What radiographic features are consistent with feline bronchiolar disease
What are some clinical signs for feline asthma and what are some other causes and how to rule out
List the two main treatment options in terms of drugs for feline asthma
1) Bronchodilations - relievers
- beta-2 adrenoceptor agonists
2) Anti-inflammatory - prevents
- Long-term administration - problem with immune systems
More effective together - give both - synergistic
What would you administer to a patient that was having an emergency asthma attack
1) Oxygen - hoping that some will go in
2) Beta-2 adrenoceptor agonist
Corticosteroids - more long-term not really in emergency
What cells produce surfactant and when does surfactant production commence
Type II pneumocytes and some surfactant lipids may be produced by Clara cells of the distal bronchi
- production commences late in foetal life
What happens to surfactant to prevent its accumulation in the lungs
surfactant can be recycled by type II pneumocytes or degraded by alveolar macrophages
What is the major function of surfactant and its other functions
1) Lower the surface tension of fluid lining alveoli to prevent complete collapse
2) opsonise infectious agents
3) bind endotoxin and have anti-oxidant activity
What impairs surfactant function or secretion
What domestic animals have grossly obvious lobulation of the lung and what is the functional significance of this
Grossly obvious in cattle and pigs
- as a result species have poor collateral ventilation (movement through pores of Kohn) in health
Benefit - inflammation may be restricted to individual lobules in disease
In which species is congenital melanosis of the lung seen and significance
piglets and young ruminants
- incidental and fade over time
What is foetal pneumonia and what are some causes
What is neonatal hyaline membrane disease
1) failure of type II penumocytes to secrete surfactant
2) increase surface tension so collapse of alveoli
3) sheer stress during inspiration
4) damage to type I pneumocytes and clara cells
5) decrease surfactant
6) diffuse pulmonary atelectasis
7) alveolar odeme and fibrin - hyaline membranes form
8) dyspnoea from birth
What are the major mechanisms responsible for atelectasis in domestic animals
1) congential ateletctasis
2) compression atelectasis
3) Obstructive atelectasis
4) Hypostatic (Dependent) Atelectasis - downside of lung recumbent for prolonged periods
What happens to atelectatic lung if the cause is not removed
may become permanent due to reduced
vascular perfusion of the collapsed lung -> local hypoxia, increased vascular permeability and oedema, and eventually fibrosis
What causes alveolar emphysema, why it is common in humans and is it common in animals
caused by exposure to other lung irritants (e.g. in coal miners), chronic bronchitis, bronchiolitis or bronchopneumonia, inherited α1-protease inhibitor deficiency, or pancreatic necrosis with release of activated proteases into circulation
Common in humans due to cigarette smoking
Rare in domestic animals, prominent in horses with heaves
What does alveolar emphysema look like grossly and what is the effect on respiratory function
appear crepitant, pale pink, bubbly or puffy and are raised above adjacent normal parenchyma
○ when severe, the air bubbles in damaged alveoli may coalesce to form large bullae (bullous emphysema)
○ spontaneous rupture of bullae -> pneumothorax
- emphysematous lung parenchyma is dysfunctional
What is the difference between alveolar emphysema and hyperinflation of alveoli
in hyperinflated lungs, there is no accompanying damage to alveolar walls (c.f. alveolar emphysema)
- hyperinflated lungs are just post mortum change due to gas trapping
interstitial emphysema which species most often seen and why, where can air in pulmonary interstitium track
most often seen in cattle, probably due to their well-developed interlobular septa and poor collateral ventilation
-○ the air tracks up the interlobular septa to beneath the visceral pleura
it may also track along lymphatics to bronchial and mediastinal lymph nodes
What are the normal functions of pulmonary alveolar macrophages, how are they replaced over time and what factors can compromise their phagocytic function?
1) rapid phagocytosis - inhaled particles, bacteria, prevent accumulation of surfactant
2) regulatory cell by releasing cytokines and other molecules
Replaced (short lifespan) by recruitment of monocytes from circulation or mitotic division of interstitial macrophages
Impaired via viral infections, hypoxia and pulmonary oedema
What are the characteristic gross general features of pneumonia
characterised by increased firmness of the affected lung parenchyma on gentle palpation
§ this change in texture is referred to as consolidation of the parenchyma and is due to replacement of air by exudate +/- scar tissue (fibrosis)
- may also have rubbery texture
Outline the difference between the acute red phase and chronic grey phase of pneumonia
Acute red phase - dominated by hyperaemia, oedema, exudation of neutrophils, and degeneration and necrosis of type I pneumocytes
Chronic grey phase - during this phase, exudate is slowly cleared by phagocytosis, epithelial repair continues and fibrosis may develop
○ atelectasis contributes to the gross pale grey “fish-flesh” appearance of the lung
What is meant by the term bronchopneumonia (lobular pneumonia) and what are its typical gross features?
List 3 causes of bronchopneumonia and exception to gross appearance rule
Mainly inhalation of bacteria
1) E.coli
2) Strep and Staph
3) nematode (lungworm) - cranioventral distribution
What is meant by the term lobar pneumonia (fibrinous pneumonia) and what are its typical gross features?