Emphysema Flashcards
(8 cards)
Emphysema
Exhalation issue. Elastin is destroyed, lungs are not elastic and can’t push air out due to lack of recoiling. It also causes collapsing of airways because of last structure previously held by Elastin
Sx - barrel chest, pursed lips (pink), slowly inhale / exhale, faster breathing rate
Emphysema pathophysiology
Loss of elasticity due to destroyed elastin by elastase, airways collapse and don’t send air out. Too much elastase is found : causes inflammation, Neutrophils gets recruited (make elastase, s more and more elastase is produced further initiating immune response ).
Lack of alpha 1 anti trypsin - unregulated elastase - no elastin
Emphysema diagnosis
Chest x ray shows inflated lungs (due to air settled ), dented neck (accessory muscles are being used to push air out), flat diaphragm (due to dented lungs )
FET - spirometers, evaluates exhalation / amount of air being pushed out. Normal reading - > 80 %, obstructive reading <50 %
Lab test for alpha 1 antitrypsin deficiency, ABG 9 amount of o2 and co2), bicarbonate (if high then Co2 high )
Diffusing capacity of lungs for carbon monoxide
Test for diffusion of gases in alveoli. CO is inhaled and holds for a sec and then blow out all of it. The computer reads amount taken in and amount breath out.
Amount in - amount out shows the amount of CO diffused in blood, efficiency of diffusion / gas exchange in alveoli.
Centriacinar emphysema vs Panacinar emphysema
Centriacinar emphysema - inflammation associated, too much elastase (produced by Neutrophils) affects larger airway, bronchioles. Triggers - smoke
Panacinar emphysema - no external factor, alpha 1 antitrypsin deficiency - elastase uncontrolled - elastin destroyed.
Emphysema treatment
Stop smoking, bronchodilators (Beta antagonists - Al uteri’s, anticholinergic - opium ), Leukotriene inhibitors - chronic
Antibiotics (to prevent ) in an exacerbation, steroids, careful administration of o2 while monitoring breathing rate- Acute / exacerbation
