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    By V. Pedar. Dallas Baptist University.

    Vascular Spasm When a vessel is severed or punctured 5 mg proscar visa, or when the wall of a vessel is damaged buy proscar 5mg line, vascular spasm occurs. The circular layers tend to constrict the flow of blood, whereas the longitudinal layers, when present, draw the vessel back into the surrounding tissue, often making it more difficult for a surgeon to locate, clamp, This OpenStax book is available for free at http://cnx. The vascular spasm response is believed to be triggered by several chemicals called endothelins that are released by vessel-lining cells and by pain receptors in response to vessel injury. Formation of the Platelet Plug In the second step, platelets, which normally float free in the plasma, encounter the area of vessel rupture with the exposed underlying connective tissue and collagenous fibers. The platelets begin to clump together, become spiked and sticky, and bind to the exposed collagen and endothelial lining. This process is assisted by a glycoprotein in the blood plasma called von Willebrand factor, which helps stabilize the growing platelet plug. As platelets collect, they simultaneously release chemicals from their granules into the plasma that further contribute to hemostasis. Plug formation, in essence, buys the body time while more sophisticated and durable repairs are being made. In a similar manner, even modern naval warships still carry an assortment of wooden plugs to temporarily repair small breaches in their hulls until permanent repairs can be made. Coagulation Those more sophisticated and more durable repairs are collectively called coagulation, the formation of a blood clot. The process is sometimes characterized as a cascade, because one event prompts the next as in a multi-level waterfall. The result is the production of a gelatinous but robust clot made up of a mesh of fibrin—an insoluble filamentous protein derived from fibrinogen, the plasma protein introduced earlier—in which platelets and blood cells are trapped. The process is complex, but is initiated along two basic pathways: • The extrinsic pathway, which normally is triggered by trauma. All three pathways are 2+ dependent upon the 12 known clotting factors, including Ca and vitamin K (Table 18. Vitamin K (along with biotin and folate) is somewhat unusual among vitamins in that it is not only consumed in the diet but is also synthesized by bacteria residing in the large intestine. Some recent evidence indicates that activation of various clotting factors occurs on specific receptor sites on the surfaces of platelets. Extrinsic Pathway The quicker responding and more direct extrinsic pathway (also known as the tissue factor pathway) begins when damage occurs to the surrounding tissues, such as in a traumatic injury. This enzyme complex leads to activation of factor X (Stuart–Prower factor), which activates the common pathway discussed below. Intrinsic Pathway The intrinsic pathway (also known as the contact activation pathway) is longer and more complex. Common Pathway Both the intrinsic and extrinsic pathways lead to the common pathway, in which fibrin is produced to seal off the vessel. As these proteins contract, they pull on the fibrin threads, bringing the edges of the clot more tightly together, somewhat as we do when tightening loose shoelaces (see Figure 18. This process also wrings out of the clot a small amount of fluid called serum, which is blood plasma without its clotting factors. During this process, the inactive protein plasminogen is converted into the active plasmin, which gradually breaks down the fibrin of the clot. Additionally, bradykinin, a vasodilator, is released, reversing the effects of the serotonin and prostaglandins from the platelets. This allows the smooth muscle in the walls of the vessels to relax and helps to restore the circulation. Several circulating plasma anticoagulants play a role in limiting the coagulation process to the region of injury and restoring a normal, clot-free condition of blood. For instance, a cluster of proteins collectively referred to as the protein C system inactivates clotting factors involved in the intrinsic pathway. And as noted earlier, basophils release heparin, a short-acting anticoagulant that also opposes prothrombin. A pharmaceutical form of heparin is often administered therapeutically, for example, in surgical patients at risk for blood clots. The coagulation cascade restores hemostasis by activating coagulation factors in the presence of an injury. How does the endothelium of the blood vessel walls prevent the blood from coagulating as it flows through the blood vessels?

    In elective surgery proscar 5 mg mastercard, patients should not eat or drink anything after midnight on the day before surgery purchase 5mg proscar with mastercard. Post-operative care, complications and their Treatment Post-operative care Post-operative care is care given to patients after an operation in order to minimize post operative complications. Early detection and treatment of post operative complications is possible if there is optimal care. Some of the care is given to all post operative patients, while the rest are specific to the type of operation. Patients encouraged to ambulate In the following sessions, we will focus on common postoperative complications. Cardiovascular complications Shock Postoperative efficiency of circulation depends on blood volume, cardiac function, neurovascular tone and adrenal secretions. Shock, or failure of the circulation, may follow: ƒ Excessive blood loss ƒ Escape of vascular fluid into the extra vascular compartments (“third spacing”) ƒ Marked peripheral vasodilatations ƒ Sepsis ƒ Adrenocortical failure ƒ Pain or emotional stress ƒ Airway obstruction Treatment includes ƒ Arresting hemorrhage ƒ Restore fluid and electrolyte balance ƒ Correct cardiac dysfunction ƒ Establish adequate ventilation ƒ Maintain vital organ function and avert adrenal cortical failure ƒ Control pain and relief apprehension ƒ Blood transfusion if required. Thrombophlebitis Superficial thrombophlebitis It is usually recognized within the first few days after operation. Clinical features A segment of superficial saphenous vein becomes inflamed manifested by: ƒ Redness ƒ Localized heat ƒ Swelling ƒ Tenderness 27 Treatment includes ƒ Warm moist packs ƒ Elevation of the extremity ƒ Analgesics Anticoagulants are rarely indicated when only superficial veins are involved. Thrombophlebitis of the deep veins Occurs most often in the calf but may also occur in the thigh or pelvis. Clinical features It may be asymptomatic or there may be dull ache or frank pain in the affected leg or calf. Treatment • Elevation of the limbs • Application of full leg gradient pressure elastic hose • Anticoagulants Prevention: Early ambulation Pulmonary embolism Pre-disposing factors ƒ Pelvic surgery ƒ Sepsis ƒ Obesity ƒ Malignancy and ƒ History of pulmonary embolism or deep vein thrombosis It usually occurs around the seventh to tenth post-operative day. The diagnosis should be suspected if cardiac or pulmonary symptoms occur abruptly. Clinical features Patients with large emboli develop chest pain; severe dyspnea, cyanosis, tachycardia, hypotension or shock, restlessness and anxiety. In small emboli, the diagnosis is suggested by the sudden onset of pleuritic chest pain sometimes in association with blood-streaked sputum, and dry cough may develop. Physical examination may elicit pleural friction rub, but in many cases there are no classical diagnostic signs. Treatment ƒ Cardiopulmonary resuscitation measures ƒ Treatment of acid-base abnormality ƒ Treatment of shock. Immediate therapy with heparin is indicated even in the absence of a definitive diagnosis. Pulmonary Complications About 30% of deaths that occur within six weeks after operation are due to pulmonary complication. Atelectasis, pneumonia, pulmonary embolism and respiratory distress syndrome from aspiration or sepsis, fluid overload or infection are the most common pulmonary complications. Atelectasis Definition Atelectasis is a pulmonary complication of early postoperative period. It is a condition characterized by areas of airway collapse distal to an occlusion. Predisposing factors Include chronic bronchitis, asthma, smoking and respiratory infection. Inadequate immediate postoperative deep breathing and delayed ambulation also increase the risk. Clinical features ƒ Fever in the immediate post operative period ƒ Increased pulse and respiratory rate ƒ Cyanosis ƒ Shortness of breath ƒ Dull percussion note with absent breath sounds Investigation X-ray findings include patchy opacity and evidence of mediastinal shift towards the atelectatic lung. Clinical features ƒ Fever in the first few postoperative days ƒ Respiratory difficulty ƒ Cough becomes productive ƒ Physical examination may reveal evidence of pulmonary consolidation Investigation Chest-x-ray may show diffuse patchy infiltrates or lobar consolidation. Prevention and treatment Chance of pulmonary aspiration can be minimized by - Fasting - Naso-gastric tube decompression If aspiration of gastric content occurs; an endotracheal tube should be placed and the air way suctioned and lavaged. This often results in re- alignments of the bowel loops and relief of the obstruction. If the obstruction doesn’t respond within 48-72 hours, re- operation is necessary. Inability of the patient to void is often due to pain caused by using the voluntary muscles to start the 31 urinary stream.

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    Quinidine: ‘Innocent bystander’ (immune complex) mechanism In some patients previously sensitized to quinidine generic 5 mg proscar free shipping, and taking it again 5 mg proscar mastercard, the drug reacts with a quinidine antibody, often IgM, to form an immune complex. This complex is then adsorbed onto the red cell membrane; the red cell is considered an “innocent stander’ because it is not the direct target of the antibody. The immune complexes often activate complement, and an abrupt and life- threatening intravascular hemolytic anemia may 294 Hematology develop. The coombs test is positive for complement; the immune complexes themselves do not bind firmly to the cell. Cephalosporins: Membrane modification These drugs cause a positive direct Coombs test through a non-immunologic mechanism. Cephalothin and other cephalosporins are capable of altering the red cell membrane so that proteins, including complement and an assortment of γ-globulins, are nonspecifically adsorbed. However, the red cell eluate does not react with any other cells, because 295 Hematology the mixture of γ-globulins does not include any predominantly red cell antigen-specific antibody. Hemolytic transfusion reactions The differential diagnosis of a positive direct antiglobulin test includes not just red cell autoantibodies but also alloantibodies-antibodies in the patient directed against foreign red cell antigens. These antibodies are either “naturally occurring,” in that individuals acquire them without specific exposure to the red cell antigen, or “immune,” form red cell transfusions. If inadvertently transfused with group A red cells, this patient’s anti-A would 296 Hematology immediately react with the donor cells. The direct Coombs test is positive due complement fixation, but may become negative within hours to days, depending on how rapidly the group a cells are destroyed. The presence of urine hemosiderin beginning 3 to 5 days after the transfusion attests to the recent presence of hemoglobinemia. If the patient then receives an antigen- positive unit, an anamnestic rise in antibody occurs over the next 3 to 21 days. Here, red cell destruction is usually leisurely, since the cells are eliminated only after they are coated with sufficient antibody, which depends on the rapidity with which it is produced. The direct Coombs test on a posttransfusion blood specimen is positive due to IgG- coated transfused red cells. The patient’s antibody screen, negative before the transfusion, becomes positive shortly 297 Hematology afterward. Hemolytic disease of the newborn This hemolytic process actually begins in utero to the baby of a mother with IgG red cell antibodies. In the past, many Rh(D)- negative women became sensitized to the red cell antigen D at the time of birth of a first Rh-positive child, because at birth it is common for a small volume of fetal cells to enter the maternal circulation. Rh-positive fetuses carried by a sensitized Rh-negative mother can be severely affected by the IgG anti-D. Some babies develop profound in utero anemia with congestive heat failure (hydrops fetalis), leading to stillbirth. Over time, some patients develop hypochromic microcytic red cells due to progressive iron deficiency, resulting form hemoglobinuria and hemosiderinuria. The Ham test involves the addition of acidified serum from a normal volunteer to the patient’s red cells. Since occasional false positives occur, positive results require confirmation with the more complex and rigorous Ham test. Leukemia The leukemias are a group of disorders characterized by the accumulation of abnormal white cells in the bone marrow. These abnormal cells may cause bone marrow failure, a raised circulating white cell count and infiltrate organs. Thus common but not essential features include abnormal white cells in the peripheral blood, a raise total white cell count, evidence of bone marrow failure (i. Other chronic types include hairy cell leukemia, prolymphocytic leukemia and various leukemia/lymphoma syndromes. In acute leukemia, in which there are over 50% myeloblasts or lymphoblasts in the bone marrow at clinical presentation, the blast cells fail to differentiate normally but are capable of further divisions. Their accumulation results in replacement of the normal hemopoietic precursor cells of the bone marrow by myeloblasts or lymphoblasts and, ultimately in bone marrow failure.

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    Telophase is characterized by the formation of two new daughter nuclei at either end of the dividing cell proven 5mg proscar. These newly formed nuclei surround the genetic material proscar 5 mg low price, which uncoils such that the chromosomes return to loosely packed chromatin. The cleavage furrow is a contractile band made up of microfilaments that forms around the midline of the cell during cytokinesis. One of these cells (the “stem cell”) enters its own cell cycle; able to grow and divide again at some future time. The other cell transforms into the functional cell of the tissue, typically replacing an “old” cell there. In some cases, a cell may divide its genetic material and grow in size, but fail to undergo cytokinesis. Cell Cycle Control A very elaborate and precise system of regulation controls direct the way cells proceed from one phase to the next in the cell cycle and begin mitosis. Precise regulation of the cell cycle is critical for maintaining the health of an organism, and loss of cell cycle control can lead to cancer. Mechanisms of Cell Cycle Control As the cell proceeds through its cycle, each phase involves certain processes that must be completed before the cell should advance to the next phase. A checkpoint is a point in the cell cycle at which the cycle can be signaled to move forward or stopped. At each of these checkpoints, different varieties of molecules provide the stop or go signals, depending on certain conditions within the cell. By interacting with many additional molecules, these triggers push the cell cycle forward unless prevented from doing so by “stop” signals, if for some reason the cell is not ready. Even during mitosis, a crucial stop2 and go checkpoint in metaphase ensures that the cell is fully prepared to complete cell division. The metaphase checkpoint ensures that all sister chromatids are properly attached to their respective microtubules and lined up at the metaphase plate before the signal is given to separate them during anaphase. These control molecules determine whether or not the cell is prepared to move into the following stage. If the abnormal cells continue to divide unstopped, they can damage the tissues around them, spread to other parts of the body, and eventually result in death. In healthy cells, the tight regulation mechanisms of the cell cycle prevent this from happening, while failures of cell cycle control can cause unwanted and excessive cell division. Failures of control may be caused by inherited genetic abnormalities that compromise the function of certain “stop” and “go” signals. The process of a cell escaping its normal control system and becoming cancerous may actually happen throughout the body quite frequently. Fortunately, certain cells of the immune system are capable of recognizing cells that have become cancerous and destroying them. If the resulting tumor does not pose a threat to surrounding tissues, it is said to be benign and can usually be easily removed. Cancer Arises from Homeostatic Imbalances Cancer is an extremely complex condition, capable of arising from a wide variety of genetic and environmental causes. Cell cycle control is an example of a homeostatic mechanism that maintains proper cell function and health. While progressing through the phases of the cell cycle, a large variety of intracellular molecules provide stop and go signals to regulate movement forward to the next phase. These signals are maintained in an intricate balance so that the cell only proceeds to the next phase when it is ready. Cruise control will continually apply just the right amount of acceleration to maintain a desired speed, unless the driver hits the brakes, in which case the car will slow down. Similarly, the cell includes molecular messengers, such as cyclins, that push the cell forward in its cycle. In addition to cyclins, a class of proteins that are encoded by genes called proto-oncogenes provide important signals that regulate the cell cycle and move it forward. In contrast, a second class of genes known as tumor suppressor genes sends stop signals during a cell cycle.

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