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104 Cards in this Set
- Front
- Back
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gram neg bacteria
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gram neg- appear pink upon gram stain
thin cell wall beta lacatamase enzymes and outer lipopolysaccharide layer with pores common gram neg: enterics, H influenzae, neisseria and psuedomonas |
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gram pos bacteria
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gram pos bacteria appear blue upon stain
thick outer wall beta lactamse enzymes on outer cell wall surface **higher internal osmotic pressure than negs *commonly cause of ocular infections |
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richettsia and chlamydia
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richettsia and chlamydia:
are intracellular parasites |
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spirochetes
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spirochetes-
flexible spiral bacteria |
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mycobacteria
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mycobacteria-
high lipid levels and slow growing |
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acitomyces
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acitomyces:
filamentous branching bacteria resembling hyphae of fungi |
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most common ocular pathogenic bacteria- gram positive cocci:
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most common ocular pathogenic bacteria- gram positive cocci:
**staph aureus -staph epidermis strep pyogenes **strep pneumiae -viridans group of streptococci |
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most common ocular pathogenic bacteria- gram positive rods
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most common ocular pathogenic bacteria- gram positive rods:
corynebacterium diphtheriae |
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most common ocular pathogenic bacteria- gram negative cocci:
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most common ocular pathogenic bacteria- gram negative cocci:
neisseria gonorrhea neisseria meningitidis |
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most common ocular pathogenic bacteria- gram negative rods:
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most common ocular pathogenic bacteria- gram negative rods:
-moraxella lacunta, H influenzae -pseudomonas aeruginosa, E coli -Enterobacter aerogenes, salmonella species -proteus mirabilis, Klebsiella Pneumoniae -serratia marcescens, shigella species -acinetobacter species |
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antibacterial drug MOAs--bacteriocidal
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antibacterial drug MOAs--bacteriocidal:
1. inhibit cell wall synthesis 2.increase cell membrane permeability 3.inhibit DNA synth |
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antibacterial drug MOAs--bacteriocidal and bacteriostatic
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antibacterial drug MOAs--bacteriocidal and bacteriostatic
-inhibit protein synth -inhibit intermediary metabolism |
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4 ways bacteria share genetic material:
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4 ways bacteria share genetic material:
1. Transformation- 2. Transduction 3.Conjugation 4.transposon insertions |
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4 ways bacteria share genetic material:
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4 ways bacteria share genetic material:
1. Transformation-DNA fragments from a lysed bacteria can be taken up into genome of living cell 2. Transduction-bacteriophage virus can carry dna from one bacteria to another 3.Conjugation-direct cell-to cell transfer of genetic info via plasmid 4.transposon insertions-pieces of DNA move from site to site within or between DNAs of bacteria/plasmids/bacteriophages **bacteria that gets acquired resistance can share with others via these means |
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4 mechanisms of bacterial resistance
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4 mechanisms of bacterial resistance
1. enzyme induction (bacteria enzymes can inactivate the drug) 2.receptor site adaption 3.conformation membrane changes (perm barrier) 4.alteration of metabolic pathway (can bypass way inhibited by the drug) |
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what are some forms of conjunctivits that may need oral administration?
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what are some forms of conjunctivits that may need oral administration?
-hyperacute -adult chlamydial -phylectenular (bleb or nodule by limbus) -reccurent corneal errosions |
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what are some forms of eyelid infections that may need oral administration?
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what are some forms of eyelid infections that may need oral administration?
-internal hordeolum (sty) -meibomianitis -preseptal cellulitis -dacrocystitis (sac) -acne rosacea -blepharitis |
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when might you need parenteral admin?
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when might you need parenteral admin?
-severe dacryocystitis (inflammation of nasolacrimal sac-usually from blockage of duct) -periorbital cellulitis |
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how do you treat endophthalmitis and panophthalmitis?
Endophthalmitis means bacterial or fungal infection inside the eye involving the vitreous and/or aqueous humors panophthalmitis- inflammation of all the eye structures or tissues (entire eye from virulent pyogenic organisms) |
how do you treat endophthalmitis and panophthalmitis?
aggressive antibacterial therapy--IM, IV, SUBCONJUNCTIVAL, INTRAVITREAL |
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*prefer cidal over static drugs
*prefer narrow spectrum |
*combine cidals=additive/synergystic
*combine statics=additive *combine cidals with statics=may be antagonistic |
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bacterial cell wall synthesis-4 stages
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4 stages of bacterial cell wall synthesis:
1. NAM associated with pentapeptide 2. Chains lengthen and carried out of cell 3.carrier recycles into cell 4. chains crosslinked **bacteria have outer peptidoglycan layer--alternating NAM and NAG links. Cross linking of polysacharide chains create rigid wall |
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Inhibitors of cell wall synthesis:
(types) |
1. Penicillins
2. Cephalosporins 3. Bacitracin 4. Vancomycin |
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Penicillins MOA
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Penicillins
-inhibit stage 4 of cell wall synth (cant crosslink) *bacteriocidal *mostly active against rapidly diving cells |
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what are the 4 groups of penicillins
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4 groups of Penicillins:
1.Highly effective against gram pos bacteria 2.Resistant to penicillinase 3. With extended spectra of activity 4.With Antipseudomonal activity |
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4 groups of Penicillins with the pencillins
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4 groups of Penicillins:
1.Highly effective against gram pos bacteria *Penicillin G and Penicillin V 2.Resistant to penicillinase *Methacillin, Oxacillin,Cloxacillin, Dicloxacillin,Nafcillin 3. With extended spectra of activity *Ampicillin and Amoxacillin 4.With Antipseudomonal activity *Carbenicillin, Ticarcillin, Pipercillin, Azlocillin, Mezlocillin |
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Group 1 penicillins
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group 1 Penicillins-
Highly effective against gram pos bacteria, and some gram neg *Penicillin G and Penicillin V *G given through parenteral or topical ocular solution *V given through oral |
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Group 2 penicillins
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Group 2 Penicillins.
Resistant to penicillinase *Methacillin, Oxacillin,Cloxacillin, Dicloxacillin,Nafcillin |
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Which group 2 penicillins for corneal ulcer?
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1. Which group 2 penicillins for corneal ulcer?
-subconjunctival methacillin -oxacillin |
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Which group 2 penicillins for internal hordeolum?
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Which group 2 penicillins for internal hordeolum?
_oral cloxacillin -dicloxacillin |
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Which group 2 penicillins for acute dacryosystitis?
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Which group 2 penicillins for acute dacryosystitis?
-oral cloxacillin -dicloxacillin -oxacillin |
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Which penicillins for preseptal cellultitis?
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Which penicillins for preseptal cellultitis?
parenteral nafcillin or oxacllin and Penicillin G with aminoglycosides |
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Group 3 penicillins
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g3 Pneicillins-
. With extended spectra of activity *Ampicillin and Amoxacillin *these are less effective against bacterial sensitive to G but active against gram negatives (like Haemophilius, e coli, and proteus) **these ARE destroyed by penicillinase[beta lactamase] (unlike group 2 which is resistant) |
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using group 3 penicillins, how do you treat hyperacute conjunctivitis?
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using group 3 penicillins, how do you treat hyperacute conjunctivitis?
with either ampicillin/amoxacillin WITH topical ciloxan |
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which group 3 penicillin for Haemophilus acute dacrocystitis?
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which group 3 penicillin for Haemophilus acute dacrocystitis?
oral amoxacillin |
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group 4 penicillin
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g4. Penicillins:
With Antipseudomonal activity *Carbenicillin, Ticarcillin, Pipercillin, Azlocillin, Mezlocillin **effective against pseudomonas, proteus, enterobacter, acinetobacter |
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how are group 4 penicillins administered?
and what is the exception? |
*all group 4 pencillins given via the parenteral route (IM/IV)
exception: Carbenicillin-oral route |
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what is the major adverse affect of penicillins?
and some other rxns? |
what is the major adverse affect of penicillins?
-ALLERGY **nonallergic rxns are CNS disturbances, hypokalemia, (low potassium), inhibition of normal platelet aggregation **superinfection if mess up normal flora |
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3 methods of bacterial resistance to penicillins
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3 methods of bacterial resistance to penicillins
1. Enzyme induction (bact enzymes inactivate drug) 2. receptor site adaption 3.conforational membrane changes |
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moa of Cephalosporins?
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Cephalosporins: are Bet-lactam antibiotics
*inhibit stage 4 of cell wall synthesis (crosslink) **CIDAL -they cause lysis of filamentous growth -they CAN be inacivated by beta lactamases (because they are BETA LACTAM DRUGS!) -**3 generations |
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what are the 1st generation of cephalosporins
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1st generation cephalosporins: (didnt name them all)
*good gram pos, and modest gram neg activity *inactivated by beta lactamases (because cephalosporins are beta lactam drugs) |
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**what is the 1st generation cephalosporin that treats corneal ulcer?
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**what is the 1st generation cephalosporin that treats corneal ulcer?
CEFAZOLIN (USE fortified drops or subconjunctival injection) **celphaloridine can be a substitute |
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what is the 1st generation cephalosporin that treats endophalmitis?
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what is the 1st generation cephalosporin that treats endophalmitis?
either CEFAZOLIN/celphaloridine with AMINOGLYCOSIDE |
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what is the 1st generation cephalosporin(s) that TXS ACUTE DACRYOCYSTITIS or preseptal cellulitis?
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what is the 1st generation cephalosporin(s) that TXS ACUTE DACRYOCYSTITIS or preseptal cellulitis?
oral cephalexin or cephadroxil |
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2nd generation cephalosporins
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2nd generation cephalosporins
**few for ocular uses (cefaclor and cefuroxime both oral avail) |
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3rd generation cephalosporins
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3rd gen cephalosprins
*more active than 1st/2nd generations against gram neg (but less against gram pos) |
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which 3rd generation cephalosporins useful for pseudomonas tx?
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which 3rd generation cephalosporins useful for pseudomonas tx?
Cefaperazone and cefatazidime |
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adverse rxns for cephalosporins
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cephalosporin rxns:
**ALLERGY MOST COMMON -vit K deficiency(can lead to bleeding) -renal impairment -normal flora--superinfection |
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Bacterial resistance to cephalosporins?
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Bacterial resistance to cephalosporins?
-ENZYME INDUCTION |
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Bacitracin--moa
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Bacitracin-
*inhibits stage 3 of cell wall synth works against gram + (staph/strep) and gram - (neisseria gonnorhea) **primarily used topically (bc of renal toxicity) |
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adverse effects of bacitracin
(big one) |
adverse effects of bacitracin
**CONTACT DERMATITS --no systemic probs with topical use |
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Vancomycin moa
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Vacomycin:
inhibits stage 2 of cell wall synth (binds to pentapeptide and inhibits elongation) --works against staph, strep, clostridium, corynebacterium, n gonnorhea) **NOT usually for topical ocular use--save for serious life threatening systemic infections |
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resistance to vancomycin MOA
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resistance to vancomycin MOA:
receptor site adaptions |
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Antibacterial drugs that increase the permeability of bacterial cell membrane:
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Antibacterial drugs that increase the permeability of bacterial cell membrane:
1. Polymyxin B 2.Gramacidin |
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permeability drugs do what?
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permeability drugs act like cationic detergents--they interact with the ppospholipids in cell membrane--cell swells and dies
**PERMEABILITY DRUGS ARE CIDAL on non dividing cells |
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Polymyxin B--MOA
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Polymyxin B--permeability drug-cationic detergent (CIDAL)
**WORKS on GRAM NEG BACTERIA-PSEUDOMONAS, E COLI, h INFLUENZAE, ENTEROBACTER **CAN USE FOR TOPICAL OCULAR/EAR/SKIN or systemic infections (serious pseugomonas) --can be neurotoxic, nephrotoxic, paresis, paralysis **no signifcant systemic effects with ocular use |
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Gramacidin
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Gramacidin-permeability drug
*similar to polymyxin B *Gram + |
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Inhibitors of protein synthesis--Aminoglycosides-name them (6)
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Aminoglycosides:(inhibitors of pr0tein synth)
1.Streptomycin 2. Neomycin 3.Gentamycin 4. Tobramycin 5. Amikacin 6. Kanamycin |
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Aminoglycoside MOA
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Aminoglycosides-
Inhibitor of protein synthesis-inhbits tRNA from binding, misreading of code, and polysome disruption *Bactericidal against gram neg (and many staph strains too) |
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what are some mechanisms of gram neg resistance to Aminoglycosides?
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what are some mechanisms of gram neg resistance to Aminoglycosides?
1. alter bacterial ribosome 2.decreased antibiotic uptake 3. Enzymatic inactivation of drug |
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Aminoglycosides administration
(synergystic with what 2?) |
Aminoglycosides administration:
-parenteral *synergystic with penicillins and cephalosporins |
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which is the most toxic of the aminoglycosides (protein synth inhibitors)?
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which is the most toxic of the aminoglycosides (protein synth inhibitors)?
NEOMYCIN |
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NEOMYCIN-
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NEOMYCIN--aminoglycosides-protein synth inhibitor
*most toxic one -works against gram pos and neg *mostly topical *allergic rxns common |
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Gentamycin
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Gentamycin-- -Aminoglycoside (protein synth inhbitor)
*works against staph, H influenzae, and gram neg rods *commonly used for surface ocular infections *can be topical, subconjunctival, intravitreal, and systemic **ALLERGY LESS COMMON THAN NEOMYCIN For serious corneal ulcers-you can use gentamycin fortified solution WITH penicillins and cephalosporins |
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Tobramycin
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Tobramycin-aminoglycoside
*a lot like gentamycin but more active against pseudomonas and less toxic than it *fortified solution for severe corneal ulcers |
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what is the drug of choice for Mycobacteria?
(an aminoglycoside) |
what is the drug of choice for Mycobacteria?
Amikacin (an aminoglycoside) |
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Aminoglycoside adverse effects:
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Aminoglycosides rxns adverse:
low therapeutic index, vestibular/auditory probs, nephrotoxic, neuromuscular blockade(inhibit CA+), ALLERGY TOPICALLY ocular |
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resistance to aminoglycosides
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resistance to aminoglycosides:
1. ezyme induction 2. receptor site adaption 3.conform. membrane change |
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Tetracyclines: name 2
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Tetracyclines:
1. Doxycycline 2. Minocycline |
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Tetracyclines: moa, etc
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Tetracyclines:
**bacteriostatic -natural or synthetic -short, long, intermediate duration *binds to 30s subunit and ihibit TRNA binding to 50s -has anticollagenolytic actvity **wide spectrum gram pos and neg, aerobic and anaerobic |
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tetracycline uses
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Tetracyclines uses-
*chlamydial inclusion conjunctivitis -nontuberculum phlyctenular keratoconjunctivitis -ocular manifestations of acne rosacea |
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Tetracyclines adverse rxns
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Tetracyclines adverse rxns:
**allergy-topical systemic low at normal dose (but some if look up, nausea, anorexia, inhibition of bone growth) |
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Tetracycline resistance mechs:
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Tetracycline resistance mechs:
1. Reduced drug uptake 2. Increased transport out of cell |
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Doxycycline (used for?)
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Doxycyline:
a tetracycline- use for chlamydial conjunctivitis and meibomianitis -like tetracycline, has anticollagenolytic effct |
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Minocycline
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Minocycline-tetracycline
similar to others but causes lightheadedness, dizzy, vertigo, etc |
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Macrolides-name 3
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Macrolides-name 3
1. Erythromycin 2.Azithromycin 3. Clarithromycin |
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Erythromycin-moa
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Erythromycin-macrolide
-inhibits protein synthesis (binds to 50s subunit) *bacteriostatic-mostly gram pos + (topical use-staph blepharitis, external horeolum, ) systemic uses: Legionaires disease |
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Azythromycin--good for what?
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Azyhtromycin-macrolide
*good for: oral administration great for adult chlamydial conjunctivitis; also good for bleph/lid infections -comes in zpac and tri-pak **Azythromycin is also available as Azasite-a topical ocular drug for bacterial conjunctivitis |
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Clarithromycin
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Clarithromycin--a macrolide
*good for adult chlamydial conjunctivitis but not as effective as azythromycin |
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Chloramphenicol-moa
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Chloramphenicol- bacteriostatic
--broad-spectrum antibiotic, alongside the tetracyclines **inhbits protein synth--binds to 50s ribosomal subunit |
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Chloramphenicol adverse rxns:
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Chloramphenicol adverse rxns:
***Gray baby syndrome-poor metab/excretion=death -hematopoetic disorders--bone marrow depression; aplastic anemia -and al sorts of other stuff |
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Chloramphenicol resistance:
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Chloramphenicol resistance:
1. Enzyme induction |
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Clindamycin-moa
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Clindamycin-protein synth inhibition
*bacteriostatic |
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Inhibitors of Folic Acid Synthesis
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Inhibitors of Folic Acid Synthesis:
1. NA sulfacetamide Sulfisoxazole 2. Short acting sulfonamides 3. Pyrimethamine and Trimethaprim |
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NA sulfacetamide Sulfisoxazole-moa
and adverse rxns- |
Inhibitors of Folic Acid Synthesis-
1. NA sulfacetamide Sulfisoxazole- *bacteriorstatic -member of sulfonamide family *inhibit bacterial conversion of para-aminobenzoic acid into dihydrofolic acid (but little effect on hman since we get folic acid from food) *topical only!! for surface infections adverse rxns: stevens johnsons syndrome (skin necrolysis), allergy, white corneal plaques |
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2. Short acting sulfonamides--moa and use
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(Inhibitors of Folic Acid Synthesis:)
2. Short acting sulfonamides -can use for trachoma and taxoplasmosis |
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3. Pyrimethamine and Trimethaprim-moa
adverse rxns? |
Inhibitors of Folic Acid Synthesis:
3. Pyrimethamine and Trimethaprim-- **inhibit dihydrofolate reductase (but not harming human) advrse rxn: WBC and platelet depression |
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Inhibitors of DNA synthesis
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--DNA is coiled, and needs dna gyrase(aka topoisomerase II) to uncoil it so that replication can occur. These drugs inhbit the gyrase/topoisomerase so this can't happen
**quinilones/fluoroquinilones |
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4 generations of Quinilones:
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4 generations of Quinilones:
-1st generation-effective against gram pos +, but no ocular applications -2nd generation-gram + activity with increase in gram neg -3rd gen: expanded gram + and effective against atypical bacteria (and inc in solubility) -4th gen:vast inc in gram + activity, anaerobic organisms, and atypical pathogens |
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4 generations of Quinilones:
-1st generation-name |
4 generations of Quinilones:
-1st generation-effective against gram pos +, but no ocular applications *nalidixic acid |
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4 generations of Quinilones:
-2nd generation-name 3 |
4 generations of Quinilones:
-2nd generation-gram + activity with increase in gram neg **ciprofloxacin, norfloxacin, ofloxoacin |
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4 generations of Quinilones:
-3rd gen: name 1 |
4 generations of Quinilones:
-3rd gen: expanded gram + and effective against atypical bacteria (and inc in solubility) **levofloxacin |
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4 generations of Quinilones:
-4th gen:name 2 |
4 generations of Quinilones:
-4th gen:vast inc in gram + activity, anaerobic organisms, and atypical pathogens **moxifloxacin and gatifloxacin |
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The Newest Quinilone:
(Fluroquinilone) |
Besifloxacin
-approved for bacterial conjunctivitis **the only flouroquinilone specifically developed for topical ocular use (no systemic counterpart that an contribute to resistance) -wide spectrum against both gram pos and negs *good because increases contact time with eye compared to solutions -same MOA as 4th generation drugs *wide spectrum bacteriocidal (against both gram pos and neg) -adverse rxns: blurry vision, eye pain, etc |
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Fluoroquinolones -moa and structure
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Fluoroquinolones inhibit the topoisomerase II ligase domain
**basic molecule is nalidixic acid---added with flourine |
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Fluoroquinolones Resistance
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1. Receptor site adaption
2. Conformational membrane change |
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first available flouroquinilone by alcon?
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first available flouroquinilone by alcon?
Ciprofloxacin |
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Ciprofloxacin
**MOA? |
Ciprofloxacin
-first available flouroquinilone by alcon -bacterCIDAL (wide spectrum) (staph, strep pseudomonas and many other gram pos and neg organisms) **IT INHIBITS DNA GYRASE |
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Resistance to Ciprofloxacin?
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Resistance to Ciprofloxacin?
chromosomal mutation **has a post antibiotic suppressive effect |
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indications for Ciprofloxacin?
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Indications for Ciprofloxacin?
1. Bacterail conjunctivitis (staph aureues, epiderm, pneumonia) 2. Bacterial Coneal ulcers (pseuomonas auriginosa, staphs,) adverse rxns of ciprofloxacin: itching, conjunctival hyperemia, bast taste in mouth, corneal staining, allergy, lid edema, etc -no significant systemic effects with topical use |
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Norfloxacin
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Norflaxacin-similar to ciprofloxacin (flouroquininlone)
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Ofloxacin-moa
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Ofloxacin similar moa, etc to ciprofloxacin (flouroquinilone-dna synth inhibits)
*use for corneal ulcer and conjunctivitis *often used after cataract or LASIK surgeries as prophylactic against bacterial infection |
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Levofloxacin-moa, etc
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Levofloxacin
*Levo-isomer of ofloxacin (flouroquinilone) -moa, etc similar to other drugs in class **BUT has better lipid solubility than others in class--so can readily penetrate cornea and reach higher aqueous concentrations **use for bacterial conjunctivitis and ulcers both gram pos and neg |
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Moxifloxacin and Gatifloxacin info
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Moxifloxacin and Gatifloxacin-newer members to flouroquinilone class
(in may, new form of Gatifloxacin= called Zymaxid) **these have greater activity against gram pos+ (than do 2nd and 3rd gen), anaerobics, and atypicals |
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Moxifloxacin and Gatifloxacin MOA and uses
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Moxifloxacin and Gatifloxacin-newer members to flouroquinilone class
*they have greater corneal penetration -block DNA gyrase and topoisomerase IV -two mechanisms decrease chance of resistance *have a large bicyclic amino chain at C7 to inhibit bacteria from pumping the drug out of the cell (furthers help preventing resistance) Moxifloxacin and Gatifloxacin approved for bacterial conjunctivitis (and off label prophylaxis and ulcers) |
