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Pharm Exam 3 > Treatment of Dermatological dz > Flashcards

Treatment of Dermatological dz Flashcards

1
Q

Classification of acne: Mild

A

Few-several papules and pustules. No nodules

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2
Q

Classification of acne: Moderate

A

Several papillose or pusutules. Few Nodules

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3
Q

Classification of acne: Severe

A

Many papules and pustules. Several Nodules

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4
Q

Tx: for Mild Acne 1st line

A

Topical retinoid. consider adding antimicrobial (benzoyl peroxide-Keratolytic)

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5
Q

Tx: for Mild Ance Alternative to 1st line

A

Salicylic acid (topical keratolytic)

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6
Q

Tx: for Mild Acne Maintenance

A

Topical retinoid

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7
Q

Tx; for moderate acne 1st line

A

Topical retinoid PLUS oral abx w/ or w/o benzoyl peroxide. (keratolytic)

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8
Q

Tx: for Moderate Acne Alternative

A

Topical ABX instead of PO

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9
Q

Tx for Moderate Acne Maintenance

A

Topical retinoid w/ or w/o benzoyl peroxide

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10
Q

Tx: for Severe Acne 1st line

A

Oral isotrenoin

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11
Q

Tx: for Severe Acne Alternative

A

Topical retinoid + po ABX + benzoyl peroxide (keratolytic)

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12
Q

Tx: for Severe Acne Maintenance

A

Topical retinoid w/or w/o benzoyl peroxide (keratolytic)

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13
Q

How are retinoids different from keratolytics?

A

Retinoids prevent formation of comedones, Keratolytics prevent the formation of comedones as well but also contribute to the rapid shedding of skin.

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14
Q

What medication form is preferred in the tx of urticaria?

A

PO is usually preferred

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15
Q

What is the difference between second generation and 1st generation antihistamines?

A

2nd gen is effective with no/minimal drowsiness (don’t enter CNS). 1st gen typically results in drowsiness (does enter CNS)

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16
Q

What are the pathogens of impetigo?

A

S. aureus, and S. pyogenes (appearance=honey crusted lesions)

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17
Q

Where might HSV 1 and 2 occur?

A

Face, mouth, genital, eyes, brain etc.

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18
Q

What are the characteristics of HSV 1/2

A

Painful pruritic vasicular lesions with periods of remission.

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19
Q

What dosage form is used for mild HSV lesions?

A

Topical

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20
Q

What dosage form is used for Genital, oral, sever or suppression HSV?

A

Oral with prophylaxis of breakouts

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21
Q

What is another name for viral Herpes Zoster?

A

Shingles

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22
Q

What virus causes Herpes zoster?

A

Recurrence of varicella zoster

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23
Q

What characterizes Herpes zozter?

A

Painful, vesicular lesions, localized along dermatome

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24
Q

What are the 5 main layers of skin?

A
  1. Cornified (stratum corneum)
  2. Clear/translucent (lucidem)
  3. Granular cell layer(granulosum)
  4. sinus (spinosum)
  5. Basal Layer (basale)
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25
Q

How many days does it take for a cell to fully keratinize to outer layer?

A

30

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26
Q

What is the most moisturizing dosage form?

A

Ointments

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27
Q

What is the most drying dosage form?

A

tinctures (second most drying is wet dressings)

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28
Q

If the problem is dry (lchenifications, scaling) use _____?

A

Wet–ointments

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29
Q

If the problem is wet (weeping, oozing, vesicular) use______

A

Dry–Tinctures and wet dressings

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30
Q

On hairy areas (including scalp) use _____?

A

tinctures, Aerosoles, lotions gels

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31
Q

If there is a cosmetic consideration for an area use____?

A

creams

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32
Q

What is the mainstay of tx for acute/chronic dermatitis?

A

Corticosteroids

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33
Q

What strength dose would be used for eczema, irritant dermatitis, seborrhea, or atopic term?

A

Low/medium

34
Q

What strength dose is used in psoriasis, lichen planus, allergic contact term?

35
Q

What is the MOA of corticosteroids?

A

Non specific anti-inflammatory. Decreases migration of PMN’s and fibroblasts. Reverses capillary permeability, controls rate of protein synth, and stabilizes lysosomes.

36
Q

Ultra High potency steroids should not be used for >____ weeks?

A

> 3 weeks.

37
Q

Low-High potency steroids should not be used for >_____?

38
Q

P’Kinetics for Corticosteroids: ADMEH

A 
A-minimal systemic (depends on dose, area, form)
D: Highly protein boudn
M: Hepatic
E: Urine
Half life: 6.5hrs
39
Q

Common ADE for Corticosteroids?

A

Cutaneous atrophy. Telangiectasia and purpura. Resolves (after months). Also-striae, acne, refractory rosacea, Adrenal suppression with increased dose/duration and in children.

40
Q

DI for Corticosteroids?

A

none if topical

41
Q

CI for corticosteroids?

A

systemic fungal infection, hypersensitivyt

42
Q

Caution for corticosteroids?

A

Pregnancy (Cat. C), Children < 12yo, ?fungal if sx worsen.

43
Q

Fingertip method?

A

Half fingertip=area of whole hand

Whole fingertip = 0.5g

44
Q

What is the etiology of Psoriasis?

A

Psoriatic plaques via hyper proliferation of keratinocytes, and inflammation (neutrophils and T-cells)

45
Q

What is considered mild-moderate psoriasis?

46
Q

What is considered Moderate-severe psoriasis?

A

> 5% or hand, feet, face or genitals

47
Q

When are corticosteroids used?

A

Mainly used in mild disease as first line. Cacipotriene + corticosteroid is more effective than mono therapy.

48
Q

What follow up is necessary for non-biologics?

A

Baseline and follow up CBC, BUN pregnancy tests etc.

49
Q

What drugs used for psoriasis are most concerning for drug interactions?

A

Methotrexate and cyclosporine.

50
Q

What is the back box warning for biologics used in psoriasis?

A

Concern for serious infections: obtain negative PPD before initiating, Malignancies have been reported.

51
Q

What form of UV is approved for use in psoriasis?

52
Q

What is the case of acne?

A
  • Seabeous gland hyperplasia-excessive sebum production.
  • Hyperkeratinization of hair follicle.
  • colonization of Propionbacterium acnes (elicits inflammatory response).
  • Formation of comedones
53
Q

MOA for topical retinoids

A
  • Prevents formation of comedones and inflammatory lesions.
  • doesn’t contribute to bacterial resistance
  • no concernes for long term use
  • negligible systemic absorption.
54
Q

ADE for topical retinoids?

A

peeling, redness, dryness, burning, pruritus

  • Avoid use in pregnancy,
  • use daily moisturizer w/ built in sunscreen
55
Q

MOA for topical Keratinolytics

A

Rapid Shedding of epidermis - prevents “clogging” and formation of comedones
-Benzoyl peroxide oxicizes bacteria, effective topical antimicrobial. not associated with resistance.

56
Q

ADE of Keratinolytics

A

Akin irritation, contact derm, dryness, erythema, peeling, stinging

57
Q

MOA for antimicrobial tx. for acne

A

Decerases bacterial load, reduces inflammation, PO reserved for severe. Combined with benzoyl peroxide (clindamycin can be compounded)

58
Q

Safety considerations for general antimicrobials?

A

Resistance: ideal length for PO=3 mos. Avoid combining topical w/ oral, and avoid switching without justification.

59
Q

contraindications for tetracycline?

A

P. acnes is resistant to tetracycline.
T-cycline is also absolutely contraindicated in pregnant women and children. Do not use t-cycline after exp. date (potency increases).

60
Q

safety considerations for Clindamycin?

A

increased risk of C. Diff

61
Q

Safety considerations for E-mycin?

A

resistance may be increasing

62
Q

Safety considerations for Dapsone?

A

severe hemolytic anemia (not yet related to topical). Test for G6PD deficiency.

63
Q

MOA for oral isotretinoin?

A

Vitamin A deriviative, Reduces 4 pathogenic factors of acne:

  • sebum production
  • comedone formation (keratinization)
  • P. acnes coloniziation
  • inflammation
64
Q

ADE isotretinoin?

A

Excessive drying burning and inflammation of skin, inflammation of lips (90%), Dyslipidemia, Arthralgias/msk pain.

65
Q

Absolute CI for isotretinoin

A

Pregnancy (

66
Q

What are REMS requirements?

A

iPLEDGE program. 2 forms of BC, monthly pregnancy test, prescriber, pt and pharm must all be registered.

67
Q

What is etiology of urticaria

A

Release of histamine

68
Q

What meds can be used in tx. of Impetigo?

A

Topical usually sufficient: single ointment (effective against MRSA), Double and triple, Neomycin is missing in double.
Oral (if needed): dicloxcilin, cephalexin, e-mycin, augmentin

69
Q

Tinea pedis

A

athlete’s foot

70
Q

Yeast infection / thrush

A

Vulvovaginal candidiasis/ oral candidiasis

71
Q

Tinea cruris

72
Q

tinea corporis / tinea capitis

73
Q

Onychomycosis

74
Q

MOA Imidazole, triazole:

A

Inhibit conversion of lanosterol to ergosterol via CYP 450 system-required in fungal cell wall, Also human steroid synth (careful with long term use)

75
Q

MOA allylamines

A

Inhibit squalene epoxidase-ergosterol synth Less effective on human steroid synthesis.

76
Q

MOA Griseofulvin

A

Binds to fungal microtubules and inhibits mitosis

77
Q

MOA Ciclopirox

A

not well understood, blocks cell membrane transport, depletes cell of substrates (AA) and ions (potassium)

78
Q

Safety with Azoles (imidazole triazole)

A

CYP P450 DI. Mainly local ADE, PT education to reduce risk of transmission.

79
Q

What is oral dosing dependent upon in tx of HSV

A
  • first episode of genital herpes
  • recurrence of g.h.
  • suppressive tx. of g.h.
  • tx of herpes zoster
80
Q

ADE for topical antivirals

81
Q

ADE for oral antivirals?

A

GI irritation, elevated LFT’s, Disorientation, hallucinations,
DI-nephrotoxic drugs.

Pharm Exam 3 (4 decks)

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