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Evolutionary important character of Selaginella is (1) strobili (2) heterosporous nature (3) ligule (4) rhizophore Ans: (2) (1) diploid (2) triploid (3) tetraploid (4) haploid Ans: (4) Q209 symptoms miscarriage prasugrel 10mg fast delivery. Prothallus (gametophyte) gives rise to fern plant (sporophyte) without fertilization symptoms zinc toxicity cheap prasugrel 10 mg mastercard. It is (1) parthenocarpy (2) apospory (3) parthenogenesis (4) apogamy Ans: (4) jo in [1989] Q211 symptoms crohns disease generic prasugrel 10mg online. The common mode of sexual reproduction in Chlamydomonas is (1) oogamous (2) isogamous (3) hologamous (4) anisogamous Ans: (2) [1990] Q212 medications gout purchase prasugrel with a mastercard. The product of conjugation in Spirogyra or fertilization of Chlamydomonas is (1) oospore (2) zygospore (3) carpospore (4) zoospore Ans: (2) [1990] Q213. Protonema occurs in the life cycle of (1) Somatogamy (2) Riccia (3) Spirogyra (4) Funaria Ans: (4) Q214. Moss peristome takes part in (1) protection (2) spore dispersal (3) absorption (4) photosynthesis Ans: (2) ht tel tp eg s: ra //t m. Apophysis in the capsule of Funaria is (1) middle part (2) lower part (3) fertile part (4) upper part Ans: (2) [1991] Q216. The plant group that produces spores and embryo but lacks vascular tissues and seeds is (1) Bryophyta (2) Pteridophyta (3) Phaeophyta (4) Rhodophyta Ans: (1) (1) Chlamydomonas (2) Pinus (3) Dryopteris (4) Selaginella Ans: (1) ht tel tp eg s: ra //t m. Bryophytes are amphibians because (1) they are mostly aquatic (2) they require a layer of water for carrying out sexual reproduction (3) all the above (4) they occur in damp places Ans: (2) in [1992] Q220. Pteridophytes differ from mosses/bryophytes in possessing (1) archegonia (2) independent gametophyte (3) flagellate spermatozoids jo (4) well developed vascular system Ans: (4) [1992] Q222. Turpentine is obtained from (1) Gymnospermous wood (2) Angiospermous wood (3) Ferns (4) Pteridophytes Ans: (1) Q223. Resin and turpentine are obtained from (1) Cedrus (2) Cycas (3) Abies (4) Pinus Ans: (4) Q224. In Pinus, the pollen grain has 6 chromosomes then in its endosperm will have (1) 6 (2) 12 (3) 24 (4) 18 Ans: (1) [1992] Q225. A plant having seeds but lacking flowers and fruits belongs to (1) Ferns (2) Pteridophytes (3) Gymnosperms (4) Mosses Ans: (3) [1993] Q226. Pinus differs from mango in having (1) ovules not enclosed in ovary (2) tree habit (3) wood (4) green leaves Ans: (1) ht tel tp eg s: ra //t m. Pyrenoids are the centres for formation of (1) fat (2) porphyra (3) starch (4) enzymes Ans: (3) Q229. Chloroplast of Chlamydomonas is (1) collar-shaped (2) stellate (3) spiral (4) cup-shaped Ans: (4) [1993] Q230. In Ulothrix/Spirogyra, reduction division (meiosis) occurs at the time of (1) zygospore germination (2) gamete formation (3) vegetative reproduction (4) zoospore formation Ans: (1) jo in [1993] Q231. The absence of chlorophyll, in the lowermost cell of Ulothrix, shows (1) cell characteristic (2) functional fission (3) beginning of labour division (4) tissue formation Ans: (3) Q232. In Chlorophyceae, sexual reproduction occurs by (1) Oogamy only (2) Isogamy and anisogamy (3) Anisogamy and oogamy (4) Isogamy, anisogamy and oogamy Ans: (4) ht tel tp eg s: ra //t m. Unique features of Bryophytes is that they (1) lack roots (2) produce spores (3) lack vascular tissues (4) have sporophyte attached to gametophyte Ans: (4) jo in [1994] Q235. In which one of these the elaters are present along with mature spores in the capsule (to help in spore dispersal)? A well developed archegonium with neck consisting of 4-6 rows of neck canal cells, characterises (1) Pteridophytes and gymnosperms (2) Gymnosperms only (3) Gymnosperms and flowering plants (4) Bryophytes and pteridophytes Ans: (4) ht tel tp eg s: ra //t m. Multicellular branched rhizoids and leafy gametophytes are characteristic of (1) all pteridophytes (2) all bryophytes (3) some peteriodphytes (4) some bryophytes Ans: (4) [1996] (1) Oscillatoria (2) Spirogyra (3) Chlorella (4) Ulothrix Ans: (3) Q243. Blue-green algae belong to (1) Rhodophyceae (2) Eukaryotes (3) Chlorophyceae (4) Prokaryotes Ans: (4) ht tel tp eg s: ra //t m. Seed-habit first originated in (1) certain monocots (2) certain ferns (3) primitive dicots (4) certain pines Ans: (2) [1997] Q246. Ulothrix can be described as a (1) membranous alga producing zoospores (2) non-motile colonial alga lacking zoospores (3) filamentous alga with flagellated reproductive stages (4) filamentous alga lacking flagellated reproductive stages Ans: (3) [1997] (1) Its xylem is mainly composed of xylem vessels (2) It does not have a well-organized female flower (3) Its roots contain some blue-green algae.

At least two cases involving impaired metabolism of imipramine have been described in the forensic literature treatment 5 alpha reductase deficiency 10mg prasugrel fast delivery. This was attempted by the toxicologist who analyzed the remains found in the basement of Dr treatment 3rd degree hemorrhoids buy prasugrel overnight. In some cases treatment for ringworm generic prasugrel 10mg without prescription, the amounts have correlated very well with the available physical evidence symptoms of buy generic prasugrel 10 mg on line. In order for such calculations to be meaningful, a number of factors must be assumed. Perhaps most important, the particular part of the tissue or blood sample analyzed must be representative of the remainder of the organ or tissue. Since most organs are not homogeneous and because uneven postmortem diffusion (as discussed later) can lead to non-homogeneity of concentration, being sure of the average concentration of drug within any one organ may be difficult without analyzing that entire organ. While it is easy to know the weight of individual organs such as the heart, lungs, liver, kidneys and brain, it is very difficult to reliably estimate the total amount of tissue into which most drugs readily distribute - the skeletal muscle. While the mass of skeletal muscle can be estimated from medical tables, given a persons height and weight, there is no assurance that the concentration of drug measured in one or two portions of skeletal muscle is representative of that in muscle from all other parts of the body. Similar arguments apply to adipose tissue, where it is more difficult to obtain representative samples and accurately assay. It should also be borne in mind that for a person chronically taking a drug with a very large volume of distribution and long half-life, the equivalent of many times the total daily dose will be normally present in the body, even after therapeutic doses. Estimation of the total body burden of a drug may not be without value in all cases; it must be done with caution and the variables well understood and acknowledged. It is the rare cases of homicidal poisoning where significant weight may be placed on such calculations and where the stakes are the highest. As discussed elsewhere in this chapter, that is often not the case, and it is very difficult to predict whether any given postmortem drug concentration represents the concentration at the time of death, even for drugs for which postmortem redistribution is not well known. Any toxicologist who has routinely analyzed drugs in multiple blood samples from the same case knows how often those concentrations unexpectedly vary from sample to sample. Even if the gastric contents contain relatively little drug, much of the drug could still be present in the ileum, or at least not attained equilibrium with muscle, adipose tissue and the major organs. Finally, the rate of absorption, bioavailability, volume of distribution, half-life, rate of metabolism and clearance are seldom known for any specific individual and can vary tremendously between subjects. The estimation of dose from postmortem blood concentrations is a practice of the foolhardy. If a person is actively absorbing an overdose, it is likely that the concentration of the drug in blood leaving the liver. This has been demonstrated in living patients and concentration differences up to about twofold recorded between arterial and venous blood. Much is still unknown about the extent to which postmortem changes in drug concentration occur and the drugs affected, however, some generalizations can be made. Postmortem redistribution is likely to be most marked for drugs that are highly protein bound, but particularly those sequestered in the major organs such as the lungs and liver. Postmortem redistribution starts to occur within an hour after death and continues as the postmortem interval increases. The most important quantitative changes in blood drug concentration occur within the first 24 h or so and are highly site dependent. In general, increases will be greater in blood from "central" sites, such as the vessels near the major organs, than in more peripheral sites, such as the femoral veins. However, blood drug concentrations can vary fivefold or more between cardiac, hepatic and pulmonary sites. Even aside from the unpredictable nature of postmortem redistribution per se, blood from the "heart", if labeled as such, could have come from either of the cardiac atria or ventricles, the pulmonary vein or artery, the aorta or the inferior vena cava. However, it should be emphasized that even if a "good" femoral blood sample is obtained, it is no guarantee that the drug concentrations subsequently measured will represent those present at the moment of death. In fact it is well established that femoral blood concentrations of many drugs can increase twofold or more after death. While it is possible that some of this increase is due to diffusion of released drug down the major vessels to the groin, it should be borne in mind that drug concentrations in skeletal muscle are often twofold or more higher than in the perimortem blood. While in many of the published studies on postmortem redistribution the vessels have been carefully ligated prior to taking blood samples, this is rarely done during routine medico-legal autopsies. Consequently, blood labeled as "femoral" may contain blood drawn down from the inferior vena cava.

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There are also indications that some of the newer benzodiazepines have a slightly smaller margin of safety medicine that makes you throw up buy 10mg prasugrel with amex. This is particularly true with reference to paediatric and geriatric patients who are more susceptible to the toxicity of these drugs symptoms you have cancer cheap prasugrel 10 mg free shipping. An area of concern with long-term benzodiazepine use is the possibility of behavioural disinhibition which may induce a person to hostile acts medications 3 times a day discount 10 mg prasugrel mastercard, aggressive behaviour medications equivalent to asmanex inhaler purchase prasugrel 10 mg with amex, and verbal indecency. Yet another important issue is with reference to the use of benzodiazepines to deliberately induce amnesia in certain individuals in order to accomplish an immoral act. Many of these drugs, particularly flunitrazepam, are capable of causing retrograde amnesia. Flunitrazepam (Rohypnol ; "Roofies") has become popular as a drug of abuse, often combined with alcohol, marijuana, or cocaine to produce an intense "high". It has been used as a "date rape" drug, both for its properties of lowering inhibitions and because it can cause retrograde amnesia. While addiction to benzodiazepines is an undeniable possibility among patients on long-term therapy, the abuse potential is much less when compared to most other sedative-hypnotics such as the barbiturates. However, abrupt cessation after prolonged use Section 5 may precipitate tachycardia, hypertension, agitation, hallucinations, delirium, and convulsions. Withdrawal syndrome is more likely if the drug has been taken at therapeutic dose for more than four months, higher dosage has been used, the drug is stopped suddenly, or a short acting benzodiazepine has been taken. Severe dysmorphism, malformations, intrauterine and extrauterine growth retardation, and central nervous system dysfunction have been described in infants born of mothers who used benzodiazepines during pregnancy. It is a white crystalline substance soluble in water or alcohol with a pungent, pear-like odour and bitter taste. Chloral hydrate is well absorbed on oral administration and is quickly metabolised to trichloroethanol in the liver by alcohol dehydrogenase. This is the active form which is later conjugated with glucuronic acid and excreted in the urine as urochloralic acid. Chlorobutanol is structurally related to trichloroethanol, and is used as a sedative/hypnotic in doses of 300 to 1200 mg/day. Chloral hydrate overdose manifests as nausea, vomiting, gastric irritation, miosis, hypotension, renal and hepatic damage, and cardiac arrhythmias (ventricular fibrillation, ventricular tachycardia, and torsades de pointes), cardiac arrest, respiratory depression, and coma. Non-cardiogenic pulmonary oedema and aspiration pneumonitis have been reported after massive overdose. The usual fatal dose is around 10 grams, but deaths have occured with doses as low as 4 grams. Chronic use of chloral hydratecan lead to a dependency syndrome with a withdrawal state similar to delirium tremens (convulsions and psychosis). A simple diagnostic test involves the instillation of a small amount of the suspected liquid in 10 ml of water, to which 2 ml of purified aniline and 4 ml of 20% sodium hydroxide are added and heated gently. The evolution of a foul odour (skunk odour) is indicative of a positive result, which also occurs with chloroform and carbon tetrachloride. Chloral hydrate and trichloroethanol in plasma can be analysed by gas chromatography. Chloral hydrate is rapidly absorbed, particularly after ingestion of liquid formulations. In the case of liquid ingestions a small flexible tube may be indicated to prevent oesophageal damage. Treatment should be mainly directed at the management of cardiac arrhythmias which are potentially life- threatening. Unfortunately the arrhythmias are usually non-responsive to conventional anti-arrhythmic drugs, and a beta-adrenergic antagonist (non-cardioselective or beta1-specific), or adrenergic neurone blocking drug such as bretylium may have to be administered. Propranolol has been the most commonly used beta adrenergic blocker for chloral hydrate-induced arrhythmias. Dose: 1 mg/dose intravenously, administered no faster than 1 mg/min repeated every 5 minutes until desired response is seen, or a maximum of 5 mg has been given. If inadequate response to initial loading dose and 4 minute maintenance dose, repeat loading dose (infuse 500 mcg/kg for one minute), followed by a maintenance infusion of 100 mcg/kg /min for 4 minutes. If response is inadequate, repeat loading dose, and increase the maintenance dose by increments of 50 mcg/ kg/min, administered as above. Torsades de pointes usually responds to magnesium sulfate or isoproterenol or amiodarone.

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It also stimulates the synthesis of lipoxygenase-derived leukotrienes causing pulmonary oedema medicine man dispensary prasugrel 10mg overnight delivery. Further medications like zovirax and valtrex generic prasugrel 10mg line, phosgene increases pulmonary vascular permeability medications you can give your cat purchase generic prasugrel line, leading to increased fluid accumulation in the interstitial and alveolar compartments treatment vertigo 10mg prasugrel free shipping. The ability of the lymphatics to clear the excess fluid is exceeded, resulting in gas diffusion abnormalities and pulmonary oedema. Clinical Features Phosgene gas has low water solubility and thus can be deeply inhaled into the lung before an individual is aware of significant exposure. Stage I: Coughing, choking, lacrimation, nausea, vomiting, headache, conjunctivitis, rhinitis, pharyngitis, bronchitis, and upper respiratory tract irritation may occur after exposure to concentrations exceeding 3 to 5 ppm. Exposures to 2 ppm may not cause eye irritation, but can result in significant, delayed respiratory effects. It is generally felt that if the victim survives 24 to 48 hours, the prognosis will be favourable. However, patients who survive exposure with pulmonary oedema may have persistent complaints of exertional dyspnoea and reduced exercise capacity and abnormal pulmonary function tests for months. Severe dermal burns or frostbite may develop following skin exposure to the liquefied material. Aminophylline 5 mg/kg loading dose followed by 1 mg/kg every 8 to 12 hours to maintain a serum level of 10 to 20 mcg/ml. Prepared for the first time in 1812, phosgene had a large scale presence in World War I as an asphyxiant war gas. The first chemical agent of warfare in modern times was chlorine, used by the German army at Ypres in 1915 against the Allies. Shortly thereafter, the Germans began mixing the chlorine with phosgene, or deployed phosgene alone as a weapon. Phosgene, together with arsenicals, blister agents, and mustard gas (also introduced during World War I) have been estimated to be responsible for approximately 1. By the time World War I concluded, mustard gas was the most widely used, but phosgene caused the most deaths. Chest X-ray may reveal incipient toxic pulmonary oedema much earlier than overt clinical manifestations. Monitor arterial blood gases and/or pulse oximetry, pulmonary function tests, and chest X-ray in patients with significant exposure. Steroid therapy: Steroids used soon after exposure may lessen the severity of pulmonary oedema. Betamethasone valerate, beclomethasone dipropionate, or dexamethasone sodium phosphate is generally recommended. The initial dose is five times that conventionally used in asthma, followed by about half the dose for 12 hours, and then standard asthma dosages for the subsequent 72 hours. Physical Appearance Pure carbon monoxide is an odourless, colourless, non-irritating gas, which is lighter than air. A carbon monoxide concentration of 5000 ppm in air is lethal to humans after five minutes of exposure. Mode of Action Carbon monoxide has an affinity for haemoglobin which is 230 to 270 times greater than that of oxygen. The net result of all this is the decreased ability of oxygen to be carried by the blood and released to tissues. In the brain this can cause further mitochondrial dysfunction, capillary leakage, leukocyte sequestration and apoptosis. This change primarily occurs during the recovery phase when lipid peroxidation occurs, which produces an overall reversible demyelination in the brain. In a study on rats, the delayed effects of neuropathology following carbon monoxide poisoning were studied. The authors suggested that these findings may have clinical application in the treatment of delayed neurotoxicity with anti-inflammatory agents. The earliest manifestations are often non-specific and may be confused with other conditions. The venous changes that develop include engorgement and tortuosity, while oedema of the optic disc may be observed.

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