Lecture 6 Circulatory Disorders I.pdf

CIRCULATORY DISORDERS I Prof. Dr. Dalya Basil IN THIS LECTURE…… ▪- Edema ▪- Hypermia and Congestion ▪- Hemorrhage ▪- Thrombosis ▪- Embolism  CIRCULATORY SYSTEM ▪ The main function of the circulatory system, which consists of the heart and blood vessels, is transport. The circulatory s...

CIRCULATORY DISORDERS I Prof. Dr. Dalya Basil IN THIS LECTURE…… ▪- Edema ▪- Hypermia and Congestion ▪- Hemorrhage ▪- Thrombosis ▪- Embolism  CIRCULATORY SYSTEM ▪ The main function of the circulatory system, which consists of the heart and blood vessels, is transport. The circulatory system delivers oxygen and nutrients needed for metabolic processes to the tissues, carries waste products from cellular metabolism to the kidneys and other excretory organs for elimination, and circulates electrolytes and hormones needed to regulate body function. ▪ The blood flow to each tissue of the body is exactly matched to tissue need. ▪ The health and well-being of cells & tissues depend not only on an intact circulation to deliver nutrients but also on normal fluid hemostasis.  EDEMA ▪ Edema is increased fluid in the interstitial tissue spaces or it is a fluid accumulation in the body cavities in excessive amount. Depending on the site, fluid accumulation in body cavities can be variously designated as: ▪ a- Hydrothorax – fluid accumulation in pleural cavity in a pathologic amount. ▪ b- Hydropericardium – pathologic amount of fluid accumulated in the pericardial cavity. ▪ c- Hydroperitoneum (ascites) – fluid accumulation in peritoneal cavity. ▪ d- Ancsarca – is a severe & generalized edema of the body with profound subcutaneous swelling.  MECHANISM OF EDEMA FORMATION ▪ Approximately 60% of the lean body weight is water, two-thirds of which is intracellular with the remainder in the extracellular compartment. ▪ The capillary endothelium acts as a semipermeable membrane and highly permeable to water & to almost all solutes in plasma with an exception of proteins. Proteins in plasma and interstitial fluid are especially important in controlling plasma & interstitial fluid volume. ▪ Normally, any outflow of fluid into the interstitium from the arteriolar end of the microcirculation is nearly balanced by inflow at the venular end. Therefore, normally, there is very little fluid in the interstitium.  MECHANISM OF EDEMA FORMATION ▪ Edema formation is determined by the following factors: ▪ 1- Hydrostatic pressure ▪ 2- Oncotic pressure ▪ 3- Vascular permeability ▪ 4- Lymphatic channels ▪ 5- Sodium and water retention HYDROSTATIC PRESSURE & THE ONCOTIC PRESSURE ▪ There are four primary forces that determine fluid movement across the capillary membrane. Each of them can be listed under the above two basic categories, the hydrostatic pressure & the oncotic pressure. These four primary forces are: ▪ a. The capillary hydrostatic pressure: This pressure tends to force fluid outward from the intravascular space through the capillary membrane to the interstitium. ▪ b. The interstial fluid hydrostatic pressure: This pressure tends to force fluid from the interstitial space to the intravascular space. ▪ c. The plasma colloid osmotic (oncotic) pressure: This pressure tends to cause osmosis of fluid inward through the capillary membrane from the interstitium. ▪ d. The interstial fluid colloid osmotic (oncotic) pressure: This pressure tends to cause osmosis of fluid outward through the capillary membrane to the interstitium.  MECHANISM OF EDEMA ▪ In addition, some fluid FORMATION is normally drained by the lymphatic channels. Usually, excess fluid will accumulate in the interstitium (i.e. edema is formed) when the capillary hydrostatic pressure is increased or when the plama oncotic pressure is decreased or when the lymphatic drainage is blocked. ▪ Hence, basically, one can divide pathologic edema into two broad categories: ▪ A. Edema due to decreased plasma oncotic pressure. The plasma oncotic pressure is decreased when the plasma proteins are decreased in various diseases such as: ▪ 1. Protein loosing glomerulopathies like nephroticsyndrome with leaky glomerulus. ▪ 2. Liver cirrhosis which leads to decreased protein synthesis by the damaged liver. ▪ 3. Malnutrition ▪ 4. Protein loosing enteropathy.  MECHANISM OF EDEMA FORMATION ▪ B. Edema resulting from increased capillary hydrostatic pressure as in the following diseases: ▪ 1. Deep venous thrombosis resulting in impaired venous return. ▪ 2. Pulmonary edema ▪ 3. Cerebral edema ▪ 4. Congestive heart failure  CLINICAL CLASSIFICATION OF EDEMA Localized Generalized ▪ - Deep venous thrombosis - Nephrotic syndrome ▪ - Pulmonary edema - Liver cirrhosis ▪ - Brain edema - Malnutrition ▪ - Lymphatic edema - Heart failure - Renal failure  LOCALIZED EDEMA ▪ A. Edema of the brain: ▪ - May be localized at the site of lesion e.g neoplasm, trauma. ▪ - May be generalized in encephalitis, & trauma ▪ - Narrowed sulci & distended gyri - ↑ Edema → compression of medulla towards foramen magnum → compression of vital centers lead to → Herniation of the brain → Patient dies. ▪ B. Pulmonary edema: ▪ - Usually occurs in left ventricular failure. ▪ - May occur in adult respiratory distress syndrome (ARDS). ▪ - lung ↑ 2.3x its weight.  GENERALIZED EDEMA ▪ Generalized edema (anasarca) occurs due to: ▪ A. Reduction of albumin due to excessive loss or reduced synthesis as is caused by: 1. Protein loosing glomerulopathies like nephrotic syndrome 2. Liver cirrhosis 3. Malnutrition 4. Protein-losing enteropathy ▪ B. Increased volume of blood secondary to sodium retention caused by congestive heart failure.  VASCULAR PERMEABILITY ▪ Increased vascular permeability usually occurs due to acute inflammation. Such edema is called inflammatory edema. Inflammatory edema differs from non-inflammatory edema by the following features: ▪ A. Inflammatory edema (exudate) - Due to inflammation-induced increased permeability and leakage of plasma proteins. - Forms an exudate [protein rich] - Specific gravity > 1.012 ▪ B. Non-inflammatory edema (transudate) - A type of edema occurring in hemodynamic derangement (i.e. increased plasma hydrostatic pressure & decreased plasma oncotic pressure). - Formed transudate [protein poor] - Specific gravity < 1.012  LYMPHATIC CHANNELS ▪ Also important is the lymphatic system which returns to the circulation the small amount of proteinaceous fluid that does leak from the blood into the interstitial spaces. Therefore, obstruction of lymphatic channels due to various causes leads to the accumulation of the proteinaceous fluid normally drained by the lymphatic channels. Such kind of edema is called lymphatic edema. ▪ Lymphatic edema occurs in the following conditions: ▪ 1. Parasitic infection. ▪ 2. Lymphatic obstruction secondary to neoplastic infiltration. E.g. breast cancer ▪ 3. post surgical or post irradiation, i.e surgical resection of lymphatic channels or scarring after irradiation  SODIUM AND WATER RETENTION ▪ Sodium & subsequently water retention occurs in various clinical conditions such as congestive heart failure & renal failure. In these conditions, the retained sodium & water result in increased capillary hydrostatic pressure which leads to the edema seen in these diseases.  HYPEREMIA AND CONGESTION Both of them can be defined as a local increase in volume of blood in a particular tissue. Hyperemia: - Is an active process resulting from an increased inflow of blood into a tissue because of arteriolar vasodilation. - Commonly occurs in exercising skeletal muscle or acute inflammation. - Affected tissue becomes red as there is engorgement with oxygenated blood.  CONGESTION ▪ Congestion - Is a passive process resulting from impaired outflow of blood from a tissue. - Occurs systemically as in cardiac failure or locally as in isolated venous obstruction. - Affected tissue appears blue-red due to accumulation of deoxygenated blood. - In long-standing congestion (also called chronic passive congestion states), poorly oxygenated blood causes hypoxia → results in parenchyma cell degeneration or cell death.  HEMORRHAGE ▪ Hemorrhage is extravasation of blood outside the blood vessel. It is caused by: ▪ 1. Physical trauma – Stabbing ▪ 2. Inadequacies in blood clotting which can be due to: qualitative & quantitative defect of platelets, missing or low amount of clotting factors prothrombin, fibrinogen, and inadequate vitamin K leads to clotting factor deficiency because this vitamin is important in the synthesis of the clotting factors by the liver.  HEMORRHAGE Terminology: 1) Haemorrhage enclosed within a tissue or a cavity is knownas hematoma. 2) Minute 1-2 mm hemorrhages occurring in the skin, mucosal membrane, or serosal surface are called petechiae. 3) Slightly > 3mm – 1 cm hemorrhage occurring in the skin is referred to as purpura. 4) Larger than 1 cm subcutaneous hemorrhage is called ecchymosis (bruises). It is typical after trauma. HEMATOMA PETECHIAE PURPURA ECCHYMOSIS (BRUISES)  HEMORRHAGE Effects of haemorrhage: depend on the rate and amount of blood loss: If > 20% the total blood volume is rapidly lost from the body, it may lead to hypovolumic shock & death. Chronic loss of blood leads to anaemia.  THROMBOSIS ▪ Thrombosis is defined as the formation of a solid or semisolid mass from the constituents of the blood within the vascular system during life. Pathogenesis: thrombus formed due to the following three factors are called ▪ Virchow’s triad:  PATHOGENESIS OF A: Endothelial injury THROMBOSIS 1. Mechanical injury: e.g rupture, torsion 2. Degeneration of endothelial cell as in atherosclerosis and aneurysm 3. Inflammation: phlebitis and arteritis B: Turbulence or Stasis (Alterations in normal blood flow): Under physiologic conditions normal blood flow is laminar, that is, the cellular elements flow centrally in the vessel lumen. Stasis & turbulence therefore: 1. Disrupt the laminar flow and bring platelets in to contact with the endothelium 2. Prevent dilution of activated clotting factors by freshly flowing blood 3. Retard or make a time lag in the inflow of clotting factor inhibitors and permit the build up of thrombi 4. Turbulence causes reduction in endothelial prostacyclin (PGI2, a vasodilator factor) and tissue-type plasminogen activator (t-PA) which has fibrinolytic activity.  PATHOGENESIS OF THROMBOSIS C: Hypercoagulablity: Hypercoagulability is any alteration of the coagulation pathway that predisposes to thrombosis. Hypercoagulability is a less common cause of thrombosis & it can be divided into: 1. Primary (Genetic), for example: mutations in factor V[Lieden factor], anti thrombin III deficiency, and protein C or S deficiency (anticoagulant proteins). 2. Secondary (Acquired) which, in turn, can be categorized into: - Myocardial infarction - Cancers (Cancers release procoagulant tissue products to cause thrombosis) - Disseminated intra vascular coagulation  TYPES OF THROMBI 1. Pale thrombus: composed mainly of platelets and fibrin strands. This type is seen in arteries 2. Red thrombus: composed of platelets, fibrin strands and red blood cells. this type seen in venous thrombosis 3. According to the presence or absence of pyogenic bacteria, thrombi can be classified to septic and aseptic respectively.  FATES (OUTCOME) OF A THROMBUS Thrombus can have one of the following fates: A: Propagation: The thrombus may accumulate more platelets and fibrin & propagate to cause vessel obstruction. B: Embolization: The thrombus may dislodge and travel to other sites in the vasculature. Such a traveling thrombus is called thromboembolism. An embolus may obstruct a vessel and lead to the death of the tissue supplied by the blood vessel. Death of a tissue due to a decreased blood supply or drainage is called infarction. Such as, Pulmonary infarction can be caused by a thromboembolus from deep venous thrombosis.  FATES (OUTCOME) OF A THROMBUS C: Dissolution: The thrombus may be removed by fibrinolytic activity. D: Organization and recanalization Organization refers to the ingrowth of endothelial cells, smooth muscle cells, and fibroblasts into the fibrin-rich thrombus. Organization is accompanied by the formation of capillary channels across the thrombus, re-establishing lumen continuity to some extent. This is known as recanalization. The recanalization eventually converts the thrombus into a vasscularized mass of tissue which is later on incorporated as a subendothelial swelling of the vessel wall.  CLINICAL SIGNIFICANCE OF THROMBI ▪ Thrombi are significant clinically because they cause obstruction of arteries and veins, also they are possible source of emboli. ▪ Venous Thrombosis (Phlebothrombosis): Venous thrombosis (clot) affects veins of the lower extremity in 90% of cases. It can be divided into superficial & deep vein thrombosis. ▪ A common form of venous thrombosis is deep vein thrombosis (DVT), when a blood clot forms in the deep veins. If a thrombus breaks off (embolizes) and flows to the lungs to lodge there, it becomes a pulmonary embolism (PE), a blood clot in the lungs. The conditions of DVT only, DVT with PE, and PE only, are all captured by the term venous thromboembolism (VTE) DEEP VEIN THROMBOSIS (DVT)  EMBOLISM An embolus is a detached intravascular solid, liquid or gaseous mass that is carried by blood to sites distant from its point of origin. After traveling via the blood, the embolus can obstruct a vessel. Causes of embolism: An embolus can arise from: o Thrombus → thromboembolism o Platelets aggregates o Fragment of material from ulcerating atheromatous plaque o Fragment of a tumor o air o Amniotic fluid o Infected foreign material  THROMBOEMBOLIS a) Pulmonary thromboembolism (PTE) : PTE is refers to the impaction of an embolus in the pulmonary arteries & their branches. 1. If the thrombus is large, it may block the outflow tract of the right ventricle or the bifurcation of the main pulumonary trunk (saddle embolus) or both of its branches, causing sudden death right side heart failure (cor pulmonale). 2. If the embolus is very small (as in 60-80% of the cases), the pulmonary emboli will be clinically silent. 3. Embolic obstruction of medium sized arteries manifests as pulmonary haemorrhage. 4. If the cardiorespiratory condition of the patient is poor (i.e., if the patient previously had cardiac or pulmonary disease), then obstruction of a medium sized pulmonary artery by a medium-sized embolus can lead to pulmonary infarction. 5. Recurrent thromboembolism can lead to pulmonary hypertension in the long run.  THROMBOEMBOLIS Deep venous thrombosis (DVT): Usually starts in deep veins within the calf muscles. Patient present with local pain, heat & edema Has higher incidence in middle aged & elderly people, after surgery or any patient have predisposing factors for thrombus formation May dislodge and cause pulmonary embolism.  THROMBOEMBOLIS b) Systemic thromboembolism: Systemic emboli arise from the left side of the heart due to prosthetic heart valve, rheumatic heart valve, arrhythmia Systemic thrombi may impact in: 1) Lower extremities (which is the commonest) 2) Brain 3) Mesenteric vessles (intestinal) 4) Spleen 5) Lower extremities (least one) THANK YOU