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Pulmonology Exam > Pharmacology of Smoking Cessation & Antimicrobials > Flashcards

Pharmacology of Smoking Cessation & Antimicrobials Flashcards

1
Q

smoking cessation - general principles

A

*need drugs + behavioral counseling
*drugs available include:
-nicotine replacement therapy (NRT) [usually long-acting (patch) + short-acting agent]
-varenicline
-bupropion

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2
Q

nicotine transdermal patch (long-acting)

A

*provides constant level of nicotine (highest strength provides nicotine plasma level ~50% of smoking 20 cigarettes per day)
*easy to use, high compliance rate
*best success if combined with short-acting product
*slow onset (about 3 hours)
*can’t adjust dose throughout day based on craving
*main ADE is local skin irritation
*sometimes used for nicotine-addicted hospitalized patients who are admitted for other reasons

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3
Q

short-acting nicotine replacement therapy (NRT) - general principles

A

*should be used in combination with a patch
*dosed multiple times during day (can adjust based on cravings & withdrawal symptoms)
*absorption needs to occur prior to nicotine getting into esophagus (nicotine is metabolized by liver and little is absorbed)
*4 options: gum, lozenge, inhalers, nasal spray

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4
Q

nicotine gum

A

*a short-acting nicotine replacement therapy (NRT) agent
*nicotine blood levels within 20 minutes
*absorption from buccal mucosa
*most ADEs are from chewing too vigorously and getting bolus release of nicotine (nausea, vomiting, abdominal pain; esophageal, oral, & gastric irritation)
*avoid acidic beverages (lowers pH, ionizes nicotine, prevents absorption)

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5
Q

nicotine lozenge

A

*a short-acting nicotine replacement therapy (NRT) agent
*similar pharmacokinetics and uses as gum
*better if dental or TMJ problems
*ADEs:
-local = mouth irritation & ulcers
-nicotine-related = nausea, vomiting, abdominal pain, headache

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6
Q

nicotine inhalers

A

*a short-acting nicotine replacement therapy (NRT) agent
*plastic that contains nicotine cartridge
*better mimics sensory aspects of smoking
*inhale nicotine vapor (not smoke)
*absorbed through oral mucosa (not lungs)
*ADEs: throat & mouth irritation, bronchospasm
*not a great choice if you have asthma

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7
Q

nicotine nasal spray

A

*a short-acting nicotine replacement therapy (NRT) agent
*absorption via nasal mucosa:
-more rapid than other products
-peak blood levels in 10 minutes
-closer to the “hit” you get from smoking
*ADEs: nasal & throat irritation, rhinitis, sneezing

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8
Q

varenicline

A

*used for smoking cessation
*partial agonist for alpha-4-beta-2 nicotinic ACh receptor
*a slight agonist effect, but mostly blocks binding of nicotine to receptor (prevents stimulation of mesolimbic dopamine system that reinforces smoking)
*start taking 1 week prior to quitting smoking
*ADEs:
-GI: nausea, vomiting
-neuro: abnormal dreams, HA, insomnia
-severe neuropsychiatric and cardiovascular concerns not born out

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9
Q

bupropion for smoking cessation

A

*MOA: weak inhibitor of DA and NE uptake
*MOA in smoking cessation not entirely understood
*start taking 1-2 weeks prior to quitting smoking
*CONTRAINDICATED IN SEIZURE DISORDERS
*blunts post-cessation weight gain
*ADEs: insomnia, agitation, dry mouth, headache, lowers seizure threshold

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10
Q

predominant treatment of viral respiratory infections

A

*mostly supportive care (treat pain, congestion, cough, etc)
*2 viruses we have antivirals for: influenza & SARS-CoV-2

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11
Q

neuraminidase inhibitors for influenza

A

*MOA: inhibit influenza virus neuraminidase; this DECREASES NEW VIRUS PARTICLE RELEASE
*3 main products:
1. oseltamivir
2. zanamivir
3. peramivir

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12
Q

oseltamivir

A

*neuraminidase inhibitor used for influenza
*ADEs: nausea, vomiting, headache

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13
Q

uses of neuraminidase inhibitors for influenza

A

*shortens duration of flu symptoms (0.5-3 days) and reduces complications in high-risk patients
*give as early as possible (hopefully within 48 hours) to at risk patients
*can consider for healthy patients if within 48 hours of symptoms
*can sometimes use oseltamivir & zanamivir for prophylaxis

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14
Q

zanamivir

A

*inhaled neuraminidase inhibitor used for influenza
*ADEs: bronchospasm, sinusitis, dizziness, ENT infections

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15
Q

peramivir

A

*IV neuraminidase inhibitor used for influenza
*ADE: diarrhea

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16
Q

remdesivir

A

*an antiviral used for COVID (infection caused by SARS-CoV-2)
*MOA: nucleotide analogue (of ATP) which inhibits RNA-dependent RNA polymerase
-competes with natural ATP for incorporation into RNA, leading to delayed chain termination during replication of viral RNA
-prodrug; needs to be activated to triphosphate
*ADEs: nausea, elevated transaminases
*best if used early in the disease

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17
Q

nirmatrelvir/ritonavir (Paxlovid)

A

*an antiviral used for COVID (infection caused by SARS-CoV-2)
*MOA: both are protease inhibitors:
-nirmatrelvir: inhibits SARS-CoV-2’s main protease (Mpro)
-ritonavir: inhibits metabolism of nirmatrelvir (acts as a booster; watch for drug interactions)
*used for symptomatic patients at risk of progressing to severe disease

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18
Q

drugs that treat/prevent inflammation associated with COVID (not the virus itself)

A

*Baricitnib (JAK inhibitor)
*Tocilizumab (IL-6 receptor antagonist)
*Dexamethasone (& other steroids)
*these treat/prevent the inflammation and tissue destruction caused by the virus, NOT the virus itself

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19
Q

beta lactam antibiotics

A

*penicillins, cephalosporins, monobactams, carbapenems
*MOA: bind to penicillin-binding proteins (PBPs), which are enzymes involved in peptidoglycan biosynthesis, which provides the cross-linking structure essential for cell wall rigidity and stability
*inhibit cell wall synthesis (inhibit transpeptidation of peptidoglycans)

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20
Q

activity of beta lactams

A

*NO beta lactams are effective against:
-MRSA
-atypical organisms (mycoplasma, legionella, chlamydia)

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21
Q

natural penicillins (Pen G & Pen V) - spectrum

A

*strep pneumo
-good; a little resistance

*strep pyogenes (group A strep)
-NO resistance

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22
Q

aminopenicillins - spectrum

A

*ampicillin (IV) & amoxicillin (PO)
*coverage: like natural penicillin (strep pneumo, strep pyogenes) PLUS:
-E. coli (60%)
-Proteus mirabilis
-H. influenzae (70%)

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23
Q

clinical uses of amoxicillin

A

*target S. pneumonia & H. flu:
-otitis media
-other community-acquired respiratory infections
*alternative for strep throat

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24
Q

amoxicillin/clavulanic acid (Augmentin)

A

*clavulanic acid is a beta-lactamase inhibitor
*expands coverage of amoxicillin:
-all H. flu and M. cat
-MSSA (non-MRSA staph)
-more gram-negatives (not pseudamonas)
-anaerobes

25
Q

piperacillin/tazobactam - spectrum

A

*covers:
-gram negatives INCLUDING PSEUDOMONAS
-anaerobes
-decent strep and MSSA coverage
*very common empiric therapy for hospital-acquired pneumonia (ventilatory-acquired pneumonia)

26
Q

cephalosporins do not kill?

A

*enterococcus
*Listeria monocytogenes
*MRSA
*atypicals

27
Q

2nd generation cephalosporins

A

*cefuroxime (oral and IV)
*activity:
-cover Staph, Strep, Proteus mirabilis, E. coli, Klebsiella (like 1st gen)
-PLUS H. flu and moraxella catarrhalis
*uses: community-acquired respiratory tract infections (usually target strep pneumo, H. flu, and M. cat)

28
Q

3rd generation cephalosporin: ceftriaxone

A

*covers gram negatives (not pseudomonas) + strep + Neisseria
*uses:
-community-acquired pneumonia
-gonorrhea
-meningitis
-gram negative infections where pseudomonas is not involved (e.g. community-acquired UTIs)

29
Q

3rd generation cephalosporin: ceftazidime

A

*covers gram negatives (INCLUDING PSEUDOMONAS)

30
Q

4th generation cephalosporin: cefepime

A

*covers gram negatives (INCLUDING PSEUDOMONAS) + strep
*uses: common empiric therapy for hospital-acquired pneumonia & ventilator-acquired pneumonia; used this instead of ceftriaxone if you need to cover Pseudomonas

31
Q

beta lactams that hit pseudomonas

A

*piperacillin/tazobactam
*ceftazidime
*cefepime
*aztreonam
*meropenem
*imipenem

32
Q

general ADEs of beta lactams

A

*hypersensitivity (rash, anaphylaxis)
*GI: diarrhea, nausea & vomiting; C. diff infection
*seizures/CNS toxicity (especially carbapenems in high doses &/or patients with risk factors):
-this is probably the most common dose-related ADE of beta-lactams

33
Q

macrolides - MOA & agents

A

*MOA: inhibit RNA-dependent protein synthesis by binding to 50S ribosomal subunit
*agents:
1. erythromycin
2. clarithromycin
3. azithromycin (most common)
*ADEs:
-prolonged QT interval, Torsades de pointes
-drug interactions
-clarithromycin: increased mortality if pt has CAD

34
Q

macrolides - spectrum

A

*staph (3rd line) & strep (2nd line; beta lactams are better)
*h. flu & m. catarrhalis
*ATYPICALS! (legionella, mycoplasma)
*non-TB mycobacteria
*B. pertussis (whooping cough)

35
Q

macrolides - uses

A

*COPD exacerbation
*added to cover atypicals in community-acquired pneumonia
*URIs in beta-lactam allergy
*non-TB mycobacterial infections

36
Q

tetracyclines - MOA & agents

A

*MOA: inhibit protein synthesis by binding to 30S ribosomal subunit
*agents:
1. tetracycline
2. doxycycline
3. minocycline

37
Q

tetracyclines - spectrum

A

*staph & strep (2nd line)
*H. flu & M. cat (2nd line)
*atypicals

38
Q

tetracyclines - uses

A

*most common: added to beta-lactam to cover atypicals in community-acquired pneumonia

39
Q

tetracyclines - kinetics

A

*well absorbed orally
*avoid di- and tri-valent cations

40
Q

tetracyclines - ADEs

A

*nausea, vomiting, diarrhea
*phototoxicity
*accumulation in growing teeth may cause pigmentation and enamel defects in teeth in children
*avoid in pregnancy & children < 8 yo if possible

41
Q

fluoroquinolones - MOA & agents

A

*MOA: inhibit DNA synthesis by binding to bacterial topoisomerase (topo II = DNA gyrase; also topo IV)
*agent: MOXIFLOXACIN

42
Q

moxifloxacin

A

*a fluoroquinolone
*spectrum:
-strep
-some gram negatives (not pseudomonas)
-H. flu, M. cat
-atypicals
*can cover typical & atypical community-acquired respiratory tract diseases with one drug

43
Q

fluoroquinolones - pharmacokinetics

A

*good oral absorption
*bind with di- and tri-valent cations (antacids, supplements, calcium-containing foods, sucralfate)

44
Q

fluoroquinolones - ADEs

A

*CNS at high doses (dizziness, HA)
*QTc prolongation
*GI, including C. diff
*risk of tendon rupture?

45
Q

drugs used to cover MRSA

A

*vancomycin
*linezolid

46
Q

vancomycin

A

*glycopeptide antibiotic
*MOA: inhibits cell wall synthesis by binding to D-Ala-D-Ala terminal of the growing peptide
*active against almost all gram-positive bacteria (COVERS MRSA)
*not absorbed orally, so oral vanc cannot treat a systemic infection
*eliminated renally
*FIRST CHOICE USED FOR MRSA

47
Q

vancomycin - ADEs

A

*fever, chills, phlebitis
*ototoxicity
*NEPHROTOXICITY (more likely if given with other nephrotoxic meds)
*leukopenia, thrombocytopenia, eosinophilia
*vancomycin infusion reaction (vancomycin flushing syndrome - not an allergic reaction)

48
Q

linezolid

A

*alternative drug used to cover MRSA pneumonia
*MOA: binds to 50S ribosomal subunit and inhibits bacterial protein synthesis
*100% oral bioavailability

49
Q

linezolid - cautions

A

*drug interactions:
-a weak monoamine oxidase inhibitor with risk for SEROTONIN SYNDROME
-watch SSRIs, cold products, meperidine, pressors, tramadol, MAOIs
*toxicities with prolonged duration:
-thrombocytopenia, anemia
-peripheral neuropathy

50
Q

why can’t we use daptomycin for MRSA pnuemonia

A

it binds to lung surfactant

51
Q

amphotericin B - MOA

A

*an antifungal
*MOA: binds to ergosterol in cell membrane to increase cell permeability

52
Q

triazoles (fluconazole, itraconazole, etc) - MOA

A

*antifungals
*MOA: inhibit fungal CYP450 enzyme systems to prevent conversion of lanosterol to ergosterol
*voriconazole is the drug of choice for aspergillus

53
Q

echinocandins (caspofungin, micafungin, andidulafungin) - MOA

A

*antifungals
*MOA: inhibit (1,3)-b-D glucan synthase, which inhibits cell wall synthesis

54
Q

flucytosine - MOA

A

*an antifungal
*pyrimidine analogue
*MOA: inhibits thymidylate synthetase, which interferes with the synthesis of nucleic acids

55
Q

amphotericin B - things to know

A

*most toxic antifungal (only use it when you have to)
*biggest concern = nephrotoxicity
*infusion reactions (fever, chills, rigors, myalgias)

56
Q

triazoles (fluconazole, etc) - things to know

A

*CYP enzyme drug interactions
*HEPATOTOXICITY (check LFTs)
*voriconazole = drug of choice for aspergillus

57
Q

flucytosine - ADEs

A

*hematological toxicity (leukopenia, thrombocytopenia)
*hepatotoxicity

58
Q

antifungals used for Candida infections

A

*fluconazole (does not cover C. krusei)

*echinocandins (more expensive)

Pulmonology Exam (36 decks)

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