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Respiratory System > Pathology of obstructive lung disease > Flashcards

Pathology of obstructive lung disease Flashcards

1
Q

Give examples of obstructive airway diseases

A

chronic bronchitis(COPD), emphysema (COPD), asthma(type 1 hypersensitivity reaction

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2
Q

Why is the following: bronchiectasis, secondary tubersclulosis, lung cancer + inhaled foreign bodies not classified as an OAD?

A

There is localised obstruction. OAD causes obstruction in all the airways

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3
Q

FEV1 vs FVC

A

FEV1: forced expiratory volume of air eaving lung in the first second
FVC: final total amount of air expired

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4
Q

What is the normal FEV1 + FVC + their ratio?

A
  • 70-80% of FVC
  • 3.5-4L
  • FVC= 5L
  • FEV1:FVC is 0.7-0.8
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5
Q

What is the normal Peak expiratory flow rate? ( PEFR)

A 
-Used to measure peak flow rate
Normal 400-600L/min
Normal range is 80-100% of best value
-50-80% is a moderate fall
<50% of best is marked fall
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6
Q

For obstructive Lung disease, state the changes in: PEFR, FEV1, FVC

A

PEFR: reduced
FEV1:reduced ( <70% of FVC)
FVC: reduced

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7
Q

Describe bronchial asthma

A

Type 1 Hypersensitivity of the airways

  • mediated by degranulation of mast cells which is percipitated. The factors released by mast cells has affects on airway by:
    1. Induction of acute inflammatory response in the airway (swelling)
    2. causes bronchial smooth muscle to constrict
  • A combination leads to reduction in airway diameter. So, airflow limitation during attack of bronchial asthma.
  • Patients will have symptoms of asthma and risk factors.
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8
Q

Is bronchial asthma/COPD reversible or irreversible?

A
  • Reversible either spontaneously or as a result of medical intervention(drugs)
  • Structural changes in airways which are irreversible by pharmacological intervention.

-COPD: irreversible but..

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9
Q

What is the main causes odf COPD ( chronic broncitis + emphysema)

A
  • Tobacco smoking
  • atmospheric pollution
  • occupation: dust
  • alpha-1-antiprotease(antritrypsin) deficiency
  • age + suceptiblity
  • men>women due to smoking/jobs
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10
Q

What is alpha-1-antiprotease(antritrypsin) deficiency?

A

-Rare cause of emphysema

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11
Q

Describe the FEV1 of a smoker compared to a non-smoker

A

FEV1 will decline with age(exposed to air pollution). In a smoker, it declines faster.
-But if you stop smoking it may be slightly reversible so FEV1 will decline slower depending on when you choose to stop smoking

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12
Q

What is the clinical definition of chronic bronchitis?

A

-cough productive sputum most days in at least 3 consecutive months for 2/+ consecutive years

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13
Q

What is complicated chronic bronchitis?

A

When yellow/mucopurulent(indicates infection) or FEV1 falls

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14
Q

State the morphological changes in chronic bronchitis

A

Large airways

  • mucous gland hyperplasia
  • Gobet cell hyperplasia = excess mucous prod.
  • Inflammation and fibrosis (minor component)

Small airways (mainly contributes to airway reduction)

  • Goblet cells appear ( not usually pressent)
  • inflammation and fibrosis(more of an issue)
  • initially inflammation is reversible which is why early smoking cessation improves symptoms

-narrowing of bronchioles is as a result of inlammation, mucous

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15
Q

What is emphysema?

A

-Increase in size of alveolar airspaces distal to the terminal bronchiole arising from either dilation / destruction of their walls WITHOUT FIBROSIS

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16
Q

State the forms of emphysema

A
  • centriacinar
  • panacinar
  • periacinar
  • scar ‘ irregular’ / ‘ bullous emphysema’
17
Q

What is centriacinar emphysema?

A
  • Loss of alveolar tissue in the middle of the acinus
  • mainly caused by cigarrete smoking
  • mainly affects apical parts of the lung
  • begins with bronchiolar dilation, then eventually alveolar tissue is lost.
18
Q

What is panacinar?

A

-wiping out of all the lung tissue
-linked with antitrypsin
deficiency
- can cause spaces in lungs ( blebs) or bulla(greater than 1cm)

19
Q

What is periacinar emphysema?

A
  • loss of tissue at edge of acinus ( acinar that are against pleura)
  • blebs/bullous formation on edge of acinus
  • leads to formation of blebs just underneath pleura. No complications unless it bursts>pneumothorax
20
Q

What is bullous emphysema?

A
  • excessive damage to alveolar structures to the point large alveolar spaces are formed
  • hyper inflated lungs
21
Q

Describe the pathogensis of emphysema

A
  • Normally, in the lung, there is macrophages and neutrophils that produces enzymes that contain proteases, elastases to break down material.
    -Everytime elastase is produced, anti-elastase(protease inhibitor) is also produced to prevent damage to the elastic framework lung.
    -Tobacco smoke e
    evokes an acute inflammatory reaction and causes immune cells to gather. It also inhibits anti-elastases which means tissue destruction occurs
  • There is repair mechanisms for elastin framework that are useless when you have emphysema.
    -You can’t grow lung alveoli back again. It is irreversible.
22
Q

Describe the pathogenesis of alpha 1 antitrypsin deficiency

A
  • there is an absence in antitrypsin, so trypsin will lead to tissue destruction of alveoli
23
Q

How can smoking lead to emphysema?

A
  • more inflammatory cells in lungs
  • induces elastases, and causes anti-elastases to now work. Repair mechanism is now poor.
  • tissue destruction
24
Q

How is COPD reversible?

A

-inflammation and smooth muscle tone respond to drugs

25
Q

How does emphysema lead to airflow limitation?

A
  • alveolar attachments; this gives a radial pull of the alveolar walls, hence maintaining the opening of airways.
  • But when alveolar attachments is destroyed ( emphysema) and the terminal bronchioles is most likely to collapse
26
Q

Why can COPD lead to hypoxaemia?

A

-Airway obstruction: leads to V/P msimatch ( V<p></p>

27
Q

Why can COPD lead to hypoxaemia?

A

-Airway obstruction: leads to V/P mismatch ( V<p></p>

28
Q

Why is COPD also classified as irreversible?

A
  • Large airways
  • Fibrosis
  • partial collapse of airway wall on expiration
  • All off this is does not respond to pharmacological intervention!
29
Q

What is meant by cor pulmonale?

A

-hypertrophy of the right ventricle of the heart that occurs due to pressure overload. Results from disease affecting function/structure of lung.

30
Q

Why can cor pulmonale lead to pulmonary hypertension?

A
  • pulmonary vasoconstriction
  • pulmonary arterioles ( muscle hypertrophy and intimal fibrosis)
  • loss of capillary bed
  • secondary polycythaemia
  • bronchopulmonary arterial anastomoses
31
Q

Long term consequences of COPD

A

Respiratory failure

Type 1: low O2, normal/low CO2( hypoxia and hypocapnia)

Type 2: low O2 and high CO2(hypoxia and hypercapnia)

Chronic hypoxia
pulmonary vasoconstriction>pul. hypertension
pul. hypertension > cor pulmonale

Respiratory System (11 decks)

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