all the antibiotics (kill me pls)

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185 Terms

1
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what are the macrolides

erythromycin, clarithromycin, azithromycin

2
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route of erythro

po and iv

3
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route of clarithro

po

4
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route of azithro

iv and po

5
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macrolides moa

bind to 50s ribosomal subunit, inhibiting protein synthesis via blocking of transpeptidation/translocation reactions

6
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are macrolides bacteiostatic or bacteriocidal

static

7
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most common macrolide resistance mechanisms

reduced permeability or active efflux. and modificstion of the ribosomal binding site by a macrolide-inducible or constitutive methylase

8
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are macrolides time or conc. dependant and why

time and idk why because they have PAEs but apparently azithro is conc

9
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are macrolides absorbed well orally

no

10
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which macrolide must be taken on an empty stomach

erythromycin base,PCE, or sterate

11
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macrolide ADRs

stomach discomfort (erythromycin worst), taste disturbances (clarithromycin), QT prolongation, drug int

12
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which macrolide has worst coverage

erythro

13
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coverage of macrolides

very poor gram +

better gram - for resp pathogens (h flu except erythro, all cover m cattarrhalis)

chlamidophilia

azithro covers salmonella shigella

14
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what is azithro DOC for

chlamydia trachomatis

15
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what are the tetracyclines

doxy,mino,tetra

16
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tetracyclines route

all po

17
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tetracyclines moa

bind to 30s ribosomal subunit, inhibiting protein synthesis

18
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most common mechanism of bacterial resistance for tetracyclines

decreased intracellular accumulation due to efflux by active transport protein pump

19
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are tetracyclines bacteriostatic or cidal

static

20
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are tetracyclines time or conc dependant

time (but they have PAEs)

21
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which tetracyclines are absorbed well orally

all except tetra

22
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which tetracyclines should be taken with food

mino,doxy - avoid milk

23
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which tetra should be taken on empty stomach

tetra

24
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tetracycline ADRs

GI upset, esophageal ulceration with doxy, photosensitivity, discolored baby teeth, vestibular side effects, bind to divalent cations (AVOID W MILK), least likely to cause c diff

25
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tetracycline coverage

MSSA, MRSA (except tetra), h flu/mcat, peptostrep, chlamydophilia and m pneumoniae

26
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what is doxy DOC in

chlamidophilia and m pneumoniae (walking pneumonia), chlamydia

27
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what are all tetracyclines DOC in

M pneumoniae

28
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what are the quinolones

ciprofloxacin, norfloxacin, levofloxacin, moxifloxacin

29
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cipro route

IV and PO

30
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norfloxacin route

po

31
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levo route

IV and PO

32
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moxi route

IV and PO

33
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what coverage do flouroquinolones widely lack

gram +

34
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flouroquinolones moa

block bacterial DNA synthesis by inhibiting bacterial topoisomerase II (DNA gyrase) and topoisomerase IV

35
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which quinolone is least likely to get resistance

moxifloxacin

36
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what leads to moxifloxacin resistance

overuse and inapropriate use of cipro and levo

37
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are quinolones bacteriocidal or static

cidal

38
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are quinolones conc or time dependant

conc

39
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which quinolone does not require renal adjustment

moxi

40
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most common ADR with quinolones

GI upset

41
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quinolones other adrs

qt prolongation, photosensitivity, binds to divalent cations, affects sugars, cns toxicity, arthropathy, tendinopathy, risk of aortic rupture

42
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quinolone coverage

strep and staph (NOT CIPRO), all easy to kill gram - except n meningitidis, all SPACE except actinobacter and moxi has no pseudomonas, chlamidophilia and m pneumonia

43
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what is cipro DOC in

shigella, pseudomonas

44
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what is levo DOC in

h flu, shigella, pseudomonas, chlamidophilia, chlamydia trachomatis

45
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what is moxi DOC in

h flu, chlamophilia,

46
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which quinolones include pseudomonas

cipro,levo

47
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which quinolone(s) (possibly) treat bfrag

moxi

48
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what are the aminoglycosides

gentamycin,tobramycin,amikacin

49
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route of aminoglycosides

IV

50
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aminoglycosides MOA

binds to 30s subunit ribosomal proteins and results in defective cell membrane

51
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are aminoglycosides bactericidal or static

cidal

52
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is aminoglycoside killing time or conc. dependant

concentration

53
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how long is aminoglycosides post antibiotic effect

6 hrs

54
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aminoglycoside ADR

nephrotoxicity (see less now due to od dosing), ototoxicity, neuromuscular blockade

55
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what type of coverage do aminoglycosides have

gram -

56
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when do aminoglycosides have gram + coverage

synergistically (ex: gentamycin + vancomycin)

57
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aminoglycosides bacteria coverage

easy to kill g-:e coli, shigella, salmonella, kleibsella, proteus

most hard to kill g- (except acinetobacter)

58
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vancomycin route

IV and PO

59
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vancomycin moa

inhibits cell wall synthesis by binding to the D-Ala-D-Ala terminus of nascent peptidoglycan pentapeptide. this inhibits transglcosylase, preventing further elongation of peptidoglycan and cross linking. peptidoglycan is weakened and the cell becomes susceptible to lysis and cell membrane is damaged

60
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is vancomycin killing time or conc dependant

time

61
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what route of vancomycin is used to treat c diff

po

62
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is vancomycin bactericidal or static

cidal

63
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vancomycin resistance mechanisms

due to synthesis of unusually thickened walls (more peptidoglycan layers), the vancomycin binds to the extra layers and becomes sequestered within the cell wall and is unable to reach site of action. (VRE, VISA)

due to modification of the D-Ala-D-Ala binding site of the peptidoglycan building block in which the terminal D-Ala is replaced by D-lactate, resulting in loss of a critical hydrogen bond that facilitates high affinity binding of vancomycin to its target (VRSA)

64
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what type of coverage does vancomycin have

gram + only basically

65
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what is vancomycin DOC for

viridians strep, MSSA, C diff (PO), MRSA, enterococcus

66
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when should vancomycin be reserved for

when other antibiotics cannot be used due to ADR/allergies, or when bacteria is resistant to other antibiotics

67
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vancomycin ADRs

infusion reactions, ototoxicity (uncommon but can occur with consistently high peaks), nephrotoxicity (uncommon)

68
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clindamycin route

PO and IV

69
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clindamycin moa

binds to 50s ribosomal subunit, inhibiting protein synthesis

70
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is clindamycin bactericidal or static

static

71
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clindamycin resistance mechanisms

mutation of the ribosomal receptor site, modification of the receptor by a constitutively expressed methylase, enzymatic inactivation of clindamycin

72
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clindamycin coverage

gram + only (strep, mssa, l mono, peptostrep)

73
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clindamycin ADR

diarrhea- most likely to cause C diff

74
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trimethoprim and sulfamethoxazole route

IV and PO

75
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TMP-SMX moa

sulfa- inhibits bacterial synthesis of dihydrofolic acid by compeititon with para-aminobenzoic acid

tmp- blocks production of tetrahydrofolic acid from dihydrofolic acid by reversibly inhibiting the required enzyme, dihydrofolate reductase, bacterial dihydrofolic acid reductase

76
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is TMP-SMX bactericidal or static

cidal together (static on own)

77
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TMP-SMX general coverage type (gram +,-,etc)

variety of gram +, gram - and other miscellaneous

78
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TMP-SMX ADR

NVD, skin rashes (SJS and TEN), photosensitivity, rash, pruritism bone marrow toxicity, increased serum creatinine, increased K, decreased Na and possible crystalluria, possible teratogenicity and increased risk for kernicterus (avoid in third trimester)

79
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nitrofurantoin MOA

drug gets reduced by bacterial flavoproteins to reactive intermediates, which inactivate or alter bacterial ribosomal proteins and other macromolecules, which causes inhibition of vital biochemical processes of aerobic energy metabolism and the synthesis of DNA, RNA, cell wall, protein

80
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where are therapeutic concentrations of nitrofurantoin achieved

urine only

81
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is nitrofurantoin bactericidal or static

cidal

82
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nitrofurantoin coverage type

some gram + and -

83
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what are nitrofurantoin exclusively used for

UTI

84
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ADR of nitrofurantoin

loss of appetite, nausea, vomiting, darkens urine, GI upset, nausea, headache, SJS/TEN (rare), hepatic reactions (rare), neuropathy/pulmonary fibrosis/hepatic fibrosis (long term use), increased risk of hemolysis in those with G6PD deficiency and in the third trimester/delivery with newborn

85
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fosfomycin MOA

inactivates enolpyruvyl transferase, ultimately inhibits bacterial cell wall synthesis. also decreases adherence of bacteria to epithelial cells of the urinary tract

86
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fosfomycin general coverage type

some gram + and some gram -

87
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fosfomycin ADRs

GI upset, diarrhea, headache, hypokalemia

88
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bacteria covered by TMP-SMX

89
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nitrofurantoin bacteria coverage

e coli and klebsiella, s saphrocytes

90
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metronidazole moa

passive diffusion into cytoplasm of anaerobic bacteria where transport proteins such as ferredoxin transfer electrons to the nitro group of metronidazole forming a nitroso free radical, creating a concentration gradient for intracellular transport of metronidazole where the free radical of metronidazole interacts with intracellular DNA resulting in inhibition of DNA synthesis and degradation and ultimately bacterial death

91
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what types of organisms is metronidazole used for

anaerobic, parasitic

92
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metronidazole ADRs

disulfiram like reactions when taken with alcohol (nausea, vomiting, ab cramps, headache), GI upsetm metallic taste, headache, vaginitis, peripheral/optic neuropathy (long term use), neurotoxicity (rare)

93
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moa of beta lactams

bind to penicillin binding proteins (PBP) which cause the peptidoglycan barrier to not form properly, causing cell lysis

94
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most common mechanisms of resistance to beta lactams

enzymatic destruction by beta lactamases and altered PBP binding sites

95
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are beta lactams bacteriocidal or static

cidal

96
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what type of killing do beta lactams have (____ dependant)

time

97
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most common ADR with beta lactams

hypersensitivity reactions

98
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other adrs of beta lactams

hematologic ADRs at high dose/long durations, neurological events at high doses, C diff

99
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what type of rash with penicillin is NOT indicative of a true IgE mediated allergy

delayed rashes after first few doses or days and no itchiness or hives

100
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if someone has non urticaria rash with penicillin can you give beta lactams

when risk of true allergy is low, can use cephalosporin with a dissimilar side chain