Respiratory System Pathology 3

Question 1

Cells present in the nasal cavities and paranasal sinuses.

Answer 1

Osteocytes - turbinates.
Chondrocytes - cartilaginous structures e.g. nasal septum.
Endothelial cells - lining blood vessels.
Fibroblasts - collagen and ECM.
Epithelial cells - lining mucosa.
– respiratory and other e.g. stratifies squamous rostrally which transitions into respiratory epithelium, olfactory epithelium.
Lymphocytes - in mucosa and w/in nasal associates lymphoid tissue.
Peripheral nerve cells - w/in mucosa.

Question 2

Animals most commonly affected by neoplastic disease of nasal cavities and paranasal sinuses.
Cell types from which they arise most commonly.
Malignant/benign?
Most common tumour type?

Answer 2

Middle-aged to elderly dogs and cats.
Epithelial in dogs.
More malignant than benign in dogs.
Carcinomas most common in dogs.
Carcinomas and lymphomas most common in cats.

Question 3

General characteristics of malignant sinonasal tumours.

Answer 3

• Slow growing.
• Space occupying.
• Locally invasive and destructive.
• Late to metastasise.
• Swelling or distortion of the face.
• Nasal discharges e.g. mucopurulent due to secondary infection, epistaxis.

Question 4

Progressive ethmoid haematoma in horses.

Answer 4

Non-neoplastic nasal mass.
Enlarging haemorrhagic nasal mass most typically arising from the ethmoid region.
Can cause obstruction of nasal passages.
Repeated haemorrhage causes progressive expansion of mucosa, forming haemorrhagic mass that starts to become organised and is encapsulated by stretched mucosa.
As mass enlarges, may cause local distortion and destruction of soft tissues and bone.
Ulceration of encapsulating mucosa may result in mild haemorrhage and epistaxis.

Question 5

Potential tumour origins at the larynx and trachea.

Answer 5

• Stratified squamous epithelium.
• Respiratory epithelium.
• Chondrocytes.
• Skeletal muscle.
• Smooth muscle.
• Fibroblasts.
• Lymphoid cells.

Question 6

Primary or secondary lung tumours more common?

Answer 6

Secondary - important to consider that there may be a primary tumour somewhere else which has spread to the lungs if neoplastic disease found in the lungs.

Question 7

In what spp. are primary lung tumours more common?

Answer 7

Sheep.
Can suffer from a neoplastic lung disease caused by Jaagsiekte sheep retrovirus.
Ovine Pulmonary Adenocarcinoma (OPA)/ Sheep Pulmonary Adenomatosis (SPA)/ Jaagsiekte.
Relatively common in UK.
Relatively long incubation period - months to years.
Clinical disease commonly in sheep ~2-4yrs old.
Multiple tumours in the alveolar epithelium in papilliform structures.
Growth causes compression of surrounding alveoli, significant increase in collagen - may result in fibrosis.
Grossly - early lesions greyish purple, nodular.
- Firm.
- later expand and coalesce.
- Cranial and ventral areas of lung affected.
- Secondary abscess formation can occur.
- Sometimes foamy fluid in airways (2/3).
– watery nasal discharge

Question 8

1. Potential primary lung tumour origins.
2. Most common type of primary lung tumour.

Answer 8

1. Respiratory epithelium - airways, glands.
   Alveolar epithelium (pneumocytes).
   Chondrocytes (and osteocytes).
   Fibrocytes.
   Mesothelium.
   Histiocytes (macrophage/dendritic cell lineages - canine histiocytic sarcoma).
   Lymphocytes.
2. Malignant epithelial tumours.
   (Carcinoma or adenocarcinoma).

Question 9

1. Where do tumours of large airway epithelial origin tend to be located?
2. Where do tumours originating from alveolar epithelium tend to be located?

Answer 9

1. Near the hilus.
2. Peripherally in the lungs.

Question 10

Routes of metastatic spread of primary epithelial lung tumours.

Answer 10

Lymphatic invasion - spread w/in lung / spread to hilar LNs (potential spread beyond these).
Intra-airway seeding by aspiration - can lead to spread w/in the lung.
Vascular invasion - metastatic spread to distant sites.
– cats –> pulmonary carcinomas can sometimes metastasise to the bones of the feet.
Transcoelomic spread - w/in pleural cavity space.

Question 11

1. Major problem with laryngeal oedema.
2. Potential causes of laryngeal oedema.

Answer 11

1. Respiratory obstruction.
2. • Local trauma (intubation, Sx.)
     - Local irritation (aspiration or inhalation of gases, fluids, solids).
     - Local inflammation (e.g. laryngeal chondritis of arytenoid cartilages and associated mucosa in horses, calves, sheep e.g. Texels).
     - Systemic conditions e.g. oedema disease in pigs – caused by some E.coli strains.
     - Anaphylaxis/allergic reactions.

Question 12

Pulmonary oedema on histology.

Answer 12

Alveolar spaces filled w/ pale pink staining fluid.
Oedematous fluid originates in alveolar walls and spills over into alveolar spaces, filling them w/ fluid.

Question 13

Mechanisms resulting in formation of pulmonary oedema.

Answer 13

Increased hydrostatic pressure.
- Passive congestion (HF), circulatory overload (e.g. excess IV fluids), inflammation.
Increased endothelial or alveolar epithelial permeability.
- Inflammation (increased vascular permeability), injury to endothelium or alveoli by infectious agents or toxins.
Decreased colloid osmotic pressure (oncotic pressure).
- Hypoproteinaemia.
Block lymphatic drainage.
- e.g. obstruction or compression of lymphatics by inflammatory or neoplastic disease.

Question 14

Gross features of pulmonary oedema.

Answer 14

Excess foamy fluid in the airways.
Fluid exuding from cut lung surfaces.
Heavy lungs.
Can be difficult to identify or differentiate from PM or agonal changes.

Question 15

1. Hydrothorax.
2. Common cause.
3. Other causes.

Answer 15

1. Oedema/transudate in the pleural space.
2. CHF.
3. Hypoproteinaemia, intra-thoracic tumours.

Question 16

1. Main sign of haemorrhage in the respiratory tract.
2. Some potential causes of haemorrhage w/in respiratory system.

Answer 16

1. Epistaxis.
2. Upper inflammatory diseases (nasal aspergillosis, guttural pouch mycosis).
   Lower inflammatory diseases (e.g. near abscessations that cause adjacent vena cava septic thrombus > thromboembolic event > septic thrombus lodges in the pulmonary arterial system > arterial septic embolic abscess > enlarges and impinges on bronchial wall > wall rupture > arterial blood flows directly into the airway > fatal haemorrhage and epistaxis.)
   Neoplastic disease.
   Non-neoplastic progressive ethmoid haematoma in horses.
   Exercise induced pulmonary haemorrhage in race horses.
   Trauma.
   Coagulopathies.

Question 17

1. Haemothorax.
2. Causes.

Answer 17

1. Blood in pleural space.
2. Trauma.
   Erosion of blood vessels by tumours.
   Clotting disorders e.g. rodenticide poisoning.

Question 18

1. How are lungs protected to some extent from infarction?
2. Potential causes of pulmonary infarction.

Answer 18

1. Extensive interconnecting capillary network.
   - blood from pulmonary artery from R heart.
   - blood from bronchial artery from aorta.
2. Lung lobe torsion.
   Massive pulmonary artery thrombus or thromboembolism causing obstruction.

Question 19

Factors predisposing to pulmonary thrombosis or thromboembolism.

Answer 19

Conditions causing activation of vascular endothelium e.g. sepsis, vasculitis, pancreatitis, bacterial pneumonia, inflammation, neoplasm.

Conditions promoting procoagulant tendencies/coagulopathies e.g. IMHA, DIC, parasites e.g. Angiostrongylus vasorum.

Conditions causing vascular stasis e.g. cardiac diseases/HF, some neoplastic diseases.

Question 20

1. Chylothorax.
2. Grossly.
3. Possible causes of chylothorax.

Answer 20

1. Chyle in pleural cavity.
2. Milky fluid (chyle).
3. Rupture of thoracic duct.
   Obstruction of the thoracic duct.
   Diseases causing occlusion of the cranial vena cava.
   CHF - elevated systemic venous pressure.

Question 21

1. Paranasal sinus cysts in horses aetiology.
2. Location of paranasal sinus cysts.
3. Cysts comprised of.

Answer 21

1. Young - congenital abnormality.
   Older - congenital abnormality progressed.
   - Acquired condition
2. Maxillary sinus.
   Ventral turbinates.
   Sometimes extension to the frontal sinus.
3. Fluid filled cavities lined by epithelium (usually respiratory). Yellow acellular fluid.

Question 22

1. Issue w/ paranasal sinus cysts.
2. Paranasal sinus clinical signs.

Answer 22

1. Airway obstruction w/ enlargement causing distortion and compression of soft tissues and bony structures e.g. facial bone, maxillary bone, nasal turbinates.
2. Facial swelling, epiphora, secondary sinusitis w/ nasal discharge.

Question 23

1. BOAS.
2. Cause.

Answer 23

1. Brachycephalic Obstructive Airway Syndrome.
2. Brachycephalic conformation.
   - size of skull reduced but soft tissue structures have not – excess soft tissues relative to skull –> airway obstruction at various sites.

Question 24

Anatomical problems associated w/ BOAS.

Answer 24

Stenotic nares.
Elongated soft palate.
Relatively large tongue.
Turbinate bones protrude into nasopharynx.
Hypoplastic trachea - narrower diameter.

Question 25

Secondary changes as a result of BOAS.

Answer 25

Inflammation and oedema e.g. palate, larynx.
- swelling and therefore further obstruction.
Everted tonsils - protrusion – obstruction.
Everted laryngeal saccules - obstruction.
Laryngeal collapse due to changes in rigidity - obstruction.

Question 26

Tracheal collapse.
- what is it?
- breeds affected?
- what happens?
- why?
- functional effects depend on?
- pressures of inspiration and expiration.

Answer 26

Dorsal ventral flattening of the trachea.
Small breed dogs - miniatures and toys.
Brachyceohalics.
Shallow shaped trachea.
Increased separation of end of the cartilage.
Tracheal membrane has to span a much wider distance - tracheal membrane prolapse into the tracheal lumen.
Aetiology may include genetic and congenital factors, degenerative changes of cartilage.
Effects depend on severity of collapse and pressures.
Pressures:
- inspiration > reduce luminal pressure of cervical trachea below the surrounding pressure > collapse.
- expiration > increase luminal pressure of cervical trachea higher than surrounding pressure > expansion.
- inspiration > increase luminal pressure of intrathoracic trachea higher than pleural pressure > expansion.
- expiration > reduce luminal pressure of intrathoracic trachea below pleural pressure > collapse.

Question 27

Clinical signs of tracheal collapse.

Answer 27

Cough - “goose honk”.
Increased RR and effort.
Exercise intolerance.
Respiratory distress.
Cyanosis.
Collapse.

Question 28

1. Most common cause of laryngeal paralysis.
2. Most commonly seen in?
3. Other names?
4. Side affected usually?
5. Other animal affected? - predisposition?

Answer 28

1. Degeneration of the recurrent laryngeal nerve.
2. Horses.
3. Equine recurrent laryngeal neuropathy / laryngeal hemiplegia / roaring.
4. Left side.
5. Dog. - large breeds. – often bilateral.

Question 29

Gross features of laryngeal paralysis?

Answer 29

Smaller and paler muscles due to atrophy due to loss of innervation due to degeneration of recurrent laryngeal nerve.
Atrophy and degree of paralysis of the dorsal, lateral and transverse cricoarytenoid muscles.
- Dorsal cricoarytenoid muscle normally abducts arytenoid cartilage during inspiration. – failure = obstruction of airway during inspiration.

Question 30

1. More common potential causes of laryngeal paralysis.
2. Less common potential causes.

Answer 30

1. Primary (idiopathic) neuronal degeneration.
   - ? underlying transport mechanism abnormality.
   Secondary to nerve trauma, compression, irritation or injury.
2. Component of a generalised polyneuropathy.
   Neurotoxins - lead, organophosphates.
   Liver failure (horse, bilateral).
   Hypothyroidism (dogs).
   Congenital nerve abnormality.