| Term | Definition |
|---|
| Body fluid | to maintain normal function each cell in the body must be surrounded by or have access to this. The composition of this is intricately regulated and depends to a large extent on the maintenance of the circulation. |
| Disturbance of blood supply and imbalance of body fluids | responsible for many commonly encountered disorders like edema, congestion, hemorrhage, and shock, as well as thrombosis, embolism and infarction. |
| Fluid compartments | approximately 60% of body weight is water. [1] Intravascular space (within vessels), [2] lymphatic space (surrounded by lymph endothelium), [3] intracellular space (66% of body water), and [4] interstitial/intercellular space (outside of vessels, outside of cells). |
| Endothelium | regulates the movement of solids, fluids, and gases across the fluid compartments by vesicular transport, filtration, and diffusion (active and passive processes). These cells: [1] provide a continuous monolayer of cells that serve as a permeability barrier, [2] synthesize several cytokines (PDGF, FGF, and IL-1), [3] generate prostacyclin, NO, and other molecules that regulate vascular tone, [4] extravasation of WBCs in tissue, [5] provides an anti-coagulant barrier between vascular space and the surrounding CT. |
| Virchow's triad of thrombosis | caused by [1] endothelial injury (most important), [2] abnormal blood flow, [3] hypercoagulability. |
| Non-inflammatory edema | can be generalized or localized. It is the net excess accumulation of fluid in the interstitial space or serous cavities (pleural, pericardial, peritoneal). Results from Starling forces that drive fluid out of the intravascular space. The balance of hydrostatic and oncotic pressure favors fluid filtration at the arterial end and absorption at the venular end of the capillary. Net outflow, fluid picked up by lymph vessels and returned to blood stream. |
| Hydrothorax | edema of the pleural space. |
| Hydropericardium | edema of the pericardial space. |
| Hydroperitoneum | edema of the peritoneal space. Ascites. |
| Causes of non-inflammatory edema | [1] increased intravascular hydrostatic pressure. Can be due to congestive heart failure (right side- pedal pitting, left side- pulmonary edema). Another example is cirrhosis of the liver can cause portal hypertension. [2] Reduced plasma osmotic pressure can occur due to albumin loss in nephrotic syndrome- usually periorbital edema. Or impaired serum protein synthesis by liver. [3] Lymphatic obstruction (Milroy disease or elephantiasis). [4] renal disease that leads to salt retention. [5] CNS failure can cause pulmonary edema by complex mech. [6] Cerebral edema results from CNS injury of disease leading to compromise of vascular supply. |
| Myxedema | a special form of non-inflammatory edema that occurs in chronic hypothyroidism. This develops insidiously due to thryoiditis or other causes of T3 and T4 insufficiency. Periorbital and peripheral edema, but differs from classic type in that it does not 'pit.' Due to accumulation of hydrophilic mucopolysaccharides in the CT. |
| Transudate | typical fluid of edema. Formation is the simplest response to inflammation or infection. Protein content is low and mostly albumin (<3gm/mL). With continued increase in vascular permeability exudates will develop (protein rich fluid). |
| Exudate | a fluid of edema. Protein rich (>3gm/mL). Implies increased vascular permeability. WBCs, RBCs, and fibrin strands are also found in the fluid due to leakage and chemotaxis. Examples include: peruitis and pleural effusion; inflammatory edema in bronchopneumonia; infected ascites; pericardial effusion following infarct or inflammation; spinal fluid in bacterial meningitis. Pus in a wound is an extreme example. |
| Congestion | engorgement of vessel with blood due to obstruction of circulatory pathways. A passive process due to impaired outflow of blood from a tissue. INFLOW obstruction- leading to the heart. Passive congestion results from capillary dilation proximal to obstruction- tissue engorged with relatively deoxygenated blood. Nutmeg liver is an example of chronic passive congestion due to cardiac inflow obstruction. OUTFLOW obstruction- in the heart- can be due to pulmonary artery or aortic stenosis or regurgitation. Cardiac hypertrophy may also result in outflow obstruction Peripheral outflow obstruction is due to vascular problems. When a major artery is obstructed its term an infarct. |
| Hemorrhage | extravasation of blood due to vessel rupture. Could be due to low platelet count or injury. Hematoma, patechiae, purpura (brown-red spots on skin), and ecchymoses are signs of this. |
| Hematoma | accumulation of blood in tissue or cavity. A sign of hemorrhage. |
| Patechiae | 2-3 mm hemorrhages, non-blanching, can be located on skin, mucus membranes, serosal surfaces. Cause by congestion or low platelet count. (also meningococcal infection). |
| Ecchymoses | large areas of black-blue discoloration due to rupture of small vessel. AKA as bruise. Can be caused by bleeding disorders, leukemia, or trauma. A sings of local hemorrhage. |
| Nutmeg liver | an example of chronic passive congestion due to cardiac inflow obsturctoin. |
| Steps of normal hemostasis | [1] vasoconstriction, [2] formation of primary plug by platelet binding to vWF and recruiting other platelets and binding to fibronogin, [3] formation of secondary plug by local activation of the coagulation cascade and former fibrin polymers, [4] anti-clotting mechanisms (plasminogen activator) confine clot to site of injury. |
| Blood coagulation | a series of events that involve the change in vessel wall, changes in the constituents of the blood, and changes in the flow patterns of the blood. Platelets bind to site of vascular injury, become activated, recruit other platelets and promote clotting reactions by PROVIDING AN ACTIVE SURFACE. A strong fibrin polymer intermixes with the aggregated platelets to form a stable plug. The clotting reactions are normally limited by glood flow, availability of procoagulant surface, the anticoagulant effects of surrounding normal endothelium, and the activation of fibrinolytic reactions. |
| Tissue factor | exposed by endothelial cells upon injury. A protein present in subendothelial tissue, platelets, and leukocytes that is necessary to initiate thrombin formation fro pro-thrombin. Thrombin then converts fibrinogen to fibrin. Thrombin also activates platelets (express fibrinogen receptors and secrete ADP). |
| Hemostatic plug | formed by activated platelets and fibrin polymer. |
| Endothelial factors that inhibit thrombosis | anti-thrombin III and thrombomodulin (inactivate thrombin), thrombin receptor that leads to secretion of vasodilators and promoters of the thrombolytic pathway) Tissue Factor inhibitor. |
| Endothelial factors that promote thrombosis | vWF, exposed collagen, and tissue factor. |
| Intrinsic pathway | Factor XII (Hagerman Factor) > Factor XI > Factor IX > Factor X > Factor II (Prothrombin to thrombin) > Factor I (Fibrinogen to fibrin). T.E.N.-X Contact activation (damaged surface). |
| Extrinsic pathway | Factor VII comes into contact with Tissue Factor > Factor X > Factor II (Prothrombin to thrombin) > Factor I (Fibrinogen to fibrin). Seven-ten. Vessel injury. |
| Thrombin (Factor IIa) activities | [1] generates fibrin monomers (cleaves fibrinogen), [2] Activates Factor Va and Factor VIII, [3] activates Factor XIIIa, [4] Activates Factor XIa, [5] activates platelets, and [6] complexes to thrombomodulin and activates protein C (anti-coagulative), [7] activates TAFI (fibrinolysis inhibitor, promotes clot formation). |
| Pathologic thrombosis | a pathologic process-inappropriate intravascular coagulation of the blood in any part of the circulatory system. Results from: [1] injury or dysfunction of the vascular system, including the endothelium, [2] cessation or reduction of blood flow, and/or [3] increased activity of the coagulation system. Important to understand the clinical consequences of this process like embolic complications and infarct. Fate of the thrombus depends on propagation, resolution/dissolution, embolization, organization and recanalization. |
| Hypercoagulable states | Genetic (e.g. mutation in Factor V) or Acquired (e.g. prolonged immobilization, myocardial infarction, tissue damage) |
| Tissue plasminogen activator (tPA) | a protein involved in the breakdown of blood clots. Catlyzes the conversion of plasminogen to plasmin, the major enzyme responsible for clot breakdown. |
| Mural thrombi | seen in heart chamber, especially in conditions that cause damage to the endothelium of the heart chambers. Myocarditis, endocarditis, and myocardial infarction predispose for these. |
| Arterial thrombi | these intravascular coagulates accumulate or build up towards the source of flow and may manifest as "lines of Zahn," which are due to alternate laying of platelets, fibrin, RBC and WBC. Contrast to venous thrombi which extend in the direction of flow. |
| Cancer | causes an increased propensity for thrombosis. Certain ones release Tissue Factor, and other cysteine proteases which promote blood coagulation and lead to endothelial injury and venous thrombosis. Trousseau's syndrome (migratory thrombophlebitis) is associated with carcinomas of the lung, pancreas, ovary, or colon. |
| Embolus | an abnormal mass of material, either solid or gaseous, which is transported in the blood from one site to a distant site where is obstructs blood flow. Such masses could be [1] thrombi (the usual source unless otherwise stated), [2] air, [3] fat (fracture of long bones), [4] bone marrow, [5] tumor, [6] debris from atherosclerotic plaque, [7] foreign body (e.g. heart valve prosthesis). |
| Pulmonary embolism | blockage of the main artery of the lung or one of its branches by a substance that has travelled from elsewhere in the body through the bloodstream. Generally due to a released thrombus that had been occluding a long segment of the venous drainage of the lower limb. Symptoms: difficulty breathing, chest pain, and palpitations. |
| Systemic embolism | generally derived from the left side of the heart (valvular endocarditis, mural thrombus in left chambers). Intracardiac (80%), aortic aneurysm, paradoxical embolus, lower extremities, brain, etc. Clinical consequences depend on extend of collateral circulation. |
| Paradoxical embolus | when an embolus arises from the venous circulation or right side of the heart and travels to the brain, kidney, or spleen on the systemic side. This is observed in patients with a right to left shunt (an atrial septal defect or patent foramen ovale). Normally such an embolus should cause a pulmonary infarct. |
| Infarct | OCCLUSION of a blood vessel by a thrombus or embolus (irrespective of nature). Leads to ischemia which will result in the necrosis of the tissue. If located in myocardium, spleen, kidney, brain, lung, etc it causes coagulative or liquefactive (brain) necrosis. Depending on extent of collateral circulation these are described as pale/white (in areas of end arterial circulation) or red. Complications: myocardial infarction may cause hemorrhage, arrhythmia, rupture (cardiac tamponade), scarring, and aneurysm. Splenic infarction can lead to sepsis and rupture with intraperitoneal hemorrhage. |
| Cardiac tamponade | an emergency condition in which fluid accumulates in the pericardium (the sac in which the heart is enclosed). If the fluid significantly elevates the pressure on the heart it will prevent the heart's ventricles from filling properly. |
| Shock | circulatory collapse that leads to inadequate perfusion and reduced oxygenation of tissue. Hypotension. The final common pathway of lethal clinical events that can follow from severe hemorrhage, large pulmonary embolism, extensive trauma or burns, a large myocardial infarction or microbial sepsis. Several varieties: [1] hypovolemic, [2] cardiogenic, [3] neurogenic, [4] anaphylactic, [5] septic. Hypovolemic shock: may result from hemorrhage, loss of fluid, severe burns, acut hemorrhagic pancreatitis, trauma, crush injury. |
| Cardiogenic shock | due to loss of myocardial contractility (infacrction, tamponade, valve rupture) |
| Neurogenic shock | due to injury of the CNS leading to vasodilation. |
| Anaphylactic shock | due to injection of foreign serum or protein (e.g. bee sting) that cause a generalized IgE mediated hypersensitivity response with vasodilation and increased vascular permeability mediated by vasoactive histamine, serotonin and kinins. |
| Septic shock | due to microbial infection, mostly G(-) endotoxin (lipid A of LPS), but also G(+) like Staph TSS. LPS is bound by LPB which bind to CD14 and stimulate the Toll-like receptors on monocytes and endothelial cells. These cells release IL-1, TNF-alpha and other vasoactive substances. The leading cause of mortality in ICUs. Results in multiorgan failure due to vasodilation, myocardial pump failure due to decreased contractility, and DIC (activates Factor XII) leads to hypoperfusion of vital organs. Not associated with hypovolemia, rather increased endothelial permeability and systemic coagulation. At first body can compensate with tachycardia, vasoconstriction and renal fluid conservation, but eventually condition progresses and tissue is injured and metabolic acidosis occurs. |
| Morphologic abnormalities of shock | result from cellular hypoxia leading to cell death. Multiple organs display tpical changes of hypoperfusion and hypoxia. DIC causes fibrin micothrombi in the microcirculation. The heart show focal subendocardial and subepicardial hemorrhages including necrosis. The brain shows hypoxic encephalophathy. Kidneys show acute tubular necrosis. The lungs how hyaline membrane disease, edema and diffuse alveolar damage- resulting in adult respiratory distress syndrome (ARDS). The adrenals show stress, depletion of lipid and hemorrhagic necrosis. The GI tract shows mucosal hemorrhage and necrosis. |
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