Obstructive Lung Diseases Flashcards
1
Q
Lab tests of obstructive lung disease
A
- Greatly decreased FEV1
- Decreased or normal FVC
- Decreased FEV1/FVC ratio ( < 0.7)
- Increased Residual Volume (RV)
- Increased Total Lung Capacity (TLC), due to increased residual volume
2
Q
Clinical Presentations of COPD - The Blue Bloater (Type B)
A
- Bronchitic” phenotype
- Long history of cough and sputum production
- Frequent exacerbations
- Less dyspnea
- Chronic hypoxemia
- Pulmonary hypertension
- Cor pulmonale – an alteration in the structure and function of the right ventricle (RV) of the heart caused by a primary disorder of the respiratory system
- Right-sided heart failure
- Normal habitus or obese
3
Q
Clinical Presentations of COPD - The Pink Puffer (Type A)
A
- “Emphysematous” phenotype
- Long history of exertional dyspnea
- Little sputum
- Infrequent exacerbations
- Hyperinflation
- Use of accessory muscle
- Pursed-lips breathing
- Normal oxygenation
- Thin; weight loss a problem
4
Q
Pathogenesis of Emphysema
A
- Smoke Induced Inflammation Drives Alveolar Destruction
- Synergistic with respiratory infections
- Neutrophilic inflammation
- Chemokines for neutrophils, e.g. interleukin-8
- Triggers an imbalance of proteases and antiproteases
- Steroid resistant
5
Q
mechanisms of airway obstruction in chronic bronchitis
A
- Intralumenal blockage (usually excessive secretions); lumen smaller
- Edema, inflammation, hypertrophy
6
Q
Lung Volumes in Asthma
A
- Typically no change in mild asthma
- Increased RV in more severe or acute disease (premature airway closure); See increase in residual volume as asthma severity increases
- FRC and TLC are usually normal, but, in more severe asthma, loss of lung elastic recoil may occur with increased TLC
7
Q
Asthma therapy as it related to the asthma cascade
A
8
Q
Asthma triggers
A
- Allergen exposure
- Viral infections
- Exercise
- Occupational exposure
- Medications
- Circadian variation (night time-sleep)
9
Q
Complications of COPD - Pulmonary Artery Hypertension
A
- predominately the result of alveolar hypoxia and resultant vasoconstriction other contributors:
- vascular bed obliteration (emphysema)
- increased blood viscosity (erythrocytosis) – thicker blood harder to get through capillaries
- compensatory right ventricular hypertrophy right ventricular failure (cor pumonale)
- peripheral edema
- jugular venous distention
- primary treatment is O2 supplementation
10
Q
Where is the obstruction?: smooth muscle hypertrophy
A
terminal bronchioles; asthma
11
Q
Airway Obstruction in Asthma
A
- Best defined by low FEV1/FVC,
- Can also have low PEFR, FEF 25-75)
- Obstruction is typically reversible (12% increase in FEV1 in response to inhaled bronchodilator = diagnostic); using albuterol to see if patient has asthma
- It is common to have normal lung function in between acute attacks
- Airway resistance is increased when obstruction is present
- Reversibility may not always result in normal lung function; can lose the reversibility over time
12
Q
Treatment of Asthma
A
Goals
- Control attacks
- Prevent attacks
- Restore normal lung function
Tools
- Medications
- Environmental control – removing triggering allergen
- Patient education
13
Q
potential protective factors of rural life
A
- Contact with animals
- Exposure to high levels of endotoxin (LPS)
- Activates innate immune responses (IL-10, IFN-γ)
- Early exposure to bacterial products – The “Microbiome” (being researched)
14
Q
Airway Remodeling in Asthma
A
- Structural airway changes in asthma include subepithelial fibrosis, increased smooth muscle mass, new vessel formation and mucus gland hyperplasia
- Remodeling can cause airway obstruction, lack of reversibility, disease progression and morbidity
- Smooth muscle hypertrophy and hyperplasia
- Submucosal gland hypertrophy → causes mucous plugging
- Basement membrane fibrosis/thickening → as a result of collagen deposition
- ↑ vascularity
- Inflammatory infiltration → most commonly eosinophils
15
Q
The Asthmatic Inflammatory Cascade
A
- Inflammatory Stimuli
- Cell Activation/Mediator Release
- Bronchial epithelial cells + dendritic cells
- T-cells
- Eosinophils
- Mast cells
- Asthmatic Inlammation
- Smooth muscle hypertrophy, bronchial hyperresponsiveness
- Clinical asthma
16
Q
Dose-Response Curves of Methacholine Challenge: healthy vs. asthma
A
- No change in normal person
- Look at “PC 20”: provocative concentration producing 20% fall in FEV1
17
Q
Eicosanoids in Asthma
A
- = 20 carbon, polyunsaturated fatty acids
- Most commonly derived from phospholipase-A2 activity on membrane phospholipids producing arachadonic acids
- Several subfamilies: prostaglandins, thromboxanes, leukotrienes, lipoxins, resolvins and eoxins
- PGD2 and cysteinyl-leukotrienes contribute to bronchoconstriction
- Enzymatic modification of cyclo-oxyganase by aspirin, NSAIDS
- Receptor antagonism by fevipiprant and montelukast respectively
18
Q
Where is the obstruction?: incomplete formation or degradation of cartilage rings, floppy airways
A
tracheomalacia or bronchomalacia (trachea or bronchi)
19
Q
examples of things that can lead to COPD
A
asthma, cystic fibrosis, bronchiectasis
20
Q
Diffusion impairment in emphysema
A
- Decreased alveolar surface area
- Decreased elastic recoil
- Increased alveolar gas volume
- Fewer capillaries
21
Q
histology of chronic bronchitis
A
- huge expansion of submucosal gland layer in patient with chronic bronchitis vs. a normal patient
22
Q
Emphysema
A
- destructive process of elastic fibers involving lung parenchyma defined anatomically
- Hard to diagnose clinically; need histology or CT scan
- destruction of alveolar walls and loss of associated capillaries
- enlargement of airspaces distal to terminal bronchioles
- universally present in advanced COPD
