Introduction to antibiotics Flashcards

1
Q

what is the main principle of antimicrobial chemotherapy?

A

drugs should be toxic to invading microorganisms but not to the host.

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2
Q

what is the key feature of bacterial cells?

A

no nucleus

peptidoglycan cell wall

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3
Q

what is the limitation of class 1 bacterial metabolism as a drug target?

A

its similar to host reactions, multiple pathways to produce energy
produce ATP and simple carbon compounds

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4
Q

what is advantage of class 2 bacterial metabolism as a drug target?

A

the folate biosynthetic pathway.

use energy and class one compounds to make small compounds

humans can make folate from diet, bacteria lack folate transporters

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5
Q

what is the main advantage of class 3 bacterial metabolism as a drug target?

A

good target as it better differentiates between pathogen and host cells

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6
Q

what is class 2 reactions

A

use ATP and class 1 compounds to make small molecules

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7
Q

what are sulphonamides?

A
are a class of antibiotics that inhibit bacteria from producing its own folate.
this can commonly cause allergic reactions so is avoided
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8
Q

what is trimethoprim?

A
a class of antibiotics that inhibits dihdryofolate reductase in bacteria .
it doesn't affect human production of tetrahydrofolate.
this can be used to treat urine infections
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9
Q

what is an advantage of trimethoprim?

A

it can be used to treat gram positive and negative bacteria.
its a broad spectrum antibiotic.

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10
Q

what is a class 3 reaction?

A

converts starch into macromolecules

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11
Q

what is an advantage of class 3 reactions as a target site?

A

better at differentiating between pathogen and host cell

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12
Q

what is penicillin and cephalosporins better at treating?

A

both used for gram positive infections

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13
Q

what infection type is harder to treat with antibiotics?

A

gram negative

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14
Q

what are the bacterial ribosomes?

A

50s and 30s

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15
Q

what are the human ribosomes?

A

60s and 40s

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16
Q

how do tetracyclines work?

A

by preventing tRNA binding to the ribosome

17
Q

how does chloramphenicol work?

A

it inhibits transpeptidation - causing premature termination of peptide chain

18
Q

how does aminoglycosides work?

A

disrupt codon ; anticodon - misreading of message

19
Q

how do macrolides work?

A

disrupt translocation (moving on of used tRNA)

20
Q

name three examples of broad spectrum antibiotics

A

trimethoprim, macrolides and tetracylclines

21
Q

what do anti-viral drugs target?

A

different stages of the viral replication stage

22
Q

what are the 7 steps of the viral replication stage?

A
  1. attachment
  2. penetration
  3. uncoating
  4. replication of nucleic acid
  5. synthesis of protein coats
  6. assembly
  7. release
23
Q

what stage of viral replication does tamiflu work on (for influenza)

A
  1. release

tamiflu is a neuraminidase inhibitor

24
Q

what stage of viral replication is acyclovirs target (drug for herpes virus)

A
  1. replication of nucleic acid
25
what stage of viral replication is the target for HIV treatment?
multiple stages 1. attachement 2. penetration 4. replication of nucleic acid 6. protease inhibitors
26
what are some of the mechanisms of bacterial antibiotic resistance?
- production of enzymes that inactivate drug e.g. beta lactamases - alteration of drug binding site e.g. penicillin - reduction of drug update by bacterium e.g. tetracylclines - alteration of enzyme pathways e.g. trimethoprim
27
what class stage is of bacterial reactions if peptidoglycan produced in?
class 3 reactions
28
what is the mechanism of action of penicillin?
penicillin forms covalent bonds with proteins with transpeptidase and carboxypeptidase activity. inhibits binding of cross linking peptides to peptidoglycan side chains
29
what class of antiviral drugs is used to treat herpes virus infection?
guanosine analogues ie. acyclovir prevents nucleic acid synthesis and are used in the treatment of herpes virus infections
30
what would be the main and most important reason drugs shouldn't be used to treat viral sore throats?
it increases antibiotic resistance - therefore decreasing the effectiveness of antibiotics