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Clin Med B 2 > COPD > Flashcards

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.

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2
Q

what are the two pathophysiologic categories of COPD

A

chronic bronchitis
emphysema

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3
Q

what are the key physiological markers of COPD

A

airflow obstruction and extensive airway destruction

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4
Q

what are the three classic respiratory symptoms of COPD

A

cough
dyspnea (SOB)
sputum production

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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

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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
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7
Q

what are risk factors for COPD

A

Fam Hx
smoking hx
environmental hx (exposure)
childhood pulmonary infections, HIV, or TB
asthma

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8
Q

How does mild COPD present

A

PE - mostly normal
may see:
prolonged expiration
faint end-expiratory wheeze w forced expiration

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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

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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
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11
Q

what are signs of heavy smoking

A

yellowing of fingers/nails

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12
Q

what is the comparison between presentations of chronic bronchitis v emphysema

A
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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
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14
Q

what are the 5 CAPTURE questions

A
  1. have you ever lived or worked in a place with dirty/polluted air, second hand smoke or dust
  2. does your breathing change with seasons, weather, or air quality
  3. does your breathing make it difficult to do things such as carry heavy loads, shovel dirt/snow, ect.
  4. compared to others of your age, do you tire easily
  5. 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)
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15
Q

what CAPTURE scores are indicative of clinically significant COPD

A

2-4

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16
Q

what is the initial workup for COPD

A

spirometry before and after bronchodilator

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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

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18
Q

what spirometry results suggest evidence of obstruction

A

FVC > 80% with FEV₁/FVC < 0.7
OR
FVC < 80% with TLC >80%

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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

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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)
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21
Q

what occurs to DLco in COPD

A

DLCO decreases in proportion to severity of disease

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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
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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

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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

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25
Q

is imaging needed to make COPD diagnosis

A

NO

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26
Q

what imaging can be CONSIDERED in evaluation of COPD

A

CXR and CT chest w/o

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27
Q

what are indications for imaging in COPD

A
  • Dyspnea/cough etiology is unclear
  • Rule out complicating process during acute exacerbations
  • Evaluate for comorbidities
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28
Q

what would a chronic bronchitis COPD chest X ray look like

A

X-ray likely to be normal unless complications or comorbidities are present

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29
Q

what would a emphysema COPD chest Xray look like

A
  • Hyperinflation
  • Flattened diaphragm
  • Increased retrosternal air space
  • Long, narrow heart shadow
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30
Q

what group determines staging in COPD

A

Global Initiative for Chronic Obstructive Lung Disease (GOLD)

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31
Q

what are the 3 dimensions of staging

A

Airflow limitations
Symptom severity
Exacerbations

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32
Q

what are the 4 stages of GOLD COPD airflow limitation staging

A
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33
Q

after GOLD category is determined, what isthe next step

A

determine symptom severity by using mMRC and CAT

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34
Q

what does Modified Medical Research Council Dyspnea Scale (mMRC) assess?

A

assesses severity of breathlessness

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35
Q

what does COPD assessment test (CAT) assess?

A

assesses multitude of symptoms present

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36
Q

what are the 4 steps of GOLD ABE assessment

A
  1. spirometry
  2. GOLD stage
  3. exacerbation hx
  4. mMRC or CAT
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37
Q

if a patient has FEV1 of 60%, 1 exacerbation, no hospitalizations, and an mMRC of 2 what is their COPD stage

A

GOLD 2B

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38
Q

if a patient has a FEV1 of 45%, 3 exacerbations, no hospitalizations and a CAT score of 13 what is thei COPD stage

A

GOLD 3E

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39
Q

what are goals of COPD management

A

improve symptoms
decreased number of exacerbations
improve patient functioning

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40
Q

what is non-pharm COPD management

A
  • smoking cessation
  • behavioral counsleing
  • vaccinations
  • adequate nutrition
  • regular exercise
  • oxygen therapy
  • pulmonary rehab
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41
Q

what vaccinations should you suggest to COPD patients

A
  • Influenza
  • COVID-19
  • PCV-20 OR PCV-13 followed by PCV-23
  • Tdap
  • Zoster in patients >50
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42
Q

how does adequate nutrition affect COPD

A
  • obese patients can improve dyspnea and exercise tolerance by losing weight
  • Vitamin D deficiency is associated with reduced lung function and increased COPD exacerbation
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43
Q

when is oxygen therapy indicated in COPD management and why

A
  • 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

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44
Q

When is pulmonary rehabilitation indicated

A

for COPD class B and E

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45
Q

what are the components of pulmonary rehabilitation therapy

A
  • exercise training
  • promotion of healthy behaviors (smoke cessation, exercise, nutrition, med use, self managment ect)
  • psychological support (coping strategies for chronis illness)
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45
Q

what are the short acting bronchidilator pharm cattegories

A

short-acting beta agonists (SABA)
short acting muscarinic antagonists (SAMA)

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46
Q

what are the long-acting bronchodilator pharm categories

A
  • Long-acting Beta Agonists (LABA)
  • Long-acting Muscarinic Antagonists (LAMA)
47
Q

what are the SABAs

A

albuterol, levabuterol

48
Q

what are the SABA SE

A
  • Tachycardia
  • Tremor
  • Cardiac arrhythmia
49
Q

what are teh SAMA meds

A

Ipratropium Bromide

50
Q

what are the SAMA SE

A
  • Dry mouth / eyes
  • metallic taste
  • prostatic symptoms
51
Q

what is the SAMA + SABA combo med

A

albuterol + ipratropium

52
Q

what are the LABAs

A

arformoterol
salmeterol
formeterol

53
Q

what are the LABA SE

A
  • tahcycardia
  • tremor
  • HA
54
Q

what are the LAMA meds

A

QD
tiotropium
umeclidinium
revefencin

BID
aclidinium
glycopyrrolate

55
Q

what are the LAMA SE

A
  • Dry mouth
  • Constipation
  • urinary retention
56
Q

what are the LAMA+LABA combo

A

QD
Olodaterol /Tiotropium
Vilanterol/Umeclidinium

BID
Formoterol/Glycopyrrolate
Formoterol/Aclidinium

57
Q

what are the LABA+ICS combo

A

Salmeterol/Fluticasone propionate
Vilanterol/Fluticasone furoate
Formoterol/Budesonide

58
Q

what are the LABA+LAMA+ICS combos

A
  • Fluticasone furoate/Umeclidinium/ Vilanterol
  • Beclometasone/Formoterol/ Glycopyrronium
  • Budesonide/Formoterol/ Glycopyrrolate
59
Q

what is initial pharm management for group E

A

LABA+LAMA

consider LAMA+LAMA_ICS if blood eosinophils >300

60
Q

what is initial pharm management for group A

A

bronchodilator

61
Q

what is initial pharm management for group B

A

LAMA + LABA

62
Q

what are factors that suggest you SHOULDN’T use an ICS with long acting bronchodilators

A
  • repeated pneumonia events
  • blood eosinophils <100
  • hx of mycobacterial infection
63
Q

what are factors that suggest you could use an ICS with long-acting bronchodilators

A
  • 1 moderate exacerbation of COPD per year
  • blood eosinophils 100 to <300
64
Q

what are factors that strongly favor the use of ICS in addition to long acting bronchodilators

A
  • Hx of hospitalizations for exacerbations of COPD
  • > 2 moderate exacerbations of COPD per year
  • blood eosinophils >300
  • history of concomitant asthma
65
Q

if a patient is on an ICS, when is removal indicated?

A
  • 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
Q

what are the two medications that we use for severe COPD

A

roflumilast and theophylline

67
Q

what is the class and MOA of roflumilast

A
  • PDE-4 inhibitor
  • suppresses cytokine release and inhibits pulmonary neutrophil infiltration which reduces inflammation, pulmonary remodeling and mucociliary malfunction
68
Q

what is the class and MOA of theophyline

A
  • non-specific PDE inhibitor
  • relaxes smooth muscle → suppresses airway response to noxious stimuli → increased diaphragm contraction force
69
Q

what is the indication for roflumilast

A

reduce exacerbations in severe COPD

70
Q

what is the indication for theophyline

A

refractory COPD

71
Q

what are the SE of roflumilast

A

psych - anxiety, depression, insomnia
GI - NVD, weight loss, dyspepsia

72
Q

what group should you avoid prescribing roflumilast to

A

patients with a mental health history

73
Q

what are the SE of theophylline

A

anxiety
temors
insomnia
nausea
cardiac arrhythmias
seizures

74
Q

who should you avoid prescribing thephylline to

A

patients with liver impatiemment

75
Q

how often should COPD patietns follow up?

A
  • 1-3 months following initial diagnosis and initiation of therapy
  • every 3-6 months once stabilized
76
Q

how often should spirometry be performed in a COPD patient

A

at least annually

77
Q

what are risk factor for acute COPD exacerbation

A

advanced age
chronic productive cough
duration of COPD
hx of prior abx therapy
COPD-related hospitalization
Comorbid conditions (CAD, CHF, DM)
respiratory infections

78
Q

what triggers 70% of COPD exacerbations

A

respiratory infections.

79
Q

what are historical and physical exam findings for an acute COPD exacerbation

A
  • worsening of respiratory symptoms over hours-days
  • wheezing and tachypnea
  • evidence of respiratory compromise
  • decreased mental status
80
Q

what is included in evidence of respiratory compromise

A
  • difficulty speaking due to respiratory effort
  • use of accessory respiratory muscles
  • paradoxical chest wall/abdominal movements
81
Q

what causes the decreased mental status during an acute COPD exacerbaiton

A

reflection of hypercapnia and hypoxemia

82
Q

what percent of acute COPD exacerbations can be managed outpatient

A

80%

83
Q

when should you consider inpatient management of Acute COPD exacerbations

A
  • 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
Q

what is included in outpatient management for acute COPD exacerbation

A
  • adjustment of bronchodilator therapy
  • consider spacers/nebulizer therapy
  • consider oral glucocorticoid therapy
  • abx for increased cough, sputum and purulence.
85
Q

what antibiotics should be considered in acute COPD exacerbation

A
  • marolide
  • 2/3rd gen cephalosporin
  • augmentin
  • respiratory flouroquinolone
86
Q

what is included in inpatient management of acute COPD exacerbation

A
  • supplemental O2
  • reverse obstruction (SABA +/- SAMA;systemic corticoseroids)
  • IV abx - levaquin, ceftriaxone, or pip-taz
  • initiate pulm rehab
87
Q

what is the target O2 during inpatient management of acute COPD exacerbation

A

88-92%

88
Q

when should you consider ICU admission for acute COPD exacerbation management

A
  • severe dyspnea not responding to therapy
  • mental status changes
  • persistent/worsening hypoxia (pO2 <40 +/- respiratory acidosis)
  • invasive mechanical ventilation needed
  • hemodynamic instability
89
Q

what is alpha-1 antitrypsin (ATT) and what is its role in the body.

A

a natural enzyme produced by the liver that migrates to the lungs through the blood.

protects the lungs from neutrophil (elastase) damage

90
Q

when does ATT deficiency occur

A

when there is a genetic defect of ATT preventing its release from the liver

91
Q

what are the two pathophysiological processes of ATT deficiency

A
  • 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
Q

how does ATT deficiency present

A
  • emphysema symptoms at younger age
  • symptoms of chronic hepatitis, cirrhosis, or hepatocellular carcinoma
  • symptoms of panniculitis (inflammation of subcutaneous tissue)
93
Q

what are symptoms of panniculitis

A

hot, painful, red nodules or plaques characteristically on the thigh or buttocks

94
Q

what factors would suggest diagnostic testing for ATT deficiency

A
  • <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
Q

what is the workup for ATT deficiency

A

low serum ATT levels (genetic testing needed to confirm phenotype)
PFT
CXR

96
Q

how do you manage a patient diagnosed with ATT deficiency

A
  • 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
Q

what is bronchiectasis

A

an irreversible focal or diffuse dilation and destruction of the bronchial walls

98
Q

what is the pathophysiology of bronchiectasis

A
  • 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
Q

what is the presentation of bronchiectasis

A
  • chronic daily productive cough of copious foul smelling thick purulent sputum
  • rales/rhonchi/wheezing
  • acute exacerbations with increased sputum volume and purulence
100
Q

why is a CXR ordered in bronchiectasis, what would it show?

A

CXR to rule out pneumonia.

may see “tram tracks” and reflected dilated airways

101
Q

what would a CT show in bronchiectasis

A

bronchial wall thickening and dilated airways with a ballooned or “honeycomb” appearance

102
Q

what labs/assessments should be ordered to evaluate bronchiectasis and why

A

sputum culture - directs abx therapy in infectious exacerbations
bronchoscopy - assess for underlying amss or foreign body in focal disease

103
Q

what is the treatment for bronchiectasis

A

non pharm management as COPD
empiric abx for acure exacerbations (amox, augmentin, doxy, bactrim)
bronchial hygiene
surgical resection
lung transplant

104
Q

when is surgical resection and lung transplant indicated in bronchiectasis

A

resection - poorly controlled focal disease
lung transplant - indicated when FEV1 <30% predicted

105
Q

what is included in bronchial hygiene

A

mucolytic therapy
bronchiodilators
chest physiotherapy

106
Q

what are the common demographics for obstructive sleep apnea

A

MC in asians, african americans, males and obese people.

107
Q

what are risk factors for OSA

A
  • Increasing age, male, obesity, smoking, craniofacial or upper airway abnormalities
  • Comorbid conditions such as pregnancy, ESRD, CHF, COPD, hx of stroke (CVA)
108
Q

what is the MC sleep related breathing disorder

A

OSA

109
Q

what is OSA

A

recurrent, functional collapse of pharyngeal airway during sleep leading to reduced airflow leading to intermittent distrubances in gas exchange and fragmented sleep.

110
Q

what is the clinical presentation of OSA

A
  • signs of disturbed sleep
  • daytime somnolence
  • obstructive apnea, hypoapnea, or respiratory related arrousels.
111
Q

what is the work up for OSA

A
  • sleep apnea questionnaire
  • in lab polysmography (sleep study) FIRST LINE
  • home sleep apnea testing
  • overnight oximetry
112
Q

what is OSA diagnostic criteria

A

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
Q

what are goals of therapy in OSA

A
  • reduce or eliminate apneas, hypoapneas or o2 desaturations during sleep
  • improve sleep quality and daytime function
114
Q

what is the management for OSA

A
  • CPAP or APAP = mainstay
  • oral appliances
  • weight loss
  • upper airway surgery
  • hypoglossal nerve stimulation

Clin Med B 2 (44 decks)

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