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PHARMA 3 > Step 1 Antibiotics 2 > Flashcards

Step 1 Antibiotics 2 Flashcards

1
Q

Front

A

Back

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2
Q

Fluoroquinolones: Drugs

A

Ciprofloxacin, ofloxacin; respiratory fluoroquinolones: levofloxacin, moxifloxacin.

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3
Q

Fluoroquinolones: Mechanism

A

Inhibit prokaryotic topoisomerase II (DNA gyrase) and topoisomerase IV. Bactericidal. Oral absorption is markedly decreased by concurrent ingestion of divalent cations (e.g., dairy, antacids).

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4
Q

Fluoroquinolones: Clinical Use

A

Effective against gram ⊝ rods of urinary and GI tracts (including Pseudomonas), some gram ⊕ organisms, otitis externa, and community-acquired pneumonia.

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5
Q

Fluoroquinolones: Adverse Effects

A
  • GI upset, superinfections, skin rashes, headache, dizziness.
  • Less commonly: leg cramps, myalgias.
  • Tendonitis or tendon rupture (especially in patients > 60 years old or on prednisone).
  • Contraindicated in pregnancy, breastfeeding, and in children < 18 years old due to possible cartilage damage.
  • May prolong QT interval.
    Mnemonic: ‘Fluoroquinolones hurt attachments to your bones.’
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6
Q

Fluoroquinolones: Mechanism of Resistance

A
  • Chromosome-encoded mutation in DNA gyrase.
  • Plasmid-mediated resistance.
  • Efflux pumps.
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7
Q

Daptomycin: Mechanism

A

Lipopeptide that disrupts gram ⊕ bacterial cell membranes by creating transmembrane channels.

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8
Q

Daptomycin: Clinical Use

A

Effective against S aureus skin infections (especially MRSA), bacteremia, infective endocarditis, and VRE.

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9
Q

Daptomycin: Adverse Effects

A
  • Myopathy.
  • Rhabdomyolysis.
    Note: Not used for pneumonia (inactivated by surfactant). Mnemonic: ‘Dapto-myo-skin’—used for skin infections but can cause myopathy.
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10
Q

Metronidazole: Mechanism

A

Forms toxic free radical metabolites in bacterial cells, damaging DNA. Bactericidal and antiprotozoal.

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11
Q

Metronidazole: Clinical Use

A

Treats:
- Giardia.
- Entamoeba.
- Trichomonas.
- Gardnerella vaginalis.
- Anaerobes (Bacteroides, C difficile).
- Can replace amoxicillin in H pylori ‘triple therapy’ for penicillin-allergic patients.
Mnemonic: ‘GET GAP on the Metro’—treats anaerobic infections below the diaphragm (vs clindamycin for above diaphragm).

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12
Q

Metronidazole: Adverse Effects

A
  • Disulfiram-like reaction with alcohol (flushing, tachycardia, hypotension).
  • Headache.
  • Metallic taste.
  • Can cause tendonitis or tendon rupture in patients > 60 years old or on prednisone.
    Note: Ciprofloxacin inhibits cytochrome P-450.
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13
Q

Linezolid: Mechanism

A

Inhibits protein synthesis by binding to the 23S rRNA of the 50S ribosomal subunit, preventing the formation of the initiation complex.

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14
Q

Linezolid: Clinical Use

A

Effective against gram ⊕ species, including MRSA and VRE.

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15
Q

Linezolid: Adverse Effects

A
  • Myelosuppression (especially thrombocytopenia).
  • Peripheral neuropathy.
  • Serotonin syndrome (due to partial MAO inhibition).
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16
Q

Linezolid: Mechanism of Resistance

A

Point mutation of ribosomal RNA.

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17
Q

Macrolides: Drugs

A

Azithromycin, clarithromycin, erythromycin.

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18
Q

Macrolides: Mechanism

A

Inhibit protein synthesis by blocking translocation (‘macroslides’); bind to the 50S ribosomal subunit. Bacteriostatic.

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19
Q

Macrolides: Clinical Use

A

Used for atypical pneumonias (Mycoplasma, Chlamydia, Legionella), STIs (Chlamydia), gram ⊕ cocci (streptococcal infections in penicillin-allergic patients), and B pertussis.

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20
Q

Macrolides: Adverse Effects

A

MACRO:
- Gastrointestinal Motility issues.
- Arrhythmia due to prolonged QT interval.
- Acute cholestatic hepatitis.
- Rash.
- Eosinophilia.
- Increases serum levels of theophylline and oral anticoagulants. Clarithromycin and erythromycin inhibit cytochrome P-450.

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21
Q

Macrolides: Mechanism of Resistance

A

Methylation of the 23S rRNA-binding site prevents drug binding.

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22
Q

Polymyxins: Drugs

A

Colistin (polymyxin E), polymyxin B.

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23
Q

Polymyxins: Mechanism

A

Cationic polypeptides that bind to phospholipids on the cell membrane of gram ⊝ bacteria, disrupting cell membrane integrity, causing leakage of cellular components, and cell death.

24
Q

Polymyxins: Clinical Use

A

Used as salvage therapy for multidrug-resistant gram ⊝ bacteria (e.g., P aeruginosa, E coli, K pneumoniae). Polymyxin B is a component of triple antibiotic ointments for superficial skin infections.

25
Q

Polymyxins: Adverse Effects

A
  • Nephrotoxicity.
  • Neurotoxicity (e.g., slurred speech, weakness, paresthesias).
  • Respiratory failure.
26
Q

Sulfonamides: Drugs

A

Sulfamethoxazole (SMX), sulfisoxazole, sulfadiazine.

27
Q

Sulfonamides: Mechanism

A

Inhibit dihydropteroate synthase, thereby inhibiting folate synthesis. Bacteriostatic (bactericidal when combined with trimethoprim).

28
Q

Sulfonamides: Clinical Use

A

Effective against gram ⊕, gram ⊝, and Nocardia. TMP-SMX is used for simple UTIs.

29
Q

Sulfonamides: Adverse Effects

A
  • Stevens-Johnson syndrome.
  • Urticaria.
  • Liver damage.
  • Folate deficiency.
  • Optic neuritis.
  • Nephrotoxicity.
  • Agranulocytosis.
  • Hemolysis if G6PD deficient.
  • Kernicterus in infants.
30
Q

Sulfonamides: Mechanism of Resistance

A

Resistance occurs through altered enzyme (dihydropteroate synthase), reduced uptake, or increased PABA synthesis.

31
Q

Dapsone: Mechanism

A

Similar to sulfonamides but structurally distinct. Inhibits dihydropteroate synthase.

32
Q

Dapsone: Clinical Use

A

Used for leprosy (both lepromatous and tuberculoid forms) and as prophylaxis or treatment for Pneumocystis jirovecii when combined with TMP.

33
Q

Dapsone: Adverse Effects

A
  • Hemolysis if G6PD deficient.
  • Methemoglobinemia.
  • Agranulocytosis.
34
Q

Trimethoprim: Mechanism

A

Inhibits bacterial dihydrofolate reductase, making it bacteriostatic.

35
Q

Cephalosporins: Mechanism

A

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

36
Q

Cephalosporins: Clinical Use (1st Generation)

A

1st generation (cefazolin, cephalexin)—gram ⊕ cocci, Proteus mirabilis, E coli, Klebsiella pneumoniae. Cefazolin is used prior to surgery to prevent S aureus wound infections.
Mnemonic: ⊕ PEcK.

37
Q

Cephalosporins: Clinical Use (2nd Generation)

A

2nd generation (cefaclor, cefoxitin, cefuroxime, cefotetan)—gram ⊕ cocci, H influenzae, Enterobacter aerogenes, Neisseria spp., Serratia marcescens, Proteus mirabilis, E coli, Klebsiella pneumoniae.
Mnemonic: ⊕ HENS PEcK (2nd graders wear fake fox fur to tea parties).

38
Q

Cephalosporins: Clinical Use (3rd Generation)

A

3rd generation (ceftriaxone, cefpodoxime, ceftazidime, cefixime)—serious gram ⊝ infections resistant to other β-lactams. Ceftriaxone is used for meningitis, gonorrhea, and disseminated Lyme disease. Ceftazidime for Pseudomonas.

39
Q

Cephalosporins: Clinical Use (4th Generation)

A

4th generation (cefepime)—effective against gram ⊝ organisms, with enhanced activity against Pseudomonas and gram ⊕ organisms.

40
Q

Cephalosporins: Clinical Use (5th Generation)

A

5th generation (ceftaroline)—broad coverage of gram ⊕ and gram ⊝ organisms. Unlike earlier generations, covers MRSA and Enterococcus faecalis but not Pseudomonas.

41
Q

Cephalosporins: Adverse Effects

A
  • Hypersensitivity reactions.
  • Autoimmune hemolytic anemia.
  • Disulfiram-like reaction.
  • Vitamin K deficiency.
  • Low cross-reactivity in penicillin-allergic patients.
  • Enhanced nephrotoxicity with aminoglycosides.
42
Q

Cephalosporins: Mechanism of Resistance

A
  • Inactivated by cephalosporinases (a type of β-lactamase).
  • Structural changes in penicillin-binding proteins (PBPs).
43
Q

Cephalosporins: Key Limitations

A

Organisms not covered by 1st–4th generation cephalosporins: LAME
- Listeria
- Atypicals (Chlamydia, Mycoplasma)
- MRSA
- Enterococci.

44
Q

β-lactamase Inhibitors: Drugs

A

Clavulanic acid, Avibactam, Sulbactam, Tazobactam.

45
Q

β-lactamase Inhibitors: Use

A

Added to penicillins to protect them from β-lactamase destruction.
Examples: amoxicillin-clavulanate, ceftazidime-avibactam, ampicillin-sulbactam, piperacillin-tazobactam (CAST).

46
Q

Carbapenems: Drugs

A

Imipenem, meropenem, ertapenem.

47
Q

Carbapenems: Mechanism

A

Broad-spectrum β-lactamase-resistant antibiotics. Bind penicillin-binding proteins, inhibiting cell wall synthesis and causing bacterial cell death.

48
Q

Carbapenems: Clinical Use

A

Effective against gram ⊕ cocci, gram ⊝ rods, and anaerobes. Reserved for life-threatening infections or when other drugs fail.
Imipenem is co-administered with cilastatin to prevent renal inactivation (‘the kill is lastin’ with cilastatin’).
Ertapenem lacks activity against Pseudomonas.

49
Q

Carbapenems: Adverse Effects

A
  • GI distress.
  • Rash.
  • CNS toxicity (seizures) at high plasma levels.
50
Q

Carbapenems: Mechanism of Resistance

A

Inactivation by carbapenemases produced by organisms such as K pneumoniae, E coli, and Enterobacter spp.

51
Q

Aztreonam: Mechanism

A

Prevents peptidoglycan cross-linking by binding penicillin-binding protein 3. Resistant to β-lactamases. Synergistic with aminoglycosides.

52
Q

Aztreonam: Clinical Use

A

Effective against gram ⊝ rods only. No activity against gram ⊕ rods or anaerobes. Used for penicillin-allergic patients and those with renal insufficiency who cannot tolerate aminoglycosides.

53
Q

Aztreonam: Adverse Effects

A

Usually well-tolerated but may cause occasional GI upset.

54
Q

Vancomycin: Mechanism

A

Inhibits peptidoglycan synthesis by binding D-Ala-D-Ala of cell wall precursors. Bactericidal (bacteriostatic for C difficile). Not susceptible to β-lactamases.

55
Q

Vancomycin: Clinical Use

A

Effective against gram ⊕ organisms, including MRSA, S epidermidis, Enterococcus species, and Clostridium difficile (oral route).

56
Q

Vancomycin: Adverse Effects

A
  • Red man syndrome (histamine-mediated flushing).
  • Nephrotoxicity.
  • Ototoxicity.
  • Thrombophlebitis.

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