1. iBSc: Question 6 - Asthma By Alan McLeod

2. Getting the best marks Read the whole question – a latter section may give you a clue about an earlier one. To see how many points you need look at the marks allocated – for example a 3 point question is generally looking for 3 salient points If giving a list answer put the best answers first – examiners will not usually mark answers too far down a list Always write something – it may get you part of a mark and is anonymised so no one will think you are stupid! If you genuinely have no clue then re-write the question to see if this sparks some ideas. If not then move on and come back at the end. And remember – always write something. Good luck!

3. Question 6 Mrs Rockley, a 67 year old smoker presents with an acute attack of breathlessness. Q6.1 List 3 differentials (3) Q6.2 Describe IMMEDIATE management on arrival at A+E (3)

4. Question 6 She has a polyphonic wheeze and a history of asthma. Q6.3 As part of your treatment you give salbutamol – this is a beta agonist. How - on a molecular level - do these drugs work? (6)

5. Question 4 The airway narrowing in asthma is multifactorial Q6.4 List the three main factors (3) Q6.5 If the radius is halved with other factors remaining equal what happens to the flow of air? (3)

6. Question 6 Most gas exchange takes place within the alveoli Q6.6 Draw and lable an alveolus showing cells and fluids present and nearby important structures (7)

7. Question 6 Mrs Rockley smokes 30 cigarettes a day – you try to persuade her to stop. Q6.7 Describe the Stages of Change model and how it may help you with getting Mrs Rockley to stop smokeing (8)

8. The Answers View these on ‘note view’ rather than on full screen – additional notes are provided for some slides

9. Generating Differentials: I’D GET VINO… I Infectious / inflammatory D Degenerative G Genetic / Idiopathic E Endocrine T Trauma V Vascular I Iatrogenic / ingested N Neoplastic O Organs

10. Acute Dyspnoea I Infectious / inflammatory Asthma, Pneumonia, COPD exacerbation (e.g. upper resp tract infection) D Degenerative G Genetic / ideopathic E Endocrine T Trauma Pneumothorax V Vascular Myocardial infarction, PE I Iatrogenic / ingested Foreign body (mostly children) N Neoplastic O Organs / other Lungs

11. Emergency Management DDanger?Check that the scene is safe RRunCheck for response HHappilyCall for HELP! AAway and Check and secure airway and C- spine BBuyCheck breathing, Resp rate CChocolate!Pulse, Heart rate

12. Emergency Management D‘Disability’ Neuro exam: minimum is pupil size / response + GCS or AVPU E‘Exposure’ 1: Expose to seek injuries 2: Keep warm + take temperature DEFGDon’t Ever Forget Glucose!!!

13. An AMPLE history AAllergies MMedications PPast med Hx LLast meal (time) EEvent – what happened

14. GPCRs Salbutamol is a beta agonist – it binds to beta receptors – the are G-protein coupled receptors http://uk.youtube.com/watch?v=tOcGbnBCdMM http://uk.youtube.com/watch?v=bU4955rLv_8&feature=rela ted

15. GPCR Summary Receptor complex + G protein G Protein has 3 subunits (alpha, beta & gamma) Receptor binds ligand Conformational change Loss of GDP from G protein alpha subunit Binding of GTP Separation of alpha subunit from beta- gamma dimer Alpha and beta-gamma freed to interact with effectors. Cascade effect. Cycle starts again

16. GPCRs in the lung Beta receptors GPCRs Gs actvates adenylate cyclase –Increased cAMP –ATP  cAMP cAMP causes relaxation of the smooth muscle Decreases sensitivity of the IP3 receptor, decreasing release of calcium from intracellular stores in response to IP3 1 Some proponents argue for a cAMP independent PKA mechanism as well 2

17. GPCRs in the heart Beta receptors GPCRs Gs activates adenylate cyclase –Increased cAMP –ATP  cAMP cAMP activates PKA PKA phosphorylates alpha-1 subunit on voltage-gated Ca ++ channels Increased Ca ++ influx Increased inotropy Increased rate Ca ++ In

18. Beta-adrenergic antagonists ‘Beta blockers’ Combat the harmful activation of the sympathetic nervous system Decrease HR Decrease contractility Examples Propranalol Sotalol Side effects Bronchoconstriction Bradycardia

19. Asthma Airway COS of Three Pathologies Constriction OedemaSecretions

20. Velocity and Flow Velocity Displacement of single particle per unit time Inversely proportional to cross sectional area –Faster in thinner tubes Aorta is thinner than total mass of capillaries –V slow capillary flow –Time for gaseous exch Flow Volume of fluid passing point A at time B Proportional to pressure difference Inversely proportional to tube length Proportional to r 4 Inversely proportional to viscosity

21. The Alveolus

22. Vessels in the Lung Pulmonary Artery –Deoxygenated blood –From Right Ventricle –Oxygenated in lungs –Affected in PE Bronchial Artery –Oxygenated blood –From systemic supply –Supplies tissues of lung Pulmonary vein –Oxygenated blood –From lungs –To Left atrium

23. Stages of Change Model AKA ‘Transtheoretical’ By Prochasta and Diclemente Patient focus Explains why some interventions don’t work Allows you to predict which ones might! Contempla- tion Mainten- ance Pre Contemplation Preparation Action

24. Two Useful Concepts Body Mass Index (BMI) 20-25: Ideal 26-30: Overweight 31-35: Obese Pack Years > 20 = increased chance complications PY= Cigs / day x Yrs 20 BMI= Wt (kg) Ht 2 (M)

25. The End The slides here should allow you to mark your own work – remember 1 mark per answer up to the maximum for the question. Multiply by 3 to get percentage points. I assume a 60% pass mark. Sorry but I am unable to give further advice on answers due to time constraints.