Flashcards in Respiratory pathology Deck (80):
Qhat is considered URT?
nasal cavity, paranasal sinus, nasopharynx, larynx, GP
What is considered LRT?
trachea, bronchi, bronchioles, alveoli
Differentiate the air conduction system from the gas exchange system
AIR CONDUCTION - nasal cavity, nasopharynx, larynx, tranchea, bronchi and bronchioles
GAS EXCHANGE - respiratory bronchioles and alveoli
What do the nasal chambers do?
50% resistance to airflow
remove particles >10-20 micromoles
humidify and warm incoming air
detect noxious irritants
Where is the mucociliary excalator present?
from terminal bronchioles to larynx. secretions include IgA and IgG, IFN and AMP (e.g defensins)
Where are alveolar macrophages?
usually 1 within the alveolus.
What are the 2 types of atelectasis
PRIMARY - failure of lung to expand at birth
SECONDARY/ACQUIRED - collapse of lung tissue that was previously expanded (ventilated)
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
permanent abnormal discolouration (melanosis)
What are the different types of circulatory disturbance?
hyperaemia, congestion and oedema
List categories of non-inflammatory diseases of the lungs -4
Atelectasis - primary or secondary
What are the different types of primary atelectasis?
TOTAL - whole lung affected
PARTIAL - area(s) of lung affected, pale = normally aerated, dark = failed to inflate
What may secondary/acquired atelectasis be secondary to?
COMPRESSION - air, mass, fluids
OBSTRUCTION - masses, FBs, thick secretions
What forms of compression can cause secondary atelectasis? 5
Prolonged recumbency (large animals)
Prolonged abdominal distension (large animals)
Outline lung collapse secondary to obstruction - 4
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.
How is emphysema divided?
What is alveolar emphysema?
permanent abnormal enlargement of airspaces distal to teh terminal bronchioles often due to destruction of alveolar walls by neutrophil elastase (RAO horses)
Outline interstitial emphysema
spetal (interstitial) lymphatics are dilated with air secondary to forced expiration (e.g. pneumonia in cattle)
Outline compensatory emphysema
emphysema is adjacent to an area of consolidation (all species, an area of lung that has become more solid)
What happens in obstructive chronic bronchitis?
SMC hypertrophy and hyperplasia.
Mucous increases in volume and viscosity
What is the predilection site for pigmentation?
lungs normally (but other sites too)
What are the 2 types of pigmentation?
MELANOSIS - depositon of melanin in alveolar walls - calves, lambs and pigs
ANTHRACOSIS - accumulation of carbon in alveolar macrophages (urban dogs and cats)
Differentiate hyperaemia and congestion
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.
Features - circulatory disturbance due to hyperameia
Localised or diffsue
Associated with acute inflammation
Affected areas of lung are dark red in colour
Cranioventral lung lobes in association with aspiration pneumonia.
Features - circulatory disturbance due to congestion
Diffuse (in HF) or dependent (may be unilateral. in hypostatic congestion)
Affected areas of lung are green/blue
How do the lungs appear in animals that have been euthanised with barbiturates?
Terminal pulmonary congestion - also known as hypostatic congestion.
Outline circulatory disturbances due to oedema
Pulmonary oedema - flooding of alveoli by fluid --> mixes with surfactant --> foam --> compromises ventilation
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.
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.
Outline gross pathology of pulmonary oedema
lungs wet and heavy.
may not collapse on opening chest and have rib impression on pleural surface
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)
Why might haemorrhage be a cause of circulatory disturbance?
Very severe congestion
As part of severe inflammation
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
What are the components of the TRIAD OF THROMBOSIS?
Abnormal blood flow
obstruction of vessels by coagulated blood components DURING LIFE
detachment of thrombi (bacteria, tumours, fat etc) which become lodged in small blood vessels
death of tissue due to an interruption (usually sudden) in its blood supply
How common are circulatory disturbances (due to pulmonary thrombosis, embolism and infarction) in veterinary species?
What are predisposing factors for this?
Predisposing factors - DIC, liver abscessation (cattle), valvular endocarditis (all species)
What may lung lobe torsion cause?
abrupt infarction in the lungs.
inflammation of the mucous membrane of the nose
inflammation of a nasal sinus.
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
What are gross and histological descriptions of pneumonia usually based on? 2
Distribution of changes in lungs
Type of inflammatory response
What are the 4 main types of pneumonia?
Bronchopneumonia (fibrinous or suppurative)
Describe location of suppurative bronchopneumonia
cranioventral distribution (of all lung lobes). associated with aspiration pneumonia
Describe location of fibrinous bronchopneumonia
cranioventral distribution (of all lung lobes). associated with aspiration pneumonia
Describe location of interstitial pneumonia
Throughout the lungs
Describe the location of embolic and granulomatous pneumonia
Both have foci of distribution
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)
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
Define 'fulminating infection'
occuring suddenly, rapidly and with great severity or intesity
= 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.
Which species is bronchiectasis principally seen in?
cattle (also sheep, goats and pigs)
Name 2 variations of bronchopneumonia
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).
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.
Sequelae - lobar pneumonia
fibrosis of affected areas in surviving anials
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.
What is the importance of bronchointerstitial pneumonia?
Mostly economic - reduced growth rate. Predisposition to the entry of more pathogenic agents.
What is interstitial pneumonia usually secondary to?
haematogenous rather than inhaled damage.
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).
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)
Aetiology - chronic interstitial pneumonia
Infections (sheep jaagsiekte)
Inhaled dusts (coal dust or silica)
Hypersensitivity reactions (Saccharopolyspora rectivirgula - farmer's lung)
What is paraquat?
If ingested (dogs/cats) --> acute interstitial pneumonia (allows exudation of fluid into alveolar lumen --> loss of respiratory function)
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).
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)
What is another name for tryptophan poisoning in cattle? 2
Acute Bovine Pulmonary Oedema and Emphysema
When does tryptophan poisoning occur?
when adult cattle are moved to lush pasture (autumn). high morbidity and mortality.
Pathogenesis - trypophan poisoning
excess tryptophan in autumn grass metabolised in rumen to 3-methyl indole which is toxic to type 1 pneumocytes.
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
Pathology - tryptophan poisoing (--> interstitial pneumonia)
lungs enlarged and wet with markedly widened septa (oedema and emphysema). flooding of alveoli with protein rich fluid.
What might embolic pneumonia be secondary to?
Endcarditis, hepatic absscessation or phlebitis
Inflammation of a vein
What causes granulomatous pneumonia?
mycobateria (TB) and fungi (aspergillosis)
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)
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.
Outline tumours in the nasal and paranasal sinus regions
Most are malignant - carcinomas or sarcomas.
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.