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MSK, rheum, derm > derm drugs > Flashcards

derm drugs Flashcards

1
Q

what is the treatment for localized BCC? advanced/metastatic?

A

topical fluorouracil, imiquimod

vismodegib

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2
Q

in general, how does imiquimod work? what four ways does it accomplish that? how is it administered?

A

topical stimulates immune response to tumor

  1. activates TLR-7/8 to initiate TH1 response
  2. inhibits adenosine receptor
  3. activates NFkB: TNF-alpha and IL’s upregulated
  4. may directly inhibit hedgehog signaling
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3
Q

what are two adverse effects of imiquimod?

A

photosensitivity

compromises condoms and diaphragms

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4
Q

describe the mechanism of action of fluorouracil

A

pyrimidine analog, antimetabolite

inhibits thymidylate synthase

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5
Q

describe the action of vismodegib. how is it administered?

A

oral SMO inhibitor (inhibits hedgehog pathway)

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6
Q

whats the most significant side effect of vismodegib? what are two other adverse effects?

A
  • intra-uterine fetal death, male-mediated teratogenecity

- alopecia most common, GI toxicities

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7
Q

what are conventional therapies usually based on for BCC and SCC?

A

cisplatin

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8
Q

what conventional cytotoxic drugs are used for melanoma?

A

dacarbazine
temozolomide
lomustine
carmustine

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9
Q

what is the mechanism of action of aldesleukin? what are the results?

A

binds IL-2 receptor

  • proliferation of immune cells
  • also stimulates TRegs which can offset this
  • stimulates cytokine cascade: IFNs, ILs, TNFs
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10
Q

what are the contraindications for aldesleukin use?

A

cardiac, pulmonary or CNS disease/dysfunction

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11
Q

what are the side effects of aldesleukin?

A

hypotension, capillary leak, pulmonary congestion, renal failure

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12
Q

what is the effect of IFN-alpha2b administration?

A

stimulates immune response by increasing ability to activate CTL’s and NK cells to lyse tumor cells

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13
Q

what are contraindications for IFN-alpha2b use?

A

autoimmune disease, cardiac dysfunciton, depression

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14
Q

what are the three major adverse effects of IFN-alpha2b use?

A
  • worsening of autoimmune disease
  • elevated LFTs
  • pulmonary toxicity
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15
Q

what is the target of ipilumumab?

A

inhibits CTLA-4

-prevents dampening effect of CTLA-4 on CD80/86, thus increasing T cell stimulation

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16
Q

what is the target of pembolizumab?

A

inhibits PD1

-prevents PD-ligand from downregulating activity of T cells

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17
Q

what is the target of nivolumab?

A

inhibits PD1

-prevents PD-ligand from downregulating activity of T cells

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18
Q

what bad adverse effects are common to checkpoint inhibitors due to too much T cell activity?

A

dermatitis, inc. TEN

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19
Q

which checkpoint inhibitors have worse adverse effects? what are two of their BBW’s?

A

ipilumumab

-endocrinopathies and peripheral neuropathy

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20
Q

what is the target of dabrafenib?

A

BRAF V600E/K/D, wild-type BRAF

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21
Q

what is the target of sorafenib?

A

multiple kinases, inc. BRAF

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22
Q

what is the target of vemurafenib?

A

BRAF V600E

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23
Q

what is the target of trametinib?

A

MEK1 and MEK2

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24
Q

what is the mechanism of new skin tumors in treatment of melanoma with kinase inhibitors?

A

loss of inhibition by the inhibited pathway on an alternative oncogenic pathway allows proliferation of new clonal line of cells

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25
Q

what drugs used in melanoma should be avoided in pregnancy?

A

checkpoint inhibitors and kinase inhibitors

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26
Q

what drugs used in melanoma should be monitored with regular chest x-rays?

A

aldesleukin and IFN-alpha2b

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27
Q

what is the primary therapy for actinic keratoses? what else is administered and their action? how are each administered?

A

topical fluorouracil and imiquimod
topical diclofenac: NSAID, anti-inflammatory
topical trichloroacetic acid: chemical peel, cauterizes skin, keratin, tissue

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28
Q

what biologic drug in psoriasis treatment is contraindicated in heart failure? what other drugs have CV side effects?

A

infliximab

-adalimumab and rituximab

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29
Q

what psoriasis biologic drug may increase LFTs?

A

infliximab

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30
Q

what three psoriasis biologics may cause lupus-like syndrome?

A

infliximab
adalimumab
etanercept

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31
Q

what molecule do retinoids mimic? what is the difference between RXR and RAR receptors?

A

Vitamin A
RAR: affects cell differentiation and proliferation
RXR: induces apoptosis

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32
Q

what are five main beneficial effects of retinoid therapy in acne/psoriasis?

A
  • increased keratinocyte turnover
  • inhibit keratinization
  • decreases sebum production/decreased gland size
  • anti-inflammatory
  • antimicrobial against P. acnes
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33
Q

describe the adverse effects of retinoids that mimic Vit A intoxication

A

dry skin/mucous membranes, conjunctivits, reduced night vision, hair loss

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34
Q

what are four adverse effects of systemic retinoids?

A
  • teratogens
  • elevated serum lipids
  • elevated LFTs
  • blood dyscrasias
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35
Q

what are three adverse effects of topical retinoid use?

A
  • increased susceptibility to sunburn
  • burning, stinging
  • desquamation
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36
Q

how are steroids used in psoriasis? acne?

A

psoriasis: topical, not oral (risk of flare on discontinuation)
acne: topical, oral for moderate/severe (move to retinoids)

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37
Q

what topical therapy should NOT be applied to face?

A

fluorinated steroids

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38
Q

what are some adverse effects of topical steroid use?

A 
dermal atrophy: cigarette-paper skin
corticoid rosacea/perioral dermatitis
steroid acne
hypopigmentation
ACD
hypertrichosis
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39
Q

what drug similar to retinoids is used in psoriasis? what is its mechanism of action? how is it administered? what is its adverse effect? what is an alternative for sensitive/intertriginous areas of skin?

A

calcipotriene
binds RXR and DNA Vit D response elements
administered with steroids, b/c topical irritant
hypercalcemia/hypercalciuria with high doses
calcitriol (hormonally active Vit D)

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40
Q

adalimumab: target, disease

A

TNF-alpha

psoriasis

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41
Q

etanercept: target, disease

A

TNF-alpha

psoriasis

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42
Q

infliximab: target, disease

A

TNF-alpha

psoriasis

43
Q

alefacept: target, disease

A

CD2 on memory T cells, promotes apoptosis/prevents activation
psoriasis

44
Q

apremilast: target, disease, unique characteristic

A

increases cellular cAMP
psoriasis
given orally

45
Q

ustekinamab: target, disease

A

inhibits IL-12 and IL-23

psoriasis

46
Q

benzoyl peroxide: mechanism, disease

A

acne
converted to benzoic acid, free radical liberation lethal for P acnes
keratolytic activity: drying and desquamative

47
Q

what are the adverse effects of benzoyl peroxide? solution?

A

too much drying/peeling: erythema, irritation, contact dermatitis (may administer with corticosteroids)
bleaching of hair, clothes

48
Q

salicylic acid: mechanism, disease

A

acne, calluses, warts, psoriasis

keratolytic: desquamation

49
Q

what are two adverse effects of salicylic acid? what are possible contraindications and why?

A

teratogen, contact irritation

hepatic/renal failure increase risk of salicylism

50
Q

what is recommended for widespread tinea infection?

A

oral:

  • terbinafine
  • itraconazole, fluconazole
  • griseofulvin
  • ketoconazole
51
Q

what is recommended for localized tinea infection?

A

topical:

  • topical azoles
  • terbinafine
  • naftifine
  • ciclopirox
52
Q

what is recommended for onychomycosis?

A

oral:

  • terbinafine
  • griseofulvin
  • itraconazole and fluconazole
53
Q

what is recommended for topical onychomycosis?

A

topical:

  • ciclopirox
  • amorolfine
54
Q

what is the mechanism of action of amorolfine? how can it be administered?

A

depletes ergosterol

only topical

55
Q

how does griseofulvin work? how can it be administered?

A

binds tubulin, inhibits microtubule formation in mitosis

oral only

56
Q

how does ciclopirox work? how can it be administered?

A

unclear: acts in nucleus to affect RNA/DNA synthesis

topical only

57
Q

what is the mechanism of action of naftifine?

A

inhibits conversion of squalene epoxide to lanosterol by 2,3-squalene epoxidase

58
Q

how does terbinafine work?

A

blocks conversion of squalene to squalene epoxide

59
Q

which antifungals are CYP3A4 inducers/inhibitors?

A

inducers: griseofulvin
inhibitors: azoles

60
Q

which azole is the only non-CYP3A4 substrate? which is the only one renally eliminated?

A

posaconazole

fluconazole

61
Q

which antifungal inhibits adrenal steroid synthesis at high doses? what are the corresponding adverse effects?

A

ketoconazole

impotence, menstrual irregularity, gynecomastia, hot flashes

62
Q

which antifungal can have cross-sensitivity with beta-lactams?

A

griseofulvin

63
Q

what are four adverse effects of griseofulvin?

A
  • teratogen
  • hepatotoxicity
  • interferes with porphyrin metabolism
  • photosensitivity
64
Q

what does malathion treat? MOA? according adverse effects and treatment of that?

A

lice
acetylcholinesterase inhibition
excessive cholinergic stimulation on systemic ingestion, give atropine

65
Q

what is permethrin used for? MOA?

A

lice

inhibits voltage-gated Na channels

66
Q

what is ivermectin used for? MOA? adverse effects?

A

lice
binds glutamate receptor, increases permeability to Cl causes hyperpolarization of cells
binds GABA, disrupts CNS transmission on systemic ingestion

67
Q

what are two physical therapy treatments for lice?

A

benzyl alcohol

dimethicone: silicone polymer, lubricates hair for nit/lice removal; suffocates louse, inhibits water secretion

68
Q

what is the first-line treatment for hyperhidrosis and what is its mechanism?

A

aluminum chloride

short-term occlusion of eccrine and aprocrine sweat glands

69
Q

what is the general target for systemic therapy of hyperhidrosis? why?

A

anticholinergics: sweat glands are stimulated by M2 stimulation by Ach

70
Q

what is the second therapy for hyperhidrosis?

A

botulinum toxin: light chain cleaves SNAP25, preventing interaction with synaptobrevin and thus fusion of Ach vesicles with membrane

71
Q

what are used as third-line therapy of hyperhidrosis?

A

antimuscarinics: atropine, oxybutynin, glycopyrrolate and propantheline

72
Q

what else is used off label for hyperhidrosis? specifically for emotion-related sweating?

A

propanolol
clonidine (alpha2-agonist)
-block sympathetic tone centrally

73
Q

which antimuscarinics don’t cross BBB and don’t cause hallucinations/drowsiness?

A

glycopyrrolate and propantheline

74
Q

how does diltiazem work in hyperhidrosis?

A

blocks vesicle release by blocking pre-synaptic rise in Ca

75
Q

minoxidil: use, MOA,

A

topical hair growth drug

-unknown MOA: alters androgen metabolism?, stimulate hair follicle?

76
Q

what is eflornithine used for

A

reduce unwanted female facial hair

77
Q

finasteride: use, MOA

A

oral hair growth drug

testosterone analog: inhibits 5-alpha-reductase thus reducing scalp/serum levels of DHT

78
Q

Saw Palmetto is used for what? what should be avoided with it?

A

benign prostatic hyperplasia

finasteride

79
Q

what is the mechanism of action of hydroquinone, used in combo with fluocinolone and tretinoin?

A

inhibits oxidation of tyrosine and thus melanin synthesis

80
Q

methoxsalen: use, MOA

A

oral, topical pigmenting agent
UVA activates it, causes cross-linking of DNA and apoptosis
delayed erythema followed by melanization and thickening of s. corneum

81
Q

what is the treatment regimen for tuberculoid and leprematous leprosy?

A

tuberculous: dapsone, rifampin
leprematous: dapson, rifampin, clofazimine

82
Q

what is second line treatment for leprosy? when do you use it?

A

clarithromycin, minocycline or ofloxacin

-when clofazimine contraindicated

83
Q

what should be monitored in patients on leprosy treatment?

A

CBC/platelets, LFTs

84
Q

dapsone:use, MOA, major toxicity and its treatment

A

leprosy
folate antagonist
methemoglobinemia: cimetidine or omeprazole (H2 inhibitors with CYP inhibition acitivity)

85
Q

rifampin: use, MOA, major adverse effect

A

leprosy
inhibits RNA synthesis by inhibiting beta-subunit of DNA-dependent RNA polymerase
red-orange body fluids

86
Q

clofazimine: use, MOA, usefulness, main adverse effect

A

leprosy
binds mycobacterial guanine/cytosine in DNA
-anti-inflammatory to offset immunologically-mediated adverse effects of treating the infection
-stains skin/body fluids red to brownish-black

87
Q

which drugs in leprosy treatment don’t require dose adjusting for renal failure?

A

rifampin: hepatic metabolism/elimination
clofazimine: hepatic elimination without metabolism

88
Q

which leprosy drug is a CYP inducer? what is the significance of this?

A

rifampin, increase toxicity of dapsone

89
Q

what is thalidomide used for and why? MOA?

A

leprosy: treat immune-mediated adverse effects of treatment

inhibits NFkB and TNF produciton

90
Q

how is uncomplicated non-MRSA treated?

A
  1. acid-stable penicillins
  2. first gen cephalosporins
  3. clindamycin or 4. vancomycin if beta-lactam allergy
91
Q

how is CA-MRSA treated?

A
  • bactrim
  • minocycline, doxycycline
  • clindamycin
  • linezolid
92
Q

what should be avoided in the treatment of MRSA?

A

fluoroquinolones

93
Q

how should serious MRSA be treated?

A
  • vancomycin
  • linezolid (esp. for toxin synthesis)
  • daptomycin
94
Q

how should polymicrobial infections be treated?

A

MRSA drug +:

  • bactrim
  • imipenem-cilastin
  • meropenem
  • ceftaroline
95
Q

what is an adverse effect of acid-stable penicillins?

A

rarely, interstitial nephritis

96
Q

what are four adverse effects of vancomycin?

A
  • Red Man syndrome
  • hypotension
  • nephrotoxicity
  • ototoxicity
97
Q

which antibiotics cause discolored teeth, photosensitivity, teratogen?

A

tetracyclines

98
Q

what antibiotic causes serotonin syndrome and optic neuropathy?

99
Q

what antibiotic can cause rhabdomyolysis?

A

daptomycin

100
Q

what is given with cidofovir and why?

A

probenecid, minimize nephrotoxicity

101
Q

which antivirals require phosphorylation by virus?

A

acyclovir, ganciclovir and their prodrugs

102
Q

what is indicated for pox viruses?

103
Q

what is indicated for VZV?

A

acyclovir/valcyclovir

famciclovir for shingles

104
Q

what is indicated for HHV-6?

A

cidofovir
foscarnet
ganciclovir/valganciclovir

MSK, rheum, derm (6 decks)

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