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The front quarter also should be perpendicular to arrhythmia greenville sc buy line terazosin the sole without medial or lateral migration arterial dissection order terazosin online. A front quarter that has migrated laterally is also an indication of an increased pronation response as the foot excessively abducts in the transverse plane arteria y vena purchase on line terazosin. Finally heart attack 80 blockage cheap 1mg terazosin with visa, check the arch and midsole to can prehypertension kill you generic 5 mg terazosin with amex make sure that the arch of the foot is not collapsing over the sole blood pressure 300200 buy 2mg terazosin. The insensate foot is unable to recognize increased shear and pressure forces that cause skin breakdown and ulceration. Skin breakdown is most common over the exposed metatarsal heads, which bear most of the weight during walking. Several research studies have shown that patients who return to normal footwear have a recurrence rate of 90%, whereas those who use modi? Redistribute and relieve high-pressure areas such as the metatarsal heads by using an accommodative total contact orthosis. A last is a three-dimensional positive model or mold from which the upper and lower aspects of the shoe are constructed. The forefoot and rear foot are in neutral alignment with a straight last, whereas a curved last is 632 the Foot and Ankle angled medially at the forefoot. In general, the straighter the last, the greater the stability and control the shoe will have; the curved last is more mobile during the gait cycle. The upper portion of the shoe includes the quarter, counter, vamp, throat, toe box, and top lining. The counter is a rigid piece of material surrounding the heel posteriorly to stabilize motion. Shoes often include an extended medial heel counter to limit midfoot motion in the overpronator. In the Balmoral style, the quarter panels are sewn together on the back edge of the vamp. The toe box then covers the end of the toes and refers to the depth of the toe region. Shank pieces are commonly used in dress and orthopaedic shoes to provide rigidity to the midsection of the shoe. The shankpiece helps to reduce the twisting or torsion of the forefoot in relation to the rear foot as well as provides support for the midfoot region. The shank refers to the portion of the shoe from the heel to the metatarsal heads. A dual density midsole uses a softer durometer material on the lateral side to decrease the lever arm ground reaction forces at heel strike and decrease the rate of pronation. The innersole attaches the upper part of the shoe to the soling and acts as a smooth? A slip-lasted shoe is sewn together at the center of the sole, much like a moccasin, and is then cemented to the midsole. Ground reaction forces also are reduced on the ankle because the take-off point is moved posteriorly. Two of the more common types of rocker soles include the forefoot rocker sole and the heel-to-toe rocker sole. A forefoot rocker sole reduces shock at toe-off by placing the apex of the rocker sole just proximal to the metatarsal heads. This type of rocker sole is able to dissipate ground reaction forces at heel strike and increase propulsion at toe-off. What is the effect of a foot orthotic on quality of life and pain in patients with patellofemoral pain syndrome? Quality evidence surrounding the use of foot orthotics for patients suffering from patellofemoral pain is limited. However, the literature does seem to weakly support the use of orthotics (custom-made and generic) as a treatment for patellofemoral pain syndrome caused by abnormal biomechanical foot function. Some of the most common theories on how foot orthotics decrease knee pain and increase function in patients with patellofemoral knee pain include the following: (1) reduction of lower limb internal rotation; (2) reduction in Q-angle; (3) decrease in laterally directed soft tissue tension forces of the vastus lateralis, iliotibial band, and patellar tendon; and (4) reduction in lateral patellofemoral contact forces. Does the use of a foot orthotic reduce the incidence of lower limb stress reactions in younger, active adults? The best designed insert is still not agreed upon; however, more important is the comfort and the ability of the wearer to tolerate the foot orthotic. Thus the use of a shock-absorbing orthotic as a preventative measure may be a wise choice for those participating in activities that often cause stress reactions of the lower limbs. Does the use of prophylactic foot orthoses have any effect on the incidence of low back pain in active individuals? It appears the use of a foot orthotic may not reduce the incidence of weight-bearing?induced low back pain in military recruits with no prior history of low back pain. Thus the use of an orthotic (custom soft or semirigid biomechanical) as a preventative measure does not appear to be of any bene? Ekenman I et al: the role of biomechanical shoe orthoses in tibial stress fracture prevention, Am J Sports Med 30:866-870, 2002. Finestone A et al: A prospective study of the effect of foot orthoses composition and fabrication on comfort and the incidence of overuse injuries, Foot Ankle Int 25:462-466, 2004. Janisse D: Introduction to pedorthics, Columbia, Md, 1998, Pedorthic Footwear Association. Milgrom C et al: A controlled randomized study of the effect of training with orthoses on the incidence of weight bearing induced back pain among infantry recruits, Spine 30:272-275, 2005. Northwestern University Medical School, Prosthetic-Orthotic Center: Management of foot disorders: theory and clinical concepts, Chicago, 1998, Northwestern University. Northwestern University Medical School, Prosthetic-Orthotic Center: Management of foot disorders: technical theory and fabrication, Chicago, 1998, Northwestern University. Stacoff A et al: Effects of foot orthoses on skeletal motion during running, Clin Biomech 15:54-64, 2000. Tiberio D: Pathomechanics of structural foot deformities, Phys Ther 68:1840-1849, 1988. C protein, 3 Boot, 630 C-reactive protein, 148, 150 Boston brace C2 sensory nerve root, 257 for isthmic spondylolisthesis, 470 C5 root lesion, 378 for scoliosis, 476 C6 root lesion, 378 Botox. Cachexia, 11 Botulinum toxin, 135, 227 Cadence in gait, 119 Boundary lubrication, 23 Cafergot. Colon disorders, 208 Coracoacromial arch, 331 Colorectal cancer, 276 Coracoacromial ligament, 328 Colton classification of olecranon fractures, 399 coracoacromial arch and, 331 Combination-lasting athletic shoes, 632 subacromial decompression and, 332 Comminuted fracture, 31 Coracobrachialis muscle, 322 Common fibular neuropathy, 591 Coracohumeral ligament, 323 Common iliac artery, 509 adhesive capsulitis and, 350 Common migraine, 260 Coronary ligament, 548 Compartment syndrome, 247-248 Coronoid process fracture, 399-400, 401 chronic, 191 Correlation coefficient, 173 foot and ankle fractures and, 623-624 Corset Complete blood count, 144 for lumbar spinal stenosis, 465 Complete cord syndrome, 487 lumbosacral, 449 Completely randomized design, 170 Cortef. Costoclavicular syndrome, 379 Dantrolene, 135 Costovertebral angle, 210 Darifenacin, 236 Cotrel-Dubousset system, 477 Darrach procedure, 51 Cotylbutazone. Deep venous thrombosis, 55-59, 207 Cubital tunnel syndrome, 403, 406 after total hip arthroplasty, 540 Cuboid subluxation, 613 after total knee arthroplasty, 577-578 Cuff test, 404 pharmacologic prevention of, 137 Cuprimine. Cyproheptadine, 262 Deltoid ligament of foot, 602 Cyriax end-feel classification, 108 Deltoid muscle, 322, 329 Cyriax transverse friction massage, 113-114 Dementia, exercise and, 301 Cyst Demerol. Dihydropyridine receptor, 8 Developmental dysplasia of hip, 225-226, 314-315 Dilantin. Deweighted treadmill ambulation in lumbar spinal Diphenylhydantoin, 262 stenosis, 464 Direct current, 77-80, 90 Dexamethasone, 133 Direct manual therapy techniques, 104 Dexone. Disability, manual therapy and, 107 Dextran, 58 Discrete variable, 169 Diabetes insipidus, 215 Disease-associated muscle atrophy, 11 Diabetes mellitus Disease-modifying antirheumatic drugs, 136 aging and, 300 Disk herniation, 454-457 Charcot deformity and, 242 classification of, 455 cold applications and, 71 effects on proprioception and postural control, 459 effects of exercise on, 44 lumbar spinal stenosis versus, 462 foot ulcer in, 242, 631 thoracic, 479 hyperglycemia and, 146 at various spinal levels, 456 metabolic syndrome and, 300 Diskectomy, exercise after, 458-459 wound healing and, 242 Diskogenic back pain, 452-460 Diagnosis, 194 Diskogenic nonradicular chronic pain, 252 Diagnostic rules of thumb, 182 Diskoid meniscus, 567-568 Diagnostic ultrasound, 303-304 Dislocation Diastasis recti abdominis, 232 elbow, 401 Diazepam, 135 foot and ankle, 617-624 for migraine, 262 avascular necrosis and, 621 for spasticity, 227 calcaneal, 619, 620-621 Diclofenac, 128 Charcot neuroarthropathy and, 622 Didronel. Distal radius, 416 Dynamic exercise, cardiovascular responses to, 298 fracture of, 293-294, 432 Dynamic receptors, 454 Distal realignment of patella, 562-563 Dysesthesia, 61, 164 Distal tibiofibular ligament rupture, 618 Dysfunction syndrome, 280 Distal transverse arch, 601 Dyskinesia, scapular, 366-368 Distention arthrography, 351 Dysphagia, 208 Distractive flexion injuries, 490 Dysplastic spondylolisthesis, 467-473 Disuse, physiologic effects on collagen, 22 Dystrophin, 3 Ditropan. Edema Dorsal intercalated segment instability, 433 in ankle sprain, 612 Dorsal interossei muscles, 417, 605 cold treatment for, 70-71 Dorsal interossei tendons, 420 in complex regional pain syndromes, 60 Dorsal proximal interphalangeal joint dislocation, 431 electrotherapeutic control of, 88 Dressings, 242-244 in integumentary disorders, 205-206 Drop-arm test, 335, 336 in posterior tibialis tendon dysfunction, 609 Drop finger, 430 in prepatellar bursitis, 557-558 Drop sign, 336 Eden-Lange procedure, 376 Drug therapy, 126-139 Effective radiating area of transducer, 92 acetaminophen and, 131-132 Effexor. Electrocardiography in pulmonary embolism, 57 Erb-Duchenne palsy, 226 Electrode Ergotamine tartrate, 262 in electrotherapy, 82-83 Error iontophoretic, 91 in clinical reasoning, 221-222 Electromotive force, 77 statistical, 169 Electromyography, 151-159 Erythrocyte disorders, 213 in carpal tunnel syndrome, 438-439, 441, 442 Erythrocyte sedimentation rate, 145, 150 classifications of nerve injuries and, 153-154 Eskalith. Implant Insall-Salvati ratio, 306 joint biomechanics and, 23 Instability, 18 magnetic resonance imaging and, 304 elbow, 386 ultrasound and, 93 patellar, 549-550, 558 Impulse, 15, 16 pubic symphysis, 515 Imuran. Hill-Sachs lesion and, 344 Indirect manual therapy techniques, 104 multidirectional, 342, 346 Indocin. Lauge-Hansen classification of ankle fractures, 617-618 Lipase, 142 Laugier fracture, 398-399 Lipid-lowering medications, 138 Le Fort-Wagstaffe fracture, 618 Lipitor. Mechanical power, 17 Mediopatellar plicae, 547 Meclofenamate, 128 Medium-frequency stimulation, 79 Meclomen. Medial collateral ligament, 570 Membrane potential, 75 injury of, 574 Meniscal cyst, 567 of rear foot, 602 Meniscal injuries, 564-568 Medial cord lesion, 378 Meniscal transplant, 567 Medial epicondyle apophysis, 229 Meniscus, 551 Medial epicondyle fracture, 401 Menopause Medial epicondylitis, 393 heart attack and stroke after, 238-239 Medial hamstring reflex, 161 osteoporosis and, 237 Medial ligamentous complex, 386 Menostar. Muscle, 3-12 Microfracture technique, 28-29 aching of, 248 Middle glenohumeral ligament, 325 actions of, 16-17 Midfoot arthrosis, 605 active insufficiency of, 7-8 Midrin. Posterior tibialis tendon dysfunction, 608-609 Piriformis muscle, 521 Posterolateral elbow dislocation, 401 Piriformis syndrome, 531-532, 591 Posterolateral rotary instability, 386, 572 Piroxicam, 128 Postherpetic neuralgia, 483-484 Index 667 Postmenopausal women Pronator teres syndrome, 404-405 calcium supplementation for, 276 Prone extension with external rotation of teres minor, 333 osteoporosis in, 237 Prone knee flexion test, 512 Postoperative hip dislocation, 539 Propoxyphene, 127 Postoperative pain Propranolol, 260, 263 cold treatment for, 70-71 Proprioception, 188 in disk herniation surgery, 459 disk herniation and, 459 Postpartum period, carpal tunnel syndrome and de gait and, 123 Quervain tenosynovitis in, 233 surgical repair of shoulder instability and, 347 Posttraumatic compartment syndrome, 247-248 Proprioceptive training, 188 Postural receptor, 454 Prostaglandins Postural syndrome, 280 inflammatory response and, 26 Posture nonsteroidal antiinflammatory drugs and, 130 cervical headache and, 258 Protein changes during pregnancy, 231 athlete need for, 190-191, 277 disk herniation and, 459 daily-recommended percentages during heavy training, lumbar pressures in, 450 277 spinal loads and, 448 Prothrombin time, 59, 144 temporomandibular joint dysfunction and, 498 Protrusion of temporomandibular joint, 497 Potassium, 146-147 Provocation elevation test, 379 Power, 15 Provocative maneuvers Predental space, 309 for chronic pain, 251-252 Prednisolone, 133 in sacroiliac joint pain, 511-512 Prednisone, 133, 262 Proximal femoral fracture, 293-294 Preemptive analgesia, 247 Proximal humeral replacement, 373, 374 Pregnancy, 230-234 Proximal humerus, 323-324 physiologic changes during, 230 average articular version of, 329 cardiovascular, 231 fracture of, 371-375 effects on collagen and, 22 Proximal interphalangeal joint, 419 effects on exercise and, 42 boutonniere deformity of, 424 respiratory, 231 lateral collateral ligament injury of, 431 Prelone. Progressive resistance exercises, 9-10, 41 Pubic symphysis Prolapse changes during pregnancy, 231 lumbar disk, 455 instability of, 515 pelvic organ, 234-235 Pubofemoral ligament, 520 Prolotherapy, 515 Pudendal nerve, 507 Pronation Pulley system of hand, 413, 428 elbow, 387, 388 Pulmonary disorders, 202-205 foot, 627 chronic obstructive pulmonary disease in, 44 rear foot, 600 exercise in older adult and, 299-300 wrist, 416 Pulmonary embolism, 57 Pronation-dorsiflexion fracture, 619 Pulsatile lavage, 244 Pronator quadratus muscle, 388 Pump, 630 Pronator teres muscle, 388 Putti-Platt procedure, 346 668 Index Q Radiography?cont?d Q-angle, 552 pelvic, 315 Q10 effect, 11 reading of radiograph, 303 Quadrangular space, 325 in rotator cuff tear, 337 Quadriceps avoidance, 122 of sacroiliac joint, 509 Quadriceps femoris reflex, 161 safety of, 302 Quadriceps muscle in spinal cord injury, 487-488 anterior cruciate ligament rehabilitation and, 88 in spondylolysis, 307 contusion of, 529 in sternoclavicular injury, 364 hip fracture and, 537 in stress fracture, 305-306 L3-4 radiculopathy and, 160 in temporomandibular joint dysfunction, 499 strain of, 525 of wrist, 310-313, 431-432 strengthening in patellofemoral disorders, 559-560, 561 Radiologic studies, 302-318 Quadriceps tendon rupture, 583 of anterior cruciate ligament, 317 Quadriga, 422 anterior humeral line and, 310 Qualitative variable, 169 of anterior shoulder dislocation, 316 Quantitative computed tomography in osteoporosis, 237 of basilar invagination, 309 Quantitative variable, 169 bone scan in, 305 in cervical headache, 258 R of cervical spine, 307, 308, 309 Radial artery, Allen test and, 422 in complex regional pain syndromes, 61 Radial collateral ligament, 386 computed tomography in, 303 Radial deviation of wrist, 416 in developmental dysplasia of hip, 314-315 Radial head diagnostic ultrasound in, 303-304 dislocation of, 310 femoral neck-shaft angle and, 315 fracture of, 34, 400, 401 of greater tuberosity fracture, 318 osteochondritis dissecans of, 390 in Hill-Sachs lesion, 344 radial nerve compression and, 406 magnetic resonance imaging in, 304-305 Radial inclination, 311, 313 of osteochondral lesion of femoral condyle, 316 Radial neck fracture, 34 in osteoporosis, 307 Radial nerve, 411 in patella alta, 306 compression of, 403-404 in patellofemoral disorders, 558-559 elbow and, 388 positron emission tomography in, 305 humeral shaft fracture and, 374, 375 predental space and, 309 injury of, 158 radiocapitellar line and, 310 Saturday night palsy and, 405-406 reading of radiograph in, 303 splinting for injury of, 422 in rotator cuff tear, 337 superficial branch of, 420 in sacroiliac joint pain, 515 Radial tunnel syndrome, 392, 403-404 safety of x-rays and, 302 Radicular disorders, 195-196 in scoliosis, 307 Radicular pain, 164, 195 in shoulder instability, 344 in spondylolisthesis, 470 in spondylolisthesis, 471 Radiculopathy, 455-456 in spondylolysis, 307 Radiocapitellar joint, 385 in stress fracture, 305-306 closed-chain upper extremity exercise and, 387 sulcus angle and, 306 Radiocapitellar line, 310 in temporomandibular joint dysfunction, 499-500 Radiocarpal joint, 419 of thoracolumbar spine, 308 Radiofrequency neurotomy, 515 ulnar variance and, 310 Radiography in whiplash, 492 in acromioclavicular injuries, 360-361 of wrist, 310-314 in adhesive capsulitis, 350 x-ray versus arthrogram in, 302 in ankle fracture, 618 Radioulnar joint, 110 in ankle sprain, 611-612 Radius in anterior shoulder dislocation, 316 distal, 416 arthrography versus, 302 radiocapitellar line and, 310 in calcaneal fracture, 619 Raloxifene, 237 in cervical headache, 258 Random error, 169 in complex regional pain syndromes, 61 Randomized controlled trial, 180 in developmental dysplasia of hip, 314-315 Rang classification, 230 in lumbar spinal stenosis, 463 Range of motion in osteoporosis, 307 active insufficiency and, 8 in patellar malalignment, 589 cervical spine, 450 Index 669 Range of motion?cont?d Rehabilitation?cont?d elbow, 387 shoulder?cont?d electrotherapy protocols and, 87-88 in anterior shoulder dislocation, 345-346 following total knee arthroplasty, 577 in long thoracic nerve palsy, 369 foot and ankle, 600 in rotator cuff tear, 334-335, 338 hip, 522, 523, 540 in total shoulder arthroplasty, 356-357 lumbar spinal stenosis and, 463 in spondylolisthesis, 471-472 manual therapy and, 107 Reiter syndrome, 52, 219, 514 of mouth opening, 496-497 Relafen. Spinal loading, 450 Snapping hip syndrome, 530 Spinal manipulation, 105-106, 107 Snapping scapula, 369-370 Spinal nerve, 448 SnNouts, 182 Spinal traction, 115-118 Sodium, 149 Spine, 443-502 Sodium hypochlorite solution, delayed healing and, 241 articular receptor distribution in, 454 Index 673 Spine?cont?d Spine?cont?d back pain and, 452-460. Trauma?cont?d Tolerance to opioid analgesics, 129 in elbow fractures and dislocations?cont?d Tolmetin, 129 distal humerus and, 394-395 Tolterodine, 236 epicondylar, 397 Tongue, resting position of, 499 intercondylar, 397-398 Topical agents, delayed healing and, 241 olecranon, 399 Topical analgesics, 132 radial head, 400-401 Topical growth factors, 245-246 supracondylar, 395-396 Toradol. Velocity, 15 Ulcer Venlafaxine, 132 plantar, 242 Venography in deep venous thrombosis, 58 venous versus arterial, 241 Venous thrombosis, 55-59 Ulcerative colitis, 514 Venous ulcer, 241 Ulnar artery, Allen test and, 422 Ventilatory threshold, 38 Ulnar deviation of wrist, 416 Vertebral fracture Ulnar nerve, 420 compression, 495 compression of, 402-403, 437 older adult and, 293-294 elbow and, 388 Vertebral landmarks, 450 injury in clavicle fracture, 371 Vertebroplasty, 495 loss of function following total elbow joint arthroplasty, Vertical compression injury, 490 406-407 Vesicare. Unipennate muscle, 7 Volar intercalated segment instability, 433 Unipolar hemiarthroplasty, 534 Volar plating of distal radius fracture, 432 Unipolar neuromuscular electrical stimulation, 83 Volar proximal interphalangeal joint dislocation, 431 Upper cervical manipulation, drug contraindications in, 137 Volar tilt of distal radius, 313 Upper extremity Voltage, nerve cell membrane depolarization and, 77 exercise-induced changes in physiology of, 39 Voltaren. The model has the potential to improve patient outcomes, reduce waiting times and ease pressure in times of high demand. Keywords scopes, practice, program, evaluation, physiotherapists, emergency, department, hwa, sub, expanded, fnal, report, projec, t Publication Details C. In particular we would like to thank the representatives of lead sites, project team members and other staff of the respective organisations involved in the evaluation of the Expanded Scopes of Practice program, as well as Clinical Advisors and members of the Project Advisory Group. The support from key staff of Workforce Innovation and Reform within Health Workforce Australia, Australian Government, is also gratefully acknowledged. Finally, the authors acknowledge the contribution made by colleagues from the Australian Health Services Research Institute during the course of the evaluation. In particular we would like to thank Kathy Eagar, Luise Lago, Milena Snoek, Elizabeth Cuthbert and Cheryl Blissett. Centre for Health Service Development, Australian Health Services Research Institute, University of Wollongong. A competency-based training pathway based on adult learning principles appears to offer most flexibility. Broader professional recognition would enhance the sustainability of this pathway. The alternative a post-graduate course delivered in a university setting has the advantage of leading to a recognised qualification but modifications are needed to ensure it is comprehensive and relevant for trainees from different jurisdictions. Both training programs include a period of supervised practice and competency assessment. Waiting times, treatment times and total time spent in the Emergency Department was also lower on these days at most sites. They felt they had been listened to, their problems were understood, and the physiotherapists were comfortable and competent in dealing with their problems. Pressures to see as many primary contact patients as possible and perform against the National Emergency Access Target were seen as barriers to collegial practice. The structure of the program, with two lead sites each leading a number of implementation sites, had a number of advantages. It reduced duplication of effort, as training pathways, modules and resources were already established. Grouping the implementation sites with lead sites in jurisdictions with similar legislative and policy structures was advantageous. The model has the potential to improve patient outcomes, reduce waiting times and ease pressure in times of high demand. The framework recognises that programs aim to make an impact at three levels consumers, providers and the system (structures and processes, networks, relationships) and is based on six domains: project delivery, project impact, sustainability, capacity building, generalisability and dissemination. The evaluation employed a range of data sources including interviews, surveys, log books, specific tools, site visits, project documentation and routine administrative data. Both lead sites were responsible for implementation in their own organisations, involving refinement of their existing models. Both models emphasised a team-based approach closely linked to the physiotherapy department in each hospital. The lead sites provided varying assistance depending on the needs of each implementation site and the project management style of the lead team. Lead sites played an important role engaging key stakeholders within their own organisations and at the implementation sites. The criteria for selecting physiotherapists to participate in the project varied slightly at each site. Physiotherapists in the Emergency Department Sub-Project Final Report Page vii the project teams worked with existing clinical governance mechanisms within their organisations and all project teams monitored patient safety and quality data and most involved their steering committee in reviewing this data. Clinicians could only increase their scope of practice upon completion of the relevant training module and assessment of clinical competencies. During the set-up phase, project teams identified a range of legislative and policy barriers to implementing aspects of the model, with impediments to prescribing most commonly reported. The program proved to be flexible, cost effective and adaptable but relies heavily on in-kind support and the allocation of non-clinical time so that participants can manage study requirements. The credentialing component involved supervised practice of the expanded scope skills and completion of a competency log book. The program relies on in-kind support from specialist physiotherapy and medical staff, without which smaller physiotherapy departments would have great difficulty sustaining the program. Feedback from participating organisations raised issues about the structure of the program, delivery, content and assessment methods. The number of unexpected deaths was similar for the baseline and implementation periods and decreased post implementation. In general, they felt they had been listened to, their problems were understood, and the physiotherapists were comfortable and competent in dealing with their problems.

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Mild degree of liver cell necrosis is seen as ballooning degeneration while acidophilic Councilman bodies (inbox) are indicative of more severe liver cell injury blood pressure natural effective 2 mg terazosin. Whereas approximately 10% of adults contracting hepatitis E it is 2-8 weeks (15-60 days) heart attack karaoke purchase terazosin 1 mg. Icteric phase: the prodromal period is heralded by the may not show changes on liver biopsy blood pressure lyrics buy cheap terazosin on-line. The Asymptomatic carriers with chronic disease may show diagnosis is based on deranged liver function tests blood pressure chart age nhs safe 5mg terazosin. Asymptomatic Infection hyperglobulinaemia) and serologic detection of hepatitis these are cases who are detected incidentally to arteria principal order terazosin 2mg without prescription have antigens and antibodies blood pressure medication with a b generic 5 mg terazosin with mastercard. Post-icteric phase: the icteric phase lasting for about 1 raised serum transaminases or by detection of the presence to 4 weeks is usually followed by clinical and biochemical of antibodies but are otherwise asymptomatic. Acute Hepatitis acute hepatitis may develop severe form of the disease the most common consequence of all hepatotropic viruses (fulminant hepatitis); and 5-10% of cases progress on to is acute inflammatory involvement of the entire liver. Grossly, the liver is Clinically, acute hepatitis is categorised into 4 phases: slightly enlarged, soft and greenish. The last named gives rise to i) Mildly injured hepatocytes appear swollen with autoimmune or lupoid hepatitis which is characterised by granular cytoplasm which tends to condense around the positive serum autoantibodies. Bridging necrosis is characterised by bands of the vulnerability of a patient of viral hepatitis to develop necrosis linking portal tracts to central hepatic veins, one chronic hepatitis are: impaired immunity and extremes of age central hepatic vein to another, or a portal tract to another at which the infection is first contracted. Inflammatory infiltrate: There is infiltration by hepatitis activity score (described below). The frequency and mononuclear inflammatory cells, usually in the portal severity with which hepatotropic viruses cause chronic tracts, but may permeate into the lobules. It is usually not possible to distinguish are as under: histologically between viral hepatitis of various etiologies, i) Necrosed hepatocytes at the limiting plate in but the following morphologic features may help in giving periportal zone. Chronic Hepatitis characterised by variable degree of changes in the portal tract. Chronic hepatitis is defined as continuing or relapsing i) Inflammatory cell infiltration by lymphocytes, plasma hepatic disease for more than 6 months with symptoms along cells and macrophages (triaditis). Majority of cases of chronic iii) Additionally, chronic hepatitis C may show lymphoid hepatitis are the result of infection with hepatotropic aggregates or follicles with reactive germinal centre and viruses?hepatitis B, hepatitis C and combined hepatitis B 612 Figure 21. Diagrammatic representation of pathologic changes in chronic hepatitis (B) contrasted with normal morphology (A). Photomicrograph on right (C) shows stellate-shaped portal triad, with extension of fibrous spurs into lobules. The portal tract is expanded due to increased lymphomononuclear inflammatory cells which are seen to breach the limiting plate. Necroinflammatory activity: vii) Cases of chronic hepatitis B show scattered ground Periportal necrosis i. The onset of fibrosis in chronic Intralobular necrosis, focal or confluent (ranging from score hepatitis from the area of interface hepatitis and bridging 0 as none to score 4 for >10 foci for focal necrosis, and necrosis is a feature of irreversible damage. Extent and depth of portal inflammation (ranging from grade necrosis in which the liver failure is rapid and fulminant 613 0 as no inflammation to grade 4 having marked portal occurring in 2-3 weeks. Fulminant hepatitis of either of the two varieties can occur from viral and non-viral etiologies: B. In addition, hepatitis are quite variable ranging from mild disease to full herpesvirus can also cause serious viral hepatitis. Non-viral causes include acute hepatitis due to drug i) Mild chronic hepatitis shows only slight but persistent toxicity. The patients present with features of hepatic failure with hepatic encephalopathy (page 602). The mortality rate is high iii) Laboratory findings may reveal prolonged prothrombin if hepatic transplantation is not undertaken. Grossly, the liver is small iv) Systemic features of circulating immune complexes due and shrunken, often weighing 500-700 gm. The sectioned surface shows diffuse complex vasculitis, glomerulonephritis and cryoglobuli or random involvement of hepatic lobes. Fulminant Hepatitis Regeneration in submassive necrosis is more orderly and (Submassive to Massive Necrosis) may result in restoration of normal architecture. Fulminant hepatitis is the most severe form of acute hepatitis ii) In massive necrosis, the entire liver lobules are in which there is rapidly progressive hepatocellular failure. As a result of loss of hepatic parenchyma, all that Two patterns are recognised?submassive necrosis having a is left is the collapsed and condensed reticulin framework less rapid course extending up to 3 months; and massive and portal tracts with proliferated bile ductules plugged Figure 21. There is wiping out of liver lobules with only collapsed reticulin framework left out in their place, highlighted by reticulin stain (right photomicrograph). Regeneration, Cholangitis is the term used to describe inflammation of the if it takes place, is disorderly forming irregular masses of extrahepatic or intrahepatic bile ducts, or both. Fibrosis is generally not a feature of main types of cholangitis?pyogenic and primary sclerosing. While primary sclerosing cholangitis is discussed later with biliary cirrhosis (page 625), pyogenic cholangitis is described the clinicopathologic course in two major forms of below. Most prevention of its spread to the contacts after detection and commonly, the obstruction is from impacted gallstone; other identification of route by which infection is acquired such as causes are carcinoma arising in the extrahepatic ducts, from food or water contamination, sexual spread or carcinoma head of pancreas, acute pancreatitis and parenteral spread. Bacteria gain entry a few hepatitis vaccines have been developed and some more to the obstructed duct and proliferate in the bile. The principle underlying either of spreads along the branches of obstructed duct and reaches these two forms of prophylaxis is that the persons who the liver, termed ascending cholangitis. The common infecting develop good antibody response to the antigen of the bacteria are enteric organisms such as E. Immunoprophylaxis and hepatitis vaccination are small beaded abscesses accompanied by bile stasis along unnecessary if the pre-testing for antibodies is positive. Passive immunisation with immune in time are replaced by chronic inflammatory cells and globulin as well as active immunisation with a killed vaccine enclosed by fibrous capsule. Current Most liver abscesses are of bacterial (pyogenic) origin; less recommendations include pre-exposure and post-exposure often they are amoebic, hydatid and rarely actinomycotic. Ascending cholangitis through ascending infection in the with combination of hepatitis B immune globulin and biliary tract due to obstruction. Amoebae multiply and block small intrahepatic portal radicles resulting in infarction necrosis of the adjacent liver parenchyma. The patients, generally from tropical and subtropical countries, may give history of amoebic dysentery in the past. Intermittent low-grade fever, pain and tenderness in the liver area are common presenting features. A positive haemagglutination test is quite sensitive and useful for diagnosis of amoebic liver abscess. Grossly, amoebic liver abscesses are usually solitary and more often located in 2. Portal pyaemia by means of spread of pelvic or gastro the right lobe in the posterosuperior portion. Amoebic intestinal infection resulting in portal pylephlebitis or septic liver abscess may vary greatly in size but is generally of emboli. The centre of the abscess contains diverticulitis, regional enteritis, pancreatitis, infected large necrotic area having reddish-brown, thick pus haemorrhoids and neonatal umbilical vein sepsis. Iatrogenic causes include liver biopsy, percutaneous biliary found in the liver tissue at the margin of abscess. The diagnosis is possible by liver right upper quadrant, fever, tender hepatomegaly and biopsy. There may be leucocytosis, elevated serum alkaline phosphatase, elevated serum alkaline phosphatase levels and hypoalbuminaemia and a positive blood culture. The basic lesion is the the cause for pyogenic liver abscess, they occur as single epithelioid cell granuloma characterised by central or multiple yellow abscesses, 1 cm or more in diameter, in an enlarged liver. There are multiple small neutrophilic abscesses with areas of extensive necrosis of the affected liver parenchyma. The adjacent viable area shows pus and blood clots in the portal vein, inflammation, congestion and proliferating fibroblasts. Direct extension from the liver may lead to subphrenic or pleuro-pulmonary suppuration or peritonitis. There may be small pyaemic abscesses elsewhere such as in the lungs, kidneys, brain and spleen. The dog is the common definite host, while man, sheep and cattle are the intermediate hosts. The infected faeces of the dog contaminate grass and farmland from where the ova are ingested by sheep, pigs and man. Thus, man can acquire infection by handling dogs as well as by eating conta minated vegetables. The ova ingested by man are liberated from the chitinous wall by gastric juice and pass through the intestinal mucosa from where they are carried to the liver by portal venous system. These are trapped in the hepatic sinusoids where they eventually develop into hydatid cyst. About 70% of hydatid cysts develop in the liver which acts as the first filter for ova. However, ova which pass through the liver enter the right side of the heart and are caught in the pulmonary capillary bed and form pulmonary hydatid Figure 21. Some ova which enter the systemic circulation give shows epithelioid granulomas with small areas of central necrosis and rise to hydatid cysts in the brain, spleen, bone and muscles. The disease is common in sheep-raising countries such as Australia, New Zealand and South America. The uncomplicated hydatid cyst of the liver may be silent or may caseation necrosis with destruction of the reticulin produce dull ache in the liver area and some abdominal framework and peripheral cuff of lymphocytes distension. Rare the peritoneal cavity, bile ducts and lungs), secondary lesions consist of tuberculous cholangitis and tuberculous infection and hydatid allergy due to sensitisation of the host pylephlebitis. The diagnosis is made by peripheral blood eosinophilia, radiologic examination and serologic tests such as indirect haemagglutination test and Casoni skin test. The cyst wall is composed of whitish membrane resembling the membrane of a hard boiled egg. Hydatid cyst grows existing liver disease, aging, female sex and genetic inability slowly and may eventually attain a size over 10 cm in to perform a particular biotransformation. Toxic liver injury produced by drugs multilocular or alveolar hydatid disease in the liver. In fact, any patient presenting with outer pericyst, intermediate characteristic ectocyst and inner liver disease or unexplained jaundice is thoroughly endocyst (Fig. Hepatotoxicity from drugs and chemicals is the consisting of fibroblastic proliferation, mononuclear cells, commonest form of iatrogenic disease. Severity of eosinophils and giant cells, eventually developing into hepatotoxicity is greatly increased if the drug is continued dense fibrous capsule which may even calcify. Ectocyst is the intermediate layer composed of Among the various inorganic compounds producing characteristic acellular, chitinous, laminated hyaline hepatotoxicity are arsenic, phosphorus, copper and iron. Endocyst is the inner germinal layer bearing daughter toxins such as pyrrolizidine alkaloids, mycotoxins and cysts (brood-capsules) and scolices projecting into the bacterial toxins. In addition, exposure Hydatid sand is the grain-like material composed of to hepatotoxic compounds may be occupational, numerous scolices present in the hydatid fluid. Hydatid environmental or domestic that could be accidental, fluid, in addition, contains antigenic proteins so that its homicidal or suicidal ingestion. The liver plays a central occur in most individuals who consume them and their role in the metabolism of a large number of organic and hepatotoxicity is dose-dependent. The main drug metabolising system resides in the drug or one of its metabolites acts as a hapten and induces microsomal fraction of the smooth endoplasmic reticulum hypersensitivity in the host. In many instances, drug of the liver cells via P-450 cytochrome and cytochrome hepatotoxicity is associated with appearance of reductase enzyme systems. The hepato cule, its active transport from the hepatocytes and ultimately toxicity by this group does not occur regularly in all its excretion in the bile or in urine depending upon the individuals and the effects are usually not dose-related. There is formation of nodules separated from one another Halothane by irregular bands of fibrosis. It occurs following hepatocellular necrosis of varying Acetaminophen etiology so that there are alternate areas of necrosis and Methyldopa regenerative nodules. Fatty change Tetracycline essential for diagnosis of cirrhosis since biliary cirrhosis and Salicylates cirrhosis in haemochromatosis have little regeneration. Hepatitis Methyldopa Isoniazid Irrespective of the etiology, cirrhosis in general is initiated Halothane by hepatocellular necrosis. Continued destruction of Ketoconazole hepatocytes causes collapse of normal lobular hepatic parenchyma followed by fibrosis around necrotic liver cells 5. Granuloma formation Sulfonamides Methyldopa and proliferated ductules and there is formation of Quinidine compensatory regenerative nodules. The mechanism of fibrosis is oral contraceptives) by increased synthesis of all types of collagen and increase Chlorpromazine in the number of collagen-producing cells. In cirrhosis, there Nitrofurantoin is proliferation of fat-storing Ito cells underlying the 7. Veno-occlusive disease Cytotoxic drugs sinusoidal epithelium which become transformed into 8. Besides collagen, two thrombosis glycoproteins, fibronectin and laminin, are deposited in excessive amounts in area of liver cell damage. Fibrosis-cirrhosis Methotrexate known, but possible candidate mediators are lymphokines 2. The cause of compensatory Sex hormones proliferation of hepatocytes to form regenerative nodules is 3. The changes produced by hepatotoxic agents may vary from mild, which are diagnosed A.

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Some experts recommend quantitative testing for fetal?maternal hemorrhage (eg arteria lacrimalis generic terazosin 5 mg on-line, Kleihauer-Betke testing) in the Rh (O) D-negative woman to blood pressure kit target buy terazosin visa identify the unusual large-volume hemorrhage (ie heart attack or heartburn order 5mg terazosin, more than 30 mL of fetal?maternal hemorrhage) pulse pressure test discount 1 mg terazosin overnight delivery, for which 300 micrograms of Rh(O) D immune globulin may be insufficient (see also Isoimmunization in Pregnancy earlier in this chapter) blood pressure medication green capsule generic terazosin 1 mg without prescription. Labor and Delivery Considerations and Complications Assessment and Management of Fetal Pulmonary Maturation ^145^258 the decision to normal pulse pressure 60 year old buy cheap terazosin 1 mg on-line deliver before 39 weeks of gestation should be based on appropriate medical (maternal or fetal) indications when the risks of continu ing the pregnancy outweigh the risks of delivery. Because of the new appreciation of the neo natal and pediatric risks associated with delivery before 39 weeks of gestation, lung maturity is not an indication for delivery before 39 weeks of gestation. Only occasionally should the knowledge of pulmonary maturity be needed to proceed with a planned delivery before 39 weeks of gestation. Antenatal Corticosteroid Therapy For women at risk of preterm birth, enhancement of fetal pulmonary function with the use of antenatal steroids lessens the prevalence and severity of neonatal Obstetric and Medical Complications 249 respiratory distress syndrome and its sequelae. A single course of corticosteroids (betamethasone or dexamethasone) is recommended for pregnant women between 24 weeks and 34 weeks of gestation who are at risk of preterm delivery within 7 days. Sparse data exist on the efficacy of corticosteroid use before fetal age of viability, and such use is not recommended. A single rescue course of antenatal corticosteroids may be considered if the antecedent treatment was given more than 2 weeks prior, the gestational age is less than 32 6/7 weeks, and the woman is judged by the physician to be likely to give birth within the next week. However, regularly scheduled repeat courses or multiple courses (more than two) are not recommended. Births at the Threshold of Viability Early preterm birth or birth of an extremely low birth weight infant (less than 1,000 g), especially those weighing less than 750 g or less than 26 weeks of gesta tion, poses a variety of complex medical, social, and ethical considerations. The effect of such births on the infants, their families, the health care system, and society is profound. Although the prevalence of such births is less than 1%, they account for nearly one half of all cases of perinatal mortality. Family Counseling When extremely preterm birth is anticipated, the estimated gestational age and weight should be carefully assessed, the prognosis for the fetus should be deter mined, and each member of the health care team should make every effort to maintain a consistent theme in their discussion with family members regarding 250 Guidelines for Perinatal Care the assessment, prognosis, and recommendations for care. Counseling from a practitioner with additional experience and expertise in extremely preterm and extremely low birth weight infants may be appropriate. In general, parents of anticipated extremely preterm fetuses can be coun seled that infants delivered before 24 weeks of gestation are less likely to survive, and those who do are not likely to survive intact. The neonatal survival rate for newborns increases from 0% at 21 weeks of gestation to 75% at 25 weeks of gestation, and from 11% at 401?500 g birth weight to 75% at 701?800 g birth weight. Disabilities in mental and psychomotor development, neuromotor function, or sensory and communication function are present in approximately one half of extremely preterm fetuses. Management Retrospective studies addressing obstetric management on outcomes of extremely premature neonates have failed to document a benefit of cesarean delivery over vaginal delivery. The effect of antenatal steroid use in the extremely preterm fetus is unclear; however, it is recommended that all women at risk of preterm delivery between 24 weeks and 34 weeks of gestation be candidates for a single course of corticosteroids (see also Assessment and Management of Fetal Pulmonary Maturation earlier in this chapter). Maternal transport to a tertiary care center before delivery should be considered whenever possible. Management regarding the extent of resuscitative and supportive efforts should be based on gestational age and birth weight but should be further individualized based on the newborns condition at birth and the parents preferences. This information may be developed by each institution and should indicate the population used in determining estimates of survivability. Chorioamnionitis Chorioamnionitis or intra-amniotic infection is largely a clinical diagnosis that often is made presumptively during labor if a laboring woman develops a Obstetric and Medical Complications 251 fever for which there is no other obvious etiology. The classic signs and symp toms include maternal fever, maternal tachycardia, uterine tenderness, fetal tachycardia, and foul-smelling amniotic fluid. Common organisms that cause chorioamnionitis include gram-negative bacteria (particularly Escherichia coli), gram-positive bacteria (particularly group B streptococci and staphylococcus), and occasionally anaerobes. It is clear that neonates born to mothers with cho rioamnionitis have less infectious outcomes if their mother is treated in utero with appropriate antibiotics. Treatment for chorioamnionitis typically is the administration of ampicillin and gentamicin; treatment with only penicillin or ampicillin is never adequate for chorioamnionitis. Endocarditis Most cases of endocarditis are not attributable to an invasive procedure, but rather are the result of randomly occurring bacteremia from routine daily activi ties. Antibiotic prophylaxis may only prevent a small number of cases of infec tive endocarditis in women undergoing genitourinary procedures, and the risk of antibiotic-associated adverse events exceeds the benefit, if any, from prophy lactic antibiotic therapy. For these reasons, the American Heart Association and the American College of Cardiology no longer recommend infective endocar ditis prophylaxis for either vaginal delivery or cesarean delivery in the absence of infection, except possibly for the small subset of patients at highest potential risk of adverse cardiac outcomes who are undergoing vaginal delivery. Only cardiac conditions associated with the highest risk of adverse outcomes from endocarditis are appropriate for infective endocarditis prophylaxis, and this is primarily for patients undergoing dental procedures that involve manipulation of gingival tissue or the periapical region of teeth, or perforation of the oral mucosa (see Box 7-3). Mitral valve prolapse is not considered a lesion that ever needs infective endocarditis prophylaxis. In patients who have one of the high-risk conditions (see Box 7-3) and an established infection that could result in bacteremia, such as chorioamnionitis or pyelonephritis, the underlying infection should be treated to prevent infec tion or sepsis, but specific additional endocarditis prophylaxis is not recom mended. For women not already receiving intrapartum antibiotic therapy for another indication that would also provide coverage against endocarditis, sin gle-dose antibiotic regimens for endocarditis prophylaxis can be administered as close to 30?60 minutes before the anticipated time of delivery as is feasible. Multiple-dose combination regimens are no longer indicated or recommended for prophylaxis. Clinically, endome tritis is characterized by fever, uterine tenderness, malaise, tachycardia, abdomi nal pain, or foul-smelling lochia. Of these, fever is the most characteristic and may be the only sign early in the course of infection. Risk factors for postpar tum endometritis include cesarean delivery, prolonged rupture of membranes, Obstetric and Medical Complications 253 prolonged labor with multiple vaginal examinations, intrapartum fever, and lower socioeconomic status. Prophylaxis Against Postcesarean Infection the single most important risk factor for infection in the postpartum period is cesarean delivery. Antimicrobial prophylaxis is recommended for all cesarean deliveries unless the patient is already receiving an antibiotic regimen with appropriate coverage (eg, for chorioamnionitis), and such prophylaxis should be administered within 60 minutes before the start of the cesarean delivery. When this is not possible (eg, need for emergent delivery), prophylaxis should be administered as soon as possible after the incision is made. A single dose of a targeted antibiotic, such as a first-generation cephalo sporin, is the first-line antibiotic of choice, unless significant drug allergies are present. For women with a history of a significant penicillin or cephalosporin allergy (anaphylaxis, angioedema, respiratory distress, or urticaria), a single-dose combination of clindamycin with an aminoglycoside is a reasonable alternative choice for cesarean delivery prophylaxis. After a single 1-gram intravenous dose of cefazolin, a therapeutic level is maintained for approximately 3?4 hours. Patients with lengthy sur geries or those who experience excessive blood loss should receive an additional intraoperative dose of the antibiotic used for preincision prophylaxis. A woman with postpartum fever should be evaluated by pertinent history, physical exam ination, blood count, and urine culture. Blood cultures rarely influence thera peutic decisions but could be indicated if septicemia is suspected. Cervical, vaginal, or endometrial cultures need not be routinely performed because the results might not indicate the infecting organism. Parenteral, broad-spectrum antibiotic treatment should be initiated according to a proven regimen and continued until the patient is afebrile. A combination of clindamycin and gentamicin, with the addition of ampicillin in refractory cases, is recommended for cost-effective therapy. If fever persists beyond antibiotic treatment for 24?48 hours, a search for alternative etiologies, including pelvic 254 Guidelines for Perinatal Care abscess, wound infection, septic pelvic thrombophlebitis, inadequate antibiotic coverage, and retained placental tissue, should be performed. Maternal Hemorrhage Hemorrhage remains one of the leading causes of maternal mortality world wide. One half of all maternal deaths occur within 24 hours of delivery and most commonly from excessive bleeding. Facilities that provide labor and delivery services should be prepared to manage maternal hemorrhage. Proper preparation and resources to manage maternal hemorrhage in a timely manner can be lifesaving. Policies to ensure the rapid availability of blood products for transfusion in the event of hemorrhage must be in place. Criteria of an esti mated blood loss of greater than 500 mL after a vaginal delivery or 1,000 mL after cesarean delivery are often used, but the average volume of blood lost at delivery can approach these amounts. Symptoms of hypotension, pallor, and oliguria typically do not occur until blood loss is substantial. Risk factors for excessive bleeding include prolonged, augmented, or rapid labor; history of postpartum hemorrhage; episiotomy, especially mediolateral; preeclampsia; overdistended uterus (macrosomia, twins, or hydramnios); operative delivery; Asian or Hispanic ethnicity; and chorioamnionitis. Other etiologies include retained placenta, placenta accreta, uterine rupture, uterine inversion, obstetric lacera tions, retained products of conception, maternal coagulopathy, and infection. In an effort to prevent uterine atony and associated bleeding, it is routine to administer oxytocin soon after delivery. Management may vary greatly among patients, depending on etiology of the hemorrhage and available treatment options, and often a multidisciplinary approach is required. Less-invasive methods should be tried initially if possible, but if unsuccessful, preservation of life may require hysterectomy. Treatment options for postpartum hemorrhage due to uterine atony include administra tion of uterotonics and pharmacologic agents, tamponade of the uterus, surgical Obstetric and Medical Complications 255 techniques to control the bleeding, and embolization of pelvic arteries. Treatment of hemorrhage due to uterine rupture should be tailored to the site of uterine injury, maternal condition, and her desire for future childbearing; hysterectomy may be necessary in a life-threatening situation. In the presence of previa or a history of cesarean delivery, the obstetric care provider must have a high clinical suspicion for placenta accreta and take appropriate precau tions. The extent (area, depth) of the abnormal attachment will determine the response?curettage, wedge resection, medical management, or hysterectomy; abdominal hysterectomy usually is the most definitive treatment. Manual replacement with or without uterine relaxants usually is successful for man agement of uterine inversion. Transfusion Transfusion therapy is used to prevent or treat hemorrhagic shock and its con sequences. Transfusion of blood products is necessary when the extent of blood loss is significant and ongoing, particularly if vital signs are unstable. Clinical judgment is an important determinant, given that estimates of blood loss often are inaccurate, determination of hematocrit or hemoglobin concentrations may not accurately reflect the current hematologic status, and symptoms and signs of hem orrhage may not occur until blood loss exceeds 15%. The purpose of transfusion of blood products is to replace coagulation factors and red blood cells for oxygen carrying capacity, not for volume replacement. To avoid dilutional coagulopathy, concurrent replacement with coagulation factors and platelets may be necessary. Accurate pregnancy dating is critical to the diagnosis (see also Estimated Date of Delivery in Chapter 5). Accurate assessment of gestational age and diagnosis of postterm gestation, as well as recognition and management of risk factors, may reduce the risk of adverse sequelae. Fetal risks include an increased perinatal mortality rate, uteroplacental insuf ficiency, meconium aspiration, intrauterine infection, low umbilical artery pH 256 Guidelines for Perinatal Care levels at delivery, and low 5-minute Apgar scores. Significant risks to the preg nant woman include an increase in labor dystocia, an increase in severe perineal injury related to macrosomia, and a doubling in the rate of cesarean delivery. Management Many authorities recommend prompt delivery in a postterm patient with a favorable cervix and no other complications. Although postterm pregnancy is defined as a pregnancy of 42 weeks or more of gestation, data suggest that rou tine induction at 41 weeks of gestation has fetal benefit without incurring the additional maternal risks of a higher rate of cesarean delivery. Women with postterm gestations who have unfavorable cervices can either be managed expectantly or undergo labor induction. Many practitioners use twice-weekly testing with some evaluation of amniotic fluid volume beginning at 41 weeks of gestation. Delivery should be initiated if there is evidence of fetal compromise or oligohydramnios. Preterm Birth ^158^241 Preterm birth is defined as birth before 37 completed weeks of gestation. Spontaneous preterm birth includes preterm labor, preterm spontaneous rup ture of membranes, and cervical insufficiency. Preterm birth is the leading cause of neonatal mortality and one of the most common reasons for antenatal hospitalization. In the United States, approximately 12% of all live births occur before term, and preterm labor preceded approximately 50% of these preterm births. The pathophysiologic events that trigger preterm parturition are largely unknown but may include decidual hemorrhage (abruption), mechanical fac tors (uterine overdistention or cervical incompetence), hormonal changes (per haps mediated by fetal or maternal stress), infection, and inflammation. Risk Factor Identification and Management A prior preterm birth is commonly reported to confer a 1. Other risk factors for preterm birth Obstetric and Medical Complications 257 include African American race, age younger than 17 years or older than 35 years, low socioeconomic status, underweight prepregnancy body mass index, smoking, vaginal bleeding in more than one trimester, bacterial infections, and short cervical length. Screening for risk of preterm birth by means other than his toric risk factors is not beneficial in the general obstetric population. Fetal fibronectin testing may be useful in women with symptoms of preterm labor to identify those with negative values and a reduced risk of preterm birth, thereby avoiding unnecessary intervention. Women with a singleton gestation and prior spontaneous pre term birth should be offered progesterone supplementation starting at 16 weeks of gestation to reduce the risk of the recurrence of preterm birth. Diagnosis of Preterm Labor the diagnosis of preterm labor is generally based upon clinical criteria of regular uterine contractions accompanied by cervical dilation, or effacement or presen tation, or both with regular contractions and at least 2 cm dilation. Fewer than 10% of women with the clinical diagnosis of preterm labor actually deliver within 7 days of presentation. It is important to recognize that preterm labor is not the only cause of preterm birth; numerous preterm births are preceded by either rupture of membranes (see also Premature Rupture of Membranes later in this chapter) or other medical problems. Patients with suspected preterm labor should be examined and observed for 1?2 hours, have their uterine activity monitored, and undergo serial cervi cal examinations to document the presence or absence of cervical change. The positive predictive value of a positive fetal fibronectin test result or a short cer vix alone is poor and should not be used exclusively to direct management in the setting of acute symptoms. Because preterm labor often is associated with urinary tract infections, a dipstick or a microscopic examination of urine and urine culture may be helpful. Ultrasound examination also may be considered to confirm gestational age, to estimate fetal weight in order to receive appro priate counseling from pediatrics, and to assess the presence of any congenital anomalies. Management of Preterm Labor Interventions to reduce the likelihood of delivery should be reserved for women likely to give birth and who are at a gestational age at which delay in delivery 258 Guidelines for Perinatal Care will provide benefit to the newborn.

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Actin consists of approximately 350 monomers and 50 molecules of each of the regulatory proteins tropomyosin and troponin blood pressure medication on empty stomach buy terazosin 5 mg line. The actin monomers are termed G-actin because they are globular and have molecular weights of approximately 42 kD blood pressure levels chart cheap 1 mg terazosin free shipping. G-actin normally is polymerized to pulse pressure locations quality terazosin 1 mg F-actin (ie arrhythmia and chest pain discount 1mg terazosin mastercard, filamentous actin) blood pressure 40 over 70 order terazosin 5 mg mastercard, which is arranged in a double helix blood pressure 5545 buy 1 mg terazosin visa. The actin filaments also join together to form the boundary between two sarcomeres in the area of the A band. A muscle shortens or lengthens because the myosin and actin myofilaments slide past each other withoutthefilamentsthemselveschanginglength. The myosincross-bridgeprojectsoutfromthemyosintail and attaches to an actin monomer in the thin filament. The cross-bridges then move as ratchets, forcing thethinfilamentstowardtheMlineandcausingasmallamountofsarcomereshortening. Themajorstructural rearrangement during contraction occurs in the region of the I band, which decreases markedly in size. List the functions of myonuclei and satellite cells, and identify the number of nuclei found in the skeletal muscle fiber. What are the major steps of fatty acid metabolism in muscle that result in the release of energy? Muscle fiber lengths range from a few millimeters in the intraocular muscles of the eye to >45 cm in the sartorius muscle. Satellite cells are normally dormant, but under conditions of stress or injury, they are essential for the regenerative growth of new fibers. Satellite cells have chemotactic properties, meaning they migrate from one location to another of higher need within a muscle fiber and then participate in the normal process of developing a new muscle fiber. The process of new fiber formation begins with satellite cells entering a mitotic phase to produce additional satellite cells. These cells then migrate across the plasma membrane into the cytosol, where they recognize each other, align, and fuse into a myotube, an immature form of a muscle fiber. Muscle growth factors are proteins that either promote muscle growth and repair or inhibit muscle protein breakdown. Examples include insulin-like growth factor, fibroblast growth factor, hepatocyte growth factor, and transforming growth factor. The variable number of myofibrils is regulated during the hypertrophy of muscle fibers that is associated with growth; for example, the number of myofibrils ranges from 50 per muscle fiber in the muscles of a fetus to approximately 2000 per fiber in the muscles of an untrained adult. The hypertrophy and atrophy of adult skeletal muscle are associated with certain types of training and disuse and result from the regulation of the number of myofibrils per fiber. The cross-sectional area of an individual muscle fiber ranges from approximately 2000 to 7500? For example, the length of the medial gastrocnemius muscle is approximately 250 mm, with fiber lengths of 35 mm, whereas the sartorius muscle is approximately 500 mm, with fiber lengths of 450 mm. The numbers of fibers range from several hundred in small muscles to >1 million in large muscles, such as those involved in hip flexion and knee extension. In a parallel-fiber muscle, the muscle fibers are arranged essentially in parallel with the longitudinal axis of the muscle itself. When muscles are designed with angles of pennation, which is the most common architecture, more sarcomeres can be packed in parallel between the origin and insertion of the muscle. As the angle of pennation increases, an increasing portion of the force developed by sarcomeres is displaced away from the tendons. As long as the angle of pennation is <30 degrees, the force lost as a result of the angle of pennation is more than compensated for by the increased packing of sarcomeres in parallel, producing an overall benefit to the force-producing capacity of muscle. The muscle shortens at different velocities depending on the load placed on the muscle. The force developed during a shortening contraction is less than the isometric force. The force developed during a lengthening contraction exceeds the isometric force by 50% to 100% because of the increased extension of the attached cross-bridges. The myosin structural state, the ratio of strong binding and weak binding cross-bridges to actin, muscle innervation, motor unit recruitment, and synchronization are all factors influencing muscle strength. Active insufficiency is the diminished ability of a muscle to produce or maintain active tension when elongated to the point at which there is no overlap between myosin and actin. When a motor neuron is activated, all the muscle fibers innervated by that motor neuron contract maximally. Excitation-contraction coupling is the physiologicmechanism whereby an electric dischargeat the muscle initiates the chemical events that lead to contraction. Acetylcholine, the neurotransmitter at the neuromuscular junction, is released from the axon terminals. Acetylcholine diffuses across the neuromuscular junction and binds with acetylcholine receptors on the sarcolemma of the muscle. The action potential (voltage change) is sensed by the dihydropyridine receptors in the transverse tubules. Calcium binds to the regulatory protein, troponin C, and the interaction between actin and myosin can occur. The myosin cross-bridges move into a strong binding state, and force production occurs. Muscle spindles provide sensory information concerning changes in the length and tension of muscle fibers. Their main function is to respond to the stretch of a muscle and, through reflex action, to produce a stronger contraction to reduce the stretch. The spindle is fusiform in shape and is attached in parallel to the regular or extrafusal fibers of the muscle. There are two sensory afferents and one motor efferent innervating the intrafusal fibers. The gamma efferent innervates the contractile portion?the striated ends of the spindle. These fibers, activated by higher cortex levels, provide the mechanism for maintaining the spindle at peak operation at all muscle lengths. When skeletal muscles contract voluntarily against a load, motor units are recruited from smallest to largest. Connected in series to 25 extrafusal fibers, these sensory receptors also are located in the ligaments of joints and are primarily responsible for detecting differences in muscle tension. Describe the adaptations in muscle structure that occur with progressive resistance exercises. Progressive resistive exercise involves 10 repetitions a day at 60% to 90% of maximal capacity; this results in an increase in strength by 0. Furthermore, neural adaptations result in an increased ability to recruit high-threshold motor units. The functional significance of this morphologic change is primarily a greater capacity for strength and power development. Endurance exercise has minimal impact on the cross-sectional area of muscle and muscle fibers. The smaller cross-sectional area allows better diffusion of metabolites and nutrients between the contractile filaments and the cytoplasm and between the cytoplasm and the interstitial fluid. The number of capillaries increases around each fiber, and there is an increase in mitochondria, especially in the type I fibers. The more extensive capillary bed improves the delivery of oxygen and circulating energy sources to the fibers, whereas the products of muscle activity are removed more efficiently. The functional significance of these changes is observed during sustained exercise, in which there is a delay in the onset of fatigue. Sarcopenia is the term used to describe age-related loss of skeletal muscle mass and strength. Apoptosis, or programmed cell death, is a regulated physiologic process critical to cellular homeostasis, which can become dysregulated, leading to disease states including muscle disease or dysfunction. Skeletal muscle structure, function, & plasticity: the physiological basis of rehabilitation (3rd ed. Molecular diversity of myofibrillar proteins: Gene regulation and functional significance. Sarcopenia is the term describing the loss of muscle mass and strength with aging. The physical activity level does not affect the changes of skeletal muscles with aging. Fast-twitch muscles show more significant age-related changes than slow-twitch muscles 2. Although two movements may appear similar (kinematics), the underlying forces causing those movements (kinetics) may be very different. This fact should be appreciated when using readily available motion analysis tools (such as recording movements on smartphones or tablets). Impulse is the area under the force-time curve and accounts not only for the magnitude of the force but also for the duration over which the force is applied. Increasing the time of the impact, which can be accomplished by cushioned shoes and/or bending the knees when making contact with the ground, can attenuate the magnitude of an impact force and may decrease the risk of injury. Elastic materials, such as bands and tubes, are often used as a form of resistance and follow Hooke?slaw (the force is proportional to the stiffness and elongation). The stiffness is determined by the manufacturer (whichusesdifferentcolorsfordifferentlevelsofstiffness)andwilldecreasewithtimeasthematerialfatigues. It is also important to keep in mind that the elongation is related to the resting length of the band or tube and not just the elongation during the exercise. In the first, an exercise starts with the band at its resting length and is elongated by a certain amount, x. In brief, if the convex surface of one bone is moving on the fixed concave surface of another bone, rotation and translation will occur in opposite directions. Additionally, if the concave surface of one bone is moving on the fixed convex surface of another bone, rotation and translation occur in the same direction. It is proposed that in order to restore rotational motion at a joint, a linear mobilization is performed in relation to the treatment plane, which is parallel to the concave joint surface. Mobilization can be performed on either segment in accordance with the convex-concave rule. For example,it has beendemonstratedthatthe glenohumeraljoint contradicts the convex-concave rule during external rotation when the humerus is abducted to 90 degrees, and there is no clear consensus that the femur translates anteriorly when the knee is flexing in a weight bearing position. However, these findings may not violate the convex-concave rule if the amount of translation in the direction of rolling is less than what the curvature of the convex segment would predict. Therefore the application of the convex-concave rule to treatment may need to be further informed by the direct method of assessing a restriction of joint gliding. Cartilage degeneration often accompanies the presence of a nonfixed axis of rotation. An absolute angle is the angle that the distal point of a segment (eg, foot, shank, thigh) makes with respect to some reference line (such as the horizontal for sagittal plane movements). A relative angle is the joint angle made by two segments (eg, the knee angle is the angle between the shank and thigh). Relative angles can be stated as either internal (included) or external (anatomic) angles. An internal angle is the angle between the longitudinal axes of the two segments comprisinga joint, while the external angle is the angular displacement from the anatomic position. If this angle were decreased by 30 degrees, the internal angle would be 150 degrees and the external angle would be 30 degrees. In observational gait analysis, for example, ankle and knee measures are usually external relative angles, while the thigh is usually an absolute angle with respect to the vertical; many motion capture systems, on the other hand, report internal angles for all three joints. In accordance with their Latin derivations, in early writings varum referred to knock knees and valgus referred to bow-legged. Because of the confusion this discrepancy can cause, it is prudent to understand how these terms are being used by various authors and not to assume that there are unambiguous and universally accepted definitions. The moment of a force (?moment for short), or torque, is the turning effect of a force. A force will have a tendency to rotate a body according to its magnitude, its direction, and the perpendicular distance between its line of application and the axis of rotation (this perpendicular distance is known as the moment arm). For example, low back injury prevention strategies are based on the premise of decreasing the moment about the low back during lifting by keeping the load as close to the spine as possible, thus reducing the moment arm of the external resistance. Similarly, flexing the elbows during abduction will decrease the moment arm about the shoulder, thus making the movement easier to perform. On the other hand, during manual muscle testing, the therapist can increase the demand on a muscle by applying the resistance as far from the axis of rotation as possible. Just as forces can be combined together to determine a resultant, they can also be broken into components. The components are useful in identifying the different effects of a force on a joint. For example, a muscle force can be divided into the component that is perpendicular to the bone (causing it to rotate and create a shear force across a joint) and the component that is parallel to the bone (usually increasing the compressive force across a joint). Therefore in addition to causing movement at a joint, all muscle forces will affect the amount of compression at a joint. During rehabilitation of certain joint pathologies, it may be necessary to identify which therapeutic exercises will increase the force of a muscle (to strengthen it) without applying excessive compressive forces across the joint. For example, performing unilateral (as opposed to bilateral) exercises for the lumbar extensors will decrease compressive forces on the spine while increasing the demand on those muscles. Over the range of motion of a joint, the magnitudes of moment arms and forces may vary. The amount of force a muscle can produce is influenced by several properties, including the length-tension relationship, which states that when a muscle is too stretched or too shortened it cannot actively produce as high amounts of force as it can when the muscle is at its optimal length. For example, when using the deltoid to abduct the shoulder from 0 to 180 degrees, the moment arm of the deltoid increases and the force-producing capabilities also increase to a position of optimal length and then decrease.

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A lung disorder caused by repeated exposure to arrhythmia books cheap 5mg terazosin fast delivery a sensitizing agent (organic and inorganic particles) and classified as acute arteria elastica terazosin 5 mg otc, subacute arteria alveolaris superior posterior buy terazosin 2mg without prescription, and chronic pulse pressure less than 10 order terazosin with visa. The acute form is characterized by respiratory symptoms that occur in a few hours after a heavy exposure heart attack jokes purchase discount terazosin on line. Treatment includes avoidance of the causative antigen and corticosteroids in severe or progressive disease heart attack restaurant buy on line terazosin. Affected groups include young and middle-aged adults, women, and African Americans. Sarcoidosis is postulated to occur in genetically susceptible individuals exposed to certain unknown environmental agents. A presentation of sarcoidosis with specific features that is usually seen in women. In the remaining patients without this classic presentation, a tissue diagnosis is required. Most commonly, the diagnosis is made by bronchial or transbronchial biopsy, mediastinal lymph node biopsy, biopsy of skin lesions, or less commonly, conjunctival or lacrimal gland biopsy. The characteristic lesion of sarcoidosis is a discrete, noncaseating epithelioid cell granuloma. However, noncaseating granulomas can be encountered in other diseases such as fungal and mycobacterial infections, foreign bodies, berylliosis, and common variable immunodeficiency. Any biopsy tissues obtained are routinely stained to exclude mycobacterial or fungal infections. Berylliosis develops after a usual latent period of years following a low-level exposure to beryllium. Other hard metal?induced lung diseases due to aluminum and cobalt exposure are also characterized by the presence of sarcoid-like granulomas. Many patients are asymptomatic and spontaneous resolution occurs in up to two thirds of them. Oral steroids, although treatment is usually not indicated in patients who are asymptomatic or in those with mild pulmonary function abnormalities. Steroid therapy is started in patients with progressive radiographic findings or moderate symptoms; hypercalcemia; and neurologic, cardiac, or ocular involvement. Other medications used in patients who cannot tolerate steroids or have progressive disease on steroid therapy include hydroxychloroquine, methotrexate, azathioprine, methotrexate, and tumor necrosis factor inhibitors. However, an elevated D-dimer level may be seen in many other conditions, such as malignancy or recent surgical procedures. In patients with allergy to contrast or who have renal failure, a nuclear medicine. V/Q scan and compression ultrasonography of the lower extremity veins may be performed. Overall, the risk of major complications is 4% and appears to be the highest in the most critically ill patients. Warfarin should be started simultaneously with any heparin, and both therapies continued for at least 4?5 days. Anticoagulation should be continued for at least 3 months, but longer treatment may be needed for patients with persistent risk factors. Warfarin is also started simultaneously with fondaparinux and continued as described. The contraindications include a history of intracranial hemorrhage, brain tumor, recent intracranial surgery or trauma, and recent (<6 mo) or active internal bleeding. Patients with uncontrolled hypertension, thrombocytopenia, bleeding tendency, recent history of nonhemorrhagic stroke, and surgery within the previous 10 days also are considered at high risk of complications of thrombolytic therapy. American Thoracic Society: the diagnostic approach to acute venous thromboembolism, Am J Respir Crit Care Med 160:1043?1066, 1999. Altered mental status, respiratory decompensation, anemia, thrombocytopenia, and petechiae that usually occur 12?36 hours after the inciting trauma. In general, these patients should be treated by a physician with expertise in the condition. In nonresponders, consider phosphodiesterase inhibitors type 5 (sildenafil or tadalafil), endothelin receptor antagonists (bosentan or ambrisentan), and prostacyclinanalogues(epoprostenol, treprostinil, or iloprost),depending onthe functional class, risk factors, and response to therapy. This intervention is considered in centers with experience for patients with central obstruction of the pulmonary arteries who have abnormal hemodynamic findings and a small number of comorbidities. Other types of pneumothorax are: & Catamenial pneumothorax: occurs in conjunction with menstruation & Traumatic pneumothorax: classified as iatrogenic (central line placement) and noniatrogenic (blunt or penetrating chest injury) Noppen M, De Keukelseir T: Pneumothorax, Respiration 76:7?15, 2008. The differentiation between these two types of effusions is important because it helps narrow the diagnostic possibilities. Transudative effusions are usually due to an imbalance in the hydrostatic or oncotic pressures or both. Exudative effusions have a broader differential diagnosis and are generally caused by inflammation, infection, malignancy, and lymphatic abnormalities. Describe the most relevant characteristic of the following exudative causes of pleural effusions. What are the diseases that can present with eosinophilic exudate (>10% eosinophils)? Hydropneumothorax Drug-induced effusions Fungal diseases Hemothorax Churg-Strauss Parasitic diseases Benign asbestos syndrome effusions 119. Lung cancer is the second most common cancer after skin cancer, but is the leading cause of cancer death in both men and women. More men than women die from lung cancer, but the gap in mortality is steadily narrowing. Lung cancer occurrence is 45% higher among African American men than among white men. Interestingly, in developed countries, the frequency of adenocarcinoma has increased while that of squamous carcinoma has decreased. The risk of lung cancer is based on the interrelationship between the exposure to etiologic agents and individual susceptibility (genetic factors). Compared with never smokers, smokers have an approximately 20-fold increase in lung cancer risk. The risk for lung cancer increases with the duration and number of cigarettes smoked per day. The risk of lung cancer decreases among those who quit smoking, but remains increased above that of nonsmokers for years after the quit date. Asbestos and cigarette smoking act synergistically to increase the risk of lung cancer. Symptoms and signs of breathlessness, bibasilar inspiratory crackles, and clubbing. Presence of interstitial pneumonia pattern with asbestos bodies on biopsy (if needed). Early studies showed that screening with chest radiographs and sputum cytology did not decrease lung cancer mortality. Independent predictors of malignancy includes older age, current or past smoking history, history of extrathoracic cancer > 5 years before nodule detection, larger nodule diameter, speculation, and upper lobe location. If the nodule is growing, tissue diagnosis should be obtained unless contraindicated by the presence of severe comorbid conditions. An exception to the 2-year rule is bronchioloalveolar carcinoma, which may be slow growing and present as nodular ground-glass opacities. At the time a nodule is found, if it has a clear-cut benign pattern such as complete calcification, no additional evaluation is needed. Depending on the type, the carcinoma can have glandular features, cytoplasmatic mucin, and extracellular keratin. A systemic disorder characterized by painful symmetrical arthropathy of the ankles, wrists, and knees with periosteal new bone formation in the distal long bones of the limbs, usually associated with clubbing. Patients with any of the paraneoplastic syndromes, and otherwise potentially treatable lung cancer, should not be excluded from potentially curative therapies. By analysis of sweat chloride by the quantitative pilocarpine iontophoresis sweat test. Patients diagnosed in adulthood usually have chronic respiratory symptoms, milder lung disease, fewer Pseudomonas infections, and more frequent pancreatic sufficiency than patients diagnosed during childhood. If the patient breathes between ventilator breaths, some pressure support is provided which augments the spontaneous breath volume. The patient may also be allowed to breathe spontaneously with pressure support, often as a transition to weaning. When only the peak inspiratory pressure increases, consider bronchospasm and endotracheal tube narrowing by secretions or occlusion due to teeth clenching of the patient. Patients develop hyperinflation and increasing intrathoracic pressure that, when extreme, can lead to hypotension (reduced venous return and increased right ventricular afterload) and even cardiopulmonary arrest. In contrast to pulmonary edema, cardiomegaly, pleural effusion, and widening of the vascular pedicle are not prominent. The Acute Respiratory Distress Syndrome Network: Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome, N Engl J Med 342:1301?1308, 2000. The occurrence of bleeding into the alveolar spaces due to disorders that disrupt the alveolar-capillary basement membrane. Up to a third of the cases are associated with the tuberous sclerosis complex of seizures, brain tumors, and cognitive impairment. Imaging studies show a combination of nodules (with or without cavitation) and thick and thin-walled cysts. Tazi A: Adult pulmonary Langerhans cell histiocytosis, Eur Respir J 27:1272?1285, 2006. A noncardiogenic form of pulmonary edema that usually occurs 2?3 days after rapid ascent to altitudes > 8500 feet. Hypoxic pulmonary vasoconstriction causes pulmonary hypertension with capillary stress fractures, release of inflammatory mediators, and decreased nitric oxide synthesis, leading to edema. Treatment includes immediate descent to lower altitude, O2, nifedipine, phosphodiesterase inhibitors, and dexamethasone. What determines if a patient with respiratory disease will need oxygen during air travel? The airplane cabin pressure is maintained at pressures that correspond to altitudes < 8000 feet. Patients cannot carry their own oxygen tank on commercial flights but can use their own battery-powered O2 concentrators. Patients have different symptoms such as skin itches, joint pain, paralysis, or unconsciousness. In addition, the upper airway dilator muscle tone decreases, favoring the development of upper airway obstruction in susceptible individuals. This index defines the severity?mild (5?15), moderate (16?30), and severe (>30)?of sleep apnea. Male gender Acromegaly Enlarged tonsils and Menopause Neuromuscular adenoids Older age disorders Medications. Excessive sleepiness, cataplexy (episodes of muscle atonia/hypotonia precipitated by intense emotions), sleep paralysis, and sleep hallucinations (at sleep onset or on awakening). Not all patients have all the components, and narcolepsy is usually diagnosed by history. Polysomnography followed by multiple sleep latency is required when cataplexy is absent. An unpleasant sensation or urge to move in the legs that increases with inactivity and at night and improves transiently with movement. Polysomnography is rarely needed because the diagnosis is obtained by clinical history. Treatment includes iron if ferritin < 50 mg/L and dopaminergic agents such as pramipexole and ropinirole. Conversely, if the patient who presents with iron-deficiency anemia, hemoccult positive stools, and stable vital signs, blood transfusions may not be needed. When the patient is stable, upper and lower endoscopy can attempt to localize the bleeding source and perform any indicated endoscopy therapies. The skin examination suggests potential bleeding sources if certain stigmata are present (Table 7-1). Visible lymphadenopathy or abdominal masses may suggest an intra-abdominal tumor or malignancy as the bleeding source. Does melena indicate a right-sided colonic source and hematochezia a left sided source? If the stool remains in contact with intestinal bacteria that degrade hemoglobin, the resulting stool is melanotic. Although right-sided lesions are usually associated with melena (dark, tarry stools) and left-sided lesions with hematochezia (the passage of bright red blood per rectum), the opposite can also be seen. Therefore, the evaluation of a patient with hematochezia must include examination of the proximal colon. Any condition that elevates the pressure in the hepatic portal system leads to varices. The normal portal venous pressure is approximately 10 mmHg but increases to > 20 mmHg in portal hypertension. The causes of portal hypertension are classified as presinusoidal, sinusoidal, and postsinusoidal. What two factors determine whether esophageal varices will develop and whether they will bleed? Beyond this level, there is poor correlation between portal pressure and likelihood of bleeding. When varices reach a large size (>5 mm in diameter), they are more likely to rupture and bleed. At any given pressure, the wall of a large varix is under greater tension than that of a small varix and must be thicker to withstand the pressure.

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