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319 final > ch 14 - antimicrobial drugs > Flashcards

ch 14 - antimicrobial drugs Flashcards

1
Q

use of antimicrobials in ancient societies

A

there is evidence that humans have been exposed to antimicrobial compounds for millennia, not just in the last century
- antimicrobial properties of certain plants were also recognized by various cultures

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2
Q

ancient brewers tapped antibiotic secrets

A

ancient Egyptians and Jordanians used beer to treat gum disease and other ailments

a chemical analysis of the bones of ancient Nubians shows that they were regularly consuming tetracycline
- most likely in their beer
- this is the strongest evidence that the art of making antibiotics which dates to the discovery of penicillin in 1928, was common practice nearly 2,000 years ago

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3
Q

first antimicrobial drugs timeline

A

the first half of the 20th century was an era of strategic drug discovery

early 1900s
- Paul Ehrlich and his assistant Sahachiro Hata found compound 606
- killed Treponema pallidum
- sold under the name of Salvarsan

1928
- Alexander Fleming discovered penicillin, the first natural antibiotic

1930s
- Klarer, Mietzsch, and Domagk disovered prontosil
- killed streptococcal and staphylococcal infections
- the active breakdown product of prontosil is sulfanilamide
- Sulfanilamide was the first synthetic antimicrobial created

early 1940s
- Dorothy Hodgkin determined the structure of penicillin using x-rays
- scientists could then modify it to produce semisynthetic penicillins

1940s
- Selman Waksman’s research team discovered several antimicrobials produced by soil microorganisms

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4
Q

first antimicrobial drugs: early 1900s

A

Paul Ehrlich and his assistant Sahachiro Hata found compound 606
- sold under the name of Salvarsan

compound 606 (Salvarsan)
- kills Treponema pallidum

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5
Q

first antimicrobial drugs: 1928

A

Alexander Fleming discovered penicillin
- first natural antibiotic

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6
Q

first antimicrobial drugs: 1930s

A

Klarer, Mietzsch, and Domagk disovered prontosil
- prontosil kills streptococcal and staphylococcal infections

prontosil’s active breakdown product is sulfanilamide
- sulfanilamide was the first synthetic antimicrobial created

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7
Q

first antimicrobial drugs: early 1940s

A

Dorothy Hodgkin determined the structure of penicillin using x-rays
- scientists could then modify it to produce semisynthetic penicillins

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8
Q

first antimicrobial drugs: 1940

A

Selman Waksman’s research team discovered several antimicrobials produced by soil microorganisms

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9
Q

chemotherapeutic agent/drug

A

any chemical agent used in medical practice

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10
Q

antibiotic agent

A

usually considered to be a chemical substance made by a microorganism
- can inhibit the growth or kill microorganisms

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11
Q

antimicrobic/antimicrobial agent

A

a chemical substance similar to an antibiotic
- but may be synthetic

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12
Q

antibiotic

A

usually has one bacterial target
- e.g. a key bacterial enzyme is blocked

develops too rapidly to be sustainable
- targets more than just DNA/membranes

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13
Q

antimicrobial

A

a broad term but often can mean multiple targets
- e.g. membranes and DNA

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14
Q

selective toxicity

A

harms microbes but not damaging the host
- e.g. harming the cell wall

antibiotics exhibit selective toxicity

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15
Q

chemotherapeutic index

A

the ratio between toxic dose to therapeutic dose
- the higher the chemotherapeutic index, the safer the drug

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16
Q

spectrum of antimicrobial activity

A

no single chemotherapeutic agent affects all microbes

antimicrobial drugs classified based on the type of organism they affect
- e.g. antibacterial, antifungal, etc

even within a group,
- one agent may have a narrow spectrum of activity
- whereas another many affect many species

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17
Q

types of spectrums of antimicrobial activity

A
  1. narrow spectrum
  2. broad spectrum
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18
Q

narrow spectrum of antimicrobial activity

A

targets only specific subsets of bacterial pathogens

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19
Q

broad spectrum of antimicrobial activity

A

targets a wide variety of bacterial pathogens
- including Gram-positive and Gram-negative species

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20
Q

opportunistic pathogen

A

microbes that usually do not cause disease in healthy people
- may become virulent with immunocompromised and unhealthy individuals

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21
Q

development of superinfections

A
  1. normal microbiota keeps opportunistic pathogens in check
  2. broad-spectrum antibiotics kill nonresistant cells
    - opportunistic pathogens still remain
  3. drug-resistant pathogens proliferate → can cause superinfection
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22
Q

types of antibiotic activity

A
  1. bacteriostatic
  2. bactericidal
  3. bacteriolytic
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23
Q

bacteriostatic

A

having the ability to inhibit bacterial growth
- generally by means of chemical or physical treatment
- reversible inhibition of a microbe’s ability to divide

total cell count & viable cell count
- increases logarithmically until reaching a still level
- this limits growth

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24
Q

bacteriocidal

A

irreversible inhibition of a microbe’s ability to divide
- dead cells are not destroyed
- total cell numbers remain constant

graph:
- total cell count and viable cell count increase logarithmically
- total cell count then hits a standstill
- viable cell count decreases logarithmically at the same time, getting killed

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25
Q

bacteriolytic

A

destruction or disintegration of bacteria
- lysis decreases both viable cell number & total cell number

graph:
- total cell count and viable cell count increase logarithmically
- then both decrease logarithmically over time

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26
Q

in vitro effectiveness

A

the effectiveness of an agent in a test tube or artificial environment
- determined by how little of it is needed to stop growth

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27
Q

the in vitro effectiveness of an agent is determined by…

A

how little of it is needed to stop growth

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28
Q

how is in vitro effectiveness measured

A

in terms of the antibiotic’s minimal inhibitory concentration (MIC)

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29
Q

minimal inhibitory concentration (MIC)

A

the lowest concentration of the drug that will prevent the growth of an organism

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30
Q

minimal inhibitory concentration (MIC) reflects…

A

antibiotic efficacy

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31
Q

minimal bactericidal concentration (MBC)

A

lowest concentration of antibacterial agent required to kill bacterium over fixed time period
- determined by doing serial tube dilution for antibiotic

can distinguish if a drug is bactericidal or bacteriostatic
- e.g. if cells grow in fresh medium without antibiotic → drug is bacteriostatic

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32
Q

determining minimum bactericidal concentration (MBC)

A

must use a serial tube dilution test for the antibiotic
- tubes with no visible growth are then inoculated onto agar media to determine MBC

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33
Q

types of antibiotic activity tests

A
  1. Kirby-Bauer disk susceptibility test
  2. E-test
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34
Q

types of antibiotic activity: Kirby-Bauer disk susceptibility test

A

determines how susceptible a bacteria is to several antibiotics
- this is shown by the zone of inhibition
- cannot distinguish whether a drug is bacteriostatic or bactericidal

antibiotic diffuses from the circular disk into the agar
- interacts with the growing bacteria

zone of inhibition is measured around filter-paper disks impregnated with antibiotics
e.g. the oxacillin disk
- MRSA has no zone of clearing because MRSA is resistant
- versus MSSA which is not resistant

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35
Q

types of antibiotic activity: E-test

A

determines MIC
- the intersection of the elliptical zone of clearing with the gradient on the drug containing strip indicates MIC
- cannot determine whether a drug is bacteriostatic or bactericidal

numbers on strip reflect the relative concentrations of antibiotic present at various points within the zone of inhibition
- the concentrations along the periphery of the clear zone are equal and reflect the MIC

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36
Q

which test can distinguish whether the drug is bacteriostatic or bactericidal, the MIC test or the Kirby-Bauer test?

A

neither, need MBC to do this

must do serial tube dilution of antibiotic
- tubes with no visible growth are inoculated onto agar media without antibiotic to determine MBC

agar plate determines if any cells survived 3x-5x above the MIC
→ if cells grow: drug is bacteriostatic
→ if cells don’t grow: drug is bactericidal

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37
Q

how to distinguish between bacteriostatic and bactericidal drugs

A

bacteriostatic
- if cells grow in the fresh medium without antibiotic

bactericidal
- if cells do not grow in the fresh medium without antibiotic

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38
Q

what are the 8 attributes of an ideal antimicrobial

A
  1. solubility
  2. selective toxicity
  3. toxicity not easily altered
  4. non-allergenic
  5. stability
  6. resistance by microorganisms not easily acquired
  7. long shelf-life
  8. reasonable cost
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39
Q

dosage

A

amount of medication given during a certain time interval
- route of administration must be considered
- half-life of antibiotic must be considered

in children
- dosage is based upon the patient’s mass

in adults
- a standard dosage is used, independent of mass

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40
Q

half-life of an antibiotic

A

the rate at which 50% of a drug is eliminated from the plasma

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41
Q

half-life of a drug

A

the rate at which 50% of a drug stays in tissue

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42
Q

when deciding which antibiotic to prescribe, the clinician needs to keep these three things in mind

A
  1. whether the organism is susceptible to the antibiotic
  2. whether the attainable tissue level of the antibiotic is higher than the MIC
    - depends on the body organs
  3. the understanding of the relationship between the therapeutic dose and the toxic dose of the drug
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43
Q

therapeutic dose

A

the minimum dose per kilogram of body weight that stops pathogen growth

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44
Q

toxic dose

A

the maximum dose that the patient can tolerate

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45
Q

route of administration: plasma concentration of drug as a function of response time

A

routes of administration:
1. IV (intravenous)
- reach peak level of plasma concentration of a drug immediately after t0
- and the magnitude is greatest out of all 3

2. IM (intramuscular)
- reach peak level of plasma concentration of drug at t1
- magnitude around half of IV’s

3. oral
- reach peak level of plasma concentration of a drug shortly after t1
- magnitude slightly lower than IM

  • this is in relation to the chemotherapeutic index
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46
Q

combinations of antibiotics can either be

A
  1. synergistic
  2. antagonistic
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47
Q

synergistic drugs may work poorly when…

A

they are given individually
- when combined, they work very well

combined effect is greater than additive effect
e.g. aminoglycoside + vancomycin

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48
Q

antagonistic drugs may work poorly when…

A

they are combined with other antagonistic drugs
- mechanisms of actions will interfere with each other → diminish their effectiveness
e.g. penicillin + macrolides

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49
Q

antibiotics exhibit selective toxicity because…

A

they disturb enzymes or structures unique to the target cell

mechanisms include:
1. cell wall synthesis
2. cell membrane integrity
3. DNA synthesis
4. RNA synthesis
5. protein synthesis
6. metabolism

50
Q

modes of action of antibiotics: targets of antibiotics

A
  1. cell wall
  2. plasma membrane
  3. DNA synthesis
  4. RNA synthesis
  5. ribosomes
  6. metabolic pathways
51
Q

antibiotics that target: cell wall

A

1. β-lactams
- penicillins
- cephalosporins
- monobactams
- carbapenems

2. glycopeptides
- vancomycin

3. bacitracin

52
Q

antibiotics that target: DNA synthesis

A

1. fluoroquinolones
- ciprofloxacin
- levofloxacin
- moxifloxacin

53
Q

antibiotics that target: RNA synthesis

A

1. rifamycins
- rifampin

54
Q

antibiotics that target: plasma membrane

A

1. polymyxins
- polymyxin B
- colistin

2. lipopeptide
- daptomycin

55
Q

antibiotics that target: ribosomes

A

30S subunit
- aminoglycosides
- tetracyclines

50S subunit
- macrolides
- lincosamides
- chloramphenicol
- oxazolidinones

56
Q

targets of antibiotics: metabolic pathways

A

folic acid synthesis
- sulfonamides
- sulfones
- trimethoprim

mycolic acid synthesis
- izoniazid

57
Q

antibiotics that target the cell wall: penicillins

A

the enzymes that attach the disaccharide units to preexisting peptidoglycan and produce peptide cross links
- collectively called penicillin-binding proteins (PBPs)

without an intact cell wall, the growing cell eventually bursts
- due to osmotic effects

penicillin is a bactericidal drug
- type of β-lactam antibiotic (has a β-lactam ring)

58
Q

antibiotics that target the cell wall: cephalosporins

A

β-lactam antibiotic originally discovered in nature but modified in the laboratory
- a type of semisynthetic drug

the basic structure of cephalosporin has been modified
- these modifications improve the drug’s effectiveness against penicillin-resistant pathogens

each modification is a new “generation” of cephalosporins
- there are currently 5 generations of this antibiotic

generation 1: Cephalexin
generation 2: Cefoxitin
generation 3: Ceftriaxone
generation 4: Cefepime
generation 5: Ceftaroline

59
Q

inhibitors of cell wall synthesis

A

polypeptide antibiotics
- bacitracin
- vancomycin

antimycobacterial antibiotics
- isoniazid (INH)
- ethambutol

60
Q

polypeptide antibiotics: bacitracin

A

topical application, works against Gram-positives
- form of inhibitor of cell wall synthesis

61
Q

polypeptide antibiotics: vancomycin

A

glycopeptide
- important “last line” against antibiotic-resistant S. aureus
- form of inhibitor of cell wall synthesis

62
Q

antimycobacterial antibiotics: isoniazid (INH)

A

inhibits mycolic acid synthesis
- form of inhibitor of cell wall synthesis

63
Q

antimycobacterial antibiotic: ethambutol

A

inhibits incorporation of mycolic acid
- form of inhibitor of cell wall synthesis

64
Q

microbial resistance to cell wall: inhibiting antibiotics

A

β-Lactamase (enzyme) is found in some bacteria
- it can break a bond in the β-lactam ring of penicillin → disables molecule

bacteria with β-Lactamase can resist the effects of penicillin
- and some other β-lactam antibiotics

Penicillin (w/ β-lactam ring) → (β-Lactamase) → Penicilloic acid

65
Q

antibiotics that target the bacterial membrane: polymyxin, tyrocidin, and platansimycin

A

act as detergents and disrupt the structure of the cell membrane
- done by binding to the phospholipids
- highly toxic
e.g. Platensimycin

mode of action
- interacts with lipopolysaccharide in the outer membrane of Gram-negative bacteria
- this kills the cell through the eventual disruption of the outer membrane and cytoplasmic membrane

66
Q

antibiotics that target the bacteria membrane: gramicidin

A

type of cyclic peptide

mode of action
- inserts into the cytoplasmic membrane of Gram-positive bacteria
- disrupting the membrane and killing the cell

67
Q

can bacterial DNA synthesis be a target for antibiotics?

A

yes, there are a few unique features of bacterial DNA synthesis that makes it a target for antibiotics

68
Q

antibiotics that affect DNA synthesis and integrity: metronidazole

A

metronidazole is activated after being metabolized by microbial protein cofactors ferredoxin
- ferredoxin is found in anaerobic and microaerophilic bacteria such as Bacterioides and Fusobacterium

aerobic microbes are resistant
- this is because they do not possess the electron transport proteins capable of reducing metronidazole

prodrug form of metronidazole → (single e- transfers) → nitrous free-radical form of metronidazole

69
Q

antibiotics that affect DNA synthesis and integrity: sulfonamides

A

sulfonamide (sulfa) drugs act to inhibit the synthesis of folic acid
- folic acid is an important cofactor in the synthesis of nucleic acid precursors

all organisms use folic acid to synthesize nucleic acids
- bacteria make folic acid from the combination of PABA, glutamic acid, and pteridine
- mammals do not synthesize folic acid and must get it from the diet or microbes

PABA: para-aminobenzoic acid
SFA: sulfanilamide

70
Q

normal folic acid formation versus formation blocked by sulfanilamide (SFA)

A

sulfanilamide (SFA) is a type of sulfonamide drug
- inhibits the synthesis of folic acid

normal folic acid formation
- P, PABA, G all enter the enzyme and synthesis occurs → folic acid

folic acid formation blocked by sulfanilamide (SFA)
- P, SFA, G all enter the enzyme → no synthesis occurs → P, SFA, G all leave the enzyme

SFA enters the enzyme in place of PABA
- PABA is needed for folic acid synthesis

71
Q

antibiotics that affect DNA synthesis and integrity: quinolones

A

DNA gyrase bound to and inactivated by a quinolone will block progression of a DNA replication fork

bacterial DNA gyrases are structurally distinct from their mammalian counterparts…
- quinolone antibiotics will not affect mammalian DNA replication

72
Q

RNA synthesis inhibiting antibiotics: rifampin (rifamycin)

A

rifampin is the best known member of the rifamycin family of antibiotics
- selectively binds to bacterial RNA polymerase and prevents transcription

rifampin is also used to treat tuberculosis and meningococcal meningitis

73
Q

antibiotics that inhibit protein synthesis: mode of action

A

the major classes of protein synthesis inhibitors target the 30S or 50S subunits of cytoplasmic ribosomes

74
Q

antibiotics that inhibit protein synthesis: drugs that affect the 30S ribosomal subunit

A
  1. aminoglycosides
    - streptomycin, gentamicin, tobramycin
  2. tetracyclines
    - doxycycline
  3. glycylcyclines
    - tigecycline
75
Q

antibiotics that inhibit protein synthesis: aminoglycosides

A

causes misreading of mRNA and inhibits peptidyl-tRNA translocation

aminoglycosides in particular:
- streptomycin
- gentamicin
- tobramycin

affects the 30S ribosomal subunit

76
Q

antibiotics that inhibit protein synthesis: tetracyclines

A

binds to the 30S subunit and prevent tRNAs carrying amino acids from entering the A site

tetracycline in particular:
- doxycycline

affects the 30S ribosomal subunit

77
Q

antibiotics that inhibit protein synthesis: glycylcyclines

A

binds to the 30S subunit and inhibits the entry of aminoacyl-tRNA into the A site
- it is able to function in tetracycline resistant cells

glycylcycline in particular:
- tigecycline

affects the 30S ribosomal subunit

78
Q

antibiotics that inhibit protein synthesis: drugs that affect the 50S ribosomal subunit

A
  1. chloramphenicol
  2. macrolides
    - erythromycin
    - azithromycin
    - clarithromycin
  3. lincosamides
    - clindamycin
  4. oxazolidinones
  5. streptogramins
    - quinupristin, dalfopristin
79
Q

antibiotics that inhibit protein synthesis: chloramphenicol

A

prevents peptide bond formation
- done by inhibiting peptidyltransferase in the 50S subunit

affects the 50S ribosomal subunit

80
Q

antibiotics that inhibit protein synthesis: macrolides

A

binds to 50S subunit and inhibit translocation of tRNA from the A site to the P site

further broken down into:
- erythromycin
- azithromycin
- clarithromycin

affects the 50S subunit of ribosomes

81
Q

antibiotics that inhibit protein synthesis: lincosamides

A

binds to peptidyltransferase and prevents peptide bond formation from the ribosome

further broken down into:
- clindamycin

affects the 50S subunit of ribosomes

82
Q

antibiotics that inhibit protein synthesis: oxazolidinones

A

binds to 50S subunit and prevent assembly of the 70S ribosome

affects the 50S subunit of ribosomes

83
Q

antibiotics that inhibit protein synthesis: streptogramins

A

bind to 50S subunit and block tRNA entry into the A site
- while blocking exit of a growing protein from the ribosome

further broken down into:
- quinupristin
- dalfopristin

affects the 50S subunit of ribosomes

84
Q

mechanisms of drug resistance

A
  1. drug modification or inactivation
  2. blocked penetration
  3. efflux pumps
  4. target modification
  5. target overproduction
  6. enzymic bypass
  7. target mimicry
85
Q

mechanisms of drug resistance: drug modification or inactivation

A

enzymes can be coded by genes that can chemically modify an antimicrobial
- which inactivates it
- or can destroy an antimicrobial through hydrolysis

inactivation of enzymes can affect:
- β-lactams
- aminoglycosides
- macrolides
- rifamycins

86
Q

mechanisms of drug resistance: blocked penetration

A

altering porins in the outer membrane

blocked penetration can affect:
- β-lactams
- tetracyclines
- fluoroquinolones

e.g. (for understanding only)
- a common mechanism of carbapenem resistance among P. aeruginosa is to decrease amount of OprD porin
- which is the primary portal of entry for carbapenems

87
Q

mechanisms of drug resistance: efflux pump

A

transport proteins that allow microorganisms to regulate their internal environment by removing toxic substances
- can export multiple antimicrobial drugs
- prevents the accumulation of drug to a level that would be antibacterial

efflux pump can affect:
- fluoroquinolones
- aminoglycosides
- tetracyclines
- β-lactams
- macrolides

88
Q

mechanisms of drug resistance: target modification

A

antimicrobial drugs have very specific targets
- structural changes to those targets can prevent drug binding
- this renders the drug ineffective

mechanism allows a formerly inhibited reaction to occur
- e.g. for understanding only: penicillin-binding proteins (PBPs) can inhibit the binding of β-lactam drugs and provide resistance to multiple drugs within this class

target modification can affect:
- fluoroquinolones
- rifamycins
- vancomycin
- β-lactams
- macrolides
- aminoglycosides

89
Q

mechanisms of drug resistance: target overproduction

A

microbe overproduces the target enzyme
- such that there is a sufficient amount of antimicrobial-free enzyme to carry out the proper enzymatic reaction

90
Q

mechanisms of drug resistance: enzymatic bypass

A

microbe develops a bypass that circumvents the need for the functional target enzyme

blocks the pathway with the functional target enzyme
- alternate route is used

91
Q

mechanisms of drug resistance: target mimicry

A

production of proteins that bind and sequester drugs
- preventing the drugs from binding to their bacterial cellular target

92
Q

fighting drug resistance

A

dummy target compounds that inactivate resistance enzymes have been developed

e.g.
- Clavulanic acid binds and ties up β-lactamases secreted from penicillin resistant bacteria

93
Q

individuals can take the following actions to help fight drug resistance

A
  • frequent hand washing
  • vaccinations
  • avoiding use of antibiotics for viral infections
  • refusing leftover antibiotics
  • take full course of antibiotics prescribed
94
Q

fighting drug resistance: effects of taking full course of antibiotics prescribed

A

day 0:
- highly sensitive organisms: moderate amount
- intermediate organisms: large amount
- highly resistant organisms: moderate amount
→ graph resembles a bell curve

day 3:
- highly sensitive organisms: low amount
- intermediate organisms: moderate amount
- highly resistant organisms: moderate amount

day 6:
- highly sensitive organisms: low amount
- intermediate organisms: low amount
- highly resistant organisms: moderate amount

day 10 (antibiotics are stopped prematurely):
- highly sensitive organisms: low amount
- intermediate organisms: low amount
- highly resistant organisms: high amount
→ relapse with resistant organisms
→ resistant organisms can also spread to other hosts, causing more drug-resistant infections

day 10 (full course of antibiotic treatment finished):
- low amount of all types of organisms
- end of successful treatment

95
Q

components of the influenza virus

A

hemagglutinin and neuraminidase
- influenza virus must be treated with antiviral agents that prevent virus uncoating or release

96
Q

hemagglutinin

A

binds to the host membrane receptors for entry by phagocytosis
- component of the influenza virus

97
Q

neuraminidase

A

cleaves sialic acid to allow virus particles to escape from infected cells
- component of the influenza virus

98
Q

antiviral agents that prevent virus uncoating or release

A
  • amantadine
  • oseltamivir (Tamiflu)
  • zanamivir (Relenza)
99
Q

antiviral agents: amantadine

A

prevents the virus from uncoating and exiting by changing the pH of the phagolysosome

100
Q

antiviral agents: oseltamivir (Tamiflu) & zanamivir (Relenza)

A

neuraminidase inhibitors prevent the virus particles from leaving the cell

101
Q

antiviral DNA and RNA synthesis inhibitors

A
  1. zidovudine
  2. acyclovir
  3. deoxyribonucleotide containing thymine
  4. deoxyguanosine
102
Q

antiviral agents: types of nucleoside and nonnucleoside reverse transcriptase inhibitors

A
  1. protease inhibitors
    - Nelfinavir (Viracept)
    - Iopinavir (Kaletra)
  2. entry inhibitors
    - CCR5 inhibitors (maraviroc)
103
Q

nucleoside and nonnucleoside reverse transcriptase inhibitors: protease inhibitors

A

targets the HIV protease enzyme
- Nelfinavir (Viracept)
- Iopinavir (Kaletra)

104
Q

nucleoside and nonnucleoside reverse transcriptase inhibitors: entry inhibitors

A

block virus envelope protein gp120 from binding to the host receptor CCR5
- CCR5 inhibitors (maraviroc)

105
Q

antifungal agents

A
  1. polyenes
    - nystatin, amphotericin B
  2. azoles
    - imidazoles, triazoles
  3. allylamines
    - terbinafine, lamisil
  4. echinocandins
    - caspofungin
  5. griseofulvin
  6. flucytosine
106
Q

antifungal agents: polyenes

A

disrupts membrane integrity
- nystatin
- amphotericin B

107
Q

antifungal agents: azoles

A

interferes with ergosterol synthesis
- imidazoles
- triazoles

108
Q

antifungal agents: allylamines

A

interferes with ergosterol synthesis
- terbinafine
- lamisil

109
Q

antifungal agents: echinocandins

A

blocks fungal cell wall synthesis
- caspofungin

110
Q

antifungal agents: griseofulvin

A

blocks cell division

111
Q

antifungal agents: flucytosine

A

inhibits DNA synthesis

112
Q

antiparasitic agents include

A
  • antiprotozoan agents
  • antihelminthic agents
113
Q

antiprotozoan agents

A

most are fairly toxic
- metronidazole
- quinine
- chloroquinine, primaquine (antimalarials)

114
Q

antiprotozoan agents: metronidazole

A

causes DNA breakage
- used to treat giardisis and Trichomonas infections

115
Q

antiprotozoan agents: quinine

A

commonly used in the past
- now used as a last resort to treat malaria

116
Q

antiprotozoan agents: chloroquinine & primaquine

A

interfere with protein synthesis
- specially RBCs
- these are antimalarials

117
Q

antihelminthic agents

A
  1. niclosamide
    - tapeworms
  2. praziquantel
    - flatworms
  3. mebendazole and albendazole
    - intestinal roundworms
  4. ivermectin
    - intestinal roundworms
118
Q

antihelminthic agents: niclosamide

A

prevents ATP generation
- targets tapeworms

119
Q

antihelminthic agents: praziquantel

A

alters membrane permeability
- targets flatworms

120
Q

antihelminthic agents: mebendazole and albendazole

A

interferes with nutrient absorption
- targets intestinal roundworms

121
Q

antihelminthic agents: ivermectin

A

causes paralysis of helminths
- targets intestinal roundworms

319 final (6 decks)

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