Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

FM2 > Protein/ DNA Inhibiting Antibiotics > Flashcards

Protein/ DNA Inhibiting Antibiotics Flashcards

1
Q

Prokaryote ribosomes contain __ and __ subunits

A

30S, 50S

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

List two antibiotic groups that target the 30S ribosomal subunit

A

aminoglycosides

tetracyclines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

List five antibiotic groups that target the 50s ribosomal subunit

A

macrolides
clindamycin
streptogramins
chloramphenicol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

List one antibiotic that targets formation of the 70S initiation complex

A

Linezolid (an oxazolidinone)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

List natural and semisynthetic aminoglycosides

A

Natural: gentamicin, neomycin, streptomycin, tobramycin

Semi-synthetic: amikacin (kanamycin + hyroxy butyric acid)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Describe the spectrum of activity of aminoglycosides

A

Enterobacteriacaea: Escherichia, Klebsiella, Enterobacter, Serratia, Proteus, Staphylococci
Tobramycin and amikacin specifically have activity against Pseudomonas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

List organisms NOT covered by aminoglycosides

A

Streptococci
Enterococci
Anaerobes- lack oxygen dependent active transport into cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How can aminoglycosides be useful in streptococcal or enterococcal infections?

A

Combination with beta lactam- usually gentamicin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

List the two aminoglycosides that are most effective against mycobacteria

A

Streptomycin

Amikacin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Aminoglycosides show ___ dependent killing; prolonged_____ effects; and are best dosed __x per day

A

concentration
postantibiotic/ persistent
high doses 1x daily

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

List mechanisms of resistance against aminoglycosides

A

enhanced efflux
inactivating enzymes (transposable genes on plasmids)
chromosomal mutation- only with streptomycin and TB

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Amikacin has less resistance than other aminoglycosides because it is inactivated by one enzyme, whereas ___ can be inactivated by 8 enzymes

A

Kanamycin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Aminoglycosides show ___ oral absorption, distribution in ECF, CNS penetration

A

Poor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Describe the two major adverse effects of aminoglycosides

A

Nephrotoxicity- reversible because renal tubular cells can regenerate. caused by drug entering from urine side of cell through pinocytosis. saturable kinetics, so less effect with 1x daily dosing

Ototoxicity- irreversible, hair cells are not regenerated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

In order to cause nephrotoxicity, aminoglycosides must first bind to _____ on the brush border of renal tubular cells. this exhibits ____ kinetics

A

Megalin

Saturable

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

List the major clinical uses for aminoglycosides

A

Plague
Tularemia
Complicated UTI with GNRs
Combined with B lactams for Psedomonas, staph, strep, enterococcal infections like endocarditis
Surgical prophylaxis
Mycobacteria (second line, always in combination)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

List two semisynthetic tetracyclines and one glycylcycline

A

Doxycycline, minocycline

tigecycline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What advantages does tigecycline have over semisynthetic tetracyclines?

A

Blocks efflux from cells

Binds better to ribosomes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Describe the spectrum of activity of tetracyclines

A

Gram positives, gram negatives, mycoplasma, chlamydia, rickettsia, spirochetes, malaria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Tetracyclines have poor activity against ____ and ______

A

enterococci

Pseudomonas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Minocycline and tigecycline are better than doxycycline against _____

A

MRSA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Why are tetracyclines bacteriostatic?

A

Binding to 30S is reversible

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Tetracycline killing is __ dependent

A

time

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

List mechanisms of resistance for tetracyclines

A

Drug efflux
Ribosomal protection
extensive cross resistance but does not apply to glycylcyclines like tigecycline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Tetracyclines have ___ oral absorption, tissue distribution, intracellular concentrations

A

good

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

List adverse effects of tetracyclines

A

Discoloration of teeth and bones- do not use in children, pregnant women
GI problems- NVD, take with food
Superinfection- oral and vaginal candidiasis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

List clinical uses of tetracyclines

A 
STIS
Borrelia
Ehrlichia
CAP
Rickettsia
Falciparum malaria 
Anthrax
MRSA
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

How can chloramphenicol be inactivated?

A

acetylation of nitro group

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Chloramphenicol is _______ because of reversible binding

A

bacteriostatic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Describe the spectrum of activity of chloramphenicol

A

Broad spectrum

Poor activity against legionella and pseudomonas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Resistance to chloramphenicol is due to production of ________________ which acetylates the nitro group

A

Chloramphenicol acetyl transferase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Chloramphenicol has ____ oral bioavailability and extensive distribution because of high ____ solubility

A

Excellent

Lipid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

List adverse effects of chloramphenicol

A

Bone marrow suppression (reversible)
Aplastic anemia, rare and non-reversible
Gray syndrome in neonates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Describe the clinical use of chloramphenicol

A

Serious salmonella, typhoid fever in developing countries

in developed countries- bacterial meningitis if penicillin allergy, anaerobic infections in CNS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

List one natural and two semisynthetic macrolides

A

Natural: erythromycin

Semi-synthetic: clarithromycin, azithromycin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Describe the spectrum of activity of macrolides

A

Streptococci, pneumococci
Legionella, Mycoplasma, Chlamydia
Helicobacteria
some atypical mycobacteria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Macrolides have weak activity against hemophilus influenzae because hemophilus has an _________

A

efflux pump

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

List mechanisms of resistance for macrolides

A

Methylation of 23s ribosome RNA- Europe, Erm genes

Enhanced efflux pumps- USA, mef genes

Chromosomal mutation of 50S
Drug inactivation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Erythromycin has modest oral absorption because it is _____ in the GI tract, but azithromycin and clarithromycin are better absorbed because they are more _________

A

ionized

acid stable

40
Q

List adverse effects of the macrolides

A

GI intolerence
Hepatitis in pregnant women
Ototoxicity, reversible

41
Q

Describe clinical use of macrolides

A

respiratory infections (sinusitis, otitis, pneumonia, bronchitis, DOC for CAP)
Strep pharyngitis and cellulitis if penicillin allergy
Atypical mycobacteria esp MAC
Helicobacter pylori, in combination with PPI
Pseudomonas exacerbations in CF (azithromycin)

42
Q

Why is azithromycin effective in Pseudomonas infections in people with CF?

A

Azithromycin is effective in biofilms but has no direct effect on Pseudomonas

43
Q

______ is a lincosamine antibiotic

A

Clindamycin

44
Q

Clindamycin is active against…

A

Staphylococci, streptococci, anaerobes incl bacteroides fragilis
moderate activity against toxoplasma, pneumocystis
poor activity against mycoplasma, chlamydia, legionella

45
Q

Resistance to macrolides and clindamycin suggests presence of ___ genes
Resistance to macrolides but susceptibility to clindamycin suggests presence of ___ genes

A

Erm

Mef

Clindamycin resistance is similar to macrolid resistance but clincamycin is not effluxed

46
Q

Clindamycin has ____ oral bioavailability and extracellular / intracellular distribution

47
Q

List two adverse effects of clindamycin

A

diarrhea

pseudomembranous colitis

48
Q

Describe clinical uses of clindamycin

A

anaerobic infections above the diaphragm
Strep (+ penicillin)
Staph (incl MRSA, better than macrolides)
alternate option for toxoplasmosis and pneumocystis

49
Q

______ was the first oxazolidonone antibiotic; ____ is a newly released oral option.

A

Linezolid

Tedizolid

50
Q

Linezolid binds to the 50S ribosome and inhibits formation of the __

A

70s initiation complex

51
Q

Describe the spectrum of activity of linezolid

A

Broad: staph, MRSA, strep, pneumococci, enterococi

52
Q

Linezolid is considered _______ but it does kill bacteria slowly

A

bacteriostatic

53
Q

Linezolid resistance is seen primarily in ___________ and is very rare but increasing in Staph aureus

A

Enterococcis faecium; resistance due to mutations near binding site of ribosome

54
Q

Linezolid has excellent ____ penetration and very good distribution to the ______ tract

A

CNS

respiratory

55
Q

List adverse effects of linezolid

A

thrombocytopenia and anemia

peripherla neuropathy

56
Q

List clinical uses for linezolid

A

VRE
MRSA
MRSE
CNS effects due to MRSA or MRSE

57
Q

_____ is a _____ antibiotic that is a combination of dalfopristin (A) and quinupristin (B).

A

Synercid

streptogramin

58
Q

When used alone, the streptogramins are ___; when used together they are ______

A

bacteriostatic

bactericidal

59
Q

Streptogramins have good activity against __________ and no activity against _________

A

Staph, strep, enterococcus faecium

no activity against e fecalis

60
Q

List clinical use of streptogramins

A

VRE (e faecium only)
MRSA
not commonly used due to adverse reactions

61
Q

List adverse reactions to streptogramins

A

Phlebitis

myalgias/ arthralgias

62
Q

______ is an antibiotic that binds to proteins involved in protein synthesis and is used in urinary tract infections

A

nitrofuratoin

63
Q

Nitrofurantoin works by ________ producing reduced derivatives that interfere with protein synthesis

A

nitrofuran reductase

64
Q

Resistance to nitrofurantoin is due to ____

A

reduced nitrofuran reductase activity

65
Q

List two adverse effects of nitrofurantoin

A

GI

Pulmonary hypersensitivity

66
Q

Describe the clinical use of nitrofurantoin

A

Treatment and prophylaxis of UTI

not effective in patients with less than 50% of normal renal function- can’t get enough active drug into urine, will be metabolized and removed

67
Q

List five nucleic acid synthesis inhibitors

A 
quinolones
rifampin
metronidazole
trimethoprim
sulfonamides
68
Q

List two quinolones

A

ciprofloxacin

moxifloxacin

69
Q

Fluoroquinolones work by inhibiting ________, enzymes involved in supercoiling of DNA

A

DNA gyrase/ topoisomerase II

Topoisomerase IV

70
Q

Quinolones are ______ and show ____ dependent killing

A

bactericidal

concentration dependent

71
Q

_____ is the only oral drug active against Pseudomonas

A

ciprofloxacin

72
Q

norfloxacin and ciprofloxacin are active against ________

A

aerobic gram negative bacilli

73
Q

Moxifloxacina nd gemifloxacin have increased activity against:

A

Gram positive cocci
atypical respiratory pathogens
mycobacteria

74
Q

List mechanisms of resistance to fluoroquinolones

A

Mutation of DNA gyrase
mutation of topoisomerase
decreased permeability-altered porins
enhanced efflux pumps

75
Q

Describe fluoroquinolone pharmacology

A

Excellent oral bioavailability
Very good serum and tissue concentrations
Norfloxacin, ciprofloxacin and levofloxacin eliminated primarily in the urine
Moxifloxacin and gemifloxacin eliminated primarily by liver

76
Q

List adverse effects of fluoroquinolones

A 
Cartilage damage, achilles tendon rupture
phototoxicity
hepatitis
QTc prolongation 
dizziness
dysglycemias
77
Q

List clinical uses of fluoroquinolones

A

Serious gram - infections including Pseudomonas
Enteric infections
Respiratory infections- CAP, HAP, DOC for legionella
Mycobacterium
UTI esp pyelonephritis
Prostatitis
Anthrax

78
Q

Rifampin works by inhibiting ______________

A

DNA dependent RNA polymerase; acts on beta subunit

79
Q

Rifampin is _______

A

bactericidal

80
Q

List spectrum of activity for rifampin

A

MSSA, MRSA, mycobacteria

81
Q

List spectrum of activity for rifaximin

A

noninvasive E colin in gut, C diff

82
Q

Resistance to rifampin is due to ____ and is very common

A

mutation of beta subunit of RNA polymerase

83
Q

Rifampin has excellent oral bioavailability but ____ does not, so it is used for infections within the bowel

84
Q

List adverse effects of rifampin

A

hepatitis
drug interactions- P450 enzyme inducer
orange discoloration of urine

85
Q

List clinical uses of rifampin

A

Mycobacterial infections, MAC

Staphylococcal infections in combination with beta lactams (active in biofilms)

86
Q

List clinical uses of rifaximin

A

traveler’s diarrhea

relapsing C diff

87
Q

Describe mechanism of action of metronidazole

A

converted to active metabolite by reduction of nitro group, binds to and damages DNA

88
Q

Describe metronidazole spectrum of activity and resistance

A

Activity: Bacteroides fragilis, C diff, entamoeba, giardia, trichomonas vaginalis

Resistance: organisms that lack nitro reductase activity

89
Q

Describe metronidazole pharmacology

A

Good oral bioavailability (very lipid soluble)

Excellent tissue distribution including CSF

Eliminated primarily by the liver

90
Q

Describe adverse effects of metronidazole

A

Peripheral neuritis

vomiting with alcohol

91
Q

Describe clinical use of metronidazole

A

Anaerobic infections below the diaphragm
C diff
Protazoan infections- entamoeba, giardia, trichomonas

92
Q

_______ inhibits dihyrdopteroate reductase and ______ inhibits dihydrofolate reductase

A

Sulfonamides

Trimethoprim

93
Q

Describe spectrum of activity of sulfonamides and trimethoprim

A

Sulfonamides: nocardia, toxoplasma, pneumocystis

Trimethoprim: E coli, Klebsiella, staph, pneumococci, pneumocystis

94
Q

List adverse effects of sulfonamides and trimethoprim

A

sulfonamides: rash, crystals in urine
trimethoprim: folate deficiency

95
Q

List clinical uses of TMP-sulfa

A

UTI, respiratory infections, pneumocystis, typhoid fever, enteric infections, MRSA, nocardia, toxoplasmosis, burns

96
Q

List oral drugs that are active against CA-MRSA

A

Doxycycline (Minocycline)
Clindamycin- particularly for children, less risk of C diff
Linezolid – very expensive
Moxifloxacin- covers less than 50% of strains
Rifampin (never use alone)
TMP/SMZ

FM2 (11 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions