chapter 10 learning objectives Flashcards

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1
Q

explain the principle of selective toxicity

A

an effective antimicrobial agent must be more toxic to a pathogen than to the pathogen’s host

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2
Q

list six mechanisms by which antimicrobial drugs affect pathogens

A
  1. inhibition of pathogen’s attachment or entry into host cell
  2. inhibition of DNA or RNA synthesis
  3. inhibition of general metabolic pathway
  4. inhibition of cell wall synthesis
  5. inhibition of protein synthesis
  6. disruption of cytoplasmic membrane
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3
Q

describe the actions of drugs that affect the cell walls of bacteria and fungi

A

bacteria and fungi have cell walls while humans and animals don’t. most common antibacterial agents prevent the cross-linkage of NAM subunits. it is common that they prevent bacteria from increasing the amount of cell wall, but don’t affect the existing layer, so it is only effective on growing cells.

fungal walls composed of various polysaccharides containing a sugar, 1,3-D-glucan. drugs inhibit the enzyme that synthesizes glucan

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4
Q

describe the basic activities of drugs that interfere with protein synthesis

A

antimicrobial agents selectively target bacterial protein translation without significantly affecting eukaryotes (remember bacteria–prokaryotes–have 70s ribosomes

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5
Q

describe the action of drugs that interfere with cytoplasmic membranes

A

some drugs act by forming a channel through the membrane. certain drugs disrupt transport across the cytoplasmic membrane while others change the permeability of cytoplasmic membranes of parasites.

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6
Q

describe the action of drugs that disrupt synthesis of folic acid

A

sulfonamides disrupt folic acid synthesis and prevent DNA and RNA from forming

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7
Q

describe the antimicrobial action of nucleotide and nucleoside analogs, quinolones, drugs that bind to DNA and RNA, and reverse transcription inhibitors

A

nucleotide/nucleoside analogs can distort shapes of nucleic acid molecules and prevent further replication, transcription, or translation.

quinolones act against prokaryotic DNA gyrase but have little effect on eukaryotes or viruses.

several drugs function by blocking DNA replication or mRNA transcription and other drugs bind to and inhibit action of RNA polymerase during transcription.

reverse transcription inhibitors act against reverse transcriptase, an enzyme HIV uses early in its replication cycle (humans lack transcriptase so it doesn’t harm them)

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8
Q

describe the action of antimicrobial attachment antagonists

A

viruses must attach to their host’s cells via chemical interaction between attachment proteins on the virus and complementary receptor proteins on a host cell.

attachment can be blocked by peptide and sugar analogs of attachment or receptor proteins

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9
Q

distinguish narrow-spectrum drugs from broad-spectrum drugs in terms of their targets and side effects

A

broad spectrum- killing of normal flora reduces microbial antagonism. it may allow for secondary infections or superinfections

narrow spectrum- more specific and target only one thing or bacteria at a time

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10
Q

discuss the advantages and disadvantages of the different routes of administration of antimicrobial drugs

A

oral- it is simple and the patient can administer to self, but it has a lower concentration and patients don’t always follow instructions

intramuscular and one-time intravenous- fast acting but requires needle and concentration less than IV

continuous intravenous- fast acting and highest drug concentration but it requires needle or catheter, and liver and kidneys breakdown drug and remove it from the body

antimicrobial agents are distributed to infected tissues by the blood. blood vessels in the brain, spinal cord, and eye are almost impermeable to many antimicrobial agents (blood-brain barrier) so infections in these areas are often difficult to treat

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11
Q

identify three main categories of side effects of antimicrobial therapy

A

toxicity, allergies, and disruption of normal microbiota

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12
Q

describe how populations of resistant microbes can arise

A

a population may contain a few organisms that are either naturally, partially, or completely resistant. resistance can be acquired either by new mutations of chromosomal genes or through acquisition of resistance genes through horizontal gene transfer (transformation, transduction, or conjugation)

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13
Q

list seven ways by which microbes can be resistant to antimicrobial drugs

A
  1. resistant cells may produce an enzyme that destroys or deactivates the drug
  2. resistant microbes may slow or prevent entry of drug into cell
  3. resistant cells may alter the target of the drug so that the drug either cannot attach to it or binds it less effectively.
  4. resistant cells may alter their metabolic chemistry or they may abandon the sensitive metabolic step altogether.
  5. resistant cells may pump the antimicrobial out of the cell before the drug can act
  6. bacteria within biofilms resist antimicrobials more effectively than free-living cells
  7. protection of the target of an antimicrobial drug
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14
Q

list two ways that genes for drug resistance are spread between bacteria

A

new mutations of chromosomal genes

acquisition of resistance genes through horizontal gene transfer

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15
Q

define cross resistance, and distinguish it from multiple resistance

A

cross resistance- resistance to one antimicrobial agent may confer resistance to similar drugs (typically when they occur in the same structure)

multiple resistance pathogens (superbugs) are resistant to three or more types of antimicrobial agents

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16
Q

describe four ways to retard development of resistance

A
  1. high concentration of drug maintained in patient long enough to kill all sensitive cells and inhibit others so immune system can destroy (finish entire prescription)
  2. use antimicrobial agents in combination (synergism- one drug enhances the effect of the second drug)
  3. limit the use of antimicrobials to necessary cases
  4. develop semisynthetic drugs, search for new antimicrobials, or synthetically design drugs