Brainscape's Knowledge GenomeTM

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


See full index

Y3 Respiratory Pathology > Diseases of the lung parenchyma > Flashcards

Diseases of the lung parenchyma Flashcards

1
Q

Compare type 1 and type 2 alveolar cells

A

Type 1:
- Flattened pneumocytes, fragile
- Have to act as the minimal barrier to gas exchange
- Terminally differentiated and can’t replicate
Type 2:
- Square shaped
- Release surfactant
- Replicate and differentiate into type 1 pneumocytes
- important for repair

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

Which species has a poor degree of collateral ventilation?

A

Cattle

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

What separates alveolar lobules, what is the function of this?

A

Septa - fibrous walls

– prevent collateral ventilation, but also prevent spread of infectious disease

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

Describe how the septa is different in:

  • Cattle, pigs, sheep
  • Horses
  • Carnivores, rodents
A
  1. Thick complete septa
  2. Incomplete, thick septa
  3. No distinct septa
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Give 3 examples of congenital abnormalities of the lung parenchyma

A
  • Congenital melanosis: black pigment
  • Agenesis of one or more of the lung lobes: failure to form
  • Ectopic lung tissue outside of the thoracic cavity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What 2 abnormalities can occur due to problems with lung inflation?

A
  • Atelectasis

- Emphysema

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

What is atelectasis?

A

Incomplete distention of the lung

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

What are the causes of atelectesis?

A
  • complete internal obstruction of the airway
  • external compression of the airway or lung
  • pneumothorax
  • defective surfactant production
  • recumbency in LAs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Define emphysema

A

Excessive inflation of the lung

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the causes of emphysema?

A
  • forced respiratory effort e.g. pneumonia

- obstructive airway disease

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

How does emphysema change the structure of the lung tissue, how does this affect gas exchange?

A

Over inflated alveolar walls break down creating larger airspaces + less area for gas exchange

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

What are the 3 main functional consequences of alveolar emphysema?

A
  1. loss of lung elasticity (early airway collapse, increased dead space)
  2. loss of pulmonary capillaries (reduced alveolar perfusion)
  3. fibrosis of remaining alveolar walls (inhibits gas exchange and reduced compliance)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Define pulmonary oedema

A

Fluid present in the airways

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

What are some consequences of pulmonary oedema?

A
  • Dyspnoea, tachypnoea: rapid, but difficult breathing
  • Hypoxia, cyanosis
  • Cough: moist and productive
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Pulmonary oedema will only occur if…?

A
  • There is damage to the alveolar epithelium

- Increased interstitial fluid volume

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

What can cause damage to the alveolar epithelium?

A

Infectious agents
Toxins
Irritants

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

How can pulmonary oedema appear grossly in the lung tissue?

A

Lungs heavy
Interlobular septa expanded
Lungs “wet” + ooze fluid (frothy)

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

How would pulmonary oedema appear histologically?

A

Eosinophilic homogenous material (fluid) diffusely present throughout alveoli

19
Q

Normal pulmonary interstitial fluid is balanced by?

A

Hydrostatic pressure
Capillary permeability
Osmotic pressure

20
Q

What are some causes of increased hydrostatic pressure?

A
  • inflammation
  • passive congestion (heart failure)
  • circulatory overload
21
Q

What are some causes of increased capillary permeability?

A
  • endothelial damage by toxins or infectious agents
  • shock
  • inflammation
22
Q

What are some causes of reduced capillary osmotic pressure?

A

Hypoproteineamia – level of plasma proteins is relatively low

23
Q

What are some causes of reduced drainage of interstitial fluid (lymphatics)?

A

Blockage of lymphatics by inflammation or tumours

24
Q

What are the different types of emboli?

A
  • Thromboemboli
  • Tumour cells: metastases
  • Fat
  • Air
25
Q

What is a thromboemboli?

A

Fragments of a blood clot that pass through the blood stream and get lodged

26
Q

What makes the lung a good site for embolism?

A
  • Fine capillary network

- Good blood supply

27
Q

Define infarction

A

Death of tissue resulting from a failure of blood supply

28
Q

How does the body react to sterile thromboemboli?

A
  • Fibrinolytic breakdown of the thrombus if it is small

- Fibrotic scarring if extensive

29
Q

How does the body react to infected thromboemboli?

A
  • Vasculitis (inflamed vessels), secondary thrombosis

- Abscess

30
Q

What are some common sources of infected thromboemboli?

A
  • Heart bacterial endocarditis
  • Joint infections
  • Liver abscesses
31
Q

Describe how liver abscesses occur in LAs

A

Focal area of infected material surrounded by a fibrous wall

  • LAs on a cereal diet have increased acidity of the rumen which decreases motility
  • Bacterial formation on the rumen wall occurs causing ulcers
  • Bacteria invade the ulcer and pass through the rumen to the hepatic portal vein => liver
32
Q

Hepatic abscesses can cause thrombosis in which major vessel?

A

Vena cava

33
Q

What are some causes of pulmonary haemorrhage

A
  • pulmonary thromboembolism
  • trauma
  • infection
  • abscesses
  • tumours
  • exercise induced e.g. racehorses
34
Q

Name the four morphologically distinct types of pneumonia

A
  • Bronchopneumonia
  • Interstitial pneumonia
  • Embolic pneumonia
  • Granulomatous pneumonia
35
Q

What are the 3 common causes of bronchopneumonia?

A
  • Bacteria
  • Aspiration of food/GI contents
  • Viruses
36
Q

What is the route of entry and distribution of bronchopneumonia in the lung?

A

Inhalation

Cranioventral

37
Q

Why is the distribution of bronchopneumonia in a cranioventral fashion?

A
  • Greater deposition of particles and organisms

- Gravitational affects and airflow

38
Q

Describe the pathogenesis of bronchopneumonia

A
  • Inhaled pathogen causes injury at bronchiole-alveolar junction
  • Loss of epithelium, blood vessels become hyperaemic (dilate)
  • inflammatory response
  • Filling of alveoli and bronchioles with exudate, cells and debris
  • inflammation and infection spreads to adjacent parts of the lungs through interlobar septae
39
Q

Describe the inflammation response of bronchopneumonia

A

Exudation of fluid + plasma proteins through spaces between epithelial cells
Recruitment of alveolar Macrophages + immigration of neutrophils

40
Q

How might bronchopneumonia appear grossly on the lung?

A

Firm
Dark pink to red-grey
Collapsed

41
Q

How does exudate change as the severity of bronchopneumonia increases?

A

Suppurative (pus = neutrophils predominantly) can become fibrinous – not black and white, continuous. Confined to lobules
Fibrinous – more damaging to tissues and vessels as it spreads. Spreads rapidly between lobules.

42
Q

Name some causes of fibrinous bronchopneumonia

A
  • Bacterial e.g. Mannheimia haemolytica in cattle

- Inhalation of a highly irritant materia

43
Q

Describe the pathogenesis of Mannheimiosis

A
  • Caused by Mannheimia haemolytica bacteria
  • Recently weaned and assembled suckled calves
  • Stress, viral infections, + other factors impair respiratory defence mechanisms
  • Bacteria colonise LRT
  • Leucotoxin production damages WBCs
  • Lysis of alveolar macrophages and neutrophils
  • Release of WBC lysosomal contents
  • Acute damage to bvs leads to fibrinous bronchopneumonia (+ toxaemia)

Y3 Respiratory Pathology (5 decks)

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