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72 Cards in this Set
- Front
- Back
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Describe the pulmonary component of COPD
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Airflow limitation that is not fully reversible
Usually progressive Abnormal inflammatory response in the lung to noxious particles (s.a. cigarette smoke) |
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Define chronic bronchitis
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Productive cough most days for at least 3 months in at least 2 consecutive years.
Initiating factor = long standing inhaled irritant |
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T/F: respiratory function can be normal for many years in patients with chronic bronchitis
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True
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What is the role of infection in chronic bronchitis?
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Not the initiating factor.
Probably significant in maintain disease and causing acute exacerbations |
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Outline major pathological changes in chronic bronchitis
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Goblet cell (bronchi and bronchioles)
->hyperplasia ->hypertrophy ->hypersecretion of mucous Basement membrane thickened Reid index > 0.4 |
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What is the Reid index?
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Compares thickness of mucous gland layer with thickness of bronchial wall from basement membrane -> inner perichondrium in cartilage
i.e. indicates disease severity and duration |
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Outline major pathological changes in small airways disease (ie. bronchiolitis)
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Inflammation in bronchioles
Airway fibrosis Hypersecretion Goblet cell metaplasia Mucous plugging (lumen occlusion) Smooth m. hypertrophy Narrow airways Unstable small airways Destruction alveolar walls |
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Can you detect small airways disease with spirometry? Why?
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No.
no significant functional change until the disease is severe– this is because the small airways have such a large volume and thus have very low resistance – contribute minimally to overall total resistance |
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What are some tests for small airways disease?
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Not used often:
Frequency dependence of dynamic compliance Single breath nitrogen test Air/helium flow volume curve |
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Define emphysema
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Abnormal permanent enlargement of airspaces (not alveoli) DISTAL to terminal bronchiole (i.e. in the respiratory zone) with destruction of their walls and without obvious fibrosis
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Describe major pathological changes in emphysema
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Protease:antiprotease imbalance
->ROS inactivate alpha-1 anti-trypsin (which is an ANTI PROTEASE) ->decreased action allows neutrophil elastase and other proteases (such as macrophage elastase and MMPs) to destroy lung tissue Also get inflammatory pathology of small airways disease (i.e. OBSTRUCTION) Loss of elastic recoil Loss of radial traction |
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T/F: Alpha-1 anti-trypsin is an anti-protease that inhibits macrophages and neutrophils from producing elastase
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FALSE!
Alpha-1 anti-trypsin is an anti-protease that inhibits neutrophils from producing elastase -> macrophages are not inhibited |
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In COPD, there is a protease:anti-protease imbalance. How do we get the neutrophils and macrophages into the lung to release their proteases and cause this damage?
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Alveolar macrophages (always present in the lungs at low concentrations) are activated by contents of the smoke
They produce cytokines which, among other things, will recruit neutrophils and other inflammatory cells to the area The neutrophils are also attracted by nicotine which is a direct chemoattractant for neutros Both macrophages and neutros will release their proteases, damaging the alveolar septum (less area for gas exchange) |
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What contributes to the loss of elastic recoil in COPD?
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1.Destruction of elastic tissue
2. ↑ alveolar size -> ↓ surface tension -> ↓ forces inward ->↓ elastic recoil |
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T/F: a smaller space has a larger surface tension.
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TRUE
(so in COPD – big alveolar spaces = less surface tension pulling the lung inwards) |
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What are the two major causes of dynamic airway collapse?
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1. pure emphysema
2. airway obstruction |
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Describe dynamic airways collapse in emphysema.
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EPP = equal pressure point, the point at which airway pressure (pushing out) equals pleural pressure (pushing in).
Airway pressure declines gradually until 0 at the mouth. EPP normally occurs at cartilagenous airways (preventing collapse). But in emphysema, you have lower initial pressure within the alveoli (less surface tension/elastic recoil), and also forced expiration (increasing pleural pressure) Net result = the EPP is moved away from the mouth, and dynamic airway collapse occurs downstream from EPP (which is at NON CARTILAGENOUS AIRWAY) NB- also get small airway collapse because they are not being held open by elastic tissue of lung |
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Describe dynamic airways collapse in airway obstruction.
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Normal driving pressure out of the alveoli (i.e. no loss of elastic recoil). Rather, have narrowed airways (incr. resistance).
This means that the airway pressure drops more rapidly on the way to the mouth, so that EPP is now before the cartilagenous airways begin -->dynamic airway collapse |
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What would happen to the following in airway obstruction?
RV FRV TLC FEV1 FVC FEV1:FVC |
RV - INCR!!
FRV - INCR TLC - INCR FEV1 - DECR!!!! FVC - DECR FEV1:FVC - DECR |
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What happens to respiratory mm. at high lung volumes?
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They are INEFFICIENT.
During hyperinflation -->inspiratory mm. are over-shortened -->expiratory mm. are over-stretched |
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T/F: When prescribing bronchodilators in COPD, the "volume effect" is more important than the airways effect
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TRUE .
symptom relief |
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What index is used to predict mortality/morbidity in COPD?
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"BODE index"
B= BODY MASS INDEX O= AIRWAYS OBSTRUCTION (FEV1) D=DYSPNOEA E=EXERCISE CAPACITY (6 min walk test) |
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Why do you use CO when testing diffusion capacity? [DLCO]
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Because it readily crosses the membrane. The limiting factor = surface area
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Why do you get a decreased TLCO/DLCO in emphysema?
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Because you have decreased the surface area for the CO to diffuse across
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What are two methods used to measure lung volume?
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1. Gas dilution method
2. Plethysomographically [prefer this] |
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What happens to respiratory capacity in emphysema?
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DECREASES.
IC = TLC - FRC The smaller the IC, the more severe the emphysema |
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COPD: What is the only reliable and consistently present finding on physical examination ?
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slowing of forced expiration
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What are the symptoms of COPD?
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breathlessness / dyspnoea (SOB) on exertion
chronic cough +/- sputum production wheeze ankle oedema orthopnoea weight loss, anorexia |
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T/F: Tidal volume can be increased by bigger breath in as well as a bigger breath out
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TRUE!
-> can recruit expiratory mm. to drop end-expiratory lung volume |
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What are some breathing changes in response to exercise?
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More outward recoil of ribcage to help inspiration
Keeps lungs at most efficient part of PV curve When tidal volume approaches ~75% TLC, lung compliance drops (stiffer), so then breathing rate increases Breathing route changes from nasal to oro-nasal Tongue and nose muscles activate to open up upper airway Lower airway diameter increases by sympathetic tone + and parasympathetic tone |
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Is peripheral muscle oxygen utilisation trainable?
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YES
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What are some limits to exercise in COPD?
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Lungs take longer to empty - so slow that they aren't fully empty by the time you take your next breath in.
Increasing ventilation (ie. exercise) leads to dynamic hyperinflation -->cannot take bigger breath in (close to TLC) -->cannot take bigger breath out (flow limitation) -->inspiratory mm. need to work harder to overcome elastic recoil forces before respiration even begins -->inspiratory mm. have reduced length-tension relationship (they are shorter so have less capacity) -->inspiratory mm. are using up more energy (i.e. O2) for the same/less result -->Exercise capacity in COPD also restricted by peripheral muscle weakness/wasting due to inactivity and cardiovascular de-conditioning ==>COPD patients try to increase ventilation by increasing breathing rate (more dynamic hyperinflation!!) |
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What happens to mm. in COPD?
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LOW GRADE CHRONIC INFLAMMATION:
--> altered regulation protein metabolism --> muscle atropy --> cachexia Reduction in strength and endurance [less type I, more type II] Reduced capillaries Reduced muscle glycogen ALSO HAVE: Decr anabolic hormones Malnutrition Myopathy Deconditioning |
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What hormonal insufficiencies are seen in COPD?
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Low testosterone
Low IGF-1 (mediates anabolic effects of growth hormone on muscle) |
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What are the 5 "limiting factors" in COPD ?
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Lung mechanics (flow limitation, hyperinflation)
Skeletal muscle dysfunction Cardiac disease Hypoxia Anxiety |
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T/F: Short-term changes in FEV1 to bronchodilators GOOD predictor of subsequent benefits with treatment
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FALSE!!!
Short-term changes in FEV1 to bronchodilators POOR predictor of subsequent benefits with treatment |
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What does giving bronchodilators do in COPD?
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Don't get much change in FEV1.
BUT get 25% change in: RV FRC [Functional Residual Capacity] Tidal vol |
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What are the effects of endurance training on skeletal mm. in normal indivs?
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Hypertrophy of Type I fibres and increase in size and number of mitochondria
Type IIb transform to IIa changes in mitochondrial enzymes (increased oxidative enzymes) Higher myoglobin levels and proliferation of muscle capillaries |
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What are the effects of endurance training on the heart in normal indivs?
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increase in cardiac chamber size and wall thickness
increase in end-diastolic volume (increased plasma volume) and increase in SV decreased body fat and increased lean body mass |
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T/F: Can patients with COPD exercise at an intensity to achieve a training effect?
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YES
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What are some options for exercise training in COPD?
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Small muscle groups at a time - less ventilatory demand
Interval training (high intensity for brief periods) Weekly increments (use Borg 4-6 for training) |
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How do exercise programs/rehab reduce SOB?
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Decreased ventilatory requirements for same Work and VO2
Decreased sensation of SOB at same expiratory vol. [?Less hyperinflation (change in breathing pattern), ?"Desensitisation”] improved resp muscle function? |
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In hypoxic patients, what can help increase exercise tolerance?
How? [Is it effective in non-hypoxic pts as well?] |
Supplemental oxygen.
Largely mediated by reduction in DYNAMIC HYPERINFLATION -->Reduced hypoxic stimulation of carotid bodies -->Incr. arterial oxygen content to go to mm. -->Same exercise at overall lower ventilation levels [yes] |
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What does Heliox do for SOB in COPD??
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80% helium, 20% oxygen
1/3 density of air so it decreased turbulent flow --> increases maximal flow rates Less hyperinflation |
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How can you judge that an association is causal?
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Compliance with the criteria is a ‘judgement call’
1. Exposure precedes outcome 2. Association unlikely to be due to chance 3. Association unlikely to be due to bias 4. Association unlikely to be due to confounding Non-absolute criteria: - The association is strong - There is a dose-response relationship - The association is consistent - The association is reversible - The association is coherent with other epidemiological data - The association is biologically plausible |
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When looking at evidence for tobacco as a cause of disease, how does "exposure precede outcome"?
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- Cigarette smoking is generally taken up in teenage and early adult life
o Lung cancer is rare under 40 years of age and peaks in frequency late in life - British doctors’ study |
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When looking at evidence for tobacco as a cause of disease, what coherence with descriptive data is there?
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Smoking in men began to rise around the turn of the century
-->lung cancer mortality began to rise in the 1940s Women started smoking much later than men -->lung cancer mortality rise began correspondingly later Smoking in women continued to increase as smoking fell in men -->lung cancer falling in men, still rising in women Reasonably good geographical correlation between smoking and lung cancer mortality |
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What is attributable risk?
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- The % of the incidence of a disease in exposed people that is due to the exposure
- The % of the incidence of a disease in exposed people that would be eliminated if exposure to the risk factor were eliminated |
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Why do people over 65 have less 'relative risk' of dying from lung cancer
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Because if they've made it that far, they have lower risk (may be less 'susceptible' to the disease)
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How did invention of the safety match and flue curing affect smoking rates?
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INCREASED
-->safety match made cigarettes more accessible -->flue curing made cigarettes milder, so people inhaled them deeper |
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What was the British Doctors' Cohort Study
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40 year follow up – ½ continuing smokers had died of tobacco-caused disease
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Around when was a decline in smoking rates first seen?
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1960s - after US General Surgeon's report, media campaigns, news
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What public indoor places within Australia are exempt from the 'no smoking' rule?
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Casino high-roller rooms are exempt in NSW, QLD, Victoria, WA
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What is a "hardcore smoker"
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o First cigarette within 30 min of waking
o Smoking lots/day o Smoke every day |
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What is meant by "smoking price elasticity"?
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For every increase in price, consumption decreases by 0.4
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T/F:Anti smoking advertising and increase in price has had a larger impact on smoking prevalence in the last 12 years in Australia than nicotine replacement therapy (NRT) advertising and sales, esp. in low and middle income groups
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TRUE
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T/F: All smokers have respiratory bronchiolitis
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TRUE!!!
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What contributes to getting COPD?
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"GET" COPD
i.e. genetics, environment, tobacco! |
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Males or females are more likely to get COPD with same amount of smoking?
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females
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What percentage of smokers develop COPD?
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15-20%
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What is the "community smoking cycle"
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Smoking is rare
Smoking is introduced as a practice of the elite - associated with high social status Smoking spreads through the rest of the community including the poor The better educated realise the health harms and reduce their smoking rates Smoking and its health harms persist in the poorer and disadvantaged |
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What are the predictors of higher smoking intensity?
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Indigenous status
Lower SES Divorce or separation Incarceration Not in employment or studying No post-school qualification English spoken at home |
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What is the only 'population' of people that exceeds Indigenous smoking rates?
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The prison population - 79% smoke
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How do rates of smoking in Indigenous people compare with non-Indigenous
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more than DOUBLE non-Indig.
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What substances affect the brain reward pathway (i.e. dopaminergic)
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Cocaine – inhibits reuptake
Opiates – enhanced neurotransmission Amphetamines – increase release & reduce reuptake Endocannabinoids – increase neuronal firing rate |
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Which has a longer occupacy time: smoke-related nicotine or ACh
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Nicotine occupies nAChR for longer.
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What benefits are seen with smoking cessation and when?
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HOURS
Improved exercise capacity - DAYS Reduced household tobacco expenditure WEEKS Safer surgery with fewer wound infections Pregnancy outcomes and healthier babies Improved control of asthma MONTHS Reduced rate of heart attacks/coronary syndrome Reduced risk of stroke Improvement in circulation to legs Less damage to lung function YEARS Reduced rates of lung cancer |
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T/F: Quit attempts are more successful in those not planning to quit
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TRUE
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What are the symptoms of nicotine toxicity?
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Nausea
Sweatiness HT |
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What is Bupropion???
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Inhibitor of neuronal reuptake of noradrenaline and dopamine
Limits nicotine CRAVING only. |
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What good would a partial agonist be in trying to quit smoking?
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Presence of smoking – reduces effect of smoking
Absence of smoking – reduces effect of withdrawal |
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What is Varenicline??
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Partial agonist at the specific nicotinic Ach receptor
Limits reward in the presence of nicotine Limits craving in the absence of nicotine Quit rate is superior to bupropion Small ‘real-life’ studies show results near those of NRT |
