Feline Allergic Bronchitis

Today is the Physiology test, and one of the questions is going to be about Feline Allergic Bronchitis (the professor said so and if he lied there will be killing).  Because of this, I have decided to write my model answer here, for all of you to read.  That’s right, all three of you get to read the answer that I am going to be writing again in a few short hours, that is how much I love you.

This is a subject near and dear to my heart, as my darling cat back home in the states has this condition.  My sweet Littl’un has been suffering from it for years, and is the main reason that I am so very good at administering pills to reluctant cats.  Littl’un was diagnosed using a history and chest x-ray, I don’t remember if blood work was done but it is highly likely.  She gets long acting shots once or twice a year when she gets really bad, and is managed with a steroid inhaler and steroid pills throughout the rest of the year.  The poor thing blew up like a balloon thanks to the side effects, but can breathe and we like her breathing.

Feline Allergic Bronchitis is a narrowing of the small passageways of the lungs due to increased sensitivity to an allergen.  The starting process for hypersensitivity begins with a particle encountered in the lungs.  This stimulates a normal immune response, eliminating the threat and setting up specific memory cells to guard against future attacks by that type of particle.  When that same particle is encountered again, the immune response is rapid and decisive.  In affected cats, it is also overblown.  The release of histamine leads to bronchoconstriction, an increase in mucus secretion, and an increase in capillary permeability (allowing more fluid to cross if not limited).  The immune response also increases the amount of prostaglandins, which leads to inflammation.  Esinophils (a type of white blood cell) act to prolong the airway injury by slowing recovery, they are jerks, and affected cats tend to have higher numbers of them hanging around.  The increased mucus secretion (accompanied by decreased cilia movement) causes mucus plugs to form, increasing resistance along the airways.

This immune response also contributes to an imbalance of sympathetic and parasympathetic signalling.  In a healthy animal, the two (which are in direct opposition) are in balance and the airway is open.  When the sympathetic side is stronger than the parasympathetic, the airways are even more open – this is the fight or flight response system.  When the parasympathetic side is stronger, the airways become constricted.  Parasympathetic stimulation causes smooth muscle in the small airways to contract which narrows the radius of the tubes.  Flow is inversely proportional to the radius to the fourth power, so even a very slight change in radius has drastic effects on flow rate.  This decreased radius also increases the velocity of the air passing through, which causes turbulence.  Turbulent air is less efficiently removed and causes problems with ventilation.

Overall, each of these things causes an increase in resistance across the airways which decreases flow of air.  In normal breathing, the diaphragm contracts to increase thoracic (chest) volume, and then relaxes to decrease thoracic volume.  When the chest volume increases it decreases the pressure surrounding the lungs, which causes air to rush in from outside (where the pressure is now higher).  When the chest volume decreases, the pressure inside the lungs increases (until it is higher than outside) and pushes the air back out.  When resistance is too high in the small airways, the passive action of the diaphragm moving is not enough to increase the pressure in the alveoli to overcome the pressure difference.  This triggers the cough reflex and air is forcibly removed by contraction of abdominal and thoracic muscles.

Treatment of this condition is based around opening airways.  Inhalers with steroids and bronchodilators are used for acute attacks, and maintenance steroid pills for longer term.  Steroids work by decreasing inflammation caused by prostaglandins during the immune response.  These are not the anabolic steroids used by athletes and body builders, they are corticosteroids that bind to receptors in cells to reduce inflammation.

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