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Obstructive Lung Diseases Flashcards

1
Q

Where are 3 areas where obstruction leading to increased resistance can occur?

A
  1. Inside the lumen
  2. in the airway wall
  3. Surrounding the airway
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2
Q

What is happening with restrictive diseases?

A

Expansion of the lung is restricted

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3
Q

What 4 things can cause expansion of the lung to be restricted?

A
  1. Alterations in the parenchyma
  2. Diseases of the pleura
  3. Diseases of the chest wall
  4. Diseases of the neuromuscular apparatus
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4
Q

What are 4 symptoms/physiological processes contributing to asthma?

A
  1. Widespread narrowing of the airways (bronchoconstriction)
    - hyper-responsiveness of the smooth muscle to contract
  2. Excessive mucous secretion
  3. Chronic inflammation
  4. Chest tightening, wheezing, and cough
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5
Q

What is the definition of airway hyper-responsiveness?

A

the capacity of the airways to undergo exaggerated narrowing in response to stimuli that do not result in a comparable degree of airway narrowing in healthy subjects

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6
Q

What is the methacholine test?

A

Methacholine given to patient via nebulised spray, and causes bronchoconstriction via muscarinic receptors. Degree of narrowing quantified by spirometry. Asthmatics will react to much lower doses.

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7
Q

Following the methocholine test, what is given to asses reversibility?

A

Bronchodilator is administered

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8
Q

Why is there thought to be extensive remodelling of airway tissue in asthmatic patients?

A

ongoing tissue injury caused by infectious agents, allergens, or inhaled particultes

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9
Q

What drives the persistence of asthma?

A

Ongoing host immune responses that generate mediators responsible for remodelling

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10
Q

Lungs are usually hyperinflated in asthma patients as a consequence of…?

A

extensive mucous plugging

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11
Q

the causes of asthma then are…

A
  1. extensive contractile response of smooth muscle = bronchoconstricion + airflow obstruction
  2. Extensive remodelling
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12
Q

What are 5 treatments for asthma?

A
  1. short acting ß antagonists to counteract bronchoconstriction
  2. corticosteroids to control inflammation
  3. Leukotriene antagonists
  4. Long acting muscarinic antagonists
  5. Anti IgG monoclonal antibody and bronchial thermoplasty
    - very expensive
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13
Q

What is the 4th leading cause of death worldwide?

A

COPD

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14
Q

What is the definition of COPD?

A

progressive loss of lung function with airflow obstruction that is not full reversible with bronchodilators

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15
Q

What is emphysema?

A

presence of permanent enlargement of the airspaces distal to the terminal bronchioles and destruction of their walls
- destroys gas exchange surfaces

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16
Q

What are the two forms of emphysema?

A
  1. centriacinar

2. panacinar

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17
Q

What is centriacinar emphysema?

A

he destruction is limited to the central part of the lobule and the peripheral
ducts and alveoli may be fine

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18
Q

What is panacinar emphysema?

A

distension and destruction of entire lobule. Throughout lung, but more common towards bottom

more severe

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19
Q

What is the role of Alpha-1 antitrypsin in emphysema?

A

inhibitor of serine proteases, including neutrophil elastase

genetic disease can cause it to accumulate in ER of liver and not make it to lung
- N.E. can then destroy connective tissue matrix of lung

People are at greater risk (especially if they smoke) of developing COPD

Can also develop paracinar emphysema early on

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20
Q

What is different between the effects of the alpha-1 antitrypsin deficiency on the liver vs. lungs?

A

liver disease: loss of function mechanism

lung disease: gain of function mechanism

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21
Q

What are 2 (and a potential third) risk factors for developing emphysema?

A
  1. Smoking (50%)
  2. Pollution
  3. potentially agricultural pesticides
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22
Q

What is the pathogenesis of emphysema?

A
  1. induction of pro-inflammatory signalling pathways results in recruitment of neutrophils and macrophages
  2. Inflammatory cells arrive at site and make more cytokines and oxidants
  3. Destruction of elastic matrix of alveoli from NE (cleaves type IV collagen)
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23
Q

What is the definition of chronic bronchitis?

A

chronic productive cough for 3 months in each of 2 successive years

24
Q

Most patients with COPD show symptoms of emphysema and bronchitis but which is more common?

A

chronic bronchitis

25
In CB, hypertrophy of the mucous glands in the large bronchi results in?
excessive mucous production | - this hypertrophy is a hallmark feature
26
What is the Reid index?
way to quantify the ratio of gland thickness to wall thickness - normally less than 0.4 but can exceed 0.7 in CB
27
Almost all cases of CB are in..
smokers!
28
what are 5 hallmark changes occuring in CB?
• Hypertrophy of sub mucosal mucus glands in trachea and bronchi • Goblet cell hyperplasia in small airways (bronchioles) • Profound increase in mucus secretion • Progression to significant inflammation • Later stages reflect changes to epithelial border of bronchioles with metaplasia, lumenal narrowing, fibrosis, mucus plugging
29
What is the most common fatal genetic disease in caucasian populations?
cystic fibrosis
30
What is the cause of CF (genetic)
loss of function mutation in gene encoding CFTR protein
31
What is the physiological result of the loss of function CF gene?
deficient epithelial anion (Cl-) permeability | - affects many organs, not just the lungs
32
What is the effect of CF on the airways?
mucopurulent material and plugging of smaller airways
33
What is the effect of CF on the sweat glands?
decreased reabsorption of NaCl by water-impermeable ductal epithelial cells = elevated sweat Cl-
34
What is the effect of CF on the pancreas?
enzyme insufficiency = malabsorption of fat and protein
35
What is the effect of CF on the small intestine
meconium becomes thickened and congested in ileum = blockage
36
What are 7 symptoms of CF?
1. Persistent cough with productive thick mucous 2. Wheezing and shortness of breath 3. Frequent chest infections, which may include pneumonia 4. Bowel disturbances, such as intestinal obstruction or frequent, oily stools 5. Weight loss or failure to gain weight despite increased appetite 6. Salty tasting sweet 7. Infertility (men) and decreased fertility (women)
37
How many classes of CFTR mutations are there? Which is the most common?
7 Class II is the most common
38
What is the class II CFTR mutation?
missense mutations and in-frame deletions disrupt CFTR folding and trafficking to the surface = degraded in golgi
39
The loss of functional CFTR results in what kinds of ion disturbances?
Increased Na+, Cl-, and water absorption across large airways - extracellular Na+ channels are released from tonic inhibition
40
What is depleted due to ion disturbances?
PCL
41
Why is the loss of PCL so disastrous in people with CF?
Lack of PCL results in mucostasis and formation of thickened mucus Plaques and plugs which adhere to CF airway surfaces
42
In addition to defective ion transport, what else is problematic in CFTR deficient cells
they exhibit innate pro-inflamatory states - more pro-inflammatory mediators - excessive activation of transcription factors, such as (NF)-κB and AP-1,
43
What is wrong with CF neutrophils?
they have reduced phagocytic activity
44
What do CF neutrophils do when they die that contributes to pathogenesis?
release DNA making the mucous more viscous as well as oxidases which increases oxidative stress
45
What is a result of the constant inflammation of the airways in CF?
Bronchiectasis - permanent enlargement of the airways
46
What are 11 therapeutic targets for CF?
1. broad inflammatory modulators: corticosteroids and ibuprofen 2. Antibacterials w anti-inflammation like Azithromycin 3. Interferon gamma to modulate intracellular signalling 4. Inhibitors of neutrophil influx 5. Inhibitors of neutrophil products 6. Anti-oxidants 7. anti-proteases 8. hyperosmolat agents 9. CFTR potentiators to improve Cl- transport 10. CFTR correctors to rescue trafficking defect 11. Gene therapy to replace CFTR
47
What is another non biological treatment for CF?
physiotherapy - vigorous massage - postural drainage - chest clapping - shaking and vibrations
48
What are ALI and ARDS?
Acute lung injury and acute respiratory distress syndrome
49
What can cause ALI and ARDS?
Direct pulmonary injury, eg pneumonia, or indirect blood-borne insults, such as sepsis
50
What is the clinical presentation of ARDS?
breathlessness and pulmonary edema
51
What distinguishes ALI from ARDS?
the more severe hypoxemia in ARDS
52
What is characteristic of the early phase of ALI?
acute inflammation of alveolar-capillary membrane, including alveolar epithelium, vascular endothelium and fibroblasts
53
What happens to the alveolar epithelial cells in ALI?
they are sloughed off, forming protein rich hyaline membranes
54
the recruitment and establishment of neutrophils in the alveoli has what effect in ALI?
disruption of epithelial fluid transport and impairment of surfactant productions
55
Most patients will recover following the acute inflammatory phase of ALI... how
proliferation of type II alveolar cells that are progenitor for both types I and II
56
What can develop if the lung injury is too severe?
the fibroproliferative phase
57
What is the fibroproliferative phase?
Mesenchymal cells proliferate, neovascularisation occurs and the alveolar space becomes filled with activated fibroblasts and myofibroblasts that synthesise excessive collagen, which is deposited to cause thickening of the alveolar walls

Human Organs and Tissues (16 decks)

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