Brainscape's Knowledge GenomeTM

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


See full index

Respiratory System > Pathology of Obstructive Lung Disease > Flashcards

Pathology of Obstructive Lung Disease Flashcards

1
Q

Which three main conditions are obstructive airway diseases?

A
  • emphysema
  • chronic bronchitis
  • asthma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

FEV1 is the…

A

Forced Expiratory Volume (FEV) of air exiting the lung in the first second of FVC.

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

FVC is the…

A

total amount of air expired after taking a maximum inspiration (FVC).

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

What factors is predicted FVC based on?

A

age, sex and height

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

FEV1 is usually about _____ of _____ in healthy persons.

A

70-80%

FVC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Normal FVC is around ____.

Normal FEV1 is _______.

Therefore, normal FEV1/FVC = ______.

A

5L

  1. 5-4L
  2. 7-0.8
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is a marked fall in PEFR?

A

<50% of best

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

What is a moderate fall in PEFR?

A

50-80% of best

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is a normal PEF in PEFR?

A

400 – 600 L/min

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

In obstructive lung disease:

  • PEFR is ________.
  • FEV1 is _________.
  • FVC ________.
  • FEV1 _______ of FVC.
A
  • reduced
  • reduced
  • normal or low
  • is less than 70% of

FEV1/FVC < 0.7

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

Outline the pathogenesis of bronchial asthma.

A
  • mast cell degranulation
  • smooth muscle contraction (immediate)
  • acute inflammatory response
  • chronic inflammation in chronic asthmatics.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

When can bronchial asthma become irreversible?

Why?

A

when it becomes chronic

In lifelong asthmatics – ultimately there may be structural changes in airways (fibrosis, scarring) which are not reversible by pharmacological intervention.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the aetiology of COPD?

A
  • SMOKING (tobacco)
  • atmospheric pollution
  • occupation e.g. dust
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What impacts your susceptibility to COPD?

A

How your metabolism handles the chemicals in cigarettes or pollution.

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

___________ deficiency is an extremely rare cause of emphysema.

A

Alpha-1-antitrypsin

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

Does congenital alpha 1 antitrypsin deficiency cause chronic bronchitis?

A

no, only emphysema

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

What is the clinical definition of chronic bronchitis?

A

Cough productive of sputum most days
in at least:
- 3 consecutive months
- for 2 or more consecutive years

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

When can chronic bronchitis become complicated? (2)

A
  • mucopurulent sputum (acute infective exacerbation)

- when FEV1 falls

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

What are the morphological changes in chronic bronchitis in the large airways (bronchi)? (3)

A
  • Mucous gland hyperplasia
  • Goblet cell hyperplasia
  • Inflammation and fibrosis is a minor component
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are the morphological changes in chronic bronchitis in the small airways (bronchioles)? (2)

A
  • Goblet cells appear (where they should not be)

- Inflammation and fibrosis in long standing disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Why do we have sputum?

When can it be problematic?

A

It is a defense mechanism - protection from things being inhaled (smoke, pollution).

It can go overboard and protect too much, goblet cells increase in number, we get inflammation and fibrosis. In more chronic cases, chronic irritation leads to chronic fibrosis.

22
Q

What is the pathological definition of emphysema?

Increase beyond the normal in the size of airspaces ______ to the ________ bronchiole arising either from ________ or from _________ of their walls and without obvious ________.

A 
distal
terminal
dilation
destruction
fibrosis
23
Q

The acinus – in human lung, 1-2cm across, supplied by 1 _______ bronchiole.

Alveolar walls _________ in emphysema.

A

terminal

disappear

24
Q

Emphysema is classified according to where the alveolar tissue is lost.

Define centri-acinar emphysema. (2)

A
  • loss of alveolar tissue around the respiratory bronchioles and the alveolar ducts.
  • Outside of the acinus – generally not affected (local).
25
Q

How does centri-acinar emphysema begin, and what does it lead to?

A
  • Begins with bronchiolar dilatation.
  • Then alveolar tissue is lost.
  • Leads to holes in the middle of the acinus.
26
Q

What are the characteristics of pan-acinar emphysema. (3)

A
  • Less common
  • Very severe
  • Wipes out huge areas of lung tissue – not just holes.
27
Q

What are the characteristics of peri-acinar emphysema. (1)

What can peri-acinar emphysema lead to? (1)

A
  • loss of tissue at the distal end or edge of acinus.

- could lead to spontaneous pneumothorax.

28
Q

What is the qualitative term, referring to patient with emphysema with really large spaces.

A

Bullous emphysema

29
Q

A _______ is an
emphysematous
space
greater than 1cm.

A

Bulla

30
Q

__________ lungs in emphysema - they have more air in their lungs, it helps to keep the ________ airways open

They suffer less airflow limitation by _________ air in their lungs.

A

Hyperinflated
small

keeping

31
Q

What type of emphysema is associated with smoking?

A

centri-acinar

32
Q

Where does centri-acinar emphyema normally occur?

A

apex

33
Q

What type of emphysema occurs in congenital alpha 1 antitrypsin deficiency?

A

pan-acinar

34
Q

How can peri-acinar emphysema cause a pneumothorax?

A

Bullae (large air spaces) rupture and air enters the pleural space form the lung.

35
Q

Outline the pathogenesis of emphysema. (4)

A
  • SMOKING
  • Protease - Antiprotease imbalance
  • Ageing
  • Alpha-1-antitrypsin deficiency
36
Q

What does smoking do to cause/worsen emphysema? (4)

A
  • increases neutrophil/macrophage production
  • increased protease/elastase production (destroy lung tissue)
  • inhibition of anti-elastase/alpha-1-antitrypsin production (homeostatic mechanism)
  • inhibits repair mechanism.

Overall, increased lung tissue destruction with reduced repair/defence mechanisms.

37
Q

What are the reversible components of COPD (with pharmacological intervention)?

A
  • smooth muscle contraction
  • inflammation

(similar to asthma)

38
Q

In COPD, which airways respond better to pharmacological intervention?

A

small

39
Q

What are alveolar attachments?

A

where alveolar tissue attaches to the bronchioles (the infrastructure).

40
Q

What causes the collapse of bronchioles on expiration in emphysema?

A
  • loss of alveolar attachments

- no longer able to hold open the bronchioles during the pressure exerted on them on expiration.

41
Q

What aspect of COPD is not able to be treated with drugs?

A

fibrosis, excess mucus in small airways.

42
Q

Which drugs can be used to treat COPD?

A
  • Beta-2 agonists

- inhaled steroids

43
Q

What can happen to COPD patients with Type II respiratory failure, in terms of resp. drive?

A
  • become desensitized to high CO2 levels in the body.
  • rely on O2 levels to drive their respiratory ventilation.
  • they end up breathing less and less and can die from resp. failure.
44
Q

Patients insensitive to hypoxia are known as what?

Explain this.

A

blue bloaters

low O2 explains blue colour, and it is due to right heart failure (increase pulmonary arterial resistance).

45
Q

Patients sensitive to hypoxia are known as what?

Explain this.

A

pink puffers

they hyperventilate heavily

46
Q

When does COPD become worse all of a sudden?

What does this lead to?

A

Acute infective exacerbation

  • secondary bacterial infection makes patients with COPD worse
  • plummet into resp. failure, resp drive decreased.
  • pus in the alveoli prevents gas exchange.
47
Q

How can hypoventilation be treated?

A

raising PIO2

48
Q

Which abnormal states cause type I respiratory failure?

A

shunt and V/Q mismatch

49
Q

Which abnormal states cause type II respiratory failure?

A

alveolar hypoventilation

50
Q

Define anatomical dead space.

A

Anatomic dead space is the total volume of the conducting airways from the nose or mouth down to the level of the terminal bronchioles, and is about 150 ml on the average in humans.

51
Q

Define alveolar dead space.

A

Alveolar dead space is sum of the volumes of those alveoli which have little or no blood flowing through their adjacent pulmonary capillaries, i.e., alveoli that are ventilated but not perfused, and where, as a result, no gas exchange can occur.

52
Q

Define physiological dead space.

A

Dead space is the volume of a breath that does not participate in gas exchange. It is ventilation without perfusion.

Respiratory System (26 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions