Chronic Obstructive Pulmonary Disease🦋 Flashcards

1
Q

What’s the function of lungs

What does gas exchange depend on?

Where can gas exchange occur

A
  • Gas exchange
  • depends on compliance( stretchability) of lungs
  • in alveoli that are both ventilated and perfused
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2
Q

What are ventilation+perfusion defects

A
  • when alveoli are ventilated but not perfused, this is ventilatory dead space
  • when alveoli are perfused but not ventilated and this leads to shunting on non-oxygenated blood from pulmonary to systemic circulation causing cyanosis
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3
Q

What causes respiratory failure

A
  • ventilation defects( CNS, neuromuscular defects, drugs)
  • perfusion defects(cardiac failure,pulmonary emboli)
  • gas exchange defects(fibrosis, consolidation, emphysema)
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4
Q

What are risk factors for COPD

A
  • nutrition
  • infections
  • socio-economic status
  • aging population
  • genes( a decrease in alpha 1 anti-trypsin)
  • cigarette smoking
  • occupational dust and chemicals(silica)
  • environmental tobacco smoke
  • indoor and out door pollution
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5
Q

What is chronic bronchitis

A

It’s a persistent productive cough for at least 3 consecutive months in at least 2 consecutive years

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6
Q

What are the forms of chronic bronchitis

A
  • simple chronic bronchitis
  • chronic asthmatic bronchitis
  • chronic obstructive bronchitis
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7
Q

Describe the features of the different forms of chronic bronchitis

A

Simple chronic bronchitis- the productive cough raises mucoid sputum but airway not obstructed

Chronic asthmatic bronchitis- has hyper responsive airways with irregular bronchospasms and wheezing

Chronic obstructive bronchitis- develops chronic outflow obstruction and is associated with emphysema

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8
Q

What cell changes take place in chronic bronchitis

A
  • mucus gland hypertrophy
  • smooth muscle hypertrophy
  • goblet cell hyperplasia
  • inflammatory infiltrate
  • excessive mucus production
  • squamous metaplasia
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9
Q

What is the morphology for chronic bronchitis

A

The trachea in the mid upper field is hyperemic

The bifurcation and bronchi contain mucopurulent exudate secretion

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10
Q

What are complications of chronic bronchitis

A
  • pulmonary hypertension and cardiac failure
  • recurrent infections
  • respiratory failure
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11
Q

What are signs and symptoms of chronic bronchitis

A
  • cough
  • sputum
  • frequent infections
  • intermittent dyspnea
  • wheeze
  • some patients develop COPD with outflow obstruction causing, hypercapnia, hypoxemia, cyanosis
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12
Q

What is emphysema

A

It is the permanent enlargement of air spaces distal to terminal bronchioles, accompanied by destruction of their walls(septa), reducing surface area of alveoli

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13
Q

What causes emphysema

A
  • smoking

- deficient of alpha 1 anti trypsin

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14
Q

What does alpha 1 antitrypsin do

A

It coats lungs,protecting them from neutrophil elastase

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15
Q

What produces neutrophil elastase

What does neutrophil elastase do

A

By white blood cell (neutrophil)

Neutrophil elastase breaks down harmful bacteria but damages lungs at the same time if they are exposed

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16
Q

What happens to alpha 1 antitrypsin when it’s deficient

A

It’s trapped in the liver causing liver cirrhosis and this leaves neutrophil elastase uninhibited causing lung damage

17
Q

What 2 imbalances cause emphysema and increase elastase

A

Protease- antiprotease imbalance

Oxidant-antioxidant imbalance

18
Q

What are the types of emphysema and their features

A
  • centriacinar (involves central/proximal parts of the acini, lesions are more common and severe in the upper lobe, this type is caused by cigarette smoking)
  • panacinar (occurs more in lower lung zones and because of alpha 1 antitrypsin deficiency)
  • distal acinar (the distal part of acinus is involved, it’s seen adjacent to pleura,along lobular margins and has cyst like structures called bullae)
  • irregular acinar (the acinus is irregularly involved, is associated with scarring, clinically asymptomatic and is the most common emphysema)
19
Q

What are complications of emphysema

A

-pulmonary hypertension (resulting in hypoxia induced pulmonary vascular spasms and loss of capillary surface area due to alveolar wall destruction)

  • right side heart failure
  • respiratory failure
20
Q

What is bronchiectasis

A

Is the abnormal fixed dilation of the bronchi

21
Q

What causes bronchiectasis

A

fibrous scarring following infection such us pneumonia, tb, cystic fibrosis (diseases that cause chronic inflammation)or it’s seen with chronic obstruction(tumour)

22
Q

What do the dilated airways in bronchiectasis do

A

Accumulate purulent secretions which can’t be removed because of damaged bronchi( cilia don’t work efficiently )

23
Q

Bronchiectasis affects which lobes normally

A

Lower lobes

24
Q

Chronic recurring infections from bronchiectasis can lead to what

A

Finger clubbing

25
What is the bronchiectasis cycle
- there is the initial insult which causes inflammation - this leads to neutrophil derived proteases - there is then airway remodeling (permanent airway dilation and loss of cilia) - then mucus accumulation which leads to bacterial colonization - then infection and the cycle continues
26
What are the complications of bronchiectasis
- Pneumonia - abscess - septicemia - empyema - metastatic abscess - amyloidosis - pulmonary hypertension
27
What are bronchiectasis symptoms
- wheezing and coughing come and go - dyspnea - foul smelling mucus - long term hypoxia can lead to finger clubbing
28
In the pathogenesis of emphysema what do the proteases and free radicals do
The proteases have a destructive effect and in patients with low anti-proteases it leads to emphysema and the free radicals deplete the lungs antioxidant mechanisms and that leads to tissue damage
29
Chemical irritants and nicotine from the tobacco cause immune cells to release what in emphysema
IL8 ,TNF, leukotriene B4