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BIOM 360 > Exam 3 chapter 9 > Flashcards

Exam 3 chapter 9 Flashcards

1
Q

What is the definition ofr antibiotic?

A

anti - life

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2
Q

definition for antimicrobial/antimicrobial agent?

A

an agent that kills microorganisms or inhibits their growth

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3
Q

definition of chemotherapy

A

use of chemical agents to treat disease

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4
Q

definition of antisepsis

A

prevention of infection or sepsis

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5
Q

definition of sepsis

A

systematic response to infection manifested by two or more of the following conditions:

  • temperature >38 C or < 36 C
  • heart rate >90 beats/min
  • respiratory rate >20 breaths/min
  • pCO2<32 mm Hg
  • WBC count >12,000 cells/mm3 or 10 % immature band forms

also been defined as the presence of pathogens or their toxins in blood and other tissues

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6
Q

What is selective toxicity?

A

ability of drug to kill or inhibit pathogen while damaging hose as little as possible

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7
Q

what is therapeutic dose?

A

drug level required for clinical reatment

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8
Q

what is toxic dose?

A

drug level at which drug becomes too toxic for patient (ie produces side effects)

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9
Q

What is therapeutic index?

A

ratio of toxic dose to therapeutic dose

guideline book

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10
Q

What are side effects?

A

undesired effects of drugs on host cells

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11
Q

define narrow-spectrum drugs

A

attack only a few different pathogens

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12
Q

define broad - spectrum drugs

A

attack many different pathogens

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13
Q

define cidal agent

A

kills microbes

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14
Q

define static agent

A

inhibits growth of microbes

slow production hoping person can build enough immunity to fight

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15
Q

Describe penicillin

Primary effect

mechanism of action

A
  • Cell wall synthesis inhibition
  • Cidal
  • inhibit traspeptidation enzymes involved in cross-linking the polysaccharide chain of peptidoglycan activate cell wall lytic enzymes
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16
Q

Describe cephalosporins

Primary effect

mechanism of action

A
  • Cell wall synthesis inhibition
  • cidal
  • same as penicilins: inhibit traspeptidation enzymes involved in cross-linking the polysaccharide chain of peptidoglycan activate cell wall lytic enzymes
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17
Q

Describe Vancomycin

Primary effect

mechanism of action

A
  • Cell wall synthesis inhibition
  • cidal
  • prevents transpeptidation of peptidoglycan subunits by binding to D-Ala-D-Ala amino acids at the end of peptide side chains. Thus it has a different binding site than that of penicilliins
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18
Q

Describe Aminoglycosides

Primary effect

mechanism of action

A
  • Protein synthesis inhibition
  • Cidal
  • Bind to small ribosomal subunit (30S) and interfere with protein synthesis by drectly causeing misreading of mRNA
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19
Q

Describe Tetracyclines

Primary effect

mechanism of action

A
  • Protein synthesis inhibition
  • Static
  • same as aminoglycosides: Bind to small ribosomal subunit (30S) and interfere with protein synthesis by drectly causeing misreading of mRNA
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20
Q

Describe macrolides

Primary effect

Mechanism of action

A
  • Protein synthesis inhibition
  • Static
  • Bind 23S rRNA of large ribosomal subunit (50s_ to inhibit peptide chain elongation during protein synthesis
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21
Q

Describe lincosamines

Primary effect

Mechanism of action

A
  • Protein synthesis inhibition
  • static
  • Act on the 50S ribosomal subunit, preventing transpeptidation by inhibiting peptidyl transferase activity
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22
Q

Describe chloramphenical

Primary effect

mechanism of action

A
  • Protein synthesis inhibition
  • static
  • (same as macrolides) Bind 23S rRNA of large ribosomal subunit (50s_ to inhibit peptide chain elongation during protein synthesis
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23
Q

Describe Quinolones and Fluoroquinolones

Primary Effect

Mechanism of action

A
  • Nucleic Acid Synthesis Inhibition
  • Cidal
  • Inhibit DNA gyrase and topoisomerase II, thereby blocking DNA replication
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24
Q

Describe Rifampin

Primary Effect

Mechanism of action

A
  • Nucleic Acid Synthesis Inhibition
  • Cidal
  • Inhibits bacteria DNA-dependent RNA polymerase
25
Q

Describe Polymyocin B

Primary effect

Mechanism of Action

A
  • Cell membrane disruption
  • cidal
  • Binds to plasma membrane and disrupts its structure and permeability properties
26
Q

Describe sulfonamides

Primary effect

Mechanism of Action

A
  • Antimetabolites
  • Static
  • Inhibit folic acid synthesis by competing with aminobenxoic acid (PABA)
27
Q

Describe trimethoprim

Primary effect

Mechanism of Action

A
  • Antimetabolites
  • static
  • Blocks folic acid synthesis by inhibiting the enzyme tetrahydrofolate reductase
28
Q

Describe Dapsome

Primary effect

Mechanism of Action

A
  • Antimetabolites
  • Static
  • Thought to interfere with folic acid synthesis
29
Q

Describe Isolazid

Primary effect

Mechanism of Action

A
  • Antimetabolites
  • Cidal if bacteria are actively crowing. static if bacteria are dormant
  • Exact mechanism is unclear, but thought to inhibit lipid synthesis (especially mycolic acid),
30
Q

Effectiveness expressed in two ways:

A
  • Minimal inhibitory concentration (MIC)
    • lowest concentration of drug that inhibits growth of pathgen
  • Minimal lethal concentration (MLC)
    • Lowes concentration of drug that kills pathgens
31
Q

How to determine the level of antimicrobial activity?

A
  • Dilution susceptibility test for MIC - time intensive
    • Inoculating media containing different concentration of drug
      • broth or agar with lowest concentration showing no growth is MIC
      • broth from which microbe can’t be recovered is MLC
  • Disk diffusion tests - kirby bauer
    • disks with specific drug placed on inoculated agar
    • observe clear sones (no growth) around disk
  • the E-test MIC and diffusion
    • convenient for use with anaerobic pathogens (Similar to disk but uses strips rather than disks)
      • Strips have gradient of antibiotic, intersection = zone of inhibition = MIC
32
Q

What are the Main modes of action for antibacterial drugs?

A
  • Inhibitors of cell wall synthesis
    • Penicillins - most are 6-aminopenicillanic acid derivatives with different side chain of amino group
      • most crucial feature = beta lactam ring (essential for bioactivity)
      • Penicillin resistant organisms produce beta lactamase - hydrolyzes a bond in ring
  • Protein synthesis inhibitors
    • ​Many antibiotics bind specifically to bacterial ribosome (Aminoacyl-tRNA binding, peptide bond formation, mRNA reading, Translocation)
    • Aminoglycoside antibiotics, Tetracyclines, Macrolides, Lincosamines, chloramphenicol
  • Metabolic antagonists
    • ​Inhibit or block metabolic pathways by competitively inhibiting metabolites by key enzymes
    • Sulfonamides, trimethoprim
  • Nucleic acid synthesis inhibition
    • ​Block DNA replication and transcription
    • Quinolones
33
Q

What are penicillin mode of actions?

A
  • Blocks the enzyme that catalyzes transpeptidation (formation of cross-links in peptidoglycan)
  • Prevents synthesis of complete cell walls leading to lysis
  • acts only on growing bacteria that are synthesizing new peptioglycans
34
Q

What are other actions and types of penicillins?

A
  • Binds to periplastic proteins (PBPs)
  • activate bacterial autolysins and murein hydrolases
  • stimulate bacterial holins to form holes or lesions in PM
  • Naturally occuring penecillins = V and G
    • semisynthetic penicillins have a broader spectrum than natural
35
Q

What are cephalosporins?

A
  • Structurally and functionally similar to penicillins
  • Broad-spectrum antibiotics that can be used by most patients that are allergic to penicillin
  • four categories based on their spectrum of activity:
    • Cephalothin
    • Cefoxitin
    • Cefoperazone
    • Ceftriaxone
36
Q

What are Vancomycin and Teicoplanin?

A

glycopeptide antibiotics

Inhibit cell wall synthesis

Vancomycin - important for treatment of antibiotic-resistant staphlocaccal and enterococcal infections

(previously cinsidered “drug of last resort” so rise in sreistance to vancomycin is great concern)

37
Q

Explain Aminoglycoside Antibiotics

A
  • Large group, all with a cyclohexane ring, amino sugars
  • bind to 30S ribosomal subunit, inhibiting protein synthesis by causing misreading of the mRNA
  • can cause hearing problems, loss of balance, kidney problems, etc
38
Q

What are tetracyclones

A
  • All have a four - ring structure to which a variety of side chains are attached
  • borad spectrum, bacteriostatic
  • combine with 30S ribosomal subunit
    • inhibit bind of aminoacyl-tRNA molecuels to the A site of the ribosome
  • sometimes used to treat acne
39
Q

What are Macrolides

A
  • Contain 12 to 22 carbon lactone rings linked to one or more sugar
    • eg. erythromycin
      • broad spectrum, usually bacteriostatic
      • binds to 23S rRNA of 50S subunit
        • inhibits peptide chain elongation
  • Used for patients allergic to penicillin
40
Q

What are Lincosamines

A
  • Interferes with protein synthesis in microbes
  • Produced by Streptomyces bacteria
  • broad spectrom antibiotic, activity against anaerobic microbes; less actively against aerobes
  • used sparingly because they can suppor (indirectly) the growth of C. difficile, which can result in other diease states
  • Clindamycin is example, and used to treate infection caused by Bacteroides fragilis, as well as some staphyloccal and streptococcal infections
41
Q

What is Chloramphenical

A
  • Now chemically synthesized
  • Binds to 23s rRNA on 50S subunit and inhibits peptidyl transferase reaction
  • Toxic with numerous side effects so only used in life threatening situations
42
Q

What are Sulfonamides or Sulfa Drugs

A

Structurally related to sulfanilamide, a para aminobenzoic acid (PABA) analog

PAGA used for synthesis of folic acid and is made by pathogens

sulfa drugs are selectively toxic due to cometative inhibition of folic acid synthesis enzymes

43
Q

What are Trimethoprim

A
  • synthetic antibiotic that also interferes with folic acid production
  • Broad spectrum
  • can be combined with sulfa to increase efficacy of treatment
    • combination blocks two steps in folic acid pathway
  • Has a variety of side effects including abdominal pain and photosentitivity reactions
44
Q

What are quinolones?

A
  • Broad spectrum, synthetic drugs containing 4-quinolone rings
  • Nalidixic acid first synthesized quinolone (1962)
  • Act by inhibiting bacterial DNA -gyrase and topoisomerase II
  • Broad spectrum, bactericidal, wide range of infections
45
Q

What are antifungal drugs?

A
  • fewer effective agents because of similarity of eukaryotic fungal cells and human cells
  • easier to treat superficial mycoses than sstemic infections
46
Q

How to treate Mycoses?

A
  • superficial mycoses
    • eg Candida
    • topical and oral
    • disrupt membrane permeability and inhibit sterol synthesis
    • disrupts mitotic spindle, may inhibit protein and DNA synthesis
  • Systemic mycoses
    • Difficult to control and can be fatal
    • Three common drugs - given IV
      • amphotericin B- binds sterols in membrane (main drug)
      • 5-flucytosin -disrupts RNA function
      • Fluconazole - low side effects, ued prophylactically
47
Q

Explain antiviral drugs

A
  • Drug development slow becaue difficult to specifically target viral replication
  • Drugs currently used inhibit virus-specific enzymes and life cycle processes
48
Q

What are antiviral drugs for influenza?

A
  • Amantidine
    • used to prevent influenza infection - ahead of time
    • Blocks penetration and uncoating of influenza virus
  • Tamiflu
    • anti-influenza agent
    • neuraminidase inhibitor
    • been shown to shorten course of illness
49
Q

What are antiviral drugs for Herpesvirus Infection?

A
  • Acyclovir
    • Inhibits herpes virus DNA polymerase
  • Adenine arabinoside (vidarabine)
    • inhibits herpes virus enzymes involved in DNA and RNA synthesis and function
  • Valacyclovir
    • prodrug form of acyclovir
  • Ganciclovir and other
    • anti-herpes virus dugs
  • Foscarnet
    • inhibits herpes virus DNA polymerase
50
Q

What are broad spectrum antiviral drugs?

A

HPMPC (cidofovir)

Inhibits viral DNA polymerase papovaviruses, adenoviruses, herpesviruses, iridoviruses, and poxviruses

51
Q

What are anti-HIV drugs?

A
  • Reverse transcriptase (RT) inhibitors
    • nuleoside RT inhibitors
    • non-nucleoside RT ingivitors
  • Protease inhibitors
    • mimic peptide bond that is normoally attacked by the protease
  • Fusion inhibitors
    • prevent HIV entry into cell

Most successful ar drug cocktails to curtail resistance

52
Q

What are antiprotozoan drugs?

A
  • The mechanism of drug action for many antiprotozoal drug is not percisely known
  • Examples of available drugs
    • some antibiotics that inhibit bacterial protein synthesis are used against protozoa
    • chloroquine and mefloquine - malaria
    • metronidazole - entramoeba infections
    • atovaquone-pneumocystis carinii and taxoplasma gondii
53
Q

What are the factors that influence antimicrobial drug effectiveness?

A
  • Ability of drug to reach site of infection
  • susceptibility of pathogen to drug
  • Ability of drug to reach concentrations in body that exceed MIC of pathogen
54
Q

Describe the ability of drug to reach site of infection

A
  • depends in part on mode of administration
    • oral: some drugs destroyed by somach acid
    • topical
    • parenteral routes
    • non-oral routes of administration
  • drug can be excluded by blood clots or necrotic tissue
55
Q

What are the factors influencing ability of drug to reach concentrations exceeding MIC?

A
  • Amount administered
  • route of administration
  • speed of uptake
  • rate of clearance (elimination) from body
56
Q

Explain drug resistance

A
  • an increaseing problem
    • once resistance originates in a population it can be transmitted to other bacteria
    • particular type of resistance mechanism is not conformed to a single class of drugs
57
Q

What are ways to overcome drug resistance?

A
  • Give drug in appropriate concentrations to destroy susceptible
  • give two or more drugs at same time
  • use drugs only when necessary
  • possible future solutions
    • continued devellopment of new drugs
    • use of bacteriophages to treat bacterial disease
58
Q
A

BIOM 360 (7 decks)

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