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p2 year > principles of infectious disease therapeutics > Flashcards

principles of infectious disease therapeutics Flashcards

1
Q

antimicrobial PKPD that is important in combatting superbugs

A
  • clinical: focus on the patient
  • translational: turning bench research into clinical guidance –> stewardship
  • interdisciplinary: pharmacy, medicine, science, pharm sci
  • global: bridge collaboration
  • trainee focused
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2
Q

interdisciplinary aspect of ID

A
  • pharmaceutics
  • pharmacometrics
  • drug delivery and design
  • drug discovery and development
  • bacterial
  • chemotherapy
  • gene therapy
  • ID
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3
Q

most common organism of infection is…

A

the one that lives in that area

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4
Q

most common eye infection

A

staph aureus

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5
Q

most common gastritis infection (stomach)

A

helicobacter pylori

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6
Q

most common food poisoning infection (intestines)

A

Escherichia coli

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7
Q

most common urinary tract infection

A

E. coli

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8
Q

most common skin infection

A

Staph aureus

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9
Q

most common community acquired pneumonia infection (lungs)

A

Strep pneumoniae

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10
Q

most common ear infection

A

strep penumoniae

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11
Q

most common bacterial meningitis infection (brain)

A

strep penumoniae

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12
Q

infectious and parasitic disease is the number __ cause of death globally

A

2

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13
Q

post-antibiotic world

A

when superbugs do not respond to the last line antibiotic defense

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14
Q

polymyxin mono therapy vs combination therapy for all-cause mortality endpoint

A

for invasive CRE (carbapenem resistant enterobacterales) infections
- combination therapy (second antibiotic causes damage in outer membrane)

for other infections
- no evidence to support combination > monotherapy
- lots of trial issues

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15
Q

ID triad

A
  • host
  • drug
  • bacteria
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16
Q

ID patient considerations

A
  • host
  • infection site and severity
  • MICs
  • treatment regimens
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17
Q

vancomycin route of administration

A

IV ONLY!!!

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18
Q

if staph aureus, which antibiotics can you NEVER USE alone even if S? why?

A
  • ciprofloxacin
  • rifampin

***will develop resistance within 24 hours!! (very susceptible to resistance)

(can use in combo therapy tho (?) (only rifampin?))

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19
Q

what is the target vanco AUC 24 hr from the guidelines?

A

400 mg*hr/L

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20
Q

what is the equation to adjust vanco dosing?

A

D target = D observed (AUC 24 target / AUC 24 obser)

aka

D target AUC 24 target
————- = ————————
D observed AUC 24 observed

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21
Q

antibiogram selection considerations

A
  • cost
  • dosage form (IV vs PO)
  • is failure okay or would it be lethal?
  • may become resistance once administer it
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22
Q

what number on an antibiogram is safe for susceptibility?

A

80
on an exam, highest wins

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23
Q

does susceptible mean it will be sucessful?

A

no

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24
Q

the primary mechanism of resistance is…

A

the primary mechanism of action of the antibiotic being used

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25
Q

mechanism of action for ciprofloxacin –> mechanism of resistance for ciprofloxacin

A

MoA: fluoroquinolone -> DNA synthesis inhibitor

MoR: mutational event in the DNA replication process

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26
Q

mechanism of action for linezolid –> mechanism of resistance for linezolid

A

MoA: oxazolodonones –> protein synthesis inhibitor

MoR: ribosomal protection (tet protein) –> allows for no inhibition and protein synthesis to continue

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27
Q

mechanism of action for vancomycin –> mechanism of resistance for vancomycin

A

MoA: glycopeptide –> cell wall agent (blocks peptidoglycan synthesis)

MoR: decrease cell wall permeability to vanco –> prevents peptidoglycan synthesis)

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28
Q

mechanism of resistance for beta lactamase bacteria enzyme

A

the beta lactamase enzyme will open the ring of the beta lactam antibiotics, thus inactivating them –> enzymatic inactivation mechanism of resistance

the beta lactamase inhibitor drugs will act as bet lactam decoys and trick the beta lactamase enzymes to break them down instead, thus saving the beta lactam ring and the action of the antibiotics

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29
Q

bacteriocidal

A

99% killing, CFU below 10^4

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30
Q

bacteriostatic

A

inhibitory, CFU above

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31
Q

HEM PEK SPACE are all…

A

gram negative aerobes

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32
Q

which HEM PEK SPACE are cocci?

A

H,M
Haemophilus influenzae
Moraxella catarrhalis

*the rest are bacilli

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33
Q

HEM PEK SPACE

A

H: Haemophilus influenzae
E: Enterobactericiae (group)
M: Moraxella catarrhalis

P: Proteus sp.
E: E. coli
K: Klebsiella sp.

S: Serratia
P: Pseudomonas aeruginosa
A: Acinetobacter
C: Citrobacter
E: Enterobacter sp.

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34
Q

what is methicillin?

A

the first penicillin that caused bacterial resistance, pulled from market for AEs –> use to determine if we can use penicillins or not

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35
Q

clindamycin is used for

A

above diaphragm anaerobes

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36
Q

metronidazole is used for

A

below diaphragm anaerobes

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37
Q

staph is

A

aerobe
gram positive
clusters

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38
Q

strep pneumoniae is

A

aerobe
gram positive
pairs

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39
Q

GAS and GBS are

A

aerobe
gram positive
chains

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40
Q

e coli is

A

aerobe
gram negative
bacilli

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41
Q

pseudomonas aeruginosa is

A

aerobe
gram negative
bacilli

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42
Q

staph aureus is

A

aerobe
gram positive
clusters
coagulase positive

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43
Q

staph epidermidis is

A

aerobe
gram positive
cluster
coagulase negative

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44
Q

what is coagulase?

A

bacterial enzyme that coagulates blood/plasma that is produced by infectious staph

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45
Q

is strep pneumoniae typical or atypical bacteria?

A

typical

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46
Q

penicillin MoA

A

beta lactams –> cell wall active

bind to transpeptidase enzymes (penicillin binding proteins) in the bacterial cell and disrupt cell wall formation

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47
Q

penicillins are bacterio…

A

cidial

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48
Q

penicillins are bacterio…

A

cidia

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49
Q

pencillin spectrum

A

gram positive aerobes
MSSA

some gram negative aerobes
some pseudomonas

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50
Q

cephalosporins MoA

A

beta lactams –> cell wall active

bind to transpeptidase enzymes in bacterial cell wall and disrupt cell wall formation (same as penicillins bc all beta lactams)

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51
Q

cephalosporins are bacterio…

A

cidal

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52
Q

cephalosporin spectrum

A

gram positive aerobes
MSSA

gram negative aerobes
some pseudomonas

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53
Q

which cephalosporins cover pseudomonas?

A

ceftazidime (3rd)
cefepime (4th)

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54
Q

which penicillins cover pseudomonas?

A

piperacillin
piperacillin/tazobactam

ticarcillin
ticarcillin/clavanute

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55
Q

which cephalosporins cover MRSA?

A

ceftaroline (5th)

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56
Q

which cephalosporin covers both MRSA and pseudomonas?

A

none

57
Q

carbapenems MoA

A

beta lactams –> cell wall active agents

58
Q

carbapenems spectrum

A

MOST BROAD SPECTRUM SINGLE AGENT!!

gram positive aerobes
MSSA

gram negative aerobes
pseudomonas (NOT ertapenem)

gram negative anaerobes

59
Q

monobactams MoA

A

beta lactam –> cell wall active agent

60
Q

monobactams spectrum

A

gram negative aerobes
pseudomonas

61
Q

aminoglycoside MoA

A

protein synthesis inhibiting agents

bind to 30S ribosomal subunit and inhibit bacterial protein synthesis

62
Q

aminoglycosides are bacterio….

A

cidal

63
Q

aminoglycoside spectrum

A

some gram positive aerobes
some MSSA
some MRSA

gram negative aerobes
pseudomonas

64
Q

aminoglycoside rank of activity against pseudomonas

A
  1. amikacin
  2. tobramycin
  3. gentamicin
65
Q

which amino glycoside covered gram positive aerobes including MSSA and MRSA and infective endocarditis

A

gentamicin + cell wall active agent

66
Q

aminoglycoside AEs

A
  • nephrotoxicity
  • ototoxicity (hearing/balance)
  • enhanced neuromuscular blockade
67
Q

which antibiotics cause nephrotoxicity?

A
  • aminoglycosides
  • polymyxins
  • vancomycin (glycopeptide – cell wall active)
    (- piperacillin/tazobactam (Zosyn))
68
Q

tetracyclines MoA

A

protein synthesis inhibiting agent

reversibly bind the 30S ribosomal subunit and inhibit bacterial protein synthesis

69
Q

tetracyclines are bacterio…

A

STATIC!

70
Q

tetracycline counseling

A

do not take with di and trivalent cations aka milk, antacids, sucralfate –> dec oral absorption

worse with tetracycline than doxycycline

71
Q

tetracycline AEs

A
  • GI intolerance
  • phototoxicity (skin or eyes become sensitive to light)
  • fanconi syndrome (dec kidney reabsorption)
72
Q

tetracycline spectrum

A

gram positive aerobes
MSSA
MRSA

gram negative aerobes

atypicals

73
Q

macrolides MoA

A

protein synthesis inhibitor

reversibly binds to 50S ribosomal subunit and inhibits bacteria protein synthesis

74
Q

macrolides are bacterio…

A

STATIC

75
Q

macrolide AEs

A
  • GI intolerance (EVEN WITH IV erythromycin)
  • IV erythromycin: phlebitis (inflammation that causes blood clot)
76
Q

macrolide spectrum

A

gram positive aerobes
MSSA

gram negative aerobes

atypical

77
Q

lincosamides MoA

A

protein synthesis inhibiting agent

reversibly bind 50S ribosomal subunit and inhibit bacteria protein synthesis

78
Q

lincosamides are bacterio…

A

STATIC

79
Q

lincosamide AEs

A
  • GI
  • pseudomembranous colitis (inflammation in colon (large intestine) bc overgrowth of C diff)
80
Q

lincosamide spectrum

A

gram positive aerobes
MSSA
MRSA

gram negative anaerobes

**excellent bone penetration

81
Q

fluoroquinolone MoA

A

DNA synthesis inhibitors –> antimetabolite and other

inhibit DNA gyrase which causes breakage of bacterial DNA –> therefore inhibits DNA

82
Q

fluoroquinolones are bacterio…

A

cidal

83
Q

fluoroquinolone counseling

A

do not take with di and trivalent cations (milk, antacids, sucralfate) bc dec oral absorption

DDI!!!

84
Q

which two antibiotic classes can you not take with milk, antacids, sucralfate? why?

A

tetracyclines (doxycycline, tetracycline)
fluoroquinolones (ciprofloxacin, levofloxacin)

dec oral absorption

85
Q

fluoroquinolone AEs

A
  • GI
  • HA
  • seizures
  • dizzy
  • QTc prolongation

NOT for children < 18 or pregnant

86
Q

fluoroquinolone spectrum

A

gram positive aerobes
MSSA

gram negative aerobes
some pseudomonas

atypicals

87
Q

which fluoroquinolones cover pseudomonas?

A

ciprofloxacin
levofloxacin

88
Q

glycopeptide MoA

A

cell wall active agent

bind to D-alanyl-D-alanine terminal residue in the growing peptidoglycan chain –> prevents further cell wall formation

89
Q

glycopeptides are bacterio…

A

cidal

90
Q

glycopeptide AEs

A
  • nephrotoxicity
  • ototoxicity
  • Red Man’s Syndrome (allergic reaction to vanco often after IV infusion, rash on face, neck, torso)
  • neutropenia
  • rash
91
Q

what is the drug of choice for MRSA?

A

glycopeptides (vanco)!

92
Q

glycopeptide spectrum

A

gram positive aerobes
MSSA
MRSA
c. diff

93
Q

lipopeptide MoA

A

cell membrane active agent

irreversibly binds to bacterial cell membrane and a calcium-dependent molecule insertion occurs –> rapidly depolarize cell membrane –> potassium efflux, ruins ion-concentration gradient –> cell death

94
Q

lipopeptide AE and monitoring

A

skeletal myopathy (loss of muscle mass)

therefore….all patients monitor for
- muscle pain/weakness, especially in distal extremities
- CPK (creatinine phosphokinase) levels weekly

if elevated CPK levels…
- monitor more frequently
- discontinue treatment for unexplained myopathy s/s + CPK > 1000 (5x ULN)
- discontinue treatment for CPK > 10x ULN

95
Q

lipopeptide spectrum

A

gram positive aerobes
MSSA
MRSA

96
Q

lipopeptide CI

A

NOT INDICATED FOR PNEUMONIA!!
- low pulmonary penetration
- microbiological activity inhibited by surfactant

97
Q

which antibiotics cover pseudomonas aeruginosa?

A

beta lactams
- piperacillin
- ticarcillin
- ceftazidime
- cefepime
- imipenem
- meropenem
- doripenem
(NOT ertapenem)

protein synthesis inhibitors
- gentamicin
- tobramycin

DNA synthesis inhibitors
- ciprofloxacin
- levofloxacin

98
Q

which antibiotics cover MRSA/MRSE?

A

beta lactams
- ceftarolin

additional cell wall active agents
- vancomycin

cell membrane active agents
- daptomycin

protein synthesis inhibitors
- gentamicin + cell wall active
- tetracycline
- doxycycline
- clindamycin
- linezolid

DNA synthesis inhibitor
- TMP/SMX

99
Q

measures/indicies of drug action

A

Cmax : MIC
%T > MIC
AUC : MIC

100
Q

which drugs are time dependent minimal/moderate persistent effects?

A

penicillins
cephalosporins
carbapenems

macrolides
oxazolidiones

101
Q

which drugs are concentration dependent prolonged persistent effects?

A

aminoglycosides
fluoroquinolones

102
Q

which drugs are time dependent prolonged persistent effects?

A

vancomycin (glycopeptide)

tetracycline (tetracyclines)
azithromycin (macrolide)

103
Q

are aminoglycosides hydrophilic or lipophilic?

A

hydrophilic

therefore…
renal CL
tissue distribution limited to extracellular space

104
Q

antibiotics without renal dose adjustment

A

NOCk a TAD on the DECk MM Lunch

nafcillin
oxacillin
ceftriaxone

tigecycline!!!
azithromycin
doxycycline

dalfopristin/quinupristin
erythromycin
clindamycin

metronidazole
moxifloxacin
linezolid

105
Q

what is the biggest factor controlling PD?

A

bacteria species!

106
Q

what is the second biggest factor for controlling PD?

A

MIC

107
Q

which drugs may be S but develop rapid resistance once used –> therefore should be avoided?

A

rifampin
ciprofloxacin (flourorquinolones)
clindamycin

108
Q

which organisms may appear S at first, but due to inducible AmpC develop rapid resistance –> may need to use less desireable antibiotics?

A

SPACE-M

Serratia
Pseudomonas aeruginosa
Acinetobacter
Citrobacter
Enterobacter
Moraxella catarrhalis

109
Q

fluoroquinolone optimal target dosing

A

AUC:MIC ratio between 125 and 250

110
Q

vancomycin optimal target dosing

A

AUC:MIC ratio above 400 mg*hr/L

111
Q

AUC:MIC is dependent on what factors?

A

dose 24 (daily dose pt recieves)
patient specific CL
bacterial specific MIC

112
Q

most purulent SSTIs are caused by

A

staph aureus
most are MSSA

113
Q

signs of systemic infection

A

fever
leukocytosis

(note that these could also be signs of other causes)

114
Q

which drugs are not reliable for MRSA empirically?

A

clindamycin
levofloxacin

115
Q

empiric treatment

A

assume most common situation bc have no labs, start broad bc don’t want to miss anything

116
Q

for empiric s. aureus, assume

A

MRSA

117
Q

defined treatment

A

once you know organism only target it

118
Q

for defined s. aureus

A

if MSSA –> deescalate therapy!

119
Q

goal vanco trough for SSTIs

A

10-15 mcg/mL

120
Q

how is vanco generally doses?

A

multiple times per day, also monitoring

121
Q

iv vancomycin AEs

A

nephrotoxicity
infusion AEs
VRE risk (vanco resistant enterococci)

122
Q

daptomycin, ceftaroline, dalbavancin, oritavancin are generally dosed

A

every 12 hours, once a day, or once a week –> longer, therefore hospitals may want to use

123
Q

how do you Dx SIRS?

A

systemic inflammatory response syndrome

NEED 2 OR MORE:
temp < 36 Celsius or >38 Celsius
> 24 breaths/min (tachypnea)
> 90 bpm (tachycardia)
WBC < 4000 or > 12000 cells/uL

124
Q

risk factors for non-purulent SSTI

A

**anything that could allow bacteria to invade deeper tissues

  • dry skin
  • fragile skin
  • obesity
  • previous skin trauma
  • previous cellulitis
  • edema from venous insufficiency
  • tinea pedis (athlete’s foot)
125
Q

non purulent SSTI cellulitis most caused by

A

streptococcus (usually group B)

126
Q

duration of purulent SSTI treatment

A

5-10 days after I and D

127
Q

not reliable for oral streptococcus non purulent SSTI?

A

doxycycline
SMX/TMP

128
Q

duration of mild cellulitis?

A

5 days

129
Q

duration of mod-severe cellulitis?

A

10-14 days, maybe longer

130
Q

what cultures do we need to do in non purulent SSTI?

A

blood!!

131
Q

necrotizing fascilitis caused by

A

monomicrobial:
strep pyogenes (GAS) (flesh eating)
s aureus
clostridium

132
Q

which cultures do you need for necrotizing facilitis?

A

blood
deep tissues

take them from surgery

133
Q

duration of necrotizing facilitis treatment

A

until..
no longer need debridement
patient clinically improved
afebrile for 48-72 hours

134
Q

which patients do you need bacteriocidal activity in?

A

CNS infections
immunocompromised
sepsis

135
Q

what inc risk of resistance

A

previous use of antibiotics long term
hospital exposure
pervious documented resistance

136
Q

linezolid serious AEs

A
  • serotonin syndrome
  • thrombocytopenia
137
Q

reasons to assume MRSA in DFI

A

Hx MRSA infection or colonization
high local prevalence
sereve infection

138
Q

DFI often caused by

A

gram positive aerobes: strep, staph, MRSA
gram negative aerobes: pseudomonas
anaerobes

polymicrobial

139
Q

reason to assume pseudomonas?

A
  • warm climate
  • frequent water exposure
  • high prevalence

p2 year (9 decks)

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