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Pharmacology > Antimicrobial Drugs > Flashcards

Antimicrobial Drugs Flashcards

1
Q

Antibiotics Definition

A

Agents produced by one organism that have some toxic or inhibitory effect on another organism or cell
Used to treat bacteria, fungi and cancer cells
NO impact on viruses

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2
Q

Selective toxicity

A

The idea that you can use toxic drugs, which as long as they are more toxic to your target than to normal tissues, can be useful

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3
Q

Bacteriocidal Antibiotics

A

Drugs that cause the death of the bacteria

Required if the patient is immunosuppressed

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4
Q

Bacteriostatic Antibiotics

A

Drugs that inhibit the growth of the bacteria
Growth resumes when the drug is removed
Success depends on there being an effective immune response

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5
Q

6 general features of bacterial cells we can attack

A
  1. A completely unique structure (ex: peptidoglycan)
  2. Pathways that are absent in mammalian cells (folic acid synthesis)
  3. Structures that differ between human and bacterial cells (ribosomal subunits)
  4. Enzymes that differ (ex: DNA gyrase)
  5. Cellular constituents that are different (certain lipids)
  6. Cellular constituents that are enriched (other lipids)
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6
Q

Transpeptidation

A

Forming the cross bridge between the 2 NAMs

Terminal Ala is removed, then first Ala can join to Gly

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7
Q

3 groups of beta lactam drugs that inhibit transpeptidation

A
  1. Penicillins
  2. Cephalosporins
  3. Cabapenems
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8
Q

Why is penicillin V better than G?

A

Penicillin G breaks down in acid

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9
Q

Narrow Spectrum vs Extended-Spectrum

A

Narrow (penicillin V): against Gram + bacteria
Extended (amoxicillin): against Gram + and some Gram - (they are better drugs - wider spectrum, better absorbed, longer half life)

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10
Q

What can we do about the beta lactamases?

A
  1. Use a beta-lactamase-resistant antibiotic (Nafcillin)

2. Combine with a beta lactamase inhibitor (Clavulanate)

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11
Q

What properties have changed from first to 4th generations cephalosporins?

A
  1. Better activity against gram negative bacteria
  2. Better ability to cross into tissue spaces
  3. Generally more resistant to beta lactamases
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12
Q

Carbapenems

A

Ex: Imipenem
Penicillin-like antibiotics in which the sulfur atom of the penicillin structure is replaced with a carbon
Altered spectrum
Resistant to beta-lactamases

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13
Q

Vancomycin

A

Cell Wall synthesis inhibitor
Binds to the growing peptide chain
Prevents subsequent ability to cross link

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14
Q

Bacitracin

A

Cell wall synthesis inhibitor
Mixture of cyclic peptides
Works inside the cell to block cell wall synthesis (stops lipid recycling - no dephosphorylation)

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15
Q

4 drugs that effect the function of ribosomes and how they work

A
  1. Erythromycin and other macrolides (binds to 50S subunit, prevents translocation-movement of ribosome along mRNA)
  2. Tetracyclines (like tetracycline) - interferes with attachment of tRNA to mRNA-ribosome complex
  3. Aminoglycosides such as gentamicin or streptomycin (changes shape of 30S subunit, causes code on mRNA to be read incorrectly)
  4. Chloramphenicol (Binds to 50S portion and inhibits formation of peptide bonds)
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16
Q

Chloramphenicol

A

Broad spectrum, active against many different bacteria
Bacteriostatic
Binds to 50S portion and inhibits formation of peptide bonds
Problems: bone marrow disturbances, common interactions with other drugs, gray baby syndrome

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17
Q

Macrolides

A

Work best against gram positive microorganisms
Bacteriostatic
Include: erythromycin, clarithromycin, azithromycin

18
Q

Erythromycin

A

Macrolide
Base is somewhat unstable in acid conditions
Food reduces absorption
Works well against gram positive organisms
Poor against gram negatives
Useful in penicillin-resistant infections

19
Q

Clarithromycin

A 
Macrolide
Chemically modified from erythromycin
Additional methyl group
Improved acid stability
Improved oral absorption
Most active against gram positives
20
Q

Azithromycin

A 
Macrolide
Further modified from clarithromycin
Additional lactone ring
Excellent tissue penetration
Released from tissue slowly
Longer half-life
Best activity against gram negative anaerobes
Acts against spirochetes
Less likely to become involved in drug interactions
21
Q

Aminoglycosides

examples, targets, route of administration, toxic to what

A

Ex: Streptomycin, gentamicin
Used mostly against gram negative enteric bacteria
Oral doses are very poorly absorbed
Usually given intramuscularly or intravenously
Toxic to ears and kidneys

22
Q

3 functions of aminoglycosides

A
  1. Block formation of the initiation complex
  2. Miscoding in the polypeptide chain
  3. Block of translocation
23
Q

Tetracyclines

A

Broad-spectrum
Active against bacteria, mycoplasma, some protozoa
bacteriostatic
Resistance is common
Chelate divalent metal ions
Adverse effects: GI irritation, accumulate in bone and teeth, teratogenic

24
Q

If macrolides, tetracyclines and aminoglycosides all block protein synthesis in bacteria, why are they different in use?

A
  1. They’re different chemically, which affects things like their stability and absorption.
  2. They interfere at different sites on the bacterial ribosomes, which means they have different therapeutic actions.
25
Q

Where can we attack bacteria?

A
  1. Interfere with their ability to synthesize materials needed for DNA (folic acid)
  2. Cell wall syntheis
  3. Protein synthesis
  4. DNA gyrase
  5. RNA elongation
  6. PM structure
  7. DNA-directed RNA polymerase
26
Q

Sulfamethoxazole/trimethoprim

A

Septra - blocks the folic acid pathway (bacteriocidal)
More effective than either drug alone
Still works if resistance develops to one drug
Used at a dose ration of 1:5, which gives a plasma concentration ratio of 1:20 (optimal)

27
Q

DNA gyrase (topoisomerase type 2)

A

Untangles the DNA in a cell (cuts it)

Fluoroquinolones block it (ex: ciprofloxacin)

28
Q

Fluoroquinolones

A

Inhibit DNA gyrase
Useful against systemic infections
Stop the bacterium form using its DNA
Overuse has lead to widespread resistance (especially respiratory pathogens)

29
Q

Polymyxins

A

Cause disruption of the bacterial membrane
Molecule has detergent like properties
Binds to phosphatidylethanolamine in PM
Problems: humans have PE too, so toxic if given systemically
Advantages: resistance and allergy is rare

30
Q

3 advantages and 3 risks of using antimicrobial drugs in combination

A 
Advantages:
1. Wider spectrum for mixed infections
2. Reduced dose for individual agents
3. Synergism between antibiotics
Disadvantages:
1. Increased possibility of adverse reactions
2. Antagonism between antibiotics
3. Greater risk of antibiotic resistance
31
Q

Example of an antagonistic combination

A

Chloramphenicol and aminoglycoside

32
Q

4 examples of synergistic combinations

A
  1. Cell wall synthesis inhibitors and amino glycosides
  2. Beta lactam drugs and beta lactamase inhibitors
  3. Beta lactams that act on different PBPs
  4. Sulfonamides and trimethoprim
33
Q

5 mechanisms of antibiotic resistance

A
  1. Decreased entry
  2. Efflux pump
  3. Altered target site
  4. Bypass pathway
  5. Enzymatic degradation
34
Q

Sulfonamide resistance may be due to (3 things)

A
  1. Decreased permeability of the cell membrane
  2. The bacteria produce a form of dihydropteroate synthetase that binds teh sulfonamide poorly
  3. Increased production of PABA by the bacteria
35
Q

Trimethoprim resistance may be due to (3 things)

A
  1. Decreased permeability of the cell membrane
  2. The bacteria produce a form of dihydrofolate reductase that binds trimethoprim poorly
  3. The bacteria produce more dihydrofolate reductase
36
Q

3 antifungals to treat candidiasis

A
  1. Ketoconazole (potentially hepatotoxic)
  2. Fluconazole (alternative to ketoconazole and less toxic)
  3. Amphotericin B (for extreme cases given IV, significantly toxic and may case renal damage)
37
Q

2 general ways antifungals work

A
  1. Bind ergosterol and form pores that leak out cell contents
  2. Inhibit enzymes that are important in making ergosterol
38
Q

Amphotericin B

A

Antifungal
Polyene macrolide antibiotic
Large molecule that is lipophilic on one side and hydrophilic on the other (so can form pores in the membrane by binding to ergosterol)
Some binding to human cell membranes so it has nephrotoxicity

39
Q

Fluconazole

A 
Azole antifungal drug
Acts by inhibiting fungal cytochrome P450 enzymes
Stops synthesis of ergosterol
Lower affinity for human P450 enzymes
Less toxic than polyene antifungals
40
Q

Therapeutic Window

A

From the minimal beneficial effects to minimal toxic effects

41
Q

Therapeutic index

A

Toxic dose 50/ Effective dose 50

Pharmacology (18 decks)

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