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

(01) Antibiotic Classes Flashcards

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.

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?

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?

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

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?
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?

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
Q

Why are aminolgycosides less effective against anaerobes?

A

Polar aminoglycosides must enter via active transport.

Anaerobes have less energy and are less likely to absorb the drug

26
Q

What does bacteriostatic mean?

A

a drug that inhibits replication but does not actively kill existing bacteria is bacteriostatic

27
Q

T or F: aminoglycosides are bacteriostatic like most other protein synthesis inhibitors

A

False, Aminoglycosides are bactericidal because they cause leaks in the membrane in addition to halting protein synthesis

28
Q

What are the classes of protein synthesis inhibitors?

A
  1. Aminoglycosides
  2. Macrolides
  3. Lincosamides
  4. Tetracyclines
  5. Streptogramins
  6. Mupirocin
29
Q

Macrolides

  • MOA
  • Common macrolides
  • Bacteriostatic or Bacteriocidal
A
  • 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
Q

Lincosamides

  • MOA
  • example of a lincosamide
  • Bacteriostatic or Bacteriocidal
A

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
Q

Why are lincosamides considered beneficial in toxin producing infections?

A
  • Toxins are proteins or are made by proteins within the bacteria
  • Since these block protein synthesis, they also block toxin production
32
Q

Tetracyclines

  • MOA
  • Bacteriostatic or Bacteriocidal
A

MOA:
- bind REVERSIBLY to 16S rRNA of 30S RSU

  • Weakens the ribosome-tRNA interaction and prevents addition of AA to growing peptide

Bacteriostatic

33
Q

What are 2 characteristics of Tetracyclines that makes them selective for bacteria over human cells?

A
  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
Q

Streptogramins

  • MOA
  • Relationship of Quinpristin and Dalfopristin
  • Bacteriostatic or bactericidal
A

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
Q

Mupirocin

- MOA

A

Inhibition of isoleucyl transfer-RNA synthetase

**Applied Topically

36
Q

Chloramphenicol

  • MOA
  • Drug-Drug interactions, why?
A

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
Q

Fluroquinolones

  • MOA
  • Bacteriostatic or Bactricidal?
A

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
Q

Why do Fluroquinolones not affect humans to any great extent?

A

we have different forms of Topoisomerase II and Topoisomerase IV

**Note: these are enzymes that relax supercoiled DNA

39
Q

What is the MOA of Rifamprins?

A

Bind PROKARYOTIC RNA polymerase, prevents initiation of RNA synthesis

**does NOT affect elongation

40
Q

What important characteristic of Rifamprin gives it access into many different enviroments?
- what are some examples of environments that it can access?

A

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
Q

Cotrimioxazole

  • Composition
  • MOA
  • uses?
A

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
Q

Why does Trimethorprim not affect human DHF reductase?

A

The drug is much more selective for the bacterial form.

100,000 times the normal dose is required to inhibit human dihydrofolate reductase

43
Q

DAPTOMYCIN

  • MOA
  • Bacteria affected
  • Bacteriostatic or Bactricidal?
  • what system can it not be used to treat and why?
A

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
Q

Fidaxomicin

  • MOA
  • Cross resistance issues?
A

MOA:
- Inhibits sigma dependent transcription of Bacterial RNA polymerases

No Cross resistance (even with rifamprin)

45
Q

Cell wall inhibitors 8 total

A

5 Penicillins

  1. Penicillin G
  2. Ampicillin
  3. Piperacillin
  4. Aztreonam
  5. Imipenem

3 others

  1. Ceftriaxone
  2. Vancomycin
  3. Cephalexin
46
Q

8 protein synthesis inhibitors

A

Aminoglycosides:
1. Gentamicin

Macrolides:

  1. Azithromycin
  2. Clarithromycin
  3. Erythromycin

Oxazolidinones:
5. Linezolid

Tetracylines:

  1. Doxycycline
  2. Tigecyline

Others:
8. Mupirocin

47
Q

7 Drugs that affect nucleic acid metabolism.

A

Fluoroquinolones
1. Ciprofloxacin

Rifamycins
2. Rifampin

Nitroimidazoles
3. Metronidazole

Dihydrofolate Reductase inhibitors
4. Cotrimoxazole

Sulfonamides
5. Cotrimoxazole

Others

  1. Daptomycin
  2. Fidaxomicin

PHARMACOLOGY - Antibiotics and Immunosuppressives (12 decks)

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