Asthma, COPD & Bronchiectasis

What is FEV1?

Forced Expiratory volume - the amount of air expired from the lungs in the first second of forced breathing.

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What is FVC?

Forced vital capacity - the maximum volume of air that someone exhales after a full inspiration beforehand

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What % of lung volume should be exhaled in the first second of expiration? In other words, what should the FEV1/FVC ratio normally be?

Normally ~75% expired within the first second. FEV1/FVC ratio of 0.75. A ratio of < 0.7 suggests asthma/COPD

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Does a normal FVC and reduced FEV1:FVC suggest an obstructive or restrictive pattern of breathing impairment? Why?

It shows obstructive because the patient expires a normal total volume of air but just not as quickly because of the obstruction (COPD)

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What does a reduced FVC and a normal FEV1:FVC suggest?

Restrictive lung disease. The patient can exhale quickly and forcefully but the FVC is lower because the lung is restricted to filling to its full capacity

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What is asthma? (briefly)

A chronic inflammatory condition of the lungs characterised by reversible airflow obstruction.

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When is asthma classically worse / what are some triggers for an attack?

At night, during exercise, cold weather, allergic component, viral infection, NSAIDs (aspirin) etc

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What does 'morning dipping' describe in asthma?

That peak flow is often worse in the morning.

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How do you confirm a diagnosis of asthma?

Take a detailed history and peak flow - often leads to 'suspected asthma'. FEV1:FVC = < 0.7 - if improves on bronchodilation then this confirms the diagnosis.

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What is the difference between intrinsic and extrinsic asthma?

Extrinsic: type I hypersensitivity (allergic-related). Intrinsic: non-immune mechanism (no causative agent) occurs in middle-aged people

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Would people with extrinsic asthma likely have a positive or negative skin ***** test?

Positive - skin ***** test checks for immediate allergic reactions to many substances. Because intrinsic asthma can normally be attributed to a particular causative allergen.

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Is late-onset asthma more likely to be intrinsic or extrinsic?

Intrinsic (develops in middle aged and generally more severe, deterioration of lung function).

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Acute episodes of bronchospasm: what is activated in this?

Mast cells are activated

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What happens in the early phase of bronchospasm (acute asthma)?

Spasmogen production (including histamine, prostaglandin D2, leukotrienes) and causes smooth muscle contraction.

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What happens in the late phase of bronchospasm (acute asthma)?

Chemotaxins attract eosinophils and mononuclear cells causing mucosal oedema which narrow the airway.

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What is chronic asthma and what condition is it very similar to?

Most asthmatics have normal resp function between acute attacks, but in chronic asthma there may be permanent narrowing (i.e. from mucus, oedema, bronchial SM)

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What is PEF?

Peak (expiratory) flow

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What % of best predicted PEF suggests a) acute, severe asthma b) life-threatening asthma

a) 33-50% of best PEF = acute & severe. b) < 33% = life-threatening asthma attack

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What are other features/signs of life-threatening asthma?

< 92% O2 sats; silent chest; cyanosis; bradycardia; confusion

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What investigation would you urgently do in severe/life-threatening asthma?

ABG (arterial blood gas)

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O2 < ? = severe hypoxia

ABG - severe hypoxia = < 8

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If you take an ABG in this situation and there is a normal PaCO2 is this a good or bad sign?

Bad - because it should be low because of hyperventilation. This shows that there is not compensation and is a bad sign

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What does raised PaCO2 suggest in acute asthma?

Near fatal - hyperventilation should be reducing CO2 normally.

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What is COPD?

Progressive airway obstruction which is characterised by longterm breathing problems and airflow problems.

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What are the two aspects of COPD which cause breakdown of lung tissue + increased airway resistance.

COPD = emphysema (decreased outflow pressure/tissue breakdown) & chronic bronchitis or bronchiolitis (increased airway resistance)

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Emphysema involves the destruction of what? What does this lead to?

Destruction of alveolar walls due to increased secretion + activation of extracellular proteases. This creates 'dilations' of acini (air spaces in the lungs)

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What are the consequences with destruction of connective tissue in the alveolar walls?

This leads to a loss of elastic recoil and there is larger alveoli with less area for gas exchange. This leads to stasis of air and reduced O2 uptake.

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What is a respiratory 'lobule'? (what does it consist of)

Lobule = the functional 'unit' of the lung - i.e. where gas exchange occurs. Each one consists of a bronchiole which becomes alveolar ducts and sacs which have alveoli.

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What is centrilobular emphysema? What risk factor is it associated with?

This is where destructive changes are limited to the central part of the lobule next to the terminal bronchiole. This is the most common form and is associated with smoking.

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What is panacinar emphysema? It is common in those with a deficiency in what?

This is were all ('pan') of the lobule features destruction and distension. It is more common in a1-antitrypsin deficiency

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Approximately what % of COPD is due to a1-antitrypsin deficiency?

2% of cases. A hereditary deficiency

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What enzyme does a1-antitrypsin normally inhibit?

Neutrophil elastase (it breaks down the alveoli walls which cause emphysema)

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What is the main abnormality seen in chronic bronchitis? (what is produced)

There is an abnormally large amount of mucus produced --> daily cough with sputum for at least 3 months out of 12 for 2 years

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What cell changes have happened to cause hypersecretion of mucus?

Hypertrophy & hyperplasia of muscus-secreting glandular cells in the bronchioles.

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What is bronchiolitis and what is it normally caused by?

Associated with smoking. It causes inflammation of the airways with marcrophage and lymphoid cell infiltration - this leads to scarring and narrowing of the airways.

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COPD causes increases airflow resistance. Is this greater on inspiration of expiration? What symptom does this lead to?

Often expiration. This means more air from the previous breath remains in the lungs. This can lead to hyperinflation of the lungs when the next breath is taken.

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What features of a history might suggest COPD and how would it be distinguished from a history of asthma?

Productive morning cough, following many years of coughing (due to mucus, dry in asthma); slowly progressive dysponeoa and relatively continuous symptoms (asthma more likely to be exarcebated with exercise than continuous). Also increased LRTIs,

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What will be the main sign in a patient with mild COPD?

Wheeze

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What features might be present in a patient with severe COPD? (Name at least 5)

tachypnoea; cyanosis; CO2 flap; hyperinflated lungs; lip pursing on expiration (to increase pressure and force airways open); signs of resp distress; poor chest expansion; hyper-resonant percussion; decreased breath sounds; auscultated wheeze etc

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What is the name for the abnormal enlargement of the R sid of the heart which may occur in resp conditions including COPD?

Cor pulmonlae

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What is polycythaemia - a complication which can occur in COPD?

An abnormally increased concentration of Hb.

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Defects in what gene normally causes polycythaemia (not necessarily in COPD)?

Usually caused by a fault in JAK2 gene which causes the bone marrow to produce too many RBCs.

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Patients with severe chronic bronchitis / COPD become insensitive to CO2 levels. What do they rely on to stimulate breathing?

They rely on their hypoxic drive (i.e. when O2 levels fall)

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These patients who rely on hypoxic drive are known as 'blue bloaters'. Are these 'blue bloaters' breathless? What other features might they have?

Blue bloaters = cyanosed and oedema (suggests cor pulmonale) - they aren't particularly breathless

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What is cor pulmonale ?

abnormal enlargement of the right side of the heart as a result of disease of the lungs or the pulmonary blood vessels.

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Would these blue bloaters show a type 1 or type 2 resp failure? What does this mean for adminstering O2?

ABG = Resp type 2 (PaO2 = low CO2 = high) - should be careful administering O2 because they are responding to hypoxic drive. If you oxygenate too high they may lose sensitivity to this. 88-92% sats aim

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'Pink puffers' - these remain sensitive to ___ levels and therefore may have a low ___ and near normal __

'Pink puffers' - these remain sensitive to CO2 levels and therefore may have low CO2 and near normal O2

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What signs and symptoms would these patients be showing?

Pink puffers - not cyanosed, working hard to keep their CO2 down so tachpnoea and tachycardia. May be using accessory muscles to increase ventilation success. More of an emphysema process than bronchitis.

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What type of resp failure could these 'pink puffers' develop if things worsen?

Type 1 - low O2 and normal/low CO2

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Name 3 investigations everyone with suspected COPD should have?

Spirometery (after bronchodilation treatment!) to confirm diagnosis & stage. CXR (to rule out other pathology). FBC

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Why must you do the spirometry after bronchodilation treatment?

If there is improvement then it may be asthma rather than COPD.

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Name 1 thing you would be checking for on the FBC in someone with suspected COPD

Polycythaemia & anaemia

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Name the % FEV1 for Stage 1 (mild) to Stage 4 (severe) COPD

Stage 1 (mild) = 80%+ FEV1. Stage 2 = 50-79% FEV1. Stage 3 = 30-49% FEV1. Stage 4 (severe) = <30% FEV1.

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What is bronchiectasis?

Chronic inflammation of the bronchi & bronchioles which causes dilatation of the airways which leads to chronic infection and inflammation.

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With repeated exacerbations of bronchiectasis what might occur in the walls of these bronchioles?

Fibrosis (scarring) which can lead to resp failure

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Where in the lung are the affected bronchi normally?

Bronchiectasis usually occurs in the base of the lung

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Intermittent haemoptysis may be the only symptom of bronchiectasis which presents. What is haemoptysis and why might it occur?

Haemoptysis is coughing up blood (from a source below the glottis). It occurs because granulation tissue formed in bronchiectasis might bleed.

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What is granulation tissue?

Granulation tissue is new connective tissue and microscopic blood vessels that form on the surfaces of a wound during the healing process

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What other symptoms may occur in bronchiectasis?

Persistent cough; copious purulent sputum; halitosis (bad breath)

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What signs may occur in bronchiectasis? (particularly during lung auscultation)

Clubbing, coarse wheeze on expiration, inspiratory crepitations

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What is the most common cause of bronchiectasis? Name 3 or 4 causes.

Mostly 'idiopathic'. Can be caused by anything which interferes with bronchioles / anything which causes multiple infections, TB, measles, pneumonia, pertussis. CF, foreign body, aspergillosis, immune deficiency.

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Connective tissue disorders often lead to bronchiectasis. What % of patients with RA (rheumatoid arthritis) develop bronchiectasis?

1/3 (33%)

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What would you look for on a CXR to indicate bronchiectasis?

Shadowing (cystic shadowing) which suggests dilated bronchioles

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What is signet ring sign which may be seen on CT for bronchiectasis?

The signet ring sign is seen in bronchiectasis when the dilated bronchus and accompanying pulmonary artery branch are seen in cross-section. The bronchus and artery should be the same size, whereas in bronchiectasis, the bronchus is markedly dilated

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What would you find when testing someone with bronchiectasis with spirometry?

Would be an obstructive spirometry (should always assess for reversibility - i.e. in asthma)

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Asthma, COPD & Bronchiectasis

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