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[[বিষয়শ্রেণী:অ্যালকোহল]]
==বিবিধ==
===১===
===বৈশিষ্ট্য===
===২===
মানুষের দেহ থেকে এলকোহল ডিহাইড্রোজিনেজ পদ্ধতিতে জারণের মাধ্যমে সীমিত ইথানল অপসারণ করা যায়। জিরো অর্ডার কাইনেটিকস বা শুন্যক্রমের মাধ্যমে রক্ত থেকে বড় আকারের এলকোহল সরিয়ে নেয়া সম্ভব।এর মানে একটি নির্দিষ্ট হারে শরীর থেকে এলকোহল বেরিয়ে যায়।<ref>{{cite journal|title=The Clinical Pharmacology of Alcohol |publisher=Ncbi.nlm.nih.gov |date=2013-08-12|pmc=1501558|last1=Becker|first1=CE|volume=113|issue=3|pages=37–45|journal=California Medicine|pmid=5457514}}</ref>
===৩===
বিশুদ্ধ বিশুদ্ধ ইথানল চামড়া ও চোখে জ্বালাপড়া সৃষ্টি করে।<ref>[http://www.nfpa.org/Assets/files/AboutTheCodes/704/CLA-AAA_ROPminutes_01-10.pdf Minutes of Meeting]. Technical Committee on Classification and Properties of Hazardous Chemical Data (January 12–13, 2010).</ref> ইথানল সেবনে মাথা ঘোরা, বমি এবং বিষক্রিয়ার সৃষ্টি হয়। দীর্ঘকাল ধরে ইথানল সেবনে মারাত্বক লিভার ড্যামেজ হতে পারে। <ref name="msdset">{{cite web|url=http://msds.chem.ox.ac.uk/ET/ethyl_alcohol.html |title=Safety data for ethyl alcohol |publisher=Msds.chem.ox.ac.uk |date=2008-05-09 |accessdate=2011-01-03}}</ref>
==তথ্য সূত্র==
{{reflist}}
===Short-term===
{| class="wikitable" style="float:right; width:25em; margin-left: 1em"
! BAC (g/L)|| BAC <br />(% v/v)|| Symptoms<ref name="Pohorecky & Brick">{{cite journal|author=Pohorecky LA, Brick J|title=Pharmacology of ethanol|journal=Pharmacol. Ther|volume=36|year=1988|pmid=3279433|doi=10.1016/0163-7258(88)90109-X|issue=2–3|pages=335–427}}</ref>
|-
| 0.5||0.05%||Euphoria, talkativeness, relaxation
|-
| 1||0.1 %||Central nervous system depression, nausea, possible vomiting, impaired motor and sensory function, impaired cognition
|-
| >1.4|| >0.14%||Decreased blood flow to brain
|-
| 3||0.3%||Stupefaction, possible unconsciousness
|-
| 4||0.4%||Possible death
|-
| >5.5|| >0.55%||Death
|}
====কেন্দ্রীয় স্নায়ুতন্ত্রের উপর প্রভাব।====
Ethanol is a central nervous system [[depressant]] and has significant psychoactive effects in sublethal doses; for specifics, see [[Effects of alcohol on the body#Effects by dosage|"Effects of alcohol on the body by dose"]]. Based on its abilities to change the [[human consciousness]], ethanol is considered a [[psychoactive drug]].<ref>[http://www.nlm.nih.gov/medlineplus/ency/article/001944.htm Alcohol use and safe drinking]. US National Institutes of Health .</ref> Death from ethanol consumption is possible when blood alcohol level reaches 0.4%. A blood level of 0.5% or more is commonly fatal. Levels of even less than 0.1% can cause [[Alcohol intoxication|intoxication]], with unconsciousness often occurring at 0.3–0.4%.<ref name="yost" />
The amount of ethanol in the body is typically quantified by [[blood alcohol content]] (BAC), which is here taken as weight of ethanol per unit volume of blood. The table at the right summarizes the symptoms of ethanol consumption. Small doses of ethanol, in general, produce euphoria and relaxation; people experiencing these symptoms tend to become talkative and less inhibited, and may exhibit poor judgment. At higher dosages (BAC > 1 g/L), ethanol acts as a [[central nervous system]] [[depressant]], producing at progressively higher dosages, impaired sensory and motor function, slowed cognition, stupefaction, unconsciousness, and possible death.
Ethanol acts in the central nervous system primarily by binding to the GABA<sub>A</sub> receptor, increasing the effects of the inhibitory [[neurotransmitter]] [[GABA]] (i.e., it is a [[positive allosteric modulator]]).<ref name="pmid17591544">{{cite journal|author = Santhakumar V, Wallner M, Otis TS|title = Ethanol acts directly on extrasynaptic subtypes of GABAA receptors to increase tonic inhibition|journal = Alcohol| volume = 41 |issue = 3|pages = 211–21|year = 2007|pmid = 17591544|pmc = 2040048|doi = 10.1016/j.alcohol.2007.04.011|url = }}</ref>
Prolonged heavy consumption of alcohol can cause significant permanent damage to the brain and other organs. See [[Alcohol consumption and health]].
According to the US National Highway Traffic Safety Administration, in 2002 about "41% of people fatally injured in traffic crashes were in alcohol related crashes".<ref>{{cite journal|author=Hingson R, Winter M|title=Epidemiology and consequences of drinking and driving|journal=Alcohol research & health : the journal of the National Institute on Alcohol Abuse and Alcoholism|volume=27|year=2003|pmid=15301401|issue=1|pages=63–78}}</ref> The risk of a fatal [[car accident]] increases exponentially with the level of alcohol in the driver's blood.<ref>{{cite journal|author=Naranjo CA, Bremner KE|title=Behavioural correlates of alcohol intoxication|journal=[[Addiction (journal)|Addiction]]|volume=88|year=1993|pmid=8448514|doi=10.1111/j.1360-0443.1993.tb02761.x|issue=1|pages=25–35}}</ref> Most [[drunk driving]] laws governing the acceptable levels in the blood while driving or operating heavy machinery set typical upper limits of [[blood alcohol content]] (BAC) between 0.02% and 0.08%.{{Citation needed|date=March 2013}}
Discontinuing consumption of alcohol after several years of heavy drinking can also be fatal. Alcohol withdrawal can cause anxiety, autonomic dysfunction, seizures, and hallucinations. [[Delirium tremens]] is a condition that requires people with a long history of heavy drinking to undertake an [[alcohol detoxification]] regimen.
The reinforcing effects of alcohol consumption are also mediated by [[acetaldehyde]] generated by [[catalase]] and other oxidizing enzymes such as [[CYP2E1|cytochrome P-4502E1]] in the brain.<ref>{{cite pmid|21332529}}</ref> Although acetaldehyde has been associated with some of the adverse and toxic effects of ethanol, it appears to play a central role in the activation of the [[Mesolimbic pathway|mesolimbic dopamine system]].<ref>{{cite pmid|18001279}}</ref>
====Effects on metabolism====
{{Main|Ethanol metabolism|Alcohol dehydrogenase}}
Ethanol within the human body is converted into acetaldehyde by [[alcohol dehydrogenase]] and then into the [[acetyl]] in [[acetyl CoA]] by [[acetaldehyde dehydrogenase]]. [[Acetyl CoA]] is the final product of both carbohydrate and fat metabolism, where the acetyl can be further used to produce energy or for biosynthesis. As such, ethanol is a nutrient. However, the product of the first step of this breakdown, acetaldehyde,<ref name="boggan1">{{cite web|url=http://chemcases.com/alcohol/alc-06.htm|accessdate=2007-09-29|author=Boggan, Bill |title=Metabolism of Ethyl Alcohol in the Body|publisher=Chemases.com}}</ref> is more toxic than ethanol. Acetaldehyde is linked to most of the clinical effects of alcohol. It has been shown to increase the risk of developing cirrhosis of the liver<ref name="boggan2">{{cite web|url=http://chemcases.com/alcohol/alc-07.htm|accessdate=2007-09-29|author=Boggan, Bill|title=Effects of Ethyl Alcohol on Organ Function|publisher=Chemases.com}}</ref> and multiple forms of cancer.
During the metabolism of alcohol via the respective dehydrogenases, NAD ([[Nicotinamide adenine dinucleotide]]) is converted into reduced NAD. Normally, NAD is used to metabolise fats in the liver, and as such alcohol competes with these fats for the use of NAD. Prolonged exposure to alcohol means that fats accumulate in the liver, leading to the term 'fatty liver'. Continued consumption (such as in [[alcoholism]]) then leads to cell death in the hepatocytes as the fat stores reduce the function of the cell to the point of death. These cells are then replaced with scar tissue, leading to the condition called [[cirrhosis]].
====Drug interactions====
Ethanol can intensify the sedation caused by other [[central nervous system]] [[depressant]] drugs such as [[barbiturate]]s, [[benzodiazepine]]s, [[opioid]]s, [[non-benzodiazepine]]s (such as [[Zolpidem]] and [[Zopiclone]]), [[antipsychotics]], [[Histamine_antagonist|sedative antihistamines]], and [[antidepressants]].<ref name="yost">{{cite journal|url=http://my.lecom.edu/library/internetresources/journal%20articles/Acute%20Care%20for%20Alcohol%20Intoxication.pdf|archiveurl=https://web.archive.org/web/20101214113109/http://my.lecom.edu/library/internetresources/journal%20articles/Acute%20Care%20for%20Alcohol%20Intoxication.pdf|archivedate=2010-12-14|title=Acute care for alcohol intoxication|publisher=Postgraduate Medicine Online|author=Yost, David A. |volume=112|issue=6|year=2002|accessdate=2007-09-29}}</ref> It interacts with [[cocaine]] in vivo to produce [[cocaethylene]], another psychoactive substance.<ref>{{cite pmid|12485948}}</ref>
'''Alcohol and metronidazole'''
One of the most important drug/food interactions that should be noted is between alcohol and metronidazole.
Metronidazole is an antibacterial agent that kills bacteria by damaging cellular DNA and hence cellular function.<ref name="cps">Repchinsky C (ed.) (2012). Compendium of pharmaceuticals and specialties, Ottawa: Canadian Pharmacists Association.{{full citation needed|date=February 2014}}</ref> Metronidazole is usually given to people who have diarrhea caused by ''[[Clostridium difficile]]'' bacteria. ''C. difficile'' is one of the most common microorganisms that cause diarrhea and can lead to complications such as colon inflammation and even more severely, death.
Patients who are taking metronidazole are strongly advised to avoid alcohol, even after 1 hour after the last dose. The reason is that alcohol and metronidazole can lead to side effects such as flushing, headache, nausea, vomiting, abdominal cramps, and sweating.<ref>{{cite pmid|2952478}}</ref><ref name="pharmaceuticals1997">SCS Pharmaceuticals. Flagyl® IV and Flagyl® I.V. RTU® (metronidazole hydrochloride) prescribing information (dated April 16, 1997). In: Physicians’ desk reference. 48th ed. Montvale, NJ: Medical Economics Company Inc; 1998:2563-5.</ref><ref name="pharmaceuticals1997" /> These symptoms are often called the [[disulfiram]]-like reaction. The proposed mechanism of action for this interaction is that metronidazole can bind to an enzyme that normally metabolizes alcohol. Binding to this enzyme may impair the liver's ability to process alcohol for proper excretion.<ref>"Ethanol/metronidazole", p. 335 in Tatro DS, Olin BR, eds. ''Drug interaction facts''. St. Louis: JB Lippincott Co, 1988, ISBN 0932686478.</ref>
==১==
==তথ্যসূত্র==
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