Week 2: COPD

Question 1

1.2 million in the UK have asthma

a. prevlence
b. incidence

Answer 1

a. prevlance

number of cases in a population at any point in time (bathtub)

Question 2

there are 795,000 new cases of asthma in the UK annually

a. prevlence
b. incidence

Answer 2

number of cases in a population at any point in time (bathtub)

Question 3

How does smoking damage the lungs

Answer 3

• Smokes – increases the activity of inflammatory cells in the lung -> increases elastase production (while the function of anti-elastase production is diminishing)
• Effect on repair system!! (Which is rubbish anyway)
• = destruction of tissues and emphysema

Question 4

A rare/inherited cause of emphysema

Answer 4

Alpha 1 anti-protease (anti-trypsin) enzyme deficiency

(alpha 1 antitrypsin) is a protease inhibitor (anti-elastase) made in the liver – which limits the damage caused by activated neutrophils releasing elastase in response to infection/cigarette smoke

onset < 45

basal predomnance to emphysema (damage seen base/all over) compared to smoking - effects seen at apex/upper lobes

Question 5

Chronic bronchitus is clinically defined as

Answer 5

having a cough productive of sputum most days for at least 3 months

in 2 consecutive years

Question 6

Lung parenchyma

Answer 6

functional tissue of organ - lungs -> parts involved in gas exchange

Each alveolus in the lung parenchyma opens directly into an alveolar duct or occasionally, in a limited number of species, into a respiratory bronchiole.

Question 7

Common COPD symptoms

Answer 7

Cough/ sputum for (3+ months in 2+ consecutive years

SOB (Dyspnoea)

Wheezing (recurrent)

Progressively getting worse

Consider (age 45+, smoking history)

Question 8

FEV1/FVC ratio of someone with COPD

Answer 8

< 0.7 (70%)

obstructive pattern

Question 9

What signs would you look for during a clinical examination on a COPD patient

Answer 9

• **breathlessness **at rest/walking into apointment
• Use of accessory muscles on expiration
• Chest wall deformities (anterior/posterior distance is larger than expected) - hyperinflation of chest
• ** Pursed lip breathing** - (trying to increase expiratory pressure)
• Cyanosis (lips, tongue, peripherals)
• Raised jugular venous pressure (later - right heart failure)
• Cachexia - severe weight loss
• Expiratory whistling - wheezing

Question 10

what chest wall deformity might you see in someone with long term COPD

Answer 10

(anterior/posterior distance is larger than expected) - hyperinflation of chest

“barrel chest”

Question 11

modified medical research council breathless scare - dyspnea related to activity

outline?

Answer 11

0 = breathless only on exercise
1 = breathless when hurrying on the level or walking up slight hill
2 = walks slower than people same age on level, due to SOB, stops for breath when walking own pace
3 = SOB walking few mins/100 yards (90m)
4= too breathless to leave house, dress, undress

not used to choose treatments of COPD

Question 12

when sputum is infected

Answer 12

mucopurulent

-> yellow/green

can indicate an infective exacerbation

Question 13

when sputum is infected

Answer 13

mucopurulent

-> yellow/green

can indicate an infective exacerbation

Question 14

how does chronic bronchitus affect the large airways

Answer 14

• hyperplasia of mucus glands (an increase in size)
• Hyperplasia of goblet cells (secrete muscus and create protective mucus layer)
• Inflammation and fibrosis are a minor component

effects on mucosa * moist inner lining - mucous membrane

Question 15

Inflammation and fibrosis in long standing bronchitus is more marked in small airways/affects small airways

a. true
b. false

Answer 15

a. true

and goblet cells appear where there should be none

Question 16

Name two things that happen pathologically to the airways in chronic bronchitus

Answer 16

1. The cells required to produce excess mucus which leads to cough and spit – increase in number -> more mucus
2. Some inflammation and fibrosis because of irritation (worse in smaller airways)

Question 17

2 anatomical changes that take place in emphysema

Answer 17

1. destruction of elastic fibres -> increases compliance (without increases in elasticity this is BAD!! cannot get the air back out as easily)
2. destruction of alveolar walls -> creates one large airspace, reducing the surface area for gas exchange

air gets trapped /increase in residual volume/hyperinflated lungs

Question 18

structures which mark the end of the conducting zone

Answer 18

terminal bronchioles

Question 19

pulomonary acinus refers to what structures/tissue

Answer 19

everything distal to the terminal bronchiole (respiratory bronchiole, alveolar ducts, alveolar sacs) – i.e., the smaller branches and grapes.

gas exchange tissue

Question 20

Respiratory bronchioles/alveolar ducts are still conducting airways

a. true
b. false

Answer 20

a. true

can participate in some gas exchange as well ->
Respiratory bronchioles have single alveoli off their walls.

Question 21

Centriacinar emphysema features

Answer 21

Upper lobes (apical parts of lobes) on both sides

Loss of lung tissue is concentrated in the centre of acinus

Associated with COPD/smoking inhalation

Question 22

Panacinar emphysema features

Answer 22

Lower zones/lobes

Takes out large areas rather than individual spots

All of the acinus is wiped out/all portions gone

Associated with alpha 1 anti-trypsin deficiency (but can be found in those without genetic abnormality)

Question 23

Periacinar emphysema features

Answer 23

tissue loss around the EDGES of the acinus

against the pleura

Airspaces visible along the edge of acinar unit, but only where it abuts against a fixed structure (pleura/vessel)

Associated with spontaneous pneumothorax when space pops or leaks air

Question 24

Type of emphysema associated with alpha 1 anti-trypsin deficiency

Answer 24

Panacinar

more severe in lower zones/lobes

Takes out large areas/entire acinus

Question 25

Type of emphysema that causes tissue loss around the edges of the acinus and is most likely to cause pneumothroax

Answer 25

Periaciner

Question 26

Bullae/Bullous emphysema

Answer 26

air spces/pockets bubble like cavities filled with air or fluid usually in UPPER LOBES take 1/3 of one side

Question 27

What might a chest xray on a patient with COPD/emphysema show after a full breath

Answer 27

- hyperinflation - flattened diaphragm - > 10 ribs showing (see all posterior parts of ribs down to 12) - increased lung volume - narrow/elongated heart - bullae

Question 28

why does hyperinflation occur in emphysema

Answer 28

When the lung tissue has been damaged and it loses its elasticity. Will appear much larger than they should be (the only way to try and stop the small airways collapsing) - The lungs may also be trapping the air after each breath - The result of this is that the person cannot make use of as much air with each breath as they otherwise would, which often leads to symptoms that include shortness of breath or difficulty breathing.

Question 29

Alpha 1 anti-trypsin deficiency

Answer 29

* We do not have a counterbalancing enzyme function -> (anti-elastase) * Results in destruction of elastin fibres /alveolar walls (in normal lungs elastases keep our lung healthy and clean, but if there is no anti-elastase production they will digest elastic fibres/lung tissue)

Question 30

what is the reversible component of COPD

Answer 30

inflammation/smooth muscle contraction will to some extent respond to bronchodilators Smooth muscle tone in SMALL AIRWAYS * Inflammations leads to an increase in smooth muscle tone (like what happens in bronchial asthma) – this will respond to the same drugs Inflammation AND smooth muscle tone respond to pharamcological intervention

Question 31

The clinical effects of COPD are mainly caused by

Answer 31

Hypoxiaemia * a below-normal level of oxygen in your blood, specifically in the arteries chronic hypoxia -> vascular changes -> Cor Pulmonale

Question 32

Cor Pulmonale

Answer 32

**- Hypertrophy of the right ventricle ** - caused by - Pulmonary vasoconstriction/hypertensionin response to chronic hypoxiathe - right ventricle must work harder and fight against increased resistance. - muscles in the vessels become hypertrophic -> the intimal surface becomes fibrotic leading a reduction in the cross-section (harder to pump blood)

Question 33

polycythaemia

Answer 33

high concentration of RBC bone marrow trys to stimulate RBC - mkaes the blood harder to pump in an already compromised system (RV hypertrophy, pulmonary hypertension, pulmonary vasocontriction) in response to hypoxia can be secondary in COPD when P02 falls

Question 34

non-pharmacological treatment of COPD

Answer 34

1. Vaccines - Flu/pneumococcal 2. Smoking cessation 3. Pulmonary rehabilitation (6 week course) 4. psychological support

Question 35

what vaccines are offered to people with COPD

Answer 35

flu (influenza) pneumococcal

Question 36

FEV1/FVC score that is evidence of airflow obstruction

Answer 36

< 70% FEV1-FVC ratio

Question 37

rare/inherited cause of emphysema

Answer 37

Alpha 1 anti-protease (anti-trypsin) enzyme deficiency

Question 38

When would you suspect alpha 1 anti-protease enzyme deficiency

Answer 38

* onset of COPD/emphysema <45 * Basal predominace to emphysema (base/all over) * Liver fibrosis or cirrhosis

Question 39

Chronic bronchitus is clinically defined as

Answer 39

Having cough and sputum for at least 3 months! Present in 2 consecutive years

Question 40

what might you find in clinical examination of someone with COPD

Answer 40

* breathlessness walking into appointment * accessory muscle use one expiration * chest wall deformities * pursed lip breathing * cyanosis (lips, tongue, peripherally - reduced -02/hypoxia) * raised jugular vein pressure (later- right heart failure) * peripheral odema * cachexia - severe weight loss * wheezing (expiratory whistling)