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PMCOL 200 > Antibiotics > Flashcards

Antibiotics Flashcards

1
Q

What are antibiotics? And 2 kinds?

A

Soluble compounds produced/released by microorganisms that inhibit growth/kill other microorganisms (bacteria for competition); synthetic and semi-synthetic

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2
Q

What are bacteria? (2)

A

Single cell organisms that are of the first life forms on Earth

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3
Q

What 4 habitats can bacteria be found in?

A

found in soil, water, acidic hot springs, Earth’s crust

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4
Q

What relationship do bacteria have w/ plants and animals?

A

symbiotic and parasitic relationship w/ plants and animals

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5
Q

Where are symbiotic bacteria found?

A

GI tract

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6
Q

What are 3 criteria for bacteria classification?

A

Aerobic/anaerobic, shape (rod, sphere, spiral, etc), cell wall

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7
Q

What are the names for rod and sphere shapes in bacteria?

A

Rod: bacillus (streptobacillus- chain)
Sphere: coccus (streptococcus-chain)

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8
Q

What are 2 types of bacterial cell walls?

A

Gram - (pink) and + (purple)

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9
Q

What is diff btwn cell walls of gram -/+ bacteria?

A

+: many layers of peptidoglycan (thick)

-: few layers of peptidoglycan (thin) w/ outer lipid memb (lipopolysacch and lipoproteins)

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10
Q

What are bacterial cell walls made of?

A

peptidoglycan (polysacch)

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11
Q

What causes the diff colours fo gram +/- bacteria?

A

Gram stain colours peptidoglycan purple
+: purple (outer peptidoglycan layers)
-: pink (lipid memb protects peptidoglycan)

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12
Q

What kind of cell wall do most bacteria have?

A

Gram - (lipid layer around peptidoglycan)

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13
Q

What is the structure of peptidoglycan?

A

Glycan strands w/ alternating N-acetylglucosamine (GlcNAc) and N-acetylmuramic acid (MurNAc) residues cross linked by peptides

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14
Q

What enzyme polymerizes individual strands of peptidoglycan chain?

A

Glycosyltransferase (GT)

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15
Q

What enzyme cross links peptidoglycan strands?

A

Transpeptidase (TP)

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16
Q

T/f: transpeptidase is targeted by antibiotics (penicillin binding protein)

A

True

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17
Q

What are normal flora?

A

Microbial species that cover our bodies (skin, mouth, lg intestine, and genitals)

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18
Q

When does normal flora cause problems? (2)

A

Immune system is weakened, gain access to normally sterile areas (perforated bowel)

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19
Q

T/f: pathogens require host to be immune-compromised/injured for infection

A

False, dont require host to be immune compromised/injured for infection

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20
Q

What are 4 diseases caused by pathogenic bacteria?

A

Food borne illnesses, STIs, skin infections, highly infectious diseases

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21
Q

T/f: prior to 1930/40s, it was common for otherwise healthy individuals to die from bacterial infections that are considered commonplace/non threatening

A

True

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22
Q

What antibiotics were developed in 1930s vs 1940s?

A

1930: sulfonamides
1940: penicillins

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23
Q

What does antibiotic “spectrum of activity” mean? And 2 types?

A

Range of bacterial species the antibiotic targets; narrow and broad

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24
Q

What does antibiotic “bacterial sensitivity” mean? 2 types?

A

Measures antibiotic ability to kill or prevent replication of bacteria;
bactericidal and bacteriostatic

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25
Q

What’s the difference btwn bacteriocidal vs bacteriostatic antibiotics?

A

Bacteriocidal: causes permanent loss of bacteria’s replicative ability
Bacteriostatic: causes temporary loss of bacteria’s growth and replication which returns after antibiotic removal

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26
Q

What does antibiotic “therapeutic index” mean?

A

Ratio of min conc needed to produce and adverse effect: min conc for desired effect (bigger is better)

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27
Q

What is an antibiotics “ability to penetrate” mean?

A

Bioavailability/ability of antibiotic to reach the site of infection

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28
Q

What is the most difficult challenge of antibiotic delivery?

A

Ability to penetrate

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29
Q

What are 4 classes of antibiotics?

A

Cell wall inhibitors, folic acid inhibitors, DNA synthesis inhibitors, protein synthesis inhibitors (pathways are diff to euk cells)

30
Q

What is penicillin derived from?

A

Penicillium notatum

31
Q

What is an ex of a cell wall inhibitor?

A

Penicillin

32
Q

Who and when was penicillin discovered?

A

Alexander Fleming in 1928

33
Q

What was the first antibiotic commercially developed?

A

Penicillin

34
Q

What are cephalosporins derived from?

A

Acremonium fungus

35
Q

What are penicillins and cephalosporins called? Why?

A

Beta lactams; have 4 membered ring

36
Q

What do beta-lactams do? (Penicillin and cephalosporins)

A

Inhibit cell wall synthesis by inhibiting DD transpeptidase that cross-links components of cells walls

37
Q

Are beta-lactams (penicillin and cephalosporins) considered bacteriocidal or bacteriostatic?

A

Bacteriocidal (inhibit cell wall synth-cause cell death)

38
Q

What is DD transpeptidase aka?

A

Penicillin binding protein

39
Q

What were cell wall inhibitors originally most effective against?

A

Gram positive (peptidoglycan on outside) but can work on gram - but less effectively

40
Q

What are beta-lactamases?

A

Bacterial enzymes (penicillinases, cephalosporinases) that hydrolize beta-lactam ring of penicillins and cephalosporins

41
Q

What are beta-lactamases made by (2) and confer?

A

Staphylococci and other gram - organisms; confers resistance

42
Q

What are beta-lactamase inhibitors? When are they used?

A

Potent inhibitors of beta-lactamases used w/ penicillins to protect from hydrolysis/inactivation

43
Q

What is vancomycin? What makes is different?

A

Cell wall inhibitor; not a beta-lactam

44
Q

How does vancomycin work?

A

Inhibits peptidoglycan cross linking

45
Q

What produces vancomycin in nature? Ex?

A

Actinobacteria species; Amycolatopsis orientalis in soil

46
Q

Why would bacteria make antibiotics?

A

For competition against other bacteria

47
Q

Why are folic acid inhibitors good antibiotics?

A

Bcse bacteria use folic acid to synthesize nucleic acids for DNA

48
Q

What is para-aminobenzoic acid (PABA)?

A

Precursor to folate in bacteria obtained from enviro

49
Q

T/f: euk also use folic acid to build folic acid, but it is obtained from diet not synthesized from PABA

A

True, only bacteria use PABA pathway for folic acid synthesis

50
Q

What are 2 folic acid inhibitors? How do they work?

A

Sulfonamides and trimethoprim; interfere w/ PABA pathway to sequentially inhibit folic acid synthesis when used together

51
Q

What do sulfonamides and trimethoprim resemble respectively?

A

Sulfonamides: PABA
Trimethoprim: dihydrofolic acid

52
Q

How does using sulfonamides and trimehtoprim inhibit folic acid synthesis?

A

Competes w/ PABA and dihydrofolic acid for enzyme, respectively

53
Q

What are 3 protein synthesis inhibitors?

A

Chloramphenicol, tetracyclines, macrolides

54
Q

Where do bacteria make proteins from mRNA?

A

70s ribosomal complex

55
Q

What transfers aa to the growing peptide chain in bacteria?

A

tRNA (t6)

56
Q

What is the process of adding aa to growing peptide chain in bacteria called?

A

Transpeptidation

57
Q

What ribosomal complex do euk have? Benefit?

A

80s; are unaffected by protein synthesis inhibitors

58
Q

What 2 antibiotic drugs bind to the 50s subunit of the 70s ribosome?

A

Chloramphenicol and macrolides

59
Q

What antibiotics bind to the 30s subunit of the 70s ribosome?

A

Tetracyclines

60
Q

What is the difference in mech of action btwn chloramphenicol/macrolides and tetracyclines?

A

(Both inhibit protein synthesis)
Chlor/macrolides: block transpeptidation
Tetracyclines: prevent binding of incoming tRNA

61
Q

What is another antibiotic that binds to the 30s subunit but blocks protein synthesis in 3 ways?

A

Aminoglycosides

62
Q

What 3 ways do aminoglycosides inhibit protein synthesis?

A
  1. Block joining of ribosomal subunits
  2. Misreading of mRNA template
  3. Block translocation (protein release from ribosome)
63
Q

Why dont protein synthesis inhibit human cells as well?

A

Difference in enzyme specificity btwn bacteria vs euk, diff shape of ribosome (70s vs 80s), diff metabolic pathways (PABA to folic acid)

64
Q

What is the most common antibiotic side effects?

A

Bacterial resistance

65
Q

What is bacterial resistance?

A

Ability of microbe to resist effects of antibiotics as a consequence of natural selection (mutation that allows survival will persist)

66
Q

What 4 ways can bacteria develop resistance? And ex (already discussed)?

A
  1. Drug inactivation/modification (beta-lactamases)
  2. Alteration of binding site (penicillin binding proteins-transpeptidases)
  3. Alteration of metabolic pathways (retrieve PABA from enviro to avoid synthesis)
  4. Reduced drug accumulation (efflux pumps to remove antibiotic from cell)
67
Q

How do antibiotics affect the GI tract causing distress? Effect?

A

Alters bacterial enviro (normal flora) which causes diarrhea or discomfort

68
Q

What can minimize GI effects of antibiotics?

A

Probiotics (active culture in yogurts)

69
Q

What is another (not GI) side effect of antibiotics? Prevention?

A

Adverse skin runs (mild rash to photo sensitivity); sunscreen

70
Q

What are Stevens-Johnsons syndrome and toxic epidermal necrolysis?

A

Rare conditions where skin becomes detached from underlying tissues and sloughs off body (can be lethal)

PMCOL 200 (27 decks)

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