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By G. Mazin. Saint Thomas Aquinas College.

An especially important purchase sinequan 10mg amex anxiety zen, although rare 25 mg sinequan with mastercard anxiety lymph nodes, problem for children re- ceiving the fatty acid antiepileptics [Depakote (divalproex sodium)] is the risk of a low platelet count and increased problems with bleeding. Drug interactions on seizure medications: (>) increases the seizure drug effect Class Generic name Trade name Major side effects (<) decreases the seizure drug effect Barbiturates Phenobarbital Luminal Sedation Propoxyphene > Acetaminophen > Primidone Mysoline Irritability Chloramphenicol > Vitamin D < Mephobarbital Mebaral Hydantoins Phenytoin Dilantin Low vitamin D Cimetidine > Vitamin D < Ethotoin Peganone Gingival hyperplasia Aspirin, ibuprofen > Meperidine < Mephenytoin Mesantoin Ataxia Antacids < Phenacemide Phenurone Sedation Increased seizures Succinimides Methsuximide Celontin Anemia Phensuximide Milontin Leukopenia Ethosuximide Zarontin Nausea and vomiting Benzodiazepines Diazepam Valium Sedation Clonazepam Klonopin Ataxia Clorazepate Tranxene Hypotonia Lorazepam Ativan Iminostilbenes Carbamazepine Tegretol Hepatitis Propoxyphene > Theophylline < Oxcarbazepine Trileptal Leukopenia Erythromycin > Doxycycline < Low thyroid Cimetidine > Low vitamin D Fatty acids Valproic acid Depakane Hepatitis Acetylsalicylic acid > Divalproex Depakote Pancreatitis Leukopenia Low platelet count Nausea and vomiting Oxazolidindione Trimethadione Tridione Paramethadione Paradione Amino acid Gabapentin Neurontin Leukopenia Phenyltriazine Lamotrigine Lamictal Hepatitis Carbonic anhydrase Acetazolamide Diamox Dicarbamate Felbamate Felbatol Aplastic anemia Hepatitis Anorexia Weight loss Insomnia Headache Source: Data abstracted from The International Consensus Handbook. Also, many anti- epileptics react with cimetidine, propoxyphene, and meperidine hydrochlo- ride. Because of these reactions, we prefer to stay with morphine and codeine (Table 3. Mobilizing the Child Many children will not want to eat or drink much in the first 24 hours post- operatively. The primary consideration at this time is to get these children comfortable; therefore, a lack of appetite is of little concern. If the amount of drugs required to make a child comfortable also makes her very sedated, 3 or 4 days may pass before she has an interest in feeding. The timing of feed- ing and the amount of feeding in the postoperative period for children who had posterior spinal fusions is a major concern because the procedure is so large that they should have only a very short period of fasting. Other chil- dren with CP generally will be eating well by 3 or 4 days postoperatively, and this is of minimal concern. Getting children out of bed and moving them in physical therapy helps their appetite to return. Patient Management 85 children who do not eat well in the hospital, and often their parents will have had prior experiences where they ate much better at home. It is appropriate to discharge these children home if they are completely stable, with careful follow-up with the parents to make sure that they do start eating sufficiently. This poor feeding can be an especially difficult problem if the family or care- takers are unreliable. In this situation, it is very important to follow these children closely as outpatients to make sure that they are not losing weight. Also, an attempt should be made to initiate bowel movements with the use of a suppository or enemas before discharge because of the chronic nature of constipation in many children with CP. Acute postoperative physical therapy is generally initiated at a child’s bedside for very gentle positioning and range of motion as tolerated on the first postoperative day. By the second postoperative day, most children are comfortable enough to be transferred to the physical therapy department and start a program of increased range, progressing to standing and gait training as determined by the specific surgical procedure and their functional abilities. Each child should have a discharge goal established, such as com- fortable range of motion and comfort when being handled by their parents to being able to independently transfer and ambulate. Once these defined goals are accomplished, the physical therapy treatment program is contin- ued on an outpatient basis. Before discharge, follow-up arrangements are made for outpatient therapy either in the child’s home or close to her com- munity, with a minimum of three visits per week for 4 to 16 weeks, until the midterm goals based on the operative procedure are accomplished. Later Postoperative Problems Some children with CP tend to have very tenuous sleep cycles. These chil- dren often have problems sleeping when conditions vary from their regular routine. For these children and occasionally for children not otherwise rec- ognized as having sleep disorders, the surgical procedure may upset their sleep routine severely. Often, a family will try for approximately a week and when unable to get the child to sleep at night, they will call the physician’s office for help. By this time the family is very tired because the child is often not only not sleeping at night, but is also most uncomfortable during the night hours. Many of these children take catnaps throughout the day. The acute treatment should be for the family to try to keep the child involved and en- gaged during the day to prevent her from falling asleep. At night, the child should be given diazepam 1 hour before bedtime, which is repeated again in 4 hours if she is not sleeping. If the child is having discomfort, acetamino- phen with codeine should be added to help with the pain.

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The blood coagulation cascade consists of a series of enzymes (such as Factor X) buy cheap sinequan 10 mg anxiety 504 plan, which are inactive until proteolytically cleaved by the preceding enzyme in the cascade generic 75mg sinequan free shipping anxiety oils. Other proteins (Factor V and Factor VIII) serve as bind- ing proteins, which assemble factor complexes at the site of injury. Ca 2+ and - carboxyglutamate residues in the proteins (formed by a vitamin K–dependent process in the liver) attach the factor complexes to phospholipids exposed on platelet membranes. Consequently, thrombus formation is rapidly accelerated and localized to the site of injury. Regulatory mechanisms within the blood coagulation cascade and antifibri- nolytic mechanisms prevent random coagulation within blood vessels that might obstruct blood flow. An x-ray showed no fractures, but a soft tissue swelling, consistent with a hematoma (bleeding into the tissues), was noted. Sloe’s mother related that soon after he began to crawl, his knees occasionally became swollen and seemed painful. The pediatrician suspected a disorder of coagulation. A screening coagulation profile suggested a possible deficiency of Factor VIII, a protein involved in the for- mation of blood clots. Sloe’s plasma Factor VIII level was found to be only 3% of the average level found in normal subjects. PLASMA PROTEINS MAINTAIN PROPER DISTRIBUTION OF WATER BETWEEN BLOOD AND TISSUES When the cells are removed from the blood, the remaining plasma is composed of water, nutrients, metabolites, hormones, electrolytes, and proteins. Plasma has essentially the same electrolyte composition as other extracellular fluids and con- stitutes approximately 25% of the body’s total extracellular fluid. The plasma pro- teins serve a number of functions, which include maintaining the proper distribution of water between the blood and the tissues, transporting nutrients, metabolites, and hormones throughout the body, defending against infection, and maintaining the integrity of the circulation through clotting. Many diseases alter the amounts of plasma proteins produced and, hence, their concentration in the blood. These The hydrostatic pressure in an changes can be determined by electrophoresis of plasma proteins over the course of arteriole is the force that “pushes” a disease. Body Fluid Maintenance between Tissues and Blood osmotic pressure, plus the tissue pressure, is the force that “pulls” water from intersti- As the arterial blood enters the capillaries, fluid moves from the intravascular space tial spaces into the venular side of the capil- into the interstitial space (that surrounding the capillaries) because of what are lary. Thus, if the hydrostatic pressure is known as Starling’s forces. The hydrostatic pressure in the arteriolar end of the cap- greater than the osmotic pressure, fluid will illaries (~37 mm Hg) exceeds the sum of the tissue pressure (~1 mm Hg) and the leave the circulation; if it is less, fluid will osmotic pressure of the plasma proteins (~25 mm Hg). At the venous end of the capillaries, the hydrostatic pressure falls to approximately 17 mm Hg while the osmotic pres- In cases of severe protein malnutri- sure and the tissue pressure remain constant, resulting in movement of fluid back tion (kwashiorkor), the concentra- from the extravascular (interstitial) spaces and into the blood. Thus, most of the tion of the plasma proteins decreases, as a result of which the osmotic force bringing water back from the tissues is the osmotic pressure mediated by the pressure of the blood decreases. The distended bellies of famine vic- As indicated in Table 45. The major protein synthesized is albumin, the extravascular tissues because of the severely decreased concentration of plasma which constitutes approximately 60% of the total plasma protein, but because of its proteins, particularly albumin. Albumin syn- relatively small size (69 kDa) is thought to contribute 70 to 80% of the total osmotic thesis decreases fairly early under condi- pressure of the plasma. Albumin, like most plasma proteins, is a glycoprotein and is tions of protein malnutrition. CHAPTER 45 / BLOOD PLASMA PROTEINS, COAGULATION AND FIBRINOLYSIS 829 Table 45. Specific Plasma Binding Proteins Synthesized in the Liver Ceruloplasmin Binds copper; appears to be more important as a copper storage pool than as a transport protein; integrates iron and copper homeostasis Corticosteroid-binding globulin Binds cortisol Haptoglobin Binds extracorpuscular heme Lipoproteins Transport cholesterol and fatty acids Retinol-binding protein Binds vitamin A Sex hormone–binding globulin Binds estradiol and testosterone Transferrin Transports iron Transthyretin Binds thyroxine (T4); also forms a complex with retinol- binding protein Many drugs also bind to albumin, which may have important pharmacologic impli- In spite of the importance of albu- cations. For example, when a drug binds to albumin, such binding will likely lower min in the maintenance of osmotic pressure in the blood, individuals the effective concentration of that drug and may lengthen its lifetime in the circula- lacking albumin (analbuminemia) have only tion. Drug dosimetry may need to be recalculated if a patient’s plasma protein con- moderate edema. The fre- quency of analbuminemia is less than one II. THE PLASMA CONTAINS PROTEINS THAT AID IN per million individuals.

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Depending on the route and timing involved order 25 mg sinequan overnight delivery anxiety girl, the acute results may be cell death through necrosis cheap sinequan 25mg mastercard anxiety chat rooms, with slower cell death through apoptosis in the surrounding tissue. In Cora Nari’s case, oxygen was restored before permanent impairment of oxidative phosphorylation had occurred and the stage of irreversible injury was reached. However, reintroduction of oxygen induced ventricular fibrillation, from which she recovered. BIOCHEMICAL COMMENTS Protection Against Ozone in Lung Lining Fluid The lung lin- Although most individuals are able ing fluid, a thin fluid layer extending from the nasal cavity to the most dis- to protect against small amounts of tal lung alveoli, protects the epithelial cells lining our airways from ozone ozone in the atmosphere, even and other pollutants. Although ozone is not a radical species, many of its toxic slightly elevated ozone concentrations pro- effects are mediated through generation of the classical ROS, as well as generation duce respiratory symptoms in 10 to 20% of the healthy population. Polyunsaturated fatty acids represent the primary target for ozone, and peroxidation of membrane lipids is the most important mechanism of ozone-induced injury. The lung lining fluid has two phases; a gel-phase that traps microorganisms and large particles, and a sol (soluble) phase containing a variety of ROS defense mech- anisms that prevent pollutants from reaching the underlying lung epithelial cells (Fig. When the ozone level of inspired air is low, ozone is neutralized prin- cipally by uric acid (UA) present in the fluid lining the nasal cavity. In the proximal and distal regions of the respiratory tract, glutathione (GSH) and ascorbic acid (AA), in addition to UA, react directly with ozone. Ozone that escapes this anti- oxidant screen may react directly with proteins, lipids, and carbohydrates (CHO) to generate secondary oxidants, such as lipid peroxides, that can initiate chain reac- tions. A second layer of defense protects against these oxidation and peroxidation products: -tocopherol (vitamin E) and glutathione react directly with lipid radi- cals; glutathione peroxidase reacts with hydrogen peroxide and lipid peroxides, and OZONE Mucus Lung lining fluid GSH AA UA ROS Neut Protein Lipid CHO α-Toc Secondary GSH-Px oxidants EC-SOD Epithelial cell Blood capillary Fig 24. GSH, glutathione; AA, ascorbic acid (vitamin C); UA, uric acid; CHO, carbohy- drate; -TOC, vitamin E; GSH-Px, glutathione peroxidase; ED-SOD, extracellular superoxide dismutase; Neut, neutrophil. However, oxidative stress may still overwhelm even this extensive defense network because ozone also promotes neutrophil migration into the lung lining fluid. Once activated, the neutrophils (Neut) produce a second wave of ROS (super- oxide, HOCl, and NO). The mitochondrial permeability transition: its molecular mechanism and role in reperfu- sion injury. Reiter RJ, Tan D-X, Wenbo A, Manchester LC, Karownik M, Calvo JR. Pharmacology and physiology of melatonin in the reduction of oxidative stress in vivo. Oxidative damage and age-related macular degener- ation. Oxidative stress and genetics in the pathogenesis of Parkinson’s disease. Which of the following vitamins or enzymes is unable to protect against free radical damage? Superoxide dismutase catalyzes which of the following reactions? The mechanism of vitamin E as an antioxidant is best described by which of the following? CHAPTER 24 / OXYGEN TOXICITY AND FREE RADICAL INJURY 457 4. An accumulation of hydrogen peroxide in a cellular compartment can be converted to dangerous radical forms in the presence of which metal? The level of oxidative damage to mitochondrial DNA is 10 times greater than that to nuclear DNA. This could be due, in part, to which of the following? The principal route for metabolism of ethanol is through hepatic alcohol dehydrogenases, which oxidize ethanol to acetaldehyde in the cytosol (Fig. Acetaldehyde is further oxidized by acetaldehyde dehy- drogenases to acetate, principally in mitochondria. Acetaldehyde, which is toxic, also may enter the blood.

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