General Pathology Resp Tract Flashcards
What does the ‘air conduction system’ consist of?
- nasal cavity
- Nasopharynx
- larynx
- trachea
- bronchi
- bronchioles
What does the upper respiratory tract consist of?
- Nasal cavity
- paranasal sinuses
- Nasopharynx
- Larynx
- Gutteral pouches (horses and great apes)
What does the gas exchange system consist of?
Respiratory bronchioles and alveoli
What provides 50% resistance to airflow as respiratory defence mechanimsms?
Nasal chambers
- remove particles >10-20nm
- humidify and warm incoming air
- detect noxious irritants
How does the pharynx/larynx protect resp tract`?
- epiglottis prevents food entering trachea
- accidental ingestion of food particles -> cough reflex
Where is the mucocilliaray escalator? what secretions?
terminal bronchioles -> larynx (not alvioli)
- secretions: IgA, IgG, interferon, antimicrobial peptides eg. defensins
What immune cells are present in the respiratory tract? Where sepcifically ?
alveolar macrophages
- resident in alveoli
- normally one sentinel macrophage per alveolus
- ingest particles
- numbers will ^ with demand eg. dusty environment
Define atelectasis
1* - failure of lung to expand at birth (lack of surfactant
> partial or total
2* - or acquired: collapse of lung tissue previouslly ventilated
> parital or total
> 2* to compression or obstruction
What colour is normal healthy lung?
Pale salmon pink
Potential causes of atelectasis 2* to compression?
- pulmonary/mediastinal masses
- hydrothorax
- pnumothorax
- prolonged recumbency in large animials
- prolonged abdo distension
Potential causes of atelactasis 2* to obstruction?
- common in cattle (lack of collateral ventilation due to thick fibrous septi)
- exudate
- distended alvilo collapse as trapped air absorbed
- collapsed alvioli contain little fluid and macrophages
Define emphysema. WHat types exist?
> excessive air in the lungs
- alveolar
- interstitial
- compensatory
How can emphysema be seen at PM?
- imprints of ribs
- lungs do not delfate
causes of alveloar emphysema? Spp?
- abnormla enlargement of airspaces distal to terminal bronchioles due to destruction of alveolar walls by neutrophil elastase (eg. RAO in horses)
- hard to exhale so permenantly inflated
- alvioli pop and merge together
- gas exchange compromised
causes of interstitial emphysema. Spp?
- septal (interstital) lymphatics dilated with air 2* to forced expiration eg. pneumonia in cattle
causes of compensatory of emphysema. Spp?
- adjacent to an area of consolidation (all species)
2 main forms of pigmentation?
- Melanosis
- melananin depoistion in alveolar walls (calves, lambs, piglets)
- normal, not pathological - Anthracosis
- carbon taken up by alveolar macrophages
- urban dogs and cats
- rarely pathological unless v severe (then defence mechanisms may be compromised)
Define hyperaemia
increased blood flow into tissue
types of hyperaemia - cause?
- localised or diffuse
- associated with acute inflammation
What colour are areas of lung affected by hyperaemia? Congestion?
Hyperaemia: Dark red
Congestion: Grey blue
- BUT cannot distinguish congestion from hyperaemia on gross analysis ??? LOOK UP
where is hyperaemia commonly seen in the lungs?
- cranioventral lulng with aspiration pnumonia
Define congestion
- decreased blood flow from tissue
what conditions is congestion seen with in the lungs?
- diffuse in cardiac failure
- dependant (may be unilateral) in hypostatic congestion
- hypostatic terminal pulmonary congestion with barbituate euthanasia (postmortem change, not pathological)
Where does lymphatic drainage flow from lungs?
thoracic duct - vena cava
How does pulmonary oedema affect repiration?
- flooding of alvioli by fluid
- mixxes with surfactant
- foam
- compromises ventilation
What factors resist pulmonary oedema?
- tight junctions between alveolar epithelium ( and capillary endothelia)
- intra-alveolar pressure > interstitial pressure
- normal conditions: fluid escaping from the blood through the endothelium passes into interstitial space and removed by lymphatic drainage
where does oedema build up in lungs?
alveolar spaces
4 main causes of pulmonary oedema
- cariogenic (Pressure overload)
- slowly developing LSCF -> high venous pressure - neurogenic (pressue overload)
- sympathetic stimulation in acute brain damage (eg. RTA) -> ^ pulmonary capillary hydrostatic pressue - excessive fluid tx (volume overload)
- damage to endothelium or epithelium
- toxic substances (eg. gases/smoke, systemic toxins: paraquat, 3-methyl indole, endotoxins from the gut)
- part of acute inflammatory process
Gross path of pulmonary oedema
- lungs wet and heavy
- may not collapse on thoracic opening
- rib impressions
micro path of pulmonary oedema
fluid usually leaches out
- may be seen as pale pink fluid when stained with H+E (eosin stain)
Causes of haemorrhage in the lungs?
- septiceamia
- bleeding disorders
- severe congestion
- severe acute inflammation
What indicates chornic haemorrhage?
Haemosiderin in alveolar macrophages
Define thrombosis
Obstruction of vessels by coagulated blood components during life
Define embolism
Detachment of thrombi or bacteria or fat or air which moves aorund cicrulation and lodges in distant small blood vessels
Define infarction
Death of tissues due to an interruption (usually sudden) in its blood supply
What are the 3 aspects of thrombosis formation?
- Endothelial injury
- Abnormal blood flow
- Hypercoagulability
> EXAM QUESTION!
Are pulmonary thrombosis, embolism and infarction common? Predisposing factors?
- rare > predisposing factors: - DIC - liver abscessation esp. cattle - valvular endocarditis (all species) > lung lobe torsion may cause abrupt infarction
How can rhinitis and sinusitis be classified?
- acute/subacute/chronic
- localised/systeic (eg. malignant catarrhal fever with herpesvirus)
- infectious or non-infectious (allergic/idiopathic)
- morphological subtype: serous, catarrhal (mucoid), purulent/supparative, necrotising, ulcerative, haaemorrhagic
Sequalae of rhinitis and sinusitis?
- resolution
- healing by scar formation
- extension to other parts of the respiratory tract
- inflammation may localise and persistn in the gutteral pouches
What are gross and histological description of pnumonia based on?
- distribution of changes in the lungs
- type of inflammatory response
4 main types of pnumonia?
- bronchopnumonia (fibrinous or supparative)
- interstitial
- embolic
- granulomatous
which type of pnumonia often has a cranioventral patten in all lunglobes?
supparative or fibrinous bronchopneumonia
what causes bronchopnuemonia and how does this affect gross pathology? how does it spread?
- bacterial infection, can be 2* to aspiration
- lesions ocour in cranioventral lung fields due to gravity ^ deposition of infectious agents here
- spread of inflammation from lobule to lobule along the airways OR by necorsis of alveoli and septa in the case of toxin producing bacteria
Sequalae of bronchopnumonia?
> resolution (mild inflammation resolves in 7d, lung back to normal 3 weeks)
deterioriation
- abscess formation with pyogenic bacteria
- pleuritis in severe fibrinous pnumonia with adhesions
- death in fulminating cases due to hypoxeamia and toxaemia (+- necrosis)
persistence (more severe inflam becomes chronic with fibrosis or bronchiectasis (sequestration))
What is bronchiectasis? When is it seen?
> permenant dilation of bronchi due to irreversible damage to bronchi wall -> nodular lung surface and large bronchioles on cut surface
- sequel to chronic bronchitis or persistent bronchopnumonia (eg. if seen at abbattoir indicates historical pnumonia problem on farm) as exuat e and inflam cells plug the bronchi and stretch them
- in severe cases bronchial wall may be destroyed resulting in abscess formation
What is lobar pneumonia? Pathogeneis?
> aggressive fulminating bronchopneumonia
common appearance of pneumonia in dogs and cats (lack of septation of lung lobules)
- invasion of highly toxic bacteria eg. pasturella
- aspiration of foreign fluids or gastric contents
-> inflammation occupies major part of/entire lobe of lung
- may follow impaired defences
Sequalae of lobar pneumonia?
- commonly death
- fibrosis of affected areas in surviving animals
Pathogenesis of bronchointerstitial pneumonia? Where does it manifest?
- inhaled mycoplasms and some viruses
- initial inflammatory reaction in bronchioles
- interstitial lymphocytic proliferation -> forms complete lymphoid follicles around the airways (cuffing)
- lymphoid follicles = cell-mediated response to chronic persistent antigenic challenge
> combination of cranioventral bronchopneumonia
Importance of broncho-interstitial pneumonia?
- mostly economic
- reduced growth rate
- predisposition to the entry of more pathogenic agents
How does interstitial pnuemonia form?
2* to haematogenous rather than inhaled damage
Which part of the lung is infected by interstitial pneumonia?
- inflammation of interstitial septa rather than airways
- distribution diffuse cf. cranioventral in brncho-pneumonia
- may be more dorsocaudal areas affected
Aetiology of interstitial pneumonia?
> acute
- infections (eg. distemper dogs)
- inhaled chemicals (eg. smoke)
- ingested toxins (eg. paraquat or tryptophan-fog fever)
- systemic conditions (eg. uraemia)
- hypersensitivity reactions (eg. lungworm infestation)
chronic
- infections (eg. jaagsiekte sheep)
- inhaled dusts (eg. coal dust, silica)
- hypersensitivity reactions (eg. saccharopolyspora rectivirgula - farmer’s lung)
What is paraquat and what pathology does it cause t low and high doses? Spp?
- paraquat herbicide (now banned but still in use illegally)
- poisoning occours in cats and dogs
> pneumotoxin that selectively damages alveolar epithelium
> allow exuation of fluid -> alveolar lumen -> loss of resp function - low doses (accdental): moderate pulm oedema, resp distress days-weeks later due to alveolar wall fibrosis
- high doses (malicious): severe fatal pulonary oedema and haemorrhage
What disease may cows ingesting lush pasture in Autumn develop? Pathogenesis?
Tryptophan poisoning -> acute bovine pulmonary oedema and emphysema (FOG FEVER)
- high morbidity and mortality
> pathogenesis
- tryptophan metabolised to 3-methyl indole
- toxic to type 1 pnumocytes
Gross and micro path of acute bovine pulmonary oedema and emphysema?
- lungs enlarged and wet
- markedly widened interlobular septa (oedema and emphysema)
- flooding of alvioli with protein rich fluid
What gross appearance does emphysema have?
Bubble wrap
What does embolic pneumonia result from?
- septic emboli in pulmonic vessels (remainder of lung relatively normal)
- 2* to endocarditis
- 2* to hepatic abscessation
- 2* to phlebitis eg. of the jugular
What causes granulomatous pnumonia?
- mycobacteria (eg. TB)
- fungi (eg. aspergillosis)
Pathogenesis and cytology of granulomatous pneumonia?
- inflammation chronic and persistent
- macrophages predominant cell type
- may be mistaken for tumours on gross examination
> micro - acid-fast bacilli stain red with ZN
- fungi stain with PAS or silver stains eg. Grocott
What is the most comon tumour-like lesion in the URT? Cause?
Polyps
- nasal or nasopharyngeal
- single or mutliple
- often pedunculated
- hyperplastic, ulcerated epithelium
- granulates to fibrous strom with varying no. inflammattory cells
> 2* to chronic irritation or inflammation
What tumours may be present in the URT?
Nasal and paranasal sinus malignant carcinomas or sarcomas
- v invasive
What are the majority of lung neoplasms?
> majority 2* (metastatic)
- mammary, haemangiosarcoma, osteosarcoma -> multiple nodules in all lung lobes
may be 1* usually invasive carcinomas, arise at hilar region and spread through lung and regional LNs
What paraneoplastic disease may be seen with lung neoplasia?
- Hypertrophic Pulmonary Osteopathy (Marie’s Disease in humans)
- extensive periosteal new bone formation in all limbs
- pathogenesis unknown, may be nervous or vascular aetiology
