Asthma and COPD

Define asthma. Sx?

Chronic inflammatory disease of the airways causing variable, reversible airflow obstruction and airway hyperresponsiveness. Sx=dyspnea, wheezing, cough, chest tightness

What cytokines drive allergic (Th2) asthma?

IL‑4, IL‑5, IL‑13.

Major effector cells in allergic asthma?

Eosinophils, mast cells, B cells (IgE).

What immunoglobulin is central to allergic asthma?

IgE.

What is airway remodeling in asthma?

Smooth muscle hypertrophy/hyperplasia, goblet cell hyperplasia, basement membrane thickening, angiogenesis, narrowed lumen.

What causes wheezing in asthma?

Turbulent airflow through narrowed small airways.

What is reversible obstruction?

FEV1 or FVC increases ≥10% after SABA(short acting beta agonist).

Name sputum findings in asthma.

Curschmann spirals, Charcot‑Leyden crystals, Creola bodies.

What are Curschmann spirals?

Mucus plugs from epithelium.

What are Charcot‑Leyden crystals?

Eosinophil breakdown crystals.

What are Creola bodies?

Desquamated epithelial cells.

What is status asthmaticus? SX? Tx?

Life‑threatening asthma exacerbation unresponsive to bronchodilators.

Sx: tachypnea, hypoxemia, silent chest, cyanosis

Tx: Bronchodilation, systemic steroids, O2

What is pulsus paradoxus?

Drop in SBP >10 mmHg during inspiration.

Aspirin‑induced asthma mechanism.

COX‑1 inhibition → ↓PGE2(PGE normally increases cAMP»bronchodilation)→ ↑leukotrienes → bronchoconstriction.

Triad of aspirin‑induced asthma.

Asthma, nasal polyps, NSAID sensitivity.

First‑line rescue therapy for asthma.

SABA (albuterol).

First‑line maintenance therapy for asthma.

Ihaled corticosteroid (fluticasone, budesonide, etc.).

Why is LABA monotherapy contraindicated in asthma?

Increases mortality because only treating bronchioles and arent doing anything to reduce inflammation that will eventually destroy the airway

Name leukotriene modifiers.

Montelukast, zafirlukast, zileuton.

Biologic for IgE‑mediated asthma.

Omalizumab (IgE antagonist)

Biologics targeting IL‑5.

Mepolizumab, reslizumab, benralizumab. (Liz is in fam of 5)

Biologic targeting IL‑4/IL‑13.

Dupilumab.

Non‑allergic asthma effector cells.

Neutrophils (Th1/Th17‑driven).

COPD definition.

Chronic, persistent, progressive airflow obstruction due to chronic inflammation from noxious particles.

Major COPD phenotypes.

Chronic bronchitis and emphysema.

Major effector cells in COPD.

Neutrophils, macrophages, CD8+ T cells.

Pathophysiology of chronic bronchitis COPD.

Goblet cell hyperplasia, mucous gland enlargement, impaired ciliary function.

Reid index definition Associated with?

Ratio of mucous gland thickness to wall thickness. Chronic Bronchitis

Chronic bronchitis (BB) clinical features.

Productive cough ≥3 months/year for ≥2 years, cyanosis, obesity, cor pulmonale(right heart failure). BLUE BLOATER

Why are chronic bronchitis patients “blue bloaters”?

Hypoxemia → cyanosis, Volume overload from right heart failure

Emphysema definition (PP)

Destruction of alveoli, alveolar ducts, respiratory bronchioles → loss of elastic recoil. PINK PUFFERs= hyperventilation and less hypoxemia

Why are emphysema patients “pink puffers”?

Hyperventilation maintains near‑normal oxygenation

Compliance in emphysema.

Increased (loss of elastic fibers).

DLCO in emphysema.

Decreased (loss of capillary beds).

Centrilobular emphysema cause.

Smoking.

Centrilobular emphysema location.

Upper lobes.

Panlobular emphysema cause.

Alpha‑1 antitrypsin deficiency.

Panlobular emphysema location.

Lower lobes.

A1AT deficiency pathophysiology.

(A1AT is a proteasome inhibitor there for deficiency)=Unopposed neutrophil elastase → destruction of elastic fibers → emphysema + cirrhosis.

Non‑pharmacologic COPD therapy.

Smoking cessation, pulmonary rehab, vaccines, oxygen, LVRS.

COPD Exacerbation Tx

Steroids, antibiotics, bronchodilators

Hyperinflation on CXR.

Flattened diaphragm, increased AP diameter.

What is barrel chest?

Increased AP diameter due to hyperinflation.