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When the sympathetic nervous system is activated discount actos 45mg without a prescription diabetes mellitus type 2 news, about half the blood volume of the liver can be expelled into the general circulation discount actos 30 mg fast delivery diabetes signs of low sugar. Because up to 15% of the total blood volume is in the liver cheap actos express control diabetes pdf, constriction of the hepatic vasculature can significantly increase the circulating blood volume during times of cardiovascular stress. At rest, the skeletal muscle vasculature accounts for about 25% of systemic vascular resistance and individual muscles receive a low blood flow of about 2 to 6 mL/min/100 g. The dominant mechanism controlling skeletal muscle resistance at rest is the sympathetic nervous system; local regulatory mechanisms become more significant with high muscle metabolism (e. Resting skeletal muscle has remarkably low oxygen consumption per 100 g of tissue, but its large mass makes its metabolic rate a major contributor to the total oxygen consumption in a resting person. Skeletal muscle blood flow is varied by both sympathetic neural and local metabolic factors. Skeletal muscle blood flow can increase 10- to 20-fold or more during the maximal vasodilation associated with high-performance aerobic exercise. During exercise, the effects of accumulation of local vasodilator agents in active skeletal muscle far exceed the effect of sympathetic neural vasoconstriction on vessels within the skeletal muscle. Under such circumstances, total muscle blood flow may increase to values three or more times higher than resting cardiac output. Cardiac output itself can increase fivefold during strenuous exercise, with most all of that increase due to an increase in skeletal muscle blood flow. Skeletal muscle arteries contain both α- and β-adrenoceptors, but the former predominate. Thus, activation of the sympathetic nervous system causes vasoconstriction in skeletal muscle. Vascular resistance can easily double from resting values as a result of increased sympathetic nerve activity, with a resulting significant decrease in muscle blood flow. Such neurogenic vasoconstriction in skeletal muscle can override local metabolic demands of the tissue to such an extent that the muscle can become modestly ischemic even though metabolism in resting skeletal muscle is very low. Fortunately, skeletal muscle cells can survive long periods with minimal oxygen supply so this low blood flow does not result in marked cell damage or death. The effects of the sympathetic nervous system on the skeletal muscle circulation is a means to exploit this very large circulation for the benefit of the body as a whole rather than to control muscle blood flow. Activation of the sympathetic nervous system to the large mass that is skeletal muscle causes a large increase in total systemic vascular resistance that is used to help maintain or limit a drop in arterial blood pressure when cardiac output is compromised (i. Like in the small intestine, this ability enables the heart and brain to be perfused in preference to other organs less critical to the acute survival of the individual. In addition, contraction of the skeletal muscle venules and veins forces blood from these vessels into the central circulation. This action helps counteract deficits in cardiac output that accompany losses of blood volume. In sum, the skeletal muscle vasculature can either place major demands on the cardiopulmonary system through massive vasodilation during exercise or respond as if expendable with intense vasoconstriction during a hypovolemic and/or hypotensive crisis. As discussed in Chapter 15, many potential local regulatory mechanisms adjust blood flow to the metabolic needs of tissues. In skeletal muscle, as in the small intestine, autoregulation efficacy is dependent on local metabolism with increased efficacy associated with high metabolism. In addition, to ensure the best possible supply of nutrients, particularly oxygen, even mild exercise causes sufficient vasodilation to perfuse virtually all of the capillaries, rather than just 25% to 50% of them as occur at rest. Like the small intestine, skeletal muscle first recruits more capillaries to enhance oxygen extraction in times of increased oxygen need and adjusts blood flow if needed after extraction is essentially maximized. The most dynamic local vascular regulatory phenomenon in skeletal muscle is the coupling of muscle blood flow to its activity (i. In fast-twitch muscles, which primarily depend on anaerobic metabolism, the accumulation of hydrogen ions from lactic acid is potentially a major contributor to active hyperemia in that muscle type. In slow-twitch skeletal muscles, oxidative metabolic requirements can increase up to 20 times during heavy exercise. It is not hard to imagine that whatever causes metabolically linked vasodilation is in ample supply at high metabolic rates and/or possesses strong + + vasodilator activity. However, none of the observed changes of these metabolites alone explains muscle active hyperemia. It is difficult to account for large active hyperemia in skeletal muscle on the vasodilatory effect of low tissue oxygen tensions alone. During rhythmic muscle contractions, the blood flow during the relaxation phase can be high, and thus it is unlikely that the muscle becomes significantly hypoxic during submaximal aerobic exercise (i. Although the tissue oxygen content likely decreases as exercise intensity increases, the reduction does not compromise the high aerobic metabolic rate except with the most demanding forms of exercise. Once the vasodilation and increased blood flow associated with exercise are established (in 1 to 2 minutes), the microvasculature is probably capable of maintaining ample oxygen for most workloads, perhaps up to 75% to 80% of maximum performance, because remarkably little additional lactic acid accumulates in the blood. The ability of skeletal muscle to meet its oxygen needs for sustained activity is not limitless. Near- maximum or maximum exercise exhausts the ability of the microvasculature to meet tissue oxygen needs, and hypoxic conditions rapidly develop, limiting the performance of the muscles. The burning sensation and muscle fatigue during maximum exercise, or at any time that muscle blood flow is inadequate to provide adequate oxygen, are partially a consequence of hypoxia. This type of burning sensation is particularly evident when a muscle must hold a weight in a steady position. In this situation, the contraction of the muscle compresses the microvessels, which severely reduces muscle blood flow. The combination of throttled flow with the energy demands of holding a weight against gravity creates marked hypoxia in muscle tissues. In all areas, an arcade of arterioles exists at the boundary of the dermis and the subcutaneous tissue over fatty tissues and skeletal muscles (Fig. From this arteriolar arcade, arterioles ascend through the dermis into the superficial layers of the dermis, adjacent to the epidermal layers. These arterioles form a second network in the superficial dermal tissue and perfuse the extensive capillary loops that extend upward into the dermal papillae just beneath the epidermis. The dermal vasculature also provides the vessels that surround hair follicles, sebaceous glands, and sweat glands. The capillary loops are essentially perpendicular to the surface of the skin such that only the tips are in close proximity to the outermost layer of that tissue. All the capillaries from the superficial skin layers are drained by venules, which form a venous plexus in the superficial dermis and eventually drain into many large venules and small veins beneath the dermis. The vascular pattern just described is modified in the tissues of the hand, feet, ears, nose, and some areas of the face, in that direct vascular connections between arterioles and venules, known as arteriovenous anastomoses, occur primarily in the superficial dermal tissues (see Fig. By contrast, relatively few arteriovenous anastomoses exist in the major portion of human skin over the limbs and torso. The anastomoses lead to a venous plexus that lies parallel to the skin surface and thus are positioned, when open, to direct blood into a large surface area of small blood vessels just underlying the surface of the skin.

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Such receptor-associated G proteins seem to represent a general frst step through which most membrane receptors operate t initiate their particular cascade of events that ultimately lead to specifc cellular responses quality actos 45mg diabetes insipidus etiology. The reader should not conclude from Figure 7-1 that all vasoactive chemical agents (chemical agents that cause vascular effects) produce their actions on the smooth muscle without changing membrane potential order actos 15mg with amex diabetes insipidus life expectancy. In fact order actos without a prescription rare diabetes in dogs, most vasoactive chemical agents do cause changes in membrane potential because their receptors can be linked, by G proteins or other means, to ion channels of many kinds. Not shown in Figure 7-1 are the processes that remove Ca2+ from the cyto­ plasm of the vascular smooth muscle, although they are important as well in determining the free cytosolic Ca2+ levels. As in cardiac cells (see Figure 2-7), smooth muscle cells actively pump calcium into the sarcoplasmic reticulum and outward across the sarcolemma. Mechanisms for Relaxation Hyperpolarization of the cell membrane is one mechanism for causing smooth muscle relaxation and vessel dilation. In addition, however, there are at least two general mechanisms by which certain chemical vasodilator agents can cause smooth muscle relaxation by pharmacomechanical means. In Figure 7-1, the spe­ cifc receptor for a chemical vasoconstrictor agent is shown linked by a specifc G protein to phospholipase C. The overall result is stimulation of Ca2+ efux, membrane hyperpolarization, and decreased contractile machinery sensitivity to Ca2+-all of which act synergistically to cause vasodilation. Nitric oxide can be produced by endothelial cells and also by nitrates, a clinically important class of vasodilator drugs. The "vascular tone" of a region can be taken as an indication of the "level of activation" of the individual smooth muscle cells in that region. As described in Chapter 6, the blood flow through any organ is determined largely by its vascular resistance, which is depen­ dent primarily on the diameter of its arterioles. Basal Tone Arterioles remain in a state of partial constriction even when all external influ­ ences on them are removed; hence, they are said to have a degree of basal tone (sometimes referred to as intrimic tone). The understanding of the mechanism is incomplete, but basal arteriolar tone may be a refection of the fact that smooth muscle cells inherently and actively resist being stretched as they continually are in pressurized arterioles. Another hypothesis is that the basal tone of arterioles is the result of a tonic production of local vasoconstrictor substances by the endo­ thelial cells that line their inner surface. In any case, this basal tone establishes a baseline of partial arteriolar constriction from which the external influences on arterioles exert their dilating or constricting effects. These influences can be separated into three categories: local infuences, neural influences, and hormonal infuences. The interstitial concentrations of many substances reflect the balance between the metabolic activity of the tissue and its blood supply. Interstitial oxygen levels, for example, fall whenever the tissue cells are using oxy­ gen faster than it is being supplied to the tissue by blood flow. Conversely, inter­ stitial oxygen levels rise whenever excess oxygen is being delivered to a tissue from the blood. Many substances in addition to oxygen are present within tissues and can affect the tone of the vascular smooth muscle. When the metabolic rate of skel­ etal muscle is increased by exercise, tissue levels of oxygen decrease, but those of carbon dioxide, H+, and K+ increase. In addition, with increased metabolic activity or oxygen deprivation, cells in many tissues may release adenosine, which is an extremely potent vasodilator agent. At present, it is not known which of these (and possibly other) metabolically related chemical alterations within tissues are most important in the local meta­ bolic control of blood fow. It appears likely that arteriolar tone depends on the combined action of many factors. For conceptual purposes, Figure 7-2 summarizes current understanding of local metabolic control. Vasodilator factors enter the interstitial space from the tissue cells at a rate proportional to tissue metabolism. These vasodilator fac­ tors are removed from the tissue at a rate proportional to blood fow. Whenever tissue metabolism is proceeding at a rate for which the blood fow is inade­ quate, the interstitial vasodilator factor concentrations automatically build up and cause the arterioles to dilate. The process continues until blood flow has risen sufciently to appropriately match the tissue metabolic rate and prevent further accumulation of vasodilator 3 An important exception to this rule occurs in the pulmonary circulation and is discussed later in this chapter. Local metabolic mechanisms represent byfr the most important meam oflocal fow control. By these mechanisms, individual organs are able to regulate their own fow in accordance with their specifc metabolic needs. As indicated below, several other types of local infuences on blood vessels have been identifed. However, many of these represent fne-tuning mechanisms and many are important only in certain, usually pathological, situations. A large number of studies have shown that blood vessels respond very differently to certain vascular infuences when their endothelial lining is missing. Acetylcholine, for example, causes vasodilation of intact vessels but causes vasoconstriction of vessels stripped of their endothelial lining. This and similar results led to the realization that endothelial cells can actively participate in the control of arterio­ lar diameter by producing local chemicals that affect the tone of the surrounding smooth muscle cells. In the case of the vasodilator effect of infusing acetylcholine through intact vessels, the vasodilator infuence produced by endothelial cells has been identifed as nitric oxide. Nitric oxide is produced within endothelial cells from the amino acid, L-arginine, by the action of an enzyme, nitric oxide syn­ thase. Nitric oxide synthase is activated by a rise in the intracellular level of the Ca2+. Acetylcholine and several other agents (including bradykinin, vasoactive intes­ tinal peptide, and substance P) stimulate endothelial cell nitric oxide production because their receptors on endothelial cells are linked to receptor-operated Ca2+ channels. Probably more importantly from a physiological standpoint, fow­ related shear stresses on endothelial cells stimulate their nitric oxide production presumably because stretch-sensitive channels for Ca2+ are activated. Such fow­ related endothelial cell nitric oxide production may explain why, for example, exercise and increased blood fow through muscles of the lower leg can cause dila­ tion of the blood-supplying femoral artery at points far upstream of the exercising muscle itsel£ Agents that block nitric oxide production by inhibiting nitric oxide synthase cause signifcant increases in the vascular resistances of most organs. For this reason, it is believed that endothelial cells are normally always producing some nitric oxide that is importantly involved, along with other factors, in reducing the normal resting tone of arterioles throughout the body. Endothelial cells have also been shown to produce several other locally acting vasoactive agents including the vasodilators "endothelial-derived hyperpolarizing factor", prostacyclin and the vasoconstrictor endothelin. Much recent evidence suggests that endothelin may play important roles in such important overall process such as bodily salt handling and blood pressure regulation. One general unresolved issue with the concept that arteriolar tone (and there­ fore local nutrient blood fow) is regulated by factors produced by arteriolr endothelial cells is how these cells could know what the metabolic needs of the downstream tissue are. This is because the endothelial cells lining arterioles are exposed to arterial blood whose composition is constant regardless of flow rate or what is happening downstream. One hypothesis is that there exists some sort of communication system between vascular endothelial cells. That way, endothelial cells in capillaries or venules could telegraph upstream information about whether the blood fow is indeed adequate. In most cases, however, definite information about the relative importance of these substances in cardiovascular regulation is lacking. Prostaglandins and thromboxane are a group of several chemically related prod­ ucts of the cyclooxygenase pathway of arachidonic acid metabolism.

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Complement is a group of serum proteins that circulate in an inactive state and can be activated by a variety of specific and nonspecific immunologic mechanisms actos 45mg cheap diabetes insipidus medications cause. Their actions actos 30 mg free shipping diabetes mellitus latin translation, sometimes called the humoral component of the innate immune system order actos 15 mg diabetes mellitus type 2 kngf, are discussed in more detail below. An important role of these chemical factors is to connect the three lines of immune system defenses. The ability of cells and tissues to respond to and to get rid of environmental challenges is an ancient evolutionary development that has persisted through vertebrate development as innate immunity. The zoologist Metchnikoff discovered that cells of a starfish could phagocytose invaders, which means that this 600-million-year-old invertebrate possesses an innate immune system. Most of these leukocytes participate in innate immune mechanisms, while lymphocytes are involved with the adaptive immune response. Innate leukocytes include phagocytes (neutrophils, macrophages, eosinophils, and dendritic cells) and nonphagocytic cells as outlined in Table 10. Phagocytic cells identify and eliminate pathogens, either by attacking larger pathogens through contact or by engulfing them. For the latter, phagocytes can directly sense the pathogens through a group of transmembrane receptors, the so-called toll-like receptors. The engulfed matter is enclosed within vacuoles and enzymatically digested, after fusion with lysosomes. Some pathogens have been coated with opsonins in a process called opsonization to render them more attractive to phagocytosis. Examples of opsonins are immunoglobulin G (IgG) antibody and the C3b molecule of the complement system. Neutrophils (one of the polymorphonuclear leukocytes) recognize chemicals produced by bacteria in a cut or scratch and migrate toward them. For killing, neutrophils use proteolytic enzymes and reactive oxygen and nitrogen species produced as part of the respiratory burst (see Chapter 9). Once monocytes migrate into tissue, they differentiate and become the larger, more powerful, phagocytic macrophages. Macrophages kill, like neutrophils, by using the respiratory burst and proteolytic enzymes. Macrophages secrete various cytokines that attract other leukocytes to the infection site and initiate the acute-phase inflammatory response. Macrophages can circulate in lymph vessels (wandering, nonfixed macrophages), or they can reside in connective tissue, in lymph nodules, along the digestive tract, in the lungs, in the spleen, and in other places (mature, fixed macrophages). For instance, the macrophages along certain blood vessels in the liver are called Kupffer cells, whereas the macrophages of the joints are called synovial A cells. Eosinophils are best known as participants in allergic reactions, where they might detoxify some of the inflammation-inducing substances. But they are also primarily evolved to secrete factors that punch small holes in worms and other parasites, causing them to die. Dendritic cells are, like macrophages, a critical link between the innate and adaptive immune systems. After phagocytosis of pathogens, the cells mature and travel to regional lymph nodes, where they activate T cells, which then activate B cells to produce antibodies against the pathogen. They release the cytolytic protein perforin, which forms a pore in the plasma membrane of the target cell. Mast cells are present in most tissues in the vicinity of blood vessels and contain many granules rich in histamine and heparin. They are especially prominent under coverings lining the body surfaces such as the skin, mouth, nose, lung mucosa, and digestive tract. Although best known for their roles in allergy and anaphylaxis of the adaptive immune system (see next section), mast cells play an important role in the innate system as well. They release factors that increase blood flow and vascular permeability, bringing components of immunity to the site of infection. In combination with IgE antibody from B cells, mast cells can also target parasites that are too large to be phagocytosed, such as intestinal worms. Adaptive immunity uses three important features in its method of attack: specificity, diversity, and memory. Microbes that escape the onslaught of cells and molecules of the innate immune system face attack by T cells, B cells, and B-cell products of the adaptive immune system, also called the acquired immune system. The adaptive immune system: Is a relatively recent evolutionary development and characteristic of jawed vertebrates Is activated by thousands of diverse antigens, which are presented as glycoproteins on the surface of bacteria, as coat proteins of viruses, as microbial toxins, or as membranes of infected cells Responds with the proliferation of cells and the generation of antibodies that specifically assault the invading pathogens Responds slowly, being fully activated about 4 days after the immunologic threat Is capable of immunologic memory, so that repeated exposure to the same infectious agent results in improved resistance against it Specificity The specificity of the adaptive immune system is created by antigen recognition molecules, which are synthesized prior to the exposure to antigen and, in B lymphocytes, can be modified during the immune response to make them even more specific to the antigen. Each class of antibody plays a unique role in immune defense and will be discussed later in the chapter. To stay with the example of antibodies, most protein antigens have several epitopes (the part of the antigen that binds the antibody) and, hence, are recognized by different B cells, which release different antibodies to mount a polyclonal antibody response. On the other hand, closely related antigens may share epitopes (cross-reactivity). Diversity The diversity of adaptive immune responses is based on a huge variety of antigen receptor configurations, essentially one receptor for each different antigen that might be encountered. The molecule diversity is mainly achieved by variable recombination of gene segments prior to exposure to antigen and, in the case of immunoglobulins, additionally by mutation of the molecules after exposure to antigen. The recognition of an antigen by the lymphocyte with the best-fitting receptor occurs mainly in the local lymph node and induces the activation, proliferation, and differentiation of the responsive cell, a process known as clonal selection. Only the clone of the lymphocyte that has the unique ability to recognize the antigen of interest proliferates and generates progenitor cells. These cells are specific to the inducing antigen but may have different functions. In the case of B cells, plasma cell clones produce antibodies, and memory cell clones enhance subsequent immune responses to the specific antigen. Clonal selection amplifies the number of T or B lymphocytes that are programmed to specifically respond to the inciting stimulus. Plasma cells are much larger and are capable of producing and secreting antibodies. Initially, the plasma cells produce IgM antibodies and later can switch to produce IgG, IgA, or IgE antibodies when antibodies with different functional capabilities are needed. Similarly, clonal proliferation of T cells can lead to the generation of more antigen-specific T cells and to the production of effector T cells, such as T helper and cytotoxic T cells, and memory T cells. Memory The memory of the adaptive immune system is based on the fact that some descendants in the expanded B- cell and T-cell clones function as memory cells (see Fig. These cells mimic the reactive specificity of the original lymphocytes that responded to the antigen and accelerate the responsiveness of the immune system when the antigen is encountered again (anamnestic response) and are the basis for immunization via vaccinations. As mentioned previously, though presented as distinct systems, no part of the immune system works separately.

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A full length cast Volkmann’s ischemic contracture in some Closed reduction under general anesthe- is applied and the bones take about 12 patients discount 45mg actos visa test your diabetes risk. To remember in Monteggia fracture disloca- ment is open reduction and internal fxation • Tis also results from a fall on the out- tion 30mg actos diabetes type 1 uk statistics, medial bone cheap 15mg actos with visa diabetic diet for kids, i. The arm is held in plaster for stretched hand and is more common than • Tis is a fracture of the upper third of ulna 6-12 weeks until union occurs. Malunion occurs in cases treated conser- It may also result from a direct blow on vatively. Tis is subluxation of the head of radius which Diagnosis Galeazzi Fracture Dislocation usually occurs in children, when the forearm is In a case with isolated fracture of the ulna (Fig. The surgeon now presses the distal frag- treatment tal to the ulnar styloid process, but they are at ment into palmar fexion and ulnar devia- • Spontaneous recovery sometimes occurs the same level afer the Colles fracture, which tion using the thumb of his other hand. X-Ray: Tis is important to diferentiate nation, palmar fexion and ulnar deviation. An X-ray is taken to check the success of the forearm and applying direct pressure Smith’s fracture, Barton’s fracture, etc. A sudden click dorsal tilt is the most characteristic displace- The patient is advised to move his fngers, is heard or felt as the head goes back to ment, best seen in the lateral X-ray. The child becomes comfort- tilt can be detected on an anteroposterior full range several times a day. Ofen the fracture is redisplaced treatment in the cast and if this happens remanipulation Treatment of Colles’ fracture is usually may be needed. The plaster is removed afer 6 weeks and It is the most common fracture of the upper • For an undisplaced fracture immobiliza- joint mobilizing and muscle strengthen- extremity and more common in elderly tion in a below elbow plaster cast for six ing exercises are started for the wrist and patients. It nearly always results from a fall on an Tis is done under regional or general • Shoulder, wrist and fnger stifness. The frst step is disimpaction of the frag- transfer (extensor indicis to extensor pol- ment of the distal fragment. Sometimes the fracture becomes visible at this stage because of resorption of fracture ends in two weeks time. Undisplaced fracture: Treatment is usu- A B C ally conservative in a scaphoid cast for 3-4 months. In widely displaced fractures open reduc- tion and internal fxation using a special compression screw (Herbert’s screw) is required. The vessels arising from the the waist, there is high probability of the superficial branch of radial artery enter the bone distally and run proximally proximal fragment becoming avascular as the blood supply enters the bone from Fracture oF scaPhoiD The fracture may be a crack fracture or a the distal fragment. Delayed and nonunion-It may result site and type of Fracture aspect of the wrist should make one suspect from either the impaired blood supply or The fracture usually occurs through the waist this type of fracture. The femoral head is forced out of its socket, Following reduction skin traction is Tere are three types of dislocations of the ofen a small or large piece of bone is broken applied and the hip is kept fully extended, hip viz. Clinical Features bearing is allowed afer three months of Majority of these injuries occur in road An isolated posterior dislocation is easy to injury. Multiple views may be needed In presence of fracture of femoral shaf to exclude a fracture of the acetabular rim or hip dislocation is quit ofen overlooked. Closed Reduction Posterior Dislocation of Hip The dislocation is reduced under general (Fig. Tis is the commonest type of hip disloca- The assistant steadies the pelvis, while the tion. The injury occurs due to force acting surgeon fexes the patient’s hip and knee at 90 along the long axis of femur when the hip is degrees and pulls the thigh vertically upwards Fig. Treatment and complications are similar Tis attachment of the capsule divides to that of posterior dislocation. If femo- cannot be manipulated or immobilized by ral head is driven into the pelvis; heavy skele- conservative means. The blood supply of the proximal frag- Tis is ofen required in the following cases: tibia is applied for six weeks. If the acetabular fragment is large and In some young patients if the fragments femoral head. The main blood supply is from the extracap- Complications sular arterial ring formed by branches of 1. Most patients who sustain this injury are extracapsular arterial ring and pass proxi- 2. Myositis ossifcans traumatica around the 75 to 80 years and female to male ratio is 4:1. The capsule of assess that in intracapsular fracture, the ascend- are forcibly abducted and externally rotated the hip joint is the key to understand the frac- ing nutrient arteries and the retinacular arteries in a road accident or fall from a tree. The distal fragment rotates laterally, while the proximal fragment rotates medially and is abducted. On examination, there is shortening and external rotation of leg due to the action of the psoas on the distal fragment. Tis not only diagnoses the fracture but also suggests the exact site and type of fracture. Some impacted femoral neck fractures may be missed in X-ray as the fracture line is invisible. The tive treatment surgery is the treatment of straight lines indicate change in direction of the medial trabecular stream of the neck choice. Multiple cancellous screws – most com- supply of the proximal fragment men- tors respectively. Multiple Knowles pins or Moore’s pins lapse of the femoral head will cause pain Tese fractures are associated with blood used in children. Clinical Features (Hemiarthroplasty) See also the long case nonunited fracture Following injury, the afected thigh is Tis is the procedure of choice in elderly neck femur, chapter 78 deformed, swollen and patient cannot lif the patients > 60 years and fractures with Garden leg. Sometimes Tompson prosthesis violence as may occur in a road trafc acci- the site and type of fracture with degree of is used. Fracture of the shaf of the femur occurs in so matoid arthritis or on steroid therapy. The fracture may occur at any site and is many diferent forms that almost all methods • Tis is also done when the treatment is equally common in the upper middle and of fracture treatment may be applicable. Extracapsular Fracture The fracture may be an oblique, transverse, • Skeletal traction Tis is best treated by open reduction and spiral or comminuted depending upon the • External fxation only in case of open internal fxation. Mobilize the patient quickly so as to avoid reduction) the complications of recumbency. Nonunion-It occurs in approximately 30 Nowadays, the most popular method of to 40 percent of intracapsular fractures. In this Treatment is done depending on the age (C) Comminuted (D) Segmental fracture method the legs of the child are tied to an of the patient – overhead beam. The hips are kept a little 373 Section 14  Orthopedics raised from the bed so that the weight of while trying to regain balance afer a the body provides the countertraction and stumble. From 2 years to 16 years-Conservative the fracture occurs by a direct violence, a treatment is done. The result is a separated fracture of the Once the fracture becomes ‘Sticky’ further patella with some comminution. Clinical Features Following injury, to front of knee or a stum- Complications ble, knee becomes swollen and painful.

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