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Exam 1 stuff Flashcards

1
Q

first generation cephalosporin activity

A

G+ (MSSA and streptococci)
Moderate activity against G- rods (E.coli, Klebsiella pneumoniae, Proteus mirabilis)

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2
Q

second-generation cephalosporin activity

A

G+ species
add G- including mortaxella catarrhalis, haemophilus influenzae, and some enterobacterales
Cephamycines: activity against many anaerobes

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3
Q

third-generation cephalosporin activity

A

lose some G+ activity (but retains good strep pneumoniae)
much more active against G-

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4
Q

fourth generation cephalosporin activity

A

CEFEPIME
broadest spectrum
good G+ and G- including pseudomonas

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5
Q

Fifth-generation cephalosporin activity

A

CEFTAROLINE
anti-MRSA activity
good G+ activity

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6
Q

NMTT group associated with

A

-hypoprothrombinemia and bleeding tendency because it inhibits Vit K epoxide reductase
-disulfiram-like reaction

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7
Q

which third-generation cephalosporin is contraindicated in neonates because it displaces bilirubin

A

ceftriaxone

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8
Q

which drug has the most potent anti-MRSA activity

A

ceftaroline fosamil (prodrug)

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9
Q

which drug binds to Fe molecules to travel through Fe channels making it a poor substrate for B lactamases

A

Cifiderocol (siderophore)
has stability to hydrolysis by all B lactamases including class B

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10
Q

first gen parenteral agents

A

cefazolin

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11
Q

first gen oral agents

A

cephalexin
cefadroxil

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12
Q

second gen parenteral agents

A

cefuroxime
cefoxitin
cefotetan

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13
Q

second gen oral agents

A

cefaclor
cefprozil

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14
Q

third gen parenteral agents

A

cefotaxime
ceftriaxone
ceftazidime w/avibactam
ceftolozane w/tazobactam

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15
Q

third gen oral agents

A

cefixime
cefpodoxime proxetil
cefdinir

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16
Q

third generation cephalosporins that maintain strep pneumoniae coverage

A

cefotaxime
ceftriaxone
cefdinir
cefpodoxime
ceftolozane/tazobactam (clinically used for G- infections)

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17
Q

helminth

A

multicellular eukaryote
complex organ systems
rudimentary NS

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18
Q

protozoa

A

single-celled eukaryotes
most free living

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19
Q

fungi

A

eukaryotes
rigid cell wall
ergosterol in membrane

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20
Q

diagnosis for fungi

A

calcofluor white stain

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21
Q

viruses

A

do not have cells
contain nucleic acid genome surrounded by a capsid

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22
Q

bacteria

A

single-celled prokaryotes

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23
Q

bacteria characteristics

A

no nucleus, flagella, cell wall, 70S ribosome, pili, capsule, G- have outer membrane

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24
Q

gram + have _______ layer of peptidoglycan in the cell wall

A

thick

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25
Gram - have _______ layer of peptidoglycan in the cell wall
thin
26
acid fast bacteria are characterized by
wax like nearly imperable cell walls contain mycolic acid
27
MIC
lowest concentration of abx that is effective against bacterial infection lowest drug concentration that stops microbial growth
28
cell wall synthesis inhibitors
beta-lactams vancomycin
29
protein synthesis inhibitors
aminoglycosides tetracyclines macrolides clindamycin chloramphenicol streptogramins
30
nucleic acid synthesis inhibitors
quinolones fluoroquinolones metronidazole
31
inhibitors of metabolism
sulfonamides trimethoprim
32
superinfections
caused by a microorganism that is resistant to abx used in initial treatment -during abx treatment, there is overgrowth of resistant strains--> leads to colonization and expansion of C.diff
33
how do abx cause C.diff
decrease diversity of microbiota and expands C.diff population increase levels of free sialic acid from host and succinate from microbiota--> expansion of C.diff population
34
innate resistance
naturally and inherently resistance
35
mechanisms of innate resistance
1. bacteria that lack peptidoglycan cell wall (mycoplasma and mycobacterium) 2. G- inherently resistant to vanc because of two membranes 3. anaerobic bacteria resistant to AMGs because O2 is required for transport across the membrane
36
acquired resistance
resistance develops in response to tx with abx
37
mechanisms of acquired resistance
DNA mutation transfer of external DNA to bacterium
38
conjugation
transfer through direct cell to cell contact through bridge/sex pilus
39
transduction
bacteria transferred from a phage that contains DNA from a previous host bacterium
40
transformation
susceptible bacteria take up DNA released into the environment and incorporate into their genome -may involve transposons
41
Mechanisms of resistance
reduced entry of abx into pathogen drug efflux drug inactivation by bacterial enzymes modification of drug target site development of alternative metabolic pathways/bypass targets
42
examples of reduced entry of abx into pathogen
change or loss of porins in G- (porins allow polar molecules in) (PCN resistance) changes to the number and structure of porins (tetracyclines and chloramphenicol resistance)
43
examples of resistance by drug efflux
overexpression of efflux pumps (MATE, MFS, SMR, SMR, RND, ABC this is MOA for bacteria, fungi, and parasites
44
examples of resistance by drug inactivation by bacterial enzymes
penicillinases or beta lactamases aminoglycoside modifying enzymes
45
examples of resistance by modification of drug target site
alteration of alternative metabolic pathways that alter binding of abx (mech for s.aureus and enterococci resistance to erythromycin)
46
examples of the development of alternative metabolic pathways/bypass targets
bacteria circumvent the synthesis of folic acid -enterococcal bacteria are dependent on thymidine but utilize exogenous from the environment so now resistant to trimethoprim
47
mechansim of resistance for carbapenems
loss of porins
48
mechanism of resistance for trimethoprim and sulfonamides
bypass targets
49
mechanism of resistance for tetracyclines and aminoglycosides
ribosomal mutation or modification
50
mechanism of resistance for polymixin antibiotics
mutations in lipopolysaccharide structure
51
mechanism of resistance for quinolones
target mutations
52
mechanism of resistance for aminoglycosides and ciprofloxacin
antibiotic modifying enzymes
53
mechanism of resistance for meropenem, quinolones, tigecycline, and chloramphenicol
overexpression of transmembrane efflux pumps
54
irreversible B lactamase inhibitors
clavulanic acid sulbactam tazobactam
55
irreversible B lactamase inhibitors work against Class
A (conventional B lactamases)
56
class A B lactamases
TEM SHV CTX-M KPC ESBLs
57
reversible covalent inhibitors work against class
A and D
58
class D B lactamases
OXA
59
reversible covalent inhibitors
avibactam durlobactam relebactam
60
reversible competitive inhibitors
vaborbactam taniborbactam (under clinical investigation)
61
reversible competitive inhibitors work against
potent inhibition of KPC and other class c
62
class C beta lactamases
AmpC
63
class B beta lactamases
NDM VIM (metallo/zinc dependent)
64
trimethoprim inhibits
DHFR (dihydrofolate reductase)
65
sulfamethoxazole inhibits
Dihydropteroate synthase
66
contraindications to sulfonamides
infants < 2 months pregnant women and mothers nursing infants less than 2 months Why? sulfonamides displace bilirubin from plasma proteins causing increased levels of bilirubin = kernicterus
67
fourth gen cephalosporin
cefepime (covers pseudomonas)
68
fifth gen cephalosporin
ceftaroline
69
siderophore
cifiderocol (stability to class B beta lactamases) travels through Fe channels
70

PDA 3 (2 decks)

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