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Pharmacology Final > Antifungals and Antivirals > Flashcards

Antifungals and Antivirals Flashcards

1
Q

what are mechanisms of antifungals?

A

target a lot of differences: ergosterol, fungal mitosis, RNA and protein synthesis, cell wall synthesis, protein synthesis

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2
Q

what do cell membrane active antifungals target?

A

ergosterol

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3
Q

allylamine drugs

A

terbinafine and naftifine

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3
Q

MOA of allylamines

A

inhibition of squalene epoxidase: blocks formation of ergosterol

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4
Q

why would inhibiting formation of ergosterol be detrimental to fungal cells?

A

Ergosterol plays a crucial role in the fungal cell membrane by maintaining its fluidity, permeability, and structural integrity, essentially acting as the primary sterol component that regulates the membrane’s function and is vital for proper fungal cell growth and survival; its structure and function are similar to cholesterol in animal cells

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5
Q

spectrum of activity of allylamines

A

broad spectrum: active against dermatophytes, yeasts, Aspergillus, dimorphic fungi

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6
Q

are allylamines fungicidal or fungiostatic?

A

fungicidal: advantage over many other drugs!

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6
Q

how do you administer allylamines?

A

available for both oral and topical use; good oral absorption

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7
Q

adverse effects of allylamines

A
  • well tolerated, low incidence of side effects
  • resistance has not been reported
  • may have synergistic activity with other drugs like fluconazole, itraconazole, voricoazole
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8
Q

polyenes

A

antifungals: amphotericin B, nystatin, natamycin (pimaricin)

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9
Q

what is amphotericin B used for?

A

systemic treatment, rarely for topical application
formulated as salts or in lipid-complex formulas

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10
Q

nystatin is available only in what formulations?

A

topical

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10
Q

nystatin is what type of drug?

A

antifungal: polyenes

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11
Q

what is the only FDA approved anti-fungal for ophthalmic use?

A

natamycin- topical only

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12
Q

what is natamycin used for?

A

only FDA approved antifungal for aphthalmic use topically

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12
Q

amphotericin B

A
  • fungicidal: binds to ergosterol, causes cell leakage and death
  • broad spectrum!
  • resistance develops slowly and doesn’t reach high levels
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12
Q

what makes amphotericin B the most toxic antifungal?

A

binds to mammalian cell cholesterol

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13
Q

is amphotericin B concentration dependent or time dependent

A

concentration dependent: Cmax:MIC of 2-4

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14
Q

what is the most toxic of all useful antifungals?

A

amphotericin B: makes a leakage hole in membrane

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15
Q

how is amphotericin B administered?

A

not absorbed from GI tract; administered IV!

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16
Q

distribution/metabolism of amphotericin B

A
  • slowly distributes to most tissues except CNS, eyes, bone.
  • accumulates in liver, kidneys, and lungs
  • lipid formulations are taken up by phagocytes with lower renal concentrations!
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16
Q

why are lipid formulations of amphotericin B safer?

A

get taken up and kept out of kidney: Lipid formulations are taken up by mononuclear phagocytes (and transported to the sites of infection) with lower renal concentrations, longer half-life, and less nephrotoxicity, less infusion-related toxicity

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16
Q

how is amphotericin B excreted?

A

small amounts are excreted in urine and bile over several weeks, fate of remainder is unknown

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17
Q

amphotericin B is synergistic with

A

flucytosine

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18
Q

what is a serious side effect of amphotericin B?

A

nephrotoxicity! need to monitor renal function weekly during therapy!
can get hypokalemia from loss of urine concentrating ability

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19
Q

what drugs can worsen side effects of amphotericin B?

A

mineralocorticoids: can worsen hypokalemia: choose one without mineralocorticoid activity: like Dex!

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19
Q

what is amphotericin B diluted in for IV administration?

A

5% dextrose
solutions are unstable and must be used within 1 week

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20
Q

what formulations of amphotericin B have lower accumulation in the kidneys?

A

liposomal or lipid-complexed formulations taken up into mononuclear phagocytic cells

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21
Q

why would combining amphotericin B be useful?

A

can be combined with other antifungals with synergistic results, allowing reduced dosage and decreased toxicity = flucytosine
allows to reduce doses of amphotericin B to reduce toxicity like leaky kidneys

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21
Q

imidazoles and triazoles

A

super broad-spectrum: antibacterial, antifungal, antiprotozoal, and anthelmintic activity

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22
Q

what is the molecular target of the azoles?

A

fungal cytochrome P450-Cyp51 or Erg 11p
structural differences in the azoles dictate binding site on the CYP system

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23
Q

what do the azoles bind to?

A

lanosterol 14a-demethylase

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24
Q

are the azoles fungistatic or fungicidal?

A

fungistatic: inhibit ergosterol synthesis

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25
Q

how are azoles often administered? why?

A

some are so poorly absorbed that use is limited to topical application for txt of superficial mycotic infections like yeast or dermatophytosis

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26
Q

what are adverse effects of imidazoles (ketocon, clotrim, micon)?

A

endocrine adverse effects through cholesterol inhibition: problem when administering phenobarb or other drugs that use P450s: these drugs inhibit P450s; will get interactions

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27
Q

what azoles are administered orally to treat systemic fungal infections?

A

fluconazole, ketoconazole, itraconazole, voriconazole

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28
Q

why do you take itraconazole with food?

A

in capsule formulation; has unpredictable absorption and bioavailability but that is improved with food intake, esp high-fat meal

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29
Q

how are azoles distributed?

A
  • ketoconazole and itraconazole are widely distributed except for CNS and bone
  • fluconazole and voriconazole penetrate the CNS very well
  • some metabolized in liver by CYP system
30
Q

how are the azoles excreted? what is the exception?

A

metabolites in bile and some drug in urine
exception is fluconazole: only one that is excreted in urine = useful for fungal cystitis!

31
Q

which drug is useful for fungal cystitis? why?

A

fluconazole: is the only azole excreted in urine as active drug!

32
Q

what are some special clinical concerns with ketoconazole?

A

may be an inhibitor or substrate of CYP system
- anorexia, V+/D+, hepatic dysfunction may occur
- suppression of adrenal or gonadal steroids (testosterone) may also occur
- reversible lightening of haircoat coloration and alopecia
- hepatotoxicity is a risk in cats

33
Q

what azole is better tolerated than ketoconazole?

A

fluconazole, only causes mild anorexia

34
Q

itraconazole clinical concerns

A
  • some dogs develop ulcerative dermatitis and edema from vasculitis
  • some develop hepatic toxicosis
  • weakens heart contractions = contraindicated in congestive heart failure
35
Q

what antifungals should pregnant animals never be given?

A

AZOLES

35
Q

what azole do cats tolerate best?

A

itraconazole&raquo_space;> keto

36
Q

when should you avoid all systemic uses of azoles?

A

PREGNANCY

37
Q

what is ketoconazole administered to treat? how is it given?

A

given orally to treat systemic mycotic infections: coccidiomycosis, blastomycosis, histoplasmosis, dermatophytosis

38
Q

what is fluconazole administered to treat?

A

candidiasis and cryptococcosis

38
Q

what is itraconazole used to treat?

A

equally effective to amphotericin B for systemic fungal agents, zygomycetes, dermatophytes, and aspergilli
broader spectrum of activity and is more potent than ketoconazole

39
Q

treatment of choice for cryptococcosis and coccidioidal meningitis

A

fluconazole

40
Q

treatment of choice for non-life threatening histoplasmosis and blastomycosis

A

itraconazole

41
Q

voriconazole

A

broadest spectrum of azole antifungals
increased activity against aspergillosis; fungicidal against some species

42
Q

griseofulvin

A

fungistatic: inhibits mitosis, but action is slow. effective only as a systemic agent against dermatophytes. resistance is rare

43
Q

pharmacokinetics of -azoles

A

slow and highly variable- increased by high-fat foods

44
Q

where does griseofulvin distribute to?

A

keratin precursor cells of skin, hair shafts and nails

44
Q

where is griseofulvin metabolized?

A

metabolized by the liver by demethylation and glucoronide conjucation

45
Q

why are cats more susceptible to griseofulvin than other animals?

A

it is metabolized to a glucoronide; longer half-life in cats and thus cats are more susceptible to toxic effects

45
Q

clinical concerns of griseofulvin

A
  • V+/D+ have been observed
  • leukopenia and anemia may occur in kittens receiving high doses
46
Q

griseofulvin should not be given to what animals?

A
  • animals with impaired liver function
  • contraindicated in pregnant animals- especially mares and queens- because it is teratogenic
  • altered spermatogenesis may occur
47
Q

what is griseofulvin used for?

A

it is administered orally for 4-6 weeks for treatment of dermatophytosis in non-food producing animals
limited availability

48
Q

why do antiviral drugs have a narrow spectrum of activity?

A

they are specific for one of the few enzymes or structural targets produced by closely related viruses

49
Q

what is the basis for most antiviral drugs?

A

nucleoside analogues- because many of the target enzymes are involved in nucleic acid replication
- protease inhibitors have been introduced that block the activity of viral proteases

50
Q

are antivirals virustatic or viruscidal?

A

virustatic: must inhibit viral replication without destroying the host cell

50
Q

what are pharmacokinetic requirements of antiviral drugs?

A

intracellular and nuclear penetration

51
Q

what is early viral infection diagnosis needed?

A

because antiviral drugs tend to be narrow-spectrum and only work against specific viruses

52
Q

amantadine and rimantadine

A

rimantadine is a derivative of amantadine, they act on an early step of viral replication after attachment of virus to cell receptors

53
Q

what is amantadine used for?

A

inhibits replication of influenza A virus, influenza C virus, Sendai virus
main clinical use has been to prevent infection with influenza A viruses in humans

54
Q

side effects of amantadine and rimantadine

A

few side effects; most of which are CNS related

55
Q

idoxuridine

A
  • nucleoside analog
  • for txt of herpesvirus infx in superficial layers of cornea and of skin, but is toxic when administered systemically!
56
Q

what form of administering idoxuridine is toxic?

A

systemically toxic, is fine to administer topically

57
Q

trifluridine

A
  • nucleoside analog
  • analog of deoxythymidine
  • agent of choice for txt of herpesvirus keratitis in humans
58
Q

treatment of choice for herpesvirus keratitis in humans

A

trifluridine
- nucleoside analog

59
Q

acyclovir

A

phosphorylated efficiently by virus-induced thymidine kinase and then is a btter substrate and inhibitor of viral polymerase
- relatively safe and is useful against a variety of DNA viruses- esp herpesvirus infections

60
Q

ribavirin

A

synthetic triazole nucleoside: broad spectrum against many RNA and DNA viruses
- inhibition of viral associated enzymes, inhibition of capping mRNA, and inhibition viral polypeptide synthesis

61
Q

ribavirin safety

A
  • well absorbed, widely distributed
  • narrow margin of safety in domestic animals: toxicity is manifested as anorexia, weight loss, bone marrow depression and anemia
61
Q

interferons and interferon-inducers

A

inferferons render cells resistant to infection by activation of cellular endonucleases that degrade viral mRNA
- also modulate the immune system of the host
- inhibit the replication of a wide variety of viruses

62
Q

clinical uses of IFN-inducers

A

effective in some model systems, but have not yet been found to be clinically useful because of their toxicity

63
Q

neuraminidase inhibitors

A

neuraminidase protein enzymatically cleaves sialic acid residues. siliac acid cleavage is required to release newly formed virus particles from infected cells - thus release of new virus is blocked

64
Q

what are neuraminidase inhibitors active against?

A

both influenza A and B

64
Q

antiviral resistance

A

infrequent

65
Q

zanamivir

A

relenza: reported to reduce flu symptoms by 1 day

66
Q

oseltamivir

A

tamiflu: reduced severity of flu symptoms by 40%, also reduces rates of secondary complications

67
Q

lysine

A

nutritional supplement- reduces frequency and severity of clinical signs of FHV-1
- herpesvirus requires arginine
- lysine is proposed to interfere with absorption of arginine in the intestine. maintain high lysine/arginine

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Pharmacology Final (9 decks)

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