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PDA 3 > Exam 1 stuff > Flashcards

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
Q

Gram - have _______ layer of peptidoglycan in the cell wall

A

thin

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26
Q

acid fast bacteria are characterized by

A

wax like nearly imperable cell walls
contain mycolic acid

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27
Q

MIC

A

lowest concentration of abx that is effective against bacterial infection
lowest drug concentration that stops microbial growth

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28
Q

cell wall synthesis inhibitors

A

beta-lactams
vancomycin

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29
Q

protein synthesis inhibitors

A

aminoglycosides
tetracyclines
macrolides
clindamycin
chloramphenicol
streptogramins

30
Q

nucleic acid synthesis inhibitors

A

quinolones
fluoroquinolones
metronidazole

31
Q

inhibitors of metabolism

A

sulfonamides
trimethoprim

32
Q

superinfections

A

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
Q

how do abx cause C.diff

A

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
Q

innate resistance

A

naturally and inherently resistance

35
Q

mechanisms of innate resistance

A
  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
Q

acquired resistance

A

resistance develops in response to tx with abx

37
Q

mechanisms of acquired resistance

A

DNA mutation
transfer of external DNA to bacterium

38
Q

conjugation

A

transfer through direct cell to cell contact through bridge/sex pilus

39
Q

transduction

A

bacteria transferred from a phage that contains DNA from a previous host bacterium

40
Q

transformation

A

susceptible bacteria take up DNA released into the environment and incorporate into their genome
-may involve transposons

41
Q

Mechanisms of resistance

A

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
Q

examples of reduced entry of abx into pathogen

A

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
Q

examples of resistance by drug efflux

A

overexpression of efflux pumps (MATE, MFS, SMR, SMR, RND, ABC
this is MOA for bacteria, fungi, and parasites

44
Q

examples of resistance by drug inactivation by bacterial enzymes

A

penicillinases or beta lactamases
aminoglycoside modifying enzymes

45
Q

examples of resistance by modification of drug target site

A

alteration of alternative metabolic pathways that alter binding of abx (mech for s.aureus and enterococci resistance to erythromycin)

46
Q

examples of the development of alternative metabolic pathways/bypass targets

A

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
Q

mechansim of resistance for carbapenems

A

loss of porins

48
Q

mechanism of resistance for trimethoprim and sulfonamides

A

bypass targets

49
Q

mechanism of resistance for tetracyclines and aminoglycosides

A

ribosomal mutation or modification

50
Q

mechanism of resistance for polymixin antibiotics

A

mutations in lipopolysaccharide structure

51
Q

mechanism of resistance for quinolones

A

target mutations

52
Q

mechanism of resistance for aminoglycosides and ciprofloxacin

A

antibiotic modifying enzymes

53
Q

mechanism of resistance for meropenem, quinolones, tigecycline, and chloramphenicol

A

overexpression of transmembrane efflux pumps

54
Q

irreversible B lactamase inhibitors

A

clavulanic acid
sulbactam
tazobactam

55
Q

irreversible B lactamase inhibitors work against Class

A

A (conventional B lactamases)

56
Q

class A B lactamases

A

TEM
SHV
CTX-M
KPC
ESBLs

57
Q

reversible covalent inhibitors work against class

A

A and D

58
Q

class D B lactamases

A

OXA

59
Q

reversible covalent inhibitors

A

avibactam
durlobactam
relebactam

60
Q

reversible competitive inhibitors

A

vaborbactam
taniborbactam (under clinical investigation)

61
Q

reversible competitive inhibitors work against

A

potent inhibition of KPC and other class c

62
Q

class C beta lactamases

A

AmpC

63
Q

class B beta lactamases

A

NDM
VIM
(metallo/zinc dependent)

64
Q

trimethoprim inhibits

A

DHFR (dihydrofolate reductase)

65
Q

sulfamethoxazole inhibits

A

Dihydropteroate synthase

66
Q

contraindications to sulfonamides

A

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
Q

fourth gen cephalosporin

A

cefepime (covers pseudomonas)

68
Q

fifth gen cephalosporin

A

ceftaroline

69
Q

siderophore

A

cifiderocol (stability to class B beta lactamases)
travels through Fe channels

70
Q
A

PDA 3 (2 decks)

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