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PMCOL 200 > 22 Antibiotic Medications > Flashcards

22 Antibiotic Medications Flashcards

1
Q

Bacteria have two different types of cell wall, how is this used by scientists?

A

Feature is used to classify bacteria into gram-positive and gram-negative

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2
Q

Where does gram-negative and gram-positive come from?

A

Reaction different bacteria cell walls have to a gram stain:

  • Old imaging technique used to label and identify bacteria strains
    • Because of structure of cell membrane
  • Gram-negative - appear pink after washing the stain off
    • have thin cell wall with few layers of peptidoglycan surrounded by second lipid membrane containing lipopolysaccharides and lipoproteins
  • Gram-Positive - appear dark purple after staining
    • thick cell wall with many layers of peptidoglycan
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3
Q

What is the difference between the celll-walls in Gram-positive and Gram-negative bacteria?

A
  • Gram-positive bacteria:
    • Possess a thick cell wall with many layers of peptidoglycan (polysaccharide chain)
    • Gram-stain binds to the peptidoglycan layer
  • Gram-negative bacteria
    • Relatively thin cell wall with few layers of peptidoglycan surrounded by a second lipid membrane containing lipopolysaccharides
    • less peptidoglycan + extra lipid membrane = absorbs less stain
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4
Q

Peptidoglycan structure consists of ______ strands made of alternating ___________ and ____________ residues cross-linked by peptides

A

Peptidoglycan structure consists of glycan strands made of alternating N-acetylglucosamine (GlcNAc) and N-acetylmuramic acid (MurNAc) residues cross-linked by peptides

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5
Q

What part of the bacteria cell membrane has the greatest contribution to the overall structure and shape of the bacterium?

A

Peptide cross-linkers between glycan strands

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6
Q

Individual strands of glycan are polymerized by the enzyme ________ into the peptidoglycan chain

A

Individual strands of glycan are polymerized by the enzyme glycosyltransferase (GT) into the peptidoglycan chain

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7
Q

What enzyme is responsible for generating the peptide cross-links that provide the structure to the bacteria cell membrane?

A

Transpeptidase (TP)

  • target of many antibiotics (aka penicillin-binding protein)
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8
Q

What are four terms used to describe the efficacy and potency of antibiotics?

A
  1. Spectrum of activity
  2. Bacterial sensitivity
  3. Therapeutic index
  4. Ability to penetrate
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9
Q

What is Spectrum of activity?

A

Spectrum of activity can be narrow or broad depending on the number of different bacterial species against which they exhibit useful activity

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10
Q

What is bacterial sensitivity?

A

Sensitivity measured by assessing the ability of the bacterial strain to replicate following antibiotic exposure

  • Bacteriocidal antibiotic leads to permanent loss of replicative ability
  • Bacteriostatic antibiotic leads to temporary loss of growth and replication that returns following the removal of antibiotics
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11
Q

________\_ antibiotic leads to permanent loss of replicative ability

A

Bacteriocidal antibiotic leads to permanent loss of replicative ability

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12
Q

_________\_ antibiotic leads to temporary loss of growth and replication that returns following the removal of antibiotics

A

Bacteriostatic antibiotic leads to temporary loss of growth and replication that returns following the removal of antibiotics

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13
Q

What is the difference between broad spectrum and narrow spectrum antibiotics?

A

Broad-spectrum: Kills off/targets a variety of bacterial species

Narrow-spectrum: targets 1-a few species of bacteria

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14
Q

What is therapeutic index?

A

Ratio of minimum concentration likely to produce an adverse effect to the minimum concentration needed to produce a desired effect

  • Wide Therapeutic index = safer
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15
Q

What is Ability to penetrate?

A

Ability of drug to get to target;

Delivery of antibiotic to site of infection is most difficult challenge of antibiotic delivery

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16
Q

What are four classes of antibiotics?

A
  1. Cell wall inhibitors
  2. Folic acid
  3. DNA synthesis inhibitors
  4. Protein synthesis inhibitors
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17
Q

How do antibiotics not target “self” (eukaryotic cells)

A

Antibiotics are designed to target pathways that are unique to bacteria (ie not found in eukaryotic cells)

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18
Q

What was the first cell-wall inhibitor developed?

A

Penicillin

-discovered by alexander fleming in 1928 - produced by fungus penicillium notatum

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19
Q

What antibiotic was derived from the fungus Acremonium in 1945 (similar to penicillin in that it is a cell-wall inhibitor)

A

Cephalosporins

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20
Q

Penicillins and cephalosporins are called ________ because they have an unusual 4-member ring

A

Penicillins and cephalosporins are called beta-lactams because they have an unusual 4-member ring

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21
Q

How do Penicillins and cephalosporins work?

A
  • Inhibit cell wall synthesis by inhibiting an enzyme (DD-transpeptidase (aka penicillin-binding protein)) responsible for cross-linking components of the cell wall (bacteriocidal)
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22
Q

Are penicillins and cephalosporins bacteriocidal or bacteriostatic?

A

Bacteriocidal - permanent destruction of the bacteria (interfering with outer structure of cell kills bacteria)

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23
Q

Do penicillins and cephalosporins target gram-negative or gram-positive bacteria?

A

Originally were only effective against gram-positive but successive generations of cephalosporins have increased activity against gram-negative (although still more effective against gram-positive bacteria)

  • Why?
    • because gram-positive bacteria have an exposed outer peptidoglycan layer = easily accessible
24
Q

What are beta-lactamases?

A

Bacterial enzymes (penicillinases, cephalosporinases) made by most staphylococci and many gram-negative organisms that hydrolyze the beta-lactam ring of certain penicillins and cephalosporins; confer resistance

  • defense mechanism
  • ARMS RACE
25
Q

What are beta-lactamase inhibitors? Provide an example.

A

Potent inhibitors of beta-lactamases used in combinations to protect hydrolyzable penicillins (antibiotics) from inactivation

eg: Clavulanic acid

26
Q

What drug named in lecture is NOT a beta-lactam but, like beta-lactams, inhibits the peptidoglycan cross-linking?

A

Vancomycin is not a beta-lactam but inhibits peptidoglycan cross-linking

27
Q

________ is produced in nature by actinobacteria species, Amycolatopsis orientalis, commonly found in soil

A

Vancomycin is produced in nature by actinobacteria species, Amycolatopsis orientalis​, commonly found in soil

28
Q

Make a flowchart of three bacterial cell wall inhibitors:

1 2 3

Narrow and/or broad

Species

A
  1. Penicillins
    • Narrow spectrum
      1. Penicillinase susceptible
      2. Penicillinase Resistant
  2. Cephalosporins
    • Narrow Spectrum
      • 1st generation
    • Wider spectrum
      • 2nd, 3rd, 4th generations
  3. Miscellaneous
    • Carbapenems
    • Aztreonam
    • Vancomycin
29
Q

Why do bacteria need folic acid?

A

Bacteria use folic acid to synthesize nucleic acids that make up their DNA

(pathway unique to bacteria)

30
Q

What is the synthesis pathway that bacteria use to make DNA?

A
  1. p-Aminobenzoic acid (PABA) - precursor for folate
  2. converted to Dihydrofolic acid using Dihydropteroate synthase
  3. Converted to Tetrahydrofolic acid by Dihydrofolate reductase
  4. Purines
  5. DNA
31
Q

What is Para-aminobenzoic acid (PABA)?

A

Nutrient obtained from the environment that is the precursor for folate in bacteria

  • converted into dihydrofolic acid and then to tetrahydrofolic acid by dihydropteroate synthase and dihydrofolate reductase respectively
32
Q

Eukaryotes don’t have PABA and must get folic acid from _____

A

Eukaryotes don’t have PABA and must get folic acid from diet

33
Q

What do folic acid inhibitors target?

A

The folate synthesis pathway in bacteria

34
Q

______ and _______ resemble PABA and dihydrofolic acid respectively and interfere with PABA metabolic pathways

A

Sulfonamides and trimethoprim (folic acid inhibitors) resemble PABA and dihydrofolic acid respectively and interfere with PABA metabolic pathways

35
Q

Which folic acid inhibitors compete with PABA

A

Sulfonamides compete with PABA

36
Q

Which folic acid inhibitors compete with Dihydrofolic acid?

A

Trimethoprim competes with dihydrofolic acid for the enzyme: Dihydrofolate reductase

37
Q

Which two folic acid inhibitors are usually given together and why?

A

Sulfonamides and trimethoprim because they block different steps in the synthesis pathway

38
Q

Bacteria make protein from ______ within the bacterial _________ complex. This is unique to bacteria (eukaryotes use 80s ribosomal complex) and so allows targeting by ____________

A

Bacteria make protein from mRNA within the bacterial 70s ribosomal complex. This is unique to bacteria (eukaryotes use 80s ribosomal complex) and so allows targeting by Protein Synthesis inhibitors

39
Q

______\_ transfers an amino acid to the growing amino acid chain (transpeptidation)

A

tRNA (t6) transfers an amino acid to the growing amino acid chain (transpeptidation)

40
Q

What is the name of the process in which amino acids are added to a growing amino acid chain?

A

Transpeptidation

41
Q

__________ and _________ bind to the 50s subunit and block transpeptidation

A

Chloramphenicol and Macrolides bind to the 50s subunit and block transpeptidation

42
Q

Chloramphenicol and Macrolides bind to the and block transpeptidation

A

Chloramphenicol and Macrolides bind to the 50s subunit and block transpeptidation

43
Q

________ bind to the 30s subunit and prevent binding of incoming tRNA

A

tetracyclines bind to the 30s subunit and prevent binding of incoming tRNA

44
Q

tetracyclines bind to the and prevent binding of incoming tRNA

A

tetracyclines bind to the 30s subunit and prevent binding of incoming tRNA

45
Q

How do the effects of Chloramphenicol, Macrolides and Tetracyclines differ?

A

Chloramphenicol and Macrolides bind to the 50s subunit and block transpeptidation

Tetracyclines bind to the 30s subunit and prevent binding of incoming tRNA

image:

C-triangle = chloramphenicol

M-triangle = Macrolides

T-triangle = tetracycline

46
Q

Like tetracyclines, ________ bind to the 30s ribosomal subunit

A

Like tetracyclines, aminoglycosides bind to the 30s ribosomal subunit

47
Q

What are three effects of aminoglycosides (where do they bind)?

A

Aminoglycosides bind the 30s ribosomal subunit and:

  1. Block the initiation of the complex
    • prevent two subunits from coming together
  2. Cause misreading of the code on the mRNA template
    • wrong aa is added (missense) (or no aa at all - nonsense)
  3. inhibit translocation
    • process of releasing protein from ribosome
48
Q

Why dont antibiotics inhibit protein synthesis in human cells as well?

A
  • Selectivity is provided by differences in protein synthesis enzymes between humans and microorganisms and the rapid growth of bacteria
  • eg: chloramphenicol doesn’t bind to the 80s ribosomal rna of mammalian cells, only the 70s ribosomal rna of bacteria
  • eg mammalian cells cannot synthesize folic acid from PABA
49
Q

What is bacterial resistance?

A

The ability of the microbe to resist the effects of antibiotics

  • arms race between antibiotics and bacteria
  • Consequence of evolution via natural selection
    • constant division = increased opportunity for mutation = some mutations may confer a survival advantage against antibioties = survive and divide
50
Q

What are four ways in which bacteria are known to develop bacterial resistance?

A
  1. Drug inactivation or modification
  2. Alteration of binding site
  3. Alteration of metabolic pathways
  4. Reduced drug accumulation
51
Q

“Beta lactamases are enzymes produced by bacteria that inactivate antibiotics”

What type of bacterial resistance is this?

A

Drug inactivation or modification

52
Q

Provide an example of “Alteration of binding site” which leads to bacterial resistance

A

Alteration of penicillin-binding proteins (aka DD-transpeptidase) in methicillin-resistant staphylococcus (MRSA)

53
Q

Provide an example of “Alteration of metabolic pathways” leading to bacterial resistance

A

Sulfonamide resistant bacteria begin to use pre-formed folic acid from the environment rather than making it from PABA

54
Q

Provide an example of reduced drug accumulation leading to bacterial resistance?

A

Develop efflux pumps to actively remove antibiotic from bacterial cell

(similar to p-glycoprotein pumps in the brain that pump drug out of brain)

55
Q

Why might antibiotic use led to gastrointestinal distress?

A

Because, particularly for broad spectrum, they can target the normal gut flora thus interfering with bacterial environment of the body

  • probiotic products can be used in conjunction to help limit/alleviate this
56
Q

What affects might antibiotics have on the skin?

A

Adverse skin reactions ranging from mild rash to photosensitivity.

  • use photoprotection (sunscreen) to help prevent UV damage
  • Stevens-johnson syndrome
  • Toxic epidermal necrolysis
57
Q

What are Stevens-johnson syndrome and toxic epidermal necrolysis?

A

rare conditions in which the skin becomes detaches from the underlying tissue and sloughs off the body

PMCOL 200 (30 decks)

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