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Drugs Flashcards

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Dermatology Board Prep flashcards
1
Q

Greatest risk factor for non-melanoma skin cancer?

Melanoma?

A 
UV radiation
UV radiation (gene damage?)
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2
Q

Effects of UV light on skin?

A

Immediate - erythema
Long-term - photo-aging, immunosuppression, carcinogenicity
*profound immune suppression (organ transplant) can increase skin cancer risk

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3
Q

Substantivity

A

Sunscreens ability to remain effective under exposure to water and sweat

  • Water resistint 40 min
  • Very water resistent 80 min
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4
Q

Imiquimod Mechanism

A

small molecule tumor-directed immune response initiator

  • direct activation of Toll-like receptor 7/8
  • involvement of adenosine receptor blockade
  • activation of NF-kappaB - upregulation of cytokines (TNF-alpha/interleukins)
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5
Q

Imiquimod Use

A

Basal Cell Carcinoma
Actinic Keratosis
HPV

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6
Q

Imiquimod Med/Toxicity

A

topical agent, limited systematization
-benzyl alcohol/paraben may be allerginic
-mild-moderate localized skin reactions common
Increased Photosensitivity
Contact compromise condom & diaphragm integrity

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7
Q

Vismodegib Mechanism

A

Oral SMO inhibitor

Lipophilic agent with extensive metabolism

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8
Q

Vismodegib Toxicity

A
  • Intrauterine fetal death
  • Male-mediated teratogenicity
  • Pregnancy-both male/female should use contraception
  • Can’t donate blood for 7 months
  • Alopecia
  • GI toxicities (N/V, diarrhea, vomiting)
  • Weight loss/fatigue
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9
Q

Vismodegib Use

A

Basal Cell Carcinoma

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10
Q

Aldesleukin Mechanism

A

Binds to cell surface IL-2 receptor
Induces proliferation/differentiation of B/T-cells, monocytes, macrophages, CTL (NK cells)
-IV or SC

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11
Q

Aldesleukin Toxicity

A

Contraindicated: CNS, cardiac, pulmonary, renal, hepatic disease/organ transplant

  • hypotension, S-TACH, peripheral vasodilation, SVT, decreased mental status, speech difficulties, cortical blindness, limb/gait ataxia, hallucinations, agitation, dyspnea, pulmonary congestion, rales, rhonchi, renal failure (capillary leak syndrome)
  • effects all systems
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12
Q

Aldesleukin Use

A

Melanoma

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13
Q

Interferon-alpha 2 beta Mechanism

A

IV or SC administered immunomodulator

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14
Q

Interferon Toxicity

A

Caution: Autoimmune Disease,Cardiac disease, depression (sucide), infection

  • flu-like symptoms, fever, fatigue
  • neutropenia, leukopenia, anemia, alopecia
  • increased hepatic enzymes (LFT)
  • cough/dyspnea, pneumonia, pneumonitis, infilatrates
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15
Q

Interferon Use

A

Melanoma

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16
Q

Ipilimumab Mechanism

A

Cytotoxic T-lymphocyte-associated antigen 4 (CTLA-4) recombinant antibody
-Bolsters antitumor response of immune system

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17
Q

Ipilimumab Toxicity

A

Severe/fatal immune-mediated adverse rxns due to T-cell activation and proliferation

  • dermatitis (toxic epidermal necrolysis)
  • most common:tiredness, diarrhea, itch, rash

Black Box: adrenal insufficiency, diarrhea, Guiliain-Barre syndrome, hepatitis, hyperthyroidism, hypopituitarism, hypothyroidism, myasthenia graivis, peripheral neuropathy, pregnancy, serious rash

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18
Q

Ipilimumab Use

A

Melanoma

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19
Q

Sorafenib Mechanism

A

Oral multi-kinase inhibitor (VEGF, PDGFR, KIT, Raf Kinase)

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20
Q

Sorafenib Toxicity

A 
Hepatic metabolism (LFT)
Hand/Foot
Rash/desquamation/anemia
Bone marrow suppression/neurtopenia (CBC)
Cat D
bleeding in GI, respiratory, brain
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21
Q

Sorafenib Use

A

Melanoma

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22
Q

Trametinib Mechanism

A

Oral reversible MEK inhibitor
Patients with BRAF V600E or V600K mutations
-can’t have received BRAF-inhibitors before

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23
Q

Trametinib Toxicity

A

Rapid skin toxicity (dermatitis, erythema, hand-foot) severe in 12%
GI:diarrhea, stomatitis, anemia
Decreased LVEF, require routine reassessment
Hypertension, hemorrhage
rare: cardiomyopathy, ILD, retinal pigment epithelial detachment

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24
Q

Trametinib Use

A

Melanoma

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25
Q

Vemurafenib Mechanism

A

Oral inhibitor of mutated BRAF (BRAFV600E)

  • genotyping required
  • can cause paradoxical ERK activation of mutated RAS-driven growth
  • resistance via alternative pathway activation
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26
Q

Vemurafenib Toxicity

A

*Hepatic metabolism, PGP/CYP interactions
Increased serum creatinine
QT prolongation and TP, ECG/ electrolyte monitoring
photosensitivity (avoid sun)
Cutaneous SCC in 1/4th
Severe dermatologic reaction (SJS)
Opthalmologic: uveitis, iritis, retinal vien occlusion

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27
Q

Vemurafenib Use

A

Melanoma

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28
Q

Carmustin Use

A

Melanoma; good b/c can cross blood brain barrier and treat brain metastases.

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29
Q

Carmustine Mechanism

A

Alkylationa and carbomoylation of amino acids

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30
Q

Carmustine Toxicity

A

Myelosuppression

CBC

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31
Q

Cisplatin Mechanism

A

Forms DNA intrastrand crosslinks

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32
Q

Cisplatin Toxicity

A

Renal tubular damage and failure

Myelosuppression

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33
Q

Cisplatin Use

A

Basal Cell Carcinoma

Squamous Cell Carcinoma

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34
Q

Cyclophosphamide Mechanism

A

Pro-drug of active alkylating moiety

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35
Q

Cyclophosphamide Toxicity

A

Myelosuppression

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36
Q

Cyclophosphamide Use

A

Basal Cell Carcinoma

37
Q

Dacarbaxine Mechanism

A

Pro-drug of active alkylating moiety

38
Q

Dacrbaxine Toxicity

A

Myelosuppression

39
Q

Dacrbaxine Use

A

Melenoma

40
Q

Trichloracetic Acid Mechanism

A

chemical peel: rapidly penetrates and cauterizeds skin, keratin, other tissue

41
Q

Tirchloracetic Acid Toxicity

A

burning, inflammation, local tenderness

42
Q

Tichloracetic Acid Use

A

Actinic Keratosis

43
Q

Acyclovir Mechanism

A

Competitively inhibits viral DNA polymerase; competes with deoxyguanosine triphosphate for incorporation into viral DNA

44
Q

Acyclovir Toxicity

A
  • O-P
  • Cross-hyper-sensitivity
  • neurotoxicity incl seizures
  • Little metabolism, renal elimination, dose adjustment in renal dysfunction or renal failure
45
Q

Acyclovir Use

A

Varicella zoster

Varicella chicken pox

46
Q

Famciclovir Mechanism

A

Competitively inhibits viral DNA polymerase; competes with deoxyguanosine triphosphate for incorporation into viral DNA

47
Q

Famciclovir Toxicity

A

-O-P
-Cross-hyper-sensitivity
Little metabolism, renal elimination, dose adjustment in renal dysfunction or renal failure

48
Q

Famciclovir Use

A

Varicella zoster

HHV-8

49
Q

Ganciclovir Mechanism

A

Competitively inhibits viral DNA polymerase; competes with deoxyguanosine triphosphate for incorporation into viral DNA

50
Q

Ganciclovir Toxicity

A

-O-P
-Cross-hyper-sensitivity
Little metabolism, renal elimination, dose adjustment in renal dysfunction or renal failure
-anemia, leukopenia, neutropenia, pancytopenia, thrombocytopenia, teratogen

51
Q

Ganciclovir Use

A

HHV-6,8

HHV-8 infection

52
Q

Valacyclovir Mechanism

A

Competitively inhibits viral DNA polymerase; competes with deoxyguanosine triphosphate for incorporation into viral DNA

53
Q

Valacyclovir Toxicity

A

-nephrotoxicity - monitor creatinine and urinary protein; probenecid hypersensitivity
Little metabolism, renal elimination, dose adjustment in renal dysfunction or renal failure

54
Q

Valacyclovir Use

A

Varicella zoster
Varicella chicken pox
HHV-8

55
Q

Cidofovir Mechanism

A

competitively inhibits viral DNA polymerase; competes with deoxyCYTOSINE triphosphate for incorpation into viral DNA

56
Q

Cidofovir Toxicity

A
  • nephrotoxicity - monitor creatinine and urinary protein; probenecid hypersensitivity
  • Little metabolism, renal elimination, dose adjustment in renal dysfunction or renal failure
57
Q

Cidofovir Use

A

Pox family

HHV-6,7,8

58
Q

Forscarnet Mechanism

A

selectively inhibits the viral specific DNA polymerases and reverse transcriptases at pyrophosphate-binding site; blocks chain elongation

59
Q

Forscarnet Toxicity

A
  • electrolyte imbalance - chelates Ca2+ ions

- Little metabolism, renal elimination, dose adjustment in renal dysfunction or renal failure

60
Q

Forscarnet Use

A

HHV-6

61
Q

Malathion Mechanism

A

Ovide: topically applied organophosphate insecticide

  • in louse, metabolized to malaoxon which inhibits acetylcholinesterase and causes neuronal hyperstimulation and paralysis
  • in human, malathion is converted to inactive metabolites and excreted by kidney
62
Q

Malathion Toxicity

A

Safe, not associated with significant topical cholinergic activity, but oral/pulmonary ingestion: increased GI peristalsis; miosis, decreased ocular accommodation/pain, rhinorrhea, chest tightness/wheezing, increased lacrimation, salivation, sweating, bradycardia, hypotension, confusion, convulsions, weakness, muscular paralysis, respiratory paralysis
Treatment is atropine & pralidoxime

63
Q

Premethrin Mechanism

A

Synthetic pyrethrin - cause hyper-excitability and paralysis by binding voltage-gated sodium channels.

64
Q

Premethrin Toxicity

A

Safe: human voltage-gated channels are not susceptible
Rare: asthma exacerbation in patients allergic to ragweed
-Systemic drug is inactivated by ester hydrolysis no effects
-Efficacy decreased b/c knock-down resistance (kdr) mutations of louse sodium channels

65
Q

Lindane Mechanism

A

Disfavored: shampoo or lotion, only patients who can’t use first line treatment
-when systemic, its a CNS stimulatent , similare effects to DDT (block GABA action)

66
Q

Lindane Toxicity

A

-Seizures and deaths
Black Box: skin disease/conditions/neonatal prematurity will increase drug systematization
not for patients with uncontrolled seizure disorders

67
Q

Lindane Use

A

Lice

68
Q

Premethrin Use

A

Lice

69
Q

Ivermectin Mechanism

A
  • Pediculicidal (must dose 3 at 1 week intervals)
  • orally and topically
  • causes hyperexcitability and paralysis by binding selectively and with high affinity to glutamate-gated chloride ion channels present in invertebrate nerve and muscle cells
  • no resistance
70
Q

Ivermectin Toxicity

A

Elevate liver transaminases & Cross BBB in children only

worsen bronchial asthma

71
Q

Minoxidil Mechanism

A

(Rogaine) Topical-potent oral vasodilator
-mechanism is unknown:activate hair follicle directly or stimulate follicular microcirculation / may alter local androgen metabolism

72
Q

Minoxidil Toxicity

A

Percutaneous abs poor, systemic effects unlikely

  • skin abrasions/irritations (sunburn, psoriasis, excoriations) increase absorption
  • must continue drug to get effect
73
Q

Finasteride Mechanism

A

Oral (1mg for hair loss, 5mg for BPH)
Testosterone analog: blocks 5-alpha-reductase activity
Decrease scalp and serum DHT conc. - no effect on cortisol, estradiol, prolactin, TSH, thyroxine, cholesterol, PTH-axis

74
Q

FInasteride Toxicity

A

Loss of libido, sexual dysfunction, feminization

palmetto/finasteride similar so don’t use together

75
Q

Eflornithine Mechanism

A

Topical to reduce unwanted female facial hair

  • related to decrease ornithine decarboxylase
  • decrease cell division & differentiation
  • produces typanostatic action, used against sleeping sickness

-limited absorption, not depilatroy, use chin/face, not eyes mucous membranes

76
Q

Eflornithine Toxicity

A

Skin effects rarely: most mild, resolve without treatment or discontination

77
Q

Methoxsalen Mechanism

A

Oral and topical pigmenting agent

  • activated by exposure to UVA 9320-400nm (peak photosensitivity within 1-2 hours, persist for days)
  • conjugation/cross-linking of DNA (Cell death)
78
Q

Methoxsalen: what happens, uses?

A
  • Delayed erythema followed over several weeks by increased epidermal melanization and thickening of stratum corneum
  • Vitiligo, symptomatic relief of psoriasis, treatment of cutaneous T-cell lymphoma (mycosis fungoides), alopecia areata, inflammatroy dermatoses, eczema, lichen planus
  • extent of topical abs is not known
79
Q

Methoxsalen Mechanism

A

Oral and topical pigmenting agent

  • activated by exposure to UVA 9320-400nm (peak photosensitivity within 1-2 hours, persist for days)
  • conjugation/cross-linking of DNA (Cell death)
80
Q

Methoxsalen: what happens, uses?

A
  • Delayed erythema followed over several weeks by increased epidermal melanization and thickening of stratum corneum
  • Vitiligo, symptomatic relief of psoriasis, treatment of cutaneous T-cell lymphoma (mycosis fungoides), alopecia areata, inflammatroy dermatoses, eczema, lichen planus
  • extent of topical abs is not known
81
Q

Daptomycin Mechanism

A
  • cyclic lipopeptide abx
  • rapidly disrupts bacterial cell membranes (depolarization and loss of membrane potential and K+ efflux)
  • bactericidal-reduce resistance (rare, no mech)
82
Q

Daptomycin Pharm

A

IV once a day (muscle toxicity in MI injection)
give after hemodialysis
Metabolism - 90% albumin bound
Elimination - renal (dose adjust for renal disease)

83
Q

Daptomycin Toxicity

A

Muscle pain/weakness
-monitor for development due to serum creatine phosphokinase elevations
Drug interactions - none with cyp P450, use cautions with co-administration of statins

84
Q

Daptomycin Uses

A

Aerobin gram +

  • multi-drug reisitant staph, strep, enterococcus (MRSA VRSA)
  • Complicated skin/soft tissue infections
  • MSSA MRSA bactermia (right endocarditis)
  • DON’T GIVE SURFACTANT*
85
Q

Linezolid (Oxazolidinones)

Mechanism

A

Inhibits protein systhesis by binding to 23S RNA on 50 ribosomal subunit

  • Bacteriostatic -staph/enterococci
  • Bactericidal-strep
86
Q

Linezolid Resistance

A
  • Point mutation in 23S RNA
  • No cross resistance with other classes
  • Emerging with enterococcal and s. aureus
87
Q

Linezolid Use

A

MRSA, enterococcus, S. aureus, S. epi, serious VRE infections

88
Q

Linezolid Pharm

A

-Oral/Parenteral use
-100% oral abs
-Food delays abs
-Met. by non-enzymatic oxidation (give 2 inactive metabolites)
-Elim: renal/non-renal
no CYP450
-more dose after hemodialysis

89
Q

Linezolid Toxicity

A

Well tolerated
diarrhea, headache, nausea/vomiting, myelosuppression if more than 2 weeks
Oral has aspartame (warn those with phenylketonuria)
*Non-selective inhibitor of monoamine oxidase, caution if coadminister with drugs metabolized by MAO
hypertension from decreased breakdown of tyramine absorbed from diet

Dermatology (9 decks)

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