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82 Cards in this Set
- Front
- Back
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Why was their an increase in lung cancers after 1935?
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People took up the habit in WWI, and this was a time lag in the lung cancer after the uptake of smoking.
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What is the smoking prevalence in Australia?
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~15%
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What sex has a higher association with smoking?
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Men
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What are the 10 steps
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Safety match and flue curing (gets into lungs better)
Hand rolling - machine = greater numbers, lesser price |
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Where does Nicotine bind to exert its effect?
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Cholinergic recepts in the autonomic ganglia(, adrenal medulla and the NMJ, as well as cholinergic receptors through the brain
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How much of an inhaled dose of nicotine reaches the systemic circulation?
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10%
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t/f... nicotine is well absorbed from the respiratory tract
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true
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t/f... nicotine in its natural form is well absorbed from the stomach
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false, nicotine is a strong base not absorbed easily from the buccal mucosa, unless formulated in chewing gum in an unionised form
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How long after smoking does it take to reach half the peak plasma concentrations?
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10 minutes after smoking, as the peak is reached during smoking due to rapid absorption.
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What is the major site for nicotine metabolism?
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Liver
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What is nicotine metabolised into?
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continine
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What can detection of continine levels in the blood tell you?
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It is a measurable chemical marker of active or passive cigarette smoking as it has a prolonged half life after being formed from nicotine in the liver.
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t/f... nicotine is not detectable in breast milk
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false
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What CNS changes does nicotine induce?
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sense of alertness and appearance of arousal on an EEG, termors and convulsions, respiration stimulation by medulla effect
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How does nicotine stimulate respiration?
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Acts on the CNS at the medulla to centrally control RR, as well as activating peripheral chemo-receptors in the carotid body and aortic arch
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t/f... large doses of nicotine cause a rebound blockade of impulse transmission
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true. Large initial doses will cause initial stimulation followed by blockade of impulse transmission
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How does nicotine effect the NMJ?
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Causes discharge of Renshaw cells in the spinal cord which inhibit motor neurones, possibly leading to a relaxation of skeletal muscle.
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How does nicotine effect your CVS?
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Increase in HR and BP due to SNS and adrenal medulla/catecholamine stimulation, but this will not usually occur in doses associated with smoking. It also stimulates peripheral chemo-receptors in carotid bodies causing a reflex vasoconstriction and tachycardia. Increases FFF in plasma.
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t/f...SNS and adrenal medulla stimulation from smoking cause an increase in HR and BP
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false.
while nicotine does cause this effect, smoking does not produce high enough nicotine concentrations generally to induce this effect through this mechanism. Reflex increase in HR and vasoconstriction in smoking is caused by nicotine action at the carotid bodies. |
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What effects does nicotine have on the GIT?
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Activates PNS to increase tone and motor activity of the bowel.
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What are the symptoms of acute tobacco toxicity?
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nausea, salivation, abdominal pain, vomiting, diarrhoea, disturbed vision, mental confusion, weakness
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What are the names of 2 non-nicotine therapies used in smoking cessation programs?
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bupropion (SRI), varenicline (champax, AchR partial agonist), clonad....,
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What is said to be the 'litmus test' to the effectiveness of a platform of tobacco control policy?
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The response of the tobacco industry. Ineffective policies are often publicly support, while effective policies are vigorously opposed.
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What is the difference in risk of dying between a smoker who quits before age 50 and one who does not?
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Half the risk of dying.
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How long does it take for the risk of dying from a heart attack to decrease by 50%? and back to ~ never-smoker rates?
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1 year, 5-10 years
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Briefly, what are the CVS benefits of smoking cessation?
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decreases the risk of fatal and non-fatal MI, stroke, thrombosis, reduces endothelial dysfunction but does not reverse atherosclerosis, improves exerces tolerance in those with arterial disease
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How much does the lung cancer risk decline after 10 years of smoking cessation?
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30-50%
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How long does it take after smoking cessation to reach a never-smoker risk of lung cancer?
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over 15 years
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What is the reduction in risk of oral, pharyngeal, laryngeal and oesophageal cancer over 5 years of smoking cessation?
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50%
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t/f... there is a risk reduction with smoking cessation for cancers of the bladder, pancreas and cervix
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true, but it is a slower risk reduction than with such cancers as oral, laryngeal etc
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What are the respiratory benefits of quitting smoking?
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Rapid improvement in pre-existing cough, wheezing and sputum production, 5% lung functional improvement within a few months, better mortality rates with chronic pulmonary diseases
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What % of chronic smoker progress to COPD?
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15%
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What are the main pathological features of COPD?
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Increased smooth muscle in airways, increased neutrophils, airway inflammation, destruction of lung tissue, hypertrophy of goblet cells
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What are the physiological disturbances seen in COPD?
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reduced FEV/VC (<70%, or <80% predicted?), hyperinflation, increased total lung volume and RV, cough, exertional dyspnoea, sputum production
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What is the most important intervention in SOPD?
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smoking cessation, the earier the better the prognosis
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What are the typical symptoms and signs of a COPD exacerbation?
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increased cough, sputum and dyspnoea, often brought about after an RTI.
CRP/Inflammation markers may be elevated |
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How do we treat COPD and what are the effects?
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Assist in cessation of smoking, long term bronchodilators and corticosteroids to reduce exacerbations and improve exercise tolerance,pulmonary rehabilitation, O2 may be given if hypoxic in an acute attack.
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What changes are seen in lower limb exercise training component of pulmonary rehabilitation?
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Increased: concentration of oxidative enzymes, capillary density, skeletal muscle myoglobin, number and density of mitochondria = better oxygen extraction in the muscle = lower lactate = reudced ventilation = reduced dyspnoea
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What is the definition for Chronic Bronchitis?
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Productive cough for 3 months in 2 consecutive years. Thickening of mucosa and hypertrophy of mucous gland and goblet cells.
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Describe small airways disease in COPD?
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respiratory bronchiolitis, lots of inflammatory cells, narrowed lumen, can have a lot before lung function/flow/resistance is affected.
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What is Emphysema?
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permanent enlargement of airspaces distal to terminal bronchioles with destruction of their wall without obvious fibrosis. This decreases available surface area for diffusion, as well as blood vessels for gas exchange. Increased Compliance/loss of elastic recoil as lung becomes floppy due to loss of surface tension in larger spaces. Pathologically, can be very big, more severe in initially the upper parts of lobes because blood flow/circulation of alpha antitrypsin is higher in base. also more surface tension on apices - damaged more easily
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t/f... as you age you get bigger alveoli
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true, this results to a decrease in elastic recoil and an increase in compliance, to a lesser extent to in emphysema
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What causes the early closure of airways in emphysema?
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lesser surface tension = lesser alveolar pressure = reduced flow to mouth = less time till alveolar pressure=pleural pressure, the point at which the airway closes. Therefore, the airway closes more distally/closer to alveoli
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What causes the early closure of airways in obstruction?
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elastic recoil normal, normal driving pressure/flow but narrowed airway, resistance is up, frictional loss is greater, therefore closure occurs sooner/more distally
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Go;d standard for pulmonary characteristics of airway obstruction?
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FEV down down
FVC down FEV1/FVC down (<70%, depends on age though) FEV1 <80% predicted |
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What is the definition of bronchodilator reversibility in pulmonary tests?
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FEV >12% of pre-bronchodilator results
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What FEV1 do people get symptomatic disability from COPD?
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70% decline from a 25 yo FEV1/ 30% of functionality
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What is the problem in FVC in people with COPD?
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Takes so long to get all of air out due to airway closure that they need to breath again before it is reached.
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What is BODE>
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Prognosis in COPD:
BMI (higher better) Obstructin of airflow (FEV1 higher better) Dyspnoea (less better) Exercise capacity (more better) |
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What happens to lung volumes in COPD?
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Hyperinflation, can't get all of air out
RV = UP UP UP FRC = UP UP TLC = UP |
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What does the flow loop look like in COPD and what does it mean?
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Scalloped expiratory phase, There is not a difference/ability to increase from the tidal/normal breathing and maximal breathing, as they lie on the same curve. In order to continue tidal breathing, the patient increases the lung volume that they breath from - lot more pressure to try to breath against this higher lung volume, takes up more energy = dyspnoea, exercise limitation
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What is DLCO and TLCO?
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Diffusing capacity/transfer factor - describes the rate of transfer of a gas between the alveoli and the blood. The area in emp
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What is required to allow exercise without breathlessness? (7 things, simple)
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Air must go in and out
Blood must go round an round Need blood and air to mix O2 to muscle muscle to be effective loads not excessive response to exercise appropriate |
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t/f... you increases respiratory rate as soon as you exercise
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False, volumes of breath increases first, but rate doesn't increase until you reach close to the max of your compacity
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What is different in an COPD patient exercising breathing?
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Can't increase volume as normal people do, so must increase rate of breathing = use more muscle/energy = dyspnoea
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Where does the equal pressure point occur in a healthy person expiring?
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Larger airways, such as the trachea, which have cartilage and so don't collapse
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Why is the end-expiratory lung volume above FRC in COPD patients?
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It takes them so long to breath out the air in the lungs, due to the obstruction, that they need to take their next breath before all the air is out. This means that they still have air in their lungs at the beginiing of the new breath, and have a more positive pressure in their lungs that they need to inspire against, which means more effort.
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Describe dynamic hyperinflation in COPD?
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As COPD patients require more oxygen in exercise etc, they are unable to increase their expiratory lung volume, so must increase their respiratory rate. This leads to even less time to empty lungs, which leads to more air being trapped behind, and the patient breathing at higher and higher end-expiratory lung volumes. these means they are breathing at sub-optimal parts of the PV curve, and have increased their work of breathing, making their muscles use up more of the oxygen they are trying to get.
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t/f... the lung is stiffer at higher lung volumes
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true
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What do stroids do to muscles?
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promote atrophy
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What leads to malnutrition in COPD?
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breathlessness (can't eat as can't breath), inflammatory processes causing cacexia?
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When is hypoxia an important determinant of ventilation?
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<60mmHg, CO2 is the driving force above this
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How do we treat COPD?
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Increase quality of life with B agonists and anti muscarinic receptor, conditioning/exercising/pulmonary rehabilitation (working on muscle not lung function, and increases mood)
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t/f... someone with severely limiting COPD will feel improvements to breather greater than someone with mild COPD when given a bronchodilator
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true - if severel COPD, bronchodilator will allow their inspiratory capacity to increse/shift so that their tidal breathing can move down to a lower volume, where as in mild COPD as their tidal breathing is not already on the maximum curve, they would only notice the benefit if they were exercising
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When do you give Oxygen to a COPD patient?
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at end of disease at home, for mortality benefit in hypoxic patients (live 1-2 years later), not for SOB.
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t/f... only heavy chronic smokers have respiratory bronchiolitis
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false, all smokers have it
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What is a risk for early onset emphysema?
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A1 anti-trypsin homozygotes
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t/f... COPD survival is similar to breast cancer at 5 years?
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true
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What is anhedonia? How is it linked to smoking?
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the inability to experience pleasure in life. Smoking causes depression/depression causes smoking
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What happens when you give smokers lesser nicotine/tar cigarettes?
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smokers take bigger puffs/deeper breaths, and go to the end of the cigarette more so than otherwise to get the same amount of nicotine in the system.
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How does brain reward work in smoking?
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nicotine binds to AchR (longer than Ach), causes a release of dopamine to cause stimulation of brain reward system. Lack of stimulation causes withdrawal.
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Why was ammonia added to cigarettes?
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Brought the pH up to a more alkaline level so that it would be more easily absorbed by the respiratory tract, leading to a bigger 'hit' and more addiction.
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What is the next cigarette smoking instance driven by in the smoker?
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fear of withdrawal rather than the pleasure.
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t/f... halving the no. of cigarettes harms the harm
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false, usually harm is only reduced by 15% as peole compensate by breathing deeper etc.
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What is the most effective cessation strategy in the community?
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Brief advice to quit by doctors etc, people won't dislike you, they know you're a professional.
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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 chances of becoming a non-smoker using NRT?
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double chance of being non-smoker in 12 months using nicotine replacement therapy
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What is a confounding factor (use smoking and pancreatic cancer assoication as an example)?
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the association found is due to a correlation between smoking and some other hazard that is a true cause of cancer of the pancreas (e.g. smoking and pancreatic cancer could be confounded by alcohol consumption)
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How do you judge something as being causative for an outcome?
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exposure precedes outcome
unlikely to be due to chance unlikely to be due to bias (design/conduct) unlikely to be due to confounders (dose response, very strong association) -with a high conifdence |
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Which sex has a higher propensity for lung cancer when exposed to cigarette smoke?
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women, though men have a higher overall incidence due to higher smoking numbers
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What is atrributable risk?
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what % incidenceof a disease is caused by the factor in those who are exposed to the risk factor
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what is population attributable risk?
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% incidence of a disease in the general population that is due to the exposure to the factor.
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