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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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What do you need to diagnosis severe CAP ?
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What is the curb 65?
27
What is the empirical txt for CAP outpt with someone who has no comorbdities or risk factors?
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What is the empirical txt for CAP outpt with someone who has comorbdities?
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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?
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HOSPITALIZED PATIENT - NON-SEVERE CAP TXT
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HOSPITALIZED PATIENT - SEVERE CAP TXT
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What are the cell wall active agents?
## Footnote Please, Come Cee My Vechial, I Hit Wall
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Skip 3rd gen because it has a separate card
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CARBAPENEMS * What are the four meds? * What is the MOA? * What makes them different?
* 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
39
CARBAPENEMS * Narrow or broad spectrum? * Which drug does not cover pseduomonas or acinetobacter? * What is doripenem for? * Should be reserved for what?
40
CARBAPENEMS * What are the SE?
* ­Nausea / vomiting (worse with imipenem) * Seizures (worse with imipenem)
41
VANCOMYCIN * What is the MOA?
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
42
What are the indications of vancomycin?
* Treatment of gram-positive organisms resistant to other antibiotics * Commonly incorporated into empiric regimens * Treatment of Clostridium difficile enterocolitis
43
Vancomycin must be given how? Why?
Not absorbed from the GI tract – must be given IV for systemic infections
44
What are the SE of Vancomycin?
* ­ Ototoxicity * ­ Nephrotoxicity * ­ Thrombophlebitis * ­ “Red-man’s syndrome
45
Dose and frequency of vancomycin is determined and monitored via what?
* Troughs – adjust per clinical pharmacy * Goal trough levels usually 15 to 20; depends on infection and MIC of bacteria
46
TETRACYCLINES * What are the different meds? * What is the MOA?
Tetracycline, doxycycline, minocycline, tigecycline MOA: inhibit bacterial protein synthesis * Binds to A-site of 30S subunit * Inhibits binding of tRNA to mRNA ribosome complex
47
Tetracylines: * What do they cover? * What is no longer used and why?
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TETRACYCLINES * What are the SE?(7)
50
Macrolides: * What are the different meds? * What is the MOA?
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
51
Macrolides: * What is the coverage? * What is less often used and why?
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MACROLIDES * What are the Interactions? * What are the SE?
54
Fluoroquinolones: * What are the different types? * What is the MOA? * How is it metabolized?
* 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
FLUOROQUINOLONES * Should not be taken with what?
Should not be taken with calcium, iron, zinc – bind quinolones and cause chelation and decreased absorption
56
What are the SE of fluoroquinolones?(6)
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What are the black box warnings about fluoroquinolones?
* 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
When should you switch from IV to PO?
61
HAP AND VAP * What are they?
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
What are the most common causes of HAP and VAP?
63
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?
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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)
## Footnote MC LAP
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HAP and VAP empiric txt: * What is the txt of a patient who is not high risk of morality and high risk of MRSA
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Fill in for MOA
inhibition of fungal agents and cell wall synthesis
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* What is first line for Histoplasmosis (mild and severe? * What are the alternatives? * What is the txt duration?
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* What is first line for Blastomyosis (mild and severe? * What are the alternatives? * What is the txt duration?
76
* What is first line for Coccidiomyosis (mild and severe? * What are the alternatives? * What is the txt duration?
77
Pneumocystis jirovecii * What type of patients do you see this in? * What does the CXR look like?
* 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 ## Footnote O2 will be lower than how bad the Xray looks
78
Pneumocystis jirovecii * What is the txt?
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
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?
* 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
Sulfamethoxazole / trimethoprim (SMX/TMp) * What are the CI? * What type of inhibitor is it?
* CI: pregnancy, infants < 2 months * CYP450 2C9 inhibitor - increases warfarin levels
81
Sulfamethoxazole / trimethoprim * What are the SE?(6)
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Tuberculosis txt * When a patient has a latent TB what test is positive? * What is the txt?
84
Fill in for TB test
85
Tuberculosis treatment * What is the txt for active disease? * HIV patients shuold get no less than what?
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When will TB treatment change?
* Regimen will change for multi-drug resistant TB
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Anti-TB medicaiton
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* Which anti-TB medications are hepatotoxic? What drugs' * MOA is inhibiting Cell wall?
* Liver:Pyrazinamide, Isoniazid, Rifampin * Cell wall:Isoniazid, Pyrazinamide and ethambutol
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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?
93
ACUTE BRONCHIOLITIS * What is the pathophysio?
* 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
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Outpatient treatment: Acute bronchiolitis * What is the supportive care?
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
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How do you use a nasal bulb suction?
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Acute bronchiolitis * What are the indications for hospitalization?
* Toxic appearing * Lethargic * Dehydrated * Poor feeding * Moderate respiratory distress * Nasal flaring, retractions, grunting * **RR > 70 bpm** * **O2 < 95% sustained** * **Apnea**
97
What is the inpatient treatment for Acute bronchiolitis?
98
What is no recommended for inpatient treatment of Acute bronchiolitis?
* 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
Palivizumab (synagis) * What is it? * What does it decrease? * What are the MC populations recommoned this? * Limited by what?
100
EPIGLOTTITIS: What is it?
inflammation of the epiglottis and adjacent supraglottic structures, potentially life- threatening condition
101
What do you see on x-ray with epiglottitis?
* Imaging: lateral neck xray * “Thumbprint Sign”
102
What are the inital interventions of epiglottitis?
* Airway management – keep airway open * AVOID irritation
103
What are the MC organisms for epiglottitis?
104
What is the first line txt of epiglottitis? What if the patient is penicillin allergic?
105
CROUP- VIRAL * What is the pathophysio? * What is the mc organism?
* 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
What is the x-ray sign in croup?
107
What are the symptoms of mild croup?
* No stridor at rest * Stridor when agitated * Barking cough * Hoarse cry * Mild to no retractions
108
What is the txt of Mild croup?
* Humidified air * Antipyretics * Hydration * Anticipatory guidance * Steroids * Dexamethasone 0.6 mg/kg PO x 1 dose * Budesonide 2 mg via nebulizer x 1 dose ## Footnote Dexamethasone reduces repeat clinic visits, emergency department visits, or hospitalizations
109
What are the symptoms of moderate croup?
* Stridor at rest * Mild retractions * ± other signs of respiratory distress * Little to no agitation
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What are the symptoms of severe croup?
* Stridor at rest * Severe retractions * Anxious, agitated, fatigued
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What is the txt for mod to severe croup? (good response, Good response with worsening during observation and Poor response)
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Racemic epinephrine * What is it? * MOA in croup?
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
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Racemic epinephrine * What is uncommon? * **What may occur?** * What is the dose?
114
Pertussis – “Whooping Cough” * What is the organism? * When is increased incidence? * How is it transmitted? * How does it cycle in the US?
* 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)
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* What is the prevent against pertussis? * What are the dosing ages?
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What is Dtap? * Who do you give it to?
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What is Tdap? * Who do you give it to?
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Pertussis: * What is the Catarrhal stage?
Catarrhal (1-2 weeks): treatment started at this phase can shorten disease course
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Pertussis: * What is the Paroxysomal stage?
Paroxysmal (2 to 4 weeks): treatment has little effect on disease course but can eradicate nasal carriage and prevent disease spread
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What is the concalscence stage?
Convalescence (1-2 weeks): Patient still infectious; treat to eradicate carriage state
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PERTUSSIS TREATMENT * When do you tx if over a year old? * When do you tx if infant < 1 year or pregnant woman,
* ­ 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
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PERTUSSIS TREATMENT * What is the supportive care? * When can patients return to school and work
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What are the three meds for pertussis?
* Azithromycin (PO or IV) * Erythromycin (cannot use under one month) * Clarithromycin (cannot use under one month)
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Pertussis treatment * What is the post exposure prophylaxis?
* 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
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Cystic Fibrosis * What is the pathophyio
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
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What is cysstic fibrosis the leading cause of?
A leading cause of bronchiectasis
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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
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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?
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RESPIRATORY DISTRESS SYNDROME (HYALINE MEMBRANE DISEASE) * What is the definition? * When does surfactant begin production? * What is the type 2 pneumocytes?
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Respiratory Distress Syndrome(Hyaline Membrane Disease) * What is the pathophysio?
* 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
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Respiratory Distress Syndrome(Hyaline Membrane Disease) * What is the txt?
* Treatment includes intratracheal surfactant therapy, supplemental O2 & mechanical ventilation as needed * Survival rate >90% with treatment
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Respiratory Distress Syndrome(Hyaline Membrane Disease) * What is the prevention?

Pharmacology (14 decks)

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