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Post-operative control of amount of fluid (not to be given more than 2/3 of the daily requirement) order 160mg malegra dxt plus with mastercard, electrolytes malegra dxt plus 160mg for sale, positioning in 20-30 degree elevation of the bed and management convulsion and of late sequel of head injury should be accomplished. Displaced bone fragments and inter-vertebral disks may herniate to the spinal cord causing compression, commonly seen in cervical and thoraco lumbar region. Brown-sequard Syndrome: Ipsilateral paresis and contra-lateral loss of pain and temperature sensation. Anterior spinal cord syndrome: Paralysis occurs below the level of the lesion with loss of temperature, touch and pain sensation. Central cord syndrome: hand and upper extremities are affected with sparing of lower extremities. Both complete and incomplete injuries of the spinal cord can result in neurogenic bladder. Immediately after injury, spinal shock ensues in which bladder reflex does not develop. There could be a finding of flaccid paralysis, depressed deep tendon reflex and sensory level. Patient assessment Early detection of spinal injury will prevent further injury to the cord. Multiple injuries, seat belt markings and neurologic findings should alert the possibility of spinal injury. In conscious patients biplanar x-rays of the symptomatic part of spine are adequate. In cervical spines, unstable injuries are easily overlooked in lateral and A-P films. It is treated symptomatically initially with rest, then with splinting and mobilization as necessary. When you assess his level of consciousness, he opens his eyes when pinched, withdraws from pain and he is confused. Although the musculoskeletal system can be affected by several conditions like congenital, metabolic or neoplastic diseases, traumatic and infectious disorders are the most important ones in developing countries. Etiology • Staphylococcus aureus is the agent in 80% of cases • Gram negative rods and Staphylococcus in neonates • H. Influenza is seen in children under 5 years of age • History of trauma is common and may predispose children to osteomyelitis Pathology Bacteria reach the bone mostly via the hematogenous route. Infection begins in the metaphysis of a long bone and spreads through the cortex and medullary cavity causing thrombosis to vessels and bone infarction. Cloxacillin + Gentamycine - Children under 5 years:- Penicillinase resistant penicillins + Anti H. Cloxacillin + Chloramphenicol - Patients above 5 years:- Penicllinase resistant penicillin E. Pathology: The dead bone (sequester) lies in an abscess cavity surrounded by a newly formed bone (Involcrum) under the elevated periosteum. There may be skin hyper pigmentation around the sinus and palpable bone thickening. Treatment Antibiotics: Used for acute exacerbation and perioperate for about six weeks. Surgery: Surgery is done to remove a dead bone (sequesterectomy) or to eliminate an abscess cavity (saucerization). Conservative treatment is considered in a patient with minimal discharge and no obvious sequestrum or bone cavity. Amputation may be considered for extensive bone involvement and heavy discharge or frequent flare-ups which incapacitate the patient. Etiology: It varies in different age groups and is similar to that of acute osteomyelitis. Bacteria may reach the joint via the blood, local extension of osteomyelitis or directly in penetrating wounds of the joint. The pus formed in the joint is chondrolytic and destroys the joint cartilage if not evacuated. Diagnosis: History: The usual presenting symptoms are joint pain, swelling and fever. Immobilize the affected joint in functional position until inflammation subsides and physiotherapy to prevent joint stiffness. The intervertebral discs, the hip and knee joints are the most frequently affected. X-ray: - Joint space narrowing - Sub chondral bone destruction - Periarticular osteoporosis Open biopsy of the joint is done if diagnosis is still in doubt. Mechanism of injury 1- Tubular bone: - Direct violence to the bone - Indirectly due to twisting or angulation 97 2- Cancellous bone: - may be fractured by compression E. Transverse fracture of the patella Bone Healing o Progresses through the phase of hematoma, cellular proliferation, callus formation and remodeling o Generally takes longer than soft tissue healing o In general, a long bone takes 6-12 weeks to heal in an adult and 3-6 weeks in children. Associated life threatening injuries may be missed if evaluation of the patient is not systematic. B) Local treatment of the fracture:- I-Reduction • Means bringing the fractured bone to normal or near normal anatomic position.

E-cadherin loss at adherens junctions is a marker of poorly differentiated carcinomas purchase malegra dxt plus 160 mg with amex. These junctions may also be disassembled by phosphorylation of proteins by activated tyrosine kinase oncoproteins (e malegra dxt plus 160 mg amex. Activation of tyrosine kinase oncoproteins or over-expression of integrin-linked kinases suppresses detached cell apoptosis (anoikis) 3. One domain maintains latency, and +2 another ligates Zn (required for activity) i. Platelet adhesion – thrombospondin acts as a bridge between tumour/platelet integrins. Homing to organs is determined by the blood flow from the primary tumour, and the extent to which the new location can provide for colonisation. Ras Æ activation of the activator protein-1 complex Æ transcription of many genes: 1. Linear energy transfer – energy transferred to the medium per unit track length of the ionising particle. Based on high dose, high dose rate exposure using a zero threshold linear extrapolation model, with correction for dose rate effects c. Note that there is a small risk of inducing fatal cancer whenever using ionising radiation in medicine – there is no threshold 2. Threshold is only because a certain number of cells must die before clinical symptoms present – the underlying process is stochastic 3. Damage to normal tissues in the radiation field, particularly haemopoetic and gastrointestinal. Late effects in most tissues due o vascular endothelium damage and chronic inflammation/fibrosis Effects of ionising radiation on individual cells: 530. Reproductive (post-mitotic) cell death – only significant for proliferating tissues. May activate a proto-oncogene or inactivate a tumour suppressor gene (Æ carcinogenesis) 4. Hypoxic cells resistant to ionising radiation – O2 sensitises, thiols protective b. It can be used to describe various immune mechanisms that harm the individual, including transplant rejection and autoimmune diseases. Mast cell release of histamine (Æ oedema), proteases, chemotoxins, cytokines, arachidonic metabolites b. Granulomatous inflammation – epithelioid and giant cells Autoimmune diseases are classified into two major groups, those affecting a single organ and those that are systemic (connective tissue or collagen diseases). Loss of self tolerance (failure of clonal deletion, failure of T-cell suppression) b. Clinical features – rash, fever, joint and pleuritic chest pain with waves of remission. Glandular destruction with infiltration of T helper and cytotoxic T cells – localisation to salivary glands unexplained 2. Salivary glands – lymphocyte infiltration Æ fibrosis, ulceration/inflammation of cornea, conjunctiva, oral mucosa 2. Lilac discoloration of the upper eyelids, periorbital oedema Vasculitis refers to (primary) inflammation of the vessels – this may occur without existing tissue damage and mediates tissue damage. Pathogenesis seems to involve hypersensitivity reactions – initiating factors unknown a. Takayasu’s arteritis (pulseless disease), females 15-40 – granulomatous inflammation of vessels including the aorta b. Acute presentation with fever and erythema of conjunctiva, mouth, hands and feetÆ skin desquamation with cervical node enlargement 2. Alimentary tract – abdominal pain, nausea, vomiting, melaena, occasional perforation 3. Wegener’s granulomatosis, middle-aged adults – necrotising respiratory tract granulomas, necrotising vasculitis, necrotising focal glomerulonephritis. Churg-Strauss syndrome (allergic granulomatosis and angiitis) – vascular lesions, bronchial asthma, eosinophilia 1. Leukocytoclastic vasculitis – Henoch-Schonlein purpura, essential cryoglobulinaemia, allergic vasculitis, serum sickness vasculitis, lupus vasculitis, hepatitis B microscopic polyarteritis Amyloidosis is the deposition of an abnormal extracellular material between cells in various tissues, leading to pressure atrophy or loss of function. The two main types are sequelae of extensive prolonged inflammatory activity (secondary amyloidosis) or due to excessive production of plasma cell derived immunoglobulin light chain (primary amyloidosis). These are derived from proteins with a β-pleated sheet configuration (stable, digestion-resistant).

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Throughout fetal development and into childhood growth and development order 160 mg malegra dxt plus with mastercard, bone forms on the cartilaginous matrix cheap 160mg malegra dxt plus visa. Some additional cartilage will be replaced throughout childhood, and some cartilage remains in the adult skeleton. Intramembranous Ossification During intramembranous ossification, compact and spongy bone develops directly from sheets of mesenchymal (undifferentiated) connective tissue. The flat bones of the face, most of the cranial bones, and the clavicles (collarbones) are formed via intramembranous ossification. The process begins when mesenchymal cells in the embryonic skeleton gather together and begin to differentiate into specialized cells (Figure 6. Some of these cells will differentiate into capillaries, while others will become osteogenic cells and then osteoblasts. Although they will ultimately be spread out by the formation of bone tissue, early osteoblasts appear in a cluster called an ossification center. The osteoblasts secrete osteoid, uncalcified matrix, which calcifies (hardens) within a few days as mineral salts are deposited on it, thereby entrapping the osteoblasts within. As osteoblasts transform into osteocytes, osteogenic cells in the surrounding connective tissue differentiate into new osteoblasts. Osteoid (unmineralized bone matrix) secreted around the capillaries results in a trabecular matrix, while osteoblasts on the surface of the spongy bone become the periosteum (Figure 6. Intramembranous ossification begins in utero during fetal development and continues on into adolescence. The last bones to ossify via intramembranous ossification are the flat bones of the face, which reach their adult size at the end of the adolescent growth spurt. In a long bone, for example, at about 6 to 8 weeks after conception, some of the mesenchymal cells differentiate into chondrocytes (cartilage cells) that form the cartilaginous skeletal precursor of the bones (Figure 6. As the matrix calcifies, 234 Chapter 6 | Bone Tissue and the Skeletal System nutrients can no longer reach the chondrocytes. Blood vessels invade the resulting spaces, not only enlarging the cavities but also carrying osteogenic cells with them, many of which will become osteoblasts. This penetration initiates the transformation of the perichondrium into the bone-producing periosteum. By the second or third month of fetal life, bone cell development and ossification ramps up and creates the primary ossification center, a region deep in the periosteal collar where ossification begins (Figure 6. While these deep changes are occurring, chondrocytes and cartilage continue to grow at the ends of the bone (the future epiphyses), which increases the bone’s length at the same time bone is replacing cartilage in the diaphyses. By the time the fetal skeleton is fully formed, cartilage only remains at the joint surface as articular cartilage and between the diaphysis and epiphysis as the epiphyseal plate, the latter of which is responsible for the longitudinal growth of bones. After birth, this same sequence of events (matrix mineralization, death of chondrocytes, invasion of blood vessels from the periosteum, and seeding with osteogenic cells that become osteoblasts) occurs in the epiphyseal regions, and each of these centers of activity is referred to as a secondary ossification center (Figure 6. The reserve zone is the region closest to the epiphyseal end of the plate and contains small chondrocytes within the matrix. These chondrocytes do not participate in bone growth but secure the epiphyseal plate to the osseous tissue of the epiphysis. The proliferative zone is the next layer toward the diaphysis and contains stacks of slightly larger chondrocytes. Chondrocytes in the next layer, the zone of maturation and hypertrophy, are older and larger than those in the proliferative zone. The longitudinal growth of bone is a result of cellular division in the proliferative zone and the maturation of cells in the zone of maturation and hypertrophy. Most of the chondrocytes in the zone of calcified matrix, the zone closest to the diaphysis, are dead because the matrix around them has calcified. Capillaries and osteoblasts from the diaphysis penetrate this zone, and the osteoblasts secrete bone tissue on the remaining calcified cartilage. When the chondrocytes in the epiphyseal plate cease their proliferation and bone replaces the cartilage, longitudinal growth stops. How Bones Grow in Diameter While bones are increasing in length, they are also increasing in diameter; growth in diameter can continue even after longitudinal growth ceases. Osteoclasts resorb old bone that lines the medullary cavity, while osteoblasts, via intramembranous ossification, produce new bone tissue beneath the periosteum. The erosion of old bone along the medullary cavity and the deposition of new bone beneath the periosteum not only increase the diameter of the diaphysis but also increase the diameter of the medullary cavity. Bone Remodeling The process in which matrix is resorbed on one surface of a bone and deposited on another is known as bone modeling. However, in adult life, bone undergoes remodeling, in which resorption of old or damaged bone takes place on the same surface where osteoblasts lay new bone to replace that which is resorbed. Those influences are discussed later in the chapter, but even without injury or exercise, about 5 to 10 percent of the skeleton is remodeled annually just by destroying old bone and renewing it with fresh bone. Those with the most severe forms of the disease sustain many more fractures than those with a mild form.

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Studies have demonstrated that mixed venous saturations are a reliable and early indicator of cardiovascular dysfunction and failure to measure this may worsen outcomes in some situations purchase malegra dxt plus 160 mg amex. Another indicator of failing oxygen delivery is the development of lactic acidosis malegra dxt plus 160 mg discount. The sequential evaluation of serum lactate levels provides important assessment of the adequacy of oxygen delivery. Lactate levels are usually high immediately after surgery but should decrease to < 2. Metabolic acidosis that is not accompanied by elevated lactate is usually a hyperchloremic metabolic acidosis (non anion gap metabolic acidosis) and generally resolves without treatment. Hematology, thrombosis and hemostasis Postoperative bleeding is the result of inadequate surgical hemostasis or of coagulopathy, either due to residual heparin, to dilutional effects, or to disseminated intravascular coagulation. If bleeding is not corrected after correction of coagulopathy or if the blood loss is greater than 10 cc/kg/hour, surgical bleeding should be considered and exploration strongly considered. Chest tubes and mediastinal drainage tubes must be kept clear and patent if there is ongoing bleeding in order to prevent the occurrence of cardiac tamponade. The onset is 5-10 days after first exposure to heparin and hours to 2-3 days with re-exposure. Use of alternative anticoagulation is imperative in pre-existing or new thrombosis and should be strongly considered for prophylaxis. Argatroban, a hepatically excreted, synthetic anti-thrombin with a t 1/2 of ~ 40-50 minutes, is presently our choice. Normal versus Abnormal Convalescence Convalescence after cardiac surgery may be characterized as normal or abnormal. Normal convalescence is recovery that is expected given the pre-operative state of the patient, the procedure performed, and the expected effects of cardiopulmonary bypass or other interventions. Abnormal convalescence is recovery that is prolonged or unexpected given what is known about the patient and the interventions that have been performed. It may be due to unknown or under appreciated abnormal pre-operative anatomy or physiology, to unexpected complications of bypass, to residual anatomic defects, or to abnormalities in other organ systems such as pneumonia or sepsis. It is crucial to identify abnormal convalescence and to characterize it thoroughly so that appropriate intervention can take place in a timely fashion. Most congenital heart defects are repaired on cardiopulmonary bypass and require a period of time during which the circulation to the heart is interrupted by aortic cross clamping and infusion of cardioplegia. This provides the surgeon with a still, flaccid heart on which to operate, however, the heart may be "ischemic" during this time. Ischemic injury to myocardium, produced (or unable to be prevented) by the protection used for operative repair, can present serious problems in the postoperative period. For the intensive care physician, knowledge of the aortic cross clamp time (ischemic time) and the period of total circulatory arrest is important. These times can be predictive of the degree of postoperative ventricular dysfunction and the amount of support that can be predicted. Patients who require extracardiac repair only and patients with simple shunting lesions who require closure (patch or ligature) without valvar involvement should require minimal inotropic support. When performed in the neonatal period, these children may require inotropic support with a single agent. Requirement of multiple agents and increasing inotropic requirements indicate abnormal convalescence. Patients with more complicated perioperative pathophysiology and those who require circulatory arrest will require more intensive myocardial and respiratory support. In the first 24 - 48 hours inotropic support may be generous and escalation of inotropic support should be anticipated in the first 24 hours due to myocardial edema/injury. Failure to respond to moderate increases in inotropic therapy and the need for high levels of inotropic therapy (Dopamine/Dobutamine > 15 µg/kg/min, Milrinone > 1. Management of pulmonary insufficiency in the postoperative period requires an understanding of the physiologic consequences of cardiopulmonary bypass. Diuresis consistent with the hemodynamic status of the child may encourage the resolution of pulmonary edema and atelectasis. The effects of cardiopulmonary bypass on renal function are not completely understood. Cardiopulmonary bypass with hypothermia, non-pulsatile perfusion, and reduced mean arterial pressure causes the release of angiotensin, renin, catecholamines and antidiuretic hormones. After total circulatory arrest, it is common to observe a period of oliguria or anuria which usually resolves after 24 hours. Treatment of renal dysfunction in the postoperative period includes increasing renal perfusion pressure using inotropic agents. Diuretics are the primary agents for promoting urinary output after cardiopulmonary bypass.

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