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Respiratory pathology Flashcards

1
Q

Qhat is considered URT?

A

nasal cavity, paranasal sinus, nasopharynx, larynx, GP

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2
Q

What is considered LRT?

A

trachea, bronchi, bronchioles, alveoli

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3
Q

Differentiate the air conduction system from the gas exchange system

A

AIR CONDUCTION - nasal cavity, nasopharynx, larynx, tranchea, bronchi and bronchioles
GAS EXCHANGE - respiratory bronchioles and alveoli

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4
Q

What do the nasal chambers do?

A

50% resistance to airflow
remove particles >10-20 micromoles
humidify and warm incoming air
detect noxious irritants

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5
Q

Where is the mucociliary excalator present?

A

from terminal bronchioles to larynx. secretions include IgA and IgG, IFN and AMP (e.g defensins)

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6
Q

Where are alveolar macrophages?

A

usually 1 within the alveolus.

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7
Q

What are the 2 types of atelectasis

A

PRIMARY - failure of lung to expand at birth

SECONDARY/ACQUIRED - collapse of lung tissue that was previously expanded (ventilated)

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8
Q

Define emphysema

A

Excessive air within the lungs (alveolar versus interstitial). In severe cases - lungs fail to deflate and there are imprints of the ribs on the pleural spaces

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9
Q

Define pigmentation

A

permanent abnormal discolouration (melanosis)

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10
Q

What are the different types of circulatory disturbance?

A

hyperaemia, congestion and oedema

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11
Q

List categories of non-inflammatory diseases of the lungs -4

A

Atelectasis - primary or secondary
Emphysema
Prigmentation
Circulating disturbances

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12
Q

What are the different types of primary atelectasis?

A

TOTAL - whole lung affected

PARTIAL - area(s) of lung affected, pale = normally aerated, dark = failed to inflate

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13
Q

What may secondary/acquired atelectasis be secondary to?

A

COMPRESSION - air, mass, fluids

OBSTRUCTION - masses, FBs, thick secretions

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14
Q

What forms of compression can cause secondary atelectasis? 5

A 
Pulmonary/mediastinal massess
Hydrothorax
Pneumothorax
Prolonged recumbency (large animals)
Prolonged abdominal distension (large animals)
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15
Q

Outline lung collapse secondary to obstruction - 4

A

Common in cattle (lack collateral circulation between lobules due to thick fibrous septae)
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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16
Q

How is emphysema divided?

A

3 types:
alveolar
interstitial
compensatory

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17
Q

What is alveolar emphysema?

A

permanent abnormal enlargement of airspaces distal to teh terminal bronchioles often due to destruction of alveolar walls by neutrophil elastase (RAO horses)

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18
Q

Outline interstitial emphysema

A

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

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19
Q

Outline compensatory emphysema

A

emphysema is adjacent to an area of consolidation (all species, an area of lung that has become more solid)

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20
Q

What happens in obstructive chronic bronchitis?

A

SMC hypertrophy and hyperplasia.

Mucous increases in volume and viscosity

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21
Q

What is the predilection site for pigmentation?

A

lungs normally (but other sites too)

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22
Q

What are the 2 types of pigmentation?

A

MELANOSIS - depositon of melanin in alveolar walls - calves, lambs and pigs
ANTHRACOSIS - accumulation of carbon in alveolar macrophages (urban dogs and cats)

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23
Q

Differentiate hyperaemia and congestion

A

HYPERAEMIA: increased blood flow in to a peripheral tissue bed but outflow same. Overall increase in oxygenated blood entering the tissue bed.
CONGESTION: normal blood flow into a peripheral tissue bed but outflow reduced.

Grossly you can’t differentiate these.

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24
Q

Features - circulatory disturbance due to hyperameia

A

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

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25
Q

Features - circulatory disturbance due to congestion

A

Diffuse (in HF) or dependent (may be unilateral. in hypostatic congestion)
Affected areas of lung are green/blue

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26
Q

How do the lungs appear in animals that have been euthanised with barbiturates?

A

Terminal pulmonary congestion - also known as hypostatic congestion.

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27
Q

Outline circulatory disturbances due to oedema

A

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

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28
Q

What factors resist pulmonary oedema? 3

A

TIGHT JUNCTIONS - b/w alveolar and capillary endothelium
INTRA-ALVEOLAR PRESSURE > interstitial pressire
LYMPHATIC DRAINAGE -removes fluid from the interstitial space.

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29
Q

What are the 4 different pathogenesis routes of pulmonary oedema?

A

CARDIOGENIC (pressure overload) - slowly developing HF, especially LSHF due to high venous pressure.
NEUROGENIC (pressure overload) - SNS stimulation in acute brain damage –> increases pulmonary capillary hydrostatic pressure
EXCESSIVE FLUID THERAPY (volume overload)
DAMAGE TO ENDOTHELIUM or EPITHELIUM - by toxic substances - gas (smoke), systemic toxins (paraquat, 3-methyl indole), endotoxins (gut). As part of an acute inflammatory process.

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30
Q

Outline gross pathology of pulmonary oedema

A

lungs wet and heavy.

may not collapse on opening chest and have rib impression on pleural surface

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31
Q

Microscopic pathology - pulmonary oedema

A

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

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32
Q

Why might haemorrhage be a cause of circulatory disturbance?

A

Septicaemias
Bleeding disorders
Very severe congestion
As part of severe inflammation

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33
Q

What does haemosiderin indicate in haemorrhage?

A

used to age how long the haemorrhage has been going on for - if haemosiderin is present, haemorrhage is not acute and may have been occuring for several days

34
Q

What are the components of the TRIAD OF THROMBOSIS?

A

Endothelial injury
Hypercoaguability
Abnormal blood flow

35
Q

Define thrombosis

A

obstruction of vessels by coagulated blood components DURING LIFE

36
Q

Define embolism

A

detachment of thrombi (bacteria, tumours, fat etc) which become lodged in small blood vessels

37
Q

Define infarction

A

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

38
Q

How common are circulatory disturbances (due to pulmonary thrombosis, embolism and infarction) in veterinary species?
What are predisposing factors for this?

A

Rare

Predisposing factors - DIC, liver abscessation (cattle), valvular endocarditis (all species)

39
Q

What may lung lobe torsion cause?

A

abrupt infarction in the lungs.

40
Q

Define rhinitis

A

inflammation of the mucous membrane of the nose

41
Q

Define sinusitis

A

inflammation of a nasal sinus.

42
Q

Outline rhinitis and sinusitis - 6

A

Acute, subacute or chronic
Localised or systemic
Infectious or non-infectious
Morphological subtypes (serous, catarrhal/mucoid, purulent/supparative, necrotising, ulcerative, haemorrhagic)
Sequelae (resolution, healing+scar, extension to other parts of the respT).
GP persistence - horses

43
Q

What are gross and histological descriptions of pneumonia usually based on? 2

A

Distribution of changes in lungs

Type of inflammatory response

44
Q

Define pneumonia

A

lung inflammation

45
Q

What are the 4 main types of pneumonia?

A

Bronchopneumonia (fibrinous or suppurative)
Interstitial
Embolic
Granulomatous

46
Q

Describe location of suppurative bronchopneumonia

A

cranioventral distribution (of all lung lobes). associated with aspiration pneumonia

47
Q

Describe location of fibrinous bronchopneumonia

A

cranioventral distribution (of all lung lobes). associated with aspiration pneumonia

48
Q

Describe location of interstitial pneumonia

A

Throughout the lungs

49
Q

Describe the location of embolic and granulomatous pneumonia

A

Both have foci of distribution

50
Q

What is bronchopneumonia?

A

bacterial infection of lungs (e.g. aspiration pneumonia
cranioventral distribution (bacteria +gravity)
inflammatory spread is lobule to lobule OR necrosis of alveoli and septa (toxin producing bacteria)

51
Q

3 possible sequelae of bronchopneumonia

A

RESOLUTION - resolves in 7 days, normal by 3 weeks
DETERIORATION - abscess (pyogenic bacteria), pleuritis (severe fibrinous pneumonia with adhesions), death (fulminating cases due to hypoxaemia and toxaemia)
PERSISTENCE - more severe inflammation becomes chronic with fibrosis or bronchiectasis

52
Q

Define ‘fulminating infection’

A

occuring suddenly, rapidly and with great severity or intesity

53
Q

Define bronchiectasis

A

= permanent dilation of some bronchi due to irreversible damage to the bronchial wall. sequel to chronic bronchitis or persistent bronchopneumonia. Severe cases –> bronchial wall destruction –> abscess formation.

54
Q

Which species is bronchiectasis principally seen in?

A

cattle (also sheep, goats and pigs)

55
Q

Name 2 variations of bronchopneumonia

A

lobar pneumonia

interstitial pneumonia

56
Q

Describe lobar pneumonia

A

aggressive fulminating bronchopneumonia. inflammation occupies a major part of entire lung lobe.

CAUSES = invasion of a highly toxic bacteria (e.g. some Pasteurella). Aspiration (foreign fluids or gastric contents).

57
Q

Why is lobar pneumonia a common appearance of pneumonia in dogs and cats?

A

because of the lack of complete lobulation and septation in these species.

58
Q

Sequelae - lobar pneumonia

A

commonly death

fibrosis of affected areas in surviving anials

59
Q

Pathogenesis - bronchointerstitial pneumonia (a type of bronchopneumonia)

A

Inhaled mycoplasmas and some viruses. Initial inflammatory 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.

60
Q

What is the importance of bronchointerstitial pneumonia?

A

Mostly economic - reduced growth rate. Predisposition to the entry of more pathogenic agents.

61
Q

What is interstitial pneumonia usually secondary to?

A

haematogenous rather than inhaled damage.

62
Q

Where is inflammation found in intersitital pneumonia?

A

inflammation is centred on interstitial septa rather than airways. Distribution is diffuse rather than cranioventral (dorso-caudal areas may be more affected).

63
Q

Aetiology - acute interstitial pneumonia - 5

A 
Infections (canine distemper)
Inhaled chemicals (smoke)
Ingested toxins (paraquat or tryptophan --> fog fever)
Systemic conditions (uraemia)
Hypersensitivity reactions (lungworm infections)
64
Q

Aetiology - chronic interstitial pneumonia

A 
Infections (sheep jaagsiekte)
Inhaled dusts (coal dust or silica)
Hypersensitivity reactions (Saccharopolyspora rectivirgula - farmer's lung)
65
Q

What is paraquat?

A 
A herbicide.
If ingested (dogs/cats) --> acute interstitial pneumonia (allows exudation of fluid into alveolar lumen --> loss of respiratory function)
66
Q

What happens if low doses (accidental) of paraquat are ingested?

A

moderate pulmonary oedema

CS - respiratory distress (days - weeks later when widespread fibrosis of alveolar walls interferes with gas exchange).

67
Q

What happens if high doses (malicious poisoning) of paraquat are ingested?

A

severe fatal pulmonary oedema and haemorrhage (overall classified as interstitial pneumonia secondary to toxins)

68
Q

What is another name for tryptophan poisoning in cattle? 2

A

Acute Bovine Pulmonary Oedema and Emphysema

‘Fog Fever’

69
Q

When does tryptophan poisoning occur?

A

when adult cattle are moved to lush pasture (autumn). high morbidity and mortality.

70
Q

Pathogenesis - trypophan poisoning

A

excess tryptophan in autumn grass metabolised in rumen to 3-methyl indole which is toxic to type 1 pneumocytes.

71
Q

Differentiate type 1 and 2 pneumocytes

A

Type 1 = squamous alveolar cells, cover 90-95% surface, involved in gas exhange

Type 2 = cover a minority of alveolar surface, function is to secrete surfactant

72
Q

Pathology - tryptophan poisoing (–> interstitial pneumonia)

A

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

73
Q

What might embolic pneumonia be secondary to?

A

Endcarditis, hepatic absscessation or phlebitis

74
Q

Define phlebitis

A

Inflammation of a vein

75
Q

What causes granulomatous pneumonia?

A

mycobateria (TB) and fungi (aspergillosis)

76
Q

Outline granulomatous pneumonia

A

macrophages = predominant cell
Granulomas may be mistaken for tumours on gross examination.
Acid fast bacilli (mycobacterial) - stain red with Ziehl Neelsen.
Fungi stain with PAS or silver stains (Grocott)

77
Q

Where may polpys be found in the RespT?

A

nasal and nasopharyngeal regions
Single or multiple (often pednculated)
Secondary to chronic irritation/inflammation
CONTAIN: hyperplastic or ulcerated epithelium, granulating to fibrous stroma and varying numbers of inflammatory cells.

78
Q

Outline tumours in the nasal and paranasal sinus regions

A

Most are malignant - carcinomas or sarcomas.

79
Q

Outline neoplasia of the lungs

A

primary or secondary
PRIMARY - usually invasive carcinomas, often arise at hilar region before spreading within lung and to regional LN
SECONDARY (most) - mammary tumours, HSA, OSA. Multiple nodules occur in all lung lobes.

80
Q

What paranaeoplastic diseases can the RespT be involved in?

A

SOLs in the lungs or thoracic cavity may be associated with periosteal thickening of long bones - Hypertrophic Pulmonary Osteopathy (Marie’s disease). Affects all bones. Unknown pathogenesis but thought to have vascular or nervous aetiology.

Respiratory (34 decks)

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