Obstructive Lung Diseases Flashcards
1
Q
list the obstructive lung diseases
A
- emphysema
- chronic bronchitis
- asthma
- bronchiectasis
2
Q
list the restrictive lung diseases
A
- acute restrictive disease
- ARDS
- chronic restrictive disease
- interstitial fibrosis
- pneumoconiosis
- granulomatous
- chest wall deformities
- neuromuscular
3
Q
summarize the differences between obstructive vs. restrictive diseases
A
4
Q
____ is a reversible anatomic airway narrowing,
while
_____ are irreversible.
A
asthma is a reversible anatomic airway narrowing,
while
CB, emphysema, bronchiectasis are irreversible.
5
Q
describe the structural change in emphysema
A
- abnormal permanent airspace enlargement distal to the terminal bronchioles accompanied by destruction of airspace walls without fibrosis
6
Q
describe the pathogenesis of emphysema
A
7
Q
describe genetic factors involved in emphysema
A
-
A1AT deficiency
- 1% of all emphysema
- Pi gene on chr. 14
- PiMM = normal, PiZZ = abnormal
- protein accumulates in the liver if abnormal
- chronic liver disease
- polymorphisms in TGFB gene
- polymorphisms in matrix metalloproteinases (MPPs)
8
Q
describe the centrilobular vs. panlobular forms of emphysema
A
-
centrilobular (centriacinar)
- smoking
- upper lung zones
- respiratory bronchioles is affected
-
panlobular (panacinar)
- A1AT deficiency
- lower lung zones
- acinus distal to RB is involved
9
Q
describe septal (distal acinar) vs. irregular (paracicatrical) forms of emphysema
A
-
septal (distal acinar) emphysema:
- rare
- next to atelectasis, along septa, margins of lobes, subpleural
- more common in upper lobes
- may form bullae
- can lead to pneumothorax
-
irregular (__paracicatrical__) emphysema
- surrounding scar
- asymptomatic
10
Q
describe the gross morphology of emphysema
A
-
gross
- hyperinflated lungs +/- bulla formation
- parenchyma has a “moth-eaten” appearance
-
histo:
-
destruction of alveolar septa without fibrosis
- free floating alveolar septa in air spaces
-
destruction of elastin within small airways
- aids in obstruction with exhalation due to airway collapse
-
destruction of alveolar septa without fibrosis
11
Q
describe what is seen in the image
A
emphysema
12
Q
describe the clinical presentation of emphysema
A
- clinical: “pink puffers”
- symptoms appear late (earlier if coexistent chronic bronchitis)
- barrel chest, dyspnea, prolonged expiration
- sitting in a forward hunched position trying to squeeze air out of the lungs
- x-ray: flat domes of diaphragm
- weak and skinny
- skinny because of excess puffing and panting due to hyperventilation
- blood gases normal until late with onset of hypoxia, hypercapnia and resp. acidosis
13
Q
chronic bronchitis is diagnosed when cough occurs ____ months in ____ years
A
chronic bronchitis is diagnosed when cough occurs in >3 consecutive months in >2 consecutive years
14
Q
describe the etiology of chronic bronchitis
A
- etiology:
- common among smokers and urban dwellers
- inhaled irritants: cigarette smoke, SO2, NO2
- can occur in conjunction with emphysema
- common among smokers and urban dwellers
15
Q
in chronic bronchitis, irritants induce…
A
- inhaled irritants induce…
- hypertrophy of seromucous glands
- increased goblet cells (via metaplasia) in surface epithelium
16
Q
describe the pathogenesis of chronic bronchitis
A
- pathogenesis:
- airflow obstruction in CB is peripheral (distal) and results from:
- small airways disease: goblet cell metaplasia at the level of the bronchioles accompanied by inflammation, smooth muscle hyperplasia and peribronchiolar fibrosis
- coexisting emphysema increases impairment
- coexistent infxn can complicate and exacerbate symptoms
- infiltrate of CD8+ T cells, macrophages and PMNs
- no eosinophils in contrast to asthma
- distinctive feature is hypersecretion of mucus
- airflow obstruction in CB is peripheral (distal) and results from:
17
Q
describe the Reid index and name a disease where it is increased
A
- Reid index = ratio of the thickness of the mucous gland layer to the thickness of the wall between the epithelium and cartilage
- this is increased in chronic bronchitis because of the seromucous gland hyperplasia
18
Q
describe the clinical presentation of chronic bronchitis
A
- clinical = blue bloaters
- hypoxia, hypercapnia, cyanosis
- persistent hypercapnia → respiratory centers insensitive to pCO2
- respiratory drive is driven by low pO2
- complicated by secondary infxns
- over time → pulm. hypertension → cor pulmonale
- common in any disease where hypoxia occurs
- hypoxia, hypercapnia, cyanosis
19
Q
A
20
Q
summarize the differences between chronic bronchitis and emphysema
A
21
Q
describe the etiology of asthma
A
- etiology:
- chronic inflammatory disease
- hyperactive airways
- recurrent wheezing, breathlessness, chest tightness and cough
- episodic, reversible bronchoconstriction
22
Q
describe the pathogenesis of type 1 hypersensitivity seen in atopic asthma
A
- pathogenesis:
- allergic sensitization; type I IgE mediated hypersensitivity rxn
- patients often have allergic rhinitis or eczema
- Th2 → cytokines
- IL-4 stimulates IgE production
- IL-5 activates eosinophils
- IL-13 stimulates mucus production and promotes IgE production by B-cells
- IgE coats mast cells which degranulate with antigen exposure
- allergic sensitization; type I IgE mediated hypersensitivity rxn
23
Q
describe the pathogenesis of mast cell degranulation in atopic asthma
A
24
Q
describe the pathogenesis of non-atopic asthma
A
- no evidence of sensitiation
- serum IgE = normal
- virus induces mucosal damage → lower threshold of subepithelial vagal receptors to irritants
- drug induced asthma
- triad: recurrent rhinitis, nasal polyps, urticaria and bronchospasm
- aspirin inhibits COX without affecting lipo-oxygenase route → bronchoconstriction mediated by leukotrienes
25
aspirin-induced asthma results in.... (4 symptoms)
* aspirin-induced asthma results in:
* recurrent rhinitis
* nasal polyps
* urticaria
* bronchospasm
26
describe occupational asthma
* asthma stimulated by fumes, organic dusts, chemical dusts and gases
* epoxy resins, plastics
* wood, cotton, platinum
* toluene
* asthma attacks following repeated exposure
27
describe what is seen in the image
* Curschmann spirals = strings of mucus with dead epithelial cells in it
28
describe the clinical presentation of asthma
* recurrent sudden attacks of resp. distress, tightness of chest
* expiratory dyspnea, wheezing/ronchi
* thick sputum
* progressive hyperinflation of lungs with air trapped distal to mucous packed bronchi
* episodic = nights and early mornings
* attacks last a couple hours and subside spontaneously or with therapy
29
describe pulmonary function tests in asthmatics
* FEV1 \<30%, hyperventilation
* hypoxia, hypercapnia, resp. acidosis
* symptom-free intervals but residual resp. defects on spirometry
30
describe the etiology of bronchiectasis
* bronchiectasis: permanent dilation of bronchi/bronchioles secondary to destruction of supporting tissue
* etiology:
* obstruction and chronic infxn
* bronchial obstruction: tumor, foreign body
* congenital/hereditary conditions
* CF, immunodeficiency states, Kartagener syndrome
* necrotizing/suppurative pneumonia
* virulent organisms (S. aureus, Klebsiella spp.)
31
describe the pathogenesis of bronchiectasis
32
describe what is seen in the image
33
describe microscopic findings in bronchiectasis
* intense acute and chronic inflammatory exudate in bronchial walls, necrotizing ulceration
* squamous metaplasia of bronchial epithelium
* lung abscesses may be present
* fibrosis of bronchial walls leading to bronchiolitis obliterans
* cultures are usually positive
34
name a hereditary cause of bronchiectasis
* primary ciliary dyskinesia (Kartagener syndrome):
* AR disorder of ciliary microtubules
* structural abnormalities of cilia impair mucociliary escalator
* persistent infxns → bronchiectasis
* decreased motility of spermatozoa → sterility in males
* 1/3 have situs inversus
