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MSK Formative 1 > Pharmacological Treatment of Skin Disorder and Fungal Infection > Flashcards

Pharmacological Treatment of Skin Disorder and Fungal Infection Flashcards

1
Q
  • MOA and MOR of Acyclovir, famiciclovir, valacyclovir?
A

MOA:

  • Monophosphorylated by HSV/VZV thymidine kinase
    • not phosphorylated in uninfected cells (so few adverse side affects)
    • Triphosphate is formed by cellular enzymes
      • preferentially inhibit viral DNA polymerase by chain termination

MOR= mutated viral thymidine kinase

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2
Q

Clinical use of Acyclovir, famciclovir and valacyclovir?

A
  • HSV and Varicella Zooster Virus (VZV)
    • (used for HSV-induced mucocutaneous and genital lesions and well as encephalitis)
  • Valacyclovir is a prodrug of acyclovir and has better oral bioavailability
    • For herpes zooster use famiciclovir
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3
Q

Adverse effects of Acyclovir, famciclovir, valacyclovir?

A

Neuropathy (headache, nausea), renal failure

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4
Q

How are Acyclovir, Valacyclovir and Famciclovir administered?

A

Orally

Acyclovir can also be given via IV

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5
Q

What is used to treat vulvar and vaginal warts?

A
  • Podophyllotoxin
  • imiquimod OTC
    • cause necrosis of warts
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6
Q

What does HAART treatment regiment for HIV?

A

2 NRTI (backbone) + 1 IN/PI/NNRTI (base)

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7
Q

In HIV what drug is the attachment inhibitor? Used for?

A
  • Maraviroc
  • CCR5 antagonist that blocks viral entry into the cell
  • For drug resistant HIV
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8
Q

What HIV drug is a fusion inhibitor?

A
  • Enfuvirtide
    • Binds HIV envelope and inhibits fusion with cell membrane
      • For multidrug resistant HIV
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9
Q

HIV NRTI (Nucleoside/Nucelotide reverse transcriptase inhibitors) drugs?

A
  • Tenofovir
  • Emtricitabine
  • Abacavir
  • Lamivudine
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10
Q

MOA of NRTI (HIV) drugs?

A
  • Intracellular triphosphate form binds to DNA and terminates reverse transcription
    • actually interacting and incorporating in the chain
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11
Q

Side effects of NRTI?

A
  • Mitochondrial toxicity
    • peripheral neuropathy
    • pancreatitis
    • hepatic steatosis
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12
Q

MOA of non-nucleoside RTI? (NNRTI)

A
  • Does not bind to the active site of reverse transcriptase but rather cause a conformational change in the RT enzyme
  • This prevents reverse transcriptase enzyme from adding nucleotides to the DNA chain
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13
Q

Side effects of NNRTI (HIV) drug?

A
  • Neurological/psych effects
    • also rash, hypersensitivity and hepatic failure
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14
Q
  • MOA of Integrases (HIV) drugs?
  • All end in?
A
  • TEGRAvir
  • Inhibit integrase enzyme
    • integrase exposes OH 3’ ends of viral DNA and covalently ligates 3’ ends to host DNA (drugs blocks this so can’t integrate into host DNA)
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15
Q
  • Protease inhibitors (HIV) drugs all end in?
  • MOA?
A
  • -navir
    • ​ inhibit cleavage of gag-poly polyproteins
      • virus makes long proteins then chops them up into protein products—>inhibits this—> inhibit viral maturation

* typically used along with 2 NRTIs

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16
Q
  • Side effects of protease inhibitors?
  • Don’t use with?
A
  • Hyperglycemia, diabetes, hyperlipidemia, hepatotoxicity
  • Don’t used with CYP inducers (ex: rifamipin); drug will be metabolized too quickly
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17
Q
  • Lyme disease infection is caused by?
  • Symptoms?
A
  • Tick borne related
  • Borrelia borgadorferi
  • erythema, migrans, flu like symptoms
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18
Q

Treatment of Lyme disease?

A
  • Doxycycline (preferred)
  • amoxcillin,
  • cefuroxime (3rd generation so can cross BBB)
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19
Q
  • Rocky Mountain Spotted Fever (RMSF) is caused by?
  • Treated with?
A
  • Tick borne illness caused by Rickettsia rickettsii
  • Treated with doxycycline
    • and if necessary chloramphenicol
      • binds to 50S ribosomal subunit and inhibits peptidyl transferase
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20
Q
  • Scabies caused by?
  • Treated with?
A
  • Caused by mite Sarcoptes scabiei

Treat with:

  • ​5% permethrin cream (topical)
    • Inhibits Na+ influx in nerve cells in insects
  • Ivermectin (oral)
    • Binds to glutamate gated Cl- channels
    • causes worm paralysis
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21
Q

MOA of Malathion to treat lice?

A
  • AchE inhibitor, organophosphate
    • Ach builds up–> muscle spasms
22
Q

What is used to treat lice?

A
  • Permethrin (topical)
  • Ivermectin
  • Malathion
23
Q

Antifungal: Cell wall inhibitor class?

A

Echinocandins

24
Q

Antifungal: Cell membrane inhibitor class?

A
  • Azoles
  • Allylamines
  • Amphotericin B / nystatin
25
Q

Antifungal: Nucleic acid synthesis inhibitor class?

A

Flucytosine

26
Q

Microtubule/mitosis inhibitor class?

A

Griseofulvin

27
Q
  • Echinocandins drug class?
  • MOA?
  • end in?
A
  • Cell wall synthesis inhibitor
    • Competitively inhibit beta glucan synthase complex
      • Fungus can’t build cell wall so it lysis (fungicidal)
  • -fungin
    • Caspofungin, micafungin, anidulafungin
28
Q
  • What are Echinocandins used against?
  • How are they administered?
A
  • Candida and Aspergillus species
  • IV only
29
Q

Side effects of Echinocandins?

A
  • Hepatotoxicity
  • Infusion related histamine release
  • GI symptoms
30
Q
  • Azoles are what class of drugs?
  • How can they be furthered subclassified?
A
  • Cell membrane synthesis inhbitiors
    • Topical
    • Systemic
31
Q

What are the topical and systemic Azoles?

A
  • Topical:
    • Miconazole,
    • Clotrimazole
  • _Systemic: (_PICK FIVE )
    • Posaconazole
    • Itraconazole
    • Ketoconazole (* also topical)
    • Fluconazole
    • Voriconazole
32
Q

What is MOA of Azoles?

A
  • Block ergosterol synthesis
    • ergosterol is fungal equivalent of cholesterol in their cell membrane
    • ergosterol is made via a cytochrome 450 enzyme Lanosterol 14 alpha-demethylase
    • Azoles inhibit Lanosterol which inhibits production of ergosterol
33
Q

MOR of Azoles?

A
  • Mutate enzyme (Lanosterol)
  • Upregulate enzyme so you still have enough to generate ergosterol
  • Efflux pump
34
Q

Topical -azoles are used for?

A

Miconazole and Clotrimazole (and Ketoconazole)

  • Topical for skin and mucous membrane infections
    • Athletes foot, ringworm, diaper rash
    • vulvovaginal candidiasis
    • Oropharyngeal candidiasis
      • tablet in mouth (swallow, don’t chew)
35
Q

Systemic -azoles are used to treat?

A
  • Fluconazole: Candida and Cryptococcus
  • Itraconazole: Fungal pnemonia, sporothrix
  • Voriconazole:Aspergillus, disseminated Cadida infection
    • (** good CSF penetration for meningitis)
  • Ketoconazole: Candida, mycoses, dermatophytes
36
Q

All -azoles inhibit metabolism of?

A

Very serious P450 inhibitors!!!

  • Side effects related to liver
37
Q

What is a drug interaction with systemic -azoles?

A

Rifampin

  • stronger P450 inducer can alter the -azole drug
38
Q

Side effects of systemic -azoles?

A

related to liver because P450 inhibitors!​

  • F: Alopecia, chapped lips
  • I: hypertension, hypokalemia, peripheral edema
  • V: vision changes, neurological issues, periostitis
  • P: possible torsades de pointes (rare)
  • K: more sever GI issues, hepatitis, headache, rash (*not first line treatment anymore)
39
Q
  • Allylamines are what class of drugs?
  • MOA?
  • all end in?
A
  • Cell membrane inhibitors
    • Inhibits squalene epoxidase
      • also inhibits ergosterol syntehsis
  • all end in -fine
    • Terbinafine, butenafine, naftifine
40
Q

What are Allylamines (Terbinafine, butenafine, naftifine) used to treat?

A
  • Dermatophyte infections
    • (tinea cruris, tinea pedis, tinea croporis)
41
Q

Terbinafine (Allylamines) is mainly used to treat?

A

given orally to treat nail dermatophytes

42
Q
  • Amphotericine B is what class of drug?
  • MOA?
  • When is it used?
A
  • Cell membrane inhibitor
  • Binds to ergosterol and facilitates the formation of leaky pores in cell membrane
  • TOXIC: used for critically ill patients with severe, invasive fungal infections
    • (*broad spectrum of candida, aspergilla, black mold)
43
Q
  • Side effects of Amphotericin B?
  • Consider premedication with?
A
  • Infusion related reactions: hypotension, nausea, vomiting
    • Consider pretreatment with diphenhydramine+acetaminophen or ibprofen
44
Q
  • Nystatin MOA?
  • Used for?
  • Side effects?
A
  • binds to ergosterol and facilitates formation of leaky pores in cell membrane
    • same as Amphotericin B
  • Topical (not IV)
    • infection by Candida
      • ​swish and swallow thrush
      • diaper rash
  • Side effects:
    • GI side effects (poor systemic absorption)
45
Q
  • Flucytosine is what class of antifungal drug?
  • MOA?
A
  • Nucleic acid synthesis inhibitor
  • 5-FC pyrimidine analog, is converted to 5-FU in fungus by cytosine deaminase (only in fungus)
  • incorporates into fungal RNA and inhibits both RNA and DNA synthesis
46
Q

When is Flucytosine used?

A
  • Only as an adjunctive treatment (with Amphotericin B) due to resistance
    • ONLY for really serious systemic fungal infections
47
Q

MOR for Flucytosine?

A
  • Fungus can get around pathway/ alter metabolic pathway to make nucleotides
  • Decrease the uptake of the drug
48
Q
  • How is Flucytosine administered/absorbed?
  • CI?
  • Side effects?
A
  • orally absorbed, widely distributed (gets into CSF)
  • CI:
    • bone marrow suppression, liver disease, kidney failure
  • Side effects:
    • alopecia*,
    • skin rash
    • GI symptoms
49
Q
  • Griseofulvin is what class of antifungal drug?
  • MOA?
A
  • Microtubule/mitosis inhibitor
  • Inhibits fungal mitosis
    • interacts with fungal microtubules and disrupts mitotic spindles
50
Q
  • How is Griseofulvin administered?
  • Treatment for what infections?
A
  • Given orally with a fatty meal (doesn’t work topically)
  • For dermatophyte infections (skin, hair, nails)
    • First line for tinea capitis ( ring worm)
51
Q
  • Side effects of Griseofulvin?
  • Other drug interactions?
A

Side effects:

  • CNS effects (confusion, dizziness, headache)
  • skin reactions
  • photosensitivity
  • hepatotoxicity

Drug inteactions

  • Induces CYP1A2, 2C9
  • Interacts with Contraceptives!
52
Q
A

MSK Formative 1 (11 decks)

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