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Drugs for Respiratory Infections Flashcards

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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
Protein Synthesis Inhibitors Mechanisms of Action Macrolides
(50S) | •Inhibits translocation
26
Protein Synthesis Inhibitors Mechanisms of Action Clindamycin
(50S) | •Inhibits translocation
27
Protein Synthesis Inhibitors Mechanisms of Action Linezolid
(50S) | •Blocks formation of initiation complex
28
Protein Synthesis Inhibitors ADRs Aminoglycosides
(30S) | •Ototoxicity, nephrotoxicity, neuromuscular block and apnea
29
Protein Synthesis Inhibitors ADRs Tetracyclines
(30S) | •GI, superinfections of C. difficile, photosensitivity, teeth discoloration
30
Protein Synthesis Inhibitors ADRs Macrolides
(50S) | •GI, hepatotoxicity, arrhythmia
31
Protein Synthesis Inhibitors ADRs Clindamycin
(50S) | •GI diarrhea, pseudomembranous colitis, skin rashes
32
Protein Synthesis Inhibitors ADRs Linezolid
(50S) | •Myelosuppression, headache, rash
33
CAP + Influenza (2005)
▫8thleading cause of death in the U.S. | ▫> 60,000 deaths due to pneumonia in U.S.
34
Community-Acquired Pneumonia (CAP) Most severe manifestations in:
Very young, elderly, chronically ill
35
Goal of CAP treatment: eradicate organism, resolve clinical disease
▫Antibiotics = mainstay of therapy ▫Therapy guided by organism and susceptibility ▫Must have knowledge of most likely infecting pathogen and local susceptibility
36
CAP –Guidelines •Infectious Disease Society of America (IDSA)/American Thoracic Society (ATS) ▫Management of Community-Acquired Pneumonia •Excluded patients:
▫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
37
CAP –Initial Assessment Assessment of severity:
Outpatient, inpatient (non-ICU), ICU
38
CAP –Initial Assessment Avoid unnecessary admissions:
▫25x greater cost inpatient vs. outpatient ▫Resume normal activities faster as outpatient ▫Hospitalization carries risks: thromboembolic events & superinfections
39
CAP –Severity of Illness Scores
•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 ```
40
CAP –CURB-65 | 30-DayMortality Based on Risk Factors
#of Risk Factors 0 0.7% 1 2.1% 2 9.2% 3 14.5% 4 40% 5 57%
41
CAP –CURB-65 what to do after scores
* Score 0-1: treat as an outpatient * Score 2: admit to hospital * Score ≥ 3: admit to ICU
42
CAP –General Medical vs. ICU
10% of hospitalized CAP patients require ICU stay
43
Use CURB-65 + minor criteria to determine need for ICU admission:
▫Multilobar infiltrates | ▫WBC
44
Two absolute indications for ICU admission:
▫Mechanical ventilation | ▫Septic shock (+ vasopressors)
45
CAP –Diagnosis Demonstrable infiltrate on CXR required:
If negative but CAP suspected, initiate antibiotics and repeat CXR in 24-48 hours
46
CAP –Diagnosis Culture
Increased mortality & risk of treatment failure –if inappropriate antimicrobials used
47
CAP –Diagnosis Additional diagnostic testing
blood and sputum culture in hospital pts cavitary infiltrates for tb and fungus recent travel legionella
48
Infecting Organisms Outpatient
Streptococcus pneumoniae Mycoplasma pneumoniae* Haemophilus influenzae Chlamydophila pneumoniae* Respiratory viruses
49
Infecting Organisms Hospitalized (Non-ICU)
S. pneumoniae M. pneumoniae* C. pneumoniae* H. influenzae Legionella spp.* Aspiration Respiratory viruses
50
Infecting Organisms Intensive-Care Unit (ICU)
S. pneumoniae Staphylococcus aureus Legionella spp. * Gram-negative bacilli H. influenzae
51
Atypical pneumonia CAP organisms
``` Mycoplasma pneumoniae* Chlamydophila pneumoniae* M. pneumoniae* C. pneumoniae* Legionella spp. * ```
52
CAP –Infecting Organisms/Disease State •Underlying bronchopulmonarydisease:
▫H. influenzae ▫Moraxella catarrhalis ▫+ S. aureus during an influenza outbreak
53
CAP –Infecting Organisms/Disease State Chronic oral steroids or severe underlying bronchopulmonary disease, alcoholism, frequent antibiotic use:
▫Enterobacteriaceae | ▫Pseudomonas aeruginosa
54
CAP –Infecting Organisms/Disease State Classic aspiration pleuropulmonary syndrome in alcohol/drug overdose or in seizures with gingival disease or esophageal motility disorders:
Anaerobes
55
CAP –Other Infecting Organisms •Common viruses:
▫Influenza ▫Respiratory syncytial virus (RSV) ▫Adenovirus ▫Parainfluenzavirus
56
CAP –Other Infecting Organisms •Other viruses:
▫Human metapneumovirus ▫Herpes simplex virus (HSV) ▫Varicella-zoster virus (VSV) ▫SARS-associated coronavirus
57
CAP –Other Infecting Organisms •2-3% incidence:
``` ▫M. tuberculosis ▫Chlamydophila psittaci(psittacosis) ▫Coxiellaburnetii(Q fever) ▫Francisellatularensis(tularemia) ▫Bordetella pertussis(whooping cough) ▫Endemic fungi Histoplasma capsulatum Coccidioidesimmitis Cryptococcus neoformans Blastomyceshominis ```
58
ohio rive fungus
histoplasmosis
59
western states fungus
coccidiomycosis
60
middle states fungus
blastomycosis
61
CAP –Resistant Organisms •Drug-resistant S. pneumoniae (DRSP)
``` ▫Age 65 years ▫B-lactam use within previous 3 months ▫Alcoholism ▫Immunosuppressive illness or therapy ▫Exposure to child at day care ```
62
CAP –Empiric Antimicrobial Guidelines •Outpatient Recommendations previously healthy
Macrolide PO (azithromycin, clarithromycin) -OR- Doxycycline PO
63
CAP –Empiric Antimicrobial Guidelines •Outpatient Recommendations DRSP risk (comorbidities, age > 65 years, use of antimicrobials within 3 months)
Respiratory fluoroquinolone PO (levofloxacin, moxifloxacin) -OR- B-lactam PO [high dose amoxicillin or amoxicillin-clavulanate preferred (alternates: ceftriaxone, cefuroxime)] PLUS a macrolide PO
64
CAP –Empiric Antimicrobial Guidelines •Inpatient, Non-Intensive Care Unit Recommendations
Respiratory FQ IV or PO (levofloxacin, moxifloxacin) -OR- B-lactam IV (ceftriaxone, cefotaxime, or ampicillin preferred) PLUSmacrolide IV (azithromycin)
65
CAP –Empiric Antimicrobial Guidelines •Inpatient, Intensive-Care Unit Recommendations
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
CAP –Modifying Empiric Regimen •Pseudomonas aeruginosarisks:
▫Structural lung disease (bronchiectasis) ▫Repeated COPD exacerbations Frequent corticosteroid and/or antibiotic use ▫Prior antibiotic therapy
67
CAP –Modifying Empiric Regimen pseudomonas treatment
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
Community-acquired methicillin-resistant Staphylococcus aureus (CA-MRSA) risks:
▫End-stage renal disease (dialysis) ▫Injection drug abuse ▫Prior influenza ▫Prior antibiotic use (especially FQ)
69
Community-acquired methicillin-resistant Staphylococcus aureus (CA-MRSA) risks: treatment
▫Add vancomycin IV or linezolid | ▫Panton-Valentine leucocidin necrotizing pneumonia: add clindamycin or use linezolid
70
CAP –Intravenous Oral Therapy | •Transition to oral therapy:
``` ▫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
CAP –Duration of Therapy
•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
HCAP
history of hospitalization or exposure to healthcare settings
73
HAP
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
VAP
arises 48-72 hours after endotracheal intubation ▫Occurs in 9-27% of all intubated patients ▫Incidence increases with longer ventilation duration
75
HCAP, HAP & VAP early onset
less than 4 days
76
HCAP, HAP & VAP late onset
5+ days
77
HCAP, HAP & VAP aerobic gram negative
P. aeruginosa E. coli K. pneumoniae Acinetobacter spp.
78
HCAP, HAP & VAP gram positive
MRSA (more common in diabetes, head trauma, those hospitalized in ICUs)
79
HCAP, HAP & VAP oropharygeal commensals
Viridansgroup streptococci Coagulase-negative staphylococci Neisseriaspp. Corynebacteriumspp.
80
Multi-Drug Resistant (MDR) Pathogens | •Pseudomonas aeruginosa
``` ▫Resistance caused by multiple efflux pumps ▫Decreased expression of outer membrane porinchannel ▫Increasing resistance to: Piperacillin Ceftazidime Cefepime Imipenem Meropenem Aminoglycosides Fluoroquinolones ```
81
Multi-Drug Resistant (MDR) Pathogens | •Klebsiella, Enterobacter, Serratia
▫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
Multi-Drug Resistant (MDR) Pathogens | •MRSA
▫> 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
Multi-Drug Resistant (MDR) Pathogens | •drsp
▫Altered PBP | ▫ALL MDR strains in US currently susceptible to vancomycin and linezolid
84
HCAP, HAP, & VAP –Diagnosis
•Radiographic infiltrate that is new or progressive •Clinical findings suggestive of infection: ▫Fever ▫Purulent sputum ▫Leukocytosis ▫Decline in oxygenation
85
Empiric Therapy –Early Onset | •Potential pathogens:
▫S. pneumoniae ▫H. influenzae ▫MSSA ▫Sensitive gram-negative: E. coli, K. pneumoniae, Enterobacterspp., Proteusspp., Serratia marcescens
86
Empiric Therapy –Early Onset Treatment:
▫Ceftriaxone OR ▫FQ (levofloxacin, moxifloxacin, ciprofloxacin) OR ▫Ampicillin/sulbactam OR ▫Ertapenem
87
Empiric Therapy –Late Onset | •Potential pathogens (MDR):
▫P. aeruginosa ▫K. pneumoniae (ESBL+) ▫Acinetobacter ▫MRSA
88
Empiric Therapy –Late Onset Treatment:
▫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
Combination vs. Monotherapy
Combination therapy recommended to ensure at least one agent is activeagainst the often MDR pathogen Use monotherapy when possible
90
Combination vs. Monotherapy Often cited reasons for combination therapy
▫To prevent resistance Evidence not well documented ▫To add synergy for treatment of P. aeruginosa Only proven valuable in neutropenia or bacteremia
91
Duration of Therapy
•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
DOC if Organism Known Streptococcus pneumoniae
``` ▫Non-resistant Penicillin G Amoxicillin ▫Resistant Chosen on basis of susceptibility: Cefotaxime, ceftriaxone, levofloxacin, moxifloxacin, vancomycin, linezolid ```
93
DOC if Organism Known Haemophilus influenzae
▫Non-B-lactamase producing Amoxicillin ▫B-lactamase producing 2ndor 3rdgeneration cephalosporin, amoxicillin/clavulanate
94
DOC if Organism Known Mycoplasma pneumoniae
Macrolide (azithromycin, clarithromycin), tetracycline (doxycycline)
95
DOC if Organism Known Chlamydophila pneumoniae
Macrolide (azithromycin, clarithromycin), tetracycline (doxycycline)
96
DOC if Organism Known Chlamydophila psittaci
Doxycycline
97
DOC if Organism Known Legionellaspp.
Fluoroquinolone, azithromycin, doxycycline
98
DOC if Organism Known Enterobacteriaceae (Klebsiella, E. coli, Proteus)
3rdor 4thgeneration cephalosporin, carbapenem (if ESBL producer)
99
DOC if Organism Known Pseudomonas aeruginosa
Antipseudomonal B-lactam PLUS ciprofloxacin, levofloxacin, or an aminoglycoside
100
DOC if Organism Known Anaerobe (aspiration): Bacteroides, Fusobacterium, Peptostreptococcus
B-lactam/B-lactamase inhibitor, clindamycin
101
DOC if Organism Known Staphylococcus aureus
▫Methicillin-sensitive Antistaphylococcalpenicillin (nafcillin, oxacillin, dicloxacillin) ▫Methicillin-resistant Vancomycin or linezolid
102
DOC if Organism Known Influenza virus
Oseltamivir, zanamivir
103
DOC if Organism Known Pneumocystis jiroveci(P. cariniipneumonia)
Trimethoprim/sulfamethoxazole
104
DOC if Organism Known Bordetella pertussis
Azithromycin, clarithromycin
105
DOC if Organism Known Coccidioidesspp.
▫No treatment necessary if normal host | Itraconazole, fluconazole
106
DOC if Organism Known Histoplasmosis and Blastomycosis
▫Itraconazole
107
Influenza overview
•Each year, 5-20% of population infected •In the U.S.: ▫36,000 deaths ▫> 200,000 hospitalizations
108
influenza transmission
▫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
influenza symptoms
``` ▫Fever ▫Myalgia ▫Headache ▫Malaise ▫Non-productive cough ▫Sore throat ▫Rhinitis ```
110
influence uncomplicated
Symptoms resolve after 3-7 days (uncomplicated) | ▫Cough/malaise can last > 2 weeks`
111
NeurominidaseInhibitors drugs
Oseltamivir(PO), zanamivir(INH)
112
NeurominidaseInhibitors moa
analogs of sialic acid, interferes with release of progeny influenza virus from infected host cell
113
NeurominidaseInhibitors pk
▫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
NeurominidaseInhibitors adrs Oseltamivir
nausea, vomiting, abdominal pain (5-10%), headache, fever, diarrhea, neuropsychiatric effects Approved for children ≥ 1 year
115
NeurominidaseInhibitors adrs Zanamivir
cough, bronchospasm, decrease in pulmonary function (reversible), nasal/throat discomfort, not recommended in underlying airway disease Approved for children ≥ 7 years
116
NeurominidaseInhibitors resistance
▫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
NeurominidaseInhibitors therapeutic use
▫Influenza prophylaxis (household and institutional) | ▫Influenza treatment
118
M2 Channel Blockers drugs
Amantadine (PO), rimantadine(PO)
119
M2 Channel Blockers moa
block M2 proton ion channels of virus inhibiting uncoatingof viral RNA within host cell ▫Active against influenza A only
120
M2 Channel Blockers pk
▫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
M2 Channel Blockers adrs
``` ▫GI (nausea, anorexia) ▫CNS (nervousness, insomnia, light-headedness) ▫Severe behavioral changes ▫Delirium ▫Agitation ▫Seizures ```
122
M2 Channel Blockers resistance
point mutations, marked resistance limiting use of these agents
123
Other Antivirals –HSV & VSV
•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
Other Antivirals –CMV
•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
Common fungi of clinical interest:
``` ▫Candida albicans ▫Histoplasma capsulatum ▫Cryptococcus neoformans ▫Coccidioidesimmitis ▫Aspergillus spp. ▫Blastomycesdermatitidis ```
126
Azole Antifungals overview
•Ergosterol found in cell membrane of fungi (compared to cholesterol used in bacteria and human cells)
127
Azole Antifungals moa
•MOA: inhibits fungal cytochrome P450, reducing production of ergosterol ▫Selective toxicity due to greater affinity for fungal rather than human cytochrome P450 enzymes
128
Azole Antifungals therapeutic use
wide spectrum of activity against Candidaspp, blastomycosis, coccidiodomycosis, histoplasmosis, and even Aspergillus(itraconazole, voriconazole)
129
Azole Antifungals adrs
minor GI upset, abnormalities in liver enzymes | •Drug interactions!!
130
Azole Antifungals drugs
Fluconazole (Diflucan) PO, IV Itraconazole PO Voriconazole (Vfend) PO, IV
131
Fluconazole (Diflucan) PO, IV
▫PK: water soluble, good CSF penetration, high PO bioavailability ~96%
132
•Itraconazole PO
PK: drug absorption increased by food and low gastric pH
133
Voriconazole (Vfend) PO, IV
▫PK: well absorbed, bioavailability > 90% | ▫ADRs: visual changes, photosensitivity
134
Amphotericin B moa
binds ergosterol, changes permeability of cell, forms pores in membrane
135
Amphotericin B pk
▫Insoluble in water, variety of lipid formulations available, poorly absorbed PO, t1/215 days, only 2-3% of blood level reaches CSF
136
Amphotericin B therapeutic use
broadest spectrum of activity, useful in life-threatening infections but very toxic
137
Amphotericin B adrs
infusion related (fever, chills, vomiting, headache), cumulative toxicity (renal damage)
138
Echinocandins
* 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
β-Lactam ADRs in genreal
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
linezolid adrs
thrombocytopenia serotonin syndrom htn vomiting headache
141
sputum culture in outpatien
no
142
cavitary infiltrates
tb and fungus
143
recent travel
legionella
144
most common cap for gramp pos
strep pneumo | staph aureas mrsa
145
gram neg cap
h flu moraxella pseudomonas
146
Enterobacterhigh frequency resistance development to cephalosporins during treatment
enduces own resistance to 1st 2nd and 3rd gens
147
methicillin causes
nephritis
148
usually on treat fungal pneumonia with
immunocompromised pts
149
influenza overview
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
m2 channel blockers in parkinsons
bc they impact dopamine in cns, so they can be used in parkinsons
151
cmv prophylaxis for
organ transplant
152
ergosterol
sterol in fungal cell membranes azoles
153
amphotericin b
plugs whole in cell membrane
154
bglucan synthase fungus
cell wall structure echocandins
155
azole drug interaction
cyp statins and antiplatelets
156
amphotericin adrs
bc release of cytokines

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