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Pharmacology > Principles of Antimicrobial Use > Flashcards

Principles of Antimicrobial Use Flashcards

1
Q

define empiric therapy

A

therapy based on knowledge of the antimicrobial spectrum

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2
Q

define broad spectrum

A

targeting a wide range of bacterial organisms

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3
Q

define narrow spectrum

A

targeted to more specific classes of bacteria

  • less impact on normal flora
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3
Q

define bactericidal

A

killing of organisms

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4
Q

define bacteriostatic

A

preventing further growth

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5
Q

define bacterial resistance

A

untreatable infections that require the use of toxic drugs

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6
Q

what activity or structure is always a potential target?

A

anything that is different from the host organism

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7
Q

list 2 beta-lactam drug classes

A
  1. penicillin
  2. cephalosporins
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8
Q

describe alexander fleming’s contribution

A

in 1928 discovered the inhibition of Staph. Aureus on agar plates of penicillium

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9
Q

what are the 2 wall synthesis inhibitors?

A
  1. beta-lactams
  2. Glycopeptides
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10
Q

beta-lactams are a broad spectrum drug that are primarily effective against

A

gram + bacteria

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11
Q

what is a characteristic of beta-lactams?

A

they are bactericidal

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12
Q

beta-lactams have poor entry into the CNS therefore they are

A

actively transported out

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13
Q

what is the most common adverse reaction to beta-lactams?

A

hypersensitivity

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14
Q

how do bacteria become resistant to beta-lactams?

A

they synthesize beta-lactamases or penicillinases

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15
Q

what is the MOA of beta-lactams?

A

to inhibit the crosslinking of peptidoglycan strands

  • peptidoglycan is a chief component for cell wall synthesis
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16
Q

penicillin’s are not active against what type of organisms?

A

those that lack a peptidoglycan cell wall

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17
Q

list examples of organisms that are resistant to penicillin

A
  1. mycobacteria
  2. protozoa
  3. fungi
  4. viruses
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18
Q

explain the concept of using beta-lactamase inhibitors in combination with other beta-lactam antibiotics

A

amoxicillin is not resistant to beta-lactamases so its combined with beta-lactamase inhibitors to increase their therapeutic value

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19
Q

list an example of a beta-lactam antibiotic that is used in combination with a beta-lactamase inhibitor

A

augmentin

amoxicillin + clavulanic acid

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20
Q

calvulanic acid is a

A

beta-lactamase inhibitor

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21
Q

explain why penicillin has such a poor oral absorption

A

due to ion trapping and stomach acidity

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22
Q

as much as 60% of penicillin that is absorbed is bound to

A

plasma proteins

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23
Q

beta-lactam drugs differ by what 3 characteristics?

A
  1. organisms inhibited
  2. pharmacokinetics
  3. bacterial resistance of certain organisms to different drugs
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24
Q

list 2 examples of inhibitors of DNA synthesis

A
  1. folate antagonists
  2. DNA topoisomerase inhibitors
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25
Q

which if the following 2 is bacteriostatic?

folate antagonists
DNA topoisomerase

A

folate antagonists

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26
Q

which of the following is bactericidal?

folate antagonists
DNA topoisomerase

A

DNA topoisomerase

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27
Q

tetrahydrofolate is the active form of

A

folic acid

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28
Q

tetrahydrofolate is a coenzyme that is required for the synthesis of what in bacteria and humans?

A
  • nucleotides
  • A.A
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29
Q

what is the difference between folate synthesis in humans and in bacteria?

A

humans: dietary dependence

bacteria: synthesized intracellularly

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30
Q

what is an additional way of inhibiting bacterial growth that involves folate?

A

inhibiting the synthesis of folate stops synthesis of a.a and nucleotides

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31
Q

drugs that affect the ____________ but not the _____________ of folic acid affects the bacteria but not the eukaryotic host

A
  • synthesis
  • utilization
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32
Q

folate antagonists can be described as being

A

bacteriostatic

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33
Q

what are 2 examples of folate antagonists?

A
  • sulfonamides
  • trimethoprim
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34
Q

sulfonamides are

A

structural analogs of para-aminobenzoic acid (PABA)

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35
Q

PABA is a substrate necessary for

A

folic acid synthesis

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36
Q

what are 2 examples of sulfonamides?

A
  • sulfanilamide
  • sulfadiazine
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37
Q

sulfonamides competitively inhibit the enzyme

A

dihydropteroate synthase

38
Q

what is the effect of inhibiting dihydropteroate synthase?

A
  • depletes folate production
  • slows bacterial division
39
Q

sulfonamides are

A

broad spectrum

40
Q

DNA topoisomerase inhibitors can be described as being

A

bactericidal

41
Q

what is an example of a DNA topoisomerase inhibitor?

A

fluoroquinolones

42
Q

what is the MOA of DNA topoisomerase inhibitors?

A

inhibits the unwinding of DNA therefore the DNA is not available for transcription or translation

43
Q

what are the 3 types of protein synthesis inhibitors?

A
  1. aminoglycosides
  2. macrolides
  3. tetracyclines
44
Q

bacterial RNA polymerase is smaller and less complex than in human therefore…

A

transcription and translation can occur within the same compartments of bacterial cells

45
Q

what are the 5 sites of action for drugs that inhibit bacterial protein synthesis?

A
  1. freeze initiation (no ribosome progression along mRNA)
  2. prevent tRNA from binding to mRNA
  3. block peptide formation
  4. block translocation step
  5. misread mRNA so wrong amino acid is inserted
46
Q

what are 2 examples of aminoglycosides?

A
  1. streptomycin
  2. gentamicin
47
Q

aminoglycosides are effective against

A

aerobic gram-negative organisms

48
Q

what is the MOA of aminoglycosides?

A

freeze the initiation of mRNA and misreads the mRNA

49
Q

aminoglycosides have a low

A

TI (therapeutic index )

50
Q

aminoglycosides are only used for serious infections that have been acquired in what settings?

A

nosocomial

hospital settings

51
Q

PHARMACOKINETICS

aminoglycosides have poor oral absorption b/c they are

A

cationic and polar

52
Q

aminoglycosides are administered

A

IM or IV

53
Q

Where are the two primary areas of potential toxicity in the body listed in your notes that may limit their use only to serious infections?

A
  • ototoxicity
  • renal toxicity
54
Q

tetracyclines prevent

A

tRNA from binding to mRNA codon

55
Q

what are the 7 characteristics and methods of viral replication?

A
  1. absorption and penetration into host
  2. uncoating of viral nucleic acid
  3. synthesis of regulatory proteins
  4. synthesis of RNA or DNA
  5. syn. of late regulatory proteins
  6. assembly & maturation of viral particles (virions)
  7. release from cells
56
Q

entry inhibitors block the

A

entry of viral products

57
Q

uncoating inhibitors inhibit the

A

release from lipid capsule

58
Q

reverse transcriptase inhibitors prevent the

A

RNA to DNA transcription

59
Q

translation disruptors promote

A
  • antisense DNA or RNA segments
  • ribosomes that cut newly translated DNA or RNA
60
Q

protease inhibitors inhibit the enzyme involved w/ the

A

final assembly of newly synthesized viral chains

61
Q

release inhibitors block

A

the release of viral replicates from the host cell

62
Q

HIV virus primarily binds to the

HIV: human immunodeficiency virus

A

GP120 site on CD4 cells

63
Q

CD4 cells are aka

A

T-helper cells

  • subtype of t-lymphocytes of the immune system
64
Q

what conditions are necessary for opportunistic infections and cancers to begin invading the body?

A
  • viral titer increases
  • [CD4] decreases
65
Q

what is known as the outward manifestation of HIV?

A

AIDS
(Acquired Immunodeficiency syndrome)

66
Q

is it possible to be HIV positive but not have AIDS by definition?

A

yes

67
Q

what are 3 treatment approached to HIV and AIDS

A
  1. antiretroviral Agents
  2. protease inhibitors
  3. fusion inhibitors
68
Q

what is an example of an antiretroviral agent?

A

zidovudine (AZT)

69
Q

what is an example of an protease inhibitor?

A

saquinavir

70
Q

what is an example of a fusion inhibitor?

A

enfuvirtide (fuzeon)

71
Q

what is the MOA of COVID

A

virus uses glycoprotein spikes to connect to ACE2 which then binds to ACE2-receptors and enters the host cell

ACE: angiotensin-converting enzyme

72
Q

the density of ACE2-receptors in a tissue is directly correlated to the

A

severity of COVID in that tissue

73
Q

what has shown to be a protective treatment/ approach to COVID?

A

decreasing/blocking ACE2 activity at its receptor sites

74
Q

ACE2 receptors are high expressed in which organ?

A

the heart

75
Q

the COVIS virus can cause

A
  • acute myocardial injury
  • chronic damage to cardiovascular system
76
Q

ACE2 is abundantly found throughout the

A

GI tract

77
Q

what type of GI issues can present from COVID?

A

pain and digestive issues w/ loss of nutrients in the body

78
Q

how does COVID affect the vascular system?

A

sets off chain of vasoconstrictive responses

79
Q

how does COVID affect the respiratory system?

A
  • constriction of blood vessels w/in the pulmonary circulation causing decreased oxygenation and viral pneumonia
80
Q

how does COVID affect the urinary system and kidneys?

A

it can lead to kidney complications that can be fetal

81
Q

what are the 7 types of treatments for COVID?

A
  1. convalescent plasma
  2. regerneron
  3. remdesivir
  4. chloroquine & hydroxycholorquine
  5. reverse transcriptase inhibitors
  6. paxlovid
  7. vaccines
82
Q

describe convalescent plasma

A

plasma that contains the antibodies from patients that have recovered from COVID

83
Q

regeneron are

A

polyclonal antibodies that bind to spike regions of the virus

84
Q

remdesivir is a broad-spectrum anti-viral drug that

A

inhibits viral replication through early termination of viral transcription

85
Q

chloroquine & hydroxychloroquine are drugs that originally were prescribed to treat

A

malaria, lupus, and rheumatoid arthritis

86
Q

chloroquine and hydroxychloroquine are drug that interfere w/ the binding of COVID virus to ACE2 receptors by inhibiting

A

glycosylation of ACE2 receptors

87
Q

chloroquine and hydroxycholorquine have to be taken under close supervision b/c

A

there’s concern for cardiotoxicity

88
Q

reverse transcriptase inhibitors are drugs that were used to treat

A

HIV by inhibiting mRNA from producing DNA for viral replicates

89
Q

paxlovid are protease enzyme inhibitors that block the replication of

A

new virons

90
Q

what are the 2 COVID vaccines?

A
  • Pfizer
  • Moderna
91
Q

the 2 covid vaccines are both

A

mRNA vaccines that contain a synthetic version of COVID genetic code

92
Q

the covid vaccines MOA can be described as

A

body synthesizing the covid spike protein -> an immune response is produce making antibodies w/ the ability to defeat the real virus

93
Q

the covid vaccines require

A

2 doses w/ 95% efficacy rate

Pharmacology (9 decks)

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