Asthma/COPD
meds ending in -ide or -sone and what's the MOA and name one AE
Inhaled corticosteroids (-ide or -sone) MOA – anti-inflammatory; blocks late rxn to allergen and reduces airway hyperresponsiveness; inhibits cytokine production, adhesion, protein activation, inflammatory cell migration/activation; reverse beta 2 down regulation; inhibits microvascular leakage
AE: cough, dysphonia, candidiasis (may need spacer and rinsing mouth), pna
meds ending in -terol and MOA and name a major AE
Beta 2 agonists (-terol) MOA: relaxes smooth muscle (stimulation of b2 adrenergic receptors -> increases cyclic AMP -> antagonizes bronchoconstriction)
SABA (albuterol or levabuterol only) = 4-6 hrs; LABA = 12+ hrs
AE: tremors, hypokalemia
leukocytosis seen in Type 2 high vs Type 2 low asthma
Type 2 High - more eosinophilic
Type 2 Low – more neutrophilic
aside from monetleukast, what is another obstructive disease med that needs to be avoided in Pts with Hx of depression/suicide?
roflumilast (PDE 4 inhibitor)
meds ending in -ium and MOA and AE
Antimuscarinics (-ium) MOA: block bronchoconstrictor effects of acetylcholine on M3 receptors => bronchdilation
SAMA (ipratropium), rest are LAMA
AE: dry mouth, bitter, metallic taste
which is characterized as having alveolar damage and which has no damage to alveoli? copd or asthma
no damage = asthma
damage = copd
COPD short term exacerbations how do you treat
Oral glucocorticosteroids 5-7 days; NO role in daily or long-term management
SABA +/- SAMA via nebulizer or inhaled
Systemic corticosteroids if severe but no more than 5 days
Abx not really recommended -> azithro or erythron do have anti-inflammatory properties
Noninvasive mechanical ventilation
Atelectasis - mediastinum shifts away or towards affected lung? (or stays midline)
Mediastinum shifts AWAY from affected lung
asthma exacerbations how do you treat mild/moderate vs severe and life threatening
Mild to moderate: SABA, prednisone, oxygen
Severe and life threatening or if mild/moderate worsens: treat at acute care facility (nebulized albuterol + ipratium; systemic corticosteroids; magnesium; oxygen)
when is oxygen indicated for COPD tx
pls dont hate me i literally dont know i think RA < 90% ??
Differentiate Chronic Bronchitis vs Emphysema
Chronic bronchitis: small airway disease
Productive cough for ≥ 3 mo/yr x 2 consecutive yrs, after excluding other causes -> inflammation + fibrosis + mucus hypersecretion
*airway narrowing and mucus secretion* impaired ventilation and V/Q mismatch
Emphysema – alveolar destruction
Increased protease activity = alveolar destruction + loss of elastic recoil -> expiratory airway collapse and air trapping and impaired gas exchange
Spirometry after bronchodilator use - what do you expect to see in asthma vs COPD?
asthma = improvement
COPD = Persistent post bronchodilator airway obstruction
Imaging signs of atelectasis
Nonspecific imaging signs, most specific sign is displacement of fissures (fissures indicate loss of lung volume)
Aggressive neuroendocrine carcinoma. Rapid growth, early spread, systemic tx, high recurrence risk. Frequently associated w paraneoplastic syndromes and smoking. 10-15% of lung cancers fall into this category
Small Cell Lung Cancer (SCLC)
hazy opacity w preserved underlying vascular markings; slow growing; think inflammation, infection, or early adenocarcinoma-spectrum lesion
ground glass nodule
What does a Plethysmography tell you
severity of copd
common comorbidity with copd (castorina emphasized this)
depression co-morbidity
mc lung cancer in women and never-smokers. may cause pleural retraction or “puckering” of overlying pleura due to associated fibrosis
40% of lung cancers. Arises from gland-forming or mucin-producing epithelial cells; often associated w type II pneumocyte or club-cell differentiation
Adenocarcinoma (type of NSCLC)
Gradually progressive dyspnea, chest pain or discomfort, wt loss, fatigue, recurrent unilateral pleural effusion.
Strongly associated w asbestos exposure (often 20-50 yrs after exposure; long latency period). Mc in older adults and men. Smoking not a RF
Malignant Mesothelioma
pulm fibrosis associated w inhalation of asbestos fibers, typically after long latency (15-20 years after exposure). on imaging, predominantly basilar/subpleural fibrosis (pleural plaques). progressive exertional dyspnea and dry cough, bibasilar inspiratory crackles, restrictive physiology and reduced DLCO
Asbestosis
walk us through GOLD ABE for COPD Groups A, B, E initial Tx
Group A = bronchodilator (alter airway smooth muscle tone; widening airways -> beta 2 agonists -erol OR antimuscaarinics -ium)
Group B = LABA + LAMA (-erol + -ium)
Group E = LABA + LAMA and consider ICS if ≥ 300 blood eos but never if < 100
walk us through the preferred GINA step up for asthma starting at steps 1-2
Track 1 GINA step up preferred: AIR-only (prn ICS-formoterol) -> MART (scheduled w low dose maintenance ICS-formoterol) -> MART w medium “ may consider prednisone course -> add LAMA, consider high dose maintenance and/or biologic
cardinal sx of hypercapnia (there's 2)
Dyspnea and headache
only type of atelectasis that is nonreversible
Contraction Atelectasis
Medication and infection-related ILD - what is the most common med that causes this AND is it restrictive or obstructive AND is it reversible
AMIODARONE; restrictive; irreversible fibrosis (progressive)