QUESTIONS

1. What is the difference between "old dog lung" & COPD/chronic bronchitis?
    
2. In this condition (bronchitis/chronic airway disease), the effort of respiration is often subtle.  If you see it, would you expect the effort to be inspiratory or expiratory & why?
    
3. What in the hell is a Clara Cell?
    
4. What anatomic features of the dog & cat lower respiratory system makes them less susceptible to respiratory compromise than other species?
    
5. The finding of bronchiectasis - say on radiographs - has been found to predispose humans w/chronic airway disease to bacterial infections in the airways.  This has been extrapolated to dogs such that when you see bronciectasis, you have an indication to run a bronchoalveolar lavage or tracheal wash for culture.  What is bronchiectasis & how do you get it (if you're a dog)?
    
6. What medication is said to be the "cornerstone of  therapy" in this disease?
    
7. When would you consider doing a bronchoalveolar lavage or tracheal wash on a dog w/airway disease?
    
8. Which is the stronger cough suppressant:  dextromethorphan or codeine?
    
9. Will it help to use bronchodilators in this disease?
   
   
   
    

ANSWERS

1. Well, er, actually "old dog lung" IS  airway disease/bronchitis/ whatever you want to call it.
   
   
   
   
    
2. Effort is expiratory.  Why?  I'll try to explain without the benefit of diagrams. Okay. Picture an airway extending from a nose into a thorax with a lung on the end.  The airway has an intrathoracic part & an extrathoracic part.  (a simplified version of the truth.)  At end expiration, there is no gas flow.  Pleural pressure is balanced by elastic recoil pressure of the thorax.  Pressure inside the airway from nose to lung is atmospheric pressure (other wise we'd have gas flow & we already said we're at end expiration when there's no gas flow.)
   
   Now we inhale.  We create a low pressure area in the thorax.  The elastic recoil of the pleura is fighting this (the lung wants to snap back rather than expand). This means the pressure w/i the lung is the intrathoracic pressure - the recoil pressure.  That's ok.  This result is still plenty lower than atmospheric pressure & air happily rushes in. In fact, the airways dilate as well as the alveoli.  Everybody that isn't held into shape w/cartilage gets bigger. Since bronchitis is an obstructive disease, inspiration works well.  In bronchitis we have nothing to fight in inspiration; our airways naturally get bigger. There's a pressure gradient from the nose down but still, the deeper down you get, the more expanded. It's easy for air to get in.
   
   Now we exhale.  Now our intrathoracic pressure is high & to it we add elastic recoil.  Well, there's still a gradient from the nose down.  At some point, the intr-airway pressure=the intrathoracic pressure (this is called "the equal pressure point").  Lower than EPP, the airway will want to dilate (intra-airway pressure is higher than intrathoracic pressure) & above the EPP the airway will want to constict (intra-airway pressure is lower than intrathoracic pressure). Now this is all we need. :(  Constriction.  Just beautiful.  In a normal dog, this is insignificant but if we alreadly had those airways plugged w/mucus we'll need some serious effort to exhale through this constriction.  This is why there is effort in exhalation in obstructive diseases where the obstruction is inside the airway.
   
   
   
   
    
3. (My husband says, "Clara cell?  Isn't that  what  you use for pimples?")
   
   The epithelium of a bronchiole has some Clara cells.  They are ciliated non-secretory cells. I believe the Clara cell has some ability to bind pneumotoxins.
   
   Other local cells include APUD cells (also called K cells) which are neuroendocrine in origin & Brush cells (function unknown).  Secretory cells are the most resitent to damage & are capable of re-differentiating into ciliated cells.
   
   
   
   
    
4. The dog & cat have tremendous "collateral ventilation."  This means that respiratory bronchioles & teritiary bronchioles (the lowest bronchioles of the tree) are linked together. This means if one branch gets obstructed, it's OK because the collateral bronchioles can get those alveoli aerated. 
   
   The species with the least collateral ventiliation is the cow.  In the cow everything is septated.  Even the lungs hardly can be divided into lobes.  They are really predisposed to pneumonia.
   
   
   
   
    
5. Bronciectasis is an abnormal dilation of bronchi.  It is felt to be a common sequela of bronchitis.  We aren't sure how it occurs but here is a favored theory.  The airway cartilage gets destroyed by all the local inflammation.  The airway collapses without its cartilage.  If atelectasis results, the remaining open bronchi dilate to take up thoracic volume.  How does this lead to a predisposition to infection?  I don't have that info specifically but I'm guessing that the normal airway defenses are just too disrupted by this process.
   
   
   
   
    
6. What drug is usually the cornerstone of therapy? :)  Glucocorticoids, of course.  This condition is based on inflammation & mucus production.  Nothing cuts inflammation & mucus production like a glucocorticoid.
   
   
   
   
    
7. Well, you might want to do it when you first make the diagnosis though it wouldn't be unreasonable to treat w/pred for a couple of weeks & see how things go.  If you had a fever, an acute exacerbation, or evidence of bronchiectasis, a culture is a good idea (though you should beware of results where multiple organisms are obtained.  Bacteria are commonly transiently present in the lungs.)  If you want to rule out a fungal infection or a parasitic infection, you might want to wash.  It is said that an eosinophilic component suggests an allergic component & portends a more favorable pred response.
   
   
   
   
    
8. Codeine is 50% stronger than dextromethorphan. (But dextromethorphan is OTC.)
   
   
   
   
    
9. We used to think that bronchoconstriction really wasn't a feature of this until Phil Padrid demonstrated that albuterol was helpful in some dogs for sure.  He recommends the use of airway dilators during flare ups & has a protocol for how to try them out in CVT XII.  Be sure to tell the owner about anxiety & muscle tremors (plus PU/PD if using a methylxanthine).  These side effects should go away after the first few days or a week but if the owner doesn't know that, they'll just blow off the medication.