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  • 1. Amy’s AsthmaScenario Briefing1. What could be the causes of instantaneous breathlessness? 12. Why is it important to examine whether the chest expands symmetrically or differentially on one side? 23. What does hyper-resonance on percussion of the chest indicate?34. What are the two main pathogenic causes of airway obstruction, and hence wheezing and where would you hear it? 45. What would crackling sounds in the airways mean? 56. Which generations of airways correspond to (i) bronchi (ii) bronchioles, (ii) respiratory bronchioles (vi) alveolar ducts and sacs67. What factors increase hemolytic tone?78. What factors decrease broncho-motor tone? 89. What are the physiological effects of asthma on the epithelium and respiratory tract?910.What are the main signs of hypercapnia?101 Pulmonary embolism or pneumothorax2 No movement on one side could indicate a tension pneumothorax or collapsed lung.3 Either surgical removal of the lung or lung collapse4Asthma and COPD, all over the lungs since these areas are not localised to particular airways (as canceror an inhaled object might). Wheezing would be most obviously heard on breathing out since this requiresmore force, in severe disease this becomes ʻgas trappingʼ.5Fluid in the small airways, if you have L ventricular failure blood wonʼt leaving the lungs adequately and sofluid may build up and cause breathlessness.6 Bronchi (2-12), bronchioles (12-16), respiratory (17-19), alveolar ducts and sacs (20-23)7 Irritant receptors and inflammatory mediators, vagal nerve stimulation (parasympathetic)8 Sympathetic stimulation through activation of B2 receptors by adrenaline9Thickening of basement membrane, smooth muscle hypertrophy, vasodilation, mucus gland hyperplasia,desquamation of epithelium, mucus plug in lumen, oedema of mucosa, white blood cells enter mucosa10Hypercapnia is having too much CO2 in the blood. Signs are flushed skin (red), vasodilation,hyperventilation
  • 2. 11.What would the oxygen saturation level of blood need to be in order for haemoglobin to lose the ability to retain oxygen?11Hypersensitivity1. What are IgE, IgM, IgG and IgA?122. What is type 1 hypersensitivity? 133. Which are the two most important types of hypersensitivity in asthma? 144. What is Der P?155. What is Atopy?166. What substance causes increased permeability of vessels to fluid and causes the localised oedema or wheal seen after a skin prick allergy test?177. What is involved in a RAST test?188. What is type 2 hypersensitivity? 199. What are the main causes of type 3 hypersensitivity (antigen-complex mediated, when there is little antibody and an excess of antigen)?2011 Around 40% or 8kPa12IgE = least abundant but plays major role in type 1 hypersensitivity, IgM = produced in the spleen by Bcells, binds to specific antigens, IgG = produced in plasma by B cells controls infection in intracellular fluidand thus responsible for what enters tissues. IgA = main antibody for mucosal linings13Immediate inflammatory/allergic response, mediated by IgE and mast cells releasing histamine, typicallyonset in 1-5 minutes and ends after 15 minutes.14 Types 1 and 415 The allergen produced by dust mite gut bacteria, the main allergen involved in asthma16 Atopy is hypersensitivity to allergens (allergy)17 Histamine18 Take patient serum containing IgE, detect bound IgE via enzyme or anti synthetic IgE antigen.19IgM antibodies to foreign cell membrane proteins, recruitment of inflammatory cells which leads to attackby killer cells, release of c3a and c5a (chemoattractants which attract inflammatory cells), antibodydependent cytotoxicity.20Incompatible blood transfusions, hemolytic disease of the newborn (where maternal IgG antibodies whichhave passed across the placenta, attack the fetal red blood cells), diabetes (antibodies to insulin/islet cellsproduced), myasthenia gravis (antibodies attack acetylcholine receptors resulting in muscle weakness).
  • 3. 10.What is the difference between type 2 (antibody) and type 3 (complex) hypersensitivities?2111.What is type 4 hypersensitivity? 2212.What is the difference between atopic/extrinsic asthma and non-atopic/intrinsic asthma? 2313.Why should NSAIDS and aspirin not be given to asthmatics?2414.Describe the type 1 and type 4 responses to an asthmatic response?25Control of Breathing1. What are the main factors which control automatic (involuntary) breathing?262. Which part of the brain has direct, higher central control which is able to bypass ANS control of breathing? 273. What is the pneumotaxic centre?284. What kinds of receptors control the lungs and breathing?2921Type 3 is a soluble complex (i.e. dissolved in blood plasma) whereas type 2 is antibodies on the skinsurface/epithelium. In type 3 large complexes activate an array of killer cells which often damage host cellswith ʻfriendly fireʼ.22 Delayed response inflammation, antibody independent, T-cell mediated, antigen presenting cells find theallergen and present it to T killer cells. This is the mechanism for delayed asthmatic response and TB.23Atopic/extrinsic has a defined (allergic) cause and usually starts in childhood, non-atopic/intrinsic has anundefined cause and is later onset.24 Because they can provoke a serious asthma attack in 5% of asthmatics.25Type 1 is the initial onset, lumen mucus increased, immune mediators released but recede again after 15minutes and breathing recovered. Hours later, the type 4 onset begins, antigen goes to dendritic cells, thenpresented to T-cell and eosinophil activation, further allergic response.26Neural controls from brainstem and lung receptors, Chemical controls from response to PCO2, PO2 andpH, as well as central chemoreceptors.27The medulla (below the pons), so cutting the medulla would mean breathing was still ok whilst awake butwould result in sleep apnoea28A network of neurons in the pons which regulates the amount of air a person can take into the body ineach breath. Ventilation needs to match metabolism.29Mechanical stretch receptors (fire when stretched to prevent over-inflation of lungs), irritant receptors,higher centres of temperature control, chemoreceptors (CO2, O2 and pH).
  • 4. 5. What is the Henring Breuer Inflation Reflex? 306. What are irritant receptors responsible for?317. What does stimulation of the arterial baroreceptors do to breathing? 328. What change occurs to the chemical ventilation control mechanism in the case of metabolic acidosis or alkalosis?339. What could be a likely source of a high level of HCO3-?3410.Where would you find the chemoreceptors which affect breathing?3511.Why would it be worse for a hypoxic patient to breathe 100% oxygen than it would to breathe normal air? 3612.What is the most likely cause of sleep apnea and why?37Pharmacology of Asthma1. What types of drug are used for the treatment of asthma? 382. How is airway smooth muscle contraction innervated/stimulated?3930 The rule that inhalation innately inhibits exhalation and vice versa.31The deep, augmented breaths you take every 5-20 minutes. Coughing and some reflex laryngeal/bronchoconstriction32 Inhibits breathing33In acidosis it takes a lower CO2 level to cause ventilation to increase, so you are more likely tohyperventilate. The reverse is true in alkalosis.34 Vomiting, loss of acid means HCO3- not used up and builds up35Chemoreceptors located mostly around the exit of cranial nerves IX and X which detect O2, CO2 and pHbased on HCO3- in the CSF.36Because this would lead to absence of CO2 and loss of the hypoxic drive, which would actually depleteoxygen levels37Most likely if patient is overweight, larynx and soft tissues in the neck become loose and breathing spacereduced. Anyone who snores has a degree of obstructive sleep apnea.38B2 agonists, anti-cholinergic, anti-inflammatory glucocorticoid, phosphodiesterase inhibitor, anti-leukotriene, cromone or ʻmast cell stabilizerʼ.39Parasympathetic vagal efferents, Excitatory non-adrenergic, non-cholinergic (an ANS transmitter which isneither noradrenaline or acetylcholine) c-fibre efferents.
  • 5. 3. How is airway smooth muscle relaxation innervated/stimulated?404. Where is airway smooth muscle located in the respiratory system? 415. Out of bronchodilators, prophylactics and anti-inflammatories, which are ‘relievers’ and which are ‘preventers’?426. Give 3 examples of ‘relievers’ and 3 of ‘preveters’437. What are the half lives of salbutamol and salmeterol? 448. What is the main mechanism of B2 receptor agonists? 459. Why are relievers such as Ipratropium Bromide not that useful for allergen induced asthma? 4610.What is the main mechanism of anti-cholinergics?4711.When would you use xanthines to treat asthma?4812.What is the main mechanism of xanthines like theophylline and aminophylline4940Sympathetic stimulation by adrenaline B2 receptors (adrenal medulla), sympathetic efferents toparasympathetic ganglia, Nitric oxide (a bronchodilator just like it is a vasodilator)41 All the way from the trachea to the respiratory bronchioles, arranged in ring structure around the lumen.42 Relievers are bronchodilators (for acute symptoms), preventers are prophylactics and anti-inflammatories(for relief of chronic symptoms)43Relievers - B2 selective agonist (e.g. Salbutamol for short acting, Salmeterol for long acting), Anti-cholinergics, Xanthines (Theophylline, Aminophylline), Preventers - Glucocorticosteriods, Cromones, Anti-leukotrienes, Xanthines44Salbutamol is a short acting reliever with a 5-6 hour half life. Salmeterol is a long acting reliever with a 17hour half life.45Increase cyclic AMP levels in target cells to induce smooth muscle relaxation, mast cell stabilisation (anti-histamine), mucus clearance by increasing cilia activity4647Its all in the name - block effects of acetylcholine released from cholinergic parasympathetic nerve fibresand so block parasympathetic induced SM contraction. Also prevent mucus hyper-secretion.48 Generally used if B2 agonists not effective, can be given in slow (for nocturnal asthma) or fast releaseforms49 Mostly as relievers as they have a short half life, mechanism is to inhibit phosphodiesterases (whichconvert cyclicAMP into AMP), so xanthines potentiate cyclic AMP production and induce relaxation of SM.Used if B2 agonists arenʼt effective. Xanthines also reduce eosinophil (WBC specifically responsible forallergic reaction, present in blood from haematopoiesis) survival.
  • 6. 13.What are beclamethosone and prednisolone?5014.What is the mechanism of glucocorticosteriods?5115.Why would you use cromones such as cromolyn sodium? 5216. What are the main side effects of glucocorticosteriods? 5317.What are the effects of cromones5418.What are two drug classes of anti-leukotrienes? 5519.Why might you use anti-leukotrienes as opposed to other preventers?5620.What is the mechanism of anti-leukotrienes? 5721.What are the side effects of B2 agonists? 5822.What are the side effects of Xanthines? 5923.What are the side effects of (oral) anti-leukotrienes?6024.What is bronchial thermoplasty?6150 Glucocorticosteriods (Preventers), take one hour before effects are seen51Suppress inflammatory gene activation by penetrating the cell nucleus and blocking the effects ofinflammatory cytokines on transcription factors in the cell nucleus. Reduces inflammatory effects such asmucosal oedema and improves airflow.52Because they produce less side effects (glucocorticosteroids can cause cough, hoarseness and evenretarded growth, weight gain, eye problems and diabetes) so are often given to children in preference53Inhaled: cough, hoarseness, Oral: retarded growth (so rarely given to children), diabetes, osteoporosis,water retention, weight gain, eye problems, diabetes, psychosis, hypertension.54Mechanism is uncertain but they block release of sensory neuropetides, stabilise mast cells and preventeosinophil (WBC specifically responsible for allergic reaction) activation55 5 Lipoxygenase Inhibitors (Zileuton, USA only) and Leukotriene receptor antagonists (e.g. Montelukast)56 In aspirin induced asthma (few unwanted side effects)575 -lipoxygenase inhibitors inhibit the enzyme converting arachidonic acid into leukotrienes and leukotrienereceptor antagonists stop the leukotrienes taking effect58 Skeletal muscle tremor, sometimes tachycardia (fast heart rate)59(Have a very narrow therapeutic range). Headaches, nausea, cardiac arrhythmia, diuresis, behaviouralchanges. (Constant therapeutic monitoring required).60 Headaches and GI disturbances61 Radiofrequency ablation of parts of the airway wall to reduce ASM contractibility
  • 7. Adherence and Placebo1. How many people (%) in the UK have a chronic illness or disability?622. What is ‘compliance’? 633. What is ‘adherence’? 644. What is ‘concordance’?655. What is the typical rate of non-adherence?666. What methods could be used to measure adherence? 677. What are the four main determinants of non-adherence (cost-benefit)?688. What 3 factors lead to increased compliance in Ley’s model? 699. How might you improve adherence?7010.What factors could affect the effectiveness of a placebo?7162 15% of the total population63 The extent to which the patientʼs behaviour matches the prescriberʼs reccomendations64 The extent to which the patientʼs behaviour matches the agreed recommendations from the prescriber. I.e.like compliance but where there has been a collective decision involved65A consultation process where the doctor and patient agree on therapeutic decisions that incorporate theirrespective views66 30-50%67Self-report questionnaire, self monitoring, pill counts or prescription refills, marked sign technique (inactivedrug markers), biochemical indicators (e.g. urine sample), clinical outcomes68 Cost: Time, side effects, Benefit: Progression, symptoms69 Understanding, satisfaction and memory70 Removing barriers (cost, repeat prescription), Identifying maladaptive illness and modifying treatmentprescriptions (e.g. symptoms, drug concerns). Improving communication (knowledge) & doctor patientrelationship, memory cues (take with food), simple well organised information.71Size, shape, colour, administration or medication. Setting: home or hospital. Patient characteristics(beliefs, anxiety, adherence), Practitioner characteristics: status, empathy, Patient-practitioner relationship