By Y. Konrad. California State University, Monterey. 2018.
Recent metallic materials for biomedical applications purchase top avana 80mg online. Kawahara H buy 80 mg top avana amex, Ochi S generic top avana 80 mg otc, Tanetani K, Kato K, Isogai M, Mizuno Y, Yamamoto H, Yamaguchi A. A biological test of dental materials, Effect of pure metals upon the mouse subcutaneous fibroblast, strain L cell in tissue culture. Corrosion of surgical implants—in vitro and in vitro tests. Evaluation of Biomaterials: John Wiley and Sons, 1980:1–34. Electronic structure and phase stability of titanium alloys. Development of a new type titanium casting technology/LEVICAST process. Fourth International Conference on Advanced Materials and Processing (PRICM 4): Japan Institute of Metals, 2001:369–372. Niinomi M, Hattori T, Morikawa K, Kasuga T, Suzuki A, Fukui H, Niwa S. Development of low rigidity -type titanium alloy for biomedical applications. Niinomi M, Akahori T, Yabunaka T, Fukui H, Suzuki A. Fretting fatigue characteristics of new biomedical type titanium alloy. Niinomi M, Kuroda D, Fukunaga K, Morinaga M, Kato Y, Yashiro T, Suzuzki A. Corrosion wear fracture of new -type biomedical titanium alloys. Niinomi M, Akahori T, Nakamura S, Fukui H, Suzuki A. Wear characteristics of surface oxidation treated new biomedical -type titanium alloy in simulated body environment. Calcium phosphate glass-ceramic joined by self- development of compositionally gradient layers on a titanium alloy. Clinical application of ceramic osseo– or soft tissue–integrated implant. Metal ion release from titanium-based prosthetic segmental replacement of long bones in baboons: a long term study. New York: Toxicology—The Basic Science of Poisons, 1986. Philadelphia: Lippincott Williams & Wilkins, 1996: 269–271. Fundamentals of Orthopaedic Biomechanics, Williams & Wilkins. Orthopaedic Biomaterials in Research and Practice, Churchill Livingstone. INTRODUCTION All metallic implants electrochemically corrode to some extent. This is disadvantageous for two main reasons: (1) the process of degradation reduces the structural integrity and (2) degradation products may react unfavorably with the host. Metallic implant degradation results from both electrochemical dissolution and wear, but most frequently occurs through a synergistic combina- tion of the two [1,2]. Electrochemical corrosion processes include both generalized dissolution uniformly affecting an entire surface and localized areas of a component.
Edematous Cellulite Edematous cellulite is primarily found in young patients who take estro-progestagens discount top avana 80mg on line. It is the so-called ‘‘youth cellulite top avana 80 mg with mastercard,’’ of the endocrine-metabolic type cheap top avana 80mg on line, with thick legs that have important physical or psychoemotional sequelae. It is frequently the expression of Dercum’s syndrome or of the traditional lipolymphoedema with lipodystrophy. The peau d’orange sign may be detected early, and a proper diagnosis is needed to discard edema- tous pathologies. It is a pathology that eventually causes serious arthritic, metabolic, and hormonal sequelae. The aesthetic condition is always affected and most difﬁcult to solve. Mixed Cellulite Normally, the forementioned cellulite pathologies are not found as pure entities but as mixed entities. For example, one may ﬁnd hard cellulite in the anterior thigh combined with edematous cellulite in the knee and leg. Bitrochanteric lipodystrophy with ﬂaccid cellulite in the internal thigh is characteristic (16,17). Metabolism alteration at the interstitial matrix level. This is frequently accompanied by recurrent lipedema. Diencephalic and endocrine dysfunction with alteration of local peripheral insulin and lipi- dic metabolism. An alteration of hyaluronic acid and mucopolysaccharides is observed with altered ground substance and extracellular ﬂuid. Tissue congestion of the lymphatic type with painful tumefaction, lipolymphoedema, and abdominal strain. Frequently, it is accompanied by the presence of herpes simplex as a result of a reduced immune function due to intestinal ﬂora disorders. There is also a local and systemic neurophysiological disorder due to the alteration of the ionic pump. They hinder veno-lymphatic microcirculation and increase lymph density as well as interstitial ground substance viscosity. Connective tissue ﬁbrosclerotic alterations derived from initial mucoid ‘‘geloide’’ (gel-like) ﬁbroedema and interstitial connective ﬁbrosclerosis may be noticed. Our therapy involves strategic, tactical, methodological, technical, and control measures. For example, a cycle of one session twice a week during the ﬁrst two months may be devised, followed by a session once a week for the remaining months. Initially, treatment may be associated with carboxytherapy before subdermic therapy techniques are applied prior to local treatments, plus a 15-day cleansing therapy and diet. The cleansing therapy will consist of hydroxycolonother- apy associated with the traditional therapy for intestinal ﬂora recovery. For subdermal 1 therapy, Endermologie should be used in programs for ‘‘edematous cellulitis’’ and ‘‘structural recovery. In the case of carboxytherapy, either the micropercutaneous approach or direct inﬁltrations may be used. Normally, there is a control visit and a therapist meeting after each six- or eight-session cycle in order to adjust diagnosis and thera- peutic conditions. These meetings and the physiotherapist’s appraisal are of utmost importance, because ultimately the therapist perceives the patient’s sensations and symptomatology as the cellulite therapy progresses. In fact, it is a chronic therapy for a disease that is frequently evolutive and gets worse, due to perpetuation and worsening of intestinal ﬂora alterations and endocrine–metabolic disorders, not to mention today’s lifestyle, usually sedentary and reckless from a nutritional or environ- mental point of view.
No further treatment and evaluation for a seizure disorder is warranted purchase 80 mg top avana amex. However cheap top avana 80mg amex, reevaluation of the management of the diabetes is of paramount importance discount top avana 80 mg. A 14-year-old boy with a history of juvenile myoclonic epilepsy is seen for recurrent seizures. His disease was very well controlled in the past with valproate, and he was seizure-free for 18 months. During the past 2 months, the patient has had eight seizures, which the patient’s father describes as being different from his usual myoclonic jerks and generalized tonic-clonic seizures. These seizures are different each time; they last from 20 to 45 minutes. On the basis of this patient’s clinical picture, what would be the most likely cause of these seizures? Nonepileptic seizure Key Concept/Objective: To recognize the clinical picture of nonepileptic seizures Approximately 20% of patients admitted to epilepsy monitoring units for diagnostic eval- uation have episodic behavioral alterations that are not caused by physiologic dysfunction of the brain. In the past, these alterations were called pseudoseizures; currently, the pre- ferred term for such seizures is nonepileptic seizures. Use of this term tends to help the patients understand their problem and facilitates referral for behavioral therapy. An important clue to the diagnosis of nonepileptic seizures is that they are periodic events that tend not to be stereotyped. Both patients and observers report varied behaviors with each event. Nonepileptic seizures may last 30 min- utes to several hours—longer than typical seizures. Patients with both nonepileptic seizures and epilepsy pose a challenging problem; this combination is occasionally found in patients undergoing assessment in epilepsy monitoring units. Treatment of nonepileptic seizures requires behavioral intervention. If both disorders are found, treatment of epilep- sy needs to be continued in parallel with behavioral therapy. A 44-year-old woman is admitted to the hospital with pneumonia. She has a medical history of epilep- sy, for which she has been receiving phenytoin for the past 10 years. She reports having fever, cough, and shortness of breath, but she denies having any neurologic symptoms. Her physical examination shows increased breath sounds at the right base, consistent with pneumonia. Her neurologic examination, including gait, is normal. In the emergency department, the patient’s phenytoin level was assessed; results show the phenytoin level to be elevated at 25 µg/ml (normal, 10 to 20 µg/ml). Which of the following would be the most appropriate way to address this patient’s elevated pheny- toin level? Hold the next dose of phenytoin, then restart the previous regimen of phenytoin C. Hold phenytoin, assess the patient’s phenytoin levels daily until they are subtherapeutic, then restart phenytoin D. Hold phenytoin, then restart before discharge and follow the patient’s phenytoin levels periodically to make sure they are therapeutic Key Concept/Objective: To recognize the general principles of epilepsy drug therapy Antiepileptic drug (AED) treatment should be directed at both controlling seizures and, when possible, correcting the underlying disease or disorder. AEDs may be used only briefly, if at all, in patients who have had a single seizure or a few seizures resulting from a transient disorder. Patients who have recurrent seizures should be treated with AEDs. Treatment with AEDs should follow certain basic principles.
In excessive amounts however generic 80mg top avana with amex, these elements are also toxic buy 80 mg top avana free shipping. Excessive cobalt may lead to polycythemia generic top avana 80mg on-line, hypothyroidism, cardiomy- opathy, and carcinogenesis [64,65]. Chromium can lead to nephropathy, hypersensitivity, and carcinogenesis [66,67]. Nickel can lead to eczematous dermatitis, hypersensitivity, and carcino- genesis. Vanadium can lead to cardiac and renal dysfunction, and has been associated with hypertension and depressive psychosis. The nonessential metallic elements also possess specific toxicities. Titanium, although generally regarded as inert, has been associated with pulmonary disease in patients with occupational exposure and in animal models. Aluminum toxicity is well documented in the setting of renal failure and can lead to anemia, osteomalacia, and neurological dysfunction, possibly including Alzheimer’s disease. However, considering the litany of documented toxicities of these elements, it is important to remember that the toxicities generally apply to soluble forms of these elements and may not apply to the chemical species that are the degradation products of prosthetic implants. Immunogenicity of Metallic Implants Some adverse responses to orthopedic biomaterial corrosion are subtle and continue to foster debate and investigation. One of these responses is ‘‘metal allergy,’’ or hypersensitivity to metallic biomaterial degradation. Dermal hypersensitivity to metal is common, affecting about 10–15% of the population [76–79]. Dermal contact and ingestion of metals have been reported to cause immune reactions, which most typically manifest as skin hives, eczema, redness, and itching [76,80,81]. As previously stated, all metals in contact with biological systems corrode [82,83 and the released soluble products, while not sensitizers on their own, can activate the immune system by forming complexes with native proteins [78,84,85]. These metal–protein complexes are considered to be candidate antigens (or, more loosely termed, allergens) for eliciting hypersensitivity responses. Metals known as sensitizers include beryllium, nickel [79–81,86], cobalt, and chromium, while occasional responses have been reported to tantalum, titanium [88,89], and vanadium. Nickel is the most common metal sensitizer in humans followed by cobalt and chromium [76,79–81]. The prevalence of metal sensitivity among the general population is approximately 10–15%, with nickel sensitivity the highest (approximately 14%). Cross-reactivity between nickel and cobalt is most common [76,78]. The amounts of these metals found in medical grade alloys were shown in Table 2. Hypersensitivity can be either an immediate (within minutes) humoral response (initiated by antibody or formation of antibody–antigen complexes of types I, II, and III reactions) or a delayed (hours to days) cell-mediated response [90,91]. It is the latter response with which implant related hypersensitivity reactions are generally associated, in particular type IV delayed type hypersensitivity (DTH). Cell-mediated delayed type hypersensitivity is characterized by antigen activation of sensi- tized TDTH lymphocytes releasing various cytokines, which result in the recruitment and activa- tion of macrophages. TDTH lymphocytes are subset populations of T helper (TH) lymphocytes purported to be of the CD4 TH-1 subtype (and in rare instances CD8 , cytotoxic T cells, TC). This TH-1 subpopulation of T cells is characterized by their cytokine release profile, e.
You have a discussion with her regarding her risk of osteoporo- sis generic top avana 80 mg overnight delivery, and you decide to obtain a dual-energy x-ray absorptiometry (DEXA) scan for screening cheap top avana 80mg mastercard. Her creatinine and albumin levels are normal discount top avana 80mg online, her liver function tests are normal except for a slightly elevated alkaline phosphatase level, and her calcium level is 11 mg/dl. What is the most appropriate step to take next in the treatment of this patient? Start bisphosphonate, calcium, and vitamin D, and reassess in 6 months 6 BOARD REVIEW B. Measure the parathyroid hormone (PTH) level with a two-site immunoradiometric assay (IRMA, or so-called intact PTH) and assess 24-hour urinary calcium output C. Order CT scans of the chest and abdomen to look for an occult malignancy D. Start hormone replacement therapy with estrogens and progestins Key Concept/Objective: To understand the appropriate initial evaluation of a patient with hyper- calcemia This patient presents with mild, asymptomatic hypercalcemia. The most common cause of hypercalcemia in outpatients is hyperparathyroidism. The differential diagnosis of hypercalcemia is extensive. Once hypercalcemia is confirmed, the next step is to measure the serum PTH concentration. Other helpful tests include blood urea nitrogen (BUN), serum creatinine, alkaline phosphatase, and serum inorganic phosphorus assays; an electrolyte panel; and an assessment of 24-hour urinary calcium output. If the levels of PTH are elevated or inappropriately normal, the hypercalcemia is said to be PTH mediat- ed. When PTH levels are suppressed, the hypercalcemia is said to be non–PTH mediated. Patients with hyperparathyroidism typically have a serum calcium concentration of less than 12 mg/dl; mild to moderate hypophosphatemia; and non–anion gap acidosis (from renal tubular acidosis). Urinary calcium excretion is usually increased; in these patients, the reduction of fractional calcium excretion by PTH is overcome by the high filtered cal- cium load, which may result in nephrolithiasis. The levels of alkaline phosphatase can be elevated as well. Before starting a more extensive evaluation in this patient, it is necessary to exclude the possibility of primary hyperparathyroidism. A 45-year-old man with a history of primary hyperparathyroidism comes to your clinic for a follow-up visit. He was diagnosed 3 years ago after routine blood tests revealed an elevation in calcium level. Review of systems is negative, and his physical examination is unremarkable. His family history is negative for similar problems. What is the most appropriate treatment regimen for this patient? Observation, with routine follow-up visits that include assessment of calcium levels and DEXA scans B. Refer to an experienced surgeon for parathyroid surgery D. Administer calcium, 1,000 to 1,500 mg/day, and vitamin D, 400 to 800 IU/day Key Concept/Objective: To understand the surgical indications for hyperparathyroidism Treatment of the patient with hyperparathyroidism must take into account the degree of the hypercalcemia, the presence of symptoms, and the severity of any end-organ damage. Because many patients with hyperparathyroidism are either asymptomatic or minimally symptomatic, there is controversy over which patients require definitive therapy with sur- gery. The 2002 National Institutes of Health Workshop on Asymptomatic Primary Hyperparathyroidism defined the following indications for surgical intervention: (1) sig- nificant bone, renal, gastrointestinal, or neuromuscular symptoms typical of primary hyperparathyroidism; (2) elevation of serum calcium by 1 mg/dl or more above the nor- mal range; (3) marked elevation of 24-hour urine calcium excretion (> 400 mg); (4) decreased creatinine clearance (reduced by 30%); (5) significant reduction in bone density (T score < –2.
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