Clin Med: Asthma and Chronic Obstructive Pulmonary Disease Flashcards
Where does gas exchange happen?
Alveoli
Asthma is
bronchial wall hyperresponsiveness and airway inflammation
two types of asthma
extrinsic and intrinsic
Extrinsic asthma is
allergic - most common
environmental vs animal allergens
Intrinsic asthma is
occupational/ pollution
cold/ humidity
stress
medications: ASA or NSAIDS
Exercise
Extrinsic Asthma pathophysiology
IgE mediated
History of _______ as a child will increase risk of developing asthma
Seasonal allergies with rashes as a child
Eczema
Step 1 management (intermittent)
SABA
ICS at beginning of infection
Step 2 management (Mild persistent)
SABA
Daily low dose ICS
alternative moteleukast
Step 2 management (mild persistent)
SABA
daily ICS
alternative moteleukast
Step 3 management (Moderate persistent)
SABA
daily ICS/LABA (combo)
Montelukast
or daily medium dose ICS
Step 4-5 management (severe persistent)
Step 4:
SABA
medium combo (ICS/LABA)
daily medium dose moteleukast
Step 5:
daily high dose ICS with LABA
daily high dose ICS with montelukast
may consider omalizumab
steroids - prednisone
Asthma risk reduction
avoid triggers
allergens - allergy meds, flonase, 1st gen antihistamines, washing face and hands
Medication management
Asthma action plan
Bronchiectasis is
irreversible inflamed and easily collapsible airways
affects medium sized bronchi and bronchioles
airways become wide (dilated) causing excess mucus
Everyday asthma
moderate persistent asthma
1-2 times a week but not everyday asthma
mild persistent asthma
a couple times per day everyday
severe asthma
Bronchiectasis presentation
chronic cough*
malodorous thich, mucopurulent*
pleuritic chest pain
digital clubbing
fever/chills
SOB
Gold standard testing for Bronchiectasis
CT scan
Best testing for bronchiectasis
bronchoscopy
assess for obstructing lesions
sputum studies are negative
can take samples
Treatment for bronchiectasis
treat and control recurrent infections
treat underlying disease
SABA and combo inhalers
duonebs (albuterol/ atrovent)
surgery (severe cases)
Bronchiectasis exacerbation treatment
antibiotics
fluoroquinolones: levofloxacin (pseudomonas coverage)
amoxicillin or augmentin
macrolides: azithromycin
parental:
ampicillin
vancomycin (concern for MRSA)
zosyn (pseudomonas coverage)
Bronchiolitis is
inflammation of the bronchioles
Types of bronchiolitis
acute - most common - pediatric pts - RSV, in adults mycoplasma
Bronchiolitis Obliterans (Constrictive) - toxic fumes - ‘popcorn lung’
Proliferative - cryptogenic (not a bacterial infection - chemical exposure, bird exposure)
Follicular - Rheumatic diseases, HIV, hypersensitivity pneumonitis
Bronchiolitis ssx
upper respiratory sxs
fever
wheezing
tachypnea
shallow respirations - rhinorrhea for kids
poor appetite
Bronchiolitis workup
CXR
nasal viral panel
PFTs
biopsy
Treatment of Acute Bronchiolitis
supportive therapy
parent education - suctioning of the nose
peaks 3-5 days
Treatment of Severe Bronchiolitis
supportive care
respiratory support - nasal suctioning, O2 prn
Trial - bronchodilator, sometimes it doesn’t work
glucocorticoids
CPAP for risk of resp failure
intubation for resp failure
COPD consists of
chronic bronchitis
emphysema
chronic obstructive asthma
Blue bloaters =
Chronic bronchitis
Pink puffers =
Emphysema
Ssx of COPD
cough
persistent progressive dyspnea (worse with exertion)
CO2 retention (chronic bronchitis)
weight loss (emphysema)
tachycardia
HTN
barrel chest (emphysema)
wheezes and crackles
Chronic bronchitis ssx
chronic productive cough for 3 or more months in 2 or more successive years
CO2 retention
more likely to be obese
cyanotic, reduced respiratory drive, hypoxic
Emphysema ssx
wt loss
hunched over, tripoding
dyspneic with prolonged expiration
permanent enlargement of alveoli - impaired gas exchange
COPD group A treatment
SABA or LABA
COPD group B treatment
LABA or LAMA
consider SABA and LABA
COPD group C treatment
add LAMA
COPD group D
LAMA or
LAMA and LABA or
ICS and LABA
treatment and education for COPD
stop smoking
exercise
health maintenance
antibiotics +/- oral steroids for exacerbation
Supplemental O2
Cystic fibrosis is a
mutation in the CFTR gene (CF transmembrane conductance regulator) - channel that transports chloride
The CFTR mutation causes
buildup of thick mucus in organs that contain mucus membranes
CF gold standard testing
Sweat chloride testing - sweat is collected and weighed/ analyzed for chloride
Definitive dx testing for CF is
genetic testing
CF treatment
inhaled dnase
Chest physiotherapy
Percussive vests
exercise
prevention of infections - immunization (not live)
bronchodilators
anti inflammatory/ bacterial prophylaxis
CFTR modulators
