General Pathology of the Respiratory Tract

Question 1

Describe the normal anatomy of the respiratory tract…

Answer 1

Upper respiratory tract:
Nasal cavity, paranasal sinuses, nasopharynx, larynx, guttural pouches (horses).

Lower respiratory tract:
Trachea, bronchi, bronchioles, and alveoli.

Air conduction system:
Nasal cavity, nasopharynx, larynx, trachea, bronchi, and bronchioles.

Gas exchange system:
Respiratory bronchioles and alveoli.

Question 2

What are the respiratory defences in the nasal chambers?

Answer 2

Nasal chambers:

50% of resistance to airflow. Therefore, brachycephalic dogs with smaller nasal structures are at greater risk.
Remove particles > 10 - 20µm.
Humidify and warm incoming air (protects LRT).
Detect noxious irritants.

Question 3

What are the respiratory defence mechanisms of the pharynx/larynx?

Answer 3

Pharynx/Larynx:
Epiglottis prevents food from entering the trachea.
Upon accidental aspiration of food particles, takes part in the cough reflex.

Question 4

Explain the respiratory defence mechanisms of the mucociliary escalator…

Answer 4

Mucociliary escalator:

• Extends from terminal bronchioles - larynx.
• Viscous mucous gel is propelled cranially by the beating of the ciliated epithelium.
• Secretions including IgA, IgG, interferon, and antimicrobial peptides, e.g: defensins.

Question 5

Explain the defence mechanisms of the alveolar macrophages….

Answer 5

Alveolar macrophages:

• Phagocytes resident within the alveolus.
• Normally one sentinel macrophage per alveolus.
• Ingest particles that reach the alveolus - if in a dusty environment, or lung haemorrhage occurs, the number of alveolar macrophages rapidly increases to clear the particles present.

Question 6

What non-inflammatory disease of the lungs that can occur?

Answer 6

Atelectasis: either primary or secondary. Primary => failure of lung tissue to expand at birth. Secondary => collapse of lung tissue that was previously expanded.

Emphysema: excessive air within the lungs.

Pigmentation: permanent abnormal discolouration (melanosis)

Circulatory disturbances: hyperaemia, congestion, oedema

Question 7

Describe primary atelectasis…

Answer 7

Failure of lung tissue to expand at birth.
Can be total or partial. Bronchi tends to stay open regardless.
Non-aerated tissue - dark red
Aerated tissue - salmon pink

Question 8

Describe secondary atelectasis…

Answer 8

‘Acquired’ atelectasis or collapse. May be secondary to:

• Compression e.g: air, masses, fluid
• Obstruction e.g: masses, FB thick secretions

Question 9

What can cause collapse of lungs secondary to compression?

Answer 9

Pulmonary or mediastinal masses
Hydrothorax
Pneumothorax
Prolonged recumbency in LAs
Prolong abdominal distention in LAs

Question 10

Describe collapse of the lungs secondary to obstruction…

Answer 10

Common in cattle and other ruminants - they have thick fibrous septae in their lungs

Due to bronchiolar obstruction by exudate
Distended alveoli collapse as trapped air is absorved
Collapsed alveoli contains a little fluid and macrophages

Question 11

Define and describe emphysema

Answer 11

Excessive air in the lungs
In severe cases, the lungs do not deflate on opening the thoracic cavity
Imprints of the ribs can be present on pleural surfaces
Subdivded:
1. Alveolar
2. Intersitial (alveolar wall, blood vessels)
3. Compensatory (neighbouring part of lung too collapsed and recieves too much air to compensate)

Question 12

What are the 3 types of emphysema…

Answer 12

1. Alveolar: permanent abnormal enlargment of airspaces distal to the bronchioles, often due to destruction of the alveolar walls by neutrophil elastase, e.g: RAO (restrictive airway disease) in horses.
2. Interstitial: septal (interstitial) lymphatics are dilated with air secondary to forced expiration, e.g: pneumonia in cattle.
3. Compensatory: emphysema is adjacent to an area of consolidation (all species).

Question 13

Define consolidation of lungs..

Answer 13

Lungs becoming more solid

i.e air replaced by fluid, neoplastic cells, fibrosis

Question 14

Describe Recurrent Airway Disease (RAO) in horses

Answer 14

Obstructive chronic bronchitis and/or emphysema

Thick, viscous mucous and inflammatory reaction, narrow airways.

Destruction of alveolar walls by neutrophil elastase - causing alveolar emphysema

Question 15

What two reasons might you get pigmentations in the lungs?

Answer 15

Melanosis

Anthracosis

Question 16

Describe melanosis of the lung..

Answer 16

Deposition of melanin in alveolar walls (calves, lambs and pigs).

No pathology

Question 17

Describe anthracosis of the lungs…

Answer 17

Accumulation of carbon in alveolar macrophages. Carbon is inert, and can’t be broken down so stay in alveolar macrophages. Secondary issues with phagocytosis may occur is they are full of carbon

Question 18

What circulatory disturbances can occur in the lungs?

Answer 18

Hyperaemia and congestion

Question 19

Describe hyperaemia (circulatory disturbance).

Answer 19

Increased blood flow into tissue.

• Localised or diffuse
• Associated with acute inflammation
• Affected areas of lung are dark red in colour
• Cranioventral lung lobes affected in association with aspiration pneumonia

Question 20

Describe congestion (circulatory disturbance).

Answer 20

Decreased blood flow out of tissue.

• Diffuse with cardiac failure.
• Dependent (may be unilateral) in hypostatic congestion - dark blue/purple lungs.Hypostatic congestion occurs after death (gravity pools blood into lowest areas). Similar effect can occur if the animal is kept in lateral recumbency for long periods of time.
• Affected areas of lung are grey/blue in colour.
• Terminal pulmonary congestion is seen in animals euthanised with barbiturates.

Question 21

Describe oedema (circulatory distrubance)

Answer 21

Pulmonary oedema - flooding of alveoli by fluid, which mixes with surfactant, creating a foam and compromising ventilation.

Question 22

What are the normal factors resisting pulmonary oedema in the lungs?

Answer 22

Tight junctions between alveolar epithelium (and capillary endothelia).

Intra-alveolar pressure > intersitial pressure.

Under normal conditions, fluid escaping from the blood through the endothelium passes into the interstitial space, and is removed by lymphatic drainage.

Question 23

Describe the pathogenesis of pulmonary oedema….

Answer 23

Cardiogenic:
Slowly-developiing heart failure (especially LHS), leading to high venous pressure

Neurogenic (pressure overload):
Sympathetic stimulation in acute brain damage - increases pulmonary capillary hydrostatic pressure.

Excessive fluid therapy (volume overload).

Damage to endothelium or epithelium:

• By toxic substances, e.g: gases (smoke), systemic toxins (paraquat, 3-methyl indole), endotoxins (gut).
• As part of an acute inflammatory process.

Question 24

Describe the pathology of pulmonary oedema…

Answer 24

Gross: lungs wet and heavy, may not collapse on opening chest, and have rib impressions on the pleural surface.

Microscopic: oedema fluid generally leaches out in tissue sections but may appear as pale pink fluid when stained with H and E.

Question 25

Describe lung haemorrhage.

Answer 25

Often occurs outside of the lungs and presses on the lungs/leaks into the lungs. - Septicaemias - Bleeding disorders - Very severe congestion - As part of severe acute inflammation. N.B: haemosiderin

Question 26

Define thrombosis

Answer 26

Obstruction of vessels by coagulated blood components during life

Question 27

Define embolism

Answer 27

Detachment of thrombi (or bacteria, tumours etc) become lodged in small blood vessels

Question 28

Define infarction

Answer 28

Death of tissue due to an interruption in blood supple

Question 29

Describe thrombosis, embolism and infarction of the respiratory system

Answer 29

``` Rare Predisposing factors include: DIC Liver abscessation Valvular endocarditis ```

Question 30

Describe rhinitis and sinusitis - inflammation of the nasal cavity and paranasal sinuses.

Answer 30

Can be acute, subacute, or chronic. Localised or part of a systemic disease (e.g: malignant catarrhal fever - bovine herpesvirus). Infectious or non-infectious (allergic or idiopathic). Morphological subtypes: serous, catarrhal (mucoid), purulent/suppurative (involves neutrophils, usually bacterial involvement), necrotising, ulcerative, haemorrhagic. Sequelae: resolution, healing by scar formation, extension to other parts of the respiratory tract. Inflammation may localise and persist in the guttural pouches (horses).

Question 31

Describe pneumonia types (inflammation of the lung)

Answer 31

Bronchopneumonia - Suppurative or Fibrinous Intersitial pneumonia Embolic pneumonia Granulomatous pneumonia

Question 32

How are different types of pneumonia classified by location?

Answer 32

Suppurative bronchopneumonia: cranio-ventral lung lobes, and cranio-ventral regions of caudal lobes, are most often affected. Fibrinous bronchopneumonia: cranio-ventral lung lobes, and cranio-ventral regions of caudal lung lobes, are most often affected. Interstitial pneumonia: bands across entire lung. Embolic pneumonia: random/nodular distribution. Granulomatous pneumonia: random/nodular distribution.

Question 33

Describe bronchopnemonia...

Answer 33

Caused by bacterial infection Lesions occur in cranioventral regions under gravity Spread of inflammation within the lung is usually by extension from lobule to lobule along the airways

Question 34

What are the potential sequelae of bronchopneumonia?

Answer 34

Resolution: mild inflammation resolves in 7 days, and the lung is back to normal within 3 weeks Deterioration: abscess formation with pyogenic bacteria. Pleuritis in sever fibrinous pneumonia with adhesions or death due to hypoxaemia Persistence: more severe inflammation becomes chronic with fibrosis.

Question 35

Describe bronchiectasis..

Answer 35

Seen principally in cattle | Permanent dilation of some bronchi due to irreversible damage to bronchi walls

Question 36

What are the two variations of bronchopneumonia?

Answer 36

1. Lobar pneumonia | 2. Broncho-interstital pneumonia

Question 37

Describe lobar pneumonia...

Answer 37

Pathogenesis: Agressive fulminating bronchopneumonia Inflammation occupies major part of the entire lung lobe May follow impaired defences Invasion of highly toxic bacteria e.g. pasteurella Aspiration of foreign fluid or gastric contensts Sequelae: Commonly death Fibrosis of affected areas

Question 38

Describe broncho-interstital pnemonia

Answer 38

Pathogenesis: Inhaled mycoplasmas and some viruses Initial inflammatory reaction in bronchioles Intersitial lymphocytic proliferation 'cuffing' Importance - mostly economic: Reduced growth rate Predisposition to entry of more pathogenic agents

Question 39

Describe intersitial pneumonia

Answer 39

Secondary to haematogenous rather than inhaled damage. Inflammation is centred on interstitial seta rather than airways Distribution is diffuse, rather than cranio-ventral

Question 40

Describe the aetiology of interstital pnemonia..

Answer 40

``` Acute: Infection (distemper) Inhaled (e.g. smoke) Ingested toxins (e.g. fog fever) Systemic conditions (e.g. uraemia) Hypersensitivity (lungworm) ``` Chronic: Infectious (e.g. jaagsiekte) Inhaled dusts (coal) Hypersensitivity (farmer's lung)

Question 41

Describe interstital pnemonia secondary to paraquat...

Answer 41

Poisoning occurs in dogs and cats: Pneumotoxin = selectively damages alveolar epithelium. Allows exudation of fluid into the alveolar lumen - loss of respiratory function. ``` Low doses (accidental ingestion): Moderate pulmonary oedema. Clinical signs of respiratory distress become evident several days to weeks later, when widespread fibrosis of alveolar walls interferes with gas exchange. ``` ``` High doses (malicious poisoning): Results in severe fatal pulmonary oedema and haemorrhages. ```

Question 42

Describe interstital pneumonia secondary to trytophan...

Answer 42

Acute Bovine Pulmonary Oedema and Emphysema ("Fog Fever"). Adult cattle moved to lush autumn pasture. High morbidity and mortality. Pathogenesis: Excess tryptophan in autumn grass, which is metabolised to 3-methyl indole. This is toxic to Type 1 Pneumocytes. Pathology: Lungs enlarged and wet, with markedly widened interlobular septa (oedema and emphysema) - gives a "bubblewrap" appearance. Flooding of alveoli with protein-rich fluid.

Question 43

Describe embolic pneumonia...

Answer 43

Pulmonary abscesses resulting from septic emboli in pulmonary vessels Secondary to endocarditis Secondary to hepatic abscessation and phlebitis

Question 44

Describe granulomatous pneumonia

Answer 44

Pneumonia caused by agents such as Mycobacterium and fungi. Inflammation is chronic and persistent with macrophages as predominant cell type

Question 45

Describe tumours and tumour-like lesions of the upper respiratory tract...

Answer 45

Nasal and nasopharyngeal polyps: - Single or multiple (often peduncluated) masses, secondary to chronic irritation/inflammation. - May follow infection, such as cat flu, which causes inflammation. - Composed of hyperplastic or ulcerated epithelium, granulating to fibrous stroma and varying numbers of inflammatory cells. Benign, hyperplastic lesions. Nasal and paranasal sinus tumours: Most are malignant - carcinomas or sarcomas.

Question 46

Describe neoplasia of the lungs...

Answer 46

May be primary or secondary. Primary tumours are usually invasive carcinomas, and often arise at the hilar region before spreading within the lung and to the regional lymph nodes. Most tumours are secondary (metastatic/metastases) - these include mammary tumours, haemangiosarcomas, and osteosarcomas. Multiple nodules occur in all lung lobes. Primary tumours tend to be one large mass (sometimes with subsequent small metastases), secondary tumours have lots of smaller nodules.