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PHRM 865 > Kays - Exam 1 > Flashcards

Kays - Exam 1 Flashcards

1
Q

Gram positive bacteria stain _____

A

(positive) purple

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2
Q

Gram negative bacteria stain _______

A

red

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3
Q

difference between bacili and cocci

A

bacili: rod shape
cocci: little circles

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4
Q

which bacteria are lactose fermenting

A 
CEEK:
Citrobacter
Enterobacter
Escherichia coli
Klebsiella
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5
Q

Which drugs/things can MASK a fever

A

Antipyretics
Corticosteroids
Antimicrobial therapy
an overwhelming infection can mask a fever

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6
Q

Systemic Signs of an infection:

Fever: Temp > _____

A

38 degrees Celsius/ 100.4 Farenheit

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7
Q

Systemic Signs of an infection:

Increased White blood count (> ________ /mm^3)

A

> 10,500

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8
Q

Normal WBC?

A

4,500 - 10,500/mm^3

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9
Q

Systemic Signs of an infection:

Tachy or Brady cardia/pnea

A

Tachy!!
HR > 90 beats/min
R > 20 breaths/min

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10
Q

Systemic Signs of an infection:

Hypo or hyper tension?

A

hypo! (SBP < 90 mmHg or an MAP < 70)

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11
Q

Normal WBC Differential:

Mature Neutrophils: _____%

A

50-70%

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12
Q

Normal WBC Differential:

Immature neutrophils: ____%

A

0 -5%

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13
Q

Normal WBC Differential:

Eosinophils: ____ %

A

0-5%

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14
Q

Normal WBC Differential:

Basophils: ____%

A

0 -2%

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15
Q

Normal WBC Differential:

Lymphocytes: _____%

A

15-40%

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16
Q

Normal WBC Differential:

Monocytes: _____%

A

2-8%

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17
Q

Which WBCs are Agranulocytes

A

Lymphocytes and Monocytes

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18
Q

Which WBCs are Granulocytes

A

the “Phils”

Neutrophils, Eosinophils, Basophils

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19
Q

Other names for mature neutrophils

A

PMNs, Polys, Segs

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20
Q

Other names for immature neutrophils

A

bands

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21
Q

Leukocytosis means ??

A

increased neutrophils (+/- bands)

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22
Q

Presence of immature forms of neutrophils means what?

A

aka a left shift = indication of bone marrow response to the infection

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23
Q

Leukocytosis generally means ______ infection

A

bacteria

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24
Q

Lymphocytosis generally means _________ infection

A

viral, fungal, or tuberculosis

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25
Q

Monocytosis usually associated with?

A

tuberclosis or lymphoma

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26
Q

Eosinophillia usually associated with?

A

ALLERGIC REACTIONS! oar protozoal/parasitic infections

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27
Q

CD4 or CD8?

depleted in HIV infection

A

CD4

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28
Q

CD4 or CD8?

bind to and directly kill tumor cells

A

CD8

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29
Q

CD4 or CD8?

help with antibody production and secrete lymphokines

A

CD4

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30
Q

ESR and CRP when elevated = _______ but not for sure ________

A

means inflammation; not always meaning infection tho…

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31
Q

Normal ESR value?

A

0 - 15 mm/hr (males)

0 - 20 mm/hr (females)

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32
Q

Normal CRP value?

A

0 - 0.5 mg/L

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33
Q

What is PCT

A

procalcitonin/precursor of calcitonin

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34
Q

Normal value of PCT

A

< 0.05 ug/L

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35
Q

PCT is more or less specific than ESR or CRP for bacterial infections

A

MORE! good for finding out if bacterial infection (PCT is not related to viral infections !)

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36
Q

What PCT value is suggestive of sepsis

A

2 - 10 ug/L

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37
Q

What PCT value means sepsis/systemic bacterial infection

A

> 10

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38
Q

what PCT value means other condition/localized infection

A

0.25 - 2 ug/L

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39
Q

Sensitivity or Specificity?

positive result in presence of disease/infection

A

Sensitivity

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40
Q

Sensitivity or Specificity?

false positive rate

A

specificity

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41
Q

Sensitivity or Specificity?

negative result in absence of disease/infection

A

specificity

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42
Q

Sensitivity or Specificity?

False negative rate

A

sensitivity

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43
Q

to give the drug abacavir – what genetic test must be done

A

HLA-B5701 = hypersensitivity

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44
Q

Empiric vs directed therapy?

A

Empiric: BROAD SPECTRUM before pathogen idenitifie

Directed: after pathogen identified/susceptibility results are known; DE-ESCALATE to agent with narrowest effective spectrum of activity

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45
Q

Want to move pts from IV to PO therapy when clinically stable and functioning GI tract annnnd ahve agents with good oral bioavaliability— what are cases where you should NOT

A

if CNS infection, endocarditis (lil Owen!), and Staph aureus bactermemia

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46
Q

what are the 3 primary reasons for combination antimicrobial therapy?

A

broad spectrum for polymicrobial infections
synergistic bactericidal activity
prevent emergence of resistance (ex: HIV drug therapy)

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47
Q

disadvantages of combo microbial therapy?

A

increased cost
greater risk of drug toxicity
superinfection with resistant bacteria
antagonism of drugs to each other

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48
Q

what 3 main things should be used to figure out empiric therapy

A
  • knowledge of the likely pathogen (body site, where infection started (hospital)
  • anticipated susceptibility pattern (antiobiogram)
  • info from pt history/PE (prior abx use, travel hx/other sick ppl at home)
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49
Q

bactericidal vs bacteriostatic

A

cidal: KILLS organism….
static: inhibits bacterial replication

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50
Q

what are 3 main ways that an antibiotic can be bactericidal

A

act on cell wall
act on cell membrane
or act on bacterial DNA

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51
Q

Antimicrobial Tissue Concentrations = mean of ________ and _____ concentrations

A

extracellular AND intracellular!

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52
Q

Gram Positive vs Gram negative Cell wall comparison:

has lots of peptidoglycan

A

Positive

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53
Q

Gram Positive vs Gram negative Cell wall comparison:

has porins

A

negative

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54
Q

Gram Positive vs Gram negative Cell wall comparison:

has lipopolysaccharide outer membrane (LPS/endotoxi)

A

negative

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55
Q

Gram Positive vs Gram negative Cell wall comparison:

has beta lactamases on the outside of the cell/towards environinment

A

gram positive

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56
Q

Gram Positive vs Gram negative Cell wall comparison:

has beta lactamases in periplasmic space

A

negative

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57
Q

what are PBPs?

A

pencillin binding proteins:

aka enzymes vital for cell wall synthesis, cell shape, and structural integrity

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58
Q

what is the most important PBP and why

A

transpeptidase:

it catalyzes final cross link between sugar and peptide in peptidoglycan molecule

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59
Q

3 types of genetic exchange that leads to resistance

A

conjugation
transduction
transformation

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60
Q

what is conjugation (genetic exchange shit)

A

direct contact or mating via sex pilli **most common

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61
Q

what is transduction (genetic exchange shit)

A

genes transferred via bacteriophages (viruses) between bacteria

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62
Q

what is transformation (genetic exchange shit)

A

uptake of “free floating” DNA from the environment then gets integrated into the hosts DNA

63
Q

Plasmids or transposons:
transferred from organism to organism
self replicating
extrachromosomal DNA

A

plasmid

64
Q

3 main mechanisms of bacterial resistance

A

enzymatic inactivation
alteration of target site
altered permeability of bacterial cell

65
Q

what are examples of abx resistance via enzymatic inacivation

A

beta lactamases

aminoglycoside modifying enzyme

66
Q

what are examples of abx resistance via alteration target site

A

PBPs
cell wall precursors
ribosomes
DNA gyrase/topoisomerase

67
Q

what are examples of abx resistance via altered permeability of bacterial cell

A

efflux pumps

porin changes

68
Q

what are beta lactamases/how do they work

A

they inactivate beta lactam abxs

work by hydrolzying/splitting amide bond = inactivate drug

69
Q

what gene in beta lactamases are we to know

A

AmpC

70
Q

what does ESBL stand for

A

Extended spectrum beta lactamases

71
Q

which bacteria typically contain AmpC

A

SPICE

serratia, pseudomonas, indole-positive proteus, citrobacter, enterobacter

72
Q

what drugs are beta lactamase inhibitors

A

tazobactam
clavulanic acid
sulbactam —- resistance to the SPICE organisms has happened!!

avibactam = lactamase inhibited in SPICE by this drug does happen tho

73
Q

how is AmpC induced?

A

the gene is normally repressed, when a beta lactam is present the gene gets DEPRESSED which cause beta lactamase production

when inducer is removed then the gene gets repressed again

74
Q

what abxs are strong inducers of AmpC

A

Penicillin G
Ampicillin
1st gen cephalosporings
Cefoxitin

*Clavulanic acid = potent induce of AmpC beta lactamases

75
Q

SPICE are typically constitutively making beta lactamases….
avoid using what abx because of developed resistance?

A

avoid 3rd gen cephalosporins

76
Q

ESBLs seen most frequently in what bacteria

A

Klebsiella pneumoniae
and
E.Coli

77
Q

ESBLs are _____ mediated and tend to hydrolyze _______ and ______

A

plasmid mediated;

hydrolyze PCNs and cephalosporins

78
Q

what drug may be useful for the CTX-M enzyme of ESBLs

A

tazobactam

79
Q

what is normally the treatment of choice for ESBLs

A

carbapenems

80
Q

what are the 3 most important carbapenemases

A

KPC (klebsiella pneumoniae carbapenemase)
Oxa-type (seen in acinetobacter)
NDM (new delhi metallo beta lactamases)

81
Q

T or F: CRE can last in the body for only 6 months

A

falseeee

carbampenemase resistant enzymes can last in the body for 12 months!! aka bacteria can get spread allllll over

82
Q

NDM-1 is resistant to all antibiotics except what?

A

Colistin

83
Q

best way to treat CRE bugs?

A

is serine carbapenemase: ceftazidime + avibactam

if the NDM-1/metallo-b lactamase = use aztreonam

84
Q

what 4 things can predispose someone to an infection

A

FLORA: alteration to normal flora of host
BARRIERS: disruption to barriers (skin, cilia, pH changes)
AGE
IMMUNOSUPPRESION: due to malnutrition, underlying disease, hormones (pregnancy or corticosteroids), drugs (cytotoxic agents)

85
Q

what does MIC stand for and its definition

A

minimum inhibitory concentration

lowest concentration of abx that prevents VISIBLE growth

86
Q

what does MBC stand for and its definition

A

minimum bactericidal concentration: lowest concentration resulting > 99.9% decrease in initial inoculum

87
Q

what is an Etest

A

epsilometer test: abx on entire strip with a continuous gradient of the drug:
an eliptical shape will form – “largest death area” = where most drug is…
MIC found where the inhibition ellipse intersects with the strip

88
Q

what is agar dilution

A

agar with two fold dilutions of abx in it;
bacteria inoculated on to them;
MIC will be agar plate with the lowest concentration and no growth of an organism

89
Q

what is broth dilution

A

two fold dilutions of abx in liquid broth;

MIC will be lowest concentration of the drug that prevents visible growth

90
Q

T or F: broth in broth dilution method has no protein in it

A

true (note because there is protein in the body tho and like drug protein binding shit)

91
Q

Definition: susceptible (for breakpoints)

A

isolated bacteria is inhibited by usually achievable concentrations when normal dosing regimens are used

92
Q

Definition: S-DD (susceptible dose dependent)

A

susceptibility is dependent on the dosing regimen used (need higher doses!!)

93
Q

Definition: intermediate (for breakpoints)

A

we guessin’
treatment MAY be successful when max doses are used or if drug is concentrated at the site of infection
MIC approaches achievable blood or tissue concentrations

94
Q

How are MIC breakpoints (aka interpretive criteria) established

A

clinical pharmacology of the drug

clinical/bacteriologic response from human studies

95
Q

Tolerance in susceptibility tests is defined as ??

A

MBC >/= to 32 x MIC

rarely identified clinically bc MBCs not routinely determined

96
Q

what is the inoculum effect

A

a laboratory phenomenon that is described as a significant increase in the minimal inhibitory concentration of an antibiotic when the number of organisms inoculated is increased

97
Q

what is MIC(50) and how do you find it

A

abx concentration that inhibits 50% of bacteria tested

ex: if you have 100 samples — put them in MIC order and find the MIC value that inhibits at least 50% of bacteria?

98
Q

what is MIC(90) and how do you find it

A

abx concentration that inhibits 90% of bacteria tested

ex: if you have 100 samples — put them in MIC order and find the MIC value that inhibits at least 90% of bacteria?

99
Q

what is Geometric mean MIC and how do you find it…

A

the antilog of the mean of the log MICs……. wut is math

100
Q

what is modal MIC and how do you find it

A

simply the most frequent MIC

101
Q

definition of synergy:

A

activity of antimicrobial combo is greater than that expected from additive activity of the individual agents

102
Q

definition of antagonism: (synergy testing)

A

activity of an antimicrobial combo is less than that expected from the additive activity of the individual agents

103
Q

Definitions additivity or indifference: (synergy testing)

A

neither synergy or antagonism

104
Q

two different tests for testing synergy

A

checkboard test (grid of using two diff abx in broth, less growth/more clear plates = synergy..)
and
time kill curves (showing effect of drugs alone vs together vs control)

105
Q

what does PAE stand for and what is the definition

A

post antibiotic effect

after abx removed, there is still some inhibitory effects on the bacterial growth still

106
Q

PAE is a phenomenon in in vivo or in vitro

A

vitro!!

not vivo!! the body has WBCs and stuff to also have extra effects after abx

107
Q

antibiotic stewardship wants rapid diagnostic testing to increase why

A

they want to detect resistant bugs faster

108
Q

what are some molecular diagnostic techniques for rapid diagnostic

A 
PCR
PNA-FISH
LAMP
MALDI-TOF
Verigene/BioFire
109
Q

aminoglycoside modifying enzyme mechanisms? (3 total)

A

acetylation
nucleotidylation
phosphorylation

110
Q

aminoglycoside modifying enzyme:
they modify the structure by transferring an indicated chemical group to a ___________
this will impair ______ and/or _______

A

to a specific side chain

impair cellular uptake/binding to ribosome

111
Q

There is a bifunctional enzyme that modifies aminoglycosides:
mainly seen in what bacteria?
the enzyme leads to high level resistance to ______ but not _______

A

mainly seen in ENTEROCOCCI
resistance to gentamicin
not resistant to streptomycin tho

112
Q

Resistance mechanisms:

what are examples of Altered target sites - PBPs

A

1 - S. Pneumoniae resistant to PCN and Cephalosporins

2 - Staphylococci is resistant to Methicillin via mecA gene

113
Q

Methicillin resistance is seen in what abx because of what gene?

A

staphylococci are resistant because of mecA gene

114
Q

the mecA gene encodes for production of a new PBP that is called ______

A

PBP2A or PBP2’

115
Q

how does vancyomyocin normally work as an antibiotic?

A

inhibits cell wall synthesis –

does this by binding to D-alanine-D-alanine terminus of pentapeptide (a peptidoglycan precursor)

116
Q

what bacteria is known to have vancomyocin resistance through the VanA gene

A

S. Aureus = VRSA

117
Q

how does the VanA gene cause resistance

A

causes the D-Ala-D-Ala part becomes D-Ala-D-Lac and vancomyocin can’t bind to the D-Ala-D-lac part

118
Q

Altered ribosomal targets lead to resistance in what antibiotics

A

macrolides, azalides, aminoglycosides, tetracyclines, clindamycin

119
Q

Altered DNA gyrase/topoisomerases lead to resistance to the drug class(es) of _______?
and this resistance is seen in what bugs most?

A

fluoroquinolones

seen in S. Pneumoniae and gram negative

120
Q

what are some drugs that have had reported chromosomal/plasmid mediated resistance with efflux pumps occur?

A

Macrolizes/Azalides

Carbapenems

121
Q

what bug has had reported efflux pump resistance to macrolides/azalides

A

S.Pneumoniae

122
Q

what bug has had reported efflux pump resistance to carbapenems

A

P.Aerugonisa

123
Q

For efflux pump resistance:
for P.Aerugonisa that has resistance to Carabapenems:
which carabapenem drug is best to use? (because it does not get effluxed out…)

A

IMIPENEM is best!! (definitely not pumped out as much as meropenem)

124
Q

P.Aeruginosa has multidrug efflux pumps… which drug(s) were bolded/in every single multidrug efflux pump…

A

Ciprofloxain/Levofloxain

125
Q

Porins will typically allow a drug to go through it when the drug is (small or large?) (more or less negative)(hydrophobic or hydrophillic?)

A

go through when small, less negative charges(aka it prefers zwitterionic charge); hydrophillic

126
Q

Mutations in porins seen most commonly in what bugs?

A

Enterobacteriaceae bois and P.Aeruginosa

127
Q

what resistance mechanisms are most common for beta lactam drugs

A

hydrolysis (aka beta lactamase);
altered target site;
efflux

128
Q

resistance mechanisms for aminoglycosides?

A

aminoglycoside modifying enzymes…..
altered target site…
efflux

129
Q

what resistance mechanisms are most common for glycopeptides (aka vancomyocin)

A

altered cell wall precursors (D-Ala-D-Lac)

130
Q

Intrinsic Resistance:

what bug has intrinsic resistance to beta lactams?

A

mycoplasma

131
Q

Intrinsic Resistance:

what bug has intrinsic resistance to vancomyocin?

A

gram negative (because they got no peptidoglycan)

132
Q

Intrinsic Resistance:

what bug has intrinsic resistance to cephalosporins

A

enterococci

133
Q

Intrinsic Resistance:

what bug has intrinsic resistance to aminoglycosides

A

anaerobes

134
Q

P.Aeruginosa: Common resistance mechanisms?

A

ESBLs
Efflux Pump
Reduced outer membrane permeability

135
Q

K.Pneumoniae Common resistance mechanisms?

A

Carbapnemases

136
Q

E.Coli: Common resistance mechanisms?

A

ESBL

137
Q

S. Aureus: Common resistance mechanisms?

A

Methicillin Resistance - mecA gene

Vanc resistance

138
Q

Enterococci: Common resistance mechanisms?

A

vancomyocin resistance via altered cell wall precursors

139
Q

what PK/PD parameter do aminoglycosides use?

A

peak/mic

140
Q

what PK/PD parameter do Beta lactams use?

A

Time above MIC

141
Q

what PK/PD parameter does Daptomyocin use?

A

AUC(0-24)/MIC or Peak/MIC

142
Q

what PK/PD parameter do Fluoroquinolones use?

A

AUC(0-24)/MIC

143
Q

what PK/PD parameter does vancomycoin use?

A

AUC(0-24)/MIC

144
Q

which abx are time dependent

A

beat lactams

vancomyocin

145
Q

what abx are concentration dependent

A

aminoglycosides
daptomyocin
fluoroquinolones

146
Q

For beta lactam abx: what are the goal %’s for time above MIC for GRAM NEGATIVES:
carabapenems: > _____%
PCNs: > ____%
cephalosporins: > ____ %

A

40%
50%
60%

147
Q

For beta lactam abx: what are the goal %’s for time above MIC for GRAM POSITIVES?

A

> 40%

148
Q

Goal AUC/MIC ratio for Fluoroquinolones?

A

> 100 for Gram negative bugs

> 30 for Gram Positive (maybe > 100…?)

149
Q

Goal Peak/MIC ratio for aminoglycosides

A

8 - 10

150
Q

Goal AUC/MIC ratio for vancomyocin

A

400 - 600

151
Q

High risk for nephrotoxicity with vancomyocin when AUC is in the range of _________

A

600 - 700 or higher of course!

152
Q

what are all the lactose fermenting bacteria

A

CEEK + VAP
citrobacter, enterobacter, e.col, kleibsella
+
vibrio cholerae, pasturella multicoda, aeromonas hydrophilia

153
Q

what bacteria are known as “atypical bacteria”? (the cell walls are difficult to stain— or maybe mycoplasma aka no cell wall)

A

chlamydophila pneumoniae
chlamydia trachomatis
legionella pneumophilia
mycoplasma pneumoniae

154
Q

what bacteria is gram variable bacilli

A

gardenerella vaginalis

PHRM 865 (59 decks)

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