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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
Features - circulatory disturbance due to congestion
Diffuse (in HF) or dependent (may be unilateral. in hypostatic congestion) Affected areas of lung are green/blue
26
How do the lungs appear in animals that have been euthanised with barbiturates?
Terminal pulmonary congestion - also known as hypostatic congestion.
27
Outline circulatory disturbances due to oedema
Pulmonary oedema - flooding of alveoli by fluid --> mixes with surfactant --> foam --> compromises ventilation
28
What factors resist pulmonary oedema? 3
TIGHT JUNCTIONS - b/w alveolar and capillary endothelium INTRA-ALVEOLAR PRESSURE > interstitial pressire LYMPHATIC DRAINAGE -removes fluid from the interstitial space.
29
What are the 4 different pathogenesis routes of pulmonary oedema?
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.
30
Outline gross pathology of pulmonary oedema
lungs wet and heavy. | may not collapse on opening chest and have rib impression on pleural surface
31
Microscopic pathology - pulmonary oedema
oedema fluid generally leaches out in tissue sections but may appear as pale pink fluid when stained with H&E (oedema fluid contains protein)
32
Why might haemorrhage be a cause of circulatory disturbance?
Septicaemias Bleeding disorders Very severe congestion As part of severe inflammation
33
What does haemosiderin indicate in haemorrhage?
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
What are the components of the TRIAD OF THROMBOSIS?
Endothelial injury Hypercoaguability Abnormal blood flow
35
Define thrombosis
obstruction of vessels by coagulated blood components DURING LIFE
36
Define embolism
detachment of thrombi (bacteria, tumours, fat etc) which become lodged in small blood vessels
37
Define infarction
death of tissue due to an interruption (usually sudden) in its blood supply
38
How common are circulatory disturbances (due to pulmonary thrombosis, embolism and infarction) in veterinary species? What are predisposing factors for this?
Rare | Predisposing factors - DIC, liver abscessation (cattle), valvular endocarditis (all species)
39
What may lung lobe torsion cause?
abrupt infarction in the lungs.
40
Define rhinitis
inflammation of the mucous membrane of the nose
41
Define sinusitis
inflammation of a nasal sinus.
42
Outline rhinitis and sinusitis - 6
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
What are gross and histological descriptions of pneumonia usually based on? 2
Distribution of changes in lungs | Type of inflammatory response
44
Define pneumonia
lung inflammation
45
What are the 4 main types of pneumonia?
Bronchopneumonia (fibrinous or suppurative) Interstitial Embolic Granulomatous
46
Describe location of suppurative bronchopneumonia
cranioventral distribution (of all lung lobes). associated with aspiration pneumonia
47
Describe location of fibrinous bronchopneumonia
cranioventral distribution (of all lung lobes). associated with aspiration pneumonia
48
Describe location of interstitial pneumonia
Throughout the lungs
49
Describe the location of embolic and granulomatous pneumonia
Both have foci of distribution
50
What is bronchopneumonia?
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
3 possible sequelae of bronchopneumonia
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
Define 'fulminating infection'
occuring suddenly, rapidly and with great severity or intesity
53
Define bronchiectasis
= 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
Which species is bronchiectasis principally seen in?
cattle (also sheep, goats and pigs)
55
Name 2 variations of bronchopneumonia
lobar pneumonia | interstitial pneumonia
56
Describe lobar pneumonia
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
Why is lobar pneumonia a common appearance of pneumonia in dogs and cats?
because of the lack of complete lobulation and septation in these species.
58
Sequelae - lobar pneumonia
commonly death | fibrosis of affected areas in surviving anials
59
Pathogenesis - bronchointerstitial pneumonia (a type of bronchopneumonia)
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
What is the importance of bronchointerstitial pneumonia?
Mostly economic - reduced growth rate. Predisposition to the entry of more pathogenic agents.
61
What is interstitial pneumonia usually secondary to?
haematogenous rather than inhaled damage.
62
Where is inflammation found in intersitital pneumonia?
inflammation is centred on interstitial septa rather than airways. Distribution is diffuse rather than cranioventral (dorso-caudal areas may be more affected).
63
Aetiology - acute interstitial pneumonia - 5
``` Infections (canine distemper) Inhaled chemicals (smoke) Ingested toxins (paraquat or tryptophan --> fog fever) Systemic conditions (uraemia) Hypersensitivity reactions (lungworm infections) ```
64
Aetiology - chronic interstitial pneumonia
``` Infections (sheep jaagsiekte) Inhaled dusts (coal dust or silica) Hypersensitivity reactions (Saccharopolyspora rectivirgula - farmer's lung) ```
65
What is paraquat?
``` A herbicide. If ingested (dogs/cats) --> acute interstitial pneumonia (allows exudation of fluid into alveolar lumen --> loss of respiratory function) ```
66
What happens if low doses (accidental) of paraquat are ingested?
moderate pulmonary oedema | CS - respiratory distress (days - weeks later when widespread fibrosis of alveolar walls interferes with gas exchange).
67
What happens if high doses (malicious poisoning) of paraquat are ingested?
severe fatal pulmonary oedema and haemorrhage (overall classified as interstitial pneumonia secondary to toxins)
68
What is another name for tryptophan poisoning in cattle? 2
Acute Bovine Pulmonary Oedema and Emphysema | 'Fog Fever'
69
When does tryptophan poisoning occur?
when adult cattle are moved to lush pasture (autumn). high morbidity and mortality.
70
Pathogenesis - trypophan poisoning
excess tryptophan in autumn grass metabolised in rumen to 3-methyl indole which is toxic to type 1 pneumocytes.
71
Differentiate type 1 and 2 pneumocytes
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
Pathology - tryptophan poisoing (--> interstitial pneumonia)
lungs enlarged and wet with markedly widened septa (oedema and emphysema). flooding of alveoli with protein rich fluid.
73
What might embolic pneumonia be secondary to?
Endcarditis, hepatic absscessation or phlebitis
74
Define phlebitis
Inflammation of a vein
75
What causes granulomatous pneumonia?
mycobateria (TB) and fungi (aspergillosis)
76
Outline granulomatous pneumonia
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
Where may polpys be found in the RespT?
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
Outline tumours in the nasal and paranasal sinus regions
Most are malignant - carcinomas or sarcomas.
79
Outline neoplasia of the lungs
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
What paranaeoplastic diseases can the RespT be involved in?
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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