Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

oseltamivir

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

zanamivir

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

peramivir

A

*IV neuraminidase inhibitor used for influenza
*ADE: diarrhea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

activity of beta lactams

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

natural penicillins (Pen G & Pen V) - spectrum

A

*strep pneumo
-good; a little resistance

*strep pyogenes (group A strep)
-NO resistance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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%)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

clinical uses of amoxicillin

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
piperacillin/tazobactam - spectrum
*covers: -gram negatives INCLUDING PSEUDOMONAS -anaerobes -decent strep and MSSA coverage *very common empiric therapy for hospital-acquired pneumonia (ventilatory-acquired pneumonia)
26
cephalosporins do not kill?
*enterococcus *Listeria monocytogenes *MRSA *atypicals
27
2nd generation cephalosporins
*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
3rd generation cephalosporin: ceftriaxone
*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
3rd generation cephalosporin: ceftazidime
*covers gram negatives (INCLUDING PSEUDOMONAS)
30
4th generation cephalosporin: cefepime
*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
beta lactams that hit pseudomonas
*piperacillin/tazobactam *ceftazidime *cefepime *aztreonam *meropenem *imipenem
32
general ADEs of beta lactams
*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
macrolides - MOA & agents
*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
macrolides - spectrum
*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
macrolides - uses
*COPD exacerbation *added to cover atypicals in community-acquired pneumonia *URIs in beta-lactam allergy *non-TB mycobacterial infections
36
tetracyclines - MOA & agents
*MOA: inhibit protein synthesis by binding to 30S ribosomal subunit *agents: 1. tetracycline 2. doxycycline 3. minocycline
37
tetracyclines - spectrum
*staph & strep (2nd line) *H. flu & M. cat (2nd line) *atypicals
38
tetracyclines - uses
*most common: added to beta-lactam to cover atypicals in community-acquired pneumonia
39
tetracyclines - kinetics
*well absorbed orally *avoid di- and tri-valent cations
40
tetracyclines - ADEs
*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
fluoroquinolones - MOA & agents
*MOA: inhibit DNA synthesis by binding to bacterial topoisomerase (topo II = DNA gyrase; also topo IV) *agent: MOXIFLOXACIN
42
moxifloxacin
*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
fluoroquinolones - pharmacokinetics
*good oral absorption *bind with di- and tri-valent cations (antacids, supplements, calcium-containing foods, sucralfate)
44
fluoroquinolones - ADEs
*CNS at high doses (dizziness, HA) *QTc prolongation *GI, including C. diff *risk of tendon rupture?
45
drugs used to cover MRSA
*vancomycin *linezolid
46
vancomycin
*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
vancomycin - ADEs
*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
linezolid
*alternative drug used to cover MRSA pneumonia *MOA: binds to 50S ribosomal subunit and inhibits bacterial protein synthesis *100% oral bioavailability
49
linezolid - cautions
*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
why can't we use daptomycin for MRSA pnuemonia
it binds to lung surfactant
51
amphotericin B - MOA
*an antifungal *MOA: binds to ergosterol in cell membrane to increase cell permeability
52
triazoles (fluconazole, itraconazole, etc) - MOA
*antifungals *MOA: inhibit fungal CYP450 enzyme systems to prevent conversion of lanosterol to ergosterol *voriconazole is the drug of choice for aspergillus
53
echinocandins (caspofungin, micafungin, andidulafungin) - MOA
*antifungals *MOA: inhibit (1,3)-b-D glucan synthase, which inhibits cell wall synthesis
54
flucytosine - MOA
*an antifungal *pyrimidine analogue *MOA: inhibits thymidylate synthetase, which interferes with the synthesis of nucleic acids
55
amphotericin B - things to know
*most toxic antifungal (only use it when you have to) *biggest concern = nephrotoxicity *infusion reactions (fever, chills, rigors, myalgias)
56
triazoles (fluconazole, etc) - things to know
*CYP enzyme drug interactions *HEPATOTOXICITY (check LFTs) *voriconazole = drug of choice for aspergillus
57
flucytosine - ADEs
*hematological toxicity (leukopenia, thrombocytopenia) *hepatotoxicity
58
antifungals used for Candida infections
*fluconazole (does not cover C. krusei) *echinocandins (more expensive)

Pulmonology Exam (36 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions