37. Obstructive and Restrictive Lung Disease Flashcards Preview

Year 1 - Term 2: Carriage of Oxygen > 37. Obstructive and Restrictive Lung Disease > Flashcards

Flashcards in 37. Obstructive and Restrictive Lung Disease Deck (18):
1

What is vital capacity measured by, and what is it a combination of?

What is it a key measurement for the diagnosis of?

 

 

Spirometer, tidal volume + inspiratory reserve + expiratory reserve

Respiratory distress. Need to compare with averages for a person's weight and height.

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2

What is peak flow the most useful measurement for?

What are forced expiratory volumes measured with?

Obstructive disease. Most useful as serial measurements each morning/night to monitor treatment effectiveness. Doesn't fluctuate in healthy person. With inhaler use, it normalises = obstructive disease diagnosis.

Vitalograph. 

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3

How do forced expiratory volumes help distinguish between obstructive and restrictive disease?

Why is the key weakness in obstructive disease during respiration?

What are the interpretations of the FEV1/FVC values?

FEV1 and FVC measured. Obstructive: FEV1 reduced due to narrowed airways but FVC normal so FEV1/FVC reducedRestrictive: FEVand FVC reduced so FEV1/FVC not decreased.

Becuase it's normally passive, so more sensitive to changes in airway diameter. Can always suck harder on diaphragm to maintain normal inspiratory time.

 

Normal: > = 70% of predicted

Mild obstruction: 61-69%

Moderate obstruction: 45-60%

Severe obstruction: <45% 

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4

How does smoking affect the lungs and FEV1?

What are the 2 main obstructive disorders?

 

Damages elasticity of lungs, gradually reduces FEV1 and creates progessive obstructive disease.

Asthma and COPD

5

What is asthma characterised by?

Describe the initial response to an antigen in asthma.

Reversible airway obstruction, smaller airways, AHR (airway hyperresponsiveness), atopy (heightened immune response - genetic). Main Features: bronchoconstriction, mucus secretion, airway inflammation 

Priming response: inhaled antigen e.g. pollen protein binds to receptor on B lymphocyte resident in bronchial submucosa -> signals to helper T cell -> releases cytokines enabling B lymphocyte to mature to plasma cell and release IgE Abs to initial antigen -> IgE Abs attach to mast cells in bronchial submucosa.

 

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6

Describe the second respose to an inhaled antigen in asthma. 

What is the response to repeated exposure to the antigen?

Asthma acute response: Next time allergen inhaled -> antigens bind to IgE on mast cells -> degranulate and release inflammatory mediators e.g. histamine -> acts on local H1 receptor ->  inflammatory response: broncoconstriction, mucus secretion, vasodilation, oedema.

Asthma chronic response: eosinophils migrate to inflamed tissue (chemotaxis) -> activated by mast cell and T helper cell's cytokines. They release enzymes and ROS that damage epithelial cells and produce hypersecretion of mucus. Damage stimulates afferent nerves which activate parasympathetic efferent nerves which increases mucus secretion and bronchoconstriction. (Eosinophils = assocaited with disease severity,, chornic asthmatic has high levels in submucosa).

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7

Why does a chronic asthmatic have to cough often, and is the cough productive?

List some signs and symptoms of asthma.

Chronic asthmatic: mucus hypersecretion and reduced ability to transport mucus due to damaged epithelium (replaced with pseudosquamous epithelium that has no cillia). Coughs often to clear it but not productive b/c mucus mainly swallowed.

Signs: wheezing, herpexpansion of thorax, increased nasal secretions, atopic dermatitis, eczema. 

Symptoms: troublesome cough, awakened by it, cough after activty, colds lasting >10 days, relief when medication used.

8

What are the long-term control medications to treat asthma?

What are the quick-relief medications to treat asthma?

What are spacers and nebulizers?

Taken daily longterm to reduce inflammation, bronchoconstriction, and improve lung function: inhaled corticosteroids, long-acting beta2 agonists, leukotriene modifiers (reduce activity of mast cells and eosiniophils). Main thng = prevent airway remodelling by eosinophils.

Short acting beta2 agonists - normally via nebulizer.

Spacer: can improve penetration of inhaled drug into lungs - produce cloud -> breathe in. Used with inhaler. Nebulizer: produces inhaled mist of medication.

9

What is COPD?

List some signs and symptoms.

Mix of chronic bronchitis (chronic productive cough (NB: asthma not) with no discernable cause for more than half the time >2 years) and emphysema (enlargement of airspaces distal to terminal bronchioles).

Easily fatigued (not enought O2), freq respiratory infections (mucus not moved b/c cillia damaged), use of accessory muscles to breathe (lift ribs), orthopneic, cor pulmonae (R HEART FAILURE DUE TO LUNG DISEASE), thin, wheezing, pursed-lip breathing, barrel chest, chronic cough, dyspnea, prolonged expiratory time, digital clubbing

10

What are the features of chronic bronchitis, and the main cause?

What are the features of emphysema, and the main cause?

Hypertrophy of bronchial glands, hypersecretion, mucus plugs and infection/inflammation. Main cause = exposure to airbourne irritants.

Destruction of lung stroma - bullae, floppy airways cause obstruction. Main cause = cigarette smoking.

11

What is the pathophysiology of bronchitis?

What is broncholitis?

What is the pathophysiology of emphysema?

Irritants damage epithelium and cause proliferation of squmous cells that don't have cillia. Also stimulate massive mucus gland enlargement. 

Selective inflammation of bronchioles.

Cigarette smoke stimulates polymorphonuclear leucocoytes (PMN) to release serine elastase. Smoke also inactivates the elastase inhibitor alpha1-antitrypsin, letting serine elastase destroy elastic tissues of alveoli walls -> emphysema. NB normally serine elastase activated when want to destroy lung CT to let WBC to site of bad infection.

12

What has happened to these alveoli? (Normal on L)

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Emphysema on R - grossly enlarged alveoli (bullae).

Lung volume isn't decreased so not a restrictive disease, but compromised O2 transpot in b/c has longer distance to diffuse -> can suffer chronic hypoxemia and hypercapnia.

13

What are the 3 things that differenetiate COPD from asthma?

Thus are COPD and asthma 2 seperate conditions?

Asthmatics: atopic and have increased airway hyperresponsiveness, eosinophills seen, steroid response 

No - there is overlap "wheezy bronchitis".

14

What are the three different categories of restrictive lung disorders? Give examples.

1) Loss of volume and increase recoil e.g. pneumonia (fluid in alveoli), pneumothorax (lung punctured and collapses), pulmonary fibrosis (elasticity loss)

2) Difficulty in production of chest movements e.g. neuromuscular weakness (diaphragm can't pull down)

3) External mechanical, limitation of lung volume e.g. kyphoscoliosis (compress lungs), ankylosing spondylitis

ALL RESTRICT GE

15

What has happened here (L = normal lung histology)? Collagen stained blue.

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R = pulmonary fibrosis. Restrictive respiratory disease.

16

What is a flow-volume loop?

Obtained from spirometer, show flow and volume during forced inspiration and expiration. Time runs around loop clockwise from downwards inspiration. Expiration always upwards. Forced expiration most useful part.

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17

What does the flow volume loop look like in:

a) obstructive disease?

b) restrictive disease?

a) Flow rate low in relation to lung volume, expiration ends prematurely b/c of early airway closure = flow collapse. Scooped out appearance after point of maximum flow. Inspiration doesn't change b/c it's active. 

b) Flow rate in inspiration and expiration normal, flow-volume loops are narrow b/c lung volume smaller so horizontal axis shrinks. 

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18

How may residual volume differ in obstructive and restrictive respiratory disease on a flow-volume loop?

Obstructive: RV may be larger than normal due to emphysema and increased functional dead space. Restrictive: flow normal but overall lung volume decreased, so RV mat be a bit smaller.

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