Obstructive lung disease: COPD-Emphysema Flashcards
(33 cards)
What is meant by obstructive lung disease
Diffuse airway disease (at any level of the respiratory tract) resulting in increase in resistance to airflow (FEV1/FVC <0.7)
List 3 obstructive lung disease
Chronic obstructive pulmonary disease
Asthma
Bronchiectasis
What is COPD
is the diseases characterised by persistant respiratory symptoms and airflow limitation due to airway and/or alveolar abnormalities caused by exposure to noxious particles or gases
List risk factors of COPD
- Strongly associated with cigarette smoking
- Poor lung development early in life
- Exposure to environmental and occupational pollutants
- Airway hyperresponsiveness
- Genetic polymorphisms
List 2 major clinicopathologic manifestation of COPD
Emphysema
Chronic bronchitis
Permanent enlargement of airspaces distal to terminal bronchiole with destruction alveolar septae and walls of airways
Emphysema
List the classifications of Emphysema
Centriacinar Emphysema
Panacinar Emphysem
Paraseptal Emphysema
Irregular Emphysema
The emphysema that affects the respiratory bronchioles and involves the upper lobes associated with smoking
Centriacinar emphysema
The emphysema that affects the alveolar and alveolar ducts and eventually the respiratory bronchioles and ivolves the lower lobes
Panacinar emphysema
The panacinar emphysema is associated with defieceny of what?
alpha 1 antitypsin defiency
The panacinar emphysema is exacerbated by?
Smoking
Name the emphysemas that causes the clinically significant airway obstruction
Panacinar and Centriacinar emphysema
The emphysema that manifests as spotaneous pneumothorax in young adults
Paraseptal emphysema
Emphysema that is clinical insignificant
Irregular emphysema
Explain the pathogenesis of emphysema in sequence
- Alpha 1 antitrypsin deficiency
- Decrease in antielastase alpha 1 antitrypsin
- Smoking causes increase in elastase PMN/Mac which results in elastic damage-emphysema
- Also the decrease in antielastase alpha 1 antitrypsin-elastic damage-emphysema
Toxic injury from inhaled smoke and other noxious particles causes what?
Damage respiratory epithelium and cause inflammation as well as oxidative stress, resulting in parencymal destruction
Both centri-acinar and panacinar emphysema are caused by imbalance of what?
Protease antiprotease
Oxidant-antioxidant
The centri-acinar is associated with what from cigarette
Nicotine
Explain the role of nicotine in Emphysema (4makrs)
- Nicotine is a chemoattractant of neutrophils by induction of nuclear factor B and resultant production pf tumour necrosis factor (TNF) and interleukin 8 (IL8)
- TNF and IL8 activate neutrophils, whihc release damaging proteases
- Nicotine causes inactivation of antiproteases
- Nicotine causes production of reactive oxygen species, which inactivates proteases and deplete antioxidants
Explain how the deifiencey of alpha 1 antirypsin causes panacinar emphysema
the normal allele encoding alpha 1 antitrypsin is PiMM but 0.012% of the population has a PiZZ allele, which is associated with a significant decrease in the amount of alpha 1 antitrypsin
Alpha 1 antitrypsin major inhibitor of proteases especially elastase secreted by netrophil during inflammation
Under mechanism of emphysema
The loss of pulomonary parenchyma results in what?
Loss of elastic tissue and recoil, increased lung compliance, increased pulmonary residual volume, increased total lung capacity
Under mechanisms of emphysema the airway obstruction results to what?
Loss of elastic tissue in the alveolar walls that surrounds respiratory bronchioles leading to decreased radial traction and functional collapse of respiratory bronchioles during expiration
What happens to diaphragmatic excursion and accessory muscles for breathing.
Mechanism of emphysema
Decreased diaphragmatic excursion and increased use of accessory muscles for breathing
Under mechanism of emphysema
With over time, with reduced ventilation and air trapping what will happen
The partial pressure of oxygen (Pa O2) decreases, the partial pressure of carbon dioxide (Pa CO2) increases, and respiratory acidosis ensues, with renal compensation. This exacerbated by small airway changes in smokers