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CR2 > Obstructive & Restrictive Lung Disease > Flashcards

Obstructive & Restrictive Lung Disease Flashcards

1
Q

What is the normal tidal volume?

A

7ml/kg, depends on mass of individual

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2
Q

Which is bigger - expiratory reserve or inspiratory reserve?

A

Inspiratory reserve volume

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3
Q

Why is it better to breathe from the bottom of your lungs than the top of your lungs?

A

if you breathe from the bottom the alveoli are small to start with so you have more room to expand and there is more room for air to go in however if you breathe at the top there is not much more expansion available and so not much more room for air to go into the alevoli

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4
Q

What should vital capacity be for a young woman?

A

3.0-3.5L

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5
Q

Why are peak flow serial measurements useful?

A

Can use to assess the effectiveness of treatment - each morning and evening

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6
Q

What is TLC =?

A

TV + IRV + ERV + RV

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7
Q

What is FVC?

A

Forced vital capacity - the maximum volume of air you can exhale after taking the deepest possible inhalation

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8
Q

What is VC?

A

The same as FVC - Forced vital capacity - the maximum volume of air you can exhale after taking the deepest possible inhalation

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9
Q

What does a vitalograph show you?

A

The time course of breathing, alternative to spirometer

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10
Q

What happens to FEV1/FVC in obstructive diseases?

A

FEV1 is reduced as you cannot breathe out as quickly
FVC stays the same as the size of the lungs is not affected
Therefore FEV1/FVC ratio is reduced

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11
Q

What happens to FEV1/FVC ratio in restrictive diseases?

A

FVC is reduced as the lung size is restricted
FEV1 is low as there is also airway constriction so you cannot breathe out as easily
Both are reduced so FEV1/FVC is not affected

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12
Q

What should FEV1/FVC normally be?

A

80-90%

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13
Q

How would you classify mild, moderate and severe obstructive diseases?

A

Normal >70% FEV1/FVC
Mild 61-69%
Moderate 45-60%
Severe <45%

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14
Q

What are key features seen in obstructive disorder?

A

Reduced peak flow

Reduced FEV1/FVC

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15
Q

What effect does smoking have on obstructive disorders?

A

Steadily reduces FEV1 further

Damages elastin in airways

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16
Q

What other things apart from obstructive disorders reduce FEV1/FVC ratio?

A

age

smoking

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17
Q

Why is it important to stop smoking regardless of age?

A

Lung function will somewhat improve at any age

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18
Q

What is the definition of asthma?

A

An Episodic limitation of airflow, reversing either spontaneously or in response to treatment

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19
Q

What is asthma characterised by?

A

Reversible airway obstruction
Smaller airways
AHR (Airway Hyper- Responsiveness)
Often atopic (allergens)

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20
Q

What are the 3 essential features of asthma?

A

Bronchoconstriction
Secretion of mucus
Airway Inflammation

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21
Q

What are some symptoms of asthma?

A

Troublesome cough, particularly at night, may be awakened by coughing
Coughing or wheezing after physical activity
Breathing problems during particular seasons
Coughing, wheezing, or chest tightness after allergen exposure
Colds that last more than 10 days
Relief when medication is used

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22
Q

What are some signs of asthma?

A

Reduced Peak Expiratory Flow!!
normal airway reflexes are hyper-responsive and prolonged!!

Wheezing sounds during normal breathing
Hyperexpansion of the thorax
Increased nasal secretions or nasal polyps
Atopic dermatitis, eczema, or other allergic skin conditions

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23
Q

What is wheezing?

A

Turbulent air flow

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24
Q

Why asthmatics cough?

A

Oversecretion of mucus, want to remove it

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25
Q

Why is airflow limited in an asthma attack?

A

bronchoconstriction
oedema
mucus hypersecretion

26
Q

What 3 things happen during an asthma attack?

A

SM around bronchioles constricts so airways narrow
Inflammation produces oedema - thickens airway wall narrowing it
Excess mucus secretion further narrows airway

27
Q

What types of substances trigger asthma?

A

Antigenic - air pollutants, pollen/mould, animal dander, medications, food

28
Q

How is IgG produced normally?

A

A antigen gets into the airways, dendritic cell (on the epithelial cell lining in the airways) recognises it as non-self and reacts to become an APC. It stimulated T helper cells (CD4+) to release interleukins IL4 and IL5 which stimulate B lymphocytes to make antibodies for the specific antigen - IgG.

29
Q

What are cytokines?

A

Small proteins secreted by one cell and cause changes in another, signalling molecules

30
Q

What are interleukins?

A

Cytokines released from WBC (leukocytes)

31
Q

What does IgG do?

A

Provides majority of antibody-based immunity against invading pathogens

32
Q

Why is the normal antigen immune response different for asthmatics?

A

Reaction with APC cells and T lymphocytes is more vigorous so T cells secrete extra IL13 which stimulate B cells to become plasms cells and make IgE as well as IgG. IgE molecules attach themselves to mast cells in connective tissue

33
Q

What do IgE antibodies do when an antigen is inhaled?

A

When antigen enters airways again, it binds to IgE antibodies on mast cells which release histamines and pro-inflammatory cytokines causing local inflammation, bronchoconstriction and mucus secretion = asthma attack

34
Q

What is mast cell degranulation?

A

Mast cell release of inflammatory mediators (histamine) to produce mucus secretion, bronchoconstriction and oedema

35
Q

What happens if an asthmatic is repeatedly exposed to the allergen?

A

Cytokines released from T cells and mast cells cause eosinophils and polymorphonuclear neutrophils to migrate to lung tissue and when exposed there is a delayed response

36
Q

Why is eosinophil production bad?

A

cause increased inflammation and epithelial damage, stimulates more powerful vagal mediated bronchoconstriction and mucus secretion, damages epithelial cells so cilia less effective in transporting mucus and even more coughing to remove

37
Q

What are the two main drug treatments fro asthma?

A

bronchodilators

anti-inflammatories

38
Q

What are the 3 main bronchodilators and how do they work?

A

Beta 2 agonists - mimic effect of adrenaline
anti-muscarinics - block PS bronchoconstriction and mucus hypersecretion
PDE - phosphodiesterase inhibitor - prevent formation and release of pro-inflammatory cytokines from mast cells and eosinophils

39
Q

What are the 3 main anti-inflammatory drugs?

A

steroids
leukotriene antagonists
anti-IgE antibodies

40
Q

What is an example of short acting beta 2 agonist? What do they do?

A

Salbutamol, relieve acute symptoms

41
Q

What is an example of a long acting beta 2 agonist? What do they do?

A

Formoterol

preventers but can be combined with short acting

42
Q

What is an example of an antimuscarinic and what do they do?

A

Antagonise M3 muscarinic receptors
Ipratropium
Tiotropium

43
Q

What is an example of a phosphodiesterase inhibitor?

A

Theophylline

Aminophylline

44
Q

Why aren’t phosphodiesterase inhibitors used much?

A

Not very effective and can have toxic side effects

45
Q

What are some other treatments for asthma, examples, what do they do?

A

Monoclonal antibodies - omalizumab, down regulates IgE receptors and stabilises mast cells, for severe allergic asthma
Magnesium - IV, emergencies, reduces SM contractility

46
Q

What do corticosteroids do?

A

Anti-inflammatory agents - reduction of bronchoconstriction, oedema and mucus formation, stimulation of beta-2 gene expression and suppression of expression of inflammatory genes

47
Q

What are some examples of corticosteroids?

A

Beclomethasone dipropionate

fluticasone dipropionate

48
Q

How do spacers and nebulisers help?

A

Spacers - improve penetration of inhaled drugs to lungs and reduced adverse effects
Nebulisers - produce inhaled mist, same effectiveness as inhalers with spaces, for severe episodes

49
Q

What is chronic bronchitis?

A

presence of chronic productive cough without discernable cause for more than half the time over two years

50
Q

What is COPD?

A

chronic bronchitis and emphysema

51
Q

What are the features of chronic bronchitis?

A

Hypertrophy of bronchial glands, hypersecretion, mucous plugs and infection/inflammation

52
Q

What is the cause of chronic bronchitis?

A

exposure to airborne irritants

53
Q

What is emphysema?

A

enlargement of airspaces distal to terminal bronchioles

54
Q

What are the features of emphysema?

A

Destruction of lung stroma - bullae,

‘Floppy Airways’ cause obstruction

55
Q

What is the main cause of emphysema?

A

Cigarette smoking

56
Q

How does bronchitis cause mucus release?

A

Irritants damage the epithelium cause squamous cell proliferation and stimulating massive mucus gland enlargement

57
Q

How does cigarette smoking cause emphysema?

A

Stimulates polymorphonuclear leucocytes to release serine elastase and inactivates elastatse inhibitor - alpha 1 antitrypsin. This means elastase can destroy elastic tissue of the lungs producing emphysema.

58
Q

Why are gross enlarged bullae a problem?

A

Gas won’t reach capillaries and won’t get transferred in or out so there is limited diffusion

59
Q

How reversible are asthma and COPD?

A

Asthma is reversible whereas COPD is not as there is lung damage

60
Q

What does a flow volume loop show?

A

Volume in spirometer machine not lungs
1 respiratory cycle
Start on right
Most important part is expiration slope at end

61
Q

How do you analyse a flow volume loop?

A

Expiration is weak point in obstructive disease so look at that
Obstructive disease will show - low expiration flow rate in relation to lung volume, ends prematurely as airways close early, scooped out appearance after point of max flow

CR2 (35 decks)

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