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Pharmacology 3001 > Antimicrobial Drugs - Dupre > Flashcards

Antimicrobial Drugs - Dupre Flashcards

1
Q

Antimicrobial chemical agents

A

Produced by one organism that have some toxic or inhibitory effect on anther organism or cell
CAN be toxic to cells too

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2
Q

Acids and alkalis

A

Prevents growth

Denatures proteins by changing pH

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3
Q

Heavy metals

A

Inhibit bacterial growth

Denatures proteins

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4
Q

Halogens

A

Hypochlorous acid used in pools with chlorine

Oxidize cell components in absence of organic matter

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5
Q

Alcohols

A

70% alcohols

Denature proteins when mixed with water

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6
Q

Phenols

A

Disrupts membranes, denatures proteins and inactivated enzymes

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7
Q

Oxidizing agents

A

Disrupt disulphide bonds and structure of memrbane

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8
Q

Alkylating agents

A

Disrupts structure of proteins and nucleic acids

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9
Q

Dyes

A

Some interfere with cell replication or block cell wall synthesis

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10
Q

Soaps and detergents

A

Lower surface tension

Make microbes accessible to other agents

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11
Q

Selective toxicity

A

Using toxic drugs, as long as they are more toxic to your target than to normal tissues
Ie. antimicrobial drugs or anticancer drugs

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12
Q

Bactericidal

A

Cells are killed

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13
Q

Bacteriostatic

A

Growth is arrested

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14
Q

Therapeutic window of antibiotics

A

Usually very safe
Large window
Main adverse effects are allergic responses (NOT toxicity) or disturbances of the normal bacterial flora

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15
Q

MIC

A

Minimal inhibitory concentration

Takes about 3 days to reach between doses

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16
Q

Antibiotics

A

Not the same as antimicrobial drugs

Agent produced by one organism that have some toxic or inhibitory effect on cancer, bacteria etc

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17
Q

Bactericidal antibiotics

A

Drugs that cause the death of the bacteria

Required if the patient is immunosuppressed

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18
Q

Bacteriostatic antibiotics

A

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

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19
Q

Features to attack on bacterial cells

A
  1. Completely unique structure (ie. peptidoglycan)
  2. Pathways that are absent in mammalian cells (ie. dihydropteroate synthetase, which produces folic acid which we get from out diet)
  3. Structure that are different between humans and bacterial cells (ie. ribosomes)
  4. Enzymes that differ between humans and bacterial cells
  5. Cellular constituents that are different in microorganisms (ie. lipid ergosterol)
  6. Cellular constituents that are enriched in microorganisms (ie. lipid phosphatiduylethanolamine)
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20
Q

Where antibiotics work

A
  1. Cell wall synthesis
  2. Folic acid metabolism
  3. Cytoplasmic membrane structure
  4. DNA gyrase
  5. RNA elongation
  6. DNA-directed RNA polymerase
  7. Protein synthesis (50S or 30S inhibition or tRNA)
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21
Q

Structure of bacterial cell wall

A

Peptidoglycan causes structure and rigidity

Protection

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22
Q

Peptidoglycan

A

Fibrous scaffold in the wall

Cross-linked network of polysaccharides (repeats of certain amino sugars) by polypeptides

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23
Q

Penicillin-binding protein

A

Enzyme that helps make scaffold in peptidoglycan

At least 6 different types

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24
Q

Beta lactamase

A

Enzyme
Causes resistance to drugs, breaks down common penicillin-like drugs
Susceptible drugs have beta lactic group in their structure

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25
Porins
Protein pores that pierce the membrane
26
Transpeptidation
Step catalyzed by PBPs | Inhibitors: penicillins, cephalosporins, carbepenems
27
Penicillin
Different modifications of core structure Penicillin V, Amoxicillin 1. Crosses wall into bacterium 2. Binds to PBP - inhibits 3. Peptidoglycan is not made 4. Cell looses rigidity 5. Fluid inside exerts outward pressure: lysis
28
Potential problems of antibiotics
1. Getting across the outer lipid membrane into gram-negative bacteria (this is why many antibiotic work against gram positive instead gram negative, unless the negative have porins) 2. Interference by beta lactamases
29
Narrow spectrum penicillins
Penicillin V ( better than G because G breaks down in acid)
30
Extended spectrum penicillins
Amoxicillin | Better absorbed, longer half life
31
Cephalosporins
4 generations, each becoming more resistance to beta lactamases, better activity against gram-negative bacteria, better ability to cross into tissue spaces
32
Carbapenems
ie. Imipenem Penicillin-like antibiotics int which the sulphur atom of the penicillin structure is replaced with carbon Altered spectrum resistant to beta-lactamases
33
Vancomycin
Binding to growing peptide chain | Prevents subsequent ability to crosslink
34
Bacitracin
Mixture of cyclic peptides | Works inside the cell to block cell wall synthesis
35
Antibiotics that block protein synthesis
``` Erythromycin and other macrocodes Tetracyclines Amino glycosides Chloramphenicol Streptomycin ```
36
Combining antibiotics
By blocking different steps, more likely for antibiotics to work overall
37
Streptomycin
Amino glycoside Changes shape of 30S protein Causes code on mRNA to be read incorrectly
38
Tetracyclines
Interfere with attachment of tRNA to mRNA-ribosome complex Broad spectrum (bacteria, mycoplasma, some protozoa) Bacteriostatic Resistance is common Differ mainly in their pharmokinetics Chelate divalent metal ions Absorption affected by milk and antacids Accumulate in developing bone and teeth Should not be used in second half of pregnancy and young children Also cause gastrointestinal irritation (mucosa and flora)
39
Erythromycin
Binds to 50s portion, preventing translation moment of ribosome along mRNA Base is somewhat unstable in acid conditions Food reduces absorption Works well against gram positive organism Generally poor against gram negatives Useful in penicillin resistant infections
40
Chloramphenicol
Broad spectrum Bacteriostatic Binds to 50S portion and inhibits formation of peptide bond Adverse effects: bone marrow disturbances, common interactions with other drugs, gray baby syndrome
41
Macrolides
Ie. erythromycin Work best with gram positive Bacteriostatic
42
Clarithromyin
Chemically modified from erythromycin, with additional methyl group Improved acid stability Improved oral absorption Most active against gram positive anaerobes
43
Azithromycin
Further modified from clarithromycin, with additional lactone ring Excellent tissue penetration Release from tissue only slowly Longer half-life Best activity against gram negative anaerobes Also acts against spirochetes Less likely to become involved in drug interactions
44
Aminoglycoside
ie. entamicin, streptomycin Used mostly against gram-negative enteric bacteria Oral doses are very poorly absorbed Usually given intramuscularly or intravenously Ototoxic and nephrotoxic Hexose ring bonded to amino sugars with glycosidic bonds Blocks formation of initiation complex Miscoding in the polypeptide chain Block of translocation
45
Why are there multiple antibiotics that block protein synthesis?
1. Different chemically, affecting their stability and absorption 2. Interfere at different sites on the bacterial ribosome, which means they have different therapeutic actions
46
Folic acid
Most bacteria make their own Made from PABA via DHPS Then reduced from folate to THF by DHFR
47
Sulfonamides
Target DHPS | Structure similar to PABA
48
Trimethoprim
Blocks DHFR
49
Sulfonamides and trimethoprim together
Synergistic bactericidal More effective than either drug alone Still works if resistance develops to one drug At dose ratio 1:5 (gives plasma ratio of 1:20)
50
DNA gyrase
Cuts DNA temporarily during DNA unwinding Bacterial topoisomerase type II Inhibitors cause replication arrest
51
Fluoroquinolones
Block DNA gyrase enzyme ie. ciprofloxacin Early drugs were quinolones, but were fluorinated as it made them more useful against systemic infections Many respiratory pathogens are now resistant
52
Polymyxins
``` Detergent-like properties Interferes with integrity of bacterial cell membrane Binds to phosphatidylethanolamine Causes disruption of the bacterial cell membrane Toxic if systemic (we have PE too) Resistance rarely develops Hypersensitivity is rare Used topically ```
53
Advantages of using antimicrobial drugs in combinations
Wider spectrum for mixed infections Reduced dose for individual agents Synergism between antibiotics
54
Risks of using antimicrobial drugs in combinations
Increased possibility of adverse reactions Antagonism between antibiotics Greater risk of antibiotic resistance
55
Septra
Combination of sulfamethoxazole and trimethoprim | Both bacteriostatic, together became bactericidal
56
Antibiotic resistance
1. Beta-lactamase 2. Mutations in proteins If antibiotics are used too freely Bacteria are agile
57
Bacterial adaptation
1. Reduced entry of the antibiotic into the bacteria 2. Increased amount of target protein 3. Lower binding to altered target protein 4. Enzyme breakdown of the drug
58
Sulfanamide resistance
1. Decreased permeability of the cell membrane 2. Bacteria produce a form of dihyropteroate synthetase (DHPS) that binds to sulfanamide poorly 3. Increase production of PABA by the bacteria
59
Trimethoprim resistance
1. Decreased permeability of the cell membrane 2. Bacteria produce a form of dihyrofolate reductase (DHFR) that binds trimethoprim poorly 3. Bacteria produce more DHFR
60
Double antibiotic resistance
Way to eradicate resistance strain infections Link two of them: beta-lactam antibiotic with quinolone If betalactamase is present, quinolone is released, if not, beta-lactam antibiotic does the work
61
Antifungals in oral candidiasis
Candidiasis is most common type of oral fungal infection | Oral ketoconazole, oral fluconazole, intravenous amphotericin B
62
Oral ketoconazole
Treatment in oral candidiasis | Potentially hepatotoxic
63
Oral fluconazole
Treatment in oral candidiasis Potentially hepatotoxic (alternative to ketoconazole, less toxic) Azole fungal drug Works through ergosterol Less toxic than polyene antifungals Acts by inhibiting fungal cytochrome P450 (lower affinity for human P450)
64
Intravenous amphotericin B
Treatment in oral candidiasis Significantly toxic and may cause renal damage Polyene macrolide antibiotics Lipophilic on one side and hydrophilic on the other, makes pore
65
Ergosterol
Main target of antifungals Lipid in fungal cell membrane (equivalent to our cholesterol) Antifungals bind and form pores that leak out contents or bind enzymes that important in making ergosterol

Pharmacology 3001 (19 decks)

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