CHAPTER 7 Flashcards

1
Q

DRUGS

A

chemicals that affect physiology in any manner

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2
Q

CHEMOTHERAPEUTIC AGENTS

A

drugs that act against diseases

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3
Q

ANTIMICROBIAL DRUGS

A

drugs that treat infections (antibiotics, synthetic chemicals, semisynthetic)

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4
Q

ANTIBIOTICS

A

substances produced by living organisms that can inhibit or destroy other microbes

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5
Q

SYNTHETIC CHEMICALS

A

antimicrobials that are completely synthesized in a lab

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6
Q

SEMISYNTHETICS

A

chemically altered antibiotics that are more effective, longer lasting, or easier to administer than naturally occurring ones

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7
Q

BETA LACTAMS

A

inhibition of cell wall synthesis, prevent bacteria from increasing amount of peptidoglycan, have no effect on existing peptidoglycan layer, effective only for growing cells

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8
Q

PENICILINS

A

a molecule that inhibits the growth of staphylococcus aureus bacteria discovered in 1928 by Alexander Fleming

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9
Q

CEPHALOSPORINS

A

beta-lactam antimicrobials used to manage a wide range of infections from gram-positive and gram-negative bacteria

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10
Q

CARBAPENEMS

A

a class of very effective antibiotic agents commonly used for the treatment of bacterial infections

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11
Q

VANCOMYCIN

A

interfere with bridges that link NAG subunits in many Gram-Positive bacteria

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12
Q

BACITRACIN

A

blocks transport of NAG and NAM from cytoplasm

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13
Q

ISONIAZID

A

disrupt mycolic acid formation in mycobacterial species

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14
Q

ETHAMBUTOL

A

disrupt mycolic acid information in mycobacterial species (treats tuberculosis)

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15
Q

PROTEIN SYNTHESIS INHIBITORS

A

two general mechanisms. Interference with bacterial ribosomes and with charging of transfer RNA molecules

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16
Q

AMINOGLYCOSIDES

A

a medicinal and bacteriologic category of traditional gram-negative antibacterial medications that inhibit protein synthesis and contain a portion of the molecule an amino-modified glycoside (sugar)

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17
Q

TETRACYCLINE

A

antibiotic that treats acne

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18
Q

CHLORAMPHENICOL

A

antibiotic that is used to treat serious infections in different parts of the body, sometimes given with other antibiotics

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19
Q

LICOSAMIDES

A

anticonvulsant that treats partial seizures

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20
Q

STREPTOGRMINS

A

a class of antibiotics that work by inhibiting the synthesis of protein in bacteria

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21
Q

MACROLIDES

A

a class of drugs used to manage and treat various bacterial infections. (Azithromycin, clarithromycin, and
erythromycin are commonly used to treat infections like pneumonia, sinusitis, pharyngitis, and tonsillitis.)

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22
Q

ANTISENSE NUCLEIC ACIDS

A

single-stranded oligonucleotides that have been specifically chemically modified which can bind to RNA expressed by target genes through base complementary pairing & affect protein synthesis at the level of
posttranscriptional processing or protein translation

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23
Q

MUPIROCIN

A

an antibiotic that treats skin infections

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24
Q

POLYMYXIN

A

disrupts the LPS and cytosolic membranes of gram-negative bacteria

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25
Q

NYSTATIN AND AMPHOTERICIN B

A

attach to ergosterol in fungal membranes

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26
Q

AZOLES AND ALLYLAMINES

A

inhibit ergosterol synthesis

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27
Q

METABOLIC ANTAGONIST

A

a type of “cytotoxic” type of drug that kills cells by mimicking the molecules that a cell needs to grow (sulfonamides and trimethoprim)

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28
Q

SULFONAMIDES

A

a class of synthetic antimicrobial drugs that are pharmacologically used as broad spectrum for the treatment of human and animal bacterial infections

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29
Q

TRIMETHOPRIM

A

an antibiotic and folate synthesis inhibitor that can treat infections including urinary tract and ear infections

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30
Q

ATOVAQUONE

A

an antifungal and anti-parasite that is used to treat and prevent Pneumocystis carinii pneumonia (PCP)

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31
Q

BLOCKERS OF UNCOATING

A

antiviral drugs that block viral un-coating and attachment

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32
Q

PROTEASE INHIBITORS

A

medications that help slow the progression of HIV, by blocking the enzyme “protease” which HIV cells need to develop and mature. (This blocks the virus from making copies of itself)

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33
Q

HEAVY METALS

A

enzymes that are denatured by drugs

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34
Q

NUCLEIC ACID SYNTHESIS INHIBITORS

A

drugs often affect both eukaryotic and prokaryotic cells, not normally used to treat infections, used in research and perhaps slow cancer cell replication

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35
Q

INHIBITORS OF DNA REPLICATION

A

gyrase inhibitors, nucleotide or nucleoside analogs, reverse transcriptase inhibitor

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36
Q

GYRASE INHIBITORS

A

quinolones (synthetic drugs) that inhibit DNA replication process

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37
Q

QUINOLONES AND FLUOROQUINOLONES

A

act against prokaryotic DNA gyrase

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38
Q

NUCLEOTIDE OR NUCLEOSIDE ANALOGS

A

interfere with function of nucleic acids, distort shapes of nucleic acid molecules and prevent further replication, transcription, or translation, most often used against viruses, effective against viruses

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39
Q

REVERSE TRANSCRIPTASE INHIBITORS

A

act against an enzyme HIV uses in its replication cycle, does not harm people because humans lack reverse transcriptase

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40
Q

INHIBITORS OF TRANSCRIPTION

A

nucleotide and nucleoside analogs, RNA polymerase inhibitors

41
Q

ATTACHEMENT ANTAGONISTS

A

block viral attachment or receptor proteins

42
Q

THERAPEUTIC INDEX

A

a quantitative measurement of the relative safety of a drug. (a comparison of the amount of a therapeutic agent that causes the therapeutic effect to the amount that causes toxicity)

43
Q

SPECTRUM OF ACTION

A

the range of bacterial types against which the antibiotic is effective, where these types often are measured in terms of inherent sensitivities

44
Q

NARROW SPECTRUM

A

effective against few organisms

45
Q

BROAD SPECTRUM

A

effective against many organisms

46
Q

DIFFUSION SUSCEPTIBILITY TESTS

A

determines which antibiotics are effective against specific species of bacteria

47
Q

MINIMUM INHIBITORY CONCENTRATION TEST (MIC)

A

test that determines the lowest concentration of an antimicrobial drug that can inhibit the growth of an organism or MIC value

48
Q

MINIMUM BACTERIAL CONCENTRATION TEST (MBC)

A

test that determine the lowest concentration of an antimicrobial drug that can kill an organism or MBC value

49
Q

TOPICAL

A

application of drug for external infections

50
Q

ORAL ROUTE

A

requires no needles and is self-administered

51
Q

INTRAVENOUS

A

administration delivers drug directly to bloodstream

52
Q

MULTIPLE DRUG RESISTANCE

A

pathogen can acquire resistance to more than one drug, common when R plasmids exchanged, develop in hospitals and nursing homes (constant use of drugs eliminates sensitive cells), multiple-drug-resistant pathogens are resistant to at least three antimicrobial agents

53
Q

This chapter focuses on which of the 3 fundamental types of antimicrobial agents?

A

Physical agents, chemical agents, and chemotherapeutic agents

54
Q

Any chemical substance that can affect the physiology of an organism is called a?

A

Drugs

55
Q

Drugs that are used to treat diseases are called?

A

Chemotherapeutic agents

56
Q

Drugs that are used to treat infections are called?

A

Antimicrobial drugs

57
Q

Antimicrobial drugs that are produced naturally by microorganisms, primarily bacteria and molds are called?

A

Antibiotics

58
Q

Antimicrobial drugs that are completely synthesized in a lab are called?

A

Synthetic chemicals

59
Q

Antimicrobial drugs that are chemically altered antibiotics that are more effective, longer lasting, or easier to administer that naturally occurring ones are called?

A

Semisynthetic

60
Q

Do chemotherapeutic agents exhibit high or low selective toxicity?

A

Low

61
Q

Antibiotics are antimicrobial drugs most associated with the treatment of what type of pathogens?

A

Microbes

62
Q

Which type of antimicrobial drugs are there more of and why?

A

Antibacterial. Because they target cell walls, which humans do not have

63
Q

What are the six main mechanisms of action for antimicrobial drugs?

A
  1. Inhibition of cell wall synthesis
  2. inhibition of protein synthesis
  3. disruption of cytoplasmic membrane
  4. inhibition of general metabolic pathways
  5. inhibition of DNA and RNA synthesis
  6. inhibition of attachment of entry into host cell
64
Q

Are bacterial cell wall inhibitors only effective against actively dividing cells or can they destroy non-dividing cells too?

A

Actively dividing cells

65
Q

Are cell wall inhibitors typically cidal or static?

A

In a clinical application, it does not matter if it is cidal or static, in a lab setting it is cidal in a low setting and static in a high setting (but it does not matter if they are cidal or static as long as they are working)

66
Q

What are the five classes of cell wall inhibitors and the basic mechanisms by which each works?

A
  1. Beta-lactams: blocks transpeptidase activity which prevents cell wall synthesis. Penicillin, cephalosporins, carbopenams
  2. Vancomycin: binds NAG in peptidoglycan and blocks transpeptidase from synthesizing new peptidoglycan
  3. Bacitracin: prevents NAG & NAM from being transported from the cytosol making the cell wall incomplete.
  4. Isoniazid: disrupt mycolic acid formation in mycobacterial species. Acid fast bacteria only, shut down the synthesis of mycolic acid (leprosy and tuberculosis)
  5. Ethambutol: disrupts mycolic acid formation in mycobacterial species. Acid fast bacteria only shut down the synthesis of mycolic acid. (Leprosy tuberculosis)
67
Q

What does the structure of a beta lactam ring look like?

A

A CARBON ring with 3 carbons, 1 Nitrogen.

68
Q

What are the four major advantages that synthetic cell wall?

A
  1. more stable in acidic environments
  2. more readily absorbed
  3. less susceptible to deactivation
  4. more active against more types of bacteria
69
Q

Are there cell wall inhibitors that are effective against fungi? If so, give an example.

A

ECHINOCANDINS; block the enzyme needed to make glucan polymer cell walls in fungi

70
Q

What are the two main targets of protein synthesis inhibitors?

A

Interference with bacterial ribosomes and interference with charging of transfer RNA molecules

71
Q

What is the limitation in selective toxicity for this group of antimicrobials?

A

We as humans, in our mitochondria have bacteria like ribosomes

72
Q

What are the 7 types of antibiotics from this group that interfere with prokaryotic ribosomes?

A

30s inhibitors 1. aminoglycosides (streptomycin & gentamycin: bind & disrupt 30s shape) 2. tetracycline (blocks tRNA docking site)
50s inhibitors 3. chloramphenicol (blocks peptidyl transferase) 4. licosamides 5. streptogramins 6. macrolides (4-6 block translocation of ribosome)
7. antisense nucleic acids (single stranded RNA or DNA that is complementary to bacterial mRNA

73
Q

the antibiotic group that block translation by binding to either the small or large ribosomal subunit?

A

AMINOGLYCOSIDES

74
Q

Which of the antibiotic groups functions by blocking the activity of peptidyl transferase?

A

CHLORAMPHENICOL

75
Q

Which of the antibiotic group/groups functions by binding to mRNA forming a double stranded molecule of RNA that prevents the initiation complex of translation from forming?

A

LICOSAMIDS, STREPTOGRAMIN, MACROLIDES

76
Q

What is the example of protein synthesis inhibitors that block the charging of tRNA molecules?

A

MUPIROCIN

77
Q

Cell membrane disruptors target which types of pathogens?

A

antifungal & antiprotozoal

78
Q

Antifungal and antiprotozoal cell membrane disruptors target what molecule in their membranes?

A

ERGOSTEROL

79
Q

What are the 2 mechanisms by which these types of antimicrobials affect this molecule?

A

Directly destroy or inhibit the synthesis of ergosterol

80
Q

What is the limitation to selective toxicity when using antifungals/antiprotozoals cell membrane disruptors that target molecule form the previous question?

A

Because there isn’t a lot

81
Q

What is the example of an antibacterial cell membrane disruptor we talked about in class?

A

Polymyxin component of Neosporin (topical)

82
Q

Which type of antifungal/antiprotozoal membrane disruptors attach to ergosterol in their membranes and create pores where ergosterol is located?

A

Nystatin; increases permeability & kills cells
Amphotericin B; antifungal affects egoistical

83
Q

Which type of antifungal/antiprotozoal membrane disruptors inhibit ergosterol synthesis?

A

Azoles, allylamines

84
Q

Metabolic inhibitors take advantage of differences in what between the host and pathogens?

A

Enzymes that carry out different metabolic pathways

85
Q

Antibacterial

A

metabolic antagonists (sulfonamides and trimethoprim)

86
Q

Antifungal and antiparasitic

A

drugs that interfere with electron transport in protozoa and fungi (atovaquone) agents that disrupt tubulin polymerization and glucose uptake by many protozoa and parasitic worms

87
Q

Antiviral

A

blockers of uncoating, protease inhibitors

88
Q

General antimicrobial

A

drugs that denature enzymes (heavy metals) low selective toxicity (denature our proteins as well, reason why we don’t us them)

89
Q

Typically include drugs that target what two processes in pathogens?

A

Inhibitors of DNA replication (DNA polymerase), inhibitors of transcription (RNA polymerase) to similar

90
Q

What is the limitation to selective toxicity for these types of antimicrobials?

A

Cause of many adverse reactions poorly understood drugs maybe toxic to kidney, liver or nerves. Consideration needed when prescribing to a pregnant woman

91
Q

What is one target in the bacterial DNA replication process that allows for high selective toxicity and why? What class of antibiotics use this target?

A

Nucleotide analogs, it mimics DNA nucleotides. Antiviral

92
Q

What are the 3 types of DNA replication inhibitors and types of pathogens effective against?

A

QUINOLONES & FLUOROQUINOLONES; act against prokaryotic DNA gyrase
NUCLEOTIDE OR NUCLEOSIDE ANALOGS; interfere with function of nucleic acids, distort shapes of nucleic acids molecules, and prevent further replication, transcription, or translation, most often used against viruses, effective against rapidly dividing cancer cells

93
Q

Why do gyrase inhibitors and reverse transcriptase inhibitors have a high level of selective toxicity?

A

We as humans lack the reverse transcriptase enzyme so it does not affect us. Gyrase is not found in humans, and it only inhibits topoisomerase

94
Q

What are nucleotide and nucleoside analogs especially effective against viral infections?

A

They can find viruses that are incorporated into DNA molecules and stop them from replicating

95
Q

What are the 2 types of transcription inhibitors and the type of pathogens they are effective against?

A

ACTINOMYCIN: low selective toxicity, not normally used in humans, but is an antibiotic
NUCLEOTIDE ANALOGS: mimics RNA nucleotides
RITAMPIN: inhibits bacterial RNA polymerase through transcription

96
Q

Any molecule that can block the attachment of viruses to human cells are called?

A

Antagonist

97
Q

Just be aware that there are antiviral drugs that block viral attachment and entry and drugs that prevent viral un-coating, which are all required steps for viral pathogenesis

A
98
Q

Possible bonus question: know at least one of the 7 mechanisms of microbial resistance

A
  1. Produce enzyme that destroys or deactivates drugs
  2. Alter their own metabolic chemistry