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PHRM 865 > Exam 4 Kays > Flashcards

Exam 4 Kays Flashcards

1
Q

what candida species is starting to emerge with multi-drug resistance

A

c. auris

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2
Q

why can aspergillus be a problem?

A

Mold can can cause disease in immunocompromised hosts and lead to neutropenia

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3
Q

What are endemic (pathogenic) fungi

A

Histoplasma
Blastomyces
Coccidioides

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4
Q

Amphotericin B MOA

A

binds to ergosterol and gets inserted into the fungal cytoplasmic membrane –> disruption of the fungal cytoplasmic membrane –> increased cell permeability –> leakage of sodium/potassium/cellular constituents, loss of membrane potential, metabolic disruption –> cell death

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5
Q

Is Amphotericin B static or cidal

A

concentration dependent cidal activity

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6
Q

Amphotericin B onset of action

A

rapid

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7
Q

Amphotericin B DOC

A

Cryptococcus
Histoplasma
Aspergillus
Mucor

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8
Q

Amphotericin B Doxycholate dosing

A

Test dose of 0.1mg/kg or 1 mg over 20-30 min

0.3-1 mg/kg/day over 4-6 hours

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9
Q

Amphotericin B L-AmB dosing

A

1.5-6 mg/kg daily over 2 hours

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10
Q

Amphotericin B ABLC dosing

A

5 mg/kg, infused at 2.5 mg/kg/hr

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11
Q

What is Amphotericin B dosing based on

A

ideal body weight or adjusted

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12
Q

Amphotericin B Deoxycholate infusion related AE

A

Headache, fever, chills, arthralgias, N/V with infusion
*Pretreat with acetaminophen or aspirin, antihistamines, mepereidine, phenothiazines, hydrocortisone

thrombophlebitis

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13
Q

Amphotericin B Deoxycholate non-infusion related AE

A

Nephrotoxicity: direct vasoconstriction –> hypokalemia and hypomagnesia

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14
Q

flucytosine MOA proteins

A

5-FC enters fungal cell –> deaminated to 5-FU –> 5FU gets incorporated into fungal RNA –> interference with protein synthesis

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15
Q

flucytosine MOA

A

5-FC enters fungal cell –> metabolized to 5-FDUMP –> inhibits thymidylate synthetase –> interfers with DNA synthesis

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16
Q

flucytosine MOA

A

cryptococcus neoformans (meningitis)

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17
Q

flucytosine excretion

A

85-95% excreted unchanged in urine

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18
Q

flucytosine AE

A

hematologic: bone marrow suppression at concentrations >100 ug/ml

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19
Q

what is flucytosine dosing based on

A

ideal if non-severe

adjusted if severe

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20
Q

flucytosine dosing

A

100 mg/kg/day PO in 4 divided doses

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21
Q

Ketoconazole MOA

A

inhibits synthesis of ergosterol via inhibition of the fungal cytochrome p-450 dependent enzyme lanosterol 14-alpha-demethylase

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22
Q

Ketoconazole SOA

A

candida albicans
crypptococcus neoformans
histoplasma
dermatophytes

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23
Q

Ketoconazole PK

A

absorption is inversely related to gastric pH

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24
Q

flucytosine distribution

A

CSF

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25
Q

ketoconazole distribution

A

throughout body minus CSF

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26
Q

ketoconazole metabolism

A

hepatic

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27
Q

can ketoconazole be used orally for first line therapy

A

no due to risk of hepatotoxicity

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28
Q

ketoconazole AE

A

hepatotoxicity

Endocrine: inhibition of adrenal steroid and testosterone synthesis

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29
Q

ketoconazole drug interaction

A

potent inhibitor of CYP3A4

gastric pH meds: decrease bioavailability
anticoag: prolonged PT
Rifampin: decreases ketoconazole
Cyclospoin- increases conce
phenytoin: increased concen
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30
Q

Itraconazole MOA

A

inhibits synthesis of ergosterol via inhibition of the fungal cytochrome P450 dependent enzyme lanosterol 14-alpha-demethylase

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31
Q

itraconazole SOA

A

aspergillus
histoplasma
sporothrix

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32
Q

itraconazole capsule absorption

A

good but dependent on gastric acidity (want low pH)

absorbed better when taking with meal or acidic cola beverage

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33
Q

itraconazole solution absorption

A

absorbed better in fasting state

not affected by gastric acidity

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34
Q

SUBA-itraconazole absorption

A

not affected by gastric acidity

give with food

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35
Q

are itraconazole capsules and suspensions interchangable

A

no

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36
Q

itraconazole distribution

A

widely distributed but poor CSF

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37
Q

itraconazole metabolism

A

active metabolite: hydroxyiraconazole

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38
Q

itraconazole elimination

A

hepatic

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39
Q

itraconazole clinical use and dosing

A

histoplasmosis: 200 TID x3 then 200 BID

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40
Q

itraconazole adverse reactions

A

hepatotoxicity
CFH
QTc prolongation

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41
Q

itraconazole black box warning

A

Contraindicated in patients with CHF: may cause negative inotropic effect

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42
Q

itraconazole drug interactions

A

H2 antagonists
PPIs
CYP3A4

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43
Q

What drugs does itraconazole increase concentrations of

A 
digoxin
quinidine
benzos
statins (minus prava)
rifabutin
cyclosporine
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44
Q

what drugs decrease concentrations of itraconazole

A

carbamazepine
phenytoin
phenobarbital
rifampin

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45
Q

what drugs increase concentrations of itraconazole

A

clarithomycin
indinavir
ritonavir

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46
Q

fluconazole MOA

A

inhibit synthesis of ergosterol via inhibition of the fungal cytochrome P-450 dependent enzyme lanosterol 14-alpha-demethylase

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47
Q

fluconazole SOA

A

candida

cryptococcus

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48
Q

what candida is fluconazole not active against

A

c. glabrata

c. krusei

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49
Q

fluconazole absorption

A

well absorbed orally independent of gastric acidity

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50
Q

fluconazole distribution

A

good concentration in CSF

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51
Q

fluconazole elimination

A

renal

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52
Q

fluconazole oropharyngeal dosing

A

200mg day 1 then 100-200 qd for 2 weeks

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53
Q

fluconazole esophageal dosing

A

400mg day 1, then 200-400 mg qd for 14-21 days

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54
Q

fluconazole vaginal dosing

A

150mg x1 dose

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55
Q

fluconazole prophylaxis dosing

A

400mg

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56
Q

fluconazole candida UTI dosing

A

100-200 mg qd

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57
Q

fluconzole cryptococcal meningitis consolidation therapy dose

A

400mg QD for 10-12 weeks after CSF negative

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58
Q

fluconazole cryptococcal meningitis maintenance therapy dose

A

200 mg qd for at least 1 year AND remains asymptomatic from infection AND CD4 count >100 for 3 months and suppressed HIV RNA in response to effective antiretroviral therapy

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59
Q

what is fluconazole dosing based off of

A

total body weight

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60
Q

fluconazole AE

A

QT prolongation

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61
Q

fluconazole DI

A

potent inhibitory of CYP2C19

moderate inhibitor of CYP3A4

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62
Q

voriconazole MOA

A

inhibits synthesis of ergosterol via inhibition of the fungal cytochrome p-450 dependent enzyme lanosterol 14-alpha-demethylase

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63
Q

voriconazole SOA

A

aspergillus

fusarium

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64
Q

voriconazole absorption

A

Great oral bioavailability

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65
Q

is voriconazole absorption affected by acid

A

NO

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66
Q

voriconazole metabolism

A

significantly metabolized by cyt p450

metabolism is saturation- non-linear PK

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67
Q

when to avoid voriconazole

A

CLCR <50

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68
Q

do you dose adjust for oral dosing of voriconazole

A

nah

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69
Q

voriconazole common dosing

A

6mg/kg q 12 for first 24 horus for loading

4mg/kg q 12 IV or 200mg Q 12 PO

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70
Q

voriconazole AE

A

visual disturbances
Elevated LFTs
QTC prolongation

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71
Q

what drugs decrease voriconazole exposure

A

rifampin
rifabutin
carbamazepine

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72
Q

posaconazole MOA

A

blocks synthesis of ergosterol

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73
Q

posaconazole SOA

A

aspergillus

mucor

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74
Q

is posaconazole affected by gastric pH

A

YES for oral suspension

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75
Q

when to avoid posaconazole

A

CrCl< 50 since IV formulation contains cyclodextrin

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76
Q

what drugs decrease dose of posaconazole

A

phenytoin
rifabutin
PPIs

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77
Q

posaconazole AE

A

QTC prolongation

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78
Q

how is isavucaonzole different than other azoles

A

prodrug- metabolized to isavuconazonium sulfate by esterases in blood

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79
Q

isavuconazole MOA

A

inhibits synthesis of ergosterol

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80
Q

isavuconazole SOA

A

aspergillus
mucor
rhizopus

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81
Q

isavuconazole PK

A

linear pk

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82
Q

is dose adjustment needed in isavuconazole

A

no

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83
Q

Isavuconazole and QTc

A

does not cause QT prolongation: can shorten QT interval

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84
Q

echinocandin MOA

A

glucan synthesis inhibit to destroy fungal cell wall

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85
Q

are echinocandins cidal or static

A

cidal

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86
Q

echinocandins SOA

A

aspergillus

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87
Q

which antifungal is CI in pregnancy

A

ibrexafunger

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88
Q

What is candida normal flora of

A

GI tract

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89
Q

most common candidasis species

A

c. albicans

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90
Q

What is the primary line of host defenses against superficial candida infections

A

cell-mediated immunity by CD4 t cells

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91
Q

OPC clinical presentation

A

“cottage-cheese” appearance with yellowish white, soft plaques that are easily removed by vigorous rubbing

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92
Q

Treatment duration of OPC

A

7-14 days but start with shorter time period first

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93
Q

OPC mild infection therapy

A

*Topical
Clotrimazole troche
Nystatin
Miconazole buccal tab

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94
Q

When is systemic therapy needed for OPC

A

Refactory OPC
patients who cannot tolerate topical agents
patients with moderate to severe disease
patients at high risk for neutropenia

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95
Q

DOC for systemic therapy OPC

A

Fluconazole

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96
Q

OPC systemic therapy options

A

fluconazole
itraconazole
posaconazole suspension

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97
Q

Treatment duration for fluconazole-refactory opc

A

> 14 days min but up to 28 days

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98
Q

Fluconazole refractory OPC treatment options

A 
itraconazole
posaconazole
amphotericin B
voriconaole
caspofungin
micafungin
anidulafungin
99
Q

what type of therapy is needed for esophageal candidiasis

A

systemic

100
Q

therapy duration for esophageal candidiasis

A

14-21 days

101
Q

esophageal candidiasis treatment options

A 
fluconazole
itraconazole
echinocandins
voriconazole
posaconazole
amphoteicin B deoxycholate
102
Q

therapy duration for esophageal candidiasis fluconazole refractory

A

21-28 days

103
Q

esophageal candidiasis fluconazole refractory treatment options

A 
itraconazole
echinocandins
voriconazole
posaconazole
amphotericin B deoxycholate
104
Q

what is uncomplicated VVC

A

sporadic infection that is susceptible to all forms of antifungal therapy regardless of treatment duration

105
Q

what is complication VVC

A

recurrent VVC
severe disease
non-candida albicans infection
host factors

106
Q

what is responsible for 80-92% of symptomatic VVC

A

candida albicans

107
Q

uncomplicated VVC treatment

A

topical/oral azoles

nystatin

108
Q

complicated VVC treatment

A

fluconazole 150mg 2-3 doses 72 hours apart

treatment 10-14 days

109
Q

what is recurrent VVC

A

> 4 episodes within a 12 months period

110
Q

recurrent VVC treatment

A

topical or oral azole for 10-14 days followed by fluconazole PO once weekly for 6 months

111
Q

antifungal-resistant VVC treatment

A

boric acid

flucytosine

112
Q

what are dermatophytoses

A

superficial mycotic infections of the skin

113
Q

what is tinea pedis

A

athletes foot

114
Q

treatment duration for tinea pedis

A

2-4 weeks of topical therapy

115
Q

what is tinea manuum

A

palmar surface infection

116
Q

what is tinea cruris

A

infection of the proximal thighs and buttocks

Jock itch

117
Q

treatment duration for tinea cruris

A

1-2 weeks of topical therapy

118
Q

what is tinea corporis

A

infection of the skin of the trunk and extremities

119
Q

what is tinea capitis

A

infection involving the scalp, hair follicles, and adjacent skin

120
Q

how to treat tinea capitis

A

terbinafine for 4-8 weeks

121
Q

what is tinea barbae

A

infection of the hairs and follicles of the beard and moustache

122
Q

how to treat tinea barbae

A

terbinafine for 4-8 weeks

123
Q

what is tinea (pityriasis) versicolor

A

hyper- or hypopigmented scaly patches on trunk and extremities

124
Q

what is onychomychosis (tinea unguium)

A

fungal infection of the toe nails (more common) and fingernails

125
Q

onychomychosis (tinea unguium) treatment

A

Terbinafine
Itraconazole
Fluconazole

126
Q

histoplasmosis pathophys

A

conidia become aerosolized when soil is distubred –> inhaled and reached bronchiioles and alveoli

organisms are phagocytized by macrophages but not killed and spread via lymph nodes –> creating tissues granulomas with central caseation and necrosis around organs

127
Q

what is important to test for when diagnosing histoplamosis

A

serologic testing

128
Q

histoplasmosis treatment: immunocompetent host-

asymptomatic or mild-moderate disease with symptoms < 4 weeks

A

No therapy required

129
Q

histoplasmosis treatment: immunocompetent host-

symptomatic with mild-moderate disease with symptoms > 4 weeks

A

Itraconazole

130
Q

histoplasmosis treatment: immunocompetent host-

moderately severe-severe disease

A

lipid amphotericin B + medrol 1-2 weeks THEN

itraconazole for a total of 12 weeks

131
Q

histoplasmosis treatment: immunocompromised host-

moderately severe-severe disseminated disease

A

Lipid amphotericin B for 1 to 2 weeks then itraconazole for at least 12 months

132
Q

histoplasmosis treatment: immunocompromised host-

less severe disease

A

itraconazole for 12 months

133
Q

blastomycosis pathophys

A

pulmmonary infection occurs secondary to inhalation of conidia –> inflammatory response with neutrophilic recruitment to lungs –> dissemination –> cell-mediated immunity –> formation of granulomas

134
Q

pulmonary blastomycosis treatment: immunocompetent host-

moderately severe-severe disease

A

Lipid amphotericin B for 1-2 weeks or until improvement, following by itraconazole for 6-12 months

135
Q

pulmonary blastomycosis treatment: immunocompetent host-

mild-moderate disease

A

itraconazole for 6 months

136
Q

disseminated or extrapulmonary blastomycosis: immunocompetent host-
CNS disease induction

A

lipid amphotericin B for 4-6 weeks, followed by an azole as consolidation therapy

137
Q

disseminated or extrapulmonary blastomycosis: immunocompetent host-
CNS disease consolidation

A

azole for 12 months
fluconazole
itraconazole
voriconazole

138
Q

blastomycosis treatment: immunocompromised host-

acute disease

A

lipid amphotericin B for 1-2 weeks or until improvement, then suppressive therapy for at least 12 months

139
Q

blastomycosis treatment: immunocompromised host-

suppressive therapy

A

itraconazole for at least 12 months

140
Q

when to treat coccidiomycosis

A

patients with large inocula, severe infection, or concurrent risk factors

141
Q

coccidiomycosis treatment duration:

primary respiratory infection

A

3-6 months

142
Q

coccidiomycosis treatment:

primary respiratory infection

A

fluconazole

itraconazole

143
Q

coccidiomycosis treatment:

symptomatic chronic cavitary pneumonia

A

fluconazole

itraconazole

144
Q

coccidiomycosis treatment:

diffuse pneumonia with bilateral or miliary infiltrates

A

Amphotericin B for several weeks; followed by an azole for 12 months total

145
Q

disseminated coccidiomycosis treatment:

nonmeningeal disease

A

itraconazole or fluconazole

amphotericin B

146
Q

disseminated coccidiomycosis treatment:

meningeal disease

A

*fluconazole
itraconazole
intrathecal amphotericin B

147
Q

cryptococcal meningitis treatment:
non-HIV infected, non-transplant host-
induction treatment

A

amphotericin B deoxycholate plus flucytosine for at least 4 weeks

148
Q

cryptococcal meningitis treatment:
non-HIV infected, non-transplant host-
consolidation treatment

A

fluconazole 400-800 for 8 weeks

149
Q

cryptococcal meningitis treatment:
non-HIV infected, non-transplant host-
maintenance treatment

A

fluconazole 200mg PO QD for 6-12 months

150
Q

cryptococcal meningitis treatment:
HIV-infected-
preferred induction treatment

A

liposomal amphotericin B plus flucytosine for at least 2 weeks

151
Q

cryptococcal meningitis treatment:
HIV-infected-
preferred consolidation treatment

A

fluconazole 400mg PO QD for equal or more than 8 weeks

152
Q

cryptococcal meningitis treatment:
HIV-infected-
preferred maintenance treatment

A

fluconazole 200 mg to complete at least 1 year of azole therapy

153
Q

cryptococcal meningitis treatment:
organ transplant recipients-
induction

A

liposomal amphotericin B plus flucytosine for at least 2 weeks

154
Q

cryptococcal meningitis treatment:
organ transplant recipients-
consolidation

A

fluconazole 400-800mg for at least 8 weeks

155
Q

cryptococcal meningitis treatment:
organ transplant recipients-
maintenance

A

fluconazole 200-400 mg for at least 6-12 months

156
Q

candidemia treatment DOC non-neutropenic adults

A

echinocandin

157
Q

candidemia treatment
non-neutropenic adults
alternative as initial therapy in selected patients who are not critically ill and who are unlikely to have fluconazole-reistant candida species

A

fluconazole

158
Q

candidemia treatment neutropenic adults

A

echinocandin

lipid formulation of amphotericin B

159
Q

C. glabrata treatment options

A

echonocandin

160
Q

c. parapsilosis treatment options

A

fluconazole or lipid amphotericin B

161
Q

c. krusei treatment options

A

echinocandin, lipid amphotericin B or voriconazole

162
Q

candidemia treatment duration: neutropenic adults

A

treat for 14 days after documented clearance of candida from blood, resolution of symptoms, and resolution of neutropenia

163
Q

chronic disseminated (heptasplenic) candidiasis treatment

A

lipid amphotericin B for several weeks followed by fluconazole

164
Q

invasive pulmonary aspergillosis treatment

A

voriconazole

165
Q

invasive pulmonary aspergillosis treatment salvage therapy

A 
amphotericin B lipid complex
caspofungin
micafungin
posaconazole
itraconazole
166
Q

prophylaxis treatment of aspergillosis

A

posaconazole

167
Q

leading cause of community acquired and hospital acquired bacteremia

A

staphylococcus aureus

168
Q

what diagnostic evaluation should you do in SAB and why?

A

Echocardiography to check for infective endocarditis

169
Q

when to perform echocardiography in SAB

A

5-7 days after onset of bacteremia

170
Q

catheter and prosthetic device management in SAB

A

consider all IV catheters and prosthetic devices to be infected in patients with SAB until infection ruled out

attempt to remove all prosthetic devices or use rifampin

171
Q

empiric treatment of SAB

A

empirically cover MSSA/MRSA

vanc 15-20 mg/kg IV q 8-12
vanc 6-10 mg/kg IV q 24

172
Q

Treatment of MSSA bacteremia

A

*cefazolin 2g Q8
nafcillin 2 g Q4
oxacillin 2 g Q8

173
Q

Treatment of MRSA batceremia

A

Vanc 15-20 mg/kg IV q8-12 h

Daptomycin 6mg/lV q 24

174
Q

Treatment of PVE

A

Vanc+rifampin for 6 weeks

gent for first 2 weeks

175
Q

duration of treatment of uncomplicated SAB

A

14 days from first negative blood culture

176
Q

duration of treatment of complicated SAB

A

4-6 weeks

177
Q

what is bacteremia

A

presence of viable bacteria (fungi) in the blood

178
Q

what is an infection

A

inflammatory response to invasion of normally sterile host tissue by the microorganisms

179
Q

what is SIRS

A

systemic inflammatory response to a variety of severe clinical insults manifested by 2 or more of the following conditions

180
Q

2 or more of the following conditions of SIRS

A 
Temp >38 or <36
HR > 90 bpm
RR >20 bpm
PaCO2 <32 mmHg
WBC >12,000, <4000
181
Q

what is sepsis

A

life-threatening organ dysfunction caused by a dysregulated host response to infection

182
Q

what is septic shock

A

subset of sepeis in which underlying circulatory, cellular, and metabolic abnormalities are associated with higher risk of mortality than sepsis alone

183
Q

sepsis characteristics

A

Pts requiring vasopressors to maintain a MAP of > 65 mm Hg and serum lactate >2 mmol/L

184
Q

what is multiple organ dysfunction syndrome

A

presence of altered organ function in an acutely ill patient so that homeostasis cannot be maintained without intervention

185
Q

What gram negative bacteria are causative pathogens in sepsis and septic shock

A

enterobacteriaceae (e. coli, klebsiella)

p. aeruginosa

186
Q

What gram positive bacteria are causative pathogens in sepsis and septic shock

A

staphylococci

187
Q

what drugs target exotoxins

A

clindamycin and linezolid

188
Q

complement systemic mechanism

A

Activated of C3a and C5a induce vasodilation and increase vascular permeability –> hemodynamic changes na platelet aggregation and activation of neturophils

189
Q

kallikrein/bradykinin system

A

fluid leakage into interstitial space due to vasodilation –> prominent feature of sepsis/septic shoc

190
Q

macrophage role in sepsis

A
  1. phagocytic cells remove and destroy bacteria and bacterial products
  2. produce potent mediators of inflammation
191
Q

tumor necrosis factor role in sepsis

A

increases vascular permeability
cause cellular damange
produce fever

primary mediator of sepsis- concentrations correlated with severity of sepsis

192
Q

IL-1 role in sepsis

A

activate monocytic cells, neutrophils, B and T lymphocutes

produce endogenous pyrogenic effect, lypolysis, cachexia

193
Q

IL-6 role in sepsis

A

stimulated the production of platelets

induces elevation in body temperature

194
Q

neutrophils role in sepsis

A

contributes to vascular and tissue injuries by releasing oxygen metabolites and lysosomal enzymes or by causing microemboli after aggregation

195
Q

what is the key target for inflammatory mediators and important producer of active mediators

A

endothelial cells

196
Q

general variables for sepsis

A 
Fever >38.3 or hypo <36
HR >90
Tachypnea
Altered mental status
Edema
Hyperglycemia
197
Q

inflammatory variables for sepsis

A

WBC >12,000
WBC <4,000
10% immature forms
Plasma CRP more than 2SD above normal value

198
Q

Community acquired infection Empiric therapy of sepsis in adults:
CAP non-neutropenic

A

Cefrtiaxone + Azithromycin

Ceftriaxone + moxi/levo

199
Q

Community acquired infection Empiric therapy of sepsis in adults:
urinary tract source non-neutropenic

A

3rd/4th gen ceph +/- AG

Pip/tazo +/- AG

200
Q

Community acquired infection Empiric therapy of sepsis in adults:
intra-abdominal non-neutropenic

A

pip/tazo
carbapenem
3rd/4th gen ceph + flagyl
cipro/evo + flagyl

201
Q

Community acquired infection Empiric therapy of sepsis in adults:
skin/soft tissue infection non-neturopenic

A

vanc
dapto
linezolid

202
Q

hospital acquired infection Empiric therapy of sepsis in adults:
HAP/VAP

A

Antipseudomonal beta lactam + AG or

AP FQ + vanc or linezolid

203
Q

hospital acquired infection Empiric therapy of sepsis in adults:
urinary tract source non-neutropenic

A

cefepime + tobra or FQ

Pip/tazo + tobra or FQ

204
Q

hospital acquired infection Empiric therapy of sepsis in adults:
intra-abdominal non-neutropenic

A

pip/tazo

carbapenem

205
Q

hospital acquired infection Empiric therapy of sepsis in adults:
skin/soft tissue infection non-neturopenic

A

vanc + pip/tazo (+ clinda if necrotizing fascitis)

206
Q

hospital acquired infection Empiric therapy of sepsis in adults:
neutropenic patient

A

pip/tazo +/- AG
AG Carbanepen +/- AG
Ceftazidime or cefepime +/- AG

207
Q

Empiric therapy of sepsis in adults:

thermal injury to at least 20% of body surface area

A

AP BL + AG+ vanc

208
Q

Empiric therapy of sepsis in adults:

suspicion of indwelling vascular catheter infection

A

vanc
dapto
linezolid

209
Q

sepsis duration of therapy

A

7-10 days

210
Q

Antibiotics are strongly discouraged when PCT is < _____

A

0.25 ng/dL

211
Q

Antibiotics are strongly encouraged when PCT is > _____

A

1 ng/dL

212
Q

Principle of sepsis therapy

A

early initiation (within first hour) of aggressive antimicrobial therapy- 1 or more drugs with in vitro activity against the most likely pathogens and that penetrate to the site presumes to be the source of sepsis

213
Q

What should be completed in the first 3 hours of septic shock presentation

A
  1. measure lactate concentration
  2. blood cultures prior to antibiotics
  3. give broad-spec antibiotics
  4. Give 30 mL/kg crystalloid (NS,LR)
214
Q

What should be completed in the first 3 hours of septic shock presentation

A

Add vasopressors

norepinephrine first line

215
Q

MAP initial resiscitation goal

A

MAP >65 mm Hg

216
Q

Is acyclovir a prodrug?

A

Yes- must be converted to acyclovir-TP by thymidine kinase in HSV

217
Q

acyclovir MOA

A

inhibits viral DNA polymerase to inhibit viral replication and is incorporated into viral DNA to cause premature chain termination

218
Q

Mechanisms of resistance for acyclovir

A

Absence or partial or altered production of viral thymidine kinase
Altered viral DNA polymerase

219
Q

Acyclovir SOA

A

HSV

VZV

220
Q

Acyclovir bioavailability

A

Oral bioavailability 10-20% (not affected by food)

Dose-dependent oral absorption (bioavailability decreases with increasing dose)

221
Q

Acyclovir distribution

A

widely distributed in tissues and body fluids

222
Q

Acyclovir metabolism/elimination

A

Eliminated renal –> adjust for renal dysfunction

223
Q

Acyclovir AE

A

N/V
Nephrotoxicity
Neurotoxicity
Thrombophlebitis with IV form

224
Q

Is valacyclovir a prodrug

A

Yes- a L-valyl ester prodrug of acyclovir

225
Q

Valacyclovir MOA

A

inhibits viral DNA polymerase to inhibit viral replication and is incorporated into viral DNA to cause premature chain termination

226
Q

Valacyclovir SOA

A

HSV

VSV

227
Q

Valacyclovir vs Acyclovir bioavailability

A

Relative bioavailability of acyclovir is 3-5 times greater with valacyclovir and may be given without regards to meals

228
Q

Is famciclovir a prodrug

A

Yes- a diester prodrug of penciclovir

229
Q

Is penciclovir a prodrug

A

Yes- becomes penciclobir triphosphate

230
Q

Famciclovir SOA

A

HSV

VZV

231
Q

Which is more potent: penciclovir or acyclovir

A

Acyclovir

232
Q

famciclovir oral bioavailability

A

Well absorbed orally but food does slow absorption but may be administered without regards to food

233
Q

Famciclovir excretion

A

Renal thus dose reduction is recommended in renal dysfunction

234
Q

famciclovir Ae

A

Headache

Nausea

235
Q

Special SOA of ganciclovir

A

CMV

236
Q

is ganciclovir a prodrug

A

Yes- in CMV infected cells, ganciclovir is mono-phosphorylated by a CMV encoded protein kinase UL97 gene then to the di- and triphosphate forms by cellular kinases

237
Q

ganciclovir MOA

A

inhibits viral DNA polymerase and/or incorporation into viral DNA to inhibit viral replication

238
Q

ganciclovir resistance

A

UL97 gene mutation which leads to viral kinase deficiency or altered viral DNA polymerase

239
Q

ganciclovir bioavailability

A

low oral bioavailability –> use IV formulation

240
Q

ganciclovir spread

A

CSF

Brain tissue

241
Q

acyclovir spread

A

brain, spinal card

CSF

242
Q

ganciclovir elimination

A

kidney –> adjust dose for renal dysfunction

243
Q

ganciclovir AE

A

bone marrow suppression

PHRM 865 (59 decks)

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