Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Respiratory > General Pathology of the Respiratory Tract > Flashcards

General Pathology of the Respiratory Tract Flashcards

1
Q

Describe the normal anatomy of the respiratory tract…

A

Upper respiratory tract:
Nasal cavity, paranasal sinuses, nasopharynx, larynx, guttural pouches (horses).

Lower respiratory tract:
Trachea, bronchi, bronchioles, and alveoli.

Air conduction system:
Nasal cavity, nasopharynx, larynx, trachea, bronchi, and bronchioles.

Gas exchange system:
Respiratory bronchioles and alveoli.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the respiratory defences in the nasal chambers?

A

Nasal chambers:

50% of resistance to airflow. Therefore, brachycephalic dogs with smaller nasal structures are at greater risk.
Remove particles > 10 - 20µm.
Humidify and warm incoming air (protects LRT).
Detect noxious irritants.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the respiratory defence mechanisms of the pharynx/larynx?

A

Pharynx/Larynx:
Epiglottis prevents food from entering the trachea.
Upon accidental aspiration of food particles, takes part in the cough reflex.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Explain the respiratory defence mechanisms of the mucociliary escalator…

A

Mucociliary escalator:

  • Extends from terminal bronchioles - larynx.
  • Viscous mucous gel is propelled cranially by the beating of the ciliated epithelium.
  • Secretions including IgA, IgG, interferon, and antimicrobial peptides, e.g: defensins.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Explain the defence mechanisms of the alveolar macrophages….

A

Alveolar macrophages:

  • Phagocytes resident within the alveolus.
  • Normally one sentinel macrophage per alveolus.
  • Ingest particles that reach the alveolus - if in a dusty environment, or lung haemorrhage occurs, the number of alveolar macrophages rapidly increases to clear the particles present.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What non-inflammatory disease of the lungs that can occur?

A

Atelectasis: either primary or secondary. Primary => failure of lung tissue to expand at birth. Secondary => collapse of lung tissue that was previously expanded.

Emphysema: excessive air within the lungs.

Pigmentation: permanent abnormal discolouration (melanosis)

Circulatory disturbances: hyperaemia, congestion, oedema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Describe primary atelectasis…

A

Failure of lung tissue to expand at birth.
Can be total or partial. Bronchi tends to stay open regardless.
Non-aerated tissue - dark red
Aerated tissue - salmon pink

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Describe secondary atelectasis…

A

‘Acquired’ atelectasis or collapse. May be secondary to:

  • Compression e.g: air, masses, fluid
  • Obstruction e.g: masses, FB thick secretions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What can cause collapse of lungs secondary to compression?

A 
Pulmonary or mediastinal masses
Hydrothorax
Pneumothorax
Prolonged recumbency in LAs
Prolong abdominal distention in LAs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Describe collapse of the lungs secondary to obstruction…

A

Common in cattle and other ruminants - they have thick fibrous septae in their lungs

Due to bronchiolar obstruction by exudate
Distended alveoli collapse as trapped air is absorved
Collapsed alveoli contains a little fluid and macrophages

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Define and describe emphysema

A

Excessive air in the lungs
In severe cases, the lungs do not deflate on opening the thoracic cavity
Imprints of the ribs can be present on pleural surfaces
Subdivded:
1. Alveolar
2. Intersitial (alveolar wall, blood vessels)
3. Compensatory (neighbouring part of lung too collapsed and recieves too much air to compensate)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the 3 types of emphysema…

A
  1. Alveolar: permanent abnormal enlargment of airspaces distal to the bronchioles, often due to destruction of the alveolar walls by neutrophil elastase, e.g: RAO (restrictive airway disease) in horses.
  2. Interstitial: septal (interstitial) lymphatics are dilated with air secondary to forced expiration, e.g: pneumonia in cattle.
  3. Compensatory: emphysema is adjacent to an area of consolidation (all species).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Define consolidation of lungs..

A

Lungs becoming more solid

i.e air replaced by fluid, neoplastic cells, fibrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Describe Recurrent Airway Disease (RAO) in horses

A

Obstructive chronic bronchitis and/or emphysema

Thick, viscous mucous and inflammatory reaction, narrow airways.

Destruction of alveolar walls by neutrophil elastase - causing alveolar emphysema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What two reasons might you get pigmentations in the lungs?

A

Melanosis

Anthracosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Describe melanosis of the lung..

A

Deposition of melanin in alveolar walls (calves, lambs and pigs).

No pathology

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Describe anthracosis of the lungs…

A

Accumulation of carbon in alveolar macrophages. Carbon is inert, and can’t be broken down so stay in alveolar macrophages. Secondary issues with phagocytosis may occur is they are full of carbon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What circulatory disturbances can occur in the lungs?

A

Hyperaemia and congestion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Describe hyperaemia (circulatory disturbance).

A

Increased blood flow into tissue.

  • Localised or diffuse
  • Associated with acute inflammation
  • Affected areas of lung are dark red in colour
  • Cranioventral lung lobes affected in association with aspiration pneumonia
20
Q

Describe congestion (circulatory disturbance).

A

Decreased blood flow out of tissue.

  • Diffuse with cardiac failure.
  • Dependent (may be unilateral) in hypostatic congestion - dark blue/purple lungs.Hypostatic congestion occurs after death (gravity pools blood into lowest areas). Similar effect can occur if the animal is kept in lateral recumbency for long periods of time.
  • Affected areas of lung are grey/blue in colour.
  • Terminal pulmonary congestion is seen in animals euthanised with barbiturates.
21
Q

Describe oedema (circulatory distrubance)

A

Pulmonary oedema - flooding of alveoli by fluid, which mixes with surfactant, creating a foam and compromising ventilation.

22
Q

What are the normal factors resisting pulmonary oedema in the lungs?

A

Tight junctions between alveolar epithelium (and capillary endothelia).

Intra-alveolar pressure > intersitial pressure.

Under normal conditions, fluid escaping from the blood through the endothelium passes into the interstitial space, and is removed by lymphatic drainage.

23
Q

Describe the pathogenesis of pulmonary oedema….

A

Cardiogenic:
Slowly-developiing heart failure (especially LHS), leading to high venous pressure

Neurogenic (pressure overload):
Sympathetic stimulation in acute brain damage - increases pulmonary capillary hydrostatic pressure.

Excessive fluid therapy (volume overload).

Damage to endothelium or epithelium:

  • By toxic substances, e.g: gases (smoke), systemic toxins (paraquat, 3-methyl indole), endotoxins (gut).
  • As part of an acute inflammatory process.
24
Q

Describe the pathology of pulmonary oedema…

A

Gross: lungs wet and heavy, may not collapse on opening chest, and have rib impressions on the pleural surface.

Microscopic: oedema fluid generally leaches out in tissue sections but may appear as pale pink fluid when stained with H and E.

25
Q

Describe lung haemorrhage.

A

Often occurs outside of the lungs and presses on the lungs/leaks into the lungs.

  • Septicaemias
  • Bleeding disorders
  • Very severe congestion
  • As part of severe acute inflammation.

N.B: haemosiderin

26
Q

Define thrombosis

A

Obstruction of vessels by coagulated blood components during life

27
Q

Define embolism

A

Detachment of thrombi (or bacteria, tumours etc) become lodged in small blood vessels

28
Q

Define infarction

A

Death of tissue due to an interruption in blood supple

29
Q

Describe thrombosis, embolism and infarction of the respiratory system

A 
Rare
Predisposing factors include:
DIC
Liver abscessation
Valvular endocarditis
30
Q

Describe rhinitis and sinusitis - inflammation of the nasal cavity and paranasal sinuses.

A

Can be acute, subacute, or chronic.

Localised or part of a systemic disease (e.g: malignant catarrhal fever - bovine herpesvirus).

Infectious or non-infectious (allergic or idiopathic).

Morphological subtypes: serous, catarrhal (mucoid), purulent/suppurative (involves neutrophils, usually bacterial involvement), necrotising, ulcerative, haemorrhagic.

Sequelae: resolution, healing by scar formation, extension to other parts of the respiratory tract.

Inflammation may localise and persist in the guttural pouches (horses).

31
Q

Describe pneumonia types (inflammation of the lung)

A

Bronchopneumonia - Suppurative or Fibrinous
Intersitial pneumonia
Embolic pneumonia
Granulomatous pneumonia

32
Q

How are different types of pneumonia classified by location?

A

Suppurative bronchopneumonia: cranio-ventral lung lobes, and cranio-ventral regions of caudal lobes, are most often affected.

Fibrinous bronchopneumonia: cranio-ventral lung lobes, and cranio-ventral regions of caudal lung lobes, are most often affected.

Interstitial pneumonia: bands across entire lung.

Embolic pneumonia: random/nodular distribution.

Granulomatous pneumonia: random/nodular distribution.

33
Q

Describe bronchopnemonia…

A

Caused by bacterial infection
Lesions occur in cranioventral regions under gravity
Spread of inflammation within the lung is usually by extension from lobule to lobule along the airways

34
Q

What are the potential sequelae of bronchopneumonia?

A

Resolution: mild inflammation resolves in 7 days, and the lung is back to normal within 3 weeks

Deterioration: abscess formation with pyogenic bacteria. Pleuritis in sever fibrinous pneumonia with adhesions or death due to hypoxaemia

Persistence: more severe inflammation becomes chronic with fibrosis.

35
Q

Describe bronchiectasis..

A

Seen principally in cattle

Permanent dilation of some bronchi due to irreversible damage to bronchi walls

36
Q

What are the two variations of bronchopneumonia?

A
  1. Lobar pneumonia

2. Broncho-interstital pneumonia

37
Q

Describe lobar pneumonia…

A

Pathogenesis:
Agressive fulminating bronchopneumonia
Inflammation occupies major part of the entire lung lobe
May follow impaired defences
Invasion of highly toxic bacteria e.g. pasteurella
Aspiration of foreign fluid or gastric contensts

Sequelae:
Commonly death
Fibrosis of affected areas

38
Q

Describe broncho-interstital pnemonia

A

Pathogenesis:
Inhaled mycoplasmas and some viruses
Initial inflammatory reaction in bronchioles
Intersitial lymphocytic proliferation ‘cuffing’

Importance - mostly economic:
Reduced growth rate
Predisposition to entry of more pathogenic agents

39
Q

Describe intersitial pneumonia

A

Secondary to haematogenous rather than inhaled damage.
Inflammation is centred on interstitial seta rather than airways
Distribution is diffuse, rather than cranio-ventral

40
Q

Describe the aetiology of interstital pnemonia..

A 
Acute:
Infection (distemper)
Inhaled (e.g. smoke)
Ingested toxins (e.g. fog fever)
Systemic conditions (e.g. uraemia)
Hypersensitivity (lungworm)

Chronic:
Infectious (e.g. jaagsiekte)
Inhaled dusts (coal)
Hypersensitivity (farmer’s lung)

41
Q

Describe interstital pnemonia secondary to paraquat…

A

Poisoning occurs in dogs and cats:
Pneumotoxin = selectively damages alveolar epithelium.
Allows exudation of fluid into the alveolar lumen - loss of respiratory function.

Low doses (accidental ingestion):
Moderate pulmonary oedema.
Clinical signs of respiratory distress become evident several days to weeks later, when widespread fibrosis of alveolar walls interferes with gas exchange.
High doses (malicious poisoning):
Results in severe fatal pulmonary oedema and haemorrhages.
42
Q

Describe interstital pneumonia secondary to trytophan…

A

Acute Bovine Pulmonary Oedema and Emphysema (“Fog Fever”).

Adult cattle moved to lush autumn pasture.
High morbidity and mortality.

Pathogenesis:
Excess tryptophan in autumn grass, which is metabolised to 3-methyl indole. This is toxic to Type 1 Pneumocytes.

Pathology:
Lungs enlarged and wet, with markedly widened interlobular septa (oedema and emphysema) - gives a “bubblewrap” appearance.

Flooding of alveoli with protein-rich fluid.

43
Q

Describe embolic pneumonia…

A

Pulmonary abscesses resulting from septic emboli in pulmonary vessels

Secondary to endocarditis
Secondary to hepatic abscessation and phlebitis

44
Q

Describe granulomatous pneumonia

A

Pneumonia caused by agents such as Mycobacterium and fungi.

Inflammation is chronic and persistent with macrophages as predominant cell type

45
Q

Describe tumours and tumour-like lesions of the upper respiratory tract…

A

Nasal and nasopharyngeal polyps:
- Single or multiple (often peduncluated) masses, secondary to chronic irritation/inflammation.
- May follow infection, such as cat flu, which causes inflammation.
- Composed of hyperplastic or ulcerated epithelium, granulating to fibrous stroma and varying numbers of inflammatory cells.
Benign, hyperplastic lesions.

Nasal and paranasal sinus tumours:
Most are malignant - carcinomas or sarcomas.

46
Q

Describe neoplasia of the lungs…

A

May be primary or secondary.

Primary tumours are usually invasive carcinomas, and often arise at the hilar region before spreading within the lung and to the regional lymph nodes.

Most tumours are secondary (metastatic/metastases) - these include mammary tumours, haemangiosarcomas, and osteosarcomas. Multiple nodules occur in all lung lobes.

Primary tumours tend to be one large mass (sometimes with subsequent small metastases), secondary tumours have lots of smaller nodules.

Respiratory (16 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions