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Respiratory BJ > Obstructive Lung Disease > Flashcards

Obstructive Lung Disease Flashcards

1
Q

How does an obstructive lung disease affect FEV1/FVC

A

Airflow is limited so FEV1 decreases
FVC may also be decreased depending on the level of obstruction
FEV1/FVC drops below 70% norm.

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2
Q

What is PEFR?

A

Peak Expiratory Flow Rate

The air exhaled in a minute

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3
Q

What are PEFR values like for someone with an obstructive lung disease?

A

Normal is between 400-600L
A normal reading would be between 80-100% of the best values
A moderate fall would be 50-80%
A marked fall would be <50% of the best value

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4
Q

Name the common obstructive ariway diseases?

A

Asthma
Chronic Bronchitis
Emphysema

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5
Q

What is COPD?

A

An amalgamation of chronic bronchitis and emphysema

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6
Q

Is asthma reversible?

A

The bronchial smooth muscle contraction and inflammation can be reversed spontaneously or with drugs

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7
Q

What kind of irritants can cause COPD?

A

Smoking is the most imporant cause

Also atmospheric pollution and occupational irriants like dusts

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8
Q

What other things can cause Emphysema without bronchitis?

A

An enzyme deficiency can cause COPD. E.g. Alpha-1-antitrypsin (antiprotease) deficiency can cause emphysema

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9
Q

What people are most likely to develop COPD?

A

The old
Men more than women. (Falling as men do less of the dirty jobs)
People in developing countries (as smoking rises there)

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10
Q

Is damage done by smoking reversible?

A

Damage to the FEV1 isnt reversible.

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11
Q

Define chronic bronchitis?

A

’ Cough productive of sputum most days in atleast 3 consecutive months for 2 or more consecutive years.’

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12
Q

What happens when acute bronchial pneumonia occurs as a complication of chronic bronchitis?

A

Infection so sputum turns yellow/green

Mucuous & pus produced (acute infective exacerbation) and FEV1 falls.

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13
Q

During chronic bronchitis what morphological changes occur in the large airways?

A
  • Mucous gland hyperplasia
  • Goblet cell hyperplasia
  • Inflammation & fibrosis (minorly)
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14
Q

During chornic bronchitis what morphological changes occur in the small airways?

A
  • Goblet cells appear

- Imflammation & fibrosis when its long standing disease

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15
Q

Define Emphysema?

A

“An increase beyond the normal size of airspaces distal to the terminal bronchiole arising either from dilatation or destruction of alveolar walls and without obvious fibrosis”

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16
Q

Whats the structure of bronchioles/alveolar?

A

Terminal bronchiole is last conduction airway sub 1mm in size and fully lined by respiratory epithelium.
Respiraotry bronchioles are part respiratory epithelium part alveolar wall
Then alveolar ducts are all alveolar wall

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17
Q

Define centriacinar emphysema?

A

The most common kind
Begins with bronchiolar dilatation then alveolar tissue loss.
Predominent in the upper half of lungs
Destroys middle of the acinus

18
Q

Why does centriacinar emphysema predominate in the upper half of lungs?

A

Lower half have greater blood supply
> Recieves more macrophages from blood
> Clearence is better at bottom

19
Q

How do centriacinar and panacinar emphysema look differnet?

A

CEntriacinar is patchy and around the center of the acinus. Upper half.
panacinar is everyfuckingwhere (lower of lungs though)

20
Q

What does panacinar emphysema work on?

A

The entire alveolus is unifromly destroyed

21
Q

What is periacinar emphysema?

A

Forms bulla (bleb), a emphysematous spacce over 1cm.

22
Q

What happens if a bulla bursts?

A

Spontaneous pneumothorax

23
Q

Where does periacinar emphysema occur?

A

In acinus close to or up against hte pleura

24
Q

How does emphysema in genral appear under a CXR?

A

A permanently hyerinflated chest is visible showing all the ribs not just the normal 10

25
Q

How does smoking cause emphysema?

A

Smoking causes a protease/antiprotease imbalance (more proteases so more elastin destruction) and damages the repair mechanisms for elastin syntehsis. This results in destruction of the elastin tissue in alveolar walls.

(PLIs irritation and imflammation)

26
Q

How does an alpha-1-antitrypsin deficiency lead to emphysema?

A

Protease-Anti-protease imbalance

27
Q

Is COPD airway obstruction reversible?

A

Traditionally no:

however the smooth muscle tone and inflammation in small airways does respond to drugs.

28
Q

What are the methods of airway obstruction in COPD?

A 
Large airways:
- Glands and mucous
Small airways:
- Smooth muscle constriction
- Inflammation
- Fibrosis
- Collapse of airway on expiration
29
Q

Why does the airway collapse on expiration in COPD?

A

The alveolar walls act like guy ropes holding the smaller airways open.
In emphysema theyre destroyed so the airway ecomes floppy.

30
Q

Whats type 1 respiratory failure?

A

Hypoxaemia with normal or low PaCO2

PaO2 <8kPa (normal 10.5-13.5kPa)

31
Q

What type 2 respiratory failure?

A

Hypercapnia with hypoxaemia

PaCO2 >6.5kPa (normal 4.8-6kPa)

32
Q

What 4 abnormal states of COPD are associated with hypoxaemia?

A
  • Ventilation/perfusion imblance (V/Q)
  • Diffusion impariment
  • Alveolar hypoventilation
  • Shunt
33
Q

Why does alveolar hypoventilation occur in those with cOPD?

A

COPD patients balance on the edge of high CO2 all the time and the central chemoreceptors lose their sensitivity to CO2 and the body comes to rely on Hypoxia to drive ventilation.
Then when you give them extra oxygen their bodies like fuck it we’ve got enough O2 lets stop breathing (hypoventilation), and CO2 builds up dangerously.

34
Q

Whats the commonest cause of hypoxaemia clinically encountered?

A

A V/Q imbalance

35
Q

Why does Increasing FIO2 improve a V/Q imbalance?

A

Abnormally functioning alveoli still haev some ventilation so increasing FIO2 increases the PAO2 in these alveoli and imporves conditions.

36
Q

Why doesnt Increasing FIO2 improve a Shunt?

A

No ventilation at all to the consolidated alveoli so no amount of oxygen will improve things

37
Q

How does diffusions impariment occur in COPD?

A

Alveolar walls are damaged by emphysema so thers a loss of alveolar surface area

38
Q

When does a shunt occur in COPD?

A

When theres acute infective exacerbation (blocks alveoli) or severe bronchopneumonia or large areas of lobar pneumonia.

39
Q

What causes Cor pulmonale? (pulmonary heart disease)

A

Pulmonary hypertension
Right ventricle hypertrophys to cope
Eventually fails

40
Q

What are some possible causes of hypertension leading to Cor Pulmonale?

A
  • Pulmonary Fibrosis
  • Loss of pulmonary capillary bed
  • Hypoxia (pulmonary vasoconstriction)
41
Q

How does hypoxia cause Cor Pulmonale?

A

Hypoxic Cor Pulmonale:

  • > Hypoxaemia causes mass pulmonary vasoconstriction
  • > Vascular resistance increases loads
  • > So pulmonary blood pressure rises (hypertension)
  • > Right ventricle has to work hard and hypertrophys
  • > heart evenutally fails.

Respiratory BJ (31 decks)

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