Respiratory Disease Flashcards

1
Q

Why is VO2 max not the best predictor of CVD?

A

Requires expensive equipment
Time-consuming

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2
Q

What are the factors controlling Vo2 max?

A

Pulmonary diffusing capacity
Cardiac output
Oxygen carrying capacity
Skeletal muscles - status of mitochondria, ability to use oxygen

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3
Q

Why is RMR not a useful marker for cardiac and/ or respiratory function?

A

Not measuring respiratory or cardiovascular capacity.
Can be used to compare different dietary interventions on the RMR

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4
Q

How does ageing effect the respiratory system?

A
  • Progressive decrease in the compliance of the lung and chest wall
  • Progressive decrease in the elastic recoil of the lung
  • Progressive decline in the strength of the respiratory muscles

Weakening of respiratory muscles lowers ability of gas exchange in the lungs

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5
Q

What is responsible for gas exchange?

A

The partial pressure of both oxygen and carbon dioxide

Partial pressure of oxygen is much higher in the alveoli than blood vessels to facilitate diffusion of oxygen from the lungs to the bloodstream.
Capillary (from tissues) –> PO2 40mmHg, PCO2 45 mm Hg
Alveolus –> PO2 104mm Hg, PCO2 40mmHg
Capillary (to tissues) –> PO2 104 mmHg, PCO2 40mm Hg

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6
Q

What can effect partial pressure?

A

Altitude
Ageing
COPD

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7
Q

How does COPD affect partial pressure

A

Higher PaCO2 –> limiting carbon dioxide release
Lower PaO2 –> damage to the lungs and airway reduces the amount of oxygen the lungs are able to take in which in turn reduces the amount of oxygen involved in gas exchange to the bloodstream

Oxygen can be measured using an oximeter and is often found to be lower than normal physiological levels because they don’t get enough partial pressure of oxygen in the lungs.

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8
Q

Why does COPD effect partial pressure in the lungs

A

It can cause alveoli damage, challenging the entry of air
Could be an airway obstruction, not allowing full amount of air to be entered –> limit amount that can enter the alveoli

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9
Q

What are the principal muscles that ensure normal, healthy respiratory function?

A

Diaphragm
Intercostal muscles –> participate in the inspiration and expiration

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10
Q

What are the secondary respiratory muscles?

A
  • Sternocleidomastoid –> long muscles that connect the sternum, clavicle and mastoid. Accessory muscles of inspiration. Act on the chest wall to affect breathing movement, causing cranial displacement
  • Scalenes –> lifts first two ribs in a forced inspiratory. Always electrically active, even not for forced breaths
  • Pectoralis Minor –> an accessory muscle of respiration when inspiration is deep and forced, will help raise ribs 3-5 to aid expanding of the thoracic cavity
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11
Q

How does calcification affect respiration/ COPD?

A

When calcification of joints occurs between ribs and spine, and ribs and the sternum, can causes a chest wall compliance to decrease by 30% (net compliance allows the lungs to achieve appropriate functional residual capacity, the volume remaining after passive expiration)

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12
Q

What is is inspiratory reserve volume?

A

Maximum amount of air that can be inspired, from forced inspiration.
Can be up to around 3 litres

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13
Q

What is tidal volume?

A

The amount of air inspired and expired in normal breathing/ resting conditions.
Around 0.5 litres

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14
Q

What is expiratory reserve volume?

A

The amount of air that can be exhaled in forced exhalation
Around 1 litre

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15
Q

What is residual volume?

A

The amount of air left in the lungs after forced expiration.
Essential to avoid lung collapse
Around 1 litre

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16
Q

How does ageing effect breathing volumes?

A

There is a decrease in the inspiratory and expiratory reserve volume.
These changes can then increasing the residual volume. This reduces the respiratory ability as residual volume is air that is not used.

Strength of primary and secondary muscle dictates gas exchange and the various volumes - exercise helps to stimulate and strengthen respiratory muscles

17
Q

What can help prevent decline of respiratory muscles?

A

Exercise

18
Q

What is spirometry?

A

A functional test to analyze respiratory function - best way to do this.
It measures all breathing parameters, paying more attention to forced expiratory volumes.
Measures the ability of the person to exhale air in the first second of the test (FEV1).

19
Q

Discuss FEV1

A

Volume expired in the first second –> measure in spirometry
In a healthy individual, it should be at 80% of the total air in forced exhalation.
Lower than 80% relates to airway obstruction, damage in the artery, or weak respiratory muscles. A large indicator of COPD.

Starts to decline around the age of 25, however depends on lifestlye and activity levels.

Factors determining FEV1 and FVC are the power of the respiratory muscles and airway diameter. Airway diameter varies little with age, main cause in the loss of muscle power however can also be due to airway obstruction.

20
Q

What is a key indicator of COPD?

A

When the FEV1 is below 80% in spirometry testing.

21
Q

What are some COPD conditions that were previously classified in terms of symptoms alone?

A

Chronic bronchitis
Chronic asthma
Emphysema

22
Q

What is Emphysema?

A

The destruction of the lung tissues
Found in COPD

23
Q

What are some causes of COPD?

A

Environmental and lifestyle factors –> most influential
- Smoking –> stopping can reduce risk significantly
- Ageing
- Obesity
- Industrial pollution

Genetic polymorphisms –> least influential

24
Q

Can COPD be reversed?

A

If the FEV1 value is between 70-80% then it is possible to reverse. Below 70% it is often irreversible.

25
Q

How does obesity influence COPD?

A

Fat can compromise function of diaphragm and ultimately disrupt breathing ability.
Reduced resting lung volumes in obese lungs due to restriction from surrounding adipose tissue and reduction in lung compliance. Adipose tissue surrounding the lungs and respiratory muscles increases pressure on the lung which can restrict their ability to work at full capacity by reducing thoracic volume.

26
Q

What is chronic bronchitits?

A

Cough with sputum for at least 3 months of the year for at least 2 consecutive years –> must occur for COPD diagnosis

Causes hypertrophy, inflammation of the alveoli and mucus production. This mucus often causes a cough.
More common in people older 50.

27
Q

What is the pathophysiology of COPD?

A

Size of alveoli increase due to hypertrophy and inflammation. Also occurs in the airway.
Size of alveoli increased to attempt to get more oxygen and maintain gas exchange in lungs. If caused by smoking or pollution. This can damage the airways.
Particles like tobacco can damage the bronchi
Inflammatory response causes the release of mucus

Bronchitis –> mucus released into the airway, increasing the size of the medium layer (hypertrophy). This leads to a smaller diameter of airway causing a lower capacity to transport gases in gas exchange.

28
Q

What is the treatment of COPD?

A

For people with a FEV1 below 70%

  • Inhaled bronchodilators (inhaler) –> open up airway to enhance transport of gases
  • Steroids –> acute use - reduce inflammation response
  • In severe cases, long term domiciliary O2 therapy may be needed (oxygen mask)
  • Exercise –> strengthening of respiratory muscles - needed to be done on a daily basis/ very regularly
29
Q

What is hypoxemia?

A

Low level of oxygen in the bloodstream.
Not an illness or a condition, its a sign of a problem tied to breathing or blood flow.

Most common causes are asthma, COPD, cystic fibrosis, pulmonary hypertension, bronchiectasis and interstitial lung diseases.

30
Q

What are the main symptoms of COPD?

A
  • Mechanical disadvantage –> rapid and frequent breathing - to try and restore low levels of oxygen. However this breathing is superstitial
  • Energy imbalance (-ve) –> breathing difficulty makes eating challenging, often don’t want to eat very much. Can cause o2 to drop more/ worsens symptoms
  • Disuse muscle atrophy –> lower energy intake, lack of activity, lower respiratory function. Lack of stimulation of respiratory muscles
  • Hypoxemia –> can lead to secondary disorders e.g. metabolic disorders, insulin resistance
  • Systemic inflammation
  • Oxidative stress
  • Insulin imbalance –> cachexia, large quantities of fat free mass can be lost, glucose uptake is modulated by adipose tissue, liver and muscle, less mass makes it harder to control blood glucose.
31
Q

Why does COPD cause oxidative stress

A

Lower oxygen levels (from hypoxemia) lead to anaerobic glycolysis which produces lactate.
High levels of lactate cause acidosis (lowering of pH) which can lead to mitochondrial damage (sensitive to chronic pH changes) and therefore cause oxidative stress –> increase synthesis of free radicals, effect function of other molecules e.g. insulin

Also related to systemic inflammation as its causes the same pathway

32
Q

Why is weight loss common in COPD patients. And what is the prevelance?

A

They often are in a negative energy balance due to eating worsening symptoms/ struggling to eat due to symptoms. The often eat little amounts which over time lead to weight loss.

70% in inpatients –> more likely to be in a worse physiological state, worse clinical scenario
20-35% in outpatients
17% patients have a BMI lower than 20 kg/m2
There is a depletion of fat free mass

33
Q

What is the best dietetic approach to treat COPD?

A

Reach energy requirements.
Calculate REE of patient
REE x 1.3-1.7 –> to attempt to provide enough energy
Use ONS if required.
Enteral or parenteral nutrition may be needed
Assess re-feeding risk
May require appetite stimulants
60% CHO, 20% protein, 20% fat

Balance FFM and functional capacity with energy expenditure and glycogen storage.

34
Q

How can fatty acid balance help manage COPD?

A

Increasing Omega 3 and reducing Omega 6 can help reduce inflammatory response and improve some of the symptoms associated with the condition