Module 2 COPD Flashcards
1
Q
LAMA
A
Long acting controller for smooth muscle relaxation and dilation.
- Slower onset w/long duration
2
Q
Is tiotropium a LAMA or SAMA?
A
LAMA
3
Q
COPD is largely caused by smoking; according to GOLD what is the more definitive cause?
A
Complex mix of genes and environment
4
Q
COPD symptoms
A
SOB
Chronic cough
Sputum
5
Q
Risk factors for COPD
A
Host Factors, but generally:
- Tobacco
- Occupation
- In/outdoor pollution
- Genetic predisposition
- COPD increases with age
6
Q
How do you test/diagnosis COPD?
A
Spirometers
(FEV1/FVC)
7
Q
COPD is formally diagnosed via spirometers to test post-bronchodilator. FEV1/ FVC ratio.
what ratio would be consistent with COPD?
A
FEV1/ FVC ratio less than 0.70
8
Q
Add slides on patient history
edit
A
9
Q
How is Spirometry used as a tool to diagnose COPD?
aka how does it work?
A
Objectively measures airflow limits
10
Q
What does normal vs obstructed airflow look like?
A
11
Q
Is COPD a obstructive or restrictive disease?
A
obstructive
12
Q
What is the difference between obstructive and restrictive lung diseases?
A
obstructive: make it hard to exhale air out of the lungs.
Restrictive: makes it hard to expand their lungs with air.
13
Q
What are 2 pathologies that make up COPD
A
Chronic bronchitis and emphysema
14
Q
What is dynamic compression?
A
Premature compression of airways.
(leading to increased airway resistance)
15
Q
What could cause increased airway resistance in a COPD patient
A
Air trapping
Increased secretions
16
Q
What direction does the equal pressure point (EPP) move in COPD?
A
Toward the alveoli into the non-cartilaginous airways.
Palv < Ppl
17
Q
Common symptoms of COPD
A
Persistent cough
Increased mucous production
Dyspnea
Muscle fatigue
18
Q
Hallmark sign of COPD
A
productive cough
19
Q
Panlobular emphysema
A
Type of emphysema involving distention and destruction of the entire primary respiratory lobule
- usually associated with 1-antitrypsin deficiency
20
Q
Centrilobular emphysema
A
Weakening and enlargement of respiratory bronchioles in the proximal portion of acinus.
- Associated with smoking.
21
Q
What criteria would classify as Chronic bronchitis?
A
presence of cough and sputum production for at least 3 months in 2 consecutive years
22
Q
What does emphysema cause?
A
- Oxidative stress
- Airway remodeling
- enzyme; enzyme inhibitor imbalance.
23
Q
Symptoms to consider a diagnosis for COPD?
A
- dyspnea
- recurrent lower resp. tract infection
- chronic cough/sputum
- history of risk factors
24
Q
GOLD diagnosis of COPD
A
FEV1/ FVC ratio < 0.70
25
How often is spirometry done for COPD
q6months to 1yr
26
GOLD 1 airflow limitation
FEV1 > 80% predicted
27
GOLD 2 airflow limitation
FEV1 50-80% of predicted
28
GOLD 3 airflow limitation
FEV1 30-50% predicted
29
GOLD 4 airflow limitation
FEV < 30% of predicted
30
mMRC grade 0
I only get breathless with strenuous exercise
31
mMRC grade 2
I walk slower than people of the same age on the level because of the breathlessness, or I have to stop for breath when walking on my own pace on the level.
32
mMRC grade 3
I stop for breath after walking about 100 meters or after a few minutes on the level
33
mMRC grade 4
I am too breathless to leave the house or I am breathless when dressing or undressing
34
Mild exacerbation treatment (Tx)
Only with Short acting bronchodilator agent (SABA)
35
Moderate COPD exacerbation Tx
SABA plus oral antibiotics or oral corticosteroids (OCS)
- OCS like prednisone or methylprednisolone
36
What are the benefit of oral corticosteroids in COPD?
- Help to improve lung function
- Improves oxygenation
- Reduces recovery time
37
Severe exacerbation Tx
Hospitalization with or without resp. failure may need NIV (very beneficial), intubation/ventilation
38
True or False: A pt who has had a COPD exacerbation in the past is at an increased risk for future exacerbations.
True.
39
Benefits of long-term supplemental oxygen therapy (LTOT)
Helps improve survival benefit
40
Indications for long-term supplemental oxygen therapy (LTOT)
Needs to have restive PaO2 < 55mmHg or <60mmHg with either cor pulmonale, edema, erythrocytosis, polycythemia
41
Pre-ganglionic receptors on the sympathetic system are comprised of?
Nicotinic receptors
(cholinergic receptors that release acetylcholine)
42
A COPD patient with a eosinophil count of 25/uL and prescribed a LABA with infrequent AECOPD continues to have dyspneic episodes:
Should be prescribed a LAMA
43
Increased airway resistance is a contributing factor to which disease process?
obstructive
44
What is Panacinar emphysema?
Involves all portions of the acinus and secondary pulmonary lobule more or less uniformly.
- It predominates in the lower lobes and is the form of emphysema **associated with 1-antitrypsin deficiency**.
- TLDR; **worsens the in the lower lobes aka alveoli!!!**
45
What does acetylcholine do to airways?
Regulates bronchoconstriction and mucus secretion
- includes inflammation and regulation of airways
46
What do anticholinergic drugs do?
Block the activity of neurotransmitter acetylcholine (Ach) at both central and peripheral nervous system synapses, reducing PNS acitivty which affects the organs differently/
- **Lungs vasodilate** by preventing bronchoconstriction
- **Increases HR** by blocking vagal tone
- GI reduces contractions for cramps
47
What are adrenergic drugs used for?
Adrenergic agonists that bind to alpha and beta receptors that depending on the receptor site affects:
- local **vasoconstriction** (for hypotension/shock)
- Relaxes (bronchodilates) (b2) **or** constricts smooth muscles (a1)
- relief of allergic states (anaphylaxis included)
- Increase HR
48
Generally, what do B1 and B2 receptors do?
B1 = excite
B2 = relax
49
Group A Combined assesment
low risk low symptoms
GOLD 1 or 2
mild to moderate airflow limitation
0-1 exacerbations per year
mMRC 0-1
CAT <10
50
Group B combined assessment
low risk more symptoms
GOLD 1 or 2
mild to moderate airflow limitations
0-1 exacerbations per year
mMRC 2-4
CAT > 10
51
Group C combined assessment
High risk less symptoms
GOLD 3 or 4
Severe to very severe airflow limitations
>2 exacerbations/yr
mMRC 0-1
CAT <10
52
Group D combined assessment
High risk more symptoms
GOLD 3 or 4
Severe or very severe airflow limitation
>2 exacerbations per year
CAT > 10
53
Group A treatment
Short acting bronchodilator (SABA)
Salbutamol or ipatropium
54
Group B treatment
LAMA or LABA
Salmeterol or Tiotropium
55
Group C treatment
LAMA or LAMA/LABA
- Add ICS to either of these if eosinophil count is > 300
- (or less than 100 after hospitalization)
- triple therapy (all 3)
56
Why would ICS not work well on COPD?
COPD has neutrophillic inflammation as opposed to eosinophilic inflammation (asthma related).
Tobacco smoke also decreases effiacy bc:
- **Has an immunosuppressive effect on lungs**
- Alters lungs response via neutrophil activity and oxidative sterss
- Increase glucocrticoid resistance (less respsonsive)
57
When to add PDE4 inhibitor
when eosinphil levels are < 100 and triple therapy is not effective
58
What can chronic inflammation result in?
small airway diseases
chronic bronchitis
destruction of lung parenchyma tissue
59
What is the pathophysiology of COPD?
Loss of elastic recoil and airway attachment
Leading to...
-> airways collapse during expiration
->Decreased surface area available for gas exchange
60
What is emphysema
Destruction of alveoli surface area
- usually due to harmful substances like cigaratte smoke
- leads to loss in elastic fibres = less recoil
61
What are 2 types of emphysema?
Panlobular
centrilobular
62
Define panlobular emphysema
Abnormal weakening and enlargement of all air spaces distal to terminal bronchioles
- aka primarily affects the alveoli
63
Define centrilobular emphysema
abnormal weakening and enlargment of resp. bronchioles and alveoli in proximal portion of acinus
64
What genetic component could cause someone to develop COPD
Alpha 1 anti trypsin deficiency
65
What is the goal of COPD treatment?
Take away what is causing the lung damage
i.e tobacco cessation
66
What are the goals of treatment for stable COPD?
Reduce symptoms
reduce risk; prevent and treat exacerbations
reduce mortality
prevent disease progression
67
What interventions are shown to decrease mortality in COPD pts w/resting hypoxemia?
tobacco cessation and O2 therapy
68
what should not be a guiding factor in treatment of COPD?
severity of airflow limitation
69
What parts assist w/reducing symptoms in COPD?
relieve symptoms
improved exercise tolerance
improve health status
70
What are the intial pharm treatments for groups
i.e ABCD?
A -> bronchodilators
B -> LABA (or LAMA's)
C -> LAMA
D -> LAMAs or [LAMA/LABA] or [ICS + LABA]
71
For pt's w/persistent long acting bronchodilator therapy, what is recommended?
Escalation to:
-LABA
-LAMA
-[LABA/ICS]
72
What predicts a low likelihood of beneficial ICS response
Blood eosinophil count < 100 cells/Ul
73
What can be done for pt who develops further exacerbations while on LABA/LAMA?
Escalation to triple therapy (LABA/LAMA/ICS)
- addition w/PDE4 inhibitor
- addition of antibiotics (azithromycin)
- w/assumption than eosinophil < 100
74
What COPD pt's receive ICS?
Those w/High risk of exacerbation
75
What COPD pt should have Pulmonary rehab (PR)?
Any that had a AECOPD should take part in PR w/1 month of AECOPD
76
What is pulmonary rehab [PR]?
Standard of care for COPD pt w/symtpoms despite optimal pharm therapy.
Improves:
- quality of life
- Dyspnea
- healthcare utilization
77
What is AECOPD?
Defined by gold as:
Acute worsening of resp. symptoms that result in requirement for additional therapy
78
What is the most common causes of COPD exacerbations?
Respiratory tract infections
79
What can prevent/treat exacerbations
- Antibiotics (when indicated) q5-7d
- NIV
80
Treatment for mild exacerbations classes?
SABA
81
Treatment for moderate exacerbations classes?
SABA w/antibiotics
82
Treatment for severe exacerbations classes?
Hospital
typically acute resp. failure
83
How long do AECOPD symptoms normally last?
7-10 days (sometimes longer)
- remember AECOPD = sustained increase in cough, sputum production, and/or dyspnea
84
What are AECOPD management options? (3)
- Inhaled bronchodilators
- PO antibiotics for sputum w/systemic corticosteroids
(keep SaO2 > 90%)
- NIV for hypercapnia (when pH < 7.3)
85
What is the success rate for NIV treatment?
80-85%
86
Indications for invasive ventilation in AECOPD?
unable to tolerate NIV
Post resp/cardiac arrest
decrease LOC
Aspiration
hemodynamic instability
87
Why do we avoid invasive ventilation?
greater morbidity risk and increased length of hospital stay
88
how can we reduce COPD progression?
smoking cessation
long term O2 therapy
lung transplant
annual flu vaccines
89
indications for O2 therapy?
resting PaO2 < 55
SaO2 < 88
PaO2 <55
sleep; same with associated complications like pulmonary hypertension and cardiac arrhythmias
90
What are some surgical interventiosn for end stage copd
lung transpant
lung vol reduction surgery
pt with aat deficency = intravenous with purified aat from human blood donor
91
What do bronchodilators do?
help reduce dyspnea
improve lung function
92
2 main classes of bronchodilators?
Beta 2 agonists
anti-muscarinics
93
What do antimuscarinic agents do?
Block the action of acetylcholine on receptors
->leads to bronchodilation and symptom reduction
94
Where are beta 2 receptors found?
bronchial and vascular smooth muscles
95
When is anti IGE therapy used?
for asthma that bypasses standard treatments.
usually in youth w/continued uncontrolled ashtma and allergies
96
3 commons LAMAs?
(actual drug names)
- Tiotropium (spirvia)
- Aclidnium Bromide (Tudorza)
- Glycopyronnium Bromide (Seebri)
97
What are 3 LABAs?
(actual drug names)
-Formoterol (oxeze)
-Salmeterol (serevent)
-Indacterol (Onbrez)
98
What are the differences between SABAs and LABAs?
long acting continuously keeps airways open
-sees long term use
shorting acting = emergencies
-"rescue inhalers"
99
What are the adrenergic receptors
Alpha and beta sympathetic receptors
100
What kind of receptors are the alpha and beta receptors?
g-coupled receptors
101
General innervation of Alpha 2 receptors result in what?
inhibitory response
102
Activation of alpha 1 receptors illicit what response?
sympathetic
Typical contractions
103
Norepinephrine is released by?
All postganglionic neurons of the sympathetic nervous system except those that stimulate sweat glands
104
Acetylcholine (AcH) stimulates what on sympathetic and parasympathetic postganglionic neurons at the neuromuscular junction?
nicotinic receptors
105
Norepi stimulates what on tissues innervated by sympathetic POSTganglionic neurons?
alpha and beta receptors
106
What are the parasympathetic receptors?
muscarinic and nicotinic
107
what degrades AcH?
cholinesterase
108
sympatholytic vs sympathomimetic drug?
mimetic = mimics effects of the sympathetic nervous system (SNS).
- elevated HR and sweating etc.
lytic = works against SNS
- used when someones heart is beating too fast
- used for high blood pressure
- i.e beta blockers
109
Examples of alpha agonists?
norepinephrine
epinephrine
dopamine (high doses)
110
Generally alpha (mostly a1) serve which function?
regulate vascular smooth muscle tone
(think peripheral vasculature)
111
mMRC is a scale that measures...
Dyspnea; via questions
112
mMRC grade 1
I get SOB when hurrying on the level or walking up a slight hill
113
For pts w/persistent exacerbations on LABA, what is the next step?
Escalation to:
-[LABA/LAMA]
-[LABA/ICS] is
114
When would a [LABA/ICS] combo be preferred?
For patients with ONE exacerbation per year, an eosinophil count >300/uL identifies a patient more likely to respond to LABA/ICS treatment
For patients with TWO exacerbations per year or one exacerbation leading to hospitalization LABA/ICS treatment can be considered at eosinophil counts >100 cells/uL
115
The most common cause of exacerbations are
Respiratory tract infections; normally triggered via bacterial infections and environmental factors (pollution)
116
Why would you use a SABD for a exacerbation rather than a LAMA?
Faster onset
117
What can improve lung function (FEV1), oxygenation, and shorten recovery time (and hospital duration)?
Systemic corticosteroids (no longer than 5-7 days of therapy)
-systemic corticosteroids are typically not good for you.
118
When would you prescribe a pt w/antibiotics?
Only w/a positive test of a bacterial infection
119
Which mode should be used in COPD pts w/acute resp. failure who have no absolute contraindications?
NIV
120
What are the benefits of NIV?
Improves gas exchange
reduce WOB
Reduce stress need needed for intubation
decreases hospital duration
Improves survival
121
what can predict future AECOPD events?
Past AECOPD
122
What is a requirement of NIV
spontaneously awake conscious patient because they need to be able to keep their air way open (Prevent aspiration)
123
CPAP/BIPAP: For positive pressure stents airways open, What does the difference between IPAP and EPAP do ?
Provides Pressure support; Augments their Vt
-helps transfer the support of the machine to improve their MV
124
Tx for mild COPD exacerbations
Treated w/SABDs
125
Tx for moderate COPD exacerbations
Treated with SABD, antibiotics, and/or oral corticosteroids.
126
Tx for Severe COPD exacerbations
Require hospital; severe are usually associated w/acute resp. failure
127
If NIV fails, what are the next steps?
intubation and mechanical ventilation
128
AECOPD Management Progessive plan
-Inhaled bronchodilators; beta 2 agonist in particular PRN
-oral antibiotics if purulent sputum is present (5-7d)
-Short course of systemic corticosteroids (5-7d)
-supplemental oxygenation to keep SaO2 > 90
-w/hypercapnia (pH < 7.3); NIV
-pay attention to 7.28
129
AECOPD: what indicator would you prescribe antibiotics?
presence of purulent sputum
130
AECOPD Management ventilation; Why do you use NIV vs invasive ventilation?
Shown to improve oxygenation and improve resp. acidosis w/o risk of vent. acquired pneumonia
-NIV can be discontinued w/o weening period
-NIV decreases RR, WOB, and severity of breathlessness
131
Indications for invasive ventilation?
Unable to handle/use to tolerate NIV
post resp. or cardiac arrest
decreased LOC
Massive aspiration/vomiting
Severe hemodynamics instability
-can reduce venous return
Life threatening hypoxemia
132
Reducing progression of COPD; how can you enhance survival?
-Smoking cessation is the first line of intervention
-Long term oxygen therapy (LTOT)
annual influenza and pneumoccal vaccinations
-some end stage may also benefit from a lung transplant or lung volume reduction surgery
133
Indications for long term oxygen therapy (LTOT)
Continuous O2;
-resting PaO2 < 55 mmHg
SaO2 @ 89% and resting PaO2 56-59 mmHg in the presence of:
-> dependant edema; suggests CHF
-> P. polmonale on the ECG (sharp peaked P waves)
-> Erythrocytosis (hematocrit > 56%)
Non continuous O2
134
SaO2 @ 89% and resting PaO2 56-59 mmHg in the presence of: what does the presence of depedant edema suggest?
CHF
135
Indications for long term O2 therapy (LTOT); what does non continuous O2 entail?
*edit*
slide 15 of COPD management
Associated with flow rate of O2 and hours per day due to factors such as exercise or exertion.
-Exercise;
PaO2 <55 or SaO2 < 88 w/low level of exertion
-During sleep; (save values as above) w/complications such as pul. hypertension, daytime sommlence or cardiac arrhythmias
136
What are surgical interventions for end stage COPD?
lung transplant
lung volume reduction surgery (LVRS)
137
For pts w/AAT deficiency and COPD what are additional therapies?
intravenous augmentation w/purified preparation of AAT from human blood donors is recommended
138
What is the most common situation to step down from a COPD medication may be considered?
when there is no improvement to dyspnea or exercise tolerance in stable COPD patients
139
What is the best intervention and general advice for a patient recently diagnosed w/mild COPD which could improve their symptoms and possibly increase their survival?
Tobacco cessation
140
What are signs of upper airway obstruction?
- Stridor
- Dyspnea
- drooling
141
When would a lobe resection be performed?
For patients w/severe COPD
142
How does a lobe resection benefit patients w/severe COPD?
Increases surface area between alveoli and pulmonary capillaries
143
Airway remodeling is a characteristic change associated w/chronic bronchitis. What is usually associated w/bronchitis?
Increased mucous viscosity and secretion
AND
reduction in elastic protiens of the lung parenchyma
144
Pathobiology of COPD
Impaired lung growth
Lung injury
Lung and systemic inflammation
-oxidative stress
-airway remodelling
-hypersecretion of mucus
145
Generally describe Empysema
Destruction and damage to alveoli decreasing alveolar surface area
146
What is panlobular empysema
Abnormal weakening/destruction and enlargement of alveoli distal to the acinus
147
What is centrilobular emphysema?
Weakening/destruction and enlargement of the alveoli near the bronchioles
*more associated w/smoking*
148
what symptoms are the common to find w/COPD?
Productive cough
Weakening of the distal airways
chronic limitation of airflow
air trapping and hyper inflammation
destruction of the lung parenchyma, including alveolar-capillary membrane.
149
Chronic Bronchitis is defined as?
THe presence of a productive cough for*atleast 3 months in 2 years*
150
Etiology of chronic bronchitis
typically from smoking
exposure to air pollution
irritants
151
Goals of treatment for COPD
Focus on tobaccos cessation; it can delay the progression of disease but lung damage is permanent
152
If a pt has a predicted FEV1 >80* their GOLD airway limitation severity would be classified as
mild
153
If a pt has a predicted FEV1 between 30-50% their GOLD airway limitation severity would be classified as
Severe
154
If a pt has a predicted FEV1 between 50-79% their GOLD airway limitation severity would be classified as
Moderate
155
If a pt has a predicted FEV1 < 30% their GOLD airway limitation severity would be classified as
Very severe
156
A pt only gets breathless w/strenuous exercise, what is his mMRC grade?
Grade o
157
A pt gets SOB when hurting on the level or walking up a slight hill. What is their mMRC grade?
Grade 1
158
A pt walks slower than people of the same age on the level because of breathlessness, or has to stop for a breath when walking on their own pace. What is their mMRC grade?
Grade 2
159
A pt has to stop for breath after walking about 100 enters or after a few mins on the level. What is their mMRC grade?
Grade 3
160
A pt is too breathless to leave the house or breathless when dressing/undressing. What is their mMRC?
Grade 4
161
mMRC evaluates what?
perception of dyspnea w/activity
162
How long do COPD exacerbation symptoms usually last?
7-10 days
163
Persistent dyspnea and SOB are strongly associated with what?
increased risk of exacerbation
164
What are the recommended initial bronchodilators to treat AECOPD?
SABA
with or w/o SAMA
165
What are 5 ways to help manage AECOPD?
Bronchodilators (SABA and SAMA)
Antibiotics if purulent sputum is present
systemic corticosteroids
supplemental oxygen
NIV if pH =<7.3
166
What are the recommended diesels for salbutamol for a MDI?
100 mcg + 2 puffs inhaled every 4 hours with a spacer
but really; 2 puffs q1h
167
What is the indication for long-term oxygen therapy?
Resting PaO2 of =< 55 mHg.
Alt.
SaO2 <88 during exercise.
168
What are some interventions for pt’s w/end stage?
Lung transplant
Lung volume reduction surgery (LVRS)
169
Lobe resections are an effective intervention for severe COPD pts. how does a lobe resection benefit these pts?
Increases surface area between alveoli and pulmonary capillaries
170
What is a complication of AAT deficiency?
Can cause emphysema
-> increasing pulmonary compliance (loss of elastic property)
171
Problems w/oxidative stress?
Breakdowns proteins and all involved enzymes (and inhibitors)
->parenchyma reduced
->causes imbalances
172
Steps for reducing progression of COPD
(enhancing survival)
1. Smoking cessation
2. Long-term oxygen therapy (LTOT)
3. Annual influenza and pneumococcal vaccinations
4. lung transplant
173
which groups of the combined COPD assessment suggest a high risk of symptoms?
C and D
*however*
1 or more hospital visits for COPD exacerbations are always high risk
174
How does smoking cessation help reduce the progression of COPD?
Slows rate of FEV1 decline to same age smokers
175
GOLD risk classification A
*Low risk ; less symptoms*
Gold 1 or Gold 2
mild to mod airflow limitations
and/or
mMRC grade 0-1
CAT < 10
176
GOLD risk classification Ç
*High Risk; less symptoms*
Gold 3 or 4
severe -> very severe airflow limitation
and/or
>2 exacerbations year
mMRC grade 0-1
CAT score < 10
177
GOLD risk classification B
Low risk ; more symptoms
Gold 1 or Gold 2
mild to mod airflow limitations
and/or
0-1 exacerbation/year
mMRC grade > 2
CAT > 10
178
GOLD risk classification D
High Risk - More symptoms
Gold 3 or Gold 4
Severe or very severe Airflow limitations
and/or
>2 exacerbations/year
mMRC grade > 2
CAT > 10
179
AECOPD management; Indicators to transition from NIV to invasive?
- Unable to tolerate NIV
- Post resp. or cardiac arrest
- Decreased LOC
- Massive aspiration/persistent vomiting
- severe hemodynamics instability
- life-threatening hypoxia
180
Group D treatment
LAMA or LAMA/LABA
Add ICS to either of these (LABA/ICS or triple therapy)
if eosinophil count is >300 or >100w/recent hospitalizations
181
When does ICS not work well on COPD?
Tobacco smoke downplays the ICS action
182
What conditions like asthma, COPD, or those associate w/chronic bronchitis, what are typical structural changes?
(5)
1. Chronic inflammation of the wall of peripheral airways
2. excessive mucous production and acclamation
3. parietal/total mucous plugging of airways
4. smooth muscle constriction of bronchial airways (bronchospasm)
5. air trapping and inflation of alveoli
183
Emphysema is characterized by what?
The weakening and permeant enlargement of air spaces distal to the terminal bronchioles; and by does turn on of the alveolar walls
-decreased SA for gas exchange
-collapse of expiration in response to increased intrapleural pressures
184
What are the alternative names for panlobular and centrilobular emphysema
Panacinar and centriacinar emphysema
185
Centriacinar emphysema involves which portion of the resp. system and alt name?
proximal portion of the acinus.
alt. name = centrilobular
186
Panacinar emphysema is involves which part of the resp. system and alt. name?
enlargement of alveoli distal to terminal bronchioles
panlobular
187
which type of emphysema is associated w/smoking?
centriacinar (centrilobular)
188
Difference between centrilobular and panlobular emphysema
189
which type of emphysema is most severe?
centrilobular
190
COPD is typically characterized by what?
**Persistent airflow limitation**
It is progressive and not fully reversible
191
Obstructive breathing pattern will do what to minimize WOB?
Minimize their WOB.
- slow down RR allows for long exhales
192
Oral corticosteroids vs inhaled corticosteroids?
Both improve dyspnea
- OCS are used primarily for flare ups
- ICS more for long term use, to prevent flare ups and make receptors available for bronchodilators
