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A frozen section (tissue that is snap-frozen and immediately sectioned in a cryostat) is indicated when the results of the study will affect management of the patient in the operating room prostate cancer radiation oncology order avodart 0.5mg mastercard. For example, the most frequent indication for a frozen section is to determine whether the resection margins are free of tumor, especially in eyelid carcinomas. When tissue is submitted for margin evaluation, appropriate orientation of the specimen, correlated with documentation (through drawings of the excision site, labeled margins, or margins of the excised tissue that are tagged with sutures or other markers) is crucial. Eyelid lesions, especially those located in the canthal areas, require tissue conservation to maintain adequate cosmetic and functional results. Other frequent indications for frozen sections are to determine whether the surgeon has obtained, through biopsy, enough representative material for diagnosis (especially of metastasis) and to submit fresh tissue for flow cytometry and molecular genetics (eg, cancers). Frozen sections are a time-intensive and costly process and should be used with discretion. A, To prepare a frozen section, the surgeon excises lesions with a surgical margin. A central cross section (C) demonstrates the distance of the tumor from the inferior surgical margin. Similarly, an elliptical excision of the tumor can be evaluated by the bread-loaf technique in which multiple cross sections (C) are prepared. B, In Mohs micrographic surgery performed on an eyelid margin tumor, the surgeon excises the visible lesion. In another variation of Mohs surgery, the surgeon performs an elliptical excision of the visible tumor. Elements of the stroma include loosely arranged collagen fibers; blood vessels and lymphatic channels; nerves; occasional accessory lacrimal glands; and resident lymphocytes, plasma cells, macrophages, and mast cells. Congenital Anomalies Choristomas Choristomatous lesions of the ocular surface range from limbal dermoid to complex choristoma. A choristoma is a benign, congenital proliferation of histologically mature tissue that is abnormal for a given topographic location. Dermoids may occur in isolation or, particularly when bilateral, as a manifestation of a congenital complex such as Goldenhar syndrome (oculoauriculovertebral dysgenesis, characterized by epibulbar dermoid, upper eyelid coloboma, preauricular skin tags, and vertebral anomalies) or linear nevus sebaceous syndrome (an oculoneurocutaneous disorder). C, Conjunctiva at the fornix may contain pseudoglands of Henle (infoldings of conjunctival epithelium with abundant goblet In contrast with dermoids, lipodermoids (or dermolipomas) occur more commonly in the superotemporal quadrant, toward the fornix; they may extend posteriorly into the orbit. Lipodermoids are composed of a significant amount of mature adipose tissue, which makes them softer and yellower than dermoids. Lipodermoids, like dermoids, may be associated with Goldenhar syndrome or linear nevus sebaceous syndrome. Clinically, complex choristomas are often indistinguishable from dermoids or lipodermoids. Hamartomas Hamartomas, like choristomas, are benign congenital proliferations; but in contrast to choristomas, they are abnormal overgrowths of mature tissue normally present at a given topographic location (hence the derivation from the Greek word for "defect or error"). In the conjunctiva, the most common variety of hamartoma is a capillary hemangioma, although this hamartoma most often involves the eyelid (see Chapter 13). E, Caruncular conjunctiva, containing sebaceous glands (S) and hair follicles (H). C, Histology shows keratinized epithelium, dense stroma, and sebaceous glands with hair follicles (arrows). D, A lipodermoid differs from a dermoid in that it contains a significant amount of mature adipose tissue (A). This lipodermoid also contains dermal adnexal structures, including sebaceous glands (S) and hair follicles (H). E, Complex choristomas combine features of multiple types of choristomas, in this case osseous (O) and lipodermoid (L) choristomas. Granulomatous Conjunctivitis Granulomatous conjunctivitis is less common than papillary conjunctivitis and follicular conjunctivitis and has both infectious and noninfectious causes. Clinically, the nodular elevations of granulomatous conjunctivitis may be difficult to distinguish from follicles, but the clinical history and systemic symptoms may point to the diagnosis. Granulomatous conjunctivitis occurring in association with preauricular lymphadenopathy is known as Parinaud oculoglandular syndrome. Bacteria such as Bartonella henselae (cat-scratch disease) and Francisella tularensis (tularemia), mycobacteria (eg, Mycobacterium tuberculosis), treponemes (eg, syphilis), and fungi (eg, sporotrichosis) are possible causes.

Nondepolarizing Relaxants In general prostate 4k discount avodart 0.5 mg buy on line, small doses of nondepolarizing relaxants antagonize a depolarizing phase I block. Dosage Because of the rapid onset, short duration, and low cost of succinylcholine, many clinicians believe that it is still a good choice for routine intubation in adults. Repeated small boluses (10 mg) or a succinylcholine drip (1 g in 500 or 1000 mL, titrated to effect) can be used during surgical procedures that require brief but intense paralysis (eg, otolaryngological endoscopies). The availability of intermediate-acting nondepolarizing muscle relaxants has reduced the popularity of succinylcholine infusions. In the past, these infusions were a mainstay of ambulatory practice in the United States. Because succinylcholine is not lipid soluble, it has a small volume of distribution. If succinylcholine is administered intramuscularly to children, a dose as high as 4­5 mg/kg does not always produce complete paralysis. Succinylcholine should be stored under refrigeration (2­8°C), and should generally be used within 14 days after removal from refrigeration and exposure to room temperature. Side Effects & Clinical Considerations Succinylcholine is a relatively safe drug-assuming that its many potential complications are under7 stood and avoided. Because of the risk of hyperkalemia, rhabdomyolysis, and cardiac arrest in children with undiagnosed myopathies, succinylcholine is considered relatively contraindicated in the routine management of children and adolescent patients. Most clinicians have also abandoned the routine use of succinylcholine for adults. Succinylcholine is still useful for rapid sequence induction and for short periods of intense paralysis because none of the presently available nondepolarizing muscle relaxants can match its very rapid onset and short duration. Children are particularly susceptible to profound bradycardia following administration of succinylcholine. Bradycardia will sometimes occur in adults when a second bolus of succinylcholine is administered approximately 3­8 min after the first dose. The dogma (based on no real evidence) is that the succinylcholine metabolite, succinylmonocholine, sensitizes muscarinic cholinergic receptors in the sinoatrial node to the second dose of succinylcholine, resulting in bradycardia. Other arrhythmias, such as nodal bradycardia and ventricular ectopy, have been reported. Stimulation of nicotinic receptors in parasympathetic and sympathetic ganglia, and muscarinic receptors in the sinoatrial node of the heart, can increase or decrease blood pressure and heart rate. Low doses of succinylcholine can produce negative chronotropic and inotropic effects, but higher doses usually increase heart rate and contractility and elevate circulating catecholamine levels. Fasciculations the onset of paralysis by succinylcholine is usually signaled by visible motor unit contractions called fasciculations. These can be prevented by pretreatment with a small dose of nondepolarizing relaxant. Because this pretreatment usually antagonizes a depolarizing block, a larger dose of succinylcholine is required (1. Hyperkalemia 8 Normal muscle releases enough potassium during succinylcholine-induced depolarization to increase serum potassium by 0. Although this is usually insignificant in patients with normal baseline potassium levels, it can be lifethreatening in patients with preexisting hyperkalemia. The increase in potassium in patients with burn injury, massive trauma, neurological disorders, and several other conditions (Table 11­5) can be large and catastrophic. Hyperkalemic cardiac arrest can prove to be quite refractory to routine cardiopulmonary resuscitation, requiring calcium, insulin, glucose, bicarbonate, and even cardiopulmonary bypass to support the circulation while reducing serum potassium levels. Intragastric Pressure Elevation Abdominal wall muscle fasciculations increase intragastric pressure, which is offset by an increase in lower esophageal sphincter tone. Therefore, despite being much discussed, there is no evidence that the risk of gastric reflux or pulmonary aspiration is increased by succinylcholine. Intraocular Pressure Elevation Extraocular muscle differs from other striated muscle in that it has multiple motor end-plates on each cell. Prolonged membrane depolarization and contraction of extraocular muscles following administration of succinylcholine transiently raise intraocular pressure and theoretically could compromise an injured eye. However, there is no evidence that succinylcholine leads to worsened outcome in patients with "open" eye injuries. The elevation in intraocular pressure is not always prevented by pretreatment with a nondepolarizing agent.

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Patients with viral hepatitis often have a 1- to 2-week mild prodromal illness (fatigue man health 2014 discount avodart 0.5 mg buy line, malaise, low-grade fever, or nausea and vomiting) that may or may not be followed by jaundice. The jaundice typically lasts 2­12 weeks, but complete recovery, as evidenced by serum transaminase measurements, usually takes 4 months. Because clinical manifestations overlap, serological testing is necessary to determine the causative viral agent. The clinical course tends to be more complicated and prolonged with hepatitis B and C viruses relative to other types of viral hepatitis. The incidence of chronic active hepatitis (see below) is 3% to 10% following infection with hepatitis B virus and at least 50% following infection with hepatitis C virus. Most patients with chronic hepatitis C infection seem to have very low, intermittent, or absent circulating viral particles and are therefore not highly infective. In addition to "universal precautions" for avoiding direct contact with blood and secretions (gloves, mask, protective eyewear, and not recapping needles), immunization of healthcare personnel is highly effective against hepatitis B infection. A vaccine for hepatitis C is not available; moreover, unlike hepatitis B infection, hepatitis C infection does not seem to confer immunity to subsequent exposure. Postexposure prophylaxis with hyperimmune globulin is effective for hepatitis B, but not hepatitis C. Drug-induced Hepatitis Drug-induced hepatitis (Table 33­2) can result from direct, dose-dependent toxicity of a drug or drug metabolite, an idiosyncratic drug reaction, or a combination of these two causes. Alcoholic hepatitis is probably the most common form of drug-induced hepatitis, but the etiology may not be obvious from the history. Chronic alcohol ingestion can also result in hepatomegaly from fatty infiltration of the liver, which reflects impaired fatty acid oxidation, increased uptake and esterification of fatty acids, and diminished lipoprotein synthesis and secretion. Acetaminophen ingestion of 25 g or more usually results in fatal fulminant hepatotoxicity. A few drugs, such as chlorpromazine and oral contraceptives, may cause cholestatic-type reactions (see below). Toxic Alcohol Acetaminophen Salicylates Tetracyclines Trichloroethylene Vinyl chloride Carbon tetrachloride Yellow phosphorus Poisonous mushrooms (Amanita, Galerina) Idiosyncratic Volatile anesthetics (halothane) Phenytoin Sulfonamides Rifampin Indomethacin Toxic and idiosyncratic Methyldopa Isoniazid Sodium valproate Amiodarone Primarily cholestatic Chlorpromazine Cyclosporine Oral contraceptives Anabolic steroids Erythromycin estolate Methimazole mushrooms (Amanita, Galerina), also may result in fatal hepatotoxicity. In addition, acute alcohol toxicity greatly complicates anesthetic management, and acute alcohol withdrawal during the perioperative period may be associated with a mortality rate as high as 50%. Only emergent surgery should be considered for patients presenting in acute alcohol withdrawal. Patients with hepatitis are at risk of deterioration of hepatic function and the development of complications from hepatic failure, such as encephalopathy, coagulopathy, or hepatorenal syndrome. A blood alcohol level is useful if the history or physical examination is compatible with ethanol intoxication. Hypokalemia and metabolic alkalosis are not uncommon and are usually due to vomiting. Concomitant hypomagnesemia may be present in chronic alcoholics and predisposes to cardiac arrhythmias. The elevation in serum transaminases does not necessarily correlate with the amount of hepatic necrosis. Bilirubin and alkaline phosphatase are usually only moderately elevated, except with the cholestatic variant of hepatitis. Hypoalbuminemia is usually not present except in protracted cases, with severe malnutrition, or when chronic liver disease is present. If a patient with acute hepatitis must undergo an emergent operation, the preanesthetic evaluation should focus on determining the cause and the degree of hepatic impairment. Information should be obtained regarding recent drug exposures, including alcohol intake, intravenous drug use, recent transfusions, and prior anesthetics. The presence of nausea or vomiting should be noted, and, if present, dehydration and electrolyte abnormalities should be anticipated and corrected. Inappropriate behavior or obtundation in alcoholic patients may be signs of acute intoxication, whereas tremulousness and irritability usually reflect withdrawal. However, benzodiazepines and thiamine are indicated in alcoholic patients with, or at risk for, acute withdrawal. Intraoperative Considerations the goal of intraoperative management is to preserve existing hepatic function and avoid factors that may be detrimental to the liver. Some patients with viral hepatitis may exhibit increased central nervous system sensitivity to anesthetics, whereas alcoholic patients will often display cross-tolerance to both intravenous and volatile anesthetics. Alcoholic patients also require close cardiovascular monitoring, because the cardiac depressant effects of alcohol are additive to those of anesthetics; moreover, alcoholic cardiomyopathy is present in many alcoholic patients.

Syndromes

• 9 - 13 years: 120 mcg/day
• Margarine (made from safflower, corn, and sunflower oil)
• Cerebral angiogram
• Raw vegetables
• Blurred vision
• Rapid growth (in the first year of life and in adolescence), when more iron is needed
• Endoscopic thoracic sympathectomy (ETS). In severe cases, a minimally-invasive surgical procedure called sympathectomy may be recommended when other treatments fail. The procedure turns off the signal that tells the body to sweat excessively. It is usually done on patients whose palms sweat much more heavily than normal. It may also be used to treat extreme sweating of the face. ETS does not work as well for those with excessive armpit sweating. See: ETS surgery
• Flank (side) pain
• Exercise or other physical stress
• Dizziness

Biotransformation Hepatic microsomal enzymes and plasma esterases rapidly hydrolyze etomidate to an inactive metabolite mens health zero excuses workout buy 0.5 mg avodart visa. Excretion the end products of etomidate hydrolysis are primarily excreted in the urine. Longterm infusion and adrenocortical suppression were associated with an increased mortality rate in critically ill (particularly septic) patients. Drug Interactions Fentanyl increases the plasma level and prolongs the elimination half-life of etomidate. A mild reduction in peripheral vascular resistance is responsible for a slight decline in arterial blood pressure. However, etomidate by itself, even in large doses, produces relatively light anesthesia for laryngoscopy, and marked increases in heart rate and blood pressure may be recorded when etomidate provides the only anesthetic depth for intubation. Respiratory Ventilation is affected less with etomidate than with barbiturates or benzodiazepines. Even induction doses usually do not result in apnea unless opioids have also been administered. Cerebral Etomidate decreases cerebral metabolic rate, cerebral blood flow, and intracranial pressure. Postoperative nausea and vomiting are more common following etomidate than following propofol or barbiturate induction. Endocrine 5 Induction doses of etomidate transiently inhibit enzymes involved in cortisol and aldosterone synthesis. This receptor, as previously noted, is coupled to a chloride channel, and activation of the receptor leads to hyperpolarization of the nerve membrane. Propofol (like most general anesthetics) binds multiple ion channels and receptors. Propofol actions are not reversed by the specific benzodiazepine antagonist flumazenil. Propofol is not water soluble, but a 1% aqueous solution (10 mg/mL) is available for intravenous administration as an oil-in-water emulsion containing soybean oil, glycerol, and egg lecithin. A history of egg allergy does not necessarily contraindicate the use of propofol because most egg allergies involve a reaction to egg white (egg albumin), whereas egg lecithin is extracted from egg yolk. This formulation will often cause pain during injection that can be decreased by prior injection of lidocaine or less effectively by mixing lidocaine with propofol prior to injection (2 mL of 1% lidocaine in 18 mL propo6 fol). Excretion Although metabolites of propofol are primarily excreted in the urine, chronic kidney failure does not affect clearance of the parent drug. Absorption Propofol is available only for intravenous administration for the induction of general anesthesia and for moderate to deep sedation (see Table 9­3). Awakening from a single bolus dose is also rapid due to a very short initial distribution half-life (2­8 min). Most investigators believe that recovery from propofol is more rapid and is accompanied by less "hangover" than recovery from methohexital, thiopental, ketamine, or etomidate. A smaller induction dose is recommended in elderly patients because of their smaller Vd. In countries other than the United States, a device called the Diprifusor is often used to provide target (concentration) controlled infusion of propofol. The device uses these data, a microcomputer, and standard pharmacokinetic parameters to continuously adjust the infusion rate. Biotransformation the clearance of propofol exceeds hepatic blood flow, implying the existence of extrahepatic metabolism. This exceptionally high clearance rate probably contributes to relatively rapid recovery after continuous infusions. Conjugation in the liver results in inactive metabolites that are eliminated by renal clearance. The pharmacokinetics of propofol do not appear to be affected by obesity, cirrhosis, or kidney failure.

Usage: q.i.d.

Bupivacaine binds open or inactivated sodium channels and dissociates from them slowly prostate cancer in men order 0.5 mg avodart mastercard. It can cause profound sinus bradycardia and sinus node arrest and malignant ventricular arrhythmias; furthermore, it can depress left ventricular contractility. Twenty percent lipid emulsions have been used to treat local anesthetic cardiac toxicity. The mechanisms of action of this therapy are unclear, although possibilities include serving as a lipid reservoir and decreasing lipophilic toxic local anesthetics in the myocardium. Calcium channel blockers are organic compounds that block Ca2+ influx through L-type but not T-type channels. Dihydropyridine blockers, such as nifedipine, simply plug the channel, whereas other agents, such as verapamil, and to a lesser extent, diltiazem, preferentially bind the channel in its depolarized inactivated state (use-dependent blockade). Cell shortening occurs when the actin and myosin are allowed to fully interact and slide over one another. This interaction is normally prevented by two regulatory proteins, troponin and tropomyosin; troponin is composed of three subunits (troponin I, troponin C, and troponin T). Troponin is attached to actin at regular intervals, whereas tropomyosin lies within the center of the actin structure. An increase in intracellular Ca2+ concentration (from about 10­7 to 10­5 mol/L) promotes contraction as Ca2+ ions bind troponin C. A series of attachments and disengagements occur as each myosin bridge advances over successive active sites on actin. Excitation­Contraction Coupling the quantity of Ca2+ ions required to initiate contraction exceeds that entering the cell through slow calcium channels during phase 2. The small amount that does enter through slow calcium channels triggers the release of much larger amounts of Ca2+ stored intracellularly (calcium-dependent calcium release) within cisterns in the sarcoplasmic reticulum. The action potential of muscle cells depolarizes their T systems, tubular extensions of the cell membrane that transverse the cell in close approximation to the muscle fibrils, via dihydropyridine receptors (voltage-gated calcium channels). This initial increase in intracellular Ca2+ triggers an even greater Ca2+ inflow across ryanodine receptors, a nonvoltagedependent calcium channel in the sarcoplasmic reticulum. The force of contraction is directly dependent on the magnitude of the initial Ca2+ influx. The quantity of intracellular Ca2+ available, its rate of delivery, and its rate of removal determine, respectively, the maximum tension developed, the rate of contraction, and the rate of relaxation. Moreover, adrenergic agonists enhance the rate of relaxation by enhancing Ca2+ reuptake by the sarcoplasmic reticulum. The new agent levosimendan is a calcium sensitizer that enhances contractility by binding to troponin C. Acidosis blocks slow calcium channels and therefore also depresses cardiac contractility by unfavorably altering intracellular Ca2+ kinetics. Halothane and enflurane seem to depress contractility more than isoflurane, sevoflurane, and desflurane. Anesthetic-induced cardiac depression is potentiated by hypocalcemia, -adrenergic blockade, and calcium channel blockers. Nitrous oxide also produces concentrationdependent decreases in contractility by reducing the availability of intracellular Ca2+ during contraction. The mechanisms of direct cardiac depression from intravenous anesthetics are not well established, but presumably involve similar actions. Of all the major intravenous induction agents, ketamine seems to have the least direct depressant effect on contractility. Local anesthetic agents also depress cardiac contractility by reducing Ca2+ influx and release in a dose-dependent fashion. The more potent (at nerve block) agents, such as bupivacaine, tetracaine, and ropivacaine, more significantly depress left ventricular contractility than less potent (at nerve block) agents, such as lidocaine or chloroprocaine. Cardiac sympathetic fibers originate in the thoracic spinal cord (T1­T4) and travel to the heart initially through the cervical (stellate) ganglia and from the ganglia as the cardiac nerves. Vagal effects frequently have a very rapid onset and resolution, whereas sympathetic influences generally have a more gradual onset and dissipation. Sinus arrhythmia is a cyclic variation in heart rate that corresponds to respiration (increasing with inspiration and decreasing during expiration); it is due to cyclic changes in vagal tone. The x descent is the decline in pressure between the c and v waves and is thought to be due to a pulling down of the atrium by ventricular contraction. The notch in the aortic pressure tracing is referred to as the incisura and is said to represent the brief pressure change from transient backflow of blood into the left ventricle just before aortic valve closure.

References

• Fukuhara N. Myoclonus epilepsy and mitochondrial myopathy. In: Scarlato G, Cerri C (eds). Mitochondrial Pathology in Muscle Diseases. Padua: Pikkin Medical Books; 1983, 88.
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• Allen T. Pathology of small airways disease. Arch Pathol Lab Med 2010;134:702-18.
• Middleton, A.W., Pfister, R.C. Stone-containing pyelocaliceal diverticulum: embryonic, anatomic, radiographic and clinical characteristics. J Urol 1974;111:2-6.