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Pulmonary system > Pathophysiology of chronic airflow limitation > Flashcards

Pathophysiology of chronic airflow limitation Flashcards

1
Q

Types of chronic obstructive airway diseases (4)

A

1) Asthma
2) COPD
3) Bronchiectasis
4) Bronchiolitis

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2
Q

What is difference between bronchus and bronchiole

A

Presence of cartilage

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3
Q

Symptoms of chronic obstructive airway diseases

A
  • cough
  • sputum
  • dyspnea
  • wheeze
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4
Q

Cough reflex - what does it involve in the nervous system

A

1) Afferent stimulation of irritant receptors in the airway - vagus nerve
2) Efferent activation of inspiration muscles including the diaphragm- phrenic nerve
3) Activation of expiatory muscles and the larynx - vagus

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5
Q

Cough reflex

A

1) mechanical/chemical stimulation of the irritant receptors within airway
2) Info goes to the brain -integration
3) Stimulation to the inspiratory muscles to take a deep breath in at the same time signal to larynx to close glottis
4) Expire against a closed glottis causing the cough reflex to occur and expel whatever was in the airway

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6
Q

Sputum -definition

A

A mixture of saliva, airway lining liquid, mucus and pus that is expelled (expectorated) from the respiratory tract during coughing

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7
Q

Phlegm

A

Airway mucus

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8
Q

Varieties of sputum

A

1) White or grey (mucoid)
2) Bloody /blood streaked (hemoptysis)
3) Rusty colored - old blood, fungal infections (aspergillus) -brown
4) purulent - containing pus - yellow-yellower-green-greener – indicated right blood cells
5) Muco-purulent
6) Foamy (pulmonary edema)

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9
Q

Sources of sputum in the airway

A

1) Bronchial mucus gland (main source)

2) Goblet cells (in the respiratory epithelium)

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10
Q

Mucus production during obstructive lung disease - sources

A

Both the bronchial mucus gland and goblet cells increase their production during obstructive lung disease
i.e in asthma get proliferation and increase in size of goblet cells

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11
Q

Dyspnea- causes

A

Increased work of breathing due to:

a) increased airway resistance
b) hypoxemia
c) hyperinflation

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12
Q

Cause of airway resistance

A
  • flow of gas goes from area of high pressure to low pressure
  • pressure gradient needs to be positive (P1-P2)
  • resistance proportional to pressure difference and inversely proportional to the flow
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13
Q

Airway resistance in obstruction/narrowing of vessels

A

If get an obstruction/narrowing of the tube

  • increase pressure
  • decrease flow
  • so overall increased resistance
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14
Q

Mechanisms of airway resistance in the lungs

A

1) Smooth muscle contraction
2) Wall thickening
3) Lumenal occlusion
4) Decreased lung elasticity
5) Obliteration

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15
Q

Smooth muscle contraction

A

1) Cause of constriction - nervous stimulation, inflammation (acetylcholine, histamine, leukotrienes, prostaglandins…)
2) Smooth muscle contraction causes reduction in radius of lumen
3) resistance proportional to 1/r^4

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16
Q

Wall thickening -how causes increased resistance

A

1) Chronic inflammation leads to remodelling wall of lumen hypertrophy and hyperplasia of the epithelium, inflammatory cell infiltration and connective tissue deposition
2) Overall thickening wall and consequently reduction of luminal radius

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17
Q

Occlusion -how causes increased resistance

A

Can’t clear mucous –> air way occluded = increased airway resistance

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18
Q

Lung elasticity- how causes increased resistance

A

1) inflammation induced proteolytic damage of the connective tissue framework of the lung and death of alveolar epithelial cells
2) loss of framework around lumen -airway collapses in on itself
3) increased resistance
ex: emphysema

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19
Q

Obliteration - how causes increased resistance

A

Significant insult to airway
Lung tries to heal
Becomes fibrosed and radius decreases over time

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20
Q

Site of inflammation in COPD (4)

A
  • central airway
  • peripheral airway
  • lung parenchyma
  • pulmonary vasculature
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21
Q

Sites of inflammation in asthma (2)

A
  • central airway

- peripheral airway

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22
Q

Sites of inflammation in bronchiectasis (2)

A
  • major bronchi

- bronchioles

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23
Q

Sites of inflammation in bronchiolities (2)

A
  • membranous and respiratory bronchioles

- immediately adjacent aveoli

24
Q

Inflammatory cells COPD (4)

A
  • neutrophils
  • macrophages
  • CD8, CD4, lymphocytes
  • B lymphocytes
25
Q

Inflammatory cells in asthma (5)

A
  • eosinophils
  • CD4 Th2 lymphocytes
  • mast cells
  • neutrophils
  • epithelial cells
26
Q

Inflammatory cells in bronchiectasis (1)

A

-neutrophils

27
Q

Inflammatory cells in bronchiolitis (5)

A
  • neutrophils
  • eosinophils
  • macrophages
  • lymphocytes
  • mast cells
28
Q

Mechanisms of increased reistance: asthma

A

1) Mainly due to smooth muscle contraction (+++)
2) Also due to wall thickening (+ to +++)
3) Lumenal occlusion (++)
Not due to
a) increased lung elasticity
b) obliteration

29
Q

Mechanisms of increased reistance: COPD

A

1) Mainly due to decreased lung elasticity and obliteration (+++)
2) Slightly due to smooth muscle contraction, wall thickening and lumenal occlusion (+)

30
Q

Mechanisms of increased reistance: Bronchiectasis

A

1) Combo of wall thickening, lumenal occlusion, obliteration (++)
2) Somewhat due to smooth muscle contraction (+)
Not due to decreased lung elasticity

31
Q

Mechanisms of increased reistance: Bronchiolitis

A

1) Mainly due to obliteration (+++)
2) Wall thickening (++)
3) Smooth muscle contraction and lumenal occlusion (+)
Not due to decreased lung elasticity

32
Q

Where does increased resistance occur + repercussions

A
  • resistance naturally decreases as one goes from central to peripheral pathway (large increase in surface area)
  • but alot of resistance changes occur in smaller airways (where damage is) - so considerable changes can occur before symptoms develop (as naturally lower resistance than larger conducting airways)
33
Q

Predominant triggers asthma

A
  • primarily allergen driven Th2 response

- also episodically by viruses and pollutants

34
Q

COPD triggers

A

-cigarette and biomass smoke exposure = oxidant damage

35
Q

Bronchiectasis triggers

A

-bacteria

36
Q

Bronchiolitis triggers

A
  • inhaled gases and fumes
  • immune rejection
  • signifcant viral infections
37
Q

Pathophysiology allergic asthma

A

1) Normally when dendritic cells present to naive T cell activate it to develop into Th1 which will secrete IFN y
2) In allergic asthma the allergen is presented to the dendritic cell which drives the naive T cell to become Th2 (people without asthma would generate mainly Th1 response to allergens)
3) Th2:
a) produces IL4, IL5, IL13
b) Leads to allergic inflammation
c) production of IgE
5) Cytokines stimulate plasma B cells
6) B cells produce further IgE, which then sensitizes the mast cells so that when the allergen represents to the mast cell activates it to release histamine and leukotrienes (degranulation)
7) leading to bronchoconstriction + inflammation = acute exacerbation of asthma

38
Q

Pathophysiology COPD

A

-multifactorial
-predominate = smoking
Then combined with…
-also genetic susceptibility (ex alpha 1 anti trypsin deficiency), respiratory infections, occupational and environmental air pollution

Leads to either of two outcomes:

1) Parenchymal inflammation, cell death leading to tissue destruction and reduced lung recoil –» leads to emphysema
2) Airway inflammation remodelling and thickening –> leads to small airway disease (wheezing, increased airway resistnace)

End result in either=

  • reduced expiratory flow
  • hyperinflation
  • gas exchange abnormalities

Which produces SYMPTOMS

39
Q

What drives development of emphysema

A
  • Proteolytic destruction of alveolar walls
40
Q

Subtypes of emphysema

A

1) Centrilobular (acinar) emphysema - affects more proximal part of respiratory bronchioles
- cigarette smoking and dust inhalation
- affecting upper lobes
2) Panlobular (acinar) emphysema - affects more of distal part of respiratory bronchioles
- affecting more of lower lobes
- honeycoming of airways
- seen more in alpha-1 antitrypsin deficiency (causing bi-basal hyperinflation and lucency)

41
Q

Bronchiectasis -definition

A

Irreversible dilation of the bronchial tree

42
Q

Cause of bronchiectasis

A
  • irreversible destruction of peripheral small airways

- due to repetitive/persistent infection of the upper or lower respiratory tract

43
Q

Effect of viral infections on cilia + consequences

A

1) Viral infection causing
- reduction in ciliary beat frequency
- increased dyskinetic beat pattern (abnormal beating)
2) Therefore start coughing -need to rely on alternative mechanisms to get mucous out

44
Q

Pathophysiology bronchiectasis

A

Cycle of infection and inflammation (usually due to underlying susceptibility or trigger

ex: primary ciliary dyskinesia-cilia don’t move
- mucous stuck down there which gets infected
- body tries to try and fight off infection get influx of inflammatory cells into lung which further disrupts mucocilliary clearance
- get more pooling of secretions and further infection
- eventually get lung damage (coughing??) - destruction of airway leading to collapse and dilation

45
Q

Causes of bronchiectasis (underlying conditions)

A

1) Cystic fibrosis - most common
2) Ciliary dysfunction syndromes
- primary cilial dyskinesia syndromes
- young’s syndrome
3) Foreign bodies
- bronchial occlusion due to foreign body
- build up of secretions which gets infected
- causes localized infection and inflammation leading to lung damage
4) Tracheomalacia
5) Relapsing polychondritis
- chronic aspiration and can’t swallow
6) Inhalation of noxious fumes/gases
ex: nitrogen mustard
6) Infection
- ex: whooping cough, TB

46
Q

Bronchiolitis

A

Home work

47
Q

Hypoxemia- how causes dyspnea

A

1) Ventilation/perfusion mismatch

2) Reduced surface area for diffusion

48
Q

Hyperinflation -how causes dyspnea

A

-increased lung volume shortens inspiratory muscles

49
Q

Wheeze -cause

A

Airway narrowing especially due to bronchoconstriction

50
Q

Detecting a wheeze

A

-detected/quantified by measuring maximal expiratory flow

51
Q

Spirometry - how, what do get

A
  1. Take a maximum breath in to fill to vital capacity
  2. Blow out to empty
  3. Get FEV1 and FVC
52
Q

What does FEV1 and FVC tell us

A

-whether airflow obstruction or restrictive lung disease
-FEV1 should be above 80% predicted
-FVC should be above 90% predicted
-ratio FEV1/FVC < 75% obstructive
>99% suggestive restrictive lung disease

53
Q

Obstructive lung disease

A
  • fall in rate of lung emptying (FEV1 decreased)
  • because exhalation at this part is effort dependent - no matter how much force develop is only a certain flow rate that will come out
  • eventually will empty out but usually with spirometry stop after 6s expriation so FVC is also increased
54
Q

Mean expiratory flow - limits

A

MEF is limited - flow will increase with increasing effort up to a point
-beyond that point increasing effort and pleural pressure does not produce increased flow

55
Q

Decrease in MEF-what can tell you

A
  • is characteristic feature of obstructive airway diseases

- serves as a relatively effort-independent measure of the severity of airway obstruction

56
Q

Restrictive lung diseases

A
  • last bit of air out not dependen on effort but on elastic property of alveoli
  • wont get increased FEV1 but will get increased FVC

Pulmonary system (19 decks)

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