Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

First Aid Microbiology > Antibiotics for micro final > Flashcards

Antibiotics for micro final Flashcards

1
Q

Penicillin G, V

A

Prototype β-lactam antibiotics (penicillinase-sensitive)

  • Penicilling G → IV and IM form
  • Penicillin V → oral
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Penicillin G, V mechanism

A
  1. Bind penicillin-binding proteins (transpeptidases).
  2. Block transpeptidase cross-linking of peptidoglycan in cell wall.
  3. Activate autolytic enzymes.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Penicillin G,V clinical use

A
  1. ​Mostly used for gram-positive organisms
    1. S. pneumoniae
    2. S. pyogenes
    3. Actinomyces
  2. Gram negative cocci
    1. N. meningitidis
  3. Spirochetes
    1. T. pallidum

Bactericidal for gram-positive cocci, gram-positive rods, gram-negative cocci, and spirochetes.

Penicillinase sensitive.

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

Penicillin G, V toxicity

A
  • Hypersensitivity reactions
  • Hemolytic anemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Penicillin G, V resistance

A

Penicillinase in bacteria (a type of β-lactamase) cleaves β-lactam ring.

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

Aminopenicillins

A
  • ​amoxicillin
  • ampicllin

Penicillinase-sensitive penicillins

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

Aminopenicillin mechanism

(and bioavailability)

A
  • Same as penicillin → wider spectrum,
  • Penicillinase sensitive.
  • Also combine with clavulanic acid to protect against destruction by β-lactamase.

(amoxicillin and ampicillin)

Note that amoxicillin has greater oral bioavailability than ampicllin.

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

Aminopenicillin clinical use

A

Exteneded spectrum penicillin

  1. H. influenzae (gram negative)
  2. H. pylori (gram negative, oxidase positive, comma shaped)
  3. E. coli (gram negative rod)
  4. Listeria monocytogenes (gram positive rod)
  5. Proteus mirabilis (gram negative rod)
  6. Salmonella (gram negative rod)
  7. Shigella (gram negative rod)
  8. enterococci (gram positive cocci)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Aminopenicillin toxicity

A
  • hypersensitivity reactions
  • rash
  • pseudomembranous colitis (ie C. dif, a gram positive rod)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Aminopenicillin resistance

A

Penicillinase in bacteria (a type of β-lactamase) cleaves β-lactam ring.

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

Penicillinase-resistant penicillins

A
  1. Dicloxacillin
  2. Nafcillin
  3. Oxacillin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Penicillinase resistant penicillins mechanism

A

(dicloxacillin, nafcillin, oxacillin)

Same as penicillin → narrow spectrum.

Penicillinase resistant because bulky R group blocks access of β-lactamase to β-lactam ring.

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

Penicillinase resistant penicillins clinical use

A

(dicloxacillin, nafcillin, oxacillin)

S. aureus (except MRSA; resistant because of altered penicillin-binding protein target site).

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

Penicillinase resistant penicillins toxicity

A
  • Hypersensitivity reactions
  • interstitial nephritis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Antipseudomonals

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

Antipseudomonal mechanism

A

(piperacillin, ticarcillin)

Same as penicillin. Extended spectrum.

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

Antipseudomonal clinical use

A

(piperacillin, ticarcillin)

Pseudomonas spp. and other gram-negative rods.

Susceptible to penicillinase; use with β-lactamase inhibitors.

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

Antipseudomonal toxicity

A

(piperacillin, ticarcillin)

Hypersensitivity reactions.

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

Beta lactamase inhibitors

A
  1. Clavulanic Acid
  2. Sulbactam
  3. Tazobactam

Often added to penicillin antibiotics to protect the antibiotic from destruction by β-lactamase (penicillinase).

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

Cephalosporins (generations 1-4) mechanism

[and what don’t they cover]

A

β-lactam drugs that inhibit cell wall synthesis but are less susceptible to penicillinases. Bactericidal.

Organisms typically not covered by cephalosporins are LAME:

  • Listeria
  • Atypicals (Chlamydia, Mycoplasma)
  • MRSA
  • Enterococci

Exception: ceftaroline covers MRSA.

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

First generation cephalosporins

A
  1. Cefazolin (IV)
  2. cephalexin (oral)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

First generation cephalosporin clinical use

A

1st generation (cefazolin, cephalexin)—

  1. gram-positive cocci
  2. gram-negative rods
    1. Proteus mirabilis
    2. E. coli
    3. Klebsiella pneumoniae

Cefazolin used prior to surgery to prevent S. aureus wound infections.

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

Second generation cephalosporins

A
  1. cefoxitin (IV)
  2. cefaclor
  3. cefuroxime
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Second generation cephalosporin clinical use

A

2nd generation (cefoxitin, cefaclor, cefuroxime)—

  1. gram-positive cocci
  2. Haemophilus influenzae
  3. Enterobacter aerogenes
  4. Neisseria spp.
  5. Proteus mirabilis
  6. E. coli
  7. Klebsiella pneumoniae
  8. Serratia marcescens
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Third generation cephalosporins
1. ceftriaxone 2. cefotaxime 3. ceftazidime
26
Third generation cephalosporin clinical use
3rd generation (ceftriaxone, cefotaxime, ceftazidime)—serious gram-negative infections resistant to other β-lactams. Ceftriaxone—meningitis, gonorrhea, disseminated Lyme disease (borrelia). Ceftazidime—Pseudomonas
27
Fourth generation cephalosporins
cefepime
28
Fourth generation cephalosporin clinical use
4th generation (cefepime)— gram-negative organisms with ↑ activity against Pseudomonas and gram-positive organisms.
29
Fifth generation cephalosporins
Ceftaroline
30
Fifth generation cephalosporin clinical use
5th generation (ceftaroline)— broad gram-positive and gram-negative organism coverage, including MRSA. Does not cover Pseudomonas.
31
Cephalosporin toxicity
1. hypersensitivity reactions 2. autoimmune hemolytic anemia 3. disulfiram-like reaction 4. vitamin K deficiency 5. Exhibit cross-reactivity with penicillins, ↑ nephrotoxicity of aminoglycosides.
32
Cephalosporin resistance
Structural change in penicillin-binding proteins (transpeptidases).
33
Carbapenems
1. imipenem 2. meropenem 3. ertapenem (limited Pseudomonas coverage) 4. doripenem
34
Carbapenem mechanism
Imipenem is a broad-spectrum, β-lactamase–resistant carbapenem. Always administered with *cilastatin* (inhibitor of renal dehydropeptidase I) to ↓ inactivation of drug in renal tubules.
35
Carbapenem clnical use
(imipenem, meropenem, ertapenem, doripenem) * ​Gram-positive cocci * Gram-negative rods * Anaerobes Wide spectrum, but significant side effects limit use to life-threatening infections or after other drugs have failed. Meropenem has a ↓ risk of seizures and is stable to dehydropeptidase I.
36
Carbapenem toxicity
* GI distress * skin rash * CNS toxicity (seizures) at high plasma levels
37
Monobactams
Aztreonam
38
Monobactam mechanism
Prevents peptidoglycan cross-linking by binding to penicillin- binding protein 3. * Less susceptible to β-lactamases. * Synergistic with aminoglycosides. * No cross-allergenicity with penicillins.
39
Monobactam clinical use
Gram-negative rods only—no activity against gram-positives or anaerobes. For penicillin-allergic patients and those with renal insufficiency who cannot tolerate aminoglycosides.
40
Monobactam toxicity
Usually nontoxic; occasional GI upset.
41
Glycopeptides
* Bacitracin * Vancomycin
42
Vancomycin mechanism
Inhibits cell wall peptidoglycan formation by binding D-ala D-ala portion of cell wall precursors. Bactericidal. Not susceptible to β-lactamases.
43
Vancomycin clinical use
Gram-positive bugs only—serious, multidrug-resistant organisms, including * MRSA * S. epidermidis * sensitive Enteroccocus species * Clostridium difficile (oral dose for pseudomembranous colitis)
44
Vancomycin toxicity
Well tolerated in general—but NOT trouble free. 1. Nephrotoxicity 2. Ototoxicity 3. Thrombophlebitis 4. diffuse flushing—red man syndrome (can largely prevent by pretreatment with antihistamines and slow infusion rate)
45
Vancomycin resistance
Occurs in bacteria via amino acid modification of D-ala D-ala to D-ala D-lac.
46
Aminoglycosides
1. Gentamicin 2. Neomycin 3. Amikacin 4. Tobramycin 5. Streptomycin
47
Aminoglycoside mechanism
Bactericidal. Irreversible inhibition of initiation complex through binding of the 30S subunit. Can cause misreading of mRNA. Also block translocation. Require O2 for uptake; therefore ineffective against anaerobes.
48
Aminoglycoside clinical use
Severe gram-negative rod infections. Synergistic with β-lactam antibiotics. Neomycin for bowel surgery.
49
Aminoglycoside toxicity
1. Nephrotoxicity 2. Neuromuscular blockade 3. Ototoxicity (especially when used with loop diuretics) 4. Teratogen.
50
Aminoglycoside resistance
Bacterial transferase enzymes inactivate the drug by * acetylation * phosphorylation * or adenylation
51
Tetracyclines
1. Tetracycline 2. Doxycycline 3. Minocycline
52
Tetracycline mechanism
Bacteriostatic. Bind to 30S and prevent attachment of aminoacyl-tRNA. Limited CNS penetration. Doxycycline is fecally eliminated and can be used in patients with renal failure. Do not take tetracyclines with * milk (Ca2+), * antacids (Ca2+ or Mg2+), * or iron-containing preparations because divalent cations inhibit drugs’ absorption in the gut.
53
Tetracycline clinical use
* Borrelia burgdorferi * M. pneumoniae Drugs’ ability to accumulate intracellularly makes them very effective against Rickettsia and Chlamydia. Also used to treat acne.
54
Tetracycline toxicity
1. GI distress 2. discoloration of teeth 3. inhibition of bone growth in children 4. photosensitivity 5. Contraindicated in pregnancy.
55
Tetracycline resistance
↓ uptake or ↑ efflux out of bacterial cells by plasmid-encoded transport pumps.
56
Chloramphenicol mechanism
Blocks peptidyltransferase at 50S ribosomal subunit. Bacteriostatic.
57
Chloramphenicol clinical use
Meningitis * Haemophilus influenzae * Neisseria meningitidis * Streptococcus pneumoniae Rocky Mountain spotted fever * Rickettsia rickettsii Limited use owing to toxicities but often still used in developing countries because of low cost.
58
Chloramphenicol toxicity
1. Anemia (dose dependent) 2. aplastic anemia (dose independent) 3. gray baby syndrome (in premature infants because they lack liver UDP-glucuronyl transferase).
59
Chloramphenicol mechanism of resistance
Plasmid-encoded acetyltransferase inactivates the drug.
60
Lincosamide
Clindamycin
61
Clindamycin mechanism
Blocks peptide transfer (translocation) at 50S ribosomal subunit. Bacteriostatic.
62
Clindamycin clinical use
Anaerobic infections (e.g., * Bacteroides spp. * Clostridium perfringens in * aspiration pneumonia * lung abscesses * oral infections. Also effective against invasive group A streptococcal infection (strep pyogenes). [Treats anaerobic infections above the diaphragm vs. metronidazole (anaerobic infections below diaphragm)]
63
Clindamycin Toxicity
1. Pseudomembranous colitis (C. difficile overgrowth) 2. fever 3. diarrhea
64
Oxazolidinones
Linezolid
65
Oxazolidinones mechanism
Inhibit protein synthesis by binding to 50S subunit and preventing formation of the initiation complex.
66
Oxazolidinones clinical use
Gram-positive species including MRSA and VRE
67
Oxazolidinones toxicity
1. Bone marrow suppression (especially thrombocytopenia) 2. peripheral neuropathy 3. serotonin syndrome
68
Oxazolidinones resistance
Point mutation of ribsomal RNA.
69
Macrolides
1. Azithromycine 2. Clarithomycin 3. Erythromycin
70
Macrolide mechanism
(Azithromycin, clarithromycin, erythromycin) Inhibit protein synthesis by blocking translocation; bind to the 23S rRNA of the 50S ribosomal subunit. Bacteriostatic.
71
Macrolide clinical use
1. Atypical pneumonias 1. Mycoplasma 2. Chlamydia 3. Legionella 2. STIs 1. Chlamydia 3. gram-positive cocci 1. streptococcal infections in patients allergic to penicillin 4. B. pertussis
72
Macrolide toxicity
1. Gastrointestinal motility issues 2. Arrhythmia caused by prolonged QT interval 3. acute cholestatic hepatitis 4. rash 5. eosinophilia. 6. Increases serum concentration of theophyllines, oral anticoagulants. 7. Clarithromycin and erythromycin inhibit cytochrome P-450.
73
Macrolide resistance
Methylation of 23S rRNA-binding site prevents binding of drug
74
Floroquinolones
1. Ciprofloxacin 2. norfloxacin 3. levofloxacin 4. ofloxacin 5. moxifloxacin 6. gemifloxacin 7. enoxacin
75
Floroquinolone mechanism
Inhibit prokaryotic enzymes topoisomerase II (DNA gyrase) and topoisomerase IV. Bactericidal. Must not be taken with antacids.
76
Floroquinolone clinical use
* Gram-negative rods of urinary and GI tracts (including Pseudomonas) * Neisseria * some gram-positive organisms
77
Floroquinolone toxicity
1. GI upset 2. superinfections 3. skin rashes 4. headache 5. dizziness 6. Less commonly, can cause leg cramps and myalgias. 7. Contraindicated in pregnant women, nursing mothers, and children \< 18 years old due to possible damage to cartilage. 8. Some may prolong QT interval. 9. May cause tendonitis or tendon rupture in people \> 60 years old and in patients taking prednisone.
78
Floroquinolone resistance
1. Chromosome-encoded mutation in DNA gyrase 2. plasmid-mediated resistance 3. efflux pumps
79
Lipopeptide
Daptomycin
80
Daptomycin mechanism
Lipopeptide that dirsupts cell membcane of gram-positive cocci.
81
Daptomycin clinical use
1. S. aureus skin infections (especially MRSA) 2. bacteremia 3. endocarditis 4. VRE (vancomycin resistant eneterococcus) Not used for pneumonia (avidly binds to and is inactivated by surfactant).
82
Daptomycin toxicity
* Myopathy * rhabdomyolysis
83
Nitroimidazole
Metronidazole
84
Metronidazole mechanism
Forms toxic free radical metabolites in the bacterial cell that damage DNA. Bactericidal, antiprotozoal.
85
Metronidazole clinical use
Treats 1. Giardia 2. Entamoeba 3. Trichomonas 4. Gardnerella vaginalis 5. Anaerobes 1. Bacteroides 2. C. difficile Used with a proton pump inhibitor and clarithromycin for “triple therapy” against H. Pylori. Treats anaerobic infection below the diaphragm vs. clindamycin (anaerobic infections above diaphragm).
86
Metronidazole toxicity
1. Disulfiram-like reaction with alcohol 1. severe flushing 2. tachycardia 3. hypotension 2. headache 3. metallic taste
87
Sulfonamides
1. ​Sulfamethoxazole (SMX) (short acting) 2. Sulfisoxazole (topical) 3. Sulfadiazine (short acting)
88
Sulfonamide mechanism
Inhibit folate synthesis. Para-aminobenzoic acid (PABA) antimetabolites inhibit dihydropteroate synthase. Bacteriostatic (bactericidal when combined with trimethoprim). (Dapsone, used to treat lepromatous leprosy, is a closely related drug that also inhibits folate synthesis.)
89
Sulfonamide clinical use
1. Gram-positives 2. gram-negatives 3. Nocardia 4. Chlamydia 5. Triple sulfas or SMX for simple UTI
90
Sulfonamide toxicity
1. Hypersensitivity reactions 2. hemolysis if G6PD deficient 3. nephrotoxicity (tubulointerstitial nephritis) 4. photosensitivity 5. kernicterus in infants 6. displace other drugs from albumin (e.g., warfarin)
91
Sulfonamide resistance
Altered enzyme (bacterial dihydropteroate synthase), ↓ uptake, or ↑ PABA synthesis.
92
Trimethoprim mechanism
Inhibits bacterial dihydrofolate reductase. Bacteriostatic.
93
Trimethoprim clinical use
Used in combination with sulfonamides (trimethoprim-sulfamethoxazole [TMP- SMX]), causing sequential block of folate synthesis. Combination used for 1. UTIs 2. Shigella 3. Salmonella 4. Pneumocystis jirovecii pneumonia treatment and prophylaxis 5. toxoplasmosis prophylaxis
94
Trimethoprim toxicity
1. Megaloblastic anemia 2. leukopenia 3. granulocytopenia (May alleviate with supplemental folinic acid)
95
30S inhibitors
* Aminoglycosides (bactericidal) * Tetracyclines (bateriostatic)
96
50S inhibitors
1. Choramphenicol 2. Clindamycin (bacteriostatic) 3. Erythromycin (macrolides) (bacteriostatic) 4. Linezolid (variable
97
Cell wall synthesis → peptidoglycan synthesis
glycopeptides → vancomycin and bacitracin
98
Cell wall synthesis → peptidoglycan cross-linking
1. Penicillinase-sensitive penicillins 2. Penicillinase-resistant penicillins 3. Antipseudomonals 4. Cephalosporins 5. Carbapenems 6. Monobactams
99
Folic acid synthesis
* Sufonamides * Trimethoprim
100
DNA topoisomerases
Floroquinolones
101
Damages DNA
Metronidazole
102
Protein Synthesis → 50s subunit
* Chloramphenicol, clindamycin, linezolid * Macrolides * Streptogramins
103
Protein synthesis → 30s subunit
* Aminoglycosides * Tetracyclines

First Aid Microbiology (11 decks)

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