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52 Cards in this Set
- Front
- Back
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What are some of the host defense mechansims against bacteria? |
normal flora skin acts as physical barrier mucosal membrane immune response chemical factors |
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what is the definition of antibiotics? |
an antibiotics is a drug used to treat bacterial infections |
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What is the major and other attributes towards a good antibiotic? |
major: selective against bacterial, not harmful to host other: - resonable cost - long shelf life - hard to develop resistance to - soluble in body fluids - not allergic - stable |
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What are the ADV and DISADV of broad spectrum antibiotics? |
ADV: kill a large range, do not have to know the bactiera DISADV: will also wipe out normal flora |
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What is the difference between bactericidal and bacteristatic? |
bactericidal - kill bacteria bacteriastatic - inhibit bacteria growth |
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Should an immunosuppressed person be giver bactericidal or bacterstatic? |
bactericidal |
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Which class of antibiotics has most broad spectrum |
tetracycline |
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What class drugs inhibit cell wall synthesis? |
beta-lactam drug = Penicillin and Cephalosporin |
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What is special about penicillin and cephalosporin? |
both contain beta-lactam ring, which is substrate analoge to D-alanine |
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WHta is the mechanism of beta-lactam drugs? |
competitive inhibitor to D-alanine. 1. beta-lactam ring bind to PBP (penicillin binding protein) 2. inhibit cross linking of cell wall 3. accumulation of cell wall pecursors 4. fungal cell produce autolytic enzymes that cause cell lysis |
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What are the two enzymes of PBP? |
transpeptidases carboxypeptidases |
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what is the function of PBP? |
to catalyze to cross linkage of cell wall precursors |
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What is required for beta-lactam drugs to work? |
the cell needs to grow, cell wall production |
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why does penicillin only work on gram +ve bacteria? |
gram +ve bacteria peptidoglycan is exposed, direct access. gram -ve bacteria peptidoglycan is covered. need to go through proin channels to reach peptidoglycan layer. penicillin molecules cannot go through porin channels. |
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Due to penicillin only lmited to gram +ve, what was done to kill gram-ve? how do they work? |
ampicillin, amoxicillin they are able to go through porins |
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When are patients given cephalosporin instead of penicillin? |
when patients have non-immediate penicillin allergic reactions |
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Define 'resistant microorg'. |
organism not killed /inhibited by antibiotics at concentrations that is achievable after normal dosage. |
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What are the mechanism of resistance? |
1. deceased permeability to drug 2. efflux pump 3. alter receptor 4. bypass pathways 5. over production of targets 5. inactivate enzymes |
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Where are most resistance genes mediated? |
plasmids |
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What is beta-lactamase? |
enzyme from fungal cells to breakdown beta-lactam ring --> antibiotics wont work |
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What drug was created to overcome beta-lamase? |
methicillin - cannot be digested by beta-lactamase |
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beta-lactamase inhibitors. give e.g. |
e.g. clavolanic acid |
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How does beta-lactamase inhibitor and beta-lactam drug work together? |
inhibitor inhibit all beta-lactamase and beta-lactam cause cell lysis |
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what is MRSA? |
MRSA = mecillin-resistant staph aureus hospital acquired infection resistance towards methicillin due to mutation to PBP |
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give e.g of innate resistance
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1. decrease permeability 2. produce beta-lactamase 3. change affinity between beta-lactam and PBP |
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What are the two protein synthesis inhibiting drugs? |
Macrolides and Cholramphenicol |
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What bacteria does macrolides cover? |
gram +ve and -ve legionellas chylamidia |
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what is special abt macrolides? |
it contains a lactone ring |
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When is macrolides used instead of penicillin |
when ppl allergic to penicillin |
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what is the mechanism of macrolides? |
1. bind to 23s of rRNA in fungal cell 2. prevent of peptide bond between two amino acids 3. prevent chain elongation (translation) 4. prevent protein synthesis |
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describe resistance to macrolides. |
methylaton of 23s RNA by 2 adenine nucleotides macrolides can no longer bind to subunit |
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what bacteria does chloramphenicol act on? |
gram +ve and -ve chylamidia rickettsia |
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what is the mechanism of chloramphenicol? |
1. bind to 23s or rRNA fungal cells 2. prevent peptidyltransterase activity 3. prevent chain elongation 4. prevent protein synthesis |
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describe resistance to chloramphenicol. |
fungal produce chloramphenicol acetyl transferase - acelylate antibiotics - no longer bind to 23s subunit |
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whatk kind of infection uses chloramphenicol? |
ear and eye infection |
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What do ppl dont like to use tetracycline |
high resistance and bad side effects |
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what are some of the side effects of tetracyclin? |
nausea, headache bad form of child teeth when taken at 18 weeks pregnant make yellow/brown teeth if taken at below 12 years of age |
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what is the mechanism of tetracyclin? |
antibiotic bind reversibly to 30s subunit cause distortion of subunit anticodons on tRNA cannot complement with codon on mRNA cannot elongation chain |
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describe resistance to tetracyclin. |
fungal have efflux pump |
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What are the two drugs of aminoglycosides? |
streptomycin and gentamicin |
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How is aminoglycosides applied? |
systemic cannot be absorbed by the gut |
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what is the mechanism of aminoglycosides |
bind to 30s subunit prevent binding of 50s subunit freeze 30s inhibit protein synthesis |
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what are the toxic effect of aminoglycosides? |
- deafness - loss of balance - kidney damage |
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Why does the use aminoglycosides need constant monitoring? |
because the therapeutic range is very small the therapeutic dosage is very close to the toxic dosage monitoring can prevent toxic effects modify dosage |
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How is aminoglycosides dosage monitored? |
measure plasma concentration of drug from 6-14 hours after infusion |
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describe the resistance of aminoglycosides |
fungal have aminoglycosides modifying enzymes which change structure of anitbiotics cannot be taken into cell - target cell alteration - alter cell wall permeability |
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How does gentamicin and penicillin work together? |
provide a synergistic effect pencillin cause break in cell wall, allow gentamicin to enter cell and bind to 30s subunit |
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What are the two types metabolic analogs? |
1. Sulphonamides 2. trimethoprim |
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What are the functions of sulphonamides? |
as an analog to Para-aminobenzoic acid - inhibit dihydropteroic reductase - inhibit folate synthesis in bacteria |
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What are the functions of trimethoprims? |
as an analog to dihydrofolic acid
- inhibit dihydrofolate reductase - inhibit folate synthesis in bacteria |
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How do you test for antibiotic sensitivity? |
1. test for MIC - minimal inhibition concentration 2. test or MBC - minimal bactericidal concentration (use concentration of from MIC that exhibit no growth) 3. Disc Diffusion Test |
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Explain the disc diffusion test. How is the CDS method used to determine antibiotic sensitivity? |
Spread the bacteria on to plate and place drop of antiobiotic the zone of inhibition shows bacteria sensitivity to the antibiotics. CDS method: if the radius of inhibition: >6mm = sensitive < 6mm = resistant |
