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General Pathology of the Respiratory Tract Flashcards

1
Q

Non-inflammatory diseases

A

Atelectasis
Emphysema
Pigmentation
Circulatory disturbances

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2
Q

primary atelectasis

A

Failure of lung tissue to expand at birth

can be total or partial

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3
Q

secondary atelectasis

A

Collapse of all or part of the lung that has previously been ventilated
May be secondary to - Compression, Obstruction

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4
Q

secondary atelectasis - compression - causes

A 
Pulmonary or mediastinal masses 
Hydrothorax 
Pneumothorax 
Prolonged recumbency in large animals 
Prolonged abdominal distension in large animals
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5
Q

secondary atelectasis - obstruction - causes

A

Common in cattle
Due to bronchiolar obstruction by exudate
Distended alveoli collapse as trapped air is absorbed
Collapsed alveoli contain a little fluid and macrophages

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6
Q

emphysema

A

excessive air in the lungs
in severe cases, the lungs do not deflate on opening the thoracic cavity
Imprints of the ribs present on pleural surfaces
3 types - Alveolar, Interstitial, Compensatory

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7
Q

alveolar emphysema

A

permanent abnormal enlargement of airspaces distal to the terminal bronchioles often due to destruction of alveolar walls by neutrophil elastase
e.g. RAO in horses

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8
Q

interstitial emphysema

A

septal (interstitial) lymphatics are dilated with air secondary to forced expiration
e.g. pneumonia in cattle

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9
Q

compensatory emphysema

A

emphysema is adjacent to an area of consolidation (all species)

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10
Q

Recurrent airway obstruction/COPD

A

obstructive chronic bronchitis - infl, swelling, thick sticky mucous blocks airways
emphysema - air exchange difficult, air becomes trapped in alveoli

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11
Q

pigmentation

A

Permanent abnormal discolouration
Melanosis - deposition of melanin in alveolar walls (calves, lambs and pigs)
Anthracosis - accumulation of carbon in alveolar macrophages (urban dogs and cats)

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12
Q

Circulatory disturbances - Hyperaemia

A

incr blood flow into tissue
localised or diffuse
associated with acute inflammation
affected areas of lung are dark red in colour
cranioventral lung lobes often affected in association with aspiration pneumonia

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13
Q

Circulatory disturbances - Congestion

A

decr blood flow from tissue
diffuse in cardiac failure or dependent (may be
unilateral) in hypostatic congestion
affected areas of lung are grey/blue in colour
terminal pulmonary congestion is also seen in animals euthanased with barbiturates

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14
Q

Circulatory disturbances - Oedema

A

Pulmonary oedema - flooding of alveoli by fluid - mixes with surfactant - foam - compromises ventilation

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15
Q

Factors resisting pulmonary oedema

A

tight junctions between alveolar epithelium (and capillary endothelia)
intra-alveolar pressure greater than interstitial pressure
under normal conditions, fluid escaping from the blood through the endothelium passes into the interstitial space and is removed by lymphatic drainage

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16
Q

Pathogenesis of Pulmonary Oedema - Cardiogenic

A

pressure overload

slowly developing heart failure – high venous pressure

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17
Q

Pathogenesis of Pulmonary Oedema - Neurogenic

A

pressure overload
sympathetic stimulation in acute brain damage
increases pulmonary capillary hydrostatic pressure

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18
Q

Pathogenesis of Pulmonary Oedema - Excessive fluid therapy

A

volume overload

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19
Q

Pathogenesis of Pulmonary Oedema - Damage to endothelium or epithelium

A

by toxic substances, systemic toxins (paraquat, 3-methyl indole), endotoxins (gut)
part of acute inflammatory process

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20
Q

Pathology of pulmonary oedema - Gross

A

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

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21
Q

Pathology of pulmonary oedema - micro

A

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

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22
Q

Circulatory disturbances - Haemorrhage - causes

A 
septicaemias 
bleeding disorders 
very severe congestion 
as part of severe acute inflammation 
Nb haemosiderin
23
Q

thrombosis - define

A

obstruction of vessels by coagulated blood components during life

24
Q

embolism - define

A

detachment of thrombi, become lodged in small blood vessels

25
infarction - define
death of tissue due to an interruption (usually sudden) in its blood supply
26
pulmonary thrombosis, embolism and infarction - predisposing factors
``` disseminated intravascular coagulation (DIC) liver abscessation (esp. cattle) valvular endocarditis (all species) Lung lobe torsion may cause abrupt infarction ```
27
rhinitis and sinusitis - types
Infectious or non-infectious (allergic or idiopathic) | morphological subtypes: serous, catarrhal (mucoid), purulent/suppurative, necrotising, ulcerative, haemorrhagic
28
rhinitis + sinusitis - sequelae
resolution healing by scar formation extension to other parts of the respiratory tract Inflammation may localise and persist in the guttural pouches (horses)
29
pneumonia
Gross + histological descriptions of pneumonia are usually based on distribution of changes in the lungs + type of inflammatory response
30
bronchopneumonia
bacterial infection lesions occur in cranioventral regions of lung due to incr deposition of infectious agents under gravity spread from lobe to lobe via airways or by necrosis of alveoli + septa with toxin producing bacteria aspiration pneumonia (after general anaesthetic)
31
bronchopneumoina - sequlae
Resolution Deterioration Persistence
32
bronchopneumoina - sequlae - resolution
mild inflammation resolves in 7 days and the lung is back to normal within 3 weeks
33
bronchopneumoina - sequlae - deterioration
abscess formation with pyogenic bacteria pleuritis in severe fibrinous pneumonia with adhesions death in fulminating cases due to hypoxaemia and toxaemia (with or without necrosis)
34
bronchopneumoina - sequlae - persistence
more severe inflammation becomes chronic with fibrosis or bronchiectasis (sequestration)
35
bronchiectasis
seen principally in cattle permanent dilation of some bronchi - irreversible damage to the bronchial wall sequel to chronic bronchitis/persistent bronchopneumonia in severe cases, the bronchial wall may be destroyed - abscess formation
36
lobar pneumonia - pathogenesis
aggressive fulminating bronchopneumonia infl occupies a major part/entire lobes of the lung may follow impaired defences invasion of a highly toxic bacterium e.g. some strains of Pasteurella aspiration of foreign fluids or gastric contents common appearance of pneumonia in dogs and cats because of the lack of complete lobulation and septation
37
lobar pneumonia - sequelae
commonly death | fibrosis of affected areas in surviving animals
38
broncho-interstitial pneumonia - pathogenesis
inhaled mycoplasmas and some viruses initial infl reaction in the bronchioles interstitial lymphocytic proliferation often to the extent of forming complete lymphoid follicles around the airways (‘cuffing’) lymphoid follicles = cell-mediated response to chronic persistent antigenic challenge
39
broncho-interstitial pneumonia - importance
mostly economic reduced growth rate predisposition to the entry of more pathogenic agents
40
interstitial pneumonia
Secondary to haematogenous rather than inhaled damage Infl centred on interstitial septa rather than airways Distribution is diffuse rather than cranioventral (dorsocaudal areas maybe more affected)
41
aetiology of acute interstitial pneumonia
Infections: e.g. distemper in dogs Inhaled chemicals: e.g. smoke Ingested toxins: e.g. paraquat or tryptophan (‘fog fever’) Systemic conditions: e.g. uraemia Hypersensitivity reactions: e.g. lungworm infestation
42
aetiology of chronic interstitial pneumonia
Infections: e.g. jaagsiekte in sheep Inhaled dusts: e.g. coal dust or silica Hypersensitivity reactions: e.g. Micropolyspora faeni (‘farmer’s lung’)
43
toxins - paraquat
pneumotoxin - selectively damages alveolar epithelium | allows exudation of fluid into the alveolar lumen - loss of respiratory function
44
toxins - paraquat - high doses
malicious poisoning | result in severe fatal pulmonary oedema and haemorrhages
45
toxins - paraquat - 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
46
toxins - tryptophan
Acute Bovine Pulmonary Oedema and Emphysema ('Fog Fever’) adult cattle moved to lush pasture (autumn) high morbidity and mortality
47
toxins - tryptophan - pathogenesis
excess tryptophan in autumn grass metabolised in the rumen to 3-methyl indole toxic to Type 1 pneumocytes
48
toxins - tryptophan - pathology
lungs enlarged and wet with markedly widened interlobular septa (oedema and emphysema) flooding of alveoli with protein-rich fluid
49
embolic pneumonia
Pulmonary abscesses resulting from septic emboli in pulmonary vessels Secondary to endocarditis Secondary to hepatic abscessation and phlebitis
50
granulomatous pnemonia
caused by mycobacteria (e.g. tuberculosis) + fungi (e.g. aspergillosis) Inflammation is chronic and persistent Macrophages = predominant cell type Granulomas may be mistaken for tumours on gross examination
51
nasal and nasopharyngeal polyps
Single or multiple (often pedunculated) masses secondary to chronic irritation/infl Composed of hyperplastic/ulcerated epithelium, granulating to fibrous stroma + varying numbers of infl cells
52
nasal + paranasal sinus tumours
most are malignant - carcinomas/sarcomas
53
neoplasia of the lungs
primary or secondary Primary usually invasive carcinomas + often arise at the hilar region before spreading within the lung and to the regional LNs Most are secondary (metastatic) - mammary tumours, haemangiosarcomas + osteosarcomas. Multiple nodules occur in all lung lobes
54
paraneoplastic disease
Space-occupying lesions in the lungs may be associated with periosteal thickening of long bones - Hypertrophic Pulmonary Osteopathy or ‘Marie’s Disease’ Extensive periosteal new bone formation affecting all limbs Unknown pathogenesis – may be nervous or vascular aetiology

Respiratory (21 decks)

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