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Pharmacology > Antimicrobials - antifungals/ anthelmintic > Flashcards

Antimicrobials - antifungals/ anthelmintic Flashcards

1
Q

Polyenes include

A

Amphotericin B
Nystatin

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2
Q

Echinocandins include

A

Caspofungin

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3
Q

Azoles include

A

Clotrimazole
Ketoconazole
Fluconazole
itraconazole
posaconazole
voriconazole

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4
Q

Allylamines include

A

terbinafine

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5
Q

MOA of amphotericin B

A

IV - disrupts the fungal cell wall synthesis binding to sterols, leading to the formation of pores in the cell membrane, causing K+ to leak out of cell resulting in cell death

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6
Q

What is Amphotericin B used to treat

A

severe invasive fungal infections - systemic
wide spectrum - widest of all antifungals
last resort - hard for people to tolerate

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7
Q

Amphotericin B onset of action?

A

rapid; not dependent on organisms growth rate

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8
Q

Amphotericin B kidney affects

A

nephrotoxicity - vasoconstrictive effect on the afferent renal arterioles, GFR usually returns to normal after cessation of medication
renal tubular acidosis

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9
Q

Amphotericin B adverse reactions

A

fever and rigors
premedicate with acetaminophen and/or diphenhydramine recommended
N/V
anemia
phlebitis

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10
Q

Flucytosine (5-FC) MOA

A

inhibits thymidylate synthesis and incorporates into fungal RNA disrupting nucleic acid and protein synthesis
Resistance can occur when fungi decrease level of enzymes targeted

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11
Q

Flucytosine is not used as

A

monotherapy; used in combo with amphotericin B or itraconazole

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12
Q

Flucytosine and Amphotericin B are used together for treatment in

A

systemic mycoses and meningitis caused by cryptococcus and candida spp.

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13
Q

Flucytosine and itraconazole are used together for treatment in

A

chromoblastomycosis infections

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14
Q

when using flucytosine you need to _____ adjust in _____ impairment

A

dose , renal

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15
Q

flucytosine adverse reactions

A

reversible neutropenia, thrombocytopenia (lab draws everyday)
dose related bone marrow suppression
reversible hepatic dysfunction
GI upset, N/V, diarrhea - m/c

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16
Q

The azoles are broken up into two different subgroups

A

imidazoles
triazoles

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17
Q

drugs included in the imidazole group

A

ketoconazole
miconazole
clotrimazole
more potent, usually topical, too toxic to be used systemically

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18
Q

drugs included in the triazoles group

A

fluconazole
itraconazole
voriconazole
posaconazole
less potent, usually IV, more systemic sx

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19
Q

the imidazoles MOA

A

inhibit C-14 alpha-demethylase (CYP450) which disrupts membrane structure

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20
Q

miconazole and clotrimazole are both ______ to be used _____

A

too toxic
systemically

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21
Q

Ketoconazole can be used _____

A

systemically

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22
Q

Ketoconazole should not be used with

A

Amphotericin B

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23
Q

Ketoconazole requires _________ for dissolution and absorption

A

gastric acid

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24
Q

Antacids and H2 histamine receptor blockers or PPI’s impair absorption of

A

ketoconazole

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25
Q

Ketoconazole adverse reactions

A

CYP450
gynecomastia, decreased libido, menstrual irregularities

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26
Q

Contraindications of ketoconazole

A

pregancy

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27
Q

the triazoles MOA

A

inhibits synthesis of cell membrane via the fungal CYP450, however does not interfere with the mammalian CYP450 enzymes involved in other steroid hormones - no endocrine side effects

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28
Q

Fluconazole indications

A

candida, cryptococcus neoformans, coccidiomycosis

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29
Q

Fluconazole does not depend on _______ for absorption

A

gastric acid

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30
Q

Fluconazole does penetrate the

A

CSF

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31
Q

Adverse reactions of fluconazole

A

N/V, rashes, alopecia, hepatitis

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32
Q

Contraindications Fluconazole

A

pregnancy - teratogenic

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33
Q

Itraconazole indications

A

histoplasmosis, blastomycosis and sporotrichosis

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34
Q

Itraconazole does require

A

gastric acid for absorption, no IV formulation

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35
Q

Itraconazole does not

A

penetrate CSF well

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36
Q

adverse reactions itraconazole

A

N/V, rash, HA, HTN, hypokalemia, edema, chronic therapy can cause alopecia, rarely hepatitis

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37
Q

Itraconazole drug-drug interactions

A

warfarin, statins, phenytoin

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38
Q

Contraindications itraconazole

A

teratogenic

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39
Q

Black box warning itraconazole

A

do not use for onychomycosis in pts with evidence of CHF or history of CHF

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40
Q

Caspofungin MOA

A

inhibits B(1,3)-D-glucan synthase, an enzyme involved in fungal cell wall synthesis

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41
Q

Caspofungin indication

A

invasive aspergillus infection (2nd line)
candidal infections
azole resistant Candida esophagitis

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42
Q

Caspofungin adverse drug reactions

A

histamine reaction with infusion
drug-drug interactions (cyclosporine, tacrolimus, rifampin)
CNS penetration is poor

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43
Q

Nystatin MOA

A

binds to ergosterol; similar mechanism to amphotericin B
too toxic for systemic use - never IV

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44
Q

Nystatin is not absorbed in

A

the GI tract

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45
Q

Nystatin is available in

A

powder, ointment, cream or suspension

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46
Q

Drug that is excellent for swish and spit or swish and swallow
topical use for skin and/or vaginal infections

A

Nystatin

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47
Q

Griseofulvin MOA

A

inhibits mitosis - accumulates in keratin containing tissues

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48
Q

Griseofulvin indications

A

dermatophytic nail infections

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49
Q

Griseofulvin treatment is required for how long

A

6-12 months

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50
Q

Griseofulvin should be avoided with

A

alcohol
increases rate of metabolism of other drugs including anticoagulants
CYP450 enzymes

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51
Q

Terbinafine MOA

A

inhibits cell wall synthesis by inhibiting fungal squalene epoxidase - decreases synthesis of ergosterol
accumulates in skin, nails and fat

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52
Q

Terbinafine contraindicated

A

nursing mothers - accumulates in breast milk

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53
Q

Terbinafine adverse reactions

A

hepatotoxicity - LFTs at baseline

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54
Q

antiprotozoal drugs include

A

trimethoprim - sulfamethoxazole
metronidazole

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55
Q

antihelmintic drugs include

A

albendazole
pyrantel pamoate
ivermectin
praziquantel

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56
Q

Metronidazole MOA

A

activated by anaerobes to metabolites that damage DNA leading to cell death

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57
Q

Metronidazole indications

A

amebiasis
giardiasis
trichomoniasis
(anaerobic bacterial infections)

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58
Q

Metronidazole adverse reactions

A

GI upset
metallic taste
seizures
neuropathy
?disulfiram effect with alcohol (sudden desire to vomit)

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59
Q

Metronidazole contraindications

A

pregnancy
breastfeeding
recent use of disulfiram

60
Q

trimethoprim - sulfamethoxazole MOA

A

synergistic blockade of folate pathway, leads to inhibition of thymidine synthesis

61
Q

trimethoprim - sulfamethoxazole avoid in pts with

A

renal disease

62
Q

trimethoprim - sulfamethoxazole contraindications

A

newborns and pregnancy

63
Q

trimethoprim - sulfamethoxazole adverse effects

A

rash
SJS
bone marrow suppression
anemia
renal impairment
hepatotoxicity

64
Q

Ascaris lumbrioides (nematodes) treatment

A

albendazole

65
Q

Trichuris trichuria (nematodes) treatment

A

albendazole

66
Q

Enterobius vermicularis (nematodes) treatment

A

albendazole

67
Q

Necator americanus (nematodes) treatment

A

albendazole

68
Q

Strongyloides stercoralis (nematodes) treatment

A

ivermectin
albendazole - 2nd line

69
Q

Onchocerca volvulus (nematodes) treatment

A

ivermectin

70
Q

cestodes (tapeworms) treatment
taenia solium (pork)
taenia saginata (beef)

A

praziquantel

71
Q

trematodes (flukes) treatment
schistosoma ssp
clonorchis sinensis

A

praziquantel

72
Q

albendazole MOA

A

binds to the microtubules in intestinal and tegmental worms and larvae; impaired glucose uptake –> glycogen depletion –> degeneration of ER and mitochondria, release of lysosomes, and depletion of ATP/ energy causing worm death

73
Q

albendazole adverse reactions

A

HA
elevated LFTs
rare = GI
alopecia
rare = liver failure, myelosuppression, seizures

74
Q

albendazole contraindications

75
Q

Pyrantel Pamoate (OTC) MOA

A

causes release of acetylcholine and inhibits cholinesterase - acts as a neuromuscular blocker, spastic paralysis, release of the helminths

76
Q

Pyrantel Pamoate adverse reactions

A

rare HA, dizziness, GI distress

77
Q

Praziquantel MOA

A

increases cell permeability to Ca2+ in schistosomes –> strong contractions and paralysis of worm musculature which leads to detachment, dislodgement and death

78
Q

Praziquantel adverse reactions

A

abdominal pain, dizziness, drowsiness

79
Q

Ivermectin MOA

A

binds and activates glutamate - gated chloride channels in invertebrate nerve and muscle cells –> hyperpolarization and death of helminth

does not cross BBB

80
Q

Ivermectin adverse reactions

A

nephrotoxicity (CNS depression, ataxia)

81
Q

Ivermectin contraindications

A

preg, meningitis

82
Q

Neuraminidase inhibitors include:

A

oseltamivir

83
Q

MOA oseltamivir

A

inhibitors of neuraminidase (enzyme that is essential for cleaving the virus from the host cell and allowing spreading of the virus from cell to cell)

84
Q

Anti-influenza agents - neuraminidase inhibitors

A

oseltamivir (PO) - active against flu A and B

85
Q

How to administer Oseltamivir for flu

A

24-48 hrs on sx onset to decrease course of disease by 1-2 days
decreases viral load
also used for prophylaxis

86
Q

How is oseltamivir metabolized and where

A

active orally as a prodrug and hydrolyzed by the liver to its active form

87
Q

Oseltamivir needs to be dose adjusted for

A

renal impairment

88
Q

SE of oseltamivir

A

N/V
recommended to take with food to minimize

89
Q

Antivirals against Herpes virus

A

acyclovir and derivatives
foscarnet

90
Q

MOA Acyclovir

A

Guanosine analogs, inhibits transcription

Activated by viral thymidine kinase (TK) - activated in infected cells
AcyclcoGTP inhibits viral DNA polymerase by chain termination

91
Q

Acyclovir spectrum of activity

A

herpes simplex 1 & 2 viruses (not effective against latent virus)
varicella-zoster virus

92
Q

Acyclovir metabolism

A

renal metabolism

93
Q

Acyclovir dose adjustment for

A

renal impairment

94
Q

Acyclovir adverse effects

A

well tolerated
mild GI upset
nephrotoxicity and neurotoxicity

95
Q

To overcome poor bioavailability of Acyclovir, _______ was developed

A

valacyclovir

96
Q

Acyclovir has poor ________ and requires ________ dosing

A

Bioavailability
frequent

97
Q

Valacyclovir is a

98
Q

How is Valacyclovir metabolized

A

hydrolyzed by first pass enzymes in the intestine and liver (99% conversion rate to acyclovir)

99
Q

Valacyclovir is more ______ than Acyclovir

100
Q

Valacyclovir has the same SE as Acyclovir but _____ is more common

101
Q

Famciclovir overcomes ________ of penciclovir

A

poor bioavailability

102
Q

How is Famciclovir metabolized

A

metabolized to penciclovir which requires phosphorylation by viral thymindine kinase in infected cells to become active

103
Q

Famciclovir MOA

A

selectively inhibits viral DNA polymerase by chain termination

104
Q

Herpes Agent Foscarnet MOA

A

directly inhibits DNA polymerase (does NOT require activation by viral kinase)
reversibly blocks the pyrophosphate binding site of viral DNA polymerase

105
Q

Foscarnet is a inorganic

A

pyrophosphate analog

106
Q

Foscarnet is used for treatment

A

of immunocompromised patients with cytomegalovirus (CMV) retinitis and mucocutaneous acyclovir-resistant HSV and VZN infections

107
Q

IV acyclovir can

A

crystalize in the renal tubules causing renal dysfunction (obstructive crystalline nephropathy)

108
Q

Foscarnet is only given in ____ form

109
Q

Foscarnet toxicity

A

requires dose adjustment in renal impairment
GI effects
electrolyte abnormalities (arrhythmias)
nephrotoxicity - reversible, worse when combined with other nephrotoxic agents

110
Q

Hep B treatment

A

entecavir
tenofovir
lamivudine

111
Q

Hep C treatment

A

Ribavirin
Ledipasvir
Sofosbuvir

112
Q

Interferons MOA

A

IFNalpha2b and alpha2a: host cytokines with complex antiviral, immunomodulatory and antiproliferative activities

113
Q

Interferons are thought to

A

induce gene transcription that inhibit viral RNA, increases phagocytic activity of macrophages, increase cytotoxicity of lymphocytes for target cell’s

114
Q

Interferons are given by

A

IV or subQ - no PO

115
Q

Interferons may be treatment for

A

HBV and HCB as combination - rarely first line

116
Q

Adverse effects of interferons

A

flu like sx shortly after administration
mood disorders, somnolence, confusion, wt loss, depression, seizures, autoimmune rxn… many more

117
Q

Interferons need to be dose adjusted in

A

severe renal disease

118
Q

Goal of HBV antiviral therapy

A

suppression of HBV DNA levels
decrease risk of liver damage
seroconversion of HBeAg+ to HBeAg-
loss of HBsAg detection

119
Q

Chronic Hepatitis B viral infection treatment

A

lamivudine
entecavir
tenofovir

120
Q

lamivudine MOA

A

cytosine analog works to inhibit viral DNA synthesis by inhibiting HBV DNA polymerase

121
Q

lamivudine has good ______ absorption

122
Q

lamivudine needs to be dose adjusted for

A

renal impairment (if CrCl < 50)

123
Q

Adverse effects of lamivudine

A

well tolerated
HA
dizziness
may cause pancreatitis

124
Q

rare SE’s of Lamivudine, Entecavir and Tenofovir

A

lactic acidosis
severe hepatomegaly

125
Q

Entecavir MOA

A

phosphorylated to guanosine triphosphate and competes as substrate for HBV DNV polymerase thereby inhibiting the enzyme

126
Q

Entecavir is not preferred for

A

lamivudine resistant strains - tenofovir is preferred

127
Q

Entecavir is not recommended for use in

A

HIV-HBV co-infection without a fully suppressive anti-HIV regimen as it may select resistance to lamivudine

128
Q

Adverse effects of Entecavir

A

increase ALT levels, mild GI upset, mild hyperglycemia, HA

129
Q

Tenofovir MOA

A

inhibits replication of HBV by inhibiting HBV DNA polymerase (also works against HIV reverse transcriptase)

130
Q

Tenofovir may be used

A

in pts who have had prior treatment or develop drug resistance - preferred if lamivudine resistance

131
Q

Tenofovir needs to be dose adjusted for

A

renal impairment

132
Q

Tenofovir adverse effects

A

GI effects, rash, hypercholesterolemia, decreased bone mineral density

133
Q

Black box warning post treatment of Tenofovir

A

post treatment exacerbation of hepatitis

monitor hepatic function closely for at least several months in pts who discontinue anti-hep B therapy

134
Q

Ribavirin MOA

A

inhibits guanine nucleotide synthesis thereby inhibiting viral transcription and RNA replication

135
Q

Ribavirin is used in treatment for

A

hep C (PO) in combination with interferon

severe pediatric RSV infections

136
Q

Serious adverse effect of Ribavirin

A

hemolytic anemia

137
Q

Ledipasvir MOA

A

inhibits NS5A protein which plays a role in both viral replication and the assembly of the hep C virus

138
Q

Ledipasvir is administered

A

PO in combination with other direct acting antivirals

139
Q

What can decrease the absorption of Ledipasvir

A

increased gastric pH levels

140
Q

Ledipasvir adverse reactions

A

well tolerated
$$$

141
Q

Sofosbuvir MOA

A

inhibits NS5B protein which plays a role in both viral replication and assembly of the hepatitis C virus

142
Q

Sofosbuvir administered

A

PO in combination formulation

143
Q

Sofosbuvir can not be coadministered with

A

Amiodarone - reports of sx bradycardia and a fatal cardiac arrest

144
Q

Ledipasvir-Sofosbuvir should be avoided in pts with

A

renal impairment

145
Q

Ledipasvir-Sofosbuvir should not be coadministered with

A

amiodarone

Pharmacology (7 decks)

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