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Dermatology Board Prep > DERM (12) Medical Therapy > Antimicrobials > Flashcards

Antimicrobials Flashcards

1
Q

What is the mechanism of bacitracin?

A

Binds to C55-prenol pyrophosphatase which leads to disruption of bacterial cell wall peptidoglycan synthesis. C55-prenol pyrophosphatase is the molecule that releases muropeptide subunits of the peptidoglycan membrane and it inhibits teichoic acid synthesis

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2
Q

What is the spectrum of bacitracin?

A

Has activity against Neisseria and gram positives but poor activity against gram negatives

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3
Q

Most common side effects of bacitracin?

A

Allergic contact dermatitis (especially in patients with stasis dermatitis or ulcer from stasis)

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4
Q

Where does bacitracin come from?

A

Bacillus subtilis

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5
Q

Where does polymyxin B come from?

A

Made by bacillus polymyxa and bacillus subtilis

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6
Q

What is the mechanism of action of polymyxin B?

A

Increased cell membrane permeability via detergent-like phospholipid interaction

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7
Q

Spectrum of polymyxin B?

A

Activity against gram negatives including pseudomonas (GN bacteria have the phospholipid membrane on the outside).

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8
Q

Where does neomycin come from?

A

Aminoglycoside made by streptomyces fadiae

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9
Q

What is the mechanism of action for neomycin?

A

Binds the 30s subunit of bacterial ribosomal RNA which leads to decreased protein synthesis

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10
Q

What is the spectrum of neomycin?

A

Activity against gram-negative and positive

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11
Q

What antibiotic does neomycin co-react with?

A

Bacitracin

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12
Q

Most common side effects of neomycin?

A

Common contact allergy, allergy more common in people with stasis derm or stasis ulcers. There is a theoretical possibility of ototoxicity/nephrotoxicity but very rare

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13
Q

What is the pregnancy safety of neomycin?

A

Pregnancy category D

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14
Q

Where does mupirocin come from?

A

pseudomonas fluorescens

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15
Q

What is the mechanism of mupirocin?

A

Binds to bacterial isoluecyl tRNA synthetase which leads to decreased RNA/protein synthesis

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16
Q

Spectrum of mupirocin?

A

Activity against MRSA and strep (resistance has been reported). It is not effective against pseudomonas

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17
Q

Where does retapamulin come from?

A

Clitopilus scyhpoides

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18
Q

What is the mechanism of retapamulin?

A

Binds to L3 protein on 50s subunit of the bacterial ribosome which leads to decreased protein synthesis

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19
Q

Spectrum of retapamulin?

A

MRSA, GBS, and anaerobes

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20
Q

Side effects of retapamulin?

A

Contact dermatitis

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21
Q

What is the primary indication for retapamulin?

A

Retapamulin (Altabax) 1% ointment is approved for impetigo (should be older than 9 months)

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22
Q

Where does gentamicin come from?

A

M. purpurea

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23
Q

What is the mechanism of gentamycin?

A

It is an aminoglycoside, so like neomycin, it binds the bacterial 30s ribosomal subunit and decreases protein synthesis

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24
Q

What is the spectrum of gentamicin?

A

Activity against gram-positive and gram negatives including pseudomonas

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25
Q

What is the mechanism of silver sulfadiazine?

A

Binds to bacterial DNA and leads to decreased DNA synthesis and disrupts cell walls and membranes

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26
Q

What is the spectrum of silver sulfadiazine?

A

Activity against gram-positive and gram-negative including MRSA and P. aeruginosa

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27
Q

Where is silver sulfadiazene mostly used?

A

Burn wounds

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28
Q

What are the side effects of silver sulfadiazene?

A

Can cross-react with sulfonamides, rare side effects include hemolysis from G6PD patients, methemoglobinemia, renal insufficiency, argyria, leukopenia, and unmasking porphyria

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29
Q

What is Iiodoquinol?

A

Quinolone-derivative with high iodine concentration

  • Has activity against GP and GN and dermatophytes/yeasts
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30
Q

What is the mechanism of benzoyl peroxide?

A

Broad-spectrum antibacterial oxidizing agent (good against p. acnes)

  • Also has keratolytic properties
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31
Q

Side effects of benzoyl peroxide?

A

Can oxidize and neutralize certain formulations of tretinoin, local irritation, can bleach hair/fabric

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32
Q

What is the mechanism of metronidazole?

A

Nitroimidazole that disrupts DNA synthesis

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33
Q

What is the spectrum of metronidazole?

A

Protozoa and anaerobes; not active against p. acnes, staphylococcus, strep, fungi, or Demodex

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34
Q

What is the mechanism of azelaic acid?

A

Dicarboxylic acid that disrupts mitochondrial respiration, decreased DNA synthesis (especially in abnormal melanocytes), and decreased reactive oxygen species production by PMN’s

  • Also inhibits tyrosinase –> decreased pigmentation
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35
Q

What is the spectrum of action for azelaic acid?

A

Activity against p. acnes; used for acne and rosacea (including perioral dermatitis)

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36
Q

Uses for azelaic acid?

A

Acne and hyperpigmentation disorders (melasma and PIH)

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37
Q

What is the action of sodium sulfacetamide?

A

Inhibits bacterial dihydropteroate synthetase (which prevents the conversion of PABA to folic acid) and leads to decreased nucleic acid/protein

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38
Q

What conditions can sodium sulfacetamide be used for?

A

Acne, rosacea, as a combination agent with or without precipitated sulfur

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39
Q

What is the mechanism of action of penicillins?

A

B-lactam ring binds to bacterial enzyme DD-transpeptidase which inhibits the formation of peptidoglycan cross-links in the bacterial cell wall and leads to cell wall breakdown

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40
Q

What are the first generation penicillins and what are they good for?

A

Dicloxacillin, oxacillin

  • good for gram-positive cocci like MSSA
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41
Q

What are the second generation penicillins and what are they good for?

A

Aminopenicillins (ampicillin and amoxicillin)

GN bacilli and GP cocci

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42
Q

What occurs when ampicillin is given in patients with mononucleosis and what is the timeline?

A

Ampicillin + mononucleosis or allopurinol or lymphocytic leukemia leads to a generalized morbilliform itchy eruption starting one week after antibiotic initiation

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43
Q

What are the 3rd and 4th generation penicillins and what are their uses?

A

Carboxypenicillins (carbenicillin and ureidopenicillins (piperacillin)

  • These have activity against pseudomonas
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44
Q

What is the mechanism of the beta-lactamase inhibitors?

A

These inhibit the beta-lactamase which prevents the breakdown of the beta-lactam ring and allows for the antibiotic to function.

  • Important for infections with MSSA, Haemophilus, Klebsiella, e. coli, proteus, and b fragilis infections
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45
Q

What is the treatment of choice for bites?

A

For animal or human bites, the tx of choice is often amoxicillin-clavulanate, think these combinations for polymicrobial infections.

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46
Q

What side effects can be seen with ticarcillin/piperacillin?

A

Hypernatremia, increased LFT’s, neutropenia, and bleeding time

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47
Q

What is the most common cause of drug-induced liver injury aside from acetaminophen?

A

Augmentin/amoxicillin + clavulanate

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48
Q

What are the symptoms of cholestatic injury (drug-induced liver injury) from Augmentin/amoxicillin + clavulanate

A

Fatigue, loss of appetite, itching, jaundice

PMID: 27003146

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49
Q

What percentage of patients with a cephalosporin allergy are penicillin-allergic?

A

2%

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50
Q

Side effects of penicillins?

A

Hypersensitivity reactions, GI side effects (common), hematology side effects, Shelley’s shoreline nails (dicloxacillin, severe expression of Beau’s lines), onychomadesis/photo-onycholysis (cloxacillin), interstitial nephritis (very rare), AGEP

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51
Q

What are some indications of penicillin-type medications in dermatology?

A

Streptococci infections, and MSSA skin infections

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52
Q

How long should streptococci infections be treated to prevent rheumatic fever?

A

10 days

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53
Q

What is the mechanism of action of cephalosporins?

A

A similar mechanism to penicillins –> beta-lactam ring that inhibits cell wall synthesis but also has 6-membered dihydrothiazine ring

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54
Q

What are some first-generation cephalosporins? and what are they used for?

A

Cefadroxil, cephalexin (good for MSSA but not MRSA or S. pneumonia)

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55
Q

What are some second-generation cephalosporins? and what are they used for?

A

Cefaclor and cefuroxime

  • Good for H. influenza, M. Catarrhalis, N. meningitides, and N. gonorrhoeae (increased GN spectrum)
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56
Q

What are some third-generation cephalosporins? and what are they used for?

A

Cefixime, cefdinir, cefotaxime, ceftazidime, cefpodoxime, and ceftriaxone

  • Good gram-negative spectrum but the decreased gram-positive spectrum
  • Good for soft tissue abscesses and diabetic foot ulcers, pneumonia etc.
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57
Q

What third-generation cephalosporin has some action against P. aeruginous?

A

Ceftazidime

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58
Q

What cephalosporins are good against B. fragilis?

A

Cefoxitin and cefotetan

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59
Q

What is a fourth-generation cephalosporin? and what is it used for?

A

Cefepime

  • Broad coverage: MSSA, nonenterococcal streptococci, and GN’s including P. aeruginosa
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60
Q

What is a fifth-generation cephalosporin? and what is it used for?

A

Ceftaroline

  • MRSA, VISA, hVISA, VRSA, MSSA, and CNS
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61
Q

Side effects of cephalosporins?

A

GI sx’s (most common), hypersensitivity reactions (cross-react / penicillins allergic pt 5-10% of the time), candida infections, hematologic SE’s (hemolytic anemia with cefotetan most common), increased LFT’s, serum sickness-like reaction (cefaclor), Jarisch-Herxheimer reaction (in Lyme disease patients receiving cefuroxime axetil), disulfiram-like reaction (cefotetan) and AGEP

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62
Q

What is the mechanism of vancomycin?

A

Tricyclic glycopeptide that inhibits bacterial cell wall synthesis

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63
Q

The spectrum of vancomycin?

A

Only gram positives, in derm most often used for MRSA infections

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64
Q

Side effects of vancomycin?

A

Red man syndrome, LABD (most common cause of drug-induced LABD), hearing loss (patients with renal failure), and nephrotoxicity (especially if given with aminoglycosides)

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65
Q

What is the mechanism of LABD from vancomycin?

A

Formation of IgA antibodies to LAD285 and IgA/IgG to BP180 [different than non-drug induced which is often LAD-1 which is a 120kd size protein cleaved from BPAG2, and LABD97 which is a 97 kd size protein cleaved from LAD-1)]

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66
Q

What is the mechanism of macrolides?

A

Inhibits 50s subunit of bacterial ribosome –> decreased protein synthesis; also has anti-inflammatory properties

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67
Q

What is the principle spectrum of macrolides?

A

Good for gram positives (except MRSA and enterococcus) used for skin and soft tissue infections in dermatology

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68
Q

What are the 3 main macrolides used?

A

Erythromycin, azithromycin, clarithromycin

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69
Q

What effect can erythromycin have on other medications?

A

Potent CYP3A4 inhibitor: increases plasma levels of warfarin, mexiletine, theophylline and statins

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70
Q

What are some indications for erythromycin?

A

Lyme disease, erythrasma/pitted keratolysis, anthrax, erysipeloid, chancroid, and LGV

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71
Q

Side effects of erythromycin?

A

GI side effects (most common and dose-limiting), ototoxicity/hearing loss, QT prolongation, hypersensitivity reactions, erythromycin estolate in pregnancy may lead to hepatotoxicity (intrahepatic cholestasis in mother, possible association of cardiovascular malforation and pyloric stenosis if fetus exposed in uterus

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72
Q

Indications for azithromycin?

A

Better than erythromycin for gram positives, often used as a second-line prophylactic antibiotic in derm surgy for PCN allergic patients.

  • Does have some GN coverage: e coli, gonorrhea, h. ducreyi, and trachomatis

activity against P. multocida (animal bites), atypical mycobacteria T. palidum, B. Burgdorferi, T. Gondii and K. Granulomatis (granuloma inguinale)

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73
Q

Side effects for azithromycin?

A

deafness, angioedema, photosensitivity, hypersensitivity, and contact derm; antiacids can decrease absorption

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74
Q

Side effects for clarithromycin?

A

metallic/bitter taste, fixed drug eruptions, LCV, and hypersensitivity reactions; contraindicated in renal dysfunction

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75
Q

What is the mechanism of fluoroquinolones?

A

Inhibits DNA gyrase (bacterial topoisomerase II) and +/- topoisomerase IV which leads to DNA fragmentation

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76
Q

What are some first and second-generation fluoroquinolones? what is the difference in their mechanism, and what is their spectrum?

A

Ciprofloxacin, ofloxacin, nalidixic acid

  • Only targets DNA gyrase (topoisomerase II)
  • Only effective against GN
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77
Q

What are some third and 4th-generation fluoroquinolones? what is the difference in their mechanism, and what is their spectrum?

A

Levofloxacin, moxifloxacin, sparfloxacin, gatifloxacin

  • Target both topoisomerase forms IV>II
  • These have improved GP coverage, decreased resistance, and slightly less efficacy against GN’s
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78
Q

What is the treatment of choice for anthrax?

A

Ciprofloxacin

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79
Q

What are some indications for fluoroquinilones?

A

Good for P. aeruginosa, may be used for some GP’s like S. aureus and GBS, mycobacterial infections

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80
Q

What is the excretion of fluoroquinolones?

A

Excreted renally except for moxifloxacin

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81
Q

What are the most common side effects of fluoroquinolones?

A

GI sx’s (most common), DNS (headache, dizziness, seizures, psychosis, and depression), tendinitis/tendon rupture, hypersensitivity, and photosensitivity/photo-onycholysis (lomefloxacin, enoxacin, and sparfloxacin >>ciprofloxacin > norfloxacin> ofloxacin>>levofloxacin

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82
Q

What fluoroquinolones are not associated with phototoxicity?

A

Levofloxacin

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83
Q

What portion of the UV spectrum triggers the fluroquinolone-related phototoxicity reaction?

A

UVA (visible spectrum too for sparfloxacin)

84
Q

What decreases the absorption of fluoroquinolones?

A

Administration of divalent cations (calcium, magnesium aluminum and zinc) decrease absorption

85
Q

What is the mechanism of tetracyclines?

A

Binds 30s subunit of bacterial ribosome (as opposed to the 50s subunit for macrolides) –> decreased protein synthesis; antiinflammatory properties (inhibits multiple matrix metalloproteinases, neutrophil migration, and decreased innate cytokines)

86
Q

What are the primary indications for tetracyclines in dermatology?

A

Acne, perioral dermatitis, rosacea, immunobullous diseases (bullous rosacea, bullous pemphigoid, CARP (minocycline), cutaneous sarcoidosis/other granulomatous diseases (minocycline), acne keloidalis nuchae, PLEVA/PLC, and acneiform eruptions secondary to EGFR inhibitors

MRSA, chlamydia, rickettsia, mycoplasma, atypical mycobacteria, spirochetes (fi PCN allergic), Lyme dz

87
Q

If a patient has an acneiform reaction from an EGFR inhibitor, what is the tx of choice?

A

Tetracyclines

88
Q

What are the subantimicrobial doses and of doxycycline?

A

modified release 40mg per day or extended-release minocycline.

  • effective for rosacea and acne and does not increase resistance in theory, and may have decreased rate of vaginal candidiasis
89
Q

What is the mechanism of tetracycline bacterial resistance?

A

Ribosomal protection and or drug efflux

90
Q

What are the most lipophilic medications of the tetracycline class?

A

Minocycline > doxycycline > tetracycline

91
Q

What can decrease the absorption of tetracyclines?

A

Metallic cations can decrease absorption via chelation (tetracycline > doxycycline > minocycline)

92
Q

Side effects of tetracyclines?

A

GI sx’s (esophagitis, nausea, and abdominal pain; most common with doxycycline but less so with enteric-coated form), acute vestibular side effects (dizziness and vertigo; usually with minocycline), benign intracranial hypertension / pseudotumor cerebri (usually minocycline; increased risk if given w/ isotretinoin), photosensitivity / photooncholysis (demeclocycline> doxycycline> tetracycline> minocycline), hyperpigmentation of skin/nail beds/teeth/mucous membranes/bone (minocycline), vaginal candidiasis, GN acne/folliculitis, serum sickness-like reactions (minocycline), drug-induced Sweet’s syndrome (minocycline) autoimmune hepatitis (minocycline), DRESS/DHS (minocycline, lupus-like syndrome (minocycline, usually ANA+, and antihitone AB+), and cutaneous PAN/Vasculitis (minocycline; pANCA+)

93
Q

What are the 3 types of minocycline-induced hyperpigmentation and what do they stain with?

A

Type I: Blue-gray pigmentation in sites of facial scarring (stains iron and melanin)

Type II: Blue-gray color on the shins and or forearms, stains for iron and melanin

Type III: Diffuse muddy brown on sun-exposed skin: stains melanin only, is a phototoxic eruption with PIH

94
Q

In what age ranges should tetracyclines not be used in?

A

Children under 8 –> tooth discoloration (note this can occur in adults too)

95
Q

Which tetracycline can be used in renal failure and why?

A

Tetracyclines are excreted renally except doxycycline which has GI tract excretion making it safe to use in renal failure

96
Q

What is the mechanism of action for Rifampin?

A

Binds the beta-subunit of bacterial DNA-dependent RNA polymerase which reduces RNA/protein synthesis

97
Q

Can rifampin be given as monotherapy?

A

No! leads to the rapid development of resistance

98
Q

What type of drug interactions are seen with rifampin?

A

CYP450 inducer, which leads to increased drug clearance/decreased efficacy (OCP’s, warfarin, azoles, CCBs, statins, and cyclosporin)

99
Q

Uses in dermatology for rifampin?

A

Mycobacterial infections, Bartonella infections (cat-scratch and bacillary angiomatosis), MRSA/MSSA, rhinoscleroma, and cutaneous leishmaniasis (all part of multi-drug regimens

100
Q

Side effects of Rifampin?

A

Orange-red discoloration of body fluids, CNS (headaches, and drowsiness), GI sx’s, rifampin-dependent antibodies which can lead to anaphylaxis, flu-like sx’s, renal failure, and hemolytic anemia; hepatotoxicity, DVT’s, pulmonary fibrosis, ocular se, worsening of porphyria (induces delta-ALA synthetase), possible hemorrhagic dz of the newborn and mother in pregnancy

101
Q

What is the mechanism of action for trimethoprim-sulfamethoxazole?

A

Dihydrofolate reductase inhibitor (trimethoprim) + dihydropteroate synthase inhibitor (sulfamethoxazole). Together, these lead to decreased tetrahydrofolic acid and decreased nucleic acid/protein synthesis

102
Q

Dermatology uses for trimethoprim-sulfamethoxazole?

A

GP cocci (not much coverage against strep in most places), acne, hidradenitis suppurativa, granuloma inguinale, actinomycetoma, cat-scratch disease, and chronic melioidosis (Burkholderia pseudomallei)

103
Q

Side effects of trimethoprim-sulfamethoxazole?

A

GI and CNS are most common, cutaneous eruptions (more common in HIV + patients, Bactrim accounts for 30% of SJS cases), hematologic SE’s (agranulocytosis, thrombocytopenia, folate deficiency + megaloblastic anemia, neutropenia, and hemolytic anemia in patients with G6PD deficiency)

104
Q

Dangers of trimethoprim-sulfamethoxazole use during pregnancy?

A

Increased risk of jaundice, hemolytic anemia, and kernicterus of baby if taken in third trimester

105
Q

What medications are particularly dangerous in dermatology when taken with trimethoprim-sulfamethoxazole?

A

Can increase dapsone levels, increase hematologic toxicity in patients taking MTX, increase renal toxicity in patients taking cyclosporin, and increase potassium in patients on ACEIs/ARBs

106
Q

What is the mechanism of clindamycin?

A

Lincosamide that binds to 50S subunit of bacterial ribosomal RNA which leads to decreased ribosomal translocation/protein synthesis

107
Q

What is the spectrum of clindamycin?

A

GP cocci, anaerobes (bacteroides, c. perfringens), but not usually GN’s (except Capnocytophaga canimorsus)

108
Q

What test can be done to test for witheter inducible resistance is present in an erythromycin-resistant, clindamycin -sensitive organism (bacteria with erm gene)?

A

“D zone test”

109
Q

What are the side effects of clindamycin?

A

Antibiotic-associated colitis, rashes, rare bone marrow suppression may increase neuromuscular blocking

110
Q

What is the mechanism for linezolid?

A

Inhibits 23S portion of 50S ribosomal subunit of bacteria

111
Q

Use and side effects of linezolid?

A
  • MRSA and VRE
  • myelosuppression in 2%, serotonin syndrome (if given with serotonergic drugs, optic/peripheral neurotoxicity
112
Q

What is the mechanism of Quinupristin and dalfopristin?

A

Diffuses through bacterial cell wall and binds 50s ribosomal subunit sites which leads to decreased protein synthesis

113
Q

Uses and side effects for quinupristin and dalfopristin?

A

Complicated skin and soft tissue infections caused by GP (MRSA, VRE)

  • Anaphylaxis, angioedema, and increased bilirubin
114
Q

What is the mechanism of action of daptomycin?

A

Depolarizes bacterial cell membrane leading to cell death

115
Q

What are some uses of daptomycin?

A

MRSA, VRE, and linezolid-resistant GP’s

116
Q

What is the mechanism of action of acyclovir, valacyclovir, famciclovir, and penciclovir?

A

Guanosine analog that requires:

Phosphorylation first by herpes-specific thymidine kinase which leads to acyclovir monophosphate. This is then phosphorylated by human cellular GMP kinase and other cellular kinases to acyclovir triphosphate.

  • In the form of acyclovir triphosphate, it competes with deoxyguanosine triphosphate as a substrate for viral DNA polymerase and incorporates into viral DNA which leads to chain termination and viral duplication

Valacyclovir and penciclovir are prodrugs of acyclovir, famciclovir is a prodrug of penciclovir

117
Q

What are the uses of topical acyclovir?

A

It is approved for HSV only, NOT VZV

118
Q

When would we consider suppressive use of acyclovir/valacyclovir?

A

If there are more than 6 episodes of HSV per year

119
Q

When should IV acyclovir be used?

A

Disseminated HSV/VZV, eczema herpeticum and in immunosuppressed patients

120
Q

What are important side effects of acyclovir?

A

When given as an IV can lead to crystalline nephropathy so give fluids

  • AZT + acyclovir can lead to drowsiness/lethargy
  • Probenecid + acyclovir increases availability and decreases clearance
121
Q

What is a potentially dangerous side effect of valacyclovir if used in patients with HIV?

122
Q

What is the difference between famciclovir and penciclovir?

A

Famciclovir is available orally, but penciclovir is only available topically

123
Q

What is the mechanism of resistance to acyclovir and valacyclovir?

A

Mutations in thymidine kinase or less commonly in DNA polymerase

124
Q

What should be used if viral resistance is seen with acyclovir/valacyclovir?

A

Foscarnet or cidofovir

125
Q

If patients have resistance to acyclovir what other medications will they be resistant to?

A

Valacyclovir, famciclovir, penciclovir

126
Q

What should be used for the VZV eruption?

A

Ideally, valacyclovir or famciclovir as this decreases VZV pain more than acyclovir

127
Q

What is the only indication for penciclovir?

A

Herpes labialis only

128
Q

What is the mechanism of action for cidofovir?

A

Nucleoside phosphate analog of deoxycytidine monophosphate.

  • Must be phosphorylated twice to cidofovir diphosphate in order to be active
  • Once active incorporates into viral DNA and blockage/termination of DNA synthesis occurs

Does not require thymidine kinase

129
Q

What forms of cidofovir are available?

A

IV and topical (not commercially available)

130
Q

What are the side effects of cidofovir?

A

Nephrotoxicity (most common), neutropenia, alopecia, uveitis/iritis, cardiomyopathy

131
Q

What is the mechanism of foscarnet?

A

IV pyrophosphate analog that binds to a pyrophosphate-binding site on viral DNA polymerase which leads to inhibition of pyrophosphate cleavage from deoxyadenosine triphosphate which leads to disruption of DNA elongation

132
Q

What is foscarnet used for?

A

Tx of choice for acyclovir-resistant HSV, CMV retinitis, and CMV skin infections in HIV patients

133
Q

Most common side effects with foscarnet?

A

Penile erosions (acute contact dermatitis from the foscarnet excreted via the urine), thrombophlebitis, nephrotoxicity, seizures, and electrolyte disturbances

134
Q

Mechanism of action for bleomycin?

A

Binds to DNA leading to single strang breaks and decreased protein synthesis, this leads to increased apoptosis/necrosis of keratinocytes

135
Q

What are the side effects of bleomycin?

A

Injection pain, Raynaud’s phenomenon, loss of nail plate/nail dystrophy, and flagellate hyperpigmentation

136
Q

What is the mechanism of action for podophyllin and podofilox?

A

An antimitotic agent that binds tubulin which leads to cell cycle arrest in metaphase

137
Q

What is the FDA approved use of podophyllin and podofilox?

A

Genital warts

138
Q

What are the side effects of podophyllin and podofilox?

A

Typically local

CAN’T use in pregnancy–>teratogenic

139
Q

Where does cantharidin come from?

A

Blister beetle/Spanish fly, Lytta vesicatoria

140
Q

What is the mechanism of action for cantharidin?

A

Disrupts desmosomes, leading to intraepidermal acantholysis leading to bullae

141
Q

How is cantharidin applied?

A

Applied in the office under occlusion for wars/molluscum; washed off at home 4 hrs later

142
Q

Side effects of cantharidin?

A

Pain from blister and ring wart formation

143
Q

What is the mechanism of action fo sinecatechins?

A

Green tea derived polyphenol epigallocatechin gallate –> apoptosis, inhibition of telomerase, and an antioxidant effect on cells

144
Q

What are sinecatechins used for and what are the side effects?

A

Approved for genital/perianal warts, SE’s are local

145
Q

What is the mechanism of action of azoles?

A

Inhibits 14alpha demethylase (catalyzes conversion of lanosterol to ergosterol) which leads to decreased ergosterol, which leads to decreased cell membrane synthesis, and increased membrane rigidity/permeability growth inhibition, and cell death

146
Q

Where is itraconazole metabolized?

A

The liver via CYP3A4

147
Q

What are the uses of itraconazole in dermatology?

A

Dermatophyte onychomycosis (12 week 200mg/day course for toenails), oropharyngeal/esophageal candidiasis, blastomycosis, histoplasmosis, and aspergillosis refractory to amphotericin B

  • Can be used off-label for extensive TV (short courses or single doses)
148
Q

What are the contraindications of itraconazole?

A

Ventricular dysfunction and CHF, active liver dz or h/o liver toxicity w/ other drugs, concurrent use of drugs metabolized via CYP3A4 (pimozide, quinidine, cisapride)

  • Caution w/ concurrent use of levomethadyl, dofetilide, statins, midazolam, triazolam, nisoldipine, and ergot alkaloids
149
Q

What are the side effects of itraconazole?

A

GI (nausea, vomiting, and abdominal pain), cutaneous (rash, more common if also using immunosuppressive medications), neurologic (headache), edema, increased LFTs, rhinitis, and fever

  • Rare: hearing loss, peripheral neuropathy, CV events (e.g. CHF), dysgeusia, pancreatitis, hepatotoxicity, neutropenia/leukopenia, pulmonary edema, and hypokalemia
150
Q

What is the metabolism of fluconazole?

A

Very little hepatic metabolism, CYP2C9 inhibitor

151
Q

What are the dermatologic uses of fluconazole?

A

vaginal / oropharyngeal / esophageal candidiasis, and cryptococcal meningitis

  • off label: tinea, systemic candida, coccidioidal meningitis, onychomycosis, and non-dermatophyte onychomycosis
152
Q

What medications should not be given with fluconazole?

A

Pimozide, quinidine, cisapride, erythromycin, terfenadine, astemizole, voriconazole, or statins

153
Q

What are the side effects of fluconazole?

A

Common: GI (nausea/abdominal pain), skin rash, headaches

Rare: CV events, cholestatis/hepatocellular damage/liver failure, severe skin reactions, seizures, leukopenia/thrombocytopenia, dysgeusia, and hyperlipidemia

154
Q

Why is ketoconazole note used orally anymore?

A

Hepatotoxicity

155
Q

What medications should ketoconazole not be used with?

A

cisapride, terfenadine, or astemizole, as interactions can lead to CV events like increased QT syndrome

156
Q

What are the side effects of ketoconazole?

A

(systemic form only): GI sx’s, idiosyncratic hepatotoxicity, pruritis, urticaria

157
Q

What is voriconazole used for?

A

New generation of azole, used primarily for serious invasive fungal infections in immunosuppressed hosts (invasive aspergillosis, candida infections, and fusarium infections)

158
Q

What are some unique side effects of voriconazole?

A

Severe phototoxicity (including pseudoporphyria, and xeroderma pigmentosum-like changes), and increase risk of SCC, visual disturbances hepatotoxicity, GI issues, and QT prolongation

159
Q

What are miconazole, clotrimazole and econazole used for?

A

These are topical azoles, active against dermatophytes, M. furfu, and C. albicans

  • good for tinea infections, TV, and cutaneous candidiasis
160
Q

What is efinaconazole?

A

Jublia and Clenafin

  • Use daily for 48 weeks for onychomycosis, only 15-20% effective
161
Q

What is luliconazole?

A

Daily 1% cream for short courses to treat various cutaneous tinea infections (interdigital candida).

  • Other topical antifungals good for cutaneous dermatophyte infections and possibly cutaneous Candida infections include oxiconazole, sulconazole and sertaconazole
162
Q

Mechanism of action for allylamines / benzylamines?

A

Inhibit squalene epoxidase (catalyzes the conversion of squalene to lanosterol) and leads to the decreased cell membrane synthesis

163
Q

Where is terbinafine metabolized?

A

It is metabolized mainly in the liver, do not give in active liver disease. Do not give if kidney function is <50 mL/min

164
Q

What is the FDA and off-label uses for terbinafine in dermatology?

A

FDA approved: Dermatophyte onychomycosis and tinea capitis

Off-label: Tinea infections, subcutaneous / systemic mycosis, histoplasmosis and chromoblastomycosis, and other types of onychomycosis (good for aspergillus but no Candida)

165
Q

What is the relative efficacy of terbinafine as compared to clotrimazole or oxiconazole in tinea pedis?

A

It is more effective

166
Q

When should terbinafine be used for tinea capitis?

A

Very effective against endothrix (T. tonsurans)

Less effective against ectothrix organisms like M. canis (griseofulvin preferred)

167
Q

What are the most common, and more rare side effects of terbinafine?

A

Common: GI (diarrhea), cutaneous (rash), headache, and increased LFT’s

Rare: Taste/smell disturbance, severe skin reactions (SJS/TEN), visual disturbance, hepatobiliary dysfunction/hepatitis/liver failure (idiosyncratic), hematologic abnormalities, neutropenia or thrombocytopenia, rhabdomyolysis, depression, exacerbation of SLE, drug-induced SCLE

168
Q

What medications should be used with caution with terbinafine?

A

Inhibits CYP2D6, so use caution with doxepin or amitriptyline

169
Q

What is naftifine?

A

A topical formulation of an allylamine/benzylamine like terbinafine, only effective for dermatophyte infections - more effective than azoles in cutaneous dermatophytoses

170
Q

What is butenafine?

A

It is a benzylamine class topical antifungal –> it is effective for cutaneous dermatophyte infections, TV, cutaneous candida

171
Q

What is the mechanism of action for griseofulvin?

A

Interferes with tubulin, inhibits mitosis and binds to keratin in keratin precursor cells, leads to resistance to fungal infections

172
Q

When should you use griseofulvin vs terbinafine?

A

Better for tinea wapitis cause by Microsporum canis

173
Q

Side effects of griseofulvin?

A

GI disturbance and headache are most common, FDE, photosensitivity, and exfoliative dermatitis; can instigate or worsen porphyria and lupus

174
Q

What is the mechanism of action for Ciclopirox olamine (Loprox)?

A

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

175
Q

What is ciclopirox used for?

A

Topical formulations are available only –> cutaneous dermatophyte infections Malassezia spp., TV, cutaneous candidiasis, and onychomycosis (in lacquer form)

176
Q

Can ciclopirox be used for candida?

A

Yes, it is more effective than allylamine/benzylamine drugs for Candida

177
Q

What are some dermatologic uses of selenium sulfide?

A

TV, seborrhea dermatitis of the scalp, and CARP

178
Q

What is the mechanism of nystatin?

A

Polyene topical agent that binds Candida cell membrane sterols and leads to increased permeability and cell death

179
Q

What are some of the echinocandins?

A

Caspofungin, micafungin, and anidulafungin

180
Q

What is the mechanism of echinocandins?

A

Inhibits beta (1,3)-D-glucan synthase which leads to decreased glucan production and leads to disruption of the cell wall synthesis

181
Q

What are the echinocandins used for?

A

Used primarily in invasive Candida infections and invasive aspergillosis (second line)

182
Q

What are the side effects of echinocandins?

A

Facial swelling (caspofungin), increased alkaline phosphatase (caspofungin), hypokalemia (caspofungin), and hematuria/proteinuria (caspofungin)

183
Q

What treatments are safe for pregnant women with scabies?

A

Permethrin and precipitated sulfur

184
Q

What is the mechanism of ivermectin?

A

Binds glutamate-gated chloride ion channels of parasite nerve/muscle cells which leads to increased membrane permeability leading to hyperpolarization and leads to death

185
Q

How does resistance to ivermectin occur?

A

Can occur due to SNP’s of P-glycoprotein-like protein

186
Q

Uses of ivermectin?

A

Onchocerciasis, intestinal strongyloidiasis, scabies (less effective for crusted form), cutaneous larva migrans, and pediculosis

187
Q

Side effects of ivermectin?

A

Rashes, pruritus, fever, and LAD (less w/ scabies infxn)

188
Q

What is the mazzotti reaction?

A

Rash/systemic sx’s/ocular rxns; occurs in patients with onchocerciasis. Doxycycline helps to reduce the reactions

189
Q

What is the mechanism of albendazole?

A

Stops tubulin polymerization which leads to immobilization and death of the parasite

190
Q

What is albendazole used for?

A

Neurocysticercosis, hydatid disesae, ascaris lumbricoides, trichuris trichiura, enterobius vermicularis, ancylostoma duodenale and necator americanus, taenia strogyloids stercoralis, giardia, scabies

191
Q

Side effects of albendazole?

A

bone marrow suppression (increased risk if pt has liver dz), aplastic anemia, agranulocytosis, hepatotoxicity, GI SE’s, rash

  • May increase eos
  • Resistance higher in pts w/ HTLV-1 infection
192
Q

What is the mechanism of thiobendazole?

A

inhibits fumarate reductase

193
Q

What are the uses of thiobendazle?

A

Cutaneous larva migrans (topical version), Strongyloides, visceral larva migrans, trichinosis, uncinariasis, necator, ancylostoma, trichuriasis, ascariasis

194
Q

Side effects of thiobendazole?

A

Hepatotoxicity, GI SE, CNS SE, SJS, may increase theophylline levels

195
Q

What is the mechanism of permethrin?

A

Disables sodium transport channels on cell membranes in arthropods leading to paralysis

196
Q

Uses for permethrin?

A

Scabies (5% cream) apply to the neck down, 2 overnight applications separated by 1 week

-Pediculosis capitis (1% solution)

197
Q

Allergies to what flowers would suggest the possibility of allergy to permethrin?

A

Asteraceae/Compositae: Chrysanthemums, ragweed, marigolds, and daisies

198
Q

What is the mechanism of action for malathion?

A

Organophosphate that inhibits acetylcholinesterase in arthropods leading to neuromuscular paralysis

199
Q

Uses for malathion?

A

0.5% solution for pediculosis capitis, most effective treatment in the united states and the treatment of choice in children over 6 years old

200
Q

What are the side effects of malathion?

A

Local SE, potentially flammable, malodorous, if ingested can give sx’s of organophosphate poisoning or decreased cholinesterase

201
Q

What is the mechanism of spinosad?

A

Instigates arthropod motor neurons leading to paralysis

202
Q

What is spinosad used for?

A

Pediculosis capitis (very rapid effect, ~10-minute application)

203
Q

What is the mechanism of lindane?

A

organochlorine leadings to decreased neurotransmission and arthropod respiratory/muscular paralysis

204
Q

What is lindane used for?

A

Scabies and pediculosis capitis

205
Q

Side effects of lindane?

A

Seizures if ingested or multiple applications, aplastic nameia leukemia (note used anymore b/c of neuro side effects)

DERM (12) Medical Therapy (7 decks)

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