Veterinary General Pathology PDF Chapter 7 Haemodynamic Derangement

## Veterinary General Pathology ### Chapter 7 Haemodynamic Derangement * Cell survival is dependent on oxygen supply and normal fluid balance * Around 60% of lean body weight is water: intracellular component (40%) and extracellular component (interstitial fluid 15% and plasma water 5%) ### Hyp...

## Veterinary General Pathology ### Chapter 7 Haemodynamic Derangement * Cell survival is dependent on oxygen supply and normal fluid balance * Around 60% of lean body weight is water: intracellular component (40%) and extracellular component (interstitial fluid 15% and plasma water 5%) ### Hyperemia (Congestion) * It refers to an increased volume of blood in the vessel of a given part. * It occurs in either of two ways: * Too much blood brought to an area (arterial or arteriolar dilatation) * Too little drained out from the area (impaired venous drainage) * Hyperemia can be active or passive (congestion) ### Active Hyperemia * It is usually due to inflammation. To bring nutrient and oxygen * All active hyperemia are acute. * Acute active hyperemia can be general and local A.G.A.H and A.L.A.H * Acute general active hyperemia: * Observed in various systemic diseases such as Pasteurellosis and Erysipelas and renal diseases (retention of body fluid) * Grossly: Organs and tissues in the body have a bright red color of arterial blood * Microscopically: arteries and capillaries throughout the body are dilated / distended and filled with blood. Disappear if cause is removed * Acute local active hyperemia ("hyperemia"): * It is the most common type of hyperemia * Etiology: physiological or pathological * Physiological acute local active hyperemia occurs for example: * in genital tract during estrus, * muscle during exercise * stomach and intestine following a meal * in lactating mammary gland and * in blushing, in humans. * Pathological acute local active hyperemia is the first stage of inflammation. Cardinal signs of inflammation and significance!!!!! ### Passive Hyperemia (Congestion) * Hindrance to the out flow of blood from an organ or region increased amount of blood in the venous side * The tissue appears blue (cyanotic), why?? * Congestion may be either localized or generalized. It can be acute or chronic, but chronic is more common. * Acute general passive hyperemia: due to a sudden obstruction to the flow of blood in the heart or lungs * Don't forget to refer books! ### Etiology: * Degeneration and necrosis of myocardium (just before death) * Sudden myocardial accidents e.g. infarct * Pneumonia: due to pulmonary exudates * Pulmonary thrombosis embolism * Hydropericardium, haemopericardium, or pyopericardium * Hydrothorax, haemothorax, and pyothorax. ### Chronic general passive hyperemia * Resulted due to permanent alterations (atrophy and fibrosis) in various tissues and organs throughout the body ### Etiology 1. Lesions involving the heart: * Stenosis of a valvular opening (usually the atrio-ventricular valves) * Valvular insufficiency * Myocardial failure especially injury on myoneural conducting system * Anomalies of the heart * Constrictive lesions of pericardium and epicardium 2. Lesions involving the lung: * Obliteration of the capillary bed (e.g. in chronic alveolar emphysema and pneumonia) * Compression of major pulmonary vessels by tumors, cysts or abscesses. * Grossly: organs will be cyanotic and edematous atrophy and fibrosis * Lungs: affected in the left-sided heart failure * heart failure cells and brown induration of the lung * Liver: affected in the right-sided heart failure (lesions on the right atrio-ventricular valve or in the lung) * Microscopic: Prominent central vein, congested centrilobular region and paler hypoxic peripheral regions nutmeg liver * Spleen: slightly enlarged and cyanotic ### Acute local passive hyperemia * As a result of sudden obstruction to the flow of blood from an organ or region * Etiology: any factor causing obstruction of the vein * 1. Mal position of the viscera (intussusception, volvulus and torsion) * 2. External pressure (ligature, bandage and rubber band ### Chronic local passive hyperemia * Etiology: any factor causing gradual or partial obstruction * 1. External pressure upon a vein (enlarging neoplasm, lymph nodes and abscesses, bandages and harnesses) * 2. Obstruction within a vein (e.g. thrombus) * Grossly: cyanotic and edematous atrophy or fibrosis * Hypostatic congestion and agonal congestion * Right sided heart failure Vs left sided heart failure * Don't forget to refer books! ### Haemorrhage * It is the escape of blood from a vessel * It can be of 2 types: haemorrhage by rhexis and haemorrhage by diapedesis ### Etiology 1. Physiological causes 2. Trauma 3. Bacterial and viral diseases (e.g. salmonellosis, clostridial disease, Pasteurellosis, swine fever) 4. Parasites (coccidiosis, strongyles, hookworms, Spirocerca lupie) 5. Necrosis or destruction of vessel well (e.g. arteriosclerosis) 6. Neoplasms 7. Toxic chemicals (phosphorus, cyanide, chloroform, arsenic etc) 8. Haemorrhagic diatheses (bleeding disorder) ### Classification of haemorrhages * Based on source: cardiac, arterial, venous and capillary hemorrhage * Based on size and shape: * Petechial (pin point and < 1mm) * Purpura (around 1cm) * Ecchymotic (over 1 to 2 cm) * Hematoma (hematocyst) * Suffusion (diffuse and irregular) * Linear hemorrhage * Based on location: * Perivascular * Perirenal * Subserous * Subcutaneous * Paranchymatous * Subcapsular * Hemothorax * Haematemesis * Hemopericardium * Enterorrhagia * Haemoperitoneum * Metrorrhagia * Haemometra * Haematuria * Epistaxis * melena * Haemoptysis * Microscopically: the presence of RBCs outside the blood vessels (intact or as hemosiderin) * Significance of hemorrhage is dependent on the volume of blood loss, the rate of loss and site of hemorrhage ### Thrombosis * Thrombosis refers to the formation of a clot from elements of the circulating blood within the vascular system during life. This clot is known as a thrombus (plural, thrombi). The development of a clot is life-saving when a large vessel ruptures or is severed. However, when a thrombus develops within the vascular system, it may be life-threatening because: * It may decrease of obstruct vascular flow causing ischemic/hypoxic injury to cells, tissues and organs. * It may become dislodged or fragmented to create emboli (an embolus is an intravascular mass carried in the bloodstream to some site removed from its origin). * Don't forget to refer books! ### "Normal Hemostasis" is influenced by components of the blood vessel wall, platelets and the clotting sequence. The integrity of the blood vessel wall is crucial in normal hemostasis as well as in thrombosis. The lining endothelium provides a nonreactive interface between the underlying reactive element of the vessel wall and the fluid blood. In addition, the endothelial cells serve to protect against thrombi formation by: * 1) releasing plasminogen activator which initiates fibrinolysis and * 2) degrading platelet-aggregating agents such as adenosine diphosphate (ADP) and certain forms of prostaglandins. Underlying the endothelial layer is the subendothelial connective tissue which contains collagen fibrils. These collagen fibrils are potent activators of clotting factors, and they promote platelet adhesion. ### In summary, the endothelial cells of the vessel wall are crucial in the maintenance of normal blood flow. If the endothelial layer is damaged, the subendothelial collagen fibrils will release "tissue factors" that activate the coagulation system. * Platelets are assigned a central role in normal hemostasis and thrombosis. They adhere to sites of endothelial injury, aggregate to form platelet masses, release granules rich in a variety of secretory products and synthesize several types of prostaglandins. In normal hemostasis, platelets adhere to the severed margins of a vessel within seconds to a few minutes. The most important stimulus to such adherence is the exposure of collagen fibrils. Once adhered, platelets release two types of granules: * 1) alpha granules which contain fibrinogen, beta thromboglobulin, cationic protein and platelet factor 4 (a heparin neutralizing protein) and * 2) dense bodies, which are rich in serotonin, ADP, ATP and ionized calcium. * The release of platelet granules is triggered by a number of substances, including collagen fibrils, thrombin, plasmin, trypsin, endotoxin and antigen-antibody complexes. It is believed that these stimuli to platelet activation inhibit membrane-bound adenyl cyclase (decreased amounts of cyclic AMP are found in aggregated platelets). Within aggregated platelets, there is increased concentration of calcium (this cation is a potent stimulus to platelet activation). In addition, platelet factor 3, which participates in the intrinsic pathway of the clotting sequence, becomes activated. Initially, the platelet aggregation forms a temporary hemostatic plug which is friable and easily dislocated in rapidly flowing bloodstreams (however, at this time, the clotting sequence leads to the formation of thrombin which is the most powerful platelet aggregator yet identified). In summary, platelets: * 1) provide a temporary plug capable of controlling blood flow in small vessels in low pressure systems, * 2) initiate the development of a permanent plug composed of aggregated platelets and fibrin, * 3) release serotonin which augments vasoconstriction and * 4) contributes to the coagulation mechanism. * Don't forget to refer books! ### The coagulation system plays a major role in normal hemostasis. Maintenance of normal fluidity of blood involves the interplay between procoagulants and anticoagulants. When the procoagulants dominate and clotting is triggered inappropriately in the intact cardiovascular system, thrombi result. Concurrent with the formation of the platelet plug, the coagulation system is activated. The critical events in blood clotting are the conversion of prothrombin to thrombin and the subsequent conversion of soluble fibrinogen into the stable fibrin polymer. ### Remember, clotting may be initiated by the intrinsic pathway when blood is exposed to a negatively charged surface (such as collagen) or by extrinsic pathway. The extrinsic pathway initiates clotting when injury exposes the blood to factors derived from injured cells and tissues. Thus, the evolution of a thrombus begins with the adherence of platelets at sites of vascular injury followed by the build-up, first of a temporary aggregation of platelets, and then the formation of a more permanent platelet mass which in turn leads to the standard clotting sequence, possibly involving both the intrinsic and extrinsic pathways. ### Thrombosis is influenced by three major factors: * 1) injury to vascular endothelium, * 2) alterations in normal blood flow and * 3) alterations in the blood (hypercoagulability). * Endothelial injury plays a dominant role in the formation of thrombi in arteries and in the heart. Once the endothelium is damaged, subendothelial collagen may be exposed and tissue thromboplastin, etc., is released and the sequence of platelet adherence and activation of the clotting sequence follows. * Alterations in normal flow as encountered with stasis and turbulence of blood contributes to the development of arterial and cardiac thrombi and are probably requisite (necessary) for venous thrombosis. In the normal flowing bloodstream, the larger particles, such as erythrocytes and leukocytes, occupy the central or more rapidly moving axial stream. The smaller platelets are carried in the more slowly moving laminar stream outside the central column. The periphery of the bloodstream adjacent to the endothelial layer moves more slowly and is free of all formed blood elements (called plasmatic stream). If stasis or turbulence occurs, this laminar flow is disrupted and platelets are brought in contact with the endothelium. Evidence suggests that stasis and turbulence assume the greatest degree of importance in the formation of venous thrombi. * Alterations in blood that induce hypercoagulability have been proposed to explain the increased incidence of thrombosis encountered in certain clinical states (E.g. following surgical procedures, parturition, accidental trauma, etc.) Hyper-coagulability has been defined as "an altered state of circulating blood that requires a smaller quantity of clot-promoting substances to induce intravascular coagulation than is required to produce comparable thrombosis in a normal host." Increased numbers of platelets, increased platelet stickiness, elevated levels of fibrinogen, increased generation of thrombin, etc., have been identified as causing hypercoagulability in various clinical conditions. * Grossly, thrombi are friable, a mixture of red and gray in irregular layers, dull, and attached to the endothelium. * Don't forget to refer books! **Arterial thrombi formed in a rapidly flowing bloodstream are usually dry, friable gray masses composed of almost regularly arranged layers of platelets and fibrin, irregularly mixed with small amounts of darker red coagulated blood (why?). The resulting laminations are known as the "lines of Zahn." Arterial thrombi are referred to as white or conglutination thrombi (why?).** **Venous thrombi, formed in a slow-moving bloodstream, appear as an intravascular clot that closely resembles the clotting of blood in a test tube. Such thrombi are red, gelatinous (why?), and they are referred to as stasis or red coagulation thrombi (why?).** ### The following terms are used to describe thrombi: * Mural thrombi - are attached to the wall of the heart or blood vessel. * Occluding thrombi - are attached to the entire circumference of the vessel. * Valvular thrombi - are attached to the heart valves. * Canalized thrombi - occur when new blood channels are formed in an organized thrombus. * Saddle thrombi - straddle the bifurcation of blood vessels. * Septic thrombi - are those which contain bacteria. * Aseptic thrombi - are those that do not contain bacteria, etc. * Microscopically, thrombi are eosinophilic masses in which leukocytes and erythrocytes may be seen. Fibrin is usually obvious, but it is seldom possible to identify platelets. ### The significance, effects and outcome of thrombi should be reviewed from any textbook (Vegad). If an animal survives the immediate ischemic effects of a newly developed thrombus, one of several pathways may be folowed. The thrombus may * 1) increase in size and, by its enlargement, eventually cause obstruction of some critical vessel, * 2) give rise to emboli (to be discussed down), * 3) be removed by fibrinolytic action or * 4) become organized. ### POSTMORTEM CLOTS * A thrombus must not be confused with postmortem clotting of blood within the vascular system. The two types of postmortem clots are: * 1) red or current jelly clots and * 2) yellow or chicken fat clots. * Red or Current Jelly Clots occur when the components of the blood are evenly distributed throughout the clot. This type develops when there is rapid clotting of blood. * Yellow or Chicken Fat Clots result from a settling and separation of erythrocytes from the fluid phase of the blood. Such clots occur when postmortem clotting is delayed. * Don't forget to refer books! ### Refer from books (preferably Vegad) about the characteristic features and difference of a thrombus and a postmortem clot. ### DISSEMINATED INTRAVASCULAR COAGULATION * Disseminated intravascular coagulation (DIC) refers to widespread microthrombi formation in capillaries, arterioles and venules. The thrombi are composed largely of fibrin and aggregated platelets. The disorder may be a complication of a diverse group of clinical diseases in which there is activation of the intrinsic pathway of blood clotting. During the widespread intravascular coagulation, fibrin is deposited throughout the vascular tree resulting in microthrombi. Although the fibrinolytic system is activated, it cannot effectively deal with the large deposits of fibrin. As a result, there is rapid consumption and eventually a deficiency of clotting factors, including fibrinogen, platelets, prothrombin and factor V, VII, and X (a deficiency of fibrinogen, platelets and prothrombin is required for the diagnosis of DIC). Therefore, animals with DIC have bleeding tendencies on hemorrhagic diathesis. Also the widespread occlusion of the microcirculation may induce signs of shock, acute respiratory distress, central nervous system depression, heart failure or renal failure (why?). Remember, affected tissues may not necessarily disclose the microthrombi because of prompt activation of the fibrinolytic system. ### EMBOLISM * Embolism refers to the movement/circulation of a foreign body (called embolus) through the circulatory system and becoming lodged in a vessel causing obstruction. An embolus (plural, emboli) is a detached intravascular solid, liquid or gaseous mass that is carried by the blood to a site distant from its point of origin. Inevitably, emboli lodge in vessels too small to permit their further passage resulting in partial or complete occlusion of the vessel. The majority of all emboli arise from thrombi (thromboembolism). These are pieces of thrombi which have been broken loose by the force of the bloodstream. Less common forms of emboli include fat emboli, gas emboli, bacterial emboli, tumor emboli and parasitic emboli. * Depending on their site of origin, emboli may come to rest anywhere within the cardiovascular system. (Unless otherwise qualified, the term "embolus" implies thromboembolism throughout this discussion). ### Pulmonary embolism: * Pulmonary emboli usually originate from thrombi in veins or in the right heart (why?). Dislodgement of venous thrombi, in part or whole, produces an embolus which flows with the venous drainage through progressively larger vessels to the right heart. Unless the embolus is very large, it passes through the spacious chambers and valve openings of the right heart and enters the pulmonary arterial circulation. Lodgement of emboli in major pulmonary vessels is commonly fatal, resulting in sudden death (why?). When pulmonary emboli occlude smaller vessels, they usually cause lung hemorrhage or infarcts. However, in animals without cardiac or circulatory insufficiency, the bronchial circulation suffices to sustain the vitality of lung tissue. Remember, pulmonary infarction results only when the bronchial circulation is inadequate to compensate, which is common in animals with impaired cardiovascular function. ### Systemic embolism: * Systemic embolism refers to emboli which travel through the arterial circulation. Such emboli usually arise from thrombi within the left heart. In contrast to venous embolism, arterial emboli travel through vessels of progressively diminishing caliber. The myocardium, spleen, kidneys, brain and lower extremities are commonly the victims of arterial embolism. ### INFARCTION * An infarct is a localized area of ischemic necrosis in an organ or tissue resulting from occlusion of either its arterial supply or venous drainage. The vascular occlusion is usually caused by thrombosis and/or embolism of the arterial blood supply. More rarely, external compression of vessels by expanding tumors, etc., may result in infarction. * Infarcts are classified on the basis of their color (red or pale infarcts) and on the presence or absence of bacterial contamination (septic or aseptic infarcts). Pale or anemic infarcts are encountered with arterial occlusion and in solid tissue. When a solid tissue is deprived of its arterial circulation, the infarct may be transiently hemorrhagic, but most become pale in a very short time. The reasons for the development of pale infarcts are as follows: >*"The arterial circulation to an area is occluded. Vessels, particularly capillaries, as well as parenchymal cells are destroyed. At the moment of vascular occlusion, blood from anastomotic peripheral vessels flows into the focus of injury, producing the initial hemorrhagic appearance. If the affected tissue is solid, seepage of blood from the anastomotic vessels is minimal. Soon after the initial blood seepage, the erythrocytes are lysed and the released hemoglobin pigment either diffuses out or is converted to hemosiderin. Therefore, in solid organs, the arterial infarct will soon (24 to 48 hours) become pale or anemic. The heart and kidneys are representative of solid, compact organs which tend to have pale infarcts." * Red or Hemorrhagic Infarcts are encountered usually under the following circumstances: > * 1) with venous occlusion, > * 2) in loose tissue, > * 3) in tissue with a dual circulation and > * 4) in tissues previously congested. * Red or hemorrhagic infarcts develop in loose tissue subsequent to arterial obstruction in the following manner. The arterial circulation to an area is obstructed. If the tissue is loose (lung, etc.), large amounts of blood collect in the spongy, loose tissue at the moment of vascular occlusion. This blood remains for long periods; thus, the arterial infarct remains red. The lungs and intestine are sites where red infarcts tend to occur. * Remember, red infarcts may occasionally be encountered in solid tissue or white infarcts in loose tissue. * Factors that influence the severity of damage resulting from infarction include the following: * Don't forget to refer books! ### General Status of the Blood and Cardiovascular System: Any alteration in the systemic circulation that reduces the oxygen-carrying capacity of the blood or the velocity and volume of blood flow through the tissues predisposes to infarction. ### Anatomic Pattern of Arterial Blood Supply: The various tissues and organs of the body receive their arterial supply through one of several patterns: * 1) a dual arterial blood supply, * 2) a "single" arterial blood supply with few anastomoses (insufficient to provide adequate bypass channels), so-called "end arteries," * 3) a "single" arterial blood supply with rich interarterial anastomoses and * 4) parallel arterial systems. * A dual blood supply is received by the lungs and liver. In animals with normal cardiac and cardiovascular status, the bronchial circulation is capable of preventing ischemic necrosis of the lungs when a branch of the pulmonary artery is obstructed. Similarly, infarction is uncommon in the liver because the portal supply of blood may be adequate, even when the hepatic arterial supply is compromised. However, in the presence of cardiac failure, severe anemia, or reduced oxygenation of the blood, occlusion of one system may precipitate ischemic necrosis. * An arterial blood supply with rich interarterial anastomoses is found in the small intestine. Here, blood is able to bypass focal areas of occlusion. * An arterial blood supply with so-called "end arteries" is found in the kidneys, for example. The major branches of the renal artery supply well-defined segments of the kidneys. Occlusion of one of the major branches, or of the main renal artery, is invariably followed by ischemic necrosis. However, if the occlusion occurs at the terminal ramification and involves subcapsular parenchyma, there may be sufficient blood flow from capsular vessels to prevent tissue damage. * Parallel arterial system is encountered in the forelimbs. Either the radial or the ulnar artery is sufficient to sustain the vitality of the tissues when one or the other is occluded. * **Rate of Development of Occlusion:** Slowly developing occlusions are better tolerated than those occurring suddenly since they provide an opportunity for alternative pathways and collateral circulation to become activated. * Microscopically, all areas of infarction undergo coagulative necrosis and resorption as discussed in chapter 2 (under necrosis) * (Remember, central nervous tissue undergoes liquefactive rather than coagulative type necrosis). * The typical coagulative appearance may be modified by extensive hemorrhage in red infarcts and by bacterial suppuration in septic infarcts. Within a few days after an infarct is initiated, an inflammatory reaction becomes well-defined. Later, a reparative process begins. * Don't forget to refer books! ### Edema (Oedema) * Edema is a condition characterized by an excessive accumulation of fluid in the intercellular (interstitial) tissue spaces or body cavities. It can occur as generalized or localized disorder. * Anasarca: is a severe and generalized edema with marked swelling of the subcutaneous tissue * Hydroperitoneum or ascites refers the collection of edema fluid in the peritoneal cavity * Hydrothorax refers the collection of edema fluid in the pleural cavity * Hydropericardium or pericardial effusion refers the collection of edema fluid in the pericardial sac * Hydrocephalus refers the collection of edema fluid in the ventricles of the brain * Hydrocele refers the collection of edema fluid in the tunica vaginalis of the testicles * Try to differentiate transudate and exudates ### Pathogenesis of edema * Edema is of two types: inflammatory and non inflammatory edema. In this chapter only non-inflammatory edema will be discussed and you are advised to refer the pathogenesis of inflammatory edema. * Edema is the result of an increase in the forces that tend to move fluids from the intravascular compartment into the interstitial fluid. The exchange between the intravascular and interstitial compartments is governed by starling's forces. This hypothesis states that the normal fluid balance is maintained by two opposing sets of forces, namely hydrostatic and osmotic pressures. At the arterial end of the capillary bed, Fluid escapes from the blood to the interstitial space largely under the influence of the hydrostatic pressure of the blood. Some amount of fluid will be returned to the vessel at the venous end of the capillary bed due to the effect of osmotic pressure of the blood. However, small amount of fluid (called lymph) will remain in the interstitial space and later on will be drained off through lymphatic vessels. There fore, the amount of interstitial fluid in a given area is dependent on the hydrostatic pressure of the blood at the arterial end of the capillary, the level of plasma protein and the adequacy of the lymphatic drainage. * The following illustration will show the relationship of hydrostatic and osmotic pressure in a normal resting leg * Hydrostatic pressure at the arterial end of the capillary = 45mmHg * Osmotic pressure at the arterial end of the capillary= 30mmHg * Net of 15mm rate of fluid flow into the tissue * Osmotic pressure at the venous end of the capillary=30mgHg * Hydrostatic pressure at the venous end of the capillary= 15mmHg * Net of 15mm rate of the fluid flow into the vein * There is a continuous circulation of fluid and no accumulation of fluid in the interstitial space. However, some amount of fluid is drained off through the lymphatics. * Generally speaking edema occur when there is * 1. an increase in intravascular hydrostatic pressure * 2. a fall in colloid osmotic pressure of the plasma * 3. an impairment in the flow of blood * However, five Pathophysiologic Mechanisms that underlie the development of edema * 1. Decrease plasma (intravascular) colloidal-osmotic pressure * 2. Increase intravascular hydrostatic pressure * 3. Lymphatic obstruction * 4. Increased microvascular permeability (reason for inflammatory edema) * 5. Sodium retention * Don't forget to refer books! ### 1. Increased hydrostatic pressure * It may result from impaired venous outflow (that is as a result of general or local passive hyperemia) and hence, it is less important cause of edema, than in humans. * Hydrostatic pressure at the arterial end = 45mmHg * Osmotic pressure at the arterial end = 30mmHg * 15mm rate of fluid flow into the tissue * Osmotic pressure at the venous end =30mmHg * Hydrostatic pressure at the venous end = 20 mmHg * 10mm rate of the fluid flow into the vein * Therefore there will be net 5mmHg rate of fluid accumulation in the tissues. This type of edema is mild and usually referred as cardiac edema since the cause is usually associated with impaired cardiac function. ### 2. Reduced osmotic pressure of plasma * It occurs when there is low plasma/serum albumin level (due to excessive loss or reduced synthesis). It is the most common cause of general edema, both in animals and man, in domestic animals it is most frequent than the previous cause. Loss of blood protein (and hence Hypoproteinemia) could be due to * a. parasites like trichostrongyles, hemonchus and intestinal parasites: referred as parasitic edema * b. renal injury, particularly on glomeruli, are common in human than in domestic animals: referred as renal edema * c. advanced liver disease (especially cirrhosis) followed by decreased synthesis of plasma proteins * d. Starvation/ malnutrition followed by reduced protein synthesis: referred as nutritional or cachectic edema. * Hydrostatic pressure at the arterial end = 45mmHg * Osmotic pressure at the arterial end = 20 mmHg * 25mm rate of fluid flow into the tissue * Osmotic pressure at the venous end =30mmHg * Hydrostatic pressure at the venous end = 15 mmHg * 5 mm rate of the fluid flow into the vein * Net result showed a 20mmHg rate of fluid accumulation in the tissues. ### 3. Lymphatic obstruction * This may result from inflammatory or neoplastic obstructions. Also occur when tumor, cyst, abscesses, bandages, rubber bands, on harnesses press upon lymph vessels or when tumors or thrombi or parasites are found within the lymphatics or lymph nodes. A good example of such edema caused by parasitic obstruction of lymphatic is elephantiasis, which is caused by Wucheraria banchrofti. If the obstruction is specific, the edema will be localized and sometimes called lymphoedema. * Hydrostatic pressure at the arterial end = 45mmHg * Osmotic pressure at the arterial end = 25mmHg * 20 mm rate of fluid flow into the tissue * Osmotic pressure at the venous end =25mm Hg * Hydrostatic pressure at the venous end = 15 mmHg * 10 mm rate of the fluid flow into the vein * The net result showed a 10 mmHg rate of fluid accumulation in the tissues. ### 4. Sodium retention * Don't forget to refer books! ### Shock (Vascular collapse) * Shock is a circulatory disturbance characterized by inadequate blood flow (hypoperfusion) to cells and tissues due to: * reduction in the total blood volume * reduction in cardiac output * inadequate effective circulating volume * The fundamental disturbance is that blood volume is too small to fill the vascular system, resulting in a fall of blood pressure and cell damage due to anoxia. ### Etiology: shock develops following any serious attack on the body's homeostasis. Depending on the causes, shock may be classified as: * hypovolemic * septic * cardiogenic and * neurogenic ### 1. Hypovolemic shock- the causes of hypovolemic shock are hemorrhage and fluid loss (extensive skin burns, exudation from large traumatic wounds, diarrhea, vomiting). The principal mechanism is inadequate blood or plasma volume and hence insufficient delivery of oxygen and nutrients to the cells and tissues and inadequate clearance of metabolic wastes. * Under normal condition more than half of the capillaries in most body part remain closed. However, if all capillary beds in the body dilate (peripheral pooling of blood), there would not be enough blood to fill the major vessels and/or heart; thus, blood pressure falls and the flow of blood is decreased. ### 2. Septic or endotoxic shock- it is mostly associated with an overwhelming infection with endotoxin producing Gram-negative bacteria (endotoxic shock) like E. coli, Proteus spp., Pseudomonas aeroginosa. It can also be caused by some gram-positive streptococci organisms. In toxic or septicemic conditions, there is some times peripheral dilatation (caused mainly by the release of vasoactive mediators such as histamine, bradykinin, prostaglandins and others) of the capillary beds which subsequently lead to shock. When capillary beds are fully dilated they have the capacity to accommodate nearly the total blood volume. The net result is peripheral pooling of blood with reduction in the effective circulating blood volume, lowered cardiac outputs and inadequate perfusion of cells and tissues. * Don't forget to refer books! ### 3. Cardiogenic shock- it can be considered or referred as "pump failure". It occurs subsequent to the sudden decrease in cardiac output which accompanies sudden extensive damage to the heart (infarct, cardiac tamponad and rupture of the heart). ### 4. Neurogenic shock- implies a state of shock mediated by the nervous system which induces peripheral vessel dilatation (dilatation of the capillary bed). It occurs in animals with severe fright, anaesthesia, pain and trauma (without hemorrhage). The principal mechanism of this type of shock is peripheral vasodilatation with pooling of blood. ### Usually shock progress through the following 3 stages * i) Early stage: if there is a small reduction in the circulating blood volume, a variety of neurohormonal mechanisms like constriction of arteriolar bed, increased heart rate and others will maintain cardiac output and blood pressure near normal. Due to vasoconstriction there body parts will be cold and pale in color. * ii) Progressive stage: in this stage despite increased heart rate there is a decline in blood pressure and cardiac output. Due to lack of oxygen tissues in the different part of the body will be forced to undertake anaerobic glycolysis leading to metabolic acidosis. Hence there will be tachypnea (abnormally rapid respiration) and oliguria (reduced urine output) * iii) Irreversible stage: this is the stage at which the condition is not reversible or stoppable even with treatment. The reduced blood flow to the brain heart and kidney leads to ischemic (hypoxic) cell death in these organs. This may lead to coma (loss of consciousness), renal failure (if kidney fails to carry out its normal function), uremia (the presence of nitrogenous waste products in the blood) and death. ### The cellular and tissue changes induced by shock are essentially those of hypoxic injury. As stated above the most vulnerable organs are brain, heart, kidneys adrenal gland and gastrointestinal organs. * Grossly the organs will have cyanotic color due to partially oxygenated (acute general passive hyperemia). Petechial hemorrhages are numerous throughout the carcass. The body cavities contain edematous fluid. * Microscopically the capillaries and small veins are distended with blood. Focall hemorrhage are present. * Clinically the animal feels cold and without strength (depressed and lethargic). The body temperature is subnormal and skin cold. Respiration is shallow and irregular. Heart and pulse rates are very rapid. * Don't forget to refer books!