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Drugs for Respiratory Infections Flashcards

1
Q

Drugs*

Aminopenicillins

A

▫Ampicillin(PO, IV, IM)

▫Amoxicillin(PO)

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2
Q

Drugs*

B-lactamase Inhibitors

A

▫Ampicillin-sulbactam[Unasyn] (IV)
▫Amoxicillin-clavulanic acid [Augmentin] (PO)
▫Piperacillin-tazobactam[Zosyn] (IV)

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3
Q

Drugs*

Third Generation Cephalosporin

A

▫Ceftriaxone[Rocephin] (IV, IM)

▫Ceftazidime[Fortaz] (IV, IM)

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4
Q

Drugs*

Fourth Generation Cephalosporin

A

Cefepime(IV, IM)

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5
Q

Drugs*

Carbapenems

A

▫Meropenem [Merrem] (IV)

▫Ertapenem[Invanz] (IV, IM)

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6
Q

Drugs*

Glycopeptides

A

Vancomycin(PO, IV)

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7
Q

Drugs*

Fluoroquinolones

A

Levofloxacin[Levaquin] (PO, IV, topical)

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8
Q

Drugs*

Aminoglycosides

A

Gentamicin(IV, IM, topical)

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9
Q

Drugs*

Tetracyclines

A

Doxycycline(PO, IV)

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10
Q

Drugs*

Macrolides

A

Azithromycin[Zithromax, Z-pak] (PO, IV, topical)

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11
Q

Drugs*

Lincosamides

A

Clindamycin[Cleocin] (PO, IV, IM, topical)

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12
Q

Drugs*

Oxazolidinones

A

Linezolid[Zyvox] (PO, IV)

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13
Q

Drugs*

Antivirals

A 
▫Oseltamivir[Tamiflu] (PO)*
▫Zanamivir [Relenza] (INH)
▫Amantadine (PO)
▫Rimantadine(PO)
▫Acyclovir (PO, IV, topical)
▫Valacyclovir[Valtrex] (PO)
▫Ganciclovir [Cytovene] (PO, IV)
▫Valganciclovir[Valcyte] (PO)
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14
Q

Drugs*

Antifungals

A 
▫Fluconazole[Diflucan] (PO, IV)*
▫Itraconazole(PO)*
▫Voriconazole[Vfend] (PO, IV)*
▫Amphotericin B (IV)
▫Caspofungin (IV)
▫Micafungin (IV)
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15
Q

β-Lactam 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

Penicillins ADR

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

Cephalosporins ADR

A
  • 1% risk of cross-reactivity to penicillins

* Diarrhea

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18
Q

Carbapenems ADR

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

Vancomycin Mechanism of Action

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

Vancomycin ADRs

A
  • Macular skin rash, chills, fever, rash
  • Red-man syndrome (histamine release): extreme flushing, tachycardia, hypotension
  • Ototoxicity, nephrotoxicity (33% with initial trough > 20 mcg/mL)
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21
Q

Fluoroquinolone Mechanism of Action

A

Concentration-dependent, targets bacterial DNA gyrase & topoisomerase IV. Prevents relaxation of positive supercoils

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22
Q

FluoroquinoloneADRs

A
  • GI 3-17% (mild nausea, vomiting, abdominal discomfort)
  • CNS 0.9-11% (mild headache, dizziness, delirium, rare hallucinations)
  • Rash, photosensitivity, Achilles tendon rupture (CI in children)
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23
Q

Protein Synthesis Inhibitors Mechanisms of Action

Aminoglycosides

A

(30S)
•Interferes with initiation
•Causes misreading & aberrant proteins

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24
Q

Protein Synthesis Inhibitors Mechanisms of Action

Tetracyclines

A

(30S)

•Blocks aminoacyl tRNAacceptor site

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25
Q

Protein Synthesis Inhibitors Mechanisms of Action

Macrolides

A

(50S)

•Inhibits translocation

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26
Q

Protein Synthesis Inhibitors Mechanisms of Action

Clindamycin

A

(50S)

•Inhibits translocation

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27
Q

Protein Synthesis Inhibitors Mechanisms of Action

Linezolid

A

(50S)

•Blocks formation of initiation complex

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28
Q

Protein Synthesis Inhibitors ADRs

Aminoglycosides

A

(30S)

•Ototoxicity, nephrotoxicity, neuromuscular block and apnea

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29
Q

Protein Synthesis Inhibitors ADRs

Tetracyclines

A

(30S)

•GI, superinfections of C. difficile, photosensitivity, teeth discoloration

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30
Q

Protein Synthesis Inhibitors ADRs

Macrolides

A

(50S)

•GI, hepatotoxicity, arrhythmia

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31
Q

Protein Synthesis Inhibitors ADRs

Clindamycin

A

(50S)

•GI diarrhea, pseudomembranous colitis, skin rashes

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32
Q

Protein Synthesis Inhibitors ADRs

Linezolid

A

(50S)

•Myelosuppression, headache, rash

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33
Q

CAP + Influenza (2005)

A

▫8thleading cause of death in the U.S.

▫> 60,000 deaths due to pneumonia in U.S.

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34
Q

Community-Acquired Pneumonia (CAP)

Most severe manifestations in:

A

Very young, elderly, chronically ill

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35
Q

Goal of CAP treatment: eradicate organism, resolve clinical disease

A

▫Antibiotics = mainstay of therapy
▫Therapy guided by organism and susceptibility
▫Must have knowledge of most likely infecting pathogen and local susceptibility

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36
Q

CAP –Guidelines
•Infectious Disease Society of America (IDSA)/American Thoracic Society (ATS)
▫Management of Community-Acquired Pneumonia
•Excluded patients:

A

▫Immunocompromised patients
▫Solid organ, bone marrow, or stem cell transplant
▫Those receiving chemotherapy
▫Long-term high dose corticosteroids (> 30 days)
▫Congenital or acquired immunodeficiency
▫HIV with CD4 count

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37
Q

CAP –Initial Assessment

Assessment of severity:

A

Outpatient, inpatient (non-ICU), ICU

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38
Q

CAP –Initial Assessment

Avoid unnecessary admissions:

A

▫25x greater cost inpatient vs. outpatient
▫Resume normal activities faster as outpatient
▫Hospitalization carries risks: thromboembolic events & superinfections

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39
Q

CAP –Severity of Illness Scores

A

•In conjunction: laboratory data, clinical evaluation, & physician interpretation

•CURB-65
   ▫Confusion
   ▫Uremia (BUN > 19 mg/dL)
   ▫Respiratory rate (≥ 30 breaths/min)
   ▫Low blood pressure
SBP
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40
Q

CAP –CURB-65

30-DayMortality Based on Risk Factors

A

of Risk Factors

0
0.7%

1
2.1%

2
9.2%

3
14.5%

4
40%

5
57%

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41
Q

CAP –CURB-65

what to do after scores

A
  • Score 0-1: treat as an outpatient
  • Score 2: admit to hospital
  • Score ≥ 3: admit to ICU
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42
Q

CAP –General Medical vs. ICU

A

10% of hospitalized CAP patients require ICU stay

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43
Q

Use CURB-65 + minor criteria to determine need for ICU admission:

A

▫Multilobar infiltrates

▫WBC

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44
Q

Two absolute indications for ICU admission:

A

▫Mechanical ventilation

▫Septic shock (+ vasopressors)

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45
Q

CAP –Diagnosis

Demonstrable infiltrate on CXR required:

A

If negative but CAP suspected, initiate antibiotics and repeat CXR in 24-48 hours

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46
Q

CAP –Diagnosis

Culture

A

Increased mortality & risk of treatment failure –if inappropriate antimicrobials used

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47
Q

CAP –Diagnosis

Additional diagnostic testing

A

blood and sputum culture in hospital pts

cavitary infiltrates for tb and fungus

recent travel legionella

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48
Q

Infecting Organisms

Outpatient

A

Streptococcus pneumoniae Mycoplasma pneumoniae* Haemophilus influenzae Chlamydophila pneumoniae* Respiratory viruses

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49
Q

Infecting Organisms

Hospitalized (Non-ICU)

A

S. pneumoniae M. pneumoniae* C. pneumoniae* H. influenzae Legionella spp.* Aspiration Respiratory viruses

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50
Q

Infecting Organisms

Intensive-Care Unit (ICU)

A

S. pneumoniae Staphylococcus aureus Legionella spp. * Gram-negative bacilli H. influenzae

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51
Q

Atypical pneumonia CAP organisms

A 
Mycoplasma pneumoniae*
Chlamydophila pneumoniae*
M. pneumoniae* 
C. pneumoniae*
Legionella spp. *
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52
Q

CAP –Infecting Organisms/Disease State

•Underlying bronchopulmonarydisease:

A

▫H. influenzae
▫Moraxella catarrhalis
▫+ S. aureus during an influenza outbreak

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53
Q

CAP –Infecting Organisms/Disease State

Chronic oral steroids or severe underlying bronchopulmonary disease, alcoholism, frequent antibiotic use:

A

▫Enterobacteriaceae

▫Pseudomonas aeruginosa

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54
Q

CAP –Infecting Organisms/Disease State

Classic aspiration pleuropulmonary syndrome in alcohol/drug overdose or in seizures with gingival disease or esophageal motility disorders:

A

Anaerobes

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55
Q

CAP –Other Infecting Organisms

•Common viruses:

A

▫Influenza
▫Respiratory syncytial virus (RSV)
▫Adenovirus
▫Parainfluenzavirus

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56
Q

CAP –Other Infecting Organisms

•Other viruses:

A

▫Human metapneumovirus
▫Herpes simplex virus (HSV)
▫Varicella-zoster virus (VSV)
▫SARS-associated coronavirus

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57
Q

CAP –Other Infecting Organisms

•2-3% incidence:

A 
▫M. tuberculosis
▫Chlamydophila psittaci(psittacosis)
▫Coxiellaburnetii(Q fever)
▫Francisellatularensis(tularemia)
▫Bordetella pertussis(whooping cough)
▫Endemic fungi
Histoplasma capsulatum
Coccidioidesimmitis
Cryptococcus neoformans
Blastomyceshominis
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58
Q

ohio rive fungus

A

histoplasmosis

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59
Q

western states fungus

A

coccidiomycosis

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60
Q

middle states fungus

A

blastomycosis

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61
Q

CAP –Resistant Organisms

•Drug-resistant S. pneumoniae (DRSP)

A 
▫Age  65 years
▫B-lactam use within previous 3 months
▫Alcoholism
▫Immunosuppressive illness or therapy
▫Exposure to child at day care
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62
Q

CAP –Empiric Antimicrobial Guidelines

•Outpatient Recommendations

previously healthy

A

Macrolide PO (azithromycin, clarithromycin)
-OR-
Doxycycline PO

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63
Q

CAP –Empiric Antimicrobial Guidelines

•Outpatient Recommendations

DRSP risk (comorbidities, age > 65 years, use of antimicrobials within 3 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

64
Q

CAP –Empiric Antimicrobial Guidelines

•Inpatient, Non-Intensive Care Unit Recommendations

A

Respiratory FQ IV or PO (levofloxacin, moxifloxacin)
-OR-
B-lactam IV (ceftriaxone, cefotaxime, or ampicillin preferred) PLUSmacrolide IV (azithromycin)

65
Q

CAP –Empiric Antimicrobial Guidelines

•Inpatient, Intensive-Care Unit Recommendations

A

B-lactam IV (ceftriaxone, cefotaxime, or ampicillin/sulbactam preferred) PLUSazithromycin IV
-OR-
B-lactam IV (ceftriaxone, cefotaxime, or ampicillin/sulbactam preferred) PLUSa respiratory FQ (levofloxacin, moxifloxacin)

66
Q

CAP –Modifying Empiric Regimen

•Pseudomonas aeruginosarisks:

A

▫Structural lung disease (bronchiectasis)
▫Repeated COPD exacerbations
Frequent corticosteroid and/or antibiotic use
▫Prior antibiotic therapy

67
Q

CAP –Modifying Empiric Regimen

pseudomonas treatment

A

Antipseudomonal B-lactam IV (piperacillin-tazobactam, cefepime, imipenem, meropenem) PLUSeither ciprofloxacin or levofloxacin
-OR-
Antipseudomonal B-lactam PLUSaminoglycoside (gentamicin) ANDazithromycin
-OR-
Antipseudomonal B-lactam PLUSaminoglycoside ANDantipneumococcal FQ

68
Q

Community-acquired methicillin-resistant Staphylococcus aureus (CA-MRSA) risks:

A

▫End-stage renal disease (dialysis)
▫Injection drug abuse
▫Prior influenza
▫Prior antibiotic use (especially FQ)

69
Q

Community-acquired methicillin-resistant Staphylococcus aureus (CA-MRSA) risks:

treatment

A

▫Add vancomycin IV or linezolid

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

70
Q

CAP –Intravenous Oral Therapy

•Transition to oral therapy:

A 
▫Hemodynamically stable
▫Improving clinically:
Temperature ≤ 37.8 ˚C
HR ≤ 100 bpm
RR ≤ 24 breaths/min
SBP ≥ 90 mmHg
Arterial 02 saturation ≥ 90%
Ability to maintain oral intake
Normal mental status
▫Tolerating oral medications
▫Normal functioning GI tract
71
Q

CAP –Duration of Therapy

A

•Minimum of 5 days treatment
▫Most patients receive 7-10 days
•Must be afebrile for 48-72 hours
•No more than 1 CAP-associated sign of clinical instability
•Exception:
▫Pseudomonas –8 day course led to more relapse compared to 15 day course

72
Q

HCAP

A

history of hospitalization or exposure to healthcare settings

73
Q

HAP

A

occurs 48 hours or more after admission
▫2ndmost common nosocomial infection in the U.S.
▫Increases hospital length of stay ~7-9 days
▫Incidence: 5-10 cases per 1000 admissions

74
Q

VAP

A

arises 48-72 hours after endotracheal intubation
▫Occurs in 9-27% of all intubated patients
▫Incidence increases with longer ventilation duration

75
Q

HCAP, HAP & VAP

early onset

A

less than 4 days

76
Q

HCAP, HAP & VAP

late onset

A

5+ days

77
Q

HCAP, HAP & VAP

aerobic gram negative

A

P. aeruginosa
E. coli
K. pneumoniae
Acinetobacter spp.

78
Q

HCAP, HAP & VAP

gram positive

A

MRSA (more common in diabetes, head trauma, those hospitalized in ICUs)

79
Q

HCAP, HAP & VAP

oropharygeal commensals

A

Viridansgroup streptococci
Coagulase-negative staphylococci
Neisseriaspp.
Corynebacteriumspp.

80
Q

Multi-Drug Resistant (MDR) Pathogens

•Pseudomonas aeruginosa

A 
▫Resistance caused by multiple efflux pumps
▫Decreased expression of outer membrane porinchannel
▫Increasing resistance to:
Piperacillin
Ceftazidime
Cefepime
Imipenem
Meropenem
Aminoglycosides
Fluoroquinolones
81
Q

Multi-Drug Resistant (MDR) Pathogens

•Klebsiella, Enterobacter, Serratia

A

▫Klebsiellaintrinsically resistant to ampicillin and can acquire resistance to cephalosporins and aztreonam ESBL production
▫Enterobacterhigh frequency resistance development to cephalosporins during treatment
▫These bacteria may carry plasmid mediated AmpC-type enzymes (ESBL) which are carbapenem susceptible but CONCERNED about resistance
May become resistant by loss of an outer membrane porin

82
Q

Multi-Drug Resistant (MDR) Pathogens

•MRSA

A

▫> 50% of ICU infections caused by S. aureus are methicillin-resistant
▫PBPs with reduced affinity for B-lactams
▫Concern for linezolid resistance but still rare

83
Q

Multi-Drug Resistant (MDR) Pathogens

•drsp

A

▫Altered PBP

▫ALL MDR strains in US currently susceptible to vancomycin and linezolid

84
Q

HCAP, HAP, & VAP –Diagnosis

A

•Radiographic infiltrate that is new or progressive
•Clinical findings suggestive of infection:
▫Fever
▫Purulent sputum
▫Leukocytosis
▫Decline in oxygenation

85
Q

Empiric Therapy –Early Onset

•Potential pathogens:

A

▫S. pneumoniae
▫H. influenzae
▫MSSA
▫Sensitive gram-negative: E. coli, K. pneumoniae, Enterobacterspp., Proteusspp., Serratia marcescens

86
Q

Empiric Therapy –Early Onset

Treatment:

A

▫Ceftriaxone OR
▫FQ (levofloxacin, moxifloxacin, ciprofloxacin) OR
▫Ampicillin/sulbactam OR
▫Ertapenem

87
Q

Empiric Therapy –Late Onset

•Potential pathogens (MDR):

A

▫P. aeruginosa
▫K. pneumoniae (ESBL+)
▫Acinetobacter
▫MRSA

88
Q

Empiric Therapy –Late Onset

Treatment:

A

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

PLUS
▫Antipseudomonal FQ (ciprofloxacin, levofloxacin) ORaminoglycoside (gentamicin, tobramycin)

PLUS
▫Linezolid ORvancomycin

89
Q

Combination vs. Monotherapy

A

Combination therapy recommended to ensure at least one agent is activeagainst the often MDR pathogen

Use monotherapy when possible

90
Q

Combination vs. Monotherapy

Often cited reasons for combination therapy

A

▫To prevent resistance
Evidence not well documented
▫To add synergy for treatment of P. aeruginosa
Only proven valuable in neutropenia or bacteremia

91
Q

Duration of Therapy

A

•VAP –good clinical response after 6 days
▫Prolonged courses leads to MDR pathogen colonization
•Shorten duration to as short as 7 days (traditional 14-21 days)
▫Unless P. aeruginosa (8 days led to relapse requires longer treatment course)

92
Q

DOC if Organism Known

Streptococcus pneumoniae

A 
▫Non-resistant
Penicillin G
Amoxicillin
▫Resistant
Chosen on basis of susceptibility:
Cefotaxime, ceftriaxone, levofloxacin, moxifloxacin, vancomycin, linezolid
93
Q

DOC if Organism Known

Haemophilus influenzae

A

▫Non-B-lactamase producing
Amoxicillin
▫B-lactamase producing
2ndor 3rdgeneration cephalosporin, amoxicillin/clavulanate

94
Q

DOC if Organism Known

Mycoplasma pneumoniae

A

Macrolide (azithromycin, clarithromycin), tetracycline (doxycycline)

95
Q

DOC if Organism Known

Chlamydophila pneumoniae

A

Macrolide (azithromycin, clarithromycin), tetracycline (doxycycline)

96
Q

DOC if Organism Known

Chlamydophila psittaci

A

Doxycycline

97
Q

DOC if Organism Known

Legionellaspp.

A

Fluoroquinolone, azithromycin, doxycycline

98
Q

DOC if Organism Known

Enterobacteriaceae (Klebsiella, E. coli, Proteus)

A

3rdor 4thgeneration cephalosporin, carbapenem (if ESBL producer)

99
Q

DOC if Organism Known

Pseudomonas aeruginosa

A

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

100
Q

DOC if Organism Known

Anaerobe (aspiration): Bacteroides, Fusobacterium, Peptostreptococcus

A

B-lactam/B-lactamase inhibitor, clindamycin

101
Q

DOC if Organism Known

Staphylococcus aureus

A

▫Methicillin-sensitive
Antistaphylococcalpenicillin (nafcillin, oxacillin, dicloxacillin)
▫Methicillin-resistant
Vancomycin or linezolid

102
Q

DOC if Organism Known

Influenza virus

A

Oseltamivir, zanamivir

103
Q

DOC if Organism Known

Pneumocystis jiroveci(P. cariniipneumonia)

A

Trimethoprim/sulfamethoxazole

104
Q

DOC if Organism Known

Bordetella pertussis

A

Azithromycin, clarithromycin

105
Q

DOC if Organism Known

Coccidioidesspp.

A

▫No treatment necessary if normal host

Itraconazole, fluconazole

106
Q

DOC if Organism Known

Histoplasmosis and Blastomycosis

A

▫Itraconazole

107
Q

Influenza overview

A

•Each year, 5-20% of population infected
•In the U.S.:
▫36,000 deaths
▫> 200,000 hospitalizations

108
Q

influenza transmission

A

▫Respiratory droplets (cough, sneeze, talk)
▫Contaminated surfaces
▫Incubation: 1-4 days (average 2 days)
▫Viral shedding: day after symptoms to 5-10 days after illness onset

109
Q

influenza symptoms

A 
▫Fever
▫Myalgia
▫Headache
▫Malaise
▫Non-productive cough
▫Sore throat
▫Rhinitis
110
Q

influence uncomplicated

A

Symptoms resolve after 3-7 days (uncomplicated)

▫Cough/malaise can last > 2 weeks`

111
Q

NeurominidaseInhibitors

drugs

A

Oseltamivir(PO), zanamivir(INH)

112
Q

NeurominidaseInhibitors

moa

A

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

113
Q

NeurominidaseInhibitors

pk

A

▫Oseltamivir–orally administered pro-drug, activated by hepatic esterases, t1/26-10 hours, glomerular filtration and tubular secretion (renallyadjust)
▫Zanamivir –10-20% reaches lungs, remainder deposits in oropharynx, t1/22.8 hours, 5-15% absorbed and excreted in urine with minimal metabolism

114
Q

NeurominidaseInhibitors

adrs Oseltamivir

A

nausea, vomiting, abdominal pain (5-10%), headache, fever, diarrhea, neuropsychiatric effects
Approved for children ≥ 1 year

115
Q

NeurominidaseInhibitors

adrs Zanamivir

A

cough, bronchospasm, decrease in pulmonary function (reversible), nasal/throat discomfort, not recommended in underlying airway disease
Approved for children ≥ 7 years

116
Q

NeurominidaseInhibitors

resistance

A

▫Point mutation in viral hemagglutinin (HA) or neuraminidase (NA) surface proteins
97.4% seasonal H1N1 resistant to oseltamivir2008-2009
Still susceptible to other drugs

117
Q

NeurominidaseInhibitors

therapeutic use

A

▫Influenza prophylaxis (household and institutional)

▫Influenza treatment

118
Q

M2 Channel Blockers

drugs

A

Amantadine (PO), rimantadine(PO)

119
Q

M2 Channel Blockers

moa

A

block M2 proton ion channels of virus inhibiting uncoatingof viral RNA within host cell
▫Active against influenza A only

120
Q

M2 Channel Blockers

pk

A

▫Amantadine –t1/212-18 hours, excreted unchanged in the urine, (renallyadjust)
▫Rimantadine–4-10x more active in vitro, t1/224-36 hours, extensive hepatic metabolism (renal and hepatic adjustment)

121
Q

M2 Channel Blockers

adrs

A 
▫GI (nausea, anorexia)
▫CNS (nervousness, insomnia, light-headedness)
▫Severe behavioral changes
▫Delirium
▫Agitation
▫Seizures
122
Q

M2 Channel Blockers

resistance

A

point mutations, marked resistance limiting use of these agents

123
Q

Other Antivirals –HSV & VSV

A

•Acyclovir (PO, IV, topical), valacyclovir(PO)
•MOA: three phosphorylation steps for activation, first step via virus specific thymidine kinase. Inhibits DNA synthesis:
▫Competition with deoxyGTPfor DNA polymerase binds DNA template irreversible complex
▫Chain termination following incorporation into viral DNA
•PK:
▫Acyclovir –bioavailability 15-20%, t1/22.3-3 hours, 20 hours in anuria, diffuses into most tissues and body fluids (including CSF)
▫Valacyclovir–L-valylester of acyclovir, rapidly hydrolyzed in liver, serum levels 3-5x greater than PO acyclovir, bioavailability 54-70%, t1/22.5-3.3 hours
•Therapeutic use: genital herpes (treatment, prophylaxis, suppression), varicella, HSV encephalitis, neonatal HSV treatment
•ADRs: nausea, diarrhea, headache

124
Q

Other Antivirals –CMV

A

•Ganciclovir (PO, IV), valganciclovir(PO)
•MOA: acyclic guanosine analog, requires activation by triphosphorylationbefore inhibiting DNA polymerase. Termination of DNA elongation.
•PK:
▫Ganciclovir –t1/24 hours, intracellular t1/216-24 hours, clearance related to CrCl
▫Valganciclovir–L-valylester, bioavailability 60%
•Therapeutic use: CMV retinitis treatment, CMV prophylaxis
•ADRs: myelosuppression, nausea, diarrhea, fever, peripheral neuropathy

125
Q

Common fungi of clinical interest:

A 
▫Candida albicans
▫Histoplasma capsulatum
▫Cryptococcus neoformans
▫Coccidioidesimmitis
▫Aspergillus spp.
▫Blastomycesdermatitidis
126
Q

Azole Antifungals

overview

A

•Ergosterol found in cell membrane of fungi (compared to cholesterol used in bacteria and human cells)

127
Q

Azole Antifungals

moa

A

•MOA: inhibits fungal cytochrome P450, reducing production of ergosterol
▫Selective toxicity due to greater affinity for fungal rather than human cytochrome P450 enzymes

128
Q

Azole Antifungals

therapeutic use

A

wide spectrum of activity against Candidaspp, blastomycosis, coccidiodomycosis, histoplasmosis, and even Aspergillus(itraconazole, voriconazole)

129
Q

Azole Antifungals

adrs

A

minor GI upset, abnormalities in liver enzymes

•Drug interactions!!

130
Q

Azole Antifungals

drugs

A

Fluconazole (Diflucan) PO, IV

Itraconazole PO

Voriconazole (Vfend) PO, IV

131
Q

Fluconazole (Diflucan) PO, IV

A

▫PK: water soluble, good CSF penetration, high PO bioavailability ~96%

132
Q

•Itraconazole PO

A

PK: drug absorption increased by food and low gastric pH

133
Q

Voriconazole (Vfend) PO, IV

A

▫PK: well absorbed, bioavailability > 90%

▫ADRs: visual changes, photosensitivity

134
Q

Amphotericin B

moa

A

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

135
Q

Amphotericin B

pk

A

▫Insoluble in water, variety of lipid formulations available, poorly absorbed PO, t1/215 days, only 2-3% of blood level reaches CSF

136
Q

Amphotericin B

therapeutic use

A

broadest spectrum of activity, useful in life-threatening infections but very toxic

137
Q

Amphotericin B

adrs

A

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

138
Q

Echinocandins

A
  • Caspofungin, micafungin, anidulafungin(IV)
  • MOA: inhibits synthesis of B(1-3)-glucan, disrupts fungal cell wall, and causes cell death
  • Therapeutic use: Candidaand Aspergillus
  • ADRs: minor GI, flushing
139
Q

β-Lactam ADRs in genreal

A

generally well tolerated

monobactram, aztreonam does not cross react but it is only gram -?

urine elimination

ceftriaxone can cause hyperbilirubinemia and kernicterus bc of protein binding

anti staph also undergo bile excretion

140
Q

linezolid adrs

A

thrombocytopenia

serotonin syndrom htn vomiting headache

141
Q

sputum culture in outpatien

A

no

142
Q

cavitary infiltrates

A

tb and fungus

143
Q

recent travel

A

legionella

144
Q

most common cap for gramp pos

A

strep pneumo

staph aureas mrsa

145
Q

gram neg cap

A

h flu
moraxella
pseudomonas

146
Q

Enterobacterhigh frequency resistance development to cephalosporins during treatment

A

enduces own resistance to 1st 2nd and 3rd gens

147
Q

methicillin causes

A

nephritis

148
Q

usually on treat fungal pneumonia with

A

immunocompromised pts

149
Q

influenza overview

A

rna eneloped virus

hemaglutting bind to ….

m2 channels are ion channels that help with viaral undcoding

neuroaminidase proteins are responsible for releasing new virus

build up immunity through vaccine or infection by getting…

flumist greater than 2 you can get it

rna enveloped bind

150
Q

m2 channel blockers in parkinsons

A

bc they impact dopamine in cns, so they can be used in parkinsons

151
Q

cmv prophylaxis for

A

organ transplant

152
Q

ergosterol

A

sterol in fungal cell membranes

azoles

153
Q

amphotericin b

A

plugs whole in cell membrane

154
Q

bglucan synthase fungus

A

cell wall structure

echocandins

155
Q

azole drug interaction

A

cyp statins and antiplatelets

156
Q

amphotericin adrs

A

bc release of cytokines

Resp (11 decks)

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