Therapeutics 523 Final Overview II

The flashcards below were created by user jannabogie on FreezingBlue Flashcards.

  1. Which SSTIs are considered uncomplicated?
    • simple abscesses
    • impetigo
    • furuncles
    • carbuncles
    • erysipelas
    • simple cellulitis
  2. Which SSTIs are considered complicated?
    • major abscesses
    • diabetic foot infx
    • pressure/decubitus ulcers
    • necrotizing fasciitis
    • severe cellulitis
    • severe animal/human bites
  3. Which SSTI-causing bacteria are frequently isolated in outpatients? In hospitalized patients?
    • Outpatients - beta-hemolytic strep, staph aureus
    • Hospitalized - Staph aureus, Pseudomonas, Enterococcus, E. coli
  4. What are the most common pathogens in animal bites?
    • Pasturella multocida
    • Staph aureus
  5. What are the most common pathogens in Human bites?
    • Eikenella corrodens
    • Oral anaerobes
  6. Describe the presentation of impetigo
    • small superficial fluid-filled vesicles
    • "honey-crusts"
  7. Treatment of impetigo
    • Topical - mupirocin, retapamulin
    • Oral - Penicillinase resistant pen (dicloxacillin) or 1st Gen Ceph (cephalexin)
    • Suspected MRSA - TMP/SMX or doxy or minocycline
  8. Describe the presentation of furuncles and carbuncles
    • Furuncle is a boil - acute inflamm of SQ skin layers and hair follicles - occurs in skin areas containing hair follicles subject to friction and perspiration
    • Carbuncle is more extensive - extends into SQ fat and develops into multiple abscesses
  9. Groups at risk for CA-MRSA
    • persons in correctional facilities
    • players of contact sports
    • military recruits
    • native-american population
    • males having sex iwth males
    • IV drug users
    • day care centers
    • tattoo recipients
  10. What are the transmission factors for CA-MRSA (5Cs)?
    • crowded living conditions
    • sharing contaminated personal items
    • compromised skin
    • frequent skin to skin contact
    • lack of cleanliness
  11. Groups/conditions that are risks for HA-MRSA
    • LTC Facility residents
    • pts with DM, HD
    • prolonged hospitalization
    • ICU
    • indwelling catheter
  12. What bugs usually cause furuncles and carbuncles?How can it be prevented?
    • Staph aureus (including CA-MRSA)
    • These are often misdiagnosed as spider bites
    • Prevention - good hygiene, keep lesions covered, avoid contact with drainage, launder shared clothing and equip
  13. Treatment for furuncles and carbuncles
    • lesions < 5 cm: only incision and drainage
    • lesions > 5 cm: incision and drainage and abx tx
    • Oral: TMP/SMX, TCs, Clindamycin (if D test neg), Rifampin, Linezolid, (no FQs)
    • Parenteral: Vanco is DOC
  14. Clinical presentation of cellulitis
    • acute inflamm of epidermis and dermis that maylater spread into the superficial fascia
    • s/s - tenderness/pain, erythema, hot, swollen
  15. Clinical presentation of erysipelas
    • type of superficial cellulitis with prominent lymphatic involvement
    • predominantly in elderly
    • lower extremeties and face involved
    • Bright red indurated lesion, raised border sharply demarcated shiny erythematous plaque, bullae formation (severe)
  16. Treatment of erysipelas
    • 5-7 d course of abx
    • Pen VK
    • if CA-MRSA suspected, use TMP/SMX, doxy or minocycline, Pen G, if pen allergy can do IV clindamycin (if D test negative) or vanco
  17. Treatment of cellulitis
    • 7-10 day antibiotic course (14 d if severe)
    • Penicillinase resistant pens: oral- dicloxacillin, parenteral- nafcillin
    • 1st Gen Cephs: oral- cephalexin, parenteral- cefazolin
    • If pen allergy - clindamycin or vanco
    • If MRSA, DOC is vanco IV, can do linezolid IV or PO, daptomycin, etc
  18. If a pt is seeking medical attention less than 8 hours after an animal or human bite, what is the treatment? What if it is 8-12 hours after?
    • < 8 hours: general wound care or rabies and/or tetanus treatment
    • 8-12 hours: treat for infx related complications
  19. What is the treatment for animal bites? For human bites?
    • Animal: copiously irrigate tear and puncture wounds, immobilize/elevate, surgical debridement if indicated; tetanus toxoid for those who need booster; consider rabies vaccine
    • Human: irrigate, debride, immobilize; may need tetanus toxoid; consider viral disease of biter (HIV); prophylaxis of non-infected wound is recommended; if infx or clenched-fist injury treat with Abx
  20. What is the duration of treatment and the abx therapy for bites?
    • 5-10 days for treatment; 3-5 d for prophylaxis
    • Oral DOC is amoxicillin/clavulanic acid
    • Parenteral DOC is ampicillin/sulbactam
  21. Describe the characteristics and s/s of necrotizing fasciitis
    • characterized by: rapid spreading inflamm, necrosis of m., fascia, and skin, extensive inflamm of SQ tissue, progressively destroys fascia and fat
    • s/s: hot, severe pain, swollen, shiny, tender, erythematous. Systemic sx are fever, chills, leukocytosis, shock, organ failure
    • characteristics suggesting necrotizing infx: diffuse swelling followed by bullae, skin necrosis, gas bubbles in soft tissue
  22. How is necrotizing fasciitis classified?
    • Type I: polymicrobial - less serious - mixed aerobic/anaerobic - bacteriodes, peptostreptococcus, MSSA/MRSA
    • Type II: truly flesh-eating - Group A Streptococcal (strep pyogenes) - without surgical interventions mortality is virtually 100%, with intervention it is 20-50%
  23. Treatment of necrotizing fasciitis
    • Surgical debridement of necrotic tissue
    • Critical care support (fluids, ventilation)
    • Empiric broad spectrum Abx - cover Streptococcus, Staphylococcus, Enterobacteriacae and anaerobes unless it is known to be Group A strep - Use a beta lactam with beta lactamase inhibitor (amp/sulbactam, pip/tazo) + cipro or gent + clindamycin + vanco
    • If Group A Strep is identified, use Pen G + clindamycin
  24. Categories of UTIs
    • Acute uncomplicated cystitis/urethritis
    • Acute uncomplicated pyelonephritis
    • Complicated
    • Recurrent
    • Asymptomatic bacteriuria
    • Symptomatic abacteriuria (not a UTI)
    • Prostatitis
  25. In males are UTIs usually complicated or uncomplicated? In females?
    • Complicated in males
    • Uncomplicated in females
  26. How is it determined that a UTI is complicated?
    • there is structural of functional abnormality of the urinary tract
    • not determined by age or organism
  27. What constitutes a recurrent UTI?
    >/= 3 episodes in a year
  28. 3 steps in treatment of UTIs
    • 1. categorize the UTI (acute uncomplicated cystitis/urethritis or pyelonephritis, complicated, recurrent, bacteriuria, or prostatitis)
    • 2. Determine patient-specific selection factors
    • 3. Consider local susceptibility patterns
  29. Which bacteria are usually the cause of uncomplicated UTIs? Complicated?
    • Uncomplicated:
    • E. coli
    • Klebsiella
    • Proteus
    • P. aeruginosa
    • Staph saprophyticus

    • Complicated:
    • E. coli
    • Klebsiella
    • Proteus
    • P. aeruginosa
    • Enterobacter spp
  30. When is single dose therapy used to treat UTIs?
    it isn't
  31. Treatment for Acute uncomplicated cystitis
    • 1. TMP/SMX x 3d
    • 2. FQ x 3d
    • 3. Nitrofurantoin x 7d
    • 4. Beta-lactams x 3d (not as effective as bactrim or FQs)

    • if pregnant
    • 1. Amox-clav x 7d (not very good)
    • 2. Ceph x 7d
    • 3. TMP/SMX x 7d (avoid in 3rd trimester)
  32. Treatment for Acute pyelonephritis - uncomplicated vs. complicated
    • Uncomplicated:
    • 1. FQ x 14d
    • 2. Bactrim x 14d
    • 3. Amox or amox/clav x 14d

    • Complicated:
    • 1. FQ x 14d
    • 2. Extended-spectrum pen + AG

    Note: "cipro sucks" especially vs E.coli
  33. Treatment for prostatitis
    • 1st choice: FQ x 4-6 weeks
    • 2nd choice: bactrim x 4-6 weeks
    • Acute may initially require IV therapy
    • Chronic prostatitis may require longer treatment periods or surgery
  34. What is the only type of oral abx that covers Pseudomonas?
  35. Which FQ shouldn't be used in a pt who has seizures?
  36. When do we follow up with patients for acute uncomplicated cystitis, pyelonephritis, prostatitis, and recurrent UTIs?
    • acute uncomplicated cystitis - no cultures needed unless pregnant, then culture at 2 weeks and monthly until delivery
    • pyelonephritis - 2 weeks after abx course is complete
    • prostatitis - f/u at 48-72 h because high failure/relapse rate. If still febrile, ultrasound. Add'ltesting for STDs in young men and partners
    • recurrent UTI - consider bactrim 1 single strength qd, or 2 DS bactrim upon sx onset or 1 DS post coitus. In older women rule out obstruction - may consider nitrofurantoin qd, but renal fx and pulmonary fibrosis a concern. Topical estrogens reduce recurrence w/o risks assoc with HRT.
  37. What are the most likely organisms to cause Meningitis?
    • in 1 mo to 29 years, the Big 3 are N meningitidis, S pneumoniae, H influenzae
    • in 30 - 70 years, N. meningitidis and S. pneumoniae are most likely
  38. Is most meningitis acute or subacute?
    • acute - this in an emergency - need abx asap
    • note- subacute forms are usually not bacterial
  39. s/s of meningitis
    • fever, chills
    • HA, backache, nuchal rigidity, mental status changes, photophobia
    • N/V, anorexia, poor feeding habits (infants)
    • Brudzinski's sign (hips and knees flex when neck is flexed)
    • Kernig's sign (cannot straighten leg when hip is flexed to 90 degrees)
    • bulging fontanel
  40. Considerations regarding antibiotic penetration into the CNS when selecting therapy to treat meningitis
    • low protein binding (more binding, harder to get into CNS)
    • lipid soluble (more lipid soluble, easier to get into CNS)
    • small molecular weight (higher weight, harder to get into CNS)
    • unionized at physiologic pH (more polar, harder to get into CNS)
    • absence or presence of meningeal inflammation (inflamm disrupts BBB making it easier to get through)
  41. Empiric therapy for meningitis
    • Neonates: ampicillin + 3rd gen ceph
    • 3 mo - 50 yr: 3rd gen ceph +/- vanco
    • > 50 years: 3rd gen ceph + ampicillin +/- vanco
  42. Treatment for meningitis d/t Strep pneumoniae
    • DOC is Pen G
    • Alternatives - ceftriaxone, cefuroxime chloramphenicol, vanco (can add rifampin if using vanco as monotx)
    • For Pen Resistant Strep pneumoniae - vanco + rifampin, FQ, linezolid
  43. What are the risks and benefits of using adjunctive corticosteroid therapy in meningitis pts?
    • significantly less hearing loss and other neurologic sequelae
    • may decrease antibiotic penetration
  44. When should corticosteroids be given when used in treatment of meningitis?
    it is crucial that they be given before or at the same time as the antibiotics
  45. Prophylaxis for meningitis
    • S. pneumoniae - no chemoprophylaxis - vaccination
    • H. influenzae - Rifampin (alt - FQs and ceftriaxone)
    • N. meningitidis - Rifampin (alt - FQs and ceftriaxone); vaccination is best (esp in ages 2-5)
  46. Therapy for meningitis d/t brain abscess
    • surgery
    • metronidazole or chloramphenicol
  47. What are the 3 most common bacteria that cause Acute Otitis Media?
    • S pneumoniae
    • H influenzae (most common)
    • M catarrhalis
  48. How do H. influenzae, M. catarrhalis, and S. pneumoniae resist antibiotics?
    • H. influenzae and M. cat produce beta-lactamases
    • S. pneumo changes its PBPs
  49. How is Certain AOM diagnosed
    • Must have 3/3 of the following:
    • Acute onset (1-2 days)
    • Presence of middle ear effusion (immobility, bulging)
    • S/S of middle ear inflammation/infx (pain, irritability, tugging on ear, difficulty sleeping, fever, gray bulging nonmotile tympanic membrane)
  50. Which risk factors for otitis media are associated with infection caused by resistant pathogens?
    • young age (< 2 y.o.)
    • previous episodes/abx exposure (within last month)
    • day care attendance
  51. What tympanic membrane findings indicate AOM?
    • bulging
    • red
    • opaque, cloudy
    • immobile or poorly mobile
  52. Who do the current AOM treatment guidelines apply to?
    • otherwise healthy children ages 2 mo - 12 years w/o underlying conditions
    • Excludes recurrent AOM or OME
  53. AOM treatment options for ages < 6 mo, 6mo-2yrs, and >/= 2 yrs for certain and uncertain diagnosis
    • < 6 mo gets antibacterial therapy for certain and uncertain
    • 6 mo to 2 yrs gets antibacterial therapy for certain diagnosis; for uncertain they get antibacterial therapy if severe illness, but if nonsevere they have the observation option
    • >/= 2 years with certain diagnosis and severe illness gets antibacterial therapy, certain diagnosis and nonsevere illness gets observation option; with uncertain diagnosis, this group always gets observation option

    Severe illness = "moderate/severe"otalgia OR fever >/= 39 degrees (102.2)
  54. Initial treatment for AOM or for kids who fail initial observation after 48-72 hours
    • If illness is not severe, first line tx is Amoxicillin 80-90 mg/kg/d divided BID.
    • If illness is severe, first line tx is Amox/clav 90 mg/kg/d divided BID.
  55. Which therapies are poor options for AOM and why?
    • Bactrim d/t high rates of resistance to S. pneumoniae
    • Erythromycin/sulfisoxazole d/t high rates of resistance to S. pneumoniae and frequent dosing
  56. Duration of therapy for AOM
    • children less than 2 years or those with severe illness - 7d
    • children greater than or equal 2 years old with moderate illness - 5-7d
  57. Which vaccines may help to prevent AOM?
    • influenza
    • conjugate pneumococcal
  58. What are the main bacteria that cause sinusitis?
    • S. pneumoniae
    • H. influenzae
    • M. catarrhalis
  59. How many days must a pt have s/s to diagnose sinusitis?
    > 10 days
  60. Treatment of sinusitis for mild symptoms lasting < 10 days
    • analgesics/antipyretics
    • nasal irrigation, humidified air
    • decongestants
    • cough suppressants and expectorants questionable
    • antihistamines NOT useful for acute
    • intranasal steroids questionable
  61. Treatment of sinusitis when sx last >/= 10 days with no relief from supportive care.
    Empiric abx for 10-14 days min

    • For mild disease with no recent abx exposure:
    • Any pt age, if not beta-lactam allergic, treat with amoxicillin or amox/clav, or cefdinir, cefpodoxime proxetil, or cefuroxime axetil
    • If pt is beta-lactam allergic, can give TMP/SMX, macrolide/azalide, or doxycycline if over 18

    • For mild disease with recent abx exposure or moderate disease:
    • If less than 18 years, give high dose amox/clav or cefdinir, cefpodoxime or cefuroxime, or ceftriaxone
    • If 18 or over, give a respiratory FQ, high dose amox/clav, ceftriaxone, or combo therapy (covering G(+) and G(-) orgs)
  62. What is the most common mechanism of resistance to penicillins for S. pneumoniae, H. influenzae, and M. catarrhalis?
  63. Under what conditions should antibiotics be initiated for a pt with sinusitis?
    • moderate disease for 10+ days
    • severe disease
    • if s/s are worsening
  64. Dosing of amox and amox/clav for sinusitis
    • 500 mg - 1 g TID or
    • 875mg - 2g BID
    • or for kids, 90 mg/kg/d divided BID
  65. Bacterial causes of pharyngitis
    Group A beta-hemolytic strep (S. pyogenes) is most common
  66. Clinical presentation of pharyngitis - the sx that are most suggestive of GAS pharyngitis
    • fever > 38 degrees
    • tonsillar exudates
    • tonsillar edema
    • cervical lymphadenopathy (tender)
    • NO cough
  67. What is the gold standard for diagnosis of pharyngitis?
    throat culture
  68. What is the DOC for GAS pharyngitis? How is it dosed?
    • penicillin
    • if less than 12 years, give 250 mg PO BID-TID x 10d
    • if older than 12 yrs, give 500 mg PO BID or 250 mg TID-QID x 10d
    • could give 1 IM dose of penicillin benzathine (600,000 or 1.2 mil units)
  69. What is the DOC for GAS pharyngitis in kids requiring a liquid formulation?
    amoxicillin x 10 d
  70. What is the most common cause of pharyngitis in 4-15 y.o. kids?
  71. Three features that distinguish GAS from viral pharyngitis
    • viral may be afebrile
    • viral usually has no exudates
    • GAS usually has no cough
  72. What commonly causes infective endocarditis (IE)?
    • bacteria (esp. G(+) aerobic orgs)
    • fungi
    • atypical microorganisms
  73. Which valves does IE commonly affect?
    • the aortic valve and the mitral valve (left-sided)
    • IV drug users have infx on the tricuspid valve more often (right-sided)
  74. Risk factors for IE - infective endocarditis
    • Hx of IE
    • Heart valve abnormalities (e.g. prosthetic valves, valvular dysfxn, mitral valve prolapse)
    • IV drug abuse
    • Hemodialysis
    • prolonged hospital stay
  75. Pathophys of infective endocarditis
    • Endocardium is damaged leading to platelet aggregation and activation of clotting cascade - fibrins deposited on endocardial surface
    • Bacteria colonize these surfaces
    • Inflamm/immune response is activated, but fails to eliminate the bacteria - bacteria, platelets, fibrins, debris entangle and vegetations grow
    • Vegetation can protect bacteria, cause more valve damage, break off and become septic emboli, or facilitate antibody formation that may lead to more inflamm and tissue damage
  76. Complications of IE
    • permanent heart valve damage
    • heart failure
    • microembolic events
    • stroke
    • death
  77. Most common pathogens that cause IE
    • gram-positive cocci (esp. strep and staph)(also enterococcus)
    • gram negative orgs - HACEK group (Haemophilus, Actinobacillus, Cardiobacterium, Eikenella corrodens, Kingella kingae)
    • For IV drug users, add MRSA, and Pseudomonas
    • Fungi and atypical orgs are uncommon - would be more in immunocompromised pt
  78. What is the mainstay of therapy for IE? What is the best management for high risk patients?
    • drug therapy is the mainstay
    • surgery is best for high risk pts
  79. Treatment for infective endocarditis
    • supportive care
    • IV antibiotics (long duration)(use BC agents)
    • Consider short-term use of rifampin and/or gent for synergy

    • Antimicrobial regimen selection depends on:
    • if the pt has their own natural (native) valves or prosthetics
    • pt-specific factors (e.g. concerns with IV drug users = co-infections and different causative organisms and polymicrobial infx)
    • etiologic organisms and their drug susceptibilities and unique properties
  80. Empiric therapy for infective endocarditis
    Vanco + Gent +/- Rifampin
  81. Antimicrobial therapy for patients with native valve IE
    • if Viridans or S. bovis, therapy is 2-4 weeks. Use Pen G, or Ceftriaxone. Can add gent SDD for synergy. Use vanco only if pt can't tolerate pens or cephs.
    • if Staphylococci (aureus or epidermidis), therapy is 6 weeks. Use Nafcillin or Oxacillin or cefazolin. Can add Gent for synergy.
    • for HACEK organisms, therapy is 4 weeks. Use ceftriaxone or amp/sulbactam or cipro
  82. What drug is FDA indicated for treatment of S.aureus bacteremia, including those with right-sided infective endocarditis caused by MRSA/MRSE?
  83. Is antimicrobial treatment of IE longer in pts with native valves or those with prosthetic valves?
  84. Care during and after the completion of antimicrobial treatments in IE
    • Get TTE
    • drug rehab referral for IVDUs
    • dental eval
    • remove IV catheter promptly
    • short-term - get 3 blood cultures, PE for evidence of CHF, eval for toxicity from abx therapy
    • long-term - get 3 blood cultures, eval valvular and ventricular fxn using echocardiography, oral hygiene and freq dentist visits very important
  85. Name conditions with the highest risk of adverse outcomes from IE for which prophylaxis with dental procedures is reasonable.
    • prosthetic cardiac valve or prosthetic material used to repair cardiac valve
    • previous IE
    • congenital heart disease (or if repaired, for the 6 months after the procedure)
    • cardiac transplant recipients with cardiac valvulopathy
  86. Dental procedures for which IE prophylaxis is reasonable for pts with cardiac condition at risk for IE
    any that involve manipulation of gingival tissue or the periapical region of teeth or perforation of oral mucosa
  87. What meds are used for IE prophylaxis regimens before dental procedures? When should the meds be taken?
    Amoxicillin is DOC - take 30-60 min before procedure
  88. A child's acid output remains low until they are how old?
    2 years
  89. Gastric emptying and intestinal transit time are prolonged in children until what age?
    6-8 months
  90. Are IM and SQ absorptions high or low in neonates?
  91. What happens to extracellular body water content and body fat as a baby ages?
    extracellular water content decreases and body fat increases
  92. Which antibiotics have larger volumes of distribution in children than in adults? Why is this important?
    • hydrophilic abx such as AGs and vanco (lipid soluble have lower Vd in children)
    • Important because they require larger doses than adults
  93. Is plasma protein binding increased or decreased in neonates?
  94. Name 2 antibiotics that displace bilirubin from albumin. What is the significance of this in neonates?
    • sulfonamides
    • ceftriaxone
    • risk of kernicterus
  95. Is membrane permeability higher or lower in neonates?
    higher (so CNS and RBC permeability may be enhanced)
  96. Limited ability of infants to perform glucuronidation may lead to what condition?
    gray baby syndrome with chloramphenicol
  97. When do GFR, tubular secretion and reabsorption reach mature levels in kids?
    by 3 years
  98. Do AGs and Vanco have a larger or smaller Vd in peds than in adults? Is their clearance increased or decreased?
    • Larger
    • Increased
  99. Antimicrobials to avoid in neonates
    • sulfonamides
    • ceftriaxone
    • chloramphenicol
    • TCs
    • FQs
    • nitrofurantoin
  100. In neonates and young infants the Vd of AGs is _____ and the renal clearance is _______ than in older children.
    • Larger
    • Slower
  101. What is CCR5 and which drug inhibits it?
    • CCR5 is the most common receptor site on the CD4 cell for the binding of HIV
    • Maraviroc is a CCR5 inhibitor
  102. What are the SEs of maraviroc?
    myopathies and rhabdomyolysis
  103. What medication is a fusion inhibitor? What are its SEs?
    • Enfuvirtide
    • skin nodules
  104. Name the NRTIs
    • Abacavir
    • Didanosine
    • Emtricitabine
    • Lamivudine
    • Stavudine
    • Tenofovir
    • Zidovudine
  105. Name the NNRTIs
    • Delaviridine
    • Efavirez
    • etravirine
    • Nevirapine
  106. What drug is an integrase inhibitor? What are its SEs?
    • Raltegravir
    • myopathy
  107. Name the protease inhibitors
    • Atazanavir
    • Darunavir
    • Fosamprenavir
    • Indinavir
    • Lopinavir
    • Nelfinavir
    • Ritonavir
    • Saquinavir
    • Tipranavir
  108. What are class effects of NRTIs?
    • lactic acidosis
    • peripheral neuropathy
  109. Class effects of NNRTIs
    • rash
    • hepatotoxicity
    • complete cross-resistance
  110. What are the class effects of protease inhibitors?
    • metabolic syndrome (lipodystropy, dyslipidemia, hyperglycemia)
    • elevated transaminases
  111. What are the fixed dose combos for HIV meds and what drugs are in each?
    • Epzicom (abacavir + lamivudine) (2 NRTIs)
    • Trizivir (abacavir + lamivudine + zidovudine) (3NRTIs)
    • Atripla (efavirenz + emtricitabine + tenofovir) (NNRTI, 2 NRTIs)
    • Truvada (emtricitabine + tenofovir) (2 NRTIs)
    • Combivir (lamivudine + zidovudine) (2 NRTIs)
  112. Which NRTI has a SE of life-threatening hypersensitivity?
  113. Which NRTI has a SE of pancreatitis?
  114. Which NRTI can exacerbate HepB infx when it is D/C'd?
  115. Which NRTI has pancreatitis and peripheral neuropathy as SEs?
  116. Which NRTI is nephrotoxic and hepatotoxic?
  117. Which NRTI causes bone marrow suppression?
  118. Why does efavirenz need to be taken on an empty stomach?
    Fatty meals increase its absorption, so CNS effects would increase
  119. Nevirapine causes liver toxicity. Don't use in pts with CD4 counts of ______?
    • females with CD4 > 250
    • males with CD4 > 400
  120. Which PIs are sulfonamides?
    • darunavir
    • tipranavir
  121. What HIV med is used as a booster for PI therapy?
  122. Which PI causes nephrolithiasis?
  123. What is the preferred PI for pregnancy?
  124. Which PI can cause intracranial hemorrhage?
  125. Which PI is used for salvage therapy and can cause QT prolongation?
  126. If an HIV regimen needs to be changed d/t suspected drug failure, how is it done?
    change all agents involved in the regimen if possible
  127. What is HAART?
    • treatment with at least 3 anti-retroviral meds
    • usually 2 NRTIs plus a NNRTI or PI or another NRTI
  128. What is the preferred NNRTI based regimen for treatment naive patients?
  129. What is the preferred PI based regimen for treatment naive patients?
    • atazanavir with ritonavir
    • plus
    • tenofovir with emtricitabine (or lamivudine)
    • OR
    • darunavir with ritonavir
    • plus
    • tenofovir with emtricitabine (or lamivudine)
  130. What is the preferred INSTI based regimen for treatment naive patients?
    • raltegravir
    • plus
    • tenofovir with emtricitabine (or lamivudine)
  131. What is the preferred antiretroviral regimen for treatment naive pregnant women?
    • lopinavir with ritonavir
    • plus
    • zidovudine with lamivudine (or emtricitabine)
  132. Things to remember for antiretroviral treatment regimens for treatment naive patients
    • Abacavir and zidovudine are never used together
    • Didanosine is not listed in the preferred or alternative regimens on the chart
    • Nevirapine must be with zidovudine
  133. What are the classes used in initiating antiretroviral treatment in a treatment naive patient?
    • a 2 NRTI backbone
    • plus either an NNRTI or a PI (boosted)
  134. What is IRIS?
    • Immune Reconstitution Inflammatory Syndrome
    • occurs when new antiretroviral regimen is started
    • may unmask undetected opportunistic infx
    • Pathogens of concern are Pneumocystis, MAC, CMV
  135. 9 common pathogens that cause opportunistic infx in HIV patients and the treatment for each
    • 1. Pneumocystis jiroveci - bactrim x 21 d
    • 2. Toxoplasma gondii - pyrimethamine (must use leukovorin with it) + sulfadiazine
    • 3. Cryptococcus neoformans - Ampho B + flucytosine, then fluconazole
    • 4. Mycobacterium tuberculosis
    • 5. MAC - clarithromycin + ethambutol +/- rifabutin
    • 6. Cytomegalovirus - Ganciclovir or valganciclovir or foscarnet
    • 7. Candida - fluconazole or nystatin or clotrimazole
    • 8. Cryptosporidiosis - immune reconstitution
    • 9. Microsporidiosis - symptomatics
  136. What is the breakpoint value for Pneumocystis jiroveci, Toxoplasma gondii, and MAC?
    • P. jiroveci is < 200
    • T. gondii is < 100
    • MAC is < 50
  137. What is the treatment for Pneumocystis jiroveci, including adjuvant tx?
    • Bactrim x 21 d
    • Pentamidine IV
    • Clindamycin + primaquine
    • Atovaquone
    • Adjuvant - glucocorticoids (methylpred)
  138. What is the treatment for Toxoplasma gondii, including adjuvant tx?
    • Pyrimethamine + sulfadiazine
    • Pyrimethamine + clindamycin
    • Bactrim
    • Adjuvant - avoid cat poop
  139. What is the treatment for MAC, including adjuvant tx?
    • clarithromycin + ethambutol + rifabutin
    • adjuvant - watch absorption of ARV
  140. What are the 1st line agents for TB?
    • isoniazid
    • rifampin/rifabutin/rifapentine
    • pyrazinamide
    • ethambutol
    • For active TB infx, use all 4 of these together
  141. What are second line agents for TB infx?
    • cycloserine
    • ethionamide
    • AGs
    • capreomycin
    • PAS (p-Aminosalicylic acid)
    • FQs
    • Linezolid
  142. Treatment of Active TB
    • 2 months with INH/RIF/EMB/PZA
    • then 4 mo with INH/RIF
    • then 3 more mo with INH/RIF if cavitation
  143. What are 5 classes of antifungals? Give examples of each.
    • azoles (fluconazole, itraconazole, posaconazole, voriconazole)
    • polyenes (Amphotericin B)
    • echinocandins (Anidulafungin, Caspofungin, Micafungin)
    • antimetabolites (flucytosine)
    • allylamines (terbinafine)
  144. Which antifungal class has nephrotoxicity as its primary toxicity?
    polyenes (Ampho B)
  145. Which azole has particularly poor activity vs. non-albican species?
  146. Which azole antifungal is renally eliminated? What is the main toxicity of the azoles?
    • fluconazole
    • hepatotoxicity
  147. Which azole antifungal may need therapeutic drug monitoring and why?
    voriconazole because it exhibits non-linear elimination
  148. Which azole antifungal has saturable oral absorption? What does this mean in terms of dosing this agent?
    • posaconazole
    • the absorption doesn't increase with doses larger than 200 mg, so even though its half life is 25-30 hours, it must be administered tid to qid
  149. What is a normal dose for each of the following? Ampho B, Fluconazole, Liposomal Ampho B, Micafungin, Flucytosine, Voriconazole, Posiconazole
    • Ampho B: 1mg/kg IV QD
    • Liposomal Ampho B: 5 mg/kg IV qd
    • Fluconazole: 400 mg IV qd
    • Micafungin: 150 mg IV qd
    • Flucytosine: 100 mg/kg PO qd
    • Voriconazole: 300 mg PO bid
    • Posaconazole: 200 mg PO tid
  150. What body parts/systems are commonly colonized by Candida spp?
    • skin
    • GIT
    • URT
    • Female genitourinary tract
  151. Do candida infx usually arise from endogenous or exogenous sources?
    • endogenous
    • compromise of host defenses/immune fxn can lead to infx
  152. Risk factors for Candida infx
    • colonization
    • exposure to broad-spectrum Abx
    • placement of a central venous catheter
    • use of parenteral nutrition
    • GI or cardiac surgery
    • prolonged hospitalization
    • ICU stay
    • thermal injury
    • premature birth
    • neutropenia
    • use of corticosteroids
    • HIV infx
    • diabetes
  153. Common Candida spp that cause human infx. Which of these are most worrisome and why?
    • C. albicans
    • C. glabrata
    • C. tropicalis
    • C. parapsilosis
    • C. krusei

    krusei and glabrata are the most concerning because they have lots of resistance - esp to azoles
  154. Which antifungals are C. glabrata and krusei resistant to? Which are they susceptible to ?
    • resistant to azoles
    • susceptible to Ampho B and echinocandins
  155. What is the best treatment for candidemia caused by Candida?
    • Echinocandins are preferred
    • Can use fluconazole if pt is hemodynamically stable, non-neutropenic, and C. glabrata or krusei is not suspected
  156. What is the treatment for invasive candidiasis?
    • if pt is hemodynamically unstable or neutropenic: use liposomal Ampho B, and echinocandin, or voriconazole
    • if pt is hemodynamically stable and non-neutropenic, but C. glabrata or krusei is suspected: use echinocandin
    • if pt is hemodynamically stable and non-neutropenic and C. glabrata and krusei are not suspected: use fluconazole or echinocandin
  157. What is the duration of therapy for candida infection?
    • at least 14 days
    • if disseminated, it is months
  158. Where is Aspergillus spp commonly found?
    • soil
    • food
    • construction sites
  159. Risk factors for acquiring Aspergillus
    • prolonged neutropenia (< 100)
    • advanced HIV
    • inherited immunodeficiency
    • transplantation pts
  160. Is Aspergillus infection usually from an endogenous or exogenous source?
  161. What type of drugs can facilitate the virulence of Aspergillus? How?
    • steroids
    • decrease the oxidative killing by macrophages
    • may promote cell growth
  162. What radiographical findings indicate a diagnosis of aspergillosis?
    • Not chest x-ray
    • CT scan - halo sign and air crescent
  163. What is the treatment for Aspergillosis?
    • Primary - Voriconazole is DOC, could also use ampho B, echinocandins (don't kill hyphae, so the Asperg. could keep growing later on), or other azoles
    • Salvage therapy - if lack of response or tolerance to another agt
    • Prophylaxis
    • Duration of treatment is at least 6-12 weeks
    • Neutropenic patients should receive colony stimulating factors
  164. What is the infecting organism for Bacterial Vaginosis and what is the treatment?
    • it is polymicrobial - mostly anaerobic bacteria like G. vaginalis, Mycoplasma, Ureaplasma
    • treatment is Metronidazole or Clindamycin
  165. Infecting organism and treatment for Chlamydia
    • Chlamydia trachomatis
    • Treatment:
    • Azithromycin 1 gram x one single dose
    • Doxycycline 100 mg BID x 1 week
  166. Infecting organism and treatment for Genital Herpes
    • HSV-1 or HSV-2
    • no cure
    • suppressive therapy - acyclovir, famciclovir, valacyclovir
  167. Infecting organism and treatment for Genital Warts
    • HPV
    • 90% of the cases are cleared by the immune system within 2 yrs
    • no cure - treat outbreaks - Podofilox, Imiquimod
    • Prevention - Gardasil Vaccine - the 6 & 11 are the ones that cause warts (16 & 18 cause cervical cancer)
  168. Infecting agent and treatment for Gonorrhea
    • Neisseria gonorrhoeae
    • Treatment is curative - Ceftriaxone 125 mg IM single dose, or Cefixime 400 mg orally in a single dose
  169. Infecting organism and treatment for pubic lice
    • Pediculosis Pubis (an ectoparasite)
    • Pediculocides - permethrin or pyrethrin
    • Alt - malathion or ivermectin
  170. Infecting organism and treatment for scabies
    • Sarcoptes scabiei
    • Permethrin or ivermectin
    • alt - lindane
  171. Infecting org and treatment for syphilis
    • Treponema pallidum
    • Penicillin - Single IM dose for infx of less than one year
  172. Infecting org and treatment for Trichimoniasis
    • Trichomonas vaginalis
    • Metronidazole 2 grams PO single dose
    • or Tinidazole 2 g PO single dose
    • or metronidazole 500 mg PO BID x 7d
  173. What is the most appropriate therapy for PID?
    Cefotetan 2 g IV q12h
Card Set:
Therapeutics 523 Final Overview II
2011-05-30 16:57:41
Therapeutics Final Overview II

Therapeutics 523 Final Overview II
Show Answers: