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Course Outline

Course Outline. Human Physiology-1. Instructor: Dr JMA Hannan Class time: ST 11.20 am - 12.50 pm Phone: 9885611 - 20 ext. 284. General Policy. Examination Mark 1st Midterm - 30% Class tests/quizzes 10% Assignment/ Presentation 10% Class participation 5% Viva 5%

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Course Outline

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  1. Course Outline Human Physiology-1 Instructor: Dr JMA Hannan Class time: ST 11.20 am - 12.50 pm Phone: 9885611 - 20 ext. 284

  2. General Policy ExaminationMark 1st Midterm - 30% Class tests/quizzes 10% Assignment/ Presentation 10% Class participation 5% Viva 5% Final exam - 40% Total marks - 100

  3. Grading Policy Numerical ScoresLetter Grade 93 and above A Excellent 90 – 92 A- 87 – 89 B+ 83 – 86 B Good 80 – 82 B- 77 – 79 C+ 73 – 76 C Average 70 – 72 C- 67 – 69 D+ 60 – 66 D Poor Below 60 “F” (Fail) If you are absent in 3 consecutive classes you will be given “F”

  4. Textbook and reference books • Text book of Medical Physiology. Guyton and Hall • Review of the Medical Physiology. William F. Ganong

  5. How to do well in this class? • Forget about your previous grade/result • Attend lectures and take notes • * Effort = Result. • Read the syllabus • Read exam questions carefully before answering • & answer all parts of a given question • 6. Turn assignments in on time • 7. Ask if you have questions

  6. The Cardiovascular System The Heart

  7. Cardiovascular System

  8. Anatomy of the Heart • Heart chambers: • Left & right atria. • Left & right ventricles. • Heart valves: • Atrioventricular valves: • Right: Tricuspid. • Left: Bicuspid • Semilunar valves • Right: Pulmonary valve. • Left: Aortic valve.

  9. Anatomy of the Heart 3 layers • Epicardium: • Outer layer • Myocardium: • middle muscle walls. • Endocardium: • Innermost surface

  10. Endocardium: lines the lumen of the heart and is composed of simple squamous epithelium and a thin layer of loose connective tissue. • Myocardium:consists of layers of cardiac muscle cells arranged in a spiral fashion about the heart’s chambers. The myocardium contracts to propel blood into arteries for distribution to the body. • Epicardium:is the outermost layer of the heart and constitutes the visceral layer of the pericardium. It is composed of simple squamous epithelium on the external surface.

  11. The Conduction System Bundle of His Purkinje fibre

  12. Intrinsic Conducting System • Sinoatrial node • Electrical pace maker. • Atrioventricular node • Receives impulses originating from SA node. • Bundle of His • Electrical link between atria and ventricles. • Purkinje fibres • Distribute impulses to ventricles.

  13. The impulse-generating and impulse conducting system of the heart comprises several specialized structures whose coordinated functions act to initiate and regulate the heartbeat. 1. The sinoatrial node, the “pacemaker” of the heart, is located within the wall of the right atrium. It generates impulses that initiate contraction of atrial muscle cells; the impulses are then conducted to the atrioventricular node. 70 - 80 impulse/min 2. The atrioventricular node is located in the wall of the right atrium, adjacent to the tricuspid valve. 40 - 60 impulse/min

  14. 3. The Bundle of His is the band of conducting tissue radiating from the AV node into the interventricular septum where it divides into two branches and continues as Purkinje fibers. 30 - 60 impulses/min 4. Purkinje fibers are large, modified cardiac muscle cells that make contact with other part of the cardiac muscle. 15 - 40 impulses/min

  15. Electrical impulses from your heart muscle (the myocardium) cause your heart to beat (contract). This electrical signal begins in the sinoatrial (SA) node, located at the top of the right atrium. The SA node is sometimes called the heart's "natural pacemaker." When an electrical impulse is released from this natural pacemaker, it causes the atria to contract. • The signal then passes through the atrioventricular (AV) node. The AV node checks the signal and sends it through the muscle fibers of the ventricles, causing them to contract. • The SA node sends electrical impulses at a certain rate, but your heart rate may still change depending on physical demands, stress, or hormonal factors. The Conduction System Mechanism of heart contraction

  16. 2 1 0 3 4 4 Cardiac Electro-Physiology • Phase 0: Rapid depolarisation of the cell membrane and it is associated with the inflow of the Na+ ions. • Phase 1: A short initial phase of rapid repolarisation due to activation of a Cl- current (inflow). K+ channel rapidly open and close causing a transient outward current. • Phase 2: Action potential plateau. A period of more gradual repolarisation in which there is a movement of Ca2+ ion into the cell. • Phase 3: Final repolarisation. A second period of rapid repolarisaion during which K+ move out of the cell. • Phase 4: A fully repolarised state during which K+ channel opens. K+ move into and Na+ out of the cell again to enable the next cycle to begin.

  17. The Cardiac Cycle • Systole: • Period of ventricular contraction. • Blood ejected from heart. • Diastole: • Period of ventricular relaxation. • Blood filling.

  18. Blood Vessels and Blood Pressure

  19. Blood Vessels • Arteries • Arterioles • Capillaries • Venules • Veins

  20. Blood Vessels • Arteries and veins consist of 3 layers. • Tunica interna (tunica intima): endothelium • Tunica media: smooth muscle layer • Tunica externa (tunica adventitia): connective tissue • Capillaries consist of simply endothelium • Single flattened layer of epithelial cells resting on basement membrane.

  21. Veins vs Arteries • Veins • Relatively thinner walls (less smooth muscle). • Less elastin fibres. • Some have valves to prevent backflow of blood. • Arteries • Thick muscular walls (more smooth muscle). • Have layers of elastin fibres. • No valves.

  22. Capillaries • Site of exchange between blood and tissues. • Thin-walled (0.2-0.4 µm). • 5-9 µm in diameter. • Arranged into capillary beds.

  23. Capillary Function • Diffusion through gaps or fenestrations. • Small molecular weight molecules (eg. Glucose). • Vesicular transport. • Endocytosis of material from blood.

  24. Blood Pressure Blood pressure is the measurement of force applied to the artery walls The pressure is determined bythe force& amount of blood pumped(CO) & the size and flexibility of the arteries(PR).

  25. Systolic & Diastolic BP Systoleheart muscle contraction. Creates high pressure in chamber. Systolic blood pressure is the pressure generated when the heart beats. Diastoleheart muscle relaxes. Drops pressure in chamber. Diastolic blood pressure is the pressure in the vessels when the heart is at rest.

  26. BP = Cardiac output x Peripheral resistance Cardiac Output Amount of blood pumped into the aorta each minute by the heart. C.O. (vol/min) = heart rate (beat/min) x stroke volume (vol/beat) = 75 beat/min x 70 ml/beat = 5250 ml/min = 5.25 L/min Venous return Quantity of blood flowing from the veins into right atrium each min. VR = CO Peripheral resistance It is the impediment (resistance) to blood flow through the vessel.

  27. Blood pressure regulation BP is directly proportional to the production of CO and PR( CO or  PR =  BP). To maintain normal BP - CO and PR are controlled by 2 overlapping control mechanisms. • Short-term BP regulation (Neural mechanisms) • Long-term BP regulation (Endocrine mechanisms) • (The renin-angiotensin-aldosterone system)

  28.  Activation of b1 adrenoceptors on heart  Cardiac output  Sympathetic activity  Activation of a1 adrenoceptors On smooth muscle  Peripheral resistance  Angiotensin II  Renin  Renal flow  Aldosterone  Glomerular filtration rate  Na+ & H2O retention  Blood volume Short-term mechanism  BP  BP Long-term mechanism Ref: Lippincott’s Pharmacologyp181

  29. Contraction of vascular smooth muscle cells & Cardiac cells & role of intracellular Ca2+. Action in vascular tissue: 3 mechanisms may be possible for the contraction of vascular smooth muscle cells. First, Voltage sensitive Ca2+ channels open in response to depolarization of the membrane and extracellular Ca2+ enters the cells. Second, hydrolysis of phosphatidylinositol to formation of inositol triphospahete (IP3) which acts as a second messenger to release intracellular Ca2+ from sarcoplasmic reticulum. Third, this intracellular Ca2+ may trigger further infloux of Ca2+ through VDC channel. This increase in cytosolic Ca2+ results in enhanced binding of Ca2+ to the protein calmodulin. The Ca2+ calmodulin complex activates myosin light-chain kinase which phosphorylates the light chain of myosin. Such phosphorylation promotes interaction between actin and myosin and contrtraction of smooth muscle. Ca2+ channel blockers inhibits the voltage dependant Ca2+ channel. Action in cardiac cells: Within the cardiac myocytes, Ca2+ binds to troponin and uncovering myosin binding sites on actin, therefore, formation of cross-linkages between actin and myosin, producing shortening and contraction of cardiac muscle.

  30. Ca2+ Channel Ca2+ Calmodulin Ca2+ calmodulin complex Myosin LC kinase (MLCK) Active MLCK Myosin LC-PO4 Myosin light chain (MLC) Actin Contraction

  31. ATPase Ca2+ Ca2+ Na+ Na+ K+ Ca2+ K+ Ca2+ Na+ Na+ SR Ca2+

  32. The renin-angiotensin-aldosterone system Blood vessel CO  BP  Blood Vol.  BP

  33. Hypertension is defined conventionally as blood pressure >140/90 mmHg.

  34. Ref: Davidson’s Medicine, p388

  35. Factors responsible for developing hypertension A. Essential Hypertension • Genetic factor (American black, Japanese; 40-60%) • Dietary factors (high salt intake, alcohol intake, obesity, lack of exercise) • Stress • Age > 60 years B. Secondary Hypertension • Pregnancy (pre-eclampsia) • Renal disease • Glomerulonephritis) • Renal vascular disease • Polycystic kidney disease • Endocrine disease • Hyperaldosteronism • Hyperthyroidism • Drugs • Oral contraceptic containing estrogens • Anabolic steroids • Corticosteroids • NSAIDS (Non-steroidal anti-inflammatory drugs)

  36. Untreated hypertension

  37. CONGESTIVE HEART FAILURE • DEFINITION • Congestive heart failure is a condition in which the heart is unable to to pump sufficient blood to meet the needs of the body. • It can be caused by an impaired ability of the heart muscle to contract or an increased workload imposed on the heart. • A clinical syndrome caused by an accumulation of fluid peripherally (right ventricular failure) or in the lungs (left ventricular failure), or both, from inadequate functioning of the heart. Congestive heart failure is a complication of an underlying disease process. • Systolic heart failure (the more common form) is due to impaired systolic pumping action of the heart. Diastolic heart failure occurs when the systolic function is normal but the filling of the heart is impaired.

  38. Signs & symptoms of congestive heart failure •  heart rate. • Rapid muscular fatigue. • Short breath due to pulmonary edema • Myocardial hypertrophy ( size of heart) • Renal output • Congestion (excessive amount of fluid) in the chest

  39. Pathology of Heart Failure Heart disease +  C.O. + -  Renal blood flow  Venous pressure  Renin release -  Angiotensin II +  Aldosterone • Na+ & H2O retension  Pre-load  After-load  Tissue perfusion Edema

  40. ANGINA PECTORIS • ‘Angina pectoris’is a Latin phrase that means"strangling in the chest."Unlike a heart attack, the heart muscle is not damaged forever, and the pain usually goes away with rest. • DEFINITION • Heart disease characterized by chest pain that occurs as a result of inadequate oxygen and blood supply to the myocardium. • Angina is characterized by a sudden, severe pressing substernal pain radiating to the left arm.

  41. TYPES 1. Stable Angina 2. Unstable Angina 3. Myocardial Infarction 1. Stable Angina Predictable pattern of exertional pressure sensation in the anterior chest relieved by rest or nitroglycerin. History:Chest pain described as tightness, pressure or aching that is typically located in the substernal area, radiating down one or both arms for 5 minutes or less, precipitated by exercise or emotional stress and relieved by rest or nitroglycerin.

  42. 2. Unstable Angina This is characyerized by pain that occurs at rest. History:More severe anginal pain that lasts more than 30 minutes or that occurs during rest and is not relieved by rest or sublingual nitroglycerin. 3. Myocardial Infarction This type of angina refer to "Emergencies of the Cardiovascular System. It is the interruption of blood supply to the heart due to block of coronary artery by thrombus, resulting in ischemic injury and necrosis of a portion of the myocardium.

  43. CAUSES OF ANGINA Angina pectorisis the result of myocardial ischemia, which occurs when the cardiac workload and myocardial oxygen demands exceed the ability of the coronary arteries to supply oxygenated blood. It is the main clinical expression of coronary artery disease(subintimal deposition of atheromas in the large and medium-sized arteries serving the heart) (atherosclerosis of coronary arteries).

  44. Risk Factors • Hypertension • Hyperlipidemia • Diabetes mellitus • Cigarette smoking • Family history of premature coronary artery disease (e.g., father died of coronary artery disease before reaching 60 years of age). • Use of oral contraceptives. • Sedentary lifestyle. • Obesity

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