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74 Cards in this Set
- Front
- Back
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What is a typical pressure in a venule?
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12-18mmHg
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How much blood is held in the venous system?
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60%, hence term 'capacitance vessels'
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What is the counter effect of raised venous pressure on the vasculature, and how does this affect capacity?
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Stress induced relaxation, capacity increases
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What is the thoracic pump?
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Lower thoracic pressure induced by movement of respiratory muscles induces air into the lungs, but it also lowers pressure in the atria of the heart, allowing more blood to be drawn in when breathing in.
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Which three mechanisms aid venous return other than simple heart pumping?
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Skeletal muscle pump, thoracic pump and the drop in atrial pressure during systole.
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What is the effect of standing up on blood pressure in the head and feet?
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Head drops around 40mmHg, feet goes up around 90mmHg
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What would be the uncompensated effect of standing on the feet?
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Oedema. Foot pressure rises by 90mmHg driving greater filtration and swelling.
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What is the skeletal muscle pump?
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Constriction of leg muscles reducing venous pressure in feet from 100mmHg to around 20-30mmHg
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How does arteriole tone aid reduction of blood pressure in feet on standing?
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Constriction reduces flow to feet on standing, both via baroreceptors and a local axon reflex.
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How does varicose veins affect the skeletal muscle pump?
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Reduces effectiveness of valves, causing oedema.
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What is the effect of standing on cardiac output, and why?
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Reduces. Veins distend a little, reducing venous return and CVP, this lowers CO and transiently lowers BP.
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Which two reflexes kick in to restore BP on standing?
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Baroreceptors in the carotid sinuses and aorta, and cardiopulmonary receptors in the atria and pulmonary vessels.
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What is the overall effect of compensatory mechanisms following standing up?
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BP rises a little.
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What is the vestibulosympathetic reflex?
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A feed forward response. Anticipation of a change in CO induces a sympathetic discharge prior to the event.
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What happens to venous pressure in most veins above the heart on standing?
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Drops to zero.
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What happens to arterial pressure above the heart on standing?
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Drops 40mmHg, lowering cerebral perfusion due to reduced hydrostatic pressure
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Which sinus does not collapse on standing?
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Dural sinus, fall in CSF pressure prevent sinus from collapsing
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What can happen after prolonged standing?
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Fall in pulse pressure after 20-30 mins as heart tires, heart rate rises to compensate as does TPR. Mean BP starts to fall. Eventually TPR falls suddenly due to increased tissue demands for O2, heart rate plummets, BP drops and cerebral perfusion drops - vasovagal syncope.
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What is the physiological advantage of feinting?
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Horizontal position restores venous return.
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What is circulatory shock?
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Inadequacy of blood flow to the tissues, which can result in tissue damage
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What are typical blood volumes for men and women?
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Men 0.77ml/kg and women 67ml/kg
Typical 80kg man = 6L Typical 60kg woman = 4L |
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What factor is more important than loss of a volume of blood?
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Speed of loss. Over 24hours a 50% loss may be tolerated, but a rapid loss of 30% can be fatal.
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How much blood loss can be tolerated before blood pressure is affected?
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Around 20% if fit and healthy.
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What is reverse stress relaxation?
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Veins shrink as blood volume reduces, begins after 10 mins and is fully developed after 1 hour.
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List responses from baroreceptors and cardiopulmonary receptors to fall in blood volume.
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Aortic and carotid baroreceptors, and atrial/atriovenous cardiopulmonary receptors reduce discharge, leading to raised SNS stimulation,
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How do arterial chemoreceptors respond to haemorrhage?
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Reduced amounts of blood will result in acidosis, chemoreceptors in aortic arch and carotid bodies will increase firing, affecting breathing
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What is the CNS ischaemic response?
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Kicks in when pressure falls below 50mmHg to divert blood to brain. Very potent, last to activate as blood is preferetially distrbuted to the brain anyway, but very short acting.
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What is the effect of compensatory mechanisms on cardiac output and perfusion?
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Preferential redirection of reduced CO to brain and heart at expense of other tissues.
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Describe how BP remains normal is a moderate haemorrhage?
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TPR increases, preferentially cutting off kidney, GI, skin and muscle to serve brain and heart. CO falls, but BP remains normal.
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How does the body respond to reduced blood volume?
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Reduced capillary pressure draws in fluid from interstitium
Thirst increases Stress and cardiopulmonary receptors increase ADH output, reducing diuresis Renal ischaemia leads to reduced GFR Renin, Angiotensin, Aldosterone system leads to increased Na+ and H2O reuptake |
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What is the result on urine output to haemorrhage?
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Reduced.
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What changes would you expect to see to [Hb] initially and then up to 6 weeks.
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[Hb] normal immediately. Falls as volume is restored. Rises sharply, then slow restoration over 6 weeks.
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Why does haemorrhage cause acidosis?
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Reduced tissue blood flow with normal metabolism leads to build up of acid in tissues and in blood.
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What causes irreversible heart failure?
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Damage to myocardium starved of O2. Low BP leads to low coronary blood flow - ischaemia
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What is isometric exercise?
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Muscle contraction without shortening - sustained
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Describe the relationship between O2 consumption and work in dynamic exercise.
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Increases linearly until VO2Max, then small increase possible anaerobically.
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How can you calculate oxygen consumption?
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Cardiac output (delivery of blood to tissues) multiplied by (arterial O2 content, minus venous O2 content)
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Describe the effect of prolonged exercise on heart rate and stroke volume.
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Heart rate rises linearly until maximum is reached, stroke volume rises initially, and then is generally stable (slight rise).
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How does fitness affect the heart response to exercise?
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Decreases both resting and submaximal heart rates.
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How does systolic and diastolic BP change in response to exercise?
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Systolic increases steadily to a maximum, diastolic remains constant, or shows a small fall/rise.
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How does arterial-venous O2 content difference alter in exercise?
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Increases as tissues remove more oxygen.
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How does O2 consumption change in maxmum exercise and how is that increased demand met?
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11 fold increase (250ml/min up to 2800ml/min)
Met by a 4x increase in cardiac output (heart rate 2.5x, stroke volume 1.25x) And a 3x increase in A-V O2 content |
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What determines VO2Max?
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Cardiac output ultimately. Arterial O2 content is constant, venous content falls as demand increases, but this cannot be changed by fitness. So CO is the main determinant.
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The trained body is able to improve A-V O2 difference slightly, how?
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Growth of new capillaries improves diffusion.
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Which metabolites control blood flow to active muscle?
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PCO2, O2, H+, adenosine
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What accounts for the small increase in stroke volume?
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Increased filling, due to raised CVP
Increased contractility due to SNS stimulation |
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Why does the increased heart rate in exercise not cause stroke volume to fall?
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CVP is sufficiently high to improve filling, even with the shorter filling period due to raised heart rate
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What accounts for the increased oxygen removal in exercise?
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Low PO2 in tissues means demand is higher, and Hb has reduced affinity for O2 due to acid pH, raised temperature and raised PCO2
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What effect does isometric exercise have on BP and how does this differ to dynamic exercise?
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Isometric exercise causes a rise in both systolic and diastolic (dynamic only changes systolic) resulting in a progressive rise in BP and HR which does not plateau.
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What causes the stimulation to breath during persistent heavy exercise?
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Change in blood pH due to lactic acid detected by arterial chemoreceptors.
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How does ventilation respond to O2 consumption?
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Increases linearly.
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What stimulates increased breathing in early exercise?
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Not PCO2 rising (as this remains constant and actually falls in heavy exercise as it is blown off)
Not PO2, as this remains constant. Not pH as this is constant until it falls later. Thought to be due to a feed fgorward mechanism centrally, plus full range of receptors. |
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What factors affect coping with illness?
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Perception of illness and the tasks to be coped with both feed into coping, which helps determine response to illness.
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What are the two main coping strategies for dealing with illness?
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Problem focussed - engage with issue, learn about it, seek info
Emotion focussed - deal with stress and anxiety, distractions, avoidance, outbursts |
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How can doctors help patients deal with psychological aspects of illness and why is this important.
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Illness outcome heavily linked to psychological factors.
Provide information, address issues and concerns, symptoms, strategies Look at motivation and behaviour change Help patient deal with emotions related to illness Look at both individual and group approaches. |
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What was the Petrie study?
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Intervention to improve long term outcomes following MI
3 x 30min sessions looing at perceptions, causes, beliefs, negative consequences and planning for recovery Patients who received intervention were 20% more likely to go to rehab, 3x less likely to suffer angina, and twice as likely to be back at work. |
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How is response to illness measured?
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Quality of life is popular, as are mood measures.
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Where do hydrogen ions come from each day?
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CO2 - produces 15000mM each day, non-carbonic acids around 40-80mM
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What is the most important buffer?
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Bicarbonate
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Describe some tell tale signs of metabolic and respiratory acidosis.
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Metabolic acidosis = Low HCO3-, low PCO2
Respiratory acidosis = High H+/PCO2 |
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Describe some tell tale signs of metabolic and respiratory alkalosis.
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Metabolic alkalosis = High HCO3-, high PCO2
Respiratory alkalosis = Low H+/PCO2 |
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What is the kidneys role in acid-base regulation?
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Reabsorbs bicarbonate (PCT) and secretes H+ ions (DCT)
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How does K+ affect H+ secretion?
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In the DCT K+ or H+ are exchanged for Na+ in. When body K+ is low, more H+ is secreted, resulting in an alkalosis.
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In a metabolic acidosis, HCO3- decreases, how does the body compensate?
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Rise in pH stimulates increased ventilation, PCO2 is reduced.
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In respiratory acidosis, PCO2 increases, how does the body compensate?
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Kidney increases production of HCO3- in tubules.
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What are the two acute and two long term defences against pH change?
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Acute - buffering and respiration
Long term - renal excretion and hepatic metabolism |
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Patient presents with high pH and low PCO2?
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Respiratory alkalosis
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Patient presents with high pH and high PCO2?
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Metabolic alkalosis
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What are three main cause of metabolic acidosis?
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Increased acid - DKA, lactic acid, ingestion
Inability to excrete - renal failure, renal tubular acidosis Loss of bicarbonate - GI loss, renal loss (proximal RTA) |
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What is the anion gap?
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Sodium and Potassium concentrations weighed against Chlorine and Bicarbonate
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Why is the anion gap relevant?
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Helps determine cause of acidosis -
Normal anion gap = Diarrhoea/vomiting High anion gap = DKA or lactic acidosis |
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What are some causes of respiratory alkalosis?
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Stress/anxiety, ventilators, trauma, drugs, hypoxia
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How does alkalosis affect Ca2+ levels?
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As pH increases, free ionised calcium is buffered by proteins, causing a drop in plasma Ca2+, this makes nerve junctions more sensitive causing tetany.
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What are some causes of metabolic alkalosis?
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Loss of H+, vomiting or diarrhoea, K+ depletion or excess of mineralocorticoids (cushing's)
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