2.6 Resp general pathology (INCOMPLETE)

How are alveolar macrophages distributed in the lung?

Normally 1 sentinel macrophage per alveolus

At what age is partial atelectasis in the lungs normal?

Up to 24-48h

• Parts of lung have not expanded

Was this animal stillborn or did it die shortly after birth?

Stillborn = total primary atelectasis

• lung has no air

3 compression causes of secondary atelectasis

• Pmeumothorax/hydrothorax

• Prolonged recumbency or abdominal distension (large animals) → presses on diaphragm

• Pulmonary/mediastinal mass → presses on lungs

Why are cattle especially prone to secondary atelectasis caused by obstructions?

Fibrous septae between lung lobules → lack of communication between lobes

• Therefore if one lobe blocked = no air goes into it

3 types of emphysema

• Alveolar (e.g. emphysema = alveolar destruction, RAO in horses)

• Interstitial (e.g. cattle pneumonia = air forced into interstitium)

• Compensatory (emphysema adjacent to area of consolidation)

Emphysema definition

Excess air in lungs

Most common cause and 2 pathological findings of this

Alveolar emphysema

• Neutrophils secrete elastase → alveolar wall destruction

• Lung feels like bubble wrap

  • Alveoli rupture and merge together

• If severe emphysema (in general) = lungs do not deflate when thoracic cavity opens

  • Imprints of ribs present on pleural surfaces

Aspiration pneumonia

• Cranioventral lung lobes are hyperaemic = gravity

Why may previously healthy animals exhibit post mortem pulmonary congestion?

Effect of barbiturate euthanasia

Why is pulmonary oedema often hard to remove?

Mixes with surfactant → foams up like detergent

3 factors resisting pulmonary oedema

• Tight junctions between alveolar + capillary endothelium

• Intra-alveolar pressure > interstitial pressure

• Interstitial lymphatic drainage removes fluid escaping from blood

4 causes of oedema

• Damage to endothelium/epithelium (inflammation, toxins)

• Cardiogenic (pressure overload)

• Neurogenic (pressure overload → excess sympathetic drive)

• Volume overload (excess fluids, renal failure)

Thrombosis

Obstruction of vessels by coagulated blood components during life within the body

• Not outside body =

5 predisposing factors for pulmonary thrombosis/embolism/infarction

• DIC

• Liver abscess (esp cows)

• Valvular endocarditis

• Lung lobe torsion → abrupt infarction

• (Jugular thrombosis from catheterisation)

6 morphological subtypes of rhinitis/sinusitis

• Serous

• Catarrhal (mucoid)

• Purulent

• Necrotising

• Ulcerative

• Haemorrhagic

5 subtypes of bronchopneumonia

• Purulent bronchopneumonia (cranioventral)

• Fibrinous bronchopneumonia (cranioventral)

• Interstitial pneumonia (diffuse)

• Embolic pneumonia (diffuse, multifocal)

• Granulomatous pneumonia (diffuse, multifocal)

Bronchopneumonia = cranioventral consolidated tissue

3 sequelae in bronchopneumonia

• Resolution

  • Mild inflammation = 7 days

  • Return to normal = 3 weeks

• Deterioriation

  • Abscess formation (if pyogenic)

  • Pleuritis (severe fibrinous pneumonia) → adhering visceral/parietal pleura

  • Fulminating cases → hypoxaemia, toxaemia, death

• Persistence

  • Becomes chronic with fibrosis and bronchiectasis

Describe the mechanism of bronchiectasis.