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PHARMACOLOGY - Antibiotics and Immunosuppressives > (01) Antibiotic Classes > Flashcards

(01) Antibiotic Classes Flashcards

(47 cards)

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1
Q

What are the 4 ways that antimicrobial agents can act through?

A
  • Inhibition of Cell Wall synthesis
  • Inhibition of Protein Synthesis
  • Inhibition of Folic Acid biosynthetic pathways
  • Inhibition of DNA/RNA synthesis
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2
Q

What type of bacteria is most sensitive to ß-lactams?

- why?

A

Gram + bacteria because they have a thick peptidoglycan cell wall

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3
Q

What protects gram - bacteria from ß-lactams?

A

Only have a thin cell wall that is protected by a LIPOPOLYSACCHARIDE layer

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4
Q

Why would you use a ß-lactimase inhibitor with penicillin?

  • how does it work?
  • what combinations are used?
A
  • Resistant bacteria may have ß-lactimase present
  • Bind to ß-lactimase to prevent them from cleaving ß-lactams

Combos:
- Clavulanic Acid + Amoxicillin

  • Tazobactam + Pipercillin
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5
Q

Narrow-Spectrum Penicillins

- structural and functional difference?

A

Structural:
- Large side chains prevent ß-lactamases from twisting the penicillin into different stereoisomers

Functional:
- Side chains limit their spectrum of activity

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6
Q

Broad Spectrum Penicillin

  • derivatives of…
  • purpose
  • administered with?
  • Example?
A

Broad Spectrum Penicillins are derived from Aminopenicillins (extra amino group to cross LPS layer on gram - bacteria)

Purpose:
- kill more types of bacteria

Administered with:
- ß-lactamase inhibitors, because they are especially sensitive

E.g. Pip/Tazo

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7
Q

Imipenem

  • what is it
  • activity
  • what is it administered with
  • why?
A

Imipenem = ß-lactam

Activity:
- Broad Spectrum

Administered with Cilastin (not and antimicrobial)

Cilastin inhibits Dehydropeptidase-1 (DHP-1) in kidney brush boarder than breaks down Imipenem

**Results in increased urinary concentrations of imipenem

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8
Q

Describe the structural differences between penicillins and cephalosporins

A

Penicillin:
- Thiazolidine attached to ß-lactam ring

Cephalosporins:
- 6 membered ring attached to ß-lactam ring

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9
Q

What do ß-lactams inhibit?

A

Inhibit Penicillin-Binding Proteins

  • This leads to breakdown of the cell wall because transpeptidases can’t do their job
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10
Q

What makes cephalosporins more user friendly?

A
  • They can be taken with or without food

- They are more acid stable

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11
Q

What is the trend as you move from the 1st generation of cephalosporins to the 4th?

A

Gram + activity is lost as Gram - activity is gained

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12
Q

What is generally treated using 1st generation cephalosporins?
- 2 examples when specific types are used

A

Treats:
- streptococcus or staphylococcus

When:

  • Cefazolin - surgical prophylaxis
  • Cephalexin - most commonly perscribed Cephalosporin for outpatient use
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13
Q

What is generally treated using 2nd generation cephalosporins?
- when are these used?

A

Mild Gram - Bacteroides infections (anaerobic)

  • intraabdominal infections
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14
Q

Would you use a second generation cephalosporin to treat a severe infection?
why or why not?

A

NO, because 3rd generation cephalosporins are more efficacious

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15
Q

When are 3rd generation cephalosporins typically used and how?
- 2 specific examples

A

Treat severe infections in combination with a drug of a different class (with a different MOA)

  1. Ceftriaxone - Treats STIs and Pediatric Meningitis
  2. Cefepime - treats pseudomonal infections
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16
Q

When are 4th generation cephalosporins used?

A

Nosocomial (hospital acquired) infections

  • These have a tendency to be antibiotic resistant, more severe, or caused by gram - organisms
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17
Q

What is the mechanism of action (MOA) of Vancomycin?

A
  • Attach to the ends of peptidoglycan precursor units (pentapeptides)
  • Transglycosylase binds and can’t let go
  • This prevents peptidoglycan synthesis
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18
Q

What kind of bacteria is Vancomycin effective against?

- why?

A

Gram + bacteria.

Effective because gram + bacteria have very thick cell walls and no new cell wall synthesis can occur

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19
Q

Compare the MOA of ß-lactam agents to Vancomycin.

Study These Flashcards
A

ß-lactam:
- inhibits transpeptidases

Vancomycin:
- inhibits transglycosylases

20
Q

When would you administer vancomycin orally vs. IV?

- why do you have to do this?

Study These Flashcards
A
  • Vancomycin is poorly absorbed by the digestive tract

Orally:
- Will kill things like C-Diff Colitis in the Colon

IV:
- Can work in blood, soft tissues, brain, heart, etc.

21
Q

What is the mechanism of action for cephalosporins?

Study These Flashcards
A

Inhibit Transpeptidases in the same way that penicillin does via the ß-lactam ring

22
Q

What is the mechanism of action of fosfomycin?

- why is this significant

Study These Flashcards
A
  • Epoxide group irreversibly inhibits enolpyruvyl transferase by binding in place of PEP
  • Blocks condensation of Uridine Diphosphate-N-acetyleglucosamine with p-enolpyruvate

**Key 1st step in bacterial cell wall synthesis

23
Q

Aminoglycosides

  • polarity
  • consequences of polarity
  • Toxicity?
Study These Flashcards
A

Aminoglycosides are polar

Consequence:

  • Poor Penetration of Biological Membranes
  • NOT GIVEN ORALLY, NOT ABSORBED IN GI TRACT

Toxicity:

  • Proximal Tubule is the only place Aminoglycosides are absorbed.
  • Aminoglycosides accumulate in kidney cells and cause Nephrotoxicity
24
Q

What is the mechanism of action of Aminoglycosides?

- what kind of infections do they treat?

Study These Flashcards
A
  1. Irreversibly bind to 30s Ribosomal subunit of bacteria

Low Concentration:
- cause misreading of mRNA by ribosomes

High Concentration:
- Halt Protein Synthesis, trapping Ribosomes at the AUG start codon

  1. Cationic Antibiotic molecules create fissures in outer membrane allowing contents to leak
    * Gram - bacterial infections
25
Why are aminolgycosides less effective against anaerobes?
Polar aminoglycosides must enter via active transport. Anaerobes have less energy and are less likely to absorb the drug
26
What does bacteriostatic mean?
a drug that inhibits replication but does not actively kill existing bacteria is bacteriostatic
27
T or F: aminoglycosides are bacteriostatic like most other protein synthesis inhibitors
False, Aminoglycosides are bactericidal because they cause leaks in the membrane in addition to halting protein synthesis
28
What are the classes of protein synthesis inhibitors?
1. Aminoglycosides 2. Macrolides 3. Lincosamides 4. Tetracyclines 5. Streptogramins 6. Mupirocin
29
Macrolides - MOA - Common macrolides - Bacteriostatic or Bacteriocidal
- Bind 23s RNA molecule of 50s subunit of bacterial ribosome and inhibit PEPTIDYLTRANSFERASE - Phagocytized by Macrophages which is a WBC and will travel to site of infection and bring drug with it 1. Erythromycin 2. Azithromycin - Bacteriostatic (bacteriocidal at high enough conc.)
30
Lincosamides - MOA - example of a lincosamide - Bacteriostatic or Bacteriocidal
MOA - bind 23S rRNA molecule of 50S RSU and block transfer of a new Aminoacid onto a growing chain Clindamycin is a Lincosaminde Bacteriostatic (bacteriocidal at high enough concentrations)
31
Why are lincosamides considered beneficial in toxin producing infections?
- Toxins are proteins or are made by proteins within the bacteria - Since these block protein synthesis, they also block toxin production
32
Tetracyclines - MOA - Bacteriostatic or Bacteriocidal
MOA: - bind REVERSIBLY to 16S rRNA of 30S RSU - Weakens the ribosome-tRNA interaction and prevents addition of AA to growing peptide Bacteriostatic
33
What are 2 characteristics of Tetracyclines that makes them selective for bacteria over human cells?
1. Active transport system by which they are taken up is present only in bacteria 2. Like the others, it is specific to prokaryotic Ribosomal subunits (30S)
34
Streptogramins - MOA - Relationship of Quinpristin and Dalfopristin - Bacteriostatic or bactericidal
MOA: - Bind to 50S RSU Synergistic Relationship: Quinupristin - binds at same place as macrolides and has similar effect Dalfopristin - binds 50S near Quinprisitin causing conformational change that ENHANCES QUINUPRISTIN BINDING - also directly interferes with chain formation **Bactericidal
35
Mupirocin | - MOA
Inhibition of isoleucyl transfer-RNA synthetase **Applied Topically
36
Chloramphenicol - MOA - Drug-Drug interactions, why?
MOA: Binds to 50S RSU and at transpeptidyl transferase and inhibits trasnpeptidation reaction Interferes with: - Macrolides and Lincosamides because they have Clindamycin because they bind near the same site
37
Fluroquinolones - MOA - Bacteriostatic or Bactricidal?
MOA: Gram - - Inhibit DNA gyrase (topoisomerase II) Gram + - Inhibit DNA gyrase (topoisomerase IV) - Prevents separation of replicated DNA into respective daughter cells *Allows Double Strand break but prevents reattachment Bactricidal: - accumulation of DNA fragments leads to cell death
38
Why do Fluroquinolones not affect humans to any great extent?
we have different forms of Topoisomerase II and Topoisomerase IV **Note: these are enzymes that relax supercoiled DNA
39
What is the MOA of Rifamprins?
Bind PROKARYOTIC RNA polymerase, prevents initiation of RNA synthesis **does NOT affect elongation
40
What important characteristic of Rifamprin gives it access into many different enviroments? - what are some examples of environments that it can access?
Rifamprin is lipofilic and can therefore penetrate into many different areas. 1. Mycobacterial walls - contain long fatty acids (mycolic acids) 2. Biofilms 3. CNS - can treat meningitis 4. Phagocytic cells - can kill bacteria that can live intracellularly
41
Cotrimioxazole - Composition - MOA - uses?
Composition: Trimethoprim and Sulfamethoxazole (sulfonamide) MOA: Sulfamethoazole -prevents PABA from entering Folic Acid Trimethoprim - prevents reduction of Dihydrofolate to Tetrahydrofolate by DIHYDROFOLATE REDUCTASE Uses: - Uncomplicated UTIs and acute exacerbations of chronic bronchitiits
42
Why does Trimethorprim not affect human DHF reductase?
The drug is much more selective for the bacterial form. 100,000 times the normal dose is required to inhibit human dihydrofolate reductase
43
DAPTOMYCIN - MOA - Bacteria affected - Bacteriostatic or Bactricidal? - what system can it not be used to treat and why?
MOA: - Lipopeptides bind to membrane and cause rapid depolarization - Protein, DNA, and RNA synthesis is halted and cell dies * Affects Gram + bacteria * Bactricidal * Doesn't treat pulmonary infections because drug is deactivated by surfactant in lungs
44
Fidaxomicin - MOA - Cross resistance issues?
MOA: - Inhibits sigma dependent transcription of Bacterial RNA polymerases No Cross resistance (even with rifamprin)
45
Cell wall inhibitors 8 total
5 Penicillins 1. Penicillin G 2. Ampicillin 3. Piperacillin 4. Aztreonam 5. Imipenem 3 others 1. Ceftriaxone 2. Vancomycin 3. Cephalexin
46
8 protein synthesis inhibitors
Aminoglycosides: 1. Gentamicin Macrolides: 2. Azithromycin 3. Clarithromycin 4. Erythromycin Oxazolidinones: 5. Linezolid Tetracylines: 6. Doxycycline 7. Tigecyline Others: 8. Mupirocin
47
7 Drugs that affect nucleic acid metabolism.
Fluoroquinolones 1. Ciprofloxacin Rifamycins 2. Rifampin Nitroimidazoles 3. Metronidazole Dihydrofolate Reductase inhibitors 4. Cotrimoxazole Sulfonamides 5. Cotrimoxazole Others 6. Daptomycin 7. Fidaxomicin

PHARMACOLOGY - Antibiotics and Immunosuppressives (12 decks)

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