By N. Kan. Westfield State College.

Bleeding from several organs within the body buy 5 mg cetirizine with amex, leading to shock & possibly death purchase cetirizine 5mg free shipping, occurs in the more severe cases generic 10 mg cetirizine with visa. The onset of the signs of poisoning may not be evident until a few days after exposure. The detection scheme utilizes post column acid- base fluorescence enhancement techniques that provide high chromatographic specificity &sensitivity. Oral absorption of cyanide is rapid and the toxic effects can present within minutes. It is widely distribution in the body & about 80% eliminated through the kidney in a form of thiocyanate. The sign and symptoms of cyanide poisoning include headache, hypoxic convulsion, and respiratory distress, cyanide odor… Laboratory analysis i) General tests 1. Chemistry Tests - Because of the blockade of aerobic biotransformation, cyanide produces an anion gap metabolic acidosis secondary to the production of lactic acid - Glucose catabolism is also altered, and the blood glucose level may be elevated 2. Blood gas analysis - PaO2 and oxygen saturation are unaltered except in severe cases where respiratory failure occurs. A spot test is a quick bedside test that can qualitatively detect the presence of cyanide using gastric aspirate. The specific cyanide level is the gold standard test and should be done even though the results may not be readily available. These levels are usually performed on whole blood but some laboratories use serum or plasma Specific laboratory tests Qualitative test Specimen Stomach contents, scene residues. Aqueous ferrous sulfate solution (100 g/l, freshly prepared in freshly boiled and cooled water). Sensitivity Cyanide, 10 mg/l Quantitative assays Specimen Heparinized whole blood (0. The samples can be stored at 4°C for 1-2 days if the analysis is delayed for any reason. Seal each well using silicone grease and carefully mix the components of the outer wells. Incubate at room temperature for 20 minutes and then add 1 ml of aqueous methanol (1:1) to the centre wells. Results The red coloration obtained with cyanide-containing solutions is stable for about 15 minutes. Measure the absorbance of the solutions from cells 2 and 3 at 560 nm against the purified water blank (cell 1). Assess the cyanide ion concentration in the sample by comparison with the reading obtained from the standard. The top household products ingested are cleaning agents, cosmetics & personal products & berries. In the stomach the presence of endogenous hydrochloric acid generates hypochlorous acid which is irritant & chlorine gas which may be inhaled causing toxic effects in the lungs. However, drugs have made & will continue to make a major contribution to human health, we must accept the risks attached to these benefit. The basic mechanisms for the toxicities arising from drugs are - Direct& predictable toxic effects due to over doses - Toxic effects occurring after repeated therapeutic doses 72 Toxicology - Direct but unpredictable toxic effects occurring after single therapeutic doses due to idiosyncratic response (peculiar response of an individual to a drug). Acetaminophen Acetaminophen is analgesics for mild &moderate pain which is very safe provided only the normal therapeutic dose. Acetaminophen is one of the drugs most commonly involved in suicide and accidental poisoning. Initial symptoms after an overdose are mild and non specific, often resulting in delayed arrival for medical care or a missed diagnosis. Acute ingestion of more than 150-200mg/kg (children) or 7gm (adults) is considered potentially toxic. Paracetamol is metabolized mainly by conjugation & minor proportion metabolized by oxidation which produces toxic products which detoxified normally. However, overdoses change the metabolic scheme giving a rise in toxic metabolite which react with liver proteins & cause tissue damage (leading to hepatic toxicity). Laboratory analysis - Severity of poisoning is determined from serum acetaminophen level. Mix 1 mL of specimen (victim or control urine, water blank) and 1 mL of concentrated hydrochloric acid. Cool and add 100 µL of the above solution to 10 mL of o- cresol reagent and then 2 mL of ammonium hydroxide, 4 mol/L 74 Toxicology Result Acetaminophen is hydrolyzed to p-aminophenol, which reacts with o- cresol and ammonium hydroxide to form an indophenol blue chromogen. Pipette 100 µL of each calibrator, control, and victim’s serum into properly labeled 13 x 100-mm glass tubes. Add 100 µL of working internal standard solution and 100 µL of phosphate buffer (0. Transfer the organic (top) layer to labeled 12 x 75-mm glass tubes and evaporate under a stream of dry air at 50 0C. Calculation Determine the peak height (or peak area) ratios of acetaminophen relative to the internal standard. Calculate the concentration of acetaminophen in the unknown by comparing its peak height ratio versus acetaminophen concentration response for the calibrator. Aspirin (salicylate) Acetylsalicylic acid, commonly known as aspirin, is still one of the most widely used minor analgesics. Salicylate poisoning is a much less common cause of childhood poisoning deaths since the introduction of child-resistant container and the reduced use of baby aspirin. Salicylates, however still accounts for numerous suicidal and accidental poisonings. Salicylate Poisoning can also result from chronic over medication; this occurs most commonly in elderly victims using salicylates for chronic pain because of impaired biotransformation, excretion & others. These conjugation steps are 76 Toxicology saturable so the half life of aspirin increases significantly with only small increase in the number of tablets. The first sign of salicylate toxicity is often hyperventilation and respiratory alkalosis due to medullary stimulation. Metabolic acidosis follows due to accumulation of intracellular lactate as well as excretion of bicarbonate by the kidney to compensate for respiratory alkalosis. Laboratory tests Urine should be tested for pH, the presence of ketone bodies and hemoglobin. Specific laboratory tests Qualitative test Specimen Urine, stomach contents, scene residues. B- To test for acetylsalicylic acid or methyl salicylate in stomach contents or scene residues, and to test for 77 Toxicology salicylamide in urine, stomach contents or scene residues, first boil 1 ml of sample with 1 ml of aqueous hydrochloric acid (0. Azide preservatives react strongly in this test, and weak false positives can be given by urine specimens containing high concentrations of ketone bodies. This test is sensitive and will detect therapeutic dosage with salicylic acid, acetylsalicylic acid, 4-aminosalicylic acid, methyl salicylate and salicylamide. Measure the absorbance of the supernatant at 540 nm against plasma blank Results Calculate the plasma salicylate concentration from the graph obtained on analysis of the salicylate standards. Some salicylate metabolites interfere, but plasma concentrations of these compounds are usually low.

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In an extensive review of epidemiological data dental caries is low in countries where the consumption of concerning the role of oral hygiene in caries prevention generic cetirizine 10 mg with amex, free sugars is below 15–20 kg/person/yr 10mg cetirizine visa. This is equival- Sutcliff concluded ‘although toothcleaning with un- ent to a daily intake of 40–55 g and the values equate to medicated agents may be expected to reduce caries 6–10% of energy intake buy 10mg cetirizine fast delivery. It is of particular importance that experience, the lack of consistent epidemiological countries which currently have low consumption of free corroboration of the relationship has led to questioning sugars (,15–20 kg/person/yr) do not increase consump- of the value of oral hygiene practices against caries. Governments should establish the means of amount of free sugars, targets for frequency of free sugars monitoring the severity and prevalence of oral diseases consumption are also important. There should be promotion of adequate fluoride exposure Governments should support research into elucidating via appropriate vehicles, for example affordable tooth- optimum fluoride intake by different age groups and paste, water, salt and milk. It is the responsibility of effective means of delivering optimum fluoride and national health authorities to ensure implementation of should also support research into nutrition and dental feasible fluoride programmes for their country. Governments should ensure that teachers, pupils and In order to minimise the occurrence of dental erosion, health professionals receive adequate education on diet, the amount and frequency of intake of soft drinks and nutrition and dental health issues. Elimination of undernutrition also provide guidelines for the use of and content of prevents enamel hypoplasia and the other potential effects educational materials to ensure they are sound and non- of undernutrition on oral health (e. Governments should set more stringent codes of practice on advertising (including advertising and infor- mation on the Internet) of sugars-rich items. Recommendations to international organisations Recommendations to private sector and industry for the prevention of dental diseases Food manufacturers should continue to produce low- The potential financial consequence of failing to prevent sugars/sugars-free alternatives to products rich in free dental diseases need to be highlighted, especially to sugars, including drinks. Manufacturers should also look governments of countries that currently have low levels of at means to reduce the erosive potential of soft drinks. The To enable individuals to make informed choices detrimental impact of quality of life throughout the life regarding the oral health/dental problems related to high course and the longer-term nutritional consequences of and frequent free sugars intake, there is a need for clear and dental disease and tooth loss also need to be highlighted. Oral health education should be promoted sugars and soft drink intake and should provide guidance alongside other forms of health education and dietary and to nations on standardised methods for data collection on nutrition advice for oral health should be integrated with appropriate study populations where necessary. This is essential if advice for fluoride toothpaste is available/affordable, individuals dental health is to be consistent with dietary advice for should be encouraged to brush their teeth with a fluoride general health. Oral health status of children and research and/or information are as follows: adults in the Republic of Niger, Africa International Dental Journal 1999; 49: 159–64. More information is needed from longitudinal studies 8 Kelly M, Steele J, Nuttall N, Bradlock G, Morris J, Nunn J, or repeated cross-sectional studies (e. Intake of non- juices and other acid-containing foods needs to be starch polysaccharide (dietary fibre) in edentulous and monitored. Nutrient intake in partially dentate patients: the effect of prosthetic rehabilita- An earlier version of this paper was prepared as a tion. Nutrition and dental caries: ten findings to be Consultation on diet, nutrition and the prevention of remembered. Pathogenesis and modifying Sweden, for their comments on an earlier draft of the factors of dental erosion. Oral health status of children Final report on the effect of sucrose, fructose and xylitol Diet, nutrition and prevention of dental diseases 223 diets on the caries incidence in man. Compendium of National Diet and Nutrition Survey: young people aged Continuing Education in Dentistry 2002; 23: 431–6. Incidence and distribution of Strep mutans in distribution and severity of tooth wear and the relationship plaque from confectionery workers. Journal of Dental between erosion and dietary constituents in a group of Research 1979; 58(Special issue): 2251. Journal of use of fluorides on caries increment in children during one Dental Research 1963; 42: 1387–99. Comparison of increment assessed over two years in 405 English dietary habits and dental health of subjects with hereditary adolescent schoolchildren. Effect of the length Community Dentistry and Oral Epidemiology 1981; 9: and number of intervals between meals on caries in rats. Longitudinal study of caries, cariogenic bacteria and diet and oral hygiene for the occurrence of caries in 3-year-olds. Dental health, Caries prevalence, Streptococcus mutans and sugar intake dental care and dietary habits in children in different among 4-year-old urban children in Iceland. Infant tion and caries experience in 12- and 13-year-old feeding and dental caries, a longitudinal study of Swedish Icelandic children. Epidemiological study of dental malocclusion, fluoride usage, toothbrushing and dietary caries experience and between-meal patterns. Community Dentistry and oral health behaviour of 12-year-old urban schoolchildren Oral Epidemiology 1992; 20: 133–7. Multiple regression cariogenicity of different dietary carbohydrates tested on analysis of dental status and related food behaviour of rats in relative gnotobiosis with a streptococcus producing French Canadian adolescents. The effects of phosphates on guidelines on sugar intake and dental caries in 3-year-olds experimental dental caries: a literature review. International Journal of Paediatric Dentistry 119 Frostell G, Birkhed D, Edwardsson S, Goldberg P, Petersson 1996; 6:81–6. Identification of low caries risk dietary com- sugar from sucrose in combination with duraphat treatment ponents. Dental caries in children one to six salivary bacterial levels in 12-year-old English school- years of ages as related to socio-economic level, food habits children. The effects of starch and sugar diets on dental glucose syrups in experiments in vitro and in the diets of caries. Journal of the American Dental other sugar analogues on acid production from sugars by Association 1980; 100: 677–81. Microbiology and Immunology 175 Gedalia I, Dakuar A, Shapiro H, Leminstein I, Goultschin 1988; 32: 25–31. Journal of the American Dental Association 1983; and bacterial composition of dental plaque in the rat. A longitudinal study of infant feeding practice, Salivary pH and glucose after consuming various beverages diet and caries related to social class in children aged 3 and including sugar-containing drinks. In vivo effects of black tea 15kg per person per year in industrialised countries; the infusion on dental plaque. Dental erosions in relation to Monthly Bulletin of the Ministry of Health 1946 (August): lactovegetarian diet. Dental Biomaterials Summary Notes Enoch Ng Lecture 1 – Intro (sections 1-5) - Biomaterials – synthetic materials for use in the body - Dental Biomaterials – synthetic materials for use in the mouth (and associated laboratory processing materials) - Biological materials – materials which occur in the body (enamel, dentin, pulp, etc) o Design of restoration or prosthesis depends on material properties - Indirect procedures require: impression, model/cast/die, pattern, mold - Priorities (best to worst) because synthetics not as good as natural tissue (prevention, conservation, longevity) a. Substitutional – same crystal structure, similar atomic size (<15% difference), similar chemical valency, no reaction to form intermetallic compounds (ex:// Au, Cu, Pt, Pd) b. Partial solid insolubility (1 or 2 phases) – solid solution formed during solidification, further cooling gives precipitation of second different solid phase (pins the movement of the dislocations) – great significance on mechanical properties, makes harder but more brittle metal 4. Intermetallic compound formation – compounds with specific and well defined stoichiometry/composition (ex:// Ag3Sn) Dental Biomaterials Summary Notes Enoch Ng Significance - Pure, untreated metals are usually too soft/weak - Strength of an alloy depends on: composition, mechanical history, thermal history - Elasticity of a metal depends on composition of the unalloyed metal (intermetallic bonding, dislocation) Selection - Metals are stronger than ceramics (not as brittle) - Must be biocompatible – resistant to corrosion and no release of metallic ions o Noble alloys (gold, platinum, palladium) o Stainless/passivated alloys – stainless steel, chromium and titanium based o Mercury Dental Biomaterials Summary Notes Enoch Ng 7 – Metallic Materials in the Mouth (Section 20) - Metals corrode in the mouth, releasing compounds into the body - [electrochemical] corrosion – physicochemical interaction between a metal and its environment to form metallic compounds, commonly oxides, resulting in metallic degradation o Metals are readily oxidized, can form ceramic materials o Ideal corrosion environment (mouth) - moisture, temp, chemical effects, fluctuating pH, food debris - Corrosion is bad – harmful by-products, galvanic pain, weakening of structure, adverse aesthetics - Corrosion Types: o Non-aqueous – tarnishing and discolouration of metals o Aqueous – electrochemical phenomenon, considered in dentistry - Electrochemistry o The anode is degraded/corroded as electrons leave it, travelling to the cathode.

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Blood supply from the kidneys flows into each renal vein proven cetirizine 10 mg, normally the largest veins entering the inferior vena cava order cetirizine 10 mg visa. Each adrenal vein drains the adrenal or suprarenal glands located immediately superior to the kidneys cetirizine 10 mg amex. The right adrenal vein enters the inferior vena cava directly, whereas the left adrenal vein enters the left renal vein. From the male reproductive organs, each testicular vein flows from the scrotum, forming a portion of the spermatic cord. The right gonadal vein empties directly into the inferior vena cava, and the left gonadal vein empties into the left renal vein. Each side of the diaphragm drains into a phrenic vein; the right phrenic vein empties directly into the inferior vena cava, whereas the left phrenic vein empties into the left renal vein. Since the inferior vena cava lies primarily to the right of the vertebral column and aorta, the left renal vein is longer, as are the left phrenic, adrenal, and gonadal veins. The longer length of the left renal vein makes the left kidney the primary target of surgeons removing this organ for donation. Major Veins of the Abdominal Region Vessel Description Inferior vena Large systemic vein that drains blood from areas largely inferior to the diaphragm; empties cava into the right atrium Series of veins that drain the lumbar portion of the abdominal wall and spinal cord; the Lumbar veins ascending lumbar veins drain into the azygos vein on the right or the hemiazygos vein on the left; the remaining lumbar veins drain directly into the inferior vena cava Largest vein entering the inferior vena cava; drains the kidneys and flows into the inferior Renal vein vena cava Table 20. The anterior tibial vein drains the area near the tibialis anterior muscle and combines with the posterior tibial vein and the fibular vein to form the popliteal vein. The fibular vein drains the muscles and integument in proximity to the fibula and also joins the popliteal vein. The small saphenous vein located on the lateral surface of the leg drains blood from the superficial regions of the lower leg and foot, and flows into to the popliteal vein. Close to the body wall, the great saphenous vein, the deep femoral vein, and the femoral circumflex vein drain into the femoral vein. The great saphenous vein is a prominent surface vessel located on the medial surface of the leg and thigh that collects blood from the superficial portions of these areas. The femoral circumflex vein forms a loop around the femur just inferior to the trochanters and drains blood from the areas in proximity to the head and neck of the femur. As the femoral vein penetrates the body wall from the femoral portion of the upper limb, it becomes the external iliac vein, a large vein that drains blood from the leg to the common iliac vein. The pelvic organs and integument drain into the internal iliac vein, which forms from several smaller veins in the region, including the umbilical veins that run on either side of the bladder. The external and internal iliac veins combine near the inferior portion of the sacroiliac joint to form the common iliac vein. In addition to blood supply from the external and internal iliac veins, the middle sacral vein drains the sacral region into the common iliac vein. Similar to the common iliac arteries, the common iliac veins come together at the level of L5 to form the inferior vena cava. Veins of the Lower Limbs Vessel Description Plantar veins Drain the foot and flow into the plantar venous arch Dorsal venous Drains blood from digital veins and vessels on the superior surface of the foot arch Plantar venous Formed from the plantar veins; flows into the anterior and posterior tibial veins through arch anastomoses Anterior tibial Formed from the dorsal venous arch; drains the area near the tibialis anterior muscle and vein flows into the popliteal vein Posterior tibial Formed from the dorsal venous arch; drains the area near the posterior surface of the tibia vein and flows into the popliteal vein Fibular vein Drains the muscles and integument near the fibula and flows into the popliteal vein Table 20. It packages nutrients absorbed by the digestive system; produces plasma proteins, clotting factors, and bile; and disposes of worn-out cell components and waste products. Instead of entering the circulation directly, absorbed nutrients and certain wastes (for example, materials produced by the spleen) travel to the liver for processing. In this case, the initial capillaries from the stomach, small intestine, large intestine, and spleen lead to the hepatic portal vein and end in specialized capillaries within the liver, the hepatic sinusoids. You saw the only other portal system with the hypothalamic-hypophyseal portal vessel in the endocrine chapter. The hepatic portal vein itself is relatively short, beginning at the level of L2 with the confluence of the superior mesenteric and splenic veins. It also receives branches from the inferior mesenteric vein, plus the splenic veins and all their tributaries. The superior mesenteric vein receives blood from the small intestine, two-thirds of the large intestine, and the stomach. The inferior mesenteric vein drains the distal third of the large intestine, including the descending colon, the sigmoid colon, and the rectum. The splenic vein is formed from branches from the spleen, pancreas, and portions of the stomach, and the inferior mesenteric vein. After its formation, the hepatic portal vein also receives branches from the gastric veins of the stomach and cystic veins from the gall bladder. The hepatic portal vein delivers materials from these digestive and circulatory organs directly to the liver for processing. Because of the hepatic portal system, the liver receives its blood supply from two different sources: from normal systemic circulation via the hepatic artery and from the hepatic portal vein. The liver processes the blood from the portal system to remove certain wastes and excess nutrients, which are stored for later use. This processed blood, as well as the systemic blood that came from the hepatic artery, exits the liver via the right, left, and middle hepatic veins, and flows into the inferior vena cava. Overall systemic blood composition remains relatively stable, since the liver is able to metabolize the absorbed digestive components. It also receives and processes blood from other organs, delivered via the veins of the hepatic portal system. It is critical to the survival of the developing human that the circulatory system forms early to supply the growing tissue with nutrients and gases, and to remove waste products. Blood cells and vessel production in structures outside the embryo proper called the yolk sac, chorion, and connecting stalk begin about 15 to 16 days following fertilization. You will learn more about the formation and function of these early structures when you study the chapter on development. These in turn differentiate into angioblasts, which give rise to the blood vessels and pluripotent stem cells, which differentiate into the formed elements of blood. Surrounding mesenchymal cells give rise to the smooth muscle and connective tissue layers of the vessels. Vascular tubes also develop on the blood islands, and they eventually connect to one another as well as to the developing, tubular heart. Thus, the developmental pattern, rather than beginning from the formation of one central vessel and spreading outward, occurs in many regions simultaneously with vessels later joining together. This angiogenesis—the creation of new blood vessels from existing ones—continues as needed throughout life as we grow and develop. Blood vessel development often follows the same pattern as nerve development and travels to the same target tissues and organs. This occurs because the many factors directing growth of nerves also stimulate blood vessels to follow a similar pattern. Whether a given vessel develops into an artery or a vein is dependent upon local concentrations of signaling proteins. The placenta—a circulatory organ unique to pregnancy—develops jointly from the embryo and uterine wall structures to fill this need. Emerging from the placenta is the umbilical vein, which carries oxygen-rich blood from the mother to the fetal inferior vena cava via the ductus venosus to the heart that pumps it into fetal circulation. Two umbilical arteries carry oxygen- depleted fetal blood, including wastes and carbon dioxide, to the placenta.