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Pharm Exam 4 > 48/49: Antibiotics II > Flashcards

48/49: Antibiotics II Flashcards

1
Q

peptidoglycan is composed of…

A

chains of repeating monomers of the disacchride subunits: NAM-NAG-pentapeptide

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2
Q

enzymes join monomers together to form NAM-NAG chains

A

transglycosylase

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3
Q

enzymes bind the NAM-NAG chains into a rigid structure by adding pentaglycine crosslinks between pentapeptide residues on adjacent chains

A

transpeptidase

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4
Q

what are peniclinin-binding proteins?

A

peptidoglycan is maintained by the enzymes that create the bonds between NAM-NAG peptidoglycan monomers and between NAM-NAG chains in the layer

selective b-lactam antibiotics bind selectively to different PBPs and this contributes to the sensitivity of bacterial strains to individual penicillins and cephalosporin antibacterial agents

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5
Q

b-lactam compounds include (4)

A

penicillins
cephalosporins
monobactams
carbapenems

these agents are bactericidial

susceptible to b-lactamase

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6
Q

MOA penicillins

A

bind to and inhibit PBP enzymes

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7
Q

key adverse effects of penicillins

A

hypersensitivity 5-7%

rash, hives, itching, respiration difficulty, anaphylaxis

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8
Q 
ampicillin
amoxicillin
piperacillin
ticarillin
azlocillin
A

all “broader” penicillins

penicillin G and V
methicillin
nafcillin
oxacillin 
= narrower spectrum
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9
Q

which penicillins are b-lactamase resistant?

A

the group of vey narrow spectrum

methicillin
nafcillin
oxacillin

all the rest are sensitive

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10
Q

______ used in combination with penicillins to increase effectiveness

A

clavulanic acid (b-lactamase inhibitor)

amoxicillin & clavulanic acid = augmentin

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11
Q

advantages of cephalosporins over penicillins

A
  • more resistant to b-lactamase
  • less % adverse effects

generally used if penicillins are not well tolerate

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12
Q

MOA cephalosporins

A

bind to and inhibit the PBPs

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13
Q

key adverse effect cephalosporins

A

hypersensitivity 2%

rash, hives, itching, respiration difficulty, anapylaxis

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14
Q

4th generation cephalosporins have a more _____ spectrum than 1st gen

A

broad

broader spectrum with increasing generation

1st g: +
2nd g: + and some -
3rd g: + and -
4th g: + and -

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15
Q

which cephalosporins can enter the CNS?

A

3rd and 4th gen

cefdinir
cfixime
ceftriaxone

cefepime

and 2g: cefuroxime

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16
Q

which cephalosporin gen is b-lactamase resistant?

A

4th gen

cefepime

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17
Q

only mono bactam agent

A

aztreonam

only gram -
penetrates CSF
b-lactamase resistant

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18
Q

MOA aztreonam

A

bind to and inhibit PBPs

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19
Q

key adverse reaction monobactams

A

hypersensitivity

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20
Q

are carbapenems resistant to b-lactamase?

A

yes but susceptible to similar enzyme carbamenemase

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21
Q

______ inactivated in kidney so it is administered with cilastatin to prevent this inactivation

A

imipenem

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22
Q

MOA carbapenems

A

bind to and inhibit the PBPs

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23
Q

key adverse effects carbapenems

A

GI

nausea, vomiting, & diarrhea

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24
Q

MOA vancomycin

A

prevents elongation of the peptidoglycan cell wall structure by binding to pentapeptide and acting as steric inhibitor

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25
Q

key adverse effect vancomycin

A

flushing “red neck” or “red man
syndrome”

also ototoxicity

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26
Q

MOA bacitracin

A

blocks incorporation of aa and nucleic acids into cell wall

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27
Q

common use fosfomycin

A

uncomplicated UTI

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28
Q

MOA fosfomycin

A

blocks an early step in cell wall synthesis by preventing syntheiss of UDP-N-acetylmuramic acid

29
Q

prtn synthesis inhibitors include…

A

aminoglycoside, macrolides, tetracycline and a few other specific compounds

30
Q

what are the steps of prtn synthesis which can be targeted by antibiotics?

A

step1: charged tRNA binds to A site
step2: peptidyl tRNA, peptide bond formation between grwoing aa chain and new aa in A site
step3: the newly uncharged tRNA exits
step4: the now-longer aa chain translocates to P site

31
Q

why target the 50S and 30S subunits?

A

unique to prokaryotes

32
Q

what ___mycins are not aminoglycosides?

A

azithromycin
clarithromycin and eryhtromycin are macrolides

fosfomycin is a phosphoenolpyruvate

daptomycin is a lipopetide

clindamycin is other

33
Q

name the aminoglycosides

A 
amikacin
gentamicin
kanamycin
neomycin
streptomycin
tobramycin
34
Q

MOA aminoglycosides

A

bind to 30S and block formation of initiation complex (step 1)

35
Q

key adverse effects aminoglycosides

A

nephrotocicity (6-7% renal tubular necrosis)

ototoxicity (2%) dizziness, ringing, fullness

36
Q

MOA macrolides

A

binds to 50S and impairs the translocation to the P site (step 4)

37
Q

name the macrolides

A

azithromycin
clarithromycin
erythromycin

38
Q

key adverse effect macrolides

A

GI stomach cramps, nausea, vomiting, diarrhea (b/c motilin receptor agonist)

39
Q

MOA tetracyclines

A

binds to 30S subunit of ribosome and prevents binding of new tRNA to A site (step 1)

40
Q

key adverse effect of tetracyclines

A

nutrient interactions : binds calcium which results in growth of calcified tissue

disrupts normal flora

photosensitivity

41
Q

MOA clindamycin

A

bind to 50S subunit of the ribosome and prevents the formation of initial complexes (step 1) and translocation to P site similar to macrolides

42
Q

key adverse effects clindamycin

A

GI: nausea, vomiting, diarrhea

**c. diff infection

43
Q

MOA chloarmphenicol

A

binds to 50S subunit of the ribosome and prevents transpeptidation or peptidyl bond formation (step 2)

44
Q

key adveres effects chloramphenicol

A

gray baby syndrome: infants lack glucuronic acid conjugation (gray color, scock, comiting, cascualr collapse)

blood: suppression of red cell production

45
Q

MOA linezolid

A

inhibits prtn synthesis by binding to the P site of the 50S ribosome and inhibiting the formation of the ribosomal-mettRNAcomplex (very first step 1)

46
Q

key adverse effect linezolid

A

blood myelosuppression

47
Q

MOA sulfonamides

A

compete with PABA for the enzyme diydropteroate synthase and block dihydrofolic acid synthesis and thus DNA synthesis

48
Q

key adverse effects sulfonamides

A

skin: hypersensitivity, photosensitivity, steven-johnson

49
Q

common use trimethoprims

A

UTIs

50
Q

MOA trimethoprims

A

inhibitor of bacterial dihydrofolate reductase resulting in impaired DNA synthesis

51
Q

key adverse effect trimethoprims

A

blood: bone marrow suppresion, megaloblastic anemia, leukopenia, granulocytopenia

52
Q

TMP-SMX =

A

trimethoprim and sulfamethoxazole

synergistic effects

commonly used to treat UTI and prostatitis

53
Q

what drug discussed is effective against anthraz?

A

fluoroquinolones

54
Q

MOA fluoroquinolones

A

disrupt the winding of DNA and the separation of DNA strands during transcription and replication. These agents specifically inhibit the enzymes topoII and topoIV

55
Q

key adverse effects fluoroquinolone

A

GI
Drug-nutrient: binds divalent cations and prevents absorption
cardio - QT prolongation

56
Q

group 1 –> 3 of fluoroquinolones

A

1 least active

2 both neg and pos, mostly neg

3 best against pos

57
Q

what organisms can metronidazole target?

A

anaerobic bacteria and protozoa

58
Q

MOA metronidazole

A

prodrug

undergoes chemical rxn in organsims and disrupts DNA

59
Q

key adverse effects metronidazole

A
  • GI

- metabolism - no alcohol!

60
Q

MOA daptomycin

A

binds to membrane and causes depolarization of membrane - bactericidial

calcium dependent insertion in membrane

61
Q

key adverse effects daptomycin

A

musculoskeletal - myopathy, rhabdomyolysis

62
Q

MOA polymyxinB

A

bind to phospholipids in cell membrane and disrupt structure “punchholes” in gram neg only

63
Q

Mechanisms of resistance for penicillins and cephalosporins

A
  1. expresion of b-lactamase
  2. alteration in PBP binding to drug
  3. alteration in porin function
64
Q

mechanisms of resistance for aminoglycosides

A
  1. expression of enzymes that alter chemical structure of drug
65
Q

mechanisms of resistance for macrolides

A
  1. transport of drug out of cell (drug efflux)

2. alterations of drug binding to 50S ribosomal subunit

66
Q

mechanisms of resistance for tetracyclines

A
  1. transport of drug out of cell (drug efflux)
67
Q

mechanisms of resistance for sulfonamides

A
  1. less sensitive drug target
  2. increased synthesis of PABA
  3. scavenge or use other sources of folic acid
68
Q

mechanisms of resistance for fluoroquinolones

A
  1. less sensitive drug target

2. drug efflux

69
Q

mechanisms of resistance for chloramphenicol

A
  1. expression of inactivating enzymes

Pharm Exam 4 (12 decks)

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