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Respiratory > General Pathology of the Respiratory Tract > Flashcards

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
Q

infarction - define

A

death of tissue due to an interruption (usually sudden) in its blood supply

26
Q

pulmonary thrombosis, embolism and infarction - predisposing factors

A 
disseminated intravascular coagulation (DIC)
liver abscessation (esp. cattle)
valvular endocarditis (all species) 
Lung lobe torsion may cause abrupt infarction
27
Q

rhinitis and sinusitis - types

A

Infectious or non-infectious (allergic or idiopathic)

morphological subtypes: serous, catarrhal (mucoid), purulent/suppurative, necrotising, ulcerative, haemorrhagic

28
Q

rhinitis + sinusitis - sequelae

A

resolution
healing by scar formation
extension to other parts of the respiratory tract
Inflammation may localise and persist in the guttural pouches (horses)

29
Q

pneumonia

A

Gross + histological descriptions of pneumonia are usually based on distribution of changes in the lungs + type of inflammatory response

30
Q

bronchopneumonia

A

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
Q

bronchopneumoina - sequlae

A

Resolution
Deterioration
Persistence

32
Q

bronchopneumoina - sequlae - resolution

A

mild inflammation resolves in 7 days and the lung is back to normal within 3 weeks

33
Q

bronchopneumoina - sequlae - deterioration

A

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
Q

bronchopneumoina - sequlae - persistence

A

more severe inflammation becomes chronic with fibrosis or bronchiectasis (sequestration)

35
Q

bronchiectasis

A

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
Q

lobar pneumonia - pathogenesis

A

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
Q

lobar pneumonia - sequelae

A

commonly death

fibrosis of affected areas in surviving animals

38
Q

broncho-interstitial pneumonia - pathogenesis

A

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
Q

broncho-interstitial pneumonia - importance

A

mostly economic
reduced growth rate
predisposition to the entry of more pathogenic agents

40
Q

interstitial pneumonia

A

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
Q

aetiology of acute interstitial pneumonia

A

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
Q

aetiology of chronic interstitial pneumonia

A

Infections: e.g. jaagsiekte in sheep
Inhaled dusts: e.g. coal dust or silica
Hypersensitivity reactions: e.g. Micropolyspora faeni (‘farmer’s lung’)

43
Q

toxins - paraquat

A

pneumotoxin - selectively damages alveolar epithelium

allows exudation of fluid into the alveolar lumen - loss of respiratory function

44
Q

toxins - paraquat - high doses

A

malicious poisoning

result in severe fatal pulmonary oedema and haemorrhages

45
Q

toxins - paraquat - low doses

A

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
Q

toxins - tryptophan

A

Acute Bovine Pulmonary Oedema and Emphysema (‘Fog Fever’)
adult cattle moved to lush pasture (autumn)
high morbidity and mortality

47
Q

toxins - tryptophan - pathogenesis

A

excess tryptophan in autumn grass metabolised in the rumen to 3-methyl indole toxic to Type 1 pneumocytes

48
Q

toxins - tryptophan - pathology

A

lungs enlarged and wet with markedly widened interlobular septa (oedema and emphysema) flooding of alveoli with protein-rich fluid

49
Q

embolic pneumonia

A

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

50
Q

granulomatous pnemonia

A

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
Q

nasal and nasopharyngeal polyps

A

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
Q

nasal + paranasal sinus tumours

A

most are malignant - carcinomas/sarcomas

53
Q

neoplasia of the lungs

A

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
Q

paraneoplastic disease

A

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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