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Pharmacology > Lecture 11 (Pulm)-Exam 6 > Flashcards

Lecture 11 (Pulm)-Exam 6 Flashcards

1
Q

Acute bronchitis
* What is it?
* What are you exposed to?
* What is the infection aspect?⭐️

A

Inflammation and irritation of the large airway epithelium

Exposure to irritating environmental trigger (tobacco, allergen)

Infection
* MCC viruses (85 to 95%) – influenza, respiratory syncytial virus (RSV), parainfluenza (RIP)
* Bacteria (5%) – M. pneumoniae, C. pneumoniae, Bordetella pertussis

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2
Q

What are the sxs of acute bronchitis?

A

Cough persisting for > 5 days
* Other symptoms (dyspnea, cyanosis, airway obstruction) rare
* ± fever
* ± transient wheezing or crackles

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3
Q

Acute Bronchitis
* How do you dx it?
* What is not recommended?⭐️

A
  • Diagnosis – clinical; CXR only if diagnosis unsure
  • Sputum cultures not recommended
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4
Q

Acute bronchitis
* What is the txt?
* Cough cont for how long?
* What does the patient need adequate of?
* What over the OTC meds that can be used?
* What should be avoided?

A
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5
Q

What are the nonpharm cough agents for bronchitis?

A
  • Lozenges
  • Hot tea (± honey)
  • Smoking cessation
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6
Q

BRONCHITIS – COUGH AGENTS
* What are all 4 of them?

A
  • Dextromethorphan
  • Benzonatate
  • Codeine/hydrocodone
  • Guaifenesin
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7
Q

Dextromethorphan
* What is the MOA?
* What are the adverse reaction?

A

MOA
* Depresses the medullary cough centers
* Decreases sensitivity of cough receptors and interrupts cough impulse transmission

SE:
* Nausea, vomiting
* Dizziness
* Drowsiness
* Hyperpyretic crisis with MAOIs

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8
Q

Benzonatate:
* What is the MOA
* What are the adverse reactions?

A

MOA
* Suppresses cough by topical anesthetic action on pulmonary stretch receptors in alveoli

Adverse Effects
* Dizziness
* Drowsiness
* Dysphagia

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9
Q

Codeine/hydrocodone
* What is the MOA?
* What are the adverse reactions?

A

MOA:
* Mu receptor antagonism; central suppression of cough center

Adverse reactions:
* Sedation
* Nausea /vomiting /constipation
* Respiratory depression

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10
Q

Guaifenesin:
* What do you take with?
* What is the MOA?
* What are the se?

A
  • Take with plenty of water
  • Stimulates the flow of respiratory secretions; decreases viscosity and increases quanity of respiratory secretions-> EASIER to cough out
  • SE: N/V, dizziness, drowsiness and HA
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11
Q

ANTI-INFLUENZA AGENTS
* What is the MOA of amantadine?
* What is the MOA of xofluza?
* What is the MOA of NA inhibitors?

A
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12
Q

ANTI-INFLUENZA AGENTS: Amantadine(PO) & Rimantadine (PO)
* What is the class and MOA
* What is the spectrum?
* What are the SE?

A
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13
Q

ANTI-INFLUENZA AGENTS: Oseltamivir & Zanamivr
* What is the class MOA?
* What is the spectrum?
* What are the SE?

A
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14
Q

ANTI-INFLUENZA AGENTS: Baloxavir marboxil
* What is the class MOA?
* What is the spectrum?
* What are the SE?

A
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15
Q

What anti-influ drug is approved for all age groups included pregnant women?

A

Neuraminidase inhibitors MC
* Oseltamivir MC – approved for all age groups including pregnant woman
* Oral tablets and suspension

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16
Q

Anti influenza agents:
* What groups need treatment and post-exposure prophylaxis?

A
  • Chronic lung disease (COPD, asthma)
  • Organ dysfunction (heart, kidney, liver)
  • Neurologic disorders
  • Immunocompromised
  • Obese
  • Extremes of age (> 65 years or < 2 years)
  • Pregnancy
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17
Q

ANTI-INFLUENZA AGENTS
* Treatment must be started within what window?
* Hospitalized patients may benefit if started within what time frame?
* What is the point of txt?

A
  • Treatment must start within 48 hours of symptoms onset – modest symptom reduction in healthy patients
  • Hospitalized patients may benefit if started within 5 days of symptom onset
  • Decrease in duration of symptoms (avg: 1 day) and severity of disease
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18
Q

Seasonal flu vaccine recommended for who?

A

all patients without vaccine contraindications > 6 months of age

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19
Q

Community-acquired Pneumonia (CAP)
* When does it occur?
* What are the two classes?

A

Occurs in the community or within first 48 hrs of hospitalization

May be typical or atypical
* Typical ”classic” Presentation: Chills, followed by fever, pleuritic pain and productive cough
* Atypical Presentation: (Often associated with Mycoplasma, Chlamydia or Legionella infection) Sore throat & Headache, followed by NON-productive cough and dyspnea

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20
Q

Nosocomial pneumonia (VAP +/- MDR & HAP)
* When does this occur?
* What are the MC bacterial pathogens?
* What is common?

A
  • Occurs during hospitalization after first 72 hours
  • MC bacterial pathogens are gram-negative rods (E. coli, Pseudomonas) and Staphylococcus aureus
  • Multidrug resistant (MDR) pathogens
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21
Q

What are the two methods of prevention of pneumonia?

A

Influenza vaccine (yearly)

Pneumococcal vaccine (>65 years and any high-risk any patients)
* High risk: [heart disease, sickle cell, pulmonary disease, diabetes, alcoholic cirrhosis or asplenic individuals)

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22
Q

MICROBIOLOGY OF CAP
* What are the pathogens for typical?
* What are the pathogens for atypical?
* What are some other organisms?

A

Typical:
* Streptococcus pneumoniae
* Hemophilus influenzae
* Staphylococcus aureus

Atypical:
* Mycoplasma pneumoniae
* Chlamydophila pneumoniae
* Legionella pneumoniae (high mortality)-> Up to 40% of CAP cases & Often undetected due to poor diagnostic tools

Other:
* Respiratory viruses – Influenza
* Aspiration – associated oral flora
* Gram-negative bacilli

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23
Q

Fill in for CAP by age

A
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24
Q

What do you need to diagnosis CAP in 18+ without immunocompromising conditions?

A
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25
Q

What do you need to diagnosis severe CAP ?

A
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26
Q

What is the curb 65?

A
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27
Q

What is the empirical txt for CAP outpt with someone who has no comorbdities or risk factors?

A
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28
Q

What is the empirical txt for CAP outpt with someone who has comorbdities?

A
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29
Q

CAP outpt txt key points
* Selection is made based on patient?
* how long is the treatment for?
* What do you want for the patient after txt (3)?
* What are the SE of macrolides?
* What is the DOC of atypicals?
* What is the issue with fluroquinolones?

A
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30
Q

HOSPITALIZED PATIENT - NON-SEVERE CAP TXT

A
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31
Q

HOSPITALIZED PATIENT - SEVERE CAP TXT

A
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32
Q

What are the cell wall active agents?

A

Please, Come Cee My Vechial, I Hit Wall

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33
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34
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35
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36
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37
Q

Skip 3rd gen because it has a separate card

A
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38
Q

CARBAPENEMS
* What are the four meds?
* What is the MOA?
* What makes them different?

A
  • Imipenem, meropenem, ertapenem, doripenem (IV only)
  • MOA: inhibit bacterial cell wall synthesis
  • Still have beta-lactam ring but slight structure change including substitution from sulfur with carbon makes them more resistant to beta lactamases
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39
Q

CARBAPENEMS
* Narrow or broad spectrum?
* Which drug does not cover pseduomonas or acinetobacter?
* What is doripenem for?
* Should be reserved for what?

A
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40
Q

CARBAPENEMS
* What are the SE?

A
  • ­Nausea / vomiting (worse with imipenem)
  • Seizures (worse with imipenem)
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41
Q

VANCOMYCIN
* What is the MOA?

A

MOA: inhibits bacterial wall synthesis

Glycopeptide antibiotic – binds tetrapeptide chains and prevents linking
* Do not bind PBPs – bypass PBP mutations
* Resistance secondary to bacterial changes in the tetrapeptide chains – vancomycin can no longer bind

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42
Q

What are the indications of vancomycin?

A
  • Treatment of gram-positive organisms resistant to other antibiotics
  • Commonly incorporated into empiric regimens
  • Treatment of Clostridium difficile enterocolitis
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43
Q

Vancomycin must be given how? Why?

A

Not absorbed from the GI tract – must be given IV for systemic infections

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44
Q

What are the SE of Vancomycin?

A
  • ­ Ototoxicity
  • ­ Nephrotoxicity
  • ­ Thrombophlebitis
  • ­ “Red-man’s syndrome
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45
Q

Dose and frequency of vancomycin is determined and monitored via what?

A
  • Troughs – adjust per clinical pharmacy
  • Goal trough levels usually 15 to 20; depends on infection and MIC of bacteria
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46
Q

TETRACYCLINES
* What are the different meds?
* What is the MOA?

A

Tetracycline, doxycycline, minocycline, tigecycline

MOA: inhibit bacterial protein synthesis
* Binds to A-site of 30S subunit
* Inhibits binding of tRNA to mRNA ribosome complex

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47
Q

Tetracylines:
* What do they cover?
* What is no longer used and why?

A
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48
Q
A
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49
Q

TETRACYCLINES
* What are the SE?(7)

A
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50
Q

Macrolides:
* What are the different meds?
* What is the MOA?

A

Erythromycin, clarithromycin, azithromycin

MOA
* ­ Inhibits bacterial protein synthesis
* ­ Bind to 50s subunit and prevent translocation; ribosome can’t slide to the next codon on the mRNA

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51
Q

Macrolides:
* What is the coverage?
* What is less often used and why?

A
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52
Q
A
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53
Q

MACROLIDES
* What are the Interactions?
* What are the SE?

A
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54
Q

Fluoroquinolones:
* What are the different types?
* What is the MOA?
* How is it metabolized?

A
  • Ciprofloxacin, levofloxacin, moxifloxacin, delafloxacin
  • MOA: Inhibits bacterial replication by inhibition of DNA gyrase (topoisomerase I and topoisomerase IV)
  • Metabolized via CYP450; also inhibitor ->Many drug interactions
55
Q

FLUOROQUINOLONES
* Should not be taken with what?

A

Should not be taken with calcium, iron, zinc – bind quinolones and cause chelation and decreased absorption

56
Q

What are the SE of fluoroquinolones?(6)

A
57
Q
A
58
Q
A
59
Q

What are the black box warnings about fluoroquinolones?

A
  • Serious, potentially irreversible adverse effects including tendinopathy and CNS effects. Avoid use / discontinue in any patients experiencing these side effects.
  • Risks > benefits for chronic bronchitis, sinusitis, uncomplicated cystitis
60
Q

When should you switch from IV to PO?

A
61
Q

HAP AND VAP
* What are they?

A

Hospital Acquired Pneumonia (HAP)
* Pneumonia that occurs ≥ 48 hours after admission; not incubating at admission

Ventilator Associated Pneumonia (VAP)
* Type of HAP that develops after endotracheal intubation

62
Q

What are the most common causes of HAP and VAP?

A
63
Q

HAP AND VAP EMPIRIC THERAPY
* Treatment should be what?
* What do you need to be worried about?
* What is the minimum duration of therapy?
* May do what?

A
64
Q
A
65
Q

HAP and VAP empiric therapy:
* What is the txt of a patient who is not high risk of mortality and not at high risk of MRSA?(5)

A

MC LAP

66
Q

HAP and VAP empiric txt:
* What is the txt of a patient who is not high risk of morality and high risk of MRSA

A
67
Q
A
68
Q
A
69
Q
A
70
Q
A
71
Q

Fill in for MOA

A

inhibition of fungal agents and cell wall synthesis

72
Q
A
73
Q
A
74
Q
  • What is first line for Histoplasmosis (mild and severe?
  • What are the alternatives?
  • What is the txt duration?
A
75
Q
  • What is first line for Blastomyosis (mild and severe?
  • What are the alternatives?
  • What is the txt duration?
A
76
Q
  • What is first line for Coccidiomyosis (mild and severe?
  • What are the alternatives?
  • What is the txt duration?
A
77
Q

Pneumocystis jirovecii
* What type of patients do you see this in?
* What does the CXR look like?

A
  • HIV/AIDS with CD4 < 200 cells/mm3
  • Solid organ and bone marrow transplant patients
  • Cancer chemotherapy patients
    * Most require primary chemoprophylaxis with TMP-SMX, pentamidine

O2 will be lower than how bad the Xray looks

78
Q

Pneumocystis jirovecii
* What is the txt?

A

TMP/SMX x 21 days (PO or IV)
* Prednisone (first dose prior to starting anti-PJP therapy)
* 40mg PO BID x 5d, 40mg PO daily x 5d, then 20mg PO daily x 11 days

79
Q

Sulfamethoxazole / trimethoprim (SMX/TMp)
* What is the MOA?
* What is the dosing based on
* What is the one double strength tablet?
* What can there be an allergic reaction to?

A
  • MOA: inhibit bacterial DNA synthesis; each inhibit different steps in bacterial folate synthesis; no folate = no nucleic acids = no DNA
  • Dosing based on TMP component
  • One double strength tablet = 160 mg TMP/ 800mg SMX
  • Allergic reaction to sulfonamide group: can cross react with other drugs with sulfonamide group including hydrochlorothiazide and glyburide
80
Q

Sulfamethoxazole / trimethoprim (SMX/TMp)
* What are the CI?
* What type of inhibitor is it?

A
  • CI: pregnancy, infants < 2 months
  • CYP450 2C9 inhibitor - increases warfarin levels
81
Q

Sulfamethoxazole / trimethoprim
* What are the SE?(6)

A
82
Q
A
83
Q

Tuberculosis txt
* When a patient has a latent TB what test is positive?
* What is the txt?

A
84
Q

Fill in for TB test

A
85
Q

Tuberculosis treatment
* What is the txt for active disease?
* HIV patients shuold get no less than what?

A
86
Q

When will TB treatment change?

A
  • Regimen will change for multi-drug resistant TB
87
Q
A
88
Q

Anti-TB medicaiton

A
89
Q
A
90
Q
A
91
Q
  • Which anti-TB medications are hepatotoxic? What drugs’
  • MOA is inhibiting Cell wall?
A
  • Liver:Pyrazinamide, Isoniazid, Rifampin
  • Cell wall:Isoniazid, Pyrazinamide and ethambutol
92
Q

Acute bronchiolitis
* What is this?
* What are the inital symptoms? What does that turn into?
* What is the MCC cause?
* What is recommended for mild disease?
* What is the recommended for patients with severe disease?

A
93
Q

ACUTE BRONCHIOLITIS
* What is the pathophysio?

A
  • Viruses replicate in the nasopharynx
  • Infects the small bronchiolar epithelium
  • Extends to the type 1 and 2 alveolar pneumocytes
  • Lower respiratory tract infection 1-3 days later
    * mucus buildup, airway obstruction, air trapping, and increased airway resistance
94
Q

Outpatient treatment: Acute bronchiolitis
* What is the supportive care?

A

Hydration

Relieve nasal congestion / obstruction

Anticipatory guidance
* Clinical course (onset, peak-> 3-5days, resolution)
* Evaluation for worsening disease (retractions, dry diapers, no tears, dipping fontelles)
* Indications to seek urgent medical care
* Use of nasal decongestants, bronchodilators is NOT recommended

95
Q

How do you use a nasal bulb suction?

A
96
Q

Acute bronchiolitis
* What are the indications for hospitalization?

A
  • Toxic appearing
  • Lethargic
  • Dehydrated
  • Poor feeding
  • Moderate respiratory distress
  • Nasal flaring, retractions, grunting
  • RR > 70 bpm
  • O2 < 95% sustained
  • Apnea
97
Q

What is the inpatient treatment for Acute bronchiolitis?

A
98
Q

What is no recommended for inpatient treatment of Acute bronchiolitis?

A
  • Routine use of beta-2 agonists (SABAs) not recommended
  • Routine use of inhaled racemic epinephrine or hypertonic saline is not recommended
  • Routine use of glucocorticoids not recommended
  • Routine use of antivirals (ribavirin) not recommended
99
Q

Palivizumab (synagis)
* What is it?
* What does it decrease?
* What are the MC populations recommoned this?
* Limited by what?

A
100
Q

EPIGLOTTITIS: What is it?

A

inflammation of the epiglottis and adjacent supraglottic structures, potentially life- threatening condition

101
Q

What do you see on x-ray with epiglottitis?

A
  • Imaging: lateral neck xray
  • “Thumbprint Sign”
102
Q

What are the inital interventions of epiglottitis?

A
  • Airway management – keep airway open
  • AVOID irritation
103
Q

What are the MC organisms for epiglottitis?

A
104
Q

What is the first line txt of epiglottitis? What if the patient is penicillin allergic?

A
105
Q

CROUP- VIRAL
* What is the pathophysio?
* What is the mc organism?

A
  • Pathophysiology – infection → inflammation of larynx, trachea, bronchi, bronchioles and lung parenchyma resulting in swelling and exudate, anatomic hallmark is narrowing of the subglottic airway
  • Organism: Parainfluenza
106
Q

What is the x-ray sign in croup?

A
107
Q

What are the symptoms of mild croup?

A
  • No stridor at rest
  • Stridor when agitated
  • Barking cough
  • Hoarse cry
  • Mild to no retractions
108
Q

What is the txt of Mild croup?

A
  • Humidified air
  • Antipyretics
  • Hydration
  • Anticipatory guidance
  • Steroids
    * Dexamethasone 0.6 mg/kg PO x 1 dose
    * Budesonide 2 mg via nebulizer x 1 dose

Dexamethasone reduces repeat clinic visits, emergency department visits, or hospitalizations

109
Q

What are the symptoms of moderate croup?

A
  • Stridor at rest
  • Mild retractions
  • ± other signs of respiratory distress
  • Little to no agitation
110
Q

What are the symptoms of severe croup?

A
  • Stridor at rest
  • Severe retractions
  • Anxious, agitated, fatigued
111
Q

What is the txt for mod to severe croup? (good response, Good response with worsening during observation and Poor response)

A
112
Q

Racemic epinephrine
* What is it?
* MOA in croup?

A

1:1 mixture of levo and dextro epinephrine

MOA in croup:
* Alpha-1 stimulation – vasoconstriction, reduce tissue edema
* Beta-1 stimulation – vasoconstriction in skin and mucosa

113
Q

Racemic epinephrine
* What is uncommon?
* What may occur?
* What is the dose?

A
114
Q

Pertussis – “Whooping Cough”
* What is the organism?
* When is increased incidence?
* How is it transmitted?
* How does it cycle in the US?

A
  • Etiology – gram-negative coccobacillus – Bordetella pertussis
  • Increased incidence summer and fall
  • Transmission via respiratory droplets
  • In US it cycles q3-5yrs – the incidence of pertussis has been rising since the 1990s (increased rates of infection in adolescents and adults)
115
Q
  • What is the prevent against pertussis?
  • What are the dosing ages?
A
116
Q

What is Dtap?
* Who do you give it to?

A
117
Q

What is Tdap?
* Who do you give it to?

A
118
Q

Pertussis:
* What is the Catarrhal stage?

A

Catarrhal (1-2 weeks): treatment started at this phase can shorten disease course

119
Q

Pertussis:
* What is the Paroxysomal stage?

A

Paroxysmal (2 to 4 weeks): treatment has little effect on disease course but can eradicate nasal carriage and prevent disease spread

120
Q

What is the concalscence stage?

A

Convalescence (1-2 weeks): Patient still infectious; treat to eradicate carriage state

121
Q

PERTUSSIS TREATMENT
* When do you tx if over a year old?
* When do you tx if infant < 1 year or pregnant woman,

A
  • ­ If over 1 year of age, treat if within 3 weeks of cough onset
  • ­ If infant < 1 year or pregnant woman, treat if within 6 weeks of cough onset
122
Q

PERTUSSIS TREATMENT
* What is the supportive care?
* When can patients return to school and work

A
123
Q

What are the three meds for pertussis?

A
  • Azithromycin (PO or IV)
  • Erythromycin (cannot use under one month)
  • Clarithromycin (cannot use under one month)
124
Q

Pertussis treatment
* What is the post exposure prophylaxis?

A
  • Household contacts
  • Others exposed within 21 days at high-risk of severe disease
  • Pregnant women, infants < 1-year, immunosuppressed, chronic lung disease, respiratory insufficiency, cystic fibrosis, persons who have close contact with infants
125
Q

Cystic Fibrosis
* What is the pathophyio

A

Affects nearly all exocrine glands = abnormal transport of chloride and sodium across secretory epithelia →thickened, viscous secretions in the bronchi, biliary tract, pancreas, intestines, and reproductive system

126
Q

What is cysstic fibrosis the leading cause of?

A

A leading cause of bronchiectasis

127
Q

Cystic Fibrosis: bacterial
* Lungs are what?
* What are the bacteria in infants and children?
* What is the bacteria for all ages?
* What is going with MRSA, Mycobacterium avium complex & M. abscessus

A
128
Q

CF managment:
* What meds are there depending on genotype and age?
* What are airway clearance therapies?
* What are the prevention measures?
* What are the bronchodilators?
* What is the anti-inflam therapy?
* What is the prevention of acute exacerbations?

A
129
Q
A
130
Q

RESPIRATORY DISTRESS SYNDROME (HYALINE MEMBRANE DISEASE)
* What is the definition?
* When does surfactant begin production?
* What is the type 2 pneumocytes?

A
131
Q

Respiratory Distress Syndrome(Hyaline Membrane Disease)
* What is the pathophysio?

A
  • Inadequate surfactant activity →high surface tension →instability of the lung at end-expiration→ low lung volume & decreased compliance
  • Surfactant deficiency → lung inflammation & respiratory epithelial injury→ increased airway resistance & possible pulmonary edema
132
Q

Respiratory Distress Syndrome(Hyaline Membrane Disease)
* What is the txt?

A
  • Treatment includes intratracheal surfactant therapy, supplemental O2 & mechanical ventilation as needed
  • Survival rate >90% with treatment
133
Q

Respiratory Distress Syndrome(Hyaline Membrane Disease)
* What is the prevention?

A

Pharmacology (14 decks)

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