L10 COPD Flashcards
small airway disease leads to
airway inflammation and remodeling
parenchymal destruction leads to
loss of alveolar attachments
decrease of elastic recoil
thick, sticky mucus is more associated with
obstructive bronchitis
air becoming trapped in damaged alveoli and air exchange becoming difficult is more associated with
emphysema
blue bloaters have
chronic bronchitis
pink puffers have
emphysema
chronic bronchitis presents more with
hypoxemia respiratory acidosis cor pulmonale from pulmonary hypertension chronic bacterial colonization airway hyper-reactivity
chronic bronchitis is defined as
chronic productive cough for 3 or more months during 2 consecutive years with no other cause
structural changes that occur with chronic bronchitis
mucous gland enlargement causes hypersecretion
bronchial squamous metaplasia
loss of ciliary transport
inflammation in chronic bronchitis is mediated by
neutrophils
due to chronic bacterial colonization
presents with inspiratory and expiratory obstruction
chronic bronchitis
impeded ventilation in chronic bronchitis results in
hypoxemia
hypercapnia
has more parenchymal damage
emphysema
destruction of the alveolar walls in emphysema leads to
pathologic enlargement of the air spaces distal to the terminal bronchioles
2 possibilites for alveolar destruction in emphysema
- too much elastase
2. too little antitrypsin
protease enzyme secreted by neutrophils and macrophages during inflammation, destroys bacteria and host tissues
neutrophil elastase
inhibits neutrophil elastase
alpha-1 antitrypsin
loss of alveolar supporting structure leads to
airway narrowing
compressed ducts
presents with expiratory airflow obstruction
emphysema
when is hypoxemia present in emphysema
later in disease
destruction of capillary bed leads to reduced DLCO
asthma is mediated by
eosinophils
what cigarette smoking do
stimulates elastase
releases cytotoxic oxygen radicals from WBCs in lung tissye
classic presentation of COPD
dyspnea
cough
sputum production
most common symptom of COPD
dyspnea on exertion
physical exam findings of COPD
tripod positioning cyanosis tobacco staining of fingers JVD accessory muscle use pursed lip breathing
for some reason Ms. Shamblen seemed to really care about this finding
tobacco staining of fingers
how does pursed lip breathing help in emphysema
resistance to outflow raises intrabronchial pressure keeping the bronchi open longer to expel more air
lung findings in COPD
barrel chest (increased AP diameter) prolonged expiration increased resonance decreased breath sounds wheezing crackles at bases
heart findings in COPD
S3 gallop
RV lift
abdominal findings in COPD
hepatomegaly
extremities findings in COPD
muscle wasting
peripheral edema
cor pulmonale is
pulmonary hypertension resulting in impaired right ventricle dysfunction
what’s unique about cor pulmonale
it’s right ventricle dysfunction (hypertrophy, dilation) that ISN’T caused by left ventricle dysfunction
required for diagnosis of COPD
spirometry
why are other labs done with COPD if spirometry is the diagnostic measure
to rule out other causes o dyspnea and comorbid diseases
spirometry consistent with obstructive pattern
FEV1/FVC
other lung test findings with COPD
increased total lung capacity
severe emphysema will have
decreased diffusing capacity of carbon monoxide
why do you do a CBC
rule out anemia
seen on CBC of chronic bronchitis
polycythemia
secondary to chronic hypoxia
may be seen on CBC during acute exacerbations of CBC
leukocytosis
when to assess pulse ox (SpO2) further when
and with what
SpO2 <92%
arterial blood gas (PaO2)
PaO2 will probs show
mild/moderate hypoxemia without hypercapnia
severe disease: hypercapnia causing respiratory acidosis
when to obtain a sputum culture
in patient unresponsive to initial antibiotic treatment
what might be found on EKG
tachycardia
right atrial enlargement
right axis deviation and/or right ventricular hypertrophy
CXR will show
signs of air trapping (increased AP diameter, hyperinflation, hyperlucency, flat diaphragms)
blebs or bullae
CXR of chronic bronchitis
cardiac enlargement
pulmonary congestion
+/- perivascular or peribronchial markings
pathognomonic for emphysema
blebs/bullae
CXR findings suggestive of emphysema
hyperinflation +/- bullae
flattening of diaphragms
enlargement of retrosternal air space
when to get a chest CT
symptoms suggest a complication of COPD (pneumonia, pneuomothorax, large bullae)
rule out alternate diagnosis (PE)
when to get a high resolution CT
considering lung volume reduction surgery
what’s the main goal of COPD management
prevent progression
group A tx
short acting bronchodilator
-or-
SABA + SAMA combo
PRN
group B tx
long acting bronchodilator (LAMA or LABA)
group C tx
LAMA
group D tx
LABA + LAMA
-or-
consider ICS + LABA
albuterol is a
short acting beta agonist bronchodilator (SABA)
2 puffs q4-6 hours
salmeterol is a
long acting beta agonist bronchodilators (LABA)
q12 hours
side effect of B2 agonists
****** palpitations tachycardia insomnia tremors ******
side effects of anticholinergic bronchodilators
dry mouth
metallic taste
headache
cough
ipratropium bromide
irpatropium + albuterol
short acting anticholinergic (SAMA)
2 puffs BID-QID
the BA in SABA/LABA is
beta agonist
the MA in SAMA/LAMA is
muscarinic antagonist (idk why they’re called anticholinergics in the lecture just to make it more confusing)
tiotropium bromide
long acting anticholinergic (LAMA)
once daily
what are anticholinergics good at
reduce air trapping
less cardiac stimulation
whats the newest combo med for COPD tx
LAMA + LABA
theophylline is
a methylxanthine
old drugs for COPD, not used much due to side effects, toxicity, drug-drug interactions
when to use theophylline
refractory COPD
Umeclidinium
long acting anticholinergic (LAMA)
once daily
formoterol is a
long acting beta agonist bronchodilators (LABA)
q12 hours
advair
inhaled corticosteroid
dulera
inhaled corticosteroid
symbicort
inhaled corticosteroid
breo ellipta
inhaled corticosteroid
corticosteroids MOA
inhibit prostaglandins –> reduced mucosal edema/inflammation –> decreased secretions
corticosteroids side effects
oral candidiasis
bruising
alpha 1 antitrypsin deficiency is defined as
serum levels <11 uM
alpha 1 antitrypsin deficiency controversial tx
antiprotease replacement injections weekly/monthly
gold stage B-D should also get
pulmonary rehab
give O2 when
to reach the goal of
for how long
chronic dyspnea at rest
SpO2 > 90% all the time
12+ hours a day
caution with O2 therapy
how to prevent it
high flow O2 may reduce drive to breath, causing respiratory acidosis
maintain O2 90-92%
educate COPD pts to
recognize early signs of pulmonary infection
early signs of pulmonary infection
increased sputum production fever worsening dyspnea chest pain hemoptysis
what is
increased dyspnea
increased cough frequency/severity
increased or purulent sputum
acute exacerbation of COPD
acute exacerbation of COPD is triggered by
respiratory illnesses (usually VIRAL) pollution
viral triggers of acute exacerbation of COPD
rhinovirus
influenza
may lead to secondary bacterial pneumonia
most common bacterial pathogens in acute exacerbation of COPD/secondary bacterial pneumonia (unclear which she meant)
H influenzae S pneumoniae Moraxella cararrhalis Mycoplasma pneumoniae Pseudomonas aeruginosa
starred bacterial pathogen
pseudomonas aeruginosa
treatment of acute exacerbation of COPD
increase dose of SABA can add ipratropium to regimen Oral steroids (40 mg/day x 5 days)
treatment of moderate/severe acute exacerbation of COPD
antibiotics:
Macrolide (azithromycin, clarithromycin)
Fluoroquinolone (moxifloxacin, gemifloxacin, levofloxacin)
treatment of severe acute exacerbation of COPD
hospitalization
indications to hospitalize
severe signs/symptoms severe underlying COPD (FEV1 <50%) significant comorbities onset of new physical symptoms (cyanosis, edema, arrhythmias) failure to respond to initial meds older age insufficient home support
