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CMOD > Sweatman Antmicrobial Drugs > Flashcards

Sweatman Antmicrobial Drugs Flashcards

1
Q

4 MOA’s of antimicrobial agents

A
  1. inhibition of cell wall
  2. inhibition of protein synthesis
  3. inhibition of folic acid biosynthetic pathways
  4. Inhibition of DNA/RNA synthesis
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2
Q

Ampicillin: DRUG CLASS

A

penicillin (beta lactam)

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3
Q

Aztreonam: DRUG CLASS

A

Penicillin (monobactam)

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4
Q

penicillin G: DRUG CLASS

A

Penicillin (beta lactam)

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5
Q

Piperacillin

A

penicillin (beta lactam)

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6
Q

Imipenem

A

penicillin (Carbapenem) also a beta lactam

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7
Q

Amoxicillin

A

penicillin

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8
Q

Clavulanic acid

A

penicillin (beta lactamase inhibitor)

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9
Q

cilastatin

A

penicillin (renal dihydropeptidase inhibitor)

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10
Q

Sulbactam

A

penicillin (beta lactamase inhibitor)

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11
Q

Tazobactam

A

penicillin (beta lactamase inhibitor)

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12
Q

Methicillin

A

penicillin

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13
Q

Nafcillin

A

penicillin

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14
Q

oxacillin

A

penicillin

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15
Q

penicllin V

A

penicillin

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16
Q

other inhibitors of cell wall synthesis

A 
ceftriaxone (IV; 3rd generation)
cephalexin (oral; 1st generation)
Vancomycin
Cefazolin (IV)
Cefepime (IV)
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17
Q

penicillins, carbapenems, and cephalosporins belong to a class of antibiotics known as….

A

Beta-lactams

4 membered ring where a N is adjacent to carboxy C–> all bind PBP’s

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18
Q

Narrow Spectrum Penicillins and their MOA

A

Oxacillin, Nafcillin
*larger molecule on penicillin side chain confers steric hindrance–>confers resistance to beta lactamase–> but also restricts their spectrum of activity (cannot conform to as many sterioisomers)

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19
Q

Aminopenicillins and their MOA’s

A

Ampicillin, Amoxicillin
*added NH2 group makes molecule more hydrophillic–>more able to cross LPS barrier and thus increased efficacy against gram-nagative bacteria

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20
Q

Broad-Spectrum Penicillins

A

Piperacillin

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21
Q

Prototypical Penicillins

A

Penicillin G and Penicillin V

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22
Q

MOA for beta lactam antibiotics

A
  1. binding to penicillin-binging proteins (transpeptidases)

2. destruction of cell wall

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23
Q

Action of transpeptidases that is disrupted by beta-lactam antibiotics

A

Cross-linking of peptidoglycan molecules in bacterial cell walls–> lack of cross-links makes them weak and the cell will lyse

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24
Q

Type of bacteria susceptible to beta lactam activity

A

Gram Positive (relies extensively on a thick, highly cross-linked cell wall)

gram negative bacteria have a LPS layer which protects the thing peptidoglycan from beta-lactam activity

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25
Q

Beta Lactamase inhibitors

A
  1. clavulanic acid (added to amoxicillin)
  2. tazobactam (added to piperacillin)
  3. Sulbactam
    * not inherently toxic to bacteria–>do not contain a beta lactam–>bind to beta lactamase and increase the duration of activity of beta lactam antibiotics
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26
Q

contains a thiazolidine ring

A

penicillins and cephalosporins

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27
Q

Monobactam with a sulfonic acid attached to beta lactam ring

A

aztreonam (bactericidal–>binds transpeptidases inside the cell wall)

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28
Q

major difference between carbapenem and other penicillins

A

carbon atom in 5 membered ring as opposed to sulfer atom

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29
Q

Why does Imipenem need cilastatin

A

in the kidneys–> cilastin inhibits an enzyme that breaks down the drug, this increases imipenem activity and decreases nephrotoxicity

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30
Q

D.O.C for Staph. Aureus and Staph epi

*Gram-positive cocci

A

Penicillinase resistant penicllins

methicillin, nafcillin, oxacillin,

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31
Q

DOC for Strep (GROUPS A,B,C,G) and S. bovis

*(Gram-Positive cocci)

A

Pen G, Pen V, Ampicillin

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32
Q

DOC for Clostridium

(*bacilli)

A

Pen G

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33
Q

DOC for E. faecalis UTI

* Gram-Positive cocci

A

ampicillin and amoxicillin

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34
Q

DOC for Strep. pneumonia

*gram-positice cocci

A

Pen G, Pen V, Ampicillin

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35
Q

DOC for E. coli

*gram-negative bacilli

A

ampicillin, (*ampicillin+sulbactam), (Amoxicillin + Clavulanate)

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36
Q

DOC for P. Aeurginosa

gram-negative bacilli

A

piperacilli n/ tazobacta m

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37
Q

Unique features of cephalosporins

A
  1. more acid stable than penicillins
  2. possess 6 membered ring attached to a beta lactam ring
  3. 4 generations (gram positive activity is lost and gram negative activity is gain with each generation)
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38
Q

List the Cephalosporins

A

Cefazolin–>1st
Cephalexin–>1st
Ceftriaxone–>3rd
Cefepime–>3rd

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39
Q

Vancomycin MOA

A

forms H+ bonds with the D-ala D-ala moeities on the NAM/NAG peptides–>prevents long NAM/NAG polymers from forming–>also disrupts cross-linking between those polymers that do form–>cell wall weakens–> bacterium lyses

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40
Q

Vancomycin is a ( ) that interupts ( ) activity during cell wall formation.

A
  1. glycopeptide

2. transglycosylase

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41
Q

Solubility of Vanc

A

VERY POORLY SOLUBLE

  • if infection is limited to GI tract–>orally because ti would not need to be absorbed to have an affect
  • if ANYWHERESE ELSE–> IV
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42
Q

Glycopeptide antibiotics are only effective against _______

A

gram-positive bacteria

gram-negatives have LPS layers that protects their peptidoglycan wall from being disrupted

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43
Q

Aminoglycosides

A 
GENTAMICIN
Amikacin
neomycin
straptamycin
tobramycin
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44
Q

lincosamides

A

clindamycin

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45
Q

macrolides

A 
AZITHROMYCIN
CLARITHROMYCIN
ERYTHROMYCIN
erythromycin
telithryomycin
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46
Q

oxazolidinones

A

LINEZOLID

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47
Q

streptogramins

A

quinipristin/dafropristin

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48
Q

tetracyclines

A

DOXYCYLINE
TIGECYCLINE
minocycline
tetracycline

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49
Q

(OTHERS) monoxycarbolic acid

A

mupriocin

50
Q

MOA for aminoglycosides

A
  1. Irreversibly bind 30s subunit
    low concentrations–Cause misreading of mRNA
    –>high conecntrations– halt protein synthesis

2.bore giant f’ing holes in the outer cell membrane
(leads to leakage of intracellular materials and increase Ab uptake)
*holes are more detrimental

51
Q

classes that inhibit cell walls

A

Penicillins, Cephalosporins & Vancomycin

52
Q

beta lactams MOA

A

disrupt transpeptidase (PBP’s), destruction of cell wall

53
Q

Beta Lactams are most potent inhibitors of which type of bacteria and why?

A 
Gram positive (thick peptidoglycan layer)
*gram negative bacteria have the LPS layer that protects the peptidoglycan layer from beta lactam activity
54
Q

Penicillin + aminoglycoside

A

Combination of cell wall and protein synthesis inhibitor

55
Q

Sulfamethexazole + trimethoprim

A

act in sequential steps in the folic acid biosynthesis pathway

56
Q

amoxicillin + clavulanic acid

A

(augmentin) beta lactam + beta lactamase inhibitor

57
Q

prokaryote ribosome

A

70S ribisomes
Small 30S subunit
Large 50S (23S and 5S and 34 other proteins)

58
Q

Aminoglycosides are bactericidal because?

A

The action on the outer bacterial membrane, in addition to its protein synthesis inhibition, is thought to be the reason that aminoglycosides are bactericidal.

59
Q

Aminoglycosides work well on which type of bacteria

A

Gram-negative

60
Q

Azithromycin (macrolide) MOA

A

Binds the 23s subunit of the 50S RSU (bacteriostatic)

61
Q

Clindamycin (lincosamide) MOA

A

binds the 23s of 50s RSU (bacteriostatic)

62
Q

Tetracycline MOA

A

bind to 16s subunit

63
Q

streptogramins MOA

A

quinipristin and dalfopristin bind the 50s (large) RSU (these two have a synergistic effect)

64
Q

mupriricin MOA

A

binding and inhibition of Isoleucyl transfer rna sythetase–> works on MRSA

65
Q

Antimicrobials

A

Antibiotics
antifungals
antiparasitics
NOT antivirals–> they are not technically alive

66
Q

MBC

A

minimum bacteriostatic concentration

*the lowest concentration of an antibacterial agent required to kill a particular bacterium

67
Q

MIC

A

minimum inhibitory concentration
*n microbiology, minimum inhibitory concentration (MIC) is the lowest concentration of an antimicrobial that will inhibit the visible growth of a microorganism after overnight incubation

68
Q

Therapeutic index

A

The therapeutic index (also known as therapeutic ratio) is a comparison of the amount of a therapeutic agent that causes the therapeutic effect to the amount that causes death (in animal studies) or toxicity (in human studies)

69
Q

Penicillin + aminoglycoside synergistic MOA

A

combination of cell wall and protein synthesis inhibition

70
Q

Sulfamethexazole + Trimethoprim (septra or bactrim) synergistic MOA

A

sulfa inhibits incorporation of PABA into folic acid
trimethoprim inhibits reduction of DHF to THF
*sequential steps

71
Q

monobactam

A

aztreonam

72
Q

carbapenem

A

impenem

73
Q

Beta Lactams…name them and their MOA

A

Penicillins, Carbapenems, Cephalosporins

  1. bind to transpeptidases and inhibit cell wall cross-linking
  2. destruction of bacterial cell wall
74
Q

end result of beta lactam activity

A

cell lysis

75
Q

why are Gram Negative bacteria more resistant to beta lactams

A

LPS layer protects the thin (2 layered) peptidoglycan wall–>BL’s cannot reach the thang

76
Q

Do beta lactamase inhibitors contain a beta lactam

A

yes–>but are not toxic to the cell

*they merely bind to beta lactamase

77
Q

BLI added to amoxicillin

A

clavulanic acid (augmentin)

78
Q

BLI added to piperacillin

A

tazobactam (zosyn)

79
Q

Narrow spectrum penicillin MOA’s

A

bulk adduct on penicllin side chain making them

  1. resistant to Beta lactamase cleavage
  2. unable to contort into may sterioisomers–> inhibiting their range of activity
80
Q

amino penicillins are best used against

A

gram negative bacteria

81
Q

Broad spectrum penicillins are modifications of…

A

amino penicillins

*inreases the range of bacteria that are susceptible to them

82
Q

Are Broad Range Penicillins sensitve to beta lactamase cleavage

A

yes–> frequently administered with beta lactamase inhibitor “pip/tazo”

83
Q

where are PBP’s located

A

inside the bacterial cell wall

84
Q

3 reasons Imipenem has a broader range spectrum of activity than other beta lactams

A

5 membered ring contains a carbon atom rather than sulfer
1. more efficient penetration thru cell wall
2 resistance to bacterial enzymes
3. affinity for all PBP’s

85
Q

renal dehydropeptidase inhibitor

A

cilistatin

*prevents renal metabolism of Imipenem, increasing the urinary concentration and minimizing nephrotoxicity o the drug

86
Q

Major advantage of cephalosporins regarding administration

A

acid stable so can be given WITHOUT FOOD

87
Q

IST GENERATION CEPHALOSPORINS ARE USEFUL FOR TREATING

A

SKIN INFECTION

CEFAZOLIN AND CEPHALEXIN

88
Q

2ND GENERATION CEPHALOSPORINS ARE USEFUL FOR TREATING?

A

GRAN NEGATIVE BACTEROIDES

89
Q

CEFTRIAXONE IS USEFUL IN TREATING

A

STD’S AND PEDIATRIC MENINGITIS

90
Q

CEFEPIME IS USEFUL in treating

A

pseudomonal infection

91
Q

Solubility of aminoglycosides

A

insoluble–> they are very polar and therefore penetration is poor

92
Q

Aminoglycosides are toxic in the

A

kidneys

93
Q

small ribosomal subunit

A

30 s

94
Q

large RSU

A

50 S

95
Q

50 S RSU is composed of

A

23 S 5 S 34 other proteins

96
Q

Aminoglycosides will not work on

A

anaerobes

*aminoglycosides require energy for uptake–> anaerobic bacteria lack much energy

97
Q

aminoglycosides are bacteriostatic/cidal

A

-cidal
*holes + protein inhibition
other protein synthesis inhibitors are mainly bacteriostatic

98
Q

macrolide nomenclature

A

-Thromycin

99
Q

Macrolide MOA

A

bind 23s of 50s–>BIND to P site inhibit peptidyl transferase–>this blocks the transfer of the new amino acid onto the growing chain
*bacteriostatic except for in high concentrations

100
Q

Macrolides are phagocytosed by?

A

macrophages at the site of infection

101
Q

MOA for lincosamides

A

23s/50s–>promote premature dissociation of peptidyl transferase

102
Q

Clinda is most useful in

A

toxin producing infections

103
Q

Tetracylin MOA

A

bind to 16 S of 30s RSU–> and inhibit amino-acyl tRNA binding

104
Q

tetracylcins static/cidal

A

cidal

they completely stop protein synthesis–>whereas other protein synthesis inhibitor stop initiation

105
Q

what are the streptogramins and how are they synergistic

BASTERICIDAL

A

Quinipristin bind to P site on 50sRSU, inhibits elongation, and promotes early termination of protein synthesis

Dalfopristin binds at a spot nearby and causes a conformation change in the 50sRSU which makes the RSU bind more tightly to quinipristin at the P site

106
Q

bactericidal protein synthesis inhibitors

A

aminoglycosides (for 2 reasons)
streptogramins (synergitic effect)
tetracycline (prevents trna from ever binding to A site
mupirocin

107
Q

Mupriocin inhibits…

A

isoleucyl tRNA synthetase

108
Q

chloramphenicol should not be given with?

A

macrolide or lincosamide Ab’s–> binds at B site as well

109
Q

floruoquinolones

A

cipro

levofloxacin

110
Q

Nitroimdazoles

A

metronidazole

111
Q

sulfonamides

A

cotromoxazole

sulfamethexazole

112
Q

rifamycins

A

rifampin

rifamixin

113
Q

DHFR inhibitors

A

cotrimoxazole

trimetoprim

114
Q

Flouroquinolones MOA

bactericidal

A

bind to and inhibit Gyrase (gram negative) and TOPO IV (gram positive)

*after the cutting step–>there is no re-anealing

115
Q

rifampin MOA

A

binds RNA polymerase–> prevents INITIATION…not ELONGATION

116
Q

RIFAMPIN is useful in treating

HIGHLY lipophillic

A 
Mycobacterium
Biofilms
Bacterial menengitis (cns penetration is high)
intracellular bacteria
abcesses
117
Q

METRONIDAZOLE IS MOST USEFUL IN TREATING

A

anaerobic bacteria–> it acts as the terminal electron acceptor (aerobic bacteria use O2 for this and metronidazole is never converted from its prodrug state

118
Q

cotrimoxazole is made up of

A

Sulfa and trimethoprim

119
Q

sulfa MOA

A

inhibits incorporation of PABA into folic acid

120
Q

trimethoprim MOA

A

inhibits DHF being reduced into THF

121
Q

in vivo concentration of sulfa to trimethoprim

A

20:1

CMOD (19 decks)

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