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
Q

What is the bronchiectasis cycle

A
  • 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
Q

What are the complications of bronchiectasis

A
  • Pneumonia
  • abscess
  • septicemia
  • empyema
  • metastatic abscess
  • amyloidosis
  • pulmonary hypertension
27
Q

What are bronchiectasis symptoms

A
  • wheezing and coughing come and go
  • dyspnea
  • foul smelling mucus
  • long term hypoxia can lead to finger clubbing
28
Q

In the pathogenesis of emphysema what do the proteases and free radicals do

A

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
Q

Chemical irritants and nicotine from the tobacco cause immune cells to release what in emphysema

A

IL8 ,TNF, leukotriene B4