COPD Flashcards
1
Q
what is COPD
A
chronic respiratory symptoms caused by airway abnormalities and/or alveoli abnormalities that cause persistent, progressive airflow obstruction.
2
Q
what are the two pathophysiologic categories of COPD
A
chronic bronchitis
emphysema
3
Q
what are the key physiological markers of COPD
A
airflow obstruction and extensive airway destruction
4
Q
what are the three classic respiratory symptoms of COPD
A
cough
dyspnea (SOB)
sputum production
5
Q
what is the difference between chronic bronchitis and emphysema
A
chronci bronchitis is more central airway - thickening of the musculature and clogging with mucous
emphysema - less sputum production, more alveolar desctruction. leading to air trapped in the alveoli
6
Q
what are the additional associated symptoms with COPD
A
- weight gain
- weight loss - associated w worse prognosis
- activity limitation (including sex)
- wheezing +/- chest tightness
- syncope
- anxiety/depression
7
Q
what are risk factors for COPD
A
Fam Hx
smoking hx
environmental hx (exposure)
childhood pulmonary infections, HIV, or TB
asthma
8
Q
How does mild COPD present
A
PE - mostly normal
may see:
prolonged expiration
faint end-expiratory wheeze w forced expiration
9
Q
how does moderate/severe COPD present
A
lung hyperinflation (barrel chest)
decreased breath sounds/wheezes
crackles at the lung bases
distant heart sounds
increased AP diameter
10
Q
How does end stage COPD present
A
- tripod posturing (calloused forearms, swollen bursae)
- accessory muscle use
- expire through pursed lips
- hoovers sign
- cyanosis
- rare nail clubbing
11
Q
what are signs of heavy smoking
A
yellowing of fingers/nails
12
Q
what is the comparison between presentations of chronic bronchitis v emphysema
A
13
Q
Who should you screen for COPD
A
- adults who present with at least 1 of 3 cardinal symptoms
- adults who have a gradual decline in activity with risk factors for COPD
14
Q
what are the 5 CAPTURE questions
A
- have you ever lived or worked in a place with dirty/polluted air, second hand smoke or dust
- does your breathing change with seasons, weather, or air quality
- does your breathing make it difficult to do things such as carry heavy loads, shovel dirt/snow, ect.
- compared to others of your age, do you tire easily
- in the past 12 months how many times did you miss work, school or ther due to a cold, bronchitis or pneumonia? (0 = no,2 or more = yes)
15
Q
what CAPTURE scores are indicative of clinically significant COPD
A
2-4
16
Q
what is the initial workup for COPD
A
spirometry before and after bronchodilator
17
Q
what is additional initial testing for COPD
A
Pulse oximetry every visit
Labs - CBC, BMP, TSH, BNP/NT-proBNP, serum alpha-1 antitrypsin
CXR
18
Q
what spirometry results suggest evidence of obstruction
A
FVC > 80% with FEV₁/FVC < 0.7
OR
FVC < 80% with TLC >80%
19
Q
if a patient has a FVC of 90% but their FEV/FVC is .68 what should you do
A
Ratio between 0.6 - 0.8 = repeat spirometry on a separate day
20
Q
when should DLco be considered for a COPD patient
A
- In presence of moderate / severe airflow limitations (FEV₁ ≤50% predicted)
- Resting O2 ≤92%
- Exertional hypoxemia (<90%)
- Severe dyspnea (mMRC ≥2)
21
Q
what occurs to DLco in COPD
A
DLCO decreases in proportion to severity of disease
22
Q
what are the indications for obtaining arterial blood gas in a COPD pt
A
- Low FEV₁ (< 40% predicted)
- Low O₂ saturation on pulse ox (< 92%)
- Depressed LOC
- Assessment of hypercapnia in “CO₂ retainers” who are given supplemental oxygen (risk of hypercapnic respiratory failure)
- Signs of right heart failure
23
Q
what are expected arterial blood gas findings in COPD
A
mild - low pO2 and normal pCO2
mod/severe - worsening pO2 and elevated pCO2
24
Q
what do the following measures mean in arterial blood gas:
pO2
pCO2
pH
SaO2
HCO3
Base excess
A
pO₂ - oxygen pressure in arterial blood
pCO₂ - amount of CO2 in arterial blood
pH - acidity or alkalinity of arterial blood
SaO₂ - oxygen saturation
HCO₃ - bicarb
Base excess - amount of acid or base required to restore a liter of blood to its normal pH at a PaCO2 of 40 mmHg
25
is imaging needed to make COPD diagnosis
NO
26
what imaging can be CONSIDERED in evaluation of COPD
CXR and CT chest w/o
27
what are indications for imaging in COPD
* Dyspnea/cough etiology is unclear
* Rule out complicating process during acute exacerbations
* Evaluate for comorbidities
28
what would a chronic bronchitis COPD chest X ray look like
X-ray likely to be normal unless complications or comorbidities are present
29
what would a emphysema COPD chest Xray look like
* Hyperinflation
* Flattened diaphragm
* Increased retrosternal air space
* Long, narrow heart shadow
30
what group determines staging in COPD
Global Initiative for Chronic Obstructive Lung Disease (GOLD)
31
what are the 3 dimensions of staging
Airflow limitations
Symptom severity
Exacerbations
32
what are the 4 stages of GOLD COPD airflow limitation staging
33
after GOLD category is determined, what isthe next step
determine symptom severity by using mMRC and CAT
34
what does Modified Medical Research Council Dyspnea Scale (mMRC) assess?
assesses severity of breathlessness
35
what does COPD assessment test (CAT) assess?
assesses multitude of symptoms present
36
what are the 4 steps of GOLD ABE assessment
1. spirometry
2. GOLD stage
3. exacerbation hx
4. mMRC or CAT
37
if a patient has FEV1 of 60%, 1 exacerbation, no hospitalizations, and an mMRC of 2 what is their COPD stage
GOLD 2B
38
if a patient has a FEV1 of 45%, 3 exacerbations, no hospitalizations and a CAT score of 13 what is thei COPD stage
GOLD 3E
39
what are goals of COPD management
improve symptoms
decreased number of exacerbations
improve patient functioning
40
what is non-pharm COPD management
* smoking cessation
* behavioral counsleing
* vaccinations
* adequate nutrition
* regular exercise
* oxygen therapy
* pulmonary rehab
41
what vaccinations should you suggest to COPD patients
* Influenza
* COVID-19
* PCV-20 OR PCV-13 followed by PCV-23
* Tdap
* Zoster in patients >50
42
how does adequate nutrition affect COPD
* obese patients can improve dyspnea and exercise tolerance by losing weight
* Vitamin D deficiency is associated with reduced lung function and increased COPD exacerbation
43
when is oxygen therapy indicated in COPD management and why
* pO2 ≤ 55 mmHg on ABG
* O2 sat ≤ 88%
* pO2 >55 <60 + RHF or erythrocytosis
* severe hypoxemia with exertion
why? - Proven to increase survival in patients with severe chronic resting arterial hypoxemia
44
When is pulmonary rehabilitation indicated
for COPD class B and E
45
what are the components of pulmonary rehabilitation therapy
* exercise training
* promotion of healthy behaviors (smoke cessation, exercise, nutrition, med use, self managment ect)
* psychological support (coping strategies for chronis illness)
45
what are the short acting bronchidilator pharm cattegories
short-acting beta agonists (SABA)
short acting muscarinic antagonists (SAMA)
46
what are the long-acting bronchodilator pharm categories
* Long-acting Beta Agonists (LABA)
* Long-acting Muscarinic Antagonists (LAMA)
47
what are the SABAs
albuterol, levabuterol
48
what are the SABA SE
* Tachycardia
* Tremor
* Cardiac arrhythmia
49
what are teh SAMA meds
Ipratropium Bromide
50
what are the SAMA SE
* Dry mouth / eyes
* metallic taste
* prostatic symptoms
51
what is the SAMA + SABA combo med
albuterol + ipratropium
52
what are the LABAs
arformoterol
salmeterol
formeterol
53
what are the LABA SE
* tahcycardia
* tremor
* HA
54
what are the LAMA meds
QD
tiotropium
umeclidinium
revefencin
BID
aclidinium
glycopyrrolate
55
what are the LAMA SE
* Dry mouth
* Constipation
* urinary retention
56
what are the LAMA+LABA combo
QD
Olodaterol /Tiotropium
Vilanterol/Umeclidinium
BID
Formoterol/Glycopyrrolate
Formoterol/Aclidinium
57
what are the LABA+ICS combo
Salmeterol/Fluticasone propionate
Vilanterol/Fluticasone furoate
Formoterol/Budesonide
58
what are the LABA+LAMA+ICS combos
* Fluticasone furoate/Umeclidinium/ Vilanterol
* Beclometasone/Formoterol/ Glycopyrronium
* Budesonide/Formoterol/ Glycopyrrolate
59
what is initial pharm management for group E
LABA+LAMA
consider LAMA+LAMA_ICS if blood eosinophils >300
60
what is initial pharm management for group A
bronchodilator
61
what is initial pharm management for group B
LAMA + LABA
62
what are factors that suggest you SHOULDN'T use an ICS with long acting bronchodilators
* repeated pneumonia events
* blood eosinophils <100
* hx of mycobacterial infection
63
what are factors that suggest you could use an ICS with long-acting bronchodilators
* 1 moderate exacerbation of COPD per year
* blood eosinophils 100 to <300
64
what are factors that strongly favor the use of ICS in addition to long acting bronchodilators
* Hx of hospitalizations for exacerbations of COPD
* >2 moderate exacerbations of COPD per year
* blood eosinophils >300
* history of concomitant asthma
65
if a patient is on an ICS, when is removal indicated?
* if the patient developed pneumonia on ICS
* inappropriate indication when ICS was first prescribed.
* lack of response to ICS (no exacerbation change)
* if patients symptoms are greatly controlled on current therapy, a trial de-escelation can be attempted with close follow up
66
what are the two medications that we use for severe COPD
roflumilast and theophylline
67
what is the class and MOA of roflumilast
* PDE-4 inhibitor
* suppresses cytokine release and inhibits pulmonary neutrophil infiltration which reduces inflammation, pulmonary remodeling and mucociliary malfunction
68
what is the class and MOA of theophyline
* non-specific PDE inhibitor
* relaxes smooth muscle → suppresses airway response to noxious stimuli → increased diaphragm contraction force
69
what is the indication for roflumilast
reduce exacerbations in severe COPD
70
what is the indication for theophyline
refractory COPD
71
what are the SE of roflumilast
psych - anxiety, depression, insomnia
GI - NVD, weight loss, dyspepsia
72
what group should you avoid prescribing roflumilast to
patients with a mental health history
73
what are the SE of theophylline
anxiety
temors
insomnia
nausea
cardiac arrhythmias
seizures
74
who should you avoid prescribing thephylline to
patients with liver impatiemment
75
how often should COPD patietns follow up?
* 1-3 months following initial diagnosis and initiation of therapy
* every 3-6 months once stabilized
76
how often should spirometry be performed in a COPD patient
at least annually
77
what are risk factor for acute COPD exacerbation
advanced age
chronic productive cough
duration of COPD
hx of prior abx therapy
COPD-related hospitalization
Comorbid conditions (CAD, CHF, DM)
respiratory infections
78
what triggers 70% of COPD exacerbations
respiratory infections.
79
what are historical and physical exam findings for an acute COPD exacerbation
* worsening of respiratory symptoms over hours-days
* wheezing and tachypnea
* evidence of respiratory compromise
* decreased mental status
80
what is included in evidence of respiratory compromise
* difficulty speaking due to respiratory effort
* use of accessory respiratory muscles
* paradoxical chest wall/abdominal movements
81
what causes the decreased mental status during an acute COPD exacerbaiton
reflection of hypercapnia and hypoxemia
82
what percent of acute COPD exacerbations can be managed outpatient
80%
83
when should you consider inpatient management of Acute COPD exacerbations
* severe symptoms such as worsening of resting dyspnea, high RR, low O2 sat, confusion, drowsiness
* acute respiratory failure
* onset of new PE findings (cyanosis, peripheral edema)
* failure to respond to initial medical management
* presence of serious comorbidities (CHF, arrhythmias)
* insufficiency home support
84
what is included in outpatient management for acute COPD exacerbation
* adjustment of bronchodilator therapy
* consider spacers/nebulizer therapy
* consider oral glucocorticoid therapy
* abx for increased cough, sputum and purulence.
85
what antibiotics should be considered in acute COPD exacerbation
* marolide
* 2/3rd gen cephalosporin
* augmentin
* respiratory flouroquinolone
86
what is included in inpatient management of acute COPD exacerbation
* supplemental O2
* reverse obstruction (SABA +/- SAMA;systemic corticoseroids)
* IV abx - levaquin, ceftriaxone, or pip-taz
* initiate pulm rehab
87
what is the target O2 during inpatient management of acute COPD exacerbation
88-92%
88
when should you consider ICU admission for acute COPD exacerbation management
* severe dyspnea not responding to therapy
* mental status changes
* persistent/worsening hypoxia (pO2 <40 +/- respiratory acidosis)
* invasive mechanical ventilation needed
* hemodynamic instability
89
what is alpha-1 antitrypsin (ATT) and what is its role in the body.
a natural enzyme produced by the liver that migrates to the lungs through the blood.
protects the lungs from neutrophil (elastase) damage
90
when does ATT deficiency occur
when there is a genetic defect of ATT preventing its release from the liver
91
what are the two pathophysiological processes of ATT deficiency
* ATT deficiency in the lungs leads to loss of elastin in the alveolar wall and early onset emphysema
* An accumulation of ATT in the liver leads to destruction of hepatocytes and liver disease
92
how does ATT deficiency present
* emphysema symptoms at younger age
* symptoms of chronic hepatitis, cirrhosis, or hepatocellular carcinoma
* symptoms of panniculitis (inflammation of subcutaneous tissue)
93
what are symptoms of panniculitis
hot, painful, red nodules or plaques characteristically on the thigh or buttocks
94
what factors would suggest diagnostic testing for ATT deficiency
* <45 years old
* non smoker or minimal smoking (<10-15)
* FH of emphysema and/or liver disease
* adult onset asthma that doesn't respond to bronchodilators
* panniculitis or unexplained liver disease
95
what is the workup for ATT deficiency
low serum ATT levels (genetic testing needed to confirm phenotype)
PFT
CXR
96
how do you manage a patient diagnosed with ATT deficiency
* refer to specializing provider for possible infusion of donor ATT
* aggressive lifestyle modifications (smoking cessation, nutritional support)
* pharm, O2, and vaccinations as indicated for COPD
* prompt management of acute respiratory infections
* pulmonary rehab
97
what is bronchiectasis
an irreversible focal or diffuse dilation and destruction of the bronchial walls
98
what is the pathophysiology of bronchiectasis
* infectious insult in addition to impaited draining / obstruction and impaired host defense (often a result of recurrent inflammation or infection of airway)
* leads to inflammation, mucosal edema, cratering, ulceration, and neovascularization of the airway.
99
what is the presentation of bronchiectasis
* chronic daily productive cough of copious foul smelling thick purulent sputum
* rales/rhonchi/wheezing
* acute exacerbations with increased sputum volume and purulence
100
why is a CXR ordered in bronchiectasis, what would it show?
CXR to rule out pneumonia.
may see "tram tracks" and reflected dilated airways
101
what would a CT show in bronchiectasis
bronchial wall thickening and dilated airways with a ballooned or "honeycomb" appearance
102
what labs/assessments should be ordered to evaluate bronchiectasis and why
sputum culture - directs abx therapy in infectious exacerbations
bronchoscopy - assess for underlying amss or foreign body in focal disease
103
what is the treatment for bronchiectasis
non pharm management as COPD
empiric abx for acure exacerbations (amox, augmentin, doxy, bactrim)
bronchial hygiene
surgical resection
lung transplant
104
when is surgical resection and lung transplant indicated in bronchiectasis
resection - poorly controlled focal disease
lung transplant - indicated when FEV1 <30% predicted
105
what is included in bronchial hygiene
mucolytic therapy
bronchiodilators
chest physiotherapy
106
what are the common demographics for obstructive sleep apnea
MC in asians, african americans, males and obese people.
107
what are risk factors for OSA
* Increasing age, male, obesity, smoking, craniofacial or upper airway abnormalities
* Comorbid conditions such as pregnancy, ESRD, CHF, COPD, hx of stroke (CVA)
108
what is the MC sleep related breathing disorder
OSA
109
what is OSA
recurrent, functional collapse of pharyngeal airway during sleep leading to reduced airflow leading to intermittent distrubances in gas exchange and fragmented sleep.
110
what is the clinical presentation of OSA
* signs of disturbed sleep
* daytime somnolence
* obstructive apnea, hypoapnea, or respiratory related arrousels.
111
what is the work up for OSA
* sleep apnea questionnaire
* in lab polysmography (sleep study) FIRST LINE
* home sleep apnea testing
* overnight oximetry
112
what is OSA diagnostic criteria
greater than 5 obstructive respiratory events (apneas ect. ) per hour of sleep plus one or more of the following:
1. sleeplessness/nonrestorative sleep/fatigue
2. waking w gasping/chokine
3. habitual snoring or breahting interuptions
4. HTN, mood disorder, cog dysfunction, CAD, CVA
ORRRR
greatter than 15 or more predominantly obstructive respiratory events per hour of sleep regardless of associated symptoms
113
what are goals of therapy in OSA
* reduce or eliminate apneas, hypoapneas or o2 desaturations during sleep
* improve sleep quality and daytime function
114
what is the management for OSA
* CPAP or APAP = mainstay
* oral appliances
* weight loss
* upper airway surgery
* hypoglossal nerve stimulation
