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Respiratory II - Exam 2 > Drugs for respiratory infections - SRS > Flashcards

Drugs for respiratory infections - SRS Flashcards

1
Q

What are the two aminopenicillins we need to know?

A

Ampicillin

Amoxicillin

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2
Q

What are three B-lactamase inhibitors Waller listed in RED?

A

Ampicillin-sulbactam

Amoxicillin-clavulanic acid

Piperacillin-tazobactam

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3
Q

What are the third generation cephalosporins?

A

Ceftriaxone

Ceftazidime

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4
Q

What is the fourth generation cephalosporin we discussed?

A

Cefepime

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5
Q

What are the two carbapenems we covered?

A

Meropenem

Etrapenem

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6
Q

What is the glycopeptide we must know?

A

Vancomycin

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7
Q

What is the fluoroquinolone we must know?

A

Levofloxacin

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8
Q

What is the aminoglycoside we must know?

A

Gentamicin

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9
Q

What is the tetracycline we must know?

A

Doxycycline

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10
Q

What is the macrolide we must know?

A

Azithromycin

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11
Q

What is the lincosamide we must know?

A

Clindamycin

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12
Q

What is the oxazolidinone we must know?

A

Linezolid

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13
Q

What antiviral was listed in RED?

A

Oseltamivir

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14
Q

What antifungals do we need to know?

A

Fluconazole

Itraconazole

Voriconazole

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15
Q

Are B-lactams time or concentration dependent?

What is their mechanism of action?

A
  • Time dependent
  • structural analogs of D-Ala-D-Ala; covalently bind penicillin-binding proteins (PBPs), inhibit transpeptidation
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16
Q

What are four ADR’s associated with penicillin?

A
  • Allergic reactions (0.7-10%)
  • Anaphylaxis (0.004-0.04%)
  • Nausea, vomiting, mild to severe diarrhea
  • Pseudomembranous colitis
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17
Q

What are the ADR’s associated with cephalosporins?

A
  • 1% risk of cross-reactivity to penicillins
  • Diarrhea
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18
Q

What are the carbapenem ADR’s? 3

A
  • Nausea/vomiting (1-20%)
  • Seizures (1.5%)
  • Hypersensitivity
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19
Q

MOA for Vancomycin?

A
  • Inhibits cell wall synthesis binding with high affinity to D-Ala-D-Ala terminal of cell wall precursor units.
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20
Q

What are the ADR’s associated with Vancomycin?

5

A
  1. Fever, chills
  2. rash
  3. Red-Man Syndrome
  4. Ototoxicity
  5. nephrotoxicity
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21
Q

What is red-man syndrome and what causes it?

A

Extreme flushing, tachycardia, hypotension

Caused by Vancomycin induced histamine release.

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22
Q

What is the mechanism of action of fluoroquinolones?

A
  1. targets bacterial DNA gyrase & topoisomerase IV.
  2. Prevents relaxation of positive supercoils
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23
Q

Are fluoroquinolones concentration or time dependent?

A

Concentration-dependent

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24
Q

Fluoroquinolone ADR’s include GI disturbances such as nausea, vomiting and abdominal discomfort. What other ADR’s are associated with these antibiotics?

A

CNS

  1. headache
  2. dizziness
  3. delirium
  4. hallucinations (rarely)

General

  1. Rash
  2. Photosensitivity
  3. Achilles tendon rupture (contraindicated in children)
    1. ​
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25
Q

What is the mechanism of action of aminoglycosides?

A
  1. Works on the 30S subunit to interfere with initiation
  2. Causes misreading and abberant protein production
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26
Q

What is the MOA of tetracyclines?

A

30S subunit- blocks aminoacyl tRNA acceptor site

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27
Q

MOA for both macrolides and clindamycin?

A

Both work on the 50S subunit to Inhibit translocation

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28
Q

MOA for Linezolid?

A

Acts at the 50S subunit to block formation of the intiation complex.

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29
Q

What are the ADR’s associated with aminoglycosides?

A
  1. Ototoxicity
  2. nephrotoxicity
  3. neuromuscular block
  4. apnea
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30
Q

What are the ADR’s we know of for tetracycline?

A
  1. GI disturbances
  2. superinfections of C. difficile
  3. photosensitivity
  4. teeth discoloration
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31
Q

What are the ADR’s for macrolides?

A
  1. GI
  2. hepatotoxicity
  3. arrhythmia
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32
Q

What are the ADR’s we should be aware of with clindamycin?

A
  1. GI disturbances
  2. pseudomembranous colitis
  3. skin rashes
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33
Q

What are the ADR’s foc linezolid?

A
  1. Myelosuppression
  2. headache
  3. rash
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34
Q

Community acquired pneumonia (CAP), is the 8th leading cause of death in the US, and manifests severely in the very young, elderly and chronically ill. What is the goal of treatement?

A

eradicate the organism, resolve clinical disease.

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35
Q

The Infectious Disease Society of America (IDSA)/American Thoracic Society (ATS) provides the guidelines for management of community acquired pneumonia, which apply to most patients.

What are some examples of patients that are excluded from these guidelines? Name up to 7

A
  1. ▫Immunocompromised patients
  2. ▫Solid organ, bone marrow, or stem cell transplant
  3. ▫Those receiving chemotherapy
  4. ▫Long-term high dose corticosteroids (> 30 days)
  5. ▫Congenital or acquired immunodeficiency
  6. ▫HIV with CD4 count < 350 cells/mm3
  7. ▫Children ≤ 18 years
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36
Q

CAP severity can be assessed with the CURB-65 score. What are the components of the CURB=65 score?

A

▫Confusion

▫Uremia (BUN > 19 mg/dL)

▫Respiratory rate (≥ 30 breaths/min)

▫Low blood pressure

– SBP < 90 mmHg, DBP ≤ 60 mmHg

▫Age (≥ 65 Years)

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37
Q

What do the varios CURB-65 scores mean for patient disposition?

A

0-1: treat as outpatient

2: admit to hospital

3 or more: admit to ICU

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38
Q

What is another Pneumonia severity index?

A

Pneumonia severity index (PSI)

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39
Q

You can use CURB-65 plus minor criteria to determine need for ICU admission. What are the minor criteria?

A

▫Multilobar infiltrates

▫WBC < 4000 cells/mm3

▫PLT < 100,000 cells/mm3

▫Core temperature < 36 ˚C

▫Hypotension requiring aggressive fluid resuscitation

40
Q

What are two absolute indications for ICU admission?

A

▫Mechanical ventilation

▫Septic shock (+ vasopressors)

41
Q

Symptoms of CAP include cough, fever, sputum production and pleuritic chest pain. What should you do to make the diagnosis?

A

chest x-ray - if negative initiate antibiotics and repeat imaging in 1-2 days

Culture - To identify organism and sensitivities/resistances

42
Q

Know the gram positive and negative organisms common to lung infections.

A

I recommend drawing out the flow chart for this one.

43
Q

What type of organisms are not detectible on gram stain?

A

Atypical ones.

44
Q

What are three infectious organisms associated with underlying bronchopulmonary disease?

A

▫H. influenzae

▫Moraxella catarrhalis

▫+ S. aureus during an influenza outbreak

45
Q

What are two examples of infectious organisms associated wtih Chronic oral steroids or severe underlying bronchopulmonary disease, alcoholism, frequent antibiotic use?

A

▫Enterobacteriaceae

▫Pseudomonas aeruginosa

46
Q

What type of infectious organisms should you be on the lookout for in classic aspiration pleuropulmonary syndrome in alcohol/drug overdose or in seizures with gingival disease or esophageal motility disorders?

A

Anaerobes - normal oral flora

47
Q

What are the CAP recommendations for empiric treatment of outpatients who were previously healthy?

A

–Macrolide PO (azithromycin, clarithromycin)

-OR-

–Doxycycline PO

48
Q

What are the CAP recommendations for empiric treatment of DRSP risk patients?

(Those with comorbidities, over 65 y/o, or used antimicrobials in past three months)

A

–Respiratory fluoroquinolone PO (levofloxacin, moxifloxacin)

-OR-

–B-lactam PO [high dose amoxicillin or amoxicillin-clavulanate preferred (alternates: ceftriaxone, cefuroxime)] PLUS a macrolide PO

49
Q

What are the CAP recommendations for empiric treatment of Inpatient, non-ICU patients?

A

–Respiratory FQ IV or PO (levofloxacin, moxifloxacin)

-OR-

–B-lactam IV (ceftriaxone, cefotaxime, or ampicillin preferred) PLUS macrolide IV (azithromycin)

50
Q

What are the CAP recommendations for empiric treatment in the inpatient, ICU setting?

A

–B-lactam IV (ceftriaxone, cefotaxime, or ampicillin/sulbactam preferred) PLUS azithromycin IV

-OR-

–B-lactam IV (ceftriaxone, cefotaxime, or ampicillin/sulbactam preferred) PLUS a respiratory FQ (levofloxacin, moxifloxacin)

51
Q

What is the CAP modifying criteria for empiric treatment regimen when there is a risk of P. aeruginosa?

A

▫Structural lung disease (bronchiectasis)

▫Repeated COPD exacerbations

–Frequent corticosteroid and/or antibiotic use

▫Prior antibiotic therapy

52
Q

If there is a risk of P, aeruginosa, what are three recommended empiric regimens?

A

–Antipseudomonal B-lactam IV (piperacillin-tazobactam, cefepime, imipenem, meropenem) PLUS either ciprofloxacin or levofloxacin

-OR-

–Antipseudomonal B-lactam PLUS aminoglycoside (gentamicin) AND azithromycin

-OR-

–Antipseudomonal B-lactam PLUS aminoglycoside AND antipneumococcal FQ

53
Q

What are four modifying criteria for patients at risk for CA-MRSA?

A

▫End-stage renal disease (dialysis)

▫Injection drug abuse

▫Prior influenza

▫Prior antibiotic use (especially FQ)

54
Q

What is the modified empiric regimen for CAP with risk of MRSA?

A

▫Add vancomycin IV or linezolid

▫Panton-Valentine leucocidin necrotizing pneumonia: add clindamycin or use linezolid

55
Q

What are the criteria for transitioning a patient from IV to oral therapy?

4

A
  1. Hemodynamically stable
  2. Improving clinically
  3. Tolerating oral medications
  4. normal functioning GI tract
56
Q

When considering transitioning patients from IV to oral therapy, “improving clinically” is listed as an indication. What are some specific criteria and the relevant baselines?

Up to 7

A
  1. –Temperature ≤ 37.8 ˚C
  2. –HR ≤ 100 bpm
  3. –RR ≤ 24 breaths/min
  4. –SBP ≥ 90 mmHg
  5. –Arterial 02 saturation ≥ 90%
  6. –Ability to maintain oral intake
  7. –Normal mental status
57
Q

What are the three guidlines that define the duration of the therapy?

For what situation is there an exception?

A
  1. Minimum 5 days treatment (usually 7-10 days)
  2. Must be afebrile for 48-72 hours
  3. No more than 1 CAP associated sign of clinical instability

Exception: psuedomonas = 15 day course of tx

58
Q

What do HCAP, HAP and VAP stand for?

A

Healthcare-Associated (HCAP),
Hospital-Acquired (HAP),
Ventilator-Associated Pneumonia (VAP)

59
Q

What does HCAP include?

A

•history of hospitalization or exposure to healthcare settings

60
Q

When does HAP occur?

A

48 or more hours after admission

61
Q

When does VAP occur?

A

48-72 hours after endotracheal intubation

62
Q

Pseudomonas aeruginosa has demonstrated increasing resistance to:

  • –Piperacillin
  • –Ceftazidime
  • –Cefepime
  • –Imipenem
  • –Meropenem
  • –Aminoglycosides
  • –Fluoroquinolones

What are the two primary mechanisms this organisms uses to defeat our weapons?

A
  1. Multiple efflux pumps
  2. Decreased expression of outer membrane porin channel
63
Q

Describe the resistance characteristics of klebsiella.

A

▫Klebsiella intrinsically resistant to ampicillin and can acquire resistance to cephalosporins and aztreonam –> ESBL production

64
Q

Describe the resistance profile of enterobacter.

A

▫Enterobacter high frequency resistance development to cephalosporins during treatment

65
Q

DRSP has an altered PBP (penicillin binding protein) that confers resistance. What are all US strains currently susceptible to?

A

Vancomycin and Linezolid

66
Q

Early onset pathogens involved in HCAP, HAP and VAP include:

  1. ▫S. pneumoniae
  2. ▫H. influenzae
  3. ▫MSSA
  4. ▫Sensitive gram-negative: E. coli, K. pneumoniae, Enterobacter spp., Proteus spp., Serratia marcescens

What are the treatment protocols for this scenario? 4 options

A
  1. ▫Ceftriaxone OR
  2. ▫FQ (levofloxacin, moxifloxacin, ciprofloxacin) OR
  3. ▫Ampicillin/sulbactam OR
  4. ▫Ertapenem
67
Q

Late onset HCAP, HAP and VAP organisms include:

  1. ▫P. aeruginosa
  2. ▫K. pneumoniae (ESBL+)
  3. ▫Acinetobacter
  4. ▫MRSA

What are the treatment options for this scenario?

A

▫Antipseudomonal cephalosporin (cefepime, ceftazidime) OR antipseudomonal carbapenem (imipenem, meropenem) OR B-lactam/B-lactamase inhibitor (piperacillin-tazobactam)

PLUS

▫Antipseudomonal FQ (ciprofloxacin, levofloxacin) OR aminoglycoside (gentamicin, tobramycin)

PLUS

▫Linezolid OR vancomycin

68
Q

DOC for Strep Pneumo?

A

▫Non-resistant

  1. –Penicillin G
  2. –Amoxicillin

▫Resistant: –Chosen on basis of susceptibility:

  1. –Cefotaxime
  2. ceftriaxone
  3. levofloxacin
  4. moxifloxacin,
  5. vancomycin,
  6. linezolid
69
Q

DOC for H. Influenza?

A

▫Non-B-lactamase producing

–Amoxicillin

▫B-lactamase producing

–2nd or 3rd generation cephalosporin, amoxicillin/clavulanate

70
Q

DOC for Mycoplasma pneumoniae?

A

Macrolide

Tetracycline

71
Q

DOC for C. pneumoniae?

A

Macrolide

Tetracycline

72
Q

DOC for C. psittaci?

A

Doxycycline

73
Q

DOC for Legionella?

A
  1. ▫Fluoroquinolone,
  2. azithromycin,
  3. doxycycline
74
Q

DOC for enterobacteriaceae?

•Enterobacteriaceae (Klebsiella, E. coli, Proteus)

A

▫3rd or 4th generation cephalosporin, carbapenem (if ESBL producer)

75
Q

DOC for P. aerugenosa?

A

▫Antipseudomonal B-lactam PLUS ciprofloxacin, levofloxacin, or an aminoglycoside

76
Q

DOC for anaerobes such as bacteroides, fusobacterium, peptostreptococcus?

A

▫B-lactam/B-lactamase inhibitor, clindamycin

77
Q

What is the DOC for staphylococcus aureus?

A

▫Methicillin-sensitive

–Antistaphylococcal penicillin (nafcillin, oxacillin, dicloxacillin)

▫Methicillin-resistant

–Vancomycin or linezolid

78
Q

What is the drug of choice for influenza virus?

A

▫Oseltamivir, zanamivir

79
Q

DOC for P. Jirovecii?

A

▫Trimethoprim/sulfamethoxazole

80
Q

DOC for Bordatella pertussis?

A

▫Azithromycin, clarithromycin

81
Q

DOC for coccidioides?

A

▫No treatment necessary if normal host

–Itraconazole, fluconazole

82
Q

DOC for histoplasmosis and blastomycosis?

A

Itraconazole

83
Q

What are the neurominidase inhibitors?

A

•Oseltamivir (PO), zanamivir (INH)

84
Q

What is the MOA of •Oseltamivir (PO), and zanamivir (INH)?

A

•analogs of sialic acid, interferes with release of progeny influenza virus from infected host cell

85
Q

What adaptation can confer resistance to neurominidase inhibitors?

A

▫Point mutation in viral hemagglutinin (HA) or neuraminidase (NA) surface proteins

86
Q

What are the M2 channel blockers we covered?

2

A

•Amantadine (PO), rimantadine (PO)

87
Q

MOA for amantadine and rimantadine?

A

Block M2 proton ion channels of virus, inhibiting uncoating of viral RNA within host cell.

88
Q

What is the only use for M2 channel blockers?

A

Influenza A only

89
Q

What are six ADR’s of M2 channel blockers?

A
  1. ▫GI (nausea, anorexia)
  2. ▫CNS (nervousness, insomnia, light-headedness)
  3. ▫Severe behavioral changes
  4. ▫Delirium
  5. ▫Agitation
  6. ▫Seizures
90
Q

What is the MOA for acyclovir?

A

three phosphorylation steps for activation, first step via virus specific thymidine kinase. Inhibits DNA synthesis.

Competes with deoxyGTP

91
Q

What is the mechanism of the azole antifungals?

A

•inhibits fungal cytochrome P450, reducing production of ergosterol (component of fungi cell membrane)

92
Q

What are the three azole antifungals we discussed?

A

Fluconazole

Itraconazole

Voriconazole

93
Q

ADR’s of voriconazole?

A

Visual changes

photosensitivity

94
Q

What is the MOA of Amphotericin B?

A

•binds ergosterol, changes permeability of cell, forms pores in membrane

95
Q

What are the ADR’s for Amphotericin B?

A

•infusion related (fever, chills, vomiting, headache), cumulative toxicity (renal damage)

96
Q

What are the three echinocandins?

A
  1. caspofungin
  2. micafungin
  3. anidulafungin
97
Q

What is the MOA of echinocandins?

A

•inhibits synthesis of B(1-3)-glucan, disrupts fungal cell wall, and causes cell death

Respiratory II - Exam 2 (13 decks)

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