Therapeutics 523 Final Overview I

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Therapeutics 523 Final Overview I
2011-05-28 21:13:59
Therapeutics Final Overview

Therapeutics 523 Final Exam Overview I
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  1. What is the cell wall of prokaryotes (like bacteria) made of?
    proteins, lipids, peptidoglycans
  2. What is the cell wall of eukaryotes (such as fungi) made of?
    • Chitin
    • mannans, glucans (polysaccharides)
  3. Which type of organisms have ergosterol, where is it, and what is its purpose?
    • eukaryotes
    • in the cell membrane
    • it is a target or binding site for many antifungals
  4. What is the difference between the cell walls of G(+) and G(-) bacteria?
    • G(+) have a thick layer of peptidoglycan with many cross links
    • G(-) have a thinner layer of peptidoglycan with fewer cross links
  5. What is a gram stain used for?
    • to classify bacteria as (+) or (-) on the basis of stain retention of the cell's peptidoglycan layer
    • G(+) stain purple
    • G(-) stain red
  6. Name the 2 different types of media used to identify or differentiate between bacteria ad some examples of each.
    • Differential - Identity of an organism - e.g. Macconkey inhibits growth of G(+) and supports G(-) growth, especially GIT orgs; CHROM differentiates betw Candida spp
    • Selective - select specific bacteria from mixed cultures - e.g. Thayer-Martin allows Neisseria to grow
  7. Name the 2 types of biochemical tests and what the results tell us.
    • 1. Coagulase - if (+) the org is S. aureus; if (-) the org is other Staph spp
    • 2. Catalase - if (+) the org is staphylococci; if (-) the org is streptococci
  8. What is the purpose of the Lancefield serogroup test?
    To group Strep spp. It can tell us where the infx came from.
  9. What do respiration/fermentation tests tell us?
    • if a bacteria has the ability to use lactose or glucose to produce acid or alcohol
    • e.g. of non-fermenters - Pseudomonas, Acinetobacter
  10. What does a hemolysis test on blood agar tell us about a bacteria?
    • If alpha, they are partially hemolytic - a small zone is cleared. e.g. S. pneumoniae
    • If beta, they are completely hemolytic - a large zone is cleared. e.g. S.pyogenes
    • If gamma, they are not hemolytic.
  11. What do serologic tests detect?
    • Nonspecific or specific antibodies
    • Presence and quantity can aid in identification of pathogen
  12. If an unknown bacteria is a cluster of G+ cocci, what test might be used to determine the identity?

    • A coagulase test.
    • If (+) they'd probably be Staph aureus
    • If (-) they'd probably be Staph epidermidis
  13. If an unknown G+ bacteria is cocci in pairs or chains, what is its likely identity?

    • Streptococci or Enterococcus
    • If they are Streptococci, they could be Alpha or Beta hemolytic.
    • If Alpha, likely identity is S. pneumoniae or Viridans group
    • If Beta, Group A may be S pyogenes, Group B may be S. agalactiae, Group D may be S. bovis, or others
  14. Gram + bacilli are unusual, but what are some of the more likely of this type of bacteria we may encounter?

    • Bacillus anthracis
    • Corynebacterium diptheriae
    • Gardnerella vaginalis
    • Listeria monocytogenes
  15. Gram negative bacilli are usually what type of bacteria?
  16. Examples of coliform enterobacteriaceae
    • E. coli
    • Klebsiella spp
    • Enterobacter
    • Serratia
  17. Examples of non-coliform enterobacteriaecae
    • Proteus spp
    • Salmonella spp
  18. Are enterobacteriaceae fermentors or non-fermentors?
  19. Name some non-fermentors
    • P. aeruginosa
    • Acinetobacter
  20. Is Neisseria G(+) or (-)? Aerobic or anaerobic? Cocci or Bacilli?
    Aerobic G(-) cocci
  21. Name 3 G(+) anaerobes
    • Clostridium
    • Peptostreptococcus
    • Propionibacterium acnes
  22. Name one G(-) anaerobe and why it is a concern
    • Bacteroides fragilis
    • Concerning because it is inherently resistant to Abx
  23. Name 3 atypical bacteria and the reason they're considered atypical

    • Chlamydia spp - cell wall similar to G- but lack peptidoglycan
    • Mycoplasma spp - lack a cell wall
    • Legionella spp - G- but difficult to stain; difficult to grow on standard media; use serologic testing to identify
  24. What is MIC? What is MBC?
    • Minimum Inhibitory Concentration - the lowest conc of an agt that inhibits the visible growth of an organism
    • Minimum Bactericidal Concentration - the lowest conc of an agt that results in a 99.9% reduction in colony forming units (kills the bacteria)
  25. What does a bimodal susceptibility distribution indicate?
  26. If the MBC is ______ times the MIC, the organism is tolerant
  27. What are breakpoint values?
    • they help evaluate MIC results and guide clinical decisions
    • based on pkin and pdyn of drug, MIC distribution in the bacteria population, clinical efficacy
    • tell if bacteria is susceptible, intermediate, or resistant to particular drugs
  28. What is an antibiogram?
    a table telling the bug, drug, % susceptibility to various drugs
  29. Is the true MIC ever determined?
  30. Define virulence and virulence factors
    • Virulence is a quantitative measurement of pathogenicity - the likelihood a pathogen will cause a disease
    • Virulence factors are factors that allow a microbe to establish itself on or in a host and enhance its potential to cause disease
  31. What are the 5 steps of pathogenesis?
    • 1. Colonize the host
    • 2. Gain access to the host
    • 3. find a niche within the host
    • 4. Evade host defenses
    • 5. Multiply within the host
  32. What are adhesions? Name 4.
    • Microbial structures that mediate adherence of binding of a microbe to the host. Susceptible hosts have receptors for the adhesions.
    • 1. fimbriae/pili
    • 2. lectins
    • 3. lipids
    • 4. mechanical
  33. Why might microbes produce biofilms? What are 2 pathogens that commonly produce biofilms?
    • to facilitate binding to target cells
    • to elude host defenses and Abx

    • Pseudomonas
    • Staph aureus
  34. How does a microbe maintain viability once inside a host?
    • Must evade host defenses by:
    • Producing antiphagocytic capsule
    • Producing toxins or destructive enzymes
    • Stealth
  35. What are exotoxins? What are endotoxins?
    • Exotoxins - bacterial proteins that the bacterium releases during exponential growth that are toxic for target cells
    • Endotoxins - intracellular and cell-associated toxic components of G(-) microbes - lipopolysaccharides
  36. List 3 factors that have contributed to the emergence of antimicrobial resistance
    • 1. Inappropriate antibiotic use by clinicians
    • 2. lack of pt education or ineffective education
    • 3. widespread antimicrobial use in the food production industry
  37. Difference between primary and secondary resistance
    • Primary is naturally occurring and no exposure to antimicrobials is required; secondary follows exposure to antimicrobials
    • Primary is predictable; secondary is not
    • Primary is also known as inherent, intrinsic, or native; secondary is also known as acquired
  38. How does secondary resistance come about?
    • Selection of resistant subpopulations
    • Genetic alterations - spontaneous mutations or acquisition of new genetic material
  39. List 3 common mechanisms of antimicrobial resistance
    • 1. antibiotic inactivating enzymes
    • 2. alteration of antimicrobial target or active site
    • 3. alterations in bacterial cellular membranes
  40. how do beta-lactamases work?
    inactivate beta-lactam antibiotics by splitting the beta-lactam ring at the amide bond
  41. What are ESBLs and what are they active against?
    • Extended-spectrum beta-lactamases
    • Active vs. all beta lactams except cephamycins, cefepime, carbapenems
    • Inhibited by beta-lactamase inhibitors such as sulbactam, clavulanate, and tazobactam
  42. Are AmpC-type beta-lactamases inhibited by beta-lactamase inhibitors?
  43. Examples of resistance by alteration of the antimicrobial target or active site
    • penicillin binding proteins (PBPs)
    • ribosomal binding sites
    • cell wall precursors
    • DNA gyrase
  44. Examples of resistance by alterations in bacterial cellular membranes
    • porin channels (change in # or size)
    • transport proteins
    • efflux pumps
  45. What is MRSA's resistance secondary to? What is the treatment of choice?
    • altered PBP
    • vancomycin (linezolid and daptomycin may also be used)
  46. What may be a good treatment option for VISA?
  47. What therapy is necessary for a cidal effect in enterococcus? Name 3 treatment strategies.
    • combo therapy with an aminoglycoside (with penicillin or vanco - these are static alone)
    • 1. vanco, linezolid, daptomycin, and streptogramins
    • 2. intermittent vs. continuous infusions of beta-lactams and vanco
    • 3. traditional vs once-daily dosing of AGs
  48. List 6 strategies to prevent the spread of antibiotic resistance
    • 1. patient education
    • 2. knowledge of local susceptibility patterns
    • 3. prescriber education
    • 4. develop guidelines for appropriate antimicrobial usage
    • 5. vaccination
    • 6. hand washing
  49. Can penicillins still work in pen-resistant S. pneumoniae?
  50. Do AGs exhibit time-dependent or concentration-dependent bactericidal activity?
  51. What are the 2 major toxicities assoc with AGs? What factor is best correlated to toxicity?
    • ototoxicity & nephrotoxicity
    • prolonged course of AG tx
  52. What are the main goals of high-dose, extended-interval (once daily) AG dosing? How is the dosing interval determined?
    • Optimize bactericidal activity
    • Minimize toxicity
    • Dosing interval determined and evaluated using a nomogram
    • (basically a LD is given every time and the conc goes down to 0 in between doses each time)
  53. How many half-lives does it take to reach steady state?
    approx 5 (assuming renal fxn is stable)
  54. How do we empirically dose vanco?
    • based on pt's weight (TBW) and CrCl
    • using nomogram
  55. Does Vanco exhibit concentration-dependent or concentration-independent killing?
    concentration-independent (time-dependent) - time above MIC
  56. What are the usual vanco target drug concentrations?
    Trough: 5-20 mg/ml
  57. What is "red man syndrome"? How can it be prevented?
    • Hypotensive rxn assoc with rapid infusion of vancomycin. D/T a vanco-induced histamine release.
    • Prevent by slowing the infusion and/or premedicating with an antihistamine
  58. A pt has a sinus infx susceptible to both amoxicillin and ampicillin. Which do you choose and why?
    Amoxicillin because it has better bioavailability, you can give it with or without food, there is less frequent dosing than with ampicillin (bid or tid as opposed to qid)
  59. An MD wants to prescribe Augmentin 500 mg TID for a pt with recurrent sinusitis. The pt can't swallow Augmentin 500 mg tabs. He writes for Augmentin 250 mg 2 tabs TID. Is this a good idea? Why?
    No. Too much clavulanic acid - leads to diarrhea.
  60. A pt has a severe pen allergy. Can the pt receive azetreonam? A carbapenem?
    • Aztreonam yes
    • Carbapenem no
  61. Which FQs inhibit DNA gyrase? Topoisomerase IV? What is the advantage of inhibiting Topo IV?
    • All FQs inhibit DNA gyrase
    • 3rd and 4th Generation FQs inhibit Topo IV
    • Advantage - less resistance and enhanced G(+) activity
  62. Why shouldn't pediatric pts generally receive FQs? Which pediatric pts sometimes receive FQs?
    • Because they can cause cartilage malformations
    • CF patients
  63. A pt develops a sternal wound infx following bypass surgery after an acute MI. He is placed on vanco. The pt is now complaining of severe itching on his face and neck. The nurse just hung the vanco bag on this pt about 10 minutes ago. He has been receiving vanco for about 7 days. What is the most plausible explanation for this event? How can you treat/prevent this rxn?
    • Red Man Syndrome
    • slow rate of infusion, give diphenhydramine, give fluids, dilute, change Abx
  64. What is the difference in indications for vanco PO and IV?
    • PO is for C. diff
    • IV is for G(+) resistant infx like MRSA and MRSE
  65. Describe the ototoxicity and nephrotoxicity that can occur with AGs
    • Ototoxicity - Cochlear and Vestibular - May or may not be reversible.
    • Nephrotoxicity - selectively toxic to proximal tubule - can cause acute tubular necrosis and glomerular nephrotoxicity
    • Related to prolonged duration of therapy or concurrent ototoxic or nephrotoxic drugs
  66. Which macrolide would you not use for bacteremia because of its extensive tissue penetration?
  67. Why should you drink a full glass of water with TCs and not take any doses at bedtime?
    to prevent esophageal ulcerations
  68. Which of the following Abx can be used to treat CAP in a pt on antiarrhythmics? moxifloxacin, azithromycin, doxycycline
    no, no, yes
  69. You have a pt on clindamycin who developed severe diarrhea and is C difficile (+) by toxin assay. How would you manage the diarrhea? List abx that can be used to treat AAD.
    • Stop the clindamycin
    • Give metronidazole 1st line PO x 10 days
    • Vanco is 2nd line x 10 days
  70. List unique SEs of metronidazole. What drug intx would you caution a pt about?
    • furry tongue feeling, abnormal taste, peripheral neuropathy
    • counsel about dirulfiram-like rxn with alcohol
  71. What are rifampin's indications for use? Why isn't rifampin ever used alone to treat an infection?
    • Indicated for TB, and for asymptomatic carriers of N. meningidites, in combo for synergy in G(+) infx
    • Combo with vanco or penicillin for endocarditis or osteomyelitis
    • Increased chance of resistance
  72. If a pt is allergic to Bactrim what other non-abx drugs may they also be allergic to?
    diuretics, celecoxib, sulfonylureas
  73. Statins should be stopped for pts on which abx because of the risk on increased CPK/myopathy
  74. Which abx has an increased risk of serotonin syndrome if given concomitantly with SSRIs or MAOIs?
  75. Which abx is available PO for the treatment of hospital-acquired MRSA/MRSE?
  76. Which abx are assoc with dysglycemia?
  77. Which abx exhibit concentration-dependent killing?
    • AGs
    • FQs
    • Metronidazole
    • Amphotericin B
    • Daptomycin
  78. Which abx exhibit concentration-independent killing?
    • Beta-lactams
    • Glycopeptides (e.g. Vanco, teicoplanin)
    • Clindamycin
    • Macrolides
    • Fluconazole
  79. What DI should you warn young women about with all antibiotics?
    • Decreased efficacy of OCs
    • Especially with rifampin
    • Use backup for duration of abx therapy plus add'l 7 days
  80. Which antibiotics interact with warfarin most significantly?
    bactrim and flagyl
  81. Which antibiotics can discolor urine?
    • nitrofurantoin
    • rifampin
    • metronidazole
  82. Which Abx cause photosensitivity?
    • FQs
    • TCs
    • sulfonamides
  83. Which Abx require therapeutic drug level monitoring?
    • AGs
    • Vanco IV
    • chloramphenicol
  84. Which abx is telithromycin related to? Which abx is tigecycline related to? Which abx is tinidazole related to?
    • telithromycin - macrolides
    • tigecycline - tetracyclines
    • tinidazole - metronidazole
  85. Which abx inhibit bacterial cell wall synthesis?
    • beta-lactams
    • vanco
  86. Which abx inhibit protein synthesis?
    • AGs
    • TCs
    • glycocyclines, chloramphenicol
    • macrolides
    • synercid
    • etc.
  87. Which abx are pregnancy category B?
    • beta-lactams
    • nitrofurantoin
    • macrolides (but not clarithromycin)
    • dlindamycin
    • metronidazole (but not in the 1st trimester)
    • sulfonamides (except in the 3rd trimester)
    • daptomycin
  88. Are beta-lactams BS or BC? What is their MOA?
    • Bactericidal
    • Inhibit cell wall synthesis by binding to PBPs leading to the bacteria having a weak cell wall which becomes leaky and then bursts
  89. What penicillin combos are antipseudomonal?
    • ticarcillin/potassium clavulanate
    • piperacillin/tazobactam sodium
  90. What is the monobactam used in combo with AGs to fight pseudomonas?
  91. Which carbapenems are antipseudomonal?
    • imipenem/cilastatin
    • meropenem
  92. Which PCN is the DOC for otitis media and acute sinusitis?
  93. What abx are the DOC in pregnancy?
  94. How do penicillins produce a DI with warfarin?
    they suppress the gut bacteria that produce Vitamin K
  95. Which cephalosporin is ok to use in neonates?
  96. Which cephs are antipseudomonal?
    • ceftazidime (3rd Gen)
    • cefepime (4th Gen)
  97. What is the purpose of cilastatin in combo with imipenem?
    • It has no antibacterial activity
    • Its role is to prevent renal tubular damage from imipenem
  98. What is the MOA of aminoglycosides?
    • Bactericidal
    • Inhibits bacterial protein synthesis
    • Has long PAE vs. G(-) organisms
  99. For G(+) aerobes gentamicin has synergy with which abx?
    vanco or a penicillin
  100. What is the MOA of fluoroquinolones?
    • Bactericidal
    • Inhibits DNA gyrase (Topo II)
    • 3rd and 4th Gen also inhibit Topo IV
    • Possess PAE for all bacteria
  101. What is the BBW for FQs?
    Tendonitis and tendon rupture
  102. Which class of Abx can cause crystalluria, QT prolongation and dysglycemia?
  103. DIs with FQs
    • Warfarin
    • multivalent cations
    • calcium
    • antiarrhythmics
    • sulfonylureas
  104. MOA of vancomycin
    • BC and BS (depending on the organism)
    • Inhibits bacterial cell wall synthesis
  105. What rate should infusion of vanco be limited to in order to avoid redman syndrome?
    give 1 gram no faster than over 1 hour
  106. What toxicities can vanco cause?
    nephro and oto
  107. MOA of macrolides/azalides and ketolides
    inhibit protein synthesis
  108. Which antibiotic classes are good for covering atypical organisms such as mycoplasma, legionella, chlamydiae, and protozoa?
    • macrolides
    • FQs
  109. clarithromycin is the DOC for which organisms?
    • MAC
    • H. pylori
  110. DOC for CAP
  111. Which abx can cause QT prolongation?
    • FQs
    • Macrolides
  112. MOA of tetracyclines
    • inhibit protein synthesis
    • bacteriostatic
  113. What class of abx is the DOC for lyme disease and rocky mountain spotted fever?
  114. Which abx have the SE of discoloration of teeth/depression of bone and teeth development?
  115. MOA of sulfonamides
    • competitive antagonism of PABA synthesis so bacteria cannot make folic acid
    • bacteriostatic
  116. DIs with sulfonamides
    • diuretics
    • celecoxib
    • sulfonylureas
  117. What is kernicterus and what abx can cause it?
    • a yellow staining of parts of the brain d/t increased unbound drug in the neonate because of neonate's inability to conjugate bilirubin
    • sulfonamides - they displace bilirubin from protein, resulting in increased free bilirubin
  118. Sulfas inhibit 2C9 which can lead to significant intx with what drug? What must be monitored?
    • warfarin
    • monitor INR carefully
  119. MOA of trimethoprim
    inhibits dihydrofolate reductase
  120. Only indication for trimethoprim
  121. MOA of lincosamides
    Inhibit bacterial protein synthesis
  122. What is the BBW on clindamycin?
    severe and possibly fatal colitis
  123. MOA of metronidazole
    • toxic to bacterial RNA and DNA
    • bactericidal to anaerobes (no activity vs. aerobes)
  124. What is the BBW on metronidazole?
    possible carcinogenicity
  125. MOA of rifampin
    • inhibits DNA-dependent RNA polymerase
    • never used alone d/t rapid development of resistance
  126. What is a unique SE of rifampin?
    reddish-orange discoloration of urine, stool, saliva, tears (permanent discoloration of contacts), sweat, sputum
  127. What abx is non-systemic and a derivative of rifamycin?
  128. Indications for nitrofurantoin
  129. SEs of nitrofurantoin
    • discolors urine brown
    • pulmonary toxicity
    • G6P deficiency hemolytic anemia
  130. BBW for chloramphenicol
    bone marrow suppression
  131. Which abx can cause gray baby syndrome?
  132. What 4 elements make up the basis of pharmacokinetics?
    • absorption
    • distribution
    • metabolism
    • elimination
  133. How does concentration-dependent bactericidal activity work? What is the goal?
    • The rate and/or extent of activity increases with increasing concentration of the antimicrobial
    • Goal is to optimize the peak:MIC ratio
    • These agents have a shallow dose-response curve
  134. How does non-concentration-dependent bactericidal activity work? What is the goal?
    • the rate and extent of bacterial killing is not significantly influenced by increasing antimicrobial concentrations - it is increased by the length of drug exposure (time-dependent killing)
    • Goal is to optimize the time above the MIC (time > MIC)
  135. Four factors that influence the PAE
    • microorganism
    • antimicrobial
    • length of antimicrobial exposure
    • antimicrobial concentration
  136. Agents that exhibit concentration-dependent bactericidal activity and have relatively long PAEs should be administered as ________________ doses to optimize the peak:MIC ratio
    large infrequent doses
  137. If a peak:MIC ratio of 10-20:1 cannot be reached, which parameter best correlates with outcome?
    • AUC:MIC
    • want it to be >100:1
  138. How should agents with concentration-independent killing and relatively short or no PAEs be dosed?
    • in order to maximize the amount of time at or above the MIC
    • small frequent doses or continuous infusion
  139. Define PAE
    post antibiotic effect - a persistent suppression of bacterial growth following a brief exposure to an antimicrobial
  140. 7 patient risk factors for pneumonia
    • 1. altered consciousness (stroke, intoxication, seizure, sleep)
    • 2. cigarette smoking
    • 3. advanced age
    • 4. underlying medical conditions
    • 5. intubation
    • 6. recent viral respiratory tract infx
    • 7. HIV/AIDS
  141. S/S of pneumonia
    • fever or hypothermia
    • rigors
    • sweats
    • new cough with or without sputum production
    • chest discomfort
    • dyspnea
  142. Can pneumonia be diagnosed based on symptoms?
  143. According to PORT scores, which risk classes treat pts as inpatients, and which treat as outpatients?
    • Risk Class I, II: outpatient
    • Risk Class III: outpatient or brief inpatient
    • Risk Class IV, V: inpatient
  144. Explain the CURB-65 Index and what it is used for
    • Used to determine need for hospitalization and need for ICU admission
    • Score based on how many of the following a patient has:
    • Confusion
    • BUN > 20 mg/dL
    • Resp Rate >/= 30 breaths/min
    • Low BP (systolic < 90 or diastolic </= 60)
    • Age >/= 65 years

    • If the score is 0-1 treat as outpatient
    • If the score is 2 admit to ward
    • If the score is 3 or more admit to ICU
  145. Risk factors for drug-resistant S.pneumoniae
    • extremes of age (< 5 or > 65)
    • antibiotic use within the past 3 months
    • exposure to a child in daycare
    • alcoholism
    • immunosuppression
    • recurrent otitis media
    • recent hospitalization
    • multiple medical comorbidities
  146. Outpatient treatment for pneumonia
    • If no recent Abx exposure, treat with macrolide (azithromycin or clarithromycin) or doxycycline
    • If pt has comorbidities or Abx exposure within last 3 months, treat with macrolide plus high-dose amoxicillin (or amox/clav) OR a FQ (levo, moxi, gemi)
  147. Inpatient treatment of pneumonia in the medical ward
    • Same if pt has had recent abx exposure or not.
    • Macrolide plus beta-lactam OR FQ
    • Options for beta-lactams - cefotaxime, ceftriaxone, ampicillin/sulbactam, ertapenem
  148. Inpatient treatment of pneumonia in the ICU
    • If Pseudomonas infx is not an issue, give a beta lactam + either a macrolide or a FQ
    • If Pseudomonas infx is an issue, give Anti-pseudomonal agt plus ciprofloxacin, OR an Antipseudomonal agt plus an AG + a FQ or macrolide Antipseudomonal agents are piperacillin/tazobactam, imipenem, meropenem, cefepime
  149. Organisms likely to cause pneumonia
    S. pneumoniae, M. pneumoniae, C. pneumoniae, H. influenzae
  150. What is the minimum duration of therapy for pneumonia? How long should a pt be afebrile?
    • Min 5 days
    • afebrile for at least 48-72 hours
  151. CAP assoc signs of clinical instability
    • temp > 37.8
    • pulse > 100 bpm
    • resp rate > 24 breaths/min
    • systolic bp < 90
    • O2 sat < 90%
    • inability to maintain oral intake
    • mental status changes
  152. What is HAP
    hospital acquired pneumonia - it occurs 48 h or more after admission and was not incubating at the time of admission
  153. What is VAP?
    ventilator-associated pneumonia - it arises more than 48-72 hours after endotracheal intubation
  154. What is HCAP?
    Healthcare associated pneumonia
  155. Risk factors for HCAP
    • pt hospitalized in an acute care hospital for > 2 days within 90 days of infection
    • pt resided in a nursing home or LTC facility
    • Pt received recent IV Abx, chemotherapy, or wound care within the past 30 days
    • pt attended a hospital or hemodialysis clinic
  156. Empiric antibiotic therapy for nosocomial pneumonia
    • if not late onset or no risk factors for MDR pathogens, treat with ceftriaxone, FQ, Amp/sulbactam, or ertapenem
    • if late onset (>/= 5 days) or risk factors for MDR pathogens, give an anti-psa ceph, or an anti-psa carbapenem, or pip/tazo PLUS an anti-psa FQ or an AG (also give vanco or linezolid if MRSA is suspected)
  157. What should be ordered in all pts with suspected pneumonia?
    • a chest x-ray - helpful with diagnosis, assessing need for hospitalization, and possible etiology
    • note: a CXR is not very valuable for monitoring pt response to therapy b/c it lags behind the clinical picture by about 3 days
  158. What are the major antigenic determinants of influenza A viruses?
    • hemagglutinin - mediates attachment and entry of virus into host cells
    • neuraminidase - facilitates the spread of virons
  159. 3 steps in the pathogenesis of influenza
    • 1. virus enters human via inhalation of virus-containing respiratory secretions
    • 2. Virus is internalized in resp tract epithelial cells
    • 3. Replicates within cells and is then released throughout the body
  160. Clinical course of influenza
    • 1-4 days of incubation
    • abrupt onset of sx
    • fever, chills, headache, myalgia, persist for about 3 days
    • resp sx may persist 3-4 d after fever subsides
    • convalescence 1-2 weeks
  161. What is the duration of infectivity for influenza?
    • 5 days after illness onset for adults
    • Children shed virus for several days before onset to > 10 days after onset of sx
  162. What is ILI?
    • influenza-like illness
    • characterized by a fever AND a cough AND/OR a sore throat in the absence of a known cause
  163. What drugs are approved for treatment and prophylaxis of influenza?
    • Neuraminidase inhibitors (oseltamivir and zanamivir)
    • must be administered within 48 h of symptom onset
  164. Which influenza medication is safe in pregnancy?
    oseltamivir (Tamiflu)
  165. Which influenza med is CI'd in asthma pts?
    zanamavir (Relenza)
  166. who should receive the influenza vaccine?
    • anyone who wants to reduce the risk of getting influenza
    • kids 6 mo - 18 yr
    • those > 50 years old
    • pregnant women
    • those with chronic medical conditions
    • immunosuppressed pts
    • residents of LTC facilities
    • those with conditions that increase risk of aspiration
    • persons who live with or care for high-risk persons (health care workers, household contacts of those < 5 and > 50 years, esp those < 6 mo, or with other high risk conditions)
  167. What are the different ways to classify intraabdominal infx?
    • 1. by location - can be localized (e.g. abscess, abdominal penetration trauma wound) or generalized (e.g. peritonitis)
    • 2. by complexity - can be uncomplicated (involving single site/organ, not into peritoneal cavity - e.g. appendicitis, cholecystitis) or complicated (involving several sites/organs in add'n to source of infx; infx extends into peritoneal cavity - e.g. peritonitis, intra-abdominal abscess)
    • 3. by acquisition locale - can be community-acquired or health-care associated (nosocomial)
  168. Which type of IAIs usually require both source control and antimicrobial therapy?
    complicated IAI
  169. Community-onset health care-associated (IAI) infx include cases involving pts with at least one of the following health care risk factors. How is hospital-onset infx different?
    • 1. presence of an invasive device at time of admission
    • 2. hx of MRSA infx or colonization
    • 3. hx of surgery, hospitalization, dialysis, or residence in a LTCF in the 12 mo preceding the culture date

    Hospital-onset infx - pts have positive culture from a normally sterile site obtained more than 48 h after admission to hospital
  170. Is appendicitis complicated or uncomplicated? How is it treated?
    • usually uncomplicated
    • managed by surgical intervention
  171. What is cholecystitis?
    sudden inflammation of gallbladder (often not infectious)
  172. When does IAI result from diverticulitis?
    When a perforation occurs and colonic contents move into the peritoneal cavity
  173. How is peritonitis classified?
    • Primary: aka SBP (spontaneous bacterial peritonitis) - no identified source - in adults with liver disease and/or ascites
    • Secondary: most common form - almost always community-acquired - may affect anyone
    • Tertiary: complication of improperly managed primary or secondary peritonitis or other abdominal medical procedures - healthcare facility-acquired - occurs in critically ill or immunocompromised pts
    • Peritoneal-dialysis associated: only in pts who receive peritoneal dialysis
  174. Common causes of peritonitis and abscess
    • appendicitis
    • diverticulitis
    • IBD
    • gastrointestinal cancer
  175. Which classes of peritonitis require urgent medical attention?
    • all of them require urgent medical attention
    • pts with secondary and tertiary are usually in acute distress and their conditions deteriorate rapidly
    • pts with primary or peritoneal dialysis-associated are not usually in acute distress
  176. What is ileus?
    the absence of peristalsis in the intestine
  177. because primary peritonitis (SBP) has highly variable and non-specific presentation, how is it diagnosed? When do we initiate empiric antibiotic treatment?
    • Must use paracentesis with lab testing of the ascites to confirm diagnosis
    • PMN cell count of > 250/mm3 is diagnostic of SBP and warrants empiric antibiotic therapy
  178. What can happen in severe cases of IAI?
    • third-spacing
    • abdominal distension
    • ileus
    • hypovolemia
    • septic shock
    • bacteremia
    • if no intervention is performed, multi-organ failures, severe systemic inflammatory response (SIRS), death
  179. What are the most common anaerobes involved in peritonitis?
    Bacteroides spp
  180. Describe the microbiology of IAI
    • Primary (SBP): usually monomicrobial, common orgs are Streptococci spp, E. coli, and Klebsiella spp
    • Secondary: usually polymicrobial with a mix of aerobic and anaerobic bacteria
    • Tertiary: associated with nosocomial microbes such as MRSA, VRE, Pseudomonas, coagulase-negative staph, candida (fungi), and those assoc with secondary
    • Peritoneal dialysis-associated: often involves enteric organisms and those found on the skin such as staph
    • Abscess: anaerobes commonly
  181. What is the typical treatment for uncomplicated IAIs?
    • surgical source control only
    • antimicrobials not required unless there is anticipated complication
    • For appendicitis only prophylactic and perioperative abx for the surgery are required - no full course of routine abx is necessary
    • For bowel injuries d/t penetrating or blunt trauma that are repaired within 12 hours and with no complications, antibiotics should be used for less than 24 hours post surgery (and prophylactic and perioperative abx)
  182. Treatment for abscess
    • surgical drainage
    • abx therapy is just an adjuvant
  183. Treatment for secondary or tertiary peritonitis
    • IV fluids
    • Infx source control
    • Empiric IV abx ASAP
    • 4-7 day course of abx therapy
  184. Treatment for SBP
    • May need IV fluids and/or surgical source control
    • If fluid from ascites confirms diagnosis of SBP (PMN > 250) abx therapy is needed
    • DOC is IV cefotaxime
    • beta lactam/beta lactamase inhibitor combos and carbapenems would work but are too broad spectrum, so are inappropriate as empiric tx. Also avoid AGs.
    • Optimal duration of therapy is 5 days minimum
  185. What is the treatment for peritoneal dialysis-assoc peritonitis?
    • may need IV fluids and surgical source control
    • culture the dialysate to id the orgs, then determine abx susceptibilities
    • empiric IV abx - followed by monotx with vanco, or a 1st gen ceph (e.g. cefazolin) given IP (would use vanco if pt is allergic to pens or if MRSA is suspected or confirmed)
    • If more severe, can add AG given IP to the ceph
    • Can admin the abx QD (intermittent dosing), and the dwell time must exceed 6 hours each time
    • Duration of tx is usually 10-14 days
  186. For IP abx therapy which abx are ok to mix in the same dialysis solution? Which should not and why?
    • vanco, AGs, cephs can all be mixed in same dialysis sol'n
    • AGs should not be mixed with pens because of chemical incompatibility (acid/base rxn)
  187. What is the duration of therapy for community-acquired peritonitis?
    4-7 days
  188. What abx is the main component in combo therapy for community-acquired IAI? Which agents should not be used?
    • metronidazole is main component (mostly used with a ceph or levo)
    • Don't use amp/sulbactam d/t E.coli resistance, cefotetan and clindamycin d/t Bacteroides resistance, AGs b/c other agents are less toxic and equally or more effective
    • Empiric antifungal tx is not necessary
    • Don't use oral agents initially
  189. Appropriate options for healthcare-acquired complicated IAI (tertiary peritonitis)
    • should have broad coverage, including Pseudomonas
    • Anti-psa B-lactam/B-lactamase inhibitor combo: piperacillin/tazobactam
    • Anti-psa carbapenems: imipenem/cilastatin, meropenem, doripenem
    • Anti-psa ceph + metronidazole: cefepime or ceftazidime
    • Anti-psa FQ + metronidazole: cipro or levo
    • Add vanco @ institutions with high incidence of MRSA/MRSE or if pt has hx of colonization
  190. When would anti-fungal therapy be indicated in healthcare-acquired complicated IAI? Which agents?
    • if pt is immunocompromised, has recurrent IAI, or failure to respond to appropriate initial therapy
    • echinocandins or azole antifungals
  191. Which type of peritonitis usually does not require culturing, speciation, and determination of antibiotic susceptibility?
    Community-acquired (secondary peritonitis) - the empiric therapy is often maintained for the full course of abx treatment unless there is intolerance or complications
  192. What is the duration of therapy for each type of peritonitis?
    • primary - 5 d minimum
    • secondary - 4-7 d
    • tertiary - 4-7 d
    • dialysis-assoc - 10-14 d
    • abscess - abx are only adjuvant
  193. What type of pneumococcal test is warranted for all pts admitted to the ICU?
    pneumococcal urinary antigen test
  194. What type of peritonitis might require prophylactic abx?
    primary (SBP)