week 2 Flashcards

1
Q

does pulmonary rehabilitation improve COPD

A

it can! There is excellent evidence for the impact of pulmonary rehab on COPD outcomes such as days spent in hospital and quality of life, and good evidence that it improves survival.

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2
Q

where does centriacinar emphysema begin

A

centri-acinar emphysema begins with dilatation of the respiratory bronchiole, and then progresses to loss of alveolar tissue.

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3
Q

is chronic hypoxaemia a feature of bronchial asthma

A

no, bronchial asthma is variable and reversible, without reduced respiratory drive and loss of alveolar area, so there is no chronic hypoxaemia. Oxygen levels should be normal.

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4
Q

what is tracheal tug

A

a sign of respiratory distress in children.abdominal breathing, subcostal recession, intercostal recession and head bobbing are all signs of respiratory distress in children, and result from trying to draw breath in through an obstructed airway.

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5
Q

does fluticasone have more severe side effects than beclomethasone

A

fluticasone is more potent and has a higher risk of serious side effects.

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6
Q

how does washing a spacer help improve its efficacy

A

washing the spacer device leaves a coating of detergent, which will decrease the static charge. This means the drug is less likely to stick to the spacer, and increases drug delivery to the lungs.

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7
Q

how do humidifiers affect asthma control

A

no evidence to suggest they have nay effect

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8
Q

what should a child under the age of 5 who has just been diagnosed with asthma and is symtomatic more than 3 times a week be started on

A

the initial preventer medication for under 5s is a LRTA. For children over 5, it is a very low dose inhaled corticosteroid.

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9
Q

is spirometry required to diagnose chronic bronchitis

A

it is a clinical diagnosis, meaning there are no specific tests for chronic bronchitis.

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10
Q

can COPD be the cause of finger clubbing

A

NO!

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11
Q

is spirometry required to diagnose COPD

A

unlike asthma, the diagnosis of COPD requires both typical symptoms and history AND typical spirometry showing airflow obstruction. Spirometry is performed pre- and post-bronchodilator therapy, to demonstrate non-reversible (or partially reversible) obstruction.

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12
Q

what is asymmetrical chest expansion indicative of

A

asymmetrical chest expansion is suggestive of lobar collapse or pleural effusion, and is not typically a finding in the asthmatic chest. Chest examination is usually normal in the clinic.

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13
Q

why should people with COPD not be treated with high flow oxygen

A

some people with advanced COPD have chronically elevated CO2 levels, which means the central chemoreceptors that detect CO2 and control the respiratory drive are desensitised and do not work. These people therefore rely on their less sensitive peripheral chemoreceptors to detect oxygen levels and generate a respiratory drive. Over-oxygenating these people can “switch off” the peripheral chemoreceptors and make their respiratory failure worse. People with severe COPD should be oxygenated carefully, with the lowest flow required to achieve acceptable oxygen saturation. In people with known Type 2 respiratory failure, this should be about 88-92%.

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14
Q

do new goblet cells appear in chronic bronchitis

A

goblet cells produce mucus. Chronic inflammation leads to new goblet cells appearing in small airways, and an increase in the number of goblet cells in larger airways.

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15
Q

can a patient still have asthma with normal spirometry

A

yes, variability is a feature of asthma. Normal spirometry cannot rule out intermittent airway obstruction.

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16
Q

how shoulds steroids be given during an acute asthma attack

A

in an acute asthma attack, steroids should be given orally, or sometimes intravenously.

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17
Q

what is the hallmark of obstructed lung disease

A

reuced FEV1:FVC (less thqn 0.7)

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18
Q

how much is height restricted in adults by brown inhalers

A

height restriction is generally about 0.5-1.0cm.

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19
Q

is the airway obstruction in asthma reversible

A

the obstruction is caused by inflammation and smooth muscle contraction, so can reverse spontaneously or with medication.

20
Q

when is someone eligible for long term oxygen therapy

A

patients are eligible for LTOT if they have a PaO2 (measured from an arterial blood sample) of <7.3 regardless of additional features. If they have complications of chronic hypoxia such as polycythaemia, pulmonary hypertension, peripheral oedema or nocturnal worsening of hypoxia, LTOT is offered sooner, at a PaO2 of <8.

21
Q

what type of drug is ipatropium

A

ipratropium bromide is a muscarinic antagonist. It works by relaxing the smooth muscle of the airways.

22
Q

is flapping tremor a sign of hypoxia

A

no, flapping tremor is a sign of hypercapnia – carbon dioxide retention.

23
Q

what is type 2 respiratory failure a sign of

A

COPD, An easy way to remember type 1 vs type 2 respiratory failure is that in type 2 failure, the movement of 2 gases is impaired. In type 1 respiratory failure, there is a failure of oxygenation, but ventilation is adequate to clear CO2 (remember that CO2 dissolves much more readily than oxygen). In type 2 respiratory failure, ventilation is impaired to the point that not only does oxygenation fail, but CO2 isn’t being cleared, and CO2 levels rise. In COPD, this is a sign of advanced disease.

24
Q

what does hypoxia lead to

A

constriction of pulmonary arterioles. When the oxygen tension in the alveoli drops, the vessels constrict, as there is no benefit to sending blood where there is no oxygen.

25
Q

what is terbutaline

A

Terbutaline is a short-acting beta agonist used as a reliever medication in asthma.

26
Q

what should co gas transfer be like in asthma

A

In asthma it should be normal or slightly increased.

27
Q

what is respiratory failure in COPD due to

A

respiratory failure in COPD is due to matched defect in ventilation and perfusion. Remember that oxygenation will be impaired in any situation where blood is not getting to the alveoli (perfusion) or air is not getting to the alveoli (ventilation). In COPD, both are affected.

28
Q

is spirometry required to diagnose asthma in adults

A

no, s in children, asthma can be diagnosed based on a highly suggestive history, and confirmed by a good response to treatment.

29
Q

what is the initial treatment of asthma in adults

A

Initial treatment of asthma in adults is with a low-dose inhaled corticosteroid.

29
Q

what uis cultural competence

A

the consideration of the diversity of cultural factors (such as language, beliefs, preferences) that are important to your patients. This results in you approaching each patient in a manner that is tailored to them and sensitive to these cultural factors, rather than treating all patients exactly the same.

30
Q

is female sex a risk factor for COPD

A

yes, although the prevalence of COPD among males has historically been higher than that among females (due to a higher prevalence of smoking), a female smoker is more likely to develop COPD than a male smoker.

31
Q

does hypoxia increase the blood pressure in the lungs in COPD

A

hypoxia leads to a reflex constriction of blood vessels in the lungs. This increases the vascular resistance, meaning the right side of the heart has to work harder, and the blood pressure rises. This is called pulmonary hypertension.

32
Q

describe FeNO in asthma

A

FeNO works like a breathalyser for airway inflammation. A high degree of inflammation will lead to a high FeNO, which would be suggestive of asthma.

33
Q

what can a deficiency in alpha-1-antitrypsin lead to

A

alpha-1 antitrypsin is an enzyme which breaks down other enzymes that break down alveolar tissue. A deficiency of this enzyme tips the balance towards tissue destruction, and can lead to emphysema

34
Q

what is the next step for a child over five on a very low dose of ICS

A

the BTS/SIGN guidelines would recommend a long-acting beta agonist (LABA) as the next step

35
Q

what causes asthma and allergies

A

an underlying abnormality in the epithelium

36
Q

what is emphysema

A

emphysema is the increase in size of the airspaces that are distal to the terminal bronchioles (i.e. the respiratory bronchioles and alveoli). This can be due to dilatation or destruction of their walls, and causes obstruction through air trapping.

37
Q

when are low dose inhaled steroids used in asthma

A

very low dose inhaled steroids are the initial treatment for paediatric asthma. Oral steroids are only used by specialists in treatment-resistant asthma.

38
Q

what is the aim when treating childhood asthma

A

aiming for minimal symptoms and good quality of life.

39
Q

what is peripheral eosonophilia suggestive of

A

while a peripheral eosinophilia may be suggestive of atopy (remember this is the cluster of conditions including asthma, eczema, hayfever, allergic rhinitis and other allergies)

40
Q

what is normal FEV1:FVC

A

0.7-0.8

41
Q

what happens to pCO2 in moderate or severe exacerbations of asthma

A

In moderate or severe exacerbations of asthma, the respiratory rate goes up, so you would expect more CO2 to be blown off, therefore the pCO2 (measurement of the amount of CO2 dissolved in the blood, shown on a blood gas analysis) should be LOW. If a patient is having an acute asthma attack with a high respiratory rate and their pCO2 is “normal”, this means they are not ventilating adequately, and this is an indication that they require specialist input urgently as their asthma is life-threatening.

42
Q

what are the majority of exacerbations of COPD

A

viral

43
Q

when is hyperinflation present

A

if more than 6 ribs are visible anteriorly, or 10 ribs posteriorly.

44
Q

where does smokimg tend to cause emphysema

A

at the apex of the lungs

45
Q

what is omalizumab

A

a specialist treatment, and is termed a “biologic” because it is an antibody. It specifically targets IgE (an antibody involved in the allergy response), compared to e.g. prednisolone which has a much more generalised anti-inflammatory action.

46
Q

what happens to Hb levels in COPD

A

COPD can cause high haemoglobin due to chronic hypoxia. This is because the body detects the low oxygen levels and attempts to improve oxygenation by making more haemoglobin, a state called polycythaemia.