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principles of disease > antimicrobial therapy week 5 > Flashcards

antimicrobial therapy week 5 Flashcards

1
Q

what is bactericidal

A

antimicrobial that kills bacteria

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2
Q

what is bacteriostatic

A

antimicrobial that inhibits growth of bacteria

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3
Q

what is M.B.C

A

minimal bactericidal concentration: minimum concentration of antimicrobial needed to kill a given organism

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4
Q

what is M.I.C

A

minimal inhibitory concentration: minimum concentration of antimicrobial needed to inhibit growth of a given organism

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5
Q

what is topical administration

A

applied to surface e.g. skin or mucuos membrane

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6
Q

what is systemic administration

A

taken internally, (orally or parenterally)

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7
Q

what is parenteral administration

A

administered intra-venously or intra-muscularly or occasionally subcutaneously

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8
Q

what are the mechanisms of action of antibiotics

A

3 ways:

  • inhibition of cell wall synthesis
  • inhibition of protein synthesis
  • inhibition of nucleic acid synthesis
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9
Q

what antibiotics use inhibition of cell wall mechanism

A
  • penicillins
  • cephalosporins
    (beta lactams) - penicillin and cephalosporins contain b lactam rings
  • effective mostly against gram positive bacteria
  • glycopeptides (bactericidal) e.g. vancomycin and teicoplanin
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10
Q

why is the inhibition of cell wall synthesis only effective in gram positive organisms

A

there is an inability to penetrate the gram negative cell wall

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11
Q

what antibiotics use the inhibition of protein synthesis mechanism

A
  1. aminoglycosides (concentration dependent bactericidal antibiotics) = useful in the treatment of serious gram negative infection e.g. coliform
    - gentamicin
  2. macrolides (depending on conc. and species bactericidal or bacteriostatic) = useful alternatives to penicillin for gram positive in those allergic
    - erythromycin
  3. tetracyclines (bacteriostatic) = treatment of gram positive
    - tetracyclines
  4. oxazolidinones (bacteriostatic or bactericidal depending on bacteria being treated) = treatment of gram positive
    - linezolid
  5. cyclic lipopeptide (strong bactericidal) = treatment of gram positive
    - daptomycin
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12
Q

what antibiotics use inhibitors of nucleic acid synthesis mechanism

A
  1. inhibition in purine synthesis (bacteriostatic, when combined bactericidal)
    - trimethoprim
    - sulphamethoxazole
    (these two are used in combination in the drug co-trimoxazole)
  2. fluroquinolones (bactericidal) = particularly effective against gram negative
    - ciprofloxacin
    - levofloxacin
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13
Q

what are the two types of antibiotic resistance

A
  • inherent or intrinsic resistance

- acquired resistance

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14
Q

what is inherent or intrinsic resistance

A
  • strains are given a natural resistance to an antibiotic
    e. g. streptococci always resistant to aminoglycosides
    e. g. gram negative organisms always resistant to vancomycin
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15
Q

how do you get acquired resistance

A

can occur in two ways:

  1. spontaneous mutation
  2. spread of resistance - gene that codes for resistance spread via plasmids or transposons from organism to organism
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16
Q

what are the types of horizontal gene transfer in bacteria

A
  1. conjugation - DNA transfer via plasmids or transposons
  2. transformation - naked DNA exchanged
  3. transduction - bacterial DNA transferred by viruses
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17
Q

what is the issue with beta lactase production in antibiotic resistance

A
  • b lactamases are bacterial enzymes which cleave the b lactam ring of the antibiotic and thus render it inactive (most hospital strains of staphylococcus aureus produce b lactamase ) (b lactamase also common in gram negative bacilli)
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18
Q

what are the two ways to combat b lactamase

A
  1. modify the antibiotic side chain, this produces new antibiotic resistance to the actions of b lactamase
    - co-amoxiclav = amoxicillin plus the b lactamase inhibitor clavulanic acid
  2. introduce a second component to the antibiotic (b lactamase inhibitor) protecting the antibiotic from enzyme degradation
    - flucloxacillin (antistaphylococcal) = a modified form of penicillin
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19
Q

what are extended spectrum b lactamases (ESBLs)

A

enzymes that mediate resistance to extended spectrum cephalosporins (an antibiotic)
- problem in hospitals by some gram negative organisms

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20
Q

what are carbapenemase producing enterobacteriaceae (CPE)

A

a bacterium that is a member of the enterobacteriaceae family, resistant to the carbapenem class of antibiotics through the production of carbapenemase

21
Q

what are carbapenem resistant enterobacteriaceae (CRE)

A

a bacterium that is a member of the enterobacteriaceae family, resistant to the carbapenem class of antibiotics by any means

  • there are some extremely resistant gram negative organisms
  • in some cases NO antimicrobial options available!!!!
22
Q

what is alteration of penicillin binding protein (PBP) target site

A
  • develop resistance to b lactams by changing the structure of their PBPs
  • mutations in PBP genes result in a modified target site to which b lactams will no longer bind
  • MRSA is any strain of s. aureus that has developed resistance to b lactam antibiotics
  • can be treated with flucloxacilin, linezolid and vancomycin
  • ALTHOUGH.. there are now vancomycin resistant enterococci
23
Q

what are some commonly used penicillins

A

benzyl penicillin - gram positive organisms
amoxicillin, ampicillin - gram negative activity
co-amoxiclav - b lactamase producing coliforms
flucloxacillin - staphylococcal infections (resistant to b lactamase)

24
Q

what are some common b lactams: cephalosporins

A

first gen. = cepharadiine
second gen. = cefuroxime
third gen. = ceftriaxone and cerftazidime
( gram negative activity increases through generations and gram positive decreases)

25
Q

what is a common aminoglycosides

A
  • gentamicin
  • gram negative organisms
  • parenteral use only
  • serum levels must be monitored because of potential toxicity
  • cheap and common
26
Q

what are some common glycopeptides

A
  • vancomycin (levels must be monitored due to toxicity)

- gram positive

27
Q

what are some common macrolides

A
  • clarithromycin (atypical pneumonia)
  • erythromycin (atypical pneumonia)
  • azithromycin (chlamydia)
  • gram positive
  • alternative to penicillin
28
Q

what are some common quinolones

A

third gen = levofloxacin

  • nearly all gram negative
  • this group is only possibility for oral therapy for pseudomonas infections
29
Q

miscellaneous common agents

A

trimethoprim - treatment of urinary infections
co-trimoxazole = trimethoprim + sulphamethoxazole (chest infections)
fusidic acid - anti-staphylococcal (should always be used in combination)
clindamycin - gram positive

30
Q

what are some newer agents

A

linezolid - treats MRSA

daptomycin - gram positive (can be used in serious MRSA infections)

31
Q

common urinary tract agents

A
  • nalidixic acid

- nitrofurantoin

32
Q

what are some side effects of antibiotics

A
  • allergic reactions (associated with b lactams)
  • immediate hypersensitivity (IgE mediated due to parenteral administration)
  • delayed hypersensitivity (immune complex or cell mediated)
  • gastrointestinal side effects (nausea and vomiting common)
  • thrush (normal flora suppressed so less competition for yeast)
33
Q

what are some toxicity effects

A
  • liver toxicity
  • renal toxicity
  • neurological toxicity (ototoxicity - hearing, optic toxicity, peripheral neurpathy - numbness, encephalopathy and convulsion - brain)
  • haematological toxicity e.g. linezolid causes bone marrow suppression
34
Q

what are some polyene anti-fungal drugs

A 
amphotericin B (extremely toxic) - only drug for IV use
nystatin - topical use only
35
Q

how do polyenes (anti-fungal) work

A

bind to ergosterol (present in fungal wall but not bacteria) and this results in increased permeability of the cell wall

36
Q

what are some anti-fungal azoles

A

fluconazole - oral and parenteral treatment of yeast infections
itraconazole - active against both yeasts and filamentous fungi
voriconazole - treats aspergillosis

37
Q

how do azoles (anti-fungals) work

A

inhibition of ergosterol synthesis (component of fungal cell wall)

38
Q

what is a allylamines anti-fungal drug

A

terbinafine - acts against dermatophyte infections

- suppresses ergosterol synthesis

39
Q

what are some anti-fungal echinocandins

A
  • caspofungin
  • micafungin
  • andulafungin
    used for serious candida and aspergillum infections
    they inhibit the synthesis of gluten polysaccharide in fungi
40
Q

what type of drugs are all anti-viral drugs

A

they are all virustatic (inhibit growth/replication)

41
Q

what are some anti-herpes virus drugs

A
  • aciclovir (low toxicity) (extremely active!)
  • valganciclovir (bone marrow toxicity)
  • gangciclovir (toxic)(IV)
  • foscarnet (highly nephrotoxic)
42
Q

anti-HIV drugs

A
  • zidovudine (nucleoside analogue)
  • nevirapine (non-nucleoside reverse transcriptase inhibitor)
  • saquinavir (viral protease inhibitor)
  • combination therapy is normal
  • usually zidovudine + nevirapine or saquinavir
43
Q

drugs for chronic hepatitis B and C

A
  • interferon-a (protein that forms part of the host immune response)
  • ribavirin
  • lamivudine + adefovir dipivoxil
44
Q

drugs for viral respiratory infections

A
  • zanamivir
  • oseltamivir
    both for influenza
  • ribavirin (occasionally for respiratory syncytial virus - RSV)
  • remdesivir (covid 19)
45
Q

what is prophylaxis

A

the administration of antimicrobials to prevent the future occurrence of infection
- e.g. in most abdominal operations

46
Q

what is empirical antimicrobial therapy

A

when the organism causing infection is not known empirical antimicrobial therapy may have to be commenced if urgent treatment is required

e. g adult with local pneumonia is likely to be infected with pneumococci and thus an agent such a benzylpenicillin or amoxicillin should be included
- intra-abdominal infection would require an agent of combination of agents that are likely to cover coliform and anaerobic organisms

47
Q

what is additive effect of combined antibiotics

A

additive 1+1=2

synergistic 1+1=5 (combined effect much greater)

48
Q

what is the simplest way to measure M.I.C

A

(minimum inhibitory concentration)
using an E-test
- paper strip

49
Q

how do labs test for susceptibility of bacteria to antibiotics

A

automated methodology

principles of disease (19 decks)

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