Respiratory Flashcards
(131 cards)
1
Q
Definition of COPD
A
Progressive lung cell destruction; characterized by persistent airflow limitation
2
Q
Is COPD reversible?
A
No, not fully
3
Q
Most common modifiable treatment to COPD?
A
Quit smoking
4
Q
What are some causes of COPD?
A
Persistent exposure to noxious particles/chemicals, which make the lung parenchyma susceptible and causes an enhanced or chronic inflammatory response
5
Q
Which disease is CHRONIC and PROGRESSIVE?
A
COPD
6
Q
How common is COPD? And is it preventable/treatable?
A
Pretty common, and yes, it is preventable and treatable
7
Q
Two presentations of COPD? Which can occur separately or together?
A
- Narrowing of small airways (obstructive bronchiolitis)
2. Parenchymal destruction (emphysema)
8
Q
What causes chronic bronchitis? (physiologically-wise?)
A
Chronic inflammation and excess mucus plugging
9
Q
Chronic inflammation leads to ______ ______ and/or ________ ________.
A
airway narrowing; parenchymal destruction
10
Q
What happens to the alveoli in emphysema?
A
Loss of alveolar membrane attachments and decreased elastic recoil
11
Q
When the airways are narrowed via obstructive bronchiolitis, there is increased ________.
A
resistance
12
Q
Breath stacking is more common in what kind of patients?
A
Asthma
13
Q
What’s one way to test whether or not a pt has COPD or asthma? And what would be the results in each case?
A
Use a bronchodilator - for an asthma pt, it will bring them back to baseline, it will have a minimal response for a COPD pt
14
Q
Which disease is reversible?
A
Asthma
15
Q
What characterizes asthma?
A
Airway hyper-responsiveness
16
Q
Patient picture for a COPD diagnosis?
A
Onset in midlife, symptoms have been slowly progressive, history of tobacco smoking or exposure to other types of smoke
17
Q
Patient picture for an asthma diagnosis?
A
Onset early in life (childhood, usually); symptoms vary widely day-to-day; symptoms worse at night and/or early morning; allergy, rhinitis, and/or eczema often present; family history of asthma
18
Q
Modifiable risk factors?
A
Smoke, occupational dusts and chemicals, air pollution
19
Q
Non-modifiable risk factors?
A
Genetic predisposition (AAT deficiency), airway hyper-responsiveness, impaired lung growth/infections
20
Q
What does AAT involve?
A
Issue with lung surfactant
21
Q
Pack history calculation?
A
cigarettes a day x years of smoking
22
Q
Percentages of smokers who develop COPD? Percentages of COPD patients who are/were smokers?
A
15-20%
85%
23
Q
Primary cause of COPD?
A
Cigarette smoking
24
Q
What could impair lung growth?
A
low birth weight, prematurity, childhood illnesses
25
Why is it bad if your lungs scar?
Because they won't be able to properly oxygenate and you get more lung rigidity (you lose elasticity and compliance) which increases risk of breath stacking
26
Repeated injury and repair of the lungs leads to what?
Inflammatory and destructive changes - leads to air trapping and airflow limitation
Disrupted normal defense/repair - leads to scarring and fibrosis
27
What can you see on a CXR by counting ribs?
Hyperinflation of the lungs
28
Hyperinflation causes what?
Flatttening of diaphragmatic muscles
29
Why is hyperinflation bad in the lungs?
less efficient ventilation; requires more work to contract; muscle fatigue; changes in lung volume; limits inspiratory reserve capacity while increases functional residual capacity; increases intrathoracic pressure
30
What is hypercapnia?
Excessive CO2 in the bloodstream due to inadequate respiration
31
Due to hyperinflation, what happens to the gas exchange in our bodies?
Reduced gas transfer including hypoxemia, hypercapnia
Reduced ventilation including obstruction, hyperinflation, ventilatory muscle impairment
Reduced ventilatory drive with CO2 retentino
32
Problems with chronic productive cough?
Impairs ciliary mobility
33
Clinical presentaitons of chronic bronchitis?
Overweight and cyanotic, elevated hemoglobin, peripheral edema, rhonchi and wheezing
34
Clinical presentations of emphysema?
Older and thin, severe dyspnea, quiet chest, CXR will show hyperinflation with flattened diaphragm
35
COPD clincial presentation
Dyspnea (progressive, worsens with activity, persistent), chronic cough** (intermittent, often productive)
Physical Exam: increased RR/shallow breathing, use of accessory respiratory muscles, cyanosis of mucosal membranes, barrel chest (due to hyperinflation)
36
Progress of COPD?
Pulmonary effects: hypoxemia, hypercapnia
Extrapulmonary effects: skeletal muscle wasting (cachexia), lower extremity edema
37
Gold standard for COPD?
Spirometry
38
Hallmark of COPD
Reduction in post-bronchodilator FEV1/FVC < 0.70
39
What is tidal volume?
Volume of air that is breathed in and out in a normal quiet breath
40
What is residual volume?
Amount of air that remains in the lungs after maximum exhalation
41
What is vital capacity?
Maximum volume of air exhaled after maximum inhalation
42
What is total lung capacity?
Maximum amount of air that the lung can hold
43
What is FEV1?
Amount of air that the patient exhales in 1 second
44
What is FEV1/FVC?
Ratio of FEV1 relative to the full volume patient exhaled in 6 seconds
45
Acute exacerbations of COPD can be due to what?
Bacterial and viral infections; tobacco or pollutant triggers
46
What occurs more frequently in severe chronic COPD?
acute exacerbations
47
What symptoms occur in an acute exacerbation?
Dyspnea, cough, sputum production and purulence, worsened hyperinflation
Worsening ABG, increased muscle fatigue
hypoxemia/hypercapnia may result in repiratory acidosis and respiratory failure
48
Why do we treat COPD agressively?
Many are readmitted, it takes several weeks to return to baseline
49
To assess COPD, what three things do you do?
1. Symptoms
2. Degree of airflow limitation
3. Risk of exacerbations
50
GOLD 1 severity and spirometry results?
Mild ; FEV1 > or = 80% predicted
51
GOLD 2 severity and spirometry results?
Moderate; 50% < or = FEV1 < 80% predicted
52
GOLD 3 severity and spirometry results?
Severe; 30% < or = FEV1 < 50% predicted
53
GOLD 4 severity and spirometry results?
Very severe; FEV1 < 30% predicted
54
COPD Stage 1 lung function?
80%
55
COPD Stage 2 lung function?
50-80%
56
COPD Stage 3 lung function?
30-50%
57
COPD Stage 4 lung function?
<30%
58
When respiratory symptoms worsen beyond normal day-day variations, what do you do for treatment?
Change in medication
59
Comorbid conditions include?
CVD, osteoporosis, depression/anxiety, skeletal muscle dysfunction, metabolic syndrome, lung cancer
60
Non-pharmalogical therapy for COPD management includes?
Quit smoking, reduce occupational exposure and indoor/outdoor pollution, possible CBT counseling to quit smoking
Nutrition counseling, education, exercising training
61
Preventative measures for COPD management?
vaccines - especially flu, pneumococcal, and covid
62
What is not generally recommended for COPD prophylaxis?
antibiotics
63
What antibiotic does seem to help with preventing COPD?
Azithromycin
Decreased exacerbations, but increases ADRs and lung resistance
64
The three goals of pharmacothearpy for COPD?
1. Reduce COPD symptoms
2. Reduced freqency and severity of symptoms
3. Improve health status and exercise tolerance
65
What medications include SABA and LABA?
Beta 2 agonists
66
What medications include SAMA and LAMA?
Anti-cholinergics
67
What combination is usually used for ICS?
LABA/ICS
68
What are the three classe of bronchodilators?
Beta 2 agonists; anti-muscarinics, methylxanthines
69
MOA for Beta 2 agonists?
Stimulate beta receptors on the lung to relax smooth muscles in the airway
70
ADRs for Beta 2 agonists?
Tachycardia, palpiations, tremor
71
SABAs?
Albuterol and levalbuterol
72
LABAs?
Salmeterol, Formoterol, Arformoterol, Indacaterol, Olodaterol, Vilanterol
73
MOA for anticholinergics?
Blocks ACh effects on muscarinic receptors leading to bronchodilation; M3 receptor on airway smooth muscle mediating bronchoconstriction and mucous secretion
74
What's the benefit of SAMAs over SABAs?
Slower onset, but typically longer duration
75
ADRs for anticholinergics?
Dry mouth, hoarseness, blurred vision, metallic taste
76
Benefit of LAMAs over LABAs?
LAMAs seem to have a greater effect in reducing exacerbations
77
SAMAs?
Ipratropium
78
LAMAs?
Tiotropium, Aclidinium, Umeclidinium
79
What is methylxanthine structurally related to?
Caffeine
80
MOA for methylxanthine?
Non-selective PDE inhibitor (3/4) causing bronchodilation, decreases airway reactivity
81
ADRs for methylxanthine?
NTD, arrhythmias, convulsions
HA, insomnia, N/V, heartburn (at thearpeutic concentrations)
Many drug interactions (smoking induces metabolism)
82
If someone stops smoking while taking methylxanthine, what do you need to do to their medication?
Reduce the dose
83
ICSs?
Fluticasone, mometasone, budesonide
84
First line asthma treatment?
ICs
85
What gets added later in COPD treatment as compared to asthma treatment?
ICs
86
Use of ICs?
Improved symptoms, lung function, reduced exacerbations
87
ADRs for ICs?
Hoarseness, oral candidiasis
Increased risk of PNA in COPD pts
88
When are oral steroids used for respiratory illnesses?
Refractor disease (really severe COPD)
89
PDE 4 Inhibitor?
Roflumilast
90
MOA for PDE 4 Inhibitors?
Anti-inflammatory effects via cAMP accumulation
91
PDE 4 inhibitors improve FEV1 in combination with what other drug?
LABAs
92
ADRs for PDE4 inhibitors?
N/V decreased appetitie, diarrhea, weight loss, mood disturbances, night terrors, suicidality
93
What virus can exacerbate asthma?
RSV
94
What is the strongest predictor of asthma?
Genetic predisoposition with atopic dermatitis
95
What is asthma?
variable airway obstruction that if often REVERSIBLE
96
What are some environmental triggers for asthma?
Secondhand smoking, urban vs rural living, RSV infection, occupational hazards
97
What two things can occur with asthma?
Airway edema (due to mast cell activation, which is elevated in allergic conditions)
Eosinophilia (releases cytokines and proinflammatory mediators)
98
Problem with asthma exacerbations?
If you have one, you'll likely have more, and if you get more, you can get permanent damage
99
Asthma presentations
Episodic dyspnea, wheezing, chest tightenss, coughing
100
Asthma symptoms occur when?
Spontanteous, allergen exposure, exercise induced
101
You can premedicate with what before exercise with asthma?
Albuterol (SABA)
102
Gold standard for asthma?
spirometry
103
Asthma reversibility indicated by spirometry?
FEV1 > 12% AFTER SABA administration
104
FEV1/FVC in both asthma and COPD
< 70%
105
Spirometry results from exercise induced bronchospasm
Drop FEV1 > 15% after an exercise challenge
| This is measured at baseline and 5 min intervals x 20-30 min
106
Asthma initial visit goals?
Diagnose, assess severity, initiate medicine and demonstrate use, develop written asthma action plan, schedule follow up
107
Why are follow-ups important for asthma patients?
Because pts will often stay on the same medication dose for a very long time, so we need to make sure they are on the right dose
108
Why don't we use LABA monotherapy for asthma?
It can reduce the pt's own susceptibility to SABA thearpy (the body develops a tolerance for it) and increases risk of DEATH
109
Treatment for asthma?
low dose ICs (can be in combination with LABAs) and SABA for rescue
110
What are the two Leukotriene receptor antagonists?
Montelukast (Singulair) and Aarfirlukast (Accolate)
111
MOA for Leukotriene receptor antagonists
Decreases response from the allergic/hypersensitivity reactions
112
When would you use a leukotriene receptor antagonist?
Asthma with allergic components
113
What biologics are available for asthma treatment?
Omalizumab, Mepolizumab
114
When would you use a biologic in asthma treatment?
pts with high amounts of eosinophils and IgE
115
Doseage for Omalizumab?
Dosed q2-4 weeks SQ based on eosinophil counts
116
Mepolizumab dosage?
q4 weeks SQ
117
ADRs for biologics?
hypersensitivity, injection site pain, HA, edema, increased risk of infection/parasitic infection
118
Preferred drug choice for asthma in pregnancy?
Albuterol
119
Preferred long term control ICs during pregnancy?
Budesonide
120
What other drugs appear to be safe in pregnancy to treat asthma?
LABAs and Montelukast (Singulair)
121
What drug can also help with allergic rhinitis in asthma with pregnancy?
Cromolyn
122
Precipitating Factors to asthma exacerbation?
allergen, pollutant exposure, respiratory infections including viral and bacterial (H. influenzae, Strep. pneumoniae, Moraxela catarrhalis), medication non-adherence
123
Treatment for COPD exacerbation?
Rapid labs and imaging work ups; treating the underlying cause, deciding outpatient vs inpatient treatment appropriation
124
AECOPD treatment?
SABA +/- SAMA treatment (Albuterol/Ipratropium nebulized solution)
Oral corticosteroid treatment - Prednisone 40mg x 5 days
Antibiotics - use with increased cough and sputum purulence, mostly azithromycin or doxycycline most commonly used
125
What are the 3 cardinal symptoms with antibiotics?
Increased dyspnea, sputum volume, sputum purulence
126
Gold standard dosing for oral contraceptives for AECOPD?
Prednisone 40 mg x 5 days
127
What is used for asthma pts to measure their PEF?
Peak flow meters
128
Early signs of asthma exacerbation
Breathlessness at rest, drowsiness, agitation, inability to speak full sentences, PEF < 50% personal best
129
Asthma exacerbation treatment?
SABA administration
Oral/IV steriod - Prednisone 40-60 mg/dose equivalent x 5-7 days
Oxygen
Increase maintenance therapy (ICs/LABA dose)
130
What drug can you also use in combination to treat an asthma exacerbation?
SAMA combination
131
Proper technique for using inhaler? MDI vs DPI?
MDI: Slowed inhalation of medication (that's why it needs a spacer)
DPI: Deep forceful inhalation to get the medication into the lungs
