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Respiratory > General Pathology Resp Tract > Flashcards

General Pathology Resp Tract Flashcards

0
Q

What does the ‘air conduction system’ consist of?

A
  • nasal cavity
  • Nasopharynx
  • larynx
  • trachea
  • bronchi
  • bronchioles
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1
Q

What does the upper respiratory tract consist of?

A
  • Nasal cavity
  • paranasal sinuses
  • Nasopharynx
  • Larynx
  • Gutteral pouches (horses and great apes)
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2
Q

What does the gas exchange system consist of?

A

Respiratory bronchioles and alveoli

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3
Q

What provides 50% resistance to airflow as respiratory defence mechanimsms?

A

Nasal chambers

  • remove particles >10-20nm
  • humidify and warm incoming air
  • detect noxious irritants
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4
Q

How does the pharynx/larynx protect resp tract`?

A
  • epiglottis prevents food entering trachea

- accidental ingestion of food particles -> cough reflex

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5
Q

Where is the mucocilliaray escalator? what secretions?

A

terminal bronchioles -> larynx (not alvioli)

- secretions: IgA, IgG, interferon, antimicrobial peptides eg. defensins

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6
Q

What immune cells are present in the respiratory tract? Where sepcifically ?

A

alveolar macrophages

  • resident in alveoli
  • normally one sentinel macrophage per alveolus
  • ingest particles
  • numbers will ^ with demand eg. dusty environment
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7
Q

Define atelectasis

A

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

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8
Q

What colour is normal healthy lung?

A

Pale salmon pink

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9
Q

Potential causes of atelectasis 2* to compression?

A
  • pulmonary/mediastinal masses
  • hydrothorax
  • pnumothorax
  • prolonged recumbency in large animials
  • prolonged abdo distension
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10
Q

Potential causes of atelactasis 2* to obstruction?

A
  • 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
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11
Q

Define emphysema. WHat types exist?

A

> excessive air in the lungs

  • alveolar
  • interstitial
  • compensatory
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12
Q

How can emphysema be seen at PM?

A
  • imprints of ribs

- lungs do not delfate

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13
Q

causes of alveloar emphysema? Spp?

A
  • 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
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14
Q

causes of interstitial emphysema. Spp?

A
  • septal (interstital) lymphatics dilated with air 2* to forced expiration eg. pneumonia in cattle
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15
Q

causes of compensatory of emphysema. Spp?

A
  • adjacent to an area of consolidation (all species)
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16
Q

2 main forms of pigmentation?

A
  1. Melanosis
    - melananin depoistion in alveolar walls (calves, lambs, piglets)
    - normal, not pathological
  2. Anthracosis
    - carbon taken up by alveolar macrophages
    - urban dogs and cats
    - rarely pathological unless v severe (then defence mechanisms may be compromised)
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17
Q

Define hyperaemia

A

increased blood flow into tissue

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18
Q

types of hyperaemia - cause?

A
  • localised or diffuse

- associated with acute inflammation

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19
Q

What colour are areas of lung affected by hyperaemia? Congestion?

A

Hyperaemia: Dark red
Congestion: Grey blue
- BUT cannot distinguish congestion from hyperaemia on gross analysis ??? LOOK UP

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20
Q

where is hyperaemia commonly seen in the lungs?

A
  • cranioventral lulng with aspiration pnumonia
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21
Q

Define congestion

A
  • decreased blood flow from tissue
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22
Q

what conditions is congestion seen with in the lungs?

A
  • diffuse in cardiac failure
  • dependant (may be unilateral) in hypostatic congestion
  • hypostatic terminal pulmonary congestion with barbituate euthanasia (postmortem change, not pathological)
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23
Q

Where does lymphatic drainage flow from lungs?

A

thoracic duct - vena cava

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24
Q

How does pulmonary oedema affect repiration?

A
  • flooding of alvioli by fluid
  • mixxes with surfactant
  • foam
  • compromises ventilation
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25
Q

What factors resist pulmonary oedema?

A
  • 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
26
Q

where does oedema build up in lungs?

A

alveolar spaces

27
Q

4 main causes of pulmonary oedema

A
  1. cariogenic (Pressure overload)
    - slowly developing LSCF -> high venous pressure
  2. neurogenic (pressue overload)
    - sympathetic stimulation in acute brain damage (eg. RTA) -> ^ pulmonary capillary hydrostatic pressue
  3. excessive fluid tx (volume overload)
  4. 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
28
Q

Gross path of pulmonary oedema

A
  • lungs wet and heavy
  • may not collapse on thoracic opening
  • rib impressions
29
Q

micro path of pulmonary oedema

A

fluid usually leaches out

- may be seen as pale pink fluid when stained with H+E (eosin stain)

30
Q

Causes of haemorrhage in the lungs?

A
  • septiceamia
  • bleeding disorders
  • severe congestion
  • severe acute inflammation
31
Q

What indicates chornic haemorrhage?

A

Haemosiderin in alveolar macrophages

32
Q

Define thrombosis

A

Obstruction of vessels by coagulated blood components during life

33
Q

Define embolism

A

Detachment of thrombi or bacteria or fat or air which moves aorund cicrulation and lodges in distant small blood vessels

34
Q

Define infarction

A

Death of tissues due to an interruption (usually sudden) in its blood supply

35
Q

What are the 3 aspects of thrombosis formation?

A
  • Endothelial injury
  • Abnormal blood flow
  • Hypercoagulability
    > EXAM QUESTION!
36
Q

Are pulmonary thrombosis, embolism and infarction common? Predisposing factors?

A 
- rare
> predisposing factors:
- DIC
- liver abscessation esp. cattle
- valvular endocarditis (all species) 
> lung lobe torsion may cause abrupt infarction
37
Q

How can rhinitis and sinusitis be classified?

A
  • 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
38
Q

Sequalae of rhinitis and sinusitis?

A
  • resolution
  • healing by scar formation
  • extension to other parts of the respiratory tract
  • inflammation may localise and persistn in the gutteral pouches
39
Q

What are gross and histological description of pnumonia based on?

A
  • distribution of changes in the lungs

- type of inflammatory response

40
Q

4 main types of pnumonia?

A
  • bronchopnumonia (fibrinous or supparative)
  • interstitial
  • embolic
  • granulomatous
41
Q

which type of pnumonia often has a cranioventral patten in all lunglobes?

A

supparative or fibrinous bronchopneumonia

42
Q

what causes bronchopnuemonia and how does this affect gross pathology? how does it spread?

A
  • 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
43
Q

Sequalae of bronchopnumonia?

A

> 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))

45
Q

What is bronchiectasis? When is it seen?

A

> 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
46
Q

What is lobar pneumonia? Pathogeneis?

A

> 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

47
Q

Sequalae of lobar pneumonia?

A
  • commonly death

- fibrosis of affected areas in surviving animals

48
Q

Pathogenesis of bronchointerstitial pneumonia? Where does it manifest?

A
  • 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
49
Q

Importance of broncho-interstitial pneumonia?

A
  • mostly economic
  • reduced growth rate
  • predisposition to the entry of more pathogenic agents
50
Q

How does interstitial pnuemonia form?

A

2* to haematogenous rather than inhaled damage

51
Q

Which part of the lung is infected by interstitial pneumonia?

A
  • inflammation of interstitial septa rather than airways
  • distribution diffuse cf. cranioventral in brncho-pneumonia
  • may be more dorsocaudal areas affected
52
Q

Aetiology of interstitial pneumonia?

A

> 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)

53
Q

What is paraquat and what pathology does it cause t low and high doses? Spp?

A
  • 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
54
Q

What disease may cows ingesting lush pasture in Autumn develop? Pathogenesis?

A

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

55
Q

Gross and micro path of acute bovine pulmonary oedema and emphysema?

A
  • lungs enlarged and wet
  • markedly widened interlobular septa (oedema and emphysema)
  • flooding of alvioli with protein rich fluid
56
Q

What gross appearance does emphysema have?

A

Bubble wrap

57
Q

What does embolic pneumonia result from?

A
  • septic emboli in pulmonic vessels (remainder of lung relatively normal)
  • 2* to endocarditis
  • 2* to hepatic abscessation
  • 2* to phlebitis eg. of the jugular
58
Q

What causes granulomatous pnumonia?

A
  • mycobacteria (eg. TB)

- fungi (eg. aspergillosis)

59
Q

Pathogenesis and cytology of granulomatous pneumonia?

A
  • 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
60
Q

What is the most comon tumour-like lesion in the URT? Cause?

A

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

61
Q

What tumours may be present in the URT?

A

Nasal and paranasal sinus malignant carcinomas or sarcomas

- v invasive

62
Q

What are the majority of lung neoplasms?

A

> 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

63
Q

What paraneoplastic disease may be seen with lung neoplasia?

A
  • Hypertrophic Pulmonary Osteopathy (Marie’s Disease in humans)
  • extensive periosteal new bone formation in all limbs
  • pathogenesis unknown, may be nervous or vascular aetiology

Respiratory (18 decks)

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