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All of medicine in 12 hours…

All of medicine in 12 hours…. Dr. Alan McLeod (F2). The Plan. Day One A systematic approach Chest Pain Acute sob Chronic sob Haemoptysis TATT Painful Limb Breast Pain Emergency management. Day Two Maximising your marks Swallowing Change in bowel habits Hepatomegaly Abdo pain

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All of medicine in 12 hours…

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  1. All of medicine in 12 hours… Dr. Alan McLeod (F2)

  2. The Plan Day One • A systematic approach • Chest Pain • Acute sob • Chronic sob • Haemoptysis • TATT • Painful Limb • Breast Pain • Emergency management Day Two • Maximising your marks • Swallowing • Change in bowel habits • Hepatomegaly • Abdo pain • Pregnancy / Birth • Recurrent Infections • Headache • Stroke • Pharmacology basics

  3. 2 Minutes 10 Causes of Chest Pain

  4. Puzzled? You Need A SYSTEM…

  5. Puzzled? What do I do?

  6. I GET VINO…

  7. 2 Minutes 10 Causes of Chest Pain

  8. Chest Pain? Where’s that wine…

  9. Ischaemic Heart Disease • Approx 1/3rd of all male deaths • Approx ¼ of all female deaths • Atheroma of coronary vessels

  10. Right: Right Ventricle, most of Right Atrium, Part of Left Atrium Left: Left Ventricle, part of Right atrium, most of Left atrium Left circumflex: Left margin of heart and its entire posterior wall, Left atrium, posterior IV septum LAD: Anterior 2/3 of IV septum, anterior portion of LV, whole apex

  11. SA Node: Right 51-65%, Left 35-45%, Bilateral <10% AV Node: Right 80-90%, Left 10-20% ALL HIGHLY VARIABLE!!!

  12. Coronary Arteries: Fill During DIASTOLE

  13. Arterial Disease Arteriosclerosis • Thickening and hardening of wall • Reduced lumen • Reduced flow • Reduced elasticity • Reduced contrractility • Diabetes • Hypertension Atherosclerosis • Commonest cause of arteriosclerosis • Specific disease • Tunica intima • Mostly large and medium vessels • Small in prolonged systemic hypertension

  14. Atherosclerosis • Changes in intima  thrombus formation • Reduced lumenal size • Poor perfusion/hypoxia • Tissue death • Loss of elasticity • Aneurysm formation Smaller vessel atherosclerosis • Ischaemic heart disease • Most strokes • Peripheral heart disease

  15. Plaque Formation

  16. Plaque Formation

  17. Plaque Formation

  18. Plaque Formation

  19. Plaque Anatomy Plaque Anatomy (early) • Free Lipid • Foam cells • Increased myointimal cells • Collagen • Disruption of internal elastic lamina Plaque Anatomy (later) • Collagen cap • Extracellular lipid mass • Foam cells • Myointimal cells • Disrupted internal elastic lamina • Pressure atrophy of muscle  collagenous replacement

  20. Atheroma – Risk factors Non-preventable • Increasing age • Male sex • Family history Preventable • Hyperlipidaemia • LDL and Cholesterol • Hypertension • Diastolic most important • Diabetes • Smoking

  21. Fold Fibrous Pericardium Myocardium Pericardial Space Layers of the Heart Endocardium Parietal Layer of Serous Pericardium Visceral Layer of Serous Pericardium

  22. Compare Skeletal and Cardiac Muscle

  23. Muscle Comparison

  24. Myocyte Action Potential NAK-CAKKK

  25. In Detail

  26. Pacemaker Action Potential Membrane potential (mV) 0 Ca++ In K+ Out -40 -80

  27. Comparison of action potentials

  28. Excitation-contraction coupling • Electrical signal • Stimulates contraction Generally • Signal causes depolarisation • CA++ entry results • Causing contraction • In The Heart • Calcium induced calcium release • Act Pot from SA Node

  29. Excitation-contraction coupling SAN L Type Calcium Channel Excitation Ca++ Ca++ Ca++ Ca++ SR Ca++ Ca++ Ca++ Ca++ Ca++ Ca++

  30. Excitation-contraction coupling L Type Calcium Channel Ca++ Ca++ Ca++ Ca++ SR Ryanodine Receptor Ca++ Ca++ Ca++ Ca++ Ca++ Ca++

  31. Excitation-contraction coupling L Type Calcium Channel Ca++ Ca++ Ca++ Ca++ SR Ryanodine Receptor Ca++ Ca++ Ca++ Ca++ Ca++ Ca++

  32. Excitation-contraction coupling Ca++ Ca++ Ca++ Tropomysin Ca++ SR Ca++ Ca++ Ca++ Ca++ Ca++

  33. Excitation-contraction coupling Ca++ Ca++ Ca++ Tropomysin Ca++ SR Ca++ Ca++ Ca++ Ca++ Ca++

  34. Excitation-contraction coupling Ca++ Ca++ Ca++ Ca++ Tropomysin Ca++ Ca++ Ca++ Ca++ SR Contraction CA++

  35. Describe Sliding Filament Theory

  36. Sliding Filament Theory http://uk.youtube.com/watch?v=gJ309LfHQ3M&feature=related • Calcium enters • Binding sites on actin uncovered by movement of Tropomyosin / troponin complex • Myosin binds to site  powerstroke • ATP binds to myosin  release from binding • ATP  ADP + Pi – cocks myosin for another Powerstroke • Continues as long as ATP and Ca present

  37. Sliding Filament Theory

  38. Normal Lead 2 A Segment is Shorter than an interval

  39. The Normal ECG PR interval: first deflection of P  first deflection of QRS • 120-200 ms (3-5 small sq) QRS interval: first deflection of QRS  end of last deflection • <100 ms (<3 small sq) QT interval (QTc is QT corrected for heart rate). Start of QRS  end of T wave • 360-440 ms (<11 small sq)

  40. Additional Abnormalities • Pathological Q wave • Duration > 1 small sq • ST Depression • 1mm or more over isoelectric line • ST Elevation • 0.5mm or more below isoelectric line • T wave abnormality • Normally upright in I, II & V1 – V3 • Normally inverted in aVr • Variable in others

  41. STEMI and NSTEMI STEMI • ST Elevation MI • ST elevation on ECG • Positive enzyme tests NSTEMI • Non ST Elevation MI • No ST elevation • Positive enzyme tests

  42. STEMI and NSTEMI A: Normal ECG B: ST Elevation C: ST Depression ST elevation in response to Isoelectric line (I) ST Segment A I P T QRS B C

  43. Evolution of ECG Changes in STEMI • Minutes to hours • Peaked T waves • Hours • ST elevation • Hours to days • T wave inversion • Loss of R wave • Days • Pathological Q wave

  44. Cardiac Enzymes

  45. Fibrinolysis • tPa • Streptokinase

  46. ACS? GO CARDIO ABCD

  47. 2 Minutes 5 Causes of acute Dyspnoea

  48. Acute Dyspnoea? Need alcohol!

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