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Even before infection hiv infection symptomatic stage valtrex 500mg visa, the vicious cycle of undernutrition and poverty in developing countries may increase vulnerability to infection: the hopelessness and despair of poverty could lead to alcohol abuse hiv infection and seizures buy cheap valtrex 500mg line, violence hiv infection rate in zambia purchase valtrex 1000mg, rape hiv infection in older adults buy valtrex online now, and irresponsible sexual behaviors, increasing exposure to the virus. In addition, malnutrition could compromise the integrity of the immune system, increasing vulnerability to infection. Stage 1: Incubation period There are no symptoms during this stage and its duration is usually 2­4 weeks. Stage 2: Acute infection (seroconversion) There is rapid viral replication during this stage. The symptoms in this stage include fever, lymphadenopathy, pharyngitis, rash, myalgia, malaise, headache, and mouth and esophageal sores. Stage 3: Asymptomatic or latency stage this stage may last from a few weeks up to 10 or 20 years, depending on the nutritional status and drug treatment of the individual. It is characterized by none or only a few symptoms, which may include subclinical weight loss, vitamin B12 deficiency, changes in blood lipids and liver enzymes, and an increased susceptibility to pathogens in food and water. Wasting is a characteristic symptom and is defined as an involuntary loss of more than 10% of baseline body weight. Nutrition interventions may help to preserve lean body mass, "strengthen" the immune system and slow progression to stage 5. The immunosuppression is severe and leads to many possible opportunistic or secondary infections with fungi, protozoa, bacteria and/or other viruses. Food and Nutrition-Related Diseases 357 Malignant diseases and dementia may develop. This is the final stage, and if not treated by antiretroviral drugs and specific drugs for the secondary infections it invariably leads to death. As mentioned above, malnutrition could contribute to increased vulnerability to infection in developing countries. The virus probably increases nutritional needs, while its effects on the nervous and digestive system lead to decreased appetite and intakes, impaired digestion, and malabsorption. The consequent loss of lean body mass gave the infection its original African name of "thin disease. Global recommendations have recently been evaluated by the Academy of Science of South Africa, and some of their conclusions are summarized in Box 15. Dietary patterns responsible for the problems the dietary patterns and nutrient intakes responsible and contributing to these problems have been intensively researched in epidemiological, clinical, and basic molecular studies. There is a huge body of scientific evidence available to identify the immediate deficiencies and excesses in intakes, as well as all the environmental factors associated with suboptimal dietary patterns that lead to the nutrition-related diseases highlighted in this chapter. Broadly, these dietary problems can be summarized as: hunger and food insecurity in developing countries, with infants, pregnant women, and older people being the most vulnerable "hidden hunger" or micronutrient deficiencies in both developed and developing countries, especially of iron, vitamin A, zinc, iodine, and all dietary antioxidants overconsumption of unfortified and refined staple foods in "low-quality diets" availability and intake of too many high-fat, sugary, and refined convenience and fast foods, increasing total fat, saturated fat, trans fat, omega-6 fatty acid, sugars, and salt intake not enough fish and other sources of omega-3 fatty acids in the diet not enough vegetables and fruit and their products in the diet not enough dietary fiber-rich foods in the diet; too little dietary variety over-reliance on dietary supplements in the developed world. Suggestions to meet the challenge In an ideal world, every human being would be able to exercise their right (often constitutionally defined) to regularly access, at affordable prices, adequate (enough, sufficient), safe (uncontaminated), and nutritious food to prevent undernutrition and to ensure optimal nutritional status for health, wellbeing, a quality life, ability to actively and productively work and play, and moreover to reach their mental and physical development potential. But we do not live in an ideal world, as the high prevalences of nutrition problems indicate. So the questions that need to be answered are what should be done and by whom to rectify the situation? What is needed is a holistic, integrated approach that will promote and make optimum nutrition possible. The challenge is huge, for there are many barriers to overcome: from war, to uncommitted political agendas, to "unhealthy" food preferences of individuals. The lessons learned from the failure of many developing countries to be on-track in reaching the Millennium Development Goals by 2015 plead for a new approach and global leadership. This could be possible in partnerships in which there is recognition and respect for different agendas, but where partners are willing to develop a common nutrition agenda and agree on steps to reach common goals. For example great strides have been made in the past few decades to reduce child undernutrition in some developing regions. The development of food-based dietary guidelines in both the developed and developing world to assist people to choose an adequate but prudent diet for optimal nutrition is an example of the latter. There is total agreement in the body of literature on the nutrition challenges of the twenty-first century that the focus should be on prevention of nutrition-related diseases to minimize their serious economic and social consequences.

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See also Trachea anti viral anti fungal herbs buy genuine valtrex on line, neoplasms of Neoplastic disorders nasal manifestations of hiv infection viral load discount valtrex online american express, 258t hiv infection rates by year generic 1000mg valtrex, 259­260 antiviral in a sentence order valtrex 1000 mg with amex, 260t of neck, 405­407, 406f Nerve(s). See also Vestibular neuronitis Neuropathy(ies), auditory, 606 Neurotologic surgery, of skull base, 813­820. See also Nasal anatomy of, 2­4, 4f, 238f congenital anomalies of, 237­247 arrhinia, 246 choanal atresia, 243­244, 244f congenital midline nasal masses, 237­240, 238f, 239f dermoid cysts, 237­240, 238f, 239f. See also Systemic disease, nasal manifestations of nerve supply of, 250 olfactory dysfunction and, 232­236, 233t. See also Computerized dynamic posturography Pott puffy tumor, sinusitis and, 281 Potter syndrome, known middle ear anomalies associated with, 650t Pregnancy hyperparathyroidism in, 575 nonallergic rhinitis during, 265 Premalignant lesions, of oral cavity and oropharynx, laser surgery of, 185 Premature caloric reversal, 616 Preponderance, directional, 615 Presbycusis, 683, 689­696. See also Frontal sinus fractures frontal fractures of, 282­286, 285f management of, in anterior skull base lesion treatment, 760 neoplasms of, 278 paranasal. See Paranasal sinus(es); Paranasal sinus neoplasms sinusitis, 273­281 Sinus histiocytosis, 405 Sinus thrombosis, lateral, otitis media and, 663t, 665 Sinus tumors. See Cutaneous neoplasms, malignant; Skin cancer in children benign neoplasms of, 214­215 malignant neoplasms in, 215­216 of external ear, 624, 625f, 626f disorders of, 632­635. See also specific disorders and External ear, disorders of, dermatologic malignant neoplasms of, 217­231. See also Skin cancer; specific types and Cutaneous neoplasms, malignant Skin cancer. See also Cutaneous neoplasms, malignant; specific types and Cutaneous melanoma adnexal tumors, 224­226, 225f basal cell carcinoma, 219­221 cutaneous melanoma, 227­231, 228t, 229f, 230t dermatofibrosarcoma protuberans, 223, 224f malignant fibrous histiocytoma, 223­224 nonmelanoma, 217­219. See Squamous cell carcinoma Skin flap, in lower blepharoplasty, 906, 906f Skin grafts postauricular, for microtia, 628 in scar revision, 892 Skin lesions benign, lasers in, 189­190 malignant, lasers in, 189 vascular, lasers in, 189, 190f Skin resurfacing ablative, 188­189 nonablative, 189 Skin slough, rhytidectomy and, 899 Skin testing, in allergic rhinitis, allergy testing in, 269 Skin-muscle flap, in lower blepharoplasty, 906 Skull base, 753­830. See also Anterior skull base, lesions of cancer of, radiographic appearance of, 795t central, imaging of, 121­127, 122f­131f. See also Sleep apnea, in children classification of, 535­536, 536t 993 sleep apnea, 536­543. See Subglottic stenosis supraglottic, pathogenesis of, 529 tracheal, 483­484, 506­510. See Glucocorticoid steroids for hemangioma of infancy, 194­195 for herpes zoster oticus, 856­857 for Meniere disease, 719 for subglottic hemangioma, 470 systemic, for sinusitis, 279 topical, for nonallergic rhinitis, 266 Stickler syndrome, 326 genes for, 699, 700t signs and symptoms of, 703 Stimulation, pulsatile, in cochlear implants, 880 Stimulated emission, defined, 177 Stimulation magnetic, of facial nerve, 841t, 845­846 pulsatile, in cochlear implants, 880 Stimulator(s), open-loop, 615 Stimulus(i), frequency-specific, 603 Stomatitis aphthous, antimicrobial therapy for, 33t herpetic, antimicrobial therapy for, 33t "Strawberry" hemangioma, 192, 193f Streptococcal pharyngotonsillitis, acute, in adenotonsillar disease, 341­342 Streptogramin(s), for head and neck infections, 39 Strial presbycusis, 692, 692t Stricture(s), anastomotic, esophageal atresia and tracheoesophageal fistula and, 485 Stridor, 422 biphasic, 462, 515 in children, 462­473 congenital laryngeal webs and, 466 inflammatory causes of, 472, 472t laryngeal cysts and, 464 laryngomalacia and, 462­464, 463f, 463t. See also Laryngomalacia laryngotracheobronchitis and, 472, 472t laryngeal foreign bodies and, 466­467 posterior laryngeal clefts and, 466, 466f respiratory papillomatosis and, 470­471 subglottic hemangiomas and, 469­470 subglottic stenosis and. See also Parotid space perivertebral space, 88­89, 92f posterior cervical space, 90, 92f retropharyngeal space, 86­88, 90f­92f spaces of, defined, 73 Suprahyoid muscles, 13 Supranuclear pathways, of facial nerve, 833­834, 833f Supraomohyoid neck dissection, 413­414, 413f, 414f Suprastomal collapse, airway reconstruction and, 531 Swallowing, problems related to , laryngeal cancer management and, 452 Swallowing process, 487f Sydenham chorea, acute adenotonsillitis and, 343 Symmetric gaze nystagmus, 614 Sympathetic chain, lesions of, imaging of, 85­86, 89f Sympathetic innervation of cranial nerves, 30 of salivary glands, 5 Sympathetic trunk, of neck, 17 Symphonix Vibrant Soundbridge SemiImplantable Device, 874­875, 875f Synchrony, neural, 603 Syndromic hearing loss, 684 Synercid, for head and neck infections, 39 Syphilis, congenital, known middle ear anomalies associated with, 648t Systemic corticosteroids, in allergic rhinitis management, 270, 271t, 272t Systemic disease age-related hearing loss vs. See also Papillary carcinoma pathogenesis of, 567 prevalence of, 567 signs and symptoms of, 567­568 thyroglossal duct carcinoma, 571 thyroid lymphoma, 571 treatment of, 571 well-differentiated, 568­569, 568t, 569t disorders of Graves disease, 562­564 hyperthyroidism, 561­562, 561t hypothyroidism, 565­566, 565t, 566t myxedema coma, 566 nonmalignant, 561­566 thyrotoxicosis, 561­562, 561t, 564­565 function of, assessment of, 550­554, 551f, 551t, 552t. See also Foreign bodies, tracheal and esophageal injuries to , 501­506 acquired tracheomalacia, 505­506 iatrogenic, 502­503 intubation injuries, 502­503 tracheoesophageal fistula, 504­505 tracheoinnominate artery fistula, 503­504 trauma-related, 501­502 neoplasms of, 510­514, 510t benign, 512­513 clinical findings in, 510­511 complications of, 512 general considerations in, 510 imaging studies in, 511 laboratory findings in, 511 malignant, 513 pathogenesis of, 510 primary, 510­514, 510t prognosis in, 513 secondary, 514 signs and symptoms of, 510­511 treatment of, 511­512 stenosis of, 483­484, 506­510 congenital anomalies, 506 extrinsic tracheal compression, 507 idiopathic, 506­507 postintubation, 507­510. See also Maxillofacial trauma middle ear, 744­745 noise-related, age-related hearing loss due to , 692, 693f to nose, 248­255. See also Nose, trauma to penetrating to neck, 474 treatment of, 478­479 to temporal bone, 750­751 physical, occupation-related, hearing loss due to , 740 skeletal, 206­213, 206f­213f. See also Skeletal trauma soft tissue, facial, treatment of, 203­205, 205f temporal bone, 744­752. See also Temporal bone, trauma to tracheal, 501­502 Traumatic bone cysts, 386­387, 387f Traumatic perinatal facial palsy, 871 Traveling wave, 591f Treacher-Collins syndrome genes for, 699, 700t known middle ear anomalies associated with, 650t Trench mouth, antimicrobial therapy for, 33t Triangles of neck, 12­13 Triangular cleft lip repair, 328­329, 329f Triangular fossa, 940 Triazole(s), for head and neck infections, 39­40 Trichilemmal cysts, proliferating, 224 Trichophytic browlift, 900 Trigeminal nerve, 27f, 28 divisions of, 27f, 28 dysfunction of, vestibular schwannoma and, 767 mandibular division of, 2 maxillary division of, 2 ophthalmic division of, 2 schwannomas of, 779 Trigeminal pain, sinusitis vs. See also Paraganglioma(s) granular cell, 310 malignant, of paranasal sinuses, 754­757 maxillary sinus, staging criteria of, 290, 291t mixed, malignant, of salivary gland, 315t, 316­317, 318f parotid, malignant, imaging of, 77t, 79­81, 80f, 81f peripheral nerve cell, of neck, 410 Pott puffy, sinusitis and, 281 sinus. See also Skull base, tumors of sternocleidomastoid, of infancy, 402 of temporal bone, 794­812. See also Vestibular testing vestibular neuronitis, 714t, 720­721 vestibular schwannoma, 765­774. See also Vocal cord paralysis polyps of, 432­433 vibration of, 417 Vocal cord contact area, in acoustic voice assessment, 425­426 Vocal cord paralysis, 456­461 anatomy related to , 456, 457t bilateral, 459­461, 460f complete vagal nerve paralysis, 460­461, 460f laser surgery of, 186 recurrent laryngeal nerve paralysis, 459­460, 460f unilateral, in children, 465­466 causes of, 456, 457t in children, 464­466, 465t causes of, 464, 465t clinical findings in, 464­465 evaluation of, 465 general considerations in, 464, 465t signs and symptoms of, 464­465 stridor and, 464­466, 465t treatment of, 465­466 patient evaluation in, 456­457 unilateral, 457­459, 457f, 459f in children, treatment of, 465 complete vagal paralysis, 458­459, 459f recurrent laryngeal paralysis, 457­458, 457f Vocal fold paralysis airway reconstruction for, 533­534 pathogenesis of, 529 Vocal problems, laryngeal cancer management and, 451 Vocal process granulomas, 433 Voice defined, 417 evaluation of, in airway reconstruction evaluation, 530 generation of, 417­418 motor and sensory control of, 418 production of, 417­421, 419f quality of, problems associated with, airway reconstruction and, 531 types of, 422­423 Voice assessment acoustic, 421­426. See also Acoustic voice assessment aerodynamic tests in, 427 laryngologic conditions in, 421 motor and sensory control of, 418 phonation in, aerodynamic properties of, 420 phonatory function studies in, 416­417 physiologic voice evaluation in, 426­428, 426f, 428f.

Currently known adiposity signals are insulin anti viral tissues kleenex buy 1000 mg valtrex with mastercard, leptin hiv infection experiences buy valtrex 1000 mg visa, and adiponectin hiv infection gif generic valtrex 500 mg visa, which are considered as long-acting signals reducing energy intake antiviral tincture safe valtrex 500 mg. Among the satiety signals are the hunger hormone ghrelin, which is secreted in the stomach, and the short-acting Various nonphysiological or external factors are also known to modify food intake, and these effects may be mediated through the intrinsic factors described above. Psychological factors such as depression may lead to either increased or decreased food intake, or changes in the consumption of specific types of foods. Environmental factors are also important, the most obvious being food availability. Even when food is available, some of the specific properties of foods make them more or less appealing, thereby modifying food intake. Important physical characteristics of food include taste, texture, color, temperature, and presentation. Other cultural influences in the environment, such as time of day, social factors, peer influence, and cultural preferences, can also play a role in influencing food intake. In this analogy, large chunks of wood are fed to the stove and the wood is gradually combusted in the presence of oxygen to release carbon dioxide, water vapor, and heat. Similarly, in the body, the food consumed is oxidized or combusted in the presence of oxygen to release carbon dioxide, water, and heat. When ingested food is used for energy, 36 Introduction to Human Nutrition however, the release and transfer of energy occur through a series of tightly regulated metabolic pathways in which the potential energy from food is released slowly and gradually over time. This process ensures that the body is provided with a gradual and constant energy store, rather than relying on a sudden release of energy from an immediate combustion of ingested food. These types of reaction occur continuously in the body and constitute energy expenditure. As discussed in more detail below, energy expenditure can be measured by assessment of total heat production in the body (direct calorimetry) or by assessment of oxygen consumption and carbon dioxide production (indirect calorimetry). Historical aspects of energy expenditure the burning or combustion of food in the body was originally described in the classic experiments of Lavoisier, who worked in France in the late eighteenth century. In addition, he was the first to describe how living organisms produced heat in a similar way, as they required oxygen for life and combusted food as they released heat. His experiments were the first to document the heat production of living organisms. Working before the invention of electricity, he built the first calorimeter in which a small animal was placed in a sealed chamber. Lavoisier packed ice into a sealed pocket around the chamber (he could only perform these studies in the winter when ice was collected from the ground), and then placed the chamber and ice layer inside an insulated chamber. Since the ice layer was insulated from the outside world, the only way that the ice could melt was by the increase in heat produced by the living animal. Lavoisier therefore measured the volume of melted ice water, and, by so doing, was able to calculate accurately the amount of heat that had to be produced by the animal to melt the measured amount of ice. This approach is termed direct calorimetry because heat production is measured directly. Direct calorimeters have been designed for measuring heat production in humans, but this approach is technically demanding, especially in human studies, and is now infrequently used. This approach is based on oxygen consumption and carbon dioxide production that occurs during the combustion (or oxidation) of protein, carbohydrate, fat, and alcohol, as shown in the example of glucose combustion. Respiratory gas analysis can easily be achieved in humans either over short measurement periods at rest or during exercise using a face mask, mouthpiece, or canopy system for gas collection, and over longer periods of 24 hours (and longer) with subjects living in a metabolic chamber. The thermic effect of a meal is typically measured by monitoring the changes in metabolic rate by indirect calorimetry for 3­6 hours following consumption of a test meal of known caloric content. The energy expended in physical activity can be measured under laboratory conditions, also using indirect calorimetry during standard activities. Energy expenditure can be assessed from indirect calorimetry in a simple, less accurate way by ignoring the contribution of protein oxidation or by collecting urine during the measurement to analyze the excreted nitrogen. The equations are produced by the insertion of the heat equivalent for carbohydrate and fat, and are valid even though there is a quantitative conversion of carbohydrate to lipid (de novo lipogenesis) or glyconeogenesis.

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Deletion of part of the short arm of chromosome 4 results in another human disorder- Wolf­Hirschhorn syndrome symptoms hiv infection after 4 years valtrex 1000 mg without a prescription, which is characterized by seizures and severe mental and growth retardation quantum antiviral formula buy valtrex 500 mg mastercard. A deletion of a tiny segment of chromosome 7 causes haploinsufficiency of the gene encoding elastin and a few other genes and leads to a condition known as Williams­Beuren syndrome antiviral vodlocker trusted valtrex 500mg, characterized by distinctive facial features hiv infection from woman to man buy discount valtrex on-line, heart defects, high blood pressure, and cognitive impairments. In individuals heterozygous for a deletion, the normal chromosome loops out during prophase I of meiosis. Deletions cause recessive genes on the homologous chromosome to be expressed and may cause imbalances in gene products. Inversions in meiosis When an individual is homozygous for a particular inversion, no special problems arise in meiosis, and the two homologous chromosomes can pair and separate normally. When an individual is heterozygous for an inversion, however, the gene order of the two homologs differs, and the homologous sequences can align and pair only if the two chromosomes form an inversion loop (Figure 9. Individuals heterozygous for inversions also exhibit reduced recombination among genes located in the inverted region. A B C D E F G E D C A B C D E F G E D C Formation of inversion loop (b) 3 In prophase I, an inversion loop forms. In prophase I of meiosis, the chromosomes form an inversion loop, which allows the homologous sequences to align. D D is not actually diminished but, when crossing over does take place, the result is abnormal gametes that result in nonviable offspring, and thus no recombinant progeny are observed. In prophase I of meiosis, an inversion loop forms, allowing the homologous sequences to pair up (see Figure 9. If a single crossover takes place in the inverted region (between segments C and D in Figure 9. The two outer chromatids, which did not participate in crossing over, contain original, nonrecombinant gene sequences. The two inner chromatids, which did cross over, are highly abnormal: each has two copies of some genes and no copies of others. Furthermore, one of the four chromatids now has two centromeres and is said to be a dicentric chromatid; the other lacks a centromere and is an acentric chromatid. In anaphase I of meiosis, the centromeres are pulled toward opposite poles and the two homologous chromosomes separate. This action stretches the dicentric chromatid across the center of the nucleus, forming a structure called a dicentric bridge (see Figure 9. Eventually, the dicentric bridge breaks, as the two centromeres are pulled farther apart. Spindle fibers do not attach to the acentric fragment, and so this fragment does not segregate into a nucleus in meiosis and is usually lost. In the second division of meiosis, the sister chromatids separate and four gametes are produced (see Figure 9. E D C Anaphase I 8 In anaphase I, the centromeres separate, stretching the dicentric chromatid, which breaks. Normal nonrecombinant gamete Nonviable recombinant gametes C E D Nonrecombinant gamete with paracentric inversion E D C Conclusion: the resulting recombinant gametes are nonviable because they are missing some genes. Thus, no recombinant progeny result when crossing over takes place within a paracentric inversion. The key is to recognize that crossing over still takes place, but, when it does so, the resulting recombinant gametes are not viable; so no recombinant progeny are observed. No dicentric bridges or acentric fragments are produced, but the recombinant chromosomes have too many copies of some genes and no copies of others; so gametes that receive the recombinant chromosomes cannot produce viable progeny. Double crossovers in which both crossovers are on the same two strands (two-strand double crossovers) result in functional recombinant chromosomes. In individuals heterozygous for a chromosome inversion, the homologous chromosomes form a loop in prophase I of meiosis. When crossing over takes place within the inverted region, nonviable gametes are usually produced, resulting in a depression in observed recombination frequencies. D C B A Translocations A translocation entails the movement of genetic material between nonhomologous chromosomes (see Figure 9. Translocation should not be confused with crossing over, in which there is an exchange of genetic material between homologous chromosomes.

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For most random flaps hiv infection statistics 2014 generic valtrex 1000mg otc, a length-to-width ratio of 1:1 is safe; however hiv infection photos buy valtrex 500mg free shipping, in the face hiv infected macrophages buy valtrex 1000 mg without a prescription, this ratio can be extended to 2:1 or even greater without significant risk of flap loss or skin necrosis antiviral x anticoncepcional 1000 mg valtrex with mastercard. Pivotal flaps may in turn be divided into transposition, rotation, and interpolated flaps. In transposition, a lifting of the flap occurs, usually across a normal bridge of tissue. Rotation flaps are curvilinear in shape, with one border of the defect being the leading border of the flap. Although transposition and rotation flaps are both pivotal flaps, they differ in that the axis of a transposition flap is linear, whereas the axis of a rotation flap is curvilinear. An interpolated flap has a linear axis and its base is removed from the defect site. This flap requires either detachment of the pedicle as a separate procedure or burying of the pedicle under a bridge of skin at the time of reconstruction. Axial flaps have a subcutaneous artery extending along the linear axis of the flap. An example of an axial flap is the paramedian forehead flap, which is based on the supratrochlear artery and vein. Pivotal Flaps Rotation Transposition Interpolation Advancement Flaps Single pedicle Bipedicle Y-V Hinged Flap In planning a reconstruction, especially for nasal defects, it may be beneficial to enlarge a defect to include an entire aesthetic region or unit and then reconstruct the entire unit with a flap. Principles of Aesthetic Subunits and Wound Dynamics Understanding the concept of aesthetic regions and the borders defining them is important in the design and performance of flap surgery. The face is divided into several aesthetic regions and each region may be divided into several units. When possible, the flap should be designed in the same aesthetic unit as the defect. When a defect involves two or more aesthetic units, it is often best to reconstruct each portion of the defect separately. This places the scars along the borders of aesthetic units and prevents the obliteration of important boundary lines between the units. The standing cutaneous deformity that is formed can be excised as a Burrow triangle to facilitate wound closure. By combining rotation and advancement tissue movement and using the principle of halving (ie, dividing the length of the closure into equal halves until the entire defect is closed), the defect may often be closed without the need for excision of a Burrow triangle. The vector of greatest tension is from the pivotal point to the most distal point along the curvilinear incision. This flap usually has a random blood supply, but depending on the location of the base of the flap, it may acquire an axial pattern. B the rotation flap is ideal for medium to large defects of the cheek, neck, and scalp. It is not useful in nasal reconstruction because of the lengthy incision required to achieve the proper tissue movement and the need to undermine and advance the pivotal point. One advantage of a rotation flap is its viability in an irradiated area or in patients with poor vascularity due to smoking or diabetes. Cheek Advancement Flaps Cheek advancement flaps have the advantage of relative mobility and elasticity of the soft tissue of the cheek area. They are useful in reconstruction of medium to large defects of the medial cheek, near the nasal-facial sulcus. The standing cutaneous deformities are excised superiorly at the junction of the cheek and lower eyelid and inferiorly along the melolabial fold. Simple Linear Closure A simple linear closure involves the undermining and movement of opposite wound margins toward each other and is the most basic of advancement flaps. Studies using animal models have demonstrated that undermining in the subcutaneous plane 2 to 4 cm provides benefit by decreasing wound tension. However, undermining tissue for distances greater than 6 cm does not alleviate wound tension and may actually increase flap tension. The classic rectangular-shaped advancement flap is created by parallel incisions extending from the border of the defect and involves a sliding movement of tissue into the defect. Two standing cutaneous deformities are created at the corners of the flap and can be corrected by excising Burrow triangles.

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