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Pharmacology Final > Antifungals and Antivirals > Flashcards

Antifungals and Antivirals Flashcards

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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
what is a serious side effect of amphotericin B?
nephrotoxicity! need to monitor renal function weekly during therapy! can get hypokalemia from loss of urine concentrating ability
19
what drugs can worsen side effects of amphotericin B?
mineralocorticoids: can worsen hypokalemia: choose one without mineralocorticoid activity: like Dex!
19
what is amphotericin B diluted in for IV administration?
5% dextrose solutions are unstable and must be used within 1 week
20
what formulations of amphotericin B have lower accumulation in the kidneys?
liposomal or lipid-complexed formulations taken up into mononuclear phagocytic cells
21
why would combining amphotericin B be useful?
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
21
imidazoles and triazoles
super broad-spectrum: antibacterial, antifungal, antiprotozoal, and anthelmintic activity
22
what is the molecular target of the azoles?
fungal cytochrome P450-Cyp51 or Erg 11p structural differences in the azoles dictate binding site on the CYP system
23
what do the azoles bind to?
lanosterol 14a-demethylase
24
are the azoles fungistatic or fungicidal?
fungistatic: inhibit ergosterol synthesis
25
how are azoles often administered? why?
some are so poorly absorbed that use is limited to topical application for txt of superficial mycotic infections like yeast or dermatophytosis
26
what are adverse effects of imidazoles (ketocon, clotrim, micon)?
endocrine adverse effects through cholesterol inhibition: problem when administering phenobarb or other drugs that use P450s: these drugs inhibit P450s; will get interactions
27
what azoles are administered orally to treat systemic fungal infections?
fluconazole, ketoconazole, itraconazole, voriconazole
28
why do you take itraconazole with food?
in capsule formulation; has unpredictable absorption and bioavailability but that is improved with food intake, esp high-fat meal
29
how are azoles distributed?
- 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
how are the azoles excreted? what is the exception?
metabolites in bile and some drug in urine exception is fluconazole: only one that is excreted in urine = useful for fungal cystitis!
31
which drug is useful for fungal cystitis? why?
fluconazole: is the only azole excreted in urine as active drug!
32
what are some special clinical concerns with ketoconazole?
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
what azole is better tolerated than ketoconazole?
fluconazole, only causes mild anorexia
34
itraconazole clinical concerns
- some dogs develop ulcerative dermatitis and edema from vasculitis - some develop hepatic toxicosis - weakens heart contractions = contraindicated in congestive heart failure
35
what antifungals should pregnant animals never be given?
AZOLES
35
what azole do cats tolerate best?
itraconazole >>> keto
36
when should you avoid all systemic uses of azoles?
PREGNANCY
37
what is ketoconazole administered to treat? how is it given?
given orally to treat systemic mycotic infections: coccidiomycosis, blastomycosis, histoplasmosis, dermatophytosis
38
what is fluconazole administered to treat?
candidiasis and cryptococcosis
38
what is itraconazole used to treat?
equally effective to amphotericin B for systemic fungal agents, zygomycetes, dermatophytes, and aspergilli broader spectrum of activity and is more potent than ketoconazole
39
treatment of choice for cryptococcosis and coccidioidal meningitis
fluconazole
40
treatment of choice for non-life threatening histoplasmosis and blastomycosis
itraconazole
41
voriconazole
broadest spectrum of azole antifungals increased activity against aspergillosis; fungicidal against some species
42
griseofulvin
fungistatic: inhibits mitosis, but action is slow. effective only as a systemic agent against dermatophytes. resistance is rare
43
pharmacokinetics of -azoles
slow and highly variable- increased by high-fat foods
44
where does griseofulvin distribute to?
keratin precursor cells of skin, hair shafts and nails
44
where is griseofulvin metabolized?
metabolized by the liver by demethylation and glucoronide conjucation
45
why are cats more susceptible to griseofulvin than other animals?
it is metabolized to a glucoronide; longer half-life in cats and thus cats are more susceptible to toxic effects
45
clinical concerns of griseofulvin
- V+/D+ have been observed - leukopenia and anemia may occur in kittens receiving high doses
46
griseofulvin should not be given to what animals?
- animals with impaired liver function - contraindicated in pregnant animals- especially mares and queens- because it is teratogenic - altered spermatogenesis may occur
47
what is griseofulvin used for?
it is administered orally for 4-6 weeks for treatment of dermatophytosis in non-food producing animals limited availability
48
why do antiviral drugs have a narrow spectrum of activity?
they are specific for one of the few enzymes or structural targets produced by closely related viruses
49
what is the basis for most antiviral drugs?
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
are antivirals virustatic or viruscidal?
virustatic: must inhibit viral replication without destroying the host cell
50
what are pharmacokinetic requirements of antiviral drugs?
intracellular and nuclear penetration
51
what is early viral infection diagnosis needed?
because antiviral drugs tend to be narrow-spectrum and only work against specific viruses
52
amantadine and rimantadine
rimantadine is a derivative of amantadine, they act on an early step of viral replication after attachment of virus to cell receptors
53
what is amantadine used for?
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
side effects of amantadine and rimantadine
few side effects; most of which are CNS related
55
idoxuridine
- nucleoside analog - for txt of herpesvirus infx in superficial layers of cornea and of skin, but is toxic when administered systemically!
56
what form of administering idoxuridine is toxic?
systemically toxic, is fine to administer topically
57
trifluridine
- nucleoside analog - analog of deoxythymidine - agent of choice for txt of herpesvirus keratitis in humans
58
treatment of choice for herpesvirus keratitis in humans
trifluridine - nucleoside analog
59
acyclovir
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
ribavirin
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
ribavirin safety
- well absorbed, widely distributed - narrow margin of safety in domestic animals: toxicity is manifested as anorexia, weight loss, bone marrow depression and anemia
61
interferons and interferon-inducers
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
clinical uses of IFN-inducers
effective in some model systems, but have not yet been found to be clinically useful because of their toxicity
63
neuraminidase inhibitors
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
what are neuraminidase inhibitors active against?
both influenza A and B
64
antiviral resistance
infrequent
65
zanamivir
relenza: reported to reduce flu symptoms by 1 day
66
oseltamivir
tamiflu: reduced severity of flu symptoms by 40%, also reduces rates of secondary complications
67
lysine
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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