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Pharmacology > Chapter 18: non-bacterial infections > Flashcards

Chapter 18: non-bacterial infections Flashcards

1
Q

what has extensive use of ABTs worldwide led to?

A

emergence of viral and fungal superinfections

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2
Q

What population is most affected by superinfections

A

immunocompromise

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3
Q

effective, specific agents are often based on

A

genetic sequencing and understanding of pathogens

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4
Q

how does a virus reproduce

A

enters a host cell and take over the cell’s protein and nucleic acid synthesis

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5
Q

effective antiviral agents need to stop one of the steps in the viral replication process

A

attachment of the virus to the host cell -release of the virus’s genes into the host cell

replication and assembly of new viral components -release of viral components into a new host cell

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6
Q

regimen of medications used to treat HIV

A

highly active antiretroviral therapy (HAART)

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7
Q

clinical syndrome review of HIV/AIDS

A

“clinical syndrome”

opportunistic infections

cancer

“set point”

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8
Q

HIV replication

A

reverse transcribe RNA genome into DNA thus reversing the usual flow of genetic information. DNA is then incorporated into host cell’s genome allowing replication

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9
Q

reasons for noncompliance with HIV treatment regimen

A

length of treatment, side effects, cost of medications,

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10
Q

Patient education regarding HAART treatment

A

how to take med

adverse effects

fitting regimen into lifestyle longterm

cost management

safe sex practices

avoiding opportunistic infections

how to live with chronic infectious disease

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11
Q

purpose of antiretrovirals in HIV treatment

A

combination of drugs to suppress viral replication to undetectable plasma HIV RNA to prevent further immune system damage as well as any possibility of emergingresistant strains

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12
Q

6 classes of antiretrovirals

A

NRTI

NNRTI

PI

CCRS

FI

INTEGRASE

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13
Q

most common combinations of antiretrovirals for treatment of HIV

A

NRTI with PI one NNRTI

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14
Q

initial antiretroviral regimen consist of

A

2 NRTIs with with either an NNRTI, PI, Integrase inhibitor, or CCR5 antagonist

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15
Q

examples of NRTIs

A

abacavir (Ziagen)

didanosine (Videx)

emtricitabine (Emtriva)

lamivudine (Retrovir)

zalcitabine (Hivid)

stavudine (Zerit)

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16
Q

NRTIs are synthetic agents thast mimic

A

natural nucleotides (building blocks of RNA)

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17
Q

NRTI mechanism of action

A

compete with natural nucleotides in the HIV virus that would otherwise be used in the reverse transcriptase enzyme in newly synthesized viral DNA chains

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18
Q

common adverse effects of NRTIs

A

rash

abdominal distress

thrombocytosis

fatigue

lactic acidosis

back pain

tremor, headache, weakness

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19
Q

things to watch for with NRTIs

A

leukopenia, anemia, anaphylaxis, heptomegaly

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20
Q

concomittent use of any 2 NRTIs

A

not recommended

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21
Q

labs that need monitored with antiretroviral treatment

A

CBC

met panal

CD4

lymphocytes

HIV levels

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22
Q

what else should HIV patients be tested for prior to initiating therapy

A

Hep B

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23
Q

patients on abacavir must be monitored for

A

signs of hypersensitivity and elevated liver function

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24
Q

target of PIs

A

later stage in viral replication cycle than NRTIs

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25
Q

PI mechanism of action

A

bind to active sites that are used by viral protease enzymes so they can’t process viral precursors critical to the maturation of an HIV virus

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26
Q

examples of PPIs

A

amprenavir (Agnerase)

atazaniavir (ATV, Reyataz)

fosamprenavir (Lexiva, Telzir)

indinavir (Crixivan)

ritonavir (Norvir)

saquinavir (Fortovase)

nelfinavir (Viracept)

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27
Q

hypersensitivity reactions of PIs

A

can be severe

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28
Q

interactions with drugs metabolized in the liver that can cause serious life threatening events

A

nonsedating antihistamines

sedative hypnotics

Astemizole, triazolam, midazolam

ergot alkaloid preparation

antiarrhythmics (amiodarone, quinidine)

CCBs

amphetamines

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29
Q

PI contraindications

A

hypersensitivity to sulfonamides

patients taking vitamin E

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30
Q

NNRTI mechanism of action

A

bind to active site of HIV reverse transcriptase

is additive or synergistic with most other antiretrovirals

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31
Q

examples of NNRTIs

A

delavirdine (Rescriptor)

evavirenz (Sustiva)

nevirapine (Viramune)

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32
Q

DERM side effect of NNRTIs

A

rash that progresses to epidermal necrosis

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33
Q

NNRTIs patient education

A

stay well hydrated to avoid renal failure

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34
Q

why should efavirenz be taken at bedtime

A

improve CNS tolerability and psychiatric effects

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35
Q

what follows initial herpes infection

A

latent state with the potential to reactivate later in life

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36
Q

efficacy of episodic therapy for herpes

A

shortens the duration of an outbreak if started within 24 hours of lesions or prodromal symptoms

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37
Q

mechanism of action for antivirals used for herpes infections

A

nucleic acid analogues host enzymes cause them to convert to active compounds and become part of the DNA chain. This inhibits viral RNA to interferen with viral DNA synthesis

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38
Q

examples of antivirals used to treat herpes infections

A

acyclovir (Zovirax)

cidofovir (Vistide)

ganciclovir (Cytovene)

famciclovir (Famvir)

penciclovir (Denavir)

foscarnet (Foscavir)

trifluridine (Viroptic)

valacyclovir (Valtrex)

valganciclovir (Valcyte)

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39
Q

interactions with antivirals used for herpes infections

A

minimal.

May affect bioavailability if acyclovir anf famciclovir are given with antihistamines

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40
Q

most important variable in selecting antiviral for herpes treatment

A

renal function

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41
Q

examples of antivirals used for respiratory infections

A

amantadine (Symmetrel)

oseltamivir (Tamiflu)

rimantadine (Flumadine)

zanamivir (Relenza)

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42
Q

zanamivir (Relenza) mechanism of action

A

prevents viral replication by inhibiting the enzyme neuraminidase

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43
Q

amantadine (Symmetrel) mechanism of action

A

dopaminergic agonsit with the ability to block the uncoating of influenza A virus

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44
Q

rimantadine (Flumadine) mechanism of action

A

tricyclic amine that affects the release of newly replicated virus strands from host cells, possibly by inhibiting uncoating of the virus

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45
Q

osteltamivir (Tamiflu)

A

analogue of sialic acid and is potent selective inhibitor of influenza A and B virus neuraminidase

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46
Q

clinical use for osteltamivir and zanamivir

A

prevention and treatment of influenza A or B

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47
Q

clinical use for amantadine and rimantadine

A

prevention and treatment for influenza A

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48
Q

susceptibility of vast majority of H1N1 strains

A

susceptible to osteltamivir and zanamivir

resistant to amantadine and rimantadine

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49
Q

antivirals for respiratory infections administered with antihistamines or antidepressants

A

cause dry mouth, blurry vision, and constipation

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50
Q

what drug causes increased toxicity if given with amantadine and rimantadine

A

triamterine

51
Q

contraindications for amantadine and rimantadine

A

pregnancy

52
Q

types of antifungals

A

polyene macrolides

azoles

terbinafine (Lamisil)

griseofluvin (Fluvicin)

53
Q

examples of polyene macrolides

A

amphotericin B

Nystatin

54
Q

examples of Azoles

A

imidazole

triazole

55
Q

patient education on antivirals used for respiratory infections

A

only shortens flu duration by 1-2 days

alcohol compounds dizziness

take 4 hours prior to bed to avoid insomnia

56
Q

drug of choice for topical fungal infections

A

nystatin

57
Q

clinical uses of amphotericin B

A

cryptococcal meningitis in HIV patients

invasive and rapidly progressing, potentially fatal fungul infections

treatment of visceral leishmaniasis

58
Q

polyene macrolides mechanism of action

A

bind to sterols in the fungal cell membrane altering the membranes permeability to K+, Mg+, and other celll components

59
Q

polyene macrolide interactions

A

synergistic nephrotoxicity with aminoglycosides or cyclosporine

60
Q

patient education about polyene macrolides

A

long term treatment may be necessary to clear infection (weeks to months)

61
Q

azoles mechanism of action

A

inhibits fungal demethylase (a CYP450 dependent enzyme present in fungi) affects the synthesis of the fungal cell wall and causes leakage of cell contents

62
Q

types of azoles

A

imidazole

triazole

63
Q

examples of imidazoles

A

fluconazole (Diflucan)

ketoconazole (Nizoral)

itraconazole (Sporanox)

64
Q

clinical uses of oral antifungals

A

superficial infections caused by yeast

dermatophytes, and invase systemic mycoses (page 351)

65
Q

clinical uses for topical antifungals

A

treat tinea infections and superficial yeast infections

66
Q

which antifungal should NOT be used with history of HF

A

itraconazole

67
Q

why should coadministration of ABTs and azoles be avoided

A

can lead to fungal resistance and fungal superinfection

68
Q

patient education: itraconazole

A

take with food to enhance absorption

avoid antacids within 2 hours of ingestion

69
Q

terbinafine (Lamisil)

mechanism of action

A

synthetic allylamine that inhibits squalene 2, 3-epoxidase

(enzyme needed for cell wall synthesis)

fungicidal to a wide variety of dermatophytes

70
Q

clinical uses for lamisil

A

superficial fungal infections of hair, nail, and skin

examples:

tinea pedic (athletes foot)

tinea cruris (jock itch)

tinea corporis (ringworm)

71
Q

lamisil interactions

A

alcohol increases liklihood of hepatotoxicity

drugs that inhibit hepatic metabolism (cimetidine, rifampin)

caffeine can increase side effects

72
Q

patient education for lamisil

A

notify clinician if dark urine, rash, pale stool appear

take same time every day for entire course

discuss OTC and herbal medications prior to use

73
Q

griseofulvin (Fulvicin)

mechanism of action

A

binds to microtubules that comprise the spindles to inhibit fungal mitosis

fungistatic

74
Q

what is griseofulvin NOT used for

A

subcutaneous or deep fungal infections

candidiasis

tinea versicolor

75
Q

clinical uses of fluvicin

A

treatment of superficial fungal infections of hair, nails, and skin

76
Q

griseofulvin interactions

A

reduces plasma salicylate levels when taken with ASA

oral contraceptives

reduces anticoagulant effect of warfarin

can increase effects of alcohol (tachycardia, diaphoresis, flushing)

77
Q

griseofulvin contraindications

A

severe liver disease

active alcoholism

pregnancy

78
Q

most common adverse effect of griseofulvin

A

skin eruptions and rash, sore throat

79
Q

types of antiprotozoals

A

metronidazole (Flagyl)

nitazoxanide (Alinia)

tinidazole (Tindamax)

80
Q

conscientious prescribing of antiprotozoals

A

include sexual partner in treatment for trichomoniasis

disulfiram-like reaction can occur to alcohol base in other preparations

efficacy unknown in immunocompromised patients

81
Q

what should be done if antiprotozoal re-treatment is necessary

A

CBC

white blood cell differential

82
Q

antiprotozoal patient education

A

avoid alcohol for at least 24 hours after last dose

expect metallic taste

may cause reddish-brown urine

take with food to avoid GI upset

83
Q

metronidazole (Flagyl)

mechanism of action

A

anaerobic bactericide, trichomonacide, amebicide

diffuses into a susceptible organisma and disrupts DNA and protein synthesis

84
Q

clinical use of flagyl

A

oral therapy for anaerobic infections, amebiasis, giardiasis, trichomoniasis, and colitis d/t C-diff

85
Q

nitazoxanide (Alinia)

mechanism of action

A

interferes with the pyruvate ferrodoxin enzyme pathway

86
Q

clinical uses of nitazoxanide (Alinia)

A

diarrhea associated with Giardia lamblia and Cryptosporidium parvum

87
Q

tinidazole (Tindamax)

mechanism of action

A

similar to flagyl but is converted to an active metabolite by cell extracts of the pathogen

88
Q

clinical uses for tinidazole (Tindamax)

A

intestinal amebiasis, giardiasis, and trichomoniasis

89
Q

clinical uses of antiprotozoals

A

topically for rosacea and bacterial vaginosis

used in combo therapy for H. pylori ulcers

90
Q

antiprotozoal interactions

A

flagyl and warfarin may induce bleeding

cimetidine may decrease metabolism of flagyl

disulfram-like reaction with alcohol

91
Q

antiprotozoals contraindications

A

first trimester of pregnancy

lactation

92
Q

antihelminthics

A

used to treat parasitic infections

93
Q

classes of antihelminths

A

benzimidazoles

pyrantel pamoate

ivermectin

94
Q

axamples of benzimidazoles

A

mebendazole (Vermox)

thiabendazole (Mintezol)

albendazole (Albenza)

95
Q

appropriate treatment for all helminthic infestations except pinworms

A

mebendazole 100mg BID x 3days

OR

albendazole 400mg daily

96
Q

most pressing concern when fighting a nematode infestation

A

seeing resistance develop

monitor patients closely

97
Q

why should patients be monitored closely when taking a banzimidazole

A

propensity of medication to cause bone marrow depression, aplastic anemia, or agranulocytosis

98
Q

benzimidazoles mechanism of action

A

each act directly on different parasites to treat systemic infections

99
Q

uses for mebendazole (Vermox)

A

treatment of ascariasis, trichuriasis, hookworm, and pinworm infections

100
Q

uses of thiabendazole (Mintezol)

A

treatment of strongyloidiasis (threadworm)

101
Q

uses of albendazole (Albenza)

A

treatment of ascariasis enterobiasis (pinworm), hookworm, and after surgical removal or aspiration of hydatid cysts

102
Q

antihelminths interactions

A

mebendazole metabolism is inhibited by cimetidine and anticonvulsants

thiabendazole and xanthine derivatives can cause toxicity

103
Q

antihelminths contraindications

A

pregnancy

renal disease

cirrhosis

104
Q

antihelminths patient education

A

chew tablets before swallowing

stool should be rechecked 3 days after treatment

strict hygiene to prevent reinfection

105
Q

pyrantel pamoate

mechanism of action

A

acts as a neuromuscular blocking agent in susceotible mature and immature helminths within the GI tract

106
Q

pyrantel pamoate is only effective where

A

within the GI lumen

107
Q

clinical uses of pyrantel pamoate

A

pinworm, roundworm, hookworm

108
Q

pyrantel and piperazine

A

mutually antagonize each other

109
Q

ivermectin (Stromectol)

mechanims of action

A

related to macrolide ABTs

causes paralysis and death of parasite by binding to chloride channels in parasite’s nerve and muscle cells

110
Q

clinical uses of ivermectin

A

river blindness (Onchocera volvulus)

control of head lice and scabies

111
Q

ivermectin interactions

A

can affect LFTs

barbituates and benzodiazepines can cause increased sedation

112
Q

ivermectin contraindications

A

pregnancy

lactation

113
Q

drugs used to treat malaria

A

chloroquine

primaquine

atovaquone/proguanil (Malarone)

114
Q

chloroquine mechanism of action

A

interfers with parasite protein synthesis and inhibits it’s growth

115
Q

what is the most widely used drug to treat malaria

A

chloroquine

(prophylaxis and treatment)

116
Q

mechanism of action for primaquine and mefloquine

A

destroy the asexual blood forms of malarial pathogens

inhibits parasite growth

117
Q

when are primaquine and mefloquine used

A

when there is known resistance to chloroquine

118
Q

malarone use

A

malria prophylaxis

119
Q

antimalarial drugs when patient is on cardiac medications such as beta-blockers

A

take cardiac medication at least 12 hours after antimalarial

120
Q

contraindications for antimalarials

A

history of seizures, psychiatric disorders, cardiac abnormalities

pregnancy

121
Q

lab values that require d/c of antimalarial medication

A

drop in LFTs, HGB concentrations, or leukocyte counts

122
Q

antimalarials in patients with G6PD

A

watch for hemolytic anemia or leukopenia

123
Q
A

Pharmacology (28 decks)

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