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IPCS > ID exam 1 > Flashcards

ID exam 1 Flashcards

1
Q

xWhat is the goal of PK

A

increase effectiveness of treatment and/or decrease the side effects of the treatment

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1
Q

____ is used to develop a model for designing individual drug regimens

A

PK

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2
Q

What is PD

A

describe characteristics of interaction between substance, active site, and action (think antimicrobial affect on pathogen)

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3
Q

What are the 2 categories that antimicrobial agents are classified as exhibiting

A

concentration dependent activity
non concentration dependent activity

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4
Q

What is concentration dependent activity of antimicrobial agents

A

rate/extent of bactericidal activity increases with increasing antimicrobial concentrations
goal to optimize peak: MIC (AUC:MIC)

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5
Q

What is non-concentration dependent activity of antimicrobial agents

A

rate/extent of killin do not increase with increasing antimicrobial concentration; instead it is increased by length of exposure
goal to optimize time concentrations remain above MIC (t>MIC)

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5
Q

What is the blood culture pathway

A

collection: sample incubated
alert: machine alerts for positive culture
gram stain: tech performs STAT stain
incubation: culture plates

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6
Q

What is the timeline for antimicrobial therapy

A

clinical illness
empiric antibiotics
culture processing
ID
targeted antibiotics

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7
Q

What is the time frame for gram stain, blood culture, EMR view

A

gram stain: 24-48 h
blood culture: additional 24-48 h
EMR view: additional 24 h

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8
Q

What are all the components of targeted antibiotics regimen

A

pathogen
indication/site of infection
dose
route
duration

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9
Q

What is MIC (minimum inhibitory concentration)

A

Lowest antimicrobial concentration that inhibits visible bacterial growth

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10
Q

What is MBC (minimum bactericidal concentration)

A

lowest antimicrobial concentration that results in microbial death

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11
Q

Broth microdilution susceptibility testing

A

inoculation with various antimicrobial concentrations (standard for testing)

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12
Q

What drugs focus on the T>MIC (time dependent killing) PD curve

A

beta lactams
tetracycline
oxazolidinones

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13
Q

What drugs focus on the AUC/MIC PD curve

A

fluoroquinolones
macrolides
ketolides
glycopeptides

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14
Q

What is the goal of beta lactams

A

keep serum concentrations above MIC for at least 40-70% of dosing interval
(max kill at 4-5x MIC, focus on T>MIC)

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15
Q

What is the Vd, half-life, and protein binding of beta lactams, excretion

A

Vd: 0.15-0.3 L/kg
half-life: 1-2 hr
protein binding: 25% or less
excretion via glomerular filtration and tubular secretion

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16
Q

Critically ill patients may have changed PK derangement what are these principles they effect

A

change in Vd
large volume of fluid resuscitation
vasopressor use
hypoalbuminemia
augmented renal clearance

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17
Q

Pharmacy to dose (PTD) - vancomycin PK/PD

A

formal pharmacy consult for pharmacist managed dosing and policy directed management

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18
Q

Therapeutic Drug Monitoring (TDM) - vancomycin PK/PD

A

assay procedures to determine drug concentrations in plasma, further interpreted and applied to develop safe and effective regimens

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19
Q

What is the difference between C1 and C2 - vancomycin PK/PD

A

C1 peak (1-2 hr after end of infusion)
C2 trough (end interval concentration)

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20
Q

What is AUC/MIC

A

integrated quantity of cumulative drug exposure for a defined period of time
average serum drug concentration during time period

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21
Q

what is the goal AUC of vancomycin

A

target: 500 mcgh/mL
range: 400-600 mcgh/mL
(500-600 for MRSA, endocarditis, menigitis)

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22
Q

Vancomycin MIC <1 and MIC >2 meaning

A

MIC >1 = 100% change of achieving goal AUC/MIC >400
MIC >2 mcg/mL - goal not achievable in patient with normal renal function

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23
Q

What is the trough level for vancomycin

A

15-20 mcg/mL

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24
Q

Vancomycin nephrotoxicity levels

A

AUC/MIC >400
trough <15 mcg/mL

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25
Q

Why is AUC in vancomycin a high variability

A

depends on dose and renal function
trough concentration explains 40% of inter0individual variability in AUC

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26
Q

For vancomycin what should the loading dose be in patients with severe infections

A

20-25 mg/kg

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27
Q

When to get trough level for vancomycin

A

30 min -1 hr prior to next dose
must be at least 6 hours after peak level

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28
Q

What is the semi-synthetic aminoglycoside

A

amikacin
(genta and tobra natural)

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29
Q

Aminoglycosides consists of _____ sugars joined by _______ bonds to an aminocyclitol nucleus

A

amino
glycosidic

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30
Q

MOA of aminoglycosides (gram negative only)

A

-inhibit protein synthesis by binding to 16S ribosomal rRNA of 30s ribosome (irreversible bond lead to PAE)
-cause cell damage by mistranslation and incorrect formation of polypeptides

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31
Q

Synergy in aminoglycosides

A

synergy: use with cell-wall active antibiotic to increase aminoglycoside uptake despite small doses

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32
Q

Amikacin is resistant to enzyme ____________

A

inactivation (remains stable against organisms resistant to genta/tobra)

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33
Q

Aminoglycoside ADME

A

a: polar
d: Vd 0.3 L/kg
m: n/a
e: urine, t1/2: 1-4 hr

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34
Q

Aminoglycosides are ______________ dependent drugs

A

concentration (higher peak = better effects) MIC 10:1

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35
Q

What is the aminoglycoside dose for hartford? urban-craig nomogram?

A

hartford: 7 mg/kg
urban-craig: 5 mg/kg
level drawn 8-12 hr after start of infusion

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36
Q

What are the common examples of antimicrobial resistance

A

MRSA
CRE (carbapenem-resistant enterococcus)
VRE (vancomycin-resistant enterococcus)
ESBLs (extended spectrum beta lactamases)

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37
Q

What is an efflux pump

A

antimicrobial actively pumped out of cell

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38
Q

What is entry inhibition

A

antimicrobial actively blocked from entering cell

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39
Q

Antimicrobial Resistance inactivation and target site modifcation

A

inactivation: breakdown of active drug
modification: active drug unable to elicit effect

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40
Q

What are gram negative pathogens commonly caused by

A

intra-abdominal infection (IAIs), urinary tract infections, ventilator-associated pneumonia (VAP), bacteremia

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41
Q

Beta-lactamases mechanism of resistance

A

cleave beta lactam ring to inactivate
ESBL are plasmid encoded
there are different types that are dependent on inactivation/hydrolysis

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42
Q

What is horizontal transfer of resistance

A

transfer of resistance genes from one organism to another
-transduction (bacteriophage/integron)
-conjugation (plasmid)
-transformation (chromosomal DNA/plasmid)

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43
Q

ESBLs may have the framework to hydrolyze/inactive all agents with ester/amide bond but what

A

this is not always the case

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44
Q

Efflux pumps/permeability

A

pumps are proteins w/in membrane that export antibiotics from intracellular matrix
outer membrane porins may decrease entry of antibiotic into cell

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45
Q

Target site modification: fluoroquinolone resistance and aminoglycoside resistance

A

fluoroquinolone resistance: target site protection/modification to alter agent binding
aminoglycoside resistance: alteration of ribosomal proteins that lead to high level resistance

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46
Q

Gram positive pathogens common cause

A

skin and structure infections, bacteremia, hospital/community acquired pneumonia

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47
Q

Staphylococci: plasmid-encoded beta lactamase nafcillin/cefazolin generally stable

A

inactivation

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48
Q

Staphylococci: PBP2a has low affinity for beta lactams (show MRSA)

A

target replacement

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49
Q

Staphylococci: leads to linezolid resistance often with other concomitant mutation

A

target modification

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50
Q

Staphylococci: repulusion of antibiotic due to increase in cell envelope charge

A

drug entry

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51
Q

Enterococci: rare-usually found in E. faecalis

A

inactivation

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52
Q

Enterococci: usually acquired resistance may differ depending on enterococcus spp

A

target replacement

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53
Q

Enterococci: reason why cephalosporins do not cover enterococcus spp

A

target modification

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54
Q

Enterococci: repulsion of antibiotic due to increase in cell envelope charge

A

drug entry

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55
Q

Streptococci: type of PBP will determine which beta lactam resistance pattern you will see

A

target modification

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56
Q

BioFire and rapid diagnostic gram negative bacteria

A

E coli
Pseudomonas aeruginosa

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57
Q

BioFire and rapid diagnostic gram positive bacteria

A

enterococcis faecalis
s. aureus

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58
Q

BioFire and rapid diagnostic yeast

A

candida albicans
candida glabrata

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59
Q

BioFire and rapid diagnostic antimicrobial resistance genes

A

methicillin resistance
-mecA/C
-MRSA

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60
Q

In a prospective audit and feedback you reports on the financial impact of interventions and feedback based on what 3 things

A

dose adjustments
alternative agents
cost of therapy

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61
Q

ID pharmacy in policy change

A

small steps
always identify key stakeholders
implement education and process change
takes time

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62
Q

Penicillin MOA

A

inhibit bacterial cell wall synthesis by binding to penicillin binding proteins
(half liver 1 hour, gets in CNS)

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63
Q

Time dependent killing of penicillins

A

Time > MIC
goal to keep serum concentration above MIC for at LEAST 50-60% OF DOSING INTERVAL)

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64
Q

Allergy for penicillin

A

range in severity
all penicillins may cause neutropenia, neurotoxicity, or renal injury (mainly nadcillin/oxacillin)

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65
Q

Cephalosporins MOA

A

inhibition of bacterial cell wall synthesis by binding to penicillin binding proteins
(half life 1-2 hr, CNS penetration)

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66
Q

Time dependent killing for cephalosporins

A

time > MIC
goal to keep serum concentration above MIC for at least 60-70% of dosing interval

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67
Q

Cephalosporins allergy

A

range in severity
less frequent than penicillins
low rate of cross reactivity especially with higher generations of 2-4

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68
Q

Cephalosporins adverse effects

A

GI
variable association with CDI
neutropenia, neurotoxicity, renal injury
local reactions are common

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69
Q

Carbapenems MOA

A

inhibition of bacterial cell wall synthesis by binding to penicillin binding proteins
(half life 1-2 hr, CNS penetration)

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70
Q

Carbapenems time dependent killing

A

time > MIC
goal to keep serum concentration above MIC for at least 40-50% of dosing interval

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71
Q

Carbapenems allergy

A

low incidence of allergy
minimal cross reactivity
neurotoxicity caution with seizure disorders in general anti epileptic drug drug interactions

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72
Q

Aminoglycosides MOA

A

inhibition of protein synthesis by binding to 30S subunit, leading to misreading in translation process (rapid bactericidal)
1-4 hr half life

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73
Q

What adverse effect of aminoglycosides can not be reversed

A

ototoxicity
(nephrotoxicity can happen and can be reversed)

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74
Q

Aminoglycoside concentration dependent killing

A

peak: MIX/AUC:MIC
goal to maximuze peak/min trough

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75
Q

Fluoroquinolones MOA

A

inhibition of bacterial topoisomerases leading to inhibition of DNA replication and transcription
(4-12 hr half life)

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76
Q

Topoisomerase II is gram ________ while Topoisomerase 4 is gram __________

A

negative
positive

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77
Q

Fluoroquinolones concentration dependent killing

A

AUC:MIC
goal to maximize AUC:MIC ratio based on organism (higher doses for gram negative organisms)

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78
Q

Fluoroquinolones adverse effects

A

GI
CNS
QT prolongation
hypo/hyperglycemia
tendonitis
increase aortic dissection
increase lft
interaction with cation

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79
Q

Macrolide MOA

A

inhibition of RNA dependent protein synthesis bind to 50S ribosomal subunit to prevent bacterial growth
(68-72 hr half life)
concentration dependent killing

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80
Q

Macrolide adverse effect

A

GI
LFT increase
potential headache
CYP3A4 inhibitors (drug-drug interactions with statin, warfarin, azithromycin inhibition weaker)

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81
Q

Lincosamide MOA

A

bind to 50S ribosomal subunit to prevent protein synthesis
half-life 3 hours
concentration dependent killing

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82
Q

Lincosamide adverse effects

A

GI
metallic tase
rash

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83
Q

Tetracycline MOA

A

bind to 30S ribosomal subunit to prevent protein synthesis
half life 12-24 h
concentration dependent killing
90-100 PO absorption

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84
Q

Tetracycline adverse effects

A

NVD
esophagitis
photosensitivity
rash
hepatotoxicity (rare)
deposition into teeth

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85
Q

TMP-SMX MOA

A

TMP: bind to dihydrofolate reductase to inhibit formation of folic acid
SMX: inhibit synthesis of dihydrofolic caid
Inhibit DNA synthesis
10 hr half life
90-100% PO absorption
time dependent killing

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86
Q

TMP-SMX adverse effects

A

rash, itching
bone marroe suppression
crystalluria of SMX component in renal tubules
hyperkalemia
caution with DDI: warfarin, anticonvulsants, ACE/ARB

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87
Q

Vancomycin MOA

A

form complex with d-ala-d-ala portion of peptide to prevent peptidoglycan syntheses
AUC: MIC PK

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88
Q

Vancomycin ADR

A

infusion related reaction
nephrotoxicity
ototoxity (rare)

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89
Q

Daptomycin MOA

A

bind to calcium and insertion into cell membrane causing rapid depolarization and cell lysis
8-10 hr half-life
urine secretion
AUC: MIC/ Peak: MIC

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90
Q

Daptomycin ADR

A

myopathies
CK elevation
injection site reaction

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91
Q

Linezolid MOA

A

inhibition of bacterial protein sysnthesis bind to 23S rRNA or 50S subunit to prevent translation complex
half life 5 hr
gets into CNS

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92
Q

Linezolid adverse effect

A

GI
myelosuppression
peripheral neuropathies
serotonin syndroms

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93
Q

Metronidazole MOA

A

intracellular reduction to produce reactive metabolites; damage DNA
half-life 8-10 hr

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94
Q

Metronidazole ADR

A

peripheral neuropathy
metallic taste
disulfiram reaction

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95
Q

Amphotericin B killing curve

A

concentration dependent killing

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96
Q

Amphotericin B Infusion Reaction

A

fever, chills, rigors, N/V, muscle pain
pre-medicate with NSAID, APAP 30-60 min before
(hypotension, bronchospasm, arrhythmia, anaphylaxis)

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97
Q

Liposomal amphotericin infusion reactions

A

Triad
-chest pain, dyspnea, hypoxia
-flank pain, ab pain, leg pain
-flushing, urticaria
Occurs within 5 minutes
-stop infusion
-give diphenhydramine
-slow infusion when re-challenged

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98
Q

Amphotericin B nephrotoxicity

A

tubular dysfunction and vasoconstriction of afferent arteriole
dose limiting toxicity
risk factors:
nephrotoxins, daily dose, cumulative dose, CKD

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99
Q

Amphotericin B nephrotoxicity prevention

A

saline loading with 500-1000 ml 0.9% NaCl before and after administering
adequate hydration
electrolyte correction
using lipid formulation when possible

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100
Q

Amphotericin B nephrotoxicity occurrence

A

Ambisome < Abelcet < Conventional

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101
Q

Azole classes

A

Imidazole (2 nitrogen)
-ketoconazole. topical
Triazoles (3 nitrogen)
-fluconazole, itrazonazole, voriconazole, posaconazole, isavuconazole

102
Q

Azole class adverse effects

A

N/V
ad pain
headache
rash
hepatotoxicity
QT prolongation

103
Q

Distribution of fluconazole

A

distributes well into CNS/ vitreous, urinary sources

104
Q

fluconazole monitoring

A

DDI
QT prolongation
increase LFT
renal
GI

105
Q

Itrazonazole administration

A

take with food, improves absorption with acid (avoid PPI)
take solution with empty stomach

106
Q

Itrazonazole BBW

A

caution use in patients with CHF

107
Q

Itrazonazole goal trough

A

0.5-1
possibily 5 in some literature

108
Q

Voriconazole monitoring

A

trough levels
DDI
increase LFT
QT prolongation
GI toxicity

109
Q

Voriconazole 30/30/30 rule

A

30% of patients, 30 min after dose, duration 30 min
abnormal vision, color vision change, photophobia, photopsia
effects subside within 1 week after stopping treatment

110
Q

Recommended intake of fluoride

A

3-4 mg/d

111
Q

Posaconazole monitoring

A

trough
DDI
BP
rigors
QT prolongation

112
Q

Monitoring for isavuconazonium

A

QT shortening**
increase LFT
DDI
GI
electrolytes

113
Q

Echinocandin PK/PD poor penetration in what

A

CNS
vitreous
urine

114
Q

Echinocandin ADR

A

infusion related reaction
rash
hepatotoxicity

115
Q

Epidemiology of beta lactam allergies

A

80% with IgE mediated lose sensitive after 10 years
10% of everyone have allergy reported

116
Q

Caution of beta lactam allergies

A

avoid penicillin and cephalosporins with documented allergy

117
Q

Inaccurate diagnosis of penicillin allergy

A

increase medical cost for patient and hospital
increase inappropriate antibiotic use
increase risk of adverse reaction

118
Q

Penicillin cross reactivity

A

low cross reactivity with cephalosporin groups
has to do with side chain

119
Q

Non professional APCs need a MHC class __ molecule coupled to a beta 2 microglobulin

A

1

120
Q

The endogenous pathway uses proteosomes and is MHC class __

A

1

121
Q

The exogenous pathway uses endosomes and is MHC class __

A

2

122
Q

MHC 1 has 8-10 amino acids with 9 being the most common. MHC 2 has how many amino acids

A

13-25 (MHC class 2 are larger)

123
Q

Non covalent drug peptide pharmacological interaction model for immune activation goes through the cell while non covalent drug peptide altered peptide repertoire model goes through what

A

it diffuses and does not have to go through the cell

124
Q

Do quinolones inhibit cutting of DNA

A

no they inhibit the repair of DNA

125
Q

What does topoisomerase IV do to DNA

A

relaxes DNA

126
Q

What does topoisomerase II / DNA gyrase do

A

supercoil DNA

127
Q

RecA causes the LexA repressor to cut itself up which frees the suppressed SOS gene. What does this mean

A

You activated an inhibitor of an inhibitor to make it work

128
Q

What is the SOS system

A

Bacteria sees damage and repairs it (gains resistance against quinolones

129
Q

Quinolones bind between the cut ends of DNA and cause what to happen

A

They do not allow the ends to come back together

130
Q

SAR of quinolone: ketone and carboxylic acid group

A

essential for gyrase binding and bacterial transport

131
Q

SAR of quinolone: R5 group

A

controls potency
G(+) activity

132
Q

SAR of quinolone: fluorine

A

controls gyrase and antibacterial potency

133
Q

SAR of quinolone: R7

A

controls potency spectrum and PK

134
Q

SAR of quinolone: X

A

controls PK and anaerobe activity

135
Q

SAR of quinolone: R1

A

controls potency
some effect on PK

136
Q

SAR of quinolone: R2

A

close to gyrase binding site

137
Q

What is the pH at which penicillin is stable

A

NONE

138
Q

In penicillins the side chains slow down or speed up rate of decomposition

A

slow down rate
(pen G is the first pencillin)

139
Q

Peptides are usually bad leaving groups except for which one

A

D-alanine transpeptidase
(D-ala-D-ala)
Penicillin is a suicide inhibitor

140
Q

On Dicloxacillin what does the two Cl groups do

A

they provide steric bluk and stop the ring from spinning

141
Q

Which is these are not an antibiotic: Clavulanic Acid, Sulbactam, Tazobactam

A

None of them are because none of them have a side chain (dont have amide side chain)

142
Q

How many places can penicillin vary? How many places can cephalosporin vary?

A

1
2

143
Q

What are the two important counseling points of cephalosporin MTT group

A

inhibit vitamin K activation (risk of bleeding)
disulfiram like reaction with alcohol (do not drink 3 days before taking and 3 days after taking)
–because of side group

144
Q

Why is there a combination of imipenem and cilastatin

A

imipenem cause kidney problems in renal tubules
cilastatin helps prevent damage

145
Q

Why is monobactam an inhaler

A

there is poor absorption from gut
(used for cystic fibrosis)

146
Q

Transfer RNA comes into which site

A

A site
blocks tRNA binding (tetracyclines)
inhibit translocation (macrolides, clindamycin)

147
Q

Why don’t you take doxycycline with calcium

A

It will cause the drug to not be absorbed
(almond milk, cow milk, etc. NONE)

148
Q

How long is azithromycin in its active form

A

100% of the time

149
Q

Erythromycin has a ketone in the 9 position and has 6, 12 hydroxy groups what does this have to do with ketals

A

they have a hemi ketal which can not bind to ribosome to inhibit it
will eventually form a full ketal
Azithromycin lacks a ketone so it does not have this intermediate

150
Q

What are the beta lactam antibiotics

A

penicillins
cephalosporins
monobactams
carbapenems

151
Q

Beta lactam MOA

A

interfere with peptidoglycan layer (mainly interrupt gram positive layers)

152
Q

Penicillin binding proteins (PBPs)

A

High molecular weight PBP (greater than 50 kD) are sensitive to both PCNs and cephalosporins
-less abundant
-activity essential for cell viability
-catalyze transpeptisase activity

153
Q

What are the 3 types of PBPs

A

PBP1: inhibited for cell lysis
PBP2: mediates transpeptidase reactions during specific portion of cell cycle
PBP3: septal peptidoglycan synthesis, blocks seperation and leads to filament formation

154
Q

What are the 4 classifications of penicillins

A

Pen G and Pen V
resistant to beta lactamase: nafcillin, dicloxacillin
broad-spectrum pen: ampicillin, amoxicillin
extended spectrum pen: piperacillin

155
Q

Beta lactamase ADME

A

depends on stability in acid and absorption with food
IM or IV
widely distributed
eliminated in kidney, tubular, glomerular, urine

156
Q

PCNs ADR

A

hypersensitivity reaction
N/V/D
injection site reactions
oral dose C. diff
avoid in people with allergy

157
Q

Injection of PCN D procaine results in what

A

dizziness, headache, seizures
-due to toxic concentrations of procaine

158
Q

PCNs entrance into CSF is inhibited by what

A

probenecid competitively inhibits this transport

159
Q

Pen G and Pen V route and dose recommendation

A

V = oral
G = IM/IV
do not take with food
procaine and benzathine used parenterally as repository forms
not stable beta lactamase

160
Q

What are the class 2 anti-staphylococcal PCNs (beta lactamase resistant and isoxazolyl pen)

A

Oxacillin (poor absorption)
Dicloxacillin (most active form)
Nafcillin (metabolized in liver no renal adjustment)

161
Q

Isoxazolyl PCN MOA

A

semistnthetic
resistant to cleavage by beta lactamase
potent inhibitors of growth of beta lactamase producing staphylococci

162
Q

Isoxazolyl PCN Absorption and Distribution

A

take without food
by liver
no dose adjustment for renal failure or hemodialysis

163
Q

What are the class 3 aminiopenicillins and dosage forms

A

ampicillin (IV, IM, PO-not for life-theatening infection)
ampicillin/sulbactam (IV, IM)
amoxicillin (oral suspension)
amoxicillin/clauvanate (suspension)

164
Q

aminiopenicillins MOA

A

destroyed by beta lactamase from both gram positive and gram negative bacteria

165
Q

Amoxicillin ADME

A

oxidation, hydroxylation, deamination processes
E: urine
co-administer with probenecid delays excretion

166
Q

Augmentin ADME

A

take with food or snack

167
Q

Class 4 antipseudomonal penicillins

A

Uredopenicillins (piperacillin)
Carboxypenicillins

168
Q

When to specifically use piperacillin

A

Klebsiella infection

169
Q

piperacillin and tazobactam ADME

A

broadest spectrum of activity
high biliary concentration
IV (both), IM (only piperacillin)
hepatic and renal elimination

170
Q

How are cephalosporins classified into generation

A

based on spectrum of action and beta lactamase stability
has a nucleus with 7-ACA

171
Q

cephalosporins MOA

A

same as penicillin
inhibits final step of peptidoglycan synthesis
no coverage against enterococci

172
Q

cephalosporins ADME

A

IM, IV
cross placenta (not for pregnancy)
cross BBB
eliminated in bile

173
Q

cephalosporins ADR

A

nephrotoxicity with aminoglycosides***
intolerance to alcohol (N/V/D with this)

174
Q

What are the first gen cephalosporins

A

cephalexin
cefazolin

175
Q

Keflex ADME

A

oral
good alternative to anti-staphylococcal penicillin
acid stable (without regard to meals)
excreted in urine by glomerular filtration and tubular secretion

176
Q

cefazolin ADME

A

IM, IV
excreted in urine or biliary

177
Q

cephalexin drug interactions

A

Metformin
Probenecid

178
Q

What are the second generation cephalosporins

A

cefuroxime (IV, oral)
cefoxitin (IV, IM)
cefotetan (oral)
cefmetazole (oral)

179
Q

second generation cephalosporins ADR

A

N-MTT side chain can inhibit vitamin K production which prolongs bleeding
disulfuram-like reaction

180
Q

second generation cephalosporins important point about BBB

A

do not cross BBB

181
Q

Does cefuroxime need a dose adjustment

A

yes in renally impaired patients

182
Q

cefuroxime ADR

A

hypersensitivity

183
Q

Third generation cephalosporins (good against pseudomona)

A

cefotaxime (IV, IM)
ceftriazone (IV, IM)
ceftazidime (IV)
ceftibuten (oral)

184
Q

Third generation cephalosporins ADR

A

C. diff

185
Q

cefotaxime drug interactions

A

nephrotoxicity aminoglycosides
cause seizures in renally impaired patients
cause GI problems

186
Q

Ceftriazone ADME

A

CSF penetration
longer half life

187
Q

Do you need dosage adjustment for ceftazidime

A

yes for renally impaired patients

188
Q

Ceftazidime ADR

A

hypersensitivity reaction

189
Q

Ceftazidime drug interactions

A

chloramphenical is antagonistic to beta lactam antibiotics
nephrotoxicity with aminoglycosides

190
Q

Ceftibuten ADR

A

hypersensitivity

191
Q

Ceftazidime drug interactions

A

antacids reduce effectiveness of ceftibuten

192
Q

What are the 4th generation cephalosporins

A

cefepime (IV, IM)

193
Q

cefepime ADME and ADR

A

in urine
require dose adjustment
local reactions
seizure with renal insufficiency

194
Q

5th generation cephalosporines

A

Ceftaroline (IV)
dose modification needed for renal impairment
hydrolysis metabolism
excreted in urine

195
Q

Monobactams (Aztreonam) ADME

A

active only against gram-negative bacteria
No cross sensitivity with PCNs
adverse effect: gram positive superinfection
dose adjustment for renal impairment

196
Q

What are the carbapenems drugs

A

Imipenem
Meropenem
Ertapenem
Doripenem

197
Q

carbapenems MOA

A

same as beta lactam antibiotics
used for serious nosocomial infections resistant to other beta lactams
(IV in hospital setting)

198
Q

carbapenems ADR

A

painful injection
allergic reaction
superinfection
seizure (unless other CNS disorders are present)

199
Q

Cilastatin is an inhibitor of what

A

dipeptidase

200
Q

Imipenem and Cilastatin drug interactions

A

cross allergy to other beta lactam antibiotics
local anesthetics
Probenecid
Valproic acid

201
Q

Meropenem considerations

A

not sensitive to renal dipeptidases (given alone, does not need cilastatin)
not for pregnancy

202
Q

Meropenem metabolism

A

liver to open beta lactam form (inactive)

203
Q

Ertapenem consideration

A

allows for once daily dosing
IM
good activity

204
Q

Doripenem ADME

A

dose adjustment for renal impairment
IV
metabolism occurs by dehydropeptidase-1

205
Q

Fluoroquinolones MOA

A

inhibit DNA topoisomerase (leading to breaks in DNA and death of cell)

206
Q

Fluoroquinolones ADME

A

no metabolism
elimination through kidneys
dose adjustment in renal dysfunction EXCEPT moxifloxacin

207
Q

Fluoroquinolones ADR

A

boxed warning for tendon rupture

208
Q

Tetracycline MOA

A

bind to bacterial ribosome at 30S subunit preventing docking of tRNA carrying new amino acid for addition to elongating protein chain

209
Q

Tetracycline ADR

A

photosensitivity
discoloration of teeth
chelate cations (do not mix with calcium, iron, antacids, multvitamins)

210
Q

Doxycycline ADME

A

100% bioavailability
with or without food
bile concentration
excreted in urine, feces
long half life

211
Q

Macrolides MOA

A

bind to 50S subunit of bacterial ribosome, preventing ribosome from shuffling along and adding new amino acids to the elongating protein chain

212
Q

Macrolides ADR

A

NVD
QT prolongation
potent inhibitors of drug-metabolizing cytochrome P450 enzymes

213
Q

Macrolide ADME

A

oral
Azithromycin not metabolized extensively
elimination in bile***
long half life

214
Q

Aminoglycosides have a narrow therapeutic window which causes what

A

high risk of toxicity (nephro and ototoxicity)
also neurologic disorders

215
Q

Aminoglycosides MOA

A

bind to bacterial ribosome 30s subunit causing mis reading of genetic code leading to incorrect proteins formation and interruption of protein synthesis

216
Q

Aminoglycosides important fact

A

have to monitor peak and through levels for correct dosing

217
Q

Sulfonamide is a general term used to describe any derivative of what

A

para-aminobenzene-sulfonamide
(para-NH2 group essential)

218
Q

TMP exerts a __________ effect when used with sulfamethoxazole

A

synergistic
(inhibitor of microbial dihydrofolate reductase which produces tetrahydrofolate)

219
Q

MOA sulfonamide

A

interfere with single carbon transfers
-folate synthesis
-de-nove purine biosynthesis
-thymidylate synthesis

220
Q

SMX common side effect

A

crystalluria (drink with water)
hematological reactions

221
Q

TMP/SMX ADME

A

widely distributed
highly absorbed
limited hepatic metabolism

222
Q

Urinary tract antiseptics inhibit the _______ of many species of ________

A

growth, bacteria
(cant be used systemically)

223
Q

Nitrofurantoin ADME

A

rapidly absorbed
discolors urine (brown color)
activity higher in acidic urine
metabolites are in active

224
Q

What are the two reasons why macrobid is selectively toxic

A

concentrations of nitrofurantoin are higher in microbial than mammalian cells
higher nitrofuran reductase activity in microbial cells

225
Q

Nitrofurantoin contraindications

A

pregnant women
children

226
Q

Fosfomycin used to treat and how to take

A

UTI and cystitis
come as granules and mixed with cold water

227
Q

Fosfomycin MOA

A

phosphoric acid derivative that inactivates the enzyme pyruvyl transferase, which inhibits bacterial wall synthesis

228
Q

Nalidixic acid MOA

A

inhibit bacterial DNA gyrase and topoisomerase IV

229
Q

Nalidixic acid pharmacokinetics

A

hepatic metabolism
urine excretion and 10 times concentration in plasma (local effect)

230
Q

Nalidixic acid ADR

A

GI
photosensitivity

231
Q

What are the types of UTIs

A

pyelonephritis
ureteritis
cystitis
prostatitis

232
Q

What are the three types of pathophysiology of UTIs

A

Ascending: bacteria from urethra up
Descending: blood stream
Lymphatic: bowel and kidney

233
Q

Risk factors for UTIs

A

female
previous UTI
sex
change in vaginal flora
pregnancy
structural abnormalities
poor hygiene

234
Q

Pathogens of community acquire UTIs

A

E. Coli (80-90%)
Klebsiella species
Staphylococcus saprophyticus
Enterococcus faecalis

235
Q

Clinical presentation of community acquires UTI

A

urgency
frequency
burning pee
-cloudy urin
-pelvic pressure

236
Q

What are the 4 urinalysis suggestive of UTI

A

bacteriurea
pyuria: WBC > 10mm^3
Nitrate positive
Leukocyte esterase positive

237
Q

What are the two types of urinalysis

A

Rapid
Complete

238
Q

What is the amount of CFUs for clinical presentation of UTI

A

> 100,000 CFU
<100,000 and symptoms
-urinalysis PRIOR to treatment

239
Q

Definition of uncomplicated UTI

A

acute cystitis in female without pregnancy, catheter, obstruction

240
Q

Non pharm treatment for UTI

A

cranberry juice (prevention only, contains proanthocyanidin)
probiotics - lactobacillus (prevention only, lower pH)
hydration

241
Q

OTC product for uncomplicated UTI

A

Azo, stops burning, preventative

242
Q

What are the treatments for uncomplicated UTI

A

nitrofurantoin: 5 days (contraindicated if CrCl <60)
bactrim: 3 days (local resistance <20)
fosfomycin: 1 day
beta lactam: 3-7 days

243
Q

What medication to use in pregnancy for UTI

A

beta lactams

244
Q

What is recurrent cystitis referred to as

A

2 episodes within the last 6 months or 3 episodes within 1 year

245
Q

Complicated UTI risk factors

A

colonization of indwelling catheter (contamination, catheter into bladder)
anatomical (VUR)
retention urine/incomplete voiding

246
Q

Most common pathogens in hospital acquired UTI

A

E. Coli
Pseudomonas aeruginose
protus vulgonis
enterobacter species
enterococcus species

247
Q

Acute complicated cystitis treatment

A

cipro: 5-7 d (renal adjusted)
bactrim: 7 d
beta lactam: 7 d
fosmycin: 7 d (ESBL e coli only)
macrobid: 7 (ESBL e coli only)

248
Q

Clinical presentation of pyelonephritis

A

fever/chills
N/V
hematuria

249
Q

Phelonephritis treatment non hospitalized

A

cipro: 3 d
bactrim: 14 d (IV first)
beta lactam: 10-14 d (IV first)

250
Q

Phelonephritis treatment hospitalized

A

fluoroquinlones (>10% give IV)
aminoglycoside
cephalosporin
cabapenems (ESBL organisms)

251
Q

Clinical presentation prostatitis

A

fever
N/V
pain
dysuria
frequency
urgency
nocturia
retention

252
Q

prostatitis common pathogens

A

E. coli
Klebsiella spp
PROTUS
enterococcus spp

253
Q

prostatitis treatment

A

2-4 weeks
fluoroquinolones
bactrim (gram negative pathogens)

254
Q

Pregnancy treatment of UTI

A

cephalexin (5-7 d, preferred)
augmentin (5-7 d)
macrobid and fosfomycin (avoid use in pyelonephritis)

IPCS (9 decks)

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