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PHRM 865 Therapeutics > Lec 4 Cephamycins/Carbapenems/Glycopeptides/Etc Cushman > Flashcards

Lec 4 Cephamycins/Carbapenems/Glycopeptides/Etc Cushman Flashcards

1
Q

the cephamycins have a _________ group which inc stability vs beta lactamases

a. oxime ether
b. pyridinium ring
c. C-3 carboxylic acid
d. 7a-methoxyl group

A

d. 7a-methoxyl group

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2
Q

drug with similar reaction to disulfiram

a. cephalexin
b. cefotetan
c. cilastatin
d. dicloxicillin

A

b. cefotetan

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3
Q

cefotetan releases _________, which can cause hypoprothrombinemia, and can also cause a disulfiram like rxn

a. 7alpha-methoxyl
b. a pyrimdine ring
c. N-methylthiotetrazole
d. a phosphate group

A

c. N-methylthiotetrazole

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4
Q

why is thienamycin not used as a drug but imipenem is?

A

too reactive to be used as a drug, since the primary amino group attacks the beta lactam intermolecularly

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5
Q

imipenim is the N-formiminoyl derivative of _______

a. azithromycin
b. daptomycin
c. thienamycin
d. plazomicin

A

c. thienamycin

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6
Q

The carbapenems are carbon analogs of the ________. The sulfur that is present in the thiazolidine ring of the penicillins is replaced by a ________ group. This increases reactivity because it is smaller than a sulfur, so the ring strain is greater in the carbapenems.

A

penicillins; methylene

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7
Q

Besides reacting with penicillin-binding proteins, imipenem reacts with and inhibits _______ _______

A

beta lactamases

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8
Q

what drug is commonly given with imipenem?

A

cilastatin

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9
Q

dehydropeptidase-1 inhibitor drug

A

cilastatin

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10
Q

Imipenems and other drugs in the carbepenem class are commonly referred to as “______ ______”, and their use is typically restricted in order to avoid widespread bacterial resistance

A

magic bullets

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11
Q

why are they called monobactams?

A

one ring, the beta lactam ring is not fused to any other ring

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12
Q

monobactams target almost completely gram _______ bacteria

A

negative

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13
Q

two glycopeptides antibiotics in clinical use

A

vancomycin (USA)
teicoplanin (Europe)

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14
Q

Vancomycin is an inhibitor of Gram _______ cell wall biosynthesis.

A

positive

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15
Q

vancomycin inhibits the _________ rxn that is required for cross-linking, but a different MOA than beta-lactam antibiotics

A

transpeptidase

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16
Q

difference between bactericidal and bacteriostatic

A

bactericidal kills bacteria, bacteriostatic slows growth

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17
Q

for vancomycin, a bacterium with an MIC ___ µg/mL is considered a susceptible strain. Staphylococcus strains that are methicillin-resistant are usually inhibited with MIC values ___-___ µg/mL.

A

4; 1-5

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18
Q

Vancomycin-resistant enterococcal (VRE) infections first appeared in Europe in connection with the use of _______

a. avoparcin
b. probenecid
c. oritavancin
d. dalfopristin

A

a. avoparcin

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19
Q

Vancomycin resistance appears to be due to a mutation of the peptidoglycan cell wall precursor from D-Ala-D-Ala to D-Ala-D-_______.

a. D-gly
b. D-pro
c. pyruvate
d. lactate

A

d. lactate

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20
Q

vanc is ___% elim by glomerular filtration with a half-life of ___-___ hours

A

90%; 4-11

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21
Q

vancomycin therapeutic uses (2)

A
  1. C diff pseudomembranous colitis (relapse or unresponsive to metronidazole tx)
  2. MRSA
22
Q

red man syndrome is assoc with which antibiotic that we talked about?

A

vanc

23
Q

nephrotoxicity and _______ are two rare potential problems of vanc

A

ototoxicity

24
Q

oritavancin, telavancin, and dalbavancin are in what drug class?

A

lipoglycopeptide antibiotics

25
Q

which of the following can be used in single dose regimens due to long half-life? (2 of them)

a. vancomycin
b. telavancin
c. dalbavancin
d. oritavancin

A

c. dalbavancin
d. oritavancin

26
Q

MOA of telavancin and dalbavancin

A

identical to vancomycin. It binds to the D-Ala-D-Ala residue on growing peptidoglycan chains and inhibits transpeptidation and transglycosylation

27
Q

synercid is a mix of ___% quinupristin and ___% dalfopristin

A

30%; 70%

28
Q

The parent natural product mixture of pristinamycins lacks suitable solubility for reliable dosages. The derivatives quinupristin and dalfopristin have amino side chains that allow salt formation and enhance the _____ _____ needed to make a useful formulation.

A

water solubility

29
Q

T or F: quinupristin and dalfopristin are each bacteriocidal alone

A

F (bacteriostatic)

30
Q

Synercid is bacteriostatic against _______ _______ (bug) and bactericidal against strains of methicillin-susceptible and methicillin-resistant _______ (bug)

A

enterococcus faecium; staphylococci

31
Q

dalfopristin MOA

A

directly interferes with peptidyl transferase forming a peptide bond between AAs

32
Q

_______ binds in the ribosomal tunnel and causes blockage of the tunnel

a. dalfopristin
b. quinupristin

A

b. quinupristin

33
Q

Synercid therapeutic use (3)

A
  1. vanc resistant enterococcus faecium bacteremia
  2. vanc-resistant enterococcus faecium UTIs
  3. skin infections caused by MRSA
34
Q

quinupristin’s MOST COMMON mech of resistance is due to:

a. A2058 methylation in 23S rRNA
b. G2576U substitution
c. inc efflux pumps
d. A2058G substitution

A

a. A2058 methylation in 23S rRNA

35
Q

Synercid significant SE

A

none (only mild ones)

36
Q

which of the following is TRUE about the PK of Synercid?

a. average half life is 10 hours
b. the blood/brain or placental barriers are penetrated
c. clearance is 75% through biliary excretion (fecal matter) and the rest in urine

A

c. clearance is 75% through biliary excretion (fecal matter) and the rest in urine

37
Q

quinupristin metabolism two products

A

quinupristin glutathione conjugate
quinupristin cysteine conjugate

38
Q

dalfopristin metabolism leads to a _____ product and a pristinamycin IIA _____ product

A

hydrolysis; reduction

39
Q

linezolid drug class

A

oxazolidinones

40
Q

linezolid MOA

A

interacts with 50S subunit which prevents formation of 70S initiation complex. Specifically interacts with 23S rRNA

41
Q

linezolid therapeutic uses (3)

A
  1. vanc-resistant enterococcus faecium
  2. nosocomial pnemonia causes by MRSA
  3. skin infections caused by MRSA
42
Q

T or F: To reduce the development of drug-resistant bacteria and maintain the effectiveness of linezolid, it should be used only to treat/prevent infections that are proven or strongly suspected to be caused by multiple drug-resistant Gram-(+) bacteria, or when patients are allergic to otherwise effective alternatives.

A

T

43
Q

linezolid resistance is due to ?

A

G to U substitution in PTC of 23S rRNA at position 2576

44
Q

T or F: linezolid-induced neuropathy was reported amongst pts receiving linezolid for more than 12 months

A

F (6 months)

45
Q

tongue discoloration and thrush are SE of which drug?

a. quinupristin
b. linezolid
c. telavancin
d. vancomycin

A

b. linezolid

46
Q

most freq SE of linezolid (3 of them)

A

N/V/D

47
Q

linezolid is metabolized via _____ _____ _____

A

morpholine ring oxidation

48
Q

how many major metabolites are there for linezolid?

A

2

49
Q

T or F: linezolid is a MAO inhibitor

A

T

50
Q

which of the following statements is FALSE about Tedizolid Phosphate?

a. Tedizolid phosphate is a second-gen oxazolidinone used for tx of acute bacterial skin and skin structure infections
b. It is less potent than linezolid vs MRSA
c. Same MOA as linezolid
d. Oral or IV
e. Prodrug
f. Don’t consume high tyramine diet when taking

A

b. It is less potent than linezolid vs MRSA (more)

PHRM 865 Therapeutics (8 decks)

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