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Pathophysiology of Cardiovascular System
Dr. Hemn Hassan Othman
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What is the circulatory system?
The circulatory system carries blood and dissolved substances to and from different places in the body. The Heart has the job of pumping these things around the body. The Heart pumps blood and substances around the body in tubes called blood vessels. The Heart and blood vessels together make up the Circulatory System.
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Our circulatory system is a double circulatory system.
This means it has two parts. Lungs Body cells the right side of the system deals with deoxygenated blood. the left side of the system deals with oxygenated blood.
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now lets look inside the heart
This is a vein. It brings blood from the body, except the lungs. These are arteries. They carry blood away from the heart. 2 atria Coronary arteries, the hearts own blood supply 2 ventricles The heart has four chambers now lets look inside the heart
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The Heart Artery to Lungs Artery to Head and Body
Vein from Head and Body Vein from Lungs Right Atrium Left Atrium valve valve Left Ventricle Right Ventricle
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blood from the heart gets around the body through blood vessels
There are 3 types of blood vessels a. ARTERY b VEIN c CAPILLARY
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Arteries carry blood away from the heart.
The ARTERY Arteries carry blood away from the heart. the elastic fibres allow the artery to stretch under pressure thick muscle and elastic fibres the thick muscle can contract to push the blood along.
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Veins carry blood towards from the heart.
The VEIN Veins carry blood towards from the heart. veins have valves which act to stop the blood from going in the wrong direction. thin muscle and elastic fibres body muscles surround the veins so that when they contract to move the body, they also squeeze the veins and push the blood along the vessel.
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The CAPILLARY Capillaries link Arteries with Veins
they exchange materials between the blood and other body cells. the wall of a capillary is only one cell thick The exchange of materials between the blood and the body can only occur through capillaries.
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The CAPILLARY A collection of capillaries is known as a capillary bed.
artery vein capillaries body cell
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what’s in BLOOD digested food red blood cells white blood cells oxygen
waste (urea) platelets carbon dioxide hormones plasma
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An Epidemiological Overview
Cardiovascular disease (CVD) is the leading cause of death in the modern world (U.S, Canada, Europe, Japan and Australia). In 2005 CVD accounted for approximately 38% percent of all deaths CVD has been the number one killer in the U.S. since 1900 except for 1918 (influenza) More that 2,500 Americans die from CVD each day most of them are men.
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Types of Cardiovascular Disease
Atherosclerosis Coronary heart disease (CHD) Chest pain (angina pectoris) Irregular heartbeat (arrhythmia) Congestive heart failure (CHF) Congenital and rheumatic heart disease Stroke
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Percentage of Deaths from Cardiovascular Disease
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Diseases of the Arteries and Veins
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Forms of arteriosclerosis Atherosclerosis
Arteriosclerosis is a general term describing hardening and loss of elasticity of the arteries. Forms of arteriosclerosis Atherosclerosis Atherosclerosis is the most common form of arteriosclerosis and it refers to hardening and loss of elasticity of large and medium-sized elastic arteries such as the aorta and coronary & cerebral arteries.
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Normal Atherosclerosis
It takes place due to formation of an atheromatous plaque (atheroma) within the tunica intima. The atheromatous plaque is composed of lipid-laden macrophages (foam cells) and free lipid (e. g., cholesterol and fatty acids) and is prone to calcification, ulceration and rupture. Normal Atherosclerosis
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Atherosclerosis Characterized by deposits of fatty substances, cholesterol, cellular waste products, calcium, and fibrin in the inner lining of the artery Hyperlipidemia – abnormally high blood lipid level Plaque – the buildup of deposits in the arteries
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Atherosclerosis Pathogenesis and progression:
Inflammation of endothelium Cellular proliferation Macrophage migration LDL oxidation (foam cell formation) Fatty streak Fibrous plaque Complicated plaque
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Atherosclerosis
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Atherosclerosis
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Atherosclerosis of the coronary artery
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Atherosclerosis Marked narrowing of the arterial lumen due to protrusion of an theromatous plaque (atheroma) from the tunica intima.
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Medial calcific sclerosis
Medial calcific sclerosis is hardening and loss of elasticity of the medium-sized muscular arteries due to deposition of calcium salts in the muscular tissue of the tunica media. Medial calcific sclerosis Deposition of calcium salts (blue color) within the tunica media of a medium-sized, muscular artery.
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It is usually more benign than other forms of arteriosclerosis because it does not cause narrowing of the lumen. It is seen mostly in the elderly.
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Types of arteriolosclerosis
Arteriolosclerosis is hardening and loss of elasticity of arterioles. It is most often associated with hypertension and/or diabetes mellitus. Types of arteriolosclerosis Types of arteriolosclerosis include hyaline arteriolosclerosis and hyperplastic arteriolosclerosis. Both are associated with vessel wall thickening and luminal narrowing that may cause ischemic injury.
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Hyaline arteriolosclerosis
Hyaline arteriolosclerosis refers to thickening of the walls of arterioles due to deposition of hyaline material. Hyaline arteriolosclerosis is seen in elderly patients, with or without hypertension and in patients with long-standing diabetes but the lesions are most common and most severe in hypertensive patients. Hyaline arteriolosclerosis Deposition of eosinophilic, homogenous hyaline substance within the walls of the arterioles in the kidney.
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Hyperplastic arteriolosclerosis
b. Hyperplastic arteriolosclerosis Hyperplastic arteriolosclerosis is a type of arteriolosclerosis associated with marked narrowing of the arteriolar lumen due to hyperplasia of the arteriolar smooth muscle cells. The term "onion-skin" is sometimes used to describe the affected arteriole. Hypertension is the principle cause in humans. Hyperplastic arteriolosclerosis Marked narrowing of the arteriolar lumen in the kidney due to hyperplasia of the arteriolar smooth muscle cells.
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Ischemic Heart Diseases
This is a generic name for a group of closely related syndromes that result from myocardial ischemia. In over 90%, this is due to a reduction in coronary blood flow. (Decrease in supply) Other conditions arise as a result of increases in demand e.g. hypertrophy, shock, increase heart rate, etc.
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Coronary Heart Disease
Myocardial infarction (MI) or heart attack – blood supplying the heart is disrupted Coronary thrombosis – blood clot in the artery Embolus – when the blood clot is dislodged and moves through the circulatory system
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Coronary Artery Disease
Any vascular disorder that narrows or occludes the coronary arteries Atherosclerosis is the most common cause Risk factors Dyslipidemia Hypertension Cigarette smoking Diabetes mellitus Obesity/sedentary lifestyle
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Coronary Artery Disease
Nontraditional risk factors Markers of inflammation and thrombosis C-reactive protein, fibrinogen, protein C, and plasminogen activator inhibitor Hyperhomocysteinemia Infections
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Coronary atherosclerosis
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Coronary atherosclerosis
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Coronary atherosclerosis
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Taken from Robbins Pathologic Basis of Disease
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Clinical Manifestations
Angina Pectoris Myocardial Infarction Chronic ischaemic heart disease Progressive heart failure consequent to previous myocardial infarction. Sudden Cardiac Death
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Angina Pectoris This is a symptom complex. Symptoms caused by transient myocardial ischemia that falls short of inducing the cellular necrosis that defines myocardial infarction. Three variants:- Stable angina Prinzmental angina Unstable angina
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Stable Angina – Most common form
Stable Angina – Most common form. Chronic stenosing coronary atherosclerosis, reaching a critical level, leaving the heart vulnerable to increased demand. Typically relieved by rest or a vasodilator
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Prinzmetal Angina Uncommon pattern Occurs at rest
Documented to be due to arterial spasm Unrelated to physical activity, heart rate or blood pressure. Generally responds to vasodilators.
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Unstable Angina Pattern here is the pain occurs with progressively increasing frequency and tends to be more prolonged Associated with disruption of the atherosclerotic plaque, with superimposed thrombosis, embolisation or spasm. Predictor of Myocardial Infarction
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Myocardial Infarction (MI)
Transmural Infarction The ischaemic necrosis involves the full or nearly the full thickness of the ventricular wall in the distribution of a single coronary artery. Usually associated with chronic coronary atherosclerosis, acute plaque change and superimposed completely obstructive thrombosis.
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Gross changes of myocardial infarction
None to occasional mottling (up to 12 hours) Dark mottling (12-24 hours) Central yellow tan with hyperemic border (3-7 days) Gray white scar (2-8 weeks)
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Varying gross appearance of myocardial infarction
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Microscopic changes of myocardial infarct
Early coagulation necrosis and oedema; haemorrhage (4-12 hours) Pyknosis of nucleic, hypereosinophilia, early neutrophilic infiltrate (12-24 hours) Coagulation necrosis, interstitial infiltrate of neutrophils (1-3 days) Dense collagenous scar (> 2 months)
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Hypereosinophilia
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Coagulative necrosis
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Interstitial infiltration of neutrophils
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Acute effects of myocardial infarction
Contractile dysfunction Arrhythmias Cardiac rupture Pericarditis Sudden death Invariably this would be due to a lethal arrhythmia (asystole or ventricular fibrillation)
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Pathological complications of myocardial infarction
Infarct extension Mural thrombus Ventricular aneurysm Myocardial rupture Ventricular free wall Septal wall in between the ventricles Papillary muscle
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Infarct extension Diagram from Robbins Pathologic Basis of Disease
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Ruptured Myocardial Infarct
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Ruptured Papillary muscle
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Fibrous scarring with compensatory hypertrophy of unaffected ventricular wall
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Ventricular wall aneurysm
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