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IPCS 3 > Pulmonary > Flashcards

Pulmonary Flashcards

1
Q

What is the definition of cystic fibrosis?

A

dysfunction in the cystic fibrosis transmembrane conductance regulator (CFTR)

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2
Q

What is the most common life-limiting genetic disorder in caucasians?

A

Cystic fibrosis

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3
Q

What organ systems are affected by cystic fibrosis?

A

lungs
digestive system
reproductive system

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4
Q

What is the most common mutation in the CFTR gene?

A

F508del

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5
Q

Cystic fibrosis is an autosomal __ disease

A

recessive

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6
Q

__ occurs in the distal airways of the lung and submucosal glands that express CFTR

A

Mucosal obstruction

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7
Q

CFTR regulates __ across the cell membrane

A

chloride transport

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8
Q

CFTR helps regulate ion transport and __ homeostasis

A

salt

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9
Q

What is the effect go a CF gene defect in the lungs?

A

decreased airway surface liquid
colliery collapse and decreased mucocilliary transport

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10
Q

CF in the lungs is a vicious cycle of mucus retention, infection, and __

A

inflammation

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11
Q

What class of mutation is categorized by no traffic?

A

Class II

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12
Q

What is the presentation of CF in the sinus and pulmonary systems?

A

chronic infections and nasal polyps
SOB and cough with sputum production daily
flat diaphragm
decreased FEV1
digital clubbing from chronic hypoxia

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13
Q

What is the presentation of CF in the GI system?

A

pancreatic insufficiency
meconium ileum, steatorrhea, and failure to thrive due to malabsorption
older patients: severe constipation and insulin deficiency

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14
Q

What is the presentation of CF in the male reproductive system?

A

Azoospermia

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15
Q

What is the presentation of CF in the female reproductive system?

A

Decreased fertility

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16
Q

T or F: all states require CF newborn screening

A

True

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17
Q

What two tests are used to diagnose CF?

A

Immunoreactive trypsinogen (IRT) screening test
Quantitative pilocarpine iontophoresis sweat test (QPIT) (or sweat chloride test)

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18
Q

What is a diagnostic level of chloride content when using the QPIT?

A

> 60 mmol/L

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19
Q

What is nonpharmacologic therapy for CF?

A

Adults: normal weight
Pediatrics: normal growth
Require 110-200% energy take

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20
Q

What medication is used to treat nutrient malabsorption due to pancreatic insufficiency?

A

Pancrelipase

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21
Q

What is a typical dose for pancrelipase?

A

500-2500 lipase units/kg/meal

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22
Q

What can happen if the patient takes too much pancrelipase?

A

Colonic strictures

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23
Q

What are risk factors for pancrelipase-induced colonic strictures?

A

<12 years old
>6000 lipas units/kg/meal for >6 months
history of meconium ileus
history of intestinal surgery
IBS

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24
Q

When should colonic stricture be considered?

A

evidence of obstruction
bloody diarrhea
abdominal pain
poor weight gain

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25
Q

What formulations does pancrelipase come in?

A

Capsules with enteric coated microspheres
Enteric coated tablets

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26
Q

What are risk factors for bone disease in CF patients?

A

malabsorption of vitamin D
poor nutritional status
physical inactivity
glucocorticoid therapy
antibiotics that require protection from sunlight exposure

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27
Q

What vitamins are fat soluble?

A

A, D, E, K

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28
Q

What is a goal vitamin D level?

A

> /=30 ng/mL

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29
Q

What test should be obtained for all adults that is related to bone health and vitamin supplementation?

A

Dual x-ray absorptiometry (DXA)

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30
Q

In a CF patient, what is the protocol is the T/Z score is >/= -1.0?

A

Optimize vitamin D, calcium, and vitamin K supplementation
Repeat in 5 years

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31
Q

In a CF patient, what is the protocol is the T/Z score is > -2.0

A

Aggressive infection treatment, minimize steroid dosing, treat CF-related diabetes
Repeat in 2-4 years

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32
Q

In a CF patient, what is the protocol is the T/Z score is </= -2.0?

A

Consider bisphosphonate
Repeat annually

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33
Q

When should airway clearance therapy be initiated in a CF patient?

A

within the first few months of life

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34
Q

What are the different examples of chest percussion?

A

Cupped hand pounding
Percussion vest
Aerobic exercise

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35
Q

What is the order of clearance therapy for patients with CF receiving chest percussion?

A

Bronchodilator
Hypertonic saline
Dornase alfa
Aerosolized antibiotic

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36
Q

What are examples of aerosolized antibiotics?

A

aztreonam
tobramycin

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37
Q

What are examples of anti-inflammatory drugs used in CF patients?

A

high-dose ibuprofen (20-30 mg/kg BID)
azithromycin

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38
Q

What bacteria is found in the early stages of CF?

A

staphylococcus aureus

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39
Q

What bacteria is found in the later stages of CF?

A

pseudomonas aeruginosa

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40
Q

What is the treatment of stenotrophomonas in CF patients?

A

Bactrim or doxycyline

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41
Q

T or F: Cf patients have larger volumes of distribution and slower clearance.

A

False
larger Vd
faster clearance
May need larger doses at shorter intervals

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42
Q

What vaccinations should CF patients get?

A

annual flu vaccine
Pneumonia
Covid

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43
Q

When does CF related diabetes usually present?

A

18-21 years

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44
Q

What is the therapy of choice in patients with CF related diabetes?

A

insulin

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45
Q

What is the indication for Ivacaftor (Kalydeco)?

A

Class III mutation
at least 1 month

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46
Q

What is the indication for Lumacaftor/Ivacaftor (Orkambi)?

A

Homozygous F508del
at least 1 year

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47
Q

What is the indication for Tezacaftor/Ivacaftor (Symdeko)?

A

Homozygous F508del
at least 6 years

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48
Q

What is the indication for Elexacafotr/Tezecaftor/Ivacaftor (Trikafta)?

A

at least one F508del mutation
at least 2 years

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49
Q

Increased oxygen uptake, blood volume, and cardiac output in pregnancy of a CF patient may lead to what complication?

A

right-sided heart failure

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50
Q

CF candidates for transplant are those with a FEV1 < __

A

30%

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51
Q

When should CF patients follow up with their provider?

A

every 1-3 months

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52
Q

What causes the increased mucus viscosity in CF patients?

A

Cl- is trapped in the cells, so no sodium or water moves out in to the lung mucus

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53
Q

What CF medication is a potentiator?

A

Ivacaftor

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54
Q

What CF medications are correctors?

A

Lumacaftor
Tezacaftor
Elexacaftor

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55
Q

Most CF medications have ___ absorption with fatty food

A

increased

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56
Q

The Cf medications are metabolized by __

A

CYP3A4/5

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57
Q

CFTR is a __-activated anion (CL-) channel

A

cAMP

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58
Q

What is the mechanism of action of Ivacaftor?

A

It binds to the defective protein at the cell surface and opens the chloride channel

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59
Q

What is the mechanism of action of Lumacaftor?

A

It corrects the processing and trafficking of defected CFTR protein

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60
Q

What are side effects of CFTR modulators?

A

headache, dizziness, skin rash, abdominal pain, diarrhea, nausea, nasal congestion, oropharyngeal pain, upper respiratory tract infection, nasopharyngitis

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61
Q

What are DDIs with CFTR modulators?

A

CYP3A4 inhibitors (Cimetidine, fluconazole, ketoconazole, grapefruit juice)

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62
Q

How is dornase alfa administered?

A

inhalation

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63
Q

What is the source of dornase alfa?

A

recombinant human DNase I

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64
Q

What are side effects of dornase alfa?

A

chest paine, voice disorder, cough, pharyngitis, rhinitis, skin rash, dyspnea

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65
Q

What is the mechanism of action of dornase alfa?

A

hydrolyzes the DNA of mucus in CF patients to decrease mucus viscosity

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66
Q

What is the source of pancrelipase?

A

contains a combination of lipase, amylase, and proteases
natural product from porcine pancreatic glands

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67
Q

What are side effects of pancrelipase?

A

headache, neck pain, abdominal pain, nasal congestion

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68
Q

What are examples of methylxanthines?

A

theophylline
caffeine

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69
Q

Theophylline has a __ therapeutic index

A

narrow

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70
Q

T or F: Theophylline has significant first pass metabolism

A

False

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71
Q

What enzyme metabolizes theophylline?

A

CYP1A2

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72
Q

A high fat meal __ absorption of theophylline

A

decreases

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73
Q

Increased cAMP causes __

A

bronchodilation

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74
Q

Increased cGMP causes __

A

decreased inflammatory cells

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75
Q

Theophylline is a __ PDE inhibitor

A

non-selective

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76
Q

Theophylline block the __ receptor and causes increased heart rate and vasoconstriction

A

adenosine

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77
Q

What medications decrease clearance of theophylline?

A

Cimetidine, macrolides, allopurinol, propranolol, quinolones

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78
Q

What medications increase clearance of theophylline?

A

Carbamazepine, phenytoin, moricizine

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79
Q

Smokers have __ clearance

A

increased

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80
Q

What are side effects of theophylline at lower concentrations?

A

headache, nausea, vomiting, insomnia

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81
Q

What are side effects of theophylline at higher concentrations?

A

arrhythmias, seizures, death

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82
Q

The side effects of theophylline at higher concentrations are due to __ effects.

A

adenosine

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83
Q

Roflumilast is metabolized by __ and __

A

CYP 3A4 and 1A2

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84
Q

Roflimulast is a __ PDE inhibitor

A

selective

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85
Q

What is the mechanism of action of roflimulast?

A

inhibition of PDE4
increases cAMP levels
Decrease inflammatory cells and cytokines, decrease bronchoconstriction, decrease vascular permeability

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86
Q

What are side effects of rolflimulast?

A

headache, insomnia, anxiety, depression, decreased appetite, weight loss, nausea, diarrhea, abdominal pain

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87
Q

Does roflumilast antagonize the adenosine system?

A

no

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88
Q

What medications decrease roflumilast concentrations?

A

CYP3A4 inducers (rifampin, dexamethasone, phenytoin, carbamazepine, rifabutin, rifapentin, phenobarbital, St John’s wort)

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89
Q

What is the definition of chronic bronchitis?

A

chronic or recurrent excessive mucus secretion with cough
Present on most days for at least 3 months of the year

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90
Q

What is the definition of emphysema?

A

Destruction of alveoli
No obvious fibrosis

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91
Q

What are possible etiologies of COPD?

A

smoking
occupational exposures
environmental air pollution
alpha antitrypsin (AAT)
Asthma and airway hyperresponsiveness are risk factors
recurrent infections increase risk

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92
Q

What are the three components of the mechanistic triad of COPD?

A

inflammation
imbalance between proteases and antiproteases
oxidative stress

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93
Q

In the central airways, inflammatory cells and mediators stimulate __

A

mucus-secreting gland hyperplasia
mucus hypersecretion

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94
Q

What is the major site of airflow obstruction in COPD?

A

peripheral airways

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95
Q

Advance COPD can lead to __

A

hypoxemia
hypercapnia

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96
Q

What is hypercapnia

A

abnormally elevated carbon dioxide levels in the blood

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97
Q

Pulmonary hypertension in a COPD patient can lead to __

A

cor pulmonale (right-sided heart failure)

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98
Q

COPD patients can get progressive loss of __ muscle

A

skeletal

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99
Q

What are symptoms of COPD?

A

variable onset
Do not correlate with severity of airflow limitation
chronic cough (>3 months)
chronic sputum production
dyspnea on exertion
as disease progresses: dyspnea at rest, ability to perform daily tasks declines

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100
Q

What are signs of COPD?

A

use of accessory muscles
pursed-lips breathing
increased respiratory rate
shallow breathing
hyperinflation of chest
auscultation: distant breath sounds, wheezing, rhonchi
Advanced: cyanosis, tachycardia
Cor pulmonale: lower extremity edema, hepatomegaly, JVD

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101
Q

What are laboratory tests for COPD?

A

polycythemia: elevated hematocrit
If FEV1 <35%, or s/sx of cor pulmonale, check pulse oximetry
If O2 sat <92%, check ABG
AAT level if <45 year and presenting with COPD s/sx, especially with FH of emphysema

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102
Q

Post bronchodilator FEV1/FVC < __ confirms presence of persistent airflow limitation

A

70%

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103
Q

What is a GOLD1 classification?

A

mild
FEV >/=80& predicted

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104
Q

What is GOLD2 classification?

A

moderate
FEV1 50-80% predicted

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105
Q

What is GOLD3 classification?

A

severe
FEV1 30-50% predicted

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106
Q

What is GOLD4 classification?

A

very severe
FEV1 <30% predicted

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107
Q

What two tests are sued to assess symptoms in COPD patients?

A

mMRC
CAT

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108
Q

How is a COPD patient classified as E?

A

> /=2 moderate exacerbations or >/=1 leading to hospitalization

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109
Q

How is a COPD patient classified as A?

A

0 or 1 moderate exacerbations not leading to hospitalization
AND CAT <10

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110
Q

How is a COPD patients classified as B?

A

0 or 1 moderated exacerbations not leading ti hospitalization
AND CAT >/= 10

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111
Q

What are the desired outcomes of treating a COPD patient?

A

reduce symptoms
reduce risk
smoking cessation

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112
Q

What is the green zone for a COPD patient?

A

usual activity level
usual amount of phlegm/mucus
take daily medications

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113
Q

What is the yellow zone for a COPD patient?

A

more breathless than usual
more coughing and increased phlegm/mucus production
continue daily medications and add reliever inhaler, oral corticosteroids, and/or antibiotic

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114
Q

What is the red zone for a COPD patient?

A

severe SOB, even at rest
coughing up blood
call 911 or seek immediate medical care

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115
Q

What is the only intervention to slow disease progression and long-term FEV1 decline?

A

smoking cessation

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116
Q

What immunizations should COPD patients get?

A

annual flu vaccine
pneumonia vaccine
Tdap
Covid

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117
Q

What are the components of pulmonary rehabilitation?

A

exercise training
breathing techniques
education
psychological and nutritional counseling

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118
Q

Optimum benefit is achieved with a pulmonary rehabilitation program lasting __

A

6-8 weeks

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119
Q

When should COPD patients do pulmonary rehabilitation?

A

at diagnosis
hospital discharge following an exacerbation
progressively deteriorating symptoms

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120
Q

What is the mainstay of treatment for symptomatic COPD?

A

bronchodilators

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121
Q

What are SABA key points in COPD?

A

rescue therapy for acute relief
avoid continuous, daily therapy

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122
Q

What are LABA key points in COPD?

A

decrease COPD exacerbations and improve exercise intolerance, dyspnea, and quality of life
patients should also receive a SABA prn

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123
Q

What are examples of combination bronchodilator products?

A

albuterol/ipratropium (Combivent)
Vilanterol/umeclidinium (Anoro)

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124
Q

What is the indication for theophylline?

A

patients who cannot use inhaled medications or are symptomatic despite appropriate use of inhaled bronchodilators

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125
Q

What is the target concentration for theophylline in COPD patients?

A

5-15 mg/L

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126
Q

What conditions increase concentrations of theophylline?

A

heart failure
liver disease

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127
Q

What conditions decrease concentrations of theophylline?

A

high protein diet

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128
Q

Theophylline should be dosed based on __

A

IBW

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129
Q

When converting from aminophylline to theophylline you __

A

multiply by 0.8

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130
Q

When converting from theophylline to aminophylline you __

A

divide by 0.8

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131
Q

Theophylline has __ kinetics

A

non-linear

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132
Q

What are key points for corticosteroids in COPD?

A

monotherapy is not recommended
avoid long-term use of oral corticosteroids

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133
Q

When is rolflumilast indicated?

A

severe or very severe COPD and a history of exacerbations

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134
Q

What is the onset for rolflumilast?

A

4 weeks

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135
Q

What is in Trelegy Ellipta?

A

fluticasone furoate
vilanterol
emclidinium

136
Q

What is in Breo Ellipta?

A

fluticasone furoate
vilanterol

137
Q

What is in Incruse Ellipta?

A

umeclidinium

138
Q

When is long-term oxygen therapy considered for COPD patients?

A

if either of the following criteria are documented twice in a 3 week period:
-PaO2 <55mmHG or SaO2 </=88% w/wo hypercapnia
-PaO2 55-60mmHg or SaO2 of 88% with evidence of right-sided heart failure, polycythemia, or pulmonary hypertension

139
Q

When is noninvasive positive pressure ventilation (NPPV) used?

A

COPD with obstructive sleep apnea

140
Q

What treatment should group E COPD patients receive?

A

LABA and LAMA
+ICS if eosinophils at least 300
+SABA pro

141
Q

What treatment should group A COPD patients receive?

A

a bronchodilator
+SABA pro

142
Q

What treatment should group B COPD patients receive?

A

LABA+LAMA
+SABA pro

143
Q

In a patient on a LAMA or LABA presenting with dyspnea, what treatment should they receive?

A

LABA or LAMA

144
Q

In a patient on a LABA with blood eos <300 experiencing an exacerbation, what treatment should they receive?

A

LABA+LAMA

145
Q

In a patient on a LABA with blood eos >300 experiencing an exacerbation, what treatment should they receive?

A

LABA+LAMA+ICS

146
Q

In a patient on LABA+LAMA with blood eos >100 experiencing an exacerbation, what treatment should they receive?

A

LABA+LAMA+ICS

147
Q

In a patient on LABA+LAMA with blood eos <100 experiencing an exacerbation, what treatment should they receive?

A

Roflumilast or azithromycin

148
Q

Ina patient on LABA+LAMA+ICS experiencing an exacerbation, what treatment should they receive?

A

Rolflumilast or azithromycin

149
Q

What are possible etiologies of COPD exacerbations?

A

respiratory tract infections
peaks of air pollution

150
Q

How is a COPD exacerbation diagnosed?

A

patient complaining of a acute change of symptoms (dyspnea, couch, and/or sputum production)

151
Q

How are COPD exacerbations treated?

A

bronchodilators (SABA)
oral corticosteroids
antibiotics?

152
Q

What is the dose of oral corticosteroids for a patients experiencing a cOPD exacerbation?

A

Prednisone 40mg PO QD 5D

153
Q

What are tests run to diagnose COPD exacerbations?

A

pulse oximetry, ABG, chest x-ray, ECG, CBC, presence of purulent sputum, biochemical tests

154
Q

When do the guidelines recommend antibiotic use in COPD exacerbations?

A

presence of three cardinal symptoms (dyspnea, sputum volume, sputum purulence)
presence of two of the carinal symptoms (one must be increase in sputum purulence)
require mechanical ventilation

155
Q

How long should a patient receive antibiotics after a COPD exacerbation?

A

5-7 days
21-42 days of P. aeruginosa or MRSA

156
Q

What antibiotics are used in uncomplicated COPD exacerbations?

A

macrolide
2nd or 3rd gen cephalosporin
doxycycline

157
Q

What antibiotics are used in complicated COPD exacerbations?

A

augmentin
levofloxacin, gemifloxacin, moxifloxacin

158
Q

What antibiotics are used in complicated COPD exacerbations with risk of P. aeruginosa?

A

levofloxacin
IV 3rd or 4th gen cephalosporin

159
Q

What is considered an uncomplicated COPD exacerbation?

A

<4 exacerbations/year
no comorbid illness
FEV1 >50% of predicted

160
Q

What is considered a complicated COPD exacerbation?

A

Age of at least 65 and >4 exacerbation/year
FEV1 35-50% of predicted

161
Q

What is considered complicated COPD exacerbation with risk of P. aeruginosa?

A

chronic bronchial sepsis
need for chronic corticosteroid therapy
resident of nursing home with <4 exacerbations/year
FEV1 <35% of predicted

162
Q

What is the target oxygen saturation for a patient with COPD?

A

88-92%

163
Q

When is assisted ventilation indicated for a patient with COPD?

A

respiratory acidosis
severe dyspnea with clinical signs suggestive of respiratory muscle fatigue such as use of accessory muscles and paradoxical motion

164
Q

What is the radiologic findings of interstitial lung disease?

A

diffuse interstitial markings

165
Q

What is the clinical presentation of interstitial lung disease?

A

shortness of breath
dyspnea on exertion

166
Q

What are risk factors for interstitial lung disease?

A

age
female gene
smoking
family history
occupation
infections

167
Q

What are causes of acute interstitial lung disease?

A

HF exacerbation
infections
drugs

168
Q

What are types of interstitial abnormality?

A

edema
diffuse inflammation
fibrosis
non-specific histologic changes

169
Q

What are causes of fluid overload interstitial lung disease?

A

HF - specifically left ventricular systolic dysfunction
renal failure
nephrotic syndrome
ascites/anasarca
capillary leak
redistribution pulmonary edema
iatrogenic

170
Q

What is the treatment for fluid overload interstitial lung disease?

A

treat underlying cause
fluid management
diuretics

171
Q

What is the steroid treatment for pneumocystis jervoeci pneumonia?

A

Prednisone 40mg BID 5D then titrate down

172
Q

What are causes of auto-immune interstitial lung disease?

A

RA
SLE
sarcoidosis
scleroderma
vasculitis
dermatomyositis
MCTD
overlap syndrome

173
Q

What is the treatment for auto-immune interstitial lung disease?

A

treat the underlying cause

174
Q

What are causes of industrial/environmental interstitial lung disease?

A

Asbestosis
berylliosis
silicosis (black lung)
hypersensitivity pneumonitis (black mold)
pollutants

175
Q

What is the treatment of industrial/environmental interstitial lung disease?

A

prevention
oxygen therapy
steroids

176
Q

When may neoplastic interstitial lung disease occur?

A

leukemia
lymphoma
metastatic cancer

177
Q

What drugs may cause interstitial lungs disease?

A

amiodarone
bleomycin

178
Q

At what doses does amiodarone cause pulmonary fibrosis?

A

long term doses >400mg per day

179
Q

What is the most common type of idiopathic interstitial pneumonias?

A

idiopathic pulmonary fibrosis

180
Q

What are risk factors for idiopathic pulmonary fibrosis?

A

smoking
occupational exposures
exposure to certain viruses
genetic predisposition?

181
Q

What is the pathophysiology of idiopathic pulmonary fibrosis?

A

alveolar epithelial injury leading to fibrotic changes

182
Q

What is the clinical presentation of idiopathic pulmonary fibrosis?

A

SOB and DOE
dry cough
fatigue and weight loss
finger clubbing

183
Q

How is idiopathic pulmonary fibrosis diagnosed?

A

diagnosis of exclusion

184
Q

What medications are used to treat idiopathic pulmonary fibrosis?

A

pirfenidone
nintedanib

185
Q

Pirfenidone is a __ substrate

A

CYP1A2

186
Q

Nintedanib is a __ substrate

A

CYP3A4

187
Q

With CYP1A2 inhibitors, pirfenidone should __

A

be monitored and adjusted as needed

188
Q

With CYP1A2 inducers, pirfenidone should __

A

be avoided

189
Q

With Pgp and CYP3A4 inhibitors, nintedanib should _

A

be monitored and adjusted as needed

190
Q

With Pgp and CYP inducers, nintedanib should __

A

be avoided

191
Q

What are side effects of pirfenidone?

A

nausea, rash, fatigue, dispepsia, photosensitivity, anorexia, increased AST and ALT

192
Q

In what patients is pirfenidone not recommended in?

A

patients with moderate-to-severe hepatic impairment

193
Q

In what patients should pirfenidone be used with caution in?

A

patients with mild hepatic impairment

194
Q

What are side effects of nintedanib?

A

diarrhea, nausea, and vomiting
small increase in risk of bleeding

195
Q

What should be monitored regularly in use of pirfenidone and nintedanib?

A

LFTs

196
Q

In what patients should nintedanib be used with caution in?

A

patients with CV disease or CV risk factors

197
Q

In what patients is nintedanib not recommended in?

A

patients with moderate-to-severe hepatic impairment

198
Q

What is the recommendation for nintedanib and patients with mild hepatic impairment?

A

decreased dose to 100mg BID

199
Q

What is non-pharmacologic therapy for idiopathic pulmonary fibrosis?

A

flu, covid, and Prevnar vaccines
nutrition
exercise
smoking cessation
support groups
early referral for lung transplant

200
Q

What is the mechanism of action of nintedanib?

A

inhibitor of the intracellular domain of tyrosine kinase receptors VEGF, FGF, and PDGF
decreases accumulation of fibrotic tissue

201
Q

What is the mechanism of action of pirfenidone?

A

reduces collagen type I expression decreasing fibrosis
downregulagtes production of growth factors

202
Q

What are examples of CYP1A2 inhibitors?

A

cimetidine
ciprofloxacin
fluvoxamine

203
Q

What are examples of CYP1A2 inducers?

A

Omeprazole
smoking

204
Q

What are SABAs?

A

Albuterol
Levalbuterol

205
Q

What are LABAs?

A

Formoterol
Salmeterol

206
Q

What are Ultra LABAs?

A

Indacaterol
Arformoterol
Olodaterol
Vilanterol

207
Q

Which beta-adrenergic agonists don’t have substrates for COMT/MAO?

A

albuterol/levalbuteral
SABAs

208
Q

What is the mechanism of action of beta adrenergic agonists?

A

smooth muscle relaxation by activating beta2 receptors and phosphorylation of proteins in smooth muscle

209
Q

What are common ADEs of SABAs?

A

muscle tremor
CNS excitement

210
Q

What are serious ADEs of SABAs?

A

tachycardia, hypokalemia

211
Q

What is an ADE of LABAs?

A

severe asthma exacerbation and asthma-related death when used as monotherapy

212
Q

What are ADEs of Indacaterol?

A

cough, headache

213
Q

What is an ADE of Olodanterol?

A

Nasopharyngitis

214
Q

What are drug interactions with SABAs?

A

nonselective beta blockers
diuretics

215
Q

What are drug interactions with LABAs?

A

nonselective beta blockers
cannabinoids
haloperidol
MAOI and TCA
loop and thiazide diuretics

216
Q

What are SAMAs?

A

ipratropium

217
Q

What are LAMAs?

A

tiotrpoium
aclidinium
umeclidinium
glycopyrrolate

218
Q

What is the mechanism of action of muscarinic antagonists?

A

block acetylcholine from binding m3 receptors

219
Q

What are side effects of muscarinic antagonists?

A

xerostemia,
blurred vision
urinary retention
headache
diarrhea, vomiting
nasopharyngitis, cough, rhinos, sinusitis
tachycardia

220
Q

Tiotropium may worsen the symptoms of __angle glaucoma

A

narrow

221
Q

Ipratropium may cause paradoxical bronchospasm because of binding to the m__ receptor

A

2

222
Q

What are inhaled corticosteroids?

A

beclomethasone
budesonide
ciclesonide
fluticasone
mometasone

223
Q

What are systemic corticosteroids?

A

prednisone
prednisolone
methylprednisolone

224
Q

Which corticosteroids are prodrugs?

A

beclomethasone
prednisone
ciclesidone

225
Q

What corticosteroids have some mineralcorticoid activity?

A

prednisone
prednisolone
mometasone

226
Q

What is the mechanism of action of corticosteroids?

A

binds to CBG
stimulates or inhibits gene transcription
inc anti inflammatory genes
dec inflammatory genes

227
Q

What are side effects of inhaled corticosteroids?

A

headache
paharyngitis
oral candidiasis
cough
dyspnea
systemic side effects with high doses

228
Q

What are side effects of systemic corticosteroids?

A

GI upset
hyperglycemia
psych disturbances

229
Q

What drugs can interact with inhaled corticosteroids?

A

azoles
macrolides
CYP3A4 inducers and inhibitors

230
Q

What drugs can interact with systemic corticosteroids?

A

antacids
fluoroquinolones
CYP3A4 inhibitors and inducers
phenytoin
warfarin

231
Q

What is the mechanism of action of omalizumab?

A

IgG monoclonal antibody that binds to IgE
decrease the release of mediators from cellsdecrease allergic inflammation

232
Q

What is the mechanism of action of dupilumab?

A

inhibits IL4 and IL13 cytokine-induced responses

233
Q

What is the mechanism of action of mepolizumab and reslizumab?

A

binds to IL5

234
Q

What is the mechanism of action of benralizumab?

A

binds to and blocks IL5 receptor

235
Q

What is the mechanism of action of tezepelumab?

A

binds to TSLP and prevents its interaction with TSLP receptor complex
inhibits inflammatory pathways

236
Q

What are the side effects of monoclonal antibodies?

A

anaphylaxis, headache, injection site reaction, antibody development

237
Q

What are leukotriene modifiers?

A

montilukast
zafirlukast

238
Q

What are side effects of montelukast?

A

dizziness, stomach pain, dyspepsia, headache, diarrhea, constipation, serious neuropsychiatric events

239
Q

What is the mechanism of action of leukotriene modifiers?

A

block the action of leukotrienes by binding to the LT1 receptors in smooth muscle cells

240
Q

What drugs interact with montelukast?

A

CYP2C9, 2C8, and 3A4/5 inhibitors and inducers

241
Q

What drugs interact with zafirlukast?

A

phenytoin
CYP2C9 substrates
food decreases bioavailability

242
Q

What are the classifications of pleural disease?

A

pleurisy
hemothorax, pneumothorax, chylothorax
pleural effusion

243
Q

What is the definition of a tension pneumothorax?

A

acute rapidly expanding pneumothorax
pressure exerted on the heart and greater vessels cause hemodynamic instability

244
Q

What is the clinical presentation of a hemothorax/pneumothorax/chylothorax?

A

SOB
DPE
chest pain and dyspnea
tachypnea
cough

245
Q

What medications should be given when a chest tube thoracostomy is performed?

A

morphine
1st gen cephalosporin (cefazoline)

246
Q

What is the definition of a pleural effusion?

A

fluid accumulation due to loss of fluid homeostasis

247
Q

What is the fluid composition of a transduative pleural effusion?

A

just fluid

248
Q

What is the fluid composition of exudative pleural effusion?

A

high protein
high cell count
high LDH

249
Q

Which type of pleural effusion involves the pleural membrane?

A

exudative

250
Q

What is the most common etiology of a transudative pleural effusion?

A

heart failure

251
Q

What is the most common etiology of exudative pleural effusion?

A

pneumonia

252
Q

What is the clinical presentation of pleural effusion?

A

SOB, DOE
cough
chest pain
tachypnea
may be asymptomatic

253
Q

Of patients with pleural effusion, who gets treatment?

A

symptomatic and/or recurrent

254
Q

What are intrapleural medication options for treatment of located effusions?

A

streptokinase
alteplase
dornase alfa

255
Q

What is the purpose of chemical pleurodesis?

A

induce scarring

256
Q

What agents are used for pleurodesis?

A

doxycycline
talc
bleomycin

257
Q

What is the common presentation of drug-induced pulmonary disease?

A

apnea
asthma
bronchospasm
pulmonary edema
pulmonary eosinophilia
pulmonary fibrosis

258
Q

What are risk factors for drug-induced pulmonary disease?

A

age
pre-existing lung disease
combination therapy
cumulative doses
oxygen therapy
radiation therapy
occupational risk factors

259
Q

What medications may induce bronchospasm?

A

aspirin
beta-blockers
sulfites and other preservatives
contrast media
ACE inhibitors
N-acetylcystiene
natural rubber latex allergies

260
Q

What is the most common drug-induced pulmonary disease?

A

bronchospasm

261
Q

What are risk factors for apnea/respiratory depression?

A

age
COPD (pre-existing pulmonary disease)
CO2 retention
dose
multiple agents

262
Q

What are symptoms of pulmonary eosinophilia?

A

fever
productive cough
dyspnea
cyanosis
bilateral pulmonary infiltrates
eosinophilia in the blood

263
Q

What drugs can cause pulmonary hypertension?

A

cocaine
oral contraceptives
amphetamines
chemotherapeutic agents
anorexic agents

264
Q

What are symptoms of aspirin-induced bronchospasm?

A

intense vasomotor rhinitis
bronchospams
flushing of head and neck
conjunctivitis

265
Q

What is the treatment for N-actylcystiene-induced pulmonary disease?

A

administer beta2 agonist with or immediately prior to N-acetylcystiene

266
Q

What drugs can cause pulmonary eosinophilia?

A

nitrofurantoin
para-aminosalicylic acid
methotrexate
sulfonamides
tetracycline
chlorpropamide
phenytoin
NSAIDs
imipramine

267
Q

What are signs and symptoms of drug-induced pulmonary fibrosis?

A

dyspnea
hypoxemia
nonproductive cough
diffuse alveolar damage
interstitial pneumonitis

268
Q

What are etiologies of asthma?

A

genetic factors
environmental factors
obesity

269
Q

What are the stages of airway obstruction?

A

airway smooth muscle constriction
airway edema
mucus hypersecretion
airway remodeling

270
Q

What are symptoms of asthma?

A

varies over time and intensity
wheezing, SOB, chest tightness, coughing
anxious and agitated
mental status changes may indicate respiratory failure

271
Q

What are signs of asthma?

A

tachypnea
tachycardia
use of accessory muscles
auscultation: end expiratory wheezing or wheezing trough inspiration and expiration

272
Q

What are laboratory test performed for asthma?

A

spirometry <80% after receiving bronchodilator
Increased IgE
RAST
FeNO

273
Q

What is considered Mild acute asthma?

A

dyspnea with activity
>/=70% PEF of personal best

274
Q

What is considered moderate acute asthma?

A

dyspnea that limits activity
40-69% PEF of personal best

275
Q

What is considered severe acute asthma?

A

dyspnea interferes with conversation or occurs at rest
25-40% PEF of personal best

276
Q

What is considered life-threatening acute asthma?

A

dyspnea where the patient can’t speak
<25% PEF of personal best

277
Q

What is nonpharmacologic therapy for asthma?

A

smoking cessation
5-10% weight loss in obese
avoid triggers
vaccination

278
Q

What is considered medium-dose fluticasone for children?

A

> 200-500

279
Q

What is considered medium-dose fluticasone for adults?

A

> 250-500

280
Q

What decreases response to inhaled corticosteroids?

A

cigarette smoking

281
Q

What is the duration for systemic corticosteroids in acute asthma?

A

3-10 days

282
Q

When is a SAMA indicated in asthma?

A

in the emergency department

283
Q

Leukotriene modifiers are beneficial in which patients?

A

allergic rhinitis
aspirin sensitivity

284
Q

What is is the preferred treatment for a patient with asthma attacks less than twice a month? What step are they?

A

Step 1
as-needed low-dose ICS-formoterol

285
Q

What is the preferred treatment for a patient with asthma symptoms twice a month or more? what step are they?

A

Step 2
as-needed low-dose ICS-formoterol

286
Q

What is the preferred treatment for a patient with asthma symptoms 4-5 days/week or waking once a week or more? What step are they?

A

Step 3
Low-dose ICS-formoterol and reliever therapy

287
Q

What is the preferred treatment for a patient with severely uncontrolled asthma initially or an acute exacerbation? What step are they?

A

Step 4
Medium-dose ICS-formoterol and reliever therapy

288
Q

When should a patient follow up after initial therapy of asthma treatment?

A

2-3 months

289
Q

What is considered mild chronic asthma?

A

well controlled with step 1 or 2 treatment

290
Q

What is considered moderate chronic asthma?

A

well controlled with step 3 or 4 treatment

291
Q

What is considered severe chronic asthma?

A

remains uncontrolled despite optimized treatment

292
Q

What are the four questions asked to assess asthma symptom control?

A

Daytime asthma symptoms more than twice/week?
Any night waking due to asthma?
SABA reliever for symptoms more than twice/week?
Any activity limitation due to asthma?

293
Q

If 1-2 of the symptom control asthma questions are yes, what is the step?

A

step up one

294
Q

If 3-4 of the symptom control asthma questions are yes, what is the step?

A

step up two

295
Q

When is a step down in therapy considered for a patient with asthma?

A

3 months controlled

296
Q

What is the target oxygen saturation for children, pregnant women, and patients with coexisting heart disease? All other patients?

A

94-98%
93-95%

297
Q

what is the core pharmacophore of beta2 adrenergic agonists?

A

substituted beta-phenyl ethylamine

298
Q

What are two key modifications of endogenous catecholamines achieving selectivity for beta2 adrenergic receptors?

A

Suitable substituents other than hydroxyls at phenyl ring
Ethyl substituent at alpha carbon

299
Q

How many carbons need to be attached to the catecholamine nitrogen to achieve a) selectivity for beta over alpha receptors b) selectivity for beta2 receptors?

A

> 1
3

300
Q

List four ways by which the duration of action of adrenergic agonists can be increased.

A

Increase affinity for the receptor
Binding to exosites of the receptor
Increase lipophilicity of inhaled drugs
Substitutions that mask sites recognized by metabolizing enzymes

301
Q

Resistance to two enzymes prolong the duration of action of adrenergic agonists. What are they?

A

COMT and MAO

302
Q

Which modifications generate resistance to metabolic inactivation of adrenergic agonists?

A

In the hydrophobic pocket on the positive nitrogen
On the alpha carbon
On the phenyl ring

303
Q

List two ways by which the retention of beta2-adrenergic agonists in the lungs can be achieved (consider Lipinski’s rule of 5).

A

High lipophilicity
High hydrophilicity

304
Q

Why has formoterol a faster onset of action than salmeterol?

A

Greater water solubility

305
Q

What is the difference between formoterol and arformoterol?

A

Arformoterol is the r,r enantoimer

306
Q

What is the main reason why olodaterol has a long duration of action in lungs?

A

Fast and high affinity association with receptor and slow dissociation

307
Q

What is the key structural modification that converts acetylcholine into an antagonist? Which structure in the receptor ligand binding site does this modification interact with (name the transmembrane helices that form that structure)?

A

Methyl group replaced with system containing at least one phenyl or dithienyl ring
VII

308
Q

What is a common structural feature of all anti-muscarinic drugs?

A

Positive quaternary amine

309
Q

Why are ipratropium and tiotropium poorly absorbed from the lungs and why do they have no oral availability? (consider charge, hydrophobicity, affinity)?

A

Highly hydrophilic, quaternary ammonium nitrogen

310
Q

Name two drugs that inhibit phosphodiesterase-4 (PDE4), one selectively and one non-selectively. You should recognize their structures and know what treatment modality they are used for.

A

Roflumilast - selective
Theophylline - nonselective

311
Q

Why is prednisone a prodrug?

A

the carbonyl must be converted to hydroxy in vivo

312
Q

Why has prednisolone more anti-inflammatory activity than hydrocortisone and a longer duration of action (a single change from hydrocortisone)?

A

The double bind at the C1-2 position

313
Q

Which of all topical glucocorticoid drugs has the highest affinity for the glucocorticoid receptor?

A

mometasone

314
Q

Explain the components of the name “omalizumab” in terms of the international Nonproprietary Names Program of the WHO. What is the meaning of LI and ZU?

A

LI: immunomodulating
ZU: humanized

315
Q

What is the main reason for the effectiveness of anti-IL-5 and antiI-IL-5R antibodies? The activation of which cell type is inhibited? Which subtype of asthma is treated with these antibodies?

A

Activation of eosinophils
Eosinophilic asthma

316
Q

What is the target of Dupilumab? What the chemical nature of this drug? To what degree it is humanized?

A

IL4 and IL13
Reduces typeII inflammation and asthma exacerbation
Fully human

317
Q

What is TSLP? What role is it playing in the pathogenesis of asthma? Name a biotechnology product that blocks this molecule.

A

Thymic stromal lymphopoietin is an alarmin released by epithelial or stromal cells
Airway inflammation and hyperresponsiveness
Tezepalumab

318
Q

Which type of mechanism underlying drug-induced pulmonary disorders (intolerance) would you expect to be specific to a particular drug molecule and which type of mechanism would lead to intolerance to an entire class of drugs?

A

Aspirin

319
Q

Which atomic element that occurs in commonly used contrast media is responsible for their high X-ray density?

A

iodine

320
Q

Which type of contrast agents have a high rate of adverse effects, which have a lower rate? What is the critical difference?

A

High osmolar, ionic
Low osmolar, nonionic

321
Q

Talc is what type of mineral?

A

silicate

322
Q

Why are toxic molecules like bleomycin and talk useful in the treatment of pleural disease? What effect do they have that is beneficial?

A

induce scarring

323
Q

When injected by intravenous drug users, talc elicits which type of response in the lung?

A

foreign body response

324
Q

What is the mechanism of toxicity common to doxycycline, other tetracyclines, and bleomycin? What other element is involved?

A

chelates ions
iron

325
Q

What is the target protein of Nintedanib (Nintedanib blocks which type of receptor)? What is the binding site?

A

Tyrosine-kinase type receptors
ATP site of FGFR

326
Q

What is the biological effect of pirfenidone?

A

decreases fibrosis

327
Q

What type of reactions occur during the metabolism of Pirfenidone?

A

Benzylic hydroxylation by CYP1A2
Cystolic oxidation to carboxylic acid

328
Q

How is pirfenidone eliminated?

A

urine

329
Q

What is the target of dornase alfa?

A

DNA

330
Q

What is the content of Pancrelipase microsphere used for the treatment of cystic fibrosis?

A

Digestive enzymes and bicarbonate buffer

331
Q

How is CFTR activated, how is it gated?

A

Activated by PKA
Gated by ATP

332
Q

What is the effect of CRTR correctors versus that potentiators?

A

Corrects misfolding, prevents degradation of CFTR proteins

333
Q

Which common mutation can be “rescued” with CFTR correctors?

A

F508del

334
Q

Which of the following cystic fibrosis drugs is/are a potentiator which is a corrector? Ivacaftor, lumacaftor, tezacaftor, elexacaftor?

A

Potentiator: Ivacaftor
Corrector: Lumacaftor, Tezecaftor, Elexacaftor

335
Q

What is a common structural feature of all cystic fibrosis drugs (answer in lecture recording, not in slides)?

A

the cyclic ring

336
Q

Name main metabolizing enzymes of the cytochrome P450 superfamily that metabolize ivacaftor, lumacaftor, and elexacaftor?

A

CYP3A4/5

IPCS 3 (4 decks)

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