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2H. Pharmacology > Principles of Antimicrobial Therapy > Flashcards

Principles of Antimicrobial Therapy Flashcards

1
Q

Use of chemicals agents against invading living organisms (cells)
Term is used for both treatment of cancer and treatment of infection

A

Chemotherapy

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2
Q

l A chemical substance capable of killing or inhibiting the growth microbes

May be naturally occurring or synthetic

A

Antimicrobia

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3
Q

A chemical substance produced by various species of organisms that is capable of killing or inhibiting the growth of other microbes or cells

A

Antibiotic

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4
Q

The ability of a drug to injure a target cell or organism without injuring other cells or organisms that are in intimate contact #choosy

A

Selective Toxicity

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5
Q

Targeting structural, physiological or metabolic difference between invading microbe and host cell

Paul Erlich(1906) “Inordertousechemotherapysuccessfully,wemustsearchforsubstancesthathaveanaffinityforthecellsofparasitesandapowerofkillingthemgreaterthanthedamagesuchsubstancescausetotheorganism(host)itself.Wemustlearntoaimwithchemicalsubstances.”

A

Selective Toxicity

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6
Q

Drugs which inactivate or destroy microbes –Antibacterial discussion is focused here

–Antiviral

–Antifungal

–Antiparasitics

A

Antimicrobials

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7
Q

Antimicrobial Targets

A

Cell wall

peptidoglycan

Cytoplasmicmembrane

Protein synthesis

Nucleic acid synthesis

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8
Q
A
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9
Q

What are drugs that inhibit CW synthesis?

A
  1. Cycloserine
  2. vancomycin
  3. bacitracin
  4. Fosfomycin
  5. Penicillins
  6. Cephalosporins
  7. Monobactams
  8. Carbapenems
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10
Q

Inhibitors of Folic Acid

A

Trimetroprim

Sulfonamides

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11
Q

inhibitors of DNA replication ( DNA gyrase)

A

Nalidixic Acid

Quinolones

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12
Q

inhibitors of DNA-Dependent RNA Polymerase

A

RifamPIN

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13
Q

Inhibitors of Protein Synthesis ( 50s Inhibitors)

A

Erythromycin

Chloramphenicol

Clindamycin

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14
Q

30s Inhibitors

A

Tetracycline

Spectinomycin

Streptomycin

Gentamycin

Tobramycin

Amikamycin

Nmemonics : GATTASS

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15
Q

Inhibits the Cell membranes

A

Polymyxins

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16
Q

Mechanism of Action

Target: Cell wall synthesis;_________

A

all β-lactam drugs

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17
Q

Target: Protein synthesis; ______________

A

macrolides, chloramphenicol,tetracycline, aminoglycosides

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18
Q

Target: RNA polymerase;

A

rifampin

“an R for R”

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19
Q

Mechanism of Action

Affecting cellular components: DNA gyraseinhibitors: _________

A

Quinolones

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20
Q

DHF reductase inhibitor: _______-

A

Trimethoprim

” Reductase : Tagabawas TTTTTT”

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21
Q

PABA: ____________

A

Sulfonamides

“P.S. “

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22
Q

Inhibit reverse transcriptase enzyme: ____________

A

Zidovudine

**” **mahilig sa baliktaran : ZOUIE”

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23
Q

Cell wall permeability:______________

A

Amphotericin B; PolymyxinB

“cell wall permeaBility: B

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24
Q

Inhibitors of biosynthetic pathways:____________-

A

Bacitracin

” Bayosynthetic:Bacitracin”

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25
Q

BacteriostaticDrugs

Protein Synthesis Inhibitors (except___________ )

–Tetracyclines

–Macrolides

–Clindamycin

–Chloramphenicol

–Linezolid

–Sulphonamides

A

** aminoglycosides**)

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26
Q

Bactericidal

A

Beta-lactamantibiotics

Vancomycin

Aminoglycosides

Fluoroquinolones

“FAVBulous napapatay lahat”

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27
Q

When to Use Bactericidal Drugs

A

Impaired host defense

Infections with poor blood flow (endocarditis, endovascular infections)

Low WBC (<500

)Cancer patients

CSF penetration (meningitis)

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28
Q

___________: Drugs which affect both Gram-pos and Gram-negbacteria;

A

Broad Spectrum

tetracycline, imipenem, 3rdgeneration cephalosporins

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29
Q

_____________: Drugs which have activity against only gram-positive bacteria

i.e. antistaphylococcalpenicillinsand 1stgeneration cephalosporins

A

Narrow Spectrum

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30
Q

____________ shows the capacity of an antimicrobial drug to inhibit the growth of bacteria after removal of the drug from the culture

provides additional time for the immune system to remove bacteria that might have survived antibiotic treatment before they can eventually regrow after removal of the drug

A

Post-Antibiotic Effect PAE

31
Q

When is antimicrobial therapy warranted for a given patient? Is an antimicrobial agent indicated on the basis of clinical findings? Or is it prudent to wait until such clinical findings become apparent? Have appropriate clinical specimens been obtained to establish a microbiologic diagnosis? What are the likely etiologic agents for the patient’s illness?

A
32
Q

-use of antimicrobial before the pathogen responsible for a particular illness or the susceptibility to a particular antimicrobial agent is known

Presumptive therapy

Based on experience with a particular clinical entity Usual justification

hope that early intervention will improve the outcome

A

Empiric Antimicrobial Therapy

33
Q

Approach to Empiric Therapy

A

Formulate clinical diagnosis of microbial infection history, PE

Obtain specimen for lab examination

Formulate microbiologic diagnosis

Determine necessity for empiric therapy

Is there a significant risk of serious morbidity if therapy is withheld until a specific pathogen is detected by the clinical laboratory?

Institute treatment

34
Q

Laboratory Investigation in Diagnosis of Infectious Agents

A
35
Q

Identification of the pathogen Collection of infected material before beginning antimicrobial therapy

Minimal inhibitory concentration (MIC)is the lowest concentration of antimicrobial that prevents visible growth of microbes

A
  1. Stains—Gram or acid-fast (which is already done)
  2. Serology
  3. Culture and sensitivity
  4. Thin layer smears
36
Q

___________-is the lowest concentration of antimicrobial that prevents visible growth of microbes

A

Minimal inhibitory concentration (MIC)

37
Q

Choosing an Antimicrobial

Three Things to Consider
Host
Organism
Drug

A

Host
Organism
Drug

38
Q

Choosing an Antimicrobial

A

Identity the infecting organism –It must be possible to make a probability assessment of the most likely culprit(s)

Likely antimicrobial susceptibility pattern of the invading organisms must be estimated PD

The presence or absence of host factors that can modify the choice of antimicrobial agents PK

–History of previous adverse reactions -must be specific as to nature of reaction

–Age of patient

39
Q

Host Factors

A

Concomitant disease states or the use of immunosuppressive medications
Prior adverse drug effects
Impaired elimination or detoxification of the drug
Age of the patient
Pregnancy status
Epidemiologic exposure

40
Q

Pharmacologic Factors

A

Kinetics of absorption, distribution, and elimination Ability of the drug to be delivered to the site of infection

Potential toxicity of an agent

Pharmacokinetic or pharmacodynamicinteractions with other drugs

41
Q

Determines not only the choice of the agent but also its dose and the route by which it should be administered –Ability to achieve effective concentration at sites of interest: e.g., CSF –Local factors that may modify drug efficacy

A

Site of Infection

42
Q

Blood-Brain Barrier Penetrability

Excellentwithorwithoutinflammation

A

Sulfonamides
Chloramphenicol
Trimethroprim
Metronidazole
Rifampicin
Isoniazid
Fluconazole
Flucytosine

FFIRM CST

43
Q

Blood-Brain Barrier Penetrability

Goodonlywithinflammation

A

Penicillins Cephalosporins:cefuroxime(2ndgen);

3rdgenparenteral(exceptcefoperazone);

4thgen Imipenem+cilastatin Meropenem Aztreonam Ciprofloxacin

44
Q

Blood-Brain Barrier Penetrability

that is good with inflammation exception in 3rd gen parenteral

A

cefoperazone

45
Q

Minimalornotgoodevenwithinflammation

A

Aminoglycosides

Tetracyclines

Lincosamides

Macrolides

“MALT”

46
Q

No passag eeven with inflammation
Polymixins
1st and 2ndgen cephalosporins
AmphotericinB

A

Polymixins
1st and 2ndgen cephalosporins
AmphotericinB

47
Q

The only 2nd gen cephalosporin that can penetrate the BBB that is good with inflamation

A

CEFUROXIME

48
Q

Local Factors

A

Pus –Aminoglycosides and polymixins bind to (and are inactivated by) pus.

Beta-lactamases produced by such organisms as Bacteroides fragiliscan cause local inactivation of beta-lactamantibiotics at the site of mixed infection.

pH –Aminoglycosideshave low activity at low pH Presence of foreign body

49
Q

Pus –_____________ bind to (and are inactivated by) pus.

A

Aminoglycosidesand polymixins

50
Q

Beta-lactamases produced by such organisms as _____________ can cause local inactivation of beta-lactamantibiotics at the site of mixed infection.

A

Bacteroides fragilis

51
Q

pH –_________________ low activity at low pH

A

Aminoglycosideshave

52
Q

Immune competence

______________ competence necessary to eradicate microorganisms

A

Immune system

53
Q

___________________- -increased problem in treatment of infection

–Need to kill infecting organism rather than just inhibit growth

–Often necessitates high dose prolonged therapy -increasing risk of toxicity and unwanted effects

A

Immune suppression

54
Q

Resistance in Some Antibiotics

Hydrolysis , mutant PBP

A

Β-lactams

55
Q

Resistance in Some Antibiotics

Active efluxfrom the cell

A

Tetracycline

56
Q

Resistance in Some Antibiotics

Inactivation by enzymes

A

Aminoglycosides

57
Q

Resistance

Overproduction of target

A

Sulfonamides

58
Q

Resistance in Some Antibiotics

Mutant DNA gyrase

A

Fluoroquinolones

59
Q

Resistance in Some Antibiotics

lReduced uptake into cell

A

Chloramphenico

60
Q

Resistance in Some Antibiotics

Reprogramingof D-ala-D-ala

A

Vancomycin

61
Q

Resistance in Some Antibiotics

Ribosomal methylation

A

Quinupristin/ dalfopristin

62
Q

Resistance in Some Antibiotics

RNA methylation, drug efflux

A

Macrolides

Erythromycin

63
Q

Combination Therapy:

Uses

A
  1. Empirical therapy
  2. Polymicrobialinfections
  3. Synergism desired To prevent development of resistance

A good combintaion: 2 bactericidal e.g. cell wall inhibitor & aminoglycosides

64
Q

 is usually defined as a four-fold or greater DECREASE in the MIC or MBC of the individual antibiotics when they are present together E.g. Aminoglycoside with a cell wall synthesis inhibitor (penicillin, cephalosporin, vancomycin). Probably due to increase entry of the AG into the bacterium where it interacts with the ribosome inhibiting protein synthesis.

A

Synergism

65
Q

Synergism Synergism may result if one drug inhibits the inactivation of the other –

E.g. ____________has little antibacterial activity but in irreversibly inhibits ß-lactamase and is used in combination with penicillins

Two drugs may act at different steps in a critical metabolic pathway –

E.g. trimthoprim and sulfamethoxazole –Sulfonamides inhibit the synthesis of folic acid and trimethoprim inhibits the reduction of folate to tetrahydrofolate

A

clavulanate

66
Q

More likely to occur when a bactericidal drug (e.g., penicillin, aminoglycoside) is combined with a primarily bacteriostatic drug (e.g. tetracycline)

A

Antagonism

67
Q

_____________require the cells to be growing or actively synthesizing protein and that the bacteriostatic drugs prevent growth or protein synthesis and thereby counter the effect of the bactericidal drug

The effect of the combination is not likely to be less than the effect of the bacteriostatic agent alone

A

Bactericidal drugs

68
Q

Combination: Disadvantages

A
  1. Antagonism of antibacterial effect
  2. Increased risk of toxicity
69
Q

Monitoring Therapeutic Response

A

Clinical assessment

Laboratory tests

Assessment of therapeutic failure

a. Due to drug selection
b. Due to host factors
c. Due to resistance

70
Q

Assessment of therapeutic failure

A

a. Due to drug selection
b. Due to host factors
c. Due to resistance

71
Q

What are the ideal characteristics of an antimicrobial ?

A
  1. Selective toxicity
  2. low toxicity to the host

3, cidal > static

  1. narrow spectrum
72
Q

Amonth the Bacteriostatic drugs this is NOT PURELY but only RELATIVELY STATIC. In INCREASE DOSAGE can become BACTERICIDAL

A

CHLORAMPHENICOL

73
Q

What are the common causes of pneumonia and CNS?

A

NBSH

  1. N. meningitidis
  2. B. fragilis
  3. S. pneumoniae
  4. H. influenzae
74
Q
A

2H. Pharmacology (17 decks)

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