosis, coccidioidomycosis, and paracoccidioidomycosis

A

Ketoconazole

255
Q

New generation of azoles used primarily for serious, invasive fungal infections in immunosuppressed hosts (invasive aspergillosis, Candida infections, and Fusarium infections)

A

Voriconazole

256
Q

SE: Voriconazole

A

Severe phototoxicity (including pseudoporphyria, and xeroderma pigmentosum-like changes)
↑risk SCC
↑risk visual disturbances

257
Q

MOA: Allylamines

A

Inhibit squalene epoxidase (catalyzes conversion of squalene to lanosterol) → ↓cell membrane synthesis

258
Q

FDA approved for dermatophyte onychomycosis and tinea capitis (granule formulation)

A

Terbinafine

259
Q

Terbinafine dosage for Onychomycosis

A

6 weeks 250 mg/day for fingernail onychomycosis

12 weeks 250 mg/day for toenail onychomycosis

260
Q

Highly effective against endothrix organisms (most commonly T. tonsurans)

A

Terbinafine

261
Q

Rare SE: Terbinafine

A 
Taste/smell disturbance
Severe skin reactions (e.g., SJS/TEN)
Sisual disturbance
Hepatobiliary dysfunction/hepatitis/liver failure (idiosyncratic)
Hematologic abnormalities
Rhabdomyolysis
Depression
Exacerbation of SLE
Drug-induced SCLE
262
Q

FDA approved for dermatophyte onychomycosis and tinea corporis/cruris/pedis/capitis; more effective in tinea capitis caused by Microsporum (e.g., M. canis) than terbinafine

A

Griseofulvin

263
Q

MOA: Griseofulvin

A

Interferes with tubulin → inhibition of mitosis; binds to keratin in keratin precursor cells → resistance to fungal infections

264
Q

MOA: Ciclopirox olamine

A

Disrupts fungal cell membrane transport of important molecules, ↓cell membrane integrity, inhibits cellular respiratory enzymes, and blocks important enzymatic cofactors

265
Q

MOA: Polyenes

A

Binds Candida cell membrane sterols → ↑permeability → cell death

266
Q

MOA: Echinocandins

A

Inhibit β-(1,3)-D-glucan synthase → ↓ glucan production → disrupt cell wall synthesis

267
Q

MOA: Ivermectin

A

Binds glutamate-gated chloride ion channels of parasite nerve/muscle cells → ↑membrane permeability → hyper-polarization → death

268
Q

SE of Ivermectin that occurs in patients with onchocerciasis, presents with rash/systemic symptoms/ocular reactions

A

Mazzotti reactions

269
Q

MOA: Albendazole

A

Stops tubulin polymerization → immobilization and death of parasite

270
Q

MOA: Thiobendazole

A

Inhibits fumarate reductase

271
Q

FDA approved for neurocysticercosis and hydatid disease

A

Albendazole

272
Q

FDA approved for strongyloides, cutaneous larva migrans, and visceral larva migrans

A

Thiobendazole

273
Q

MOA: Permethrin

A

Disables sodium transport channels on cell membranes of arthropods → paralysis
Related to pyrethrins, which come from flowers of genus Compositae

274
Q

Dosage of Permethrin for Scabies

A

Scabies (5% cream is the treatment of choice; neck down application – 2 overnight applications separated by 1 week

275
Q

MOA: Malathion

A

Organophosphate that inhibits acetylcholinesterase in arthropods → neuromuscular paralysis

276
Q

MOA: Lindane

A

Organochlorine → ↓neurotransmission → arthropod respiratory/muscular paralysis

277
Q

MOA: Spinosad

A

Instigates arthropod motor neurons → paralysis

278
Q

Topical anti parasite that may cause seizures if ingested or multiple applications

A

Lindane

279
Q

Ultraviolet A spectrum

A

320–400 nm

280
Q

Ultraviolet B spectrum

A

280–320 nm

281
Q

MOA: Psoralen + UVA

A

Photoactivated psoralen molecules form 3,4 or 4’,5’ cyclobutane monofunctional adducts to pyrimidines in DNA → interstrand DNA cross-link → ↓DNA synthesis/cell cycle arrest

282
Q

UVA-1

A

340–400nm

283
Q

MOA: UVB

A

↓DNA synthesis (i.e., in psoriatic epidermis) and ↑p53 → cell cycle arrest/keratinocyte apoptosis; ↓proinflammatory cytokines, ↓Langerhans cells in skin

284
Q

Narrowband UVB

A

311–313nm

285
Q

Broadband UVB

A

280–320

286
Q

Excimer laser

A

308 nm

287
Q

Treatment of choice for Vitiligo

A

NB-UVB

288
Q

Pheresis via venous catheter in arm vein → blood cells separated into leukocyte-rich buffy coat and RBCs (returned back to patient) → 8-methoxypsoralen added to leukocytes → UVA radiation → reinfusion

A

Extracorporeal photochemotherapy

289
Q

Contraindication: ECP

A

Severe cardiac disease - because of difficulty in handling added fluid volume

290
Q

Activated by blue light (Blu-U device); no need for occlusion

A

Aminolevulinic acid (ALA)

291
Q

Activated by red light (Aktilite) and is more lipophilic; occlusion recommended

A

Methyl aminolevulinate (MAL)

292
Q

MOA: Photodynamic therapy

A

Photosensitizers are ultimately converted to protoporphyrin IX within cells → activated to a higher energy state (along with production of reactive oxygen species, including singlet O2) primarily with light ≈ 410 nm (Soret band, blue), but also has other peaks (e.g., 635 nm, red) → localize by mitochondria → necrosis/apoptosis of malignant cells

293
Q

T/F: Neoplastic cells accumulate more porphyrins than normal cells

A

True

294
Q

Aromatic compounds that absorb radiation and convert it into longer, lower-energy wavelengths

A

Chemical sunscreen

295
Q

Chemically inert compounds that reflect/scatter radiation

A

Physical sunscreen

Zinc oxide and titanium dioxide

296
Q

MOA: Hydroquinone

A

Competes with tyrosine as substrate for tyrosinase; production of ROS → melanocyte damage

297
Q

MOA: Pimecrolimus and tacrolimus

A

bind to FK506-binding protein forming a complex → complex binds to enzyme calcineurin → prevention of calcineurin from dephosphorylating transcription factor NFAT-1 → ↓transcription of cytokine IL-2 → ↓T-cell activation/proliferation

298
Q

MOA: Pimecrolimus and tacrolimus

A

Bind to FK506-binding protein forming a complex → complex binds to enzyme calcineurin → prevention of calcineurin from dephosphorylating transcription factor NFAT-1 → ↓transcription of cytokine IL-2 → ↓T-cell activation/proliferation

299
Q

MOA: Vitamin D analogs

A

Product binds to vitamin D receptors → drug-receptor complex + RXR-α binds to DNA at vitamin D response elements → ↓keratinocyte proliferation/epidermal differentiation, ↓IL-2/IL-6/IFN-γ/GM-CSF, ↓NK-cell and cytotoxic T-cell activity, ↑involucrin/transglutaminase → enhanced cornified envelope formation

300
Q

MOA: Thalidomide

A

Inhibits TNF-α and IFN-γ, ↓IL-12 production, ↓helper T-cells, ↑suppressor T-cells, ↑IL-4/5 production, ↓PML chemotaxis, and ↓histamine/acetylcholine/prostaglandins

301
Q

Anticholinergic agent used orally or topically for hyperhidrosis which blocks acetylcholine’s effects on sweat glands

A

Glycopyrrolate

302
Q

Antichlolinergic agent which is approved for overactive bladder but can be used for hyperhidrosis

A

Oxybutinin

303
Q 
Phosphodiesterase inhibitor that:
↑erythrocyte/leukocyte deformability
↓platelet aggregation
↓TNF-α
↓neutrophil adhesion
A

Pentoxifylline

304
Q

Used for erythema nodosum leprosum (FDA approved), HIV-related disorders, lupus erythematosus, GVHD, prurigo nodularis, and neutrophilic dermatoses (e.g., Behcet’s disease)

A

Thalidomide

305
Q

MOA: Nicotinamide

A

Inhibits PARP-1 →↓NFκB transcription → ↓leukocyte chemotaxis; ↓lysosomal enzyme release; stabilizes leukocytes by inhibiting PDE → immunomodulation; ↓lymphocytic transformation/antibody production; ↓mast cell degranulation

306
Q

MOA: Colchicine

A

Binds tubulin dimers in leukocytes → mitotic arrest in metaphase and ↓chemotaxis

307
Q

Riminophenazine dye used for antibiotic (i.e., antimycobacterial, especially multibacillary leprosy and erythema nodosum leprosum) and antiinflammatory (e.g., SLE, pyoderma gangrenosum, erythema dyschromicum perstans, and discoid LE) purposes

A

Clofazimine

308
Q

Has the SE of reversible orange-brown skin and body fluid discoloration

A

Clofazimine

309
Q

CYP1A2 substrates

A

theophylline/caffeine, warfarin, and pimozide

310
Q

CYP1A2 inhibitors

A

fluoroquinolones, macrolides (e.g., erythromycin), and ketoconazole

311
Q

CYP1A2inducers

A

phenytoin, barbiturates, rifampin, and cigarette smoke

312
Q

CYP2C9 substrates

A

phenytoin, sulfonamides, warfarin, fluvastatin, and losartan

313
Q

CYP2C9 inhibitors

A

fluconazole and TMP-SMX

314
Q

CYP2C9 inducers

A

carbamazepine and rifampin

315
Q

CYP2D6 substrates

A

tricyclic antidepressants (e.g., doxepin and amitriptyline), metoprolol/propranolol, antidysrhythmics (e.g., encainide and propafenone), antipsychotics (e.g., clozapine and pimozide)

316
Q

CYP2D6 inhibitors

A

SSRIs (e.g., fluoxetine and sertraline), pimozide, and terbinafine

317
Q

CYP2D6 inducers

A

carbamazepine, phenytoin, and rifampin

318
Q

CYP3A4 substrates

A

warfarin, carbamazepine, doxepin, sertraline, antidysrhythmics (e.g., amiodarone, digoxin, and quinidine), CCBs (e.g., diltiazem and nifedipine), chemotherapy (e.g., doxorubicin, vinblastine, and cyclophosphamide), H1 antihistamines, HMG CoA reductase inhibitors (lovastatin and simvastatin), oral contraceptives/estrogens, cyclosporine, tacrolimus, corticosteroids, dapsone, pimozide, benzodiazepines, protease inhibitors, and colchicine

319
Q

CYP3A4 inhibitors

A

azole antifungals (e.g., ketoconazole and itraconazole), clarithromycin/erythromycin, metronidazole, protease inhibitors, SSRIs (e.g., sertraline), grapefruit juice, cimetidine, and CCBs

320
Q

CYP3A4 inducers

A

rifampin, griseofulvin, anticonvulsants (e.g., phenytoin and carbamazepine), dexamethasone, and St. John’s wort

Dermatology Board Review (2 decks)

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