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Exam 2 > Antibiotics Lecture 12 > Flashcards

Antibiotics Lecture 12 Flashcards

1
Q

Gram Positive

A

Staphylococcus (CoNS, aureus, MRSA)

streptococcus (pyogenes, pneumonia, PCN-resistant)

enterococcus (faecalis, faecium, VRE)

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2
Q

Gram Negative

A

Piddly: Haemophilus, morexella, morganella, shigella, salmonella (provedencia, neisseria)

fence (pek): proteus, eschericia coli, klebsiella

SPACE: serratia, pseudomonas, acinetobacter, citrobacter, enterobacter

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3
Q

Atypicals

A

chlamydia, mycoplasma, legionella

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4
Q

Anaerobes

A

peptostreptococcus, bacteroides, clostridium

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5
Q

Bactericidal agent

A

kill bacteria

penicillins, cephalosporins

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6
Q

bacteriostatic agent

A

works but may have limitations

inhibitory to growth of susceptible microorganisms: sulfonamides

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7
Q

Narrow spectrum of activity

A

effective against a small number of microorganisms

Pen G: gram positive organisms (strep)

nafcillin: staph and strep

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8
Q

broad spectrum of activity

A

effective against a large number of microorganisms

piperacillin/ tazobactam

imipenem: gram positive, gram negative, and anaerobic organisms

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9
Q

Synergy

A

enhancement of action of one drug by another

trimethoprim/sulfamethoxazole: sequential inhibition of folic acid synthesis

penicillin/aminoglycoside: increased penetration of aminoglycoside as penicillin breaks down cell wall (enterococcus)

different site for mechanism of action (psedomonas)

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10
Q

antagonism

A

decreased action of one drug by another

bacteriostatic/bactericidal: most cidal agents require active cell division or acitve protein synthesis for expression of their bactericidal activity.

many static agents inhibit these “active” processes

may be more in vitro than in vivo

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11
Q

postantibiotic effect

A

persistent effect of an antimicrobial on bacterial growth following brief exposure of organisms to a drug

aminoglycosides and fluoroquinolones

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12
Q

pharmacodynamics: concentration and time dependent killing

A

concentration dependent killing: killing dependent on peak concentration. Optimal kill occurs when conc exceeds 10x MIC. Quinolones, aminoglycosides

time dependent killing: Killing is dependent on amount of time the concentration stays above the MIC (40-50%). B-lactam antibiotics

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13
Q

Mechanism of action of antimicrobial agents

A

inhibitors of cell wall synthesis

inhibitors of protein synthesis or structure

interferes with cell membrane function

interferes with DNA/RNA syntehsis

inhibitors of metabolism

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14
Q

Inhibitors of cell wall synthesis

A

Penicillins/cephalosporins/carbapenems/aztreonam: prevents cross linking of peptidoglycan strands by inhibiting transpeptidases

vancomycin: inhibits peptidoglycan synthetase and polymerization of linear peptide

bacitracin

cycloserine

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15
Q

Inhibitors of protein synthesis/structure

A

aminoglycosides: inhibits 30s ribosomes; causes misreadings of mRNA
chloramphenicol: inhibits peptidyl transferase and peptide formation

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16
Q

Inhibitors of protein synthesis/structure 2

A

erythromycin, clindamycin, lincomycin: inhibits 50s

tetracyclines: inhibits binding of aminoacyl tRNA to ribosome. 30s

streptogramins/linezolid: 23s

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17
Q

interference with cell membrane function

A

polymixin B, colistin: cationic detergent

fungal section: azole and polyene antifungals

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18
Q

interference with DNA/RNA synthesis

A

rifampin: inhibits DNA dependent RNA polymerase
fluoroquinolones: intereres with super coiling of DNA by action of DNA gyrase topoisomerase II

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19
Q

Inhibitors of metabolism

A

isoniazid, ethambutol: inhibits lipid synthesis

sulfonamides, trimethoprim: prevents synthesis of folic acid

20
Q

confirm presence of infection

A

antimicrobial stwardship

fever

signs and symptoms: physical findings (cackles, SOB, erythema, dysuria), leukocytosis/left shift, pain, blood

predisposing factors: disruption of natural barriers, immunosuppressive state, age

21
Q

basic steps in therapy

A

determine the site of infection

determine the causative organisms: which antimicrobial agents are effective against it (them)

select a drug based on: sensitivity of the microorganism, physiochemical properties, toxicities of the drug, patient characteristics

follow patient for clinical response

alter therapy as necessary

22
Q

Starting empiric ABX coverage

A

site of infection difficult to culture: cellulitis, pneumonia, brain abscesses, middle ear infection

serious or life-threatening infections: timing to collect cultures

empiric therapy: culture site before starting antibiotics. Gram stains very informative for selection of empiric antibiotic

23
Q

Pharmacologic considerations

A

route of administration, distribution, routes of elimination, drug interactions, allergies

24
Q

routes of administration

A

oral candidates: mild to moderate infections

intravenous candidates: moderate to severe infections. patient unable to take oral agents. afebrile for 2-3 days consider change to oral

intramuscular: IV access is not obtainable. Short term solution

25
distribution
consider site of infection and distribution of agent to that site urine concentration, bone penetration, lung tissue penetration, skin and osft tissue concentration, meningitis (penetration into CNS when meninges are inflamed vs uninflammed (ceftriaxone vs unasyn))
26
route of elimination
renal vs hepatic: dose reduction for renal insufficiency. Recommendation for dialysis patient. Many drugs are eliminated through the renal system. urinary tract infection: renal excretion is desired. High concentration of drugs are eliminated unchanged.
27
drug interactions
concurrent medication interferes with antibiotic: antacids with quinolones and tetracycle antibiotic interferes with concurrent agent: bactrim or erythromycin with warfarin. Ciprofloxacin with theophylline, and linezolid with selective serotonin reuptake inhibitor (SSRIs)
28
microbial resistance
certain organisms inherit resistance patterns from environmental exposure to ABX resistance may be natural or may result from mutation, adaptation, or gene transfer multiple resistance-plasmids
29
mechanisms of resistance
increased drug inactivating enzyme activity (b-lactamases) alter cell wall/ membrane permeability: alteration of the porin channel altered binding site/ receptor of drug drug efflux increase endogenous metabolite: sulfonamides (bacteria may synthesize PABA to antagonize drug)
30
MoR Penicillins/cephalosporins
B lactamases PBP changes Porin channel changes
31
MoR aminoglycosides
enzyme inactivation
32
MoR Macrolides
Methyltransferases that alter drug binding sites on 50S ribosomal subunit
33
MoR tetracyclines
transport systems that pump drugs out of the cell
34
MoR sulfonamides
Increased PABA formation target enzyme sensitivity
35
MoR Fluroquinolones
target enzyme changes drug efflux
36
Combination therapy Pros and cons
advantages: treatment of mixed bacterial infections. treatment of severe infections when organism is unknown. Enhancement of antibacterial activity (synergy: endocarditis tx; pseudomonas spp) disadvantage: added risk of toxicity
37
Adverse effects
allergic reactions dose related toxicities: imipenem: seizures, amphotericin: nephrotoxicitiy, cefazolin: neutropenia (dose and duration) idiosyncratic reactions: aplastic anemia: chloramphenicol alteration of normal flora (superinfection)
38
Cost
the least expensive agent that will treat the patient's infection should be used de escalation from broad spectrum to narrow side effect profile required monitoring of therapy: vancomycin peak/trough, very expensive (CBC, SCR/BUN, trough levels)
39
delays in beginning therapy
initiate therapy as soon as possible first dose in ER (mixed research 2, 4, 6, 8 hours) balance overuse vs timely administration important to culture suspected sites before beginning antibiotics check gram stain and results of cultures for verification of appropriate antibiotics
40
inadequate drug or drug levels
patient not culture before initiating therapy meningitis: inadequate penetration of drug into the CNS pneumonia: aminoglycosides concentration of 8-10 mcg/ml necessary to penetrate the lung (40% of blood conc reaches lung) balance high enough peak with low enough trough call pharmacy to dose and monitor
41
host defenses inadequate
immunocomrpomised host: cancer patients or HIV/AIDS patients success dependent on achieving a level of antibacterial activity: sufficient to tip the balance in favor of the host. dWhile preventing toxicities, resistance and superinfection
42
abscess
antibiotic therapy, in most cases, is not adequate drainage of involved area necessary to resolve infection antibiotic cleans up the remaining infection and/or cellulitis
43
Other factors
drug interactions: binding and compliance microbial resistance: developed during therapy. intrinsic lab error viral infection
44
superinfection
alterations in normal flora results in removal of inhibitory influences in the body usually due to broad spectrum antibiotics enterobacteriaceae (PEK, SE) candida spp. clostridium difiicile (pseudomembranous colitis)
45
SPACE bug coverage: Box and one coverage
cell wall inhib: PCN (piperacillin, ticarcillin), Ceph (cetazadime, cefepime), Carbapenem (imipenem, meropenem), Monobactam DNA gyrase: FQN (ciprofloxacin, levofloxacin) 30S: aminoglycosides (gentamicin, tobramycin, amikacin)
46
SPACE: Ace in the Hole and the last resort
Azetreonam (Anaphylaxis) Colistin

Exam 2 (23 decks)

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