Obstructive Lung Diseases- Baker 1 Flashcards Preview

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Flashcards in Obstructive Lung Diseases- Baker 1 Deck (83)
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1: What is FVC?
2: What is FEV?
3: What is PEF?
4: What is FEF?
5: What is TLC
6: What is RV?
7: What is DLCO?

1: Total amount of air exhaled during the forced expiration
2: Amount of air expired per second
3: How fast air is coming out
4: Measures airflow halfway through an exhale
5: Measures amount of air in your lungs after you inhale as deeply as possible
6: Amount of air left in your lungs after complex exhalation
7: Measures the ability of the lungs to transfer gas from inhaled air to RBCs in pulmonary capillaries


What does the spirometry test show in obstructive pulmonary disease?

-decreased FEV1
-decreased FEV1/FVC ratio
-decreased FEF 25-75
-normal to increased TLC
-Increased RV


What will a flow-volume loop look like with an obstruction?

decreased expiration showing scooped out pattern


What are the 2 components of COPD?
What are 2 other obstructive pulmonary diseases?

-emphysema and chronic bronchitis


What is the biggest risk factor of obstructive pulmonary disease?
What is the prevalence?
What percent of smokers develop COPD?


-6.2% total (5.2% male and 7.2% female)

-10-15% of smokers develop COPD


Who is more likely to get COPD, females or males?

females :(


Is COPD killing more or less people as of late?

more people :(


What is the trend of tobacco use?

less people are using them now


Where is COPD most common?

in the south eastern states


Where do most people die of COPD?

mid east states and montana and wyoming


Whats happening for the rates of women with COPD?

its been increasing since 200 and is now more common in females than males


What are the top 4 causes of death?
What is a risk factor for all of these?

1. heart problems
2. Cancer
3.COPD, asthma
4. Cerebrovascular

Cigarette smoking


How is emphysema defined, clincally or anatomically?



What is emphysema?
Is there fibrosis in this disorder?

the irreversible enlargement of airspaces distal to the terminal bronchioles
-no, there is airspace wall destruction without fibrosis


What are the four types of emphysema?



What is the most common type of emphysema?

Centriacinar but a lot are a combo of this


What is the type of emphysema seen with smokers? What is it?

-damage of the bronciole which results in damage and loss of the alveolar/bronchiole septum.


What is panacinar emphysema?

get destruction of the alveolar septum which results in large and fused alveoli


What is this:
initial sparring of the distal acinus. (Involved later)
affects upper lobes/apical segments

Centriacinar emphysema


What is this:
associated with chronic bronchitis and smoking (walls with black pigment)

centriacinar emphysema


If you see dilated alveoli with destroyed alevolar septum, what are you looking at?



What is this:
less common
-airspace enlargement from respiratory bronchiole to alveoli (no sparring)
-effects lower lobes/ anterior margins

Panacinar Emphysema


What type of emphysema is most severe at lung bases?
What is this emphysema associated with?

Panacinar emphysema
-alpha 1 anti-trypsin deficiency


What is the pathogenesis of emphysema?

Irritant (such as tobacco)-> ROS-> reduced capacity of antioxidants-> inflammation w/ more neutrophils-> increase elastase + alpha 1 antitrypsin deficiency -> emphysema

***Note elastic in lungs is what makes you expire and elastase will destroy this and alpha 1 anti-trypsin will decrease elastase, so without this you will get emphysema***


How can you get alpha 1 antitrypsin deficiency that results in emphysema?

due to the increase ROOS can lead to oxidative inactivation of it
you can have a congenital deficiency


A1 antitrypsin is a proteinase inhibitor (destroys the protein elastase) and the gene for this is found on the locus of chromosome (blank)



What is the normal config for a1-antitrypsin?

PiM X 2 copies=PiMM


What is the panacinar emphysema config for a1-antitrypsin?

PiZ X 2copies=PiZZ (2 messed up copies of the gene)


What happens if you are heterozygote for a1-antritrypsin deficiency (PiM +PiZ=PiMZ)?

Typically have reduced levels of alpha1AT but asymptomatic
HOWEVER, add smoking and risk increases significantly


Why do people with emphysema use accessory respiratory muscle for inspirations and expirations?

Serine elastase breaksdown the elastin in the alveoli-> destruction of the alveoli->lose elasticity of the lungs (ie. Loss of elastic recoil of the lungs) ->must use accessory respiratory muscles for inspirations and expirations.